|Year : 2020 | Volume
| Issue : 2 | Page : 220-229
Relation between central venous pressure values and outcome in critically ill patients
Amr Abdalla, Amr H Dahroug, Ahmed Rashad
Department of Critical Care Medicine, Faculty of Medicine, Alexandria University, Alexandria, Egypt
|Date of Submission||21-Mar-2019|
|Date of Acceptance||18-Nov-2019|
|Date of Web Publication||27-Jun-2020|
Lecturer Amr H Dahroug
Critical Care Medicine, 4 Adm Street, Ibrahimia, Alexandria
Source of Support: None, Conflict of Interest: None
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 (<8 mmHg), intermediate CVP (8–12 mmHg), and elevated 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.
Keywords: central venous pressure, hemodynamic monitoring, ICU admission, mortality, organ dysfunction
|How to cite this article:|
Abdalla A, Dahroug AH, Rashad A. Relation between central venous pressure values and outcome in critically ill patients. Res Opin Anesth Intensive Care 2020;7:220-9
|How to cite this URL:|
Abdalla A, Dahroug AH, Rashad A. Relation between central venous pressure values and outcome in critically ill patients. Res Opin Anesth Intensive Care [serial online] 2020 [cited 2020 Sep 25];7:220-9. Available from: http://www.roaic.eg.net/text.asp?2020/7/2/220/287988
| Introduction|| |
Intravenous fluids are infused mainly to restore intravascular volume in patients with distributive and hypovolemic shock. The benefits of the appropriate use of fluids in ICUs and hospitals are described well, but there are potential risks of volume overload, and it affects organ dysfunction and mortality .
In the early stages of shock, assessment of fluid status is usually easy and ordering fluid administration is helped by clinical signs of hypovolemia. Recognizing low central blood volume is difficult because of the unreliability of clinical signs of hypovolemia in the ICU setting. About fifty percent of shocked patients can respond to fluid infusion by increase in cardiac output .
Central venous pressure represents an index of cardiac preload which is strictly related to the right ventricular end-diastolic pressure.
CVP is influenced by changes in the transmural pressure (difference between the pressure within the vessel and outside the vessel) and vessel distensibility. Hence, changes in pericardial, intrathoracic (positive end-expiratory pressure), and intra-abdominal pressure; vascular resistance and compliance; blood volume; and cardiac pump function all affect CVP .
Since the introduction of the Frank-Starling law, the volume state is often thought of in terms of preload measures, such as CVP. Indeed, international clinical guidelines recommended the use of CVP as the end point of fluid resuscitation based on the belief that CVP reflects intravascular volume status ,.
According to Guyton , venous return is determined by the gradient between mean capillary filling pressure (MCFP) and CVP. An increase in the CVP or a fall in the MCFP will reduce venous return, stroke volume, and cardiac output. In addition to influencing venous return, a high CVP is transmitted backward increasing venous pressure. The increase in venous pressure has a profound effect on microcirculatory flow and organ function.
According to studies, CVP more than 8 mmHg is independently associated with a higher mortality and increased risk of acute kidney injury (AKI) in patients with sepsis and heart failure ,,.
The kidney is affected by congestion that leads to decreased renal blood flow, increased renal interstitial pressure which compromise lymph flow ,.
| Aim|| |
The aim of this work is to assess effect of CVP over 7 days after ICU admission on clinical prognosis and mortality.
| Patients and methods|| |
Our study was carried out on 218 adult patients (older than 18 years) requiring hemodynamic monitoring who were admitted to Critical Care Medicine Department in Alexandria Main University Hospital during 6 months period from the start of September 2017 to the end of February 2018, after approval of medical ethics committee, and an informed consent from the patients or their next of kin was taken before their enrollment in the study. We excluded pregnant women and patients who died within 24 h after admission.
Methods and measurements
All patients included in the study were subjected to proper history taking, and demographics (age, sex, medical history, drug history, etc.) were collected.
Complete physical examination; Glasgow coma scale, systolic blood pressure, diastolic blood pressure, mean arterial pressure (MAP), heart rate, surface body temperature (T), and chest auscultation were collected.
