Reduction In Central Venous Pressure Research Articles

Infrahepatic Inferior Vena Cava Clamping for Reduction of Central Venous Pressure and Blood Loss During Hepatic Resection

Infrahepatic Inferior Vena Cava Clamping for Reduction of Central Venous Pressure and Blood Loss During Hepatic Resection

Impact of reverse remodeling on cardiac function.

Left ventricular assist devices (LVADs) have become the standard of care for treatment of patients with refractory end-stage heart failure (1-5). An LVAD results in decompression of the left ventricle, which promotes reverse remodeling, as manifested by decreased ventricular size, decreased mitral and tricuspid valve regurgitation and improved ventricular function. This process may play an important role in inducing left ventricular recovery with eventual explantation of the device. Right ventricular function and right-sided hemodynamics are also improved with LVAD therapy. Along with unloading of the right ventricle, there is a substantial reduction in central venous pressure (CVP), pulmonary artery pressure (PAP) and tricuspid regurgitation (TR). Consistent with the macroscopic changes seen on echocardiography as well as intracardiac pressures measured on right heart catheterizations, there are microscopic changes in the heart that are consistent with reverse remodeling after placement of an LVAD. These microscopic changes include changes in myocyte size, regression of fibrosis, cellular hypertrophy, collagen content, gene expression and various biomarkers of recovery, such as cardiac tumor necrosis factor-alpha (6-10).

Preliminary experience with combined inhaled milrinone and prostacyclin in cardiac surgical patients with pulmonary hypertension.

To retrospectively evaluate the effects of combined inhaled prostacyclin and milrinone to reduce the severity of pulmonary hypertension when administered prior to cardiopulmonary bypass. Retrospective case control analysis of high-risk patients undergoing cardiac surgery. Single cardiac center. Sixty one adult cardiac surgical patients with pulmonary hypertension, 40 of whom received inhalation therapy. Inhaled milrinone and inhaled prostacyclin were administered before cardiopulmonary bypass (CPB). Administration of both inhaled prostacyclin and milrinone was associated with reductions in central venous pressure, and mean pulmonary artery pressure, increases in cardiac index, heart rate, and the mean arterial-to-mean pulmonary artery pressure ratio (p<0.05), with no significant change in mean arterial pressure. The rate of difficult and complex separation from CPB was 51% in the inhaled group and 70% in the control group (p = 0.1638). Postoperative vasoactive requirement was reduced at 12 hours (35.9 v 73.7% p<0.01) and 24 hours (25.6 v 57.9% p<0.05) postoperatively in the combined inhaled agent group. Hospital length of stay and mortality were similar between the groups. Preemptive treatment of pulmonary hypertension with a combination of inhaled prostacyclin and milrinone before CPB was associated with a reduction in the severity of pulmonary hypertension. In addition, a significant reduction in vasoactive support in the intensive care unit during the first 24 hours after cardiac surgery was observed. The impact of this strategy on postoperative survival needs to be determined.

Nitroglycerine and patient position effect on central, hepatic and portal venous pressures during liver surgery.

To reduce blood loss during liver surgery, a low central venous pressure (CVP) is recommended. Nitroglycerine (NG) with its rapid onset and offset can be used to reduce CVP. In this study, the effect of NG on portal and hepatic venous pressures (PVP and HVP) in different body positions was assessed. Thirteen patients undergoing liver resection were studied. Cardiac output (CO), mean arterial pressure (MAP) and CVP were measured. PVP and HVP were measured using tip manometer catheters at baseline (BL) in horizontal position; during NG infusion, targeting a MAP of 60 mmHg, with NG infusion and the patient placed in 10 head-down position. NG infusion reduced HVP from 9.7 ± 2.4 to 7.2 ± 2.4, PVP from 12.3 ± 2.2 to 9.7 ± 3.0 and CVP from 9.8 ± 1.9 to 7.2 ± 2.1 mmHg at BL. Head-down tilt during ongoing NG resulted in increases in HVP to 8.2 ± 2.1, PVP to 10.7 ± 3 and CVP to 11 ± 1.9 mmHg. CO at BL was 6.3 ± 1.1, which was reduced by NG to 5.8 ± 1.2. Head-down tilt together with NG infusion restored CO to 6.3 ± 1.0 l/min. NG infusion leads to parallel reductions in CVP, HVP and PVP at horizontal body position. Thus, CVP can be used to guide NG dosage and fluid administration at horizontal position. NG infusion can be used to reduce HVP. Head-down tilt can be used during NG infusion to improve both blood pressure and CO without substantial increase in liver venous pressure. In head-down tilt, CVP dissociates from HVP and PVP.

