Download Cardiac Disorders

Anatomy and Physiology
of the Heart
Anatomy
• Chambers
– Two upper atria (right and left)
– Two lower ventricles (right and left)
• Muscle layers
– Endocardium, myocardium, and epicardium
• Valves
– Atrioventricular valves
• Mitral and tricuspid
– Semilunar valves
• Aortic and pulmonic
Heart Sounds
• The first heart sound (S1), referred to as lub,
occurs when the ventricles contract during
systole and when the mitral and tricuspid
valves close
• The second heart sound (S2), called dub,
occurs during ventricular relaxation or
diastole and is caused by the closing of the
aortic and pulmonic valves
Figure 35-1
Coronary Blood Flow
• Left coronary artery and the right coronary
artery
– Left coronary artery branches into the left
anterior descending and circumflex arteries
– Right coronary artery branches to supply the
sinoatrial (SA) and the atrioventricular (AV)
nodes, the RA and RV, and the inferior part of
the LV
Coronary Blood Flow
• Venous system parallels the arterial system:
the great cardiac vein follows the left
anterior descending artery and the small
cardiac vein follows right coronary artery
• Veins meet to form the coronary sinus
(largest coronary vein), which returns
deoxygenated blood from the myocardium
to the right atrium
Figure 35-2
Figure 35-3
Conduction
• SA node, called the pacemaker, initiates the impulse
• The impulse is carried throughout the atria to the AV node,
located on the floor of the RA
• Impulse is delayed in the AV node, then transmitted to the
ventricles through the bundle of His
• The bundle is made up of Purkinje cells and is located where
the atrial and ventricular septa meet
• Bundle of His divides into left and right bundle branches
• Left branch divides into anterior and posterior branches:
fascicles
• Terminal ends of right and left branches: the Purkinje fibers
• When impulse reaches Purkinje fibers, ventricles contract
Figure 35-4
Conduction
• Cardiac innervation
– Heart innervated by sympathetic and
parasympathetic fibers of the autonomic nervous
system
• Sympathetic fibers distributed throughout the heart
• Sympathetic stimulation results in increased heart rate,
increased speed of conduction through the AV node, and
more forceful contractions
• Parasympathetic fibers (part of the vagus nerve) found
primarily in the SA and AV nodes and the atrial tissue
• Parasympathetic stimulation results in slowing of heart
rate, slowing of conduction through the AV node, and
decreased strength of contraction
Cardiac Function
• Cardiac cycle
– Contraction and relaxation of the heart make up one
heartbeat
• Cardiac output
– Amount of blood (in liters) ejected per minute
– Factors that affect stroke volume: preload,
contractility, and afterload
• Myocardial oxygen consumption
– Myocardial tissue routinely needs 70% to 75% of the
oxygen delivered to it by the coronary arteries
Age-Related Changes
• Heart
– Increased density of connective tissue and
decreased elasticity
– Number of pacemaker cells in the SA node
decreases, as does the number of nerve fibers in
the ventricles
• Blood vessels
– Changes in connective tissue and elastic fibres in
arteries cause them to become stiffer.
– Veins stretch and dilate, leading to venous stasis
and sometimes impaired venous return.
