sodium-bicarbonate has been researched along with Shock--Septic* in 13 studies
2 review(s) available for sodium-bicarbonate and Shock--Septic
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Is there a role for sodium bicarbonate in treating lactic acidosis from shock?
Bicarbonate therapy for severe lactic acidosis remains a controversial therapy.. The most recent 2008 Surviving Sepsis guidelines strongly recommend against the use of bicarbonate in patients with pH at least 7.15, while deferring judgment in more severe acidemia. We review the mechanisms causing lactic acidosis in the critically ill and the scientific rationale behind treatment with bicarbonate.. There is little rationale or evidence for the use of bicarbonate therapy for lactic acidosis due to shock. We agree with the Surviving Sepsis guidelines recommendation against the use of bicarbonate for lactic acidosis for pH at least 7.15 and we further recommend a lower target pH of 7.00 or less. If bicarbonate is used, consideration must be given to slow infusion and a plan for clearing the CO2 that is produced and measuring and correcting ionized calcium as the resultant 10% drop may decrease cardiac and vascular contractility and responsiveness to catecholamines. When continuous renal replacement therapy is used during severe acidosis, we recommend bicarbonate-based replacement fluid over citrate as citrate may increase the strong ion gap. Effective therapy of lactic acidosis due to shock is to reverse the cause. Topics: Acidosis, Lactic; Humans; Shock, Septic; Sodium Bicarbonate | 2008 |
[Treatment of toxico-infectious shock].
Topics: Animals; Anti-Bacterial Agents; Bicarbonates; Drug Therapy, Combination; Heparin; Histamine H1 Antagonists; Humans; Hydrocortisone; Hypertonic Solutions; Rabbits; Shock, Septic; Sodium Bicarbonate; Vasodilator Agents | 1984 |
1 trial(s) available for sodium-bicarbonate and Shock--Septic
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[The use of sodium bicarbonate in stages in treating hypoperfusion induced lactic acidemia in septic shock].
To explore the use of sodium bicarbonate in stages in treating hypoperfusion induced lactic acidemia due to septic shock.. In this prospective randomized, double-blind, controlled clinical trial, a total of 65 patients of hypoperfusion induced lactic acidemia due to septic shock admitted between April 2006 and April 2010 were assigned to two groups. Thirty-five patients of "stage" group sodium bicarbonate was used in two stages: in first stage sodium bicarbonate was given by venous drip until pH≥7.15, and in second stage sodium bicarbonate was given by intravenous drip till pH≥7.25 after 6 hours. Thirty patients in control group intravenous drip of sodium bicarbonate was used till pH≥7.15. Early goal-directed therapy(EGDT) was used in the first 6 hours of fluid resuscitation. The number of dysfunction organ, time of mechanical ventilation, maximum sequential organ failure assessment (SOFA) score, delta SOFA score, durations of stay in intensive care unit (ICU) and in hospital, and mortality were recorded in two groups. Blood gas analysis and index of hemodynamics were monitored at 0 hour and 8 hours in both groups.. Compared with control group, "stage" group was associated with a lower number of dysfunction organ, time of mechanical ventilation, maximum SOFA score, delta SOFA score, durations of stay in ICU and in hospital, and mortality (number of dysfunction organ: 2.68±0.79 vs. 3.28±0.80, time of mechanical ventilation: 10.32±2.26 days vs. 13.80±2.56 days, maximum SOFA score: 11.01±2.26 vs. 13.11±2.26, delta SOFA score: 1.71±1.25 vs. 3.43±1.27, duration of stay in ICU: 14.0±3.6 days vs. 20.0±3.7 days, duration of stay in hospital: 28.3±12.9 days vs. 41.9±13.2 days, mortality: 34.28% vs. 60.00%, P<0.05 or P<0.01). There were no significant differences in blood gas analysis and index of hemodynamics at 0 hour, and they were improved at 8 hours. Compared with control group, in "stage" group, lactic acid (Lac) was significantly lowered (1.50±1.08 mmol/L vs. 2.93±1.09 mmol/L), and pH, mixed venous oxygen saturation (SvO2), oxygen extraction ratio (O2ER), cardiac index (CI), oxygen delivery (DO2) were significantly increased (pH:7.29±0.05 vs. 7.20±0.05, SvO2: 0.75±0.18 vs. 0.66±0.17, O2ER: 0.32±0.06 vs. 0.25±0.06, CI: 113.36±13.34 ml×s(-1)×m(-2) vs. 83.35±13.34 ml×s(-1)×m(-2), DO2: 840±170 ml×min(-1)×m(-2) vs. 630±171 ml×min(-1)×m(-2), all P<0.01).. The use of sodium bicarbonate in stages in treating hypoperfusion induced lactic acidemia as a result of septic shock can lower the occurrence rate of multiple organ dysfunction syndrome, time of mechanical ventilation, durations of stay in ICU and in hospital, and mortality. Topics: Acidosis, Lactic; Adult; Aged; Double-Blind Method; Female; Humans; Male; Middle Aged; Multiple Organ Failure; Prospective Studies; Shock, Septic; Sodium Bicarbonate | 2013 |
10 other study(ies) available for sodium-bicarbonate and Shock--Septic
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Prognostic value of neglected biomarker in sepsis patients with the old and new criteria: predictive role of lactate dehydrogenase.
