External Phonocardiograms Research Articles

Reinvestigation of the relationship between the amplitude of the first heart sound to cardiac dynamics

The relationships between the amplitude of the first heart sound (S1) and the rising rate of left ventricular pressure (LVP) concluded in previous studies were not consistent. Some researchers believed the relationship was positively linear; others stated the relationship was only positively correlated. To further investigate this relationship, this study simultaneously sampled the external phonocardiogram, electrocardiogram, and intracardiac pressure in the left ventricle in three anesthetized dogs, while invoking wide hemodynamic changes using various doses of epinephrine. The relationship between the maximum amplitude of S1 and the maximum rising rate of LVP and the relationship between the amplitude of dominant peaks/valleys and the corresponding rising rate of LVP were examined by linear, quadratic, cubic, and exponential models. The results showed that the relationships are best fit by nonlinear exponential models.

The First Heart Sound Immediately after Exercise as an Index of Exercise Stress

INTRODUCTION. This study investigated whether the amplitude of the first heart sound (AHS-1) and the diastolic time (DT) recorded immediately after exercising could be related to those values during exercise.METHODS. Nine male volunteers (24.6±2.9 years old) participated in this study. A discontinuous graded exercise test was performed on an electrically braked cycle ergometer. The external phonocardiograms were recorded during the test. The 10 highest AHS-1 during the last 30 sec at each stages and 10 consecutive AHS-1 immediately after each stage of exertion were measured. The DT was calculated as the systolic time subtracted from the cardiac cycle time interval assessed by the waveform of the heart sounds in the same time range as the above analysis.RESULTS. The change of AHS-1 during exercise and immediately after exercise at each stage demonstrated a significant correlation (r=0.979, p<0.01). The workloads at the breaking point during and immediately after exercise were the same. There were significant correlations between the DT during exercise and immediately after exercise in all (r=0.951 to 0.993, p<0.01).CONCLUSION. The results of this study clarified that AHS-1 and DT during exercise can be estimated from the phonocardiogram that is recorded immediately after exercise.

Relationship Between The First Heart Sound Amplitude And Blood Lactate Concentration During A Ramp Exercise

CONCLUSIONS: These results indicated that the HS monitoring during a ramp test is useful protocol in order to measure the HSBP. This could provide valuable information regarding exercise stress and effectively apply for an exercise prescription. PURPOSE: Heart sound (HS) is a convenient, noninvasive approach for evaluating cardiac performance. Valuable information regarding exercise stress may thus be detectable using the heart sound. Obara et al.(2005) reported that the amplitude of first HS (S1) accelerates above blood lactate threshold (LT) during a discontinuous graded exercise. However, monitoring heart sound during exercise has inherent limitation such as noises from chest movements. The purpose of this study was to investigate whether the S1 can continuously be recorded during a ramp exercise test. In addition, the possibility to be an application of an exercise prescription was explored. METHODS: Twenty volunteers underwent a continuous ramp test using a cycle ergometer. This test consisted of 4 minutes at 10 watts followed by a ramp slope at 1 watt every 4 or 6 seconds (i. e. 15 or 10 watts/minute) until exhaustion to measure the maximum oxygen consumption (VO2max). The external phonocardiograms were recorded both at rest and during the test. A microphone was placed in the manubrium of sternum. The amplitude of the S1 was measured beat-by-best throughout the exercise in millivolts and then averaged for 10 consecutive cycles. Moreover, the lactate concentration was measured in blood samples from an earlobe in order to determine the LT. RESULTS: The S1 steeply increased at a workload and the S1 breaking point (HSBP) was observed in all subjects. The slope of regression line of the S1 amplitude against workload was found to be steeper above the HSBP (double to 40 times of the slope before HSBP). HSBP and LT had significant relationships with VO2max (r=0.769, 0.872;p<0.01). There was no significant difference in the work rates corresponding to LT and HSBP (79.1±31.3 vs 80.4±20.0, p=0.470), and a significant relationship was observed between them (r=0.779,p<0.01). However, Bland-Altman plots showed an important bias (r=−0.548, p<0.05). A stepwise regression analysis revealed that HSBP and age contributed to 69.4% of variability in LT.

Noninvasive index of cardiac contractility during stress testing: a collaborative study.

