digoxin and Heart-Arrest

In this focused update, the American Heart Association provides updated guidance for resuscitation of patients with cardiac arrest, respiratory arrest, and refractory shock due to poisoning. Based on structured evidence reviews, guidelines are provided for the treatment of critical poisoning from benzodiazepines, β-adrenergic receptor antagonists (also known as β-blockers), L-type calcium channel antagonists (commonly called calcium channel blockers), cocaine, cyanide, digoxin and related cardiac glycosides, local anesthetics, methemoglobinemia, opioids, organophosphates and carbamates, sodium channel antagonists (also called sodium channel blockers), and sympathomimetics. Recommendations are also provided for the use of venoarterial extracorporeal membrane oxygenation. These guidelines discuss the role of atropine, benzodiazepines, calcium, digoxin-specific immune antibody fragments, electrical pacing, flumazenil, glucagon, hemodialysis, hydroxocobalamin, hyperbaric oxygen, insulin, intravenous lipid emulsion, lidocaine, methylene blue, naloxone, pralidoxime, sodium bicarbonate, sodium nitrite, sodium thiosulfate, vasodilators, and vasopressors for the management of specific critical poisonings.

Topics: Adrenergic beta-Antagonists; American Heart Association; Benzodiazepines; Cardiopulmonary Resuscitation; Digoxin; Heart Arrest; Humans; United States

Different foeticide techniques and pharmacological agents have been used to achieve foetal asystole. This study aimed to compare the success of intraamniotic digoxin, intracardiac potassium chloride (KCl), and funic KCl in achieving foetal asystole and discuss procedural difficulties for physicians and clinical outcomes. This prospective observational study included 124 patients who received foeticide at 22-31 weeks of gestation. All procedures were performed transabdominally, and 1 mg of intraamniotic digoxin, funic KCl, or intracardiac KCl was administered. Procedure times, procedural difficulty scores, patient pain scores, decrease in haematocrit levels, induction and hospitalisation times, and the presence of chorioamnionitis were recorded. The foeticide success rates were 93.0, 95.1, and 97.5% for intraamniotic digoxin, intracardiac KCl, and funic KCl, respectively. Intraamniotic digoxin was associated with shorter procedure times, lower procedural difficulty scores, and lower patient pain scores (

Topics: Abortion, Induced; Chorioamnionitis; Digoxin; Female; Fetal Death; Fetal Heart; Heart Arrest; Humans; Potassium Chloride; Pregnancy; Prospective Studies

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Topics: Anti-Arrhythmia Agents; Cardiopulmonary Resuscitation; Child; Digoxin; Heart Arrest; Humans

Although the mechanism of action is not well known, intravenous lipid emulsion (ILE) has been shown to be effective in the treatment of lipophilic drug intoxications. It is thought that, ILE probably separates the lipophilic drugs from target tissue by creating a lipid-rich compartment in the plasma. The second theory is that ILE provides energy to myocardium with high-dose free fatty acids activating the voltage-gated calcium channels in the myocytes. In this study, effects of ILE treatment on digoxin overdose were searched in an animal model in terms of cardiac side effects and survival. Forty Sprague-Dawley rats were divided into five groups. As the pre-treatment, the groups were administered saline, ILE, DigiFab and DigiFab and ILE. Following that, digoxin was infused to all groups until death except the control group. First arrhythmia and cardiac arrest observation times were recorded. According to the results, there was no statistically significant difference among the group in terms of first arrhythmia time and cardiac arrest times. However, when the saline group compared with ILE-treated group separately, significant difference was observed. DigiFab, ILE or ILE-DigiFab treatment make no significant difference in terms of the first arrhythmia and cardiac arrest duration in digoxin-intoxicated rats. However, it is not possible to say that at the given doses, ILE treatment might be successful at least as a known antidote. The fact that the statistical significance between the two groups is not observed in the subgroup analysis, the study should be repeated with larger groups.

Topics: Animals; Antidotes; Arrhythmias, Cardiac; Cardiotoxicity; Chemical and Drug Induced Liver Injury; Cytoprotection; Digoxin; Disease Models, Animal; Fat Emulsions, Intravenous; Fatty Liver; Heart Arrest; Immunoglobulin Fab Fragments; Kidney; Liver; Rats, Sprague-Dawley

Previous studies have shown that cyclodextrin group medicines bind to various drugs. The hypothesis of our study is to determine whether sugammadex could bind to digoxin and delay the cardiovascular toxicity of that drug. Twenty-eight sedated Wistar rats were infused with digoxin at 3 mg/h (0.25 mg/ml). Five minutes after the start of infusion, animals were treated with a bolus of either 16 mg/kg (Sgdx16), 100 mg/kg (Sgdx100), or 1000 mg/kg (Sgdx1000) sugammadex. The control group infusion did not contain sugammadex. Heart rate, electrocardiography, and respiratory rate were monitored. The primary endpoint was time to asystole. Digoxin infusion continued until the animals arrested. The time to asystole for the Sgdx1000 group was significantly longer compared to that for the control group (p < 0.05). The mean lethal dose of digoxin was 5.35 ± 2.06 mg/kg in the saline-treated rats. On the other hand, the mean lethal dose of digoxin was 8.54 ± 1.51 mg/kg in the sugammadex 1000 group (p < 0.05). The mean lethal dose of digoxin was significantly higher than control group (p < 0.05). We found that the 1000 mg/kg dose of sugammadex delayed digoxin cardiotoxicity in a rat model of digoxin toxicity. We conclude that further research must be conducted on the interaction between digoxin and sugammadex.

