sodium-bicarbonate and Heart-Arrest

The effectiveness of pharmacologic management of cardiac arrest patients is widely debated; however, several studies published in the past 5 years have begun to clarify some of these issues. This article covers the current state of evidence for the effectiveness of the vasopressor epinephrine and the combination of vasopressin-steroids-epinephrine and antiarrhythmic medications amiodarone and lidocaine and reviews the role of other medications such as calcium, sodium bicarbonate, magnesium, and atropine in cardiac arrest care. We additionally review the role of β-blockers for refractory pulseless ventricular tachycardia/ventricular fibrillation and thrombolytics in undifferentiated cardiac arrest and suspected fatal pulmonary embolism.

Topics: Anti-Arrhythmia Agents; Atropine; Epinephrine; Heart Arrest; Humans; Sodium Bicarbonate

The use of sodium bicarbonate to treat metabolic acidosis is intuitive, yet data suggest that not all patients benefit from this therapy.. In this narrative review, we describe the physiology behind commonly encountered nontoxicologic causes of metabolic acidosis, highlight potential harm from the indiscriminate administration of sodium bicarbonate in certain scenarios, and provide evidence-based recommendations to assist emergency physicians in the rational use of sodium bicarbonate.. Sodium bicarbonate can be administered as a hypertonic push, as a resuscitation fluid, or as an infusion. Lactic acidosis and cardiac arrest are two common scenarios where there is limited benefit to routine use of sodium bicarbonate, although certain circumstances, such as patients with concomitant acute kidney injury and lactic acidosis may benefit from sodium bicarbonate. Patients with cardiac arrest secondary to sodium channel blockade or hyperkalemia also benefit from sodium bicarbonate therapy. Recent data suggest that the use of sodium bicarbonate in diabetic ketoacidosis does not confer improved patient outcomes and may cause harm in pediatric patients. Available evidence suggests that alkalinization of urine in rhabdomyolysis does not improve patient-centered outcomes. Finally, patients with a nongap acidosis benefit from sodium bicarbonate supplementation.. Empiric use of sodium bicarbonate in patients with nontoxicologic causes of metabolic acidosis is not warranted and likely does not improve patient-centered outcomes, except in select scenarios. Emergency physicians should reserve use of this medication to conditions with clear benefit to patients.

Topics: Acidosis; Acidosis, Lactic; Bicarbonates; Child; Heart Arrest; Humans; Sodium Bicarbonate

The 2010 Advanced Cardiac Life Support guidelines stated that routine sodium bicarbonate (SB) use for cardiac arrest patients was not recommended. However, SB administration during resuscitation is still common.. To evaluate the effect of SB on return of spontaneous circulation (ROSC) and survival-to-discharge rates in adult cardiac arrest patients.. We searched Medline, Scopus, and Cochrane Central Register of Controlled Trials (CENTRAL) from inception to December 2019. We included trials on nontraumatic adult patients after cardiac resuscitation and SB treatment vs. controls.. A meta-analysis was performed with six observational studies, including 18,406 adult cardiac arrest patients. There were no significant differences in the ROSC rate (odds ratio [OR] 1.185; 95% confidence interval [CI] 0.680-2.065) and survival-to-discharge rate (OR 0.296; 95% CI 0.066-1.323) between the SB and no-SB groups. In the subgroup analysis based on the year factor, there were no significant differences in the mortality rate in the After-2010 group. In the subgroup analysis based on the continent, the ROSC rate (OR 0.521; 95% CI 0.432-0.628) and survival-to-discharge rate (OR 0.102; 95% CI 0.066-0.156) were significantly lower in the North American group.. SB use was not associated with improvement in ROSC or survival-to-discharge rates in cardiac resuscitation. In addition, mortality was significantly increased in the North American group with SB administration.

Topics: Adult; Advanced Cardiac Life Support; Cardiopulmonary Resuscitation; Heart Arrest; Humans; Out-of-Hospital Cardiac Arrest; Patient Discharge; Sodium Bicarbonate

Local anaesthetic systemic toxicity (LAST) gives rise to symptoms from the central nervous and cardiovascular systems. Knowledge about symptoms and risk factors is crucial in preventing LAST. Treatment of severe symptoms should often include vasopressors and sodium bicarbonate. In cardiac arrest the guidelines for advance life support including high-quality cardiopulmonary resuscitation (CPR) should be followed - emphasising prolonged CPR and extracorporeal life support (ECLS) in case of LAST. The conclusion of this review is that intravenous lipid emulsion should only be considered, when other interventions fail, and ECLS is unavailable.

Topics: Anesthetics, Local; Cardiopulmonary Resuscitation; Extracorporeal Membrane Oxygenation; Heart Arrest; Humans; Sodium Bicarbonate

The goal of treating patients who present with cardiac arrest is to intervene as quickly as possible to affect the best possible outcome. The mainstays of these interventions, including early activation of the emergency response team, early initiation of cardiopulmonary resuscitation, and early defibrillation, are essential components with demonstrated positive impact on resuscitation outcomes. Conversely, the use of the code drugs as a component of advanced life support has not benefited these patients to the same extent as the basic interventions in a general. Although short-term outcomes are improved as a function of these medications, the final outcome has not been altered significantly in most instances.

Topics: Anti-Arrhythmia Agents; Calcium; Cardiopulmonary Resuscitation; Fibrinolytic Agents; Heart Arrest; Humans; Magnesium; Parasympatholytics; Sodium Bicarbonate; United States; Vasoconstrictor Agents

Topics: Advanced Cardiac Life Support; Algorithms; Anti-Arrhythmia Agents; Arrhythmias, Cardiac; Calcium; Cardiopulmonary Resuscitation; Child; Defibrillators; Drug Administration Routes; Electric Countershock; Glucose; Heart Arrest; Humans; Magnesium; Parents; Sodium Bicarbonate; Sweetening Agents; Vasoconstrictor Agents

Common clinical practices often are unsupported by experimental evidence. One example is the administration of sodium bicarbonate to neonates. Despite a long history of widespread use, objective evidence that administration of sodium bicarbonate improves outcomes for patients in cardiopulmonary arrest or with metabolic acidosis is lacking. Indeed, there is evidence that this therapy is detrimental. This review examines the history of sodium bicarbonate use in neonatology and the evidence that refutes the clinical practice of administering sodium bicarbonate during cardiopulmonary resuscitation or to treat metabolic acidosis in the NICU.

Topics: Acidosis, Respiratory; Cardiopulmonary Resuscitation; Evidence-Based Medicine; Heart Arrest; Humans; Infant, Newborn; Intensive Care Units, Neonatal; Sodium Bicarbonate; Treatment Outcome

No specific drug therapy has been shown to improve long-term survival after cardiac arrest, and only few drugs have a proven benefit for short-term survival. This study reviews recent studies on drugs during cardiopulmonary resuscitation.. Epinephrine is the first-line vasopressor during cardiopulmonary resuscitation. Arginine vasopressin may be more effective than epinephrine in patients presenting with asystole or as a second vasopressor 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 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 cardiac arrest.. Epinephrine is the vasopressor of first choice for routine use 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 used in shock-refractory ventricular fibrillation. Although not recommended for routine use, thrombolytic therapy during cardiopulmonary resuscitation may be considered in patients with suspected pulmonary embolism or after unsuccessful conventional cardiopulmonary resuscitation in patients with a presumably thrombotic cause of cardiac arrest.

Topics: Anti-Arrhythmia Agents; Arginine Vasopressin; Atropine; Cardiopulmonary Resuscitation; Epinephrine; Fibrinolytic Agents; Heart Arrest; Humans; Sodium Bicarbonate; Vasoconstrictor Agents

To date, there is no evidence showing a benefit from any advanced cardiac life support (ACLS) medication in out-of-hospital cardiac arrest (OOHCA), despite animal data to the contrary. One explanation may be a difference in the time to first drug administration. Our previous work has shown the mean time to first drug administration in clinical trials is 19.4min. We hypothesized that the average time to drug administration in large animal experiments occurs earlier than in OOHCA clinical trials.. We conducted a literature review between 1990 and 2006 in MEDLINE using the following MeSH headings: swine, dogs, resuscitation, heart arrest, EMS, EMT, ambulance, ventricular fibrillation, drug therapy, epinephrine, vasopressin, amiodarone, lidocaine, magnesium, and sodium bicarbonate. We reviewed the abstracts of 331 studies and 197 full manuscripts. Exclusion criteria included: non-peer reviewed, all without primary animal data, and traumatic models. From these, we identified 119 papers that contained unique information on time to medication administration. The data are reported as mean, ranges, and 95% confidence intervals. Mean time to first drug administration in animal laboratory studies and clinical trials was compared with a t-test. Regression analysis was performed to determine if time to drug predicted ROSC.. Mean time to first drug administration in 2378 animals was 9.5min (range 3.0-28.0; 95% CI around mean 2.78, 16.22). This is less than the time reported in clinical trials (19.4min, p<0.001). Time to drug predicted ROSC (odds ratio 0.844; 95% CI 0.738, 0.966).. Shorter drug delivery time in animal models of cardiac arrest may be one reason for the failure of animal studies to translate successfully into the clinical arena.

Topics: Amiodarone; Animals; Anti-Arrhythmia Agents; Clinical Trials as Topic; Disease Models, Animal; Drug Administration Schedule; Epinephrine; Heart Arrest; Humans; Lidocaine; Life Support Care; Magnesium Sulfate; Regression Analysis; Sodium Bicarbonate; Time Factors; Vasoconstrictor Agents; Vasopressins

For adults and pediatric age patients, high-dose intravenous epinephrine was recommended if standard-dose epinephrine failed to achieve return of spontaneous circulation. More recent trials suggest that high-dose epinephrine is not beneficial and may result in increased harm. There are no randomized clinical studies of high-dose versus standard-dose intravenous epinephrine in neonates. Routine use of high-dose epinephrine during neonatal resuscitation cannot be recommended. Although sodium bicarbonate has been used during neonatal resuscitation, the only randomized controlled trial of its use during brief neonatal resuscitation showed no benefit. Sodium bicarbonate infusion during neonatal cardiopulmonary resuscitation (CPR) has several known and potential side effects. The use of sodium bicarbonate infusion should be discouraged during brief CPR. Whether sodium bicarbonate is beneficial for infants who require prolonged CPR despite adequate ventilation is unknown.

Topics: Adrenergic Agonists; Animals; Cardiopulmonary Resuscitation; Dose-Response Relationship, Drug; Epinephrine; Heart Arrest; Humans; Infant, Newborn; Infusions, Intravenous; Sodium Bicarbonate

Topics: Acidosis; Bicarbonates; Buffers; Cardiopulmonary Resuscitation; Coronary Circulation; Heart Arrest; Humans; Myocardial Contraction; Practice Guidelines as Topic; Sodium Bicarbonate; Tromethamine

To review available investigations describing the properties of the buffer mixture Tribonat.. Original reports published in peer-reviewed medical journals.. Review of 76 citations, including four original studies on the effect of Tribonat performed by or supervised by the author, and six original studies concerning Tribonat originating from the institution to which the author is affiliated.. Computer search of the literature regarding treatment with alkaline buffers during cardiopulmonary resuscitation.. Routine buffering of acidosis has been questioned, but clinical situations still exist where such treatment is regarded as indicated. In such cases, a buffer with advantageous qualities and few side-effects is desirable. The hitherto commonly used buffers do not always fulfill these requirements, and a more profound knowledge of the alternative Tribonat may therefore be warranted.. The reviewed articles support the assumption that Tribonat may offer important advantages over previously used buffers in situations where administration of an alkalinizing agent is indicated.

Topics: Acidosis; Bicarbonates; Buffers; Cardiopulmonary Resuscitation; Heart Arrest; Humans; Sodium Bicarbonate; Treatment Outcome; Tromethamine

The use of bicarbonate is rooted in three decades of clinical experience and observational studies. For many years, bicarbonate passed the tried and true test for clinical therapies; however, administration of sodium bicarbonate during cardiac arrest and hypoxic acidosis has become increasingly controversial. The controversy provides an excellent opportunity to evaluate the impact an evidence-based approach might have on a common clinical practice. Is bicarbonate efficacious in the treatment of the severe acidosis that accompanies cardiac arrest during cardiopulmonary resuscitation (CPR)? Are the deleterious effects of bicarbonate clinically relevant? What is the evidence upon which a rational decision may be based? This review evaluates and ranks the evidence supporting the use of sodium bicarbonate in the therapy of acidosis associated with cardiac arrest during CPR.

Topics: Acidosis, Respiratory; Animals; Cardiopulmonary Resuscitation; Critical Care; Evidence-Based Medicine; Heart Arrest; Humans; MEDLINE; Sodium Bicarbonate

A combined hypercarbic and metabolic acidosis develops during the low flow state of cardiac arrest treated with cardiopulmonary resuscitation. Several negative consequences of the acidosis have been demonstrated, two of the most important being reduced contractility of the ischaemic but still beating myocardium and impaired resuscitability of the arrested heart. Even though interventions to re-establish a spontaneous circulation should be the number one priority during cardiopulmonary resuscitation, attempts to treat the acidosis are often carried out in order to avoid the reported negative inotropic effect. Different alkaline buffers have been used, but it has been demonstrated over the years that such treatment may aggravate the situation due to a variety of deleterious side-effects of the buffers. A mixture of THAM, acetate, sodium bicarbonate and phosphate registered as Tribonat has been suggested as a suitable alternative to conventional buffer substances. The problems preceding the designation of Tribonat as well as studies evaluating its effects are reviewed in this article. Tribonat seems to offer a more well-balanced buffering without any major disadvantages compared with previously used alkaline buffers, even though improved survival has not been reported.

Topics: Acidosis; Bicarbonates; Buffers; Carbonates; Cardiopulmonary Resuscitation; Controlled Clinical Trials as Topic; Drug Combinations; Heart Arrest; Humans; Sodium Bicarbonate; Survival Rate; Treatment Outcome; Tromethamine

Topics: Aged; Buffers; Clinical Trials as Topic; Combined Modality Therapy; Drug Administration Schedule; Drug Therapy, Combination; Electric Countershock; Epinephrine; Heart Arrest; Humans; Sodium Bicarbonate; Vasoconstrictor Agents

The resuscitation of children from cardiac arrest and shock remains a challenging goal. The pharmacologic principles underlying current recommendations for intervention in pediatric cardiac arrest have been reviewed. Current research efforts, points of controversy, and accepted practices that may not be most efficacious have been described. Epinephrine remains the most effective resuscitation adjunct. High-dose epinephrine is tolerated better in children than in adults, but its efficacy has not received full analysis. The preponderance of data continues to point toward the ineffectiveness and possible deleterious effects of overzealous sodium bicarbonate use. Calcium chloride is useful in the treatment of ionized hypocalcemia but may harm cells that have experienced asphyxial damage. Atropine is an effective agent for alleviating bradycardia induced by increased vagal tone, but because most bradycardia in children is caused by hypoxia, improved oxygenation is the intervention of choice. Adenosine is an effective and generally well-tolerated agent for the treatment of supraventricular tachycardia. Lidocaine is the drug of choice for ventricular dysrhythmias, and bretylium, still relatively unexplored, is in reserve. Many pediatricians use dopamine for shock in the postresuscitative period, but epinephrine is superior. Most animal research on cardiac arrest is based on models with ventricular fibrillation that probably are not reflective of cardiac arrest situations most often seen in pediatrics.

Topics: Adult; Anti-Arrhythmia Agents; Calcium Chloride; Child; Dopamine; Drug Monitoring; Drug Therapy; Heart Arrest; Humans; Pediatrics; Resuscitation; Sodium Bicarbonate; Vasoconstrictor Agents

Topics: Anti-Arrhythmia Agents; Atropine; Calcium; Cardiopulmonary Resuscitation; Drug Administration Routes; Epinephrine; Heart Arrest; Humans; Magnesium; Sodium Bicarbonate; Vasoconstrictor Agents

The routine use of sodium bicarbonate in patients with cardiac arrest has been discouraged, with the benefit of outcome evaluation. Current recommendations include an elaborate stratification of circumstances in which bicarbonate is to be used. The physiological and clinical aspects of bicarbonate administration during cardiopulmonary resuscitation in animal and human studies were reviewed. The onset of significant acidemia or alkalemia is associated with adverse system specific effects. The administration of bicarbonate may mitigate the adverse physiological effects of acidemia, improve response to exogenously administered vasopressor agents, or simply increase venous return due to an osmolar effect, resulting in increased coronary perfusion pressure. Likewise, bicarbonate may have adverse effects in each of these areas. The preponderance of evidence suggests that bicarbonate is not detrimental and may be helpful to outcome from cardiac arrest. An objective reappraisal of the empirical use of bicarbonate or other buffer agents in the appropriate "therapeutic window" for cardiac patients may be warranted.

Topics: Acid-Base Equilibrium; Acidosis; Animals; Central Nervous System; Disease Models, Animal; Heart; Heart Arrest; Hemodynamics; Humans; Lung; Myocardium; Sodium Bicarbonate

The metabolic acidosis resulting from poor tissue perfusion is considered to have several significant hemodynamic effects. Correction of the acidosis with sodium bicarbonate seems to be a rational approach to this problem. However, the current medical literature shows little clinical benefit to this tactic. In fact, indiscriminate bicarbonate administration may, itself, have deleterious effects. Concurring with the absence of a consistent therapeutic advantage to the use of sodium bicarbonate in the treatment of lactic acidosis due to inadequate tissue perfusion, the American Heart Association removed the routine use of sodium bicarbonate from the treatment of cardiac arrest in the algorithms of the Advanced Cardiac Life Support course. Although the debate continues, a detailed review of the medical literature does not support the use of sodium bicarbonate in this setting.

Topics: Acidosis, Lactic; Heart Arrest; Hemodynamics; Humans; Respiratory Transport; Sodium Bicarbonate

Topics: Carbonates; Drug Combinations; Heart Arrest; Humans; Sodium Bicarbonate; Tromethamine

Topics: Acidosis, Lactic; Bicarbonates; Clinical Protocols; Evaluation Studies as Topic; Heart Arrest; Humans; Infant, Newborn; Neonatology; Osmolar Concentration; Resuscitation; Sodium; Sodium Bicarbonate

Topics: Anti-Arrhythmia Agents; Bicarbonates; Cardiotonic Agents; Cardiovascular Agents; Drug Therapy, Combination; Fluid Therapy; Heart Arrest; Hemodynamics; Humans; Resuscitation; Shock, Cardiogenic; Sodium; Sodium Bicarbonate; Vasoconstrictor Agents

Topics: Acidosis; Bicarbonates; Blood Gas Analysis; Heart Arrest; Humans; Resuscitation; Sodium; Sodium Bicarbonate

It is generally believed that metabolic acidosis prevails during cardiac arrest. However, recent experimental and clinical studies have demonstrated that respiratory acidosis in mixed venous blood and respiratory alkalosis in arterial blood with only minor increases in lactic acid characterize the early acid-base changes that follow cardiac arrest and cardiopulmonary resuscitation (CPR). While continued CO2 production with critical reduction in systemic perfusion explains the accumulation of CO2 in the venous side, the reduction of pulmonary blood flow with maintenance of constant minute ventilation explains the decreases in expired CO2 and therefore arterial PCO2. In the heart, marked increases in CO2 tension and lactic acid are associated with dramatic decreases in myocardial pH with consequent depression of contractile function. Administration of sodium bicarbonate, however, neither increases resuscitability nor improves long term outcome. Moreover, adverse effects stemming from increases in plasma osmolality, increases in hemoglobin-O2 affinity, induction of alkalemia and generation of CO2 are potentially deleterious for myocardial and cerebral function. Consequently, the American Heart Association has recently discouraged the routine administration of bicarbonate during the initial 10 minutes of CPR in which interventions with proven efficacy such as artificial ventilation, precordial compression, electric defibrillation and epinephrine administration take place. Alternative experimental buffer therapy with agents that consume CO2 have also failed to alter the outcome of cardiac arrest.

