Central venous pressure, pulmonary artery occlusion pressure, intrathoracic blood volume, and right ventricular end-diastolic volume as indicators of cardiac preload

Central venous pressure (CVP), pulmonary artery occlusion pressure (PAOP) and right ventricular end-diastolic volume (RVEDV) are often regarded as indicators of both circulating blood volume and cardiac preload. To evaluate these relationships, the response of each variable to induced volume shifts was tested. The relationships between these variables and cardiac index (CI) and stroke volume index (SVI) was also recorded to assess the utility of each variable as an indicator of cardiac preload. The responses of the new variable intrathoracic blood volume (ITBV) to the same maneuvers was also tested. To examine the effects of changes in cardiac output alone on ITBV, the effects of infusing dobutamine were studied.

Ten anesthetized piglets were studied during conditions of normovolemia, hypovolemia, and hypervolemia. The effects of an infusion of dobutamine were examined under normovolemia and hypovolemia. Cardiac output was measured by thermodilution, and ITBV was measured by double-indicator dilution.

CI was correlated to CVP with r² = .42 (P ≤ .01), to PAOP with r² = .43 (P ≤ 5.01), to RVEDV index with r² = .21 (P ≤ .01), and to ITBV with r² = .78 (P ≤ .01) (pooled absolute values). Bias (mean difference of the percent changes with NORMOVOLEMIA = 100%) ± 1 SD; for SVI - ITBV index was 1 ± 22%, for SVI — CVP it was −128 ± 214%; for SVI — PAOP it was −36 ± 46%; and for SVI -RVEDV index it was 1 ± 29%. Dobutamine infusion increased heart rate (to about 190 × min⁻¹) and CI by 30% in normovolemia and hypovolemia, while ITBV remained basically unchanged.

Under the experimental conditions choosen neither CVP, PAOP, nor RVEDV reliably indicated changes in circulating blood volume, nor were they linearly and tightly correlated to the resulting changes in SVI. ITBV reflected both changes in volume status and the resulting alteration in cardiac output. The possibility that ITBV might be cardiac output-dependent was not supported. ITBV, therefore, shows potential as a clinically useful indicator of overall cardiac preload.     

Pulmonary artery pressure versus pulmonary capillary wedge pressure and central venous pressure in shock

Evidence is presented from 43 dogs and 30 patients that under conditions of severe hemorrhagic, traumatic or septic shock, there may be partial obstruction of the pulmonary microcirculation due to disseminated intravascular coagulation (DIC) particularly in the pulmonary venules. This may cause the left atrial pressure to fall and the pulmonary artery pressure to rise, in some cases drastically. Pulmonary edema may result. This dangerous rise in pulmonary artery pressure is not reflected by the wedged pulmonary artery catheter which will monitor only the status of the left heart. Central venous pressure (CVP) may remain within normal limits even after pulmonary artery pressure has risen to dangerous levels with the development of pulmonary edema. It is only with right ventricle failure against the high pulmonary pressure that CVP rises. It is concluded that pulmonary artery pressure measurements are very important in monitoring intravenous fluid administration in severe shock. Wedged pulmonary artery pressures monitor the left heart but may be misleading if taken alone. Central venous pressure gives a delayed response to fluid overload.     

Evaluation of mean systemic filling pressure from pulse contour cardiac output and central venous pressure

Objective  

The volemic status of a patient can be determined by measuring mean systemic filling pressure (Pmsf). Pmsf is obtained from the venous return curve, i.e. the relationship between central venous pressure (Pcv) and blood flow. We evaluated the feasibility and precision of Pmsf measurement.     

