Lung Expansion Therapy Protocol

Lung expansion measures (e.g., positive end-expiratory pressure [PEEP] or continuous positive airway pressure [CPAP]) may be administered to attempt to offset the alveolar consolidation and atelectasis associated with ARDS (see Lung Expansion Protocol, Protocol 9-3).

Mechanical Ventilation Protocol

Mechanical ventilation is often needed to provide and support alveolar gas exchange and eventually return the patient to spontaneous breathing. Continuous mechanical ventilation is justified when the acute ventilatory failure is thought to be reversible (see Protocols 9-5, 9-6, and 9-7).

Ventilation Strategy for Adult Respiratory Distress Syndrome*

Today, the ventilation strategy for most patients with ARDS entails low tidal volumes and high respiratory rates. The initial tidal volume is usually set at 5 to 7 mL/kg, and the rate is set at 20 to 25. Ventilatory rates as high as 35 breaths/min may be needed to maintain an adequate minute volume. The plateau pressure should be less than 30 cm H₂O. PEEP and CPAP are used with small tidal volumes to reduce atelectasis.

The patient’s Paco₂ often is allowed to increase (permissive hypercapnia) as a tradeoff to protect the lungs from high airway pressures. In most cases, an increased ventilatory rate adequately offsets the decreased tidal volume used in the management of ARDS. The Paco₂, however, should not be permitted to increase to the point of severe acidosis (e.g., a pH below 7.2).

The therapeutic goal of low tidal volume ventilation is to (1) decrease high transpulmonary pressures, (2) reduce overdistention of the lungs, and (3) decrease barotrauma. (See Mechanical Ventilation Protocols, Protocol 9-5, Protocol 9-6, and Protocol 9-7.)

Antibiotics are commonly administered in an effort to treat secondary bacterial infections (see Appendix III).

Respiratory Assessment and Plan

The patient was admitted to the intensive care unit, intubated, and mechanically ventilated with these settings: V_T 500 mL, rate 12 breaths/min, Fio₂ 0.4, and 10 cm H₂O of PEEP. An arterial line was placed in her left radial artery, and an intravenous infusion was started with lactated Ringer’s solution.

Over the next 72 hours, the patient’s oxygenation status continued to deteriorate; in spite of a progressive increase in the delivered Fio₂, PEEP, and pressure-controlled mechanical ventilation. When the arterial oxygen tension did not improve appreciably on an Fio₂ of 1.0 and a PEEP of 20 cm H₂O, a Swan-Ganz catheter was placed in the pulmonary artery. In view of the PEEP, the pressure readings were difficult to interpret. A mean pulmonary artery pressure of 27 mm Hg, however, did suggest increased pulmonary vascular resistance.

A chest x-ray examination confirmed severe ARDS with extensive, diffuse infiltrates and atelectasis; worse on the right side. At this time, the respiratory practitioner immediately decreased the tidal volume on the ventilator to 350 mL (7 mL × 50 kg) and increased the rate to 20 breaths/min. The Fio₂ remained at 1.0, and the PEEP was still at 20 cm H₂O. The patient’s arterial blood gas values 20 minutes later were pH 7.31, Paco₂ 49, 25, and Pao₂ 38. Her Spo₂ was 70%. She had crackles, wheezes, and rhonchi in all lung fields. Moderate to large amounts of purulent sputum frequently were suctioned from the endotracheal tube. Her blood pressure was 90/60, and her heart rate was 130/min. Her temperature was 100.2° F. At this time, the respiratory care practitioner charted the following SOAP note:

Respiratory Assessment and Plan

After 3 hours it was apparent that current management would not be successful; the physician decided to alert the extracorporeal membrane oxygenation (ECMO) team and place the patient on extracorporeal membrane oxygenation. This was done, and the patient was maintained on ECMO for 13 hours, when she developed ventricular tachycardia followed by ventricular fibrillation. Attempts to reestablish normal cardiac function were not successful, and the patient was pronounced dead 45 minutes later.

Discussion

This was possibly a preventable death. Gastric lavage never should be performed on an unconscious patient unless the airway is first protected with a cuffed endotracheal tube. This is one of the very few categoric imperatives in pulmonary medicine. The following three causative factors known to produce ARDS may have been operative in this patient: (1) drug overdose, (2) aspiration of gastric contents, and (3) breathing an excessive Fio₂ for a long period. As time progressed, the patient’s lungs became stiffer and physiologically nonfunctional as a result of the anatomic alterations associated with ARDS. Careful measurement of the alveolar-arterial oxygen tension difference (P[A-a]O₂) would have detected this (see page 72).

As documented in the first assessment, her crackles, rhonchi, refractory hypoxemia, and x-ray findings all reflected the pathophysiologic changes seen in patients with Atelectasis (see Figure 9-8) and/or Increased Alveolar-Capillary Membrane Thickening (see Figure 9-10). Aggressive Lung Expansion Therapy (see Protocol 9-3), in the form of PEEP, was used with mechanical ventilation right from the start. When the chest radiograph confirmed severe ARDS after 72 hours of therapy, the immediate changes in the mechanical ventilator settings—the reduction in the patient’s tidal volume to 350 mL, the increased respiratory rate of 20 breaths/min, and permissive hypercapnia—were all clearly indicated and appropriate. Unfortunately, these therapeutic techniques and use of ECMO to manage the condition were not enough in the final analysis.