Acidosis: Difference between revisions

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(/* Causes in Alphabetical Order Sailer, Christian, Wasner, Susanne. Differential Diagnosis Pocket. Hermosa Beach, CA: Borm Bruckmeir Publishing LLC, 2002:77 ISBN 1591032016 Kahan, Scott, Smith, Ellen G. In A Page: Signs and Symptoms. Malden, Massa...)
(/* Causes in Alphabetical Order Sailer, Christian, Wasner, Susanne. Differential Diagnosis Pocket. Hermosa Beach, CA: Borm Bruckmeir Publishing LLC, 2002:77 ISBN 1591032016 Kahan, Scott, Smith, Ellen G. In A Page: Signs and Symptoms. Malden, Massa...)
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*Hypotension
*Hypotension
*Hypotensive state
*Hypotensive state
*[[Hypothermic shivering ]]
*Hypothermic shivering  
*[[Hypovolemia]]  
*[[Hypovolemia]]  
*[[Hypoxia]]  
*[[Hypoxia]]  
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*[[Isopropyl alcohol]]  
*[[Isopropyl alcohol]]  
*[[Ketoacidosis]]
*[[Ketoacidosis]]
*[[Kidney disorders]]
*Kidney disorders
*[[Leukemia]]
*[[Leukemia]]
*[[Liver disease  ]]  
*[[Liver disease  ]]  
*[[Loss of bicarbonate or bicarbonate precursors   ]]
*Loss of bicarbonate or bicarbonate precursors  
*[[Lymphoma]]  
*[[Lymphoma]]  
*[[Malignant hyperpyrexia ]]  
*[[Malignant hyperpyrexia ]]  
*[[Malignant hypertension]]  
*[[Malignant hypertension]]  
*[[Malignant neoplastic conditions Myeloma ]]  
*Malignant neoplastic conditions [[Myeloma]]
*[[Maple syrup urine disease]]  
*[[Maple syrup urine disease]]  
*[[Mesenteric insufficiency]]
*Mesenteric insufficiency  
*[[Methanol]]  
*[[Methanol]]  
*[[Mitochondrial encephalomyopathy]]
*Mitochondrial encephalomyopathy
*[[Mitochondrial myopathy]]
*[[Mitochondrial myopathy]]
*[[Mitochondrial toxicity]]  
*[[Mitochondrial toxicity]]  
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*[[Pheochromocytoma ]]  
*[[Pheochromocytoma ]]  
*[[Pickwickian syndrome]]
*[[Pickwickian syndrome]]
*[[Posttreatment of ketoacidosis ]]  
*Posttreatment of [[ketoacidosis ]]  
*[[Propylene glycol      ]]  
*[[Propylene glycol      ]]  
*[[Proximal renal tubular acidosis]]
*[[Proximal renal tubular acidosis]]
*[[Pseudohypoaldosteronism type 1, autosomal dominant ]]
*Pseudohypoaldosteronism type 1, autosomal dominant  
*[[Pseudohypoaldosteronism type 1, autosomal recessive ]]
*Pseudohypoaldosteronism type 1, autosomal recessive
*[[Pseudohypoaldosteronism type 2 ]]
*Pseudohypoaldosteronism type 2  
*[[Pulmonary Embolism]]  
*[[Pulmonary Embolism]]  
*[[Pulseless electrical activity]]  
*[[Pulseless electrical activity]]  
*[[Reduced oxygen utilization ]]
*Reduced oxygen utilization
*[[Renal circulatory insufficiency]]
*Renal circulatory insufficiency  
*[[Renal failure]]
*[[Renal failure]]
*[[Renal tubular acidosis]]  
*[[Renal tubular acidosis]]  
*[[Salicylate]]  
*[[Salicylate]]  
*[[Sepsis]]  
*[[Sepsis]]  
*[[Severe anaemia]]
*Severe [[anaemia]]
*[[Severe asthma ]]  
*Severe [[asthma ]]  
*[[Severe burns]]
*Severe [[burns]]
*[[Severe diarrhoea]]
*Severe [[diarrhoea]]
*[[Severe exercise]]
*Severe exercise
*[[Severe hepatopathy]]
*Severe hepatopathy  
*[[Severe hypoxemia (PO2 <25 to 30 mmHg) ]]
*Severe hypoxemia
*[[Severe liver disease]]
*Severe liver disease
*[[Shock]]  
*[[Shock]]  
*[[Short bowel syndrome ]]
*[[Short bowel syndrome ]]
*[[Small intestine fistula]]
*Small intestine [[fistula  
*[[Splenic infarction]]
*[[Splenic infarction]]
*[[ST Elevation Myocardial Infarction Complications]]
*[[ST Elevation Myocardial Infarction Complications]]

Revision as of 21:24, 26 June 2013

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List of terms related to Acidosis

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Overview

For acidosis referring to acidity of the urine, see renal tubular acidosis.

Acidosis is an increased acidity (i.e. an increased hydrogen ion concentration). If not further qualified, it refers to acidity of the blood plasma.

Generally, acidosis is said to occur when arterial pH falls below 7.35, while its counterpart (alkalosis) occurs at a pH over 7.45. Arterial blood gas analysis and other tests are required to separate the main causes.

Strictly speaking, the term acidemia would be more appropriate to describe the state of low blood pH, reserving acidosis to describe the processes leading to these states. Nevertheless, most physicians use the terms interchangeably. The distinction may be relevant where a patient has factors causing both acidosis and alkalosis, where the relative severity of both determines whether the result is a high or a low pH.

