The mouth-to-bag resuscitator during standard anaesthesia induction in apnoeic patients.

AIM: Ventilation of a non-intubated emergency patient by inexperienced rescuers with a standard bag-valve device may result in high inspiratory flow rates and subsequently high airway pressures with stomach inflation. Therefore, a self-inflating bag has been developed that requires lay rescuers to blow up a single-use balloon inside an adult bag-valve device, which, in turn, displaces air within the bag towards the patient. This concept has been compared to standard adult bag-valve devices earlier in bench models but not in patients. METHODS: An anaesthetist who was blinded to all monitor tracings ventilated the lungs of 40 apnoeic patients during routine anaesthesia induction either with a standard bag-valve device or with the mouth-to-bag resuscitator in a random order. Study endpoints were peak inspiratory flow rates, peak airway pressure, tidal volumes and inspiratory time. RESULTS: Peak inspiratory flow was 40+/-10lmin(-1) for the standard bag-valve device versus 33+/-13lmin(-1) for the mouth-to-bag resuscitator (P<0.0001); peak airway pressure was 17+/-5cmH(2)O versus 14+/-5cmH(2)O (P<0.0001); inspiratory tidal volume was 477+/-133ml versus 644+/-248ml (P<0.001) and inspiratory time was 1.1+/-0.3s versus 1.9+/-0.6s (P<0.0001). CONCLUSION: Employing the mouth-to-bag resuscitator during simulated ventilation of a non-intubated patient in respiratory arrest significantly decreased peak inspiratory flow and peak airway pressure and increased inspiratory tidal volume and inspiratory times compared to a standard bag-valve device.

A suction laryngoscope facilitates intubation for physicians with occasional emergency medical service experience--a manikin study with severe simulated airway haemorrhage.

INTRODUCTION: We developed a suction laryngoscope, which enables simultaneous suction and laryngoscopy in cases of airway haemorrhage and evaluated its potential benefits in physicians with varying emergency medical service experience. METHODS: Eighteen physicians with regular and 24 physicians with occasional emergency medical service experience intubated the trachea of a manikin with severe simulated airway haemorrhage using the suction laryngoscope and the Macintosh laryngoscope in random order. RESULTS: In physicians with regular emergency medical service experience, there was neither a difference in time needed for intubation [median (IQR, CI 95%)]: 34 (18, 30-46) vs. 34 (22, 30-52) s; P=0.52, nor in the number of oesophageal intubations [0/18 (0%) vs. 3/18 (16.7%); P=NS] when using the suction vs. the Macintosh laryngoscope. In physicians with occasional emergency medical service experience, there was no difference in time needed for intubation [median (IQR, CI 95%)]: 42 (25, 41-57) vs. 45 (33, 41-65) s; P=0.56, but the number of oesophageal intubations was significantly lower when using the suction laryngoscope [4/24 (16.7%) vs. 12/24 (50.0%); P=0.04]. CONCLUSIONS: In a model of severe simulated airway haemorrhage, employing a suction laryngoscope significantly decreased the likelihood of oesophageal intubations in physicians with occasional emergency medical service experience.

Arginine vasopressin during sinus rhythm: effects on haemodynamic variables, left anterior descending coronary artery cross sectional area and cardiac index, before and after inhibition of NO-synthase, in pigs.