Correlations between cardiac output, stroke volume, central venous pressure, intra-abdominal pressure and total circulating blood volume in resuscitation of major burns

The purpose of this study was to observe the interactions between cardiac index (CI), stroke volume index (SVI), central venous pressure (CVP), intra-abdominal pressure (IAP) and total circulating blood volume index (TBVI) during resuscitation of major burns. Sixteen patients with an average TBSA of 46% (26-67%) and an average abbreviated burn severity index of 8.9 (7-11) were included into an intra-individual comparative prospective study over an 18-month period. The COLD Z-021 system (Pulsion Medical Systems, Munich, Germany) was used to obtain CI, SVI and TBVI. Two hundred and thirty-four to 278 intra-individually comparative measurements were performed for the analyses during the first 4 days after the burn injury. Correlations were shown for the interactions between CI and TBVI (r = 0.550; rs = 0.518), SVI and TBVI (r = 0.606; rs = 0.626) and for CVP versus IAP (r = 0.487; rs = 0.474). Poor or no correlations were demonstrated for the comparisons CI versus CVP (r = 0.401; rs = 0.352), CVP-PEEP versus IAP (r = 0.255; rs = 0.272). TBVI versus IAP (r = -0.120; rs = -0.169), TBVI versus CVP (r = 0.025; rs = -0.036), TBVI versus CVP-PEEP (r = -0.046; rs = -0.101), CI versus CVP-PEEP (r = 0.088; rs = 0.092) as well as for IAP versus CI (r = 0.050; rs = 0.034). An additional analysis demonstrated no correlation between TBVI and MAP (r = -0.095; rs = -0.136). Our data provide evidence that the CVP is influenced more by external pressures (IAP) than by the actual intravascular volume status of the patient. Thus, the CVP is not a suitable tool to guide fluid resuscitation during burns with shock. The TBVI may be an ideal value to guide resuscitation because the augmentation of TBVI during fluid resuscitation correlated well with improved cardiac output and stroke volume. Future randomised studies are required to demonstrate whether TBVI guided resuscitation of burns has an impact on outcome.     

Effect of large volume infusion on left ventricular volumes,performance and contractility parameters in normal volunteers

Objective Characterize the normal human cardiovascular response to large volume infusion of normal saline.Design: Prospective, interventional trial.Setting ICU procedure room.Participants Healthy male volunteers (n=32).Interventions Volumetric echocardiography during 4-L saline infusion (3 L over 3 h followed by 1 L over 2 h).Measurements and results Following 3-L saline infusion, stroke volume and cardiac output increased approximately 10% without a significant change in heart rate or blood pressure. A decrease in end-systolic volume contributed to the increase in stroke volume to an extent similar to that provided by the increase in end-diastolic volume. All contractility indices except end-systolic wall stress/end-systolic volume index were increased at 3 h post-initiation of saline infusion. Stroke volume but not cardiac output remained elevated at 5 h with persistence of ventricular volume responses; only ejection fraction was significantly elevated among the contractility indices. Afterload measures including total peripheral resistance and end-systolic wall stress were significantly decreased after 3-L infusion but were unchanged compared to baseline following infusion of an additional 1 L over 2 h. Modeled blood viscosity studies demonstrate that changes in apparent contractility after 3-L saline infusion can be explained solely by viscosity reduction associated with hypervolemic hemodilution.Conclusion The initial increase in stroke volume associated with high volume saline infusion in normal volunteers is associated with increases of most load-dependent and ostensibly load-independent parameters of left ventricular contractility. This phenomenon is unlikely to represent a true increase in contractility and appears to be caused by reduced afterload as a consequence of decreased blood viscosity. This decrease in blood viscosity may complicate analysis of some previous in vivo studies examining the effect of volume loading on cardiac function using low-viscosity solutions.Electronic Supplementary Material Supplementary material is available in the online version of this article at An editorial regarding this article can be found in the same issue ()     

Optimal level of the reference transducer for central venous pressure and pulmonary artery occlusion pressure monitoring in supine,prone, and sitting position

