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Temporary transveous pacing and femoral vein thrombosis
ABSTRACTS
TEMPORARY TRANSVEOUS PACING AND FEMORAL VEIN THROMBOSIS Andre J. Nolewajka, MD; Michele D. Goddard, MD; Thomas C. Brown, MD, Univer3ity of Western Ontario, London, Canada. The true incidence of deep vein thrombosis with subsequent pulmonary embolism in patients requiring temporary transvenous pacing via the femoral vein is unknown. Thirty consecutive patients, mean age 66+ 10 years (38-79) requiring temporary transvenous paczng were studied by bilateral contrast venography.and perfusion lung scans within 4 hours of removing the pacing wire. The patients were subdivided,into two subgroups based on their hemodynamic status. There "as no statistical difference between the two groups with respect to mean age or the length of time.the pacer wire was in place and all patients were placed on subclinical heparin therapy. Eleven or 37% iif the patients had venogram evidence of thrombosis with 6 (55%) showing lung scan evidence of The hemodynamically compromised pulmonary emboli. subgroup (7 patients) had 6 (85%) patients with thrombosis with 3 (50%) having subsequent pulmonary emboli. The hemodynamically stable subgroup (23 patients) had a 22% incidence of thrombosis and a 40% incidence of emboli. Deep venous thrombosis with subsequent pulmonary emboli is a serious cpmplication of temporary transvenous pacing using the percutaneous femoral approach, despite prophylactic heparin anticoagulation.
AN ANALYSIS OF MALFUNCTION AND COMPLICATIONS OF TEMPORARY PACING Joseph L. Austin, MD; Lehman K. Preis, MD; Richard S. Crampton, MD, FACC; Randolph P. Martin, MD, University of Virginia, Charlottesville, VA. Temporary pacing is a common treatment for bradyarrhythmias, but few studies have dealt with pacer malfunction (MF) and complications. We reviewed the medical records of 100 consecutive patients (pts) who received 113 temporary pacemakers (PM). MF was defined as failure to capture and/or sense, and occurred in 37% (42/113) of PM. The initial MF occurred within 48 hrs in 86% (36/42) and within 24 hrs in 50% (21/42). The incidence of MF "as 35% (32/91) in femoral catheters and 42% (B/19) in brachial (p=not significant (NS)). In pts witti acute myocardial infarction (AMI), 50% (9/18) of PM developed MF vs 35% (33/95) of PM in pts without AM1 (NS). Thirty-seven complications occurred in 20% (23/113) of PM: ventricular tachycardia during insertion:7, bleeding or hematoma at the site:4, cardiac perforation:4, fever: 7, sepsis:3, phlebitis:6, local infection:3, and pulmonary embolus (PE) :3. No deaths resulted from these complications. In pts with AMI, 28% (5/18) of PM produced complications vs 19% (18/95) of PM in pts without AM1 (NS). While theincidence of total complications, especially perforation, was signigicantly higher in brachial (7/19) vs femoral (16/91) PM (p<.O5), sepsis, local infection, and PE were seen In all pts with sepsis, local infeconly in femoral PM. tion, and PE, and in 5/6 pts with phlebitis, the PM were in place 2 72 hrs (p <.OOOS). We conclude: 1) Since MF is common after pacemaker insertion and tends to occur early, close monitoring is advisable. 2) The incidence of MF does not seem influenced by site of insertion or presence of AMI. 3) Complications are also not infrequent and in pts prone to thromboembolism and/or infection, sites other than femoral should be considered. It may be advisable to terminate temporary pacing by 72 hrs.
THE RHYTHMS UNDERLYING THE FIXED RATE PACING OF LONG-TERM TRANSTGLEPHONE MONITORING Doris J.W.Escher, MD, FACC; Seymour Furman, MD, FACC; John D. Fisher, MD. FACC. Montefiore Hosnital and Medical Center, Bronx, New York
ATRIO-VENTRICULAR NODAL "MEMORY" STUDIED BY RANDOM ATRIAL STIMULATION Frederik M.A. Harms, MD; Robert M. Heethaar, PhD; Etrenne 0. Robles de Medina, MD, FACC; Frits L. Meijler, MD, FACC, University Hospital, Utrecht, the Netherlands.
