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To assess the value of precordial percussion in detecting cardiomegaly, and to compare it with palpation of the apical impulse.Descriptive study.Hospitals and clinics of a university medical center.Light indirect percussion of the precordium was performed on 72 inpatients and 28 outpatients. All patients had a posteroanterior radiograph of the chest. Percussors were unaware of the clinical history and of chest roentgenogram results.Thirty-six patients (36%) had cardiomegaly, defined as a cardiothoracic ratio of greater than 0.5 on chest roentgenogram. The cardiothoracic ratio was significantly correlated with percussion distance from the midsternal line in the left fourth (r = 0.35, p less than 0.0006), fifth (r = 0.65, p less than 0.00001), and sixth (r = 0.40, p less than 0.0001) intercostal spaces. After adjustment for clinical symptoms and systolic and diastolic blood pressures, percussion distance in the left fifth intercostal space remained a significant independent predictor of the cardiothoracic ratio. Percussion distance in the left fifth interspace discriminated cardiomegaly with a receiver-operating characteristic (ROC) area of 0.95. Percussion dullness more than 10.5 cm from the midsternal line in the left fifth interspace had a sensitivity of 94.4% (95% confidence interval [CI], 79.9% to 99.0%) and a specificity of 67.2% (CI, 54.2% to 78.1%). Distance of the apical impulse from the midsternal line discriminated with an ROC area of 0.95, but an impulse was palpated in only 40% of cases.Percussion in the left fifth intercostal space accurately discriminates patients with and without cardiomegaly, and adds information beyond that obtainable from the history and other parts of the physical examination.

The vena cava and the pulmonary vein, as well as the atrioventricular (A-V) valves, emit loud sounds over a wide range of frequencies when tensed, under water, by application of moderate force. Much larger forces are required to elicit low-pitched sounds from the large arteries, strips of atrial or ventricular walls or even from most aneurysms of the left ventricle. Only the A-V valves seem capable of causing the heart sounds heard over the precordium, but the jugular and pulmonic veins could emit the sounds heard above the clavicles or from the esophagus at the level of the left atrium, synchronous with the venous atrial wave. Some ventricular aneurysms could contribute to low-pitched gallop sounds. The diastolic sounds recorded from patients with mitral Starr-Edwards prostheses have the high pitch and brief duration characteristic of the opening and closing sounds of the metal valves, and vary in the same way as third and fourth sounds from normal valves. This proves that third and fourth sounds usually are purely valvular in origin. Rapid ventricular filling, protodiastolic or presystolic, leads to kinetic forces from deceleration in the ventricles adequate to tense the A-V valves or force the ball into the atrial orifice of the prosthesis with sufficient force to evoke loud, high-pitched sounds. Lesser forces yield faint, low-pitched noises.

W E recently stumbled onto the fact that loud sounds could be recorded during atria1 systole over the jugular veins of patients with large P waves and elevated pressure in the right atrium. This led us to review the previous reports on auscultation over the jugular veins and finally to the conclusion that this phenomenon had escaped the notice even of those who had an intense interest in venous pulses and sounds. The published jugular phonograms do not show any presystolic sounds similar to those we have obtained, although faint sounds due to atria1 systole have been recorded repeatedly in the last four decades. Our first observation was the result of noting huge presystolic ballistocardiographic waves, headward and rightward, in a man with mitral stenosis, mild failure of the right side of the heart and a P-R interval of 0.26 seconds. (Fig. 1.) Routine precordial phonocardiograms showed a faint apical first sound, ascribable to the long A-V interval, together with classical presystolic murmurs and loud pulmonic second sounds. (Fig. 2.) No gallop could be detected over the precordium but as there were large spiked P waves, giant jugular a waves and minimal venous collapse in either systole or early diastole, the possibility of a tight tricuspid stenosis was considered. Phonograms taken from the right jugular bulb exhibited a loud, split presystolic sound. (Fig. 2.) The first and second sounds, faint in this area, were quite loud just below the clavicle where no presystolic sound was recorded. (Fig. 2.) Later, catheterization established the presence of tricuspid stenosis with normal pulmonary arterial pressure, and angiocardiograms showed a large right auricle which failed to empty in twenty seconds. In brief, seeing huge presystolic gallop waves in the ballistocardiograms with no gallop in routine precordial sound traces, led to recording a jugular gallop sound and establishing the diagnosis of tricuspid disease in a patient long considered to have pure mitral stenosis. The next day the same sound was recorded in a young woman returning for study after a mitral valvulotomy. Here, too, the gallop was not apparent just caudal to the right clavicle but the first and second sounds, together with a loud systolic murmur, also could be heard over the jugular vein, so that there was a local gallop rhythm not audible over the precordium. (Fig. 3.) In this patient there was no functional stenosis or insufficiency of the tricuspid valve since the jugular pressure falls sharply after the c and u waves. (Fig. 3.) Thus we learned that the presystolic gallop over the jugular bulb was not pathognomonic of tricuspid stenosis. Within a few days opportunity arose to seek this sound in two patients with congenital heart disease who had previously been catheterized and known to have high right auricular pressure without mitral or tricuspid disease. Both had a presystolic gallop of great intensity, recorded only over the jugular bulb. (Fig. 4.) Failure to record anything but faint sounds or inaudible vibrations from the jugular bulb of normal subjects or from patients with left ventricular failure and normal venous pressures, forced us to conclude that a loud presystolic sound limited to the veins was pathognomonic of right atria1 hypertension. The main facts concerning the first twelve subjects with loud presystolic jugular sounds are

TAGGED RED CELLS IN SELECTION OF PATIENTS FOR SPLENECTOMY. Paul R. McGurdy, Charles E. Roth and Benedict J. Dy three have improved. These patients had maximum spleen/ precordium ratios of 1.5 or more and increases in spleeni’precordium ratios over the initial readings (sequestration index) of 0.5 or more. The unimproved patient had a maximum spleen/precordium ratio of 0.7 and a sequestration index of 0.25. Improvement following splenectomy coincides with the results predicted. In five of the remaining eight patients the test results did not favor splenectomy. Two of the others are now being prepared for surgery. It is concluded that the technic of body scanning described may be helpful in selecting patients with hemolytic anemia for splenectomy.