Pulmonary Artery Pressure Waveform Research Articles

Impact of respiratory cycle during mechanical ventilation on beat-to-beat right ventricle stroke volume estimation by pulmonary artery pulse wave analysis.

The same principle behind pulse wave analysis can be applied on the pulmonary artery (PA) pressure waveform to estimate right ventricle stroke volume (RVSV). However, the PA pressure waveform might be influenced by the direct transmission of the intrathoracic pressure changes throughout the respiratory cycle caused by mechanical ventilation (MV), potentially impacting the reliability of PA pulse wave analysis (PAPWA). We assessed a new method that minimizes the direct effect of the MV on continuous PA pressure measurements and enhances the reliability of PAPWA in tracking beat-to-beat RVSV. Continuous PA pressure and flow were simultaneously measured for 2-3min in 5 pigs using a high-fidelity micro-tip catheter and a transonic flow sensor around the PA trunk, both pre and post an experimental ARDS model. RVSV was estimated by PAPWA indexes such as pulse pressure (SVPP), systolic area (SVSystAUC) and standard deviation (SVSD) beat-to-beat from both corrected and non-corrected PA signals. The reference RVSV was derived from the PA flow signal (SVref). The reliability of PAPWA in tracking RVSV on a beat-to-beat basis was enhanced after accounting for the direct impact of intrathoracic pressure changes induced by MV throughout the respiratory cycle. This was evidenced by an increase in the correlation between SVref and RVSV estimated by PAPWA under healthy conditions: rho between SVref and non-corrected SVSD -0.111 (0.342), corrected SVSD 0.876 (0.130), non-corrected SVSystAUC 0.543 (0.141) and corrected SVSystAUC 0.923 (0.050). Following ARDS, correlations were SVref and non-corrected SVSD -0.033 (0.262), corrected SVSD 0.839 (0.077), non-corrected SVSystAUC 0.483 (0.114) and corrected SVSystAUC 0.928 (0.026). Correction also led to reduced limits of agreement between SVref and SVSD and SVSystAUC in the two evaluated conditions. In our experimental model, we confirmed that correcting for mechanical ventilation induced changes during the respiratory cycle improves the performance of PAPWA for beat-to-beat estimation of RVSV compared to uncorrected measurements. This was demonstrated by a better correlation and agreement between the actual SV and the obtained from PAPWA.

Feasibility of a Composite Measure of Pulmonary Vascular Impedance and Application to Patients with Chronic RV Failure Post LVAD Implant.

Pulmonary vascular impedance (PVZ) describes RV afterload in the frequency domain and has not been studied extensively in LVAD patients. We sought to determine (1) feasibility of calculating a composite (c)PVZ using standard of care (SoC), asynchronous, pulmonary artery pressure (PAP) and flow (PAQ) waveforms; and (2) if chronic right ventricular failure (RVF) post-LVAD implant was associated with changes in perioperative cPVZ.PAP and PAQ were obtained via SoC procedures at three landmarks: T(1), Retrospectively, pre-operative with patient conscious; and T(2) and T(3), prospectively with patient anesthetized, and either pre-sternotomy or chest open with LVAD, respectively. Additional PAP's were taken at T(4), following chest closure; and T(5), 4-24h post chest closure. Harmonics (z) were calculated by Fast Fourier Transform (FFT) with cPVZ(z) = FFT(PAP)/FFT(PAQ). Total pulmonary resistance Z(0); characteristic impedance Zc, mean of cPVZ(2-4); and vascular stiffness PVS, sum of cPVZ(1,2), were compared at T(1,2,3) between +/-RVF groups.Out of 51 patients, nine experienced RVF. Standard hemodynamics and changes in cPVZ-derived parameters were not significant between groups at any T.In conclusion, cPVZ calculated from SoC measures is possible. Although data that could be obtained were limited it suggests no difference in RV afterload for RVF patients post-implant. If confirmed in larger studies, focus should be placed on cardiac function in these subjects.

