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
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
3
Q
normal anatomical variants
A
- coronary dominance
- single/extra ostia (start of coronary arteries)
- LCX connected to RCA
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
5
Q
LCX
A
-supplies free wall of LV b/n ant and post pap muscle
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
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
8
Q
coronary dominance
A
- where post descending comes from
- 70% from RCA
- 20% from both
- 10 % from LCX
9
Q
post pap
A
-RCA and LCX
10
Q
ant pap
A
-LAD and LCX
11
Q
borders of perfusion territories
A
- irregular and complex
- deeply interdigitated
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
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
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
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
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
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
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
