ANATOMY & PHYSIOLOGY

BLOOD

Heart Anatomy ▪ Atrium and sinus venosus form left

• Located within mediastinum of thoracic and right atria
cavity • Embryonic heart folds on itself at 24 and 35
• Pericardium surrounds heart, forming days of gestation
pericardial cavity
• Base - posterior site where great vessels
attach to heart
• Apex - inferior tip of heart
▪ Just left of the sternum
▪ Indention forms cardiac notch of left
lung • Walls form to separate chambers of the
heart
▪ Interatrial septum between the atria
▪ Interventricular septum between the
ventricles
• Congenital heart defects (CHDs) may occur
if development proceeds incorrectly

Chambers of the Heart

Atria
• superior chambers
• Receives
• Right atrium -receives deoxygenated blood
from systemic circuit
▪ Via superior vena cava, inferior vena
cava, and coronary sinus
• Left atrium - receives oxygenated blood
from pulmonary circuit
▪ Via pulmonary veins
Ventricles
• inferior chambers
• Ejects
• Right ventricle - ejects deoxygenated blood
into pulmonary trunk
▪ Pulmonary trunk divides
into pulmonary arteries and sends
Embryonic Development of the Heart blood to lungs
• Prior to 24 days gestation, the heart is a five- • Left ventricle - ejects oxygenated blood into
section tube aorta
▪ Truncus arteriosus forms aorta and ▪ Sends blood to systemic tissues
pulmonary trunk
▪ Bulbus cordis and ventricle form the
left and right ventricles
 Pericardium
• Membranous sac that surrounds heart
Fibrous pericardium
• Attaches heart to diaphragm
Serous pericardium
• reduces friction as heart beats
▪ Parietal layer
▪ Visceral layer
Pericardial cavity
• Cavity in between parietal and visceral
layers

Circulation through the Heart

• Deoxygenated blood is received by right
atrium
▪ Via superior vena cava, inferior vena
cava, and coronary sinus
• Blood enters right ventricle and is ejected
into pulmonary trunk
• Pulmonary trunk divides to form
pulmonary arteries that deliver blood to
lungs
• Pulmonary veins carry oxygenated blood
from lungs to left atrium Formation of Serous Pericardium
• Oxygenated blood enters left ventricle and • Serous pericardium begins as a fluid-filled
is ejected into aorta and systemic arteries sac
• As heart enlarges, it pushes into the sac
Human Circulation ▪ Like a fist pushing into a balloon
• Two systems of blood vessels in human • Results in a double-layered sac with a fluid-
circulation. filled cavity between the heart and the
Systemic circuit pericardium
• Transports oxygenated blood to tissues and
returns deoxygenated blood back to heart.
Pulmonary circuit
• Transports deoxygenated blood from heart
to lungs and returns oxygenated blood back
to heart.
 Surface Features of the Heart Epicardium
Auricles • most superficial
• pouch-like extensions of each atrium ▪ Same as visceral layer of serous
▪ Allow atria to accept extra amounts pericardium
of blood Myocardium
Sulci • contains cardiac muscle
• grooves that contain coronary blood ▪ Thickest layer of heart wall
vessels ▪ Contains collagenous framework of
▪ Coronary sulcus heart, blood vessels, and nerves
▪ Anterior interventricular sulcus Endocardium
▪ Posterior interventricular sulcus • deepest layer
▪ Simple squamous epithelium
▪ Continuous with endothelium of
blood vessels

Orientation of Cardiac Muscle Fibers

• Cardiac muscle fibers are oriented for
effective contraction
• Fibers wrap around each atrium
▪ Contraction of cardiac muscle
forces blood into the ventricles
• Fibers swirled from apex toward great
arteries around ventricles
▪ Contraction at apex forces blood
into the great vessels

Anterior Surface of Heart

• Left and right ventricles are prominent on Myocardial Thickness
anterior surface • Transverse and coronal sections of the heart
• Fat deposits protect the heart and blood show myocardial thickness
vessels within sulci • Left ventricle has a thicker myocardium
compared to the right ventricle
▪ Hypertrophies early in life
▪ Due to increased resistance of the
aorta (to systemic circuit), which
must be overcome

