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Original ORIGIAL Article ARTICLE Korean Circulation J ;3:33-353 ISS 173-55 c, The Korean Society of Circulation 전기자극으로조성한심실및상실성빈맥의혈역학연구 가톨릭대학교의과대학내과학교실 노태호 이만영 오용석 진승원 신우승 김희열 조은주 김재형 최규보 홍순조 Hemodynamic Effects of Simulated Ventricular Tachycardia and Suraventricular Tachycardia in Dogs Tai Ho Rho, MD, Man Young Lee, MD, Yong Sok Oh, MD, Seung Won Jin, MD, Woo Seung Shin, MD, Hee Yul Kim, MD, Eun Ju Cho, MD, Jae Hyung Kim, MD, Kyu Bo Choi, MD and Soon Jo Hong, MD Deartment of Internal Medicine, College of Medicine, The Catholic University of Korea, Seoul, Korea ABSTRACT Background and Objectives:Tachycardias have various clinical features according to the heart rate, the left ventricular systolic function, the site of origin and the mechanisms of the tachycardias. The rimary urose of this study was to evaluate the role of the origin site and cycle length on the ventricular tachycardia (VT) hemodynamics. Our secondary urose was to exlore the ossible hemodynamic differences between the two common suraventricular tachycardias (SVT). Materials and Methods:VT was simulated in 1 dogs that had there chests oened by using ventricular acing (VP) at 3 different sites: the left ventricular aex (), the right ventricular outflow tract (), and the right ventricular aex (). The mean arterial ressure (MAP), the mean left atrial ressure (MLAP) and the mean ulmonary artery ressure (MPAP) were monitored during VP. To simulate SVT, the right atrial aendage and the right ventricular basal setum were stimulated at different cycle lengths with different ventriculo-atrial (VA) time intervals in another 11 dogs that had their chests oened. The arterial ressure, the ulmonary caillary wedge ressure and the cardiac outut was observed during simulated atrial tachycardia (Grou I), AVRT (Grou II) and AVRT (Grou III). Results:In the VT study, at the same acing site as of the VP, the MAP was significantly decreased with the VP, and the ΔMAP was significantly increased as the length of the VP cycle shortened. At the same acing cycle length of the VP, the ΔMAP was significantly greater at the or than at the. At the same acing site of the VP, the MLAP and the ΔMLAP were significantly increased as the VP cycle length shortened. In the SVT study, MAP was highest in Grou I and it decreased with the decreasing VA interval, but this was not significant. The systolic arterial ressure was significantly higher in Grou II than in Grou III. The CO was higher in Grou I than in the other two grous, with a significant difference, and the CO decreased with shortening of the VA interval, but this was not significant. Conclusion:The above results suggest that in addition to the tachycardia rate, the origin site could be an indeendent factor of the VT hemodynamics. Eisodes of AVRT and AVRT may have a different hemodynamic imact that robably originates from the different timing of the ventricular and atrial contraction. (Korean Circulation J ;3:33-353) KEY WORDS:Tachycardia, ventricular;tachycardia, atrioventricular nodal reentry. 논문접수일 :3 년 월 17 일수정논문접수일 :5 년 3 월 3 일심사완료일 :5 년 7 월 11 일교신저자 : 노태호, -9 서울동대문구전농동 -5 가톨릭대학교의과대학내과학교실전화 :() 95- 전송 :() 9-75 E-mail:tairho@catholic.ac.kr 33