Coronary Artery Disease (CAD)
Arteriosclerosis
–Abnormal thickening, hardening, loss
of elasticity of arterial walls
Atherosclerosis
–Form of arteriosclerosis;
inflammatory disease that begins
with endothelial injury and
progresses to the complicated lesion
seen in advanced stages of the
disease process
Coronary Artery Disease (CAD)
Risk factors
– Nonmodifiable
• Age, gender, heredity, and race
– Modifiable
• Increased serum lipids, high blood
pressure, cigarette smoking (nicotine),
diabetes mellitus with elevated blood
glucose, obesity, sedentary lifestyle
– Other factors
• Stress, sex hormones, birth control pills,
excessive alcohol intake, high
homocysteine levels
Progression of lesions
Fatty streak
Fibrous plaque
Complicated lesions
Collateral circulation
Branches grow from existing
arteries; provide increased blood
flow
Figure 35-3
http://www.youtube.com/watch?v=SjRPxGNOt
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Angina Pectoris
The most common symptom of CAD
Demand for oxygen by myocardial cells exceeds
supply
Stable angina
– Occurs with exercise or activity and usually
subsides with rest
Unstable angina
– Pain more severe, occurs at rest or with minimal
exertion, is often not relieved by NTG or requires
more frequent NTG administration, and is not
predictable
Variant angina
Caused by coronary artery
spasm; may not be associated
with CAD
Unpredictable and often occurs
at rest
Angina Pectoris
Medical treatment
– Initial therapy for patients with angina
• A Aspirin and antianginal therapy
• B Beta-blocker and blood pressure
• C Cigarette smoking and cholesterol
• D Diet and diabetes
• E Education and exercise
Acute Myocardial Infarction
Risk factors for AMI
–Obesity, smoking, a high-fat diet,
hypertension, family history, male
gender, diabetes mellitus, sedentary
lifestyle, and excessive stress
Acute Myocardial Infarction
Pathophysiology
– Begins with occlusion of a coronary artery
– Over 4-6 hours, ischemia, injury, infarction
develop
– Ischemia results from a lack of blood and oxygen
to a portion of the heart muscle
– If ischemia is not reversed, injury occurs
– Deprived of blood and oxygen, the affected
tissue becomes soft and loses its normal color
– Continued ischemia: infarction of myocardial
tissue
– Ischemia lasting 20 minutes or more is sufficient
to produce irreversible tissue damage
Acute Myocardial Infarction
Complications
– Heart failure, cardiogenic shock,
thromboembolism, and ventricular
aneurysm/rupture
Signs and symptoms
Pain
• Heavy or constrictive pain located below or
behind sternum
• May radiate to the arms, back, neck, or jaw
– Patient becomes diaphoretic and lightheaded
and may experience nausea, vomiting, and
dyspnea
– The skin is frequently cold and clammy
– Patient experiences great anxiety; feeling of
impending doom
Acute Myocardial Infarction
Medical diagnosis
– History and the physical signs and symptoms
– Laboratory evidence and ECG changes
• Cardiac markers
–Troponin, myoglobin, and cardiac enzymes
• Electrocardiogram
–Ischemia: ST segment depressed; T wave is
inverted
–If there has been total occlusion of a
coronary artery, the ECG will show ST
elevation (STEMI)
–Following infarction, another change often
seen on the ECG waveforms is a significant
Q wave
Figure 35-8
Acute Myocardial Infarction
Medical treatment
– Drug therapy
• Sublingual or intravenous nitroglycerin
• Morphine or Demerol
• Oxygen
• Fibrinolytic therapy
• Aspirin and beta-adrenergic blockers
– Percutaneous coronary intervention (PCI)
• Intracoronary stents
• Coronary atherectomy
• Laser angioplasty
• Radiation therapy
– Coronary artery bypass graft surgery
Figure 35-9
http://www.youtube.com/watch?v=S9AqBd4R
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Figure 35-10
Figure 35-11
Acute Myocardial Infarction
Assessment
– Ask patient to describe the pain, including
type, location, duration, and severity
Interventions
– Pain
– Decreased cardiac output
– Anxiety
Cardiac rehabilitation
Heart Failure
Etiology and risk factors
– Two types
• Disorders that increase the workload of
