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

• Published in: British journal of anaesthesia : BJA Vol. 125; no. 6; p. 1018
• Main Authors: Morelli, Andrea, Romano, Salvatore M, Sanfilippo, Filippo, Santonocito, Cristina, Frati, Giacomo, Chiostri, Marco, Agrò, Felice E, Ertmer, Christian, Rehberg, Sebastian W, Vieillard-Baron, Antoine
• Format: Journal Article
• Language: English
• Published: England 01-12-2020
• Subjects: 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; septic shock; haemodynamic monitoring; arterial elastance; ventricular–arterial coupling; tachycardia; dicrotic notch; beta blockers; esmolol
• ISSN: 1471-6771
• DOI: 10.1016/j.bja.2020.05.058

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 (SDP
), which reflects the coupling between myocardial contractility and a given afterload, in discriminating the origin of tachycardia.
In this post hoc analysis of 45 patients with septic shock with persistent tachycardia, we characterised features of haemodynamic response focusing on SDP
, classifying patients according to variations in arterial dP/dt
after 4 h of esmolol administration to maintain HR <95 beats min
. A cut-off value of 0.9 mm Hg ms
was used for group allocation.
After reducing HR, arterial dP/dt
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
; mean [SD], P<0.001). At baseline, patients with decreased dP/dt
after esmolol had lower SDP
than those with higher dP/dt
(40 [19] vs 53 [16] mm Hg, respectively; P=0.01). The SDP
remained unchanged after esmolol in the higher dP/dt
group (49 [16] mm Hg), whereas it decreased significantly in patients with lower dP/dt
(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/dt
SV increased (from 48 [12] to 67 [14] ml; P<0.001) with maintained cardiac output.
A decrease in SDP
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.
NCT02188888.