Valsalva Termination of Ventricular Tachycardia

MENASHE B. WAXMAN, M.D., ROBERT W. WALD, M.D., JOHN P. FINLEY, M.D.,

JORGE F. BONET, M.D., EUGENE DOWNAR, M.D., AND ARJUN D. SHARMA, M.D.
SUMMARY Nine patients with recurrent ventricular tachycardia (VT) that could be repeatedly terminated
by a Valsalva nmaneuver are described. In two, the tachycardia would cease for only a few seconds and then
resume, whereas in seven, the tachycardia could be permanently and reproducibly terminated with a Valsalva
maneuver. In all patients the tachycardia ended during the strain phase of the Valsalva maneuver, when blood
pressure and radiographic measurement indicated that cardiac dimensions had been reduced dramatically. The
speed with which the Valsalva maneuver terminated VT increased in direct proportion to the strain pressure.
Maneuvers such as standing or nitroglycerin, which independently reduce cardiac dimensions, enhanced the
potency of the Valsalva maneuvers. Pretreatment with atropine or propranolol in four patients did not alter the
response of VT to the Valsalva maneuver. Thus, it appears that a strong Valsalva maneuver can terminate
some forms of VT, most likely related to an abrupt reduction in cardiac dimensions.

in whom the Valsalva maneuver was attempted met

the following additional criteria: (1) They suffered
from recurrent, morphologically identical episodes of
VT for more than 1 year. (2) They tolerated the
episodes well and exhibited no hypotension, heart
failure or signs of myocardial ischemia during VT. (3)
They were capable of executing a proper Valsalva
maneuver. Nine of the 15 patients could terminate
episodes of VT with the Valsalva maneuver. In these
nine patients, all attacks consistently broke when a
Valsalva maneuver of sufficient intensity and duration
was performed, and attacks of VT could be easily reinduced, thereby allowing multiple observations on the
effects of the Valsalva maneuver.

PATIENTS WHO SUFFER from tachycardia are

often instructed to perform a Valsalva maneuver in an
effort to modify or terminate their rhythm disturbance.", 2 A regular tachycardia that breaks with a
Valsalva maneuver is presumed to be paroxysmal
supraventricular tachycardia (PSVT)3 because it
usually involves the atrioventricular (AV) node,4'
which is vagally responsive. A Valsalva maneuver is
one way to promote a strong increase in cardiac vagal
traffic,6 which in turn can depress AV nodal conduction and terminate PSVT.2 Three patients were
referred to us because of tachycardias that were
difficult to manage. Each patient was thought to be
suffering from PSVT with aberrant ventricular conduction because they were able to terminate their
arrhythmias at least intermittently with a Valsalva
maneuver. Careful analysis of these records proved
the presence of ventricular tachycardia (VT). We
systematically studied the effect of a Valsalva
maneuver in 15 selected cases of VT. In this report we
describe nine patients who could repeatedly terminate
VT by performing a Valsalva maneuver.

Physiologic Studies

Valsalva maneuvers were performed with the

patients lying on an electric bed whose position could
be accurately controlled. The Valsalva maneuver was
performed in two ways. In the first, quantitation was
not attempted, and the patients simply inspired to a
moderate volume, closed their glottis and raised intrathoracic pressure for as long as 15 seconds. When
quantitation of the intrathoracic pressure was desired,
the patient respired through a mouthpiece with a unidirectional valve. The inspiratory side of the valve was
open to room air and the expiratory side was connected to a manometer and a Statham P23Db straingauge transducer. The manometer was in full view of
the patient. To perform the Valsalva maneuver, the
patient again inspired to a moderate intrathoracic
volume and expired against the manometer in such a
way as to hold a constant pressure. To prevent the
patient from achieving pressure by closing the glottis
and generating pressure in the mouth only, a small
leak was introduced in the system to prevent closure
of the glottis.7 Thus, the recorded pressure reflected
the intrathoracic pressure. The transducer signal was
conditioned by a Hewlett-Packard preamplifier
(model 8805C).
The ECG, beat-to-beat heart rate, blood pressure,
intrathoracic pressure and chest wall movement were
simultaneously recorded on heat-sensitive paper using
a Hewlett-Packard recorder (model 7758). Episodes

Materials and Methods

Patient Population

The effect of the Valsalva maneuver on VT was explored in 15 patients selected from 123 consecutive
patients with VT seen by one of the authors from
1973-1978. The cardiac diagnoses of these patients
are summarized in table 1. Patients with coronary
artery disease and heart failure were excluded from
the study. VT was recurrent and sustained in only 32
of the remaining patients. Fifteen of these 32 patients

From the Department of Medicine, University of Toronto

Faculty of Medicine, and the Division of Cardiology, Toronto
General Hospital, Toronto, Ontario, Canada.
Supported in part by grants-in-aid from the Ontario Heart Foundation and the Canadian Heart Foundation.
Address for correspondence: Menashe B. Waxman, M.D., Cardiovascular Unit, Toronto General Hospital, 101 College Street,
Toronto, Ontario, Canada M5G 1 L7.
Received October 17, 1978; revision accepted April 4, 1980.
Circulation 62, No. 4, 1980.

