Number of Credits: 1 CME Credit
Marsha M. Neumyer, BS, RVT, FSDMS, FSVU, FAIUM
Vascular Diagnostic Educational Services
The Institute for Advanced Medical Education is accredited by the Accreditation Council for Continuing Medical Education (ACCME) to provide continuing medical education for physicians.
The Institute for Advanced Medical Education designates this enduring material for a maximum of 1 AMA PRA Category 1 Credits™. Physicians should only claim credit commensurate with the extent of their participation in the activity.
These credits are accepted by the American Registry for Diagnostic Medical Sonography (ARDMS).
For information on applicability and acceptance of continuing education credit for this activity, please consult your professional licensing board or other credentialing organization.
Physicians, sonographers and others who perform and/or interpret vascular ultrasound.
In order to complete this program you must have a computer with a recent browser version. You must also have the capability to display and print PDF files in order to view and print out your certificate. (Note: Your CME certificate is stored in your account and is available at any time.)
For any questions or problems concerning this program or for problems related to the printing of the certificate, please contact IAME at 802-824-4433 or firstname.lastname@example.org.
This activity is designed to be completed within the time designated. To successfully earn credit, participants must complete the activity during the valid credit period. To receive AMA PRA Category 1 Credit™, you must receive a minimum score of 70% on the post-test.
Follow these steps to earn CME credit:
Your CME credits will be archived in the account you create and can be accessed at any time.
Estimated Time for Completion: approximately 1 hour
Date of Release and Review: January 31, 2013; February 19, 2016
Expiration Date: February 28, 2019
In compliance with the Essentials and Standards of the ACCME, the author of this CME tutorial is required to disclose any significant financial or other relationships they may have commercial interests.
Marsha Neumyer discloses a relationship with Unetixs Vascular, Inc as consultant and member of the Speaker’s Bureau.
No one at IAME who had control over the planning or content of this activity has relationships with commercial interests.
Atherosclerosis is recognized as a major cause of systemic arterial disease which quite often leads to critical sequelae including stroke, heart attack and limb loss. With respect to the peripheral arterial system, it has been estimated that more than 9 million people in the United States alone have stenosis or occlusion of one or more of their lower limb arteries. While many of those with arterial blockage have symptoms as a consequence of flow-limiting disease, surprisingly the majority will remain asymptomatic. It must be recognized that the absence of symptoms does not preclude future risk for compromised ambulation, arterial ulceration, and the need for revascularization.1,2 As such, it is important to define test procedures that are capable of detecting and localizing arterial disease, confirming the presence of flow-limiting lesions, determining the potential for healing, and distinguishing patients who may benefit from medical therapy alone from those who require intervention for limb salvage.
Historically, clinicians have used digital subtraction angiography (DSA), three-dimensional magnetic resonance angiography, or computed tomographic angiography for confirmation of arterial disease affecting the lower limb and for planning reconstructive surgery or endovascular procedures. While the benefits and limitations of each of these imaging technologies have been well defined, it must be recognized that none are capable of accurately detailing the functional impact of pressure-flow reducing lesions on tissue perfusion.
More than half a century ago, investigators demonstrated that significant pressure and flow gradients developed distal to obstructions that narrowed the diameter of an artery by more than 50%-60%. Based on this knowledge they applied a variety of diagnostic tools to document the physiologic alterations in pressure and flow that are associated with hemodynamically significant arterial disease. While many of the earlier techniques are no longer used, modern vascular laboratories employ indirect, physiologic testing as the primary diagnostic method for confirming the presence of hemodynamically significant lesions and for defining the involved arterial segment(s). These non-imaging studies are often complemented with duplex sonography to precisely localize obstructions and to differentiate stenoses from occlusions.
The following paragraphs describe the instrumentation, technical applications and diagnostic criteria used for indirect, physiologic assessment of peripheral arterial disease.