Topics: Acid-Base Imbalance; Animals; Bicarbonates; Blood Gas Analysis; Dogs; Heart Arrest; Humans; Resuscitation; Sodium; Sodium Bicarbonate; Swine

The belief that defibrillation of unwitnessed ventricular fibrillation frequently results in asystole, combined with perceived low survival rates, led to deviation from "standard" advanced cardiac life support (ACLS) by physicians directing paramedics in the field. In nonstandard ACLS, intubation or drug therapy preceded defibrillation. This study retrospectively compared standard and nonstandard ACLS for ventricular fibrillation. The long-term survival rates were 12.3% (7/57) and 3.6% (6/168) for the two forms of ACLS, respectively (p = 0.03). The incidence of postcountershock asystole was 35% and 28% (p = 0.45). The survival rates for patients with a postcountershock rhythm and a pulse were 83% and 17% after standard and nonstandard ACLS (p less than 0.0001). Other factors reported to have a significant effect on survival were compared, and no significant differences (p greater than 0.05) were noted for mean age, sex, cardiopulmonary resuscitation (CPR) initiated by a bystander, ACLS response time, time to CPR, lay-witnessed arrest, or time to definitive care. The significant difference in the time to defibrillation (14 and 26 minutes) was expected. This is the first clinical study to clearly confirm the ACLS recommendation of early defibrillation before drug therapy in ventricular fibrillation.

Topics: Aged; Bicarbonates; Electric Countershock; Epinephrine; Female; Heart Arrest; Humans; Male; Middle Aged; Resuscitation; Retrospective Studies; Sodium; Sodium Bicarbonate; Time Factors; Ventricular Fibrillation

Topics: Anti-Arrhythmia Agents; Arrhythmias, Cardiac; Bicarbonates; Child; Child, Preschool; Electrocardiography; Epinephrine; Heart Arrest; Humans; Infant; Infant, Newborn; Injections; Prognosis; Respiration, Artificial; Resuscitation; Sodium; Sodium Bicarbonate

Cardiopulmonary resuscitation is effective if established early and coupled with specific therapeutic interventions. Most cardiopulmonary arrest is due to ventricular fibrillation and early defibrillation offers the highest probability of success. External cardiac compression alone is inadequate to provide adequate perfusion to vital organs and, therefore, cannot sustain life unless coupled with advanced therapeutic interventions. Many new techniques for increasing flow have been developed, but have not been established clinically. The American Heart Association guidelines for CPR are still valid and are the basis for our current CPR. A practical perspective is presented whereby the therapeutic interventions are pursued systematically in an expeditious and coordinated fashion so that the key interventions are made within the first 10 to 15 minutes of the arrest.

Topics: Anti-Arrhythmia Agents; Atropine; Bicarbonates; Brain Diseases; Calcium; Cardiac Pacing, Artificial; Catheterization; Electric Countershock; Heart Arrest; Heart Massage; Humans; Intubation, Intratracheal; Resuscitation; Sodium; Sodium Bicarbonate; Sympathomimetics; Tachycardia; Veins; Ventricular Fibrillation

We are currently witnessing the emergence of a physiologic approach to cardiopulmonary resuscitation. The algorithms and recommendations provided by the AHA provide an excellent framework for managing cardiac emergencies. As new knowledge becomes available, these recommendations should be modified and expanded. Continued assessment of the patient is a critical factor in managing cardiac arrest. As more complex technology and newer medications crowd the resuscitation scene, it is extremely important not to lose sight of the patient and the basics of good resuscitation: airway, breathing, and circulation. Technology provides helpful adjuncts to our assessment but cannot replace direct contact with the patient and the information gathered by direct observation. Students often fix their attention on the cardiac monitor, treating the electrical activity but ignoring the patient. Only by bringing together our observations from the patient, the laboratory, and our diagnostic tools will our knowledge of resuscitation develop to the point where we can improve survival from cardiac arrest.

Topics: Airway Obstruction; American Heart Association; Bicarbonates; Bretylium Tosylate; Calcium; Catheterization; Electric Countershock; Esophagus; Heart Arrest; Humans; Intubation; Respiration, Artificial; Resuscitation; Sodium; Sodium Bicarbonate; United States

Topics: Airway Obstruction; Bicarbonates; Cardiac Pacing, Artificial; Electric Countershock; Heart Arrest; Humans; Intraoperative Complications; Intubation, Intratracheal; Respiration, Artificial; Resuscitation; Sodium Bicarbonate

Topics: Adult; Anti-Arrhythmia Agents; Arrhythmias, Cardiac; Bicarbonates; Blood Circulation; Brain Ischemia; Cardiotonic Agents; Child; Electric Countershock; Heart Arrest; Heart Massage; Humans; Hypoxia, Brain; Infant, Newborn; Resuscitation; Sodium Bicarbonate; Ventricular Fibrillation

Topics: Airway Obstruction; Assisted Circulation; Bicarbonates; Calcium; Cardiac Pacing, Artificial; Cardiovascular Diseases; Coronary Artery Bypass; Electric Countershock; Emergency Medical Services; Epinephrine; Heart Arrest; Heart Diseases; Heart Valve Prosthesis; Humans; Respiration, Artificial; Resuscitation; Sodium Bicarbonate

To evaluate associations between sodium bicarbonate use and outcomes during pediatric in-hospital cardiac arrest (p-IHCA).. Prespecified secondary analysis of a prospective, multicenter cluster randomized interventional trial.. Eighteen participating ICUs of the ICU-RESUScitation Project (NCT02837497).. Children less than or equal to 18 years old and greater than or equal to 37 weeks post conceptual age who received chest compressions of any duration from October 2016 to March 2021.. None.. Child and event characteristics, prearrest laboratory values (2-6 hr prior to p-IHCA), pre- and intraarrest hemodynamics, and outcomes were collected. In a propensity score weighted cohort, the relationships between sodium bicarbonate use and outcomes were assessed. The primary outcome was survival to hospital discharge. Secondary outcomes included return of spontaneous circulation (ROSC) and survival to hospital discharge with favorable neurologic outcome. Of 1,100 index cardiopulmonary resuscitation events, median age was 0.63 years (interquartile range, 0.19-3.81 yr); 528 (48.0%) received sodium bicarbonate; 773 (70.3%) achieved ROSC; 642 (58.4%) survived to hospital discharge; and 596 (54.2%) survived to hospital discharge with favorable neurologic outcome. Among the weighted cohort, sodium bicarbonate use was associated with lower survival to hospital discharge rate (adjusted odds ratio [aOR], 0.7; 95% CI, 0.54-0.92; p = 0.01) and lower survival to hospital discharge with favorable neurologic outcome rate (aOR, 0.69; 95% CI, 0.53-0.91; p = 0.007). Sodium bicarbonate use was not associated with ROSC (aOR, 0.91; 95% CI, 0.62-1.34; p = 0.621).. In this propensity weighted multicenter cohort study of p-IHCA, sodium bicarbonate use was common and associated with lower rates of survival to hospital discharge.

Topics: Cardiopulmonary Resuscitation; Child; Cohort Studies; Heart Arrest; Humans; Infant; Intensive Care Units; Prospective Studies; Sodium Bicarbonate

To determine whether time to prepare IV medications for hyperkalemia varied by 1) drug, 2) patient weight, 3) calcium salt, and 4) whether these data support the Advanced Cardiac Life Support recommended sequence.. Prospective randomized simulation-based study.. Single pediatric tertiary medical referral center.. Pediatric nurses and adult or pediatric pharmacists.. Subjects were randomized to prepare medication doses for one of four medication sequences and stratified by one of three weight categories representative of a neonate/infant, child, or adult-sized adolescent: 4, 20, and 50 kg. Using provided supplies and dosing references, subjects prepared doses of calcium chloride, calcium gluconate, sodium bicarbonate, and regular insulin with dextrose. Because insulin and dextrose are traditionally prepared and delivered together, they were analyzed as one drug. Subjects preparing medications were video-recorded for the purpose of extracting timing data.. A total of 12 nurses and 12 pharmacists were enrolled. The median (interquartile range) total preparation time for the three drugs was 9.5 minutes (6.4-13.7 min). Drugs were prepared significantly faster for larger children (50 kg, 6.8 min [5.6-9.1 min] vs 20 kg, 9.5 min [8.6-13.0 min] vs 4 kg, 16.3 min [12.7-18.9 min]; p = 0.001). Insulin with dextrose took significantly longer to prepare than the other medications, and there was no difference between the calcium salts: (sodium bicarbonate, 1.9 [0.8-2.6] vs calcium chloride, 2.1 [1.2-3.1] vs calcium gluconate, 2.4 [2.1-3.0] vs insulin with dextrose, 5.1 min [3.7-7.7 min], respectively; p < 0.001). Forty-two percent of subjects (10/24) made at least one dosing error.. Medication preparation for hyperkalemia takes significantly longer for smaller children and preparation of insulin with dextrose takes the longest. This study supports Pediatric Advanced Life Support guidelines to treat hyperkalemia during pediatric cardiac arrest similar to those recommended per Advanced Cardiac Life Support (i.e., first, calcium; second, sodium bicarbonate; and third, insulin with dextrose).

Topics: Adolescent; Advanced Cardiac Life Support; Body Weight; Calcium Chloride; Calcium Gluconate; Child; Child, Preschool; Critical Care; Drug Compounding; Female; Glucose; Heart Arrest; Humans; Hyperkalemia; Infant; Infant, Newborn; Insulin; Male; Prospective Studies; Sodium Bicarbonate; Time Factors; Water-Electrolyte Balance

This study evaluates the effect of early administration of an empirical (1 mEq/kg) sodium bicarbonate dose on survival from prehospital cardiac arrest within brief (<5 minutes), moderate (5-15 minutes), and prolonged (>15 minutes) down time.. Prospective randomized, double-blinded clinical intervention trial that enrolled 874 prehospital cardiopulmonary arrest patients managed by prehospital, suburban, and rural regional emergency medical services. Over a 4-year period, the randomized experimental group received an empirical dose of bicarbonate (1 mEq/kg) after standard advanced cardiac life support interventions. Outcome was measured as survival to emergency department, as this was a prehospital study.. The overall survival rate was 13.9% (110/792) for prehospital arrest patients. There was no difference in the amount of sodium bicarbonate administered to nonsurvivors (0.859 +/- 0.284 mEq/kg) and survivors (0.8683 +/- 0.284 mEq/kg) (P = .199). Overall, there was no difference in survival in those who received bicarbonate (7.4% [58/420]), compared with those who received placebo (6.7% [52/372]) (P = .88; risk ratio, 1.0236; 0.142-0.1387). There was, however, a trend toward improved outcome with bicarbonate in prolonged (>15 minute) arrest with a 2-fold increase in survival (32.8% vs 15.4%; P = .007).. The empirical early administration of sodium bicarbonate (1 mEq/kg) has no effect on the overall outcome in prehospital cardiac arrest. However, a trend toward improvement in prolonged (>15 minutes) arrest outcome was noted.

Topics: Advanced Cardiac Life Support; Aged; Aged, 80 and over; Double-Blind Method; Emergency Medical Services; Heart Arrest; Humans; Middle Aged; Prospective Studies; Sodium Bicarbonate; Survival Analysis; Treatment Outcome

This study correlated the delay in initiation of bystander cardiopulmonary resuscitation (ByCPR), basic (BLS) or advanced cardiac (ACLS) life support, and transport time (TT) to survival from prehospital cardiac arrest. This was a secondary endpoint in a study primarily evaluating the effect of bicarbonate on survival.. Prospective multicenter trial.. Patients treated by urban, suburban, and rural emergency medical services (EMS) services.. Eight hundred and seventy-four prehospital cardiac arrest patients.. This group underwent conventional ACLS intervention followed by empiric early administration of sodium bicarbonate noting resuscitation times. Survival was measured as the presence of vital signs on emergency department (ED) arrival. Data analysis utilized Student's t-test and logistic regression (p<0.05).. Survival was improved with decreased time to BLS (5.52 min versus 6.81 min, p=0.047) and ACLS (7.29 min versus 9.49 min, p=0.002) intervention, as well as difference in time to return of spontaneous circulation (ROSC). The upper limit time interval after which no patient survived was 30 min for ACLS time, and 90 min for transport time. There was no overall difference in survival except at longer arrest times when considering the primary study intervention bicarbonate administration.. Delay to the initiation of BLS and ACLS intervention influenced outcome from prehospital cardiac arrest negatively. There were no survivors after prolonged delay in initiation of ACLS of 30 min or greater or total resuscitation and transport time of 90 min. This result was not influenced by giving bicarbonate, the primary study intervention, except at longer arrest times.

Topics: Adolescent; Adult; Advanced Cardiac Life Support; Aged; Aged, 80 and over; Cardiopulmonary Resuscitation; Child; Child, Preschool; Emergency Medical Services; Heart Arrest; Humans; Middle Aged; Outcome Assessment, Health Care; Prospective Studies; Sodium Bicarbonate; Survival Rate; Time Factors

This study associated survival from prehospital cardiac arrest to patient historical variables including presenting complaint, medications used, and medical history as a secondary end point in a trial evaluating the effect of bicarbonate administration. This raises issues concerning extensive prehospital historical assessment that may potentially delay care and transport.. This prospective multicentre trial enrolled 874 prehospital cardiac arrest patients encountered by urban, suburban, and rural emergency medical services. This group underwent conventional ACLS intervention followed by empiric early administration of sodium bicarbonate (1mEq/l). Survival was measured as the presence of vital signs on emergency department arrival. Data analysis used Student's t test, Fisher's exact test, chi2 with Pearson correlation, and logistic regression (p<0.05). Secondary end points were analysed including an association with common historical variables such as medical history, presenting complaint, or drugs used.. The overall survival rate was 13.9% (110 of 793) of prehospital arrest patients. There was no correlation between historical factors, such as chief complaint or history of present illness (p = 0.277), medical history (p = 0.425), presence of specific disease conditions (p = 0.1125-0.956), or overall drug use (p = 0.002-0.9848). However, there was an adverse association between specific antiarrhythmic use (p = 0.003) and outcome.. There is little relation of patient historical factors on the outcome from prehospital cardiac arrest raising issues of efficiency with history taking in prehospital care and transport.

Topics: Advanced Cardiac Life Support; Aged; Anti-Arrhythmia Agents; Comorbidity; Emergencies; Emergency Medical Services; Female; Heart Arrest; Humans; Logistic Models; Male; Middle Aged; Prospective Studies; Sodium Bicarbonate; Survival Rate; Treatment Outcome

This study correlated the effect of witnessing a cardiac arrest and instituting bystander CPR (ByCPR), as a secondary end point in a study evaluating the effect of bicarbonate on survival.. This prospective, randomised, double blinded clinical intervention trial enrolled 874 prehospital cardiopulmonary arrest patients encountered in a prehospital urban, suburban, and rural regional emergency medical service (EMS) area. This group underwent conventional advanced cardiac life support intervention followed by empiric early administration of sodium bicarbonate (1 mEq/l), monitoring conventional resuscitation parameters. Survival was measured as presence of vital signs on emergency department (ED) arrival. Data were analysed using chi(2) with Pearson correlation and odds ratio where appropriate.. The overall survival rate was 13.9% (110 of 792) of prehospital cardiac arrest patients. The mean (SD) time until provision of bystander cardiopulmonary resuscitation (ByCPR) by laymen was 2.08 (2.77) minutes, and basic life support (BLS) by emergency medical technicians was 6.62 (5.73) minutes. There was improved survival noted with witnessed cardiac arrest-a 2.2-fold increase in survival, 18.9% (76 of 402) versus 8.6% (27 of 315) compared with unwitnessed arrests (p<0.001) with a decreased risk ratio of mortality of 0.4534 (95% CI, 0.0857 to 0.1891). The presence of ByCPR occurred in 32% (228 of 716) of patients, but interestingly did not correlate with survival. The survival rate was 18.2% (33 of 181) if ByCPR was performed within two minutes and 12.8% (6 of 47), if performed >two minutes (p = 0.3752).. Survival after prehospital cardiac arrest is more likely when witnessed, but not necessarily when ByCPR was performed by laymen.

Topics: Adult; Cardiopulmonary Resuscitation; Double-Blind Method; Emergency Medical Services; First Aid; Heart Arrest; Humans; Prognosis; Prospective Studies; Sodium Bicarbonate; Survival Rate; Time Factors

Carbicarb, sodium bicarbonate, and 5% dextrose were compared for effects on resuscitability in a canine model of electromechanical dissociation after ventricular fibrillation.. 21 healthy mongrel dogs were anesthetized with pentobarbital, intubated, and mechanically supported. They were instrumented to measure heart rate, arterial pressure, pulmonary artery pressure, right atrial pressure, cardiac output, and arterial and mixed venous blood gases. The dogs were then subjected to a protocol that consisted of three successive CPR episodes. During each episode they were treated with repeated injections of one of the three substances, randomly chosen. After two minutes of ventricular fibrillation and four minutes of electromechanical dissociation, CPR was started with a thumper (rate, 60; duty cycle, 50%). If recovery was not obtained after five minutes of CPR, 1 mEq/kg carbicarb or sodium bicarbonate or 5 mL D5W was injected in the right atrium. Half the dose of the same substance was injected every five minutes thereafter; 1 mg epinephrine was also injected every five minutes until recovery. Hemodynamic and gasometric evaluations were performed five and 20 minutes after recovery. This later evaluation served as baseline for the next CPR episode.. The duration and success rates of CPR are similar in the three CPR groups. Hemodynamic parameters were also similar during recovery. Bicarbicarb and sodium bicarbonate increased bicarbonate levels and corrected pH in the arterial and mixed venous blood. There was no difference in the blood gas values after carbicarb and sodium bicarbonate.. In this model of cardiac arrest, carbicarb was not superior to sodium bicarbonate in the correction of metabolic acidosis during CPR.