3 Korean Circulation J ;3:33-353 서 론 가혈역학적으로미치는영향에대해알아보고자하였다. 빈맥성부정맥으로인한임상양상은부정맥발생의해부학적위치, 빈맥주기, 빈맥의지속정도, 빈맥발생의기전, 좌심실기능상태, 자율신경계반응의신속성등여러인자에의해영향받음이이미잘알려져있고, 1-) 그정도에따라, 또개인에따라, 별증상을느끼지못하는경우도있고, 약간의혈압하강에그치는것으로부터, 지속적인저혈압, 심혈관계의허탈, 쇽및급사에이르기까지다양하다. 부정맥발생의해부학적위치는그중가장중요한요인으로간주되는데상실성빈맥은심실성빈맥에비해혈역학적장애가덜심하다고알려져있는데이는심실의전기흐름과수축과정이정상적이기때문이다. 같은심실빈맥에있어서도심실빈맥의발생위치가혈역학에어떠한식으로든영향을미칠것임을짐작할수있으나이에대하여는별로연구가이루어져있지않다. 다만, 최근에심부전의새로운치료로서등장한양심실동시자극 (biventricular acing) 의효과를관찰한연구에서보인바와같이 5-) 심실자극부위가혈역학에영향을갖고있음이알려지며심실빈맥의경우에도빈맥발생의위치에따라유사한영향이있을가능성이제시되었다. 그외에도심실빈맥발생초기의급격한동맥압하강은자율신경계에영향을미침이분명하고따라서심실빈맥시자율신경조작이혈역학에미치는영향을관찰함도필요하다. 임상에서흔히접하는상실성빈맥의양대기전인방실결절회귀 (AV node reentry) 와방실회귀 (AV reentry) 는모두체표심전도상좁은폭의 QRS 파를보이며심실박동수에있어서도큰차이가없으므로임상양상이나혈역학적인면에서도차이가없다고일반적으로생각하기쉽다. 그러나방실결절회귀와방실회귀는심전도상의유사함에도불구하고심방과심실의수축시점에는적지않은차이가존재하며이로인해심박출량중심방수축의기여에차이가발생하며따라서여러혈역학적지수에차이가있을가능성이크나이에대하여도보고된것이드물다. 본연구는 부로구성되어있으며, 심실빈맥및상실성빈맥과유사한상황을실험개에서전기자극으로인위적으로조성함으로써, 이들부정맥이어떠한혈역학적변화를일으키며또한이러한혈역학적변화에어떠한변수들이관여하는지를알아보고자하였다. 구체적으로, 1부에서는심실빈맥의발생부위와빈맥주기가심실빈맥시의혈역학적변화에미치는영향과심실빈맥초기의혈압하강에대한자율신경계의역할등을연구하고자, 조성된심실빈맥하에서의동맥압, 폐동맥압및좌심방압의변화를관찰하여위의인자들과혈역학적변화와의관계를규명하고자하였다. 부에서는상실성빈맥에서발생하는혈역학적변화를규명하고특히실방간격이서로다른방실결절회귀빈맥과방실회귀빈맥에서심실충만에대한심방수축시기의변화 재료및방법 실험동물실험동물은한국산잡견 (1~15 kg) 9마리를암, 수구별없이사용하였다. 이들중 1마리를심실빈맥군으로하여이중 1마리에서우심실유출로, 우심실첨부및좌심실첨부에서심실조율을시행하여동맥압, 폐동맥압및좌심방압의변화를관찰하였고심실빈맥시심장의자율신경계의영향을검사하기위해별도의 마리를사용하였다. 나머지 11마리는상실성빈맥군으로하였으며여러자극주기로심실과심방을연차적으로자극하여동맥압, 폐동맥쐐기압및심박출량의변화를관찰하였다, 자극하는동안시간이지남에따라발생하는혈역학변화가실험결과에미칠수있는영향을고려해각각자극방법의순서는그빈도가서로같도록하였다. 마취마취는 thioental sodium( 치오닐, 대한약품, 대한민국 ) 15 mg/kg 을정맥주사한후기관내삽관을시행하고인공호흡기 (Tiberius, Dräger AG Lubeck, Hannover, Germany) 를통해기계적호흡을유지시켰다. α-chloralose(sigma, St. Louis, Missouri, U.S.A) mg/kg 을정맥내로주사하여유도마취한후마취를유지시키기위해시간당 α- chloralose 1 mg/kg 을추가로투여하였다. 실험동물은산소와공기를혼합하여기계적으로호흡시키면서주기적으로동맥혈가스검사를시행하여 H 7.3~7., PCO 33~3 mmhg, PO > mmhg 로유지하였다. 또한표준심전도를기록하기위해사지체표에전극을부착하였다. 동맥압, 좌심방압, 폐동맥압및폐동맥쐐기압을측정하기위해각각대퇴동맥, 좌심방이와주폐동맥에위치한도관을압력변환기에연결시키고 hysiograhy(evr13, PPG, ew York, USA) 에압력곡선이나타나게하였으며압력곡선의기록속도는 1 mm/sec 로하고 scale factor 는동맥압은 1 mmhg/ mm, 좌심방압.1 mmhg/mm 그리고폐동맥압은. mmhg/ mm로설정하였다. 정맥도관으로는마취제및약제를투여하였고 lactated Ringer s solution 5~1 ml/kg/ hr 로수액을유지시키면서출혈시동량의 entastarch(pen-tasan, 제일, 대한민국 ) 를투여하여교정하였다. 체온은직장내에체온계를거치하여측정하였고전기담요를이용하여 3-39 를유지하였다. 심실빈맥군수술적처치서혜부의피부를절개하여대퇴동맥과대퇴정맥을노출하고

Tai Ho Rho, et al:hemodynamics of Arrhythmias 35 각각 F의도관을삽입하였다. 동맥도관을통해동맥압을측정하였고정맥도관으로는마취제, 수액및약제를투여하였다. 제 늑간에서횡절개로개흉술후심막을절개하여심막요람을만든후심장을노출시켰다. 좌심방압을측정하기위해서는좌심방이에도관을, 폐동맥압을측정하기위해주폐동맥에도관을삽입하였다. 심실을조율하기위해우심실유출로 (), 우심실첨부 (, 심실중격우측 1 cm) 및좌심실첨부 (, 심실중격좌측 1 cm) 에각각 개씩 5 mm 간격으로심외막에전극선 (TME -ZA Stericlin, PAPIER, Germany) 을부착하였다. 심실조율심실조율을위해외부심장자극기 (external cardiac stimulator, 3F51, SA-EI, Jaan) 를각부위의심외막하에부착한전극선에연결하고각부위의조율역치 (acing threshold) 를측정하였으며모든조율은조율역치의두배로시행하였다. 조율주기는수술적처치후혈역학적으로안정된상태에서실험동물의분당기초심박수를측정하여그수치의 배, 배와 배의조율횟수로정하여환산하였다. 우심실유출로, 우심실첨부및좌심실첨부에서각각 초간조율하여동일조율부위에서빈맥의주기에따른혈역학적변화와동일조율주기에서조율부위에따른혈역학적변화를관찰하기위해평균동맥압, 평균좌심방압과평균폐동맥압을조율 1초전부터조율후혈역학적변화가안정될때까지동시에기록하였다 (Fig. 1). 평균동맥압의최대감소치는심실조율전의평균동맥압과심실조율후평균동맥압의최저치와의차이로구하였고평균좌심방압의최대증가치는심실조율후평균좌심방압의최고치와조 율전의평균좌심방압과의차이로구하였다. 각조율사이에는혈역학적지표들이안정될때까지최소 5분간의휴식기를두었다. 