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Paradoxical Intracellular Acidosis Definition

Treatment Of Acidosis: Sodium Bicarbonate And Other Drugs

Treatment Of Acidosis: Sodium Bicarbonate And Other Drugs

Treatment of Acidosis: Sodium Bicarbonate and Other Drugs Lactic acidosis, defined as a lactate level > 5 mmol/1 and a pH 7.35, is far and away the most-important acidosis during critical illness and most of this discussion of acidosis treatment will focus on treatment of lactic acidosis. Even in the face of maximal supportive therapy, lactic acidosis is associated with a mortality of 60-90% [ 1 , 2 , 3 , 4 ], so physicians have long relied on treatments to lower the [H+], such as sodium bicarbonate. Less common than lactic acidosis, and much more amenable to conventional treatments, are ketoacidoses and respiratory acidosis, but these too occasionally prompt consideration of alkalinizing therapies. Lowering the [H+] in blood depends on manipulating the strong ion difference ([SID]), total concentration of non-volatile weak acid buffer (ATOT), or arterial CO2 tension (PaCO2), or raising the total concentration of weak bases, BTOT (normally sufficiently small that it can be ignored). Therefore, potential treatments include: 1. Raise [SID]: a) add strong cations: bicarbonate, carbicarb, dialysis b) remove strong anions: dichloroacetate (DCA), dialysis, thiamine, riboflavin, vasoactive drugs? 2. Lower the paCO2: raise VE or lower VD/VT or VCO2 3. Reduce ATOT: remove albumin, but very limited effect Acute Lung InjurySodium BicarbonateAcute Respiratory Distress SyndromeLactic AcidosisDiabetic Ketoacidosis These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves. This is a preview of subscription content, log in to check access Unable to display preview. Download preview PDF. Weil MH, Afifi AA (1970) Experimental and clinical studies on lactate and pyruvate as indicators of th Continue reading >>

8.7 Use Of Bicarbonate In Metabolic Acidosis

8.7 Use Of Bicarbonate In Metabolic Acidosis

8.7 Use of Bicarbonate in Metabolic Acidosis Metabolic acidosis causes adverse metabolic effects (see Section 5.4 ). In particular the adverse effects on the cardiovascular system may cause serious clinical problems. Bicarbonate is an anion and cannot be given alone. Its therapeutic use is as a solution of sodium bicarbonate. An 8.4% solution is a molar solution (ie it contains 1mmol of HCO3- per ml) and is the concentration clinically available in Australia. This solution is very hypertonic (osmolality is 2,000 mOsm/kg). The main goal of alkali therapy is to counteract the extracellular acidaemia with the aim of reversing or avoiding the adverse clinical effects of the acidosis (esp the adverse cardiovascular effects). Other reasons for use of bicarbonate in some cases of acidosis are: to promote alkaline diuresis (eg to hasten salicylate excretion) 8.7.2 Undesirable effects of bicarbonate administration In general, the severity of these effects are related to the amount of bicarbonate used. These undesirable effects include: 8.7.3 Important points about bicarbonate 1. Ventilation must be adequate to eliminate the CO2 produced from bicarbonate Bicarbonate decreases H+ by reacting with it to to produce CO2 and water. For this reaction to continue the product (CO2) must be removed. So bicarbonate therapy can increase extracellular pH only if ventilation is adequate to remove the CO2. Indeed if hypercapnia occurs then as CO2 crosses cell membranes easily, intracellular pH may decrease even further with further deterioration of cellular function. 2. Bicarbonate may cause clinical deterioration if tissue hypoxia is present If tissue hypoxia is present, then the use of bicarbonate may be particularly disadvantageous due to increased lactate production (removal of acidotic i Continue reading >>

