Pulse pressure respiratory variation in experimental hemorrhage and resuscitation

Background

Pulse pressure (Pp) is strongly coupled with left ventricular stroke volume (SV). Therefore, pulse pressure respiratory variation (ΔPp) reflects SV variation during the respiratory cycle. ΔPp accentuation identifies hypovolemia, and this parameter is recommended to guide volume replacement. Recent reports alert to other clinical situations that accentuate ΔPp, such as pulmonary hypertension and right ventricular dysfunction. ΔPp during and after massive resuscitation has not been determined.

Objective

To observe ΔPp alterations during aggressive volume resuscitation after experimental hemorrhage.

Methods

In 12 ventilated and anesthetized dogs (19 ± 2.5 kg), the CO, MPAP and PAWP were measured by Swan–Ganz catheter; pulmonary resistance (PVR) was calculated using standard formulae. Arterial pressure traces were recorded by a multi-parametric monitor (Datex-Ohmeda, Finland) and ΔPp was calculated according to the following formula: ΔPp (%) = 100 × (Pp_ins - Pp_exp) / [(Pp_ins + Pp_exp) / 2]. Graded hemorrhage (20 ml/min) was produced to a MAP of 40 mmHg. The total shed blood volume was retransfused over 30 min at a rate of 50 ml/min (T10–T30).

Results

During shock we observed the predicted MPAP and PAWP drop and ΔPp amplification, due to a decreased preload, and, consequently, cardiac output decreased. After total shed blood reinfusion and volume expansion (T30), ΔPp increased when compared with either BL (P = 0.02) or T20 (P = 0.003). This increase was associated with increased PVR (P = 0.01) and MPAP (P = 0.05), when compared with BL (Table 1).

Table 1

Conclusion

We conclude that ΔPp can increase after rapid volume infusion as in hypovolemic states. An acute increase in pulmonary pressure and resistance may be responsible for the observed increment in ΔPp.