the heart
• Disorders that interfere with heart’s
pumping ability
– Patients at risk for HF: those with CAD,
AMI, cardiomyopathy, hypertension, COPD,
pulmonary hypertension, anemia, disease
of the heart valves, and fluid volume
overload
Heart Failure
Pathophysiology
– The LV, RV, or both fail as pumps
– Usually left side of heart fails first; right
side fails as a result of the left-sided failure
Compensation
– Sympathetic compensation
– Renal compensation
– Natriuretic peptides
– Ventricular hypertrophy
Heart Failure: Signs and Symptoms
Left-sided heart failure
– Anxious, pale, and tachycardic
– Consecutive blood pressure readings may
show a downward trend
– Auscultation of the lung fields reveals
crackles, wheezes, dyspnea, and cough
– S3 and S4 heart sounds heard
Heart Failure: Signs and Symptoms
Right-sided heart failure
–Increased central venous pressure,
jugular venous distention, abdominal
engorgement, and dependent edema
–Anorexia, nausea, and vomiting from
the abdominal engorgement
–Fatigue, weight gain, decreased
urinary output
http://www.youtube.com/watch?v=JXA6LjmKs
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Heart Failure
Medical diagnosis
– History, physical examination, radiographs,
and laboratory test results
Heart Failure
Medical treatment
– Drug therapy
• ACE inhibitors, diuretics, beta-adrenergic
blockers, inotropic agents, cardiac glycosides,
and nitrates. In addition, certain patients will
benefit from B-type natriuretic peptide
– Intra-aortic balloon pump (IABP)
– Ventricular assist devices (VADs)
– Biventricular pacing
– Surgery
• Coronary artery bypass grafting, valve repair
or replacement, partial left ventriculectomy,
Heart Failure
Assessment
– Heart sounds, rate, and rhythm
– Jugular vein distention
– Baseline respiratory assessment of rate,
rhythm, and breath sounds is vital
– Measure weight and blood pressure
accurately
– Inspect skin and palpate for turgor and
edema
– Intake and output records and daily
weights
Heart Failure
Interventions
–Decreased Cardiac Output
–Impaired Gas Exchange
–Fluid Volume Excess
–Activity Intolerance
–Anxiety
Infective Endocarditis
Etiology and risk factors
–Primarily affect the valves
–Incidence has decreased with the use
of antibiotics, but there has been a
resurgence of the problem in
intravenous drug abusers
–Patients with valvular disease also at
risk
Infective Endocarditis
Pathophysiology
–Pathogens, usually bacteria, enter the
bloodstream by any of the previously
mentioned means
–The pathogen accumulates on the
heart valves and/or the endocardium
and forms vegetations
Infective Endocarditis
Complications
– Heart failure and embolization
Signs and symptoms
– Fever, chills, malaise, fatigue, and weight
loss
– Chest or abdominal pain; may indicate
embolization
– Petechiae inside the mouth and on the
ankles, feet, and antecubital areas
– Osler’s nodes on the patient’s fingertips or
toes
Infective Endocarditis
Medical diagnosis
– History, physical examination, results of
lab studies
– Echocardiography
– Serial blood cultures; elevated WBC
Medical treatment
– Antimicrobials, rest, limitation of activities
– Prophylactic anticoagulants
– Surgery to replace an infected prosthetic
valve
Infective Endocarditis
Assessment
–Review patient’s history for risk
factors, recent invasive procedures,
pathologic cardiac conditions, and
onset of symptoms
–Assess for temperature elevation,
heart murmur, evidence of HF (cough,
peripheral edema), and embolization
Infective Endocarditis
Interventions
–Administer prescribed antibiotics
–Assess cardiac output and monitor for
complications
–Teach patient about the medications
prescribed and any restrictions
imposed
–Encourage adequate rest
Pericarditis
Etiology and risk factors
– Inflammation of the pericardium
– May be primary disease or associated with
another inflammatory process
– The disease may be acute or chronic
• Acute pericarditis caused by viruses,
bacteria, fungi, chemotherapy, or AMI
(Dressler’s syndrome)
• Chronic pericarditis caused by
tuberculosis, radiation, or metastases
