DOPPLER US
GENERAL
interpretation_of_peripheral_arterial_and_venous_doppler_waveforms-_a_consensus_statement_vm2020.pdfNOTES
Spectral waveform:
Y axis: range of frequency shifts/velocities
Thickness of line represents range of velocities sampled
Low thickness = low range of values, think center of aorta.
X axis: time
Resistive index: resistance of vascular bed DISTAL to interrogated vessel.
If RI <1 = End diastolic flow must be above 0 = forward EDF
As RI increases from low to high resistance vascular beds the forward flow decreases.
Reporting arterial waveforms: direction of flow, phasicity, resistance.
Higher diastolic flow = lower resistance waveform = lower RI
Lower diastolic flow = higher resistance waveform = higher RI
ARTERIAL DOPPLER GENERAL
FLOW DIRECTION
PHASICITY
PEAK SYSTOLIC VELOCITY
PSV is the most accurate method of evaluating the degree of arterial stenosis.
PSV is elevated proximal to and at the site of stenosis.
PSV may be decreased distal to a hemodynamically significant stenosis.
ELEVATED PSV
Downstream (distal) stenosis
Compensatory flow, contralateral to an obstruction or severe stenosis.
Physiologic hyperdynamic state in healthy pt
DECREASED PSV
Upstream (more proximal) stenosis
Poor cardiac pump function
Near-total occlusion
RESISTANCE
High resistive waveforms: sharp upstroke and brisk downstroke; multi or monophasic.
Low resistive waveforms: prolonged downstroke in late systole w continuous forward flow throughout diastole; monophasic
Biphasic waveform: hybrid waveform that is monophasic w features of both high/low resistivity as it contains both brisk downstroke and also continuous forward flow throughout diastole.
Intermediate resistive waveforms: sharp upstroke, brisk downstroke, continuous forward flow during diastole above zero flow baseline but with end-systolic notch.
In absence of disease, the diastolic component in the arterial waveform reflects the vascoconstriction present in the resting muscular beds. Normal waveforms in a high resistive bed will display a retrograde (reflected) wave in early diastole.
HIGH RESISTANCE
Key features: sharp upstroke and brisk downstroke, with or without diastolic flow reversal. Can be multi or monophasic.
LOW RESISTANCE
Key features: a prolonged downstroke in late systole and continuous forward flow throughout diastole. monophasic.
Prolonged diastolic downslope with the presence of pandiastolic flow. In contrast to intermediate resistance, the low-resistive waveform contains a continuous and prolonged diastolic forward flow without the presence of an end-systolic notch.
INTERMEDIATE RESISTANCE
Key features: sharp upstroke, brisk downstroke, visible presence of an end-systolic notch and continuous forward flow throughout diastole that is above the zero-flow baseline.
In contrast to low resistance, the intermediate resistive waveform contains a rapid deceleration at end systole followed by a diastolic acceleration with continuous forward flow.
The waveform pattern suggests vasodilation and can be the result of exertion (exercise), increased temperature, vasodilator drugs, or a severe arterial obstruction distal to the point of Doppler insonation.
WAVEFORM CHARACTERISTICS
VENOUS DOPPLER GENERAL
WAVEFORM TERMS
WAVERFORM MODIFIERS
PERIPHERAL VASCULATURE
NORMAL ARTERIAL WAVEFORMS
Peripheral arterial circulation supplies mm tissues of upper/lower extremities
Can be anterograde and retrograde waves
Pulse wave reflection can occur at branch sites (Ao bifurcation, branches)
Systolic component is produced by LV contraction via ascending aorta resulting in rapid increase in volume and velocity.
Diastolic component reflects the vasoconstriction present in the resting mm beds.
High resistive beds can display a retrograde/reflected wave in early diastole.
A small antegrade component may be present in mid- to late- diastole as a result of an antegrade wave generated by proximal compliant large and medium arteries.
Conditions that increase flow to limb do so via arteriole dilation in the mm bed allowing forward flow throughout diastole
Exercise
Increased limb temperature
AVF
Although Doppler waveform generally demonstrates a narrow spectral bandwidth, some light incrase in spectral broadening may be noted
INFLOW ARTERIES
Lower: common, external, and internal iliac artery
Upper: innominate, subclavian
Minimally increased spectral boadening may be seen in internal iliac artery 2/2 size of Doppler sample volume and smaller vessel diameter compared to common and external iliac arteries.
