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Biomedical subjects

G C Kramer

Publications and source records attributed to G C Kramer.

At least 37 records · Page 2Linked to original sources
PubMed1997

Effects of hypertonic saline on regional function and blood flow in canine hearts during acute coronary occlusion.

Small-volume resuscitation using hypertonic saline (7.5%) is effective for various types of shock. Recently, hypertonic saline has been proposed for fluid management in patients with impaired cardiovascular function. Whether hypertonic saline is safe in the compromised heart during coronary occlusion is not known. We examined the effects of hypertonic saline at 4 mL.kg-1 on myocardial function and blood flow during acute coronary occlusion. In anesthetized dogs, the left ventricle (LV) was instrumented with pressure and ultrasonic dimension transducers. Myocardial contractility was assessed using percent of systolic shortenings measured in both normal or ischemic regions. Blood flow distribution was measured using radioactive microspheres. Percent of systolic shortening and blood flow in the normal myocardium, unaltered by coronary occlusion, increased significantly after hypertonic saline from 11.0 +/- 1.1% to 13.7 +/- 1.4% and from 120 +/- 13 mL.min-1.100 g-1 to 169 +/- 13 mL.min-1.100 g-1, respectively. In the ischemic myocardium, occlusion of the left anterior descending coronary artery markedly decreased percent of systolic shortening from 13.0 +/- 1.2% to 9.3 +/- .9% and blood flow from 98 +/- 13 mL.min-1.100 g-1 to 19 +/- 10 mL.min-1.100 g-1. At peak effect of hypertonic saline contractility and blood flow in the ischemic myocardium decreased to 7.4 +/- .8% and 12 +/- 5 mL.min-1.100 g-1, respectively. Five of the nine dogs developed premature ventricular beats during hypertonic saline infusion. However, no significant changes were observed when normal saline was given at equivalent volumes to hypertonic saline in six dogs. Hypertonic saline was associated with significant increases in heart rate (from 116 +/- 3 beats.min-1 to 129 +/- 5 beats.min-1) and cardiac output (from 2.54 +/- .17 L.min-1 to 3.32 +/- .26 L.min-1). Except for an improved perfusion in the skin, hepatic arterial, and coronary beds, blood flow to the muscle, spleen, jejunum, kidney, and brain was not significantly altered by hypertonic saline. Our data demonstrates variant effects of hypertonic saline on either normal or ischemic myocardium. Whereas contractile function and blood flow in the normal myocardium were improved after hypertonic saline infusion, further decreases in blood flow and contractile function in region distal to coronary occlusion could lead to worsening of ischemic injury. These data suggest that hypertonic saline may be deleterious in hearts with impaired contractile function caused by ischemia.

Animals↗
PubMed1997

Hypertonic saline dextran (HSD) and intraosseous vascular access for the treatment of haemorrhagic hypotension in the far-forward combat arena.

Battlefield statistics show that 50% of deaths are due to acute haemorrhage. Hypertonic (7.5% saline)/hyperoncotic (6% Dextran-70) solution (HSD) for the treatment of haemorrhagic hypotension may have physiologic and logistic advantages over conventional fluid therapy for use in the far-forward combat arena. HSD rapidly expands plasma volume and stabilizes haemodynamic variables in various animal models of haemorrhage, at a volume dose of about 1/10 of conventional lactated Ringers solution. However, combat conditions, as well as the physiological status of the patient may result in time delays or failure to achieve vascular access. Over the past 5 years we have investigated intraosseous infusion of HSD via the sternum or tibia, as a possible means of achieving rapid vascular access and plasma volume expansion. These data in experimental animals and one clinical study show that HSD can be safely and rapidly infused via the intraosseous route achieving the same haemodynamic benefit as observed with intravenous administration.

Animals↗
PubMed1996

Future directions for resuscitation research. IV. Innovative advanced life support pharmacology.