This study examined the pH, lactate dehydrogenase (LDH), and heart rate values on the first day of hospitalization in patients with a prediagnosis of sepsis and biomarkers that may predict mortality.. Patients hospitalized in an emergency intensive care unit with a diagnosis of systemic inflammatory response syndrome were classified as having sepsis (n = 28), septic shock (n = 8), or severe sepsis (n = 8) according to International Sepsis Guidelines (old criteria). Forty-four patients were classified as having sepsis (n = 4), septic shock (n = 30), or infection (n = 10) according to The Third International Consensus Definitions for Sepsis and Septic Shock (new criteria). The effects of these patients' laboratory values on survival between groups were compared. Significant values were evaluated by χ. When the patients were categorized according to the new classification criteria, there was an increase in the number of septic shock patients and a decrease in the number of sepsis patients. In addition, 10 patients were removed from the sepsis category. There was a significant difference between ex and discharged patients in terms of heart rate, pH, sodium bicarbonate, lactate, and LDH (P= .007, P= .002, P= .034, P= .009, and P= .002, respectively). Based on a χ. Systemic pH, LDH, and heart rate values may be used to determine the best time to discharge patients from intensive care to other, more affordable hospital units. Topics: Aged; Aged, 80 and over; Biomarkers; Clinical Enzyme Tests; Female; Heart Rate; Hospitalization; Humans; Hydrogen-Ion Concentration; L-Lactate Dehydrogenase; Lactic Acid; Male; Practice Guidelines as Topic; Predictive Value of Tests; Prognosis; Sepsis; Shock, Septic; Sodium Bicarbonate; Survival Rate | 2016 |
Bicarbonate therapy in the treatment of septic shock: a second look.
The use of supplemental sodium bicarbonate for the treatment of patients with septic shock and elevated blood lactate levels remains a controversial therapy. We conducted a retrospective study between March 2004 and February 2009 of 36 consecutive patients diagnosed with septic shock who received continuous infusion of bicarbonate therapy. A control group was matched 1:1 for age, site of infection, and predicted mortality by APACHE II. All patients were managed according to standard protocols. The median time until reversal of shock did not achieve statistical significance between the bicarbonate group (44.5 h [95% confidence interval [CI] 34-54] and the control group (55.0 h [95% CI 39-60] (p = 0.09). The median time to liberation of mechanical ventilation was significantly reduced in the bicarbonate group (10 days [95% CI 5.0-13.0] compared to the control group (14 days [95% CI 9.0-19.0], p = 0.02). The length of intensive care unit (ICU) stay was also shorter in the surviving patients who received bicarbonate compared to controls (median 11.5 days (95% CI 6.0-16.0) vs. 16.0 days (95% CI 13.5-19.0), respectively; p = 0.01). However, there was no difference in 28-day mortality between the two study groups (28%; 95% CI 14-45% vs. 33%; 95% CI 19-51%, respectively; p = 0.79). Infusion of sodium bicarbonate in septic patients with arterial hyperlactatemia may facilitate weaning from mechanical ventilation and reduce length of ICU stay. Topics: Aged; Aged, 80 and over; APACHE; Female; Humans; Intensive Care Units; Male; Middle Aged; Retrospective Studies; Shock, Septic; Sodium Bicarbonate; United States | 2010 |
Effect of fluid resuscitation on ryanodine receptor in macaques with endotoxic shock.
