External Phonocardiograms Research Articles

Unusual hemodynamic findings of diagnostic value in a case of left atrial myxoma ∗

Unusual laboratory findings in a case of left atrial myxoma are presented. The end-diastolic pressure gradient between the left ventricle and wedge position ranged from 0 to 21 mm. Hg with no relation to heart rate or rhythm, respiration, or wedge position. The y descent was slow rather than the usual rapid y descent associated with mobile atrial myxomas. These findings probably were caused by left atrial inflow obstruction rather than outflow obstruction. Pressure transients owing to sudden acceleration and deceleration of the tumor and surrounding blood, with subsequent oscillations of the heart and great vessels, were recorded in the left ventricle, aorta, external carotid pulse, and external phonocardiogram during the phase of isovolumic contraction and during a period beginning with isovolumic relaxation through rapid ventricular filling. These findings, when present, strongly suggest the presence of a mobile atrial tumor.

Effect of respiration on pansystolic regurgitant murmurs as studied by biatrial intracardiac phonocardiography

Twelve patients have been studied in an attempt to delineate the effect of continuous accentuated respiration on the intracardiac murmurs of mitral and tricuspid insufficiency. External phonocardiographic and stethoscopic observations have been made in order to demonstrate the correlation between internal and external acoustical events and to derive some knowledge regarding the validity of Carvallo's observations. Of the eleven patients with mitral insufficiency, eight were studied by left atrial phonocardiography. In none did respiration result in an altered intensity of the murmur of mitral insufficiency when recorded in the left atrium. In eight patients with mitral insufficiency and associated tricuspid insufficiency, marked inspiratory augmentation of the regurgitant murmur was recorded in the right atrium. Thus, the two premises upon which Carvallo's sign rest are valid, namely, that respiration does not affect the intensity of the murmur of mitral insufficiency while inspiration results in augmentation of the tricuspid regurgitant murmur in every case when these murmurs are recorded at their source. The external phonocardiogram clearly demonstrated inspiratory augmentation of the tricuspid regurgitant murmur in four patients with tricuspid insufficiency. A less obvious but similar response was noted in an additional three patients. However, stethoscopic examination of these seven patients clearly demonstrated inspiratory augmentation of the systolic regurgitant murmur in every case. Thus, careful auscultatory examination may be more reliable than external phonocardiography in detecting changes in intensity of the tricuspid regurgitant murmur. In the eighth case of combined mitral and tricuspid insufficiency, neither the external phonocardiogram nor the stethoscopic observation demonstrated external augmentation of the regurgitant murmur. In this instance, the diagnostic value of intracardiac phonocardiography is clearly demonstrated. In addition, observations concerning the importance of selective augmentation of the regurgitant murmur in the diagnosis of tricuspid insufficiency have been discussed and an additional pitfall of confusing a long ejection murmur with a regurgitant murmur has been demonstrated. It is apparent from these studies that selective inspiratory augmentation of a pansystolic regurgitant murmur, when present, continues to be a useful sign of tricuspid insufficiency.

Rate of rise of left ventricular pressure: Indirect measurement and physiologic significance

An indirect measurement of the maximum rate of rise of left ventricular pressure (dP/dt Max.) was derived by dividing aortic diastolic pressure (Pd) by the interval between the first rapid vibration of the first sound and the beginning of ventricular ejection (S 1X), using appropriate recordings of aortic and ventricular pressures and external phonocardiograms from intact anesthetized dogs. A very close correlation of Pd/S 1X with the direct measurement of dP/dt Max. was found (R = 0.92) under a variety of experimental conditions designed to alter aortic pressure and ventricular filling pressure, output and contractile capacity. Pd/S 1X, the interval S 1X, and the mean systolic ejection rate (MSER) were compared as indices of ventricular contractile capacity under various experimental circumstances. All indices reflected the inotropic effects of epinephrine and hypocalcemia, but S 1X and MSER were more misleading than Pd/S 1X when the circulatory alteration included a change of aortic diastolic pressure.

