[ 71 ]

72 | 1st year MBBS – Block-3

Chapter – 04
PHYSIOLOGY
• Explain the physiological anatomy of cardiac muscle. Physiology Cardiac
CV- • Explain the functional importance of intercalated discs. Muscle
P-001 • Discuss the properties of cardiac muscles.
• Describe and draw the phases of action potential of ventricle.
• Describe and draw the phases of action potential of SA node along with
explanation of the mechanism of self-excitation/ Auto rhythmicity of SA node.
• Define and give the duration of the Absolute and relative refractory period
in cardiac muscle.
• Describe the mechanism of excitation-contraction coupling and relaxation
in cardiac muscle.
• Draw & explain pressure & volume changes of left ventricle during cardiac
cycle.
• Explain & draw relationship of ECG (Electrocardiography) with cardiac cycle.
• Explain & draw the relationship of heart sounds with cardiac cycle. Enlist,
draw, and explain the physiological basis of atrial pressure waves in relation
to cardiac cycle.
• Define & give the normal values of the cardiac output, stroke volume, end
diastolic volume & end systolic volume

CARDIAC MUSCLE
• The heart is composed of three major types of cardiac muscle: atrial muscle, ventricular muscle, and specialized
excitatory and conductive muscle fibers
• Cardiac muscles striated in the same manner as skeletal muscles
• Contain actin and myosin filaments
Cardiac muscle as syncytium
Intercalated Discs
↓ (separate individual cardiac muscle cells)
Cardiac Muscle Fibers
↓ (individual cells connected in series and parallel)
Gap Junctions (Communicating Junctions)
↓ (rapid diffusion of ions)
Ion Movement in Cardiac Muscle
↓ (moves easily along the longitudinal axis)
Action Potential Travel
↓ (easily travels from one cell to the next via intercalated discs)
Cardiac Syncytium
↓ (many interconnected heart muscle cells)
Excitation Spread
↓ (when one cell becomes excited, action potential spreads to all)
• Two Syncytiums
• Atrial Syncytium (walls of the atria)
• Ventricular Syncytium (walls of the ventricles)
Properties of Cardiac Muscles
• Contractility & Conductivity
• Excitability
 Chapter-4: Physiology (Cardiovascular Module) | 73

• Rythmiticity
• Automaticity
Phases of Action Potential
Phase 0 (Depolarization):
• Fast Sodium Channels Open. When the cardiac cell is stimulated and depolarizes, the membrane potential
becomes more positive.
• Voltage- gated sodium channels (fast sodium channels) open and permit sodium to rapidly flow into the cell and
depolarize it.
• The membrane potential reaches about +20 millivolts before the sodium channels close.
Phase 1 (Initial Repolarization):
• Fast Sodium Channels Close. The sodium channels close, the cell begins to repolarize, and potassium ions leave
the cell through open potassium channels
Phase 2 (Plateau):
• Calcium Channels Open and Fast Potassium Channels Close. A brief initial repolarization occurs and the action
potential then plateaus as a result of increased calcium ion permeability and decreased potassium ion permeability.
• The voltage- gated calcium ion channels open slowly during phases 1 and 0, and calcium enters the cell. Potassium
channels then close, and the combination of decreased potassium ion efflux and increased calcium ion influx
causes the action potential to plateau.
Phase 3 (Rapid Repolarization):
• Calcium Channels Close and Slow Potassium Channels Open.
• The closure of calcium ion channels and increased potassium ion permeability, permitting potassium ions to exit
the cell rapidly, ends the plateau and returns the cell membrane potential to its resting level.
Phase 4 (resting membrane potential)
• The heart muscles undergo Resting membrane potential before the beginning of new contraction

Relative refractory period

Join Medico Express Free Guidelines Group

03346072846
74 | 1st year MBBS – Block-3

• The refractory period of the heart is the interval of time during which a normal cardiac impulse cannot re- excite
an already excited area of cardiac muscle.
• The normal refractory period of the ventricle is 0.25 to 0.30 second, which is about the duration of the prolonged
plateau action potential.
Absolute refractory period
• There is an additional relative refractory period of about 0.05 second during which the muscle is more difficult to
excite than normal but can be excited by a very strong excitatory signal.

Excitation Contraction Coupling in Cardiac Muscle

Action Potential spread to T tubules →opening of voltage dependent L type Calcium channels in T tubules →activation
of ryanodine receptor channels in Sarcoplasmic reticulum →release of calcium from sarcoplasm also →muscle contraction

Cardiac Cycle:
 Chapter-4: Physiology (Cardiovascular Module) | 75

• The cardiac events that occur from the beginning of one heartbeat to the beginning of the next are called
the cardiac cycle.
• Each cycle is initiated by spontaneous generation of an action potential in the sinus node
• The cardiac cycle consists of a period of relaxation called diastole, during which the heart fills with blood,
followed by a period of contraction called systole
• The total duration of the cardiac cycle, including systole and diastole, is the reciprocal of the heart rate.
• For example, if heart rate is 72 beats/min, the duration of the cardiac cycle is 1/72 min/beat—about 0.0139
minutes per beat, or 0.833 second per beat.
Phases of Cardiac Cycle
1-Atrial Systole
2-Ventricular Systole
I. Isovolumetric Contraction
II. Rapid Ejection
III. Slow Ejection
3-Ventricular Diastole
I. Protodiastole
II. Isovolumetric relaxation
III. Rapid Filling
IV. Slow Filling
Pressure and Volume Changes of the Left Ventricle During the Cardiac Cycle
Phase I: Period of Filling
• Start of Phase I:
o Ventricular Volume: About 50 ml (end-systolic volume).
o Diastolic Pressure: 2 to 3 mm Hg.
• Filling Process:
o End-Diastolic Volume: Increases to about 120 ml (an increase of 70 ml).
o Volume-Pressure Diagram: Extends from point A to point B, with volume increasing to 120 ml and
diastolic pressure rising to 5 to 7 mm Hg.
Phase II: Period of Isovolumic Contraction
• Characteristics:
o Volume: Remains unchanged because all valves are closed.
o Pressure: Increases until it equals the aortic pressure, reaching about 80 mm Hg (depicted by point C).
Phase III: Period of Ejection
• Ejection Process:
o Systolic Pressure: Rises further due to continued ventricular contraction.
o Volume: Decreases as the aortic valve opens and blood is ejected into the aorta.
Phase IV: Period of Isovolumic Relaxation
• End of Ejection:
o Aortic Valve: Closes.
o Ventricular Pressure: Falls back to diastolic pressure levels.
o Volume: Remains unchanged during this phase.
o Return to Starting Point: The ventricle ends with about 50 ml of blood and a diastolic pressure of 2 to
3 mm Hg.

Join Medico Express Free Guidelines Group

03346072846
76 | 1st year MBBS – Block-3

The relationship of ECG with cardiac cycle

• P Wave
o Caused by the spread of depolarization through the atria.
o Followed by atrial contraction.
o Results in a slight rise in the atrial pressure curve immediately after the P wave.
• QRS Complex
o Appears about 0.16 seconds after the onset of the P wave.
o Represents electrical depolarization of the ventricles.
o Initiates ventricular contraction.
o Causes ventricular pressure to begin rising.
o Begins slightly before the onset of ventricular systole.
• T Wave
o Represents the stage of repolarization of the ventricles.
o Occurs when ventricular muscle fibers begin to relax.
o Occurs slightly before the end of ventricular systole.
Heart Sounds
• Valve Opening
o Not typically heard with a stethoscope.
o Opening is a relatively slow process and does not produce noise.
• Valve Closure
o Heard as sound due to vibration of the valves and surrounding fluids from sudden pressure changes.
• First Heart Sound (S1)
o Caused by the closure of the A-V (atrioventricular) valves.
o Low pitch and relatively long-lasting.
• Second Heart Sound (S2)
o Caused by the closure of the aortic and pulmonary valves at the end of systole.
o Rapid snap with a short-lasting vibration.
 Chapter-4: Physiology (Cardiovascular Module) | 77

Pressure Changes in the Atria—a, c, and v Waves

Pressure Changes in the Atria: a, c, and v Waves
• Atrial Pressure Waves
o a Wave:
▪ Caused by atrial contraction.
▪ Right atrial pressure increases by 4 to 6 mm Hg.
▪ Left atrial pressure increases by 7 to 8 mm Hg.
o c Wave:
▪ Occurs when the ventricles begin to contract.
▪ Caused by:
▪ Slight backflow of blood into the atria at the onset of ventricular contraction.
▪ Bulging of the A-V valves backward into the atria due to increasing ventricular
pressure.
o v Wave:
▪ Occurs toward the end of ventricular contraction.
▪ Results from slow flow of blood into the atria from the veins while the A-V valves are closed
during ventricular contraction.

End diastolic volume

• During diastole, normal filling of the ventricles increases the volume of each ventricle to about 110 to 120
ml. This volume is called the end- diastolic volume.
Stroke volume output
• the ventricles empty during systole, the volume decreases by about 70 ml, which is called the stroke volume
output
End systolic volume
• The remaining volume in each ventricle, about 40 to 50 ml, is called the end- systolic volume.
Ejection Fraction
• The fraction of the end- diastolic volume that is ejected is called the ejection fraction
• About 0.6 (or 60%). The ejection fraction percentage is often used clinically to assess cardiac systolic
(pumping) capability
Relation of EF and EDV and SV
EF= SV/EDV
SV = EDV - ESV
EF= EDV – ESV / EDV

Join Medico Express Free Guidelines Group

03346072846
78 | 1st year MBBS – Block-3

• Describe the Frank starling mechanism. Physiology Regulation of

CV- • Describe the autonomic regulation of heart pumping. heart
P-002 • Describe the effect of potassium, calcium ions & temperature on heart
pumping
function.
• Define chronotropic effect- positive and negative.
• Define the inotropic effect: positive and negative.
• Define dromotropic effect: positive and negative.
• Describe the location of adrenergic & cholinergic receptors in heart.
• Name the receptors present in coronary arterioles.
• Explain sympathetic & parasympathetic effects on heart rate &
conduction velocity

Frank starling mechanism

• The heart automatically pumps all the blood coming into Atria
• The intrinsic ability of the heart to adapt to increasing volumes of inflowing blood is called the Frank-Starling
mechanism.
Mechanism of Frank Starling

Extra amount of blood flows into the ventricles, the

cardiac muscle is stretched to a greater length

Stretching causes the muscle to contract with

increased force

The ventricle, because of its increased pumping,

automatically pumps the extra blood into the arteries.

Autonomic regulation of heart pumping

Mechanisms of Excitation of the Heart by the Sympathetic Nerves
• Effect of Sympathetic Stimulation
o Increased Heart Rate:
▪ Can raise heart rate from a normal 70 beats/min to 180-200 beats/min.
o Increased Force of Contraction:
▪ Doubling of force of contraction.
▪ Increased volume of blood pumped.
▪ Elevated ejection pressure.
o Increased Cardiac Output:
▪ Maximum cardiac output can increase twofold to threefold.
o Effects of Sympathetic Inhibition:
▪ Decreases cardiac pumping by about 30% when sympathetic activity is depressed below
normal.
 Chapter-4: Physiology (Cardiovascular Module) | 79

Parasympathetic (Vagal) Stimulation

• Effect of Strong Vagal Stimulation
o Heart Rate Reduction:
▪ Can cause the heart to stop briefly; subsequently, the heart may "escape" and beat at 20-40
beats/min as long as stimulation continues.
o Reduction in Strength of Contraction:
▪ Can decrease the strength of heart muscle contraction by 20% to 30%.
o Distribution of Vagal Fibres:
▪ Mainly distributed to the atria.
▪ Less impact on ventricles, which explains why vagal stimulation primarily reduces heart rate
rather than greatly decreasing contraction strength.
Effect of calcium potassium and temperature on heart functions
Effect of calcium
• Increased calcium cause spastic contraction pf heart
• Decreased calcium causes spastic flaccidity
Effect of potassium
• Increased potassium concentration in ECF
• Heart become dilated
• Heart rate decreases
• Impulse transmission through AV bundle blocked
• Heart become weak which leads to death
Effect of temperature
• Moderate increase in temperature increase contractile strength of heart
• Prolonged increase in temperature exhaust metabolic system of heart and cause cardiac weakness
• Sympathetic stimulation of heart cause increase in nor epinephrine
• Cardiac membrane permeability increased to Na+ and Ca+
• Increased rate of SA nodal discharge
• Increased heart rate
• Increased rate of impulse transmission
Aspect Chronotropic Effect Ionotropic Effect Dromotopic Effect
Definition Chronotropic effects are those An inotropic effect is when A Dromotropic effect is one
that change the heart rate. medication changes the which affects the conduction
contractility of the heart. speed in the AV node, and
Positive Positive chronotropic effect A positive inotrope increases Positive dromotropy increases
Effect increases the heart rate (e.g. contractility. conduction velocity (e.g.
epinephrine stimulation) (e.g. epinephrine stimulation) epinephrine stimulation)
Negative Negative chronotropic effect are A negative inotrope decreases Negative dromotropy decreases
Effect those that decreases the heart rate contractility. (e.g. Vagal velocity (e.g. vagal stimulation).
(e.g. Vagal Stimulation) Stimulation)

Location of adrenergic and cholinergic receptors in the heart

Adrenergic receptors (sympathetic)
• Alpha 1 adrenoceptor present on myocytes of heart
• Beta 1 adrenoceptors on cardiac muscles
• Beta 2 adrenoceptors on cardiac muscles

Join Medico Express Free Guidelines Group

03346072846
80 | 1st year MBBS – Block-3

Cholinergic receptors (parasympathetic)

• M2 muscarinic receptors on cardiac muscles especially on SA and AV Node
Sympathetic and parasympathetic effect on heart rate and conduction velocity
Sympathetic NS
➢ Sympathetic stimulation of the heart
➢ Norepinephrine secreted
➢ Increase permeability of cardiac fibres membrane to Na+ and K+
➢ Increase rate of SA nodal discharge
➢ Increase heart rate
➢ Increase rate of impulse transmission
➢ Increase conduction velocity
Parasympathetic NS
➢ Parasympathetic stimulation of heart
➢ Acetylcholine secreted
➢ Act on cholinergic receptors of heart
➢ Increase permeability of cardiac fibres membrane to K+ Hyperpolarization
➢ Longer time required to reach threshold by Na+ leakage
➢ Decrease rate of SA nodal discharge
➢ Decrease Heart rate
➢ Decrease rate of impulse transmission
➢ Decrease force of contraction
➢ Decrease velocity
 Chapter-4: Physiology (Cardiovascular Module) | 81

• Draw and explain the conducting system of heart. Physiology Conducting system of
CV-P- • Describe the physiological basis and significance of heart
003 AV nodal delay.

Conducting system of heart

The conducting system of heart consists of:
➢ SA node (pace maker)
➢ Internodal fibres and atria
➢ AV Node (delay)
➢ AV bundle bundle of hiss
➢ Right and Left branches
➢ Purkinjie fibres (from apex to base of ventricles)
SA node
• It acts as pacemaker of heart
• Generate rhythmic self-excitatory impulses
Mechanism of action Potential in Heart:
Resting membrane potential is -55 to -60 → Sodium channels have already become deactivated at -55 → sodium leaks
inward through leaky channels (also called funny channels) → RMP comes to -40 (threshold value) → Opening of Calcium
channels → depolarization followed by opening of K+ channels and repolarization

Internodal pathway
• 3 Bundles of atrial fibres containing Purkinjie fibres
• Conduct impulses from SA node to AV node
• Anterior posterior and middle internodal pathways
AV node
AV node causes delay in transmission from atria to ventricles due to
• Slow conduction
• Less number of gap junctions
• Slow Na+ and Ca+ channels
• Small size
Cause of Delay in AV node:
• The slow conduction is caused by diminished numbers of gap junctions between successive cells in conducting
pathway

Join Medico Express Free Guidelines Group

03346072846
82 | 1st year MBBS – Block-3

• The total delay of AV node and AV bundle is about 0.13 seconds

• Due to this delay atria contract 1/6th ahead of ventricles
• It allows proper filling of ventricles before pumping blood into aorta and pulmonary trunk
AV Bundle and Purkinjie fibres
• Purkinjie fibres originate in AV node
• Makes AV bundle in fibrous tissue
• Divide into right and left branches which run downward and divide into other small fibres
• Transmit cardiac impulses very rapidly from AV node throughout ventricles in 0.03 seconds
• Transmission of cardiac impulse is very rapid due to decrease gap junctions.
• Av bundle is one way conduction pathway
 Chapter-4: Physiology (Cardiovascular Module) | 83

• Explain the ectopic pacemaker Physiology Fundamentals of

CV-P- • Enlist, draw, and explain the physiological basis & give ECG
004 durations of waves, intervals, and segments of normal ECG.
• Physiology
• Describe the standard limb leads, Augmented limb leads &
precordial leads.
• Define Einthoven's Triangle & Einthoven's law.
• Explain the physiological basis of upright T wave in normal
ECG.
• Describe the location and significance of J point in ECG.
• Explain the physiological basis of current of injury.
• Enlist the ECG changes in angina pectoris.
• Enlist the ECG changes in myocardial infarction.
• Plot the mean cardiac axis.
• Physiology Enlist the physiological & pathological causes of
right axis deviation of heart.
• Enlist the physiological & pathological causes of left axis
deviation of heart
• Describe the abnormalities of T wave and their cause

Ectopic Pacemaker of heart

• Sa Node is natural pacemaker of heart
• The conduction by SA node is 70-80 times per minute
• The conduction by AV node is 40-60 while by Purkinje system is 15-40 times per minute
• A pacemaker elsewhere than the sinus node is called an ectopic pacemaker.
Causes of Ectopic pacemaker
• Abnormal sequence of contraction of the different parts of the heart and can cause weakening of heart pumping.
• Blockage of transmission of the cardiac impulse from the sinus node to the other parts of the heart.
The new pacemaker then usually occurs at the A- V node or in the AV bundle
When A- V block occurs— a new pacemaker develops in the Purkinje system of the ventricles and drives the ventricular
muscle at a new rate at 15 and 40 beats per minute
Stokes Adam Syndrome:

Purkinje fibers
No blood to
doesn’t conduct
Sudden AV block brain during this Person faints
impulse until 15-
time
20 seconds

Waves of ECG
➢ P wave produced by atrial depolarization
➢ QRS Complex v is formed by Ventricular depolarization
➢ ST segment and T wave represents ventricular repolarization
➢ Atrial T wave, if present, represent atrial repolarization.
➢ U wave, If present, represent slow repolarization of papillary muscles

Join Medico Express Free Guidelines Group

03346072846
84 | 1st year MBBS – Block-3

Intervals
PQ or PR intervals
➢ Time interval b/w onset of atrial conduction and onset of ventricular conduction
➢ It represent AV nodal delay
➢ Value 0.16sec
QT interval
➢ Duration of ventricular contraction from start of Q wave to T wave
➢ Value 0.35sec

Standard limb lead augmented limb lead and precordial lead

3 standard bipolar limb leads
Lead l
• The negative terminal of the electrocardiograph is connected to the right arm
• The positive terminal is connected to the left arm.
• The electrocardiograph records positively—that is, above the zero- voltage line in the ECG.
Lead ll
• The negative terminal of the electrocardiograph is connected to the right arm
• The positive terminal is connected to the left leg.
• The electrocardiograph records positively.
Lead III
• The negative terminal of the electrocardiograph is connected to the left arm,
 Chapter-4: Physiology (Cardiovascular Module) | 85

• The positive terminal is connected to the left leg.

• The electrocardiograph records positively.

Einthoven’s triangle
• It is an equilateral triangle which is drawn arbitrarily around area of heart in which apices represent right arm left
arm and left leg
Einthoven’s Law
• Einthoven’s law states that if the ECGs are recorded simultaneously with the three limb leads, the sum of the
potentials recorded in leads I and III will equal the potential in lead II
Lead I potential+ Lead III potential= Lead II potential
Precordial limb leads
Positive electrode connected to six separate positions on chest and negative electrode to right arm, left arm and left leg.
➢ V1= connected to 4rth intercostal space 1 inch away from right sternal border
➢ V2= 4rth intercostal space 1 inch away from left sternal border
➢ V3= midpoint b/w V2 and V4
➢ V4= 5th intercostal space at left midclavicular line
➢ V5= point where anterior axillary line cut perpendicularly from horizontal line extended from V4
➢ V6=point where mid axillary line cut perpendicularly the same horizontal line extended from V4

Join Medico Express Free Guidelines Group

03346072846
86 | 1st year MBBS – Block-3

Augmented unipolar limb leads

Two leads connected to negative terminal and 3 rd lead to positive terminal
➢ aVR lead when positive terminal connected to right arm
➢ aVL lead when positive terminal connected to left arm
➢ aVF Lead when positive terminal connected to left leg.
Physiological basis of upright T wave in normal ECG
• The T wave is caused by potentials generated as the ventricles recover from depolarization.
• This process normally occurs in ventricular muscle 0.25 to 0.35 second after depolarization.
• The T wave is known as a repolarization wave
Location and significance of J point in ECG
The point at which ECG potential is always zero is called J point
Location of J point
➢ At the end of QRS complex
➢ When no current flows through heart
➢ And depolarization waves have completed their passage through heart.
Importance of J point
➢ By the help of J point we can find the injured area of heart by
➢ Plotting axis of current of injury
Current of injury
Many cardiac abnormalities that damage the heart muscle cause part of the heart to remain partially or totally depolarized
all the time.
➢ When this condition occurs, current flows between the pathologically depolarized and normally polarized areas.
➢ This condition is called a current of injury.
➢ The injured part of the heart is negative and depolarized
➢ The normal part of the heart is neutral or in positive polarity
Causes
➢ Mechanical trauma
➢ Infectious processes
➢ Ischemia of local areas of heart muscle caused by local coronary occlusions.
Plot the mean cardiac axis
 Chapter-4: Physiology (Cardiovascular Module) | 87

Causes of left axis deviation of heart Causes of right side deviation of heart
• Left ventricular hypertrophies due to • Hypertrophy of right ventricle
hypertension • Congenital pulmonary valve stenosis
• Aortic valvular stenosis • Tetralogy of fallout
• Aortic valvular regurgitation • Interventricular septal defect
• Congenital heart conditions • Inspiration when person stands up
• Expiration • tall person
• When person lies down • right bundle branch block
• Left bundle branch block
• Obesity

Abnormalities of T waves and causes

• Inverted T wave caused by ischemia of ventricles. Medications such as antiarrhythmic and digoxin cause T wave
inversion
• Opposite polarity of T wave caused by delayed impulse transmission through ventricles
• Bundle branch block
• Biphasic T wave due to digitalis toxicity
ECG changes in myocardial infarction
➢ ST segment elevation
➢ T wave inversion
➢ Deep Q wave
Management
• On arrival in emergency patient should immediately receive Oxygen by nasal prongs.
• Sublingual nitro-glycerine
• Analgesics for pain relief
• Aspirin 160 to 325mg orally
ECG changes in angina pectoris
➢ ST segment depression
➢ Prolonged QT interval
➢ Negative T wave
Management
• Sublingual nitroglycerin is the effective medication for the acute relief of angina patient.
• B blockers
• Ca+ channel blockers

Join Medico Express Free Guidelines Group

03346072846
88 | 1st year MBBS – Block-3

Describe the effect of hypokalemia and hyperkalemia on ECG. Integrate with Effect of
CV-P- Describe the effect of hypocalcemia and hypercalcemia on ECG. Biochemistry electrolyte on
005 ECG

Effect of hyperkalemia on ECG Effect of hypokalemia on ECG

Flattened P wave Peaked P wave
Peaked T wave Shallow T wave
Prolonged PR interval Prolonged PR interval,
Prolonged QRS duration Prominent U wave
ST Depression

Effect of hypercalcemia on ECG Effect of hypocalcaemia on ECG

ST segment elevation Lengthening of the ST segment.
Biphasic T waves Prolongation of the QT interval
Prominent U waves.
 Chapter-4: Physiology (Cardiovascular Module) | 89

• Define tachycardia and enlist its causes. Physiology Cardiac

CV- • Define bradycardia and enlist its causes. arrhythmia
P-006 • Classify arrhythmias.
• Explain the physiological basis of sinus arrhythmia.
• Explain the physiological basis of reflex bradycardia in Athletes. Explain
the carotid sinus syndrome.
• Enlist the causes of atrioventricular block.
• Explain the types of atrioventricular blocks.
• Explain the ECG changes in 1st, 2nd & 3rd degree heart block.
• Explain the cause, physiological basis & ECG changes in Stokes Adam
syndrome/ventricular escape.
• Enlist the causes of premature contractions.
• Explain the causes and ECG changes of premature atrial contractions.
• Explain the physiological basis of pulses deficit.
• Explain the causes and ECG changes in Premature Ventricular
Contraction (PVC).
• Enlist the causes and ECG findings in Long QT syndrome.
• Explain the causes, physiological basis, features, ECG changes &
management of premature heartbeat.
• Explain the causes, physiological basis, features, ECG changes &
management of atrial fibrillation.
• Explain the causes, physiological basis, features & ECG changes of
ventricular fibrillation.
• Explain the physiological basis, features & ECG changes of atrial flutter.
• Compare Flutter and Fibrillations
Arrhythmias
• Abnormal rhythm of heart beat is called cardiac arrhythmia
• It can be classified as

Join Medico Express Free Guidelines Group

03346072846
90 | 1st year MBBS – Block-3

Tachycardia
The term tachycardia means fast heart rate, which usually is defined as faster than 100 beats/min in an adult
Causes
• Fever
• Exercise
• Sympathetic stimulation
• Emotions
• Pregnancy
• High altitude
• Theophylline (coffee)
• Anaemia
• Hyperthyroidism
• Hypersecretion of catecholamines
• Cardiomyopathy
• Valvular heart disease
• Haemorrhagic shock.
Management:
• Benign conditions such as stress do not require any specific treatment
• If sinus tachycardia is due to any medical condition the patient should be admitted for urgent evaluation.
Bradycardia
The term bradycardia means slow heart rate usually less than 60 beats/min
Causes
• Sleep
• Vagal stimulation
• Athletes
• Hypothermia
• Hypothyroidism
• Heart attack
• Congenital heart disease
• Degenerative process of aging
• Obstructive jaundice
• Increased intracranial pressure
• Carotid sinus syndrome
Management
• Maintain patent airway.
• Assist breathing give oxygen
• Monitor ECG and BP
• In case of poor perfusion proper medication is required such as atropine
Bradycardia in athletes
• The well- trained athlete’s heart is often larger and stronger than that of a normal person.
• This allows the athlete’s heart to pump a large stroke volume output per beat even during periods of rest.
Sinus Arrhythmias
o Sinus arrhythmia can arise from various circulatory conditions affecting the sympathetic and
parasympathetic nerve signals to the heart’s sinus node.
 Chapter-4: Physiology (Cardiovascular Module) | 91

• Respiratory Type of Sinus Arrhythmia:

o Cause: Results from signals spilling over from the medullary respiratory center into the adjacent
vasomotor center during the inspiratory and expiratory phases of respiration.
o Effect: Causes alternating increases and decreases in impulses transmitted through the sympathetic and
vagus nerves to the heart.
• Mechanisms:
o Inspiration:
▪ Lung Inflation: Decreases intrathoracic pressure.
▪ Venous Return: Increases.
▪ Stretch Receptors: Activated, sending impulses to the vasodilator area (cardio inhibitory
center) via vagus nerve afferent fibers.
▪ Vagal Tone: Decreases due to reflex inhibition of the vasodilator area.
o Expiration:
▪ Lung Deflation: Increases intrathoracic pressure.
▪ Venous Return: Decreases.
▪ Stretch Receptors: Not stimulated, so the vasodilator area is not inhibited.
▪ Vagal Tone: Increases, leading to a decreased heart rate.

