Respiratory Acidosis

The respiratory system is responsible for eliminating the volatile acid carbon dioxide (CO2), which is produced via aerobic metabolism. The body produces approximately 15,000 mmol of CO2 daily, which is the majority of daily acid production; the remainder of the daily acid load (only about 70 mmol of nonvolatile acids) is excreted through the kidneys. In the setting of hypoventilation, this acid load is not adequately blown off, and respiratory acidosis occurs. Renal compensation occurs after 3–5 days, as the kidneys attempt to increase the serum bicarbonate levels. Patients are often asymptomatic, or they may present with neuropsychiatric manifestations or mild dyspnea. Diagnosis is made with arterial blood gas measurement. Management involves treating the underlying etiology, stabilizing the patient, and avoiding respiratory sedatives.

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Overview

Definition

Respiratory acidosis is the process that results in an accumulation of carbon dioxide (CO2) due to abnormal gas exchange in the lungs. In primary respiratory acidosis, the arterial blood gas will show:

  • pH < 7.4 
  • PCO2 (partial pressure of carbon dioxide) > 40 mm Hg (i.e., hypercapnia)

Epidemiology

  • Incidence: varies based on the etiology
  • More common in:
    • End-stage chronic obstructive pulmonary disease (COPD)
    • Surgical patients

Acid–Base Review

Acid–base disorders are classified according to the primary disturbance (respiratory or metabolic) and the presence or absence of compensation.

Identifying the primary disturbance

Look at the pH, PCO2 (partial pressure of CO2), and HCO3 (bicarbonate) to determine the primary disturbance. 

  • Normal values:
    • pH: 7.35–7.45
    • PCO2:  35–45 mmHg
    • HCO3: 22–28 mEq/L
  • “-emia” versus “-osis”:
    • “-emia” refers to “in the blood”:
      • Acidemia: more hydrogen ions (H+) in the blood = pH < 7.35
      • Alkalemia: more hydroxide ions (OH) in the blood = pH > 7.45 
    • “-osis” refers to a process:  
      • Acidosis and alkalosis refer the processes that cause acidemia and alkalemia. 
      • pH may be normal in acidosis and alkalosis.
  • Primary (uncompensated) respiratory disorders: 
    • Disorders caused by abnormalities in PCO2
    • Both the pH and PCO2 are abnormal, in opposite directions.
    • Primary respiratory acidosis:  pH < 7.35 and PCO2 > 45 
    • Primary respiratory alkalosis: pH > 7.45 and PCO2 < 35
  • Primary (uncompensated) metabolic disorders: 
    • Disorders caused by abnormalities in HCO3 
    • Both the pH and PCO2 are abnormal, in the same direction. 
    • Primary uncompensated metabolic acidosis:  
      • pH < 7.35 and PCO2 < 40 
      • Think: “So the acidosis is not due to ↑ CO2 … it must be due to ↓ serum HCO3 → metabolic acidosis”
      • Confirm by looking at HCO3: will be low (< 22 mEq/L)
    • Primary uncompensated metabolic alkalosis: 
      • pH > 7.45 and PCO2 > 40
      • Think: “So the alkalosis is not due to ↓ CO2… it must be due to ↑ serum HCO3 → metabolic alkalosis”
      • Confirm by looking at HCO3: will be high (> 28 mEq/L)
  • Simple disorders:
    • The presence of one of the above disorders with appropriate compensation
    • Respiratory disorders are compensated by renal mechanisms.
    • Metabolic disorders are compensated by respiratory mechanisms
  • Mixed disorders: two primary disorders present

Compensation

When acidosis or alkalosis develops, the body will try to compensate. Often, compensation will result in a normal pH.

  • In primary respiratory acid–base disorders, the kidney may try to compensate in an attempt to normalize the pH.
    • Kidneys respond to respiratory acidosis by increasing serum HCO3 through ↑ secretion of H+.
    • Kidneys respond to respiratory alkalosis by decreasing serum HCO3 through:
      • ↓ Secretion of H+
      • Urinary excretion of HCO3 (normally bicarbonate is 100% absorbed)
  • In primary metabolic acid–base disorders, the lungs may try to compensate in an attempt to normalize the pH.
    • Lungs respond to metabolic acidosis by ↑ ventilation.
    • Lungs respond to metabolic alkalosis by ↓ ventilation.
  • Interpreting the serum HCO3:
    • Normal range: 22–28 mEq/L
    • ↑ HCO3 is due to either:
      • Metabolic alkalosis, or
      • Compensated chronic respiratory acidosis
    • ↓ HCO3 is due to either:
      • Metabolic acidosis, or
      • Compensated chronic respiratory alkalosis