843

Downloaded from http://circ.ahajournals.org/ by guest on August 27, 2015

CIRCULATION

844

TABLE 1. Clinical Data in 123 Patients with Ventricular

Tachycardia

Coronary artery disease

Acute myocardial infarction
(< 4 weeks)
Postmyocardial infarction (> 4 weeks)
Postmyocardial infarction + LV
aneurysm

Angina pectoris without infarction

Subtotal

Hypertensive heart disease

LVH
LVHI + congestive heart failure
Subtotal
Cardiomyopathy
Acute myocarditis (viral ?)
Chronic congestive cardiornyopathy
Hypertrophic nonobstructive
cardiomyopathy
Hypertrophic obstructive
cardiomyopathy
Subtotal
Rheumatic heart disease
Aortic valve disease
Mitral valve disease
Combined aortic and mitral valve
disease
Subtotal

17
32
15
7

(1)

5
4
2 (1)
2

2 (1)

3(1)
3

(1)

Miscellaneous
Digitalis intoxication
2
Obstructive pulmonary disease
2 (1)
Malignant hyperthermia
2 (1)
Mitral valve prolapse
3 (1)
Calcified cardiac cyst
1 (1)
Normal
15 (6)
Subtotal
25
The numbers in parentheses indicate the source and
the number of cases of ventricular tachycardia in whom
a Valsalva maneuver was attempted.
Abbreviations: LV = left ventricular; LVH - LV hypertrophy.

of VT were reinduced during these studies by right

ventricular stimulation using an endocardial electrode. Valsalva maneuvers were performed in horizontal (00), upright (+60) and dependent (-40)
positions. The maneuvers were also repeated 10
minutes after 0.3-0.6 mg of sublingual nitroglycerin.
In each case, the Valsalva pressure and time required
to terminate the VT were monitored.
In four patients, the effects of Valsalva maneuvers
were measured during control conditions and after
1.2-2.4 mg of i.v. atropine and 0.15 mg/kg of i.v.
propranolol. To assess the adequacy of vagal

VOL 62, No 4, OCTOBER 1980

blockade, the effect of carotid sinus massage on sinus

rate and on AV conduction time after termination of
the tachycardia was determined after administration
of atropine. Right- or left-sided carotid sinus massage
failed to slow the sinus rate or prolong or block AV
conduction. Further, carotid sinus massage during VT
after administration of atropine did not slow the dissociated atrial activity in two patients or prolong or
block the associated atrial activity in two other
patients. The adequacy of d blockade after propranolol was also assessed after termination of the tachycardia. Administration of a 5-,U intravenous bolus of
isoproterenol did not increase the sinus rate.
To estimate cardiac dimensions at the time of VT
termination, roentgenographic images of the heart
were obtained using R-wave synchronized exposures
during full inspiration both before and during the
strain phase of a Valsalva maneuver that resulted in
termination of the tachycardia.
Intracardiac Electrophysiologic Studies
Using multipolar electrode catheters, we recorded
electrograms from the high right atrium, the His bundle region and the right ventricle. The right atrium or
right ventricle was stimulated through adjacent poles
on the same catheter. Antegrade conduction intervals
were studied during sinus rhythm by incremental
atrial pacing to the point of AV Wenckebach conduction. Antegrade refractoriness was determined by introduction of atrial premature complexes. Antegrade
conduction was also studied in the presence of vagal
stimulation produced by carotid sinus massage during
constant atrial pacing at a cycle length of 500 msec.
Retrograde conduction was studied during right ventricular pacing. His bundle escape beats were
produced by abrupt cessation of rapid atrial pacing or
by vagal stimulation using carotid sinus massage during conditions of sinus rhythm or a combination of
both. Tachycardia was induced by driving the right
ventricle at a rate just above the spontaneous sinus
rate and introducing one or two premature complexes
after 10 basic cycles. The premature complexes were
delivered at 1.5 times the late diastolic threshold, and
scanned the entire cardiac cycle at 5-10-msec intervals
until the tachycardia was initiated. When a single
premature complex failed to initiate the tachycardia,
this stimulus was kept fixed at the earliest point in the
cardiac cycle that produced a propagated response
and a second premature ventricular complex was then
introduced. The coupling interval of the second
premature stimulus was shortened until the tachycardia was initiated. Tachycardia initiation was also
tested by trains of right ventricular pacing at cycle
lengths of 350-250 msec. Once the tachycardia was
initiated and shown to be sustained, the response to
ventricular stimulation was tested. Single ventricular
premature stimuli were introduced after every 10
cycles of the tachycardia, and the entire cycle was
scanned at 5-10-msec intervals until the tachycardia
stopped. Short trains of rapid ventricular pacing at
rates 10-50% above the tachycardia rate were also
applied to terminate the tachycardia. After each

Downloaded from http://circ.ahajournals.org/ by guest on August 27, 2015

VALSALVA TERMINATION OF VT/Waxman et al.

845

study, antegrade conduction was restudied after the

administration of 1.2-2.4 mg of i.v. atropine. The dose
chosen was sufficient to permit 1:1 conduction to the

VT had a left bundle branch block morphology. The

Valsalva maneuver produced permanent conversion of
the VT in seven patients and transient conversion in

ventricles at a rate at least 10% above the tachycardia

rate. Intracavitary electrograms and surface ECG
signals were recorded on photographic paper using an
Electronics for Medicine recorder (model DR 12).
Timing of administered pulses was achieved by a
Digitimer (model 4020). The timer was coupled to a
Grass stimulator (model S88) that delivered pulses to
the heart through Grass stimulation isolation units
(model SIU5). The purpose of the study was carefully
explained, and verbal and written consent were obtained from each patient.

two.

Results
Clinical data and characteristics of the VT in each
patient are summarized in table 2. In each patient, the

Electrophysiologic Studies During Sinus Rhythm

and Atrial and Ventricular Pacing (table 3)

In all nine patients the PR interval, AV nodal conduction time (AH), His-Purkinje conduction time
(HV) and QRS morphology and duration were normal during sinus rhythm. During atrial pacing or introduction of premature atrial complexes, the AH interval increased inversely with the cycle length, but the
HV interval and QRS duration and morphology did
not change from control. Early premature atrial complexes and rapid atrial pacing caused progressive AH
delay and eventual AV block proximal to the His bun-

TABLE 2. Clinical Patient Data and Characteristics of Ventricullar Tachycardia

VT
AV
VT
Termination
Age
rate
Cardiac status
by Valsalva
morphology relationship
Sex (years)
Pt
LBBB
AVD
175
Permanent
F
Calcified cardiac
26
MP
cyst
AVA
LBBB
180
Transient
M
26
Normal
AN
AVD
LBBB
165
Transient
m
18 Malignant
DC
hyperthermia
LBBB
AVD
170
Permanent
M
Normal
11
RE
AVD
LBBB
160
Permanent
COPD
63
M
OD
AVA
LBBB
175
Permanent
Normal
M
36
DC
LBBB
AVD
190
Permanent
F
Mitral stenosis
49
MO
Mitral insufficiency
Aortic insufficieincy
LBBB
AVD
180
Permanent
F
40
Aortic insufficiency
TB
LBBB
AVI)
170
Permanent
m
24
Normal
MB
Abbreviations: COPI) = chronic obstructive pulmonary disease; VT = ventrictular tachycardia; LBBB
left bundle branch block patterin; AV = atrioventricular; AVD = AV dissociation; AVA = AV association.

TABLE 3. Electrophysiologic Data

RA pacing
Tachycardia Tachycardia
initiation
termination
Before
RV
Normal sinus rhythm
Wenckebach
RV
CL for
HV QlS PVC pacing PVC pacing
AH
HV QRS Wenckebach AH
Pit
Pt
40
240
400
+
80 +(1)
+
80
+(2)
40
100
160
MP
260
45
+
350
80 80
+(2)
100
45
170
AN
90 50
290
+
430
90
40
+(1)
100
160
DC
80 +(2)
300
53
420
+
+
80
+(1)
40
95
150
RE
90 +(2)
+
40
270
400
+
90
+(1)
40
100
180
OD
80 +(2)
45
280
+
390
+
+(2)
80
45
110
170
DC
90
50
+
410
280
+
+(1)
90
50
110
+(1)
180
MO
+
45
270
+
370
+(3)
45
80
80 +(1)
120
180
TB
40
80 +(1)
+
290
380
+(1)
+
40
80
100
160
MB
to
of
PVCs
needed
the
number
in
denote
brackets
All
numbers
in
All intervals and dturations are msec.
initiate or terminate the tachycardia.
Abbreviations: AH = atrioventricular node conduction interval; HV - His-Purkinje conduction interval;
CL = cycle length; PVC = premature ventricular complex (paced); RV = right ventricular; + = successful
induction or terinination of tachycardia; - = tachycardia started spontaneously.
Downloaded from http://circ.ahajournals.org/ by guest on August 27, 2015

846

CIRCULATION

dle in each patient. Vagal stimulation accomplished

by carotid sinus massage during constant atrial pacing
at a cycle length of 500 msec produced AH interval
prolongation in all patients and second-degree AV
block proximal to the His bundle in five, without
change in the HV interval or QRS morphology. Atrial
pacing at rates in excess of the tachycardia was accomplished in each case after pretreatment with
atropine; in no patient did the QRS morphology or
HV interval change from control.
Attempts to stimulate the His bundle directly failed
in all nine patients. His bundle escape beats were induced in four patients and had an HV interval and
QRS morphology identical to those under control
conditions. Ventricular pacing produced ventriculoatrial (VA) conduction in only two of the nine
patients, who also had retrograde conduction during
the tachycardia. In the two patients with intact VA
conduction, rapid pacing produced incremental VA
conduction delay and eventual VA block. Similarly,
VA delay and block could be produced by vagal
stimulation using carotid sinus massage during constant ventricular stimulation at a cycle length of 500
msec.
Induction and Termination of VT (table 3)