Systolic pressure normally increases as blood flows from the heart to arteries in the lower extremities.3,4 In contrast, diastolic and mean pressures decrease. The increase in systolic pressure is a consequence of several factors. Among the most important are the effects of energy loss associated with arterial branching and the difference in wall compliance and vessel diameter when the aorta is compared to the small caliber limb arteries. It is also important to remember that resting muscle requires only sufficient blood flow to satisfy its metabolic needs. Therefore, in the absence of a flow demand created by significant arterial obstruction or exercise, the resistance to arterial inflow to the muscular beds of the resting lower limb is elevated and, as a consequence, ankle systolic blood pressures are normally equal to or greater than the central aortic pressure measured at brachial level. Given this, a decrease in ankle pressure compared to brachial pressure signifies the presence of pressure-reducing obstruction in the more proximal arteries of the lower limb. This hemodynamic feature allows for a simple, accurate, rapid means for detecting the presence of lower limb arterial disease that is also predictive of disease severity.
Tibial and brachial artery pressures are measured using pneumatic cuffs, a sphygmomanometer, and a tool for sensing arterial flow distal to the cuff. It has been shown in multiple studies that accurate measurement of limb systolic pressures is achieved when care is taken to ensure that the width of the pneumatic cuff bladder exceeds the diameter of the limb segment beneath the cuff by at least 20% .9 Use of narrower cuffs will result in artifactual elevation of the measured arterial pressure. While some laboratories may employ photoplethysmography or pulsed Doppler as tools for sensing arterial flow, most commonly, continuous wave (CW) Doppler is used to ensure a complete and accurate examination.
The brachial systolic pressure is measured by placing an appropriately-sized blood pressure cuff around the upper arm. Using a CW Doppler probe, an arterial signal is recorded in any non-diseased artery distal to the cuff. The brachial artery is most commonly used as the recording site as it is easily accessible and provides a brisk, audible signal. The blood pressure cuff is inflated to suprasystolic pressure. This results in transient occlusion of the brachial artery and loss of the audible arterial signal. The cuff is then slowly deflated until the arterial signal is again noted, signifying the opening pressure of the artery. It is important to use a deflation rate of only 2-3 mmHg per second as a faster rate may result in underestimation of the opening pressure. The study is repeated using the contralateral brachial artery. The higher of the two arm pressures will be used in calculation of the ankle-brachial index (ABI). While brachial systolic pressures may be identical, there is often a side-to-side pressure difference. Arterial inflow obstruction (subclavian, axillary, and/or brachial artery) should be suspected in patients with a brachial systolic pressure gradient exceeding 20 mmHg.
The systolic pressure is next measured in the dorsalis pedis (DP) artery by applying an appropriate-sized blood pressure cuff around the ankle. The arterial signal in the DP artery is recorded using a CW Doppler probe. Cuff inflation and deflation are performed in a manner identical to that used for measurement of the brachial systolic pressure. The procedure is repeated using the posterior tibial (PT) artery as the target vessel (Figure 1 A and B). The process is repeated on the contralateral side. The pressures in both the DP and PT are retained for calculation of the ankle-brachial index.
The ankle-brachial index (alternatively called the ankle-arm index) is calculated as a ratio of the higher of the two ankle systolic pressures to the higher of the two brachial systolic pressures (Figure 2). Because the ankle pressures normally equal or exceed the brachial pressure, the ankle-brachial index should be equal to or greater than 1.0. Error may be introduced if the brachial pressure exceeds 200 mmHg or the ABI is greater than 1.3 as a result of medial calcinosis of the tibial arteries.
Figure 2. Diagram illustrating brachial and tibial artery pressures and the calculated ankle-brachial index (ABI). Note that the ABI on each side is obtained by dividing the higher of the two tibial pressures by the highest brachial pressure.
Rather than measuring specific pressures in the DP and PT, some investigators prefer to obtain a global ankle pressure. This can be achieved by placing a photoplethysmographic sensor (PPG) on the great toe and recording the arterial signal from the digital cutaneous circulation (Figure 3). Photoplethysmography is discussed in a later section.
Figure 3. Technique for recording digital pressures. Note the photoplethysmograph placed directly on the skin and the position of the digital blood pressure cuff.
