The accuracy of Pleth Variability Index for directed fluid optimization in donors in living donor liver transplantation

Background Fluid management strongly affects hepatic resection and aims to reduce intraoperative bleeding during living donation. The Pleth Variability Index (PVI) is a tool to assess the fluid responsiveness from the pulse oximeter waveform; we evaluated the efficacy and accuracy of finger PVI compared to pulse pressure variation (PPV) from arterial waveform in predicting the fluid response in donor hepatectomy patients with the guide of non-invasive cardiac output (CO) measurements. We recruited forty patients who were candidates for right lobe hepatectomy for liver transplantation under conventional general anesthesia methods. During periods of intraoperative hypovolemia not affected by surgical manipulation, PVI, PPV, and CO were recorded then compared with definitive values after fluid bolus administration of 3–5 ml/kg aiming to give a 10% increase in CO which classified the patients into responders and non-responders. Results Both PPV and PVI showed a significant drop after fluid bolus dose (P < 0.001) leading to an increase of the CO (P < 0.0001), and the area under the curve was 0.934, 0.842 (95% confidence interval, 0.809 to 0.988, 0.692 to 0.938) and the standard error was 0.0336, 0.124, respectively. Pairwise comparison of PPV and PVI showed non-significant predictive value between the two variables (P = 0.4605); the difference between the two areas was 0.0921 (SE 0125 and 95% CI − 0.152 to 0.337). Conclusions PVI is an unreliable indicator for fluid response in low-risk donors undergoing right lobe hepatectomy compared to PPV. We need further studies with unbiased PVI monitors in order to implement a non-invasive and safe method for fluid responsiveness.

Physiologic cardiovascular studies in resuscitated normotensive septic shock with persistent hyperlactatemia.

Background: To study effects of increasing vasopressor dosage and fluid resuscitation on ventriculoarterial (VA) coupling and venous return (VR)-related parameters in resuscitated normotensive septic shock patients with persistent hyperlactatemia. Methods: We performed a prospective experimental study in patients with septic shock who was admitted to medical intensive care unit and still had hyperlactatemia even received initial resuscitation to maintain mean arterial pressure (MAP) >65 mmHg. All patients received incremental dose of norepinephrine (NE) to increased MAP, then NE was titrated to baseline dosage and waited for 15 mins, then fluid bolus was given. VA coupling-related parameters [arterial elastance (Ea), left ventricular end-systolic elastance (Ees), left ventricular stroke work (SW), potential energy (PE), stroke volume (SV), and Ea/Ees], and VR-related parameters [central venous pressure (CVP), mean systemic pressure analogue (Pmsa), venous return pressure (Pvr)] were measured at 4 time points including pre-increased NE phase, post-increased NE phase, pre-fluid bolus phase, and post-fluid bolus phase. Primary outcome was average of Ea/Ees. Secondary outcomes were differences in VA coupling-related parameters and VR-related parameters between pre- vs. post- interventions. Results: All 20 patients were normotensive [MAP 74 (66-80) mmHg] with elevated blood lactate [2.7 (2.4-3.6) mmol/L] at enrollment. Average Ea/Ees was 0.89 (0.61-1.16). Compared to pre-increased NE phase, post-increased NE phase had significantly higher MAP, CVP, SV, SW, PE, Pmsa, and Pvr. Likewise, compared to pre-fluid bolus phase, post-fluid bolus raised MAP, CVP, SV, Ees, SW, Pmsa, and Pvr significantly. No difference in Ea/Ees compared between before- vs. after- received both interventions. Conclusions: In resuscitated normotensive septic shock patients with persistent hyperlactatemia, we found an average Ea/Ees of 0.89. Increasing NE dosage or fluid bolus increased most of VA coupling-related parameters and VR-related parameters, but not Ea/Ees. Further large study is warranted to validate these findings.

