Afterload reduction with phentolamine in patients with acute pulmonary edema.

Phentolamine in amounts of 10 to 40 microgram/kg/min was infused intravenously for the emergency treatment of acute pulmonary edema due to left ventricular failure. Fourteen patients with arteriosclerotic heart disease, ranging in age from 52 to 87 years, had clinical and roentgenographic signs of pulmonary edema. The pulmonary artery wedge pressure was increased to an average of 24 mm Hg and the cardiac index was decreased to 1.9 liters/min/m2 or less prior to the administration of phentolamine. A reduction in the pulmonary artery wedge pressure to 14 mm Hg and an increase in the cardiac index to 2.5 liters/min/m2 was observed in response to this alpha adrenergic blocking agent. Reduction in peripheral resistance with phentolamine was associated with reversal of pulmonary edema.

Oxygen delivery, anoxic metabolism and hemoglobin-oxygen affinity (P50) in patients with acute myocardial infarction and shock.

Changes in systemic oxygen delivery after acute myocardial infarction were investigated in 21 patients. In seven patients with shock, circulatory failure was characterized by a significant reduction in cardiac index, a decrease in oxygen transport and oxygen consumption and an increase in concentration of blood lactate; a decrease in the affinity of hemoglobin for oxygen (increased P50) was also noted. The P50 averaged 28.8 plus or minus 0.87 (standard error of the mean) torr in patients with shock and 26.0 plus or minus 0.45 torr (P less than 0.05) in patients without circulatory failure. However, there was no significant difference in oxygen extraction from arterial blood between the two groups. The time course of the changes in P50, cardiac index and oxygen consumption was separately examined in 12 patients. In six patients with shock, P50 increased by an average of 4.6 plus or minus 2.05 torr (P less than 0.05) and this augmentation accounted for an estimated 18 percent increase in oxygen release. Maximal P50 values were observed after 24 hours of circulatory failure. In the absence of shock, no consistent changes in P50, cardiac index or oxygen consumption were observed. These data indicate that a reduction in oxygen delivery after acute myocardial infarction is followed by a compensatory increase in P50. This change in P50 accounts for increases in oxygen availability independently of changes in cardiac output.

Relationship between pulmonary hemodynamics and arterial pH and carbon dioxide tension in critically ill patients.

To ascertain the clinical significance of derangements in arterial pH and arterial carbon dioxide tension (PaCO2) in modifying pulmonary arterial pressures and pulmonary vascular resistance in critically ill patients, the relationship between these two sets of variables was evaluated in 75 patients. No significant differences in pulmonary hemodynamic values were found among patients with acidemia, a normal pH, or alkalemia, even at extreme pH values; and there was no consistent relationship between PaCO2 and each of the pulmonary hemodynamic measurements. In patients who initially had a normal pH but subsequently developed acidemia or alkalemia, there was also no significant correlation between changes in pH and pulmonary hemodynamic values. We conclude that abnormalities of pulmonary hemodynamic values in seriously ill patients are usually due to factors other than acid-base derangements. Of practical importance is the observation that the predictability of the pulmonary arterial wedge pressure from the pulmonary arterial diastolic pressure is not invalidated by acid-base disturbances.

Oxygen transport, consumption and utilization during barbiturate intoxication.

Factors related to oxygen availability and requirements were measured on 51 occasions in 14 patients intoxicated with short-acting barbiturates. Patients had no clinical signs of circulatory shock. The cardiac index was normal (3.4 +/- 1.1 1/min/m2) but there was a slight decrease of the mean arterial oxygen content (17.2 +/- 3.0 ml/100 ml). Oxygen transport was normal (571 +/- 199 ml/min/m2). However, the arteriovenous oxygen differences were decreased (3.4 +/- 1.0 ml/100 ml). Oxygen consumption was reduced (110 +/- 42 ml/min/m2) and the oxygen extraction ratio (oxygen consumption/oxygen transport) was decreased (0.20 +/- 0.05), thus confirming a decreased oxygen utilization. Arterial concentration of lactate was normal. Accordingly the observed decrease in oxygen consumption was related to a reduction in oxygen requirements during barbiturate intoxication rather than due to an imbalance between availability and metabolic requirements for oxygen.