MundaHoshiarpuriya
Maavan Thandiyan Shavaan
Respiratory Acidosis
Author: Wael El Minaoui, MBBS, Fellow in Pulmonary/Critical Care Medicine, East Tennessee State University
Coauthor(s): Ryland P Byrd Jr, MD, Professor, Department of Internal Medicine, Division of Pulmonary Medicine and Critical Care Medicine, Program Director of Pulmonary Diseases and Critical Care Medicine Fellowship, James H Quillen College of Medicine, East Tennessee State University; Medical Director of Respiratory Therapy, James H Quillen Veterans Affairs Medical Center
Introduction
Background
Respiratory acidosis is a clinical disturbance due to alveolar hypoventilation. Production of carbon dioxide occurs rapidly, and failure of ventilation promptly increases the partial arterial pressure of carbon dioxide (PaCO2). The normal reference range for PaCO2 is 36-44 mm Hg. Alveolar hypoventilation leads to an increased PaCO2 (ie, hypercapnia). The increase in PaCO2, in turn, decreases the bicarbonate (HCO3 -)/PaCO2, decreasing the pH. Hypercapnia and respiratory acidosis ensue when impairment in ventilation occurs and the removal of carbon dioxide by the lungs is less than the production of carbon dioxide in the tissues.
Respiratory acidosis can be acute or chronic. In acute respiratory acidosis, the PaCO2 is elevated above the upper limit of the reference range (ie, >45 mm Hg) with an accompanying acidemia (ie, pH <7.35). In chronic respiratory acidosis, the PaCO2 is elevated above the upper limit of the reference range, with a normal or near-normal pH secondary to renal compensation and an elevated serum bicarbonate value (ie, >30 mm Hg).
Acute respiratory acidosis is present when an abrupt failure of ventilation occurs. This failure in ventilation may be caused by depression of the central respiratory center by cerebral disease or drugs, an inability to ventilate adequately owing to a neuromuscular disease (eg, myasthenia gravis, amyotrophic lateral sclerosis, Guillain-Barré syndrome, muscular dystrophy), or airway obstruction related to asthma or chronic obstructive pulmonary disease (COPD).
Chronic respiratory acidosis may be secondary to many disorders, including COPD. Hypoventilation in COPD involves multiple mechanisms, including decreased responsiveness to hypoxia and hypercapnia, increased ventilation-perfusion mismatch leading to increased dead space ventilation, and decreased diaphragmatic function due to fatigue and hyperinflation.
Chronic respiratory acidosis also may be secondary to obesity-hypoventilation syndrome (ie, pickwickian syndrome), neuromuscular disorders such as amyotrophic lateral sclerosis, and severe restrictive ventilatory defects as observed in interstitial fibrosis and thoracic deformities.
Lung diseases that primarily cause abnormalities in alveolar gas exchange usually do not cause hypoventilation; however, they tend to cause stimulation of ventilation and hypocapnia secondary to hypoxia. Hypercapnia only occurs if severe disease or respiratory muscle fatigue is present.
Pathophysiology
Metabolism rapidly generates a large quantity of volatile acid (carbon dioxide) and nonvolatile acid. The metabolism of fats and carbohydrates leads to the formation of a large amount of carbon dioxide. The carbon dioxide combines with water to form carbonic acid (H2 CO3). The lungs excrete the volatile fraction through ventilation, and acid accumulation does not occur. A significant alteration in ventilation that affects elimination of carbon dioxide can cause a respiratory acid-base disorder. The PaCO2 is normally maintained within the range of 35-45 mm Hg.1,2
Alveolar ventilation is under the control of the central respiratory centers, which are located in the pons and the medulla. Ventilation is influenced and regulated by chemoreceptors for PaCO2, PaO2, and pH located in the brainstem, as well as by neural impulses from lung-stretch receptors and impulses from the cerebral cortex. Failure of ventilation quickly increases the PaCO2.
