naloxone and Heart-Arrest

Opioids are effective analgesics, but they can have harmful adverse effects, such as addiction and potentially fatal respiratory depression. Naloxone is currently the only available treatment for reversing the negative effects of opioids, including respiratory depression. However, the effectiveness of naloxone, particularly after an opioid overdose, varies depending on the pharmacokinetics and the pharmacodynamics of the opioid that was overdosed. Long-acting opioids, and those with a high affinity at the µ-opioid receptor and/or slow receptor dissociation kinetics, are particularly resistant to the effects of naloxone. In this review, the authors examine the pharmacology of naloxone and its safety and limitations in reversing opioid-induced respiratory depression under different circumstances, including its ability to prevent cardiac arrest.

Topics: Analgesics, Opioid; Drug Overdose; Heart Arrest; Humans; Naloxone; Narcotic Antagonists; Opiate Overdose; Respiratory Insufficiency

This review comprises the most extensive literature search and evidence evaluation to date on the most important international BLS interventions, diagnostics, and prognostic factors for cardiac arrest victims. It reemphasizes that the critical lifesaving steps of BLS are (1) prevention, (2) immediate recognition and activation of the emergency response system, (3) early high-quality CPR, and (4) rapid defibrillation for shockable rhythms. Highlights in prevention indicate the rational and judicious deployment of search-and-rescue operations in drowning victims and the importance of education on opioid-associated emergencies. Other 2015 highlights in recognition and activation include the critical role of dispatcher recognition and dispatch-assisted chest compressions, which has been demonstrated in multiple international jurisdictions with consistent improvements in cardiac arrest survival. Similar to the 2010 ILCOR BLS treatment recommendations, the importance of high quality was reemphasized across all measures of CPR quality: rate, depth, recoil, and minimal chest compression pauses, with a universal understanding that we all should be providing chest compressions to all victims of cardiac arrest. This review continued to focus on the interface of BLS sequencing and ensuring high-quality CPR with other important BLS interventions, such as ventilation and defibrillation. In addition, this consensus statement highlights the importance of EMS systems, which employ bundles of care focusing on providing high-quality chest compressions while extricating the patient from the scene to the next level of care. Highlights in defibrillation indicate the global importance of increasing the number of sites with public-access defibrillation programs. Whereas the 2010 ILCOR Consensus on Science provided important direction for the “what” in resuscitation (ie, what to do), the 2015 consensus has begun with the GRADE methodology to provide direction for the quality of resuscitation. We hope that resuscitation councils and other stakeholders will be able to translate this body of knowledge of international consensus statements to build their own effective resuscitation guidelines.

Topics: Adult; Age Factors; Analgesics, Opioid; Cardiopulmonary Resuscitation; Child; Defibrillators; Electric Countershock; Emergencies; Emergency Medical Services; Health Education; Heart Arrest; Heart Massage; Humans; Naloxone; Near Drowning; Observational Studies as Topic; Randomized Controlled Trials as Topic; Ventricular Fibrillation

Topics: Adult; Anaphylaxis; Cardiac Tamponade; Cardiopulmonary Resuscitation; Emergency Medical Services; Fat Emulsions, Intravenous; Female; Heart Arrest; Humans; Hypothermia; Naloxone; Near Drowning; Percutaneous Coronary Intervention; Pregnancy; Pregnancy Complications, Cardiovascular; Pulmonary Embolism; Water-Electrolyte Imbalance; Wounds and Injuries

Topics: Analgesics, Opioid; Emergency Service, Hospital; Female; Heart Arrest; Humans; Methadone; Middle Aged; Naloxone; Narcotic Antagonists

Pharmacologic agents are used to improve conditions that may contribute to the development of cardiac arrest such as dysrhythmias, hypotension, shock, or anoxia. The authors review the clinical application of several specific agents in resuscitation.

