Light levels of anaesthesia after relaxation for tracheal intubation - comparison of succinylcholine and cis-atracurium.

BACKGROUND: Use of a single bolus of a hypnotic together with non-depolarizing muscle relaxants for anaesthesia induction may cause inappropriate light levels of anaesthesia (ILLA). The purpose of this study was to compare the incidence of ILLA during anaesthesia induction using either cis-atracurium (CIS) or succinylcholine (SUC). METHODS: Patients (n = 65) received fentanyl and propofol. Relaxants were randomly chosen and were either CIS 0.15 mg/kg, or SUC 1 mg/kg. After achieving relaxation, ILLA were assessed double-blinded by the isolated forearm technique and electroencephalogram -derived values. RESULTS: Time from induction to complete relaxation was 335 ± 55 s with CIS and 141 ± 26 s with SUC. Nine patients in the CIS group (26%), but no patient in the SUC group responded to commands before endotracheal intubation (P < 0.01). During the entire induction up to 1 min after intubation in the CIS group, 24 of 35 patients (68%) showed 31 episodes of ILLA, as defined as responsiveness to commands and spontaneous movements. With SUC, 8 of 30 patients (27%) showed 11 episodes of ILLA (P < 0.01). In patients with ILLA, state entropy (SE) and spectral edge frequency (SEF) were 68 ± 10 (mean ± standard deviation) and 17 ± 4 Hz, respectively, and in patients without ILLA, SE and SEF were 40 ± 14 and 12 ± 3 Hz, respectively (P < 0.01). CONCLUSION: The onset time of a muscle relaxant has substantial impact on the incidence of ILLA during induction of anaesthesia. Entropy and SEF may indicate the presence of ILLA.

A comparison of the endotracheal tube and the laryngeal mask airway as a route for endobronchial lidocaine administration.

Drug administration via the endotracheal tube is recommended as a second-line approach in emergency settings such as cardiac arrest. It is unknown what amount of drugs are absorbed when they are given through the laryngeal mask airway as compared with the endotracheal tube. We administered lidocaine at a dose of 2 mg/kg diluted in 10 mL normal saline to 20 anesthetized patients undergoing routine surgical procedures. Ten patients received lidocaine into the endotracheal tube and 10 patients received lidocaine into the laryngeal mask airway. Blood samples were taken for measurement of lidocaine plasma concentrations, and the pharmacokinetics were calculated. Therapeutic plasma concentrations (>1.4 microg/mL) could be achieved in 10 of 10 patients after endotracheal tube instillation but in only 4 of 10 patients after laryngeal mask instillation (P < 0.05). Peak lidocaine concentrations (2.47 and 1.09 microg/mL) (P < 0.05) and the area under the time versus plasma concentration curve (117.7 and 91.2 microg x min x mL(-1)) (P < 0.05) were higher after lidocaine administration into the endotracheal tube than into the laryngeal mask airway. In conclusion, the laryngeal mask airway is not a reliable route for the recommended dose of endobronchial lidocaine administration compared with the endotracheal tube.

Vasopressin-mediated adrenocorticotropin release increases plasma cortisol concentrations during cardiopulmonary resuscitation.

OBJECTIVE: Vasopressin is a possible stimulus for both adrenocorticotropin (ACTH) and endothelin-1 release. The aim of this study was to compare plasma concentrations of ACTH, cortisol, and endothelin-1 after epinephrine or vasopressin administration in an experimental animal model of cardiopulmonary resuscitation (CPR). DESIGN: Prospective, randomized, controlled animal study. SETTING: A university research laboratory. SUBJECTS: Fourteen 12- to 14-wk-old domestic pigs. INTERVENTIONS: After 4 mins of cardiac arrest and 3 mins of external chest compression, the pigs were randomly assigned to receive either 0.045 mg/kg epinephrine (n = 7) or 0.4 units/kg vasopressin (n = 7). At 5 mins after drug administration, defibrillation was attempted. MEASUREMENTS AND MAIN RESULTS: Coronary perfusion pressure, ACTH, cortisol, and endothelin-1 were measured before cardiocirculatory arrest, during CPR before drug administration, and at 90 secs and 5 mins after drug administration. Coronary perfusion pressure was comparable between groups. All seven animals in the vasopressin group survived, but only one pig in the epinephrine group survived (p = .005). ACTH and cortisol concentrations remained unchanged in epinephrine-treated animals, but increased significantly after vasopressin administration and were significantly higher than in epinephrine-treated animals 5 mins after drug administration. Endothelin-1 concentrations remained unchanged during the study period and were comparable between both groups. CONCLUSIONS: Vasopressin is a potent stimulus for ACTH secretion, but does not trigger endothelin-1 release from vascular cells during cardiac arrest and CPR. The increased plasma cortisol concentrations caused by the enhanced ACTH release after vasopressin may be one factor contributing to the improved outcome repeatedly observed with vasopressin in animal models of CPR.

