Differences in circulating blood volume changes during emergence from general anesthesia in transcatheter aortic valve implantation and MitraClip implantation.

PURPOSE: We aimed to compare changes in the circulating blood volume (CBV) during emergence from general anesthesia in patients undergoing transcatheter aortic valve implantation (TAVI) and MitraClip implantation. METHOD: We included 97 patients who underwent TAVI or MitraClip implantation. The primary outcome was the rate of change in the estimated CBV associated with emergence from general anesthesia. The secondary outcomes were hemoglobin and hematocrit values before and after emergence from anesthesia for each procedure. Additionally, the independent factors associated with changes in the estimated CBV were assessed using multiple regression analysis. RESULTS: In the TAVI group, the hemoglobin concentration increased from 9.6 g/dL before emergence from anesthesia to 10.8 g/dL after emergence (P < 0.001; mean difference, 1.2 g/dL, 95% confidence interval [CI] 1.1-1.3 g/dL). Conversely, no statistically significant change was observed in the hemoglobin concentration before and after emergence from anesthesia in the MitraClip group. The mean rate of change in the estimated CBV was - 15.4% (standard deviation [SD] 6.4%) in the TAVI group and - 2.4% (SD, 4.7%) in the MitraClip group, indicating a significant decrease in the estimated CBV in the former than in the latter (P < 0.001; mean difference, 13.0%; 95% CI 9.9-16.1%). CONCLUSION: Emergence from general anesthesia increased the hemoglobin concentration and decreased the estimated CBV in patients undergoing TAVI but did not elicit significant changes in patients undergoing MitraClip implantation. These results may provide a rationale for minimizing blood transfusions during general anesthesia in patients undergoing these procedures.

Maternal body weight and estimated circulating blood volume: a review and practical nonlinear approach.

Postpartum haemorrhage continues to be a leading cause of morbidity and mortality in the obstetric population worldwide, especially in patients at extremes of body weight. Quantification of blood loss has been considered extensively in the literature. However, these volumes must be contextualised to appreciate the consequences of blood loss for individual parturients. Knowledge of a patient's peripartum circulating blood volume is essential to allow accurate interpretation of the significance of haemorrhage and appropriate resuscitation. Greater body weight in obesity can lead to overestimation of blood volume, resulting in inappropriately high thresholds for blood product transfusion and delays in treatment. The most recent Mothers and Babies: Reducing Risk through Audits and Confidential Enquiries across the UK (MBRRACE-UK) surveillance report demonstrated the risk to this population, with more than half of all maternal mortality recorded in parturients who were either overweight or obese. Current linear calculations used to estimate circulating blood volumes based on patients' weights could be contributing to this phenomenon, as blood volume increases at a disproportional rate to body composition. In this review, we summarise the relevant physiology and explore the existing literature on the estimation of circulating blood volume, both during pregnancy and in obesity. Building on key works and principal findings, we present a practical, nonlinear approach to the adjustment of estimated blood volume with increasing body mass. This clinical tool aims to reduce the clinical bias influencing the management of obstetric haemorrhage in a population already at increased risk of morbidity and mortality. Discussion of the limitations of this approach and the call for further research within this field completes this review.

Cardiovascular determinants of resuscitation from sepsis and septic shock.

BACKGROUND: We hypothesized that the cardiovascular responses to Surviving Sepsis Guidelines (SSG)-defined resuscitation are predictable based on the cardiovascular state. METHODS: Fifty-five septic patients treated by SSG were studied before and after volume expansion (VE), and if needed norepinephrine (NE) and dobutamine. We measured mean arterial pressure (MAP), cardiac index (CI), and right atrial pressure (Pra) and calculated pulse pressure and stroke volume variation (PPV and SVV), dynamic arterial elastance (Eadyn), arterial elastance (Ea) and left ventricular (LV) end-systolic elastance (Ees), Ees/Ea (VAC), LV ejection efficiency (LVeff), mean systemic pressure analogue (Pmsa), venous return pressure gradient (Pvr), and cardiac performance (Eh), using standard formulae. RESULTS: All patients were hypotensive (MAP 56.8 ± 3.1 mmHg) and tachycardic (113.1 ± 7.5 beat min-1), with increased lactate levels (lactate = 5.0 ± 4.2 mmol L-1) with a worsened VAC. CI was variable but > 2 L min-1 M-2 in 74%. Twenty-eight-day mortality was 48% and associated with admission lactate, blood urea nitrogen (BUN), and creatinine levels but not cardiovascular state. In all patients, both MAP and CI improved following VE, as well as cardiac contractility (Ees). Fluid administration improved Pra, Pmsa, and Pvr in all patients, whereas both HR and Ea decreased after VE, thus normalizing VAC. CI increases were proportional to baseline PPV and SVV. CI increases proportionally decreased PPV and SVV. VE increased MAP > 65 mmHg in 35/55 patients. MAP responders had higher PPV, SVV, and Eadyn than non-responders. NE was given to 20/55 patients in septic shock, but increased MAP > 65 mmHg in only 12. NE increased Ea, Eadyn, Pra, Pmsa, and VAC while decreasing HR, PPV, SVV, and LVeff. MAP responders had higher pre-NE Ees and lower VAC. Dobutamine was given to 6/8 patients who remained hypotensive following NE. It increased Ees, MAP, CI, and LVeff, while decreasing HR, Pra, and VAC. At all times and all steps of the protocol, CI changes were proportional to Pvr changes independent of treatment. CONCLUSIONS: The cardiovascular response to SSG-based resuscitation is highly heterogeneous but predictable from pre-treatment measures of cardiovascular state.