약물을이용한자율신경차단실험동물 마리를대상으로 roranolol(ici, England) 1 mg/kg 을정맥주사하고 1분후에 atroine sulfate( 대한약품, 대한민국 ).5 mg/kg 을정맥주사함으로써, 심장의자율신경지배를차단하여내인성심박수 (intrinsic heart rate) 상태로유지시켰다. 이후자율신경차단상태를유지하기위해한시간간격으로 roranolol 1 mg/kg 과 atroine sulfate.5 mg/kg 을투여하였다. 약물투여전과후에우심실유출로, 우심실첨부및좌심실첨부를기초심박수의 배에해당되는조율주기로 초동안전기적으로조율하여평균동맥압, 평균좌심방압의변화를기록하여자율신경차단전, 후의혈역학적차이를관찰하였다. 상실성빈맥군수술적처치서혜부의피부를절개하여대퇴동맥과대퇴정맥을노출시켜각각 F의도관을삽입하였다. 동맥도관을통해동맥압을측정하였고정맥도관으로는마취제, 수액및약제를투여하였다. 폐동맥쐐기압은우측외경정맥을통해 7.5 F Swan-Ganz 도관을주폐동맥에거치하여풍선을팽창시킨후측정하였고심박출량은열희석법을이용하여측정하였다 (Patient monitor, Hewllet Packard, U.S.A.). 정중으로흉골절개를시행하고심막을절개하여심막요람을만든 15 MAP. MAP (mmhg) 5 MPAP MLAP 1 MPAP/MLAP (mmhg) MAP (mmhg) 15 5 MAP MPAP MLAP VP sec 1 MPAP/MLAP (mmhg) Fig. 1. An examle of simultaneous recordings of mean arterial ressure (MAP), mean ulmonary artery ressure (MPAP), and mean left atrial ressure (MLAP) before, during, and after ventricular acing (VP) in a dog. Uer anel: recordings of MAP, MLAP & MPAP during VP at the heart rate of,, & of BHR (from the left) at a single site (). Lower anel: recordings of MAP, MLAP & MPAP during VP at,, & (from the left) at a single acing rate ( of BHR). BHR: baseline heart rate, : left ventricular aex, : right ventricular outflow tract, : right ventricular aex.

3 Korean Circulation J ;3:33-353 후심장을노출시켰다. 심방을자극하기위해전극선을우심방이의심외막에고정하였다. 심실을자극하기위해서는우선심실중격의위치를확인한뒤전극선의피복을벗겨 5G 주사바늘에통과시키고그끝을구부려바늘과함께심실중격상부의심근에수직으로꽂은뒤구부려진전극선은심근에박힌채고정되도록하고바늘만당겨제거하는방법을이용하였는데이는되도록히스속과가까운심근을자극하여정상적인경로의심실탈분극과유사한상태로만들어상실성빈맥과유사하게하기위함이었다. 자발적인동율동을억제하기위해동결절을분쇄하여동정지 (sinus arrest) 상태를만들었다. 심방및심실조율외부심장자극기를각부위의심외막하에고정시킨전극선에연결하고각부위의자극역치를측정하였으며모든자극은자극역치의두배로시행하였다. I군에서는심방빈맥상태를실현하기위해분당 1 회의 AOO mode 로우심방을조율하면서혈역학적지수의변화가안정화될때까지 초간기다린후동맥압, 폐동맥쐐기압, 및심박출량을측정하였다. II군에서는방실회귀빈맥을실현하기위해역시분당 1 회의 DOO mode 로실-방간격을 msec 로조율하였으며 III군에서는방실결절회귀빈맥을실현하기위해서실-방간격을 5 msec, msec 로조율하여같은방법으로측정하였다. 자극방법이바뀔때마다 1분간의회복시간을두어각자극시작시의혈역학적수치를같도록하였다. 통계적분석모든결과는평균 ± 표준편차로표시하였다. 심실빈맥군에서평균동맥압, 평균좌심방압과평균폐동맥압의조율주기및조율부위에따른차이및조율시작후각시점에서측정치의비교에는 -tailed aired t test 를이용하였다. Pearson 씨의상관분석을이용하여심실조율후최저평균동맥압과조율중단후최고평균동맥압과의상관관계를분석하였다. 상실성빈맥군에서동맥압, 평균폐동맥쐐기압과심박출량의자극방법및자극간격에따른각각의차이를비교하는데는역시 tailed aired t test 를이용하였다. 상실성빈맥군내의세 (I, II, III) 군간의차이를비교하는데는일원분산분석및 Bonferroni test 와 Scheffe test 를통한사후검증을이용하였다. 자극시각군에서각혈역학적 arameter 차이의상관관계를분석하기위해역시 Pearson Correlation analysis 를시행하였다. 모든통계분석은 <.5 인경우를유의한차이가있는것으로판정하였다. 결과 심실빈맥군안정시혈역학심실빈맥군에서안정시기초심박수는평균 1±1.7 회 / 분이었고평균동맥압은 11±.1 mmhg, 평균좌심방압은.3±. mmhg 였고평균폐동맥압은 1±. mmhg 였다. 우심실유출로, 우심실첨부및좌심실첨부의조율역치는모두 1.5 mv 이하로측정되었다. 평균동맥압평균동맥압의최대감소치는동일한조율부위에서는세부위모두조율주기가짧아질수록높게나타났다 (<.1). 동일한조율주기에서는좌심실첨부조율시보다우심실유출로와우심실첨부조율시에평균동맥압의감소가현저했으며 ( vs ; <.1, vs ; <.5), 우심실첨부와우심실유출로간에는유의한차이가없었다 (Table 1, Fig. ). 최저치에도달한후심실조율이계속됨에도불구하고평균동맥압은서서히회복되었으며최대감소치의 1/ 수준까지회복된시간은조율주기가짧을수록유의하게지연되었으나 (<.1), 동일조율주기에서는조율부위에따른차이는없었다. 조율중단후평균동맥압은급상승하여평균 7초후에최고치에도달하였고최고평균동맥압은 배로조율시에는 1±5.3 mmhg(x), 배로조율시에는 1±9.5 mmhg(<.1 vs X), 배로조율시에는 15±1.1 mmhg(<.1 vs X) 정도조율전보다증가되었다. 심실조율시작후최저평균동맥압과조율중단후최고평균동맥압간에는기초심박수의 배와 배의조율주기에서조율부위에관계없이유의한상관관계를보였다 (r=.57, r=., <.1). 평균좌심방압평균좌심방압은평균 3초에최고치에도달하였고심실 Table 1. Maximum mean arterial ressure differences (ΔMAP) at the three different sites at the same acing rate Pacing rate (XBHR) ΔMAP (mmhg) ±.9 (.%) 31±. (31.%) 9±1. (9.%)*. 3±9.3 (35.5%) ±1.1 (.5%) 1±11.3 (39.%)* 9±1.9 (7.%) 5±13. (5.%) 57±1. (53.%) Values are mean±sd from 1 dogs. ΔMAP: {baseline mean arterial ressure (MAP)}-{lowest MAP during ventricular acing (VP)}, (%): Δ MAP/baseline MAP, BHR: baseline heart rate, : left ventricular aex, : right ventricular outflow tract, : right ventricular aex. vs ; : <.1, vs ; *: <.5, : <.1, vs ; all =S