Topics: Animals; Antidotes; Cardiotoxicity; Digoxin; Heart Arrest; Heart Rate; Infusions, Intravenous; Injections, Intravenous; Myocardial Contraction; Rats, Wistar; Sugammadex; Time Factors

Digoxin is a cardiac glycoside that is frequently prescribed in atrial fibrillation and heart failure. Symptoms such as nausea, hyperkalaemia, cardiac arrhythmias and cardiac arrest are seen in digoxin toxicity. The treatment focuses on reduction of digoxin absorption, prevention of hypokalaemia and hyperkalaemia, treatment of symptoms and, in severe toxicity, administration of digoxin antibodies.. A 73-year-old man with a history of extensive cardiac disease was seen 45 minutes after ingesting 20 mg of digoxin. The patient developed ventricular fibrillation within 3 hours of ingestion, before arrival of the digoxin antibodies. The patient passed away despite resuscitation and administration of an insufficient amount of digoxin antibodies.. The national supply of digoxin antibodies in the Netherlands proved to be too limited for the treatment of a patient with severe digoxin toxicity. An increase in the supply, and central storage, of digoxin antibodies could promote faster administration of an adequate amount of the antibodies. Timely transportation to an extra corporeal membrane oxygenation centre should also be considered.

Topics: Aged; Arrhythmias, Cardiac; Atrial Fibrillation; Digoxin; Fatal Outcome; Heart Arrest; Humans; Male; Netherlands; Ventricular Fibrillation

Intravenous lipid emulsion eliminates the toxicity-related symptoms of several drugs. We hypothesized that intravenous lipid emulsion prolongs the survival time in digoxin-intoxicated rats.. Electrocardiograms of 14 anesthesized Wistar rats were monitored. All of the rats received digoxin infusion at a rate of 12 mL/h (0.25 mg/mL). Five minutes after the start of digoxin infusion, animals were treated either with 12.4 mL/kg intravenous lipid emulsion (group L) or saline (group C). The primary outcome variable was time elapsed until asystole development. Cumulative dose of digoxin required to induce asystole was also recorded.. Mean time until asystole development in groups C and L were 21.28 ± 8.61 and 32.00 ± 5.41 minutes, respectively (P< .05). The mean lethal doses of digoxin in the groups C and L were 3.97 ± 1.54 and 6.09 ± 0.96 mg/kg, respectively (P< .05).. Intravenous lipid emulsion prolonged the time until asystole development and increased cumulative lethal dose in rats intoxicated with digoxin.

Topics: Animals; Anti-Arrhythmia Agents; Digoxin; Dose-Response Relationship, Drug; Fat Emulsions, Intravenous; Heart Arrest; Infusions, Intravenous; Rats; Rats, Wistar

Topics: Aged; Anti-Arrhythmia Agents; Body Weight; Digoxin; Drug Interactions; Drug Monitoring; Electrocardiography; Emergency Nursing; Emergency Treatment; Female; Heart Arrest; Heart Block; Humans; Immunoglobulin Fab Fragments; Medical History Taking; Nursing Assessment; Practice Guidelines as Topic

We report the first case of a child with known cardiac disease who presented in full cardiac arrest secondary to digoxin poisoning and was successfully resuscitated. A 12-week-old female presented 1-week status post surgical repair of a congenital heart anomaly in asystolic cardiac arrest. The patient was successfully resuscitated with standard Advanced Pediatric Life Support. A toxic digoxin level returned, Digoxin-specific antibody fragments (Digibind, Fab) were administered, and all signs and symptoms of toxicity resolved. The patient was discharged 6 days after presentation with full neurological recovery.

Topics: Child; Diagnosis, Differential; Digoxin; Electrocardiography; Emergency Treatment; Female; Heart Arrest; Humans; Poisoning

