Peripheral arterial evaluation


On completion of this chapter, you should be able to:

  • Describe the anatomy encountered during a venous duplex imaging examination

  • Understand arterial physiology as it relates to the development of peripheral arterial disease

  • Recognize the risk factors associated with peripheral arterial disease

  • Discuss the changes that occur to segmental pressures and pulse volume waveforms in the presence of occlusive arterial disease

  • Outline the proper instrument control settings used during arterial duplex imaging

  • Describe the characteristics of arterial spectral Doppler signals obtained during arterial duplex imaging

  • Discuss the imaging characteristics associated with arterial narrowing

The noninvasive evaluation of patients with peripheral arterial disease (PAD) has evolved greatly. With today’s sophisticated technology, sonographic examinations can provide both an anatomic and a physiologic evaluation of patients presenting with symptoms of PAD. Capabilities have advanced from simple oscillometric measurements to segmental pressures, pulse volume recordings, stress testing, and direct evaluation of arteries and associated surgical interventions by duplex imaging. Originally, noninvasive testing was used to offer objectivity in the diagnosis of arterial disease. Recently indications have been expanded, and the current noninvasive evaluation is tailored to patients’ specific needs, depending on their clinical presentation and the suspected pathology.

PAD affects an estimated 12 million people in the United States and approximately 20% of individuals 55 or older. , This results in 750,000 office visits and 63,000 hospitalizations annually. PAD can present with a wide variety of symptoms, as well as remain asymptomatic, even in patients with advanced stages. Therefore the physical examination alone has poor sensitivity and specificity. Thus the noninvasive arterial evaluation complements a patient history and physical examination, as the detection of PAD has been reported in up to 3 times as many individuals using noninvasive testing compared with self-reported symptoms.

The noninvasive arterial examination is an important component in the evaluation of a patient with signs and symptoms of arterial occlusive disease. Although not required for diagnosis, noninvasive arterial testing is valuable to many patients and their physicians, as it can confirm a PAD diagnosis, stage disease severity, and be used to longitudinally evaluate disease progression ( Box 39-1 ).

BOX 39-1

Purposes of Noninvasive Arterial Testing

  • Provide objective documentation of the severity of the arterial disease

  • Aid in diagnosis of exercise-induced pain caused by occlusive arterial disease

  • Supplement clinical judgment regarding healing of foot ulcers and amputation sites

  • Evaluate pulsatile masses (aneurysms, pseudoaneurysms)

  • Evaluate suspected arterial trauma

  • Evaluate surrounding arterial anatomy

  • Evaluate angioplasty/stent placement (planning and follow-up)

  • Serve as a baseline study before operative reconstruction

  • Provide postoperative follow-up, including bypass and dialysis graft surveillance

Noninvasive arterial testing is made up of two different types of ultrasound technology: (1) indirect and (2) direct testing or duplex imaging. Although indirect tests and peripheral arterial duplex imaging are discussed separately in this chapter, a combination of tests is typically indicated, depending on the patient and the clinical presentation. By combining the two types of testing, a better, more holistic representation of the disease can be made.

Anatomy associated with peripheral arterial testing

The peripheral arterial system is made up of arteries, arterioles, and capillaries in the most distal portion. The main function of the arterial system is to transport oxygen-rich blood from the heart to the organs and tissues throughout the body. After exiting the left ventricle of the heart, blood travels through the central arteries until it reaches the arteries of the periphery. The peripheral arteries are located in the upper and lower extremities and transport blood to the microcirculation of the arterial system, made up of the arterioles and capillaries. After the capillaries, blood exits the arterial system and enters the venous system for its return to the heart.

The wall of an artery consists of three layers: (1) tunica intima (innermost), (2) tunica media (middle), and (3) tunica adventitia (outermost). The tunica media layer primarily consists of smooth muscle and connective tissue and provides the vessel with structure and support.

