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.

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

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.

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).

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.