February 17, 2021Open Access

Left ventricular-arterial coupling as a predictor of stroke volume response to norepinephrine in septic shock – a prospective cohort study

XZXiaoyang ZhouChina Mobile (China)JPJianneng PanNingbo No. 2 Hospital YWYang WangJohnson & Johnson (United States)

Structured PICO

Does baseline left ventricular-arterial coupling predict stroke volume response to norepinephrine in patients with septic shock?

Population

34 adult patients (age > 18 years) with septic shock, persistent hypotension despite fluid resuscitation, requiring norepinephrine to maintain MAP > 65 mmHg. Mean age 70, 71% male, based in China. Excluded: refractory shock not reaching target MAP, atrial fibrillation, receiving vasoactive agents or cardiac assist devices at enrollment, and poor echogenicity.

Intervention

Norepinephrine infusion adjusted to reach and maintain target mean arterial pressure (MAP) > 65 mmHg

Outcome

Stroke volume (SV) response to norepinephrine (defined as ≥ 15% increase in SV after NE infusion), predicted by baseline left ventricular-arterial coupling (Ea/Ees ratio)surrogate

Baseline left ventricular-arterial coupling (Ea/Ees ratio) can accurately predict which patients with septic shock will have a clinically significant increase in stroke volume in response to norepinephrine.

Abstract

BACKGROUND: Left ventricular-arterial coupling (VAC), defined as the ratio of arterial elastance (Ea) to left ventricular end-systolic elastance (Ees), is a key determinant of cardiovascular performance. This study aims to evaluate whether left VAC can predict stroke volume (SV) response to norepinephrine (NE) in septic shock patients. METHODS: This was a prospective cohort study conducted in an intensive care unit of a tertiary teaching hospital in China. We recruited septic shock patients who had persistent hypotension despite fluid resuscitation and required NE to maintain mean arterial pressure (MAP) > 65 mmHg. Those patients in whom the target MAP was not reached after NE infusion were ineligible. Echocardiographic variables were measured before (baseline) and after NE infusion. SV responder was defined by a ≥ 15% increase in SV after NE infusion. RESULTS: Of 34 septic shock patients included, 19 (56%) were SV responders. Before NE infusion, SV responders had a lower Ees (1.13 ± 0.24 mmHg/mL versus 1.50 ± 0.46 mmHg/mL, P = 0.005) and a higher Ea/Ees ratio (1.47 ± 0.40 versus 1.02 ± 0.30, P = 0.001) than non-responders, and Ea in SV responders was comparable to that in non-responders (1.62 ± 0.36 mmHg/mL versus 1.43 ± 0.28 mmHg/mL, P = 0.092). NE significantly increased Ea and Ees in both groups. The Ea/Ees ratio was normalized by NE administration in SV responders but unchanged in non-responders. The baseline Ea/Ees ratio was positively correlated with NE-induced SV increases (r = 0.688, P < 0.001). Logistic regression analysis indicated that the baseline Ea/Ees ratio was a predictor of SV increases induced by NE (odd ratio 0.008, 95% confidence interval (CI): 0.000 to 0.293), with an area under the receiver operating characteristic curve of 0.816 (95% CI: 0.646 to 0.927). CONCLUSIONS: The left VAC has the ability to predict SV response to NE infusion in septic shock patients. TRIAL REGISTRATION: Chinese Clinical Trial Registry, ChiCTR1900024031, Registered 23 June 2019 - Retrospectively registered, http://www.chictr.org.cn/edit.aspx?pid=40359&htm=4 .

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