Lower extremity

The descending aorta is the continuation of the aorta beyond the aortic arch. The descending aorta is divided into a thoracic and an abdominal section. The thoracic portion terminates at the aortic opening in the diaphragm, where the abdominal aorta begins at the approximate level of the twelfth thoracic vertebra as it passes through the aortic hiatus of the diaphragm. At the approximate level of the fourth lumbar vertebra, the abdominal aorta bifurcates to become the right and left common iliac arteries ( Figure 39-1 ). Each common iliac artery bifurcates into an internal iliac artery (hypogastric artery), which perfuses the pelvis, and an external iliac artery, which continues distally to supply blood to the lower extremity. The external iliac artery terminates at the level of inguinal ligament, where it becomes the common femoral artery.


​The arteries of the lower extremity.

The common femoral artery (CFA) originates beneath the inguinal ligament and travels distally with the common femoral vein. In the distal portion of the groin, the CFA bifurcates into the femoral and profunda femoris (deep femoral) arteries. The profunda femoris artery is located posterior and lateral to the femoral artery. It begins at the CFA bifurcation and terminates in the lower third of the thigh. The profunda femoris artery travels deep within the leg in close associate with the profunda femoris vein and supplies blood to the muscles of the thigh and the hip. The femoral artery (FA) originates from the common femoral artery bifurcation and travels through the adductor (Hunter’s) canal, and continues along the length of the medial thigh in close proximity to the femoral vein. The proximal FA is superficial, but it dives deep in the distal portion of the thigh. The FA terminates at the opening of the adductor magnus muscle, at which point it becomes the popliteal artery. The popliteal artery travels behind the knee in the popliteal fossa with the popliteal vein. Major branches of the popliteal artery are the sural and genicular arteries. The popliteal artery terminates distally into the anterior tibial artery and the tibioperoneal trunk.

The anterior tibial artery (ATA) arises from the popliteal artery in the proximal calf and travels distally along the lateral calf, into the anterior compartment of the ankle. At this level it courses superficially and becomes the dorsalis pedis artery. The dorsalis pedis artery (DPA) is located on the dorsal foot. At its distal portion, the DPA joins with branches of the posterior tibial artery to form the plantar arch. Arising off the plantar arch are the metatarsal arteries that divide into the digital branch arteries.

The tibial-peroneal trunk (tibial-fibular trunk) begins in the proximal calf from the bifurcation of the popliteal artery. The tibial-peroneal trunk briefly travels distal until its bifurcation into the posterior tibial artery and the peroneal artery. The posterior tibial artery (PTA) travels down the medial calf in the posterior compartment, parallel to the posterior tibial veins. The PTA terminates between the ankle and the heel into the medial and lateral plantar arteries. The peroneal artery is located deep within the calf and travels with the peroneal veins near the medial aspect of the fibula, parallel and deep to the PTA. The peroneal artery terminates in the distal third portion of the calf. Its branches communicate with branches of the PTA and ATA.

Upper extremity

The ascending aorta originates from the left ventricle. The transverse aortic arch is located in the superior mediastinum and is formed as the aorta ascends and curves posteroinferiorly from right to left, superior to the left mainstem bronchus. Three main branches arise from the superior convexity of the arch in its normal configuration. The first branch is the innominate artery (brachiocephalic), which divides into the right subclavian and the right common carotid artery. Next, the left common carotid artery arises, followed by the left subclavian artery ( Figure 39-2 ).


​The arteries of the upper extremity.

The subclavian artery originates at the inner border of the scalenus anterior muscle in close proximity to the subclavian vein, and travels beneath the clavicle to the outer border of the first rib. Here it becomes the axillary artery. Major branches of the subclavian artery are the vertebral artery, thyrocervical trunk, costocervical trunk, internal mammary, and dorsal scapular artery. The axillary artery is a continuation of the subclavian artery, which begins at the outer border of the first rib and travels through the axilla in close association with the axillary vein. The axillary artery terminates at the lower border of the tendon of the teres major muscle where it becomes the brachial artery. The brachial artery travels close and parallel to the paired brachial veins along medial portion of the upper arm. The brachial artery typically terminates just below the antecubital fossa into the radial and ulnar arteries, but anatomic variations in this area are common.