Carotid sinus syndrome:

• In these patients, the pressure receptors (baroreceptors) in the carotid sinus region of the carotid artery walls
are extremely sensitive.
• Even mild external pressure on the neck initiate a strong baroreceptor reflex
• Intense vagal- acetylcholine effects on the heart, including extreme bradycardia.
• Sometimes this reflex is so powerful that it actually stops the heart for 5 to 10 seconds, leading to loss of
consciousness
Heart Block:
Heart block is the blockage of impulses generated by SA node in the conductive system. Because of the blockage, the
impulses cannot reach the cardiac musculature, resulting in ectopic arrhythmia. Based on the area affected, the heart block
is classified into two types
1. Sinoatrial block
2. Atrioventricular block

Join Medico Express Free Guidelines Group

03346072846
92 | 1st year MBBS – Block-3

AV Block
• The only means by which impulses ordinarily can pass from the atria into the ventricles is through the A-V bundle,
also known as the bundle of His
• Blockage of AV bundle can leads to serious clinical conditions
Causes of AV bundle block
• Ischemia of AV node or AV bundle fibres
• Compression of AV bundle by scar tissue
• Inflammation of AV node or AV bundle
• Extreme stimulation of heart by vagus nerve
• Degeneration of AV conduction system
• Medications causes AV bundle block such as Digitalis
• B blockers
• Ca+ channel blockers
• Digoxin
Types of AV bundle block
Incomplete AV Block
1st degree block
• All impulses travel very slowly from atria to ventricles
• ECG changing shows prolonged PR interval
• The usual lapse of time between the beginning of the P wave and the beginning of the QRS complex is about 0.16
second when the heart is beating at a normal rate.
• In general, when the P-R interval increases to greater than 0.20 second, the P-R interval is said to be prolonged
and the patient is said to have first-degree incomplete heart block.
nd
2 degree block
• When conduction through the A-V bundle is slowed enough to increase the P-R interval to 0.25 to 0.45 second,
the action potential is sometimes strong enough to pass through the bundle into the ventricles and sometimes not
strong enough to do so.
• In this instance, there will be an atrial P wave but no QRS-T wave, and it is said that there are “dropped beats” of
the ventricles. This condition is called second-degree heart block
• There are two types of second-degree A-V block
Type I Type 2
It is also known as Wenckebach periodicity or mobitz It is also known as mobitz type II heart block
type I
Type I block is characterized by progressive prolongation In type II block there is usually a fixed number of non-
of the PR interval until a ventricular beat is dropped conducted P waves for every QRS complex
Type I block is almost always caused by abnormality of At other times, rhythms of 3 : 2 or 3 : 1 may develop. Type
the A-V node. II block is generally caused by an abnormality of the bundle
of His-Purkinje system
In most cases, this type of block is benign and no specific It may require implantation of a pacemaker to prevent
treatment is needed. progression to complete heart block and cardiac arrest

Complete AV Block
3rd degree block
• When the condition causing poor conduction in the A-V node or A-V bundle becomes severe, complete block of
the impulse from the atria into the ventricles occurs
• Impulses do not pass from atria to ventricles
• Atria contract at rhythm of SA node
 Chapter-4: Physiology (Cardiovascular Module) | 93

• Ventricle contract at their own slow rhythm

• Atria and ventricles beat independently
• All four classes of anti-arrhythmic drugs and digoxin cause 3rd degree heart block
Management
• Initial management of bradycardia patient is IV atropine
• If the patient on medication reduce the dose of B blockers, Ca+ channel blockers, antiarrhythmic, digoxin.
• Patient with 3rd degree heart block require cardiac pacing
• Patient with Mobitz 2 or 3rd degree block require urgent admission in hospital for cardiac monitoring.
ECG changes in 1st 2nd 3rd degree heart block.
1st degree heart block: prolonged PR interval >220msec
nd
2 degree heart block:
Mobitz 1( wenckebach): PR interval lengthens, Drop beat
Mobitz 2: no lengthening of PR interval, Heart contracts at ratio
of 2:1, 3:2, 3:1 etc.
3rd degree heart block: No correlation b/w P wave and QRS, Frequency of P
wave is greater than QRS.

Stokes Adam syndrome/ventricular escape

Causes
• 3rd degree complete block
Physiological Basis
• In patients with 3rd degree block impulse transmission is blocked at AV node.
• Atria continue to contract at SA node rhythm

Join Medico Express Free Guidelines Group

03346072846
94 | 1st year MBBS – Block-3

• A new ventricular pacemaker develop in Purkinjie system after 5 to 30 seconds

• Ventricles do not start their own beating until 5 to 30 seconds (ventricular escape) this phenomenon is due to
overdrive suppression.
• Brain does not receive blood for 4 to 7 seconds results in cerebral ischemia.
• Some people faint due to lack of blood supply. This condition is called stokes Adam syndrome.
ECG changes
• No correlation b/w P wave and QRS complex.
• Frequency of P wave is greater than QRS.
Atrial premature contraction and ECG changes
A premature contraction is a contraction of the heart before the time that normal contraction would have been expected.
This condition is also called extra systole, premature beat, or ectopic beat.
Causes of premature atrial contraction:
• Smoking
• Lack of sleep
• Ingestion of too much coffee
• Alcoholism
• Drugs, Asthma medicine
• High blood pressure
• Hyperthyroidism
• Pregnancy
ECG CHANGES
• P wave occur too soon
• PR interval shortened
• Compensatory pause in ECG
Management
• Avoid triggers
• B Blocker at Low doses 1st line treatment
• Atrial pacing can also be done

Pulse deficit
• When the heart contracts ahead of schedule, the ventricles do not filled with blood normally
• The stroke volume output is depressed or absent.
• The pulse wave passing to the peripheral arteries after a premature contraction is so weak that it cannot be felt in
the radial artery.
• There is decrease in the number of radial pulses occurs compared with the actual number of contractions of the
heart.
Premature ventricular contraction
Causes of PVC
• Smoking
• Lack of sleep
 Chapter-4: Physiology (Cardiovascular Module) | 95

• Emotional irritability
• Mild toxic states
• Strayed impulses
ECG changes in PVC
• QRS complex prolonged
• QRS complex high voltage
• Opposite polarity of T wave
Management
• Lifestyle changes
• Avoid PVC triggers such as smoking caffeine
• BP medication prescribed

Long QT syndrome LQTS

Causes
• Delayed repolarization of ventricular muscles
• Mutation of Na+ or K+ channel genes
• Acquired form of LQTS due to hypokalaemia hypomagnesemia hypocalcaemia
• Excessive use of anti-arrhythmic drugs such as Quinidine, antibiotics like fluoroquinolones and erythromycin
ECG changes
• Torsade’s di points due to delayed repolarization and prolonged ventricular depolarization.
• Long QT interval on ECG.
Management
• Magnesium sulphate for acute LQTS
• Antiarrhythmic medications such as B blockers
• Surgical implantation of cardiac defibrillator for long term LQTS
Atrial fibrillation
Causes
• Dilation of ventricles
• Block of impulse through Purkinjie system.
• Myocardial ischemia
Pathophysiology
• Cardiac impulses stimulate first one portion of the ventricular muscle, then another portion
• Re-excite the same ventricular muscle again and again.
• Many small portions of the ventricular muscle contract at the same time.

Join Medico Express Free Guidelines Group

03346072846
96 | 1st year MBBS – Block-3

ECG
• ECG shows irregular waves.
• No repetitive ECG pattern
Features
• Heart palpitation
• Dizziness
• Chest pain
Management
• CPR
• Defibrillation
• Medication
• Catheter ablation
Atrial fibrillation
Causes
• Over Dilation of atria
Pathophysiology
• Many unsynchronized impulses travel through atria & cause re excitation
ECG changes
• No P waves from atria
• QRS T complex normal
Features
• Irregular heartbeat
• Palpitations
• Fluttering in chest
Atrial flutter
Pathophysiology
• Atrial flutter caused by a circus movement in the atria. Atrial flutter is different from atrial fibrillation.
• Electrical signals travel as a single large wave but only in one direction.
• Rapid contraction of one side of atria 200 to 350 beats/minute.
ECG changes
• P waves are strong
 Chapter-4: Physiology (Cardiovascular Module) | 97

• QRS T complex follow P wave after every 2 beats of atria

Causes
• High blood pressure
• Coronary artery disease
• Congenital heart defect
Features
• Stroke
• Palpitation
• Dizziness
Compare flutter and fibrillation

Atrial Fibrillation Atrial flutter

In atrial fibrillation atria beat irregularly In atrial flutter atria beat regularly and faster.
Electrical activity in atrial fibrillation is not coordinated. Electrical activity in atrial flutter is coordinated.
Both atrial flutter & fibrillation effect the upper chamber Both atrial flutter & fibrillation effect the upper chamber
of heart of heart

Join Medico Express Free Guidelines Group

03346072846
98 | 1st year MBBS – Block-3

Explain the functional parts of circulation (arteries, arterioles, Physiology Organization of

CV-P- capillaries, veins, venules). Circulation
007
Arteries Veins Capillaries
Function Carry blood away from heart Carry blood toward heart Carry blood from artery to vein and
exchange material with the tissue
Pressure High Pressure Low Pressure Low pressure
Lumen diameter Narrow Wide Extremely narrow (one cell thick)
Wall thickness Thick Thin
Wall layers Three Three One
• Tunica Adventitia • Tunica Adventitia • Only Tunica intima
• Tunica Media • Tunica Media
• Tunica Intima • Tunica Intima
Elastic fibers Large amount Small amount None
Valves No Yes No
Composition Oxygenated blood except Deoxygenated blood except Gaseous exchange occurs
pulmonary artery pulmonary veins
 Chapter-4: Physiology (Cardiovascular Module) | 99

• Explain the pressures in systemic & pulmonary circulation. Physiology Blood

CV-P- • Explain the types of Blood flow and significance of Reynolds flow
008 number

Systemic circulation
• Systemic circulation refers to the circulation other than Pulmonary system
• The pressure in systemic capillaries varies from 35 mm Hg near the arteriolar end.
• It becomes 10 mm Hg near the venous ends
• Average functional pressure = about 17 mm Hg.
• This low pressure causing leakage of plasma from capillary pores.
• In the kidneys, the pressure is about 60 mm Hg causing high filtration.
• The arterial pressure ranges from 80 to 120 mm Hg while the venous pressure ranges from 15 to 20 mmHg
• The Systolic pressure is 120 while diastolic pressure is 80mm Hg
• Mean arterial pressure is 94mm Hg
Pulmonary circulation
• Pulmonary artery systolic pressure = 25 mm Hg
• Diastolic pressure = 8 mm Hg
• Mean pulmonary arterial pressure =16 mm Hg.
• The mean pulmonary capillary pressure averages only 7 mm Hg

Blood Flow
• Definition:
o Blood Flow: The quantity of blood passing a given point in the circulation per unit of time.
o Units: Commonly expressed in milliliters per minute (ml/min) or liters per minute (L/min), but can also
be measured in other units like milliliters per second.
• Cardiac Output:
o Resting Flow: Approximately 5000 ml/min in an adult at rest.
o Definition: The amount of blood pumped into the aorta by the heart each minute.

Join Medico Express Free Guidelines Group

03346072846
100 | 1st year MBBS – Block-3

1. Turbulent Flow
• Characteristics:
o Occurrence: Happens when blood flow rate is too high, encounters an obstruction, makes a sharp turn,
or flows over a rough surface.
o Pattern: Blood flow becomes disorderly, forming eddy currents or whorls similar to whirlpools in a
rapidly flowing river.
o Resistance: Greater resistance due to increased friction caused by eddy currents, compared to
streamlined flow.
2. Laminar Flow
• Characteristics:
o Steady Flow: Occurs when blood flows at a steady rate through a long, smooth vessel.
o Streamlines: Blood flows in parallel layers, with each layer maintaining a consistent distance from the
vessel wall.
o Central Flow: The central portion of the blood stays in the center of the vessel.
o Pattern: Known as laminar or streamline flow.
Reynold’s number
➢ Measure of tendency for turbulence to occur
Re= νdρ/n
• It is Directly proportional to velocity diameter density of blood
• It is Inversely proportional to viscosity of blood
 Chapter-4: Physiology (Cardiovascular Module) | 101

• Describe local control of blood flow according to tissue needs. Physiology Local &
CV- • Discuss humoral control of local blood flow. Humoral
P-009 • Explain long term control of local blood flow.
Control of
Blood flow
• Describe vascular control by ions and other chemical factors.
• Name the organs in which auto regulation of blood flow occurs during
changes in arterial pressure (metabolic & myogenic mechanisms).

Local control of blood flow

Vasodilator theory

Decreased blood flow or greater rate of metabolism

Decreased Oxygen and other nutrients supply

Increase rate of formation of vasodilator substances i.e. 2

Lactic acid histamine K+ H+

Vasodilation of local vascular bed

Increase blood flow

Oxygen or nutrient demand theory

Decreased blood flow or greater rate of metabolism

Oxygen supply decrease

Smooth muscles in precapillary sphincter dilate

(because they need O2 to contract)

Increase blood flow

Humoral control of local blood flow

Vasodilator agents Vasoconstrictor agent
Histamine Epinephrine
Norepinephrine
Serotonin Vasopressin
Bradykinin Angiotensin
Prostaglandin Endothelin
Epinephrine Calcium ions
Na+ K+ Mg++ Slightly increase pH
Decrease pH OR rapid increase in pH Decreased CO2
Anions
Increase CO2
NO

Join Medico Express Free Guidelines Group

03346072846
102 | 1st year MBBS – Block-3

Long-Term Control of Local Blood Flow

1. Growth of New Vessels: Angiogenesis
• Mechanism:
o Regulation: Changes the vascularity of tissues to regulate long-term local blood flow.
o Trigger: Lack of oxygen and nutrients stimulates the secretion of angiogenic factors, leading to new
vessel growth.
• Key Factors:
o Angiogenic Factors: Over a dozen factors, mostly small peptides, promote new blood vessel growth.
o Characterized Factors:
▪ Vascular Endothelial Growth Factor (VEGF)
▪ Fibroblast Growth Factor
▪ Platelet-Derived Growth Factor (PDGF)
▪ Angiogenic Factor
• Process of Angiogenesis:
o Sprouting: New vessels sprout from existing small vessels.
o Basement Membrane Dissolution: Initial step involves dissolving the basement membrane of
endothelial cells at the sprouting site.
o Endothelial Cell Reproduction: New endothelial cells rapidly reproduce and extend outward through
the vessel wall in cords directed toward the angiogenic factor.
o Formation of Tubes: Cells in the cords fold over and form tubes.
o Capillary Loop Formation: Tubes connect with others from donor vessels, forming capillary loops
through which blood begins to flow.
o Result: Increase in local blood flow.
2. Collateral Circulation
• Overview:
o When an artery or vein is blocked, new vascular channels develop around the blockage to partially
resupply blood to the affected tissue.
• Process:
o Initial Dilation: Small vascular loops connecting vessels above and below the blockage dilate within
the first minute or two, likely due to metabolic factors.
o Further Opening:
▪ Hours: Blood flow increases but may still be less than required.
▪ 1 Day: Up to half of the tissue’s needs may be met.
▪ Few Days: Blood flow usually meets tissue needs.
o Long-Term Growth: Collateral vessels continue to grow for months, forming multiple small channels
rather than a single large vessel.
o Resting Conditions: Blood flow may return nearly to normal, but new channels may not meet the
demands during strenuous activity.
• Example:
o Coronary Artery Thrombosis: Development of collateral blood vessels after thrombosis of a coronary
artery is a significant example.
Autoregulation of blood flow occurs during changes in arterial pressure.
Effective autoregulation of blood flow occurs during changes in arterial pressure in following tissues
• Brain
• Heart
• Kidney
• All of these organs show excellent autoregulation in body.
 Chapter-4: Physiology (Cardiovascular Module) | 103

Metabolic Theory

Excess flow
provide O2 and Blood flow returns
Arterial pressure constriction of
other nutrients to normal despite
increase vessels
and remove increase in BP
vasodilation

Myogenic Theory

stretch induced
Myogenic Myogenic
Increase in vascular
Stretching of contraction contraction
arterial depolarization
Blood vessels of smooth of smooth
pressure occurs in smooth
muscles muscles
muscles of vessels

Join Medico Express Free Guidelines Group

03346072846
104 | 1st year MBBS – Block-3

• Explain the role of autonomic nervous system for regulating the Physiology Nervous
CV- circulation. Regulation of
P-010 • Explain the vasomotor center. circulation
• Explain the control of vasomotor center by higher nervous centers.
• Explain emotional fainting / vasovagal syncope.
• Identify vessels constituting micro-capillaries.
• Enumerate hydrostatic and osmotic factors that underlie starling’s
hypothesis for capillary function

Role of autonomic nervous system for regulating the circulation

Sympathetic stimulation
• It supplies both blood vessels and heart
• Sympathetic nerve fibres causes contraction of vascular muscles increasing the tone of vessel walls
• It increases Heart Rate and Contractility.
• It enhances its strength volume and pumping
• Inhibition of sympathetic system causes vasodilation
Parasympathetic stimulation
• Has minor effect on blood flow
• It effects heart only, not blood vessels
• Parasympathetic stimulation causes decrease in heart rate and a slight decrease in heart muscle contractility
Vasomotor centre of brain
Location
It is located bilaterally in the reticular substance of the medulla and lower third of the pons is an area called the vasomotor
centre.
Function
• This centre transmits parasympathetic impulses through the vagus nerves to the heart
• and sympathetic impulses through the spinal cord
• And peripheral sympathetic nerves to virtually all arteries, arterioles.
It is consist of 3 areas
1. A vasoconstrictor area
Location
• It is located bilaterally in the anterolateral portions of the upper medulla.
• The neurons originating in this area distribute their fibres to all levels of the spinal cords
Function
• They excite preganglionic vasoconstrictor neurons of the sympathetic nervous system.
2. A vasodilator area
Location
• A vasodilator area located bilaterally in the anterolateral portions of the lower half of medulla
Function
• Inhibit the vasoconstrictor activity of this area and cause vasodilation.
3. A sensory area
Location
• It is located bilaterally in the nucleus tractus solitarius in the posterolateral portions of the medulla and lower
pons.
 Chapter-4: Physiology (Cardiovascular Module) | 105

Functions
• It helps control activities of the vasoconstrictor and vasodilator areas of the vasomotor centre
• It provides reflex control of many circulatory functions.
• An example is the baroreceptor reflex for controlling arterial pressure.
Control of vasomotor centre by higher nervous centre
Reticular substance of pons mesencephalon diencephalons
• The reticular substance of the pons mesencephalon diencephalons can excite or inhibit the vasomotor centre.
• The neurons in the more lateral and superior portions of the reticular substance cause excitation
• Medial and inferior portions cause inhibition.
Hypothalamus
• The hypothalamus exert powerful excitatory or inhibitory effects on the vasomotor centre
• The posterolateral portions causes excitation.
• Anterior portion can cause mild excitation or inhibition.
Cerebral cortex
• Stimulation of the motor cortex excites the vasomotor centre.
• Stimulation of the anterior temporal lobe, orbital areas of the frontal cortex, anterior part of the cingulate gyrus,
amygdala, septum, and hippocampus can all excite or inhibit the vasomotor centre.

Emotional fainting /vasovagal syncope

• Vasodilatory reaction occurs in people who experience intense emotional disturbances that cause fainting.
• In this case, the muscle vasodilator system becomes activated.
• At the same time, the vagal cardio inhibitory centre transmits strong signals to the heart to slow the heart rate.
• The arterial pressure falls rapidly, which reduce the blood flow to the brain.
• As a result person loses consciousness. This overall effect is called vasovagal syncope.
Starling’s hypothesis for capillary function
“States that fluid movement between capillaries is the result of balance between hydrostatic and osmotic forces.”
Hydrostatic and osmotic factors
1. The capillary pressure (Pc), which tends to force fluid outward through the capillary membrane.

Join Medico Express Free Guidelines Group

03346072846
106 | 1st year MBBS – Block-3

2. The interstitial fluid pressure (Pif), which tends to force fluid inward through the capillary membrane when Pif is
positive but outward when Pif is negative
3. The capillary plasma colloid osmotic pressure (Πp), which tends to cause osmosis of fluid inward through the
capillary membrane.
4. The interstitial fluid colloid osmotic pressure (Πif), which tends to cause osmosis of fluid outward through the
capillary membrane.

These forces collectively are called Starling forces

➢ If the sum of these forces—the net filtration pressure— is positive, there will be a net fluid filtration across
the capillaries.
➢ If the sum of the Starling forces is negative, there will be a net fluid absorption from the interstitial spaces
into the capillaries.
➢ The net filtration pressure (NFP) is calculated as
NFP = Pc - Pif - p - if
 Chapter-4: Physiology (Cardiovascular Module) | 107

• Explain the role of nervous system in rapid control of arterial blood Physiology Rapid
CV- pressure. control of
P-011 • Explain the regulation of arterial blood pressure during exercise. arterial
blood
• Enlist different mechanisms for short term regulation of arterial blood pressure
pressure.
• Explain the role of baroreceptors in regulation of arterial blood
pressure.
• Explain the role of chemoreceptors in regulation of arterial blood
pressure.
• Make a flow chart to discuss the role of Atrial volume reflexes /
Bainbridge reflex in control of blood pressure.
• Make a flow chart to show the reflex responses to increased blood
volume which increase blood pressure and atrial stretch.
• Describe the role of CNS ischemic response in regulation of the blood
pressure.
• Explain the Cushing reflex.
• Explain the role of abdominal compression reflex to increase the arterial
blood pressure.

Role of nervous system in rapid control of blood pressure

For rapid increase in arterial pressure sympathetic nervous system is stimulated and at the parasympathetic nervous system
is inhibited.
Following changes take place
1. Most arterioles of the systemic circulation are constricted, which greatly increases the total peripheral resistance.
2. The veins are strongly constricted. This constriction displaces blood out of the large peripheral blood vessels
toward the heart.
3. The heart is directly stimulated by the autonomic nervous system which increases cardiac pumping.

Regulation of arterial blood pressure during exercise

During heavy exercise, the muscles require greatly increased blood flow. → It is fulfilled by local vasodilation of the
muscles and sympathetic nervous response → Motor areas of the brain become activated → Reticular areas also activated
→ Vasoconstriction & cardio acceleration of vasomotor areas increased → Arterial pressure is increased

Short term regulation of blood pressure

Following mechanisms plays role in short term regulation
➢ Baroreceptor reflex
➢ Chemoreceptor reflex
➢ Abdominal compression reflex
➢ Arterial and pulmonary artery reflex
➢ Arterial reflex to kidney
➢ Bainbridge reflex
➢ CNS ischemic response
Baroreceptor Arterial Pressure Control System—Baroreceptor Reflexes
This reflex is initiated by stretch receptors, called baroreceptors → these receptors are located at specific points in the
walls of several large systemic arteries → A rise in arterial pressure stretches the baroreceptors → Baroreceptors are
activated and send stimulatory impulses to nucleus of tractus solitarius through glossopharyngeal and vagus nerves.
Nucleus of tractus solitarius inhibits the vasoconstrictor area and excites the vasodilator area → Dilation of blood vessels
→ Pressure comes back to normal

Join Medico Express Free Guidelines Group

03346072846
108 | 1st year MBBS – Block-3

Chemoreceptors in Regulation of Blood Pressure

• Function:
o Response: Chemoreceptors respond to changes in the chemical constituents of blood.
o Location:
▪ Peripheral Chemoreceptors: Situated in the carotid body and aortic body.
• Sensitivity:
o Stimuli: Sensitive to:
▪ Lack of oxygen (hypoxia)
▪ Excess carbon dioxide (hypercapnia)
▪ Increased hydrogen ion concentration (acidosis)
• Mechanism:
o Decreased Arterial Pressure:
▪ Leads to reduced blood flow to chemoreceptors.
▪ Results in decreased oxygen, increased carbon dioxide, and increased H+ concentration.
o Chemoreceptor Activation:
▪ Stimulated by changes in blood chemistry.
▪ Sends signals through the glossopharyngeal or vagus nerve to the vasoconstrictor area of the
brain.
o Response:
▪ Vasoconstriction: Peripheral vessels constrict, increasing arterial pressure.
Bainbridge reflex:
Blood volume increase → Arterial pressure increase → Stretch receptors of atria stretched → Send afferent signals to
medulla → Efferent signals send back to heart → Heart rate and contractility increases → Prevent accumulation of blood
in atria and veins.
 Chapter-4: Physiology (Cardiovascular Module) | 109

CNS ischemic response:

Decrease blood flow to brain → Results in ischemia → Increase CO2 lactic acid → Decrease pH of vasomotor centre →
Vasoconstrictor area excited → Intense vasoconstriction of peripheral nerves → Increase in Blood pressure to normal
Cushing reflex:
It is a special type of CNS ischemic response.
CSF pressure increased than that of arterial pressure → Brain arteries compressed → Blood flow to the brain cut off →
Ischemia of CNS due to lack of blood supply → Arterial pressure increased than CSF pressure → Compressed brain
arteries opened.
Abdominal compression reflex in control of BP:
Arterial pressure decrease due to blood loss → Sympathetic fibres to abdominal muscles stimulated → Contraction of
abdominal muscles → Veins of abdomen compressed → Venous return to heart increased → Cardiac output increased
→ Arterial pressure increased

Join Medico Express Free Guidelines Group

03346072846
110 | 1st year MBBS – Block-3

• Make a flow chart to discuss the role of renin angiotensin Physiology Kidneys in long
CV- system for long term control of blood pressure. term Regulation of
P-012 • Make a flow chart to show the regulation of blood pressure in Arterial Blood
response to increase in ECF (Extra Cellular Fluid) volume. Pressure
• Make a flow chart to show the regulation of blood pressure in
response to increase in salt intake.
Renin-Angiotensin System
• Renin Production:
o Synthesis and Storage:
▪ Form: Synthesized and stored as prorenin in juxtaglomerular (JG) cells of the kidneys.
▪ Location: JG cells are modified smooth muscle cells in the walls of the afferent arterioles near
the glomeruli.
o Activation:
▪ Trigger: When arterial pressure falls, prorenin is activated to release renin through intrinsic
reactions in the kidneys.
• Renin Action:
o Enzymatic Function:
▪ Substrate: Acts on angiotensinogen (renin substrate), a plasma globulin.
▪ Product: Converts angiotensinogen to angiotensin I, a 10-amino acid peptide.
• Angiotensin I to Angiotensin II:
o Conversion:
▪ Process: Within seconds to minutes, angiotensin I is converted to angiotensin II by the removal
of two additional amino acids.
▪ Product: Angiotensin II is an 8-amino acid peptide.
• Effects of Angiotensin II:
o Vasoconstriction:
▪ Action: Extremely powerful vasoconstrictor.
▪ Outcome: Raises arterial pressure, helping to correct the initial fall in pressure.
 Chapter-4: Physiology (Cardiovascular Module) | 111

Angiotensin performs several functions.

