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Biomedical subjects

Volker Wenzel

Publications and source records attributed to Volker Wenzel.

At least 19 recordsLinked to original sources
PubMed2006

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.

Airway Resistance↗
PubMed2006

Terlipressin as an adjunct vasopressor in refractory hypotension after tricyclic antidepressant intoxication.

AIM OF STUDY: To report the management of cardiovascular failure refractory to standard catecholamine therapy with terlipressin in a patient with tricyclic antidepressant (TCA) intoxication. CASE REPORT: A 41-year-old woman, with suicidal ingestion of 11.25 g amitriptyline and 1500 mg diclofenac, was admitted to the emergency department. After 30 min in ventricular fibrillation, with ongoing CPR, she regained a potentially perfusing rhythm, but with hypotension refractory to standard catecholamine therapy with adrenaline, 2 microg/kg/min (norepinephrine); adrenaline, 1 microg/kg/min (epinephrine) until 55 min after admission. An injection of 1 mg terlipressin restored mean arterial blood pressure >65 mmHg within 10 min. Ten hours after admission to the intensive care unit, catecholamine support could be withdrawn because of a stable haemodynamic state. Within 7 days, all organ function recovered, and the patient regained full neurological function. CONCLUSIONS: Successful management of cardiovascular failure with terlipressin after TCA intoxication refractory to catecholamines suggests a potential role for terlipressin as an adjunct vasopressor in severely hypotensive patients.

Adult↗
PubMed2006

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.

Animals↗
PubMed2006

Arginine vasopressin in advanced cardiovascular failure during the post-resuscitation phase after cardiac arrest.

Arginine vasopressin (AVP) has been employed successfully during cardiopulmonary resuscitation, but there exist only few data about the effects of AVP infusion for cardiovascular failure during the post-cardiac arrest period. Cardiovascular failure is one of the main causes of death after successful resuscitation from cardiac arrest. Although the "post-resuscitation syndrome" has been described as a "sepsis-like" syndrome, there is little information about the haemodynamic response to AVP in advanced cardiovascular failure after cardiac arrest. In this retrospective study, haemodynamic and laboratory variables in 23 patients with cardiovascular failure unresponsive to standard haemodynamic therapy during the post-cardiac arrest period were obtained before, and 30 min, 1, 4, 12, 24, 48, and 72 h after initiation of a supplementary AVP infusion (4 IU/h). During the observation period, AVP significantly increased mean arterial blood pressure (58+/-14 to 75+/-19 mmHg, p < 0.001), and decreased noradrenaline (norepinephrine) (1.31+/-2.14 to 0.23+/-0.3 microg/kg/min, p = 0.03), adrenaline (epinephrine) (0.58+/-0.23 to 0.04+/-0.03 microg/kg/min, p = 0.001), and milrinone requirements (0.46+/-0.15 to 0.33+/-0.22 microg/kg/min, p < 0.001). Pulmonary capillary wedge pressure changed significantly (p < 0.001); an initial increase being followed by a decrease below baseline values. While arterial lactate concentrations (95+/-64 to 21+/-18 mg/dL, p < 0.001) and pH (7.27+/-0.14 to 7.4+/-0.14, p < 0.001) improved significantly, total bilirubin concentrations (1.12+/-0.95 to 3.04+/-3.79 mg/dL, p = 0.001) increased after AVP. There were no differences in the haemodynamic or laboratory response to AVP between survivors and non-survivors. In this study, advanced cardiovascular failure that was unresponsive to standard therapy could be reversed successfully with supplementary AVP infusion in >90% of patients surviving cardiac arrest.

Aged↗
PubMed2006

Brain tissue oxygen pressure and cerebral metabolism in an animal model of cardiac arrest and cardiopulmonary resuscitation.

OBJECTIVE: Direct measurement of brain tissue oxygenation (PbtO2) is established during spontaneous circulation, but values of PbtO2 during and after cardiopulmonary resuscitation (CPR) are unknown. The purpose of this study was to investigate: (1) the time-course of PbtO2 in an established model of CPR, and (2) the changes of cerebral venous lactate and S-100B. METHODS: In 12 pigs (12-16 weeks, 35-45 kg), ventricular fibrillation (VF) was induced electrically during general anaesthesia. After 4 min of untreated VF, all animals were subjected to CPR (chest compression rate 100/min, FiO2 1.0) with vasopressor therapy after 7, 12, and 17 min (vasopressin 0.4, 0.4, and 0.8 U/kg, respectively). Defibrillation was performed after 22 min of cardiac arrest. After return of spontaneous circulation (ROSC), the pigs were observed for 1h. RESULTS: After initiation of VF, PbtO2 decreased compared to baseline (mean +/- SEM; 22 +/- 6 versus 2 +/- 1 mmHg after 4 min of VF; P < 0.05). During CPR, PbtO2 increased, and reached maximum values 8 min after start of CPR (25 +/- 7 mmHg; P < 0.05 versus no-flow). No further changes were seen until ROSC. Lactate, and S-100B increased during CPR compared to baseline (16 +/- 2 versus 85 +/- 8 mg/dl, and 0.46 +/- 0.05 versus 2.12 +/- 0.40 microg/l after 13 min of CPR, respectively; P < 0.001); lactate remained elevated, while S-100B returned to baseline after ROSC. CONCLUSIONS: Though PbtO2 returned to pre-arrest values during CPR, PbtO2 and cerebral lactate were lower than during post-arrest reperfusion with 100% oxygen, which reflected the cerebral low-flow state during CPR. The transient increase of S-100B may indicate a disturbance of the blood-brain-barrier.