UNLABELLED: We have shown previously that arginine vasopressin (AVP) given during sinus rhythm increases mean arterial blood pressure (MAP) and left anterior descending (LAD) coronary artery cross sectional area. AVP was assumed to result in vasodilatation via activation of the endothelial nitric oxide system. The purpose of the present study was to assess the effects of AVP before and after NO-inhibition. Nine domestic pigs were instrumented for measurement of haemodynamic variables using micromanometer-tipped catheters, and measurement of LAD coronary artery cross sectional area employing intravascular ultrasound (IVUS). Haemodynamic variables, LAD coronary artery cross sectional area and cardiac output were measured at baseline, 90 s and 5, 15, and 30 min after AVP (0.4 U kg (-1) IV) before and after blockade of nitric oxide synthase with N(G)-nitro L-arginine methyl ester (L-NAME). Compared with baseline, AVP significantly increased MAP after 90 s (89+/-4 versus 160+/-5 mm Hg), increased LAD coronary artery cross sectional area (11.3+/-1 versus 11.8+/-1 mm(2)) and decreased cardiac index (138+/-6 versus 53+/-6 mL/min kg(-1)). After blockade of nitric oxide synthase, AVP significantly increased MAP after 90 s (135+/-4 versus 151+/-3 mm Hg), increased LAD coronary artery cross sectional area (8.7+/-1 versus 8.9+/-1 mm(2)), and significantly decreased cardiac index (95+/-6 versus 29+/-4 mL/min kg (-1)). IMPLICATIONS: During sinus rhythm, AVP increased MAP and LAD coronary artery cross sectional area, but decreased cardiac index.

Vasopressin improves survival in a porcine model of abdominal vascular injury.

INTRODUCTION: We sought to determine and compare the effects of vasopressin, fluid resuscitation and saline placebo on haemodynamic variables and short-term survival in an abdominal vascular injury model with uncontrolled haemorrhagic shock in pigs. METHODS: During general anaesthesia, a midline laparotomy was performed on 19 domestic pigs, followed by an incision (width about 5 cm and depth 0.5 cm) across the mesenterial shaft. When mean arterial blood pressure was below 20 mmHg, and heart rate had declined progressively, experimental therapy was initiated. At that point, animals were randomly assigned to receive vasopressin (0.4 U/kg; n = 7), fluid resuscitation (25 ml/kg lactated Ringer's and 25 ml/kg 3% gelatine solution; n = 7), or a single injection of saline placebo (n = 5). Vasopressin-treated animals were then given a continuous infusion of 0.08 U/kg per min vasopressin, whereas the remaining two groups received saline placebo at an equal rate of infusion. After 30 min of experimental therapy bleeding was controlled by surgical intervention, and further fluid resuscitation was performed. Thereafter, the animals were observed for an additional hour. RESULTS: After 68 +/- 19 min (mean +/- standard deviation) of uncontrolled bleeding, experimental therapy was initiated; at that time total blood loss and mean arterial blood pressure were similar between groups (not significant). Mean arterial blood pressure increased in both vasopressin-treated and fluid-resuscitated animals from about 15 mmHg to about 55 mmHg within 5 min, but afterward it decreased more rapidly in the fluid resuscitation group; mean arterial blood pressure in the placebo group never increased. Seven out of seven vasopressin-treated animals survived, whereas six out of seven fluid-resuscitated and five out of five placebo pigs died before surgical intervention was initiated (P < 0.0001). CONCLUSION: Vasopressin, but not fluid resuscitation or saline placebo, ensured short-term survival in this vascular injury model with uncontrolled haemorrhagic shock in sedated pigs.

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.

Influence of negative expiratory pressure ventilation on hemodynamic variables during severe hemorrhagic shock.

