IACC VolV ta . No. 2 Augunt 1991 957-99

587

Repetitive Sinoatrial Exit Block as the Major Mechanism of DrugProvoked Long Sinus or Atrial Pause SAN-JOU YEH, MD, TOSHIO YAMAMOTO, MD," FUN-CHUNG LIN, MD, CHUN-CHIEH WANG, MD, DELON %4U, MD, FACC Taipei, Taiwan

Prolonged sinus er atrial pause occurred in six patients with paroxysmal sup" ventricul-tachycardia after drug administra. tint,, All six patients had normal sinus node function during control electrophysiologic study; the sinus cycle length ranged from 310 to 900 ms (mean 743 ± 141) and the Ingest sinus node recovery time ranged from 800 to 1,230 mS (mean 1,018 ± 168) . A long sinus or atria) pause occurring at the teminatian of taehyeardla or cessation of atrial pacing, ranging from 3,100 to 8,200 ms (mean 6,270 ± 1,674), was provoked by the administration of various drags. These included an intravenous bolus injection of adenosine triphosphate (5 mg ; one patient), intravenous bolus injection of verapamil (5 mg ; one patient), a combination of a single oral dose of diltiazem 1120 mg) and propranolol (20 to 40 mg; three patients), oral diltiazem (240 mg/day ; one patient) and a combination of oral diltiazem (240 mg/day) and propranolol (160 mg/day; one patient) .

Termination of an acute episode of paroxysmal supraventricular tachycardia frequently requires parenteral drug administration, whereas prevention of recurrence of

paroxysmal supraventricular tachycardia usually ,cgtdrca long-term oral drug administration (1 .2) . Although parentcral and long-term oral drug administration are safe, they may occasionally cause syncope as a result of prolonged sinus or atria) pauses (3-8), The mechanism of a drug-provoked long sinusoratrial pause is unclear . In this study, we investigated the mechanisms of drug-provoked sinus or atrial pauses using a sinus node electrogram recording in a group of patients with paroxysmal supraventricular tachycardia to whom a long sinus or atrial pause was provoked by drug

administration.

From the Section of Cardiology . Department of Medicine . Coal; Gung Medical College. Taipei. Taiwan . This study Was ,ipportcd in pan by Drool NSC79-0412-8182 .37 from the Notional Science Council of the Republic of China . Taipei . 'Dr . Y- role h at, intcrnadonal Fellow from the Sceend Dcpenmcnt of Interval Medicine, S ., ama Medical School, Sadama. Japan . Manuscript received October 12, 1990 ; rre-did manuscript received January Ie, 1991 . accepted February 15.1991 . Addy- for mnrintq: Dclon Wu, MD, Chang Genii Mcmooal Hospital . 199 Tang Had North Road . Taipei . Taiwan . 1991 by the American College of Cardiology

In five patients, low frequency deflections suggestive of sinus note activity with a cycle length between 620 and 3,500 ms were recorded during pauses. These findings suggest that repetitive sinoatrial exit block was responsible for the pause. Sinus slowing

with a lung arrest suggesting suppression of sinus automaticity was also noted in three of these five patient'; the longest sinus arrest in these three patients was 4,160, 4,800 and >41,910 ms, respectively . The remaining patient with a pause of 6,840 rns had no recordable sinus activity, either reflecting suppression of sinus automaticity or technical failure . In conclusion, this study suggests that both sinoatrial exit block and suppression of sinus automaticity are mechanisms for drug. provoked long sinus or atrial pauses, fJ Am Call Cardiol 1991 ;18x587-95)

