Standardization of Baseline and Provocative Invasive Hemodynamic Protocols for the Evaluation of Heart Failure and Pulmonary Hypertension

Authors, Journal, Affiliations, Type, DOI

• Authors: Mark N. Belkin (Chair), Marat Fudim (Vice Chair), Claudia Baratto, Jonathan Grinstein, Ian Hollis, Nkechinyere Ijioma, Rachna Kataria, Gregory D. Lewis, Susanna Mak, Ryan J. Tedford, Jennifer T. Thibodeau, Hidenori Yaku; on behalf of AHA Fellow-In-Training and Early Career Committee of the Council on Clinical Cardiology
• Journal: Circ Heart Fail. 2026;19:e000088. February 2026
• Affiliations: University of Chicago; Duke University; Harvard/MGH; University of Bergamo (Italy); Medical University of South Carolina; Brown University; Mount Sinai (Canada); Ohio State University; UT Southwestern; Northwestern University
• Type: AHA Scientific Statement (consensus)
• DOI: 10.1161/HHF.0000000000000088

Overview

This 2026 AHA Scientific Statement addresses a critical operational gap: while guidelines specify when to perform invasive hemodynamic studies, there has been limited consensus on how to conduct them standardly and how to perform provocative maneuvers. The document provides evidence-based protocols for baseline RHC technique (transducer positioning, PAWP measurement, CO methodology), four categories of provocative studies (vasodilator challenge for PH reversibility in HF, PAH acute vasoreactivity testing, volume challenge, and invasive exercise hemodynamics), LVAD ramp and reverse ramp studies, and guidance on serial/remote hemodynamic monitoring. It directly updates several haemodynamic thresholds and supersedes earlier procedural guidance across the HFpEF, PH, and advanced HF spectra.

Keywords

AHA Scientific Statements · cardiac catheterization · dyspnea paroxysmal · heart failure diastolic · heart failure systolic · hemodynamics · hypertension pulmonary

Key Takeaways

Baseline RHC Standardization

• Patient preparation: Fasting not required; continue prescribed medications; defer IV sedation — sedation alters breathing patterns and vascular tone, distorting target hemodynamic measures; topical/local anaesthesia preferred; oral premedication if anxiolysis required
• Transducer zeroing (supine): Level at mid-chest, approximating the right atrium; zero by opening system to air to equilibrate with atmospheric pressure
• Transducer zeroing (upright exercise): Level at the phlebostatic axis (intersection of 4th intercostal space and mid-chest); mark the RA level on the chest wall fluoroscopically before patient moves to upright
• Pressure readings: Take at end-expiration, without breath-holding (inadvertent Valsalva decreases preload); avoid use of automatically displayed monitor averages (algorithms do not account for respiration or ectopy)
• Wide respiratory variation (mechanical ventilation, obesity, severe lung disease): Average across the respiratory cycle, or report both end-expiratory and average values
• PAWP timing — sinus rhythm: Measure at end-diastole (mean of the a-wave); avoid measurement during/just after ectopic beats
• PAWP timing — atrial fibrillation: Measure 130–160 ms after QRS onset, before the V-wave
• PAWP verification: Obtain saturation in the wedged position (discard first 5–10 mL); within 3–5% of systemic pulse oximetry confirms correct wedge position — critical when PAWP is elevated (misclassification of PAH risk)
• V-waves: In significant AV regurgitation or non-compliant atria: use mean PAWP (incorporating V-waves) for PVR calculations; use mean PAWP excluding V-waves to estimate ventricular end-diastolic pressure

Cardiac Output Methodology

• Direct Fick (VO₂ measured directly): Gold standard; requires metabolic cart or Douglas bag — not available in most catheterisation laboratories
• Thermodilution: Reliable alternative; inject 10 mL saline at known temperature; average 3 consistent values within 10% of each other; performing injections at the same respiratory phase improves precision; remains accurate even in the presence of tricuspid regurgitation (contrary to common belief); unreliable in intracardiac shunts or ECMO
• Indirect Fick (VO₂ estimated by nomogram): Demonstrated to be inaccurate in numerous studies — formulae derived from infants/children or selected healthy adults do not reflect cardiac disease patients; should not be used; thermodilution preferred
• During exercise: Indirect Fick cannot be estimated — PA saturation falls with exercise oxygen uptake in ways not captured by fixed formulae; use direct Fick (metabolic cart) or thermodilution

