Acidosis
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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
- Traumatic shock
- Sepsis
- Severe hypoxemia
- Severe diarrhoea
- Renal failure
- Multiple organ dysfunction syndrome
- Nausea and Vomiting
- Mesenteric insufficiency
- Ketoacidosis
- Ischemic colitis
- Hypotension
- Ethanol ingestion
- Cardiogenic shock
- Alcohol
- Acetylsalicylic acid
Causes by Organ System
| Cardiovascular |
Acute pulmonary edema, beriberi heart disease, cardiac arrest, cardiogenic shock, cardiogenic shock, cardiomyopathy hypotonia, cataract and cardiomyopathy, congestive heart failure, hemorrhagic shock, hypoperfusion , hypotension, hypotensive state malignant hypertension, myocardial Infarction, pulseless electrical activity, shock, ST Elevation myocardial infarction complications, torsade de pointes, ventricular arrhythmias, ventricular fibrillation |
| Chemical/Poisoning | Salicylate , Propylene glycol , Methanol , Isopropyl alcohol , Diethylene glycol , Cyanide intoxication , Cocaine , Carbon monoxide poisoning , Alcohol , Ethylene glycol |
| Dental | No underlying causes |
| Dermatologic | No underlying causes |
| Drug Side Effect | Zidovudine Oral , Zalcitabine , Therapy with carbonic anhydrase inhibitor , Phenformin , Paracetamol , Glyburide and Metformin , Ethylene glycol ,Ethanol ingestion , Didanosine , Carbonic anhydrase inhibitors , Biguanide , Aspirin , Acetylsalicylic acid , Acetazolamide, Pergolide |
| Ear Nose Throat | No underlying causes |
| Endocrine | Thyrotoxicosis , Pseudohypoaldosteronism type 2 , Pseudohypoaldosteronism type 1, autosomal recessive , Pseudohypoaldosteronism type 1, autosomal dominant , Posttreatment of ketoacidosis , Pheochromocytoma , Ketoacidosis , Hypoglycemia , Hyperosmolar non-ketotic diabetic coma , Diabetic Ketoacidosis , Diabetes , Adrenal cortex insufficiency |
| Environmental | Hypothermic shivering, Drowning |
| Gastroenterologic | Volvulus , Small intestine fistula , Short bowel syndrome , Severe liver disease , Severe hepatopathy , Severe diarrhoea , Pancreatic fistula , Nausea and Vomiting , Mesenteric insufficiency , Liver disease , Ischemic colitis , Ileus , Diarrhea , Biliary fistula , Acute liver failure |
| Genetic | No underlying causes |
| Hematologic | Splenic infarction , Severe anaemia |
| Iatrogenic | No underlying causes |
| Infectious Disease | Sepsis , Infection , Fever , Disseminated Intravascular Coagulation , Clostridium Difficile , Cerebral Malaria |
| Musculoskeletal/Orthopedic | No underlying causes |
| Neurologic | Grand mal seizure , Epilepsy , Coma , CNS depression , Cerebral hypoxia , Cerebral edema |
| Nutritional/Metabolic | Total parenteral nutrition , Starvation |
| Obstetric/Gynecologic | No underlying causes |
| Oncologic | Tumor , Myeloma , Lymphoma , Leukemia |
| Ophthalmologic | No underlying causes |
| Overdose/Toxicity | Toluene , Salicylates , Ethylene glycol , Ethanol ingestion , Alcohol , Isopropyl alcohol , Diethylene glycol |
| Psychiatric | No underlying causes |
| Pulmonary | Status asthmaticus , Severe asthma , Pulmonary Embolism , Infant respiratory distress syndrome , Hypercapnia , Following chronic hyperventilation CO2 intoxication , Chronic obstructive lung disease , Apnea , Acute Respiratory Distress Syndrome |
| Renal/Electrolyte | Uremic , Type 4 RTA (hypoaldosteronism)]] , Type 2 (proximal) renal tubular acidosis (RTA) , Type 1 (distal) RTA , Renal tubular acidosis , Renal failure , Renal circulatory insufficiency , Proximal renal tubular acidosis , Kidney disorders , Hypokalaemic distal renal tubular acidosis , Hyperkalaemic distal renal tubular acidosis , Hyperkalaemia , Distal renal tubular acidosis , Decreased renal acid excretion , Chronic kidney disease , Chronic interstitial nephritis , Acute renal failure , Acute glomerulonephritis |
| Rheumatology/Immunology/Allergy | No underlying causes |
| Sexual | No underlying causes |
| Trauma | Traumatic shock |
| Urologic | Ureterosigmoidostomy , Ureteral diversion |
| Miscellaneous | Mitochondrial myopathy , Mitochondrial encephalomyopathy , Maple syrup urine disease , Malignant hyperpyrexia , Loss of bicarbonate or bicarbonate precursors , Hypoxia , Hypovolemia , Hyperchloremic acidosis , Heavy physical work , Glutathione synthase deficiency , Glutaric aciduria type 1 , Glutaric acidemia type 2 , Glomerular/tubular retention acidosis , Galactose-1-phosphate uridyltransferase deficiency , Fistula , Fanconi syndrome , Enzymatic defects in glycogenolysis or gluconeogenesis (as with type 1 glycogen storage disease) , Enhanced metabolic rate , Drug-induced mitochondrial dysfunction due to zidovudine or stavudine , Dieting , Decreased oxygen delivery , Decreased activity of pyruvate dehydrogenase or pyruvate carboxylase , Complications During and Following Cardiac Catheterization, Acute Disseminated Encephalomyelitis , 4-hydroxyphenylpyruvate hydroxylase deficiency , 3-Methylcrotonyl-CoA carboxylase deficiency , Altered redox state favoring pyruvate conversion to lactate , |
Causes in Alphabetical Order [1] [2]
Respiratory Acidosis
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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
External Links
cs:Acidóza da:Acidose de:Azidose gl:Acidose nl:Acidose no:Acidose sk:Acidóza fi:Asidoosi sv:Acidos tl:Acidosis