Figure 2 - uploaded by Alun David Hughes
Content may be subject to copyright.
Wave intensity pattern 

Wave intensity pattern 

Source publication
Article
Full-text available
Key points: Wave travel plays an important role in cardiovascular physiology. However, many aspects of pulmonary arterial wave behaviour remain unclear. Wave intensity and reservoir-excess pressure analyses were applied in the pulmonary artery in subjects with and without pulmonary hypertension during spontaneous respiration and dynamic stress tes...

Contexts in source publication

Context 1
... pattern in the pulmonary artery in health and disease has been described previously ( Lau et al., 2014). Briefly, a FCW -the incident wave -is observed in early systole corresponding to right ventricular (RV) ejection ( Figure 2A). This is followed by a FDW in late systole corresponding to ventricular relaxation prior to the closure of the pulmonary valve. ...
Context 2
... of ensemble-averaged pressure and velocity waveforms and the corresponding WIA pattern during Valsalva manoeuvre and handgrip exercise are shown in Figure 2B and 2C, respectively. During Valsalva manoeuvre, the ejection period was significantly shorter compared to baseline (Table 3). ...

Similar publications

Article
Full-text available
Background In contrast to systemic hypertension, the significance of arterial waves in pulmonary hypertension (PH) is not well understood. We hypothesized that arterial wave energy and wave reflection are augmented in PH and that wave behavior differs between patients with pulmonary arterial hypertension (PAH) and chronic thromboembolic pulmonary h...