Effect of phased chest and abdominal compression-decompression cardiopulmonary resuscitation on myocardial and cerebral blood flow in pigs.

OBJECTIVE: This study was designed to assess the effects of a phased chest and abdominal compression-decompression cardiopulmonary resuscitation (CPR) device, Lifestick, vs. standard CPR on vital organ blood flow in a porcine CPR model. DESIGN: Prospective, randomized laboratory investigation using an established porcine model with instrumentation for measurement of hemodynamic variables, vital organ blood flow, blood gases, and return of spontaneous circulation. SETTING: University hospital research laboratory. SUBJECTS: Twelve domestic pigs. INTERVENTIONS: After 4 mins of untreated ventricular fibrillation, either the Lifestick CPR device (n = 6) or standard CPR (n = 6) was started and maintained for an additional interval of 6 mins before attempting defibrillation. MEASUREMENTS AND MAIN RESULTS: During CPR, but before epinephrine, use of the Lifestick CPR device resulted in significantly higher (p < .05) mean (+/- SD) coronary perfusion pressure (23+/-9 vs. 10+/-7 mm Hg), cerebral perfusion pressure (29+/-11 vs. 18+/-10 mm Hg), mean arterial pressure (49+/-10 vs. 36+/-13 mm Hg), end-tidal carbon dioxide (32+/-11 vs. 20+/-7 mm Hg), left ventricular myocardial blood flow (44+/-19 vs. 19+/-12 mL x min(-1) x 100 g(-1)), and total cerebral blood flow (29+/-10 vs. 14+/-12 mL x min(-1) x 100 g(-1)). After 45 microg/kg epinephrine, hemodynamic and vital organ blood flow variables increased to comparable levels in both groups. CONCLUSIONS: Compared with standard CPR, the Lifestick CPR device increased significantly hemodynamic variables and vital organ blood flow during CPR before epinephrine administration.

Intraosseous vasopressin improves coronary perfusion pressure rapidly during cardiopulmonary resuscitation in pigs.

OBJECTIVE: Intravenous administration of vasopressin during cardiopulmonary resuscitation (CPR) may be more effective than optimal doses of epinephrine. The main purpose of this study was to determine whether intraosseous vasopressin achieves serum drug levels comparable with intravenous doses during CPR and, additionally, to evaluate the effects of intraosseous vasopressin during CPR. DESIGN: Prospective, randomized laboratory investigation using an established porcine model with instrumentation for measurement of hemodynamic variables, blood gases, and return of spontaneous circulation. SETTING: University hospital laboratory. SUBJECTS: Twelve domestic pigs. INTERVENTIONS: After 4 mins of untreated ventricular fibrillation and 3 mins of CPR, 12 pigs were randomized to be treated with intravenous administration of vasopressin (0.8 unit/kg vasopressin; n = 6) or intraosseous vasopressin (0.8 unit/kg vasopressin; n = 6). Defibrillation was performed 5 mins after drug administration to attempt the return of spontaneous circulation. MEASUREMENTS AND MAIN RESULTS: At both 90 secs and 5 mins after drug administration, intravenous and intraosseous administration of vasopressin resulted in comparable mean (+/-SEM) coronary perfusion pressure (43+/-4 vs. 44+/-3 and 30+/-2 vs. 37+/-2 mm Hg, respectively) and vasopressin plasma concentrations (13,706+/-1,857 vs. 16,166+/-3,114 pg/mL and 10,372+/-883 vs. 8246+/-2211 pg/mL, respectively). All animals in both groups were successfully resuscitated; pigs that received intraosseous vasopressin had a significantly higher (p < .05) mean arterial (92+/-6 vs. 129+/-12 mm Hg) and coronary perfusion pressure (84+/-11 vs. 119+/-11 mm Hg) at 5 mins of return of spontaneous circulation. CONCLUSIONS: Intraosseous vasopressin resulted in comparable vasopressin plasma levels, hemodynamic variables, and return of spontaneous circulation rates as did intravenous vasopressin. Intraosseous vasopressin may be an alternative for vasopressor administration during CPR, when intravenous access is delayed or not available.

