Case submitted by Chanigan Nilubol, MD, Columbia University, New York, NY, USA
OUR EXPERT: Jennifer MacRae, MSc, MD, FRCPC
Dr MacRae is currently an Assistant Professor of Medicine at the University of Calgary and a nephrologist with the Calgary Health Region. Her clinical and research interests include cardiovascular physiology and vascular access in kidney patients. She is the Medical Director of Hemodialysis and Vascular Access for the Southern Alberta Renal Program.
Full size image(224.7 KB)Case Presentation
A 67-year-old male with end-stage renal failure who has been on three times a week hemodialysis for the past 3 years via a left brachiocephalic AV fistula, was admitted to the hospital for an evaluation for aortic valve replacement for his severe aortic stenosis.
His other medical problems include hypertension, ischemic cardiomyopathy, history of ventricular tachycardia S/P pacemaker/AICD and chronic obstructive lung disease. A Transthoracic echo upon admission showed:
- Markedly dilated left atrium
- Moderately dilated right and left ventricle
- Estimated left ventricular ejection fraction (LVEF) 13%
- Severely thickened aortic valve, mean pressure gradient of 32 mmHg, valve area 0.8 cm2.
His hospital course during the evaluation process for aortic valve intervention was complicated with intradialytic hypotension, bilateral lower extremities cellulitis, low-grade sepsis with DIC.
On hospital day 5, he was transferred to the intensive care unit for continuous renal replacement therapy (CRRT) with vasopressor support. A double-lumen hemodialysis catheter was placed in femoral vein as an access for CRRT.
On hospital day 11 he was considered a poor candidate for aortic valve replacement and underwent an percutaneous aortic valvuloplasty. Post-valvuloplasty echocardiogram showed aortic valve area 1.2 cm2 with mean pressure gradient 31 mmHg and estimated LVEF 35%. Post-procedure, he remained hypotensive needing continuous vasopressin infusion. Ultrafiltration via CRRT was limited due to hypotension. The pt later developed line infection, and a new double lumen catheter was placed on the other femoral vein. Pt became delirious and incoherent, and eteriorated over the 2-wk hospital course.
Physical exam at this point revealed a chronically ill male, BP 90/60 on vasopressin, P 90 beats/min, coarse breathsound bilaterally, regular heart rhythm with loud systolic ejection murmur, bilateral lower extremity erythema and edema. There was a large functioning left braciocephalic AV fistula.
Question to the Expert
Does fistula takedown (and placement of a tunneled dialysis catheter) help hemodynamically in patients with critical aortic outflow obstruction?
the expert replies
Background: AVF hemodynamics
Unfortunately there is a lack of literature surrounding the hemodynamic impact of arteriovenous fistula (AVF) in chronic kidney disease (CKD) patients without cardiac disease let alone those patients with cardiac structural abnormalities like valvular heart disease. However, we can draw upon several physiology studies to extrapolate the possible impact that [1]AVF may have in a patient with critical aortic stenosis (AS). Guyton and Sagawa [2] demonstrated the short term influence of AVF on cardiac hemodynamics by creating small and large AVF in a dog model. They found that AVF creation increases the cardiac output (CO) immediately, decreases the total peripheral resistance (TPR) and subsequently drops the systemic arterial pressure. The heart achieves the increased CO with an increase in heart rate (HR), contractility and stroke volume. Studies in CKD patients ([3, 4] are consistent with the above and have also demonstrated that AVF creation increases the CO. The increase in CO is modulated by several mechanisms including: increased sympathetic activity (resulting in increased HR and contractility) and neurohormal changes (such as increased ANP and BNP and decreased renin) that produce a reduction in TPR and increased blood volume. Thus, clearly AVF are associated with changes in cardiac hemodynamics even in patients with normal cardiac function. What these studies do not demonstrate is the long term impact of these changes on cardiac structure and function and it has been postulated that over time the LV and LA dilate in response to AVF creation. Left ventricular end diastolic dimension (LVEDD) reduction and LV hypertrophy (LVH) regression have been demonstrated with AVF ligation in post renal transplant patients[5-7]; providing indirect evidence of AVF contribution to LVH[8]. Unfortunately there are no published studies looking at prospective changes in LVH or LVEDD in patients with AVF.
