Transient ventricular tachycardia following the valsalva maneuver in a patient with paroxysmal atrial tachycardia

TRANSIENT VALSALVA

WILLIAM

VENTRICULAR MANEUVER ATRIAL HOLLANDER,

TACHYCARDIA IN A PATIENT TACHYCARDIA M.D.,

AND

BOSTON,

GEORGE

WITH

FOLLOWING THE PAROXYSMAL

M.D.

ENTWISLE,

MASS.

T

HE Valsalva maneuver is occasionally useful in the treatment of paroxysmal tachycardia.’ To our knoweldge, this is the first case report in which this maneuver appeared to produce transient ventricular tachycardia while it simulIt is of interest that taneously relieved the paroxysmal auricular tachycardia. spontaneous reversion of paroxysmal auricular tachycardia to normal sinus rhythm is sometimes accompanied by transient ventricular arrhythmias.2J More common methods used to convert paroxysmal auricular tachycardia, such as carotid sinus stimulation, ocular pressure, Mecholyl, and neostigmine, also at times produce ventricular arrhythmias.4-6 CASE

REPORT

A 37-year-old white widow was admitted to the Massachusetts Memorial Hospitals because of “pounding pain in the chest” of six hours’ duration. The patient was known to have had hypertension for two years, and her chief complaint was migrainelike headaches. Six months prior to admission she had a sudden attack of pounding in the chest, later associated with pressing substernal pain radiating down the left arm. The attack lasted three to five hours and ended after either carotid sinus pressure or ocular pressure was applied. A similar episode of palpitation without chest pain occurred one month before admission. This attack was recorded electrocardiographically as auricular tachycardia and was terminated by ocular pressure. At this time prophylactic quinidine, 0.2 Gm., three times a day, was begun. Since ocular and Six hours before admission the third episode of pounding in the chest began. carotid sinus stimulation were without effect, hospitalization was advised. The positive physical findings were confined to the cardiovascular system. Blood pressure was 190/115 mm. Hg, pulse 180, respirations 26, temperature 98.6” F. The heart was enlarged The rate was rapid and 2 cm. to the left of the midclavicular line in the fifth intercostal space. the rhythm regular. A Grade 3 apical systolic murmur was heard. The second pulmonic sound was accentuated. The lungs were clear to auscultation and percussion. The laboratory data showed a normal urine analysis and hemogram. Electrocardiographic tracing was interpreted as auricutar tachycardia. H&tal Course.-On admission, repeated the auricular tachycardia. Likewise 0.8 mp. apparent immediate effect. Two hours after neuver was employed. During this maneuver,

ocular and carotid sinus stimulation failed to affect Cedilanid administered intravenously was without the administration of Cedilanid, the Valsalva main the phase of forced expiration, the paroxysmal

From the Evans Memorial of the Massachusetts Memorial Medicine, Boston University School of Medicine, Boston. Received for publication Dec. 21. 1955. 799

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auricular tachycardia terminated, but was unexpectedly replaced by a bout of ventricular cachycardia. Immediately, however, as deep inspiratory breathing began, the unexpected arrhythmia reverted to a normal sinus rhythm which persisted throughout the two-day hospital course. One month after discharge, the patient was admitted to the surgical service. Transthoracic sympathectomy from DI to I& was advised for treatment of hypertension and prevention of future attacks of paroxysmal auricular tachycardia. Since the operation, performed three years ago, the patient has been normotensive and has had no attacks of parox!;smal auricular tachycardia. DISCUSSION

The Valsalva experiment or maneuver was first described in 17407 and is named for its investigator, Antonio Maria Valsalva. The effect of this maneuver on the brachial arterial pressure may be divided into four phases as illustrated in Fig. 1. The first phase occurs immediately after forced expiration begins, the second during the course of sustained forced expiration, the third immediately after the end of forced expiration and the return of deep inspiratory breathing, and the fourth lasts until the blood pressure returns to control levels.

Fig.

l.-Normal

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During the Valsalva maneuver in normal individuals, premature beats sometimes occur, expecially during the inspiratory effort, Phase 3. The premature beats arising in this phase are attributed to a vagal reflex that occurs secondary to a rise in the systemic blood pressure. This same mechanism may also explain the appearance of premature beats and ventricular tachycardia which have been observed during the conversion of paroxysmal auricular tachycardia.4-6 The work of Scherf and Chick* on the topical effects of acetylcholine on the dog’s heart lends support to this hypothesis. The efficacy of Mecholyl (acetyl beta-methylcholine), carotid sinus pressure, ocular pressure, and neosynephrine in the conversion of paroxysmal auricular tachycardia depend on direct cholinergic action, or on reflex vagal stimulation.17 Reflex vagal stimulation is also believed to be the mechanism for reversion during or following the Valsalva maneuver in patients with paroxysmal auricular tachycardia, and for this reason the Valsalva maneuver can be grouped with the

