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PubMed1999

Antioxidative resuscitation solution prevents leukocyte adhesion in the liver after hemorrhagic shock.

BACKGROUND: The generation of iron-dependent toxic oxygen radicals during the initial resuscitation from hemorrhagic shock was shown to be a relevant factor for the initiation of the inflammatory cascade. Therefore, this experimental study was designed to evaluate the effects of a deferoxamine-conjugated hydroxyethyl-starch solution (HES-DFO) on oxygen radical induced injury and microcirculatory alterations in the rat liver compared with resuscitation with regular hydroxyethyl-starch, lactated Ringer's solution (RL), or a gelatin-based solution. METHODS: After hemorrhage and random assignment to 1 hour of blood-free resuscitation with the aforementioned solutions, hepatic microcirculation and leukocyte adhesion characteristics were assessed by intravital fluorescence microscopy in anesthetized rats. Oxygen radical activity was estimated by determination of glutathione levels in liver homogenate and determination of thiobarbituric acid-reactive substances in plasma as markers of lipid peroxidation. RESULTS: Resuscitation by HES-DFO resulted in restoration of hemodynamic parameters compared with gelatin-based solution and HES. The hepatic microcirculation was severely altered 1 hour after resuscitation from shock in all groups indicated by sinusoidal narrowing and reduced sinusoidal blood flow. HES-DFO, however, attenuated leukocyte adhesion and improved velocity index in sinusoids as well as sinusoidal perfusion. The shock-associated generation of oxygen radicals during resuscitation was prevented by HES-DFO as indicated by restored glutathione and reduced thiobarbituric acid-reactive substances. CONCLUSION: The results suggest that HES-DFO effectively reduces oxygen radical formation during the initial resuscitation period, thus, attenuating pathologically enhanced leukocyte adhesion and improving hepatic microcirculation.

Animals↗
PubMed2000

Hypertonic saline resuscitation abrogates neutrophil priming by mesenteric lymph.

OBJECTIVE: Neutrophil (PMN) priming after hemorrhagic shock is predictive of the subsequent development of multiple organ failure, but the mechanism remains unknown. Recently, we and others have demonstrated that mesenteric lymph from shock animals resuscitated with lactated Ringer's solution (LR) is not only a potent PMN priming agent but also causes lung injury. Work by others has shown that resuscitation with hypertonic saline (HTS) protects animals from lung injury after hemorrhagic shock. Therefore, we hypothesize that resuscitation with HTS will abolish PMN priming by postshock mesenteric lymph. METHODS: After mesenteric lymph duct catheterization, male rats underwent hemorrhagic shock (mean arterial pressure of 40 mm Hg for 90 minutes) and resuscitation with shed blood plus either LR (2x volume of shed blood) or 4 mL/kg of 7% HTS (isonatremic). Priming for superoxide by PMN was measured after fMLP (1 microM) activation. RESULTS: Shock significantly decreased mesenteric lymph flow from preshock levels in both groups. LR resuscitation produced significantly more mesenteric lymph than HTS resuscitation. Mesenteric lymph from LR animals primed PMN for superoxide production, whereas, HTS eliminated this priming. CONCLUSION: HTS not only decreases postshock mesenteric lymph production, it eliminates PMN priming by mesenteric lymph, suggesting a mechanism for the beneficial effects of HTS resuscitation.

Animals↗
PubMed2000

Maintaining survivors' values of left ventricular power output during shock resuscitation: a prospective pilot study.

