Cardiovascular and Circulatory Function

Anatomy of the Heart

 Hollow, muscular organ
 Location: center of the thorax, mediastinum
 Weight: 300 g (10.6 oz)
 Function: pumps blood to the tissues, supplying them with oxygen and other nutrients

Layers of the Heart

1. Endocardium
 inner layer
 endothelial tissue that lines the inside of the heart and valves
2. Myocardium
 middle layer, made up of muscle fibers and is responsible for the pumping action
 composed of specialized cells called myocytes
 forms an interconnected network of muscle fibers (intercalated discs)

3. Epicardium
 exterior layer

Pericardium
 thin, fibrous sac that encases the heart
 2 layers: visceral and parietal
o Visceral Pericardium
 Adheres to the epicardium
o Parietal Pericardium
 Envelopes the visceral pericardium
 tough fibrous tissue that attaches to the great vessels, diaphragm, sternum, and vertebral
column
 supports the heart in the mediastinum
Pericardial space
 space between parietal and visceral
 filled with about 20 mL of fluid
 lubricates the surface of the heart and reduces friction during systole

Chambers of the Heart

2 atria – Right and Left
2 Ventricles - Right and Left
Note!! The pumping action of the heart is accomplished by the rhythmic relaxation and
contraction of the muscular walls
1. Diastole
 Relaxation phase
 All four chambers relax simultaneously
 Known as the period of ventricular filling
2. Systole
 contraction of the atria and the ventricles
 Atrial and ventricular systole are not simultaneous events

Valves of the Heart

  permit blood to flow in only one direction
 composed of thin leaflets of fibrous tissue
 open and close in response to the movement of blood and pressure changes within the chambers
 atrioventricular (AV) and semilunar
1. Atrioventricular Valves - separate the atria from the ventricles
a. Tricuspid valve - composed of three cusps or leaflets, separates the right atrium from the
right ventricle
b. Mitral or bicuspid valve - two cusps, between the left atrium and the left ventricle
2. Semilunar Valves - composed of three leaflets, which are shaped like half-moons
a. Pulmonic valve - between the right ventricle and the pulmonary artery
b. Aortic valve - between the left ventricle and the aorta

Diastole - AV valves are open, semilunar valves are closed

Systole - AV valves are closed, semilunar valves are open

Coronary Arteries
 The heart has high metabolic requirements
 Left and right coronary arteries and their branches supply arterial blood to the heart
 Myocardial ischemia - inadequate oxygen supply
1. Right Coronary Artery
Supplies the right side of the heart
Posterior descending artery – supplies the posterior wall of the heart
2. Left Coronary Artery
Has 3 branches
 Left main coronary artery
 Left anterior descending artery
 Circumflex artery

Coronary Veins
 Superficial to the coronary arteries
 Returns blood to the heart through the coronary sinus, located posteriorly in the right atrium

Cardiac Conduction System

 generates and transmits electrical impulses that stimulate contraction of the myocardium
 The heart is innervated by the ANS
 ANS does not initiate contraction
 2 specialized electrical cells:
o Nodal cells
o Purkinje cells
 3 characteristics of these cells:
 Automaticity: ability to initiate an electrical impulse
 Excitability: ability to respond to an electrical impulse
 Conductivity: ability to transmit an electrical impulse from one cell to another

Sinoatrial (SA) node

 primary pacemaker
 Location: junction of the SVC and the RA
  Bachmann’s Bundle
o myocardial strands connecting the right and left atrial walls
o pathway of interatrial conduction

(SA) node generates electrical impulses

Conducted along the myocardial cells of the atria (Internodal Pathways)

Electrical stimulation and subsequent contraction of the atria

Atrioventricular (AV) node

 Secondary pacemaker of the heart
 Location: Right atrial wall located near tricuspid valve
 Coordinates the incoming electrical impulses from the atria
 Relays the impulse to the ventricles

Receives electrical impulses from SA Node

Relays the impulse to the ventricles

Via the Bundle of His

Bundle of His
 bundle of specialized conducting tissue that relays impulse from AV node to ventricles
 2 branches:
o Right bundle branch
o Left bundle branch

Purkinje fibers
 terminal point in the conduction system
 composed of Purkinje cells that rapidly conduct impulses throughout the thick walls of the ventricles
 Ventricular contraction

Cardiac Action Potential

 Stimulation of the myocytes occurs due to the exchange of electrically charged particles – ions
(sodium, potassium, and calcium)
 The repeated cycle of depolarization and repolarization
 Resting or polarized state
o Na+ is the primary extracellular ion
o K+ is the primary intracellular ion
o The inside of the cell has a negative charge
o The outside of the cell has a positive charge

Resting/Polarized State

Stimulation from the Conduction System

 Exchange of Ions

Na and Ca will move inside and K will move outside

Depolarization (Inside +, Outside –)

Depolarization
 electrical activation of a cell caused by the influx of sodium into the cell while potassium exits the
cell

Depolarization is completed

Exchange of ions reverts

Na and Ca will move outside and K will move inside

Repolarization (Inside -, Outside +)

Repolarization
 return of the cell to resting state, caused by reentry of potassium into the cell while sodium exits
the cell

Blood Circulation

Cardiac Cycle
 events that occur in the heart from the beginning of one heartbeat to the next
 3 major sequential events:
o Diastole
o Atrial systole
o Ventricular systole
  Diastole
o all chambers are relaxed
o AV valves are open
o Semilunar valves are closed
o Pressures in all of the chambers are the lowest which facilitates ventricular filling
o Venous blood returns to the right atrium from the superior and inferior vena cava, then into the
right ventricle
o oxygenated blood returns from the lungs via the four pulmonary veins into the left atrium and
ventricle
 Atrial Systole
o Atrial muscles contract in response to an electrical impulse initiated by the SA node
o Increased pressure inside the atria, ejecting the remaining blood into the ventricles
o Also known as atrial kick
 Ventricular Systole
o pressure inside the ventricles rapidly increases
o AV valves close
o Pulmonic and aortic valves are open
o Blood is ejected into the pulmonary artery and aorta
o At the end of systole, pressure within the right and left ventricles rapidly decreases.
o As a result, pulmonary arterial and aortic pressures decrease, causing closure of the semilunar
valves.
o These events mark the onset of diastole, and the cardiac cycle is repeated.

Cardiac Output
 refers to the total amount of blood ejected by one of the ventricles in liters per minute

Stroke Volume
 amount of blood ejected from one of the ventricles per heartbeat.

Cardiac Output = Stroke Volume x HR

ANS Influence on Cardiac Activity

 SNS
o Release of norepinephrine which increases the heart rate and contraction of the heart
 PNS
o Release of acetylcholine from the vagal fibers causing slow heart rate and slight decrease in
cardiac contractility (vagal stimulation)

Effect of Heart Rate on Cardiac Output

 The cardiac output responds to changes in the metabolic demands of the tissues associated with
stress, physical exercise, and illness.
 Changes in heart rate are due to inhibition or stimulation of the SA node mediated by the
parasympathetic and sympathetic divisions of the autonomic nervous system
o PNS – its branches travel to the SA node by the vagus nerve. Stimulation of the vagus
nerve slows the heart rate
o SNS - increases heart rate by innervation of the beta-1 receptor sites located within the
SA node. The heart rate is increased by the sympathetic nervous system through an
increased level of circulating catecholamines (secreted by the adrenal gland) and by
excess thyroid hormone, which produces a catecholaminelike effect
 In addition, the heart rate is affected by central nervous system and baroreceptor activity
o Baroreceptors - specialized nerve cells located in the aortic arch and in both right and left
internal carotid arteries.
 Sensitive to changes in blood pressure (BP)
 Elevations in BP Baroreceptors increase their rate of transmission
Impulses are transmitted to cerebral medulla Initiation of PNS and inhibition of
SNS Decreased HR and BP
  Low BP Less b`aroreceptor stimulation Decrease in parasympathetic
activity Enhancement of sympathetic response BP elevation through
vasoconstriction and increased HR

Effect of Stroke Volume on Cardiac Output

 Stroke volume is primarily determined by three factors: preload, afterload, and contractility.
1. Preload - degree of stretch of the ventricular cardiac muscle fibers at the end of diastole.
 The volume of blood within the ventricle at the end of diastole determines preload, which
directly affects stroke volume
 Commonly referred to as left ventricular end diastolic pressure
 Frank–Starling (or Starling) law - as the volume of blood returning to the heart
increases,
muscle fiber stretch also increases (increased preload), resulting in
stronger contraction and a greater stroke volume
2. Afterload - resistance to ejection of blood from the ventricle
 Systemic vascular resistance - resistance of the systemic BP to left ventricular
ejection
 Pulmonary vascular resistance - resistance of the pulmonary BP to right ventricular
ejection
 There is an inverse relationship between afterload and stroke volume
 For example, afterload is increased by arterial vasoconstriction, which leads to decreased
stroke volume. The opposite is true with arterial vasodilation, in which case afterload is
reduced because there is less resistance to ejection, and stroke volume increases.
3. Contractility - force generated by the contracting myocardium
 Enhanced by circulating catecholamines, sympathetic neuronal activity, and certain
medications (e.g., digoxin [Lanoxin], dopamine, or dobutamine)
 Increased contractility results in increased stroke volume
 Contractility is depressed by hypoxemia, acidosis, and certain medications (e.g., beta-
adrenergic blocking agents such as metoprolol [Lopressor]).
 Ejection fraction - percentage of the end-diastolic blood volume that is ejected with each
heartbeat
o The ejection fraction of the normal left ventricle is 55% to 65%
o Used as a measure of myocardial contractility
o An ejection fraction of less than 40% indicates that the patient has decreased left
ventricular function and likely requires treatment of HF

Assessment of the Cardiovascular System

Past Health, Family, and Social History
1. Non-modifiable Risks
 Increasing age –age above 40 y/o due to physiologic changes of the heart and blood
vessels
 Sex – Men are prone to CVD before age 65. Women are more prone after age 65.
o Heart of a woman tends to be smaller than that of a man
o Coronary arteries of a woman are also narrower in diameter than a man’s arteries
o Women have the benefit of the female hormone estrogen and its cardioprotective
effects
 Increases high-density lipoprotein (HDL) that transports cholesterol out of arteries
 Reduces low-density lipoprotein (LDL) that deposits cholesterol in the artery
 Dilates blood vessels
 Heredity
 Race
2. Modifiable Risks
 Stress – stimulates SNS
 Diet - high sodium and high fat diet
 Exercise - Sedentary lifestyle predisposes patients to have CVD
 Smoking - Nicotine causes vasoconstriction and vasospasms of the arteries, increases
myocardial oxygen demand and decreases level of HDL
  Alcohol – causes vasoconstriction
 Hypertension
 Hyperlipidemia/Hypercholesterolemia
 Diabetes mellitus
 Obesity - Increase cardiac workload, increase LDL
 Personality type or behavior - Type A behavior pattern (competitiveness, aggressiveness,
impatience)
 Contraceptive pills (estrogen) - Increase blood viscosity – risk for thromboembolism;
Stimulates liver to produce angiotensinogen - hypertension

Common Symptoms
1. Chest Pain
 Due to decrease coronary tissue perfusion and oxygenation

Decrease coronary tissue perfusion and oxygenation

Anaerobic metabolism

Lactic acid

Irritation of the nerve endings in myocardium

 Pain Assessment (SOCRATES)

o Site
o Onset
o Character
o Radiation
o Associated Symptoms
o Timing
o Exacerbating factors
o Severity
2. Shortness of breath or dyspnea
 Dyspnea on exertion (DOE) - Indicates decreased cardiac reserve
 Orthopnea - Advanced heart failure indicating pulmonary congestion
 Paroxysmal Nocturnal Dyspnea - Severe SOB that occurs 2-5 hrs after the onset of sleep
3. Edema - Due to increase hydrostatic pressure
4. Syncope - Generalized muscle weakness with inability to stand upright, followed by loss of
consciousness. Due to decreased cerebral perfusion
5. Palpitations - Unpleasant awareness of the heartbeat. May be described by patient as “pounding”,
“racing” or “skipping”
6. Fatigue - Due to inadequate cardiac output, sometimes referred to as vital exhaustion

Past Health, Family, and Social History

 Medications
 Nutrition
 Elimination
 Activity and Exercise
 Sleep and Rest
 Self-Perception and Self-Concept
 Roles and Relationships
 Sexuality and Reproduction
 Coping and Stress Tolerance