Topics: Acidosis, Lactic; Animals; Bicarbonates; Blood Gas Analysis; Carbonates; Clinical Protocols; Disease Models, Animal; Dogs; Drug Combinations; Glucose; Heart Arrest; Hemodynamics; Resuscitation; Sodium; Sodium Bicarbonate

One hundred ninety-nine patients with out-of-hospital cardiac arrest persisted in ventricular fibrillation after the first defibrillation attempt and were then randomly assigned to receive either epinephrine or lidocaine before the next two shocks. The resulting electrocardiographic rhythms and outcomes for each group of patients were compared for each group and also compared with results during the prior 2 years, a period when similar patients primarily received sodium bicarbonate as initial adjunctive therapy. Asystole occurred after defibrillation with threefold frequency after repeated injection of lidocaine (15 of 59, 25%) compared with patients treated with epinephrine (four of 55, 7%) (p less than 0.02). There was no difference in the proportion of patients resuscitated after treatment with either lidocaine or epinephrine (51 of 106, 48% vs. 50 of 93, 54%) and in the proportion surviving (18, 19% vs. 21, 20%), respectively. Resuscitation (64% vs. 50%, p less than 0.005) but not survival rates (24% vs. 20%) were higher during the prior 2-year period in which initial adjunctive drug treatment for persistent ventricular fibrillation primarily consisted of a continuous infusion of sodium bicarbonate. The negative effect of lidocaine or epinephrine treatment was explained in part by their influence on delaying subsequent defibrillation attempts. Survival rates were highest (30%) in a subset of patients who received no drug therapy between shocks. We conclude that currently recommended doses of epinephrine and lidocaine are not useful for improving outcome in patients who persist in ventricular fibrillation.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Bicarbonates; Electric Countershock; Electrocardiography; Epinephrine; Evaluation Studies as Topic; Heart Arrest; Humans; Lidocaine; Sodium; Sodium Bicarbonate; Survival Analysis; Ventricular Fibrillation

Topics: Cardiopulmonary Resuscitation; Emergency Service, Hospital; Heart Arrest; Humans; Sodium Bicarbonate

Topics: Cardiopulmonary Resuscitation; Heart Arrest; Humans; Resuscitation; Sodium Bicarbonate

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

To investigate whether the effects of sodium bicarbonate (SB) during cardiopulmonary resuscitation (CPR) would be influenced by blood pH and administration timing. Adult patients experiencing in-hospital cardiac arrest (IHCA) from 2006 to 2015 were retrospectively screened. Early intra-arrest blood gas data were obtained within 10 min of CPR. Multivariable logistic regression analysis and generalised additive models were used for effect estimation and data exploration, respectively. A total of 1060 patients were included. Only 59 patients demonstrated favourable neurological status at hospital discharge. Blood pH ≤ 7.18 was inversely associated with favourable neurological outcome (odds ratio [OR], 0.24; 95% confidence interval [CI], 0.11-0.52; p value < 0.001) while SB use was not. In the interaction analysis for favourable neurological outcome, significant interactions were noted between SB use and time to SB (SB use × time to SB ≥ 20 min; OR 6.16; 95% CI 1.42-26.75; p value = 0.02). In the interaction analysis for survival to hospital discharge, significant interactions were noted between SB use and blood pH (Non-SB use × blood pH > 7.18; OR 1.56; 95% CI 1.01-2.41; p value = 0.05). SB should not be empirically administered for patients with IHCA since its effects may be influenced by blood pH and administration timing.

Topics: Aged; Cardiopulmonary Resuscitation; Female; Heart Arrest; Humans; Inpatients; Male; Middle Aged; Sodium Bicarbonate; Treatment Outcome

Cardiopulmonary resuscitation is common in the United States, with >200,000 people experiencing an in-hospital cardiac arrest (IHCA) annually. Recent medication shortages have raised the question of the frequency and type of medication used during cardiac arrest resuscitation. We sought to determine the frequency and quantity of medications used during IHCA.. This retrospective, single-center, medical record review was performed at a large, urban teaching hospital. Adults ≥18 years old who had an IHCA with confirmed loss of pulse between January 2017 and March 2018 were identified. A standardized data collection tool was used to extract data from the electronic medical record. The primary outcome was the frequency and quantity of medications used during the IHCA. Secondary outcomes included median time to defibrillation and frequency of sodium bicarbonate use, including among patients with end-stage renal disease (ESRD).. Criteria were met for 181 IHCA events. Demographic characteristics were 71% black, 17% white, mean age of 65 years, and 46% women. Epinephrine was given in 86.7% of the arrests, with a mean cumulative dose of 4.2 mg. Sodium bicarbonate was given in 63.5% of the arrests, with a mean cumulative dose of 9.0 g (1.9 amps). Amiodarone was given in 30.9% of the arrests, with a mean cumulative dose of 311.8 mg. Median time to defibrillation was 2 min (interquartile range, 1-4 min). Preexisting ESRD was present in 24.8% of patients, of whom 71.1% received sodium bicarbonate. Sodium bicarbonate administration was associated with a lower likelihood of survival to discharge (odds ratio [OR] = 0.27; 95% CI, 0.11-0.66) as well as a lower rate of return to spontaneous circulation (ROSC) (OR = 0.35; 95% CI, 0.13-0.95). Magnesium administration was associated with a lower rate of ROSC (OR = 0.39; 95% CI, 0.15-0.98). Of note, in patients with preexisting ESRD, no medications were significantly associated with a change in likelihood of survival to discharge or rate of ROSC. In patients without preexisting ESRD, magnesium was associated with a lower rate of ROSC (OR = 0.23; 95% CI, 0.08-0.77).. We found that in a hospital with established rapid response and code blue teams, numerous medications that are not recommended for routine use in cardiac arrest are still administered at significant frequencies. Furthermore, substantial amounts of drugs with known recent shortage are used in IHCA. Inc.

Topics: Advanced Cardiac Life Support; Aged; Aged, 80 and over; Amiodarone; Anti-Arrhythmia Agents; Drug Utilization; Electric Countershock; Epinephrine; Female; Heart Arrest; Hospitals, Teaching; Humans; Male; Middle Aged; Odds Ratio; Patient Discharge; Sodium Bicarbonate; United States

We describe a 27-year-old female with repeated episodes of pulseless electrical activity due to intoxication with a substance that was unidentified at presentation. Severe QRS widening was observed and empiric treatment with sodium bicarbonate and intravenous lipid emulsion was administered. In this case, intraosseous administration of lipid emulsion failed to improve haemodynamic parameters, suggesting that this dose remained in the bone marrow compartment. We recommend that physicians become aware of this possibility and to avoid intraosseous administration of lipid emulsion.

Topics: Adult; Antimalarials; Buffers; Calcium Gluconate; Cardiovascular Agents; Chloroquine; Critical Care; Drug Overdose; Electrocardiography; Fat Emulsions, Intravenous; Female; Heart Arrest; Humans; Infusions, Intraosseous; Sodium Bicarbonate; Suicide, Attempted; Treatment Outcome

Yew leaves poisoning is a rare life-threatening intoxication, whose diagnosis can be difficult. Initial symptoms are nausea, vomiting, abdominal pain, dizziness, tachycardia, muscle weakness, confusion, beginning within 1 hr from ingestion and followed by bradycardia, ventricular arrhythmias, ventricular fibrillation, severe hypotension, and death. Taxine-derived alkaloids are responsible for the toxicity of the yew leaves, blocking sodium and calcium channels, and causing conduction abnormalities. Because of lack of a specific antidote and limited efficacy of common antiarrhythmic drugs, prompt diagnosis, detoxification measures, and immediate hemodynamic support (also with transvenous cardiac stimulation) are essential.

Topics: Adrenergic alpha-Agonists; Adult; Aged; Amiodarone; Anti-Arrhythmia Agents; Arrhythmias, Cardiac; Cardiopulmonary Resuscitation; Cephalotaxus; Charcoal; Electrocardiography; Female; Gastric Lavage; Heart Arrest; Humans; Magnesium Sulfate; Male; Middle Aged; Norepinephrine; Pacemaker, Artificial; Plant Extracts; Plant Leaves; Sodium Bicarbonate; Treatment Outcome

Topics: Adult; Antidepressive Agents, Tricyclic; Antidotes; Bradycardia; Diagnosis, Differential; Drug Overdose; Electric Countershock; Electrocardiography; Female; Heart Arrest; Humans; Sodium Bicarbonate; Substance-Related Disorders; Suicide, Attempted

Anesthesia for lung transplantation remains one of the highest risk surgeries in the domain of the cardiothoracic anesthesiologist. End-stage lung disease, pulmonary hypertension, and right heart dysfunction as well as other comorbid disease factors predispose the patient to cardiovascular, respiratory and metabolic dysfunction during general anesthesia. Perhaps the highest risk phase of surgery in the patient with severe pulmonary hypertension is during the induction of anesthesia when the removal of intrinsic sympathetic tone and onset of positive pressure ventilation can decompensate a severely compromised cardiovascular system. Severe hypotension, cardiac arrest, and death have been reported previously. Here we present 2 high-risk patients for lung transplantation, their anesthetic induction course, and outcomes. We offer suggestions for the safe management of anesthetic induction to mitigate against hemodynamic and respiratory complications.

Topics: Adrenergic alpha-Agonists; Anesthesia; Bronchodilator Agents; Calcium Chloride; Cardiopulmonary Resuscitation; Cardiotonic Agents; Epinephrine; Fatal Outcome; Female; Heart Arrest; Humans; Hypertension, Pulmonary; Lung Transplantation; Male; Middle Aged; Milrinone; Nitric Oxide; Norepinephrine; Sodium Bicarbonate; Vasoconstrictor Agents; Vasopressins

We report a rare fatal case of acute metformin overdose in a 19-year-old woman.

Topics: Acidosis; Blood Gas Analysis; Cardiotonic Agents; Drug Overdose; Fatal Outcome; Female; Heart Arrest; Humans; Hypoglycemia; Hypoglycemic Agents; Hypotension; Long QT Syndrome; Metformin; Sodium Bicarbonate; Young Adult

Calcium and sodium bicarbonate (SB) are frequently used in treating patients with severe hyperkalaemia. We evaluated the efficacy of these medications for the treatment of severe hyperkalaemia during cardiopulmonary resuscitation (CPR). We also hypothesised that the effects of these medications might be associated with serum potassium level during CPR.. We conducted a retrospective observational study in a single medical centre. From adult patients who had suffered an in-hospital cardiac arrest from 2006 through 2012, we included those with a serum potassium level>6.5 mEq/L measured during CPR. We used multivariable logistic regression analysis to study the association of calcium/SB with sustained return of spontaneous circulation (ROSC).. Among the 109 patients included in our analysis, 40 (36.7%) patients achieved sustained ROSC, and only four (3.7%) patients survived to hospital discharge. The mean serum potassium level was 7.8 mEq/L. The analysis indicated that administration of SB was positively associated with sustained ROSC when serum potassium level was <7.9 mEq/L (odds ratio [OR]: 10.51; 95% confidence interval [CI]: 1.50-112.89; p: 0.03); administration of calcium and SB was also positively associated with sustained ROSC when serum potassium level was <9.4 mEq/L (OR: 51.11; 95% CI: 3.12-1639.16; p: 0.01).. The use of calcium and SB might be effective in the treatment of severe hyperkalaemia during cardiac arrest. The efficacy of SB/calcium correlated with serum potassium level. However, because the number of patients included in the analysis was small, this conclusion should be further examined in the future.

Topics: Adult; Aged; Calcium; Cardiopulmonary Resuscitation; Female; Heart Arrest; Humans; Hyperkalemia; Inpatients; Male; Middle Aged; Retrospective Studies; Sodium Bicarbonate; Taiwan; Treatment Outcome

The purpose was to determine prognosis of patients presenting extreme acidosis (pH <7) on admission to the intensive care unit (ICU) and to identify mortality risk factors.. We retrospectively analyzed all patients who presented with extreme acidosis within 24 hours of admission to a polyvalent ICU in a university hospital between January 2011 and July 2013. Multivariate analysis and survival analysis were used.. Among the 2156 patients admitted, 77 patients (3.6%) presented extreme acidosis. Thirty (39%) patients suffered cardiac arrest before admission. Although the mortality rate predicted by severity score was 93.6%, death occurred in 52 cases (67.5%) in a median delay of 13 (5-27) hours. Mortality rate depended on reason for admission, varying between 22% for cases linked to diabetes mellitus and 100% for cases of mesenteric infarction (P = .002), cardiac arrest before admission (P < .001), type of lactic acidosis (P = .007), high Simplified Acute Physiology Score II (P = .008), and low serum creatinine (P = .012).. Patients with extreme acidosis on admission to ICU have a less severe than expected prognosis. Whereas mortality is almost 100% in cases of cardiac arrest before admission, mortality is much lower in the absence of cardiac arrest before admission, which justifies aggressive ICU therapies.

Topics: Acidosis; Acidosis, Lactic; Acidosis, Respiratory; Adult; Aged; Diabetes Mellitus; Extracorporeal Membrane Oxygenation; Female; Heart Arrest; Hemorrhage; Hospital Mortality; Hospitalization; Hospitals, University; Humans; Hypoglycemic Agents; Infarction; Intensive Care Units; Male; Mesenteric Ischemia; Metformin; Middle Aged; Multivariate Analysis; Prognosis; Renal Dialysis; Respiration, Artificial; Retrospective Studies; Risk Factors; Severity of Illness Index; Sodium Bicarbonate; Survival Analysis; Vasoconstrictor Agents

Topics: Calcium; Cardiopulmonary Resuscitation; Heart Arrest; Humans; Hyperkalemia; Sodium Bicarbonate

Topics: Heart Arrest; Humans; Out-of-Hospital Cardiac Arrest; Sodium Bicarbonate

Despite limited recommendations for using sodium bicarbonate (SB) during cardiopulmonary resuscitation (CPR), we hypothesized that SB continues to be used frequently during pediatric in-hospital cardiac arrest (IHCA) and that its use varies by hospital-specific, patient-specific, and event-specific characteristics.. We analyzed 3719 pediatric (<18 years) index pulseless CPR events from the American Heart Association Get With The Guidelines-Resuscitation database from 1/2000 to 9/2010.. SB was used in 2536 (68%) of 3719 CPR events. Incidence of SB use between 2000 and 2005 vs. 2006 and 2010 was 71.1% vs. 66.2% (P=0.002). The primary outcome was survival to discharge. Secondary outcomes included 24-h survival and neurologic outcome. Multivariable logistic regression analyzed the association between SB use and outcomes. SB had increased use an ICU location, metabolic/electrolyte disturbance, prolonged CPR, pVT/VF, and concurrently with other pharmacologic interventions. Adjusting for confounding factors, SB use was associated with decreased 24-h survival (aOR 0.83, 95% CI: 0.69, 0.99) and decreased survival to discharge (aOR 0.80; 95% CI: 0.65, 0.97). Inclusion of metabolic/electrolyte abnormalities, hyperkalemia, and toxicologic abnormalities only (n=674), SB use was not associated with worse outcomes or unfavorable neurologic outcome.. SB is used frequently during pediatric pulseless IHCA, yet there is a significant trend toward less routine use over the last decade. Because SB is more likely to be used in an ICU, with prolonged CPR, and concurrently with other pharmacologic interventions; its use during CPR may be associated with poor prognosis due to an association with "last ditch" efforts of resuscitation rather than causation.

Topics: Adolescent; American Heart Association; Cardiopulmonary Resuscitation; Child; Child, Preschool; Critical Care; Female; Heart Arrest; Hospitalization; Humans; Infant; Logistic Models; Male; Outcome Assessment, Health Care; Practice Guidelines as Topic; Pulse; Registries; Sodium Bicarbonate; Survival Rate; United States

Flecainide is a Class Ic antiarrythmic agent associated with adverse events due to its pro-arrythmic effects. We report the case of a 33-year-old female presenting in cardiac arrest after a flecainide overdose treated with intravenous fat emulsion (IFE), sodium bicarbonate (NaHCO₃), and extracorporeal membrane oxygenation (ECMO). This case reviews the pathophysiology and management of flecainide toxicity including novel strategies of IFE and ECMO.

Topics: Adult; Anti-Arrhythmia Agents; Drug Overdose; Electrocardiography; Extracorporeal Membrane Oxygenation; Fat Emulsions, Intravenous; Female; Flecainide; Heart Arrest; Humans; Sodium Bicarbonate

Lacosamide treats partial seizures by enhancing slow inactivation of voltage-gated sodium channels. The described cardiac toxicity of lacosamide in the literature to date includes atrioventricular blockade (PR prolongation), atrial flutter, atrial fibrillation, sinus pauses, ventricular tachycardia and a single cardiac arrest. We report a second case of cardiac arrest following an intentional lacosamide overdose.. A 16 year-old female with a seizure disorder was found unresponsive in pulseless ventricular tachycardia after intentionally ingesting 4.5 g (76 mg/kg) lacosamide, 120 mg (2 mg/kg) cyclobenzaprine and an unknown amount of levetiracetam. Exact time of ingestion was unknown. Her initial electrocardiogram (ECG) demonstrated sinus tachycardia at 139 beats per minute, QRS duration 112 ms, and terminal R-wave in lead aVR > 3 mm. Despite treatment with 150 mEq of sodium bicarbonate, she had persistent EKG findings eight hours after presentation. Her serum lacosamide concentration nine hours after presentation was elevated at 22.8 μg/mL, while serum cyclobenzaprine concentration was 16 ng/mL (therapeutic: 10-30 ng/mL), and serum levetiracetam concentration was 22.7 μg/mL (therapeutic: 12-46 μg/mL). On hospital day three, ECG demonstrated resolution of the terminal R-wave with QRS of 78 ms. The patient recovered without physical or neurologic sequelae.. The patient's lacosamide, cyclobenzaprine and levetiracetam overdose was associated with QRS prolongation and terminal right axis deviation--suggesting sodium channel blockade as a likely etiology for her cardiac arrest. Cyclobenzaprine has potential for sodium channel blockade and ventricular dysrhythmias although cardiac toxicity due to cyclobenzaprine alone is rare. The combination of cyclobenzaprine with lacosamide may have resulted in cardiovascular collapse. In conclusion, overdose of lacosamide combined with therapeutic concentrations of sodium channel blocking xenobiotics may cause cardiac conduction delays and cardiac arrest.

Topics: Acetamides; Adolescent; Amitriptyline; Anticonvulsants; Drug Interactions; Drug Overdose; Electrocardiography; Epilepsy; Female; Heart Arrest; Humans; Lacosamide; Levetiracetam; Piracetam; Risk Factors; Sodium Bicarbonate; Sodium Channel Blockers; Sodium Channels; Suicide, Attempted; Tachycardia, Ventricular; Treatment Outcome

Features consistent with the syndrome known as excited delirium (ExDS) have been associated with law enforcement restraint-related death. The pathophysiology and exact causative factors of restraint-related death associated with ExDS remain unclear. We present a case of successful field resuscitation of a man with ExDS who experienced cardiopulmonary arrest while being restrained by law enforcement officers. Despite the presence of a severe lactic acidosis on emergency department admission, the patient recovered following prehospital treatment with advanced cardiac life support measures and intravenous sodium bicarbonate, likely in part due to early recognition of the disease process.

Topics: Acidosis; Adult; Advanced Trauma Life Support Care; Delirium; Electric Stimulation; Emergency Medical Services; Forensic Medicine; Heart Arrest; Humans; Male; Police; Psychomotor Agitation; Restraint, Physical; Resuscitation; Sodium Bicarbonate; Syndrome

The present study tested the hypothesis that addition of an inhibitor of Na(+)/H(+) exchanger (NHE1) to sodium bicarbonate might improve the response to base therapy from prolonged asphyxial cardiac arrest in piglets.. Asphyxial cardiac arrest was induced by endotracheal tube clamping. Animals were randomly assigned to four study groups: (i) vehicle control, (ii) administration of sabiporide (NHE1 inhibitor), (iii) administration of sodium bicarbonate, and (iv) administration of sabiporide and sodium bicarbonate.. Administration of sodium bicarbonate alone did not affect survival, hemodynamic measures, and regional blood flow to critical tissues such as brain, heart, kidney, liver, and spleen. In contrast, sabiporide given alone or combined with sodium bicarbonate improved these. Furthermore, treatment with sabiporide reduced accumulation of neutrophils, reduced cytokine production in the lung, and reduced plasma levels of cardiac troponin-I, alanine aminotransferase, aspartate aminotransferase, and urea. In addition, the combined use of sabiporide and sodium bicarbonate had more profound reduction in interleukin (IL)-6 and IL-10, compared to sabiporide alone.. These results suggest that addition of sabiporide to the administration of sodium bicarbonate might improve hemodynamic response and dampen the inflammatory cascade noted with cardiac arrest, and therefore being an attractive option in the treatment of cardiac arrest.

