carbon dioxide acidosis
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carbon dioxide acidosis
acidosis(as?i-do'sis) [ acid + -osis]
carbon dioxide acidosisRespiratory acidosis.
diabetic acidosisDiabetic ketoacidosis.
hypercapnic acidosisRespiratory acidosis.
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.
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 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 acidosisAbbreviation: RTA
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.
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.