Chapter 5 / Precordial Pulsations 113 5 Precordial Pulsations CONTENTS MECHANICS AND PHYSIOLOGY OF THE NORMAL APICAL IMPULSE PHYSICAL PRINCIPLES GOVERNING THE FORMATION OF THE APICAL IMPULSE NORMAL APICAL IMPULSE AND ITS DETERMINANTS ASSESSMENT OF THE APICAL IMPULSE LEFT PARASTERNAL AND STERNAL MOVEMENTS RIGHT PARASTERNAL MOVEMENT PULSATIONS OVER THE CLAVICULAR HEADS PULSATIONS OVER THE SECOND AND/OR THIRD LEFT INTERCOSTAL SPACES SUBXIPHOID IMPULSE PRACTICAL POINTS IN THE CLINICAL ASSESSMENT OF PRECORDIAL PULSATIONS REFERENCES In this chapter the pulsations of the precordium will be discussed in relation to their identification, the mechanisms of their origin, and their pathophysiological and clinical significance. Precordial pulsations include the “apical impulse,” left parasternal movement, right parasternal movement, pulsations of the clavicular heads, pulsations over the second left intercostal space, and subxiphoid impulses. MECHANICS AND PHYSIOLOGY OF THE NORMAL APICAL IMPULSE Since during systole the heart contracts, becoming smaller and therefore moving away from the chest wall, why should one feel a systolic outward movement (the apical impulse) at all? Logically speaking there should not be an apical impulse. Several different methods of recording the precordial motion have been used to study the apical impulse going back to the late 19th century (1,2). Among the more modern methods, the notable ones are the recordings of the apexcardiogram (3–17), the impulse cardiogram (18), and the kinetocardiogram (19–21). While apexcardiography records the relative displacement of the chest wall under the transducer pickup device, which is often held by the examiner’s hands, the proponents of the impulse cardiography and kinetocardiography point out that these methods allow the recording of the absolute movement of the chest wall because the pickup device is anchored to a fixed point held 113 114 Cardiac Physical Examination in space away from the chest. Kinetocardiography uses a flexible metal bellows probe coupled by air transmission to the manometer. The impulse cardiogram, on the other hand, utilizes a light metal rod with a flag at one end, held by light metal springs attached to a Perspex cone. The light metal rod with the flag is coupled directly to a photoelectric cell, the instrument being held rigidly in a metal clamp fixed to a stand. Despite its limitations, apexcardiography has been extensively studied with simultaneous left ven- tricular pressures obtained through high-fidelity recordings with the use of catheter- tipped micromanometers (8,14,15). These studies have demonstrated clearly that the upslope of the apexcardiogram corresponds closely to the rise of the pressure in the left ventricle during the isovolumic phase of systole. The summit of the systolic upstroke of the apexcardiogram (the E point) occurs about 37 ms after the opening of the aortic valve and roughly 40 ms after the development of the peak dP/dt of the left ventricular pres- sure in normal subjects (15). These observations are also consistent with the findings obtained using kinetocardiography (20). When the apical impulse is recorded by kineto- cardiography, it is seen to begin about 80 ms after the onset of the QRS in the electro- cardiogram and about 10 or 20 ms before the carotid pulse upstroke. These observations indicate, therefore, that the apical impulse begins to rise during the pre-ejection phase of the left ventricular contraction and must therefore involve part of the isovolumic phase of systole, and the peak movement must involve the early rapid ejection phase of systole. Timed angiographic studies of Deliyannis and co-workers (22) show that the portion of the heart underlying the apex beat is usually the anterior wall of the left ventricle, which moves forward during early systole and moves away and backward from the chest wall during mid-late systole. They suggest that the forward movement of the left ven- tricle in early systole is caused by the contraction of the middle circular fibers, which are confined to the upper three-fifths of the normal heart. The falling away of the apex of the left ventricle in late systole is attributed to the contraction of the spirally oriented fibers overlying the apex of the left ventricle, since in the normal heart the middle circular fibers do not extend to the apex. They further suggest that in left ventricular hypertrophy, the middle circular fibers extend to the apex completely, thereby preventing the movement away of the apex from the chest wall in mid-late systole (according to these authors accounting for a sustained duration of the apical movement when there is underlying left ventricular hypertrophy). A variety of explanations have been given for the presence of the normal apical impulse. The common explanation is that the heart rotates counterclockwise along its long axis during contraction, causing the left ventricle to swing forward to hit the chest wall (23–25). This twisting motion has been observed in the beating heart when exposed at surgery. This rotation is along the