Do2 [Hb x Sao2 x 134 00031 x Pao2 x CO

It is necessary to secure the airway in patients with neurological compromise. Positive-pressure mechanical ventilation is indicated in the presence of pulmonary edema, acute lung injury or acute respiratory distress syndrome, severe bronchospasm, or therapeutic hyperventilation. Ventilatory support is titrated to minimize the work of breathing and ensure adequate arterial oxygen saturation ( SaO2) and PaCO2. In spontaneously breathing patients continuous positive airway pressure with inspiratory pressure support will decrease the work of breathing and assist ventilation. Inspired oxygen concentration (FiO 2), positive end-expiratory pressure, mean airway pressure, inspiratory-to-expiratory ratio, and flow characteristics of ventilated breaths can be manipulated in order to recruit atelectatic alveoli, increase ventilation-perfusion matching, and increase blood oxygenation. Pulmonary management is largely empirical. Care must be used to ensure that positive airway pressure does not depress cardiac output, cause barotrauma, or increase intracranial pressure by impeding venous return. Ideally, the lowest inspired concentration of oxygen should be used to minimize hyperoxia and reperfusion injury (Rosenthal eí@L 1995). Although controversial, hyperbaric oxygen therapy (2-3 atm at minimally acceptable FiO2) may prevent neutrophil accumulation and lipid peroxidation associated with hyperoxia, oxygen free-radical toxicity, and reperfusion injury (Haywood. etal 1996).

Steroids have not been shown to be effective in acute lung injury or acute respiratory distress syndrome due to drowning. Likewise, antibiotic prophylaxis for pneumonia due to water-borne pathogens or for aspiration pneumonitis is not indicated. Instead, directed antibiotic therapy based on clinical signs of infection and culture results is more appropriate. The administration of artificial surfactant has been described in animal drowning models and in children with acute respiratory distress syndrome (Perez-Benavides eLâL 1995), but has not been shown to improve survival in either group.

The management of the tissue perfusion deficit and pulmonary edema may necessitate invasive monitoring with either a pulmonary artery catheter or transesophageal echocardiography (Fig 1). Lactic acidosis following drowning can be prolonged, and ensuring optimal oxygen delivery can aid in the management of metabolic acidosis. Although transesophageal echocardiography visualizes cardiac function and ventricular volumes better, a pulmonary artery catheter can be used to measure mixed venous oxygen saturation and calculate the oxygen extraction ratio. Although defibrillation is often necessary during the initial phases of resuscitation, the continued use of inotropic therapy in drowning victims is associated with a poor prognosis since most drowning victims had good pre-existing cardiac function. The management of oliguria in the face of pulmonary edema is another indication for the invasive monitoring of volume status.

Fig. 1 Chest radiograph of a 36-year-old victim of drowning in freshwater. Bilateral infiltrates correlate clinically with the acute respiratory distress syndrome. A pulmonary artery catheter can be seen in the left main pulmonary artery and was used to optimize oxygen delivery.

Hypothermia increases the incidence of cardiac arrhythmias, coagulopathy, and metabolic acidosis due to peripheral vasoconstriction and hypoperfusion. In general, forced-air convective heating is the most practical treatment of hypothermia. However, sudden vasodilation can precipitate hypotension and acid-base and electrolyte abnormalities from the washout of metabolic products following peripheral reperfusion. Shivering increases oxygen consumption and must be avoided in situations of tenuous oxygen delivery.

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Eliminating Stress and Anxiety From Your Life

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