Changes of pulse wave transit time after haemodynamic manoeuvres in healthy adults: a prospective randomised observational trial (PWTT volunteer study).

Background: Pulse wave transit time (PWTT) shows promise for monitoring intravascular fluid status intraoperatively. Presently, it is unknown how PWTT mirrors haemodynamic variables representing preload, inotropy, or afterload. Methods: PWTT was measured continuously in 24 adult volunteers. Stroke volume was assessed by transthoracic echocardiography. Volunteers underwent four randomly assigned manoeuvres: 'Stand-up' (decrease in preload), passive leg raise (increase in preload), a 'step-test' (adrenergic stimulation), and a 'Valsalva manoeuvre' (increase in intrathoracic pressure). Haemodynamic measurements were performed before and 1 and 5 min after completion of each manoeuvre. Correlations between PWTT and stroke volume were analysed using the Pearson correlation coefficient. Results: 'Stand-up' caused an immediate increase in PWTT (mean change +55.9 ms, P-value <0.0001, 95% confidence interval 46.0-65.7) along with an increase in mean arterial pressure and heart rate and a drop in stroke volume (P-values <0.0001). Passive leg raise caused an immediate drop in PWTT (mean change -15.4 ms, P-value=0.0024, 95% confidence interval -25.2 to -5.5) along with a decrease in mean arterial pressure (P-value=0.0052) and an increase in stroke volume (P-value=0.001). After 1 min, a 'step-test' caused no significant change in PWTT measurements (P-value=0.5716) but an increase in mean arterial pressure and heart rate (P-values <0.0001), without changes in stroke volume (P-value=0.1770). After 5 min, however, PWTT had increased significantly (P-value <0.0001). Measurements after the Valsalva manoeuvre caused heterogeneous results. Conclusion: Noninvasive assessment of PWTT shows promise to register immediate preload changes in healthy adults. The clinical usefulness of PWTT may be hampered by late changes because of reasons different from fluid shifts. Clinical trial registration: German clinical trial register (DRKS, ID: DRKS00031978, https://www.drks.de/DRKS00031978).

Non-invasive assessment of Pulse Wave Transit Time (PWTT) is a poor predictor for intraoperative fluid responsiveness: a prospective observational trial (best-PWTT study).

BACKGROUND: Aim of this study is to test the predictive value of Pulse Wave Transit Time (PWTT) for fluid responsiveness in comparison to the established fluid responsiveness parameters pulse pressure (ΔPP) and corrected flow time (FTc) during major abdominal surgery. METHODS: Forty patients undergoing major abdominal surgery were enrolled with continuous monitoring of PWTT (LifeScope® Modell J BSM-9101 Nihon Kohden Europe GmbH, Rosbach, Germany) and stroke volume (Esophageal Doppler Monitoring CardioQ-ODM®, Deltex Medical Ltd, Chichester, UK). In case of hypovolemia (difference in pulse pressure [∆PP] ≥ 9%, corrected flow time [FTc] ≤ 350 ms) a fluid bolus of 7 ml/kg ideal body weight was administered. Receiver operating characteristics (ROC) curves and corresponding areas under the curve (AUCs) were used to compare different methods of determining PWTT. A Wilcoxon test was used to discriminate fluid responders (increase in stroke volume of ≥ 10%) from non-responders. The predictive value of PWTT for fluid responsiveness was compared by testing for differences between ROC curves of PWTT, ΔPP and FTc using the methods by DeLong. RESULTS: AUCs (area under the ROC-curve) to predict fluid responsiveness for PWTT-parameters were 0.61 (raw c finger Q), 0.61 (raw c finger R), 0.57 (raw c ear Q), 0.53 (raw c ear R), 0.54 (raw non-c finger Q), 0.52 (raw non-c finger R), 0.50 (raw non-c ear Q), 0.55 (raw non-c ear R), 0.63 (∆ c finger Q), 0.61 (∆ c finger R), 0.64 (∆ c ear Q), 0.66 (∆ c ear R), 0.59 (∆ non-c finger Q), 0.57 (∆ non-c finger R), 0.57 (∆ non-c ear Q), 0.61 (∆ non-c ear R) [raw measurements vs. ∆ = respiratory variation; c = corrected measurements according to Bazett's formula vs. non-c = uncorrected measurements; Q vs. R = start of PWTT-measurements with Q- or R-wave in ECG; finger vs. ear = pulse oximetry probe location]. Hence, the highest AUC to predict fluid responsiveness by PWTT was achieved by calculating its respiratory variation (∆PWTT), with a pulse oximeter attached to the earlobe, using the R-wave in ECG, and correction by Bazett's formula (AUC best-PWTT 0.66, 95% CI 0.54-0.79). ∆PWTT was sufficient to discriminate fluid responders from non-responders (p = 0.029). No difference in predicting fluid responsiveness was found between best-PWTT and ∆PP (AUC 0.65, 95% CI 0.51-0.79; p = 0.88), or best-PWTT and FTc (AUC 0.62, 95% CI 0.49-0.75; p = 0.68). CONCLUSION: ΔPWTT shows poor ability to predict fluid responsiveness intraoperatively. Moreover, established alternatives ΔPP and FTc did not perform better. TRIAL REGISTRATION: Prior to enrolement on clinicaltrials.gov (NC T03280953; date of registration 13/09/2017).

