We evaluated the hemodynamic response of 12% shed blood replacement with 7.5% sodium chloride after a nonlethal hemorrhage in chronically instrumented swine. Compared to no treatment or Ringer's lactate infusion, the hypertonic salt solution was followed by increased cardiac output. We then evaluated the effect of hypertonic sodium chloride on survival after an otherwise lethal hemorrhage in chronically instrumented and unanesthetized swine. Survival was significantly greater after replacement of 25% of the shed blood with 7.5%, but not with 0.9%, 5.0%, or 10.0% sodium chloride solution. The mechanism appears to be by increased tissue perfusion as indicated by lower lactate values. Resuscitation with low-volume hypertonic sodium chloride may be life saving and life supporting during the initial treatment of trauma patients when conventional therapy is not available.

Animals↗

PubMed1987

A computer model of hemorrhagic shock in domestic swine.

We used a modified version of the computer model of the circulation developed by C.V. Greenway (Pharmacol Rev 33:213-251, 1982) to study the volume-pressure relationship of the systemic venous circulation during and immediately after massive blood loss. Our theoretical predictions were based on experimental measurements performed in conscious, chronically instrumented swine subjected to massive and rapid loss of a predetermined amount of blood. These animals were subjected to an exponential removal of either 50% of their calculated blood volume in 1 hour or a linear removal of 60% in 15 minutes. Our computer model indicates a hysteresis effect between the volume-pressure curves during and immediately following hemorrhage. The results emphasize the importance of venous capacitance changes as a compensatory response to blood loss.

Animals↗

PubMed1986

Regional blood flow during hypothermic arrest.

Little is known about the efficacy of CPR in the setting of hypothermia-induced cardiac arrest. We measured organ blood flow produced by conventional closed-chest CPR in eight swine following normothermic KCl-induced cardiac arrest and in seven swine surface-cooled until cardiac arrest occurred. Radiomicrospheres were injected in the unanesthetized basal state, after five minutes of CPR, and after 20 minutes of CPR. After five minutes of CPR, the cardiac output and cerebral and myocardial blood flows (mean +/- SD) of hypothermic animals were 15.3 +/- 7.5 mL/min/kg, 0.16 +/- 0.11 mL/min/g, and 0.20 +/- 0.15 mL/min/g, respectively. Mean percentage flows were 7%, 15%, and 8%, respectively, of those measured in the unanesthetized prearrest state, and 50%, 55%, and 31%, respectively, of the flow produced during CPR in normothermic animals. Blood flow during hypothermic CPR did not change significantly over time; however, during normothermic CPR, cardiac output and cerebral and myocardial flows decreased so that at 20 minutes there were no significant differences from those values measured in hypothermic animals. The reduction in organ flow produced by external chest compression in hypothermic animals may be a result of the changes in the viscoelastic properties of the thorax that occur during profound hypothermia.

Animals↗

PubMed1986

Small-volume infusion of 7.5% NaCl in 6% Dextran 70 for the treatment of severe hemorrhagic shock in swine.

In the initial treatment of the hypovolemic trauma patient, commonly used crystalloids have little clinical benefit in the small volumes generally infused during transport. We evaluated the efficacy of a small-volume infusion of 7.5% NaCl in 6% Dextran 70 as a treatment modality for an otherwise lethal hemorrhage in swine. Sixty chronically instrumented swine were randomized into one of four treatment groups: 0.9% NaCl (NS, n = 15), 7.5% NaCl (HS, n = 15), 6% Dextran 70 (DEX, n = 16), and 7.5% NaCl in 6% Dextran 70 (HSD, n = 14). Each animal was bled 46 mL/kg in 15 minutes. Five minutes after the completion of hemorrhage, the animals were infused with their respective treatment in a volume (11.5 mL/kg) equal to 25% of the shed blood. Of those animals receiving HSD, 100% survived until euthanized at 96 hours. In comparison, animals infused with NS, HS, and DEX had 96-hour survival values of 13%, 53%, and 69%, respectively. The survival rate of the HSD group was significantly better than that of the NS group (P less than .001) and the HS group (P less than .01). The infusion of HSD increased mean arterial pressure, PCO2, and plasma bicarbonate to a significantly greater extent than NS alone (P less than .05). These results demonstrate that a small-volume infusion of the hypertonic sodium chloride/dextran solution is superior to equal volumes of a standard crystalloid in resuscitating animals from hemorrhagic shock.

