Cardio #98
Monday, February 3, 2003 1:00
Dr. Tune
Ashleigh McClendon
Page 1 of 5
Coronary Circulation
I. Coronary Anatomy
A. Major Arteries
1. Right Coronary Artery
a. Branches: branch to SA node, right marginal branch, posterior descending artery
2. Left Coronary Artery
a. Branches: circumflex branch, left anterior descending artery
B. Major Veins
1. Coronary sinus
2. Great cardiac vein
3. Middle cardiac vein
4. Small cardiac vein
C. Basic Structure
1. Arteries and veins are on the outside of the heart. They give off branches which travel down into the tissue and branch further.
D. Coronary Microcirculation
1. Heart does have a small collateral circulation, which serves to provide an alternative route to capillary beds
2. Thebesian vein: drains venous blood directly into ventricles, which is a normal right to left shunt
II. Phasic Coronary Flow (IMPORTANT!)
A. Left Side
1. The left ventricle contracts and compresses it’s own blood supply
2. Results
a. LOW flow during SYSTOLE (can reach zero)
b. HIGH flow during DIASTOLE
3. Left ventricle veins, however, have the opposite pattern of flow (high flow in systole and low flow in diastole)
4. The phasic pattern of flow is due to changes in myocardial tissue pressures
B. Right Side
1. Right sided flow is the opposite from the left side because there is less tissue and therefore, less tissue pressure
2. Results
a. HIGH flow during SYSTOLE
b. LOW flow during DIASTOLE
III. Endocardial vs. Epicardial Blood Flow
A. Endocardium (innermost layer)
1. Has the highest tissue pressure, so it receives flow only during diastole
2. Most vulnerable to ischemia
3. Coronary resistance is lower here because of increased metabolic demands of the tissue
a. Because of this, the endocardial flow is not impaired and the endocardial flow is slightly greater than that of the epicardium
B. Epicardium
1. Lowest tissue pressure
IV. Changes in Coronary Flow
A. Tachycardia
1. Has a dual effect on coronary flow
a. Flow is decreased by shortening the amount of time the heart spends in diastole because of increase heart rate (mechanical reduction)
b. Flow is increased due to an increase in local metabolic vasodilation (metabolic dilation)
2. Even though we have two effects, the main effect is metabolic dilation
V. Coronary Autoregulation
A. Definition
1. the intrinsic tendency of an organ to maintain constant blood flow despite changes in arterial perfusion pressure
B. How does this happen?
1. we really don’t know, but there are two thoughts on it
a. myogenic mechanisms
i. means that the stretch of the vascular smooth muscle causes a contraction
b. local metabolic mechanisms
i. this is a feedback relationship between metabolism and flow
C. Normal limits
1. Autoregulation works best within pressure of 60-140 mmHg
D. Think about Ohm’s law
1. In order to keep flow constant, we need to change pressure and resistance (flow = P/R)
E. Effect of Metabolism
1. Metabolism is measured by measuring oxygen consumption
2. the normal cardiac oxygen consumption is about 8-10 mL/min/ 100g
a. cardiac oxygen consumption is effected by the rate of flow (delivery) and how fast the oxygen is used
3. Myocardial oxygen consumption (MVO2) = flow (arterial O2 content – coronary venous O2 content)
4. Normal coronary venous O2 content = 5; Normal arterial O2 content= 20; Normal systemic venous O2 content = 15
5. Under normal resting conditions, the rate of extraction of O2 for cardiac muscle is high (75%)
a. The PO2 of coronary venous blood is about 20 mmHg, which is lower than normal
i. As a result, this leaves very little extraction reserve
6. The fact that there is very little extraction reserve (room for error) means that increases in metabolic demand must be met primarily by increases in coronary blood flow
F. Supply and Demand
1. In a normal conditions, the supply (how much O2 gets to the tissue) must equal the tissue’s demand for O2
2. When demand is greater than supply, ischemia results
3. Influencers of demand
a. Heart rate
b. Contractility
c. Systolic wall tension
4. Influencers of supply
a. O2 carrying capacity
b. Coronary blood flow
i. This is influenced by vascular resistance (arteriole diameter)
5. Anemia
a. In this disease, coronary blood flow must increase because of fewer red blood cells to carry oxygen
b. Cardiac output also increases
G. Local Metabolic Coronary Vasodilation
1. definition: intrinsic local mechanism that controls coronary blood flow to match changes in myocardial metabolism
2. how it works: the hypothesis is that a decrease in cardiac tissue oxygen tension (PO2) is the stimulus for the production of local vasodilators that will increase coronary flow and oxygen delivery to the heart muscle
3. In some books you will read that adenosine is the prime vasodilator, but this is probably not true. Adenosine participates in a negative feedback mechanism in which as oxygen consumption goes up, the PO2 goes down and adenosine increases because of the breakdown of ATP. Adenosine binds to receptors and this causes vasodilation
a. One of the reasons Dr. Tune said this doesn’t work is because of his own research. Caffeine blocks adenosine receptors; however, upon exercise, the vessels still dilate.
