Phys- Coronary Flow Flashcards
Oxygen delivery equation
Oxygen Deliivery = Blood Flow x Oxygen Content
Flick Equation
VO2= Blood Flow x (CaO2 - CvO2)
Extraction equation
Difference between what goes in and what comes out CaO2-CvO2
If coronary O2 extraction is nearly maximal at rest how does the heart match O2 delivery with increases in myocardial VO2?
increased blood flow
Control of coronary blood flow
Primarily under local metabolic control
Intramural arteries
penetrate the myocardium and are subject to high transmural pressure during systole (surround pressure)
capillary to fiber ratio in cardiac muscle
(number or capillaries per muscle fiber) 1 capillary/fiber
Cardiac Capillary density
VERY high (~3500 capollaries/mm^2 ) to support the metabolism of the heart
describe cardiac capillary perfusion at rest
heterogeneous- not all are well perfused at rest
Capillary recruitment
increased myocardial work increases blood flow and more uniform perfusion of capillaries
How do we get more uniform perfusion of capillaries during capillary recruitment
Increased myocardial work causes 1.) Increased “Functional” capillary density 2.) Decreased diffusion distances 3.)Enhanced capillary exchange
Coronary Collateral Vessels
Arterial-to arterial anastamoses: Coronary arteries form collateral channels to ensure myocardial perfusion and help protect the mycoardium against ischemia
Native coronary collateral vessels
exist in all hearts - relatively small and few in number
Mature (or stimulated) coronary collaterals
Myocardial ischemia stimulates collarteral growth. The lumen of collateral vesslesl enlarges followed by significant wall thickening.
Myocardial Oxygen Consumption depends on what variables
Blood flow (Q) and coronary oxygen extraction (CaO2-CvO2) where MVO2 = Q x (CaO2-CvO2)
In the heart, when is oxygen extraction nearly maximal
under resting conditions
what is the only way to increase MVO2
by increasing blood flow (remember: oxygen extraction is at near max under resting conditions)
MVO2 increases in proportion to what
Myocardial work- Maximal MVO2 can increase 5-6 fold from resting MVO2
Determinants of MVO2 “The Big 3”
1.) Contractility 2.) Heart Rate 3.) Wall Tension
Theory behind how increases in ionotropy increases MVO2
thought to be related to the metabolic cost of Ca release and uptake
Discuss the increase in MVO2 as a result of wall tension
MVO2 increases linearly with peak systolic pressure (or peak systolic wall tension) developed by the left ventricle (Law of LaPlace Wall tension = (pressure x radius)/2thickness)
Discuss tratments if there is a mismatch between MVO2 and the ability to deliver O2 to the tissue
1.) B-Blockers (decreases HR and Contractility= decrease Myocardial work by decreasing MVO2) 2.) Ca channel blockers (decrease contractility = decrease MVO2) 3.) Nitrates (decrease afterload by causing peripheral vasodilation and decrease preload through venodilation)
Determinants of MVO2 “The Little 3”
1.) Basal requirements (cellular metabolism) 2.) Activation Energy (cost of electrical activation) 3.) Ejection of Blood (Cost of shortening muscle)
Myocardial Metabolic Substrate Utilization
1.) ATP (used for contraction ) is in dynamic equilibrium with a pool of creatine phosphate 2.) Oxidative Metabolism (fatty acids) - 60% of substrate utilization- balance is glucose and lactate 3.) Glycolysis - 40% of substrate metabolism
Discuss situations where Glycolysis predominates in myocardial substrate utilization
During ischemia and hypoxemia - glycolysis predominates and the heart switched from net lactate uptake to net lactate production. NOTE: more predominant but less efficient
How does the heart meat increased O2 demands (increased MVO2)
almost entirely though increasing blood flow
Does the percentage of cardiac output used changed when MVO2 is increased?
NO. Flow increases up to 5 fold as MVO2 increased but cadiac output remains ~5% (as it is in resting conditions)
What is the drivig pressure for coronary flow
Aortic diastolic pressure
Describe the coronary flow in ventricular systole
Coronary flow decreased due to “systolic squeeze” (Psurround > Pdiastolic in coronaries) Flow begins to increase again in diastole
When does coronary perfusion occur
Diastole
Describe the phasic nature of coronary flow
Flow increases during early diastole and follows aortic pressure
Where does “systolic Squeeze” have the greatest effect
the left ventricle (occurs to a lesser extent in the low pressure right ventricle)
Is phasic flow more pronounced in subendocardium or subepicardium?
Subendoardium due to systolic squeeze (still occurs in the subepicardium but to a lesser extent)
Effect of Aortic Stenosis and coronary perfusion
Increases left ventricular work but will NOT increase coronary perfusion pressure or flow - creates and unfavoralble supply/demand ratio
What is the most important determinant of Coronary Blood Flow
Myocardial oxygen consumption
Autonomic control of coronary flow
1.) Direct effects - innervated by both sympathetic (vasoconstriction) and parasympathetic (modest vasodilatio) 2.) Indirect effects- MORE IMPORTANT- Metabolic vasoregulation
Coronary Vasoregulation
Changes in metabolic demand due to changes in HR, contractility, or blood pressure are far more important in determining vascular caliber and myocardial blood flow
Adenosine Hypotheis
Adenosine causes vasodilation in hypoxia
what substrates can induce vasodilation in coronary arteries
Adenosine, hyperkalemia (K) , hypercapnia (high CO2), acidosis (H) , lactate, and prostaglandins
Vascular Reserve (Coronary Autoregulation)
How much we can increase flow at a given pressure (difference between the autoregulating curve and the maximally vasodilated curve)
Conditions of reduced coronary reserve
1.) Lower perfusion pressures (low diastolic pressure) 2.) Chronically higher MVO2 (increased flow) 3.) Increased fixed resistance (eg: atherosclerosis)
Which has less fow reserve, subendo or subepi? What is the risk of this?
Subendo has less flow reserve - greater risk of ischemia, injury, and infarction