Topics: Alanine Transaminase; Animals; Aspartate Aminotransferases; Asphyxia; Cytokines; Echocardiography; Guanidines; Heart Arrest; Hemodynamics; Neutrophils; Regional Blood Flow; Sodium Bicarbonate; Sodium-Hydrogen Exchangers; Swine; Troponin I; Urea

Amniotic fluid embolism (AFE) is a rare and potentially fatal complication of pregnancy. In this case report, we highlight the successful use of sodium bicarbonate in a patient with an AFE. We present a case of a 38-year-old mother admitted for an elective caesarean section. Following the delivery of her baby, the mother suffered a cardiac arrest. Following a protracted resuscitation, transoesophageal echocardiography demonstrated evidence of acute pulmonary hypertension, with an empty left ventricle and an over-distended right ventricle. In view of these findings and no improvement noted from on-going resuscitation, sodium bicarbonate was infused as a pulmonary vasodilator. Almost instantaneous return of spontaneous circulation was noted, with normalisation of cardiac parameters. We propose that in patients suspected with AFE and who have been unresponsive to advance cardiac life support measures, and where right ventricular failure is present with acidosis and/or hypercarbia, the use of sodium bicarbonate should be considered.

Topics: Adult; Embolism, Amniotic Fluid; Female; Heart Arrest; Humans; Hypertension, Pulmonary; Pregnancy; Sodium Bicarbonate; Vasodilator Agents

To evaluate the preferences and self-reported practices of pediatric acute care physicians with respect to sodium bicarbonate administration to infants and children in shock or cardiac arrest.. National survey study utilizing a self-administered questionnaire.. Thirteen Canadian pediatric tertiary care centers.. Canadian pediatric critical care physicians, pediatric emergency physicians, and trainees in these subspecialties.. None.. Survey items were evaluated based on Yes/No responses, frequency responses, and Likert scales. Overall response rate was 53% (151/284) with 49.0% (74/151) citing pediatric critical care as their primary practice. 82.0% of respondents (123/150) indicated they would administer sodium bicarbonate as part of ongoing resuscitation for septic shock, whereas 58.3% (88/151) would administer sodium bicarbonate in a cardiac arrest scenario (p=0.004). 47.3% (71/150) selected a pH threshold at or below which they would administer sodium bicarbonate (mean, 6.94±0.013; median, 7.00; range, 6.50-7.20; interquartile range, 6.90-7.00), whereas 20.5% (31/151) selected a base excess threshold (mean, -15.62±0.78; median, -16; range, -20 to -4; interquartile range, -20 to -14). Both pH and duration of resuscitation were strongly associated with the decision to administer sodium bicarbonate (p<0.0001). Respondents' perceptions regarding a colleague's likelihood of administering sodium bicarbonate to the same patient under the same circumstances reflect an acknowledgment of disparate practices with respect to sodium bicarbonate use. 53.0% (79/149) felt current American Heart Association guidelines help them in deciding whether to administer sodium bicarbonate to critically ill patients, and 84% would support a randomized trial.. Differences of opinion exist among pediatric acute care physicians with respect to the timing and appropriateness of sodium bicarbonate administration during resuscitation. Most indicated they would support moving forward with a clinical trial.

Topics: Acidosis, Lactic; Attitude of Health Personnel; Canada; Child; Child, Preschool; Emergency Service, Hospital; Health Care Surveys; Health Knowledge, Attitudes, Practice; Heart Arrest; Hospitals, Pediatric; Humans; Infant; Practice Patterns, Physicians'; Resuscitation; Shock; Sodium Bicarbonate

Topics: Acidosis, Lactic; Heart Arrest; Humans; Practice Patterns, Physicians'; Shock; Sodium Bicarbonate

We report a unique case of diabetic ketoacidosis in which a relatively low potassium level on admission was associated with consequent life-threatening and refractory arrhythmia secondary to inappropriate use of intravenous insulin and bicarbonate therapy. The latter was reversed by rapid bolus potassium injection. Although we do not advocate this approach in every case, we emphasise that a bolus injection of potassium may be life saving in such cases. The lessons from this case have led to multidisciplinary meetings and modification of the institute's diabetic ketoacidosis clinical pathway.

Topics: Adult; Diabetic Ketoacidosis; Female; Heart Arrest; Humans; Hypoglycemic Agents; Hypokalemia; Insulin; Potassium Chloride; Sodium Bicarbonate; Young Adult

Topics: Adrenergic Agonists; Adrenergic alpha-Agonists; Adrenergic beta-Antagonists; Anesthetics, Local; Blood Pressure; Cardiomyopathy, Hypertrophic; Electric Countershock; Epinephrine; Female; Heart Arrest; Heart Rate; Humans; Hypophysectomy; Lidocaine; Middle Aged; Nasal Mucosa; Norepinephrine; Propanolamines; Sodium Bicarbonate

Topics: American Hospital Association; Cardiopulmonary Resuscitation; Emergency Medical Services; Guidelines as Topic; Heart Arrest; Humans; Sodium Bicarbonate; United States

Intravenous sodium bicarbonate (SB) administration during cardiopulmonary arrest (CPA) is intended to counteract lactic acidosis due to hypoxia, poor perfusion, and anaerobic metabolism. Despite a lack of documented efficacy and a level III recommendation from the American Heart Association, SB is widely used during resuscitation events. SB has both theoretical and measurable adverse effects. Excess or poorly timed administration during a CPA may elevate a patient's pH, inducing alkalemia. Despite decades of controversy surrounding use of this drug, the prevalence of SB-induced alkalemia has not been previously documented.. To estimate the prevalence of SB-induced alkalemia in inpatients after CPA and to investigate the pattern of SB administration.. Medical records were retrospectively reviewed with attention to SB administration and arterial blood gas (ABG) data. After application of inclusion and exclusion criteria to 264 CPA patients, the study group comprised 88 patients. When measured, if PCO(2) and pH were above normal limits after SB administration, we concluded that SB contributed to the alkalemia.. Twenty-seven (31%) patients received SB without any ABG data, and 70 (79%) patients received at least one empiric SB dose. Of the 61 patients with ABG data, alkalemia occurred in 10, a prevalence of 16%. Administration of SB increased pH in only 9 (15%) other CPA patients and had no effect in the 42 (69%) remaining patients.. Administration of SB during CPA was causally linked with inducing alkalemia in 16% of patients. Early collection of ABG samples may assist in optimizing pH during CPA and thus reduce unwarranted empiric use of SB.

Topics: Adult; Aged; Aged, 80 and over; Alkalosis; Blood Gas Analysis; Carbon Dioxide; Cardiopulmonary Resuscitation; Drug Administration Schedule; Female; Heart Arrest; Humans; Hydrogen-Ion Concentration; Male; Middle Aged; Prevalence; Retrospective Studies; Sodium Bicarbonate

A 19-year-old woman was brought by ambulance to the emergency department (ED) from a police holding cell. Less than 3 hours earlier, the patient had been a passenger in a car stopped for a traffic violation. As the police officer approached the car, the patient was noted to hurriedly stuff 2 plastic bags containing a white powdery substance into her mouth. On questioning, it was reported that the packets contained cocaine. Less than an hour after being taken to the police station, the patient was witnessed to have a generalized seizure. What is the pharmacological basis of acute cocaine intoxication? What are the cardiovascular manifestations of acute cocaine intoxication? What is the basis for using sodium bicarbonate in cocaine-induced wide-complex dysrhythmias? What is the basis for the use of lidocaine in cocaine-induced wide-complex dysrhythmias? Is there any evidence for the use of amiodarone to treat cocaine-induced wide-complex dysrhythmias?

Topics: Amiodarone; Anti-Arrhythmia Agents; Anticonvulsants; Antidotes; Arrhythmias, Cardiac; Charcoal; Cocaine; Electrocardiography; Emergency Medical Services; Female; Heart Arrest; Humans; Lidocaine; Lorazepam; Pulse; Seizures; Sodium Bicarbonate; Sympathomimetics; Tachycardia, Ventricular; Young Adult

Topics: Acidosis, Lactic; Angiography, Digital Subtraction; Blood Gas Analysis; Contrast Media; Diabetes Mellitus, Type 2; Fatal Outcome; Heart Arrest; Humans; Hypoglycemic Agents; Intubation, Intratracheal; Iohexol; Male; Metformin; Middle Aged; Postoperative Complications; Radiographic Image Enhancement; Renal Insufficiency; Respiration, Artificial; Respiratory Distress Syndrome; Sodium Bicarbonate; Subarachnoid Hemorrhage; Tomography, X-Ray Computed

Topics: Advanced Cardiac Life Support; Data Interpretation, Statistical; Emergency Medical Services; Heart Arrest; Humans; Sodium Bicarbonate; Survival Analysis

We describe a case of a 2-year-old boy who ingested 35 mg.kg(-1) of amitriptyline. He developed central nervous system toxicity, as demonstrated by coma and seizures and cardiac toxicity (cardiac arrest) within 1 h of ingestion. The cardiac toxicity was refractory to standard therapy. His cardiac rhythm alternated between ventricular tachycardia and pulseless ventricular tachycardia/ventricular fibrillation for a period of 17 h. Following prolonged cardiopulmonary resuscitation and aggressive supportive management, the patient recovered both cardiovascularly and neurologically. An echocardiogram and MRI brain were subsequently performed and were normal. The patient was discharged 2 weeks later with normal cognitive, behavioral and motor function. We discuss the benefit of prolonged and effective cardiopulmonary resuscitation in the management of this potentially fatal poisoning.

Topics: Adrenergic beta-Agonists; Amitriptyline; Analgesics, Non-Narcotic; Anticonvulsants; Blood Gas Analysis; Cardiopulmonary Resuscitation; Child, Preschool; Coma; Drug Overdose; Heart Arrest; Humans; Hypnotics and Sedatives; Kidney; Magnesium Sulfate; Male; Seizures; Sodium Bicarbonate; Time Factors; Treatment Outcome; Vasodilator Agents

Topics: Acetaminophen; Adult; Alcohol Drinking; Analgesics, Non-Narcotic; Critical Care; Dextropropoxyphene; Drug Combinations; Heart Arrest; Humans; Lactic Acid; Male; Prognosis; Sodium Bicarbonate

Topics: Adult; Cardiopulmonary Resuscitation; Diabetic Ketoacidosis; Heart Arrest; Humans; Male; Sodium Bicarbonate; Survivors; Treatment Outcome

Topics: Advanced Cardiac Life Support; Data Interpretation, Statistical; Emergency Medical Services; Heart Arrest; Humans; Sodium Bicarbonate; Survival Analysis; Treatment Outcome

We report two drowning victims with hypothermic circulatory arrest who were resuscitated with the use of extracorporeal circulation (ECC). The first patient developed severe post-bypass pulmonary oedema and inspired us to use a leucocyte-depletion filter in the second patient to attenuate leucocyte-mediated pulmonary reperfusion injury.. In the first patient, a standard extracorporeal circuit was used. In the second patient, systemic leucocyte depletion was applied using leucocyte-depletion filters (Pall RS 1, Pall, Portsmouth, UK), in the venous side of the extracorporeal circuit. Circulating leucocyte counts were measured and arterial blood gas analysis and chest X-rays were performed.. Both patients showed a decrease of the circulating leucocyte counts during rewarming and had nearly similar leucocyte counts on arrival at the intensive care unit (ICU). The first patient developed severe pulmonary oedema, with poor arterial blood gases, whereas the second patient, who had leucocyte-depletion by filtration, did not develop severe pulmonary oedema, and had good arterial blood gases.. Profound leucocyte-depletion by means of filtration may have contributed to limit leucocyte-mediated pulmonary reperfusion injury.

Topics: Accidents, Traffic; Acidosis; Adult; Cardiotonic Agents; Child, Preschool; Dopamine; Extracorporeal Circulation; Fatal Outcome; Heart Arrest; Humans; Hypothermia; Leukocyte Reduction Procedures; Male; Multiple Organ Failure; Near Drowning; Polymerase Chain Reaction; Pulmonary Edema; Reperfusion Injury; Rewarming; Sodium Bicarbonate

Topics: Buffers; Cardiopulmonary Resuscitation; Clinical Trials as Topic; Emergency Medical Services; Heart Arrest; Humans; Sodium Bicarbonate; Treatment Outcome

The use of sodium bicarbonate (SB) in cardiopulmonary resuscitation (CPR) is controversial. This study analyzes the effects of SB use on CPR outcome in the Brain Resuscitation Clinical Trial III (BRCT III), which was a multicenter randomized trial comparing high-dose to standard-dose epinephrine during CPR. Sodium bicarbonate use in BRCT III was optional.. The entire BRCT III database was reviewed. Analysis included only patients who arrested out of the hospital and whose time from collapse to initiation of ACLS was no longer than 30 min (total n = 2122 patients). Sodium bicarbonate use by the 16 participating study sites was analyzed. The study sites were divided according to their SB usage profile: 'low SB user' sites administered SB in less than 50% of CPRs and their first epinephrine to SB time exceeded 10 min; and 'high SB user' sites used SB in over 50% of CPRs and their first epinephrine to SB time was <10 min.. Sites' SB usage rates ranged between 3.1% and 98.2% of CPRs. Sodium bicarbonate usage rates correlated inversely with the sites' intervals from collapse (r = - 0.579 P = 0.018) from initiation of ACLS (r = - 0.685 P = 0.003) and from first epinephrine (r = - 0.611 P = 0.012) to SB administration. Mean ROSC rate in the 'high SB user' sites was 33.5% (CI = 30.0-37.0) compared to 25.7% (CI = 23.1-28.4) in the 'low SB user' sites. In the 'high SB user' sites, hospital discharge rate was 5.3% (CI = 3.6-7.0) compared to 3% (CI = 2.0-4.0) in the 'low SB user' sites, and 5.3% (CI = 3.6-7.0) had a favorable neurological outcome compared to 2.1% (CI = 1.2-3.0) in the 'low SB user' sites. Collapse to ACLS interval was 8.5 min (CI = 8.1-9.0) in the 'high SB user' sites compared to 10.2 min (CI = 9.8-10.6) in the 'low SB user' sites, and their ACLS to first epinephrine interval was 7.0 min (CI = 6.5-7.5) compared to 9.7 min (CI = 9.3-10.2). Multivariate regression analysis found that belonging to 'high SB user' sites independently increased the chances for ROSC (OR 1.36, CI 1.08-1.7) and for achieving a good neurological outcome (OR 2.18, CI 1.23-3.86).. Earlier and more frequent use of SB was associated with higher early resuscitability rates and with better long-term outcome. Sodium bicarbonate may be beneficial during CPR, and it should be subjected to a randomized clinical trial.

Topics: Acidosis; Aged; Brain; Buffers; Cardiopulmonary Resuscitation; Dose-Response Relationship, Drug; Emergency Medical Services; Epinephrine; Female; Heart Arrest; Humans; Male; Middle Aged; Randomized Controlled Trials as Topic; Sodium Bicarbonate; Sympathomimetics; Tachycardia, Ventricular; Treatment Outcome; Ventricular Fibrillation

Evaluate the efficacy of advanced life support interventions using the pediatric Utstein guidelines.. Charts from all patients for whom a cardiorespiratory arrest code was called during a six-year period in a university affiliated centre were reviewed. Data were recorded according to the pediatric Utstein guidelines and a P < 0.05 was considered significant.. Of the 234 calls, 203 were retained for analysis. The overall survival rate at one year was 26.0% of which 10% had deterioration of their neurologic status compared to the pre-cardiorespiratory arrest evaluation. Time to achieve sustained return of spontaneous circulation (ROSC; P < 0.0001) and sustained measurable blood pressure (P = 0.002), to perform endotracheal intubation (P = 0.04) and the dose of sodium bicarbonate (P < 0.0001) were indicators of long-term survival. Two patients were alive at one year with unchanged neurologic status despite a time to achieve sustained ROSC longer than 30 min (38 and 44 min). The mean first epinephrine dose of patients for whom ROSC was achieved but unsustained was higher than those for whom ROSC was achieved and sustained (0.038 +/- 0.069 mg*kg(-1) vs 0.011 +/- 0.006 mg*kg(-1); P = 0.004). Survival rate and mean first epinephrine dose of patients who received their first epinephrine dose endotracheally (13.3%; 0.011 +/- 0.004 mg*kg(-1)) were comparable to those of patients who received their first epinephrine dose intravenously (7%; 0.015 +/- 0.027 mg*kg(-1)).. For intravenously administered epinephrine, a dose of 0.01 mg*kg(-1) seems appropriate as the first dose. The endotracheal route is a valuable alternative for epinephrine administration and, for infants, the dose does not need to be increased. A minimal resuscitation duration time of 30 min can be misleading if ROSC is used as the indicator.

Topics: Academic Medical Centers; Adolescent; Adult; Analysis of Variance; Cardiopulmonary Resuscitation; Child; Child, Preschool; Dose-Response Relationship, Drug; Epinephrine; Female; Heart Arrest; Hospitalization; Humans; Infant; Intubation, Intratracheal; Life Support Care; Male; Quebec; Retrospective Studies; Sodium Bicarbonate; Survival Rate; Treatment Outcome; Vasoconstrictor Agents

NEW RECOMMENDATIONS: for cardio-pulmonary resuscitation Methods such as mouth to mouth or the search for a pulse, until now the fundamental preliminaries, have now become second line. Everything must be organised to allow for defibrillation as rapidly as possible. NEW MODALITIES FOR CARDIAC MASSAGE: The frequency of compressions recommended is currently 100 per minute in the adult with a rhythm of compression-ventilation reaching 15/2 before intubation. Concerning the haemodynamic agents for cardiac arrest, the efficacy of high doses of adrenalin is not greater than with conventional doses. Vasopressin is not superior to intravenous adrenalin regarding survival at 24 hrs exepet in case of asystoly. Dopamine at a "renal" dose is no longer used. ANTIARRYTHMICS: Amiodarone is part of the decisional tree in the case of ventricular fibrillation or ventricular tachycardia without a pulse. Semi-automatic defibrillator accessibility should be generalized. INFUSED SOLUTIONS: Sodium bicarbonate does not improve the survival except in particular cases. Physiological serum should be preferred to glucosed serum during reanimation.