OBJECTIVE: Maintaining left ventricular power output (LVP) > 320 mm Hg x L/min/m2 during resuscitation has been retrospectively associated with faster resolution of acidosis and survival after posttraumatic shock. The purpose of this prospective study was to evaluate the effects of maintaining LVP above this threshold during resuscitation on base deficit clearance, organ failure, and survival. METHODS: This was a study of a consecutive series of critically injured patients (PWR) monitored with a pulmonary artery catheter during initial resuscitation. LVP, calculated as cardiac index-(mean arterial pressure-central venous pressure), was maintained >320 mm Hg x L/min/m2 via a predefined protocol by using ventricular pressure-volume diagrams. Outcome was assessed by base deficit clearance (<6 mEq/L) in <24 hours, lowest base deficit in the first 24 hours after admission (24-hr base deficit), organ dysfunctions/patient, and survival. Results were compared with 39 control patients (OXY) with identical enrollment criteria from a previous prospective study who were resuscitated based on oxygen transport criteria. RESULTS: Twenty patients were studied over a 6-month period. Mean LVP during resuscitation in the PWR group was 360 +/- 100 mm Hg x L/min/m2. Admission base deficit was similar between the two groups (PWR 11 +/- 4.2 vs. OXY 11 +/- 5.8 mEq/L;p = 0.66). More PWR patients cleared base deficit in < 24 hours than OXY patients (16 of 20 vs. 17 of 39, p = 0.009, Fisher's exact test), and the PWR patients had a significantly lower 24-hr base deficit (3.9 +/- 3.7 vs. 7.1 +/- 4.6 mEq/L, p = 0.01). Organ dysfunction rate was lower in the PWR group (2.1 +/- 1.5 vs. 3.2 +/- 1.4 organ dysfunctions/patient, p = 0.007). Survival in the PWR group was 15 of 20, versus 21 of 39 in the OXY group (p = 0.10). CONCLUSION: Prospectively maintaining LVP above 320 mm Hg x L/min/m2 during resuscitation is an achievable goal. It is associated with improved base deficit clearance and a lower rate of organ dysfunction after resuscitation from traumatic shock.

Acid-Base Equilibrium↗
PubMed2001

Irreversible shock is not irreversible: a new model of massive hemorrhage and resuscitation.

BACKGROUND: Existing shock models do not address the patient with massive hemorrhage (> 1 blood volume). Such patients often die from irreversible shock. This model simulates the clinical scenario of massive hemorrhage and resuscitation (MHR) to determine if irreversible shock can be reversed. METHODS: Lewis rats were bled at a rate of 1 estimated blood volume (EBV) per hour for 2 hours with simultaneous infusion of resuscitation mixture (RM) consisting of red blood cells and crystalloid. Blood pressure was maintained at a mean arterial pressure (MAP) of 50 mm Hg during the 2 hours of hemorrhage. Hemorrhage was stopped and resuscitation continued for 1 hour until 6, 8, or 10 x EBV of RM was infused. Control animals were subjected to a traditional fixed pressure hemorrhage to MAP of 50 mm Hg for 2 hours followed by resuscitation to MAP > 90 mm Hg for 1 hour with crystalloid alone. Two-week survival was compared using a chi2 test. RESULTS: Control animals (n = 13) were hemorrhaged 48% +/- 5% of EBV and had a mortality rate of 23%. MHR animals had severity and duration of hypotension identical to that of controls but were hemorrhaged 214% +/- 8% of EBV. Despite receiving 390 mL/kg of RM and a final hematocrit of 37%, 14 of 15 animals resuscitated with 6 x EBV died from "irreversible" shock (mortality, 93%; p < 0.001 vs. controls). When very large volumes of resuscitation were used, survival rates improved significantly. The 10 x EBV group received 120% of lost red blood cells and 530 mL/kg of crystalloid and had 64% survival at 2 weeks (p < 0.01 vs. 6 x EBV group). CONCLUSION: This MHR model is much more lethal than a traditional severe hemorrhage model and reproduces the clinical picture of irreversible shock. This irreversible shock can be reversed with very large volumes of resuscitation.

Animals↗
PubMed2001

Hypotensive resuscitation using a polymerized bovine hemoglobin-based oxygen-carrying solution (HBOC-201) leads to reversal of anaerobic metabolism.

