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Failure of subclavian venepuncture: the internal jugular vein as a useful alternative
International Journal of Cardiology, 35 (1992) 275-278 0 1992 Elsevier Science Publishers B.V. All rights reserved
CARD10
275 0167-5273/92/$05.00
14317
Failure of subclavian venepuncture: the internal jugular vein as a useful alternative S.A.M. Said a, J.J.J. Bucx a and C.M. Stassen
b
Departments of n Cardiology and b Radiodiagnostics, Streekziekenhub Midden-Twente, Hengelo, Netherlands (Received
13 September
1991; revision
accepted
7 November
1991)
After several attempts, temporary and permanent pacing for post-infarction symptomatic tachybradyarrhythmias, was finally achieved via the left internal jugular vein. Failure of bilateral subclavian venepuncture was experienced by two different operators. Partial right-sided pneumothorax developed following several attempts of subclavian puncture, and it resolved spontaneously. Upper extremity contrast venography revealed signs compatible with antecedent thrombotic disease of unknown etiology. Antiarrhythmic drug therapy was safely and successfully instituted. Key words: Failure of subclavian venepuncture; tion of subclavian venepuncture
Temporary and permanent
Introduction
The subclavian vein is the most commonly used portal for implantation of pacemaker lead. It is expeditious both for single- and dual-chamber pacing and, in general, the method is safe. The subclavian venous approach has achieved great popularity as central access, but the internal jugular approach has also become popular since complications, such as pneumothorax, may be less [l]. Failure of subclavian venepuncture and the rate of complications, however, has been attributed to the experience of the operator [2], may be secondary to healed clavicular fracture, or may occur when the patient is severely hypovolemic or vasospastic. We report here a case in whom puncture of both subclavian veins was unsuccessful, due to previous bilateral silent thrombotic lesions strongly suggested by upper extremity contrast venography. Recognition of this possible cause of failure may help others to avoid the delay and
Correspondence to: S.A.M. Said M.D., Department of Cardiology, Streekziekenhuis Midden-Twente, Geerdinksweg 141, 7555 DL Hengelo Ov, Netherlands.
complications pacing. Case
pacing; Internal jugular vein; Complica-
we experienced
in achieving permanent
Report
A 71-year-old man was admitted to the Coronary Care Unit suffering from a one-day-old inferopostero-lateral myocardial infarction. He received conventional treatment regimen. Two days after admission, he developed atria1 fibrillation/ flutter with rapid ventricular response, necessitating therapy with sotalol 80 mg twice a day, which resulted in ventricular standstill of 7 seconds. On physical examination, he was acutely ill, the blood pressure was 130/70 mmHg, the pulse was regular at 90 beats/min. The jugular venous pressure was not elevated. He had an immobile facial expression, rigid musculature and tremor of both hands. The heart was clinically not enlarged and the auscultatory findings were normal. His antecedent medical history included endogenous depression, Parkinson’s disease and transurethral prostate resection. The admission electrocardiogram showed sinus rhythm with Q waves in the inferior leads, prominent R wave in V2 and ST-segment elevation in M-6. The laboratory
276
Fig. 1. Contrast venography demonstrating thrombotic occlusion with recanalization and collateral formation (0 (arrow, Fig. a) and hazy aspect of the left subclavian veins ( * , Fig. b). le = lead; cl = clavicle; pg = pulse generator.
elevation of the cardiac enzymes. Successful access via the left jugular vein was achieved for temporary pacing after failure of the left subclavian venous route. Three weeks after the date of the infarction, permanent pacing was attempted due to second-degree atrioventricular block Mobitz type II. The procedure was unsuccessful due to failure of puncture of the right subclavian vein. After this procedure the chest X-ray revealed a small right-sided pneumothorax which spontaneously resolved. One week later, puncture of the left subclavian vein was also unsuccessful. The left internal jugular vein was then punctured and a permanent lead was inserted and positioned in the right ventricular apex. Permanent pacing was then established. The further clinical course was uneventful and the patient was discharged in a good clinical condition. Venography of the subclavian veins showed an intraluminal filling defect with data showed
of the right
recanalization and collateral formations of the right and hazy appearance of the left subclavian veins (Fig. 11. Discussion
In this case, temporary and permanent pacing was indicated due to development of tachybradyarrhythmias following myocardial infarction. Several attempts at subclavian venous puncture were unsuccessful. Ultimately, both temporary and permanent pacing were achieved using the internal jugular venous approach. Reasons for failure of subclavian venous puncture include inexperience of the operator [2], vascular abnormalities, chest deformity and old thrombotic occlusions [3]. Although “percutaneous subclavian vein catheterization provides a golden route for support of patients”, many complications have been reported. They include
Fig. 1. (continued).
