Effect Of Central Venous Pressure Research Articles

Effect of central venous pressure on fluid delivery during start-up of syringe infusion pumps for microinfusion.

Intravenous administration of highly concentrated and potent drugs at low flow rates is common practice, particularly in critically ill children. Drug delivery during infusion start-up can be considerably delayed by intrinsic factors of syringe infusion pump assemblies. The impact of central venous pressures on the course of start-up fluid delivery of such microinfusions remains unknown. Infusion volumes delivered after activation of the start button in a conventional 50 mL syringe infusion pump assembly equilibrated (representing classical in vitro testing) and not equilibrated (representing real clinical conditions) to central venous pressure levels of 0, 10 and 20 mmHg at a set infusion flow rate of 1 mL/h were measured using a fluidic flow sensor. The experimental setup mimicking real life conditions demonstrated considerable differences in fluid delivery during pump start-up depending on central venous pressure. A central venous pressure of 0 mmHg resulted in massive fluid delivery at infusion start-up, while central venous pressure levels of 10 and 20 mmHg resulted in retrograde flows with related mean (95% CI) zero-drug delivery times of 3.22 (2.98-3.46) min and 4.51 (4.33-4.69) min, respectively (p < .0001). Depending on central venous pressure level, connection and starting a new syringe pump can result in significant antegrade or retrograde fluid volumes. In clinical practice, this can lead to hemodynamic instability and hence requires clinical alertness. Further research and methods to improve start-up performance in syringe infusion pump systems are desirable.

Association Between the Central Venous Pressure and All-Cause Mortality in Critically Ill Patients with Acute Kidney Injury.

PurposeElevated central venous pressure (CVP) plays an important role in the occurrence of acute kidney injury (AKI) and it is also independently associated with the prognosis of critically ill patients. However, the effect of CVP on critically ill AKI patients remains unclear. In this study, we analyzed the relationship between CVP and all-cause mortality of critically ill patients with AKI.Patients and MethodsThe clinical data of patients in intensive care unit (ICU) were retrieved from the Medical Information Mart for Intensive Care III (MIMIC-III) database and retrospectively analyzed. The all-cause mortality for up to 90 days was the main observed outcome. We used the minimum CVP value obtained during the first 72 hours after ICU admission for our analysis and patients were grouped according to this parameter. Patients were also analyzed after being further divided according to stages 1, 2 and 3 of AKI. Multiple Cox regression and Kaplan–Meier analyses were used to explore the association between CVP measurements and death of ICU patients with AKI.ResultsA total of 1986 ICU patients with AKI were studied. A total of 527 (26.5%) patients died by day 90. The high CVP group (patients with ≥10 mmHg) had the lowest 90-day survival rate (P =0.001 by log rank test) when according to Kaplan–Meier analysis. By using Cox regression analysis, high CVP was found to be linked to an increase in mortality (CVP ≥10 mmHg versus ≤5 mmHg, HR, 1.336, 95% CI, 1.064 to 1.677, P trend=0.014). Furthermore, when using in a multivariate Cox regression analysis with CVP as a continuous variable, the higher CVP levels were still an independent risk factor for 90-day all-cause mortality (per 1 mmHg increase, HR, 1.031, 95% CI, 1.013–1.049, P=0.001). In subgroup analysis, a similar trend was observed in patients with AKI stages 2 and 3.ConclusionThe minimum CVP level during the first 72h after ICU admission was positively associated with mortality in critically ill patients with AKI and this more marked in cases with severe AKI.