Pericarditis
Pathophysiology
– In acute pericarditis, inflammatory process
increases amount of pericardial fluid and
inflammation of the pericardial
membranes
– In chronic pericarditis, scarring of the
pericardium fuses the visceral and parietal
pericardia together
– Loss of elasticity results from the scarring
– Constrictive process prevents adequate
ventricular filling
Pericarditis
Complications
– Pericardial effusion or accumulation of fluid in
the pericardial space
• May lead to cardiac tamponade
Signs and symptoms
– Chest pain
• Most severe on inspiration
• Sharp and stabbing but may be described as
dull or burning
• Relieved by sitting up and leaning forward
– Dyspnea, chills, and fever
Pericarditis
Medical diagnosis
– Serial ECGs
– Echocardiogram
– CPK-MB
– Blood cultures
Medical treatment
– Analgesics, antipyretics, anti-inflammatory
agents, and antibiotics
– Surgical creation of a pericardial window
for chronic pericarditis with effusion
Pericarditis
Assessment
– Assessment of heart sounds especially important
Interventions
– Rest and reduction of activity
– Administer and teach patient about medications
– Emotional support
– Vital signs; auscultate for pericardial friction rub
– Note pain characteristics and response to
analgesics and anti-inflammatory agents
– Monitor the ECG for dysrhythmias
Cardiomyopathy
Disease of the heart muscle
Cause often unknown; may be secondary to another
disease process
Usually leads to heart failure
Three types: dilated, hypertrophic, and restrictive
Risk factors with dilated CMP are excessive use of
alcohol, pregnancy, and infections
Hypertrophic CMP: common in younger individuals
Amyloidosis, sarcoidosis, and other
immunosuppressive disorders may predispose
individuals to restrictive cardiomyopathy
Figure 35-12
Cardiomyopathy
Pathophysiology
– Dilated cardiomyopathy: dilation of the
ventricle and severely impaired systolic
function
– Hypertrophic cardiomyopathy: LV
hypertrophies and there is thickening of
the ventricular septum
– Restrictive cardiomyopathy: the
myocardium becomes rigid and
noncompliant
Cardiomyopathy
Signs and symptoms
– Dilated cardiomyopathy: dyspnea, fatigue,
left-sided heart failure, and moderate-tosevere cardiomegaly
– Hypertrophic cardiomyopathy: dyspnea,
orthopnea, angina, fatigue, syncope,
palpitations, ankle edema, and S4 sounds
– Restrictive cardiomyopathy: dyspnea,
fatigue, right-sided HF, S3 and S4 sounds,
and mitral valve regurgitation
Cardiomyopathy
Medical diagnosis
– Echocardiography
– Chest radiography
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Cardiomyopathy
Medical treatment
– Dilated cardiomyopathy: positive inotropic
drugs, diuretics, ACE inhibitors and
vasodilators; heart transplant
– Hypertrophic cardiomyopathy:
antidysrhythmics, antibiotics,
anticoagulants, calcium channel blockers,
beta-blockers; surgical interventions;
implantable cardioverter-defibrillator
– Restrictive cardiomyopathy: similar to that
of HF therapy. Heart transplantation may
be considered
Cardiomyopathy
Assessment
– Primarily for heart failure
– Be alert for dyspnea, cough, edema,
dysrhythmias, and decreased cardiac output
Interventions
– Similar to that of patients with HF
– A hopeful atmosphere and careful explanation of
care requirements
– Encourage the family to support the patient
– Guide the patient to make lifestyle changes
– Encourage patient to make decisions and choices
Figure 35-13
Sudden Cardiac Death
When heart activity and respirations cease abruptly
Most common reason is coronary heart disease
Often preceded by ventricular tachycardia or
ventricular fibrillation and occasionally by severe
bradydysrhythmias
Sudden cardiac death may be the first indication of
CAD
Other causes: left ventricular dysfunction,
cardiomyopathy, hypokalemia, antidysrhythmics,
liquid protein diets, and high alcohol consumption
Those who survive sudden cardiac death need
extensive testing to determine its nature and cause
Sudden Cardiac Death
Implantable cardioverter/defibrillator
– For patients with life-threatening
recurrent ventricular fibrillation who are