Methods Study patients . Criteria for inclusion of patients in this study were I) induction of sustained tachycardia in patients with clinically documented paroxysmal supraventricular tachycardia: 2) normal sinus nude function during control electrophysiolugic study; and 3) provocation of a prolonged sinus or ainal pause, defined as an interval >3 s after parcuteral or oral drug administration . From September 1986 to December 1989, a total of 121 consecutive patients with sustained paroxysmal supraventricular tachycardia were prospective)) studied. Six of the 121 patients developed a prolonged sinus or atrial pause after drug administration . There were five women and one man, aged 46 to 62 years (mean . 51) 56 . 6). None had demonstrable organic hear[ disease Electruphyslokigic study . The study protocol was approved by the Hospital Research Ethics Committee and written informed consent was obtained from all subjects . F.lecirnphysiologic study was performed with patients in a postabsorptive nonsedated state. All cardiac medication was discontinued x72 h (or 5 plasma half-lives) before study . Multiple electrode catheters were positioned in the high right atrium, coronary sinus, right ventricular apex and across the tricuspid valve for recording of intracardiac electrograms and pacing from different sites of the heart . Surface electroon5-109"wta2,5o



01 :lf r :1 '.1 DRLG-I'R(Wr1RliIi 51Nr5 PAL SE

588

IACC Vat . 18, No . 2 August 1991 :587-95

I . Clinical . Elccirocardiugraphic and Electrophyslnlogic Chararlerisrics cf Six Reicnl, Tafile

Case1aI 3 5 6

Aem lyrr' Gender

Dun,aon ofSV]'

99:F ? :;F 9 0 411.1 61 'M 650

ion

haslPPlmsl

4 ' 10 13 4 20

720 1 .100 1 .000 91x1 870 680

MechaNSm if SVT AVRT

I.nnpol SN51 (ms) 800 1,000 1 . 1 34 1.1101 1 .1711 940

AVRT AVR1 AVRT AVRT AVNRf

AVNRT -,o iownlrkular node rwolranl tachycardla ; AVRT = alnoe PP = Into cycle emricular rcrnlront lachFeardw'. r = Female ; M = kg81h 11'9 m-11 : SNRI =onus node recovery Imp : 5VT Ssarraoenl ricalar hake oordo

cardiographic (ECG) leads 1, aVF and V I and intracardiac

electrograms were simultaneously displayed and recorded on a mullichanncl oscilloscopic recorder (VR-16: Electronic : for Medicine) as paper speeds of 50, 100 and 150 mm/s . A stimulus of 2 ms duration and approximately twice diastolic threshold was provided by a digital programmable stimulator (DTU PG 100 ; Bloom and Associates) . Anlerograde and retrograde conduction properties were evaluated with atria) and ventricular incremental and extrastimulus testing techniques . The sinus node recovery time was evaluated otter sudden termination of overdrive atria) pacing tore, minimum of 30 s . It was measured as the interval from the last stimulus artifact to the first returning P wave that was consistent with sinus origin . The upper limit of normal for maximal sinus node recovery time was 1 .600 ms in our laboratory. Conduction intervals, refractory periods and echo zone were doused and measured as previously described R). Electrophysiulogic diagnosis of dual pathway atriovcntricutar (AV) node reentrant tachycnrdia and orthodromic AV reentrant Iachycardie was made using previously described criteria (2) .

Drug therapy tar induced supraventrieular tachyeardia . Afterthe control study, sustained supraventricular lachycardin was induced, adenosine lriphosphate (5 to IS mg) was given intravenously as a bolus injection and the patient was monitored conuonously with recording of the sinus node elcctrograms. Ten to 20 min later, a second dose of adeno . sine triphosphate was administered to reconfirm the effects . After this, verapamil (5 to 10 mg) was administered intravenously during an induced episode of sustained supraventricular ruchycardia while the patient was monitored conlinunusly . This concluded the initial study . All electrode Catheters were removed ; a hexaputar electrode catheter was introduced through the right anlecubital vein, advanced to the right ventricular apex and secured for subsequent eice trophysiologic studies . The followinr drugs were tested sequentially on separate days : a single oral dose of combined diltiazem (90 to 120 mg) and propranolol (20 to 80 mg) ; diltiazem (240 mg(day in four divided doses): verapamil (320 mg/day in four divided doses) ; quiaidine sulfate (1,600 mg/day in four divided doses) ; procainamide (4,000 mg/day in four divided doses) ; disopyramide phosphate (800 mg/day in four divided doses) ; propranolol (160 mg/day in four divided doses) ; a combination of diltiazem (240 mg/day in four divided doses) and propranelel 1160 mg/day in four divided doses) ; digoxin (1 .75 mg over a period of 24 h) ; and a combination of propranolol (160 mg/day in four divided doses) and digoxin (0.25 mg/day after a loading dose of 1 .75 mg) . When a prolonged atriat pause (re3 s) that occurred at termination of tachycardia or cessation of rapid atria) pacing was noted during the studies, a sinus node electrogram was recorded either by the four proximal electrodes (interelectrode distance of I cm) of the hexapolar electrode catheter (three patients) or by a newly introduced quadripolar electrode catheter if the hexapolar electrode catheter was unable to record a sinus node electrogram (three patients).