Pathophysiology and Etiology

Review of relevant pulmonary concepts

  • Tidal volume (TV): volume of air moved into and out of the lungs per breath
  • Hypercapnia: elevated levels of CO2 in the blood
  • Dead space: air in the respiratory tree that does not participate in gas exchange
    • Anatomic dead space:
      • Upper airway down to the terminal bronchioles
      • Fixed volume of air
    • Alveolar dead space:
      • Refers to certain alveoli that are ventilated but not perfused
      • Normally very small total volume, unless there is a pathologic process
    • Physiologic dead space = anatomic dead space + alveolar dead space 
  • Effects of deep versus shallow breaths:
    • Deep breath:  ↑ TV + fixed volume of dead space
      • Dead space is a smaller fraction of total ventilation.
      • Better gas exchange → no hypercapnia
    • Shallow breath = ↓ TV + fixed volume of dead space
      • Dead space is a higher fraction of total ventilation.
      • Worse gas exchange → risk for hypercapnia
  • Minute ventilation:
    • Volume of air moved into and out of the lungs per minute
    • Minute ventilation = tidal volume × respiratory rate
  • Alveolar ventilation (VA):
    • The fraction of the minute ventilation that participates in gas exchange 
    • VA is inversely related to PaCO2 
      • As ventilation ↑ → PaCO2 ↓ 
      • As ventilation ↓ → PaCO2 ↑ 
    • VA = (tidal volume – dead space) × respiratory rate

Relationship between alveolar ventilation and PCO2

Image by Lecturio.

Pathophysiology

Respiratory acidosis occurs when the PCO2 is elevated. 

  • Causes of respiratory acidosis:
    • ↓ Alveolar ventilation (VA):
      • ↓ Respiratory rate
      • ↓ Tidal volume
      • ↑ Dead space
    • Severe ↓ lung diffusion capacity 
    • Severe ventilation–perfusion mismatch
  • These conditions may occur because of abnormalities in the respiratory pathway affecting CO2 elimination:
    • CNS
    • Peripheral nervous system
    • Respiratory muscles and the chest wall
    • Upper airways 
    • Lungs
Table: Respiratory pathway affecting CO2 elimination
How is CO2 elimination affected?Disruption of CO2 elimination is caused by disorders of the:
“Won’t breathe”CNS
“Can’t breathe”
  • Peripheral nervous system
  • Respiratory muscles and chest wall
  • Upper airways
Abnormal gas exchange: “can’t breathe enough”Lungs

Etiology

Table: Etiologies of respiratory acidosis
EtiologyExamples
↓ Respiratory rate: ↓ respiratory drive
  • Medications:
    • Opiates
    • Benzodiazepines
  • Primary brain disorders:
    • Stroke
    • Encephalitis
    • Brainstem disease
  • Obstructive sleep apnea
↓ Tidal volume: impaired ability to fully expand the lungs
  • Respiratory muscle weakness:
    • Guillain–Barré syndrome
    • Myasthenia gravis
    • ALS
    • Muscular dystrophy
    • Cervical spine injury above C3
    • Metabolic disorders: hypophosphatemia, hypomagnesemia, hypokalemia
  • Decreased chest wall compliance:
    • Obesity
    • Kyphoscoliosis
    • Ankylosing spondylitis
    • Pectus excavatum
↑ Alveolar dead space: impaired ability for gas exchange
  • Pulmonary fibrosis: Scar tissue prevents gas exchange.
  • Pulmonary edema: Fluid in alveoli prevents gas exchange.
  • Pulmonary embolus: Blood clot prevents perfusion of alveoli.
  • Chronic obstructive pulmonary disease (COPD): alveoli destruction
  • Asthma: airway obstruction preventing effective alveolar ventilation

Renal compensation

The kidneys respond to respiratory acidosis by increasing serum HCO3.

