Proximal pulmonary arterial obstruction decreases the time constant of the pulmonary circulation and increases right ventricular afterload

2013 ◽  
Vol 114 (11) ◽  
pp. 1586-1592 ◽  
Author(s):  
Alberto Pagnamenta ◽  
Rebecca Vanderpool ◽  
Serge Brimioulle ◽  
Robert Naeije
Keyword(s):  
Pulmonary Hypertension ◽  
Right Ventricular ◽  
Time Constant ◽  
Pulse Pressure ◽  
Pulmonary Circulation ◽  
Characteristic Impedance ◽  
Ventricular Afterload ◽  
Hydraulic Load ◽  
Distal Obstruction ◽  
Pulmonary Arterial

The time constant of the pulmonary circulation, or product of pulmonary vascular resistance (PVR) and compliance (Ca), called the RC-time, has been reported to remain constant over a wide range of pressures, etiologies of pulmonary hypertension, and treatments. We wondered if increased wave reflection on proximal pulmonary vascular obstruction, like in operable chronic thromboembolic pulmonary hypertension, might also decrease the RC-time and thereby increase pulse pressure and right ventricular afterload. Pulmonary hypertension of variable severity was induced either by proximal obstruction (pulmonary arterial ensnarement) or distal obstruction (microembolism) eight anesthetized dogs. Pulmonary arterial pressures (Ppa) were measured with high-fidelity micromanometer-tipped catheters, and pulmonary flow with transonic technology. Pulmonary ensnarement increased mean Ppa, PVR, and characteristic impedance, decreased Ca and the RC-time (from 0.46 ± 0.07 to 0.30 ± 0.03 s), and increased the oscillatory component of hydraulic load (Wosc/Wtot) from 25 ± 2 to 29 ± 2%. Pulmonary microembolism increased mean Ppa and PVR, with no significant change in Ca and characteristic impedance, increased RC-time from 0.53 ± 0.09 to 0.74 ± 0.05 s, and decreased Wosc/Wtot from 26 ± 2 to 13 ± 2%. Pulse pressure increased more after pulmonary ensnarement than after microembolism. Concomitant measurements with fluid-filled catheters showed the same functional differences between the two types of pulmonary hypertension, with, however, an underestimation of Wosc. We conclude that pulmonary hypertension caused by proximal vs. distal obstruction is associated with a decreased RC-time and increased pulsatile component of right ventricular hydraulic load.

scholarly journals Decreased time constant of the pulmonary circulation in chronic thromboembolic pulmonary hypertension

2013 ◽  
Vol 305 (2) ◽  
pp. H259-H264 ◽  
Author(s):  
Robert V. MacKenzie Ross ◽  
Mark R. Toshner ◽  
Elaine Soon ◽  
Robert Naeije ◽  
Joanna Pepke-Zaba
Keyword(s):  
Pulmonary Hypertension ◽  
Time Constant ◽  
Pulmonary Circulation ◽  
Wave Reflection ◽  
Arterial Compliance ◽  
Chronic Thromboembolic Pulmonary Hypertension ◽  
Left Heart Failure ◽  
Thromboembolic Pulmonary Hypertension ◽  
Pulmonary Arterial ◽  
Rc Time Constant

This study analyzed the relationship between pulmonary vascular resistance (PVR) and pulmonary arterial compliance ( Ca) in patients with idiopathic pulmonary arterial hypertension (IPAH) and proximal chronic thromboembolic pulmonary hypertension (CTEPH). It has recently been shown that the time constant of the pulmonary circulation (RC time constant), or PVR × Ca, remains unaltered in various forms and severities of pulmonary hypertension, with the exception of left heart failure. We reasoned that increased wave reflection in proximal CTEPH would be another cause of the decreased RC time constant. We conducted a retrospective analysis of invasive pulmonary hemodynamic measurements in IPAH ( n = 78), proximal CTEPH ( n = 91) before (pre) and after (post) pulmonary endarterectomy (PEA), and distal CTEPH ( n = 53). Proximal CTEPH was defined by a postoperative mean pulmonary artery pressure (PAP) of ≤25 mmHg. Outcome measures were the RC time constant, PVR, Ca, and relationship between systolic and mean PAPs. The RC time constant for pre-PEA CTEPH was 0.49 ± 0.11 s compared with post-PEA-CTEPH (0.37 ± 0.11 s, P < 0.0001), IPAH (0.63 ± 0.14 s, P < 0.001), and distal CTEPH (0.55 ± 0.12 s, P < 0.05). A shorter RC time constant was associated with a disproportionate decrease in systolic PAP with respect to mean PAP. We concluded that the pulmonary RC time constant is decreased in proximal CTEPH compared with IPAH, pre- and post-PEA, which may be explained by increased wave reflection but also, importantly, by persistent structural changes after the removal of proximal obstructions. A reduced RC time constant in CTEPH is in accord with a wider pulse pressure and hence greater right ventricular work for a given mean PAP.