Advanced Hemodynamic Metrics

• Cardiac power output (CPO): Reflects combined LV and RV function; low LV CPO predicts poor outcomes in AMI-cardiogenic shock; reincorporating RAP into CPO formula (original calculation included RAP) improves prognostic value in acute decompensated HF and HF-CS
• Aortic pulsatility index (API): Reflects LV ejection efficiency and ventriculoarterial coupling; predictor of myocardial recovery and ability to wean from temporary MCS; principal components: pulse pressure and PAWP
• PA pulsatility index (PAPI): Identifies severe RV dysfunction in AMI; predicts RV failure after LVAD implantation
• RV stroke work index (RVSWI): Beat-to-beat RV workload; prognostic in HF-CS and post-LVAD RV failure
• Myocardial performance score: Combines API and CPO; reflects ventricular power efficiency; correlates with ventriculoarterial coupling and overall energetic state

Vasodilator Challenge for PH Reversibility in Advanced HF (Table 1)

Indications (ISHLT 2024): PA systolic pressure >50 mmHg + (TPG ≥15 mmHg OR PVR ≥3 WU) during HTX candidacy evaluation; also consider if TPG/PVR is elevated even if PASP <50 mmHg in low-CO states
Hemodynamic targets: TPG ≤12–15 mmHg + PVR ≤2.5–3 WU + SBP >85 mmHg

• Sodium nitroprusside (SNP):

  • Mechanism: releases NO → SVR reduction → LV afterload reduction → CO↑ + PAWP↓ → secondary PA pressure and PVR reduction
  • Protocol: start 0.25–0.5 μg/kg/min; titrate ↑0.5 μg/kg/min every 3–5 min; reassess at each dose; max 10 μg/kg/min
  • Contraindications: SBP <85 mmHg; use milrinone instead if SBP <85, low SVR, or low-CO state; consider iNO if PAWP <12 mmHg; stop if PAWP <12 mmHg
  • Use infusion pump only (light-sensitive infusion bag)
  • Caution in PAH with RV dysfunction — acute BP drop may precipitate decompensation

• Milrinone:

  • Mechanism: PDE3 inhibitor → increased cAMP → enhanced contractility + systemic vasodilation; higher LV peak dP/dt and stroke work index vs SNP; less BP-dependent mechanism for PAWP reduction
  • Protocol: bolus 25–50 μg/kg over 5–10 minutes; reassess hemodynamics 5 min after bolus (no uptitration required)
  • Preferred over SNP when: hypotension, low SVR, or PVR elevation driven by low CO state
  • Cautions: unstable tachyarrhythmias; use with caution if eGFR <30 mL/min (prolonged half-life)

PAH Acute Vasoreactivity Testing (Table 2)

Indication: Patients with PAH (most commonly idiopathic, heritable, or drug-induced) with mPAP >20 mmHg + PAWP <15 mmHg
Positive response (current definition): mPAP decrease ≥10 mmHg to absolute value ≤40 mmHg with maintained or increased CO (replaces older 20% PVR reduction criterion)
Responders: ~10%; positive response has predictive/prognostic value only in idiopathic, heritable, or drug-induced PAH — not other PH forms; long-term CCB responders now have their own WSPH subclassification

• iNO: 10–20 ppm initial; titrate every 5 min; max 40–80 ppm; measure after 10–15 min; taper before cessation; avoid if PAWP elevated (risk of pulmonary oedema); Class I (ESC 2022)
• Inhaled iloprost: 5–17 μg nebulized over 15 min; measure after 10–15 min; no contraindications for short-term testing; Class I (ESC 2022)
• IV epoprostenol: 2 ng/kg/min initial; titrate 2 ng/kg/min every 10 min; max 12 ng/kg/min; contraindicated if pulmonary oedema; Class I (ESC 2022)
• Adenosine: Initial 50 μg/kg/min; titrate by 50 μg/kg/min every 2–5 min; max ~350–500 μg/kg/min; no longer recommended in ESC 2022 guidelines due to frequent adverse effects (AV block, bronchospasm, hypotension); contraindicated in 2nd/3rd degree AV block, sick sinus, bronchospastic lung disease, preexcited AF
• Preferred agents: iNO and inhaled prostacyclin analogs preferred over IV epoprostenol and adenosine (similar response rates with better systemic safety profile)
• PA compliance during AVT: Estimating PA compliance (SV / pulmonary pulse pressure) during AVT may further aid long-term CCB response prediction

Volume Challenge and Passive Leg Raise

Standard fluid bolus challenge: 7–10 mL/kg (~500 mL) of 0.9% saline at minimum 100 mL/min infusion rate
PLR in cath lab: "Feet on pedals" (for potential exercise follow-up) or wedge at ~45°; complete hemodynamic measurements 20 seconds to 3 minutes after completion

Expected response in normal (compliant) hearts:

• RAP: ~+5 mmHg
• PAWP: ~+6 mmHg
• mPAP: ~+7–8 mmHg
• CO: +1.5–2 L (primarily stroke volume +12–13 mL rather than HR +6 bpm)
• Note: elderly patients (especially older women) may show steeper filling pressure responses