Sodium Bicarbonate

Sodium Bicarbonate

Indications Metabolic Acidosis Diabetic Ketoacidosis (DKA) (see Diabetic Ketoacidosis and Hyperosmolar Hyperglycemic State) Indications: pH <6.9-7.0 (however, evidence for this recommendation is lacking) Patients with Hemodynamic Compromise (Due to Impaired Myocardial Contractility and Vasodilation) or Life-Threatening Hyperkalemia May Particularly Benefit from Bicarbonate Administration to Correct the pH Lactic Acidosis (see Lactic Acidosis) Adverse Effects of Acidemia: these (selected adverse effects) provide a rationale for administering bicarbonate with pH <7.1 Arrhythmias Arterial Vasodilation and Venoconstriction Decreased Left Ventricular Contractility Impaired Responsiveness to Catecholamine Vasopressors (Nat Rev Nephrol, 2012) [MEDLINE] Indications: pH <7.1 (however, evidence for this recommendation is lacking) This is due to the fact that at pH <7.1, small changes in pCO2 and serum bicarbonate result in large changes in the serum pH Clinical Efficacy: neither of these trials demonstrated clinical benefit with bicarbonate administration in patients with pH >7.1 Trial of Sodium Bicarbonate in Critically Ill Patients with Lactic Acidosis (Ann Intern Med, 1990) [MEDLINE] Sodium Bicarbonate Did Not Improve Hemodynamics in Critically Ill Patients with Metabolic Acidosis and Hyperlactatemia Sodium Bicarbonate Did Not Increase the Cardiovascular Response to Infused Catecholamines in in Critically Ill Patients with Metabolic Acidosis and Hyperlactatemia Sodium Bicarbonate Decreased Plasma Ionized Calcium and Increased the pCO2 Trial of Sodium Bicarbonate in Lactic Acidosis (Crit Care Med, 1991) [MEDLINE] Administration of sodium bicarbonate did not improve hemodynamic variables in patients with lactic acidosis, but did not worsen tissue oxygenation Non-Anion Gap Metabo Continue reading >>

Physiological Effects Of Hyperchloraemia And Acidosis

Physiological Effects Of Hyperchloraemia And Acidosis

Physiological effects of hyperchloraemia and acidosis Chelsea and Westminster NHS Foundation Trust Chelsea and Westminster NHS Foundation Trust BJA: British Journal of Anaesthesia, Volume 101, Issue 2, 1 August 2008, Pages 141150, J. M. Handy, N. Soni; Physiological effects of hyperchloraemia and acidosis, BJA: British Journal of Anaesthesia, Volume 101, Issue 2, 1 August 2008, Pages 141150, The advent of balanced solutions for i.v. fluid resuscitation and replacement is imminent and will affect any specialty involved in fluid management. Part of the background to their introduction has focused on the non-physiological nature of normal saline solution and the developing science about the potential problems of hyperchloraemic acidosis. This review assesses the physiological significance of hyperchloraemic acidosis and of acidosis in general. It aims to differentiate the effects of the causes of acidosis from the physiological consequences of acidosis. It is intended to provide an assessment of the importance of hyperchloraemic acidosis and thereby the likely benefits of balanced solutions. Hyperchloraemic acidosis is increasingly recognized as a clinical entity, a new enemy within, that had gone otherwise unnoticed for decades. Although any associated morbidity may be subtle at present, there is a trend in current evidence to suggest that hyperchloraemic acidosis may have adverse consequences which may be circumvented by the use of balanced solutions. These consequences, both theoretical and clinical, may result from hyperchloraemia, acidosis, or both. There is some evidence of hyperchloraemia causing problems, but at present the clinical relevance is uncertain. The literature does appear to be unified in stating that acidosis results in adverse physiological effects bu Continue reading >>

Response To 100mmol Of Sodium Bicarbonate

Response To 100mmol Of Sodium Bicarbonate

Response to 100mmol of Sodium Bicarbonate These are the physiological effects of infusing 100mmol of concentrated (8.4%) sodium bicarbonate into a patient. A 1 molar solution of sodium bicarbonate is what you are giving. The osmolality is 2000mosm/L. Let us unfocus from the movements of water and sodium, as they are predictable, and their patterns already well rehearsed. Let us instead observe the traffic of the HCO3- anion. Let us pretend that suddenly 100mmol of this anion is dumped into the extracellular fluid (and being easily water soluble, it frolics merrily through the extracellular fluid compartments, distributing evenly among them). This means 25mmol of HCO3- is now in the vascular compartment and 75 mmol is in the interstitial fluid. The extracellular concentration of bicarbonate pre-infusion in our model is 24mmol/L, which gives us 336 mmol overall. A sudden increase by 100mmol (to a total content of 436 mmol) would cause the concentration to rise to 31.1mmol/L. The change in extracellular bicarbonate concentration following a bicarbonate infusion From the above calculations, it would seem that the volume of distribution for bicarbonate is the same as the extracellular fluid, 14L or about 0.2L/Kg. Experimental findings demonstrate that this is not the case. Simplistic fluid-filled cylinder models of distribution do not do justice to the complexity of bicarbonate distribution. The major source of complexity, is the tendency of the bicarbonate to buffer hydrogen ions and become "lost" in the process, converting to water and carbon dioxide. This tendency, as one might imagine, is dependent on the presence of acidosis or alkalosis. An excellent article has examined this relationship, and I will clumsily paraphrase Figure 5 from it below. The figure describes the Continue reading >>