Vasopressin improves vital organ blood flow after prolonged cardiac arrest with postcountershock pulseless electrical activity in pigs.

OBJECTIVE: Although a benefit of vasopressin when compared with epinephrine was shown during cardiopulmonary resuscitation (CPR) after a short duration of ventricular fibrillation cardiac arrest, the effect of vasopressin during prolonged cardiac arrest with pulseless electrical activity is currently unknown. DESIGN: Prospective, randomized laboratory investigation using an established porcine model with instrumentation for measurement of hemodynamic variables, vital organ blood flow, blood gases, and return of spontaneous circulation. SETTING: University hospital laboratory. SUBJECTS: Eighteen domestic pigs. INTERVENTIONS: After 15 mins of cardiac arrest and 3 mins of chest compressions, 18 animals were randomly treated with either 0.8 units/kg vasopressin (n = 9) or 200 microg/kg epinephrine (n = 9). MEASUREMENTS AND MAIN RESULTS: Compared with epinephrine, vasopressin resulted, at both 90 secs and 5 mins after drug administration, in significantly higher (p < .05) median (25th-75th percentiles) left ventricular myocardial blood flow (120 [range, 96-193] vs. 54 [range, 11-92] and 56 [range, 41-80] vs. 21 [range, 11-40] mL/min/100 g, respectively) and total cerebral blood flow (85 [78-102] vs. 24 [18-41] and 50 [44-52] vs. 8 [5-23] mL/min/100 g, respectively). Spontaneous circulation was restored in eight of nine animals in the vasopressin group and in one of nine animals in the epinephrine group (p = .003). CONCLUSIONS: Compared with a maximum dose of epinephrine, vasopressin significantly increased left ventricular myocardial and total cerebral blood flow during CPR and return of spontaneous circulation in a porcine model of prolonged cardiac arrest with postcountershock pulseless electrical activity.

Vasopressin combined with nitroglycerin increases endocardial perfusion during cardiopulmonary resuscitation in pigs.

Although vasopressin increases vital organ blood flow during cardiopulmonary resuscitation (CPR), endocardial perfusion remains suboptimal. This study was designed to assess the effects of vasopressin versus a combination of vasopressin and nitroglycerin on vital organ blood flow in a porcine model of CPR. After 4 min of cardiac arrest, and 3 min of closed-chest compressions, 14 animals were randomly treated with either 0.4 U/kg vasopressin (n = 7) or 0.4 U/kg vasopressin combined with 5 microg/kg nitroglycerin (n = 7). Coronary and cerebral perfusion pressure as well as left ventricular myocardial blood flow was comparable between groups throughout the experiment. Ninety seconds after drug administration, vasopressin combined with nitroglycerin resulted in comparison with vasopressin alone in significantly higher mean (+/- standard error of the mean) left ventricular endocardial blood flow (78+/-7 vs 51+/-5 ml x min(-1) x 100 g(-1); P < 0.05), and a significantly higher endocardial/epicardial perfusion ratio (0.93+/-0.09 vs 0.57+/-0.06; P < 0.05). Seven of seven animals in the vasopressin group, and four of seven animals in the vasopressin and nitroglycerin group (NS) were resuscitated successfully and survived the 2-h observation period. We conclude that, when compared with vasopressin therapy alone, combined vasopressin and nitroglycerin improved endocardial perfusion significantly immediately after drug administration during CPR.

Splanchnic and renal blood flow after cardiopulmonary resuscitation with epinephrine and vasopressin in pigs.

In laboratory investigations, vasopressin given during CPR resulted in improved vital organ blood flow when compared with epinephrine. Given the profound and long lasting vasopressor effects of vasopressin, we tested the hypothesis that vasopressin given during CPR would result in renal and splanchnic hypoperfusion in the post-resuscitation period when compared with epinephrine. After 4 min of ventricular fibrillation, 16 pigs were randomly assigned to receive either 0.045 mg x kg(-1) epinephrine or 0.4 U X kg(-1) vasopressin before defibrillation. Splanchnic and renal blood flow were measured 30, 90, and 240 min after restoration of spontaneous circulation (ROSC) in the epinephrine and vasopressin groups and in a control group of eight pigs using radiolabeled microspheres. Hepatic blood flow was measured before arrest and 30, 90, and 240 min after ROSC by means of indocyanine green infusion. Thirty minutes after ROSC, renal and adrenal blood flow were significantly lower in the vasopressin group (300 [273-334] and 256 [170-284] ml X min(-1) x 100 g(-1)) (median and 25th and 75th percentile) as compared with the epinephrine group (370 [346-429] and 360 [326-420] ml x min(-1) x 100 g(-1); P < 0.05). Pancreatic, intestinal, and hepatic blood flow were not significantly different in animals after receiving epinephrine or vasopressin. In comparison to epinephrine, vasopressin given during cardiac arrest impairs renal and adrenal perfusion temporarily but does not lead to intestinal or hepatic hypoperfusion in the post-resuscitation phase.

