Respiratory acidosis acute

Acute respiratory acidosis i Increased3 -Normal AHCO3- = 0.1 x APaCC)/... 

Severe, acute respiratory acidosis produces a variety of neurologic abnormalities. Initially these include headache, blurred vision, restlessness, and anxiety. These may progress to tremors, asterixis, somnolence, and/or delirium. If untreated, terminal manifestations include peripheral vasodilation leading to hypotension and cardiac arrhythmias. Chronic respiratory acidosis is typically associated with cor pulmonale and peripheral edema. 

Hypercapnia (abnormally high concentration of carbon dioxide in the blood) can develop as a result of overfeeding with both dextrose and total calories.1,37 Excess carbon dioxide production and retention can lead to acute respiratory acidosis. The excess carbon dioxide also will stimulate compensatory mechanisms, resulting in an increase in respiratory rate in order to eliminate the excess carbon dioxide via the lungs. This increase in respiratory workload can cause respiratory insufficiency that may require mechanical ventilation. Reducing total calorie and dextrose intake would result in resolution of hypercapnia if due to overfeeding. 

The early compensatory response to acute respiratory acidosis is chemical buffering. If respiratory acidosis is prolonged (more than 12 to 24 hours), renal excretion of H+ increases, which generates new bicarbonate. 

In a patient with chronic respiratory acidosis (e.g., chronic obstructive pulmonary disease), treatment is essentially similar to that for acute respiratory acidosis with a few important exceptions. Oxygen therapy should be initiated carefully and only if the Pao2 is less than 50 mm Hg because the drive to breathe depends on hypoxemia rather than hypercarbia. 

In most cases of acute respiratory acidosis, such as following cardiopulmonary arrest, sodium bicarbonate therapy is not indicated and may be detrimental. Blood gas analysis should guide therapy. 

The body responds to acute respiratory acidosis with chemical buffering. The increase in PaC02 results in increased carbonic acid levels. 

The carbonic acid dissociates, releasing hydrogen ions, which are buffered by nonbicarbonate buffers (i.e., proteins, phosphate, and hemoglobin) and bicarbonate. Thus on the basis of physicochemical factors, increases in PaC02 raise the serum bicarbonate concentration. In general, in acute respiratory acidosis, the bicarbonate concentration increases by 1 mEq/L above 24 for each 10-mm Hg increase in PaC02 above 40 (see Table 51 ). 

ACUTE RESPIRATORY ACIDOSIS IN A COMPENSATED CHRONIC RESPIRATORY ACIDOTIC PATIENT... 

Patients with a history of chronic respiratory acidosis (e.g., those with chronic obstructive pulmonary disease) may experience an acute worsening of their respiratory acidosis. This may result in severe life-threatening hypoxemia. As with acute respiratory acidosis, the goals... 

Respiratory acidosis may be acute or chronic. Acute conditions occur within minutes or htnirs. They are uncompensated. Renal compensation has no time to develop as the mechanisms which adjust bicarbonate reabsorption take 48-72 h to become fully effective. The primary problem in acute respiratory acidosis is alveohir hypoventilation. If airflow is completely or partially reduced, the PCO, in the bltHtd will rise immediately and the H ) will rise quickly (Fig. 2). A resulting low PO, and high PCO. causes coma. If this is not reliev ed rapidly, death results. 

Acute respiratory acidosis is a medical emergency and needs to be dealt with by removing the source of the respiratory problem. 

Arieff AI, Kerian A, Massry SG DeLima J. (1976). Intracellular pH of brain alterations in acute respiratory acidosis and alkalosis. Am J Physiol 230, 804-812. 

B. For arterial blood from a subject with acute respiratory acidosis, the graph lies higher. 

B. No. The graphs would be coincident because acute respiratory acidosis means exposure of the subject to a high PCO2 with no compensation. 

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