Use of an inspiratory impedance threshold valve during chest compressions without assisted ventilation may result in hypoxaemia.

INTRODUCTION: Although the concept of intermittent airway occlusion with the inspiratory impedance threshold valve (ITV) is a well-recognised strategy for improving efficiency of cardiopulmonary resuscitation (CPR), little is known about possible pulmonary side effects. METHODS: After a baseline chest CT-scan, 24 pigs with beating hearts undergoing apnoeic oxygenation received an injection of a contrast medium and were then assigned randomly to either active compression-decompression CPR with ITV (ACD ITV CPR), ACD CPR alone, or standard-CPR with ITV (standard-ITV CPR), or standard-CPR alone. After a maximum of 5 min of chest compressions or if oxygen saturation dropped below 70%, the experiment was stopped, haemodynamic variables and blood gas values were measured, and another CT-scan was performed; all animals underwent a 30 min recovery-period and a third subsequent CT-scan. RESULTS: At baseline arterial oxygen saturation by pulse oxymetry was 99% in all four groups; in both the ACD ITV CPR and the standard-ITV CPR groups, arterial oxygen saturation dropped below 70% within 126+/-9s, whereas chest compressions in all ACD CPR and standard-CPR pigs were performed over 5 min (P<0.001). Before stopping chest compressions arterial oxygen pressure decreased in the ACD ITV CPR group from 426+/-96 to 42+/-8 mmHg while it decreased in the ACD CPR group only from 415+/-116 to 197+/-127 mmHg (P<0.001 between groups); in the standard-ITV CPR group arterial oxygen partial pressure decreased from 427+/-109 to 34+/-5 mmHg while oxygen partial pressure decreased only from 467+/-44 to 144+/-98 mmHg in the standard-CPR group (P<0.004 between groups). After the second CT scan arterial oxygen partial pressure decreased further to 19+/-2 mmHg in the ACD ITV CPR versus 210+/-41 mmHg in the ACD CPR group; to 20+/-2 mmHg in the standard-ITV CPR versus 148+/-33 mmHg in the standard-CPR group. Lung-density values (Hounsfield units) were significantly higher in the ACD ITV CPR versus ACD CPR group (-134+/-54 versus -330+/-77) and standard-ITV CPR versus standard-CPR group (-98+/-50 versus -387+/-42). After a 30 min recovery-period, there were no significant differences in arterial oxygen partial pressure (ACD ITV CPR 275+/-110 mmHg versus ACD CPR 379+/-111 mmHg and standard-ITV CPR 265+/-138 mmHg versus standard CPR 367+/-55 mmHg). Furthermore, there were no differences in lung density values between groups after 30 min of recovery. CONCLUSION: In this animal model with a beating heart, intermittent airway obstruction through an ITV combined with apnoeic oxygenation and without active ventilation resulted in hypoxaemia due to transiently impaired lung function.

An observational study of vasopressin infusion during uncontrolled haemorrhagic shock in a porcine trauma model: Effects on bowel function.

The effects of vasopressin on the gut in a porcine uncontrolled haemorrhagic shock model are described. In eight anaesthetised pigs, a liver laceration was performed; when haemorrhagic shock was decompensated, all animals received 0.4 IU/kg vasopressin, followed by 0.08 IU/kg min over 30 min, which maintained a mean arterial blood pressure >40 mmHg. Subsequent surgical intervention, infusion of whole blood and fluids resulted in a stable cardiocirculatory status. Three hours after stabilisation, all pigs developed non-bloody diarrhoea which converted into normal bowel movements within 24 h. All histological samples retained 7 days after the experiment revealed no histopathological changes. In conclusion, in this small observational study of uncontrolled porcine haemorrhagic shock, a resuscitation strategy that included high dose vasopressin was associated with transient diarrhoea and good long term survival.

Detrimental hemodynamic effects of assisted ventilation in hemorrhagic states.