Effects of sildenafil on hypoxic pulmonary vascular function in dogs

2006 ◽  
Vol 101 (4) ◽  
pp. 1085-1090 ◽  
Author(s):  
Pierre Fesler ◽  
Alberto Pagnamenta ◽  
Benoit Rondelet ◽  
François Kerbaul ◽  
Robert Naeije
Keyword(s):  
Arterial Pressure ◽  
Right Ventricular ◽  
Vascular Function ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Characteristic Impedance ◽  
Systemic Arterial Pressure ◽  
Pulmonary Vasodilators ◽  
Hydraulic Load ◽  
Pulmonary Arterial ◽  
Inhaled No

Sildenafil has been shown to be an effective treatment of pulmonary arterial hypertension and is believed to present with pulmonary selectivity. This study was designed to determine the site of action of sildenafil compared with inhaled nitric oxide (NO) and intravenous sodium nitroprusside (SNP), known as selective and nonselective pulmonary vasodilators, respectively. Inhaled NO (40 ppm), and maximum tolerated doses of intravenous SNP and sildenafil, (5 μg·kg−1·min−1 and 0.1 mg·kg−1·h−1), respectively, were administered to eight dogs ventilated in hypoxia. Pulmonary vascular resistance (PVR) was evaluated by pulmonary arterial pressure (Ppa) minus left atrial pressure (Pla) vs. flow curves, and partitioned into arterial and venous segments by the occlusion method. Right ventricular hydraulic load was defined by pulmonary arterial characteristic impedance (Zc) and elastance (Ea) calculations. Right ventricular arterial coupling was estimated by the ratio of end-systolic elastance (Ees) to Ea. Decreasing the inspired oxygen fraction from 0.4 to 0.1 increased Ppa − Pla at a standardized flow of 3 l·min−1·m−2 from 6 ± 1 to 18 ± 1 mmHg (mean ± SE). Ppa − Pla was decreased to 9 ± 1 by inhaled NO, 14 ± 1 by SNP, and 14 ± 1 mmHg by sildenafil. The partition of PVR, Zc, Ea, and Ees/Ea was not affected by the three interventions. Inhaled NO did not affect systemic arterial pressure, which was similarly decreased by sildenafil and SNP, from 115 ± 4 to 101 ± 4 and 98 ± 5 mmHg, respectively. We conclude that inhaled NO inhibits hypoxic pulmonary vasoconstriction more effectively than sildenafil or SNP, and sildenafil shows no more selectivity for the pulmonary circulation than SNP.

scholarly journals Successful treatment of severe combined post- and pre-capillary pulmonary hypertension in a patient with idiopathic restrictive cardiomyopathy

2018 ◽  
Vol 8 (3) ◽  
pp. 204589401877013
Author(s):  
Satomi Ishihara ◽  
Hidetaka Kioka ◽  
Tomohito Ohtani ◽  
Yoshihiro Asano ◽  
Osamu Yamaguchi ◽  
...  
Keyword(s):  
Heart Failure ◽  
Pulmonary Hypertension ◽  
Right Ventricular ◽  
Restrictive Cardiomyopathy ◽  
Assist Device ◽  
Heart Failure Treatment ◽  
Ventricular Assist ◽  
Failure Treatment ◽  
Ventricular Afterload ◽  
Pulmonary Arterial