Physical Assessment
1. General Appearance – assess the following:
 LOC - alert, lethargic, comatose
 Mental status - oriented to person, place, time; coherence
 Signs of distress which include pain or discomfort, shortness of breath, or anxiety
 Size of the patient - normal, overweight, underweight, or cachectic
  Height and weight are measured to calculate BMI as well as the waist circumference
2. Assessment of the Skin and Extremities
 Skin color, temperature, and texture
 6 P’s (pain, pallor, pulselessness, paresthesia, poikilothermia [coldness], and paralysis)
 Peripheral edema - edema of the feet, ankles, or legs
 Pitting edema - an indentation in the skin created by this pressure
 Capillary refill time – prolonged indicates inadequate arterial perfusion to the extremities.
Reperfusion occurs within 2 seconds
3. Blood Pressure
 pressure exerted on the walls of the arteries during ventricular systole and diastole
 Normal BP: <120 mmHg systolic, <80 mmHg diastolic
 Pulse Pressure - difference between the systolic and the diastolic pressures
o reflection of stroke volume
o Normal: 30 to 40 mm Hg
o Decreased pulse pressure reflects reduced stroke volume
4. Arterial Pulses
 Pulse rate
o 60-100 bpm
o Anxiety frequently raises the pulse rate during the physical examination
o If the rate is higher than expected, the nurse should reassess the pulse near the end of the
physical examination, when the patient may be more relaxed
 Pulse Rhythm
o Normal: Regular
o if the pulse rhythm is irregular, the heart rate should be counted by auscultating the apical
pulse, the PMI, for a full minute while simultaneously palpating the radial pulse
o Apical impulse
 Also called point of maximal impulse - pulsation created during normal ventricular
contraction
 Location: intersection of the midclavicular line of the left chest wall and the
fifth intercostal space
 Pulse Rhythm
o Pulse deficit - difference between the apical and radial pulse rates
 Pulse Amplitude
o used to assess peripheral arterial circulation
o indicative of the BP in the artery
o Interpretation: absent, diminished, normal, or bounding
 0 - Not palpable or absent
 +1 - Diminished—weak, thready pulse; difficult to palpate; obliterated with pressure
 +2 - Normal
 +3 - Moderately increased—easy to palpate, full pulse
 +4 - Markedly increased—strong, bounding pulse
 Palpation of Arterial Pulses
o Temporal, common carotid, brachial, radial, femoral, popliteal, dorsalis pedis, and posterior
tibial arteries
o NOTE!!! Light palpation is essential
o Do not simultaneously palpate both the temporal and carotid arteries, because it is possible
to decrease the blood flow to the brain.
5. Jugular Venous Pulsations
o reflects central venous pressure (CVP)
o CVP - pressure in the RA or the RV at the end of diastole
o Normal Adult: normally visible in the supine position with the head of the bed elevated to
30
o Abnormal: obvious distention of the veins with the patient’s head elevated 45° to 90°
indicates an abnormal increase in CVP
6. Heart Inspection and Palpation
o Six Areas
 o Aortic area
o Pulmonic area
o Erb point
o Tricuspid area
o Mitral (apical) area
o Epigastric area

Aortic area - second intercostal space to the right of the sternum

Pulmonic area – 2nd intercostal space to the left of the sternum
Erb point – 3rd intercostal space to the left of the sternum
Tricuspid area – 4th and 5th intercostal spaces to the left of the sternum
Mitral (apical) area - left 5th intercostal space at the midclavicular line
Epigastric area - below the xiphoid process

 Normal Heart Sounds

o S1 and S2
o S1 - closure of the AV valves
o S2 - closure of the semilunar valves
o Normally, the S1 and S2 are the only sounds heard during the cardiac cycle
 S1 -First Heart Sound
o Tricuspid and mitral valve closure
o “lub”
o heard the loudest at the apical area
 S2 - Second Heart Sound
o Closure of the pulmonic and aortic valves
o “dub”
 S3 - Third Heart Sound
o heard early in diastole during the period of rapid ventricular filling
o “DUB”
o heard immediately after S2 - “Lub-dub-DUB”
o normal finding in children and adults up to 35 or 40 years of age - referred to as a
physiologic S3
o Older adults - HF
o best heard with the bell of the stethoscope
 S4 - Fourth Heart Sound
o occurs late in diastole
o heard just before S1 is generated
o “LUB”
o “LUB lub-dub”
o auscultated using the bell of the stethoscope over the apical area with the patient in the left
lateral position
 There are times when both S3 and S4 are present, creating a quadruple rhythm, which sounds like
“LUB lub-dub DUB.” Example: tachycardia, all four sounds combine into a loud sound, referred to
as a summation gallop
 Murmurs - created by turbulent flow of blood in the heart
 Friction Rub - harsh, grating sound that can be heard in both systole and diastole
o caused by abrasion of the inflamed pericardial surfaces from pericarditis
o can be heard best using the diaphragm of the stethoscope, with the patient sitting up
and leaning forward
7. Assessment of Other Systems
 Hemoptysis - Pink, frothy sputum
 Cough - dry, hacking cough from irritation of small airways
 Crackles – pulmonary congestion
 Wheezes - Compression of the small airways by interstitial pulmonary edema
 NOTE!!! Beta-adrenergic blocking agents such as propranolol (Inderal), may cause
airway narrowing, especially in patients with underlying pulmonary disease

Diagnostic Evaluation for Cardiovascular System

1. Serum Laboratory Tests

 Complete Blood Count
o Elevated RBC - Hypoxia – inadequate tissue perfusion
o Increased WBC - Infections, myocardial infarction
o Decreased hemoglobin and hematocrit - Anemia
 BUN - Indicator of renal function
o Elevated - Decreased cardiac output leading to decrease kidney perfusion
 Prothrombin Time (PT)
o Time required for clotting to occur after thromboplastin and calcium are added to decalcified
plasma
o Measures effectiveness of Coumadin – therapeutic range is 1.5 – 2 times the normal value
o Normal: 9.5 – 12 secs
 Partial Thromboplastin Time (PTT) and APTT
o Time required for clotting to occur after thromboplastin reagent is added to the blood plasma
o Measures effectiveness of Heparin - 2 – 2.5 times the normal value
o Normal PTT: 60-70 secs
o Normal APTT: 20-39 secs
 Serum Cholesterol
o NPO 10-12 hours
o Normal: 150 – 200 mg/dl
 Serum Triglycerides
o NPO 10-12 hours
o Normal: 140 – 200 mg/dl
 Blood Cultures
o Diagnosis of infectious heart diseases
o Caution: avoid contamination of the specimen to provide accurate results
 Serum Electrolytes:
o Sodium – 135 – 145 mEq/L
o Potassium – 3.5 – 5 mEq/L
o Calcium – 8.6 – 10.4 mg/dl
2. Serum Enzyme Studies
  AST – Aspartate Aminotransferase
o Formerly SGOT
o Elevated level indicates tissue necrosis
o Normal: 7-40 mu/mL
o Used for diagnosis of MI
 Initial elevation: 4-6 hrs
 Peaks: 24-36 hrs
 Returns to normal: 5-7 days
 Creatinine Phosphokinase (CK-MB)
o Most cardiac specific enzyme
o Accurate indicator of myocardial damage
o Normal: Male – 50-325 mu/mL (2-6ng/mL)
o Normal: Female – 50-250 mu/mL (2-5 ng/mL)
o Diagnosis for MI
 Onset: 3-6 hrs
 Peaks: 12-18 hrs
 Returns to normal: 3-4 days
 Lactic Dehydrogenase (LDH)
o LDH1 – most sensitive indicator of myocardial damage among the 5 LDH
o Normal: 100-225 mu/mL
o Diagnosis for MI
 Onset: 12 hrs
 Peaks: 48 hrs
 Returns to normal: 10-14 days
 Troponin I, C, T
o Most specific to detect MI
o Troponin I has high affinity for myocardial injury. It rises within 3 hours and persists for up to
7-10 days
o Normal: Troponin I - <0.3 ng/mL, Troponin T - <0.2 ng/mL
 Hydroxybutyrate Dehydrogenase (HBD)
o Elevation accompanies elevation of LDH
o Valuable in detecting “silent MI”
o Normal: 140-350 u
o Diagnosis for MI
 Onset: 10-12 hrs
 Peaks: 48-72 hrs
 Returns to normal: 12-13 days
3. Serologic Tests
 VDRL – Venereal Disease Research Lab
o Detection of syphilis
o Syphilis can cause some aortic disorders
4. Imaging Studies
 Chest X-ray
o Radiography of the chest is done to determine anatomical changes such as the size and
position of the heart
o Nursing Interventions:
 Prepare the client, explain procedure and purpose
 Remove jewelry
 Ensure that the client is not pregnant
 Magnetic Resonance Angiography
o noninvasive, painless technique that is used to examine both the physiologic and anatomic
properties of the heart
o uses a powerful magnetic field and computer-generated pictures to image the heart and
great vessels
o Nursing Interventions:
  Contraindicated to patients with pacemaker, metal plates, prosthetic joints, or other
metallic implants
 Remove any jewelry, watches, or other metal items
 Transdermal patches that contain a heat-conducting aluminized layer must be
removed
 Assess for presence of claustrophobia – sedative can be given
 An intermittent clanking or thumping can be heard during the procedure
 Advise patient to remain still during the procedure
 Cardiac Catheterization
o Invasive procedure used to diagnose structural and functional diseases of the heart and great
vessels
o Involves the percutaneous insertion of radiopaque catheters into a large vein and an artery
o 2 types:
 Right Sided - Insertion is via a large vein: medial cubital or brachial vein
 Left Sided - Passing a catheter into the aorta via brachial or femoral artery
o Tests performed prior to the test:
 Renal Function
 CBC
 Coagulation studies
o Nursing Interventions: Pre-procedure
 Informed consent
 Psychosocial support to allay anxiety
 Assess for allergy to iodine/seafood – if allergic patient can be premedicated with
antihistamines and corticosteroids
 Obtain initial VS
 NPO - 8 to 12 hours
 Ask client to void
 Done under local anesthesia
 Mark distal pulses
 Expected duration: less than 2 hrs which includes lying in a hard table
 Check lab values
 Skin prep on the insertion site
 Inform what to feel during the procedure: occasional pounding sensation
(palpitation) may be felt in the chest (fluttering sensation) and warm or
flushed feeling throughout the body and a sensation similar to the need to
void
 If the client is taking metformin, withhold the medication 24 hours prior to the
procedure because of the risk of lactic acidosis. Medication is not resumed until
prescribed by the physician
o Nursing Interventions: Post-procedure
 Observe the catheter access site for bleeding or hematoma formation
 Assess peripheral pulses q15mins for 1hr, q30mins for 1hr, and q1 for 4 hrs
 Monitor V/S and cardiac rhythm
 Assess presence of 6P’s on the affected extremity
 Bed rest for 2 to 6 hours after the procedure
 For femoral approach using mechanical device and manual approach – bed rest for 6
hours, with the affected leg straight and the head of the bed elevated no greater
than 30°
 If the radial artery was accessed, the patient remains on bed rest for 2 hours or
until the effects of sedation have dissipated
 Avoid sleeping on the affected arm for 24 hours
 Avoid repetitive movement of the affected extremity for 24 to 48 hours
 Analgesic medication is given as prescribed for discomfort
 Report chest pain and bleeding or sudden discomfort from the catheter insertion sites
promptly
 Monitor I and O - contrast-induced nephropathy
 Monitor for bleeding from the catheter access site and for orthostatic hypotension
  If bleeding occurs, apply manual pressure immediately and notify HCP
 Apply sandbag or compression device to the insertion site as ordered
 Encourage fluid intake, if not contraindicated
 Monitor for any signs of hypersensitivity