Tai Ho Rho, et al:hemodynamics of Arrhythmias 37 Mean arterial ressure (mmhg) 3 9 1 3 9 1 3 9 1 Mean arterial ressure (mmhg) 3 9 1. 3 9 1 3 9 1 Fig.. Changes of mean arterial ressure (MAP) at 3 different sites during and after ventricular acing for seconds at 3 different rates (,, & of baseline heart rate). indicates nadir MAP.P: eak MAP, : left ventricular aex, : right ventricular outflow tract, : right ventricular aex, BHR: baseline heart rate. Uer anel shows a greater MAP dro at a shorter cycle length at the same acing site (all <.1). Lower anel shows a greater MAP dro at or than at the same acing rate; vs : all <.1 at 3 different rates, vs : <.5 at & BHR, <.1 at of BHR. There is no significant difference of MAP between and. 조율이계속됨에도불구하고더이상증가되지않고오히려감소되었다. 평균좌심방압은조율중단후 1초이내에모든경우에서조율전수준으로회복되었다 (Fig. 3). 평균좌심방압의최대증가치는좌심실첨부에서는.±1.1 mmhg (X), 5.1±1.3 mmhg(x), 7.±.9 mmhg(x), 우심실유출로에서는 3.±1.15 mmhg(x), 5.±.17 mmhg(x), 7.7±3.13 mmhg(x), 우심실첨부에서는 3.1±1.3 mmhg(x), 5.±1.1 mmhg(x), 7.±. mmhg(x) 로동일한조율부위에서는세부위모두조율주기가짧아질수록높게나타났으나 (<.1), 동일한조율주기에서는조율부위에따른차이가관찰되지않았다. 평균폐동맥압평균폐동맥압은조율시작직후평균 5초안에세부위모두에서일시적으로감소되었다가서서히증가되었으며조율 동안지속적으로상승되었다. 평균폐동맥압은조율중단직후에는급상승되었다가수초안에조율전수준으로감소하였다 (Fig. ). 평균폐동맥압의조율시작직후일시적감소는좌심실첨부에서는.±.71 mmhg(x),.7 ±.3 mmhg(x), 1.1±.7 mmhg(x), 우심실유출로에서는 1.±. mmhg(x), 1.7±.55 mmhg(x), 1.9±.73 mmhg(x), 우심실첨부에서는 1.±.33 mmhg(x), 1.±.3 mmhg(x),.9±.9 mmhg (X) 로동일주기에서는세부위모두우심실유출로에서좌심실첨부와우심실첨부에비해높았으나 (<.5), 좌심실첨부와우심실첨부간에는유의한차이는없었다. 자극중단직후폐동맥압의급상승정도는좌심실첨부에서는.7±.3 mmhg(x), 1.±.51 mmhg(x),.±.7 mmhg(x), 우심실유출로에서는.±.5 mmhg (X), 1.7±.5 mmhg(x),.5±. mmhg(x),

3 Korean Circulation J ;3:33-353 Mean left atrial ressure (mmhg) 3 9 3 9 3 9. Mean left atrial ressure (mmhg) 3 9 3 9 3 9 Fig. 3. Changes of mean left atrialressure (MLAP) at 3 different sites during and after ventricular acing for seconds at 3 different rates (,, & of baseline heart rate). : left ventricular aex, : right ventricular outflow tract, : right ventricular aex. Uer anel shows a greater MLAP increase at a shorter cycle length at the same acing site. There are significant MLAP differences at each time oint (all <.1). Lower anel shows no significant regional differences of MLAP at the same acing cycle length at each time oint (all =S). 13 13. 13 Mean ulmonary artery ressure (mmhg) 11 9 11 9 11 9 7 3 9 7 3 9 7 3 9 Fig.. Changes of mean ulmonary artery ressure (MPAP) at 3 different sites during and after ventricular acing for seconds at 3 different rates (,, & of baseline heart rate). : left ventricular aex, : right ventricular outflow tract, : right ventricular aex. After initiation of ventricular acing, there are greater decreases of MPAP in than / ( vs /: all <.5, vs : all =S). After termination of ventricular acing, greater increases of PMAP are found at shorter cycle length ( vs : <.5, vs : <.1).

