Diastolic Function and Peripheral Venous Pressure as Indices for Fluid Responsiveness in Cardiac Surgical Patients.

OBJECTIVE: Identifying fluid responsiveness is critical to optimizing perfusion while preventing fluid overload. An experimental study of hypovolemic shock resuscitation showed the importance of ventricular compliance and peripheral venous pressure (PVP) on fluid responsiveness. The authors tested the hypothesis that reduced ventricular compliance measured using transesophageal echocardiography results in decreased fluid responsiveness after a fluid bolus. DESIGN: Prospective observational study. SETTING: Two-center, university hospital study. PARTICIPANTS: The study comprised 29 patients undergoing elective coronary revascularization. INTERVENTION: Albumin 5%, 7 mL/kg, was infused over 10 minutes to characterize fluid responders (>15% increase in stroke volume) from nonresponders. MEASUREMENTS AND MAIN RESULTS: Invasive hemodynamics and the ratio of mitral inflow velocity (E-wave)/annular relaxation (e'), or E/e' ratio, were measured using transesophageal echocardiography to assess left ventricular (LV) compliance at baseline and after albumin infusion. Fifteen patients were classified as responders and 14 as nonresponders. The E/e' ratio in responders was 7.4 ± 1.9 at baseline and 7.1 ± 1.8 after bolus. In contrast, E/e' was significantly higher in nonresponders at baseline (10.7 ± 4.6; p = 0.04) and further increased after bolus (12.6 ± 5.5; p = 0.002). PVP was significantly greater in the nonresponders at baseline (14 ± 4 mmHg v 11 ± 3 mmHg; p = 0.02) and increased in both groups after albumin infusion. Fluid responsiveness was tested using the area under the receiver operating characteristic curve and was 0.74 for the E/e' ratio (95% confidence interval 0.55-0.93; p = 0.029) and 0.72 for the PVP (95% confidence interval 0.52-0.92; p = 0.058). CONCLUSION: Fluid responders had normal LV compliance and lower PVP at baseline. In contrast, nonresponders had reduced LV compliance, which worsened after fluid bolus. E/e,' more than PVP, may be a useful clinical index to predict fluid responsiveness.

A prospective case series evaluating use of an in-line air detection and purging system to reduce air burden during major surgery.

BACKGROUND: Intravascular air embolism (AE) is a preventable but potentially catastrophic complication caused by intravenous tubing, trauma, and diagnostic and surgical procedures. The potentially fatal risks of arterial AE are well-known, and emerging evidence demonstrates impact of venous AEs on inflammatory response and coagulation factors. A novel FDA-approved in-line air detection and purging system was used to detect and remove air caused by administering a rapid fluid bolus during surgery. METHODS: A prospective, randomized, case series was conducted. Subjects were observed using standard monitors, including transesophageal echocardiography (TEE) in the operating room. After general anesthesia was induced, an introducer and pulmonary artery catheter was inserted in the right internal jugular to administer fluids and monitor cardiac pressures. Six patients undergoing cardiac surgery were studied. Each patient received four randomized fluid boluses: two with the in-line air purging device, two without. For each bolus, a bulb infuser was squeezed three times (10-15 mL) over 5 s. The TEE was positioned in the mid-esophageal right atrium (RA) to quantify peak air clearance, and images were video recorded throughout each bolus. Air was quantified using optical densitometry (OD) from images demonstrating maximal air in the RA. RESULTS: All subjects demonstrated significantly lower air burden when the air reduction device was used (p = 0.004), and the average time to clear 90% of air was also lower, 3.7 ± 1.2 s vs. 5.3 ± 1.3 s (p < 0.001). CONCLUSION: An air purging system reduced air burden from bolus administration and could consequently reduce the risk of harmful or fatal AEs during surgery.

Multivariate physiological recordings in an experimental hemorrhage model.

In this paper we describe a data set of multivariate physiological measurements recorded from conscious sheep (N = 8; 37.4 ± 1.1 kg) during hemorrhage. Hemorrhage was experimentally induced in each animal by withdrawing blood from a femoral artery at two different rates (fast: 1.25 mL/kg/min; and slow: 0.25 mL/kg/min). Data, including physiological waveforms and continuous/intermittent measurements, were transformed to digital file formats (European Data Format [EDF] for waveforms and Comma-Separated Values [CSV] for continuous and intermittent measurements) as a comprehensive data set and stored and publicly shared here (Appendix A). The data set comprises experimental information (e.g., hemorrhage rate, animal weight, event times), physiological waveforms (arterial and central venous blood pressure, electrocardiogram), time-series records of non-invasive physiological measurements (SpO2, tissue oximetry), intermittent arterial and venous blood gas analyses (e.g., hemoglobin, lactate, SaO2, SvO2) and intermittent thermodilution cardiac output measurements. A detailed explanation of the hemodynamic and pulmonary changes during hemorrhage is available in a previous publication (Scully et al., 2016) [1].