Animals↗

PubMed1986

Epidemiology of trauma: military experience.

Battle injuries sustained in conventional warfare are more likely to be lethal than are injuries sustained by civilians. Depending on the tactical situation, mortality may range from 20% to more than 80% of all casualties. The American experience indicates that about 90% of the total mortality occurs on the battlefield. Such casualties, those classified as killed in action, die before reaching medical care. More than 90% of all battle injuries (morbidity) are caused by penetrating missiles. Exsanguination from wounds of the heart/great vessels and penetrating/perforating wounds of the skull cause the majority of battlefield deaths. The frequency distribution of injury severity appears to be bimodal. A large peak occurs at low injury severity and indicates a population of casualties with relatively benign soft tissue wounds. A smaller peak at high injury severity represents those killed in action.

Adult↗

PubMed1986

Current shock models and clinical correlations.

No useful purpose is served by developing therapeutic interventions that are applicable only in nonexistent patient populations. The history of laboratory hemorrhagic shock research may be a case in point because although many interventions have been proposed on the basis of animal experimentation, few if any have found a place in the treatment of human beings. For a laboratory shock model to have clinical relevance, it must replicate important aspects of shock as seen in human beings during or following massive blood loss. The difficulty in developing an animal model that incorporates these human aspects--hypothermia, hypoxia, hypotension, acidosis, coagulopathy, etc--must not be underestimated. Four methodological factors to consider are animal species, anesthesia, tissue trauma, and nociceptive effects. The development of an animal shock model will require several compromises and the results, whether dealing with mechanisms or therapeutic outcomes, must be considered suspect until confirmatory data are obtained from human studies.

Animals↗

PubMed1986

Hypertonic sodium chloride solutions for the prehospital management of traumatic hemorrhagic shock: a possible improvement in the standard of care?

Acute hemorrhage is a major cause of death in both civilian and military trauma. The suboptimal effect of the volume of standard crystalloids that can be infused during transport has resulted in a need for a more efficacious fluid for the prehospital management of both civilian and military trauma. Markedly hypertonic sodium chloride solutions have been shown to improve transiently the hemodynamic consequences of shock in animal models. The use of small volumes of 7.5% NaCl in 6% dextran 70 has resulted in a solution superior to equal volumes of standard crystalloids in the ability to resuscitate animals from hemorrhagic shock. The hypertonic sodium chloride/dextran solution has the potential advantages of improving survival, producing a beneficial hemodynamic effect with smaller fluid volumes, reducing total fluid requirements during resuscitation, and being stored easily. This solution may prove valuable in the early resuscitation of the hypovolemic trauma patient and merits further clinical trials.

Animals↗

PubMed1986

Wounding mechanism of projectiles striking at more than 1.5 km/sec.

In 1976 Charters and Charters (2) described experiments intended to study effects of projectiles with a striking velocity greater than 1 km/sec. They postulated that the projectiles at higher velocity would cause shallow wounds with wide tissue destruction on the surface, especially when striking velocity exceeded the speed of sound in tissue (about 1.5 km/sec). We found no other studies reported dealing with projectiles in this velocity range, the conclusions and assumptions of Charters and Charters have been quoted by others and accepted as fact. We designed and performed experiments to test the hypothesis of Charters and Charters by comparing temporary cavity morphology and penetration in gelatin. We fired two types of blunt projectiles over a velocity range from 650 m/sec (2,137 ft/sec) to 2,016 m/sec (6,614 ft/sec). In these studies we found no evidence to indicate that shape and characteristics of the disruption in ordnance gelatin change significantly when missile striking velocity exceeds sonic speed in the target.

Forensic Medicine↗