Tai Ho Rho, et al:hemodynamics of Arrhythmias 39 우심실첨부에서는.±.31 mmhg(x), 1.±.5 mmhg(x),.3±.59 mmhg(x) 로동일주기에서는조율부위에따른차이는없었지만동일부위에서는세부위모두조율주기가짧을수록높게나타났다 (X vs X, <.5; X vs X, <.1). 약물을이용한심장자율신경차단정맥내로 roranolol 과 atroine 주사후분당심박수는 15±11.9 회에서 1±.3 회로감소되었으나평균동맥압과평균좌심방압에는유의한차이가없었다. 기초심박수의 배로심실을조율했을때자율신경차단제투여전에평균동맥압은 1±13.9 mmhg 에서 ±1. mmhg 로감소하였고자율신경차단후에는평균동맥압은 1±1.9 mmhg 에서 ±1.5 mmhg 로감소하여자율신경차단제투여전에비해자율신경차단후에동맥압이현저하게감소되었으며 (<.1), 조율이지속되는동안과조율중단후에도동맥압의회복이둔화되었다. 조율시작후 초의평균동맥압은차단제투여전이 1±1.3 mmhg, 자율신경차단후에 1±1.9 mmhg 로유의한차이를보였으며 (<.1), 각각조율전평균동맥압의 77.9% 와 5.3% 까지회복되었다. 또한평균좌심방압도차단제투여전에비해현저하게증가되었으며 (<.1), 심실조율을중단할때까지지속적으로상승되었다. 평균동맥압의최대감소치와평균좌심방압의최대증가치는심장의자율신경차단후유의하게높아졌지만동일조율주기에서조율부위에따른차이는관찰되지않았다 (Table ). 동맥압평균동맥압은심방만조율했던심방빈맥군 (I 군 ) 에서 7. ±. mmhg 로가장높았고실-방간격 msec 로조율하여실현했던방실회귀빈맥군 (II 군 ) 에서.±17. mmhg 로나타나실-방간격 5msec 와 msec 로조율하여실현했던방실결절회귀빈맥군 (III 군 ) 에서각각 7.3±. mmhg,.3±. mmhg 로나타난것에비해높았으나통계적인의의는없었다. 수축기동맥압은실-방간격 msec 인방실회귀빈맥군 (II 군 ) 에서 19.±. mmhg 로방실결절회귀빈맥군 (III 군 ) 중특히실방간격 5 msec 로조율했을때 95.3±7.1 mmhg 로나타난것에비해유의하게높았으며 (<.5) 역시심방빈맥군 (I군 ) 에서 113.±19.7 mmhg 로가장높았다 (Fig. 5). 이완기동맥압은실-방간격의변화에대해일정한경향을보이지않았다. 평균폐동맥쐐기압평균폐동맥쐐기압은심방빈맥군에서 3.7±.3 mmhg 으로가장낮았으나실- 방간격의점차적인감소에대해일정한경향을보이지않았다 (Table 3). 심박출량심박출량은심방빈맥군 (I군 ) 에서 1.1±.3 L/min 로방실결절회귀빈맥군 (III군) 중특히실- 방간격 msec로조율한방실결절회귀빈맥군의.9±. L/min 와실-방간격 msec 로조율한방실회귀빈맥군 (II 군 ) 의.99±.1 L/min 보다유의하게높게관찰되었다 (<.1). 통계적인의 상실성빈맥군 안정시혈역학상실성빈맥군에서실험동물의안정시기초심박수는 1 ±11.7 회 / 분이었고평균동맥압은 11±11.1 mmhg, 평균폐동맥쐐기압은.5±7. mmhg 였다. 우심방첨부와심실중격부의자극역치는모두 1.5 mv 이하로측정되었다. Table. Effect of cardiac autonomic blockade on mean arterial ressure (MAP) and mean left atrial ressure (MLAP) during ventricular acing ( of baseline heart rate) at the three different sites Pacing site ΔMAP(mmHg) Before blockade After blockade ΔMLAP(mmHg) Before blockade After blockade 3±5.1 59±11.* 7.5±1.97 15.±.* 5±5. 1±9.9* 7.7±3.15 1.7±5.1* 3±. 5±5.* 7.5±.5 1.9±.3* Values are mean±sd from six dogs. ΔMAP: baseline MAP- lowest MAP during ventricular acing (VP), ΔMLAP: highest MLAP during VP-baseline MLAP, : left ventricular aex, : right ventricular outflow tract, : right ventricular aex. Autonomic blockade by roranolol (1 mg/kg and then 1 mg/kg/hr, iv) and atroine (.5 mg/kg and then.5 mg/kg/hr, iv). *: <.1 Systemic arterial ressure mmhg 15 5 Grou I Grou II Grou III Mean Systole Diastole Fig. 5. Comarison of mean, systolic and diastolic arterial ressure in 3 grous of simulated suraventricular tachycardia. Grou I: AOO acing mode that simulated atrial tachycardia (AT), Grou II: DOO mode acing with VA interval of msec that simulated atriventricular reentrant tachycardia (AVRT), Grou III: DOO mode acing with VA interval of 5 msec or aced ventricle and atrium simultaneously that simulated atrioventricular nodal reentrant tachycardia (AVRT). Diastole; diastolic arterial ressure, Mean: mean arterial ressure, Systole; systolic arterial ressure. Error bars indicate mean±sd. *: <.5, comared with Grou II. *