Topics: Adult; Aftercare; Algorithms; Amiodarone; Cardiopulmonary Resuscitation; Cardiovascular Agents; Decision Trees; Electric Countershock; Electrocardiography; Epinephrine; Fluid Therapy; France; Heart Arrest; Hemodynamics; Humans; Physical Examination; Practice Guidelines as Topic; Respiration, Artificial; Sodium Bicarbonate; Survival Analysis; Treatment Outcome; United States; Vasopressins

Topics: Acidosis; Cardiopulmonary Resuscitation; Heart Arrest; Humans; Randomized Controlled Trials as Topic; Sodium Bicarbonate; Survival Rate; Thrombolytic Therapy

To explore the effects of alkaline buffers on cerebral perfusion and cerebral acidosis during and after cardiopulmonary resuscitation (CPR), 45 anaesthetized piglets were studied. The animals were subjected to 5 min non-interventional circulatory arrest followed by 7 min closed chest CPR and received either 1 mmol/kg of sodium bicarbonate, 1 mmol/kg of tris buffer mixture, or the same volume of saline (n=15 in all groups), adrenaline (epinephrine) boluses and finally external defibrillatory shocks. Systemic haemodynamic variables, cerebral cortical blood flow, arterial, mixed venous, and internal jugular bulb blood acid-base status and blood gases as well as cerebral tissue pH and PCO(2) were monitored. Cerebral tissue acidosis was recorded much earlier than arterial acidaemia. After restoration of spontaneous circulation, during and after temporary arterial hypotension, pH in internal jugular bulb blood and in cerebral tissue as well as cerebral cortical blood flow was lower after saline than in animals receiving alkaline buffer. Buffer administration during CPR promoted cerebral cortical reperfusion and mitigated subsequent post-resuscitation cerebral acidosis during lower blood pressure and flow in the reperfusion phase. The arterial alkalosis often noticed during CPR after the administration of alkaline buffers was caused by low systemic blood flow, which also results in poor outcome.

Topics: Acidosis; Animals; Bicarbonates; Brain; Buffers; Carbon Dioxide; Cardiopulmonary Resuscitation; Cerebrovascular Circulation; Disease Models, Animal; Heart Arrest; Hydrogen-Ion Concentration; Isotonic Solutions; Sodium Bicarbonate; Sodium Chloride; Sus scrofa; Tromethamine

Topics: Animals; Cardiopulmonary Resuscitation; Dogs; Heart Arrest; Sodium Bicarbonate

Controversy surrounds the use of buffers during cardiac arrest to correct acidosis. The objective of this study was to determine whether attenuation or neutralization of cerebral acidosis by Carbicarb alters hippocampal glutamate levels, neuronal cell death, and neurologic deficits after reperfusion from asphyxial cardiac arrest in rats.. Rats were prospectively randomized to either a control (n=45), low-dose Carbicarb (LDC; 3 mL/kg, n=45), or high-dose Carbicarb (HDC; 6 mL/kg, n=45) group in a blinded fashion during resuscitation after 8 minutes of asphyxial cardiac arrest. Microdialysis was used to assess brain pH and glutamate. A neurologic deficit score and neuronal cell death in the hippocampus were determined at day 7.. Resuscitation was greatest in LDC rats (42/45) and least in HDC rats (28/45) versus that in control rats (34/45). Brain pH was higher in the LDC and HDC rats 10 minutes after resuscitation and remained higher than that of control rats for 120 minutes after resuscitation. Glutamate levels at 10 to 120 minutes after reperfusion were lowest in the LDC rats. LDC rats had the lowest neurologic deficit score (1+/-2) versus that of control rats (13+/-8) and HDC rats (19+/-6). Hippocampal neuronal cell death was lowest in LDC rats (30+/-20) versus that in control rats (86+/-47) and HDC rats (233+/-85).. LDC administered during resuscitation from asphyxial cardiac arrest attenuated acidosis, improved resuscitation, and reduced neurologic deficits and the number of dead hippocampal neurons. Neutralization of cerebral acidosis with HDC increased the number of dead hippocampal neurons and neurologic deficits after resuscitation from cardiac arrest in rats.

Topics: Acidosis; Animals; Asphyxia; Brain; Brain Ischemia; Carbonates; Cell Death; Disease Models, Animal; Drug Combinations; Glutamic Acid; Heart Arrest; Hippocampus; Neurons; Rats; Recovery of Function; Reperfusion Injury; Sodium Bicarbonate; Treatment Outcome

This study retrospectively analyzed the pattern of sodium bicarbonate (SB) use during cardiopulmonary resuscitation (CPR) in the Brain Resuscitation Clinical Trial III (BRCT III). BRCT III was a prospective clinical trial, which compared high-dose to standard-dose epinephrine during CPR. SB use was left optional in the study protocol. Records of 2915 patients were reviewed. Percentage, timing and dosage of SB administration were correlated with demographic and cardiac arrest variables and with times from collapse to Basic Life Support, to Advanced Cardiac Life Support (ACLS) and to the major interventions performed during CPR. SB was administered in 54.5% of the resuscitations. The rate of SB use decreased with increasing patient age-primarily reflecting shorter CPR attempts. Mean time intervals from arrest, from start of ACLS and from first epinephrine to administration of the first SB were 29+/-16, 19+/-13, and 10.8+/-11.1 min, respectively. No correlation was found between the rate of SB use and the pre-ACLS hypoxia times. On the other hand, a direct linear correlation was found between the rate of SB use and the duration of ACLS. We conclude that when SB was used, the time from initiation of ACLS to administration of its first dose was long and severe metabolic acidosis probably already existed at this point. Therefore, if SB is used, earlier administration may be considered. Contrary to physiological rationale, clinical decisions regarding SB use did not seem to take into consideration the duration of pre-ACLS hypoxia times. We suggest that guidelines for SB use during CPR should emphasize the importance of pre-ACLS hypoxia time in contributing to metabolic acidosis and should be more specific in defining the duration of "protracted CPR or long resuscitative efforts", the most frequent indication for SB administration.

Topics: Advanced Cardiac Life Support; Age Factors; Aged; Cardiopulmonary Resuscitation; Emergency Medical Services; Female; Heart Arrest; Humans; Life Support Care; Male; Middle Aged; Practice Guidelines as Topic; Retrospective Studies; Sodium Bicarbonate; Time Factors

Severe acidemia (blood pH < 7.1 to 7.2) suppresses myocardial contractility, predisposes to cardiac arrhythmias, causes venoconstriction, and can decrease total peripheral vascular resistance and blood pressure, reduce hepatic blood flow, and impair oxygen delivery. These alterations in organ function can contribute to increased morbidity and mortality. Although it seemed logical to administer sodium bicarbonate to attenuate acidemia and therefore lessen the impact on cardiac function, the routine use of bicarbonate in the treatment of the most common causes of severe acidemia, diabetic ketoacidosis, lactic acidosis, and cardiac arrest, has been an issue of great controversy. Studies of animals and patients with these disorders have reported conflicting data on the benefits of bicarbonate, showing both beneficial and detrimental effects. Alternative alkalinizing agents, tris-hydroxymethyl aminomethane and Carbicarb, have shown some promise in studies of animals and humans, and reevaluation of these buffers in the treatment of severe acidemic states seems warranted. The potential value of base therapy in the treatment of severe acidemia remains an important issue, and further studies are required to determine which patients should be administered base therapy and what base should be used.

Topics: Acidosis; Acidosis, Lactic; Animals; Arrhythmias, Cardiac; Bicarbonates; Buffers; Calcium; Carbonates; Cardiac Output; Diabetic Ketoacidosis; Drug Combinations; Heart Arrest; Humans; Myocardial Contraction; Oxygen; Potassium; Sodium Bicarbonate; Tromethamine; Vascular Resistance; Water-Electrolyte Balance

Although cocaine is one of the leading causes of drug-related deaths, there is little clinical information describing the precise sequence of events leading to death in the cocaine intoxication. Usually, cocaine-related sudden deaths are unwitnessed, its electrocardiographic features are not attainable, and the majority of these patients have a rapidly fatal course and die before arriving at the hospital. We report a patient with massive cocaine ingestion who developed psychomotor agitation and generalized seizures followed by asystolic cardiac arrest. Ventilation with supplemental oxygen by endotracheal intubation immediately restored spontaneous heart beat. After resuscitation, a severe metabolic acidosis (pH 6.65) and cardiac dysrrhythmias consistent with sodium channel poisoning were detected. The electrocardiogram showed accelerated junctional rhythm at 85 beats/min with right bundle branch block and left anterior hemiblock configuration, prolongation of QRS (0.16 sec) and QTc (0.52 sec) intervals, and terminal J wave associated with coved ST-segment elevation in leads V(1) and V(2) resembling the Brugada syndrome. Sodium bicarbonate administration was quickly followed by normalization of the cardiac conduction disturbances. This article discusses the clinical and electrophysiologic implications of these findings.

Topics: Acidosis; Adult; Cocaine; Death, Sudden, Cardiac; Dopamine Uptake Inhibitors; Electrocardiography; Heart Arrest; Heart Conduction System; Humans; Male; Sodium Bicarbonate; Syndrome

The likelihood of successful defibrillation and resuscitation decreases as the duration of cardiac arrest increases. Prolonged cardiac arrest is also associated with the development of acidosis. These experiments were designed to determine whether administration of sodium bicarbonate and/or adrenaline in combination with a brief period of cardiopulmonary resuscitation (CPR) prior to defibrillation would improve the outcome of prolonged cardiac arrest in dogs. Ventricular fibrillation (VF) was induced by a.c. shock in anaesthetised dogs. After 10 min of VF, animals received either immediate defibrillation (followed by treatment with bicarbonate or control) or immediate treatment with bicarbonate or saline (followed by defibrillation). Treatment with bicarbonate was associated with increased rates of restoration of spontaneous circulation. This was achieved with fewer shocks and in a shorter time. Coronary perfusion pressure was significantly higher in NaHCO3-treated animals than in control animals. There were smaller decreases in venous pH in NaHCO3-treated animals than in controls. The best outcome in this study was achieved when defibrillation was delayed for approximately 2 min, during which time NaHCO3 and adrenaline were administered with CPR. The results of the present study indicate that in prolonged arrests bicarbonate therapy and a period of perfusion prior to defibrillation may increase survival.

Topics: Animals; Cardiopulmonary Resuscitation; Dogs; Electric Countershock; Epinephrine; Heart Arrest; Sodium Bicarbonate; Time Factors; Ventricular Fibrillation

A 52-year-old man developed an out-of-hospital cardiac arrest complicating a myocardial infarction. After prolonged cardiopulmonary resuscitation, he was admitted to an intensive care unit, where 25 episodes of cardiac arrests occurred within a few hours. Finally the outcome was favourable. This case raises the question of the duration a cardiopulmonary resuscitation in case of out-of-hospital and in-hospital cardiac arrest. The question is to determine how long resuscitation efforts must be prolonged after recurrent cardiac arrests.

Topics: Anti-Arrhythmia Agents; Cardiopulmonary Resuscitation; Coma; Combined Modality Therapy; Coronary Care Units; Critical Care; Dopamine; Drug Therapy, Combination; Echocardiography; Electric Countershock; Epinephrine; Euthanasia, Passive; Fibrinolytic Agents; First Aid; Glasgow Coma Scale; Heart Arrest; Humans; Hypnotics and Sedatives; Lidocaine; Male; Middle Aged; Myocardial Infarction; Recurrence; Reflex, Pupillary; Renal Dialysis; Sodium Bicarbonate; Thrombolytic Therapy; Time Factors; Tissue Plasminogen Activator; Treatment Outcome; Ventricular Fibrillation

Topics: Acid-Base Equilibrium; Animals; Cardiopulmonary Resuscitation; Heart Arrest; Humans; Sodium Bicarbonate; Treatment Outcome

To compare intraosseous with central venous blood samples for biochemical analyses and hemoglobin levels during cardiopulmonary resuscitation (CPR) and during cardiopulmonary resuscitation with infusion of sodium bicarbonate, epinephrine, and saline boluses through the intraosseous site.. Prospective, complete repeated measures study.. An animal laboratory at a university medical center.. Thirty-two piglets (mean weight, 30 [range, 24-35] kg).. Animals were anesthetized, instrumented, and subjected to hypoxic cardiac arrest. An intraosseous cannula was inserted into the tibia, and animals were randomly assigned to one of five groups: heparinized saline (n = 6), epinephrine infusions only (n = 6), saline infusions only (n = 6), sodium bicarbonate infusions only (n = 8), and epinephrine, saline, and sodium bicarbonate infusions through the same site (n = 6). CPR (chest compressions and mechanical ventilation) was performed in all groups. Simultaneous blood samples were taken from the central venous and intraosseous sites before arrest and after 5 and 30 mins of CPR.. There were no differences (p < .05) in sodium, potassium, magnesium, lactate, and calcium values of intraosseous and central venous blood at the baseline and during 5 mins of CPR with infusions through the intraosseous cannula. At 30 mins, differences were apparent in magnesium, potassium, and sodium values between groups when the intraosseous cannula was used for infusions as well as sampling. Intraosseous potassium, glucose, and magnesium values were lower and sodium values were higher than central venous blood levels. No differences were seen at all sampling intervals if small-volume heparinized saline was given through the intraosseous site. Hemoglobin values were lower in the intraosseous group after 30 mins of CPR and infusions through the intraosseous site. After 30 mins of CPR, all hemoglobin values from the intraosseous site were <10 g/100 mL.. Intraosseous and central venous blood biochemical and hemoglobin values were similar during hemodynamic stability and throughout 30 mins of resuscitation if no drugs were given through the intraosseous site. However, differences existed after 30 mins of CPR and infusions through the intraosseous site. Laboratory values may be erroneous when intraosseous blood is used during periods of resuscitation of >5 mins if drugs and fluid boluses have also been infused through the site. For reliable values, an intraosseous site for sampling only may be reasonable.

Topics: Animals; Blood Chemical Analysis; Blood Glucose; Blood Specimen Collection; Cardiopulmonary Resuscitation; Drug Therapy, Combination; Electrolytes; Epinephrine; Heart Arrest; Hemodynamics; Hemoglobins; Infusions, Intraosseous; Random Allocation; Sodium Bicarbonate; Sodium Chloride; Swine

Severe cocaine toxicity causes acidemia and cardiac dysfunction. These manifestations are described in 4 patients who presented with seizures, psychomotor agitation, and cardiopulmonary arrest. Their initial laboratory values demonstrated acidemia and electrocardiographic findings that included a prolonged QRS complex and QTc duration and a rightward T40 ms axis deviation. Treatment of the patients with hyperventilation, sedation, active cooling, and sodium bicarbonate infusion led to the normalization of their blood pHs and reversal of their cardiac conduction disorders. Acidemia can contribute to cocaine cardiac disorders by promoting conduction delays, dysrhythmias, and depressed myocardial contractility. Good supportive care corrects the blood pH and cardiac conduction disorders and remains the major focus in the management of patients with cocaine toxicity.

Topics: Acid-Base Imbalance; Adult; Akathisia, Drug-Induced; Alkalies; Apnea; Arrhythmias, Cardiac; Cocaine; Cocaine-Related Disorders; Crack Cocaine; Electrocardiography; Heart; Heart Arrest; Humans; Hydrogen-Ion Concentration; Hypnotics and Sedatives; Hypothermia, Induced; Male; Myocardial Contraction; Narcotics; Respiration, Artificial; Seizures; Sodium Bicarbonate

a) To determine the relationship of acid-base balance (pH, PCO2) of blood samples from the intraosseous and the mixed venous route during prolonged cardiopulmonary resuscitation; b) to compare the effect of separate infusions of epinephrine, fluid boluses, or sodium bicarbonate through the intraosseous sites on the acid-base status of intraosseous and mixed venous blood during cardiopulmonary resuscitation; and c) to compare pH and Pco2 of intraosseous and mixed venous blood samples after sequential infusions of fluid, epinephrine, and sodium bicarbonate through a single intraosseous site.. Prospective, randomized study.. Animal laboratory at a university center.. Thirty-two mixed-breed piglets (mean weight, 30 kg).. Piglets were anesthetized and prepared for blood sampling and cardiopulmonary resuscitation. After anoxic cardiac arrest, ventilation was resumed and chest compression was resumed. Blood gas samples from the pulmonary artery and both intraosseous sites were obtained simultaneously at baseline, at cardiac arrest, and at 5, 10, 15, 20, and 30 mins of cardiopulmonary resuscitation for group 1 (control group) and after drug (epinephrine and sodium bicarbonate) and saline infusions via one of the intraosseous cannulas in groups 2 through 5.. We found no differences between intraosseous and mixed venous pH and Pco2 during periods of <15 mins of cardiopulmonary resuscitation. However, this relationship was not maintained during prolonged cardiopulmonary resuscitation and after bicarbonate infusion. After large volume saline infusion, the pH and Pco2 of mixed venous and intraosseous blood were similar. During epinephrine infusion, the relationship between intraosseous and mixed venous pH and Pco2 was similar to that found in the control group.. The intraosseous blood sample could be used to assess central acid-base balance in the early stage of arrest and cardiopulmonary resuscitation of <15 mins. However, during cardiopulmonary resuscitation of longer duration, drug infusions may render the intraosseous site inappropriate for judging central acidosis.

Topics: Acid-Base Equilibrium; Acidosis; Adrenergic Agonists; Animals; Blood Gas Analysis; Blood Specimen Collection; Bone and Bones; Cardiopulmonary Resuscitation; Child; Epinephrine; Fluid Therapy; Heart Arrest; Humans; Prospective Studies; Random Allocation; Sodium Bicarbonate; Swine; Time Factors; Veins

Topics: Animals; Buffers; Carbonates; Cardiopulmonary Resuscitation; Disease Models, Animal; Dogs; Drug Combinations; Heart Arrest; Humans; Sodium Bicarbonate; Tromethamine; Ventricular Fibrillation

During cardiopulmonary resuscitation (CPR), elimination of CO2 was shown to be limited by low tissue perfusion, especially when very low perfusion pressures were generated. It has therefore been suggested that sodium bicarbonate (NaHCO3), by producing CO2, might aggravate the hypercarbic component of the existing acidosis and thereby worsen CPR outcome. The objectives of this study were to evaluate the effects of CO2 producing and non-CO2 producing buffers in a canine model of prolonged ventricular fibrillation followed by effective CPR.. Prospective, randomized, controlled, blinded trial.. Experimental animal research laboratory in a university research center.. Thirty-eight adult dogs, weighing 20 to 35 kg.. Animals were prepared for study with thiopental followed by halothane, diazepam, and pancuronium. Ventricular fibrillation was electrically induced, and after 10 mins, CPR was initiated, including ventilation with an FIO2 of 1.0, manual chest compressions, administration of epinephrine (0.1 mg/kg every 5 mins), and defibrillation. A dose of buffer, equivalent to 1 mmol/kg of NaHCO3, was administered every 10 mins from start of CPR. Animals were randomized to receive either NaHCO3, Carbicarb, THAM, or 0.9% sodium chloride (NaCl). CPR was continued for up to 40 mins or until return of spontaneous circulation.. Buffer-treated animals had a higher resuscitability rate compared with NaCl controls. Spontaneous circulation returned earlier and at a significantly higher rate after NaHCO3 (in seven of nine dogs), and after Carbicarb (six of ten dogs) compared with NaCl controls (two of ten dogs). Spontaneous circulation was achieved twice as fast after NaHCO3 compared with NaCl (14.6 vs. 28 mins, respectively). Hydrogen ion (H+) concentration and base excess, obtained 2 mins after the first buffer dose, were the best predictors of resuscitability. Arterial and mixed venous Pco2 did not increase after NaHCO3 or Carbicarb compared with NaCl.. Buffer therapy promotes successful resuscitation after prolonged cardiac arrest, regardless of coronary perfusion pressure. NaHCO3, and to a lesser degree, Carbicarb, are beneficial in promoting early return of spontaneous circulation. When epinephrine is used to promote tissue perfusion, there is no evidence for hypercarbic venous acidosis associated with the use of these CO2 generating buffers.