 Computed Tomography
o Form of cardiac imaging that uses x-rays to provide accurate cross-sectional “virtual” slices of
specific areas of the heart and surrounding structures
o 2 types of cardiac CT scanning:
 Coronary CT angiography
 Electron beam CT (EBCT) - for coronary calcium scoring
o Coronary CT angiography
 requires the use of an IV contrast agent
 used to evaluate coronary arteries for stenosis, the aorta for aneurisms or dissections,
graft patency after coronary artery bypass grafting (CABG), pulmonary veins in
patients with atrial fibrillation, and cardiac structures for congenital anomalies
 Interventions:
Assess for any contrast medium allergy, seafood allergy, iodine allergy
Corticosteroids and antihistamines if there is a history of allergy
Beta blockers prior to the scan to control heart rate and rhythm
Caution in patients with renal insufficiency
Administer IV hydration before and after the scan to minimize the effect of the
contrast on renal function
Encourage fluid intake
Assess for hypersensitivity reaction
Remain still during the procedure
Expect transient flushing, metallic taste, nausea, or bradycardia during the
contrast infusion
 Transthoracic Echocardiography
o noninvasive ultrasound test that is used to measure the ejection fraction and examine the
size, shape, and motion of cardiac structures
o involves transmission of high-frequency sound waves into the heart through the chest
wall and the recording of the return signals
o Interventions:
 Inform the patient about the test, explaining that it is painless
 Gel applied to the skin helps transmit the sound waves
 Patient is asked to turn onto the left side or hold a breath
 Test takes about 30 to 45 minutes
 Transesophageal Echocardiography
o Threading a small transducer through the mouth and into the esophagus
o Provides clearer images because ultrasound waves pass through less tissue
o A topical anesthetic agent and moderate sedation are used
o Preprocedural Interventions:
 Provide preprocedure education and ensures that the patient has a clear
understanding
 NPO for 6 hrs
 Informed consent
 Start an IV line
 Remove dentures
 Provide emotional support
 Monitor level of consciousness, BP, ECG, respiration, and oxygen saturation
o Postprocedural Interventions:
 Maintain bed rest with the head of the bed elevated to 45°
 Monitor the patient for dyspnea and assess vital signs, SpO2, level of consciousness
 NPO until fully awake and gag reflex returns
  Sore throat may be present for the next 24 hours
 Report the presence of a persistent sore throat, shortness of breath, or difficulty
swallowing
 Electrocardiography
o Graphic representation of the electrical currents of the heart
o Obtained by placing disposable electrodes in standard positions on the skin of the chest wall
and extremities
o Useful for detecting cardiac dysrhythmias, location and extent of MI, cardiac hypertrophy and
effectiveness of medication
o Example: Standard 12-lead ECG
o Interventions:
 Advise client to lie still, breathe normally and refrain from talking
 Reassure that an electrical shock will not occur
 Document any medication that the client is taking
 Gently abrade the skin with a clean dry gauze pad
 Cleansing the skin with alcohol hinders detection of the cardiac electrical signal
 If the amount of chest hair prevents the electrode from having good contact with the
skin, the hair may need to be clipped
o Components of the Electrocardiogram
 Waveforms - P wave, QRS complex, T wave, U wave)
 Segments and intervals - PR interval, ST segment, QT interval
 ECG records the electrical activity at the speed of 25 mm/sec
 Each small square represents 0.04 second
 Each large square represents 0.20 second
ii.

o P wave
electrical impulse starting in the SA node and spreading through the atria
Atrial depolarization
Normal: 2.5 mm or less in height and 0.11 seconds or less in duration
o QRS complex
Ventricular depolarization
Normal: less than 0.12 seconds in duration
o T wave
Ventricular repolarization - when the cells regain a negative charge; called the
resting state
Normal: less than 0.12 seconds in duration
o U wave
Represents repolarization of the Purkinje fibers
Hypokalemia
o PR interval
measured from the beginning of the P wave to the beginning of the QRS complex
represents the time needed for sinus node stimulation, atrial depolarization, and
conduction through the AV node before ventricular depolarization
Normal: 0.12 to 0.20 seconds in duration
 o ST segment
early ventricular repolarization
lasts from the end of the QRS complex to the beginning of the T wave
o QT interval
represents the total time for ventricular depolarization and repolarization
measured from the beginning of the QRS complex to the end of the T wave

Coronary Artery Disease

A. Coronary Atherosclerosis
 abnormal accumulation of lipid, or fatty substances, and fibrous tissue in the lining of arterial blood
vessel walls
 Risk Factors
o Family history of CAD
o Increasing age
o Gender
o Race (higher incidence of heart disease in African Americans than in Caucasians)
o Elevated low-density lipoprotein (LDL)
o Hyperlipidemia
o Cigarette smoking
o Tobacco use
o Hypertension
o Diabetes
o Metabolic syndrome
o Obesity
o Physical inactivity
 Metabolic syndrome - cluster of metabolic abnormalities. Diagnosis is made in the presence of 3
on the following conditions:
o Insulin resistance (fasting plasma glucose more than 100 mg/dL or abnormal glucose
tolerance test)
o Central obesity (waist circumference more than 35 inches in females, more than 40 inches
in males)
o Dyslipidemia (triglycerides more than 150 mg/dL, HDL less than 50 mg/dL in females, less
than 40 mg/dL in males)
o Blood pressure persistently greater than 130/85 mm Hg
o Proinflammatory state (high levels of C-reactive protein [CRP])
o Prothrombotic state (high fibrinogen level)
 Clinical Manifestations:
o According to the location and degree of narrowing of the arterial lumen, thrombus
formation, and obstruction of blood flow to the myocardium
o Impediment to blood flow is usually progressive, causing an inadequate blood supply that
deprives the cardiac muscle cells of oxygen needed for their survival (ischemia)
 can be asymptomatic
 chest pain
 epigastric distress and pain that radiates to the jaw or left arm
  shortness of breath
 indigestion
 nausea
 palpitations
 numbness
 Prevention and Management
o Controlling Cholesterol Abnormalities
 Dietary Measures
Diet low in saturated fat and high in soluble fiber
Mediterranean diet - vegetables and fish and restricts red meat
 Physical Activity
Weight reduction and increased physical activity
Regular, moderate physical activity
 Medications
HMG-CoA Reductase Inhibitors (Statins)
o Atorvastatin (Lipitor), Simvastatin (Zocor)
o Inhibits enzyme involved in lipid synthesis (HMG-CoA)
o Administer in the evening
o Monitor liver function test
o Myalgia and arthralgia are common adverse effects
Fibric Acids (Fibrates)
o Fenofibrate (Tricor), Gemfibrozil (Lopid)
o Decreases synthesis of TGs and other lipids
o Adverse effects include diarrhea, flatulence, rash, myalgia
o Contraindicated in severe renal and liver disease
Bile Acid Sequestrants
o Cholestyramine (Questran), Colestipol (Colestid)
o Oxidize cholesterol into bile acids, which decrease fat absorption
o Used when statin alone has not been effective in controlling lipid levels
o Taken before meals
o Promoting Cessation of Tobacco Use
 Educational programs, counseling, consistent motivation and reinforcement messages,
support groups, and medications
 Complementary therapies (e.g., acupuncture, guided imagery, hypnosis)
o Managing Hypertension
 Hypertension is defined as blood pressure measurements that repeatedly exceed
140/90 mm Hg
 Early detection of high blood pressure and adherence to a therapeutic regimen
o Controlling Diabetes
 Diabetes is known to accelerate the development of heart disease
 Hyperglycemia fosters dyslipidemia, increased platelet aggregation, and altered red
blood cell function, which can lead to thrombus formation
 Treatment with insulin, metformin (Glucophage), and other therapeutic interventions
that lower plasma glucose levels
B. Angina Pectoris
 Clinical syndrome usually characterized by episodes or paroxysms of pain or pressure in the
anterior chest
 Cause: insufficient coronary blood flow (the need for oxygen exceeds the supply)
 Factors Associated with Typical Angina Pain
o Physical exertion (increase myocardial oxygen demand)
o Exposure to cold (vasoconstriction and elevated blood pressure, with increased oxygen
demand)
o Eating a heavy meal (increases the blood flow to the mesenteric area for digestion, reducing
the blood supply available to the heart muscle)
o Stress or any emotion-provoking situation (release of catecholamines)
 Types of Angina
 o Stable angina - predictable and consistent pain that occurs on exertion and is relieved by
rest and/or nitroglycerin
o Unstable angina - also called preinfarction angina or crescendo angina; symptoms
increase in frequency and severity; may not be relieved with rest or nitroglycerin
o Intractable or refractory angina -severe incapacitating chest pain
o Variant angina - also called Prinzmetal’s angina; pain at rest with reversible ST-segment
elevation; thought to be caused by coronary artery vasospasm
o Silent ischemia - objective evidence of ischemia (such as electrocardiographic changes with
a stress test), but patient reports no pain

 Clinical Manifestations
o Chest pain – patient might describe it as:
 Mild indigestion to a choking or heavy sensation in the upper chest
 Severity ranges from discomfort to agonizing pain
 May be accompanied by severe apprehension and a feeling of impending death
 Felt deep in the chest behind the sternum (retrosternal area)
 Poorly localized and may radiate to the neck, jaw, shoulders, and inner aspects of the
upper arms, usually the left arm
 Tightness or a heavy choking or strangling sensation
 Stable: subsides with rest or administering nitroglycerin
 Unstable angina: increase in frequency and severity and are not relieved by rest and
administering nitroglycerin; require medical intervention
o Weakness or numbness in the arms, wrists, and hands
o Shortness of breath
o Pallor
o Diaphoresis
o Dizziness or lightheadedness
o Nausea and vomiting
o ECG: T-wave inversion, ST segment elevation, or the development of an abnormal Q wave
 Medical Management
o Pharmacologic Therapy
 Nitrates – Nitroglycerin
Potent vasodilator that improves blood flow to the heart muscle and relieves pain
Relax the systemic arteriolar bed, lowering blood pressure and decreasing
afterload therefore decreasing myocardial oxygen requirements
Route: sublingual tablet or spray, oral capsule, topical agent, IV
Common adverse effect of nitroglycerin is headache
Self-Administration of Nitroglycerin
o Instruct the patient to make sure that the mouth is moist, the tongue is still,
and saliva is not swallowed until the nitroglycerin tablet dissolves
o Advise the patient to carry the medication at all times as a precaution
o Should be carried securely in its original container (e.g., capped dark glass
bottle); tablets should never be removed and stored in metal or plastic
pillboxes
o Nitroglycerin is volatile and is inactivated by heat, moisture, air, light, and
time. Instruct the patient to renew the nitroglycerin supply every 6 months
o Best taken before pain develops
o Note how long it takes for the nitroglycerin to relieve the discomfort
o Advise the patient that if pain persists after taking three sublingual tablets
at 5-minute intervals, emergency medical services should be called
o Side effects of nitroglycerin, including flushing, throbbing headache,
hypotension, and tachycardia
o Advise the patient to sit down for a few minutes when taking nitroglycerin to
avoid hypotension and syncope
 Beta-Adrenergic Blocking Agents
 Reduce myocardial oxygen consumption by blocking beta-adrenergic sympathetic
stimulation to the heart
Results are reduction in heart rate, slowed conduction of impulses through the
conduction system, decreased blood pressure, and reduced myocardial
contractility
Metoprolol (Lopressor)
Cardiac side effects and possible contraindications include hypotension,
bradycardia, advanced atrioventricular block, and acute heart failure
If given IV for an acute cardiac event, the ECG, blood pressure, and heart rate are
monitored closely
Not to stop taking abruptly, because angina may worsen and MI may develop
Patients with diabetes who take beta-blockers are instructed to monitor their
blood glucose levels as prescribed because beta-blockers can mask signs of
hypoglycemia
Causes bronchoconstriction, and therefore are contraindicated in patients with
significant chronic pulmonary disorders, such as asthma
 Calcium Channel Blocking Agents
Decrease sinoatrial node automaticity and atrioventricular node conduction,
resulting in a slower heart rate and a decrease in the strength of myocardial
contraction
Increase myocardial oxygen supply by dilating the smooth muscle wall of the
coronary arterioles
Amlodipine (Norvasc) and diltiazem (Cardizem)
Watch out for hypotension
Side effects may include atrioventricular block, bradycardia, and constipation
 Antiplatelet
Prevents platelet aggregation and reduces the incidence of MI and death in
patients with CAD
Aspirin may cause GI upset and bleeding – given with H2 blocker and PPI for
continued aspirin therapy
 Anticoagulant Medications
Prevents the formation of new blood clots
Route: IV or SC
Dose of heparin given is based on the results of the activated partial
thromboplastin time (aPTT)
Therapeutic when the aPTT is 2 to 2.5 times the normal aPTT value
Monitor for signs and symptoms of external and internal bleeding
Bleeding precautions
o Applying pressure to the site of any needle puncture for a longer time than
usual
o Avoiding intramuscular (IM) injections
o Avoiding tissue injury and bruising from trauma or use of constrictive
devices
Antidote: Protamine Sulfate

o Oxygen Administration
 Initiated at the onset of chest pain in an attempt to increase the amount of oxygen
delivered to the myocardium and to decrease pain
 Observe the rate and rhythm of respirations and the color of skin and mucous
membranes
 Pulse oximetry
 Normal oxygen saturation (SpO2) level is greater than 95% on room air

