Pulse-pressure variation and hemodynamic response in patients with elevated pulmonary artery pressure: a clinical study
1 Department of Intensive Care Medicine, Bern University Hospital and University of Bern (Inselspital), Freiburgstrasse 10, 3010 Bern, Switzerland
2 Department of Anesthesiology and Pain Therapy, Bern University Hospital and University of Bern (Inselspital), Freiburgstrasse 10, 3010 Bern, Switzerland
Critical Care 2010, 14:R111 doi:10.1186/cc9060
See related commentary by Madger, http://ccforum.com/content/14/5/197Published: 11 June 2010
Pulse-pressure variation (PPV) due to increased right ventricular afterload and dysfunction may misleadingly suggest volume responsiveness. We aimed to assess prediction of volume responsiveness with PPV in patients with increased pulmonary artery pressure.
Fifteen cardiac surgery patients with a history of increased pulmonary artery pressure (mean pressure, 27 ± 5 mm Hg (mean ± SD) before fluid challenges) and seven septic shock patients (mean pulmonary artery pressure, 33 ± 10 mm Hg) were challenged with 200 ml hydroxyethyl starch boli ordered on clinical indication. PPV, right ventricular ejection fraction (EF) and end-diastolic volume (EDV), stroke volume (SV), and intravascular pressures were measured before and after volume challenges.
Of 69 fluid challenges, 19 (28%) increased SV > 10%. PPV did not predict volume responsiveness (area under the receiver operating characteristic curve, 0.555; P = 0.485). PPV was ≥13% before 46 (67%) fluid challenges, and SV increased in 13 (28%). Right ventricular EF decreased in none of the fluid challenges, resulting in increased SV, and in 44% of those in which SV did not increase (P = 0.0003). EDV increased in 28% of fluid challenges, resulting in increased SV, and in 44% of those in which SV did not increase (P = 0.272).
Both early after cardiac surgery and in septic shock, patients with increased pulmonary artery pressure respond poorly to fluid administration. Under these conditions, PPV cannot be used to predict fluid responsiveness. The frequent reduction in right ventricular EF when SV did not increase suggests that right ventricular dysfunction contributed to the poor response to fluids.