These includes
1- Vasoconstriction
2- Salt retention by kidney
3- Release of Aldosterone by adrenal gland
4- Activation of Thirst centre
Regulation of blood volume in response to increase in increase in ECF

Regulation of blood volume in response to increase in salt intake

Increased
osmolality
Both
Excess salt in Increased also causes
mechansim osmolality
ECF increases osmolality posterior
increases returns to
ECF activates pituitary to
total body normal
osmolality thirst centre secrete large
water
amount of
ADH

Join Medico Express Free Guidelines Group

03346072846
112 | 1st year MBBS – Block-3

• Define cardiac output, cardiac index & venous return Integrate with Cardiology Cardiac
CV-P- with their normal values. / Medicine output
013 • Discuss the factors regulating cardiac output.
• Discuss factors regulating venous return

Cardiac output
• Cardiac output is the quantity of blood pumped into the aorta each minute by the heart.
• CO= Stroke Volume X Heart Rate
• Normal Range= 5 to 6 L/min
Factors Regulating Cardiac Output
• Increase venous return increases cardiac output
• Increased contractility increases Cardiac output by increasing Stroke volume
• Increased Afterload causes heart to pump against greater resistance which decreases cardiac output
• Increased heart rate also increases Cardiac output
• Increase tissue metabolism causes increased Cardiac output by increasing Venous return
• Increase blood volume causes Increase mean systemic filling pressure which results in increase venous return. As
result Cardiac output increased
• Increase Sympathetic stimulation increases heart rate and increases venous tone
• Contraction of abdomen causes compression of venous reservoir which increases venous return and cardiac output

Venous return
• It is the quantity of blood flowing from the veins into the right atrium each minute.
• Venous return = cardiac output (Frank Starling mechanism)
Factors Regulating Venous return
• Increased Mean systemic filling pressure increases venous return
• It increases with increased in venous tone
• Increase right arterial pressure decrease venous return
• Increase pressure gradient increases venous return.
• Increase resistance to venous return decreases venous return
• Increase negative intra thoracic pressure increases venous return
 Chapter-4: Physiology (Cardiovascular Module) | 113

Cardiac index
• It is cardiac output per square meter of body surface area.
• Cardiac Index =3L/min/m2 of total body area in 70 kg man
Pathological causes of high and low cardiac output
Pathological causes of high cardiac output Pathological causes of low cardiac output
Anemia Myocardial infarction
Hyperthyroidism Myocarditis
Arterio venous fistula Valvular heart diseases
Beri Beri disease Cardiac tamponade.
Hemorrhage
Acute venous dilation
Obstruction of veins
Myocardial infarction

Join Medico Express Free Guidelines Group

03346072846
114 | 1st year MBBS – Block-3

Explain the regulation of skeletal muscle blood flow at rest Physiology Skeletal muscle
CV-P- & during exercise. circulation
014
• During rest, skeletal muscle blood flow =3 to 4 ml/ min/100 g of muscle.
• During extreme exercise in athletes= 100 to 200 ml/min/100 g of muscle
FACTORS REGULATING BLOOD FLOW TO SKELETAL MUSCLE
Blood flow through skeletal muscle is regulated by three factors:
1-Mechanical factors
• During contraction of the muscle, blood vessels are compressed and the blood flow decreases.
• And during relaxation of the muscle, compression of blood vessels is relieved and the blood flow increases.
2-Chemical factors
• Important chemical factors, which regulate the blood flow through skeletal muscles, are lack of oxygen, excess
of carbon dioxide and increased hydrogen ion concentration.
• All these chemical factors increase the blood flow to muscle by causing vasodilatation
3-Nervous Factors
• Blood vessels of the skeletal muscles are mostly innervated by sympathetic nerve fibers and few parasympathetic
nerve fibers are also seen.
• Special feature of sympathetic nerve fibers supplying the skeletal muscles is that these nerve fibers are
vasodilators and not constrictors
During Exercise Sympathetic stimulation of heart and parasympathetic inhibition of heart occurs → Increased heart rate
& contractility → Peripheral blood vessels constricted → Vasodilation of muscle blood vessels → Mean systemic filling
pressure increase → Venous return increased → Cardiac output increased
 Chapter-4: Physiology (Cardiovascular Module) | 115

• Explain the physiological anatomy of coronary circulation. Physiology Coronary

CV-P- • Explain the regulation of coronary blood flow. circulation
015 • Explain the physiological basis of angina, myocardial &
subendocardial infarction

Physiological anatomy of coronary circulation

Arterial blood supply
• The left coronary artery supplies mainly the anterior and left lateral portions of the left ventricle
• The right coronary artery supplies most of the right ventricle and the posterior part of the left ventricle in
80% to 90% of people
Venous supply
• Coronary sinus drain left ventricle
• Anterior cardiac veins drain right ventricle
• Thebesian veins drain small amount of blood from all chambers of heart.
Regulation of coronary blood flow
Metabolic control

Increase work Increase

load on heart Increase oxygen vasodilation of Increase coronary
leads to increase usage coronary blood blood flow
metabolism vessels

Nervous regulation

Sympathetic stimulation
increases heart rate and It leads to Increased Increased coronary blood
contractility causes vasodilation flow
increased metabolism

Angina Pectoris
• Angina is the chest pain that is caused by myocardial ischemia.
• It is the common manifestation of coronary artery disease.
• Pain starts beneath the sternum and radiates to the surface of left arm and left shoulder.
Pathophysiology
• During myocardial ischemia, there is accumulation of anaerobic metabolic end products such as uric acid
• Metabolites and other pain producing substances like substance P, histamine and kinin stimulate the sensory nerve
endings, leading to pain
Treatment:
• Vasodilator drugs
• Calcium channel blockers
• Beta Blockers
Myocardial infarction
Myocardial infarction is the necrosis of myocardium caused by insufficient blood flow due to embolus, thrombus or
vascular spasm.
It is also called heart attack.
In myocardial infarction, death occurs rapidly due to ventricular fibrillation

Join Medico Express Free Guidelines Group

03346072846
116 | 1st year MBBS – Block-3

Pathophysiology:

Obstruction of
Area of
coronary artery by Myocardial
Local ischemia coagulative
thrombus or infarction
necrosis
embolus

Symptoms:
• Cardiac pain
• Nausea
• Vomiting
• Palpitations
• Difficulty in breathing
• Extreme weakness
• Sweating
• Anxiety
Treatment:
• Aspirin
• Nitroglycerine
• Morphine
• Beta blockers
• Oxygen
Subendocardial infarction
• Myocardial infarction that occurs in subendocardial muscles due to decrease diastolic arterial pressure is called
Subendocardial infarction
• Death occurs due to decrease cardiac output, fibrillation and rupture of heart
 Chapter-4: Physiology (Cardiovascular Module) | 117

• Define & enlist different types of shock. Physiology Circulatory

CV- • Explain the causes, features, and pathophysiology of hypovolemic / shock
P-016 hemorrhagic shock.
• Explain the causes, features, and pathophysiology of septic shock.
• Explain the causes, features, and pathophysiology of neurogenic
shock.
• Explain the causes, features, and pathophysiology of anaphylactic
shock.
• Discuss the treatment of different types of shock.
• Explain the different stages of shock.
• Explain the mechanisms that maintain the cardiac output & arterial
blood pressure in non-progressive shock.
• Enlist different types of positive feedback mechanisms that can lead to
the progression of shock

Circulatory Shock
“Circulatory shock means insufficient blood flow through the body to the extent that the body tissues are damaged because
too little oxygen and nutrients are delivered to the tissue cells”
Types of shock
➢ Hypovolemic shock
➢ Neurogenic shock
➢ Anaphylactic shock
➢ Septic shock
➢ Cardiogenic Shock

Hypovolemic shock
Shock due to decreased blood volume is called hypovolemic shock or cold shock.
It occurs when there is acute loss of at least 10% to 15% of blood
CAUSES
➢ Haemorrhage.
➢ Plasma loss due to burn.
➢ Dehydration.
➢ Diarrhoea vomiting sweating

Join Medico Express Free Guidelines Group

03346072846
118 | 1st year MBBS – Block-3

PATHOPHYSIOLOGY

Blood volume Venous return Cardiac output

Shock
decrease decrease decrease

FEATURES
• Rapid and Shallow breathing: Due to S.N.S activation
• Cold and clammy Skin: Due to compensatory vasoconstriction
• Rapid, Thready Pulse: Due to decrease blood flow with tachycardia
• Thirst and dry mouth: Due to decreased body fluid
• Low temperature: Due to decrease perfusion and evaporation of sweating
Septic Shock
Sepsis is the pathological condition characterized by the presence of pathogenic organisms or their toxins in blood or
tissues.
Shock developed during sepsis is known as septic shock

Pathophysiology

In septic shock bacterial Infection may spread

Cause destruction of
infection develops in from one tissue to
tissue
body another tissue

CAUSES
➢ Streptococcal infection
➢ Staphylococcal infection
➢ Gangrenous infection
➢ Infection by colon Bacilli
FEATURES
➢ High fever
➢ High cardiac output
➢ Vasodilation
➢ Sluggish blood flow
➢ Disseminated intravascular coagulation
Neurogenic Shock
Sudden loss of vasomotor tone throughout the body, resulting especially in massive dilation of the veins
The resulting condition is known as neurogenic shock

Pathophysiology

Sudden Loss Massive dilation Decrease Decrease

Neurogenic
of vasomotor causing Increased Venous Cardiac
Shock
tone vascular capacity return output
 Chapter-4: Physiology (Cardiovascular Module) | 119

Causes
➢ Deep general anaesthesia
➢ Vasomotor anaesthesia
➢ Brain damage cause of vasomotor paralysis
Features
Instability in
• Blood pressure
• Temperature regulation
• Heart rate
Anaphylactic shock
Anaphylaxis is an allergic condition in which the cardiac output and arterial pressure often decrease drastically
Pathophysiology
Antigen antibody complex formation → Release of histamine and slow reacting substance bradykinin → Increase vascular
capacity → Increase capillary permeability → Loss of fluid into interstitial spaces → Venous return decrease → Cardiac
output decrease.
Causes
➢ Antigens entering blood
➢ Food especially nuts and shell fish
➢ Latex found in disposable gloves and syringes
➢ Medication penicillin and aspirin
Clinical features
• Skin reaction hives and itching
• Hypotension
• Nausea vomiting diarrhoea
Treatment in different types of shock
• Blood and plasma transfusion
• Dextrose solution.
• Sympathomimetic drugs in neurogenic and anaphylactic shock
• Head down position
• Oxygen therapy
• Glucocorticoid treatment
Stages of different types of shock
1- Non progressive stage: In which the normal circulatory compensatory mechanisms cause full recovery without help
from outside therapy
2- A progressive stage: In which the shock becomes worse without therapy until death occurs
3- An irreversible stage: Shock has progressed to such an extent that all forms of known therapy are inadequate to save
the person’s life
Mechanisms that lead to non-progression of shock
• Baroreceptor reflexes, which initiate powerful sympathetic stimulation of the circulation
• Central nervous system ischemic response, which initiate even more powerful sympathetic stimulation
throughout the body
• Reverse stress- relaxation of the circulatory system, which causes the blood vessels to contract around the
diminished blood volume
• Increased secretion of renin by the kidneys and formation of angiotensin II, which constricts the peripheral
arterioles and also causes decreased output of water and salt by the kidneys.
• Increased secretion by the adrenal medullae of epinephrine and norepinephrine.

Join Medico Express Free Guidelines Group

03346072846
120 | 1st year MBBS – Block-3

• Compensatory mechanisms that return the blood volume back towards normal

Progression of shock
 Chapter-4: Physiology (Cardiovascular Module) | 121

• Enlist the different types of heart sounds and explain the physiological Physiology Heart
CV- basis of each. sounds
P-017 • Enlist the causes of 3rd and 4th heart sounds.
• Explain the causes & physiological basis of murmurs caused by valvular
lesions.
• Enumerate abnormal heart sounds and describe the physiological basis of
each.

Heart sound:
First Heart Sound Second Heart Sound
Due to closure of AV valve Due to closure of Semilunar Valve
First heart sound is produced during isometric contraction Second heart sound is produced at the end of Systolic
period and earlier part of ejection period period
First heart sound is a long, soft and low-pitched sound Second heart sound is a short, sharp and high-pitched sound
It resembles the spoken word ‘LUBB’ It resembles the spoken word ‘DUBB’
Duration of first heart sound is about 0.14 seconds Duration of second heart sound is about 0.11 seconds. The
reason for shorter duration is that Semilunar valves are
tauter than AV valves

3rd Heart Sound 4th Heart Sound

It is due to oscillation of blood back and forth b/w walls of It is due to contraction of Atria and rushing of blood
ventricle
Third heart sound is produced at middle third of diastole Fourth heart sound is produced during Atrial systole
It maybe physiological or pathological It is always Pathological
Normal: Exercise Pathological: ventricular hypertrophy
Pathological: Systolic heart failure

Splitting of 2nd Heart Sound:

Physiological: Inspiration split 2nd heart sound because pulmonary valve closes later than aortic
Pathological: Defect in Bundle branch especially right bundle branch
Heart Murmurs
Systolic murmur of aortic stenosis
Blood flows with difficulty from ventricles to aorta → Pressure rise to 300 mmHg in left ventricle →Blood flow with high
velocity from left ventricle to aorta →this phenomenon cause severe turbulence of blood in aorta.
Systolic murmur of mitral regurgitation.
Backward flow of blood through mitral valve into left atrium during systole creates systolic murmur of mitral regurgitation.
Diastolic murmur of mitral regurgitation
Blood flow backward from high pressure aorta into left ventricle
Diastolic murmur of mitral stenosis.
Blood flow with difficulty from atria into ventricles during mitral stenosis →Pressure in left atrium rise above 30 mmHg
→this create diastolic murmur of mitral stenosis

Join Medico Express Free Guidelines Group

03346072846
122 | 1st year MBBS – Block-3

Abnormal heart sounds

Abnormal heart sounds is known as murmur.
• Systolic murmur
• Pansystolic murmur due to mitral regurgitation.
• Ejection murmur arise from pulmonary and aortic outflow tract
• Late systolic murmur due to mitral valve prolapse
• Diastolic murmur
• Early diastolic murmur due to aortic or pulmonary regurgitation
• Mid diastolic murmur arise from mitral valve
 Chapter-4: Physiology (Cardiovascular Module) | 123

MCQ PEARLS
CV-P-001 (Cardiac Muscle)
1. What type of muscle is the heart composed of? Cardiac muscle
2. Which of the following is NOT a property of cardiac Rigidity
muscles?
3. Which phase of the cardiac action potential involves Phase 0
the opening of fast sodium channels?
4. What occurs during Phase 2 of the cardiac action Calcium channels open and potassium channels close
potential?
5. During which phase of the cardiac cycle does the Isovolumetric Relaxation
aortic valve close?
6. What is the ejection fraction (EF) of the heart if the 0.6
end-diastolic volume (EDV) is 120 ml and the end-
systolic volume (ESV) is 40 ml?
7. The refractory period during which the heart muscle Relative refractory period
is more difficult to excite than normal but can be
excited by a very strong signal is called:
8. Which of the following is NOT a phase of the Ventricular Diastole
cardiac cycle?
9. What is the approximate duration of the cardiac 0.833 seconds
cycle if the heart rate is 72 beats per minute?
10. The 'T wave' in an ECG represents: Repolarization of the ventricles
11. What causes the second heart sound (S2)? Closure of the aortic and pulmonary valves
12. The end-diastolic volume (EDV) is 110-120 ml
approximately:
13. What causes the 'a wave' in atrial pressure Atrial contraction
changes?
14. During which phase does the ventricle reach its Period of Isovolumetric Relaxation
end-systolic volume?
15. What is the stroke volume output if the end- 70 ml
diastolic volume is 120 ml and the end-systolic
volume is 40 ml?

CV-P-002 (Regulation of heart pumping)

1. What is the intrinsic ability of the heart to adapt to Frank-Starling mechanism
increasing volumes of inflowing blood called?
2. How much can the heart rate increase with From 70 beats/min to 180-200 beats/min
sympathetic stimulation?
3. What effect does sympathetic inhibition have on Decreases cardiac pumping by about 30%
cardiac pumping?
4. What can strong vagal stimulation do to the heart Can cause the heart to stop briefly, then beat at 20-40
rate? beats/min
5. What is the main impact of vagal stimulation on the Less impact on ventricles
ventricles?
6. How does increased calcium affect heart Causes spastic contraction
contraction?

Join Medico Express Free Guidelines Group

03346072846
124 | 1st year MBBS – Block-3

7. What is the effect of increased potassium Heart becomes dilated, heart rate decreases, impulse
concentration on the heart? transmission through AV bundle blocked
8. What happens to cardiac function with a moderate Increases contractile strength of heart
increase in temperature?
9. What is the definition of a chronotropic effect? Changes the heart rate
10. What does a positive dromotropic effect do? Increases conduction velocity
11. Where are Alpha 1 adrenoceptors located in the On myocytes of heart
heart?
12. What effect does sympathetic stimulation have on Increases conduction velocity
the conduction velocity of the heart?
13. Which receptors are primarily affected by M2 muscarinic receptors on SA and AV Node
parasympathetic stimulation in the heart?
14. What effect does acetylcholine have on cardiac Increases permeability to K+, causing
fibers' membrane permeability? hyperpolarization
15. What effect does a positive inotrope have on the Increases contractility
heart?

CV-P-003 (Conducting system of heart)

1. What acts as the pacemaker of the heart? SA node
2. What causes the delay in transmission at the AV Slow conduction, fewer gap junctions, slow Na+ and
node? Ca+ channels
3. What is the approximate delay caused by the AV About 0.13 seconds
node and AV bundle?
4. What pathway conducts impulses from the SA node Internodal pathway
to the AV node?
5. How do Purkinje fibers contribute to cardiac Transmit impulses very rapidly from AV node
impulse transmission? throughout ventricles
6. What is the resting membrane potential of the heart? -55 to -60 mV
7. Why is the transmission of cardiac impulses very Decreased number of gap junctions
rapid in Purkinje fibers?

CV-P-004 (Fundamentals of ECG)

1. What is a pacemaker elsewhere than the sinus node Ectopic pacemaker
called?
2. How many times per minute does the AV node 40-60 times per minute
conduct impulses?
3. What causes the delay in the AV node? Slow conduction, fewer gap junctions, and slow Na+
and Ca+ channels
4. What syndrome is associated with a new pacemaker Stokes-Adams Syndrome
developing in the Purkinje system?
5. What does the P wave on an ECG represent? Atrial depolarization
6. What is the duration of the QT interval? 0.35 seconds
7. What is the purpose of Einthoven’s Law? To relate the potentials recorded in leads I, II, and III
8. Where is the J point located on an ECG? At the end of the QRS complex
9. What is the significance of a biphasic T wave on an Digitalis toxicity
ECG?
10. What are the typical ECG changes in myocardial ST segment elevation, T wave inversion, Deep Q
infarction? wave
 Chapter-4: Physiology (Cardiovascular Module) | 125

CV-P- 005 (Effect of electrolyte on ECG)

1. What ECG change is typically associated with Flattened P wave and peaked T wave
hyperkalemia?
2. What ECG finding is indicative of hypokalemia? Shallow T wave and prominent U wave
3. What effect does hypercalcemia have on the ST ST segment elevation
segment of an ECG?
4. How does hypocalcemia typically affect the QT Prolongation of the QT interval
interval on an ECG?
5. What ECG change is associated with hyperkalemia Prolonged QRS duration
and hypocalcemia?

CV-P- 006 (Cardiac arrhythmia)

1. What is the typical heart rate associated with Faster than 100 beats/min
tachycardia in an adult?
2. What is a common cause of bradycardia? Hypothyroidism
3. Which type of arrhythmia is characterized by Respiratory type of sinus arrhythmia
alternating increases and decreases in impulses?
4. What is a key ECG finding in 1st-degree AV block? Prolonged PR interval (>220 msec)
5. Which ECG change is associated with 3rd-degree No correlation between P wave and QRS complex
AV block?
6. What condition is characterized by a premature Premature atrial contraction (PAC)
contraction of the heart before the expected time?
7. What is a common management approach for atrial Medication, CPR, defibrillation, catheter ablation
fibrillation?
8. Which arrhythmia is associated with rapid Atrial flutter
contraction of the atria at 200 to 350 beats per minute?
9. In which arrhythmia are P waves typically absent Atrial fibrillation
on the ECG?
10. What is the main difference between atrial flutter Atrial flutter has coordinated electrical activity; atrial
and atrial fibrillation? fibrillation does not.

CV-P-007 (Organization of Circulation)

1. Which type of blood vessel has a narrow lumen Arteries
diameter?
2. What is the primary function of capillaries? Carry blood from arteries to veins and exchange
material with tissues
3. Which blood vessel type has valves to prevent Veins
backflow?
4. What is a key characteristic of the walls of veins Veins have thinner walls than arteries
compared to arteries?
5. Which blood vessel type is characterized by having Arteries
a thick wall with three layers: Tunica Adventitia,
Tunica Media, and Tunica Intima?

CV-P-008 (Blood flow)

1. What is the average functional pressure in systemic 17 mm Hg
capillaries?

Join Medico Express Free Guidelines Group

03346072846
126 | 1st year MBBS – Block-3

2. Which pressure measurement is characteristic of the 25 mm Hg

pulmonary artery systolic pressure?
3. In which type of blood flow does the blood move in Laminar Flow
parallel layers with minimal disruption?
4. What does Reynolds number measure in the context The tendency for turbulence to occur
of blood flow?
5. Which of the following is NOT a factor directly Viscosity of blood
proportional to Reynolds number?
6. What is the systolic pressure in systemic 120 mm Hg
circulation?
7. What is the mean pulmonary arterial pressure? 16 mm Hg
8. What type of flow occurs when blood encounters an Turbulent Flow
obstruction and forms eddy currents?
9. Which pressure in systemic circulation is 80 mm Hg
considered the diastolic pressure?
10. How does Reynolds number relate to blood flow Inversely proportional
in terms of viscosity?

CV-P-009 (Local & Humoral Control of Blood

flow)
1. What theory suggests that blood vessels dilate in Oxygen or nutrient demand theory
response to increased oxygen or nutrient demand?
2. Which of the following is a vasodilator agent? Histamine
3. Which vasoconstrictor agent is associated with Epinephrine
increasing blood pressure and vasoconstriction?
4. What process involves the growth of new blood Angiogenesis
vessels in response to low oxygen levels?
5. Which key factor is involved in the process of Vascular Endothelial Growth Factor (VEGF)
angiogenesis?
6. How do collateral vessels respond to an artery or Initial dilation of small vascular loops
vein blockage in the short term?
7. What is a significant example of collateral Coronary Artery Thrombosis
circulation development?
8. Which organ shows excellent autoregulation of All of these organs
blood flow during changes in arterial pressure?
9. What theory explains blood flow regulation based Myogenic Theory
on muscle responses to pressure changes?
10. Which metabolic condition would increase blood Increase CO2
flow due to increased CO2 levels?

CV-P-010 (Nervous Regulation of circulation)

1. Which type of autonomic stimulation increases Sympathetic stimulation
heart rate and contractility?
2. What is the primary effect of parasympathetic Decrease in heart rate
stimulation on the heart?
3. Where is the vasomotor center located? Medulla and lower pons
4. Which area of the vasomotor center is responsible Vasoconstrictor area
for vasoconstriction?
 Chapter-4: Physiology (Cardiovascular Module) | 127

5. The vasodilator area of the vasomotor center Vasoconstrictor activity

inhibits which type of activity?
6. Which higher nervous center can exert powerful Hypothalamus
effects on the vasomotor center?
7. What is the role of the sensory area of the Provides reflex control and helps control the
vasomotor center? vasoconstrictor and vasodilator areas
8. What causes vasovagal syncope? Intense emotional disturbances leading to rapid fall in
arterial pressure
9. According to Starling’s hypothesis, which factor Capillary plasma colloid osmotic pressure (Πp)
tends to force fluid inward through the capillary
membrane?
10. What is the net filtration pressure (NFP) in the NFP = Pc - Pif - Πp + Πif
capillaries calculated as?

CV-P-011 (Rapid control of arterial blood

pressure)
1. What happens to systemic arterioles during a rapid They are constricted, increasing total peripheral
increase in arterial pressure? resistance.
2. How does the sympathetic nervous system affect Veins are strongly constricted, displacing blood
veins during a rapid increase in arterial pressure? towards the heart.
3. What is the role of the autonomic nervous system It stimulates the heart, increasing cardiac pumping.
in the heart during rapid increases in arterial pressure?
4. During heavy exercise, what primarily fulfills the Local vasodilation and sympathetic nervous response.
increased blood flow requirement of muscles?
5. Which reflex is initiated by stretch receptors in Baroreceptor reflex
large systemic arteries?
6. Where are peripheral chemoreceptors located? Carotid body and aortic body
7. What triggers the chemoreceptors to send signals to Lack of oxygen, excess carbon dioxide, or increased
the brain? hydrogen ion concentration.
8. What is the primary response of the Bainbridge Increased heart rate and contractility to prevent blood
reflex? accumulation.
9. In the CNS ischemic response, what causes intense Decreased blood flow to the brain, leading to ischemia
vasoconstriction of peripheral nerves? and increased CO2.
10. What occurs during the Cushing reflex? Increased CSF pressure causes brain arteries to be
compressed, leading to increased arterial pressure.

CV-P-012 (Role of kidneys in long term Regulation

of Arterial Blood Pressure)
1. Where is prorenin synthesized and stored? In the juxtaglomerular (JG) cells of the kidneys.
2. What triggers the activation of prorenin to release A fall in arterial pressure.
renin?
3. What does renin act on to convert it to angiotensin Angiotensinogen (renin substrate).
I?
4. What is the product of the conversion of Angiotensin I.
angiotensinogen by renin?
5. How is angiotensin I converted to angiotensin II? By the removal of two additional amino acids.
6. What is the primary effect of angiotensin II on It acts as a powerful vasoconstrictor, raising arterial
blood vessels? pressure.

Join Medico Express Free Guidelines Group

03346072846
128 | 1st year MBBS – Block-3

7. Which hormone is released by the adrenal gland in Aldosterone.

response to angiotensin II?
8. What role does angiotensin II play in the regulation It activates the thirst center.
of thirst?
9. How does the body respond to an increase in By regulating blood volume through mechanisms like
extracellular fluid (ECF) volume? increased salt retention and fluid balance.
10. What is a common response to increased salt Increased blood volume due to enhanced salt
intake in terms of blood volume regulation? retention.

