Contribution of left ventricle and small bowel in irreversible hemorrhagic shock

¹ Department of Medicine, Seton Hall College of Medicine; Thomas J. White Cardiopulmonary Institute; and B. S. Pollak Hospital for Chest Diseases, Jersey City, New Jersey

To determine if alterations taking place in the heart itself contribute to the development of an irreversible stage in hemorrhagic shock, 16 intact anesthetized dogs were bled until mean arterial blood pressure reached 30 mm Hg; the blood was reinfused 4–5 hr later, and the animals were observed for an additional 7 hr or until demise. The ratio of maximal systolic rate of left ventricular pressure rise (MRPR) (in mm Hg/sec) to end-diastolic pressure (LVEDP) was used as an index of contractility. All animals exhibited a rise in contractility within 90 min, but in nine dogs who developed irreversible shock there occurred a progressive rise in LVEDP beginning at 2 hr of hypotension. Simultaneously there was a rise in transaminases (SGOT) level in coronary sinus blood, presumably due to muscle necrosis. Contractility was not restored after reinfusion and declined until death. No decrease in contractility was found in seven dogs whose circulatory failure proved to be reversible except for a brief period following retransfusion. Enterectomy, reported to protect against irreversibility, was performed in five additional dogs. An early decline in contractility, which progressed until demise, indicated that bowel pathology was not essential for irreversible shock. Thus, it would appear that an early decline in ventricular function, initiated within the first 2 hr of hypotension, reflects a potential contribution of the heart to the development of an irreversible stage in hemorrhagic shock.

Key Words: irreversible shock • reversible shock • left ventricular end-diastolic pressure • left ventricular contractility in oligemic shock • enterectomy and shock • cardiac enzyme release

Submitted on October 21, 1964