Topics: Adrenal Cortex Hormones; Anti-Arrhythmia Agents; Arrhythmias, Cardiac; Atropine; Bretylium Tosylate; Calcium Channel Blockers; Cardiotonic Agents; Dobutamine; Dopamine; Heart Arrest; Humans; Isoproterenol; Lidocaine; Naloxone; Norepinephrine; Resuscitation; Vasoconstrictor Agents

Noninvasive positive pressure ventilation (NIPPV) may improve postoperative lung function and reduce postoperative complications in patients undergoing abdominal surgery. The purpose of our study was to determine whether the timing of postoperative NIPPV affects lung function 1 day postoperatively.. Forty morbidly obese patients with known obstructive sleep apnea undergoing laparoscopic bariatric surgery with standardized anesthesia care were randomly assigned to receive NIPPV immediately after tracheal extubation (immediate group) or supplemental oxygen (standard group). All patients had continuous positive airway pressure initiated 30 minutes after extubation in the postanesthesia care unit (PACU) via identical noninvasive ventilators. Spirometry was performed by a blinded observer in the perioperative holding area 1 hour after admission to the PACU and 1 day postoperatively. The primary outcome was the change in forced vital capacity (FVC) from baseline to 24 hours (FVC baseline-FVC 24 hours).. Forty patients, 20 in each group, were enrolled in the study. Forced expiratory volume in 1 second, FVC, and peak expiratory flow rate were significantly reduced in both groups from perioperative values throughout the study. At 24 hours, the intervention group had lost only 0.7 L FVC, versus 1.3 L for the intervention group (P = 0.0005). An analysis of covariance confirmed this and indicated that the immediate postoperative NIPPV better preserved spirometric function at 1 and 24 hours postoperatively. Specifically, the differences in the primary outcome were statistically significant.. NIPPV given immediately after extubation significantly improves spirometric lung function at 1 hour and 1 day postoperatively, compared with continuous positive airway pressure started in the PACU, in morbidly obese patients with obstructive sleep apnea undergoing laparoscopic bariatric surgery.

Topics: Adult; Anesthesia, Inhalation; Bariatric Surgery; Critical Care; Female; Heart Arrest; Humans; Intubation, Intratracheal; Laparoscopy; Lung; Male; Middle Aged; Naloxone; Narcotic Antagonists; Obesity, Morbid; Oximetry; Oxygen; Peak Expiratory Flow Rate; Positive-Pressure Respiration; Respiration, Artificial; Respiratory Insufficiency; Sleep Apnea, Obstructive; Spirometry; Treatment Outcome; Vital Capacity

Naloxone is standard medication for the treatment of heroin intoxications. No large-scale studies have yet been carried out to determine its toxicity in heroin intoxications.. We have undertaken an investigation as to the frequency, type and degree of severity of complications attributable to naloxone administration. Subjects treated between 1991 and 1993 with naloxone for intravenous drug intoxications were prospectively evaluated.. Development of ventricular tachycardia or fibrillation; atrial fibrillation; asystole; pulmonary edema; convulsions; vomiting; and violent behavior within ten minutes after parenteral administration of naloxone.. Six of 453 intoxicated subjects (1.3%; 95% confidence interval 0.4%-3%) suffered severe adverse effects within ten minutes after naloxone administration (one asystole; three generalized convulsions; one pulmonary edema; and one violent behavior). After the ten minute period, no further complications were observed.. The short time between naloxone administration and the occurrence of complications, as well as the type of complications, are strong evidence of a causal link. In 1000 clinically diagnosed intoxications with heroin or heroin mixtures, from 4 to 30 serious complications can be expected. Such a high incidence of complications is unacceptable and could theoretically be reduced by artificial respiration with a bag valve device (hyperventilation) as well as by administering naloxone in minimal divided doses, injected slowly.

Topics: Adolescent; Adult; Aggression; Cocaine; Confidence Intervals; Drug Overdose; Female; Heart Arrest; Heroin; Humans; Illicit Drugs; Injections, Intramuscular; Injections, Intravenous; Male; Middle Aged; Naloxone; Narcotic Antagonists; Prospective Studies; Pulmonary Edema; Seizures; Substance Abuse, Intravenous

