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Hypercapnia

ISSN 2398-2950

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Introduction

  • Hypercapnia is an elevation above normal of the arterial pressure of carbon dioxide (CO2) ( PaCO2 >45 mm Hg).
  • Most cases of hypercapnia are a result of hypoventilation. Sequelae of prolonged hypercapnia include respiratory acidosis Acid base imbalance  and increased intracranial pressure Intracranial pressure measurement.  Mechanical ventilation may be required to correct hypercapnia until the underlying condition can be corrected.

Presenting signs

  • Rapid, shallow breathing associated with hypoventilation.
  • Tachycardia, hypertension, or arrhythmias secondary to increased sympathetic tone associated with respiratory acidosis.
  • Slow respiratory rate; CNS depression, obtundation, or coma may occur secondary to increased intracranial pressure.
  • Other clinical signs may be present depending on the underlying disease such as CNS disease, neuromuscular disease, drugs, toxins, respiratory fatigue, etc.
  • Patients receiving general anesthesia: no apparent signs. Normal respiratory rate, low tidal volume.

Acute presentation

  • Depends on underlying disease, but often associated with rapid shallow breathing or signs of respiratory distress if associated with hypoxemia Hypoxemia.

Geographic incidence

  • No specific geographic predispositions.

Age predisposition

  • No age predisposition.

Breed/Species predisposition

  • No breed predisposition.

Public health considerations

  • No public health concerns.

Cost considerations

  • Animals with hypoventilation, hypoxemia and/or hypercapnia all require intensive monitoring and supportive care which is likely to be expensive.
  • If mechanical ventilation is required, the costs associated with the intensive monitoring are extremely expensive.

Special risks

  • Animals with hypercapnia are marked anesthetic risks because many anesthetics blunt the normal regulatory response mechanisms.

Pathogenesis

Etiology

  • Hypercapnia is almost exclusively a result of hypoventilation, which can be a result of numerous underlying disease states.

Predisposing factors

General

  • Chronic pulmonary disease.
  • CNS or neuromuscular disease.
  • Prolonged hypoxemia which may result in respiratory fatigue.
  • Respiratory depressant drugs.

Pathophysiology

  • Carbon dioxide (CO2) metabolism:
    • Produced by cellular metabolism.
    • In the bloodstream CO2 combines with water to form carbonic acid, which dissociates to form hydrogen and bicarbonate ions.  While the hydrogen ions combine with intracellular buffers such as Hb, the bicarbonate moves into the extracellular space.  Metabolically produced CO2 is carried in the bloodstream primarily as bicarbonate while effecting little change on the extracellular pH.
    • The reverse process results in CO2 excretion from the RBC when Hb is oxygenated, thus ventilation allows for removal of CO2 from the bloodstream.
  • Control of Ventilation:
    •  Main stimuli to respiration are decreased arterial PO2 (hypoxemia) and increased arterial PCO2 (hypercapnia).
    • CO2 is the major stimulus via effects on chemoreceptors of the respiratory center in the medulla which respond to changes in CSF pH:
      • Ventilation will increase by 1-4 L/min for every 1 mm Hg rise in PCO2.
    • O2 plays a lesser role via effects on the chemoreceptors located in the carotid bodies:
      • Hypoxemia does not substantially promote ventilation until the PaO2 is less than 50-60 mm Hg.
  • Development of hypercapnia:
    • Decreased ventilation:
      • Most common reason for development of hypercapnia by far.
    • Increased CO2 production:
      • Increased metabolic CO2 production may occur with hyperthermia.
      • Increased inspired CO2 is usually an anesthetic accident.

Diagnosis

Presenting problems

  • Usually respiratory-related (rapid, shallow breathing) or related to the effects of prolonged hypercapnia (CNS depression, coma).

Client history

  • Complaints of respiratory disease such as rapid, shallow breathing.  There may also be a history of chronic respiratory disease or of neurologic disease.
  • Primary complaint may be related to the sequelae of hypercapnia such as CNS depression.