Table 2 . Drag-Provoked Long Sinus or Atria) Pause n Six f atients Post-Tadlycardia ar Postpacinx Pause (ms) BoO

Cae No . I

2 3 4

Drug0 ATP . 5 In IA DZ. NO mg day + Pro, I60 mgldas S mgle dose of DZ. I d0 mg - FI r. 40 mg Single dose at DZ. 120 era + No. 20 m8 Single dose of DZ. 120 M. + pro . 40 mg Verapamih 5 mg IV D2 . 240 n yd.,

Rhythm Imo

Sinus CL

SACt

870

170

Longeu Parse

No- of SAB

CL of Sinus Flectrogram

1 .100 7,800

1 4

JER

06 .050

4

900-1 .300

JER

8 .200

3

1,090-3,500

6.200

5

040-1 .100

750-1 .000

Type I SAB nod 2 .1 S.4B 1110 210 Idrl

520-1 .400

Longest Sinus Arrest

First Returning Beat

4,160

Sinus Sinus

-

Jundional

4,800

Anial or junainnal

-

Sinus

Alrial erjuncticeal lunclional adenosine teiphosphate ; CL = cycle lengl h : DL = II-IV = ivm asxnauri J ER junaianal escape rhythm : Pro =propranolol: SAB = sinualual ATP = exit block . SAC I = sinoatrial conduction time . 5 6

5150-720 780

*5.700 6 .840

1 -

-

X4.910 -



(ACC Vol la. No . 2 Augur1 1991 :557.95

YE11 EL AL . DRUGPROVOKEO SINUS PAUSE

589

A

Figure I, Case 4 . 0-currence of type I and 2:1 sinoarrial exit block after oral administration of a single dose of dilliazem (120 mgt and propranolol (40 mg) . Panels A and B are continuous . Armor indicate the sinus node electragram ISNE)t high right atria) /PIRA) imcrsals are labeled . The tirs6 fifth and seventh sinus deflections were the first sinus ac . tivity after a blocked impulse and were barely visible. The second . third and eighth sinus deflections became apparent when sinoatrial conduction time lengthened to allow more exposure of the sinus electrogram in be recorded before aural depolarization . Note that type I sinoatria( exit dock or-c erred between the first and the fourth sinus def .elio :t . The fourth and s,xth sinus deflections w ere blocked . 1, .AV F and VI = eleetrcrcardingraphic leads,

VI ----J` HRA

rte

r w,

J am • /u,u rao 77 "

raze

SNEJ

i -w --_

Validation of sinus node electrugram . The sinus node elecirogram was validated by recording of multiple repetitive, identical, low frequency deflections free of beseli re drifting during an atria( pause that was noted on both the surface ECG and the high right atral electrogram (9-14) . These low frequency deflections were recorded only at the critical area of rhejunclion of the superior vena cava and the right atrium . Moving the electrode catheter a few millimeters away from this area resulted in disappearance of these deflections . All measurements are presented as mean values SD, Results Clinical and ECG findings (Table 1). Although all six patients had recurrent palpitation, none had syncope during palpitation or after spontaneous termination of palpitation . In one patient (Case 5) . two episodes of a prolonged atrial pause of 2.6 and 2 .8 s, respectively, were noted after termination of supraventricular tachycardia after a single oral dose of diltiazem (120 mgt and after an intravenous bolus injection of verapamil (4 mg) in the emergency room . The sinus cycle length at rest in these six patients ranged from 680 to (,000 ms (mean 853 Y 137). The QRS complexes

