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Cardiology > Pathophysiology of MI and Ischemia 1 and 2 > Flashcards

Pathophysiology of MI and Ischemia 1 and 2 Flashcards

1
Q

How does ischemia differ from anoxia?

A

oxygen deprivation with no perfusion vs impalance between oxygen supply/demand due to impaired or inadequate perfusion (ischemia)

*ischemia includes hypoxia and accumulation of waste products

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2
Q

What is reactive hyperemia?

A

ability to augment coronary blood flow under conditions of increased oxygen demand via vasodilation –> maximal/resting CBF = coronary flow reserve

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3
Q

What does ischemia do to metabolite demand in the heart?

A

shift from oxphos to anaerobic metabolism leading to

  1. lactic acid buildup which inhibits glycolysis
  2. toxic TG buildup (acts like a detergent)
  3. falling ATP stores lead to irreversibly injury to sarcolemma, cell death w/sodium accumulation and calcium depletion
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4
Q

Why is the subendocardium vulnerable to the effects of ischemia?

A

intramural compressive forces increase resistance in these areas and autoregulation is more effective in epicardium than subendocardium

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5
Q

What are the electrophysiologic effects of ischemia?

A
  1. increase in extracellular K+ –> depolarization
  2. increase in intracellular Na+ –> reduced AP conduction velocity
  3. acidosis due to H+/Ca2+ exchange –> reduced action potential amplitude and duration
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6
Q

What contributes to ST segment depression during ischemia?

A

voltage gradient between normal and ischemic zones of muscle lead to current flow between these regions

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7
Q

What are the diastolic contractile effects of ischemia?

A
  1. impairs active relaxation in early diastole

2. causes regional stiffness (decreased compliance) = higher EDP and impairs filling

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8
Q

What are the systolic contractile effects of ischemia?

A

contraction decreases proportionately to decrease in flow

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9
Q

Where is there dyskinesis, hypokineses/akinesis, and hyperkinesis in ischemia?

A

dyskinesis: central zone
hypo/akinesis: adjacent areas
hyperkinesis: compensatory areas due to adrenergic stim and starling mech

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10
Q

Prolonged ischemia leads to irreversible contractile dysfunction called ____

A

infarction

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11
Q

Acute ischemia with reperfusion can cause prolonged contractile dysfunction called ____

A

stunning

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12
Q

chronic hypoperfusion causing reversible contractile dysfunction

A

hibernation

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13
Q

What causes angina?

A

ischemia leading to anaerobic byproducts that have an effect on cervicothoracic receptors

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14
Q

What kind of angina? chronic, transient, demand-related

A

stable

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15
Q

What kind of angina? increased frequency, reduced precipitants, supply-related

A

unstable

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16
Q

What kind of angina? vasospasm

A

variant or printzmetal’s –> often happens at night/not necessarily w/exertion

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17
Q

What kind of angina? diabetics, transplant

A

silent

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18
Q

Dx of angina

A

symptoms + diaphoresis/CHF +

  1. ECG: St depression, twave inversion, transient ST elevation
  2. Echo abnormalities
  3. Cath occlusion
  4. Stress testing
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19
Q

What is the ST segment?

A

period of relative inactivity between end of systole and beginning of repolarization//isoelectric

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20
Q

What accounts for ST depression in angina?

A

ischemic cells have decreased resting membrane potential w/ current flowing from normal myocardium to ischemic zone leading to ST segment depression in leads opposite to the area of the ischemia (no longer isoelectric) –> b/c its the subendocardium that is more likely to be damaged the flow is from the chest wall side of the ventricle to the inner part of the ventricle AKA away from chest lead

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21
Q

St difference in ischemia vs infarction

A

ST depression vs ST elevation

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22
Q

Pharmacologic tx of ischemia

A

goal is to restore supply/demand:

demand:

  1. nitrates to reduce LVEDP/vasodilate coronary
  2. beta blockers to reduce HR, contractility, BP
  3. calcium channel blockers to reduce preload, afterload, HR, BP, contractility

supply:

  1. anti-platelet agents (aspirin, clopidogrel)
  2. anti-coagulants (heparin, DTI, LMWH)
23
Q

Surgical tx of ischemia

A

PCI, stents, CABG

24
Q

Pathophysiology of MI

A

usually preceded by unstable angina –> plaque rupture due to macrophage derived MPs degrading fibrous cap –> release of lipids –> thrombosis, platelet activation, vasoconstriction, luminal obstruction, ischemia –> infarction

*also emboli, vasospasm

25
Q

Irreversible heart muscle necrosis from prolonged ischemia

A

infarction

26
Q

factors affecting extent of infarction

A

location of plaque, size of vascular bed, collaterals, local tissue factors, time occlusion/reperfusion

27
Q

Dx of MI

A

chest pain, diaphoresis, tachycardia, dyspnea +

  1. ST segment elevation, late Q waves
  2. serum enzyme elevatin
  3. akinesis on echo, cath
28
Q

Why is there ST segment elevation in infarction?

