Pathophys. of MI and Ischemia Flashcards Preview

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Flashcards in Pathophys. of MI and Ischemia Deck (29):
0

What's the rationale behind a stress test?

Resting coronary blood flow doesn't deteriorate until a lesion hits about 80% occlusion of the vessel.
But maximum coronary blood slow deteriorates sooner, which can only be assessed by increasing the metabolic demands of the heart.

1

Bad cellular events in ischemia?

Toxic TG buildup...
Lactic acid...
ATP depletion - ion pumps stop working.

2

Is the endocardium or the epicardium more susceptible to ischemia?

The endocardium is more susceptible.

3

How does extracellular K+ change in ischemia? What does this do to resting membrane potentials?

There's more extracellular K+ in ischemia.
This makes the resting membrane potential more positive. (the slides... confused this. See Rachel's email!)

4

3 electrophysiologic consequences of ischemia at the individual myocyte level?
What effect does ischemia have on conduction velocity?

Increased membrane potential.
Slower phase 4 upstroke.
Reduced AP amplitude and duration.
Conduction velocity will be reduced.

5

Why is there ST segment depression in (non-transmural) ischemia?

So the ischemic area is in subendothelium, and has a higher membrane potential, meaning less + charge outside. Current will flow from normal areas to the ischemic areas... which produces ST depression in some leads.

6

Which is impaired first in ischemia: contraction or relaxation?

Relaxation- it's a more active, energy-dependent process with all those pumps.
Causes decreased compliance -> increased LVEDP, decreased EDV

7

3 outcomes of prolonged ischemia?

Stunning, hibernation, infarction (cell death)

8

When does "hibernation" occur?

With slowly developing CAD that impairs resting coronary flow.

10

How is "hibernation"distinct from "stunning"?

Hibernation is reduced contractility due to chronic reduced coronary flow.
Stunning is the slow return of function after an acute ischemic event.

11

4 kinds of angina?

Stable
Unstable
Variant (aka vasospasm or Printzmetal's)
Silent

12

What "silent" angina? What kinds of conditions is it typically associated with?

Ischemic pain isn't felt because afferents from the heart are severed/damaged.
This happens in diabetic with neuropathy, and in transplanted hearts.

13

3 ECG changes seen in cardiac ischemia?

ST depression.
T wave inversion.
Transient ST elevation.

14

What does ischemia look like on echo?

Abnormal wall motion.

15

What non-invasive imaging study can assess perfusion in a stress test?

thalium 201 or "MIBI" imaging

16

2 goals of medical treatment of cardiac ischemia (aka angina)?

Reduce metabolic demands/increase perfusion of heart. (nitrates, beta blockers, Ca++ channel blockers)
Prevent/lyse clots (anticoagulants, anti-platelet agents)

17

What enzymes are largely responsible for plaque ruptures? Which cells make them?

Matrixmetalloproteinases that degrade the fibrous cap.
Made by macrophages.

18

What causes most MI?

Thrombus generated by plaque rupture.
Emboli and vasospasm are rare causes.

19

Signs of MI on ECG?

ST elevation.
"Later Q waves"

20

What causes the ST changes in MI?

In MI, current flows out of the affecting area.
Has to do with delayed depolarization and rapid repolarization.

21

Which cardiac enzymes would be most useful for assessing if someone had an MI in the past few days?

Troponins
..and CK to a lesser degree.

22

Most common "arrhythmia" associated with MI?

Sinus tachycardia

23

How can MI cause sinus bradycardia?

Lesion to vagal *efferents* in an inferior MI.

24

3 processes that can lead to increased risk of ventricular arrhythmia in MI?

Acidosis.
Reentry.
Autonomic tone.

25

4 complications of LV dysfunction in MI?

Diastolic failure -> pulm. edema.
Systolic failure -> cardiogenic shock.
Pericarditis.
Mechanical ruptures (septum, free wall, papillary muscle).

26

What can PO2 measurement tell you about ventricular septal defects?

An abnormally high (or abnormally normal, if the pt seems shocky) PA PO2 suggests oxygenated blood is flowing from the LV back to the right heart / lungs.
(you might also see this in distributive shock, though.)

27

Consequences of ventricular wall thinning post-MI?

Can become very thin and prone to aneurysm. Remainder of ventricle may hypertrophy.

28

What med can you give to make post-MI remodeling occur in a more favorable manner?

ACE-inhibitors

29

2 methods of reperfusion?
What is the time window for reperfusion?

Thrombolytics.
PCI (percutaneous intervention)
< 6hrs from start of symptoms is best, can be done up to 12hrs later.