P041: TREATMENT OF LIFE THREATENING PULMONARY EMBOLISM: THE ANESTHESIOLOGISTâS PERSPECTIVE.
Ferenc Rabai, MD, Lawrence Caruso, MD; University of Florida
Introduction: Massive pulmonary embolism (PE) is associated with acute right heart failure and life-threatening cardiorespiratory compromise. Systemic thrombolytic therapy is the mainstay of treatment. However, when this is contraindicated or not effective, patients may present emergently for catheter-guided interventional therapies (e.g. intraarterial thrombolysis, mechanical- and suction thrombectomy). The combination of the serious pathophysiological derangements and the availability of various interventional techniques creates a management conundrum. In this case report we highlight important issues and management considerations of this disease process from the anesthesiologist’s perspective.
Case: A 61 year old female that had a right basal ganglia hemorrhagic stroke 3 weeks prior presented with respiratory distress (Fig. 1). She had sinus tachycardia, hypotension, tachypnea, troponinemia and type 1 respiratory failure with hypoxemia and hypocapnia. Computed tomography angiogram (CTA) showed large clot burden in bilateral proximal pulmonary arteries with signs of right heart strain and severely reduced blood flow, diagnostic of massive PE (Fig. 2 and Fig. 3). Due to her recent stroke, she was not a candidate for systemic thrombolysis or surgical thrombectomy. Therefore emergent catheter-guided thrombectomy was indicated. No sedation was administered in order to maximize patient cooperation and avoid the detrimental effects of positive pressure ventilation (PPV), but one hour into the procedure general endotracheal anesthesia needed to be induced due to progressive dyspnea, hypotension and agitation. Epinephrine, milrinone and vasopressin infusions were titrated and inhaled nitric oxide was added to maintain hemodynamics and optimize pulmonary blood flow. An increase in deadspace caused by mechanical ventilation resulted in impeded gas exchange and severe respiratory acidosis with a PaCO2-EtCO2 gradient approaching 75mmHg, but the patient was deemed not a candidate for extracorporeal membrane oxygenation (ECMO). The patient suffered PEA cardiac arrest twice in conjunction with suction thrombectomy but was resuscitated successfully both times. Despite repeated attempts at thrombectomy there was only modest improvement in blood flow (Fig. 4). Therefore a single dose of intraarterial tPA (25 mg) was administered after carefully balancing the added risks associated with her recent stroke. Fortunately, the patient improved postoperatively in the ICU and follow-up CTA showed reduced clot burden bilaterally. Patient was discharged two weeks later. Echocardiogram one month later showed no evidence of pulmonary hypertension.
Discussion: The severely compromised right heart function and reduced cardiac output in patients with massive PE increases the risk for hemodynamic instability in response to even small doses of sedatives and anesthetic medications. Although maintenance of spontaneous breathing is critical in preserving cardiac preload and gas exchange, intubation and PPV may be unavoidable during catheter-guided procedures. Careful selection of agents for anesthetic induction and hemodynamic support to optimize inotropy and pulmonary blood flow is vital. Catheter-guided thrombectomy maneuvers are geared towards resolving proximal obstruction, but may cause sudden and profound hemodynamic perturbations leading to cardiac arrest. A thorough understanding of the interplay between these catheter-guided interventions and the brittle hemodynamic state of massive PE in conjunction with careful anesthetic management and aggressive hemodynamic support including contingency planning for ECMO are vital elements for achieving optimal outcomes.