Respiratory Acidosis Clinical Presentation

Updated: Apr 03, 2017
  • Author: Ryland P Byrd, Jr, MD; Chief Editor: Zab Mosenifar, MD, FACP, FCCP  more...
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Presentation

History

The clinical manifestations of respiratory acidosis are often those of the underlying disorder. Manifestations vary, depending on the severity of the disorder and on the rate of development of hypercapnia. Mild to moderate hypercapnia that develops slowly typically has minimal symptoms.

Patients may be anxious and may complain of dyspnea. Some patients may have disturbed sleep and daytime hypersomnolence. As the partial arterial pressure of carbon dioxide (PaCO2) increases, the anxiety may progress to delirium, and patients become progressively more confused, somnolent, and obtunded. This condition is sometimes referred to as carbon dioxide narcosis.

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Physical Examination

Physical examination findings in patients with respiratory acidosis are usually nonspecific and are related to the underlying illness or the cause of the respiratory acidosis.

Thoracic examination of patients with obstructive lung disease may demonstrate diffuse wheezing, hyperinflation (ie, barrel chest), decreased breath sounds, hyperresonance on percussion, and prolonged expiration. Rhonchi may also be heard.

Cyanosis may be noted if accompanying hypoxemia is present. Digital clubbing may indicate the presence of a chronic respiratory disease or other organ system disorders.

The patient’s mental status may be depressed if severe elevations of PaCO2 are present. Patients may have asterixis, myoclonus, and seizures.

Papilledema may be found during the retinal examination. Conjunctival and superficial facial blood vessels may also be dilated.

A study by Zorrilla-Riveiro et al of 212 patients indicated that in persons with dyspnea, nasal flaring is a sign of respiratory acidosis. [9]

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Complications

Patients with chronic respiratory acidosis, by definition, have a component of alveolar hypoventilation. Partial arterial pressure of carbon dioxide (PaCO2) and bicarbonate levels are increased, and obligatory decreases in partial pressure of arterial oxygen (PaO2) also occur.

Complications are often related to the chronic hypoxemia, which can result in increased erythropoiesis, leading to secondary polycythemia.

Chronic hypoxia is a cause of pulmonary vasoconstriction. This physiologic response can, in the long term, lead to pulmonary hypertension, right ventricular failure, and cor pulmonale.

Hypopneas and apneas during sleep lead to impaired sleep quality and cerebral vasodilation, causing morning headaches, daytime fatigue, and somnolence.

High levels of CO2 can lead to confusion, often referred to as carbon dioxide narcosis. As a late complication of cerebral vasodilation, patients may have papilledema. [10]

A study by Lun et al indicated that in patients with acute exacerbation of COPD, those with either compensated or decompensated respiratory acidosis tend to have poorer lung function and a greater risk for future life-threatening events than do normocapnic patients. [11]

A study by de Miguel-Díez et al indicated that respiratory acidosis is one factor increasing the risk of rehospitalization for patients within 30 days of initial hospitalization for acute exacerbation of COPD and is also a risk factor for inhospital mortality in these readmitted patients. Other factors associated with rehospitalization and inhospital mortality included older age, malnutrition, nonobesity, and treatment with noninvasive ventilation. [12]

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