From Dyspnea to Respiratory Failure in a Flash

Jessica L. Bunin, MD; Christopher J. Lettieri, MD

Disclosures

September 22, 2011

Clinical Presentation

A 66-year-old black woman was admitted to the medical wards for dyspnea. One week prior, the patient had been admitted to the same hospital with a large right-sided pulmonary embolism that was the result of prolonged immobility. She responded well to treatment with enoxaparin and was transitioning to treatment with warfarin at the time of her second admission. Her dyspnea now occurred at rest and worsened with any movement. She reported an increase from 2-pillow to 4-pillow orthopnea as well as a mild increase in her lower-extremity edema. She denied chest pain, cough, fever, weight gain, nausea, and lightheadedness.

Initially her admission was unremarkable. Her shortness of breath responded to albuterol nebulizers. Workup was initiated to determine a primary cause. The shortness of breath did not return and cardiac enzymes were negative. She was to be discharged on hospital day 3, but overnight she developed acute worsening shortness of breath that progressed to respiratory failure. She was intubated and transferred to the intensive care unit. The acute decompensation was thought to be due to recurrent pulmonary embolism vs a cardiac source. Cardiac enzymes were negative and a transthoracic echocardiogram showed good systolic function, moderate mitral regurgitation, and mild diastolic dysfunction. A repeat CT angiogram revealed only minimal resolving embolism burden. Over the next 48 hours, she did well and her ventilator settings were decreased, but on day 5 in the hospital, she again decompensated and at that time was found to have an anterior non-ST elevation myocardial infarction with a troponin peak of more than 10. She required increased ventilator settings and vasopressor support. She tolerated rapid titration of her vasopressor support, and decrease of ventilator settings was attempted once again.

The patient did well for 2 days, but on day 8 in the hospital, she developed severe hypertension (230/130 mm Hg), tachycardia (130 beats/min), tachypnea (35 breaths/min), and oxygen desaturations to the 70s. She had copious pink frothy sputum in her endotracheal tube. After maximizing her ventilator settings, she required bag-valve masking to raise her oxygen saturation above 90%. This event was managed with furosemide, nitroglycerine, labetalol, and sedation, which she initially seemed to tolerate, but she then progressed to hypotension and pulseless electrical activity arrest. She returned to normal sinus rhythm after approximately 10 minutes of cardiopulmonary resuscitation. By the next morning, the patient returned to her baseline status. No trigger was identified for this event.

Chest radiograph showed severe pulmonary edema, focal cardiac ultrasound showed good cardiac function without right ventricular strain, and cardiac enzymes were negative. Over the course of the next several days, the patient experienced 3 similar episodes of hypertension, tachycardia, and desaturation with copious frothy pink secretions. In each instance, the patient was stable without complaints 5-10 minutes prior to the episode. Minor triggers in some incidents were identified, such as laying the patient flat in bed or cleaning the patient, but other incidents had no trigger. After each episode, she became temporarily hypotensive but did not again progress to pulseless electrical activity and did not require vasopressor support.

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