were narrow in four of these six patients, intermittently pre-excited in one patient and persistently pre-excited in the

remaining patient. The cycle length of clinically documented suprauentricular tachycardia ranged from 300 to 400 ms (mean 343 ± 35) . Electraphysiolugic studies (Table 1) . During control study . the basic sinus cycle length ranged from 5101o 900 ms (mean 743 ± 141) . The sinoatrial conduction time ranged from 50 to 100 ms (mean 80 C 19) . The longest sinus node recovery time ranged from 800 to 1,230 ms (mean 1,019 t

1601 and corrected sinus node recovery time ranged from 140 to 3511 (mean 275 ± 86) . Sustained supraventricular (achy cardia was inducible in all six patients, including five with orlhodromic AV reentrant tachycardia and one patient with slow-fast dual pathway AV node reentrant tachycardia . The Induced tachycardia had a cycle length ranging from 260 to 400 ms (mean 358 ± 5S) . No patient had a prolonged atria) page after electrical termination of tachycardia by overdrive pacing . Drug provocation of prolonged atria( pause (Table 2) . All six patients had a prolonged atrial pause at termination of supraventncular tachycardia or cessation of rapid atria) pacing after drug administration . The drugs that provoked a long atral pause included adenosine triphusphate (5 mg by intravenous bolus injection) (Patient I) ; combination of diltiazem (20 mg in a single oral dose) and propranolol (20 to 40 mgt (Patients 2 to 4) ; verapamil (5 mg by intravenous bolus injection) (Patient 5) : a combination of diltiazem



YEH ET AL. DRUG-PROVOKED SINUS PAUSE

5 90

JACC V.I . IS . No . 2 August I9YI :SX7-95

A

H- Taut

-i

Ftomaticity igure 2 . Case I . Sappree ioa of sinus noand occurrence of repetitive

sinoatrial exit block resulting in a prolonged aerial pause after oral administration of diltiazem (240 mg/day) and proprnolol (160 mg/day). Panel A is . . recording during control cleetrophysiulogic study ; panels B and C are recordings after diltia.. unit propmnolol . Panel A shows a sinus node recovery time of 750 ms after cessation of rapid atria) pacing that was delivered during an induced episode of supraventricular tachycardia . The paced cycle length was 220 ms and the pacing site was the coronary I sinus (CS) . Panel B shows a prolonged atrial pause due to A long sinus arrest of 4,160 ms after cessation of ventricular pacing with 1 :1 retrograde ventriculoatrial conduction at a cycle length of 400 ms. The sinus arrest was followed by a sinus deflection (arrow) before subsequent ventricular pacing . Panel C I I shows an episode of prolonged atrial pause ----J `,' J of 4.960 ms due to repetitive sinoatral exit block )arrows) that occurred after cessation of rapid a trial pacing at a paced cycle length of 330 ms. The fifth sinus deflection is conducted with an atria] response . A, CS and V = low septa) right atria), coronary sinus and ventricular response to the basic rhythm or -na-- pacing: Ae and HRAe = low septa] right ratria) and high right atria) response to the induced supraventricular tachycnrdia : HBE. HBE,, and HBEJ, = His bundle. distal I) His bundle, and proximal His bundle electrograms ; 5 = stimulus artifact . Other abbreviations as in Figure 1 . The paper speed is 100 mmls in panel A and 50 trials in panels B and C . --V

B

I

1AVF 400

If

I SNEI

.

f

/r f r J

V

HRAT-,4-~ .a HBE-fW - ~'Y~-rf

l am SNg .i 1

HRAf

P

~-.

