Path_12.txt

ischemic heart disease

• valve disease
• HTN, cor pulmonale
• congenital heart disease

• disruption of circulation; rupture of a vessel
• abnormal cardiac conduction; heart block, v fib
• blood flow obstruction; coronary atheroslerosis, thrombosis, aortic valve stenosis
• regurgitant flow causing output from contraction to be directed backward; causes volume overload and diminishes forward flow
• shunts bypassing the lungs and causing volume overload
• failure of myocardium; congestive heart failure

pathologic state in which impaired cardiac function renders the heart unable to maintain output sufficient for metabolic requirements of the body

• diminished cardiac output
• accumulation of blood in the venous system
• both

• progressive deterioration of myocardial contractile function
• usually due to ischemic disease, pressure or volume overload, dilated cardiomyopathy
• the damaged muscle contracts weakly and the chamber does not empty properly

• myocyte hypertrophy
• it is initially adaptive but can make myocyte vulnerable to injury

• inability of the ventricle to relax so it can not properly fill
• occurs in massive LV hypertrophy, fibrosis, amyloid deposits, constrictive pericarditis

• ventricular dilation; improves contraction my myofiber stretching, frank starling law.
• blood volume expansion
• tachycardia
• these changes all impose there own burden on the heart. They combine with the original cardiac disease and cause dilation in excess of optimal tension generating point and cause progressive CHF

• ischemic heart disease
• hypertension
• aortic and mitral valve disease
• myocardial disease

• pulmonary congestion and edema due to impaired pulmonary outflow
• reduced renal perfusion due to diminished cardiac output; causes salt retention to expand volume, ischemic acute tubular necrosis (ATN), impaired waste excretion causing prerenal azotemia
• reduced central nervous system perfusion; often causes hypoxic encephalopathy ( coma to irritability)

high levels of nitrogen containing compounds; urea, creatinine and various other body waste

left sided heart failure

• tricuspid and pulmonary valve disease
• pulmonary vascular disease causing cor pulmonale

• portal, systemic, and peripheral congestion and edema with effusions
• hepatomegly with centrilobular congestion and atrophy of central hepatocytes. Produces a nutmeg appearance
• centrilobular necrosis with sever hypoxia, can create cardiac sclerosis
• congestive splenomegaly with sinusoidal dilation, focal hemorrhage, hemosiderin deposits and fibrosis

supply vs demand

• reduced coronary blood flow due to a combination of coronary athersclerosis, vasospasm, and shock (systemic hypotension)
• Increased myocardial demand; hypertrophy and tachycardia
• hypoxia due to diminished oxygen transport; less severe since the flow of nutrients other then oxygen os not affected

hypoxia

• anemia
• advanced lung disease
• cyanotic congenital diseases
• CO poisoning
• cigarette smoking

• MI
• angina pectoris
• chronic ischemic heart disease
• sudden cardiac death

MI

when duration and severity of ischemia is sufficient to cause heart muscle death

• paroxysmal substernal pain
• the duration and severity of ischemia are not sufficient to cause MI

• stable; symptoms occur with exertion and go away with rest. 75% or greater stable stenosis of coronary arteries
• Prinzmetal; due to vasospasms. Usually without atheroslerosis
• Unstable; due to atherosclerotic plaque disruption. Not related to exertion

• seen in elderly people with moderate multivessel coronary atherosclerosis
• usually develop CHF, may result from postinfarct cardiac decompensation or slow ischemic myocyte degeneration
• cells usually have lipofusion

• death within 1 hour of the onset of symptoms
• predominant cause is IHD
• most victims have atherosclerosis with acute plaque disruption
• fatal arrhythmia is the most common etiology ( asytole, V Fib)

• conduction system scaring
• acute ischemic injury
• electrical instability resulting from an electrolyte imbalance or an ischemic focus

• transmural
• Subendocardial

• involves the full thickness of the cardiac muscle
• caused by severe coronary atherosclerosis with acute plaque rupture and superimposed thombotic occlusion

