Ischemic Heart Dz Flashcards
IHD pathogenesis in 90%?
reduced coronary blood flow d/t atherosclerotic narrowing
causes of decreased blood flow (4)?
- fixed atherosclerotic narrowing
- acute plaque change
- thrombosis overlying ruptured plaque
- vasospasm
how much narrowing causes stx w/ exercise? at rest?
70%. 90% at rest.
what is the most common artery affected? 2 others also affected?
first several cm of LAD. also left circumflex, entire R coronary artery.
what are things that could happen to plaques resulting in myocardial ischemia?
- rupture/fissures/ulcerations (exposes underlying thrombogenic substances)
- hemorrhage into atheroma (expands plaque and further narrows lumen)
what is the result of acute plaque change?
acute coronary syndromes: acute MI, unstable angina, sudden cardiac death
what are influences that contribute to acute plaque changes? intrinsic and extrinsic factors
intrinsic: structure and composition of plaque (foam cells/lipids, thin fibrous cap, MODERATELY STENOTIC LIPID RICH ATHEROMAS W SOFT CORE, abundant inflammation, few SMCs, and mechanical stress at jxn of fibrous cap and adjacent normal wall
extrinsic: adrenergic stimulation (upon awakening, emotional)
how does coronary thrombosis decrease blood flow?
can be partial or total. total = acute transmural MI or sudden death. incomplete (mural thrombus) causes unstable angina, acute subendocardial infarction, sudden death, or emboli
how does vasoconstriction lead to decreased blood flow?
compromises lumen size, increases mechanical forces that contribute to plaque rupture, leads to severe but TRANSIENT reduction in coronary blood flow
what are some stimulators of vasoconstriction?
adrenergic agonists, locally released platelet contents, endothelial dysfunction leading to impaired secretion of endothelial relaxing factors, mediators released from mast cells
4 basic syndromes of IHD?
angina pectoris, MI, chronic IHD, sudden cardiac death
clinical angina pectoris? grossly?
15 seconds to 15 minutes of chest pain caused by transient myocardial ischemia. no cell necrosis.
3 patterns of angina pectoris?
stable: attributed to chronic stenosing coronary AS
prinzmetal: due to coronary artery spasm, at rest
unstable: becomes more frequent, often at rest, induced by disruption of plaque with superimposed partial thrombosis (often prodrome of acute MI)
MI risk factors
increasing age and predisposition to atherosclerosis: HTN, cigarettes, DM, increased cholesterol and or lipids
pathogenesis of MI?
90%: acute plaque change resulting in thrombus and occlusion of coronary artery
10%: vasospasm, emboli or unexplained
types of MI?
transmural, subendocardial
transmural MI qualities?
- full thickness of ventricular wall
- confined to distribution of 1 vessel
- fixed coronary obstruction w superimposed acute plaque change and complete obstructive thrombosis
subendocardial MI qualities?
- necrosis limited to inner 1/3 (watershed area)
- may extend laterally beyond perfusion of 1 vessel
- fixed coronary obstruction w acute plaque change but w non-occlusive thrombus or lysis of thrombus or hypotension
how long till irreversible damage is done?
20-40 minutes (coagulative necrosis)
effect of early thrombotic therapy?
3-4 hrs. trying to reperfuse and limit size of infarct.
gross morphology of MI at under 12 hours?
not apparent. with tetrazolium stain, see pale areas 2-3 hrs post occurrence.
gross morphology of MI at 12 - 24 hrs
dark red-blue mottling (d/t stagnant blood)
gross morphology of MI at 1-14 days
early: sharply defined yellow-tan area
late: still central yellow-tan area but hyperemic peripheral zone (d/t repair)
gross morphology of MI at over 2 weeks?
gray-white scar begins to form