BACKGROUND: Traditional resuscitation regimens have been recently challenged. This study evaluates hypotensive resuscitation with a hemoglobin-based oxygen-carrying (HBOC) solution after severe hemorrhage in a porcine model. We hypothesized that HBOC-201 restores tissue perfusion at a lower mean arterial pressure than standard resuscitation fluids. METHODS: Yorkshire swine (55-65 kg, n = 30), were rapidly hemorrhaged to a mean arterial pressure (MAP) of 30 mm Hg, maintained hypotensive for 45 minutes, and randomized into groups. Group I was resuscitated with an HBOC solution to a MAP of 60 mm Hg. Groups II and III were resuscitated to a MAP of 80 mm Hg with lactated Ringer's solution (LR) alone or LR (40 mL/kg) followed by shed blood, respectively. Group IV was resuscitated with shed blood alone to a MAP of 60 mm Hg. Group V received an HBOC solution to a MAP of 50 mm Hg. Hemodynamic variables, Swan-Ganz parameters, blood gas samples, and lactate levels were followed for 5 hours. Data were analyzed by analysis of variance/Duncan multiple range test. RESULTS: There were no significant differences in mortality between any groups. Groups I, IV, and V had lower (p < 0.05) cardiac output, pulmonary artery wedge pressure, and MAP than either group II or group III. Svo2 was significantly lower in the HBOC groups. There were no significant differences in arterial pH or lactate between groups I, III, and IV. Lactate levels, base excess, and arterial pH were significantly worse in the LR-alone and HBOC-50 groups. CONCLUSION: Hypotensive resuscitation with HBOC-201 at a MAP of 60 mm Hg after a controlled hemorrhage in swine provides sufficient tissue perfusion and oxygen delivery to reverse anaerobic metabolism on the basis of global physiologic markers despite continued hypotension, hypovolemia, and low cardiac output.

Analysis of Variance↗
PubMed2002

Dalteparin sodium treatment during resuscitation inhibits hemorrhagic shock-induced leukocyte rolling and adhesion in the mesenteric microcirculation.

BACKGROUND: Ischemia/reperfusion-induced polymorphonuclear neutrophil leukocyte (PMN) adhesion and extravasation are pivotal for the development of postinjury multiple organ failure. We hypothesized that the deleterious microcirculatory consequences of hemorrhagic shock (HS) could be altered by low-molecular-weight heparin (LMWH) therapy. Our aim was to investigate the effects of dalteparin sodium on leukocyte-endothelial cell interactions when LMWH treatment was initiated before HS or during resuscitation. METHODS: Anesthetized dogs underwent HS (40 mm Hg mean arterial pressure for 60 minutes) and resuscitation either with shed blood or with lactated Ringer's (LR) solution. LMWH or conventional heparin sodium pretreatment was administered subcutaneously before hemorrhage; or LMWH was given intravenously during resuscitation. Mesenteric postcapillary venules were observed by intravital video microscopy before and after HS, and 60 minutes, 120 minutes, and 180 minutes after resuscitation, and leukocyte rolling and firm adherence were determined. RESULTS: HS significantly increased PMN rolling and adhesion in the mesenteric microcirculation. LMWH, but not heparin sodium pretreatment, significantly inhibited both primary and secondary interactions. LMWH treatment was also effective when initiated during resuscitation. LMWH exerted the same inhibitory effect regardless of the type of resuscitation. CONCLUSION: LMWH treatment during resuscitation effectively inhibits PMN rolling and adhesion.

Animals↗
PubMed2002

Improving ventricular-arterial coupling during resuscitation from shock: effects on cardiovascular function and systemic perfusion.

