Acid-Base Balance

Effros, Richard M.; Swenson, Erik R.

doi:10.1016/b978-1-4557-3383-5.00007-5

Cited by 8 publications

(3 citation statements)

References 76 publications

(75 reference statements)

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“…Healthy people at high altitude [ 54 ] or persons hyperventilating to non-hypoxic stimuli (drugs with respiratory stimulant activity, severe anxiety, hepatic encephalopathy, brain lesions) can become quite alkalotic and alkalemic with arterial pH acutely rising as high as 7.7 and PaCO 2 falling to as low 10 mmHg (reviewed in Ref. [ 43 ]). Respiratory alkalosis alters, both negatively and positively, many hypoxic responses involved in enhancing tissue O 2 delivery and utilization .…”

Section: Hypoxia and Respiratory Alkalosis At High Altitudementioning

confidence: 99%

Hypoxia and Its Acid–Base Consequences: From Mountains to Malignancy

Swenson

2016

Advances in Experimental Medicine and Biology

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Hypoxia, depending upon its magnitude and circumstances, evokes a spectrum of mild to severe acid-base changes ranging from alkalosis to acidosis, which can alter many responses to hypoxia at both non-genomic and genomic levels, in part via altered hypoxia-inducible factor (HIF) metabolism. Healthy people at high altitude and persons hyperventilating to non-hypoxic stimuli can become alkalotic and alkalemic with arterial pH acutely rising as high as 7.7. Hypoxia-mediated respiratory alkalosis reduces sympathetic tone, blunts hypoxic pulmonary vasoconstriction and hypoxic cerebral vasodilation, and increases hemoglobin oxygen affinity. These effects and others can be salutary or counterproductive to tissue oxygen delivery and utilization, based upon magnitude of each effect and summation. With severe hypoxia either in the setting of profound arterial hemoglobin desaturation and reduced O2 content or poor perfusion (ischemia) at the global or local level, metabolic and hypercapnic acidosis develop along with considerable lactate formation and pH falling to below 6.8. Although conventionally considered to be injurious and deleterious to cell function and survival, both acidoses may be cytoprotective by various anti-inflammatory, antioxidant, and anti-apoptotic mechanisms which limit total hypoxic or ischemic-reperfusion injury. Attempts to correct acidosis by giving bicarbonate or other alkaline agents under these circumstances ahead of or concurrent with reoxygenation efforts may be ill advised. Better understanding of this so-called "pH paradox" or permissive acidosis may offer therapeutic possibilities. Rapidly growing cancers often outstrip their vascular supply compromising both oxygen and nutrient delivery and metabolic waste disposal, thus limiting their growth and metastatic potential. However, their excessive glycolysis and lactate formation may not necessarily represent oxygen insufficiency, but rather the Warburg effect-an attempt to provide a large amount of small carbon intermediates to supply the many synthetic pathways of proliferative cell growth. In either case, there is expression and upregulation of many genes involved in acid-base homeostasis, in part by HIF-1 signaling. These include a unique isoform of carbonic anhydrase (CA-IX) and numerous membrane acid-base transporters engaged to maintain an optimal intracellular and extracellular pH for maximal growth. Inhibition of these proteins or gene suppression may have important therapeutic application in cancer chemotherapy.

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Section: Hypoxia and Respiratory Alkalosis At High Altitudementioning

confidence: 99%

Hypoxia and Its Acid–Base Consequences: From Mountains to Malignancy

Swenson

2016

Advances in Experimental Medicine and Biology

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“…The respiratory alkalosis was the result of compensation for the metabolic acidosis. Usually, in physiology, the result of compensation is moving the pH back to the normal range but would never move to the side of alkalemia [ 9 , 10 ]. In other words, the body never overcompensates for the primary process.…”

Section: Discussionmentioning

confidence: 99%

Detecting Concealing Heart Failure in a Young Alcohol-Related Liver Failure Patient Using the Most Basic Pathophysiological Principle

