JACC Vol. 4 No. I July 1984:65 '1 65 Electrophysiologic Testing in the Upright Position: Improved Evlution of Ptients With Rhythm Disturbnces Using Tilt Tble STEPHEN C. HAMMILL, MD, FACC, DAVID R. HOLMES, JR., MD, FACC, DOUGLAS L. WOOD, MD, MICHAEL J. OSBORN, MD, FACC, CHRISTOPHER McLARAN, MB, DECLAN D. SUGRUE, MB, BERNARD J. GERSH, MB, CHB, DPHIL, FACC Rochester Minnesot Ptients re trditionlly evluted in the supine position in the electrophysiology lbortory, lthough due to crdic rhythm disturbnce re often mximl cliniclly during stnding. The ssumption of the upright position results in dependent displcement of blood, followed by prompt vsoconstriction to mintin rteril pressure. This norml response my ggrvte tchyrrhythmis by incresing ctecholmine levels or my precipitte vsodepressor if the vsoconstrictor response is bsent. The use of tilt tble during electrophysiologictesting ws evluted over 12 month period in 104 ptients hving men ge of 60 yers (rnge 37 to 81): 59 with suprventriculr tchycrdi, 6 with vsovgl nd 39 with crotid sinus hypersensitivity. Twenty-three ptients (22%) hd significnt bnormlities when upright tht were not present when supine: eight ptients with suprventriculr tchycrdi who hd their clinicl syndromes of nd when upright, but only miniml when supine; two ptients with suprventriculr tchycrdi who hd sustined trioventriculr reentry when upright, but only two to eight bets of tchycrdi when supine; six ptients with nd norml crdic evlution before electrophysiologic testing who hd their typicl spells only fter being plced upright during vsovgl event nd seven ptients with crotid sinus hypersensitivity who hd their clinicl syndromes with crotid sinus mssge only when upright, developing hypotension despite mintiningtheir hert rte with sinus rhythm or pcing (vsodepressor response). In 22% of ptients, electrophysiologic testing in the upright position provided cliniclly importnt informtion tht ws not evident during stndrd testing in the supine position. The crdiovsculr response to stnding my ggrvte disturbnces in crdic rhythm by reflex ltertions in hert rte nd blood pressure. The physiologic effects of ssuming the upright posture hve been well described (1-4). With upright tilting, the centrl blood volume is diminished nd the crdic output is reduced by 20 to 30%. There is incresed venous volume in the dependent limbs, prompt vsoconstriction nd reduction in peripherl blood flow by the resistnce vessels nd n increse in hert rte to mintin rteril pressure ner the supine levels. If the compenstory vsoconstriction is delyed or insufficient, rteril pressure will decrese nd person my experience lighthededness or. From the Division of Crdiovsculr Diseses nd Internl Medicine, Myo Cl:nic nd Myo Foundtion, Rochester, Minnesot. Mnuscript received 'Iovember 14, 1983; revised mnuscript received Jnury 18, 1984. ce epted Jnury 27, 1984. Address for reprints: Stephen C. Hmmill, MD, Myo Clinic, Rochester, Minnesot 55905. 1984 by the Americn College of Crdiology Electrophysiologic testing is usully performed with the ptient in the supine position. The ssumption of the upright position by use of tilt tble during electrophysiologic testing cn significntly ffect disturbnces in crdic rhythm (5,6). Ptients with tchyrrhythmis my develop n enhnced hert rte nd trioventriculr (AV) conduction in response to the increse in sympthetic stimultion nd prsympthetic withdrwl (5), while ptients with vsodepressor my hve their clinicl syndromes by pssive tilting (7-10), Being plced in the upright position using the tilt tble is similr to the physiologic mneuver of stnding, except tht musculr contrction is not required to mintin the upright posture, resulting in less venous return from the lower limbs (4). Becuse of the potentil usefulness of the tilt tble s physiologic stress during routine electrophysiologic testing, we evluted the use of tilt tble in ll ptients with suprventriculr tchycrdi. crotid sinus hypersensitivity nd. We describe our experience with the use of the tilt tble in 104 ptients seen during 12 month period. 0735-1097/84/$3.00