An artificial intelligence-based noninvasive solution to estimate pulmonary artery pressure.

AimsDesign to develop an artificial intelligence (AI) algorithm to accurately predict the pulmonary artery pressure (PAP) waveform using non-invasive signal inputs.Methods and resultsWe randomly sampled training, validation, and testing datasets from a waveform database containing 180 patients with pulmonary atrial catheters (PACs) placed for PAP waves collection. The waveform database consisted of six hemodynamic parameters from bedside monitoring machines, including PAP, artery blood pressure (ABP), central venous pressure (CVP), respiration waveform (RESP), photoplethysmogram (PPG), and electrocardiogram (ECG). We trained a Residual Convolutional Network using a training dataset containing 144 (80%) patients, tuned learning parameters using a validation set including 18 (10%) patients, and tested the performance of the method using 18 (10%) patients, respectively. After comparing all multi-stage algorithms on the testing cohort, the combination of the residual neural network model and wavelet scattering transform data preprocessing method attained the highest coefficient of determination R2 of 90.78% as well as the following other performance metrics and corresponding 95% confidence intervals (CIs): mean square error of 11.55 (10.22–13.5), mean absolute error of 2.42 (2.06–2.85), mean absolute percentage error of 0.91 (0.76–1.13), and explained variance score of 90.87 (85.32–93.31).ConclusionThe proposed analytical approach that combines data preprocessing, sampling method, and AI algorithm can precisely predict PAP waveform using three input signals obtained by noninvasive approaches.

A Novel Non-Invasive Method for Estimating Elevated Pulmonary Vascular Resistance Based on Echocardiographic Assessment of Pulmonary Artery Wave Reflection.

Several non-invasive methods for pulmonary vascular resistance (PVR) measurement are proposed, but none are sufficiently accurate for use in clinical practice. This study proposes a new echocardiographic method of pulmonary artery wave reflection and investigates its efficacy in managing patients with pulmonary hypertension.Methods and Results:In total, 83 patients with left heart disease, pulmonary arterial hypertension, and chronic thromboembolic pulmonary hypertension (CTEPH), who underwent Doppler echocardiography and right heart catheterization, were included in the study. Pulmonary artery wave reflection was characterized by separating the pulmonary artery pressure waveform into forward and backward (Pb) waves, based on wave intensity. Pulmonary artery pressure waveforms were estimated from continuous Doppler tracings of tricuspid regurgitation velocity, and flow velocity was measured using pulsed Doppler of the right ventricular outflow tract. Pb-peak was compared with catheter hemodynamic indices, and with PVR by Abbas 2003, 2013 and Haddad in relation to increased catheter PVR. Catheter PVR and Pb were strongly correlated (r=0.77, P<0.001). The areas under the receiver operator characteristic curve for Pb-peak, PVR by Abbas 2003, 2013 and Haddad were 0.91, 0.72, 0.80, and 0.80, respectively, and were used to detect an increase in PVR (>3 Woods units). This study describes a novel, simple, and non-invasive echocardiography method to assess pulmonary wave reflected pressure to identify patients with pulmonary hypertension due to increased PVR.

Ambulatory factors influencing pulmonary artery pressure waveforms and implications for clinical practice.

CardioMEMS, a remote pulmonary artery pressure monitoring system, provides waveform patterns for the ambulatory heart failure patient. These waveforms provide significant insights into patient volume and clinical management. We aim to provide a foundation for understanding the determinants of waveform characteristics and provide practical examples illustrating how to interpret and integrate common scenario waveforms into clinical decision-making. A total of three groups of relevant scenarios were included namely (a) location and activity at time of waveform transmission, (b) impact of contemporary interventions, and (c) arrhythmias. We illustrate that waveform analysis can be individualized to each patient's care strategy in the appropriate clinical context to help guide clinical decision-making.