Animals↗
PubMed2006

Copeptin and arginine vasopressin concentrations in critically ill patients.

CONTEXT: Determination of arginine vasopressin (AVP) concentrations may be helpful to guide therapy in critically ill patients. A new assay analyzing copeptin, a stable peptide derived from the AVP precursor, has been introduced. OBJECTIVE: Our objective was to determine plasma copeptin concentrations. DESIGN: We conducted a post hoc analysis of plasma samples and data from a prospective study. SETTING: The setting was a 12-bed general and surgical intensive care unit (ICU) in a tertiary university teaching hospital. PATIENTS: Our subjects were 70 healthy volunteers and 157 ICU patients with sepsis, with systemic inflammatory response syndrome (SIRS), and after cardiac surgery. INTERVENTIONS: There were no interventions. MAIN OUTCOME MEASURES: Copeptin plasma concentrations, demographic data, AVP plasma concentrations, and a multiple organ dysfunction syndrome score were documented 24 h after ICU admission. RESULTS: AVP (P < 0.001) and copeptin (P < 0.001) concentrations were significantly higher in ICU patients than in controls. Patients after cardiac surgery had higher AVP (P = 0.003) and copeptin (P = 0.003) concentrations than patients with sepsis or SIRS. Independent of critical illness, copeptin and AVP correlated highly significantly with each other. Critically ill patients with sepsis and SIRS exhibited a significantly higher ratio of copeptin/AVP plasma concentrations than patients after cardiac surgery (P = 0.012). The American Society of Anesthesiologists' classification (P = 0.046) and C-reactive protein concentrations (P = 0.006) were significantly correlated with the copeptin/AVP ratio. CONCLUSIONS: Plasma concentrations of copeptin and AVP in healthy volunteers and critically ill patients correlate significantly with each other. The ratio of copeptin/AVP plasma concentrations is increased in patients with sepsis and SIRS, suggesting that copeptin may overestimate AVP plasma concentrations in these patients.

Adult↗
PubMed2006

Arteriolar vasoconstrictive response: comparing the effects of arginine vasopressin and norepinephrine.

INTRODUCTION: This study was designed to examine differences in the arteriolar vasoconstrictive response between arginine vasopressin (AVP) and norepinephrine (NE) on the microcirculatory level in the hamster window chamber model in unanesthetized, normotonic hamsters using intravital microscopy. It is known from patients with advanced vasodilatory shock that AVP exerts strong additional vasoconstriction when incremental dosage increases of NE have no further effect on mean arterial blood pressure (MAP). METHODS: In a prospective controlled experimental study, eleven awake, male golden Syrian hamsters were instrumented with a viewing window inserted into the dorsal skinfold. NE (2 microg/kg/minute) and AVP (0.0001 IU/kg/minute, equivalent to 4 IU/h in a 70 kg patient) were continuously infused to achieve a similar increase in MAP. According to their position within the arteriolar network, arterioles were grouped into five types: A0 (branch off small artery) to A4 (branch off A3 arteriole). RESULTS: Reduction of arteriolar diameter (NE, -31 +/- 12% versus AVP, -49 +/- 7%; p = 0.002), cross sectional area (NE, -49 +/- 17% versus AVP, -73 +/- 7%; p = 0.002), and arteriolar blood flow (NE, -62 +/- 13% versus AVP, -80 +/- 6%; p = 0.004) in A0 arterioles was significantly more pronounced in AVP animals. There was no difference in red blood cell velocities in A0 arterioles between groups. The reduction of diameter, cross sectional area, red blood cell velocity, and arteriolar blood flow in A1 to A4 arterioles was comparable in AVP and NE animals. CONCLUSION: Within the microvascular network, AVP exerted significantly stronger vasoconstriction on large A0 arterioles than NE under physiological conditions. This observation may partly explain why AVP is such a potent vasopressor hormone and can increase systemic vascular resistance even in advanced vasodilatory shock unresponsive to increases in standard catecholamine therapy.

