sodium-bicarbonate and Shock

This article reviews the current body of knowledge regarding lactic acidosis in critically ill patients. The classification of disordered lactate metabolism and its pathogenesis are examined. The utility of lactate as a metabolic monitor of shock is examined and current therapeutic strategies in the treatment of patients suffering from lactic acidosis are extensively reviewed. The paper is designed to integrate basic concepts with a current approach to lactate in critical illness that the clinician can use at the bedside.. Comprehensive review of the available, basic science, medical, surgical, and critical care literature.. The severity of lactic acidosis in critically ill patients correlates with overall oxygen debt and survival. Lactate determinations may be useful as an ongoing monitor of perfusion as resuscitation proceeds. Therapy of critically ill patients with lactic acidosis is designed to maximize oxygen delivery in order to reduce tissue hypoxia by increasing cardiac index, while maintaining hemoglobin concentration. Buffering agents have not been shown to materially affect outcome from lactic acidosis caused by shock. The benefits of other specific therapies designed to reduce the severity of lactic acidosis remain unproven.

Topics: Acidosis, Lactic; Bicarbonates; Blood Gas Analysis; Carbonates; Citric Acid Cycle; Critical Illness; Drug Combinations; Fluid Therapy; Glycolysis; Hemodynamics; Humans; Lactates; Lactic Acid; Metabolic Clearance Rate; Monitoring, Physiologic; Oxygen Consumption; Predictive Value of Tests; Severity of Illness Index; Shock; Sodium; Sodium Bicarbonate; Survival Rate

Iron poisoning continues to be a major toxicologic problem, with major impact on the gastrointestinal and circulatory systems. Failure to recognize the severity of iron intoxication may result in an inappropriate level of intervention. By using estimates of the total body burden of iron, clinical symptoms, and the serum iron concentration, an appropriate decision can be made to initiate aggressive chelation therapy with deferoxamine. In severe intoxication, the use of intravenous deferoxamine is indicated, along with supportive care, with particular attention to maintaining the intravascular volume. Other important measures include correction of acidosis and disorders of coagulation and replacement of blood components when there is evidence of gastrointestinal hemorrhage. Under rare circumstances in which large numbers of iron tablets are present in the gastrointestinal tract, surgical removal may be indicated. In addition, measures such as hemodialysis and exchange transfusion should be reserved for those unusual poisonings in which more conservative therapy is unsuccessful. In rare cases of iron intoxication, late sequelae such as hepatic necrosis and gastrointestinal scarring with obstruction may occur. The prompt recognition and initiation of management of children with acute iron poisoning is the single most critical element in decreasing the morbidity and mortality associated with these products.

Topics: Absorption; Bicarbonates; Chemical and Drug Induced Liver Injury; Child, Preschool; Deferoxamine; Diarrhea; Female; Fluid Therapy; Gastric Lavage; Gastrointestinal Hemorrhage; Humans; Infant; Ipecac; Iron; Necrosis; Renal Dialysis; Shock; Sodium; Sodium Bicarbonate; Vomiting

Topics: Acidosis; Airway Obstruction; Apgar Score; Bicarbonates; Blood Transfusion; Calcium Gluconate; Heart Massage; Humans; Infant, Newborn; Infant, Premature; Respiratory Distress Syndrome, Newborn; Resuscitation; Shock; Sodium Bicarbonate; Time Factors

