Acute Hypercapnic Respiratory Failure Following Initiation of Hemodialysis

Abstract

INTRODUCTION:Patients receiving hemodialysis are prone to rapid changes in acid-base status with modern high-flux dialyzer membranes. These changes are rarely consequential but may be problematic in patients with hypoventilation. We present a case of acute hypercapnic respiratory failure following initiation of hemodialysis in a man with oliguric acute kidney injury (AKI) and morbid obesity with obstructive sleep apnea (OSA) and obesity hypoventilation syndrome (OHS).CASE PRESENTATION: A 75 y.o. man with CKD Stage 4 due to hypertension and diabetes was admitted for oliguric AKI. He had multiple comorbidities including morbid obesity, OSA, OHS and prior strokes. He required initiation of hemodialysis for progressive azotemia and acidemia. He had a baseline ABG this admission of pH 7.35, pCO2 47 mmHg, pO2 132 mmHg on 4 L/ min NC with a serum HCO3 25 mmol/L. He was eupneic without respiratory distress. During dialysis, he was observed to develop progressive hypoventilation with increasingly worse mentation. He was found to have acute hypercapnic respiratory failure (pH 7.01, pCO2 123 mmHg, pO2 83 mmHg while on 4 L/min NC) and placed on BiPAP with improvement. The serum HCO3 at the time of ABG was 30 mmol/L by Henderson-Hasselbach equation. Acute hypercapnic respiratory failure due to hemodialysis was suspected and he was placed on NIPPV prior to subsequent hemodialysis sessions without further episodes of acute hypercapnic respiratory failure.DISCUSSION: Dialysate prescriptions contain supraphysiologic [HCO3] that may predispose patients with underlying hypoventilation to acute hypercapnia via multiple mechanisms. Abrupt bicarbonate influx from dialysate acutely increases blood pH which can cause hypoventilation via effects on central and peripheral chemoreceptors [1]. Furthermore, the nonvolatile acids in blood react with exogenous HCO3 in the dialysate producing CO2 which then returns to the patient via venous line and transiently increases pCO2 which further contributes to hypercapnia in patients with OSA or OHS [2]. The rapid reduction in circulating [Hþ] also transiently reduces ionized calcium which may cause diaphragmatic weakness and further promote hypoventilation.CONCLUSIONS: Hemodialysis may precipitate acute hypercapnic respiratory failure in patients with known hypoventilation due to OSA and/or OHS. Identifying patients at risk of this phenomenon can facilitate early intervention or adjustment of dialysate prescription to reduce likelihood of developing acute hypercapnic respiratory failure due to rapid flux of nonvolatile acids and bicarbonate as discussed previously. We suspect that this phenomenon is underreported and further investigation is of interest.