The topics discussed in this session include a partial review of laboratory and clinical studies examining the effects of adrenergic agonists on restoration of spontaneous circulation after cardiac arrest, the effects of varying doses of epinephrine, and the effects of novel vasopressors, buffer agents (NaHCO3, THAM, 'Carbicarb') and anti-arrhythmics (lidocaine, bretylium, amiodarone) in refractory ventricular fibrillation. Novel therapeutic approaches include titrating electric countershocks against electrocardiographic power spectra and of preceding the first countershocks with single or multiple drug treatments. These approaches need to be investigated further in controlled animal and patient studies. Epidemiologic data from randomized clinical outcome studies can give clues, but cannot document pharmacologic mechanisms in the dynamically changing events during attempts to achieve restoration of spontaneous circulation from prolonged cardiac arrest. Also, rapid drug administration by the intraosseous route was compared with intratracheal and intravenous (i.v.) drug administration. Many studies on the above treatments have yielded conflicting results because of differences between healthy hearts of animals and sick hearts of patients, differences in arrest (no-flow) times and cardiopulmonary resuscitation (CPR) (low-flow) times, different pharmacokinetics, different dose/response requirements, and different timing of drug administration during low-flow CPR versus during spontaneous circulation. The need to stabilize normotension and prevent rearrest by titrated novel drug administration, once spontaneous circulation has been restored, requires research. Most of the above topics require some re-evaluation in clinically realistic animal models and in cardiac arrest patients, especially by titration of old and new drug treatments against variables that can be monitored continuously during resuscitation.

Adrenergic Agonists↗
PubMed1996

Intraosseous resuscitation of hemorrhagic shock in a pediatric animal model using a low sodium hypertonic fluid.

OBJECTIVE: To study the efficacy of a low sodium hypertonic resuscitation fluid for resuscitation of severe hemorrhage in a pediatric animal, using the intraosseous route. DESIGN: Prospective, randomized, controlled animal study. SETTING: University physiology laboratory. SUBJECTS: Seventeen immature (6- to 9-wk-old) piglets, weighing 10.6 +/- 0.4 kg, were studied under anesthesia. INTERVENTIONS: A new 2400 mosm/L hypertonic fluid, "Isosal" was formulated with reduced (3.45%) sodium content compared with a 2400-mosm/L (7.5%) hypertonic saline solution. This formulation was accomplished by substituting glucose and mixed amino acids for sodium. Piglets were subjected to 1 hr of hemorrhage, reducing the cardiac output to 50% of baseline value. Resuscitation was carried out through the intraosseous route with an initial 6 mL/kg bolus of either hypertonic saline, Isosal, or lactated Ringer's solution. After the initial bolus, additional test fluid was given to maintain the cardiac output at baseline value for a 2-hr period. MEASUREMENTS AND MAIN RESULTS: Total resuscitation volumes, hemodynamic variables, and electrolytes were measured. Intraosseous vascular access was easily established in all animals, and fluid resuscitation was carried out effectively through this route. Resuscitation volumes were significantly lower for both of the hypertonic fluids (12.7 +/- 1.2 mL/kg for hypertonic saline, and 12.5 +/- 1.7 mL/kg for Isosal solution) compared with lactated Ringer's solution (75.3 +/- 11.6 mL/kg) (p = .01). Both hypertonic saline and Isosal solution resulted in an immediate supranormal response in cardiac output that lasted 20 mins. In contrast, when lactated Ringer's solution was used, multiple boluses were required over a 20-min period to normalize cardiac output. Serum sodium was significantly higher in the hypertonic saline group compared with the Isosal or lactated Ringer's groups (p = .001). CONCLUSIONS: Isosal solution was as effective as hypertonic saline in "small volume" resuscitation of severe hemorrhagic shock in a pediatric animal model through the intraosseous route, and produced significantly less hypernatremia when compared with hypertonic saline.

Amino Acids↗
PubMed1996

Burn resuscitation: crystalloid versus colloid versus hypertonic saline hyperoncotic colloid in sheep.