Citations

... 13 Su et al. have studied WIA in patients with primary pulmonary arterial hypertension (PAH) and chronic thromboembolic pulmonary hypertension. [14][15][16][17] There are no studies of WIA in the pulmonary artery in heart failure and PHLHD. ...
Article
Full-text available
Wave intensity analysis (WIA) uses simultaneous changes in pressure and flow velocity to determine wave energy, type, and timing of traveling waves in the circulation. In this study, we characterized wave propagation in the pulmonary artery in patients with pulmonary hypertension associated with left‐sided heart disease (PHLHD) and the effects of dobutamine. During right heart catheterization, pressure and velocity data were acquired using a dual‐tipped pressure and Doppler flow sensor wire (Combowire; Phillips Volcano), and processed offline using customized Matlab software (MathWorks). Patients with low cardiac output underwent dobutamine challenge. Twenty patients with PHLHD (all heart failure with reduced left ventricular ejection fraction) were studied. Right ventricular systole produced a forward compression wave (FCW), followed by a forward decompression wave (FDW) during diastole. Wave reflection manifesting as backward compression wave (BCW) following the FCW was observed in 14 patients. Compared to patients without BCW, patients with BCW had higher mean pulmonary artery pressure (28.7 ± 6.12 vs. 38.6 ± 6.5 mmHg, p = 0.005), and lower pulmonary arterial capacitance (PAC: 2.88 ± 1.75 vs. 1.73 ± 1.16, p = 0.002). Pulmonary vascular resistance was comparable. Mean pulmonary artery pressure of 34.5 mmHg (area under the curve [AUC]: 0.881) and PAC of 2.29 mL/mmHg (AUC: 0.833) predicted BCW. The magnitude of the FCW increased with dobutamine ( n = 11) and correlated with pulmonary artery wedge pressure. Wave reflection in PHLHD is more likely at higher pulmonary artery pressures and lower PAC and the magnitude of reflected waves correlated with pulmonary artery wedge pressure. Dobutamine increased FCW but did not affect wave reflection.
... Although we avoided measuring tidal volume during the IME protocols, we can infer that the volunteers in the sham protocol had higher tidal volume with each inspiration due to the lack of resistance of inspiratory action. Thus, greater pulmonary volume would mechanically hinder ventricular filling during cardiac diastole, decreasing the final diastolic volume and, thus, SV 21,22 . However, we observed no difference between SV deltas in our comparison between sessions. ...
Article
Full-text available
The literature on hemodynamic responses during inspiratory muscle exercise (IME) lacks a consensus. To evaluate and compare hemodynamic responses during an IME session with and without resistive load, 15 sedentary men were subjected to two randomized IME sessions: one with 40% of maximal inspiratory pressure (IME 40%) and another without a resistive load (Sham), both of which were performed for two minutes over eight sessions with one-minute intervals. Systolic blood pressure (SBP), diastolic blood pressure (DBP), mean blood pressure (MBP), total peripheral resistance (TPR), stroke volume (SV), cardiac output (CO), and heart rate (HR) were measured by infrared digital photoplethysmography during five basal minutes and during the IME sessions. One-way analysis of variance and the Student’s t test for paired data were used to analyze hemodynamic response and delta values between sessions. Effect size was evaluated by Cohen’s D. A 5% significance level was adopted. SBP responses (sham: ∆−1±2 vs. 40%: ∆−4±2mmHg, p=0.27), DBP (sham: ∆2±1 vs. 40%: ∆1±2mmHg, p=0.60) and MBP (sham: ∆2±1 vs. 40%: ∆0±2mmHg, p=0.28) were similar between sessions. HR increases were higher in the 40% IME session than in the sham session (sham: ∆9±2 vs. 40%: ∆3±2bpm, p=0.001). SV only decreased during the sham session but responses were similar between sessions (sham: ∆−2±2 vs. IME 40%: ∆−6±2ml, p=0.13). Both sessions did not change SBP, DBP, MBP, CO, and TPR, but we observed a greater increase in HR in the IME 40% session. Only the Sham session decreased SV. Keywords: Breathing Exercises; Hemodynamics; Young Adult
... Aortic reservoir function assessed by WIA is a predictor of cardiovascular events in patients with systemic arterial hypertension [21,22]. In the pulmonary circulation, several small human studies have explored the utility of WIA and reservoir-wave analysis, in PAH and chronic thromboembolic PH [23][24][25][26], but none have used WIA and cardiovascular magnetic resonance (CMR) to assess the effect of PH on cardiopulmonary physiology. ...
... In our study, PH patients had a significantly reduced pulmonary compliance and prominent reflected waves within the pulmonary circulation compared to non-PH patients. Our findings are in agreement with previous data from animal models [32,33] and human studies [25,34,35]. In our cohort, wave speed in the PA was correlated to haemodynamic parameters, including mean PA pressure and PVR, but also to the distensibility of the MPA. ...
... Our findings also provide physiological explanation to characteristic findings of PH on non-invasive imaging modalities, building on insights from previous studies [25,32,33,35,36]. The short acceleration time in pulmonary flow seen on echocardiography and CMR in these patients [33,37] relates to the prominent FCW in early systole, a marker of rapid early systolic flow acceleration. ...
Article
Full-text available
