Coronary Circulation Flashcards
where do the 2 coronary arteries arise?
from the aortic sinuses behind the left and right coronary aortic valve cusps at the root of the aorta
what are the 2 major arteries and their major branches, and what they all follow??
- right coronary
- acute marginal - left main coronary travels 1-1.5 cm before branching
- left anterior descending (anterior interventricular artery) follows anterior interventricular groove to apex of heart
- circumflex artery (LCX) follows left atrioventricular groove posteriorly
- ramus intermedians (optional) between LAD and LCX
what are the major branches of the LAD?
- diagonal branches distributing over free wall of left ventricle
- septal branches penetrating into anterior portion of ventricular septum
what are the major branches of the LCX?
obtuse marginals
to where is myocardium drained?
venous drainage is mostly to right atrium via long coronary sinus
- opens into RA near IVC and tricuspid valve
- CS rests in posterior AV groove and gets venous blood from left ventricle through middle cardiac vein, posterior interventricular vein, great cardiac vein, anterior interventricular vein, and (from RV) small cardiac vein
how does venous blood from right ventricle return to the RA?
anterior cardiac veins empty directly and individually into the RA
-small cardiac veins enter coronary sinus, which enter RA
thebesian vessels and where they drain most
connect cardiac chambers to arterioles, capillaries, and venules
- coronary flow may return from typical route or via Thebesian vessels
- mostly drain into RA, but also LV and RV
what is the typical route of coronary flow?
artery –> arteriole –> capillary –> venule –> vein –> right atrium
normal anatomical heart variants
- coronary dominance
- abnormal branching
- all three major arteries have same ostia in aortic root
- each major coronary artery has its own ostia in the aortic root
typical blood distribution of coronary arteries (right dominant pattern)
LCX: free wall of LV between anterior and posterior papillary muscle
LAD: free wall of LV, anterior 2/3 of ventricular septum, and small part of free wall of RV
RCA: free wall of RV, posterior 1/3 of interventricular septum, and posterior wall of LV to posterior papillary muscle
there is significant overlap
coronary dominance of posterior descending artery
travels in posterior interventricular groove to apex of heart
- 70% of PDAs are supplied by RCA (right dominance)
- 20% are co-dominant
- 10% are supplied by LCX (left dominant)
what are leaflets of mitral valve tethered to? what happens if they fail?
anterior and posterior papillary muscles in left ventricle
-failure causes acute mitral regurgitation and pulmonary edema
what are the anterior and posterior papillary muscles supplied from?
anterior: supplied by LAD and LCX arteries
posterior: supplied by RCA and LCX arteries
are the borders of cardiac perfusion territories irregular or regular?
they are very irregular and complex, b/c very interdigitated border
when does coronary perfusion happen?
it occurs during (early) diastole, b/c aortic diastolic pressure is transmitted w/o resistance to coronary ostia
- aortic arch and coronary sinuses act as a miniature reservoir to maintain uniform coronary inflow
- in RCA, force of external compression is much less from weaker RV, to keep even flow during diastole and systole
what is the major variable controlling blood flow?
change in coronary vascular resistance
what do epicardial coronary arteries act as?
conductance/conduit vessels
- 0.3 to 5 mm diameter
- no appreciable resistance to blood flow w/ no detectable pressure drop along length of epicardial arteries
what do arterioles act as?
resistance vessels
- 10-200 micron diameter with large pressure drops
- -those less than 300 um account for 95% of resistance across coronary bed
- -those less than 100 um account for 50% of total coronary resistance
is diastole longer or shorter when heart rate is high?
diastole is shorter when HR is high
-left ventricular coronary flow is reduced during tachycardia
when is the pressure differential between aorta and RV, and aorta and atria greater?
during systole
-thus, coronary flow here is not appreciably reduced during systole
where does no blood flow occur during systole? and what does this mean?
subendocardial part of left ventricle
-most prone to ischemic damage, so most common site of MI
3 components to resistance to coronary blood flow
R1 - epicardial conduit artery resistance (pathologic)
R2 - arterioles and resistance arteries (metabolic)
R3 - compressive resistance (mechanical)
R1
epicardial conduit artery resistance
- insignificant normally
- if over 50% stenosis, it starts contributing to total coronary resistance, and may resting reduce flow with over 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 (mechanical) resistance
- varies with time through cardiac cycle
- related to cardiac contraction and systolic pressure
- higher in subendocardial than subepicardial layers
how is blood flow to LV affected in patients with stenotic aortic valves?
blood flow is decreased b/c pressure in LV must be much higher in the aorta to eject the blood
-vessels are severely compressed during systole
what happens to coronary flow when aortic diastolic pressure is low?
flow decreases b/c the rise in venous pressure decreases effective coronary perfusion pressure
myocardial O2 consumption
myocardium extracts nearly all of O2 delivered to it from coronary blood flow
- normal venous O2 saturation of coronary sinus is 30% (so myocardium extracts 70% of O2 supplied to it at rest)
- any increase in O2 consumption needs increase in blood flow
what is coronary blood flow determined by?
