Describing pulsatile fluid systems mathematically is very complex. Hemodynamics can be defined as the physical factors that influence blood flow which is based on fundamental laws of physics, namely Ohm’s law: Voltage (Δ V) equals the product of current (I) and resistance (R), i.e.,

In relating Ohm’s law to fluid flow, the voltage is the pressure difference between two points (δ P), the resistance is the resistance to flow (R), and the current is the blood flow (F):

Resistance to blood flow within a vascular network is determined by the length and diameter of individual vessels, the physical characteristics of the blood (viscosity, laminar flow versus turbulent flow), the series and parallel arrangements of vascular network, and extravascular mechanical forces acting upon the vasculature. This is expressed in Poiseuille’s law:

Poiseuille’s Law relates the rate at which blood flows through a small blood vessel (Q) with the difference in blood pressure at the two ends (Δ P), the radius (r) and the length (L) of the artery, and the viscosity (η) of the blood.

Of the above factors, changes in vessel diameter are most important quantitatively for regulating blood flow as well as arterial pressure within an organ. Changes in vessel diameter, either by constriction or dilatation, enable organs to adjust their own blood flow to meet the metabolic requirements of the tissue. Flow velocity increases as the pressure gradient increases and flow volumes are relatively preserved, only to a point though.

Osborne Reynolds determined how viscosity, vessel radius, and pressure/volume relations influenced the stability of flow through a vessel:

Density and viscosity are relatively constant, therefore the development of turbulence depends mainly on the velocity and size of the vessel. Density is defined as mass per unit volume and viscosity is defined as a measure of the resistance of a fluid to being deformed by either shear stress or extensional stress. A Reynolds number >2000 causes turbulence and vessel wall vibration producing a bruit. High velocities cause turbulence and hinder volumes flow, creating eddies.

Basics of Vascular Ultrasound

Ultrasonic waves entering human tissue are absorbed, reflected, and scattered to produce images of anatomic structures. The transmission properties of the sound waves depend on the density and elasticity of the tissues. Density and speed of propagation of ultrasound waves determine a tissue’s acoustic impedance. The larger the differences in acoustic impedance between tissues, the more ultrasound waves are reflected. The reflection further depends on the angle of insonation. Strong reflective interfaces, such as air or bone, prevent imaging of weaker echoes from deeper tissue and cast shadows behind them. Tissues that strongly reflect ultrasound are termed hyperechoic, whereas poorly reflective tissues are termed hypoechoic.

The transducer repeatedly emits pulses of sound at a fixed repetition frequency. A detector records echoes originating from interfaces and scatterers in the sound beam. Echo signals are then amplified and processed into a format for display. If ultrasound is continuously transmitted along a particular path, the energy will also be continuously reflected back from any source in the path of the beam, making it difficult to predict the depth of the returning echoes. With pulse-echo techniques, it is possible to predict the distance of a reflecting surface from the transducer if the time between the transmission and reception of the pulse is measured and the velocity of the ultrasound along the path are known.

When the ultrasound pulse returns to the transducer, it causes the transducer to vibrate and will generate a voltage across the piezoelectric element. The amplitude of the returning pulse depends on several factors, including the proportion of the ultrasound reflected to the transducer and by which the signal has been reflected along its path. The amplitude of the pulse received back to the transducer can be displayed (A-mode) against time and then can be calibrated to time, thus showing the depth of the boundary in the tissue. The varying amplitude of the signal can be displayed as a spot of varying brightness. This type of display is known as a B-mode scan.

B-Mode Imaging

Structures imaged by B-mode, or brightness mode, are displayed proportionally to the intensity of returning echoes. The ultrasonic beam scanning through a tissue plane produces a two-dimensional gray-scale image. In clinical practice, the beam is swept quickly through the field of view, and the image is continuously renewed, allowing visualization of the underlying tissue anatomy.