Investigation of treatment volume versus circulating blood volume during Rheocarna treatment.

INTRODUCTION: Rheocarna's therapeutic effect is associated with fibrinogen (Fib) and low-density lipoprotein cholesterol (LDL-C) adsorptive removal. This study aimed to retrospectively investigate the association between treatment volume (TV) and circulating blood volume (CBV) and the Fib removal rate (Fib-RR) and LDL-C-RR. METHODS: CBV and TV/CBV, cut-off value (CO value), and area under the receiver operating characteristic (ROC) curve (AUC) were calculated. The Fib-RR and LDL-C-RR at the midterm and end of treatment were compared. The groups were further categorized into three groups with TV/CBV lower than or higher than the CO value at the midterm and end (midterm/end; Group L: lower than/lower than CO; Group L/H: lower than/higher than CO; Group H: higher than/higher than CO), and the Fib-RR and LDL-RR of each group at the midterm and end were compared. RESULTS: ROC analysis revealed a TV of 1.480 times the BV as CO value, which showed a maximum Youden index predicting a Fib-RR of 20% (AUC: 0.828). Among the three groups, Group L and Group L/H demonstrated significantly higher Fib-RR and LDL-C-RR at the end of the study than in the midterm, while Group H exhibited no difference. CONCLUSION: The results reveal that a treatment volume of 1.5 times the circulating blood volume is a sufficient solute removal capacity in the Rheocarna-enabled cases.

A sensitive method for the simultaneous UHPLC-MS/MS analysis of milrinone and dobutamine in blood plasma using NH4F as the eluent additive and ascorbic acid as a stabilizer.

The purpose of this work was to develop and validate an HPLC-MS/MS method suitable for quantifying two important cardiovascular drugs, milrinone and dobutamine, in neonatal and paediatric patients' blood plasma samples. Sufficiently low LLOQ levels were required to obtain adequate pharmacokinetic data for the evaluation of optimal dosing. Since the specifics of the patient group set some restrictions on the available sample volume, the method was designed to use only 20 µL of plasma for the analysis. Analytes were separated chromatographically in a biphenyl column using a conventional water-methanol-formic acid eluent with the addition of ammonium fluoride. The latter provided a significant signal enhancement in positive ion mode detection for both analytes allowing the LLOQ to reach below 1 ng/mL. Matrix matched calibration was linear in the range of 1-300 ng/mL, between-run accuracy remained within 107-115%, and precision within 4.8-7.4% for both analytes over the calibration range (including LLOQ level). Dobutamine degradation in plasma samples was prevented by the usage of ascorbic acid. The method was applied to plasma samples of neonates from two pharmacokinetic/pharmacodynamics studies (n = 38).

Applied Physiology of Fluid Resuscitation in Critical Illness.

Fluids during resuscitation from shock increase mean systemic pressure and venous return. The pressure gradient for venous return must increase. Mean systemic pressure is the amount of vascular space in unstressed and stressed volume, mostly unstressed. Shock states can decrease mean systemic pressure by increasing unstressed volume, decreasing total blood volume, or decreasing the pressure gradient for venous return. Crystalloids across bodily spaces restore normal volume, whereas colloids remain in the intravascular space. Electrolyte content of fluids matters and excess chloride impairs renal blood flow. Albumin seems to be more effective at restoring blood volume in severe sepsis, but not in other conditions.

Investigating the ability of non-invasive measures of cardiac output to detect a reduction in blood volume resulting from venesection in spontaneously breathing subjects.