66 HAMMILL ET AL. JACC Vol. 4. No. I July 1984:65-71 Methods Study group. Ptients were studied from Februry I, 1982 through Jnury 31, 1983. During tht time, 251 consecutive ptients were evluted. Ptients with hemodynmiclly unstble ventriculr tchycrdi, primry disese of the conduction system or norml studies were excluded. A totl of 104 ptients were studied with the tilt tble. In the 104 ptients, the following rhythm disturbnces were identified during electrophysiologic testing: suprventriculr tchycrdi (59 ptients), crotid sinus hypersensitivity (39 ptients) nd vsovgl (6 ptients). The men ge of the 104 ptients (46 women nd 58 men) ws 60 yers (rnge 37 to 81). Electrophysiologic evlution. When brought to the electrophysiology lbortory, the ptient ws in nonsedted postbsorptive stte. Ech ws lightly sedted with dizepm, nd three electrode ctheters were plced percutneously. One ctheter ws dvnced to the right trium, the second to the region of the His bundle nd the third to the right ventriculr pex. In selected ptients, fourth electrode ctheter ws dvnced to the coronry sinus. Incr ementl tril pcing ws performed with rtes rnging from just fster thn sinus rhythm up to 200 bets/min. At ech rte, the ptient ws pced for 30 seconds, fter which pcing ws terminted. Pcing ws decresed in 50 ms decrements until cycle length of 400 ms ws reched; therefter, pcing ws decresed in 20 ms decrements. After tril pcing, premture tril bets were introduced, scnning distole being decresed by 20 ms to tril refrctoriness during sinus rhythm nd during tril pcing of 100 bets/min. Right crotid sinus mssge followed by left crotid sinus mssge ws performed for 5 seconds unless clinicl exmintion ws suggestive of crotid rtery or cerebrovsculr disese. Crotid sinus mssge ws performed with the ptient in the supine nd upright positions, nd hert rte nd blood pressure were monitored. Ventriculr pcing ws then performed from the right ventriculr pex nd right ventriculr outflow trct using incrementl ventriculr pcing (five bets) to 2: 1 ventriculr cpture or cycle length of 200 ms. Distole ws scnned with single ventriculr stimuli until ventriculr refrctoriness occurred. This ventriculr stimulus ws then fixed t 40 ms beyond refrctoriness. Distole ws gin scnned by second ventriculr stimulus until refrctoriness occurred. The ventriculr extrstimuli were introduced during sinus rhythm nd ventriculr pcing t 100 nd 150 bets/min. Blood pressure ws monitored with cuff. nd the mesurements reported with represent the mximl chnge observed. Posturl evlution. Ech ptient ws evluted in the supine nd upright positions t tilt ngle of pproximtely 60 using stndrd tilt tble. The ptient ws plced in the upright position during crotid sinus mssge nd during ny induced or spontneous suprventriculr rrhyth mi. In ddition, if the ptient experienced spontneous suggestive of vsovgl event during the electrophysiologic study, he or she ws plced in the upright position. Crotid sinus hypersensitivity. Ptients demonstrting vsodepressor response to crotid sinus mssge were evluted with temporry pcing in the upright position to determine if the decrese in blood pressure with crotid sinus mssge could be eliminted by pcing. thereby distinguishing between the crdioinhibitory nd vsodepressor components of crotid sinus hypersensitivity. An bnorml crdioinhibitory response to crotid sinus mssge ws defined s n RR intervl of greter thn 3 seconds (11). An bnorml vsodepressor response to crotid sinus mssge ws defined s decrese in blood pressure greter thn 30 mm Hg t time when the hert rte ws mintined in norml rnge, either by sinus rhythm or by pcing. Pcing ws performed using AV sequentil or ventriculr pcing, mking certin