Myocardial depressant effects of sodium acetate

Kirkendol, Paul L.; Pearson, James E.; Bower, John D.; Holbert, Robert D.

doi:10.1093/cvr/12.2.127

Cited by 56 publications

(28 citation statements)

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“…After haemodialysis the cardiac output fell to much lower levels during tilt than before dialysis. This may be secondary to a decrease in plasma volume following ultrafiltration during haemo dialysis or to negative inotropic effects of substances such as acetate on the myocardium [34], Acetate may also cause peripheral vasodilatation [35,36], but this is un likely to have occurred in our patients, as peripheral vas cular resistance increased after haemodialysis. In haemo dialysis patients PRA is largely uninfluenced by changes in dietary sodium, posture, or reduction in extracellular fluid volume [37,38].…”

Section: Discussionmentioning

confidence: 99%

Effect of Haemodialysis on the Control of the Circulation in Patients with Chronic Renal Failure

1985

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The mechanisms of hypotension during haemodialysis were investigated by studying cardiovascular reflexes, body fluid volumes, and osmolality in 11 patients with renal failure before and after haemodialysis and in 17 normal subjects before and after furosemide diuresis. Blood pressure and heart rate responses to tests of autonomic nervous function were unaffected in either group except that in the patients, head-up tilt after haemodialysis caused a fall in blood pressure. This was associated with a greater fall in cardiac output than before haemodialysis but with a similar rise in peripheral vascular resistance. Resting plasma noradrenaline levels were higher than normal, and the rise in plasma noradrenaline levels in response to tilt was unaffected by haemodialysis. Plasma renin activity rose in response to head-up tilt in normal subjects, but not in patients either before or after haemodialysis. Our studies indicate that changes in plasma potassium and osmolality or the possible peripheral circulatory effects of acetate do not impair the regulation of the circulation in response to haemodialysis. Haemodialysis does not reduce plasma noradrenaline levels. Impaired myocardial function in response to fluid depletion or unresponsiveness of the renin-angiotensin system may contribute to haemodialysis hypotension.

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Section: Discussionmentioning

confidence: 99%

Effect of Haemodialysis on the Control of the Circulation in Patients with Chronic Renal Failure

1985

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“…Early evidence suggested that sodium acetate solution was effective in restoring blood pH and plasma bicarbonate in patients suffering from metabolic acidosis [2]; however, a more recent study suggested that acetate was associated with hemodynamic instability, vasodilatation and negative inotropic affects in patients undergoing high volume renal replacement therapy (RRT) [3]. Concern about the potential for myocardial depression with acetate is supported by studies suggesting that acetate decreases myocardial contractilityand blood pressure in dogs [4] and impaired contractile function in anisolated perfused rat heart model [5]. Even the small quantity of acetate present in various dialysis fluids (usually 35 mmol/l) can result in plasma acetate concentrations of 10 to 40 times the physiological level (50 to 100 μmol/l) [6].…”

Section: Unbuffered/unbalanced Crystalloidsmentioning

confidence: 99%

Crystalloid Fluid Therapy

Reddy¹,

Weinberg²,

Young³

2016

Annual Update in Intensive Care and Emergency Medicine

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“…Sodium acetate has fallen into disuse as a dialysate buffer due to adverse events associated with its administration, including myocardial depression, hypotension, and hypopnea resulting in hypoxemia [22][23][24]. Sodium acetate, when given in excess during dialysis, is funneled to alternative metabolic pathways, leading to increased nitric oxide concentrations and resulting hemodynamic instability [25].…”

Section: Adverse Events From Sodium Acetatementioning

confidence: 99%

Sodium Acetate as a Replacement for Sodium Bicarbonate in Medical Toxicology: a Review

et al. 2013

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Sodium bicarbonate is central to the treatment of many poisonings. When it was placed on the FDA drug shortage list in 2012, alternative treatment strategies to specific poisonings were considered. Many hospital pharmacies, poison centers, and medical toxicologists proposed sodium acetate as an adequate alternative, despite a paucity of data to support its use in medical toxicology. The intention of this review is to educate the clinician on the use of sodium acetate and to advise them on the potential adverse events when given in excess. We conducted a literature search focused on the pharmacology of sodium acetate, its use as a buffer in pathologic acidemia and dialysis baths, and potential adverse events associated with excess sodium acetate infusion. It appears safe to replace sodium bicarbonate infusion with sodium acetate on an equimolar basis. The metabolism of acetate, however, is more complex than bicarbonate. Future prospective studies will be needed to confirm the efficacy of sodium acetate in the treatment of the poisoned patient.

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Myocardial depressant effects of sodium acetate

Cited by 56 publications

References 0 publications

Effect of Haemodialysis on the Control of the Circulation in Patients with Chronic Renal Failure

Effect of Haemodialysis on the Control of the Circulation in Patients with Chronic Renal Failure

Crystalloid Fluid Therapy

Sodium Acetate as a Replacement for Sodium Bicarbonate in Medical Toxicology: a Review

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