B-mode ultrasound takes reflected signals and converts them to a series of dots on a display. A transducer, whose resonant frequency is between roughly 2 and 10 MHz, is used to transmit a short pulse of sound into a patient. The sound is reflected from a tissue interface where there are differences in acoustic impedance. The reflected pulse is received by the ultrasound instrument and the pulse amplitude is encoded as brightness and depth on a monitor. The time that is required for the pulse to travel from the transducer to the interface and back is directly proportional to its depth. The acoustic velocity is 1540 m/s. As the sound pulse propagates through tissue, it is attenuated and this would darken the parts of the image that correspond to regions further from the probe. In order to compensate for this attenuation, echoes originating from deeper tissues are amplified more than echoes originating near the probe. Because different tissues have different attenuation coefficients, the amplification can be varied as a function of depth. The exact manner in which the amplification depends on depth is usually displayed on the ultrasound instruments monitor as a depth-gain curve or time-gain curve. Usually, 100 to 200 separate ultrasound beam lines are used to construct each image.

Doppler Display Modes

Doppler ultrasound is a technique for recording noninvasive velocity measurements. The difference in frequency between emitted and returning ultrasonic echoes is the Doppler frequency shift.¹ As the blood is moving, the sound undergoes a frequency (Doppler) shift that is described by the Doppler equation^2,3:

where c is the acoustic velocity in blood, 1540 m/s; F₀ is the transmitted frequency; θ is the Doppler angle; v is the velocity of the blood. The shift is measured only for the component of motion occurring along the ultrasound beam. Therefore, absolute velocity measurements require that a correction be made for the angle (θ) between the vessel and the beam as

Color Doppler Imaging

Color Doppler ultrasound is a technique for visualizing the velocity of blood within an image plane. Color is superimposed on a conventional gray-scale image to enhance the image of the Doppler frequency shift. A color Doppler instrument measures the Doppler shifts in a few thousand sample volumes located in an image plane. For each sample volume, the average Doppler shift is encoded as a color and displayed on top of the B-mode image. The way in which the frequency shifts are encoded is defined by the color bar located to the side of the image. By convention, positive Doppler shifts, caused by blood moving toward the transducer, are encoded as red and negative shifts are encoded as blue. Color Doppler images are updated several times per second, thus allowing the flowing blood to be easily visualized.

In healthy individuals, arterial flow is pulsatile and laminar, whereas stenoses, angles, or elevated velocities may cause the laminar flow pattern to be distrupted.⁴ Additionally, turbulence at the stenosis and distal to the area causes an increase in the rage of flow velocities known as spectral broadening.² As the degree of stenosis progresses, flow velocities increase at the point of maximum narrowing. In very stenotic areas, marked reductions in the residual lumen cause flow velocities to fall, leading to flow cessation with complete lumen obliteration. Doppler insonation proximal to an occluded vessel assumes a stump flow pattern.

Continuous Wave Doppler

Continuous wave Doppler uses two piezoelectric crystal transducers where one crystal continuously emits toward the region of interest and the other continuously receives reflected echoes. Flow toward the transducer produces an increase in the received frequency, whereas flow away from the transducer causes a drop. Continuous Doppler does not provide information about the depth of the tissue.

Power Doppler

Power Doppler ultrasonography emphasizes the display of amplitude information rather than the relative velocity or direction of flow. This method of display has some advantages in that the power Doppler display is not dependent on the angle of insonation and has better sensitivity when compared with conventional Doppler frequency. Advantages of power Doppler include independence from the angle of insonation, absence of aliasing, and the ability to detect very low flows.

Lower extremity peripheral arterial disease (PAD) is associated with an amplified risk of cerebrovascular and cardiovascular morbidity and mortality, including stroke, myocardial infarction, and even death. The prevalence of PAD in North America and Europe is currently estimated to affect approximately 27 million people.⁵

Noninvasive tests are preformed to confirm and define the extent of obstruction in patients with suspected lower extremity PAD based upon the history (e.g., symptoms of intermittent claudication) or in patients with risks factors for vascular disease (e.g., older age, smoking, diabetes mellitus).⁶ The establishment of successful patient stratification in vascular medicine is through a thorough clinical evaluation and accurate noninvasive testing. In this chapter, the focus is on the functional mechanics of normal and abnormal vascular flow, types of noninvasive imaging, limitations of noninvasive imaging, and recommendations and guidelines in lower extremity, carotid, renal artery, cerebral, mesenteric, upper extremity, and vertebral vascular diseases.