The present study was conducted in parallel in three different institutions with a similar purpose but using different technical setups. Based on the experimental demonstration that the external phonocardiogram is similar to the rate of acceleration (d3P/d3t) of the left ventricular pressure, and that catecholamines in a similar way increase the early positive wave of the left ventricular pressure and the first heart sound (S1) of the external phonocardiogram; knowing that exercise causes secretion of catecholamines and sympathetic reflexes, we have studied the S1 changes as a result of exertion in 34 normal young subjects. Blood pressure, heart rate, electrocardiograph, and phonocardiograph recordings of each subject were taken. In 10 subjects, cardiac output was also recorded by impedance cardiography. The result of the study was that the first heart sound increased routinely 4-5 times the normal amplitude; in a few subjects the increase was up to 15 times greater. While the extent of increase of S1 was proportional to the severity and duration of the effort and was usually proportional to the increase of other parameters, exceptions were noted as having marked increase of S1 with moderate increase of either blood pressure or heart rate. This was explained by the different receptors activated by the catecholamines and by the complexity of hormonal and neural influences acting on various organs in a stress test. The amplitude of S1 was found to be a reasonably reliable index for following changes of cardiac contractility during exercise, and the suggestion was made that this parameter should be studied in parallel with the others in routine stress tests.

The genesis of the third and fourth heart sounds. A pressure-flow study in dogs.

To examine the mechanism of mitral flow deceleration in diastole and its potential influence on the genesis of third (S3) and fourth (S4) heart sounds, we simultaneously recorded left atrial and left ventricular pressures (micromanometers), mitral flow velocity (electromagnetic catheter-tip flow velocity meter), and internal and external phonocardiograms in 25 open-chest dogs. Diastolic time intervals, transmitral pressure gradients (planimetry), maximum mitral flow velocity, and acceleration and deceleration of flow were measured under different loading conditions. It was found that deceleration of mitral flow in early and late diastole is always caused by a negative transmitral pressure gradient. After volume loading, diastolic pressures, positive (forward) and negative (backward) transmitral pressure gradients, and acceleration and deceleration of flow increased, and an S3 or S4 appeared (20:25 dogs). These sounds occurred during the phase of flow deceleration and could be recorded from the chest wall, inside the left ventricle, and directly from the epicardial surface of the freely exposed left ventricular wall. After balloon occlusion of the inferior vena cava (17:25 dogs), the opposite changes were observed and gallop sounds disappeared. The results indicate that the left ventricular pressure rise in response to filling reverses the transmitral pressure gradient and decelerates flow. Deceleration of inflow by the left ventricular wall in early and late diastole may represent a key mechanism in the genesis of S3 and S4.

Systolic Time Intervals in Isolated Septal Defects before and after Corrective Surgery

Systolic time intervals (STI) were analyzed in 34 patients with isolated ventricular septal defect (VSD) and undirectional left-to-right shunt. 14 of the patients who underwent corrective surgery were followed-up for at least 10 years. The measurements were obtained from simultaneous high speed photographic recordings of electrocardiogram, external carotid pulse and phonocardiogram. Before the operation the Q-I sound interval and, consequently, the pre-ejection period were significantly prolonged and the left ventricular ejection time significantly abbreviated, the degree of abbreviation relating with the magnitude of the shunt. The above deviations persisted after corrective surgery, and only several years after the operation the parameters studied became normal. It is concluded that the most likely explanation for these abnormalities is the depressed contractility of the left ventricle, secondary to the long-standing volume overload, which tends to persist after corrective surgery.

Systolic Time Intervals in Isolated Septal Defects before and after Corrective Surgery in Female Patients

Systolic time intervals (STI) were evaluated in 19 female patients with uncomplicated ostium secundum atrial septal defect (ASD), before, shortly after (within 2 months) and a long time after the corrective surgery (mean 13.2 years). The measurements were obtained from simultaneous high speed photographic recordings of electrocardiogram, external carotid pulse and phonocardiogram. Before the operation, a significant prolongation of Q-I heart sound interval was detected, together with a less prominent but statistically significant shortening of the left ventricular ejection time; the above alterations were not correlated with the magnitude of the shunt and disappeared shortly after corrective surgery. The STI were still normal a long time after surgical closure of ASD. In accordance with hemodynamic studies reported by other authors, our results confirm that the deviations of STI observed in ASD are due to a reduced diastolic filling of the left ventricle secondary to an apparent decreased distensibility.

