Disappearance
of Tricuspid
Systolic Murmur
with Nodal Rhythm* &X)RCE
A.
b_lPVhROS,
London.
T
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EFFECT
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England
these findings with the exception of the diastolic murmur which, as is often the case with faint diastolic murmurs, was not recorded. There was evidence of left atria1 enlargement and right ventricular hypertrophy in the electrocardiogram. Chest x-ray films showed enlargement of the left atrium, right ventricle and ~~lllnonary arteries with tapered peripheral branches suggestive of pulmonary arterial hypertension. .-L-it combined right und ieft heart &ath~?ter~~fft~orl, a mean pulmonary wedge pressure of 33 mm. Hg above the level of midthorax, pulmonary arterial pressure of 126, 58 mm. Hg and a systemtc pressure of 115/70 mm. Ng were obtained. The mean right atria1 pressure was elevated (13 mm. Hg), but the wave form showed a good x descent, excluding significant triruspid insuffici~ncy.3 The mean left atria1 pressure was 32 mm. Hg, mean diastolic gradient across the mitral valve 20 mm. Hg, the cardiac output 2.5 L. per minute and the calculated mitral valve area 0.45 sq. cm. ‘I’ht- left atria1 pressure pulse did not suggest significant mitral insufficiency, and the possibility of even trivial reflux was also excluded by retrograde all~iogra~hy of the left ventricle. 7%~ preoperative diagnosis, therefore, was severe mitral stenosis with pulmonary hypertension and slight tricuspid insufficiency. During the operation the valve was found severely stenosed (3 by 4 mm.) and without incompetence; it was readily split digitally. Postoperatively, the size of the heart diminished, and the abnormal auscultatory findings disappeared. Phonocardiographic Observc&‘ons: Following the recording of the control phonocard~ogram, the patient was given a single, slow intravenous injection of 40 pg. of norepinephrine (8 fig. per ml. of isotonic saline) in order to observe the effect of the drug on the tricuspid systolic murmur.g Accentuation of the murmur was initially observed (Fig. l), a condition consistent with previous observations.4 The murmur was seen to diminish and disappear on the oscilloscope; this was confirmed by auscultation. It reappeared one and a half minutes later. Analysis of the phonocardiogram showed that the attenuation of the mur-
on to
M.D.I.
been
in patients with aortic stenosis and auricular fil~rillation due to corresponding changes of stroke volume, whereas the murmur of mitral insufficiency remained reiativel) In the following case attenuation unaffected.” complete disappearancf of a an d virtually tricuspid systolic murmur occurred with a period of nodal rhythm, which did not affect the pressure or the stroke volume in the right ventriclc. observed
CZASE KEPORT n 22 year old woman
was admitted to the hospital with a history of progressive limitation of effort tolerance for four years. Eighteen months before admittance she had had pulmonary embolism witft infarction associated with manifestations of congestive heart failure which responded slowly to treatment. The patient was subsequently left with almost total disability. On cxaminution, she was found to be dyspneic at rest Thr juguwith sinus tachycardia and a small pulse. lar venous pulse was efevated 10 cm. above the sternal angle with prominent .4 and I’ waves. There were moderate enlargement of the liver and dependent edema, but the bases of both lungs were clear. Marked pulsation at the upper and lower left sternal border suggested enlargement of the right ventricle and of the pulmonary artery. Auscultation revealed a loud first heart sound and a closely split second sound with an accentuated pulmonary component. A loud pansystolic murmur, maximal at the tricuspid area and the apex of the heart, showed no appreciable change with respiration; a faint middiastolic murmur was audible at the apex. So opening snap was heard. A phonocardiogram confirmed
* From the Cardiac Department, Guy’s Hospital, London, England. t Present address: Royal Victoria Hospital, Montreal, Canada. 278
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and Nodal Rhythm
The systolic murmur was first accentuated during and after injection of norepinephrine. FIG. 1. Phonocardiograms (30 seconds) ; it then diminished considerably (60 seconds), and the opening snap became apparent for the first time. Sinus rhythm was The murmur returned to control ampliLude,“and the opening snap disappeared at 180 seconds. 2 = secondisound, OS = openpresent in the control tracing and at 180 seconds and nodal rhythm in the meantime. ing snap, TA = tricuspid area, MA = mitral area. HF = high frequency tracing.