Restrictive cardiomyopathy (RCM) is a rare form of cardiomyopathy that is characterized by restrictive ventricular filling. Elevated filling pressure leads to pulmonary hypertension (PH), which often progresses to combined post- and pre-capillary PH (Cpc-PH) with increased diastolic pulmonary vascular pressure gradient (DPG) and pulmonary vascular resistance (PVR) caused by longstanding backward hemodynamic consequences of left heart disease (LHD) leading to morphological changes in the pulmonary vasculature. Patients with high PVR undergoing left ventricular assist device (LVAD) implantation are at increased risk of postoperative right-sided heart failure requiring concomitant implantation of a right ventricular assist device (RVAD). We report a case of RCM with severe Cpc-PH due to extremely elevated DPG and PVR. The patient presented recurrent syncope caused by severe PH. Right heart catheterization (RHC) revealed highly elevated DPG 30 mmHg and PVR 25.3 Wood units (WU) and subsequent significant reduction of right ventricular afterload during vasoreactivity testing with inhaled nitric oxide (NO) to DPG 5 mmHg and PVR 10.5 WU. During the administration of pulmonary vasodilators, pulmonary congestion worsened. Second RHC revealed elevated pulmonary arterial wedge pressure (PAWP) and modest decrease of pulmonary arterial pressure (PAP) 87 mmHg and PVR 9.6 WU. Therefore, an inotropic agent and systemic vasodilator were added for the treatment of left-sided heart failure. Targeting elevated filling pressures with both PAH-specific and heart failure treatment, a further decrease of right ventricular afterload with DPG of 5 mmHg and PVR of 3.8 WU was achieved. In a next step, LVAD was successfully implanted, without need for RVAD, as a bridge to transplantation. This is the first reported case of Cpc-PH that revealed the potential reversibility of extremely elevated DPG and PVR, and suggests the importance of preoperative RHC-guided optimized medical PAH-specific and heart failure treatment before LVAD implantation.

Quantification of right ventricular afterload in patients with and without pulmonary hypertension

2006 ◽  
Vol 291 (4) ◽  
pp. H1731-H1737 ◽  
Author(s):  
Jan-Willem Lankhaar ◽  
Nico Westerhof ◽  
Theo J. C. Faes ◽  
Koen M. J. Marques ◽  
J. Tim Marcus ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Artery ◽  
Right Ventricular ◽  
Pulmonary Artery Pressure ◽  
Arterial Compliance ◽  
Characteristic Impedance ◽  
Peripheral Resistance ◽  
Windkessel Model ◽  
Artery Pressure ◽  
Pulmonary Arterial

Right ventricular (RV) afterload is commonly defined as pulmonary vascular resistance, but this does not reflect the afterload to pulsatile flow. The purpose of this study was to quantify RV afterload more completely in patients with and without pulmonary hypertension (PH) using a three-element windkessel model. The model consists of peripheral resistance ( R), pulmonary arterial compliance ( C), and characteristic impedance ( Z). Using pulmonary artery pressure from right-heart catheterization and pulmonary artery flow from MRI velocity quantification, we estimated the windkessel parameters in patients with chronic thromboembolic PH (CTEPH; n = 10) and idiopathic pulmonary arterial hypertension (IPAH; n = 9). Patients suspected of PH but in whom PH was not found served as controls (NONPH; n = 10). R and Z were significantly lower and C significantly higher in the NONPH group than in both the CTEPH and IPAH groups ( P < 0.001). R and Z were significantly lower in the CTEPH group than in the IPAH group ( P < 0.05). The parameters R and C of all patients obeyed the relationship C = 0.75/ R ( R2 = 0.77), equivalent to a similar RC time in all patients. Mean pulmonary artery pressure P and C fitted well to C = 69.7/P (i.e., similar pressure dependence in all patients). Our results show that differences in RV afterload among groups with different forms of PH can be quantified with a windkessel model. Furthermore, the data suggest that the RC time and the elastic properties of the large pulmonary arteries remain unchanged in PH.