OBJECTIVE: Our goal was to demonstrate explicitly that lower-frequency positive-pressure ventilation not only preserves adequate oxygenation and acid-base status in hemorrhagic states, but also that "normal" or higher respiratory rates significantly compromise hemodynamics, even with moderate degrees of hemorrhage. DESIGN AND SUBJECTS: Eight intubated pigs (ventilated with 12 mL/kg tidal volume, 28% FIO2, respiratory rate = 12 breaths/min) were hemorrhaged to <65 mm Hg of systolic blood pressure. Respiratory rates were then sequentially changed every 10 mins to 6, 20, 30, and 6 breaths/min. MEASUREMENTS AND MAIN RESULTS: With respiratory rates at 6 breaths/min, all subjects maintained pH of >7.25 and SaO2 of >99% while increasing systolic blood pressure (mean, 65-84 mm Hg; p < .05), time-averaged coronary perfusion pressure (50 +/- 2 to 60 +/- 4 mm Hg; p < .05), and cardiac output (2.4 to 2.8 L/min; p < .05). With respiratory rates of 20 and 30 breaths/min, systolic blood pressure (73 +/- 4 and 66 +/- 5 mm Hg, respectively), coronary perfusion pressure (47 +/- 3 and 42 +/- 4 mm Hg), and cardiac output (2.5 and 2.4 L/min) diminished. When returned to 6 breaths/min, systolic blood pressure (95 mm Hg), coronary perfusion pressure (71 + 6 mm Hg), and cardiac output (3.0 L/min) improved significantly (p < .05 for all comparisons). CONCLUSIONS: After moderate hemorrhage, animals maintain adequate oxygenation and acid-base status with lower-frequency respiratory rates, whereas increasingly higher respiratory rates progressively and significantly impair hemodynamics. Current ventilatory protocols for trauma resuscitation should be re-examined and considered a possible cause of worsened clinical outcomes and unrecognized confounded study results.

Treatment of hypotension in pigs with an inspiratory impedance threshold device: a feasibility study.

OBJECTIVE: An inspiratory impedance threshold device was evaluated in spontaneously breathing animals with hypotension to determine whether it could help improve systemic arterial pressures when fluid replacement was not immediately available. DESIGN: Prospective, randomized. SETTING: Animal laboratory. SUBJECTS: Thirty-nine female farm pigs (weight, 28-33 kg). INTERVENTIONS: A total of 39 anesthetized spontaneously breathing pigs were treated with an impedance threshold device, with cracking pressures from 0 to -20 cm H2O. Four separate experimental protocols were performed: protocol A, in which the hemodynamics of seven pigs were examined during application of an impedance threshold device at various levels of inspiratory impedance (-5, -10, -15, and -20 cm H(2)O), both before and after a severe, controlled hemorrhage to a systolic blood pressure of 50 - 55 mm Hg; protocol B, in which nine pigs bled to systolic blood pressure of 50 -55 mm Hg were treated with an impedance threshold device set at -12 cm H2O and were compared with nine others treated with a sham device; protocol C, in which the effects of the impedance threshold device on mixed venous gases were measured in seven hemorrhaged pigs; and protocol D, in which the effects of the impedance threshold device on cardiac output in seven hemorrhaged pigs were measured. METHODS AND MAIN RESULTS: During initial studies with both normovolemic and hypovolemic pigs, sequential increases in inspiratory impedance resulted in a significant increase in systolic blood pressure, whereas diastolic left ventricular and right atrial pressures decreased significantly and proportionally to the level of impedance. When comparing the sham vs. active impedance threshold device (-12 cm H(2)O) in hypotensive pigs, systolic blood pressure (mean +/- sem) with active impedance threshold device treatment increased from 70 +/- 2 mm Hg to 105 +/- 4 mm Hg (p <.01). Pressures in the control group remained at 70 +/- 4 mm Hg (p <.01). Cardiac output increased by nearly 25% (p <.01) with the active impedance threshold device when calculated using the mixed gas equation and when determined by thermodilution. CONCLUSIONS: These studies demonstrate that it is feasible to use a device that creates inspiratory impedance in spontaneously breathing normotensive and hypotensive pigs to increase blood pressure and enhance cardiopulmonary circulation in the absence of immediate fluid resuscitation. Further studies are needed to evaluate the potential long-term effects and limitations of this new approach to treat hypovolemic hypotension.

Treatment of uncontrolled hemorrhagic shock after liver trauma: fatal effects of fluid resuscitation versus improved outcome after vasopressin.