Animals↗
PubMed2006

Effects of face mask ventilation in apneic patients with a resuscitation ventilator in comparison with a bag-valve-mask.

Bag-valve-mask ventilation in an unprotected airway is often applied with a high flow rate or a short inflation time and, therefore, a high peak airway pressure, which may increase the risk of stomach inflation and subsequent pulmonary aspiration. Strategies to provide more patient safety may be a reduction in inspiratory flow and, therefore, peak airway pressure. The purpose of this study was to evaluate the effects of bag-valve-mask ventilation vs. a resuscitation ventilator on tidal volume, peak airway pressure, and peak inspiratory flow rate in apneic patients. In a crossover design, 40 adults were ventilated during induction of anesthesia with either a bag-valve-mask device with room air, or an oxygen-powered, flow-limited resuscitation ventilator. The study endpoints of expired tidal volume, minute volume, respiratory rate, peak airway pressure, delta airway pressure, peak inspiratory flow rate and inspiratory time fraction were measured using a pulmonary monitor. When compared with the resuscitation ventilator, the bag-valve-mask resulted in significantly higher (mean+/-SD) peak airway pressure (15.3+/-3 vs. 14.1+/-3 cm H2O, respectively; p=0.001) and delta airway pressure (14+/-3 vs. 12+/-3 cm H2O, respectively; p<0.001), but significantly lower oxygen saturation (95+/-3 vs. 98+/-1%, respectively; p<0.001). No patient in either group had clinically detectable stomach inflation. We conclude that the resuscitation ventilator is at least as effective as traditional bag-valve-mask or face mask resuscitation in this population of very controlled elective surgery patients.

Apnea↗
PubMed2006

[Arginine-vasopressin in septic and vasodilatorial shock].

Current therapy of septic/vasodilatory cardiovascular failure includes volume resuscitation and infusion of inotropic and vasopressor agents. Norepinephrine is the first-line vasoconstrictor, and can stabilize hemodynamic variables in most patients. Nonetheless, irreversible cardiovascular failure which is resistant to conventional hemodynamic therapies still is the main cause of death in patients with severe sepsis and septic shock. In such advanced, catecholamine-resistant shock states, arginine-vasopressin (AVP) has repeatedly caused an increase in mean arterial blood pressure, a decrease in toxic norepinephrine-dosages, as well as further beneficial hemodynamic, endocrinologic and renal effects. Although AVP exerted negative inotropic effects in previous clinical trials and in selected animal experiments, a continuous low-dose AVP infusion during advanced septic/vasodilatory shock caused a decrease in cardiac index only in patients with a hyperdynamic circulation. Adverse effects on gastrointestinal circulation and the systemic microcirculation can not be excluded, but have not yet been confirmed in clinical prospective trials. Negative side effects of a supplementary AVP therapy are an increase in total bilirubin concentrations, and a decrease in platelet count. A transient increase in hepatic transaminases during AVP infusion is most likely related to preceding hypotensive episodes. Important points which must be considered when using AVP as a "rescue vasopressor" in septic/vasodilatory shock states are: 1) AVP infusion only in advanced shock states that can not be adequately reversed by conventional hemodynamic therapy (e.g. norepinephrine >0,5-0,6 mug/kg/min), 2) presence of normovolemia, 3) AVP infusion only in combination with norepinephrine, 4) strict avoidance of bolus injections and dosages >4 IU/h. Effects of a supplementary AVP infusion in advanced vasodilatory shock on survival are currently examined in a large, prospective multicenter trial in North America and Australia.

Arginine Vasopressin↗
PubMed2006

Drug treatment and thrombolytics during cardiopulmonary resuscitation.

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

Cardiopulmonary Resuscitation↗
PubMed2006

Serum vasopressin concentrations in critically ill patients.

