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Vascular Laboratory: Arterial Physiologic Assessment
Arterial physiologic testing adds a degree of objectivity to the subjective clinical evaluation of peripheral arterial disease (PAD). The advances in direct physiologic testing of specific arterial sites by duplex scanning and noninvasive imaging evaluation provide the approximate localization of extent of disease and therefore indirect physiologic testing is now less critical (see Chapter 22 , Vascular Laboratory: Arterial Duplex Scanning). However, physiologic testing is helpful when the diagnosis is uncertain, such as in patients with possible neurogenic claudication. These tests are also useful in determining the extent to which arterial disease limits walking in patients who have concomitant orthopedic or neurologic problems contributing to their disability. Noninvasive testing can be used to detect PAD in otherwise asymptomatic patients, and this can be valuable since PAD is an independent risk factor for cardiac events and the early diagnosis of PAD can initiate risk factor modification. In patients with advanced disease, physiologic testing helps to determine the ability of ischemic ulcers to heal or provides guidance for the optimal level of amputation. This chapter reviews the theory, methods, interpretation, and applications of the various indirect physiologic arterial tests available in the vascular laboratory.
Doppler Ultrasonography
The development of Doppler ultrasound to detect blood flow and analyze velocity waveforms revolutionized the ability to detect and quantitate peripheral vascular disease noninvasively. This chapter discusses the use of basic continuous wave Doppler and waveform analysis.
Principles of Doppler Ultrasound
The handheld continuous wave “pocket Doppler” devices typically have a transmitting frequency between 5 and 10 MHz, suitable for more superficial arteries due to the limited penetration depth of ultrasound waves at this frequency. The tip of the probe has a transmitting piezoelectric crystal that converts electrical energy into ultrasound waves, as well as a receiving piezoelectric crystal that detects reflected ultrasound waves. The probe converts detected frequency shift and sends it to the speakers for an audible signal. A fluid interface, generally an aqueous gel, is required between the probe and the skin to allow penetration of ultrasound waves into the tissue without significant loss of energy from impedance mismatch (difference in density causing significant reflection of ultrasound waves, thus preventing further tissue penetration). Moving red blood cells act as reflectors that backscatter ultrasound waves. The frequency of the reflected ultrasound wave is shifted from the transmitted frequency in direct proportion to the velocity of the blood flow due to the Doppler effect ( Fig. 21.1 ). The magnitude of the frequency shift (Δf) is given by the following Doppler equation:
where V is blood velocity in centimeters per second, f 0 is the transmitted frequency, θ is the angle between the velocity vector and the path of the ultrasound beam (known as the Doppler angle), and C is the velocity of sound through blood (1.54 × 10 5 cm/s). This equation can be rearranged to solve for V when the Doppler angle is known, or it can be estimated, as it is in duplex scanning.
Aural Interpretation of the Doppler Waveform
The velocity of blood flow is proportional to the frequency shift, which is heard as a change in pitch of the audio signal. Loudness (amplitude) is proportional to the volume of red blood cells moving through the Doppler signal path. Turbulence causes nonuniform velocities and imparts a harsh quality to the audible Doppler signal. An experienced listener can identify increased pitch, which corresponds to luminal narrowing causing increased velocity of flow. One can also assess the contour of the velocity waveform. Normal peripheral arteries at rest have a triphasic or biphasic quality with a brisk upstroke of forward flow in systole, a brief reverse flow component in diastole caused by the reflection of the flow wave from the high resistance periphery, and finally, in most, but not all peripheral arteries, a small forward component in late diastole ( Fig. 21.2A and B ). When the peripheral vascular resistance is low, either due to the arterial bed downstream such as the kidneys, brain, or liver, or after exercise, hyperemia, or intraarterial administration of vasodilating drugs, the velocity waveform loses the reverse flow component and becomes monophasic with forward flow throughout the entire cardiac cycle.
Arterial obstruction causes dampening of the waveform, which becomes monophasic ( Fig. 21.2C ). The low-amplitude, monophasic Doppler signals that result from extensive occlusive disease may be difficult to distinguish from venous signals. Gentle compression of the foot causes a rush of venous blood from emptying the veins that is easy to appreciate in the Doppler signal. Directional Doppler can also be useful to distinguish arterial from venous signals because it will indicate whether blood is flowing toward or away from the ultrasound probe.
Qualitative and Quantitative Waveform Analysis
The earliest change at the site of stenosis is widening of the waveform (spectral broadening) in early diastole, when flow is decelerating and least stable. More severe stenosis produces a marked increase in systolic velocity in addition to spectral broadening. Critical stenosis limits flow and pressure and generally occurs when the lumen is narrowed by 50% or more. Waveforms at the site of stenosis are associated with a doubling of peak systolic velocity when compared with the adjacent segments ( Fig. 21.3 ). Downstream from significant stenoses, waveforms become blunted and monophasic with widening as a result of turbulence.