The Identification of Mild Mitral Regurgitation: Its Separation from Innocent Murmurs by Intracardiac and Esophageal Phonocardiography Combined with Pharmacologic Response.

s1 October 1964The Identification of Mild Mitral Regurgitation: Its Separation from Innocent Murmurs by Intracardiac and Esophageal Phonocardiography Combined with Pharmacologic Response.Richard F. Leighton, M.D., William L. Page, M.D., Richard S. Goodwin, M.S., Charles F. Wooley, M.D., Joseph M. Ryan, M.D., F.A.C.P.Richard F. Leighton, M.D.Search for more papers by this author, William L. Page, M.D.Search for more papers by this author, Richard S. Goodwin, M.S.Search for more papers by this author, Charles F. Wooley, M.D.Search for more papers by this author, Joseph M. Ryan, M.D., F.A.C.P.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-61-4-797_1 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptNine patients, aged 19 to 48, with apical systolic murmurs, without radiologic or electrocardiographic evidence of cardiac enlargement, were studied. An innocent murmur was frequently suspected. All had external phonocardiograms with pharmacologic studies. Phonocardiograms were also recorded from within the esophagus at the atrial level in eight, and from within the left and right sides of the heart in five and seven patients, respectively. Right heart and pulmonary artery murmurs were thereby excluded and mitral regurgitation was diagnosed in all patients. Confirmation was obtained in three who had left ventricular angiography.These murmurs were of high frequency and either pansystolic... This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Columbus, Ohio PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 October 1964Volume 61, Issue 4Page: 797-797KeywordsAngiographyElectrocardiographyEsophagusHeartMitral insufficiencyPatient advocacyPulmonary arteriesSystolic ejection murmur Issue Published: 1 October 1964 PDF downloadLoading ...

An Atlas of Hemodynamics of the Cardiovascular System.

Modem devices for detecting pressure and sound in the cardiovascular system have added much to our understanding of normal and abnormal heart action. In this volume the authors describe their own observations of these phenomena, mainly in dogs with experimental valvular heart disease. The effects of acute valvular lesions on pressure pulses simultaneously recorded from several cardiac chambers occupies most of the first half of the book, while other topics, principally intracardiac pressure pulses in experimentally produced arrhythmias, are dealt with in the remaining pages. Intracardiac and external phonocardiograms frequently are related to events in the pressure tracings. A few angiocardiograms also are included. The illustrations carry the burden of the book's message. Each takes up a full page opposite a descriptive block of text in which the causes, hemodynamic consequences, clinical manifestations, and therapy of the lesions are discussed. Since the pressure recordings were obtained with manometric systems free

Hemodynamic correlates of the various components of the first hear sound.

Previous studies in this laboratory having demonstrated that AV valve closure is not directly responsible for the rapid vibrations of the first heart sound, the mechanism of production of this "sound" was studied further in 30 experiments in dogs. The experiments were performed with multiple pressure catheterization, and intracardiac phonocatheterization, and were compared with external phonocardiograms and electrocardiograms. In 10 experiments, the first derivatives of the left and right ventricular pressures were also recorded. In four experiments, direct epicardial and arterial sound tracings were obtained. These experiments revealed that three groups of vibrations, or components, were often visible in the external phonocardiogram, and in intracardiac and epicardial tracings. The first component follows the onset of left ventricular pressure rise and closure of the mitral valve but coincides with the rapid rise of the first derivative of LV pressure. The second component has no relationship with right heart events, occurs before aortic valve opening, and coincides with the sudden change of course of the first derivative of LV pressure. The third component occurs slightly after aortic valve opening, and seems related to sudden increase of aortic wall tension. It is probably the physiological equivalent of the aortic "ejection sound." Thus, the first two components are both left ventricular in origin while the third is of aortic origin.