BACKGROUND: Efficacy of circulation depends on interactions between the heart and the vascular system. Ventricular-arterial coupling (VAC) has been described as an important determinant of cardiovascular function during resuscitation from shock. However, no prospective studies examining VAC and systemic perfusion have been performed. VAC is measured by the ratio of afterload (aortic input impedance [E ]) to contractility (end-systolic elastance [E ]). Lowering E /E is associated with better VAC and improved myocardial work efficiency. Our hypothesis was that optimizing VAC during resuscitation results in improved myocardial work efficiency while simultaneously improving systemic perfusion. METHODS: This was a prospective study in a consecutive series of critically injured patients. Hemodynamic variables, including E, E, and myocardial work efficiency were evaluated by constructing ventricular pressure-volume loops at the bedside during resuscitation. After pulmonary artery catheterization and adequate fluid resuscitation, left ventricular power output and E /E were optimized with inotropic agents and/or afterload reduction. Efficiency was calculated as stroke work/total left ventricular energy expenditure. Tissue perfusion was estimated by calculating base deficit clearance per hour. RESULTS: Twenty-three patients were studied over a 9-month period. Fifteen patients required inotropic support or afterload reduction. Improvements were seen in E /E (from 1.0 +/- 0.4 to 0.6 +/- 0.2 mm Hg/mL/m, p = 0.0004), and left ventricular power output (from 280 +/- 77 to 350 +/- 81 L/min/m. mm Hg, p = 0.003) with resuscitation. A concomitant improvement in myocardial efficiency (from 70% +/- 8.0% to 77% +/- 5.0%, p = 0.0001) and base deficit clearance (from 0.1 +/- 0.4 to -0.2 +/- 0.1 mEq/L/h, p = 0.006) was seen. CONCLUSION: Improved ventricular-arterial coupling during resuscitation is associated with improved myocardial efficiency and systemic tissue perfusion. Perfusion can be improved at lower energy cost to the heart by focusing on thermodynamic principles during resuscitation.

Acid-Base Equilibrium↗
PubMed2002

Tolerance of family presence during pediatric cardiopulmonary resuscitation: a snapshot of military and civilian pediatricians, nurses, and residents.

BACKGROUND: Family presence during cardiopulmonary resuscitation is becoming a more common and accepted practice. OBJECTIVES: We wanted to determine the views held by pediatricians on family presence during pediatric cardiopulmonary resuscitation. We hypothesized that physicians who had more experience with critical illness and death would be more willing to allow parental presence. Additionally, we hypothesized that recently trained physicians, who may have had more educational exposure to family presence, would be more open to the practice than physicians who had been practicing longer. METHODS: A 10-question survey was distributed to attendees of the American Academy of Pediatrics annual Uniformed Services Pediatric Seminar meeting, as well as pediatric staff and residents at both Tripler Army Medical Center and Kapiolani Women's and Children's Medical Center, Honolulu, Hawaii. Responses were compared using chi analysis, with significance indicated by a value < 0.05. RESULTS: Of the 245 respondents, 65% indicated that they would not allow parental presence. There was no significant difference in the responses based on gender, military affiliation, or years of experience. Those involved in inpatient-oriented specialties and residents were significantly more likely to allow parental presence during resuscitation than respondents involved in outpatient-oriented specialties (57.5%, 50%, and 26.4%, respectively; < 0.01). Although only one third of respondents had been involved in a resuscitation during which parents were allowed to be present, the majority (63%) indicated that they would be willing to repeat the practice. CONCLUSIONS: Although in the minority, one third of the pediatricians surveyed are comfortable allowing parental presence during cardiopulmonary resuscitation. We conclude that pediatricians who have more frequent contact with seriously ill children are more likely to accept parental presence. Additionally, the exposure to parental presence during resuscitation efforts increases the likelihood of allowing parental presence in future resuscitation efforts.

Attitude of Health Personnel↗
PubMed1998

Hemodynamic and metabolic responses to repeated hemorrhage and resuscitation with hypertonic saline dextran in conscious swine.

Previous work in our laboratory has demonstrated that HSD is an effective small-volume resuscitation fluid for the treatment of hemorrhagic hypotension, but limitations to its usefulness in severe hemorrhage have not been explored. In the present study, animals (N = 12) were bled from an arterial line at a rate of 1 mL/kg/min until continuously monitored aortic blood flow was reduced to one-half its baseline value, and then they were immediately resuscitated with 7.5% NaCl/6% dextran 70 (hypertonic saline dextran, 4 mL/kg) administered intravenously over 3 min. After recording the maximum improvement in blood pressure, blood samples were obtained and the hemorrhage-resuscitation sequence was repeated until no further measurable increase in cardiac index or blood pressure could be elicited by resuscitation. In the majority of the animals, cardiac index and right and left ventricular stroke work could be improved at least through two bleedings and resuscitation. These improvements sufficed to increase oxygen delivery and consumption, despite the decreases in hematocrit induced by bleeding, transcapillary refill, and asanguinous fluid administration. Under these severe hemorrhage conditions, the acid-base imbalance was not improved by hypertonic saline dextran, and the rate of increase in acidosis was not affected by its administration. We observed a progressive decrease in base excess from +1.35+/-3.19 (mean +/- standard error) to -12.9+/-2.1 mEq/L even when resuscitation improved oxygen consumption significantly by 95+/-20%. In animals that survived as many as three bleedings and resuscitation, the depletion of buffering capacity of the blood was most predominant, and bicarbonate reached a nadir of 7.62 mEq/L with a base excess of -22.4 mEq/L. It is evident that restoration of perfusion in shock treats only a portion of the physiologic dysfunction, leaving major metabolic derangements uncorrected.