CV-P-013 (Cardiac output)

1. What is the formula for calculating cardiac output? Cardiac Output = Stroke Volume × Heart Rate.
2. What is the normal range of cardiac output in 5 to 6 L/min.
adults?
3. Which factor increases cardiac output by increasing Increased contractility.
stroke volume?
4. How does increased afterload affect cardiac output? It decreases cardiac output by increasing resistance.
5. What happens to cardiac output when there is an It increases due to increased venous return.
increase in tissue metabolism?
6. What is the relationship between venous return and Venous return = Cardiac Output.
cardiac output according to the Frank-Starling
mechanism?
7. How does an increase in mean systemic filling It increases venous return.
pressure affect venous return?
8. What is the cardiac index and what is its normal Cardiac Output per square meter of body surface area;
value for a 70 kg man? Normal value = 3 L/min/m².
9. Which condition is a pathological cause of high Hyperthyroidism.
cardiac output?
10. Which condition is a pathological cause of low Myocardial infarction.
cardiac output?

CV-P-014 (Skeletal muscle circulation)

1. What is the blood flow to skeletal muscle during 3 to 4 ml/min/100 g
rest?
2. During muscle contraction, how does blood flow Decreases
through skeletal muscles change?
3. Which chemical factors contribute to increased Increased hydrogen ion concentration
blood flow to skeletal muscles?
4. What is a unique feature of sympathetic nerve fibers They are vasodilators
supplying skeletal muscles?
5. During exercise, what happens to the mean Mean systemic filling pressure increases, cardiac
systemic filling pressure and cardiac output? output increases

CV-P-015 (Coronary circulation)

1. Which artery primarily supplies the anterior and left Left coronary artery
lateral portions of the left ventricle?
2. What is the primary venous drainage route for the Anterior cardiac veins
right ventricle?
 Chapter-4: Physiology (Cardiovascular Module) | 129

3. What is the common manifestation of coronary Angina pectoris

artery disease characterized by chest pain and left arm
radiation?
4. What substances are known to stimulate sensory Substance P, histamine, kinin
nerve endings and cause pain during myocardial
ischemia?
5. What are common treatments for angina pectoris? Vasodilator drugs, calcium channel blockers, beta
blockers
6. What is myocardial infarction also commonly Heart attack
known as?
7. What is a common cause of myocardial infarction? Embolus, thrombus, vascular spasm
8. What are the common symptoms of myocardial Cardiac pain, nausea, vomiting, palpitations,
infarction? difficulty in breathing, extreme weakness, sweating,
anxiety
9. Which treatment options are used for myocardial Aspirin, nitroglycerine, morphine, beta blockers,
infarction? oxygen
10. What type of myocardial infarction occurs in Subendocardial infarction
subendocardial muscles due to decreased diastolic
arterial pressure?

CV-P-016 (Circulatory shock)

1. What is the primary characteristic of hypovolemic Decreased blood volume
shock?
2. What are common causes of hypovolemic shock? Hemorrhage, plasma loss due to burns, dehydration,
diarrhea, vomiting, sweating
3. What is septic shock associated with? Presence of pathogenic organisms or toxins in blood
or tissues
4. Which type of shock is characterized by sudden loss Neurogenic shock
of vasomotor tone and massive dilation of veins?
5. What causes anaphylactic shock? Antigen-antibody complex formation leading to
histamine and bradykinin release
6. Which type of shock is associated with high fever, Septic shock
high cardiac output, and vasodilation?
7. What are common clinical features of anaphylactic Skin reactions (hives, itching), hypotension, nausea,
shock? vomiting, diarrhea
8. What is a common treatment method for different Blood and plasma transfusion, dextrose solution,
types of shock? oxygen therapy, glucocorticoids
9. In which stage of shock do compensatory Non-progressive stage
mechanisms allow for full recovery without external
therapy?
10. Which mechanisms lead to non-progression of Baroreceptor reflexes, CNS ischemic response,
shock? reverse stress-relaxation, renin-angiotensin system,
increased epinephrine/norepinephrine secretion

CV-P-017 (Heart sounds)

1. Which heart sound is produced by the closure of the First heart sound
AV valves?
2. What is the characteristic duration of the second 0.11 seconds
heart sound?

Join Medico Express Free Guidelines Group

03346072846
130 | 1st year MBBS – Block-3

3. The third heart sound is usually produced during Middle third of diastole
which phase of the cardiac cycle?
4. Which of the following is true about the fourth heart It is associated with ventricular hypertrophy
sound?
5. What causes the physiological splitting of the Delayed closure of the pulmonary valve
second heart sound during inspiration?
6. Which type of murmur is associated with a Systolic murmur of mitral regurgitation
backward flow of blood through the mitral valve
during systole?
7. What is the cause of a diastolic murmur in mitral Blood flow difficulty from atria into ventricles
stenosis?
 Chapter-4: Physiology (Cardiovascular Module) | 131

UNIVERSITY QUESTIONS
HEART
Q1: What is sinus arrhythmia and its mechanism? (Annual 2007)
Q2: What are the features and cause of second and third heart sounds? (Supple 2007)
Q3: Define refractory period and its types. What is its mechanism? Give the normal value of absolute refractory period of
ventricular muscle. (Annual 2008)
Q4: Draw the normal ECG. Show its waves and intervals. Give two changes in ECG in a patient of acute myocardial
infarction. (Annual 2008)
Q5: What are the pressure changes in the Atria during the cardiac cycle? Give the relationship of these atrial pressure
changes with the juglar venous pulse. (Supple 2008).
Q6: A 60 yr. old lady falls down while climbing stairs. On examination in a hospital emergency here B.P 60/40 mmHg,
Pulse rate 300/min and irregular, ECG dissociation b/w P waves and QRS complex.
(a) What is type this heart block?
(b) Give further Management.
(c) What is stoke Adam Syndrome.
Q7: A woman of 50 yr presents with irregularly irregular pulse, pulse deficit. Her ECG shows small irregular waves
replacing P waves and QRS complexes at unequal distance. (Annual 2010).
a. Name the condition?
b. What is mechanism of this condition?
c. What are the features of this condition?
Q8: What are volume changes in the ventricles during the cardiac cycle? What is ejection fraction? Give its normal value.
(Supple 2010)
Volume changes in ventricles during cardiac cycle
Q9: What are the pressure changes in atria during the cardiac cycle? How are these atrial pressure changes related to the
juglar venous pulse? (Annual 2011)
Q10: Explain the spread of cardiac impulse after its origin. (Annual 2012)
Q11: (a) Draw and label ventricular muscles action potential.
(b) Specify role of different ionic channels in production of action potential. (Annual 2013)
Q12: (a) What is frank starling law of hart and its significance? (Supple 2013)
(b) Write briefly about premature ventricular contractions (PVCs).
Q13: (a) Give mechanism of production of different waves in right atrial pressure tracing during cardiac cycle. (Annual
2014)
(b) How will you correlate these waves with different heart sounds production during cardiac cycle?
Q14: Draw ventricular muscle action potential; give role of different ionic channels in this action. (Supple 2014).
Q15: (a) Define cardiac index and cardiac reserve. Give their normal values. (Annual 2015)
(b) What are volume changes in the ventricles during the cardiac cycle?
Q16: (a) Give features and causes of 1st and second heart sounds.
(b) What are effects of sympathetic stimulation on the heart? (Supple 2015)
Q18. Draw one ECG complex and show a U-wave on it. What is the cause of this occasional wave? (Supple 2016)
Q19. a) Describe the transmission of cardiac impulse through the heart. Elaborate your answer with a labeled diagram.
(Annual 2017)
b) What is the effect of parasympathetic (vagal) stimulation on SA node and AV node.
Q20. Draw, label and describe the aortic and left ventricular pressure changes during the cardiac cycle. (Supplementary
2017 held in 2018)
Q21. a) Describe the transmission of cardiac impulse through the heart. (Annual 2018)

Join Medico Express Free Guidelines Group

03346072846
132 | 1st year MBBS – Block-3

Elaborate your answer with a labeled diagram.

b) What is the effect of parasympathetic system stimulation on SA node and AV node?
Q22. Give brief outline of: (Supplementary 2018 held in 2019)
(a) Effect of vagal stimulation on SA nodal action potential. 2.5
(b) Ventricular excitation by action potential. 2.5
Q23. a) Enlist the left ventricular pressure changes during all phases of cardiac cycle. Elaborate your answer with the help
of a diagram. 2,1 (Annual 2019)
b) Compare the effects of hyperkalemia and hypercalcemia on heart pumping. 2
Q24. a) Give the physiological basis and ECG changes of complete Atrioventricular Heart Block.
b) Explain the features and pathophysiology of Stokes Adams syndrome. (Supply 2019 held in 2020)
Q25. a) Explain the pathophysiology of Adam-Stokes syndrome.
b) Classify and explain the atrioventricular (AV) heart blocks. Illustrate your answer with the help of diagrams.
(Annual 2020)
Q26. a) Describe the first second- and third-degree heart blocks and draw their ECG pictures. (Supply 2020 held in 2021)
b) Draw and label aortic pressure changes during different phases of cardiac cycle.
Q27. a) Enumerate the mechanism of absolute refractory period that develops just after the onset of an action potentiaí.
What is the significance of prolonged refractory period in cardiac muscle? (Annual 2022 held in 2023)
Q28. a) Enlist different types of heart blocks. (Supply 2022 held in 2023)

CIRCULATION
Q1: How is coronary blood flow regulated? (Annual 2007)
Q2: What is the role of baroreceptors in the body? (Supple 2007)
Q3: A middle aged man riding on a bicycle was hit by speedy car. He got multiple injuries and fell on the ground. He was
taken to emergency department of the hospital after 1 hour. He was bleeding profusely from wounds. He was drowsy. On
examination radial pulse was rapid. Skin was pale, cold and clammy. Arterial B.P was 70/50 mmHg. (Annual 2008)
(a) Which type of was he having?
(b) Why was radial pulse rapid & thready?
(c) Why was skin pale, cold & clammy?
(d) Why was arterial pressure low?
Q4: Enlist different mechanisms of arterial blood pressure regulation. What is the role of barorecptors for maintaining the
arterial blood pressure? (Supple 2008).
Q5: A 50 yr old barber gradually develops elongated, tortuous and dilated veins in the legs.
a. What is the condition? (Annual 2009)
b. Enlist factors that affect venous return
c. How are veins controlled by nervous system?
d. How do inspiration and expiration affect venous return?
Q6: During the medical checkup of a healthy man of 20 years, which heart sounds can be auscultated? Give their features
and mechanism of production. (Annual 2010).
Q7: A man 45 years old was injured during a road accident. He had profuse bleeding from his wound. When he was
brought to emergency department of the nearly hospital, he was drowsy. His arterial pulse was 130/min and thread. Blood
pressure was 70/50mmHg, skin was pale, cold clammy. (Supple 2010).
a. Which condition the man was having?
b. Why was his skin pale, cold clammy?
c. Give the mechanisms which could raise his blood pressure.
Q8: A middle aged man had profuse bleeding from multiple injuries during a road side accident. His PB dropped to
70/50mmHg. Give mechanisms which helped to raise his BP. (Annual 2011).
 Chapter-4: Physiology (Cardiovascular Module) | 133

Q9: A middle aged man was hit by a speedy car infliciting multiple injuries. He had profuse bleeding from his wound.
When he was brought to emergency department of the nearby hospital, he was drowsy. His arterial pulse was 130/min and
thread. Blood pressure was 60/4 0mmHg, skin was pale, cold clammy. (Supple 2011).
a. Which condition the man was having?
b. Why was his skin pale, cold clammy?
c. Give the mechanisms which could raise his blood pressure.
Q10: Write notes on: (Annual 2012)
a) Oxygen lack (nutrient lack) theory for control of local blood flow
b) Central nervous system ischemic response
Q11: (a) Define cardiac output and ejection fraction, (Annual 2013)
Q12: (a) A young man at rest has blood pressure 120/75 mmHg. After exercise it becomes 130/85 mmHg. Find out his
pulse pressure and mean blood pressure at rest and after exercise.
(b) What is role of rennin angiotensin mechanism in the body? (Supple 2013)
Q13: A student fainted upon listening to the shocking news of the failure in an examination.
(a) Give the pathophysiology basis of fainting in this case.
(b) What happen to the mean systemic filling pressure and venous return in this case?
(c) How total peripheral resistance is altered in a patient having septic shock? (Annual 2014)
Q14: Explain pathophysiology of progressive shock. (Supple 2014)
Q15: A young man bleeds profusely during a road traffic accident. His blood pressure falls to 80/55mmHg. Outline
mechanism which will help to raise his blood pressure. (Annual 2015)
Q16: (a) A man has high cerebrospinal fluid pressure. Give the mechanism by which cerebrospinal blood flow in
maintained?
(b) What is electromagnetic flow meter? (Supple 2015)
Q17: A middle aged male bleeds profusely due to a Road Traffic Accident. His blood pressure falls to 70/55 mmHg.
(Annual 2016)
a) Calculate his mean blood pressure. 03
b) Give mechanisms by which his blood pressure will be raised. 02
Q18: a) Enlist all the mechanisms controlling Arterial Blood Pressure. What is Cushing’s Reaction? 02,1.5
(b) Intermediate Time period Pressure Control Mechanism: 1.5
(a) Rapidly acting pressure control Mechanisms:
Q19: a) Define Cardiac Output and Cardiac Index. Give normal value. 02
b) How the Cardiac Output is measured by using the Oxygen-Fick principle. (Supple
Q20: During clinical rounds, the Medical Consultant presented a patient who had mean arterial pressure reduced to
70mmHg. He explained to the students that the baroreceptor reflex mechanism can normalize the arterial pressure. How
does this mechanism normalize reduced arterial pressure? 5 (Annual 2017)
Q21: a) Give four observations in favour of the fact that true interstitial fluids pressure in loose subcutaneous tissue is sub
atmospheric. 2 (Supplementary 2017 held in 2018)
b) Draw and enlist the factors that can cause a hypereffective and hypoeffective heart. 3
Q22: a) How do baroreceptors normalize reduced arterial pressure in a patient who has mean arterial blood pressure
reduced to 65 mm of Hg. (Annual 2018)
b) How Total Peripheral Resistance (TPR) is altered in a patient having septic shock?
Q23: Define circulatory shock. Write down the mechanism of myocardial depression and vasomotor failure in progressive
state of Hypovolemic (Hemorrhagic) shock. (Supplementary 2018 held in 2019)
Q24: a) Make a list of all the blood pressure control mechanisms according to the timeframe within which they come into
play and discuss only stress relaxation and capillary fluid shift mechanism in detail. 1.5, 0.5, 0.5
Q25: a) Explain pathophysiology and causes of neurogenic shock. (Supple 2019 held in 2020)
b) Give the physiological basis of vasovagal syncope.
Q26: a) What is the role of Baroreceptors in controlling the blood pressure?

Join Medico Express Free Guidelines Group

03346072846
134 | 1st year MBBS – Block-3

b) What is Bainbridge reflex?

c) Briefly describe Cushing reaction. (Annual 2020)
Q27: Explain the role of kidney in the regulation of blood pressure, when the mean arterial
pressure falls to 80 mmHg due to hemorrhage. (Supply 2020 held in 2021)
Q28: a) Give the mechanism of production of different waves in right atrial pressure tracing during a cardiac cycle. (Annual
2021 held in 2022)
b) Draw and label SA node action potential and ventricular action potential. How is it
different from ventricular action potential?
Q29: a) Explain the spread of cardiac Impulse through the heart. Why this impulse delays at the AV node? (Supply 2021
held in 2022)
b) Draw the ECG of a person with complete atrioventricular (AV) block and briefly mention the pathophysiology of
Stokes-Adam Syndrome.
Q30: A middle aged man riding on a bicycle was hit by a speedy car. He got multiple injuries and fell on the ground. He
was taken to emergency department of the hospital after an hour. He was bleeding profusely from wounds and was drowsy.
On examination radial pulse was rapid and thread. Skin was pale, cold and clammy. Arterial blood pressure was 70/50 mm
of Hg. (Annual 2021 held in 2022)
a) Name the condition he is suffering from.
b) Why was radial pulse rapid and thready?
c) Why was skin pale, cold and clammy?
d) Give mechanisms which helped to raise his blood pressure.
Q31: a) Describe the nervous reflex which is initiated when the cerebrospinal fluid pressure rises to equal the arterial
pressure. (Supply 2021 held in 2022)
b) What is phonocardiogram? Contrast the features of first and second heart sounds.
Q32. a) What are baroreceptors? How they minimize blood pressure fluctuations In changing posture? (Annual 2022 held
in 2023)
b) A guard at mausoleum of Allama Iqbal gets tortuous distended veins of legs.
i. What Is this condition called?
ii. What is significance of venous valves and venous pumps?
Q33. A 30 years old man was brought to emergency after a road traffic accident. He was bleeding from his right leg and
his pulse was rapid and slightly weak. His mean blood pressure was 80 mm of mercury. Briefly outline the various
compensatory mechanisms that prevent further deterioration of the circulation in this case. (Annual 2022 held in 2023)
Q34. How a vicious cycle of cardiovascular deterioration makes a shock progressive? (Supply 2022 held in 2023)
 Chapter-4: Physiology (Cardiovascular Module) | 135

Chapter – 04
PHYSIOLOGY
Enlist the muscles of inspiration and expiration in quiet breathing Physiology Breathing
Re-P- Enlist the muscles of inspiration and expiration in labored breathing
001 Explain the components of the work of breathing Discuss the mechanics of
pulmonary ventilation Explain periodic breathing Explain the causes and
pathophysiology of sleep apnea

Respiration
“Exchange of O2 and CO2 between environment and organism is called respiration”
Muscles involved in quiet breathing:
Normal quiet breathing is accomplished almost entirely by diaphragm.
Muscles involved in laboured breathing:
During forced inspiration:
1. External intercostal (raise the rib cage)
2. Sternocleidomastoid (elevated sternum)
3. Anterior serrati
4. Scalene (elevates first two ribs)
During forced expiration:
1. Abdominal recti (primary muscle)
2. Internal intercostal (pull ribs downward and inward)
Components of Respiration:
• Pulmonary ventilation which means inflow and outflow of air b/w atmosphere and lung alveoli
• Diffusion of O2 and CO2 b/w alveoli and blood
• Transport of O2 and CO2 in the blood and body fluids to and from the body's tissue cells
• Regulation of ventilation
Work of breathing:
During normal quiet breathing, all respiratory muscle contraction occurs during inspiration; expiration is almost entire
passive process caused by elastic recoil of the lungs and chest cage
The work of inspiration can be divided into three fractions:
1. That required to expand the lungs against the lung and chest elastic forces called compliance work or elastic
work
2. That required to overcome viscosity of the lung and chest wall structure called tissue resistance work.
3. That required to overcome airway resistance to movement of air into the lungs called airway resistance work.
Mechanics of Pulmonary ventilation:
• During inspiration, contraction of ribs and diaphragm causes ribs to elevate and diaphragm moves downward
and less domelike, space increases and pressure decreases hence, inward movement of gases.
• Antero-posterior and vertical diameter also increases.
• During expiration, relaxation of ribs and diaphragm causes ribs to move downward and diaphragm upward and
more domelike, space decreases and pressure increases hence, outward movement of gases.

Join Medico Express Free Guidelines Group

03346072846
136 | 1st year MBBS – Block-3

• Antero-posterior and vertical diameter also decreases.

Periodic Breathing:
• An abnormality of respiration in which a person breathes deeply for a short interval and then breathes slightly or
not at all for an additional interval, with the cycle repeating itself over and over.
• Cheyne-Stokes breathing is one type of periodic breathing.
Basic mechanism of Cheyne-stokes Breathing:
Step Description
Initial Increase in Breathing rate increases, causing more CO2 to be expelled from the body.
Respiration
Decrease in CO2 As CO2 levels drop, the inflow of O2 continues but takes time to stimulate the respiratory
center.
Delayed Response The respiratory center becomes depressed due to low CO2 when the over-ventilated blood
reaches the brain.
Cycle Reversal As CO2 levels start to increase and O2 levels decrease, the respiratory center becomes less
inhibited.
Breathing Resumes The person starts breathing harder again due to the delayed response from the brain.
Cycle Repeats The cycle of increased and decreased respiration continues, leading to the characteristic pattern.
Causes:
1. Heart failure
2. Hypoxemia
3. Hypo-perfusion of brain
4. Poor positioning in sleep
Sleep Apnea:
• During sleep, breathing stops suddenly.
• May be repeated 100’s of times in severe cases lasting for 10 seconds or longer.
Causes
1. Airway obstruction
2. Disease of CNS
3. Obesity
Pathophysiology of Obstructive sleep apnea:
• Caused by blockage of upper airway.
 Chapter-4: Physiology (Cardiovascular Module) | 137

Sleep

Upper airway tone decrease

Upper airway tone decrease

Obstructive apnea ( snoring)

Hypoxia and hypercapnia ( automatic stimulation )

Arousal (daytime sleepiness)

Upper airway tone increases

Breathing resumes and the cycle repeats itself over and

over again .

Associated factors:
Obstructive sleep apnea usually occurs:
1. In older obese persons in whom there is increased fat deposition in soft tissues of the pharynx
2. The compression of pharynx due to excessive fat masses in the neck
3. Nasal obstruction

Join Medico Express Free Guidelines Group

03346072846
138 | 1st year MBBS – Block-3

4. Enlarged tonsils
5. A very large tongue
6. Certain shapes of palate that increase resistance to the flow of air
Treatment:
• Surgery to remove excess fat tissue at the back of throat ( a procedure called uvulo-palatopharyngo-plasty) ,
remove enlarged tonsils or adenoids or create an opening in the trachea ( tracheostomy )
• Nasal ventilation with continuous positive airway pressure (CPAP)
Pathophysiology of central sleep apnea:
• Occurs when the neural drive to respiratory muscles transiently abolished.
Associated factors:
1. Damage to the central respiratory centres
2. Abnormalities of the respiratory neuromuscular apparatus
3. Patients with this disease are extremely sensitive to small doses of sedative narcotics, which further reduce the
responsiveness of the respiratory centres to the stimulatory effects of co2.
Treatment:
• Medications that stimulate the respiratory centres can sometimes be helpful, but ventilation with CPAP at night
is usually necessary
• Pure central sleep apnea accounts for less than 1% of case
 Chapter-4: Physiology (Cardiovascular Module) | 139

• Define and explain lung compliance. Physiology Lung

Re-P- • Enlist the factors that affect lung compliance. Compliance
002 • Draw the compliance diagram of air filled and saline filled lungs.
• Enlist the components of surfactant.
• Describe the role of surfactant in lung compliance.
• Explain the role of surfactant in premature babies

Lung Compliance:
• The extent to which the lungs will expand for each unit increase in transpulmonary pressure is called lung
compliance.
• It is the stretch ability of lungs and inverse of Elastance.
• Compliance of both lungs is 200 ml of air /cm H2O transpulmonary pressure.
• Compliance of lungs and thorax is less because thorax cage prevents the lungs from expansion. It's value is 110
ml of air/cm3 H20 transpulmonary pressure
Compliance Increase Compliance Decrease
Emphysema Pulmonary fibrosis
Old Age TB
Pleural thickening
Heart Diseases like LHF

Compliance diagram of lungs

Compliance diagram of lungs is a diagram relating lung volume changes to changes in pleural pressure which in turn,
alters transpulmonary pressure.
It consists of two curves:
• Expiratory compliance curve
• Inspiratory compliance curve
Characteristics:
• Elastic forces of the lung tissue (determined by elastin and collagen fibers)
• Elastic forces caused by surface tension of the fluid that lines the inside walls of alveoli
• Following figure compares the compliance diagram of lungs filled with saline solution and filled with air

Join Medico Express Free Guidelines Group

03346072846
140 | 1st year MBBS – Block-3

• When the lungs are filled with air, there is an interface between the alveolar fluid and the air in the alveoli.
• In the lungs filled with saline solution, there is no air-fluid interface and therefore the surface tension affect us
not present; only tissue elastic forces are operating in the lung filled with saline solution.
Surfactant:
It is a complex mixture of phospholipids (most important is dipalmitoyl phosphatidylcholine called lecithin) surfactant
lipoproteins and calcium ions secreted by type II alveolar epithelial cells.
Function:
• It is responsible for reducing surface tension thus causes lungs to collapse.
Role in premature babies:
• In fetus, surfactant synthesis begins from 24th to 35th gestational week.
• A Lecithin: Sphingomyelin ratio greater than 2:1 in amniotic fluid reflects mature levels of surfactant.
• In premature babies, due to lack of surfactant a disease occurs called healing membrane disease or
respiratory distress syndrome of newborn.
• Therefore, alveoli of these babies collapse which makes lung expansion difficult.
• Without immediate treatment, these babies die due to inadequate ventilation
 Chapter-4: Physiology (Cardiovascular Module) | 141

• Define the different lung volumes and capacities and their clinical Physiology Lung
Re-P- significance. volumes and
003 • Discuss Forced Expiratory Volume 1/ Forced Vital Capacity Capacities
(FEV1/FVC) ratio and its clinical significance.
• Enlist the lung volumes and capacities that cannot be measured by
spirometer.
• Define dead space & explain its types.
• Discuss FEV1/FVC ratio in relation to Bronchial Asthma.
• Discuss FEV1/FVC ratio in relation to Chronic Pulmonology
Obstructive Pulmonary disease/restrictive lung

Pulmonary Volumes:
Four pulmonary lung Volumes are the volumes that when added together, equal the, maximum volume to which the
lungs can be expanded.
The significance of each of these lung Volumes is the following:
i. The tidal volume is the volume of air inspired of expired with each normal breath. Its average amount is 500 ml
ii. The inspiratory reserve volume is the extra volume of air that can be inspired over and above the normal tidal
volume when the person inspires with full force. Average amount is 3000 ml.
iii. The expiratory reserve volume is the maximum extra volume of air that can be expired by forceful expiration
after the end of a normal tidal expiration. Amount is 1100 ml.
iv. The residual volume is the volume of air remaining in the lungs after the most forceful expiration. Amount is
1200 ml.
Pulmonary Capacities:
Combinations of two or more of the Volumes together called pulmonary capacities.
Important pulmonary capacities are the following:
i. The inspiratory capacity equals the tidal volume plus inspiratory reserve volume. It is the amount of air that a
person can breathe in beginning at the normal expiratory level and distending the lungs to maximum amount.
Amount is 3500 ml.
ii. The functional residual capacity equals the expiratory reserve volume plus the residual volume. This capacity is
the amount of air that remains in the lungs at the end of normal expiration. Amount is 2300 ml.
iii. The vital capacity equals the inspiratory reserve volume plus the tidal volume plus expiratory reserve volume.
This capacity is the maximum amount of air a person can expel from the lungs after first filling the lungs to
their maximum extent and then expiring to the maximum extent. Amount is 4600 ml.
iv. The total lung capacity is the max volume to which the lungs can be expanded with the greatest possible effort.
It is equal to the vital capacity plus the residual volume. Amount is 5800 ml.