OBJECTIVES: The present study was undertaken to assess the fluid balance and hemodynamic effects during the first 8 hrs of resuscitation in animals with a large body surface area burn, using lactated Ringer's solution, 6% hetastarch, and hypertonic saline dextran. DESIGN: A prospective, blinded, controlled, terminal study, using anesthetized animals. The initial baseline period was followed by scald injury, and three different treatment regimens were administered from coded bags to achieve a physiologic end point. SETTING: University laboratory. SUBJECTS: Eighteen female sheep (35 to 45 kg) were anesthetized with isoflurane. INTERVENTIONS: Test solutions (10 mL/kg of either lactated Ringer's solution, hetastarch, or hypertonic saline dextran) were infused 30 mins after the scald injury at a rate to restore and maintain the baseline oxygen delivery (DO2) value. MEASUREMENTS AND MAIN RESULTS: Cardiovascular hemodynamics, plasma sodium concentration, plasma colloid osmotic pressure, and fluid balance were measured before and after scalding and resuscitation. After the initial 10-mL/kg test solution dose was given, lactated Ringer's solution was infused to achieve the same end point of baseline DO2 for the remainder of the 8 hrs. The scald caused an initial 30% reduction in cardiac output, a 20% reduction in mean arterial pressure, and 10% to 15% increase in hematocrit. All three test solutions restored and maintained baseline DO2 within 1 hr. However, hetastarch and hypertonic saline dextran reduced the net fluid volume over 8 hrs by 48% and 74%, respectively, compared with lactated Ringer's solution. Edema in the burn wound was not affected by treatment, while hypertonic saline dextran reduced edema in nonburned skin compared with both lactated Ringer's solution and hypertonic saline dextran. Plasma colloid osmotic pressure was significantly higher in the hetastarch and hypertonic saline dextran groups. A continuous decrease in plasma sodium concentrations from baseline values (140 to 145 mmol/L) was measured in the lactated Ringer's solution and hetastarch groups (130 to 133 mmol/L) over 8 hrs. Plasma sodium concentrations in the group receiving hypertonic saline dextran were increased (150 to 155 mmol/L) at 4 hrs, but returned toward baseline by 8 hrs. CONCLUSIONS: Net volume loading can be reduced markedly by initial resuscitation of large body surface area burn injury using a colloid (hetastarch), and can be further reduced by use of hypertonic saline colloid. Hyponatremia was apparent in the isotonic crystalloid- and colloid-treated animals, but not in those animals treated with hypertonic saline colloid.

Animals↗
PubMed1996

Fluid compartments in hemorrhaged rats after hyperosmotic crystalloid and hyperoncotic colloid resuscitation.

Postresuscitation organ failure may be associated with detrimental changes in body fluid compartments. We measured how shock and resuscitation acutely alters the interstitial, cellular, and plasma compartments in different organs. Nephrectomized, anesthetized rats were bled to 50 mmHg mean arterial pressure for 1 h, followed by 60 min of resuscitation to restore blood pressure using 0.9% normal saline (NS,n = 10), 7.5% hypertonic saline (HS,n = 8), 10% hyperoncotic albumin (HA, n = 8), or 7.5% hypertonic saline and 10% hyperoncotic albumin (HSA, n = 7). A 2-h 51Cr-EDTA distribution space estimated extracellular fluid volume (ECFV), and a 5-min 125I-labeled albumin distribution space measured plasma volume (PV). Total tissue water (TW) was measured from wet and dry weights; interstitial fluid volume (ISFV) and cell water were calculated. NS resuscitation required 7 times more fluid (50.9 +/- 7.7 vs. 8.6 +/- 0.7 for HA, 5.9 +/- 0.4 for HS, and 3.9 +/- 0.5 ml/kg for HSA), but there were no differences between solutions in whole animal PV, ECFV, or ISFV. Fluid shifts within tissues depended on resuscitation solution and type of tissue. TW was significantly reduced by hypertonic saline groups in heart, muscle, and liver (P < 0.05). ISFV was significantly reduced by HA groups in the skin. In all tissues, mean cell water in groups receiving HS was smaller; this was significant for heart, lung, muscle, and skin. In conclusion, 1) HS solutions mobilize fluid from cells while expanding both PV and ISFV, and 2) TW and cellular water increase with both isotonic crystalloids and hyperoncotic colloids in many tissues.

Albumins↗
PubMed1996

Resuscitation from severe hemorrhage.