While this method affords a rapid means for determining the ankle pressure, deficiencies should be noted. Because the foot receives blood flow from the DP, PT, peroneal and collateral circulations, disease isolated to the individual tibial arteries cannot be detected. Proximal arterial disease, inflammation, changes in body temperature, medication and other factors may result in vasoconstriction or vasodilation of the arterial microcirculation. As a consequence, the plethysmographic waveform morphology may be altered- a situation which may potentially impact accurate determination of arterial pressure. It should be noted that the current reimbursement mandates require documentation of pressures and waveforms recordings from both the dorsalis pedis and posterior tibial arteries.
As noted, ankle systolic pressure normally equals or exceeds the brachial systolic pressure. A normal ankle-brachial index, therefore, exceeds 1.0 with a mean value of 1.11+/- 0.10.10 As such, the ABI is the procedure of choice for identification of hemodynamically significant arterial disease proximal to the ankle and serves as a reliable indicator of the severity of disease. Given this, determination of the ankle-brachial index should be the initial test in evaluation of a patient suspected of lower limb arterial disease and compared to the clinical presentation. In general, an ABI in the range of 0.5 to 0.8 would most likely be documented in patients presenting with mild to moderate claudication. Patients with rest pain most often have indices less than 0.5 while those with tissue loss commonly have ankle pressures less than 35 mmHg, multi-segmental occlusive disease and an ABI less than 0.3.
Absolute ankle pressures yield valuable diagnostic information. Ischemic rest pain is unlikely in a non-diabetic patient with an absolute ankle pressure > 60 mmHg and in a diabetic patient with an ankle pressure > 80 mmHg but is probable when the ankle pressure is < 40 mmHg. It has been demonstrated in multiple studies that ischemic ulcers are unlikely to heal with an ankle pressure < 40-50 mmHg.
Because of the overlap in ankle pressures, it is important to relate the clinical presentation to the resting pressures and ABI. For example, a patient with a resting ABI exceeding 0.5 but complaints of 50 yard claudication would be best served diagnostically with alternative noninvasive testing (e.g., constant-load treadmill exercise evaluation) to differentiate true vascular claudication from pain associated with other pathology, such as spinal stenosis.
Interpretation of Toe Pressures. In cases where tibial artery systolic pressures cannot be determined due to arterial calcification, systolic pressure in the great toe should be substituted for the tibial pressure and a toe-brachial index (TBI) should be calculated.11 In the absence of flow-limiting proximal atherosclerotic disease, mean toe-brachial indices in normal diabetic and non-diabetic patients are similar because the digital arteries infrequently calcify.
Digital pressure measurement in the great toe requires an appropriately-sized blood pressure cuff (2.5-3.0 cm) and a sensor for arterial flow. Most commonly, photoplethysmographic sensors are used but CW Doppler flow meters may also be employed (Figure 3).
Normally, the great toe pressure approximates 80% of the systemic pressure and a TBI = 0.80 is consistent with the absence of proximal flow-reducing disease.12 As proximal arterial disease increases in severity, toe pressure decreases proportionally and values less than 0.5 signify moderately severe disease.
An index < 0.2 and toe pressures less than 30mmHg are consistent with critical ischemia and poor potential for healing. According to the recommendations of the Trans-Atlantic Intersociety Consensus (TASC) group, an absolute toe pressure less than 30-50 mmHg is consistent with chronic limb ischemia.13 In accordance with this study, toe pressures are best used to predict the absence of chronic limb ischemia rather than to identify its presence.
As previously noted, systolic pressure and flow volume decrease distal to arterial segments where the luminal diameter is narrowed by more than 50%-60% as a result of disease or extrinsic compression. The presence and location of pressure-flow reducing lesions can be detected quite easily using segmental pressure techniques.
Limb systolic pressures are measured segmentally in a manner similar to that used for measurement of the tibial artery pressures taking care to completely occlude arteries beneath the cuff during cuff inflation.