tht pcing did not induce hypotension. Finlly. ptients were evluted in the supine nd upright positions fter tropine (2.4 mg) or n ntirrhythmic drug ws given intrvenously, s dictted by the study. Sttisticl nlysis. Dt were nlyzed using Student's t test for pired observtions. Vlues re expressed s men vlues ± stndrd devition. Results The tilt tble ws helpful in 23 of the 104 cses. Control hert rte nd blood pressure did not chnge significntly when ptients chnged from the supine to the upright position. Suprventriculr tchycrdi. Ten (17%) of the 59 ptients with suprventriculr tchycrdi hd few other thn while in the supine position (Tble 1). In the upright position. ll ptients but one (Cse 7) experienced light-hededness, ner or within I to 2 minutes. Their clinicl syndromes were nd ssocited with significnt (p = 0.01) increse in the rte of suprventriculr tchycrdi (160 ± 37 bets/min in the supine position to 193 ± 29 bets/min in the upright position) nd with significnt (p = 0.001) decrese in blood pressure during suprventriculr tchycrdi (120 ± 12 mm Hg in the supine position to 77 ± 18 mm Hg in the upright position). The supine nd upright blood pressures during sinus rhythm were not significntly different (130 ± 18 nd 125 ± 12 mm Hg, respectively). nd the supine blood pressure during sinus rhythm ws not different from tht during suprventriculr tchycrdi. Two ptients (Cses 4 nd 7) experienced sustined pr-
JACC Vol. 4. No.1 July 1984:6;71 HAMMILL ET AL. ELECTROPHYSIOLOGIC TESTING IN THE UPRIGHTPOSITION 67 Tble 1. Ptients With Suprventriculr Tchycrdi Cse Age (yr) &Sex Clinicl Presenttion Findings During Electrophysiologic Study Supine Upright 2 3 4 5 48M WPW, proxysml lighthededness 6 79F Syncope, wide QRS tchycrdi on 24 hour monitoring 7 58M WPW. 8 9 10 81M 75F 72F 37F 39F 70F 49F Syncope, nonsustined proxysml tril fibrilltion nd PVCs on 24 hour monitoring Syncope, norml crdiovsculr evlution, history of Syncope, four bets of wide QRS tchycrdi on 24 hour monitoring WPW, PSVT, ner Syncope, Syncope, nonsustined wide QRS tchycrdi on 24 hour monitoring Ner, Atril fibrilltion: HR 170, BP 130 (BP 140 in NSR), no Atril flutter: HR 140, BP 110 (BP 170 in NSR), no Sinus node reentry: HR 85 (2:1 AV block), BP 110 (BP 115 in NSR), no AV reentry (nonsustined, 8 bets): HR 160, BP 120 (BP 130 in NSR), AVreentry: HR 194, BP 130 (BP 130 in NSR), AV reentry: HR 200, BP 100 (BP 110 in NSR), AV reentry (nonsustined, 2 to 6 bets): HR 160, BP 120 (BP 120 in NSR). no Atril reentry: HR 200. BP 120 (BP 120 in NSR), Atril flutter: HR 150 (2:1 AV block), BP 140 (BP 150 in NSR). no Atril flutter: HR 150, BP 120 (BP 120 in NSR). Atril fibrilltion: HR 200, BP 65 (BP 135 in NSR), ner Atril flutter: HR 150, BP 60 (BP 140 in NSR), ner Sinus node reentry: HR 188 (1:1 AV conduction), BP 75 (BP 115 in NSR), ner AV reentry (sustined): HR 175, BP 55 (BP 130 in NSR), AV reentry: HR 230, BP 90 (BP 125 in NSR), light-hededness AV reentry: HR 200, BP 60 (BP 100 in NSR), ner AV reentry (sustined): HR 190, BP 110 (BP 120 in NSR). clinicl Atril reentry: HR 240. BP 75 (BP 120 in NSR), ner Atril flutter: HR 155 (2: I AV block), BP 90 (BP 140 in NSR), ner Atril flutter: HR 210, BP 90 (BP 120 in NSR),. ner --_._--------------------------------------- AV = trioventriculr; BP = blood pressure (mm Hg); F = femle; HR = hert rte (bets/min); M = mle; NSR = norml sinus rhythm; PSVT = proxysml suprventriculr tchycrdi; PVC = premture ventriculr complex; WPW = Wolff-Prkinson-White syndrome. oxysml suprventriculr tchycrdi due to trioventriculr (AV) reentry on ssuming the upright position, but hd only nonsustined proxysml suprventriculr tchycrdi (two to eight bets) in the supine position. Ptient 3 presented with history of nd four bets of wide QRS tchycrdi during 24 hour monitoring. The electrophysiologic study demonstrted proxysml suprventriculr tchycrdi due to reentry in the sinus node