Relation between central venous pressure values and outcome in critically ill patients

Background Central venous pressure (CVP) was the most commonly used parameter to guide fluid responsiveness. However, recent studies showed that there is no correlation between CVP and circulating blood volume, and CVP more than 8 mmHg is independently associated with a higher mortality and increased risk of acute kidney injury in patients with sepsis and heart failure. Objective The aim of this study was to assess the effect of CVP over 7 days after ICU admission on clinical prognosis and mortality. Patients and methods The study was conducted on 218 patients in whom hemodynamic monitoring was required, and CVP was measured from the first day of ICU admission. Three values of CVP were selected to be measured (the values once inserted, the peak values, and the mean values of CVP) throughout the monitoring process over 7 days of ICU admission. Acute Physiology and Chronic Health Evaluation II score was calculated on admission, and Sequential Organ Failure Assessment (SOFA) score was calculated every other day. Length of ICU stay, mechanical ventilation days, and mortality at days 7 and 28 were recorded. Results Although the initial CVP values were only correlated with mean of SOFA scores, mean and peak CVP values were correlated with Acute Physiology and Chronic Health Evaluation II score, mean SOFA score, mechanical ventilation days, and mortality. Only peak CVP showed correlation with mean creatinine, and only mean CVP values were correlated with length of ICU stay. According to mean CVP values, patients were classified as low CVP ( 12 mmHg). The elevated mean CVP group was associated with increased 28-day mortality, and regarding further investigations such as renal function, duration of mechanical ventilation, and laboratory results related to organ dysfunction, it also demonstrated that higher mean CVP group was associated with poor ICU outcome for patients in ICU settings. Conclusion The study showed that for patients in ICU settings, elevated mean CVP load was associated with poor clinical outcome and prolonged treatment in ICU. Level and duration of elevated mean CVP should be evaluated, and more effort should be made to establish the cause and appropriate treatment for elevated mean CVP.

The correlation between CVP-derived parameters and the prognosis of critically ill patients

ObjectiveTo investigate the effect of central venous pressure on the organ dysfunction and prognosis of critically ill patients. MethodsWe conducted a retrospective observational cohort study of 488 ICU patients with central venous pressure and its derived parameters in a half-year period in one single ICU centre to compare the length of ICU stay, critical illness scores (SOFA and APACHE II), serum creatinine and lactate levels. ResultsThe initial, peak and mean CVP levels of critically ill patients and length of ICU stay, peak lactate levels and SOFA scores were significantly correlated. While the peak CVP and peak creatinine levels were significantly correlated, the correlation of initial and mean CVP levels with peak creatinine was not significant. Subgroup analysis showed that in the patients with a peak CVP value above 12mmHg, the length of stay was significantly prolonged, organ function was significantly worse, and the SOFA score was significantly higher. ROC analysis showed peak levels of CVP above 11.5mmHg had the greatest ability to predict mortality of critically ill patients. ConclusionExposure to higher levels of central venous pressure in critically ill patients is associated with a poorer prognosis and worse organ function. Therefore, central venous pressure should be kept as low as possible during hemodynamic therapy in critically ill patients.

Congestive kidney failure in cardiac surgery: the relationship between central venous pressure and acute kidney injury.

Acute kidney injury (AKI) in cardiac surgery has traditionally been linked to reduced arterial perfusion. There is ongoing evidence that central venous pressure (CVP) has a pivotal role in precipitating acute renal dysfunction in cardiac medical and surgical settings. We can regard this AKI driven by systemic venous hypertension as 'kidney congestive failure'. In the cardiac surgery population as a whole, when the CVP value reaches the threshold of 14 mmHg in postoperative period, the risk of AKI increases 2-fold with an odds ratio (OR) of 1.99, 95% confidence interval (95% CI) of 1.16-3.40. In cardiac surgery subsets where venous hypertension is a hallmark feature, the incidence of AKI is higher (tricuspid disease 30%, carcinoid valve disease 22%). Even in the non-chronically congested coronary artery bypass population, CVP measured 6 h postoperatively showed significant association to renal failure: risk-adjusted OR for AKI was 5.5 (95% CI 1.93-15.5; P = 0.001) with every 5 mmHg rise in CVP for patients with CVP <9 mmHg; for CVP increments of 5 mmHg above the threshold of 9 mmHg, the risk-adjusted OR for AKI was 1.3 (95% CI 1.01-1.65; P = 0.045). This and other clinical evidence are discussed along with the underlying pathophysiological mechanisms, involving the supremacy of volume receptors in regulating the autonomic output in hypervolaemia, and the regional effect of venous congestion on the nephron. The effect of CVP on renal function was found to be modulated by ventricular function class, aetiology and acuity of venous congestion. Evidence suggests that acute increases of CVP should be actively treated to avoid a deterioration of the renal function, particularly in patients with poor ventricular fraction. Besides, the practice of treating right heart failure with fluid loading should be avoided in favour of other ways to optimize haemodynamics in this setting, because of the detrimental effects on the kidney function.