A woman in her fifties was admitted to hospital with decreased awareness and circulatory failure. She had been treated with left atrial cryoablation a few weeks before admission and had been cardioverted a few days after the procedure because of relapse of atrial fibrillation.. On admission, the patient had systolic blood pressure of 80 mm Hg and an ECG with broad QRS-complexes at 380 ms. We suspected intoxication and she was intubated to administer activated charcoal after gastric lavage. She was cardiovascularly unstable and in need of intravenous infusion of noradrenaline and adrenaline. Further investigations at her home suggested that she had poisoned herself with 4-5 g flecainide, 0.3 g oxazepam and 0.5 g meclizine. After administration of 500 mmol sodium bicarbonate and 5 mmol calcium chloride, the QRS complexes narrowed temporarily. On day 2, due to sustained bradycardia and hypotension despite receiving adrenergic medications, a temporary pacemaker was implanted, leading to improved heart rate and blood pressure. She experienced several complications including hypertensive pulmonary oedema, atrial fibrillation, extensively prolonged QT interval because of polypharmacy and Takotsubo cardiomyopathy. She was discharged from the hospital in good health on day 17. At a follow-up visit at the outpatient clinic 12 weeks later, cardiac function had normalised. The QT interval was now normal; however, there were persistent T-wave inversions in leads I, aVL and V4-6.. Flecainide blocks sodium channels in cardiomyocytes. Intoxication with flecainide is rare, with mortality rates of about 10 %. Sodium bicarbonate in larger doses has been reported to stabilise patients with flecainide intoxication due to modification of the binding of flecainide to sodium receptors in cardiomyocytes, and due to alkalisation which makes flecainide detach from sodium receptors. Our patient had a temporary effect with narrowing of QRS complexes after receiving sodium bicarbonate. She also showed a beneficial effect from implantation of a temporary pacemaker, although earlier case reports have described problems with high thresholds and capture failure.

Topics: Anti-Arrhythmia Agents; Charcoal; Drug Overdose; Electrocardiography; Female; Flecainide; Humans; Middle Aged; Pacemaker, Artificial; Shock; Sleepiness; Sodium Bicarbonate

Lactic acidosis is a very common biological issue for shock patients. Experimental data clearly demonstrate that metabolic acidosis, including lactic acidosis, participates in the reduction of cardiac contractility and in the vascular hyporesponsiveness to vasopressors through various mechanisms. However, the contributions of each mechanism responsible for these deleterious effects have not been fully determined and their respective consequences on organ failure are still poorly defined, particularly in humans. Despite some convincing experimental data, no clinical trial has established the level at which pH becomes deleterious for hemodynamics. Consequently, the essential treatment for lactic acidosis in shock patients is to correct the cause. It is unknown, however, whether symptomatic pH correction is beneficial in shock patients. The latest Surviving Sepsis Campaign guidelines recommend against the use of buffer therapy with pH ≥7.15 and issue no recommendation for pH levels <7.15. Furthermore, based on strong experimental and clinical evidence, sodium bicarbonate infusion alone is not recommended for restoring pH. Indeed, bicarbonate induces carbon dioxide generation and hypocalcemia, both cardiovascular depressant factors. This review addresses the principal hemodynamic consequences of shock-associated lactic acidosis. Despite the lack of formal evidence, this review also highlights the various adapted supportive therapy options that could be putatively added to causal treatment in attempting to reverse the hemodynamic consequences of shock-associated lactic acidosis.

Topics: Acidosis, Lactic; Carbon Dioxide; Hemodynamics; Hospital Mortality; Humans; Shock; Sodium Bicarbonate

Intravenous lipid emulsion (ILE) has been shown to ameliorate toxicity from lipophilic xenobiotics, attributed in part through sequestration to circulating lipid droplets (sink). We postulated additional benefit with plasma exchange therapy undertaken subsequent to lipid injection, hypothesising enhanced blood carriage of lipophilic toxin to increase yield when combined with an extracorporeal method of elimination.. Instrumented rabbits underwent clomipramine infusion at 3.2 mg/kg/min to target mean arterial pressure (MAP) of 50% baseline, then continuously at 2 mg/kg/min to death or 90 min. Resuscitation with saline (Control), sodium bicarbonate (BIC), ILE, or lipid emulsion plus cycled plasma exchange (LEPE), was commenced on attaining target MAP.. Greater survival was observed in animals receiving lipid emulsion from both LE and LEPE groups (Control median 12.0 [IQR 10.5 – 20] min, BIC median 30 [IQR 19 – 33] min, LE 85 [IQR 30 – 90] min, LEPE 90 min; P 0.0001). No difference was observed in MAP, Heart Rate, or Electrocardiograph QRS duration between surviving LE and LEPE animals at 90 min. Mean plasma exchange of 52%circulating plasma volume returned only 0.04% of the administered clomipramine load in LEPE group animals.. Infusion of lipid emulsion resulted in greater survival in this rabbit model of intravenous clomipramine toxicity. Plasma exchange performed in conjunction with administration of lipid emulsion failed to result in significant extracorporeal clomipramine elimination. Intravascular lipid sequestration of clomipramine appears an inadequate sole explanation for the beneficial effects of lipid emulsion.