A variety of noninvasive examinations are available to provide an objective diagnostic tool to assess the presence and degree of PAD. The noninvasive vascular evaluation includes ankle and toe brachial index, exercise treadmill test, segmental limb pressures (SLPs), segmental volume plethysmography, and color duplex imaging. These examinations allow the clinician to objectively determine the presence of disease, localize lesions, and establish the severity of disease to determine the progression or its response to therapeutics. This section will review the evidence-based benefits, limitations, quality assurance, and guidelines of each of these vascular diagnostic techniques.

Patients should be evaluated for PAD if they are at increased risk from their age, presence of atherosclerotic risk factors, have leg pain suggestive of ischemia, or have distal limb ulceration (Table 17-1).

Many vascular practices use various algorithms for the diagnosis of PAD; however a thorough historical review of symptoms and atherosclerotic risks factors, physical examination, and the use of noninvasive vascular tests are paramount in diagnosing PAD. The most cost-effective tool for lower extremity PAD detection is the ankle-brachial index (ABI) and should be performed in every patient suspected of having lower extremity PAD (Figure 17-1).⁸

Many vascular practices simultaneously obtain ABIs, SLPs, and pulse volume recordings (PVRs) in patients with suspected PAD as initial diagnostic tests.

The ABI is a relatively simple, inexpensive, and reproducible method to confirm the clinical suspicion of arterial occlusive disease. Despite the increasing use of more sophisticated diagnostic tests, the ABI has been shown through epidemiology studies to predict future cardiovascular ischemic events. This has led to increasing use of the ABI examination in office practice. The sensitivity and specificity associated with an ABI threshold of 0.90 or less have ranged from a sensitivity of 79% to 95% and specificity of 96% to 100% compared with contrast angiography. Fowkes et al.⁹ demonstrated that with an ABI diagnostic threshold of 0.90, the sensitivity of the ABI was 95% and specificity was 100% compared with angiography. Feigelson et al.¹⁰ demonstrated using only posterior tibial measurements in assessing the ABI, that with an ABI diagnostic threshold of 0.8, the sensitivity of the ABI was 89% and specificity was 99% with a overall accuracy of 98% compared with angiography. Lijmer et al.¹¹ evaluated the ABI by using a receiver operating characteristic (ROC) to determine its diagnostic accuracy depending on the localization of the disease. This study demonstrated patients with significant PAD (lesions ≥50%), that with an ABI diagnostic threshold of 0.91, the sensitivity of the ABI was 79%, and specificity was 96%. Multiple investigations have also evaluated the interobserver variability of the ABI measurement. Endres et al.¹² tested the variability of a measured ABI with six angiologists, six primary care physicians, and six trained medical office assistants. They performed two ABI measurements: each measurement on six individuals from a group of 36 unselected subjects aged 65 to 70 years and found mean differences between the ABI measurements very close to zero.¹²

Several studies have shown that the ABI is associated with functional capacity, even in asymptomatic patients. The Women’s Health and Aging Study evaluated disabled women 65 years or older and used the ABI as a measure of lower extremity function. The results showed that decreasing ABI values were associated with worsening functional scores, even after adjustment for age, race, smoking status, and comorbidities.¹³ Even lower ABI scores in the asymptomatic women in this study correlated with slower walking velocities, poorer standing balance scores, slower time to rise, and fewer blocks walked per week.¹³ In the Study of Osteoporotic Fractures, 1492 women 65 years or older were evaluated to compare the relationship between ABI (≤0.90) and extremity function.¹⁴ This study showed patients with an ABI greater than 0.90 had significantly higher hip abduction force, knee extension force, walking velocity, and number of blocks walked than those with ABI of less than 0.90.

Studies have also shown that an abnormal ABI is predictive of both cardiovascular and cerebrovascular disease. Newman et al.¹⁵ has shown an inverse relation between cardiovascular disease and ABI. For example, participants with an ABI <0.8 were more than twice as likely as those with an ABI of 1.0 to 1.5 to have a history of myocardial infarction, congestive heart failure, stroke, angina, or a transient ischemic attack in a cohort of 5084 participants. Mortality and morbidity in patients with lower extremity PAD has been quantitated by McKenna et al.,¹⁶ who demonstrated a 5-year mortality of 50% and 30% in patients with an ABI of 0.40 and 0.70, respectively. It also has been shown that those with an ABI less than 0.50 demonstrated a 5-year mortality of 37%, 29% for patients with an ABI between 0.50 and 0.69, and 9% for patients with an ABI between 0.70 and 0.89.¹⁷ Resnick et al.¹⁸ demonstrated that patients with an ABI of less than 0.90 had an all cause mortality of 1.69 and cardiovascular mortality of 2.52, while patients with an ABI of 1.40 or greater had a all-cause mortality of 1.77 and cardiovascular mortality of 2.09.