In response to a surge of deaths from synthetic opioid overdoses, there have been increased efforts to distribute naloxone products in community settings. Prior research has assessed the effectiveness of naloxone in the hospital setting; however, it is challenging to assess naloxone dosing regimens in the community/first-responder setting, including reversal of respiratory depression effects of fentanyl and its derivatives (fentanyls). Here, we describe the development and validation of a mechanistic model that combines opioid mu receptor binding kinetics, opioid agonist and antagonist pharmacokinetics, and human respiratory and circulatory physiology, to evaluate naloxone dosing to reverse respiratory depression. Validation supports our model, which can quantitatively predict displacement of opioids by naloxone from opioid mu receptors in vitro, hypoxia-induced cardiac arrest in vivo, and opioid-induced respiratory depression in humans from different fentanyls. After validation, overdose simulations were performed with fentanyl and carfentanil followed by administration of different intramuscular naloxone products. Carfentanil induced more cardiac arrest events and was more difficult to reverse than fentanyl. Opioid receptor binding data indicated that carfentanil has substantially slower dissociation kinetics from the opioid receptor compared with nine other fentanyls tested, which likely contributes to the difficulty in reversing carfentanil. Administration of the same dose of naloxone intramuscularly from two different naloxone products with different formulations resulted in differences in the number of virtual patients experiencing cardiac arrest. This work provides a robust framework to evaluate dosing regimens of opioid receptor antagonists to reverse opioid-induced respiratory depression, including those caused by newly emerging synthetic opioids.

Topics: Analgesics, Opioid; Drug Overdose; Fentanyl; Heart Arrest; Humans; Naloxone; Narcotic Antagonists; Opiate Overdose; Receptors, Opioid; Receptors, Opioid, mu; Respiratory Insufficiency

Benzonatate is a local anesthetic-like sodium channel antagonist that is widely prescribed as an antitussive. While it may be reasonable to assume that patients would present with a prolonged QRS interval following benzonatate overdose, the published literature does not support this. We report a case of a patient presenting following a benzonatate overdose with a prolonged QRS on her initial electrocardiograph (ECG) rhythm strip with rapid normalization of QRS duration.. A 14-year-old girl presented in cardiac arrest following a benzonatate overdose. The patient was found in cardiac arrest within minutes of last being known well. Bystanders immediately provided cardiopulmonary resuscitation (CPR), and she was in asystole on emergency medical services (EMS) arrival. Return of spontaneous circulation (ROSC) was obtained following administration of intraosseous epinephrine and naloxone. EMS obtained an ECG rhythm strip following ROSC demonstrating a sinus rhythm with a QRS duration of 160 ms. Over the ensuing 30 minutes, there was progressive narrowing of the QRS. A 12-lead ECG obtained on arrival in the emergency department (ED) 44 minutes later demonstrated a QRS duration of 94 ms. Initially, EMS ECG rhythm strips were unavailable and an isolated benzonatate ingestion was considered less likely as ECG intervals were normal. Benzonatate exposure was later confirmed with a urine benzonatate concentration, which was 8.5 mcg/mL. The patient made a full recovery.. Cases of pediatric benzonatate overdose with rapid development of cardiac arrest and full recovery have been previously reported. In this case, evidence of cardiac sodium channel blockade was demonstrated with a prolonged QRS interval on initial ECG rhythm strip analysis. However, unlike previous cases, rapid resolution of QRS prolongation occurred in this case. While transient QRS prolongation may be observed, finding a normal QRS interval should not discount the possibility of benzonatate overdose.

Topics: Adolescent; Anesthetics, Local; Antitussive Agents; Arrhythmias, Cardiac; Butylamines; Child; Drug Overdose; Epinephrine; Female; Heart Arrest; Humans; Naloxone; Sodium Channels

Resuscitations in neonates and infants present caregivers with challenging decisions in a highly stressful environment. Consideration of the pathophysiology of cardiac arrest and respiratory failure prior to an emergency allows for thoughtful utilization of pharmacotherapy. It is vital to remember that establishment of an airway and delivery of breaths and chest compressions should be prioritized. Epinephrine is first-line pharmacotherapy for severe bradycardia or cardiac arrest unresponsive to the provision of respiratory support and chest compressions. Sodium bicarbonate may be considered based on the intrinsic links between cardiac arrest, respiratory failure, and mixed acidosis. However, experimental and clinical data suggest that sodium bicarbonate worsens myocardial performance by several mechanisms (decreased intramyocardial pH, reduced oxygen delivery to tissues, reduced coronary perfusion pressure). Additionally, rapid administration of this hyperosmolar therapy may contribute to intracranial hemorrhage. With no clear benefit and multiple risks, sodium bicarbonate has been excluded from neonatal resuscitation algorithms. Opioids may produce respiratory depression in neonates, whether given to the mother prior to delivery or in neonatal intensive care; therefore, naloxone may be considered to restore respiratory drive. However, 50 years of neonatal utilization has not produced clinical studies documenting efficacy and safety. On the contrary, clinical studies fail to detect clear benefit and numerous concerning adverse reactions have been reported, including acute withdrawal, cardiorespiratory decompensation, and death. For these reasons, naloxone has also been removed from neonatal resuscitation algorithms. Clear understanding of pathophysiology, pharmacology, and clinical data support the use of multiple pharmacotherapies in neonatal resuscitation, including epinephrine, normal saline, intravenous glucose, adenosine, and calcium gluconate as reviewed in a previous column. The same pathways inform confident exclusion of sodium bicarbonate and naloxone.