Topics: Animals; Blood Gas Analysis; Buffers; Carbonates; Cardiopulmonary Resuscitation; Disease Models, Animal; Dogs; Drug Combinations; Epinephrine; Heart Arrest; Hemodynamics; Infusions, Intravenous; Prospective Studies; Random Allocation; Sodium Bicarbonate; Treatment Outcome; Tromethamine; Ventricular Fibrillation

Topics: Cardiopulmonary Resuscitation; Child; Heart Arrest; Humans; Sodium Bicarbonate

Serious complications from tricyclic antidepressant (TCA) overdose are uncommon. We present a case of massive imipramine overdose complicated by ventricular fibrillation and a prolonged period of cardiovascular collapse. A total of 400 mmol of sodium bicarbonate, 5 mg of adrenaline and 80 mg of sotalol were given during 50 minutes of cardiac arrest. The patient made a full recovery with no apparent neurological sequelae. The highest TCA plasma level we could find in the published literature was 4873 ng/ml4; our patient's peak TCA level was 6000 ng/ml. Tricyclic antidepressant overdose is a common cause of intensive care unit admission. It has a low mortality rate.

Topics: Adrenergic Agonists; Adult; Anti-Arrhythmia Agents; Antidepressive Agents, Tricyclic; Critical Care; Depression; Drug Overdose; Electric Countershock; Epilepsy, Tonic-Clonic; Epinephrine; Female; Heart Arrest; Humans; Imipramine; Puerperal Disorders; Shock; Sodium Bicarbonate; Sotalol; Ventricular Fibrillation

Topics: Animals; Dogs; Drug Evaluation, Preclinical; Heart Arrest; Humans; Sodium Bicarbonate; Time Factors

Application of sodium bicarbonate is still an option when resuscitation efforts remain unsuccessful. Despite this, there are no recommendations on how long resuscitation should be performed after administration of this drug. Here we describe a case in which prehospital resuscitation efforts were terminated about 35 min after cardiac arrest. Seven minutes after all efforts had been discontinued, spontaneous sinus rhythm appeared from a zero-line ECG, giving normal hemodynamic values. The underlying reason might be unexpected and unrecognized hyperkalemia, which was diminished by administration of sodium bicarbonate, even under the conditions of cardiocirculatory arrest.

Topics: Cardiopulmonary Resuscitation; Electrocardiography; Heart Arrest; Hemodynamics; Humans; Hyperkalemia; Male; Middle Aged; Myocardial Contraction; Sodium Bicarbonate; Time Factors

Organ malfunction often occurs following cardiac arrest and resuscitation. Renal function, inulin clearance (Cln), was examined in 27 dogs before and after (days 2, 4, and 6) cardiac arrest and resuscitation. Group A (n = 7) had no ventricular fibrillation (VF), but cardiopulmonary support was applied for 20 min, and three transthoracic countershocks were delivered. In groups B (n = 7), C (n = 7), and D (n = 6) VF was induced for 2.5, 5.0, and 7.5 min, respectively, followed by cardiopulmonary support for 20, 20, and 15 min, respectively. When necessary, epinephrine and sodium bicarbonate were given during resuscitation. Countershock was applied for defibrillation. Kidneys were examined histologically in groups C and D. Following cardiac arrest, Cln was significantly less in the arrested groups compared to the nonarrested group. Within group C, which received the most epinephrine, Cln correlated negatively with epinephrine administration, and with the energy applied for defibrillation. Histologically, group C showed the highest incidence of cortical tubular cytoplasmic vacuolization, regeneration, inflammation, and tubular casts. Groups C and D showed outer medullary tubular cytoplasmic vacuolization, renal vascular changes, and calcification. In conclusion, cardiac arrest and resuscitation may precipitate acute renal hypofunction as well as reversible and irreversible morphological changes in normal functioning canine kidneys. The confounding effect of pre-existing renal disease remains to be examined experimentally.

Topics: Animals; Cardiopulmonary Resuscitation; Dogs; Electric Countershock; Epinephrine; Heart Arrest; Hypertrophy; Insulin; Kidney; Sodium Bicarbonate

Earlier studies demonstrated that hypertonic buffer agents administered during cardiopulmonary resuscitation (CPR) altered neither myocardial pH nor cardiac resuscitability. The rationale for the routine use of buffer agents for CPR has therefore been challenged. However, when these buffer agents are administered during CPR, they may have favorable effects on the postresuscitation course. Postresuscitation myocardial dysfunction has more recently emerged as a potentially fatal complication after successful cardiac resuscitation. Options for prevention and management of this complication have prompted the present studies, in which the effects of buffer agents administered during CPR are evaluated as to their effects on postresuscitation myocardial function and survival.. Prospective, randomized, controlled animal study.. University animal laboratory.. Forty male Sprague-Dawley rats (450 to 570 g).. Ventricular fibrillation was induced electrically. Mechanical Ventilation and percordial compression were initiated after either a 4- or an 8-min interval of untreated cardiac arrest. Sodium bicarbonate as a CO2-generating buffer, Carbicarb and tromethamine as CO2-consuming buffers, or hypertonic saline placebo were injected as a bolus into the right atrium during CPR. Defibrillation after 10 mins of cardiac arrest and CPR was successful in each instance. No differences in the electric power required for successful resuscitation were documented. Left ventricular pressure, rate of left ventricular pressure increase measured at a left ventricular pressure of 40 mm Hg (dP/dt40), rate of left ventricular pressure decline (-dP/dt), and end-tidal PCO2 were continuously measured for 240 mins after successful resuscitation.. Decreases in coronary perfusion pressure were observed after each buffer or placebo injection. As anticipated, end-tidal PCO2 increased after bicarbonate and decreased after Carbicarb or tromethamine. Postresuscitation left ventricular function was significantly decreased in all animals. However, there was significantly less depression in rate of left ventricular pressure increase measured at a left ventricular pressure of 40 mm Hg (dP/dt40), rate of left ventricular pressure decline (-dP/dt), and a lower left ventricular diastolic pressure with both Carbicarb and tromethamine in association with significant increases in postresuscitation survival rate. When the duration of untreated cardiac arrest was increased to 8 mins, the severity of postresuscitation left ventricular dysfunction was magnified and postresuscitation myocardial function and survival were significantly improved with both CO2-generating and CO2-consuming buffer agents.. Although buffer agents may not improve the success of resuscitation when administered during CPR, they may ameliorate postresuscitation myocardial dysfunction and thereby improve postresuscitation survival.

Topics: Animals; Buffers; Cardiopulmonary Resuscitation; Heart Arrest; Hydrogen-Ion Concentration; Male; Myocardial Contraction; Rats; Rats, Sprague-Dawley; Sodium Bicarbonate; Tromethamine

We investigated the factors associated with cerebral dysfunction in patients undergoing extracorporeal life support (ECLS) following conventional advanced cardiac life support (ACLS). The subjects were 9 patients in whom ECLS was started following ACLS because of intractable cardiac arrest. We investigated whether the irreversibility of cerebral dysfunction during ECLS was related to the cardiopulmonary resuscitation (CPR) time, arterial pH and blood gases, hemoglobin concentration (Hb), peak arterial pressure (PAP) before the start of ECLS and total doses of epinephrine and sodium bicarbonate administered during CPR. Two of the 3 patients who recovered consciousness were weaned from ECLS and survived, while all 6 patients who did not recover from coma were not weaned and died. There was no difference in the CPR time, Hb and PAP before the start of ECLS along with total doses of epinephrine and sodium bicarbonate administered during CPR between the patients who recovered consciousness and those who did not. In addition, there was no difference in arterial pH and blood gases except the arterial oxygen tension (PaO2) between the groups. The PaO2 values before the start of ECLS in the patients who remained in coma ranged from 34 to 58 mmHg, whereas those in the patients who recovered consciousness ranged from 132 to 442 mmHg. The PaO2 values before the start of ECLS in the patients who remained in coma were less than 60 mmHg, whereas those in the patients who recovered consciousness were over 60 mmHg. The present study suggests that hypoxemia during CPR may play a major role in severe cerebral dysfunction in patients undergoing ECLS and PaO2 during CPR.

Topics: Adult; Blood Gas Analysis; Blood Pressure; Brain Ischemia; Cardiopulmonary Resuscitation; Case-Control Studies; Coma; Epinephrine; Extracorporeal Membrane Oxygenation; Female; Heart Arrest; Hemoglobins; Humans; Hydrogen-Ion Concentration; Hypoxia; Male; Middle Aged; Risk Factors; Sodium Bicarbonate; Time Factors

Although high-dose epinephrine during CPR improves coronary perfusion pressure (CoPP) and rate of return of spontaneous circulation (ROSC) in some models, its impact on long term outcome (> or = 72 h) has not been evaluated. Previous studies of sodium bicarbonate (NaHCO3) therapy during CPR indicate that beneficial effects may be dependent on epinephrine (EPI) dose. We hypothesized that EPI and NaHCO3 given during CPR have a significant impact on long term outcome. One hundred male Sprague-Dawley rats were prospectively studied in a block randomized placebo controlled trial. Rats were anesthetized, paralyzed, mechanically ventilated, instrumented, and each underwent 10 min of asphyxia, resulting in 6.8 +/- 0.4 min of circulatory arrest. Resuscitation was performed by mechanical ventilation and manual external chest compressions. EPI 0.0 (placebo), 0.01, 0.1, or 1.0 mg/kg IV was given at the onset of CPR, followed by NaHCO3 0.0 (placebo) or 1.0 mEq/kg IV. Successfully resuscitated rats were monitored and ventilated for 1 h without hemodynamic support. Neurologic deficit scores (NDS), cerebral histopathologic damage scores (CHDS) and myocardial histopathologic damage scores (MHDS) were determined in rats that survived 72 h. EPI improved CoPP and ROSC in a dose-dependent manner up to 0.1 mg/kg. Rats receiving EPI 0.1 and 1.0 mg/kg during CPR exhibited prolonged post-ROSC hypertension and metabolic acidemia, increased A-a O2 gradient, and an increased incidence of post-ROSC ventricular tachycardia or fibrillation. Overall survival was lower with EPI 0.1 and 1.0 mg/kg compared to 0.01 mg/kg. Although NDS was significantly less with EPI 0.1 mg/kg compared to placebo, there was no difference in CHDS between groups. In contrast, MDS was significantly higher with EPI 0.1 mg/kg compared to placebo or EPI 0.01 mg/kg. There was an overall trend toward improved survival at 72 h in rats that received NaHCO3 which was most evident in the EPI 0.1 mg/kg group. We conclude that (1) EPI during CPR has a biphasic dose/response curve in terms of survival, when post-resuscitation effects are left untreated and (2) NaHCO3 doses greater than 1.0 mEq/kg may be necessary to treat the side-effects of high-dose EPI. Further work is needed to determine if treating the immediate post-resuscitation effects of high-dose EPI can prevent detrimental effects on long-term outcome.

Topics: Animals; Asphyxia; Cardiopulmonary Resuscitation; Central Nervous System Diseases; Dose-Response Relationship, Drug; Epinephrine; Heart Arrest; Male; Rats; Rats, Sprague-Dawley; Sodium Bicarbonate; Survival Rate; Time Factors; Treatment Outcome

Cardiopulmonary resuscitation (CPR) generating low perfusion pressures and beginning immediately after cardiac arrest maintains cerebral ATP but not cerebral pH or arterial pH. We tested the hypothesis that preventing severe arterial acidemia prevents cerebral acidosis, whereas augmenting arterial acidemia augments cerebral acidosis.. In dogs anesthetized with pentobarbital and fentanyl, cerebral pH and ATP were measured with 31P MR spectroscopy and blood flow was measured with radiolabeled microspheres. A pneumatically controlled vest was placed around the thorax, and chest compressions were begun immediately after electrically induced cardiac arrest. Cerebral perfusion pressure was maintained with epinephrine at 30 mm Hg for 90 minutes. The arterial acidemia observed during CPR was untreated in a control group, corrected to a pH of 7.3 with the use of sodium bicarbonate, or maintained below pH 6.5 with intravenous lactic acid after 14 minutes of CPR.. At 10 minutes of CPR, cerebral ATP (99 +/- 1.5%, control), blood flow (35 +/- 3 mL/min per 100 g), O2 consumption (4.0 +/- 0.2 mL/min per 100 g), and cerebral pH (7.05 +/- .03) were unchanged from prearrest values (mean +/- SEM). After 10 minutes of CPR in the control group, cerebral pH progressively fell (6.43 +/- 0.10 at 90 minutes) in parallel with cerebral venous pH. In the bicarbonate group cerebral pH was maintained higher (6.91 +/- 0.08). Cerebral blood flow, O2 consumption, and ATP were sustained near prearrest values in both groups. In the lactate group, however, the rate of decrease of cerebral pH was augmented (6.47 +/- 0.06 by 30 minutes), and cerebral blood flow and metabolism were significantly reduced.. Cerebral pH decreased in parallel with blood pH when resuscitation was started immediately upon arrest even when cerebral O2 consumption and blood flow were near normal. Although cerebral metabolism was near normal during the first hour of CPR, systemic bicarbonate administration ameliorated the cerebral acidosis. This finding indicates that the blood-brain pH gradient is important at the subnormal cerebral perfusion pressures seen in CPR.

Topics: Acidosis; Adenosine Triphosphate; Analysis of Variance; Animals; Brain; Brain Stem; Cardiopulmonary Resuscitation; Cerebrovascular Circulation; Coronary Circulation; Dogs; Heart Arrest; Hydrogen-Ion Concentration; Infusions, Intravenous; Lactates; Lactic Acid; Magnetic Resonance Spectroscopy; Male; Oxygen Consumption; Regional Blood Flow; Sodium Bicarbonate; Spinal Cord; Time Factors

Despite the absence of outcome evaluation, the use of sodium bicarbonate in cardiac arrest has declined based on advanced cardiac life-support guidelines. The effects of bicarbonate therapy on outcome in a canine model of ventricular fibrillation cardiac arrest of brief (5-min) and prolonged (15-min) duration were examined.. Prospective, randomized, controlled trial.. Experimental animal laboratory in a university medical center.. Thirty-two adult dogs, weighing 10 to 17 kg.. The animals were prepared with ketamine, nitrous oxide/oxygen, halothane, and pancuronium. Ventricular fibrillation was then electrically induced and maintained in arrest for 5 mins (n = 12) or 15 mins (n = 20). Canine advanced cardiac life-support protocols were instituted, including defibrillation, cardiopulmonary resuscitation (CPR), and the administration of epinephrine (0.1 mg/kg), atropine, and lidocaine. The bicarbonate group received 1 mmol/kg of sodium bicarbonate initially, and base deficit was corrected to -5 mmol/L with additional bicarbonate, whereas acidemia was untreated in the control group. Cardiopulmonary values were recorded at intervals between 5 mins and 24 hrs, and the neurologic deficit score was determined at 24 hrs after CPR.. The treatment group received an additional 2 to 3 mmol/kg of bicarbonate in the early postresuscitation phase. Compared with controls, the bicarbonate group demonstrated equivalent (with brief arrest) or improved (with prolonged arrest) return of spontaneous circulation and survival to 24 hrs, with lessened neurologic deficit. The acidosis of arrest was decreased in the prolonged arrest group without hypercarbia. Improved coronary and systemic perfusion pressures were noted in the bicarbonate group with prolonged arrest, and the epinephrine requirement for return of spontaneous circulation was decreased.. The empirical administration of bicarbonate improves the survival rate and neurologic outcome in a canine model of cardiac arrest.

Topics: Acidosis; Animals; Atropine; Blood Circulation; Dogs; Epinephrine; Heart Arrest; Hemodynamics; Hydrogen-Ion Concentration; Hypercapnia; Lidocaine; Prospective Studies; Resuscitation; Sodium Bicarbonate; Time Factors; Ventricular Fibrillation

To generate hypotheses regarding the association of standard Advanced Cardiac Life Support (ACLS) drugs with human cardiac arrest survival.. This observational cohort study was conducted over a two-year period in the wards, intensive care units, and EDs of two tertiary care hospitals. Included werc adult patients who suffered cardiac arrest either inside or outside the hospital and who required epinephrine according to standard ACLS guidelines. Six standard ACLS drugs (given while CPR was in progress) were assessed for association with survival from resuscitation to one hour and to hospital discharge by univariate and multivariate logistic regression analyses.. In the 529 patients studied, initial cardiac rhythm had no impact on the association between drug administration and survival. The time of drug administration (quartile of ACLS period) was associated with resuscitation for atropine (p < 0.05) and lidocaine (p < 0.01). The odds ratios (95% CIs) for successful resuscitation, after multivariate adjustment for potential confounders, were: a respiratory initiating cause, 3.7 (2.1 -6.4); each 5-minute increase in CPR-ACLS interval, 0.5 (0.4-0.7); each 5-minute duration of ACLS. 0.9 (()1.8- 1.0; atropine, 1.2 (1.0-1.3); bretylium. (0.4 (0.1-1.1); calcium 0.8 (0.2-2.4); lidocaine, 0.9 (0.7-1.1); procainamide. 21.0 (5.2-84.0) d sodium bicarbonate 1.2 (1.0-1.6). All other potential confounding variables entered into the model were not significantly associated with resuscitation.. Initiating cause of arrest, time to ACLS, and duration of ACLS were important correlates of survival. Other than procainaimide, standard ACLS drugs had relatively little association with survival, but timing of administration may be an important factor. Further research using definitive large randomized controlled trials is warranted to assess the role of drug therapy in improving cardiac arrest survival.