Background Right ventricular (RV) coupling to the pulmonary circulation influences the response of the RV to the increased afterload caused by pulmonary hypertension (PH), which ultimately determines prognosis. A methodology that accounts for pulsatile flow is required when assessing ventriculo-arterial coupling. We applied wave intensity analysis (WIA) methods to assess the compliance of the main pulmonary artery (PA) in patients with or without PH and compared this to PA distensibility, RV function and clinical outcomes. Methods High-fidelity blood pressure and Doppler flow velocity tracings were obtained simultaneously during cardiac catheterisation for suspected PH. RV volumes, main PA distensibility and ventriculo-arterial coupling (Emax/Ea) were analysed utilising cardiovascular magnetic resonance. Results The study included 17 PH patients and 6 controls. Wave speed, reservoir and excess pressure were higher in PH patients compared to controls (p < 0.01 for all). Waveforms relating to RV ejection, microvascular wave reflection and late systolic proximal deceleration were higher in PH patients compared to controls (p < 0.01 for all) and related to echocardiographic findings, including PA Doppler notching and shortened acceleration time. Wave speed, reservoir pressure and excess pressure were strongly correlated to main PA distensibility, RV function and Emax/Ea. A higher total pressure integral was associated with an increased risk of death (all-cause mortality). Conclusion The reservoir-excess pressure model, in combination with conventional clinical imaging, provides valuable information on the pathophysiology of PH that standard haemodynamic parameters do not. Future studies should further investigate the prognostic implications of WIA in PH, and its potential role in clinical practice.
... Recently, several studies have reported that PAWR might influence right ventricular afterload and provide additional information regarding the severity and progression of PH [13][14][15][16][17]. The pulmonary artery (PA) blood flow consists of two waves; forward and reflection. ...
Article
Full-text available
Pulmonary hypertension (PH) is a complex syndrome that has been frequently diagnosed in dogs and humans and can be detected by Doppler echocardiography and invasive catheterization. Recently, PAWR attracts much attention as a noninvasive approach for the early detection of PH. The present study aims to investigate the PAWR changes in acute pulmonary embolism (APE) and highlight the response of PAWR variables to vasodilator therapy in dogs. For this purpose, anesthesia and catheterization were performed in 6 Beagle dogs. After that, APE was experimentally conducted by Dextran microsphere administration, followed by vasodilator (Nitroprusside; 1μg/kg/min/IV) administration. The hemodynamics, echocardiography, PVR and PAWR variables were evaluated at the baseline, after APE and after administration of nitroprusside. The result showed a significant increase in PVR, PAP, tricuspid regurgitation (TR) as well as PAWR variables following APE induction compared with the baseline (p < 0.05). Vasodilation caused by administration of nitroprusside reduced the mean atrial pressure, PVR and PAWR parameters. There were a significant correlation and linear regression between PAWR indices and PVR as well as right ventricular function parameters. In conclusion, PAWR is not only correlated with PVR but also the right ventricular function parameter, which indicates that PAWR may be useful as a new evaluation method in PH, considering that PAWR can assess both right ventricular afterload and right ventricular function.
... Sundblad et al. [52], who studied subjects during rest and leg exercise, as they were suddenly tilted from upright to supine, found an initial drop in SV, which they attributed to ventricular interdependence [15,[50][51][52]. Moreover, pulmonary circulation, a remarkable blood reservoir, may act as a buffer [53], further attenuating the effect of venous return on left ventricular contraction. On the other hand, Elstad et al. [43], who performed exercise with small proximal muscle masses, stressed the role of muscle vasodilation and the ensuing rapid TPR fall in determining the φ1 increase in SV. ...
Article
Full-text available
We hypothesised that vagal withdrawal and increased venous return interact in determining the rapid cardiac output (CO) response (phase I) at exercise onset. We used lower body negative pressure (LBNP) to increase blood distribution to the heart by muscle pump action and reduce resting vagal activity. We expected a larger increase in stroke volume (SV) and smaller for heart rate (HR) at progressively stronger LBNP levels, therefore CO response would remain unchanged. To this aim ten young, healthy males performed a 50 W exercise in supine position at 0 (Control), −15, −30 and −45 mmHg LBNP exposure. On single beat basis, we measured HR, SV, and CO. Oxygen uptake was measured breath-by-breath. Phase I response amplitudes were obtained applying an exponential model. LBNP increased SV response amplitude threefold from Control to −45 mmHg. HR response amplitude tended to decrease and prevented changes in CO response. The rapid response of CO explained that of oxygen uptake. The rapid SV kinetics at exercise onset is compatible with an increased venous return, whereas the vagal withdrawal conjecture cannot be dismissed for HR. The rapid CO response may indeed be the result of two independent yet parallel mechanisms, one acting on SV, the other on HR.
... Also, arterial aging and pathologies (e.g. hypertension) affect both the magnitude and timing of arterial reflected waves and, therefore, the features of the pressure waveform (3,4). ...
... WIA was performed essentially as described previously, 2 but values were normalized to cardiac cycle length to make it independent of sampling rate. 20 With the knowledge of the local wave speed, waves were separated into their forward (shown as WI + ) and backward (shown as WI À ) components (Equation 6): ...
... ACEI indicates angiotensinconverting enzyme inhibitor; BMI, body mass index; Cp, global pulmonary compliance; CTEPH, chronic thromboembolic pulmonary hypertension; DBP, diastolic blood pressure; PA, pulmonary artery; PAH, pulmonary arterial hypertension; PAPd, diastolic pulmonary arterial pressure; PAPm, mean pulmonary arterial pressure; PAPs, systolic pulmonary arterial pressure; PDE-5, phosphodiesterase type 5; RV, right ventricle; SBP, systolic blood pressure; TPR, total pulmonary resistance; WU, wood unit. *Previously published data.20 ...
Article
Full-text available