Hemodynamic Consequences Of Severe Lactic Acidosis In Shock States: From Bench To Bedside

Hemodynamic Consequences Of Severe Lactic Acidosis In Shock States: From Bench To Bedside

Hemodynamic consequences of severe lactic acidosis in shock states: from bench to bedside Kimmoun et al.; licensee BioMed Central.2015 The Erratum to this article has been published in Critical Care 2017 21:40 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 Continue reading >>

Efficient Extra- And Intracellular Alkalinization Improves Cardiovascular Functions In Severe Lactic Acidosis Induced By Hemorrhagic Shock | Anesthesiology | Asa Publications

Efficient Extra- And Intracellular Alkalinization Improves Cardiovascular Functions In Severe Lactic Acidosis Induced By Hemorrhagic Shock | Anesthesiology | Asa Publications

Efficient Extra- and Intracellular Alkalinization Improves Cardiovascular Functions in Severe Lactic Acidosis Induced by Hemorrhagic Shock From the CHU Nancy, Service de Ranimation Mdicale Brabois, Pole Cardiovasculaire et Ranimation Mdicale, Hpital Brabois, Vandoeuvre les Nancy, France; Institut National de la Sant Et de la Recherche Mdicale (INSERM) U1116, Equipe 2, Facult de Mdecine, Vandoeuvre les Nancy, France; Universit de Lorraine, Nancy, France (A.K., N.D., and B.L.); INSERM U1116, Equipe 2, Facult de Mdecine, Vandoeuvre les Nancy, France; Universit de Lorraine, Nancy, France (N.S., K.I., and C.S.); and Critallographie, Rsonnance Magntique et Modlisation (CRM2), Unit Mdicale de Recherche (UMR), Centre National de la Recherche Scientifique (CNRS), Institut Jean Barriol, Facult des Sciences et Technologies, Vandoeuvre les Nancy, France; Universit de Lorraine, Nancy, France (J.-M.E. and S.L.). From the CHU Nancy, Service de Ranimation Mdicale Brabois, Pole Cardiovasculaire et Ranimation Mdicale, Hpital Brabois, Vandoeuvre les Nancy, France; Institut National de la Sant Et de la Recherche Mdicale (INSERM) U1116, Equipe 2, Facult de Mdecine, Vandoeuvre les Nancy, France; Universit de Lorraine, Nancy, France (A.K., N.D., and B.L.); INSERM U1116, Equipe 2, Facult de Mdecine, Vandoeuvre les Nancy, France; Universit de Lorraine, Nancy, France (N.S., K.I., and C.S.); and Critallographie, Rsonnance Magntique et Modlisation (CRM2), Unit Mdicale de Recherche (UMR), Centre National de la Recherche Scientifique (CNRS), Institut Jean Barriol, Facult des Sciences et Technologies, Vandoeuvre les Nancy, France; Universit de Lorraine, Nancy, France (J.-M.E. and S.L.). From the CHU Nancy, Service de Ranimation Mdicale Brabois, Pole Cardiovasculaire et Ranimation Mdicale, Hpital Bra Continue reading >>

Effect Of Sodium Bicarbonate On Intracellular Ph Under Different Buffering Conditions - Sciencedirect

Effect Of Sodium Bicarbonate On Intracellular Ph Under Different Buffering Conditions - Sciencedirect