The potential to be successfully resuscitation from severe traumatic hemorrhagic shock is not only limited by the "golden 1 hr", but also by the "brass (or platinum) 10 mins" for combat casualties and civilian trauma victims with traumatic exsanguination. One research challenge is to determine how best to prevent cardiac arrest during severe hemorrhage, before control of bleeding is possible. Another research challenge is to determine the critical limits of, and optimal treatments for, protracted hemorrhagic hypotension, in order to prevent "delayed" multiple organ failure after hemostasis and all-out resuscitation. Animal research is shifting from the use of unrealistic, pressure-controlled, hemorrhagic shock models and partially realistic, volume-controlled hemorrhagic shock models to more realistic, uncontrolled hemorrhagic shock outcome models. Animal outcome models of combined trauma and shock are needed; a challenge is to find a humane and clinically realistic long-term method for analgesia that does not interfere with cardiovascular responses. Clinical potentials in need of research are shifting from normotensive to hypotensive (limited) fluid resuscitation with plasma substitutes. Topics include optimal temperature, fluid composition, analgesia, and pharmacotherapy. Hypotensive fluid resuscitation in uncontrolled hemorrhagic shock with the addition of moderate resuscitative (28 degrees to 32 degrees C) hypothermia looks promising in the laboratory. Regarding the composition of the resuscitation fluid, despite encouraging results with new preparations of stroma-free hemoglobin and hypertonic salt solutions with colloid, searches for the optimal combination of oxygen-carrying blood substitute, colloid, and electrolyte solution for limited fluid resuscitation with the smallest volume should continue. For titrating treatment of shock, blood lactate concentrations are of questionable value although metabolic acidemia seems helpful for prognostication. Development of devices for early noninvasive monitoring of multiple parameters in the field is indicated. Molecular research applies more to protracted hypovolemic shock followed by the systemic inflammatory response syndrome or septic shock, which were not the major topics of this discussion.

Animals↗
PubMed1995

Gut mucosal ischemia during normothermic cardiopulmonary bypass results from blood flow redistribution and increased oxygen demand.

Impaired gut mucosal perfusion has been reported during cardiopulmonary bypass. To better define the adequacy of gut blood flow and oxygenation during cardiopulmonary bypass, we measured overall gut blood flow and ileal mucosal flow and their relationship to mucosal pH, mesenteric oxygen delivery and oxygen consumption in immature pigs (n = 8). Normothermic, noncross-clamped, right atrium-to-aorta cardiopulmonary bypass was maintained at 100 ml/kg per minute for 120 minutes. Animals were instrumented with an ultrasonic Doppler flow probe on the superior mesenteric artery, a mucosal laser Doppler flow probe in the ileum, and pH tonometers in the stomach, ileum, and rectum. Radioactive microspheres were injected before and at 5, 60, and 120 minutes of cardiopulmonary bypass for tissue blood flow measurements. Overall gut blood flow significantly increased during cardiopulmonary bypass as evidenced by increases in superior mesenteric arterial flow to 134.1% +/- 8.0%, 137.1% +/- 7.5%, 130.3% +/- 11.2%, and 130.2% +/- 12.7% of baseline values at 30, 60, 90, and 120 minutes of bypass, respectively. Conversely, ileal mucosal blood flow significantly decreased to 53.6% +/- 6.4%, 49.5% +/- 6.8%, 58.9% +/- 11.6%, and 47.8% +/- 10.0% of baseline values, respectively. Blood flow measured with microspheres was significantly increased to proximal portions of the gut, duodenum and jejunum, during cardiopulmonary bypass, whereas blood flow to distal portions, ileum and colon, was unchanged. Gut mucosal pH decreased progressively during cardiopulmonary bypass and paralleled the decrease in ileal mucosal blood flow. Mesenteric oxygen delivery decreased significantly from 67.0 +/- 10.0 ml/min per square meter at baseline to 42.4 +/- 4.6, 44.9 +/- 3.5, 46.0 +/- 3.6, and 42.9 +/- 3.9 ml/min per square meter at 30, 60, 90, and 120 minutes of bypass. Despite the decrease in mesenteric oxygen delivery, mesenteric oxygen consumption increased progressively from 10.8 +/- 1.4 ml/min per square meter at baseline to 13.4 +/- 1.2, 15.9 +/- 1.2, 16.7 +/- 1.4, and 16.6 +/- 1.54 ml/min per square meter, respectively. We conclude that gut mucosal ischemia during normothermic cardiopulmonary bypass results from a combination of redistribution of blood flow away from mucosa and an increased oxygen demand.