Paradoxical and Retrograde Air Embolism from Pressurized Peripheral Bolus

Introduction. Cerebral air embolism is a rare, yet serious neurological occurrence with unclear incidence and prevalence. Here, we present a case of fatal cerebral arterial and venous cerebral gas embolism in a patient with infective endocarditis and known large right-to-left shunt and severe tricuspid regurgitation following pressurized fluid bolus administration. Case Presentation. A 32-year-old female was admitted to the medical intensive care unit from a long-term acute care facility with acute on chronic respiratory failure. Her medical history was significant for intravenous heroin and cocaine abuse, methicillin-sensitive Staphylococcus aureus tricuspid valve infective endocarditis on vancomycin, patent foramen ovale, septic pulmonary embolism with cavitation, tracheostomy with chronic ventilator dependence, multifocal cerebral infarction, hepatitis C, nephrolithiasis, anxiety, and depression. After intravenous fluid administration, she became unresponsive with roving gaze, sluggish pupils, and hypotensive requiring vasopressors. CT of the brain showed diffuse arterial and venous cerebral air embolism secondary to accidental air administration from fluid bolus. Magnetic resonance imaging of the brain showed diffuse global anoxic injury and flattening of the globe at the optic nerve insertion. Given poor prognosis, her family chose comfort measures and she died. Conclusions. Fatal cerebral air embolism can occur through peripheral intravenous routes when the lines are inadequately primed and fluids administered with pressure. Caution must be exercised in patients with right-to-left shunting as air may gain access to systemic circulation.

Changes in central venous-to-arterial carbon dioxide tension induced by fluid bolus in critically ill patients

Background In this prospective observational study, we evaluated the effects of fluid bolus (FB) on venous-to-arterial carbon dioxide tension (PvaCO2) in 42 adult critically ill patients with pre-infusion PvaCO2 > 6 mmHg. Results FB caused a decrease in PvaCO2, from 8.7 [7.6−10.9] mmHg to 6.9 [5.8−8.6] mmHg (p < 0.01). PvaCO2 decreased independently of pre-infusion cardiac index and PvaCO2 changes during FB were not correlated with changes in central venous oxygen saturation (ScvO2) whatever pre-infusion CI. Pre-infusion levels of PvaCO2 were inversely correlated with decreases in PvaCO2 during FB and a pre-infusion PvaCO2 value < 7.7 mmHg could exclude a decrease in PvaCO2 during FB (AUC: 0.79, 95%CI 0.64–0.93; Sensitivity, 91%; Specificity, 55%; p < 0.01). Conclusions Fluid bolus decreased abnormal PvaCO2 levels independently of pre-infusion CI. Low baseline PvaCO2 values suggest that a positive response to FB is unlikely.

Rapid 500 mL albumin bolus versus rapid 200 mL bolus followed by slower continuous infusion in post-cardiac surgery patients: a pilot before-and-after study

OBJECTIVE: To evaluate the haemodynamic effects of rapid fluid bolus therapy (FBT) (500 mL of 4% albumin over several minutes) versus combined FBT (rapid 200 mL FBT followed by a 300 mL infusion over 30 minutes). DESIGN: Single centre, prospective, before-and-after trial. SETTING: A tertiary intensive care unit in Australia. PARTICIPANTS: Fifty mechanically ventilated post-cardiac surgery patients. INTERVENTIONS: Rapid 4% albumin FBT versus combined FBT. MAIN OUTCOME MEASURES: We recorded haemodynamic parameters from before FBT to 30 minutes after FBT. A mean arterial pressure (MAP) response was defined by a MAP increase > 10%, and a cardiac index (CI) response was defined by a CI increase > 15%. RESULTS: Immediately after rapid FBT versus combined FBT, there was a CI response in 13 patients (52%) compared with five patients (20%) respectively (P = 0.038), and a MAP response in 11 patients (44%) in each group. However, from FBT administration to 30 minutes, there was a time and group interaction such that MAP was higher in the rapid FBT group (P = 0.003), as was the case for central venous pressure (P = 0.002) and mean pulmonary artery pressure (P < 0.001). Body temperature fell immediately and was lower with rapid FBT but became warmer than with combined FBT later (P < 0.001). At 30 minutes, a MAP response was seen in ten patients (40%) compared with nine patients (36%) (P < 0.99) and a CI response was present in eight patients (32%) compared with 11 patients (44%) (P = 0.56) in the rapid versus combined FBT groups respectively. CONCLUSION: Rapid FBT was superior to combined FBT in terms of mean MAP levels and immediate CI response. However, the number of MAP responders or CI responders was similar at 30 minutes.