Abstract
Optimisation of preload is an essential component of clinical management and is frequently guided by pulmonary artery occlusion pressure (PAOP). We have examined the relationship between changes in PAOP and left ventricular end-diastolic volume (LVEDV) in septic and non-septic patients. Fifteen patients were studied. PAOP was measured during apnoea. Transthoracic echocardiography was used to acquire standard four-chamber apical views of the heart. Digital image storage was initiated with the onset of apnoea and a standard method used to calculate LVEDV [1]. Fifteen cardiac cycles were recorded before ventilation recommenced. Measurements were repeated after rapid fluid infusion of 500 ml Gelofusine without change to end-expiratory pressure. Two independent observers, who were blinded to clinical data, recorded LVEDV for each cardiac cycle. The mean value of LVEDV from the last five cycles from both observers was used for calculations. The Mann-Whitney-U test was used for group comparison (SPSS 11.0). Results are expressed as median (25th–75th percentiles). Images from 13 patients were suitable for analysis, six with severe sepsis and seven without sepsis. Baseline values were not significantly different between groups. For septic and non-septic patients, respectively, these were as follows: LVEDV 141.4 (96.9–194.2) vs 188.1 (145.0–220.8) ml (p = 0.23); PAOP 12.5 (8.7–13.7) vs 9.0 (3.0–16.0 ) mmHg (p = 0.45). Median responses to rapid fluid infusion (RFI) in septic and non-septic patients were as follows: PAOP 7.0 (4.2–9.7) vs 3.0 (1.0–3.0) mmHg (p = 0.02) and for LVEDV −9.6 (−28.7 to 21.9) vs 28.1 (18.2–77.6) ml (p = 0.02). The increase in PAOP tended to be > 3 mmHg in septic patients and ≤3 mmHg in non-septic patients. These results suggest that preload (measured as LVEDV) responds poorly to rapid fluid infusion in patients with sepsis despite large increases in PAOP. This is not explained by baseline differences of values for PAOP or LVEDV.
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