Ventriculo-arterial Decoupling in Acutely Altered Hemodynamic States

Abstract

Th e dynamic interaction between the heart and the systemic circulation allows the cardiovascular system to be effi cient in providing adequate cardiac output and arterial pressures necessary for suffi cient organ perfusion [1]. Th e cardiovascular system provides adequate pressure and fl ow to the peripheral organs in diff erent physiological (rest and exercise) and pathological conditions because of the continuous modulation of the arterial system compliance, stiff ness and resistance with respect to left ventricular (LV) systolic performance [2]. Card iac output is the fi nal result of this dynamic modulation. Because LV stroke volume depends on myocardial contractility and loading conditions (preload and afterload), both cardiac and arterial dysfunction can lead to acute hemodynamic decompensation and shock. According to the underlying pathophysiological mechanisms, altered hemodynamic profi les can be classifi ed as primarily refl ecting cardiogenic, hypovolemic, obstructive or distributive shock.Low cardiac output resulting in systemic hypoperfusion requires prompt and adequate treatment to restore cardio vascular function and prevent organ hypo perfusion. Current clinical guidelines recommend resuscitation with intravascular fl uid infusions supplemented with selective use of inotropes and vasopressors to reverse shock in critically ill patients [3,4]. Howe ver, the treatment of acute he modynamic impairment should be tailored based on the etiological mechanism of the cardiovascular dysfunction. Herein lies a major problem with present guidelines: Th ey cannot distinguish the underlying causes of impaired LV stroke volume leading to impaired cardiac output. Ventriculo-arterial couplingTh e concept that the cardiovascular system works better when the heart and the ar terial system are coupled has been well demonstrated [5,6]. When t he h eart pumps blood into the vascular tree at a rate and volume that matches the capability of the arterial system to receive it, both cardiovascular performance and its associated cardiac energetics are optimal [7,8]. A cont ract ility or arterial tone that is too high or too low decouples these processes and can lead to cardiac failure independent of myocardial ischemia or the toxic eff ects of sepsis and related systemic disease processes. Th is optimization means that the LV workload and the arterial system optimally match when the left ventricle ejects the blood into the arterial system and is quantifi ed by ventriculo-arterial (V-A) coupling analysis. Th is process is optimized without excessive changes in LV pressure, and the mechanical energy of LV ejection is completely transferred from the ventricle to the arterial system [9,10]. Th e ro le o f V-A coupling in the management of critically ill patients with severe hemodynamic instability and shock is becoming increasingly clear.V-A coupling can be defi ned as the ratio of the arterial elastance (Ea) to the ventricular elastance (Ees). Th is ratio was fi rst proposed by Suga [11] as a method t o evaluate the mechanica...