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At NURSING.com, we believe Black Lives Matter ✊🏿, No Human Is Illegal 🤝, Love Is Love 🏳️🌈, Women`s Rights Are Human Rights 👩, Science Is Real 🔬, Water Is Life 🌊, Injustice Anywhere Is A Threat To Justice Everywhere ☮️. AccessibilitySitemapDrug List Overview Practice EssentialsRespiratory acidosis is an acid-base balance disturbance due to alveolar hypoventilation. Production of carbon dioxide occurs rapidly and failure of ventilation promptly increases the partial pressure of arterial carbon dioxide (PaCO2). [1] The normal reference range for PaCO2 is 35-45 mm Hg. [2, 3] Alveolar hypoventilation leads to an increased PaCO2 (ie, hypercapnia). The increase in PaCO2, in turn, decreases the bicarbonate (HCO3–)/PaCO2 ratio, thereby decreasing the pH. Hypercapnia and respiratory acidosis ensue when impairment in ventilation occurs and the removal of carbon dioxide by the respiratory system is less than the production of carbon dioxide in the tissues. Lung diseases that cause abnormalities in alveolar gas exchange do not typically result in alveolar hypoventilation. Often these diseases stimulate ventilation and hypocapnia due to reflex receptors and hypoxia. Hypercapnia typically occurs late in the disease process with severe pulmonary disease or when respiratory muscles fatigue. (See also Pediatric Respiratory Acidosis, Metabolic Acidosis, and Pediatric Metabolic Acidosis.) Acute vs chronic respiratory acidosisRespiratory 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 levels (ie, >30 mEq/L). Acute respiratory acidosis is present when an abrupt failure of ventilation occurs. This failure in ventilation may result from depression of the central respiratory center by one or another of the following:
Chronic respiratory acidosis may be secondary to many disorders, including COPD. Hypoventilation in COPD involves multiple mechanisms, including the following:
Chronic respiratory acidosis also may be secondary to obesity hypoventilation syndrome (OHS—ie, Pickwickian syndrome), neuromuscular disorders such as ALS, and severe restrictive ventilatory defects such as are observed in interstitial fibrosis and thoracic skeletal deformities. Workup in respiratory acidosisArterial blood gas (ABG) analysis is necessary in the evaluation of a patient with suspected respiratory acidosis or other acid-base disorders. [4] The most common abnormal serum electrolyte finding in chronic respiratory acidosis is the presence of a compensatory increase in serum bicarbonate concentration. A thyrotropin and a free T4 level should be considered in selected patients, since hypothyroidism may cause obesity, leading to obstructive sleep apnea (OSA) and sleep apnea–related hypoventilation. Many patients with chronic hypercapnia and respiratory acidosis are also hypoxemic. These patients may have secondary polycythemia, as demonstrated by elevated hemoglobin and hematocrit values. In patients without an obvious source of hypoventilation and respiratory acidosis, a drug screen should be performed. The effects of sedating drugs such as narcotics and benzodiazepines in depressing the central ventilatory drive and causing respiratory acidosis should be considered. These sedative drugs should be avoided, if possible, in patients with respiratory acidosis. Radiography, computed tomography (CT) scanning, and fluoroscopy of the chest may provide helpful information in determining causes of respiratory acidosis. Radiologic studies (CT scanning and magnetic resonance imaging [MRI]) of the brain should be considered if a central cause of hypoventilation and respiratory acidosis is suspected. Pulmonary function test measurements are required for the diagnosis of obstructive lung disease and for assessment of the severity of disease. Forced expiratory volume in 1 second (FEV1.0) is the most commonly used index of airflow obstruction. Electromyography (EMG) and measurement of nerve conduction velocity (NCV) are useful in diagnosing neuromuscular disorders (eg, myasthenia gravis, Guillain-Barré syndrome, and amyotrophic lateral sclerosis [ALS]), which can cause ventilatory muscle weakness. Measurement of transdiaphragmatic pressure is a useful diagnostic test for documenting respiratory muscle weakness. However, it is difficult to perform and is usually carried out only in specialized pulmonary function laboratories. Management of respiratory acidosisPharmacologic therapies are generally used as treatment for the underlying disease process. Oxygen therapy is employed to prevent the sequelae of long-standing hypoxemia. Therapeutic measures that may be lifesaving in severe hypercapnia and respiratory acidosis include endotracheal intubation with mechanical ventilation and noninvasive positive pressure ventilation (NIPPV) techniques such as nasal continuous positive-pressure ventilation (NCPAP) and nasal bilevel ventilation. The latter techniques of NIPPV are preferred treatment for obesity hypoventilation syndrome (OHS) and neuromuscular disorders, because they help to improve partial pressure of arterial oxygen (PaO2) and decrease the partial pressure of arterial carbon dioxide (PaCO2). Noninvasive external negative-pressure ventilation devices are also available for the treatment of selected patients with chronic respiratory failure. Rapid correction of the hypercapnia by the application of external noninvasive positive-pressure ventilation or invasive mechanical ventilation can result in alkalemia. Accordingly, these techniques should be used with caution. Etiology and PathophysiologyAs noted (see Background), respiratory acidosis may have a variety of different causes, including the following:
A study by Alfano et al of over 200 patients with coronavirus disease 2019 (COVID-19) found the rate of respiratory acidosis to be 3.3%. Among the acid-base disturbances in this cohort, metabolic alkalosis had the highest prevalence (33.6%), followed by respiratory alkalosis (30.3%), combined alkalosis (9.4%), respiratory acidosis, and metabolic acidosis (2.8%). In addition, 3.6% of patients had other compensated acid-base derangements (3.6%). Overall, about 80% of patients in the cohort had an acid-base condition. [10] MetabolismMetabolism 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 normally acid accumulation does not occur. [11] 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. [12, 13] Alveolar ventilationAlveolar 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, partial pressure of arterial oxygen (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 results in an increase in the PaCO2. Physiologic compensationIn acute respiratory acidosis, the body’s compensation occurs in 2 steps. The initial response is cellular buffering that takes place 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:
The expected change in pH with respiratory acidosis can be estimated with the following equations:
Electrolyte levelsRespiratory acidosis does not have a great effect on serum electrolyte levels. Some small effects occur in calcium and potassium levels. Acidosis decreases binding of calcium to albumin and tends to increase serum ionized calcium levels. In addition, acidemia causes an extracellular shift of potassium. [14] Respiratory acidosis, however, rarely causes clinically significant hyperkalemia.