Multiple studies have shown the importance of the ABI as a predictor of cardiovascular or all-cause mortality in asymptomatic patients. Criqui et al.¹⁹ has evaluated a 10-year follow up of 67 patients with a diagnosis of PAD and a ABI of 0.80 or less, showing a dramatic increase in rate of mortality in both men (61.8%) and women (33.3%) when compared with men (16.9) and women (11.6%) without disease (Figure 17-2).

Thus, the accuracy in establishing the diagnosis and 5-year survival in patients with lower extremity PAD is well predicted by the ABI value. The American Diabetes Association and American Heart Association have long endorsed the ABI, suggesting that the procedure be preformed in all individuals with diabetes who are aged 50 years and older, in individuals with diabetes who are younger than 50 years of age and have other atherosclerosis risk factors, and in individuals with diabetes of more than 10 years duration.^20,21

Assessing the ABI

The ABI is performed after the patient has been at rest in the supine position for 10 minutes. The systolic blood pressure should then be measured with appropriately sized cuffs from both brachial arteries and from both the posterior tibial arteries and the dorsalis pedis with a handheld Doppler instrument (Figure 17-3).⁸

The cuff is then rapidly inflated above systolic pressures, thereby obliterating flow to the part under study. As the pressure in the cuff is gradually deflated, the point at which flow is resumed is taken as the opening or systolic pressure at that level. The ABI is calculated by dividing the highest systolic ankle pressure by the higher of the two systolic brachial pressures. Calculated values should be recorded to two decimal places. The average time required to perform the ABI is approximately 5 to 10 minutes. With increasing degrees of arterial stenosis, there is a progressive fall in systolic blood pressure distal to the sites of involvement. This extent to which the pressure falls is dependent on the extent of involvement. The interarm systolic pressure gradient during a routine examination should be less than 12 mm Hg in a normal individual. The ankle pressure in healthy individuals is usually 10 to 15 mm Hg higher than the brachial arterial systolic pressure caused by pulse wave reflections. Subclavian or axillary arterial stenosis is presumed to be present if the blood pressures in the arms are not equal, and the higher blood pressure should then be used for ratio calculations.

ABI values have been categorized to determine the presence and the severity of PAD. The National Heart, Lung, and Blood Institute initiated The Multi-Ethnic Study of Atherosclerosis (MESA) to further understand the pathogenesis of atherosclerosis by providing quantifiable measures of cardiovascular disease, characterization of cardiovascular disease to disrupt its natural course, and to optimize study of the progression of subclinical disease. The MESA cohort consists of 6814 men and women aged 45 to 84 years (38% whites, 28% African Americans, 23% Hispanics, 11% Asians, and approximately 50% females) who were enrolled at six US field centers. They all were free of clinically evident cardiovascular disease at the time of enrollment. Five ABI categories were defined: <0.90 (definite PAD), 0.90 to 0.99 (borderline ABI), 1.00 to 1.09 (low-normal ABI), 1.10 to 1.29 (normal ABI), and 1.30 (high ABI) (Table 17-2).²²

Previous studies showed that an ABI less than 0.90 is 94% sensitive and 99% specific for angiographically diagnosed PAD.²³ Some studies have used ABI 1.50 to define the upper limit of normal, but generally an ABI of 1.3 is indicative of medial arterial calcinosis and noncompressible arteries.^24,25,26,27 Mild claudication or obstruction occurs with an ABI <0.9–0.75. Moderate to severe claudication occurs with an ABI <0.75–0.4. Jelnes et al.²⁸ demonstrated that an ABI value <0.50 suggests that progression to critical leg ischemia is likely in the subsequent 6.5 years of follow-up (Table 17-2). Thus, patients with severely decreased ABIs are at particularly high risk for the development of rest pain, ischemic ulceration, and gangrene. Absolute levels of tissue ischemia are typically associated with ankle blood pressure recordings of 35 mm Hg or less in nondiabetic subjects, and of less than 55 mm Hg in diabetic subjects.²⁹