Survival following out-of-hospital cardiac arrest (OHCA) from ventricular fibrillation (VF) is poor and dependent on a rapid emergency response system. Improvements in emergent early response have resulted in a higher percentage of patients surviving to admission. However, the admission variables that predict both short- and long-term survival in a region with high discharge survival following OHCA require further study in order to identify survivors at subsequent highest risk.. All patients with OHCA arrest in Olmsted County Minnesota between 1990 and 2000 who received defibrillation of VF by emergency services were included in the population-based study. Baseline patient admission characteristics in survivor and nonsurvivor groups were compared. Survivors to hospital discharge were prospectively followed to determine long-term survival.. Two hundred patients suffered a VF arrest. Of these patients, 145 (73%) survived to hospital admission (7 died within the emergency department) and 79 (40%) were subsequently discharged. Sixty-six (83%) were male, with an average age of 61.9 +/- 15.9 years. Univariate predictors of in-hospital mortality included call-to-shock time (6.6 vs. 5.5 min, p = 0.002), a nonwitnessed arrest (75.4 vs. 92.4%, p = 0.008), in-field use of epinephrine (27.8 vs. 93.4%, p < 0.001), age (68.1 vs. 61.9 years, p = 0.017), hypertension (36.1 vs. 14.1%, p = 0.005), ejection fraction (32.4 vs. 42.4, p = 0.012), and use of digoxin (34.9 vs. 12.7%, p = 0.002). Of all these variables, hypertension [hazard ratio (HR) 4.0, 95% CI 1.1-14.1, p = 0.03], digoxin use (HR 4.5, 95% CI 1.3-15.6, p = 0.02), and epinephrine requirement (HR 62.0, 95% CI 15.1-254.8, p < 0.001) were multivariate predictors of in-hospital mortality. Nineteen patients (24%) had died prior to the survey follow-up. Five patients experienced a cardiac death, resulting in a 5-year expected cardiac survival of 92%. Multivariate variables predictive of long-term mortality include digoxin use (HR 3.02, 95% CI 1.80-5.06, p < 0.001), hypertension (HR 2.06, 95% CI 2.12-3.45, p = 0.006), and call-to-shock time (HR 1.18, 95% CI 1.01-1.38, p = 0.038).. A combined police/fire/EMS defibrillation program has resulted in an increase of patients surviving to hospital admission after OHCA. This study confirms the need to decrease call-to-shock times, which influence both in-hospital and long-term mortality. This study also identifies the novel demographic variables of digoxin and hypertension, which were also independent risk factors of increased in-hospital and long-term mortality. Identification of these variables may provide utility in identifying those at high-risk of subsequent mortality after resuscitation.

Topics: Aged; Aged, 80 and over; Anti-Arrhythmia Agents; Digoxin; Electric Countershock; Emergency Medical Services; Female; Heart Arrest; Hospital Mortality; Humans; Hypertension; Male; Middle Aged; Patient Admission; Predictive Value of Tests; Research Design; Risk Factors; Survival Analysis; Time Factors; Treatment Outcome; Ventricular Fibrillation

The cardiac safety of digoxin therapy for congestive heart failure (CHF) is a source of concern, especially among those with renal impairment.. Using a case-control design, we examined the risk of primary cardiac arrest (PCA) associated with digoxin therapy within three levels of renal function.. After adjustment for other clinical characteristics, digoxin therapy for CHF was not associated with an increased risk of PCA [odds ratio (OR)=0.97, 95% confidence interval (CI) 0.59-1.62] among patients with normal renal function (serum creatinine

Topics: Aged; Cardiotonic Agents; Case-Control Studies; Creatinine; Digoxin; Female; Heart Arrest; Heart Failure; Humans; Kidney; Male; Middle Aged; Odds Ratio; Risk Factors

We experienced sudden cardiac arrest after induction of general anesthesia using isoflurane. The patient had had paroxysmal atrial fibrillation for one year and had been treated with digoxin and cibenzoline succinate. Sinus rhythm appeared soon after the start of closed chest compression. However cardiac arrest recurred, and we inserted a temporary pacemaker catheter to stabilize the circulatory status. She awoke from anesthesia without any complications. The diagnosis of sick sinus syndrome (SSS) was made postoperatively and she had a permanent pacemaker implanted. We thought that the hidden SSS had been the cause of this sudden cardiac arrest.

Topics: Aged; Anesthesia, General; Anesthetics, Inhalation; Anti-Arrhythmia Agents; Atrial Fibrillation; Breast Neoplasms; Digoxin; Female; Heart Arrest; Humans; Imidazoles; Isoflurane; Mastectomy; Pacemaker, Artificial; Sick Sinus Syndrome

A 79-year 65 kg male called the ambulance service 4 h after ingestion of 100 tablets of digoxin 0.1 mg complaining of nausea and vomiting. The ECG showed an idioventricular escape rhythm with a heart rate of 30/min. After 0.5 mg atropine, heart rate increased to 80/min. Soon after admission to the emergency department, the patient developed electromechanical dissociation. Due to persistent cardiac arrest, percutaneous cardiopulmonary bypass was started, and the ECG rhythm changed to ventricular fibrillation. Several attempts to terminate ventricular fibrillation by electrical defibrillation failed. Fifty-eight minutes after cardiac arrest, antidigoxin-Fab was administered and 1 h 25 min after cardiac arrest, ventricular fibrillation was terminated by the tenth electrical defibrillation attempt. Initially, the patient's overall status improved over the next 2 days, but then he developed a severe adult respiratory distress syndrome and died of unresponsive septic shock 12 days after ingestion of digoxin. This case demonstrates that percutaneous cardiopulmonary bypass may provide support in patients with cardiac arrest due to massive digoxin overdose. This temporary support can maintain adequate tissue perfusion during the time required for drug neutralization in order to achieve successful defibrillation. Percutaneous cardiopulmonary bypass should be considered in patients with severe, but temporary cardiac dysfunction due to a life-threatening drug overdose.