Volume 49, Issue 5 , May 1996, Pages 1262-1267 Effect of sodium bicarbonate on intracellular pH under different buffering conditions Author links open overlay panel JacquesLevrautDr. Effect of sodium bicarbonate on intracellular pH under different buffering conditions. Previous in vitro studies have reported a paradoxical exacerbation of intracellular acidosis following bicarbonate therapy due to the generated CO2 entering the cytoplasm. However, these studies were conducted in nonphysiological Hepes-buffered media. We compared the effect of a sodium bicarbonate load on the intracellular pH (pHi) of hepatocytes placed in nonbicarbonate (NBBS) or bicarbonate (BBS) buffering systems. The pHi of isolated rat hepatocytes was measured using the fluorescent pH sensitive dye BCECF and a single-cell imaging technique. Cells were placed in medium buffered with or Hepes. All media were adjusted to pH 7 with L-lactic acid or HCl. An acute 45mM sodium bicarbonate load was added to each medium and the changes in pHi were measured every three seconds for 90 seconds. The sodium bicarbonate load caused rapid cytoplasmic acidification of cells in NBBS (N = 50, P < 0.001). In contrast, hepatocytes in BBS underwent a marked increase in pHi (N = 50, P < 0.001) without any initial decrease in pHi. These differences were highly significant for the buffer (P < 0.01), but not for the acid used. We conclude that sodium bicarbonate exacerbates intracellular acidosis only in a NBBS. Hence, in vitro studies reporting a paradoxical intracellular acidosis following bicarbonate therapy cannot be extrapolated to the in vivo buffering conditions, and should not be used to argue against bicarbonate therapy. Continue reading >>

Bicarbonate Therapy And Intracellular Acidosis.

Bicarbonate Therapy And Intracellular Acidosis.

1. Clin Sci (Lond). 1997 Dec;93(6):593-8. Bicarbonate therapy and intracellular acidosis. (1)Renal Laboratory, St Thomas' Hospital, London, U.K. 1. The correction of metabolic acidosis with sodium bicarbonate remainscontroversial. Experiments in vitro have suggested possible deleterious effectsafter alkalinization of the extracellular fluid. Disequilibrium of carbon dioxideand bicarbonate across cell membranes after alkali administration, leading to thephenomenon of 'paradoxical' intracellular acidosis, has been held responsible forsome of these adverse effects. 2. Changes in intracellular pH in suspensions ofleucocytes from healthy volunteers were monitored using a fluorescentintracellular dye. The effect in vitro of increasing extracellular pH with sodiumbicarbonate was studied at different sodium bicarbonate concentrations. Lacticacid and propionic acid were added to the extracellular buffer to mimicconditions of metabolic acidosis. 3. The addition of a large bolus of sodiumbicarbonate caused intracellular acidification as has been observed previously.The extent of the intracellular acidosis was dependent on several factors, being most evident at higher starting intracellular pH. When sodium bicarbonate wasadded as a series of small boluses the reduction in intracellular pH was small.Under conditions of initial acidosis this was rapidly followed by intracellularalkalinization. 4. Although intracellular acidification occurs after addition of sodium bicarbonate to a suspension of human leucocytes in vitro, the effect isminimal when the conditions approximate those seen in clinical practice. Wesuggest that the observed small and transient lowering of intracellular pH isinsufficient grounds in itself to abandon the use of sodium bicarbonate in human acidosis. Continue reading >>

Bicarbonate Therapy And Intracellular Acidosis

Bicarbonate Therapy And Intracellular Acidosis

1. The correction of metabolic acidosis with sodium bicarbonate remains controversial. Experiments in vitro have suggested possible deleterious effects after alkalinization of the extracellular fluid. Disequilibrium of carbon dioxide and bicarbonate across cell membranes after alkali administration, leading to the phenomenon of 'paradoxical' intracellular acidosis, has been held responsible for some of these adverse effects. 2. Changes in intracellular pH in suspensions of leucocytes from healthy volunteers were monitored using a fluorescent intracellular dye. The effect in vitro of increasing extracellular pH with sodium bicarbonate was studied at different sodium bicarbonate concentrations. Lactic acid and propionic acid were added to the extracellular buffer to mimic conditions of metabolic acidosis. 3. The addition of a large bolus of sodium bicarbonate caused intracellular acidification as has been observed previously. The extent of the intracellular acidosis was dependent on several factors, being most evident at higher starting intracellular pH. When sodium bicarbonate was added as a series of small boluses the reduction in intracellular pH was small. Under conditions of initial acidosis this was rapidly followed by intracellular alkalinization. 4. Although intracellular acidification occurs after addition of sodium bicarbonate to a suspension of human leucocytes in vitro, the effect is minimal when the conditions approximate those seen in clinical practice. We suggest that the observed small and transient lowering of intracellular pH is insufficient grounds in itself to abandon the use of sodium bicarbonate in human acidosis. Do you want to read the rest of this article? ... However, an experimental study by Benjamin et al. on dogs subjected to hemorrhagic shoc Continue reading >>