Lyu¹,

Miskovsky²

2022

Cureus

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Long-term alcohol abuse can cause alcohol-related liver injury (acute alcoholic hepatitis, acute liver failure, hepatic steatosis, fibrosis, or cirrhosis), as well as cardiac injury. Alcoholic cardiomyopathy is a severe consequence of chronic alcohol abuse. Incidence of alcoholic cardiomyopathy ranges from 1-2% of all heavy alcohol users. In the United States, excess alcohol consumption contributes to more than 10% of cases of heart failure. Here, we present a case of a 41-year-old male patient with severe alcohol abuse who presented with signs and symptoms of liver failure and was found to have severe left ventricular systolic dysfunction and dilated cardiomyopathy. More interestingly, the detection of heart failure in this patient was convoluted but also represented an amazing example of how the most basic pathophysiological principles help answer clinical questions in a perplexing scenario. The patient is a 41-year-old Caucasian male with severe alcohol abuse who presented with complaints of diffuse yellowish discoloration of skin, fatigue, and "feeling not like himself” for six weeks. A review of systems revealed mild exertional dyspnea and bilateral lower extremity swelling. Physical exam was remarkable for diffuse jaundice involving the whole body, tachycardia, and trace edema in the lower extremity bilaterally. Otherwise, lungs were clear to auscultation, normal heart sounds with regular heart rate and rhythm, no Jugular vein distention, and no carotid bruits were appreciated. Labs showed elevated total bilirubin, aspartate aminotransferase (AST), alanine aminotransferase (ALT), ammonia, and lactate levels. Notably, venous blood gas (VBG) showed metabolic acidosis with compensating respiratory alkalosis with normal potential Hydrogen (pH). An electrocardiogram showed sinus tachycardia. Treatment was started for acute alcoholic liver failure, with intravenous fluids, intravenous prednisolone, and Clinical Institute Withdrawal Assessment for Alcohol (CIWA) protocol. The patient’s liver function markers went down stably. However, the patient’s mental status got worse and his lactate levels continued to rise. He was prescribed empirical antibiotics with a pan Computed tomography (CT) scan to look for any source of infection which revealed no meaningful positive findings. Surprisingly and interestingly, the venous blood gas pH started to trend up demonstrating alkalotic pH which contrasted the initial normal pH on admission. The metabolic acidosis was seemingly “over-compensated” by respiratory alkalosis. It was speculated that another underlying pathology existed to count for respiratory alkalosis. Chest X-ray (CXR) showed cardiomegaly but no pneumonia. An echocardiogram showed severe left ventricular systolic dysfunction with an Ejection Fraction of 20% and dilated left ventricle. The treatment direction was switched from treating liver failure to targeting heart failure with intravenous diuretics. The patient’s mental status improved remarkably after three days of diuresis and the patient wa...

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“…The pathophysiology of metabolic alkalosis consists mainly of 2 parts: (1) loss of hydrogen and (2) increase of bicarbonate. The primary causes of the maintenance of metabolic alkalosis include (1) reduction of effective circulating volume, (2) chloride deficiency, (3) hypokalemia, and (4) decreased renal function [ 3 – 5 ]. In the present case, the main cause of metabolic alkalosis may have been volume depletion or chloride deficiency.…”

Section: Discussionmentioning

confidence: 99%

Aldosterone Response in Severe Hypokalemia and Volume Depletion: A Case Report and Review of the Recent Research

Kai

Tominaga

Uchida

et al. 2016

Case Reports in Nephrology

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We report a case of severe hypokalemia and volume depletion complicated by chronic watery diarrhea resulting from chronic alcoholism in a 57-year-old man. Prompt replacement of normal saline with potassium chloride and cessation of alcohol intake resulted in a favorable outcome. We discuss the pathophysiology of the case, emphasizing the response of aldosterone in both hypokalemia and volume depletion, and provide a review of recent research.

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Acid-Base Balance

Cited by 8 publications

References 76 publications

Hypoxia and Its Acid–Base Consequences: From Mountains to Malignancy

Hypoxia and Its Acid–Base Consequences: From Mountains to Malignancy

Detecting Concealing Heart Failure in a Young Alcohol-Related Liver Failure Patient Using the Most Basic Pathophysiological Principle

Aldosterone Response in Severe Hypokalemia and Volume Depletion: A Case Report and Review of the Recent Research

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