4. Other Local Metabolic Vasodilators
a. Includes: K ATP channels, ATP-ADP, nitric oxide, ANP, O2-CO2, K, H (lactic acid), EDHF (EETs), and prostaglandins
5. Endothelial control
a. Endothelial Derived Relaxing Factor (EDRF)
i. This is nitric oxide
ii. it’s release is stimulated by acetylcholine (parasympathetics) and shear stress (increased velocity causes increased sheer)
iii. this mediates large epicardial coronary dilation
b. Endothelial Derived Constricting Factor
i. This is endothelin
ii. Endothelin is a potent vasoconstrictor with a long duration of action
iii. The levels of this chemical are increased in atherosclerosis, MI, and CHF ( which makes it a possible drug target in treating these diseases)
VI. Neural Control of Coronary Circulation
A. Sympathetic
1. Results in increase of heart rate and contractility ( which decreases coronary flow due to mechanics)
2. Also results in increased metabolic activity (which increases coronary flow and actually wins out over the mechanical problems)
3. Two receptors are
a. Alpha adrenoceptors- cause vasoconstriction of medium/large arteries (helps maintain normal transmural flow distribution)
b. Beta adrenoceptors- vasodilate primarily coronary arterioles (norepinephrine)
c. Stimulation of the Beta receptors overrides the alpha stimulation
B. Parasympathetic
1. the release of acetylcholine increases coronary blood flow by augmenting nitric oxide release, resulting in vasodilation
2. patients with atherosclerosis have endothelial dysfunction, which results in a decrease in acetylcholine mediated coronary vasodilation
VII. Coronary Collaterals
A. Role
1. serve to provide nutritive flow to ischemic region following a severe or complete coronary artery occlusion
B. Structure
1. can be a single or interconnecting network of channels
2. only a small amount of pre-existing collaterals are in the human heart
C. If coronary stenosis develops slowly over time (like weeks to months), the pre-existing collaterals develop into mature arteries (a process called arteriogenesis) and new capillary networks also develop (a process called angiogenesis)
VIII. Cardiac Efficiency
A. Definition: the amount of work done per amount of energy consumed
B. The heart has a low efficiency (about 14%)
C. Efficiency can be improved with exercise
IX. Substrate Utilization
A. The heart uses whatever you give it
B. Substrate uptake is proportional to arterial concentration
C. Specifics
1. Carbohydrates account for 35-40%
2. Fatty acids account for 60% (especially during times of fasting)
3. During ischemia or hypoxia, the heart prefers glucose as a fuel
a. Why? Because you get the most ATP per O2 consumed
X. End of Lecture Questions
A. The true statement is D. (Coronary artery blood flow is proportional to myocardial oxygen demands)
B. Endothelin (E) causes an increase in coronary resistance- the rest cause a decrease in resistance