Clinical Feature of Respiratory Failure-Hypoxia and Hypercapnia

The clinical features of respiratory failures are hypoxia and hypercapnia. The manifestations of hypoxia and hypercapnia vary from each other.

Manifestations of hypoxia
Hypoxia is more harmful to tissues than hypercapnia. Vital organs such as the brain, heart, liver and kidney and the pulmonary vessels are adversely affected. Neurological symptoms include headache, irritability, insomnia, drowsiness, mental confusion, and coma. Objective evidence of cerebral dysfunction can be demonstrated by the electroencephalogram. If hypoxia is severe, fatty change, tissue necrosis, and focal hemorrhages develop in the myocardium. Cardiac arrhythmias are precipitated. Constriction of pulmonary arteries leads to pulmonary hypertension and this may precipitate right-sided heart failure. Liver cells become edematous and necrosed. In chronic hypoxia the liver shows fatty change and fibrosis. Severe hypoxia may give rise to renal tubular damage. Secondary polycythemia develops in chronic hypoxia states.

Manifestations of hypercapnia
In the initial stages hypercapnia stimulates the respiratory centre and the resultant hyperventilation helps to lower the PaCO2 to normal levels. In established hypercapnia the respiratory centre becomes insensitive to raised PaCO2. In such cases the stimulus for the respiratory centre is hypoxia. Injudicious administration of oxygen may abolish this hypoxic stimulus and give rise to depression of respiration and carbon-dioxide narcosis results. Hypercapnia causes cerebral vasodilation, headache, and rise in intracranial tension. As a result, papilledema may occur in severe cases. Peripheral vasodilatation develops and this gives rise to warm extremities, flushing and rapid high volume pulse. When PCO2 levels exceed 50mm Hg, drowsiness, confusion, muscle twitching, and flapping tremors develop. The deep tendon reflexes become sluggish and the patient lapses into coma when PCO2 rises above 80 mm Hg.

Acute respiratory failure should be managed as an emergency in an intensive respiratory care unit if facilities are available. Proper monitoring includes the record of heart rate, respiratory rate, blood pressure, temperature, serum electrolytes and blood gas levels. In addition to general supportive care, special attention should be paid to the airways and proper oxygenation.

Maintenance of the airway
Irrespective of the cause, in all cases of respiratory failure, the upper air passages should be fully inspected and foreign bodies and secretions should be removed. In the recumbent comatose patient, the chin should be pulled up to prevent the tongue from falling back and obstructing the pharynx. If the patient cannot expectorate freely, secretions should be aspirated. If the patient can cooperate, removal of secretions should be aided by postural coughing, gentle tapping on the chest, steam inhalations and administration of drugs like bromhexine hydrochloride. Bromhexine hydrochloride can be administered orally in a dose of 8 mg thrice orally. Mucolytic agents can be administered as aerosols, eg, acetylcysteine. Adequate hydration is necessary, since it helps in loosening the secretions for easy expectoration. If bronchospasm is present, it can be relieved by drug-like salbutamol given 2-4 mg Orally or 0.5 mg intramuscularly. Parenteral corticosteroids (betamethasone 4mg) may have to be given if bronchospasm is not relieved by simple measures. Salbutamol and beclomethasone can also be given as metered aerosols.

Since infection is a very common precipitating factor, antibiotic therapy is indicated. Preliminary assessment of the infecting agents can be made by Gram-staining of the sputum and the suitable antibiotic can be started. In the acute case, crystalline penicillin and in the chronic case a broad-spectrum drug such as ampicillin or chloramphenicol may be required. Antibiotic therapy may have to be reviewed when microbiological results are obtained.