The requirement that the width of the cuff bladder must exceed 20% of the diameter of the limb works well for all limb segments with the exception of the upper thigh. When the diameter of the limb is large in relation to the width of the cuff, the pressure in the cuff bladder may not be transmitted completely to the depth of the arteries in the central part of the thigh. Variation in the girth and shape of the thigh contributes to a range of pressures in both normal patients and those with significant arterial disease. As a consequence, arterial pressure may be over-or underestimated. To overcome this problem and to better differentiate inflow (ilio-femoral) from outflow (femoro-popliteal) obstruction, clinicians have employed blood pressure cuffs that are less than the recommended width for assessment of high thigh pressures
Most often, arterial pressure is measured bilaterally at four levels: high thigh, above knee, below knee and ankle (Figure 4).
Figure 4. Location of the lower limb blood pressure cuffs using a 4-cuff technique. Courtesy of Unetixs Educational Publishing, North Kingstown, RI.
The blood pressure cuffs are inflated to supra-systolic levels at each location beginning at ankle level and progressing cephalad. CW Doppler is used to sense the presence of arterial flow in an artery distal to a cuff. In the absence of proximal occlusive disease, flow is most often recorded in the dorsalis pedis or posterior tibial artery.
Recognizing the potential for errors associated with cuff artifact at high thigh, many laboratories use a single thigh measurement rather than obtaining pressures at both upper and lower thigh. This three-cuff method employs a single broad (19 cm x 40 cm) contoured cuff that encircles the thigh (Figure 5).
Figure 5. Location of lower limb blood pressure cuffs using a 3-cuff technique. Courtesy of Unetixs Educational Publishing, North Kingstown, RI.
Considering that inflation of such a large cuff results in compression of the common femoral, superficial femoral and profunda femoris arteries, it is understandable that the 3-cuff method may cause differentiation of inflow from outflow lesions to be difficult.
Using the four-cuff technique for measuring segmental pressures, and assuming the use of appropriately-sized blood pressure cuffs, the high thigh pressure should exceed the brachial pressure by at least 30 mmHg.15 It is important to note that when a narrow high thigh cuff is used, the thigh pressure will be artifactually elevated and will normally exceed the brachial pressure by at least 40 mmHg. A low high thigh blood pressure signifies arterial compromise proximal to or beneath the high thigh cuff. Pressure-reducing aorto-iliac lesions can be detected by using a calculated high thigh to brachial systolic pressure index. Normally, the thigh-brachial index exceeds 1.2 16 whereas an index between 0.8 and 1.2 signifies a pressure-reducing inflow lesion. An index < 0.8 is commonly associated with iliac artery occlusion.
Similarly, pressure gradients exceeding 20-30 mmHg between cuffs on the same limb are associated with pressure-reducing lesions proximal to the cuff with the lower pressure or beneath the cuffs (Figure 6). Larger pressure gradients are commonly associated with arterial occlusion.
Figure 6. Diagram illustrating a significant pressure gradient across the femoral-popliteal arterial segment on the right. On the left, global perfusion pressure at ankle level is sustained by flow through the posterior tibial, peroneal and collateral channels even though the dorsalis pedis artery is diseased.
In the absence of lower extremity arterial disease, blood should flow symmetrically from the abdominal aorta into the arterial trees of the lower extremities and segmental pressures should be comparable at the same level side-to-side. A pressure difference exceeding 20-30 mmHg compared to the pressure in the contralateral cuff highlights the possibility of hemodynamically significant disease on the side with the lower pressure (Figure 7).
Figure 7. Accurate interpretation of lower extremity segmental pressures is achieved by comparing pressures side-to side as well as vertically. Pressure gradients in excess of 20-30 mmHg signify flow-limiting disease on the side with the lower pressure.
Using the three-cuff technique, a normal thigh pressure should approximate the systemic pressure. Given that the cuff encompasses all the thigh arteries, a decrease in thigh pressure > 30 mmHg compared to the systemic pressure suggests significant disease in the aorto-iliac, ilio-femoral, or femoro-popliteal segment. Quite often, additional testing (e.g.,CW Doppler, duplex sonography) is required to localize the occlusive lesions.