Topics: Epinephrine; Heart Arrest; Humans; Infant; Infant, Newborn; Naloxone; Respiratory Insufficiency; Resuscitation; Sodium Bicarbonate

Topics: Antidotes; Drug Overdose; Heart Arrest; Humans; Naloxone; Opiate Overdose

Topics: Antidotes; Drug Overdose; Heart Arrest; Humans; Naloxone; Opiate Overdose

At our institution, we observed an increase in opioid-related adverse events after instituting a new pain treatment protocol. To prevent this, we programmed the Omnicell drug dispensing system to page the RRT whenever naloxone was withdrawn on the general wards.. Retrospective review of a prospectively collected database with a before and after design.. When comparing the two 12-month periods, there was a decrease in monthly opioid-related cardiac arrests from 0.75 to 0.25 per month (difference = 0.5; 95% CI, 0.04-0.96, P = 0.03) and a nearly significant decrease in code deaths from 0.25 to 0 per month (difference = -0.25; 95% CI, -0.02-0.52, P = 0.07) without a significant decrease in pain satisfaction scores (difference = -2.3; 95% CI, -4.4 to 9.0, P = 0.48) over the study period. There were also decreased RRT interventions from 7.3 to 5.6 per month (difference = -1.7; 95% CI, -0.31 to -3.03, P = 0.02) and decreased inpatient transfers from 2.9 to 1.8 transfers per month (difference = -1.2; 95% CI, -0.38 to -1.96, P = 0.005). When adjusting for inpatient admissions and inpatient days, there was a decrease in opioid-related cardiac arrests from 2.9 to 0.1 per 10,000 admissions (difference = -2.0; 95% CI, -0.2 to -3.8, P = 0.03) and a decrease in cardiac arrests from 0.5 to 0.2 per 10,000 patients (difference = -0.34; 95% CI, -.02 to -0.65, P = 0.04).. Naloxone-triggered activation of the RRT resulted in reduced opioid-related inpatient cardiac arrests without adversely affecting pain satisfaction scores.

Topics: Analgesics, Opioid; Antidotes; Heart Arrest; Hospital Mortality; Hospital Rapid Response Team; Hospitalization; Humans; Inpatients; Naloxone; Narcotic Antagonists; Pain Management; Retrospective Studies

To evaluate the hemodynamic and metabolic effects of terlipressin and naloxone in cardiac arrest.. Cardiac arrest in rats was induced by asphyxia and maintained for 3.5 minutes. Animals were then resuscitated and randomized into one of six groups: placebo (n = 7), epinephrine (0.02 mg/kg; n = 7), naloxone (1 mg/kg; n = 7) or terlipressin, of which three different doses were tested: 50 µg/kg (TP50; n = 7), 100 µg/kg (TP100; n = 7) and 150 µg/kg (TP150; n = 7). Hemodynamic variables were measured at baseline and at 10 (T10), 20 (T20), 30 (T30), 45 (T45) and 60 (T60) minutes after cardiac arrest. Arterial blood samples were collected at T10, T30 and T60.. The mean arterial pressure values in the TP50 group were higher than those in the epinephrine group at T10 (165 vs. 112 mmHg), T20 (160 vs. 82 mmHg), T30 (143 vs. 66 mmHg), T45 (119 vs. 67 mmHg) and T60 (96 vs. 66.8 mmHg). The blood lactate level was lower in the naloxone group than in the epinephrine group at T10 (5.15 vs. 10.5 mmol/L), T30 (2.57 vs. 5.24 mmol/L) and T60 (2.1 vs. 4.1 mmol/L).. In this rat model of asphyxia-induced cardiac arrest, terlipressin and naloxone were effective vasopressors in cardiopulmonary resuscitation and presented better metabolic profiles than epinephrine. Terlipressin provided better hemodynamic stability than epinephrine.

