• Am. J. Cardiol. · Jun 1990

    Hemodynamic and oxygen transport variables in cardiogenic shock secondary to acute myocardial infarction, and response to treatment.

    • J E Creamer, J D Edwards, and P Nightingale.
    • Intensive Care Unit, University Hospital of South Manchester, United Kingdom, England.
    • Am. J. Cardiol. 1990 Jun 1; 65 (20): 1297-300.

    AbstractThere are few data on oxygen transport in cardiogenic shock after acute myocardial infarction. This prospective study examined oxygen transport variables in 19 such patients and assessed their responses to treatment. Femoral and pulmonary arterial catheters were inserted before any therapy except correction of hypoxemia by mechanical ventilation in 8 patients, defibrillation (3 patients) or pacing (5 patients). In 3 patients mean arterial pressure was greater than 80 mm Hg and cardiac index greater than 2.1 liters/min/m2 with normal mixed venous oxygen saturation despite simultaneous clinical shock. They recovered with no further treatment. Sixteen patients were treated with varying combinations of intravenous fluids and dobutamine (37 +/- 25 mu/kg/min) and 14 survived long enough for a second set of measurements to be completed. Mean heart rate increased from 83 +/- 22 to 101 +/- 20 beats/min and mean cardiac index from 1.4 +/- 0.5 to 2.5 +/- 0.4 liters/min/m2 (p less than 0.001). Oxygen consumption (VO2) was maintained even when oxygen delivery (DO2) was less than 330 ml/min/m2. After treatment DO2 increased from 230 +/- 69 to 397 +/- 60 ml/min/m2 (p less than 0.001) and VO2 from 103 +/- 31 to 124 +/- 27 ml/min/m2 (p less than 0.05). Mean mixed venous oxygen saturation increased from 54 +/- 16 to 69 +/- 8% (p less than 0.001) and mean oxygen extraction ratio decreased from 48 +/- 16 to 31 +/- 6% (p less than 0.001). There was no correlation between cuff systolic blood pressure and mean arterial pressure before or after resuscitation. Thirteen patients survived to hospital discharge. When cardiogenic shock responds to treatment, large increases in DO2 lead to small increases in VO2 but large increases in mixed venous oxygen saturation, reflecting improved tissue oxygen availability.

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