The natural history (Nhx) of the underlying rhythm (UR) of paced (P) patients (pts) on long term transtelephone monitoring (TTM) is unknown, particularly when always paced on ?TM (apparent pacemaker (PM) dependence), as is the level of risk for syncope (real PM dependence) in event of sudden failure. One hundred consecutive pts (48 male, 52 female; usual age distribution) with WI pulse generators (PG) on TTM were reviewed for Nhx of LJR. Duration of pacing "as 2-122 (av 50) months: duration of TTM the last 1-63 (av 16) months of followup. Forty six pts were 100% P on day of entry to study; 32 of these, always P on TTM, revealed on PM inhibition UR of 3O block (B) 10, atria1 fibrillation (AF)without bradycardia (BA) 5, with BA 5, Sick Sinus Syndrome (SSS) with BA 5* incomplete B5, other 2. Of 36 pts initially P for 3 B, the 28 always P on TTM had UR of 3O B 14, AF 7, intermittent B 5. sinus BA 2. Of 31 pts initially P for SSS, UR broke through intermittently or regularly in 14, 7 were always P. Those pts not P on entry to study ran gamut from original UR of SSS, AF with bradycardia and 3O B to RSR.
To study AV junctional function, ventricular responses were correlated with atria1 intervals during random atria1 stimulation. Methods: Five patients with normal AV conduction -documented by incremental atria1 pacing- were studied during random high right atria1 stimulation (interval range 350 to 700 msec) using a computer controlled stimulator. Right atria1 and His bundle electrograms were used to document the AV nodal transmission characteristics. In all patients random atria1 stimulation "as repeated following I mg atropine i.v. and 20 minutes after 5 mg propranolol i.v. Cross-correlograms were computed between atria1 intervals and AH conduction times, before and after drug administration, Results : I) The first correlation coefficient showed a strong negative correlation (-0.8) between the last atria1 interval preceeding the conducted atria1 complex and AH conduction time. 2) Second and higher order coefficients showed no significant correlation between atria1 intervals and AH conduction times. 3) In spite of observed changes in AV nodal refractoriness similar results "ere obtained after atropine and propranolol administration. Conclusions: 1) Adaptation of AV nodal conduction to random changes in atria1 intervals does not exceed two cycles, suggesting no, or a minimal effect of AV nodal "memory" on AV transmission characteristics. 2) This AV nodal behaviour "as not affected by the autonomic nervous system.
Many pts apparently shift UR post implantation, often, in the short run of brief inhibition, to less serious patterns. TO evaluate the relatively small but siqnificant (10% or less) true risk for syncope in event of recalls, traveling, scheduling of PG changes, etc., pacemaker center visits, with inhibition of pacing to reveal UR must be interpolated with long term TTM. A schedule of Q 6-12 months will provide a good Nhx of the UR.
February 1990
The American Journal of CARDIOLOGY
Volume 45
459
TEMPORARY TRANSVEOUS PACING AND FEMORAL VEIN THROMBOSIS Andre J. Nolewajka, MD; Michele D. Goddard, MD; Thomas C. Brown, MD, Univer3ity of Western Ontario, London, Canada. The true incidence of deep vein thrombosis with subsequent pulmonary embolism in patients requiring temporary transvenous pacing via the femoral vein is unknown. Thirty consecutive patients, mean age 66+ 10 years (38-79) requiring temporary transvenous paczng were studied by bilateral contrast venography.and perfusion lung scans within 4 hours of removing the pacing wire. The patients were subdivided,into two subgroups based on their hemodynamic status. There "as no statistical difference between the two groups with respect to mean age or the length of time.the pacer wire was in place and all patients were placed on subclinical heparin therapy. Eleven or 37% iif the patients had venogram evidence of thrombosis with 6 (55%) showing lung scan evidence of The hemodynamically compromised pulmonary emboli. subgroup (7 patients) had 6 (85%) patients with thrombosis with 3 (50%) having subsequent pulmonary emboli. The hemodynamically stable subgroup (23 patients) had a 22% incidence of thrombosis and a 40% incidence of emboli. Deep venous thrombosis with subsequent pulmonary emboli is a serious cpmplication of temporary transvenous pacing using the percutaneous femoral approach, despite prophylactic heparin anticoagulation.