Exercise training improves lung gas exchange and attenuates acute hypoxic pulmonary hypertension but does not prevent pulmonary hypertension of prolonged hypoxia

2006 ◽  
Vol 100 (1) ◽  
pp. 20-25 ◽  
Author(s):  
Fabrice Favret ◽  
Kyle K. Henderson ◽  
Julie Allen ◽  
Jean-Paul Richalet ◽  
Norberto C. Gonzalez
Keyword(s):  
Pulmonary Hypertension ◽  
Cardiac Output ◽  
Gas Exchange ◽  
Exercise Training ◽  
Right Ventricular ◽  
Acute Hypoxia ◽  
Male Rats ◽  
Hypoxic Pulmonary Hypertension ◽  
Ventricular Afterload ◽  
Pulmonary Arterial

Our laboratory has previously shown an attenuation of hypoxic pulmonary hypertension by exercise training (ET) (Henderson KK, Clancy RL, and Gonzalez NC. J Appl Physiol 90: 2057–2062, 2001), although the mechanism was not determined. The present study examined the effect of ET on the pulmonary arterial pressure (Pap) response of rats to short- and long-term hypoxia. After 3 wk of treadmill training, male rats were divided into two groups: one (HT) was placed in hypobaric hypoxia (380 Torr); the second remained in normoxia (NT). Both groups continued to train in normoxia for 10 days, after which they were studied at rest and during hypoxic and normoxic exercise. Sedentary normoxic (NS) and hypoxic (HS) littermates were exposed to the same environments as their trained counterparts. Resting and exercise hypoxic arterial Po2 were higher in NT and HT than in NS and HS, respectively, although alveolar ventilation of trained rats was not higher. Lower alveolar-arterial Po2 difference and higher effective lung diffusing capacity for O2 in NT vs. NS and in HT vs. HS suggest ET improved efficacy of gas exchange. Pap and Pap/cardiac output were lower in NT than NS in hypoxia, indicating that ET attenuates the initial vasoconstriction of hypoxia. However, ET had no effect on chronic hypoxic pulmonary hypertension: Pap and Pap/cardiac output in hypoxia were similar in HS vs HT. However, right ventricular weight was lower in HT than in HS, although Pap was not different. Because ET attenuates the initial pulmonary vasoconstriction of hypoxia, development of pulmonary hypertension may be delayed in HT rats, and the time during which right ventricular afterload is elevated may be shorter in this group. ET effects may improve the response to acute hypoxia by increasing efficacy of gas exchange and lowering right ventricular work.

P4690Effects of pulmonary artery wedge pressure on right ventricular pulsatile loading in pulmonary hypertension: a reappraisal based on pulmonary arterial isobaric stiffness

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
D Chemla ◽  
E Berthelot ◽  
J Weatherald ◽  
E Lau ◽  
P Attal ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Artery ◽  
Stroke Volume ◽  
Right Ventricular ◽  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Pulse Pressure ◽  
Pulmonary Artery Wedge Pressure ◽  
Pulmonary Arterial ◽  
Wedge Pressure