To guarantee accurate measurement of central venous pressure (CVP) or pulmonary artery occlusion pressure (PAOP), proper positioning of a reference transducer is a prerequisite. We investigated ideal transducer levels in supine, prone, and sitting position in adults. Chest computed tomography images of 113 patients, taken in supine or prone position were reviewed. For supine position, distances between the back and the uppermost blood level of both atria and their ratios to the largest anteroposterior (AP) diameter of thorax were calculated. For prone position, same distances and ratios were calculated from the anterior chest. For sitting position, distances between the mid-sternoclavicular joint and the most cephalad blood level of both atria and their ratios to the sternal length were calculated. The ratio of the uppermost blood level of right atrium (RA) and left atrium (LA) to the largest AP diameter of thorax was 0.81 ± 0.04 and 0.59 ± 0.03 from the back in supine position. That calculated from the anterior chest in prone position was 0.54 ± 0.03 and 0.46 ± 0.03. The ratio of the most cephalad blood level of RA and LA to the sternal length was 0.70 ± 0.10 and 0.68 ± 0.09 from the mid-sternoclavicular joint in sitting position, which corresponded to the upper border of 4th rib. Optimal CVP transducer levels are at four-fifths of the AP diameter of thorax in supine position, at a half of that in prone position, and at upper border of the 4th sternochondral joint in sitting position. PAOP transducer levels are similar in prone and sitting position, except for supine position which is at three-fifths of the AP diameter of thorax.     

Combination of continuous pulse pressure variation monitoring and cardiac filling pressure to predict fluid responsiveness

To assess if combining central venous pressure (CVP) and/or pulmonary capillary wedge pressure (PCWP) information with arterial pulse pressure variation can increase the ability to predict fluid responsiveness in patients under general anesthesia. This study is a retrospective analysis of patients scheduled for coronary artery bypass surgery and monitored with a pulmonary artery catheter who underwent a volume expansion after induction of general anesthesia. Among the 46 patients studied, 31 were responders to volume expansion. CVP similar to PCWP, was a poor predictor of fluid responsiveness, as indicated by low values of areas under the receiver operating characteristic curves [0.585 (95?% CI 0.389–0.780) and 0.563 (95?% CI 0.373–0.753) respectively, p?=?0.76]. The area obtained for PPV was 0.897 (95?% CI 0.801–0.992) with a threshold value of 12?%. The sensitivity, specificity, positive likelihood ratio, and negative likelihood ratio was 83.9?%, 86.7?%, 6.29 and 0.19 respectively. Combining information on right and/or left cardiac filling pressures with PPV did not increase the ability to predict whether a patient will be a responder or a non-responder to volume expansion. The ability to identify a potentially fluid responsive patient was no better using PPV plus cardiac filling pressures when compared to using PPV alone. Therefore, if PPV values are being monitored in a patient, CVP and PCWP values do not provide additional information to predict fluid responsiveness.     

Central venous pressure and shock index predict lack of hemodynamic response to volume expansion in septic shock: A prospective,observational study

Purpose

Volume expansion is a common therapeutic intervention in septic shock, although patient response to the intervention is difficult to predict. Central venous pressure (CVP) and shock index have been used independently to guide volume expansion, although their use is questionable. We hypothesize that a combination of these measurements will be useful.

Methods

In a prospective, observational study, patients with early septic shock received 10-mL/kg volume expansion at their treating physician's discretion after brief initial resuscitation in the emergency department. Central venous pressure and shock index were measured before volume expansion interventions. Cardiac index was measured immediately before and after the volume expansion using transthoracic echocardiography. Hemodynamic response was defined as an increase in a cardiac index of 15% or greater.

Results

Thirty-four volume expansions were observed in 25 patients. A CVP of 8 mm Hg or greater and a shock index of 1 beat min^− 1 mm Hg^− 1 or less individually had a good negative predictive value (83% and 88%, respectively). Of 34 volume expansions, the combination of both a high CVP and a low shock index was extremely unlikely to elicit hemodynamic response (negative predictive value, 93%; P = .02).

Conclusions

Volume expansion in patients with early septic shock with a CVP of 8 mm Hg or greater and a shock index of 1 beat min^− 1 mm Hg^− 1 or less is unlikely to lead to an increase in cardiac index.     

