ABSTRACT
In undertaking the work described in this book, one of our goals was to develop a better clinical hydraulic measure of left ventricular load than was currently provided. This was available at the end of the twentieth century as arterial blood pressure measured non-invasively from brachial (or radial) cuff sphygmomanometry or from direct cannulation of the radial artery. The cuff is widely applied in clinical practice, in epidemiology, and in drug studies. Radial cannulation is frequently used by intensivists and anesthetists in operating rooms or intensive care wards. The pressure that one wishes to obtain is that in the ascending aorta, since this approximates that in the left ventricle during systole, and that at the coronary ostia during the period of diastole. We expected that such pressures (aortic systolic and pulse pressures) would be more relevant to left ventricular load and central artery circumferential stress than systolic and pulse pressures measured in the upper limb. We also expected that other indices derived from the aortic pressure wave, including its amplification to the upper limb, its augmentation from peripheral wave reflection, its integral during the periods of systole and diastole would provide more information on vascular load, cardiac function, and ventricular-vascular interaction. Results of such application are described later in this chapter and elsewhere, including Chapters 14 and 15. Initially, however, it is desirable to examine theoretic and practical implications which may detract from our ability to apply this information, and the approximations that are made in attempting to do so. The initial approximation was to use the carotid artery pressure waveform as a surrogate of the aortic pressure waveform. The carotid pressure waveform was rarely used by pioneers of sphygmography in the nineteenth century (although Mahomed (1872) published one tracing to show its different contour to the radial – see
Fig. 10.34). Mackenzie and Lewis used carotid waveforms, measured through tambours applied to the neck to identify and understand cardiac arrhythmias prior to availability of the ECG (Snellen, 1983). Carotid tracings were later used by Weissler (1968) and colleagues at Ohio State University for measurement of systolic time intervals as a measure of left ventricular (LV) function. This work was overtaken by introduction of echocardiography in the 1970s, but was reintroduced following development of arterial tonometry (Drzewiecki et al., 1983), and introduction of accurate instruments by Huntly Millar as a modification of his high fidelity catheter manometer (Murgo and Millar, 1972). Ray Kelly (O’Rourke and Kass, 2001) was responsible for the seminal studies with this instrument including calibration and validation (Kelly et al., 1989b; Kelly et al., 1989f) and the first drug study to show benefit of a vasodilating bblocker (dilevalol) over atenolol on carotid systolic pressure despite similar effects of both drugs on brachial systolic pressure and aortic pulse wave velocity (PWV) (Kelly et al., 1989d). Pressure and diameter waveforms are similar though not identical in the carotid artery and proximal aorta, so that one can be used as a surrogate of the other (van Bortel et al., 2001b). Pressure waves are basically similar in the ascending aorta and carotid artery (Kelly et al., 1989b; Chen et al., 1997), although amplitude of the augmented pressure wave is almost twice as high in the ascending aorta as in the carotid artery (Kelly et al., 1989a; Takazawa et al., 1998). The carotid pressure wave is widely used as a surrogate of ascending aortic pressure and a measure of central pressure (Kelly et al., 1989b; Chen et al., 1997; Kass et al., 1998; Mitchell et al., 2002; Mitchell et al., 2003; Mitchell et al., 2004a; Mitchell et al., 2004b; Mitchell et al., 2005a; Mitchell et al., 2005b; Dart et al., 2006; Mitchell et al., 2006; Dart et al., 2007; Mitchell et al., 2007a; Mitchell et al., 2007b; Segers et al., 2007b; Mitchell et al., 2008; Segers et al., 2009; Mitchell et al., 2010).
