Myocardial Flow & Oxygen Supply
Vessels on the epicardial surface of the heart are considered to be conductance vessels and under normal conditions offer little resistance for blood flow and perfusion.
The four factors influencing blood flow and resistance dynamics for intramural coronary vasculature are: aortic root pressure, extravascular compression, myocardial metabolic requirement, and neural control.
Aortic root pressure represents the driving force for coronary blood flow. Extravascular compression affects subendocardial and intramural perfusion during diastole and is sensitive to changes in preload, inotropic stimulation, and heart rate. Myocardial oxygen consumption stimulates increased coronary blood flow while autonomic stimulation of sympathetic (vasoconstriction) or parasympathetic (vasodilation) interact to impact supply and demand.
The pressure gradient facilitating perfusion through the myocardium is maintained by the balance of the driving force at the proximal coronaries (aortic end-diastolic pressure) overcoming native resistance (wall resistance, coronary sinus resistance, and left ventricular end-diastolic pressure) thus providing antegrade flow. Anesthetic measures should incorporate efforts to reduce left ventricular end-diastolic pressure while increasing the diastolic arterial blood pressure.
Constant coronary perfusion is maintained by autoregulation. Anemic states, coronary artery stenosis, hypotension, and hypertension can create an environment that exceeds the limits of autoregulation to meet accelerated myocardial oxygen demand. Aortic root diastolic pressure then becomes the driving force for coronary perfusion under these circumstances. Hypotension associated with coronary artery stenosis should be avoided as it may lead to hypoperfusion refractory to decreased vasodilatory reserve, decreased diastolic perfusion pressure, and increased resistance in the coronary vessels.
Tachycardia-induced reductions in diastolic filling time are significant considering that diastolic perfusion provides the majority of blood flow to the epicardial, endocardial, and subendocardial regions of the left ventricle, while the right ventricle receives a portion of it’s coronary blood supply during systole. This role in attenuating diastolic intervals makes tachycardia detrimental during the course of treatment for the cardiac patient.
While subendocardial and sub-epicardial layers have the same determinants for blood flow, subendocardial layers are at greater risk from ischemia and infarction.
The deeper subendocardium is subjected to greater wall tension which then expresses as a metabolic requirement 10-20% greater than the more superficial epicardium. Higher oxygen demand and greater resistance to flow, diminishes the vasodilatory reserve in this layer making it vulnerable and pressure dependent when perfusion pressures fall below 70 mm Hg. In conditions such as coronary stenosis where a pressure drop dictates pressure mediated flow to the subendocardium, blood flow to the epicardium may still be autoregulated (assuming a pressure in the outer layer of 40-60 mm Hg) and facilitate transmural coronary steal of blood flow to the epicardium.
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