Assessments for Acute Physiology and Chronic Health Evaluation (APACHE II) score on admission and the Sequential Organ Failure Assessment (SOFA) score on first day of study and every 48 h for 7 days were performed.
Routine laboratory investigations included complete blood count, urea, creatinine, serum glutamic oxaloacetic transaminase, serum glutamic pyruvic transaminase, total protein, serum albumin, electrolytes such as Na and K, prothrombin time, partial thromboplastin time, and total and direct bilirubin. Hypoxic index (PaO2/FiO2) was calculated using arterial blood gases assessment on first day of study and every 24 h for 7 days.
Assessment of CVP from an internal jugular or subclavian central venous line was manually done using a manometer. Its value was read on the manometer scale, which was marked in centimeters; therefore gave a value for the CVP in centimeters of water, which was then changed to millimeter mercury using the equation, 1 mmHg=1.36 cmH2O.
Three values were selected to be measured (the values once inserted, the peak values, and the mean values of CVP). Four readings of CVP were taken daily from patient chart with 6 h apart; the highest of them was recorded as the peak value, and mean of them was recorded as the mean value of the day throughout the monitoring process over 7 days of ICU admission.
Chest radiography on the first day of the study after central venous line insertion was done.
Outcome data like mortality at days 7 and 28, ICU stay days, and days of mechanical ventilation were recorded.
Statistical analysis 
Data were fed to the computer and analyzed using IBM SPSS software package, version 20.0. (IBM Corp., Armonk, New York, USA) . Qualitative data were described using number and percent. The Kolmogorov–Smirnov test was used to verify the normality of distribution. Quantitative data were presented using range, mean, standard deviation and median. The level of significance of the results was considered at 5%.
| Results|| |
The CVP was monitored in 218 patients; half of them were diagnosed as having septic shock, whereas cardiogenic shock represented ∼16% of cases and traumatic brain injury was the diagnosis in 11% of cases. Other cases include upper gastrointestinal bleeding, AKI, cerebrovascular stroke, intracerebral hemorrhage, hypertensive pulmonary edema, burn, and alleged intoxication. Mean age was 50.93±14.87 years, and males had slightly higher percentage than females (50.5 vs. 49.5%). MAP was 57.78±10.50 mmHg, mean creatinine was 1.56±1.22 mg/dl, and mean values of initial, peak, and mean CVP were 13.95±4.69, 14.34±11.59, and 11.9±2.72 mmHg, respectively.
Regarding the outcome of studied cases, 206 of the 218 cases were mechanically ventilated and length of ICU stay was 9.62±4.14. A total of 87 cases died within 28 days, with mortality rate of 39.9%, and of those died, 46 cases were within 7 days of admission ([Table 1]).
Correlation analysis of central venous pressure-derived parameters with organ function and outcome of critically ill patients
Both peak CVP and mean CVP were significantly correlated with APACHE II scores (P<0.001). The initial CVP value and APACHE II score showed no significant correlation (P=0.129).
Initial, mean, and peak CVP values were significantly correlated with SOFA score (P=0.017, <0.001, <0.001, respectively).
The peak levels of CVP and mean creatinine values were significantly correlated, with a correlation coefficient of 0.160 (P=0.018). However, there was no significant correlation between the initial value of CVP and mean creatinine levels (P=0.764). The mean level of CVP and mean creatinine value also showed no significant correlation (P=0.098).
Only mean values of CVP were significantly correlated with the length of stay in the ICU, with correlation coefficient 0.133 and P=0.049, whereas mean and peak values of CVP were significantly correlated with mechanical ventilation days of critically ill patient with correlation coefficient of 0.292 and 0.236 and P values of less than 0.001 and 0.001, respectively.
The nonsurvivor group of patients showed relatively higher initial, mean, and peak CVP, with mean values of 10.78±3.34, 12.97±2.96, 14.79±3.48 mmHg, respectively, compared with survivors group, with mean values of 9.91±3.49 mmHg for initial CVP, 11.18±2.29 mmHg for mean CVP, and 12.87±2.58 mmHg for peak CVP.