UNLABELLED: In a porcine model of uncontrolled hemorrhagic shock, we evaluated the effects of vasopressin versus an equal volume of saline placebo versus fluid resuscitation on hemodynamic variables and short-term survival. Twenty-one anesthetized pigs were subjected to severe liver injury. When mean arterial blood pressure was <20 mm Hg and heart rate decreased, pigs randomly received either vasopressin IV (0.4 U/kg; n = 7), an equal volume of saline placebo (n = 7), or fluid resuscitation (1000 mL each of lactated Ringer's solution and hetastarch; n = 7). Thirty minutes after intervention, surviving pigs were fluid resuscitated while bleeding was surgically controlled. Mean (+/- SEM) arterial blood pressure 5 min after the intervention was significantly (P < 0.05) higher after vasopressin than with saline placebo or fluid resuscitation (58 +/- 9 versus 7 +/- 3 versus 32 +/- 6 mm Hg, respectively). Vasopressin improved abdominal organ blood flow but did not cause further blood loss (vasopressin versus saline placebo versus fluid resuscitation 10 min after intervention, 1343 +/- 60 versus 1350 +/- 22 versus 2536 +/- 93 mL, respectively; P < 0.01). Seven of 7 vasopressin pigs survived until bleeding was controlled and 60 min thereafter, whereas 7 of 7 saline placebo and 7 of 7 fluid resuscitation pigs died (P < 0.01). We conclude that vasopressin, but not saline placebo or fluid resuscitation, significantly improves short-term survival during uncontrolled hemorrhagic shock. IMPLICATIONS: Although IV fluid administration is the mainstay of nonsurgical management of trauma patients with uncontrolled hemorrhagic shock, the efficacy of this strategy has been discussed controversially. In this animal model of severe liver trauma with uncontrolled hemorrhagic shock, vasopressin, but not saline placebo or fluid resuscitation, improved short-term survival.

A comparison of epinephrine and vasopressin in a porcine model of cardiac arrest after rapid intravenous injection of bupivacaine.

UNLABELLED: In a porcine model, we compared the efficacy of epinephrine, vasopressin, or the combination of epinephrine and vasopressin with that of saline placebo on the survival rate after bupivacaine-induced cardiac arrest. After the administration of 5 mg/kg of a 0.5% bupivacaine solution i.v., ventilation was interrupted for 3 +/- 1 min (mean +/- SD) until asystole occurred. Cardiopulmonary resuscitation (CPR) was initiated after 1 min of cardiac arrest. After 2 min of CPR, 28 animals received, every 5 min, epinephrine; vasopressin; epinephrine combined with vasopressin; or placebo i.v.. Three minutes after each drug administration, up to 3 countershocks (3, 4, and 6 J/kg) were administered; all subsequent shocks were 6 J/kg. Blood was drawn throughout the experiment for the determination of plasma bupivacaine concentration. In the vasopressin/epinephrine combination group, all pigs survived (P < 0.01 versus placebo); in the vasopressin group 5 of 7, in the epinephrine group 4 of 7, and in the placebo group none of 7 swine survived. The plasma concentration of total bupivacaine showed no significant difference among groups. In this model of bupivacaine-induced cardiac arrest, CPR with a combination of vasopressin and epinephrine resulted in significantly better survival rates than in the placebo group. IMPLICATIONS: Although cardiovascular collapse occurs mostly immediately after rapid injection of a local anesthetic in the presence of anesthesiologists, resuscitation may be difficult, and the outcome is usually poor. In this model of bupivacaine-induced cardiac arrest, cardiopulmonary resuscitation with a combination of vasopressin and epinephrine resulted in significantly better survival rates than in the placebo group.

Brain metabolism during cardiopulmonary resuscitation assessed with microdialysis.

