RPVI cheat sheet

Doppler equation: f_d = (2·f_0·v·cosθ)/c; velocity is proportional to the cosine of the Doppler angle, so error grows sharply above 60 degrees.

Angle correction should be kept at or below 60 degrees; at 60 degrees a 5-degree angle error produces roughly a 15% velocity error.

Bernoulli relationship: pressure gradient ≈ 4v², so a peak velocity of 4 m/s corresponds to about 64 mmHg of gradient.

Resistive index RI = (PSV − EDV)/PSV; values above ~0.7 indicate high distal resistance and below ~0.5 low resistance.

Pulsatility index PI = (PSV − EDV)/TAMV; it reflects the entire waveform rather than a single point.

Spectral broadening indicates a range of velocities within the sample volume and is seen with turbulence or nonuniform flow.

Aliasing occurs when the Doppler shift exceeds the Nyquist limit (PRF/2); raising PRF, lowering frequency, or increasing the angle can correct it.

Color Doppler shows mean velocity and direction, not peak velocity; a color bruit or aliasing jet suggests locally elevated velocity.

Wall filter removes low-frequency, high-amplitude signals from vessel wall motion but can obscure slow flow if set too high.

Normal ICA PSV is generally below ~125 cm/s; PSV above ~230–250 cm/s with elevated EDV supports ≥70% ICA stenosis.

The ICA/CCA PSV ratio above ~4.0 supports a ≥70% ICA stenosis; ratio helps correct for systemic flow state.

Near-occlusion (string sign) shows markedly reduced PSV with high resistance distally; velocity criteria for stenosis do not apply.

The ophthalmic artery normally flows toward the probe; reversed flow suggests severe ipsilateral ICA disease or external carotid collateral supply.

Vertebral artery flow reversal or a high-resistance waveform can reflect subclavian steal or proximal stenosis.

TCD uses a 2 MHz pulsed probe through temporal, orbital, foraminal, and suboccipital windows; temporal window is absent in a minority of adults.

A microembolic signal on TCD is brief, high-intensity, unidirectional, and random, distinct from the lower-intensity background.

Cerebral autoregulation and collateral flow mean a unilateral severe stenosis may be accompanied by contralateral velocity increase.

Ankle-brachial index = highest ankle pressure (dorsalis pedis or posterior tibial) divided by the higher of the two brachial pressures.

ABI interpretation: >1.40 noncompressible; 1.00–1.40 normal; 0.91–0.99 borderline; ≤0.90 abnormal; ≤0.50 severe.

Toe-brachial index is useful when ABI is falsely elevated by medial calcinosis; TBI below ~0.70 is abnormal.

Segmental pressures drop of ≥20–30 mmHg between adjacent cuffs localizes disease to that segment.

Pulse volume recordings show dampened or flattened waveforms distal to stenosis; loss of the dicrotic notch is an early sign.

Exercise testing with a post-exercise ABI drop of ≥20% or ≥30 mmHg increases diagnostic yield when resting ABI is normal.

Biphasic and monophasic waveforms indicate progressively more proximal or severe disease; triphasic is normal.

TcPO2 below ~30–40 mmHg suggests poor wound healing potential in critical limb ischemia evaluation.

Normal lower-extremity venous flow is spontaneous, phasic with respiration, and augments with distal compression.

Reflux criteria commonly used: >0.5 s in superficial veins and >1.0 s in deep veins after distal augmentation.

Venous thrombosis shows absent or partial compressibility, intraluminal echoes, and absent spontaneous or phasic flow.

Valsalva maneuver assesses proximal (femoral/iliac) competency; distal compression assesses more distal segments.

Continuous nonphasic flow suggests proximal obstruction; pulsatile venous flow suggests right heart dysfunction or AV fistula.

Acute thrombus is typically hypoechoic and distends the vein; chronic thrombus is echogenic, retracted, and may show collaterals.

Calf vein thrombosis is often isolated and may propagate; serial follow-up is a recognized management strategy for isolated muscular calf vein thrombosis.

Upper-extremity DVT evaluation focuses on compressibility of internal jugular, subclavian, axillary, and brachial veins; subclavian is often assessed indirectly by waveform.

Normal renal artery PSV is generally below ~180–200 cm/s; higher values with turbulent flow suggest stenosis.

The renal-aortic ratio (renal PSV divided by aortic PSV) above ~3.5 suggests significant renal artery stenosis.

The tardus-parvus waveform (delayed systolic upstroke, low RI) indicates downstream flow from a proximal stenosis.

Normal superior mesenteric artery waveform is low resistance with high diastolic flow; fasting vs postprandial states alter the pattern.

Median arcuate ligament syndrome shows a focal celiac artery stenosis with a characteristic hook and velocity increase that varies with respiration.

Aortic aneurysm is measured outer wall to outer wall; a diameter ≥3.0 cm defines an aneurysm in the infrarenal aorta.

Endoleak after EVAR is detected as flow within the aneurysm sac outside the stent graft.

Portal hypertension signs include dilated portal vein, reduced or reversed portal flow, and recanalized paraumbilical veins.

Doppler equation relates shift to velocity and angle; cosine dependence makes angle accuracy critical.

RI and PI quantify downstream resistance and waveform pulsatility.

Aliasing reflects exceeding the Nyquist limit.

Color displays mean velocity; spectral Doppler measures peak and mean.

Wall filter and gain settings affect detection of slow flow.

Spectral broadening suggests turbulence or sampling across a velocity range.

Bernoulli estimate converts peak velocity to pressure gradient.

ICA PSV and ICA/CCA ratio form the basis of stenosis grading.

Near-occlusion yields low velocities and high distal resistance.

Ophthalmic and vertebral flow direction reveal collateral pathways.

TCD uses specific acoustic windows and identifies microembolic signals.

Contralateral velocity may rise with unilateral severe stenosis.

Normal ICA PSV is generally under 125 cm/s.

ABI uses highest ankle pressure over higher brachial pressure.

ABI thresholds classify normal, borderline, abnormal, and severe disease.

TBI is used when medial calcinosis elevates ABI.

Segmental pressure gradients localize disease.

Pulse volume recordings show waveform damping distal to stenosis.

Exercise testing increases sensitivity when resting ABI is normal.

TcPO2 aids wound healing assessment.

Normal venous flow is spontaneous, phasic, and augmentable.

Reflux thresholds differ for superficial and deep veins.

Noncompressibility is the hallmark of acute DVT.

Valsalva tests proximal competency.

Continuous or pulsatile flow suggests obstruction or right heart disease.

Acute and chronic thrombus differ in echogenicity and vein size.

Upper-extremity evaluation relies on compressibility and waveform analysis.

Renal artery PSV and renal-aortic ratio define stenosis.

Tardus-parvus waveform indicates proximal stenosis.

SMA waveform varies with fasting and postprandial state.

Median arcuate ligament syndrome shows respiratory-variable celiac stenosis.

Aortic aneurysm is measured outer wall to outer wall.

Endoleak is flow in the sac outside the graft.

Portal hypertension alters portal vein caliber and flow direction.