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Cardiology > Pathophys of MI and Infarction > Flashcards

Pathophys of MI and Infarction Flashcards

1
Q

What determines myocardial O2 demand?

A
  • Wall Tension
  • HR
  • Contractility
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2
Q

What determines myocardial O2 supply?

A
  • Coronary blood flow (diastolic perfusion P, coronary vasc resistance)
  • O2 carrying cap of blood
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3
Q

What is coronary flow reserve (CFR)?

A

Coronary flow reserve=maximal coronary blood flow/resting CBF
–>ie the maximum inc in blood flow through the coronary arteries above the normal resting volume

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4
Q

What is reactive hyperemia?

A

Transient increase in blood flow that occurs during a brief period of ischemia

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5
Q

What happens to the CFR in stenosis?

A

It decreases. The vessels maintain normal resting CBF by dilating to a greater degree at rest. When an inc in demand occurs, they cannot dilate as much in response now. This lowers the max CBF and also decreases the CFR.

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6
Q

What are the biochemical effects of ischemia?

A

-Decrease in O2 means dec in ox phos so cells use glucose. (remember FA ox is the preferred mech of energy production in the heart)

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7
Q

What happens to the sarcolemma if ATP stores fall?

A

If they fall <30%, there is irrev injury to sarcolemma resulting in cell death, Na accumulation and calcium depletion

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8
Q

What layer of the heart is most vulnerable to ischemia and why?

A

Subendocardium

  • Intramural compressive forces inc resistance on these vessels
  • Autoregulation is more effective in the epicardium
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9
Q

What are the electrophysiologic effects of ischemia?

A
  • Sarcolemma integrity is disrupted
  • Na/K ATPase fails
  • extracellular K+ levels rise as do intracellular Na+ levels
  • Ca/H+ exchange leads to acidosis
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10
Q

What are the consequences of the electrophys effects of ischemia?

A

Reductions in:

  • Resting potential
  • Phase 4 upstroke
  • AP amplitude and duration
  • Conduction velocity
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11
Q

What causes ST segment depression?

A

The voltage gradient between normal and ischemic zones lead to current flow between these regions (toward the inner subendo layer) causing ST segment depression in the ECG opposite the area of ischemia

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12
Q

What are the mechanical effects if ischemia?

A

Diastolic effects:

  • Impaired active relaxation in early diastole–>regional stiffness, higher EDP, impaired vent filling
  • Very sensitive to ischemia, early measure
  • ->remember diastole is an active process where isovol relaxation req energy to re-sequester Ca2+

Systolic effects:
-Contractile forces dec proportionally to dec in O2 flow due to impaired Ca2+ fxn

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13
Q

Where on the P/V curve does diastolic ischemia shift it?

A

Up/Left (more P req for less vol, due to inc end diastolic Ps)

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14
Q

Where on the P/V curve does systolic ischemia shift it?

A

Down/Right (decreased contractility, higher vol produces lower P)

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15
Q

What is hypokineses?

A

dec capacity for contraction

–>in adjascent areas

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16
Q

What is akinesis

A

Absence of contraction

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17
Q

What is dyskinesis

A

Bulging of ischemic area that occurs as a result of dec capacity for contraction (spastic). Contraction during diastole, relaxation during systole. Increases incidence of aneurysms
–>in central zone

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18
Q

compensatory hyperkinesis

A

due to adrenergic stimulation and starling mech, everything else kicks into high gear to maintain CO

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19
Q

What is infarction?

A

Irreversible cell death

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20
Q

What is stunning?

A

Tissue is reperfused after acute ischemia before the cells die. Eventually, contractile fxn can be restored, but this can take a while. Prolonged period of contractile dysfxn that will eventually recover is labeled as stunned tissue

–>accumulation of toxins, altered ca uptake

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21
Q

Hibernation

A

Chronic hypoperfusion that leads to contractile dysfxn, but that can also be repaired by fully restoring perfusion.
-Occurs with severe CAD impairing resting coronary blood flow, non-acute

Note a heart can have elements of both hibernating and stunning

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22
Q

What is angina?

A

Chest discomfort produced by ischemia due to anaerobic byproducts effects on cervicothroacic receptors
–>chest tightness radiating to left arm, neck and jaw

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23
Q

What is stable angina?

A

Chronic transient and demand related

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24
Q

What is unstable angina?

A

Often a progression from stable. Angina occurs more often . Usually result of sudden change in atherosclerotic plaque that more severely occludes the vessel.