Topics: Animals; Antidepressive Agents, Tricyclic; Blood Pressure; Clomipramine; Electrocardiography; Fat Emulsions, Intravenous; Heart Rate; Kaplan-Meier Estimate; Plasma Exchange; Rabbits; Resuscitation; Shock; Sodium Bicarbonate; Survival

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

Topics: Aged, 80 and over; Anti-Arrhythmia Agents; Atrial Fibrillation; Confusion; Female; Flecainide; Hallucinations; Humans; Shock; Sodium Bicarbonate

Topics: Acidosis; Ampicillin; Animals; Anti-Bacterial Agents; Atropine; Blood Cell Count; Blood Chemical Analysis; Cephalosporins; Electrolytes; Female; Fluid Therapy; Gentamicins; Glucose; Horse Diseases; Horses; Hydrogen-Ion Concentration; Hypoglycemia; Infusions, Intravenous; Sepsis; Shock; Sodium Bicarbonate; Uveitis

Sodium bicarbonate is the most physiological alkalinizing agent. The effect of a new bicarbonated Ringer's solution (BRS) containing Mg2+, on metabolic acidosis and serum magnesium abnormality were evaluated and compared with those of acetated Ringer's (ARS), lactated Ringer's (LRS) and Ringer's (RS) solutions in an experimental haemorrhagic shock model with dogs.. Animals were randomly divided into six groups (n = 6 in each group), a sham-operated group, an operated group without infusion, and 4 operated groups with infusion (BRS, ARS, LRS and RS groups). Each RS was intravenously administered at 60 mL kg(-1) h(-1) for 1.5 h. Arterial blood gases, plasma electrolytes and cardiovascular parameters were analysed.. BRS significantly improved blood base excess values, which were decreased by blood-letting, faster and more markedly than did LRS and RS (BRS--6.3 +/- 0.5 mEq L(-1); LRS--9.2 +/- 1.1 mEq L(-1); RS--12.4 +/- 1.0 mEq L(-1) at the end of infusion). The alkalinizing effect of BRS tended to be better than that of ARS but not significantly so. The serum Mg2+ concentration was well-maintained by BRS as compared to other RS (BRS 1.5 +/- 0.0 mgdL(-1); ARS 1.2 +/- 0.0mgdL(-1); LRS 1.1 +/- 0.0mgdL(-1); RS 1.3 +/- 0.1 mgdL(-1), at the end of infusion).. These results suggest that BRS is a suitable perioperative solution for metabolic acidosis and serum electrolyte balance among RS tested.

Topics: Acid-Base Equilibrium; Acidosis; Animals; Blood Pressure; Carbon Dioxide; Disease Models, Animal; Dogs; Heart Rate; Hematocrit; Hemoglobins; Hemorrhage; Infusions, Intravenous; Isotonic Solutions; Lactic Acid; Magnesium; Male; Oxygen; Random Allocation; Ringer's Lactate; Ringer's Solution; Shock; Sodium Bicarbonate; Time Factors

To report a case of reversible blindness associated with severe alcoholic ketoacidosis.. Observational case report.. A 44-year-old male presented with gradual bilateral blindness that developed within a 24-hour period. He suffered from ethanol-induced severe ketoacidosis and shock and was resuscitated with epinephrine and sodium bicarbonate.. The treatment of acidosis led to a rapid resolution of the patient's blindness.. It is important to understand the role of severe acidosis as the sole causative factor of reversible bilateral blindness.