  • Mechanism of ↑ HCO3: ↑ renal secretion of H+ 
    • H+ exists in the nephrons as H2CO3 (carbonic acid).
    • For each H+ secreted, one HCO3 is left over (i.e., regenerated).
    • This HCO3 is then reabsorbed into circulation → ↑ serum HCO3  
  • Level of HCO3 increases:
    • Initially by approximately 1 mEq/L per 10 mmHg ↑ in PaCO2
    • By approximately 4 mEq/L per 10 mm Hg ↑ in the partial pressure of arterial CO2 (PaCO2) in patients with chronic respiratory acidosis
  • Process takes 3–5 days to complete:
    • Cells must undergo physical changes to allow increased H+ secretion.
    • Serum HCO3 and pH rise slowly during this time.
    • pH improves.

Acute versus chronic respiratory acidosis

Acute versus chronic respiratory acidosis is defined by the degree of renal compensation.

  • Acute respiratory acidosis is uncompensated:
    • Not enough time for renal compensation to occur
    • More likely to be symptomatic because of hypercapnia
    • High risk for acute respiratory failure within minutes to hours
  • Chronic respiratory acidosis is compensated:
    • Renal compensation is complete.
    • Usually asymptomatic, despite chronic hypercapnia
    • Low risk for acute respiratory failure within the next minutes to hours
    • Significant long-term risk for acute respiratory failure if exposed to additional insults

Clinical Presentation, Diagnosis, and Management

Clinical presentation and diagnosis

Diagnosing a respiratory acidosis typically requires an arterial blood gas.

  • Clinical presentation of hypercapnia:
    • Neurologic:
      • Anxiety/paranoia
      • Headaches
      • Somnolence
      • Delirium
      • Coma
    • Pulmonary: dyspnea (usually mild)
  • Diagnosis: primarily with an arterial blood gas (ABG):
    • Acute respiratory acidosis: 
      • pH < 7.35
      • PaCO2 > 45 mmHg
      • Normal HCO3
    • Chronic respiratory acidosis (compensated):
      • pH < 7.4 (low or near-normal)
      • PaCO2 > 45 mmHg
      • HCO3 elevated

Management

  • Assess the ABCs:
    • Ensure that the airway is secure.
    • Administer supplemental O2.
    • Ventilatory support as needed
  • Treat the underlying etiology; examples include:
    • COPD exacerbation: bronchodilators and corticosteroids
    • Pneumonia in neuromuscular disorders: antibiotics
  • Avoid respiratory sedatives.

Clinical Relevance

  • Myasthenia gravis: an autoimmune disorder characterized by abnormalities in neuromuscular conduction that results in fluctuating weakness and can lead to acute hypercapnic respiratory failure 
  • Guillain–Barré syndrome: a postinfectious acute, immune-mediated polyneuropathy of the peripheral nerve roots characterized by progressive, symmetrical, and ascending paralysis that ultimately affects the patient’s ability to breath 
  • Chronic obstructive pulmonary disease (COPD): a spectrum of conditions characterized by irreversible airflow limitation due to chronic inflammation of small airways: Exacerbations of COPD can impair alveolar ventilation, raise PaCO2, and induce an acidotic state.
  • Asthma: a chronic inflammatory condition of the airways, characterized by bronchial hyperreactivity, which presents as wheezing, cough, and dyspnea: Acute exacerbations of asthma cause a sudden impairment of alveolar ventilation and can lead to respiratory acidosis.

References

  1. Emmett, M., Palmer B. F. (2020). Simple and mixed acid-base disorders. UpToDate. Retrieved April 1, 2021, from https://www.uptodate.com/contents/simple-and-mixed-acid-base-disorders 
  2. Feller-Kopman, D. J., Schwartzstein, R. M. (2021). Mechanisms, causes, and effects of hypercapnia. UpToDate. Retrieved April 1, 2021, from https://www.uptodate.com/contents/mechanisms-causes-and-effects-of-hypercapnia
  3. Theodore, A. C. (2020). Arterial blood gases. UpToDate. Retrieved April 1, 2021, from https://www.uptodate.com/contents/arterial-blood-gases
  4. Feller-Kopman, D. J., Schwartzstein, R. M. (2021). The evaluation, diagnosis, and treatment of the adult patient with acute hypercapnic respiratory failure. UpToDate. Retrieved April 8, 2021, from https://www.uptodate.com/contents/the-evaluation-diagnosis-and-treatment-of-the-adult-patient-with-acute-hypercapnic-respiratory-failure

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