Effects of a newly designed paediatric pulmonary heart valve on hemodynamic function

Congenital heart disease is one of the most common types of birth defect. If there is an obstruction of the right ventricular outflow tract, it is often necessary to provide a reconstruction of this outflow tract which is normally performed in the neonatal period. However, in Japan there is no commercially-available prosthetic valve of the appropriate size. Senior Assistant Professor Kenji Suzuki is a paediatric cardiac surgeon based within the Nippon Medical School Musashikosugi Hospital, Japan, who is working to develop a pulmonary valve prosthesis in the paediatric field. He and his team are working to develop a new design of pulmonary valve prosthesis that avoids dysfunction such as thrombus formation and reduced mobility of valve leaflets and the researchers are investigating the effects of a newly designed paediatric pulmonary heart valve on hemodynamic function. To do this, the team will construct a circulatory simulator that mimics the right heart system and measure the right ventricular pressure and pulmonary artery pressure waveform, which will enable them to calculate the regurgitation rate. The researchers will observe valve leaflet motion by video recording. In preliminary experiments, Suzuki and the team have already shown that the regurgitation rate and pressure gradient are lower than those of the prosthetic valve they previously developed and, looking ahead, the researchers plan to gather more data and fine-tune the structure.

Right ventricular and pulmonary artery pulse pressure variation and systolic pressure variation for the prediction of fluid responsiveness: an interventional study in coronary artery bypass surgery patients.

Predicting fluid responsiveness is essential when treating surgical or critically ill patients. When using a pulmonary artery catheter, pulse pressure variation and systolic pressure variation can be calculated from right ventricular and pulmonary artery pressure waveforms. We conducted a prospective interventional study investigating the ability of right ventricular pulse pressure variation (PPVRV) and systolic pressure variation (SPVRV) as well as pulmonary artery pulse pressure variation (PPVPA) and systolic pressure variation (SPVPA) to predict fluid responsiveness in coronary artery bypass (CABG) surgery patients. Additionally, radial artery pulse pressure variation (PPVART) and systolic pressure variation (SPVART) were calculated. The area under the receiver operating characteristics (AUROC) curve with 95%-confidence interval (95%-CI) was used to assess the capability to predict fluid responsiveness (defined as an increase in cardiac index of > 15%) after a 500 mL crystalloid fluid challenge. Thirty-three patients were included in the final analysis. Thirteen patients (39%) were fluid-responders with a mean increase in cardiac index of 25.3%. The AUROC was 0.60 (95%-CI 0.38 to 0.81) for PPVRV, 0.63 (95%-CI 0.43 to 0.83) for SPVRV, 0.58 (95%-CI 0.38 to 0.78) for PPVPA, and 0.71 (95%-CI 0.52 to 0.89) for SPVPA. The AUROC for PPVART was 0.71 (95%-CI 0.53 to 0.89) and for SPVART 0.78 (95%-CI 0.62 to 0.94). The correlation between pulse pressure variation and systolic pressure variation measurements derived from the different waveforms was weak. Right ventricular and pulmonary artery pulse pressure variation and systolic pressure variation seem to be weak predictors of fluid responsiveness in CABG surgery patients.

Pulmonary arterial wave reflection as a novel estimate of pulmonary vascular resistance