Sodium Bicarbonate Use

Sodium Bicarbonate Use

metabolic acidosis leads to adverse cardiovascular effects bicarbonate must be administered in a solution as sodium bicarbonate 8.4% solution contains 1mmol of HCO3-/mL and is very hypertonic (2,000mOsm/kg) goal of NaHCO3 administration in severe metabolic acidosis to counteract the negative cardiovascular effects of acidaemia alternatives to NaHCO3 include carbicarb, dichloroacetate, Tris/THAM Treatment of sodium channel blocker overdose (e.g. tricyclic overdose) Urinary alkalinisation (salicylate poisoning) Metabolic acidosis (NAGMA) due to HCO3 loss (RTA, fistula losses) Cardiac arrest (in prolonged resuscitation + documented severe metabolic acidosis) Diabetic ketoacidosis (very rarely, perhaps if shocked and pH < 6.8) Severe pulmonary hypertension with RVF to optimize RV function Severe ischemic heart disease where lactic acidosis is thought to be an arrhythmogenic risk hypernatraemia (1mmol of Na+ for every 1mmol of HCO3-) hyperosmolality (cause arterial vasodilation and hypotension) impaired oxygen unloading due to left shift of the oxyhaemoglobin dissociation curve removal of acidotic inhibition of glycolysis by increased activity of PFK hypercapnia (CO2 readily passes intracellularly and worsens intracellular acidosis) severe tissue necrosis if extravasation takes place bicarbonate increases lactate production by: increasing the activity of the rate limiting enzyme phosphofructokinase and removal of acidotic inhibition of glycolysis shifts Hb-O2 dissociation curve, increased oxygen affinity of haemoglobin and thereby decreases oxygen delivery to tissues POINTS TO REMEMBER WHEN USING BICARBONATE it is generally better to correct underlying cause of acidosis and give supportive care than to give sodium bicarbonate ensure adequate ventilation to eliminate CO2 pro Continue reading >>

Bicarbonate Therapy In Severe Metabolic Acidosis

Bicarbonate Therapy In Severe Metabolic Acidosis

Abstract The utility of bicarbonate administration to patients with severe metabolic acidosis remains controversial. Chronic bicarbonate replacement is obviously indicated for patients who continue to lose bicarbonate in the ambulatory setting, particularly patients with renal tubular acidosis syndromes or diarrhea. In patients with acute lactic acidosis and ketoacidosis, lactate and ketone bodies can be converted back to bicarbonate if the clinical situation improves. For these patients, therapy must be individualized. In general, bicarbonate should be given at an arterial blood pH of ≤7.0. The amount given should be what is calculated to bring the pH up to 7.2. The urge to give bicarbonate to a patient with severe acidemia is apt to be all but irresistible. Intervention should be restrained, however, unless the clinical situation clearly suggests benefit. Here we discuss the pros and cons of bicarbonate therapy for patients with severe metabolic acidosis. Metabolic acidosis is an acid-base disorder characterized by a primary consumption of body buffers including a fall in blood bicarbonate concentration. There are many causes (Table 1), and there are multiple mechanisms that minimize the fall in arterial pH. A patient with metabolic acidosis may have a normal or even high pH if there is another primary, contravening event that raises the bicarbonate concentration (vomiting) or lowers the arterial Pco2 (respiratory alkalosis). Metabolic acidosis differs from “acidemia” in that the latter refers solely to a fall in blood pH and not the process. A recent online survey by Kraut and Kurtz1 highlighted the uncertainty over when to give bicarbonate to patients with metabolic acidosis. They reported that nephrologists will prescribe therapy at a higher pH compared with Continue reading >>