- driving pressure through coronary vessel
- extravascular compression of coronary arteries by heart contraction
- resistance of coronary vessels
autoregulation of coronary flow
intrinsic ability of heart to maintain constant blood flow over wide range of coronary perfusion pressures
- basal flow is constant despite fluctuations in coronary artery pressure
- increases in MVO2 increase blood flow
- require metabolic and myogenic mechanisms
coronary flow reserve (CFR)
maximal increase in coronary blood flow (CBF) above its resting level for a given perfusion pressure when coronary vasculature is maximally dilated (usually 5 times more than rest flow)
-reductions usually due to epicardial coronary artery stenosis or coronary microvascular dysfunction, but must be up to 75% to see any difference
when is autoregulation impaired?
critical fall in aortic pressure
chronic HTN
LV hypertrophy
how do hyperaemic CBF values compare to resting CBF values?
hyperaemic CBF are 2-3 fold greater than resting
what are the metabolic and myogenic control mechanisms for autoregulation
meta: may be due to NO-mediated dilation when endothelial cells of coronary arteries sense changes in pressure via sensitive ion channels
myo: arteriolar VSM contracts with increased intraluminal pressure
different sites of microvasculature may have different dominant mechanisms of control
what does the endothelium produce?
powerful vasodilators:
-EDRF - endothelium derived relaxing factor
-NO
-prostacyclin
-EDHF - endothelium derived hyperpolarizing factor
powerful vasoconstrictors
-ED-1
how can endothelium be damaged?
athersclerosis and cardiac risk factors
-dysfunction leads to imbalance of coronary flow, pathogenesis of myocardial ischemia, and is a central factor in evolution of athersclerosis and thrombosis
what is preload and when is it affected?
filling pressure; amount of stretch on a muscle just before contraction
-affected by MV stenosis or regurgitation, and aortic insufficiency
what is afterload and when is it affected?
pressure/resistance the heart is working against while it is squeezing (what heart has to push against)
-affected by HTN and aortic stenosis
supply (low flow) ischemia
reduction in blood flow
- increased coronary vascular tone
- intracoronary platelet aggregation
- thrombus formation
demand (high flow) ischemia
increase in coronary blood flow that is insufficient to meet increased myocardial O2 demand
- usually in presence of coronary obstruction
- brought about by exercise, emotional stress, or tachycardia
hypoxia
reduced O2 supply
-due to asphyxiation, CO poisoning, cyanotic congenital heart disease, or cor pulmonale
how is max myocardial perfusion determined?
coronary pressure distal to stenosis
how much resistance to surface arteries offer to blood flow?
very little
stenosis of which valve will cause ventricular hypertrophy?
stenosis of the aortic valve
- increased muscle needs more O2
- CFR is reduced b/c of change in ration of blood supply to mass of tissue
how does left ventricle hypertrophy affect coronary flow?
myocardial mass increases w/o increase in microcirculatory resistance arteries
- max flow per minute during vasodilation is unchanged, so max flow per gram of tissue falls inversely with change in LV mass
- increased LV also needs higher resting flow
- net effect is decreased CFR at any pressure
how can coronary blood flow be assessed?
- coronary angiogram in cardiac catheterization lab
- MRA - magnetic resonance angiogram
- CTA - computed tomography angiogram
physiologic assessment of heart
echo doppler
cardiac MRI or PET scan
FFR in cath lab
how is ischemia tested?
exercise stress tests (echo or nuclear, SPECT, PET)
pharmocological stress dests (Dobutamine, vasodilators)
what are pharmacologic methods of improving coronary blood flow?
nitroglycerine, adenosine, dipyrimadamole, papaverine, nitric oxide
what are invasive methods of improving coronary blood flow?
angioplasty with stent, CABG (coronary artery bypass graft), IABP (intra-aortic balloon pump)
how can controlled arrest be done?
cardioplegia or transplant
what can coronary angiograms be used to look at?
injection of iodinated contrast selectively into coronary ostia by catheter (from radial or femoral nerve)
- coronary anatomy (dominance, vascular territories, anomalous vessels, collaterals)
- coronary lumen obstruction and resulting blood flow
- invasive, may have underestimation of severity, and no info on hemodynamic significance or vessel wall
how does IABP improve cardiac function?
- afterload reduction
- deflation of balloon acutely reduces patient’s ABP prior to systole, so heart can pump against lower pressure, reducing work of heart - diastolic augmentation
- balloon inflation just after aortic valve closure increases diastolic pressure in aorta and improves coronary blood flow during diastole, increasing O2 supply to heart
does coronary artery epithelium participate in coronary vascular resistance regulation
yes, coronary artery endothelium is a primary regulator of coronary vascular resistance
is coronary blood flow autoregulated?
yes, coronary blood flow is autoregulated
how does blood flow differ in left and right coronary arteries in systole and diastole?
LCA: more flow during diastole than systole (may even go to zero or below during systole)
RCA: flow is fairly even during both
does systolic compression have a larger effect on flow through RV or LV myocardium?
systolic compression has less of an effect on the right ventricular myocardium flow, meaning a bigger effect on the left
what do nitrates do?
first line treatment for angina
- stimulate release of NO in smooth muscle to increase cGMP for relaxation, to reduce ventricular wall stress via venodilation (NOT arteriolar dilation), and minimize myocardial O2 consumption
- coronary arterioles are usually already dilated
what do beta-blockers like NE do?
they are used to treat angina
-decrease HR and contractility to reduce myocardial O2 consumption
what are vasodilators of the coronary artery system, and which is the major one?
major: adenosine
others: bradykinin, prostaglandins, CO2, K+
how do the decreases in blood flow differ between endocardium and epicardium in systole?
subendocardial flow decreases a lot more than the minor change in epicardial flow