Prediction of fluid challenge effect: filling pressure when left ventricular function is abnormal, diastolic volume when left ventricular function is normal

Fluid resuscitation is a cornerstone of intensive care unit patient care, but prediction of the cardiovascular response remains difficult, despite many efforts in clinical research. The concept of responders and nonresponders illustrates such a difficulty. Many techniques have been tested, from strictly non-invasive to invasive, delivering various parameters related to the fluid challenge response. Considering the physical parameters available, such as pressure, volume and flow generated by right and left pumps circulating in elastic or compliant tubes, it sounds useful to go back to the basic knowledge to discuss the results of the present article. This published study tested in the postoperative period of cardiovascular surgery the prediction obtained with filling pressures and the diastolic volume. When left ventricular function (global ejection fraction) is adequate, the volume before fluid administration seems to predict well the fluid challenge response; whereas when the global ejection fraction is poor, the filling pressure seems more suitable. The present commentary discusses the main physiological issues related to these findings, with some methodological aspects.     

Dynamic arterial elastance to predict arterial pressure response to volume loading in preload-dependent patients

Introduction  

Hemodynamic resuscitation should be aimed at achieving not only adequate cardiac output but also sufficient mean arterial pressure (MAP) to guarantee adequate tissue perfusion pressure. Since the arterial pressure response to volume expansion (VE) depends on arterial tone, knowing whether a patient is preload-dependent provides only a partial solution to the problem. The objective of this study was to assess the ability of a functional evaluation of arterial tone by dynamic arterial elastance (Ea_dyn), defined as the pulse pressure variation (PPV) to stroke volume variation (SVV) ratio, to predict the hemodynamic response in MAP to fluid administration in hypotensive, preload-dependent patients with acute circulatory failure.     

Diagnostic accuracy of central venous saturation in estimating mixed venous saturation is proportional to cardiac performance among cardiac surgical patients

Purpose

Advanced hemodynamic monitoring in cardiac surgery translates into improvement in outcomes. We evaluated the relationship between central venous (ScvO₂) and mixed venous (SvO₂) saturations over the early postoperative period. The adequacy of their interchangeability was tested in patients with varying degrees of cardiac performance.

Methods

In this prospective observational study, we evaluated 156 consecutive cardiac surgical patients in an academic center. The ScvO₂ and SvO₂ data were harvested from 468 paired samples taken preoperatively (T0), after weaning from cardiopulmonary bypass (T1) and on postoperative day 1 (T2).

Results

The relationship between ScvO₂ and SvO₂ was inconsistent, with inferior correlations in patients with lower cardiac indices (CI) (Pearson r² = 0.37 if CI ≤2.0 L/min per square meter vs r² = 0.73 if CI >2.0 L/min per square meter, both P < .01). Patients with lower CI also had wider 95% limits of agreement between SvO₂ and ScvO₂. The proportion of patients with a negative SvO₂-ScvO₂ gradient increased over time (48/156 [31%] at T0 to 73/156 [47%] at T2; P < .01). This subgroup more frequently required inotropes at T2 than patients with a positive SvO₂-ScvO₂ gradient (odds ratio, 6.46 [95% confidence interval, 0.81-51.87], P = .06) and also had higher serum lactate levels (1.5 ± 0.8 vs 1.0 ± 0.4; P < .01).

Conclusions

The diagnostic accuracy of ScvO₂ for estimating SvO₂ is proportional to cardiac performance. A negative SvO₂-ScvO₂ gradient at T2 correlated with inotropic support requirement, higher operative risk score, age, lactate level, and duration of cardiopulmonary bypass.     

静脉应用甘露醇及速尿后中心静脉压变化

经临床观察,应用升压药病人在静脉输入甘露醇后,1h~2h内血压明显升高,而使升压药用量暂时减少。为了进一步了解这一现象,我们观察了84例静脉输入甘露醇、速尿或二者联用后中心静脉压的变化。现报道如下。1对象及方法选择2001年6月—2004年12月测量中心静脉压且应用甘露醇、速尿病人84例,排除观察过程中药物、躁动、咳嗽及腹内压突然增高[1]等影响中心静脉压测量的因素,保持监测中心静脉压及其他外部条件一致,其中36例在20min~30min内静脉输入20%甘露醇250mL,32例静脉注射速尿20mg,16例静脉注射速尿20mg后半小时至1h又静脉输入20%甘露醇250m…     