Vasopressin combined with epinephrine decreases cerebral perfusion compared with vasopressin alone during cardiopulmonary resuscitation in pigs.

BACKGROUND AND PURPOSE: It is unknown whether a combination of vasopressin and epinephrine may be superior to vasopressin alone by targeting both nonadrenergic and adrenergic receptors. METHODS: After 15 minutes of cardiac arrest (13 minutes of ventricular fibrillation and 2 minutes of pulseless electrical activity) and 3 minutes of chest compressions, 16 animals were randomly treated with either 0.8 U/kg vasopressin (n = 8) or 0.8 U/kg vasopressin combined with 200 microg/kg epinephrine (n = 8). RESULTS: Comparison of vasopressin with vasopressin and epinephrine at 90 seconds and 5 minutes after drug administration resulted in comparable mean (+/-SEM) coronary perfusion pressure (54+/-3 versus 57+/-5 and 36+/-4 versus 35+/-4 mm Hg, respectively), cerebral perfusion pressure (59+/-6 versus 65+/-8 and 40+/-6 versus 39+/-6 mm Hg, respectively), and median (25th to 75th percentiles) left ventricular myocardial blood flow [116 (81 to 143) versus 108 (97 to 125) and 44 (35 to 81) versus 62 (42 to 74) mL x min(-1) x 100 g(-1), respectively], but significantly increased (P<0.05) total cerebral blood flow [81 (77 to 95) versus 39 (34 to 58) and 50 (43 to 52) versus 28 (16 to 35) mL x min(-1) x 100 g(-1), respectively]. Return of spontaneous circulation rates in both groups were comparable (vasopressin, 7 of 8; vasopressin and epinephrine, 6 of 8). CONCLUSIONS: Comparison of vasopressin with vasopressin and epinephrine resulted in comparable left ventricular myocardial blood flow but significantly increased cerebral perfusion.

Endobronchial vasopressin improves survival during cardiopulmonary resuscitation in pigs.

BACKGROUND: Intravenous administration of vasopressin during cardiopulmonary resuscitation (CPR) has been shown to be more effective than optimal doses of epinephrine. This study evaluated the effect of endobronchial vasopressin during CPR. METHODS: After 4 min of untreated ventricular fibrillation and 3 min of CPR, 21 pigs were randomized to be treated with 0.8 U/kg intravenous vasopressin (n = 7), 0.8 U/kg endobronchial vasopressin (n = 9), or an endobronchial placebo of normal saline (n = 5). Defibrillation was performed 5 min after drug administration to attempt return of spontaneous circulation. RESULTS: All animals in the intravenous and endobronchial vasopressin group were resuscitated successfully, but only two of five animals in the placebo group were. At 2 and 5 min after drug administration, coronary perfusion pressure in the intravenous and endobronchial vasopressin group was significantly higher than in the placebo group (50 +/- 10, 34 +/- 5 vs. 16 +/- 6 mmHg, respectively; and 35 +/- 10, 39 +/- 10 vs. 19 +/- 5 mmHg, respectively; P < 0.05). CONCLUSIONS: Endobronchial vasopressin is absorbed during CPR, coronary perfusion pressure is increased significantly within a short period, and the chance of successful resuscitation is increased in this porcine model of CPR. Endobronchial vasopressin may be an alternative for vasopressor administration during CPR, when intravenous access is delayed or not available.

Regulation of beta 2-adrenergic receptors on mononuclear leukocytes in patients with acute ischemic heart disease.

