Respiratory Failure

Respiratory failure occurs when the respiratory system fails in oxygenation and/or carbon dioxide elimination. Respiratory failure may be:¹

• Hypoxaemic respiratory failure (type I respiratory failure): PaO₂ is less than 60 mmHg (8kPa) with a normal or low PaCO₂. This is caused by ventilation-perfusion mismatch with either/both:
  • Under-ventilated alveoli (e.g. pulmonary oedema, pneumonia or acute asthma).
  • Venous blood bypasses ventilated alveoli (e.g. right to left cardiac shunts).
  Hyperventilation increases CO₂ removal but does not increase oxygenation as blood leaving unaffected alveoli is almost fully saturated.
• Hypercapnic respiratory failure (type II respiratory failure): PaCO₂ is more than 50 mmHg (6.5kPa) and indicates inadequate alveolar ventilation. Any ventilation-perfusion mismatch will affect PaO₂ and therefore hypoxaemia is also common.

Respiratory failure may be acute or chronic. The clinical markers of long-standing hypoxaemia include polycythaemia and cor pulmonale.

Common causes of type I respiratory failure

• Chronic obstructive pulmonary disease
• Pneumonia
• Pulmonary oedema
• Pulmonary fibrosis
• Asthma
• Pneumothorax
• Pulmonary embolism
• Pulmonary arterial hypertension
• Cyanotic congenital heart disease
• Bronchiectasis
• Adult respiratory distress syndrome
• Kyphoscoliosis
• Obesity

Common causes of type II respiratory failure

• Chronic obstructive pulmonary disease
• Severe asthma
• Drug overdose, poisoning
• Myasthenia gravis
• Polyneuropathy
• Poliomyelitis
• Muscle disorders
• Head and neck injuries
• Obesity
• Pulmonary oedema
• Adult respiratory distress syndrome
• Myxoedema

The cause of respiratory failure is often clear from the history and physical examination.

Symptoms

• The history may indicate the underlying cause, e.g. paroxysmal nocturnal dyspnoea, and orthopnoea in pulmonary oedema.
• Both confusion and reduced consciousness may occur.

Signs

• Localised pulmonary findings are determined by the underlying cause.
• Neurological features may include restlessness, anxiety, confusion, seizures, or coma.
• Tachycardia and cardiac arrhythmias may result from hypoxaemia and acidosis.
• Cyanosis
• Polycythaemia is a complication of long-standing hypoxaemia.
• Cor pulmonale: pulmonary hypertension is frequently present and may induce right ventricular failure, leading to hepatomegaly and peripheral oedema.

• Arterial blood gas analysis: confirmation of the diagnosis.
• Chest x-ray
• Full blood count: anaemia can contribute to tissue hypoxia; polycythaemia may indicate chronic hypoxaemic respiratory failure.
• Renal and hepatic function: may provide clues to the aetiology or identify complications associated with respiratory failure. Abnormalities in electrolytes such as potassium, magnesium, and phosphate may aggravate respiratory failure and other organ function.
• Serum creatine kinase and troponin I: to help exclude recent myocardial infarction. An elevated creatine kinase may also indicate myositis.
• Thyroid function tests
• Echocardiography: if a cardiac cause of acute respiratory failure is suspected.
• Pulmonary function tests are useful in the evaluation of chronic respiratory failure.
• ECG: to evaluate a cardiovascular cause and may also detect dysrhythmias resulting from severe hypoxaemia or acidosis.
• Right heart catheterisation: should be considered if uncertainty about cardiac function, adequacy of volume replacement, and systemic oxygen delivery.
• Pulmonary capillary wedge pressure may be helpful in distinguishing cardiogenic from non-cardiogenic oedema.

• A patient with acute respiratory failure generally needs prompt admission to hospital. Most patients with chronic respiratory failure can be treated at home with oxygen as well as therapy for their underlying disease.
• Immediate resuscitation may be required.
• Correction of hypoxaemia: ensure adequate oxygen delivery to tissues, generally achieved with a PaO₂ of 60 mmHg or an arterial oxygen saturation (SaO₂) of greater than 90%.
• Beware the prolonged use of high concentration oxygen in chronic sufferers who have become reliant on their hypoxic drive to maintain an adequate ventilation rate. Elevating the PaO₂ too much may reduce the respiratory rate so that the PaCO₂ may rise to dangerously high levels.
• Hypercapnia and respiratory acidosis: correct the underlying cause and/or provide assisted ventilation.
• Mechanical ventilation is used to increase PaO₂ and to lower PaCO₂. Mechanical ventilation also rests the respiratory muscles and is an appropriate therapy for respiratory muscle fatigue. Weaning patients with chronic respiratory failure off of mechanical ventilation may be very difficult.
• Appropriate management of the underlying disease.

• Pulmonary: e.g. pulmonary embolism, pulmonary fibrosis, and complications secondary to the use of mechanical ventilation.
• Cardiovascular: e.g. cor pulmonale, hypotension, reduced cardiac output, arrhythmias, pericarditis, and acute myocardial infarction.
• Gastrointestinal: e.g. haemorrhage, gastric distention, ileus, diarrhoea, and pneumoperitoneum. Stress ulceration is common in patients with acute respiratory failure.
• Polycythaemia.
• Hospital acquired infection: e.g. pneumonia, urinary tract infections, and catheter-related sepsis, are frequent complications of acute respiratory failure.
• Renal: acute renal failure and abnormalities of electrolytes and acid-base homeostasis are common in critically ill patients with respiratory failure.
• Nutritional: including malnutrition and complications related to administration of enteral or parenteral nutrition. Complications associated with naso-gastric tubes, e.g. abdominal distention and diarrhoea.

• The mortality rate associated with respiratory failure varies according to the underlying aetiology.
• The mortality rate for adult respiratory distress syndrome is approximately 40%.
• In patients with COPD and acute respiratory failure, the overall mortality rate is approximately 10%.