The result is a noisy, high-pitched Doppler signal at the site of stenosis. This signal can be heard for several vessel diameters downstream from the site of stenosis because of transmission of the high-velocity jet over this distance. A few centimeters upstream from the stenosis, the waveform is affected by the high resistance of the stenosis. This results in less forward flow and a large, reflected wave following the lower frequency systolic peak. It is heard as a “to-and-fro” signal pattern. Extremely low flow may not be detectable by handheld Doppler instruments because of inadequate signal generation or cutoff of very low frequencies by the filter that is used to eliminate wall motion artifacts.
To overcome the subjective, operator-dependent nature of qualitative waveform analysis, spectrum analyzers can be used. These instruments have a frequency analyzer that uses fast Fourier analysis or similar methods to give a full picture of the entire spectrum of frequencies present in each sampling interval. Frequency shifts are displayed on the vertical axis and time on the horizontal axis. The amplitude of the reflected signal at each frequency is represented by a gray scale (see Fig. 21.2 ). The intensity of the gray scale is proportional to the number of red blood cells traveling at a particular velocity at each point in time. These devices, which are used in all duplex scanners, permit identification of features, such as uniformity of flow (narrow band of velocities) or nonuniformity (widening of the velocity waveform, known as spectral broadening). When the angle of insonation is known, the output can be displayed as velocity over time and various parameters can be measured, such as peak and end-diastolic velocity and ratios of various velocity components. Duplex scanners also use pulsed Doppler with time-gated reception of the reflected ultrasound to allow the operator to select the depth at which velocity information is obtained. This permits interrogation of Doppler information within a visualized vessel and thereby more precise categorization of the degree and location of stenosis. In the absence of Duplex scanning, indirect analysis of waveforms obtained at the common femoral artery level such as peak-to-peak pulsatility index (calculated as (V max − V min )/V mean where V stands for velocity, max for maximum, and min for minimum), Laplace transform, power frequency spectral analysis, pulse wave velocity, and pulse transit time have been used to determine whether significant aortoiliac occlusive disease is present. However, these indirect methods are prone to false-negative interpretations because waveforms can return to a normal contour within only a few vessel diameters downstream from a significant stenosis. ,
Pressure Measurements
Strandness and coworkers developed noninvasive pressure measurement in the 1960s when continuous wave Doppler instruments became available to detect blood flow. Since pressure differentials drive flow, decreased pressure results in decreased flow. In most instances, therefore, pressure is an acceptable surrogate measure for flow and is easier to measure.
The higher-frequency components of the pressure waveform are more sensitive to the dampening effect of stenoses, and therefore decreases in systolic pressure are more sensitive than changes in mean or diastolic pressure for detecting stenosis. The reduction in pressure is caused by viscous losses from flow through narrow channels and by kinetic energy losses secondary to turbulence (which is the dominant source of loss in all but the smallest arteries). Turbulence occurs when kinetic forces are much greater than the viscous forces that produce ordered, laminar flow. The relationship between these forces is estimated by the Reynold number (Re):
where V is velocity in centimeters per second, d is diameter of the vessel, and ν is viscosity (which varies with velocity; in other words, blood is a non-Newtonian fluid). As flow increases, velocity increases, and flow becomes less stable as both viscous and kinetic losses increase. Greater than Reynold numbers of approximately 2500, turbulence develops (at least in straight tubes with nonpulsatile flow, conditions that are not met in the normal human vasculature) and energy is lost (as imperceptible heat generation). Thus resting flow and velocity may not be associated with a reduction in pressure. However, a pressure gradient may develop when flow increases, resulting in increased turbulence.
A mild stenosis that does not cause a drop in pressure at rest may become evident when flow is increased. A peak systolic pressure drop across an arterial segment of 10 mm Hg at rest or 15 mm Hg after hyperemia induced by exercise, ischemia, or the administration of vasodilators indicates increased resistance in this segment sufficient to reduce flow by a clinically meaningful amount. Conversely, significant proximal lesions (e.g., in the aortoiliac system) may not be evident even after vasodilation if the outflow vessels (superficial and profunda femoral arteries) are so diseased that outflow is severely restricted. If there is minimal flow, there is no pressure drop across a vessel no matter how stenotic.
Ankle–Brachial Index Measurement
Basic Technique
The simplest noninvasive method for documenting the presence of lower extremity arterial occlusive disease is the ankle–brachial index (ABI). The cuff is placed as low as possible on the leg above the ankle, inflated above systolic pressure, and then slowly deflated while the Doppler probe is held over the posterior tibial artery, just behind the medial malleolus ( Fig. 21.4A ), or the dorsalis pedis artery, slightly lateral to the extensor hallucis longus tendon approximately a centimeter distal to the ankle joint. The ankle pressure is recorded as the highest pressure at which the Doppler signal returns. If no signal can be obtained over these arteries, the examiner should check for the terminal branch of the peroneal artery (the lateral tarsal artery), which is just anterior and medial to the lateral malleolus. However, pressure in this artery may not be as good a measure of pedal flow as in the other two tibial arteries because it is often not in continuity with the pedal arch.