The radial artery begins at the brachial artery bifurcation and travels distally along the lateral forearm. At the level of the palm, the radial artery terminates to form the deep palmar arch. The ulnar artery originates at the brachial artery bifurcation and travels distally along the medial forearm. At the level of the palm, the ulnar artery terminates to form the superficial palmar arch. Both palmar arches supply blood to the digital arteries.

Arterial physiology

The arterial portion of the circulatory system functions to transport oxygenated, nutrient-rich blood from the heart to the various organs and tissues of the body. On cardiac contraction, the left ventricle ejects a stroke volume of arterial blood into the arterial system. This is done under a large amount of pressure, providing the blood within the arterial system with a large amount kinetic energy. Therefore the arterial system is characterized as a closed, high-pressure system. Being a closed system preserves the amount of kinetic energy the blood possesses, allowing it to travel far distances within the arterial system quickly and efficiently.

In general, artery diameter size decreases the farther it is located in the periphery. The diameter of an artery influences the way in which the blood flows within it, as diameter has the greatest effect on vessel flow volume. The diameter of an artery and the resistance that is placed on the blood within it are inversely related. Therefore as the diameter of an artery decreases, arterial resistance increases. To this end, in circumstances in which a constant blood flow volume exists, a decrease in artery diameter will result in an increase in arterial blood flow velocity, as conveyed by Bernoulli’s principle (velocity = flow/area). Blood flow velocity is represented as peak systolic velocity (PSV) and end-diastolic velocity (EDV), typically measured in centimeters per second (cm/sec). Arterial PSV increases can be used for the detection of arterial pathology. Arterial occlusive disorders, such as PAD, cause a reduction in arterial lumen, which in turn causes PSV to rise. Detection of a PSV increase can then be used to diagnose, stage, and categorize arterial diseases. This is a main principle on which noninvasive testing relies. Measuring true lumen diameter, and comparing it to the diameter of the residual lumen, can also be used for the detection of arterial disease. This is known as a diameter reduction measurement.

Arterial pathophysiology

PAD and other occlusive disorders are characterized by a reduction in arterial lumen diameter. This reduction causes an increase in arterial resistance and does not allow the optimal blood volume to flow through that segment(s) of the vessel. The result is an inadequate supply of arterial blood to the muscles and/or tissues of the body. When in use, muscle tissue requires a higher level of arterial perfusion to meet its increased oxygen demand. Therefore using muscles that are perfused by an artery that is affected by PAD will cause symptoms arising from muscle tissue oxygen deficiency to be experienced. This is common in the lower extremities, as muscles require an increase in perfusion during ambulation. The inability to receive the extra arterial blood required for muscle use is known as intermittent claudication. Intermittent claudication is characterized by muscle cramps during ambulation, which subside on rest. In more severe circumstances, arterial perfusion is diminished to the point at which it can no longer meet the oxygen demands of tissues, even while at rest. This results in tissue ischemia and death, which may present as tissue ulceration or gangrene.

Atherosclerosis is the primary disease process that leads to PAD. Atherosclerosis is characterized by the buildup of atherosclerotic plaque on the arterial endothelium as a result of excess lipids in the blood. Over time the plaque hardens, while continual buildup reduces the lumen area. Atherosclerosis can also cause an arterial embolism, which can occur when plaque dislodges from the arterial wall, and propagates distally in the arterial system. The embolism can travel to the brain and cause a stroke, or travel to the extremities where it may occlude small vessels, causing ischemia.

Peripheral arterial disease


​Treatment methods for PAD aim to decrease patient symptoms and improve prognosis by preventing the risk of further cardiovascular events. Treatments can be categorized into three types: (1) medical management/conservative, (2) endovascular, and (3) surgical.

