RVS

• Tunica:
• Intima=Innermost layer (endothelial cells)
• Media=Middle layer (thickest)
• Externa (Adventitia)= Outermost layer

• Tiny vessels that carry bl to the walls of larger arteries
• Feed Adventitial layer and some of medial layer

• aka Duplex U/S
• 2 elements: Gray Scale & Color doppler
• Both displays are presented on the same screen ("duplex") to facilitate interpretation.

• Visualizes the structure or architecture of the body part. 
• No motion or bl flow is assessed. 
• This is the way plaque is dir imaged in a bl vessel, w/ the reader typically commenting on cross-sectional narrowing (>70% is typically considered worthy of treatment)

• Visualize the flow or movement of a structure, typically used to image blood w/in an art. 
• We see bl flow vel incr through a region of narrowing, like a finger pressing up against the end of a running garden hose. 
• Incr vel indicate a region of narrowing or resistance (vel >250 cm/s typically considered worthy of treatment).

• Descrip.   DR   PSV cm/s EDVcm/s  Ratio
• Normal   <50%      <125         <40       <2
• Mild      50-69%    125-230    40-100     2-4
• Severe   >75%      >230         >100      >4
• Occlusion          Flow not detected

• Anechoic / Echo lucent: Complete absence of returning sound waves, area is black.
• Hypo echoic: Structure has very
• few echoes and appears darker than
• surrounding tissue.
• Hyperechoic/Echogenic: structure appears
• brighter than surrounding tissue
• Inflow, Outflow, Runoff: refer respectively to Aortoiliac, Femoropopliteal and trifurcation art

• Abd AO bif @ the level of the 4th lumbar vertebrae creating the CIA's (Common Iliac Art)RT CIA is longer than the LT & crosses over the LT Iliac Vns
• CIA bif into Internal/External Iliac Art

• Anterior Tibial Art
• ↳Dorsalis Pedis Art (DPA) major branch is Deep Plantar Art (dpa)

• Post Tibial Art
• ↳2 major distal branches: Lateral plantar art w/c unites w/ Deep Plantar art to form the Plantar arch

After arising fr the dist Pop A, ATA passes superficial to Interosseous membrane

• Ant Tibia: ATA & paired ATV's
• Post Tibia: PTA & paired PTV's
• Medial to Fibula: Peroneal Art & paired Pero Vns

• Arises from the bifurcation of the common iliac art 
• EIA travels inferolateral along medial side of Psoas Major muscle
• EIA → CFA when passing under the Inguinal Ligament

• aka Hypogastric Art
• Supplies bl to the walls & viscera of the pelvic, genitals, gluteal region, upper thigh & perineum
• Mult branches provide important collaterals in the presence of EIA obstruction

• Formed fr the EIA under the Inguinal Lig coursing Lat to the CFV
• It is approximately 4cm long and
• bifurcates into the SFA & the DFA

• Arises fr the LAT side of the CFA & courses down the thigh in closer proximity to the femur than the SFA (Posterolateral to SFA)
• aka Profunda Femoris
• Supplies bl to thigh muscles & hip joint
• Its branches are a critical collateral source in case of SFA obstruction

• Originates 4cm below the Inguinal Lig arising fr the CFA
• Courses along mid aspect of thigh at the level of adductor Hiatus/Hunter's canal and enters POP fossa (behind knee) and becomes POP A

• -Begins @ Adductor Hiatus
• -Continuation of the SFA.
• -Descends lateral & bif just below the knee into the ATA & Tibioperoneal Trunk
• -Supplies bl to knee section & calf muscles

• First branch of POP A
• Courses betw Tibia & Fibula terminating in the DPA on the ANT surf of the foot
• Feeds ANT lateral aspect of leg & medial aspect of the foot

• aka Proximal/Post Tibial Art
• 2nd branch off distal POP A w/c divides into PTA & Pero Art

• Post to Tibia, behind Medial Malleolus
• Terminates into medial/lateral Plantar art of the foot
• Feeds medial aspect of lower leg & foot

• Adjacent to the border of Fibula (small bone)
• Supplies Lateral aspect of leg & foot
• Courses deep in the post compartment of the leg.

ATA comes on lateral aspect of ankle and → DPA w/c branches into Deep Plantar Art & part of Plantar arch

• AVF: may be due to surgery
• Pseudo Aneurysm: due to needle, trauma, surg, catherization
• Peripheral Art Aneurysm: ↑ BP. Most likely occur in the Dist SFA/POP A

• Diabetes is the major risk factor
• PPG in leg does NOT diagnose superficial thrombophlebitis

• Adequately visible
• Appropriate position so it can be uniformly & completely compressed
• Size
• Location
• Monitor Ankle Po

• Pt currently on bl thinning meds
• Pt has discomfort; no sedation available

• Caused by an abnormal insertion of the gastrocnemius muscle compressing on the Pop Art
• Repeated trauma can lead to aneurysm w/c are found bilat in >10% of cases; thrombosis
• Usually occurs in young athletic men

• Obstruction of a section of the leg esp in the calf creating ↑ Po due to DVT, lymphatic fl leak, hemorrhage (trauma) or edema w/in osteofascial membrane
• Can lead to Ischemia & ultimately muscle necrosis
• Sudden occurrence is a result of bleeding in compartment
• Treatment usually incl fasciotomy

• When embolic material moves distally & gets lodged in the digital art
• Causes cyanosis (bluish discoloration)
• May be caused by any of the ff:
• Aneurysmal disease, arteritis, Ulcerated &/or atherosclerotic lesions, some angiographic procedures

Caused by thrombosis, intraplaque hemorrhage, embolization

• Smoking
• Hyperlipidimia
• Family Hx
• Diabetes
• Hypertension
• Sedentary lifestyle

• -Aortic Bifurcation
• -Iliac/Femoral Bifurcation
• -Tibial Trifurcations
• -SFA @ the level of the adductor Hiatus (important site in diabetic pts.)

• Peripheral Art Disease or PAD--1st stage
• Pain in muscles during exercise occuring in buttocks, thigh & calf relieved by rest
• Inadequate bl supply to the muscle
• Leg pain, cramps, tightness & fatigue
• Disease is usually Proximal to the location of symptoms

• Mimics vascular symptoms
• Usually orthopedic or neurogenic in origin

• Buttock: Aorto-iliac art occlusive disease if bilat pain. If pain is on 1 side=Unilat art occlusive disease
• Thigh: EIA &/or Common Femoral occlusive disease
• Calf:  Popliteal/Tibial occulusive disease

• -Leg pain after walking a certain distance in pts w/atherosclerosis
• -Symptoms incl. pain, aching, cramping, or fatigue of the muscles in the lower limbs
• -Quickly relieved by rest
• -Typically occur in the calf  
• -Po drops distal to the obstructed segment after exercise

• 2nd stage---Persistent
• Severe symptom of diminished bl flow
• Occurs when limb is not dependent (ie pain occurs @ night when at rest but helps when pt sits on side of bed or stand) gravitational effect

• 3rd Stage---Most Severe
• Tissue death
• Revascularization or amputation is usually required

• Loss of hair on affected extremity
• Thickening/discoloration on toe nails
• change in skin texture (Shiny/tight)
• Redness in the foot
• Art Ulcers
• Pedal Ulcer

• Atherosclerosis Obliterans (ASO)
• Plaque build up on intima leading to hardening of the vessel
• 99% of Chronic vascular disease=ASO (plaque)

• Inflammation of Art/Veins
• Prevents bl flow to distal sections of the body (ie fingers, toes, nose)
• Occurs equally in UE/LE
• Common in heavy smoking men
• Starts distally→ proximally= NO collaterals

• aka Pulselessness Disease
• Inflammation of Tunica Media/Intima
• Inflammation of AO/AO arch

• Occlusion in ART of Abd AO
• Assoc. w/ claudication of LE w/c can cause Male impotency

• Mult art are swollen/painful
• Related to trauma/surgery

Idiopathic of Superficial Temp Art

• Results from trauma, embolism, thrombus
• No Collaterals develop w/ Acute Art Occlusion

• Near lat malleolus, toes & over dorsum of the foot
• Deep & more regularly shaped
• Trophic changes: Dryness, scaly skin, loss of hair, thickened toenails
• Severe pain but very little bleeding

• Pain
• Pallor
• Pulselessness
• Paresis (weakness)
• Paresthesia (numbness/tingling)
• Polar (cold)

*An acute occlusion is an ER situation due to abrupt onset w/c does NOT provide collaterals

• Thrombus
• Plaque
• Dissecting Aneurysm
• Trauma
• Tumors
• Entrapment of vessel
• Hypercoagulability
• Raynaud's Phenomenon

Abnormal vasospasm of the digital art in hand/feet due to exposure to cold

Pain, Paresthesia, Skin color changes:

• Pallor: Paleness or whiteness of skin due to deficient bl supply
• Rubor: Reddening of the skin suggestive of vessel damage or dilatation secondary to reactive hyperemia 
• Cyanosis: Bluish discoloration usually caused by presence of deoxygenated hemoglobin in the bl

• Physical Exam
• Doppler Waveform
• Doppler segmental pressures
• Palpation
• Auscultation
• CWD

• Skin color changes
• Temp (warm vs. cold)
• Lesions (ie ulcerations)
• Capillary filling indicates obst in art perfusion
• Elevation/dependency changes (elevation turns pallor) and dependency turns rubor

• Pulses/aneurysms
• AO
• CFA
• POP A
• DPA
• PTA/ATA

0-4 (0:No pulse; 4:Aneurysmal/bounding)

• Stethoscope used to listen for a bruit (mainly after stenosis) heard over an art
• Bruit is a vibration transmitted to surround tissue.

• Noise heard thru stethoscope
• Results in turbulence causing tissue vibration Distal to stenosis
• Assoc w/ hemodynamically significant lesion
• Absence of Bruit may be due to a very tight stenosis (ie >90%)

• AVF
• AVM
• Cardiac murmur
• Dissecting Aneurysm
• Post stenotic turbulence
• Patent Hemodialysis graft

• CCA
• AO
• Femoral A
• POP A

W/ severe stenosis (>90% DR), bruit disappears bec art bl flow ↓ (aka Pre-occlusive) & there is no longer tissue vibration w/c would usually occur distal to a >50% stenosis

• Eval plaque, stenosis, narrowing disease
• Approximate location of plaque/disease
• Follow up post surgery
• Less expensive

• Wounds, dressing, casts
• Obesity
• Less definite location of disease
• Ca++ vessels yield falsely elevated doppler po
• Has trouble discriminated betw obstructive disease of CFA and EIA

• Pt Supine, slight oblique & knee extended
• Use 8-10 MHz 
• Obtain waveforms fr: CFA, SFA, POPA, PTA, DPA, PERO art

Malleolus: prominent bony portion in ankle

• Normal: Triphasic waveform w/diastolic reversal of flow
• Abnormal: Monophasic waveform

Abnormal post exercise: Slow upstroke w/ rounded peak, slow down slope w/ reversal of flow

• Improper probe position 
• Incorrect angle s/b 45-60
• Inadequate amt of gel used
• Excessive Po on end of probe
• Inadvertent probe motion

• Extrinsic compression fr tight clothing, tumors, ascites, pregnancy, obesity, improper pt positioning or pain causing muscle contraction
• Peripheral Art occlusive disease (PAD): poor inflow=poor outflow
• COPD  due to elevated central venous Po
• Improper probe angle or probe Po

• Partial obstruction
• Collateralization
• Paired vns of lower extremity
• Bi-fed sys (mult. deep vns)

• Supine position w/ knee slightly bent
• Use 5-7 MHz linear probe
• For obese pts use curved linear probe, ↓ F

Obtain images from CFA, DFA (prox), SFA (P/M/D), POPA, PTA, PERO, ATA

Obtain long, TRV, Gray, Color, PWD signals (45-60), measure PSV

• Normal Analog Doppler Waveform uses a Qualitative approach (reverse flow component)
• Gray: anechoic vessel w/ clean lumen
• Color: filled up & flow seen wall to wall
• PW: Triphasic waveform