In acute respiratory acidosis, the body's compensation occurs in 2 steps. The initial response is cellular buffering that occurs over minutes to hours. Cellular buffering elevates plasma bicarbonate values, but only slightly, approximately 1 mEq/L for each 10-mm Hg increase in PaCO2. The second step is renal compensation that occurs over 3-5 days. With renal compensation, renal excretion of carbonic acid is increased and bicarbonate reabsorption is increased.
The expected change in serum bicarbonate concentration in respiratory acidosis can be estimated as follows:
Mortality/Morbidity
The morbidity and mortality of respiratory acidosis depends on the underlying cause of the respiratory acidosis, associated conditions, the patient's compensatory mechanisms, and effectiveness of medical care.
Clinical
History
The clinical manifestations of respiratory acidosis often are 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 usually has minimal symptoms.
Patients may be anxious and may complain of dyspnea. Some patients may have disturbed sleep and daytime hypersomnolence. As the 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.
Physical
The findings upon physical examination in patients with respiratory acidosis usually are 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 also may be heard.
Cyanosis may be noted if accompanying hypoxemia is present. Digital clubbing may indicate the presence of a chronic respiratory tract disease or other organ system disorders.
The patient's mental status may be depressed if he or she has severe elevations of PaCO2. Patients may have asterixis, myoclonus, and seizures.
Papilledema may be found during the retina examination. Conjunctival and superficial facial blood vessels also may be dilated.
Causes
Respiratory acidosis may occur due to a variety of etiologies, including the following:
Author: Wael El Minaoui, MBBS, Fellow in Pulmonary/Critical Care Medicine, East Tennessee State University
Coauthor(s): Ryland P Byrd Jr, MD, Professor, Department of Internal Medicine, Division of Pulmonary Medicine and Critical Care Medicine, Program Director of Pulmonary Diseases and Critical Care Medicine Fellowship, James H Quillen College of Medicine, East Tennessee State University; Medical Director of Respiratory Therapy, James H Quillen Veterans Affairs Medical Center
Introduction
Background
Respiratory acidosis is a clinical disturbance due to alveolar hypoventilation. Production of carbon dioxide occurs rapidly, and failure of ventilation promptly increases the partial arterial pressure of carbon dioxide (PaCO2). The normal reference range for PaCO2 is 36-44 mm Hg. Alveolar hypoventilation leads to an increased PaCO2 (ie, hypercapnia). The increase in PaCO2, in turn, decreases the bicarbonate (HCO3 -)/PaCO2, decreasing the pH. Hypercapnia and respiratory acidosis ensue when impairment in ventilation occurs and the removal of carbon dioxide by the lungs is less than the production of carbon dioxide in the tissues.
Respiratory acidosis can be acute or chronic. In acute respiratory acidosis, the PaCO2 is elevated above the upper limit of the reference range (ie, >45 mm Hg) with an accompanying acidemia (ie, pH <7.35). In chronic respiratory acidosis, the PaCO2 is elevated above the upper limit of the reference range, with a normal or near-normal pH secondary to renal compensation and an elevated serum bicarbonate value (ie, >30 mm Hg).
Acute respiratory acidosis is present when an abrupt failure of ventilation occurs. This failure in ventilation may be caused by depression of the central respiratory center by cerebral disease or drugs, an inability to ventilate adequately owing to a neuromuscular disease (eg, myasthenia gravis, amyotrophic lateral sclerosis, Guillain-Barré syndrome, muscular dystrophy), or airway obstruction related to asthma or chronic obstructive pulmonary disease (COPD).
Chronic respiratory acidosis may be secondary to many disorders, including COPD. Hypoventilation in COPD involves multiple mechanisms, including decreased responsiveness to hypoxia and hypercapnia, increased ventilation-perfusion mismatch leading to increased dead space ventilation, and decreased diaphragmatic function due to fatigue and hyperinflation.
Chronic respiratory acidosis also may be secondary to obesity-hypoventilation syndrome (ie, pickwickian syndrome), neuromuscular disorders such as amyotrophic lateral sclerosis, and severe restrictive ventilatory defects as observed in interstitial fibrosis and thoracic deformities.
