Search

Pulmonary hypertension (PH) is defined by a sustained increase in mean pulmonary arterial pressure > 25 mmHg. Due to its widespread availability, echocardiography (ECHO) is used as the first-line imaging modality to detect pulmonary PH and assess right ventricular (RV) function in daily routine. As such, ECHO is the key examination to detect the presence of PH, to provide valuable prognostic information and to give an orientation to therapeutic strategies. In addition to detection and screening, ECHO also provides clues for the differential diagnosis of PH. The present document, based on a consensus of experts, provides practical recommendations for the use of ECHO in the evaluation of PH and of its consequences on the right ventricle.

The article discusses the study which examines the contribution of pulmonary vascular resistance (PVR) to decrease the capacity in hypoxic healthy respondents. The study used ergometer cardiopulmonary exercise test and echocardiographic estimation of pulmonary artery pressure and cardiac to calculate total PVR for healthy volunteers in normoxia and hypoxic breathing. It found that hypoxic pulmonary hypertension restricts exercise capacity in healthy subjects and prevent therapy.

Aerobic exercise capacity is decreased at altitude because of combined decreases in arterial oxygenation and in cardiac output. Hypoxic pulmonary vasoconstriction could limit cardiac output in hypoxia. We tested the hypothesis that acetazolamide could improve exercise capacity at altitude by an increased arterial oxygenation and an inhibition of hypoxic pulmonary vasoconstriction. Resting and exercise pulmonary artery pressure (Ppa) and flow (Q) (Doppler echocardiography) and exercise capacity (cardiopulmonary exercise test) were determined at sea level, 10 days after arrival on the Bolivian altiplano, at Huayna Potosi (4,700 m), and again after the intake of 250 mg acetazolamide vs. a placebo three times a day for 24 h. Acetazolamide and placebo were administered double-blind and in a random sequence. Altitude shifted Ppa/Q plots to higher pressures and decreased maximum O2 consumption (VO2max). Acetazolamide had no effect on Ppa/Q plots but increased arterial O2 saturation at rest from 84 ± 5 to 90 ± 3% (P < 0.05) and at exercise from 79 ± 6 to 83 ± 4% (P < 0.05), and O2 consumption at the anaerobic threshold (V-slope method) from 21 ± 5 to 25 ± 5 ml·min-1kg-1 (P < 0.01). However, acetazolamide did not affect VO2max (from 31 ± 6 to 29 ± 7 ml·kg-1 min-1) and the maximum respiratory exchange ratio decreased from 1.2 ± 0.06 to 1.05 ±0.03 (P < 0.001). We conclude that acetazolamide does not affect maximum exercise capacity or pulmonary hemodynamics at high altitudes. Associated changes in the respiratory exchange ratio may be due to altered CO2 production kinetics. [ABSTRACT FROM AUTHOR]

Hypoxia has been reported to alter left ventricular (LV) diastolic function, but associated changes in right ventricular (RV) systolic and diastolic function remain incompletely documented. We used echocardiography and tissue Doppler imaging to investigate the effects on RV and LV function of 90 min of hypoxic breathing (fraction of inspired O2 of 0.12) compared with those of dobutamine to reproduce the same heart rate effects without change in pulmonary vascular tone in 25 healthy volunteers. Hypoxia and dobutamine increased cardiac output and tricuspid regurgitation velocity. Hypoxia and dobutamine increased LV ejection fraction, isovolumic contraction wave velocity (ICV), acceleration (ICA), and systolic ejection wave velocity (S) at the mitral annulus, indicating increased LV systolic function. Dobutamine had similar effects on RV indexes of systolic function. Hypoxia did not change RV area shortening fraction, tricuspid annular plane systolic excursion, ICV, ICA, and S at the tricuspid annulus. Regional longitudinal wall motion analysis revealed that S, systolic strain, and strain rate were not affected by hypoxia and increased by dobutamine on the RV free wall and interventricular septum but increased by both dobutamine and hypoxia on the LV lateral wall. Hypoxia increased the isovolumic relaxation time related to RR interval (IRT/RR) at both annuli, delayed the onset of the E wave at the tricuspid annulus, and decreased the mitral and tricuspid inflow and annuli E/A ratio. We conclude that hypoxia in normal subjects is associated with altered diastolic function of both ventricles, improved LV systolic function, and preserved RV systolic function. [ABSTRACT FROM AUTHOR]