• Abnormal
• Gray: Plaque, aneurysm, bl clot
• Color: filling defect
• DR calculation in both planes
• PW: Mono/bi-phasic w/ Tardus Parvus

• As the obstruction increases, the
• waveforms will become flatter 
• Normal PSV:
• Femoral Arteries = 80-100 cm/s
• Pop = 60-80 cm/s
• Tibial Arteries =40-60 cm/s
• Abnormalities in the PV may be
• indicative of stenosis and occlusion.
• In early stages of stenosis and occlusion, the PV distal to the occlusion may actually
• increase.
• first sign of abnormality is the absence of the dicrotic notch  

• -Waveform Shape
• -PSV
• -Spectral Window/Envelope
• -Look for focal acceleration of Velocities & Distal Turbulence

• -Absence of flow
• -Proximal flow is High Resistance
• -Distal flow is Low Resistance w/ Tardus Parvus
• -Collateral Flow

• -Low Vel Monophasic waveforms
• -Lose Triphasic character
• -Tardus Parvus appearance
• -Low Resistance to degree of Ischemia

• PI=Max Vel - Min. Vel    
•            Mean Vel

Peak Systolic to peak end diastolic vel divided by Mean vel

• Normal PI
• CFA: >5.5 (leg)
• POP: >8.0 (calf)
• If no SFA disease, PI of <5=Aorto-Iliac disease
• -Fist clenching ↑ distal Resistance causing more pulsatility; therefore, a closed fist will 
•  also ↓ diastolic flow

• Time fr onset of systole to the maximum peak velocity
• Helps diff Inflow fr. Outflow disease
• ↑ or prolonged amt of time=proximal disease
• Not affected when stenosis is distal to US beam

• AT <133 m/s = No significant disease
• AT >133 m/s = Proximal disease

In severe stenosis, pre stenotic flow may be having ↓ diastolic flow & ↑ resistance but have short AT

• A. Outflow: Femoral
• Bl is going to obstructed site
• Proximal to disease (High Resistance)

• B. Inflow: Aorto-Iliac Bl coming fr obstructed site
• Dist to disease (Low Resistance)

Compares Brachial systolic BP to the ankle Po to identify lower extremity art disease

• ABI=Ankle (↑est of either PTA or DPA)                   ↑Brachial
• BP taken Bilat on Brachial Art (BA)
• Inflate Po cuffs 20-30 mmhg > than last pulse
• Release Po--->1st sound heard is PS(peak systolic) Po
• BP is also taken bilat @ the ankles w/ a CW probe on PTA & DPA

• >1.0      NORMAL
• 0.9-1.0   ASYMPTOMATIC, Mild disease
• 0.5-0.9   CLAUDICATION, Moderate disease
• <0.5      REST PAIN, severe Art disease
•              s/b <60 mmHg

• Taking BP (only systolic components) of the diff segments of the body
• Part of ABI exam, but helps narrow down area of disease

• Supine
• Bilat BA & ankle Po & calculate ABI
• Bilat BP of LE w/ help of 4 cuff or 3 cuff technique

• Bilat Brachial Po
• Ankle Po (DPA & PTA)
• Calf (below knee)
• Above Knee (low thigh)High Thigh

*If thigh Po done first=false BP for lower cuffs

• High Thigh
• Low Thigh (above knee)
• Below knee
• Ankle
• Can diff betw inflow/outflow disease
• Thigh Po is >30 mmhg than the highest Brachial Po

• Thigh cuff
• Below knee
• Ankle
• More accurate 
• Cant diff betw inflow/outflow disease
• Thigh Po ≥ Brachial Po

Small "narrow" cuff= falsely ↑ elevated bpLarge cuff= falsely ↓ decr bp

• 1. Brachial to HT: HT s/b @ least 30 mmhg > than the higher brachial BP
• 2. Vert Po: (Comp adj segments in same extremity)  BP s/b w/in 20 mmhg diff
• 3. Horiz Po: (Comp segments Rt ->Lt) No more than 20 mmhg

• If Po diff betw HT & BA is > 30 mmhg= disease is in Iliac section & probably Proximal Femoral section
• If Po fr AK & BK is >20 mmhg=Femoral disease
• If Po fr BK to calf is >20 mmhg= Popliteal/Tibial section
• If Po diff betw adj segments (up/down) or LT/RT is >20 mmhg=disease is on lower Po leg

• Cant discriminate betw Stenosis/Occlusion
• Can't pinpoint exact location
• Difficulty distinguishing betw CFA & EIA disease
• Ca++ vessels yield falsely elevated bp

• -Ca++ vessels can't be compressed (obliterated) such as Diabetic pts
• -To r/o PAD perform TBI
• -Are falsely elevated less frequently than Tibial ankle Po
• -Useful in assessing small vessel disease in toes & foot
• -Air Plethysmography can also be used but PPG is easier to use

0.6-0.8 (60-80% of ↑ Brachial Po)

Toe Po ÷ ↑ Brachial Po

• ≥ 0.8 = NO Significant PAD
• 0.2-0.5 = CLAUDICATION
• <0.2 = REST PAIN

• -Used in conjunction w/DSP
• -Bl flow moves thru art vessels under the cuff
• -Vol changes occur during systole in extremity
• -Vol change displace air cuff bladder
• -Po change in air filled bladder cuff is converted into analog waveform by Po tx

Waveform represents how much blood is flowing thru the extremities

• Thigh/ankle: >15mm
• Calf: >20 mm
• If AMP is lower, disease is probably present
• -It is only marginally meaningful diagnostically
• -Usual cuff Po in ART Vol recording=65 mmHg

• Air Cuff
• Strain Gauge
• PPG

Uses mercury filled silicon like tube that has electrodes on both ends

• Detects cutaneous bl flow & records pulsations
• Photo cell attaches on digital underside of hand/foot
• Photo cell sends infrared light into tissue w/ light emitting diode
• Photo cell rvs back scattered light & measures its reflection
• ↑Blood=↓reflection

• Checks for blood clot in LE/UE
• Checks Volume Changes
• Most optimal exam for digit Po

• Do DSP
• Do PVR   
• First upper & lower thighs   
• Calves then feet
• Use table values of DSP

• Normal: Sharp Systolic PeakProminent Dicrotic Notch (reflected wave)
• Mildly Abnormal: Sharp Systolic Peak
• No DN and diastolic flow moves away fr baseline
• Moderately Abnormal: Flattened Systolic peak, Upstroke/Dwnstroke are =, No DN
• Severely Abnormal: PW severely low or absent

• For Pts w/ classic symptoms of Claudication
• For pts free of heart problems & is able to tolerate exercise
• Used to determine if symptoms are due to Ischemia (lack of bl supply)
• Help diff betw True & Pseudo Claudication
• Helps determine presence/absence of collaterlization
• Resting vol can be obtained post exercise

• Do DSP/PVR
• 1. Leave Brachial/ankle cuffs on & remove others
• 2. Have pt walk on treadmill @ 1.5-2 MPH w/ a 10-12% incline for 5 mins or until leg hurts
• 3. Quickly lay pt back & obtain Bilat ABI w/in 3 mins
• If ABI ↑ or stays same=Normal test
• If ABI ↓ repeat only ankle Po in 2 mins & repeat every 5 mins until ABI returns to pre-exercise level
• If after 20 mins Po are not normal, STOP exam

During exercise, Peripheral Resistance ↓ diminishing or eliminating diastolic reversal flow (vasodilated)

• If ankle Po ↓ post exercise, but recovers w/in 2-6 mins=Single segment or mild disease
• If ankle Po ↓ post exercise & stays low for 10-12 mins=Multi segment disease or multi-level
• Above 10 mins=Severe disease aka Pseudoclaudication (neurospinal problems)

*Normally bp ↑ post exercise

• aka Post Occlusive Reactive Hyperemia (PORH)
• Uncomfortable exam for pt

• If Pt can't walk
• Heart Disease
• Pulmonary problems (ie COPD)
• Poor Cardiac Output
• If DSP w/in Normal limit (WNL) but symptoms are present
• Alt method to PORH is TOE Raises

• Do DSP/PVR then;
• Place occlusive cuff on HT 20-30 mmhg higher than systolic Po for 3-5 mins
• Maintaining Po in suprasystolic level will cause Ischemia at the site of cuff to cause symptoms of Claudication
• Deflate cuff and immediately take ABI every 1-2 min intervals

• If ankle Po stays same or ↓ by up to 20%=NORMAL (>100% incr in mean vel)
• If ankle Po ↓ more than 20%=Abnormal Test (bl takes longer to return)

Treadmill testing is preferred bec. it induces physiologic stress

Diff between the 2 testing is speed & elevation

• LT Subc A branches off AO Arch on LT side
• On the RT, Innominate art/Brachiocephalic A branches dir off AO Arch and turns into RT Subc A w/c turns → Axillary Art @ Lateral Level of 1st rib
• Axillary Art → Brachial art & Bif into Radial/Ulnar

*Internal Mammary Art (aka Internal Thoracic Art) is a branch of the Subc A

Brachial Art→ laterally→Radial Art→Superficial Palmar arch→Deep Palmar arch (joins the deep branch of ulnar art)

Brachial art→medially→Ulnar art→Deep Palmar arch→Superficial Palmar arch

• -An extra rib in the thorax (cervical rib)
• -Causes extrinsic compression on dist. subc or prox axillary art
• -It can affect the brachial plexus (nerves that
• pass into the arms from the neck) 
• -Common in Females 20-40 y/o
• -Anatomical structural deformity

ATOS: Art TOS caused by compression of the Subc Art

VTOS: Venous TOS caused by compression or blockage of the Subc Vn

• Neck pain
• UE pain, weakness or clumsiness
• Numbness & tingling in shoulder/arm
• Intermittent pain/weakness during exercise
• Headache

• Adison's Test: arm extended 90
• Costo clavicular Maneuver
• Hyper abduction
• EAST: Elevated Arm Stress Test

• 1.Arm @ rest, hand in lap
• 2.Arm raised to 90 angle (same plane as torso)
• 3.Arm raised to 120 or 180 angle
• 4.Exaggerated military stance
• 5.Adison maneuver position: same as #4 and head turned sharply to RT then w/ head turned sharply to LT

*Only ART component of TOS can be evaluated.  Symptoms due to Neurogenic Compression of brachial plexus

Normal: PVR waveform does not change (DN)and BP remains constant

Abnormal: opposite

• Carpel Tunnel
• Cervical Disk condition

• -Caused by Art obstruction proximal to origin of Vert Art
• -Stenosis/Occlusion in the origin of the SUBC ART
• -Pt presents symptoms of POST circulation insufficiency
• -So during arm exercise, a pt w/ subclavian steal syndrome can experience not only claudication of the affected arm, but also symptoms related to insufficient bl flow to the brain.

