Respiratory acidosis resident survival guide
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Qasim Khurshid.M.B.B.S
Overview
Respiratory acidosis occurs when carbon dioxide production exceeds the elimination mainly due to alveolar hypoventilation. Respiratory acidosis is associated with concurrent increases in Paco2, decreases in pH and compensatory increases in blood HCO3- concentration.Respiratory acidosis can be acute or chronic, with initial metabolic compensation to increase HCO3- concentrations by intracellular buffering. Chronic respiratory acidosis results in longer lasting increases in renal reabsorption of HCO3-. Alveolar hypoventilation and resulting respiratory acidosis may also be associated with hypoxemia, especially evident when patients are inspiring room air (20.9% O2).
Causes
Life-Threatening Causes
Life-threatening causes include the following:[1][2]
- Sedative overdose (eg, narcotic or benzodiazepine, some anesthetics, tricyclic antidepressants)
- Epiglottitis
- Foreign body aspiration
- Angioedema
- Pulmonary embolism (usually severe)
- Respiratory muscle fatigue
- Periodic paralysis
- Phrenic nerve injury
- Organophosphates poisoning
- Procainamide toxicity
Common Causes
Most common causes include the following:[3][2]
- Sedative overdose (eg, narcotic or benzodiazepine, some anesthetics, tricyclic antidepressant
- Encephalitis
- Brainstem disease
- Central and obstructive sleep apnea
- Amyotrophic lateral sclerosis
- Dynamic hyperinflation (eg, upper and lower airway disorders including chronic obstructive pulmonary disease, severe asthma)
- Endstage interstitial lung disease
- Pulmonary embolism (usually severe)
- Thyrotoxicosis
- Foreign body aspiration
- Retropharyngeal disorders
- Obstructive goiter
- Vocal cord paralysis
- Hypophosphatemia
- Hypomagnesemia
- Hyperthyroidism
- Tetanus
- Botulism
- Succinylcholine and neuromuscular blockade
Diagnosis
Shown below is an algorithm summarizing the diagnosis of respiratory acidosis.[4][5]
Suspected acid base disorder | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Acidemia pH<7.35 | Normal pH | Alkalemia pH>7.45 | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Metabolic acidosis HCO3<24mmol/L CO2:HCO3 12:10 | Respiratory acidosis pCO2>40mmHg | Metabolic alkalosis HCO3>28mmol/L CO2:HCO3 7:10 | Respiratory alkalosis pCO2<35mmHg | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Anion gap | Non anion gap | Acute CO2:HCO3 10:1 | Chronic CO2:HCO3 10:3 | Acute CO2:HCO3 10:2 | Chronic CO2:HCO3 10:4 | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Appropriate compensation Ratio(CO2:HCO3) Metabolic acidosis 12:10 Metabolic alkalosis 7:10 Acute respiratory acidosis 10:1 Chronic respiratory acidosis 10:3 Acute respiratory alkalosis 10:2 Chronic Respiratory alkalosis 10:4 | |||||||||||||||||||||||||||||||||||||||||||||||||||
Treatment
Shown below is an algorithm summarizing the treatment of acute respiratory acidosis.[6][7]
Apnea or Respiratory distress(of recent onset) | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||
{{{ }}} | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Airway patency scured | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Yes | NO | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Oxygen-rich mixture delivered | Airway patent | Remove dentures,foreign bodies, or food particles Consider tracheal intubation | |||||||||||||||||||||||||||||||||||||||||||||||||||||||
Mental status and blood gas evaluated | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Patient alert, Blood pH>7.10 or PaCO2<80mmHg | Patient obtunded,Blood pH<7.10 or PaCO2>80mmHg | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Administer O2 via nasal mask or prongs to maintain pO2>60mmHg Correct reversible causes of pulmonary dysfunction with antibiotics,bronchodilators,and corticosteriods as needed Monitor patient with abnormal arterial blood gases at 20-30 minutes of interval initially and less frequently thereafter If PaO2 does not increase to >60mmHg or PaCO2 rises to >80mmHg,proceed to therapy for obtunded | Consider use of non invasive ventilation through a nasal or full face mask Consider intubation or initiation of mechanical ventilation if non invasive ventilation fails or contraindicated If arterial pH<7.10 on ventilatory support, administer sodium bicarbonate to maintain blood pH between 7.10 to 7.20 Correct reversible causes of pulmonary dysfunction with antibiotics,bronchodilators,and corticosteriods as needed | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Dos
- Respiratory acidosis should be considered in patients with limited respiratory reserve (COPD exacerbation) and present with increasing shortness of breath, new hypoxemia, change in mental status or hypersomnolence.[8][9]
- When patients present with suspected acute respiratory acidosis, the physician should simultaneously assess and stabilize the airway, breathing, and circulation, perform a brief clinical bedside assessment with telemetry and oxygen monitoring, draw an arterial blood gas (ABG), and administer initial empiric bedside therapies.
