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Flashcards in Cardio Mod 5 Deck (27):

myocardial infarction
-myocardial cells become ischemic within how many seconds of blood flow occlusion

10 seconds


myocardial infarction-
what is the backup when blood flow initially becomes occluded?

attempt to rely on myoglobin O2 stores for first 6-10seconds


myocardial infarction -
what are the cellular changes as myocardial cells become oxygen deprived

1. loss of contractility followed by drop in cardiac output
2. conduction abnormalities (EKG changes) leading to dysrhythmias
3. anaerobic metabolism is only mechanism to provide energy with lactic acid accumulation


two options after blood flow obstruction

1. blood flow restored - return to aerobic metabolism, contractility returns followed by cellular repair
2. flow is not restored - then myocardial infarction occurs (damage and potential tissue necrosis)


what is the main cause of myocardial ischemia

atherosclerosis in the form of CAD


initially impairment from MI be only be evident when?
but as time progresses impairment happens when?

1. initially under increased demand
2. as pathology impairment becomes evident at low levels of demand (at rest)


other causes of myocardial ischemia - decreased delivery of blood to myocardium

1. coronary spasm (prinzmetal angina)
2. hypotension
3. arrhythmias
4. decreased O2 capacity of blood (anemia, hypoxemia, altitude)


other causes of myocardial ischemia - increased demand for O2 by mycardium

1. tachycardia and exercise - both more work for the heart
2. HTN ( more work to overcome increased afterload)
3. cardiac hypertrophy (bigger muscle demands more O2)
4. valve dysfunction/disease


-what is stable angina?
-what is happening?
-how long does it last?
-when is the onset? what relieves it?

-transient episode of blood flow impairment in relation to O2 demand of the cardiac muscle
-usually happens with gradual narrowing of the lumen and stable plaque development
-lasts 3-5 min
-onset usually some form of exercise/exertion or stress, relieved with rest


myocardial ischemia
-narrowing of what artery by what percentage will result in impairment of cellular metabolism

coronary artery by >50%


s/s of stable angina

angina pectoris - substernal chest discomfort (heaviness - pressure -pain: all three)


what is silent angina?
-when does it usually happen?

myocardial ischemia that dose not cause obvious s/s
common following conditions/surgical procedures that may impair innervation - ex. heart transplant, CABG, emotional stress, diabetes


acute coronary syndromes - unstable angina

thrombus breaks up before cell death - allows return of blood flow
"reversible MI with no cell damage

**increases likelihood of MI within relative near future (20% of patients with unstable angina will ahve MI or death from MI within 20 days)


what is an MI

thrombus occludes blood flow for prolonged period and causes irreversible cardiac nercrosis


initial pathophys of MI from immediate to 10-20 minutes
-immediate effects?
-accumulation of what due to anaerobic metabolism
-EKG effects
-sympathetic response?
-angiotensin 2 effect?
-metabolic response?

-immediate loss of contractility and dysrhythmia
-lactic acid accumulation - after 6-10 seconds of anaerobic metabolism (mechanism for survival)
-EKG changes within 30-60 seconds (electrolyte changes and lactic acid accumulation alter conduction - dysrhythmia)
-sympathetic - increased catecholamine release (clinical beta blockers)
-angiotensin 2 release - increases BP/cardio exertion,sympathetic response - also increases collagen/scar formation (clinical - ACE inhibitors or angiotensin receptor antagonists
-above processes lead to increase metabolic response = increases glucose & FFA into circulation - 72hr post hyperglycemia


MI pathophys at 20 minutes

process of necrosis begins at 20 minutes
necrosis usually begins in sub-endothelium
cellular/histological changes aren't grossly visible until 6 hours


MI pathophys 3-6 hours

-necrosis expands outward toward epicardium
-gradual expansion through thickness of ventricular wall
-transmural infarct = infarct effects complete thickness of ventricular wall - basis for STEMI classification


MI pathophys at 6-12 hours

-degree of cell damage becomes increasingly irreversible over 12 hours
-window of opportunity to minimize damage - thrombolysis/reperfusion
-coagulation necrosis occurring - cell swells/protein breakdown
-biomarkers begin to be released into bloodstream


what biomarkers are released by the heart in an MI from 6-12 hours after

1. myoglobin - very early marker, rise in 2 hours
2. troponin (T and I) - marker of choice, may begin to rise in 3 hours, peak at 18-48 hrs depending on MI size **best predictor stats of all markers
3. CK-MB - used to be marker of choice prior to troponins, may rise in 3 hours peak 18-24 hrs


MI pathophys at 18hrs to 3-5 days

inflammatory cascades bring leukocytes/proteolytic enzymes accumulate to remove damaged/necrotic cells


MI pathophys at 3-4 days

soft scar formation begins
granulation appears - microphages and fibroblasts accumulate
soft scar formation is potential risk of fatal rupture during first 1-2 weeks - 10% of MI mortality


what do fibroblasts produce

immature fibrous scar tissue


MI pathophys for 2-3 months

mature scar formation
thin, noncontractile area of ventricular wall (very strong tissue)
dilation and cardiac hypertrophy may result - excess collagen formation bw myocytes in wall


what is myocardial stunning

myocardial cell unable to contract after reperfusion. contractile dysfunction occurs even though the myocardial cell has not suffered irreversible damage and coronary blood flow is normal
-transient - hours to days


what is hibernating myocardium

contractile function is reduced in a healthy myocardial cell that is experiencing ischemia but returns to normal contractile function after perfusion is restored


what is ischemic preconditioning

myocardial cell adapts to brief episodes of ischemia by increasing ischemic tolerance to infarction


what is reperfusion injury

-may occur after a hypoxic area of myocardium is re perfused
-the reintroduction of blood flow may create excess oxygen free radical production leading to a cascade of cell damage and inflammation
-reperfusion injury contributes to the final infarct size - up to 50% of total infarct size