The effect of metabolic alkalosis on the ventilatory response in healthy subjects

Abstract

A B S T R A C TBackground: Patients with acute respiratory failure may develop respiratory acidosis. Metabolic compensation by bicarbonate production or retention results in posthypercapnic alkalosis with an increased arterial bicarbonate concentration. The hypothesis of this study was that elevated plasma bicarbonate levels decrease respiratory drive and minute ventilation. Methods: In an intervention study in 10 healthy subjects the ventilatory response using a hypercapnic ventilatory response (HCVR) test was assessed, before and after administration of high dose sodium bicarbonate. Total dose of sodiumbicarbonate was 1000 ml 8.4% in 3 days. Results: Plasma bicarbonate increased from 25.2 ± 2.2 to 29.2 ± 1.9 mmol/L. With increasing inspiratory CO 2 pressure during the HCVR test, RR, V t , Pdi, EAdi and V E increased. The clinical ratio ΔV E /ΔP et CO 2 remained unchanged, but Pdi, EAdi and V E were significantly lower after bicarbonate administration for similar levels of inspired CO 2 . Conclusion: This study demonstrates that in healthy subjects metabolic alkalosis decreases the neural respiratory drive and minute ventilation, as a response to inspiratory CO 2 .

The Effects of Furosemide usage on Organ System Failure Status based on Modified Sequential Organ Failure Assessment Score in Critically ill Patient

“…[13] is is because of a serum bicarbonate level 2 mEq/L more than others, in which metabolic alkalosis could also affect the respiratory drive and minute ventilation. [14] e result of this study is not supported by DOSE-AHF study that shows diuretic benefits on curing organ system dysfunction caused by fluid overload (including cerebral edema, pulmonary edema, myocardial edema, hepatic congestion, renal interstitial edema, and intestinal edema). [8] However, previous research supports the result of the study, stating that diuretic usage causes acute kidney injury and increases the mortality of patients with 1.68 odd ratios.…”

Prolonged Weaning: S2k Guideline Published by the German Respiratory Society

“…All organs including the respiratory muscles have a basal metabolic supply, whose impairment through metabolic disorders (hypo/hyperthyroidism, adrenal insufficiency, hyperglycaemia), electrolyte disorders (hyperkalaemia, magnesium and phosphate deficiencies), albumin deficiency, or exogenous endocrine factors such as glucocorticoidsteroid therapy, can lead to functional disorders [17, 45, 121]. Furthermore, metabolic alkalosis can promote weaning failure by attenuating respiratory drive with compensatory hypercapnia [122, 123]. Similarly, metabolic acidosis should also be considered as a cause of prolonged weaning, since it places a further strain on the already overloaded respiratory pump through ventilatory compensation [124].…”

SARS-CoV-2 (COVID-19) and intravascular volume management strategies in the critically ill

“…41 Since patients receiving diuretics had a serum bicarbonate level of 2 mEq/L above others, and metabolic alkalosis can reduce the neural respiratory drive and minute ventilation, the authors argued that the metabolic side effect of diuretics could contribute to the observed mechanical ventilation weaning difficulties. 41,42 In the face of positive fluid balance during the de-escalation phase of sepsis management, one might consider earlier application of renal replacement therapy (RRT), especially in those patients with more severe volume overload, progressive metabolic alkalosis with diuretic use, suboptimal diuretic response or diuretic refractoriness, and development of oliguric AKI. In light of evidence on the detrimental impact of RRT use for treatment of sepsis (through clearance of inflammatory mediators and cytokines), 43 RRT should be considered only if indicated for optimization of volume status or treatment of azotemia.…”