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. Author manuscript; available in PMC: 2021 Nov 1.
Published in final edited form as: Circ Heart Fail. 2020 Oct 3;13(11):e007981. doi: 10.1161/CIRCHEARTFAILURE.120.007981

Role of Pulmonary Artery Wedge Pressure Saturation During Right Heart Catheterization: A Prospective Study

Michael C Viray 1, Eric L Bonno 1, Nicholas D Gabrielle 1, Bradley A Maron 2, Jessica Atkins 1, Nicholas S Amoroso 1, Valerian LC Fernandes 1, Anbukarasi Maran 1, Christopher D Nielsen 1, Eric R Powers 1, Daniel H Steinberg 1, Thomas M Todoran 1, Thomas G Di Salvo 1, Gregory R Jackson 1, Brian A Houston 1, Ryan J Tedford 1
PMCID: PMC7674188  NIHMSID: NIHMS1634595  PMID: 33016102

Diagnosis and proper classification of PH is challenging. Even when gold-standard right heart catheterizations (RHC) are performed, PH is often misdiagnosed, resulting in inappropriate and potentially harmful treatment approaches.1 Additionally, the definition of PH has expanded recently, putting even more emphasis on accurate hemodynamic assessment during RHC.24 A critical component of the hemodynamic evaluation is measurement of pulmonary artery wedge pressure (PAWP) since this is the sole parameter that delineates pre-capillary PH (PCPH) from PH due to left heart disease (PH-LHD), conditions with disparate therapeutic strategies. The PAWP is also a key determinant of pulmonary vascular resistance (PVR) that is used to delineate the two PH-LHD subgroups: isolated post-capillary PH (IpcPH) and combined pre- and post-capillary PH (CpcPH).2 Importantly, PAWP only reflects left atrial pressure if a complete occlusion of the PA occurs. If the occlusion is incomplete, the measured pressure will include contributions from the PA, falsely elevating the recorded PAWP and possibly leading to misdiagnosis.5 To address this point, recently published consensus statements recommend confirming an elevated PAWP and complete occlusion by measuring the oxyhemoglobin saturation (SaO2) of blood from the distal tip of the PA catheter when in the wedge position.2 With complete occlusion, SaO2 will approximate that of the left atrium whereas lower SaO2 values may indicate incomplete occlusion and should prompt additional PAWP measurement attempts.

Accordingly, we instituted a standard of care clinical protocol at our institution as follows: SaO2 level is measured from a wedge blood sample for all RHC where PAWP is >15mmHg. If the initial PAWP is confirmed to be occlusive (SaO2 >90% or within 5% of systemic arterial saturation), it is the final reported value. However, if PAWP saturation suggests an incomplete occlusion, up to 2 additional attempts are made to obtain PAWP with an occlusive SaO2. The final reported PAWP is the value associated with an occlusive SaO2.

Because data regarding the feasibility and clinical impact of this method are lacking, we sought to prospectively study the overall success rate of obtaining an occlusive PAWP SaO2, the differences between the initial and final reported hemodynamics, and any clinically-relevant PH re-classification. After Institutional Review Board approval, and several months after instituting the standard of care protocol, investigators not performing the RHC enrolled and observed subjects undergoing clinically-indicated RHC from September 2019 to June 2020. Demographic, clinical, echocardiographic, procedural and hemodynamic data were collected. Subjects undergoing routine post-transplant RHC and those with PAWP ≤15mmHg were excluded. All hemodynamics were measured in a standardized fashion and were reported by the proceduralists (not investigational observers). Initial and final hemodynamics were compared using the Signed-Rank Test.

A total of N=111 consecutive subjects were enrolled. One subject was excluded due to incomplete data. The cohort was 58±14 years old, 60% male, 60% Caucasian/35% Black race, and had body mass index of 31±7 kg/m2. The average left ventricular ejection fraction (LVEF) was 41±23%, with 47/110(43%) having LVEF ≥50%. Clinical indications for RHC included assessment of advanced heart failure therapy candidacy (38%), uncertain volume/perfusion status (26%), pre-operative optimization/risk stratification (24%), and evaluation of known/suspected PCPH(12%). RHC were performed by interventional cardiologists (52/110; 47%) and heart failure cardiologists (58/110; 53%).

