scholarly journals Acute volume loading exacerbates direct ventricular interaction in a model of COPD

2017 ◽  
Vol 123 (5) ◽  
pp. 1110-1117 ◽  
Author(s):  
William S. Cheyne ◽  
Alexandra M. Williams ◽  
Megan I. Harper ◽  
Neil D. Eves

Volume loading increases left ventricular (LV) stroke volume (LVSV) through series interaction, but may paradoxically reduce LVSV in the presence of large increases in right ventricular (RV) afterload because of direct ventricular interaction (DVI). RV afterload is often increased in chronic obstructive pulmonary disease (COPD) as a result of pathological changes to respiratory mechanics, namely increased negative intrathoracic pressure (nITP), dynamic lung hyperinflation (DH), and increased pulmonary vascular resistance (PVR). These hallmarks of COPD negatively impact LV hemodynamics in normovolemia. However, it is unknown how these heart-lung interactions are impacted by acute volume loading. Twenty healthy subjects (23 ± 2 yr) completed the study protocol, involving acute volume loading via 20° head-down tilt (HDT) in isolation and with 1) inspiratory resistance of −20 cmH2O (HDT+nITP) and 2) nITP, expiratory resistance to induce DH and hypoxic-mediated increases in PVR (HDT+COPD model). LV volumes and geometry were assessed using triplane echocardiography. HDT significantly increased LVSV by 10 ± 10% through an 8 ± 6% increase in LV end-diastolic volume (LVEDV). HDT+nITP paradoxically decreased LVSV by 11 ± 12% and LVEDV by 6 ± 9% from supine baseline, or −14 ± 10% LVSV and −15 ± 13% LVEDV from HDT ( P < 0.001). HDT+COPD model decreased LVSV (21 ± 10% and 28 ± 11%) and LVEDV (16 ± 10% and 22 ± 10%) from both supine and HDT, respectively ( P < 0.001). Under all conditions, significant septal flattening (increased radius of septal curvature) occurred, indicating DVI. Thus, when RV afterload is increased and/or an external constraint to ventricular filling exists, acute volume loading appears to paradoxically reduce LVSV. These findings have important implications for understanding how volume status impacts cardiopulmonary interactions in COPD. NEW & NOTEWORTHY Volume loading may exacerbate adverse cardiopulmonary interaction in COPD; however, the mechanisms remain unclear. We found that when negative intrathoracic pressure is increased, acute volume loading paradoxically reduces stroke volume. This reduction in stroke volume is considerably greater in a model of COPD, owing to the effects of lung hyperinflation.

2018 ◽  
Vol 315 (3) ◽  
pp. H474-H481 ◽  
Author(s):  
William S. Cheyne ◽  
Jinelle C. Gelinas ◽  
Neil D. Eves

Dynamic hyperinflation (DH) is common in chronic obstructive pulmonary disease and is associated with dyspnea and exercise intolerance. DH also has adverse cardiac effects, although the magnitude of DH and the mechanisms responsible for the hemodynamic impairment remain unclear. We hypothesized that incrementally increasing DH would systematically reduce left ventricular (LV) end-diastolic volume (LVEDV) and LV stroke volume (LVSV) because of direct ventricular interaction. Twenty-three healthy subjects (22 ± 2 yr) were exposed to varying degrees of expiratory loading to induce DH such that inspiratory capacity was decreased by 25%, 50%, 75%, and 100% (100% DH =  inspiratory capacity of resting tidal volume plus inspiratory reserve volume ≈ 0.5 l). LV volumes, LV geometry, inferior vena cava collapsibility, and LV end-systolic wall stress were assessed by triplane echocardiography. 25% DH reduced LVEDV (−6 ± 5%) and LVSV (−9 ± 8%). 50% DH elicited a similar response in LVEDV (−6 ± 7%) and LVSV (−11 ± 10%) and was associated with significant septal flattening [31 ± 32% increase in the radius of septal curvature at end diastole (RSC-ED)]. 75% DH caused a larger reduction in LVEDV and LVSV (−9 ± 7% and −16 ± 10%, respectively) and RSC-ED (49 ± 70%). 100% DH caused the largest reduction in LVEDV and LVSV (−13 ± 9% and −18 ± 9%) and an increase in RSC-ED (56 ± 63%). Inferior vena cava collapsibility and LV afterload (LV end-systolic wall stress) were unchanged at all levels of DH. Modest DH (−0.6 ± 0.2 l inspiratory reserve volume) reduced LVSV because of reduced LVEDV, likely because of increased pulmonary vascular resistance. At higher levels of DH, direct ventricular interaction may be the primary cause of attenuated LVSV, as indicated by septal flattening because of a greater relative increase in right ventricular pressure and/or mediastinal constraint. NEW & NOTEWORTHY By systematically reducing inspiratory capacity during spontaneous breathing, we demonstrate that dynamic hyperinflation (DH) progressively reduces left ventricular (LV) end diastolic volume and LV stroke volume. Evidence of significant septal flattening suggests that direct ventricular interaction may be primarily responsible for the reduced LV stroke volume during DH. Hemodynamic impairment appears to occur at relatively lower levels of DH and may have important clinical implications for patients with chronic obstructive pulmonary disease.