In two patients, VT repeatedly resumed spontaneously after termination, and induction of VT

could not be studied in them. In these two patients, VT
was permanently converted to sinus rhythm by i.v. administration of 500 mg of procaineamide, after which
VT could not be evoked with electrical stimulation.
VT could be induced repeatedly by introduction of a
single early premature ventricular stimulus in four
patients and by introduction of two consecutive early
stimuli in three patients. These premature complexes
were introduced during constant ventricular pacing at
cycle lengths 20% shorter than the control sinus rate.
Also, short trains of rapid ventricular pacing at cycle
lengths of 350-250 msec started VT in all seven
patients so tested. In all nine patients, VT could be terminated by premature ventricular stimuli or bursts of
rapid ventricular pacing at cycle lengths of 380-250
msec. VT was terminated by a single early premature
1 SEC

VOL 62, No 4, OCTOBER 1980

ventricular complex in five patients, by two early

premature ventricular complexes in three patients and
by three early premature ventricular complexes in one
patient. Induced VT had the same morphology as
spontaneous VT.
Electrophysiologic Studies During VT

The tachycardia in all nine cases met the following

criteria8 for VT: (1) The QRS morphology during the
tachycardia differed from that during sinus conducted
beats and the QRS was 120 msec or longer in all
patients. (2) AV dissociation was present in seven of
the nine patients; in the remaining two patients with
AV association, VA block could be induced by carotid
sinus massage without altering the tachycardia. (3)
Fusion beats and normal capture beats were observed
spontaneously in six patients, and could be induced by
atrial pacing at rates in excess of the tachycardia after
atropine in the remaining three. (4) Atrial pacing at
rates in excess of the tachycardia did not produce
aberrant ventricular conduction in any of the patients.
(5) There was no His bundle potential preceding the
QRS complex during the tachycardia, and a clear H
potential with a normal HV interval (40-50 msec) was
seen during sinus rhythm without catheter repositioning (fig. 1).
Phase of VT Termination

At least four consecutive episodes of VT in each

patieht were terminated by a Valsalva maneuver. In
all patients, the VT terminated during the strain phase
(phase II) of the Valsalva maneuver.9 In no instance
did the VT break during phase I, III or IV (fig. 2).
Phase II of the Valsalva maneuver is characterized by
a reduction in cardiac size.7 9 10 Chest roentgenograms were obtained to verify that the VT terminated
when the cardiac size decreased (fig. 3).
Time Required to Break VT Related to
the Intensity of the Valsalva Maneuver,
Body Position and Nitroglycerin

The intensity of the Valsalva maneuver was inversely related to the time required to terminate the
VT. Figure 4 shows two episodes of VT termination in
VAILSALVA