Mean and peak values of CVP were significantly related with mortality (P<0.001 for both), whereas initial values of CVP were not related with mortality, with P value of 0.066.
Receiver operating characteristic analysis of mortality
A receiver operating characteristic analysis was carried out for peak and mean CVP values, APACHE II score, and mean SOFA score to predict death within 28 days. We measured the area under the curve (AUC) of these data, and AUC of peak CVP was 0.670 and of mean CVP was 0.685 whereas AUC of mean SOFA score was 0.818 and that of APACHE II was 0.598, as shown in the table. Mean SOFA score was the best predictor of mortality within 28 days followed by mean CVP values. Cut-off values were analyzed, and the best peak CVP cutoff value is 13.4 mmHg, with sensitivity of 63.22% and specificity of 67.18%, and the best mean CVP cutoff value is 12.5 mmHg with sensitivity of 56.32% and specificity of 74.05% ([Figure 1]).
|Figure 1 ROC curve for different parameters to predict mortality for total sample (n=218). ROC, receiver operating characteristic.|
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The patients included in this study were divided into three groups according to the level of CVP (<8, 8–12, and >12 mmHg) to observe the corresponding average MAP, APACHE II score, mean SOFA score, mean creatinine (mg/dl), days of mechanical ventilation, the length of stay in the ICU, and mortality at different mean CVP levels ([Figure 2],[Figure 3],[Figure 4] and [Table 2]).
|Figure 2 Distribution of the studied cases according to mean CVP (mmHg) (n=218). CVP, central venous pressure.|
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|Figure 3 Correlation between APACHE II (a), mean SOFA (b), days of mechanical ventilation (c), length of ICU stay (d), and mortality (e) and mean CVP (mmHg) (n=218). APACHE, Acute Physiology and Chronic Health Evaluation; CVP, central venous pressure; SOFA, Sequential Organ Failure Assessment.|
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|Figure 4 Correlation between APACHE II (a), mean SOFA (b), mean creatinine mg/dl (c), days of mechanical ventilation (d), and mortality (e) and peak CVP (mmHg) (n=218). APACHE, Acute Physiology and Chronic Health Evaluation; CVP, central venous pressure; SOFA, Sequential Organ Failure Assessment.|
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|Table 2 Correlation between central venous pressure and different parameters (N=218)|
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The APACHE II score of the highest CVP group (>12 mmHg) increased significantly compared with the other two groups (CVP <8 and 8–12 mmHg), with mean scores of 19.78±5.98 vs. 10.78±1.79 and 16.71±5.38, respectively; P2 and P3 <0.001). The APACHE II score between the CVP less than 8 mmHg and CVP 8–12 mmHg groups also showed significant differences (P1=0.006).
The mean creatinine levels (mg/dl) of the highest CVP group (<12 mmHg) increased significantly compared with the other two groups (CVP <8 and 8–12 mmHg) (P2=0.007 and P3=0.001, respectively).
The CVP more than 12 mmHg group exhibited the highest SOFA score and that was statistically significantly compared with the CVP less than 8 and 8–12 mmHg groups (mean value, 11.11±4.73 vs. 5.71±2.78 and 8.03±2.87 points; P2 and P3>0.001, respectively).
The length of ICU stay in the CVP more than 12 mmHg group increased significantly relative to the CVP 8–12 mmHg group (P3=0.004). Days of mechanical ventilation were significantly longer in the CVP more than 12 mmHg group in comparison with the CVP 8–12 mmHg group (mean values, 8.24±3.87 vs. 6.14±3.17 days, respectively; P3<0.001) ([Figure 5]).
|Figure 5 Relation between APACHE II (a), mean creatinine (mg/dl) (b), mean SOFA (c), length of ICU stay (d), days of mechanical ventilation (e), and 28-day mortality (f) and mean CVP groups. APACHE, Acute Physiology and Chronic Health Evaluation; CVP, central venous pressure; SOFA, Sequential Organ Failure Assessment.|
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Mean CVP group analysis showed a statistically significant higher 28-day mortality in CVP more than 12 mmHg group compared with the CVP 8–12 mmHg group, with a mortality rate of 55.4 and 28.2%, respectively (P3>0.001). There was no statistically significant difference among the three mean CVP groups regarding 7-day mortality, with MCp=0.417 ([Figure 5]).
| Discussion|| |
Elevated CVP is common in ICU settings ,, and may be caused by several conditions, such as congestive heart failure syndrome, constrictive pericardial disease, tension pneumothorax, and resuscitation/evacuation phases of septic shock. Although CVP has been utilized to assess intravascular volume in ICU patients, studies have challenged the validity of elevated CVP in ICU settings ,,,,.