Abstract Funding Acknowledgements Type of funding sources: Public hospital(s). Main funding source(s): International Medical Research and Development Fund Background Measuring pulmonary vascular resistance (PVR) is essential for diagnosing pulmonary hypertension. PVR can be estimated from a simple ratio of tricuspid regurgitation velocity (TRV) to time-velocity integral of flow through right ventricular outflow tract (RVOT) (Abbas equation), but this relationship has been shown to be unreliable in patients with high PVR. Once PVR is elevated, there is an increased pressure wave reflected from the peripheral of pulmonary artery (PA). We tested the hypothesis that assessing PA wave reflection could be an alternative method for estimating PVR. Methods This study recruited 83 patients (69 ± 14 years old, 44 men), including 41 patients with left-sided heart disease, 23 patients with pulmonary arterial hypertension and 19 patients with chronic thromboembolic pulmonary hypertension. PA wave reflection was assessed by separating PA pressure waveform derived from a Doppler tracing of TRV into forward and backward pressure (Pf and Pb), using a velocity profile at RVOT. This separation was based on the concept of wave intensity. PVR was estimated using Abbas equation. Pb and PVR by Abbas equation were compared for the correlations with direct measurement of PVR by right heart catheterisation within 48 hours after echocardiography. Results Figure A illustrates Pb and Pf waveforms obtained from a patient with chronic thromboembolic pulmonary hypertension. Pb increased from mid systole and formed a late peak of PA pressure waveform. Pb correlated strongly with PVR by catheter (figure B), whereas PVR by Abbas equation underestimated PVR especially when PVR was high, resulting in a moderate correlation (figure C). Receiver-operator characteristic curves showed a higher accuracy of Pb for identifying PVR &amp;gt; 3WU as well as 6WU, compared with PVR by Abbas equation (figure D and E). Conclusions This novel echocardiographic method for assessing PA wave reflection helps diagnose the severity of pulmonary hypertension. Abstract Figure.

Damage to Pulmonary Artery Catheter in Cardiac Surgery Causing Inadequate Pulmonary Artery Pressure Waveform

Damage to Pulmonary Artery Catheter in Cardiac Surgery Causing Inadequate Pulmonary Artery Pressure Waveform

Implementing CardioMEMS Monitoring and Interventions into Clinical Practice

Heart failure is a complex clinical syndrome and its management can be challenging. Recurrent hospitalizations cannot always be avoided and the mortality and morbidity rates in this population are higher with each hospital admission. Current technological advances have focused on exploring intra-vascular or intra-cardiac devices as an option to monitor hemodynamics remotely in patients with heart failure to guide and optimize their medical therapy. This review discusses the implementation of the CardioMEMS monitoring system and its use into clinical practice in patients with heart failure. Over time, several devices have been studied to monitor hemodynamics in heart failure patients. The CardioMEMS is the only monitoring technology that has demonstrated the ability to significantly reduce heart failure hospitalizations approved by the FDA. Research has showed that it could potentially lead to improved outcomes through hemodynamic guidance of medical therapy in this population. Data collected by the device includes pulmonary artery (PA) pressure values (systolic, diastolic, and mean), PA pressure wave forms, and heart rate. Information is sent remotely to physicians via a secure web-based site. After a provider analyzes the information, medication titration can be done according to the different PA readings. This approach has been very convenient for patients and physicians since patients do not need to undergo repeat invasive hemodynamic testing in order to obtain intracardiac pressures. The CardioMEMS system has showed promising results in heart failure patients and there are encouraging signs that it might be of benefit in special populations such as patient with ventricular assist devices and pulmonary hypertension. Heart failure is a major public health issue generating increasing annual costs in the United States health care system every year. Pulmonary artery pressure monitoring with the CardioMEMS monitoring system can help physicians tailor medical therapy in patients with heart failure remotely. Monitoring patients in the outpatient setting could reduce the need for hospitalizations for acute decompensated heart failure; and hence, reduce the mortality and morbidity rates in this population.

Significance and prognostic impact of v wave on pulmonary artery pressure in patients with heart failure: beyond the wedge pressure