HBE

L2J

K\^, 4,
VALSALVA
~~~~~~~~~~~~~

L2

.....

FIGURE 1. Simultaneous recordings of

lead 2 and His bundle electrogram (HBE)
during ventricular tachycardia (VT) in
patient AI. During the strain phase of the
Valsalva maneuver, the tachycardia terminated transiently and a sinus beat was
noted. A clear His bundle potential (arrow)
preceded this QRS complex with an HV interval of 40 msec.

Downloaded from http://circ.ahajournals.org/ by guest on August 27, 2015

847

VALSALVA TERMINATION OF VT/Waxman et al.

VALSALVA

Li
L2
L3
BAE

.vr t

-1

-I

100BP

mmHg

-IGlURE 22. Simultaneous recordings of

surfac,e EC'G leads 1, 2, 3. bipolar right
atrial electrogranm (BAE) and aortic blood
pressure (BP) in patient DC. Atrioventricular dissociation wasv present during ventriciular tachicardia (VT). During the initial
phase of the Valsalva mzaneuver (phase I),
the BP ro.se transiently. After several beats
o)f the strain phase (phase IIt the BP
amplitude decreased (arrow) and VT termiinlated. When the BP returned toward control seveural secunds later, the tachlcardia
res uimed.

U
1 SEC

the same patient at different Valsalva pressures. A

small but distinct difference in the time required to terminate the VT was observed in these two instances.
This relationship in another patient is plotted in figure
5. The VT broke sooner at higher Valsalva pressures.
This relationship was studied in horizontal, upright
and dependent positions as well as after nitroglycerin.
The upright position and nitroglycerin both greatly
reduced the time required to terminate VT at any
Valsalva pressure, while the dependent position
prolonged the time for termination of VT.
Effects of Atropine and Propranolol
on lermination of VT

Pretreatment with atropine alone, propranolol

alone or a combination of these agents did not alter
Valsalva termination of VT (figs. 6 and 7).
INSP.

K*M
fl_U

Discussion
The nine patients described fulfilled criteria for VT.8
Yupraventricular tachycardia with aberrant venricular conduction was ruled out because the atria
ould be paced at rates in excess of the tachycardia
ind gain capture of the ventricles with a normal
?RS morphology and AH and HV intervals that
lemonstrated normal AV conduction during this inervention. By contrast, during tachycardia the QRS
omplexes were wide, had a left bundle branch block
norphology and were not preceded by a His bundle
)otential. Moreover, atrial activity during the
achyeardia was dissociated in seven patients and in
he two patients in whom it was associated, VA conluction could be blocked without affecting the tachyardia. There was no evidence of an accessory AV
nuscle bundle11 (Kent bundle) bridging the atria and

INSP.+VALSALVA
s

roentgenoFFcs
graphic expo.sure on the upper left was obtained during VT after a deep inspiration
(INSPJ. The exposure on the upper right
was obtained after an identical inspiration
followed by a strong Valsalva maneuver and
Ri

was

3.

Patient

obtained

DC.

during

the

The

last

VT

beat

(corresponding to the arrow infigure 2). The

bottonm diagram is a superimposition of the
cardiac silhouettes in the two roentgenogramis at the top. The interrupted line
denotes the Valsalva exposure, and the solid
line represents the control inspiratorY film.
The heart size was considerably reduced
during the Valsalva maneuver.
1

Downloaded from http://circ.ahajournals.org/ by guest on August 27, 2015

CIRCULATION

848

HR

(B/M)

VOL 62, No 4, OCTOBER 1980

T | 4I 11_

il IIZ.
1f1 *1 PiW;1l I;[fIfT1
il 2I T 1
w`2fl!:StHT||flE
a4
l_-7Il
v-,!1,,~~~ ~~~t
1h1a1-.Jil*1lllll{'t.l0
IWI

P1

hltI

Uwf11M1 P

tlE

i1il

til

lltINl It
fU

MUl
Wii

1 1

_1 1

RgmMgj

11 _

"t|||||

RESP g

VP 30mmHg
Time to Break VT 2.5 Sec

VP 5OmmHg
Time to Break VT 1 Sec

FIGURE 4. Simultanteous recordings of lead I J beat-to-beat heart rate (HR) blood pressure and chest wall
movement (RESP) in patient TB. (left) Termination of ventricular tachycardia (VT) during a Valsalva
strain of 50 mm Hg. (right) Termination of VT during a Valsalva strain of 30 mm Hg. In both cases, VT terminated as soon as the blood pressure decreased (arrows), but VT terminated sooner at the higher pressure.

Both terminations shown here were permanent. VP

Valsalva pressure.

ventricles, because the QRS morphology and the con-

15r
A

o O UPRIGHT(+60)
-A- DEPENDENT (-40)
| HORIZONTAL (0)

duction always proceeded over normal AV connections."1, 13 The possibility of a reciprocating supraven-

tricular tachycardia proceeding antegradely over such

a bypass tract is excluded by the presence of AV dissociation during the tachycardia.14 The possibility of
an accessory nodoventricular or fasciculoventricular
accessory connection` seems unlikely for the aboveU)
101
stated reasons and because the His bundle escape
beats were not aberrant and had normal HV inter-U)
Co
I -N.
vals.15
n
VT could be terminated in nine of 15 patients. Thus,
0
we wondered whether these patients differ significantly
from those described by other investigators.'6 18 The
A~~~^
0
series of 123 patients with VT from which our 15 cases
were drawn had cardiac diagnosis similar to those in
L ..,
E 5
series reported from other laboratories. Despite this,
"8..,
the true incidence of Valsalva termination of VT was
not tested in this study because of the rigorous selection criteria. The 15 patients who met the criteria for
