The Effects of Vasoactive Medications on Mean Circulatory Filling Pressure, Venous Resistance, Systemic Vascular Resistance, Cardiac Index, and Oxygen Extraction After Pediatric Heart Transplant: Leveraging High-Fidelity Physiologic Data

TL;DR

This study shows how high-fidelity data can reveal how vasoactive drugs affect venous circulation in pediatric heart transplant patients, helping guide medication choices.

Contribution

The study introduces a method to estimate venous parameters at the bedside using high-fidelity data and demonstrates how vasoactive drugs affect venous tone.

Findings

Vasoactive medications like vasopressin and norepinephrine significantly influence mean circulatory filling pressure and venous resistance.

High-fidelity physiologic data can explain nearly 60% of the variance in venous resistance and mean circulatory filling pressure.

Venous parameters derived from these data can guide the selection and titration of vasoactive medications in clinical settings.

Abstract

What are the main findings?
High-fidelity physiologic data can help estimate venous parameters such as mean circulatory filling pressure, venous resistance, and venous return.Vasoactive medications have different effects on the arterial and venous systems.

High-fidelity physiologic data can help estimate venous parameters such as mean circulatory filling pressure, venous resistance, and venous return.

Vasoactive medications have different effects on the arterial and venous systems.

What is the implication of the main finding?
Venous parameters can be estimated at the bedside and can help clarify the physiology.Venous parameters can help select appropriate vasoactive medications.

Venous parameters can be estimated at the bedside and can help clarify the physiology.

Venous parameters can help select appropriate vasoactive medications.

Background: The physiologic effects of vasoactive medications on the venous circulation remain incompletely understood. Contemporary bedside management often emphasizes the arterial circulation, whereas Guytonian physiology emphasizes the venous circulation and mean circulatory filling pressure in determining steady-state cardiac output. The primary aim of this study was to characterize the effect of vasoactive medications on mean circulatory filling pressure and venous resistance. Methods: Demographic data and vasoactive data were collected from the electronic health record and collated with high-fidelity physiologic monitoring data. Mean circulatory filling pressure and venous resistance were calculated using clinically validated equations and then were modeled using a random forest regression incorporating postoperative time and infusion doses of epinephrine, norepinephrine, milrinone, vasopressin, phenylephrine, calcium, sodium nitroprusside, and nicardipine. Similar models were constructed for indexed systemic vascular resistance, cardiac index, cerebral oxygen extraction, and renal oxygen extraction. Results: Data from a total of 57 unique patients comprising 9,654,239 data points were analyzed. The model explained 57% of the variance in mean circulatory filling pressure and 59% of the variance in venous resistance. Vasopressin and norepinephrine were the most influential for mean circulatory filling pressure and venous resistance. Conclusions: Vasoactive medications appear to modulate venous tone and impact mean circulatory filling pressure and venous resistance. High-fidelity physiologic data allow for characterizing these effects and guide titration of vasoactive medications at the bedside.

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