Respiratory Alkalosis

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. When hypoventilation occurs, excess carbon dioxide is blown off and respiratory alkalosis develops. The kidneys respond by decreasing serum bicarbonate (HCO3) through increased HCO3 excretion or decreased excretion of H+. Patients present with an increased respiratory rate, dyspnea, light-headedness and potentially psychologic symptoms. Diagnosis involves a thorough history, an exam, and an arterial blood gas measurement. Management focuses on addressing the underlying abnormalities, stabilizing patients in acute distress, and potentially a small dose of short-acting benzodiazepines.

 

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Overview

Definition

Respiratory alkalosis refers to the process that results in a decreased level of carbon dioxide (CO2) within the blood.

Epidemiology

  • Gender bias: male = female
  • Incidence: dependent on the etiology
  • Incidence of hyperventilation syndrome: 25%–80% in adults with anxiety

Etiology

Table: Etiologies of respiratory alkalosis
EtiologyExamples
Physiologic (not pathologic)
  • Pregnancy
  • High altitude
Hypoxia-induced
  • Pulmonary embolism
  • Pulmonary edema
  • COPD or asthma exacerbations
Medications
  • Aspirin overdose
  • Nicotine overdose
  • Progesterone
Intracranial processes
  • Stroke
  • Encephalitis
  • Traumatic brain injury
Psychologic etiologies
  • Anxiety
  • Psychosis
Other processes
  • Pain
  • Fever

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

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 alkalosis is a process that results in a decreased level of carbon dioxide. 

  • Almost always due to hyperventilation (↑ respiratory rate)
  • The arterial blood gas will show:
    • pH > 7.40 
    • PCO2 < 30 mmHg 
  • The hyperventilation may be caused by:
    • ↑ Drive from the CNS (pathologic or physiologic)
    • Hypoxemia-induced causes → body attempts to correct the hypoxia at the expense of CO2 loss

Renal compensation

  • Kidneys respond to respiratory alkalosis by decreasing serum HCO3:
    • Excretion of HCO3 is increased → threshold for HCO3reabsorption is changed 
    • Decreased secretion of H+ 
  • Process takes 3–5 days to complete:
    • Cells must undergo physical changes.
    • Serum HCO3 and pH decrease slowly during this time.
  • Degree of compensation defines acute versus chronic respiratory alkalosis.

Renal compensation of respiratory alkalosis:
In respiratory alkalosis, the PCO2 is decreased, shifting the PCO2 curve to the right (1). As HCO3– levels are decreased by the kidneys, the pH improves along the PCO2 line (2)

Image by Lecturio.

Acute versus chronic respiratory alkalosis

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

  • Acute respiratory alkalosis is uncompensated:
    • Not enough time for renal compensation to occur
    • More likely to be symptomatic from hypocapnia
  • Chronic respiratory alkalosis is compensated:
    • Renal compensation is complete.
    • HCO3 decreases by approximately 4 mEq/L per 10-mmHg decrease in PaCO2
    • Usually asymptomatic, despite chronic hypocapnia
    • Hypocapnia is usually mild and pH may be very near normal.

Clinical Presentation, Diagnosis, and Management

Clinical presentation

  • Tachypnea
  • Dyspnea
  • Dizziness/light-headedness
  • Paresthesias (perioral, hands/feet) due to decreased ionized calcium
  • Psychologic symptoms:
    • Anxiety
    • Fear
    • Impending doom
  • Highly variable presentation, based on underlying etiology; for example:
    • High-altitude illness: findings consistent with pulmonary and/or cerebral edema
    • Sepsis: fever, hypotension, findings consistent with originating infection (e.g., cough or dysuria)
    • Pulmonary embolism: calf pain, unilateral lower-extremity edema

Diagnosis

Diagnosing a respiratory alkalosis typically requires a thorough history and exam and an arterial blood gas measurement.

  • Arterial blood gas:
    • Acute respiratory alkalosis (uncompensated): 
      • pH > 7.45
      • PaCO2 < 35 mmHg
      • Normal HCO3
    • Chronic respiratory alkalosis (compensated):
      • pH > 7.4 (slightly high or near-normal)
      • PaCO2 < 35 mmHg
      • HCO3 decreased
  • Electrolytes: Abnormalities are common and may lead to complications.
    • Basic metabolic panel
    • Magnesium
    • Phosphate
  • Chest X-ray: to rule out other causes of tachypnea

Management

  • Assess and address the ABCs (airway, breathing, and circulation) if patient is in acute distress.
  • Attempt to correct the underlying abnormality.
  • Small dose of short-acting benzodiazepine

Clinical Relevance

  • Hyperventilation syndrome: an inappropriate increase in minute ventilation beyond basic needs, typically associated with panic disorder: Patients will typically present with intermittent episodes of spontaneously resolving hyperventilation, often with mild dyspnea, dizziness, and chest tightness. Metabolic alkalosis may develop. Diagnosis involves excluding physiologic causes of tachypnea. Management involves reassurance and possibly short-acting benzodiazepines.
  • High-altitude illness: a collective term for conditions involving cerebral and pulmonary symptoms that occur initially at high altitude: Hypoxia at higher altitudes stimulates hyperventilation, which can lead to respiratory alkalosis. These conditions are characterized by fluid shifts out of the vessels into the extravascular fluid space, leading to cerebral and pulmonary edema. Management involves descent to a lower elevation and oxygen therapy.
  • Salicylate toxicity: a complex mechanism that results in a mixed acid–base disorder, involving both respiratory alkalosis and metabolic acidosis: Activation of the respiratory center in the medulla results in hyperventilation, while interference with cellular metabolism can lead to metabolic acidosis. The patient can also have significant vomiting, and gastric ulcers and platelet dysfunction may develop. After initial stabilization, patients can be treated with activated charcoal to absorb the aspirin.

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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