* S~ study, including the nine who successfully terminated
VT with a Valsalva maneuver, were unique in that
none had coronary artery disease or heart failure and
all had stable, well-tolerated VT. The 108 other cases
II
50
40
0
30
of VT were not tested. We suspect that most other in20
60
10
vestigators have not endeavored to terminate VT with
Valsalva Pressure (mmHg)
Valsalva maneuvers in the majority of patients they
FIGUR E 5. Patient MB. Time required for ventricular
examined. Thus, we cannot determine how unusual
tachyc,ardia (VT) to break plotted against the Valsalva
the observed response really is. VT had a left bundle
pressuire generated. The Valsalva maneuvers were perbranch block morphology in the 15 patients in this
forme d in the horizontal () dependent (-40) and upright
study. The significance of this is not known, but it may
(+600') positions as well as after nitroglycerin. VT terpoint to a special locus of these tachycardias. Inducminatied sooner with a stronger Valsalva strain. The upright
tion and termination of VT by programmed electrical
positicmn and nitroglycerin increased the Valsalva potency,
stimulation was similar to that described in other
where as the dependent position reduced the Valsalva poPOST

tency.

0.3mg NTG

reports.'7-21

Downloaded from http://circ.ahajournals.org/ by guest on August 27, 2015

VALSALVA TERMINATION OF VT/Waxman et al.

CONTROL
L3

FIGURE 6. Recordings of lead 3 during

ventricular tachycardia (VT) in patient AN.
Two applications of a strong Valsalva
maneuver before and after atropine broke
the tachycardia transiently. In the top strip
there is 1:1 ventriculoatrial (VA) conduction. During the initial Valsalva maneuver,
VA block developed. After atropine, VA
block was prevented yet the VT was interrupted. The arrows denote retrograde activity.

VALSALVA

POST 2.4 mg ATROPINE

849

VALSALVA

; ~ ~ ~ ~ ~I

Valsalva maneuvers produce pronounced changes in

autonomic tone.7' 9, 22 The Valsalva termination of VT
in our cases did not appear to be mediated through a
vagal mechanism because pretreatment with atropine
did not modify the response. Similarly, the failure of
propranolol to alter the response suggests that
alterations in sympathetic tone did not play a prominent role. These observations do not completely exclude a partial role of changing autonomic tone.
Atropine and propranolol are competitive receptor-

blocking drugs, and, at the dosages used, some effects

from vagal and sympathetic tone change might still
have occurred during the Valsalva maneuver. The
completeness of cardiac vagal or sympathetic
blockade was tested by observing attenuation in the
response of supraventricular structures, such as the
sinus node rate or AV nodal conduction, to autonomic
stimulation. Figure 6 illustrates a Valsalva maneuver
terminating VT after atropine pretreatment had
prevented vagally induced retrograde block in conduc-

Li

250
HR (B/M)
0.
250

BP (mmHg)

RESP
VP = 40 mmHg
FIGURE 7. Recordings of lead 1, beat-to-beat heart rate (HR), blood pressure (BP) and chest wall movement (RESP) in patient TB, illustrating Valsalva termination of ventricular tachycardia (VT) after pretreatment with atropine and propranolol. VT terminated when blood pressure began to decrease during the strain
phase (arrow). VP = Valsalva pressure.
Downloaded from http://circ.ahajournals.org/ by guest on August 27, 2015

850

CIRCULATION

tion to the atria. However, there are no simple

markers for judging the adequacy of vagal or sympathetic blockade of ventricular tissue.
Although the mechanism of Valsalva termination
remains uncertain, an acute reduction in heart size
probably played a central role. VT always broke during the strain phase at a time when a decreasing blood
pressure and a reduction in the size of the x-ray
silhouette indicated that cardiac dimensions were
greatly reduced. The relationship between various
body positions and nitroglycerin and Valsalva potency
supports the role of cardiac size. Body position and
nitroglycerin have known effects on cardiac size,23-25
and predictably influenced the potency of the Valsalva
maneuver; specifically, reduction in cardiac size induced by upright position or by nitroglycerin
enhanced, while a dependent position reduced, the
potency of the Valsalva maneuver.
A reduction in cardiac size might have a specific action in cases where VT is initiated and maintained by
stretch, whereas in other cases a reduction in cardiac
size may not be related in any specific way to the
mechanism of spontaneous initiation or maintenance
of VT. Insufficient information on the mode of spontaneous onset of VT in these cases is available. The
observations made in the two patients in whom the
Valsalva maneuver only transiently stopped VT are
perhaps pertinent. In both patients VT resumed
several seconds later, when blood pressure returned to
control (fig. 2). This probably reflects a return of cardiac dimensions to their original size. Similarly, a
reduction in cardiac size by digitalis, bed rest,
diuretics or afterload reduction may often contribute
to termination of a ventricular tachyarrhythmia. A
reduction in the frequency of premature ventricular
complexes has been reported with the use of digitalis.26
The hemodynamic role of digitalis in producing this
effect has not been assessed. Acute cardiac stretch is