Join Medico Express Free Guidelines Group

03346072846
142 | 1st year MBBS – Block-3

Forced expiratory volume (FEV-1):

It is the volume of air expelled in 1st second during determination of forced vital capacity.
Clinical Significance
• Decreased in obstructive lung disease.
• Decreased in those non-obstructive diseases which decreases vital capacity
Vital capacity Forced Vital Capacity (FVC):
It is the volume of air that can be forcefully expelled from the lungs after maximum inspiration.
Clinical significance
• Normal or decreased in obstructive lung disease.
• Always decreased in restrictive lung disease.
FEV-1/FVC ratio and clinical significance:
• Normal value is 75%
• It is characteristically decreased to below 60% in obstructive lung disease & not in restrictive.
• It is normal or increased in restrictive lung disease.
• In obstructive disease, fall in FEV-1 is greater than fall in FVC. So FEV-1/FVC ratio decreases up to 30%
• In restrictive disease, fall in FEV-1 and FVC are usually proportional & so FEV-1/FVC % remains within
normal limit up to 80%.
Type Disease Structures Involved
Restrictive Respiratory Diseases Polio myelitis CNS
Myasthenia gravis CNS and thoracic cavity
Flail chest (broken ribs) Thoracic cavity
Paralysis of diaphragm CNS
Spinal cord diseases CNS
Pleural effusion Thoracic cavity
Obstructive Respiratory Diseases Asthma Lower respiratory tract
Chronic bronchitis
Emphysema
Cystic fibrosis
Laryngotracheobronchitis Upper respiratory tract
Epiglottis
Tumors Upper and/or lower respiratory tract
Severe cough and cold with phlegm Upper respiratory tract

Lung Volumes and capacities that can't be measured with spirometer:

• Almost all Volumes and capacities are measured by Spirometry
• Functional residual capacity & Residual volume Total lung capacity cannot be measured by spirometry
• These are measured by helium dilution method.
Dead space
• Areas of lungs where gas exchange does not occur called dead space and air that fills these areas called dead
space air
• Its value is 150ml
Types:
Anatomical dead space:
• Volume of all the space of the respiratory system other than the alveoli and closely related gas exchange areas is
called anatomical dead space.
 Chapter-4: Physiology (Cardiovascular Module) | 143

Physiological dead space:

• In some alveoli gas exchange doesn't occur due to poor blood supply or any pathological condition called
alveolar dead space.
• If this space added to anatomical dead space called physiological dead space.

Join Medico Express Free Guidelines Group

03346072846
144 | 1st year MBBS – Block-3

• Define alveolar ventilation. Physiology Pulmonary ventilation

Re-P-004 • Define minute respiratory volume.
• Describe the pressures in the pulmonary system.

Alveolar ventilation:
The rate at which volume of new air reaches respiratory passage for gaseous exchange is called alveolar ventilation.
VA = Freq × (VT – VD)
Where VT = tidal volume, VD = physiological dead space
VA = 12 × (500 – 150) = 4200 ml /min
Minute Respiratory Volume:
It is the total amount of new air moved into the respiratory passages each mint.
MRV = tidal vol. × freq. = 500 × 12 = 6000 ml / min or 6 L /min
Pressures in Pulmonary circulation:
• Pulmonary blood vessels include pulmonary artery, which carries deoxygenated blood to alveoli of lungs and
bronchial artery, which supply oxygenated blood to other structures of lungs, and Pulmonary Vein which carry
blood from lungs to Heart
• The systolic pulmonary arterial pressure normally averages about 25 mm Hg in the human being
• The diastolic pulmonary arterial pressure is about 8 mm Hg
• The mean pulmonary arterial pressure is 15 mm Hg.
• The mean pulmonary capillary pressure is about 7 mm Hg
• The blood volume of the lungs is about 450 millilitres, about 9 percent of the total blood volume of the entire
circulatory system.
• Approximately 70 millilitres of this pulmonary blood volume is in the pulmonary capillaries, and the remainder
is divided about equally between the pulmonary arteries and the veins.
 Chapter-4: Physiology (Cardiovascular Module) | 145

• Describe the blood volume of the Lungs. Physiology Pulmonary

Re-P- • Describe the distribution and regulation of blood flow through the Circulation
005 lungs.
• Describe the mechanics of blood flow in the three blood flow zones
of the lung.
• Describe the effect of heavy exercise on pulmonary arterial pressure.
• Describe the function of pulmonary circulation when left atrial
pressure rises as a result of left-sided heart failure.
• Explain pulmonary capillary dynamics.

Blood Volume of Lungs

• The blood volume of the lungs is about 450 millilitres, about 9 percent of the total blood volume of the entire
circulatory system.
• Approximately 70 millilitres of this pulmonary blood volume is in the pulmonary capillaries, and the remainder
is divided about equally between the pulmonary arteries and the veins
• Under various physiological and pathological conditions, the quantity of blood in the lungs can vary from as
little as one-half normal up to twice normal.
• Failure of the left side of the heart or increased resistance to blood flow through the mitral valve as a result of
mitral stenosis or mitral regurgitation causes blood to dam up in the pulmonary circulation, sometimes
increasing the pulmonary blood volume as much as 100 percent and causing large increases in the pulmonary
vascular pressure
Blood Flow through Lungs
• The blood flow through the lungs is essentially equal to the cardiac output
• Under most conditions, the pulmonary vessels act as distensible tubes that enlarge with increasing pressure and
narrow with decreasing pressure.
• For adequate aeration of the blood to occur, the blood must be distributed to the segments of the lungs where
the alveoli are best oxygenated
• When the concentration of O2 in the air of the alveoli decreases below normal, especially when it falls below 70
percent of normal (i.e., below 73 mm Hg Po2), the adjacent blood vessels constrict, with vascular resistance
increasing more than fivefold at extremely low O2 levels.
• This effect is opposite to the effect observed in systemic vessels, which dilate rather than constrict in response
to low O2 levels
• Low O2 concentration may stimulate release of vasoconstrictor substances or decrease release of a vasodilator,
such as nitric oxide, from the lung tissue
• Hypoxia may directly induce vasoconstriction by inhibition of oxygen-sensitive potassium ion channels in
pulmonary vascular smooth muscle cell membranes.
• With low partial pressures of oxygen, these channels are blocked, leading to depolarization of the cell
membrane and activation of calcium channels, causing influx of calcium ions.
• The rise of calcium concentration then causes constriction of small arteries and arterioles
• Nervous stimulation of sympathetic system also increases vascular resistance hence decreasing blood flow
Regional pulmonary blood flow
• In the upright adult, the lowest point in the lungs is normally about 30 cm below the highest point, which
represents a 23 mm Hg pressure difference, about 15 mm Hg of which is above the heart and 8 below.
• That is, the pulmonary arterial pressure in the uppermost portion of the lung of a standing person is about 15
mm Hg less than the pulmonary arterial pressure at the level of the heart, and the pressure in the lowest portion
of the lungs is about 8 mm Hg greater
• Under different normal and pathological lung conditions, one may find any one of three possible zones
(patterns) of pulmonary blood flow, as follows:

Join Medico Express Free Guidelines Group

03346072846
146 | 1st year MBBS – Block-3

Zone 1: No blood flow during all portions of the cardiac cycle because the local alveolar capillary pressure in that area of
the lung never rises higher than the alveolar air pressure during any part of the cardiac cycle
Zone 2: Intermittent blood flow only during the peaks of pulmonary arterial pressure because the systolic pressure is then
greater than the alveolar air pressure, but the diastolic pressure is less than the alveolar air pressure
Zone 3: Continuous blood flow because the alveolar capillary pressure remains greater than alveolar air pressure during
the entire cardiac cycle
• Normally, the lungs have only zones 2 and 3 blood flow—zone 2 (intermittent flow) in the apices and zone 3
(continuous flow) in all the lower areas.
• Zone 1 blood flow, which means no blood flow at any time during the cardiac cycle, occurs when either the
pulmonary systolic arterial pressure is too low or the alveolar pressure is too high to allow flow
Effect of heavy exercise on pulmonary arterial pressure
• During heavy exercise, blood flow through the lungs may increase fourfold to sevenfold. This extra flow is
accommodated in the lungs in three ways:
(1) by increasing the number of open capillaries, sometimes as much as threefold
(2) by distending all the capillaries and increasing the rate of flow through each capillary more than twofold
(3) By increasing the pulmonary arterial pressure.
• Normally, the first two changes decrease pulmonary vascular resistance so much that the pulmonary arterial
pressure rises very little, even during maximum exercise
• The ability of the lungs to accommodate greatly increased
blood flow during exercise without increasing the pulmonary
arterial pressure conserves the energy of the right side of the
heart.
• This ability also prevents a significant rise in pulmonary
capillary pressure and the development of pulmonary edema.
Function of the pulmonary circulation when the left atrial pressure
rises as a result of left-sided heart failure
• The left atrial pressure in a healthy person almost never rises
above +6 mm Hg, even during the most strenuous exercise.
• These small changes in left atrial pressure have virtually no
effect on pulmonary circulatory function
• When the left side of the heart fails, however, blood begins to
dam up in the left atrium.
• As a result, the left atrial pressure can rise on occasion from its
normal value of 1 to 5 mm Hg all the way up to 40 to 50 mm
Hg.
• The initial rise in atrial pressure, up to about 7 mm Hg, has little
effect on pulmonary circulatory function.
• However, when the left atrial pressure raises to greater than 7 or 8 mm Hg, further increases in left atrial pressure
cause almost equally great increases in pulmonary arterial pressure, thus causing a concomitant increased load on
the right heart.
• Any increase in left atrial pressure above 7 or 8 mm Hg increases capillary pressure almost equally as much.
• When the left atrial pressure rises above 30 mm Hg, causing similar increases in capillary pressure, pulmonary
edema is likely to develop
Pulmonary capillary dynamics
• No direct measurements of pulmonary capillary pressure have ever been made.
• However, “isogravimetric” measurement of pulmonary capillary pressure, using a technique described in Chapter
16, has given a value of 7 mm Hg.
• This measurement is probably nearly correct because the mean left atrial pressure is about 2 mm Hg and the mean
pulmonary arterial pressure is only 15 mm Hg, so the mean pulmonary capillary pressure must lie somewhere
between these two values.
 Chapter-4: Physiology (Cardiovascular Module) | 147

• The dynamics of fluid exchange across the lung capillary membranes are qualitatively the same as for peripheral
tissues.
• However, quantitatively, there are important differences, as follows:
(1) The pulmonary capillary pressure is low, about 7 mm Hg, in comparison with a considerably higher functional
capillary pressure in the peripheral tissues of about 17 mm Hg
(2) The interstitial fluid pressure in the lung is slightly more negative than that in peripheral subcutaneous tissue.
(This pressure has been measured in two ways: by a micropipette inserted into the pulmonary interstitium, giving
a value of about −5 mm Hg, and by measuring the absorption pressure of fluid from the alveoli, giving a value of
about −8 mm Hg.)
(3) The colloid osmotic pressure of the pulmonary interstitial fluid is about 14 mm Hg, in comparison with less than
half this value in the peripheral tissues.
(4) The alveolar walls are extremely thin, and the alveolar epithelium covering the alveolar surfaces is so weak that
it can be ruptured by any positive pressure in the interstitial spaces greater than alveoli air pressure (>0 mm Hg),
which allows dumping of fluid from the interstitial spaces into the alveoli

Join Medico Express Free Guidelines Group

03346072846
148 | 1st year MBBS – Block-3

• Discuss pathophysiology and common causes of pulmonary Physiology Pulmonary

Re-P- edema. Edema, and
006 • Explain the safety factors that prevent pulmonary edema. Pleural Fluid
• Explain the physiological basis of the presence of fluid normally
in the pleural cavity.
• Define pleural effusion and give its causes.

Pulmonary Edema
• Pulmonary edema occurs in the same way that edema occurs elsewhere in the body.
• Any factor that increases fluid filtration out of the pulmonary capillaries or that impedes pulmonary lymphatic
function and causes the pulmonary interstitial fluid pressure to rise from the negative range into the positive range
will cause rapid filling of the pulmonary interstitial spaces and alveoli with large amounts of free fluid.
Pathophysiology:

Rise in Pulmonary
hydrostatic pressure of Fluid leaks out from
Edema
combined filtering Pulmonary vessels
hydrostatic pressure

Causes
The most common causes of pulmonary edema are as follows:
(1) Left-sided heart failure or mitral valve disease, with consequent great increases in pulmonary venous pressure
and pulmonary capillary pressure and flooding of the interstitial spaces and alveoli
(2) Damage to the pulmonary blood capillary membranes caused by infections such as pneumonia or by breathing
noxious substances such as chlorine gas or sulphur dioxide gas.
Safety Factor in Acute Conditions:
• In the human being, whose normal plasma colloid osmotic pressure is 28 mm Hg, the pulmonary capillary
pressure must rise from the normal level of 7 mm Hg to more than 28 mm Hg to cause pulmonary edema, giving
an acute safety factor against pulmonary edema of 21 mm Hg.
Safety Factor in Chronic Conditions:
• When the pulmonary capillary pressure remains elevated chronically (for at least 2 weeks), the lungs become
even more resistant to pulmonary edema because the lymph vessels expand greatly, increasing their capability of
carrying fluid away from the interstitial spaces perhaps as much as 10-fold.
• Therefore, in patients with chronic mitral stenosis, pulmonary capillary pressures of 40 to 45 mm Hg have been
measured without the development of lethal pulmonary edema
Fluid in the pleural cavity
• When the lungs expand and contract during normal breathing, they slide back and forth within the pleural cavity.
• To facilitate this movement, a thin layer of mucoid fluid lies between the parietal and visceral pleurae.
• The pleural membrane is a porous, mesenchymal, serous membrane through which small amounts of interstitial
fluid transude continually into the pleural space.
• These fluids carry with them tissue proteins, giving the pleural fluid a mucoid characteristic, which is what allows
extremely easy slippage of the moving lungs
• The total amount of fluid in each pleural cavity is normally slight—only a few milliliters. .
• A negative force is always required on the outside of the lungs to keep the lungs expanded.
• This force is provided by negative pressure in the normal pleural space.
• The basic cause of this negative pressure is pumping of fluid from the space by the lymphatics (which is also the
basis of the negative pressure found in most tissue spaces of the body)
 Chapter-4: Physiology (Cardiovascular Module) | 149

Pleural Effusion
• Collection of Large Amounts of Free Fluid in the Pleural Space is called Pleural effusion
• Pleural effusion is analogous to edema fluid in the tissues and can be called “edema of the pleural cavity.”
Causes
(1) Obstruction of Lymphatic drainage from the pleural cavity
(2) Cardiac failure, which causes excessively high peripheral and pulmonary capillary pressures
(3) Greatly reduced plasma colloid osmotic pressure
(4) Infection or any other cause of inflammation of the surfaces of the pleural cavity, which increases permeability
of the capillary membranes

Join Medico Express Free Guidelines Group

03346072846
150 | 1st year MBBS – Block-3

• Explain the ultrastructure of respiratory membrane. Physiology Principles of

Re-P- • Discuss the factors affecting diffusion of gases across the respiratory Gaseous
007 membrane. Exchange
• Explain the diffusion capacity of respiratory membrane for oxygen
and carbon dioxide.
• Define alveolar, pleural and transpulmonary pressure.
• Explain differences in the partial pressures of atmospheric,
humidified, alveolar air and explain physiological basis of change in
each pressure

Structure of Respiratory Membrane:

Membrane of respiratory unit through which gas exchange takes place are collectively called respiratory or pulmonary
membrane.
Layers of membrane:
(1) A layer of surfactant lining the alveoli
(2) The alveolar epithelium
(3) An epithelial basement membrane
(4) A thin interstitial space b/w alveolar epithelium and capillary membrane
(5) A capillary basement membrane
(6) The capillary endothelial membrane.
Factors affecting gas diffusion through membrane:
(1) Thickness of membrane (inversely)
(2) Surface area of membrane (directly)
(3) Diffusion coefficient of gas (directly)
(4) Partial pressure difference of gas b/w two sides of the membrane (directly)
Diffusing capacity of respiratory membrane:
The volume of gas that will diffuse through the membrane each minute for a partial pressure difference of 1 mm Hg is
called respiratory membrane’s diffusing capacity
For Oxygen:
• Under resting conditions = 21 ml /min /mm Hg
• It increases to about three times during exercise due to opening up of previously dormant capillaries and increased
ventilation perfusion ratio.
For Carbon dioxide:
• Under resting conditions = 400 to 450 ml /min/mm Hg
• During exercise = 1200 to 1300 ml/min /mm Hg
Pleural pressure:
• It is the pressure of the fluid in the thin space b/w the lung pleural and chest wall pleural.
• It is a slight suction means slightly negative pressure
Value:
• At the beginning of inspiration = - 5 cm of H20
• During inspiration = - 7.5 cm of H20
• During expiration = - 5 cm of H20
Alveolar pressure:
It is the air pressure inside the lung alveoli
 Chapter-4: Physiology (Cardiovascular Module) | 151

Value:
• During normal inspiration, alveolar pressure decreases to about – 1 cm H20
• During expiration, it rises to about + 1 cm H20
Transpulmonary pressure:
It is the difference b/w alveolar and pleural pressure
Significance:
• It is a measure of the elastic forces in the lungs that tend to collapse the lungs at each instant of respiration celled
recoil pressure.

Difference in composition of alveolar and atmospheric air:

Reasons:
(1) Alveolar air is only partially replaced by atmospheric air with each breath
(2) O2 is constantly being absorbed into the pulmonary blood from alveolar air
(3) Dry atmospheric air that enters the respiratory passages is humidified even before it reaches the alveoli.
Normal Composition of Gases in Air:

Join Medico Express Free Guidelines Group

03346072846
152 | 1st year MBBS – Block-3

Physiological Basis
• The atmospheric air is entirely composed of nitrogen and O2, almost no CO2 and little water vapour
• However, when passes through respiratory passages, it becomes totally humidified.
• Likewise, expired air is mostly composed of CO2 and water vapour, with little oxygen due to exchange of gases
at alveolar level
• It's a combination of dead space air and alveolar air
• Alveolar air is slowly renewed by atmospheric air: only 350 ml of new air is brought into the alveoli with each
normal inspiration and the same is expired.
• So half of alveolar air is renewed in 17 sec
Importance:
• Prevents sudden changes in gas concentrations in the blood
• Prevents excessive increase and decrease in tissue oxygenation, tissue O2 concentration and pH
• Helps to stabilize respiratory control
 Chapter-4: Physiology (Cardiovascular Module) | 153

Explain the different forms of transport of oxygen in Physiology Transport of oxygen in the
Re-P- the blood blood
008
Transport of O2 in blood:
Oxygen is taken up by blood & then transported in 2 forms:
(1) Dissolved form = 3 %
(2) In combination with haemoglobin = 97 % ( as oxy-Hb)
Dissolved form
• Oxygen dissolves in water of plasma and is transported in this physical form.
• Amount of oxygen transported in this way is very negligible.
• It is only 0.3 mL/100 mL of plasma.
• It forms only about 3% of total oxygen in blood
In combination with haemoglobin
• Oxygen combines with haemoglobin in blood and is transported as oxyhemoglobin.
• Transport of oxygen in this form is important because, maximum amount (97%) of oxygen is transported by this
method.

Join Medico Express Free Guidelines Group

03346072846
154 | 1st year MBBS – Block-3

• Draw and explain oxyhemoglobin dissociation curve Physiology oxyhemoglobin

Re-P- oxyhemoglobin dissociation curve. dissociation curve ,
009 • Enlist the factors that cause the rightward shift of Bohr`s effect &
Cyanosis
oxyhemoglobin dissociation curve.
• Enlist the factors that cause the leftward shift of
oxyhemoglobin dissociation curve.
• Explain the Bohr`s effect.
• Define, enlist the types and causes of cyanosis

Oxygen-Hb dissociation curve:

• A plot of the degree of saturation of Hb measured at different partial pressure of oxygen is called oxygen-HB
dissociation curve
• Because the blood leaving the lungs and entering the systemic arteries usually has a PO2 of about 95 mm Hg, one
can see from the dissociation curve that the usual O2 saturation of systemic arterial blood averages 97 percent.
• Conversely, in normal venous blood returning from the peripheral tissues, the PO2 is about 40 mm Hg, and the
saturation of haemoglobin averages 75 percent.

• The blood of a normal person contains about 15 grams of haemoglobin in each 100 milliliters of blood, and each
gram of haemoglobin can bind with a maximum of 1.34 milliliters of O2 (1.39 milliliters when the haemoglobin
is chemically pure)
• Therefore, 15 times 1.34 equals 20.1, which means that, on average, the 15 grams of haemoglobin in 100 milliliter
of blood can combine with a total of about 20 milliliters of O2 if the haemoglobin is 100 percent saturated. This
is usually expressed as 20 volumes percent.
Factors that shift the oxygen-haemoglobin dissociation curve
Left Shift Right Shift
Decreased hydrogen ions Increased hydrogen ions
Decreased CO2 Increased CO2
Decreased temperature Increased temperature
Decreased BPG Increased BPG
Increased pH Decreased pH
Decrease in metabolic rate Increase in Metabolic Rate
Fetal Hb
 Chapter-4: Physiology (Cardiovascular Module) | 155

Bohr’s Effect:
• Effect of increase in pCO2 or increase in Hydrogen ion concentration to shift the curve to right side, to decrease
the affinity of Hb for oxygen is called Bohr’s Effect
• This effect can be applied at tissue level and at lung level
Application of Bohr’s Effect:
At tissue level:
Increase in pCO2 & Increase in hydrogen ion concentration → shift to right → easy dissociation of oxygen from Hb at
tissue level
At lung level
Decrease in pCO2 & decrease in hydrogen ion concentration → shift to left → more association of oxygen with Hb at lung
level
Cyanosis:
• Bluish discoloration of skin & mucus membrane, when concentration of deoxy-Hb in small blood vessels like
capillaries is more than 5 g /dl
Types of Cyanosis:
Peripheral cyanosis: Central Cyanosis :
Seen in exposed skin only (at ear lobules, nose and Seen in skin & mucous membranes ( at lips and tongue)
nails)
Exposed area is cold (rubbing helps) Exposed area is warm
No clubbing Clubbing may be +ive
Arterial PO2 remains normal Mostly Arterial PO2 is below normal (due to hypoxic
hypoxia )
Causes: cold, obstruction and decreased cardiac output Causes polycythemia, altitude, lung diseases

Join Medico Express Free Guidelines Group

03346072846
156 | 1st year MBBS – Block-3

• Enlist different forms in which Carbon dioxide CO2 is transported in Physiology Transport of
Re-P- the blood. CO2 in blood
010 • Explain carboxyhemoglobin dissociation curve.
• Explain the Haldane effect.
• Explain the chloride shift / Hamburger phenomenon.
• Define the respiratory exchange ratio (RER)

Transport of CO2 in blood:

• Dissolved in plasma = 7%
• As bicarbonate in plasma = 70%
• As Carboxyhaemoglobin = 23%

Carboxyhaemoglobin dissociation curve:

• A curve denoting relationship between quantity of CO2 combined with blood in all forms and partial pressure of
CO2 is called CO2 dissociation curve.
Special features of dissociation curve:
• Normal blood PCO2 range: 40 mm Hg in arterial blood to 45 mm Hg in venous blood = very narrow range
• Normal concentration of CO2 in blood in all its different forms is 50 volumes percent.
• Only 4% of this is exchanged during normal transport of CO2 from the tissues to the lungs
• Concentration rises to 52 volume % as the blood passes through the tissues & falls to 48 volume % as it passes
through the lungs.
 Chapter-4: Physiology (Cardiovascular Module) | 157

Haldane Effect:
Haldane effect is the effect by which combination of oxygen with haemoglobin displaces carbon dioxide from haemoglobin
Binding of O2 with Hb →displace CO2 from the blood • It operates at lung level. • It applies on carbon dioxide transport
Significance of Haldane effect
(1) Release of carbon dioxide from blood into the alveoli of lungs
(2) Uptake of oxygen by the blood
Chloride shift:
When HCO3- diffuses out of RBC, Cl- diffuses in to RBC to maintain electrical potential balance of RBC; this is carried
out by bicarbonate-chloride carrier protein.
This phenomenon is called chloride shift / Hamberger's shift.
At tissue level, RBCs in systemic capillary gains chloride and water → size in venous blood > size in arterial blood At
lung level, RBCs in pulmonary capillary loss water and chloride → size of RBC is smaller.
Respiratory exchange ratio:
• It is the ratio between the volume of CO2 output & the volume of O2 consumed
• R = volume of CO2 output / volume of O2 consumed = 4 ml / 5 ml = 0.8
• R increases from 0.8 to 1 with carbohydrate diet and decreases from 0.8 to 0.6 with fat-rich diet

Join Medico Express Free Guidelines Group

03346072846
158 | 1st year MBBS – Block-3

Explain the alveolar oxygen and carbon dioxide pressure when Physiology VA/Q
Re-P- Pulmonary ventilation (V) and Perfusion (Q), VA/Q= infinity, zero (ventilation
011 normal and Explain the concept of physiological shunt when VA/Q ratio perfusion ratio)
is above normal Explain the concept of physiological dead space when
VA/Q ratio is above normal

Ventilation perfusion ratio:

• It is the ratio of alveolar ventilation (V) to pulmonary blood flow (Q)
• If the frequency, tidal volume, and cardiac output are normal, the V/Q ratio is approximately 0.8.
NORMAL V/Q RATIO:
• When alveolar ventilation (V) & blood flow (Q) is normal for an alveolus:
• PO2=104mmHg
• PCO2=40mmHg
ZERO V/Q RATIO:
• When the ventilation(V) is zero yet there is still perfusion(Q) , the air in the alveolus comes to equilibrium with
the blood oxygen and carbon dioxide because these gases diffuse between the blood and the alveolar air
• Po2 of 40 mm Hg
• Pco2 of 45 mm Hg.
• The normal partial pressures of these two gases in alveoli that have blood flow but no ventilation.
Shunt Flow
• Venous blood passing through the pulmonary capillaries which do not become oxygenated is called the Shunted
Blood.
• The total quantitative amount of shunted blood per minute is called the physiological shunt.
• When airways are blocked then ventilation is zero and if blood flow is normal then V/Q= 0 which is called a
shunt.
• Greater the physiological shunt, the greater the amount of blood that fails to be oxygenated as it passes through
the lungs.
INFINITY V/Q RATIO:
• There is no capillary blood flow to carry oxygen away or to bring carbon dioxide to the alveoli
• Alveolar air becomes equal to the humidified inspired air.
• The air that is inspired loses no oxygen to the blood and gains no carbon dioxide from the blood
• Po2 of 149 mm Hg
• Pco2 of 0 mm Hg
• If ventilation is normal then VA/Q = infinite, which is called a dead space, there is no gas exchange in a lung that
is ventilated but not perfused.
• The PO2 & PCO2 of alveolar gas will approach their values in inspired.
 Chapter-4: Physiology (Cardiovascular Module) | 159

• Enlist the respiratory and non-respiratory functions of the lung. Physiology Protective
Re-P- • Explain the nervous control of bronchiolar musculature. Reflexes
012 • Trace the reflex arc of cough reflex and sneeze reflex

Respiratory functions of the lungs:

1. Exchange of gasses in the lungs
Non-respiratory functions of the lungs
1. Synthetic function
2. Removal of some substances including amines
3. Filtering function
4. Reservoir function
5. Acid base balance
6. Temperature regulation
7. Water balance of body
8. Route of drug administration
9. Involved in phonation
10. Metabolic and endocrine function
11. Defence function
12. Miscellaneous function
Nervous control of bronchiolar musculature:
• Bronchiolar walls are made up of smooth muscles.
• It is supplied by both sympathetic and parasympathetic system
Sympathetic dilation of bronchioles:
• Direct control by sympathetic nerve fibers is relatively weak, however, bronchioles much exposed to
norepinephrine and epinephrine released by sympathetic stimulation of adrenal gland medullae.
• These caused dilation of bronchioles, an effect which is opposite to smooth muscles of vessels
Parasympathetic constriction of bronchioles:
• Parasympathetic nerve fibers from vagus nerve penetrate the lung parenchyma and secrete acetylcholine which
causes mild to moderate constriction of bronchioles.
Cough reflex:
• Stimulus: foreign particle causes irritation
• Receptor organ: the terminal bronchioles, larynx, trachea and carina.
• Afferent: vagus nerve
• Centre: medulla
Response/Reflex:
Up to 2.5 litters of air are rapidly inspired → the epiglottis and vocal cords shut tightly → the abdominal muscles contract
forcefully → pressure in the lungs raises to 100 mm Hg or more → then the vocal cords and epiglottis suddenly open and
air is expelled at velocities ranging from 75 to 100 miles / hour → The rapidly moving air carries with it foreign matter
Sneeze reflex:
• Stimulus: foreign particle causes irritation
• Receptor organ: nasal passageways
• Afferent: fifth cranial nerve
• Centre: medulla
Response/Reflex:
Same series of reactions takes place but the uvula is depressed so large amounts of air pass rapidly through the nose thus
clearing the nasal passages of foreign matter.