Diagnostic thresholds for occult postcapillary PH:

• PAWP ≥19 mmHg after fluid bolus or PLR = positive test for occult postcapillary PH (excellent PPV in single-centre study; larger multicenter validation needed)
• PLR with PAWP ≤11 mmHg can rule out postcapillary PH
• High proportion of intermediate results (PAWP 12–18 mmHg) limits diagnostic utility in many patients
• Positive fluid challenge may provide insight on CO reserve and RV reserve in HFrEF; predict long-term outcomes after advanced therapies

Important caveat: Results must be interpreted in context of clinical phenotype, comorbidities, and imaging — not used in isolation for diagnosis

Invasive Exercise Hemodynamic Testing

Supine vs upright (Table 3):

• Supine advantages: higher venous return, more stable hemodynamics, validated with an established HFpEF treatment (dapagliflozin); majority of HFpEF diagnostic data based on peak PAWP or PAWP/CO slope
• Upright advantages: closer representation of daily activities (gravitational pooling); improved rate-responsiveness in pacemaker-dependent patients; higher achievable workload; more repeated measures; better for peak VO₂ and peripheral impairment assessment
• Upright: lower PAWP cutoffs apply; focus on PAWP/CO and mPAP/CO slopes

Exercise protocol:

• No sedation; exercise-appropriate clothing; start at 0 W, 60–80 rpm; increase 10–20 W per stage every 1–3 min
• Measure at each stage: RAP, PA pressure, PAWP, systemic BP, arterial saturation, CO (thermodilution or direct Fick with metabolic cart)
• Maximal effort: patient-reported maximum OR respiratory exchange ratio >1.05 (if metabolic cart available)
• Goal: complete within ~10 minutes at peak workload

HFpEF invasive diagnostic criteria (Table 4) — at least ONE required:

1. Resting PAWP ≥15 mmHg
2. PAWP ≥20 mmHg with fluid bolus or passive leg raise
3. Peak exercise PAWP ≥25 mmHg (supine) OR ≥20 mmHg (upright)
4. PAWP/CO slope >2 mmHg·L·min (regardless of body position)

Exercise-induced PH: mPAP/CO slope >3 mmHg·L·min — predicts outcomes independently from resting haemodynamics; both precapillary and postcapillary components can contribute; may uncover postcapillary PH in presumed precapillary PH

Additional exercise variables:

• Chronotropic incompetence: HRR <0.80 (or <0.62 on beta-blockers); HRR = (peak HR − rest HR) / (predicted peak HR − rest HR); predicted peak HR = 220 − age
• Impaired peripheral O₂ extraction: Peak VO₂ <80% predicted + peak CO ≥80% predicted OR peak C(a-v)O₂ <14 mg/dL
• Preload insufficiency: Peak VO₂ <80% predicted + peak CO <80% predicted + adynamic/minimal filling pressure increment (ΔPAWP <7 mmHg) during exercise with reduced stroke volume and CO
• PCWL (PAWP indexed to workload/body weight): >25.5–34.7 mmHg·W·kg = higher mortality risk in both HFrEF and HFpEF
• Ventilatory efficiency: Submaximal exercise best period to assess VE/VCO₂ (prognostic in HFpEF); dapagliflozin improved ventilatory abnormalities in supine exercise testing

Supine vs upright PAWP discordance (20% rate):

• PAWP/CO slope <2 but absolute PAWP ≥25 mmHg: higher BMI, more AF, higher resting filling pressures, higher exercise CO (12.3 L/min)
• PAWP/CO slope >2 but PAWP <25 mmHg: lower peak CO (7.7 L/min), same comorbidities
• PAWP/CO slope (not absolute PAWP) consistently differentiates HFpEF from controls across meta-analysis (n=2,180 HFpEF + 682 controls) and multicenter study (n=764, predicted outcomes)

Arteriovenous fistula assessment: AVF flow >1–1.5 L/min or >20% CO = high-output; temporary AVF compression: modest reductions in RAP, CO, PVR; consider IVC saturation and PA saturation to estimate AVF shunt flow via Fick principle

LVAD Hemodynamic Studies

Ramp study (speed optimization):

• Incrementally increase pump speed; examine cardiac and pump measures at each stage
• Combined echo + invasive hemodynamics required for current centrifugal flow pumps (less predictable LV echo changes vs older axial pumps)
• Target hemodynamics: CVP <12 mmHg + PAWP <18 mmHg + CI >2.2 L/min/m²
• RAMP-IT-UP study (hemodynamic ramp optimization for HVAD): trend toward higher event-free survival with hemodynamic optimization; reduced readmissions and hemocompatibility-related adverse events with HeartMate 3 optimization
• CO by thermodilution preferred over estimated Fick in LVAD patients
• Additional uses: PVR assessment; LVAD complication diagnosis; volume assessment; exercise intolerance evaluation

