Use Vasopressors Instead of Large-Volume Resuscitation in the Treatment of Shock from Massive Pulmonary Embolism Andrew L. Rosenberg MD Massive pulmonary embolism (PE) occurs when more than 50% of the pulmonary circulation is acutely obstructed by a venous embolus, usually originating in the lower extremities. In massive PE, severe hemodynamic derangements result from pulmonary artery obstruction; profound pulmonary vasoconstriction due to local mediator release; and hypoxemia-induced vasoconstriction. The resulting increased right ventricular (RV) afterload results in acute right ventricular dilatation as the normally thin-walled RV is tasked with overcoming high pulmonary vascular resistance. Other consequences of acutely increased RV pressures include tricuspid regurgitation and sometimes a significantly shifted intraventricular septum. This can lead to impaired left ventricular (LV) filling and ultimately decreased cardiac output and hypotension. In addition, decreased aortic diastolic pressures and increased RV pressure may result in RV ischemia due to poor coronary perfusion, further reducing RV work and exacerbating the shock state. This scenario may occur so rapidly that the patient immediately experiences syncope or death manifested by pulseless electrical activity. The diagnosis of this physiological process is made by recognizing the clinical scenario of an acutely ill patient, with agitation, dyspnea, shock, and hypoxemia in an appropriate host with risk factors for deep venous thrombosis including immobility, major surgeries, bed rest, malignancy, family history, oral contraceptives use, and/or trauma. Usually, in massive PE, there is scant time for confirmatory tests; often the patient is too unstable for transport. However, a variety of modalities exist if time permits, the patient is stable, and the clinical situation is uncertain. Probably the most important noninvasive exam would be an emergent computed tomography (CT) scan to both suggest and/or rule out other mimics of PE. Other tests that can be used to suggest the presence of a PE are an echocardiogram, arterial blood gases (may reveal hypoxemia and hypocarbia due to increased minute ventilation), and a d-dimer (may be of some value in ruling out a PE if it is negative, although a positive does not confirm the diagnosis in all cases). What to Do The usual initial treatment for suspected or confirmed massive pulmonary embolism is intravenous (IV) fluid administration. An initial bolus of 500 mL to 1,000 mL of isotonic crystalloid may be especially helpful if/when patients are intubated with resulting decrease in right ventricular preload due to increased intrathoracic pressures from positive pressure ventilation. However, intravenous fluids, especially if given too quickly or in too large a volume, may worsen RV dilatation, increase RV wall stress, decrease RV perfusion, and shift the ventricular septum leftward, resulting in decreased LV output and worsening the cycle of RV failure. An alternative treatment is to judiciously initiate a vasoconstrictor with some inotropic effect, such as norepinephrine at 0.05 to 0.2 mcg/kg/min or perhaps dopamine at 5 to 15 mcg/kg/min. Several animal studies have suggested that these agents improve systemic blood pressure, cardiac output, pulmonary vascular resistance, and right ventricular pressure compared with volume resuscitation alone in models of massive PE. Ultimately, thrombolytic agents, surgical or interventional radiologic clot removal, and/or anticoagulation are the treatments of choice in the setting of massive pulmonary embolism with hypotension and/or severe hypoxemia. Source:Avoiding Common ICU Errors, 1st Edition Copyright 2007
Posted on: Thu, 12 Sep 2013 21:01:02 +0000