- A brief history and examination should be performed at the bedside so that therapies targeted at a specific underlying cause can be administered quickly
- In addition to ABGs, a complete blood count, serum chemistries including bicarbonate and electrolytes, and a chest radiograph should be performed
- Always treat the underlying cause of respiratory acidosis.
Don'ts
- Do not use non-invasive ventilation if patient is unable to protect the airway.[10]
- Do not use non-invasive ventilation if patient have cardiac or pulmonary arrest or impending respiratory muscle fatigue
References
- ↑ Davidson AC, Banham S, Elliott M, Kennedy D, Gelder C, Glossop A, Church AC, Creagh-Brown B, Dodd JW, Felton T, Foëx B, Mansfield L, McDonnell L, Parker R, Patterson CM, Sovani M, Thomas L (April 2016). "BTS/ICS guideline for the ventilatory management of acute hypercapnic respiratory failure in adults". Thorax. 71 Suppl 2: ii1–35. doi:10.1136/thoraxjnl-2015-208209. PMID 26976648.
- ↑ 2.0 2.1 Johnson RA (2017). "A Quick Reference on Respiratory Acidosis". Vet Clin North Am Small Anim Pract. 47 (2): 185–189. doi:10.1016/j.cvsm.2016.10.012. PMID 27939862.
- ↑ Epstein SK, Singh N (2001). "Respiratory acidosis". Respir Care. 46 (4): 366–83. PMID 11262556.
- ↑ O'Driscoll BR, Howard LS, Earis J, Mak V (June 2017). "BTS guideline for oxygen use in adults in healthcare and emergency settings". Thorax. 72 (Suppl 1): ii1–ii90. doi:10.1136/thoraxjnl-2016-209729. PMID 28507176.
- ↑ Celli BR, MacNee W (June 2004). "Standards for the diagnosis and treatment of patients with COPD: a summary of the ATS/ERS position paper". Eur. Respir. J. 23 (6): 932–46. doi:10.1183/09031936.04.00014304. PMID 15219010.
- ↑ Rudolf M, Banks RA, Semple SJ (September 1977). "Hypercapnia during oxygen therapy in acute exacerbations of chronic respiratory failure. Hypothesis revisited". Lancet. 2 (8036): 483–6. doi:10.1016/s0140-6736(77)91606-3. PMID 70692.
- ↑ Durrington HJ, Flubacher M, Ramsay CF, Howard LS, Harrison BD (July 2005). "Initial oxygen management in patients with an exacerbation of chronic obstructive pulmonary disease". QJM. 98 (7): 499–504. doi:10.1093/qjmed/hci084. PMID 15955796.
- ↑ Joosten SA, Koh MS, Bu X, Smallwood D, Irving LB (March 2007). "The effects of oxygen therapy in patients presenting to an emergency department with exacerbation of chronic obstructive pulmonary disease". Med. J. Aust. 186 (5): 235–8. PMID 17391084.
- ↑ Bone RC, Pierce AK, Johnson RL (December 1978). "Controlled oxygen administration in acute respiratory failure in chronic obstructive pulmonary disease: a reappraisal". Am. J. Med. 65 (6): 896–902. doi:10.1016/0002-9343(78)90740-4. PMID 742628.
- ↑ Campbell EJ (October 1967). "The J. Burns Amberson Lecture. The management of acute respiratory failure in chronic bronchitis and emphysema". Am. Rev. Respir. Dis. 96 (4): 626–39. doi:10.1164/arrd.1967.96.4.626. PMID 6057604.