Topics: Adult; Aged; Aged, 80 and over; Anti-Arrhythmia Agents; Atropine; Bretylium Compounds; Calcium; Cardiopulmonary Resuscitation; Cohort Studies; Dose-Response Relationship, Drug; Epinephrine; Female; Heart Arrest; Humans; Lidocaine; Life Support Care; Logistic Models; Male; Middle Aged; Procainamide; Sodium Bicarbonate; Survival Analysis; Sympathomimetics; Treatment Outcome

Topics: Electric Countershock; Emergencies; Epinephrine; Heart Arrest; Heart Massage; Humans; Resuscitation; Sodium Bicarbonate

Topics: Anti-Arrhythmia Agents; Atropine; Bicarbonates; Calcium; Epinephrine; Heart Arrest; Humans; Sodium; Sodium Bicarbonate

Systemic acidosis occurs during cardiac arrest and cardiopulmonary resuscitation (CPR). The present study investigated the effect of different modes of sodium bicarbonate administration on blood gas parameters during CPR. Arterial and venous blood gases were obtained during 10 minutes of CPR which was preceded by 3 minutes of unassisted ventricular fibrillation in 36 dogs. Following 1 minute of CPR, the animals received one of four treatments in a randomized and blinded manner: normal saline (NS), sodium bicarbonate bolus dose 1 mEq/kg (B), sodium bicarbonate continuous infusion 0.1 mEq/kg/min (I), and sodium bicarbonate bolus dose (0.5 mEq/kg) plus continuous infusion 0.1 mEq/kg/min (L+I). Eleven dogs completed NS, 8 B, 8 I, and 9 L+I protocol. Following NS infusion, both arterial and venous pH declined consistently over time. Significant differences compared with NS treatment in venous pH were observed at 12 minutes of ventricular fibrillation (L+I, 7.27 +/- 0.05; NS, 7.15 +/- 0.05; B, 7.20 +/- 0.05; I, 7.24 +/- 0.04, each bicarbonate treatment versus NS, and L+I versus B, (P < .05). The B group had an elevated venous PCO2 (mm Hg) concentration following 6 minutes of ventricular fibrillation compared with NS, L+I, and I groups (81 +/- 14 versus 69 +/- 10 versus 68 +/- 10 versus 71 +/- 8, respectively, (P = .07). Arterial pH and PCO2 values showed a similar trend as the venous data with the L+I group demonstrating arterial alkalosis (pH > 7.45) at 12 minutes of ventricular fibrillation.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Acidosis; Animals; Bicarbonates; Blood; Carbon Dioxide; Cardiopulmonary Resuscitation; Disease Models, Animal; Dogs; Heart Arrest; Hydrogen-Ion Concentration; Infusions, Intravenous; Injections, Intravenous; Random Allocation; Sodium; Sodium Bicarbonate; Sodium Chloride

Twenty-seven patients in cardiopulmonary arrest had simultaneous measurements of arterial and central venous blood gases during cardiopulmonary resuscitation (CPR) with a pneumatic chest comparison and ventilation device. Mean central venous and arterial hydrogen ion concentrations, PCO2 and calculated bicarbonate concentrations were significantly different (P less than 0.01) at all sampling times (0, 10 and 20 min). Central venous blood samples predominantly showed a respiratory acidosis in contrast to a mixed disturbance in arterial samples inclined towards a metabolic acidosis. The mean difference between central venous PCO2 (pcv CO2) and arterial PCO2 (pa CO2) ranged from 5.18 to 5.83 kPa reflecting the low blood flow in patients undergoing CPR. Measurement of arterial Po2 indicated adequate oxygenation using the pneumatic device. Arterial blood gas analysis alone does not reflect tissue acid base status. Bicarbonate administration during CPR may have adverse effects and any decision as to its use should be based on central venous blood gas estimations.

Topics: Acid-Base Imbalance; Acidosis, Respiratory; Adult; Aged; Aged, 80 and over; Arteries; Bicarbonates; Blood Gas Analysis; Carbon Dioxide; Cardiopulmonary Resuscitation; Female; Heart Arrest; Humans; Hydrogen-Ion Concentration; Male; Middle Aged; Prospective Studies; Sodium; Sodium Bicarbonate; Veins

The objective of this study was to assess the changes in outcome of cardiac arrest due to ventricular fibrillation, asystole and electromechanical dissociation in relation to the changing guidelines for drug therapy set by the U.K. Resuscitation Council. It was a retrospective study of 667 resuscitation records for the years 1982, 1986, 1988, 1989, 1990 and 1991. It took place in a large district general hospital with a regional cardio-thoracic centre. We have audited the asystolic cardiac arrests (N = 271) which occurred outside the cardiac care unit (CCU). Adrenaline (intravenous 1 mg) is now the first line drug followed by atropine at an increased dose (2 mg intravenously); calcium is no longer recommended and sodium bicarbonate should be reserved for cases in which an acidosis has been documented. Atropine use has increased over the 9-year period. Bicarbonate use did not change from 1982 to 1986 but fell progressively to no use at all in 1991. Calcium use has declined since 1982. Adrenaline use has remained unchanged. Survival from asystolic arrests (hospital discharge) has remained unchanged at 0-5.5%. Asystole as a primary event in the CCU was uncommon (N = 17) and no patient was discharged. Over the same period, 60% of patients (N = 92) with a cardiac arrest on CCU due to ventricular fibrillation (VF) were discharged and 55% were alive after 6 months. For VF on the wards (N = 192), only 20% of patients were discharged from hospital. A similar proportion was successful for each year.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Atropine; Bicarbonates; Calcium; Cardiology Service, Hospital; Cardiopulmonary Resuscitation; Drug Utilization; Epinephrine; Heart Arrest; Heart Block; Hospitalization; Humans; Outcome and Process Assessment, Health Care; Retrospective Studies; Sodium; Sodium Bicarbonate; Treatment Outcome; United Kingdom; Ventricular Fibrillation

Topics: Acidosis; Animals; Bicarbonates; Cardiopulmonary Resuscitation; Heart Arrest; Humans; Hypertonic Solutions; Sodium; Sodium Bicarbonate; Swine

This study attempted to determine the effect of bicarbonate administration on resuscitation in a porcine model of prolonged cardiac arrest.. After instrumentation, 26 swine were subjected to ventricular fibrillation for 15 minutes (16 animals) or 20 minutes (ten animals) with no resuscitative efforts.. Resuscitation attempts with open-chest cardiac massage and epinephrine were used in all animals after the arrest period. The experimental group was given sodium bicarbonate (3 mEq/kg), and the control group received 3% saline (5 mL/kg) at the initiation of cardiac massage.. Resuscitation success, hemodynamics, and arterial and mixed venous gases were compared in the bicarbonate and hypertonic saline-treated groups.. There was no difference in resuscitation rates between bicarbonate and nonbicarbonate-treated swine. After 15 minutes of ventricular fibrillation, six of eight bicarbonate-treated swine were resuscitated successfully compared with five of eight hypertonic saline-treated animals. None of the five bicarbonate-treated or five hypertonic saline-treated swine that underwent 20 minutes of ventricular fibrillation were resuscitated. The arterial and mixed venous pH values were significantly different in the bicarbonate-treated animals from values in the control group. There was no difference in systolic or diastolic blood pressures or myocardial perfusion pressure between the bicarbonate and hypertonic saline-treated animals.. Despite correlation of arterial and venous acidemia, the use of sodium bicarbonate did not improve resuscitation from prolonged cardiac arrest.

Topics: Animals; Arteries; Bicarbonates; Blood Pressure; Carbon Dioxide; Heart; Heart Arrest; Hydrogen-Ion Concentration; Resuscitation; Saline Solution, Hypertonic; Sodium; Sodium Bicarbonate; Swine; Time Factors; Veins

Topics: Bicarbonates; Cytoplasm; Heart Arrest; Humans; Hydrogen-Ion Concentration; Sodium; Sodium Bicarbonate

Recent studies have demonstrated an increase in carbon dioxide (CO2) tension (PCO2) in both mixed venous and coronary vein blood early in the course of cardiac arrest and cardiopulmonary resuscitation. Because increased PCO2 in the myocardium correlates with both ischemic injury and depression of contractile function, the effects of hypertonic solutions of either the CO2-"generating" sodium bicarbonate (NaHCO3) buffer, a mixture of sodium carbonate (Na2CO3) and sodium bicarbonate (carbicarb) acting as a CO2-"consuming" buffer, or saline placebo (NaCl) were compared during cardiopulmonary resuscitation in 25 healthy minipigs. Both buffer agents significantly increased the pH and HCO3- of arterial, mixed venous and coronary vein blood. Bicarbonate increased whereas carbicarb reduced blood PCO2 in the systemic circuit as anticipated. However, neither the PCO2 nor the lactate content of coronary vein blood was favorably altered by buffer therapy. Four of eight animals treated with bicarbonate, five of eight treated with carbicarb and six of nine placebo-treated animals were successfully resuscitated and had a comparable 24 h survival rate. Coronary perfusion pressure during precordial compression, a critical determinant of resuscitability, was transiently decreased by each of the hypertonic solutions. Accordingly, neither CO2-generating nor CO2-consuming buffers mitigated increases in coronary vein PCO2 or improved the outcome of cardiopulmonary resuscitation under these experimental conditions.

Topics: Acid-Base Equilibrium; Animals; Bicarbonates; Buffers; Carbon Dioxide; Carbonates; Drug Combinations; Heart; Heart Arrest; Hemodynamics; Osmolar Concentration; Resuscitation; Saline Solution, Hypertonic; Sodium Bicarbonate; Swine; Swine, Miniature

In a cardiological department (Coronary Care Unit) routine treatment of asystole and electromechanical dissociation has comprised intracardiac injection (ICI) of drugs, usually given by trained nurses, using the parasternal approach into the right ventricle, followed by continued external cardiac massage. A 7-year experience is presented with 543 consecutive ICIs to 247 patients. Cardiac action was restored in half of the patients (125/247); 7.7% (19/247) were discharged alive. Autopsy was done in 80% of fatal cases (182/228). A left-sided pneumothorax was demonstrated in 9 of the 80 patients surviving ICI for greater than 1 h, a minor haemopericardium in three, but serious consequences in none. Lesions of the coronary artery or of the myocardium attributable to the ICI were never seen. Asystole in some patients was converted into ventricular fibrillation or ventricular tachycardia which in six patients proved intractable, but other serious cardiac arrhythmias having a possible connection with the ICI were not observed. It is concluded that during a cardiac standstill, drug treatment by ICI with good technique carries a low risk, quite acceptable in these circumstances, and from a theoretical point of view can be expected to have advantages over administration of the drug into a peripheral vein.

Topics: Bicarbonates; Electrocardiography; Epinephrine; Feasibility Studies; Heart Arrest; Heart Ventricles; Humans; Injections; Isoproterenol; Lidocaine; Sodium; Sodium Bicarbonate

Cardiac arrest in infants and children is usually not unexpected. All efforts, therefore, should be made to recognize a high risk situation soon enough and to apply the emergency therapeutic measures that are mandatory. When the drama occurs, cardiopulmonary resuscitation (CPR) must be instituted at once according to a well-defined sequence: first, elementary CPR performed by any occasional rescuer, including 1. clearing of the airways, 2. mouth-to-mouth breathing, and 3. closed cardiac massage (CCM); then, medical CPR applied by a professional rescuer pursuing the same objectives and consisting of 1. tracheal intubation, 2. manual or mechanical ventilation with pure oxygen, 3. controlled efficacy CCM, and 4. intratracheal, then intravenous or intraosseous injection of adrenaline. As this sequence cannot be improvised, no effort should be spared to teach and organize CPR outside and within hospitals.

Topics: Bicarbonates; Child; Child, Preschool; Epinephrine; Heart Arrest; Heart Massage; Humans; Infant; Respiration, Artificial; Resuscitation; Sodium; Sodium Bicarbonate

We investigated the effects of carbon dioxide-producing and carbon dioxide-consuming buffers on intramyocardial pH and on cardiac resuscitability. In 29 pigs, intramyocardial pH was continuously measured with a glass electrode advanced into the midmyocardium of the posterior left ventricle through a diaphragmatic window. Ventricular fibrillation (VF) was electrically induced by alternating current applied to the epicardium of the left ventricle. After 3 minutes of VF, precordial compression was begun and continued for an interval of 8 minutes. Sodium bicarbonate (a carbon dioxide-generating buffer), Carbicarb (a carbon dioxide-consuming buffer), and hypertonic sodium chloride (control solution) were infused into the right atrium during cardiac resuscitation. Defibrillation was attempted by transthoracic direct-current shock after 11 minutes of VF. Intramyocardial pH progressively decreased from an average value of 7.26 before VF to 6.87 before infusion of buffers. Systemic circulation and great cardiac vein pH significantly increased after administration of the two buffer agents. However, intramyocardial pH continued to decline to an average of 6.62 after 11 minutes of VF, and this decline was not altered by either buffer solution or by the saline control. As in previous studies, resuscitability was closely related to coronary perfusion pressure at the time of direct-current countershock but not to pH. Accordingly, the rationale of reversing acidosis by the administration of these buffer agents is not supported. Even more important, neither carbon dioxide-consuming nor carbon dioxide-producing buffers altered myocardial acidosis or improved myocardial resuscitability under controlled experimental conditions of cardiac arrest.

Topics: Acidosis; Animals; Bicarbonates; Blood; Buffers; Carbon Dioxide; Carbonates; Disease Models, Animal; Drug Combinations; Heart Arrest; Hydrogen-Ion Concentration; Lactates; Lactic Acid; Myocardium; Resuscitation; Saline Solution, Hypertonic; Sodium; Sodium Bicarbonate; Swine

A model of hypothermic circulatory arrest has been developed in the newborn dog. Ten puppies were anesthetized with halothane, paralyzed, and artificially ventilated with 70% nitrous oxide 30% oxygen to arterial oxygen pressure greater than 8.0 kPa (60 mm Hg), arterial carbon dioxide pressure of 4.4-5.6 kPa (33-42 mm Hg), and arterial pH of 7.35-7.42. Animals were surface cooled to 20 degrees C, after which cardiac arrest was produced with i.v. KCl. Dogs remained asystolic without ventilation for 1.0 (n = 4), 1.5 (n = 3), or 2.0 (n = 3) h. Resuscitation was accomplished with closed-chest compression, mechanical ventilation, i.v. epinephrine and NaHCO3, and rewarming to 37 degrees C. Postarrest recovery was maintained for 3-4 h; thereafter, the puppies underwent perfusion-fixation of their brains for pathologic analysis. Plasma glucose (control = 8.3 mmol/L) increased slightly during hypothermic cardiac arrest (+36%) but was markedly elevated at 15 min postarrest (20 mmol/L). Blood lactate (control = 1.1 mmol/L) increased almost 200% during hypothermic circulatory arrest, with a further rise to 9.0 mmol/L at 15 min postarrest. Thereafter, lactate decreased in the 1-h arrested dogs but increased progressively in the other groups. Mean arterial blood pressure returned to baseline (73 mm Hg) by 15 min postarrest, remained stable in the 1-h dogs, but fell at 3 h to 62 and 34 mm Hg in the 1.5- and 2.0-h groups, respectively. No neuropathologic alterations were seen in puppies arrested for 1 h, whereas all puppies arrested for 1.5 or 2 h had varying degrees of cerebral cortical and hippocampal damage.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Animals; Animals, Newborn; Bicarbonates; Blood Glucose; Cerebral Cortex; Dogs; Dopamine; Glucose; Heart Arrest; Hemodynamics; Hydrogen-Ion Concentration; Hypothermia; Resuscitation; Sodium; Sodium Bicarbonate

We compared the administration of sodium bicarbonate via a catheter inserted in the external jugular and extending to the junction with the subclavian vein (group 1) and a peripheral hindpaw vein (group 2) in puppies. During spontaneous cardiac activity, the increases in pH (0.12 +/- 0.04 in group 1 vs. 0.08 +/- 0.04 in group 2) and PCO2 (11 +/- 2.8 torr in group 1 vs. 6 +/- 3.2 torr in group 2) in blood from the right atrium 10 sec after the injection of bicarbonate differed significantly. However, the increases in pH (0.31 +/- 0.07 in group 1 vs. 0.30 +/- 0.15 in group 2) and PCO2 (86 +/- 33 torr in group 1 vs. 72 +/- 35 torr in group 2) in blood from the right atrium during closed chest CPR were similar in the two groups. We found that the sodium bicarbonate reached the central circulation more rapidly when administered in the external jugular vein as compared to a peripheral site, but this difference was small and did not reach the level of significance during CPR. Our findings do not provide evidence of any advantage to obtaining central venous access (a potentially complicated procedure) in children with cardiac arrest in regard to the delivery of medications to the heart.

Topics: Animals; Bicarbonates; Blood Gas Analysis; Blood Pressure; Body Temperature; Catheterization, Central Venous; Catheterization, Peripheral; Dogs; Foot; Heart Arrest; Jugular Veins; Monitoring, Physiologic; Resuscitation; Sodium; Sodium Bicarbonate; Veins

There is controversy regarding the use of alkalinizing agents during reperfusion after cardiac arrest. The potential deleterious effects of sodium bicarbonate (bicarb) administration, including paradoxic cerebral acidosis, have led to the search for alternative agents. Tromethamine (tris) is a non-CO2-generating buffer that has been proposed for use during cardiopulmonary resuscitation. The purpose of this experiment was to compare the ability of tris with bicarb to correct brain pH (pH B) during reperfusion after a 12-minute cardiac arrest. Adult mongrel dogs were instrumented and placed in the bore of a Bruker Biospec 1.89 tesla superconducting magnet system. Ventricular fibrillation was induced; after 12 minutes, cardiopulmonary bypass was initiated and maintained for two hours with minimum flows of 80 mL/kg/min. Bicarb (n = 5) or tris (n = 5) were administered to correct arterial pH as rapidly as possible. 31P NMR spectra were obtained at baseline and throughout ischemia and reperfusion. The pH B was determined with the inorganic phosphate relative to the phosphocreatine resonance signal shift. Profile analysis indicates a difference between groups (P less than .02) related to an initial delay in pH B correction in the tris group. By 48 minutes of reperfusion, pH B did not differ between the groups. Moreover, there was no evidence of paradoxic cerebral acidosis in the bicarb group. Although tris corrects blood pH as quickly as bicarb, it is less effective in correcting pH B. Absence of paradoxic acidosis may be caused by efficient elimination of CO2 by cardiopulmonary bypass.

