Stressing the right ventricular-pulmonary vascular unit: beyond pulmonary vascular resistance

Pulmonary arterial hypertension is a progressive disease of the pulmonary vasculature, ultimately leading to right heart failure and death. Current treatment is aimed at targeting three different pathways: the prostacyclin, endothelin and nitric oxide pathways. These therapies improve functional class, increase exercise capacity and improve haemodynamics. In addition, data from a meta-analysis provide compelling evidence of improved survival. Despite these treatments, the outcome is still grim and the cause of death is inevitable – right ventricular failure. One explanation for this paradox of haemodynamic benefit and still worse outcome is that the right ventricle does not benefit from a modest reduction in pulmonary vascular resistance. This article describes the physiological concepts that might underlie this paradox. Based on these concepts, we argue that not only a significant reduction in pulmonary vascular resistance, but also a significant reduction in pulmonary artery pressure is required to save the right ventricle. Haemodynamic data from clinical trials hold the promise that these haemodynamic requirements might be met if upfront combination therapy is used.

Download Full-text

Effect of increased pulmonary vascular resistance on right ventricular systolic performance in dogs

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1984.246.3.h339 ◽

1984 ◽

Vol 246 (3) ◽

pp. H339-H343 ◽

Cited By ~ 1

Author(s):

M. Ghignone ◽

L. Girling ◽

R. M. Prewitt

Keyword(s):

Pulmonary Artery ◽

Right Ventricular ◽

Pulmonary Vascular Resistance ◽

Vascular Resistance ◽

Diastolic Pressure ◽

Systolic Pressure ◽

Glass Beads ◽

Ventricular Systolic Pressure ◽

Bead Injection ◽

The Right

We tested the possibility that for a given contractile state and right ventricular systolic pressure (RVSP), rate and extent of ventricular shortening would be reduced as resistance to ejection increased. In eight anesthetized, ventilated dogs, we measured RV and pulmonary artery pressure (Ppa), blood pressure, heart rate, cardiac output (CO), and RV dP/dt before (condition 1) and after (condition 2) pulmonary vascular resistance (PVR) was increased by injection of small (80 micron) glass beads. Glass beads caused a large increase (P less than 0.001) in Ppa and in RVSP and, despite increased RV end-diastolic pressure (EDP), CO and stroke volume (SV) were reduced. A third set of measurements was obtained following a further increase in resistance (condition 3). A comparison of condition 2 with condition 3, despite constant RVSP, constant mean Ppa, and increased EDP, showed a marked fall in CO and SV (P less than 0.001) when glass bead injection increased calculated resistance from 21 (condition 2) to 34 (condition 3) mmHg X 1(-1) X min. RV contractility, as assessed by Vmax and peak dP/dt was similar in both conditions. In five additional dogs, we measured the same parameters as before plus instantaneous pulmonary artery flow in all conditions. In a comparison of conditions 2 and 3, despite constant RVSP and increased EDP, peak and total flow (P less than 0.05) were reduced as resistance to RV ejection increased. We conclude that the right ventricle shortens more slowly and to a smaller extent against the same systolic pressure when its resistive afterload increases.

Download Full-text

Impact of successful percutaneous balloon mitral valvuloplasty on pulmonary vascular resistance and right ventricular functions

The Egyptian Heart Journal ◽

10.1016/j.ehj.2013.12.035 ◽

2014 ◽

Vol 66 (1) ◽

pp. 12

Author(s):

Mohammad Gouda Mohammad

Keyword(s):

Right Ventricular ◽

Pulmonary Vascular Resistance ◽

Vascular Resistance ◽

Mitral Valvuloplasty ◽

Percutaneous Balloon Mitral Valvuloplasty ◽

Percutaneous Balloon ◽

Ventricular Functions

Download Full-text

Effects of Inspired Oxygen on Echocardiographic Assessment of Pulmonary Vascular Resistance and Myocardial Contractility in Bronchopulmonary Dysplasia

PEDIATRICS ◽

10.1542/peds.65.3.536 ◽

1980 ◽

Vol 65 (3) ◽

pp. 536-540 ◽

Cited By ~ 3

Author(s):

Henry L. Halliday ◽

Fe M. Dumpit ◽

June P. Brady

Keyword(s):

