Reply to Mezidi et al.: Assessment of Airway Closure and Expiratory Airflow Limitation to Set Positive End-Expiratory Pressure in Morbidly Obese Patients with Acute Respiratory Distress Syndrome.

From the Authors:

We appreciate the thoughtful letter of Dr. Mehdi Mezdi and colleagues addressing our recent manuscript (1). The authors have raised several key pulmonary and hemodynamic questions on the ventilation of patients with obesity that should be investigated further. Our discussion here is limited and is focused on the apparent paradoxical hemodynamic response to lung recruitment in patients with severe obesity with an average body mass index (BMI) of 57 ± 12 kg/m2 and an average esophageal pressure range of 17–20 cm H2O. To address this point, we present novel data, documenting the hemodynamic effects of a lung-recruitment maneuver in two patients who were hemodynamically unstable, had severe obesity, and were treated by the Massachusetts General Hospital Lung Rescue Team (2).

Case 1

A 59-year-old woman with a BMI of 59 kg/m2 (predominantly gynoid in distribution) was intubated because of aspiration pneumonia. The Lung Rescue Team was consulted in the setting of worsening hypoxemia (PaO/FiO of 55 mm Hg with positive end-expiratory pressure [PEEP] of 15 cm H2O) in septic shock requiring infusion of four inotropic-vasopressor medications. Before the recruitment maneuver was performed, the patient had a mean arterial pressure (MAP) of 70 mm Hg and a heart rate of 126 beats/min (bpm). After the recruitment maneuver and PEEP titration were performed and a best PEEP of 23 cm H2O was found, the patient’s MAP increased to 84, and her heart rate was 132 bpm. During the ventilatory procedure, inotropic-vasopressor agents were not adjusted. Figure 1 (case 1) shows that increased positive airway pressures translated into a progressive increase in arterial pressure. In the following hours at a PEEP of 23 cm H2O, inotropic-vasopressor requirements were reduced by more than 50% (no fluid challenges were administered).

Figure 1.

Case 1: Continuous recording of esophageal pressure (centimeters of water), airway pressures (centimeters of water), and invasive arterial pressure (millimeters of mercury) during the recruitment maneuver (RM) and positive end-expiratory pressure (PEEP) titration by the Lung Rescue Team is shown. Note that the driving pressure decreased from 17 cm H2O (baseline) to 10 cm H2O after the RM, suggesting lung recruitment. Doses of intravenous inotropic-vasopressor medications were unchanged before, during, and after RM and PEEP titration. The doses of inotropic-vasopressor medications were as follows: epinephrine, 5 μg/min; norepinephrine, 33 μg/min; phenylephrine, 25 μg/min; and vasopressin, 0.04 U/min. After 2 hours at 23 cm H2O of PEEP, epinephrine and phenylephrine were stopped, norepinephrine was decreased to 25 μg/min, and vasopressin was unchanged. After 4 hours, norepinephrine was decreased further to 21 μg/min, and vasopressin was unchanged. Case 2: CO (L/min), stroke volume (SV; ml/min) (both measured by transpulmonary thermodilution), MAP (millimeters of mercury), and PEEP (centimeters of water) before, during, and after the Lung Rescue Team intervention are shown. Open circles indicate CO values. Solid circles indicate SV values. Intravenous inotropic-vasopressor medication requirements before the RM were as follows: epinephrine, 3 μg/min; norepinephrine, 50 μg/min; and vasopressin, 0.08 U/min. Epinephrine was reduced to 2 μg/min during alveolar recruitment because of systemic hypertension. After 2 and 4 hours at 20 cm H2O of PEEP, epinephrine was decreased to 1 μg/min, and norepinephrine and vasopressin were unchanged (50 μg/min and 0.08 U/min, respectively). CO = cardiac output; MAP = mean arterial pressure.

Case 2

A 58-year-old man with a BMI of 40 kg/m2 (predominantly android in distribution) was intubated in the setting of pneumothorax and pulmonary contusions after a high-velocity motor-vehicle accident. The Lung Rescue Team was requested because of worsening oxygenation (PaO/FiO of 99 mm Hg with PEEP of 14 cm H2O) in the setting of requiring three inotropic-vasopressor medications (MAP of 72 mm Hg and heart rate of 94 bpm). During the recruitment maneuver, increased by 2.7 L/min, stroke volume increased by 8 ml/beat (both measured by transpulmonary thermodilution), and MAP increased by 20 mm Hg (Figure 1 [case 2]). We also observed a decreased stroke volume variation (from 16% to 6%) and no changes in central venous pressure (13–14 cm H2O). His heart rate was 103 bpm. PEEP was set at 20 cm H2O. The improved blood pressure allowed the epinephrine dose to be decreased rapidly during and in the hours after lung recruitment (no fluid challenges were administered).

Taken together, both the data presented in our manuscript and these two cases make us hypothesize that high pleural pressure acts like a shield for the cardiovascular system against high ventilator pressures. Prior investigations of the effects of positive-pressure ventilation on heart–lung interactions did not examine the role of high baseline pleural pressure (3–5).

As shown in the patients represented in Figure 1, the counterbalance of high pleural pressure due to obesity permitted the use of high airway pressures that not only improved respiratory system compliance (reduced driving pressure) and lung volumes but also raised and systemic blood pressure. The increased pleural pressure prevents high-airway-pressure lung injury (6) and hemodynamic collapse (7) that might otherwise occur during high-pressure ventilation in patients with low baseline pleural pressures. Future studies are needed to determine the validity of our hypothesis.