BACKGROUND: Monitoring cardiac output (CO) in shocked patients provides key etiological information and can be used to guide fluid resuscitation to improve patient outcomes. Previously this relied on invasive monitoring, restricting its use in the Emergency Department (ED) setting. The development of non-invasive devices (such as LiDCOrapidv2 with CNAP™ and USCOM 1A), and ultrasound based measurements (Transthoracic echocardiography, inferior vena cava collapsibility index (IVCCI), carotid artery blood flow (CABF) and carotid artery corrected flow time (FTc)) enables stroke volume (SV) and CO to be measured non-invasively in the ED. We investigated the ability of these techniques to detect a change in CO resulting from a 500 ml reduction in circulating blood volume (CBV) following venesection in spontaneously breathing subjects. Additionally, we investigated if using incentive spirometry to standardise inspiratory effort improved the accuracy of IVC based measurements in spontaneously breathing subjects. METHODS: We recorded blood pressure, heart rate, IVCCI, CABF, FTc, transthoracic echocardiographic (TTE) SV and CO, USCOM 1A SV and CO, LIDCOrapidv2 SV, CO, Stroke volume variation (SVV) and pulse pressure variation (PPV) in 40 subjects immediately before and after venesection. The Log-Odds and coefficient of variation of the difference between pre- and post-venesection values for each technique were used to compare their ability to consistently detect CO changes resulting from a reduction in CBV resulting from venesection. RESULTS: TTE consistently detected a reduction in CO associated with venesection with an average decrease in measured CO of 0.86 L/min (95% CI 0.61 to 1.12) across subjects. None of the other investigated techniques changed in a consistent manner following venesection. The use of incentive spirometry improved the consistency with which IVC ultrasound was able to detect a reduction in CBV. CONCLUSIONS: In a population of spontaneously breathing patients, TTE is able to consistency detect a reduction in CO associated with venesection.

Effect of acute endotoxemia on analog estimates of mean systemic pressure.

Dynamic estimates of mean systemic pressure based on a Guytonian analog model (Pmsa) appear accurate under baseline conditions but may not remain so during septic shock because blood volume distribution and resistances between arterial and venous beds may change. Thus, we examined the effect of acute endotoxemia on the ability of Pmsa, estimated from steady-state cardiac output, right atrial pressure, and mean arterial pressure, to reflect our previously validated instantaneous venous return measure of mean systemic pressure (Pmsi), derived from beat-to-beat measures of right ventricular stroke volume and right atrial pressure during positive pressure ventilation. We studied 6 splenectomized pentobarbital-anesthetized close chested dogs. Right ventricular stroke volume was measured by a pulmonary arterial electromagnetic flow probe. Instantaneous venous return measure of mean systemic pressure and Pmsa were calculated during volume loading and removal (±100-mL bolus increments×5) both before (control) and 30 minutes after endotoxin infusion (endo). Cardiac output increased (2628±905 vs 3560±539 mL/min; P<.05) and mean arterial pressure decreased (107±16 vs 56±12 mm Hg; P<.01) during endo. Changes in Pmsi and Pmsa correlated during both control and endo (r2=0.7) with minimal bias by Bland-Altman analysis (mean difference±95% confidence interval, 0.47±5.04 mm Hg). We conclude that changes in Pmsa accurately tracts Pmsi under both control and endo.

Analysis of peripheral artery velocity tracing in a porcine model.

BACKGROUND: The aim of the study was to trace the peripheral artery velocity with ultrasound in pigs and provide inference on diagnosis of the type, location and severity of vascular diseases. MATERIALS AND METHODS: Limb tightening, adrenaline administration and arterial wall pinching were performed independently in six pigs, and then the evolution of the external iliac artery or femoral artery velocity tracing were monitored. RESULTS: With the increase of the extents of hindlimb tightening, peak systolic velocity (PSV) of ipsilateral external iliac artery turned from 36.33±1.77 cm/s to 59.72±2.67 cm/s, minimum post-principal wave velocity (MPV from 13.68±1.11 cm/s to -7.48±0.82 cm/s, peak diastolic velocity (PDV) from 19.31±0.86 cm/s to 8.98±0.45 cm/s, and, end diastolic velocity (EDV) from 13.2±0.45 cm/s to 0. With the increase of the dose of the epinephrine injection, PSV increased from 36.33±1.77 cm/s to 43.97±2.15 cm/s but then decreased to 35.43±3.01 cm/s, and MPV negatively increased to -23.53±0.82 cm/s after decreasing from 13.68±1.11 cm/s to 0. PDV and EDV gradually decreased to zero. With the increase of the stenosis severity in the abdominal aortic wall pinching, PSV was reduced and had a linearly negative correlation with the stenosis severity (R=0.983, R2=0.967). MPV gradually increased, and its direction reversed when the stenosis severity increased, then diminished when the blood flow was occluded by more than 2/3. CONCLUSIONS: The formation of peripheral artery velocity is the result of concurrent effects of cardiac ejection, vascular resistance, effective circulating blood volume and elastic recoil. Vascular resistance exerts pronounced effects on the diastolic waveform, and the occurrence of backward wave indicates that the downstream circulation resistance significantly increases.