I

f

-

(240 mg/day orally) and propranolol (160 mg/day orally) (Patient 1) and diltiazem (240 mg/day orally) (Patient 6). Four patients (Patients I and 4 to 6) had sinus rhythm and two (Patients 2 and 3) had junetional rhythm with 1 :1 retrograde conduction . Of the four patients with sinus rhythm, three had I :I sinoatrial conduction ; their sinoatrial conduction time was 170, 210 and 140 ms, respectively . The other had intermittent type I and 2 :1 sinoatrial exit block (Fig. I) . A prolonged atria) pause (duration 3,100 to 8,200 ms [mean 6,270 '- 1,674]) was noted in all six patients after cessation of overdrive pacing or termination of supraventricular tachycardia. During the long atrial pause, low frequency deflections reflecting sinus activity and having a cycle length

between 620 and 3,500 ms were observed in five patients (Patients I to 5 ; Fig. 2 to 5). Marked sinus slowing with a long arrest was also noted in three of these five patients ; the longest sinus arrest in the three patients was 4,160, 4,800 and >4,910 ms . respectively (Fig. 2B, 6A and 6B). In the remaining patient (Patient 6), tow frequency deflections were not recorded after a long sinus pause of 6,840 ms when junctional escape rhythm with 1 :1 retrograde atrial conduction handicapped the recording of the sinus node clectrograms . In the six patients, the first returning beat after the atrial pause was of sinus origin in two patients (Patients I and 4; Fig . 2C and 5C), junctional origin in two patients (Patients 2 and 6 ; Fig. 4B) and atria) or junctional, or both, in the remaining two patients (Patients 3 and 5; Fig. 3B and 6B) .



IACC Vol . Is . Na t Augmi I991SRT-SS

V £H ET AL. DRUG-PROVOKED SINUS PAUSE

RRIFlg1iPiIITH1111#'I141il'Ii'f1MIIi"

,

II'

591

11111M

B n AV F-

V,_

rW 2340

SNEJk13]p

Discussion Syncope and paroxysmal supraventricular tachyeardia . Paroxysmal supraventricular tachycardia is a benign clinical arrhythmia. The acute attack is frequently terminated by a simple vagal maneuver or parenleral drug administration ; long-term prophylaxls is usually achieved by mainrrm nce oral drug administration (I). Patients with paroxysmal supraventricular tnchycardia may occasiortally experience sym cope at either the onset or the termination of an episode of tachyeardia . The former results from hyputensiun due to a sudden decrease in stroke volume (15) cr secondary to a vasovagal reflex triggered by tnchycardia-induced ealecholamlne secretion (16) . The latter results from a prolonged sinus or atria) pause at the termination of tachyeardia, especially in patients with sick sinus syndrome (17). Autiarrhythmic agents and sinus node function . Betaadrenergic blockers . digitalis, calcium channel blockers, class I antiairhythmic drugs and adenosine are known to depress sinus node function, causing sinus bradycardia, prolongation of sinus node recovery time and lengthening of sinoatrial conduction time (18-22) . They are usually safe in clinical usage; symptomatic sinus node dysfunction occurs only rarely with acute parenteral administration or long-term oral administration of these agents . Nonetheless, cardiac

Figure 3. Case

i Slowing of

single sineatrial exit

block.

sinus automaticity accompanied by a

resulting in a prolonged aerial pause after

an intravenous bolus injection of verapamil IS mgt . Panel

A shows a

sinus node recovery time of 500 ms after cessation of rapid atpal pacing at a paced cycle length of 350 ms before drug administration . Pond B shows a long aerial pause of

2370

ms due to slowing of sinus

Jummatieny sod occurrence of a single sinoatrial exit block after urapam0 . The blocked sinus deflection occurred 1,320 ms after cessation of atrial pacing at a paced cycle length of 460 ms.