Care must be taken in measuring segmental systolic pressures when the arterial flow rate is so slow that it is difficult to differentiate it from venous flow. In such cases it is helpful to augment the venous flow signal by compressing the limb distally; the arterial signal will either diminish or remain unchanged. In some cases it may be helpful to obliterate the venous flow signal so that the arterial signal becomes more apparent. Potential for pressure measurement error also exists in hypertensive patients who may demonstrate increased pressure gradients and in patients with low cardiac output where the gradient may be lower than expected.
While systolic pressure measurements have shown value for identification of hemodynamically significant lesions in the lower limb, it must be noted that this test defines the segment of the limb where a pressure gradient exists. It does not define the precise site of the lesion(s) nor does it accurately differentiate flow-reducing stenosis from arterial occlusion. Similar pressures may be obtained distal to critical stenoses that are poorly collateralized and arterial occlusions that are well collateralized. Pressure measurements should be avoided in limbs with arterial stents and/or evidence of acute deep or superficial venous thrombosis. Artifactually elevated pressures are quite often obtained in patients with evidence of medial calcification of the peripheral arteries.
Chronic flow-limiting lesions are most commonly associated with exercise-induced limb pain (intermittent claudication). The metabolic demands of exercising muscle require at least a 5-fold increase in limb blood flow volume compared to the resting state. This increase is accomplished through vasodilation of the high resistance collaterals and muscular arterioles which control the distribution of flow to the capillary bed.18 When a significant lesion is present in a lower extremity artery, blood must bypass the obstruction by way of high resistance collateral channels. During exercise the flow rate is increased to meet the muscle demand and a pressure gradient develops across the lesion because the collateral circulation cannot maintain distal perfusion pressures. Pain occurs in the exercising muscle body as a result of inadequate collateral compensatory flow.
Constant-load treadmill exercise testing and measurement of post-exercise ankle pressures have shown value for detection of pressure-flow reducing lesions and determining if the severity of circulatory compromise is consistent with vascular ischemia. There are multiple reasons to consider treadmill exercise testing in patients with symptoms of intermittent claudication: (1) the exercise simulates the activity that produces the symptoms, (2) the severity of pain can be determined and localized to one or more limb segments, (3) it can be determined whether post-exercise ankle pressures deteriorate to ischemic levels, (4) the duration of post-exercise hyperemia (recovery time) can be determined, (5) true vascular claudication can be differentiated from pseudoclaudication caused by venous insufficiency, neurospinal or musculoskeletal conditions, and (6) disease progression and/or response to therapy can be determined. Constant-load treadmill exercise testing is contraindicated in patients with gait disturbances, poorly controlled hypertension, or history of cardiac disorders.
Prior to treadmill exercise, ankle pressures are measured at rest and an ankle-brachial index is calculated. While the degree of treadmill elevation and the walking speed may be reduced, most often the patient will perform treadmill exercise at an elevation of 12% and a constant speed of 2 mph. This elevation and speed simulate the circulatory response induced by normal ambulation. It is important that the same speed and elevation are consistent for each patient on follow-up evaluations. The patient exercises to the point of claudication, but does not exercise for longer than 5 minutes. Ankle pressures are measured immediately post-exercise and at 3-minute intervals until the pressures return to pre-exercise levels (Figure 8A and B).
Normally, post-exercise ankle pressures remain unchanged or increase slightly because vasodilation provides the required volume increase. When post-exercise ankle pressures initially decrease but return to baseline values within 3-5 minutes, a single-segment lesion is most often indicated. Reconstitution of distal vessels is significantly delayed when multi-segmental disease is present. In such cases, ankle pressures return to baseline values within 10-12 minutes dependent on the extent of collateral compensatory flow. Critical ischemia and vascular claudication cause a dramatic decrease in the post-exercise ankle pressure to 60 mmHg or less. It is important to document the recovery time, the symptoms that are experienced during exercise, and the pre-and post-exercise pressures as this information yields valuable clues to the location and severity of disease and the extent of collateral compensatory flow. Consideration must be given to the patient’s motivation, tolerance for pain, and/or symptoms that precede claudication such as shortness of breath or back or hip pain as these factors may impact the duration of exercise.
