Respiratory failure

It is estimated that nearly 2,000,000 people with the acute respiratory failure are hospitalized annually in the US.

Acute case of respiratory failure costs exceed $50 billion a year.

Respiratory failure has two main components: ventilatory dysfunction and hypoxemia. 

Ventilatory dysfunction leads to dyspnea, increased work of breathing, use of accessory muscles, and hypercapnia: this situation is best managed with the use of a method that offers ventilatory support. 

Hypoxemia reflects inadequate gas exchange and warrants different forms of oxygen therapy and specific device settings, mostly positive pressure, to improve gas exchange.

Clinical respiratory distress and severe hypoxemia often go together in various combinations because injuries that cause abnormal gas exchange often result in abnormal mechanics and high work of breathing, but they can also be dissociated.

Classified into two groups depending upon the component of the respiratory system that is involved: hypercapnic respiratory failure a consequence of ventilatory failure and associated with an elevated Paco2 above 45 mm Hg, or hypoxic respiratory failure a consequence of gas exchange failure and associated with Pao2 less than 60 mm Hg with or without widening of the alveolar arterial O2 gradient.

Hypercapnic respiratory failure can occur from three processes including an increase in co2 production, decreased minute ventilation and an increase in dead-space ventilation.

Acute onset of hypercapnea determines the management as an acute change of Paco2 of 10mm Hg decreases the pH by .08, while with chronic hypercapnea renal compensation occurs with bicarbonate retention and corrects the pH towards normal.

A patient with hypercapnea should not be sedated.

The use of supplemental oxygen can worsen hypercapnea by worsening V/Q matching, the Haldane effect and suppressing central hypoxemic drive.

In the presence of hypercapnea oxygen utilization should be given to keep hemoglobin saturated with oxygen to greater than 90%.

In the presence of hypercapnea rapid efforts must be made to improve ventilation by noninvasive or mechanical intubation methods.

Hypoxia associated respiratory failure occurs because of impaired gas exchange or hypoventilation with a Pao2 of less 60 mm Hg.

In a randomized clinical study of patients with acute hypoxemic respiratory failure without hypercapnia comparing high flow oxygen therapy, standard oxygen therapy through a facemask or noninvasive positive pressure ventilation did not result in significant different intubation rates (Frat JP et al).

Approximately half of the patients with acute respiratory failure require invasive mechanical ventilation, and in-hospital mortality exceeds 20% in these patients.

A major cause of mortality in patients with severe respiratory failure is iatrogenic injury due to the ventilator itself-ventilatory induced lung injury (VILI).

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