The brachial pressure, measured with a manual blood pressure cuff and continuous wave Doppler at the distal brachial or radial artery, is used as the denominator for the ABI and serves as a surrogate for central aortic pressure, which cannot be measured noninvasively. As upper extremity occlusive disease may lower brachial pressure, the higher of the two arm measurements should be used. Bilateral upper extremity occlusive disease renders the ABI nondiagnostic. The ABI for each lower extremity is the highest of the detectable ankle pressures divided by the higher of the two brachial pressures (see Fig. 21.4B ). The ABI is less variable than ankle pressure, with a standard deviation of approximately 0.07, so a measurement greater than two standard deviations is considered significant. Normalizing to the brachial pressure accounts for the normal variation in central pressure and allows a better appreciation of the extent of arterial occlusive disease in the presence of systemic hypotension or hypertension.
The pressure waveform changes as it moves distally through the vasculature ( Fig. 21.5 ). Peak systolic pressure is accentuated by the additive effect of reflected pressure waves from the periphery. In addition, the lower extremity vasculature remodels in reaction to increased intraluminal pressure from gravity and upright posture to have increased wall thickening and unchanged inner radius, leading to increased arterial stiffness. Thus, although mean pressure decreases as the pressure wave travels distally, peak systolic pressure increases. As a result, ankle systolic pressure is normally approximately 10% higher than brachial pressure (ABI of 1.1). Significant PAD decreases this ratio. Because of the known variance of this test, ABIs in the range of 0.9 to 1.29 are considered normal. However, a value of 0.9 to 1 should be considered borderline because these patients have been demonstrated to have increased lower extremity and cardiovascular risk. As the extent and severity of PAD increases, ABI decreases ( Fig. 21.6A ).
ABI has been well validated against contrast-enhanced angiography for its ability to detect stenosis of greater than 50%. , , The sensitivity of this test depends on the lower limit of normal that is chosen, with higher limits detecting more disease, as well as the population being tested, with lower sensitivity in more elderly populations or with a higher percentage of diabetic or chronic kidney disease patients. Using an average of the two measurements has been found to correlate better with walking distance than using either the lower or higher ankle pressure. In general, the sensitivity of ABI in detecting PAD ranges from 80% to 95% and the specificity from 95% to 100%, with positive and negative predictive values in excess of 90%. ,
The automated blood pressure instruments commonly used in hospitals and clinics to determine arm blood pressures may also be used at the ankle level. The machine detects oscillations of pressure, caused by changes in volume in the extremity as a result of influx of blood with each systolic pulse, in the cuff as it deflates. Oscillation begins while the cuff is well above systolic pressure and continues until it is well below diastolic pressure. Maximum oscillation occurs at mean arterial pressure. Each manufacturer has its own proprietary algorithm, empirically derived, to determine systolic and diastolic pressure from oscillometry. These algorithms were developed for measurement of arm pressure but can also be used for ankle pressure. Like standard Doppler methods, oscillometry has good concordance for normal ankle pressure, but it overestimates pressure when there is moderate disease and is unable to determine pressure in severe disease due to the significantly diminished pulse pressure. Nevertheless, this method may be useful to screen for PAD in primary care clinics because it is rapid and requires no specialized training or equipment. ,
Noninvasive tests can help to make the diagnosis of popliteal entrapment syndrome. A change in ankle plethysmography and ABI with stress maneuvers suggests popliteal entrapment. The limb is examined with the knee extended and the foot in the neutral, forced plantar-flexed, and forced dorsiflexed positions. The test is considered positive if the ABI drops more than 0.5 or there is flattening of the plethysmographic tracing with forced dorsiflexion or plantar flexion , (see Ch. 144 , Nonatherosclerotic Popliteal Artery Diseases).
Prognostic Value of Ankle–Brachial Index
The ABI has predictive value; measurements greater than 0.5 are infrequently associated with progression to critical limb ischemia over the next 6 years. Decreased ABI and the presence of diabetes mellitus were the two factors associated with the development of chronic limb ischemia in a 15-year study of 1244 patients with claudication. An abnormal ABI (either <0.60 or >1.30) has been associated with increased overall mortality, as has decline in ABI over time. The ABI is useful as an office screening tool for PAD in asymptomatic patients older than 65 years of age, for whom an ABI <0.90 is associated with an increased mortality and vascular event risk. The American Diabetes Association has recommended similar screening with ABI for diabetic patients older than 50 years of age. Although detection of PAD can identify patients at risk for cardiac events, there are no data demonstrating that screening leads to prevention of such events. Further, there is no evidence that ABI adds significantly to Framingham Risk Score or other assessments of cardiovascular risk. Routine surveillance of ABI is not indicated in untreated patients with PAD unless they develop new or worsening symptoms.
However, cardiovascular mortality, all-cause mortality, and major coronary event rates by gender have not been well defined in population-based studies. There are no known gender-based differences in diagnostic testing of any of the physiologic PAD tests, and all noninvasive studies may be used to document the presence of PAD in women. A trend exists that suggests higher event rates for women than for men for individuals with an ABI <0.90. Women suffer the consequences of PAD at rates at least as high as those observed in men ( Fig. 21.7 ).
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