Background In contrast to systemic hypertension, the significance of arterial waves in pulmonary hypertension (PH) is not well understood. We hypothesized that arterial wave energy and wave reflection are augmented in PH and that wave behavior differs between patients with pulmonary arterial hypertension (PAH) and chronic thromboembolic pulmonary hypertension (CTEPH). Methods and Results Right heart catheterization was performed using a pressure and Doppler flow sensor–tipped catheter to obtain simultaneous pressure and flow velocity measurements in the pulmonary artery. Wave intensity analysis was subsequently applied to the acquired data. Ten control participants, 11 patients with PAH, and 10 patients with CTEPH were studied. Wave speed and wave power were significantly greater in PH patients compared with controls, indicating increased arterial stiffness and right ventricular work, respectively. The ratio of wave power to mean right ventricular power was lower in PAH patients than CTEPH patients and controls. Wave reflection index in PH patients (PAH: ≈25%; CTEPH: ≈30%) was significantly greater compared with controls (≈4%), indicating downstream vascular impedance mismatch. Although wave speed was significantly correlated to disease severity, wave reflection indexes of patients with mildly and severely elevated pulmonary pressures were similar. Conclusions Wave reflection in the pulmonary artery increased in PH and was unrelated to severity, suggesting that vascular impedance mismatch occurs early in the development of pulmonary vascular disease. The lower wave power fraction in PAH compared with CTEPH indicates differences in the intrinsic and/or extrinsic ventricular load between the 2 diseases.
Article
Full-text available
The literature on hemodynamic responses during inspiratory muscle exercise (IME) lacks a consensus. To evaluate and compare hemodynamic responses during an IME session with and without resistive load, 15 sedentary men were subjected to two randomized IME sessions: one with 40% of maximal inspiratory pressure (IME 40%) and another without a resistive load (Sham), both of which were performed for two minutes over eight sessions with one-minute intervals. Systolic blood pressure (SBP), diastolic blood pressure (DBP), mean blood pressure (MBP), total peripheral resistance (TPR), stroke volume (SV), cardiac output (CO), and heart rate (HR) were measured by infrared digital photoplethysmography during five basal minutes and during the IME sessions. One-way analysis of variance and the Student’s t test for paired data were used to analyze hemodynamic response and delta values between sessions. Effect size was evaluated by Cohen’s D. A 5% significance level was adopted. SBP responses (sham: ∆−1±2 vs. 40%: ∆−4±2mmHg, p=0.27), DBP (sham: ∆2±1 vs. 40%: ∆1±2mmHg, p=0.60) and MBP (sham: ∆2±1 vs. 40%: ∆0±2mmHg, p=0.28) were similar between sessions. HR increases were higher in the 40% IME session than in the sham session (sham: ∆9±2 vs. 40%: ∆3±2bpm, p=0.001). SV only decreased during the sham session but responses were similar between sessions (sham: ∆−2±2 vs. IME 40%: ∆−6±2ml, p=0.13). Both sessions did not change SBP, DBP, MBP, CO, and TPR, but we observed a greater increase in HR in the IME 40% session. Only the Sham session decreased SV. Keywords: Breathing Exercises; Hemodynamics; Young Adult
Article
High wave speed and large wave reflection in the pulmonary artery have previously been reported in patients with chronic thromboembolic pulmonary hypertension (CTEPH). We assessed the impact of pulmonary endarterectomy (PEA) on pulmonary arterial wave propagation and reservoir function in CTEPH patients. Right heart catheterization was performed using a combined pressure and Doppler flow sensor tipped guidewire to obtain simultaneous pressure and flow velocity measurements in the pulmonary artery in eight CTEPH patients before and 3 months after PEA. Wave intensity and reservoir-excess pressure analyses were then performed. Following PEA, mean pulmonary arterial pressure (PAPm, ~49 versus ~32 mmHg), pulmonary vascular resistance (PVR, ~11.1 versus ~5.1 Wood Units) and wave speed (~16.5 versus ~8.1 m/s), i.e. local arterial stiffness, markedly decreased. The changes in the intensity of the reflected arterial wave and wave reflection index (pre: ~28%; post: ~22%) were small and post-PEA patients with and without residual pulmonary hypertension (i.e. PAPm ≥25 mmHg) had similar wave reflection index (~20 versus ~23%). The reservoir and excess pressure decreased post-PEA and the changes were associated with improved right ventricular afterload, function and size. In conclusion, while PVR and arterial stiffness decreased substantially following PEA, large wave reflection persisted, even in patients without residual pulmonary hypertension, indicating lack of improvement in vascular impedance mismatch. This may continue to affect the optimal ventriculo-arterial interaction and further studies are warranted to determine whether this contributes to persistent symptoms in some patients.
Article
Full-text available
Arterial stiffness and wave reflection are important components of the ventricular afterload. Therefore, we aimed to assess the arterial wave characteristics and mechanical properties of the proximal pulmonary arteries (PAs) in the hypoxic pulmonary hypertensive rat model. After 21 days in normoxic or hypoxic chambers (24 animals/group), animals underwent transthoracic echocardiography and PA catheterization with a dual-tipped pressure and Doppler flow sensor wire. Wave intensity analysis was performed. Artery rings obtained from the pulmonary trunk, right and left PAs, and aorta were subjected to a tensile test to rupture. Collagen and elastin content were determined. In hypoxic rats, proximal PA wall thickness, collagen content, tensile strength per unit collagen, maximal elastic modulus, and wall viscosity increased, whereas the elastin-to-collagen ratio and arterial distensibility decreased. Arterial pulse wave velocity was also increased, and the increase was more prominent in vivo than ex vivo. Wave intensity was similar in hypoxic and normoxic animals with negligible wave reflection. In contrast, the aortic maximal elastic modulus remained unchanged, whereas wall viscosity decreased. In conclusion, there was no evidence of altered arterial wave propagation in proximal PAs of hypoxic rats while the extracellular matrix protein composition was altered and collagen tensile strength increased. This was accompanied by altered mechanical properties in vivo and ex vivo. NEW & NOTEWORTHY In rats exposed to chronic hypoxia, we have shown that pulse wave velocity in the proximal pulmonary arteries increased and pressure dependence of the pulse wave velocity was steeper in vivo than ex vivo leading to a more prominent increase in vivo.