Editing Arterial physiological assessment


== '''Doppler ultrasonography''' ==

* [[File:Doppler.png|right|frameless|365x365px]]Indications:
** Suspected symptomatic chronic PAD
** Suspected acute limb ischaemia
** Pedal infected without a palpable pulse
** Atheroembolic or thromboembolic disease states
** Surveillance post-revascularisation
* Criteria for critical flow-limiting stenosis:
** Loss of triphasic waveform
** Spectral broadening with an increase in velocity (PSV >200cm/s, EDV > 0cm/s)
** Vr greater than 3 across the stenosis
* Principles
** The velocity of blood flow is proportional to the frequency shift, which is heard as a change in pitch of the audio signal
** Amplitude (loudness) is proportional to the volume of red blood cells moving through the Doppler signal path[[File:Doppler 1 .png|right|frameless]]
** Turbulence imparts a harsh quality to the signal via non-uniform velocities
** Contour of the waveform is also important
*** Normal arteries a triphasic or biphasic quality, with brisk upstroke in systole, a brief reverse stroke in diastole (caused by the reflection of the flow wave from the high resistance periphery), and mostly a small forward component in late diastole
*** [[File:Doppler 2.png|right|frameless]]When peripheral vascular resistance is low, the velocity waveform loses the reverse flow component and becomes monophasic with forward flow throughout the entire cardiac cycle
*** Arterial obstruction causes dampening of the waveform which becomes monophasic

* Changes in stenosis
** Early: spectral broadening (widening of the waveform in early diastole)
** Late: increase in systolic velocity + spectral broadening
** Critical: doubling of PSV when compared with adjacent segments, with blunted and monophasic segments distally
** Proximal to the stenosis, you get a 'to and fro' pattern, as the resistance distally increases, and you get a large reflected wave
**[[File:Doppler - changes in waveform.png|frameless|388x388px]]

* Technical
** Colour-flow Doppler is the image with coloured velocities over the region - pixel encoding of blood flow. Set gain by increasing it until noise appears in the flow, then reducing it slightly. You don't want to see flow beyond the artery wall.
*** Arterial stenosis is seen as mosaicism within the lumen (turbulence) and reduction in colour-encoded flow in the lumen.
*** When you find a region of stenosis, put spectral Doppler on to quantify it.
** Spectral Doppler is a graph of velocity over time, which can show quantitative velocity too
** Should be at an angle of <60 degrees
** Pulsatility index
*** Divide peak-to-peak velocity spectral shift by the mean velocity
*** Normal values:
**** Femoral >6
**** Popliteal >8
**** Normal peripheral arteries >4
*** PI < 4 may reflect proximal inflow/occlusive disease
*** Change in PI or spectral waveform damping is diagnostic of multilevel occlusive disease
** 'Damping factor'
*** Division of distal artery PI by proximal artery PI
*** <0.9 is diagnostic of occlusive disease
** If assessment of mesenteric arteries is planned, should fast for 4 hours prior

[[File:Flow vs velocity.png|frameless|720x720px]]

[[File:Velocity vs ABI.png|frameless|362x362px]]


== '''Duplex ultrasonography''' ==

* Refers to the combination of Doppler USS with anatomic USS
* Left side is orientated towards patient's head

== '''Pressure measurements''' ==

* Background
** Pressure differentials drive flow, and therefore decreased pressure results in decreased flow
** In most instances, pressure is an acceptable surrogate measure for flow
** Decreases in systolic pressure are more sensitive than changes in mean or diastolic pressure for detecting stenosis
** Mild stenoses that do no cause a drop in pressure at rest may become evident when flow is increased
** A pressure drop of 10mm Hg at rest or 15mm Hg after exercise/ischaemia/administration of vasodilators indicates increased resistance in this segment sufficient to reduce flow by a clinically meaningful account
* Ankle-brachial index measurement[[File:ABI.png|right|frameless]]
** Simplest way to demonstrate lower extremity occlusive arterial disease. Detects stenosis >50%. Sensitivity 80-95%, specificity >95%.
** Numerator: Place cuff as low as possible on the leg, above the ankle. Inflate above systolic pressure, then slowly deflate while the Doppler probe is held over PTA/DP (if no pressure here, can try lateral tarsal artery, just anterior and medial to the lateral malleolus). The ankle pressure is recorded as the highest pressure at which the Doppler signal returns.
** Denominator: highest arm pressure at brachial artery
** Patient should be supine for 5 minutes prior to measurement
** ABI >1.3 should raise suspicion that the arterial wall is stiffened, as can occur in diabetes/CKD. Other reasons to suspect this in the patient with seemingly high ankle pressures:
*** Pulse not palpable
*** Monophasic waveform
*** Remainder of clinical picture strongly suggestive of PAD
*** Doppler signal diminishes while the ankle is elevated
** Toe pressure measurements can be useful when you suspect calcified arteries, as they are less commonly calcified. Normal toe pressure is 20-40mm Hg less than ankle pressure. Toe-brachial index <0.7 is abnormal. Pressures of 30mm Hg or lower are a/w ischaemic symptoms. Foot lesions usually heal when the toe pressures are >50mm Hg, or slightly higher in diabetics.
* Exercise testing:
** [[File:Exercise testing.png|right|frameless]]Rest supine for 20 minutes then test ABI. Walk for 5 minutes or until symptoms prevent further exertion, then lie down and measure ABI again immediately and every 2 minutes for 10 minutes or until it returns to normal.
** Clinically significant lower extremity PAD can be reliably ruled out in patients who can walk for the full five minutes without symptoms or a decrease in ABI.
** This can also be done by induction of reactive hyperaemia (with a tourniquet) or with vasodilators, when walking is not possible

[[Category:Vascular]]