Why are collateral coronary arteries not a great solution to overcoming myocardial ischemia?
The collateral arteries branch off of the main arteries upstream where occlusion would block all downstream flow.
What happens to coronary blood flow differ at rest vs while exercising?
At rest it is about 1mL/min per gram of myocardium and can increase to 3-4mL/min per gram.
A patient comes to see you because he has pain in his chest while exercising. You diagnose him with angina pectoris and order a myocardial perfusion scan which is seen below. What do these results tell you?
During exercise the patient has decreased blood flow to the apex of the heart that gets better with rest. This leads you to the interventricular branch of the left coronary artery (LAD).
How do you determine the amount of oxygen being delivered to the myocardium?
Coronary blood flow (mL/min) x (arterial [O2] - venous [O2])
Why can you essentially eliminate the venous [O2] in the equation that determines the amount of oxygen reaching the myocardium?
The heart extracts nearly all of the oxygen out of the arterial blood and the blood is near black when it returns to the right atrium.
Why must the heart increase coronary blood flow any time exercise happens?
It cannot possibly extract any more oxygen from arterial blood than it already does. So it must increase the amount of arterial blood delivered.
How do lung diseases and anemia affect coronary blood flow?
They increase it because these conditions decrease the amount of oxygen delivered to tissue by the blood.
A patient comes to see you complaining of shortness of breath while walking followed by chest pain that radiates down her arm. What is causing her chest pain?
With heart failure, the heart has to pump faster which allows for less relaxation time during diastole. This causes back up and pulmonary congestion. When the patient walks they already have heart disease and by increasing O2 demand the heart just can't keep up, gets ischemic and feels angina pectoris.
When is myocardial ischemia no longer reversible?
What are the determinants of myocardial O2 consumption?
Heart rate, Chamber wall stress and Myocardial contractility.
What mechanisms normally control coronary blood flow?
Metabolic (O2 consumption), Physical (perfusion pressure, intramyocardial pressure, intravascular pressure) and Physiological (NO,NE).
How does heart muscle contraction stimulate vasodilation?
Adenosine is released as a byproduct of ATP dephosphorylation during contraction.
When does most coronary blood flow occur and why?
During diastole. During systole ventricular contraction collapses epicardial blood vessels and impedes flow.
Why does tachycardia often have a side effect of angina pectoris?
Decreased diastole = decreased flow through coronary vessels. Increased heart rate = increased O2 consumption.
Why does a patient with atherosclerosis have difficulties with vasodilation?
Atherosclerosis obliterates healthy endothelial cells. Healthy endothelial cells sense shear stress from blood flow, make and release NO that causes vasodilation. Without these cells, vessels stay vasoconstrictor.
At what point does coronary atherosclerosis obstruction start to cause symptoms?
70%. This is not as good of a measure of coronary heart disease as the FFR (functional flow reserve).
Why is pressure gradient lost downstream of an atherosclerotic plaque?
As blood passes the plaque it must accelerate through the narrowed space. Eddys are created which decreases pressure on the downstream side of the plaque.
How can you quantify coronary arterial obstruction?
Functional flow reserve. It is a measure of the pressure loss in the artery due to the stenosis. The if there is > 25% pressure loss the patient is at high risk for ischemic heart disease.