The aim of our study was to investigate the association between CVP load and outcome of patients in ICU setting.
In this study, 218 patients were enrolled with a mean of age of 50.39 years. Overall, 50.5% of the enrolled patients were males. The most common cause of admission was septic shock (50.9%). Initial CVP represents the venous loading at the first contact, while peak CVP represents the peak exposure to the venous loading of critical ill patients; both of them were acquired at one point. Mean CVP represents the long duration of venous loading; it was acquired by calculation.
According to studies, values of CVP did not correlate with the values of blood volume or with prediction of fluid responsiveness ,,.
The differences between the changes in CVP and changes in circulating blood volume were assessed by trials, and there were no significant correlation ,. Dramatic changes in systemic hemodynamics may not be associated with any significant changes in CVP ,,.
Elevation in the CVP or a decrease in the mean capillary filling pressures (MCFP) will reduce venous return, stroke volume and cardiac output as described by Cecconi and colleagues following a fluid challenge in postsurgical ICU patients .
The pathophysiological changes that occur with elevated CVP, as manifestation of systemic venous congestion, generally have acute consequences in patients being treated in ICU settings .
According to results of our study, mean and peak CVP values were correlated with APACHE II score, mean SOFA score, and mechanical ventilation days. Although only peak CVP showed correlation with mean creatinine, mean CVP was the only parameter significantly correlated with length of ICU stay. Mean CVP subgroup analysis showed that duration of mechanical ventilation and laboratory results related to organ dysfunction demonstrated that higher mean CVP level was associated with poor ICU outcome for patients in ICU settings.
Wang et al. (2017) demonstrated in a retrospective study on 488 ICU patients with central venous pressure that the initial, peak and mean CVP levels of critically ill patients and length of ICU stay, SOFA score and peak lactate levels were significantly correlated. Peak CVP levels were significantly correlated with peak creatinine levels, while initial and mean CVP levels were not significant with peak creatinine. Additionally, patients with a peak CVP value above 12 mm Hg showed significantly prolonged length of stay, worse organ function and higher SOFA score .
Vellinga et al.  performed a post-hoc analysis of a prospective study in septic patients who were resuscitated according a strict non-CVP guided treatment protocol. They observed a significant association between an elevated mean CVP and impairment of microcirculatory blood flow.
Pilcher and colleagues investigated retrospectively CVP values in 118 patients after lung transplantation. Elevated CVP was associated with prolonged mechanical ventilation (odds ratio, 2.31; 95% confidence interval, 1.31–4.07; P=0.004). Duration of ventilation (P<0.001), ICU mortality (P=0.02), hospital mortality (P=0.09), and 2-month mortality (P=0.02) were higher in patients with CVP of greater than 7 mmHg .
In our study, peak CVP values showed significant correlation with mean creatinine, and based on comparison of different mean CVP groups, patients with elevated CVP showed a significantly higher serum creatinine (median, 1.43 mg/dl) than patients with low CVP (0.9 mg/dl, P=0.007) and patients with intermediate CVP (1.0 mg/dl, P=0.001).
In 1931, Winton found that renal venous pressure may affect urine flow. The higher the pressure, the lower the urine flow. In clinical settings, cardiorenal syndrome represents an example of the influence of CVP on the kidney ,.
In patients with chronic heart failure, high CVP was an independent risk factor for kidney injury ,. It is clear that most of the studies on the association between CVP and kidney function were in patients with heart failure, with few studies in patients with septic shock.