OBJECTIVE: Outcome after trauma with severe hemorrhagic shock is still dismal. Since the majority of blood is present in the venous vessels, it might be beneficial to perform venous recruiting via the airway during severe hemorrhagic shock. Therefore, the purpose of our study was to evaluate the effects of negative expiratory pressure ventilation on mean arterial blood pressure, cardiac output, and short-term survival during severe hemorrhagic shock. DESIGN: Prospective study in 21 laboratory animals. SETTING: University hospital research laboratory. SUBJECTS: : Tyrolean domestic pigs. INTERVENTIONS: After induction of controlled hemorrhagic shock (blood loss approximately 45 mL/kg), 21 pigs were randomly ventilated with either zero end-expiratory pressure (0 PEEP; n = 7), 5 cm H2O positive end-expiratory pressure (5 PEEP; n = 7), or negative expiratory pressure ventilation (up to -30 cm H2O at the endotracheal tube during expiration; n = 7). MEASUREMENTS AND MAIN RESULTS: Mean (+/-sd) arterial blood pressure was significantly higher in the negative expiratory pressure ventilation swine when compared with the 0 PEEP (38 +/- 5 vs. 27 +/- 3 mm Hg; p = .001) and the 5 PEEP animals (38 +/- 5 vs. 20 +/- 6 mm Hg; p < .001) after 5 mins of the experiment. Cardiac output was significantly higher in the negative expiratory pressure ventilation swine when compared with the 0 PEEP (3.1 +/- .4 vs. 1.9 +/- .9 L/min; p = .001) and 5 PEEP animals (3.1 +/- .4 vs. 1.2 +/- .8 L/min; p < .001) after 5 mins of the experiment. All seven negative expiratory pressure ventilation animals, but only three of seven 0 PEEP animals (p = .022), survived the 120-min study period, whereas all seven of seven 5 PEEP animals were dead within 35 mins (p < .001). Limitations include that blood loss was controlled and that the small sample size limits the evaluation of survival outcome. CONCLUSIONS: When compared with pigs ventilated with either 0 PEEP or 5 PEEP, negative expiratory pressure ventilation during severe hemorrhagic shock improved mean arterial blood pressure and cardiac output.

Vasopressin during cardiopulmonary resuscitation and different shock states: a review of the literature.

Vasopressin administration may be a promising therapy in the management of various shock states. In laboratory models of cardiac arrest, vasopressin improved vital organ blood flow, cerebral oxygen delivery, the rate of return of spontaneous circulation, and neurological recovery compared with epinephrine (adrenaline). In a study of 1219 adult patients with cardiac arrest, the effects of vasopressin were similar to those of epinephrine in the management of ventricular fibrillation and pulseless electrical activity; however, vasopressin was superior to epinephrine in patients with asystole. Furthermore, vasopressin followed by epinephrine resulted in significantly higher rates of survival to hospital admission and hospital discharge. The current cardiopulmonary resuscitation guidelines recommend intravenous vasopressin 40 IU or epinephrine 1mg in adult patients refractory to electrical countershock. Several investigations have demonstrated that vasopressin can successfully stabilize hemodynamic variables in advanced vasodilatory shock. Use of vasopressin in vasodilatory shock should be guided by strict hemodynamic indications, such as hypotension despite norepinephrine (noradrenaline) dosages >0.5 mug/kg/min. Vasopressin must never be used as the sole vasopressor agent. In our institutional routine, a fixed vasopressin dosage of 0.067 IU/min (i.e. 100 IU/50 mL at 2 mL/h) is administered and mean arterial pressure is regulated by adjusting norepinephrine infusion. When norepinephrine dosages decrease to 0.2 microg/kg/min, vasopressin is withdrawn in small steps according to the response in mean arterial pressure. Vasopressin also improved short- and long-term survival in various porcine models of uncontrolled hemorrhagic shock. In the clinical setting, we observed positive effects of vasopressin in some patients with life-threatening hemorrhagic shock, which had no longer responded to adrenergic catecholamines and fluid resuscitation. Clinical employment of vasopressin during hemorrhagic shock is experimental at this point in time.

Effects of thrombolysis during out-of-hospital cardiopulmonary resuscitation.