• Dist Subc Art is being fed by reversed flow in Ipsilateral Vert Art (normal flow s/b Antegrade) in Carotid duplex &/or TCD
• Higher resistance flow will show in vert art bec its now supplying bl to the arm rather than the brain
• Proximal occlusion or high grade stenosis in Ipsilateral Innominate or SCA
• Color-flow doppler will show retrograde filling of ipsilateral vert
• Steal is in area of ↓ BP w/ a diff of >20mmhg seen in the same side of the affected arm

• Plaque build-up on intimal layer causing hardening of the vessel
• Rare condition

• aka Buerger's Disease
• Occurs equally in UE/LE
• Starts distally→Proximally (NO collaterals)
• Rest pain in both hands/feet

• aka Pulselessness Disease
• Inflammation of Intima/media causes narrowing of the lumen
• USA: Intimal thickening >0.08 cm
• PVR waveform abnormal

• Common in young women <40 y/o
• Bilat involvement
• Often the cause isn't known
• Benign w/ excellent prognosis
• Intermittent digital ischemia due to digital art spasm bec of stress, exposure to cold, etc

• -Vasospastic w/c vasoconstriction ↑ and dist resistance ↓ due to arterioles & capillaries dilation
• -Vasospasm of the arteries reduces
• blood flow to the fingers and toes

• Most severe form of Raynauds
• First manifestation of Buerger's disease
• Normal vasoconstrictive response in arterioles & capillaries are superimposed on a previous disease or obstruction
• Ischemia is constantly present

• -Hands/feet always stay cold & may lead to Rest pain
• -Digital color changes from pallor→cyanosis & as blood flow returns becomes rubor w/ Throbbing pain & burning sensation
• -Numbness & tingling in hands/feet
• -

• PPG is used to obtain PVR waveforms (DN)
• Quality of w/c is used to differentiate obstructive vs. vasospastic

• Bulge or dilation of vessel diameter
• Ulnar aneurysms
• Subclavian/Axillary aneurysm→ fusiform

• Pt Supine
• Do PVR waveforms & DSP by applying Po cuffs to:
• Upper arms (BA)
• Forearms (below elbow) radial/ulnar
• All 10 fingers using PPG method (reflection of light) and FBI

• Brachial to Brachial: If Po diff is >20 mmhg in adj or RT/LT side= disease is in ↓ Po side
• Upper Arm: If Po is >30 mmhg betw upper arm Po (RT/LT)= Severe Po reducing stenosis w/@ least 50% DR or occlusion of Subc Art/Axillary Art
• Brachial & Forearm: Po diff betw adj cuff sites on same arm should not differ by >10 mmhg
• Radial & Ulnar: Po diff s/b 5 mmhg to one another

• -Evaluate standard features of PVR waveforms
• -Peripheral Resistance is usually LOWER in the UE than in the LE
• -BA waveform w/o flow reversal is a common finding

≥0.8 (80% of ↑ Brachial Po)

• 0.75-1.05 =Normal
• <0.75 =Abnormal
• ≤0.29 =Occlusion

Finger Po ÷ ↑ Brachial Po

• Pt Supine
• Arm moved laterally away fr body w/ palm up (anatomical position)
• Use 8-12 Mhz linear tx
• For Axillary Art, place pt arm above their head
• For rest of exam, return pts arm to normal anatomical position (palms up)

• SCA
• AXILLARY ART
• BRACHIAL ART
• RADIAL ART
• ULNART ART
• PALMAR ARCHES (optional)

Eval for signs & symptoms of Aneurysm such as pseudo-aneurysm or discoloration

• Tri-phasic waveform
• Bi-phasic waveform can be considered normal in pts 65-70 y/o
• Clear, spectral windows w/ narrow BW

• Monophasic waveform (low resistance)
• Non-pulsatile flow pattern
• Spectral broadening & window filling
• Aliasing w/ color doppler (Mosaic)
• Flow dist to a critical stenosis = Monophasis w/ a sluggish upstroke to peak systole & ↓ diastolic flow along w/ spectral broadening (Tardus Parvus)
• W/50% DR Stenosis--->PSV will ↑ by 100% over PSV prox to stenosis

*Ratio of PSV (@Stenosis) to proximal segments PSV will be a ratio >2 w/ a Stenosis >50% DR

Used to determine if Radial/Ulnar Art is occluded

• Pt Clenches his/her hands tightly
• Pinch off radial or ulnar art w/ ur thumb
• Allow pt to open their hand while still compressing on art

If hand turns red then art that is not  compressed is NOT obstructed

If hand turns white after opening then art that is not compressed IS occluded

• PPG sensor applied to ea of 2/3 finger tips
• Waveforms obtained b4 and during manual compression of ipsilateral (same side)radial art
• Continuation of waveforms during manual compression of radial art=hand/fingers are receiving bl flow via palmar arches & normal ulnar art

• Excessive dorsiflexion of hand = false +
• Extension of hand/fingers= Pallor

• -When ART disease is extremely severe
• Surgical intervention can save the limb, bypass grafts are recommended
• -Used to treat Peripheral Vascular Disease

• Synthetic (man-made): Goretex & Dacron
• Autologus (fr body of same person)

• -PTFE aka Goretex is a double line appearance of the graft walls in U/S imaging
• -Connection betw art & vn by a synthetic material either in Upper arm, forearm or LE
• -Reliable for a Bypass operation where the
• distal anastomosis is placed above the knee in the POPA
• -Not likely to stay open if placed below the knee

• 1. Reversed Vn (Saphenous) graft:   
• Pts own vn is used w/o removing the         valves w/c allows bl to flow w/o obstruction
• *Surgical removal of GSV & ligation of all branches  
• *VFR must be the same throughout the graft
• *Distal end of graft being larger in diameter may have ↓ vel than at the proximal end
• *Possible mismatch in size is a disadvantage
• (distal anastamosis where a large diameter vn is anastomosed to a small diameter art)
• VFR: Volume Flow Rate

• 2. In-Situ (In place) Grafts: GSV is left in place & connected to affected arm
• Valves are removed & branches ligated
• Uses "Valvulatome"

• Angioplasty and/or stenting,
• atherectomy, or cryoplasty

Grafts provide good inflow, outflow, and adequate conduit of blood flow

• Aortobifemoral graft 
• Axillofemoral femerofemoral graft
• Femoral-popliteal graft
• Popliteal-tibial graft
• Femoral-tibial graft

• -Pseudoaneurysm @ the anastamosis site
• -Surgical distention of vessel @ the anastamosis site unintentional retained valve
• -Retained valve can cause blockage & failure of graft due to tubular necrosis

• -Atherosclerosis
• -Scar tissue may compress graft & occlude flow
• -Pseudoaneurysm
• -Intimal Hyperplasia @ anastamosis site

• Pt Supine
• Use 7-10 MHz linear probe
• Observe for aneurysms, thrombus & infection

• Obtain color, PW doppler w/ PSV measurements of:
• 1.Native Art   (inflow art)
• 2.Art anastamosis
• 3.Art end of graft
• 4.Midgraft
• 5.Venous end of graft
• 6.Venous anastamosis
• 7.Native Vn (outflow vn)

• 1: Low Resistance
• 2-6: HR (100-200 cm/s) normal
• 7: ↑ Vol may be pulsatile & risk for clotting

• PSV betw 100-200 cm/s w/ organized turbulence
• Vel tends to be higher in the first 6 mos after placement of graft

• High grade stenosis w/ PSV <50 cm/s = graft inflow disease
• Dampened signal = Proximal to a disease
• A 100% ↑ in Vel ff by a distal ↓ in vel =50% DR stenosis

• Direct connection between high pressure arterial sys and low pressure venous sys
• There are marked anatomic & hemodynamic changes

Dialysis grafts or AVFs are placed in the arm for easy access on dialysis pts & to ↓ infection

BP should NOT be taken at the site of a dialysis fistula; You can on the contralateral side

• Fistula is a direct connection betw art & vn
• 2 types: Congenital (Mult Channels) & Traumatic
• 4 components: Prox Art, Dist Art, Prox Vn, Dist Vn

• Characteristics of Congenital AVF:
• BP in the DIST art may be reduced
• Fistula ↓ Flow Resistance
• Proximal flow is ↑
• Characteristics of Traumatic AVF:
• -Art Resistance Proximal to fistula is ↓ (lots of diastolic flow; ↑ in vol of bl flow in the feeding art)
• -Venous Po in draining (proximal) Vn Flow ↑ (pulsatile)
• -Distal Po will be Reduced
• -No Collaterals develop

• Present @ birth
• Not a dir connection between art/vns

• Looped Synthetic Graft: BA to Axillary Vn
• Straight Synthetic Graft: BA to Antecubital Vn
• Brescia-Cimino: Radial A to Cephalic Vn (300ml/min)

BA: Brachial Art

• Prolonged dialysis time (3+ years)
• Abnormal lab val (Kidney val: Creatinine/BUN)
• Arm Swelling
• Digital pain
• ↑ Venous Po= ↑ Venous Vol
• Change in the bruit of the graft

• Venous anastamosis site or outflow vn becomes stenotic & thrombus appears due to ↑ volume
• Pseudoaneurysm (Ying-yang sign)@ dialysis site
• Hematoma
• If Art flow is >400 cm/s then graft has 75%DR=96%AR
• CHF can develop due to ↑ venous flow return from dialysis graft
• Perigraft fluid collections (infection)

• Analog Doppler uses a CW tx
• Signal is easily affected
• Display is less sensitive than spectral analysis
• High Vel=Underestimated
• Low Vel= Overestimated

*FFT converts Doppler signals to analog waveforms 

• Low resistant has diastolic patterns
• Art that carry low resist bl flow are those that provide continuous bl supply in the vascular bed (ie ICA, Renal art, Celiac art, post-prandial SMA)

• High resistant flow have little or no flow in diastole (more pulsatile in nature)
• (ie AO, CFA, PTA, Pre-prandial SMA)

• -Causes vasoconstriction & an "inotrope" ↑ the force of cardiac contraction. Both work
• via the Autonomic Nervous System. 
• -Pharmacology of Vasopressors & Inotropes:

• Adrenaline: the most commonly available
• inotrope and is given by IV (in many cases the
• most appropriate drug to maintain blood
• pressure).
• Dopamine: ↑ mean art Po & cardiac output
• Epinephrine (Epi) administration can
• ↑ BP in patients who are unresponsive
• to traditional agents. It ↑ heart rate & has the potential to induce tachyarrhythmia’s, Ischemia & hypoglycemia.

• ↑ in pulsatility in small & med size art
• Dilates arterioles to maintain continuity of flow
• ↑ Po & ↓ in Resistance

• Caused by: cold temp, anxiety, certain hormones & drugs, atherosclerosis, caffeine
• *Peripheral Resistance is controlled by Vasoconstriction & Vasodilatation of the Arterioles

• ↓ in pulsatility in small & medium size art causing in more flow
• Widening of the bl vessel

Caused by: temp, hormones & exercises

*Art Obstructive disease & Distal Ischemia causes ↑ Vasodilatation & ↓ Peripheral Resistance

• -Relaxation of the vascular smooth muscle & dilatation of peripheral art & vns.
• -Dilatation of the vns promotes peripheral pooling of bl & ↓ venous ret to the heart,
• thereby reducing LT ventricular end-diastolic
• pressure and pulmonary capillary wedge
• pressure (preload).
• -Nitroglycerin Transdermal Delivery Syst
• is a unit designed to provide continuous
• controlled release of nitroglycerin through
• intact skin.

• Triphasic: FWD, Reverse flow in systole, FWD flow in diastole, no flow @ end of diastole
• Biphasic: FWD, Reverse flow in systole and no flow @ end of diastole
• Monophasic: FWD flow during systole alone & no flow @ end of diastole

• Has abnormal:
• Doppler Art signals
• Systolic segmental Po
• PPG tracings

• Has normal:
• Doppler Art signals
• Systolic segmental Po
• &/or PPG tracings
• Abnormal findings after cold stimulation

• (TcP02) measures the oxygen level of tissue beneath the skin (60-80 mmHg)
• -is an indirect measure of blood flow 
• -Determines whether healing can occur @ a wound site or @ a specific amputation level

• Inability to keep electrode on surface of skin
• It can NOT be applied to non-intact skin (ie ulceration)

Manual Calibration prior to obtaining a reading at any portion of the extremity

• ABD AO can be distinguished from
• the vena cava by its thicker wall, pulsations,
• non-compressible nature, and ability to detect
• pulsatile Doppler flow 
• PROX AO: Sup to or @ the level of celiac Axis (2.5-3 cm) (Low Resistance Waveform)
• MID AO: Below Celiac Axis & above Renal Bif (1.5-2.5 cm)
• DIST AO: Just above the bif (1-1.5 cm) (HR)

HR: High Resistance

No vessel course POST to the AO

• AO Root: starts @ aortic annulus w/c inc. aortic sinus & valves and ends @ Sinuotubual junction
• Ascending AO:Starts @ sinotubual junction & ends @ innominate art
• AO Arch:cont after innominate art ends at the SUBC Art
• Descending AO:starts at the LT proximal SUBC Art
• Abdominal AO:starts once it passes thru the diaphragm & ends at the Bif of the Iliacs