Aortic valve closure and cardiac vibrations in the genesis of the second heart sound

Simultaneous M-mode echocardiograms and external phonocardiograms were recorded in 15 healthy subjects to evaluate the genesis of the second heart sound. The onset of the second sound was found synchronous with the coaptation of the aortic valve cusps and a sharp vibration on the aortic wall. The closed valve was oscillating for 30 to 45 ms after the coaptation of the cusps. Magnified echocardiographic studies of the interventricular septum revealed a consistent, momentary quiver across the septal myocardium a mean of 4 ms after the onset of the second sound. In most subjects, a transient myocardial vibration was observed in temporal association with the first heart sound as well. The present observations suggest that the aortic valve closure initiates the production of the second heart sound, the main audible component resulting, however, from vibrations in the cardiac structures after the valve closure.

Phonocardiography in the Horse: 2. The Relationship of the External Phonocardiogram to Intracardiac Pressure and Sound

The paper describes observations during individual cardiac cycles on the changing pressures and sounds recorded from the various chambers of the heart and aorta, related to phonocardiograms from an external microphone hand-held over the cardiac area. The majority of the first sound appears to arise from the left side of the heart after the AV valves have closed and the second sound is a consequence of sudden deceleration of blood against already closed semilunar valves. Systolic murmurs at the aortic root may be benign from increased flow and turbulence at the peak of ejection but these may not be recorded externally.

PHONOCARDIOGRAPHIC RECORDING OF HETEROTOPIC CARDIAC GRAFT FUNCTION IN THE RAT I. DIAGNOSIS OF REJECTION

Daily simultaneous recordings of an electrocardiogram and an external thorax phonocardiogram and abdominal phonocardiogram were obtained in 24 rats with abdominal heart grafts so that rejection could be studied. The sounds recorded above the heterotopic heart are the result of a pressure differential between host and graft ventricle competing with one another. As soon as the contractility of the graft ventricle decreases below the contractility of the host ventricle, characteristic and specific changes occur in the abdominal phonocardiogram: the amplitude of the first sound becomes smaller while the timing of the second heart sound (aortic valve closure) is subsequently controlled by the host ventricle. These observations coincide with clinical and histological symptoms of rejection and are, therefore, of diagnostic value. In addition, a rough quantitative record of graft function is obtained by abdominal phonocardiography using the host's own cardiac function as a reference parameter.

Clinical Study on the Acoustic Phenomena in Coronary Venous System with Intracardiac Phonocardiography

In order to study the intracardiac murmurs in coronary venous system, right heart catheterization was carried out on 35 patients with or without mitral regurgitation. The double-lumen phonocatheter of A. E. L. was used for 33 cases but for 2 the microtip phonocatheter of Millar was employed. As a rule, simultaneous recording of intracardiac and external phonocardiograms was made with the pressure tracing in the majority of cases. The examined subjects were divided into 3 groups; 9 cases with mitral regurgitation confirmed by left ventriculography (Group I), 20 without mitral regurgitation (Group II), and 6 with functional systolic murmur (Group III). In Group I, a loud systolic murmur was recorded in 7 cases (MR 5, MR + AR 1, ECD 1), but in none of IHSS in the coronary sinus or great coronary vein. In Group II, no systolic bruit was noted in VSD and other lesions except ASR in the coronary venous system. The same was true in patients with functional systolic murmur (Group III). Intracardiac phonocardiography is thought to be useful to record mitral regurgitant murmurs in the coronary venous system, since the latter is in the close proximity to the mitral posterior commissure or mitral annulus.

Possible Mechanism of Wide Splitting of the Second Sound in Idiopathic Dilatation of the Pulmonary Artery

A patient with idiopathic dilatation of the pulmonary artery is presented. Simultaneous pressure tracings of the ventricles (right and left) and the two arteries (aortic and pulmonary) together with an external phonocardiogram, revealed no asynchronism in the closure of the two semilunar valves. The mechanism of the wide splitting of the second sound is discussed and is related to peripheral factors.

Sound pressure correlates of the second heart sound. An intracardiac sound study.

The sound pressure correlates of the second heart sound were studied in 22 patients during diagnostic cardiac catheterization. Simultaneous right ventricular and pulmonary artery pressures were recorded with equisensitive catheter-tip micromanometers together with the external phonocardiogram and ECG. In 12 patients having normal pulmonary vascular resistance (group 1), pulmonic closure sound was coincident with the incisura of the pulmonary artery pressure curve which in turn was separated from the right ventricular pressure trace by an interval denoted hangout. The duration of this interval varied (33-89 msec), was independent of pulmonary artery pressure or resistance and was felt to be primarily a reflection of the capacitance of the pulmonary vascular tree. The absolute value of this interval during inspiration was very similar to the splitting interval and, when subtracted from the Q-P 2 interval, the remaining interval (QRV) was almost identical to the Q-A 2 interval, indicating that the actual duration of right and left ventricular systole is nearly equal. Awareness of the existence of the hangout interval and its hemodynamic determinants offers a reasonable mechanism to explain the audible expiratory splitting of the second heart sound found in patients with idiopathic dilatation of the pulmonary artery following atrial septal defect repair and in one additional patient studied with mild valvular pulmonic stenosis. In nine patients with elevated pulmonary vascular resistance approaching systemic levels (group 2), the absolute value of the hangout interval was markedly reduced (15-28 msec) consistent with the decrease in capacitance of the pulmonary vascular bed and the increased pulmonary vascular resistance known to occur in pulmonary hypertension. In those patients where the duration of right and left ventricular systole were nearly equal, narrow splitting of the second heart sound was present. In those patients where selective prolongation of right ventricular systole occurred, the narrow hangout interval persisted, but the splitting interval was prolonged proportionate to the increased duration of right ventricular systole.

