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Acute Hypercapnic Respiratory Failure Associated With Hemodialysis

Acute Hypercapnic Respiratory Failure Associated With Hemodialysis

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Published by Mahmoud Diaa

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Published by: Mahmoud Diaa on Aug 28, 2011
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02/20/2014

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P
atients undergoing chronic hemo-dialysis are regularly subject toacute shifts in extracellular acid-base balance. In the intervalbetween dialysis treatments, they accu-mulate non-volatile acidic metabolites andbecome progressively acidemic. Theseacids are acutely neutralized and “cleanedoff” at each dialysis session. Routinelyused superphysiological bicarbonate con-centration (37 meq/L HCO
3
) in dialysatecorrects the acidosis and creates an initialmild metabolic alkalosis at the end of eachdialysis. Such acid-base changes are rapidwith modern-day high-flux dialyzers.In patients with adequate pulmonaryreserve, the dialysis-associated acid-baseshift is overcome primarily via respira-tory compensation. In general, blood pH(with compensation) at the end of eachdialysis is kept at near physiological range.However, in patients with severe underly-ing pulmonary structural and functionalabnormalities, routinely employed dialysisprescription may not be tolerated and canbe potentially detrimental.We present a case of acute respiratoryfailure temporally associated with hemo-dialysis initiation, consistent with acutehypercapnia triggered by rapid bicar-bonate influx from dialysis. This caseunderscores the importance of individual-izing dialysis prescriptions for patientswith compromised pulmonary ventilatoryreserve.
Case Report
A 55-year-old man with kidney failure dueto diabetes and hypertension, on intermit-tent hemodialysis thrice weekly for theprior 5 years, was admitted for acute pneu-mococcal pneumonia. He had multiplemedical comorbidities including morbidobesity (weight: 136 kg, body mass index:44), chronic obstructive pulmonary disease(COPD) with hypercapnia (baseline arterialblood gas on room air: pH 7.37, PCO
2
48mmHG, PO
2
84 mmHG [on a non-dialysisday] and pre-dialysis blood HCO
3
: 24-29 mEq/L), and heart failure (ejectionfraction: 44%). He required mechanicalventilation, and infection was effectivelycontrolled with antibiotics.By hospital day 5, he was weaned off ventilation and resumed oral intake (fromNG tube feeds). He had been maintainedon his regular dialysis schedule and pre-scription of 37 mEq/L dialysate bicarbon-ate since admission. At his first dialysispost extubation (hospital day 7), he wasnoted to be exceedingly drowsy, but awak-able, and his digital O
2
saturations werestable (
90%). On his subsequent dialysis(hospital day 9), he developed acute hypop-nea and hypoxia (O
2
saturation
50%)at ~15-20 minutes after being connectedto the dialyzer. The dialysis was prompt-ly discontinued, and oxygen provided.However, he remained hypopneic andbecame unresponsive, requiring resuscita-tion and intubation. His arterial blood gasduring resuscitation (~10 minutes after thediscontinuation of the dialysis) was pH7.22, PCO
2
78 mmHg, PO
2
66 mmHg, andcalculated HCO
3
32 mEq/L. The patientwas transferred to the medical intensivecare unit (ICU).On examination in the ICU, he wasresponsive, with a pulse of 92/min, respi-ratory rate 18/min, O
2
saturation 96% onmechanical ventilation (assist control, rateof 14, low tidal volume of 500 mL toprevent lung injury, PEEP of 5 and FIO
2
of 40%), blood pressure 112/52 mmHg,and temperature 37.5ºC. His breath soundswere reduced, and scattered crackles werenoted at bilateral lung bases. His heartrate was regular, without murmurs orrubs, abdomen obese and non-tender, andextremities without edema. His chest x-rayshowed cardiomegaly, pulmonary infil-trates, and vascular congestion, which wasnot significantly different from the x-rayon the prior day. Laboratory study resultsafter ICU arrival were as follows: WBCcount 8.5
10
9
 /L, hemoglobin 9.2 g/dL,sodium 130 mEq/L, potassium 5.1 mEq/L,
Acute Hypercapnic Respiratory FailureAssociated With Hemodialysis
Carlos R. Franco Palacios, MD; Abdullah Altayeh, MD; Qi Qian, MD Drs. Palacios and Qian are with the Department of Medicine, Division of Nephrology and Hypertension, and Dr. Altayehis with the Department of Critical Care Medicine, Mayo Clinic, College of Medicine, Rochester, Minnesota.
Patients undergoing hemodialysis are subject to recurrent acid-base perturbations. Prior to each dialysis treatment,they are relatively acidemic, which is corrected rapidly during dialysis. We report a patient with obesity, obstructivelung disease, and pneumonia who developed acute respiratory failure triggered by an influx of high bicarbonateduring dialysis. This case emphasizes that in patients with severely compromised respiratory reserve, a largeamount of bicarbonate influx during hemodialysis may cause acute CO
2
accumulation and ventilatory distress. Anindividualized approach with judicious adjustment of the dialysate bicarbonate concentration may be necessary.
DOI: 10.1002/dat.20506
February 2011
Dialysis & Transplantation
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Case Report
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
2
60 mmHg,PO
2
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.
Discussion
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.
1
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.
2
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.
3
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
2
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.
4,5
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
2
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
Figure 1A
, his baseline COPD/chronicCO
2
retention and the recent lung paren-chymal injury (pneumonia) rendered him
FIGURE 1.
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.
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