inadvertent arterial puncture, hemothorax, hydrothorax, hemomediastinum, brachial plexus and phrenic nerve injury, hematoma formation and pneumothorax
El. The jugular venous access carries a small risk of pneumo- or hemothorax. Other causes of failure of subclavian venepuncture may include subclavian ve-
nous thrombosis secondary to toxic and harmful effects of drugs or indwelling catheters [3], “effort” thrombosis, thoracic outlet syndrome, previous surgery, trauma and malignancy. Subclavian venography is recommended when failure of venepuncture occurs in an attempt to clarify the cause.
278 Acknowledgements
We are greatly indebted to Mr. E. Bartelink, Mr. F.T. Zwienenberg and Mrs. H.E. Blijdenstein for their assistance. References 1 Martin C, Auffray JP, Saux P, Albanese J, Gouin F. The axillary vein: an alternative approach for percutaneous pulmonary artery catheterization. Chest 1986;90:694-697.
2 Lockwood AH. Percutaneous subclavian vein catheterization. Too much of a good thing? Arch Intern Med 1984; 144:1407-1408. 3 Surratt RS, Picus D, Hicks ME, Darcy MD, Kleinhoffer M, Jendrisak M. The importance of preoperative evaluation of the subclavian vein in dialysis access planning. Am J Radio1 1991;156:623-625. 4 Linos DA, Mucha P Jr, Van Heerden JA. Subclavian vein: a golden route. Mayo Clin Proc 1980;55:315-321. 5 Herbst CA Jr. Indications, management, and complications of percutaneous subclavian vein catheters: an audit. Arch
Surg 1987;113:1421-1425.
International Journal of Cardiology, 35 (1992) 278-280 0 1992 Elsevier Science Publishers B.V. All rights reserved 0167-5273/92/$05.00
CARD10 14318
Antiadrenergic
cardiovascular adverse effects of high-dose amiodarone loading regimen
Giinter Steurer, Herwig Schmidinger and Bernhard Frey Departments of Cardiology and Pharmacology, University of Henna, Austria
(Received 11 October 1991; revision accepted 7 November 1991)
A 55year-old patient with inferior wall infarction was treated effectively for ventricular tachycardia with high-dose oral amiodarone loading regimen (5 g within 16 hours). Serial pharmacokinetic studies demonstrated a rapid temporary increase in amiodarone plasma concentration to a maximum of 3.40 pg/ml 17 hours after initiation of therapy followed by a return to normal plasma concentration within 8 hours. During fast drug evasion the patient developed acute low-output syndrome with syncope successfully controlled with intravenous catecholamine administration. Our findings suggest that the cardiovascular collapse was caused by the non-competitive adrenoceptor antagonism of amiodarone resulting in secondary autonomic insufficiency. Key words: Amiodarone;
Loading regimen; Antiadrenergic
Introduction
Amiodarone is a highly lipid-soluble class III antiarrhythmic agent with unique pharmacokinetic properCorrespondence to: G. Steurer, c/o Prof. Pedro Brugada, Cardiovascular Center, OLV Hospital, Moorselbaan 164, B-9300 Aalst, Belgium. This study was supported by the Fonds zur Fiirderung der wissenschaftlichen Forschung WWF), Erwin Schrodinger Auslandsstipendium Nr. J0544-MED.
cardiovascular
adverse effect
ties. Arniodarone is absorbed slowly, the bioavailability ranges from 30 to 60% with marked interpatient variability. Plasma elimination is triphasic with a distribution rate of 4 hours, a peripheral compartment with a steady state reached in days and a deep compartment, where steady state is reached in months [l]. These unfavorable pharmacokinetic properties cause a delayed onset of drug action. Therefore, loading regimens designed to achieve antiarrhythmic drug efficacy in a short period of time have gained clinical importance [2].