Topics: Aged; Anti-Arrhythmia Agents; Cardiopulmonary Bypass; Digoxin; Drug Overdose; Electric Countershock; Fatal Outcome; Heart Arrest; Humans; Male; Retreatment

Topics: Adolescent; Bone Marrow Transplantation; Digoxin; Drug Therapy, Combination; Electrocardiography, Ambulatory; Heart Arrest; Humans; Immunosuppressive Agents; Long QT Syndrome; Male; Tachycardia, Sinus; Tacrolimus

Topics: Adolescent; Arrhythmia, Sinus; Bone Marrow Transplantation; Digoxin; Heart Arrest; Heart Failure; Humans; Immunosuppressive Agents; Male; Tacrolimus

During February 1993-May 1995, the New York City Poison Control Center (NYCPCC) was informed about onset of illness in five previously healthy men after they ingested a substance marketed as a topical aphrodisiac; four of the men died. These cases were investigated by the New York City Department of Health, the New York City Department of Environmental Protection, and the Food and Drug Administration (FDA). Four cases were referred to the NYCPCC and one case to the New York City medical examiner's office. The decedents died from cardiac dysrhythmias, and all five patients had measurable levels of digoxin* detected in their serum. Digoxin had not been prescribed for therapeutic purposes for any of these patients, and none had medical conditions associated with endogenous digoxin-like immunoreactive substances. The purported aphrodisiac contains bufadienolides, naturally occurring cardioactive steroids that have digoxin-like effects. This report describes three of the five case reports, summarizes the investigations of the five cases, and underscores the health risks associated with inappropriate use of preparations containing digoxin-like substances.

Topics: Adolescent; Adult; Aphrodisiacs; Arrhythmias, Cardiac; Bufanolides; Digoxin; Fatal Outcome; Heart Arrest; Humans; Hyperkalemia; Hypotension; Male; New York City; Poisoning

Topics: Adolescent; Adult; Arrhythmias, Cardiac; Bufanolides; Digoxin; Fatal Outcome; Heart Arrest; Humans; Hyperkalemia; Hypotension; Male; New York City; Poisoning

Topics: Analysis of Variance; Animals; Binding, Competitive; Calcium; Digoxin; Drug Synergism; Heart; Heart Arrest; In Vitro Techniques; Lead; Myocardium; Organometallic Compounds; Ranidae

We describe a patient with unexpectedly high serum digoxin after cardiac surgery. To control atrial fibrillation in the immediate postoperative period, she was given a brief trial of digoxin (four 0.25-mg doses) over 12 h. Serum digoxin 6 h later was 2.5 micrograms/L. Two days later, the patient developed ventricular fibrillation, which progressed to cardiac arrest. During or immediately after resuscitation, blood was drawn for a digoxin measurement, and the concentration reported was 9.3 micrograms/L; this result was verified by repeated analysis. Digoxin decreased rapidly and progressively to near 4.0 micrograms/L over the next several hours and thereafter decreased slowly to 1.0 microgram/L over the next 11 days, despite no digoxin being administered. The unexpectedly high digoxin raised questions about the accuracy of the digoxin measurement, particularly about the possible influence of the digoxin-like immunoreactive factor. Analytical approaches to distinguishing true digoxin from this factor and other artifacts of digoxin measurement were applied to this patient, with unanticipated results.

Topics: Aged; Cardiac Surgical Procedures; Digoxin; False Positive Reactions; Female; Fluoroimmunoassay; Heart Arrest; Humans; Radioimmunoassay; Ventricular Fibrillation

Interaction of frusemide and digitalis on frog heart has been studied. It was found that like digitalis, frusemide did not have any effect on normal heart, but restored the normal myocardial contraction of the hypodynamic frog heart. Frusemide induced cardiac arrest when administered during digoxin infusion. It is suggested that interaction of frusemide and digoxin has additive effect.

Topics: Animals; Digoxin; Drug Interactions; Furosemide; Heart; Heart Arrest; In Vitro Techniques; Ranidae

Topics: Animals; Calcium; Digoxin; Drug Interactions; Heart; Heart Arrest; Lead; Perfusion; Ranidae

