Introduction to Cardiac Pathology Flashcards
Describe cardiac muscle
branching, striated fibers; organized into parallel units (sarcomeres); sarcolemma arranged to deliver calcium for rapid conduction; intercalated discs; central nuclei; main fuel is fatty acids
Where do coronary arteries run
run in connective tissue on surface of heart, supply blood from outer to inner layers of myocardium; originate in coronary ostia behind aortic valve
Most of the coronary blood flow occurs during
diastole
LAD supplies
apex of heart, anterior left ventricle, anterior two thirds of ventricular septum
Right coronary artery supplies
entire right ventricular free wall, posterior third of ventricular septum; posterior left ventricle
Left circumflex supplies
lateral left ventricular wall; in 1/5 people, also supplies posterior aspect of left ventricle
Results in damage to the left ventricular wall and ventricular septum
occlusions to either the right or left coronary arteries
Part of the endocardium at greatest risk of ischemia
subendocardial region
Describe the heart’s conduction system
specialized myofibers; myocytes have a certain automaticity; without impulse conduction, will either fire aberrantly or contract in an unorganized fashion
SA node
located at the junction of the SVC and right atrium; serves as the pacemaker
AV node
near the atrium-ventricular junction; organizes and fires impulse into the bundle of his
Bundle of His
runs thru ventricular septum to insure coordinated contraction of both ventricles, movement of contraction in a wave of depolarization to maximize pumping action
Pericardial sac
potential space, usually holds 50-60 ml of serous fluid
Pericardial sac is lined by
lined on both sides with mesothelial layers of the serous pericardium
Visceral layer/epicardium
reflection of the pericardium which covers the surface
heart and serous pericardium are encased in what
several layers of the fibrous pericardium
Chamber function
left/right synchronous; dependent on directional wave of depolarizaton; sequential upper chamber to lower chamber contraction to help in directional flow
Valvular function
essentially one-directional flow valves to prevent backflow; essential for maintaining stroke volume and attaining chamber pressure; passive action
Primary causes of cardiovascular dysfunction
hypovolemia; arrhythmia; pressure overload; volume overload; cardiac muscle failure
pressure overload caused by
hypertension, valvular stenosis
volume overload caused by
fluid overload, valvular insufficiency
Cardiac muscle failure caused by
ischemia, metabolic, cardiomyopathy
myocardium response to increased work demands
pressure overload -> concentric hypertrophy
volume overload -> eccentric hypertrophy
Microscopic changes in hypertrophied myocytes
cellular and nuclear enlargement; increased myocyte size and myofibril content; some disorganization of sarcomeres; expression of fetal proteins
Hypertrophy leads to
enlargement/dilation and eventual heart failure; increased myocardial demands for oxygen
Mechanisms involved in cardiac decompensation
Starling law; inadequate oxygenation; fibrosis; loss of myocytes; abnormal calcium homeostasis; adrenergic densesitization; amyloidosis
Symptoms and signs of left sided heart failure
cardiac enlargement; left atrium enlargement; pulmonary congestion; hypoxic encephalopathy; coronary insufficiency and cardiac ischemia
Symptoms and signs of right sided heart failure
engorgement of systemic and portal vasculature; hypoxia; liver congestion; kidney congestion; splenic congestion; dependent peripheral edema
Nutmeg liver
right sided heart failure; chronic passive congestion; centrilobular necrosis leading to cardiac sclerosis;local hemorrhage; phagocytosis of red cells
Etiology of global heart failure
long-standing right or left-sided failure; constrictive disease; massive infarct; shock
Signs and symptoms of global heart failure
degree of symptomology depends on the rapidity of development of cardiac failure
Causes of Cor pulmonale
pulmonary hypertension secondary to primary disease of the lungs or pulmonary vasculature; acute: pulmonary embolism; chronic: COPD, compression/obliteration of pulmonary arteries; fibrosis of lungs
Criteria for hypertensive heart disease
- left ventricular hypertrophy (usually concentric) in the absence of other cardiac pathology
- history of hypertension
Microscopic features of myocyte hypertrophy
increased myocyte size with prominent and sometimes reduplicated nuclei; decreased capillary density; increased deposition of ECM
Microscopic features of myocardial atrophy/apoptosis
decreased cell numbers; increased fibrosis
Microscopic features of cardiac necrosis/inflammation
coagulative necrosis with evolving inflammatory infiltrate; eventual replacement by fibrosis and scar
Microscopic features of reperfusion injury
contraction bands
Microscopic features of cardiac aging
fewer myocytes; increased collagen; amyloid; basophilic degeneration; brown atrophy (lipofuschin)
Microscopic features of acute of chronic inflammatory response to infection of the heart
depends on the nature of the infectious agent; variable infiltration of inflammatory cells and myocyte damage
