Diastolic ventricular interaction in chronic heart failure

Atherton, J.; Moore, Thomas; Lele, Suhas S.; Thomson, Helen L.; Galbraith, Andrew; Belenkie, Israel; Tyberg, John V.; Frenneaux, Michael

doi:10.1016/s0140-6736(96)05109-4

Cited by 202 publications

(118 citation statements)

References 20 publications

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“…25 In patients with CHF, marked external constraint to LV filling was present in the majority of patients with LVEDP/pulmonary capillary wedge pressure Ͼ15 mm Hg. 14,26 In accordance with our hypothesis, LV pacing significantly reduced this external constraint, presumably by causing a phase shift in LV filling relative to RV filling, as recently demonstrated in the LV pacing canine model, 17 in which LV relaxation and filling occurred relatively early compared with RV relaxation and filling. If so, RV diastolic pressure and pericardial pressure are likely to be lower at any given LV diastolic volume.…”

Section: Bleasdale Et Al LV Pacing Reduces Ventricular Interactionsupporting

confidence: 89%

“…13 We hypothesized that at least part of the acute hemodynamic benefit from LV pacing may be due to reduced external constraint to LV filling. In previous work, we demonstrated that in CHF patients with high pulmonary capillary wedge pressure, LV filling was markedly impeded by external constraint from the right ventricle (RV) via the shared interventricular septum (direct diastolic ventricular interaction) 14 and from the stretched pericardium (pericardial constraint). Lower-body negative pressure reduced RV volume but increased LV volume and stroke volume.…”

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confidence: 99%

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Left Ventricular Pacing Minimizes Diastolic Ventricular Interaction, Allowing Improved Preload-Dependent Systolic Performance

et al. 2004

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Background-Left ventricular (LV) pacing improves hemodynamics in patients with heart failure. We hypothesized that at least part of this benefit occurs by minimization of external constraint to LV filling from ventricular interaction. Methods and Results-We present median values (interquartile ranges) for 13 heart failure patients with LV pacing systems implanted for New York Heart Association class III/IV limitation. We used the conductance catheter method to measure LV pressure and volume simultaneously. External constraint was measured from the end-diastolic pressure-volume relation recorded during inferior vena caval occlusion, during LV pacing, and while pacing was suspended. External constraint to LV filling was reduced by 3.0 (4.6 to 0.6) mm Hg from 4.8 (0.6 to 7.5) mm Hg (PϽ0.01) in response to LV pacing; effective filling pressure (LV end-diastolic pressure minus external constraint) increased by 4.0 (2.2 to 5.8) mm Hg from 17.7 (13.3 to 22.6; PϽ0.01). LV end-diastolic volume increased by 10 (3 to 11) mL from 238 (169 to 295) mL (Pϭ0.01), whereas LV end-systolic volume did not change significantly (Ϫ1 [Ϫ2 to 3] mL from 180 [124 to 236] mL, Pϭ0.97), which resulted in an increase in stroke volume of 11 (5 to 13) mL from 49 (38 to 59) mL (PϽ0.01). LV stroke work increased by 720 (550 to 1180) mL ⅐ mm Hg from 3400 (2110 to 4480) mL ⅐ mm Hg (Pϭ0.01), and maximum dP/dt increased by 120 (2 to 161) mm Hg/s from 635 (521 to 767) mm Hg/s (Pϭ0.03). Conclusions-This study suggests a potentially important mechanism by which LV pacing may produce hemodynamic benefit. LV pacing minimizes external constraint to LV filling, resulting in an increase in effective filling pressure; the consequent increase in LV end-diastolic volume increases stroke volume via the Starling mechanism. (Circulation.

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Section: Bleasdale Et Al LV Pacing Reduces Ventricular Interactionsupporting

confidence: 89%

mentioning

confidence: 99%

Left Ventricular Pacing Minimizes Diastolic Ventricular Interaction, Allowing Improved Preload-Dependent Systolic Performance

et al. 2004

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“…Other studies observed an inverse relation in left and right ventricular ejection dynamics that was very close to 180u out of phase and a septal swing with the dynamics, i.e. parallel ventricular interdependence [5][6][7][8]. The experimental study by Gonzalez et al [9] and our experimental and clinical studies [10][11][12] do not support ''lung pooling'' hypothesis, but could be easily explained by the parallel ventricular interdependence.…”