The present work investigated the effect of preperfusion of ascending concentrations of lead acetate (LA) (10(-9), 10(-7) and 10(-5) M) on digoxin (DGN) cardiotoxicity in isolated frog heart, in order to look for any consequent variations in its lead-induced potentiation. The DGN perfusion time(s) and DGN exposure (micrograms DGN/10 mg heart weight) for, and myocardial DGN level (ng DGN/g wet tissue) at, cardiac arrest were the parameters evaluated so as to assess cardiotoxicity. Both sodium acetate and LA (10(-7) M) preperfusion led to a diminution in cardiac rate at 10 min of DGN perfusion without altering the contractility compared to the DGN alone group. With regard to DGN perfusion time for cardiac arrest, preperfusion of ascending concentrations of LA induced a corresponding decrease which was statistically significant (P < 0.05). On the other hand, in the experimental group that received preperfusion of 10(-9) M LA, the DGN exposure for cardiac arrest was not significantly different from that of the control, whereas in the 10(-7) and 10(-5) M groups, it was significantly lower (P < 0.05). In the experimental group that received preperfusion of 10(-7) M LA, the significant reduction in DGN perfusion time and DGN exposure was well corroborated by a diminution in the myocardial DGN level (4.01 +/- 0.17 ng/g wet tissue in comparison with the control value of 5.72 +/- 0.4 ng/g wet tissue, P < 0.05) at cardiac arrest. Taken together, these data reveal that with the preperfusion of LA in ascending concentrations, there is a relative increase in LA-induced potentiation of DGN cardiotoxicity.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Acetates; Acetic Acid; Animals; Digoxin; Dose-Response Relationship, Drug; Drug Synergism; Heart Arrest; Myocardial Contraction; Organometallic Compounds; Perfusion; Ranidae

Topics: Animals; Digoxin; Drug Interactions; Ethylenediamines; Heart Arrest; In Vitro Techniques; Lead; Perfusion; Ranidae

Digoxin (DGN) and aminophylline (theophylline ethylenediamine, APH) being frequently prescribed cardioactive drugs, the present study investigated the effect of APH (10(-4) M) preperfusion on DGN-cardiotoxicity employing the isolated frog heart preparation. The mean DGN perfusion time (sec) and mean DGN exposure (microgram/10 mg heart wt.) for cardiac arrest were the parameters studied. APH preperfusion caused a significant elevation in both the parameters, signifying that it afforded protection against DGN-cardiotoxicity. This protective effect was not observed with the preperfusion of ethylenediamine (EDA) instead of APH, which led to the inference that the protective effect of APH was solely due to its theophylline component. The present finding that APH-pretreatment might modulate DGN-cardiotoxicity, of considerable pharmaco-toxicological interest.

Topics: Aminophylline; Animals; Digoxin; Heart; Heart Arrest; In Vitro Techniques; Perfusion; Ranidae

Although electrolyte levels are commonly determined during inhospital CPR, the clinical usefulness of these measurements is questionable. Electrolyte and digoxin levels were obtained from 99 patients during resuscitative efforts. Measurements were examined for association with pre and postarrest values, outcome from arrest, and presence or absence of refractory ventricular arrhythmias. While BUN and creatinine (Cr) values correlated closely with pre and postarrest levels (r2 greater than 50%), Na, K, and Ca measurements were less reflective (r2 less than 50%). When electrolyte levels obtained during CPR were correlated with outcome, linear regression showed a consistent trend for higher levels in patients who subsequently died (K p less than .001; Mg p less than .02; Na p less than .025; Ca p less than .02; BUN p less than .02; Cr p less than .025). Finally, among the 12 patients with documented refractory ventricular arrhythmias, there appeared to be little association with K, Mg, and digoxin abnormalities observed during resuscitative efforts. These results suggest that electrolyte levels during CPR are strongly affected by metabolic disturbances and therapeutic interventions, and consequently, the clinical usefulness of these measurements may be limited.

Topics: Blood Urea Nitrogen; Creatine; Digoxin; Electrolytes; Female; Heart Arrest; Humans; Male; Middle Aged; Reference Values; Resuscitation

The effect of empiric antiarrhythmic therapy with quinidine and procainamide on long-term mortality was examined in 209 patients with coronary artery disease resuscitated after out-of-hospital cardiac arrest. The antiarrhythmic agent used was determined by the patient's private physician without knowledge of the study ambulatory electrocardiogram. Of the 209 patients, procainamide was prescribed in 45 (22%), quinidine in 48 (23%) and no antiarrhythmic therapy in 116 (55%). Digoxin therapy was initiated in 101 patients. The 2-year total survival rate for the quinidine, procainamide and nontreated patients was 61, 57 and 71% (p less than 0.05), and for sudden death was 69, 69 and 89% (p less than 0.01), respectively. These observations suggest that empiric antiarrhythmic therapy in survivors of out-of-hospital cardiac arrest did not affect total mortality and was associated with an increased frequency of sudden death.

Topics: Aged; Anti-Arrhythmia Agents; Coronary Disease; Death, Sudden; Digoxin; Heart Arrest; Humans; Middle Aged; Procainamide; Quinidine; Resuscitation; Retrospective Studies

Digoxin therapy can cause important toxic events when elevated drug levels occur. Interpreting drug levels can be hampered by artifactual errors such as poor assay quality, incorrect timing or drawing of blood samples, and, as has been demonstrated for tobramycin, errors due to drawing blood through drug administration catheters. A case is reported in which a correctly timed and analyzed digoxin level of 33.60 ng/ml may have been due to drawing the blood sample through a line used to administer digoxin eight hours earlier. Subsequent measurements by venipuncture documented much lower concentrations.

