American Journal of Respiratory and Critical Care Medicine

From the Author:

Berlin proposes an alternative mechanism to explain refractory shock and pulmonary edema about the patient we have reported in the Journal (1). The patient was on mechanical ventilation with an obstruction of the expiratory ventilator limb. We agree that hemodynamic consequences of PEEPi with dynamic hyperinflation due to an increase of expiratory impedance can cause acute cor pulmonale. PEEPi increases right ventricle outflow impedance by increasing vascular pulmonar resistance, which can decrease the left ventricular compliance due to leftward shift and thus decrease cardiac output (2, 3). Also, its effect on intra-abdominal pressure may collapse inferior vena cava and impair the venous return to right heart and decrease cardiac output (2).

During the severe complication developed by our patient, airway pressures were high (peak pressure of 60 cm H2O, and plateau pressure of 55 cm H2O) (1). In this scenario, it is likely that PEEPi could have been increased and exceeded the extrinsic PEEP set on the ventilator, which was of 16 cm H2O. Although the mechanism proposed by Berlin and colleagues could have caused acute cor pulmonale, we found that transthoracic echocardiography revealed a mean pulmonary arterial pressure of 12 mm Hg, right atrium and ventricle were of normal size and the ejection fraction was 65%. Furthermore, the intra-abdominal pressure was 8 mm Hg. These findings are not compatible with PEEPi as a cause of shock in this patient.

After changing the ventilator tubing set in our patient and correcting the severe acute hypercapnic acidosis, the patient improved, hemodynamic status stabilized, and the patient recovered from pulmonary failure (1). Therefore, we believe that our case represents an unusual example of acute severe hypercapnia with extreme acidemia, where hypercapnic acidosis is associated with development of severe shock and pulmonary edema. Because of the temporal relationship between hemodynamic parameters and values of CO2, we believe that severe hypercapnia with extreme acidemia was the cause of shock and respiratory failure in our patient.

1. Manzanares W, Cancela M, Berrutti D. Shock and pulmonary edema secondary to severe acute hypercapnic acidosis. Am J Respir Crit Care Med 2010;182:1455.
2. Ranieri VM, Dambrosio M, Brienza N. Intrinsic PEEP and cardiopulmonary interaction in patients with COPD and acute ventilatory failure. Eur Respir J 1996;9:12831292.
3. Rossi A, Gottfried SB, Zocchi L, Higgs BD, Lennox S, Calverley PM, Begin P, Grassino A, Milic-Emili J. Measurement of static compliance of the total respiratory system in patients with acute respiratory failure during mechanical ventilation: the effect of intrinsic positive end-expiratory pressure. Am Rev Respir Dis 1985;131:672677.

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