Section: Introductioncontrasting

confidence: 64%

Mechanism Study of Pulsus Paradoxus Using Mechanical Models

Cao

Xing

Yuan

et al. 2013

Ultrasound in Medicine & Biology

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Pulsus paradoxus is an exaggeration of the normal inspiratory decrease in systolic blood pressure. Despite a century of attempts to explain this sign consensus is still lacking. To solve the controversy and reveal the exact mechanism, we reexamined the characteristic anatomic arrangement of the circulation system in the chest and designed these mechanical models based on related hydromechanic principles. Model 1 was designed to observe the primary influence of respiratory intrathoracic pressure change (RIPC) on systemic and pulmonary venous return systems (SVR and PVR) respectively. Model 2, as an equivalent mechanical model of septal swing, was to study the secondary influence of RIPC on the motion of the interventriclar septum (IVS), which might be the direct cause for pulsus paradoxus. Model 1 demonstrated that the simulated RIPC had different influence on the simulated SVR and PVR. It increased the volume of the simulated right ventricle (SRV) when the internal pressure was kept constant (8.16 cmH 2 O), while it had the opposite effect on PVR. Model 2 revealed the three major factors determining the respiratory displacement of IVS in normal and different pathophysiological conditions: the magnitude of RIPC, the pressure difference between the two ventricles and the intrapericardial pressure. Our models demonstrate that the different anatomical arrangement of the two venous return systems leads to a different effect of RIPC on right and left ventricles, and thus a pressure gradient across IVS that tends to shift IVS left-and rightwards. When the leftward displacement of IVS reaches a considerable amplitude in some pathologic condition such as cardiac tamponade, the pulsus paradoxus occurs.

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“…This is almost certainly caused by a decrease in the volume of the right ventricle and a decrease in pericardial pressure, which increases effective LV distending pressure despite a decrease in LVEDP (ie, diastolic ventricular interaction). 28 ANP infusion reduces cardiac filling pressures too rapidly to be solely accounted for by a fluid shift into the interstitial space and, in HF, in absence of significant diuresis or changes in hematocrit. 2,3,27 These observations re-emphasize the potentially important venous effects of ANP.…”

Section: Clinical and Pathophysiological Implicationsmentioning

confidence: 99%

Effects of Exogenous and Endogenous Natriuretic Peptides on Forearm Vascular Function in Chronic Heart Failure

Schmitt

Gunaruwan

Payne

et al. 2004

ATVB

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Objective-Natriuretic peptides (NPs) reduce central venous pressure in patients with chronic heart failure (cHF) despite attenuation of arterial, renal, and humoral effects. This suggests a preserved venodilator response. This study had 4 aims: to compare the venodilator effects of human NPs in patients with cHF; to assess the contribution of basal ANP and BNP levels to regulation of forearm vascular volume (FVV); to test the hypothesis that venous ANP responsiveness is preserved in cHF; and to assess the involvement of endothelial nitric oxide-synthase (eNOS) in NP-induced vascular effects. Methods and Results-Venous and arterial forearm vascular responses to incremental intra-arterial doses of ANP, Urodilatin, BNP, CNP, or the ANP receptor antagonist A71915 were studied in 53 patients and 11 controls. ANP receptor antagonism reduced FVV by 4.4%Ϯ1.2% (PϽ0.05). The forearm blood flow (FBF) response to ANP was significantly blunted in patients versus controls (PϽ0.01), whereas FVV increased similarly in both groups (maximum 14.7% and 13.4%, both PϽ0.001). The eNOS blockade reduced ANP-induced FBF changes in controls but not in patients (PϽ0.05), whereas similar reductions in FVV changes were seen in groups (both PϽ0.001). Conclusions-In

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Diastolic ventricular interaction in chronic heart failure

Cited by 202 publications

References 20 publications

Left Ventricular Pacing Minimizes Diastolic Ventricular Interaction, Allowing Improved Preload-Dependent Systolic Performance

Left Ventricular Pacing Minimizes Diastolic Ventricular Interaction, Allowing Improved Preload-Dependent Systolic Performance

Mechanism Study of Pulsus Paradoxus Using Mechanical Models

Effects of Exogenous and Endogenous Natriuretic Peptides on Forearm Vascular Function in Chronic Heart Failure

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