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Heart
Special Pathology
• The human heart is a remarkably efficient, durable, and reliable pump; – propels over 6000 liters of blood through the body
daily – beats more than 40 million times a year during an
individual's lifetime, thereby – providing the tissues with a steady supply of vital
nutrients and – facilitating the excretion of waste products.
• The normal heart weight varies with body height and weight;
• 250 to 300 g in females • 300 to 350 g in males.
– The usual thickness of the free wall of;• right ventricle is 0.3 to 0.5 cm • left ventricle 1.3 to 1.5 cm • increases in cardiac size and weight accompany many forms of
heart disease. – Greater heart weight or ventricular thickness indicates hypertrophy, – enlarged chamber size implies dilation. – An increase in cardiac weight or size (owing to hypertrophy and/or
dilation) is termed cardiomegaly.
• Cardiac myocytes – Basic to the heart's function is the near-inexhaustible cardiac muscle, the
myocardium, – composed primarily of a collection of specialized muscle cells (Fig.).
• They are arranged largely in a circumferential and spiral orientation around the left ventricle – chamber that pumps blood to the systemic circulation
• Cardiac myocytes have five major components: – (1) cell membrane (sarcolemma) and T-tubules, for impulse conduction; – (2) sarcoplasmic reticulum, a calcium reservoir needed for contraction; – (3) contractile elements; – (4) mitochondria; and – (5) nucleus
• Cardiac muscle cells contain many more mitochondria between myofibrils than do skeletal muscle cells – (approximately 23% of cell volume vs. 2%),– almost complete dependence of cardiac muscle on aerobic metabolism
• Cardiac muscle cells each usually contain one spindle-shaped nucleus – Ventricular muscle contracts during systole and relaxes during diastole
• Three major epicardial coronary arteries;– (1) right coronary artery (RCA)– (2) left anterior descending (LAD) – (3) left circumflex (LCX) arteries,
• both arising from left (main) coronary artery, – Branches of the LAD
» diagonal and septal perforators– Branches of the LCX
» obtuse marginals
– Most coronary arterial blood flow to the myocardium occurs during ventricular diastole,
• microcirculation is not compressed by the cardiac contraction
• The right and left coronary arteries function;– End arteries– Although anatomically most hearts have numerous intercoronary
anastomoses (collateral circulation)• Little blood courses through these channels in the normal heart
– When one artery is severely narrowed, • blood flows via collaterals from the high to the low pressure system• causes the channels to enlarge
– Progressive dilation of collaterals; • stimulated by ischemia, • play a role in providing blood flow to areas of the myocardium otherwise
deprived of adequate perfusion
– When the principal blood flow is compromised and collateral blood flow is inadequate,
• subendocardium (myocardium adjacent to the ventricular cavities) • area most susceptible to ischemic damage
• Aging – knowledge of changes in the cardiovascular system that are
expected to occur with aging is important; • With an increasing number of persons surviving into their eighth
decade and beyond, • number of individuals aged 65 years and older will approximately
double from 2000 to 2050 – (from 35 million to 79 million in the United States)
– Changes associated with aging occur in;• pericardium,• cardiac chambers,• valves, • epicardial coronary arteries, • conduction system, • myocardium, • aorta
• With advancing age;– amount of epicardial fat increases,
• particularly over the anterior surface of the right ventricle and in the atrial septum.
– A reduction in the size of the left ventricular cavity; • particularly in the base-to-apex dimension, accentuated
by systemic hypertension• sigmoid septum
– rightward shift and tortuosity of a dilated ascending aorta, this chamber alteration causes the basal ventricular septum to bend leftward, bulging into the left ventricular outflow tract
• Such reduction in the size of the left ventricular cavity can simulate the obstruction to blood leaving the left ventricle
– often occurs with hypertrophic cardiomyopathy
• Several changes of the valves;– Calcification of the mitral annulus and aortic valve,
the latter frequently leading to aortic stenosis– Valves can develop fibrous thickening,
• mitral leaflets tend to buckle back toward the left atrium during ventricular systole,
• simulating a prolapsing (myxomatous) mitral valve
– Many older persons develop small filiform processes (Lambl excrescences) ;
• closure lines of aortic and mitral valves;• arising from the organization of small thrombi on the
valve contact margins
• Compared with younger myocardium, "elderly" myocardium also has;– fewer myocytes, increased collagenized connective tissue
and, in some individuals, deposition of amyloid– In the muscle cells, lipofuscin deposits, and basophilic
degeneration, an accumulation within cardiac myocytes of a gray-blue byproduct of glycogen metabolism, may be present.
