SM 134a - Coronary Blood Flow Flashcards

1
Q

What is the “double product?”

How is it calculated?

A

The double product estimates the oxygen needs of the heart.

Double product = Systolic blood pressure * Heart Rate

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2
Q

What is R1, as it relates to coronary blood flow?

What governs it?

A

R1 is the resistance in conduit arteries

It is ususally small, and governed by endothelial and autonomic factors

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3
Q

What is R2, as it relates to coronary blood flow?

What governs it?

A

Microcirculatory (aka autoregulatory) resistance in vessels usually <200 uM. R2 is the primary mechanism for maintaining the balance of oxygen supply and demand in the myocardium

  • Metabolic factors predominate at rest
  • Endothelial and neurohormonal factors are activated during exercise
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4
Q

What is R3, as it relates to coronary blood flow?

What governs it?

A

R3 is compressive resistance

It is governed by the compression of coronary blood vessles during systole

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5
Q

What is the primary governer of resistance to blood flow in the endocardium?

A

R3: compressive resistance

There are more R3 mechanisms in the endocardium than in the epicardium

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6
Q

What is the primary governer of resistance to blood flow in the epicardium?

A

R2: Microcirculatory resistance

There are more R2 mechanisms in the epicardium than in the endocardium

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7
Q

Under basal conditions, is R2 in the myocardium high or low?

Why is this important?

A

At rest, R2 is high.

This means there is a lot of “stretch” reserved for vasodilation if the heart needs it (i.e. during exercise)

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8
Q

What metabolic factors govern R2?

When do they predominate?

A

Metabolic factors adenosine and PO2 govern R2 during rest

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9
Q

What endothelial factors actively impact R2 during exercise?

A
  • Nitric Oxide (aka Endothelial-derived relaxing factor, EDRF)
    • Greatest impact in vessels <100 um
    • Increased flow = increased synthesis
  • Endothelial derived hyperpolarizing factor (EDHF)
    • Increased flow = increased synthesis
  • Prostacyclins
    • Synthesized continuously (via the cyclooxygenase pathway
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10
Q

What neurohormonal factors actively govern R2 during exercise?

A
  • Autonomic nervous system
    • Alpha-adrenergic constriction to non-essential capilary beds
    • Beta-adrenergic dilation to essential capillary beds (ex: the heart)
  • Vasoactive agents
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11
Q

Which resistance mechanism is the primary mechanism for maintaining oxygen supply and demand in the heart?

A

R2: Resistance in microcirculatory (<200 uM) vessels

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12
Q

What is endothelial-derived hyperpolarizing factor (EDHF)?

When is it synthesized?

A

A vasodilator synthesized by endothelial cells during periods of increased flow (ex: during exercise)

It decreases R2, allowing for increased blood flow to the endocardium

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13
Q

What is Endothelial-Derived Relaxing Factor (EDRF)?

When is it synthesized?

A

EDRF is nitric oxide. It is synthesized by endothelial cells (especially coronary vessels between 100-200 uM) during periods of increased flow (ex: during exercise)

It decreases R2, allowing for increased blood flow to the endocardium

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14
Q

Where is R2 the greatest?

A

Epicardium, during rest

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15
Q

Where is R3 the greatest?

A

Endocardium

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16
Q

How would you calculate the total resistance to blood flow through the coronary arteries?

A

RTotal = R1 + R2 + R3

The vessels are in series

17
Q

What is the equation for coronary flow reserve?

A

(Flow during maximum coronary vasodilation)/(Flow under resting conditions)

Normally, the reserve is 4-5 due to R2-mediated vasodilation during exersise

18
Q

During an exercise stress test, what are some signs that coronary reserve is exhausted?

A

Chest pain

ST segment depression on ECG

19
Q

What happens if coronary reserve is low?

What might cause this?

A

If coronary reserve is low, the coronary arteries cannot adequately expand to increase flow in response to exercise

This can be caused by anatomic abnormalities or atherosclerosis, that require decreases in R2 during rest, such that it is already “used up” when oxygen demand increases during exercise

20
Q

What additional information would you learn by adding nuclear imaging to an exercise stress test?

A

You can identify and localize regional limitations in flow reserve

(Find out which tissues are not adequately perfused during exercise)

21
Q

What additional information would you learn by adding echocardiography to an exercise stress test?

A

Identify and localize stress-induced abormalities in left ventricular contractile function

Can see wall motion abnormalities

22
Q

What are the endothelium-independent components of coronary blood flow?

A

Increased metabolic demand during exercise causes vasodilation via increased adenosine, expecially in microvessels <100 uM

[Directly dilateds R2 microvessels]

23
Q

What are the endothelium-dependent components of coronary blood flow?

A

Increased Nitric Oxide production in larger R2 vessels (100-200uM)

Increased EDHF promotes relaxation of vascular smooth muscle

24
Q

What disease states reduce the efficacy of the endothelium-dependent components of coronary flow? (Nitric oxide and EDHF)

A
  • Diabetes
  • Hypercholesterolemia
  • Smoking

The result is decreased maximum flow to coronary arteries

25
Q

A patient with partially occluded coronary arteries may still have a normal exercise stress test.

What percent occlusion puts the patient in the “danger zone” for angina pectoris and myocardial ischemia?

A

70% occlusion at rest

At this point, the resistance mechanisms (especially R2) are as relaxed as possible during rest to allow for adequate perfustion. There is no remaining coronary reserve

Exercise increase demand for oxygen, but the mechanisms to increase supply are already maxed out, leading to ischemia

26
Q

Where in the myocardium does the R2 vasodilator reserve run out first?

A

Subendocardium

There are fewer R2 reserve mechanisms in the endocardium than the epicardium

There are more R3 reserve mechanisms in the endocardium than the epicardium

27
Q

If a conduit artery is partially occluded due to atherosclerosis, what mechanisms will compensate to maintain coronary blood flow?

A

Conduit artery stenosis = increased R1

R2 mechanisms will cause microvascular dilation to compensate

Howerver, when this happens the coronary reserve is decreased, reducing the ability of R2 mechanisms to compensate for increased demand (ex: exercise)