Our recent study demonstrated that sodium bicarbonate improved cardiac function in macaque models with early-phase endotoxic shock. In the present study, we investigated further the ryanodine receptor/calcium release-channel (RyR) and calcium pump after fluid resuscitation of macaques with early-phase endotoxic shock.. Twenty-four anaesthetised macaques were assigned to four groups. Nineteen animals were given an intravenous dose of 2.8 mgkg(-1) lipopolysaccharide (LPS). Sixty minutes after the LPS challenge, the animals were given (i) 5 mLkg(-1) normal saline (Ns group, n = 6), (ii) 5 mLkg(-1) of 5% sodium bicarbonate (Sb group, n = 6) or (iii) 5 mLkg(-1) of 3.5% hypertonic sodium chloride (Hs group, n = 7). The control group (Co group, n = 5) received 1 mLkg(-1) normal saline and then with 5 mLkg(-1) normal saline 60 min later.. Endotoxin produced a reduction of the density of RyR but did not alter the affinity of RyR. Compared with normal saline, sodium bicarbonate or hypertonic saline induced a restoration of density of RyR but did not influence the affinity of RyR and the calcium pump.. Up-regulation of RyR performance in myocardium following administration of sodium bicarbonate contributes to the improvement of cardiac function in macaques in the early phase of endotoxic shock. Topics: Animals; Calcium-Transporting ATPases; Disease Models, Animal; Escherichia coli; Female; Fluid Therapy; Lipopolysaccharides; Macaca; Male; Myocardium; Resuscitation; Ryanodine Receptor Calcium Release Channel; Saline Solution, Hypertonic; Shock, Septic; Sodium Bicarbonate; Up-Regulation | 2006 |
Endotoxic shock model with fluid resuscitation in Macaca mulatta.
These studies established a macaque model of early-phase endotoxic shock, and investigated the resuscitation effects of three different solutions. Twenty-four macaques were assigned to four groups. Nineteen animals were given an intravenous dose of 2.8 mg/kg lipopolysaccharide (LPS). At 60 min after LPS challenge, the animals were given (i) 5 mL/kg normal saline (Ns group, n=6), (ii) 5% of 5 mL/kg sodium bicarbonate (Sb group, n=6), (iii) hypertonic 3.5% sodium chloride of 5 mL/kg (Hs group, n=7). The control group (Co group, n=5) was first injected with 1 mL/kg Ns and with 5 mL/kg Ns 60 min later. Haemodynamic parameters and blood gases were measured during the experiment, and myocardial morphology was examined on termination of the experiment. Administration of LPS caused hypotension and decreases of the left ventricular work index (LVWI). In the Sb group, mean arterial pressure, cardiac index, systemic vascular resistance index, LVWI and right ventricular work index were significantly higher than those of the Ns group. Pathological changes of myocardium were identified in all of the LPS groups. The studies suggest that macaques are suitable models for studying endotoxic shock and potential fluid therapies. Topics: Analysis of Variance; Animals; Blood Gas Analysis; Disease Models, Animal; Hemodynamics; Heparin; Hydrogen-Ion Concentration; Lipopolysaccharides; Macaca mulatta; Myocardium; Saline Solution, Hypertonic; Shock, Septic; Sodium Bicarbonate; Ventricular Function, Left | 2005 |
Amrinone combined with dobutamine improves hemodynamics and oxygen delivery without down-regulation of cardiac beta-adrenergic receptor density in porcine endotoxemia.