BACKGROUND AND PURPOSE: Microdialysis is an established tool to analyse tissue biochemistry, but the value of this technique to monitor cardiopulmonary resuscitation (CPR) effects on cerebral metabolism is unknown. The purpose of this study was to assess the effects of active-compression-decompression (ACD) CPR in combination with an inspiratory threshold valve (ITV) (=experimental CPR) vs. standard CPR on cerebral metabolism measured with microdialysis. METHODS: Fourteen domestic pigs were surfaced-cooled to a body core temperature of 26 degrees C and ventricular fibrillation was induced, followed by 10 min of untreated cardiac arrest; and subsequently, standard (n=7) CPR vs. experimental (n=7) CPR. After 8 min of CPR, all animals received 0.4 U/kg vasopressin IV, and CPR was maintained for an additional 10 min in each group; defibrillation was attempted after a total of 28 min of cardiac arrest, including 18 min of CPR. RESULTS: In the standard CPR group, microdialysis measurements showed a 13-fold increase of the lactate-pyruvate ratio from 7.2+/-1.3 to 95.5+/-15.4 until the end of CPR (P<0.01), followed by a further increase up to 138+/-32 during the postresuscitation period. The experimental group developed a sixfold increase of the lactate-pyruvate ratio from 7.1+/-2.0 to 51.1+/-8.7 (P<0.05), and a continuous decrease after vasopressin. In the standard resuscitated group, but not during experimental CPR, a significant increase of cerebral glucose levels from 0.6+/-0.1 to 2.6+/-0.5 mM was measured (P<0.01). CONCLUSION: Using the technique of microdialysis we were able to measure changes of brain biochemistry during and after the very special situation of hypothermic cardiopulmonary arrest. Experimental CPR improved the lactate-pyruvate ratio, and glucose metabolism.

Early identification of bacteria leading to central venous catheter contamination.

UNLABELLED: Catheter-related bloodstream infections (CRBSI) are a common problem in patients after central venous catheterization. Using DNA analysis we compared bacteria found on the tip of central venous catheters removed because of clinical signs of CRBSI with bacteria found on needle, dilator, and guidewire used for insertion of these catheters. In five of seven central venous catheters removed because of clinical signs of CRBSI, bacteria on the catheter tip were genetically identical to bacteria found on the insertion device, proving that catheter contamination in these cases was caused by contacting bacteria during the initial puncture. These findings may be important for antibiotic prophylaxis or therapy in patients at risk for CRBSI. IMPLICATIONS: In five of seven central venous catheters removed because of clinical signs of catheter-related blood infections, DNA analysis showed bacteria found on the catheter tip to be identical with bacteria found on the puncture kits used for insertion of these catheters.

The effects of nifedipine on ventricular fibrillation mean frequency in a porcine model of prolonged cardiopulmonary resuscitation.

UNLABELLED: We assessed the effects of a calcium channel blocker versus saline placebo on ventricular fibrillation mean frequency and hemodynamic variables during prolonged cardiopulmonary resuscitation (CPR). Before cardiac arrest, 10 animals were randomly assigned to receive either nifedipine (0.64 mg/kg; n = 5) or saline placebo (n = 5) over 10 min. Immediately after drug administration, ventricular fibrillation was induced. After 4 min of cardiac arrest and 18 min of basic life support CPR, defibrillation was attempted. Ninety seconds after the induction of cardiac arrest, ventricular fibrillation mean frequency was significantly (P < 0.01) increased in nifedipine versus placebo pigs (mean +/- SD: 12.4 +/- 2.1 Hz versus 8 +/- 0.7 Hz). From 2 to 18.5 min after the induction of cardiac arrest, no differences in ventricular fibrillation mean frequency were detected between groups. Before defibrillation, ventricular fibrillation mean frequency was significantly (P < 0.05) increased in nifedipine versus placebo animals (9.7 +/- 1.2 Hz versus 7.1 +/- 1.3 Hz). Coronary perfusion pressure was significantly lower in the nifedipine than in the placebo group from the induction of ventricular fibrillation to 11.5 min of cardiac arrest; no animal had a return of spontaneous circulation after defibrillation. In conclusion, nifedipine, but not saline placebo, prevented a rapid decrease of ventricular fibrillation mean frequency after the induction of cardiac arrest and maintained ventricular fibrillation mean frequency at approximately 10 Hz during prolonged CPR; this was nevertheless associated with no defibrillation success. IMPLICATIONS: This study evaluates the effects of a calcium channel blocker on ventricular fibrillation mean frequency, hemodynamic variables, and resuscitability during prolonged cardiopulmonary resuscitation (CPR) in pigs. Nifedipine, but not saline placebo, prevented a rapid decrease of ventricular fibrillation mean frequency after the induction of cardiac arrest and maintained ventricular fibrillation mean frequency at approximately 10 Hz during prolonged CPR but did not improve resuscitability.

Emergency ventilatory management in hemorrhagic states: elemental or detrimental?

