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Abstract Respiratory distress is a type of respiratory failure resulting from many different disorders that cause fluid to accumulate in the lungs and oxygen levels in the blood to be too low. Respiratory failure is a syndrome in which the respiratory system fails in one or both of its gas exchange functions. Many other causes besides respiratory muscle weakness contribute to respiratory failure. The ability to sustain normal respiration depends on the integration of many systems that are involved in breathing. Disruption of any one or a combination of these systems can induce failure. Failure of oxygen exchange results in the development of severe hypoxemia with cellular anoxia and tissue asphyxia. This can occur with all forms of lung disease. While, failure of carbon dioxide exchange results in hypercapnic respiratory failure, causing increased carbon dioxide in arterial blood and respiratory acidosis. On the basis of pathophysiology and ABGs, 2 classical patterns of RF have been described. Type I RF, results from failure of the gas-exchanging organ, while Type II RF is the result of decreased alveolar ventilation. Continuous monitoring of pulse oximetry has become an important tool for respiratory assessment and monitoring. Both laboratory and radiographic investigations are important tools for assessing and monitoring the response to the management of respiratory failure as arterial blood gases, complete blood picture, chest X-ray, as well as pulmonary function tests. Treatment of ARF includes the following: First, respiratory rescue therapy that includes (1) Prone positioning, (2) Extracorporeal life support (ECLS), (3) Inhaled nitric oxide (iNO) and (4) High frequency oscillatory ventilation (HFOV). Second, pharmacological adjuvant therapies which include corticosteroid treatment and neuro-muscular blocking agents (NMBAs). Thirdly, non-invasive ventilation (NIV) which is a ventilatory support method without endotracheal or tracheostomy tube. Fourthly, mechanical ventilatory support. Lastly, treatment of the underlying cause. Surfactant reduces surface tension in the alveolar spaces, facilitating lung expansion and preventing alveolar collapse during expiration in the human neonate. After its administration, exogenous surfactant rapidly improves arterial oxygenation and the alveolar-arterial oxygen difference, reducing the requirements of ventilatory support. |