OUTFLOW ARTERIES
Lower: common femoral, profunda femoris (deep femoral), superficial femoral, and popliteal artery
Upper: axillary and brachial artery
In normal thigh arteries, there may be a slight decrease in PSV compared to PSV in the normal inflow arteries.
RUN-OFF ARTERIES
Lower: anterior tibial, posterior tibial, peroneal artery
Upper: radial, ulnar artery
Spectral bandwidth remains consistent w laminar flow although a slight increase in spectral broadening may be noted secondary to the size of the Doppler sample volume and small vessel diameters.
No significant difference is noted in PSV among the 3 calf or 2 forearm arteries.
PLANTER, PALMAR, DIGITAL ARTERIES
The flow pattern remains laminar, although a slight increase in the PW spectral bandwidth may be noted secondary to the size of the Doppler sample volume and the small diameter of the plantar and digital arteries.
PHYSIOLOGIC EFFECTS
The increased flow demand and decreased vascular resistance associated with exercising muscle, increased body temperature, or focal inflammation results in continuous forward flow.
PSV can increase significantly (e.g. external iliac artery) as a result of exercise, even when the artery is normal.
ABNORMAL ARTERIAL WAVEFORMS
Severity of arterial lumen diameter reduction is reflected in continual increase in PSV and EDV velocities to a critical value consistent w a pre-occlusive lesion.
Minimal diameter reduction can result in slight disruption to laminar flow without significant increase in PSV or change in early diastolic reverse flow.
Loss of reverse flow component and transition from a multiphasic to monophasic flow pattern are apparent when a pressure-flow gradient is formed at site of stenosis.
The waveform also indicates the location of arterial obstruction.
Delayed systolic upstroke suggests flow-limiting disease proximal to the recording site.
Distal to a stenosis, ischemia in the tissue bed will result in vasodilation and decreased resistance. Additionally, there is a decrease in distal pressure due to the pressure drop across the stenosis. This pressure drop, along with the lower resistance, results in increased diastolic flow throughout the cardiac cycle distal to a stenosis.
Proximal to an occlusion or high-grade stenosis, the resistance will increase. The reflected wave or any antegrade diastolic flow, if normally present, may be reduced or absent and sequential flow-limiting lesions and collateral vessel capacity can affect waveform morphology at a given Doppler sampling location.
<50% STENOSIS
PSV increases slightly but is less than double that in the normal adjacent proximal segment (velocity ratio < 2).
Typically, there is a multiphasic waveform with rapid upstroke and no appreciable increase in diastolic velocity.
Spectral broadening is pansystolic.
50-74% STENOSIS
When arterial lumen is significantly narrowed, a pressure-flow gradient is present at the stenotic site.
PSV increases by more than 100% (velocity ratio > 2) compared to the normal adjacent proximal segment.
The early diastolic reverse flow component is commonly lost (may be residual in a high-velocity state with extensive collateralization) with continuous, pandiastolic forward flow in response to decreased vascular resistance in the distal tissue bed. Spectral broadening is present.
>75% STENOSIS
Severe arterial narrowing results in at least a fourfold increase in PSV (velocity ratio > 4) compared to the normal proximal adjacent segment.
The waveform is monophasic, diastolic velocity may be increased, and a spectral bruit is commonly noted adjacent to the zero-flow baseline.
DISTAL TO FLOW REDUCING STENOSIS
Waveform is monophasic with prolonged upstroke and PSV is decreased.
Spectral broadening is present.
DISTAL TO OCCLUSION
Waveform is dampened and monophasic
PROXIMAL TO OCCLUSION
In the absence of flow-limiting stenosis proximal to the site of Doppler sampling, the waveform is characterized by rapid upstroke and may be high resistive or intermediate resistive.
Area of high-velocity flow b/n an artery and vein is usually seen as area of aliasing on color doppler.
PSEUDOANEURYSM
Flow is bidirectional (to-fro) through the neck or tract of the arterial pseudoaneurysm. The waveform has a rapid systolic upstroke with exaggerated deceleration, and an elongated and prominent reverse flow component.
AVF
Blood flow from a high-pressure artery into a low-pressure vein results in spectral broadening and elevated systolic and diastolic velocities. Continuous forward flow is noted throughout the cardiac cycle.
NORMAL VENOUS WAVEFORMS
Normal venous flow in the larger peripheral and more central veins is spontaneous with low-velocity Doppler waveforms that reflect pressure gradient changes produced by respiratory and cardiac function.
