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Flashcards in Myocardial Ischemia Deck (14):

1. Increasing levels of adenosine occurs in ischemia is indicative of what process?

aerobic metabolism slows with ischemia and ATP is degraded successively to ATP, AMP and then adenosine, loss of ATP also leads to increased creatine phosphate and slowing Na/K ATPase.


1. How does Katp channel act in cellular protection from ischemia?

low ATP concentration can trigger Katp channel to shuttle K+ out of the cell causing hyperpolarization of the membrane

hyper polarization causes cell to loose contractile force but does result in self-preservation by inactivating many other channels


3. Describe the progression of damage in the electrical and pump actions of the heart due to ischemia.

because there is ion channel dysfunction there is further dysfunction of sinus or AV notes leading to changes in conduction velocity (arrhythmias)

ion channel dysfunction also leads to (1) impaired relaxation and (2) impaired contraction


2. How does reperfusion cause cellular injury?

increased O2 leads to radicals which reduce NO

abrupt rise in intracellular Ca+++ from damage to sarcolemmal membrane and SR due oxidative stress

rapid return to normal pH facilitates hypercontracture (Kapt channels close, removing local protection)


4. How is myocardial tissue "stunned" and what does this mean for the tissue?

prolonged ischemia (20min) with restored blood flow can cause alterations in troponin response to Caa++ and reduce cellular function

cells can repair damage over the course of 7-14 and can restore their functionality


What is the cause of "no reflow"?

microvascular injury means the structural components of the vessel have been damaged to such an extent that they can no longer perfuse the tissue


Why might arrhythmia after reperfussion be a good thing regarding the myocardial tissue?

repercussion can causes electrolyte imbalance after a thrombolytic agent busts a clot, it is usually a signal that the blood flow has been restored to the tissue


What is the effect of stuttering angina to protect the heart in MI?

short periods of ischemia may help to condition the heart before a major MI and limit the damage due to ischemia


4. What is cardiac hibernation?

chronic partial occlusion can result in "hibernation" that reduce myocyte function but keep cells alive, this is different from stunning because is longer but is caused by ischemia not infarction

characteristically, it is muscle that would work better if it had better blood flow (still viable) and its function will increase if blood flow improves


4. Contrast stunning and hibernation.

stunning is transient total occlusion
hibernation is constant partial flow


4. List 4 factors that can lead to no re-flow.

vascular occlusion due to debris
vascular constriction in response to debris
destruction of ischemic tissues
tissue edema


5. Name 4 ways to test for ischemia while at rest.

measure electrical impact with ECG (ST seg)
observe wall function with Echo
evaluate perfusion with nuclear imaging
evaluate anatomical structures with CT or angiogram


5. Name 3 ways to test for ischemia caused by stress.

induce stress by (and measure response):
exercise (ECG +/- echo or nuclear)
vasodilator (nuclear medicine)
beta agonist (echo)


5. Discuss 4 key changes of the heart that can be used in diagnosis of MI.

electrical changes (EKG)
anatomic changes in wall (Echo, MRI)
functional changes (Echo/ventriculogram)
perfusion changes (nuclear imaging)