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Background Obese and overweight body habitus are common among patients undergoing right heart catheterization for suspected pulmonary hypertension, but previous studies have described only patients with severe obesity. This study examined the effect of body habitus on intracardiac pressures, thermodilution cardiac output (TDCO), indirect Fick (iFick) cardiac output (CO), and pulmonary vascular resistance (PVR) in subjects with normal cardiopulmonary hemodynamics. Methods A retrospective analysis was conducted on healthy volunteers and patients referred for right heart catheterization for dyspnea of unknown origin with normal hemodynamics. Of the 65 subjects (53 ± 14 years; 51% female), 31% were normal weight, 49% were overweight, and 20% had obesity, as defined by a body mass index of 30-39.9 kg/m 2 . Mixed venous oxygen saturations and intracardiac pressures were compared across body mass index categories. Agreement between iFick CO calculated by 3 formulae, and TDCO and PVR was examined. Results No differences in intracardiac pressures were observed, but mixed venous oxygen saturations were lower in the obese group. iFick CO underestimated TDCO, particularly with the LaFarge formula, with a systematic difference of 0.33 L/min for every 1 L/min increase in CO. This difference was largest in the obese group—on average by 23% ± 10%, translating to an overestimation of PVR by 34% ± 16% on average. Conclusions In individuals without severe obesity, intracardiac pressures are not different, but mixed venous oxygen saturations are lower. Obesity confounds estimations of CO and PVR by iFick methods, which could result in inappropriate hemodynamic classification. These data can inform best practices in hemodynamic assessment of populations with obesity.

Exercise imposes increased pulmonary vascular afterload based on rises in pulmonary artery (PA) wedge pressure, declines in PA compliance, and resistance‐compliance time. In health, afterload stress stabilizes during steady‐state exercise. Our objective was to examine alterations of these exercise‐associated stresses in states of pre‐ and post‐capillary pulmonary hypertension (PH). PA hemodynamics were evaluated at rest, 2 and 7 min of steady‐state exercise at moderate intensity in patients who exhibited Pre‐capillary (n = 22) and post‐capillary PH (n = 22). Patients with normal exercise hemodynamics (NOR‐HD) (n = 32) were also studied. During exercise in all groups, PA wedge pressure increased at 2 min, with no further change at 7 min. In post‐capillary PH and NOR‐HD, increases in PA diastolic pressure and diastolic pressure gradient remained stable at 2 and 7 min of exercise, while in pre‐capillary PH, both continued to increase at 7 min. The behavior of the diastolic pressure gradient was linearly related to the duration of resistance‐compliance time at rest (r2 = 0.843) and exercise (r2 = 0.760). Exercise resistance‐compliance time was longer in pre‐capillary PH associated with larger increases in diastolic pressure gradient. Conversely, resistance‐compliance time was shortest in post‐capillary PH compared to pre‐capillary PH and NOR‐HD and associated with limited increases in exercise diastolic pressure gradient. During steady‐state, modest‐intensity exercise‐specific patterns of pulmonary vascular afterload responses were observed in pre‐ and post‐capillary PH relative to NOR‐HD. Longer resistance‐compliance time related to greater increases in PA diastolic pressure and diastolic pressure gradients in pre‐capillary PH, while shorter resistance‐compliance time appeared to limit these increases in post‐capillary PH.

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At a given level of oxygen consumption, cardiac output is similar at high altitude compared to at sea level; however it is achieved with a greater heart rate and lesser stroke volume (SV), which is related to reduced left ventricular (LV) end-diastolic volume (EDV). In turn, the reduced LV SV mediated by the Frank-Starling mechanism has been suggested to occur secondarily to a decreased circulating blood volume and/or increased pulmonary vascular resistance. At high altitude, total blood volume decreases secondarily to an acute plasma volume loss, and as the partial pressure of oxygen in inspired air decreases, alveolar hypoxia stimulates pulmonary vasoconstriction and increases pulmonary vascular resistance. However, correction of either has not been consistently shown to entirely return SV to sea level values. Further, the maximal value of both oxygen consumption and cardiac output is lower, although the directionality of the association remains unclear.In a recent issue of The Journal of Physiology, Stembridge et al. (2019) aimed to determine the contributions of high altitude-induced hypovolaemia and hypoxic pulmonary vasoconstriction to LV function and maximal oxygen consumption. The authors' main hypotheses were that both plasma volume expansion (saline infusion) and pulmonary vasodilatation (phosphodiesterase-5 inhibition) would increase LV EDV at rest and exercise; however, only the reversal of hypoxic pulmonary vasoconstriction would increase the maximum oxygen consumption. To this end, 12 healthy male participants were prospectively recruited. Maximal oxygen consumption was determined through a graded exercise test, and cardiac function was assessed by echocardiography at rest and during constant work-rate exercise at 50% peak power. These assessments were then repeated after 5-10 days at high altitude (3800 m) without and with plasma volume expansion to achieve sea level haematocrit values, without and with administration of the pulmonary vasodilator sildenafil, and with both in combination. At high altitude, resting LV EDV and SV were not significantly different compared to at sea level following plasma volume expansion or sildenafil administration. However, neither intervention elicited a significant improvement in LV EDV and SV during exercise at 50% peak power, nor on maximal oxygen consumption. From these findings, the authors concluded that at 3800 m, hypovolaemia and hypoxic pulmonary vasoconstriction contribute to a reduction in LV EDV, yet interventions which normalize LV EDV at rest do not yield improvements during exercise. The study design utilized by Stembridge et al. (2019) has several strengths and some limitations which merit discussion. Study participants were appropriately selected after screening to ensure they had minimal risk factors for cardiovascular disease; however, the study group was relatively small and did not include female participants. Although the sample size limited statistical power, particularly given the inclusion of several repeated measures, the authors effectivel...

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