Cardio Mod 5 Flashcards

1
Q

myocardial infarction

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

A

10 seconds

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2
Q

myocardial infarction-

what is the backup when blood flow initially becomes occluded?

A

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

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3
Q

myocardial infarction -

what are the cellular changes as myocardial cells become oxygen deprived

A
  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
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4
Q

two options after blood flow obstruction

A
  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)
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5
Q

what is the main cause of myocardial ischemia

A

atherosclerosis in the form of CAD

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6
Q

initially impairment from MI be only be evident when?

but as time progresses impairment happens when?

A
  1. initially under increased demand

2. as pathology impairment becomes evident at low levels of demand (at rest)

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7
Q

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

A
  1. coronary spasm (prinzmetal angina)
  2. hypotension
  3. arrhythmias
  4. decreased O2 capacity of blood (anemia, hypoxemia, altitude)
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8
Q

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

A
  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
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9
Q
  • what is stable angina?
  • what is happening?
  • how long does it last?
  • when is the onset? what relieves it?
A
  • 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
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10
Q

myocardial ischemia

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

A

coronary artery by >50%

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11
Q

s/s of stable angina

A

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

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12
Q

what is silent angina?

-when does it usually happen?

A

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

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13
Q

acute coronary syndromes - unstable angina

A

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)

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14
Q

what is an MI

A

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

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15
Q

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?
A
  • 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
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16
Q

MI pathophys at 20 minutes

A

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

17
Q

MI pathophys 3-6 hours

A
  • 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
18
Q

MI pathophys at 6-12 hours

A
  • 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
19
Q

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

A
  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
20
Q

MI pathophys at 18hrs to 3-5 days

A

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

21
Q

MI pathophys at 3-4 days

A

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

22
Q

what do fibroblasts produce

A

immature fibrous scar tissue

23
Q

MI pathophys for 2-3 months

A

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

24
Q

what is myocardial stunning

A

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

25
Q

what is hibernating myocardium

A

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

26
Q

what is ischemic preconditioning

A

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

27
Q

what is reperfusion injury

A
  • 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