Systolic-dicrotic notch pressure difference can identify tachycardic patients with septic shock at risk of cardiovascular decompensation following pharmacological heart rate reduction

Br J Anaesth. 2020 Dec;125(6):1018-1024. doi: 10.1016/j.bja.2020.05.058. Epub 2020 Jul 18.

Abstract

Background: During sepsis, heart rate (HR) reduction could be a therapeutic target, but identification of responders (non-compensatory tachycardia) and non-responders (compensatory for 'fixed' stroke volume [SV]) is challenging. We tested the ability of the difference between systolic and dicrotic pressure (SDPdifference), which reflects the coupling between myocardial contractility and a given afterload, in discriminating the origin of tachycardia.

Methods: In this post hoc analysis of 45 patients with septic shock with persistent tachycardia, we characterised features of haemodynamic response focusing on SDPdifference, classifying patients according to variations in arterial dP/dtmax after 4 h of esmolol administration to maintain HR <95 beats min-1. A cut-off value of 0.9 mm Hg ms-1 was used for group allocation.

Results: After reducing HR, arterial dP/dtmax remained above the cut-off in 23 patients, whereas it decreased below the cut-off in 22 patients (from 0.99 [0.37] to 0.63 [0.16] mm Hg ms-1; mean [SD], P<0.001). At baseline, patients with decreased dP/dtmax after esmolol had lower SDPdifference than those with higher dP/dtmax (40 [19] vs 53 [16] mm Hg, respectively; P=0.01). The SDPdifference remained unchanged after esmolol in the higher dP/dtmax group (49 [16] mm Hg), whereas it decreased significantly in patients with lower dP/dtmax (29 [11] mm Hg; P<0.001). In the latter, the HR reduction resulted in a significant cardiac output reduction with unchanged SV, whereas in patients with higher dP/dtmax SV increased (from 48 [12] to 67 [14] ml; P<0.001) with maintained cardiac output.

Conclusions: A decrease in SDPdifference could discriminate between compensatory and non-compensatory tachycardia, revealing a covert loss of myocardial contractility not detected by conventional echocardiographic parameters and deteriorating after HR reduction with esmolol.

Clinical trial registration: NCT02188888.

Keywords: arterial elastance; beta blockers; dicrotic notch; esmolol; haemodynamic monitoring; septic shock; tachycardia; ventricular–arterial coupling.

Publication types

  • Observational Study

MeSH terms

  • Adrenergic beta-Antagonists / therapeutic use
  • Adult
  • Aged
  • Arterial Pressure
  • Blood Pressure / drug effects
  • Cardiac Output / drug effects
  • Echocardiography
  • Female
  • Heart Failure / diagnostic imaging
  • Heart Failure / physiopathology*
  • Heart Rate / drug effects*
  • Humans
  • Male
  • Middle Aged
  • Myocardial Contraction / drug effects
  • Norepinephrine / therapeutic use
  • Propanolamines / therapeutic use
  • Prospective Studies
  • Shock, Septic / diagnostic imaging
  • Shock, Septic / physiopathology*
  • Tachycardia / diagnostic imaging
  • Tachycardia / drug therapy
  • Tachycardia / etiology
  • Tachycardia / physiopathology*
  • Vasoconstrictor Agents / therapeutic use

Substances

  • Adrenergic beta-Antagonists
  • Propanolamines
  • Vasoconstrictor Agents
  • esmolol
  • Norepinephrine

Associated data

  • ClinicalTrials.gov/NCT02188888