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Physiology Week 3 > Coronary Circulation > Flashcards

Coronary Circulation Flashcards

1
Q

thebesian vessels

A
  • connect cardiac chambers to arterioles, capillaries, and venules
  • can follow normal route-arteries-arteriole-cap-venule-vein- RA
  • or can drain right from arterioles, cap, venules to chambers
  • RA receives most but L and R vent can receive some
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2
Q

interconnections

A
  • arterial to venous shunts
  • arterial/arterial connections
  • venous/venous connections
  • become prominent on diseased hearts
  • not a simple loop
  • clinical techniques exploit the interconnectivity in an effort to force perfusion into territories whose primary route is compromised-during surgery can give cardiologic soln to coronary arteries and sinus simultaneously
  • some patients have 3 vessel occlusion and no symptoms
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3
Q

normal anatomical variants

A
  • coronary dominance
  • single/extra ostia (start of coronary arteries)
  • LCX connected to RCA
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4
Q

distribution of blood flow

A
  • coronary perfusion territories
  • coronary dominance
  • redundancy of blood distribution to papillary muscle- make sure mitral valve is ok/no regurgitation
  • interdigitated borders
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5
Q

LCX

A

-supplies free wall of LV b/n ant and post pap muscle

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6
Q

LAD

A

supplies the free wall of the LV, anterior 2/3 of the vent septum and a small portion of the free wall of the RV

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7
Q

RCA

A

supplies the free wall of the RV, post 1/3 of the vent septum and the posterior wall of the LV to the post pap muscle

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8
Q

coronary dominance

A
  • where post descending comes from
  • 70% from RCA
  • 20% from both
  • 10 % from LCX
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9
Q

post pap

A

-RCA and LCX

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10
Q

ant pap

A

-LAD and LCX

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11
Q

borders of perfusion territories

A
  • irregular and complex

- deeply interdigitated

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12
Q

perfusion

A
  • flow/ Q
  • influenced by pressure (diastolic b/c perfusion occurs then) and resistance-mechanical/metabolic/pathologic
  • P=QR
  • Q=P/R
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13
Q

myocardial oxygen consumption

A
  • extracts nearly all of the oxygen delivered to it form coronary blood flow
  • normal venous oxygen saturation of coronary sinus is 30% (compared to 75% in RA/RV
  • increase in oxygen consumption requires increase in flow
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14
Q

coronary perfusion

A
  • occurs during diastole-reduced diastolic pressure can reduce perfusion
  • during diastole, aortic diastolic pressure is transmitted without resistance to coronary ostia
  • aortic arch and coronary sinuses act as mini reservoir, facilitating maintenance of uniform coronary inflow
  • epicardial coronary arteries act as conductance of conduit vessels (0.3-5mm d)-no appreciable resistance to blood flow/ no pressure drop along the length of the epicardial arteries
  • arterioles are 10-200 microns in diameter-resistance vessels with large pressure drop
  • LCA extracardial pressure greater-greater increase during diastole
  • RCA pressure not as bad- flow even in systole/diastole
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15
Q

autoregulation

A
  • intrinsic ability of the heart to maintain a constant blood flow over a wide range of coronary perfusion pressures
  • increases in consumption require more flow
  • impaired in presence of fall in aortic pressure and chronic HTN and LV hypertrophy
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16
Q

coronary flow reserve

A
  • maximal increase in coronary blood flow above its resting level for a given perfusion pressure when vasculature is maximally dilated
  • hyperaemic CBF increase 2-3x nomal
  • reduction of coronary flow reserve is due to epicardial stenosis or microvascular dysfunction
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17
Q

R1

A
  • epicardial conduit artery resistance
  • insignificant in normal
  • in presence of >50% stenosis, starts contributing to total coronary resistance and may reduce resting flow with >90% stenosis
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18
Q

R2

A
  • arterioles and resistance arteries
  • dynamic resistance from metabolic and autoregulatory adjustments to flow
  • changes in response to physical forces and metabolic needs of tissue
19
Q

R3

A

compressive resistance

  • varies with time through cardiac cycle
  • related to cardiac contraction and systolic pressure
  • higher in subendocardial and then epicardial layers
20
Q

normal blood flow

A
  • no flow in subendocardial portion of LV in systole, most common site of MI
  • decreased LV flow in stenotic aortic valves because Pressure in LV must be much higher than aorta to eject blood- have to get it out to fill LAD- if aorta is stenotic can’t do that
  • decreased when aortic diastolic pressure is too low- CHF- decreases effective perfusion pressure (diastolic pressure needs to be high enough to get to LV)
21
Q

coronary flow during cycle

A
  • LV subendocardial only during diastole ( pressure in LV is higher than aorta during systole)
  • flow in RV and atria not appreciably reduced during systole, aortic pressure is much higher than them
  • Left can’t get blood during systole because LV contracting still and too high pressure
  • aortic pressure is higher than RV and A, so blood gets there throughout the whole cycle
  • LV flow reduced during tachy because diastole shorter
22
Q

mechanism of autoregulation

A
  • metabolic and myogenic

- different sites in microvasculature have different dominant mechanisms of control