tht could be initited nd terminted by criticlly timed tril premture complexes (Fig. I). In the supine position, the ptient hd tchycrdi rte of 170 bets/min with 3:2 nd 2:I AV block nd systolic blood pressure of 110 mm Hg with no ssocited. On being plced in the upright position, the ptient hd n increse in hert rte to 188bets/min, n increse in AV conduction to I: I rtio nd decrese in systolic blood pressure to 75 mm Hg; she lso experienced, including ner, tht were comptible with her clinicl syndrome. Vsovgl. Six ptients (Tble 2) experienced diphoresis nd nxiety in the supine position, with significnt (p = 0.01) decrese in hert rte (72 ± 10 bets/min when free of with decrese to 48 ± 14 bets/min during in the supine position). During, their supine blood pressures decresed from the men vlue before developed (from 123 ± 13 to 106 ± 14 mm Hg, p = 0.02). On ssuming the upright position during, the ptients hd no significnt decrese in hert rte (men 42 ± 20 bets/min); however, blood pressure decresed drmticlly (men 48 ± 8 mm Hg) from the supine vlue during (p = 0.001) nd from the
68 HAMMILL ET AL. JACC Vol. 4, No. J July 1984:65-71 A H1 H ' ~ v ~ V V1 II AVF Figure 1. A (bove), Criticlly timed tril premture complex (APC) termintes proxysml suprventriculr tchycrdi due to sinus node reentry. B (t right), With the ptient in the supine position, the tchycrdi cycle length is 350 ms (170 bets/min) with 3:2 AV conduction nd blood pressure of 110 mm Hg. C (t right), With the ptient erect, the tchycrdi cycle length (CL) is decresed to 320 ms (188 bets/min), AV conduction is incresed \0 1: I nd blood pressure is decresed to 75 mm Hg. The ptient experienced her clinicl syndrome including ner. HRA, H.. Hz nd V = high right tril, His nd right ventricu lr recording electrodes, respectively;, h nd v = tril, His nd ventriculr depolriztions, respectivel y. Tble 2. Ptients With Spontneous (Vsovgl) Syncope Age (yr) Cse &Sex Clinicl Presenttion Supine Findings During Vsovgl Episode Upright II 59M Syncope, PVCs on 24 hour monitoring 12 38M Syncope, sid to hve crdic rrest elsewhere, no rhythm recorded 13 38M Syncope, ventriculr demnd pcemker elsewhere 14 51F Syncope, AV pcemker elsewhere 15 69M Syncope. norml crdic evlution 16 12M Syncope, crotid sinus hypersensitivity Abbrevitio ns s in Tble I. HR 50, BP 100 (BP 120 control), nuse HR 40, BP 120 (BP 135 control), no HR 50, BP 125 (BP 130 control), nuse, nxiety HR 72, BP 90 (BP 120 control), light-hededness HR 30, BP 100 (BP 130 control), nxiety HR 45, BP 100 (BP 100 control). diphoresis HR 30, BP 40 (BP 100 control),, clinicl syndrome HR 30, BP 50 (BP 130 control),, clinicl syndrome HR 50, BP 60 (BP 130 control),, clinicl syndrome HR 78, BP 50 (BP 120 control)., clinicl syndrome HR 25, BP 40 (BP 110 control),, clinicl syndrome HR 40, BP 50 (BP 95 control),, clinicl syndrome
JACC Vol 4. No. I July 1984:';5-71 HAMMILL ET AL. ELECfROPHYSIOLOGIC TESTING IN THE UPRIGHT POSITION 69 B SUPINE TACHYCARDIA CL BP 110 350ms,\.'I.-_...:;;",rl ~: ~.I\: IV'-"l" '---y/~ '-- H, v -'--.--- H 2 -.- _- 1~ '.-l~, ~~---+~ V l~ 1~ II c AVF ERECT BP 75.JI'--...---JI:'HR~ '~"\I '----.li'\..--~-j '-_-J upright vlue before (p = 0.001). All ptients experienced in the upright position tht ws resolved on ssuming the supine position. This symptom complex the sme symptom complex experien ced cliniclly by ll six ptient s. Two ptients (Cses 13 nd 14) continued to experience fter receiving permnent ventriculr demnd pcing system implnted t nother institution. The spontneou s occurrence of in the upright position during the electrophysiologic study the ptients' clinicl syndrome nd ws the result of vsodepressor mechnism, s evidenced by decrese in blood pressure, despite mintennce of the hert rte with the permnent pcemker. Neither of these ptients demonstrted ventriculotril conduction or decrese in blood pressure with ventricul r pcing.