Closed-Loop Control of FiO2 Rapidly Identifies Need For Rescue Ventilation and Reduces ARDS Severity in a Conscious Sheep Model of Burn and Smoke Inhalation Injury.

Pulmonary injury can be characterized by an increased need for fraction of inspired oxygen or inspired oxygen percentage (FiO2) to maintain arterial blood saturation of oxygenation (SaO2). We tested a smart oxygenation system (SOS) that uses the activity of a closed-loop control FiO2 algorithm (CLC-FiO2) to rapidly assess acute respiratory distress syndrome (ARDS) severity so that rescue ventilation (RscVent) can be initiated earlier. After baseline data, a pulse-oximeter (noninvasive saturation of peripheral oxygenation [SpO2]) was placed. Sheep were then subjected to burn and smoke inhalation injury and followed for 48 h. Initially, sheep were spontaneously ventilating and then randomized to standard of care (SOC) (n = 6), in which RscVent began when partial pressure of oxygen (PaO2) < 90 mmHg or FiO2 < 0.6, versus SOS (n = 7), software that incorporates and displays SpO2, CLC-FiO2, and SpO2/CLC-FiO2 ratio, at which RscVent was initiated when ratio threshold < 250. RscVent was achieved using a G5 Hamilton ventilator (Bonaduz, Switzerland) with adaptive pressure ventilation and adaptive support ventilation modes for SOC and SOS, respectively. OUTCOMES: the time difference from when SpO2/FiO2 < 250 to RscVent initiation was 4.7 ±â€Š0.6 h and 0.2 ±â€Š0.1 h, SOC and SOS, respectively (P < 0.001). Oxygen responsiveness after RscVent, defined as SpO2/FiO2 > 250 occurred in 4/7, SOS and 0/7, SOC. At 48 h the SpO2/FiO2 ratio was 104 ±â€Š5 in SOC versus 228 ±â€Š59 in SOS (P = 0.036). Ventilatory compliance and peak airway pressures were significantly improved with SOS versus SOC (P < 0.001). Data suggest that SOS software, e.g. SpO2/CLC-FiO2 ratio, after experimental ARDS can provide a novel continuous index of pulmonary function that is apparent before other clinical symptoms. Earlier initiation of RscVent translates into improved oxygenation (reduces ARDS severity) and ventilation.

Effect of hemorrhage rate on early hemodynamic responses in conscious sheep.

Physiological compensatory mechanisms can mask the extent of hemorrhage in conscious mammals, which can be further complicated by individual tolerance and variations in hemorrhage onset and duration. We assessed the effect of hemorrhage rate on tolerance and early physiologic responses to hemorrhage in conscious sheep. Eight Merino ewes (37.4 ± 1.1 kg) were subjected to fast (1.25 mL/kg/min) and slow (0.25 mL/kg/min) hemorrhages separated by at least 3 days. Blood was withdrawn until a drop in mean arterial pressure (MAP) of >30 mmHg and returned at the end of the experiment. Continuous monitoring includedMAP, central venous pressure, pulmonary artery pressure, pulse oximetry, and tissue oximetry. Cardiac output by thermodilution and arterial blood samples were also measured. The effects of fast versus slow hemorrhage rates were compared for total volume of blood removed and stoppage time (whenMAP < 30 mmHg of baseline) and physiological responses during and after the hemorrhage. Estimated blood volume removed whenMAPdropped 30 mmHg was 27.0 ± 4.2% (mean ± standard error) in the slow and 27.3 ± 3.2% in the fast hemorrhage (P = 0.47, pairedttest between rates). Pressure and tissue oximetry responses were similar between hemorrhage rates. Heart rate increased at earlier levels of blood loss during the fast hemorrhage, but hemorrhage rate was not a significant factor for individual hemorrhage tolerance or hemodynamic responses. In 5/16 hemorrhages MAP stopping criteria was reached with <25% of blood volume removed. This study presents the physiological responses leading up to a significant drop in blood pressure in a large conscious animal model and how they are altered by the rate of hemorrhage.