Flow velocities are very low in the smaller veins distally in the extremities and may not produce discernable Doppler signals in the resting state.
Throughout the periphery, flow velocities vary with respiration 2/2 changes in intrathoracic and intraabodiminal pressures (respirophasic). These patterns of respiratory variations in flow velocity can be suspended, severely dampened or absent with shallow breathing or breath holding.
Peripheral veins that are most distal to the heart (calf or forearm veins) demonstrate less spontaneity and respirophasicity compared to the veins closer to the heart. Cardiac filling and contraction also draws and pushes venous flow, with this influence normally stronger in veins closest to the heart termed pulsatile flow.
ABNORMAL VENOUS WAVEFORMS
Evaluation includes appraisal of flow direction, responses to respiration and cardiac function, and response to physiologic maneuvers.
Symmetry is your friend! Changes 2/2 central or systemic conditions are seen bilaterally. Use contralateral side for comparison.
Normal antegrade flow direction in the venous system may become retrograde when there is valvular incompetence or occlusion in more central venous segment.
Continuous venous flow suggests a more central obstruction.
Pulsatility is not normally seen in lower extremity peripheral veins 2/2 distance from heart. Loss of pulsatility in central upper extremity and abdominal veins however is abnormal.
Interpretation of venous waveform morphology is most often done w/o reporting angle corrected velocity data although measuring velocities is essential when evaluating a fistula or venous stenosis.
Three components to carotid artery exam:
Plaque morphology
Hemodynamic evaluation
Waveform analysis
CEREBROVASCULAR WAVEFORMS
Bilateral extracranial cerebral vessels include CC, EC, IC and vertebral arteries.
Inflow depends on Ao valve, Ao arch, brachiocephalic, and subclavian arteries. When normal, waveform reflects the resistance of the distal vascular bed.
Outflow depends on status of basal cerebral arteries (CoW) and rest of intracranial cerebral circulation.
PLAQUE MORPHOLOGY
Evaluated on grayscale w/o Doppler and described in terms of absolute percent stenosis
<50%: no hemodynamic significant
>50%: luminal plaque expected to show increased PSV
Morphology:
Residual lumen: concentric, eccentric, irregular
Echogenicity: uniformly echolucent, predominantly echolucent (>50% plaque), predominantly echogenic (>50% of plaque), uniformly echogenic
+/- ulceration
HEMODYNAMICS
Normal PSV in large arteries is 60-100 cm/sec
<125 cm/s normal
>125 cm/sec ~>50% stenosis
>230 cm/sec ~>70% stenosis
Occluded or nearly occluded artery can have no detectable flow
End diastolic velocity >100 cm/sec suggests >70% stenosis
PSVR ratio (ICA stenosis: normal distal CCA) is more useful than absolute PSV in high and low flow states (poor cardiac function or tandem stenosis underestimates, crossover collateralization in contralateral arteries overestimates).
<2 normal
>2 suggests >50% ICA stenosis
>4 suggests >70% ICA stenosis
WAVEFORM ANALYSIS
Normal flow:
Rapid systolic upstroke, reflecting normal prox vessels and cardiac function
Diastolic portion is determined by resistance of distal vascular bed.
Waveform changes can occur w/ proximal occlusive lesions, focal lesions in specific arterial segments and changes in the resistance of the distal vascular bed.
Brain tissue normally has a low vascular resistance, a normal ICA waveform shows a low resistive pattern with relatively high diastolic velocities and forward flow throughout the cardiac cycle. In contrast, the EC supplies a high resistive vascular bed (skin, mm, bone) similar to that of peripheral arteries
Parvus tardus waveforms: diminished and delayed arterial pulsations characterized by increased systolic acceleration time (longer intervals b/n the bringing of systolic upstroke and the systolic peak. Observed distal to locations of severe stenosis.
COMMON CAROTID ARTERY
NORMAL
AORTIC VALVE / CARDIAC DISEASE
AoV STENOSIS
Bilateral parvus tardus waveforms seen throughout the carotid and vertebral arteries
Ao REGURGITATION
Pulsus bisferiens: two prominent systolic peaks w an interposed mid-systolic retraction.
First sytolic peak may represent initial high volume ejection of blood followed by abrupt midsystolic flow deceleration caused by the regurgitant valve; second peak may be related to relaxation of the distended aorta.