Layers of the Heart Wall

 Interatrial Septum of the Heart Heart Valves
• Interatrial septum located between atria • Valves prevent blood from moving in the
• Contains fossa ovalis wrong direction
▪ Oval shaped depression Atrioventricular (AV)
▪ Remnant of foramen ovale of fetal • Valves located between atria and
heart that allowed blood to bypass ventricles
pulmonary circuit ▪ Tricuspid valve on right
o Lungs don’t oxygenate blood ▪ Bicuspid valve on left
in fetus Semilunar (SL)
▪ Septum primum closes foramen • Valves located at exit points of heart
ovale at birth ▪ Pulmonary valve on right
Interventricular Septum of the Heart ▪ Aortic valve on left
• Interventricular septum located between
ventricles Heart Valve Functioning
▪ More muscular than interatrial • Valves open and close in response to
septum pressure differences
▪ Aids in ventricular contraction • When ventricles contract, blood rushes
toward atria and AV valves close
Fibrous Skeleton of Heart • When ventricles relax, blood attempts to
• Fibrous skeleton separates atria from reenter heart and SL valves close
ventricles
• Four openings allow blood to move through
the heart
▪ Each opening has a valve to ensure
one-way blood flow through the
heart
• Atrioventricular (AV) valves between atria
and ventricles
• Semilunar (SL) valves between ventricles
and great vessels (pulmonary trunk and
aorta)
Internal Ventricular Features
Interventricular septum
• wall between ventricles
Chordae tendineae
• anchor AV valves
Papillary muscles
• large bundles of muscle attached to chordae
tendineae
Trabeculae carneae
• large ridges on interior of ventricular walls

AV Valve Features
• AV valves contain cusps that ensure one-
way flow of blood
• Chordae tendineae anchor cusps to
papillary muscles on the ventricular walls
Right - DEOXYGENATED • Failure to function properly leads to valvular
Right Atrium heart disease
• Receives deoxygenated blood from the • Regurgitation occurs when valves allow
systemic circuit blood to move in wrong direction (e.g., from
▪ Via the super vena cava, inferior vena ventricle into the atrium)
cava, and coronary sinus Valve stenosis
• Fills with venous blood during atrial • Valve stenosis occurs when valves become
relaxation calcified
▪ Venous return ▪ Valve may be harder to open causing
• Contains pectinate muscles within auricle heart to work harder
and anterior wall of chamber

Right Ventricle
• Receives deoxygenated blood from the right
atrium
▪ Blood initially passes through the
open tricuspid valve first
• Walls contain ridges of muscle called
trabeculae carneae
• Pressure increases during ventricular
contraction
▪ Increased pressure closes tricuspid
valve yet opens pulmonary
semilunar valve
• Deoxygenated blood ejected into pulmonary
trunk Coronary Arteries
• Left and right coronary arteries
Left - OXYGENATED ▪ Arise from ascending aorta and
Left Atrium travel in coronary sulcus
• After gas exchange in the lungs, oxygenated ▪ Fill during ventricular relaxation
blood returns to left atrium • Left coronary artery branches to form
▪ Via pulmonary veins circumflex artery and anterior
• Auricle contains pectinate muscles interventricular artery
• Fills during atrial relaxation • Right coronary artery branches to form
• Ejects blood through open bicuspid (mitral) marginal arteries and posterior
valve into left ventricle interventricular arteries

Left Ventricle Coronary Veins

• Receives oxygenated blood from left atrium • Great cardiac vein
• Contraction closes bicuspid valve and ▪ Travels in anterior interventricular
opens aortic semilunar valve sulcus
• Ejects oxygenated blood into the aorta and • Posterior cardiac vein accompanies the
into the systemic circuit circumflex artery
• Small cardiac vein accompanies right
coronary artery
• Anterior cardiac veins accompany small
cardiac artery
• Most cardiac veins drain into coronary
sulcus

Heart Valve Disorders

 Cardiac Muscle
• Capable of initiating action potentials
independently
▪ Referred to as autorhythmicity
• Heart continues to beat when removed from
body
• “Heart-in-a-Box” machine
circulates oxygenated blood through donor
hearts
• Heart rate can be manipulated by nervous
and endocrine systems

