Percutaneous Creation of Arteriovenous Shunts
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Abstract
Reductions in systemic vascular resistance and increased cardiac output are thought to help maintain tissue oxygen delivery during hypoxia. Here we discuss the rationale for creating arteriovenous (AV) shunts in humans and we describe novel techniques for percutaneous creation of AV shunts in patients. Although large AV shunts have been associated with cardiac failure, we believe that the creation of a moderate arteriovenous fistula (AVF) might benefit selected patients with respiratory disease. Here we study the acute effects of an AVF on mixed venous oxygen content and arterial oxygenation during hypoxia in pigs. Closure of the AVF resulted in a 15% reduction in cardiac output (p < 0.01), associated with a 10% reduction in arterial oxygen saturation (p < 0.05), and a 20% reduction in mixed venous oxygen saturation (p < 0.01). We conclude that creation of an AVF improves oxygen delivery during hypoxia and might benefit patients with respiratory disease.
Introduction
In the 1960s, Holman and colleagues at Stanford described a series of experiments revealing that small-to-moderate fistulae with rigid borders typically remain stationary in size without a deleterious effect on hemodynamics.1,2 In contrast, fistulae with a distensible rim progressively dilate, leading ultimately to cardiac dilatation and, in some cases, cardiac failure.3 Generally, except for vascular access in dialysis patients, the presence of an arteriovenous (AV) shunt promotes discussion about the merits and risks of surgical closure. Recently, we have explored the concept that the creation of a moderate-sized AV shunt might benefit selected patients with cardiac and respiratory disease. In this paper we will first explain the rationale behind the therapeutic potential of AV shunts; then, we will describe novel techniques for the percutaneous creation of AV shunts; and finally, we hope to balance the benefits against possible risks associated with AV shunts.
The rationale for creating AV shunts to improve exercise capacity. Since exercise performance is related to cardiac output, our rationale for creating AV shunts to improve exercise capacity is based on a triad of physiology principles. (Q is cardiac output, P is the mean arterial pressure minus the central venous pressure, SVR is systemic vascular resistance, HR is heart rate, SV is stroke volume, VO2 is oxygen consumption, CaO2 is the oxygen content of arterial blood, and CvO2 is the oxygen content of mixed venous blood).
Equation 1:
Q liters per minute-1 = dP Pascals / SVR Dynes.
Equation 2:
Q liters. minute-1 = HR beats per minute -1 x SV liters. beat -1.
Equation 3:
Q liters. minute -1 = VO2 grams per minute-1 / CaO2 – CvO2 (grams. liter -1).
In engineering terms, an AV fistula is a low-resistance circuit allowing flow from a high-pressure arterial system to a low-pressure venous system, thus bypassing the higher resistance capillary beds. Creation of an AV shunt lowers systemic vascular resistance (and to a lesser extent arterial diastolic blood pressure), resulting in an increased cardiac output (Equation 1). A chronic increase in cardiac output increases stroke volume, thus allowing an amplified cardiac output response to changes in heart rate (Equation 2). An amplified cardiac output response to exercise-induced tachycardia allows for greater oxygen delivery and consumption, which is essential for exercising muscles (Equation 3). Maximal cardiac output is closely related to maximal oxygen consumption, which in turn is related to maximum exercise capacity.
In a hypothetical example, a 40-year-old, 70 kg, man has a resting heart rate of 70 beats per minute (bpm)-1 and a stroke volume of 70 ml, and a cardiac output of 4.9 liters per min (lpm).-1 During maximal exercise his heart rate increases to a maximum of 180 bpm-1 (220 minus age bpm-1), and his cardiac output increases to approximately 12.6 lpm-1 After the creation of an AV fistula, his resting heart rate remains approximately 70 bpm.-1 His stroke volume will have increased to 85 ml, so that his resting cardiac output will be 5.95 lpm-1 (approximately 1 lpm-1 will flow through the AV shunt, so that the effective cardiac output to the body at rest will remain at approximately 4.9 lpm;-1 and the pulmonary blood flow will effectively increase by approximately 1 lpm-1). However, during maximal exercise when his heart rate increases to 180 bpm,-1 his cardiac output will be 15.3 lpm.-1 Since approximately 1 lpm-1 will still flow through the AV shunt, the effective cardiac output to the body would be 14.3 lpm-1: an increase of 1.7 lpm-1 over the maximum of 12.6 lpm-1 before the creation of the AV shunt. This will allow for an increased oxygen consumption of 250 ml per min-1 (since the ratio of change in cardiac output to change in oxygen consumption is generally about 6:1). The normal cardiovascular response to hypoventilation is to increase cardiac output and reduce systemic vascular resistance — related in part to the effects of hypoxemia and hypercarbia on the autonomic nervous system.4 The net result is to increase cardiac output and hence tissue oxygen delivery to compensate for the hypoventilation. We believe that a moderate AV fistula might replicate or even amplify this response and thus benefit patients with respiratory disease. Interestingly, the increase in cardiac output in these circumstances does not lead to a measurable increase in cardiac oxygen consumption because the workload of the contracting heart is reduced because of a drop in afterload.5 A controlled afterload reduction (approximately 10 mmHg reduction in diastolic pressure) could theoretically increase cardiac power output, another index that is related to exercise capacity.
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