Analysis of Variance↗
PubMed1995

Mixed venous oxygen saturation during cardiopulmonary bypass poorly predicts regional venous saturation.

Mixed venous oxygen saturation is generally accepted as an indicator of adequacy of systemic oxygen delivery; however, cardiopulmonary bypass (CPB) may alter this relationship. Major postoperative complications potentially secondary to inadequate oxygen delivery during CPB indicate that mixed venous oxygen saturation may not detect regional venous desaturation during CPB. We therefore tested the hypothesis that mixed venous oxygen saturation and pH did not predict regional venous oxygen saturations and pH during 2 h of bypass in a swine model. Six immature swine (27-34 kg) received standard normothermic CPB. Sagittal sinus and portal vein oxygen saturations and blood gases were measured at 30, 60, 90, and 120 min of bypass. Although the venous reservoir oxygen saturation remained unchanged during 2 h of bypass, sagittal sinus saturation and pH decreased significantly (66% +/- 3.3% to 33% +/- 2.2% and 7.38 +/- 0.04 to 7.23 +/- 0.05, respectively). Likewise in the portal vein, oxygen saturation and pH also decreased (82% +/- 2.4% to 59.3% +/- 3.9% and 7.39 +/- 0.03 to 7.27 +/- 0.06, respectively). We conclude that profound regional venous desaturation and progressive regional acidemia may go undetected even when a standard pump flow rate of 100 mL.kg-1.min-1 is used and mixed venous oxygen saturation is normal.

Animals↗
PubMed1995

Hypertonic saline-dextran resuscitation from hemorrhagic shock induces transient mixed acidosis.

OBJECTIVE: To evaluate the magnitude and mechanism of potential metabolic acidosis after resuscitation with 7.5% sodium chloride/6% dextran-70. DESIGN: Blinded, randomized, control trial. SETTING: Laboratory setting. SUBJECTS: Sixteen healthy Yorkshire swine. INTERVENTIONS: Anesthetized, mechanically ventilated swine underwent 90 mins of hemorrhagic hypotension (mean arterial pressure of 50 to 55 mm Hg), and a lactic acid infusion (1.5 to 2.4 mmol/kg) was given during the last 60 mins of hemorrhage to produce pretreatment acidosis. The pigs were then given either 4 mL/kg of intravenous normal saline (n = 8) or 7.5% sodium chloride/6% dextran-70 (n = 8). Groups then received isotonic lactated Ringer's solution to restore and maintain cardiac output for 120 mins. MEASUREMENTS AND MAIN RESULTS: There was no difference between groups during baseline or shock for any parameter. At the end of shock, arterial pH and base balance were below baseline values. During resuscitation, cardiac output was reached and maintained in both groups. One minute after infusion of hypertonic saline/dextran, there was a significant but transient decrease in arterial pH (from 7.407 +/- 0.015 to 7.339 +/- 0.025) and base balance (from -6.5 +/- 0.7 to -9.9 +/- 1.0 mmol/L). These changes returned to shock levels by 10 mins and then normalized to baseline levels. Hypertonic saline dextran resulted in an immediate hypernatremia, hyperchloremia, and hypokalemia, a decrease in inorganic strong ion difference (calculated as sodium plus potassium minus chloride concentrations), and no immediate change in anion gap. The normal saline group did not show an initial transient decrease in pH and base balance during resuscitation. Plasma lactate, total protein, and hemoglobin concentrations decreased equally in both groups, although they decreased more quickly with hypertonic saline/dextran. CO2 temporarily and insignificantly increased in arterial blood slightly more after the administration of hypertonic saline/dextran. By 120 mins, acid-base, electrolyte and protein changes were normalizing with hypertonic saline/dextran, while pH, base balance, and protein were decreasing below shock values in animals initially treated with normal saline. CONCLUSIONS: Hypertonic saline/dextran caused an immediate, transient acidemia, which was primarily due to a hyperchloremic, hypokalemic, metabolic acidosis with normal anion gap and decreased inorganic strong ion difference, but which was partially due to a mild transient respiratory acidosis. The acidemia was transient because of the offsetting alkalotic effects of decreasing serum protein, normalization of electrolytes, and transient nature of the increase in CO2. Lactic acidosis was not the cause of the acidemia. Over time, the acid-base status appeared to be improved more effectively with hypertonic saline/dextran than with isotonic saline resuscitation.