 Nursing Interventions:
1. TREATING ANGINA
o Stop all activities and sit or rest in bed in a semi-Fowler’s position to reduce the oxygen
requirements
 o Assess the patient’s angina - a change may indicate a worsening of the disease
o Monitor vital signs and observe for signs of respiratory distress
o ECG monitoring
o Administer Nitroglycerin as ordered
o Oxygen therapy if the patient’s respiratory rate is increased or if the oxygen saturation
level is decreased - 2 L/min by nasal cannula
o Follow a diet low in saturated fat, high in fiber, and, if indicated, lower in calories
2. REDUCING ANXIETY
o Provide information about the illness, its treatment, and methods of preventing its
progression
o stress reduction methods, such as guided imagery or music therapy
o Address the spiritual needs of the patient and family
3. PREVENTING PAIN
o Identify the level of activity that causes the patient’s pain or prodromal symptoms
o Alternate the patient’s activities with rest periods
o Balancing activity and rest is an important aspect of the educational plan for the patient
and family
C. Acute Coronary Syndrome and Myocardial Infarction
 Emergent situation characterized by an acute onset of myocardial ischemia that results in
myocardial death if definitive interventions do not occur promptly
 Coronary occlusion, heart attack, and myocardial infarction are used synonymously, the preferred
term is myocardial infarction
 Includes unstable angina, NSTEMI, and ST-segment elevation myocardial infarction (STEMI)
 Clinical Manifestations
o Chest pain or discomfort not relieved by rest or nitroglycerin
o Heart sounds may include S3, S4, and new onset of a murmur
o Increased jugular venous distention may be seen if the myocardial infarction (MI) has caused
heart failure
o Blood pressure may be elevated because of sympathetic stimulation or decreased because
of decreased contractility, impending cardiogenic shock, or medications
o ST-segment and T-wave changes
o Shortness of breath, dyspnea, tachypnea, and crackles if MI has caused pulmonary
congestion. Pulmonary edema may be present
o Nausea, indigestion, and vomiting
o Decreased urinary output may indicate cardiogenic shock
o Cool, clammy, diaphoretic, and pale appearance due to sympathetic stimulation may
indicate cardiogenic shock
o Anxiety, restlessness, and lightheadedness may indicate increased sympathetic stimulation
or a decrease in contractility and cerebral oxygenation
 Assessment and Diagnostic Findings
o based on the presenting symptoms
o 12-lead ECG
 should be obtained within 10 minutes from the time a patient reports pain or arrives
in the ED
 T-wave inversion, ST-segment elevation, and development of an abnormal Q wave
 Unstable angina: The patient has clinical manifestations of coronary ischemia, but
ECG and cardiac biomarkers show no evidence of acute MI
 STEMI: The patient has ECG evidence of acute MI with characteristic changes in two
contiguous leads on a 12-lead ECG. In this type of MI, there is a significant damage to
the myocardium.
 NSTEMI: The patient has elevated cardiac biomarkers (e.g., troponin) but no definite
ECG evidence of acute MI. In this type of MI, there may be less damage to the
myocardium
o Troponin - An increase in the level of troponin in the serum can be detected within a few
hours during acute MI.
o Creatine Kinase - increases when there has been damage to the myocardium
o Myoglobin - heme protein that helps transport oxygen
  found in cardiac and skeletal muscle
 starts to increase within 1 to 3 hours and peaks within 12 hours after the onset of
symptoms
 not very specific in indicating an acute cardiac event
 Medical Management
o Initial Management: Immediately give:
 Oxygen
 Aspirin
 Nitroglycerin
 Morphine
drug of choice to reduce pain and anxiety
decreases the work of the heart
assess for hypotension or decreased respiratory rate
 Beta-blockers
 Heparin and antiplatelet
 Emergent Percutaneous Coronary Intervention
o patient with STEMI is taken directly to the cardiac catheterization laboratory for an
immediate PCI
o procedure used to open the occluded coronary artery and promote reperfusion to the area
that has been deprived of oxygen
 Thrombolytics (Fibrinolytics)
o initiated when primary PCI is not available or the transport time to a PCI-capable hospital is
too long
o use to dissolve (i.e., lyse) the thrombus in a coronary artery (thrombolysis), allowing blood to
flow through the coronary artery again (reperfusion), minimizing the size of the infarction
and preserving ventricular function
o Alteplase (Activase), reteplase (Retavase), and tenecteplase (TNKase)
o Absolute Contraindications
 Active bleeding
 Known bleeding disorder
 History of hemorrhagic stroke
 History of intracranial vessel malformation
 Recent major surgery or trauma
 Uncontrolled hypertension
 Pregnancy
o Nursing Considerations
 Minimize the number of times the patient’s skin is punctured.
 Avoid intramuscular injections.
 Draw blood for laboratory tests when starting the IV line.
 Start IV lines before thrombolytic (fibrinolytic) therapy; designate one line to use for
blood draws.
 Avoid continual use of noninvasive blood pressure cuff.
 Monitor for acute dysrhythmias and hypotension.
 Monitor for reperfusion: resolution of angina or acute ST-segment changes.
 Check for signs and symptoms of bleeding: decrease in hematocrit and hemoglobin
values, decrease in blood pressure, increase in heart rate, oozing or bulging at
invasive procedure sites, back pain, muscle weakness, changes in level of
consciousness, complaints of headache.
 Treat major bleeding by discontinuing thrombolytic (fibrinolytic) therapy and any
anticoagulants; apply direct pressure and notify the primary provider immediately.
 Treat minor bleeding by applying direct pressure if accessible and appropriate;
continue to monitor.
 Antidote: Aminocaproic Acid
 ACE inhibitors
o prevent the conversion of angiotensin I to angiotensin II
o blood pressure decreases and the kidneys excrete sodium and fluid (diuresis), decreasing
the oxygen demand of the heart
 oBlood pressure, urine output, and serum sodium, potassium, and creatinine levels need to
be monitored closely
 Cardiac Rehabilitation
o an important continuing care program for patients with CAD that targets risk reduction by:
 providing patient and family education
 offering individual and group support
 encouraging physical activity and physical conditioning
o Goals: Extend life and improve the quality of life
o 3 Phases of Cardiac Rehabilitation
 Phase I
begins with the diagnosis of atherosclerosis
patient education focuses on the essentials of self-care rather than instituting
behavioral changes for risk reduction
Priorities for in-hospital education include the signs and symptoms that indicate
the need to call 911 (seek emergency assistance), the medication regimen, rest–
activity balance, and follow-up appointments with the primary provider
 Phase II
occurs after the patient has been discharged
patient attends sessions three times a week for 4 to 6 weeks but may continue for
as long as 6 months
The outpatient program consists of supervised, often ECG monitored, exercise
training that is individualized
At each session, the patient is assessed for the effectiveness of and adherence to
the treatment
includes educational sessions for patients and families that are given by
cardiologists, exercise physiologists, dietitians, nurses, and other health care
professionals
 Phase III
a long-term outpatient program that focuses on maintaining cardiovascular
stability and long-term conditioning
The patient is usually self-directed during this phase and does not require a
supervised program

NURSING INTERVENTIONS:
 RELIEVING PAIN AND OTHER SIGNS AND SYMPTOMS OF ISCHEMIA
o Medication therapy
o Oxygen as ordered - flow rate of 2 to 4 L/min via nasal cannula
o Vital signs monitoring
o Physical rest in bed with the head of the bed elevated or in a supportive chair helps
decrease chest discomfort and dyspnea
 IMPROVING RESPIRATORY FUNCTION
o Regular and careful assessment of respiratory function
o monitor fluid volume status to prevent fluid overload
o encourage the patient to breathe deeply
o change position frequently to maintain effective ventilation throughout the lungs
o Pulse oximetry
 PROMOTING ADEQUATE TISSUE PERFUSION
o Bed or chair rest
o Skin temperature and peripheral pulses must be checked frequently to monitor tissue
perfusion
 REDUCING ANXIETY
o Develop a trusting and caring relationship with the patient
o Provide information to the patient and family in an honest and supportive manner
o Ensure a quiet environment
o preventing interruptions that disturb sleep
o providing spiritual support consistent with the patient’s beliefs
 MONITORING AND MANAGING POTENTIAL COMPLICATIONS
o Acute pulmonary edema
 o Heart failure
o Cardiogenic shock
o Dysrhythmias and cardiac arrest
o Pericardial effusion and cardiac tamponade

INVASIVE CORONARY ARTERY PROCEDURES

 Percutaneous Coronary Interventions
o Percutaneous Transluminal Coronary Angioplasty
 a balloon-tipped catheter is used to open blocked coronary vessels and resolve
ischemia
 used in patients with angina and as an intervention for ACS
 purpose of PTCA is to improve blood flow within a coronary artery by compressing the
atheroma
o Coronary Artery Stent
 A stent is a metal mesh that provides structural support to a vessel at risk of acute
closure
 When the balloon is inflated, the mesh expands and presses against the vessel wall,
holding the artery open. The balloon is withdrawn, but the stent is left permanently in
place within the artery
 risk of thrombus formation - patient receives antiplatelet medications, usually
aspirin and clopidogrel

D. Pulmonary Edema
 Abnormal accumulation of fluid in the interstitial spaces and alveoli of the lungs
 Clinical Manifestations
o Restlessness and anxious
o Sudden onset of breathlessness and a sense of suffocation
o Tachypnea with noisy breathing
o Low oxygen saturation rates
o Skin and mucous membranes may be pale to cyanotic, cool and moist
o Tachycardia and JVD
o Incessant coughing producing increasing quantities of foamy sputum
o Orthopnea
 Assessment and Diagnostic Findings
o Airway and breathing
o Vital signs
o Cardiac monitoring
o IV access
o Arterial blood gases, electrolytes, BUN, and creatinine
o Chest x-ray
 Medical Management
o Oxygen Therapy
 To relieve hypoxemia and dyspnea
  A nonrebreathing mask is used initially
 Endotracheal (ET) intubation and mechanical ventilation maybe required
 Oxygenation is monitored by pulse oximetry and by measurement of arterial blood
gases
o Diuretics
 Furosemide or another loop diuretic
 Monitor BP, UO, electrolytes, daily weights
o Vasodilators
 IV nitroglycerin or nitroprusside may enhance symptom relief in pulmonary edema
 Monitor BP
 Nursing Management
o Position: Upright legs dangling over the side of the bed - reduce venous return to the
heart
o Provide Psychological Support - simple, concise information in a reassuring voice about what
is being done to treat the condition and the expected results
o Monitoring Medications
E. Cardiogenic Shock
 decreased CO leads to inadequate tissue perfusion and initiation of the shock syndrome
 a life-threatening condition with a high mortality rate
 Clinical Manifestations
o Pain of angina
o Dysrhythmias
o Complaints of fatigue
o Express feelings of doom
o Signs of hemodynamic instability (hypotension)
 Medical Management
o Goals:
 To limit further myocardial damage
 Preserve the healthy myocardium
 Improve cardiac function by increasing cardiac contractility
o Oxygenation
 supplemental oxygen is given by nasal cannula at a rate of 2 to 6 L/min
 oxygen saturation exceeding 95%
 Monitor arterial blood gas values, pulse oximetry values, and ventilatory effort
o Pain Control - IV morphine – pain, vasodilation, reduces anxiety
o Hemodynamic Monitoring
 To assess the patient’s response to treatment
 Performed in the intensive care unit (ICU), where an arterial line can be inserted
 A multilumen central venous and pulmonary artery catheter may be inserted to
allow measurement of myocardial filling pressures, pulmonary artery pressures,
cardiac output, and pulmonary and systemic resistance
o Fluid Therapy
 Administration of fluids must be monitored closely to detect signs of fluid overload
 Incremental IV fluid boluses are cautiously given to determine optimal filling
pressures for improving cardiac output
 A fluid bolus should never be given rapidly, because rapid fluid administration in
patients with cardiac failure may result in acute pulmonary edema.
o Pharmacologic Therapy
 Inotropic agents and vasodilators
 Inotropic medications increase cardiac output by mimicking the action of the
sympathetic nervous system, activating myocardial receptors to increase myocardial
contractility (inotropic action), or increasing the heart rate (chronotropic action).
 Vasodilators are used primarily to reduce the workload of the heart and oxygen
demand
 Dobutamine - inotropic effects by stimulating myocardial betareceptors, increasing
the strength of myocardial activity and improving cardiac output
  Nitroglycerin
 Dopamine - sympathomimetic agent that has varying vasoactive effects depending
on the dosage
 Doses of 2 to 8 µg/kg/min improve contractility (inotropic action), slightly increase
the heart rate (chronotropic action), and may increase cardiac output
 Doses that are higher than 8 µg/kg/min predominantly cause vasoconstriction
F. Pericardial Effusion and Cardiac Tamponade
 Pericardial effusion (accumulation of fluid in the pericardial sac)
 An increase in pericardial fluid raises the pressure within the pericardial sac and compresses the
heart resulting to
o Elevated pressure in all cardiac chambers
o Decreased venous return due to atrial compression
o Inability of the ventricles to distend and fill adequately
 Clinical Manifestations
o Chest pain, tachypnea, and dyspnea
o JVD results from poor right atrial filling and increased venous pressure
o Hypotension
o Feeling of pressure in the chest
o Patients with cardiac tamponade typically have tachycardia in response to low CO
o Pulsus paradoxus, a systolic blood pressure that is markedly lower during inhalation. Abnormal
difference of at least 10 mm Hg in systolic pressure between the point that it is heard during
exhalation and the point that it is heard during inhalation
 Medical Management:
o Pericardiocentesis
 Puncture of the pericardial sac to aspirate pericardial fluid
 Patient is monitored by continuous ECG and frequent vital signs
 Performed using echocardiography to guide placement of the drainage catheter
 Complications of pericardiocentesis include coronary artery puncture, myocardial trauma,
dysrhythmias, pleural laceration, and gastric puncture
 After pericardiocentesis, the patient’s heart rhythm, blood pressure, venous pressure, and
heart sounds are monitored frequently to detect possible recurrence of cardiac tamponade
o Pericardiotomy
 Pericardial window
 Under general anesthesia, a portion of the pericardium is excised to permit the exudative
pericardial fluid to drain into the lymphatic system

