Mechanical Function of the Left Atrium

Abstract

tile chamber that actively empties immediately before the onset of LV systole and establishes final LV end- diastolic volume.1,2 The LA is a reservoir that stores pulmonary venous return during LV contraction and isovolumic relaxation after the closure and before the opening of the mitral valve.3 Lastly, the LA is a conduit that empties its contents into the LV down a pressure gradient after the mitral valve opens4 and continues to passively transfer pulmonary venous blood flow during LV diastasis. These contraction, reservoir, and conduit func- tions of the LA mechanically facilitate the transition be- tween the almost continuous flow through the pulmonary venous circulation and the intermittent filling of the LV.5 The contractile activity of the LA was initially de- scribed by William Harvey in 1628.6 This “booster pump” contribution to cardiac output7–10 normally ac- counts for approximately 20% of LV stroke volume11 but becomes increasingly important to the preservation of cardiovascular performance in patients with reduced LV compliance.12,13 The enhanced significance of atrial sys- tole to LV filling in patients with LV dysfunction is emphasized by the frequently observed development of clinical signs and symptoms of heart failure when LA contraction is improperly timed14–16 or eliminated with the onset of atrial tachyarrhythmias.11 These adverse effects are reversed with the subsequent restoration of normal sinus rhythm and LA contraction.11 The relative impact of LA reservoir function on early LV filling was initially recognized by Henderson et al.,17 and the de- pendence of reservoir function on LA compliance was later identified by Suga.5 While these and other early studies provided seminal information about LA function, comprehensive evaluation of LA performance in the nor- mal and diseased heart was limited by lack of effective techniques for reproducibly measuring continuous LA volume and pulmonary venous blood flow until the 1980s. This objective has subsequently been facilitated by the application of pressure–volume theory adapted from LV function analysis and by the widespread use of two-dimensional and Doppler echocardiography. This article critically reviews recent advances in the under- standing of LA physiology derived from pressure–volume relations and echocardiography, discusses the mechanical consequences of primary LA dysfunction, examines LA mechanical adaptation to LV dysfunction, and describes current knowledge about the actions of volatile and intravenous anesthetics on LA function in vivo.