• Celiac Art:Stomach, spleen, liver, panc, duodenum
• ↳Lt Gastric Art
• ↳Splenic Art
• ↳Hepatic Art
• SMA: Small Intestine, Cecum, ascending colon, part of TRV colon
• Renal: Kidneys
• IMA: Lt 1/2 of TRV colon, descending colon, iliac & sigmoid colon, part of the rectum
• GONADALS: OV & Testes

• Hepatic/Splenic Art (both have low resistance)
• "Seagull" sign: Hepatic Art/Splenic Art/Celiac Trunk

• AO does not taper inferiorly
• Loss of elasticity may result in tortuous AO
• AO is not dilated to the point of aneurysm

• Normal: up to 3 cm
• Abnormal: >3cm → aneurysmal

Thickening, hardening & deposition of plaque in the intimal wall

• Common sites: Infrarenal
• Origin of renal art → Proximal edge
• Bif of AO into CIA

↑ w/ age, mostly affects men, assoc w/ aneurysm

• Narrowing of AO due congenital or external compression & may affect Abd AO/Thoracic AO
• Assoc w/ hypertension & symptoms of LE ischemia & claudication

• -It is often caused by Congenital Art wall weakness and atherosclerosis
• -Focal dilation of ART walls involving all 3 layers

• True- found in infrarenal, CIA, Circle of Willis
• Fusiform: diffuse, circumferential, dilation
• Saccular: localized out-pouching

• Dissecting: Found in thoracic AO, ABD AO
• Small tear in intima allowing bl to form in "blind-pocket" betw 2 layers
• Pseudo-aneurysm: Defect in main art wall (ie post-catheter insertion or puncture)

• -90% of Infrarenal AAA is degenerative
• -Abdominal Aortic Aneurysm is the most common reason for ABD vascular exam caused by:
• Trauma, smoking, infection, atherosclerosis, congenital weakness or hyperlipidimia
• -Normal measurement: 2-3 cm
• >5 cm is considered medical/surgical ER
• -60% of all aneurysms over 7 cm will rupture w/in a year

• -ABD AO is scanned fr the midline to determine the presence or absence of an aneurysm 
• -Determines whether an aneurysm is infrarenal or suprarenal & if there is any thrombus or heterogeneous plaque features w/in the dilated lumen.
• -Longitudinal View is the preferred plane in measuring AAA

• Rupture is the most frequent complication of Aortic anuerysm
• Distal embolization is the most frequent complication of peripheral arterial aneurysm

• *Thrombosis can occur w/ either type
• AAA's gold standard is Ultrasound exam

• Weakness of the ART wall may result in Aneurysm of AO arch and may lead to Dissection of the AO
• Usually found in tall, skinny & white people

Commonly found in Infrarenal / Bif

• Obtain A/P and TRV measurement
• Location of aneurysm---Infrarenal, Suprarenal & Bif
• Wall thickening s/b <0.08 cm
• Look for dissecting vessel "intimal flap" in lumen
• Triphasic/Biphasic waveforms (Normal)
• High resistance, high Vel, Triphasic flow

• *Remember that a diameter >3cm is considered to represent abnormal
• dilatation. 

• Curvilinear prob 3.5-4.5 MHz
• Obtain images in Long and TRV of:
• Prox AO
• Mid AO
• Dist AO
• R/L CIA's

Use color/PW

• 50% DR = 100% ↑ in PSV across adj segments
• -Prestenotic to stenotic PSV ratio >4:1 = >75%DR
• -PSV >400 cm/s= >75% DR

• Renal Art arise w/in 1.5 cm from SMA laterally off of the AO
• RT Renal Art courses POST to the RT Kidney
• LT Renal Vn courses ANT to AO but POSt to SMA to enter the IVC & Inferior to LT Renal Art

• 1.Removing waste products from the blood and
• 2. Regulating the water fluid levels.
• Kidney Art are low resistant and there is a
• constant vasodilation of the artery branches.
• Normal pole to pole length is 10-12 cm.
• *Most common anatomic variations of the RA is Mult RA

Direct/Indirect 

• Direct approach: involves Doppler interrogation along the entire length of the main RA and any accessory RA (RA:renal Art)
• Eval Celiac and mesenteric Art

• Indirect: involves eval of the segmental or interlobar art w/in the kidney 
• This technique infers stenosis of the main RA thru recognition of abnormal waveform shape obtained from the
• intrarenal arteries.

• -A low resistance waveform with sharp systolic upstroke is expected in the normal main RA
• -The systolic upstroke is rapid with an AT of
• 0.07 seconds or less.
• 

• Native kidney is not removed in transplant cases
• Lt Renal Vn serves as  the landmark 
• Use 3.5-5 MHz curved tx
• Measure in long & TRV
• Obtain color/PW images of:
• Segmental art @ the Sup, Mid, Inf poles of the kidney
• Get acceleration time measurements
• MRA @ hilum →PSV
• MRA @ origin near AO →PSV
• AO @ the level of kidneys→PSV

• Renal to Aortic Ratio is used for checking renal hypertension 
• AO stenosis will lead to Renal inflow problem & result in Renovascular Hypertension.
• *Maximum RA PSV ÷ Max AO PSV obtained @ the level of the MRA

• Normal RAR=<3.5
• PSV of MRA = 100-180 cm/s

• Abnormal:
• >60% DR: RAR >3.5  PSV >200 cm/s w/PST
• AT >70 m/s (Tardus parvus)= significant stenosis

*If unable to rely on AO PSV (ie AO stenosis), PSV of 180-200 cm/s in Renal Art is another reliable predictor

2 main criteria used to determine if Resistance has ↑ in the kidney &/or Renal art

Resistive Index (RI) indicates Resistance of blood flow in the vessels

RI=PSV-EDV ÷ PSV (normal=<0.75)

PR= End diastolic V ÷ PSV (normal=>0.2)

Hypoechoic to the liver or same echogenecity

• -5% of Pts w/ Renal Art Stenosis are assoc w/ HTN
• -75% of pts w/ Renovascular HTN is due to Atherosclerosis (found @ PROX RA)
• -25% of pts w/ FMD (found MID-DIST RA) It may also be assoc w/ Cerebrovascular disease 
• -Other findings in the renal vascular exam incl:
• intrinsic renal parenchymal disease, mesenteric stenosis or extrinsic compression, and aneurysm.

• HTN (new onset or uncontrollable)
• Follow-up post PTA/stenting 
• Follow-up bypass grafting
• Follow-up renal allograft

• Duplex/color scanning is utilized to eval renal artery & kidney parenchymal bl flow for
• hemodynamically significant renal art stenosis (>60%) and occlusions. 
• Examination of the Abd AO & the origins of the celiac and superior mesenteric art are
• routinely incl.

• May be the result of thrombus/emboli
• If MRA (main renal art) is affected, entire kidney is affected
• Branches of MRA: Segmental art, Interlobar art, Arcuate art

May be caused by plaque or fibromuscular hyperplasia or Renal hypertension

• Bypass graft
• Angioplasty:ballooning of art wall
• Stent

Can cause obstruction to the drainage

Infra (BELOW) renal aneurysms

• Donor Art is anastamosed to either the External/Internal Iliac Art 
• Internal Iliac Art aka Hypogastric art
• Renal V is → EIV
• Renal transplants are usually located in the RT Iliac fossa
• Low Resistance flow pattern

• Acute Rejection
• Renal Vn thrombosis
• Infection
• Tubular necrosis
• AVF
• perinephric fluid accumulations &
• hydronephrosis

• Connection sites
• Distal donor art
• Recepient art

Abnormal texture of kidney w/ ↑ cortical echogenecity

• Abnormal size >13cm
• Hypoechoic area w/in the kidney (signs of failure)

• Smaller size kidney <9cm
• ↑ in RI (Resistive Index)

• Normal Arcuate Art Resistance: 0.6-0.8 cm
• Abnormal: >0.9 cm

• Normal PSV: ≤180 cm/s
• Abnormal: >180 cm/s indicates Stenosis

SMA found 1 cm distal to Celiac Axis

Deficiency of bl being sent to the Intestines

Symptoms: Dull, crampy pain 15-20 mins after meal

• Pre-prandial→ High Resistance w/ RI= 0.75
• Post prandial→Low Resistance w/ RI= 0.6
• PSV <275 cm/s

• SMA Abnormal: PSV ≥275 cm/s(fasting) = ≥70-99%DR
• High Resistance waveform

If SMA is occluded, Inferior Mesenteric (IMA) may become collateral, dilated, prominent, indicating disease (occlusion, ischemia) of SMA

Median Arcuate Ligament of the diaphragm compresses the celiac axis during exhalation

Normal: Low Resistance waveform

Abnormal: High Resistance waveform w/ PSV ≥ 200 cm/s = ≥70-99% DR indicating ↑ velocity and turbulence

*Observe for post-stenotic turbulence

• Incl Hepatic Art, PV, Splenic Vn
• Liver has 2 sources of bl:
•  1. Hepatic Art=brings oxygenated bl → 25% 
•  2. Portal Vn (echogenic walls)=nutrient rich bl → 75%
• Bl is drained fr liver by 3 HV (dark walls) that enter the IVC just below the diaphragm (R/M/L HV)
• HA gives rise to the GDA (gastroduodenal art), RT Gastric art & Supraduodenal art

• -Elevated venous Po in portal sys due to obstruction to bl flow
• -Po becomes too high, the blood backs
• up and finds other ways to flow back to the
• heart, where it is pumped to the lungs, where
• it gets rid of waste products and picks up
• oxygen 
• -bl can travel to the vns in the esophagus (esophageal varices), in the skin of the abdomen & the vns of the rectum
• & anus (hemorrhoids) to get around the
• blockages in the liver. 
• -Usually related to advanced chronic liver disease called Cirrhosis
• -Severely elevated Po w/in liver may result in reversed flow (hepato-fugal) in portal vn & ↑ flow in hepatic art

• Enlarged coronary vn
• Subcapsular varices
• Esophageal varices
• Hemorrhoids
• Patent Umbilical Vn (Caput Medussa)
• Splenic Varices (Pleural Effusion)
• Generalized Ascites

• -Results fr scarring of a liver injury caused by hepatitis, alcohol abuse, or other
• causes of liver damage. 
• -Scar tissue blocks the flow of bl through the liver.

• Any ↑ in portal bl flow caused by:
• PV thrombosis
• Splenic V thrombosis
• Compression of PV due to lymph node
• Pancreatitis
• Splenomegaly

• Absence of flow on color doppler
• Dilated PV w/ internal echoes
• Make sure vel scale ↓ to detect slow flow

• Can be caused by:
• Inflammatory process, Portal Hypertension, Post Surgicalcomplications, Pregnancy, Contraceptives, Smoking, Tumors, Idiopathic (dont know)

• ↓ in capacity of liver to transmit bl to IVC causes incl:
• Fatty liver
• Cirrhosis of the liver
• Parasitic infections called Shistosomiasis
• METS

• Budd Chiari Syndrome-Obst of HV
• Cardiac abnormalities
• Tumor in IVC (clot or compression)

• Non-visualization of flow in HV or IVC
• Echogenic intraluminal thrombus
• Flat continuous flow in PROX HV

• Transjugular Intrahepatic Portosystemic Shunt (TIPSS) procedure
• Under Fluoroscopic guidance, radiologist threads a catheter fr RT IJV to IVC → RT HV
• Bridge is percutaneously created in the PV"
• Bridge" (tract) is stented using metallic endoprosthesis
• Shunting bl fr PV → HV decompresses the PV sys

• Color fill in lumen
• Meas Vel in main PV, (P/M/D) shunt, IVC or draining Vn
• ↑ Vel/pulsatile flow in PV, HA
• PSV= 125-200 cm/s 
• Hepatopetal flow in MPV, Reversed flow in RPV, LPV

• Stenosis/occlusion in the shunt usually @ the hepatic end
• Absent flow
• Hepatofugal flow in PV & HA
• PSV <50 cm/s
• PV >13 mm in quiet respiration
• Loss of Resp variation

