Left ventricle is 4.5 cm across internally. At 8-15 mm thick, it is both thicker and larger than the RV.
The most basic measure of systolic function is cardiac output, which is usually indexed to body surface area (normal cardiac index [CI] is 2.5 to 3.5 L/min/m2). During high-stress situations CO can increase to as high as 30 L/min in some individuals.
Stroke volume is a superior to CI as a measure of systolic function because it corrects for changes in heart rate. Stroke volume is determined by contractility, preload, and afterload. It should be kept in mind that while contractility, preload, and afterload can be thought of independently, in the intact cardiovascular system all three variables are related/interdependent.
Technically defined as the amount of work produced by the heart given certain loading conditions (preload and afterload). Unfortunately, most readily available indices of contractility (ex. ejection fraction) and even some more invasive indices (ex. ventricular dP/dt) are load-dependent. More complex metrics, such as the slope of the end-systolic pressure-volume relation (ESPVR) (developed by Suga and colleagues, relates maximal end-systolic elastance [Ees] under various loading conditions) appear to be less load dependent. Note also that contractility is dependent on heart-rate, with increased heart rate leading to increased contractility (Bowditch Phenomena).
According to Kaplan, preload is technically defined as ventricular wall stress at end-diastole [Kaplan JA, ed. Essentials of Cardiac Anesthesia. Saunders, 2008 p 60; however, ventricular volume at end-diastole may be a more clinically useful definition – first, it is more easily measured (by echocardiography) and second, it is the geometrical configuration of the ventricle (in particular, interactions between actin and myosin) that determines the maximum amount of wall-stress generated.
Ventricular preload can be altered by blood volume, intrathoracic (and pericardial) pressure, body position, venous tone, exercise, atrial function, valvular stenosis, and ventricular thickness.
Normally related to contractility via the Frank-Starling curve, whether or not there is a descending portion of the Frank-Starling curve in humans is a matter of debate [Parker JO and Case RB. Circulation 60: 4, 1979; FREE Full-text at Circulation]
Afterload is most commonly defined as either left ventricular wall stress during systole (which, by Laplace’s law, is equal to [Pr/2h]) or as aortic input impedance (a biphasic descriptor [modulus and phase] of the forces which oppose pulsatile flow, primarily vascular resistance, aortic compliance, and wave reflections). Proponents of wall stress point out that myocardial VO2 is related to wall stress, whereas proponents of impedance point out that wall stress is to some degree determined by the ventricle itself (since S = Pr/2h) and thus cannot represent an external load (which is what afterload is supposed to be) [Nichols WW, Pepine CJ. Prog Cardiovasc Dis 24: 293, 1982]. SVR is a drastic oversimplification of afterload and has been shown to be poorly related to wall stress [Lang RM et al. Circulation 74: 1114, 1986; FREE Full-text at Circulation]
The relaxation phase of the cardiac cycle is just as important as the contractile phase (systole) in overall cardiac function. In fact, isolated diastolic dysfunction is present in up to 50% of patients who have congestive heart failure [Kaplan JA, ed. Essentials of Cardiac Anesthesia. Saunders, 2008 p 56]. Ventricular relaxation, formerly thought to be a passive process, is an active, energy-consuming process (called lusitropy) that involves redistribution of calcium from the cytosol into the sarcoplasmic reticulum.
Adequacy of ventricular filling is related to transmural pressure (pressure across the ventricular wall), ventricular compliance, and filling time (inversely related to HR). According to Barash, increasing the HR from 60 bpm to 160 bpm can decrease filling time from 400 ms to 10 ms [Barash, PG. Clinical Anesthesia, 5th ed. (Philadelphia), p. 863, 2006
Until recently, very few pharmacologic agents were known to improve diastolic relaxation, thus modification (when possible) of the traditional causes of impaired relaxation (aging, coronary artery disease, ventricular hypertrophy, and a variety of pharmacologic agents), combined with appropriate management of physiologic parameters (ex. filling pressures) were the only options available to the practitioner.
The recent appreciation for the importance of active relaxation is the basis for the development of novel pharmacologic agents (called lusitropes) that are designed to improve myocardial relaxation. Levosimendan (a calcium sensitizer [Jörgensen K et al. Circulation 117: 1075, 2008; FREE Full-text at Circulation]) and istaroxime (inhibits the Na+/K+ ATPase and stimulates sarcoplasmic reticulum calcium ATPase [Shah SJ et al. Am Heart J 157: 1035, 2009]) are two lusitropic agents recently developed and under investigation – the former has been studied in the intraoperative setting, the latter has not.
TEE Assessment of Diastolic Function
Can be assessed by examining mitral inflow velocities (E and A wave) during apnea and end-Valsalva, tissue doppler imaging of the mitral annulus (E/e’ > 15 implies moderate dysfunction) and pulmonary venous inflow. For a thorough discussion on echocardiographic assessment of diastolic function and the importance of diastolic function in cardiac anesthesia, please see [Sanders D et al. Anesthesiol Clin 27: 497, 2009; FREE Full-text at PubMed Central]