35 Korean Circulation J ;3:33-353 Table 3. The mean value of ulmonary artery wedge ressure in three grous of different cardiac stimulation Suraventricular tachycardia AT grou AVRT grou AVRT grou Stimulation mode and VA interval AOO DOO VA ms DOO VA 5 ms DOO VA ms Mean PAWP 3.73±.3 1.±..91±3.1 7.±.3 >.1 AT: atria tachycardia, AVRT: atriventricular reentrant tachycardia, AVRT: atrioventricular nodal reentrant tachycardia, PAWP: ulmonary artery wedge ressure, VA interval: ventriculoatrial interval Cardiac outut L/min 1.5 1.5 Grou I Grou II Grou III Fig.. Comarison of cardiac outut in 3 grous of simulated suraventricular tachycardia. Grou I: AOO acing mode that simulated atrial tachycardia (AT), Grou II: DOO mode acing with VA interval of msec that simulated atriventricular reentrant tachycardia (AVRT), Grou III: DOO mode acing with VA interval of 5 msec or aced ventricle and atrium simultaneously that simulated atrioventricular nodal reentrant tachycardia (AVRT). Error bars indicate mean±sd. *: <.1, comared with Grou I. 의는없었으나방실회귀빈맥군 (II군 ) 에서방실결절회귀빈맥군 (III군) 에서보다심박출량이높게측정되는양상을보였다 (Fig. ). 고 심실빈맥은심실에서이상자동능발생, 회귀, 후분극등의기전으로생성되는비정상적인전기현상으로심전도상빠른횟수의광폭의 QRS 파를나타내는부정맥이다. 심실빈맥시의혈역학적변화는정상생리적인심방심실수축의순차적인조화가깨어지며구축율이감소하고더불어빠른심실수축횟수로말미암아동맥압의하강이발생한다. 9) 심실빈맥시의임상양상은매우다양하여약간의혈압하강에그치는것으로부터지속적인저혈압, 심혈관계의허탈, 쇼크및급사에이르기까지다양하다. 이와같이심실빈맥시나타나는일련의다양한혈역학적반응에관여하는인자들에대해서는아직도명확하게규명되어있지않다. 이러한인자로서는, 수축에참여하는심근의이상유무, 심실빈맥의발생부위, 빈맥주기, 역행성실방전도 (ventriculoatrial conduction) 유무, 1) 빈맥초기혈압하강에대한자율신경계의반응등이작용할것으로추측할수있다. 심실 * 찰 * 조기수축시맥압은심실조기수축의발생부위와연결간격 (couling interval) 에의해결정되며연결간격이짧을수록, 우심실보다는좌심실에서발생하는경우에맥압이현저하게감소된다. 11-13) 혈역학적인면에서심실조기수축시연결간격의중요성은기초맥박수와심실확장기의지속기간에따라달라진다. 즉연결간격이짧을수록확장기가짧아지고좌심실충만양이감소되어결과적으로심박출량이감소된다. 1) 이연구결과는심실빈맥의경우에도빈맥의주기길이와발생부위가혈역학적변화의중요한결정인자가될것을강력히시사한다. 이전의연구 1) 에서도심실빈맥시혈역학적인변화에짧은빈맥주기가중요한인자임이밝혀져있으나심실빈맥시어느정도로짧은빈맥주기가결정적인혈역학적변화를일으키는가에대한정량적연구는이루어지지않았으며또한동일한빈맥주기에서빈맥의발생부위에따른혈역학적변화에대한연구또한보고된바가없다. 본연구의결과에의하면심실조율시평균동맥압의하강과평균좌심방압의상승은조율주기가짧을수록현저하였으며동일한조율주기에서는평균좌심방압은조율부위에따른차이가없었지만평균동맥압은좌심실조율보다는우심실조율시감소가심한것을알수있었다. 이상의결과로빈맥주기가빈맥초기혈역학적변화의주된결정인자로간주되며동일한빈맥주기에서는빈맥의발생부위에따라유의한혈역학적인차이를나타내므로빈맥발생부위도심실빈맥발생시혈역학적변화에영향을주는중요한인자로생각된다. 적절한심박출량을유지하기위해서는심방과심실의수축이순차적으로조화를이루는것이중요하며심실의연쇄수축이유지되는경우에는그렇지않은경우에비해약 15% 까지동맥압이증가됨이알려져있다. 15) 심실빈맥시에는빠른심실수축으로인해심실의확장기동안심실충만이상실될뿐아니라역행성실방전도가발생하여심방수축이승모판이닫힌상태에서일어나게된다. 또한심실빈맥시는전기의비정상적인전도로심실의수축과이완의부조화와승모판역류가동반된다. ) 본연구에서심실조율시작직후동맥압의감소와동시에좌심방압의급격한상승이관찰되었다. 폐동맥압은조율시작직후일시적으로감소되었다가조율이지속되면서서서히상승되었다. 폐동맥압의상승은좌심방압상승의반향으로추정되나 초의짧은심실조율에서는임상적으로의미있는상승은관찰되지않았다. 이결과로빈맥주기나빈맥의발생부위는심실빈맥발생