Reductions in central venous pressure by lower body negative pressure or blood loss elicit similar hemodynamic responses.

The purpose of this study was to compare hemodynamic and blood analyte responses to reduced central venous pressure (CVP) and pulse pressure (PP) elicited during graded lower body negative pressure (LBNP) to those observed during graded blood loss (BL) in conscious humans. We hypothesized that the stimulus-response relationships of CVP and PP to hemodynamic responses during LBNP would mimic those observed during BL. We assessed CVP, PP, heart rate, mean arterial pressure (MAP), and other hemodynamic markers in 12 men during LBNP and BL. Blood samples were obtained for analysis of catecholamines, hematocrit, hemoglobin, arginine vasopressin, and blood gases. LBNP consisted of 5-min stages at 0, 15, 30, and 45 mmHg of suction. BL consisted of 5 min at baseline and following three stages of 333 ml of hemorrhage (1,000 ml total). Individual r(2) values and linear regression slopes were calculated to determine whether the stimulus (CVP and PP)-hemodynamic response trajectories were similar between protocols. The CVP-MAP trajectory was the only CVP-response slope that was statistically different during LBNP compared with BL (0.93 ± 0.27 vs. 0.13 ± 0.26; P = 0.037). The PP-heart rate trajectory was the only PP-response slope that was statistically different during LBNP compared with BL (-1.85 ± 0.45 vs. -0.46 ± 0.27; P = 0.024). Norepinephrine, hematocrit, and hemoglobin were all lower at termination in the BL protocol compared with LBNP (P < 0.05). Consistent with our hypothesis, LBNP mimics the hemodynamic stimulus-response trajectories observed during BL across a significant range of CVP in humans.

Venous air embolism during major liver surgery

Editor, Venous air embolism is a potentially fatal event, but its prevalence during liver resection is unknown. Although major gas embolisms have been reported during liver surgery, liver resection has not been documented as a procedure bearing a serious risk of this complication.1 Lodging of air in the pulmonary vessels results in the elevation of pulmonary arterial pressure and a rapid decrease in end-tidal carbon dioxide concentration (EtCO2).2 The sudden onset of this symptom during an operation usually raises the suspicion of possible venous air embolism. The aim of this study was to assess the incidence of embolic events during liver resection with the use of transoesophageal echocardiography (TOE), the most sensitive method for detection of pulmonary air embolism.3 Ethical approval for this study (Ethical Committee No. RNN/369/12/KB) was provided by the Ethical Committee of the Medical University of Lodz, Poland (Chairperson Prof Przedzisław Polakowski) on 22 May 2012. Intraoperative visualisation of heart chambers was obtained by inserting a TOE probe (model 6T GM Medical System, complementary with VIVID 7 PRO; General Electric, Milwaukee, USA) into the oesophagus. All the TOE examinations were made along the interatrial septum. The data were analysed using software for quantitative analysis of signal intensity (Q-analyse; General Electric, Milwaukee, WI, USA). Using the time intensity curves, data were analysed in two regions of interest: right atrium (RA) and left atrium. All statistical calculations were performed using SigmaPlot version 12.0 (Systat Software Inc., San Jose, CA, USA). To compare the differences in maximum and minimum EtCO2, heart rate and mean arterial pressure in groups with and without gas embolism on TOE, we applied the parametric t-test and nonparametric Mann–Whitney test. All data are given in the text as mean and standard deviation Thirty-eight consecutive patients scheduled for hemihepatectomy (right: 29, left: 9) for metastatic tumours of the liver were enrolled in the study. The average age was 56.3 years (range 22 to 75 years). Combined general and epidural anaesthesia was undertaken in all patients. Minor [defined as several air bubbles in the RA and right ventricle (RV)] and major air embolisms (air bubbles filling at least 50% of the RA and RV) were identified in 23 (60%) and five (13%) patients, respectively. Air embolism was accompanied by cardiorespiratory changes including a decrease in minimum EtCO2 (to 3.2 ± 0.4 versus 3.8 ± 0.4 kPA; P = 0.005) and increase in maximum heart rate (101.1 ± 12.0 versus 87.3 ± 12.1 beats per minute; P = 0.003). The difference in signal intensity (dB) between the RA and the left atrium is shown in Fig. 1.Fig. 1: No captions available.Furthermore, all serious complications, including early postoperative myocardial infarction (one case; 2.6%) and bleeding requiring intraoperative blood transfusion (six cases; 15%) occurred in patients with air embolism. Finally, the mean length of hospital stay tended to be longer in this group than in patients without air embolism (13.1 ± 7.7 versus 8.5 ± 1.7 days; P = 0.123). The prevalence of venous air embolism during liver surgery is underestimated.4 Liver resection requires intraoperative reduction of central venous pressure to minimise bleeding from transected parenchyma. The combination of general and epidural anaesthesia used for this purpose results in arterial hypotension, masking the main signs of pulmonary embolism.5,6 To the best of our knowledge, this is the first study investigating the prevalence of pulmonary air embolism during major liver surgery with the routine use of TOE. The results show that air embolism is common and generally asymptomatic. However, further studies elucidating its influence on the postoperative course of patients after liver resection are needed. Acknowledgements relating to this article Assistance with the letter: none. Financial support and sponsorship: none. Conflicts of interest: none. Presentation: none.

