Ramping Up the Pressure on the Right Ventricle.

Abstract

HomeCirculation: Heart FailureVol. 15, No. 6Ramping Up the Pressure on the Right Ventricle Free AccessResearch ArticlePDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyRedditDiggEmail Jump toFree AccessResearch ArticlePDF/EPUBRamping Up the Pressure on the Right Ventricle Simone L. Savaris, MD, MSc, Isaac S. Chang, PhD, Stephen P. Wright, MSc, PhD and Susanna Mak, MD, PhD Simone L. SavarisSimone L. Savaris Correspondence to: Simone L. Savaris, MD, MSc, Division of Cardiology, Mount Sinai Hospital, 600 University Ave, Toronto, ON M5G 1X5, Canada. Email E-mail Address: [email protected] https://orcid.org/0000-0002-9049-1805 Division of Cardiology, Mount Sinai Hospital, Toronto, ON, Canada (S.L.S., S.M.). Search for more papers by this author , Isaac S. ChangIsaac S. Chang Mount Sinai Hospital, Toronto, ON, Canada (I.S.C.). Search for more papers by this author , Stephen P. WrightStephen P. Wright Centre for Heart, Lung, and Vascular Health, School of Health and Exercise Sciences, University of British Columbia, Kelowna, Canada (S.P.W.). Search for more papers by this author and Susanna MakSusanna Mak https://orcid.org/0000-0003-2193-602X Division of Cardiology, Mount Sinai Hospital, Toronto, ON, Canada (S.L.S., S.M.). Search for more papers by this author Originally published21 Apr 2022https://doi.org/10.1161/CIRCHEARTFAILURE.122.009671Circulation: Heart Failure. 2022;15Other version(s) of this articleYou are viewing the most recent version of this article. Previous versions: April 21, 2022: Ahead of Print A 49-year-old man underwent Heartmate 3 left ventricular assist device implantation as bridge to transplant candidacy for cardiogenic shock due to an ischemic cardiomyopathy which was complicated by a flail mitral valve leaflet resulting in severe regurgitation.Right heart catheterization was performed to assess residual pulmonary hypertension. Right ventricular (RV) and pulmonary artery (PA) pressures were recorded continuously. At baseline, mean PA pressure was 24 mm Hg and pulmonary vascular resistance was 3.0 WU at a speed of 5600 rpm. PA wedge pressure was altered by adjusting speed from 4600 to 5800 rpm. Further increases in speed did not change hemodynamics. Vasoreactivity testing with sodium nitroprusside was also used, based on recent evidence that even mildly elevated PA loading confers increased mortality risk.1,2 Pmax, a theoretical maximal RV systolic pressure derived by extrapolating the isovolumic portions of the waveform, was averaged over 10 cardiac cycles to calculate a single-beat estimate of RV end-systolic elastance, along with PA elastance and the end-systolic elastance:elastance ratio.3The incremental decline in the PA wedge pressure with attenuation of the V wave can be seen as left ventricular assist device speed was increased, and then with infusion of the vasodilator sodium nitroprusside (Figure and Table from left to right). Concomitant reductions in PA pressure and elastance were associated with shortening of the time to peak RVSP, and improved RV-PA coupling as reflected by increasing end-systolic elastance:elastance ratio. Importantly, mixed venous O2 saturation, stroke volume, and cardiac output increased steadily with afterload reduction.Table. Hemodynamics and Values Derived From Single-Beat Estimation of the Ees:Ea RatioUnsupportedRelatively unsupportedBaselineSNP (0.75 μg/kg per min)SNP (1.5 μg/kg per min)Speed4600 rpm5000 rpm5600 rpm5600 rpm5600 rpmMAP, mm Hg9492969065PAWP (a/v/mean), mm Hg18/37/1817/35/1710/24/1011/28/115/9/3PAP (S/D/M), mm Hg51/14/3047/13/2941/10/2441/9/2432/5/17RAP, mm Hg44320PVR, d/s per cm5192200240176168SVR, d/s per cm51532143613781193765MVO2, %61.663.365.168.573.3CO, L/min4.74.95.45.96.8SVi, mL/m2 per beat3941454955RVSP, mm Hg4946424334Time to RVSP, ms318226221210146Pmax, mm Hg166136143147142Ea, mm Hg/mL0.60.470.370.340.2Ees:Ea ratio2.72.73.63.76.7CO indicates cardiac output; Ea, pulmonary artery arterial elastance; Ees, RV end-systolic elastance; MAP, mean arterial pressure; MVO2, mixed venous oxygen saturation; PAP, pulmonary artery pressure; PAWP, pulmonary artery wedge pressure; Pmax, maximal predicted RV pressure; PVR, pulmonary vascular resistance; RAP, right atrium pressure; RV, right ventricle; RVSP, right ventricle systolic pressure; SNP, sodium nitroprusside; SVi, stroke volume index; and SVR, systemic vascular resistance.Download figureDownload PowerPointFigure. The figure shows that with alterations in speed and with a vasodilator challenge (from left to right), pulmonary artery wedge pressure (PAWP) and pulmonary artery pressure (PAP) declined, with measurable changes in the morphology of the right ventricular pressure (RVP) waveform. Pmax, the theoretical maximal RVP, and graphical representations of the coordinates employed for single-beat estimation of RV end-systolic elastance (Ees) are also illustrated. Ea indicates pulmonary artery arterial elastance; Pes, estimated end-systolic pressure; Pmax, maximal predicted RVP; RVSP, right ventricle systolic pressure; SNP, sodium nitroprusside; and SV, stroke volume.This case reinforces the effect of systemic vasodilation and venodilation to optimize hemodynamics in the setting of heart failure with reduced ejection fraction, mitral regurgitation, and a continuous flow left ventricular assist device. The upstream effects of adequate unloading of the left ventricle to improve the function of the RV-PA circulatory unit are also illustrated.Article InformationSources of FundingNone.Disclosures None.FootnotesFor Sources of Funding and Disclosures, see page 645.Correspondence to: Simone L. Savaris, MD, MSc, Division of Cardiology, Mount Sinai Hospital, 600 University Ave, Toronto, ON M5G 1X5, Canada. Email simonelouise.[email protected]ca