Join Medico Express Free Guidelines Group

03346072846
160 | 1st year MBBS – Block-3

• Explain the principle means by which acclimatization Physiology Aviation and

Re-P- occurs. space
013 • Explain the events that occur during acute mountain
sickness.
• Enlist the features of chronic mountain sickness

Acclimatization:
• Acclimatization refers to the adaptations or the adjustments by the body in high altitude.
• While staying at high altitudes for several days to several weeks, a person slowly gets adapted or adjusted to the
low oxygen tension, so that hypoxic effects are reduced.
• It enables the person to ascent further.
How does the acclimatization occurs:
• A great increase in pulmonary ventilation
• Increased numbers of red blood cells
• Increased diffusing capacity of the lungs
• Increased vascularity of the peripheral tissues
• Increased ability of the tissue cells to use O2 despite low PO2.
Acute mountain sickness:
• People who ascend rapidly to high altitude become acutely sick and can die if not given O2 or rapidly moved to
a low altitude.
• Two events frequently occur:
1. Acute cerebral edema
2. Acute pulmonary edema
Chronic mountain sickness:
Occasionally, a person who remains at high altitude too long experiences chronic mountain sickness in which following
events occur:
1. The red blood cell mass and haematocrit become exceptionally high
2. The pulmonary arterial pressure becomes elevated
3. The right side of the heart becomes greatly enlarged
4. The peripheral arterial pressure begins to fall
5. Congestive heart failure ensues
6. Death
 Chapter-4: Physiology (Cardiovascular Module) | 161

• Explain the pathophysiology, features, prevention and treatment of Physiology Deep sea
Re-P- decompression sickness. diving
014
Decompression Sickness
Decompression sickness occurs when a person rapidly returns to normal atmospheric pressure from a high-pressure
environment, such as deep sea.
Cause:
• High Pressure: At deep sea, high barometric pressure compresses gases in the body, reducing their volume.
• Gas Utilization and Expiration: Oxygen is used by tissues, and carbon dioxide is expired, but nitrogen, which
makes up 80% of the respiratory gases, remains inert—neither utilized nor expired.
• Nitrogen Solubility: Compressed nitrogen dissolves in tissues, especially fat, while the person is at depth.
• Rapid Ascent: A sudden return to atmospheric pressure causes the nitrogen to decompress and form bubbles.
• Bubble Formation: These bubbles obstruct blood flow, leading to air embolism and decompression sickness.
Symptoms:
• Mainly due of the escape of nitrogen from tissues in the form of bubbles
• Symptoms are:
1. Severe pain in tissues, particularly the joints, produced by nitrogen bubbles in the myelin sheath of sensory nerve
fibers
2. Sensation of numbness, tingling or pricking and itching
3. Temporary paralysis due to nitrogen bubbles in the myelin sheath of motor nerve fibers
4. Muscle cramps associated with severe pain
5. Occlusion of coronary arteries followed by coronary ischemia, caused by bubbles in the blood
6. Occlusion of blood vessels in brain and spinal cord
7. Damage of tissues of brain and spinal cord because of obstruction of blood vessels by the bubbles Dizziness,
paralysis of muscle, shortness of breath and choking occur
8. Finally, fatigue, unconsciousness and death.
Prevention:
• While returning to mean sea level, the ascent should be very slow with short stay at regular intervals
• Stepwise ascent allows nitrogen to come back to the blood, without forming bubbles
• It prevents the decompression sickness
Treatment:
• Recompression should be done
• Keeping the person in a recompression chamber
• Brought back to atmospheric pressure b reducing the pressure slowly
• Hyperbaric oxygen therapy may be useful

Join Medico Express Free Guidelines Group

03346072846
162 | 1st year MBBS – Block-3

• Draw and explain the effect of CO poisoning on Physiology Carbon monoxide

Re-P- oxyhemoglobin dissociation curve. poisoning
015 • Explain the pathophysiology, features, and treatment of CO
poisoning.

CO Poisoning
Incomplete combustion of carbon produces CO → Hb has 250x more affinity to bind with CO, than to O2 → Carbon-
monoxy Hb shifts the oxy-Hb curve to left → O2 dissociation becomes difficult → CO also inhibits cytochromes →Death
• CO is colorless & odourless
• In CO poisoning, skin is cherry red coloured
Effect of CO poisoning on oxyhemoglobin dissociation curve
• Carbon-monoxy Hb shifts the oxy-Hb curve to left

Treatment:
• Remove the subject from source of exposure.
• 100% oxygen therapy can help
• Hyperbaric O2 can help (O2 with increased pressure = 2-3 atmospheric pressure )
 Chapter-4: Physiology (Cardiovascular Module) | 163

• Enumerate the components of respiratory centers and explain Physiology Nervous

Re-P- their functions. regulation of
016 • Explain the inspiratory RAMP signal. respiration
• Explain the Herring Breuer reflex/lung inflation reflex and its
clinical significance.

Respiratory Center:
• The respiratory centre is composed of several groups of neurons located bilaterally in the medulla oblongata and
pons of the brain stem.
• Four major collections of neurons are:
1. Dorsal respiratory group
2. Ventral respiratory group
3. Pneumotaxic center
4. Apneustic Center

Dorsal respiratory group of neurons:

• Its neurons are located within the nucleus of the tractus solitarius (NTS)
• It is the sensory termination of both vagal and glossopharyngeal nerves
• It receive impulses from:
1. Peripheral chemoreceptors
2. Carotid and aortic baroreceptors
3. Other receptors in the lungs.
Rhythmical inspiratory discharges from the dorsal respiratory group:
• It is the Pacemaker of respiratory signals

Join Medico Express Free Guidelines Group

03346072846
164 | 1st year MBBS – Block-3

• It generates basic rhythm of respiration

• It emits Repetitive inspiratory neuronal action potentials.
Inspiratory “ramp” signal
• To start with, the amplitude of action potential is low.
• It is due to the activation of only few neurons.
• Later, more and more neurons are activated, leading to gradual increase in the amplitude of action potential
in a ramp fashion.
• Impulses of this type discharged from dorsal group of neurons are called inspiratory ramp signals.
• Ramp signals are not produced continuously but only for a period of 2 seconds, during which inspiration
occurs.
• After 2 seconds, ramp signals stop abruptly and do not appear for another 3 seconds.
• Switching off the ramp signals causes expiration.
• At the end of 3 seconds, inspiratory ramp signals reappear in the same pattern and the cycle is repeated.
• Normally, during inspiration, dorsal respiratory group neurons inhibit expiratory neurons of ventral group.
• During expiration, the expiratory neurons inhibit the dorsal group neurons.
• Thus, the medullary respiratory centers control each other.
Significance of inspiratory ramp signals
• Significance of inspiratory ramp signals is that there is a slow and steady inspiration, so that the filling of
lungs with air is also steady
Pneumotaxic center:
Locations:
• It is present dorsally in the nucleus parabrachialis of the upper pons.
Functions:
• Controls rate and duration of breathing by terminating inspiratory signals
• Control the “switch-off” point of the inspiratory ramp
• Limits the Duration of Inspiration and Increases the Respiratory Rate
Mechanism:
• Strong pneumotaxic signal → inspiration is of 0.5 seconds
• Weak signals → inspiration might continue for 5 or more seconds
Ventral respiratory group of neurons:
Location:
• Ventral respiratory group of neurons are present in nucleus ambiguous and nucleus retroambiguous.
• These two nuclei are situated in the medulla oblongata, anterior and lateral to the nucleus of tractus solitarius.
• Ventral respiratory group has both inspiratory and expiratory neurons.
• Inspiratory neurons are found in the central area of the group.
• Expiratory neurons are in the caudal and rostral areas of the group.
Function:
• Active when there is need to increase pulmonary ventilation providing the powerful expiratory signals to the
abdominal muscles during very heavy expiration especially in exercise.
• Inactive during normal quiet respiration ^ Do not participate in the basic rhythmical oscillation that controls
respiration.
• Electrical stimulation of a few of the neurons in the VG causes inspiration, whereas stimulation of others causes
expiration.
Apneustic center:
• Apneustic center is situated in the reticular formation of lower pons.
 Chapter-4: Physiology (Cardiovascular Module) | 165

Function
• Apneustic center increases depth of inspiration by acting directly on dorsal group neurons.
Medullary Centers
Feature Dorsal Group Ventral Group
Situation Diffusely situated in nucleus of tractus In nucleus ambiguous and nucleus
solitarius retroambiguous
Type of Inspiratory neurons Inspiratory and expiratory neurons
Neurons
Function − Always active − Inactive during quiet breathing
− Generate inspiratory ramp − Active during forced breathing
− Has autorhythmic property

Hering-Breuer reflex:
When lungs become overly inflate → stretch receptors in bronchi and bronchioles stimulated → signals through vagus
into dorsal respiratory area → switch off of the inspiratory ramp signal → limits period of inspiration → Increase Rate of
respiration.
Advantage:
• In humans, it is not activated until the tidal volume Increases to more than three times normal
• It is mainly a protective mechanism for preventing excess lung inflation.

Join Medico Express Free Guidelines Group

03346072846
166 | 1st year MBBS – Block-3

• Explain the location of chemo sensitive area (central Physiology Chemical

Re-P- chemoreceptors) and peripheral chemoreceptors. control of
017 • Explain the effect of hydrogen ions & carbon dioxide on the respiration
chemo- sensitive area.
• Explain the role of oxygen in the control of respiration/peripheral
chemoreceptors

Central Chemosensitive area:

• Located bilaterally beneath the ventral surface of medulla.
Function:
• Sensitive to change in either blood PCO2 or H+ concentration, and it in turn excites the other portions of
respiratory center to increase rate and intensity of respiration.
Primary stimulus:
• H+ ion is the primary stimulus for chemosensitive area.
Effects of H+ and CO2 in chemosensitive area:
1. Effect of blood H+: H+ ions don’t cross the blood-brain barrier so blood H+ ions cannot affect chemosensitive area
directly.
2. Effect of blood CO2: Blood CO2 has potent indirect effect. Blood CO2 cross blood-brain Barrier. CO2 combines with
H20 to form H2CO3 which dissociates into HCO3- and H+. This H+ ion stimulates chemosensitive area. Thus, blood CO2
can effect chemosensitive area indirectly.
3. Effect of CSF CO2: CSF CO2 has more potent effect on chemosensitive area than blood CO2 because CSF has less
protein buffers, H+ ions resulting from the dissociation of H2CO3 are not removed rapidly.

Peripheral chemoreceptor area:

• Most of the chemoreceptors are in carotid bodies at bifurcation of common carotid arteries and a few in aortic
bodies along arch of aorta
• Afferents from carotid bodies pass through Hering’s nerve to glossopharyngeal nerve and then to dorsal
inspiratory area.
 Chapter-4: Physiology (Cardiovascular Module) | 167

• Afferents from aortic bodies pass through vagus nerve to dorsal medullary inspiratory area.
Stimulus:
• Decreased arterial oxygen, in the range of 60 mm Hg down to 30 mm Hg, stimulates the chemoreceptors.
Mechanism:
Bodies have multiple glandular like cells called gliomas cells which
have O2 – sensitive potassium channels become inactivated when
blood PCO2 decreases.

This causes to open voltage gated calcium channels and increases

intracellular ca2+ concentration

Send impulses to dorsal inspiratory area

Causes switch-off of inspiratory ramp signal

Limits period of inspiration

Increase rate of inspiration.

Join Medico Express Free Guidelines Group

03346072846
168 | 1st year MBBS – Block-3

• Explain the regulation of Respiration during Exercise Physiology Exercise and Respiration
Re-P-
018
Regulation of respiration during exercise:
1. Motor cortex, while transmitting impulses to contracting muscle, also sends collateral impulses to excite dorsal
inspiratory area.
2. Receptors for position & movement present around joints, in the muscles, tendons and joint ligaments excite
dorsal inspiratory area.
3. During exercise → metabolism increases → body temperature increases → stimulates respiration directly &
indirectly
Neuro-genic drive from respiratory centre during heavy exercise:
• Arterial PCO2 remain normal (40mm Hg) at rest & during heavy exercise.
• If PCO2 does change from 40, there is stimulation of ventilation above 40 & depression of ventilation below 40.
• This shift in exercise is partly a learned response that involves cerebral cortex.
• Neurogenic factor shifts the curve about 20- fold in upward direction so that vent. Matches the rate of CO2 release
keeping normal level of Arterial PCO2
 Chapter-4: Physiology (Cardiovascular Module) | 169

• Enlist the effects of acute hypoxia. Physiology Hypoxia

Re-P- • Explain the hypoxia inducible factor a master switch for body response
019 to hypoxia.
• Define and explain different types of hypoxias.

Hypoxia:
• Decrease O2 supply to tissues below physiological levels is called hypoxia.
Effects of acute hypoxia
• Drowsiness
• Depressed
• Mental activity
• Decreased work capacity of muscles
• Headache, nausea and sometimes euphoria.
Types of Hypoxia:
1. HYPOXIC HYPOXIA:
• Decreased arterial partial pressure of oxygen.
Causes:
• High altitude
• Depression of respiratory centre
• Respiratory muscle paralysis
• Obstructive and restrictive lung disease
• Congenital heart disease.
TREATMENT:
• O2 treatment is most effective in this type of hypoxia.
2. ANEMIC HYPOXIA:
• Anaemic hypoxia is the condition characterized by the inability of blood to carry enough amount of oxygen.
• Oxygen availability is normal But the blood is not able to take up sufficient amount of oxygen due to anaemic
condition
Causes:
• Decreased number of RBCs
• Decreased haemoglobin content in the blood
• Formation of altered haemoglobin
• Combination of haemoglobin with gases other than oxygen and carbon dioxide
3. STAGNANT / ISCHEMIC HYPOXIA:
Stagnant hypoxia is the hypoxia caused by decreased velocity of blood flow. It is otherwise called hypokinetic hypoxia.
Causes
• Decreased cardiac output
• Sluggish blood flow due to heart failure
• Haemorrhage
• Circulatory shock
• Venous obstruction.
4.HISTOTOXIC HYPOXIA:
• Histotoxic hypoxia is the type of hypoxia produced by the inability of tissues to utilize oxygen.

Join Medico Express Free Guidelines Group

03346072846
170 | 1st year MBBS – Block-3

Causes
• Cyanide poisoning (it inhibits cytochrome oxidases →oxidative process is inhibited)
• Narcotic over-dosage (it inactivates the enzyme dehydrogenase → inhibition of tissue oxygenation).
• Beriberi (it is deficiency of thymine co-enzyme which is required for many oxidative reactions).
TREATMENT:
• Methylene blue or nitrites.
Characteristics features of different types of hypoxia
Feature Hypoxic Anemic Stagnant Histotoxic
Hypoxia Hypoxia Hypoxia Hypoxia
1. PO₂ in Arterial Blood Reduced Normal Normal Normal
2. Oxygen Carrying Capacity of Normal Reduced Normal Normal
Blood
3. Velocity of Blood Flow Normal Normal Reduced Normal
4. Utilization of Oxygen by Tissues Normal Normal Normal Reduced
5. Efficacy of Oxygen Therapy 100% 75% < 50% Not useful
 Chapter-4: Physiology (Cardiovascular Module) | 171

• Explain the pathophysiology of Tuberculosis. Integrate with Pathology Tuberculosis

Re-P-020
Tuberculosis:
Causative organism: Tubercle bacilli or Mycobacterium tuberculosis
Pathophysiology:

Infected area is invaded by macrophages

Walling-off of the lesion by fibrous tissue forms

tubercle

This walling-off process helps to limit further

transmission of the tubercle bacilli in the lungs

Protective process against extension of the infection

However, in about 3 percent of all people in whom tuberculosis develops, if the disease is not treated, the walling off
process fails and tubercle bacilli spread throughout the lungs, often causing extreme destruction of lung tissue with
formation of large abscess cavities
Effects:
• Decrease Vital capacity
• Decrease Total respiratory membrane surface area
• Increase thickness of respiratory membrane
• Abnormal ventilation perfusion ratio

Join Medico Express Free Guidelines Group

03346072846
172 | 1st year MBBS – Block-3

• Describe the pathophysiology of Pneumonia. Integrate with Pathology Pneumonia

Re-P-021
Pneumonia:
• Any inflammatory condition of the lungs in which alveoli are filled with fluid and blood cells.
Example: Bacterial pneumonia caused by pneumococci.
Pathophysiology

pulmonary membrane
fluid, RBCs and WBCs
Infection in alveoli becomes inflamed and
leak out into alveoli
porous

Effects
• Decreased surface area of respiratory membrane
• Hypoxemia
 Chapter-4: Physiology (Cardiovascular Module) | 173

• Define Dyspnea Enlist different causes of dyspnea General Dyspnea

Re-P- • Differentiate between cardiac and respiratory dyspnea Outline Medicine
022 management strategies for dyspnea

Dyspnea:
• Dyspnea means difficulty in breathing.
• It is otherwise called the air hunger.
• Normally, the breathing goes on without consciousness. When breathing enters the consciousness and produces
discomfort, it is called dyspnea.
• Dyspnea is also defined ‘as a consciousness of necessity for increased respiratory effort
Causes
• Pneumonia
• Pulmonary edema
• Pulmonary effusion
• Poliomyelitis
• Pneumothorax
• left ventricular failure
• Decompensated mitral stenosis
• Severe asthma
Aspect Cardiac Dyspnea Respiratory Dyspnea
Primary Cause Heart-related issues (e.g., heart failure, coronary Lung-related issues (e.g., asthma,
artery disease) chronic obstructive pulmonary disease)
Onset Often gradual but can be sudden in acute conditions Typically gradual but can also be sudden
in acute conditions
Symptoms Shortness of breath, often worsens with exertion, Shortness of breath, wheezing, chest
orthopnea (difficulty breathing when lying flat), tightness, often related to specific
paroxysmal nocturnal dyspnea (sudden nighttime triggers or activities
shortness of breath)
Physical Exam Edema (swelling of legs), jugular vein distention, Wheezing, decreased breath sounds,
Findings crackles or rales in lungs, irregular heartbeat signs of increased work of breathing
(e.g., use of accessory muscles)
Associated Congestive heart failure, myocardial infarction, Asthma, chronic bronchitis, emphysema,
Conditions valvular heart disease pneumonia
Response to Improvement with heart failure management, Improvement with bronchodilators,
Treatment medications like diuretics, ACE inhibitors, or beta- corticosteroids, or antibiotics, depending
blockers on the specific respiratory condition
Effect on Activity Typically worsens with physical exertion or lying Worsens with physical exertion or
flat; improved with rest and sitting up exposure to triggers (e.g., allergens,
irritants)
Clinical Features
Cough Not prominent after dyspnea Prominent and often precedes dyspnea
Orthopnea Common Not present
Paroxysmal Common Not present
Nocturnal
Dyspnea (PND)
Edema Present (e.g., swelling in legs) Not typically present

Join Medico Express Free Guidelines Group

03346072846
174 | 1st year MBBS – Block-3

Raised Jugular Present Not present

Venous Pressure
(JVP)
Evidence of Often present Not present
Valvular Heart
Defect
Urine Output Reduced Normal
Benefit with Significant improvement No significant change
Diuretics
Sputum Not present Common
Production and
Wheezing

1. General Approaches
• Assessment and Diagnosis: Accurate diagnosis of the underlying cause through history, physical examination,
and diagnostic tests.
• Patient Education

2. Pharmacological Management
• Bronchodilators: For conditions like asthma and COPD, to open airways and improve airflow.
• Corticosteroids: To reduce inflammation in conditions such as asthma and COPD.
• Diuretics: For cardiac dyspnea, to reduce fluid overload and improve symptoms of heart failure.
• Oxygen Therapy: For hypoxemic patients to increase oxygen levels and alleviate dyspnea.
• Antibiotics: For infections that are causing or contributing to respiratory symptoms.
3. Non-Pharmacological Management
• Positioning:
o Orthopnea: Sit upright or use pillows to support sitting position.
o Pulmonary Dyspnea: Elevate the head of the bed or use a comfortable position that eases breathing.
• Breathing Techniques:
o Pursed-Lip Breathing: Helps to keep airways open longer.
 Chapter-4: Physiology (Cardiovascular Module) | 175

o Diaphragmatic Breathing: Encourages efficient breathing and reduces the work of breathing.
• Pulmonary Rehabilitation: Includes exercise training, breathing exercises, and education for chronic respiratory
conditions.
• Lifestyle Modifications:
o Weight Management: To reduce the burden on the heart and lungs.
o Smoking Cessation: To prevent further respiratory damage and improve lung function.
4. Management of Specific Causes
• Cardiac Dyspnea:
o Heart Failure Management: Includes medications (e.g., ACE inhibitors, beta-blockers), lifestyle
changes, and sometimes surgical interventions.
o Valvular Disease: Management may include medications or surgical repair/replacement of heart valves.
• Pulmonary Dyspnea:
o Asthma: Regular use of inhalers, avoiding triggers, and monitoring peak flow.
o COPD: Long-acting bronchodilators, inhaled corticosteroids, and regular monitoring.
o Infections: Appropriate antibiotics or antivirals as needed.
5. Advanced Interventions
• Mechanical Ventilation
• Surgical Interventions
6. Supportive Care
• Psychological Support
• Palliative Care

Join Medico Express Free Guidelines Group

03346072846
176 | 1st year MBBS – Block-3

• Enlist the causes of Pneumothorax. Integrate with Pneumothorax

Re-P- • Describe the signs and symptoms of Pneumothorax Surgery
023
Pneumothorax:
• Pneumothorax is the presence of air in pleural space.
• Intrapleural pressure, which is always negative, becomes positive in pneumothorax and it causes collapse of lungs.
Causes
• Air enters the pleural cavity because of damage of chest wall or lungs during accidents, bullet injury or stab injury.
Sign and Symptoms:
• Sharp and stabbing chest pain
• Shortness of breath
• Bluish skin
• Fatigue
• Rapid Breathing
• Dry, hacking cough
• Rapid Heart Rate
• Shock and collapse
 Chapter-4: Physiology (Cardiovascular Module) | 177

• Enlist the causes of Pleuritis Integrate with Surgery Pleuritis

Re-P-024 • Describe the signs and symptoms of Pleuritis
• Discuss the management of Pleuritis

Pleuritis
Pleuritis (or pleurisy) is inflammation of the pleura, the lining surrounding the lungs.
1. Infectious Causes:
o Viral Infections: nfluenza or adenovirus.
o Bacterial Infections: pneumonia, tuberculosis, or bacterial infections following chest surgery.
o Fungal Infections: immunocompromised individuals.
2. Inflammatory Causes:
o Autoimmune Diseases: rheumatoid arthritis, lupus, or systemic sclerosis.
o Rheumatic Fever: Can follow streptococcal infections.
3. Other Causes:
o Trauma or Injury: Chest trauma or recent chest surgery.
o Pulmonary Embolism: Blood clot in the lungs can cause pleuritic pain.
o Malignancy: Tumors involving the pleura, such as lung cancer or mesothelioma.
o Pneumothorax: Air in the pleural space can cause inflammation.
Signs and Symptoms of Pleuritis
Signs:
• Pleuritic Rub: A friction rub heard on auscultation of the chest, characteristic of pleuritis.
• Reduced Breath Sounds: Over the affected area of the pleura.
Symptoms:
• Sharp, Stabbing Pain: Typically localized to one side of the chest, worsens with deep breathing, coughing, or
movement.
• Dyspnea: Difficulty breathing due to pain or inflammation.
• Cough: Often dry and non-productive.
• Fever: If the pleuritis is due to an infection.
• Chest Tightness: Sensation of pressure or discomfort in the chest.
Management of Pleuritis
1. Treatment of Underlying Cause:
• Infectious Causes:
o Antibiotics: For bacterial infections.
o Antivirals: For viral infections if indicated.
• Autoimmune Diseases:
o Corticosteroids: To reduce inflammation.
• Malignancy:
o Oncological Treatment: Such as chemotherapy or radiation.
2. Symptomatic Relief:
• Pain Management:
o Non-Steroidal Anti-Inflammatory Drugs (NSAIDs): Such as ibuprofen or naproxen to reduce pain
and inflammation.
o Acetaminophen: For pain relief if NSAIDs are contraindicated.
• Analgesics: Opioids may be used for severe pain, but with caution due to potential side effects.