Can the temporary use of right ventricular assist devices bridge patients with acute right ventricular failure after cardiac surgery to recovery?

A best evidence topic in cardiac surgery was written according to a structured protocol. The question addressed was: Can the temporary use of right ventricular assist devices (RVADs) bridge patients to recovery who suffer acute right ventricular failure after cardiac surgery? More than 183 papers were found using the reported search, of which 13 represented the best evidence to answer the clinical question. The authors, journal, date and country of publication, patient group studied, study type, relevant outcomes and results of these papers are tabulated. Indications for surgical intervention included coronary artery bypass surgery, valve replacement, post-heart transplant and left ventricular assist device insertion. Significant reductions in central venous pressure (P = 0.005) and mean pulmonary artery pressures (P < 0.01) were reported during and after RVAD support. Furthermore, increases in right ventricular cardiac output (P < 0.05), right ventricular ejection fraction (P < 0.05), right ventricular stroke work (P < 0.05) and pulmonary artery oxygen saturations (P < 0.05) were also seen. Assessment by one study showed that on Day 7 after RVAD removal, the right ventricular ejection fraction had increased by up to 40%. Dynamic echocardiography studies performed before, during and after RVAD placement demonstrated that after RVAD implantation, right ventricular end-diastolic dimensions (P < 0.05) and right atrial dimensions decreased (P < 0.05) and right ventricular ejection fraction (P < 0.05) increased. Although several studies successfully weaned patients from an RVAD, there were several complications, including bleeding requiring surgical intervention. However, this may be reduced by using percutaneous implantation (bleeding incidence: 4 of 9 patients) rather than by a surgically implanted RVAD (bleeding incidence: 5 of 5 patients). However, mortality is higher in percutaneous RVAD patients rather than in surgical RVAD (80-44%) patients. Causes of death cited for patients on an RVAD included multiorgan failure, sepsis, thromboembolic events, reoccurring right heart failure and failure to wean due to persistent right ventricular failure. We conclude that RVADs have been successfully used to bridge patients to recovery after cardiac surgery; however, RVADs carry numerous risks and a high mortality rate.