Topics: Animals; Arterial Pressure; Asphyxia; Cardiopulmonary Resuscitation; Epinephrine; Heart Arrest; Hemodynamics; Lypressin; Male; Models, Animal; Naloxone; Random Allocation; Rats; Rats, Wistar; Reference Values; Reproducibility of Results; Terlipressin; Time Factors; Vasoconstrictor Agents

Naloxone's use in cardiac arrest has been of recent interest, stimulated by conflicting results in both human case reports and animal studies demonstrating antiarrhythmic and positive ionotropic effects. We hypothesized that naloxone administration during cardiac arrest, in suspected opioid overdosed patients, is associated with a change in cardiac rhythm.. From a database of 32,544 advanced life support (ALS) emergency medical dispatches between January 2003 and December 2007, a retrospective chart review was completed of patients receiving naloxone in cardiac arrest. Forty-two patients in non-traumatic cardiac arrest were identified. Each patient received naloxone because of suspicion by a paramedic of acute opioid use.. Fifteen of the 36 (42%) (95% confidence interval [CI]: 26-58) patients in cardiac arrest who received naloxone in the pre-hospital setting had an improvement in electrocardiogram (EKG) rhythm. Of the participants who responded to naloxone, 47% (95% CI: 21-72) (19% [95% CI: 7-32] of all study subjects) demonstrated EKG rhythm changes immediately following the administration of naloxone.. Although we cannot support the routine use of naloxone during cardiac arrest, we recommend its administration with any suspicion of opioid use. Due to low rates of return of spontaneous circulation and survival during cardiac arrest, any potential intervention leading to rhythm improvement is a reasonable treatment modality.

Topics: Adult; Aged; Confidence Intervals; Drug Overdose; Electrocardiography; Emergency Medical Services; Female; Heart Arrest; Humans; Male; Middle Aged; Naloxone; Narcotic Antagonists; Narcotics; Retrospective Studies; Treatment Outcome

Naloxone is a pure opioid antagonist specifically indicated for respiratory depression due to opioid exposure. There is not enough data on safety of naloxone, especially in extremely preterm neonates. We report the case of a preterm neonate (gestation 27 weeks and 3 days, birth weight 485 g) who developed cardiac arrest following treatment with naloxone (dose 100 mcg/kg) for a tenfold morphine overdose on day 7 while being ventilated for respiratory distress syndrome. Asystolic cardiac arrest occurred immediately after administering naloxone and required full resuscitation, including adrenaline and external chest compression. Recovery from the cardiac arrest was complete. However, the neonate died on day 45 of life due to unrelated causes. Reports of similar adverse effects of the drug in adults as well as data from animal models raise concerns about safety of naloxone, especially in preterm neonates, given the lack of data on the pharmacokinetics of the drug in this high-risk population. Possible explanations for the adverse event under such a scenario include an idiosyncratic reaction, hypoxia, direct myocardial depressant effect and sympathoadrenal interactions. Awareness of this rare but potentially lethal complication of naloxone is necessary to optimise the response to such an adverse event.

Topics: Female; Heart Arrest; Humans; Infant, Newborn; Naloxone; Narcotic Antagonists; Respiratory Insufficiency

Topics: Adrenergic Agonists; Advanced Cardiac Life Support; Animals; Clinical Trials as Topic; Drug Therapy, Combination; Epinephrine; Heart Arrest; Humans; Naloxone; Shock

To investigate if naloxone combined with epinephrine can increase the resuscitation rate in cardiac arrest rat models induced by asphyxia.. Twenty-four rats were allocated into SA group (treated with 1 mL of saline, n = 8), EP group (treated with epinephrine 5 microg/100g, n = 8), and NA group (treated with epinephrine 5 microg/100g in combination with naloxone100 microg/100g, n = 8). Eight minutes after asphyxia, cardiopulmonary resuscitation was initiated, and different drugs were used in different groups at the same time.. Rates of restoration of spontaneous circulation (ROSC) were 25%, 75%, and 87.5% in SA, EP, and NA groups, respectively. The rate of ROSC in the NA group was significantly higher than that in the other 2 experimental groups (P < .05). The average resuscitation time in the NA group was much lower than that in the other 2 cohorts.. The administration of epinephrine alone may increase early resuscitation rate in a cardiac arrest model compared with placebo group. Moreover, the combination of naloxone and epinephrine may significantly increase resuscitation rate. The duration of ROSC in combination group is much shorter than that in the other 2 groups.

