Reg. of Coronary Circulation Flashcards Preview

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Flashcards in Reg. of Coronary Circulation Deck (26)
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1
Q

Is coronary blood flow able to make big changes in response to increased demand?

A

Yeah.

2
Q

Which epicardial coronary arteries provide blood to the anterior and lateral portions of the heart?

A

the LAD and circumflex a. (Cx), mainly

3
Q

Which coronary artery provides blood to the SA node? (note that it’s not always the same)

A

60% of time: proximal RCA

40% of time: circumflex a. (Cx)

4
Q

Which coronary artery provides blood to the AV? (note that it’s not always the same)

A

90% of time: RCA

10% of time: Cx

5
Q

What small vessels are an important source of collateral blood supply in CAD?

A

Small penetrating aa.

6
Q

What vessels are responsible for the majority of coronary vascular resistance?

A

Intramyocardial aa.

7
Q

What are the 2 parts of the pressure gradient that drives coronary blood flow?

A

High pressure: central aortic pressure (120ish mmHg)
Low pressure: LVEDP (about 10mmHg)
*This doesn’t seem that intuitive, but it’s important.

8
Q

When in the cardiac cycle does most flow in coronary arteries occur? Why?

A

During (ventricular) diastole.

Because of myocardial compressive forces during systole. “extravascular resistance”

9
Q

What effect do extravascular forces have ont he transmural distribution of coronary flow?

A

They cause more restriction on the subendocardial area -> subendocardium is more vulnerable to ischemia.

10
Q

What does “autoregulation” refer to in coronary blood flow?

A

Flow remains constant over a wide range of perfusion pressures. (60 - 150mmHg).
(vascular smooth muscle contracts when pressure is high, relaxes when pressure is low)

11
Q

Flow decreases proportional to r^4 as the radius decreases, so what happens when there’s stenosis of epicardial arteries?

A

Due to impressve ability of coronary vessels to adapt, you can actually maintain consistent normal flow despite significant stenosis - especially for resting flow.
Resting flow - pretty good until about 80-90% occlusion (asymptomatic until exertion).
Maximum flow - really starts to drop off at about 60% occlusion.

12
Q

What does “vasodilator reserve” refer to? What’s the formula, and what are R1 and R2?

A

If epicardial flow decreases, small arteries can dilate to compensate.
Q = P / (R1 + R2)
Where R1 coronary a. resistance.
R2 is resistance of small arteries.
(if R1 increases, R2 can decrease to maintain same flow)

13
Q

2 ways to measure vasodilator reserve?

A

Doppler flow probe (measure flow after vasodilator given).

Fractional flow reserve (delta mean pressure after vasodilator applied).

14
Q

4 broad ways in which coronary blood flow is regulated?

A

Myogenic (response to changes in pressure)
Endothelial (release of substances)
Metabolic (adenosine build up)
Neurohumoral effects

15
Q

What’s the mechanism for myogenic regulation of coronary blood flow?

A

Stretch receptors induce depolarization of vascular smooth muscle cells. Flow is kept constant despite changes in perfusion pressure.

16
Q

What’s the main molecule involved in endothelial regulation of coronary blood flow (for vasodilation)? Mediators of its release?

A

NO

Release mediated by pulsatile stress, Ach, others.

17
Q

Why does inhibition of NO synthase lead to vasoconstriction of the coronary vessels?

A

Because NO is constantly being produced at a low basal level

18
Q

3 molecules that stimulate Endothelin-1 release?

A

Thrombin, A-II, epinephrin, (and some cytokines)

19
Q

When is adenosine released from myocardial cells?

What cells does it act on?

A

Adenosine is release when O2 demand exceeds reply. (it’s produced from AMP)
It diffuses to coronary artery smooth muscle, and causes relaxation -> vasodilation.

20
Q

Difference between the effect of beta1 vs. beta2 adrenergic agonism on coronary arteries?

A

Beta1: vasodilation via increased metabolic demand.
Beta2: direct vasodilatory effects
(note that alpha agonism usu. causes vasoconstriction)

21
Q

Review: How does Ach’s effect on vascular tone vary between vessels with intact and damaged endothelium?

A

Intact: vasodilation via NO.
Damaged: vasonconstriction via muscarinic receptors.
(Ach can be used to assess if vascular damage is present.)

22
Q

What is significant about treatment with statins making patients’ coronary arteries not constrict in response to Ach (vs. placebo)?

A

It means that the endothelium is healthier.

exercise makes the vessels dilate more in response to Ach

23
Q

3 meds for angina pectoris (ischemic pain from CAD)?

A

Nitrates, anti-platelet agents, and beta-blockers.

24
Q

Unstable angina vs. acute MI?

A

Unstable angina is blockage that’s severe enough to be symptomatic, but acute MI is complete blockage of the artery.

25
Q

Treatment of coronary artery spasm?

A

nitrates or Ca++ channels blockers to prevent spasm

26
Q

What’s small-vessel disease? (in the context of CAD)

A

It’s poorly defined.

Angina with decreased vasodilator reserve, but no obvious narrowing of epicardial arteries.