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Acute Systemic Hypotension After Arteriovenous Fistula Construction In Clin Exp Nephrol (2011) 15:788–790 DOI 10.1007/s10157-011-0484-3 CASE REPORT Acute systemic hypotension after arteriovenous fistula construction in a patient with severe aortic stenosis Naobumi Mise • Lisa Uchida • Mototsugu Tanaka • Shinji Tanaka • Hiroyoshi Nakajima • Tokuichiro Sugimoto Received: 7 January 2011 / Accepted: 13 June 2011 / Published online: 2 July 2011 Ó Japanese Society of Nephrology 2011 Abstract We report the case of a 53-year-old hemodial- Introduction ysis patient with severe aortic stenosis, who developed acute systemic hypoperfusion after arteriovenous fistula An arteriovenous fistula (AVF) may impose a cardiac (AVF) construction. He presented with hypotension and burden, and occasionally causes heart failure (HF) [1]. repeated syncope soon after distal radiocephalic AVF High-output HF is a well-known AVF-associated disorder, construction, and finally developed a respiratory arrest. His and may be suspected when an AVF flow is excessive, blood pressure and hemodynamics recovered promptly by usually [3 L/min or 30% of cardiac output (CO) [1]. sub-emergent aortic valve replacement surgery. In the However, when a patient’s cardiac function is extremely present case, the heart with severe aortic stenosis could not low, HF may develop even with a moderate AVF flow increase cardiac output in response to the reduction in [1, 2]. peripheral vascular resistance caused by the AVF. High- We report on a patient with severe aortic stenosis who output heart failure, a relatively rare AVF-associated dis- developed acute systemic hypoperfusion after distal radi- order, occurs with an excessive AVF flow, usually more ocephalic AVF construction and recovered after aortic than 3 L/min or 30% of cardiac output. However, heart valve replacement (AVR) surgery. failure may develop soon after construction of an AVF with a moderate blood flow if a patient’s cardiac function is severely impaired. In addition, heart failure may improve Case report with AVF preservation if the underlying heart disease is treatable. In December 1997, a 53-year-old man with 5 year history of hemodialysis due to chronic glomerulonephritis was Keywords Aortic stenosis Á Aortic valve replacement Á referred to our cardiovascular surgery department due to Arteriovenous fistula Á Hemodialysis Á severe aortic stenosis. He had presented symptomatic HF High-output heart failure for 1 month and surgical intervention was indicated. On admission, an echocardiography after a hemodialysis ses- sion demonstrated a markedly elevated pressure gradient of 110 mmHg between the aorta and the left ventricle, severe left ventricular hypertrophy and decreased left ventricular N. Mise (&) Á L. Uchida Á M. Tanaka Á S. Tanaka Á ejection fraction (LVEF) of 25%. Detailed echocardio- T. Sugimoto graphic data were as follows: aortic valve area 0.8 cm2, left Division of Nephrology, Department of Medicine, Mitsui Memorial Hospital, 1 Kanda-izumi-cho, ventricular diastolic diameter (LVDD) 43 mm, diastolic Chiyoda-ku, Tokyo 101-8643, Japan posterior wall thickness (PWT) 18 mm, interventricular e-mail: [email protected] septum thickness (IVS) 18 mm, and E/A ratio 0.51. Serum hemoglobin concentration was 8.3 g/dl and intact para- H. Nakajima Division of Cardiology, Department of Medicine, thyroid hormone was 218 pg/ml. His left snuff box AVF Mitsui Memorial Hospital, Tokyo, Japan was obstructed at the anastomotic site. 123 Clin Exp Nephrol (2011) 15:788–790 789 AVF flow did not exceed 1.0 L/min. In the present case, the AVF flow was not excessive according to physical examination. High-output HF was thought to be relevant only with an AVF of long duration [6]; however, it has been shown that AVFs can reach their maximum flow as early as 6 weeks [7] and AVF construction has immediate cardiac effects [8]. Thus, this disorder can occur sooner than initially thought [6]. In the present case, the heart with severe aortic stenosis could not increase CO in accordance with the reduction in peripheral vascular pressure caused by the AVF. An AVF reduces peripheral vascular resistance because blood flows preferentially through the vessel of least resistance, namely the AVF [9], and, in our case, total peripheral resistance Fig. 1 Change in predialysis systolic blood pressure. After the decreased after AVF creation [10]. In normal subjects, arteriovenous fistula (AVF) creation, systolic blood pressure dropped systemic resistance falls with creation of an AVF, but CO and continuous intravenous administration of norepinephrine was required during hemodialysis (HD) sessions. The patient finally increases and maintains necessary blood flow for essential developed a cardiac arrest. After aortic valve replacement (AVR) organs [3]. However, in the present case, the increase in surgery, his blood pressure rose significantly. The AVF was preserved CO after the AVF construction might have been insuffi- cient because of marked aortic stenosis and therefore the Two days later, a radiocephalic