Effects of systemic-pulmonary shunts on regional myocardial blood flow in experimental pulmonary stenosis.
The pulmonary artery of anesthetized dogs was constricted until right ventricular failure occurred (decreased cardiac output and aortic blood pressure; elevated right ventricular end-diastolic pressure). Coronary blood flow distribution was measured by means of an electromagnetic flowmeter and radioactive microspheres. With moderate levels of pulmonary stenosis (right ventricular pressure to 60 per cent of systemic pressure), right ventricular coronary flow increased (30 per cent, p smaller than 0.01) despite a significant fall in right ventricular driving pressure (aorto-right atrial pressure). Right ventricular failure occurred when right ventricular coronary flow did not increase sufficiently to meet raised oxygen requirements. Opening a pulmonary-systemic shunt during right ventricular failure increased pulmonary blood flow but lowered coronary driving pressure further, as blood was diverted into the lungs through the low-resistance fistula. Consequently, right ventricular coronary flow fell 50 per cent (p smaller than 0.01) and right ventricular failure with pulmonary stenosis resulted in a 362 per cent (p smaller than 0.01) increase in right coronary flow plus improved cardiac output. We made the following conclusions: (1) Right ventricular failure with pulmonary stenosis and intact ventricular septum is due to inadequate right ventricular blood flow to meet raised oxygen demands; (2) opening a pulmonary-systemic shunt may potentiate this failure and exaggerate ischemia by lowering coronary driving pressure and reducing right ventricular coronary flow.
D000818:Animals; D002302:Cardiac Output; D002306:Cardiac Volume; D003326:Coronary Circulation; D003327:Coronary Disease / Q000378:metabolism / Q000503:physiopathology*; D003331:Coronary Vessels / Q000503:physiopathology*; D004285:Dogs; D006333:Heart Failure / Q000378:metabolism / Q000503:physiopathology*; D006439:Hemodynamics; D006801:Humans; D007223:Infant; D009206:Myocardium / Q000378:metabolism; D010101:Oxygen Consumption; D011651:Pulmonary Artery / Q000503:physiopathology*; D011652:Pulmonary Circulation; D011666:Pulmonary Valve Stenosis / Q000503:physiopathology*; D011877:Radionuclide Imaging; D014655:Vascular Resistance