Functional hepatic venous outflow and its correlation with early graft function in live donor liver transplantation

Introduction: To evaluate the effect of central venous pressure (CVP) on early graft function in live donor liver transplantation (LDLT). Methods: 61 Recipients of LDLT without any technical complications from May 2013 to November 2014 were included. CVP was measured at five time points – before surgery, anhepatic phase, 30 minutes after reperfusion, end of surgery and post operatively (days 1–5). Patients were divided into two groups based on CVP ≤10, >10 mm Hg at various time points for analysis. Results: Elevated postoperative CVP (p ≤ 0.001) and drain culture positivity in the first week (p < 0.001) were found to be independent predictors of mortality on multivariate analysis. Optimum cut off of CVP in predicting mortality is 10.8. High cardiac output at the end of surgery (p = 0.005), high MELD scores (p = 0.011) and culture proven infection at any site (p = 0.002) were all independent predictors of early graft dysfunction (EGD) on multivariate analysis. There was an inverse correlation between CVP and SVR at the beginning of surgery which reversed to a positive correlation at the end of surgery. Conclusions: Elevated CVP in the postoperative period in recipients is a risk factor of mortality in the setting of LDLT. EGD is associated with high MELD scores, higher cardiac output at the end of surgery and infection at any site. A restrictive fluid management protocol aiming for a CVP <11 seems beneficial.

The Effect of Central Retinal Venous Pressure in Patients with Central Retinal Vein Occlusion and a High Mean Area of Nonperfusion

To evaluate the effect of central venous pressure (CVP) on visual outcomes and retinal ischemic consequences in patients with central retinal vein occlusion (CRVO). Prospective, single-center cohort study. Eighty-eight patients with CRVO and a high overall mean area (21.6 disc areas) of capillary nonperfusion (CNP) who were followed for 18 months before the availability of intravitreal therapy and who were offered standard care of the time. Patients were evaluated at baseline and at 3, 8, and 18 months. At each study visit, measurements of CVP, best-corrected visual acuity (BCVA), area of CNP, retinal fluorescein transit time (FTT), and an evaluation for rubeosis iridis were performed. Evaluation of the effect of different levels of CVP on BCVA, retinal blood flow, and the development of retinal ischemia and rubeosis iridis. Mean BCVA was significantly higher in patients with lower CVP at all time points (P<0.0001). The area of CNP increased significantly with higher levels of CVP and progressed with time. The development of rubeosis iridis was significantly associated with CVP at all time points and was present in 5.6%, 27.9%, and 88.9% of those with low, moderate, and high CVP levels, respectively (P<0.0001), at the 18-month conclusion. Retinal blood flow as measured by FTT was reduced with higher levels of CVP. Spontaneous lowering of CVP had beneficial effects on BCVA, although this diminished with time. Eyes with increased CVP after more severe CRVO demonstrate significantly reduced vision, reduced retinal blood flow, a higher incidence of rubeosis iridis, and larger areas of CNP that correlate with the degree of CVP elevation.

Assessment effect of central venous pressure in fluid resuscitation in the patients with shock: a multi-center retrospective research