• limited to the inner third of the ventricle
• caused by increased cardiac demand in the setting of limited blood supply due to fixed atherosclerosis
• can occur in an evolving transmural infarct when the obstruction is relieved in enough time to prevent transmural infarction

transmural infarct

collateral circulation

erosion, ulceration, fissuring, rupture, or hemorrhage expansion of an atherosclerotic plaque

• ready to rupture
• plaques involved in coronary events have a large lipid pool, thin fibrous cap, macrophage rich inflammation

• changes in blood pressure and platelet reactivity, both occur in the morning when awakening
• exercise and smoking, both release catecholomines

• protein c or s deficiency, factor V laiden
• increase risk of cardiovascular event

20-40 minutes

repercussion to ischemic tissue may restore viability but leave cell inn functional for 1-2 days

• mostly left ventricle
• 15% left and right ventricle
• 1-3% isolated right ventricle

• diffuse coronary atherosclerosis and borderline perfusion made transiently critical by increased myocardial demand, vasospasm, or hypotension but without superimposed thrombus
• plaque disruption with overlaying thrombus that spontaneously lyses, this limits the extent myocardial injury

• reversible; glycogen depletion, mitochodrial swelling, relaxation of myofibrils
• irreversible; sarcolemmal disruption, mitochondrial amorphous densities (solid)

• TTC staining defect
• TTC is a substrate for lactate dehydrogenase. non viable areas are pale, viable are red brown

• before 6-12 hours they are inapparent, 3-6 hour changes can be highlighted by TTC staining techniques
• 18-24 hours pale cyanotic areas
• first week; lesions become more defined, yellow and softened
• 7-10 days; hyperemic (increase in the amount of blood flow) granulation tissue appears at the edge of the infarct and grown in with time
• 6 weeks; white fiberous scar

• 1 hour; intracellular edema, and myocytes at the edge of the infarct become wavy and buckled, stretching of non contractile tissue
• 12-72 hours; dead myocytes become hypereosinophilic with loss of nuclei. Neutrophils invade necrotic tissue
• 3-7 days; dead myocytes are digested by macrophages
• 7-10 days; granulation tissue replaces necrotic tissue generating a dense fibrous scar

• symptoms; chest pain, nausea, diaphoresis, dyspnea
• ECG changes;
• elevation in serum cardio-myocyte specific proteins; MB-CK, troponins

• depend on size and location of injury.
• death in first year post MI IS 30% 5-10% EVERY YEAR THEREAFTER
• arrhythmias
• CHF
• shock; 40% LV infarct
• ventricular rupture; within 10 days. In free wall causes tamponade, in septum causes left to right shunt
• rare papillary muscle rupture; cause severe mitral regurge
• fibrous paricarditis 2-3 post infarct but not usually clinically significant
• thrombus from non contractile area with risk of embolism
• stretch of infarcted area leading to aneurysm
• repedative extenuation of infarct

• history of of hypertension
• LV hypertrophy
• absence of other lesion that induce cardiac hypertrophy; aortic stenosis or coarctation

• hypertrophic enlargement occurs in response to increased work
• thickened myocytes reduce compliance, impairing diastolic filling while increasing oxygen demand
• hypertrophy increases the distance oxygen must travel to myocyte
• atherosclerosis can add to ischemia

• thick LV wall, >2cm
• heart weigh >500gm
• enlarged myocyte
• chronically fibrosis and focal atrophy leading to degeneration with LV dilation and thinning

• CHF
• hypertrophy
• renal disease
• stroke

• pulmonary hypertension causes right ventricular hypertrophy or dilation
• hypoxia and acidosis, pneumonia or PE, cause vasoconstriction in the lung vasculature that exacerbates any baseline hypertension

right ventricle dilation following PE

chronic right ventricle pressure overload

• RV hypertrophy >1cm
• RV dilation
• tricuspid regurg
• pulmonary arterial wall thickening and atherosclerosis

cardiac symptoms are usually masked by the obstructive lung disease