胸内正压对正常人左室充盈的直接影响及其力学机制

目的 探讨胸内正压对正常人左室充盈的直接影响及其力学机制.方法 超声心动图检测30例成正常人初始时与标准乏氏动作张力期10 s时左室舒张早期、舒张晚期血流速度（E峰、A峰）、二尖瓣环舒张早期运动速度（e）,计算左室舒张功能（E/A）、舒张早期充盈压（E/e）的变化.结果 与初始时比较,标准乏氏动作张力期10 s时,E峰、E/A及E/e减低,差异均有统计学意义（P＜0.05）.结论 胸内正压的力学作用会阻碍左室舒张运动,引起E峰及E/A减低;胸内正压增加血流阻力可能是导致E峰及E/e减低的一个原因.     

Variability of Doppler echocardiographic indexes of left ventricular filling in transplant recipients and in normal subjects

This study examines the reproducibility and variability of pulsed wave Doppler versus continuous wave Doppler ultrasound indexes of left ventricular filling in cardiac allograft recipients and in normal subjects. The following indexes were studied: isovolumic relaxation time, pressure half-time, peak early mitral flow velocity, and peak mitral flow velocity after atrial systole. Intraobserver and interobserver variability were assessed by regression analysis. Individual components of variance (subject, reader, beat, day, and tracing) were estimated in a subset of five patients and five normal subjects, and estimated total variance defined for each group. Temporal (day-to-day) variability for 95% confidence was estimated for these patients and for normal subjects. Temporal variability in the group from which the subsets were drawn was measured from absolute and percent change in values on two occasions. Estimated and observed 95% confidence limits were compared. Intersubject variability was the largest component of variance in both transplant recipients and in normal subjects. For all indexes in transplant recipients (in the absence of rejection) and normal subjects, observed absolute mean differences (+/- 2 standard deviations) between values from recordings taken on two different days were larger than the 95% confidence limits estimated from the components of variance analysis. The observed 95% limits for transplant recipients versus normal subjects were as follows: isovolumic relaxation time, 20 msec versus 6 msec; pressure half-time, 16 msec versus 9 msec; peak early mitral flow velocity, 32 cm per second versus 17 cm per second; and peak mitral flow velocity after atrial systole, 28 cm per second versus 10 cm per second.(ABSTRACT TRUNCATED AT 250 WORDS)     

The use of respiratory variations in right atrial pressure to predict the cardiac output response to PEEP

PURPOSE: The purpose of this study was to determine whether the pattern of respiratory variation in right atrial pressure (Pra) predicts the cardiac output response to positive end-expiratory pressure (PEEP). MATERIALS AND METHODS: We studied 18 patients with a variety of cardiac and pulmonary disorders requiring ventilatory support. A pulmonary artery flotation catheter was in place as part of their routine management. Changes in PEEP were made from 0 to 14 cm H2O to determine the level of PEEP, which increased PO(2) without decreasing cardiac output (ie, assessment of best PEEP). Static lung compliance and auto-PEEP were obtained from the pressure signal on the ventilator. The change in Pra with a spontaneous inspiratory effort (ie, triggered breath) was used to determine whether patients had a restrictive (ie, operating on the flat part of the Starling curve), or nonrestrictive pattern (acting on the ascending part of the Starling curve) as previously described. RESULTS: Cardiac output decreased 0.7 +/- 0.8 L/min (change from baseline P <.05) in the group with an inspiratory decrease in Pra and -0.04 +/- 1.50 L/min (P = NS) in the group without an inspiratory decrease in Pra. The groups were not significantly different. However, the variance in cardiac output was large and, in contrast to our hypothesis, two patients in the group with an inspiratory decrease in Pra did not have a decrease in cardiac output. Pra and pulmonary artery occlusion pressure after the PEEP trial were greater than before, indicating that reflex circulatory adjustments occurred in response to the PEEP. CONCLUSIONS: The inspiratory pattern in Pra does not predict the response to cardiac output to PEEP in individual patients. This is most likely because of reflex adaptations in the circuit that occur with the application of PEEP. The response of a patient to PEEP is affected by the patient's volume reserves, filling status of the right atrium, and neurosympathetic activity.     