OBJECTIVE: To investigate relationships between acute adrenergic stress, plasma catecholamine concentrations, and beta 2-adrenergic receptors. DESIGN: Prospective, descriptive study. SETTING: Emergency medical service at a university hospital. PATIENTS: Twenty-seven patients with out-of-hospital cardiac arrest (n = 11), myocardial infarction (n = 6), and angina pectoris (n = 10), and 12 control subjects. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Mononuclear leukocyte beta 2-adrenergic receptor density and affinity were measured in patients 15 mins after successful cardiopulmonary resuscitation and after the diagnosis of myocardial infarction or angina pectoris, respectively, and were measured as well in control subjects. Plasma concentrations of catecholamines, glucose, and lactate were simultaneously measured with heart rate and blood pressure. After cardiac arrest, the density of beta 2-adrenergic receptors (1858 +/- 188 sites/cell [p < .01]), plasma epinephrine concentration (31,990 +/- 14,526 pg/mL [174.6 +/- 79.3 nmol/L] [p < .01]), heart rate (100 +/- 6 beats/min [p < .01]), glucose concentration (14.9 +/- 0.8 mmol/L [p < .01]), and lactate concentration (10.9 +/- 0.6 mmol/L [p < .01]) were increased in patients compared with those values in healthy controls. CONCLUSION: Acute maximal stress, such as after cardiac arrest, is associated with an increase in the density of beta 2-adrenergic receptors on mononuclear leukocytes derived from patients after successful cardiopulmonary resuscitation.

Randomised comparison of epinephrine and vasopressin in patients with out-of-hospital ventricular fibrillation.

BACKGROUND: Studies in animals have suggested that intravenous vasopressin is associated with better vital-organ perfusion and resuscitation rates than is epinephrine in the treatment of cardiac arrest. We did a randomised comparison of vasopressin with epinephrine in patients with ventricular fibrillation in out-of-hospital cardiac arrest. METHODS: 40 patients in ventricular fibrillation resistant to electrical defibrillation were prospectively and randomly assigned epinephrine (1 mg intravenously; n = 20) or vasopressin (40 U intravenously; n = 20) as primary drug therapy for cardiac arrest. The endpoints of this double blind study were successful resuscitation (hospital admission), survival for 24 h, survival to hospital discharge and neurological outcome (Glasgow coma scale). Analyses were by intention to treat. FINDINGS: Seven (35%) patients in the epinephrine group and 14 (70%) in the vasopressin group survived to hospital admission (p = 0.06). At 24 h, four (20%) epinephrine-treated patients and 12 (60%) vasopressin-treated patients were alive (p = 0.02). Three (15%) patients in the epinephrine group and eight (40%) in the vasopressin group survived to hospital discharge (p = 0.16). Neurological outcomes were similar (mean Glasgow coma score at hospital discharge 10.7 [SE 3.8] vs 11.7 [1.6], p = 0.78). INTERPRETATION: In this preliminary study, a significantly larger proportion of patients created with vasopressin than of those treated with epinephrine were resuscitated successfully from out-of-hospital ventricular fibrillation and survived for 24 h. Based upon these findings, larger multicentre studies of vasopressin in the treatment of cardiac arrest are needed.

[Ventilation during cardiopulmonary resuscitation (CPR). A literature study and analysis of ventilation strategies]. / Beatmung während der kardiopulmonalen Reanimation (CPR). Eine Literaturstudie und Analyse von Beatmungsstrategien.

In a recently published German multicenter study, 25% of the patients with witnessed cardiac arrest outside the hospital were resuscitated successfully and discharged from the hospital. Approximately 100,000 people suffer a fatal cardiac arrest in Germany annually, which is approximately tenfold the number of deaths from motor vehicle accidents. Cardiopulmonary resuscitation (CPR) performed by bystanders is an important part of the chain of survival to minimize the time interval without artificial circulation and ventilation in a cardiac arrest victim. This is especially important in areas with long response times of the emergency medical service (EMS). Early examples of ventilation have been described throughout history. References to mouth-to-mouth ventilation (MTMV) are found in the Bible, in a description of the resuscitation of a coal miner in 1744, and in an experiment in 1796 demonstrating that exhaled gas was safe for breathing. In 1954, Elam and colleagues described artificial respiration with the exhaled gas of a rescuer using a mouth-to-mask ventilation method. The modern CPR era started with the combination of MTMV and chest compressions 35 years ago. However, the value of MTMV is currently under discussion because of a widespread fear of transmission of infectious diseases. Healthcare professionals have stated in several studies that they may withhold MTMV when confronted with a cardiac arrest in a stranger. Although an infection with Mycobacterium tuberculosis is more likely than one with HIV via MTMV, the fear of the public is understandable. An expert committee of the American Heart Association stated that MTMV may be omitted in the initial phase of cardiac arrest, and considered recommending chest compressions only if the EMS will arrive rapidly. In paralyzed volunteers, however, ventilation induced by chest compressions was not able to provide sufficient gas exchange, especially when the airway was not protected. Laboratory investigations studying ventilation during CPR showed controversial results; in one animal model of cardiac arrest with muscle paralysis, chest compressions were not sufficient for adequate gas exchange, but active compression-decompression CPR achieved reasonable ventilation. Animal models that prevented gasping during cardiac arrest required ventilation during CPR, whereas gasping animals seemed to be satisfactorily ventilated with chest compressions alone. The question whether spontaneous gasping after cardiac arrest in humans may be sufficient for oxygenation and carbon dioxide elimination is debatable and remains unanswered at this time. When cardiac arrest is monitored, frequent coughing by the patient may maintain artificial ventilation and circulation for 30 s. The strategy to compress the thorax first and then maintain the airway and perform ventilation may only have an advantage for the first 30 s of CPR. Therefore, MTMV remains the therapy of choice to ventilate the victim of cardiac arrest. If a rescuer chooses to not perform MTMV, at least chest compressions should be administered. During ventilation with an unprotected airway, tidal volumes of 0.5 l instead 0.8-1.2 l may have an advantage. This strategy would decrease the inspiratory flow rate and, therefore, peak airway inflation pressure, which is associated with stomach inflation. Animal models indicate that lower esophageal sphincter pressure may decrease rapidly to 5 cm H2O during cardiac arrest, which may further increase the importance of a low peak airway pressure during ventilation with an unprotected airway. Gastric inflation may cause, besides regurgitation, aspiration, and pneumonia, an increased intragastric pressure, which may push up the diaphragm, decrease lung compliance, and induce a vicious circle of hypoventilation and stomach inflation.(ABSTRACT TRUNCATED)