Additional noninvasive vascular studies can be preformed in patients with abnormal ABIs. Patients with leg pain on exertion who have ABI values of 0.91 to 1.30 should be considered for an exercise test, while patients less than 0.90 at rest needs no additional tests for the diagnosis of PAD (though maybe performed to assess functional limitations). If a patient’s ABI value is above 1.30, then one should perform additional test such as pulse-volume recording, measurement of a toe-brachial index (TBI), or duplex ultrasonography to determine whether PAD exists (Figure 17-4).⁸

Toe blood pressure analysis is useful to screen for PAD in diabetic patients who may have medial calcinosis of medium-sized arteries or to evaluate for the presence of pedal and digital arterial disease in patients with nonhealing ulcers, rest pain, and gangrene. Patients with unaffected arteries to the level of the ankle but severe PAD in the arteries of the feet and digits may have normal ABIs but a depressed TBI. TBIs less than 0.7 are abnormal, claudication indexes range from 0.35 to 0.69, and those with rest ischemia have indexes ranging from 0.11 to 0.24.^30,31,32 A toe blood pressure less than 30 mm Hg has 80% sensitivity for detecting limbs with rest ischemia.³¹

Transcutaneous oxygen and carbon dioxide pressure (PO₂ and PCO₂) foot monitoring has been compared with ankle Doppler-derived systolic pressure regarding their abilities to discriminate the severity of limb ischemia before vascular reconstruction and to predict surgical outcome early in the postoperative period. Transcutaneous PO₂ (TcPCO₂), foot-chest TcPO₂ index, transcutaneous PCO₂ (TcPCO₂), foot TcPO₂/TcPCO₂ index (TcPO₂/TcPCO₂), ankle Doppler systolic pressure (AP), and ABI have been evaluated with revascularized limbs. The measurement of TcPO₂ and foot-chest TcPO₂ has been found to be more sensitive to the degrees of severity of limb ischemia and more closely associated with the outcome of revascularization than AP and ABI. TcPCO₂ and TcPO₂/TcPCO₂ have not been useful in the assessment of the vascular patient undergoing reconstructive surgery. Before operation, TcPO₂ less than or equal to 22 torr and foot-chest TcPO₂ index less than or equal to 0.46 indicate severe limb ischemia requiring urgent revascularization. After operation, TcPO₂ less than or equal to 22 torr and foot-chest TcPO₂ index less than or equal to 0.53 indicate that revascularization is likely to fail.

Limitations of the ABI

The ABI is an effective diagnostic tool, however it does not measure the effectiveness of preventive treatment. The ABI also may not be accurate in individuals whom have noncompressible arteries. The incidence of noncompressible arteries is higher in individuals with diabetes, those with renal insufficiency, and elderly patients as a result of calcified arteries that prevent occlusion of blood flow by the blood pressure cuff. This may result in an unusually high ABI reading, thus, for patients in whom symptoms strongly suggest PAD, the presence of a normal or high ABI should not be resumed to rule out the diagnosis. Also, patients with occlusions or severely stenotic iliofemoral arteries may also occasionally present with a normal ABI at rest because of the presence of collateral arterial networks. In these cases, an alternative diagnostic test (e.g., toe-brachial pressure, Doppler waveform analysis, PVR, exercise ABI test, or duplex ultrasound) should be performed.

ABI and Exercise Treadmill Testing

When the resting ABI is normal, but there is a high clinical suspicion for arterial disease, measurement of ABI coupled with exercise testing can be used to determine whether a patient’s symptoms are caused by PAD (Table 17-3).^33,34

When the patient exercises, this produces significant peripheral vasodilatation in the presence of arterial stenosis, resulting in significant blood pressure gradients. These blood pressure gradients cause the ABI to drop in patients with PAD, whereas in individuals without stenosis will have a slight increase or no change in the ABI.

When performing the test, a baseline ABI is obtained, then the patient is placed on a treadmill using a constant speed and grade until the patient has walked to maximal discomfort or a predefined end point. The patient’s leg symptoms, location of symptoms, and their intensity should be recorded at symptom onset and at the time of maximal discomfort. Immediately after exercise, the patient is asked to lie in a supine position and the ABI should be measured at 1-minute intervals until the preexercise baseline is reached. ABI <0.90 at 1 minute after exercise indicates hemodynamically significant PAD (Table 17-4).