Objectives: Right ventricular (RV) afterload is best described by a pulmonary arterial impedance (PVZ) spectrum, which integrates pulmonary vascular resistance (PVR), elastance, and wave reflection. We evaluated the feasibility of PVZ determinations in patients with pulmonary arterial hypertension (PAH) during routine right heart catheterization and Doppler echocardiography. Design: Prospective study. Setting: Academic hospital. Patients: Twenty-two patients with PAH. Interventions: Right heart catheterization with a fluid-filled Swan-Ganz catheter, Doppler echocardiography, and administration of inhaled nitric oxide (NO) [10 to 20 ppm; 17 patients], maximum tolerated dose of IV epoprostenol (average, 8.5 ng/kg/min; 5 patients), and IV dobutamine (8 µg/kg/min; 8 patients). Measurements and results: PVZ was calculated from the spectral analysis of synchronized pulmonary artery pressure (Ppa) and flow waves. The mean (± SE) Ppa was 63 ± 3 mm Hg, and the mean PVR was 16 ± 2 Wood units. The PVZ spectrum was markedly shifted to higher than normal pressures and frequencies, with a mean 0-Hz impedance (Z0) of 1,506 ± 138 dyne · s · cm-5, and a mean characteristic impedance (Zc) of 124 ± 11 dyne · s · cm-5, which are in keeping with data from previous studies. Inhaled NO levels decreased Ppa, PVR, Z0, and Zc without a change in cardiac output. Epoprostenol administration did not affect Ppa, increased cardiac output, and decreased Z0 and Zc. Dobutamine administration increased cardiac output and Ppa, and decreased PVR and Z0, without changing Zc. Conclusions: The determination of PVZ to quantify RV afterload is feasible during routine right heart catheterization and Doppler echocardiography. The measurement is sensitive to pharmacologic interventions. [ABSTRACT FROM AUTHOR]

Abstract: Lung carbon monoxide (CO) transfer and pulmonary capillary blood volume (Vc) at high altitudes have been reported as being higher in native highlanders compared to acclimatised lowlanders but large discrepancies appears between the studies. This finding raises the question of whether hypoxia induces pulmonary angiogenesis. Eighteen highlanders living in Bolivia and 16 European lowlander volunteers were studied. The latter were studied both at sea level and after acclimatisation to high altitude. Membrane conductance (DmCO) and Vc, corrected for the haemoglobin concentration (Vccor), were calculated using the NO/CO transfer technique. Pulmonary arterial pressure and left atrial pressures were estimated using echocardiography. Highlanders exhibited significantly higher NO and CO transfer than acclimatised lowlanders, with Vccor/VA and DmCO/VA being 49 and 17% greater (VA: alveolar volume) in highlanders, respectively. In acclimatised lowlanders, DmCO and DmCO/VA values were lower at high altitudes than at sea level. Echocardiographic estimates of cardiac output and pulmonary arterial pressure were significantly elevated at high altitudes as compared to sea level. The decrease in DmCO in lowlanders might be due to altered gas transport in the airways due to the low density of air at high altitudes. The disproportionate increase in Vc in Andeans compared to the change in DmCO suggests that the recruitment of capillaries is associated with a thickening of the blood capillary sheet. Since there was no correlation between the increase in Vc and the slight alterations in haemodynamics, this data suggests that chronic hypoxia might stimulate pulmonary angiogenesis in Andeans who live at high altitudes. [ABSTRACT FROM AUTHOR]