CARD10
275 0167-5273/92/$05.00
14317
Failure of subclavian venepuncture: the internal jugular vein as a useful alternative S.A.M. Said a, J.J.J. Bucx a and C.M. Stassen
b
Departments of n Cardiology and b Radiodiagnostics, Streekziekenhub Midden-Twente, Hengelo, Netherlands (Received
13 September
1991; revision
accepted
7 November
1991)
After several attempts, temporary and permanent pacing for post-infarction symptomatic tachybradyarrhythmias, was finally achieved via the left internal jugular vein. Failure of bilateral subclavian venepuncture was experienced by two different operators. Partial right-sided pneumothorax developed following several attempts of subclavian puncture, and it resolved spontaneously. Upper extremity contrast venography revealed signs compatible with antecedent thrombotic disease of unknown etiology. Antiarrhythmic drug therapy was safely and successfully instituted. Key words: Failure of subclavian venepuncture; tion of subclavian venepuncture
Temporary and permanent
Introduction
The subclavian vein is the most commonly used portal for implantation of pacemaker lead. It is expeditious both for single- and dual-chamber pacing and, in general, the method is safe. The subclavian venous approach has achieved great popularity as central access, but the internal jugular approach has also become popular since complications, such as pneumothorax, may be less [l]. Failure of subclavian venepuncture and the rate of complications, however, has been attributed to the experience of the operator [2], may be secondary to healed clavicular fracture, or may occur when the patient is severely hypovolemic or vasospastic. We report here a case in whom puncture of both subclavian veins was unsuccessful, due to previous bilateral silent thrombotic lesions strongly suggested by upper extremity contrast venography. Recognition of this possible cause of failure may help others to avoid the delay and
Correspondence to: S.A.M. Said M.D., Department of Cardiology, Streekziekenhuis Midden-Twente, Geerdinksweg 141, 7555 DL Hengelo Ov, Netherlands.
complications pacing. Case
pacing; Internal jugular vein; Complica-
we experienced
in achieving permanent
Report
A 71-year-old man was admitted to the Coronary Care Unit suffering from a one-day-old inferopostero-lateral myocardial infarction. He received conventional treatment regimen. Two days after admission, he developed atria1 fibrillation/ flutter with rapid ventricular response, necessitating therapy with sotalol 80 mg twice a day, which resulted in ventricular standstill of 7 seconds. On physical examination, he was acutely ill, the blood pressure was 130/70 mmHg, the pulse was regular at 90 beats/min. The jugular venous pressure was not elevated. He had an immobile facial expression, rigid musculature and tremor of both hands. The heart was clinically not enlarged and the auscultatory findings were normal. His antecedent medical history included endogenous depression, Parkinson’s disease and transurethral prostate resection. The admission electrocardiogram showed sinus rhythm with Q waves in the inferior leads, prominent R wave in V2 and ST-segment elevation in M-6. The laboratory
276
Fig. 1. Contrast venography demonstrating thrombotic occlusion with recanalization and collateral formation (0 (arrow, Fig. a) and hazy aspect of the left subclavian veins ( * , Fig. b). le = lead; cl = clavicle; pg = pulse generator.
elevation of the cardiac enzymes. Successful access via the left jugular vein was achieved for temporary pacing after failure of the left subclavian venous route. Three weeks after the date of the infarction, permanent pacing was attempted due to second-degree atrioventricular block Mobitz type II. The procedure was unsuccessful due to failure of puncture of the right subclavian vein. After this procedure the chest X-ray revealed a small right-sided pneumothorax which spontaneously resolved. One week later, puncture of the left subclavian vein was also unsuccessful. The left internal jugular vein was then punctured and a permanent lead was inserted and positioned in the right ventricular apex. Permanent pacing was then established. The further clinical course was uneventful and the patient was discharged in a good clinical condition. Venography of the subclavian veins showed an intraluminal filling defect with data showed
of the right
recanalization and collateral formations of the right and hazy appearance of the left subclavian veins (Fig. 11. Discussion
In this case, temporary and permanent pacing was indicated due to development of tachybradyarrhythmias following myocardial infarction. Several attempts at subclavian venous puncture were unsuccessful. Ultimately, both temporary and permanent pacing were achieved using the internal jugular venous approach. Reasons for failure of subclavian venous puncture include inexperience of the operator [2], vascular abnormalities, chest deformity and old thrombotic occlusions [3]. Although “percutaneous subclavian vein catheterization provides a golden route for support of patients”, many complications have been reported. They include
Fig. 1. (continued).