Abstract Background Pulmonary hypertension (PH) is associated with stiffening of pulmonary arteries. Previous studies have suggested that high pulmonary artery wedge pressure (PAWP) in postcapillary PH (Pc-PH) further augments PA stiffness at a given level of pulmonary vascular resistance as compared to pulmonary arterial hypertension (PAH). However, these studies do not take into account differences in distending pressure (mean PA pressure, mPAP), which has an effect on stiffness due to non-linear stress-strain behavior of arteries. Purpose To compare total PA stiffness between Pc-PH and idiopathic PAH (iPAH) studied at similar mPAP (isobaric stiffness). Methods This was an analysis of right heart catheterization results obtained in 112 Pc-PH and 112 iPAH patients extracted from the French PAH network registry and matched for mPAP (median 38 vs 39 mmHg, P=NS), age (70.5 years each) and sex (64% female each). Total PA stiffness was calculated as the ratio of PA pulse pressure to indexed stroke volume. Results Total PA stiffness (n=224) increased with mPAP (Spearman's rho = 0.66) and decreased with PAWP (rho = - 0.17) (each P<0.01). The isobaric stiffness was lower in Pc-PH (median (IQR) = 0.91 (0.64–1.39) mmHg/mL/m2) than in iPAH (1.18 (0.83–1.62) mmHg/mL/m2, P<0.01). The patients were then stratified according to their mPAP (25–35 mmHg, n=74 (37/37); 36–43 mmHg, n=75 (34/41); and 44–66 mmHg, n=75 (41/34)). The isobaric stiffness was lower in Pc-PH than iPAH in the 1st mPAP tertile (0.62 vs 0.83 mmHg/mL/m2, P=0.06), in the 2nd mPAP tertile (0.76 vs 1.22 mmHg/mL/m2, P<0.01) and in the 3rd mPAP tertile (1.41 vs 1.77 mmHg/mL/m2, P<0.01). The pulmonary vascular resistance was lower in Pc-PH than iPAH in every mPAP tertile (each P<0.01). Finally, Pc-PH had a higher indexed stroke volume than iPAH (37 (29–48) vs 32 (27–40) mL/m2, P<0.01) while systolic PA pressure and PA pulse pressure were similar. Conclusion Unexpectedly, the isobaric pulmonary arterial stiffness was lower in Pc-PH than iPAH patients. It is proposed that PAWP attenuates the increase in RV pulsatile loading in PH when the natural high-strain-induced stiffening was accounted for. This may contribute to a less impaired right ventricular-PA coupling leading to higher indexed stroke volume in Pc-PH than iPAH despite similar PA pressure. At every mPAP level, both the lower PA stiffness and lower pulmonary vascular resistance in Pc-PH than in iPAH may contribute to explain differences in the pressure overload-induced right ventricular adaptation between the two diseased groups, a point that deserves to be confirmed by further studies. Acknowledgement/Funding University regular funds

Right ventricular pressure-volume loop shape and systolic pressure change in pulmonary hypertension

2021 ◽  
Author(s):  
Manuel Jonas Richter ◽  
Steven Hsu ◽  
Athiththan Yogeswaran ◽  
Faeq Husain-Syed ◽  
István Vadász ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Right Ventricular ◽  
Pulse Pressure ◽  
Augmentation Index ◽  
Systolic Pressure ◽  
Pressure Differential ◽  
Stroke Work ◽  
Loop Shape ◽  
Pulmonary Arterial ◽  
Rv Function

Right ventricular (RV) function determines outcome in pulmonary arterial hypertension (PAH). RV pressure-volume loops - the gold standard for measuring RV function - are difficult to analyze. Our aim was to investigate whether simple assessments of RV pressure-volume loop morphology and RV systolic pressure differential reflect PAH severity and RV function. We analyzed multi-beat RV pressure-volume loops (obtained by conductance catheterization with preload reduction) in 77 patients with PAH and 15 patients without pulmonary hypertension in two centers. Patients were categorized according to their pressure-volume loop shape (triangular, quadratic, trapezoid, or notched). RV systolic pressure differential was defined as end-systolic minus beginning-systolic pressure (ESP−BSP); augmentation index as ESP−BSP/pulse pressure; pulmonary arterial capacitance (PAC) as stroke volume/pulse pressure; and RV-arterial coupling as end-systolic/arterial elastance (Ees/Ea). Trapezoid and notched pressure-volume loops were associated with the highest afterload (Ea), augmentation index, pulmonary vascular resistance (PVR), mean pulmonary arterial pressure, stroke work, and B-type natriuretic peptide, and the lowest Ees/Ea and PAC. Multivariate linear regression identified Ea, PVR, and stroke work as the main determinants of ESP−BSP. ESP−BSP also significantly correlated with multi-beat Ees/Ea (Spearman's rho: −0.518, P < 0.001). A separate retrospective analysis of 113 patients with PAH showed that ESP−BSP obtained by routine right heart catheterization significantly correlated with a non-invasive surrogate of RV-arterial coupling (tricuspid annular plane systolic excursion/pulmonary arterial systolic pressure ratio; rho: −0.376, P < 0.001). In conclusion, pressure-volume loop shape and RV systolic pressure differential predominately depend on afterload and PAH severity and reflect RV-arterial coupling in PAH.

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