Characteristics of Cardiac Muscle

Coronary Artery Disease • Branching fibers connected by intercalated
• Leading cause of death worldwide discs
• Plaque buildup decreases coronary blood Striated
flow • contractile unit is sarcomere
▪ Blockages visible on coronary Myocardial contractile cells
angiogram • pass action potentials from one cell to
▪ Begins as fatty streak during another
childhood and continues throughout Myocardial conducting cells
life • generate and conduct action potential
• Can lead to hypoxia and myocardial through heart
ischemia
Structure of Contractile Cardiac Muscle
• Contain myofilaments arranged into
sarcomeres
• T (transverse) tubules conduct action
potentials into cells
• Sarcoplasmic reticulum stores calcium ions
• Plentiful mitochondria produce ATP
• Intercalated discs connect cells
▪ Desmosomes and tight junctions
anchor cells together
▪ Gap junctions allow action
potentials to conduct quickly from
cell to cell
 Cardiac Muscle Metabolism
• Produce ATP mainly by aerobic respiration
▪ Highly dependent on oxygen to make
ATP
▪ Oxygen supplied by coronary
arteries
▪ Also store oxygen with myoglobin
• Can use lactic acid, fatty acids, and glucose
to generate ATP

Conduction System of the Heart

• Generates and conducts action potentials in
the heart
1. Sinoatrial (SA) node—pacemaker of the
heart
2. Atrioventricular (AV) node
3. AV bundle (Bundle of His)
4. AV bundle branches
Heart Disease and Cardiac Muscle 5. Purkinje fibers
• Heart disease and heart attacks cause
damage to cardiac muscle
• Cardiac muscle does not regenerate yet is
replaced by non-contractile scar tissue
▪ Decreases pumping ability of heart

Propagation of Cardiac Action Potential

• SA node depolarizes spontaneously
• Depolarization spreads quickly over both
atria
• AV node slows down movement and
conducts depolarization into ventricle
• AV Bundle, left and right AV bundle
branches, Purkinje fibers depolarize
ventricles
Sinoatrial (SA) Node ▪ Phase 3—at +5 mV calcium
• Specialized group of conducting cells channels close and potassium
located in superior/posterior wall of right voltage-gated channels open
atrium • Potassium outflow brings membrane
▪ Highest rate of depolarization potential to –60 mV and cell depolarizes
establishes normal sinus rhythm again
• Known as the "pacemaker" of the heart
• Action potential spreads through both atria
downward toward atrioventricular (AV) node
▪ Spreads through cardiac muscle
cells and internodal pathway
▪ Can only reach ventricles through AV
node
• Depolarization leads to contraction of atria
as a unit
• Extreme SA node stimulation produces
maximal heart rate
▪ Around 220 beats per minute
Atrioventricular (AV) Node
• Located in inferior floor of right atrium
• Slows down depolarization from SA node
▪ Pause allows atria to fully contract
before depolarization enters
ventricles below
Atrioventricular Bundle
• Atrioventricular (AV) bundle emerges from
AV node and travels along the superior
portion of the interventricular septum
Rates of Conduction System Firing
Bundle Branches
• SA has the highest rate of depolarization
• Bundle divides into left and right bundle
within cardiac conduction system
branches in interventricular septum
▪ This is why it is the pacemaker
▪ Left bundle branch is larger than the
right • Rate slows as depolarization moves through
▪ Right bundle branch communicates remaining components
with papillary muscles in right • Damage to SA node may cause bradycardia
ventricle ▪ Bradycardia—slow heart rate
Purkinje Fibers ▪ Possible requires artificial
• Bundle branches connect with Purkinje pacemaker to take over job of SA
fibers at apex of heart node
▪ Purkinje fibers spread depolarization
upward from apex through
ventricular walls

Depolarization in Nodal Cells

• Nodal cells spontaneously depolarize at –60
mV
▪ Phase 1—at –60 mV, voltage-gated
sodium channels open moving
membrane toward threshold
▪ Phase 2—voltage-gated calcium
channels open when sodium ions
depolarize to threshold
Depolarization of Cardiac Contractile Cells
• Rapid depolarization followed by plateau
phase and repolarization
• Long refractory period to allow time for
movement of blood
• Resting membrane potential is -80mV in
atria and -90mV in ventricles
• Movement of ions through gap junctions
spreads action potential from conduction
system
• As ions move, contractile cells will reach
threshold Skeletal Muscle Action Potentials and Tetany
• At threshold sodium voltage-gated channels • Skeletal muscle cells can continue to
open generate action potentials during
• Influx of Na+ brings membrane potential to contraction
+30 mV ▪ This is summation
• Potassium voltage-gated channels open and • Continual stimulation (i.e., summation) can
potassium exits cell lead to tetany
• Slow opening calcium voltage-gate ▪ Sustained contraction
channels open at same time and calcium • Tetany would be bad for cardiac muscle as
enters cell relaxation is required for ventricular filling
▪ This leads to plateau phase
• At 0 mV, calcium channels close while
potassium channels remain open, and cell
repolarizes