Acid-Base Equilibrium↗
PubMed2000

Kinetics of P-selectin expression in regional vascular beds after resuscitation of hemorrhagic shock: a clue to the mechanism of multiple system organ failure.

Leukocyte-endothelial cell interactions play an important role in mediating organ dysfunctions observed after hemorrhagic shock. P-selectin is the first endothelial cell adhesion molecule to be upregulated after an ischemic insult. The objective of this study was to define kinetics of P-selectin expression in different regional vascular beds of mice exposed to hemorrhagic shock. In-vivo P-selectin expressions were determined using dual radiolabeled monoclonal antibody technique in lungs, heart, liver, kidneys, intestinal mesentery, stomach, small bowel, and colon 0.5, 1, 2, 5, 10, and 24 h after resuscitation of 40 mmHg hemorrhagic shock. In another group, P-selectin expression was determined in same organs 5 h after resuscitation of 30 mmHg hemorrhagic shock. Hemorrhagic shock of 40 mmHg caused significant upregulation of P-selectin in lungs and liver at 30 min after resuscitation (P < 0.001). There was a second and more pronounced upregulation of P-selectin in lungs and liver at 5 h after resuscitation (P < 0.001). In heart, intestinal mesentery, stomach, small bowel, and colon, P-selectin was not upregulated until 5 h after resuscitation from 40 mmHg hemorrhagic shock (P < 0.001). While hemorrhagic shock of 40 mmHg did not cause P-selectin upregulation in kidneys, hemorrhage to 30 mmHg did elicit a significant increase at 5 h after resuscitation (P < 0.001). We conclude that P-selectin is upregulated after resuscitation of hemorrhagic shock in lungs, liver, heart, stomach, and intestines. P-selectin upregulation in kidneys only takes place after more severe hemorrhagic shock.

Animals↗
PubMed2000

Does the timing of hypertonic saline resuscitation affect its potential to prevent lung damage?

Hypertonic saline (HS) resuscitation has been reported to prevent lung damage by suppressing neutrophil activation in animal models. Data on the effectiveness of HS to prevent organ damage in the clinical setting are inconsistent. We investigated whether the timing of HS administration relative to neutrophil activation could affect its potential to block neutrophil responses. Different likely clinical circumstances were simulated in vitro by exposing human neutrophils to HS at different time points before and after activation with N-formyl-methionyl-leucyl-phenylalanine (fMLP). The in vivo effect of using HS as a secondary resuscitation fluid was determined with a mouse model of hemorrhage. BALB/c mice were hemorrhaged (40 +/- 5 mmHg) for 1 h and partially resuscitated with HS or Lactated Ringer's (LR) 20 min before completing resuscitation with LR or HS, respectively. Neutrophil activation parameters were determined 2 h after complete resuscitation and lung damage was assessed after 24 h. The length of exposure to physiologically relevant HS levels (20 mM) determined the suppressive effect on in vitro neutrophil superoxide formation. HS treatment caused a transient state of suppression during which neutrophil activation was suppressed; however, HS was unable to suppress cells that were stimulated with fMLP before HS was added. Accordingly, in vivo lung damage was greater in animals that received HS after they had been partially resuscitated with LR compared to mice that received HS before LR (P < 0.05). We conclude that timing of exposure to HS affects neutrophil responses in vitro and may reduce the potential of HS resuscitation to prevent lung injury in vivo.

Animals↗
PubMed2000

Hypertonic/hyperoncotic resuscitation after intestinal superior mesenteric artery occlusion: early effects on circulation and intestinal reperfusion.

