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Phonocardiography and Venous Pulsations
@I
GRAPHIC TECHNIQUES IN CARDIOLOGY
Phonocardiography and Venous Pulsations
The Use of the Jugular Pulse in the Diagnosis of Atrial Septa1 Defect Alorton E . Tauel, M.D., F.C.C.P.'
In the evaluation of patients of almost all ages, one often asks the question: Could an atrial septal defect (ASD) account for clinical picture? Among the various simpler techniques of assessment, phonocardiography in conjunction with jugular pulse recording often can be of considerable help in answering this question. An illustrative case follows:
A 54-year-old woman was admitted to the hospital for cardiac evaluation. Nine years earlier, she had developed ankle edema and mild exertional dyspnea and had, therefore, received digitalis and diuretics, with a good response following this treatment. She remained asymptomatic until one year before admission, when she again developed dyspnea on exertion and experienced two episodes of substernal pressure-type pain together with nausea and diaphoresis. She was hospitalized elsewhere for the second of these episodes and was told that she had had a myocardial infarction. She remained in the hospital for three weeks, but subsequently c ~ n t i n u e dto have intermittent chest pain, increasing fatigability. increasing dyspnea on exertion, noctuna, orthopnea, nocturnal dyspnea, and persistent ankle edema. Physical examination, when we saw her, disclosed normal blood pressure and pulse rate. She had slight dyspnea while sitting upright. The lungs contained persistent diffuse bilateral moist rales, particularly in the lung bases. One found, on cardiac examination, an apical impulse in the fifth intercostal space at the anterior axillary line, with considerable activity in the left parasternal region. A pulmonic shock was felt. and, on auscultation, the second sound was widely split; this splitting varied little with respiration. A grade II/VI systolic, crescendo-decrescendo murmur was heard at the left sternal border and ~ulmonarvarea. A third heart sound gallop was present at the lower left sternal border. The liver edge was palpable 2 cm below the right subcostal margin, and a trace of ankle edema was detected. The electrocardiogram showed an intraventricular condnction defect (QRS 0.12 second duration) suggestive of 'From the Department of Medicine, Indiana University School of Medicine, and the Krannert Institute of Cardiology, Marion County General Hospital, Indianapolis, Indiana. Supported in part by the Herman C. Krannert Fund, U.S.P.H.S. Grants HE-6308, and HE-5749 and the Indiana Heart Association.
58
complete right bundle branch block. Left axis deviation was present. Roentgenograms of the chest and cardiac fluoroscopy showed congested lung fields. The right and left atria, right ventricle, and pulmonary outfiow tract were all enlarged. Pulmonary artery pulsations were prominent. Phonocardiogram and pulse tracings are discussed below. Sr~mmaryof the results of right and left-heart catherization is as follows: oximetric studies, indicator dilution curves, and cineangiocardiography revealed evidence of a large atrial septal defect, ostium secundum in type, with left-to-right shunt flow sufficient in magnitude to produce pulmonary blood flow twice that of the systemic flow. There was also elevation of the left-ventricular end-diastolic Dressure (18 mm Hg), and coronary cineangiograms showed fairly severe arteriosclerotic narrowing of all major vessels. The pulmonary artery pressure was elevated (68/21 rnrn Hg). but the pulmonary vascular resistance was within normal limits. There was no evidence of tricuspid insufficiency.
Figure 1 shows the salient graphic features: the second heart sound (recorded at the lower left sternal border) is widely split, and P p is abnormally prominent. Additional tracings taken during normal quiet respiration indicated that the splitting interval increased by about 0.01 second with each inspiration, and this was, therefore, within the range of "fixed" splitting. The normal individual generally shows splitting variation of greater than 0.02 second. A crescendo-decrescendo systolic murmur can be seen at the left sternal border and pulmonary area. The jugular pulse tracing shows high, peaked V waves, which slightly exceed the A waves in height. Both the X and Y descents are quite pronounced. Normally the V wave is substantially smaller than the A wave, with a V/A ratio of less than 0.9 (average 0.66).' Figure 2 shows a typical normal jugular pulse tracing.
