Key result
In pulmonary hypertension, the exercise response is limited by restricted maximum cardiac output due to massively increased right ventricular afterload, despite doubled contractility compared to controls.
Why the study?
How does exercise affect cardiovascular and ventilatory responses in patients with pulmonary hypertension compared to healthy subjects?
How does exercise affect cardiovascular and ventilatory responses in patients with pulmonary hypertension compared to healthy subjects?
Exercise capacity in pulmonary hypertension is fundamentally limited by restricted maximum cardiac output due to increased right ventricular afterload.
Guides exercise hemodynamics interpretation in PH; leaves open whether afterload reduction augments peak cardiac output in trials.
In healthy subjects, exercise causes a complex cardiovascular and ventilatory response that allows for a 20-fold increase of oxygen consumption as compared to rest. In pulmonary hypertension (PH) this response is very much limited by a restriction of the maximum cardiac output (CO). This restriction is caused by a massively increased afterload of the right ventricle (RV) despite an adaptation that doubles right ventricular contractility as compared to normal controls.1
No takes yet. Share an insight, caveat, or question.
Horst Olschewski (2012) conducted a review in Pulmonary hypertension. Exercise vs. Normal controls was evaluated. In pulmonary hypertension, the exercise response is limited by restricted maximum cardiac output due to massively increased right ventricular afterload, despite doubled contractility compared to controls.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: