Respiratory acidosis

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] ; Associate Editor(s)-in-Chief: Vamsikrishna Gunnam M.B.B.S [2] Nasrin Nikravangolsefid, MD-MPH [3]

Respiratory acidosis is a clinical condition that occurs when the lungs are not able to remove enough of the carbon dioxide (CO2) produced by the body. Respiratory acidosis can be encountered in the inpatient units and emergency department , as well as in intensive care and postoperative units.Respiratory acidosis may become life-threatening if left untreated.

Respiratory acidosis was first described by Henderson–Hasselbalch and Bronsted–Lowry In the early 1950s.

Respiratory acidosis is an result of imbalance between acid-base due to alveolar hypoventilation.The normal range is 35-45 mm Hg for PaCO₂.Increase in the production of carbon dioxide due to failure of ventilation results in sudden increase of the partial pressure of arterial carbon dioxide (PaCO₂) above the normal range. Alveolar hypoventilation is one of the cause to increased PaCO₂ which is is called hypercapnia. Hypercapnia and respiration acidosis occur while impairment in air flow happens and the elimination of carbon dioxide by the respiratory system is much less than the production of carbon dioxide in the tissues

Common causes of respiratory acidosis include chronic obstructive pulmonary disease (COPD), neuromuscular diseases, chest wall disorders, obesity-hypoventilation syndrome, obstructive sleep apnea (OSA), the central nervous system (CNS) depression, lung, airway diseases, laryngeal and tracheal stenosis, Interstitial lung disease. Respiratory acidosis seen with past history of chronic lung disease, sleep problems, neuromuscular disorder, smoking history, travel history and any history of recent trauma.

Respiratory acidosis may be classified into two groups: Acute respiratory acidosis and Chronic respiratory acidosis.

The prevalence of respiratory acidosis in patients with acute COPD is approximately 75 (95% CI 61 to 90) per 100 000/year in men aged 45-79 and 57 (95% CI 46 to 69) per 100 000 in women. The incidence of respiratory acidosis increases with age because the range for a normal gradient increases with age.

Respiratory acidosis (primary hypercapnia), is the acid–base ailment that consequences from an increase in carbon dioxide in the body. Acute respiratory acidosis happens with respiratory failure, which could result from any unexpected respiratory parenchymal, airways (eg, chronic obstructive pulmonary disease), pleural, chest wall, neuromuscular eg, spinal cord injury, or central nervous system disorders. Chronic respiratory acidosis can result from several procedures and is typified by way of a sustained increase in arterial partial pressure of carbon dioxide, ensuing in renal adaptation, and an extra marked increase in plasma bicarbonate. Different mechanisms of respiratory acidosis include increased carbon dioxide production, alveolar hypoventilation, abnormal breathing drive, abnormalities of the chest wall and respiratory muscles. Common complications of respiratory acidosis include pulmonary, neurologic and cardiovascular complications such as Anxious, Dyspnea, Daytime somnolence, Alterations in sensorium like delirium and paranoia, Asterixis, Myoclonus, Seizures and Papilledema. Depending on the level of the carbon-dioxide levels at the time of diagnosis and the disease causing the respiratory acidosis defines the prognosis.

Respiratory acidosis or acute hypercapnia is often asymptomatic, leading to delayed diagnosis of the condition. Symptoms may include confusion, fatigue, lethargy, shortness of breath, sleepiness or daytime somnolence.The medical manifestations of respiratory acidosis are regularly the ones of the underlying disorder.

Physical examination may vary, relying on the severity of the disorder and on the rate of development of hypercapnia. Mild to moderate hypercapnia that develops slowly generally has minimum symptoms.

Laboratory findings consistent with the diagnosis of respiratory acidosis include arterial blood gas (ABG), complete blood count(CBC), toxicology screen, thyroid function tests, creatine phosphokinase which are helpful in the diagnosis of respiratory acidosis.

An x-ray may be helpful in the diagnosis of respiratory acidosis which underlying lung pathology. Findings of an x-ray suggestive respiratory acidosis include hyperinflation, diaphragmatic flattening, Infiltrates, Pneumothorax.