Reply to Simpson

We appreciate the comments from D. Simpson that, in addition to intensive medical management for a reduction in central venous pressure (CVP) [1], a drop of oncotic pressure due to hypoalbuminaemia in Fontan patients with protein losing enteropathy (PLE) is another explanation for the absence of difference in the CVP between the ‘excellent’ and chronic phase of PLE Fontan patients [2]. In fact, when we looked into our recent data on consecutive 275 stable Fontan patients, including 21 PLE patients, there were no patients with severe hypoalbuminaemia (≤2.5 g/dl) with a CVP of ≥13 mmHg as Bull [3] noted, although there was a significant inverse correlation between the plasma albumin concentration and CVP (r = −0.23, P< 0.0001). Pathophysiological mechanisms of hypoalbuminaemia may be multifactorial in Fontan patients with PLE, although the precise mechanism(s) remains unclear. As demonstrated in patients with heart failure, malnutrition, reduced synthesis of albumin in the congested liver with chronic inflammation and increased transcapillary escape rate of albumin may be additional causes of hypoalbuminaemia [4]. We may have to take those into consideration to care for sicker Fontan patients with long-affected PLE because those patients have some pathophysiological conditions similar to those in heart failure patients, such as chronic inflammation [5]. Thus, once PLE occurred, small CVP decline that we observed due to intensive managements and the hypoalbuminaemia-associated low oncolic pressure may not be sufficient to decrease the high rate of albumin transcapillary escape, leading to sustained hypoalbuminaemia, making the situation more susceptible to oedema [6] and intractable to treat. Those sicker PLE patients require repeated hospitalizations, resulting in poor quality of life after the Fontan operation. Our PLE experience reminds us of an importance of selection criteria for the operation and we have to be aware that a role of Fontan operation is to offer a better quality of life in patients with complex congenital heart disease because of its palliative nature.

Cardiovascular responses to lower body negative pressure before and after 4 h of head-down bed rest and seated control in men and women

Cardiovascular deconditioning after a 4-h head-down bed rest (HDBR) might be a consequence of the time of day relative to pre-HDBR testing, or simply 4 h of confinement and inactivity rather than the posture change. Ten men and 11 women were studied during lower body negative pressure (LBNP) before and after 4-h HDBR and 4-h seated posture (SEAT) as a control for time of day and physical inactivity effects to test the hypotheses that cardiovascular deconditioning was a consequence of the HDBR posture, and that women would have a greater deconditioning response. Following HDBR, men and women had lower blood volume, higher heart rate with a greater increase during LBNP, a greater decrease of stroke volume during LBNP, lower central venous pressure, smaller inferior vena cava diameter, higher portal vein resistance index with a greater increase during LBNP, but lower forearm vascular resistance, lower norepinephrine, and lower renin. Women had lower vasopressin and men had higher vasopressin after HDBR, and women had lower pelvic impedance and men higher pelvic impedance. Following SEAT, brachial vascular resistance was reduced, thoracic impedance was elevated, the reduction of central venous pressure during LBNP was changed, women had higher angiotensin II whereas men had lower levels, and pelvic impedance increased in women and decreased in men. Cardiovascular deconditioning was greater after 4-h HDBR than after SEAT. Women and men had similar responses for most cardiovascular variables in the present study that tested the responses to LBNP after short-duration HDBR compared with a control condition.

Central versus peripheral control of cardiac output in humans: insight from atrial pacing

Central <i>versus</i> peripheral control of cardiac output in humans: insight from atrial pacing

Infrahepatic Inferior Vena Cava Clamping for Reduction of Central Venous Pressure and Blood Loss During Hepatic Resection

To evaluate the effectiveness and safety of infrahepatic inferior vena cava (IVC) clamping for reduction of central venous pressure (CVP) and blood loss during hepatic resection. Low CVP during parenchymal transection has been widely accepted to reduce intraoperative hemorrhage via the hepatic veins and is commonly achieved by anesthesiological interventions such as fluid restriction. We hypothesized that infrahepatic clamping of the IVC may lower the intraoperative blood loss more effectively and, moreover, prevent potential adverse effects of fluid restriction such as hemodynamic instability. Patients scheduled for elective hepatic resection were enrolled and allocated randomly to CVP reduction by infrahepatic IVC clamping or anesthesiological interventions including primarily fluid restriction with additional use of diuretics, nitro compounds, and opioids (control group). The primary efficacy endpoint was total intraoperative blood loss. Analyses were done following intention-to-treat principles. The protocol was submitted to the clinicaltrials.gov registry (NCT00732979). From April 2007 to December 2009, a total of 152 patients were randomized and 128 were eligible for final analyses. Baseline data were similar between both study groups. Despite higher CVP values during resection (4.0 ± 3.2 vs. 2.6 ± 1.8 mm Hg; P = 0.003), infrahepatic IVC clamping significantly reduced total intraoperative blood loss [550 (350.0-1150) mL vs. 900 (500-1500) mL; P = 0.02] and blood loss during parenchymal transection [150 (85-500) mL vs. 400 (200-700) mL; P = 0.006] compared with the control group. Postoperative mortality [4 (6.1%) vs. 2 (3.2%); P = 0.42] and total morbidity rates [38 (58.5%) vs. 37 (58.7%); P = 0.97] were comparable between both study groups. Although intraoperative hemodynamic instability occurred less frequently in patients with infrahepatic IVC clamping [0 vs. 4 (6.3%); P = 0.04], the incidence of pulmonary embolism was increased in this study arm [4 (6.1%) vs. 0; P = 0.04]. Infrahepatic IVC clamping is associated with significantly less intraoperative blood loss and may reduce the incidence of intraoperative hemodynamic instability. The potential association with postoperative pulmonary embolism represents a significant concern.

