Physiology, Respiratory Acidosis


Article Author:
Shivani Patel


Article Editor:
Sandeep Sharma


Editors In Chief:
Linda Lindsay


Managing Editors:
Avais Raja
Orawan Chaigasame
Carrie Smith
Abdul Waheed
Khalid Alsayouri
Frank Smeeks
Kristina Soman-Faulkner
Trevor Nezwek
Radia Jamil
Patrick Le
Sobhan Daneshfar
Anoosh Zafar Gondal
Saad Nazir
William Gossman
Pritesh Sheth
Hassam Zulfiqar
Navid Mahabadi
Steve Bhimji
John Shell
Matthew Varacallo
Heba Mahdy
Ahmad Malik
Mark Pellegrini
James Hughes
Beata Beatty
Nazia Sadiq
Hajira Basit
Phillip Hynes
Tehmina Warsi


Updated:
5/4/2019 1:39:16 PM

Introduction

Respiratory acidosis is a state in which there is usually a failure of ventilation and an accumulation of carbon dioxide. The primary disturbance of elevated arterial PCO2 is the decreased ratio of arterial bicarbonate to arterial PCO2, which leads to a lowering of the pH. In the presence of alveolar hypoventilation, 2 features commonly are seen are respiratory acidosis and hypercapnia. To compensate for the disturbance in the balance between carbon dioxide and bicarbonate (HCO3-), the kidneys begin to excrete more acid in the forms of hydrogen and ammonium and reabsorb more base in the form of bicarbonate. This compensation helps to normalize the pH.[1]

Etiology

The respiratory centers in the pons and medulla control alveolar ventilation. Chemoreceptors for PCO2, PO2, and pH regulate ventilation. Central chemoreceptors in the medulla are sensitive to changes in the pH level. A decreased pH level influences the mechanics of ventilation and maintains proper levels of carbon dioxide and oxygen. When ventilation is disrupted, arterial PCO2 increases and an acid-base disorder develop. Another pathophysiological mechanism may be due to ventilation/perfusion mismatch of dead space.

Respiratory acidosis can be subcategorized as acute, chronic, or acute and chronic. In acute respiratory acidosis, there is a sudden elevation of PCO2 because of failure of ventilation. This may be due to cerebrovascular accidents, use of central nervous system (CNS) depressants such as opioids, or inability to use muscles of respiration because of disorders like myasthenia gravis, muscular dystrophy or Guillain-Barre Syndrome. Because of its acute nature, there is a slight compensation occurring minutes after the incidence. On the contrary, chronic respiratory acidosis may be caused by COPD where there is a decreased responsiveness of the reflexes to states of hypoxia and hypercapnia. Other individuals who develop chronic respiratory acidosis may have fatigue of the diaphragm resulting from a muscular disorder. Chronic respiratory acidosis can also be seen in obesity hypoventilation syndrome, also known as Pickwickian syndrome, amyotrophic lateral sclerosis, and in patients with severe thoracic skeletal defects. In patients with chronic compensated respiratory disease and acidosis, an acute insult such as pneumonia or disease exacerbation can lead to ventilation/perfusion mismatch.

Respiratory acidosis may cause slight elevations in ionized calcium and an extracellular shift of potassium. However, the hyperkalemia is usually mild. In chronic respiratory acidosis, renal compensation occurs gradually over the course of days.[2][3]

Epidemiology

The frequency of respiratory acidosis in the United States and worldwide varies based on the etiology. End-stage COPD patients are more prone to develop this acid-base disorder. It has also been noted that surgical patients are at a greater risk of developing respiratory acidosis.

Pathophysiology

Carbon dioxide plays a remarkable role in the human body mainly through pH regulation of the blood. The pH is the primary stimulus to initiate ventilation. In its normal state, the body maintains CO2 in a well-controlled range from 38 to 42 mm Hg by balancing its production and elimination. In a state of hypoventilation, the body produces more CO2 than it can eliminate, causing a net retention of CO2. The increased CO2 is what leads to an increase in hydrogen ions and a slight increase in bicarbonate, as seen by a right shift in the following equilibrium reaction of carbon dioxide:

  • CO2 + H2O -> H2CO3- -> HCO3- + H+

The buffer system created by carbon dioxide consists of the following three molecules in equilibrium: CO2, H2CO3-, and HCO3-. When H+ is high, HCO3- buffers the low pH. When OH- is high, H2CO3 buffers the high pH. In respiratory acidosis, the slight increase in bicarbonate serves as a buffer for the increase in H+ ions, which helps minimize the drop in pH. The increase in hydrogen ions inevitably causes a decrease in pH, which is the mechanism behind respiratory acidosis.[4][5]