CT scan may be helpful in the diagnosis of respiratory acidosis. Findings on CT scan help in identifying etiologies of specific condition that include Central nervous system tumor, Stroke,CNS trauma and Brainstem lesions.

MRI may be helpful in identifying abnormalities that not found on CT scans, especially in the brainstem.

Other diagnostic studies for respiratory acidosis include pulmonary function tests, which are necessary for the diagnosis of the chronic obstructive lung disease.

The mainstay of treatment for respiratory acidosis is treating the underlying disorder which is responsible for the condition. While correcting hypercapnia extra care should be taken because rapid correction of the hypercapnia can result in metabolic alkalemia and can result in seizures especially when cerebrospinal fluid (CSF) becomes alkaline. Indications for admitting the patient in intensive care unit (ICU) when a patient presents with a low pH of (< 7.25), confusion, lethargy and respiratory muscle weakness.

Pharmacologic medical therapy is recommended for patients who are taking sedatives. For patients suspected of drug overdose, administration of antidote should be considered. Supportive therapy for respiratory acidosis includes bag-valve-mask ventilation. In patients with severe hypoxemia it is necessary to administer oxygen to avoid life threatening complications.

Surgical intervention is not recommended for the management of respiratory acidosis.

There are no established measures for the primary prevention of respiratory acidosis.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Vamsikrishna Gunnam M.B.B.S [2]

Respiratory acidosis is a clinical condition associated with lungs dysfunction in order to remove excess carbon dioxide (CO2) from the body. Respiratory acidosis may be classified into two groups: Acute respiratory acidosis and Chronic respiratory acidosis.

• Respiratory acidosis is classified into acute and chronic groups, depending on the duration.

• Acute respiratory acidosis occurs when PaCO2 is increased above the upper limit of the reference range >45 mmHg with an accompanying acidemia (ie, pH <7.35).

• In patients with pure acute respiratory acidosis, the levels of hypercapnia and bicarbonate correctly predicts the pH.
• In contrast, in patients who develop acute respiratory acidosis, the measured pH will be higher than predicted.
• Acute respiratory acidosis occurs due to the result of sudden failure of ventilation. This failure may be due to central nervous system(CNS) disease or any drug-induced respiratory depression.
• Inability to ventilate sufficiently , due to respiratory muscle paralysis disorders including myasthenia gravis, amyotrophic lateral sclerosis [[[Amyotrophic lateral sclerosis|ALS]]], guillain-Barré syndrome, muscular dystrophy.
• Airway obstruction, usually seen in patients with asthma or chronic obstructive pulmonary disease (COPD).^[1][2]

• Chronic respiratory acidosis occurs when PaCO₂ is elevated above the upper limit of the reference range ie >45 mmHg.
• But the pH is at the lower limit of normal or near-normal pH (eg, pH 7.33 to 7.35) secondary to renal compensation (secretion of acid from the distal tubule).
• Chronic respiratory acidosis may occur secondary to many diseases such as chronic obstructive pulmonary disease(COPD) and Obesity hypoventilation syndrome (OHS) that involve multiple mechanisms including^[3][4][5][6]
  • In conditions with hypoxia and hypercapnia, the responsiveness is decreased .
  • Increased in dead space ventilation due to increased ventilation-perfusion mismatch.
  • Function of Diaphragm decreased due to hyperinflation and fatigue.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Vamsikrishna Gunnam M.B.B.S [2]

Respiratory acidosis is an result of imbalance between acid-base due to alveolar hypoventilation.The normal range is 35-45 mm Hg for PaCO₂.Increase in the production of carbon dioxide due to  failure of ventilation results in sudden increase of the partial pressure of arterial carbon dioxide (PaCO₂) above the normal range. Alveolar hypoventilation is one of the cause to increased PaCO₂ which is is called hypercapnia. Hypercapnia and respiration acidosis occur while impairment in air flow happens and the elimination of carbon dioxide by the respiratory system is much less than the production of carbon dioxide in the tissues.Respiratory acidosis encountered in the emergency department and inpatient patients, as well as in intensive care units and postoperative patients.