PAD is not the cause of the symptoms if the exercise produces discomfort or pain and the ABI remains unchanged or normal. Exercise treadmill tests should not be preformed in patients with lower extremity rest pain, noncompressible vessels on a resting study, acute deep venous thrombosis, shortness of breath at rest or with minimal exertion, uncontrolled angina, or a physical disability that limits the patient’s ability to ambulate on a treadmill.

An alternative form of exercise testing is active pedal plantar flexion. The patients raise their heels as high as possible and then immediately lower them, repeating the cycle for up to 50 consecutive repetitions. ABIs are measured immediately after completing the exercise with the patient in a supine position. McPhail et al.³⁵ compared the active pedal plantarflexion technique with the standard lower extremity vascular laboratory treadmill exercise. This study demonstrated an excellent correlation (r = 0.95, 95% confidence interval 0.93 to 0.97) between mean postexercise ankle-brachial systolic blood pressure indices for treadmill exercise and active pedal plantar flexion, while producing zero symptoms of angina or dyspnea (Figure 17-5).

The reactive hyperemia test is an alternative to the baseline ABI or treadmill test. If one is unable to walk on a treadmill, the reactive hyperemia test can be performed to diagnose PAD. Standard blood pressure cuffs are placed around the thighs and ankles. The thigh cuffs will be inflated above the patient’s normal systolic blood pressure for 3 to 5 minutes. Once the thigh cuffs are deflated, the ankle cuffs are inflated briefly above the patient’s systolic blood pressure, so that using the Doppler instrument, blood pressure measurements can be immediately taken at both ankles. A significant (50% or greater) decrease in ankle blood pressure indicates that there is a blockage in the leg arteries and thus is a diagnosis of PAD.

When further detection, localization, or characterization of PAD is necessary, the measurement of segmental pressures and PVRs can be used. The ABI cannot determine the location of proximal arterial lesions or the relative significance of lesions at multiple levels. In contrast to ABI studies, the segmental pressure analysis is able to make measurement of systolic blood pressure along selected segments of each extremity and accurately determine the presence and severity of stenosis in the peripheral arteries. When SLP measurements are used in combination with PVRs, a 97% diagnostic accuracy is demonstrated when compared with angiography.³⁶

Assessing SLP

The SLPs are preformed after the patient has been at rest in the supine position for 20 minutes. A series of pneumatic cuffs are placed on the upper and lower portions of the thigh, the calf, above the ankle, and often over the metatarsal area of the foot and great toe. Likewise, in the upper extremity, pneumatic cuffs are placed on the upper arm over the biceps, on the forearm below the elbow, and at the wrist. Systolic pressure is determined at each level using a continuous-wave Doppler probe. In the upper extremities, the Doppler probe can be placed over the brachial artery in the antecubital fossa or over the radial and ulnar arteries at the wrist. The ABI is calculated, and then the pressure is sequentially inflated in each cuff to 20 to 30 mm Hg above the systolic pressure, or beyond the last audible Doppler arterial signal. The systolic pressure is recorded as the pressure at which the first audible Doppler arterial signal returns. If pressure measurements need to be repeated, the cuff should be fully deflated for about 1 minute prior to repeat inflation. The average time required to perform SLPsis approximately 15 to 20 minutes.

In normal individuals, the difference in systolic pressure between any two adjacent levels (vertical) in the leg should be less than 20 mm Hg. A blood pressure gradient in excess of 20 mm Hg between successive cuffs usually signifies significant occlusive disease between the cuffs. The horizontal gradients between corresponding segments of the two legs may also indicate the presence of occlusive lesions. As the limb girth decreases from the thigh to the ankle, pressure measurements also decrease. The high-thigh pressure in the average sized limb is normally at least 20 to 30 mm Hg greater than the highest brachial pressure. If this difference is less than this amount from the high-thigh to brachial, then this would suggest an aortoiliac obstruction (or, CFA stenosis/CFA equivalent). In further determining the level at which there may be stenosis or occlusion, a thigh pressure index (ratio of high thigh systolic pressure to brachial systolic) can be calculated. The thigh pressure index is normally greater than 1.2, however an index between 0.8 and 1.2 suggests aortoiliac stenosis (Table 17-5). A complete iliac occlusion is consistent with a thigh pressure index less than 0.8.³⁷

Significant reduction in blood pressure cuff positions³⁸

• 
  

  between the brachial artery and the upper thigh reflects aortoiliac, common femoral or both proximal superficial femoral artery and profunda disease,

  
  
• 
  

  between the upper and lower thigh reflects femoral artery disease,

  
  
• 
  

  between the lower thigh and upper calf reflects distal femoral artery or popliteal disease, and

  
  
• 
  

  between the upper and lower calf reflects tibial disease.