70 HAMMILL ET AL. JACC Vol. 4. No. I July 1984:65-71 Crotid sinus hypersensitivity. Seven (18%) of ptients with crotid sinus hypersensitivity experienced few in the supine position during crotid sinus mssge (blood pressure 128 ± 27 mm Hg during sinus rhythm nd 116 ± 21 mm Hg during crotid sinus mssge, p = 0.07) (Tble 3). In the upright position, ll seven ptients experienced ner or comptible with their clinicl syndromes, ssocited with decrese in systolic bloodpressure (from 117 ± 16mm Hg during sinus rhythm to 69 :±; 13 mm Hg during crotid sinus mssge, p = 0.001), lthoughhert rte ws mintined in normlrnge by sinus rhythm or pcing. This represents vsodepressor crotid sinus hypersensitivity tht ws not observed when the ptient ws in the supine position. Discussion Electrophysiologic study llows the induction of crdic rhythm bnormlities in ptients whose presumed rhythm disturbnce my be proxysml nd insufficiently frequent to be documented by stndrd electrocrdiogrm or 24 hour mbultory monitoring. However, becuse the electrophysiologic study is usully performed with the ptient in the supine position, the typicl clinicl syndrome my not be during n induced rrhythmi. The physicin must then ssume tht the induced rrhythmi is the cuse of the ptient's. The use of the tilt tble to plce the ptient in the upright position closely simultes common physiologic stress plced on the crdiovsculr system during spontneous clinicl rhythm disturbnce nd is more likely to reproduce the ptient's typicl clinicl syndrome. Of the 104 ptients evluted in this study, 23 (22%) experiencedtheir typicl clinicl syndrome only fter being plced in the upright position, thus llowing correltion between the nd the rhythm disturbnce. Suprventriculr tchycrdi. The crdiovsculr response to being plced in the upright position ws similr, with ll ptients developing hypotension shortly fter upright posturing. Eight ptients with suprventriculr tchycrdi demonstrted more rpid rtes of the tchycrdi or Tble 3. Ptients With Vsodepressor Crotid Sinus Hypersensitivity Cse 17 18 19 20 21 22 23 Age (yr) &Sex 70M 67F 68M 4lM 79F 48M 65M Clinicl Presenttion Syncope, ventriculr tchycrdi Syncope. norml crdic evlution Syncope. norml crdic evlution Syncope. ventriculr demnd pcemker plced elsewhere Syncope. norml crdic evlution Syncope. norml crdic evlution Syncope, PVCs Findings Associted With Crotid Sinus Mssge Supine BP control 110. sinus puse with CSM 6.0 seconds; BP fter CSM 105, no BP control 150. sinus puse with CSM 2.0 seconds; BP fter CSM 150. no BP control 11 2. sinus puse with CSM 1.6 seconds; BP fter CSM 100. no BP control 115. sinus puse with CSM 3.6 seconds:" BP fter CSM 100. no BP control 11 0. sinus puse with CSM 7.0 seconds; BP fter CSM 100. no BP control 120. sinus puse with CSM 4.5 seconds; BP fter CSM 120, no BP control 180, sinus puse with CSM 9.0 seconds; BP fter CSM 140, no *Permnent pcemker inhibited. CSM = crotid sinus mssge; other bbrevitions s in Tble I. Upright BP control 11 0, sinus puse with CSM 5.5 seconds; BP fter CSM 70. ner ; BP with pcing 11 0; BP with pcing fter CSM 75. ner BP control 130. sinus puse with CSM 1.8 seconds; BP fter CSM 60 (HR 70). ner BP control 110. sinus puse with CSM 1.6 seconds; BP fter CSM 60 (HR 65). BP control IDS. sinus puse with CSM 4.0 seconds; BP fter CSM 70, ner ; BP with pcing 105; BP with pcing fter CSM 70, ner BP control 100. sinus puse with CSM 7.6 seconds; BP fter CSM 70. ner ; BP with pcing 95; BP with pcing fter CSM 75. ner BP control 122. sinus puse with CSM 5.0 seconds; BP fter CSM 50 (HR 55). BP control 145. sinus puse with CSM 8.2 seconds; BP fter CSM 90. ner ; BP with pcing 140; BP with pcing fter CSM 90. ner
