Critical Care Medicine-Neurologic Disorders>>>>>Respiratory Failure
Question 5#

A 60-year-old thin female smoker presents to the ED with several days of worsening dyspnea, productive cough, and high fevers. She remains hypotensive despite fluid resuscitation and develops worsening hypoxemia/ARDS requiring intubation and mechanical ventilation. A central line is placed in the right internal jugular vein for vasopressor administration, and she is admitted to the ICU and placed on low tidal volume ventilation protocol using the high PEEP/FiO₂ grid studied in the ALVEOLI trial. Twenty-four hours later admission blood cultures are positive for Streptococcus pneumonia and her respiratory status has continued to deteriorate, now on 6 mL/kg IBW with FIO₂ of 0.8 and PEEP of 20 cm H₂O with plateau pressure of 29 cm H₂O. ScVO₂ is 75% while on moderate dose of norepinephrine and ABG is 7.32/40/65. Using volumetric capnography you measure dead space to be 75%. Several hours later she desaturates, and the FiO₂ is raised to 1.0 with PEEP 24 cm H₂O. Because making the ventilator change she has worsening hypotension and SpO₂ remains in the low 90s. SCVO₂ is remeasured at 55% and repeat ABG is 7.24/48/59 with no change in minute ventilation from the prior ABG. In another 10 minutes, SpO₂ drops to the low 80s and you are adding a second vasopressor.

Which of the following should you do next?

 

A. Increase the PEEP
B. Start inhaled nitric oxide
C. Order urgent echocardiogram
D. PE protocol chest CT
E. Transiently disconnect the patient from the ventilator

Correct Answer is E

Comment:

Correct Answer: E 

High levels of PEEP can lead to increased Zone 1 conditions in the lung while simultaneously reducing cardiac output (by reducing venous return into the heart and increasing pulmonary vascular resistance). This can be life threatening if presence of this positive feedback loop is not quickly recognized.

• Dead space increases and results in worsening hypercarbia despite increase in minute ventilation, causing pH to drop (which will tend to worsen ventilator dyssynchrony and hypotension). In patients with obstructive lung disease, dyssynchrony and tachypnea may further predispose to auto-PEEP, which will tend to exaggerate this problem.
• Lower cardiac output leads to lower central venous oxygen content. Given that the lungs are injured, they will be less effective in fully oxygenating the blood, which will result in a lower arterial oxygen content.
• The clinician or respiratory care practitioner may respond by increasing the PEEP further causing further hypoxemia.

The only option that is absolutely incorrect in this setting is (A). The intensivist should recognize this scenario and that the deteriorating hemodynamics is likely to produce cardiovascular collapse if quick action is not taken. Thus (C) and (D) would be wasting precious time. Nitric oxide may marginally improve V/Q matching and oxygenation but will not help with the hemodynamics, if the primary problem is reduced venous return. The intensivist must maintain a high index of suspicion for presence of this feedback loop and recognize that sometimes decreasing the PEEP will improve systemic oxygenation in addition to improving dead space and cardiac output. Intravascular volume expansion may also improve the above physiology but may not be necessary if hemodynamics rapidly improve with reduced airway pressure. Transient disconnection from ventilator and resuming ventilation at a lower PEEP would be the most appropriate intervention.

Reference:

1. Luecke T. Pelosi P. Clinical review: positive end-expiratory pressure and cardiac output. Crit Care. 2005;9(6):607-621.