Acidaemia reduces cardiac output and left ventricular contractility in conscious XXXX .

@entity209 @entity26 @entity742 @entity998
We studied the effects of HCI-induced @entity209 on cardiac output, contractile function, myocardial blood flow, and myocardial @entity26 consumption in nine unanaesthetized newborn @entity742 . Through a left thoracotomy, catheters were placed in the aorta, left atrium and coronary sinus. A pressure transducer was placed in the left ventricle. Three to four days after surgery, we measured cardiac output, dP/dt, left ventricular end diastolic and aortic mean blood pressures, heart rate, aortic and coronary sinus blood @entity26 contents, and left ventricular myocardial blood flow during a control period, during @entity209 , and after the aortic pH was restored to normal. We calculated systemic vascular resistance, myocardial @entity26 consumption and left ventricular work. Acidaemia was associated with @entity998 , maximal dP/dt, and aortic mean blood pressure. Left ventricular end diastolic pressure and systemic vascular resistance increased, and heart rate did not change significantly. The reduction in myocardial blood flow and @entity26 consumption was accompanied by fall in cardiac work. Cardiac output returned to control levels after the pH had been normalized but maximal dP/dt was incompletely restored. Myocardial blood flow and @entity26 consumption increased beyond control levels. This study demonstrates that HCI-induced @entity209 in conscious newborn @entity742 is associated with a @entity998 which could have been mediated by the reduction in contractile function and/or the increase in systemic vascular resistance. The decreases in myocardial blood flow and @entity26 consumption appear to reflect diminished cardiac work. The restoration of a normal cardiac output after normalization of the pH appears to have resulted from the increases in heart rate and left ventricular filling pressures in conjunction with an incomplete restoration of contractile function.