Effects of amrinone (AMR), a phosphodiesterase inhibitor, alone and in combination with dobutamine (DOB), on hemodynamics and O2 delivery were studied during porcine endotoxemia. Pentobarbital-anesthetized pigs were randomly administered either Escherichia coli lipopolysaccharide (endotoxin) or equivolumetric .9% NaCl (control) as a continuous infusion for 4 h. From 2 to 4 h (T = 120-240 min) of endotoxin infusion, pigs were randomly administered one of the following treatments; AMR infusion (40 micrograms/kg/min) (AMRlow); DOB (10 micrograms/kg/min) (DOB); AMR infusion (40 micrograms/kg/min) + DOB (AMRlow+DOB); AMR bolus (.75 mg/kg) followed by AMR infusion (40 micrograms/kg/min) (AMRhigh); or AMR bolus (.75 mg/kg) followed by infusion (40 micrograms/kg/min) + DOB (AMRhigh+DOB). Myocardial samples were obtained at the end of the experiment and flash-frozen for beta-adrenergic receptor analysis. Endotoxin significantly (p < .05) decreased cardiac index, right ventricular ejection fraction, stroke volume index, maximum rate of rise of left ventricular pressure (dP/dtmax), mean arterial pressure, and O2 delivery, and increased pulmonary vascular resistance and mean pulmonary arterial pressure (p < .05). AMRlow+DOB significantly (p < .05) increased cardiac index, dP/dtmax, right ventricular ejection fraction, stroke volume index, O2 delivery and consumption, and decreased mean pulmonary arterial pressure, pulmonary vascular resistance, mean arterial pressure, and systemic vascular resistance. beta-Adrenergic receptor density (Bmax) and binding equilibrium dissociation constant (KD) for [3H]dihydroalprenolol were not affected by endotoxin or any treatment (p < .05). Endotoxin-induced hemodynamic deterioration and decreased O2 delivery was attenuated by AMRlow+DOB. Potential applications of this combination may exist in treatment of septic patients with inadequate myocardial performance and reduction in O2 delivery complicated by pulmonary hypertension. Topics: Amrinone; Animals; Disease Models, Animal; Dobutamine; Down-Regulation; Drug Therapy, Combination; Hemodynamics; Hydrogen-Ion Concentration; Oxygen Consumption; Radioligand Assay; Receptors, Adrenergic, beta; Shock, Septic; Sodium Bicarbonate; Swine; Ventricular Function, Right | 1995 |
Effects of sodium bicarbonate on striated muscle metabolism and intracellular pH during endotoxic shock.
The effects of HCO3Na load on acid-base balance and muscle intracellular bioenergetics have been investigated using 31P-magnetic resonance spectroscopy in an experimental model of endotoxinic shock. Anesthetized, mechanically ventilated, and paralyzed rats (n = 16) were given an intravenous bolus of Escherichia coli lipopolysaccharide (15 mg/kg). When shock was established they were randomly assigned to receive either HCO3Na intravenously (2 mmol/kg in 2 min) or an equimolar saline injection. Lipopolysaccharide induced a significant decrease in the levels of mean arterial pressure (58 +/- 6 vs. 120 +/- 8 mmHg), arterial pH (7.20 +/- .03 vs. 7.35 +/- .01), intracellular pH (6.86 +/- .04 vs. 7.08 +/- .01), a marked hyperlactatemia (7 +/- 3 vs. 1.2 +/- .2 mmol/L) and a drop in the phosphocreatine-inorganic phosphate ratio. In the bicarbonate-loaded rats, mean arterial pressure further decreased whereas it remained unchanged in the saline group. Bicarbonate increased arterial pH and PaCO2 transiently. In the saline group, arterial pH decreased and PaCO2 remained stable. In both groups, intracellular pH and high energy phosphates had a similar evolution. In this model of septic shock, partial correction of arterial pH using HCO3Na did not reduce the metabolic cellular injury in skeletal muscle. Based on these results, HCO3Na may be of limited therapeutic value in severe septic metabolic acidosis. Topics: Acidosis, Lactic; Animals; Blood Pressure; Disease Models, Animal; Hindlimb; Hydrogen-Ion Concentration; Lipopolysaccharides; Magnetic Resonance Spectroscopy; Muscle, Skeletal; Physical Phenomena; Physics; Rats; Rats, Sprague-Dawley; Shock, Septic; Sodium Bicarbonate; Sodium Chloride | 1994 |
Blood biochemical response to sodium bicarbonate infusion during sublethal endotoxemia in ponies.