History and Physical

The clinical presentation of respiratory acidosis is usually a manifestation of its underlying cause. Signs and symptoms vary based on the length, severity, and progression of the disorder. Patients can present with dyspnea, anxiety, wheezing, and sleep disturbances. In some cases, patients may present with cyanosis due to hypoxemia. If the respiratory acidosis is severe and accompanied by prolonged hypoventilation, the patient may have additional symptoms such as altered mental status, myoclonus, and possibly even seizures. Respiratory acidosis leads to hypercapnia, which induces cerebral vasodilation. If severe enough, increased intracranial pressure and papilledema may ensue, increasing the risk of herniation and possibly even death. Cases of chronic respiratory acidosis may cause memory loss, impaired coordination, polycythemia, pulmonary hypertension, and heart failure. Persistence of apnea during sleep can lead to daytime somnolence and headaches. In patients with an obvious source of respiratory acidosis, the offending agent needs to be removed or reversed.[6]

Evaluation

An arterial blood gas (ABG) and serum bicarbonate level is necessary to evaluate patients with suspected respiratory acidosis. Other tests can be conducted to evaluate the underlying causes. In respiratory acidosis, the ABG will show an elevated PCO2 (>45 mmHg), elevated HCO3- (>30 mmHg), and decreased pH (<7.35). The respiratory acidosis can be further classified as acute or chronic based on the relative increase in HCO3- with respect to PCO2. In cases of acute respiratory acidosis, HCO3- will have increased by one mEq/L for every ten mmHg increase in PCO2 over a few minutes. In cases of chronic respiratory acidosis, HCO3- will have increased by four mEq/L for every ten mmHg increase in PCO2 over a time course of days. If the compensation does not occur in this pattern, a mixed respiratory-metabolic disorder may be present. In a patient who presents with unexplained respiratory acidosis, a drug screen may also be warranted.[7][8]

Treatment / Management

Once the diagnosis has been made, the underlying cause of respiratory acidosis has to be treated. The hypercapnia should be corrected gradually because rapid alkalization of the cerebrospinal fluid (CSF) may lead to seizures. Pharmacologic therapy can also be used to help improve ventilation. Bronchodilators like beta agonists, anticholinergic drugs, and methylxanthines can be used in treating patients with obstructive airway diseases. Naloxone can be used in patients who overdose on opioid use.[9][10]

Differential Diagnosis

  • Botulism
  • Bronchitis
  • Diaphragm Disorders
  • Diaphragmatic Paralysis
  • Asthma
  • Opioid Abuse
  • Sedative, Hypnotic, Anxiolytic Use Disorder
  • Chronic Obstructive Pulmonary Disease (COPD)
  • Obesity

Pearls and Other Issues

Patients who are moribund, lethargic or confused need to be monitored in the intensive care unit (ICU). Those who exhibit hypoventilation will need endotracheal intubation and mechanical ventilation. The use of respiratory stimulants has not been shown to be effective in treating respiratory acidosis. Medroxyprogesterone has been used to stimulate the respiratory drive, but its benefits are questionable. Hypoxic patients, of course, need supplemental oxygen.

Enhancing Healthcare Team Outcomes

The diagnosis of respiratory acidosis is easily made from an arterial blood gas but its management is complex. All healthcare workers including the nurse practitioners must be familiar with the management of respiratory acidosis. Once the diagnosis has been made, the underlying cause of respiratory acidosis has to be treated. The hypercapnia should be corrected gradually because rapid alkalization of the cerebrospinal fluid (CSF) may lead to seizures. Pharmacologic therapy can also be used to help improve ventilation. Bronchodilators like beta agonists, anticholinergic drugs, and methylxanthines can be used in treating patients with obstructive airway diseases. Naloxone can be used in patients who overdose on opioid use.

Patients who are moribund, lethargic or confused need to be monitored in the intensive care unit (ICU). Those who exhibit hypoventilation will need endotracheal intubation and mechanical ventilation. The use of CNS stimulants has not been shown to improve the condition and thus empirical prescription of these drugs should be avoided.


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Physiology, Respiratory Acidosis - Questions

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A 17-year-old male patient is seen in the emergency department after being involved in a motor vehicle accident. He has suffered multiple injuries to his chest. He has stable vital signs but has significant chest pain. The chest x-ray reveals multiple rib fractures and evidence of pulmonary contusion. His initial blood gasses are PCO2 51, PO2 64, pH 7.24 and bicarbonate 21. The arterial blood gas most likely represents which of the following conditions?



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Which of the following acid-base disorders is most likely in a 56-year-old with chronic obstructive pulmonary disease? (pH/bicarbonate/PO2/PCO2)



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What is the best treatment for a patient on the ventilator with acute respiratory acidosis?



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What is the correct interpretation of an arterial blood gas with a pH 7.36, PCO2 48, and bicarbonate 26?

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A patient has chronic respiratory acidosis. The differential is between central nervous system induced hypoventilation or a pulmonary parenchymal or airway cause. Which test would be most helpful?



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An arterial blood gas (ABG) reveals the following values: pH 7.35, PO2 63 mmHg, PCO2 48 mmHg, and bicarbonate 36 mEq/L. What is the interpretation of the ABG?