often important in generating experimental dysrhythmias.27' 28 The results of programmed stimulation suggest that reentry is the most likely mechanism, as the tachycardias could be reliably started and
stopped by electrical stimulation.29 Cardiac stretch
can enhance Purkinje fiber automaticity,30 31 which
can lead to a loss of membrane potential and reduce
conduction velocity.32 The latter property is essential
in the initiation and maintenance of reentry.33 An
abrupt reduction in cardiac dimensions might reduce
Purkinje fiber stretch, lessen automaticity and improve conduction velocity. Such changes could cause a
reentrant arrhythmia to stop.33 A conclusive arrhythmic mechanism cannot be offered, because recent
work has shown that electrical stimulation can elicit
or stop automatic activity in a variety of cardiac
tissues.34-37
Our observations are clinically significant. First,
Valsalva termination of an unknown tachycardia can
no longer be assumed to indicate that the tachycardia
is supraventricular in origin.1-3 All cases of VT terminated during phase II of the Valsalva maneuver,
whereas a supraventricular tachycardia would be expected to slow or stop during phase IV, when a reflex

VOL 62, No 4, OCTOBER 1980

increase in vagal drive is induced by a rise in arterial

79 Second, blood pressure, roentgenographic and body position data all suggest that a
reduction in cardiac size is central to termination. This
has many implications because many drugs or other
interventions can affect cardiac size and hence
facilitate or retard VT termination. Third, the capacity of Valsalva to terminate VT may explain many
episodes of spontaneous termination when the patient
performs a Valsalva maneuver unconsciously or unnoticed. Two cases of VT were recently described in
pressure.6

which sinus rhythm was restored by retching.38 It

would seem reasonable that retching could produce

cardiovascular actions similar to those seen during the
strain phase of a Valsalva maneuver.
Future studies should endeavor to use more refined
methods, such as two-dimensional ultrasound, to
quantitate the degree of volume change in each cardiac chamber. It would be of interest to examine cases
of VT that do not break with the Valsalva maneuver
to see if an insufficient ventricular volume change explains the failure of the tachycardia to break. The
overall incidence of Valsalva termination of VT as
well as the usefulness of our observations will depend
on testing the Valsalva maneuver on a much wider
variety of cases of VT. If observations and experiments firmly establish that volume reduction is the
central mechanism of Valsalva termination of VT, we
will have identified a specific clinical physiologic instrument with great potential.
Addendum
Since submission of this manuscript, a case of a 64year-old man with severe hypertensive and ischemic
heart disease was reported in whom 33 episodes of VT
were converted by repeated forceful coughs.39 Several
brief coughs in close succession were needed to terminate the tachycardia. The hemodynamic effects of
coughing closely resemble those of a Valsalva
maneuver.9 Thus, this cough-terminated VT may have
occurred through a mechanism similar to that in our
report.

References
1. Friedberg CK: Diseases of the Heart, 3rd ed. Philadelphia, WB
Saunders, 1966, pp 514-582
2. Bellet S: Essentials of Cardiac Arrhythmias: Diagnosis and
Management. Philadelphia, WB Saunders, 1972, pp 102-114
3. Kistin AD: Problems in the differentiation of ventricular
arrhythmias with abnormal QRS. Prog Cardiovasc Dis 9: 1,
1966
4. Bigger JT, Goldreyer BN: The mechanism of supraventricular
tachycardia. Circulation 42: 673, 1970
5. Wu D, Denes P, Fernando A, Dhingra R, Wyndham CRC,
Bauernfeind R, Latif P, Rosen KM: Clinical, electrocardiographic and electrophysiologic observations in patients with
paroxysmal supraventricular tachycardia. Am J Cardiol 41:
1045, 1978
6. Levin AB: A simple test of cardiac function based upon the
heart rate changes induced by the Valsalva maneuver. Am J
Cardiol 18: 90, 1966
7. Korner PI, Tonkin AM, Uther JB: Reflex and mechanical circulatory effects of graded Valsalva maneuvers in normal man. J
App] Physiol 40: 434, 1976

Downloaded from http://circ.ahajournals.org/ by guest on August 27, 2015

VALSALVA TERMINATION OF VT/Waxman et al.

8. Peuch P, Grolleau R, Fijac E, Posner J: The diagnosis of
supraventricular tachycardias and the differentiation between
supraventricular tachycardias with aberrant conduction and
ventricular tachycardias. In Symposium on Cardiac
Arrhythmias, edited by Sandoe E, Flensted-Jensen E, Olesen
KH. Sodertalje, Sweden, AB Astra, 1970, p 199
9. Sharpey-Schafer EP: Effect of respiratory acts on the circulation. In Handbook of Physiology, vol III, edited by Hamilton
WF, Dow P. Washington DC, American Physiological Society,
1965, pp 1875-1886
10. Robertson D, Stevens RM, Friesinger GC, Oates JA: The effect
of the Valsalva maneuver on echocardiographic dimensions in
man. Circulation 55: 596, 1977
11. Anderson RH, Becker AE, Brechenmacher C, Davies MJ,
Rossi L: Ventricular preexcitation. A proposed nomenclature
for its substrates. Eur J Cardiol 3: 27, 1975
12. Dhingra RC, Rosen KM, Rahimtoola SH: Normal conduction
interval and responses in sixty-one patients using His bundle
recording and atrial pacing. Chest 64: 55, 1973
13. Denes P, Wu D, Dhingra RC, Pietras RJ, Rosen KM: The
