John M. Whitley

Regional Cerebral Blood Flow Following Resuscitation from Hemorrhagic Shock with Hypertonic Saline Influence of a Subdural Mass

After severe hemorrhage, hypertonic saline restores systemic hemodynamics and decreases intracranial pressure (ICP), but its effects on regional cerebral blood flow (rCBF) when used for resuscitation of experimental animals with combined shock and intracranial hypertension have not been reported. We compared rCBF changes (by radiolabeled microsphere technique) after resuscitation from hemorrhage with either 0.8 or 7.2% saline in animals with and without a right hemispheric subdural mass. We studied 24 mongrel dogs anesthetized with 0.5% halothane and 60% nitrous oxide. In group 1 (n = 12), hemorrhage reduced mean arterial pressure (MAP) to 45 mmHg for 30 min. In group 2 (n = 12), ICP was increased and maintained constant at 15 mmHg, whereas hemorrhage reduced MAP to 55 mmHg for 30 min (cerebral perfusion pressure [CPP] approximately 40 mmHg in each group). After the 30-min shock period, 6 animals in each group received one of two randomly assigned resuscitation fluids over a 5-min interval: 1) 7.2% hypertonic saline (HS; sodium 1,232 mEq.l-1, volume 6.0 ml.kg-1); or 2) 0.8% isotonic saline (SAL; sodium 137 mEq.l-1, volume 54 ml.kg-1). Once fluid resuscitation began, ICP was permitted to vary independently in both groups. Data were collected at baseline (before subdural balloon inflation in group 2), midway through the shock interval (T15), immediately after fluid infusion (T35), and 60 and 90 min later (T95, T155). In groups 1 and 2, ICP was significantly less in animals resuscitated with HS compared to those receiving SAL (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Small-volume resuscitation from hemorrhagic shock in dogs: Effects on systemic hemodynamics and systemic blood flow

Background and Methods.This study compared canine systemic hemodynamics and organ blood flow (radioactive microsphere technique) after resuscitation with 0.8% saline (Na+ 137 mEq/L), 7.2% hypertonic saline (Na+ 1233 mEq/L), 20% hydroxyethyl starch in 0.8% saline, or 20% hydroxyethyl starch in 7.2% saline, each in a volume approximating 15% of shed blood volume. Twenty-four endotracheally intubated mongrel dogs (18 to 24 kg) underwent a 30-min period of hemorrhagic shock, from time 0 to 30 min into the shock period, followed by fluid resuscitation.Data were collected at baseline, 15 min into the shock period, immediately after fluid infusion, 5 min after the beginning of resuscitation, and at 60-min intervals for 2 hr, (65 min after the beginning of resuscitation, and 125 min after the beginning of resuscitation). The animals received one of four randomly assigned iv resuscitation fluids: saline (54 mL/kg), hypertonic saline (6.0 mL/kg), hy-droxyethel starch (6.0 mL/kg) or hypertonic saline/hydroxyethyl starch (6.0 mL/kg). Results.Mean arterial pressure increased in all groups after resuscitation. Cardiac output increased with resuscitation in all groups, exceeding baseline in the saline and hypertonic saline/hydroxyethyl starch groups (p < .05 compared with hypertonic saline or hydroxyethyl starch). Sixty-five minutes after the beginning of resuscitation, cardiac output was significantly (p < .05) greater in either of the two colloid-containing groups than in the hypertonic saline group. After resuscitation, hypertonic saline and hydroxyethyl starch produced minimal improvements in hepatic arterial flow, hypertonic saline/ hydroxyethyl starch increased hepatic arterial flow to near baseline levels, and saline markedly increased hepatic arterial flow to levels exceeding baseline (p < .05, saline vs. hydroxyethyl starch). One hundred twenty-five minuutes after the beginning of resuscitation, hepatic arterial flow had decreased in all groups; hepatic arterial flow in the hypertonic saline group had decreased to levels comparable with those during shock. Myocardial, renal, and brain blood flow were not significantly different between groups. Conclusions.Small-volume resuscitation with the combination of hypertonic saline/ hydroxyethyl starch is comparable with much larger volumes of 0.8% saline, and is equal to hypertonic saline or hydroxyethyl starch in the ability to restore and sustain BP and improve organ blood flow after resuscitation from hemorrhagic shock. (Crit Care Med 1991; 19:364)