While the location of disease impacts the magnitude of the pressure drop and the recovery time,19 the precise location of arterial occlusive disease may be difficult to determine based on the post-exercise ankle pressure response alone. Investigators have shown that a post-exercise ABI in the range of 0.9 to 0.6 is most often predictive of isolated infra-popliteal disease while inflow (aorto-iliac) disease reduces the distal pressures to a greater degree. A post-exercise ABI < 0.3 and an absolute ankle pressure less than 60 mmHg are consistent with multi-segmental disease in non-diabetic patients.
Reactive hyperemia testing is a noninvasive technique that is occasionally used for patients who are not able to perform constant-load treadmill exercise testing due to cardiopulmonary disease, amputation or gait disturbance. The test employs cuff occlusion methods to induce vasodilation and, as a consequence, increased extremity blood flow.
To perform the test a wide, contoured blood pressure cuff is placed around each thigh and appropriately-sized cuffs are placed at ankle level. The thigh cuffs are inflated to supra-systolic pressure (20-30 mmHg pressure higher than the brachial pressure) for 3-7 minutes to occlude the thigh arteries, inducing local hypoxia and vasodilation. Following cuff deflation, ankle pressures are measured at 30 second intervals for 3 to 6 minutes or until ankle pressures return to pre-occlusion level.
Immediately following cuff deflation, ankle pressures decrease 20% - 30% in patients with no significant extremity disease and return to approximately 90% of baseline within 1 minute. This is in sharp contrast to the normal response to treadmill exercise where a post-exercise drop in ankle pressure signifies flow-limiting disease. Patients with single-segment arterial disease most often demonstrate less than 50% decrease in ankle pressure, whereas those with multi-segmental disease have a post-occlusive decease in pressure that exceeds 50%. Because similar results may be found in normal patients and those with flow-limiting arterial disease, caution is warranted in the interpretation of reactive hyperemia studies.
While infrequently utilized in the modern vascular laboratory, there are recognizable benefits associated with reactive hyperemia testing. It can be performed portably using appropriately-sized blood pressure cuffs, a sphygmomanometer, and a hand-held Doppler and is less time-consuming than a treadmill exercise study. The major deficiency is that it does not simulate the physiologic response to exercise-associated claudication that is achieved with treadmill exercise. Additionally, the test is very uncomfortable and thigh compression should be avoided in patients with suspected extremity venous thrombosis, femoro-popliteal bypass grafts and/or femoral artery stents.
Some vascular laboratories have chosen alternative methods of stress testing for patients who are unable or unwilling to perform treadmill exercise or reactive hyperemia testing. The more commonly chosen methods include heel raises, hall walking, plantar and dorsiflexion, and use of a pedal ergometer. While these tests elicit increased flow to the calf muscles, the exercise load cannot be standardized. Given this, these tests have little value for evaluation of therapeutic response or disease progression.
Plethysmographic techniques are used to record changes in the blood flow volume of the limb and/or digits that occur throughout the cardiac cycle and as a consequence of obstructive disease in the major limb arteries. Plethysmographic studies have value for assessment of peripheral arterial disease because they a) reflect global tissue perfusion, b) provide an indirect assessment of the extent of collateral compensatory flow and c) are not affected by vessel calcification. It must be recognized, however, that they do not provide information about flow in specific arteries or flow direction. Air-calibrated plethysmography, otherwise known as pulse volume recording, and photoplethysmography are the most commonly used methods in modern vascular laboratories.
In the absence of significant disease in the lower limb arteries, blood should flow symmetrically from the aorta into both extremities. The volume of blood in the tissues and, therefore, limb volume, should increase during systole and decrease during diastole equally in both limbs These cyclic alterations in limb volume can be demonstrated with pulse volume recording (PVR), a technique that utilizes pneumatic cuffs which serve as sensors for arterial flow and changes in limb volume.
The cuffs are calibrated by injecting air into the cuff bladder to achieve a cuff pressure approximating 65 mmHg and a volume of cuff air sufficient to ensure that the cuff bladder fits snuggly against the skin.21 Unlike segmental systolic pressure measurements, the study is performed simultaneously in both limbs. Because comparison of wave contour and amplitude will be made side-to-side at the same level, care must be taken to ensure that the gain remains constant at all cuff levels, cuff pressure has stabilized, and that air volume within the cuff bladder is within 10%-15% in both cuffs at the same level.