HEART FAILURE
 Clinical syndrome resulting from structural or functional cardiac disorders that impair the ability of
the ventricles to fill or eject blood
 Often referred to as congestive heart failure (CHF), because many patients experience pulmonary
or peripheral congestion with edema
 Clinical syndrome characterized by signs and symptoms of fluid overload or inadequate tissue
perfusion
 Indicates myocardial disease in which impaired contraction of the heart (systolic dysfunction) or
filling of the heart (diastolic dysfunction) may cause pulmonary or systemic congestion
 Two major types of HF
 Systolic heart failure - alteration in ventricular contraction characterized by a weakened
heart muscle
 Diastolic heart failure - characterized by a stiff and noncompliant heart muscle, making it
difficult for the ventricle to fill

Etiology
 Coronary artery disease
 Hypertension
 Cardiomyopathy
 Valvular disorder
 Renal dysfunction with volume overload
  Diabetes

Clinical Manifestations
A. Left-Sided Heart Failure
 Pulmonary congestion
 Dyspnea, cough, pulmonary crackles, and low oxygen saturation levels
 S3, or “ventricular gallop,” may be detected on auscultation - caused by abnormal ventricular
filling
 Dyspnea on exertion
 Orthopnea - may use pillows to prop themselves up in bed, or they may sit in a chair and even
sleep sitting up
 Paroxysmal nocturnal dyspnea - sudden attacks of dyspnea at night
 Cough initially dry and nonproductive -dry hacking cough
 Cough may become moist over time - Large quantities of frothy sputum (pink or tan (blood
tinged))
 Bibasilar crackles that do not clear with coughing
 Oliguria when awake
 Frequent urination at night (nocturia) – decrease workload of the heart during sleeping
 Increase blood pressure
 Dizziness, lightheadedness, confusion, restlessness, and anxiety
 Heart rate (tachycardia) and palpitations
 Peripheral pulses become weak
 Easily fatigued and has decreased activity tolerance
B. Right-Sided Heart Failure
 Congestion in the peripheral tissues and the viscera predominates
 Jugular venous distention (JVD)
 Edema of the lower extremities (dependent edema)
 Hepatomegaly (enlargement of the liver)
 Ascites (accumulation of fluid in the peritoneal cavity)
 Weight gain due to retention of fluid
 Anorexia (loss of appetite), nausea, or abdominal pain
 Generalized weakness

Assessment and Diagnostic Findings

 Echocardiogram - to determine the EF, identify anatomic features and confirm the diagnosis of HF
 Chest x-ray and a 12-lead electrocardiogram (ECG)
 Serum electrolytes, blood urea nitrogen (BUN), creatinine, liver function tests, complete blood count
(CBC), BNP, and routine urinalysis

Medical Management
 Goals
o To relieve patient symptoms
o To improve functional status and quality of life
o To extend survival
 Objectives of guideline-directed patient management
o Improvement of cardiac function with optimal pharmacologic management
o Reduction of symptoms and improvement of functional status
o Stabilization of patient condition and lowering of the risk of hospitalization
o Delay of the progression of HF and extension of life expectancy
o Promotion of a lifestyle conducive to cardiac health

Pharmacologic Therapy
 Angiotensin-Converting Enzyme Inhibitors
o Promote vasodilation and diuresis, ultimately decreasing afterload and preload
o Decrease the secretion of aldosterone, a hormone that causes the kidneys to retain
sodium and water
o Monitor for hypotension, hyperkalemia (increased potassium in the blood), and alterations
in renal function
o ACE inhibitors may be discontinued if the potassium level remains greater than 5.5 mEq/L
or if the serum creatinine rises
 Angiotensin Receptor Blockers
 o Similar hemodynamic effects and side effects with ACE inhibitors
o Block the vasoconstricting effects of angiotensin II at the angiotensin II receptors
o Alternative to ACE inhibitors
 Beta-Blockers
o Block the adverse effects of the sympathetic nervous system
o Relax blood vessels, lower blood pressure, decrease afterload, and decrease cardiac
workload
 Diuretics
o To remove excess extracellular fluid by increasing the rate of urine produced
o Loop diuretics - inhibit sodium and chloride reabsorption mainly in the ascending loop of
Henle
o Thiazide diuretics - inhibit sodium and chloride reabsorption in the early distal tubules
o Aldosterone antagonists - block the effects of aldosterone in the distal tubule and
collecting duct (Aldactone)
 Digitalis
o An essential agent for the treatment of HF
o Increases the force of myocardial contraction and slows conduction through the
atrioventricular node
o Positive inotropic and negative chronotropic effect
o Patients with renal dysfunction and older patients should receive smaller doses of digoxin,
as it is excreted through the kidneys
o Key concern associated with digoxin therapy is digitalis toxicity
o Watch out for anorexia, nausea, visual disturbances, confusion, and bradycardia
o Serum potassium level is monitored because the effect of digoxin is enhanced in the
presence of hypokalemia and digoxin toxicity may occur
o Serum digoxin level is obtained if the patient’s renal function changes or there are
symptoms of toxicity
 Intravenous Infusions
o IV inotropes (milrinone [Primacor], dobutamine [Dobutrex])
o Increase the force of myocardial contraction
o Used for patients who do not respond to routine pharmacologic therapy and are reserved
for patients with severe ventricular dysfunction

Nutritional Therapy
 Low-sodium (no more than 2 g/day) diet
 Avoiding excessive fluid intake
 Consider good nutrition as well as the patient’s likes, dislikes, and cultural food patterns
 Patient adherence is important because dietary indiscretions may result in severe exacerbations
of HF requiring hospitalization

NOTE: Give Supplemental Oxygen

Nursing Interventions
A. PROMOTING ACTIVITY TOLERANCE
 Avoid prolonged physical inactivity - pressure ulcers (especially in edematous patients) and
venous thromboembolism
 Exercise training - daily walking regimen
 Schedule should alternate activities with periods of rest
 Small, frequent meals decrease the amount of energy needed for digestion while providing
adequate nutrition
 Nurse helps the patient identify peak and low periods of energy, planning energy-consuming
activities for peak periods
 Patient’s response to activities needs to be monitored
 Limit physical activities to only 3 to 5 minutes at a time, one to four times per day
B. MANAGING FLUID VOLUME
 Oral diuretics should be given early in the morning
 Assist the patient to adhere to a low-sodium diet by reading food labels and avoiding high-
sodium foods such as canned, processed, and convenience foods
 Assist the patient to plan fluid intake throughout the day while respecting the patient’s dietary
preferences
  Amount of fluid needs to be monitored closely
 Patient is positioned or taught how to assume a position that facilitates breathing - number of
pillows may be increased, the head of the bed may be elevated, or the patient may sit in a
recliner
 Assess for skin breakdown and institute preventive measures
 Positioning to avoid pressure and frequent changes of position help prevent pressure ulcers
C. CONTROLLING ANXIETY
 Promote physical comfort and provide psychological support
 When patients with HF are delirious, confused, or anxious, restraints should be avoided.
Restraints are likely to be resisted, and resistance inevitably increases the cardiac workload.
D. MONITORING AND MANAGING POTENTIAL COMPLICATIONS
 Pulmonary edema, kidney injury, and life-threatening dysrhythmias
 Excessive and repeated diuresis can lead to hypokalemia
 Hyperkalemia may occur, especially with the use of ACE inhibitors, ARBs, or spironolactone
 Prolonged diuretic therapy may produce hyponatremia (deficiency of sodium in the blood),
which can result in disorientation, weakness, muscle cramps, and anorexia
 Volume depletion from excessive fluid loss may lead to dehydration and hypotension. ACE
inhibitors and beta-blockers may contribute to the hypotension
 Other problems associated with diuretics include increased serum creatinine (indicative of
renal dysfunction) and hyperuricemia (excessive uric acid in the blood), which leads to gout

Management of Patients With Dysrhythmias and Conduction Problems

Definition of Terms:
 Depolarization - Electrical Stimulation
 Systole - Mechanical Contraction
 Repolarization - Electrical Relaxation
 Diastole - Mechanical Relaxation

Normal Sinus Rhythm

 electrical impulse starts at a regular rate and rhythm in the SA node and travels through the normal
conduction pathway

Characteristics of Normal Sinus Rhythm

 Ventricular and atrial rate: 60 to 100 bpm
 Ventricular and atrial rhythm: Regular
 QRS shape and duration: Usually normal
 P wave: Normal and consistent shape; always in front of the QRS
 PR interval: Consistent interval between 0.12 and 0.20 seconds
 P:QRS ratio: 1:1

Dysrhythmias
 disorders of the formation or conduction (or both) of the electrical impulse within the heart
 diagnosed by analyzing the ECG waveform
 treatment is based on the frequency and severity of symptoms produced
 named according to the site of origin of the electrical impulse and the mechanism of formation or
conduction involved

Types of Dysrhythmias:
 Sinus
 Atrial
  Junctional
 Ventricular

Sinus Dysrhythmias
A. Sinus Bradycardia
 SA node creates an impulse at a slower-than-normal rat

Characteristics:
o Same with normal sinus rhythm except Ventricular and atrial rate which is Less than 60
Management:
o depends on the cause and symptoms
o If there are signs and symptoms of clinical instability (acute alteration in mental status, chest
discomfort, hypotension)
Rapid IV bolus of 0.5 mg of atropine Repeated every 3 to 5 minutes
Until maximum dosage of 3 mg
Administer O2 as prescribed for symptomatic
 If unresponsive to atropine
o Emergency transcutaneous pacing
o Catecholamines (dopamine or epinephrine)

B. Sinus Tachycardia
 sinus node creates an impulse at a faster-than-normal rate

Characteristics:
o Same with normal sinus rhythm except Ventricular and atrial rate which is greater than 100, but
usually lesser than 120

Heart rate increases

Diastolic filling time decreases

Reduced cardiac output

Syncope and low blood pressure

Management:
o determined by the severity of symptoms
o directed at identifying and abolishing its cause
 o Synchronized cardioversion - treatment of choice if persistent and causing hemodynamic
instability
o Vagal maneuvers
Carotid sinus massage
Gagging
Bearing down against a closed glottis
Forceful and sustained coughing
Applying a cold stimulus to the face
o Beta-blockers and calcium channel blockers
o Adenosine (Adenocard)
o Procainamide (Pronestyl), amiodarone, and sotalol (Betapace)

C. Sinus Arrhythmia
 sinus node creates an impulse at an irregular rhythm
 rate usually increases with inspiration and decreases with expiration

Characteristics:
 Same with normal sinus rhythm except Ventricular and atrial rhythm: Irregular
Management:
 Sinus arrhythmia does not cause any significant hemodynamic effect and therefore is not typically
treated.