Conservative treatments first aim to reduce controllable risk factors for PAD, such as tobacco use and poor diet, through lifestyle modification. Exercise is also recommended, as increases in walking ability ranging from 50% to 200% have been reported. Medical management can also be implemented using pharmacologic agents, but this generally results in only mild to moderate improvement of symptoms. Common types of agents prescribed are anticoagulants, antiplatelets, antihypertensives, and lipid-lowering agents.

Endovascular treatments aim to revascularize the limbs of individuals of patients with PAD. Endovascular procedures are becoming a popular treatment strategy, as this technique is much less invasive than other surgical options. In this technique a catheter is introduced into the arterial system, typically the femoral artery at the groin, and is advanced to the atherosclerotic lesion, where a variety of revascularization methods can be performed. Common types of endovascular revascularization interventions are percutaneous transluminal angioplasty (increases artery diameter in cases of focal lesions), endograft placements (for aneurysm repair), atherectomy (removes plaque), and thrombin injections (for pseudoaneurysm treatment). Although the long-term effects of endovascular revascularizations are debated, it is typically attempted initially, followed by surgical intervention in case of failure.

Surgical interventions, like endovascular interventions, mainly focus to revascularize the afflicted limb, but are typically more invasive. The most common vascular surgical intervention is bypass graft surgery, which aims to create a new arterial conduit, providing blood flow with an alternative route. This conduit is typically anastomosed with the affected artery proximal, and distal to the atherosclerotic lesion. A variety of bypass graft types can be used, ranging from native vessels to synthetic materials. Other common vascular surgical interventions aimed at revascularization are thrombectomy (removal of a thrombus or embolus) and endarterectomy (surgical removal of plaque and the intima and media layers of an artery). In severe cases of PAD, vascular surgeries aimed at preventing disease progression may be necessary. The most common form of this is limb amputation.

It is important for sonographers practicing arterial imaging to understand the different vascular treatment strategies. Familiarization with different types of medical management may aid while obtaining patient histories. Furthermore, many of the aforementioned endovascular surgical interventions, such as percutaneous angioplasty, thrombin injections, and some bypass graft placements, are performed under ultrasound guidance. If needed, the sonographer may be asked to assist in these surgeries and perform the ultrasound guidance imaging. If this occurs, an understanding of the surgery, and why it is being performed, will aid in providing the vascular surgeon with accurate and relevant information.

Risk factors and symptoms of peripheral arterial disease.

​Several risk factors have been associated with peripheral occlusive arterial disease, some of which are controllable and others uncontrollable. Controllable risk factors include diabetes mellitus, hyperlipidemia, hypertension, tobacco use, and poor diet. Uncontrollable risk factors include increasing age, genetic predisposition (family history of atherosclerosis), documented atherosclerosis in the coronary and/or carotid system, gender (males at a higher risk than females), and thrombophilia.

Symptoms of lower extremity occlusive arterial disease include claudication and rest pain. Claudication is defined as walking-induced muscular discomfort of the calf, thigh, hip, or buttock, due to ischemia caused by the lack of arterial muscle perfusion. Most patients describe claudication as a cramping or aching in the muscles of their legs as they walk or exercise, which is relieved by resting for approximately 2 to 5 minutes. As PAD progresses, the distance afflicted individuals are able to walk before the onset of symptoms decreases. In more severe cases, perfusion is so diminished that muscles are unable to obtain an adequate amount of oxygenated blood even when they are not being used. This is known as rest pain. Further disease progression from this point can result in tissue loss, ulceration, gangrene, and critical limb ischemia, leading to limb amputation.

Over a 5-year period, one study reported that only 1% to 2% of individuals presenting with PAD developed critical limb ischemia or required amputation. Furthermore, in the first year of the same study, just 3% of individuals developed critical limb ischemia. However, PAD pathophysiologic processes caused a decreased quality of life and mobility loss.

Ischemic rest pain points to critical ischemia of the distal limb. Typical patient complaints include discomfort in the toes while lying down, which often awakens them from sleep, with relief found by placing the affected limb in a dependent position. This permits gravity to assist in delivering blood flow to the foot.