Tai Ho Rho, et al:hemodynamics of Arrhythmias 351 직후혈역학적변화에주로관여되며심실빈맥이지속되면서혈역학적회복에는다른인자들이관련될것으로생각된다. 심실빈맥이시작되면순간적으로혈압이감소되고심실의충만압이상승되는데동맥압의감소는경동맥동과대동맥에존재하는압반사수용체를자극하여중추신경계로부터교감신경성유출이증가되어교감신경흥분효과를유발하게되고, 1)17) 결과적으로심실의수축성이증가되고말초혈관이수축되면서전신혈관저항이상승되어혈압상승이일어나게된다. 1) 본연구에서 roranolol 과 atroine 으로심장의자율신경을차단하고심실조율을시행하였을때평균동맥압이자유신경차단제투여전에비해현저하게감소되었으며조율이지속되는동안과조율중단후에도동맥압의회복이둔화되었다. 이는 Feldman 등 19) 의관찰결과와일치한다. 이결과는말초혈관의수축반응이존재함에도불구하고 roranolol 로인해좌심실의수축성이감소되어나타났으며따라서심실빈맥초기혈역학적회복에는 α 및 β 교감신경반응이모두필요한것을알수있다. 또한자율신경차단후차단전과달리좌심방압이지속적으로상승되는것으로보아심실빈맥시 β 교감신경반응에의한심실기능의개선정도가심실충만압과관련성이있을것으로추정된다. 이연구에서는 β 차단제인 roranolol 외에부교감신경차단제인 atroine 이추가로투여되었는데본연구결과에 atroine 의영향은알수없으며이후추가연구가필요할것으로생각된다. 발작성상실성빈맥은규칙적이고좁은 QRS 파를보이는빈맥이갑자기발생하고정지하는특징을가지며심계항진이나어지럼증을가장흔하게호소하는비교적예후가양호한부정맥으로알려져있으나 ) 적지않은경우에서실신등의심각한증세가보고되었다. 1) Ogawa 등 ) 은특히구혈전기 (re-ejection eriod) 에선행하여심방수축이일어나는것이심실기능을최대화함을규명하였고, Samet 등 3) 은정상심장을가진동물과사람에서심박출량이최대로유지되기위해서는적절한시기에심방수축이일어나는것이중요함을밝혔다. 심실의이완기동안에심방의수축이이루어지면심실수축전에실방압력차가증가하게되어심실이수축하기전에방실판막이닫히게된다. 만약심방수축없이심실이수축하게되면심각한판막역류현상이초래되고 ) 심방수축이심실의수축기후기, 즉방실판막이열리기직전에일어나면이완말기용적이현저히감소하고심실수축도감소함이밝혀졌다. DiCarlo 등 3) 은정상심장에서심방과심실간의자극간격이감소할수록심박출계수와박출량계수가유의하게감소함을밝혔다. Wood 등 5) 은상실성빈맥에서심계항진이나어지럼증, 실신등의증세가나타날수있다고하였으나방실결절회귀빈맥과방실회귀빈맥에서실제로이들증세의빈도에는의의있는차이가없었다. 그러나 Matsui 등 ) 이발표한바에따르면발작성상실 성빈맥에서전구혈시간 (re-ejection time: PET) 과구혈시간 (ejection time: ET) 및이들의비율 (PET/ET) 이서로다르며방실결절회귀빈맥에서전구혈시간이유의하게증가하여혈역학적인장애가더심하리라고예견하였으며이는실방전도간격이방실결절회귀빈맥에서짧아지기때문이라고하였다. 방실결절회귀빈맥에서는심주기중등용성수축기와최초심실구혈기도중에심방수축이발생한다. 심방의수축은박출량의 15~% 를기여하며이는역시심주기중어느시기에심방수축이이루어지는가에따라심박출량에차이가있음을시사하는것이다. 7) 본연구에서도심방과심실의수축이시간적으로적절히이루어지도록심방만자극한경우 ( 심방빈맥군, I군 ) 수축기동맥압이가장높았고심박출량이가장컸다. 심방의수축과동시혹은거의동시에심실의수축이이루어지도록설정한경우 ( 방실결절회귀빈맥군, III군 ) 에서보다, 실-방수축이얼마간의시간간격을두고이루어지도록설정한경우 ( 방실회귀빈맥군, II군 ) 에수축기동맥압이더높고심박출량도더컸다. 따라서시간적으로더적절한실- 방수축이이루어지는방실회귀빈맥이그렇지않은방실결절회귀빈맥보다혈역학적으로유리한효과를내리라는추측을할수있다. 폐동맥쐐기압은일정한경향을보이지않았는데이는자극기간이충분히길지않았기때문으로여겨지며실제임상에서관찰되는바와같이빈맥의지속시간이수시간정도로자극기간이길어지거나반복해서자극하면두군에서차이가발생할가능성이있으리라생각되나추후연구가필요한부분이다. 요약 배경및목적 : 빈맥은빈맥발작시분당심실수축횟수, 좌심실수축기능, 발생위치, 기전등의요소에의해다양한증상이발현된다. 본연구의목적은실험개를이용하여심실빈맥및여러기전의상실성빈맥을인위적으로조성하여혈역학적변화를관찰하고또한, 이러한혈역학적변화에어떠한인자들이관여하는지탐구하였다. 방법 : 1마리의개흉견에서, 좌심실첨부, 우심실유출로와우심실첨부를전기적으로조율하여심실빈맥과유사한조건을조성한후동맥압, 폐동맥압및좌심방압의변화를관찰하였다. 다른 11마리의개흉견에서, 우심방이와우심실의중격기시부를다양한실-방간격으로조율하여상실성빈맥을조성하였다. 우심방이만조율하여심방빈맥 (I군 ) 을, 실-방간격 msec 으로조율하여방실회귀빈맥 (II 군 ) 을, 실-방간격 5 msec, msec로조율하여방실결절회귀빈맥 (III 군 ) 과유사하게설정한후동맥압, 폐동맥쐐기압및심박출량을관찰하였다.