The Role of Calcium in Contractile Cells

• Calcium comes from both sarcoplasmic
reticulum and extracellular fluid
• Calcium serves two important roles in
contractile cells:
1. Influx through slow calcium channels
Skeletal Muscle Versus leads to plateau phase
Cardiac Muscle Action Potentials ▪ Ensures relaxation between
• Skeletal muscle action potential ends contractions
immediately before contraction 2. Binds to troponin to expose myosin
▪ Allows for summation binding sites on thin filaments
• Cardiac muscle remains in plateau phase
until end of contraction
▪ Prevents summation
▪ Allows cell to relax fully so that
ventricular filling can occur
 Electrocardiogram • Membrane Potential and ECGs:
• Electrocardiogram - Leads on surface of ▪ Changes in the membrane potential
body monitor electrical signals as they of contractile cardiac muscle cells of
move through the body and cardiac muscle the ventricles corresponds with the
QRS complex

• An ECG evaluates ionic movement through

the body
• In contrast, a recording
microelectrode evaluates ionic movement • ECG segments and intervals are regions
across a cellular membrane between waves
▪ PR interval—from beginning of P
wave to beginning of QRS complex
o Delay usually indicates heart
block
▪ ST segment
o Elevation usually indicates
heart attack

• Major components of a healthy ECG:

▪ P wave — atrial depolarization
▪ QRS complex — ventricular
depolarization
o Atrial repolarization occurs
at the same time
▪ T wave — Ventricular repolarization

Events of Heart Contraction and ECGs

• P wave = atrial depolarization
• Baseline segment following P wave = atrial
contraction
• QRS complex = ventricular depolarization
• S-T segment = ventricular contraction
• T wave = ventricular repolarization
 Fibrillation on Heart Rate
• Patches of dead or nonconductive cardiac Sympathetic stimulation
muscle can cause fibrillation • increases heart rate and strength of
▪ Uncoordinated beating of the heart contraction
Atrial fibrillation ▪ Cardioaccelerator region sends
• not always life-threatening signals to SA node, AV node, and
Ventricular fibrillation ventricular myocardium
• life-threatening due to ineffective pumping Parasympathetic stimulation
of blood • decreases heart rate and strength of
Defibrillator contraction
• A defibrillator can be used to correct ▪ Cardioinhibitory center sends
abnormal heart rhythms signals to SA and AV nodes

Nervous System Influence on Heart Activity

• Autonomic nervous system influences heart Stages of the Cardiac Cycle
activity • Period of time and set of events that occur
• Control centers in medulla oblongata during one complete beat of the heart
Cardiac accelerator nerves ▪ Systole = contraction
• sympathetic ▪ Diastole = relaxation
▪ Increase heart rate and force of 3. Total diastole
contraction 4. Atrial systole
Vagus nerves (CN X) 5. Early ventricular systole
• parasympathetic 6. Late ventricular systole
▪ Decrease heart rate 7. Early ventricular diastole

Pressures and Flow

• Blood flow is due to pressure gradients
▪ Blood flows from areas of higher to
lower pressure
• Water flows from high to low as a balloon is
filled
• Squeezing the balloon causes water to move
due to higher pressure
• Pressure increases with systole
• Pressure decreases with diastole
•
•
•
•

Total Diastole
Effect of Autonomic Nervous System
• Myocardium is completely relaxed • Referred to as isovolumetric contraction
• Blood passively fills chambers of heart phase
• AV valves open and SL valves are closed • Ventricles contract and ventricular
pressure increases
▪ Sends blood back toward atria
• AV valves close and produce S1 heart sound
• SL valves closed
• Since all four valves are closed there is no
change in ventricular volume

Atrial Systole
• Contraction of atria adds blood to
ventricular volume Late Ventricular Systole
▪ Ventricles fill to End Diastolic • Ventricular ejection phase
Volume (EDV) of ~130mL • Ventricular pressure increases and SL
• AV valves are open, and SL valves are closed valves open; AV valves remain closed
• Aortic pressure decreases as blood flows • Blood is ejected into pulmonary trunk and
into systemic circuit aorta
▪ Stroke Volume (SV)—amount of
blood ejected per beat; ~70mL
▪ End Systolic Volume (ESV)—amount
of blood remaining in ventricle after
systole; ~60mL
• Atria are relaxed