Topics: Animals; Cardiopulmonary Resuscitation; Epinephrine; Heart Arrest; Male; Naloxone; Random Allocation; Rats; Rats, Sprague-Dawley

Cardiac arrest was induced with asphyxia to identify if naloxone alone increases resuscitation rate during cardiopulmonary resuscitation in a rat asphyxia model. The animals were randomized into either a saline group (Sal-gro, treated with normal saline 1 ml iv, n = 8), a low-dose naloxone group (treated with naloxone 0.5 mg/kg iv, n = 8), or a high-dose naloxone group (HN-gro, treated with naloxone 1 mg/kg iv, n = 8) in a blinded fashion during resuscitation. At the end of 10 minutes of asphyxia, cardiopulmonary resuscitation was started, and each drug was administered at the same time. The rate of restoration of spontaneous circulation was seen in 1 of 8, 3 of 8, and 7 of 8 animals in the Sal-gro, LN-gro, and HN-gro, respectively. The rate of restoration of spontaneous circulation in HN-gro was significantly higher than that in Sal-gro (P < .05). Naloxone (1 mg/kg) alone can increase resuscitation rate following asphyxial cardiac arrest in rats.

Topics: Animals; Asphyxia; Blood Pressure; Cardiopulmonary Resuscitation; Disease Models, Animal; Dose-Response Relationship, Drug; Female; Heart Arrest; Heart Rate; Male; Naloxone; Narcotic Antagonists; Prospective Studies; Random Allocation; Rats; Rats, Sprague-Dawley; Reference Values; Respiration; Time Factors; Treatment Outcome

It is not known whether naloxone is as efficacious as epinephrine during cardiopulmonary resuscitation (CPR). The aim of the study was to compare the effects of naloxone and epinephrine on the outcomes of CPR following asphyxial cardiac arrest in rats.. Cardiac arrest was induced with asphyxia by clamping the tracheal tubes. Twenty-four Sprague-Dawley rats were randomized prospectively into a saline group (treated with normal saline, 1 ml intravenously, n = 8), an epinephrine group (treated with epinephrine, 0.04 mg/kg intravenously, n = 8) or a naloxone group (treated with naloxone, 1 mg/kg intravenously, n = 8) in a blind fashion during resuscitation after asphyxial cardiac arrest. After 5 min of untreated cardiac arrest, conventional manual CPR was started and each drug was administered at the same time.. The rates of restoration of spontaneous circulation (ROSC) were one of eight (12.5%), seven of eight (87.5%) and seven of eight (87.5%) in the saline, epinephrine and naloxone groups, respectively. The rates of ROSC in the epinephrine and naloxone groups were equal and significantly greater than that in the saline group (P = 0.01 and P = 0.01, respectively).. The administration of naloxone or epinephrine alone may increase the resuscitation rate, and both drugs are equally effective for CPR in a rat asphyxia model. However, the mechanism by which naloxone produces its efficacy during CPR remains unclear and further experimentation will be necessary.

Topics: Animals; Asphyxia; Blood Pressure; Cardiopulmonary Resuscitation; Electrocardiography; Epinephrine; Female; Heart Arrest; Heart Rate; Male; Naloxone; Narcotic Antagonists; Rats; Rats, Sprague-Dawley; Survival; Vasoconstrictor Agents

Topics: Acetaminophen; Adult; Dextropropoxyphene; Drug Combinations; Emergencies; Female; Heart Arrest; Humans; Naloxone; Narcotic Antagonists; Resuscitation; Suicide, Attempted

We report a patient who presented palatal myoclonus (PM) after anoxic brain damage that was completely abolished by the administration of opioid agonists. This suggests the involvement of peptide systems in the development of PM.

