Right Ventricular Dysfunction During Endurance Exercise as Determined by Pressure-Volume Analysis

Abstract

A 37-year-old athlete completed invasive endurance (90 km) bicycle exercise testing for right ventricular pressure-volume analysis. Increased right ventricular afterload caused declines in ventricular-arterial coupling and cardiac output, causing increased arteriovenous oxygen difference to maintain oxygen uptake. These findings demonstrate effects of changes in right ventricular performance on exercise capacity. (Level of Difficulty: Intermediate.)

Central Illustration

Invasive exercise testing with pressure-volume (PV) analysis demonstrates that the healthy right ventricle (RV) has substantial contractile reserve, with a 3- to 4-fold increase in metrics of contractility during short bouts of exercise.¹ That said, prolonged exercise may precipitate RV dysfunction caused by sustained increases in afterload.^2,3 However, there have not been any invasive hemodynamic assessments of RV performance during extended duration exercise. Herein, we present a first-ever analysis of RV function during prolonged exercise using conductance catheters to generate RV PV loops, a gold standard method of characterizing ventricular function (Cardiopulmonary and Right Ventricular Function in Health and Disease; NCT04147299).

Clinical Vignette

A healthy 37-year-old male endurance athlete (187 cm, 78 kg) with maximal oxygen consumption (Vo₂ max) of 47.9 mL/kg/min and hemoglobin of 14.1 g/dL completed invasive hemodynamic testing during 90 km of exercise on upright stationary cycle ergometry. Immediately before exercise, hemodynamic evaluation was completed with pulmonary arterial (PA) catheterization and Fick cardiac output (Qc) was determined. Thereafter, the PA catheter was exchanged for a conductance catheter for RV PV analysis, which was left in place for the duration of testing. Cardiac magnetic resonance (CMR) was obtained 1 hour before invasive testing began and immediately following completion of exercise. RV PV loop volume was calibrated from CMR and loop width (ie, stroke volume) was calibrated from Fick Qc derived from PA catheterization. Single beat loop estimation was used to estimate end-systolic elastance (E_ES), obtained from determination of maximum isovolumic pressure, from which E_ES is derived.⁴ End-systolic pressure is obtained from the second derivative of the pressure waveform (Figure 1).³ Effective arterial elastance (E_A) was defined as the ratio of end-systolic pressure and stroke volume during exercise.⁵ Peripheral oxygen extraction was directly measured by assessing arterial and mixed venous uptake throughout the study.

Figure 1.

Schematic Overview of Single-Beat Modeling Technique for Determining Ees

(Left) A sinusoid is fitted to the rising and falling isovolumic portions of the pressure waveform; the resulting peak of this sinusoid is known as the maximum isovolumic pressure. On the right, the line between maximum isovolumic pressure, at end-diastolic volume, and the end-diastolic pressure models the end-systolic pressure-volume relation, the slope of which is end-systolic elastance (E_ES). Effective arterial elastance is simply the slope of the line connecting end-diastolic pressure and no pressure (0) at end-diastolic volume.⁶ The occurrence of end systole (and in turn, end-diastolic pressure) may be measured directly, or it may be inferred from waveform features of the second time derivative of pressure.

Supine resting hemodynamics were normal: heart rate, 54beats/min; blood pressure, 134/84 mm Hg; right atrial pressure, 5 mm Hg; systolic, diastolic, and mean PA pressure, 24, 10, and 15 mm Hg, respectively; pulmonary capillary wedge pressure, 9 mm Hg; PA saturation, 76%; Fick Qc, 6.5 L/min; and cardiac index, 3.25 L/min/m².

The participant maintained a cycling speed of ∼21-23 km/h throughout the test and total exercise time was 4 hours, 20 minutes. RV PV analysis demonstrated an early initial increase in contractility and Qc (Figure 2A). Sustained increases in RV afterload (E_A) were associated with reductions in ventricular-arterial coupling (E_ES/E_A ratio), as well as reductions in Qc and contractility particularly during the final hours of exercise. CMR demonstrated an increase in RV end-systolic volume by 20 mL after exercise (Figure 2B). RV ejection fraction was preserved. Left ventricular ejection fraction and volumes were preserved.

Figure 2.

Longitudinal Change in RV PV Analysis and Ventricular Structure and Function Derived From CMR

(A) Longitudinal changes in the right ventricular (RV) pressure-volume (PV) analysis are shown. (B) Ventricular structure and function are derived from the cardiac magnetic resonance (CMR) data. avO2_diff = peripheral oxygen extraction; E_A = end-arterial elastance; EDV = end-diastolic volume; E_ES = end-systolic elastance; EF = ejection fraction; ESV = end-systolic volume; HR = heart rate; LV = left ventricle; PRSW = preload recruitable stroke work; SV = stroke volume; Vo₂ = oxygen consumption.

Discussion

This case represents the first invasive analysis of RV performance during endurance exercise. We found that after several hours of increased RV afterload in response to sustained exercise, RV contractility declined, and despite an increase in heart rate, Qc declined. This reduction in Qc was partially offset by an increase in peripheral oxygen extraction to maintain Vo₂ and overall workload throughout the duration of exercise. Preload recruitable stroke work (product of stroke work and end-diastolic volume), a marker of cardiac function that is independent of preload and afterload, initially increased but declined after several hours of exercise, which is also indicative of a decline in RV contractility and coinciding with the decline in stroke volume.

The RV historically has been referred to as a passive conduit and a mere bystander.^2,5 However, our findings demonstrate the impact of RV function on overall exercise capacity, as well as the body’s attempt to compensate for reductions in RV cardiac output during prolonged exercise, such as by increases in HR and peripheral oxygen extraction as described. These observations describe the contributions of the RV to overall cardiac performance during prolonged exercise.

Funding Support and Author Disclosures

Dr Cornwell has received funding by a National Institutes of Health/National Heart, Lung, and Blood Institute Mentored Patient-Oriented Research Career Development Award (1K23HLI32048), as well as the National Institutes of Health/National Center for Advancing Translational Sciences (UL1TR002535). All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.