COMMENT Initially, we suspected that this patient was suffering from severe arteriosclerotic heart disease with congestive heart failure. The complete right
DIS. CHEST, VOL. 54, NO. 6, DECEMBER 1968
DIAGNOSIS OF ATRIAL SEPTAL DEFECT
FIGURE1. Graphic features of patient described in text. High peaked jugular V waves are readily apparent. Note also wide splitting of second heart sound and systolic ejection mrlrmur.
bundle branch block could be invoked to explain the widely split second heart sound. The fixation of splitting of this sound could be ascribed to the coexisting congestive heart failure, as has been noted by a previous study.2 The jugular pulse tracing
provided us with a major clue to the proper diagnosis of atrial septal defect.'," High, peaked V waves following a prominent X descent have been observed in 41 per cent of uncomplicated atrial septal defects and tend to indicate a fairly large left-to-right atrial shunt.' Tricuspid regurgitation, another condition which can cause increased V waves, causes obliteration of the X descent, thus producing a pattern significantly different from that of uncomplicated atrial septal defect. When the pulmonary vascular resistance becomes greatly elevated in ASD, the jugular A waves generally become dominant again, and this sign is lost. The presence of this type of V wave accentuation is virtually specific for ASD and, with practice, can be recognized at the bedside. The cause of this curious jugular abnormality in ASD is not completely understood, but the following explanation appears plausible: in ASD, the right atrium, filling rapidly from both the systemic veins 'and left atrium, receives a tremendous quantity of blood. During ventricular diastole, this blood can be transferred readily into the dilated right ventricle. During ventricular systole, however, when the bicuspid valve is closed, the rapidly filling right atrium is momentarily over-distended, resulting in a sharp rise of pressure during the time of the V waves. An alternative explanation for the V wave dominance in ASD is that the left atrial pressure contour is transmitted through the septal defect into the right atrium and thence to the jugular veins. The normal left-atrial contour shows dominant V waves. In summary, then, the case described above represents an example of a patient with arteriosclerotic heart disease in whom a fairly large ASD contributed to the occurrence of congestive heart failure. The jugular pulse provided one of the most readily discernible indicators of the presence of the ASD, this pulse manifesting high, peaked V waves. Following establishment of the proper diagnosis, the patient underwent surgical repair of the ASD, and was discharged after showing considerable improvement. 1 TAVEL,M. E., BARD, R. A., FRANKS, L. C., FEICENBAUXI, H., FISCH,C.: The jugular venous pulse in atrial septal defect, A.M.A. Arch. Int. Med., l21:524, 1968. 2 PERLOFF,J. K. AND HARVEY, W. P.: Mechanisms of splitting of the second heart sound, Circulation, 18:998, 1958. 3 REINHOLD, J.: Venous pulse in atrial septal defect: A clinical sign, Brit. Med. J., 1:695, 1955.
FIGURE2. Normal jugular pulse. Note relatively small V wave and short Y descent.
DIS. CHEST, VOL. 54, NO. 6, DECEMBER 1968
Reprint requests: Dr. Tavel, Indiana University School of Medicine, Indianapolis 46202.
59
GRAPHIC TECHNIQUES IN CARDIOLOGY
Phonocardiography and Venous Pulsations
The Use of the Jugular Pulse in the Diagnosis of Atrial Septa1 Defect Alorton E . Tauel, M.D., F.C.C.P.'
In the evaluation of patients of almost all ages, one often asks the question: Could an atrial septal defect (ASD) account for clinical picture? Among the various simpler techniques of assessment, phonocardiography in conjunction with jugular pulse recording often can be of considerable help in answering this question. An illustrative case follows:
A 54-year-old woman was admitted to the hospital for cardiac evaluation. Nine years earlier, she had developed ankle edema and mild exertional dyspnea and had, therefore, received digitalis and diuretics, with a good response following this treatment. She remained asymptomatic until one year before admission, when she again developed dyspnea on exertion and experienced two episodes of substernal pressure-type pain together with nausea and diaphoresis. She was hospitalized elsewhere for the second of these episodes and was told that she had had a myocardial infarction. She remained in the hospital for three weeks, but subsequently c ~ n t i n u e dto have intermittent chest pain, increasing fatigability. increasing dyspnea on exertion, noctuna, orthopnea, nocturnal dyspnea, and persistent ankle edema. Physical examination, when we saw her, disclosed normal blood pressure and pulse rate. She had slight dyspnea while sitting upright. The lungs contained persistent diffuse bilateral moist rales, particularly in the lung bases. One found, on cardiac examination, an apical impulse in the fifth intercostal space at the anterior axillary line, with considerable activity in the left parasternal region. A pulmonic shock was felt. and, on auscultation, the second sound was widely split; this splitting varied little with respiration. A grade II/VI systolic, crescendo-decrescendo murmur was heard at the left sternal border and ~ulmonarvarea. A third heart sound gallop was present at the lower left sternal border. The liver edge was palpable 2 cm below the right subcostal margin, and a trace of ankle edema was detected. The electrocardiogram showed an intraventricular condnction defect (QRS 0.12 second duration) suggestive of 'From the Department of Medicine, Indiana University School of Medicine, and the Krannert Institute of Cardiology, Marion County General Hospital, Indianapolis, Indiana. Supported in part by the Herman C. Krannert Fund, U.S.P.H.S. Grants HE-6308, and HE-5749 and the Indiana Heart Association.