Cardiovascular function during the postresuscitation phase after cardiac arrest in pigs: a comparison of epinephrine versus vasopressin.

OBJECTIVE: The administration of vasopressin during cardiopulmonary resuscitation (CPR) provides significantly more vital organ blood flow when compared with epinephrine during cardiac arrest in pigs. The effects of this potent vasoconstrictor on postresuscitation cardiovascular function remain unknown. The purpose of this study was to compare the effects of vasopressin and epinephrine on cardiovascular function in the postresuscitation phase after CPR. DESIGN: Prospective, randomized, experimental study. SETTING: University research laboratory. SUBJECTS: Domestic pigs, 12 to 14 wks of age. INTERVENTIONS: Sixteen pigs were randomly allocated to receive either 0.045 mg/kg of epinephrine or 0.4 U/kg of vasopressin after 4 mins of cardiac arrest. MEASUREMENTS AND MAIN RESULTS: Hemodynamics, left ventricular contractility, and myocardial blood flow were measured for an interval of 240 mins after successful CPR. Differences between animals treated with epinephrine vs. vasopressin were most pronounced 15 mins after restoration of spontaneous circulation. At this time, mean aortic pressure was 64 +/- 6 (SEM) mm Hg in the epinephrine group and 84 +/- 6 mm Hg (p < .05) in the vasopressin group. Systemic vascular resistance was 1285 +/- 72 dyne.sec/cm5 in the epinephrine group and 2314 +/- 130 dyne.sec/cm5 (p < .001) in the vasopressin group. Cardiac index was 140 +/- 9 mL/min/kg in animals treated with epinephrine and 99 +/- 9 mL/min/kg (p < .01) in animals treated with vasopressin. Myocardial contractility (dp/ dtmax/P) was 52.8 +/- 3.4/sec with epinephrine as compared with 36.3 +/- 2.9 sec-1 (p < .01) with vasopressin. Left ventricular epicardial blood flow was 241 +/- 35 mL/min/100 g with epinephrine and 142 +/- 22 mL/min/100 g (p < .05) with vasopressin. Four hours after CPR, no significant differences were observed between groups. CONCLUSIONS: In the early postresuscitation phase, vasopressin provided higher systemic blood pressures and there was a reversible depressant effect on myocardial function when compared with epinephrine. Overall cardiovascular function was not irreversibly or critically impaired after the administration of vasopressin in this pig model of cardiac arrest.

Cerebral oxygenation during cardiopulmonary resuscitation with epinephrine and vasopressin in pigs.