Topics: Aged; Blood Specimen Collection; Digoxin; False Positive Reactions; Female; Heart Arrest; Humans

Topics: Digoxin; Drug Interactions; Halothane; Heart Arrest; Humans; Intraoperative Complications; Verapamil

Topics: Amiodarone; Arrhythmias, Cardiac; Digoxin; Drug Interactions; Electrocardiography; Heart Arrest; Humans; Male; Middle Aged

A 1-month-old infant suffered cardiac arrest shortly after presentation to the emergency department. The child had a history of heart disease treated with digoxin. The infant died despite intensive resuscitative efforts, including the use of digoxin-specific Fab antibodies. A brief discussion of this case and the use of digoxin-specific antibodies is presented.

Topics: Antibodies; Digoxin; Emergencies; Heart Arrest; Heart Failure; Humans; Infant, Newborn; Male; Resuscitation

To determine the relative value of clinical findings, results of low-level treadmill electrocardiographic (ECG) exercise testing and left ventricular (LV) ejection fraction (EF) for predicting cardiac events in the year after an acute myocardial infarction (AMI), 72 patients who had had an uncomplicated AMI were studied with either radionuclide angiography or 2-dimensional echocardiography to assess LVEF and a low-level treadmill exercise test before hospital discharge. All patients were followed for 1 year. Nineteen patients (26%) had at least 1 cardiac event: coronary artery bypass grafting (11 patients), recurrent AMI (6 patients) or cardiac death (6 patients). Multiple logistic regression analysis revealed that total cardiac events were predicted by exercise ECG ST-segment depression or angina, prior AMI, ventricular ectopic activity during exercise and digoxin therapy (cumulative r = 0.58, p less than 0.001). Coronary artery bypass grafting was predicted by exercise ECG ST-segment depression or angina (r = 0.29, p = 0.01). Recurrent AMI was predicted by exercise ECG ST-segment depression or angina, prior AMI and ventricular ectopic activity during exercise (cumulative r = 0.49, p less than 0.001). Cardiac death was predicted by an LVEF of 40% or less (r = 0.38, p = 0.01). The presence of both an LVEF of 40% or less and ECG ST-segment depression on treadmill exercise testing defined a subgroup of patients with a high incidence of early cardiac death (33%).(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Adrenergic beta-Antagonists; Angina Pectoris; Coronary Artery Bypass; Digoxin; Exercise Test; Female; Heart; Heart Arrest; Humans; Male; Myocardial Infarction; Prognosis; Radionuclide Imaging; Stroke Volume

During treatment with amiodarone, digoxin and nadolol, asystole occurred repeatedly in a patient with chronic persistent automatic atrial tachycardia. Asystole did not occur after discontinuation of drug therapy, and rechallenge with amiodarone alone produced marked overdrive suppression of all pacemakers resulting in asystole. Amiodarone serum level was within therapeutic range. The possible electrophysiologic mechanisms by which amiodarone might suppress both normal and abnormal pacemakers are discussed. The occurrence of asystole at therapeutic serum concentration of amiodarone suggests that this drug should be used with caution.

Topics: Adult; Amiodarone; Anti-Arrhythmia Agents; Arrhythmias, Cardiac; Benzofurans; Digoxin; Drug Therapy, Combination; Electrocardiography; Female; Heart Arrest; Heart Atria; Heart Rate; Humans; Nadolol; Propanolamines; Tachycardia

Topics: Animals; Arrhythmias, Cardiac; Chick Embryo; Digoxin; Fetal Heart; Heart; Heart Arrest; Medigoxin; Myocardial Contraction

Topics: Aged; Coronary Disease; Digoxin; Drug Interactions; Drug Therapy, Combination; Female; Heart Arrest; Humans; Male; Ventricular Fibrillation; Verapamil

Documentation of the mechanism of sudden death is described in a patient with a prolonged QT interval. Ventricular tachycardia was initiated by a ventricular premature beat (VPB) with a prematurity index similar to previous isolated VPBs. This event occurred despite the fact that the patient was receiving phenytoin sodium, a drug known to shorten the QT interval.

Topics: Aged; Death, Sudden; Diabetes Complications; Digoxin; Electrocardiography; Epilepsy, Tonic-Clonic; Furosemide; Heart Arrest; Heart Failure; Humans; Male; Phenytoin; Potassium Chloride; Ventricular Fibrillation

There are a number of important drug interactions with amiodarone. This agent appears to have a marked effect on the kinetics of some commonly used cardiovascular drugs, such as warfarin, digoxin, quinidine, and procainamide, and has dynamic interactions with others, such as the beta blockers and some calcium antagonists. Bleeding has been reported, apparently caused by a potentiation of the anticoagulant effect of warfarin by amiodarone. Torsades de pointes has been observed when quinidine, propafenone, or mexiletine is given together with amiodarone. Furthermore, amiodarone may interact with beta-blocking agents and some of the calcium antagonists to produce symptomatic sinus bradycardia and sinus arrest, especially in a latent or overt sick sinus syndrome. During surgery, amiodarone may induce hypotension and an atropine-resistant bradycardia, possibly by interacting with anesthetic agents. A knowledge of the time of onset, extent, duration, and possible mechanisms of the interactions of amiodarone with other cardioactive drugs is still incomplete, but further studies are of great therapeutic importance.