Join Medico Express Free Guidelines Group

03346072846
178 | 1st year MBBS – Block-3

3. Supportive Care:
• Rest: Reducing physical activity to minimize pain and allow healing.
• Breathing Exercises: Gentle breathing exercises to help maintain lung function and reduce discomfort.
4. Drainage (if necessary):
• Thoracentesis: If there is a significant pleural effusion, fluid may be drained to relieve pressure and improve
symptoms.
• Chest Tube: For persistent or large pleural effusions or pneumothorax.
5. Follow-Up:
• Monitoring: Regular follow-up to assess response to treatment and adjust as necessary.
 Chapter-4: Physiology (Cardiovascular Module) | 179

• Enlist the causes of Bronchitis. Integration with General Bronchitis

Re-P- • Discuss the signs and symptoms of Bronchitis. Medicine
025 • Discuss the management of Bronchitis

Bronchitis
Bronchitis is the inflammation of the bronchial tubes
1. Acute Bronchitis:
• Viral Infections: Often following a cold or influenza (e.g., rhinovirus, influenza virus, coronavirus).
• Bacterial Infections: Mycoplasma pneumoniae, Chlamydia pneumoniae, or Haemophilus influenzae.
• Irritants: Exposure to environmental pollutants, tobacco smoke, or fumes.
• Allergens: Allergic reactions to environmental triggers.
2. Chronic Bronchitis:
• Smoking: The primary cause, leading to chronic inflammation and mucus production.
• Air Pollution: Exposure to pollutants, dust, and fumes in certain occupational settings.
• Chronic Respiratory Infections: Repeated infections that lead to persistent inflammation.
• Genetic Factors: Conditions like alpha-1 antitrypsin deficiency can contribute to chronic bronchitis.
• Other Environmental Exposures: Long-term exposure to irritants or allergens.
Signs and Symptoms of Bronchitis
Acute Bronchitis:
• Cough: Often persistent, starting dry and becoming productive with mucus.
• Sputum Production: Mucus that may be clear, yellow, or green.
• Chest Discomfort: May include a feeling of tightness or soreness.
• Fatigue: General feeling of tiredness or malaise.
• Fever: Often mild to moderate.
• Shortness of Breath: Usually mild and related to the cough.
Chronic Bronchitis:
• Persistent Cough: Lasting for at least three months in two consecutive years.
• Excessive Mucus Production: Thick, often discolored sputum.
• Frequent Respiratory Infections: Increased susceptibility to colds and flu.
• Shortness of Breath: Particularly with exertion or during respiratory infections.
• Wheezing: High-pitched whistling sound during breathing.
• Cyanosis: Bluish color of lips or fingertips due to low oxygen levels (in severe cases).
Management of Bronchitis
1. Acute Bronchitis:
• Rest: Adequate rest to help the body recover.
• Hydration: Increased fluid intake to help loosen mucus.
• Pain and Fever Relief:
o NSAIDs: Such as ibuprofen or acetaminophen for pain and fever.
• Cough Suppressants: If cough is severe and interfering with sleep, but generally should be avoided if it’s
productive.
• Expectorants: To help loosen mucus.
• Avoid Irritants: Such as smoking or exposure to environmental pollutants.

Join Medico Express Free Guidelines Group

03346072846
180 | 1st year MBBS – Block-3

• Antibiotics: Reserved for bacterial infections if indicated, though most cases are viral and do not require
antibiotics.
2. Chronic Bronchitis:
• Smoking Cessation: The most crucial step to slow disease progression and improve symptoms.
• Bronchodilators: To relax and open airways.
• Inhaled Corticosteroids: To reduce inflammation in the airways.
• Expectorants: To help clear mucus from the lungs.
• Pulmonary Rehabilitation: Includes exercise training and education to improve lung function and quality of
life.
• Oxygen Therapy: For patients with significant hypoxemia.
• Vaccinations: Annual influenza vaccination and pneumococcal vaccine to prevent infections.
• Managing Exacerbations: Prompt treatment of respiratory infections and exacerbations with medications or
hospital care if necessary.
 Chapter-4: Physiology (Cardiovascular Module) | 181

• Classify different types of pneumonia. Integration with General Medicine Pneumonia

Re-P-026 • Discuss the sign symptoms of pneumonia.
• Discuss the management of pneumonia

Pneumonia:
• Pneumonia is the inflammation of lung tissues, followed by the accumulation of blood cells, fibrin and exudates
in the alveoli.
• Affected part of the lungs becomes consolidated.
Causes:
• Bacterial or viral infection
• Inhaling noxious chemical substance
Types:
• Pneumonia is of two types, namely lobar pneumonia and lobular pneumonia.
• When it is lobular and associated with inflammation of bronchi, it is known as bronchopneumonia
• It can also be classified into Typical and Atypical pneumonia
Symptoms:
• High fever
• Cough with yellow, green or bloody mucus.
• Tiredness (fatigue)
• Rapid breathing
• Shortness of breath
• Rapid heart rate
• Sweating or chills
• Chest pain and/or abdominal pain especially with coughing or deep breathing
Management:
• Oxygen Therapy
• Antiviral, Antifungal, Antibacterial drugs
• Cough Suppressants

Join Medico Express Free Guidelines Group

03346072846
182 | 1st year MBBS – Block-3

• Classify different types of asthma. Integration with General Medicine Asthma

Re-P-027 • Discuss the signs and symptoms of asthma.
• Discuss the management of asthma

Asthma:
Spastic contraction of bronchioles, resulting in difficult breathing is called asthma.
Causes:
• The usual cause is allergic hypersensitivity of bronchioles to foreign substances in air
• In older people, the cause is almost always hypersensitivity to non-allergic types of irritants in the air such as
irritants in smog
Effects:
• Localized edema in smalls bronchioles
• Secretion of thick mucus into the bronchiolar lumen
• Spasm of the bronchiolar smooth muscle
Symptoms:
• Wheezing
• Coughing and chest tightness becoming severe and
• Breathing faster
• Fast heartbeat
• Drowsiness
• Confusion
• Exhaustion or dizziness
• Fainting
Management:
• Bronchodilators including Beta agonist and anti-muscarinic agents
• Anti-Inflammatory drugs
• Avoiding Allergic agents
 Chapter-4: Physiology (Cardiovascular Module) | 183

• Classify different types of Tuberculosis. Integration with General Tuberculosis

Re-P- • Discuss the signs and symptoms of tuberculosis. Medicine
028 • Discuss the management of Tuberculosis

Tuberculosis
1. Clinical Classification:
• Primary Tuberculosis:
o Initial Infection: Typically occurs in children or adolescents.
o Ghon Complex: Involves a pulmonary focus and regional lymphadenopathy.
• Secondary Tuberculosis (Reactivation TB):
o Reactivation: Often occurs in adults, particularly in those with weakened immune systems.
o Lung Apices: Typically affects the upper lobes of the lungs.
• Latent Tuberculosis Infection (LTBI):
o Asymptomatic: The person is infected with Mycobacterium tuberculosis but does not exhibit active
disease.
o Not Infectious: Cannot spread TB to others.
• Active Tuberculosis:
o Pulmonary TB: Affects the lungs and is the most common form.
o Extrapulmonary TB: Affects other organs such as lymph nodes, kidneys, bones, and the central
nervous system.

2. Site of Infection:
• Pulmonary TB: Involves the lungs.
• Extrapulmonary TB: Involves organs other than the lungs.
3. Drug Resistance:
• Drug-Sensitive TB: Responsive to standard TB treatment regimens.
• Multidrug-Resistant TB (MDR-TB): Resistant to at least isoniazid and rifampin, the two main TB drugs.

Join Medico Express Free Guidelines Group

03346072846
184 | 1st year MBBS – Block-3

• Extensively Drug-Resistant TB (XDR-TB): Resistant to isoniazid, rifampin, any fluoroquinolone, and at least
one of the three injectable second-line drugs.
Signs and Symptoms of Tuberculosis
1. Pulmonary Tuberculosis:
• Cough: Persistent, often with sputum production. May become bloody (hemoptysis) in advanced cases.
• Chest Pain: Sharp or dull pain in the chest.
• Fever: Low-grade fever, often occurring in the evenings.
• Night Sweats
• Unintentional weight loss.
• Fatigue
• Loss of Appetite
2. Extrapulmonary Tuberculosis:
• Lymphatic TB: Swelling of lymph nodes.
• Skeletal TB: Back pain, joint pain, or deformities if the spine or other bones are involved.
• Genitourinary TB: Painful urination, blood in urine, or kidney pain.
• Central Nervous System TB: Headaches, confusion, or meningitis symptoms.
• Abdominal TB: Abdominal pain, swelling, or gastrointestinal symptoms.
Management of Tuberculosis
1. Treatment:
• Standard Regimen for Drug-Sensitive TB:
o First-Line Drugs:
▪ Isoniazid (INH)
▪ Rifampin (RIF)
▪ Ethambutol (EMB)
▪ Pyrazinamide (PZA)
o Duration: Typically 6 months for drug-sensitive TB.
• Multidrug-Resistant TB (MDR-TB):
o Second-Line Drugs:
▪ Fluoroquinolones (e.g., levofloxacin, moxifloxacin)
▪ Injectable Agents (e.g., amikacin, kanamycin)
▪ Additional Agents: Such as linezolid or clofazimine.
o Duration: Longer treatment duration, often 18-24 months.
• Extensively Drug-Resistant TB (XDR-TB):
o Complex Regimen: Combination of second-line drugs and newer agents.
2. Supportive Measures:
• Nutritional Support
• Monitoring
• Psychosocial Support
3. Preventive Measures:
• Vaccination: BCG vaccine.
• Infection Control: Proper ventilation, use of masks, and isolation of infectious cases in healthcare settings.
• Contact Screening: Testing and monitoring individuals who have been in close contact with TB patients.
4. Management of Latent TB Infection (LTBI):
• Preventive Therapy: Isoniazid or a combination of isoniazid and rifapentine to prevent the progression to active
TB.
 Chapter-4: Physiology (Cardiovascular Module) | 185

• Classify different types of acute respiratory distress Integration with Acute respiratory
Re-P- syndrome. General distress
029 • Discuss the signs and symptoms of acute respiratory Medicine syndrome
distress syndrome.
• Discuss the management of acute respiratory distress
syndrome

Classification of Acute Respiratory Distress Syndrome (ARDS)

1. Severity of ARDS:
• Mild ARDS:
o PaO₂/FiO₂ Ratio: 200-300 mmHg.
o Examples: Early stages or less severe presentations.
• Moderate ARDS:
o PaO₂/FiO₂ Ratio: 100-200 mmHg.
o Examples: Moderate impairment of oxygenation.
• Severe ARDS:
o PaO₂/FiO₂ Ratio: <100 mmHg.
o Examples: Severe impairment of oxygenation with significant clinical impact.
2. Based on Cause (Pathophysiology):
• Direct ARDS: Resulting from direct injury to the lung parenchyma.
o Examples: Pneumonia, aspiration of gastric contents, toxic inhalation.
• Indirect ARDS: Resulting from systemic processes that affect the lungs.
o Examples: Sepsis, severe trauma, pancreatitis.
3. Timing (Berlin Definition):
• Early ARDS: Onset within 1 week of a known clinical insult or worsening respiratory symptoms.
• Moderate ARDS: Onset 1-2 weeks after insult.
• Late ARDS: Onset more than 2 weeks after the initial insult.
Signs and Symptoms of Acute Respiratory Distress Syndrome (ARDS)
1. Signs:
• Tachypnea: Rapid breathing.
• Cyanosis: Bluish discoloration of the skin and mucous membranes due to low oxygen levels.
• Use of Accessory Muscles: Increased work of breathing, noticeable use of neck and chest muscles.
• Diffuse Crackles: Rales heard on auscultation due to fluid in the alveoli.
2. Symptoms:
• Severe Dyspnea: Shortness of breath that develops quickly.
• Hypoxemia: Low blood oxygen levels, often refractory to supplemental oxygen.
• Confusion or Agitation: Due to hypoxia and impaired gas exchange.
• Fatigue: General weakness and tiredness due to respiratory distress.
Management of Acute Respiratory Distress Syndrome (ARDS)
1. Supportive Care:
• Oxygen Therapy: Supplemental oxygen to maintain adequate oxygen saturation.
• Mechanical Ventilation:
o Ventilation Strategy: Low tidal volume ventilation to reduce further lung injury (e.g., ARDSnet
protocol).

Join Medico Express Free Guidelines Group

03346072846
186 | 1st year MBBS – Block-3

o Positive End-Expiratory Pressure (PEEP): To prevent alveolar collapse and improve oxygenation.
2. Pharmacological Management:
• Antibiotics: For underlying infections, such as pneumonia.
• Corticosteroids: May be used in some cases to reduce inflammation and improve outcomes (e.g.,
dexamethasone).
• Neuromuscular Blockers: In severe cases, to reduce the work of breathing and improve ventilation (e.g.,
cisatracurium).
3. Fluid Management:
• Careful Fluid Resuscitation: To avoid fluid overload while maintaining adequate blood pressure and organ
perfusion.
4. Supportive Therapies:
• Prone Positioning: To improve ventilation and oxygenation in severe ARDS.
• Nutritional Support: Ensuring adequate nutrition to support recovery.
5. Treatment of Underlying Cause:
• Sepsis Management: Broad-spectrum antibiotics and source control.
• Trauma Care
• Management of Other Conditions
6. Advanced Interventions:
• Extracorporeal Membrane Oxygenation (ECMO): For severe cases unresponsive to conventional ventilation.
• Surgical Interventions: Rarely, in cases where other treatments fail.
7. Monitoring and Follow-Up:
• Continuous Monitoring: Regular assessment of oxygenation, ventilation, and hemodynamic status.
• Long-Term Follow-Up
 Chapter-4: Physiology (Cardiovascular Module) | 187

• Define respiratory failure. Integration with Respiratory

Re-P- • Describe various types of respiratory failure. General Medicine Failure
030 • Enlist various causes of respiratory failure.
• Outline management strategies of respiratory failure

Respiratory Failure: Respiratory failure is a condition in which the respiratory system fails in one or both of its gas
exchange functions: oxygenation and carbon dioxide elimination. It results in inadequate oxygenation of blood
(hypoxemia) and/or insufficient elimination of carbon dioxide (hypercapnia).
Types of Respiratory Failure:
1. Type 1 Respiratory Failure (Hypoxemic):
o Definition: Characterized by a low partial pressure of oxygen in the blood (PaO₂ < 60 mmHg) with
normal or low partial pressure of carbon dioxide (PaCO₂).
o Causes: Pneumonia, pulmonary edema, acute respiratory distress syndrome (ARDS), pulmonary
embolism, asthma, and interstitial lung disease.
2. Type 2 Respiratory Failure (Hypercapnic):
o Definition: Characterized by a high partial pressure of carbon dioxide in the blood (PaCO₂ > 50 mmHg)
with or without hypoxemia.
o Causes: Chronic obstructive pulmonary disease (COPD), severe asthma, neuromuscular disorders (e.g.,
myasthenia gravis), central respiratory depression (e.g., drug overdose), and obesity hypoventilation
syndrome.
3. Type 3 Respiratory Failure (Perioperative):
o Definition: Typically occurs in the postoperative period due to atelectasis or impaired respiratory
mechanics.
o Causes: Post-surgical atelectasis, abdominal surgery, thoracic surgery, and inadequate pain control
leading to shallow breathing.
4. Type 4 Respiratory Failure (Shock-related):
o Definition: Associated with circulatory shock, where respiratory failure occurs due to inadequate
perfusion of the respiratory muscles, leading to fatigue and failure.
o Causes: Septic shock, cardiogenic shock, hypovolemic shock, and neurogenic shock.
Causes of Respiratory Failure:
1. Lung Diseases:
o COPD
o Asthma
o Pneumonia
o Pulmonary edema
o ARDS
o Interstitial lung disease
2. Airway Obstruction:
o Foreign body aspiration
o Laryngeal edema
o Severe bronchospasm
3. Neuromuscular Disorders:
o Guillain-Barré syndrome
o Myasthenia gravis
o Amyotrophic lateral sclerosis (ALS)
o Spinal cord injury

Join Medico Express Free Guidelines Group

03346072846
188 | 1st year MBBS – Block-3

4.Central Nervous System Disorders:

o Drug overdose (opioids, sedatives)
o Stroke
o Traumatic brain injury
o Brainstem lesions
5. Thoracic and Chest Wall Disorders:
o Rib fractures
o Flail chest
o Severe kyphoscoliosis
o Obesity hypoventilation syndrome
6. Cardiovascular Causes:
o Pulmonary embolism
o Left heart failure
o Shock (septic, cardiogenic, hypovolemic)
Management Strategies of Respiratory Failure:
1. Oxygen Therapy:
o Administer supplemental oxygen to correct hypoxemia.
o Methods include nasal cannula, face mask, non-rebreather mask, or high-flow nasal cannula.
2. Ventilatory Support:
o Non-Invasive Ventilation (NIV): CPAP or BiPAP for patients with mild to moderate respiratory
failure.
o Invasive Mechanical Ventilation: Endotracheal intubation and ventilation for severe respiratory
failure.
3. Treat Underlying Cause:
o Antibiotics for infections (e.g., pneumonia).
o Bronchodilators and corticosteroids for asthma or COPD.
o Anticoagulation for pulmonary embolism.
o Diuretics for pulmonary edema.
4. Pharmacologic Therapy:
o Bronchodilators (e.g., beta-agonists, anticholinergics).
o Corticosteroids to reduce inflammation.
o Sedatives or analgesics to reduce anxiety and pain, facilitating ventilation.
o Neuromuscular blockers in severe cases requiring mechanical ventilation.
5. Supportive Care:
o Positioning (e.g., semi-recumbent or prone positioning in ARDS).
o Fluid management to avoid overload and worsening pulmonary edema.
o Nutritional support to prevent muscle wasting and maintain respiratory muscle function.
6. Monitoring and Follow-Up:
o Continuous monitoring of oxygenation (pulse oximetry, arterial blood gases).
o Regular assessment of ventilatory parameters if on mechanical ventilation.
o Adjust treatment based on clinical progress and test results.
 Chapter-4: Physiology (Cardiovascular Module) | 189

Describe ABC in a trauma patient Integration with Surgery First Aid in Surgical Patients
Re-P-031
ABC in a Trauma Patient:
The ABCs refer to the primary assessment and management steps in trauma care. They stand for Airway, Breathing, and
Circulation.
1. Airway with Cervical Spine Protection (A):
• Objective: Ensure the airway is open and clear to allow for adequate oxygenation while protecting the cervical
spine.
• Assessment:
o Check for patency of the airway: Look for signs of obstruction such as stridor, hoarseness, or inability
to speak.
o Inspect for foreign bodies, blood, vomit, or swelling that could obstruct the airway.
o Consider the risk of cervical spine injury in all trauma patients, especially those with head, neck, or high-
impact injuries.
• Management:
o If the airway is compromised, use techniques such as a jaw-thrust or chin-lift maneuver to open the
airway while maintaining cervical spine alignment.
o Suction to clear any obstructions.
o In cases of severe airway compromise, consider advanced airway management (e.g., endotracheal
intubation).
o Apply a cervical collar or other stabilization devices to protect the cervical spine.
2. Breathing and Ventilation (B):
• Objective: Ensure adequate breathing and oxygenation to support vital organ function.
• Assessment:
o Inspect the chest for movement, symmetry, and signs of trauma (e.g., flail chest, penetrating injuries).
o Auscultate for breath sounds: Check for equal and bilateral breath sounds.
o Palpate for any deformities or tenderness in the chest wall.
• Management:
o Administer supplemental oxygen via a non-rebreather mask or other appropriate devices.
o Address any life-threatening conditions such as:
▪ Tension pneumothorax: Immediate needle decompression followed by chest tube placement.
▪ Open pneumothorax: Apply an occlusive dressing and prepare for chest tube insertion.
▪ Flail chest: Provide ventilatory support, which may include positive pressure ventilation.
▪ Hemothorax: Insert a chest tube to drain blood and allow lung re-expansion.
3. Circulation with Hemorrhage Control (C):
• Objective: Ensure adequate circulation and control hemorrhage to maintain organ perfusion.
• Assessment:
o Check for pulse: Assess the rate, rhythm, and quality.
o Inspect for signs of shock: Look for pale, cool, clammy skin, altered mental status, or decreased urine
output.
o Identify any obvious sources of bleeding.
o Assess blood pressure and capillary refill time.
• Management:
o Control external bleeding with direct pressure, tourniquets, or hemostatic agents as needed.
o Establish IV access with two large-bore IV catheters.

Join Medico Express Free Guidelines Group

03346072846
190 | 1st year MBBS – Block-3

o Begin fluid resuscitation with crystalloids or blood products if necessary, based on the patient’s
hemodynamic status.
o Treat for shock: Consider the use of vasopressors if indicated, and continue monitoring for signs of
internal bleeding (e.g., abdominal trauma, pelvic fractures).
 Chapter-4: Physiology (Cardiovascular Module) | 191

MCQ PEARLS
Re-P-001 (Breathing)
1. Which muscle is primarily involved in normal quiet Diaphragm
breathing?
2. What is the primary muscle involved during forced Abdominal recti
expiration?
3. What does pulmonary ventilation refer to in the context Inflow and outflow of air between atmosphere and lung
of respiration? alveoli
4. What type of work is required to overcome airway Airway resistance work
resistance during inspiration?
5. Which respiratory abnormality is characterized by Cheyne-Stokes breathing
alternating deep and shallow breathing cycles?
6. Which condition is associated with airway obstruction Obstructive sleep apnea
during sleep?
7. What type of sleep apnea occurs due to blockage of the Obstructive sleep apnea
upper airway?
8. What is the most common treatment for obstructive sleep Nasal ventilation with CPAP
apnea?
9. What is a characteristic cause of central sleep apnea? Damage to the central respiratory centers
10. What procedure involves creating an opening in the Tracheostomy
trachea for obstructive sleep apnea?

Re-P-002 (Lung Compliance)

1. What is the definition of lung compliance? The extent to which the lungs will expand for each unit
increase in transpulmonary pressure
2. What is the relationship between lung compliance and Inverse
elastance?
3. What is the lung compliance value for both lungs? 200 ml of air/cm H2O transpulmonary pressure
4. Which condition is associated with increased lung Emphysema
compliance?
5. Which condition is associated with decreased lung Pulmonary fibrosis
compliance?
6. What type of cells secrete surfactant in the lungs? Type II alveolar epithelial cells
7. What is the most important phospholipid in surfactant? Dipalmitoyl phosphatidylcholine (lecithin)
8. What disease occurs in premature babies due to lack of Respiratory distress syndrome of newborn
surfactant?
9. At what gestational week does surfactant synthesis begin From the 24th to 35th week
in the fetus?
10. What is the significance of a Lecithin: Sphingomyelin Reflects mature levels of surfactant
ratio greater than 2:1 in amniotic fluid?

Re-P-003 (Lung volumes and Capacities)

1. What is the volume of air inspired or expired with each Tidal volume
normal breath called?
2. Which pulmonary volume refers to the extra air that can Inspiratory reserve volume
be inspired beyond the normal tidal volume?

Join Medico Express Free Guidelines Group

03346072846
192 | 1st year MBBS – Block-3

3. What is the volume of air remaining in the lungs after the Residual volume
most forceful expiration?
4. Which pulmonary capacity equals the tidal volume plus Inspiratory capacity
inspiratory reserve volume?
5. What is the vital capacity equal to in terms of pulmonary Inspiratory reserve volume + tidal volume + expiratory
volumes? reserve volume
6. What is the clinical significance of a decreased FEV- Indicates obstructive lung disease
1/FVC ratio?
7. Which disease is classified as a restrictive respiratory Polio myelitis
disease?
8. What is the anatomical dead space? Volume of all spaces in the respiratory system other than
alveoli and closely related gas exchange areas
9. What method is used to measure functional residual Helium dilution method
capacity, residual volume, and total lung capacity?
10. What is the normal value of dead space air? 150 ml

Re-P-004 (Pulmonary ventilation)

1. What is the formula for alveolar ventilation (VA)? VA = Freq × (VT – VD)
2. What is the minute respiratory volume (MRV) when the tidal volume is 500 ml and the 6000 ml/min or 6 L/min
frequency is 12 breaths/min?
3. What is the systolic pulmonary arterial pressure in a healthy human? 25 mm Hg
4. What is the mean pulmonary arterial pressure? 15 mm Hg
5. What percentage of the total blood volume is found in the lungs? 9 percent

Re-P-005 (Pulmonary Circulation)

1. What is the approximate blood volume of the lungs? 450 milliliters
2. What condition can increase pulmonary blood volume Failure of the left side of the heart
by 100% and cause large increases in pulmonary vascular
pressure?
3. What is the pulmonary arterial systolic pressure in a 25 mm Hg
healthy human?
4. What effect does a decrease in alveolar oxygen Causes vasoconstriction
concentration below 73 mm Hg have on pulmonary blood
vessels?
5. Which zone of pulmonary blood flow is characterized by Zone 3
continuous blood flow throughout the cardiac cycle?
6. During heavy exercise, how do the lungs accommodate By increasing the number of open capillaries and
increased blood flow without significantly raising distending them
pulmonary arterial pressure?
7. What happens to left atrial pressure when the left side of It rises, potentially up to 40 to 50 mm Hg
the heart fails?
8. What is the normal pulmonary capillary pressure? 7 mm Hg
9. What is the pulmonary capillary pressure in comparison Pulmonary capillary pressure is lower (7 mm Hg vs. 17 mm
to the peripheral tissues? Hg in peripheral)
10. What is the interstitial fluid pressure in the lung Slightly more negative in the lung (around -5 mm Hg to -8
compared to peripheral subcutaneous tissue? mm Hg)
 Chapter-4: Physiology (Cardiovascular Module) | 193

Re-P-006 (Pulmonary Edema, and Pleural Fluid)

1. What is the most common cause of pulmonary edema? Left-sided heart failure or mitral valve disease
2. What can cause damage to pulmonary blood capillary Infections like pneumonia or inhaling noxious substances
membranes leading to pulmonary edema?
3. What happens to pulmonary interstitial fluid pressure in It rises from negative to positive
pulmonary edema?
4. What is the safety factor against pulmonary edema in 21 mm Hg
acute conditions?
5. How does the body increase resistance to pulmonary Expansion of lymph vessels increases fluid drainage
edema in chronic conditions? capability
6. What is the usual pulmonary capillary pressure in 40 to 45 mm Hg
patients with chronic mitral stenosis without developing
lethal pulmonary edema?
7. What is the normal function of the thin layer of mucoid Facilitates easy slippage of the lungs during breathing
fluid in the pleural cavity?
8. What is pleural effusion? Collection of large amounts of free fluid in the pleural
space
9. What is a common cause of pleural effusion related to Cardiac failure
heart function?
10. What condition increases the permeability of capillary Infection or inflammation of the pleural cavity surfaces
membranes leading to pleural effusion?

Re-P-007 (Principles of Gaseous Exchange)

1. What is the function of the respiratory membrane? It is the membrane through which gas exchange takes place
2. Which layer lines the alveoli in the respiratory Surfactant
membrane?
3. How does the thickness of the respiratory membrane Inversely
affect gas diffusion?
4. What is the diffusing capacity of the respiratory 21 ml/min/mm Hg
membrane for oxygen under resting conditions?
5. What is the value of pleural pressure at the beginning of -5 cm H2O
inspiration?
6. What is transpulmonary pressure? The difference between alveolar and pleural pressure
7. What happens to alveolar pressure during normal It decreases to about -1 cm H2O
inspiration?
8. Why is alveolar air only partially replaced by To prevent sudden changes in gas concentrations in the
atmospheric air with each breath? blood
9. What is the significance of transpulmonary pressure? It measures the elastic forces in the lungs that tend to
collapse the lungs
10. How much alveolar air is renewed with each normal 350 ml
inspiration?

Re-P-008 (Transport of oxygen in the blood)

1. What percentage of oxygen is transported in dissolved form in the 3%
blood?
2. How much oxygen is transported per 100 mL of plasma in dissolved 0.3 mL
form?
3. What percentage of oxygen is transported in combination with 97%
hemoglobin?

Join Medico Express Free Guidelines Group

03346072846
194 | 1st year MBBS – Block-3

4. What is the main form of oxygen transport in the blood? In combination with hemoglobin
5. Why is the transport of oxygen in combination with hemoglobin It transports the maximum amount of oxygen
important?