Coupling of Central Venous Pressure and Intracranial Pressure in a 6-Year-Old Patient With Fontan Circulation and Intracranial Hemorrhage

A sharp rise in intracranial pressure (ICP) was noted in a 6-year-old girl with Fontan circulation after surgical removal of a hematoma associated with intracranial hemorrhage. Inhalation of nitric oxide resulted in reduction of central venous pressure (CVP) and precipitous fall in ICP, which was otherwise resistant to conventional therapy. Specifically, the rate of fall of ICP (9 mm Hg) exceeded that of the CVP (3 mm Hg), indicating disproportionate CVP-ICP coupling. The present case provides not only a novel insight into cardio-cerebral interaction in Fontan physiology but also useful information regarding the treatment of Fontan patients in the setting of increased ICP.

Heat-stress-induced changes in central venous pressure do not explain interindividual differences in orthostatic tolerance during heat stress

The extent to which heat stress compromises blood pressure control is variable among individuals, with some individuals becoming very intolerant to a hypotensive challenge, such as lower body negative pressure (LBNP) while heat stressed, while others are relatively tolerant. Heat stress itself reduces indexes of ventricular filling pressure, including central venous pressure, which may be reflective of reductions in tolerance in this thermal condition. This study tested the hypothesis that the magnitude of the reduction in central venous pressure in response to heat stress alone is related to the subsequent decrement in LBNP tolerance. In 19 subjects, central hypovolemia was imposed via LBNP to presyncope in both normothermic and heat-stress conditions. Tolerance to LBNP was quantified using a cumulative stress index (CSI), and the difference between normothermic CSI and heat-stress CSI was calculated for each individual. The eight individuals with the greatest CSI difference between normothermic and heat-stress tolerances (LargeDif), and the eight individuals with the smallest CSI difference (SmallDif), were grouped together. By design, the difference in CSI between thermal conditions was greater in the LargeDif group (969 vs. 382 mmHg × min; P < 0.001). Despite this profound difference in the effect of heat stress in decreasing LBNP tolerance between groups, coupled with no difference in the rise in core body temperatures to the heat stress (LargeDif, 1.4 ± 0.1°C vs. SmallDif, 1.4 ± 0.1°C; interaction P = 0.89), the reduction in central venous pressure during heat stress alone was similar between groups (LargeDif: 5.7 ± 1.9 mmHg vs. SmallDif: 5.2 ± 2.0 mmHg; interaction P = 0.85). Contrary to the proposed hypothesis, differences in blood pressure control during LBNP are not related to differences in the magnitude of the heat-stress-induced reductions in central venous pressure.

Changes in central venous pressure during heat stress as a possible predictor of compromised blood pressure control during simulated hemorrhage

The extent to which heat stress compromises blood pressure control is quite variable between individuals; some are intolerant to a simulated hemorrhagic challenge while heat stressed, with others being relatively tolerant. The objective of this study was to identify if the magnitude of reduction in central venous pressure (CVP) during heat stress explains the variability in tolerance to a hemorrhagic challenge. Simulated hemorrhage was imposed via lower body negative pressure to pre‐syncope on 20 subjects during passive heating. Tolerance was quantified with a cumulative stress index (CSI), and the 8 subjects with the lowest and the 8 with the highest CSI were categorized as low‐ and high‐tolerant, respectively. The increase in core body temperature was similar between groups (1.45 ± 0.11 versus 1.41 ± 0.09°C, P = 0.44), and by design CSI was greater for the high tolerant group (439 ± 183 vs 86 ± 39 CSI units; P &lt; 0.001). Although heat stress decreased CVP in the low (6.6 ± 2.6 to 0.8 ± 2.1 mmHg) and the high (7.6 ± 2.0 to 2.0 ± 3.0 mmHg) tolerant groups (P &lt; 0.001), the magnitude of this reduction was not different between groups (low: 5.9 ± 1.4; high: 5.6 ± 2.1 mmHg; P=0.53). Contrary to our hypothesis, differences in blood pressure control during simulated hemorrhage are not related to differences in the magnitude of the heat stress‐induced reduction in CVP.Supported by NIH Grants HL61388 &amp; HL84072 &amp; TREi