Background Central venous pressure (CVP) and intrathoracic blood volume index (ITBVI) were used to assess the fluid status. It has previously been shown that CVP is not as accurate as ITBVI for all the shock patients. We therefore hypothesized that the change of CVP has the ability to predict fluid responsiveness in some clinical cases of shock. Methods From September 1st 2009 to September 1st 2011, sixty-three patients with shock from different Intensive Care Unit (ICU) were collected into this retrospective study. All the patients received fluid challenge strategy (infusing 300 ml hydroxyethyl starch in 20 minutes), were monitored with CVP and pulse-indicated continuous cardiac output (PICCO). The correlation between changes in cardiac index (ΔCI), CVP (ΔCVP) and ITBVI (ΔITBVI) were analyzed. Fluid responsiveness was defined as an increase in CI ≥10%. Receiver operating characteristic (ROC) curves were generated for ΔCVP and ΔITBVI. Results For all the patients, there was no correlation between ΔCI and ΔCVP (P=0.073), but in the subgroup analysis, the correlation between ΔCI and ΔCVP was significant in those younger than 60 years old (P=0.018) and those with hypovolemic shock (P=0.001). The difference of areas under the ROC curves of ΔCVP and ΔITBVI were not statistically significant in the group younger than 60 years old or hypovolemic shock group (P &gt;0.05, respectively). However, no similar results can be found in the group older than 60 years old and the other two shock type groups from ROC curves of ΔCVP and ΔITBVI. Conclusions ΔCVP is not suitable for evaluating the volume status of the shock patients with fluid resuscitation regardless of their condition. However, in some ways, ΔCVP have the ability to predict fluid responsiveness in the younger shock patients or in the hypovolemic shock patients.

Effects of central venous pressure on acute kidney injury in septic shock

To investigate the effects of central venous pressure on acute kidney injury (AKI) in septic shock. A total of 86 septic shock patients with PiCCO (pulse indicator continuous cardiac output) monitoring admitted at our department from January 2009 to January 2011 were retrospectively studied. They were divided into 2 groups based on central venous pressure (CVP) at 24 hs after PiCCO monitoring. There were 41 cases in low CVP group (CVP ≤ 10 mm Hg and 45 cases in high CVP group (CVP > 10 mm Hg). Their hemodynamic data, lactate concentration, ScvO₂ (central venous oxygen saturation), APACHEII (acute physiology & chronic health evaluation II) score and serum creatinine were obtained at the beginning and 24 hours after PiCCO monitoring. The incidence and mortality of AKI, the outcome of these patients in ICU and at Day 28 post-diagnosis were recorded. (1) The incidences of AKI were 51.2% (21/41) and 75.6% (34/45) in low and high CVP groups respectively; (2) Nine cases (22.0%) died in ICU in low CVP group and 20 cases (44.4%) in high CVP group. And 12 cases (29.3%) died within 28 days in low CVP group while 21 cases (46.7%) in high CVP group. A high CVP may increase the incidence and morbidity of AKI in septic shock. And an excessively high CVP should be prevented.

Akira Takeshita, MD, PhD

Akira Takeshita, MD, PhD, 69, Professor Emeritus of Cardiovascular Medicine and Director Emeritus of the Institute of Angiocardiology, Kyushu University Graduate School of Medicine, Japan, died on March 15, 2009 after a long illness. Dr Takeshita was an internationally recognized leader in cardiovascular medicine. His research focused on neural regulation and vascular biology. Dr Takeshita was born on January 24, 1940. He earned his MD degree from Kyushu University School of Medicine in 1965. His unique and international career started immediately after his graduation when, unlike many other Japanese physicians, especially at that time, he moved to the Tachikawa U.S. Air Force Hospital near Tokyo, where he was an intern and resident. He met Makiko, who was performing her externship in anesthesiology at the Hospital, and they married in 1968. They helped each other as the best partners in life and also as medical professionals, for 41 years until his death. In 1967, Dr Takeshita returned to Kyushu University where he trained in the Department of Cardiovascular Medicine. He then moved to Mount Sinai Hospital, Cleveland, in …