Abureviatlons as in Figure I .

asystole and a prolonged sinus or aerial pause have been described (3-8,23) . Benaim (3) described a 57 year old man

with supraventricular tachyeardia taking practotol (600 mg/ day) who developed cardiac asystole after intravenous administraltan of practotol 120 mg) and verapamil (7 mg), Tonkin et al . (4) observed marked prolongation of sinus node recovery time (4,040 ms) in a 70 year old patient with sick sinus syndrome and AV node reentrant tnchycardia after intravenous administration of verapamil (0.15 mglkg). Belhassen et al . (5) observed a 5 s sinus arrest after an inrave nous bolus injection of adenosine in terminating AV reentrant tachyeardia 15) . DiMarco el al. 16) reported a 2 to 5 s sinus arrest after an intravenous bolus injection of



5 92

YFH FT AI .. D RUG.P R(VORFD SINUS

JACC Vol . Iv. Na . 2 August 1991 rcr95

Paws

A

HRAes

HRA-' 17 4n5D

Figure 4. Case 2. Repetitive sinoatrial exit block resulting in a

prolonged atriol pause aver administration or a single oral dose of diltiazem (120 mg) and prapmnnlol 140 mg) . Panel A shows a sinus node recovery lime of EM ms atterecssation of rapid aerial pacing at a paced cycle length of 360 ms before drug administmrion . Panel B shows a prolonged atria] pause of 4 .690 ms due in repetitive

sinoatrial exit block after cessation of ventricular pacing with 1 :1 retrograde vcntticutoahial conducliua at a paced cycle length of 400 ms after dilnazem and proprnotol . The Faust was followed by a junclional escape rhythm with 1 :1 retrograde eondu iiun- H = His bundle potential : other abbreviations as in Fiputes I and 2.

adenosine in three patients with paroxysmal supravenlricutarIachycardia . Yen ct A . (7) observed severe sinus brady cardia with junctional escape rhythm in a patient after a single oral dose of a combination of dilliazem and propranclol was administered to terminate paroxysmal supravenlricular tachycardia . Koo el al . (8) reported on a 27 year old woman with automatic atria) lachycardia and no previous sinus node dysfunction who developed a sinus pause of8 .920 ms 5 days after treatment with digoxin (0 .25 mg)day), nadolol (80 mgdday) and amiodarone (I giday), A long sinus pause did not occur after discontinuation of drug therapy, but

rechallenge with amiodaruae caused prolonged cardiac asys • tole . Gould et

al .

(231 described a 77 year old woman who

developed 2 :1 sinoatrial exit block while taking tocainide (400 mg three times daily) for premature ventricular beats . These previously reported episodes in patients with druginduced severe sinus depression usually occurred with preexisting sinus node dysfunction . The six patients in the present study had no clinical evidence of sinus node dysfunction or a history of syncope- In five of these six patients, the long sinus pause occurred after oral drug administration. Mechanisms or drug-provoked prolonged sinus or aerial pause . Several studies (11-14) have demonstrated that sinoatrial exit block rather than sinus node suppression is the major mechanism responsible for the abnormally prolonged sinus or atrial pause that occurs spontaneously after termination of supraventriculartachyarrhylhmia, after rapid atrial pacing or during carotid sinus massage . In these cases, Mobitz type 11 or type l exit block with repetitive sinoatrial exit block is the mechanism of the prolonged pause (11-13) • Complete sinoatrial exit block with atria) escape rhythm has also been shown (l4) to be present in some patients with the bradycardia-tachycardiasyndrome . Whether a similar mechanism is also responsible for the drug-provoked long sinus or atria] pause has not been clarified previously .



YEN ET At,, DRUG-PRiVOKen SINUS PAUSE

IACC Vol. 18 . No. 2 :ucan !991 .`. 3::5

A

202

IIII11,111

AVF

ao

s

s

a

t:, l ti S, Case 4. Repetitive siaoalrial exil block resulting in a prolonged a trial pause after administration of a singtt oral dose of diltiazrm 11211 mgt and propranalol (40 mgt Panel A shows a sinus node recovery time of 1 .000 ms after cessation of rapid atrial pacing at a paced cycle length of 330 ms before drug administration . Panels B and C are continuous recordings after diltiazem and propranolol, showing a prolonged atrial pause of 4.220 ms due to repetitive sine, atdal exit block (arrows) after cessation of ventricular pacing with 1 :1 retrograde ventriculoatria) conduction at a paced cycle length of 400 ms . The last sinus deflection is conducted with an atrial response . Abbreviations as in Figures 1 and 2 . Figure