unresponsive to medications or
pacemakers
– The device senses heart rate, diagnoses
rhythm changes, and treats ventricular
dysrhythmias
Nursing Care
Promote psychosocial adaptation
– Body image change and a fear of shocks
Patients and families need teaching and
support
Family instructed in CPR
ID bracelet and a card with instructions about
the ICD setting carried at all times
Advise to avoid strong magnetic fields
Valvular Disease
Mitral stenosis: narrowing of the opening in the mitral
valve that impedes blood flow from the LA into the
LV
Mitral regurgitation: allows blood to flow back into
the LA during diastole
Mitral valve prolapse: one or both leaflets enlarges
and protrudes into the LA during systole
Aortic stenosis: valve cusps become fibrotic and
calcify
Aortic regurgitation: fibrosis and thickening of the
aortic cusps progress until the valve no longer
maintains unidirectional blood flow
Cardiac Transplantation
The first heart transplantation was performed
in 1967 in South Africa by Dr. Christiaan
Barnard
Today in the United States, approximately 2500
are done annually for end-stage heart
disease
Donor must meet the criteria for brain death,
have no malignancies outside the central
nervous system, be free of infection, and not
have experienced severe chest trauma
Cardiac Transplantation
Donor and recipient organs carefully matched
Recipient must be free of infection at the time
of transplantation
– Patient prepped as any open-heart
procedure
– Cardiopulmonary bypass initiated;
recipient’s heart is removed except for the
posterior portions of the atria
– Donor heart trimmed and anastomosed to
the remaining native heart
– Patient removed from bypass, heart
restarted, and chest is closed
Cardiac Transplantation
Aftercare similar to that of coronary artery
bypass surgery
– Hemodynamic monitoring, ventilation, cardiac
assessment, care of chest tubes, and accurate
intake and output measurements are vital
Modified protective isolation used
Patients and families taught sign/symptoms of
infection, to avoid crowds and others with
infections
Lifelong immunosuppression
Rejection monitored by endomyocardial
biopsies
Electrocardiogram Monitoring
12-lead electrocardiogram
– Looks at heart from 12 directions or
perspectives
– Permits more precise evaluation of the
heart’s electrical activity
Continuous ECG monitoring
– Most units that perform continuous
monitoring use the five-lead system with
four limb electrodes and a chest electrode
Figure 35-15
Electrocardiogram Monitoring
Interpretation of electrocardiograms
– Heart’s electrical activity represented by
deflections, positive and negative, from
the baseline
• P wave, QRS complex, and T wave
– Criteria for interpreting
electrocardiograms
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•
•
•
•
•
•
Rate calculation
Rhythm
P waves
PR interval
QRS complex
T waves
QT interval
Electrocardiogram Monitoring
Interpretation of electrocardiograms
– Normal sinus rhythm
• The most common cardiac rhythm is sinus in
origin because the impulse originates in the
SA node; is conducted normally
– Common dysrhythmias (rhythm disturbance
from problem in the conduction system)
• Atrial dysrhythmias
• Junctional or escape rhythms
• Ventricular dysrhythmias
Figure 35-17
Figure 35-18
Figure 35-19
Figure 35-20
Figure 35-22
Figure 35-25
Figure 35-26
Figure 35-27
Figure 35-28
Figure 35-29
Figure 35-30
Hemodynamic Monitoring
• Central venous catheter
–Placed through the skin, into a
venous access (brachial, femoral,
subclavian, or jugular sites), and
threaded into the RA
–Catheter may have 1 to 3 lumens
–Mixed venous oxygen saturation
Hemodynamic Monitoring
• Pulmonary artery catheter
– Swan-Ganz catheter
– Longer than the central venous catheter
– Inserted like the central venous catheter
and is threaded through the RA, tricuspid
valve, RV, pulmonic valve, and into
pulmonary artery
– Cardiac output
• Measured continuously or by
thermodilution
Hemodynamic Monitoring
• Arterial line
–Provides a direct measurement of
systolic and diastolic blood
pressures