Respiratory failure is categorized into hypoxemic, hypercapnic, or a combination of the two. It may also be further divided into acute or chronic. Anesthesiologists more consistently encounter acute respiratory failure.
Acute hypoxemic respiratory failure, defined as PaO2 < 60 mmHg, may be secondary to low FiO2, V/Q mismatch, alveolar hypoventilation, diffusion difficulty, and/or shunt. Hypercapnic or combined acute respiratory failure may be due to obstructive lung disease, reduced respiratory effort from drug, brain stem lesion, or obesity, neuromuscular disease such as myasthenia gravis or Guillain–Barré syndrome, or deformed anatomy from scoliosis or flail chest. Treatment of respiratory failure focuses on underlying causes.
NONVENTILATORY RESPIRATORY MANAGEMENT
Nonventilatory modalities for treatment of acute respiratory failure include oxygen therapy, tracheobronchial toilet with incentive spirometer and percussive therapy, continuous positive airway pressure (CPAP), and respiratory system-targeted medications.
Oxygen supplementation is provided by low- and high-flow systems. Low-flow systems include nasal cannulas, simple mask, and reservoir mask. These systems do not ensure exact patient FiO2. Alternatively, high-flow systems, such as venture mask, provide at least 40 L/min of a gas mixture, allowing precise FiO2 delivery.
Oxygen therapy is appropriate for mild to moderate hypoxemia; however, ventilator support and oxygenation are required when the respiratory failure is due to poor ventilation and oxygenation. Furthermore, take care to avoid excessive oxygen administration, which harms the lungs. Oxygen toxicity results from 60% FiO2 > 48 hours. Oxygen free radicals induce the release of inflammatory mediators that cause tissue damage and cellular injury. In addition, when nitrogen is replaced by oxygen in the lungs from delivery of large O2 volumes, subsequent flow of oxygen into the bloodstream causes alveolar collapse known as absorption atelectasis. Therefore, restrict oxygen supplementation and aggressively wean as tolerated to minimize exposure.
Tracheobronchial toilet and incentive spirometry use help improve respiratory impairment from atelectasis and mucous plugging. Positive airway pressure, administered by a high-flow nasal cannula or by mask using a ventilator, also helps improve atelectasis and increase functional residual capacity (FRC). FRC is the lung volume remaining at the end of normal exhalation. Anesthesia and supine position decrease FRC, resulting in hypoxia. Positive airway pressure, CPAP when noninvasive and positive end-expiratory pressure (PEEP) when invasive ventilation, improves FRC and reduces V/Q mismatching.
Despite the range of modalities available for nonventilatory management, some patients eventually need ventilatory support as respiratory insufficiency progresses and spontaneous respiratory effort is inadequate to ensure optimal ventilation and oxygenation. Mechanical ventilation may be provided with a mask noninvasively or through endotracheal tube or tracheostomy tube invasively.
Noninvasive ventilation is appropriate if the cause of the respiratory failure is readily reversible. However, for patients with altered mental status, hemodynamic instability, copious secretions, or airway challenges such as poor mask seal or angioedema, invasive mechanical ventilation with ...