BACKGROUND AND PURPOSE: Administration of vasopressin during cardiopulmonary resuscitation (CPR) improves vital organ blood flow compared with epinephrine, but the effect of vasopressin on cerebral oxygenation and cerebral venous hypercarbia during CPR has not previously been studied. METHODS: Fourteen pigs were allocated to receive either epinephrine (0.2 mg/kg) or vasopressin (0.4 U/kg) after 4 minutes of ventricular fibrillation and 3 minutes of CPR. Cerebral blood flow was determined by radiolabeled microspheres, and arterial and cerebral venous blood gases were measured. RESULTS: Cerebral blood flow, measured before and 90 seconds and 5 minutes after drug administration, was 9 (3; 12), 25 (19; 27), and 18 (10; 23) mL/min per 100 g (median and 25th and 75th percentiles, respectively) in the epinephrine group and 12 (5; 16), 51 (48; 70), and 53 (45; 63) mL/min per 100 g in the vasopressin group (P<.05 at 90 seconds, P<.01 at 5 minutes between groups). Five minutes after drug administration, cerebral venous Pco2 was 63 (59; 68) mm Hg in the epinephrine group and 47 (43; 55) mm Hg in the vasopressin group (P<.01); at the same time cerebral venous pH was 7.18 (7.17; 7.20) and 7.26 (7.22; 7.36) (P<.01) in the epinephrine and vasopressin groups, respectively. Cerebral oxygen extraction ratio, calculated before and 90 seconds and 5 minutes after drug administration, was 0.42 (0.32; 0.57), 0.47 (0.41; 0.57), and 0.56 (0.56; 0.64) in the epinephrine group and 0.43 (0.38; 0.45), 0.38 (0.25; 0.44), and 0.35 (0.33; 0.49) in the vasopressin group (P<.05 at 90 seconds and 5 minutes). CONCLUSIONS: Compared with epinephrine, vasopressin not only increases cerebral blood flow but also improves cerebral oxygenation and decreases cerebral venous hypercarbia when administered during CPR in pigs.

Regulation of right atrial beta-adrenoceptors after cardiopulmonary resuscitation in pigs.

OBJECTIVE: to test the hypothesis that right atrial beta-adrenoceptors are down-regulated after CPR and administration of beta-adrenergic agents. METHODS: after 3 min of ventricular fibrillation and 3 min of cardiac massage, 6 pigs received adrenaline (45 micrograms/kg) intravenously before defibrillation. After restoration of spontaneous circulation, dopamine was given in order to maintain the mean arterial blood pressure stable. Right atrial beta-adrenergic binding sites were determined by an equilibration binding assay using (-)-125Iodocyanopindolol. RESULTS: plasma adrenaline (mean +/- S.E.M.) was 1.1 +/- 0.9 ng/ml (6.0 +/- 4.9 nmol/l) pre-arrest and increased to 63.8 +/- 45.8 (348.2 +/- 250.0 nmol/l) (P < 0.05) and 1034 +/- 344 ng/ml (5644 +/- 1878 nmol/l) (P < 0.05) during CPR before and after adrenaline administration. At points in time 30 and 120 min after successful CPR, plasma adrenaline was 2.4 +/- 0.5 and 1.3 +/- 0.3 ng/ml (13.1 +/- 2.7 and 7.1 +/- 1.6 nmol/l). Compared to pre-arrest, the density of high-affinity beta-adrenoceptors was 29.0 +/- 12.8 fmol/mg pre-arrest and was 69.4 +/- 21.6 and 84.2 +/- 16.7 fmol/mg (P < 0.05 vs. pre-arrest) 30 and 120 min after CPR. The density of low-affinity as well as of total binding sites was not significantly changed after CPR. CONCLUSIONS: it is concluded that markedly elevated plasma catecholamine concentrations after CPR and administration of adrenaline and dopamine do not lead to a decrease in the total density of beta-adrenoceptors but to an increase in high-affinity beta-adrenoceptors in right atrial cells.

Vasopressin administration in refractory cardiac arrest.

BACKGROUND: Successful outcomes after cardiopulmonary resuscitation remain disappointingly infrequent, in animal studies, administration of exogenous vasopressin during closed- and open-chest cardiopulmonary resuscitation has recently been shown to be more effective than optimal doses of epinephrine in improving vital organ blood flow. OBJECTIVE: To describe the clinical effects and outcomes of administering vasopressin to patients in cardiac arrest refractory to current medical therapies. DESIGN: Case reports. SETTING: University hospital. PATIENTS: 8 adults with in-hospital cardiac arrest. INTERVENTIONS: After intravenous epinephrine (administered according to American Heart Association guidelines) and defibrillation efforts had failed, patients in cardiac arrest who were having cardiopulmonary resuscitation received 40 U of vasopressin intravenously and then defibrillation. MEASUREMENTS: Return of spontaneous circulation and hospital discharge rates. RESULTS: After administration of vasopressin, spontaneous circulation was promptly restored in all patients. Three patients were discharged from the hospital with intact neurologic function; the other five lived for between 30 minutes and 82 hours. CONCLUSION: In the presence of ventricular fibrillation with severe hypoxia and acidosis, vasopressin seems to be more potent and effective than adrenergic vasopressors for restoring spontaneous cardiovascular function. These results do not justify the widespread use of vasopressin for refractory cardiac arrest. However, on the basis of these cases, further studies comparing vasopressin with epinephrine are warranted in an effort to improve the currently dismal prognosis of patients after cardiac arrest.

