No abstract

To evaluate hemodynamic, angiographic, and biological effects of a single bolus of urokinase, an open descriptive trial was conducted in a homogeneous group of 14 patients with acute life-threatening pulmonary emboli and without prior cardiopulmonary disease. For every patient the efficacy of the treatment was evaluated by comparing control and posttherapeutic values after the bolus injection of 15,000 IU/kg body weight urokinase (urinary source) administered in 10 min in the right atrium, followed by continuous intravenous full-dose heparin therapy. In two patients clinical status, hemodynamics, vascular obstruction, and biological (fibrinogen and plasminogen levels) parameters remained unchanged. One of these two patients died, making the mortality rate for the whole group 7%. Twelve of 14 patients showed rapid clinical improvement. Evaluation at 12 hr demonstrated significant decreases in pulmonary vascular obstruction (Miller index, 34%), total pulmonary vascular resistances (37%), and fibrinogen and plasminogen levels (41% and 40%, respectively), without any significant change in cardiac index. The hemodynamic sequential measurements performed (1, 3, 6, and 12 hr) in seven of the 12 improved patients showed that the greatest percentage of the total hemodynamic improvement occurred within the first 3 hr after bolus administration of urokinase. No severe hemorrhagic complications were observed. Because of its rapid efficacy and its low cost, the bolus technique appeared particularly useful in the treatment of patients with acute life-threatening pulmonary emboli.Circulation 70, No. 5, 861-866, 1984. SEVERE, life-threatening pulmonary emboli associated with clinical shock, right ventricular failure, seizures, or syncope require early, rapid, and effective therapy.Under

No abstract

The haemodynamic changes following the administration of morphine 0.15 and 0.30 mg kg" 1 i.v. were studied in 11 patients, free from known cardiac disease. All patients were acutely ill and their lungs were being ventilated mechanically. In those patients receiving 0.15 mg kg" 1 , the only haemodynamic change was a slight and transitory decrease in the systolic arterial pressure. In contrast, several changes were observed in patients receiving 0.30 mg kg" 1 : an immediate and prolonged decrease in the cardiac index was noted along with transient decreases in heart rate, stroke volume index, arterial pressure and left stroke work index. These results suggest that the haemodynamic cost of morphine 10 mg is negligible but could be significant when 20 mg has been administered and must be weighed against its beneficial effects in the critically ill patient.