A

current basically escapes from the infarct out of the heart b/c of transmural cell death causing rapid repolarization and delayed depolarization so there is flow towards the chest leads

29
Q

What is the role of enzyme tests in dx of MI?

A

cells release enzymes (like troponin, CK-MB, myoglobin) over 6-24 hours and these can be measured in the bloodstream –> indication of cellular damage

30
Q

What kind of arrhythmia is most common complication of MI?

A

sinus tachycardia

31
Q

What kind of arrhythmia is most common complication of inferior MI?

A

sinus bradycardia (vagal efferents in inferior wall)

32
Q

What is the consequence of acute diastolic dysfunction due to LV dysfunction post-MI?

A

pulmonary edema

33
Q

What is the consequence of acute systolic dysfunction due to LV dysfunction post-MI?

A

systemic hypoperfusion –> extensive myonecrosis can cause shock//highest mortality with extensive damage w/combined pulmonary congestion and hypoperfusion

34
Q

Which ventricular complications can occur 3-6 days after an MI?

A

ventricular free wall rupture, septal rupture, papillary muscle rupture

35
Q

How can we identify a VSD due to wall rupture post MI?

A

oxygen in PA increases (RV has more oxygenated blood)

presents as cardiogenic shock, chest pain, bp drop

36
Q

How can we identify a free wall rupture post MI?

A

equal pressures, effusion

37
Q

How can we identify a papillary muscle rupture post MI?

A

v wave, flail leaflet

38
Q

How do aneurysms form post-MI?

A

dead cells bulge out b/c of contractile forces from rest of healthy heart –> can rupture and be walled off (pseudoaneurysm)

39
Q

Which drugs favorably alter remodeling of LV after MI?

A

ACE inhibitors

40
Q

Tx of MI

A
  1. thrombolysis
  2. PTCA- percutaneous transluminal coronary angioplasty –> better mortality b/c doesn’t cause bleeding, but takes longer and requires special teams
  3. adjuncts like aspirin, clopidogrel, heparin, beta blockers, oxygen, morphine

*can save tissue if <6h from MI

41
Q

lethal ischemia leads to what histologic finding?

A

coagulative necrosis

42
Q

T/F there is a lot of collateral circulation among coronary arteries

A

F –> but can develop in the context of occlusion

43
Q

Earliest changes in ischemic injury to myocardium

A
  1. aerobic –> anaerobic metabolism
  2. cessation of contraction
  3. altered electrical activity
  4. relaxation of myofibrils –> thin wavy stretched myocytes
44
Q

How long do we have to reverse the early changes of ischemia?

A

20-40 mins –> reperfusion

45
Q

How long does it take to have necrosis of the entire myocardium after ischemic injury?

A

6-12 hours (but it’s a continuous process with death beginning locally at 20 minutes and progressing as a wave front reaching the full thickness within 6-12 hours)

46
Q

How long does it take for myocytes to die in the context of ischemic injury to the myocardium,?

A

after 20-40 minutes, cells begin coagulative necrosis –> unless reperfused, contraction band necrosis

47
Q

What follows necrosis post ischemia to the myocardium?

A

phagocytosis by polys (max at 3 days) and then macrophages –> healing with granulation tissue –> scarring

48
Q

What leads to acute coronary syndromes?

A

plaque rupture and consequent super-imposed thrombi

*unstable angina, acute MI, sudden cardiac death

49
Q

What kind of obstruction leads to subendocardial MI? transmural MI?

A 
incomplete = subendocardial
complete = transmural
50
Q

What stain allows us to distinguish dead from living myocardium <12 hours after infarct?

A

LDH

51
Q

What causes contraction band necrosis?

A

reperfusion of lethally injured myocytes –> leaky membranes allow calcium ion influx and hypercontraction

52
Q

What causes reperfusion injury?

A

oxygen-derived free radicals kill additional myocytes and injure endothelium of microvessels –> interstitial hemorrhage = red infarct

53
Q

What is dressler’s syndrome?

A

autoimmune pericarditis post infarct due to formation of abs against cardiac proteins // pericarditis can occur w/o autoimmune etiology as well –> friction rub or pericardial effusion/tamponade

54
Q

Where does wall perforation occur?

A

where the polys are (3-5 days after MI) –> border of living/dead myocardium

Cardiology (41 decks)

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