Sodium Bicarbonate Therapy In Patients With Metabolic Acidosis

Sodium Bicarbonate Therapy In Patients With Metabolic Acidosis

The Scientific World Journal Volume 2014 (2014), Article ID 627673, 13 pages Nephrology Division, Hospital General Juan Cardona, Avenida Pardo Bazán, s/n, Ferrol, 15406 A Coruña, Spain Academic Editor: Biagio R. Di Iorio Copyright © 2014 María M. Adeva-Andany et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Abstract Metabolic acidosis occurs when a relative accumulation of plasma anions in excess of cations reduces plasma pH. Replacement of sodium bicarbonate to patients with sodium bicarbonate loss due to diarrhea or renal proximal tubular acidosis is useful, but there is no definite evidence that sodium bicarbonate administration to patients with acute metabolic acidosis, including diabetic ketoacidosis, lactic acidosis, septic shock, intraoperative metabolic acidosis, or cardiac arrest, is beneficial regarding clinical outcomes or mortality rate. Patients with advanced chronic kidney disease usually show metabolic acidosis due to increased unmeasured anions and hyperchloremia. It has been suggested that metabolic acidosis might have a negative impact on progression of kidney dysfunction and that sodium bicarbonate administration might attenuate this effect, but further evaluation is required to validate such a renoprotective strategy. Sodium bicarbonate is the predominant buffer used in dialysis fluids and patients on maintenance dialysis are subjected to a load of sodium bicarbonate during the sessions, suffering a transient metabolic alkalosis of variable severity. Side effects associated with sodium bicarbonate therapy include hypercapnia, hypokalemia, ionized hypocalcemia, and QTc inter Continue reading >>

Sodium Bicarb For Treatment Of Acidosis?

Sodium Bicarb For Treatment Of Acidosis?

SDN members see fewer ads and full resolution images. Join our non-profit community! Was in a case the other day (Im an intern, so I was basically shadowing a CA-3) and we got an intraop ABG which showed a pH of 7.18. Attending asked for sodium bicarb to correct acidosis. Its my understanding that when you give bicarb youre basically just dumping CO2 in the patient, and that any increase in pH is secondary to an increase in SID (i.e. increasing strong cation ion sodium, while not increasing strong anion.) Do you guys use bicarb to correct metabolic acidosis? Was in a case the other day (Im an intern, so I was basically shadowing a CA-3) and we got an intraop ABG which showed a pH of 7.18. Attending asked for sodium bicarb to correct acidosis. Its my understanding that when you give bicarb youre basically just dumping CO2 in the patient, and that any increase in pH is secondary to an increase in SID (i.e. increasing strong cation ion sodium, while not increasing strong anion.) Do you guys use bicarb to correct metabolic acidosis? except, when a sudden intolerable decrease in pH is expected (ie release of a clamp or tourniquet), or when all else is failing (ie during a code when i want the pressors to work long enough to gain a foothold - little evidence for this). Agreed. Bicarb is only masking the acidosis and it is better to treat the cause rather than correct the pH. However, if things are beginning to go south in a hurry and you can't correct the problem rapidly enough then bicarb can be a benefit. Mostly by increasing the effectiveness of your inotropes, as Slavin said. Remember, some of the criticism of bicarb came from codes where removal of CO2 was impaired. We don't usually have that issue so some say it won't harm anything to give bicarb. I disagree, CO2 will Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

I. Review of normal lipid metabolism Triglycerides in adipose ==lipolysis==> Long-chain FAs Long-chain FAs==hepatic beta-oxidation==>Acetyl CoA Acetyl CoA==hepatic ketogenesis==>ketone bodies Ketone bodies are Beta-hydroxybutyrate and Acetoacetate Beta-OHB is oxidized to AcAc-; their relative concentrations depend on redox state of cell; Beta-OHB predominates in situation favoring reductive metabolism (e.g. decreased tissue perfusion, met. acidosis, catabolic states--like DKA!) Typical ratio Beta-OHB:AcAc- is 3:1; us. increases in DKA II. Hormonal influences on glucose and lipid metabolism Insulin In liver, increases glu uptake from portal blood; stimulates glycogenesis, inhibits glycogenolysis and gluconeogenesis In skeletal muscle, increases glu uptake from blood, stimulates protein synth, inhibits proteolysis In adipose tissue, required for glu and lipoprotein uptake from blood; stimulates lipogenesis, inhibits lipolysis Tissues which don't require insulin to transport glucose into cells: brain, renal medulla, formed blood elements Counterregulatory hormones: glucagon (major player in DKA), epi/norepi, cortisol, growth hormone (no acute effects, only over days-weeks) Glucagon: increases hepatic beta-oxidation, ketogenesis, gluconeogenesis and glycogenolysis; decreases hepatic FA synth. Epi/Norepi: increase hepatic gluconeogenesis & glycogenolysis; increases adipose lipolysis; decreases peripheral glu utilization Cortisol: major effect is decreased peripheral glu utiliz; little effect on production Growth hormone: increases hepatic gluconeogenesis and glycogenolysis; increases adipose lipolysis In high counterreg. hormone states (see above), require high levels of insulin to avoid progressive hyperglycemia and ketoacidosis--glucagon levels in DKA are 5-6 x nl* III. Pa Continue reading >>

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