carbon dioxide acidosis

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res·pi·ra·to·ry ac·i·do·sis

acidosis caused by retention of carbon dioxide; due to inadequate pulmonary ventilation or hypoventilation, with decrease in blood pH unless compensated by renal retention of bicarbonate.

carbon dioxide acidosis


(as?i-do'sis) [ acid + -osis]
An actual or relative increase in the acidity of blood due to an accumulation of acids (as in diabetic acidosis or renal disease) or an excessive loss of bicarbonate (as in renal disease). The hydrogen ion concentration of the fluid is increased, lowering the pH. See: acid-base balance; acidemia; buffer; pHacidotic (-dot'ik), adjective

carbon dioxide acidosis

Respiratory acidosis.

compensated acidosis

Acidosis in which the pH of body fluids has returned to normal. Compensatory mechanisms maintain the normal ratio of bicarbonate to carbonic acid (approx. 20:1) in blood plasma even though the bicarbonate level is decreased or the carbon dioxide level is elevated.

diabetic acidosis

Diabetic ketoacidosis.

dialysis acidosis

Metabolic acidosis due to prolonged hemodialysis in which the pH of the dialysis bath has been inadvertently reduced by the action of contaminating bacteria.

D-lactate acidosis

An anion gap metabolic acidosis in patients with malabsorption, e.g., secondary to short gut syndrome or jejunoileal bypass. In this syndrome the delivery of glucose and starch to the colon without prior digestion in the small intestine results in the absorption of the D-isomer of lactate into the blood stream. Patients may experience intoxication or encephalopathy as a result, especially after a carbohydrate-rich meal.

hypercapnic acidosis

Respiratory acidosis.

hyperchloremic acidosis

Acidosis in which there is an abnormally high level of chloride in the blood.

lactic acidosis

An accumulation of lactic acid in the blood, often due to inadequate perfusion and oxygenation of vital organs (e.g., in cardiogenic, ischemic, or septic shock), drug overdoses (commonly, salicylates or ethanol), skeletal muscle overuse (e.g., after heavy exercise or seizures), or other serious illnesses (some cancers; diabetes mellitus). Lactic acid is produced more quickly than normal when there is inadequate oxygenation of skeletal muscle and other tissues. Thus any disease that leads to tissue hypoxia, exercise, hyperventilation, or some drugs (e.g., oral hypoglycemic agents) may cause this condition. In general, when blood pH is less than 7.35 and lactate is greater than 5 to 6 mmol/L (5 to 6 mEq/L), lactic acidosis is present.

metabolic acidosis

Any process that causes a decrease in the pH of the body as a result of the retention of acids or the loss of bicarbonate buffers. Metabolic acidosis is usually categorized by the presence or absence of an abnormal anion gap. The anion gap metabolic acidoses include diabetic, alcoholic, and lactic acidoses; the acidosis of renal failure; and acidoses that result from the consumption of excess acids e.g., salicylates, methanol, or ethanol. Non-anion gap metabolic acidoses occur in diarrhea, renal tubular acidosis, and multiple myeloma.


Possible causes include excessive ingestion of acids, salicylates, methanol, or ethylene glycol; failure of the kidneys to excrete acids, e.g., in renal failure or renal tubular acidosis; ketoacidosis (diabetic, alcoholic, owing to starvation); severe dehydration; diarrhea; rhabdomyolysis; seizures; and shock.

Patient care

A history is obtained, focusing on the patient's urine output, fluid intake, dietary habits (including recent fasting), associated disorders (e.g., diabetes mellitus and kidney or liver dysfunction), and the use of medications (including aspirin) and alcohol. Arterial blood gas values, serum potassium level, and fluid balance are monitored. The patient is assessed for lethargy, drowsiness, and headache, diminished muscle tone, and deep tendon reflexes. The patient is also evaluated for hyperventilation, cardiac dysrhythmias, muscle weakness and flaccidity, and gastrointestinal distress (e.g., nausea, vomiting, diarrhea, and abdominal pain). Prescribed intravenous fluids, medications, e.g., sodium bicarbonate or insulin, and other therapies, e.g., oxygen or mechanical ventilation, are administered. The patient is positioned to promote chest expansion and repositioned frequently. Frequent oral hygiene with sodium bicarbonate rinses will neutralize mouth acids, and a water-soluble lubricant will prevent lip dryness. A safe environment with minimal stimulation is provided, and preparations should be available if seizures occur. Both patient and family are given oral and written information about prescribed medication and managing related diseases.