Topics: Adrenergic beta-Antagonists; Amiodarone; Anti-Arrhythmia Agents; Arrhythmia, Sinus; Benzofurans; Blood Coagulation Disorders; Calcium; Digoxin; Drug Interactions; Drug Synergism; Heart Arrest; Humans; Kinetics; Quinidine; Tachycardia; Warfarin

Topics: Amiodarone; Benzofurans; Digoxin; Drug Interactions; Heart Arrest; Humans

An elderly woman allegedly ingested oleander leaves and died. Ventricular arrhythmias and asystole were unresponsive to cardiopulmonary resuscitation, pharmacologic agents, and cardioversion. The patient, who had no access to digoxin, had an initial serum digoxin concentration of 5.8 ng/mL. Cross-reactivities between oleander extract and pure oleandrin and digoxin in the digoxin radioimmunoassay were 100:1 and 29,000:1, respectively. We postulate that glycosides in oleander leaves produced the elevated serum digoxin concentration. Based on an assumed volume of distribution of the oleander glycosides of 1 L/kg, the calculated lethal dose absorbed by our patient was 200 times greater than lethal doses in several animal species and corresponded to the absorption of 4 g of oleander leaves.

Topics: Aged; Cardenolides; Cross Reactions; Digoxin; Female; Heart Arrest; Humans; Plant Extracts; Plant Poisoning; Plants, Medicinal; Radioimmunoassay; Ventricular Fibrillation

A case of cardiac arrest due to digitalis toxicity is described. The patient had normal serum digoxin levels and hypokalemia, and treatment with potassium chloride, phenytoin, and pacing was successful. Comment is made on the serum digoxin levels in relation to serum potassium.

Topics: Digoxin; Female; Heart Arrest; Humans; Hypokalemia; Middle Aged

Digoxin therapy was withdrawn over a four-year period in the geriatric wards of Skellefteå Hospital, if the indications for it were not clear, the medication was of doubtful value and there were no contraindications to withdrawal. Contraindications comprised symptoms of cardiac failure at rest or during light physical activity, X-ray signs of pulmonary congestion, a proven need for digoxin therapy following earlier withdrawal, or atrial fibrillation with a ventricular rate higher than 95 beats/min. A patient, who within two months presented signs of cardiac failure or an arrhythmia requiring digoxin, was considered to be in need of digoxin. Digoxin was withdrawn from a total of 141 patients, of whom 134 were examined after two months. According to our criteria, 108 (81%) of these 134 patients did not require digoxin treatment.

Topics: Age Factors; Aged; Arrhythmias, Cardiac; Digoxin; Drug Utilization; Female; Heart Arrest; Humans; Male; Middle Aged

Topics: Arrhythmia, Sinus; Arrhythmias, Cardiac; Digoxin; Drug Synergism; Female; Heart Arrest; Humans; Middle Aged; Verapamil

Topics: Digoxin; Drug Evaluation; Heart Arrest; Heart Conduction System; Humans

Overdosage with cardiac glycosides is well documented, but not usually fatal. A case is described in which cardiac arrest in asystole was associated with a serum digoxin level of 50-4 microgram/1, the highest concentration yet reported after oral administration.

Topics: Administration, Oral; Digoxin; Female; Heart Arrest; Humans; Middle Aged; Suicide

On isolated guinea-pig papillary muscles as well as on electrically driven atria digoxin was infused into the bath fluid until cardiac arrest occurred. The concentration of digoxin which caused standstill is defined as the toxic one. The toxicity was determined under various Ca2+-concentrations. On the papillary muscle the increase of extracellular Ca2+ from 0.9 to 7.2 mM increased the toxicity of digoxin, i.e. significantly diminished its toxic concentrations. Likewise, on electrically driven atria an increase of Ca2+ from 0.45 to 7.2 mM increased the toxicity of digoxin. These results demonstrate that with regard to the toxicity Ca2+ and digoxin act synergistically.

Topics: Animals; Calcium; Digoxin; Drug Synergism; Electric Stimulation; Guinea Pigs; Heart; Heart Arrest; Heart Atria; In Vitro Techniques; Male; Myocardial Contraction; Papillary Muscles

Forty-nine patients admitted to a Coronary Care Unit with myocardial infarction complicated by left ventricular failure, were treated with 1.75 mg Lanoxin over 36 hours. Serum digoxin levels were measured by radioimmunoassay at 8, 24, and 48 hours. No difference in serum levels was observed between those patients who received 'old' (reduced bioavailability) and those who received 'new' Lanoxin. Serum levels were significantly higher at 8 and 24 hours in those patients who received their first dose intramuscularly compared with those who received their first dose orally, irrespective of the bioavailability of the oral preparation used. No correlation was observed between serum digoxin levels and serum urea or creatinine during the 48-hour period of study. The incidence of arrhythmias is reported, but no conclusion can be drawn as to whether or not the glycoside contributed to this in any way. The use of digoxin in patients with acute myocardial infarction complicated by left ventricular failure is justifiable in the light of available evidence. However, in view of the possible predisposition of such patients to toxicity, lower serum levels than were achieved in many of our patients seem desirable and a modified dosage schedule is suggested.