axis of the left ventricle. Torsional deformation of the left ventricular midwall in human hearts with intramyocardial markers has in fact been demonstrated. This appears to have some regional nonuniformity. Torsional defor- mation appears to be maximal in the apical lateral wall, intermediate in the apical inferior wall, and minimal in the anteroapical wall. Torsional changes were less at the midven- tricular level compared to the apical segments with similar regional variation. The exact cause of the regional variations is not defined. The possible causes suggested by these authors include variations in the left ventricular fiber architecture as well as the asym- metrical attachment of the left ventricle to the mitral annulus posteriorly and the aortic root anteriorly (26). The papillary muscles together with the underlying left ventricular Chapter 5 / Precordial Pulsations 115 myocardium contract during systole to keep the mitral leaflets together in the closed position, preventing their evertion into the left atrium with the rising intraventricular pressure. In the process, the closed mitral apparatus must exert an opposite pull on the individual papillary muscle groups. It is possible that the asymmetrical attachment of the mitral apparatus to the left ventricle may result in an asymmetrical pull on the papillary muscles with a stronger pull on the antero-lateral papillary muscle group and the under- lying left ventricular myocardium compared to the pull exerted on the postero-medial papillary muscle group. This might also be a contributory factor in the accentuated torsional changes seen in the apical lateral walls. In addition, during the phase of iso- volumic contraction, it has been shown that there is an increase in the external circum- ference of the left ventricle together with a decrease in the base-to-apex length (27). However, these changes during systole alone are still insufficient to explain the apical impulse, which must result from hitting of the inside of the chest by the left ventricle. Because during systole all fibers contract and the ventricular walls thicken all around, the overall size becomes smaller the moment ejection begins, and therefore the heart would not be expected to come closer to the chest wall. Thus, the genesis of the apical impulse is poorly explained by these mechanisms alone. The formation of the apical impulse is perhaps better understood when simple prin- ciples of physics are also considered, since they are applicable in relation to the heart and the great vessels. Stapleton refers to these indirectly when he states that the apical impulse “probably represents recoil movement which develops as left ventricular output meets aortic resistance”(20). PHYSICAL PRINCIPLES GOVERNING THE FORMATION OF THE APICAL IMPULSE The heart is essentially a pump connected to the aorta and the pulmonary artery, both of which are conduits of fluid (blood). Therefore, pure physical principles of hydrody- namics should be sufficient to explain the mechanism of the apical impulse formation with one important anatomical consideration, which is the fact that the aorta is essen- tially a coiled pipe (aortic arch) and fixed posteriorly at the descending segment. Newton’s third law of motion indicates that for every action there is equal and oppo- site reaction. This effect is easily demonstrated in a simple physics experiment (Figs. 1A,B and 2). Similarly, as the left ventricle contracts and the intracavitary pressure rises during the isovolumic contraction phase (after the mitral valve closure and before the aortic valve opening), this pressure is equally distributed on all the walls of the left ventricle, including the apex and the closed aortic valve. There could be some change in shape and possibly torsional deformation during the time of the peak acceleration of the left ventricular pressure development. No appreciable motion of the heart occurs, how- ever, because forces on the opposing walls balance out. This equilibrium is disturbed once the aortic valve opens and ejection begins. As in the physics experiment, similar to the beaker’s movement in the direction opposite to the flow of water, the unopposed force on the apex of the left ventricle will move the left ventricle downward (Figs. 3A,B). Ejection of fluid under pressure into a coiled pipe will have a tendency to straighten out the pipe as is commonly observed with the coiled garden hose as the water is turned on. With the aorta representing a coiled pipe, ejection of the left ventricular stroke volume into the aorta under pressure will have a tendency to straighten the aortic arch. 116 Cardiac Physical Examination Fig. 1. (A) Atmospheric pressure (bold arrows) exerted on water in the beaker is evenly distrib- uted on all sides of the beaker (short arrows in beaker), and the system is in equilibrium. (B) When the tap on the beaker is opened and the water runs out, the forces pushing on the left side of the beaker are no longer balanced by equal and opposite forces; therefore, the beaker and the cork it is sitting on will move to the left.