Pulmonary Artery Pulsatility Index: Physiological Basis and Clinical Application

Authors, Journal, Affiliations, Type, DOI

• Hoong Sern Lim (University Hospital Birmingham NHS Foundation Trust, UK)
• Finn Gustafsson (Rigshospitalet, University of Copenhagen, Denmark)
• European Journal of Heart Failure, 2020; 22:32–38
• Review article
• DOI: https://doi.org/10.1002/ejhf.1679

Overview

PAPi (pulmonary artery pulsatility index) is widely used in advanced heart failure and cardiogenic shock management, yet its physiological basis had received little formal attention before this review. Lim and Gustafsson demonstrate that PAPi is not a direct measure of RV function but rather a composite index governed by RV stroke volume, pulmonary arterial capacitance (PAC), and right atrial pressure (RAP) — all of which vary with loading conditions and disease state. Because PAC has a hyperbolic inverse relationship with pulmonary vascular resistance (PVR) and falls disproportionately at elevated PAWP, the same PAPi value can arise from vastly different hemodynamic states. This renders population-specific PAPi thresholds non-interchangeable and limits application of a single universal cutoff.

Keywords

Heart failure • Pulmonary artery pulsatility index

Key Takeaways

Background

• Invasive hemodynamic monitoring is recommended in advanced HF and cardiogenic shock unresponsive to initial therapy
• PAPi = pulmonary artery pulse pressure (PAPP) / right atrial pressure (RAP); where PAPP = PASP − PADP
• PAPi was incorporated into the Tehrani et al. cardiogenic shock management algorithm as a central parameter

Right Heart Failure

• RHF defined as a clinical syndrome from alteration of structure/function of the right heart circulatory system causing sub-optimal pulmonary blood flow or elevated venous pressures
• RV failure is a cause but not a prerequisite for RHF (e.g. RA compression can produce RHF without RV contractile impairment)
• Echocardiographic assessment of RV function is challenging due to retrosternal position, complex geometry, and limited windows post-cardiac surgery
• TAPSE reduction post-cardiac surgery may lack clinical significance despite measurable change

Physiological Determinants of PAPi

Pulmonary Arterial Capacitance (PAC) and Pulse Pressure

• PAC estimated clinically as RV stroke volume / PAPP; this overestimates true capacitance but correlates well with Windkessel models
• Rearranged: PAPP = RV stroke volume / PAC — lower PAC produces higher PAPP (and therefore higher PAPi) at the same stroke volume
• The slope of the PAPP–stroke volume relationship is steeper at lower PAC: at low PAC, even small changes in stroke volume produce large changes in PAPP
• PAC has a hyperbolic inverse relationship with PVR; their product (RC time constant) is relatively constant under diverse conditions
• Exception: increasing PAWP disproportionately reduces PAC (shifts PVR–PAC hyperbola leftward and downward), raising PAPi even if PVR, RAP, and stroke volume are unchanged
• Augmentation of pulmonary wave reflection proposed as mechanism for the disproportionate PAC reduction at higher PAWP — not fully elucidated
• Normal PAC ≈ ≥4 mL/mmHg (assuming SV 60 mL, PAPP 15 mmHg)
• PAC in advanced HF: median ~2.5 mL/mmHg; lower still with severe pulmonary hypertension due to left heart disease (~1.3 mL/mmHg)

RAP Determinants

• RAP is determined by the cardiac function–venous return function intersection
• Drop in RV contractility → increased RAP even without change in venous return
• Volume loading (increased stressed volume) → rightward shift of venous return curve → higher RAP and stroke volume; in poor RV function, primarily increases RAP without meaningful stroke volume increase → PAPi falls
• Venoconstriction → reduces slope of venous return curve → reduces RAP and cardiac output; resistance to venous return has a larger effect on venous return and CO than arterial resistance