Right-sided austin flint murmur: Documentation by intracardiac phonocardiography, echocardiography and postmortem findings

A 25 year old man with multiple congenital cardiac defects, pulmonary hypertension, pulmonary reguritation had a loud mid-diastolic rumbling murmur with presystolic accentuation, heard best at the lower left sternal border and cardiac apex. Intracardiac and external phonocardiograms, echocardiograms and postmortem findings documented that the rumble represented a “right-sided Austin Flint” murmur.

Temporal relation of the second heart sound to aortic flow in various conditions

To establish the temporal relation of the second heart sound to left ventricular ejection during various conditions of preload, afterload and ventricular function, the electromagnetic aortic flow, aortic pressure, left atrial pressure, external phonocardiogram and electrocardiogram were recorded in 15 open chest chloralose-anesthetized dogs. Propranolol and atropine were infused to hold heart rate and contractility relatively constant. Preload was varied by volume changes, afterload by aortic constriction or angiotensin or methoxamine infusion, and ventricular function by citrate or barbiturate infusion. Fifteen-hundred cycles were analyzed using photographic recordings at 200 mm/sec with 0.04 or 0.004 second time lines. The onset of the second heart sound occurred an average of 5.2 ± 2.6 msec before the nadir of flow reversal and 23.2 ± 5.7 msec after the onset of rapid deceleration of flow. The latter interval could be varied by preload, afterload or changes in ventricular function without changes in the relation of the second sound to flow reversal. Recordings of the first derivative of aortic flow revealed the onset of the second heart sound to occur simultaneously with peak deceleration of aortic flow (0.3 ± 2 msec) under all hemodynamic conditions. External and internal systolic intervals correlated well during all maneuvers ( r = 0.90, P <0.001). These data indicate that the second sound is temporally related to flow reversal, not the onset of rapid deceleration, and support the hypothesis that the second sound results from the peak deceleration of forward flow and from the acceleration of backflow in the aorta.

Left atrial myxoma: Hemodynamic and phonocardiographic features

Two cases of left atrial myxoma are presented, with a review of clinical clues which may help in distinguishing this disease from mitral valve disease. Suggestive features in the apexcardiogram and internal and external phonocardiograms are discussed, together with related hemodynamic events indicated on the pulmonary capillary wedge, left atrial and left ventricular pressure tracings. The origins of various auscultatory features are analyzed in the light of specific hemodynamic events. Hemolytic anemia was present in one case, and ruptured chordae tendineae with scarring and myxomatous degeneration of the mitral leaflets in the other. Possible mechanisms for these lesions related to myxoma are discussed. The role of cardiac fluoroscopy, left ventricular cineangiography and the levophase of pulmonary angiography in helping to delineate left atrial myxoma is also mentioned.