AVS & REGURG
DEVICES
Monophasic parvus tardus waveforms w slow systolic upstroke and rounded systolic peak (thought to be 2/2 intrinsic residual myocardial reserve pumping some of the blood.
Constant antegrade flow w no flow reversal
Reduced PSVs. Be cautious in pts w LVAD as they may have carotid stenosis w/o elevated PSV
IABP alters doppler waveforms due to sequential inflation and deflation of balloon which can lead to over/underestimation of true flow velocities.
A second peak of forward flow during systole corresponds to balloon inflation.
Transient reversal of flow corresponds to balloon deflation at end of diastole immediately preceding the next hearbeat.
INTERNAL CAROTID ARTERY
NORMAL
ABNORMAL
EXTERNAL CAROTID ARTERY (ECA)
NORMAL
ABNORMAL
VERTEBRAL ARTERY (VA)
SUBCLAVIAN STEAL SYNDROME
VA provides collateral BF to upper extremity bc of vascular blockage 2/2 stenosis/occlusion of prox subclavian or brachiocephalic artery.
Leads to reverse flow in VA to perfuse SCA distal to stenosis/occlusion
Exacerbated by demand for increased arterial BF in affected arm.
SCA obstruction is most likely 2/2 atherosclerosis tho must exclude vasculitis, dissection, adjacent neoplasm.
Findings:
Normal waveform of one VA w signal systolic peak followed by a diastolic component.
Contralateral VA demonstrates 2 systolic peaks: Initial systolic peak followed by sharp deceleration and second systolic peak (bunny rabbit sign)
Evocation maneuvers can be performed to accentuate steal
BP cuff inflated: minimal restoration toward normal waveform
Sudden BP cuff deflation: accentuation of steal w/ flow reversal during mid systole.
Subclavian steal is likely if cerebral sx are exacerbated w arm exercise.
RENAL DOPPLER
GENERAL / NORMAL
The kidneys are high flow demand end-organs, which receive blood from one or more renal arteries.
Doppler waveform demonstrates a rapid upstroke, sharp peak, and a low resistive monophasic waveform consistent with continuous diastolic forward.
Normal aortic and renal artery velocity is 60-100 cm/sec
RESISTIVE INDEX
RI = PSV-EDV/PSV
Measured in segmental arteries of the upper, mid and lower poles
Useful and sensitive noninvasive marker of renal function.
Healthy patients show significant dependence on age and area sampled; normal 0.5-0.7
Elevated >0.7 indicates pathologic impedance to flow
Nonspecific but may indicate renal artery stenosis, acute urinary obstruction, or medical renal disease.
Increased intrarenal RI is considered a marker of intrarenal arterial stiffness and worsening tubulointerstitial damage.
Normal RI higher in elderly patients w/o renal insufficiency and neonates <6months
Measure interlobar renal arteries (adjacent to medullary pyramids) in 3 locations of each kidney (upper pole, interpolar region, lower pole) and reported as average.
RENAL ARTERY STENOSIS (RAS)
RAS findings from renal artery (renal artery only)
PSV >200 cm/sec
Renal artery: aortic velocity ratio > 3.5
Reduced/absent EDV suggests stenosis distal to area of interest.
Focal areas of aliasing
Like carotid artery, tardus et parvus waveform suggests stenosis proximal to the transducer, known as inflow lesion.
RAS findings via interlobular artery
Early systolic acceleration <300 cm/sec
Limitations:
Decreased sensitivity w/ borderline stenosis
Cant distinguish high grade from complete occlusion w collateral flow
Unable to localize stenosis
Variation in cursor location for measurement of systolic acceleration
Dependent on compliant vessels
Intrarenal doppler cannot solely be used to dx RAS
RENAL VEIN THROMBOSIS
Usually w/n 1st week post tx (48 hrs MC); <5% of Tx pts
Untreated venous occlusion prone to renal rupture and hemorrhage. If graft infarction and infection -> explantation.
Findings
Enlarged edematous hypoechoic kidney 2/2 obstructed venous outflow; renal vein distention by thrombus; loss of corticomedullary differentiation.
Absent venous waveform at hilum and parenchyma
Reversed diastolic flow in renal arterial waveform
PERINEPHRIC HEMATOMA
RENAL AVF/AVM
RENAL INFARCT
RENAL VEIN NUTCRACKER
TRANSPLANT KIDNEY
Typically implanted in the R > L iliac fossa; usually single but en-bloc transplant of both kidneys into recipient can be occasionally performed (pediatric donor to adult recipient)
Goal is to determine whether there is treatable surgical or vascular complication. US cannot reliably differentiate b/n various cuases of parenchymal rejection and requires bx for definite diagnosis.