PVR provide a method to evaluate the arterial pressure waveform with the use of pneumoplethysmograph. This allows one the ability to assess the change in limb volume between diastole and systole in a segmental manner from the thigh to the ankle. The magnitude of the pulse volume correlates with blood flow and provides an index of large vessel patency. The device uses a large thigh cuff placed proximally and a calf and ankle cuffs used distally. A brachial cuff is also placed and PVR tracings are recorded to provide an index of normal pulsatility in a normal limb. The magnitude of the pulse amplitude and pulse upstroke provides a global physiological measurement of large-vessel patency and correlates with blood flow. Any deviation in the amplitude or upstroke signifies the presence of a flow limiting stenosis in the more proximal segment (Figure 17-6).^39,40

Measurement of low PVR amplitude has been shown to correlate with arterial segmental pressure gradients of 10 mm Hg at rest or gradients of 20 mm Hg by injection with papaverine.⁴¹ The accuracy of the combined PVR and segmental pressure measurements has been assessed by comparison to the angiographic gold standard in a prospective study of 50 patients with lower extremity PAD.⁴² The overall accuracy ranged from 90% to 95% and the PVR-segmental pressure technique accurately predicted the severity of iliac and superficial femoral artery obstruction, distinguishing iliac from proximal superficial femoral artery disease (Figure 17-7).

PVR has been evaluated for its ability to predict limb prognosis and have correlated well with ankle systolic blood pressure. Kaufman et al.⁴³ evaluated the relationship of PVR tracings to limb outcome in 517 patients with lower extremity PAD and demonstrated 41.9% of patients with minimal symptoms with nearly flat recordings required surgical intervention, 85.7% of patients with nearly flat tracings with jeopardized limbs underwent surgery, and 97.9% of patients with jeopardized limbs and flat tracings underwent limb salvage surgery. Makisalo et al.⁴⁴ evaluated the prognostic value of PVR tracings in predicting risk of amputation in 129 diabetics and nondiabetic renal transplant patients and took noninvasive measurements on lower limb amputations and found a low PVR amplitude prior to transplantation in 82% of the diabetic patients and 36% of the nondiabetic patients. The 5-year follow-up demonstrated that abnormal PVR values and TBI were the greatest predictors for proximal foot amputations.

PVR is a useful diagnostic test for patients with suspected lower extremity PAD and assesses limb perfusion after revascularization procedures. It also can predict limb ischemia and the risk of amputation. PVR can provide information regarding small-vessel disease when applied to the feet and is also useful in patients with noncompressible vessiles in whom ABIs and segmental pressures are spuriously elevated.

Limitations of SLPs and PVR

Segmental limb pressure measurements have the same limitations as the ABI in individuals whom have noncompressible arteries, resulting in erroneously high indices. The incidence of noncompressible arteries is higher in individuals with diabetes and elderly patients as a result of calcified arteries that prevent occlusion of blood flow by the blood pressure cuff. Another limitation is that one cannot distinguish occlusions with collaterals from stenosis. Also, the true brachial pressure cannot be measured in patients with bilateral subclavian artery stenosis, making this a major limitation of the SLP, and the ABI.

