Computer simulation of the hemodynamic determinants of myocardial oxygen supply and demand.
A computer program was developed that uses a mathematical model of the cardiovascular system to predict myocardial oxygen supply and demand as well as cardiac hemodynamics. This model combines the time-varying elastance model of the left ventricle, the modified Windkessel model of the arterial system, and the left ventricular pressure-volume area prediction of myocardial oxygen demand. The computer simulation permits independent control of variables, thus providing the opportunity to design "experiments" and to observe the results. The model predicts that tachycardia leads to reduced myocardial oxygen supply and increased demand. Hypertension caused by increased systemic vascular resistance increases supply more than it increases demand. On the other hand, increased contractility or left ventricular end-diastolic pressure increases demand more than supply, and may cause ischemia in the presence of coronary artery stenosis. The model is an aid in understanding how hemodynamic variables affect the balance between myocardial oxygen supply and demand. It can be used for education and to analyze study protocols prior to animal experimentation.
Schwid
H A
HA
Department of Anesthesiology, University of Washington, Seattle.
Buffington
C W
CW
Strum
D P
DP
D000818:Animals; D001011:Aorta / Q000502:physiology; D001794:Blood Pressure / Q000502:physiology; D002302:Cardiac Output / Q000502:physiology; D002306:Cardiac Volume / Q000502:physiology; D003198:Computer Simulation; D003326:Coronary Circulation / Q000502:physiology; D003327:Coronary Disease / Q000503:physiopathology; D003331:Coronary Vessels / Q000502:physiology; D006339:Heart Rate / Q000502:physiology; D006439:Hemodynamics; D006801:Humans; D007022:Hypotension / Q000503:physiopathology; D008955:Models, Cardiovascular; D009200:Myocardial Contraction / Q000502:physiology; D009206:Myocardium / Q000378:metabolism*; D010101:Oxygen Consumption / Q000502:physiology*; D013610:Tachycardia / Q000503:physiopathology; D014655:Vascular Resistance / Q000502:physiology; D016277:Ventricular Function, Left / Q000502:physiology