Evidence-based review of the use of the pulmonary artery catheter: impact data and complications

The pulmonary artery catheter (PAC) was introduced in 1971 for the assessment of heart function at the bedside. Since then it has generated much enthusiasm and controversy regarding the benefits and potential harms caused by this invasive form of hemodynamic monitoring. This review discusses all clinical studies conducted during the past 30 years, in intensive care unit settings or post mortem, on the impact of the PAC on outcomes and complications resulting from the procedure. Although most of the historical observational studies and randomized clinical trials also looked at PAC-related complications among their end-points, we opted to review the data under two main topics: the impact of PAC on clinical outcomes and cost-effectiveness, and the major complications related to the use of the PAC

Cross-comparison of cardiac output trending accuracy of LiDCO, PiCCO, FloTrac and pulmonary artery catheters

Introduction: Although less invasive than pulmonary artery catheters (PACs), arterial pulse pressure analysis techniques for estimating cardiac output (CO) have not been simultaneously compared to PAC bolus thermodilution CO (COtd) or continuous CO (CCO) devices.Methods: We compared the accuracy, bias and trending ability of LiDCO™, PiCCO™ and FloTrac™ with PACs (COtd, CCO) to simultaneously track CO in a prospective observational study in 17 postoperative cardiac surgery patients for the first 4 hours following intensive care unit admission. Fifty-five paired simultaneous quadruple CO measurements were made before and after therapeutic interventions (volume, vasopressor/dilator, and inotrope).Results: Mean CO values for PAC, LiDCO, PiCCO and FloTrac were similar (5.6 ± 1.5, 5.4 ± 1.6, 5.4 ± 1.5 and 6.1 ± 1.9 L/min, respectively). The mean CO bias by each paired method was -0.18 (PAC-LiDCO), 0.24 (PAC-PiCCO), -0.43 (PAC-FloTrac), 0.06 (LiDCO-PiCCO), -0.63 (LiDCO-FloTrac) and -0.67 L/min (PiCCO-FloTrac), with limits of agreement (1.96 standard deviation, 95% confidence interval) of ± 1.56, ± 2.22, ± 3.37, ± 2.03, ± 2.97 and ± 3.44 L/min, respectively. The instantaneous directional changes between any paired CO measurements displayed 74% (PAC-LiDCO), 72% (PAC-PiCCO), 59% (PAC-FloTrac), 70% (LiDCO-PiCCO), 71% (LiDCO-FloTrac) and 63% (PiCCO-FloTrac) concordance, but poor correlation (r2 = 0.36, 0.11, 0.08, 0.20, 0.23 and 0.11, respectively). For mean CO < 5 L/min measured by each paired devices, the bias decreased slightly.Conclusions: Although PAC (COTD/CCO), FloTrac, LiDCO and PiCCO display similar mean CO values, they often trend differently in response to therapy and show different interdevice agreement. In the clinically relevant low CO range (< 5 L/min), agreement improved slightly. Thus, utility and validation studies using only one CO device may potentially not be extrapolated to equivalency of using another similar device. © 2010 Hadian et al.; licensee BioMed Central Ltd

The effects of vasoactive drugs on pulse pressure and stroke volume variation in postoperative ventilated patients

Introduction: Although pulse pressure variation (PPV) and stroke volume variation (SVV) during mechanical ventilation have been shown to predict preload responsiveness, the effect of vasoactive therapy on PPV and SVV is unknown. Methods: Pulse pressure variation and SVV were measured continuously in 15 cardiac surgery patients for the first 4 postoperative hours. Pulse pressure variation was directly measured from the arterial pressure waveform, and both PPV and SVV were also calculated by LiDCO Plus (LiDCO Ltd, Cambridge, United Kingdom) before and after volume challenges or changes in vasoactive drug infusions done to sustain cardiovascular stability. Results: Seventy-one paired events were studied (38 vasodilator, 10 vasoconstrictor, 14 inotropes, and 9 volume challenges). The difference between the measured and LiDCO-calculated PPV was 1% ± 7% (1.96 SD, 95% confidence interval, r2 = 0.8). Volume challenge decreased both PPV and SVV (15% to 10%, P < .05 and 13% to 9%, P = .09, respectively). Vasodilator therapy increased PPV and SVV (13% to 17% and 9% to 15%, respectively, P < .001), whereas increasing inotropes or vasoconstrictors did not alter PPV or SVV. The PPV/SVV ratio was unaffected by treatments. Conclusion: Volume loading decreased PPV and SVV; and vasodilators increased both, consistent with their known cardiovascular effects. Thus, SVV and PPV can be used to drive fluid resuscitation algorithms in the setting of changing vasoactive drug therapy. © 2011 Elsevier Inc