ACUTE AND CHRONIC RESPIRATORY ACIDOSIS (CARBONIC ACID EXCESS)
Respiratory acidosis is a clinical disorder in which the pH is less than 7.35 and the PaCO2 is greater than 42mm Hg. It may be either acute or chronic.
Respiratory acidosis is always due to inadequate excretion of CO2 with inadequate ventilation, resulting in elevated plasma CO2 levels and thus elevated carbonic acid (H2CO3) levels (Epstein & Singh, 2001). In addition to an elevated PaCO2, hypoventilation usually causes a decrease in PaO2. Acute respiratory acidosis oc-curs in emergency situations, such as acute pulmonary edema, as-piration of a foreign object, atelectasis, pneumothorax, overdose of sedatives, sleep apnea syndrome, administration of oxygen to a patient with chronic hypercapnia (excessive CO2 in the blood), severe pneumonia, and acute respiratory distress syndrome. Res-piratory acidosis can also occur in diseases that impair respira-tory muscles, such as muscular dystrophy, myasthenia gravis, and Guillain-Barré syndrome.
Mechanical ventilation can be associated with hypercapnia if the rate of effective alveolar ventilation is inadequate. Ventilation is fixed in these patients, and CO2 may be retained if the rate of CO2 production is increased.
Clinical signs in acute and chronic respiratory acidosis vary. Sud-den hypercapnia (elevated PaCO2) can cause increased pulse and respiratory rate, increased blood pressure, mental cloudiness, and feeling of fullness in the head. An elevated PaCO2 causes cere-brovascular vasodilation and increased cerebral blood flow, particularly when it is higher than 60 mm Hg. Ventricular fibrilla-tion may be the first sign of respiratory acidosis in anesthetized patients.
If respiratory acidosis is severe, intracranial pressure may in-crease, resulting in papilledema and dilated conjunctival blood vessels. Hyperkalemia may result as hydrogen concentration overwhelms the compensatory mechanisms and moves into cells, causing a shift of potassium out of the cell.
Chronic respiratory acidosis occurs with pulmonary diseases such as chronic emphysema and bronchitis, obstructive sleep apnea, and obesity. As long as the PaCO2 does not exceed the body’s ability to compensate, the patient will be asymptomatic. However, if the PaCO2rises rapidly, cerebral vasodilation will in-crease intracranial pressure; cyanosis and tachypnea will develop. Patients with chronic obstructive pulmonary disease who gradu-ally accumulate CO2 over a prolonged period (days to months) may not develop symptoms of hypercapnia because compen-satory renal changes have had time to occur.
Arterial blood gas evaluation reveals a pH less than 7.35, a PaCO2 greater than 42 mm Hg, and a variation in the bicarbonate level, depending on the duration of the acidosis in acute respiratory aci-dosis. When compensation (renal retention of bicarbonate) has fully occurred, the arterial pH may be within the lower limits of normal. Depending on the cause of respiratory acidosis, other di-agnostic measures would include monitoring of serum electrolyte levels, chest x-ray for determining any respiratory disease, and a drug screen if an overdose is suspected. An ECG to identify any cardiac involvement as a result of chronic obstructive pulmonary disease may be indicated as well.
Treatment is directed at improving ventilation (Epstein & Singh, 2001); exact measures vary with the cause of inadequate ventila-tion. Pharmacologic agents are used as indicated. For example, bronchodilators help reduce bronchial spasm, antibiotics are used for respiratory infections, and thrombolytics or anticoagulants are used for pulmonary emboli.
Pulmonary hygiene measures are initiated, when necessary, to clear the respiratory tract of mucus and purulent drainage. Ade-quate hydration (2–3 L/day) is indicated to keep the mucous membranes moist and thereby facilitate the removal of secretions. Supplemental oxygen is used as necessary.
Mechanical ventilation, used appropriately, may improve pul-monary ventilation. Inappropriate mechanical ventilation (eg, increased dead space, insufficient rate or volume settings, high fraction of inspired oxygen [FiO2] with excessive CO2 production) may cause such rapid excretion of CO2 that the kidneys will be un-able to eliminate excess bicarbonate quickly enough to prevent al-kalosis and seizures. For this reason, the elevated PaCO2 must be decreased slowly. Placing the patient in a semi-Fowler’s positionfacilitates expansion of the chest wall. Treatment of chronic res-piratory acidosis is the same as for acute respiratory acidosis.
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