Sound, pressure and motion correlates in mitral stenosis

Fifteen patients with mitral stenosis were studied during diagnostic cardiac catheterization in an effort to correlate the heart sounds of mitral stenosis with the corresponding mitral valve motion and intracardiac pressure events. In seven patients, mitral valve motion during cineangiography was correlated with a simultaneously recorded external phonocardiogram using the cine trace system. In seven additional patients, mitral valve motion during cineangiography was correlated with simultaneous sound and pressure events recorded with a catheter tip micromanometer using the cine trace system. The mitral component of the first heart sound occurred when the ascent of the mitral valve abruptly stopped at the point of maximal upward excursion which was coincident with the left atrial C wave. The mitral opening snap occurred when the descent of the mitral valve was abruptly halted at the point of maximal downward excursion which was coincident with the notch on the y descent of the left atrial pressure. Simultaneous equisensitive micromanometer pressures were obtained from the left atrium and the left ventricle in three patients. The mitral first heart sound occurred 18 msec after pressure crossover while a pressure gradient of 14 mm Hg developed between the left atrium and the left ventricle. The opening snap occurred 28 msec after pressure crossover while a pressure gradient of 11 mm Hg developed between the left atrium and the left ventricle. No flow occurred across the mitral valve until the point of maximal descent was reached. Following the opening snap, the initiation of flow into the left ventricle corresponded with the onset of the diastolic murmur. Subtle pressure transients recorded from the left atrium, left ventricle and central aorta using the catheter tip micromanometer were coincident with the mitral first heart sound and opening snap and could be clearly identified in the first derivative of these pressures. These data support the principle that sudden acceleration and deceleration of blood within the cardiohemic system is responsible for the production of heart sound transients. At the point of maximal ascent and descent of the mitral valve, a sudden change in the momentum of blood as it is arrested by the stenotic mitral valve sets the entire cardiohemic system into vibration. The higher frequency vibrations are appreciated as the mitral first heart sound and opening snap, whereas the lower frequency components are recorded as pressure transients.

Isovolumic contraction and left ventricular ejection times: External measurements at rest and after exercise in normal men

Sixty normal men, aged 26 to 64, had simultaneous external phonocardiograms at the apex, external right carotid arterial pulse tracings and electrocardiograms obtained in the supine position at rest, immediately after exercise and 3 minutes after exercise. Each subject exercised in the upright position on a bicycle ergometer at a load of 60 watts. The mean external isovolumic contraction time (EICT) was 0.041 ± 0.006 second at rest, 0.025 ± 0.005 second immediately after exercise and 0.036 ± 0.006 second 3 minutes after exercise. The mean left ventricular ejection time/external isovolumic contraction time (LVET/EICT) ratio was 7.4 ± 1.3 at rest, 11.0 ± 2.2 immediately after exercise and 8.2 ± 1.5 3 minutes after exercise.

The ejection click of valvular pulmonic stenosis.

Ten patients with valvular pulmonic stenosis were studied by simultaneous external phonocardiograms and intracardiac pressure recordings during successive respiratory cycles to examine the mechanism of the respiratory variation in the ejection click. Selective cineangiograms were performed in four. During inspiration right ventricular end-diastolic pressure (RVEDP) exceeded the pressure in the pulmonary artery (+2.7 mm) and no ejection click was recorded. During expiration RVEDP was lower than the pressure in the pulmonary artery (-3.6 mm) and a click was recorded. The click was present throughout the respiratory cycle when pulmonary artery diastolic pressure consistently exceeded RVEDP. Clicks were associated with sudden "doming" of the valve demonstated by cineangiography. These data support the valvular origin of the ejection click in pulmonic stenosis and provide the following explanation for the respiratory variation: Inspiratory increase in venous return causes the valve leaflets to move to an open or "domed" position. Ventricular systole at this time produces no sound since there is no slack. With expiration pulmonary artery pressure exceeds RVEDP. Ventricular systole at this time produces an opening motion of the closed, slack leaflets. The click occurs when the opening motion is suddenly checked.

Sound-pressure correlates of the aortic ejection sound. An intracardiac sound study.

The sound-pressure correlates of the aortic ejection sound (AES) were studied in six patients without aortic valve disease (group 1) and in nine patients with valvular aortic stenosis (group 2) during diagnostic left heart catheterization. Aortic root sound and pressure events were recorded by a catheter-tip micromanometer simultaneously with the external phonocardiogram, indirect carotid pulse, and electrocardiogram. The AES in group 1 patients was coincident with the onset of pressure rise in the aortic root. This relationship was not altered by drug administration, although variations in the amplitude of the AES occurred. It was concluded that the AES in patients without aortic valvular disease is an exaggerated ejection component of the normal first heart sound, and that it is a root phenomenon related to the forceful ejection of blood into the aorta. The AES in group 2 patients was delayed 24 to 40 msec after the onset of pressure rise in the aortic root, was coincident with the anacrotic notch, and introduced the aortic ejection murmur. Aortic root sound and pressure were recorded simultaneously with aortic valve motion during angiography in two patients utilizing a cine trace system. The AES occurred when the domed valve reached its maximal excursion, and the interval between the onset of aortic pressure rise and the AES was equal to the total time required for the piston-like ascent of the dome. It was concluded that the AES in valvular aortic stenosis is valvular in origin. The amplitude of the valvular AES correlated best with valve mobility on the angiogram, and no correlation existed between its presence and the severity of the valvular stenosis.