The objective of the study was to determine the early effects of hypertonic/hyperoncotic starch resuscitation after 2 h occlusion of the superior mesenteric artery (SMA) in comparison to animals reperfused without treatment and isotonic resuscitation. SMA was clamped (18 pigs, 19-23 kg) for 2 h followed by a 2-h reperfusion period, which was initiated with isotonic (ISO) (35 mL/kg 0.9% NaCl and 5 mL/kg 10% hydroxyethyl starch within 30 min) or hypertonic/hyperoncotic resuscitation (HHES) (7.5% NaCl/10% hydroxyethyl starch within 5 min). Cardiac output (CO), mean arterial blood pressure (MAP), serum lactate, antimesenteric serosal Laser-Doppler values (LD), and intramural pHi (tonometry) were measured. Without resuscitation at the onset of reperfusion MAP (70 +/- 3 mmHg) decreased to 40 +/- 3 mmHg and CO to 31% of baseline values after 30 min. Serum lactate increased to 5.1 +/- 1.6 mmol/L without improvement. The decrease of CO was attenuated only during the initial 30 min of reperfusion in the ISO group, but significantly better counteracted by hypertonic/hyperoncotic resuscitation. Without treatment, LD flow of the ileum (baseline 23-27 LD units) recovered but intramural pH (pHi) remained significantly decreased (7.26 +/- 0.05). With isotonic resuscitation LD values (21.8 +/- 2.1 LD units) and intramural pHi (7.09 +/- 0.14) decreased even more (P < 0.05) whereas the HHES group showed a significant hyperemic reaction and a normalization of the intramural pHi and serum lactate within 30 min. Hypertonic/hyperoncotic resuscitation significantly improves MAP and CO during reperfusion shock and induces an immediate hyperemic reperfusion reaction of the intestinal microcirculation. Adequate isotonic fluid replacement in order to restore the postischemic plasma volume loss may cause a pronounced deterioration of intestinal perfusion.

Animals↗
PubMed2004

Preload optimization using "starling curve" generation during shock resuscitation: can it be done?

Preload-directed resuscitation is the standard of care in U.S. trauma centers. As part of our standardized protocol for traumatic shock resuscitation, patients who do not respond to initial interventions of hemoglobin replacement and fluid volume loading have optimal preload determined using a standardized algorithm to generate a "Starling curve." We retrospectively analyzed data from 147 consecutive resuscitation protocol patients during the 24 months ending August 2002. Fifty (34%) of these patients required preload optimization, of which the optimization algorithm was completed in 36 (72%). The average age of those who required preload optimization was 44 +/- 3 years vs. 34 +/- 1 years for patients who did not. Execution of the algorithm caused PCWP to increase from 18 +/- 1 mmHg to a maximum of 25 +/- 2 mmHg and CI to increase from 3.2 +/- 0.1 L/min m(-2) to 4.5 +/- 0.4 L/min m(-2). Algorithm logic determined PCWP = 24 +/- 2 to be optimal preload at the maximum CI = 4.8 +/- 0.4, and as the volume loading threshold for the remaining time of the resuscitation process. Starling curve preload optimization was begun 6.5 +/- 0.8 h after start of the resuscitation protocol and required 36 +/- 5 min and 4 +/- 0.4 fluid boluses (1.6 +/- 0.2 L). Comparison of early response of those patients who required preload optimization and those who did not indicated hemodynamic compromise apparent in the 1st 4 h of standardized resuscitation. We conclude that preload optimization using sequential fluid bolus and PCWP-CI measurement to generate a Starling curve is feasible during ICU shock resuscitation, but that there is the disadvantage that increasing and maintaining high PCWP may contribute to problematic tissue edema.

Abdominal Injuries↗
PubMed2003

Myocardial protection during resuscitation from cardiac arrest.