A v wave on pulmonary artery wedge (PAW) pressure sometimes augments and appears on pulmonary artery (PA) pressure wave in patients with heart failure (HF). However, the significance of PA v wave in HF remains to be elucidated. We retrospectively analyzed pressure waveforms in 61 HF patients (left ventricular ejection fraction 35 ± 15%). On the PAW and PA pressure waveforms, mean pressure as well as peak and amplitude of v waves (ampPAWv and ampPAv, respectively) were measured. Occurrence of worsening HF and cardiac death was recorded for 2years after the catheterization. The ampPAWv did not correlate with ampPAv. When the patients were divided into 4 groups: I (high-ampPAWv/high-ampPAv), II (high-ampPAWv/low-ampPAv), III (low-ampPAWv/high-ampPAv), and IV (low-ampPAWv/low-ampPAv), the prevalence of group III was low (I: 13, II: 17, III: 4, IV: 27). Mean pressures of PAW and PA were similarly elevated in groups I and II. Cardiac index was lowest (I: 2.0 ± 0.4, II: 2.8 ± 0.6, III: 2.2 ± 0.2, IV: 2.4 ± 0.6L/min/m2, ANOVA P < 0.01, P < 0.01 for I vs II) and tricuspid annular plane systolic excursion / systolic PA pressure was impaired (I: 0.27 ± 0.07, II: 0.48 ± 0.22, III: 0.59 ± 0.35, IV: 0.68 ± 0.35mm/mmHg, ANOVA P < 0.01) in group I. During the follow-up, 13 events were observed. Kaplan-Meier analysis showed that patients in group I were at highest risk of cardiac events. PA v was observed mainly in patients with augmented PAW v wave and decreased cardiac index, suggesting an advanced stage of HF. Moreover, augmented PAv was associated with worse outcome in HF patients.

Towards a Multi‐Scale Model of Ventilation‐Perfusion Matching

Ventilation‐Perfusion (V/Q) matching is a critical determinant of efficient gas exchange in the pulmonary circulation. The regulatory mechanisms that control V/Q matching under normal and pathological scenarios are incompletely understood. In this study we present the derivation and validation of a multi‐scale computer model of hemodynamics and gas exchange accounting for the fractal‐like pattern of pulmonary vascular branching, mechanical coupling of blood‐tissue interactions, gas exchange, hemoglobin biochemistry, and vasoregulatory mechanisms. By simulating the regional distribution of V/Q ratios, this model serves as an in‐silico platform to test and refine hypotheses regarding the contributions of vasoregulatory mechanisms to regional perfusion and V/Q matching in the lung. Figure 1 depicts the various model “blocks” and how they are interconnected. The complete model is formulated as an algebraically constrained system of ordinary and partial differential equations and is parameterized to represent function in an adult Sprague Dawley rat. Block (A) illustrates the whole‐lung vascular network model. The network geometry is generated by a space‐filling algorithm and is validated by comparing anatomical predications (length, radius, and connectivity) to morphometric data (from existing literature). Block (B) shows how the mechanics of each vessel segment is represented as a lumped system. Mechanics are validated by comparing model predictions to macro‐scale pressure‐flow relationships and pulmonary artery pressure waveforms (from existing literature and our own in vivo studies). Block (C) depicts a representative gas exchange unit. Block (D) portrays oxygen‐sensitive vasoregulatory mechanisms that have been implicated in the maintenance of pulmonary vasomotor tone. Model simulations illustrate that perfusion heterogeneity is governed by the geometry of the vascular tree, and local interaction between alveolar and vascular pressures. Moreover, conducted vascular responses (hypoxic pulmonary vasoconstriction, and the hypoxia‐mediated/mechanically‐transduced release of ATP from red blood cells) modulate the redistribution of blood flow in response to pathological insults such as a pulmonary embolism. Taken together, our results suggest that more homogenous blood flow distributions increase the bulk oxygen content entering the systemic circulation.Support or Funding InformationNIH/NINDS R01 NS087147NIH/NHLBI R01 HL127151This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

ABNORMAL RIGHT VENTRICULAR - PULMONARY VASCULAR COUPLING AT REST AND EXERCISE IN PATIENTS WITH DYSPNEA OF UNKNOWN ORIGIN AND/OR SUSPECTED PULMONARY HYPERTENSION