BACKGROUND: A study was performed to demonstrate that slower respiratory rates (RRs) of positive-pressure ventilation can preserve adequate oxygenation and acid-base status in hemorrhagic states, whereas "normal" or higher RRs worsen hemodynamics. METHODS: Eight swine (ventilated with 12 mL/kg tidal volume, 0.28 Fio(2); RR of 12 breaths/min) were hemorrhaged to < 65 mm Hg systolic arterial blood pressure (SABP). RRs were then sequentially changed every 10 minutes to 6, 20, 30, and 6 breaths/min. RESULTS: With RRs at 6 breaths/min, the animals maintained pH > 7.25/Sao(2) > 99%, but increased mean SABP (from 65 to 84 mm Hg; p < 0.05), time-averaged coronary perfusion pressure (CPP) (from 50 +/- 2 to 60 +/- 4 mm Hg; p < 0.05), and cardiac output (Qt) (from 2.4 to 2.8 L/min; p < 0.05). With RRs of 20 and 30 breaths/min, SABP (73 and 66 mm Hg), CPP (47 +/- 3 and 42 +/- 4 mm Hg), and Qt (2.5 and 2.4 L/min) decreased, as did Pao(2) and Paco(2) (< 30 mm Hg), with p < 0.05 for each comparison, respectively. When RR returned to 6 breaths/min, SABP (95 mm Hg), CPP (71 +/- 6 mm Hg), and Qt (3.0 L/min) improved significantly (p < 0.05). CONCLUSION: After even moderate levels of hemorrhage in animals, positive-pressure ventilation with "normal" or higher RRs can impair hemodynamics. Hemodynamics can be improved with lower RRs while still maintaining adequate oxygenation and ventilation.

Arginine vasopressin, but not epinephrine, improves survival in uncontrolled hemorrhagic shock after liver trauma in pigs.

OBJECTIVE: Epinephrine is widely used for treatment of life-threatening hypotension, although new vasopressor drugs may merit evaluation. The purpose of this study was to determine the effects of vasopressin vs. epinephrine vs. saline placebo on hemodynamic variables, regional blood flow, and short-term survival in an animal model of uncontrolled hemorrhagic shock and delayed fluid resuscitation. DESIGN: Prospective, randomized, laboratory investigation that used a porcine model for measurement of hemodynamic variables and regional abdominal organ blood flow. SETTING: University hospital laboratory. SUBJECTS: A total of 21 pigs weighing 32 +/- 3 kg. INTERVENTIONS: The anesthetized pigs were subjected to a penetrating liver injury, which resulted in a mean +/- sem loss of 40% +/- 5% of estimated whole blood volume within 30 mins and mean arterial pressures of <20 mm Hg. When heart rate declined progressively, pigs randomly received a bolus dose and continuous infusion of either vasopressin (0.4 units/kg and 0.04 units.kg-1.min-1, n = 7), or epinephrine (45 microg/kg and 5 microg.kg(-1).min(-1), n = 7), or an equal volume of saline placebo (n = 7), respectively. At 30 mins after drug administration, all surviving animals were fluid resuscitated while bleeding was surgically controlled. MEASUREMENTS AND MAIN RESULTS: Mean +/- sem arterial blood pressure at 2.5 and 10 mins was significantly (p <.001) higher after vasopressin vs. epinephrine vs. saline placebo (82 +/- 14 vs. 23 +/- 4 vs. 11 +/- 3 mm Hg, and 42 +/- 4 vs. 10 +/- 5 vs. 6 +/- 3 mm Hg, respectively). Although portal vein blood flow was temporarily impaired by vasopressin, it was subsequently restored and significantly (p <.01) higher when compared with epinephrine or saline placebo (9 +/- 5 vs. 121 +/- 3 vs. 54 +/- 22 mL/min and 150 +/- 20 vs. 31 +/- 17 vs. 0 +/- 0 mL/min, respectively). Hepatic and renal artery blood flow was significantly higher throughout the study in the vasopressin group; however, no further bleeding was observed. Despite a second bolus dose, all epinephrine- and saline placebo-treated animals died within 15 mins after drug administration. By contrast, seven of seven vasopressin-treated animals survived until fluid replacement, and 60 mins thereafter, without further vasopressor therapy (p <.01). Moreover, blood flow to liver, gut, and kidney returned to normal values in the postshock phase. CONCLUSIONS: Vasopressin, but not epinephrine or saline placebo, improved short-term survival in a porcine model of uncontrolled hemorrhagic shock after liver injury when surgical intervention and fluid replacement was delayed.