Acid-Base Equilibrium↗
PubMed1995

Hypertonic acetate dextran achieves high-flow-low-pressure resuscitation of hemorrhagic shock.

OBJECTIVE: For resuscitation of hemorrhagic hypovolemia, we compared the effectiveness of (1) isotonic lactated Ringer's solution (LRS), (2) 2400 mOsm of 7.5% NaCl:6% dextran 70 (HSD), and (3) 2400 mOsm of 7.9% sodium acetate:1.9% NaCl:6% dextran 70 (HAD). DESIGN: In six randomized, blinded experiments for each solution, conscious instrumented adult sheep were hemorrhaged by removing approximately 1.8 L (42 +/- 3 mL/kg) of blood, while maintaining the mean arterial pressure (MAP) at 50 mm Hg for 2 hours. METHODS: Test solutions were infused as needed to restore the cardiac index to baseline. RESULTS: Volume requirements with HAD (236 +/- 29 mL) and HSD (244 +/- 39 mL) were significantly less (p < 0.05) than LRS (3463 +/- 234 mL). Mean arterial pressure was normalized with HSD and LRS, but not with HAD, which resulted in MAPs of 20 to 25 mm Hg less than baseline resulting from a reduced peripheral resistance. Oxygen delivery, however, was significantly higher with HAD during the resuscitation period. Acid-base balance (pH) and oxygen consumption were normalized within 5 minutes of infusion only with HAD. CONCLUSIONS: Small-volume infusion with HAD resulting in "high-flow-low-pressure" resuscitation may offer unique hemodynamic and metabolic advantages for the initial treatment of hemorrhage from trauma.

Acetates↗
PubMed1995

Limiting initial resuscitation of uncontrolled hemorrhage reduces internal bleeding and subsequent volume requirements.

We tested the hypothesis that full or "standard resuscitation" (SR) with lactated Ringer's solution (LRS) results in increased bleeding in uncontrolled hemorrhagic shock, compared with a "limited prehospital resuscitation" (LPR) regimen and a control group of "no resuscitation" (NR). Cardiac output was used as physiological endpoint for resuscitation. Twenty swine had 25 mL/kg of blood withdrawn during a 30-minute controlled hemorrhage, followed by a 20-minute "prehospital" resuscitation regimen was conducted in three groups: the SR group (n = 6), LRS infused as needed to restore cardiac index (CI) to 100% baseline; the LPR group (n = 8), with resuscitation using LRS to 60% of baseline CI, with volume limited to 10 mL/kg; and the NR group (n = 6). After aortotomy repair, intraoperative resuscitation was continued for 120 minutes using LRS to achieve and maintain 80% of baseline mean arterial pressure. Blood pressure and cardiac index were greatly reduced, to 34% and 39% of baseline, respectively, by hemorrhage. During prehospital resuscitation, the SR group required 48.8 +/- 6.5 mL/kg of LRS, whereas the LPR group received 9.4 +/- 0.6 mL/kg (p < 0.05). Mean arterial pressure increased in all three groups during prehospital resuscitation (p < 0.05). Pulse pressures increased in the SR and LPR groups only (p < 0.05). The increment in oxygen delivery was significantly greater in the SR group, compared with the LPR group (p < 0.05), which in turn was significantly greater than the NR group (p < 0.05). Peritoneal blood volume was significantly higher in the SR group (20.6 +/- 5.6 mL/kg), versus the LPR (7.3 +/- 1.3 mL/kg; p < 0.05) and NR groups (3.0 +/- 0.9 mL/kg; p < 0.05). Crystalloid and whole blood requirements during the intraoperative resuscitation phase were significantly higher in the SR group (193 +/- 16.0 and 9.0 +/- 2.5 mL/kg), than in LPR (111.8 +/- 15.6 and 4.5 +/- 1.8 mL/kg; p < 0.05) and NR groups (128.5 +/- 32.3 and 3.9 +/- 2.3 mL/kg; p < 0.05). In the presence of uncontrolled hemorrhagic shock, LPR and NR can significantly reduce internal hemorrhage and subsequent intraoperative crystalloid and blood requirements.

