Quantification of Ventricular Hydraulic Output Using Pressure/Flow Analysis: A Single-Animal Proof-of-Concept Study During Dobutamine Stress

Introduction: Ventricular pressure and arterial flow are commonly evaluated separately, although their instantaneous product represents hydraulic power. This study examined whether synchronized ventricular pressure and arterial flow recordings can be used to describe ventricular pressure/flow coupling and hydraulic output at baseline and during dobutamine stress. Materials and Methods: This was a descriptive reanalysis of an acute experiment in one anesthetized 35 kg male swine. Left ventricular pressure, aortic pressure, and ascending aortic transit-time flow were acquired simultaneously at 200 Hz. Pressure/flow loops were constructed by plotting instantaneous left ventricular pressure against aortic flow. Ventricular hydraulic output power was calculated as P_LV(t)Q_Ao(t), and hydraulic energy per beat was calculated by time integration over the defined ejection interval. The ratio of integrated hydraulic energy to the pressure/time integral was reported as pressure-weighted mean flow. Repeated beats were treated as subsamples from one experimental unit; the results are therefore descriptive and no population-level inference was performed. Results: In total, 27 baseline beats and 32 dobutamine beats were analyzed. Mean cycle duration decreased from 461 to 381 ms, corresponding to approximately 130 and 158 beats/min. Peak left ventricular pressure increased from 87.4 to 116.3 mmHg, peak aortic flow from 6.87 to 12.43 L/min, and dP/dt_max from 1770 to 4089 mmHg/s. Ventricular hydraulic energy output increased from 0.104 ± 0.016 to 0.134 ± 0.030 J/beat, while hydraulic energy delivered to the aorta increased from 0.087 ± 0.014 to 0.116 ± 0.027 J/beat. The pressure-weighted mean flow increased from 3.72 ± 0.26 to 6.24 ± 0.88 L/min. The geometric pressure/flow loop integral increased from 139.7 ± 27.2 to 649.3 ± 275.4 mmHg·L/min. Forward ejected volume was similar between conditions, at 10.1 and 10.6 mL/beat. Conclusions: Synchronized ventricular pressure and arterial flow recordings permit descriptive quantification of ventricular hydraulic power, energy per beat, pressure-weighted mean flow, and pressure/flow trajectory geometry. In this single preparation, dobutamine was associated with higher pressure, flow, and hydraulic output over a shorter cycle. These findings demonstrate analytical feasibility but do not establish a validated biomarker, valve efficiency metric, or population-level effect.

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Journal
Fluids
Published
2026-10-05
DOI
https://doi.org/10.3390/fluids11100247
Primary Topic
Cardiovascular Function and Risk Factors
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article

Quantification of Ventricular Hydraulic Output Using Pressure/Flow Analysis: A Single-Animal Proof-of-Concept Study During Dobutamine Stress

Filip A Konecny
Fluids
Cardiovascular Function and Risk Factors
article

Quantification of Ventricular Hydraulic Output Using Pressure/Flow Analysis: A Single-Animal Proof-of-Concept Study During Dobutamine Stress

Filip A Konecny
article en

Abstract

Introduction: Ventricular pressure and arterial flow are commonly evaluated separately, although their instantaneous product represents hydraulic power. This study examined whether synchronized ventricular pressure and arterial flow recordings can be used to describe ventricular pressure/flow coupling and hydraulic output at baseline and during dobutamine stress. Materials and Methods: This was a descriptive reanalysis of an acute experiment in one anesthetized 35 kg male swine. Left ventricular pressure, aortic pressure, and ascending aortic transit-time flow were acquired simultaneously at 200 Hz. Pressure/flow loops were constructed by plotting instantaneous left ventricular pressure against aortic flow. Ventricular hydraulic output power was calculated as P_LV(t)Q_Ao(t), and hydraulic energy per beat was calculated by time integration over the defined ejection interval. The ratio of integrated hydraulic energy to the pressure/time integral was reported as pressure-weighted mean flow. Repeated beats were treated as subsamples from one experimental unit; the results are therefore descriptive and no population-level inference was performed. Results: In total, 27 baseline beats and 32 dobutamine beats were analyzed. Mean cycle duration decreased from 461 to 381 ms, corresponding to approximately 130 and 158 beats/min. Peak left ventricular pressure increased from 87.4 to 116.3 mmHg, peak aortic flow from 6.87 to 12.43 L/min, and dP/dt_max from 1770 to 4089 mmHg/s. Ventricular hydraulic energy output increased from 0.104 ± 0.016 to 0.134 ± 0.030 J/beat, while hydraulic energy delivered to the aorta increased from 0.087 ± 0.014 to 0.116 ± 0.027 J/beat. The pressure-weighted mean flow increased from 3.72 ± 0.26 to 6.24 ± 0.88 L/min. The geometric pressure/flow loop integral increased from 139.7 ± 27.2 to 649.3 ± 275.4 mmHg·L/min. Forward ejected volume was similar between conditions, at 10.1 and 10.6 mL/beat. Conclusions: Synchronized ventricular pressure and arterial flow recordings permit descriptive quantification of ventricular hydraulic power, energy per beat, pressure-weighted mean flow, and pressure/flow trajectory geometry. In this single preparation, dobutamine was associated with higher pressure, flow, and hydraulic output over a shorter cycle. These findings demonstrate analytical feasibility but do not establish a validated biomarker, valve efficiency metric, or population-level effect.

FluidsVol. 11(10)
Moffitt Cancer Center (US), McMaster University (CA)
Openalex Percentile: Top 11%
Cardiovascular Function and Risk Factors
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