2016 ◽  
Vol 311 (6) ◽  
pp. H1367-H1374 ◽  
Author(s):  
William S. Cheyne ◽  
Alexandra M. Williams ◽  
Megan I. Harper ◽  
Neil D. Eves

Chronic obstructive pulmonary disease (COPD) is associated with dynamic lung hyperinflation (DH), increased pulmonary vascular resistance (PVR), and large increases in negative intrathoracic pressure (nITP). The individual and interactive effect of these stressors on left ventricular (LV) filling, emptying, and geometry and the role of direct ventricular interaction (DVI) in mediating these interactions have not been fully elucidated. Twenty healthy subjects were exposed to the following stressors alone and in combination: 1) inspiratory resistive loading of −20 cmH2O (nITP), 2) expiratory resistive loading to cause dynamic hyperinflation (DH), and 3) normobaric-hypoxia to increase PVR (hPVR). LV volumes and geometry were assessed using triplane echocardiography. LV stroke volume (LVSV) was reduced during nITP by 7 ± 7% (mean ± SD; P < 0.001) through a 4 ± 5% reduction in LV end-diastolic volume (LVEDV) ( P = 0.002), while DH reduced LVSV by 12 ± 13% ( P = 0.001) due to a 9 ± 10% reduction in LVEDV ( P < 0.001). The combination of nITP and DH (nITP+DH) caused larger reductions in LVSV (16 ± 16%, P < 0.001) and LVEDV (12 ± 10%, P < 0.001) than nITP alone ( P < 0.05). The addition of hPVR to nITP+DH did not further reduce LV volumes. Significant septal flattening (indicating DVI) occurred in all conditions, with a significantly greater leftward septal shift occurring with nITP+DH than either condition alone ( P < 0.05). In summary, the interaction of nITP and DH reduces LV filling through DVI. However, DH may be more detrimental to LV hemodynamics than nITP, likely due to mediastinal constraint of the heart amplifying DVI.


2020 ◽  
Vol 44 (1) ◽  
pp. 12-16
Author(s):  
I. M. Fushtey ◽  
K. L. Nikolaieva

