Treatment of lactic acidosis: Appropriate confusion

Rachoin, Jean‐Sebastien; Weisberg, Lawrence S.; McFadden, Christopher B.

doi:10.1002/jhm.600

Cited by 40 publications

(26 citation statements)

References 126 publications

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“…This is of special importance in sepsis and shock, where acid accumulation can occur, despite adequate oxygen delivery [46]. Hypermetabolic conditions are observed in shock states like septic shock that are characterized by insulin resistance, hyperlactatemia, and increased oxygen demand, resulting from both enhanced mitochondrial oxygen utilization and oxygen radical production, which may coincide both with compromised tissue microcirculatory perfusion and mitochondrial dysfunction [47].…”

Section: Acidosis Results From Excessive Aerobic Metabolismmentioning

confidence: 99%

Rethinking Heart Failure

Fürstenwerth¹

2012

Cardiol Res

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An increasing body of clinical observations and experimental evidence suggests that cardiac dysfunction results from autonomic dysregulation of the contractile output of the heart. Excessive activation of the sympathetic nervous system and a decrease in parasympathetic tone are associated with increased mortality. Elevated levels of circulating catecholamines closely correlate with the severity and poor prognosis in heart failure. Sympathetic over-stimulation causes increased levels of catecholamines, which induce excessive aerobic metabolism leading to excessive cardiac oxygen consumption. Resulting impaired mitochondrial function causes acidosis, which results in reduction in blood flow by impairment of contractility. To the extent that the excessive aerobic metabolism resulting from adrenergic stimulation comes to a halt the energy deficit has to be compensated for by anaerobic metabolism. Glucose and glycogen become the essential nutrients. Beta-adrenergic blockade is used successfully to decrease hyperadrenergic drive. Neurohumoral antagonists block adrenergic over-stimulation but do not provide the heart with fuel for compensatory anaerobic metabolism. The endogenous hormone ouabain reduces catecholamine levels in healthy volunteers, promotes the secretion of insulin, induces release of acetylcholine from synaptosomes and potentiates the stimulation of glucose metabolism by insulin and acetylcholine. Ouabain stimulates glycogen synthesis and increases lactate utilisation by the myocardium. Decades of clinical experience with ouabain confirm the cardioprotective effects of this endogenous hormone. The so far neglected sympatholytic and vagotonic effects of ouabain on myocardial metabolism clearly make a clinical re-evaluation of this endogenous hormone necessary. Clinical studies with ouabain that correspond to current standards are warranted.

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Section: Acidosis Results From Excessive Aerobic Metabolismmentioning

confidence: 99%

Rethinking Heart Failure

Fürstenwerth¹

2012

Cardiol Res

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“…The use of sodium bicarbonate to correct lactic acidosis remains controversial because sodium bicarbonate can increase lactate production14. Recent studies have suggested that therapy be guided by changes in lactate level15.…”

Section: Discussionmentioning

confidence: 99%

Epinephrine-induced lactic acidosis in orthognathic surgery: a report of two cases

Son

Park

Cho

et al. 2016

J Korean Assoc Oral Maxillofac Surg

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Submucosal infiltration and the topical application of epinephrine as a vasoconstrictor produce excellent hemostasis during surgery. The hemodynamic effects of epinephrine have been documented in numerous studies. However, its metabolic effects (especially during surgery) have been seldom recognized clinically. We report two cases of significant metabolic effects (including lactic acidosis and hyperglycemia) as well as hemodynamic effects in healthy patients undergoing orthognathic surgery with general anesthesia. Epinephrine can induce glycolysis and pyruvate generation, which result in lactic acidosis, via β2-adrenergic receptors. Therefore, careful perioperative observation for changes in plasma lactate and glucose levels along with intensive monitoring of vital signs should be carried out when epinephrine is excessively used as a vasoconstrictor during surgery.

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“…Four PD solutions were used each day: two 1.5% PhysionealTM PD solutions, one 4.25% PhysionealTM PD solution, and one overnight exchange using 7 We hypothesized that lactate-containing PD solution was one of the causes of her lactic acidosis.…”

Section: Casementioning

confidence: 99%

A Case of Lactate Containing Peritoneal Dialysis Solution Induced Lactic Acidosis Corrected by Changing to Hemodialysis

Kim

Lee

et al. 2017

KMJ

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Elevated lactate levels are associated with acute illnesses, and the mortality is high. Here, we report a case of lactate-containing peritoneal dialysis (PD) solution inducing lactic acidosis corrected by changing to hemodialysis (HD). This 70-year-old female patient was treated with PD 8 months previously for end-stage renal disease caused by diabetes mellitus. She was admitted complaining of general weakness. Initial lactate level was 22.1 mg/dL and increased to 62.4 mg/dL showing high anion gap metabolic acidosis and compensatory hyperventilation. There are no definite causes of lactic acidosis besides the use of PD solutions containing a lactate component. The patient's lactate level was decreased after temporarily changing the dialysis modality to HD. Her lactate level was increased again after restarting PD, and decreased to normal after restarting HD. We report this case because physicians should consider lactate-containing PD solution as a possible cause of lactic acidosis.

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Treatment of lactic acidosis: Appropriate confusion

Cited by 40 publications

References 126 publications

Rethinking Heart Failure

Rethinking Heart Failure

Epinephrine-induced lactic acidosis in orthognathic surgery: a report of two cases

A Case of Lactate Containing Peritoneal Dialysis Solution Induced Lactic Acidosis Corrected by Changing to Hemodialysis

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