IVC CLAMP: infrahepatic inferior vena cava clamping during hepatectomy - a randomised controlled trial in an interdisciplinary setting

BackgroundIntraoperative haemorrhage is a known predictor for perioperative outcome of patients undergoing hepatic resection. While anaesthesiological lowering of central venous pressure (CVP) by fluid restriction is known to reduce bleeding during transection of the hepatic parenchyma its potential side effects remain poorly investigated. In theory it may have negative effects on kidney function and tissue perfusion and bears the risk to result in severe haemodynamic instability in case of profound intraoperative blood loss. The present randomised controlled trial evaluates efficacy and safety of infrahepatic inferior vena cava (IVC) clamping as an alternative surgical technique to reduce CVP during hepatic resection.Methods/DesignThe proposed IVC CLAMP trial is a single-centre randomised controlled trial with a two-group parallel design. Patients and outcome-assessors are blinded for the treatment intervention. Patients undergoing elective hepatic resection due to any reason are enrolled in IVC CLAMP. All patients admitted to the Department of General-, Visceral-, and Transplant Surgery, University of Heidelberg for elective hepatic resection are consecutively screened for eligibility and written informed consent is obtained on the day before surgery. The primary objective of this trial is to assess and compare the amount of blood loss during hepatic resection in patients receiving surgical CVP reduction by clamping of the IVC as compared to anaesthesiological CVP without infrahepatic IVC clamping reduction. In addition to blood loss a set of general as well as surgical variables are analysed.DiscussionThis is a randomised controlled patient and observer blinded two-group parallel trial designed to assess efficacy and safety of infrahepatic IVC clamping during elective hepatectomy.Trial registrationClinicalTrials NCT00732979

Hemodynamic Effects and Safety of Nesiritide in Neonates with Heart Failure

Evaluate effects and safety of nesiritide (Natrecor, Scios Inc.) human B-type natriuretic peptide, in neonates with heart failure. Seventeen neonates, not responding to conventional therapy, treated with nesiritide were retrospectively reviewed. Average age 16 + 8 days; weight 3.2 + 0.6 kg. Fifteen treated with concomitant inotropic therapy; all with diuretics. Twelve received loading dose; followed by continuous infusions of 0.005 mcg/kg/min (2); 0.01 mcg/kg/min (12); 0.02 mcg/kg/min (3). Length of therapy 5 + 4 days. No change in heart rate or blood pressure between baseline, 1 hour or 24 hours of nesiritide infusion. Decrease central venous pressure (CVP) 24 hours after infusion (p = 0.03). Ins-out ratio improved in 29%. No difference in pre and post therapy BUN and creatinine (Cr). 18% had hypotension requiring intervention. Nesiritide use in neonates may improve hemodynamics as demonstrated by reduction in CVP. All patients tolerated bolus dosing, however, transient hypotension occurred in 18% of neonates with continuous infusion.

Comment on Point:Counterpoint: “Cardiovascular variability is/is not an index of autonomic control of circulation”