OBJECTIVE: To measure arginine vasopressin (AVP) serum concentrations in critically ill patients. DESIGN: Prospective study. SETTING: Twelve-bed general and surgical intensive care unit in a tertiary, university teaching hospital. PATIENTS: Two-hundred-thirty-nine mixed critically ill patients and 70 healthy volunteers. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Demographic data, hemodynamic variables, vasopressor drug requirements, blood gases, AVP serum concentrations within 24 hrs after admission, multiple organ dysfunction score, and outcome were recorded. Twenty-four hours after admission, study patients had significantly higher AVP concentrations (11.9 +/- 20.6 pg/mL) than healthy controls (0.92 +/- 0.38 pg/mL; p < .001). Males had lower AVP concentrations than females (9.7 +/- 19.5 vs. 15.1 +/- 20.6 pg/mL; p = .014). Patients with hemodynamic dysfunction had higher AVP concentrations than patients without hemodynamic dysfunction (14.1 +/- 27.1 vs. 8.7 +/- 10.8 pg/mL; p = .042). Patients after cardiac surgery (n = 96) had significantly higher AVP concentrations when compared to patients admitted for other diagnoses (n = 143; p < .001). AVP concentrations were inversely correlated with length of stay in the intensive care unit (correlation coefficient, -0.222; p = .002). There was no correlation between serum AVP concentrations and the incidence of shock or specific hemodynamic parameters. Four (1.7%) of the 239 study patients met criteria for an absolute AVP deficiency (AVP, <0.83 pg/mL), and 32 (13.4%) met criteria for a relative AVP deficiency (AVP, <10 pg/mL, and mean arterial pressure, <70 mm Hg). In shock patients, relative AVP deficiency occurred in 22.2% (septic shock), 15.4% (postcardiotomy shock), and 10% (shock due to a severe systemic inflammatory response syndrome) (p = .316). CONCLUSIONS: AVP serum concentrations 24 hrs after intensive care unit admission were significantly increased in this mixed critically ill patient population. The lack of a correlation between AVP serum concentrations and hemodynamic parameters suggests complex dysfunction of the vasopressinergic system in critical illness. Relative and absolute AVP deficiency may be infrequent entities during acute surgical critical illness, mostly remaining without significant effects on cardiovascular function.

Case-Control Studies↗
PubMed2006

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.

Animals↗
PubMed2006

Cutaneous vascular reactivity and flow motion response to vasopressin in advanced vasodilatory shock and severe postoperative multiple organ dysfunction syndrome.

INTRODUCTION: Disturbances in microcirculatory homeostasis have been hypothesized to play a key role in the pathophysiology of multiple organ dysfunction syndrome and vasopressor-associated ischemic skin lesions. The effects of a supplementary arginine vasopressin (AVP) infusion on microcirculation in vasodilatory shock and postoperative multiple organ dysfunction syndrome are unknown. METHOD: Included in the study were 18 patients who had undergone cardiac or major surgery and had a mean arterial blood pressure below 65 mmHg, despite infusion of more than 0.5 microg/kg per min norepinephrine. Patients were randomly assigned to receive a combined infusion of AVP/norepinephrine or norepinephrine alone. Demographic and clinical data were recorded at study entry and after 1 hour. A laser Doppler flowmeter was used to measure the cutaneous microcirculatory response at randomization and after 1 hour. Reactive hyperaemia and oscillatory changes in the Doppler signal were measured during the 3 minutes before and after a 5-minute period of forearm ischaemia. RESULTS: Patients receiving AVP/norepinephrine had a significantly higher mean arterial pressure (P = 0.047) and higher milrinone requirements (P = 0.025) than did the patients who received norepinephrine only at baseline. Mean arterial blood pressure significantly increased (P < 0.001) and norepinephrine requirements significantly decreased (P < 0.001) in the AVP/norepinephrine group. Patients in the AVP/norepinephrine group exhibited a significantly higher oscillation frequency of the Doppler signal before ischaemia and during reperfusion at randomization. During the study period, there were no differences in either cutaneous reactive hyperaemia or the oscillatory pattern of vascular tone between groups. CONCLUSION: Supplementary AVP infusion in patients with advanced vasodilatory shock and severe postoperative multiple organ dysfunction syndrome did not compromise cutaneous reactive hyperaemia and flowmotion when compared with norepinephrine infusion alone.

Aged↗
PubMed2006

Vasopressin combined with epinephrine during cardiac resuscitation: a solution for the future?

Epinephrine given during cardiopulmonary resuscitation (CPR) may cause beta-mimetic complications in the postresuscitation phase. Vasopressin may be an alternative vasopressor drug during CPR. A subgroup analysis of a large prospective CPR investigation and of retrospective CPR studies suggests that vasopressin may be especially beneficial when combined with epinephrine. Beneficial effects of adding vasopressin were observed in other catecholamine-refractory shock states as well, such as vasodilatory shock and haemorrhagic shock. In order to maximize effects of any vasopressor during CPR, rapid aggressive chest compressions must be ensured to maximize blood flow and to enable advanced cardiac life support drugs to reach the arterial vasculature. We suggest alternating injections of 1 mg epinephrine i.v. and 40 IU vasopressin i.v. every 3-5 minutes during CPR until spontaneous circulation can be achieved or CPR efforts are terminated.

Cardiopulmonary Resuscitation↗
PubMed2006

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.

Animals↗