Right Ventricular ◽

Pulmonary Vascular Resistance ◽

Bronchopulmonary Dysplasia ◽

Vascular Resistance ◽

Myocardial Contractility ◽

Blood Gases ◽

Venous Admixture ◽

Ejection Time ◽

Ventricular Ejection Time ◽

Inspired Oxygen

We studied the effects of minor changes of inspired oxygen in ten preterm infants (birth weight: 700 to 1,780 gm; postnatal age: 4 to 18 weeks) with severe bronchopulmonary dysplasia. We compared the echocardiogram, capillary blood gases, and calculated venous admixture when the oxygen level was raised or lowered by 10% of the initial value. Mean ambient inspired oxygen was 0.31, capillary Po2 was 62 torr, and calculated venous admixture was 40%. The ratio of right ventricular preejection period to right ventricular ejection time (RPEP/RVET) was 0.32, suggesting mild increase in pulmonary vascular resistance. In all instances, there was echocar-diographic evidence of further increase in pulmonary vascular resistance with a minor decrease in inspired oxygen. Lowering the inspired oxygen to 0.28 resulted in a reduction in Pao2 to 54 torr, an increase in calculated venous admixture to 47%, and an increase in RPEP/RVET to 0.36 (P <.001). Raising the inspired oxygen to 0.34 increased Pao2 to 72 torr but had no effect on RPEP/RVET. Calculated venous admixture decreased to 33% (P <.001). Myocardial contractility did not change with decrease in inspired oxygen but improved slightly with increase in inspired oxygen. These preliminary findings suggest that in infants with bronchopulmonary dysplasia the Pao2 should be kept > 55 torr and the RPEP/RVET < 0.35 to avoid the development of right heart failure.

Download Full-text

Echocardiographic Pulmonary to Left Atrial Ratio (ePLAR): A Comparison Study between Ironman Athletes, Age Matched Controls and A General Community Cohort

Journal of Clinical Medicine ◽

10.3390/jcm8101756 ◽

2019 ◽

Vol 8 (10) ◽

pp. 1756 ◽

Cited By ~ 1

Author(s):

Tran ◽

Kwon ◽

Holt ◽

Kierle ◽

Fitzgerald ◽

...

Keyword(s):

Right Ventricular ◽

Pulmonary Vascular Resistance ◽

Vascular Resistance ◽

Left Atrial ◽

Systolic Pressure ◽

Exercise Stress ◽

Control Group ◽

Right Ventricular Systolic Pressure ◽

Ventricular Systolic Pressure ◽

General Community

Background: During exercise there is a proportionally lower rise in systemic and pulmonary pressures compared to cardiac output due to reduced vascular resistance. Invasive exercise data suggest that systemic vascular resistance reduces more than pulmonary vascular resistance. The aim of this study was the non-invasive assessment of exercise hemodynamics in ironman athletes, compared with an age matched control group and a larger general community cohort. Methods: 20 ironman athletes (40 ± 11 years, 17 male) were compared with 20 age matched non-athlete controls (43 ± 7 years, 10 male) and a general community cohort of 230 non-athletes individuals (66 ± 11 years, 155 male), at rest and after maximal-symptom limited treadmill exercise stress echocardiography. Left heart parameters (mitral E-wave, e’-wave and E/e’) and right heart parameters (tricuspid regurgitation maximum velocity and right ventricular systolic pressure), were used to calculate the echocardiographic Pulmonary to Left Atrial Ratio (ePLAR) value of the three groups. Results: Athletes exercised for 12.2 ± 0.53 minutes, age matched controls for 10.1 ± 2.8 minutes and general community cohort for 8.3 ± 2.6 minutes. Mitral E/e’ rose slightly for athletes (0.9 ± 1.8), age matched controls (0.6 ± 3.0) and non-athletes (0.4 ± 3.2). Right ventricular systolic pressure increased significantly more in athletes than in both non-athlete cohorts (35.6 ± 17 mmHg vs. 20.4±10.8mmHg and 18 ± 9.6 mmHg). The marker of trans-pulmonary gradient, ePLAR, rose significantly more in athletes than in both non-athlete groups (0.15 ± 0.1 m/s vs. 0.07 ± 0.1 m/s). Conclusions: Pulmonary pressures increased proportionally four-fold compared with systemic pressures in ironman athletes. This increase in pulmonary vascular resistance corresponded with a two-fold increase in ePLAR. These changes were exaggerated compared with both non-ironman cohorts. Such changes have been previously suggested to lead to right ventricle dysfunction, arrhythmias and sudden cardiac death.

Download Full-text