• -Hepatic artery occlusion and infarct, portal vein and IVC thrombosis 
• -RT HA shows a typical tardus parvus waveform=PROXIMAL disease (ART thrombosis or severe stenosis)
• -Occlusion at the hepatic arterial anastomosis
• is present

• Dark walls
• Hepatofugal flow (away)
• Phasic, Bi-dir/pulsatile flow due to pulsations from the heart
• Same flow is seen in IVC

• Cant see HV due to bl clot/tumor w/in lumen
• Atrophy of RT lobe & hypertrophy of Caudate lobe
• Monophasic waveform (in case of cirrhosis)

• Echogenic walls
• Hepatopetal flow (towards)
• Phasic w/ respiration consistent w/ Splenic & mesenteric vns
• Size is up to <1.3 cm or <13 mm

• MPV size >1.3 cm
• Hepatofugal flow
• Patent umbilical vn/Ligamentum Teres (LT)
• Tumor/bl clot w/in the vessel

• Normal: Low Resistance, pulsatile flow
• Abnormal: ↓ flow or absent flow after liver transplant indicates obstruction of HA

• AO: Never touches the liver
• Has thicker/ stronger medial layer
• Triphasic, pulsatile/ high vel plug flow
• Tapers inferiorly
• 

• Wraps around the left lobe of liver
• Thinner walls
• Steady flow that changes w/ respiration
• Gets bigger in diameter closer to the heart

1. Superior epigastric art it is the terminal branc of the → Internal mammary art aka Internal Thoracic Art.  It is mapped to identify location & patency

• 2. Deep Inf epigastric art → External Iliac art 
• Anastomostic region is known as "watershed area"
• Both arteries incl. perforators contribute bl supply to Rectus Abdomnis muscle
• Main reason for mapping is TRAM flap used for breast reconstruction after mastectomy and also as a graft to the Lt Ant descending (LAD) coronary art

3.Radial Art used for bypass graft in coronary art

• Aka Internal Thoracic Art
• The use of the left internal mammary artery (LIMA) to bypass the left anterior descending artery (LAD) is the “gold standard” of coronary artery revascularization

• Veins are mapped with duplex imaging to
• determine suitability to use as a bypass
• conduit.
• Check for: 
• Normal vn wall compressibility
• Absence of wall thickness
• Patency throughout an acceptable length of vn
• >2mm in diameter (TRV approach)

• GSV
• Cephalic Vn
• Basilic Vn
• less often, Lesser Saphenous Vn

*Once determined suitable, vns are used as a bypass graft for extremity or coronary & for use in dialysis access

• Defect in the area that would normally fill with
• contrast medium in an X-ray or MRI
• examination 
• Filling defects=presence, location & extent of disease

• A defect in the contour part of the
• GI tract, as seen by x-ray after
• contrast medium has been introduced may indicate presence of a tumor or foreign
• body

• Puncture site hematoma
• Pseudoaneurysm
• Local Art occlusion
• Neurologic complications

• Angioplasty (PTA)
• STENT

• -Percutaneous Transluminal Angioplasty (PTA)
• -Balloon tipped catheter is brought to region of stenosis, its slowly inflated (dilating lumen)
• -Expanding the balloon compresses the plaque against the art wall & reduces the blockage 
• -Balloon is deflated, catheter removed
• -"Kissing Stent" angioplasty/Stent technique is used for Bifurcations

-Performed in art (renal, iliac, femoral, POP)

(Types of Stent: balloon expandable, self-expanding; stent grafts used in larger art)

• Stents help prevent the art fr. becoming narrowed or blocked again in the mos/yrs after angioplasty
• It is placed in a weakened art to
• improve bl flow & to help prevent the art fr bursting 
• Made of metal mesh
• Similar techniques as in angiography utilized to insert stent

• EXTRA: Cervical
• INTRA: Petrous, Cavernous Siphon (Carotid Siphon), Supraclinoid → ICA terminates into ACA/MCA

• Central Retinal Art
• Supra Orbital Art
• Frontal Art

• Ophthalmic art coming off Carotid Siphon (Cavernous Siphon)
• Curvature of Carotid Siphon makes it susceptible to the formation of a flow-reducing lesion

Supplies the Ant portion of the brain

• Superior Thyroid Art
• Ascending Pharyngeal Art
• Lingual Art
• Facial Art →Angular Art
• Occipital Art
• Posterior Auricular Art
• Maxillary Art
• Superficial Temporal Art

Supplies the neck, face & scalp

Bl flow in ECA is cephalad (toward head); flow in Superior Thyroid is caudal (toward tail)

• Low Resistance: Constant supply of bl flow during systole & diastole.  Normally seen in vessels feeding organs (ICA, Vert, celiac, hepatic, post prandial SMA, renal art)
• >80% of bl fr CCA flows → ICA

High Resistance: Does NOT require a constant supply of bl flow (ECA, pre-prandial SMA, peripheral art)

*BL FLOW FR HIGH TO LOW

• B-mode: 
• More PosteroLateral
• Usually larger
• No branches in neck
• Prominent dilatation @ take off

• Doppler flow:
• More continuous flow
• Low-resistance signal (↑ flow in diastole)
• Absent-to-very little response in Temp Art tapping

• B-mode: 
• More medial
• Usually smaller
• Branches evident

• Doppler flow:
• More pulsatile flow
• High-resistance signal (↓ flow in diastole)
• Oscillates w/ Temp art tapping

• Presence of dressings, skin staples or sutures
• Edema or hematoma
• Abnormal size or contour of neck
• Depth or course of the vessel
• Acoustic shadowing fr Ca++
• Inadequate optimization of machine controls

• -Bright yellow spot w/in an Art Branch in Ophthalmologic exam
• -Pts have a 75% risk of TIA w/ this incident

• Vert Art branch off the Subc Art
• It unites after entering the skull fr Basilar Art
• RT Vert art is usually smaller than LT Vert art

• Ant system: Consists of carotid art & their branches
• Post system: Consists of Vert & Basilar art & their branches
• Circle of Willis is the most important intracranial comm. channel that connects the 2 systems

• It receives its blood supply from the Carotid & Vert Art
• Ant Cerebral Art
• Middle Cerebral Art
• Post Cerebral Art
• Basilar Art
• Distal ICA
• Ant. Comm. Art
• Post Comm. Art

• Brain is divided in 2 halves or hemispheres, one on either side of midline
• LT Hemi=Dominant & controls speech
• RT Hemi=Controls LT side of body

Hemispheric stroke affects MCA distally & contralateral side of body

*A pt presenting w/ aphasia & weakness of RT arm & leg may be due to LT hemispheric infarct.  The term Lateralizing symptoms may also be used instead of Hemispheric symptoms.

• Intracranial: ACA & MCA
• Extracranial: CCA, ECA, ICA

• Unilateral effects on the body
• Hemiparesis: 1 sided weakness
• Hemiparesthesia: prickling or tingling of the skin
• Aphasia
• Behavior changes
• Peripheral vision loss
• Amaurosis Fugaux

• Hemiparesis
• Amaurosis Fugax
• Aphasia
• *Stenosis of the ICA has the highest risk of TIA
• Either paresis &/or paresthesia may be on the contralateral side of the lesion

• Temp partial or total blindness
• "shade coming down over the involved eye"
• Affects the same or ipsilateral side of the lesion

• Absence of speech/garbled speech
• May be present if dominant hemisphere is affected

*Since most people are RT-handed, it is suggestive of a LT Hemispheric infarct

• Aphasia
• More severe hemiparesis or hemiplegia (one-side) of face & arm than of the leg
• Behavioral changes

• Disrupts vision in 1/2 the visual field of both eyes
• Obstruction of MCA branch

• Severe leg hemiparesis or hemiplegia
• Incontinence & loss of coordination

• Intracranial: PCA & Basilar Art
• Extracranial: Vert Art

• Bilateral effects on the body
• Bilat Paresthesia
• Bilat Paresis
• Vertigo (loss of bal)
• Diplopia (double vision)
• Drop attack
• Ataxia (loss of muscle coord)
• Dysphagia (difficulty swallowing)
• Horner Syndrome (Ptosis) drooping of upper eyelid

• Nonlocalizing or nonlateralizing sysmptoms not related to either RT or LT hemispheres of the brain:
• Dizziness
• Syncope (transient loss of consciousness)
• Dysarthia (disturbance of speech)
• Severe headache

• Reversible Ischmeic Neurologic Deficit 
• Completely resolves after 24 hrs
• Opposite of RIND is CVA

• TIA (Transient Ischemic Attack): Neurological deficit w/ symptoms lasting <24 hrs 
• "Mini stroke" but Temporary (Transient)
• Affects the side of the body opposite that of the Ischemic hemisphere

CVA (Cerebrovascular Accident): Stroke with Neurological deficit w/ symptoms lasting >24 hrs

• Sudden:
• -numbness or weakness of the face, arm or leg, especially on one side of the body
• -confusion, trouble speaking or understanding
• -trouble seeing in one or both eyes
• -trouble walking, dizziness, loss of balance or coordination
• -severe headache with no known cause

rtPA: most common medical treatment of acute ischemic stroke

• Sudden death of some brain cells due to lack of oxygen when the blood flow to the brain is
• impaired by blockage or rupture of an artery to the brain.

• Atheromatous plaque
• Thromboembolic diseases

• Affects primarily the intima & may extend to media
• In Cerebrovascular system, occurs commonly in origin of ICA
• Diabetes is a risk factor
• In LE circulation, Hunter's canal or adductor hiatus is the most common site

• Accumulation of lipid-containing material, smooth muscle cells, collagen, fibrin & platelets
• Causes thickening, hardening & loss of elasticity of art walls that form w/in & beneath intima

• Leading cause of morbidity and mortality worldwide
• Caused when a blood vessel is obstructed by a blood clot (embolus) that has been carried in the bloodstream from the site of its formation
• Incl. both venous thromboembolism (VTE)
• and arterial thrombosis

Is a general term w/c refers to mainly 2 conditions: DVT and its potentially fatal acute complication, pulmonary embolism (PE).

Is a frequent complication in pts with atrial fibrillation (AF) (irreg/very fast heart rate, ie palpitations) and can lead to stroke or systemic embolism.

• Aneurysm
• Dissection
• Fibromuscular Dysplasia (FMD)
• Carotid Body Tumor (CBT)
• Neointimal Hyperplasia

• Causes tearing injury to AO/Art (ie Car accident)
• Causes RT side weakness & aphasia

• Abnormal, and usually abrupt, formation of a tear along the inside wall of an art
• As the tear becomes larger,  it  forms  a small pouch  called  a  “false  lumen.”  The  blood that  accumulates  inside  this  false lumen can lead to a stroke

• Growing pool of blood in the wall of the
• artery  is  known  as  a  “pseudo  aneurysm.” Pseudo aneurysms can lead to symptoms of
• stroke by pressing on brain structures located
• nearby
• They can also burst and cause major
• bleeding into the brain (hemorrhagic strokes)
• When this occurs, it is referred to as “dissecting pseudo aneurysm.”