Exercise during right heart catheterization (RHC) is employed in select centers to demonstrate the extent to which pulmonary artery (PA) hemodynamics and/or left heart filling pressures may be abnormal. Both lesions may increase the effective PA elastance (Ea), which is a measure of afterload to the right ventricle (RV) as it ejects during systole. RV contractile performance can be expressed as the RV end-systolic elastance (Ees), and the ratio of Ees:Ea reflects ventricular-vascular coupling. We examined the Ees:Ea ratio at rest and during exercise in patients with dyspnea and/or suspected pulmonary hypertension, grouped by their exercise hemodynamic classification. Patients referred for an exercise hemodynamic study underwent a submaximal cycle-ergometry challenge during diagnostic RHC. RV and PA pressures were simultaneously transduced, and thermodilution cardiac output was determined. The RV and PA pressure waveforms were analyzed offline to determine Ees using the single-beat method and calculate Ea as [mean PA pressure/stroke volume]. Exercise hemodynamic classifications have been defined a priori by our laboratory from previous prospective studies of exercise hemodynamics in healthy volunteers. Exercise hemodynamic classifications include: 1) left heart disease (Ex-LHD) based on an increased slope of the PA wedge pressure/cardiac output relationship; 2) pulmonary vascular disease (Ex-PVD) based on an elevated end-diastolic pulmonary pressure gradient; 3) combined (Ex-CPH) if both criteria are met; 4) hemodynamically Ex-Normal if neither criteria are met. Preliminary data and descriptive statistics were available for 42 consecutive patients (17M/25F; Age = 58±15); exercise hemodynamic classifications comprised 14 Ex-Normal, 15 Ex-LHD, 8 Ex-PVD, and 5 Ex-CPH. At baseline, mPAP ≥25 mmHg was present in 0/14 Ex-Normal, 5/15 Ex-LHD, 5/8 Ex-PVD, and 5/5 Ex-CPH (Table 1). Ex-LHD had similar Ees and modestly higher Ea compared to Ex-Normal. Ex-PVD had substantially higher Ees and Ea compared to Ex-Normal. Ex-PVD also had substantially higher Ees and Ea compared to Ex-LHD. However, Ees:Ea appeared similarly depressed in both Ex-LHD and Ex-PVD compared to Normal. This was despite normal pulmonary pressures at baseline in Ex-LHD. During exercise, Ees:Ea appeared to augment modestly in Ex-Normal, but remained stable in other groups (Figure 1). Systolic RV performance augmented in proportion with increased load during exercise; however, less favorable ventricular-vascular coupling in patients with pulmonary vascular and/or left heart disease persisted during exercise. Despite mostly normal at rest hemodynamics, ventricular-vascular coupling appears abnormal in patients with left heart disease exposed by exercise.View Large Image Figure ViewerDownload Hi-res image Download (PPT)

0985. Open lung ventilation improves conditions for right ventricle performance by decreasing pulmonary vascular wave reflections in an experimental model of ARDS

Impaired right ventricle (RV) function is associated with worse outcome in ARDS. Pulmonary artery pressure waveform analysis provides information about phenomena that affect RV performance. In particular, pulmonary vascular wave reflection (WR) is directly related with RV stress. We hypothesised that open lung ventilation (OLV), compared with conventional ARDS-net ventilation (CV), would improve conditions for RV performance in an ARDS model. This hypothesis was tested by measuring pulmonary vascular wave reflection (WR).

Cryoballoon pressure waveform change during balloon inflation is not a reliable predictor of adequate pulmonary vein occlusion.