When the volume of the limb increases during systole, air in the cuff bladder is displaced. The air is replaced when the limb volume decreases in diastole. The changes in cuff volume and pressure are sensed by a pressure transducer and translated into an analog recording that displays the amplitude and contour of the pulse wave throughout the cardiac cycle (Figure 9).
Figure 9. Physiologic study demonstrating segmental pulse volume recording. Note the alterations in waveform morphology that occur throughout the cardiac cycle.
As expected, the pulse volume wave contour parallels the intra-arterial pressure contour. In the absence of flow-limiting disease proximal to a cuff or beneath the cuff, the PVR waveform should exhibit rapid systolic rise time, a sharp peak at systole, a reflected wave (dicrotic notch) during systolic deceleration, and gradual diastolic run-off (Figure 10). The reflected wave is an expression of the reverse flow component resulting from elevated peripheral vascular resistance, a finding that is expected in normal resting muscles. The reverse flow causes a momentary increase in the volume of blood beneath the cuff. This increased volume is reflected in the waveform contour as a slight increase in amplitude.
Figure 10. Normal pulse volume waveforms recorded at ankle level. A normal waveform exhibits rapid systolic rise time, a sharp systolic peak, a reflected wave on the systolic deceleration slope and gradual diastolic run-off.
Any situation that produces a flow demand (>50% stenosis or occlusion, exercise, or inflammation) in the muscular bed of the limb will elicit a change in the waveform contour and amplitude. In such cases, the waveform will be characterized by delayed systolic rise time, rounded systolic peak, loss of the dicrotic notch and delayed run-off (Figure 11).
Figure 11. An abnormal pulse volume waveform recorded at ankle level. The waveform reflects flow-limiting proximal arterial disease and is characterized by delayed systolic rise time, a rounded systolic peak, absence of the reflected wave, and delayed run-off.
The amplitude of the waveform is proportional to the total flow and pulse pressure at any given limb segment. As such, the waveform amplitude serves as a reliable marker for flow-limiting disease and the extent of compensatory flow in the collateral bed. A decrease in the amplitude of the waveform reflects the reduction in blood flow volume noted distal to hemodynamically significant lesions. It should be noted that the offending lesion may be proximal to, beneath, or between cuffs. When analyzing the amplitude of PVR waveforms, it is important to keep in mind that the amplitude maybe affected by blood pressure, vasomotor tone, ventricular stroke volume, patient positioning, edema and body habitus.
An elevation in waveform amplitude may be noted in situations where there is increased tissue flow (e.g., extensive collaterals, arteriovenous fistulas or malformations, inflammation). This is commonly seen in the waveform recorded at the below knee level as a result of normal increased flow at thigh and knee levels through the profunda femoris and geniculate arteries (Figure 12). Absence of the increase suggests flow-limiting disease in the superficial femoral artery.
Figure 12. Physiologic study demonstrating increased waveform amplitude in the below knee tracing on the left suggesting that the femoro-popliteal lesions are well collateralized. The femoro-popliteal pressure gradient on the right is supported by abnormal pulse volume recording waveform morphology.
Photoelectric plethysmography is used as a tool for indirect assessment of the volume of blood in the microcirculation and is often used for measurement of digital pressures and assessment of healing potential for wounds, ulcers and amputation sites.
The study is performed by attaching a light-emitting diode to the skin with clear double-stick tape. The diode transmits infra-red light into the underlying tissue. The light is reflected from blood cells coursing through the tissue capillary bed and detected by a phototransistor, within the diode, as alterations in electrical impedance. The changes in electrical resistance, expressed as an analog waveform, are proportional to the number of red cells in the microcirculation. It should be recognized that unlike PVRs, photoplethysmographs do not truly measure volume changes in the limb or digit caused by alterations in blood flow. Even so, the plethysmographic waveform morphology closely resembles that of a PVR waveform and the same principles of analysis apply. Even so, consideration must always be given to the potential for waveform alterations that occur as a result of vasodilation or vasoconstriction associated with inflammation, variations in skin temperature, or pharmacologics.