The rate of cellular metabolic activity affects and, at the same time, is affected by the pH of the body fluids. In mammals, the normal pH of arterial blood lies between 7.35 and 7.50 depending on the species (e.g. healthy human-arterial blood pH varies between 7.35 and 7.45). Blood pH values compatible with life in mammals are limited to a pH range between 6.8 and 7.8. Changes in the pH of arterial blood (and therefore the extracellular fluid) outside this range result in irreversible cell damage (Needham, 2004).

Classification

  • Acidosis can either be metabolic or respiratory.
    • Both are caused by low arterial pH.
    • Metabolic acidosis is due to an increased accumulation of acid equivalents through impairment of the regulatory ability of the liver, kidneys, or metabolism.
    • Respiratory acidosis is caused by a retention of carbon dioxide due to inadequate hypoventilation or pulmonary ventilation.

Pathophysiology

Respiratory acidosis

Respiratory acidosis results from a build-up of carbon dioxide in the blood (hypercapnia) due to hypoventilation. It is most often caused by pulmonary problems, although head injuries, drugs (especially anaesthetics and sedatives), and brain tumors can also bring it on. Emphysema, chronic bronchitis, asthma, severe pneumonia, and aspiration are among the most frequent causes. It can also occur as a response to chronic metabolic alkalosis.

Blood gases show pH below 7.35 as above mentioned, and PaCO2 will be high (>45 mmHg / 6 kPa).

The key to distinguish between respiratory and metabolic acidosis is that in respiratory acidosis, the CO2 is increased while the bicarbonate is either normal (uncompensated) or increased (compensated). Compensation occurs if respiratory acidosis persists for days or longer and a chronic phase is entered with partial buffering of the acidosis through renal bicarbonate retention.

Metabolic acidosis

Metabolic acidosis may result from disturbances in the ability to excrete acid via the kidneys. Renal acidosis is associated with an accumulation of urea and creatinine as well as metabolic acid residues of protein catabolism.

An increase in the production of metabolic acids may also produce metabolic acidosis. For example, lactic acidosis may occur from 1) severe (PaO2 <36mm Hg) hypoxemia causing a fall in the rate of oxygen diffusion from arterial blood to tissues, or 2) hypoperfusion (e.g. hypovolemic shock) causing an inadequate blood delivery of oxygen to tissues. A rise in lactate out of proportion to the level of pyruvate, e.g. in mixed venous blood, is termed "excess lactate" and is the best indicator of an inadequate flow of oxygen into the body's mitochondria from either cause. Oxygen debt (and muscle excess lactate) is also seen in strenuous exercise. Once oxygenation is restored, the acidosis clears quickly. Another example of increased production of acids occurs in starvation and diabetic acidosis. It is due to the accumulation of ketoacids (ketosis) and reflects a severe shift from glycolysis to lipolysis for fuel needs.

Acidic poisons, iron etc., and decreased production of bicarbonate may also produce metabolic acidosis.

Metabolic acidosis can result in stimulation of chemoreceptors and so increase alveolar ventilation, leading to respiratory compensation, otherwise known as Kussmaul breathing, which is a specific type of hyperventilation. Should this situation persist the patient is at risk for exhaustion leading to respiratory failure.

Mutations to the V-ATPase 'a4' or 'B1' isoforms result in distal renal tubular acidosis—a condition that leads to metabolic acidosis—in some cases with sensorineural deafness.

In blood gas tests, it is characterised by a low pH, low blood HCO3, and normal or low PaCO2. In addition to arterial blood gas one can use the anion gap to differentiate between possible causes.

The Henderson-Hasselbalch equation is useful for calculating blood pH, because blood is a buffer solution. The amount of metabolic acid accumulating can also be quantitated by using buffer base deviation, a derivative estimate of the metabolic as opposed to the respiratory component. In hypovolemic shock for example, approximately 50% of the metabolic acid accumulation is lactic acid, which disappears as blood flow and oxygen debt are corrected.

Causes

Common causes of acidosis


Causes by Organ System

Cardiovascular No underlying causes
Chemical/Poisoning No underlying causes
Dental No underlying causes
Dermatologic No underlying causes
Drug Side Effect No underlying causes
Ear Nose Throat No underlying causes
Endocrine No underlying causes
Environmental No underlying causes
Gastroenterologic No underlying causes
Genetic No underlying causes
Hematologic No underlying causes
Iatrogenic No underlying causes
Infectious Disease No underlying causes
Musculoskeletal/Orthopedic No underlying causes
Neurologic No underlying causes
Nutritional/Metabolic No underlying causes
Obstetric/Gynecologic No underlying causes
Oncologic No underlying causes
Ophthalmologic No underlying causes
Overdose/Toxicity No underlying causes
Psychiatric No underlying causes
Pulmonary No underlying causes
Renal/Electrolyte No underlying causes
Rheumatology/Immunology/Allergy No underlying causes
Sexual No underlying causes
Trauma No underlying causes
Urologic No underlying causes
Miscellaneous No underlying causes


Causes in Alphabetical Order [1] [2]


Respiratory Acidosis


Treatment

Treatment of any of the varieties of metabolic acidosis is focused upon correction of the underlying problem. However, neutralizing the acidosis with infusions of bases like sodium bicarbonate may be temporarily helpful in some critical emergencies.

References

  1. Sailer, Christian, Wasner, Susanne. Differential Diagnosis Pocket. Hermosa Beach, CA: Borm Bruckmeir Publishing LLC, 2002:77 ISBN 1591032016
  2. Kahan, Scott, Smith, Ellen G. In A Page: Signs and Symptoms. Malden, Massachusetts: Blackwell Publishing, 2004:68 ISBN 140510368X

External Links

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