effect of cycle length on cardiac refractory periods in man. Circulation 49: 32, 1974
14. Wellens HJJ, Durrer D: The role of an accessory atrioventricular pathway in reciprocal tachycardia: observations in
patients with and without the Wolff-Parkinson-White syndrome. Circulation 52: 58, 1975
15. Gallagher JJ, Sealy WC, Kasell J, Wallace AG: Multiple
accessory pathways in patients with the pre-excitation syndrome. Circulation 54: 571, 1976
16. Wellens HJJ, Bar FHM, Lie KI: The value of the electrocardiogram in the differential diagnosis of a tachycardia with a
widened QRS complex. Am J Med 64: 27, 1978
17. Josephson ME, Horowitz LN, Farshidi A, Kastor JA:
Recurrent sustained ventricular tachycardia. 1. Mechanisms.
Circulation 57: 431, 1978
18. Denes P, Wu D, Dhingra RC, Amat-y-Leon F, Wyndham C,
Mautner RK, Rosen KM: Electrophysiologic studies in patients
with chronic recurrent ventricular tachycardia. Circulation 54:
229, 1976
19. Wellens HJ, Schuilenburg RM, Durrer D: Electrical stimulation of the heart in patients with ventricular tachycardia. Circulation 46: 216, 1972
20. Fisher JD, Cohen HL, Mehra R: Cardiac pacing and
pacemakers. II. Serial electrophysiologic-pharmacologic testing of recurrent tachyarrhythmias. Am Heart J 93: 658, 1977
21. Wellens HJJ, Duren DR, Lie KI: Observations on mechanisms
of ventricular tachycardia in man. Circulation 54: 237, 1976
22. Baldora VS, Ewing DJ: Heart rate response to Valsalva

23.

24.
25.
26.

27.

28.
29.
30.
31.
32.
33.
34.

35.
36.
37.
38.

39.

851

maneuver: reproducibility in normals, and relation to variation

in resting heart rate in diabetics. Br Heart J 39: 641, 1977
Bevegard S, Holmgren A, Johnsson 13: Circulatory studies in
well-trained athletes at rest and during heavy exercise, with
special reference to stroke volume and influence to body position. Acta Physiol Scand 57: 26, 1963
Mason DT, Zelis R, Amsterdam EA: Actions of the nitrites on
the peripheral circulation and myocardial oxygen consumption:
significance in the relief of angina pectoris. Chest 59: 296, 1971
Burggral GW, Parker JO: Left ventricular volume changes
after amyl nitrite and nitroglycerin in man as measured by ultrasound. Circulation 49: 136, 1974
Lown B, Graboys TB, Podrid PJ, Cohen BH, Stockman MB,
Gaughan CE: Effect of digitalis on ventricular premature beats.
N Engl J Med 296: 301, 1977
Moe GK, Malton SD, Rennick BR, Freyburger WA: The role
of arterial pressure in the induction of idioventricular rhythms
under cyclopropane anaesthesia. Pharmacol Exp Ther 94: 319,
1948
Dresel DE, Sutter MC: Factors modifying cyclopropaneepinephrine cardiac arrhythmias. Circ Res 9: 1284, 1961
Wellens HJJ: Value and limitations of programmed electrical
stimulation of the heart in the study and treatment of tachycardias. Circulation 57: 845, 1978
Dudel VJ, Trautwein W: Das Aktionspotential und Mechanogramm des Herzmiuskels unter dem Einfenss der Dehnung. Cardiologia 25: 344, 1954
Kaufmann R, Theophile U: Automatie fordernde Dehnungseffekte an Purkinje-Faden, Papillarmuskeln und Vorhoftrabekeln von Rhesus-Affen. Pfluegers Arch 297: 174, 1967
Singer DH, Lazzara R, Hoffman BF: Interrelationships
between automaticity and conduction in Purkinje fibers. Circ
Res 21: 537, 1967
Cranefield PF, Wit AL, Hoffman BF: Genesis of cardiac
arrhythmias. Circulation 47: 190, 1973
Cranefield PF: The Conduction of the Cardiac Impulse: The
Slow Response and Cardiac Arrhythmias. Mount Kisco, New
York, Futura, 1975, pp 199-265
Wit AL, Cranefield PF: Triggered activity in cardiac muscle
fibers on the simian mitral valve. Circ Res 38: 85, 1976
Wit AL, Cranefield PF: Triggered and automatic activity in the
canine coronary sinus. Circ Res 4: 435, 1977
Ferrier GR: Digitalis arrhythmias: role of oscillatory after
potentials. Prog Cardiovasc Dis 19: 459, 1977
Lyon LJ, Nevins MA: Retching and termination of ventricular
tachycardia. Chest 74: 110, 1978
Wei JY, Greene HL, Weisfeldt ML: Cough facilitated conversion of ventricular tachycardia. Am J Cardiol 45: 174, 1980

Downloaded from http://circ.ahajournals.org/ by guest on August 27, 2015

Valsalva termination of ventricular tachycardia.

M B Waxman, R W Wald, J P Finley, J F Bonet, E Downar and A D Sharma
Circulation. 1980;62:843-851
doi: 10.1161/01.CIR.62.4.843
Circulation is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231
Copyright 1980 American Heart Association, Inc. All rights reserved.
Print ISSN: 0009-7322. Online ISSN: 1524-4539

The online version of this article, along with updated information and services, is located on
the World Wide Web at:
http://circ.ahajournals.org/content/62/4/843

Permissions: Requests for permissions to reproduce figures, tables, or portions of articles originally
published in Circulation can be obtained via RightsLink, a service of the Copyright Clearance Center, not the
Editorial Office. Once the online version of the published article for which permission is being requested is
located, click Request Permissions in the middle column of the Web page under Services. Further
information about this process is available in the Permissions and Rights Question and Answer document.
Reprints: Information about reprints can be found online at:
http://www.lww.com/reprints
Subscriptions: Information about subscribing to Circulation is online at:
http://circ.ahajournals.org//subscriptions/

Downloaded from http://circ.ahajournals.org/ by guest on August 27, 2015