Key result
Procedural sedation during RHC is linked to ~2 mmHg lower baseline PAWP but worse post-milrinone RV hemodynamics.
Why the study?
Procedural sedation during right heart catheterization in patients with advanced heart failure is not standardized and its hemodynamic effects are poorly characterized.
Does procedural sedation affect baseline and post-milrinone hemodynamic measurements during right heart catheterization in patients with advanced heart failure?
Observational (n=223)
Does procedural sedation affect baseline and post-milrinone hemodynamic measurements during right heart catheterization in patients with advanced heart failure?
Procedural sedation during right heart catheterization in advanced heart failure alters baseline hemodynamics and may mask left ventricular dysfunction while unmasking right ventricular strain during inotropic stress.
Answers are grounded in this paper and cite their sources.
Sedation may confound RHC hemodynamic interpretation in advanced HF; leaves open whether protocols should standardize or avoid it in future studies.
Background Right heart catheterization (RHC) is common in assessing patients with advanced heart failure (AHF). Procedural sedation is not standardized, and its effects in patients with AHF are poorly characterized. Methods Retrospective chart review of patients undergoing RHC and qualifying for milrinone drug study with our AHF team from 2014 to 2019 was conducted. Criteria for drug study: pulmonary artery wedge pressure (PAWP) >15mmHg and/or cardiac index (CI) <2.2L/min 2 . 5mcg/kg/min of milrinone was infused over 10 minutes with pre- and post-infusion hemodynamic measurements recorded. Measurements were compared within groups (before vs after milrinone) and between groups; analysis was performed with Chi square and t-test. Results 223 patients were included: median age 57 years-old (IQR 48-66), 33% women, and 52% African-American. 121 patients (54%) received sedation and 102 (46%) did not. Baseline characteristics were similar, but the sedation group had a higher LVEF (LVEF 24% vs 21%, p<0.05). All hemodynamic variables are presented (sedation vs no sedation). Median sedation administered was 25mcg of fentanyl and 1mg of midazolam. Significant baseline hemodynamic differences are: PAWP (24.74 vs 26.95, p<0.05), indirect Fick CI (1.92 vs 1.77, p<0.05, systemic vascular resistance (1540 vs 1753, p<0.05), and right atrial to PAWP ratio (RA:PAWP) (0.59 vs 0.51, p<0.05). After milrinone infusion, only RA:PAWP remained significant (0.57 vs 0.49, p<0.05), but pulmonary artery pulsatility index (PAPI) (2.64 vs 3.81 p<0.05) and RV Myocardial Performance Score (RV-MPS) (1.38 vs 2.10, p<0.05) developed statistical significance. Conclusions Left ventricular performance may initially benefit from hemodynamic effects of sedation, but the difference relative to no sedation counterparts is not sustained after milrinone infusion. Conversely, sedation may strain the right ventricle, initiating uncoupling further exacerbated by milrinone infusion. Given the implications of invasive hemodynamics in AHF patients, short-term procedural comfort should be weighed against potentially deleterious hemodynamic effects.
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Mundkur et al. (2026) conducted an observational in Advanced Heart Failure (n=223). Procedural sedation vs. No sedation was evaluated on Baseline pulmonary artery wedge pressure (PAWP) (p=<0.05). Procedural sedation during right heart catheterization was associated with lower baseline PAWP (24.74 vs 26.95, P<0.05) but worsened right ventricular hemodynamics after milrinone infusion.
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