JACC VJI. 4. No.1 July 198t65-71 HAMMILL ET AL. 71 more rpid conduction through the trioventriculr (AV) node, presumbly becuse of n increse in sympthetic stimultion nd of prsympthetic withdrwl (5), while in two ptients, nonsustined tchycrdi becme sustined. The incresed rte of the tchycrdi ws not sufficient to mintin blood pressure, nd nine of the ptients experienced their clinicl syndrome with hypotension nd ner or. Ptients with rpid suprventriculr tchycrdi hve shortened ventriculr distolic filling time nd chnge in norml tril nd ventriculr synchrony tht cn decrese crdic output (12,13); however, reflex peripherl vsculr mechnisms re usully sufficient to prevent. The present study reveled no reltion between the hypotensive response to upright posturing nd the tchycrdi rte while the ptient ws supine or upright. Vsovgl. The six ptients with vsovgl were studied becuse ech hd history of repeted episodes of profound. All six developed their typicl svncopl syndrome only fter being plced in the upright position. Ptients with vsovgl hve previously been demonstrted (7-10) to decrese their hert rte, crdic output nd peripherl resistnce, resulting in hypotension.md ner or in response to ssuming the upright position. All six ptients immeditely returned to consciousness fter being returned to the supine position. Crotid sinus hypersensitivity. The evlution of ptients with crotid sinus hypersensitivity ws significntly improved by use of the tilt tble. These ptients hve crdioinhibitory nd vsodepressor responses to crotid sinus mssge, with bout 10% of them hving pure vsodepressor responses (11,14). Becuse n bnorml response to crotid sinus mssge is present in 60% of persons more thn 60 yers old nd usully is not ssocited with. the physicin should demonstrte tht the ptient's is ssocited with crotid sinus hypersensitivity nd not with nother neurologic or crdic bnormlity (15). In this study, the ptients with vsodepressor crotid sinus hypersensitivity continued to demonstrte hypotension with despite mintennce of norml hert rte nd AV synchrony by temporry pcing or sinus rhythm. Such ptients hve vsodepressor, either lone or with crdioinhibitory, nd require therpy imed t preventing the decrese in blood pressure tht is ssocited with their crotid sinus hypersensitivity. Pcemker implnttion lone would not be expected to relieve the symptom, of vsodepressor. This 12 month experience with the use of the tilt tble in 104 ptients undergoing electrophysiologic testing provided useful informtion in 22% of ptients by creting physiologic stress tht ccentuted both tchyrrhythmi nd brdy rrhythmi nd llowed the physicin to correlte n induced rhythm with the clmicl. References I. Robinson BF, Epstein SE, Beiser GO. Brunwld E. Control of hert rte by the utonomic nervous system: studies in mn on the interreltion between broreceptor mechnisms nd exercise. Circ Res 1966;19:400-11. 2. Wng Y. Mrshll RJ, Shepherd JT. The effect of chnges in posture nd of grded exercise on stroke volume in mn. J Clin Invest 1960;39:105 I-61. 3. Loeppky JA, Greene ER, Hoekeng DE, Cprihn A, Luft DC. Betby-bet stroke volume ssessment by pulsed Doppler in upright nd supine exercise. J Appl Physiol 1981;50:1173-82. 4. Rushmer RF. Effects of posture. In: Rushmer RF, ed. Structure nd Function of the Crdiovsculr System. 2nd ed. Phildelphi: WB Sunders, 1976;217-46. 5. Curry PVL. Rowlnd E. Fox KM. Krikler OM. The reltionship between posture. blood pressure nd electrophysiologicl properties in ptients with proxysml suprventriculr tchycrdi. Arch Ml Coeur 1978;71:293-9. 6. Wxmn MB. Shrm AD. Cmeron DA. Huert F, Wld RW. Reflex mechnisms responsible for erly spontneous termintion of proxysml suprventriculr tchycrdi. Am J Crdiol 1982;49:259-72. 7. Epstein SE. Stmpfer M, Beiser GO. Role of the cpcitnce nd resistnce vessels in vsovgl. Circultion 1968;37:524-33. 8. Goldstein OS. Spnrkel M. Pittermn A. et t. Circultory control mechnisms in vsodepressor. Am Hert J 1982;104: 1071-5. 9. Glick G. Yu PN. Hemodynmic chnges during spontneous vsovgl rections. Am J Med 1963;34:42-51. 10. Weissler AM. Wrren JV. Estes EH Jr. Mcintosh HD. Leonrd 11. Vsodepressor : fctors influencing crdic output. Circultion 1957;15:875-82. II. Frnke H. Uber ds Krotissinus-Syndrom und den sogennnten hyperktiven Krotissinus-Reftex. Stuttgrt: Schttuer, 1963:75-8. 12. Goldreyer BN. Kstor JA. Kershbum KL. The hemodynmic effects of induced suprventriculr tchycrdi in mn. Circultion 1976;54:783-9 13. Mclntosh HD. Morris 11 Jr. The hemodynmic consequences of rrhythmis. Prog Crdiovsc Dis 1966;8:330-63. 14. Weiss 5, Bker JP. The crotid sinus reflex in helth nd disese: its role in the custion of finting nd convulsions. Medicine (Bltimore) 1933;12:297-354. 15. Nthnson MH. Hyperctive crdioinhibitory crotid sinus reflex. Arch Intern Med 1946;77:491-503.