Cryoballoon ablation of pulmonary veins (PVs) is widely used to treat atrial fibrillation (AF). Successful ablation requires occluding the PVs by cryoballoon. Angiography is a standard method of assessing PV occlusion. To decrease contrast doses and overcome potential contraindications (e.g., allergy to contrast, renal disease), alternative methods have been tested, including intracardiac echocardiography, transesophageal echocardiography-color flow Doppler, and distal cryoballoon pressure monitoring. We evaluated pressure monitoring’s accuracy in detecting PV occlusion during cryoballoon ablation. We studied 72 PVs in 18 nonconsecutive patients (mean age 68 ± 8 years; 13 male) who underwent cryoballoon ablation for paroxysmal AF. In 67 PVs, we documented the point at which the recorded pressure waveform at the distal tip of the inflated cryoballoon transformed from a left atrial into a pulmonary arterial pressure waveform. PV occlusion was confirmed by concurrent PV angiography through the distal balloon channel. Occlusion was rated on a I–IV scale in which I indicated poor occlusion with major leakage and IV indicated complete occlusion without leakage. In 43 of 67 PVs (64%), the change in the pressure waveform from left atrial to pulmonary arterial was associated with complete PV occlusion (grade IV), confirmed by angiography. In the other 24 PVs, complete occlusion was achieved by further movement of the cryoballoon under intracardiac echocardiographic guidance and angiographic confirmation. All 67 PVs were electrically isolated with cryoballoon. The change in pressure waveforms at the distal tip of inflated cryoballoon is not a reliable predictor of complete PV occlusion during cryoballoon ablation.

Hemodynamic Monitoring in the ICU

This review examines the most commonly used hemodynamic monitoring devices in the intensive care unit. After a brief review of some important issues in hemodynamic monitoring, a variety of monitoring systems are considered, including arterial catheters, pulmonary artery catheters (PACs), less invasive hemodynamic monitors, central venous oxygen saturation (ScvO2) monitors, and point-of-care (POC) echocardiography. For each system, the basic operating principles, indications and limitations of use, complications, key issues in data interpretation, and evidence regarding utility in patient care are reviewed. Figures depict the distinction between correlation and agreement, a representative Bland-Altman plot, a square wave test, PAC waveforms, principles of pulmonary artery occlusion pressure measurement, measuring pulmonary artery occlusion pressure at end-exhalation, right atrial and ventricular pressure waveform, pulmonary artery pressure waveform, potential pulmonary artery occlusion waveforms, west zones of the lung and the pulmonary artery occlusion pressure measurements, and POC echocardiography. Tables outline landmarks during insertion of the PAC from the internal jugular and subclavian vein insertion sites; indications, contraindications, and complications of PAC insertion; a comparison of less invasive hemodynamic monitors; reasons for decreased mixed or ScvO2; and indications and contraindications for transesophageal echocardiography. This review contains 12 highly rendered figures, 7 tables, and 95 references.

Beat-to-beat estimation of the continuous left and right cardiac elastance from metrics commonly available in clinical settings

IntroductionFunctional time-varying cardiac elastances (FTVE) contain a rich amount of information about the specific cardiac state of a patient. However, a FTVE waveform is very invasive to directly measure, and is thus currently not used in clinical practice. This paper presents a method for the estimation of a patient specific FTVE, using only metrics that are currently available in a clinical setting.MethodCorrelations are defined between invasively measured FTVE waveforms and the aortic and pulmonary artery pressures from 2 cohorts of porcine subjects, 1 induced with pulmonary embolism, the other with septic shock. These correlations are then used to estimate the FTVE waveform based on the individual aortic and pulmonary artery pressure waveforms, using the “other” dysfunction’s correlations as a cross validation.ResultsThe cross validation resulted in 1.26% and 2.51% median errors for the left and right FTVE respectively on pulmonary embolism, while the septic shock cohort had 2.54% and 2.90% median errors.ConclusionsThe presented method accurately and reliably estimated a patient specific FTVE, with no added risk to the patient. The cross validation shows that the method is not dependent on dysfunction and thus has the potential for generalisation beyond pulmonary embolism and septic shock.