Topics: Adult; Alcoholism; Blindness; Cardiopulmonary Resuscitation; Drug Therapy, Combination; Epinephrine; Glucose; Humans; Infusions, Intravenous; Isotonic Solutions; Ketosis; Male; Ringer's Solution; Shock; Sodium Bicarbonate; Visual Acuity; Vitamin B Complex

Topics: Acidosis, Lactic; Cell Hypoxia; Humans; Lactic Acid; Severity of Illness Index; Shock; 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

To examine factors determining the haemodynamic and metabolic responses to treatment of diabetic ketoacidosis with alkali, groups of anaesthetised and ventilated rats with either diabetic ketoacidosis (mean arterial pH 6.86-6.96, mean arterial blood pressure 63-67 mm Hg) or hypovolaemic shock due to blood withdrawal (mean pHa 7.25-7.27, mean arterial blood pressure 36-41 mm Hg) were treated with sodium chloride ('saline'), sodium bicarbonate or 'Carbicarb' (equimolar bicarbonate plus carbonate). In the diabetic ketoacidosis series, treatment with either alkali resulted in deterioration of mean arterial blood pressure and substantial elevation of blood lactate, despite a significant rise in myocardial intracellular pH determined by 31P-magnetic resonance spectroscopy. These effects were accompanied by falling trends in the ratios of myocardial phosphocreatine and ATP to inorganic phosphate. Erythrocyte 2,3-bisphosphoglycerate was virtually absent in animals with diabetic ketoacidosis of this severity and duration. In contrast, in shock due to blood withdrawal, infusion of saline or either alkali was accompanied by a transient elevation of mean arterial blood pressure and no significant change in the already elevated blood lactate; erythrocyte 2,3-bisphosphoglycerate was normal in these animals. The effect of alkalinization in rats with severe diabetic ketoacidosis was consistent with myocardial hypoxia, due to the combination of very low initial erythrocyte 2,3-bisphosphoglycerate, alkali-exacerbated left shift of the haemoglobin-oxygen dissociation curve and artificial ventilation. No evidence was found for any beneficial effect of 'Carbicarb' in either series of animals; 'Carbicarb' and sodium bicarbonate could be deleterious in metabolic acidosis of more than short duration.

Topics: 3-Hydroxybutyric Acid; Animals; Blood Pressure; Carbon Dioxide; Carbonates; Diabetes Mellitus, Experimental; Diabetic Ketoacidosis; Drug Combinations; Hemodynamics; Hydrogen-Ion Concentration; Hydroxybutyrates; Lactates; Magnetic Resonance Spectroscopy; Male; Partial Pressure; Rats; Rats, Wistar; Shock; Sodium Bicarbonate; Sodium Chloride; Time Factors

Rats rendered hypotensive and acidotic by withdrawal of blood were treated by infusion of either an equimolar mixture of sodium bicarbonate and sodium carbonate ("Carbicarb"), sodium bicarbonate alone, or sodium chloride. Skeletal muscle intracellular pH (pHi) was measured using magnetic resonance spectroscopy from the chemical shift of the carbon-2 (C2) proton resonance of the imidazole ring of anserine. In the groups treated with alkali, arterial blood pH (pHa) was restored to normal, but no change was observed in the sodium chloride-treated animals. Despite an elevation of arterial blood partial pressure of CO2 (PaCO2) in the group treated with sodium bicarbonate, no significant change in pHi was observed in any group. Blood lactate levels, initially elevated in all groups, underwent only minor changes. In all three groups a transient and similar elevation of arterial blood pressure was observed after infusion. Differential effects of Carbicarb and sodium bicarbonate in metabolic acidosis may be dependent on the model of metabolic acidosis used, and an alteration in PaCO2 induced by alkali therapy may not be a major determinant of changes in pHi.