Metabolism

• Metabolism in the body tissues rapidly generates a big quantity of volatile acids which are like eg carbon dioxide and nonvolatile acid.^[1]
• The metabolism of fats and carbohydrates ends up in the formation of a huge quantity of carbon dioxide.
• The carbon dioxide combines with water to form carbonic acid (H2CO3). The lungs excrete the unstable fraction via ventilation, and generally acid accumulation does not occur.
• A considerable alteration in ventilation that affects elimination of carbon dioxide can cause a respiratory acid-base disease. The partial arterial pressure of carbon dioxide (PaCO2) is normally maintained in between 35-45 mm Hg.

Alveolar ventilation

• Alveolar air flow is under the control of the central breathing centers, which can be placed in the pons and the medulla.^[2]
• Ventilation is prompted and controlled by using chemoreceptors for PaCO2, partial pressure of arterial oxygen (PaO2), and pH placed inside the brainstem, as well as by means of neural impulses from lung-stretch receptors and impulses from the cerebral cortex.
• Failure of air flow quickly results in an increase within the PaCO2.

Physiologic compensation^[3][4]

Acute cellular compensatory stage

• In acute respiratory acidosis, the body’s compensation happens in two steps.
• The preliminary reaction is cellular buffering that takes place within minutes to hours.
• Cellular buffering results in elevation of plasma bicarbonate values, but only slightly (approximately 1 mEq/L for every 10-mm Hg increase in PaCO2).

Chronic renal compensatory stage

• The second step occurs because of the renal compensation that occurs within 3-5 days.^[5]
• With renal compensation, renal excretion of carbonic acid is elevated, and bicarbonate reabsorption is accelerated.

• The predicted alternate in serum bicarbonate concentration in respiratory acidosis can be estimated as follows:
  • Acute respiration acidosis – Bicarbonate increases via 1 mEq/L for each 10-mm Hg upward push in % 2.the extreme exchange in bicarbonate is, therefore, pretty modest and is generated via the blood, extracellular fluid, and cellular buffering machine.
  • chronic respiratory acidosis – Bicarbonate will increase by means of 3.5 mEq/L for every 10-mm Hg upward push in % 2. The more change in bicarbonate in chronic respiratory acidosis is accomplished by means of the kidneys. The reaction starts soon after the onset of respiration acidosis however calls for three-five days to turn out to be whole.
  • The change in pH in respiratory acidosis can be estimated with the following equations:
    • Acute respiratory acidosis – Change in pH = 0.008 × (40 – PaCO ₂)
    • Chronic respiratory acidosis – Change in pH = 0.003 × (40 – PaCO ₂)

Electrolytes^[6]

• Respiratory acidosis does no longer have a outstanding effect on serum electrolyte levels.
• Some small results arise in calcium and potassium levels.
• Acidosis decreases binding of calcium to albumin and has a tendency to increase serum ionized calcium levels.
• Similarly, acidemia causes an extracellular shift of potassium.
• Respiratory acidosis, but, rarely causes clinically significant hyperkalemia.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Vamsikrishna Gunnam M.B.B.S [2]

Common causes of respiratory acidosis include chronic obstructive pulmonary disease (COPD), Neuromuscular diseases, Chest wall disorders, obesity–hypoventilation syndrome, Obstructive sleep apnea (OSA), the Central nervous system (CNS) depression, lung and airway diseases etc.

Respiratory acidosis may be caused by:

• Patients suffering from COPD conditions like Emphysema, chronic bronchitis, asthma.^[1][2][3][4]
• Chest wall disorders like amyotrophic lateral sclerosis (ALS), Paralysis and dysfunction of diaphragm, Guillain-Barré syndrome(Ascending paralysis), Myasthenia gravis(Acetylcholine receptor antibodies), Muscular dystrophy, Botulism(food poisoning caused by a bacterium)
• Obesity–hypoventilation syndrome: A condition which is seen most commonly in which severely overweight people who fail to breathe deeply enough, which results in low blood oxygen levels and high blood carbon dioxide (CO₂) levels.^[5][6]
• Obstructive sleep apnea (OSA): OSA frequency increases with age and obesity. In this condition, breath can become very shallow or one may even stop breathing.^[7]
• Central nervous system (CNS) depression:
  • Drugs: Drugs like narcotics, barbiturates, benzodiazepines which depress the central respiratory system.
  • Neurologic disorders: like trauma, brainstem disease, and encephalitis.
  • Primary alveolar hypoventilation: Its a disorder in which it results in respiratory arrest during sleep.
  • Congenital central alveolar hypoventilation syndrome: It is rare but lifelong and life-threatening disorder. It affects both central and autonomic nervous system which controls heart rate, blood pressure, sensing of oxygen and carbon dioxide levels in the blood, temperature etc.Congenital central alveolar hypoventilation syndrome is also called as Ondine curse.

