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Peripheral Venous Pressure as a Surrogate for Central Venous Pressure under General Anaesthesia: An Experimental Study

This experimental study on anesthetized beagles demonstrates that peripheral venous pressure (PVP) correlates linearly with central venous pressure (CVP) across a broad range, and that incorporating tissue pressure into an estimation formula significantly improves CVP prediction accuracy, particularly in low-pressure states.

Original authors: Hiroki Matsushita, Takuya Nishikawa, Yuta Nakamura, Kazumasu Sasaki, Kei Sato, Hidetaka Morita, Yuki Yoshida, Nana Hiraki, Masahiro Otake, Kenta Oba, Masafumi Fukumitsu, Toru Kawada, Kazunori Uemura

Published 2026-07-06

📖 5 min read🧠 Deep dive

CC BY 4.0

Original authors: Hiroki Matsushita, Takuya Nishikawa, Yuta Nakamura, Kazumasu Sasaki, Kei Sato, Hidetaka Morita, Yuki Yoshida, Nana Hiraki, Masahiro Otake, Kenta Oba, Masafumi Fukumitsu, Toru Kawada, Kazunori Uemura, Keita Saku

Original paper licensed under CC BY 4.0 (https://creativecommons.org/licenses/by/4.0/). ✨ This is an AI-generated explanation of the paper below. It is not written or endorsed by the authors. For technical accuracy, refer to the original paper. Read full disclaimer

The Big Idea: A "Backdoor" Pressure Check

Imagine you are trying to check the water pressure in the main tank of a house (the Central Venous Pressure, or CVP). Usually, to get an accurate reading, you have to drill a hole right into the main tank near the heart. This is invasive, requires a specialist, and can be risky.

The researchers wanted to know if they could just check the pressure in a garden hose connected to the house (the Peripheral Venous Pressure, or PVP). If the hose pressure matches the tank pressure, doctors could use a simple needle in a patient's arm instead of a complex tube in their neck to monitor how much fluid the body has.

The Problem: The "Squeeze" Factor

In previous studies, this "garden hose" idea worked great when the water pressure was high. But when the pressure was low, the hose reading was often higher than the tank reading.

The researchers discovered why: Tissue Pressure (TP).
Think of the veins in your arm like a soft, collapsible straw. When the water pressure inside is low, the soft flesh (muscle and skin) surrounding the straw squeezes it shut. This "squeeze" makes the pressure inside the straw read higher than it actually is in the main tank because the straw is being crushed from the outside.

The Experiment: A Doggy Test Drive

The team tested this theory on 25 beagle dogs under general anesthesia. They did three main things:

The Pressure Range Test: They slowly filled the dogs with fluid (like turning up the water tap) and then drained fluid out (like opening a drain). They measured the pressure in the main tank (CVP) and the arm hose (PVP) at every single step, from very low pressure to very high pressure.
The Drug Test: They gave some dogs drugs that tighten blood vessels (like norepinephrine) and others drugs that relax them (like trinitroglycerin) to see if the "hose vs. tank" relationship changed.
The Simulation Test: They simulated two scary hospital scenarios:
- Vasodilation: Using a drug to widen blood vessels (like a sudden drop in blood pressure).
- Hemorrhage: Draining blood to simulate a bleed.

The Findings: When the Hose Lies and When it Tells the Truth

1. The "Squeeze" Only Happens at Low Pressure
When the pressure was low (below about 10 mmHg), the "garden hose" (PVP) read higher than the "main tank" (CVP). This is because the surrounding tissue was squeezing the vein.

The Analogy: Imagine stepping on a garden hose. Even if the water pressure is low, the spot where you step feels "hard" or pressurized because of your foot.
The Fix: Once the pressure got high enough to push the vein open against the tissue squeeze, the hose reading matched the tank reading perfectly.

2. Drugs Didn't Change the Rules
Surprisingly, whether the dogs were given drugs to tighten or relax their blood vessels, the relationship between the hose and the tank stayed the same. The "squeeze" from the tissue was the main factor, not the drugs.

3. The New Formula
The researchers created a math formula to fix the "lie" the hose tells at low pressure.

The Formula Logic: If the pressure is low, the formula subtracts a bit of the "tissue squeeze" value to get the real number. If the pressure is high, it just uses the hose reading directly.
The Result: When they tested this new "Estimated CVP" (eCVP) during the simulated bleeding and drug scenarios, it was much more accurate than just looking at the raw hose pressure. It was like having a smart calculator that knows when the garden hose is being squeezed and corrects the number automatically.

The Catch (Limitations)

The study admits a few things they couldn't fully test yet:

The "Open Chest" Surprise: When they opened the chest of a few dogs (simulating major surgery), the relationship flipped at very high pressures. The main tank pressure actually became higher than the hose pressure. This happened because the heart valve (tricuspid) started leaking backward, sending a pressure wave up the hose that didn't match the main tank.
Species Difference: This was tested on dogs. Humans have different body shapes and vein structures, so the "squeeze" factor might be different for people.

The Bottom Line

This study shows that checking the pressure in a vein in the arm is a very good way to guess the pressure near the heart, but only if you know how to correct for the "squeeze" of the surrounding tissue when the pressure is low.

They built a simple equation that accounts for this squeeze. If you use this equation, you can get a much more accurate reading of the heart's fluid status than just looking at the raw number from the arm vein. However, before doctors can use this on humans, they need to prove it works in people, not just dogs.

