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A 72-year-old woman is admitted to the intensive care unit (ICU) with a 9-hour history of left-sided weakness and tachypnea. She has had hypertension for over 15 years. There is no history of current chest pain or previous neurologic illness. Physical examination shows that she is awake and mildly lethargic. Pulse is regular at 80 bpm. Blood pressure is 210/110 mm Hg in both arms. Respiratory rate is 34 breaths/min. Temperature is 37°C. There is no pallor or jaundice. Jugular venous pressure is not elevated. Carotid pulses are brisk. Lungs show rales bilaterally. Cardiac examination shows normal heart tones without murmur. There is an S3 gallop. Abdomen is soft without mass. There is no peripheral edema. Neurologic examination shows the patient to be lethargic. There is a left hemiparesis.

Laboratory shows normal complete blood cell count and chemistry profile. Serum B-natriuretic peptide (BNP) is elevated at 700 pg/mL. Serum troponin I is elevated at 0.10. Electrocardiogram (ECG) shows sinus rhythm with left ventricular hypertrophy and repolarization abnormality. Chest radiography shows cardiomegaly with signs of pulmonary edema. Emergency computed tomography scan of the head shows signs of acute right hemisphere ischemic infarction.


What are the initial steps in the therapy for this patient's cardiac and medical illness?


This patient has evidence of an acute cerebrovascular accident involving the right hemisphere. In addition, tachypnea, pulmonary rales, and S3 gallop on examination are consistent with the diagnosis of heart failure, which is confirmed by abnormalities of the chest radiograph and serum BNP level. The immediate goals of therapy for heart failure are to improve dyspnea, optimize blood pressure, reduce lung congestion, and improve cardiac output. Medical treatments to reverse or prevent myocardial injury are instituted, and a search for reversible causes of heart failure needs to occur (see the box below). Drug therapy is initiated in order to improve hemodynamic status while preserving neurologic and renal function. Therapies should not increase the risk of myocardial ischemia and necrosis or promote the occurrence of arrhythmia. Careful serial assessment of patient status is mandatory to guide pharmacologic therapy following signs of heart failure on physical examination. Pulmonary rales, S3 gallop, elevated jugular venous pressure, urine output, and pulse oximetry are important signs to follow.


Unlike chronic systolic heart failure, there is a paucity of controlled study data and few evidence-based guidelines for the treatment of acute heart failure. Strategies are based on small studies, experience, observation, and consensus of opinion. Initial therapies include supplemental oxygen and assessment of the need for ventilatory assistance with external positive airway pressure (continuous positive airway pressure or bilevel positive airway pressure) or endotracheal intubation with mechanical ventilation. External positive pressure ventilation improves oxygenation and pulmonary compliance and decreases work of breathing. This may prevent the need for endotracheal intubation. The latter may be required for patients with severe hypercapnia, acidosis, and respiratory muscle fatigue.1



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