Despite apparent confirmation of PAWP occlusion by fluoroscopy and/or typical hemodynamic waveform appearance, an occlusive PAWP SaO2 was obtained on the first attempt only 50% of the time (55/110; Figure). There was no difference in initial success rate between interventional and heart failure cardiologists or based on LVEF. With up to two additional attempts, an occlusive PAWP SaO2 was obtained in 91% of subjects. In subjects in whom additional attempts were successful in obtaining occlusive PAWP SaO2 (n=45; initial SaO2 68.8±14.3% vs 94.5±2.7%; p <0.001), 29 had a lower final PAWP compared to the initial PAWP [20±6 vs. 25±7 mmHg; p<0.001], and 14 of the 45 subjects (31%) had ≥4 mmHg difference between final and initial PAWP values. This also led to significant differences in final vs. initial PVR (3.8±3.5 vs. 2.4±1.8 WU; p<0.001). Re-classification from PH-LHD to PCPH was made in 6 subjects and from IpcPH to CpcPH in 4 subjects. Additionally, of the 10 subjects without an occlusive PAWP SaO2 after three attempts, 5(50%) were noted to have a lower final reported PAWP compared to the initial PAWP, which resulted in re-classification of three additional subjects. This suggests that even the attempt to obtain a PAWP saturation, with deflation and re-inflation of the balloon, may lead to lower and likely more accurate PAWP values. In total, 13 subjects (12%) were ultimately re-classified. There were no observed complications.

Figure.

Figure.

Study Flow Chart. * = p < 0.001, # = p > 0.05, PH-LHD = pulmonary hypertension due to left heart disease, PCPH = pre-capillary pulmonary hypertension, IpcPH = isolated post-capillary pulmonary hypertension, CpcPH = combined pre- and post-capillary pulmonary hypertension

In this prospective, single-center study, half of initial PAWP measurements were not occlusive when the initial measured PAWP was >15mmHg. The practice of obtaining a PAWP saturation resulted in significantly lower PAWP, higher PVR, and clinically-relevant disease re-classification. A PAWP saturation is a simple, safe and effective technique to verify complete PAWP occlusion during RHC and should be considered in clinical practice.

Acknowledgments

Disclosures: All authors report no direct conflicts relevant to this manuscript. Dr. Todoran receives consulting fees from Medtronic and GE Healthcare. Dr. Maron receives research funding from the NIH (NIH U01HL125215-01; 1R01HL139613-01; R01HL153502; R21HL134320; U54HL119145), Cardiovascular Medical Research Education Foundation, and Boston Biomedical Innovation Center; is a co-inventor on US patent 9,605,047, US pending patent PCT/US2019/059890, and provisional patent applications 62475955 and 029672; and is a member of the steering committee for a research grant supported by Actelion Pharmaceuticals. Dr. Maran serves a consultant and speaker for Boston Scientific, Medtronic and Phillips. Dr. Houston receives grant funding from Medtronic. Dr. Tedford reports general conflicts include consulting relationships with Medtronic, Aria CV Inc., Acceleron, Arena Pharmaceuticals and United Therapeutics. Dr. Tedford is on a steering committee for Medtronic and Abbott, and a research advisory board for Abiomed. He also does hemodynamic core lab work for Actelion and Merck.

Footnotes

Presented at the Heart Failure Society of America Annual Meeting, September 30, 2020 – October 6, 2020

References

  • 1.Deaño RC, Glassner-Kolmin C, Rubenfire M, Frost A, Visovatti S, McLaughlin VV and Gomberg-Maitland M. Referral of Patients With Pulmonary Hypertension Diagnoses to Tertiary Pulmonary Hypertension Centers: The Multicenter RePHerral Study. JAMA Internal Medicine. 2013;173:887–893. [DOI] [PubMed] [Google Scholar]
  • 2.Vachiery JL, Tedford RJ, Rosenkranz S, Palazzini M, Lang I, Guazzi M, Coghlan G, Chazova I and De Marco T. Pulmonary hypertension due to left heart disease. European respiratory journal. 2019;53:1801897. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 3.Maron BA, Brittan EL, Hess E, Waldo SW, Barón AE, Huang S, Goldstein RH, Assad T, Wertheim BM, Alba GA, Leopold JA, Olschewski H, Galiè N, Simonneau G, Kovacs G, Tedford RJ, Humbert M and Choudhary G. Pulmonary vascular resistance and clinical outcomes in patients with pulmonary hypertension: a retrospective cohort study. Lancet Respiratory Medicine. 2020;8:873–884. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 4.Maron BA, Hess E, Maddox TM, Opotowsky AR, Tedford RJ, Lahm T, Joynt KE, Kass DJ, Stephens T, Stanislawski MA, Swenson ER, Goldstein RH, Leopold JA, Zamanian RT, Elwing JM, Plomondon ME, Grunwald GK, Baron AE, Rumsfeld JS and Choudhary G. Association of Borderline Pulmonary Hypertension With Mortality and Hospitalization in a Large Patient Cohort: Insights From the Veterans Affairs Clinical Assessment, Reporting, and Tracking Program. Circulation. 2016;133:1240–1248. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 5.Johnson S, Witkin A, Rodriguez-Lopez J and Channick R. Room For Improvement in Pulmonary Capillary Wedge Pressure Reporting: a review of hemodynamic tracings at a large academic medical center. Pulmonary Circulation. 2020. doi: 10.1177/2045894020929157 [DOI] [PMC free article] [PubMed] [Google Scholar]

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