![]() Naloxone can be used in patients who overdose on opioids. Bronchodilators like beta-agonists, anticholinergic drugs, and methylxanthines can be used in treating patients with obstructive airway diseases. Pharmacologic therapy can also be used to help improve ventilation. The hypercapnia should be corrected gradually because rapid alkalization of the cerebrospinal fluid (CSF) may lead to seizures. Once the diagnosis has been made, the underlying cause of respiratory acidosis has to be treated. All healthcare workers including the nurse practitioners must be familiar with the management of respiratory acidosis. The diagnosis of respiratory acidosis is easily made from an arterial blood gas but its management is complex. In patients with an obvious source of respiratory acidosis, the offending agent needs to be removed or reversed. ![]() Persistence of apnea during sleep can lead to daytime somnolence and headaches. Cases of chronic respiratory acidosis may cause memory loss, impaired coordination, polycythemia, pulmonary hypertension, and heart failure. If severe enough, increased intracranial pressure and papilledema may ensue, increasing the risk of herniation and possibly even death. Respiratory acidosis leads to hypercapnia, which induces cerebral vasodilation. If the respiratory acidosis is severe and accompanied by prolonged hypoventilation, the patient may have additional symptoms such as altered mental status, myoclonus, and possibly even seizures. ![]() In some cases, patients may present with cyanosis due to hypoxemia. Patients can present with dyspnea, anxiety, wheezing, and sleep disturbances. Signs and symptoms vary based on the length, severity, and progression of the disorder. The clinical presentation of respiratory acidosis is usually a manifestation of its underlying cause. In chronic respiratory acidosis, renal compensation occurs gradually over the course of days. Respiratory acidosis may cause slight elevations in ionized calcium and an extracellular shift of potassium. In patients with chronic compensated respiratory disease and acidosis, an acute insult such as pneumonia or disease exacerbation can lead to ventilation/perfusion mismatch. Chronic respiratory acidosis can also be seen in obesity hypoventilation syndrome, also known as Pickwickian syndrome, amyotrophic lateral sclerosis, and in patients with severe thoracic skeletal defects. Other individuals who develop chronic respiratory acidosis may have fatigue of the diaphragm resulting from a muscular disorder. On the contrary, chronic respiratory acidosis may be caused by COPD where there is a decreased responsiveness of the reflexes to states of hypoxia and hypercapnia. ![]() Because of its acute nature, there is a slight compensation occurring minutes after the incidence. This may be due to cerebrovascular accidents, use of central nervous system (CNS) depressants such as opioids, or inability to use muscles of respiration because of disorders like myasthenia gravis, muscular dystrophy or Guillain-Barre Syndrome. Respiratory acidosis can be subcategorized as acute, chronic, or acute and chronic. In acute respiratory acidosis, there is a sudden elevation of PCO2 because of failure of ventilation. Another pathophysiological mechanism may be due to ventilation/perfusion mismatch of dead space. When ventilation is disrupted, arterial PCO2 increases and an acid-base disorder develop. A decreased pH level influences the mechanics of ventilation and maintains proper levels of carbon dioxide and oxygen. Central chemoreceptors in the medulla are sensitive to changes in the pH level. Chemoreceptors for PCO2, PO2, and pH regulate ventilation. The respiratory centers in the pons and medulla control alveolar ventilation.
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