Topics: Administration, Oral; Arrhythmias, Cardiac; Creatinine; Digoxin; Heart Arrest; Humans; Injections, Intramuscular; Middle Aged; Myocardial Infarction; Radioimmunoassay; Urea

Topics: Animals; Arrhythmias, Cardiac; Barbiturates; Bemegride; Biopharmaceutics; Blood Pressure; Cardiac Output; Digoxin; Dose-Response Relationship, Drug; Electrocardiography; Heart; Heart Arrest; Heart Rate; Specific Gravity; Vascular Resistance; Ventricular Fibrillation

Topics: Arrhythmias, Cardiac; Digoxin; Female; Furosemide; Heart Arrest; Heart Failure; Humans; Lidocaine; Middle Aged

Topics: Adenosine; Animals; Bradycardia; Bufanolides; Cardiac Glycosides; Cardiac Output; Digitalis Glycosides; Digitoxin; Digoxin; Guinea Pigs; Heart Arrest; Heart Block; Infusions, Parenteral; Lethal Dose 50; Mathematics; Ouabain; Plants, Medicinal; Time Factors

Topics: Adolescent; Adrenal Cortex Hormones; Brain Edema; Cardiomegaly; Central Venous Pressure; Cerebrovascular Circulation; Digoxin; Diuretics; Heart Arrest; Heart Atria; Heart Injuries; Hematoma; Humans; Male; Mediastinum; Oxygen Inhalation Therapy; Postoperative Complications; Radiography; Rupture; Thrombosis; Time Factors; Ventilators, Mechanical

Topics: Acidosis; Alkalosis; Anti-Bacterial Agents; Blood Transfusion; Body Temperature; Digoxin; Diuretics; Drainage; Glucose; Heart Arrest; Heart Defects, Congenital; Humans; Hypoglycemia; Hypoproteinemia; Infant, Newborn; Intubation, Intratracheal; Isoproterenol; Parenteral Nutrition; Positive-Pressure Respiration; Postoperative Care; Serum Albumin; Thrombocytopenia; Water-Electrolyte Balance

Topics: Arrhythmias, Cardiac; Atropine; Bradycardia; Digoxin; Electrocardiography; Heart Arrest; Heart Atria; Heart Block; Heart Conduction System; Humans; Hyperkalemia; Male; Middle Aged; Pacemaker, Artificial; Time Factors

Topics: Arrhythmias, Cardiac; Child, Preschool; Digoxin; Female; Follow-Up Studies; Heart Arrest; Heart Block; Hemorrhage; Humans; Hypotension; Infant; Male; Methods; Postoperative Complications; Propranolol; Transposition of Great Vessels

Topics: Digoxin; Erythroblastosis, Fetal; Exchange Transfusion, Whole Blood; Female; Heart Arrest; Humans; Infant, Newborn; Injections, Intramuscular; Pregnancy; Radioimmunoassay

Topics: Amitriptyline; Animals; Antidepressive Agents; Desipramine; Digoxin; Dose-Response Relationship, Drug; Drug Interactions; Heart; Heart Arrest; Imipramine; Male; Nortriptyline; Rats; Reserpine; Stress, Physiological

Topics: Aged; Atrial Fibrillation; Digoxin; Edrophonium; Female; Heart Arrest; Humans; Neuromuscular Nondepolarizing Agents; Quaternary Ammonium Compounds

Topics: Animals; Aorta; Blood Pressure; Blood Volume; Cardiac Output; Digoxin; Dogs; Electrocardiography; Female; Heart Arrest; Heart Rate; Hemodynamics; Male; Phenytoin; Vascular Resistance; Ventricular Fibrillation

Topics: Anticoagulants; Arrhythmias, Cardiac; Atropine; Digoxin; Electric Countershock; Heart Arrest; Humans; Intensive Care Units; Isoproterenol; Levallorphan; Lidocaine; Medical Staff, Hospital; Meperidine; Myocardial Infarction; New Zealand; Nursing Service, Hospital; Oxygen Inhalation Therapy; Procainamide; Quinidine; Sympathomimetics; Ventricular Fibrillation

Topics: Adams-Stokes Syndrome; Bradycardia; Digitalis; Digoxin; Electrocardiography; Heart Arrest; Heart Rate; Humans; Myocardial Infarction; Plants, Medicinal; Plants, Toxic; Procainamide; Propranolol; Quinidine; Sympathomimetics

Topics: Arrhythmias, Cardiac; Digitoxin; Digoxin; Heart Arrest; Humans; Infant