mur coincided with the onset of nodal rhythm, and its reappearance, with resumption of sinus rhythm. During the nodal rhythm a high frequency sound also appeared, probably an opening snap (Fig. 1). The test was repeated during right heart catheterization with simultaneous recording of the phonocardiogram and of the right ventricular and systemic pressures. The tracing showed that the patient had nodal rhythm when norepinephrine was administered; the presence of an atria1 A wave before the rise in systolic pressure in the right ventricle suggested that atria1 preceded the ventricular contraction. Accentuation of the systolic murmur was initially observed (Fig. 2), and this was followed by attenuation and almost complete disappearance. No coincident change of the pressure in the brachial artery or right ventricle was evident, but the atria1 A wave disappeared, probably because of simultaneous occurrence AUGUST
1962
of atria1 and ventricular contractions. On closer scrutiny of the record, a hump on the ascending limb of the right ventricular pressure wave is apparent which, if not an artifact, might represent the pulse of atria1 systole. With the receding effect of norepmephrine the A wave reappeared and the murmur assumed its control amplitude and configuration (Fig. 2).
COMMENTS Attenuation of the systolic murmur with shifting of the pacemaker from the sinus into the A-V node and, on a second occasion, from the upper into the middle region of the A-V node, and its restoration with resumption of the control rhythm suggest a phenomenon of cause and effect. There was no change in right
280
FIG. 2. Cot~/x~l: Pansystoiic murmur of tricuspid insufficiency recorded tog&her with right ventricular (RV pr) and brachial arterial (BA pr) pressure during right heart catheterization. .?O s~on~fs: Peak right ventricular and systemic Ippc~ance nf the opening snap (OS) and LXpressux elevation coincident to the end of norepinephrine injection. (8 srcondr: lL)isappeararm: of A wave and cnnsiderabIc centuation of the rmmnur. Diminutive ~1 wave still prtsent. !&I ccuads: .ilmost complete disappearance of the murmur. 150 to I80 seconds: The attenuation of the murmur. murmur has I-CCOV~TC.~ its control ampiitudc coincident to rccordinp; of the A wave before that of the ventricle. The opening snxp is nu lun.~~r x-isiblr. 2 = second sound.
associated ventricular or systemic pressure with this, nor, presumably, in stroke ~~Jurne~ Consequently, it seems reasonable to conclude that the s~l~~uitaneous occurrence of right atria1 and right ventricular systole reduced the In the absence of a simulregurgitant flow. taneous record of right auricular pressure, it is impussil)le to know whether the hump on the ascending limb uf right ventricular pres-
sure wave is an artifact or whether it represents she pressure geP;erated into the right atrium with the midnodal beats. The latter possibility seems hard to believe in view of the high level indicated ii 10 mm. Hg). In any case, it is unlikely that the atrium was capable of reducing the reflux lly opposing ventricular pressure, whereas it is conceivable that auriculx contraction could approximate the valve THE
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Tricuspid
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leaflets and thus reduce regurgitation of trivial degree. It is doubtful, however, whether this could happen if the incompetence were more than slight. Indeed, in the presence of significant mitral insufficiency, even small left ventricular stroke volumes are capable of providing regurgitant flows adequate enough to keep the intensity of the regurgitant murmur relatively constanL2 A similar explanation has been presented by Caloh for the decrease or disappearance of the murmur of mitral insufficiency in A-V block. SUMMARY In a patient with severe mitral stenosis, pulmonary hypertension and slight functional tricuspid incompetence, administration of norepinephrineproduced nodal rhythm that resulted in the disappearance of the tricuspid pansystolic murmur. Since there was no significant change in right ventricular and systemic pressure during the transition to and from nodal rhythm, the phenomenon was ascribed to simultaneous auricular and ventricular contraction.
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281
ACKNOWLEDGMENT Thanks are due to Dr. Charles G. Baker and Sir Russell Brock for permission to study and report on this case and to Dr. C. A. MacLeod for valuable help in the preparation of the manuscript.
REFERENCES V. Cardiovascular Sound in Health and Disease, p. 434. Baltimore, 1958. Williams & Wilkins Co.
1. MCKIJSICK,
2. HENKE, R. An aid stenosis 60: 354,
P.. MARCH, H. W. and HULTGREN. H. N. to identification of the murmur of aortic with atypical localization. Am. Heart J., 1960.
3. MCMICHAEL, J. and SHILLINGFORD, J. valvular incompetence in heart failure. 1: 537, 1957.
The role of
Brit. M.
J.,
4. BOUSVAROS, G. A. Effect of norepinephrine on the phonocardiographic, auscultatory and hemodynamic features of congenital and acquired heart disease. Am. J. Cardiol., 8: 328, 1961. 5.
Phonocardiography in arrhythmias and A. blocks. In: Cardiology. An Encyclopedia of the Cardiovascular System, vol. 3, chapt. 2, p. 55. Edited by Luisada, A. A. New York, Toronto and London, 1959. McGraw-Hill Co.
CALO,