Atrial Dysrhythmias
A. Atrial Fibrillation
 most common sustained dysrhythmia
 rapid, disorganized, and uncoordinated twitching of the atrial musculature causing the atria to
quiver or fibrillate instead of fully squeezing. As a result, blood is collected in atria increasing the risk
for clot formation
 Rapid and irregular ventricular response reduces the time for ventricular filling, resulting in a smaller
stroke volume
 Risk of heart failure, myocardial ischemia, and embolic events such as stroke

Characteristics:
 Ventricular and atrial rate: Atrial rate is 300 to 600 bpm; ventricular rate is usually 120 to 200
bpm in untreated atrial fibrillation
 Ventricular and atrial rhythm: Highly irregular
 P wave: No discernible P waves; irregular undulating waves that vary in amplitude and shape are
seen and referred to as fibrillatory or f waves
 PR interval: Cannot be measured
 P:QRS ratio: Many:1
Management:
  Antithrombotic Medications
o Anticoagulants and antiplatelet drugs - to reduce risk of embolic stroke
o Patients with low stroke risk – Aspirin
o Patients with at least moderate risk - warfarin (Coumadin)
 Administer O2 as prescribed
 Medications That Control the Heart Rate
o Beta-blocker
o Calcium channel blocker
 Medications That Convert the Heart Rhythm or Prevent Atrial Fibrillation
o Flecainide, propafenone, amiodarone, dofetilide, or sotalol
 Cardioversion

B. Atrial Flutter
 conduction defect in the atrium and causes a rapid, regular atrial impulse at a rate between 250
and 400 bpm
 Atrial rate is faster than the AV node can conduct, not all atrial impulses are conducted into the
ventricle, causing a therapeutic block at the AV node

Characteristics:
 Ventricular and atrial rate: Atrial rate ranges between 250 and 400 bpm; ventricular rate usually
ranges between 75 and 150 bpm.
 P wave: Saw-toothed shape; these waves are referred to as F waves.
 PR interval: Multiple F waves may make it difficult to determine thePR interval.
 P:QRS ratio: 2:1, 3:1, or 4:1
Management:
 Can cause chest pain, shortness of breath, and low blood pressure
 Adenosine
o causes sympathetic block and slowing of conduction through the AV node
o IV rapid administration, followed by a 20-mL saline flush, elevation of the arm with the IV
line
 Antithrombotic therapy
 Electrical cardioversion
 Vagal maneuvers

Ventricular Dysrhythmias

A. Premature Ventricular Complex

 impulse that starts in a ventricle and is conducted through the ventricles before the next normal
sinus impulse
 PVCs can occur in healthy people, especially with intake of caffeine, nicotine, or alcohol.
 The patient may feel nothing or may say that the heart “skipped a beat.”

Management:
 If asymptomatic - usually is not serious
  Frequent and persistent may be treated with amiodarone or sotalol (short term)
B. Ventricular Tachycardia
 three or more PVCs in a row, occurring at a rate exceeding 100 bpm
 emergency because the patient is nearly always unresponsive and pulseless

Management:
 Procainamide – pt’s who do not have acute MI or severe HF
 IV amiodarone - medication of choice for a patient with impaired cardiac function or acute MI
 Lidocaine - medication most commonly used for immediate, short-term therapy, especially for
patients with impaired cardiac function
 Cardioversion or defibrillation

C. Ventricular Fibrillation
 most common dysrhythmia in patients with cardiac arrest
 rapid, disorganized ventricular rhythm that causes ineffective quivering of the ventricles
 No atrial activity is seen on the ECG
 most common cause of ventricular fibrillation is coronary artery disease and resulting acute MI

Management:
 Always characterized by the absence of an audible heartbeat, a palpable pulse, and respirations
 no coordinated cardiac activity, cardiac arrest and death are imminent if the dysrhythmia is not
corrected
 Early defibrillation
 Cardiopulmonary resuscitation (CPR) until defibrillation is available
 Administration of amiodarone and epinephrine may facilitate the return of a spontaneous pulse
after defibrillation

D. Ventricular Asystole
 Commonly called flatline
 Characterized by absent QRS complexes
 no heartbeat, no palpable pulse, and no respiration

Management:
 CPR
  Hs and Ts: hypoxia, hypovolemia, hydrogen ion (acid–base imbalance), hypo- or hyperglycemia,
hypo- or hyperkalemia, hyperthermia, trauma, toxins, tamponade (cardiac), tension pneumothorax,
or thrombus (coronary or pulmonary)
 intubation and establishment of IV access

Adjunctive Modalities and Management Of Dysrhythmias

Cardioversion and Defibrillation
 used to treat tachydysrhythmias by delivering an electrical current that depolarizes a critical mass
of myocardial cells
 When the cells repolarize, the SA node is usually able to recapture its role as the heart’s pacemaker
 Defibrillator, is used for both cardioversion and defibrillation
 Electrical voltage required to defibrillate the heart is usually greater than that required for
cardioversion
 One major difference between is the timing of the delivery of electrical current
 In cardioversion, the delivery of the electrical current is synchronized with the patient’s
electrical events; in defibrillation, the delivery of the current is immediate and
unsynchronized.
Cardioversion
 Synchronized countershock to convert an undesirable rhythm to a stable rhythm
 Elective or emergency
 set to synchronize with the ECG on a cardiac monitor so that the electrical impulse discharges
during ventricular depolarization (QRS complex)
o prevents the discharge during the vulnerable period of repolarization (T wave), which could
result in VT or ventricular fibrillation
 Lower amount of energy is used than defibrillation
 50 to 360 joules, depending on the defibrillator’s technology, the type and duration of the
dysrhythmia, and the size and hemodynamic status of the patient

Nursing Interventions
 Pre-procedure
 If elective – consent
 NPO at least 4 hours if elective
 Sedation as ordered
 If elective, hold digoxin for 48 hours preprocedure as prescribed to prevent
postcardioversion ventricular irritability
 If elective for atrial fibrillation or atrial flutter, client should receive anticoagulant therapy
for 4-6 weeks prior to the procedure and TEE should be performed
 Respiration is then supported with supplemental oxygen delivered by a bag-valve mask device
with suction equipment readily available
 Although patients rarely require intubation, equipment is nearby in case it is needed

 During the Procedure

 Ensure that the skin is clean and dry in the area where the electrode pads/hands-off pads will
be placed
 Be sure that no one is touching the bed of the client when delivering the countershock
 Gels or pastes with poor electrical conductivity (e.g., ultrasound gel) should not be used
 Paddles or pads should be placed so that they do not touch the patient’s clothing or bed linen
and are not near medication patches or in the direct flow of oxygen
 Women with large breasts should have the left pad or paddle placed underneath or lateral to
the left breast
 Monitor leads must be attached to the patient in order to set the defibrillator to the
synchronized mode (“in sync”)
 When it is time to defibrillate, whomever is delivering the charge should announce, “charging
to (number of joules)” prior to discharging.
 “Clear!” must be called three times before discharging
o 1st: discharger must visually check that he or she is not touching the patient, bed, or
equipment
 o 2nd: discharger must visually check that no one else is touching the bed, the patient, or
equipment
o 3rd: discharger must perform a final visual check to ensure that everyone is clear of the
patient and anything touching the patient
 The delivered energy and resulting rhythm are recorded
 Post Procedure
o Priority assessment includes ability of the client to maintain the airway and breathing
o Resume O2 administration as ordered
o Assess v/s
o Assess LOC
o Monitor cardiac rhythm
o Monitor for indications of successful response - sinus rhythm, strong peripheral pulses,
normal BP, adequate urine output
o Assess the skin on the chest for evidence of burns

Defibrillation
 Used in emergency situations as the treatment of choice for ventricular fibrillation and pulseless VT
 Asynchronous countershock
 Not used for patients who are conscious or have a pulse
 The sooner defibrillation is used, the better the survival rate
 The defibrillator is charged to 120-200 joules (biphasic) or 360 joules (monophasic) for one
countershock from the defibrillator, CPR is resumed immediately and continued for 5 cycles or
about 2 minutes
 Epinephrine is given after initial unsuccessful defibrillation to make it easier to convert the
dysrhythmia to a normal rhythm with the next defibrillation
o Epinephrine increases cerebral and coronary artery blood flow
 Antiarrhythmic medications such as amiodarone, lidocaine, or magnesium may be given if
ventricular dysrhythmia persists

Conduction Abnormalities
 PR interval is assessed for the possibility of an AV block
 AV blocks occur when the conduction of the impulse through the AV nodal or bundle of His area is
decreased or stopped
 AV block may be temporary and resolve on its own, or it may be permanent and require permanent
pacing

A. First-Degree Atrioventricular Block

 all the atrial impulses are conducted through the AV node into the ventricles at a rate slower than
normal
 PR interval: Greater than 0.20 seconds; PR interval measurement is constant

B. Second-Degree Atrioventricular Block, Type I (Wenckebach)

 repeating pattern in which all but one of a series of atrial impulses are conducted through the AV
node into the ventricles
 Each atrial impulse takes a longer time for conduction than the one before, until one impulse is
fully blocked.
  PR interval: The PR interval becomes longer with each succeeding ECG complex until there is a P
wave not followed by a QRS. The changes in the PR interval are repeated between each “dropped”
QRS, creating a pattern in the irregular PR interval measurements.

C. Second-Degree Atrioventricular Block, Type II

 occurs when only some of the atrial impulses are conducted through the AV node into the
ventricles.

D. Third-Degree Atrioventricular Block

 occurs when no atrial impulse is conducted through the AV node into the ventricles
 two impulses stimulate the heart: one stimulates the ventricles and one stimulates the atria
 P waves may be seen, but the atrial electrical activity is not conducted down into the ventricles to
cause the QRS complex

Medical Management of Conduction Abnormalities

 treatment is directed toward increasing the heart rate to maintain a normal cardiac output
 No symptoms, no treatment may be indicated or it may simply consist of decreasing or
eliminating the cause (e.g., withholding the medication or treatment).
 Initial treatment of choice is an IV bolus of atropine
o not effective in second-degree AV block, type II, or third-degree AV block
 Temporary transcutaneous pacing
 Permanent Pacemaker

Pacemakers
 Temporary or permanent device that provides electrical stimulation and maintains the heart rate
when the clint’s intrinsic pacemaker fails to provide perfusing rhythm.

A. Noninvasive Transcutaneous Pacing

  Used as temporary emergency measure in profoundly bradycardic or asystolic client until invasive
pacing can be initiated
 Large electrode pads are placed on the client’s chest and back and connected to an external pulse
generator
Nursing Considerations:
 Wash the skin with soap and water before applying electrodes
 It is not necessary to shave the hair or apply alcohol or tinctures to the skin
 Do not take BP and pulse on the left side
 Electrodes should be in good contact with the skin
 If loss of capture occurs, assess the skin contact of the electrodes
 Evaluate client for discomfort
B. Invasive Transvenous Pacing
 Pacing lead wire is place through the vein into the right atrium or right ventricle
Nursing Considerations:
 Monitor the pacemaker insertion site
 Restrict client movement to prevent wire displacement
 Monitor v/s and cardiac monitor
C. Permanent Pacemakers
 Pulse generator is internal and surgically implanted in a subcutaneous pocket below the clavicle
 The leads are passed transvenously via the cephalic or subclavian vein to the endocardium on the
right side of the heart
Client Education:
 Instruct the client about the pacemaker
 Instruct the client in the signs of battery failure and when to notify the HCP
o Fainting, losing consciousness
o Chest pain with weakness, dizziness, nausea and vomiting
o Palpitations
o Bradycardia
o Frequent hiccups
 Instruct the client to report any fever, redness, swelling or drainage from the insertion site
 Report signs of dizziness, weakness or fatigue, swelling of the ankle, chest pain or SOB
 Always wear a MedicAlert Bracelet
 Loose fitting clothes
 No contact sports
 Inform all HCP’s that pacemaker has been inserted
 Most electrical appliances can be used without any interference with the functioning of the
pacemaker; however, do not operate electrical appliances directly over the pacemaker site
 Avoid transmitter towers and antitheft devices in store
 Instruct the client to inform airport security that he/she has a pacemaker because the
pacemaker may set off the security detector
 If any unusual feelings occur when near electrical devices, move 5-10 feet away and check the
pulse
 Emphasize the importance of follow up
 Use cellphones on the opposite side of the pacemaker

