PROLONGED CONTROLLED HEMORRHAGIC SHOCK IN LARGE ANIMALS - POTENTIAL FOR VENTRICULAR ASSIST SUPPORT?:

Despite novel pharmacological strategies and modified protocols for aggressive fluid resuscitation management, the event of prolonged hemorrhagic shock still represents a life-threatening event resulting in high mortality rates. Purpose of the experimental study was a) to develop a hemorrhagic shock model in large animal species which leads to a delayed death despite pharmacological intervention within 24 hours (hrs); b) to investigate the possibility of a potential benefit of acute implantation of a left ventricular assist device (LVAD). Methods: Domestic swine (n=13) underwent surgery including removal of the spleen. The animals were instrumented with flow probes on the cranial mesenteric artery (SMA) and left ascending coronary artery (LAD). Additionally, complete invasive hemodynamic monitoring was established. Hemorrhage was induced by extraction of arterial blood from the carotid artery to a mean pressure (MAP) of either 35mmHg (Group I, n=3) or 40mmHg (n=10) over a 30min period. After an additional 30min to simulate response time, fluid resuscitation was initiated (crystalloid solution: blood loss = 2:1). In the MAP40 group, pigs received either fluid resuscitation only (Group II) or underwent implantation of a left ventricular assist device (LVAD, Group III, n=5 each). Results: During hemorrhage, a total blood volume of 1037±212 cc (I), 862±387 cc (II), and 681±117 cc (III) was extracted [pI-III < .05]. Shorter survival was observed in Group I (230±25.5 min) vs. Group II (709±251 min; pI-II < .05) and vs. Group III (662±428 min; pI-III < .05; pII-III=n.s.). Cause of death in most animals was due to cardiac arrhythmias. Blood parameters increased in all animals progressively: creatinine 2.3±0.3 mg/dL, lactic acid 50.1±28.4 mg/dL, SGPT 48.4±23.9 U/L (after 6 hrs), indicating the severity of shock. Although similar amounts of fluids were given over 5 hrs, LAD flow in the non-pump group (II) was fairly constant (51±24cc), but increased in the pump group (74±28cc; n.s.). The SMA flow reached baseline level (495±191cc; II) or was even elevated (750±446cc; III; n.s., 5 hrs each). The cardiac output in both groups did not differ significantly. Interestingly, we found a significant difference in SGOT levels between groups II and III (750±135 U/L, II vs. 359±157 U/L, III; p < .005). Summary: We developed a pressure-fixed hemorrhagic shock model in pigs which is prolonged, reproducible, and leads to certain death despite the use of drugs and fluid resuscitation. This large animal model represents an excellent opportunity to investigate future therapeutic approaches including the use of ventricular assist systems to prevent further progression of shock consequences.