Physiologic acid-base and electrolyte changes in acute and chronic renal failure patients.

Patients with acute and chronic renal failure are vulnerable to a wide variety of acid–base and electrolyte disturbances. The variety is related not only to predictable disturbances that arise as a consequence of impaired urinary excretion, but also to associated factors, such as intercurrent disease processes, chronic medications, and renal replacement therapy. For the sake of simplicity, this review emphasizes the pathogenesis, diagnosis, and treatment of common problems, including metabolic acidosis, hyponatremia, hypernatremia, hyperkalemia, hyperphosphatemia, and hypocalcemia. Dialytic management, addressed elsewhere in this issue, will not be discussed in detail. As background for this discussion, consider the following clinical example (pertinent aspects of the case will be discussed in the conclusion to this chapter): A 48-year-old white man was scheduled for laparoscopic repair of a paraesophageal hernia. His past medical history included hypertension, gastroesophageal reflux disease, hiatal hernia, heavy ethanol use, anxiety, and depression. Chronic medications included benazepril, potassium chloride, hydrochlorothiazide, and buspirone. He reported the ability to walk two blocks comfortably and stated that he had had a negative treadmill test. On examination in the preanesthesia testing area, he was 73 in tall and weighed 97 kg. His blood pressure was 136/94 mm Hg, his heart rate was 103 beats/min, and his respiratory frequency was 20 breaths/min. Preoperative laboratory values included hemoglobin (Hb) 15.4 g/dL, prothrombin time 13.7 seconds, partial thromboplastin time 28 seconds, serum sodium concentration ([Na+]) 138 mEq/L, serum chloride concentration ([C1−]) 92 mEq/L, potassium concentration ([K+]) 4.6 mEq/L, carbon dioxide content (CO2) 26 mEq/L, blood urea nitrogen (BUN) 17 mg/dL, serum creatinine (SCr) 1.52 mg/dL, anion gap 20 mEq/L, total calcium (Ca) 11.4 mg/dL, total magnesium (Mg) 1.8 mg/dL, total phosphate (PO4) 7.5 mg/dL. Preoperatively, he received diazepam 10 mg po, sodium citrate/citric acid 30 mL po, and midazolam 2 mg iv. In the operating room, an 18-ga peripheral intravenous catheter was inserted and a noninvasive blood pressure monitor and pulse oximeter were placed. Induction of anesthesia included fentanyl, sodium thiopental, lidocaine, and succinylcholine, followed by endotracheal intubation. Maintenance of anesthesia consisted of isoflurane, nitrous oxide, and oxygen. Cisatracurium was used for muscle relaxation. The intraoperative course was characterized by labile blood pressure, an increase in peak inspiratory pressure to 38 cm H2O after abdominal insufflation, and oliguria, with 30 mL of urine during the first 4 hours of anesthesia. Total fluids during the initial four hours consisted of 4 L of 0.9% saline. The urinary bladder catheter appeared to be patent. Because of concern about oliguria and labile blood pressure, an arterial catheter was inserted and 500 mL of 6% hetastarch was infused. At the time of arterial catheterization, arterial blood gases were as follows: pH 7.18, PaCO2 48 mm Hg, PaO2 159 mm Hg (FiO2 0.5), and HCO3− 18 mEq/L. Other laboratory values included Hb 14.2 g/dL, [Na+] 142 mEq/L, [K+] 4.7, and ionized calcium concentration [Ca2+] 3.7 mEq/L. One hour later, after receiving 50 mEq of sodium bicarbonate, 1000 mL of 0.9% saline, and another 500 mL of 6.0% hetastarch and increasing tidal volume from 930 mL to 1000 mL, repeat arterial blood gases were as follows: pH 7.13, PaCO2 60 mm Hg, PaO2 192 mm Hg (FiO2 0.5), and HCO3− 19 mEq/L. Hb had decreased to 11.9 g/dL. He remained oliguric. Further interventions included 500 mL of 6.0% hetastarch, 50 mEq of sodium bicarbonate, 1.0 g of CaCl2, and 25 g of mannitol. Despite a total crystalloid infusion of 6.5 L, urinary output remained negligible. The last two intraoperative arterial blood gases were pH 7.18, PaCO2 51 mm Hg, PaO2 197 mm Hg (FiO2 0.5), HCO3− 19 mEq/L; one hour before the end of surgery, pH 7.19, PaCO2 46 mm Hg, PaO2 203 mm Hg (FiO2 0.5), and HCO3− 17 mEq/L. At the end of surgery, Hb was 10.3 g/dL. A central venous catheter was placed, revealing that central venous pressure was 14 mm Hg. During the last 30 minutes of anesthesia, urinary output exceeded 200 mL. Total intraoperative fluids included 8 L of crystalloid and 1 L of hetastarch. Estimated blood loss was 250 mL. At the conclusion of surgery, muscle relaxation was reversed and he was extubated and transferred to the recovery room. Fifteen minutes after arrival in the postanesthesia care unit, he required reintubation for respiratory distress and received esmolol for acute hypertension (blood pressure 240/150 mm Hg). Arterial blood gases obtained shortly after intubation were pH 7.09, PaCO2 49 mm Hg, PaO2 127 mm Hg (FiO2 0.5), and HCO3− 17 mEq/L. He was transferred to the surgical intensive care unit. His blood pressure remained elevated (210/100 mm Hg). On admission to the surgical intensive care unit, laboratory values included [Na+] 141 mEq/L, [Cl−] 109 mEq/L, [K+] 4.7 mEq/L, CO2 15 mEq/L, BUN 21 mg/dL, SCr 1.74 mg/dL, anion gap 17 mEq/L, [Ca2+] 4.7 mg/dL, Mg 0.9 mg/dL, PO4 9.1 mg/dL. Arterial blood gases were pH 7.12, PaCO2 45 mm Hg, PaO2 122 mm Hg (FiO2 0.5), and HCO3− 14 mEq/L. Over the next 24 hours, metabolic acidosis resolved. He was weaned from mechanical ventilation and extubated without difficulty. The remainder of his hospital course was uneventful.