sodium-bicarbonate and Respiratory-Insufficiency

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

Duchenne muscular dystrophy (DMD) leads to progressive paresis, respiratory failure and premature death. Long-term positive pressure ventilation can improve quality of life and survival, but previously unrecognized complications may arise. We analyzed the characteristics of severe metabolic acidosis occurring in 8 of 55 DMD patients, of 20-36 years of age, observed over a 5-year period. All patients were on positive pressure ventilation and were being treated for chronic constipation. Before admission, they had had a reduced intake of fluids and food. Upon examination, they were severely ill, dyspneic and suffering from abdominal discomfort. Metabolic acidosis with a high anion gap was noted in 5 of the 8 patients and with a normal anion gap in the other 3. They all recovered after the administration of fluids and nutrition, the regulation of bowel movements and treatment with antibiotics, as appropriate. Metabolic acidosis is a life-threatening, potentially preventable complication in older DMD patients. Early recognition, subsequent administration of fluids, nutrition and antibiotics and regulation of bowel movements seem to be essential.

Topics: Acid-Base Equilibrium; Acidosis; Adult; Buffers; Constipation; Disease Management; Female; Hemofiltration; Humans; Laxatives; Male; Malnutrition; Muscular Dystrophy, Duchenne; Positive-Pressure Respiration; Quality of Life; Respiratory Insufficiency; Respiratory Tract Infections; Severity of Illness Index; Sodium Bicarbonate; Treatment Outcome

A 68-year-old man presented to the Emergency Department with a severe metabolic alkalosis after ingesting large quantities of baking soda to treat his dyspepsia. His underlying pulmonary disease and a progressively worsening mental status necessitated intubation for respiratory failure. Laboratory studies revealed a hyponatremic, hypochloremic, hypokalemic metabolic alkalosis. The patient was successfully treated after cessation of the oral bicarbonate, initiation of intravenous hydration, and correction of electrolyte abnormalities.

Topics: Aged; Alkalosis; Dyspepsia; Emergency Service, Hospital; Humans; Male; Respiratory Insufficiency; Self Medication; Sodium Bicarbonate

To report diagnostic, clinical and therapeutic aspects of cyanide intoxication resulting from ingestion of cyanogenic glucoside-containing apricot seeds.. Thirteen patients admitted to the Pediatric Intensive Care Unit (PICU) of Erciyes University between 2005 and 2009 with cyanide intoxication associated with ingestion of apricot seeds were reviewed retrospectively.. Of the 13 patients, four were male. The mean time of onset of symptoms was 60 minutes (range 20 minutes to 3 hours). On admission, all patients underwent gastric lavage and received activated charcoal. In addition to signs of mild poisoning related to cyanide intoxication, there was severe intoxication requiring mechanical ventilation (in four cases), hypotension (in two), coma (in two) and convulsions (in one). Metabolic acidosis (lactic acidosis) was detected in nine patients and these were treated with sodium bicarbonate. Hyperglycaemia occurred in nine patients and blood glucose levels normalised spontaneously in six but three required insulin therapy for 3-6 hours. Six patients received antidote treatment: high-dose hydroxocobalamin in four and two were treated with a cyanide antidote kit in addition to high-dose hydroxocobalamin. One patient required anticonvulsive therapy. All patients recovered and were discharged from the PICU within a mean (SD, range) 3.1 (1.7, 2-6) days.. Cyanide poisoning associated with ingestion of apricot seeds is an important poison in children, many of whom require intensive care.

Topics: Acidosis; Antidotes; Charcoal; Child; Child, Preschool; Coma; Cyanides; Eating; Female; Gastric Lavage; Hematinics; Humans; Hydroxocobalamin; Hyperglycemia; Insulin; Male; Poisoning; Prunus; Respiratory Insufficiency; Retrospective Studies; Seeds; Seizures; Sodium Bicarbonate; Turkey