Physical signs of peripheral occlusive arterial disease are elevation pallor, dependent rubor, ischemic ulcers, gangrene, bruits, and decreased peripheral pulses (femoral, popliteal, dorsalis pedis, posterior tibial, axillary, brachial, radial, and ulnar). Pulses are compared with the contralateral side and are graded on a scale from 0 to 3+; 0 = no pulse, 1+ = questionable pulse, 2+ = weak pulse, and 3+ = normal pulse. Additional physical findings include a decrease in temperature (poikilothermia), loss of skin integrity, and/or hair loss at the affected site.

In the acute stages of arterial occlusion or arterial occlusive disease, common manifestations include pain, pallor, decreased peripheral pulses, paresthesias, paralysis, and a localized decrease in skin temperature.

Indirect (physiologic) arterial testing

Segmental doppler pressures

The objective of segmental Doppler testing is to obtain systolic blood pressures at different levels of the extremities. This provides a quantitative value that offers physiologic information of the segment of the vessel from which it is obtained. Comparison of pressures can be with others obtained at different segments (levels) within the ipsilateral or contralateral limb, to determine disease severity and relative location. Segmental Doppler pressures are often repeated longitudinally to provide information regarding disease progression. This testing also serves to differentiate arterial disease from other disorders, such as neurologic or musculoskeletal disease, as these symptoms often overlap.

Before beginning the examination, the patient should rest for 15 minutes to allow the blood pressure to stabilize and legs to recover from walking to the examination room. During this time, the patient’s chart can be reviewed and history obtained. The patient’s history should focus on risk factors of PAD, documenting current severity and location of symptoms, and a history of any previous arterial testing, diagnoses, or interventions. Knowledge of prior vascular intervention is imperative, as pressure cuffs should not be placed over graft or stent placements.

Segmental pressures are obtained with the patient in the supine position, with the legs at the same level as the heart. This prevents hydrostatic pressure (gravity-induced) artifact. While performing segmental pressure testing on the lower extremities, blood pressure cuffs are placed bilaterally on the upper arm (brachial pressure), proximal thigh, low thigh (above the knee), calf (below the knee), and ankle just above the medial malleoli. Using a flow detector (continuous wave Doppler transducer), an audible and visual Doppler waveform is obtained at the level of the ankle. Ankle pressures are obtained in the posterior tibial artery and dorsalis pedis artery. Proximal thigh, low thigh, and calf pressures are then recorded using the strongest distal Doppler signal (posterior tibial artery or dorsalis pedis artery). This is done bilaterally.

To accurately obtain a systolic pressure measurement, each cuff is independently inflated from 20 to 30 mm Hg above systolic pressure, and then slowly deflated. As cuff pressure decreases, the systolic pressure recorded at that cuff location is the pressure at which the audible and/or visual arterial Doppler signal returns. If no distal Doppler signals are noted (no measurable blood flow or occlusion of the distal vessels), thigh pressures are obtained using the Doppler signal from the popliteal artery.

A continuous wave (CW) Doppler instrument is used to perform segmental limb pressures. An 8-MHz CW transducer can be used for most patients. If the Doppler signal is attenuated due to vessel depth, a 4-MHz CW transducer may be necessary to improve penetration. A generous amount of ultrasound gel should be used to ensure good transducer-to-skin contact. The CW transducer should insonate at an angle of 45 to 60 degrees to provide optimal Doppler signals. Transducer pressure applied to the skin must maintain good contact but cannot be excessive, as it may obliterate the Doppler signal.

To obtain pressures comparable with direct intraarterial measurements, the blood pressure cuff must have a width 20% greater than the diameter of the limb. The cuff should fit snug, but not too tight as to occlude the artery being investigated. It is also important that the bladder of the cuff be placed directly over the artery to ensure its accurate compression. In situations where the width of the cuff is small compared with the girth of the limb, the pressure in the cuff may not be completely transmitted to the arteries, resulting in falsely elevated values. Therefore falsely elevated pressures may exist in obese patients. Conversely, proximal thigh pressures may be falsely decreased in extremely thin patients, as the pressure cuff may be too large. The cuff-to-limb ratio should be kept in mind when the patient’s legs are abnormally large or small.