• Bl inside the false lumen can clot and extend
• slowly into the area where bl normally
• flows.
• Small pieces fr the growing bl clot can break off, flow upstream & become trapped inside a
• smaller art in the brain

• An abnormal fibrous tissue develops along medial layer w/ overgrowth of collagen
• Usually seen in carotid or renal art in young women
• Affects the mid to distal aspect of the Renal Art
• Bead-like or string of pearls appearance

• Highly vascular
• Develops above carotid bif betw ICA & ECA 
• Usually fed by ECA

• Intimal thickening fr overproduction of smooth muscle cells
• Usually seen in vascular injury/reconstruction (post carotid endarterectomy)

• Sharp upstroke/Short AT not consistent w/Proximal disease
• Low flow in diastole=blood going into a high resistance vascular bed

Findings: Pre-occlusive/occlusive lesion is distal (carotid siphon, termination of ICA → Middle & Ant Cerebral art)

*Pattern of bl flow in systole and diastole tells you where bl is coming from

• Look at all info available by duplex (spectral analysis), B-mode & color flow doppler before determining significance of flow
• Comparing findings Bi-lat is also critical

• ↑ Cardiac output
• Tortuosity of the vessel
• Collateralizing for ipsi/contra lateral disease
• Inappropriate doppler angle (ie >60⁰)

• Low cardiac output
• ↑ flow vel NOT detected
• Long, smooth plaque formation
• Stenosis @ area of dilatation (ie carotid bulb)
• Inappropriate doppler angle

• Fatty streaks
• Fibrous (soft) plaque
• Complex plaque
• Ca++
• Thrombus
• Surface characteristics

Hypoechoic & homogenous (low-level echoes of similar appearance)

Low, medium & high level echoes that have heterogeneous (non-uniform) appearance

• Bright, highly reflective echoes
• Acoustic shadowing fr Ca+ deposit

• Same echogenicity as flowing bl
• Bl clot

aka Bruise

Blockage

*Occluded vessels do NOT produce a Bruit

Narrowing of a vessel

• Pre-stenosis: Flow may or may not be altered. HIGH Resistance, LOW Diastole=Dist Disease
• @ Stenosis: High Vel or F; spectral broadening; loss of spectral or F window
• Distal to stenosis: Low flow, Low vel
• Tardus Parvus waveform=dampened signal indicating Proximal to disease.  Post stenotic Turbulence

• Low flow vel in systole & diastole=abnormal flow
• Almost continuous flow throughout the cardiac cycle suggests its going to a low resistance vascular bed
• Slow acceleration time (AT)=Proximal high grade stenosis/occlusion

• Dampened signal=proximal disease
• 

• Frequencies exceeding Nyquist limit cannot be accurately displayed.  Nyq=1/2 PRF
• Can be eliminated by:
• Incr Scale
• Decr F
• Lower baseline
• Switch to CW
• Change view to decr vessel depth (SV)

• Uses 2 MHz Pulsed doppler w/ spectral analysis
• It uses a non-invasive modality for imaging bl flow in cerebral art and vns 
• Exam requires Sample Vol @ varying depths
• 0 angle of insonation in TCI
• Used to eval Intracranial stenosis, Occlusion, vasospasm or collateralization
• Sound waves transmitted through these
• windows are reflected by bl cells in the
• intracranial vasculature.
• The frequency shift of the reflected sound waves recorded at the
• probe is used to estimate bl flow vel or flow vol
• Acoustic windows utilized: Transtemporal, transorbital, and tranforaminal windows.
• Submandibular may also be used to eval extradural ICA
• Technique measures Time Averaged Maximum Vel (TAMV) not PSV or EDV

• Identify IC (Intracranial) emboli and assess
• vasomotor reactivity
• Diagnosis and management of IC occlusive disease.
• Eval effects of extracranial stenosis on intracranial hemodynamics
• Identification and monitoring of vasospasm ff subarachnoid hemorrhage.

• Evaluation of IC flow ff:
• -head trauma
• -during surg to incl emboli detection and
• documentation of intraoperative and
• postoperative hemodynamic changes
• -Assessment of vasomotor reactivity for
• specific indications
• -Identification of IC vasculopathy in pts w/ Sickle Cell Anemia
• -Quantification of degree of IC stenosis (>65%) in the major basal cerebral art
• -Monitor flow patterns w/in AVM & identify the vascular supply to these malformations  
• -Assess the vertebrobasilar (POST) circulation so that collateral pathways & pathology can be identified.

• V      Window  Depth     Dir     Vel       Angle
•                      (mm)            (cm/s)
• MCA     TT     30-60    Ante  55+/-12 Ant/Sup

• Terminal
• ICA      TT     55-65    BI     55+/-12    same

• ACA     TT     60-80   Retro  50+/-11   same
• PCA     TT     60-70   Ante   39+/-10   same
• ICA     TO     60-80  Varies  47+/-14   varies
• Opht   TO     40-60  Ante    21+/-5    Medial
• VA      TF     60-90  Retro   38+/-10   R/L mid
• BA      TF     80-120 same  41+/-10    Midline

• Cross-over
• External-to-internal 
• Post-to-Ant

• Antegrade flow is evident in ACA.  
• Flow is crossing over from the contralateral ACA via a patent Ant Comm Art

ACA: Ant Cerebral Art

• Retrograde flow seen in Ophthalmic Art
• Flow results fr ECA to ICA collateralization → distal branches of Superficial Temp Art that connect w/ dist branches of Ophthalmic art
• Intracranial flow is via Ipsilat Ophthalmic art

• ↑ flow vel found in PCA
• Ant circulation is via Post Comm Art

PCA: Post Cerebral Art

• Requires serial recordings to monitor alterations in mean vel over time
• *TCD most accurate when evaluating spasms of MCA (middle cerebral art)
• MCA >120 cm/s consistent w/ Vasospasm

• Hemispheric Index (HI) >3=vasospasm
• HI=MCA vel ÷ distal extracranial ICA vel

↓ Po on the Rt side

Chest pain, sometimes w/ radiation to jaw & or arm

• Inflammation of the Temp art
• May produce severe headaches &/or sudden unilat blindness
• Type of Giant Cell arteritis 
• Affects frontal &/or parietal branches of Superficial Temp Art

• -Thickened intimal structures evident on B-mode
• -PSV being doubled of 58+/-9 cm/s due to intimal thickening
• -Halo anechoic area around art wall from edema of the intima

DR=[1- d÷D] x 100

• d=Residual Lumen
• D=True Lumen

50%DR = 75%AR

• -MRA is often used to evaluate the
• art of the neck & brain, the thoracic and
• abdominal aorta, the renal arteries, and the
• legs
• -Radio f energy & strong magnetic field produce multi-plane images
• -Able to quantitate bl flow
• -Non-Ionizing radiation
• -CT & MRA may be used for better
• indication when presence of a univocal US
• study, identify aneurysms and hemorrhage. 
• -Sensitive to presence of stenosis but overestimate the disease process
• -Presence of metal precludes imaging
• -Requires great skill

• Special kind of X-ray machine
• Ionizing radiation used to obtain cross-sectional images
• Evaluates nature of cerebral infarctions & intracranial aneurysms, hemorrhage & AVM's
• Degraded image by pt motion & presence of metallic surgical clips
• Only one plane

• Categories are: 
• Medical
• Surgical
• Endovascular

• Life style modifications such as:
• Stop smoking, Wt control & low cholesterol diet
• Aspirin may be prescribed to ↓ thrombolic activity

• -Endarterectomy, is a removal of the atherosclerotic material
• -Your physician may recommend endarterectomy to treat one or more of the following:
• Carotid art disease
• Peripheral arterial disease, such as leg or arm art disease
• Renal (kidney) art disease
• Aortic arch conditions
• Aortoiliac occlusive disease
• Visceral (intestines, spleen and liver) art disease.

Stenting continues to be an emerging technology w/ extensive clinical investigation continuing

• 1. Confluence of venules of the deep digital vns →Metatarsal vns
• 2. Metatarsal vns →Deep venous arches = Tibial Vns
• 3. Paired PTV + Paired Pero Vns drain →Tibioperoneal trunk 
• 4. ANT Tibial + TibioPeroneal trunk and LSV = Pop V
• 5. Pop V becomes Superficial Femoral Vn @ the Adductor hiatus (distal thigh)
• 6. SFV becomes CFV w/c is medial to the CFA and is formed by the confluence of the SFV, DFV & GSV below the Inguinal Lig
• 7. CFV becomes EIV above Inguinal Lig
• 8. EIV unites w/ the IIV (Internal Iliac Vn) to form the Common Iliac Vn (CIV) 
• 9. CIV's join to form IVC @ the level of the 5th lumbar vertebra to the RT atrium

• CFV
• SFV
• DFV
• POP VN
• Paired ATV's
• Paired PTV's
• Paired Peroneal Vns

• 1. Small Saphenous Vn
• 2. Great Saphenous Vn (GSV)

• Located Post to Lateral malleolus and ascends the Post surf of the calf
• It joins the Pop V @ or near Pop crease or fossa
• Its confluence w/ the deep sys varies and may occur anywhere fr the Pop fossa → Post thigh

• -Longest Vn in body
• -Originates on dorsum of foot Ant to Medial Malleolus
• -Ascends medially ff the tibia bone & along medial surface of the thigh
• -Ends in the groin @ the Saphenofemoral junction (CFV)
• -A normal GSV meas. 3-4 mm (0.3-0.4cm) in the mid- thigh. When reflux is present, it is usually larger, but there is NO dir. association betw the size of the GSV and the severity of the disease.

• -As bl flow moves proximally → heart it goes fr the Superficial sys → Deep sys via the Perf  
• -Perforator vns have one-way valves designed
• to prevent backflow of blood towards the
• superficial veins.
• -When those valves no longer function properly, reflux occurs, and can
• enlarge the perforators and the superficial
• veins they lead to 

aka: Communicating Vns

• Hunters → Medial aspect of leg
• Dobbs → Above the knee
• Boyds → Behind the knee
• Cockett's → Calf (1,2,3)
• LSV has lateral perf branches

• PTV's have 2 important perforators near medial malleolus.  
• Post comm branch of GSV in the medial lower calf is connected to a 3rd perforator
• Post arch vn provides superficial connection to 3 perforating vns @ the ankle level w/c are important in the development of venous stasis ulcers (Cockett perforators)

• -Perforator veins in the lower leg and ankle are particularly vulnerable to distention and incompetence, and the
• -Resultant circulatory problems create an
• increased likelihood of edema, skin
• discoloration, dermatitis and skin ulcers in the
• immediate area.
• -Like primary superficial veins that become incompetent, perforator veins
• can be treated.

• -Dilated vessels in the soleal & gastrocnemius muscle of the calf w/c serves as "Reservoir" for venous bl
• -Gastrocnemial Vns drain→POP VN
• -Soleal Vns drain→PTV & PERO VNS

-SOLEAL Sinus is the #1 location for DVT

• aka Soleus pump is An action of the calf (soleus) muscles in w/c the muscles contract and squeeze the popliteal and tibial veins,
• bl is propelled →deep sys & moves cephalad toward the heart (aka Venous ♥)

• Vns as reservoirs for bl collection
• Contracting muscles of the legs
• Competent valves to maintain unidirectional bl flow

Bl → heart resulting in ↓ in venous pooling & venous Po & ↑ in venous return

*If valves are incompetent, opposite occurs: Venous pooling & venous Po ↑ while venous return ↓

• Chronic Venous Insufficiency
• Unilat LE swelling, aching & a sense of heaviness
• Usually from a previous DVT

*Prolonged return to pre-exercise

Commonly occur on the dorsum of the foot

Contains synovial fluid from the knee joint

• 1. Confluence of the venules of Deep digital veins → Metacarpal vns
• 2. Metacarpal vns→Deep venous arches→forearm vns
• 3. Radial & Ulnar Vns join near the antecubital fossa in front of the elbow to form the Paired Brachial Vn
• 5. Brachial Vns paired w/ BA joins the Basilic Vn to becomes Axillary Vn 
• Axillary Vn travels adj to Axillary Art and crosses the 1st rib to become the Subc Vn
• 6. Subc Vn is inf/ant to Subc Art and courses Medially
• It joins IJV (Internal Jugular Vn) & forms & drains→Brachiocephalic/Innominate Vns
• 7. RT & LT Innominate Vns unite to form SVC (Superior Vena Cava)
• 8. SVC carries bl → RT atrium

• Cephalic Vn
• Travels superficially up the Lat aspect of arm
• Joins prox Subc Vn or distal axillary vn

• Basilic Vn (Largest Vn in the UE)
• Travels superficially up the Medial aspect of arm
• Joins w/ Paired Brachial vn to form Axillary vn

• Cephalic & Basilic Vns connect @ Antecubital fossa through Median Cubital Vn
• They are paired closer to the wrist

• Cephalic Vn
• Radial Vns
• Ulnar Vns w/ the Basilic Vn most medial

*Many pts have extensive branches of the Basilic vn in the forearm & one main vessel may not be found at the wrist level

• Basilic Vn
• Brachial Vns w/ Cephalic Vn most Lateral

• Means corresponding veins & refers to their close proximity to the accompanying Art (usually same name)
• Usually found with certain smaller arteries,
• especially those in the extremities. 