Elevated RI (>0.7) suggests renal dysfunction
5 categories to look for when evaluating: artery, vein, parenchyma, collecting system, area around tx (collections)
SURGICAL COMPLICATIONS
Collecting system obstruction -> hydronephrosis
Causes: ureteral anastomotic stricture, mass (lymphocele), or ureteral stone.
Fluid collection (blood, pus, urine) is dependent on timing:
Immediate postop: hematoma
1-2 weeks postop: urinoma
3-4 weeks postop: abscess
2nd month and beyond: lymphocele
VASC COMPLICATIONS
Renal vein thrombosis: renal ARTERY doppler may show reversal of diastolic flow
Renal artery stenosis: elevated flow velocities @ stenosic site w/ parvus et tardus waveform distal to the stenosis. Usually takes several weeks to months to develop.
Pseudoaneurysm 2/2 renal bx
MEDICAL COMPLICATIONS
Generally cannot be differentiated on US. Bx is needed.
Hyperacute rejection: w/n first few hrs of tx (very rare, ABO blood type incompatibility.
Acute tubular necrosis: immediate few postoperative days; usually sequela of preimplantation ischemia.
Acute rejection: w/n 3 months of tx
Chronic rejection: after 3 months of tx
Drug toxicity: cyclosporine is nephrotoxic
HEMODIALYSIS
A) radiocephalic fistula @ wrist
B) brachiocephalic fistula @ antecubital fossa
C) brachiobasilic vein transposition
D) forearm loop graft
E) upper arm straight graft
F) axillary loop graft
G) thigh graft
BASICS
2 options for HD
AVF: anastomosis b/n artery and vein allowing vein to enlarge and arterialize to become accessible and provide adequate flow for HD; takes 8-12 weeks to mature (~50% never mature)
Radiocephalic/forearm (preferred)
Low rates of maturation
Typical stenosis at juxtaanastomotic segment (w/n 2 cm).
Brachiocephalic/upper arm (2nd preferred)
Used when radial artery or forearm cephalic vein are unsuitable for RC creation
High rate of dialysis associated steal syndrome which precludes subsequent ipsilateral forearm fistula creation
Typical stenosis at cephalic arch.
Brachiobasilic/upper arm (requires 2 surgeries)
Used when upper arm cephalic vein unsuitable for AVF creation.
Difficult surgery; high rate of steal syndrome
Typical stenosis at proximal swing segment.
HD graft: artificial graft with prosthetic conduit that connects artery to vein like AVF; takes less time to mature but poorer long-term patency and higher rates of infection.
Forearm loop
Upper arm
Thigh
Vessels must be a minimum diameter to be used:
Veins: 2.5 mm AVF; 4.0 mm for AVG
Measured after dilation via tourniquet or BP cuff.
Artery for both 2.0 mm
MATURE FISTULA
High volume, low resistance, monophasic flow.
Rule of 6s
Flow >600 mL/min in draining vein measured 10 cm from anastamosis over 3 cardiac cycles.
Diameter >0.6 cm in draining vein
No more than 0.6 cm deep
Should mature by 6 weeks
IMMATURE FISTULA
Occurs in >50% of newly created AVFs; investigate if no maturation by 6 weeks.
Causes:
Inflow stenosis: MCC; does not allow for dilation and arterialization of fistula.
Competing outflow veins:
Accessory veins: naturally occurring branches arising from venous outflow tract; treat with ligation and embolization.
Collateral veins: alternative drainage pathways; develop in setting of downstream stenosis; treat by addressing underlying stenosis.
Fistula maturity can be diagnosed clinically but if maturity is not obvious can undergo US.
PSV should be assessed at
- 2 cm cranial to arterial anastomosis w/n feeding artery
2 cm caudal to venous anastomosis w/n graft
At arterial and venous anastomoses
Mid graft
Any site of abnormal narrowing or color/pulsed doppler aliasing.
AVF STENOSIS
Decreased flow <500 mL/min
PSV ratio = PSV @ stenosis / PSV 2 cm upstream
Stenosis at anastomosis PSVR > 3:1; PSV >400-500 cm/s
Inflow arterial or draining vein stenosis PSV ratio >2:1