In a healthy individual, pressure measurements will increase from the ankle to the proximal thigh because of the relationship between constant cuff width and the increase in limb size. Blood pressure cuffs with bladders that measure 12 × 40 cm should be used to obtain ankle and calf pressures, whereas cuffs with longer bladders (12 × 55 cm) should be used for proximal and distal thigh pressures. This may vary depending on institutional protocol.

After all lower extremity pressures are obtained bilaterally, brachial pressures are obtained in both arms, using a Doppler signal from the brachial artery at the antecubital fossa. If a difference of ≥20 mm Hg occurs between arms, an arterial obstruction of the innominate, subclavian, axillary, or proximal brachial artery is suspected on the side with the lower systolic pressure. In the absence of this discrepancy (a healthy subclavian artery is assumed), brachial pressures provide a baseline measure with which lower extremity pressures can be compared.

The proximal thigh pressure should be at least 30 mm Hg greater than the brachial pressure. This is due to cuff size artifact rather than an actual increase in intraarterial pressure. A proximal thigh pressure equal to or less than the brachial pressures suggest disease at or proximal to the femoral artery. While comparing pressure measurements within a limb, there should be no more than a 20 mm Hg pressure gradient between adjacent segments. If a 20 mm Hg pressure gradient between adjacent cuff placements does occur, the limb is abnormal and indicates intercurrent disease. A significant pressure gradient (20 mm Hg) between the proximal and distal thigh cuffs suggests disease of the femoral artery. Disease of the distal femoral artery, the popliteal artery, or both is suspected if a significant pressure gradient is present between the low thigh and calf. Disease of the tibial arteries is suspected if a 20 mm Hg pressure gradient is present between the calf and ankle. Similarly, pressure measurements obtained at the same level in the contralateral limb also should not differ by more than 20 mm Hg. Like brachial pressures, a 20 mm Hg discrepancy is suggestive of arterial disease at or proximal to the segment with the lower systolic pressure. When interpreting segmental pressures, it may be difficult to localize disease when multilevel pathology is present. Proximal arterial obstruction or stenosis can cause a significant pressure gradient that may mask distal disease. Additionally, segmental pressure gradients are unable to distinguish between a stenosis and an occlusion.

Because systemic pressures vary by the individual, and from examination to examination, absolute pressures are not used to categorize or monitor disease progression. Instead, all pressures are divided by the highest brachial pressure and expressed as a ratio. This is known as the pressure index (PI). Although PIs are reported at each level that pressures are obtained, the most commonly used are those obtained at the level of the ankle (from the posterior tibial artery or dorsalis pedis artery). This is known as the ankle-brachial index (ABI), and it is one of the most commonly ordered segmental pressure examination.

In 2013 the American College of Cardiology and the American Heart Association published standardized guidelines for the interpretation of ABI studies. Normal ABI results range from 1.00 to 1.40. Noncompressiblity of vessels, due to calcification, is defined as ABI greater than 1.40. , , Although this finding is not able to accurately assess limb perfusion, it is associated with an increased risk of a cardiovascular event. ABI values between 0.91 and 0.99 are considered borderline. If borderline ABI values are found in a patient in with suspected PAD, further testing is warranted. ABI values ≤0.90 are abnormal and suggestive of disease. This is the most commonly used ABI threshold for PAD detection, which has been found to have a sensitivity and specificity of greater than 90%. , The value of the ABI correlates to disease severity, with a high risk of amputation when ABI values are less than 0.50. ABI values can be divided into four main categories representative of patient symptoms ( Table 39-1 ). Most patients’ clinical symptoms and their ABIs fit into these four categories, but there tends to be some overlap between groups. While conducting longitudinal ABI monitoring, it has been reported that a decrease in ABI values of greater than 0.15 is significant and is suggestive of PAD progression.

