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Weekly Echo

# 20260314
Author
Author Photo
Dr.Kumar.C
viji_vairavan@yahoo.com

Institute: Senior Consultant Cardiac Anaesthesiologist, The Madras Medical Mission, Chennai, Tamilnadu.

Decoding elevated transvalvular gradients following aortic valve replacement – part 2 (The Scenarios)

Mid Week Quiz

# 00444
Author
Quiz Author
Dr. Sucharita Das
drsucharita.das@gmail.com

Institute: Narayana Hrudayalaya

Quiz Question:

A 65-year-old male with anterior wall myocardial infarction (MI) presents in shock. His systolic blood pressure (BP) = 90 mmHg, diastolic BP = 50 mmHg. Left ventricular outflow tract (LVOT) velocity time integral (VTI)= 10cm, LVOT diameter =2.0 cm End systolic LV volume = 120 ml, ejection fraction (EF) 35%, pre- ejection time 110 milliseconds, total ejection time is 233 milliseconds. All the following interpretations are correct except:

Winner of the Quiz:
Sridevi Natarajan
srinut01@gmail.com

Institute: Frontier Lifeline Hospital

Media:
Answers Submitted
a (4)
b (4)
c (17)
d (7)
Explanation:

a.    Ventriculo-arterial coupling (VAC) is calculated as a ratio of the arterial elastance (Ea, afterload) to LV  end systolic elastance (Ees, contractility). A normal ratio (Ea/ Ees) ranges from 0.5 to 1, representing optimal cardiac VAC efficiency ratio.


a. Arterial Elastance (Ea): =   (Where ESP is End systolic pressure, stroke volume SV (single beat method by Chen, et al)

             SV= = 3.14x 12 x 10 = 31.4 ml

             Ea= 0.9x 90/ 31.4= 81/31.4= 2.6mmHg/ ml

 Ea is elevated here.

Ventricular end systolic elastance (Ees)

     

 

End(est) is the estimated normalized ventricular elastance at the onset of ejection (1)

Manual calculation of Ees is prone for error and unnecessary.

Clinicians should use validated digital tools like the i Elastance App. This application was developed by Pietro Bertini to assist clinicians (Bertini P, et al 2016, i Elastance, research gate).

 

 

Calculated Ees is 0.71mmHg/ ml

Ees is markedly reduced here.

Ea/ Ees ratio=  2.6/.71=3.6

So, there is severe uncoupling


b. Yes, this statement is correct. In cardiogenic shock, there is typically high afterload relative to poor contractility. Also,  most commonly due to LV dysfunction, eg: post-MI, primary problem is decrease in contractility.  The failing myocardium can not generate adequate force which leads to decrease in stroke volume and cardiac output. As a result of compensatory mechanism, the body tries to maintain perfusion via sympathetic activation along with vasoconstriction. This causes increased systemic vascular resistance and afterload.  So, yes, afterload is disproportionately high compared to contractility.


c. No, this statement is not correct.  In cardiogenic shock the Ea/Ees ratio is high, not low. Ea reflects afterload and Ees reflects contractility. In cardiogenic shock, there is decrease in contractility, so Ees will be reduced. This decrease in contractility causes compensatory increase in vasoconstriction. So the ratio of Ea/ Ees will be high. Low Ea / Ees is seen in vasodilatory state like septic shock (early stage).

d. Yes, inotropes help to improve coupling. In cardiogenic shock, contractility reduces, and afterload is high. Ea/ Ees ratio increases and there is uncoupling. Inotropes increase contractility (Ees). This reduces Ea/Ees ratio toward normal. So best initial strategy is to start inotropes (e.g. d obutamine) to increase Ees and restore the coupling.

References:

 1. Holm H, Magnusson M, Jujic A, et al. How to calculate ventricular-arterial coupling? Eur J Heart Fail 2022;24:600-2.  

Correct Answer: c)Low arterial elastance (Ea)/ LV end-systolic elastanace (Ees) ratio is seen in cardiogenic shock.