Endocarditis
 inflammation of the endothelial surface of the heart
 can be either infective (caused by microorganisms such as bacteria and fungi) or non-infective
(autoimmune disorders)
 Infective: staphylococci or streptococci
 Ports of entry for the infecting organism include the oral cavity (especially if the client has had a
dental procedure in the previous 3 to 6 months), infections (cutaneous, genitourinary,
gastrointestinal, and systemic), and surgery or invasive procedures, including IV line placement.
 Risk factors:
o Presence of prosthetic heart valves and cardiac devices (e.g., pacemaker)
o Presence of structural cardiac defects
 o Older adults
o IV drug abuse
o Hospital acquired (hemodialysis or prolonged IV fluid or antibiotic therapy)
o Immunosuppressive medications
o Body piercing (especially oral, nasal, and nipple), branding, and tattooing

Deformity or injury of the endocardium

Accumulation of fibrin and platelets (clot formation) on the endocardium

Infectious organisms invade the clot and endocardial lesion

Vegetation of microorganism

Vegetations may embolize to other tissues throughout the body (systemic emboli)

Infection may erode through the endocardium into underlying structures

Tears or other deformities of valve leaflets, dehiscence of prosthetic valves,

deformity of chordae tendineae, or mural abscesses

 Clinical Manifestations
o Fever (intermittent or absent)
o Heart murmur
o Clusters of petechiae may be found on the body
 Osler nodes - small, painful nodules on pads of fingers or toes
 Janeway lesions - irregular, red or purple, painless flat macules on palms, fingers,
hands, soles, and toes
 Roth spots - hemorrhages with pale centers in fundi of the eyes
 Splinter hemorrhages - under the proximal half of fingernails and toenails.
 Petechiae may appear in conjunctiva and mucous membranes
o Malaise
o Anorexia
o Weight loss
o Back and joint pain
o Cardiomegaly
o Heart failure
o Tachycardia
o Splenomegaly
o Headache
o Temporary or transient cerebral ischemia (stroke)
 Diagnostic Findings
o 2 sets of blood cultures – definitive diagnosis, before administration of any antimicrobial
agents
o Elevated white blood cell (WBC) counts
o Positive rheumatoid factor
o Elevated ESR
o Echocardiography
 Prevention
o Antibiotic prophylaxis - for high-risk patients immediately before and sometimes after dental
procedures
o Good oral hygiene
o Avoid using toothpicks or other sharp objects in the oral cavity
o Avoid nail biting
o Avoid body piercing, branding, tattooing
 oMinimize outbreaks of acne, psoriasis
oAddiction treatment programs
oAvoid IUD
oMeticulous hand hygiene, site preparation, and aseptic technique during insertion and
maintenance procedures
o All catheters, tubes, drains, and other devices are removed as soon as they are no longer
needed or no longer function
 Medical and Surgical Management
o Antibiotic therapy - 2 to 6 weeks every 4 hours or continuously by IV infusion
 Penicillin – DOC for bacterials
 Amphotericin B– DOC for fungal
o Surgery – if nonresponsive to medications
 Valve debridement or excision
 Debridement of vegetations
 Debridement and closure of an abscess
 Closure of a fistula
 Aortic or mitral valve debridement, excision, or replacement
 Nursing Management
o Assess heart sounds - new or worsening murmur may indicate complications
o Administer antibiotic, antifungal, or antiviral medication as prescribed
o Adherence or medication compliance
o Increase OFI
o Balance rest and activities – rest periods due to fatigue
o Good infection control and prevention practices
o Administer NSAIDs or antipyretics as prescribed
o Maintain antiembolism stockingsifprescribed.
o Manage fever with cooling techniques such as with a fan, tepid water baths, or cloth
compresses - if
shivering or piloerection occurs, these interventions should be discontinued due to increased
oxygen consumption and potential to further increase of body temperature
o Monitor for signs and symptoms of systemic embolization
 Splenic emboli - as evidenced by sudden abdominal pain radiating to the left
shoulder and the presence of rebound abdominal tenderness on palpation
 Renal emboli - as evidenced by flank pain radiating to the groin, hematuria, and
pyuria.
 Central nervous system emboli - confusion, aphasia, or dysphasia
 Pulmonary emboli - as evidenced by pleuritic chest pain, dyspnea, and cough
o All invasive lines and wounds must be assessed daily for redness, tenderness, warmth,
swelling, drainage, or other signs of infection

Myocarditis
 inflammatory process involving the myocardium, can cause heart dilation, thrombi on the heart wall
(mural thrombi), infiltration of circulating blood cells around the coronary vessels and between the
muscle fibers, and degeneration of the muscle fibers themselves
 caused by:
o Infection (viral, bacterial, rickettsial, fungal, parasitic, metazoal or protozoal, spirochetal)
o Immune related (immunosuppression therapy)
o Inflammatory reaction to toxins (ethanol, radiation therapy)
 Clinical Manifestations
o May be asymptomatic, with an infection that resolves on its own
o Fatigue and dyspnea
o Tachycardia
o Syncope
o Palpitations
o Discomfort in the chest and upper abdomen
 o Flulike symptoms (most common)
o Pericardial friction rub
o Gallop rhythm
o Murmur that sounds like fluid passing an obstruction
o Pulsus alternans
o Complications: sudden cardiac death and severe CHF
 Diagnostic Findings
o MRI with contrast
o CBC – increased WBC
o ECG - dysrhythmias or ST–T-wave changes
o Increase ESR or CRP
 Prevention
o Appropriate immunizations (e.g., influenza, hepatitis)
o Early treatment
 Medical Management
o Bed rest to decrease cardiac workload
o Activities, especially athletics, should be limited for a 6-month period or at least until heart
size and function have returned to normal
o Physical activity is increased slowly, and the patient is instructed to report any symptoms
that occur with increasing activity, such as a rapidly beating heart
o Antibiotics as prescribed (penicillin for hemolytic streptococci)
o NSAIDs should not be used for pain control - ineffective in relieving the inflammatory process
in myocarditis and have
been linked to worsening inflammation of the myocardium. This also can contribute to an
increased mortality from increased virulence of the pathogen
 Nursing Management
o Assess for signs and symptoms of heart failure and dysrhythmias
o Continuous cardiac monitoring with personnel and equipment readily available to treat life-
threatening dysrhythmias
o Assist the client to a position of comfort, such as sitting up and leaning forward.
o Administer oxygen as prescribed
o Patients with myocarditis are sensitive to digitalis – monitor for toxicity (WOF new onset of
dysrhythmia, anorexia, nausea, vomiting, headache, and malaise)
o Anti-embolism stockings
o Passive and active exercises
Pericarditis
 inflammation of the pericardium, which is the membranous sac enveloping the heart
 may be acute, chronic, or recurring
 may occur 10 days to 2 months after acute myocardial infarction
 may be a primary illness, or it may develop during various medical and surgical disorders
 Classifications:
o Adhesive (constrictive) - the layers of the pericardium become attached to each other
and restrict ventricular filling
o Serous – accumulation of serum in the pericardial sac
o Purulent - accumulation of pus in the pericardial sac
o Calcific - accumulation of calcium deposits in the pericardial sac
o Fibrinous - accumulation of clotting proteins in the pericardial sac
o Sanguinous - accumulation of blood in the pericardial sac
o Malignant – cancer
 Causes:
o Idiopathic or nonspecific causes
o Infection: usually viral, rarely bacterial, fungal or parasitic
o Disorders of connective tissue – SLE, RA, rheumatic fever
o Sarcoidosis
o Hypersensitivity states: immune reactions, medication reactions, and serum sickness
 o Disorders of adjacent structures: myocardial infarction, dissecting aneurysm, pleural and
pulmonary disease (pneumonia)
o Neoplastic disease – due to metastasis
o Radiation therapy of chest and upper torso (peak occurrence 5–9 months after treatment)
o Trauma: chest injury, cardiac surgery, cardiac catheterization, implantation of pacemaker, or
implantable cardioverter defibrillator

Inflammation of the pericardium

Accumulation of fluid in the pericardial sac (pericardial effusion)

Increased pressure on the heart (cardiac tamponade)

Frequent or prolonged episodes of pericarditis

Thickening and decreased elasticity of the pericardium

Fusion of the visceral and parietal pericardium

Ventricular expansion during ventricular filling is restricted (constrictive pericarditis)

Decreased cardiac output (heart failure)

Increased systemic venous pressure

Systemic congestion and hepatic failure

 Clinical Manifestations
o May be asymptomatic
o Chest pain
 may be located beneath the clavicle, in the neck, or in the left trapezius (scapula)
region
 remains fairly constant, but it may worsen with deep inspiration and when lying down
or turning
 pain is grating and is aggravated by breathing (particularly inspiration), coughing,
and swallowing
 Pain is worse when in the supine position and may be relieved by leaning forward
o Creaky or scratchy friction rub heard most clearly at the left lower sternal border at the end
of exhalation (pericardial friction rub)
 place the diaphragm of the stethoscope tightly against the patient’s thorax
 auscultate the left sternal edge in the fourth intercostal space
 heard best when a patient is sitting
 to differentiate pericardial friction rub from a pleural friction rub, the patient is asked
to hold their breath; a pericardial friction rub will continue to be heard
o Mild fever
o Fatigue and malaise
o Nonproductive cough or hiccup
o Dyspnea
o Respiratory splinting – because of pain upon inspiration
o Elevated white blood cell count
 Diagnostic Findings
o Echocardiogram - may detect inflammation, pericardial effusion or tamponade, and heart
failure
o TEE
o CT imaging - best diagnostic tool for determining size, shape, and location of pericardial
effusions
 oCardiac MRI may assist with detection of inflammation and adhesions
oVideo-assisted pericardioscope-guided biopsy of the pericardium or epicardium - to obtain
tissue samples for culture and microscopic examination
o 12-lead ECG - ST elevations. depressed PR segments or atrial dysrhythmias
 Medical Management
o Analgesic medications and NSAIDs - pain relief during the acute phase. Indomethacin
(Indocin) is contraindicated because it may decrease coronary blood flow.
o Colchicine (Colcrys) or corticosteroids (e.g., prednisone) - if the pericarditis is severe or if the
patient does not respond to NSAIDs
o Pericardiocentesis
o Pericardial window - a small opening made in the pericardium to allow continuous drainage
into the chest cavity
o Pericardiectomy - Surgical removal of tough encasing pericardium to release both ventricles
from constrictive and restrictive inflammation and scarring
 Nursing Management
o Administer analgesics as prescribed
o Administer oxygen.
o Educate and reassure patient that the pain is not due to a heart attack
o Forward-leaning or sitting position – to relieve pain and discomfort
o Activity restrictions until pain and fever subside
o Encourage gradual increase of activity as condition improves
o Be alert to cardiac tamponade