Mullens et al. (2009) studied 145 patients with acute decompensated heart failure. Patients who developed AKI had higher mean CVP on admission (18 vs. 12, P<0.001) and after intensive care (11 vs. 8, P=0.04). Patients with CVP <8 mmHg had less frequent development of AKI (P=0.01) . The results of this study were consistent with those of Guglin et al. , who showed that renal dysfunction in heart failure is owing to congestion but not low output.
Damman and colleagues investigated the relationship between elevated CVP and renal function and mortality in 2557 cardiovascular patients. They found that higher CVP levels were associated with renal function impairment and reduced survival (hazard ratio: 1.03 per mmHg increase, 95% CI: 1.01–1.05, P=0.0032). They confirmed that CVP could affect kidney function in patients with normal heart as in patients with heart failure .
Legrand and colleagues performed a retrospective study between 2006 and 2010 in a surgical ICU. They studied the relationship between hemodynamic parameters and AKI and found that high CVP, independent of systolic blood pressure, diastolic blood pressure, MAP, central venous oxygen saturation, or cardiac output, was associated with AKI. The association of the level of CVP and the risk of developing AKI suggests a role of venous congestion in the development of AKI. Patients with AKI had a higher mortality (38 vs. 15%, P=0.003) than those with no AKI or improving AKI .
However, Uthoff et al.  demonstrated that a low CVP can also result in kidney injury because low CVP can decrease the cardiac output. Another study showed that low CVP and intraoperative fluid administration less than 2,250 mL were risk factors for delayed kidney graft function . Thus, it is necessary to monitor for a reduction in cardiac output in patients with decreased CVP with reduced fluid volume.
Results of our study showed that there was a statistically significant higher 28-day mortality in CVP more than 12 mmHg group compared with the CVP 8–12 mmHg group, with a mortality rate of 55.4 and 28.2%, respectively (P3>0.001), whereas the CVP less than 8 mmHg group showed no statistically significant difference in 28-day mortality compared with the other two groups (P values were P1=0.714 and P2=0.297, respectively). There was no statistically significant difference among the three mean CVP groups regarding 7-day mortality, with MCp=0.417.
Dong-ki Li et al. (2017) evaluated the association between 28-day mortality and mean CVP level after ICU admission in a retrospective analysis of more than 9000 patients. At 28 days, 1645 patients were died. Secondary outcomes were also poor in patients with higher quartiles of elevated mean CVP . Boyd and colleagues investigated whether CVP and fluid balance after resuscitation for septic shock were associated with mortality. They conducted a retrospective review of the use of intravenous fluids during the first 4 days of care. Results showed that patients with low CVP had the lowest mortality rate followed by those with CVP of 8–12 mmHg. The highest mortality rate was observed in those with elevated mean CVP more than 12 mmHg .
Beside fluid overload, there were various aspects affecting CVP, including intrathoracic pressure and pericardial pressure. During mechanical ventilation, intrathoracic pressure was determined by airway plateau pressure. Higher plateau pressure or transalveolar pressure is associated with higher CVP levels. Intra-abdominal hypertension during critical ill process poses a potential to have higher intrathoracic pressure, which could be transmitted to elevate CVP .
From all the above, it may be considerable to avoid high CVP levels and shortening the duration of CVP above 12 mmHg, which, in some way might, improve outcomes.
The main limitation of this study is the relatively small sample size for a survival study, the study design was noninterventional, and no causal relationships could be established.
This study had multiple sources of confounding. Sex, age, ethnicity, congestive heart failure, cardiac arrhythmias, hypertension, valvular disease, pulmonary circulation disease, and renal failure are all contributing factors to mortality.
Unlike the other studies on elevated mean CVP in certain patient populations and disease processes, this study included critically ill patients in general.
| Conclusion|| |
In the light of this study, we conclude that higher mean levels of CVP (cut off=12.5 mmHg) were associated with higher SOFA scores, APACHE II scores, prolonged mechanical ventilation days, longer ICU stay, and increased 28-day mortality.
SOFA score was the best predictor for 28-day mortality (AUC=0.818) compared with peak and mean CVP levels and APACHE II score.
Higher peak CVP levels were associated with impaired renal function.
Prevention of high CVP values (mean and peak) and detection and treatment of the cause are recommended.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
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[Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5]
[Table 1], [Table 2]