B Al: V.~ p HM

,1111

f }

f

I

I

I

SNE

41 I

h

1

AVF V. HRA 4220

SNE

The present study demonstrates that repetitive sinoalnal exit block is the major mechanism responsible for the drug-provoked long sinus or atria] pause in patients without evidence of previous sinus node dysfunction . However, it is usually accompanied by suppression of sinus automaticity with sinus arrest . Sinoatrial exit block was documented in five of the six patients with a recordable sinus node etect,ogram, whereas slowing of sinus automaticity with a long sinus arrest was noted in three of these five patients . In the remaining patient with no recordable scans node electrogram during a long p •s ase, inability to record the sinus node electrogram could reflect either suppression of sinus automaticity or technical failure .

Clinical implications. This study has several clinical implications. Firs, both sinoatrial exit block and suppression of sinus automaticity are mechanisms of a drug-provoked long sinus or atria] pause in patients with paroxysmal supraventricular tachycardia without previous sick sinus syndrome, However, sinoatrial exit block appears to be the major mechanism. Second . a long sinus or atria) pause could he the mechanism of syncope in patients with paroxysmal supraventricular tachycardia when the combination of a beta-blacker and a calcium channel blacker is administered . Third, a long sinus or atria) pause could be a potential mechanism of syncope in patients with coronary artery disease when the patient is treated with the combination of a



YEH ET 11 . DRUG-PN(WVr1KED

594

IACC V.I . In, No . 2 Augu,, 1001¶47-95

SINUS PAUSE



B

r SNF1

_

375tJ --

_.

__



C 1

Figure 6 . Case 5. Suppression of sinus aatn,aalicily acrompanicd by sinoatrial exit block resulting in a prolonged atria) pause oiler an intravenous bolus tniccesen of verupamil 15 mgr . Pinch A, B and C arc conUnuaas recordings- Note that after cessation of rapid soul pacing at a paced cycle length of 5011 ms, the first sinus deflection an- aired 1 .380 ms later and was blocked (piu el A). The second sinus deflection occurred 3 .750 ms after the first deflection and was also blocked panel B) . It was futlocoed by two junclional escape beats wish retrograde conduction to the atria until sinus rhythm costumed (panel CJ. Abbreviations as in Fguee 1 .

AVF'

SNE---tam a.

beta-blocker and a calcium channel blacker- This may occur particularly if the patient has paroxysmal supravenlricular tachyarrhythmias such as atrial fibrillation or Butler .

References

Suprnvenlrirol r -h,-d- tAMA 1993 5493357-r0 2 . WIt a. Dorm P . AInot.3 .t.are 1. it at. CloSrat . elrolim rdiographrtand eiectruphysmlegm observations n pasieals with paroxysmal surravtnlnc ular lachycardir. Am) Cardio[ 1970:71' 11145-51 . 5 . Benaim ME. Asyslale allot verapamil . lA MW 1 1972 :2' 169-70 . 4. Tonkin Ahi . Aylward PE. Joel SE . Hedge WFVerapamil in prophslaxis arparaxy amel ama.mtidraler each) mnmmnl mrh ynaraia . 1 Ca:dnvasc Pharmaco11980 :2:Y1-86. 5. Belhresen B, Pell,$ A . Shoshanl0. Co. B, Lani'do S. ElsetrophysioIrgic eflecd nr ode.-,--5'aripheephere nn vin-l-, pr n

Repetitive sinoatrial exit block as the major mechanism of drug-provoked long sinus or atrial pause.

Prolonged sinus or atrial pause occurred in six patients with paroxysmal supraventricular tachycardia after drug administration. All six patients had ...
419KB Sizes 0 Downloads 0 Views