Pathophys. of MI and Ischemia

Question 0

Bad cellular events in ischemia?

Answer 0

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

Question 1

What’s the rationale behind a stress test?

Answer 1

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.

Question 2

Is the endocardium or the epicardium more susceptible to ischemia?

Answer 2

The endocardium is more susceptible.

Question 3

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

Answer 3

There’s more extracellular K+ in ischemia.

This makes the resting membrane potential more positive. (the slides… confused this. See Rachel’s email!)

Question 4

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

Answer 4

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

Question 5

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

Answer 5

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.

Question 6

Which is impaired first in ischemia: contraction or relaxation?

Answer 6

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

Question 7

3 outcomes of prolonged ischemia?

Answer 7

Stunning, hibernation, infarction (cell death)

Question 8

When does “hibernation” occur?

Answer 8

With slowly developing CAD that impairs resting coronary flow.

Question 10

How is “hibernation”distinct from “stunning”?

Answer 10

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

Question 11

4 kinds of angina?

Answer 11

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

Question 12

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

Answer 12

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

Question 13

3 ECG changes seen in cardiac ischemia?

Answer 13

ST depression.
T wave inversion.
Transient ST elevation.

Question 14

What does ischemia look like on echo?

Answer 14

Abnormal wall motion.

Question 15

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

Answer 15

thalium 201 or “MIBI” imaging

Question 16

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

Answer 16

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

Question 17

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

Answer 17

Matrixmetalloproteinases that degrade the fibrous cap.

Made by macrophages.

Question 18

What causes most MI?

Answer 18

Thrombus generated by plaque rupture.

Emboli and vasospasm are rare causes.

Question 19

Signs of MI on ECG?

Answer 19

ST elevation.

“Later Q waves”

Question 20

What causes the ST changes in MI?

Answer 20

In MI, current flows out of the affecting area.

Has to do with delayed depolarization and rapid repolarization.

Question 21

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

Answer 21

Troponins

..and CK to a lesser degree.

Question 22

Most common “arrhythmia” associated with MI?

Answer 22

Sinus tachycardia

Question 23

How can MI cause sinus bradycardia?

Answer 23

Lesion to vagal efferents in an inferior MI.

Question 24

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

Answer 24

Acidosis.
Reentry.
Autonomic tone.

Question 25

4 complications of LV dysfunction in MI?

Answer 25

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

Question 26

What can PO2 measurement tell you about ventricular septal defects?

Answer 26

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.)

Question 27

Consequences of ventricular wall thinning post-MI?

Answer 27

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

Question 28

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

Answer 28

ACE-inhibitors

Question 29

2 methods of reperfusion?

What is the time window for reperfusion?

Answer 29

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