Current reimbursement and accreditation mandates for arterial physiologic testing require measurement of pressures and documentation of waveforms. In some cases, single-segment pressure studies may be all that is required for diagnostic purposes while other clinical scenarios will necessitate multi-segmental testing. Waveforms may be recorded using continuous-wave Doppler, pulsed Doppler (with imaging) or plethysmography. By customizing each test based on the clinical queries relevant to the patient’s medical history and presenting symptoms, accurate evaluations can be achieved in a time and cost-effective manner.
As noted in Figure 13, the diagnostic pathway is based on the resting ankle pressures and ankle-brachial index coupled with knowledge of the technical applications of the physiologic test procedures. The subsequent choice of noninvasive studies is focused on defining the location and severity of disease.
For example, a patient presents with symptoms of thigh and buttock claudication but has a resting ABI of 1.2 and multi-phasic continuous wave Doppler waveforms over the dorsalis pedis and posterior tibial arteries. In this case, it is unlikely that significant pressure gradients would be apparent in the resting limb. As such, accurate and time-efficient diagnostic information would not be achieved by initially performing segmental studies. Based on the patient’s presenting symptoms, the goal should be to unmask an inflow lesion by increasing the flow rate over the narrowed arterial segment. In the absence of a current cardiopulmonary disorder or gait disturbance, this can be achieved by having the patient perform constant-load treadmill exercise testing. If the exercise test is positive, disease location could be identified by analysis of continuous-wave Doppler waveforms recorded at the common femoral and popliteal arteries. Evidence of delayed systolic rise time in the CW Doppler waveform will signify flow-reducing disease in the iliac and/or femoro-popliteal arterial segment.
Toe pressures should be obtained and a toe-brachial index calculated when the tibial arteries are noncompressible. Because arterial calcification proximal to the ankle cannot be discounted, segmental systolic pressure measurements may be misleading. In such cases, segmental pulse volume recording could be used to identify flow-limiting disease and to define the extent of collateral compensatory flow.
If ankle pressure measurements are abnormal, without indication of tibial artery medial calcinosis, the diagnostic algorithm would lead to segmental systolic pressure measurements. Constant-load treadmill exercise would be included in the diagnostic pathway if the resting ABI was > 0.5. Duplex scanning would also be included if there was a need to define the specific location and/or length of the lesion(s) or to differentiate stenosis from occlusion. Imaging may be added to the pathway in cases where aneurysm, pseudoaneurysm or arteriovenous fistula was suspected.
Figure 13. A diagnostic algorithm for evaluation of peripheral arterial disease demonstrating selective use of ankle-brachial index, toe-brachial index, continuous wave (CW) Doppler, segmental systolic pressure measurement, pulse volume recording, constant-load treadmill exercise and duplex imaging.
Noninvasive physiologic studies serve as a valuable adjunct to the physical examination and medical history. Pressure and volume flow studies provide confirmation of hemodynamically significant disease, detection of critical ischemia at rest or post-exercise, definition of the involved limb segment(s), and assessment of response to therapy. A diagnostic algorithm, which uses a combination of pressures and waveforms, ensures accurate, time-efficient and cost-effective testing. If site-specific, morphologic information is required, arterial physiologic testing may be complemented with duplex sonographic evaluations.
As with all areas of noninvasive vascular assessment, the accuracy of the study is dependent on the knowledge, experience and expertise of the examiner and the physician interpreter. Studies have demonstrated that high quality patient care is best achieved when the testing is performed and interpreted by credentialed sonographers and physicians in accredited vascular facilities.
1 Voucher = 1 CME Credit
|10 or More||$9.50 each*|
Buy 10 or more credits and get the best pricing around. If you don't need them all now they'll be waiting for you later because they never expire.
Once purchased, your CME credits are available at any time in your Online CME Control Panel. Just log back into your account.
"Information is very informative and valuable to my area of practice."
Angela Dorosky-Lisauskas, RDMS