PULMONARY CIRCULATION IN LOW CARDIAC OUTPUT SYNDROME FOLLOWING OPEN HEART SURGERY

  • KUMON KEIJI
    Department of Intensive Care Unit and Cardiovascular surgery, National Cardiovascular Center, Associate director of Intensive care unit
  • TANAKA KAZUHIKO
    Department of Intensive Care Unit and Cardiovascular surgery, National Cardiovascular Center, Director of Intensive care unit
  • NAKAJIMA NOBUYUKI
    Department of Intensive Care Unit and Cardiovascular surgery, National Cardiovascular Center, Director of vascular surgery
  • NAITO YASUAKI
    Department of Intensive Care Unit and Cardiovascular surgery, National Cardiovascular Center, Director of cardiac surgery
  • FUJITA TSUYOSHI
    Department of Intensive Care Unit and Cardiovascular surgery, National Cardiovascular Center, Chief director of cardiovascular surgery

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The pulmonary circulation of 41 patients with low cardiac output syndrome (LOS) in the recovery period following open heart surgery was studied. Cardiac indices (CI) of these patients in LOS was 1.64±0.28 (Mean ± SD) L/min・m^2 and increased to 2.60±0.50 L/min・m^2 after the stabilization of hemodynamic conditions. Mean pulmonary arterial pressure, pulmonary arteriolar resistance index (PARI) and total pulmonary resistance index (TPRI) in the condition of LOS were very high and significantly decreased after recovery from LOS, although the mean left atrial pressure showed no significant change. The correlation coefficient (r) between CI and PARI was found to be -0.574. High Pao_2 with reductions of alveolar-arterial oxygen tension difference (A-aDo_2) and physiological pulmonary shunt ratio (Qs/Qt) in LOS significantly decreased concomitant with significant increases in both A-aDo_2 and Qs/Qt after the stabilization of the hemodynamic condition. Moderate correlations were obtained between CI and Pao_2 (r=-0.478), and high correlations were established between CI and physiological pulmonary shunt flow Q^^.ps) (r=0.747). These studies showed that pulmonary vaso-construction was playing a major role in the elevation of pulmonary vascular resistance in LOS, which eventually leads to the reduction of intrapulmonary shunting.

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