Abstract Chronic obstructive pulmonary disease (COPD) greatly affects the quality of life, significantly limiting the physical capabilities of people suffering from it. The prevalence of COPD worldwide is about 7,6 %, and it is one of the main causes of morbidity and mortality in today’s society. An urgent medical and social problem of our time is the development of pulmonary hypertension (PH) in patients with COPD. Transthoracic echocardiography is important for PH screening. It has the highest sensitivity and specificity among non-invasive examinations, and unlike catheterization of the right heart, it does not require special equipment and centers for dynamic monitoring of patients with PH. When pulmonary hypertension, there is a pronounced remodeling of the heart. At the first stage, it occurs in the right parts of the heart, and in the future, as a consequence, it is accompanied by a violation of systolic inter-ventricular interactions. Purpose of the study. To determine the characteristics of left ventricular systolic function in patients with pulmonary hypertension on the background of COPD. Materials and methods. Results of the study are based on data from a comprehensive survey of 170 COPD patients aged 40 to 65 years, 123 of which had pulmonary hypertension and 47 ones had no pulmonary hypertension. Results and discussion. In the group of patients with PH on the background of COPD, the shock volume was 74,72 cm3 (64,60–83,09) and it was significantly lower compared to the level of 82,04 cm3 (75,20–87,76) of the COPD group without PH (p < 0,05). Such echocardiographic index as left ventricular ejection fraction in groups of patients with COPD with PH and without it, was 57,59% (53,84–62,19) and 59,44% (56,67–61,88), respectively, and it was significantly lower compared to the level of 64,62% (62,86–67,91) of healthy individuals (p < 0,05). There was a straight increase in end-diastolic volume and end-systolic volume in the subgroup of patients with COPD duration > 12 years compared to the subgroup ≤ 12 years, 134,17 cm3 (117,00–150,15) versus 125,52 cm3 (105,20–139,60) and 57,37 cm3 (51,70–65,60) versus 51,40 cm3 (43,08–59,84), respectively (p < 0,05). The impact volume had no significant differences between subgroups depending on the duration of COPD (p > 0,05). The level of LV ejection fraction was significantly lower in the subgroup of COPD duration > 12 years 56,64% (52,65–59,73) against the subgroup ≤ 12 years (p < 0,05). There were no significant differences between the levels of systolic heart function indicators: end-diastolic volume, end-systolic volume, shock volume, and LV EF depending on the stage of COPD (p > 0,05). Correlation analysis revealed significant relationships between the following indicators: duration of COPD and ESV (R = +0,24, p = 0,008); duration of COPD and LV EF (R = –0,25, p = 0,006); MPAP and EDV (R = –0,22, p = 0.02);MPAP and SV (R = –0,26, p = 0,004); MPAP and LV EF (R = –0,21, p = 0,02). Keywords: left ventricular systolic function, pulmonary hypertension, chronic obstructive pulmonary disease, mean pulmonary artery pressure.


Author(s):  
Stephen P. Wright ◽  
William Spencer Cheyne ◽  
Jinelle C. Gelinas ◽  
Megan I. Harper ◽  
John P. Sasso ◽  
...  

Augmented negative intrathoracic pressures (nITP) and dynamic hyperinflation (DH) are adverse breathing mechanics (ABM) associated with chronic obstructive pulmonary disease that attenuate left ventricular (LV) preload and augment afterload. In COPD, hypertension (elevated systemic arterial load) commonly adds additional afterload to the LV. Combined ABM and hypertension may profoundly challenge ventricular-vascular coupling and attenuate stroke volume (SV), particularly if LV systolic reserve is limited. However, even in the healthy heart, the combined impact of ABM and systemic arterial loading on LV function and ventricular-vascular coupling has not been fully elucidated. Healthy volunteers (10M/9F, 24±3 years) were challenged with Mild (-10cmH2O nITP and 25% DH) and Severe (-20cmH2O nITP and 100% DH) ABM, without and with post-exercise ischemia (PEI) at each severity. LV SV, chamber geometry, and end-systolic elastance (Ees), arterial elastance (Ea), and ventricular-vascular coupling (Ees:Ea) were quantified using echocardiography. Compared to resting Control (58±13mL), SV decreased during Mild ABM (51±13mL), Mild ABM+PEI (51±11mL), Severe ABM (50±12mL), and Severe ABM+PEI (47±11mL) (P<0.001); similar trends were observed for LV end-diastolic volume. The end-diastolic radius of septal curvature increased, indicating direct ventricular interaction, during Severe ABM and Severe ABM+PEI (P<0.001). Compared to Control (1.99±0.41mmHg/mL), Ea increased progressively with Mild ABM (2.21±0.47mmHg/mL) and Severe ABM (2.50±0.56mmHg/mL); at each severity Ea was greater with superimposed PEI (P<0.001). However, well-matched Ees increases occurred, and Ees:Ea was unchanged throughout. ABM pose a challenge to ventricular-vascular coupling that is accentuated by superimposed PEI; however, in healthy younger adults, the LV has substantial systolic reserveto maintain coupling.


2020 ◽  
Vol 7 (1) ◽  
pp. e000741
Author(s):  
Felix Herth ◽  
Jens M Hohlfeld ◽  
Johannes Haas ◽  
Alberto de la Hoz ◽  
Xidong Jin ◽  
...  