• Extremity                        Paired Vns
• Upper                              Brachial
•                                       Radial
•                                       Ulnar

• Lower                              Ant Tibial
•                                       Post Tibial
•                                       Peroneal

• Joining of the ATV+Tibial Peroneal trunk Vns=Pop V @ the Adductor Hiatus
• From the Adductor Hiatus, SFV joins w/the Profunda Femoris Vn (DFV)
• Fr the Inguinal Lig, EIV joins w/ IIV
• Confluence of the CIV joins the IVC to the RT Atrium
• Fr the medial arm vn, Basilic (superficial vn) joins the Brachial Vn
• Fr the lateral arm vn, Cephalic (superficial vn) joins the Axillary vn
• Joining of the Innominate Vns, SVC ends @ the RT atrium

• SVC is joined by the LT & RT innominate vns
• IVC is joined by the LT & RT CIV
• PORTAL VN is formed by vessels carrying bl → liver (ie Superior Mesenteric & Splenic Vns)
• HEPATIC VN are vessels that carry bl out of the liver → IVC

*INSPIRATION & EXHALATION have little, if any, affect on Central Vessels

• Thin-walled collapsible tubes that carry bl away from the periphery → heart
• Has the same 3 layers as Art wall (medial layer is the thinnest)
• Walls do not have the same elasticity as Art wall (it allows for some dilatation &/or constriction)
• Venous sys starts at the capillary level w/progressive ↑ in size as vessels carry bl → RT atrium
• Venous valves are evident in some vessels

• -64% of our blood volume is carried in the veins.
• -It can expand to hold large amts of
• bl.
• -Veins are bl vessels that carry bl fr the body back to the heart.
• -Bl return fr the legs occurs mainly through the deep veins.
• -Within the veins, especially those of the
• legs are valves.

• -Extensions of Intimal layer that provide unilateral flow fr Superficial to deep & fr the Periphery to Central venous sys
• -They are bicuspid, essential to the muscle pump & consist of endothelial tissue
• -When the muscle is at rest, the valves close helping to prevent the backward flow of blood

• W/o Valves:
• Innominate Vns
• Sup Vena Cava (SVC)

• W/Valves:
• Jugular Vn
• Cephalic & Basilic Vns

• Soleal Sinuses
• EIV: contains valves 25% of the time
• CIV
• IIV
• IVC

• GSV (most below knee) : 12
• Small Saphenous Vn: 6-12
• Perforators: 1 ea
• Infrapopliteal: 7-12 ea
• Pop & Femoral: 1-3 ea
• CFV: 1 
• EIV

• Venous Vol
• Venous Resistance
• Venous Po

• -Thin walled collapsible nature of the veins
• affect venous volume 
• Low vol = dumbbell shape
• High vol = Circular shape

Flattened shape allows ↑ flow resistance than circular shape

Compliance: Ability of vns to accomodate large shifts in vol w/ limited changes in venous Po

• The shape of the vn determines transmural
• pressure (distension pressure) 
•  
• Low bl vol=low Po
• High vol=High Po

• -Muscle contraction (ie, walking, swimming, running) promotes venous return by muscle pump
• -Sympathetic activation of vns ↓ venous compliance, ↑ central venous Po & promotes venous return indir by augmenting cardiac output through the Frank-Starling mechanism, w/c ↑ the total bl flow thru the circulatory system
• -During respiratory inspiration, the venous return ↑ because of a ↓ in RT atrial Po 
• -An ↑ in the resistance of the vena cava, as occurs when the thoracic vena cava becomes compressed during a Valsalva maneuver or during late pregnancy, ↓ return 
• -Gravity

• 1. Respiratory cycle - Central venous pressure
• (CVP) ↓ w/ inspiration thereby ↑ venous return.
• (look @ inspiration)
• 2. Venous tone 
• 3. Right heart function - The bl reaching the RT ventricle is pumped to the pulmonary
• circulation and therefore will not be damped
• backward in the venous system.
• 4) Gravity
• 5) Muscle pump

• -Develops when venous return is impaired for any reason, and can arise fr abnormalities w/in the deep veins, superficial veins, or a combination 
• -Normal Po w/in the vns of the LE is extremely low.
• -Normal inflow to the LE vns is purely via arterial inflow
• -When the entire venous system is filled, valves float open & venous PO rises to
• a maximum exactly equal to the height of the
• standing column of venous blood from RT
• atrium to foot.
• -This triggers an urge to move the legs, activating the muscle pumps and emptying the leg veins.

• -Thoracic Po ↓ (CVP ↓ & Venous Return ↑)
• CVP: Central Venous Po
• -Abd Po ↑
• -Bl moves fr abd to thoracic section
• -Bl fr legs ↓/stops
• -Inflow fr UE is allowed (↑) & →SVC drains

• -Thoracic Po ↑ (CVP ↑ & Venous Return ↓)
• -Abd Po ↓
• -Bl fr legs ↑ in flow → IVC
• -Bl fr arms ↓/stops due to high Po in that region

• -Evaluates status of EIV, CIV and IVC
• -Used to check for Valvular incompetence & Superficial venous system
• -As pt takes a deep breath & holds it then bears down Both Thoracic & Abd Po ↑ w/c leads to ↓ bl flow in both lower/upper extremities
• -While thoracic Po ↑ in Arterial sys, ↓ Venous return (flow & vel) occurs causing Doppler venous signal @ the CFV to cease (stop).  
• -As pt releases the breath & stops bearing down, a decline in art BP resulting fr impaired
• atrial filling w/c involves an ↑ in BP after a
• sympathetic response & augmentation of venous signal should be visible
• -After the strain is released a ↓ in art BP is followed by another sympathetic restoration

• Diminished augmentation=proximal obstruction
• Augmentation of signal as pt bears down=flow reversal consistent w/ Valvular incompetence

• -Diminishes Venous bl flow everywhere in the body  
• As pt releases the breath & stops bearing down, there s/b a brief ↑ in flow

If a prolonged flow reversal/reflux occurs=Incompetent valves 

In color, red flow lasting 0.5 a second then blue flow on release of valsalva= Incompetence  

Compress or squeeze proximal in the leg to check Competency of valves

-Cessation of flow w/ proximal compression, resuming on release

-Augmentation w/proximal compression or on release of distal compression=insufficiency

-If color flow display lights up blue w/ calf compression then red for 2-3 seconds on release=Venous Reflux

• Extrinsic compression of the lower left iliac
• vein as it passes under the right iliac artery.
• LT Iliac Vn crosses Post to the RT CIA distal to the AO Bif

• -Extrinsic compression of the LT Iliac vn as it passes under the RT Iliac art
• -causes ↑ incidence of acute DVT of LT lower extremity
• -It is also known as iliac vein compression syndrome & as  ‘Crockett syndrome’.  
• -Should not be confused w/ external compression leading to ilio-femoral DVT.

• -Pain/swelling in the ankles & legs but not the feet
• -Sometimes accompanied by redness & warmth
• -Relieved by elevation
• + Homans sign: pain in calf upon Dorsiflexion
• -Clinical exam is neither specific/sensitive
• -Diabetes is NOT a risk factor
• -With DVT high up in the leg (iliofemoral vein), superficial vns may become visible over the thigh and hip areas as well as over the lower abdomen

• Muscle strain
• Superficial Thrombophlebitis
• Dir inj to leg
• Varicose veins
• Muscle tear
• Baker's cyst
• Cellulitis
• Lymphangitis
• Heart failure
• Extrinsic compression
• Complications of chronic venous insufficiency

• A blood clot that forms in an inflamed part of
• a vein near the surface of the body (i.e., not a
• deep vein)
• -Attributed to a thrombosed saphenous vn
• -Results in significant incapacitation of pt
• -Responds to ambulation, warm soaks & aspirin
• -Frequently recurrent
• -NOT diagnosed by PPG

• -Venous insufficiency is the most common venous disease w/c presents w/ a range of skin changes 
• -Skin edema fr fluid accumulation
• -Redness (rubor) → (ie cellulitis)
• -Brownish discoloration (brawny) fr venous stasis
• -Whiteness (pallor)
• -Bluish discoloration (cyanosis)

• Infection of dermal tissue causing abscess on skin
• Red, warm tissue commonly seen on the shin/foot

• -↑ capillary Po fr an obstructive process (excessive fl accumulation in tissues)
• -Can also be related to electrolyte imbalance, renal dysfunction or congestive heart failure
• -Pitting edema of BOTH LE is related to cardiac or systemic origin (CHF)

• Chronic Condition
• Painless, swelling due to obstruction in the lymphatic system

Evident in the medial surface of lower leg-to-ankle area (gaiter zone)

fr arterial spasm secondary to extensive, acute ilio-femoral thrombosis called Phlegmasia alba dolens

fr severely reduced venous obstruction called Phlegmasia Cerulea Dolens

• Trauma to the vessel aka endothelial damage
• Venous stasis
• Hypercoagulability

Could be intrinsic (ie drugs, indwelling catheter) or extrinsic (ie following a fall, Paget-Schroetter Syndrome)

• Can result fr a variety of causes incl:
• bed rest
• immobility
• myocardial infarction
• congestive heart failure
• hypotension
• COPD 
• SVC syndrome
• Obesity
• Pregnancy
• Previous DVT
• Extrinsic compression
• Surgery
• Paraglegia

Can be related to pregnancy, cancer treatment, estrogen intake, hyperviscosity, deficiency of antithrombin III, nephrotic syndrome, changes after severe trauma or burn, race, age, smoking, and obesity.

Chronic Venous insufficiency-typical rusty brown color at ankles & calves

• -Occurs bec obstruction created by DVT prevents adequate venous outflow
• -LE ulcers are caused by CVI
• -↑ venous vol results in ↑ Po
• -Weak Calf muscle
• -Congenital defect of the valves
• -Previous DVT
• -Valvular incompetence
• -Post Phlebetic
• -Results from Calf-vein, pop v, iliac vn thrombosis and superficial insufficiency

Pulmonary embolism

• A piece of thrombus breaks loose & travels centrally through the heart where it lodges in smaller vessels of the pulmonary circulation
• -It can lead to even more serious complications, including: Heart palpitations, heart failure or cardiogenic shock. ↑ BP in the lung art (pulmonary hypertension).

• -Pulmonary angiography is the definitive diagnostic tool although spiral CT is the most widely used (Gold Standard Test)
• -Radioisotope test w/c involves both breathing & injection of the isotope is the V/Q scan
• -Heparin is the drug of choice to manage PE

• -Tachypnea: rapid respiration
• -chest pain
• -Sudden cough, which
• may produce bloody sputum 
• -↓ Art bl gas
• -shortness of breath (diaphoresis/dyspnea)
• -Pleural Effusion

*90% of PE come fr LE DVT

• -Valvular incompetence causes venous hypertension
• -When venous hypertension exists, arteries no longer have significantly higher pressure than veins, blood is not pumped as effectively, and it pools. 
• -Alteration in energy gradient across capillary bed ↓ bl flow
• -Stagnant bl ↑ capillary Po causing fluid, RBC's & other products leak into surrounding tissue
• -Hemosiderin fr breakdown of stagnant RBC's causes brawny discoloration
• -Breakdown of other substances can prevent surrounding tissue fr rcvng proper tissue nutrition & oxygenation leading → ulceration
• -Wounds may not properly heal if there is an underlying venous disease

• Near medial malleolus cephalad to the foot
• Shallow & irreg shaped & located in bony prominences 
• Stasis dermatitis: Infection/inflammation, brawny, LE varicosities, edema
• Mild Pain
• Venous ooze
• Commonly occur in the LE
• *Venous ulcers tend to develop near medial malleolus bec of perforators @ that location
• LE ulcers are the result of Venous Disease

• -Varicose veins are actually just normal veins that have dilated due to high pressure becoming "Incompetent valves"
• -Symptoms include aching pain, burning,
• cramping, throbbing, leg fatigue, and swelling.
• -Standing for long periods and heat aggravate
• symptoms. 
• -Pregnancy and the menstrual cycle also tend to worsen symptoms
• -Walking, cool temperatures and elevation
• improves them.