 Author Nazir A Lone, MD, MBBS, MPH, FACP, FCCP Physician in Pulmonary and Critical Care Medicine, Peconic Bay Medical Center, Northwell Health Nazir A Lone, MD, MBBS, MPH, FACP, FCCP is a member of the following medical societies: American Association for Bronchology and Interventional Pulmonology, American College of Chest Physicians, American College of Physicians, International Association for the Study of Lung Cancer, Medical Society of the State of New York, Society of Critical Care Medicine Disclosure: Nothing to disclose. Coauthor(s) Laurel Whitney MD Candidate, Columbia University College of Physicians and Surgeons Disclosure: Nothing to disclose. Chief Editor Zab Mosenifar, MD, FACP, FCCP Geri and Richard Brawerman Chair in Pulmonary and Critical Care Medicine, Professor and Executive Vice Chairman, Department of Medicine, Medical Director, Women's Guild Lung Institute, Cedars Sinai Medical Center, University of California, Los Angeles, David Geffen School of Medicine Zab Mosenifar, MD, FACP, FCCP is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, American Federation for Medical Research, American Thoracic Society Disclosure: Nothing to disclose. Additional Contributors Ryland P Byrd, Jr, MD Professor of Medicine, Division of Pulmonary Disease and Critical Care Medicine, James H Quillen College of Medicine, East Tennessee State University Ryland P Byrd, Jr, MD is a member of the following medical societies: American College of Chest Physicians, American Thoracic Society Disclosure: Nothing to disclose. Thomas M Roy, MD Chief, Division of Pulmonary Disease and Critical Care Medicine, Quillen Mountain Home Veterans Affairs Medical Center; Professor of Medicine, Division of Pulmonary Disease and Critical Care Medicine, Fellowship Program Director, James H Quillen College of Medicine, East Tennessee State University Thomas M Roy, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, American Medical Association, American Thoracic Society, Southern Medical Association, Wilderness Medical Society Disclosure: Nothing to disclose. Acknowledgements Wael El Minaoui, MBBS Fellow in Pulmonary/Critical Care Medicine, East Tennessee State University, James H Quillen College of Medicine Disclosure: Nothing to disclose. Jackie A Hayes, MD, FCCP Clinical Assistant Professor of Medicine, University of Texas Health Science Center at San Antonio; Chief, Pulmonary and Critical Care Medicine, Department of Medicine, Brooke Army Medical Center Jackie A Hayes, MD, FCCP is a member of the following medical societies: Alpha Omega Alpha, American College of Chest Physicians, American College of Physicians, and American Thoracic Society Disclosure: Nothing to disclose. Oleh Wasyl Hnatiuk, MD Program Director, National Capital Consortium, Pulmonary and Critical Care, Walter Reed Army Medical Center; Associate Professor, Department of Medicine, Uniformed Services University of Health Sciences Oleh Wasyl Hnatiuk, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, and American Thoracic Society Disclosure: Nothing to disclose. Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference Disclosure: Medscape Salary Employment What nursing interventions are appropriate to prevent respiratory acidosis?Nursing Interventions & Considerations
Maintain adequate hydration. Maintain patent airway and provide humidification if acidosis requires mechanical ventilation. Perform tracheal suctioning frequently and vigorous chest physiotherapy, if ordered.
What is the priority of management in respiratory acidosis?Treatment is aimed at the underlying disease, and may include: Bronchodilator medicines and corticosteroids to reverse some types of airway obstruction. Noninvasive positive-pressure ventilation (sometimes called CPAP or BiPAP) or a breathing machine, if needed. Oxygen if the blood oxygen level is low.
What nursing interventions should be done for patient with acidMedical Management / Nursing Interventions:
Encourage the anxious patient to verbalize fears. Administer sedation as ordered to relax the patient. Keep the patient warm and dry. Encourage the patient to take deep, slow breaths or breathe into a brown paper bag (inspire CO2).
What precautions should the nurse implement for the patient with metabolic acidosis to prevent potential injury?Nursing Interventions & Considerations
Keep sodium bicarbonate ampules handy for emergency administration. Monitor vital signs, laboratory results and level of consciousness frequently. Watch out for signs of decreasing level of consciousness. Record intake and output accurately to monitor renal function.
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What is a nursing priority to prevent complications in clients with respiratory acidosis
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