Animals↗
PubMed1995

Dose response effects of hypertonic saline and dextran on cardiovascular responses and plasma volume expansion in sheep.

Despite the established efficacy of 7.5% NaCl/6% dextran-70 in the treatment of hypovolemia, the optimal formulation of a hyperosmotic/hyperoncotic small volume resuscitation solution has yet to be defined. The present study investigates the cardiovascular effects of hypertonic saline ranging from 3.75%-25% NaCl (HS) and dextran-70 (D-70) ranging from 3 to 24%. HS and D-70 were studied alone or in specific combinations at a dose of 4 mL/kg, in euvolemic sheep. Blood samples were collected before, during and up to 60 min after infusion of the test solutions. Dose-dependent effects of HS were immediate increases in cardiac output (CO) of 30-85%, falling to 10-35% over baseline after 60 min. HS concentrations over 3.75% significantly reduced systemic vascular resistance, but HS had no significant effect on mean arterial pressure (MAP). Plasma volume (PV) expansion with HS was an immediate, but transient increase of 12-35%. Infusion of D-70 induced sustained 10-20% increases in CO and 10-30% increases in PV, peaking 10 min post-infusion. D-70 also resulted in small (5-12 mmHg) increases in MAP. Cardiovascular effects of D-70 correlated with a dose-dependent increase in plasma dextran concentrations. All HS solutions significantly increased plasma Na, which peaked at > or = 200 mEq/L in the 25% group. The effects of D-70 and HS combined were additive on PV expansion and CO. These data indicate that concentrations of HS and D-70 which are higher than those currently used have a greater capability for expanding PV, but use of HS > 7.5% may be limited by resulting hypernatremia.

Animals↗
PubMed1994

Hypertonic saline/dextran for cardiopulmonary bypass reduces gut tissue water but does not improve mucosal perfusion.

Gut mucosal ischemia has been associated with cardiopulmonary bypass (CPB) and may contribute to postoperative systemic inflammatory response and multiorgan dysfunction. Hypertonic saline/dextran (HSD) has been previously shown to selectively increase mucosal blood flow in circulatory shock. To determine whether adding HSD to the prime solution for CPB improves gut mucosal blood flow and oxygenation, we performed normothermic, non-cross-clamped CPB in pigs with 1 ml/kg of HSD (25% NaCl/24% dextran 70) (HSD group, n = 9) or lactated Ringer's solution (LRS group, n = 9) as control added to a standard prime. Animals were instrumented with ultrasonic flow probes on the superior mesenteric artery (SMA), laser Doppler mucosal flow probes in the ileum, and indwelling portal vein catheters and tonometers for mucosal hydrogen ion measurements and pH calculations in the stomach, ileum, and rectum. The total infused volume and net fluid balance was significantly lower in the HSD than in the LRS group (649 +/- 171 ml vs 2075 +/- 385 ml and 502 +/- 182 ml vs 1891 +/- 363 ml, respectively, P < 0.01). SMA flow in the LRS group increased to 110-123% of baseline during CPB and was significantly higher than that in the HSD group which remained unchanged. Ileal mucosal blood flow decreased significantly to 70-50% of baseline in both groups with no difference between groups. Gut oxygen (O2) delivery decreased during CPB in both groups, but O2 consumption remained unchanged. Gastric, ileal, and rectal mucosal pH decreased progressively, and portal venous blood pH also decreased in both groups, but there was no significant difference between groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Design of an intraosseous infusion system.