– Extensive lipofuscin deposition in a small, atrophied heart is called brown atrophy;
• often accompanies cachectic weight loss, as seen in terminal cancer. Although the
– morphologic changes described are common in elderly patients at necropsy, and they may mimic disease,
• Only in a minority are they associated with clinical cardiac dysfunction.
CHANGES IN THE AGING HEARTChambers Myocardium
Increased left atrial cavity size Increased mass
Decreased left ventricular cavity size Increased subepicardial fat
Sigmoid-shaped ventricular septum Brown atrophy
Valves Lipofuscin deposition
Aortic valve calcific deposits Basophilic degeneration
Mitral valve annular calcific deposits Amyloid deposits
Fibrous thickening of leaflets Aorta
Buckling of mitral leaflets toward the left atrium
Dilated ascending aorta with rightward shift
Lambl excrescences Elongated (tortuous) thoracic aorta
Epicardial Coronary Arteries Sinotubular junction calcific deposits
Tortuosity Elastic fragmentation and collagen accumulation
Increased cross-sectional luminal area Atherosclerotic plaque
Calcific deposits
Atherosclerotic plaque
Cardiac pathology• Although many diseases can involve the heart
and blood vessels,
– cardiovascular dysfunction results from one or more of five principal mechanisms:
• Failure of pump• Obstruction to flow• Regurgitant flow• Disorders of cardiac conduction• Disruption of the continuity of the circulatory system
• Failure of the pump;– cardiac muscle contracts weakly or inadequately, and the
chambers cannot empty properly– In some conditions, however, the muscle cannot relax sufficiently
to permit ventricular filling
• Obstruction to flow;– owing to a lesion preventing valve opening or otherwise causing
increased ventricular chamber pressure (e.g., aortic valvular stenosis, systemic hypertension, or aortic coarctation).
– The increased pressure overworks the chamber that pumps against the obstruction.
• Regurgitant flow;– causes some of the output from each contraction to flow backward, – adding a volume workload to each of the chambers, which must
pump the extra blood – (e.g., left ventricle in aortic regurgitation; left atrium and left
ventricle in mitral regurgitation).
• Disorders of cardiac conduction; – Heart block or arrhythmias owing to uncoordinated generation of
impulses – (e.g., atrial or ventricular fibrillation) – lead to nonuniform and inefficient contractions of the muscular
walls.
• Disruption of the continuity of the circulatory system; – permits blood to escape – (e.g., gunshot wound through the thoracic aorta).
• The major categories of cardiac diseases– congenital heart abnormalities, – ischemic heart disease, – heart disease caused by systemic hypertension, – heart disease caused by pulmonary diseases
(corpulmonale)– diseases of the cardiac valves, – primary myocardial diseases
• Manifestations of Cardiac Diseases;– Pain
• Ischemic Pain• Pericardial Pain
– Cardiac Enlargement• Hypertrophy • Dilatation
– Abnormal Cardiac Rhythm • Arrhythmia• Dysrhythmia
• Ischemic Pain;– The most common cause of cardiac pain is myocardial ischemia– caused by stimulation of nerve endings by the lactic acid
produced during anaerobic glycolysis – classically is retrosternal – usually described as constricting in nature– may radiate to the back, to either arm (especially the left), or up
the neck into the jaw. Pain varies in severity from mild to excruciating
– Angina pectoris;• ischemic pain • induced by exercise sometimes by stress or cold• relieved by rest.
• Pericardial Pain;– Inflammation of the parietal pericardium– sharp lower retrosternal pain – vary with posture and respiration. It is often – accompanied by signs of pericardial inflammation
• pericardial rub and effusion.
