Assessment of left and right ventricular function in out-of-hospital cardiac arrest

Abstract Background Patients resuscitated after out-of-hospital cardiac arrest (OHCA) may be hemodynamically compromised and suffer from cardiac stunning, often requiring interventions with vasoactive drugs. Aortic pulse pressure- and pulmonal artery pressure index (APi, PAPi) may be used to assess cardiovascular function. APi reflects left ventricular stroke volume and arterial compliance and therefore serve as an indirect, load-dependent marker of left ventricular function. PAPi reflects right ventricular pulsatile output and is an invasive indicator of right ventricular function, where low values (1.0–1.5) suggest RV failure. Methods This post-hoc study was based on the sub-cohort monitored with a standard pulmonary artery catheter (PAC) in the BOX-trial (n=730, 93 % of the total cohort). Patients were randomized to a MAP of 63 vs 77 mmHg and two oxygen targets. APi and PAPi were derived from arterial line and PAC measurements at pre-specified time points. PAPi and APi were calculated as: PAPi = (Pulmonary artery pulse pressure) / (Right atrial pressure) APi = (Mean arterial pulse pressure) / (Pulmonary capillary wedge pressure, PCWP) Linear mixed models were used to assess associations with the MAP target (63 vs. 77 mmHg) according to the intention-to-treat groups from the BOX trial. Spearman correlation and multivariable logistic regression analyses were used to examine associations of median APi and PAPi with age, sex, and markers of cardiac arrest severity (no-flow and low-flow time, initial lactate level), and one-year all-cause mortality. Results The included patients were mainly male (~81%) with a median age of 64 years (IQR: 54-72.2) and left ventricular ejection fraction of 35% (IQR: 25-45). Median of the first measured cardiac index was 1.67 L/min/m² (IQR 1.33–2.05). PAPi was similar between patients randomized to a MAP of 63 or 77 mmHg and increased steadily the next 48h, independent of MAP target (Figure 1A). Initial APi was 2.7 (95% CI: 2.5-3.0) and 2.9 (95% CI: 2.7-3.1) in MAP 63 and 77 groups respectively. API increased steadily by 60% (43-77%) at 48 hours. From 6 hours to 36 hours the MAP 77 mmHg target was associated with a 11-22% higher APi (all pair-wise P 0.05) (Figure 1B). Median APi and PAPi during the first 48 hours correlated weakly with age, low-flow time, and admission lactate (all rho 0.19, P 0.05). Median APi 3.0 was associated with higher one-year mortality (aOR 1.61, 95% CI 1.15–2.24, P = 0.005), as was median PAPi 1.0 (aOR 2.10, 95% CI 1.33–3.31, P = 0.001), Figure 2. Conclusion In this OHCA cohort, both APi and PAPi were associated with cardiac arrest severity and all-cause mortality. While only APi increased in response to a higher MAP target, both indices rose steadily during the first days of ICU admission, suggesting progressive restoration of biventricular function during early intensive care after resuscitation.