Hypertonic/hyperoncotic fluid resuscitation after hemorrhagic shock in dogs

We compared canine systemic and cerebral hemodynamics after resuscitation from hemorrhagic shock with 4 mL/kg (a volume approximating 12% of shed blood volume) of 7.2% saline (HS; 1233 mEq/L sodium), 20% hydroxyethyl starch (HES) in 0.8% saline, or a combination fluid consisting of 20% hydroxyethyl starch in 7.2% saline (HS/HES). Eighteen endotracheally intubated mongrel dogs (18-24 kg) were ventilated to maintain normocarbia with 0.5% halothane in nitrous oxide and oxygen (60:40). After a 30-min period of hemorrhagic shock (mean arterial blood pressure = 40 mm Hg), extending from time T0 to T30, animals received one of three randomly assigned intravenous resuscitation fluids: HS, HES, or HS/HES. Data were collected at baseline, at the beginning and end of the shock period (T0 and T30), immediately after fluid infusion (T35), and at 60-min intervals for 2 h (T95, T155). After resuscitation, mean arterial blood pressure and cardiac output increased similarly in all groups, but failed to return to baseline. Intracranial pressure decreased during shock and increased slightly, immediately after resuscitation in all groups. During shock, cerebral blood flow (cerebral venous outflow method) declined in all groups. After resuscitation, cerebral blood flow increased, exceeding baseline in the HS and HS/HES groups but remaining low in the HES group (P less than 0.05 HS vs HES at T35). We conclude that small-volume resuscitation (4 mL/kg) with HS, HS/HES, or HES does not effectively restore or sustain systemic hemodynamics in hemorrhaged dogs. In dogs without intracranial pathology, the effects on cerebral hemodynamics are also comparable, except for transiently greater cerebral blood flow in the HS group in comparison with the HES group.

Bedside blood gas and electrolyte monitoring in critically ill patients.

A major advantage of near-patient testing is time savings that facilitate important diagnostic and therapeutic decisions. Recent technologic advances have made available a number of systems that allow for near-patient testing. The reliability of these instruments must be validated in the clinical setting in the hands of their intended users. We evaluated the Gemstat blood gas, electrolyte, and Hct portable analyzer in the critical care setting when used by numerous individuals with no previous laboratory training. Blood gas, Na, K, and Hct results were highly correlated with those from the clinical laboratories (PaO2, r = .96; PaCO2, r = .92, pH, r = .96; Na, r = .93; K, r = .95; Hct, r = .91). The Gemstat represents a new generation of portable, rapid, safe, and accurate instruments that are well suited for ICU settings. The instrument can facilitate clinical management of patients, and may improve patient care.

Rebound intracranial hypertension in dogs after resuscitation with hypertonic solutions from hemorrhagic shock accompanied by an intracranial mass lesion

We compared intracranial pressure (ICP) and cerebral blood flow (CBF) in dogs after inflating a subdural intracranial balloon to increase ICP to 20 mm Hg, inducing hemorrhagic shock (mean arterial pressure [MAP] of 55 mm Hg), and infusing a single bolus of fluid consisting of either 54 mL/kg of 0.8% saline (SAL), 6 mL/kg of 7.2% hypertonic saline (HS), 20% hydroxyethyl starch (HES) in 0.8% SAL, or a combination fluid (HS/HES) containing 20% HES in 7.2% saline. Twenty-six dogs were ventilated with 0.5% halothane in N2O and O2 (60:40 ratio). As ICP was maintained at 20 mm Hg, rapid hemorrhage reduced MAP to 55 mm Hg (time interval of zero [T0]) which was maintained at that level for 30 minutes (until T30). Subsequently, over a 5-minute interval (T30-T35), one of the four randomly assigned resuscitation fluids was infused. Data were collected at baseline; after subdural balloon inflation; at T0, T30, T35, and 30-minute intervals thereafter for 2 hours (T65, T95, T125, and T155). CBF and ICP were compared using repeat-measure ANOVA. Cerebral blood flow was greater at T35 in the HS and HS/HES groups than in the HES group (P = .025). In the SAL group, ICP increased significantly from T0 to T35, remaining unchanged thereafter. At T35, ICP in the HS group was significantly lower than in the SAL group (P < .05) but subsequently increased. ICP in the HS/HES group exceeded that in all other groups at T95 and T125 (P < .05). After a severe reduction in cerebral perfusion pressure (CPP), HS solutions (both HS and HS/HES) were associated with a delayed rise in ICP and did not improve global forebrain CBF in comparison with conventional saline solutions.

Hemorrhage and intracranial hypertension in combination increase cerebral production of thromboxane A2.

Background and MethodsTo determine the effects of reduced cerebral perfusion pressures produced by hemorrhage alone or in combination with intracranial hypertension on thromboxane A2 (TxA2) production, we undertook a randomized study in 38 anesthetized, mongrel dogs. Animals were subjected to 30 mins of hemorrhagic shock with normal (group 1) or increased (group 2) intracranial pressure (ICP). Group 1 animals (n = 22) were hemorrhaged to reduce cerebral perfusion pressure to 40 mm Hg for 30 mins. In group 2 (n = 16), cerebral perfusion pressure was reduced by the combination of less severe hypotension and intracranial hypertension (20 mm Hg). Cerebral and systemic hemodynamic measurements were recorded, including cerebral blood flow (sagittal sinus outflow method); ICP; cerebral perfusion pressure; and arterial and cerebral venous concentrations of TxB2 (double-antibody radioimmunoassay technique), the major metabolite of TxA2. Data were obtained at baseline and at the beginning and end of the 30-min shock period. ResultsHemorrhagic shock significantly (p < .05) decreased cerebral blood flow in both groups. At the beginning of the shock period, cerebral blood flow was higher in group 1 than in group 2 (p < .05) and venous-arterial differences in TxB2 increased significantly (p < .05) in group 2, but not in group 1. At the end of the 30-min shock period, venous-arterial levels of TxB2 remained significantly (p < .05) higher in group 2. ConclusionsIncreased cerebral production of TxA2 during hypotension accompanied by intracranial hypertension may contribute to the severity of neural damage produced by the combination of head trauma and shock. (Crit Care Med 1991; 19:532)