The effect of omeprazole (2 mg kg-1 i.v.) on respiratory depression induced in rats by acute oral methadone administration (5 mg kg-1) was examined and compared with control animals that only received methadone. Quantitative assessments of arterial Pco2,Po2, pH, and respiratory rate were employed as criteria for evaluation. Intragastric pH was measured in each rat immediately before and 2 h after methadone. Plasma concentration of methadone was measured for 3 h. The relationship between drug effect and the systemic bioavailability of methadone, measured as the area under the plasma concentration-time curve (AUC0-180), was also evaluated. The intensity of the methadone-induced respiratory depression was significantly greater in the omeprazole group than in control rats. A significant variation (p < 0.01) in all respiratory parameters was detected from 30 to 120 min after methadone. Omeprazole caused a significant increase in methadone levels (Cmax = 156 +/- 6.5 ng mL-1 against 51 +/- 5.8 ng mL-1 in control; p < 0.05). AUC0-180 was higher (p < 0.05) after omeprazole treatment (18.6 +/- 1.4 micrograms mL-1 min) than in control (6.8 +/- 0.6 microgram mL-1 min). Two hours after treatment with omeprazole, intragastric pH values were significantly elevated (4.7 +/- 0.1 against 2.2 +/- 0.04) and continued increasing, being 6.4 +/- 0.1 at the end of the experiment. Correlation was observed between intragastric pH and the area under the effect- (respiratory depression-) time curve (r = 0.74; p < 0.001). A relationship between plasma methadone levels at 120 min and gastric pH (r = 0.92; p < 0.001) was detected. A significant correlation between the area under the effect-time curve (0-120 min) and AUC0-180 has been also observed (r = 0.90; p < 0.01). These pharmacokinetic and pharmacodynamic changes could be gastric pH dependent because they were mimicked when gastric pH was experimentally modified by bicarbonate whereas opposite results were obtained with acidic pH2 solution.

Topics: Administration, Oral; Animals; Area Under Curve; Drug Interactions; Female; Gastric Mucosa; Hydrogen-Ion Concentration; Intestinal Absorption; Methadone; Omeprazole; Pulmonary Gas Exchange; Rats; Rats, Sprague-Dawley; Respiration; Respiratory Insufficiency; Sodium Bicarbonate

We retrospectively evaluated the clinical and laboratory findings of all patients admitted to our facility during a 6.5-year period with a history of cyclic antidepressant ingestion (CAD). Outcome parameters [admission CAD concentration, arterial pH, and corrected QT (QTc) and QRS intervals] used in adult populations to predict morbidity after CAD ingestion were applied to our study population. During the study period, 45 patients (mean +/- SD age of 11.8 +/- 5.6 years) were admitted with CAD ingestion. Conduction delays were present in 17 patients, 9 of whom had QTc intervals greater than 0.43 seconds. Seven patients had generalized seizures; 7 required mechanical ventilation; 14 had Glasgow Coma Scores of 8 or lower on presentation; and one required pharmacologic support for hypotension. In our cohort, the mean admission serum CAD concentration was 461.5 +/- 477.4 ng/mL. Correlations were found between the arterial pH, the QRS interval, the QTc interval, and the admission CAD serum concentration. In an analysis of three subsets of patients (i.e., those with seizures, coma, and respiratory insufficiency), only patients who presented with seizures were found to have a significant prolongation in the QRS and QTc intervals. Pediatric patients who have ingested CADs and present with seizures would appear to be at increased risk for having conduction delays, cardiac dysrhythmias, and, presumably, attendant morbidity and mortality associated with an ingestion.

Topics: Adolescent; Anticonvulsants; Antidepressive Agents, Tricyclic; Arkansas; Child; Child, Preschool; Female; Humans; Infant; Intensive Care Units, Pediatric; Male; Poisoning; Respiration, Artificial; Respiratory Insufficiency; Retrospective Studies; Seizures; Sodium Bicarbonate

Topics: Adult; Asthma; Bicarbonates; Female; Humans; Male; Respiratory Insufficiency; Sodium; Sodium Bicarbonate; Ventilators, Mechanical

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

Topics: Acidosis; Acidosis, Respiratory; Bicarbonates; Blood Circulation; Dogs; Heart Function Tests; Hemodynamics; Infusions, Parenteral; Pharmacology; Pulmonary Circulation; Research; Respiratory Insufficiency; Sodium Bicarbonate