To reduce the emergency treatment time of shock victims, resuscitation fluids can be infused into a patient via their sternum rather than through a peripheral vein. Successful use of this method requires manual infusion because available medical equipment is not capable of infusing the preferred resuscitation fluids into the sternum at the required flow rates. This article describes the process and results of the design of a high pressure infusion system specifically intended for automating emergency sternal infusions. Infusion requirements for the human sternum were clearly defined, and were followed by the development and evaluation of many infusion system ideas, including numerous commercially available pump designs. The options were narrowed down to five schemes that were studied in depth. Finally, two schemes were picked, a compressed gas bag-within-a-bag design and a peristaltic design.

Decision Trees↗
PubMed1994

Resuscitation from hypovolemia in swine with intraosseous infusion of a saturated salt-dextran solution.

Prehospital fluid resuscitation of traumatic injury is limited by difficulty in delivering large volumes of fluid in the field and time delays associated with gaining vascular access. We addressed these limitations in 14 anesthetized swine by evaluating a highly efficient volume expander, a near-saturated salt-dextran solution (SSD) administered through a new device, which gains vascular access via intraosseous (IO) infusion into the sternal bone marrow. After a steady-state baseline was achieved, all animals were hemorrhaged to 45 mm Hg for one hour. Half of the hemorrhaged animals were infused intraosseously with either normal saline (NS) or SSD until cardiac output was restored to the baseline value. No further infusion was given and animals were monitored for 2 hours. Both regimens were able to restore cardiac output to the baseline value, but only 1.3 +/- 0.1 mL/kg of SSD was required vs. 31.6 +/- 6.3 mL/kg for NS. In addition, cardiac output was better sustained after 2 hours with SSD than with NS. No deleterious effects of IO infusion of SSD were observed. From the improvement in cardiovascular variables and the lack of significant sternal or pulmonary pathologic perturbations, these data suggest that IO infusion of SSD can effectively treat hypovolemia and may allow field treatment when logistic considerations make conventional resuscitation impractical.

Animals↗
PubMed1994

Effects of isotonic crystalloid resuscitation on fluid compartments in hemorrhaged rats.

Redistribution of fluid after isotonic crystalloid resuscitation from hemorrhage may result not only in interstitial edema but also in cellular edema. We measured the extent to which shock and resuscitation altered fluid compartments in different organs. Nephrectomized, anesthetized rats were randomly divided into a Control group (n = 10) and a Hemorrhage plus Resuscitation group (H/R, n = 10). Rats were subjected to 60 min hemorrhagic hypotension (50 mmHg) followed by a 60 min resuscitation period with .9% NaCl infused as needed to maintain mean arterial pressure at 80% of baseline. A 2 h 51Cr-EDTA distribution space was used to estimate extracellular fluid volume (ECFV) and a 5 min 125I-albumin distribution space was used to measure plasma volume (PV). After euthanasia, total tissue water was measured by wet/dry weight analysis and interstitial fluid volume (ISFV) and cell water were calculated for selected organs. Resuscitation volume was two times the shed blood volume, but resulted in a PV equal to that of the Controls. There were no significant differences in whole animal ECFV or ISFV, although the mean values in the H/R group were greater than that of the Control group. The mean values for total tissue water for each tissue in the H/R group were larger than the respective means of the Control tissues but was significantly greater for only the heart (3639 +/- 56 microL/g vs. 3493 +/- 24 microL/g, mean +/- S.E., p < .05). In all H/R tissues, mean values for ISFV were also larger; this difference was significant for only the liver and small intestines (744 +/- 62 vs. 518 +/- 29 microL/g and 1117 +/- 155 vs. 706 +/- 58 microL/g, respectively). Heart cell water was significantly larger in H/R than Controls (2900 +/- 60 microL/g vs. 2738 +/- 27 microL/g). These data suggest that resuscitation of hemorrhage using isotonic crystalloid normalizes overall PV and ECFV but also causes interstitial expansion in selected gut tissues and cellular edema in the heart.

Animals↗