Technical Summary: Peripheral Venous Pressure as a Surrogate for Central Venous Pressure under General Anaesthesia

Problem Statement
Central venous pressure (CVP) is a critical parameter for assessing systemic fluid status and diagnosing right heart failure, particularly in anaesthetic and intensive care settings. However, its clinical utility has declined due to the invasiveness of central line placement. While peripheral venous pressure (PVP) has been proposed as a less invasive surrogate, existing literature presents conflicting data. Some studies suggest PVP reliably tracks CVP, while others indicate significant discrepancies, particularly at low pressure values where PVP frequently exceeds CVP. Furthermore, the physiological mechanisms driving these discrepancies across broad pressure ranges within the same individual remain uncharacterized. Specifically, the role of tissue pressure (TP)—the external compression exerted by surrounding tissues on veins—has not been systematically assessed in vivo as a contributor to the PVP–CVP gradient.

Methodology
This experimental study utilized 25 beagle dogs under general anaesthesia to characterize the PVP–CVP relationship across a wide pressure spectrum (0–30 mmHg). The experimental design included three distinct protocols:

Protocol 1 (Characterization & Formula Derivation): In 15 dogs, a wide pressure range was induced by withdrawing blood to induce hypovolaemic shock (CVP ≤ 5 mmHg) followed by aggressive fluid and blood reinfusion until PVP exceeded 30 mmHg. This was performed under three vascular conditions: no drug, continuous norepinephrine (NE) infusion, and continuous trinitroglycerin (TNG) infusion. PVP, CVP, and TP were measured simultaneously. A mathematical model was derived to estimate CVP (eCVP) by accounting for the difference between PVP and TP in the low-pressure range.
Sensitivity Analysis: To assess the impact of intrathoracic constraints, the PVP–CVP relationship was measured in three additional dogs following median sternotomy (open-chest condition).
Protocol 2 (Validation): In seven dogs (distinct from Protocol 1), the derived eCVP formula was validated under simulated clinical haemodynamic fluctuations. This included vasodilation induced by sodium nitroprusside (SNP) and haemorrhage induced by controlled blood withdrawal.

Data analysis involved calculating the maximum cross-correlation coefficient ( $\gamma_{max}$ ) to assess waveform similarity and using Bland–Altman analysis and mean absolute error (MAE) to evaluate the accuracy of eCVP against measured CVP.

Key Contributions and Results

Linearity and Pressure Dependence: Across the 0–30 mmHg range, PVP and CVP demonstrated a strong linear correlation (correlation coefficient = 0.99). However, the relationship is pressure-dependent. At pressures below approximately 10 mmHg, PVP consistently exceeded CVP, and PVP waveforms appeared flattened with reduced pulsatility. As pressures increased beyond 10 mmHg, the discrepancy diminished, and PVP and CVP converged, eventually tracking closely once both pressures surpassed the measured tissue pressure (TP).
Role of Tissue Pressure (TP): The study identified TP as a primary factor causing PVP to exceed CVP in the low-pressure range. The authors hypothesize that at low intravascular pressures, veins behave as "collapsible tubes," where external TP narrows the lumen, increasing resistance and elevating measured PVP relative to CVP. Once intravascular pressure exceeds TP, the vein dilates, resistance drops, and the pressures equalize.
Vasoactive Drug Influence: The administration of vasoactive agents (NE or TNG) had minimal impact on the linearity of the PVP–CVP relationship. The correlation remained strong (CC = 0.99) regardless of whether the vascular tone was increased or decreased.
Estimation Formula: A two-part estimation formula was derived to correct PVP for TP effects in the low-pressure range:
- When $PVP < TP^*$ : $eCVP = 1.19 \times PVP - 0.19 \times TP^*$
- When $PVP \geq TP^*$ : $eCVP = PVP$
  (Where $TP^*$ is the baseline tissue pressure).
Validation Accuracy: In Protocol 2, the eCVP formula significantly outperformed raw PVP in estimating CVP. During both SNP-induced vasodilation and haemorrhage, eCVP demonstrated a lower bias and a significantly smaller mean absolute error (MAE) compared to uncorrected PVP. For instance, during vasodilation, the MAE for eCVP was significantly lower than for PVP (median paired difference −0.61 mmHg, p < 0.05).
Open-Cest Sensitivity: Under open-chest conditions, the relationship remained linear, but at high pressures (>10 mmHg), CVP occasionally exceeded PVP. This was associated with the appearance of tricuspid regurgitation (TR) and prominent v-waves in the CVP waveform, suggesting that valvular pathology can alter the PVP–CVP gradient in the high-pressure range.

Significance and Claims
The authors claim that this study provides the first systematic in vivo characterization of the PVP–CVP relationship across a broad pressure range within the same individuals, explicitly accounting for tissue pressure. The primary significance lies in the demonstration that while PVP is a linear surrogate for CVP, its accuracy is compromised in the low-pressure range typical of general anaesthesia due to TP.

The study concludes that incorporating TP into a correction formula enables a more accurate, continuous, and minimally invasive estimation of CVP than PVP alone. The authors posit that this approach could facilitate continuous CVP monitoring in perioperative and ICU settings without the need for central lines. However, the paper maintains a modest stance regarding clinical application, noting that the findings are derived from a canine model. The authors explicitly state that species-specific anatomical differences (e.g., venous valve distribution) and the dynamic nature of TP in humans necessitate further clinical validation before the estimation formula can be practically applied to patient care. They also highlight that conditions involving rapid sympathetic activation or acute valvular regurgitation may limit the formula's accuracy.