Effect of Central Venous Pressure on Spinal Cord Oxygenation

To analyze the effect of central venous pressure on cerebrospinal fluid oxygen tension and intrathecal pressure, multiparameter sensors were introduced into the intrathecal space for continuous monitoring of cerebrospinal fluid Po(2), Pco(2), and intrathecal pressure in 15 pigs. After 20 min of aortic clamping, hypervolemia was established for 20 min, followed by normovolemia. The animals were divided into 3 groups: in group 1, cerebrospinal fluid Po(2) = 0% at some time during crossclamping; in group 2, cerebrospinal fluid Po(2) was <50%; and in group 3, cerebrospinal fluid Po(2) remained > or = 50%. Mean decreases in cerebrospinal fluid Po(2) during the initial 20 min of crossclamping were 82%, 57%, and 15% in groups 1, 2, and 3, respectively. Following induction of hypervolemia, central venous and cerebrospinal fluid pressures increased simultaneously; this caused a significant decrease in cerebrospinal fluid Po(2) in group 2 only. In this model, aortic clamping did not increase cerebrospinal fluid pressure if central venous pressure was not elevated. The detrimental effect of elevated intrathecal pressure on cerebrospinal fluid oxygenation was seen only in animals with an intermediate degree of spinal cord ischemia. This might have important implications for the prevention of paraplegia during thoracoabdominal aortic replacement.

Changes in human plasma atrial natriuretic polypeptide concentration in normal subjects during passive leg raising and whole-body tilting.

The effect of central venous pressure on release of human atrial natriuretic polypeptide (hANP) was studied by measuring the plasma hANP levels during passive leg raising to 60 degrees and head up whole-body tilt at 60 degrees in normal volunteers. In ten subjects, after at least 1 h recumbency, both legs were raised passively 60 degrees for 20 min. While the legs were raised the plasma hANP level increased significantly from a basal level of 101 +/- 10 pg/ml (mean +/- SE) to a peak of 165 +/- 15 pg/ml after 10 min, and returned to the basal level 10 min after the legs were lowered. The blood pressure and pulse rate were not affected by raising the legs. The effect of head up whole-body tilt of 60 degrees from the supine position, for 20 min, was examined in nine normal subjects. Their plasma hANP decreased transiently at 5 min in five of them and at 10 min or later in the remaining four subjects. Their blood pressure did not change but their pulse rate increased significantly while their body was being tilted. These results suggest that secretion of hANP is regulated physiologically by changes in the central venous pressure.

Continual monitoring of intraocular pressure: effect of central venous pressure, respiration, and eye movements on continual recordings of intraocular pressure in the rabbit, dog, and man.

A new method has been devised for continual monitoring of intraocular pressure by radiotelemetry. The use of this instrument for monitoring intraocular pressure by a variety of ophthalmic conditions is described.

Effect of central venous pressure on arterial baroreflex control of heart rate

There is considerable evidence that the level of afferent cardiopulmonary receptor activity modulates sinus node responses to arterial baroreflex stimulation in experimental animals. We tested the hypothesis that this reflex interaction occurs also in man by measuring sinus node responses to arterial baroreceptor stimulation with phenylephrine injection or neck suction, before and during changes of central venous pressure provoked by lower body negative pressure or leg and lower trunk elevation. Variations of central venous pressure between 1.1 and 9.0 mmHg did not influence arterial baroreflex mediated bradycardia. Baroreflex sinus node responses were augmented by intravenous propranolol, but the level of responses after propranolol was comparable during the control state, lower body negative pressure, and leg and trunk elevation. Sinus node responses to very brief baroreceptor stimuli applied during the transitions of central venous pressure also were comparable in the three states. We conclude that physiological variations of central venous pressure do not influence sinus node responses to arterial baroreceptor stimulation in man.

Effect of central venous pressure on brain tissue pressure and brain volume.

In cats, brain tissue pressure (BTP) was measured by the wick-catheter method. The BTP was positive, but lower than cerebrospinal fluid pressure. Elevation on central venous pressure led only to a transient proportional increase of BTP. When the calvaria and dura of one hemisphere were removed, the rise of BTP was even less. Water content of the brain was normal in either case, even after prolonged venous hypertension. Venous hypertension led in all cases to a marked increase of the brain volume which was caused by vessel dilatation. In brain edema, produced by rinsing the brain surface with ouabain and concentrated saline, BTP was increased permanently by venous hypertension. The water content of the brain was much greater than normal. From these results it was concluded that congestive edema does not occur in the brain unless the tissue is damaged. However, venous hypertension does cause brain swelling.