23
Q

metabolic autoregulation

A
  • result of local metabolism
  • may be due to NO mediated dilation
  • endothelium senses changes in pressure through pressure sensitive ion channels
24
Q

myogenic autoregulation

A

-arteriolar smooth muscle contracts with increased intraluminal pressure

25
Q

endothelial control of coronary vascular tone

A
  • produces powerful vasodilators:
  • EDRF (endo derived relaxing factor)
  • NO
  • prostacyclin
  • EDHF (hyperpolarizing factor)
  • powerful vasoconstrictors- endothelin 1
  • endothelium can be damaged by atherosclerosis and cardiac risk factors-imbalance of flow, ischemia
26
Q

risk factors associated with endothelial dysfunction

A
  • dyslipidemia-dense LDL, Lpa, oxidized LPL
  • HTN
  • diabetes mellitus
  • smoking
  • menopause
  • hyperhomocystenemia
  • aging
  • family history of CAD
  • mutation in eNOS
27
Q

nitric oxide

A
  • produced from L arginine by nitric oxide synthase (NOS) in vascular endothelium
  • under normal conditions, continually produced
  • increased flow stimulates NO because shear force on vascular endo causes release of Ca
  • inhibition of NO causes vasoconstriction
  • NO increases blood flow during metabolic stimuli
  • inhibition of NO reduces the magnitude of metabolic dilation
  • NO production increased in response to hypoxia
  • NO principal mediator of flow mediated dilation
28
Q

preload

A
  • filling pressure
  • amount of stretch on muscle just before contraction
  • MV stenosis causes understretching-can’t get blood into LV
  • MV regurgitation causes overstretching- backflow and then right back in again
  • aortic insufficiency-LV hypertrophy, stretch
29
Q

afterload

A
  • pressure/resistance the heart is working against while it is squeezing
  • HTN
  • aortic stenosis
  • TPR
30
Q

oxygen consumption effectors-all 50% inc

A
  • wall stress increases o2 consumption by 25%
  • contractility by 45%
  • pressure work by 50%
  • heart rate by 50%
  • volume work by 4%
31
Q

pathologies influencing perfusion and MVO2

A
  • CAD
  • Vent hypertrophy
  • vent dilation
  • coronary fistula
32
Q

CAD

A
  • imbalance between supply and demand
  • reduction in flow-supply ischemia/low flow ischemia- increased vascular tone, platelet agg, thrombus
  • demand/high flow ischemia-increase in flow but insufficient to meet increase in myocardial o2 demand-obstruction, brought on by exercise, stress, tachy
  • hypoxia-CO, asphyxiation, cyanotic congenital heart disease
33
Q

effects of stenosis on flow

A
  • maximum perfusion ultimately determined by coronary pressure distal to stenosis (if too high, won’t get there)
  • autoregulation maintains constant flow with increasing stenosis by decreasing other resistance
  • need to be vasodilated to detect
  • normal coronary flow reserve is up to 5x rest flow
  • no significant pressure drop up to 50% severity
  • worsening causes increased pressure drop, decreased flow
  • at >90%, resting flow decreased
34
Q

coronary flow reserve 2

A
  • healthy heart can increase flow to myocardium in response to local metabolic demand by reducing resistance
  • if arteries become blocked and therefore resistant, we must dilate arterioles
  • eventually flow will suffer
35
Q

ventricular hypertrophy

A
  • reduces coronary flow reserve
  • stenosis of aortic valve- LV works harder
  • increased mass needs more oxygen, but coronary flow reserve reduced because change in ration to mass of tissue
  • mass increases without increase in microcirculatory resistance
  • max flow during vasodilation doesnt change, max flow per gram decreases as mass increases
  • resting flow increases with increase in mass
  • decreased flow at any pressure
  • mild stenosis can even be ischemic
36
Q

clinical notes

A

-assessment of coronary blood flow:
-angiogram in cath lab
-MRA-magnetic resonance angiogram
-CTA- CT angio
Physiologic assessment:
-echo doppler
-cardiac MRI
0cardiac PET scan
-FFR in cath lab
-ischemia testing-stress test with echo or nuclear
-pharmacological stress tests-dobutamine or vasodilators

37
Q

methods of improving coronary blood flow

A
  • pharm-nitroglycerine, adenosin
  • invasive-angioplasty with stent or CABG
  • other-IABP, controlled arrest-cardioplegia, transplant
38
Q

nitroglycerin

A
  • dilates epicardial conduit arteries and small coronary resistance vessels
  • improves subendocardial perfusion by reducing LV end diastolic pressure by venodilation
  • dilates coronary collateral vessels
39
Q

adenosine

A

coronary dilator

  • relaxes VSM cells
  • released from cardiac myocytes when rate of ATP hydrolysis exceeds its synthesis during ischemia or increased metabolic demand
  • short half life
  • binds to A2 receptors, increases cAMP and opens intermediate Ca activated K channels
  • endothelium independent
40
Q

dipyridamole

A
  • inhibits the myocyte reuptake of adenosine
  • mechanism similar to adenosine
  • reversed adenosine receptor antagonists-aminophylline
41
Q

papaverine

A

-causes endothelium independent relaxatoin of VSM by inhibiting phosphodiesterase and increasing cAMP

42
Q

invasive coronary flow modification

A
  • 1958
  • injected iodinated contrast selectively into coronary ostia by catheter
  • contrast fills vessel lumen
  • x ray radiation releases photons from iodine, taken up by camera
  • angiogram
  • anatomy, vessel dominance, territories, anaomalous
  • coronary lumen obstruction
  • coronary blood flow
  • limitations-invasive, underestimates lesion severity, no info on hemodynamic significance, no info on vessel wall
43
Q

IABP

A
  • intra aortic balloon pump
  • improves cardiac function
  • afterload reduction-deflation of the balloon reduces ABP immediately prior to systole and allow heart to pump against a lower pressure
  • diastolic augmentation-balloon inflation just after aortic valve closure increases diastolic pressure and increases flow to heart

Physiology Week 3 (9 decks)

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