Algorithmic processing of pressure waveforms to facilitate estimation of cardiac elastance

BackgroundCardiac elastances are highly invasive to measure directly, but are clinically useful due to the amount of information embedded in them. Information about the cardiac elastance, which can be used to estimate it, can be found in the downstream pressure waveforms of the aortic pressure (Pao) and the pulmonary artery (Ppa). However these pressure waveforms are typically noisy and biased, and require processing in order to locate the specific information required for cardiac elastance estimations. This paper presents the method to algorithmically process the pressure waveforms.MethodsA shear transform is developed in order to help locate information in the pressure waveforms. This transform turns difficult to locate corners into easy to locate maximum or minimum points as well as providing error correction.ResultsThe method located all points on 87 out of 88 waveforms for Ppa, to within the sampling frequency. For Pao, out of 616 total points, 605 were found within 1%, 5 within 5%, 4 within 10% and 2 within 20%.ConclusionsThe presented method provides a robust, accurate and dysfunction-independent way to locate points on the aortic and pulmonary artery pressure waveforms, allowing the non-invasive estimation of the left and right cardiac elastance.

Assessment of right ventricular afterload by pressure waveform analysis in acute pulmonary hypertension

To characterize hydraulic right ventricle (RV) afterload by pulmonary arterial pressure waveform analysis in an acute pulmonary hypertension (PH) model. Pulmonary artery (PA) flow and pressure were recorded in six anesthetized sheep. Acute isobaric PH was induced by phenylephrine (active) and PA mechanical constriction (passive). We estimated the amplitude of the forward and reflected pressure waves according to the inflection point. In most cases the inflection pressure was smooth, thus the inflection point was defined as the time at which the first derivative of pulmonary arterial pressure reached its first minimum. We calculated the input and characteristic (Z(C), time-domain Li method) impedances, the capacitance index (stroke volume/pulse pressure), the augmentation index (AI) (reflected pressure/pulse pressure), the fractional pulse pressure (pulse pressure/mean pressure) and the wasted energy generated by the RV due to wave reflection during ejection (E(W)). Pulse pressure, fractional pulse pressure, AI and Z(C) increased and capacitance index decreased during passive PH with respect to control (P < 0.05). In contrast, Z(C) and the capacitance index did not change and E(W) and the AI decreased during active PH. Pulse pressure correlated with E(W) and Z(C) and the AI was correlated with E(W) (r > 0.6, P < 0.05). PA pressure waveform analysis allows the quantification of the dynamic RV afterload. Prospective clinical studies will be necessary to validate this time-domain approach to evaluate the dynamic RV afterload in chronic PH.

Doppler Echocardiography Can Provide a Comprehensive Assessment of Right Ventricular Afterload

The purpose of this study was to evaluate novel Doppler echocardiographic methods for a comprehensive assessment of right ventricular afterload, including pulmonary artery (PA) mean pressure (PAMP) and the PA pressure waveform. The study comprised 109 patients who underwent right-heart catheterization simultaneously (group A, n = 31) with Doppler echocardiography on 35 occasions or nonsimultaneously (group B, n = 78) within 24 hours of Doppler echocardiography. Right ventricular afterload variables were obtained using pulsed Doppler in the PA and continuous Doppler of tricuspid regurgitation. The intervals from QRS to the opening and closing of the pulmonary valve and to the peak velocity of tricuspid regurgitation were measured. PA end-diastolic pressure, PA systolic pressure, and PA notch pressure were calculated. The Doppler-derived pressure curve was separated into 3 parts with fitted second-order curves. Catheter PAMP and Doppler PA systolic pressure in group A were strongly related (R = 0.85). The regression equation from group A (PAMP = 0.65 x Doppler PA systolic pressure - 1.2 mm Hg) was used to calculate PAMP in group B. There was no difference between catheter PAMP (mean, 39 +/- 18 mm Hg; range, 8-95 mm Hg) and Doppler PAMP (mean, 39 +/- 15 mm Hg; range, 12-83 mm Hg) (P = .85). The systolic areas under the curves for catheter and Doppler PAMP in group A were 20 +/- 4.7 and 20 +/- 4.0 mm Hg s, respectively (P = .52), and the diastolic areas were 21 +/- 5.7 and 22 +/- 6.3 mm Hg s, respectively (P = .21). A comprehensive assessment of right ventricular afterload that includes PAMP and the PA pressure waveform can be provided by Doppler echocardiography in patients with a wide range of PA pressures and different diagnoses.