What is the pulmonary artery pulsatility index, how is it calculated, what values indicate right‑ventricular dysfunction, and how should a low PAPi be managed?

Pulmonary Artery Pulsatility Index (PAPi)

Definition and Calculation

The pulmonary artery pulsatility index (PAPi) is calculated as (pulmonary artery systolic pressure − pulmonary artery diastolic pressure) / right atrial pressure, and serves as a hemodynamic marker of right ventricular function. 1

• PAPi reflects the pulse pressure generated by the right ventricle relative to the filling pressure, providing insight into RV contractile function and coupling to the pulmonary circulation 2, 3
• The calculation requires three invasive measurements obtained during right heart catheterization: PA systolic pressure, PA diastolic pressure, and right atrial pressure (central venous pressure) 1
• PAPi can also be estimated non-invasively using transthoracic echocardiography, though the invasive measurement remains the gold standard 4

Threshold Values Indicating Right Ventricular Dysfunction

A PAPi value <2.0 indicates significant right ventricular dysfunction and predicts adverse outcomes across multiple clinical contexts. 1, 3

Critical Thresholds by Clinical Context:

• Cardiogenic shock: PAPi <1.0 defines RV-dominant or biventricular cardiogenic shock and indicates refractory shock requiring consideration of mechanical circulatory support 1
• LVAD implantation: PAPi <2.0 predicts right ventricular failure and need for RVAD support after left ventricular assist device placement, with optimal sensitivity and specificity at this threshold 3
• Acute myocardial infarction with cardiogenic shock: PAPi <2.0 identifies patients at high risk for RV dysfunction, particularly in the setting of inferior MI 1
• Pulmonary arterial hypertension: PAPi <5.3 predicts increased mortality risk in PAH patients (adjusted hazard ratio 2.23) 5
• Advanced heart failure: Lower PAPi values independently predict death or hospitalization at 6 months (hazard ratio 0.91 per unit increase) 2
• Acute pulmonary embolism: Lower PAPi measurements correlate with increased 30-day mortality and higher rates of RV failure 4

Physiologic Context:

• Normal PAPi values are typically >2.0, with median values around 2.35 in advanced heart failure populations 2
• PAPi values between 1.0-2.0 represent intermediate RV dysfunction 1
• The prognostic strength of PAPi appears driven primarily by the right atrial pressure component, with elevated RAP being the strongest predictor of adverse outcomes 5

Management of Low PAPi

When PAPi is <1.0 in cardiogenic shock, immediate escalation to mechanical circulatory support should be considered after optimizing medical therapy and ensuring adequate filling pressures. 1

Algorithmic Approach to Low PAPi Management:

Step 1: Confirm Hemodynamic Profile

• Verify cardiac power output <0.6 W, which combined with PAPi <1.0 defines refractory shock 1
• Assess right atrial pressure: RAP >15 mmHg with PAPi <1.0 indicates RV-dominant shock 1
• Measure pulmonary capillary wedge pressure to distinguish biventricular (PCWP >15 mmHg) from isolated RV failure (PCWP <15 mmHg) 1

Step 2: Optimize Medical Therapy Before MCS

• Maintain mean arterial pressure >65 mmHg with minimum necessary vasopressor dose 1
• Exercise caution with positive pressure ventilation in RV-dominant failure, as initiation can abruptly lower systemic arterial pressure 1
• Correct metabolic acidosis and hypoxemia, which worsen RV function 1
• Ensure adequate but not excessive volume status—elevated RAP drives low PAPi and worsens outcomes 5

Step 3: Risk Stratification for MCS

• PAPi <1.0 with cardiac power output <0.6 W indicates need for mechanical circulatory support consideration 1
• Assess for contraindications: anoxic brain injury, irreversible end-organ failure, prohibitive vascular access, DNR status 1
• In LVAD candidates, PAPi measured on inotropes is more predictive of post-LVAD RV failure than measurements off inotropes (OR 0.21 vs 0.49) 3

Step 4: Serial Monitoring and Dynamic Assessment

• Repeat PAPi measurements during optimization provide incremental risk stratification beyond single time-point values 6
• The "optimal PAPi" (initial PAPi + PAPi at optimized hemodynamics) independently predicts early RV failure after LVAD (OR 0.64 per unit increase) 6
• Serial measurements identify dynamic RV reserve and guide timing of advanced therapies 6

Context-Specific Management:

In acute pulmonary embolism with low PAPi:

• Low PAPi predicts RV failure and 30-day mortality better than TAPSE 4
• Consider escalation to systemic thrombolysis or catheter-directed therapy based on hemodynamic compromise 4

In pulmonary arterial hypertension with PAPi <5.3:

• Intensify PAH-specific therapies and consider earlier referral for advanced therapies including lung transplantation 5
• The low PAPi reflects elevated mean RAP, which is the strongest mortality predictor in this population 5

In pre-LVAD optimization with persistently low PAPi despite medical therapy:

• Consider alternative strategies including biventricular support or total artificial heart rather than isolated LVAD 6, 3
• Time from catheterization to LVAD (up to 6 months) does not significantly affect PAPi's predictive value 3

Common Pitfalls to Avoid:

• Do not rely on PAPi alone—integrate with cardiac power output, cardiac index, and clinical perfusion markers 1
• Avoid aggressive diuresis based solely on elevated RAP when this would compromise systemic perfusion; the elevated RAP in low PAPi reflects RV failure, not necessarily volume overload 5
• Do not delay right heart catheterization in cardiogenic shock to obtain PAPi and other hemodynamic parameters, though RHC should not delay urgent revascularization 1
• Recognize that PAPi is more predictive when measured on inotropic support in LVAD candidates, reflecting stressed hemodynamics 3