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JOURNAL ARTICLE
RESEARCH SUPPORT, NON-U.S. GOV'T
Cardiopulmonary manifestations of hantavirus pulmonary syndrome.
Critical Care Medicine 1996 Februrary
OBJECTIVE: To describe the clinical characteristics of a group of patients infected with the newly recognized hantavirus in the Southwestern United States.
DESIGN: Case series.
SETTING: Tertiary referral center.
PATIENTS: All patients with confirmed hantavirus infection admitted to the University of New Mexico Hospital between May 1, 1993 and January 1, 1994.
INTERVENTIONS: Records of patients with hantavirus infection were reviewed to collect all pertinent clinical data.
MEASUREMENTS AND MAIN RESULTS: Pulmonary disease in these patients was characterized by hypoxemia covering a wide range of severity. The cause of hypoxemia was an increased permeability (noncardiac) pulmonary edema which could be differentiated from hydrostatic (cardiac) pulmonary edema by its association with low pulmonary artery occlusion pressures and increased protein content of edema fluid. Hemodynamic measurements in severe cases showed a shock state characterized by a low cardiac index (range 1.6 to 3.0 L/min/min2), a low stroke volume index (range 10.5 to 29 mL/m2), and high systemic vascular resistance index (range 1,653 to 2,997 dyne.sec/cm5.m2). Progression to death was associated with worsening cardiac dysfunction unresponsive to treatment and causing oxygen debt and lactic acidosis.
CONCLUSIONS: The two major life-threatening pathophysiologic changes in Hantavirus Pulmonary Syndrome are increased permeability pulmonary edema, and an atypical form of septic shock caused by myocardial depression and hypovolemia.
DESIGN: Case series.
SETTING: Tertiary referral center.
PATIENTS: All patients with confirmed hantavirus infection admitted to the University of New Mexico Hospital between May 1, 1993 and January 1, 1994.
INTERVENTIONS: Records of patients with hantavirus infection were reviewed to collect all pertinent clinical data.
MEASUREMENTS AND MAIN RESULTS: Pulmonary disease in these patients was characterized by hypoxemia covering a wide range of severity. The cause of hypoxemia was an increased permeability (noncardiac) pulmonary edema which could be differentiated from hydrostatic (cardiac) pulmonary edema by its association with low pulmonary artery occlusion pressures and increased protein content of edema fluid. Hemodynamic measurements in severe cases showed a shock state characterized by a low cardiac index (range 1.6 to 3.0 L/min/min2), a low stroke volume index (range 10.5 to 29 mL/m2), and high systemic vascular resistance index (range 1,653 to 2,997 dyne.sec/cm5.m2). Progression to death was associated with worsening cardiac dysfunction unresponsive to treatment and causing oxygen debt and lactic acidosis.
CONCLUSIONS: The two major life-threatening pathophysiologic changes in Hantavirus Pulmonary Syndrome are increased permeability pulmonary edema, and an atypical form of septic shock caused by myocardial depression and hypovolemia.
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