Topics: Acidosis; Animals; Bicarbonates; Brain; Carbon Dioxide; Cardiopulmonary Bypass; Dogs; Heart Arrest; Hydrogen-Ion Concentration; Magnetic Resonance Spectroscopy; Phosphorus Isotopes; Sodium; Sodium Bicarbonate; Tromethamine

The hospital of Brugge relies on selection of the emergency calls and sends a Mobile Intensive Care Unit (MICU) whenever cardiac arrest (CA) is suspected. The University Hospital of Leuven does no selection of calls and responds to every emergency call by sending an ambulance with an advanced life support (ALS) trained nurse. The MICU is called when the ambulance crew recognizes the emergency to be a CA. The Leuven system is a so-called tiered system. Although MICU-response times are significantly longer in Leuven than in Brugge, no difference is found as to the success of CPCR. The immediate response to all emergency calls by specialized E.D. nurses (paramedic) capable of ALS, seems to make up for the difference in MICU-response times. The University Hospital of Jette has a higher success-rate for CPCR for in-hospital CA, than the University Hospitals of Leuven. Due to size and lay-out differences, the MICU-response times are shorter in Jette than in Leuven. Basic life support (BLS) provided by doctors and nurses present at the scene, does not seem to be able to compensate for longer MICU-arrival times. The introduction of semi-automatic or automatic defibrillators, to be used by the BLS trained medical and nursing personnel, might be able to make up for the longer MICU-intervention times. Inter-center differences were witnessed as far as the amount of sodium-bicarbonate infused during CPR. Within each group of total duration of CPR an inverse correlation exists between the amount of bicarbonate infused and the success rate of CPCR. Partial correlation between the bicarbonate infused and the survival with regaining of consciousness at 14 days post-CPR, with constant CPR-time, is statistically significant. This indicates that long-term CPCR success is inversely correlated with increasing amounts of sodium-bicarbonate infused. Short duration of CPR and low adrenaline dosage correlate with immediate and long-term success of CPR. On the contrary, low versus high bicarbonate dosage has hardly any influence on immediate success (restoration of spontaneous circulatory activity) but low bicarbonate dosage favours long-term success (survival accompanied by recuperation of brain function). Our data support a negative effect on long-term survival with recuperation of consciousness from infusion of more than 1 mEq/kg body weight of sodium-bicarbonate during CPR. No final conclusions can be drawn so far as to the mechanisms of this negative effect at the level of the

Topics: Ambulances; Bicarbonates; Emergency Medical Services; Heart Arrest; Humans; Intensive Care Units; Physicians; Resuscitation; Sodium; Sodium Bicarbonate; Time Factors

This study examined plasma epinephrine (E) and norepinephrine (NE) concentrations, pH, and mean arterial blood pressure (MAP) in a cardiac arrest model. Twenty-three domestic swine (15-26 kg) were anesthetized with ketamine 20 mg/kg, i.m. and alpha-chloralose 25 mg/kg, i.v. and ventilated with a respirator. Catheters were placed in the right ventricle, left ventricle and femoral arteries for MAP recordings and blood pH sampling every 2 min. Catecholamine samples were taken from the femoral artery every 2 min. Cardiac arrest was induced by endocardial stimulation with a Grass S88 stimulator. Five minute post arrest resuscitation was initiated with a mechanical resuscitator. Ten minute post arrest NaHCO3 1 mEq/kg was administered by the peripheral i.v. (P; n = 6), central (CE; n = 5), or intraosseous, via the tibia, (I; n = 6), route. Controls (C; n = 6) did not receive NaHCO3. MAP (mean +/- S.D.) prior to arrest was: C 144 +/- 16, P 139 +/- 11, CE 137 +/- 13 and I 133 +/- 11 mmHg. Five and 25 min post arrest it was: C 21 +/- 5 and 17 +/- 6, P 34 +/- 8 and 23 +/- 7, CE 17 +/- 7 and 14 +/- 10 and I 26 +/- 6 and 11 +/- 3 mmHg, respectively. A 2-way analysis of variance did not reveal any difference in MAP values in the four groups. In all groups the blood pH from the femoral artery demonstrated a respiratory alkalosis that peaked at approximately 7.48 5 min after initiation of mechanical resuscitation. In the groups receiving NaHCO3, it peaked at 7.77 +/- 0.09 CE and 7.65 +/- 0.06 P 2 min post infusion and at 7.71 +/- 0.06 I 8 min post infusion. An analysis of variance revealed that the CE and I routes were significantly different (P less than 0.05) from the P group and that all three groups were different (P less than 0.05) from the C. Plasma E and NE concentrations at 0, 6, 10, 12, 20 and 30 min post arrest in the C group were, respectively: 3 and 10, 94 and 327, 119 and 329, 92 and 234, 33 and 135, and 127 and 62 ng/ml, respectively. All 3 groups receiving NaHCO3 demonstrated similar patterns and were not significantly different from C when compared with a 2-way analysis of variance.(ABSTRACT TRUNCATED AT 400 WORDS)

Topics: Animals; Bicarbonates; Blood Pressure; Epinephrine; Female; Heart Arrest; Hydrogen-Ion Concentration; Male; Norepinephrine; Resuscitation; Sodium; Sodium Bicarbonate; Swine

A case of severe metabolic alkalosis (MA) resulting from ingestion of baking soda (sodium bicarbonate) is presented. On admission to the emergency department, the patient was alert and stable with an initial examination that was remarkable only for carpopedal spasm. Shortly thereafter, the patient had a sudden, unexpected cardiopulmonary arrest. Following resuscitation, without administration of sodium bicarbonate, the arterial blood gas revealed a pH of 7.73, pO2 of 51 mm Hg, and pCO2 of 52 mm Hg. After admission to the intensive care unit, the patient's MA was corrected using IV 0.25 N hydrochloric acid. The patient remained comatose as a result of severe anoxic encephalopathy and died two weeks after admission. We believe this is the first reported case of severe MA resulting in sudden cardiopulmonary arrest in a previously ambulatory patient.

Topics: Acute Disease; Alkalosis; Bicarbonates; Emergencies; Heart Arrest; Humans; Male; Middle Aged; Sodium; Sodium Bicarbonate

Topics: Aged; Bicarbonates; Heart Arrest; Humans; Male; Resuscitation; Sodium; Sodium Bicarbonate

Topics: Acetates; Bicarbonates; Electric Countershock; First Aid; Heart Arrest; Hemodynamics; Humans; Hypoxia, Brain; Resuscitation; Sodium; Sodium Bicarbonate; Tromethamine

Central to the controversy that surrounds the treatment of accidental severe hypothermia is the question of how the method of rewarming affects myocardial performance, and therefore survival. We induced severe hypothermia and cardiac arrest in 15 mongrel dogs. Each dog was rewarmed by one of three methods: partial cardiac bypass (Group I); peritoneal dialysis (Group II); or external rewarming with a fluid-circulated blanket (Group III). The cardiac arrest state was supported by partial cardiac bypass in Group I and by standard mechanical cardiopulmonary resuscitation (CPR) in Groups II and III. In all dogs, the hypothermically depressed myocardial performance returned to normal upon rewarming. Groups I and II had similar rewarming times and required similar volumes of crystalloid and bicarbonate solutions to maintain adequate cardiac filling pressures and arterial pH. However, Group III had a significantly slower rewarming time and required significantly greater volumes of crystalloid and bicarbonate solutions. The sole procedural death occurred in Group III. Our results show that partial cardiac bypass, peritoneal dialysis, and the fluid-circulated blanket are equally effective in rewarming severely hypothemic dogs with cardiac arrest, provided that the cardiac arrest is relieved by partial cardiac bypass or standard mechanical CPR and that physiologic levels of intravascular volume, oxygenation, and pH are maintained.

Topics: Accidents; Animals; Bicarbonates; Body Temperature; Cardiac Output; Crystalloid Solutions; Disease Models, Animal; Dogs; Electrocardiography; Heart Arrest; Heart Rate; Hypothermia; Infusions, Parenteral; Isotonic Solutions; Peritoneal Dialysis; Plasma Substitutes; Resuscitation; Sodium; Sodium Bicarbonate

The case of a 3-month-old male infant who was found unresponsive and cyanotic in a crib at home is presented. On arrival in the emergency department the child was receiving basic cardiopulmonary resuscitation (CPR) by a rescue squad and was without vital signs in asystole. The patient achieved a stable rhythm and blood pressure before intravenous access was obtained. Epinephrine and atropine were given via the endotracheal route and sodium bicarbonate through intraosseous infusion.

Topics: Atropine; Bicarbonates; Emergency Medical Services; Epinephrine; Heart Arrest; Humans; Infant; Infusions, Parenteral; Intubation, Intratracheal; Male; Resuscitation; Sodium; Sodium Bicarbonate; Sudden Infant Death; Tibia; Time Factors

Topics: Atropine; Bicarbonates; Calcium Chloride; Child; Child, Preschool; Dopamine; Electric Countershock; Epinephrine; Equipment and Supplies, Hospital; Heart Arrest; Humans; Infant; Intubation, Intratracheal; Isoproterenol; Life Support Care; Patient Care Planning; Patient Care Team; Pediatric Nursing; Professional-Family Relations; Resuscitation; Sodium; Sodium Bicarbonate

Topics: Arrhythmias, Cardiac; Atropine; Bicarbonates; Calcium Chloride; Epinephrine; Heart Arrest; Humans; Sodium; Sodium Bicarbonate

Topics: Acidosis; Acidosis, Lactic; Animals; Bicarbonates; Calcium; Dogs; Heart Arrest; Humans; Hydrogen-Ion Concentration; Sodium; Sodium Bicarbonate

Lactic acidosis is seen frequently after severe anoxia and circulatory failure. Because dichloroacetate (DCA) has been shown to be effective in the treatment of lactic acidosis, we studied its effect on lactate levels and pH in arterial and sagittal sinus blood specimens in a pediatric canine model of anoxic cardiac arrest followed by CPR. Lactate levels rose steadily in all puppies receiving DCA alone (group 1), DCA plus bicarbonate (group 2), bicarbonate alone (group 3), or neither drug (group 4). Arterial and sagittal-sinus lactate levels were in the range of 2 mmol/L during the baseline period, 6 mmol/L after anoxic arrest, and 10 mmol/L after 20 min of CPR. Bicarbonate, but not DCA, significantly raised arterial pH. Neither drug reversed the progression of acidosis in the sagittal sinus; mean pH ranged from 6.85 to 6.92 among the four groups after 20 min of CPR. We speculate that DCA did not decrease lactate levels or raise the pH in either the peripheral circulation or the CNS (sagittal sinus) because of poor perfusion achieved during closed-chest cardiac compression.

Topics: Acetates; Acidosis, Lactic; Animals; Bicarbonates; Carbon Dioxide; Dichloroacetic Acid; Dogs; Heart Arrest; Hydrogen-Ion Concentration; Lactates; Lactic Acid; Models, Biological; Oxygen; Resuscitation; Sodium; Sodium Bicarbonate

CO2 kinetics during CPR was investigated in 15 anesthetized piglets. BP, blood gases, and acid-base balance were monitored through catheters in the carotid artery and a central vein, as well as in cerebrospinal fluid. Cardiac arrest was induced by a transthoracic direct current shock. CPR was begun immediately by artificial ventilation and simultaneous external chest compressions. Epinephrine was administered after 8 min of CPR. One group (n = 5) of animals received no buffer treatment while another (n = 5) received an infusion of 75 mmol sodium bicarbonate and a third group (n = 5) received an equivalent amount of tris-buffer mixture. The results of these experiments, as well as previously described circulatory variables during CPR, were analyzed using a computer model describing the CO2 kinetics of the pig. Our main finding was that PaCO2 was positively correlated to cardiac output during CPR; improved cardiac output during CPR resulted in more efficient tissue CO2 elimination and was associated with increased survival rates. PaCO2 was also somewhat reduced by efficient alveolar hyperventilation. The arterial PCO2 and pH did not reflect the acid-base balance in peripheral tissues. During CPR, bicarbonate and tris-buffer mixture both quickly passed through the blood-brain barrier. When buffer treatment is indicated during CPR, a buffer which does not increase tissue PCO2 may be the drug of choice.

Topics: Acid-Base Equilibrium; Animals; Bicarbonates; Blood Pressure; Carbon Dioxide; Cardiac Output; Computers; Heart Arrest; Hydrogen-Ion Concentration; Kinetics; Resuscitation; Sodium; Sodium Bicarbonate; Sodium Chloride; Swine; Tromethamine

Clinical techniques for artificial perfusion have not previously been examined directly for their effects on brain high-energy metabolism. Our study involved 24 large mongrel dogs that were anesthetized, instrumented for central venous intravenous access, and subjected to craniotomy to expose the dura and underlying parietal cortex. The animals were divided into the following six experimental groups of four animals each: nonischemic controls; 15-minute cardiac arrest without resuscitation; 45-minute cardiac arrest without resuscitation; 15-minute cardiac arrest plus 30 minutes resuscitation with conventional cardiopulmonary resuscitation (CPR); 15-minute cardiac arrest plus 30 minutes resuscitation with interposed abdominal compression (IAC) CPR; and 15-minute cardiac arrest plus 30 minutes resuscitation with internal cardiac massage. Cardiac arrest was induced by central venous injection of KCl 0.6 mEq/kg, and it was confirmed by continuous ECG monitoring. The three active resuscitation models included administration of NaHCO3 and epinephrine, but no attempt was made to restart the heart by defibrillation during resuscitation. At the indicated time in each group, a 4- to 5-g sample of brain was removed through the craniotomy, immediately cooled to 0 C and processed for isolation of mitochondria. The mitochondria were studied for their content of superoxide dismutase and for quantitative oxygen consumption with glutamate/malate substrate during resting and ADP-stimulated respiration. Our results show a significant drop in brain mitochondrial superoxide dismutase activity during the first 15 minutes of cardiac arrest. There is minimal injury to brain mitochondrial oxygen consumption during both 15 and 45 minutes of complete ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Animals; Bicarbonates; Brain; Coronary Disease; Dogs; Epinephrine; Heart Arrest; Heart Massage; Mitochondria; Oxygen Consumption; Perfusion; Resuscitation; Sodium Bicarbonate; Superoxide Dismutase; Time Factors

Topics: Animals; Bicarbonates; Blood Pressure; Blood Vessels; Dogs; Epinephrine; Heart Arrest; History, 20th Century; Hydrogen-Ion Concentration; Methoxamine; Resuscitation; Sodium; Sodium Bicarbonate

Results obtained during animal investigations cannot be directly applied to patients because of the anatomical and physiological differences present. Experience has shown that cases of sudden cardiac arrest can only be effectively helped if cardiac massage and artificial ventilation are carried out as soon as possible, and that no sodium bicarbonate need be given when resuscitation measures are begun immediately, or very soon after arrest. In this situation it is better to use adrenaline only, in order to improve organ perfusion. The examples presented show that giving bicarbonate can alter potassium kinetics. Very low serum potassium concentrations are often measured during and following successful resuscitation, and giving too large an amount of buffer solution can worsen this hypokalaemia and lead to a further arrest. The infusion of sodium bicarbonate and the rapid increase in blood sugar levels during resuscitation can lead to a marked rise in serum osmolality which in turn can jeopardize the return of cerebral function. Because in the presence of reduced cerebral perfusion, high blood glucose levels increase the degree of cerebral lactacidosis blood glucose levels should be measured and corrected as necessary.

Topics: Acid-Base Equilibrium; Bicarbonates; Blood Glucose; Calcium; Carbon Dioxide; Child; Epinephrine; Heart Arrest; Hematocrit; Humans; Male; Middle Aged; Oxygen; Potassium; Resuscitation; Sodium; Sodium Bicarbonate; Water-Electrolyte Balance

Cardiac output using the currently recommended closed-chest cardiopulmonary resuscitation (CPR) technique is marginal (less than 30% of control), and eventually will result in tissue hypoperfusion and lactic acidemia. Intermittent sodium bicarbonate administration currently is recommended for treatment of this metabolic acidemia, and based on available data recommended dosages are empiric but sound. In this review the potential complications of acidemia and sodium bicarbonate administration are considered from the viewpoint of resuscitation outcome. In our opinion, available data are limited, and further evaluation and consideration of sodium bicarbonate requirements in the resuscitation setting are required.

Topics: Acidosis, Respiratory; Animals; Bicarbonates; Dogs; Heart Arrest; Humans; Hydrogen-Ion Concentration; Lactates; Sodium Bicarbonate

A prospective study of advanced cardiopulmonary resuscitation (CPR) was carried out on 226 patients in order to examine factors predicting successful resuscitation and 6 month survival. The mean age of all patients was 70 years and median age was 74. Cardiopulmonary resuscitation was successful in 40.5% (137) of all arrests and in 48.7% (110) of the first arrests. Thirty of 207 patients with one or more cardiac arrests were discharged alive (14%). Twenty-one of our patients were alive at 6 months (10.3%). Patients in ventricular fibrillation and/or ventricular tachycardia at the time of arrest were more likely to have successful outcomes. When the patient required Isuprel or bicarbonate, cardiopulmonary resuscitation was significantly less successful. We found no correlation of immediate outcome with the following variables: location of arrest; time of day; pre-existence of shock; coma; stroke; malignancy. Uremia and/or chronic obstructive pulmonary disease was not significantly associated with failed resuscitation. Most notable in our results of specific treatments was the evidence for the need to improve the initial pH, particularly when it was less than 7.2. Failure to do so by the time the second blood gas was drawn was associated with failure of cardiopulmonary resuscitation. Our results also suggest that the adequate treatment of metabolic acidosis, and improved ventilatory management with improved PO2 and optimization of PCO2, play a role in the better outcome of cardiopulmonary resuscitation.

Topics: Acid-Base Equilibrium; Adolescent; Adult; Aged; Bicarbonates; Child; Child, Preschool; Female; Heart Arrest; Hospitalization; Humans; Hydrogen-Ion Concentration; Infant; Isoproterenol; Male; Middle Aged; Prognosis; Prospective Studies; Resuscitation; Risk; Sodium Bicarbonate; Time Factors

Topics: Bicarbonates; Heart Arrest; Humans; Sodium Bicarbonate

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

This study compares the effect of epinephrine (11 dogs) with that of the combination of epinephrine with calcium (10 dogs) in CPR after anoxial cardiac arrest. In the epinephrine group resuscitation was successful in all 11 dogs within 4 minutes. In the calcium group only 7 out of 10 dogs could be resuscitated: 3 dogs died during CPR in cause of irreversible fibrillation (2 cases) and "stone heart" (1 case). High CPK-activity reflected severe myocardial cell damage. In the survivors of the calcium group cardiac function was significantly impaired: 1. decreased left ventricular pressure (LVP) and contractility (dp/dt max), 2. increased afterload, 3. decreased cardiac output inspite of increased heart rate, 4. as a consequence, reduced perfusion of the vital organs. - These results foster the conclusion that calcium should not be used henceforth in CPR. Epinephrine was and is still the drug of choice in resuscitation after cardiac arrest.

Topics: Animals; Bicarbonates; Calcium; Combined Modality Therapy; Creatine Kinase; Dogs; Drug Therapy, Combination; Epinephrine; Heart Arrest; Hemodynamics; Resuscitation; Sodium Bicarbonate

Topics: Analgesics; Anesthesiology; Bicarbonates; Calcium; Electric Countershock; Emergencies; Epinephrine; First Aid; Heart Arrest; Heart Massage; Humans; Intubation, Intratracheal; Lidocaine; Oxygen; Plasma Substitutes; Respiratory Insufficiency; Resuscitation; Shock; Sodium Bicarbonate; Ventilators, Mechanical

Learning to effectively treat cardiac emergencies is not an easy task. It is my opinion that mastery of material presented herein will ensure minimal competency. Finding practical experiences to help develop the necessary medical skills will require imagination and creativity. The following are offered as possible resources:1. Attend the American Heart Association's basis and advanced life support classes. (CPR training must be repeated at six-month intervals.) 2. Spend several days and/or nights in the emergency room at a local hospital observing (helping with(emergency care. #. Spend time with a mobile coronary care unit if available in your community. 4. Watch and do venipunctures at the local blood bank or donor center. 5. Observe in the intensive care unit at a local hospital. 6. Assist an oral surgeon in preparing intravenous lines and monitor a patient during sedation. 7. Observe administration of oxygen by an anesthesiologist in the operating room at a local hospital.

Topics: Angina Pectoris; Bicarbonates; Electric Countershock; Emergencies; Epinephrine; Heart; Heart Arrest; Heart Diseases; Humans; Myocardial Infarction; Resuscitation; Sodium Bicarbonate

Direct-air ventilation, external cardiac compression, and external defibrillation are established techniques for patients who unexpectedly develop cardiac arrest. The proper use of drugs can increase the incidence of successful resuscitation. Intracardiac adrenaline (epinephrine) acts as a powerful stimulant during cardiac standstill and, in addition, converts fine ventricular fibrillation to a coarser type, more responsive to electrical defibrillation. Routine use of intravenous sodium bicarbonate is recommended to combat the severe metabolic acidosis accompanying cardiac arrest. Lidocaine is particularly useful when ventricular fibrillation or ventricular tachycardia tends to recur. Analeptics are contraindicated, since they invariably increase oxygen requirements of already hypoxic cerebral tissues. The following acrostic is a useful mnemonic for recalling the details of the management of cardiac arrest in their proper order: A (Airway), B (Breathing), C (Circulation), D (Diagnosis of underlying cause), E (Epinephrine), F (Fibrillation), G (Glucose intravenously), pH (Sodium bicarbonate), I (Intensive care).

Topics: Acidosis; Arrhythmias, Cardiac; Bicarbonates; Brugada Syndrome; Cardiac Conduction System Disease; Critical Care; Drug Therapy; Electric Countershock; Epinephrine; Glucose; Heart Arrest; Heart Conduction System; Humans; Intensive Care Units; Lidocaine; Resuscitation; Sodium Bicarbonate; Tachycardia, Ventricular; Ventricular Fibrillation