In this post hoc analysis, we assessed effects of thrombolysis during out-of-hospital cardiopulmonary resuscitation. The original study was designed as a double-blinded, prospective, multicenter, randomized, controlled clinical trial. In this report, 1,219 patients were randomized, but 33 patients were excluded due to missing study drug codes. Thus, 1,186 patients were analyzed based on receipt (n = 99) versus nonreceipt (n = 1,087) of thrombolysis; the primary end point was hospital admission, and the secondary end point was hospital discharge. Patients who received thrombolysis versus those who did not were significantly younger (mean +/- SD 62.7 +/- 13.3 vs 66.5 +/- 14.3 years of age, p = 0.01) and more likely to have had an acute myocardial infarction (75.3% vs 54.6%, p < 0.01) or pulmonary embolism (20.2% vs 12.0%, p = 0.03) as the suspected underlying cause for cardiac arrest. In patients who underwent thrombolysis versus those who did not, cardiac arrest was more often witnessed (86.9% vs 77.5%, p = 0.03), initial ventricular fibrillation was more likely (59.6% vs 38.0%, p < 0.01), and a short estimated interval (0 to 5 minutes) between collapse and initiation of basic life support was more likely (51.3% vs 29.2%, p < 0.01). In patients who received thrombolysis, sodium bicarbonate (45.5% vs 33.0%, p = 0.01), lidocaine (32.3% vs 18.1%, p < 0.01), and amiodarone (30.3% vs 12.2%, p < 0.01) were administered significantly more often. Hospital admission rates were significantly higher in patients who underwent thrombolysis than in patients who did not (45.5% vs 32.7%, p = 0.01), and there was a trend to higher hospital discharge rates (14.1% vs 9.5%, p = 0.14). In patients who had suspected myocardial infarction, hospital admission and discharge rates were significantly higher in patients who underwent thrombolysis than in patients who did not. In logistic regression models after adjusting for confounding variables (e.g., age, initial electrocardiographic rhythm, and initiation of basic life support), hospital admission and discharge rates did not differ significantly. In conclusion, even when being employed in patients with a potentially better chance to survive, thrombolysis in patients with cardiac arrest resulted in an increased hospital admission but not discharge rate in this post hoc analysis.

Signs of inflammation after sciatic nerve block in pigs.

Nerve stimulators are widely used to assist with peripheral nerve blocks but do not eliminate the risk of nerve injury. We evaluated the histologic findings 6 h after sciatic nerve block with bupivacaine in pigs. When a motor response was still obtained with a current <0.2 mA (n = 10), the postmortem microscopic evaluation revealed lymphocytes and granulocytes sub-, peri-, and intraneurally in 5 (50%) of 10 pigs. No signs of inflammation were observed when the muscle contraction was achieved with a current between 0.3 and 0.5 mA (P = 0.03). In conclusion, the current required to elicit a motor response, the position of the needle tip, and the subsequent likelihood of nerve damage merit further evaluation.

Influence of positive end-expiratory pressure ventilation on survival during severe hemorrhagic shock.

STUDY OBJECTIVE: Although a moderate positive end-expiratory pressure (PEEP) level is widely recommended, it is unknown whether moderate PEEP during mechanical ventilation has adverse effects during severe hemorrhagic shock. Therefore, the purpose of our study was to evaluate the effects of 0 cm H2O PEEP versus 5 cm H2O PEEP versus 10 cm H2O PEEP on short-term survival in a porcine model of severe hemorrhagic shock. Secondary study endpoints were hemodynamic variables and blood gases. METHODS: Twenty-four anesthetized pigs were bled approximately 45 mL/kg, randomized into 3 groups, and then ventilated with 0, 5, or 10 cm H2O PEEP. Survival rates were compared using Kaplan-Meier methods with log rank (Mantel Cox) comparison of cumulative survival by treatment group. RESULTS: Seven of 8 0 cm H2O PEEP animals survived the 120-minute study period, but 8 of 8 5 cm H2O PEEP animals died within 30 minutes, and 8 of 8 10 cm H2O PEEP animals were dead within 20 minutes (P<.0001). Ventilation with 0 cm H2O PEEP prevented a further reduction of mean arterial blood pressure and cardiac output. When compared with the 0 cm H2O PEEP group, end-tidal CO2 declined in the 5 cm H2O PEEP and 10 cm H2O PEEP animals. Compared with the 0 cm H2O PEEP animals, those ventilated with 5 or 10 cm H2O PEEP had higher lactate levels after 10 minutes. CONCLUSION: When compared with pigs ventilated with either 5 or 10 cm H2O PEEP, those ventilated with 0 cm H2O PEEP during untreated, severe hemorrhagic shock had significantly improved short-term survival.