Arterial duplex ultrasonographic examination of the lower extremities can be used to noninvasively diagnose the anatomic location and degree of occlusions.⁴⁵ Duplex ultrasound also can be used to evaluate aneurysms, arterial dissection, AV fistulas, popliteal artery entrapment syndrome, evaluation of lymphoceles, and assessment of soft tissue masses in individuals with vascular disease. Gauthier and Dieter demonstrated a case of a pseudoaneurysm, mimicking the presentation of a deep venous thrombosis by causing extrinsic compression of the venous system. The patient had complete resolution of the pseudoaneurysm and his symptoms following treatment with ultrasound-guided percutaneous thrombin injection.⁴⁶ Duplex ultrasound can determine artery wall thickness, degree of flow turbulence, vessel morphologic characteristics, and changes in blood flow velocity in areas of stenosis. The specificity of the duplex ultrasound ranges from 92% to 98% and its sensitivity ranges from 92% to 95%.⁴⁷ A meta-analysis comparison of the accuracy of the duplex Doppler performed with or without color imaging guidance demonstrated a sensitivity of 93% using a color-guided duplex technique compared with 83% for noncolor duplex.⁴⁸ Peripheral arterial ultrasound is indicated in patients with claudication, leg pain, ulcers, and lower extremity revascularization.

Duplex ultrasound can predict if a patient’s anatomy is suitable for angioplasty with an accuracy of 84% to 94%.^49,50 It has been used as a substitute for arteriography for infrainguinal bypass grafting to select the most appropriate tibial vessel for anastomosis.^51,52,53 Proia et al.⁵¹ demonstrated no difference in patency of infrapopliteal bypass grafts in patients evaluated by preoperative duplex versus angiographic methods. However, Larch et al. demonstrated that color duplex sonography is inferior to angiography for evaluation of tibial arteries for distal bypass.⁵⁴ Even though there are discrepancies between studies, duplex ultrasonography can be used for prerevascularization decision making.

In patients who have undergone surgical bypass graft revascularization, especially with saphenous vein, failure may recur because of the development of stenoses. These stenoses develop at the anastomosis site, within the body of the graft, or proximal or distal from the graft in the native artery. Duplex ultrasound surveillance allows detection of these stenoses before the graft becomes thrombosed. Figure 17-8 represents a mid-SFA stenosis.

Most studies demonstrate that 80% of grafts can be salvaged if the stenosis is detected and repaired prior to graft thrombosis. Mattos et al.⁵⁵ showed that vein grafts that were revised secondary to positive findings on duplex ultrasound had a 90% 1-year patency rate. Graft stenoses that had not been revised despite the presence on duplex ultrasound had a 1-year patency rate of only 66%. Lundell et al.⁵⁶ reported a 3-year patency rate of vein grafts monitored with duplex ultrasound of 78% compared to a 53% patency rate for those followed up with the ABI. Vein bypass grafts should be studied within 4 to 6 weeks after graft placement, then 3, 6, 9, 12 months, and annually for venous conduits. Other studies have found no improvement in the patency of synthetic grafts when using surveillance intervals with duplex ultrasound.^50,57,58

Assessing Duplex Ultrasonography

Peripheral arterial stenosis is characterized using a 5 to 7.5 MHz transducer. The vessels are studied in the sagittal plane and Doppler velocities are obtained using a 60-degree angle. Angles above 60 degrees can result in significant overestimation of the velocity and should be avoided. Vessels are classified into one of five categories⁵⁹ (Table 17-6): Graft surveillance is preformed in manner identical to their use in native vessel arterial duplex ultrasonography (Figure 17-9).

Peak systolic velocities and end-diastolic velocities are determined at each segment and compared to the segment of graft proximal to it. Doubling of the peak systolic velocity (PSV) within a stenotic segment relative to the normal segment indicates significant graft stenosis of greater than 50%, with a sensitivity of 95% and specificity of 100%.⁶⁰ Also, low-flow states (peak systolic velocities <45 cm/s) within a graft indicates an increased propensity for graft failure.⁶¹

Limitations of Duplex Ultrasonography

Although duplex ultrasonography is an accurate test, accuracy of the duplex examination depends on the ability of the technique to image the vessel. Difficulties in imaging can be attributed to body habitus, bowel gas, calcified vessels, and stenosis in the presence of tandem lesions. Stenoses in tandem lesions decrease the sensitivity range from 92% to 95% to approximately 60% to 65%.^62,63

Symptomatic arterial disease of the upper extremity accounts for approximately 5% of all cases of extremity ischemia.⁶⁴ In contrast to lower extremity ischemia, ischemia in the upper extremity may be caused by a variety of systemic diseases (Tables 17-7 and 17-8). Upper extremity disease can often be diagnosed using noninvasive diagnostic tests.