ACUTE PULMONARY-EMBOLISM - CLINICAL, PATHOPHYSIOLOGICAL, DIAGNOSTIC, AND THERAPEUTIC ASPECTS

Pulmonary embolism must often be considered as a differential diagnosis, especially in the perioperative period. Only prompt therapeutic measures can reduce the high early mortality in the acute phase of this condition. Diagnostic and therapeutic measures are dependent on the severity of the symptoms. If pulmonary embolism is suspected, heparin is administered. In the case of cardiovascular deterioration, other measures have to be taken. Following confirmation of the diagnosis of pulmonary embolism, several thrombolytic regimens are applicable. Low-dose urokinase (bolus 250,000 U followed by 60,000-80,000 U/h) is associated with a relatively low incidence of bleeding complications. A more rapid reduction of the right ventricular afterload will be achieved via short-term thrombolysis. Newer findings suggest that bolus thrombolysis with 3 million U urokinase is as effective as 100 mg tissue plasminogen activator (rt-PA) administered over a 2-h period. When the patient is found to be in a state of shock, confirmation of the diagnosis has to be delayed. Recommendations include the bolus application of 1.5-3 million U urokinase when right ventricular decompensation is prominent or during cardiopulmonary resuscitation. In case of existing contraindications or postoperatively, low-dose urokinase treatment (bolus 250,000 U followed by 40,000-60,000 U/h, rarely up to 2,200 U/kg per hour) may be initiated when the situation is urgent and there are no treatment alternatives. Bolus application of 1-2 million U urokinase should be considered depending on the severity of the symptoms and the underlying disease. In some hospitals, alternative treatment modalities include catheter-assisted procedures with subsequent local thrombolysis and surgical embolectomy. Pathophysiological aspects as well as therapeutic options in the intensive care unit are discussed in depth. In addition to adequate oxygenation, right ventricular coronary perfusion and contractility may be maintained using various catecholamine infusions. The importance of phosphodiesterase inhibitors, mediator antagonists such as acetylsalicylic acid or ketanserin, and dilators of the pulmonary vascular bed are discussed.