Topics: Acidosis; Animals; Carbonates; Drug Combinations; Hemodynamics; Hydrogen-Ion Concentration; Lactates; Male; Muscles; Rats; Rats, Wistar; Shock; Sodium Bicarbonate; Sodium Chloride

To examine: a) the rate and extent of delivery of radioactive tracers to the central circulation from the tibial, medial malleolar, distal femoral, and humeral intraosseous sites, as well as from a peripheral intravenous site; and b) the end-tidal CO2 response to injected sodium bicarbonate at these sites.. Prospective, descriptive study.. Animal laboratory at a university medical center.. Twenty anesthetized and mechanically ventilated piglets were cannulated with 18-gauge bone marrow needles at intraosseous sites and 22-gauge Teflon catheters in peripheral veins. A 22-gauge angiocath was placed in the right carotid artery of each subject. Drug kinetics were studied in the normovolemic and hypovolemic (acute bleeding of 25 mL/kg) states.. Sodium bicarbonate (1 mEq/kg) was injected into each of the three intraosseous and one intravenous sites with simultaneous monitoring of end-tidal CO2. A 10-min period for stabilization was allowed between injections. Aliquots of 99mtechnetium were injected at randomly selected sites and blood samples were obtained at 1.5-sec intervals via carotid artery for radioactive counts. Experiments were repeated after withdrawal of 25 mL/kg of blood.. Assessment by end-tidal CO2 monitoring after 1-mEq/kg injections of bicarbonate demonstrated a mean initial end-tidal CO2 increase at 12.8 secs and a mean maximal end-tidal CO2 increase of 8 torr (1.06 kPa), with no significant site differences noted. Radioactive tracer injections were detected in the carotid artery after 15.4 secs in normovolemic animals and after 21.4 secs in hypovolemic animals, with no significant site differences detected. The proportion of injected tracer at 2, 5, 10, 20, 30, and 40 mins identified no significant differences between various intraosseous and intravenous sites.. Our study demonstrated similar rapid transit and proportion of bicarbonate and radioactive tracers, reaching the central circulation from multiple intraosseous sites and a peripheral intravenous site. This finding suggests that adjustments in drug dosage may not be required, using various intraosseous locations as an alternative to peripheral intravenous drug therapy.

Topics: Animals; Blood Circulation; Breath Tests; Carbon Dioxide; Catheterization, Peripheral; Evaluation Studies as Topic; Indium Radioisotopes; Infusions, Intraosseous; Infusions, Intravenous; Shock; Sodium Bicarbonate; Swine; Swine, Miniature; Technetium Tc 99m Pentetate; Tidal Volume; Time Factors

A fatal case of fulminant hepatic failure that occurred in the neonatal period is reported in a premature infant born after 27 4/7-weeks' gestation. Immediately after birth the infant had severe hypoxia and hypotension resulting from birth asphyxia, hypovolemic shock, and septicemia. At autopsy, histological appearance of the liver showed virtually total hepatocellular necrosis without features of fibrosis. Although the exact cause of hepatocellular injury cannot be fully ascertained, it is assumed that hypoxia and hypotension must have been the predominant factors leading to massive hepatic necrosis.

Topics: Acyclovir; Alanine Transaminase; Aspartate Aminotransferases; Bicarbonates; Cloxacillin; Dopamine; Female; Fetal Hypoxia; Fetal Membranes, Premature Rupture; Humans; Infant, Newborn; Infant, Premature, Diseases; Liver; Male; Necrosis; Netilmicin; Pancuronium; Partial Thromboplastin Time; Penicillins; Pregnancy; Prothrombin Time; Sepsis; Shock; Sodium; Sodium Bicarbonate

Metabolic acidosis is the most frequent acid-base abnormality observed in the critically ill. Although there are many different causes, in the absence of ketosis and renal failure lactic acidosis is the most likely underlying disturbance. Controversy continues to surround the relative roles of the liver and the kidneys in the control of acid-base balance. There is no consensus concerning the use of bicarbonate in the treatment of a life-threatening metabolic acidosis.

Topics: Acidosis; Bicarbonates; Blood; Dichloroacetic Acid; Hemodynamics; Humans; Hydrogen-Ion Concentration; Renal Dialysis; Shock; Sodium; Sodium Bicarbonate; Vasodilator Agents

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: Acid-Base Equilibrium; Animals; Bicarbonates; Blood Volume; Dogs; Hyperbaric Oxygenation; Hypotension; Research; Shock; Shock, Hemorrhagic; Sodium Bicarbonate; Vascular Resistance