THE EFFECT IN HUMANS OF EXTRACELLULAR pH CHANGE ON THE RELATIONSHIP BETWEEN SERUM POTASSIUM CONCENTRATION AND INTRACELLULAR POTASSIUM

Burnell, James M.; Mf, Villamil; Uyeno, Ben T.; Scribner, Belding H.

doi:10.1097/00132586-195706000-00006

Cited by 44 publications

(63 citation statements)

References 2 publications

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“…Similarly, the relationship of potassium concentration to blood pH observed in human subjects with disturbances in acid-base balance (34) was not apparent in this study. It seems likely that respiratory acidosis does in fact cause a transfer of potassium into the extracellular space, but in our chronic studies renal losses probably prevent the usually observed hyperkalemia.…”

Section: Discussioncontrasting

confidence: 75%

Tissue and Renal Response to Chronic Respiratory Acidosis*

Carter¹,

Seldin²,

Teng³

1959

J. Clin. Invest.

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Section: Discussioncontrasting

confidence: 75%

Tissue and Renal Response to Chronic Respiratory Acidosis*

Carter¹,

Seldin²,

Teng³

1959

J. Clin. Invest.

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“…Table 2. Rates of renal acid excretion, PO 4 excretion, and urinary pH during control, acid infusion, equilibration, and recovery periods patient in a single creditable report (13,14). Thus, based largely on animal data exhibiting an extraordinary variance (⌬[K]p/ ⌬pH ranged from Ϫ2.4 to Ϫ16.7), it was concluded that AMA was associated with consistent hyperkalemia, but of uncertain magnitude.…”

Section: Discussionmentioning

confidence: 99%

“…Based largely on studies in anesthetized dogs but supported by an often-cited report of acute HCl and NH 4 Cl treatment of preexisting metabolic alkalosis in a single patient (13), it has been widely accepted that human AMA (of mineral acid origin) is characterized by statistically and clinically significant acute hyperkalemia of varying magnitude (14,15) and is even thought to represent a major adverse consequence of the disorder (16).…”

mentioning

confidence: 99%

Acute Metabolic Acidosis

Wiederseiner

Muser²,

Lutz

et al. 2004

Journal of the American Society of Nephrology

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Abstract. Despite the high incidence of acute metabolic acidosis, there are no reliable human data to enable physicians to accurately diagnose this disorder. In addition, there is uncertainty about the direction and magnitude of plasma potassium changes in acute metabolic acidosis. The systemic and renal acid-base, electrolyte, and endocrine response to acute acid loads (imposed by three timed NH 4 Cl infusions into the duodenum, 0.9 mmol of NH 4 Cl per kg of body weight over 30 min each) was characterized in six healthy male subjects in whom a metabolic steady-state had been established. Arterialized blood CO 2 tension decreased by 0.85 mmHg per mmol/L decrease in plasma bicarbonate concentration and blood hydrogen ion concentration increased by 0.45 nmol/L per mmol/L decrease in plasma bicarbonate concentration. Plasma potassium did not change significantly (ϩ0.02 Ϯ 0.02 mmol/L per mmol decrease in plasma bicarbonate concentration). Plasma insulin increased and plasma glucagon levels decreased in acute metabolic acidosis, while catecholamines and aldosterone were not affected significantly. These data provide the first diagnostic criteria for the diagnosis of acute metabolic acidosis in humans. The finding of a hyperinsulinemic response in acute metabolic acidosis suggests that an insulin response counterregulates any acidemia-induced cellular potassium efflux, resulting in stable plasma potassium concentrations.

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“…Alkalosis causes an intracellular shift of potassium [13,14]. Excessive urinary excretion of bicarbonate takes sodium along with it, followed by potassium as sodium is depleted [15].…”

mentioning

confidence: 99%

Baking Soda Can Settle the Stomach but Upset the Heart: Case Files of the Medical Toxicology Fellowship at the University of California, San Francisco

Al-Abri

Olson

2013

J. Med. Toxicol.

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A 50-year-old man with a past medical history of diabetes mellitus, hypertension, and Zollinger-Ellison syndrome came to the emergency department (ED) with a history of increasing vomiting and diarrhea for 1 week and poor oral intake for a few days. He described generalized weakness and lethargy the day before presentation. During the initial ED evaluation, he suddenly had an episode of ventricular tachycardia treated with a single synchronized cardioversion followed by an amiodarone drip. His initial laboratory investigation revealed marked hypokalemia (potassium 2.0 mEq/L), hyponatremia (sodium 122 mEq/L), hypochloremia (59 mEq/L), and elevated serum bicarbonate (46 mEq/L). The BUN was 8 mg/dL, creatinine was 0.9 mg/dL, and glucose was >600 mg/dL. Arterial blood gases revealed a pH of 7.6, pO 2 100 mm Hg, pCO 2 59 mm Hg, and calculated bicarbonate 60 mEq/L. Serum calcium was 8.1 mg/dL, magnesium 1.6 mg/dL, phosphate 1.3 mg/dL, and albumin 2.7 g/L.On further questioning, it was discovered that the patient had been experiencing persistent heartburn and gastric upset for the past 7 years following gastrinoma removal. He had not been compliant with his usual medication regimens for hypertension, diabetes, and gastric hyperacidity and had been using baking soda as an antacid, adding a teaspoon of the white powder to his drinks on an as-needed basis daily for years.

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THE EFFECT IN HUMANS OF EXTRACELLULAR pH CHANGE ON THE RELATIONSHIP BETWEEN SERUM POTASSIUM CONCENTRATION AND INTRACELLULAR POTASSIUM

Cited by 44 publications

References 2 publications

Tissue and Renal Response to Chronic Respiratory Acidosis*

Tissue and Renal Response to Chronic Respiratory Acidosis*

Acute Metabolic Acidosis

Baking Soda Can Settle the Stomach but Upset the Heart: Case Files of the Medical Toxicology Fellowship at the University of California, San Francisco

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