RESPIRATORY FAILUREA
sudden and life threatening deterioration of the gas exchange of the lung. It exists when the exchange oxygen for carbon dioxide in the lungs cannot keep up with the rate of oxygen consumption and carbon dioxide production by the cells of the body.
a decrease in arterial oxygen tension (PaO2) to less than 50 mmHg, and an increase of arterial carbon dioxide tension (PaCO2) to greater than 50 mmHg with an arterial pH of 7.35.
deterioration
in the gas exchange of the lung period after that has developed insidiously or has persisted for a long period after an episode of ARF.
ETIOLOGY
Decreased
respiratory drive- may occur with severe brain injury, large lesions of the brainstem (multiple sclerosis), use of sedative medications and metabolic disorders.
Dysfunction
of the chest wall- may occur due to any disease or disorder of the nerves, spinal cord, muscle or neuromuscular junction involved in respiration.
Dysfunction
of lung parenchyma- pleural effusion, hemothorax, pneumothroax and upper airway obstruction are conditions that interfere with ventilation by preventing expansion of the lungs.
Other
causes- may occur due to effects of anesthetic agents, analgesics and sedatives which may depress respiration or enhance the effect of opioid leading to hypoventilation
CLINICAL MANIFESTATIONS
Hypoxemia-
restlessness, agitation, dyspnea, disorientation, confusion, delirium, loss of consciousness Hypercapnia- headache, somnolence, dizziness, confusion
Tachypnea
initially: then when no longer able to compensate, bradypnea Accessory muscle use Asynchronous respirations
Pathophysiology
Insufficient respiratory center stimulation or insufficient chest wall movement, resulting in alveolar hypoventilation
Limitaion of carbon dioxide release combining with water forming carbonic acid (H2CO3)
- Acidemia and fall in pH - Tachypnea then eventually bradypnea - Use of accessory muscles - Asynchronous respirations
Hypoxemia occurs as a consequence of hypercapnia. Fall in PaO2 unless increased amount of oxygen are added to inspired air.
DIAGNOSTIC EVALUATION
ABG
analysis- show changes in PaO2, PaCO2 and pH from patients normal; or PaO2 less than 50 mmHg, PaCO2 greater than 50 mmhg, pH less than 7.35 Pulse oximetry- decreasing PaO2 End tidal CO2 monitoring- elevated
Complete
blood count, serum electrolytes, chest X-ray, urinalysis, electrocardiogram, (ECG), blood and sputum cultures- to determine underlying cause and patients condition.
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