Reverse ramp (recovery assessment):

• Perform when patient meets functional and echocardiographic recovery criteria
• Protocol: obtain baseline hemodynamics at patient's usual speed → ensure full anticoagulation → incrementally decrease speed to nominal LVAD flow (net zero flow through LVAD) → obtain hemodynamics at each stage
• Traditional recovery thresholds (minimal acceptable at nominal flow):
  • PAWP ≤12–15 mmHg
  • CI ≥2.4–2.6 L/min/m²
  • MAP ≥65 mmHg
• Emerging: API (reflects LV efficiency/ventriculoarterial coupling) may be more prognostic than standard thresholds; stable/rising pulse pressure or persistently low PAWP at nominal flow predicts sustained recovery

Temporal Hemodynamic Assessment

PAC in ICU/cardiogenic shock:

• Growing evidence for routine PAC in cardiogenic shock; particularly helpful in HF-CS; nonrandomized studies show lower mortality vs non-PAC use
• PACCS trial (NCT05485376): RCT of early PAC vs no/delayed PAC in HF-CS — currently enrolling; will provide definitive RCT evidence
• ISHLT Class I indication for PAC perioperatively in patients with advanced PH/RV dysfunction undergoing intermediate-to-high-risk procedures

Repeat outpatient RHC:

• PAH: every 3–6 months after diagnosis or when clinical worsening occurs
• Intermediate-risk PAH: further risk stratification using RAP, SV index, CI, SvO₂
• PAH with positive vasoreactivity: evaluate long-term CCB response
• Borderline PH with BMPR2 variant or systemic sclerosis: detect PH development
• LVAD: every 3–6 months to assess PVR changes (bridge-to-transplant) or myocardial recovery
• Heart transplant candidates: ISHLT Class I for RHC every 3–6 months; especially if reversible PH or worsening HF

Remote PA pressure monitoring:

• Recommended for high-risk HF (NYHA Class II–III + recent HF hospitalisation or elevated natriuretic peptides)
• CHAMPION trial (CardioMEMS): PA-guided management → reduced HF hospitalisations and urgent visits
• GUIDE-HF and MONITOR-HF: Consistent reduction in HF-related hospitalisations across varying ejection fractions
• PROACTIVE-HF (Cordella PA Sensor, Edwards Lifesciences): Significant reductions in HF-related hospitalisations; confirmed safety of seated PA pressure monitoring in high-risk patients
• Detection of rising PA pressures often occurs days to weeks before clinical congestion — enables proactive outpatient therapy adjustments (diuretic titration, GDMT optimization)
• Limited data in PAH specifically

Limitations of the Document

• Provocative testing protocols (especially volume challenge thresholds) are largely derived from single-centre studies; require broader multicentre validation
• Optimal PAWP cutoffs for exercise hemodynamics (absolute vs slope, supine vs upright) are not yet fully standardized — ~20% discordance rate between methods
• Translating dynamic hemodynamic phenotyping into effective targeted interventions has not been consistently demonstrated (e.g., pacing for chronotropic incompetence did not improve VO₂)
• Remote PA monitoring data are primarily from CardioMEMS; limited data in PAH or in non-HF populations
• API and advanced hemodynamic metrics lack prospective RCT evidence for routine use in guiding therapy decisions
• PACCS RCT (NCT05485376) is not yet complete — routine PAC in cardiogenic shock remains evidence-based but not RCT-proven

Key Concepts Mentioned

• concepts/Right-Heart-Catheterization — primary concept updated
• concepts/HFpEF — invasive diagnostic criteria; exercise hemodynamic thresholds
• concepts/PAH-Risk-Stratification — vasoreactivity testing indications
• concepts/RV-PA-Coupling — exercise-induced PH; RV adaptation during exercise

Key Entities Mentioned

• entities/Pulmonary-Hypertension — AVT protocols; PH reversibility testing
• entities/Heart-Failure — remote monitoring; exercise hemodynamics; LVAD ramp protocols
• entities/CTEPH — PAC perioperative guidance

Wiki Pages Updated

• Created: wiki/sources/hemodynamic-hf-pht-aha-2026.md
• Updated: wiki/concepts/Right-Heart-Catheterization.md — major update (provocative protocols, HFpEF criteria, LVAD ramp, remote monitoring)
• Updated: wiki/entities/Pulmonary-Hypertension.md — AVT protocol detail (adenosine caveat, updated positive response definition)
• Updated: wiki/entities/Heart-Failure.md — remote PA monitoring, exercise hemodynamics
• Updated: wiki/sourceindex.md
• Updated: wiki/wikiindex.md