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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
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
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,
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.
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.
Initially, we suspected that this patient was suffering from severe arteriosclerotic heart disease
with congestive heart failure. The complete right
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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.
H., FISCH,C.: The jugular venous pulse in atrial septal
defect, A.M.A. Arch. Int. Med., l21:524, 1968.
W. P.: Mechanisms of splitting of the second heart sound, Circulation, 18:998, 1958.
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.
Reprint requests: Dr. Tavel, Indiana University School of
Medicine, Indianapolis 46202.
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