Acute and Chronic Respiratory Acidosis (Carbonic Acid Excess) PDF

2/22/24, 2:23 PM Realizeit for Student 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 45 mm Hg and a compensatory increase in the plasma HCO3 occurs. It may be either acute or c...

2/22/24, 2:23 PM Realizeit for Student 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 45 mm Hg and a compensatory increase in the plasma HCO3 occurs. It may be either acute or chronic. Pathophysiology Respiratory acidosis is due to inadequate excretion of CO2 with inadequate ventilation, resulting in elevated plasma CO2 concentrations and, consequently, increased levels of carbonic acid. In addition to an elevated PaCO2, inadequate ventilation usually causes a decrease in PaO2. Acute respiratory acidosis occurs in emergency situations, such as acute pulmonary edema, aspiration of a foreign object, atelectasis, pneumothorax, and overdose of sedatives, as well as in nonemergent situations, such as sleep apnea associated with severe obesity, severe pneumonia, and acute respiratory distress syndrome. Respiratory acidosis commonly occurs in patients with severe chronic obstructive pulmonary disease (COPD) when patients acutely decompensate due to respiratory infection or heart failure. Respiratory acidosis can also occur in diseases that impair respiratory muscle function and cause hypoventilation. These disorders include severe scoliosis, muscular dystrophy, multiple sclerosis, myasthenia gravis, and GuillainBarré syndrome (Feller-Kopman & Schwartzstein, 2017). Clinical Manifestations Clinical signs in acute and chronic respiratory acidosis vary. Acute respiratory acidosis can occur due to sudden hypercapnia (elevated PaCO2) that will increase pulse, blood pressure, and respiratory rate. The patient may complain of confusion, disorientation, or may exhibit diminished level of consciousness. An elevated PaCO2, greater than 60 mm Hg causes reflexive cerebrovascular vasodilation and increased cerebral blood flow. Ventricular fibrillation may be the first sign of respiratory acidosis in anesthetized patients (Feller-Kopman & Schwartzstein, 2017). If respiratory acidosis is severe, intracranial pressure may increase, resulting in papilledema and dilated conjunctival blood vessels. Acidosis can cause hyperkalemia as the hydrogen ion concentration overwhelms the compensatory mechanisms. Acidosis causes H+ ion to move into the cells, causing a shift of potassium out of the cell. The bloodstream then gains increased potassium ions (i.e., hyperkalemia) (Mount, 2017c). Chronic respiratory acidosis occurs with pulmonary diseases such as COPD, including emphysema and chronic 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 PaCO2 increases rapidly, reflexive cerebral vasodilation will increase intracranial pressure, and cyanosis and tachypnea will develop. Patients with slowly progressive COPD gradually accumulate CO2 over a prolonged period of time (months to years) and the body becomes used to high CO2 levels. Patients with longterm COPD may not develop symptoms of hypercapnia because compensatory renal changes have had time to occur (Feller-Kopman & Schwartzstein, 2017). Quality and Safety Nursing Alert If the PaCO2 is chronically greater than 50 mm Hg, the respiratory center becomes relatively insensitive to CO2 as a respiratory stimulant, leaving hypoxem respiration. Patients with long-term COPD breathe independently based on a hypoxic drive. High oxygen concentration administration can remove the stim can lose the independent stimulus to breathe and incur respiratory failure. Therefore, oxygen is given with extreme caution in patients with long-term COP Assessment and Diagnostic Findings In respiratory acidosis, ABG analysis reveals a pH less than 7.35, a PaCO2 greater than 45 mm Hg, and variation in the bicarbonate level, depending on the duration of the acute respiratory acidosis. When compensation occurs over a prolonged period and renal retention of bicarbonate has fully occurred, the bicarbonate neutralizes the acidosis. Arterial pH is within the lower limits of normal (e.g., pH 7.35). Depending on the cause of respiratory acidosis, other diagnostic measures include monitoring of serum electrolyte levels, chest x-ray for determining respiratory infection or other disease, and a drug screen if an overdose is suspected. ECG monitoring is recommended to identify any cardiac involvement as a result of COPD (Feller-Kopman & Schwartzstein, 2017). Medical Management Treatment is directed at improving ventilation in acute and chronic respiratory acidosis. Exact measures vary according to the cause of inadequate ventilation. Pharmacologic agents are commonly used. For example, bronchodilators help reduce bronchial spasm and increase ventilation, antibiotics are used for respiratory infections, and thrombolytics or anticoagulants are used for pulmonary emboli (Stoller, 2019). Pulmonary physiotherapy and nebulizer treatment can be used to clear the respiratory tract of mucus and purulent drainage. Adequate hydration (2 to 3 L/day) is indicated to keep the mucous membranes moist and decrease viscosity of mucous, thereby facilitating removal of secretions. Low concentration of supplemental oxygen is given as necessary (Aboussouan, 2018). https://herzing.realizeithome.com/RealizeitApp/Student.aspx?Token=lqf9HhURQ5RqpgqAkzH2zRrdbUNNMKTSTb3II3pEltD4s%2fPbBdKcWtJFoZ4TUro%2b%… 1/2 2/22/24, 2:23 PM Realizeit for Student Mechanical ventilation, used appropriately, may be necessary to improve pulmonary ventilation. PaCO2 should be reduced slowly and gradually using a mechanical ventilator. Mechanical ventilation can cause too rapid ventilatory loss of CO2, which pulls H+ out of the bloodstream too rapidly. If there is a rapid loss of H+ the bloodstream becomes too alkalotic. The kidneys are unable to eliminate bicarbonate quickly enough to prevent alkalosis and seizures (Feller-Kopman & Schwartzstein, 2017). https://herzing.realizeithome.com/RealizeitApp/Student.aspx?Token=lqf9HhURQ5RqpgqAkzH2zRrdbUNNMKTSTb3II3pEltD4s%2fPbBdKcWtJFoZ4TUro%2b%… 2/2