Pulmonary venous flow in cardiac tamponade: influence of left ventricular dysfunction and the relation to pulsus paradoxus.

The pattern of left atrial filling was studied in nine closed-chest dogs during cardiac tamponade before and after production of microembolic left ventricular dysfunction produced by intracoronary injection of 54 +/- 4 microns (SD) microspheres. With cardiac tamponade, a significant increase in the ratio of systolic/diastolic pulmonary venous flow velocity integral both before (1.65 +/- 0.24 versus 2.77 +/- 0.43 [SE], p less than 0.05) and after production of left ventricular dysfunction (0.57 +/- 0.12 versus 1.77 +/- 0.44, p less than 0.05) was seen. Compared with baseline, cardiac tamponade caused a significant inspiratory decrease in systolic pulmonary venous velocity both before (7.3 +/- 2.0 versus 1.2 +/- 1.4 cm/sec) and after left ventricular dysfunction (3.4 +/- 0.4 versus 1.0 +/- 0.9 cm/sec, both p less than 0.05). The magnitude of respiratory variation (expiration-inspiration) of the pulmonary venous flow velocity integral with tamponade was significantly greater before than after left ventricular dysfunction (1.6 +/- 0.2 cm versus 0.8 +/- 0.2 cm, p less than 0.05). A significant correlation was found between the inspiratory fall in aortic systolic pressure and the flow velocity integral of pulmonary venous flow before left ventricular dysfunction (r = 0.58, p less than 0.05). After coronary embolization, neither pulsus paradoxus nor significant respiratory variation (expiration-inspiration) of the pulmonary venous flow integral was observed with cardiac tamponade. In this model of cardiac tamponade and left ventricular dysfunction, left atrial filling occurs predominantly during ventricular systole. These changes may be helpful in recognizing hemodynamically significant pericardial effusion and have implications for the pathophysiology of cardiac tamponade.     

Some aspects of the arterial response to venous occlusion in man

1. Plethysmographic blood flow records made after venous occlusion of the forearm showed a biphasic response which was first vasodilator and then vasoconstrictor. 2. The myogenic nature of the vascoconstrictor phase was confirmed in eight subjects after total autonomic blockade with atropine, propranolol, phentolamine and guanethidine. 3. Forearm venous blood demonstrated a rise in hydrogen ion concentration and a fall in oxygen tension during venous occlusion, which may contribute to the vasodilatation phase.     

Relation of epicardial fat to central aortic pressure and left ventricular diastolic function in patients with known or suspected coronary artery disease

The present study tested the hypothesis that epicardial fat may be associated with augmented central aortic pressure and impaired left ventricular (LV) function. We studied 134 consecutive patients undergoing left-sided cardiac catheterization for coronary artery disease (CAD) and examined the relation of epicardial fat volume measured by multi-detector computed tomography to ascending aortic pressure and LV ejection fraction determined by cardiac catheterization as well as indices of LV diastolic function assessed by Doppler echocardiography [early diastolic mitral annular velocity (e′) and a ratio of early diastolic mitral inflow to annular velocities (E/e′)]. Epicardial fat volume indexed to body surface area correlated positively with age (r = 0.24, P < 0.01), body mass index (r = 0.38, P < 0.001), systolic aortic pressure (r = 0.21, P < 0.05), aortic pulse pressure (r = 0.23, P < 0.01), LV ejection fraction (r = 0.22, P < 0.05) and E/e′ (r = 0.24, P < 0.05) and did negatively with e′ (r = ?0.31, P < 0.05). In multivariate linear regression including potential confounders, increased epicardial fat volume index correlated with aortic systolic and pulse pressure and LV diastolic function indices, but not LV ejection fraction. In conclusion, we found that epicardial fat was associated with augmented central aortic pressure and LV diastolic dysfunction in patients with known or suspected CAD.