Less Common Causes

Less common causes of disease name include:

• Laryngeal and tracheal stenosis
• Interstitial lung disease

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Eiman Ghaffarpasand, M.D. [2]

Abbreviations: ABG (arterial blood gas); ACE (angiotensin converting enzyme); BMI (body mass index); CBC (complete blood count); CSF (cerebrospinal fluid); CXR (chest X-ray); DOE (dyspnea on exercise); ECG (electrocardiogram); FEF (forced expiratory flow rate); FEV1 (forced expiratory volume); FVC (forced vital capacity); JVD (jugular vein distention); MCV (mean corpuscular volume); Plt (platelet); RV (residual volume); SIADH (syndrome of inappropriate antidiuretic hormone); TSH (thyroid stimulating hormone); Vt (tidal volume); WBC (white blood cell);

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Respiratory acidosis is an acid-base balance disturbance because of alveolar hypoventilation. Production of carbon dioxide takes place rapidly and failure of air flow directly increases the partial pressure of arterial carbon dioxide (PaCO2). The regular reference range for PaCO2 is 35-45 mm Hg.

• The prevalence of respiratory acidosis in patients with acute COPD is approximately  75 (95% CI 61 to 90) per 100 000/year for men aged 45-79 and 57 (95% CI 46 to 69) per 100 000 for women.^[1]

• The incidence of respiratory acidosis increases with age because the range for a normal gradient increases with age.
• The gradient can be estimated with the help of equation A-a gradient = age x 0.3.

Template:WH Template:WS

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Vamsikrishna Gunnam M.B.B.S [2]

Respiratory acidosis is an result of imbalance between acid-base due to alveolar hypoventilation.The normal range is 35-45 mm Hg for PaCO₂.Increase in the production of carbon dioxide due to  failure of ventilation results in sudden increase of the partial pressure of arterial carbon dioxide (PaCO₂) above the normal range. Alveolar hypoventilation is one of the cause to increased PaCO₂ which is is called hypercapnia.Hypercapnia and respiratory acidosis occur while impairment in air flow happens and the elimination of carbon dioxide by the respiratory system is much less than the production of carbon dioxide in the tissues.Respiratory acidosis encountered in the emergency department and inpatient patients, as well as in intensive care units and postoperative patients.

Natural History^[1][2]

• Respiration acidosis(primary hypercapnia), is the acid–base ailment that consequences from an increase in carbon dioxide in the body.
• Acute respiratory acidosis happens with respiratory failure, which could result from any unexpected respiratory parenchymal, airways (eg, chronic obstructive pulmonary disease ), pleural, chest wall, neuromuscular eg, spinal cord damage, or central nervous system disorders.
• Chronic respiratory acidosis can result from several procedures and is typified by way of a sustained increase in arterial partial pressure of carbon dioxide, ensuing in renal adaptation, and an extra marked increase in plasma bicarbonate.
• Different mechanisms of respiratory acidosis include increased carbon dioxide production, alveolar hypoventilation, abnormal breathing drive, abnormalities of the chest wall and respiratory muscles.
• Despite the fact that the symptoms, signs, results of respiratory acidosis are numerous, the major effects are seen on the central nervous and cardiovascular systems which are life threating.

Common complications of respiratory acidosis include:

Depending upon the level and rate of CO2 accumulation in arterial blood the complications of respiratory acidosis are pulmonary, neurologic and cardiovascular complications like

• Anxious
• Dyspnea
• Daytime somnolence
• Alterations in sensorium like delirium and paranoia
• Asterixis
• Myoclonus
• Seizures
• Papilledema

Depending on the level of the carbon-dioxide levels at the time of diagnosis and the disease causing the respiratory acidosis defines the prognosis.

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