Cerebrovascular effects of small volume resuscitation from hemorrhagic shock: Comparison of hypertonic saline and concentrated hydroxyethyl starch in dogs

To determine if hypertonic and hyperoncotic resuscitation solutions exerted comparable effects on cerebral hemodynamics following hemorrhagic shock, we compared randomly assigned, equal volumes (6.0 ml/kg) of hypertonic (7.2%) saline (HS) and hyperoncotic (20%) hydroxyethyl starch (HES) for resuscitation from acute experimental hemorrhage in 12 anesthetized dogs. Regional cerebral blood flow (radiolabeled microspheres), intracranial pressure (cisternal catheter), and systemic hemodynamics were recorded. Rapid hemorrhage reduced the mean arterial pressure to 45 mm Hg for 30 min. Resuscitation fluids were infused over 5 min. Both fluids restored mean arterial pressure and cardiac output equally. However, at 60 min following resuscitation, cardiac output decreased in the HS group in comparison to the HES group (1.7 +/- 0.1 vs. 3.1 +/- 0.2 L/min, p <0.05). Cardiac output rapidly declined, however, in the HS group in comparison to the HES group (p <0.05 60 min following resuscitation). Intracranial pressure and cerebral perfusion pressure were similar at all intervals. Regional cerebral blood flow was similar following both fluids. Neither fluid restored cerebral oxygen transport to baseline values. Based on these data, the authors conclude that, following severe hemorrhagic shock of brief duration, systemic and cerebral hemodynamic values are restored equally well by highly concentrated colloid or by hypertonic saline, although hypertonic saline only transiently improves cardiac output.

Thromboxane A2 receptor antagonist SQ29548 does not improve canine postischemic cerebral hypoperfusion.

The thromboxane receptor antagonist SQ29548 was administered to mongrel dogs after an 11-min period of global cerebral ischemia to test the hypothesis that it would improve delayed postischemic cerebral hypoperfusion (PIH) during concurrent elevations in cerebral venous thromboxane B2 (TxB2), the stable metabolite of thromboxane A2 (TxA2). Immediately following an 11-min period of aortic root cross-clamping, six dogs received 0.2 mg/kg of SQ29548 intravenously followed by continuous infusion of 0.2 mg/kg/h (TRA group) and six received a saline placebo (control). Over the next 120 min, cerebral venous outflow was measured from the confluence of the sagittal and lateral sinuses, while arterial and cerebral venous samples were obtained for measurement of TxB2. Delayed postischemic cerebral hypoperfusion, confirmed in the control group (p < 0.05) (16 +/- 2.7 vs. 32 +/- 2.4 ml/min baseline), was nearly identical in the TRA group (14 +/- 0.9 vs. 30 +/- 2.5 ml/min baseline). Cerebral venous TxB2 levels rose dramatically in both groups after ischemia (3670 +/- 440 vs. 1100 +/- 350 pg/ml baseline, control and 2720 +/- 170 vs. 580 +/- 100 pg/ml baseline, TRA group) (p < 0.05). There were no significant group mean differences in any of the other hemodynamic data except mean arterial pressure (MAP) at T120 and Hgb at baseline. We conclude that postischemic intravenous administration of the thromboxane receptor-specific antagonist SQ29548 fails to improve delayed postischemic cerebral hypoperfusion and does not alter cerebral venous TxB2 release in this canine model of global cerebral ischemia.

Effects On Intracranial Pressure In a Clinically Derived Fluid Resuscitation Protocol Following Hemorrhagic Shock with an Accompanying Intracranial Mass

We have previously shown, in a hemorrhagic shock — intracranial mass model, that isotonic crystalloid results in a greater and more rapid increase in ICP immediately following resuscitation than hypertonic crystalloid, colloid or a combination of crystalloid and colloid (Whitley 1988). This rapid increase in ICP may exacerbate the neurological sequelae of the shock episode by decreasing CBF following resuscitation. While the effects of resuscitation on ICP have been extensively studied, they have dealt only with the effects of a single resuscitation fluid bolus, unlike the clinical protocol where systemic hemodynamics are maintained. The present study compared the cerebrovascular effects of resuscitation with isotonic and hypertonic crystalloid, each with and without colloid (10% Pentastarch), while maintaining cardiac output above baseline levels in a hemorrhagic shock — intracranial mass model.