Re-P-009 (oxyhemoglobin dissociation curve, Bohr`s effect, Cyanosis)

1. What is the usual O2 saturation of systemic arterial blood, given a PO2 97%
of about 95 mm Hg?
2. What is the average O2 saturation of hemoglobin in normal venous blood 75%
with a PO2 of about 40 mm Hg?
3. How much oxygen can 15 grams of hemoglobin in 100 mL of blood bind 20 milliliters (20 volumes percent)
if fully saturated?
4. What factor causes a right shift in the oxygen-hemoglobin dissociation Increased CO2
curve?
5. What effect does Bohr’s Effect have at the tissue level? Shifts the curve to the right
6. What is the effect of increased hydrogen ion concentration on the Right shift
oxygen-hemoglobin dissociation curve?
7. What does peripheral cyanosis indicate about the skin and mucous Bluish discoloration in exposed skin only
membranes?
8. What is a common cause of central cyanosis? Lung diseases
9. What is the primary reason for clubbing in central cyanosis? Hypoxic hypoxia
10. Which factor decreases the affinity of hemoglobin for oxygen according Increased pCO2
to Bohr’s Effect?

Re-P-010 (Transport of CO2 in blood)

1. What percentage of CO2 is transported in the blood as bicarbonate? 70%
2. What is the normal PCO2 range in arterial and venous blood? 40 mm Hg to 45 mm Hg
3. How much CO2 is exchanged during normal transport from the tissues to the 4%
lungs?
4. What is the effect of oxygen binding with hemoglobin on carbon dioxide? Displaces CO2 from hemoglobin
5. What is the primary effect of the Haldane effect? Release of CO2 into the alveoli
6. What is the chloride shift? Exchange of Cl- for HCO3- in RBC
7. What happens to RBC size at the tissue level due to chloride shift? Increases in venous blood
8. What is the respiratory exchange ratio (R) on a carbohydrate diet? Increases to 1
9. What percentage of CO2 is transported in the blood as carboxyhemoglobin? 23%
10. How does the respiratory exchange ratio change with a fat-rich diet? Decreases to 0.6

Re-P-011 (VA/Q (ventilation perfusion ratio)

1. What is the normal ventilation-perfusion (V/Q) ratio? Approximately 0.8
2. What are the partial pressures of O2 and CO2 in alveoli with a normal PO2 = 104 mm Hg, PCO2 = 40 mm Hg
V/Q ratio?
3. What is the PO2 and PCO2 in alveoli with a zero V/Q ratio? PO2 = 40 mm Hg, PCO2 = 45 mm Hg
4. What is the term for venous blood passing through pulmonary capillaries Shunted Blood
without becoming oxygenated?
5. What is the physiological shunt? Total amount of shunted blood per minute
6. What occurs when the ventilation (V) is zero and there is still perfusion V/Q ratio = 0, called a shunt
(Q)?
 Chapter-4: Physiology (Cardiovascular Module) | 195

7. What are the PO2 and PCO2 in alveoli with an infinite V/Q ratio? PO2 = 149 mm Hg, PCO2 = 0 mm Hg
8. What is the condition called when there is no capillary blood flow but Dead Space
normal ventilation?
9. What does an infinite V/Q ratio indicate about the alveolar gas No gas exchange occurs
exchange?
10. What are the partial pressures of inspired air in a dead space situation? PO2 = 149 mm Hg, PCO2 = 0 mm Hg

Re-P-012 (Protective reflexes)

1. Which of the following is a respiratory function of the Exchange of gases in the lungs
lungs?
2. Which non-respiratory function of the lungs involves Temperature regulation
regulation of body temperature?
3. What is the primary nervous control of bronchiolar Sympathetic stimulation with norepinephrine and
musculature for dilation? epinephrine
4. What neurotransmitter causes constriction of bronchioles Acetylcholine
through parasympathetic stimulation?
5. What is the receptor organ involved in the cough reflex? Terminal bronchioles, larynx, trachea, and carina
6. What nerve carries the afferent signal for the cough Vagus nerve
reflex?
7. During the cough reflex, what is the maximum pressure 100 mm Hg or more
achieved in the lungs?
8. Which cranial nerve is involved in the sneeze reflex? Fifth cranial nerve
9. What is the receptor organ involved in the sneeze reflex? Nasal passageways
10. During the sneeze reflex, what happens to the uvula? The uvula is depressed

Re-P-013 (Aviation and space)

1. What does acclimatization refer to? Adaptations or adjustments by the body to high altitude
2. What is one of the primary physiological changes that Increased pulmonary ventilation
occur during acclimatization?
3. What does chronic mountain sickness often lead to in The red blood cell mass and hematocrit become
terms of red blood cell mass? exceptionally high
4. What is a common acute condition that can occur due to Acute cerebral edema
rapid ascent to high altitude?
5. What condition is associated with elevated pulmonary Right-sided heart enlargement
arterial pressure in chronic mountain sickness?
6. How does acclimatization affect the diffusing capacity It increases
of the lungs?
7. What is a significant risk of ascending to high altitude Acute pulmonary edema
too quickly without acclimatization?
8. What happens to the ability of tissue cells to use oxygen It increases
during acclimatization?
9. What can be a consequence of chronic mountain sickness The peripheral arterial pressure begins to fall
related to peripheral arterial pressure?
10. What is a possible outcome of chronic mountain Congestive heart failure and death
sickness if left untreated?

Re-P-014 (Deep sea diving)

1. What primarily causes decompression sickness? Rapid ascent from high-pressure environment

Join Medico Express Free Guidelines Group

03346072846
196 | 1st year MBBS – Block-3

2. Which gas is primarily responsible for decompression Nitrogen

sickness when it forms bubbles?
3. What happens to nitrogen in tissues during a high- It dissolves in tissues, especially fat
pressure environment?
4. What is a common symptom of decompression sickness Severe pain in tissues, particularly joints
due to nitrogen bubbles in the sensory nerve fibers?
5. What is a recommended prevention method for Stepwise ascent with regular intervals
decompression sickness during ascent?
6. What treatment is commonly used for decompression Recompression in a hyperbaric chamber
sickness?
7. What symptom may occur due to bubbles in the coronary Coronary ischemia
arteries?
8. What is a possible effect on the brain and spinal cord due Damage to tissues from obstruction of blood vessels
to decompression sickness?
9. How should a person be brought back to atmospheric Slowly reducing the pressure in a recompression chamber
pressure after decompression sickness?
10. What is a symptom that could indicate severe Fatigue, unconsciousness, and death
decompression sickness leading to unconsciousness?

Re-P-015 (Carbon monoxide poisoning)

1. What is a key characteristic of carbon monoxide (CO) in terms of its Colorless and odorless
physical properties?
2. What color change is typically observed in the skin of someone suffering Cherry red
from CO poisoning?
3. How does carbon monoxide affect the oxyhemoglobin dissociation curve? Shifts the curve to the left
4. What is a primary treatment method for CO poisoning? 100% oxygen therapy
5. How can hyperbaric oxygen therapy be beneficial in treating CO It provides oxygen at increased pressure
poisoning?

Re-P-016 (Nervous regulation of respiration)

1. Where is the Dorsal Respiratory Group of neurons Nucleus of the tractus solitarius (NTS)
located?
2. What is the primary function of the Dorsal Respiratory Generates basic rhythm of respiration
Group of neurons?
3. What is the role of inspiratory ramp signals? Provides a slow and steady inspiration
4. Where is the Pneumotaxic Center located? Nucleus parabrachialis of the upper pons
5. What effect does the Pneumotaxic Center have on Controls rate and duration of breathing
breathing?
6. Which group of neurons is active during forced Ventral Respiratory Group
breathing?
7. What is the primary function of the Apneustic Center? Increases depth of inspiration
8. What happens during the Hering-Breuer reflex? Limits period of inspiration to prevent excess lung inflation
9. How does the Ventral Respiratory Group influence Provides powerful expiratory signals during heavy
respiration? expiration
10. What occurs during inspiration due to the activity of the Inspiratory ramp signals are generated
Dorsal Respiratory Group?
 Chapter-4: Physiology (Cardiovascular Module) | 197

Re-P-017 (Chemical control of respiration)

1. Where is the Central Chemosensitive Area located? Beneath the ventral surface of the medulla
2. What is the primary stimulus for the Central H+ ions
Chemosensitive Area?
3. How does blood CO2 indirectly affect the Central Blood CO2 crosses the blood-brain barrier and forms
Chemosensitive Area? H2CO3, which dissociates into H+ ions
4. Why does CSF CO2 have a more potent effect on the CSF has less protein buffers and H+ ions from H2CO3 are
Central Chemosensitive Area compared to blood CO2? not removed rapidly
5. Where are the majority of peripheral chemoreceptors Carotid bodies at the bifurcation of common carotid
located? arteries
6. Which nerve carries afferents from the carotid bodies to Hering’s nerve
the dorsal inspiratory area?
7. Which nerve carries afferents from the aortic bodies to Vagus nerve
the dorsal medullary inspiratory area?
8. What range of arterial oxygen levels stimulates the 60 mm Hg down to 30 mm Hg
peripheral chemoreceptors?
9. How does the Central Chemosensitive Area respond to Blood H+ ions cannot cross the blood-brain barrier directly,
changes in blood H+ concentration? so they do not affect it directly
10. What is the role of the Central Chemosensitive Area in It excites other portions of the respiratory center to increase
respiration? rate and intensity of respiration

Re-P-018 (Exercise and Respiration)

1. What does the motor cortex do in addition to transmitting Sends collateral impulses to excite the dorsal inspiratory
impulses to contracting muscles during exercise? area
2. What types of receptors excite the dorsal inspiratory area Receptors for position and movement around joints,
during exercise? muscles, tendons, and joint ligaments
3. How does an increase in body temperature during It stimulates respiration directly and indirectly
exercise affect respiration?
4. How does arterial PCO2 change during heavy exercise? It remains normal at 40 mm Hg
5. What is the role of the neurogenic factor during heavy Shifts the ventilation curve about 20-fold upward to match
exercise? CO2 release and maintain normal arterial PCO2

Re-P-019 (Hypoxia)
1. What is the primary characteristic of hypoxic hypoxia? Decreased arterial partial pressure of oxygen
2. What is the most effective treatment for hypoxic Oxygen treatment
hypoxia?
3. What type of hypoxia is characterized by a reduced Anemic Hypoxia
oxygen carrying capacity of blood?
4. What is a common cause of stagnant hypoxia? Decreased cardiac output
5. In which type of hypoxia is the PO₂ in arterial blood Anemic Hypoxia, Stagnant Hypoxia, Histotoxic Hypoxia
normal?
6. Which type of hypoxia is caused by an inability of tissues Histotoxic Hypoxia
to utilize oxygen?
7. Which type of hypoxia is characterized by normal Hypoxic Hypoxia, Stagnant Hypoxia, Histotoxic Hypoxia
oxygen carrying capacity of blood?
8. What treatment is effective for histotoxic hypoxia? Methylene blue or nitrites
9. What type of hypoxia involves decreased velocity of Stagnant / Ischemic Hypoxia
blood flow?

Join Medico Express Free Guidelines Group

03346072846
198 | 1st year MBBS – Block-3

10. Which type of hypoxia has the lowest efficacy of Stagnant / Ischemic Hypoxia, Histotoxic Hypoxia
oxygen therapy?

Re-P-020 (Tuberculosis)
1. What is the causative organism of tuberculosis? Mycobacterium tuberculosis
2. What is one of the effects of tuberculosis on lung Decrease vital capacity
function?
3. What happens to the respiratory membrane surface area Decrease total respiratory membrane surface area
in tuberculosis?
4. What is an effect of tuberculosis on the thickness of the Increase thickness of respiratory membrane
respiratory membrane?
5. In severe cases of untreated tuberculosis, what can Extreme destruction with formation of large abscess
happen to the lung tissue? cavities

Re-P-021 (Pneumonia)
1. What is pneumonia characterized by? Inflammatory condition of the lungs with alveoli filled with
fluid and blood cells
2. What is an effect of pneumonia on the surface area of the Decreased surface area of respiratory membrane
respiratory membrane?
3. What is a common consequence of pneumonia related to Hypoxemia
blood oxygen levels?

Re-P-022 (Dyspnea)
1. What is dyspnea commonly referred to as? Air hunger
2. Which condition is not a cause of dyspnea? Diabetes mellitus
3. What is a common symptom of cardiac dyspnea? Orthopnea
4. Which physical exam finding is typically associated with Wheezing
respiratory dyspnea?
5. What is a prominent clinical feature of cardiac dyspnea but not Edema
respiratory dyspnea?
6. How does dyspnea related to cardiac issues generally respond Significant improvement
to diuretics?
7. What is the typical effect of bronchodilators in managing Opens airways and improves airflow
dyspnea?
8. Which treatment is most effective for hypoxic hypoxia? Oxygen therapy
9. What non-pharmacological management technique helps to Sit upright or use pillows to support sitting position
ease breathing in patients with orthopnea?
10. Which of the following is a characteristic of pulmonary Sputum production and wheezing
dyspnea but not cardiac dyspnea?

Re-P-023 (Pneumothorax)
1. What is pneumothorax characterized by? Presence of air in the pleural space
2. What effect does pneumothorax have on intrapleural pressure? Intrapleural pressure becomes positive
3. Which symptom is commonly associated with pneumothorax? Sharp and stabbing chest pain
4. What can cause a pneumothorax? Damage to the chest wall or lungs
5. Which sign or symptom is NOT typically associated with pneumothorax? Persistent, productive cough
 Chapter-4: Physiology (Cardiovascular Module) | 199

Re-P-024 (Pleuritis)
1. What is pleuritis? Inflammation of the pleura
2. Which infection is NOT a common cause of pleuritis? Chickenpox
3. What type of pain is typically associated with pleuritis? Sharp, stabbing pain
4. Which diagnostic sign is characteristic of pleuritis? Pleuritic rub on auscultation
5. Which medication is commonly used to manage pain in Non-Steroidal Anti-Inflammatory Drugs (NSAIDs)
pleuritis?
6. What is the treatment approach for pleuritis caused by Corticosteroids
autoimmune diseases?
7. What condition may require thoracentesis or a chest tube for Significant pleural effusion
management?
8. Which symptom is typically NOT associated with pleuritis? Productive cough
9. What type of breathing exercise is recommended for Gentle breathing exercises
symptomatic relief in pleuritis?
10. What type of infection is managed with antivirals in the case Viral infections
of pleuritis?

Re-P-025 (Bronchitis)
1. What is the primary cause of chronic bronchitis? Smoking
2. Which type of bronchitis is often associated with exposure to Chronic Bronchitis
environmental pollutants?
3. What symptom is common in both acute and chronic bronchitis but may Cough
differ in duration?
4. Which medication is typically used to manage pain and fever in acute NSAIDs (e.g., ibuprofen, acetaminophen)
bronchitis?
5. What is a key management strategy for chronic bronchitis? Smoking cessation
6. What type of bronchitis is associated with persistent cough lasting for at Chronic Bronchitis
least three months in two consecutive years?
7. What is a common symptom of acute bronchitis that may not be present Fever
in chronic bronchitis?
8. Which treatment is specifically used to help open airways in chronic Bronchodilators
bronchitis?
9. What is a significant non-pharmacological intervention for chronic Pulmonary rehabilitation
bronchitis?

Re-P-026 (Pneumonia)
1. What is a primary cause of pneumonia? Bacterial or viral infection
2. What type of pneumonia involves inflammation of bronchi and is also Lobular pneumonia
known as bronchopneumonia?
3. What is a common symptom of pneumonia related to mucus Cough with yellow, green, or bloody mucus
production?
4. What is a common management strategy for pneumonia? Oxygen Therapy
5. Which type of pneumonia is associated with consolidation of the Lobar pneumonia
affected lung area?
6. What is a symptom of pneumonia that may cause discomfort during Chest pain and/or abdominal pain
coughing or deep breathing?
7. What is the typical treatment for a bacterial cause of pneumonia? Antibacterial drugs

Join Medico Express Free Guidelines Group

03346072846
200 | 1st year MBBS – Block-3

8. What symptom might indicate a more severe case of pneumonia or a High fever
systemic response?
9. What type of pneumonia can also be classified as atypical? Lobar pneumonia
10. What type of medication is used to relieve symptoms of coughing in Cough Suppressants
pneumonia?

Re-P-027 (Asthma)
1. What is the primary cause of asthma? Allergic hypersensitivity to foreign substances
2. What type of irritants are associated with asthma in older people? Non-allergic types of irritants in the air
3. What is a common effect of asthma on bronchioles? Spasm of the bronchiolar smooth muscle
4. Which medication class includes beta agonists and anti-muscarinic Bronchodilators
agents?
5. What symptom of asthma involves a high-pitched whistling sound Wheezing
during breathing?
6. What is a common symptom of asthma that relates to difficulty Chest tightness
breathing and sensation of tightness?
7. What effect does asthma have on the secretion within the Secretion of thick mucus
bronchiolar lumen?
8. What is a potential symptom of severe asthma that may affect Drowsiness or confusion
consciousness?
9. What type of drugs are used to reduce inflammation in asthma? Anti-inflammatory drugs
10. What is a recommended management strategy for asthma related Avoiding allergic agents
to allergens?

Re-P-028 (Tuberculosis)
1. What is a second-line drug used in the treatment of TB? Second-line drugs and newer agents
2. What type of support is essential in TB management besides medication? Nutritional Support
3. What preventive measure is recommended to protect against TB in Proper ventilation and use of masks
healthcare settings?
4. What is the purpose of the BCG vaccine? Vaccination against TB
5. What is involved in contact screening for TB? Testing and monitoring close contacts
6. What drug combination is used for preventive therapy in latent TB infection Isoniazid and rifapentine
(LTBI)?
7. What type of support is provided to patients to help them cope with TB? Psychosocial Support
8. What is a key component of managing latent TB infection (LTBI)? Preventive Therapy
9. What measure helps prevent the spread of TB in public settings? Isolation of infectious cases
10. What monitoring practice is essential in the management of TB? Regular Monitoring

Re-P-029 (Acute respiratory distress syndrome)

Statement Answer
1. What is the PaO₂/FiO₂ ratio range for mild ARDS? 200-300 mmHg
2. Which ARDS type results from systemic processes affecting the lungs? Indirect ARDS
3. What is a common example of direct ARDS? Pneumonia
4. What is the PaO₂/FiO₂ ratio for severe ARDS? <100 mmHg
5. Which timing category of ARDS onset occurs within 1 week of a known clinical Early ARDS
insult?
 Chapter-4: Physiology (Cardiovascular Module) | 201

6. What symptom is characterized by a bluish discoloration of the skin due to low Cyanosis
oxygen levels?
7. What ventilation strategy is recommended to reduce further lung injury in ARDS? Low tidal volume ventilation
8. Which medication may be used to reduce inflammation in ARDS? Corticosteroids
9. What is a supportive therapy that improves ventilation and oxygenation in severe Prone Positioning
ARDS?

Re-P-030 (Respiratory Failure)

1. What is the PaO₂ threshold for Type 1 Respiratory Failure PaO₂ < 60 mmHg
(Hypoxemic)?
2. Which type of respiratory failure is characterized by PaCO₂ > 50 Type 2 Respiratory Failure (Hypercapnic)
mmHg?
3. What is a common cause of Type 3 Respiratory Failure Post-surgical atelectasis
(Perioperative)?
4. Which type of respiratory failure is associated with inadequate Type 4 Respiratory Failure (Shock-related)
perfusion of respiratory muscles?
5. What is a typical management method for Type 1 Respiratory Oxygen Therapy
Failure?
6. Which disorder is a common cause of Type 2 Respiratory Failure Chronic obstructive pulmonary disease (COPD)
(Hypercapnic)?
7. What type of ventilatory support is used for mild to moderate Non-Invasive Ventilation (NIV)
respiratory failure?
8. Which medication is used to reduce inflammation in respiratory Corticosteroids
failure management?
9. What supportive care measure can be used to avoid fluid overload Fluid management
in respiratory failure?
10. What is an example of a central nervous system disorder that can Stroke
cause respiratory failure?

Re-P-031 (First Aid in Surgical Patients )

1. What is the primary objective of the Airway component in Ensure the airway is open and clear.
trauma care?
2. Which maneuver is used to open the airway while protecting Jaw-thrust maneuver
the cervical spine?
3. What should be done if the airway is severely compromised? Consider endotracheal intubation.
4. What is a common sign of a tension pneumothorax that Tracheal deviation or absent breath sounds.
requires immediate intervention?
5. How is a flail chest typically managed in trauma care? Provide ventilatory support.
6. What is the purpose of administering supplemental oxygen To ensure adequate oxygenation.
in trauma care?
7. How should external bleeding be controlled in a trauma With direct pressure, tourniquets, or hemostatic agents.
patient?
8. What is the recommended IV access approach in trauma Establish two large-bore IV catheters.
care?
9. What signs indicate the need for fluid resuscitation in a Signs of shock such as altered mental status and
trauma patient? decreased urine output.
10. What should be done if signs of internal bleeding are Monitor closely and manage based on hemodynamic
suspected? status.

Join Medico Express Free Guidelines Group

03346072846
202 | 1st year MBBS – Block-3

UNIVERSITY QUESTIONS
TOPIC: TRANSPORT OF OXYGEN IN THE BLOOD
Q1. Draw and label oxygen hemoglobin dissociation curve. Enumerate factors which shift the curve to left. What is bohrs
effects? (Annual 2007)
Q2. a) Draw and label oxygen hemoglobin dissociation curve. Enumerate the causes which shift the curve to right and left
sided?
b) What is Haldene’s effect? (Supple 2015)
Q3: a) Enlist FOUR factors that determine the gas exchange through respiratory membrane. 2.5
b) Draw and label the Oxyhemoglobin Association-Dissociation curve and define Bohr’s effect and P50− (Supple
2016)
Q4: a) Draw and label oxygen hemoglobin dissociation curve. List the factors that shift the curve to right and to the left
side.
b) Describe the role of peripheral chemoreceptors in control of breathing. (Supply 2020 held in 2021)

TOPIC: LUNG VOLUMES AND CAPACITIES

Q1. Define dead space. What are tits types? Give the advantages of dead space. (Supple 2007) (5)
Q2. A middle aged man has aterial PCO2 = 65mmHg (normal 40mmHg) and arterial pH = 7.3. Explain the mechanism by
which these changes can effects the respiration. (Annual 2010).
Q3. Which pulmonary volumes and capacilities can be determined by a spirometer? Give their details
and normal values: (Supple 2010
Q4. A man of 45 years is suffering from bronchial asthma with asthma. What changes in the following lung function
parameters are likely in this man: (Annual 2011) (5)
a) Surface area of respiratory membrane
b) Lung compliance
c) Residual volume
d) Functional residual capacity
Q5. A man 50 year old is suffering from bronchial asthma since ten years. His lung function tests were done. How
following parameters are affected and why? (Annual 2012)
a. FEV1
b. FEV1/FVC %
c. residual volume
d. Functional residual capacity
Q6: A 45 years old man has respiratory rate =16 per minute. His tidal volume is 600 mL and dead space volume is 150
mL. What is the minute respiratory volume and alveolar ventilation rate of this man? 2
b) Draw and label normal Oxygen-Hemoglobin dissociation curve and discuss its shift during strenuous exercise. 3
(Supplementary 2017)
Q7: Define lung Compliance. How the surfactant increases lung compliance? (Supplementary 2018)
Q8: A 50 years old smoker progressively developed dyspnea and cough over a few months. After clinical examination and
performing his Lung Function Tests, he was diagnosed to be suffering from pulmonary emphysema. How following
parameters will be altered in this patient. (Supplementary 2018 held in 2019)
(a) Ventilation perfusion ratio.
(b) Pulmonary compliance.
(c) Functional residual capacity.
Q9: a) What is lung compliance? (Annual 2019)
 Chapter-4: Physiology (Cardiovascular Module) | 203

Enumerate four conditions in which lung compliance decreases. 1, 1

Q:10 a) What is the compliance of lungs. Explain the forces that determine the compliance of lungs in a healthy person.
(SUPPLY 2023 HELD IN 2024)
b) Explain why saline filled lungs have more compliance than that of air filled lungs with the help of a diagram

TOPIC: CHEMICAL CONTROL OF RESPIRATION

Q1. What are peripheral chemoreceptors? Give their role in the control of respiration. (Annual 2008) (5)
Q2. What is the major form of transport of carbon dioxide in the blood? Explain the Haldane’s effect. (Supple 2008) (5)
Q3. Give chemical regulation of the respiration. (Annual 2015).

TOPIC: RESPIRATORY DISTRESS SYNDROMDE

Q1. A premature is brought to Pediatric emergency with marked difficulty in breathing, bluishness of the skin and
tachypnoea of 30 breaths / min. (Annual 2009)
a. What is Disorder? (1)
b. What are Physiological basis of this disorder? (3)

TOPIC: HYPOXIA
Q1. Define hypoxia. What are its types? (Supple 2011) (5)

TOPIC: TRANSPORT OF CARBONDIOXIDE IN BLOOD

Q1. a. What are different forms in which carbon dioxide is transported in the blood?
b. What is Haldane effect? (Annual 2013)
Q2: a) How is Carbon Dioxide transported in the blood? 3.5
b) What is Functional Residual Capacity? (Annual 2016) 1.5

TOPIC: NERVOUS CONTROL OF RESPIRATION

Q1. a. What is respiratory Ramp signal? (Supple 2013) (2.5)
b. Give effects of changes in extracellular fluid of hydrogen ion, partial pressure of CO2 & partial pressure of O2 on
respiration. (2.5)
Q2. How respiration is stimulated secondary to changes in the: (Annual 2014)
a. Arterial oxygen tension
b. Brain interstitial fluid hydrogen ion concentration

TOPIC: DEEP SEA DIVING

Q1: Enlist symptoms of Decompression sickness. 2.5 (Annual 2017)
Q2: Write down the causes, symptoms and treatment of CAISSON DISEASE. 2.5 (Supplementary 2017)
Q3: a) Enlist symptoms of decompression sickness. Why these symptoms in this condition? (Annual 2018)

TOPIC: BREATHING
Q1: a) Arterial blood gas analysis of a patient revealed arterial PCO2= 67 mmHg and arterial pH=7.33. How these changes
can affect his respiration?
b) What are the components of "Work" of Breathing? (Supple 2019 held in 2020)
Q2: A four-hours-old 28,-week gestation, 2.3 kg male infant was born to a 25 year old healthy woman. The infant
developed progressively severe respiratory distress after birth. Doctors referred the baby to neonatal nursery where he was
put on continuous positive airway pressure therapy.
a) Do premature babies have any lung problem?

Join Medico Express Free Guidelines Group

03346072846
204 | 1st year MBBS – Block-3

b) What is the principle of surface tension?

c) Explain the importance of surfactant in reducing alveolar surface tension in air filled lung.
d) Define the “Laplace’s Law”. How is this applied to lung mechanism if air passage leading from alveoli is blocked?
(Annual 2020)
Q3. a) Draw and label a graph showing changes in alveolar pressure, pleural pressure and transpulmonary pressure during
normal breathing. (Annual 2022 hel in 2023)
b) What is surfactant? What is its significance?
Q4. a) What are the components of “Respiratory Unit”? (Supply 2022 held in 2023)
b) Describe the factors affecting rate of gas diffusion through the respiratory membrane.
 Chapter-4: Physiology (Cardiovascular Module) | 205

Join Medico Express Free Guidelines Group

03346072846
206 | 1st year MBBS – Block-3