inadvertent arterial puncture, hemothorax, hydrothorax, hemomediastinum, brachial plexus and phrenic nerve injury, hematoma formation and pneumothorax
El. The jugular venous access carries a small risk of pneumo- or hemothorax. Other causes of failure of subclavian venepuncture may include subclavian ve-
nous thrombosis secondary to toxic and harmful effects of drugs or indwelling catheters [3], “effort” thrombosis, thoracic outlet syndrome, previous surgery, trauma and malignancy. Subclavian venography is recommended when failure of venepuncture occurs in an attempt to clarify the cause.
278 Acknowledgements
We are greatly indebted to Mr. E. Bartelink, Mr. F.T. Zwienenberg and Mrs. H.E. Blijdenstein for their assistance. References 1 Martin C, Auffray JP, Saux P, Albanese J, Gouin F. The axillary vein: an alternative approach for percutaneous pulmonary artery catheterization. Chest 1986;90:694-697.
2 Lockwood AH. Percutaneous subclavian vein catheterization. Too much of a good thing? Arch Intern Med 1984; 144:1407-1408. 3 Surratt RS, Picus D, Hicks ME, Darcy MD, Kleinhoffer M, Jendrisak M. The importance of preoperative evaluation of the subclavian vein in dialysis access planning. Am J Radio1 1991;156:623-625. 4 Linos DA, Mucha P Jr, Van Heerden JA. Subclavian vein: a golden route. Mayo Clin Proc 1980;55:315-321. 5 Herbst CA Jr. Indications, management, and complications of percutaneous subclavian vein catheters: an audit. Arch
Surg 1987;113:1421-1425.
International Journal of Cardiology, 35 (1992) 278-280 0 1992 Elsevier Science Publishers B.V. All rights reserved 0167-5273/92/$05.00
CARD10 14318
Antiadrenergic
cardiovascular adverse effects of high-dose amiodarone loading regimen
Giinter Steurer, Herwig Schmidinger and Bernhard Frey Departments of Cardiology and Pharmacology, University of Henna, Austria
(Received 11 October 1991; revision accepted 7 November 1991)
A 55year-old patient with inferior wall infarction was treated effectively for ventricular tachycardia with high-dose oral amiodarone loading regimen (5 g within 16 hours). Serial pharmacokinetic studies demonstrated a rapid temporary increase in amiodarone plasma concentration to a maximum of 3.40 pg/ml 17 hours after initiation of therapy followed by a return to normal plasma concentration within 8 hours. During fast drug evasion the patient developed acute low-output syndrome with syncope successfully controlled with intravenous catecholamine administration. Our findings suggest that the cardiovascular collapse was caused by the non-competitive adrenoceptor antagonism of amiodarone resulting in secondary autonomic insufficiency. Key words: Amiodarone;
Loading regimen; Antiadrenergic
Introduction
Amiodarone is a highly lipid-soluble class III antiarrhythmic agent with unique pharmacokinetic properCorrespondence to: G. Steurer, c/o Prof. Pedro Brugada, Cardiovascular Center, OLV Hospital, Moorselbaan 164, B-9300 Aalst, Belgium. This study was supported by the Fonds zur Fiirderung der wissenschaftlichen Forschung WWF), Erwin Schrodinger Auslandsstipendium Nr. J0544-MED.
cardiovascular
adverse effect
ties. Arniodarone is absorbed slowly, the bioavailability ranges from 30 to 60% with marked interpatient variability. Plasma elimination is triphasic with a distribution rate of 4 hours, a peripheral compartment with a steady state reached in days and a deep compartment, where steady state is reached in months [l]. These unfavorable pharmacokinetic properties cause a delayed onset of drug action. Therefore, loading regimens designed to achieve antiarrhythmic drug efficacy in a short period of time have gained clinical importance [2].