- What is Respiratory failure (types I and II)
- Statistics on Respiratory failure (types I and II)
- Risk Factors for Respiratory failure (types I and II)
- Progression of Respiratory failure (types I and II)
- Symptoms of Respiratory failure (types I and II)
- Clinical Examination of Respiratory failure (types I and II)
- How is Respiratory failure (types I and II) Diagnosed?
- Prognosis of Respiratory failure (types I and II)
- How is Respiratory failure (types I and II) Treated?
- Respiratory failure (types I and II) References
What is Respiratory failure (types I and II)
Respiratory failure is a disease of the lungs. The respiratory system basically consists of a gas exchanging organ (the lungs) and a ventilatory pump (respiratory muscles and the thorax). Either or both of these can fail and cause respiratory failure. Respiratory failure occurs when gas echange at the lungs is sufficiently impaired to cause a drop in blood levels of oxgyen (hypoxaemia); this may occur with or without an increase in carbon dioxide levels. The definition of respiratory failure is PaO27kPa (55mmHg). Respiratory failure is divided into type I and type II.
- Type I respiratory failure involves low oxygen, and normal or low carbon dioxide levels.
- Type II respiratory failure involves low oxygen, with high carbon dioxide.
Statistics on Respiratory failure (types I and II)
Respiratory failure is common, as it occurs in any severe lung disease – it can also occur as a part of multi-organ failure.
Risk Factors for Respiratory failure (types I and II)
Causes of Type I respiratory failure: disease that damage lung tissue, including pulmonary oedema, pneumonia, acute respiratory distress syndrome, and chronic pulmonary fibrosing alveoloitis. Causes of Type II respiratory failure: the most common cause is chronic obstructive pulmonary disease (COPD). Others include chest-wall deformities, respiratory muscle weakness (e.g. Guillain-Barre syndrome) and central depression of the respiratory centre (e.g. heroin overdose).
Progression of Respiratory failure (types I and II)
- Type I respiratory failure occurs because of damage to lung tissue. This lung damage prevents adequate oxygenation of the blood (hypoxaemia); however, the remaining normal lung is still sufficient to excrete the carbon dioxide being produced by tissue metabolism. This is possible because less functioning lung tissue is required for carbon dioxide excretion than is needed for oxygenation of the blood.
- Type II respiratory failure is also known as ‘ventilatory failure’. It occurs when alveolar ventilation is insufficient to excrete the carbon dioxide being produced. Inadequate ventilation is due to reduced ventilatory effort, or inability to overcome increased resistance to ventilation – it affects the lung as a whole, and thus carbon dioxide accumulates. Complications include: damage to vital organs due to hypoxaemia, CNS depression due to increased carbon dioxide levels, respiratory acidosis (carbon dioxide retention). This is ultimately fatal unless treated. Complications due to treatment may also occur.
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How is Respiratory failure (types I and II) Diagnosed?
The following basic investigations are useful to monitor patients with respiratory failure:
- Tidal volume and vital capacity – these measurements can be taken by simple ‘spirometry’. They are especially useful to monitor progress in patients with respiratory inadequacy due to neuromuscluar problems, such as Guillain-Barre syndrome, in which the vital capacity decreases as the weakness increases.
- Blood gas analysis – blood gas measurements are required for diagnosis of respiratory failure by definition (see Disease Site). Alterations in oxygenation are also useful in monitoring respiratory failure. In addition, blood gas analysis enables disturbances in acid-base balance (acidosis or alkalosis) to be identified.
- Pulse oximetry – a light clip placed on the finger or earlobe gives a measure of blood oxygen saturation. This is not as reliable as arterial blood gas analysis, but is much easier and gives a continuous reading.
Prognosis of Respiratory failure (types I and II)
Respiratory failure is a severe condition that is generally terminal unless treated. Patients can be given supplemental oxygen, and mechanically ventilated if needed – although long-term ventilation has significant consequences. This may be because the patient’s respiratory muscles become weak, or difficulties weaning the patient from the respirator – they may not be able to breathe for themselves (especially COPD patients).
How is Respiratory failure (types I and II) Treated?
The treatment of respiratory failure involves the following measures:
- supplemental oxygen – given initially via face mask
- control of secretions (physiotherapy)
- treatment of lung infection (antibiotics)
- control of airways obstruction (e.g. using bronchodilators, corticosteroids)
- limiting pulmonary oedema
- reducing load on respiratory muscles
Finally, if the above measures are not effective, some form of respiratory support needs to be considered. There are many different devices and techniques used in providing respiratory support; they will not be discussed in detail. Broadly speaking, respiratory support techniques can be split into non-invasive and invasive techniques.
- Non-invasive techniques are used in conscious, cooperative patients, and are administered via face mask or nasal prongs.
- Invasive respiratory support is administered via an endotracheal tube or tracheostomy. The endotracheal tube is passed through the mouth, down the throat and through the larynx. A balloon is inflated at its tip to keep it lodged in the trachea, just under the larynx. Tracheostomy involves making an incision in the neck, and placing the tube directly into the trachea.
Invasive respiratory support may cause significant complications, including: cardiac failure, lung infection, and barotrauma (e.g. Pneumothorax). Respiratory support also weakens the respiratory muscles, so spontaneous respiration has to be resumed gradually.
Respiratory failure (types I and II) References
 Kumar P, Clark M. Clinical Medicine. Fourth Ed. WB Saunders, 1998. pp849-856