To the Editor:—
We read with interest the recent review by Dr. Gelman on venous function and central venous pressure. In the paragraph on systolic blood pressure and pulse pressure variations, Dr. Gelman describes the effects of positive-pressure ventilation on ventricular and stroke volumes and states that during inspiration, a temporary increase (as compared with end of expiration) in left ventricular (LV) stroke volume, pulse pressure, and systolic blood pressure occurs.1
This deflection is called “delta-up” and is usually around 2–4 mmHg.1
Delta-up has effectively been described as reflecting the inspiratory increase in LV stroke volume.2
However, delta-up actually quantifies the inspiratory increase in systolic blood pressure2
and may thus result either from an increase in LV stroke volume or an increase in extramural aortic pressure related to the increase in pleural pressure.3
Unlike the systolic blood pressure, the pulse pressure is directly proportional to LV stroke volume.3
It is thus the inspiratory increase in pulse pressure (which could be called “deltaPP-up”) that reflects the inspiratory increase in LV stroke volume. No study, however, has investigated whether delta-up and deltaPP-up behave similarly among ventilated patients. We recently reviewed 298 arterial blood pressure curves recorded immediately before or after fluid challenges in 35 mechanically ventilated patients (21 men and 14 women, mean [± SD] age of 55 ± 14 yr) in the intensive care unit (n = 17) or in the operating room (n = 18). Delta-up was measured as previously described (fig. 1
For each patient, the arterial pressure curve recording with the largest delta-up was then selected. In these 35 recordings, pulse pressure and deltaPP-up (the difference between maximal pulse pressure at inspiration and pulse pressure at end-expiratory pause; fig. 1
) were then also measured. We found that deltaPP-up (1.6 ± 1.8 mmHg) was smaller than delta-up (5.3 ± 2.4 mmHg; P
< 0.01 vs.
deltaPP-up). All 35 patients had a positive delta-up (range, 2–13 mmHg), whereas deltaPP-up ranged between −1 and 8 mmHg and was positive (≥ 1 mmHg) in only 23 patients (P
< 0.01 vs.
delta-up). Among the 16 patients where delta-up was 6 mmHg or greater, deltaPP-up was 2 mmHg or less in 12 patients. These data show that inspiratory increases in systolic blood pressure (delta-up) and pulse pressure (deltaPP-up) are not equivalent. Extramural aortic pressure seems to be the primary determinant of delta-up in many patients. Using delta-up as an indicator of inspiration-induced increase in LV stroke volume may thus be misleading. Finally, it has been suggested that the pulse pressure variation, because it includes this inspiratory increase in LV stroke volume that is not related to fluid responsiveness, may falsely predict positive responses to volume expansion.3,5
In the current study, where the criterion for selection of arterial curves was a large delta-up, deltaPP-up was large enough to potentially result in such false-positive pulse pressure variation in only one patient (deltaPP-up = 8 mmHg [13% of the pulse pressure]; pulse pressure variation = 15%; delta-up = 13 mmHg; delta-down = 3 mmHg). This strongly suggests that this theoretical limitation of pulse pressure variation may be relevant in only a small proportion of patients. In any case, deltaPP-up, but not delta-up, should be measured to detect such occurrence.
Emmanuel Robin, M.D., Ph.D.
Fabrice Granet, M.D.
*Centre Hospitalier Universitaire de Lille, Lille, France. email@example.com