Vasopressin, but not fluid resuscitation, enhances survival in a liver trauma model with uncontrolled and otherwise lethal hemorrhagic shock in pigs.

BACKGROUND: The authors compared the effects of vasopressin fluid resuscitation on survival in a liver trauma model with uncontrolled and otherwise lethal hemorrhagic shock in pigs. METHODS: A midline laparotomy was performed on 23 domestic pigs, followed by an incision, and subsequent finger fraction across the right medial liver lobe. During hemorrhagic shock, animals were randomly assigned to receive either 0.4 U/kg vasopressin (n = 9), or fluid resuscitation (n = 7), or saline placebo (n = 7), respectively. A continuous infusion of 0.08 U x kg(-1) x min(-1) vasopressin in the vasopressin group, or normal saline was subsequently administered in the fluid resuscitation and saline placebo group, respectively. After 30 min of experimental therapy, bleeding was controlled by surgical intervention, and blood transfusion and rapid fluid infusion were subsequently performed. RESULTS: Maximum mean arterial blood pressure during experimental therapy in the vasopressin-treated animals was significantly higher than in the fluid resuscitation and saline placebo groups (mean +/- SD, 72 +/- 26 vs 38 +/- 16 vs 11 +/- 7 mmHg, respectively; P< 0.05). Subsequently, mean arterial blood pressure remained at approximately 40 mmHg in all vasopressin-treated animals, whereas mean arterial blood pressure in all fluid resuscitation and saline placebo pigs was close to aortic hydrostatic pressure (approximately 15 mmHg) within approximately 20 min of experimental therapy initiation. Total blood loss was significantly higher in the fluid resuscitation pigs compared with vasopressin or saline placebo after 10 min of experimental therapy (65 +/- 6 vs 42 +/- 4 vs 43 +/- 6 ml/kg, respectively; P< 0.05). Seven of seven fluid resuscitation, and seven of seven saline placebo pigs died within approximately 20 min of experimental therapy, while 8 of 9 vasopressin animals survived more than 7 days (P < 0.05). CONCLUSIONS: Vasopressin, but not fluid resuscitation or saline placebo, ensured survival with full recovery in this liver trauma model with uncontrolled and otherwise lethal hemorrhagic shock in pigs.

Vasopressor response in a porcine model of hypothermic cardiac arrest is improved with active compression-decompression cardiopulmonary resuscitation using the inspiratory impedance threshold valve.

UNLABELLED: During normothermic cardiac arrest, a combination of active compression-decompression (ACD) cardiopulmonary resuscitation (CPR) with the inspiratory threshold valve (ITV) significantly improves vital organ blood flow, but this technique has not been studied during hypothermic cardiac arrest. Accordingly, we evaluated the hemodynamic effects of ACD + ITV CPR before, and after, the administration of vasopressin in a porcine model of hypothermic cardiac arrest. Pigs were surface-cooled until their body core temperature was 26 degrees C. After 10 min of untreated ventricular fibrillation, 14 animals were randomly assigned to either ACD CPR with the ITV (n = 7) or to standard (STD) CPR (n = 7). After 8 min of CPR, all animals received 0.4 U/kg vasopressin IV, and CPR was maintained for an additional 10 min in each group; defibrillation was attempted after 28 min of cardiac arrest, including 18 min of CPR. Before the administration of vasopressin, mean +/- SEM common carotid blood flow was significantly higher in the ACD + ITV group compared with STD CPR (67 +/- 13 versus 26 +/- 5 mL/min, respectively; P < 0.025). After vasopressin was given at minute 8 during CPR, mean +/- SEM coronary perfusion pressure was significantly higher in the ACD + ITV group, but did not increase in the STD group (29 +/- 3 versus 15 +/- 2 mm Hg, and 25 +/- 1 versus 14 +/- 1 mm Hg at minute 12 and 18, respectively; P < 0.001); mean +/- SEM common carotid blood flow remained higher at respective time points (33 +/- 8 versus 10 +/- 3 mL/min, and 31 +/- 7 versus 7 +/- 3 mL/min, respectively; P < 0.01). Without active rewarming, spontaneous circulation was restored and maintained for 1 h in three of seven animals in the ACD + ITV group versus none of seven animals in the STD CPR group (not significant). During hypothermic cardiac arrest, ACD CPR with the ITV improved common carotid blood flow compared with STD CPR alone. Moreover, after the administration of vasopressin, coronary perfusion pressure was significantly higher during ACD + ITV CPR, but not during STD CPR. IMPLICATIONS: New strategies are needed to improve the efficiency of cardiopulmonary resuscitation (CPR) in hypothermic cardiac arrest. Active compression-decompression CPR with the inspiratory threshold valve improved carotid blood flow (and coronary perfusion pressure with vasopressin) compared with standard CPR.