Effects of decreasing peak flow rate on stomach inflation during bag-valve-mask ventilation.

Reducing inspiratory flow rate and peak airway pressure may be important in order to minimise the risk of stomach inflation when ventilating an unprotected airway with positive pressure ventilation. This study was designed to yield enough power to determine whether employing an inspiratory gas flow limiting bag-valve device (SMART BAG, O-Two Medical Technologies Inc., Ontario, Canada) would also decrease the likelihood of stomach inflation in an established bench model of a simulated unintubated respiratory arrest patient. The bench model consists of a training lung (lung compliance, 50 ml/cm H2O; airway resistance, 4 cm H2O/l/s) and a valve simulating lower oesophageal sphincter opening at a pressure of 19 cm H(2)O. One hundred and ninety-one emergency medicine physicians were requested to ventilate the manikin utilising a standard single-person technique for 1 min (respiratory rate, 12/min; Vt, 500 ml) with both a standard adult bag-valve-mask and the SMART BAG. The volunteers were blinded to the experimental design of the model until completion of the experimental protocol. The SMART BAG versus standard bag-valve-mask resulted in significantly (P < 0.001) lower (mean +/- S.D.) mean airway pressure (14 +/- 2 cm H2O versus 16 +/- 3 cm H2O), respiratory rates (13 +/- 3 breaths per min versus 14 +/- 4 breaths per min), incidence of stomach inflation (4.2% versus 38.7%) and median stomach inflation volumes (351 [range, 18-1211 ml] versus 1426 [20-5882 ml]); lung tidal volumes (538 +/- 97 ml versus 533 +/- 97 ml) were comparable. Inspiratory to expiratory ratios were significantly (P < 0.001) increased (1.7 +/- 0.5 versus 1.5 +/- 0.6). In conclusion, the SMART BAG reduced inspiratory flow, mean airway pressure and both the incidence and actual volume of stomach inflation compared with a standard bag-valve-mask device while maintaining delivered lung tidal volumes and increasing the inspiratory to expiratory ratio.

Vasopressin during cardiopulmonary resuscitation: a progress report.

OBJECTIVE: In patients undergoing cardiopulmonary resuscitation, circulating endogenous vasopressin concentrations were significantly higher in successfully resuscitated patients than in patients who died. These observations have prompted several investigations to assess the role of vasopressin to improve cardiopulmonary resuscitation management. DESIGN: Literature review. RESULTS: In the cardiopulmonary resuscitation laboratory, vasopressin improved vital organ blood flow, cerebral oxygen delivery, the probability of restoring spontaneous circulation, and neurologic recovery better than epinephrine. In pediatric preparations with asphyxia, epinephrine was superior to vasopressin, whereas in both pediatric pigs with ventricular fibrillation and adult porcine models with asphyxia, combinations of vasopressin and epinephrine proved to be highly effective. In addition, vasopressin enabled short- and long-term survival in a porcine model of uncontrolled hemorrhagic shock. In a recently published European, multiple-center trial, 1,219 adult patients with out-of-hospital cardiac arrest were randomized to receive two injections of either 40 IU of vasopressin or 1 mg of epinephrine followed by additional epinephrine if needed. The clinical study did not confirm laboratory data showing vasopressin to be more effective than epinephrine in ventricular fibrillation and pulseless electrical activity, but vasopressin was superior to epinephrine in patients with asystole. Vasopressin followed by epinephrine was more effective than epinephrine alone in the treatment of refractory cardiac arrest. CONCLUSIONS: According to new data from the European vasopressin study, we suggest, first, the administration of 1 mg of epinephrine, followed alternately by 40 IU of vasopressin and 1 mg of epinephrine every 3 mins in adult cardiac arrest victims, regardless of the initial electrocardiographic rhythm.