TABLE 39-1

Interpretation of Ankle-Brachial Pressure Index (ABI)

Clinical Presentation Ankle-Brachial Index
Normal >0.90
Claudication 0.50–0.89
Rest pain 0.21–0.49
Tissue loss <0.21

Modest variability in measuring ankle pressures is likely to be associated with normal patient or observer variability. The importance of body temperature in recording ABIs in claudicators has been demonstrated. Variability in the ankle pressure index was documented as being higher after body cooling (0.79 ± 0.04) than during routine testing (0.69 ± 0.03) or after warming (0.65 ± 0.04).

As mentioned previously, lower extremity pressures may be falsely elevated because of medial calcinosis and/or medial sclerosis, causing the artery to become noncompressible during pressure measurements. This is suspected when pressure indices exceed 1.40, and is most commonly seen in the diabetic population. , , In these situations, toe pressures and pulse volume recordings provide particularly valuable additional information for the evaluation of the patient’s ischemia, as these tests are not affected by a noncompliant arterial wall.

Alternative to the four-cuff method of performing lower extremity segmental pressures, a three-cuff method may also be used. This is done in the same way as the four-cuff technique, but only one blood pressure cuff is used in the thigh. This method requires less time, as one less pressure measure is required. However, it is not able to differentiate between inflow disease and femoral artery disease, as it provides only one thigh pressure. For this reason it is not as commonly used as the four-cuff technique.

Segmental pressure measurements in the lower extremity tend to underestimate the extent of the disease. Reasons for underestimation include the following: (1) narrowing of the arterial lumen must be significant enough to cause a pressure change (not able to detect very mild disease), (2) proximal disease may mask distal disease, and (3) calcified vessels may falsely elevate the pressures recorded. The purpose of indirect testing, however, is to provide information regarding the overall hemodynamics of the limb, instead of the status of an individual vessel. Vessel-specific information is obtained using direct (duplex imaging) testing. Therefore the data provided by pressure measurements during indirect testing are used in combination with findings from direct testing to provide a holistic representation of extremity perfusion.

Segmental pressure testing can also be performed in the upper extremity, but it is uncommon. Arterial disease in the upper extremity does not occur as often as in the lower extremity, although problems of stenosis and/or obstruction of the inflow arteries (innominate, subclavian) can occur. Arterial embolization (cardiac origin) is another reason for upper extremity testing. Small emboli from atrial fibrillation or aortic valve disease can cause ischemic reactions in the fingers and hands. Upper extremity segmental pressures are performed using three blood pressure cuffs, one each on the upper arm, forearm, and wrist. Upper arm pressures are obtained with the CW transducer on the brachial artery. Forearm and wrist pressures are obtained using the distal radial or ulnar artery. Just as in the lower extremity, pressures are obtained bilaterally, with a pressure gradient of greater than 20 mm Hg between adjacent or contralateral segments being suggestive of disease.

Arterial stress testing

In individuals without occlusive arterial disease, blood perfusion will increase to muscles that are being used during exercise to meet their elevated oxygen demands. This is facilitated by a decrease in peripheral vascular resistance. However, in individuals suffering from intermittent claudication, the increased perfusion to the muscles used for ambulation needed during exercise is not achieved. Yet these individuals may experience no symptoms while at rest (normal resting ABIs) because their resting systolic pressure is sufficient to meet muscle tissue oxygen demands while they are not in use. An alternative explanation could also be that collateral vessels have formed that are able to meet resting level oxygen demands, but may not be able to sufficiently meet elevated oxygen demands. These patients should be stressed with exercise testing in an attempt to reduce peripheral resistance, thereby increasing the pressure gradient across the arterial segment and unmasking a hemodynamically significant lesion. The goal of this type of testing is to induce claudication symptoms, so that a determination of PAD severity can be made.