58
complete right bundle branch block. Left axis deviation was present. Roentgenograms of the chest and cardiac fluoroscopy showed congested lung fields. The right and left atria, right ventricle, and pulmonary outfiow tract were all enlarged. Pulmonary artery pulsations were prominent. Phonocardiogram and pulse tracings are discussed below. Sr~mmaryof the results of right and left-heart catherization is as follows: oximetric studies, indicator dilution curves, and cineangiocardiography revealed evidence of a large atrial septal defect, ostium secundum in type, with left-to-right shunt flow sufficient in magnitude to produce pulmonary blood flow twice that of the systemic flow. There was also elevation of the left-ventricular end-diastolic Dressure (18 mm Hg), and coronary cineangiograms showed fairly severe arteriosclerotic narrowing of all major vessels. The pulmonary artery pressure was elevated (68/21 rnrn Hg). but the pulmonary vascular resistance was within normal limits. There was no evidence of tricuspid insufficiency.
Figure 1 shows the salient graphic features: the second heart sound (recorded at the lower left sternal border) is widely split, and P p is abnormally prominent. Additional tracings taken during normal quiet respiration indicated that the splitting interval increased by about 0.01 second with each inspiration, and this was, therefore, within the range of "fixed" splitting. The normal individual generally shows splitting variation of greater than 0.02 second. A crescendo-decrescendo systolic murmur can be seen at the left sternal border and pulmonary area. The jugular pulse tracing shows high, peaked V waves, which slightly exceed the A waves in height. Both the X and Y descents are quite pronounced. Normally the V wave is substantially smaller than the A wave, with a V/A ratio of less than 0.9 (average 0.66).' Figure 2 shows a typical normal jugular pulse tracing.
COMMENT Initially, we suspected that this patient was suffering from severe arteriosclerotic heart disease with congestive heart failure. The complete right
DIS. CHEST, VOL. 54, NO. 6, DECEMBER 1968
DIAGNOSIS OF ATRIAL SEPTAL DEFECT
FIGURE1. Graphic features of patient described in text. High peaked jugular V waves are readily apparent. Note also wide splitting of second heart sound and systolic ejection mrlrmur.
bundle branch block could be invoked to explain the widely split second heart sound. The fixation of splitting of this sound could be ascribed to the coexisting congestive heart failure, as has been noted by a previous study.2 The jugular pulse tracing
provided us with a major clue to the proper diagnosis of atrial septal defect.'," High, peaked V waves following a prominent X descent have been observed in 41 per cent of uncomplicated atrial septal defects and tend to indicate a fairly large left-to-right atrial shunt.' Tricuspid regurgitation, another condition which can cause increased V waves, causes obliteration of the X descent, thus producing a pattern significantly different from that of uncomplicated atrial septal defect. When the pulmonary vascular resistance becomes greatly elevated in ASD, the jugular A waves generally become dominant again, and this sign is lost. The presence of this type of V wave accentuation is virtually specific for ASD and, with practice, can be recognized at the bedside. The cause of this curious jugular abnormality in ASD is not completely understood, but the following explanation appears plausible: in ASD, the right atrium, filling rapidly from both the systemic veins 'and left atrium, receives a tremendous quantity of blood. During ventricular diastole, this blood can be transferred readily into the dilated right ventricle. During ventricular systole, however, when the bicuspid valve is closed, the rapidly filling right atrium is momentarily over-distended, resulting in a sharp rise of pressure during the time of the V waves. An alternative explanation for the V wave dominance in ASD is that the left atrial pressure contour is transmitted through the septal defect into the right atrium and thence to the jugular veins. The normal left-atrial contour shows dominant V waves. In summary, then, the case described above represents an example of a patient with arteriosclerotic heart disease in whom a fairly large ASD contributed to the occurrence of congestive heart failure. The jugular pulse provided one of the most readily discernible indicators of the presence of the ASD, this pulse manifesting high, peaked V waves. Following establishment of the proper diagnosis, the patient underwent surgical repair of the ASD, and was discharged after showing considerable improvement. 1 TAVEL,M. E., BARD, R. A., FRANKS, L. C., FEICENBAUXI, H., FISCH,C.: The jugular venous pulse in atrial septal defect, A.M.A. Arch. Int. Med., l21:524, 1968. 2 PERLOFF,J. K. AND HARVEY, W. P.: Mechanisms of splitting of the second heart sound, Circulation, 18:998, 1958. 3 REINHOLD, J.: Venous pulse in atrial septal defect: A clinical sign, Brit. Med. J., 1:695, 1955.
FIGURE2. Normal jugular pulse. Note relatively small V wave and short Y descent.
DIS. CHEST, VOL. 54, NO. 6, DECEMBER 1968
Reprint requests: Dr. Tavel, Indiana University School of Medicine, Indianapolis 46202.
59