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 vasopressin and epinephrine for out-of-hospital cardiopulmonary resuscitation.

BACKGROUND: Vasopressin is an alternative to epinephrine for vasopressor therapy during cardiopulmonary resuscitation, but clinical experience with this treatment has been limited. METHODS: We randomly assigned adults who had had an out-of-hospital cardiac arrest to receive two injections of either 40 IU of vasopressin or 1 mg of epinephrine, followed by additional treatment with epinephrine if needed. The primary end point was survival to hospital admission, and the secondary end point was survival to hospital discharge. RESULTS: A total of 1219 patients underwent randomization; 33 were excluded because of missing study-drug codes. Among the remaining 1186 patients, 589 were assigned to receive vasopressin and 597 to receive epinephrine. The two treatment groups had similar clinical profiles. There were no significant differences in the rates of hospital admission between the vasopressin group and the epinephrine group either among patients with ventricular fibrillation (46.2 percent vs. 43.0 percent, P=0.48) or among those with pulseless electrical activity (33.7 percent vs. 30.5 percent, P=0.65). Among patients with asystole, however, vasopressin use was associated with significantly higher rates of hospital admission (29.0 percent, vs. 20.3 percent in the epinephrine group; P=0.02) and hospital discharge (4.7 percent vs. 1.5 percent, P=0.04). Among 732 patients in whom spontaneous circulation was not restored with the two injections of the study drug, additional treatment with epinephrine resulted in significant improvement in the rates of survival to hospital admission and hospital discharge in the vasopressin group, but not in the epinephrine group (hospital admission rate, 25.7 percent vs. 16.4 percent; P=0.002; hospital discharge rate, 6.2 percent vs. 1.7 percent; P=0.002). Cerebral performance was similar in the two groups. CONCLUSIONS: The effects of vasopressin were similar to those of epinephrine in the management of ventricular fibrillation and pulseless electrical activity, but vasopressin was superior to epinephrine in patients with asystole. Vasopressin followed by epinephrine may be more effective than epinephrine alone in the treatment of refractory cardiac arrest.

A pilot study to evaluate the SMART BAG: a new pressure-responsive, gas-flow limiting bag-valve-mask device.

UNLABELLED: Reducing inspiratory flow rate and peak airway pressure may be important to minimize the risk of stomach inflation when ventilating an unprotected airway with positive pressure ventilation. In this study, we assessed the effects of a standard self-inflating bag compared with a new pressure-responsive, inspiratory gas flow-limiting device (SMART BAG) on respiratory mechanics in 60 adult patients undergoing routine induction of anesthesia. Respiratory variables were measured using a pulmonary monitor. The SMART BAG resulted in significantly decreased inspiratory flow rate and peak airway pressure while providing adequate tidal volume delivery. IMPLICATIONS: The SMART BAG, a new pressure-responsive, peak inspiratory gas flow-limiting bag-valve mask device, limits inspiratory gas flow from up to 120 L/min in a standard self-inflating bag to approximately 40 L/min. It is designed for use by all levels of health care professionals and has been proven in a clinical pilot study to effectively ventilate patients in respiratory arrest.

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.

Survival with full neurologic recovery after prolonged cardiopulmonary resuscitation with a combination of vasopressin and epinephrine in pigs.

