bicarbonate 28 mEq/L, and creatinine4.5 mg/dL.His ventilatory status was stabilized,and 4 hours later he was transitioned tobi-level positive airway pressure ventila-tion (BIPAP). About 8 hours later, hisABG was pH 7.32, PCO
75 mmHg, and serum bicarbonate30 mEq/L. Based on his previouspre-dialysis blood bicarbonate, we pro-vided hemodialysis for him with a reduceddialysate bicarbonate concentration,28 mEq/L for his ﬁrst ICU dialysis runand 30 mEq/L for the second run on thefollowing day. He tolerated both runswithout any adverse respiratory event. Hewas weaned off BIPAP after the seconddialysis and transferred back to the regularmedical unit. During his subsequenthemodialysis, the dialysate bicarbonateconcentration was adjusted to between27 and 30 mEq/L according to his status.He was discharged 2 weeks later. Hisin-patient dialysis history was conveyedto his out-patient dialysis unit.
Acute bicarbonate inﬂux during dialysis,although traditionally considered a benigncondition, can potentially be detrimental.In our patient, the tight temporal asso-ciation of the dialysis initiation and onsetof acute hypercapnic respiratory failure,and the subsequent tolerability of dialysiswith a reduced bicarbonate concentration,indicate that the abrupt bicarbonate inﬂuxduring dialysis was the initial trigger of hisrespiratory decompensation.Pre-dialysis metabolic acidosis is aprominent feature in dialysis patients. Ananuric, non-hypercatabolic dialysis patientretains ~70-80 mEq of H
daily. The aniongap is typically elevated in this settingas the retained anions (phosphate, sul-fate, urate, and hippurate) are non-vola-tile. Adverse sequelae from sustainedmetabolic acidosis are multiple, includingnegative nitrogen balance, protein wast-ing, anorexia, fatigue, bone loss, depres-sion of cardiac contractility, arrhythmias,gastrointestinal disturbances, hormonalderangements, insulin resistance, hyperka-lemia, altered gluconeogenesis and triglyc-eride metabolism, and (in children) growthretardation.
Hemodialysis corrects acidosis andmitigates the academia-associated detri-mental effects. However, abrupt bicarbon-ate inﬂux through this mechanism cantrigger several adverse effects. First
anacute raise in blood pH can cause hypoven-tilation and respiratory depression. Thiseffect is well known and is mediated viaboth central and peripheral chemorecep-tors.
Second, alkalosis depresses tissueoxygen delivery by inducing vasoconstric-tion and by shifting the oxygen disso-ciation curve to the left, thereby impairinghemoglobin’s ability to release oxygen.
Alkalosis-induced tissue hypoxemia canthus adversely affect vital organs, includingcerebral, cardiovascular, and pulmonaryfunctions. Third, abrupt reduction in thecirculating H
concentration (neutralized bybicarbonate inﬂux) acutely reduces the cir-culating ionized pool of calcium, leading tofunctional hypocalcemia and ensuing neu-romuscular/end-organ functional impair-ment, including diaphragmatic muscleweakness.Although bicarbonate administration-related disadvantages are well known,they have not been the focus of our dailypractice because bicarbonate providedthrough routine dialysis has not beenshown to be overtly consequential. Twofactors are likely attributable to such asubclinical presentation: 1) the bicarbon-ate load with dialysis, although high, isnot extremely excessive; and 2) the body’scompensatory mechanisms, including CO
exhalation (which was compromised inour patient), are able to buffer the acutebicarbonate-mediated effects. Thus, bicar-bonate inﬂux via dialysis is generally welltolerated, although cases of extremelyhigh alkali/bicarbonate administrationabove and beyond the capacity of com-pensatory mechanisms have been reportedand are associated with serious clinicalconsequences.
In our patient, the initial bicarbon-ate-loading triggered adverse effectswere augmented by his severely compro-mised reserve (morbid obesity, underlyingCOPD, congestion, and recent pneumo-nia). The arterial blood gas obtained dur-ing resuscitation already showed that hehad developed CO
retention and respi-ratory acidosis. Nonetheless, his calcu-lated bicarbonate concentration at thattime was still high, consistent with highbicarbonate inﬂux from dialysis. If theblood gas were obtained before the onsetof respiratory failure, he would most cer-tainly have been alkalemic. As shown in
, his baseline COPD/chronicCO
retention and the recent lung paren-chymal injury (pneumonia) rendered him
Proposed pathogenesis of the patient’s acute respiratory failure. A, The sequelaeof abrupt bicarbonate infusion at dialysis. B, The genesis of acute CO
accumulation. COPD,chronic obstructive pulmonary disease.
Dialysis & Transplantation
2/10/11 9:57:32 AM