Volume 11 Supplement 3

Fourth International Symposium on Intensive Care and Emergency Medicine for Latin America

Open Access

Pharmacological vasodilatation increased pulse pressure variation mimicking hypovolemic status in rabbits

  • GA Westphal1, 2,
  • ARR Gonçalves1, 2,
  • A Bedin1, 2,
  • R Steglich1, 2,
  • E Silva1, 2 and
  • LF Poli de Figueiredo1, 2
Critical Care200711(Suppl 3):P9

https://doi.org/10.1186/cc5796

Published: 19 June 2007

Background

Pulse pressure respiratory variation (PPV), which is the difference between the maximal and minimal arterial pulse pressure values after one positive-pressure breath, is largely used for early identification of hypovolemic status. Increased PPV, as seen in hypovolemia, results from exaggerated respiratory variation in transpulmonary blood flow that results in corresponding left ventricular preload variations during respiratory cycles. Hence, any factor that affects left ventricular preload can be associated with PPV amplification.

Objective

To test the hypothesis that PPV amplification observed in hypovolemia can also be observed during pharmacological vasodilatation, induced by sodium nitroprusside (SN).

Methods

Ten anesthetized, mechanically ventilated rabbits, underwent progressive hypotension by either controlled hemorrhage (CH) or intravenous SN infusion. CH group: five rabbits were submitted to graded hemorrhage of 10%, 20%, 30%, 40% and 50% of their blood volume. Mean arterial pressure steps were registered and assumed as pressure targets. SN group: five rabbits were submitted to a progressive SN dose infusion to reach similar pressure targets observed in the CH group (Table 1). PPV was measured at each arterial pressure step.
Table 1

Pulse pressure respiratory variation values in every step in both groups

 

BL

T1

T2

T3

T4

T5

Hemorrhage

3.9 ± 1.2

6.7 ± 1.8

9.7 ± 2.4

13.5 ± 1.6

15.1 ± 0.9

19.6 ± 2.4

Nitroprusside

5.6 ± 2.1

10.7 ± 2.4

10.7 ± 2.4

16.3 ± 4

22.1 ± 5.3

22.6 ± 5.4

Results

The heart rate was significantly greater in the SN group than in the CH group (P < 0.05). PPVs were similar among the experimental models in all steps (P = 0.17).

Conclusion

Pharmacologic vasodilatation by SN induced a PPV amplification similar to that observed in hypovolemia. Our results reinforce the idea that PPV amplification may be associated with potential cardiovascular response and not necessarily hypovolemic status. Hence, caution should be exercised before assuming that PPV is a marker of intravascular volume status.

Authors’ Affiliations

(1)
Division of Experimental Surgery, Joinville University (Univille) Medical School
(2)
Division of Applied Physiology, Heart Institute, InCor, University of São Paulo Medical School

Copyright

© BioMed Central Ltd 2007

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