Lung diseases that primarily cause abnormalities in alveolar gas exchange usually do not cause hypoventilation; however, they tend to cause stimulation of ventilation and hypocapnia secondary to hypoxia. Hypercapnia only occurs if severe disease or respiratory muscle fatigue is present.
Pathophysiology
Metabolism rapidly generates a large quantity of volatile acid (carbon dioxide) and nonvolatile acid. The metabolism of fats and carbohydrates leads to the formation of a large amount of carbon dioxide. The carbon dioxide combines with water to form carbonic acid (H2 CO3). The lungs excrete the volatile fraction through ventilation, and acid accumulation does not occur. A significant alteration in ventilation that affects elimination of carbon dioxide can cause a respiratory acid-base disorder. The PaCO2 is normally maintained within the range of 35-45 mm Hg.1,2
Alveolar ventilation is under the control of the central respiratory centers, which are located in the pons and the medulla. Ventilation is influenced and regulated by chemoreceptors for PaCO2, PaO2, and pH located in the brainstem, as well as by neural impulses from lung-stretch receptors and impulses from the cerebral cortex. Failure of ventilation quickly increases the PaCO2.
In acute respiratory acidosis, the body's compensation occurs in 2 steps. The initial response is cellular buffering that occurs over minutes to hours. Cellular buffering elevates plasma bicarbonate values, but only slightly, approximately 1 mEq/L for each 10-mm Hg increase in PaCO2. The second step is renal compensation that occurs over 3-5 days. With renal compensation, renal excretion of carbonic acid is increased and bicarbonate reabsorption is increased.
The expected change in serum bicarbonate concentration in respiratory acidosis can be estimated as follows:
- Acute respiratory acidosis: Bicarbonate increases 1 mEq/L for each 10-mm Hg rise in PaCO2.
- Chronic respiratory acidosis: Bicarbonate increases 3.5 mEq/L for each 10-mm Hg rise in PaCO2.
- Acute respiratory acidosis: Change in pH = 0.008 X (40 - PaCO2)
- Chronic respiratory acidosis: Change in pH = 0.003 X (40 - PaCO2)
Mortality/Morbidity
The morbidity and mortality of respiratory acidosis depends on the underlying cause of the respiratory acidosis, associated conditions, the patient's compensatory mechanisms, and effectiveness of medical care.
Clinical
History
The clinical manifestations of respiratory acidosis often are 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 usually has minimal symptoms.
Patients may be anxious and may complain of dyspnea. Some patients may have disturbed sleep and daytime hypersomnolence. As the 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.
Physical
The findings upon physical examination in patients with respiratory acidosis usually are 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 also may be heard.
Cyanosis may be noted if accompanying hypoxemia is present. Digital clubbing may indicate the presence of a chronic respiratory tract disease or other organ system disorders.
The patient's mental status may be depressed if he or she has severe elevations of PaCO2. Patients may have asterixis, myoclonus, and seizures.
Papilledema may be found during the retina examination. Conjunctival and superficial facial blood vessels also may be dilated.
Causes
Respiratory acidosis may occur due to a variety of etiologies, including the following:
- Chronic obstructive pulmonary disease - Emphysema, severe asthma3,4 , chronic bronchitis
- Neuromuscular diseases - Amyotrophic lateral sclerosis, diaphragm dysfunction and paralysis, Guillain-Barré syndrome, myasthenia gravis, muscular dystrophy
- Chest wall disorders - Severe kyphoscoliosis; status post thoracoplasty; flail chest; less commonly, ankylosing spondylitis, pectus excavatum, or pectus carinatum
- Obesity-hypoventilation syndrome
- Obstructive sleep apnea
- CNS depression - Drugs (eg, narcotics, barbiturates, benzodiazepines, other CNS depressants), neurologic disorders (eg, encephalitis, brainstem disease, trauma), primary alveolar hypoventilation
- Other lung and airway diseases - Laryngeal and tracheal stenosis
- Lung-protective ventilation in ARDS
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