Contraindications to lower extremity arterial stress testing include forms of cardiac disease, severe pulmonary disease, severe hypertension, inability to walk on the treadmill, and in cases of calcified vessels (unreliable pressure measurements; the use of pulse volume recordings may be helpful in some patients). If the patient is unable to safely use a treadmill, the patient may perform calf raises as an alternative method to induce claudication symptoms.

Arterial stress testing begins by first obtaining brachial and ankle pressures at rest, bilaterally. The cuffs are then left in place as exercise testing is performed on a treadmill at 1.5 to 2 miles per hour on a 10% to 12% grade (this may vary by institution and should be documented to ensure appropriate testing reproducibility and comparison). After walking for 5 minutes, or until symptoms develop and prevent further exercise, brachial and ankle pressures are quickly taken. A brachial pressure is obtained unilaterally on the side that demonstrated the higher resting pressure. Ankle pressures are obtained bilaterally using the artery (posterior tibial or dorsalis pedis) that demonstrated the highest resting pressure in each limb. (This means that the posterior tibial artery may be used in one limb while the dorsalis pedis artery is used on the other.) In total, this yields three locations at which postexercise pressures are recorded. These pressures should be obtained within 2 minutes following exercise and then repeated every 2 minutes for 10 minutes, or until pressure values return to baseline (resting). The time it takes for the onset of symptoms during exercise, symptom location, total walking time, and the pressure values obtained at each location and time point are documented and used to monitor changes in an individual on repeat examination.

The magnitude of ankle pressure decrease following exercise and the time required for the ankle pressure to return to baseline reflect the severity of the underlying arterial disease. In general, ankle pressures that fall after exercise and return to baseline within 5 minutes are suggestive of single-segment occlusive disease. Multisegment arterial disease is usually associated with reduced ankle pressures that persist for longer than 10 minutes after exercise. If ankle pressures are unchanged or are improved (elevated) after exercise, underlying arterial disease (even if present) can be excluded as a cause of the patient’s symptoms.

Digit pressures

Toe pressures are a more accurate method of evaluating distal limb and foot perfusion in individuals with falsely elevated limb pressures. Toe pressures may also be used to determine whether there is obstructive disease involving the pedal arch and digital arteries. A digital cuff is placed at the base of the hallux (big toe), and its blood pressure is obtained by placing a photoplethysmography sensor on the distal portion of the toe. Similar to the ankle-brachial index, a toe-brachial index (TBI) is reported. A toe pressure is commonly accepted as normal with a TBI ≥0.80. However, one review of the literature has found a TBI value of 0.71 as the lower limit of normal to demonstrates high levels of sensitivity (90% to 100%) and specificity (65% to 100%).

Plethysmography testing

Two types of plethysmography testing are typically used for indirect testing of the peripheral arterial system: pulse volume recordings and photoplethysmography. These are typically used in conjunction with other indirect testing measures, such as segmental pressures. Although this form of testing does not directly measure blood pressure within the limb, it does provide valuable information regarding overall limb perfusion, allowing for a more accurate representation of disease.

Pulse volume recordings.

​Pneumoplethysmography, more commonly known as pulse volume recording (PVR), is used to measure changes in segmental limb volume that occur with each cardiac cycle. This can be performed in the upper or lower extremity. PVRs are obtained using blood pressure cuffs and are therefore often obtained at the same levels as segmental pressure testing. Each cuff is independently inflated between 20 and 30 mm Hg above systolic pressure and slowly deflated. As the cuff deflates, changes in limb volume are represented visually as a PVR waveform. These waveforms are interpreted qualitatively, with a normal waveform demonstrating a rapid rise (acceleration) to a sharp peak during systole, followed by a slower fall (deceleration) during diastole ( Figure 39-3 ). The downslope of a normal PVR waveform contains a dicrotic notch that reflects the brief period of retrograde flow that occurs in arteries during diastole.

May 29, 2019 | Posted by in ULTRASONOGRAPHY | Comments Off on Peripheral arterial evaluation
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