PAPi Summary

• PAPi is influenced by: RAP, PAWP, PAC, and stroke volume
• Example: patient A (normal PAC 5 mL/mmHg, SV 50 mL, RAP 5 mmHg) and patient B (abnormal PAC 1.5 mL/mmHg, SV 40 mL, RAP 14 mmHg) can both have PAPi ≈ 2.0 — illustrating that the same PAPi value reflects entirely different hemodynamic states
• In homogeneous populations (similar PAC and PAWP), stroke volume/RAP ratio dominates PAPi → PAPi becomes a proxy for the Frank-Starling relationship

Clinical Studies Summary

Clinical Application

Population-Specific Thresholds Are Non-Interchangeable

• No single PAPi threshold applies across diverse populations; the same PAPi can reflect different loading conditions
• Isolated acute RV infarction (normal PAWP/PAC): PAPi significantly lower than biventricular failure from end-stage HF (high PAWP, high PVR, low PAC)
• Restrictive vs dilated cardiomyopathy: at same PAWP and stroke volume, restrictive CMP has higher RAP (steeper LV diastolic PV relationship/myocardial stiffness) → lower PAPi

Where PAPi Is Useful

• Homogeneous/defined groups where PAC and PAWP are relatively similar → stroke volume/RAP ratio dominates PAPi
• Progressive RHF in advanced HF + pulmonary hypertension: low PAC makes PAPP highly sensitive to stroke volume changes → PAPi falls significantly even if RAP is unchanged

Post-LVAD Setting: PAPi Less Sensitive

• LVAD implantation rapidly improves PAWP and PAC due to LV unloading → stroke volume–PAPP slope flattens → PAPP less sensitive to stroke volume changes
• After LVAD, significant PAPi drop may only occur if there is concurrent RAP increase — not just stroke volume change
• PAPi may not be a sensitive measure of post-LVAD RHF in absence of device malfunction

Pulmonary Vasodilator Effect on PAPi

• PVR-PAC hyperbolic relationship means: at very elevated PVR, reducing PVR produces minimal increase in PAC (right-side plateau of hyperbola)
• Sodium nitroprusside in severe pulmonary hypertension due to left heart disease: PAPi decreased slightly from 2.43 to 2.01 in responders (reduction in both PA and RA pressures); no change in non-responders (2.41 to 2.40)
• Effect of diuretics/fluid on PAPi is variable and depends on net effect on RAP, stroke volume, and PAC from PAWP changes

Limitations of the Document

• Narrative review; no primary data generated
• Studies in Table 1 have significant risk of selection bias (post-hoc analyses with incomplete datasets — e.g. ESCAPE: only 190 of 433 patients had complete RHC data; SHOCK trial: less than half had complete data)
• PAPi thresholds in all cited studies are unvalidated across populations
• No prospective studies documenting serial PAPi changes over time in any population
• Effect of therapeutic interventions (vasodilators, inotropes, exercise) on PAPi unstudied
• SHOCK trial/registry finding (no PAPi–mortality association) limits PAPi's role in acute MI-related cardiogenic shock

Key Concepts Mentioned

• concepts/Pulmonary-Artery-Pulsatility-Index — primary subject of the review
• concepts/Right-Ventricular-Failure — pathophysiology and clinical context
• concepts/Cardiogenic-Shock — clinical application of PAPi
• concepts/Pulmonary-Hypertension — PAC-PVR relationship and PAH data
• concepts/Right-Heart-Catheterization — derived measurement context
• concepts/RV-PA-Coupling — physiological context

Key Entities Mentioned

• entities/Heart-Failure — advanced HF as primary clinical population
• entities/HFrEF — ESCAPE trial population

Wiki Pages Updated

• wiki/sources/papi-ejhf-2020.md — created (this file)
• wiki/concepts/Pulmonary-Artery-Pulsatility-Index.md — significantly expanded with physiological framework
• wiki/concepts/Right-Ventricular-Failure.md — added source reference and PAPi physiological context
• wiki/sourceindex.md — new entry added
• wiki/wikiindex.md — PAPi entry updated