Effect of the cardioselective ATP-sensitive potassium channel inhibitor HMR 1883 in a porcine model of cardiopulmonary resuscitation.

OBJECTIVE: HMR 1883 (the free acid form of HMR 1098) selectively inactivates myocardial ATP sensitive potassium channels, which may be a potential important therapeutic approach to prevent life-threatening arrhythmias. This study was designed to assess the effects of HMR 1883 combined with adrenaline on haemodynamic variables, blood gases, and cardiac arrhythmias in a porcine cardiac arrest model. METHODS: After 8 min of untreated cardiac arrest, followed by 1 min of cardiopulmonary resuscitation (CPR), 12 pigs weighing 30-40 kg were assigned randomly to receive either 45 microg/kg adrenaline alone (n=6), or 45 microg/kg adrenaline combined with 3 mg/kg HMR 1883 (n=6), followed by up to three defibrillation attempts 2 min later. Five minutes after return of spontaneous circulation, cardiac arrest was induced for 1 min, with the CPR protocol following as described above. All animals subsequently underwent four cardiac arrest intervals of 1, 2, 3, and 4 min duration which were separated by four episodes of 5 min of return of spontaneous circulation. RESULTS: Haemodynamic variables, cardiac arrhythmias in the acute resuscitation phase between termination of chest compressions and return of spontaneous circulation, and after return of spontaneous circulation in both groups were comparable throughout the experiment. Survival rates throughout the experiment were comparable between groups. Arterial blood gases, electrolyte, glucose, and lactate levels in both groups during the experiment indicated comparable severe metabolic acidosis, with increasing levels after each episode of simulated refibrillation, and subsequent return of spontaneous circulation. CONCLUSION: Combining HMR 1883 with adrenaline during CPR resulted in comparable haemodynamic variables, return of spontaneous circulation rates, cardiac arrhythmias, lactate and glucose levels compared with adrenaline alone. This indicates that injection of HMR 1883 was safe under these conditions.

Vasopressin improves survival in a pig model of hypothermic cardiopulmonary resuscitation.

OBJECTIVE: During hypothermic cardiopulmonary resuscitation with a body core temperature <30 degrees C administration of a vasopressor to support coronary perfusion pressure is controversial. The purpose of the current study was to assess the effects of a single 0.4-unit/kg dose of vasopressin on coronary perfusion pressure, defibrillation success, and 1-hr survival in a pig model of hypothermic closed-chest cardiopulmonary resuscitation combined with rewarming. DESIGN: Prospective, randomized study in an established pig model. SETTING: University hospital research laboratory. SUBJECTS: Fifteen 12- to 16-wk-old domestic pigs. INTERVENTIONS: Pigs were surface cooled to a body core temperature of 26 degrees C and ventricular fibrillation was induced. After 15 mins of untreated cardiac arrest, manual closed-chest cardiopulmonary resuscitation and thoracic lavage with 40 degrees C warmed tap water were started. After 3 mins of external chest compression, animals were assigned randomly to receive vasopressin (0.4 units/kg, n = 8; or saline placebo, n = 7). Defibrillation was attempted 10 mins after drug administration. MEASUREMENTS AND MAIN RESULTS: Compared with saline placebo treated-animals, coronary perfusion pressure in vasopressin-treated pigs was significantly higher 90 secs (36 +/- 5 mm Hg vs. 7 +/- 4 mm Hg, p =.000) to 10 mins (24 +/- 4 mm Hg vs. 8 +/- 4 mm Hg, p =.000) after drug administration. Restoration of spontaneous circulation and 1 hr survival were significantly higher in vasopressin animals compared with saline placebo (8 of 8 vasopressin pigs vs. 0 of 7 placebo pigs, p <.001). CONCLUSIONS: A single 0.4-unit/kg dose of vasopressin administered at a body core temperature <30 degrees C significantly improved defibrillation success and 1-hr survival in a pig model of hypothermic cardiopulmonary resuscitation.