Hypertonic NaHCO3 infusion caused blood volume expansion, increased blood bicarbonate concentration, and delayed the onset of hypophosphatemia in ponies with endotoxemia. However, NaHCO3 infusion did not normalize blood pH, and it increased blood L-lactate concentration, and caused hypokalemia, hypernatremia, and hyperosmolality. The deleterious effects of NaHCO3 infusion in endotoxemia ponies outweighed the beneficial effects. The role of hypertonic NaHCO3 given IV for treatment of endotoxemia in equids must be reevaluated. Topics: Animals; Bicarbonates; Endotoxins; Escherichia coli; Escherichia coli Infections; Female; Horse Diseases; Horses; Hydrogen-Ion Concentration; Infusions, Intravenous; Lactates; Lactic Acid; Male; Shock, Septic; Sodium; Sodium Bicarbonate | 1990 |
Hemodynamic and renal advantages of dual cyclooxygenase and leukotriene blockade during canine endotoxic shock.
The decline in mean arterial pressure (MAP), cardiac output (CQ), and renal blood flow (RBF) that accompany endotoxic shock is partly ameliorated by cyclooxygenase or leukotriene blockade. This study determined whether dual cyclooxygenase and leukotriene blockade provided greater hemodynamic protection than either single blockade alone. Mongrel dogs were pretreated with either ibuprofen or LY171883 alone or dual blockade consisting of ibuprofen combined with LY171883 or propylgallate, then given Escherichia coli endotoxin, and monitored for 10 hr. Postendotoxemic MAP was equally maintained with dual blockade and with ibuprofen. For the first 5 hr postendotoxin, CQ was best maintained by dual blockade. However, by 9 hr postendotoxin, CQ in LY171883-treated animals was 88 +/- 8% of control. LY171883 provided the greatest protection of RBF, while dual blockade provided the least protection for both RBF and urine flow rates (V). Ibuprofen-treated dogs required less NaHCO3 for acid-base maintenance than did dual-blocked animals. In summary, dual cyclooxygenase and leukotriene blockade was advantageous in protecting MAP and CQ during the early phases of shock but provided no greater protection of RBF, GFR, V or acid-base balance than did single blockade. Overall, LY171883 provided the best protection from circulatory dysfunction. Topics: Acetophenones; Animals; Bicarbonates; Blood Pressure; Cardiac Output; Cyclooxygenase Inhibitors; Diuresis; Dogs; Endotoxins; Escherichia coli; Glomerular Filtration Rate; Hemodynamics; Ibuprofen; Kidney; Leukotriene Antagonists; Renal Circulation; Shock, Septic; Sodium; Sodium Bicarbonate; Tetrazoles | 1990 |
[New therapeutic aspects in the treatment of diffuse peritonitis].
The diffuse peritonitis is a syndrome during the course of which biochemical reactive chains are activated according to a cascade principle. Most of these biochemical reactive chains develop within an acid environment. The solutions applied for abdominal lavage so far had neutral pH value. The present acute peritonitis experiment has shown that a peritoneal pH increase during lavage therapy stopped the septic reactive chain and thus improved significantly the rate of survival in the test animals. These experimental findings ar now subject for clinical examination. Topics: Animals; Bicarbonates; Blood Pressure; Hydrogen-Ion Concentration; Peritoneal Lavage; Peritonitis; Rats; Rats, Inbred Strains; Shock, Septic; Sodium; Sodium Bicarbonate; Sodium Chloride | 1987 |
SEVERE SEPTIC SHOCK TREATED SUCCESSFULLY WITH SODIUM BICARBONATE.
Topics: Acidosis; Bicarbonates; Blood Volume; Child; Drug Therapy; Femur; Humans; Hypotension; Infusions, Parenteral; Osteomyelitis; Resuscitation; Sepsis; Shock, Septic; Sodium Bicarbonate; Staphylococcal Infections | 1964 |