Pathology 2-1

• Male: 300-350 g
• Female: 250-300 g

• Left: 1.3-1.5 cm
• Right: .3-.5 cm

Subendocardium b/c its the most distal myocardium, most vulnerable to ischemia and least well perfused area.

• tachycardia - increased HR
• brachycardia- decreased HR
• both decrease cardiac output over time

futter or fibrillation- extremely rapid rates, chambers don't fully fill, also decreases cardiac output

Cardiac Hypertrophy; due to increased work

• 1) elevated pressure
• -from systemic hypertension
• - or aortic valve stenosis

• 2) increased blood volume
• - valvular regurgitation
• - congenital effects from shunting blood

• 3) Exercise ( not detrimental)
• 4) slowly developing severe anemia
• 5) hyperthyroidism
• 6) post infarction
• 7) idiopathic

normal myocyte( 10-15 micronswide, 100 microns long) increase 25 or more micro

nuclei become large, hyperchromatic, rectangular "box-car" shape

Concentric Hypertrophy

increased heart weight and wall thickniss to cavity ratio

eccentric hypertrophy

• increased hypertrophy with increased dilation
• wall thickness to cavity increase proportionate

Extracellular CT increases relative to myocytes

collagen type changes and there is decreased compliance

no change in capillary growth so there is impaired diffusing capacity and increased susceptibility to ischemia

B/c there is an increase in ECM and microvessels with myocyte: its proportionate

• Underlying causes: systolic dysfunction- decrease myocardial contractility
• diastolic dysfunction- decrease ability myocardium to expand and allow adeq. filling

• common etiologies:
• 1) L. vent hypertrophy from pressure overload or volume overload
• 2) chronic ischemic heart disease
• 3) cardiomyopathies
• 4)constrictive pericarditis

big, dilated and floppy. increased weight, chamber dilation, wall thinning, myocyte hypertrophy

• 1) Lungs- increased pulmonary venous pressure leads to edema
• 2) Kidneys- decreased perfusion
• 3) Brain- cerebral hypoxia

• 1) Liver- increased weight, nutmeg liver
• 2) Kidneys
• 3) Portal system- spleen-ascites
• 4) peripheral tissues- ankle edema
• 5) pleura/pericardium
• 6) brain-hypoxia
• 7) jugular venous distention

• -Angina pectoris
• -sudden cardiac death
• -myocardial infarction
• -chronic ischemic heart disease

Paroxysmal episodic pain- radiating, transient, induced by exertion

coronary atherosclerosis, valvular dysfunction, arrhythmias that impair coronary perfusion

It is a variant of angina pectoralis, can occur at rest, increased frequency, prolonged and merging attacks

related to thrombus formation and transient ischemia. increase MI risk

It's collapse and death w/i 24 hrs, related to ischemia, arrhythmias, absence of clinical history of ischemic heart disease

It's ischemic necrosis of myocardium with prolonged chest pain that can radiate

• due to sudden occlusion coronary art flow
• mismatch in myocardial oxygen demands and coronary diffusion
• myocyte necrosis

gradual or episodic coronary insufficiency with development congestive heart failure, preceding or following MI

• chronic ischemia
• history angina/MI

Men peak 55-64, women 8th decade; the older women get the closer the ratio gets

• hemorrhage, rupture of plaque
• thrombosis
• vacospasm
• sudden increased myocardial oxygen demand
• hypotension
• tachycardia, or valve dysfunction

• 1) Transmural infarction-most common
• entire wall necrosis, acute plaque disruption with thrombosis lead to occlusion of flow, sharply defined by distrib. affected vessel

• 2) Subendocardial infarction
• necrosis inner 1/2-1/3 vent wall, not defined by single vessel, diffuse reduction coronary flow by atherosclerosis affect multiple vessels, subendocardium suffers ischemic necrosis