Topics: Carcinoma; Endorphins; Glasgow Coma Scale; Heart Arrest; Humans; Laryngeal Neoplasms; Male; Middle Aged; Muscle Contraction; Myoclonus; Naloxone; Palate, Soft

We performed a retrospective review to investigate the safety of prehospital naloxone administration by paramedics as part of a protocol for all patients presenting with an acutely depressed level of consciousness (LOC). The prevalence of naloxone-induced vomiting, seizures, hypotension, hypertension, and cardiac arrest was sought from the prehospital records of 813 patients treated during a 12-month period. The mean age of the treated patients was 42.4 +/- 9.7 years. The initial dose of naloxone was 0.4 to 0.8 mg, and the mean total dose was 0.9 +/- 0.6 mg. No patients lost a pulse within ten minutes of receiving naloxone. Two patients (0.2%) experienced a significant drop in systolic blood pressure, and one patient (0.1%) demonstrated a significant rise in systolic blood pressure within five minutes of naloxone administration. Vomiting occurred in two patients (0.2%), and one patient (0.1%) suffered a tonic-clonic seizure within five minutes of naloxone administration. Of the 813 patients treated, 60 patients (7.4%: mean age, 32.3 +/- 6.7 years) were judged to have an improved LOC after naloxone, with 27 (3.3%) regaining a normal LOC. We conclude that in the above doses, naloxone is safe as part of prehospital protocols for paramedics treating patients with an acutely depressed LOC. However, the vast majority of patients treated empirically with naloxone in the field demonstrated no benefit.

Topics: Adult; Emergencies; Emergency Medical Services; Female; Heart Arrest; Humans; Hypotension; Male; Middle Aged; Naloxone; Pennsylvania; Retrospective Studies; Safety; Seizures; Unconsciousness; Vomiting

Topics: Adult; Facial Bones; Fractures, Bone; Heart Arrest; Humans; Male; Naloxone; Orthopedic Fixation Devices; Pulmonary Edema

To determine the effects of naloxone, an opiate antagonist, on the adrenomedullary response to cardiac arrest, plasma epinephrine and norepinephrine levels were measured before, during, and after cardiac arrest in dogs. Ventricular fibrillation was induced in 12 dogs anesthetized with pentobarital sodium (30 mg/kg) and standard American Heart Association cardiopulmonary resuscitation (CPR) was begun using a mechanical device. At 6.5 minutes of CPR, naloxone (10 mg/kg) or 0.9% saline (10 ml) was given intravenously. At 12 minutes of CPR, the cardiac ventricles were electrically defibrillated. Plasma epinephrine and norepinephrine levels were measured before ventricular fibrillation; at 2.5, 4.5, 9.5, and 11.5, minutes of CPR; and at 5, 10, 15, and 20 minutes after resuscitation. Epinephrine and norepinephrine increased from prearrest levels of 3.66 +/- 0.67 (+/- SE) and 24.02 +/- 3.67 ng/ml to 66.67 +/- 9.65 and 74.00 +/- 9.91 ng/ml, respectively, at 4.5 minutes of CPR. After resuscitation, norepinephrine levels remained slightly elevated, while epinephrine fell to prearrest levels. Naloxone did not cause a significant change in either epinephrine or norepinephrine from 6.5 minutes of CPR (time of treatment) through 20 minutes postresuscitation. In addition, naloxone had no effect on either the end-diastolic pressure difference during CPR or resuscitation outcome. We conclude that cardiac arrest causes significant increases in plasma epinephrine and norepinephrine levels, which remain elevated for the duration of the arrest, and that naloxone has no effect on these levels.

Topics: Adrenal Medulla; Animals; Dogs; Epinephrine; Heart Arrest; Hemodynamics; Naloxone; Norepinephrine; Resuscitation

The effects of pre- and post-treatment with naloxone on the cardiotoxicity of ouabain in the guinea-pig were studied. After pretreatment with naloxone, the dose of ouabain required to induce ventricular arrhythmias and cardiac arrest were significantly increased, in a dose-dependent manner, compared with the control, indicating a protective effect of naloxone against digitalis intoxication. Administration of naloxone at the onset of cardiac arrhythmias induced by a lethal dose of ouabain restored the cardiac rhythm and consequently saved life in seven out of eight animals, indicating an antiarrhythmic effect of naloxone in digitalis-intoxicated guinea-pigs. The protective and antiarrhythmic effects of naloxone against digitalis intoxication have clinical implications.