PURPOSE OF REVIEW: Successful treatment of cardiac arrest requires that an electrically stable and mechanically competent cardiac activity be promptly reestablished. However, many interventions used to attempt to reestablish cardiac activity may also inflict additional myocardial injury and, in turn, compromise resuscitability. In this review, we examine mechanisms of such myocardial injury and discuss potential new strategies for myocardial protection during resuscitation from cardiac arrest. RECENT FINDINGS: Efforts are currently directed at understanding underlying mechanisms of myocardial injury associated with current resuscitation methods, with the purpose of developing alternative approaches that are safer and more effective. These new approaches include, among others, the development of alternative low-energy defibrillation waveforms, methods for optimizing the timing for attempting defibrillation, and the use of vasopressor agents devoid of beta-agonist effects. There is also interest in understanding the role that activation of pathways of ischemic and reperfusion injury could play during resuscitation from cardiac arrest. To this end, activation of the sarcolemmal sodium-hydrogen exchanger isoform 1 seems to play an important role. Other potentially important pathways involve adenosine metabolism, activation of potassium ATP channels, and generation of oxygen radical species. These pathways may become novel pharmacologic targets for cardiac resuscitation. SUMMARY: The growing body of research in these areas is bringing hope that in a not so distant future new approaches and interventions for cardiac resuscitation could be available for resuscitation of humans in various clinical settings.

Anti-Arrhythmia Agents↗
PubMed2006

Drug treatment and thrombolytics during cardiopulmonary resuscitation.

PURPOSE OF REVIEW: During cardiopulmonary resuscitation, no specific drug therapy has been shown to improve survival to hospital discharge after cardiac arrest, and only few drugs have a proven benefit for short-term survival. This article reviews recent experimental and clinical data about vasopressor, antiarrhythmic and thrombolytic agents. RECENT FINDINGS: General use of high-dose epinephrine (>1 mg) can not be recommended, whereas it should be considered during prolonged cardiopulmonary resuscitation. No catecholamine superior to epinephrine has been identified. Arginine vasopressin has been shown to be as effective as epinephrine in patients with ventricular fibrillation and pulseless electrical activity, and may be more effective in patients presenting with asystole or as the second vasopressor (after epinephrine) in refractory cardiac arrest. Sodium bicarbonate should not be 'blindly' administered during cardiopulmonary resuscitation unless an arterial blood gas analysis can be obtained, or after prolonged unsuccessful cardiopulmonary resuscitation. Amiodarone should be preferred over lidocaine, since it may improve short-term survival. Thrombolytic therapy during cardiopulmonary resuscitation may be beneficial if a pulmonary embolism or acute myocardial infarction is suggested to be the cause of the cardiac arrest. SUMMARY: Epinephrine still represents the first-line vasopressor during cardiopulmonary resuscitation. Arginine vasopressin may be considered in patients presenting with asystole or who are unresponsive to initial treatment with epinephrine. Amiodarone should be preferred to other antiarrythmic agents in patients with cardiac arrest. Thrombolytic therapy during cardiopulmonary resuscitation is a promising new therapeutic option, but its general use in cardiac arrest cannot be recommended until the results of a large multicentre trial become available.

Cardiopulmonary Resuscitation↗
PubMedDate not supplied

The 2003 Carl A Moyer Award: real-time metabolic monitors, ischemia-reperfusion, titration endpoints, and ultraprecise burn resuscitation.

Real-time metabolic monitoring of varied vascular beds provides the raw data necessary to conduct ultraprecise burn shock resuscitation based on second-by-second assessment of regional tissue perfusion. It also illustrates shortcomings of current clinical practices. Arterial base deficit was continuously monitored during 11 clinical resuscitations of patients suffering burn shock using a Paratrend monitor. Separately, in a 30% TBSA rat burn model (N = 70), three Paratrend monitors simultaneously recorded arterial blood gas and tissue pCO2 of the burn wound and colonic mucosa during resuscitation at 0, 2, 4, 6, and 8 ml/kg/%TBSA. Paratrend data were analyzed in conjunction with previously reported laser Doppler images of actual burn wound capillary perfusion. With current clinical therapy, continuous monitoring of arterial base deficit revealed repetitive cycles of resolution/worsening/resolution during burn shock resuscitation. In the rat model, tissue pCO2 in both burn wounds and splanchnic circulation differed depending on the rate of fluid resuscitation (P <.01 between sham and 0 ml/kg/%TBSA and between 2 ml/kg/%TBSA and 4 ml/kg/%TBSA). Burn wound pCO2 values correlated well with laser Doppler determination of actual capillary perfusion (rho = -.48, P <.01). The following conclusions were reached: 1). Gratuitous and repetitive ischemia-reperfusion-ischemia cycles plague current clinical therapy as demonstrated by numerous "false starts" in the resolution of arterial base deficit; 2). in a rat model, real-time monitoring of burn wound and splanchnic pCO2 demonstrate a dose-response relationship with rate of fluid administration; and 3). burn wound and splanchnic pCO2 are highly correlated with direct measurement of burn wound capillary perfusion by laser Doppler imager. Either technique can serve as a resuscitation endpoint for real-time feedback-controlled ultraprecise resuscitation.

