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CV > Myocardial oxygen supply, demand, and ischemia > Flashcards

Myocardial oxygen supply, demand, and ischemia Flashcards

1
Q

determinants of myocardial oxygen supply

A
  • heart rate
  • contractility
  • ventricular wall stress (blood pressure, ventricular chamber radius, ventricular wall thickness)
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2
Q

relationship between blood pressure and wall stress

A

increase in blood pressure- increase in wall stress

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3
Q

relationship between radius of ventricle wall and wall stress

A

increase in radius of ventricle- increase in wall stress

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4
Q

relationship between ventricular wall thickness and wall stress

A

increased ventricular wall thickness- less wall stress (less stress on each individual myocyte)

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5
Q

determinants of myocardial oxygen supply

A

oxygen content (hemoglobin level, oxygen saturation); oxygen extraction; coronary blood flow

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6
Q

list the components of coronary blood flow

A 
coronary perfusion pressure
coronary resistance (myocardial R, arteriolar R, epicardial R)
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7
Q

list factors that contribute to arteriolar resistance

A

vascular tone, local metabolites, endothelial function

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8
Q

list factors that affect epicardial resistance

A

atherosclerosis

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9
Q

write an equation for calculating coronary blood flow

A

CBF = (Postium-PCS)/(Rart + Rmyo + REpi)

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10
Q

highest flow through the left coronary artery is during early ______

A

diastole (aortic valve open, muscles not contracting)

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11
Q

myocardial resistance is greater in the ____ than in the _________

A

subendocardium; epicardium

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12
Q

arteriolar resistance is adjusted in response to metabolic factors, including…

A

adenosine, prostaglandins, NO, endothelin, potassium, oxygen

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13
Q

explain autoregulation in the context of arteriolar resistance

A

resistance, R- art, is dynamic and varies in response to local conditions to titrate the blood flow into the local tissue

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14
Q

describe coronary flow reserve

A

Ability to increase blood flow is related to the ability to reduce R-art. When the arterioles are not maximally dilated (R-art is not maximally reduced) there remains some coronary flow reserve
If an artery is temporarily occluded, metabolic substances build up and dilate the arterioles/ decrease arteriolar resistance.

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15
Q

R-myo is due to compression of the perforating arteries within ventricular muscle in ________.

A

systole

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16
Q

R-epi can become important in the case of ________

A

atherosclerosis

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17
Q

the only way to meaningfully increase oxygen supply to the heart is to increase__________

A

coronary blood flow

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18
Q

what is the primary mechanism of regulating coronary blood flow

A

alter resistance to flow in coronary arteries (R-art)

19
Q

describe reactive hyperemia and how it relates to coronary flow reserve

A

If an artery is temporarily occluded, metabolic substances build up and dilate the arterioles/ decrease arteriolar resistance. When occlusion is removed, CBF increases above baseline due to low resistance that that was developed during occlusion. The amount of flow increase above baseline is called reactive hyperemia and represents the amount of available coronary flow reserve.

20
Q

what compound is considered the primary link between myocardial oxygen consumption and coronary blood flow

A

adenosine

21
Q

describe the impact of epicardial stenosis on coronary flow reserve

A

As R-epi increases, R-art must decline in order to maintain constant flow rates in the myocardium and keep total coronary resistance the same. This “uses up” coronary flow reserve

22
Q

most arteriolar reserve is lost at around ____% stenosis, and coronary blood flow becomes strictly dependent on ____________

A

90%; perfusion pressure

* there will be ischemia at rest

23
Q

list mechanisms of increased myocardial oxygen demand

A

increased heart rate, increased contractility, increased ventricular wall stress

24
Q

list mechanisms of decreased myocardial oxygen supply

A

ex in anemia, low coronary perfusion pressure, increased perssure in coronary sinus, reduced arterial oxygen saturation, atherosclerotic plaque rupture with thrombus, endothelial dysfunction

25
Q

CAD leads to limited coronary blood flow by:

A

fixed narrowing, endothelial dysfunction, increased R-epi

26
Q

list initial cellular effects of ischemia

A
  • reduced ATP, initially ADP and creatinine phosphate preserve ATP
  • anaerobic metabolism, increases lactic acid production and decreases pH
  • elevated H+ in the cell opens the K-ATPase channels
27
Q

list effects of opening the K-ATPase channel

A

loss of potassium gradient, contractile dysfunction. likely self-protective mechanism allowing cell to survive transient periods of ischemia

28
Q

later cellular effects of ischemia

A
  • ATP depletion–> loss of Na/K ATPase pump function
  • cell membrane loses integrity, Na and water flow in
  • proteases leak out, degrade myofibrils
  • ## inflammatory infiltration of neutrophils
29
Q

list electrical and mechanical effects of ischemia

A

electrical: dysfunction of SA/AV nodes, arrhythmias
mechanical: impaired muscle relaxation, increases filling pressure, decreases compliance, impaired contraction

30
Q

list four types of myocardial reperfusion injury

A

myocardial stunning
no reflow
reperfusion arrhythmia
fatal reperfusion injury

31
Q

define myocardial stunning

A

ventricular dysfunction that persists after reperfusion despite absence of irreversible damage and despite restoration of normal blood flow. Likely because cell is intact but torponin mechanism is damaged due to Ca changes, so the cell won’t beat for a while. After 7-14 days protein synthesis= new troponin, cell can recover function

32
Q

what is the likely cause of no reflow after opening an occluded epicardial artery

A

edema, destruction of small vascular structures in myocardium

33
Q

what is the role of O2 in reperfusion injury

A

oxygen radicals injure cells, reduce NO

34
Q

what is the role of calcium in reperfusion injury

A

Abrupt rise in intracellular Ca++ is caused by damage to sarcolemmal membrane and SR
High Ca++ leads to myocyte hypercontracture, increasing O2 demand

35
Q

describe the phenomenon of ischemic pre-conditioning

A

people with previous “stuttering angina” have smaller MIs

likely involves the K-ATP channel

36
Q

list clinical effects of ischemia

A
  • chest pain
  • decreased ventricular relaxation- decrease in diastolic compliance of ventricle, elevation of diastolic ventricular pressure, because ventricle is stiffer.
  • S4 sound may be heard as a result of reduced ventricular compliance
  • decreased myocardial contractility: anaerobic metabolites depress myofibrilar function- protons decease affinity of calcium binding to troponin C, thus decrease sensitivity of myofibrils to calcium
37
Q

differentiate between myocardial stunning and hibernating myocardium

A
  • Stunning: transient total occlusion- ventricular dysfunction that persists after reperfusion despite absence of irreversible damage and despite restoration of normal blood flow
  • Hibernation: constant partial flow -result of chronic partial occlusion, reduced function but myocytes are alive and will recover function if blood flow improves
38
Q

what diagnostic study is best to clarify chest pain

A

history

39
Q

what diagnostic study is best to clarify cellular electrical changes

A

ECG, stress ECG

40
Q

what diagnostic study is best to clarify reduction in coronary blood flow

A

myocardial perfusion stress test, coronary angiography, stress echocardiogram, stress MRI

41
Q

what diagnostic study is best to clarify conversion to anaerobic metabolism

A

PET scan

42
Q

what diagnostic study is best to clarify systolic dysfunction/ impaired contractility

A

echocardiogram, MRI, CT, physical exam

43
Q

what diagnostic study is best to clarify diastolic dysfunction/ impaired relaxation

A

echocardiogram, MRI, physical exam

CV (7 decks)

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