Coronary Circulation Flashcards
thebesian vessels
- 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
interconnections
- 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
normal anatomical variants
- coronary dominance
- single/extra ostia (start of coronary arteries)
- LCX connected to RCA
distribution of blood flow
- coronary perfusion territories
- coronary dominance
- redundancy of blood distribution to papillary muscle- make sure mitral valve is ok/no regurgitation
- interdigitated borders
LCX
-supplies free wall of LV b/n ant and post pap muscle
LAD
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
RCA
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
coronary dominance
- where post descending comes from
- 70% from RCA
- 20% from both
- 10 % from LCX
post pap
-RCA and LCX
ant pap
-LAD and LCX
borders of perfusion territories
- irregular and complex
- deeply interdigitated
perfusion
- flow/ Q
- influenced by pressure (diastolic b/c perfusion occurs then) and resistance-mechanical/metabolic/pathologic
- P=QR
- Q=P/R
myocardial oxygen consumption
- 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
coronary perfusion
- 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
autoregulation
- 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
coronary flow reserve
- 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
R1
- 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
R2
- arterioles and resistance arteries
- dynamic resistance from metabolic and autoregulatory adjustments to flow
- changes in response to physical forces and metabolic needs of tissue
R3
compressive resistance
- varies with time through cardiac cycle
- related to cardiac contraction and systolic pressure
- higher in subendocardial and then epicardial layers
normal blood flow
- 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)
coronary flow during cycle
- 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
mechanism of autoregulation
- metabolic and myogenic
- different sites in microvasculature have different dominant mechanisms of control
metabolic autoregulation
- result of local metabolism
- may be due to NO mediated dilation
- endothelium senses changes in pressure through pressure sensitive ion channels
myogenic autoregulation
-arteriolar smooth muscle contracts with increased intraluminal pressure