Aortic Stenosis Hemodynamics
One may speculate that a patient with baseline severe aortic stenosis and an AVF probably has a more rapid time course of the development of subsequent LVH. With aortic stenosis there is a large pressure gradient between the LV and aorta: the LV is pressure increased, the LV wall stress is increased and the LV hypertrophies over time. This results in increased LV stiffness and decreased compliance which leads to diastolic impairment and increased LVEDP. Diastolic filling of the LV becomes very dependent on the atrial component and anything that impairs atrial contraction (such as atrial fibrillation) results in increased LVEDP and reduced CO which may precipitate heart failure.[9] In AS patients the CO is normal initially but later on as the stenosis progresses the CO may remain normal at rest but cannot accommodate the increased demand with exercise. As heart failure develops there is a further reduction in the resting CO and an increase in heart rate. The myocardial oxygen demands are increased with severe AS due to the LVH, increased LVEDP and increased afterload. Blood flow to the subendocardium may be inadequate at rest and the coronary blood flow is reduced.
Impact of AVF on Aortic Stenosis and Progression of Heart Failure
The presence of an AVF contributes to additional output requirements for the heart. In the presence of AS the load is additive which creates excessive demands on the heart. AVF increase myocardial oxygen demands[10] and decrease subendocardial perfusion which adds to the reduction in coronary blood flow that occurs with AS. Therefore, considering the impact of AVF and the effect of severe aortic stenosis, ligation of the AVF in this case should improve the hemodynamics. In practice, when AVF are ligated, the hemodynamics improve and the heart failure resolves.
A Few Words on Size of AVF Flow
The degree to which an AVF impacts the hemodynamics is unknown but probably related to the size of the blood flow through the fistula, Qa. A high flow AVF (> 2 000 ml/min ) in the presence of underlying cardiac disease likely contributes to heart failure [8, 11] and probably accelerates the time course at which this occurs. Knowledge of the access flow in this case would be helpful in predicting the degree of improvement post ligation.
References:
- Young P, Rohr M, Marterre W: High output cardiac failure secondary to a brachiocephalic arteriovenous hemodialysis fistula: two cases. The American Surgeon 64:239-241, 1998.
- Guyton A, Sagawa K: Compensations of cardiac output and other circulatory functions in areflex dogs with large AV fistulas. Am J Physiol 200:1157-1163, 1961.
- Iwashima Y, Horio T, Takami Y, et al.: Effects of the creation of arteriovenous fistula for hemodialysis on cardiac function and natriuretic peptide levels in CRF. American Journal of Kidney Diseases 40:974-982, 2002.
- Ori Y, Korzets A, Katz M, et al.: Hemodialysis arteriovenous access: a prospective hemodynamic evaluation. Nephrol Dial Transplant 1:94-97, 1996.
- Unger P, Velez-Roa S, Wissing K, et al.: Regression of left ventricular hypertrophy after arteriovenous fistula closure in renal transplant recipients: A long term follow-up. American Journal of Transplantation 4:2038-2044, 2004.
- Unger P, Wissing K, de Pauw L, et al.: Reduction of left ventricular diameter and mass after surgical arteriovenous fistula closure in renal transplant recipients. Transplantation 74:73-79, 2002.
- van Duijnhoven EC, Cheriex EC, Tordoir JH, et al.: Effect of closure of the arteriovenous fistula on left ventricular dimensions in renal transplant patients. Nephrol Dial Transplant 16:368-372, 2001.
- MacRae J, Levin A, Belenkie I: The cardiovascular effects of arteriovenous fistula in chronic kidney disease: A cause for concern? Seminars in Dialysis 19:349-352, 2006.
- Rahimtoola S: Chapter 63 Aortic Valve Disease. Hurst's The Heart:1759-1765, 1998.
- Savage M, Ferro C, Sassano A, et al.: The impact of arteriovenous fistula formation on central hemodynamic pressures in chronic renal failure patients: a prospective study. American Journal of Kidney Diseases 40:753-759, 2002.
- MacRae J: Vascular access and cardiac disease: Is there a relationship? Current Opinions in Nephrology and Hypertension 15:577-582, 2006
FOLLOW UP PROVIDE BY DR. NILUBOL
The patient underwent ligation of his L brachial fistula.
His systolic blood pressure immediately increased by 20mmHg, and was able to come of pitressin. He resumed hemodialysis two days later.
His further hospital course was unfortunately complicated by line sepsis two months later, which necessitated ICU admisssion with resumption of pressors and CRRT.
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