Topics: Animals; Arrhythmias, Cardiac; Digitonin; Dose-Response Relationship, Drug; Drug Interactions; Female; Guinea Pigs; Heart; Heart Arrest; Naloxone; Ouabain

Topics: Heart Arrest; Humans; Naloxone; Resuscitation

Naloxone has been shown to increase arterial pressure in hemorrhagic and septic shock. To determine if naloxone has salutary effects during cardiac arrest with conventional closed-chest cardiopulmonary resuscitation (CPR), ten dogs were studied during 20 minutes of ventricular fibrillation (VF) and CPR and during a 30-minute postcountershock period. Central aortic (Ao) and right atrial (RA) systolic and end-diastolic (EDP) pressures, instantaneous Ao-RA pressure difference (coronary perfusion pressure), and electromagnetic Ao flow were measured. Ao and RA samples were analyzed during a control period and at five-minute intervals during CPR for PO2, PCO2, and pH. During VF, a piston-cylinder device was used to perform anteroposterior sternal depressions and positive pressure ventilations (100% O2) at standard rates and ratios. After 15 minutes of CPR, animals were randomized and given either naloxone (5 mg/kg) or epinephrine (1 mg). Defibrillation was attempted five minutes later using 1 J/kg and then, if necessary, 2, 4, 8, 12, and 16 J/kg until VF was terminated or the maximum energy dose was reached. If VF persisted or if countershock resulted in asystole or a nonperfusing rhythm (electrical-mechanical dissociation [EMD]), the alternate drug (naloxone or epinephrine) was then given. Measured systolic pressures, coronary perfusion pressures, aortic flow, and blood gases were not significantly different during the control period or at five, ten, and 15 minutes of VF and CPR between animal groups prior to drug administration. When compared to hemodynamic values measured at 15 minutes, naloxone had no significant effect on pressures or aortic flow measured five minutes after administration.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Animals; Blood Pressure; Carbon Dioxide; Coronary Circulation; Dogs; Electric Countershock; Epinephrine; Female; Heart Arrest; Hemodynamics; Male; Naloxone; Oxygen; Resuscitation; Stroke Volume; Ventricular Fibrillation

Topics: Female; Heart Arrest; Humans; Middle Aged; Naloxone

The endotracheal route for drug administration provides a rapid means of accessing the systemic circulation when intravenous routes cannot be established in emergent situations. This route is relatively free of significant complications and has been documented as being successful numerous times in various clinical settings. Currently, the following drugs have been studied by this route: epinephrine, atropine, lidocaine, naloxone, bretylium, and diazepam. The paper reviews the current state of the art of endotracheal drug administration.

Topics: Atropine; Bradycardia; Diazepam; Electrocardiography; Emergencies; Epinephrine; Heart Arrest; Humans; Intubation, Intratracheal; Lidocaine; Naloxone; Respiratory Insufficiency

When vascular access is delayed or unreliable in emergency situations, an endotracheal tube provides a rapid and reliable route for administration of medication. Epinephrine, lidocaine, and atropine have shown clinical efficacy when given by the endotracheal route. There is evidence that other medications including naloxone and diazepam may also be suitable for endotracheal use, but clear-cut recommendations await further studies of pharmacokinetics and toxicity.

Topics: Adult; Anaphylaxis; Anti-Arrhythmia Agents; Atropine; Bicarbonates; Diazepam; Emergencies; Epinephrine; Heart Arrest; Humans; Intubation, Intratracheal; Lidocaine; Naloxone; Pharmaceutical Preparations; Sodium Bicarbonate

Topics: Heart Arrest; Heroin; Humans; Male; Middle Aged; Naloxone; Ventricular Fibrillation

Topics: Heart Arrest; Humans; Naloxone

Topics: Aged; Carbon Dioxide; Female; Heart Arrest; Humans; Monitoring, Physiologic; Naloxone; Partial Pressure; Phenoperidine

Topics: Adult; Anesthesia; Arteriovenous Fistula; Atropine; Carotid Artery Diseases; Cavernous Sinus; Dexamethasone; Diazepam; Droperidol; Female; Fentanyl; Heart Arrest; Humans; Hypothermia, Induced; Naloxone; Neostigmine; Neuroleptanalgesia; Pancuronium; Preanesthetic Medication; Thiopental