- Describes the ratio of PA pulse pressure and RAP (CVP)
Background
- Originally evaluated in patients with RV infarction (2012) who went on to have an RVAD fitted. PAPi was developed as an attempt to determine suitability for weaning. It has now found utility in managing patients with advanced heart failure and those with LVAD who develop concmmitant RV failure.
Physiology
PAPi is a surrogate marker of RV function although the context of RV impairment is very important (Acute RV infarction vs chronic biventricular failure) as eloquently described in the systematic review referenced below.
- PA pulse pressure (PA-pp) should increase with increasing RV stroke volume in normal individuals
- PA-pp Increases by an exaggerated quantity if pulmonary capacitance (PAC) is LOW. Note that normal capacitance should be around 4ml/mmHg and this decreases to 2.5 or less in established HF (see graph above) This decrease in capacitance is a progressive disorder caused by loss of elastin and collagen in the pulmonary vessels.
- Excessive increase in PA-pp coupled with increased CVP suggests the RV is unable to “process” a given venous return (stroke volume) resulting in LOW levels of PAPi.
- Found to be a predictive risk index for mortality in patients with PAH
- ePAPi was significantly associated with 60 day mortality in one study looking at echo-derived parameters in patients with cardiogenic shock
- Can also be used to assess responsiveness to treatment e.g. PAPi changes pre and post administration of pulmonary vasodilator therapy.
References