POINT-COUNTERPOINT COMMENTSComment on Point:Counterpoint: “Cardiovascular variability is/is not an index of autonomic control of circulation”Catherine F. Notarius, and John S. FlorasCatherine F. Notarius, and John S. FlorasPublished Online:01 Jun 2007https://doi.org/10.1152/japplphysiol.00283.2007MoreSectionsPDF (27 KB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations The following letter is in response to Point:Counterpoint “Cardiovascular variability is/is not an index of autonomic control of circulation” that appeared in the August issue (vol. 101, pages 676–682, 2006).To the Editor: Changes in heart rate variability (HRV) or blood pressure variability (BPV) may well track qualitatively changes in vagal or sympathetic nerve traffic induced by some interventions in experimental models or human volunteers (6). However, contextual and interpretive limitations to their broader application to between-person comparisons or cardiovascular disease states have not been emphasized sufficiently in prior correspondence.HRV is a marker of sinoatrial node responsiveness to oscillations in sympathetic and vagal nerve traffic, not necessarily of nerve firing rates (5). Thus conditions of high but relatively invariate sympathetic nerve firing and heart rates, such as exercise (2) or advanced heart failure (4), are characterized by loss, rather than gain, of low frequency (LF) HRV spectral power. Even within healthy subjects, a very modest (1.6 mmHg) reduction in central venous pressure without effect on stroke volume or blood pressure elicits marked discordance between muscle sympathetic nerve firing rates (increased) and both LF power and the LF/HF ratio (unchanged; Ref. 3). Although BPV in the LF range tracks sympathetic nerve discharge within healthy subjects (6), it is not increased, but similar in subjects with and without heart failure (1). There is evidence from large population studies that low HRV increases the risk of premature cardiovascular death, but as yet none that such data quantify reliably risk in a specific individual or that selectively increasing HRV pharmacologically or non-pharmacologically without affecting other known modifiable risk markers improves outcome.Thus HRV and BPV analyses are best reserved for focused within-subject mechanistic investigations.REFERENCES1 Butler GC, Ando S, Floras JS. Fractal component of variability of heart rate and systolic blood pressure in congestive heart failure. Clin Sci (Colch) 92: 543–550, 1997.Crossref | Google Scholar2 Casadei B, Cochrane S, Johnston J, Conway J, Sleight P. Pitfalls in the interpretation of spectral analysis of the heart rate variability during exercise in humans. Acta Physiol Scand 153: 125–131, 1995.Crossref | PubMed | Google Scholar3 Floras JS, Butler GC, Ando S, Brooks SC, Pollard MJ, Picton P. Differential sympathetic nerve and heart rate spectral effects of nonhypotensive lower body negative pressure. Am J Physiol Regul Integr Comp Physiol 281: R468–R475, 2001.Link | ISI | Google Scholar4 Notarius CF, Butler GC, Ando S, Pollard MJ, Senn B, Floras JS. Dissociation between microneurographic and heart rate variability estimates of sympathetic tone in normal subjects and patients with heart failure. Clin Sci (Colch) 96: 557–565, 1999.Crossref | Google Scholar5 Notarius CF, Floras JS. Limitations of the use of spectral analysis of heart rate variability for the estimation of cardiac sympathetic activity in heart failure. Europace 3: 29–38, 2001.Crossref | PubMed | ISI | Google Scholar6 Parati G, Mancia G, Di Rienzo M, Castiglioni J, Taylor A, Studinger P. Point:Counterpoint: Cardiovascular variability is/is not an index of autonomic control of circulation. J Appl Physiol 101: 676–682, 2006.Link | ISI | Google Scholar Download PDF Previous Back to Top Next FiguresReferencesRelatedInformation Cited ByDifferent equestrian sports horses’ reactivity to startleJournal of Veterinary Behavior, Vol. 57Mild Hypothermia Attenuates Circulatory and Pulmonary Dysfunction During Experimental Endotoxemia*Critical Care Medicine, Vol. 41, No. 12 More from this issue > Volume 102Issue 6June 2007Pages 2406-2406 Copyright & PermissionsCopyright © 2007 the American Physiological Societyhttps://doi.org/10.1152/japplphysiol.00283.2007PubMed17551108History Published online 1 June 2007 Published in print 1 June 2007 Metrics

Intraoperative Blood Salvage During Liver Resection

A randomized controlled trial was conducted to clarify the effectiveness of intraoperative blood salvage in reducing blood loss. Although reduction of central venous pressure (CVP) is thought to decrease blood loss during liver resection, no consistently effective and safe method for obtaining the desired reduction of CVP has been established. Living liver donors scheduled to undergo liver graft procurement were randomly assigned to a blood salvage group, in which a blood volume equal to approximately 0.7% of the patient's body weight was collected before the liver transection, or a control group. The surgeons were blinded to the randomization results. The primary outcome measure was blood loss during liver parenchymal division. A multivariate analysis was also performed. Seventy-nine donors were allocated intraoperatively to the blood salvage group (n = 40) or the control group (n = 39). The amount of blood loss during liver transection was significantly smaller in the blood salvage group than in the control group (median loss during transection, 140 mL vs. 230 mL, P = 0.034). The CVP at the beginning of the liver parenchymal division was significantly lower in the blood salvage group than in the control group (median, 5 cm H2O vs. 6 cm H2O, P = 0.005). The results of a multivariate analysis revealed that intraoperative blood salvage offered the advantage of reduced blood loss during liver parenchymal division (adjusted OR, 0.31; 95% CI, 0.11-0.85, P = 0.025). Modest intraoperative blood salvage significantly and safely reduced blood loss during hepatic parenchymal transection.