renal acidosis

Acidosis caused either by kidney failure, in which phosphoric and sulfuric acids and inorganic anions accumulate in the body, or by renal tubular diseases. The acidosis is induced by urinary wasting of bicarbonate and inability to excrete phosphoric and sulfuric acids.

Patient care

Renal acidosis due to one of the renal tubular acidoses responds to treatment either with sodium bicarbonate or with citrated salts (e.g., potassium citrate). The acidosis of chronic renal failure may require therapy with sodium bicarbonate or may be treated by dialysis with a bicarbonate-rich dialysate. Diets are adjusted for patients with renal failure to limit the metabolic production of acids (these usually rely on limitations of daily dietary protein). Foods rich in potassium and phosphate are restricted. Patients with renal failure should be monitored for signs and symptoms of renal acidosis, including loss of appetite, changes in levels of consciousness, or alterations in respiratory rate or effort. Laboratory monitoring may include frequent assessments of arterial blood gas values, serum electrolytes, carbon dioxide levels, and blood urea nitrogen and creatinine. Prescribed intravenous fluids are given to maintain hydration.

renal tubular acidosis

Abbreviation: RTA
Any of a group of non-anion gap metabolic acidoses marked by either loss of bicarbonate or failure to excrete hydrogen ions in the urine. Type I (distal RTA) is marked by low serum potassium, elevated serum chloride, a urinary pH greater than 5.5, nephrocalcinosis, and nephrolithiasis. Alkalis such as sodium bicarbonate or Shohl's solution are effective treatments.

Type II (proximal RTA) is caused by impaired reabsorption of bicarbonate by the proximal tubules. Its hallmarks include preserved glomerular filtration, hypokalemia, excessive bicarbonate excretion in the urine during bicarbonate loading, and a urinary pH less than 5.5. Osteopenia and osteomalacia are common. Treatments include volume restriction and potassium and bicarbonate supplementation.

Type IV (hyperkalemia RTA) is usuallyassociated with hyporeninemic hypoaldosteronism due to diabetic nephropathy, nephrosclerosis associated with hypertension, or chronic nephropathy. Patients have high serum potassium levels and low urine ammonia excretion but no renal calculi. The hyperkalemia may be managed by mineralocorticoids with furosemide. Glomerular filtration is reduced in this disorder.

respiratory acidosis

Acidosis caused by inadequate ventilation and the subsequent retention of carbon dioxide. Synonym: carbon dioxide acidosis; hypercapnic acidosis

Patient care

The patient suspected of developing acute respiratory acidosis is monitored using arterial blood gases, level of consciousness, and orientation to time, place, and person. The patient is also evaluated for diaphoresis, a fine or flapping tremor (asterixis), depressed reflexes, and cardiac dysrhythmias. Vital signs and ventilatory effort are monitored, and ventilatory difficulties such as dyspnea are documented. Prescribed intravenous fluids are given to maintain hydration. The patient is oriented as often as necessary, and information and reassurance are given to allay the patient's and family's fears and concerns. Prescribed therapies for associated hypoxemia and underlying conditions are provided, responses are evaluated, and related patient education is given.

The respiratory therapist (RT) works with the attending physician to determine when to intubate and mechanically ventilate the patient with acute respiratory acidosis. Once the patient is intubated and is receiving mechanical ventilation, the RT monitors and maintains the patient's airway and tolerance of the positive pressure ventilation. This requires the RT to perform frequent q1-2m assessments of the patient and the ventilator and report side effects to the attending physician. Some patients with advanced chronic obstructive lung disease develop chronic respiratory acidosis (as a result of CO2 retention), usually with a compensatory metabolic (renal) alkalosis.


Acute respiratory acidosis is a medical emergency in which immediate efforts to improve ventilation are required.