1. 80% of cardiac death are due to?
    ischemic heart disease
  2. 5-10% of cardiac deaths are due to?
    • valve disease
    • HTN, cor pulmonale
    • congenital heart disease
  3. Cardiac disease occurs as a consequence of?
    • 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
  4. What is congestive heart failure?
    pathologic state in which impaired cardiac function renders the heart unable to maintain output sufficient for metabolic requirements of the body
  5. Characteristics of CHF?
    • diminished cardiac output
    • accumulation of blood in the venous system
    • both
  6. Heart failure is mostly due to ?
    • 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
  7. How does the heart respond to pressure or volume overload?
    • myocyte hypertrophy
    • it is initially adaptive but can make myocyte vulnerable to injury
  8. Heart failure due to diastolic dysfunction
    • inability of the ventricle to relax so it can not properly fill
    • occurs in massive LV hypertrophy, fibrosis, amyloid deposits, constrictive pericarditis
  9. How does the heart compensate for inadequate output in CHF
    • 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
  10. Major cause of left sided heart failure?
    • ischemic heart disease
    • hypertension
    • aortic and mitral valve disease
    • myocardial disease
  11. manifestation of left sides heart failure
    • 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)
  12. What is azotemia
    high levels of nitrogen containing compounds; urea, creatinine and various other body waste
  13. Most common cause of right sided heart failure
    left sided heart failure
  14. Cause of pure right heart failure
    • tricuspid and pulmonary valve disease
    • pulmonary vascular disease causing cor pulmonale
  15. manifestation of right heart failure
    • 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
  16. ischemic heart disease is caused by an imbalance in?
    supply vs demand
  17. Three causes of ischemia
    • 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
  18. What can exacerbate ischemia
  19. Hypoxia is secondary to
    • anemia
    • advanced lung disease
    • cyanotic congenital diseases
    • CO poisoning
    • cigarette smoking
  20. Four ischemic syndromes
    • MI
    • angina pectoris
    • chronic ischemic heart disease
    • sudden cardiac death
  21. Most important for of IHD
  22. When does MI occur
    when duration and severity of ischemia is sufficient to cause heart muscle death
  23. Angina pectoris
    • paroxysmal substernal pain
    • the duration and severity of ischemia are not sufficient to cause MI
  24. Three types of angina
    • 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
  25. Chronic ischemic heart disease
    • 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
  26. sudden cardiac death
    • 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)
  27. What triggers an arrhythmia
    • conduction system scaring
    • acute ischemic injury
    • electrical instability resulting from an electrolyte imbalance or an ischemic focus
  28. Two types of MI
    • transmural
    • Subendocardial
  29. Tansmural MI
    • involves the full thickness of the cardiac muscle
    • caused by severe coronary atherosclerosis with acute plaque rupture and superimposed thombotic occlusion
  30. subendocardial infarct
    • 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
  31. Consequence of one or more disrupted plaques
    transmural infarct
  32. How can a coronary occlusion not result in an MI
    collateral circulation
  33. What is the initial event in transmural MI
    erosion, ulceration, fissuring, rupture, or hemorrhage expansion of an atherosclerotic plaque
  34. Vulnerable plaques
    • ready to rupture
    • plaques involved in coronary events have a large lipid pool, thin fibrous cap, macrophage rich inflammation
  35. What may increase the risk of plaque rupture?
    • changes in blood pressure and platelet reactivity, both occur in the morning when awakening
    • exercise and smoking, both release catecholomines
  36. Hypercoagulabilty
    • protein c or s deficiency, factor V laiden
    • increase risk of cardiovascular event
  37. Time between complete myocardial ischemia and irreversible damage
    20-40 minutes
  38. Cardiac stunning?
    repercussion to ischemic tissue may restore viability but leave cell inn functional for 1-2 days
  39. What tissues do transmural MIs affect
    • mostly left ventricle
    • 15% left and right ventricle
    • 1-3% isolated right ventricle
  40. Causes of subendocardial infarcts
    • 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
  41. Electron microscopy of an MI
    • reversible; glycogen depletion, mitochodrial swelling, relaxation of myofibrils
    • irreversible; sarcolemmal disruption, mitochondrial amorphous densities (solid)
  42. Histochemistry of MI tissue
    • TTC staining defect
    • TTC is a substrate for lactate dehydrogenase. non viable areas are pale, viable are red brown
  43. Gross changes after an MI
    • 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
  44. Microscopic change with MI
    • 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
  45. Diagnosis of MI is based on?
    • symptoms; chest pain, nausea, diaphoresis, dyspnea
    • ECG changes;
    • elevation in serum cardio-myocyte specific proteins; MB-CK, troponins
  46. Complication of an MI
    • 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
  47. Diagnosis of HHD
    • history of of hypertension
    • LV hypertrophy
    • absence of other lesion that induce cardiac hypertrophy; aortic stenosis or coarctation
  48. Pathogenesis of HHD
    • 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
  49. Morphology of HHD
    • thick LV wall, >2cm
    • heart weigh >500gm
    • enlarged myocyte
    • chronically fibrosis and focal atrophy leading to degeneration with LV dilation and thinning
  50. Clinical features of HHD
    • CHF
    • hypertrophy
    • renal disease
    • stroke
  51. Pulmonary heart disease, cor pulminale
    • 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
  52. Acute cor pulminale
    right ventricle dilation following PE
  53. Chronic cor pulminale
    chronic right ventricle pressure overload
  54. morphology of cor pulmonale
    • RV hypertrophy >1cm
    • RV dilation
    • tricuspid regurg
    • pulmonary arterial wall thickening and atherosclerosis
  55. clinical features of cor pulmonale
    cardiac symptoms are usually masked by the obstructive lung disease
Card Set
heart disease