This exploratory, randomised, double-blind, double-dummy, multicentre, cross-over study explored the effect of 6 weeks of treatment with tiotropium/olodaterol (T/O) versus fluticasone propionate/salmeterol (F/S) on left ventricular filling in patients with chronic obstructive pulmonary disease with functional residual capacity (FRC) >120% predicted and postbronchodilator improvement of FRC ≥7.5%. Overall, 76 patients were randomised across nine sites. Treatment with T/O or F/S increased left ventricular end-diastolic volume index from baseline (adjusted mean change: T/O: 2.317 mL/m2, F/S: 2.855 mL/m2), with no statistically significant difference between treatments. However, T/O resulted in a significantly greater reduction in lung hyperinflation versus F/S (FRC plethysmography absolute change from baseline: F/S: –0.329 L, T/O: –0.581 L).


2006 ◽  
Vol 290 (4) ◽  
pp. H1528-H1533 ◽  
Author(s):  
C. Tji-Joong Gan ◽  
Jan-Willem Lankhaar ◽  
J. Tim Marcus ◽  
Nico Westerhof ◽  
Koen M. Marques ◽  
...  

The aim of this study was to investigate the contribution of direct right-to-left ventricular interaction to left ventricular filling and stroke volume in 46 patients with pulmonary arterial hypertension (PAH) and 18 control subjects. Stroke volume, right and left ventricular volumes, left ventricular filling rate, and interventricular septum curvature were measured by magnetic resonance imaging and left atrial filling by transesophageal echocardiography. Stroke volume, left ventricular end-diastolic volume, and left ventricular peak filling rate were decreased in PAH patients compared with control subjects: 28 ± 13 vs. 41 ± 10 ml/m2( P < 0.001), 46 ± 14 vs. 61 ± 14 ml/m2( P < 0.001), and 216 ± 90 vs. 541 ± 248 ml/s ( P < 0.001), respectively. Among PAH patients, stroke volume did not correlate to right ventricular end-diastolic volume or mean pulmonary arterial pressure but did correlate to left ventricular end-diastolic volume ( r = 0.62, P < 0.001). Leftward interventricular septum curvature was correlated to left ventricular filling rate ( r = 0.64, P < 0.001) and left ventricular end-diastolic volume ( r = 0.65, P < 0.001). In contrast, left atrial filling was normal and not correlated to left ventricular end-diastolic volume. In PAH patients, ventricular interaction mediated by the interventricular septum impairs left ventricular filling, contributing to decreased stroke volume.


Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Bertrand Ebner ◽  
Jennifer Maning ◽  
Louis Vincent ◽  
Jelani Grant ◽  
neal olarte ◽  
...  

Background: Chronic obstructive pulmonary disease (COPD) is well-known cause of ventricular dysfunction. However, in the setting of patients with advanced heart failure undergoing left ventricular assist device (LVAD) implantation, there is paucity data on COPD influence on in-hospital outcomes. Methods: This retrospective cohort study based on the Nationwide Inpatient Sample included all patients above 18 years all who underwent LVAD implantation from 2011 to 2017. All data was weight as recommended by Healthcare Cost and Utilization Project.Multivariate logistic regression was used to evaluate the impact of COPD on in-hospital outcomes. Results: A total of 25,503 patients underwent LVAD implantation, of those 13.8% had a pre-existing diagnosis of COPD. Individuals with COPD were older (median 62 vs. 58 years, p<0.001), more commonly male (82% vs. 76.4%, p<0.001). Patient with COPD had a greater burden of comorbidities confirmed by significant higher rate of hypertension, diabetes, atrial tachyarrhythmias, dyslipidemia, prior stroke, coronary and peripheral artery diseases, pulmonary hypertension, and chronic kidney disease (p<0.001 for all). No significant difference was found in in-hospital stroke, infections, short-term percutaneous mechanical circulatory support, implant related complications, and LVAD thrombosis. There was a significant higher rate of inpatient acute kidney injury, major bleeding, cardiac complications, thromboembolism, and cardiac arrest in patients without COPD (p<0.05 for all outcomes). Compared to patients without COPD, individuals with COPD had a lower mortality (6.2% vs. 12.4%; OR 0.59; C.I. 0.512-0.685; p<0.05). Conclusion: Patients with COPD undergoing LVAD implantation have higher comorbidities, however, it is not associated with increase in-hospital all-cause mortality.Further studies are needed to analyze the differences found between these two groups in more detail.


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