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above methods of treatment. In the case presented, however, the ventricular arrhythmia definitely took place during the expiratory phase of the Valsalva maneuver. The blood pressure in this patient was not being followed during this maneuver, nor was the patient’s expiratory pressure being measured. It is possible that the intrathoracic pressure was low before the onset of the ventricular arrhythmia (Fig. 2) and the arterial pressor response was occurring while the patient was exerting inadequate forced expiration. If this is true, then reflex vagal stimulation can be postulated as the mechanism for both the reversion and the ventricular arrhythmia. During the forced expiratory phase of the Valsalva maneuver, sympathetic rather than vagal discharge probably occurs secondary to a fall in the systemic blood pressure. During this phase, epinephrine is probably released by the sympathetic nervous system and this may produce ventricular tachycardia. This effect of epinephrine appears to require either coexisting myocardial ischemia or reflex vagal inhibition of the higher pacemakers of the heart .g-12 Myocardial ischemia, during forced expiration when intrathoracic pressure is high, is postulated on the basis of a decrease in coronary blood flow due to an increased resistance to flow and to a fall both in the cardiac output and diastolic blood pressure. Since there is no evidence for inhibition of the higher pacemakers during the blowing effort, the combination of myocardial ischemia and sympathoadrenal discharge seems a plausible mechanism to explain the appearance of ventricular tachycardia in this case. It is recognized that digitalis, an agent often recommended, and used in this case for the treatment of paroxysmal auricular tachycardia, has been reported to produce ventricular tachycardia .13J4 The digitalis given to this patient would be having significant effect at the time of the Valsalva maneuver. The close temporal relationship between the Valsalva maneuver and changes in rhythm, however, implicates the maneuver. The electrocardiographic tracing during the forced expiration (Fig. 2) reveals the dominant rhythm to be ventricular tachycardia for five beats. The ectopic auricular focus at this time appeared to be replaced because (1) it was either completely suppressed by the faster ventricular pacemaker, or (2) it was independently discharging and concealed in the ventricular complexes. The reversion to a normal sinus rhythm during the inspiratory phase of the Valsalva maneuver was likely related to a restoration of neurogenic balance between the cardioaccelerator and cardioinhibitor nerves. CONCLUSIONS

1. A case of paroxysmal auricular tachycardia, converted during the Valsalva maneuver to a normal sinus rhythm, is presented, in which transient ventricular tachycardia preceded the conversion. 2. The mechanism of the conversion and the appearance of the ventricular arrhythmia have been discussed. REFERENCES

1. 2.

Linenthal, A. J., and Freedberg, A. S. : Measures Used in the Prevention Cardiac Arrhythmias, New England J. Med. !241:570-578, 1949. Barker, P. S.: Ventricular Tachycardia During an Attack of Paroxysmal cardia, Heart 11:67-69, 1924.

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N. A.: Fibrillation of the Ventricles at the End of an Attack of Paroxvsmal , -Tachycardia in Man, Heart 3:213-218, 1911-1912. Levine, S. A., and Harvey, W. P.: Clinical Auscultation of the Heart, Philadelphia, 1950, W. B. Saunders Company, p. 327. Meredith, H. C., Jr., and Beckwith, J. R.: Development of Ventricular Tachycardia Following Carotid Sinus Stimulation in Paroxysmal Supraventricular Tachycardia, AM. HEART J. 39:604-606, 1950. Landman, M. E., and Ehrenfeld, I.: Ventricular Fibrillation Following Eyeball Pressure in a Case of Paroxysmal Supraventricular Tachycardia, AM. HEART J. 43:791, 1952. Luisada, Aldo A. : Heart, Baltimore, 1948, Williams & Wilkins Company, 653 pp. Scherf, D., and Chick, F. B.: Abnormal Cardiac Rhythms Caused by Acetylcholine, Circulation 3:764-769, 1951. Wilburne, M., Surtshin, A., Rodbard, S., and Katz, L. N.: Inhibition of Paroxysmal Ventricular Tachycardia by Atropme, AM. HEART J. 34:860-870, 1947. Hoff, H. E., and Nahum! L. H.: The Role of Adrenaline in the Production of Ventricular Rhythms and Then Suppression by Acetyl-B-Methylcholine Chloride, J, Pharmacol. & Exper. Therap. 52:235-245, 1934. Lenel. R.. Vanloo. A.. Rodbard. S.. and Katz. L. N.: Factors Involved in the Production ‘of Paroxysmal ‘Ventricular Tachycardia Induced by Epinephrine, Am. J. Physiol. 153:553-557, 1948. Nathanson, M. H., and Miller, H.: The Action of Norepinephrine, Epinephrine, and Isopropyl Norepinephrine on the Rhythmic Function of the Heart, Circulation 6:238-244, 1952. Marvin, H. M.: Paroxysmal Ventricular Tachycardia With Alternating Complexes Due to Digitalis Intoxication, AM. HEART J. 4:21, 1928. Lundy, C. J., and McLellan, L. L.: Paroxysmal Ventricular Tachycardia: An Etiological Study With Special Reference to the Type, Ann. Int. Med. 7:812-836, 1934. Starr, I., Jr.: Acetyl-B-Methylcholin, Further Studies of Its Action in Paroxysmal Tachycardia and in Certain Other Disturbances of Cardiac Rhythm, Am. J. M. SC. 191:210-225, 1936. Doneean. C. K.. and Townsend. C. V.: Phenvleohrine Hvdrochloride in Paroxvsmal Suora-ventricular Tachycardia,‘J. A. M. A. 157:716-718, 1955. Kennamer, R., and Prinzmetal, M.: The Cardiac Arrhythmias, New England J. Med. 250:509-520, 1954.