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Which of the following should not be given to a patient with respiratory acidosis?



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Which abnormal lab is expected with respiratory acidosis?

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Respiratory acidosis may not result from which one of the following conditions?



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To which of the following do neurons in the central chemoreceptors of the respiratory center in the brainstem respond most strongly?



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What is the major form in which carbon dioxide is carried in the blood?



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A 66-year-old male patient presents to the emergency department. Laboratory findings reveal a blood pH of 7.33, HCO3- of 25 millimol, and a pCO2 of 50 mmHg. Which of the following is the most likely disorder?



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A 28-year-old female presents with shortness of breath for 3 days which is progressively getting worse. In the emergency department, the blood workup shows white cell count of 14,000 with 78% neutrophils 78% and 11% eosinophils. Basic metabolic profile shows sodium of 136 mmol/L, potassium 4.1 mmol/L, chloride 100 mmol/L, and bicarbonate 20 mmol/L. The patient has seasonal allergies, and family history is positive for asthma in her mother. Chest x-ray is normal, EKG shows sinus tachycardia. Arterial blood gas (ABG) shows pH of 7.2, PCO2 of 60, and bicarbonate of 20. Initially, the patient was given albuterol and Ipratropium nebulization and intravenous corticosteroids, was put on BiPAP, but she did not improve. Her shortness of breath increased, and she was using accessory muscles. She is intubated and placed on a ventilator with settings AC mode tidal volume of 400, rate of 24, PEEP of 5, and FiO2 40%. ABG was drawn after 1 hour which shows pH 7.16, PCO2 66, and bicarbonate of 25. What is the acid-base disorder patient has on last ABG and how should the ventilator settings be adjusted?



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A 58-year-old female with the past medical history of very severe chronic obstructive pulmonary disease (FEV1 0.9L less than 30% predicted) and chronic carbon dioxide retention presents to the hospital complaining of worsening shortness of breath and cough productive of greenish-yellow phlegm without blood. Her oxygen saturation is 72% on room air. There is bilateral wheezing on the physical examination, and she is using accessory muscles to breath. She is alert awake oriented. Before she is placed on supplemental oxygen, a room air arterial blood gas is drawn which reveals pH 7.26, PCO2 68, PO2 48, and HCO3- 32. The chest x-ray is normal. EKG is normal. She is given corticosteroids, antibiotics, and ipratropium bromide/albuterol via nebulizer. What acid-base disorder does she have and what is the next step in treatment?



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Which of the following is not a cause of acidosis?



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A 27-year-old female presents to the emergency department with shortness of breath. Upon ordering an arterial blood gas, the findings were as follows: pH of 7.29, HCO3- of 24 millmol, and a pCO2 of 51 mmHg. Which of the following acid-base disorders is most likely seen in this patient?



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A 59-year-old female presents to the emergency room. Laboratory findings reveal a blood pH of 7.28, bicarbonate of 24.1 mmol/L, and a pCO2 of 49 mmHg. Which of the following is the most likely disorder?



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A 45-year-old male presents to the emergency department by ambulance. According to the paramedics, he was found with a needle in his arm on the side of the road unresponsive. His respiratory rate is 6 breaths per minute. What acid-base order is this patient likely experiencing?



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A patient has been admitted to a medical unit with multiple medical problems. His blood gas reveals that he has developed acute respiratory acidosis. Which of the following disorders are known to cause this disturbance? Select all that apply.



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In a client with respiratory acidosis, there may be alterations in which serum electrolyte? Select all that apply.



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Physiology, Respiratory Acidosis - References

References

CO2 pulse and acid-base status during increasing work rate exercise in health and disease., Kisaka T,Cox TA,Dumitrescu D,Wasserman K,, Respiratory physiology & neurobiology, 2015 Nov     [PubMed]
[Acid-base status in patients treated with peritoneal dialysis]., Katalinić L,Blaslov K,Pasini E,Kes P,Bašić-Jukić N,, Acta medica Croatica : casopis Hravatske akademije medicinskih znanosti, 2014 Apr     [PubMed]
Veno-venous extracorporeal CO2 removal for the treatment of severe respiratory acidosis., Cove ME,Federspiel WJ,, Critical care (London, England), 2015 Apr 17     [PubMed]
Permissive hypercapnia: what to remember., Contreras M,Masterson C,Laffey JG,, Current opinion in anaesthesiology, 2015 Feb     [PubMed]
Carbon dioxide in the critically ill: too much or too little of a good thing?, Marhong J,Fan E,, Respiratory care, 2014 Oct     [PubMed]
Gallo de Moraes A,Surani S, Effects of diabetic ketoacidosis in the respiratory system. World journal of diabetes. 2019 Jan 15;     [PubMed]
Castro D,Keenaghan M, Arterial Blood Gas 2018 Jan;     [PubMed]
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Brinkman JE,Sharma S, Physiology, Respiratory Drive 2018 Jan;     [PubMed]
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