Acid-Base Equilibrium↗
PubMedDate not supplied

Enteral resuscitation of burn shock using World Health Organization oral rehydration solution: a potential solution for mass casualty care.

Enteral resuscitation could provide a means to resuscitate burn shock when intravenous (IV) therapy is unavailable, such as in mass disasters. We evaluated the extent of intestinal absorption and resuscitative effects of World Health Organization Oral Rehydration Solution after a 40% TBSA burn in anesthetized swine compared with the IV infusion of lactated Ringer's infused by Parkland formula. Plasma volume (PV) was measured using indocyanine green dye dilution. Intestinal absorption was assessed using phenol red as a nonabsorbable marker. Changes in hematocrit, hemodynamics, and measured PV showed equivalent resuscitative effects of enteral and IV resuscitation. The duodenal fluid absorption rate started at 77 +/- 32 ml/hr per meter of intestine during the first hour and increased to 296 +/- 40 ml/hr during the fourth hour of resuscitation, with a total of 93 +/- 2% of World Health Organization Oral Rehydration Solution infused into the intestine being absorbed. Intestinal absorption rates after burn injury are sufficient to resuscitate a 40% TBSA burn.

Animals↗
PubMed2005

Amiloride combined with small-volume resuscitation with hypertonic saline is superior in ameliorating trauma-hemorrhagic shock-induced lung injury in rats to the administration of either agent alone.

OBJECTIVE: Recognition of the limitations of standard crystalloid resuscitation has led to exploration for alternative resuscitation strategies that might better prevent the development of trauma-hemorrhage-induced organ dysfunction and systemic inflammation. Thus, the goal of this study was to compare the effects of two resuscitation strategies alone and in combination with that of standard resuscitation with Ringer's lactate. These two strategies were intravenous injection of amiloride, an inhibitor of Na/H exchange and epithelial Na channels, and resuscitation with hypertonic saline. DESIGN: Prospective animal study with concurrent control. SETTING: Small animal laboratory. SUBJECTS: Adult male Sprague-Dawley rats. INTERVENTIONS: Rats injected with amiloride or its vehicle were subjected to trauma-hemorrhagic shock (T/HS) or trauma sham-shock (T/SS) and resuscitated with Ringer's lactate or hypertonic saline. The T/HS model consisted of a laparotomy plus 90 mins of shock (mean arterial pressure 30 mm Hg). Three hours after the end of the shock or sham-shock period, lung permeability, lung histology, pulmonary neutrophil sequestration, neutrophil CD11b expression, gut injury, and red blood cell rigidification were assessed. MEASUREMENTS AND MAIN RESULTS: Both amiloride and hypertonic saline reduced T/HS-induced pulmonary permeability and neutrophil sequestration, and coadministration of these two agents was more efficacious than administration of the individual agents. In contrast, whereas gut injury was attenuated by both amiloride and hypertonic saline, combined administration of amiloride and hypertonic saline failed to further protect the gut. Additionally, hypertonic saline reduced both neutrophil CD11b expression and red blood cell rigidification, whereas amiloride was without effect. CONCLUSIONS: Combined administration of amiloride and small-volume resuscitation with hypertonic saline may be a strategy worthy of further evaluation in the therapy of shock-induced distant organ injury.

Amiloride↗