4.7 Article

Early Cardiac Arrest in Patients Hospitalized With Pneumonia A Report From the American Heart Association's Get With the Guidelines-Resuscitation Program

Journal

CHEST
Volume 141, Issue 6, Pages 1528-1536

Publisher

AMER COLL CHEST PHYSICIANS
DOI: 10.1378/chest.11-1547

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Funding

  1. National Institutes of Health
  2. National Heart, Lung, and Blood Institute [K23 HL097157-01]

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Background: Pneumonia is the leading infectious cause of death. Early deterioration and death commonly result from progressive sepsis, shock, respiratory failure, and cardiac complications. Recent data suggest that cardiac arrest may also be common, yet few previous studies have addressed this. Accordingly, we sought to characterize early cardiac arrest in patients who are hospitalized with coexisting pneumonia. Methods: We performed a retrospective analysis of a multicenter cardiac arrest database, with data from >500 North American hospitals. We included in-hospital cardiac arrest events that occurred in community-dwelling adults with pneumonia within the first 72 h after hospital admission. We compared patient and event characteristics for patients with and without pneumonia. For patients with pneumonia, we also compared events according to event location. Results: We identified 4,453 episodes of early cardiac arrest in patients who were hospitalized with pneumonia. Among patients with preexisting pneumonia, only 36.5% were receiving mechanical ventilation and only 33.3% were receiving infusions of vasoactive drugs prior to cardiac arrest. Only 52.3% of patients on the ward were receiving ECG monitoring prior to cardiac arrest. Shockable rhythms were uncommon in all patients with pneumonia (ventricular tachycardia or fibrillation, 14.8%). Patients on the ward were significantly older than patients in the ICU. Conclusions: In patients with preexisting pneumonia, cardiac arrest may occur in the absence of preceding shock or respiratory failure. Physicians should be alert to the possibility of abrupt cardiopulmonary collapse, and future studies should address this possibility. The mechanism may involve myocardial isehemia, a maladaptive response to hypoxia, sepsis-related cardiomyopathy, or other phenomena. CHEST 2012; 141(6):1528-1536

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