Early Ventricular Systole

Early Ventricular Diastole
• Referred to as isovolumetric relaxation • The waves and segments of an ECG
phase correlate with the mechanical events of the
• Ventricles begin to relax and pressure cardiac cycle: Systole and Diastole
decreases • Systolic blood pressure is measured during
• Blood attempts to flow back into ventricles ventricular systole
and SL valves close • Diastolic blood pressure is measured
▪ Produces S2 heart sound during ventricular diastole
▪ Momentary dip in aortic pressure
called dicrotic notch
• All valves closed so no change in ventricular
volume
• Atria fully relaxed and beginning to fill

Heart Sounds
• Normal heart sounds are produced by
closure of atrioventricular (AV) or
semilunar (SL) valves
▪ First heart sound (S1) is produced
by closure of AV valves during
isovolumetric contraction
▪ Second heart sound (S2) is
produced by closure of SL valves
during isovolumetric relaxation
• Murmurs may be caused by turbulent blood
flow across a valve
▪ Auscultation is done to listen for
murmurs

Late Ventricular Diastole

• Second phase of ventricular diastole
• Ventricles continue to relax, pressure
decreases
• When ventricular pressure decreases lower
than atrial pressure, AV valves open
▪ Blood flows from the atria into the
ventricles
▪ When both chambers are in diastole
and the semilunar valves are closed,
ventricular filling begins

ECG Correlation to the Cardiac Cycle Events of the Cardiac Cycle

Wiggers diagram
• A Wiggers diagram illustrates the pressures
within the atria, ventricles, and aorta during
the cardiac cycle
• It also displays the valve and heart sound
events of the cardiac cycle

Ejection Fraction
• Only part of the end diastolic volume (EDV)
is ejected
▪ Ejection fraction—percentage of
EDV ejected per beat
o Usually around 55–70%
• Greater SV possible if ejection fraction and
heart rate are increased
• Increasing SV and heart rate

Exercise and Cardiac Function

• During exercise it is necessary to increase
cardiac output to use cardiac reserve
▪ Cardiac reserve - difference
Cardiac Output between maximum and resting CO
• The amount of blood ejected by each • This is done by:
ventricle per minute ▪ Increasing HR
• Changes in response to body’s metabolic o Autonomic nervous system
demands increases HR above 100
▪ Increases during exercise or beats per minute (bpm)
physical activity ▪ Increasing SV
• Cardiac output (CO) is calculated by o Increased EDV, contractility,
multiplying heart rate by stroke volume and decreased resistance
▪ CO = HR × SV during exercise
• At rest CO is approximately the entire blood
volume of an adult Factors Influencing Heart Rate and
▪ ~5L/min Contractility
Chronotropic factors
Regulation of Cardiac Output • influence HR
• Both stroke volume and heart rate can be • Positive chronotropic factors increase HR
regulated to control cardiac output • Negative chronotropic factors decrease HR
• Multiple factors affect heart rate and stroke Inotropic factors
volume • influence contractility
▪ Factors that increase HR or SV will • Positive inotropic factors increase
increase CO contractility
▪ Factors that decrease HR or SV will • Negative inotropic factors decrease
decrease CO contractility
 Factors That Influence Heart Rate Afterload
• The force that the ventricles must overcome
to open the SL valves
▪ Equivalent to the resistance of the
vascular system
• If afterload decreases, SL valves open
sooner and SV increases
• If afterload increases, SL valves open later
and SV decreases

Factors That Affect Stroke Volume (SV)

Stroke Volume Regulation

Factors that influence stroke volume are:
Preload
• determined by EDV
▪ As EDV increases, ventricles stretch Flow Chart of Factors
more That Affect Cardiac Output
▪ EDV increases with increased
venous return
▪ Increased stretch causes increased
contraction strength and SV
increases
▪ Frank-Starling mechanism states
there is an upper limit to this
relationship
o Excessive stretch of
sarcomeres beyond optimal
length leads to weaker
contraction

Contractility
• force of contraction
▪ Positive inotropic agents—
increase force of contraction
o Increase SV
o Epinephrine, norepinephrine, T3,
T4
▪ Negative inotropic agents—
decrease force of contraction
o Decrease SV
o Elevated extracellular
potassium, elevated levels of
acid