Clinical signs

  • Rapid, shallow breathing associated with hypoventilation.
  • Tachycardia, hypertension, or arrhythmias secondary to increased sympathetic tone associated with respiratory acidosis.
  • Slow respiratory rate; CNS depression, obtundation, or coma may occur secondary to increased intracranial pressure.
  • Other clinical signs may be present depending on the underlying disease such as CNS disease, neuromuscular disease, drugs, toxins, respiratory fatigue, etc.

Diagnostic investigation

  • Arterial blood gas analysis Arterial blood gas sampling is the best way to assess ventilation. In the conscious patient, PaCO2 values >45 mm Hg are abnormal.
  • Chest radiographs Radiography: thorax are often useful to elucidate the underlying disease process.  Further diagnostics aimed at diagnosing the underlying problem will depend on the results of initial diagnostic workup.
  • End-tidal CO2 monitoring can be useful in intubated animals. 
    Bear in mind that the end-tidal CO2 normally is 2-5 mm Hg lower than the PaCO2 and that the end-tidal CO2 may underestimate the PaCO2 under many circumstances, especially when severe hypercapnia is present.
  • Venous PCO2 may give a general idea about whether hypercapnia may be present.  The venous PCO2 normally is 5-10 mm Hg higher than the arterial PCO2. 
    A normal venous CO2 confirms the absence of systemic hypercapnia, but an elevated venous CO2 does not confirm its presence due to local effects on venous blood.

Definitive diagnostic features

Gross autopsy findings

  • Depends on underlying disease.

Histopathology findings

  • Depends on underlying disease.

Differential diagnosis

  • Hypoventilation:
    • CNS disease.
    • Neuromuscular disease.
    • Pulmonary parenchymal disease.
    • Respiratory muscle fatigue.
    • Pleural space disease.
    • Chest wall damage.
    • Upper airway disease.
  • Increased dead space ventilation:
    • Increased physiologic dead space.
      • Pulmonary thromboembolism.
    • Increased anatomic equipment dead space:
      • Usually anesthetic accident, eg ET tube far beyond dental arcade.
  • Increased CO2 production:
    • Increased metabolic production.
    • Increased inspired CO2:
      • Usually anesthetic accident.

Treatment

Initial symptomatic treatment

  • Ensuring a patent airway followed by mechanical ventilation are the most effective means for correcting hypercapnia due to hypoventilation, however this requires specialized equipment and staff and is very expensive.
    Hand ventilating is just as effective.
  • Bag squeezing for GA patients.
  • Supplemental oxygen Nasal oxygen administration, only in those animals that are also hypoxemic. 
    This may worsen the hypercapnia in some cases.
  • Respiratory stimulating drugs have questionable efficacy:

Subsequent management

Treatment

  • Will be aimed at correcting the underlying condition when possible.

Monitoring

Prevention

Outcomes

Prognosis

  • Ultimately depends on underlying disease, but is guarded in most cases.
  • Animals requiring mechanical ventilation typically have a poor prognosis, though it can be a life-saving measure with a positive outcome when the underlying disease is reversible (eg drug overdose, cervical intervertebral disk disease).

Expected response to treatment

  • Most animals will respond well to appropriate supportive treatment, but the underlying disease must ultimately be corrected.

Reasons for treatment failure

  • Untreatable underlying disease.
  • Unavailability of specialized equipment or staffing required for mechanical ventilation.

Further Reading

Publications

Refereed papers

Other sources of information

  • King L G (2004) Textbook of Respiratory Disease in Dogs and Cats. Saunders, St. Louis.
  • West J B  (2000) Respiratory Physiology The Essentials. 6th edn. Lippincott Williams & Wilkins, Baltimore.
  • Rose B D (1994) Clinical Physiology of Acid-Base and Electrolyte Disorders. 4th edn.  McGraw-Hill, Inc., New York.