Respiratory Acidosis and Alkalosis

Introduction

Key Concepts

• PCO₂ is inversely proportional to alveolar ventilation.
• ⩒_E = Respiratory Rate x Tidal Volume (Minute Ventilation)
• ⩒_D = Dead space

• Therefore, a decrease in minute ventilation results in increased PCO₂, leading to acidosis.
• An increase in minute ventilation decreases PCO₂, thereby causing alkalosis.¹
• This equation also demonstrates how changes in dead space contribute to PCO₂ levels.

Overview

• The respiratory system is a critical component of the physiological regulation networks governing systemic acid-base homeostasis.
• The body relies on peripheral chemoreceptors (found in the carotid bodies, the bifurcations of the carotid arteries, and the aortic arch) and central chemoreceptors (found in the medulla and the pons) to detect changes in PCO₂ by monitoring blood pH.²
• Activation of central chemoreceptors increases minute ventilation.
• The ideal systemic pH is 7.35-7.45, allowing for proper function of intracellular and extracellular biological functions.³
• Changes in ventilation help maintain a buffer system, allowing proper excretion of CO₂.

Please refer to the OA summary on “Normal Acid-Base Balance” for further details. Link.

Definitions

• Respiratory acidosis is a hypoventilation-driven acid-base disorder defined by a decreased ratio of arterial bicarbonate to arterial PCO₂, with laboratory findings of:⁴
  • PCO₂ >45mmHg
  • pH <7.35
• Respiratory alkalosis is a hyperventilation-driven acid-base disorder defined by an increased ratio of arterial bicarbonate to arterial PCO₂, with laboratory findings of:⁵
  • PCO₂ <35 mmHg
  • pH >7.45

Evaluation and Diagnosis

• Respiratory acidosis and alkalosis are physiologically defined disorders that are diagnosed exclusively on the basis of laboratory values.
• Arterial blood gas (ABG) analysis is the most accurate method for determining systemic pH and gas exchange; however, it requires arterial puncture, which carries a higher procedural risk and is more time-intensive than venous blood gas obtained from a peripheral site.²
• Venous blood gas samples offer a faster, simpler approach to collection via peripheral venipuncture; however, they have been shown to be less accurate overall than ABGs.
• The modality of blood gas determination should be guided by clinical urgency, safety, and resource availability
• Intraoperatively, end tidal CO₂ may be used as a surrogate for PCO₂; however, the dead space from the ventilator must be considered

Acute vs Chronic Differentiation

• Further classification of respiratory acidosis and alkalosis as acute or chronic is determined by the degree of metabolic (renal) bicarbonate compensation.
• Acute compensation occurs in minutes, while chronic compensation occurs over days.
• Failure of expected compensation indicates the presence of a mixed metabolic-respiratory acid-base disorder.⁴

Respiratory Acidosis

Chronic vs Acute Metabolic Compensation

• Acute respiratory acidosis: HCO₃^– increase of 1 mEq/L for every incremental increase (10 mmHg) of PCO₂.
• Chronic respiratory acidosis: HCO₃^– increase of 4 mEq/L for every incremental increase (10 mmHg) of PCO₂.

Predominant Etiologies of Acute Respiratory Acidosis

• There are 3 main pathophysiologic drivers of respiratory acidosis
  • Dysfunction of alveolar ventilation
  • Respiratory muscle/chest wall dysfunction
  • Central nervous system (CNS) dysfunction

Predominant Etiologies of Chronic Respiratory Acidosis

• Common causes of chronic respiratory acidosis include
  • Chronic obstructive pulmonary disease
  • Obesity hypoventilation syndrome
  • Chronic neuromuscular weakness

Clinical Presentation

The main driver of respiratory acidosis clinical presentation is the effects of elevated PCO₂.

Neurologic

• Neurologic sequelae are caused by CO₂-mediated cerebral vasodilation results in increased intracranial pressure (ICP).
• Clinical manifestations of increased ICP include altered mental status, headache, and sedation.

Cardiopulmonary

• Cardiopulmonary consequences include pulmonary vasoconstriction, pulmonary hypertension, systemic vasodilation, and decreased cardiac output.
• The resultant decrease in cardiac output is opposed by sympathetic activity, causing systemic hypertension
• In severe cases of respiratory acidosis, patients may develop cor pulmonale.³

Treatment

Treatment of respiratory acidosis is the identification and treatment of the underlying cause, which may include:

• Antimicrobial treatment for infectious processes
• Corticosteroids for inflammatory processes
• Reversal agents for substance ingestion
• Bronchodilators or ventilation support if necessary

Perioperative Considerations

• Permissive hypercapnia
  • Permissive Hypercapnia is lung protective ventilation (LPV) strategy where intentional mechanical hypoventilation is utilized to minimize volutrauma, atelectotrauma, and biotrauma.³
  • The main principle of LPV is maintaining small tidal volumes; in this case, minute ventilation is the only provider-controlled component for PCO₂ regulation.
  • Please see the OA summary on permissive hypercapnia. Link
• Dead space ventilation
  • Dead space is an area of the lung that does not participate in gas exchange.
  • Conditions resulting in increased dead space, including pulmonary embolism, severe hypertension, and decreased cardiac output, increase hypercapnia and resultant
    acidosis.³
• Ventilator management
  • Reduction of ventilator-associated dead space (excessive tubing) allows for reduction of PCO₂.
  • Increased tidal volume (with consideration of LPV) promotes greater CO₂ elimination.
  • An increase in respiratory rate facilitates greater CO₂ clearance per minute.
• Other Considerations
  • For patients with chronic respiratory acidosis, medications that depress respiratory rate, such as opioids and sedatives, should be avoided/limited in the pre- and postoperative stages to prevent exacerbation of the existing respiratory acidosis.
  • Individuals with chronic respiratory acidosis (i.e., chronic obstructive pulmonary disease) should not undergo rapid normalization of PCO₂, as this would disrupt the compensatory hypoxemic drive for respiration, leading to worsening hypercapnia and acidosis.
  • Correction of acidemia should be made gradually to prevent rapid alkalinization of the cerebral spinal fluid, leading to seizures.⁴

Respiratory Alkalosis

Acute vs Chronic

• Acute respiratory alkalosis: HCO₃^– decrease of by 2 mEq/L per incremental decrease (10 mmHg) of PCO₂.
• Chronic respiratory alkalosis: HCO₃^– decrease of by 5 mEq/L per incremental decrease (10mmHg) of PCO₂.¹

Predominant Etiologies: Acute

• Alveolar hyperventilation
• Hypoxemia driven hyperventilation
• Cardiopulmonary receptor stimulation

Predominant Etiologies: Chronic

• Long-term hyperventilation (pregnancy)
• Chronic liver disease
• Long-term high-altitude exposure

Clinical Presentation

• Clinical manifestations of respiratory alkalosis are heavily influenced by the resulting decrease in ionized calcium, resulting in paresthesia, muscle spasms, and tetany2
• Alkalosis also results in systemic vasoconstriction, resulting in tissue hypoperfusion and cardiac arrhythmias.
• Alkalosis may lead to electrolyte abnormalities manifesting as life-threatening arrhythmias, altered mental status, or muscular dysfunction.

Treatment and Perioperative Considerations

• Intraoperative respiratory alkalosis is typically precipitated by mechanical hyperventilation and inadequate analgesia.
• Treatment of respiratory alkalosis is the identification and treatment of the underlying cause, which may include²
  • Pain management
  • Anxiety management
  • Discontinuation of causative medications
  • Antimicrobials for infectious processes

Important Consideration: Rapid correction of alkalosis may lead to reperfusion injury, depending on the severity.