Hematologic Function

Anatomic and Physiologic Overview

Blood
 Connective tissue
 7% to 10% of the normal body weight
 Amounts to 5 to 6 L of volume
 Functions:
o Carries oxygen and nutrients to the body cells for cellular metabolism
o Carries hormones, antibodies, and other substances
o Carries waste products produced by cellular metabolism to the lungs, skin, liver, and kidneys,
where they are transformed and eliminated from the body
o Prevents bleeding
 Three primary cell types - 40% to 45% of the blood volume
o Erythrocytes (RBC) – carries hemoglobin to provide oxygen to the tissues. It has an average
lifespan of 120 days
o Leukocytes (WBC) – fights infection
  Neutrophil – prevents or limits bacterial infection via phagocytosis
 Monocyte – enters tissue as macrophage; highly phagocytic especially fungus; immune
surveillance
 Eosinophil – allergic reactions (neutralizes histamine); digests foreign particles;
phagocytosis of parasites
 Basophil – contains histamine; integral part of hypersensitivity reactions
 T Lymphocyte – cell mediated immunity, example: delayed allergic reactions, rejection of
foreign tissue (e.g., transplanted organs), and destruction of tumor cells
 B lymphocyte – humoral immunity, example: production of immunoglobulins
o Thrombocytes (Platelets) – fragment of megakaryocyte; coagulation; hemostasis; average
lifespan of 10 days
 Hematopoiesis – process of blood cell formation.
o Primary site is the bone marrow though the liver and spleen may also be involved during
embryonic development and in other conditions (extramedullary hematopoiesis)
o Under normal conditions, the adult bone marrow produces about 175 billion erythrocytes, 70
billion neutrophils (a mature type of WBC), and 175 billion platelets each day.
o Limited to the pelvis, ribs, vertebrae, and sternum
o Stem cells - primitive cells of the bone marrow, have the ability to self-replicate, thereby
ensuring a continuous supply of stem cells throughout the life cycle
 When stimulated to do so, stem cells can begin a process of differentiation into either
myeloid or lymphoid stem cells
 Lymphoid stem cells - produce either T or B lymphocytes
 Myeloid stem cells - differentiate into three broad cell types: erythrocytes, leukocytes,
and platelets
 Erythrocytes (Red Blood Cells)
o biconcave disc that resembles a soft ball compressed between two fingers
o has a diameter of about 8 mcm and is so flexible that it can pass easily through capillaries that
may be as small as 2.8 mcm in diameter
o membrane of the red cell is very thin so that gases, such as oxygen and carbon dioxide, can
easily diffuse
across it
o have no nuclei and they have many fewer metabolic enzymes than do most other cells
o the disc shape provides a large surface area that facilitates the absorption and release of
oxygen molecules
o consist primarily of hemoglobin, which contains iron and makes up 95% of the cell mass
 Hemoglobin - made up of four subunits (heme portion attached to a globin chain)
 Iron is present in the heme component of the molecule
 Heme has the ability to bind to oxygen loosely and reversibly
o FUNCTION: transport of oxygen between the lungs and tissues
o Reticulocytes - slightly immature forms of erythrocytes
o Erythropoiesis - erythrocyte production, entire process takes less than 5 days
o Erythropoietin - hormone produced primarily by the kidney to stimulate the bone marrow to
produce RBC
o For normal erythrocyte production, the bone marrow also requires iron, vitamin B12, folate,
pyridoxine (vitamin B6), protein, and other factors
o Red Blood Cell Destruction
 average lifespan of a normal circulating erythrocyte is 120 days
 aged erythrocytes lose their elasticity and become trapped in small blood vessels and the
spleen
 they are removed from the blood by the reticuloendothelial cells, particularly in the liver and
the spleen
 as the erythrocytes are destroyed, most of their hemoglobin is recycled
 some hemoglobin also breaks down to form bilirubin and is secreted in the bile
 Iron Stores and Metabolism
o Iron is normally absorbed from the small intestine
 o Additional amounts of iron, up to 2 mg daily, must be absorbed by women of childbearing age to
replace that lost during menstruation
o Total body iron content in the average adult is approximately 3 g
o Iron is stored as ferritin and when required, the iron is released into the plasma, binds to
transferrin, and is transported into the membranes of the normoblasts (erythrocyte precursor
cells) within the marrow, where it is incorporated into hemoglobin
o Iron is lost in the feces, either in bile, blood, or mucosal cells from the intestine
o Iron deficiency in the adult generally indicates blood loss (e.g., from bleeding in the GI tract or
heavy menstrual flow)
o Lack of dietary iron is rarely the sole cause of iron deficiency anemia in adults
o The source of iron deficiency should be investigated promptly, because iron deficiency in an
adult may be a sign of bleeding in the GI tract or colon cancer
 Vitamin B12 and Folate Metabolism
o Vitamin B12 and folate are required for the synthesis of deoxyribonucleic acid (DNA) in RBCs
o Both vitamin B12 and folate are derived from the diet
o Folate is absorbed in the proximal small intestine, but only small amounts are stored within the
body
o Vitamin B12 is found only in foods of animal origin, strict vegetarians may ingest little vitamin
B12
o Vitamin B12 combines with intrinsic factor produced in the stomach - absorbed in the distal
ileum
 Leukocytes (White Blood Cells)
o two general categories: granulocytes and lymphocytes
o total leukocyte count is 4000 to 11,000 cells/mm3
o approximately 60% to 80% are granulocytes and 20% to 40% are lymphocytes
o Granulocytes - defined by the presence of granules in the cytoplasm of the cell
 Eosinophils
 Basophils
 Neutrophils
o Agranulocytes
 Monocytes - largest of the leukocytes
 Lymphocytes
o FUNCTION: protect the body from invasion by bacteria and other foreign entities
 Platelets (Thrombocytes)
o not technically cells; rather, they are granular fragments of giant cells in the bone marrow called
megakaryocytes
o FUNCTION: essential role in the control of bleeding
o Platelets have a normal lifespan of 7 to 10 days
 Plasma and Plasma Proteins
o Liquid portion of the blood
o More than 90% of plasma is water; remainder consists primarily of plasma proteins; clotting
factors (particularly fibrinogen); and small amounts of other substances, such as nutrients,
enzymes, waste products, and gases
o Plasma proteins consist primarily of albumin and globulins.

Bone Marrow Aspiration and Biopsy

 Performed when additional information is needed to assess how a patient’s blood cells are being
formed and to assess the quantity and quality of each type of cell produced within the marrow
 These tests are also used to document infection or tumor within the marrow
 Normal bone marrow is in a semifluid state and can be aspirated through a special large needle
 SITES: iliac crest and occasionally from the sternum
 Nursing Management
o Informed consent
o Skin prep using aseptic technique
o Done under local anesthesia
 o Explain sensation:
 Patients typically feel a pressure sensation as the needle is advanced into position
 Actual aspiration always causes sharp but brief pain
 DBE and relaxation techniques often helps ease the discomfort
o Assist the patient in maintaining a comfortable position and encourage relaxation and deep
breathing throughout the procedure
o Complications: bleeding and infection
o Apply pressure to the site for several minutes and cover with a sterile dressing
o Warm tub baths and a mild analgesic agent as prescribed
o Aspirin-containing analgesic agents should be avoided in the immediate post-procedure period
because they can aggravate or potentiate bleeding

ANEMIA
 condition in which the hemoglobin concentration is lower than normal
 amount of oxygen delivered to body tissues is diminished
 most common hematologic condition
 Classifications:
o Hypoproliferative - bone marrow does not produce adequate numbers of erythrocytes
o Hemolytic - premature destruction of erythrocytes results in the liberation of hemoglobin from
the erythrocytes into the plasma; released hemoglobin is converted in large part to bilirubin
and, therefore, the bilirubin concentration rises
o Bleeding – resulting from RBC loss

A. Iron Deficiency Anemia

 Most common type of anemia in all age groups, and it is the most common anemia in the world
 Causes
o Intake of dietary iron is inadequate for hemoglobin synthesis
o Blood loss - bleeding from ulcers, gastritis, inflammatory bowel disease, or GI tumors (most
common cause of IDA among men and postmenopausal women)
o Menorrhagia (excessive menstrual bleeding) and pregnancy with inadequate iron
supplementation (most common cause of IDA among premenopausal women)
o Chronic alcoholism
o Prolonged use of medications such as aspirin, steroids, or nonsteroidal anti-inflammatory drugs
(NSAIDs)
o Iron malabsorption - gastrectomy, bariatric surgery, or with celiac or other inflammatory bowel
disease
 Clinical Manifestations
o Smooth, red tongue
o Tachycardia
o Fatigue
o Brittle and ridged nails
o Angular cheilosis
 Diagnostic Findings
o Bone marrow aspiration - definitive method of establishing the diagnosis
o MCV - measures the size of the erythrocytes, decreased in IDA
o Decrease hematocrit and RBC levels
o Decreased hemoglobin level
 Medical Management
o Oral iron supplementation – ferrous sulfate, ferrous gluconate, and ferrous fumarate
 Taken on an empty stomach - an hour before meals
 GI side effects (primarily constipation, but also cramping, nausea, and vomiting)
 Taking iron with vitamin C increases absorption of the iron
 Iron absorption is reduced with food, especially dairy products.
 Eat foods high in fiber to minimize problems with constipation
 Remember that stools will become dark in color
  Prevent staining the teeth with a liquid preparation by using a straw or placing a spoon at
the back of the mouth to take the supplement. Rinse the mouth thoroughly afterward.
o Parenteral Iron Formulations
 Nursing Management
o Preventive education
o Food sources high in iron - taking iron-rich foods with a source of vitamin C (e.g., orange juice)
enhances the absorption of iron
 Organ meats (e.g., beef or calf’s liver, chicken liver)
 Meats
 Beans (e.g., black, pinto, and garbanzo)
 Leafy green vegetables
 Raisins
 Molasses
o Balance rest and activity
B. Aplastic Anemia
 Rare disease caused by a decrease in or damage to marrow stem cells, damage to the
microenvironment within the marrow, and replacement of the marrow with fat
 Stem cell damage is caused by the body’s T cells mediating an inappropriate attack against the
bone marrow, resulting in bone marrow aplasia (i.e., markedly reduced hematopoiesis)
 Significant neutropenia and thrombocytopenia also occur
 Causes:
o Idiopathic
o Viral infections
o Medications, chemicals, or radiation damage
o Benzene and benzene derivatives (e.g., airplane glue, paint remover, dry-cleaning solutions)
o Toxic materials, such as inorganic arsenic, glycol ethers, plutonium, and radon
 Clinical Manifestations
o Anemia - fatigue, pallor, dyspnea
o Leukopenia – risk for infection (repeated throat infections – lymphadenopathy)
o Thrombocytopenia – risk for bleeding (Purpura or bruising, retinal hemorrhages)
 Diagnostic Findings
o CBC – pancytopenia (a decrease in all myeloid stem cell–derived cells)
o Bone marrow aspirate shows an extremely hypoplastic or even aplastic (very few to no cells)
marrow replaced with fat
 Medical Management
o Hematopoietic stem cell transplant (HSCT)
o Immunosuppressive therapy - combination of antithymocyte globulin (ATG) and cyclosporine or
androgens
o ATG - purified gamma-globulin solution, is obtained from horses or rabbits immunized with
human T lymphocytes
 Side effects - fever and chills during infusion
 WOF anaphylaxis - sudden onset of a rash or bronchospasm
o Transfusions of PRBCs and platelets as necessary
 Nursing Management
o Assess for signs of infection and bleeding
o Monitor for side effects of therapy, particularly for hypersensitivity reaction while administering
ATG
o Long-term cyclosporine therapy - monitor for long-term effects, including renal or liver
dysfunction, hypertension, pruritus, visual impairment, tremor, and skin cancer
o Do not stop medications abruptly
C. Megaloblastic Anemias
 anemia caused by deficiencies of vitamin B12 or folic acid
 identical bone marrow and peripheral blood changes occur because both vitamins are essential for
normal DNA synthesis
 the erythrocytes that are produced are abnormally large and called megaloblastic red cells
 other cells derived from the myeloid stem cell (nonlymphoid leukocytes, platelets) are also
abnormal
 A bone marrow analysis reveals hyperplasia (an abnormal increase in the number of cells), and the
precursor erythroid and myeloid cells are large and bizarre in appearance
 Many of these abnormal erythroid and myeloid cells are destroyed within the marrow, so the
mature cells that do leave the
marrow are actually fewer in number (pancytopenia can develop)
 Folic Acid Deficiency
o Deficient intake of folic rich foods (green vegetables and liver)
o Alcoholism
o Liver disease
o Chronic hemolytic anemias
o Pregnancy
o Malabsorption
 Vitamin B12 Deficiency (Pernicious Anemia)
o Inadequate dietary intake (vegans)
o Faulty absorption from the GI tract
o Crohn’s disease or after ileal resection, bariatric surgery, or gastrectomy
o Chronic use of histamine blockers, antacids, or proton pump inhibitors to reduce gastric acid
production can also inhibit
B12 absorption
o Absence of intrinsic factor
 Clinical Manifestations - symptoms of folic acid and vitamin B12 deficiencies are similar, and the
two anemias may coexist
o Pernicious Anemia
 Neurologic manifestations
 Weakness
 Listlessness
 Fatigue
 Smooth, sore, red tongue
 Extremely pale, particularly in the mucous membranes
 Paresthesias in the extremities
 Difficulty maintaining balance
 Loss of position sense (proprioception)
 Medical Management
o Folate deficiency
 Increase amount of folic acid in the diet
 Administer 1 mg of folic acid daily
 Folic acid IM only to people with malabsorption problems
o Vitamin B12 deficiency
 Oral supplements with vitamins or fortified soy milk
 Monthly intramuscular injections of vitamin B12 (lack of intrinsic factor)
 Nursing Management
o Inspect skin, mucous membranes, and tongue
o Mild jaundice may be apparent and is best seen in the sclera without using fluorescent lights
o Vitiligo (patchy loss of skin pigmentation) and premature graying of the hair are often seen in
patients with pernicious
anemia
o Careful neurologic assessment is important
o If sensation is altered, the patient needs to be instructed to avoid excessive heat and cold
o Pay particular attention to ambulation and assess the patient’s gait and stability
o Eat small amounts of bland, soft foods frequently
POLYCYTHEMIA