Hemodynamic parameters change earlier than tissue oxygen tension in hemorrhage.

BACKGROUND: Untreated hypovolemia results in impaired outcome. This study tests our hypothesis whether general hemodynamic parameters detect acute blood loss earlier than monitoring parameters of regional tissue beds. MATERIALS AND METHODS: Eight pigs (23-25 kg) were anesthetized and mechanically ventilated. A pulmonary artery catheter and an arterial catheter were inserted. Tissue oxygen tension was measured with Clark-type electrodes in the jejunal and colonic wall, in the liver, and subcutaneously. Jejunal microcirculation was assessed by laser Doppler flowmetry (LDF). Intravascular volume was optimized using difference in pulse pressure (dPP) to keep dPP below 13%. Sixty minutes after preparation, baseline measurements were taken. At first, 5% of total blood volume was withdrawn, followed by another 5% increment, and then in 10% increments until death. RESULTS: After withdrawal of 5% of estimated blood volume, dPP increased from 6.1% +/- 3.0% to 20.8% +/- 2.7% (P < 0.01). Mean arterial pressure (MAP), mean pulmonary artery pressure (PAP) and pulmonary artery occlusion pressure (PAOP) decreased with a blood loss of 10% (P < 0.01). Cardiac output (CO) changed after a blood loss of 20% (P < 0.05). Tissue oxygen tension in central organs, and blood flow in the jejunal muscularis decreased (P < 0.05) after a blood loss of 20%. Tissue oxygen tension in the skin, and jejunal mucosa blood flow decreased (P < 0.05) after a blood loss of 40% and 50%, respectively. CONCLUSIONS: In this hemorrhagic pig model systemic hemodynamic parameters were more sensitive to detect acute hypovolemia than tissue oxygen tension measurements or jejunal LDF measurements. Acute blood loss was detected first by dPP.

Assessing intravascular volume by difference in pulse pressure in pigs submitted to graded hemorrhage.

We assessed changes in intravascular volume monitored by difference in pulse pressure (dPP%) after stepwise hemorrhage in an experimental pig model. Six pigs (23-25 kg) were anesthetized (isoflurane 1.5 vol%) and mechanically ventilated to keep end-tidal CO2 (etCO2) at 35 mmHg. A PA-catheter and an arterial catheter were placed via femoral access. During and after surgery, animals received lactated Ringer's solution as long as they were considered volume responders (dPP>13%). Then animals were allowed to stabilize from the induction of anesthesia and insertion of catheters for 30 min. After stabilization, baseline measurements were taken. Five percent of blood volume was withdrawn, followed by another 5%, and then in 10%-increments until death from exsanguination occurred. After withdrawal of 5% of blood volume, all pigs were considered volume responders (dPP>13%); dPP rose significantly from 6.1+/-3.3% to 19.4+/-4.2%. The regression analysis of stepwise hemorrhage revealed a linear relation between blood loss (hemorrhage in %) and dPP (y=0.99*x+14; R2=0.7764; P<.0001). In addition, dPP was the only parameter that changed significantly between baseline and a blood loss of 5% (P<0.01), whereas cardiac output, stroke volume, heart rate, MAP, central venous pressure, pulmonary artery occlusion pressure, and systemic vascular resistance, respectively, remained unchanged. We conclude that in an experimental hypovolemic pig model, dPP correlates well with blood loss.

Hypothermia--it's more than a toy.

PURPOSE OF REVIEW: Perioperative hypothermia triples the incidence of adverse myocardial outcomes in high-risk patients; it significantly increases blood loss and augments allogeneic transfusion requirements. Even mild hypothermia increases the incidence of surgical wound infection following colon resection and therefore the duration of hospitalization. Hypothermia adversely affects antibody- and cell-mediated immune defenses, as well as the oxygen availability in the peripheral wound tissues. Mild perioperative hypothermia changes the kinetics and action of various anesthetic and paralyzing agents, increases thermal discomfort, and is associated with delayed postanesthetic recovery. RECENT FINDINGS: On the other hand however, therapeutic hypothermia may be an interesting approach in various settings. Lowering core temperature to 32-34 degrees C may reduce cell injury by suppressing excitotoxins and oxygen radicals, stabilizing cell membranes, and reducing the number of abnormal electrical depolarizations. Evidence in animals indicates that even mild hypothermia provides substantial protection against cerebral ischemia and myocardial infarction. Mild hypothermia has been shown to improve outcome after cardiac arrest in humans. Randomized trials are in progress to evaluate the potential benefits of mild hypothermia during aneurysm clipping and after stroke or acute myocardial infarction. SUMMARY: This article reviews recent publications in the field of accidental as well as therapeutic hypothermia, and tries to assess what evidence is available at the present time.