AVF was reconstructed patient developed systemic severe hypotension and cere- at a proximal site near his left wrist, because the patient’s bral hypoperfusion. This disorder may be considered as HF was well controlled and his hemodynamics were tem- low-output HF, rather than congestive HF. Once his aortic porally stable. Soon after AVF creation, his systolic blood stenosis was resolved by an AVR, his blood pressure rose pressure dropped from 140 to 100 mmHg, although he was dramatically and he never demonstrated symptoms of HF asymptomatic (Fig. 1). During hemodialysis sessions on again. successive days, a continuous intravenous infusion of a In patients with impaired cardiac function, AVF con- noradrenergic agent was needed to maintain blood pres- struction may worsen HF. MacRae et al. [6] suggested that sure. In the ward, he developed syncope 3 times. The third certain patients with intrinsic cardiac diseases may be more syncopal episode culminated in a respiratory arrest, and susceptible to developing high-output HF. However, mechanical ventilation was started. Thus, 3 days later he aggravation of HF by AVF may be overlooked because HF underwent a sub-emergent AVR using a 23-mm mechani- is very common in dialysis patients and they have multiple cal valve. The native aortic valve was a congenital bicuspid risk factors for HF, including anemia, volume overload, or valve and showed marked calcification. His blood pressure pre-existing cardiac disease [11]. In the present case, rose promptly after AVR, and intravenous infusion of ni- occlusion of the pre-existing AVF suggested severe low cardipine was needed to control the blood pressure in the CO and peripheral circulatory failure, although HF was postoperative period. On the 12th postoperative day, an temporally controlled and the heart rate increase after the echocardiograph after a hemodialysis session showed that AVF construction was 4/min, which did not seem to be the LVEF had recovered to 61%. Detailed echocardio- excessive. The postponement of AVF construction should graphic data were as follows: LVDD 47 mm, diastolic have been considered until an AVR was performed. In such PWT 11 mm, and IVS 12 mm. The newly constructed cases, dialysis access which does not create a new arte- wrist AVF was preserved. riovenous shunt flow might be preferable, such as a per- manent catheter or arterial superficialization [3], although an AVF should be considered the vascular access of choice Discussion for most stable dialysis patients. HF caused by excessive AVF flow may be cured by High-output HF typically occurs when a large proportion of treatment of pre-existing cardiac diseases. Reduction of CO flows through the AV access [3] and is considered a AVF flow with closure or banding is usually considered in rare entity [2]; however, this disorder may occur even with such circumstances [2]. Closure of the AVF resulted in a normal access flows if cardiac function is poor [2], prob- significant reduction in the LVDD and left ventricular ably because access flow becomes relatively excessive to mass. In our case, however, the AVR dramatically the impaired CO. It was reported that HF improved by improved HF with AVF preservation. This result suggests closure [4], banding, or revision of AVF [5], even when that HF improvement might be expected with AVF 123 790 Clin Exp Nephrol (2011) 15:788–790 preservation if the cardiac disease is treatable. In previous 5. Ahearn DJ, Maher JF. Heart failure as a complication of he- reports, improvement in LVEF was reported after AVR modialysis arteriovenous fistula. Ann Intern Med. 1972;77:201–4. [12, 13]. 6. MacRae JM, Pandeya S, Humen DP, Krivitski N, Lindsay RM. In summary, we experienced a patient with severe aortic Arteriovenous fistula-associated high-output cardiac failure: a stenosis, who developed acute systemic hypoperfusion due review of mechanisms. Am J Kidney Dis. 2004;43:e17–22. to AVF construction. An AVR improved the hemody- 7. Begin V, Ethier J, Dumont M, Leblanc M. Prospective evaluation of the intra access flow of recently created native arteriovenous namics promptly and the patient recovered without any fistulae. Am J Kidney Dis. 2002;40:1277–82. sequelae. Excessive cardiac burden due to AVF must be 8. Guyton AC, Sagawa K. Compensations of cardiac output and considered in patients with severely impaired cardiac other circulatory functions in areflex dogs with large AV fistulas. function. Am J Physiol. 1961;200:1157–63. 9. Japanese Society for Dialysis Therapy, Scientific Committee. Guidelines for the construction and repair of vascular access. J Jpn Soc Dial Ther. 2005;38:1491–551 (in Japanese). 10. Korsheed S, Eldehni MT, John SG, Fluck RJ, Mclntyre CW. References Effects of arteriovenous fistula formation on arterial stiffness and cardiovascular performance and function. Nephrol Dial Trans- 1. K/DOQI clinical practice guidelines for cardiovascular disease in plant. 2011. doi:10.1093/ndt/gfq851. dialysis patients. Am J Kidney Dis. 2005;45:S1–153. 11. Engelberts I, Tordoir JH, Boon ES, Schreij G.
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