Effect of skin surface cooling on central venous pressure during orthostatic challenge

Orthostatic stress leads to a reduction in central venous pressure (CVP), which is an index of cardiac preload. Skin surface cooling has been shown to improve orthostatic tolerance, although the mechanism resulting in this outcome is unclear. One possible mechanism may be that skin surface cooling attenuates the drop in CVP during an orthostatic challenge, thereby preserving cardiac filling. To test this hypothesis, CVP, arterial blood pressure, heart rate, and skin blood flow, as well as skin and sublingual temperatures, were recorded in nine healthy subjects during lower body negative pressure (LBNP) in both normothermic and skin surface cooling conditions. Cardiac output was also measured via acetylene rebreathing. Progressive LBNP was applied at -10, -15, -20, and -40 mmHg at 5 min/stage. Before LBNP, skin surface cooling lowered mean skin temperature, increased CVP, and increased mean arterial blood pressure (all P < 0.001) but did not change mean heart rate (P = 0.38). Compared with normothermic conditions, arterial blood pressure remained elevated throughout progressive LBNP. Although progressive LBNP decreased CVP under both thermal conditions, during cooling CVP at each stage of LBNP was significantly greater relative to normothermia. Moreover, at higher levels of LBNP with skin cooling, stroke volume was significantly greater relative to normothermic conditions. These data indicate that skin surface cooling induced an upward shift in CVP throughout LBNP, which may be a key factor for preserving preload, stroke volume, and blood pressure and improving orthostatic tolerance.

Hypotension during hemodialysis results from an impairment of arteriolar tone and left ventricular function

Hypotensive episodes are a major complication of hemodialysis. Hypotension during dialysis could be directly related to a reduction in blood volume or to a decrease in cardiovascular activation as a response to decreased cardiac filling. A decreased cardiovascular activation could be due to patient-related or to dialysis-related factors. In order to study the isolated effect of a reduction in filling pressure, lower body negative pressure (LBNP) causes activation of the cardiovascular reactivity with a decrease in cardiac filling, but without the influence of the dialysis procedure that could affect cardiovascular reactivity. We studied the relationship between relative blood volume (RBV), central venous pressure (CVP), systolic arterial pressure, heart rate, stroke volume index (SI), and total peripheral resistance index (TPRI) during a combined dialysis/ultrafiltration and during LBNP to -40 mmHg in 21 hemodialysis patients with a high incidence of hypotension. Systolic arterial pressure, heart rate, SI and TPRI were measured by Finapres. CVP was measured after cannulation of the jugular vein. During dialysis RBV was measured by a blood volume monitor (BVM). In order to study the conditions in which hypotension occurred after dialysis, we divided the patients into 2 groups: hypotensive (H) and non-hypotensive (NH) during dialysis. Baseline levels did not show any significant differences. During dialysis systolic arterial pressure declined gradually in the H group from 30 minutes before the onset of hypotension. There was a similar decrease of RBV and increase of heart rate in both groups with a large interindividual variation. At hypotension, H patients showed a significantly smaller increase in TPRI as compared to NH patients. The reduction in SI tended to be greater at hypotension, while CVP decreased to a similar extent in both groups. Moreover, during LBNP, a similar reduction in CVP resulted in a much smaller decrease in SI. Systolic arterial pressure was only slightly lowered due to a much greater increase in TPRI. We conclude that dialysis-related hypotension in our patient group did not result from an inability to maintain blood volume or from decreased cardiac filling. Hypotension appeared to result from the inability to adequately increase arteriolar tone and a reduction in left ventricular function. Both vascular tone and left ventricular function appeared to be impaired by the dialysis procedure.