UNLABELLED: We sought to determine the effects of a combination of vasopressin and epinephrine on neurologic recovery in comparison with epinephrine alone and saline placebo alone in an established porcine model of prolonged cardiopulmonary resuscitation (CPR). After 4 min of cardiac arrest, followed by 3 min of basic life support CPR, 17 animals were randomly assigned to receive, every 5 min, either a combination of vasopressin and epinephrine (vasopressin [IU/kg]/epinephrine [ micro g/kg]: 0.4/45, 0.4/45, and 0.8/45; n = 6), epinephrine alone (45, 45, and 200 micro g/kg; n = 6), or saline placebo alone (n = 5). After 22 min of cardiac arrest, including 18 min of CPR, defibrillation was attempted to achieve the return of spontaneous circulation. Aortic diastolic pressure was significantly (P < 0.01) increased 90 s after each of 3 vasopressin/epinephrine injections versus epinephrine alone versus saline placebo alone (mean +/- SEM: 69 +/- 3 mm Hg versus 45 +/- 3 mm Hg versus 29 +/- 2 mm Hg, 63 +/- 4 mm Hg versus 27 +/- 3 mm Hg versus 23 +/- 1 mm Hg, and 52 +/- 4 mm Hg versus 21 +/- 3 mm Hg versus 16 +/- 3 mm Hg, respectively). Spontaneous circulation was restored in six of six vasopressin/epinephrine pigs, whereas six of six epinephrine and five of five saline placebo pigs died (P < 0.01). Neurologic evaluation 24 h after successful resuscitation revealed only an unsteady gait and was normal 5 days after the experiment in all vasopressin/epinephrine-treated animals. In conclusion, in this porcine model of prolonged CPR, repeated vasopressin/epinephrine administration, but not epinephrine or saline placebo alone, ensured long-term survival with full neurologic recovery. IMPLICATIONS: We present a study to evaluate the effects of a combination of vasopressin and epinephrine during prolonged cardiopulmonary resuscitation on neurological outcome in pigs. We found that all pigs treated with a combination of vasopressin and epinephrine could be resuscitated and had full neurologic recovery observed over an entire period of 5 days.

Decreasing peak flow rate with a new bag-valve-mask device: effects on respiratory mechanics, and gas distribution in a bench model of an unprotected airway.

Reducing inspiratory flow rate and peak airway pressure may be important in order to minimise the risk of stomach inflation when ventilating an unprotected airway with positive pressure ventilation. The purpose of this study was to assess the effects of a newly developed bag-valve-mask device (SMART BAG), O-Two Systems International, Ont., Canada) that limits peak inspiratory flow. A bench model simulating a patient with an unintubated airway was used consisting of a face mask, manikin head, training lung (lung compliance, 100 ml/cm H(2)O, airway resistance 4 cm H(2)O/l/s, lower oesophageal sphincter pressure 20 cm H(2)O and simulated stomach). Twenty nurses were randomised to each ventilate the manikin using a standard single person technique for 1 min (respiratory rate, 12/min) with either a standard adult self-inflating bag, or the SMART BAG. The volunteers were blinded to the experimental design of the model until completion of the experimental protocol. The SMART BAG vs. standard self-inflating bag resulted in significantly (P<0.05) lower mean+/-S.D. peak inspiratory flow rates (32+/-2 vs. 61+/-13 l/min), peak inspiratory pressure (12+/-2 vs. 17+/-2 cm H(2)O), lung tidal volumes (525+/-111 vs. 680+/-154 ml) and stomach tidal volumes (0+/-0 vs. 17+/-36 ml), longer inspiratory times (1.9+/-0.3 vs. 1.5+/-0.3 s), but significantly higher mask leakage (26+/-13 vs. 14+/-8%); mask tidal volumes (700+/-104 vs. 785+/-172 ml) were comparable. The mask leakage observed is not an uncommon factor in bag-valve-mask ventilation with leakage fractions of 25-40% having been previously reported. The differences observed between the standard BVM and the SMART BAG are due more to the anatomical design of the mask and the non-anatomical shape of the manikin face than the function of the device. Future studies should remove the mask to manikin interface and should introduce a standardized mask leakage fraction. The use of a two-person technique may have removed the problem of mask leakage. In conclusion, using the SMART BAG during simulated ventilation of an unintubated patient in respiratory arrest significantly decreased inspiratory flow rate, peak inspiratory pressure, stomach tidal volume, and resulted in a significantly longer inspiratory time when compared to a standard self-inflating bag.

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.