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The state in which the lungs cannot perform the function of gas exchange adequately during rest and exercise is called respiratory failure. In this condition, the resting PaO2 falls below 60mm Hg (60 torr or 8 KPa) and/or the PaCO2 rises above 49mm Hg (49 torr or 7 KPa), when breathing room air at sea level. Lowered PaO2 alone is not adequate to make the diagnosis of respiratory failure, in right to left shunt lesions the PaO2 may be lowered without its occurrence. Respiratory failure has been divided into type I and type II. These may be acute or Chronic. Its causes are many. Interference with any of the major processes-ventilation, perfusion or diffusion- may result in its occurrence.
Causes of respiratory failure
1. Interference with the mechanics of the chest wall: severe kyphoscoliosis, obesity, flail chest injury with multiple rib fractures, paralysis of the chest wall muscles and diaphragm, immobility of the chest wall as in progressive systemic sclerosis.
2. Pleural disorders: Large collection of pleural fluid, tension pneumothorax, gross thickening of the pleura.
3. Diseases of the airways: Severe asthma, advanced chronic bronchitis and emphysema, laryngeal edema, mechanical obstruction of air passages.
4. Pulmonary diseases: Pulmonary interstitial fibrosis, neonatal and adult respiratory distress syndrome, allergic alveolitis, extensive malignancy, bilateral pneumonia.
5. Diseases of pulmonary vasculature Primary pulmonary hypertension, polyarteritis nodosa, repeated pulmonary embolism.
6. Metabolic Metabolic alkalosis
7. Depression of the respiratory centre: Intracranial tension, narcotic poisoning.
The clinical picture depends on the speed of onset, cause and severity. Acute respiratory failure produces more dramatic symptoms whereas chronic respiratory failure may even remain asymptomatic. Respiratory failure may or may not be associated with dyspnea. Though in the early stages CO2 retention causes dyspnea, with the passage of time the respiratory centre becomes adapted and unresponsive to elevated levels of CO2. At this stage the lowered PaO2 (60 mm Hg or below) is the effective stimulus for respiration. There is no direct correlation between the blood gas levels and severity of dyspnea.
In the majority of cases the patient has a long-standing respiratory problem such as chronic obstructive airway disease and respiratory failure is precipitated by infection. The increased secretions and mucosal edema caused by infection aggravate the airway obstruction and these result in alveolar hypoventilation. As a result hypoxia and hyper-capnia (rise in level of arterial carbon-dioxide) develop. As the respiratory failure progresses the PaO2 falls from 60 mm Hg (mild) to 20 mm Hg (severe).
Type I respiratory failure: This type is characterized by lowered PaO2 and normal or low PaCO2. This is usually the result of conditions in which ventilation is normal, but there is defective diffusion or ventilation- perfusion imbalance. Conditions like pulmonary edema, respiratory distress syndrome, extrinsic allergic alveolitis and interstitial pulmonary fibrosis lead to type I respiratory failure.
Type II respiratory failure: In this condition, PaO2 is reduced and PaCO2 is elevated. Hypoxia is the more prominent feature. This results from conditions characterized by defective ventilation occurring along with ventilation-perfusion imbalance. Alveolar hypoventilation occurs in chronic bronchitis and emphysema, asthma, respiratory paralysis, etc. Hypercapnia develops only when the FEV goes down below 1.2 liters. With higher values of FEV, hypercapnia is rare. If the respiratory failure is of acute onset, retention of carbon-dioxide leads to acidosis and fall of pH. If the respiratory failure becomes chronic, compensatory mechanisms come into play. Renal conservation of bicarbonate restores the pH to near-normal.
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