• Cardiac Enlargement;– Dilation of the cardiac chambers
• heart failure, myocarditis
– hypertrophy of the walls • hypertension, many valvular defects
• Cardiac dilation and hypertrophy do not cause clinical symptoms– useful indications of the presence of cardiac disease– recognized by clinical examination, radiography, or
electrocardiography• Documentation of cardiac hypertrophy at autopsy is
usually done by measuring the thickness of the walls– Right ventricle thickness exceeding 0.5 cm - RVH– left ventricular thickness exceeding 1.5 cm - LVH
• Abnormal Cardiac Rhythm; – Arrhythmia; Dysrhythmia
• Normal cardiac contraction;– Sinoatrial (SA) – initiate the impulse in right atrium– Atrioventricular (AV) node – conduct impulse from
atria to ventricles– His-Purkinje system - Spread impulse in the ventricular
mass• Ventricular contractions are coordinated by the
branches of the AV node. – Arrhythmias reflect;
• (1) altered activity of the SA node, • (2) the development of "new" ectopic foci that drive the
heart at an accelerated or irregular rate, • (3) conduction defects
• Methods of Evaluating Cardiac Structure & Function; – Physical Examination
• Arterial Pulse• Jugular Venous Pulse• Cardiac Apex Beat• Auscultation of the Heart
– Electrocardiography– Imaging studies– Cardiac Catheterization– Endomyocardial Biopsy
• Arterial Pulse;– Palpation of the carotid and radial artery
pulses permits recognition of;• rate and rhythm of ventricular contraction • subtle changes in the pressure wave associated
with certain cardiac diseases;– sustained low-volume pulse in aortic valve stenosis – bounding pulse in aortic valve incompetence
• Jugular Venous Pulse;– The height of the internal jugular vein pulse wave – clinical estimate of central venous pressure– increased in right heart failure, volume overload,
and pericardial tamponade or constriction– Alteration of the wave form of the jugular venous
pulse also provides important information• accentuation of the first, or a wave indicates that the
pressure in the right side of the heart is increased• absence of the a wave is a sign of atrial fibrillation
• Cardiac Apex Beat;– Localization of the cardiac apex beat by palpation
• rough evaluation of cardiac enlargement
– A sustained heave at the apex is characteristic of left ventricular hypertrophy;
– a heave at the left parasternal border occurs with right ventricular hypertrophy
• Auscultation of the Heart– Normal heart usually has two sounds;
• first due to closure of the atrioventricular valves• second due to closure of the semilunar valves (
– usually perceived as slightly split because of asynchronous closure of pulmonary and aortic valves
– Various additional sounds may signify disease• third heart sound (triple, or gallop, rhythm) may occur as a result of rapid
ventricular filling in diastole and is seen in heart failure and mitral incompetence.
• An opening snap suggests;• mitral stenosis; a fourth heart sound, pulmonary or systemic hypertension;
and a friction rub, pericarditis.
– Cardiac murmurs;• turbulence of blood flow through the heart, • usually across damaged valves and abnormal pressure gradients• Soft, innocent ejection systolic murmurs occur in high-output states
– fever or anemia and during vigorous exercise
• Murmurs signifying congenital and valvular heart disease
• Electrocardiography– Graphic display of the electrical activity of the heart as recorded
on the body surface by appropriately placed electrodes. – Normal electrocardiographic tracing can be divided into;
• (1) the P wave, due to atrial depolarization; • (2) the PR interval, which is a rough measure of conduction time
through the atrioventricular node; • (3) the QRS complex, due to ventricular depolarization; and • (4) the T wave, due to ventricular repolarization. The ST segment is
isoelectric (ie, level with the baseline) in the normal physiologic state.
– The ECG provides valuable information for assessment of • (1) cardiac hypertrophy, • (2) arrhythmias and conduction delays, • (3) myocardial ischemia and infarction, • (4) pericardial disease, • (5) electrolyte abnormalities (especially K+, Mg2+, Ca2+) and some drug
effects (eg, digitalis).
• Imaging studies – Echocardiography;
• (M-mode, two-dimensional, Doppler, stress, and transesophageal)
• means of evaluation of cardiac structure with sound waves reflected from the heart
– Chest radiography;• gross cardiac structure and size
– Magnetic resonance imaging (MRI), radionuclide imaging, cine-computed tomography (CT), and positron emission tomography (PET)
• newer modalities.
• Cardiac Catheterization– insertion of a catheter through;
• a vein - right heart • an artery - to the left heart
– evaluation of pressures and oxygen saturation in the various chambers
– angiography • Injection of radiopaque dye • visualization and photography of the contracting heart
and the coronary arteries.
• Endomyocardial Biopsy;– Tissue can be taken from the inner surface of the
heart with a biopsy forceps passed in a manner similar to a cardiac catheter.
– The main indications for endomyocardial biopsy are diagnosis of suspected;
• myocarditis• cardiomyopathy• organ rejection after heart transplantation
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