Pulmonary Artery Pulsatility Index

Physiological Basis

The Pulmonary Artery Pulsatility Index (PAPi) is derived from the pressure changes in the pulmonary artery, reflecting the pulsatile nature of blood flow and RV function. It is calculated using systolic and diastolic pulmonary artery pressures as measured on a pulmonary artery catheter and right atrial pressure.

Consider the components of right ventricular output - preload as determined by venous return, contractility as determined by right ventricular function, and afterload as determined by pulmonary vascular compliance and resistance. Similar to the left ventricle and systemic pulse pressure, the right ventricular pulse pressure can act as a surrogate for the contractility of the right ventricle. When faced with increased afterload, a functioning right ventricle will compensate by increasing its contractility and subsequently pulse pressure to maintain an adequate stroke volume. A failing right ventricle will not be able to compensate in this way, leading to the principle of RV-PA uncoupling as talked about in our hemodynamic interfaces calculator.

When the RV can no longer compensate, right atrial pressure rises early, and PA pulse pressure falls, subsequently decreasing PAPi even prior to clinical signs of right heart failure. This makes PAPi a sensitive, and early indicator of a failing right ventricle. Similar to TAPSE/RVSP, PAPi assesses load-dependent RV function, not just an isolated measure of RV contractility, providing greater physiologic context and a more nuanced assessment of the right ventricle.

Clinical Application

PAPI is used to assess RV function, particularly in conditions like pulmonary hypertension and RV failure. It can be applied to a variety of RV pathologies, and be serially assessed with treatment interventions to monitor for therapeutic benefit.

Different clinical cutoffs can be used for a PAPi that indicates poor prognosis depending on the underlying condition. In advanced biventricular failure and pulmonary hypertension values from <1.85 to <3.65 can be used as cutoffs, in the ICU we typically use values of <0.9 derived from the RV infarction literature. If faced with an index <0.9, we know there is RV dysfunction contributing to a patient's shock state, and can therefore consider inodilators, diuresis, inhaled pulmonary vasodilators (all depending on clinical context) and reassess a PAPi in short intervals for improvement. At the same time, it may be beneficial to assess cardiac outputs/indices to assess for interval improvement of these indices as well, to assess how well improving RV function improved cardiac output.

Generally speaking, the numbers I use as guides are: PAPi >2 = normal, PAPi 1-2 is non-specific but worth noting as an indicator of trouble, and PAPi <0.9-1 as a specific indicator or RV dysfunction warranting intervention.

Evidence Base

The benefit of PAPi is in its sensitivity to RV dysfunction, and its validation across many RV pathologies where other echocardiographic parameters no longer work. For example, in the post-cardiac surgery world, patients often have a reduced tricuspid annular plane systolic excursion (TAPSE) but this is not associated with reduced RV function. If the etiology of a patients shock is unclear, and a patient has underlying RV dysfunction from pulmonary hypertension, RV infarct or are post-cardiac surgery, PAPi provides useful insight on the contributions of the right ventricle to someones shock state.

PAPi has been validated as a prognostic indicator across advanced heart failure, RV infarction, prior to LVAD insertion and pulmonary hypertension. As above, values vary as low as 0.9 to 3.65, with these cutoffs representing the chronicity of each pathology and the loading conditions of that ventricle. For example, in a patient with pulmonary hypertension the right ventricle has likely been working against a higher afterload for months to years, meaning it has adapted somewhat to compensate for the higher pulmonary pressures. This can be contrasted to the right ventricle that has acutely infarcted, with reduced myocardial contractility that has happened within minutes and an inability to compensate.

Our Suggestion

PAPi is a useful, sensitive clinical tool to evaluate for RV dysfunction as a contributor to shock. When interpreting PAPi, consider the acute vs chronic nature of the right ventricular dysfunction, specific load state of the right ventricle, and apply this to the broader clinical context to the indexed value itself. With interventions, reassess your PAPi for improvement as a short interval guide on if management strategies are successful.