35 Korean Circulation J ;3:33-353 결과 : 심실빈맥군 : 동일한심실조율부위에서조율주기가짧아질수록평균동맥압이감소하는정도가컸으며, 동일한조율주기에서평균동맥압의최대감소치는좌심실첨부보다우심실유출로와우심실첨부에서높게나타났으나우심실첨부와우심실유출로간에유의한차이가없었다. 동일한심실조율부위에서조율주기가짧아질수록평균좌심방압이증가하는정도가높게나타났으나, 동일한조율주기에서평균좌심방압의최대증가치는심실내조율부위에따른차이는없었다. 심장의자율신경차단후평균동맥압의최대감소치와평균좌심방압의최대증가치는차단제투여전에비해유의하게높아졌으며, 조율이지속되는동안과조율중단후에도평균동맥압의회복이둔화되었다. 상실성빈맥군 : 평균동맥압은 I군 ( 심방조율군 ) 에서가장높았고실-방조율간격을점차감소시키며동맥압의감소하였으나통계적으로유의하지않았다. 수축기동맥압은실- 방조율간격을 msec 로조율했을때 (II 군 ), 5 msec 나 msec 로조율했을때 (III 군 ) 보다통계적으로유의하게높았다. 심박출량은 I군에서 II군이나 III 군에서보다유의하게높았고, II군에서 III 군에서보다높은양상을보였으나유의하지는않았다. 결론 : 위의결과로볼때, 심실빈맥시빈맥주기외에도빈맥의발생부위가혈역학적변화에영향을줄수있는독립적인다른한인자로생각된다. 또한동일심박수를가진상실성빈맥에서혈역학적변화의정도가그기전에따라차이가있을수있고그차이는심방과심실의수축시점과관련이있을가능성을보여준다. 중심단어 : 심실빈맥 ; 방실회귀빈맥. 본논문은 1999 년도대한순환기학회산학협동연구비의지원에의하여이루어졌음. 또한일부가톨릭중앙의료원의연구비보조로이루어졌음. REFERECES 1) Hamer AW, Stanley SA, Thomas P, Mandel WJ. Factors that redict syncoe during ventricular tachycardia in atients. Am Heart J 19;17:997-5. ) Lima JA, Weiss JL, Guzman PA, Weisfeldt ML, Reid PR, Traill TA. Incomlete filling and incoordinate contraction as mechanisms of hyotension during ventricular tachycardia in man. Circulation 193;:9-3. 3) DiCarlo LA Jr, Morady F, Krol RB, et al. The hemodynamic effects of ventricular acing with and without atrioventricular synchrony in atients with normal and diminished left ventricular function. Am Heart J 197;11:7-5. ) Ellenbogen KA, Smith ML, Thames MD, Mohanty PK. Changes in regional adrenergic tone during sustained ventricular tachycardia associated with coronary artery disease or idioathic dilated cardiomyoathy. Am J Cardiol 199;5:133-. 5) Auricchio A, Stellbrink C, Block M, et al. Effect of acing chamber and atrioventricular delay on acute systolic function of aced atients with congestive heart failure. Circulation 1999;99:993-31. ) Ihm SH, Rho TH, Cho EJ, et al. Hemodynamic benefits of atriobiventricular acing in oen chest dogs. Korean Circ J 1;31: -. 7) Lee MY, Rho TH, Yoo KD, et al. The relationshi between QRS duration and LV systolic function in aced atients. Korean Circ J 1;31:37-3. ) Kim YH, Kim JS. Clinical characteristics in atients with imlantable cardioverter-defibrillator (ICD). Korean Circ J ; 3:395-. 9) Steinbach KK, Merl O, Frohner K, et al. Hemodynamics during venticular tachyarrhythmias. Am Heart J 199;17:11-. 1) Peuhkurinen KJ, Uusimaa PA, Ruskoaho H, Linnaluoto M, Huikuri H. Hemodynamic recovery, atrial natriuretic etide, and catecholamines during simulated ventricular tachycardia: Effect of ventriculoatrial conduction. Pacing Clin Electrohysiol 1995;1:75-. 11) Levy JM, Mesel E, Rudolh AM. Unequal right and left ventricular ejection with ectoic beats. Am J Physiol 19;3:111-. 1) Millar K, Eich RH, Abildskov JA. Relation of variations in activation order to intraventicular ressures during remature beats. Circ Res 19;19:1-. 13) Eber LM, Berkovits BV, Maltloff JM, Gorlin R. Dynamic characterization of remature venticular beats and ventricular tachycardia. Am J Cardiol 197;33:37-3. 1) Otsuji Y, Toda H, Kisanuki A, et al. Influence of left ventricular filling rofile during receding control beats on ulse ressure during ventricular remature contractions. Eur Heart J 199; 15:-7. 15) Maloney J, Khoury D, Simmons T, et al. Effect of atrioventricular synchrony on stroke volume during ventricular tachycardia in man. Am Heart J 199;13:151-. 1) Kendrick E, Oberg B, Wennergren G. Vasoconstrictor fibre discharge to skeletal muscle, kidney, intestine, and skin at varing levels of arterial barorecetor activity in the cat. Acta Physiol Scand 197;5:-7. 17) Rea RF, Eckberg DL. Carotid barorecetor-muscle symathetic relation in human. Am J Physiol 197;53:R99-3. 1) Ogilvie RI, Zborowska-Sluis D. Effect of chronic raid ventricular acing on total vascular resistance. Circulation 199;5:15-3. 19) Feldman T, Carroll JD, Munkenbeck F, et al. Hemodynamic recovery during simulated ventricular tachycardia: role of adrenergic recetor activation. Am Heart J 19;115:57-7. ) Dhala A, Bremner S, Blanck Z, et al. Imairment of driving abilities in atients with suraventricular tachycardias. Am J Cardiol 1995;75:51-. 1) Leitch JW, Klein GJ, Yee R, Leather RA, Kim YH. Syncoe associated with suraventricular tachycardia: an exression of tachycardia rate or vasomotor resonse? Circulation 199;5: 1-71. ) Ogawa S, Dreifus LS, Shenoy P, Brockman SK, Berkovits BV. Hemodynamic consequences of atrioventricular and ventriculoatrial acing. Pacing Clin Electrohysiol 197;1:-15. 3) Samet P, Castello C, Bernstein W. Hemodynamic sequelae of atrial, ventricular, and sequential atrioventricular acing in cardiac atients. Am Heart J 19;7:75-9. ) Little RC. Effect of atrial systole on ventricular ressure and closure of the A-V valve. Am J Physiol 1951;1:9-95. 5) Wood KA, Drew BJ, Scheinman MM. Frequency of disabling

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