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Flashcards in Reg. of Coronary Circulation Deck (26)
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Is coronary blood flow able to make big changes in response to increased demand?



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

the LAD and circumflex a. (Cx), mainly


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

60% of time: proximal RCA
40% of time: circumflex a. (Cx)


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

90% of time: RCA
10% of time: Cx


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

Small penetrating aa.


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

Intramyocardial aa.


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

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


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

During (ventricular) diastole.
Because of myocardial compressive forces during systole. "extravascular resistance"


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

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


What does "autoregulation" refer to in coronary blood flow?

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)


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

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.


What does "vasodilator reserve" refer to? What's the formula, and what are R1 and R2?

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)


2 ways to measure vasodilator reserve?

Doppler flow probe (measure flow after vasodilator given).
Fractional flow reserve (delta mean pressure after vasodilator applied).


4 broad ways in which coronary blood flow is regulated?

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


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

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


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

Release mediated by pulsatile stress, Ach, others.


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

Because NO is constantly being produced at a low basal level


3 molecules that stimulate Endothelin-1 release?

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


When is adenosine released from myocardial cells?
What cells does it act on?

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


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

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


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

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


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

It means that the endothelium is healthier.
(exercise makes the vessels dilate more in response to Ach)


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

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


Unstable angina vs. acute MI?

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


Treatment of coronary artery spasm?

nitrates or Ca++ channels blockers to prevent spasm


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

It's poorly defined.
Angina with decreased vasodilator reserve, but no obvious narrowing of epicardial arteries.