Left heart studies in mitral stenosis with special reference to intracardiac phonocardiography

1. 1. A study was made of 33 patients with mitral valve disease by means of left and right heart catheterization, conventional phonocardiography and intracardiac phonocardiography of the right and left heart. The intracardiac phonocardiogram was recorded by the electronic method from the catheter used for recording pressures. Fourteen cases were operated upon, and 2 of them were examined at autopsy. The severity of the diagnosis was confirmed by the surgeon. 2. 2. A minor delay (10 milliseconds) was found in the vibrations of the intracardiac phonocardiogram over those of the external phonocardiogram. These are inherent in the method used. 3. 3. The intracardiac phonocardiogram proved of great utility in identifying the murmurs, their point of origin, their phase and mechanism. Greater amplitude of the third or fourth sound, and of the opening snap, was often found. 4. 4. A comparative study of the intracardiac sounds and pressures revealed that the first sound is delayed over the point of crossing of the ventricular and atrial pressures, and that the opening snap is delayed over the point of crossing of the atrial and ventricular pressures, confirming data already gathered in an experimental study. 5. 5. The first sound of the left side of the heart often followed that of the right side. This was particularly evident in cases with atrial fibrillation after a short diastole, and was true only in severe mitral stenosis. This confirms previous statements by others. 6. 6. Even though a relationship was found between Q-1 and 2-OS, respectively, and both the values of the left atrial mean pressure and the left atrial-left ventricular diastolic gradient, this relation was not as close as stated by previous authors, possibly because their data were based on right heart catheterization alone or catheterization plus surgical findings.

Hemodynamic correlates of the fourth heart sound.

Intracardiac phonocardiographic characteristics of the atrial sounds and the relation of these vibrations to mechanical and electrical events of the cardiac cycle were studied in 21 dogs. Simultaneous recordings of intracardiac (from RA, LA, RV, and LV) and external phonocardiograms and equisensitive intracardiac pressures confirmed that the atrial sound is commonly formed by two main sets of vibrations: the first coincident with the onset of the atrial "a" wave, the second with its highest pressure peak. It is suggested that the first group of vibrations is usually due to atrial contraction and the second to ventricular filling. A short reversal of presystolic AV pressures after atrial relaxation occurred in some of the cases, suggesting that here a valvular mechanism was involved in the production of the late component of the atrial sound. The rapid intravenous infusion of saline generally increased the amplitude of the atrial sound and made evident the presence of a second component. The administration of drugs inducing systemic or pulmonary hypertension failed to give consistent changes in the amplitude and timing of the atrial sound. An asynchronism between right and left atrial sounds was demonstrated, the right-sided presystolic vibrations preceding those of the left heart by 0.026 sec (AS1) and 0.023 sec (AS2), respectively, in accordance with the earlier electrical activation and contraction of the right atrium.

Hemodynamic correlates of the first heart sound

The temporal relationship between the "crossing" of equisensitive atrial and ventricular pressure tracings and the initial components of the first heart sound of the homolateral intracardiac phonocardiogram was analyzed in 35 dog experiments. These studies showed that the first component of the first heart sound followed the atrioventricular valve closure (AV crossing) in all instances by an average time interval of 23 msec and that, at the time of its occurrence, there was a ventricular-atrial pressure gradient of 5 mm Hg in the right side and of 14 mm Hg in the left side of the heart. It is concluded that valvular closure, per se, does not cause the first component of the first heart sound. Actually the first heart sound occurs later during the period of isometric ventricular contraction, suggesting that the rise of ventricular pressure is responsible for its vibrations. Comparative analyses of right and left intracardiac and external phonocardiograms showed that the right side component of the first heart sound follows the left in about three-fourths of the cases and is coincident with it in the remainder and that these events are reflected in the same order in the external phonocardiogram.

