Vasodilation increases pulse pressure variation, mimicking hypovolemic status in rabbits

Glauco A Westphal, Anderson Roman Gonçalves, Antônio Bedin, Raquel Bissacotti Steglich, Eliezer Silva, Luiz Francisco Poli-de-Figueiredo, Glauco A Westphal, Anderson Roman Gonçalves, Antônio Bedin, Raquel Bissacotti Steglich, Eliezer Silva, Luiz Francisco Poli-de-Figueiredo

Abstract

Objective: To test the hypothesis that pulse pressure respiratory variation (PPV) amplification, observed in hypovolemia, can also be observed during sodium nitroprusside (SNP)-induced vasodilation.

Introduction: PPV is largely used for early identification of cardiac responsiveness, especially when hypovolemia is suspected. PPV results from respiratory variation in transpulmonary blood flow and reflects the left ventricular preload variations during respiratory cycles. Any factor that decreases left ventricular preload can be associated with PPV amplification, as seen in hypovolemia.

Methods: Ten anesthetized and mechanically ventilated rabbits underwent progressive hypotension by either controlled hemorrhage (Group 1) or intravenous SNP infusion (Group 2). Animals in Group 1 (n = 5) had graded hemorrhage induced at 10% steps until 50% of the total volume was bled. Mean arterial pressure (MAP) steps were registered and assumed as pressure targets to be reached in Group 2. Group 2 (n = 5) was subjected to a progressive SNP infusion to reach similar pressure targets as those defined in Group 1. Heart rate (HR), systolic pressure variation (SPV) and PPV were measured at each MAP step, and the values were compared between the groups.

Results: SPV and PPV were similar between the experimental models in all steps (p > 0.16). SPV increased earlier in Group 2.

Conclusion: Both pharmacologic vasodilation and graded hemorrhage induced PPV amplification similar to that observed in hypovolemia, reinforcing the idea that amplified arterial pressure variation does not necessarily represent hypovolemic status but rather potential cardiovascular responsiveness to fluid infusion.

Keywords: Volume replacement; cardiac function; hemodynamics; hemorrhagic shock; vasodilation.

Figures

Figure 1
Figure 1
The representative trace shows the arterial pressure fluctuations during mechanical ventilation. The systolic pressure is maximal during inspiration and declines in expiration. Similarly, arterial pulse pressure is maximal during inspiration and minimal during expiration. Ppmax, maximal arterial pulse pressure; Ppmin, minimal arterial pulse pressure; Psmax, maximal arterial systolic pressure; Psmin, minimal arterial systolic pressure.
Figure 2
Figure 2
Hemodynamic variables measured during experiment steps in the hemorrhage and nitroprusside (SNP) groups. Steps T1, T2, T3, T4 and T5 correspond to 10%, 20%, 30%, 40% and 50% of blood removal from estimated volemic state (hemorrhage group). In the SNP group, mean arterial pressure (MAP) achieved corresponds to the MAP observed at each bleeding step set in the hemorrhage group. Bars “a” (Hemorrhage) and “b” (SNP) correspond to p t-test). An asterisk shows statistical differences (p < 0.05) between groups (ANOVA test).

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