The assessment of ventricular systolic performance is one of the most important roles of perioperative echocardiography. Ventricular function is a key determinant of cardiac output, and global or regional dysfunction may be present before surgery or develop de novo perioperatively. Patients with coronary disease are particularly at risk. The ability of the echocardiographer to recognize such abnormalities is critical to optimal patient care.
In most clinical settings, the assessment of ventricular systolic function is performed qualitatively and relies heavily on the scanning ability and trained interpretive eye of the echocardiographer. The ability to accurately assess global and regional ventricular systolic function is one of the most difficult transesophageal echocardiographic (TEE) skills to acquire, and there is no shortcut to supervised training and ongoing continuous quality improvement, ideally with access to an independent gold standard.1 Paradoxically, whereas quantitative methods may require more time for image acquisition and processing, interpretation of the results of such approaches may be relatively straightforward.
All the methods presented in this chapter were first described using transthoracic imaging methods and have been extrapolated to the transesophageal approach. However, it is worth noting that, in some situations, studies directly validating TEE-based applications have not been performed. Because right ventricular (RV) performance is arguably equally important, methods of assessing RV function are discussed in Chapter 9.
THE PHYSIOLOGY OF VENTRICULAR FILLING AND CONTRACTION: PRESSURE-VOLUME RELATIONS
A basic understanding of ventricular physiology, in particular pressure-volume relations, is essential to appropriate utilization of available methods of assessing left ventricular (LV) systolic performance.
The cardiac cycle includes three basic phases: ventricular contraction, relaxation, and filling. LV contraction is initiated when, as a result of rising cytosol calcium levels, the actin and myosin filaments increase the degree to which they overlap, resulting in sarcomere shortening. As more and more cardiomyocytes are activated, the LV begins to contract and LV pressure rises. The LV pressure continues to rise until it overcomes the left atrial pressure, at which point the mitral valve closes. During isovolumic contraction, the period between mitral closure and aortic opening, the LV pressure continues to rise. When it exceeds the aortic pressure, the aortic valve opens and blood is ejected. As ejection continues, LV pressure peaks and begins to decrease. When it decreases below the aortic pressure, the aortic valve closes and ejected blood continues to be propagated through the systemic circulation. On a cellular level, calcium is taken up by the sarcoplasmic reticulum, and the myofilaments enter a state of relaxation. Because the mitral and aortic valves are in a closed position, ventricular volume remains constant. This period is known as isovolumic relaxation. With continued relaxation, LV pressure decreases further and the mitral valve opens. LV filling occurs in response to the gradient between the left atrium and the ventricle. This first period of filling is known as the early diastolic filling ...