Effects of epinephrine and vasopressin on median fibrillation frequency and defibrillation success in a porcine model of cardiopulmonary resuscitation.

OBJECTIVE: This study was designed to assess whether median frequency of ventricular fibrillation (VF) correlates with myocardial blood flow and defibrillation success during cardiopulmonary resuscitation (CPR) after epinephrine or vasopressin administration. METHODS AND RESULTS: After 4 min of VF and 3 min of CPR, 14 pigs received 0.045 mg/kg epinephrine or 0.4 U/kg vasopressin. Using radio-labeled microspheres, median myocardial blood flow during CPR before, and 90 s and 5 min after drug administration (DA) was 15.5 (12.6, 23.1; 25th percentile, 75th percentile), 26.4 (18.5, 29.1), 16.9 (14.9, 19.1) mL min-1 100 g-1, respectively, in the epinephrine, and 16.9 (15.4, 18.9), 48.1 (36.9, 68.9) (P < 0.05 vs. before DA), 52.3 (38.5, 65.0) mL min-1 100 g-1, respectively, in the vasopressin group. Using spectral analysis of VF, median frequency of VF was 11.0 (10.7, 11.8), 11.3 (9.6, 13.1), 10.2, (8.8, 11.4) Hz, respectively, in the epinephrine, and 10.1 (10.0, 10.5), 11.7 (11.1, 14.2) (P < 0.05 vs. before DA), 13.2 (11.5, 13.9) Hz, respectively, in the vasopressin group at the same points in time. Median frequency correlates significantly with myocardial blood flow in the epinephrine (n = 21); rs = 0.772; P < 0.001) and in the vasopressin group (n = 21; rs = 0.905; P < 0.001). Median fibrillation frequency before the first defibrillation was 13.0 (12.2, 13.2) Hz in resuscitated (n = 8) and 9.2 (8.3, 10.2) Hz (n = 6) in non-resuscitated animals (P < 0.01). CONCLUSIONS: We conclude that median frequency of VF reflects myocardial blood flow and the chance of successful defibrillation during closed-chest CPR after vasopressor treatment in a porcine model of VF.

Effects of ventilation on hemodynamics and myocardial blood flow during active compression-decompression resuscitation in pigs.

BACKGROUND: Active compression-decompression (ACD) improves hemodynamics and vital organ blood flow during cardiopulmonary resuscitation. The effects of intermittent positive pressure ventilation (IPPV) on ACD have not been studied. This study was designed to compare the effects of ACD with and without IPPV on gas exchange, hemodynamics, and myocardial blood flow. METHODS: After 30 s ventricular fibrillation, 14 tracheally intubated pigs were allocated to receive either ACD combined with IPPV (ACD-IPPV) or ACD alone. In animals treated with ACD-IPPV, the lungs were ventilated using a servo ventilator. Animals treated with ACD received 100% oxygen by a reservoir but ventilation was not assisted. RESULTS: Minute ventilation (median) was 6.5 and 6.1 l/min after 1 and 7 min of ACD-IPPV, and was 4.2 and 1.6 l/min after 1 and 7 min of ACD. In contrast to ACD-IPPV, PaO2 was less and PaCO2 was greater with ACD. Mean arterial (53 and 40 mmHg; P < 0.05) and mean central venous pressure (25 and 14 mmHg; P < 0.01) were greater during ACD-IPPV as compared with ACD. After administration of epinephrine 0.2 mg/kg, myocardial blood flow increased only in ACD-IPPV treated animals, and 5 min after epinephrine administration, myocardial blood flow was greater during ACD-IPPV (33 ml.min-1.100 g-1) as compared with ACD (15 ml.min-1.100 g-1; P < 0.05). Restoration of spontaneous circulation could be achieved only in animals subjected to ACD-IPPV. CONCLUSIONS: Gas exchange was critically impaired during the late phase of ACD. Compared with ACD-IPPV, myocardial blood flow was less preserved with ACD and was too low to achieve restoration of spontaneous circulation.