The effects of amyl nitrite and phenylephrine on the intracardiac murmurs of small ventricular septal defects

1. 1. Synchronous external and internal phonocardiographic tracings were recorded in 8 patients who had small ventricular septal defect (less than 45 per cent left-to-right shunt) and normal pulmonary arterial pressure, and were without pulmonary stenosis. The external phonocardiograms showed a widely radiating pansystolic murmur, either plateau shaped or with a late crescendo. The internal phonocardiogram showed a similar murmur in the right ventricle. In 3 patients the murmur due to the ventricular septal defect radiated widely into both pulmonary arteries but was not equally loud at all sites in the right ventricle, suggesting jet flow of shunted blood down the pulmonary arteries. In 3 patients the septal-defect murmur was confined to the ventricle, and a separate pulmonary ejection murmur was recorded beyond the pulmonary valve. 2. 2. Amyl nitrite softened the pansystolic regurgitant murmur recorded in the right ventricle. In the pulmonary artery, however, the short ejection murmur was intensified, but this had no influence on the externally recorded murmur, which also softened. 3. 3. Phenylephrine produced marked intensification and prolongation of the murmur in the right ventricle and of the externally recorded murmur, and in one subject the intrapulmonary ejection murmur intensified. 4. 4. Since changes in the chest-wall murmur closely parallel changes in the right ventricular murmur, variation in intensity of the chest-wall murmur alone provides information of the change in volume rate of shunt flow. 5. 5. In the case of minute ventricular septal defect the tracings recorded at the fourth left intercostal space and in the right ventricle both showed the characteristic crescendo-decrescendo murmur which softened after amyl nitrite and intensified and lengthened after phenylephrine. The intrapulmonary ejection murmur increased with amyl nitrite. Since the septal-defect murmur is softer and more localized in the case of minute septal defect, a separate pulmonary ejection murmur may be heard in the pulmonary area. Unless auscultation is made at the correct site, the diagnostic effect of amyl nitrite may not be detected. 6. 6. This study has thrown some light on the different behavior of the regurgitant systolic murmur of ventricular septal defect and the pulmonary ejection murmur under the influence of vasoactive drugs. It has clarified the interpretation of these murmurs when they are heard at the chest wall.

On the mechanism of production of the heart sounds

The mechanisms of the heart sounds have been investigated by means of animal experiments and the recording of tracings in normal human subjects. Simultaneous tracings of pressure have been recorded in dogs from the two ventricles, from one ventricle and its respective atrium, and from the aorta and pulmonary artery. The time relationship of the motion of the various valves was revealed by these tracings plus simultaneous external phonocardiograms. Simultaneous intracardiac phonocardiograms confirmed these data. Selective phonocardiograms have been recorded through various filters in man, together with low-frequency tracings of the precordium, carotid and aortic tracings, and jugular tracings. The following conclusions have been reached (Fig. 11): 1. 1. The first sound is made of 3 phases: low-pitched beginning, due to 2. myocardial tension; higher-pitched central phase, due to valvular events; lowpitched final phase, due to vascular phenomena. The central phase contains at least 4 vibrations which correspond to the motion of the 4 valves in the following order: mitral closure, tricuspid closure, pulmonic opening, aortic opening. Whenever one or more large vibrations correspond to the phase of ejection, they are likely to be of a vascular nature. 3. 2. The second sound is made of 3 phases: low-pitched beginning, due to eddies preceding the valvular closure; higher-pitched central phase, due to closure of the semilunar valves; and low-pitched final phase, due to final vibrations plus opening of the A-V valves. The central and final phases correspond, firt, to the closure of the semilunar valves and, then, to the opening of the A-V valves, in this order: aortic closure, pulmonic closure, tricuspid opening, mitral opening. 4. 3. Rapid filling of the ventricles is usually nonsimultaneous, in this order: rapid filling of right ventricle, rapid filling of left ventricle. These data confirm some interpretations of previous workers but exclude others. Time intervals for the various phases are given for large dogs. Measurements taken in phonocardiograms of normal persons, recorded with a technique which is identical to that used in dogs, indicate that similar figures can be used in man.