  • inc frequency, reduced precipitants, supply related
  • Medical emergency
25
Q

What is variant angina?

A

Arteries close due to vasosoasm, not atherosclerosis. Results in transient occlusion

26
Q

What is silent angina?

A

There is transient ischemia, but the patient is unaware. Usually due to impaired neural sensation. Increased incidence in diabetes and transplants

27
Q

ECG signs of MI

A

ST depression, T wave inversion, transient ST elevation

28
Q

What does the ST segment reflect?

A

Reflects period of relative inactivity between the end of systole and the beginning of repolarization (normally this is isoelectric)

29
Q

Why do ischemic cells change ST segment?

A

They have decreased resting membrane potential with current flowing from normal myocardium into the ischemic zone. this results in ST segment depression in the leads opposite the area of ischemia

30
Q

What type of ischemia causes ST depression?

A

Subendocardial injury

31
Q

What pharma agents are used to dec demand?

A

Nitrates, beta blockers, Ca channel blockers

32
Q

What pharma agents are used to improve supply

A

Anti-platelet agents, anticoagulants

33
Q

What kind of mechanical approaches are used to improve supply?

A
  • Percutaneous coronary intervention (PCI)
  • Stent implantation
  • CABG
34
Q

Goal of treatment of ischemia

A

focus on restoraton of supply/demand by improving flow or reducing demand

35
Q

What happens to ST segment in ischemia?

A

depression (current is going through the area of ischemia)…due to decreased resting membrane pot, current flows from the normal myocardium towards the ischemic zone

36
Q

What happens to ST segment in infarction?

A

elevation (current is going away from the area of infarction, in the opp direction as ischemia), (there is an excess of voltage flow out of the necrosed area)

37
Q

What is the most common cause of infarction?

A

plaque rupture

38
Q

MMPs role in plaque rupture

A

They are macrophage derived and degrade the fibrous cap. This releases lipids into the lumen, exposing the subendothelium and promoting thrombosis, platelet activation and vasoconstriction.

39
Q

Define MI

A

Irrev heart muscle necrosis resulting from prolonged ischemia

40
Q

ECG findings on MI

A

ST seg elevation, later Q waves

41
Q

Chemical findings in MI

A

serum enzyme elevation

42
Q

Imaging findings with MI

A

Akinesis

43
Q

In ischemia, what happens to the resting membrane potential

A

It decreases

44
Q

In ischemia, what happens to the current flow?

A

it goes into the area of ischemia or subendo infarct

45
Q

In ischemia, what happens to the ST segment?

A

depressed

46
Q

In MI, what happens to the AP?

A

Rapid repolarization, delayed depolarization

47
Q

In MI, what happens to the current flow?

A

Goes out of the infarct

48
Q

In MI, what happens to the ST segment?

A

elevated

49
Q

What is the difference between where on the heart the injury occurs in ischemia vs MI?

A

Ischemia: subendo
MI: transmural

50
Q

What is a Q wave?

A

Area of already infarcted territory, not ongoing like in ST elevation areas

51
Q

Why does MI often lead to arrhythmias ?

A

Changes in electrophys make them common. Dead tissue does not conduct normally

52
Q

Why is troponin elevated in MI?

A

It along with other cardiac enzymes are released into the blood by dead myocytes

53
Q

Most common arrhythmia associated with MIs?

A

Sinus tachycardia

54
Q

Other arrhythmias associated with MIs?

A

I-nferior: sinus bradycardia

  • conduction block
  • vent arrhythmias
55
Q

When do we treat arrhythmias?

A

If they inc O2 demand or cause hemodynamic instability (ie maintain adequate CO and BP)

56
Q

What mechanical complications can occur due to MI and when do they occur?

A
  • vent free wall rupture (anterior or inferior MI)
  • vent septum rupture (anterior MI)
  • pap m rupture (inferior MI), leads to flail leaflet
  • ->occurs 3-6 days after MI
57
Q

What are the complications of MI?

A
  • Dec compliance
  • CO dec
  • Pericarditis (immune system attempts to clear out tissue)
  • Mechanical complications
  • Aneurysms due to dyskinesis and remodeling (thinning of wall)
  • LV remodeling (use ACE inhib to alter remodeling, dec scars–>only thing used to help current issue, rest of treatments are to prevent future events)
58
Q

Treatment of MI

A

Reperfusion is the ultimate goal!

  • drugs (aspirin, heparin, beta blockers, etc)
  • PCI/stents (take more time to initiate)
  • ->best if <6 hrs after symp onset

Cardiology (16 decks)

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