AN ANALYSIS OF MALFUNCTION AND COMPLICATIONS OF TEMPORARY PACING Joseph L. Austin, MD; Lehman K. Preis, MD; Richard S. Crampton, MD, FACC; Randolph P. Martin, MD, University of Virginia, Charlottesville, VA. Temporary pacing is a common treatment for bradyarrhythmias, but few studies have dealt with pacer malfunction (MF) and complications. We reviewed the medical records of 100 consecutive patients (pts) who received 113 temporary pacemakers (PM). MF was defined as failure to capture and/or sense, and occurred in 37% (42/113) of PM. The initial MF occurred within 48 hrs in 86% (36/42) and within 24 hrs in 50% (21/42). The incidence of MF "as 35% (32/91) in femoral catheters and 42% (B/19) in brachial (p=not significant (NS)). In pts witti acute myocardial infarction (AMI), 50% (9/18) of PM developed MF vs 35% (33/95) of PM in pts without AM1 (NS). Thirty-seven complications occurred in 20% (23/113) of PM: ventricular tachycardia during insertion:7, bleeding or hematoma at the site:4, cardiac perforation:4, fever: 7, sepsis:3, phlebitis:6, local infection:3, and pulmonary embolus (PE) :3. No deaths resulted from these complications. In pts with AMI, 28% (5/18) of PM produced complications vs 19% (18/95) of PM in pts without AM1 (NS). While theincidence of total complications, especially perforation, was signigicantly higher in brachial (7/19) vs femoral (16/91) PM (p<.O5), sepsis, local infection, and PE were seen In all pts with sepsis, local infeconly in femoral PM. tion, and PE, and in 5/6 pts with phlebitis, the PM were in place 2 72 hrs (p <.OOOS). We conclude: 1) Since MF is common after pacemaker insertion and tends to occur early, close monitoring is advisable. 2) The incidence of MF does not seem influenced by site of insertion or presence of AMI. 3) Complications are also not infrequent and in pts prone to thromboembolism and/or infection, sites other than femoral should be considered. It may be advisable to terminate temporary pacing by 72 hrs.
THE RHYTHMS UNDERLYING THE FIXED RATE PACING OF LONG-TERM TRANSTGLEPHONE MONITORING Doris J.W.Escher, MD, FACC; Seymour Furman, MD, FACC; John D. Fisher, MD. FACC. Montefiore Hosnital and Medical Center, Bronx, New York
ATRIO-VENTRICULAR NODAL "MEMORY" STUDIED BY RANDOM ATRIAL STIMULATION Frederik M.A. Harms, MD; Robert M. Heethaar, PhD; Etrenne 0. Robles de Medina, MD, FACC; Frits L. Meijler, MD, FACC, University Hospital, Utrecht, the Netherlands.
The natural history (Nhx) of the underlying rhythm (UR) of paced (P) patients (pts) on long term transtelephone monitoring (TTM) is unknown, particularly when always paced on ?TM (apparent pacemaker (PM) dependence), as is the level of risk for syncope (real PM dependence) in event of sudden failure. One hundred consecutive pts (48 male, 52 female; usual age distribution) with WI pulse generators (PG) on TTM were reviewed for Nhx of LJR. Duration of pacing "as 2-122 (av 50) months: duration of TTM the last 1-63 (av 16) months of followup. Forty six pts were 100% P on day of entry to study; 32 of these, always P on TTM, revealed on PM inhibition UR of 3O block (B) 10, atria1 fibrillation (AF)without bradycardia (BA) 5, with BA 5, Sick Sinus Syndrome (SSS) with BA 5* incomplete B5, other 2. Of 36 pts initially P for 3 B, the 28 always P on TTM had UR of 3O B 14, AF 7, intermittent B 5. sinus BA 2. Of 31 pts initially P for SSS, UR broke through intermittently or regularly in 14, 7 were always P. Those pts not P on entry to study ran gamut from original UR of SSS, AF with bradycardia and 3O B to RSR.
To study AV junctional function, ventricular responses were correlated with atria1 intervals during random atria1 stimulation. Methods: Five patients with normal AV conduction -documented by incremental atria1 pacing- were studied during random high right atria1 stimulation (interval range 350 to 700 msec) using a computer controlled stimulator. Right atria1 and His bundle electrograms were used to document the AV nodal transmission characteristics. In all patients random atria1 stimulation "as repeated following I mg atropine i.v. and 20 minutes after 5 mg propranolol i.v. Cross-correlograms were computed between atria1 intervals and AH conduction times, before and after drug administration, Results : I) The first correlation coefficient showed a strong negative correlation (-0.8) between the last atria1 interval preceeding the conducted atria1 complex and AH conduction time. 2) Second and higher order coefficients showed no significant correlation between atria1 intervals and AH conduction times. 3) In spite of observed changes in AV nodal refractoriness similar results "ere obtained after atropine and propranolol administration. Conclusions: 1) Adaptation of AV nodal conduction to random changes in atria1 intervals does not exceed two cycles, suggesting no, or a minimal effect of AV nodal "memory" on AV transmission characteristics. 2) This AV nodal behaviour "as not affected by the autonomic nervous system.
Many pts apparently shift UR post implantation, often, in the short run of brief inhibition, to less serious patterns. TO evaluate the relatively small but siqnificant (10% or less) true risk for syncope in event of recalls, traveling, scheduling of PG changes, etc., pacemaker center visits, with inhibition of pacing to reveal UR must be interpolated with long term TTM. A schedule of Q 6-12 months will provide a good Nhx of the UR.
February 1990
The American Journal of CARDIOLOGY
Volume 45
459