• -Caused by Valvular incompetence of the superficial venous sys in the presence of an intact deep venous sys
• -Varicosities result fr hereditary weakness or absence of venous valves
• -Aggravating factors include pregnancy, obesity & occupations w/c require long periods of standing

• -Pain during walking
• -Secondary varicose veins are those due to
• obstruction and valvular incompetence of the
• deep veins. 
• -This is the more serious form.

• -Pt is seated w/ legs dangling
• -Sensor applied above medial malleolus
• -Pt does 5 foot dorsiflexions to empty vns
• If Venous refill time (VRT) is ≥20 sec=Normal
• If VRT <20 sec, a tourniquet is applied to eliminate infl of superficial venous sys & study is repeated
• If repeat VRT >20 sec=Superficial sys has Venous IcompetenceIf repeat VRT remains <20 sec=Deep sys is incompetent

• -They are all capacitance/outflow modalities and utilizes a scoring grid to plot them
• -All used in detecting significant DVT

• -Documents Chronic Venous Insufficiency by quantifying the changes in venous outflow, venous reflux, calf muscle pump function & ambulatory venous pressure (↑)
• in pts w/ chronic swelling, venous ulcers &/or varicose veins
• -Can't be performed in pts w/ Acute DVT
• -Inaccurate results will be obtained if PPG sensor is not place @ right site (ie over a varicose vein or if skin is very thick or not intact)

• Plethysmography measure Vol changes from all vessels under the sensor
• Capable of utilizing either DC or AC coupling monitor flow patterns fr either Venous or Arterial sys

• Dir Current that is either + or -
• Only flows in 1 direction (ie battery)
• DC power evaluates relatively slow changes in bl content of the skin, it used for VENOUS eval

• Alternating current of 60 cycles/sec (reverses current fr + to - 60 times per sec)
• With AC power, intense flow changes are required to produce measurable signal
• It is used for ART studies

*Tech must set equipment to the appropriate coupling depending on study 

• Pt supine & leg passively raised=Venous sys is emptied
• When pt quickly stands=↑ Venous Vol (VV) is seen
• When pt completes 1 tiptoe exercise=↓ in calf VV is seen & calculated as the ejection vol (EV)
• VFT is measured after a series of 10 tiptoe exercise
• As pt quickly go back to supine position; same leg is elevated, Vns should empty

• VFI (Venous Filling Index): rate of venous filling
• EF (Ejection fraction): measures function of calf muscle pump & s/b >60%
• RVF (Residual Vol Fraction): is percentage of VV remaining after 10 tiptoe exercise

• Pt Supine
• 7-10 MHz linear probe
• Obtain compression, non-comp gray scale, color & PW images on the ff:
• IJV, SCV, AXILLARY V, BRACHIAL V, CEPHALIC V, BASILIC V, RADIAL/ULNAR VS

*Sniff to compress SCV

• Pt Supine in a Semi-Fowler or Reverse Trendlenberg position
• Leg bent
• 5-7 MHz linear probe
• -Use AUG to prove there is NO thrombus
• -Obtain TRV, gray scale on the same screen w/ & w/o comp of:
• CFV, DFV (P), SFV (P/M/D), POPV, ATV, PERO V, PTV

• Grayscale & color w/ PWD 
• Make sure color is filled from wall to wall,
• if there are filling defects:
• ↓ scale to show slow flow
• ↑ color gain, ↑ persistence, ↓ F, ↓ filter, ↓ box size, distal squeeze, lift Po fr vessel

• Spontaneity: flow is immediately seen when probe is placed over vessel
• Phasicity: related to respiration
• -During inspiration venous
• signals stop, during expiration venous signals return in an augmented state. 
• Augmentation w/ distal compression & proximal release
• Patency: open vessel throughout

Venous incompetence or Valvular incompetence can be assessed w/ handheld CW doppler

-Nonspontaneous flow seen in PTVs or GSV is common in pts that are nervous and/or cold & therefore, Vasoconstricted (less flow in venous side due to closed down arterioles)

• -The key ultrasound finding in excluding venous clot is the complete compressibility of the vein w/ downward pressure of the U/S probe 
• -With thrombosis and lumen obstruction, downward probe Po will fail to compress the vein image
• -failure to collapse the vn w/ enough pressure to deform the artery is considered a positive
• finding for venous occlusion 
• -Incomplete or partial collapse is also considered an abnormal finding

• To r/o DVT, to check compressibility & spontaneous signal
• Shallow breathing → Cont flow (NO phasicity)
• Ask PT to breathe deep & check for phasicity (spontaneous, or steady flow) to r/o DVT

• -Surgical removal of a vn clot.
• -This procedure, most commonly
• used to treat a rare complication of DVT called Phlegmasia cerulea dolens 
• -When combined with one or more of the ff treatments there is a 70-100% success rate: Thrombolysis; Anticoagulant medications; Angioplasty and stenting; and Placement of a vena cava filter.

• >65 y/o; Have bleeding tendencies; Have HTN, CHF, or poor kidney function; or Are allergic to contrast dye. 
• -Other complications for treatment of DVT include: PE; Post-thrombotic syndrome;
• Phlegmasia cerulea dolens, hemorrhage,
• Stroke.
• -Has been assoc to repeat clotting

• Indicates venous or pulmonary HTN, CHF, or the presence of an AVF 
• If Bilat =Systemic Venous HTN
• (EXCEPT: Flow in JUGULAR, SUBC & INNOM is pulsatile due to close proximity to the heart
• SUBC VN will usually Augment w/ Inspiration

• -No Collateralization 
• -No color filling
• -Attachment of thrombus may be poorly attached to the wall (like a tail)
• -Vessel not completely compressible
• -Anechoic or sonolucent (absence of echoes) or very low-level echoes
• -Dilated (compared to accompanying art)
• -Abnormal flow patterns

• -Vessel may not be completely compressible
• -Hyperechoic
• -Retracted vessel size
• -May be abnormal flow patterns
• -Collateralization may be evident
• -Vessel fills; color shift indicating Reflux may be seen
• -Thrombus very well adhered to wall
• -Assoc w/ pigmentation, brawny edema
• -Subcutaneous fibrosis
• -Cutaneous atrophy

• -INVASIVE Procedure that provides x-ray visualization of the veins, particularly in the LE 
• -A special dye is injected that is visible upon x-ray 
• -Pt position is on an exam table tilted 60⁰upright
• -It allows the physician to evaluate the size and condition of the veins
• -It is the gold standard for diagnosis of DVT
• -Several methods are used to visualize the Vns: Ascending Venography, Descending Venography, Venography of the UE, Venacavography

• -Assesses Acute DVT 
• -Identifies the presence and location of DVT.   -Venous puncture site is on the dorsum of the foot
• -Capable of identifying filling defects consistent w/ an acute DVT, anatomic variations & development of collateral channels

*This info may be helpful in determining if pt is a candidate for surgical intervention

• -Is performed to diagnose Valvular Insufficiency
• -Identifies specific Valvular Incompetence
• -Venous puncture site is @ the CFV

• Highly technical in technique & interpretation
• Expensive
• Uncomfortable
• Adverse effects of the contrast media
• Not for pts w/ severe peripheral vascular occlusive disease (PVOD)
• Not for pts w/ allergies to iodine

-Assesses blockage, lesions, or thrombosis in the veins of the neck and axillary (armpit) region

• ↓ in platelets
• Causes bleeding complication (hematoma) in pts w/ heparin treatment

If no contraindications (ie active bleeding) pt usually rcvs a 5-10 day dose of IV heparin

• Coumadin: interferes w/ formation of bl clot. It is taken on a reg basis for 3-6 mos
• Heparin: interferes w/ formation of bl clot
• Lytic therapy: ie streptokinase or urokinase, breaks down thrombus & is usually recommended when DVT is limb threatening (ie phlegmasia cerulea dolens & phlegmasia alba dolens)

• Placement of IVC interruption device to prevent PE (pulmonary embolism)
• Iliofemoral thrombectomy may also be considered for impending limb loss

• -A substance that prevents coagulation (it stops blood from clotting).
• -These anticoagulants are used to treat pts.
• with DVT, PE, atrial fibrillation (AF), and
• mechanical prosthetic heart valves.
• -Warfarin (Coumadin) is the most common used agent
• -Heparin is another agent used w/c
• works by activating antithrombin III, w/c
• blocks thrombin from clotting blood. It can be used in vivo (by injection), and also in
• vitro to prevent blood or plasma clotting in or
• on medical devices.

• -It hinders the effect of anticoagulant Coumadin
• -Vitamin K laden foods (generally leafy green
• vegetables) and diuretics (↑ clotting
• factor concentration) reduce the anticoagulant
• effect and ↓ the turnover of clotting factors.

• -sometimes called "water pills."    
• -used to treat CHF, high BP or edema (water
• retention) 
• -lower the amt of salt or sodium and water in your body, w/c helps to lower your BP
• -Lasix, Aquatensen, Diucardin, Diulo, Diuril,
• Enduron and Hydro are are commonly used
• diuretics.

• IVC interruption devices: placed below the Renal Vns & are bright echogenic lines on B-mode
• Systemic Venous Hypertension: Persistent dilated vessels consistent w/ Venous Hypertension
• Portal Hypertension: ↑ Portal Venous Po = in variety of flow alterations like reversed flow in PV (hepato-fugal instead of hepato-petal) ↑ flow in HA & development of collateral channels

• Sensitivity
• Specificity
• +Predictive value
• - Predictive value
• Accuracy

• Ability of a test to detect disease when it is present
• Divide # of true + noninvasive studies by # of all false - = # of + gold standard studies

• Ability of a test to exclude disease when no disease is present
• Divide # of true - noninvasive studies by # of all false + studies= # of - gold standard studies

• How often a + study is correct
• Divide the # of True+ noninvasive studies by total # of Abnormal + noninvasive studies whether studies were correct or incorrect in picking up disease

• How often a - study is correct
• Divide the # of true - noninvasive studies by total # of Normal - noninvasive studies whether studies were correct or incorrect in excluding disease

• Overall ability of a test to identify disease as well as to exclude it
• Indicates how confident you are that the noninvasive study is correct
• Divide # of true positive + true negative noninvasive studies by total # of noninvasive studies whether they were correct or not

• True + : study is + (disease detected thru radiology, surg, pathology, etc)
• False + : study is + but pt does not have disease state. Findings not confirmed (by gold standard) or wrong
• True - : study is - (no disease findings thru radiology, surgery, etc)
• False - : study is - but pt has the disease state & was missed. Findings not confirmed (by gold standard) or wrong

• 1. Compare noninvasive results w/ gold standard
• 

• aka Average
• Add the numbers together
• Divide by how many numbers were added together
• The mean
• of 4,7,10,3,3,3 is 5.

• Mode-Arrange the numbers in order by size
• Determine the number of instances of each
• numerical value
• The numerical value that has the most instances or most common occurring is the Mode

• The mode of 2, 4, 5, 5, 5, 7,
• 8, 8, 9, 12 is 5. 

• Arrange the numbers in order by
• size
• If there is an odd number of terms; the
• median is the center term
• If there is an even
• number of terms, add the two middle terms
• and divide by 2

• ↓ SA Node rate (natural pacemaker of the ♥)
• -Parasympathetic innervation of
• the heart is controlled by the vagus nerve; therefore, vagus nerve lowers the
• heart rate.

*Sympathetic nervous system of the ♥ ↓ AV conduction time & ↑ the heart rate & contractility

• Inertia: when flow accelerates/decelerates (due to change in dir)
• Kinetic: Energy of something in motion
• Potential: form of BP
• Hydrostatic: Gravity
• Viscosity: Friction or resistance of bl & by its Inertia
• Stasis: Stagnant

• Acidosis: build up of carbon dioxide (Ph=7.4 normal) Ph=7.3 acidosis (hypoventilation)
• Alkalosis: Deficient carbon dioxide (PCo2=40 normal) PCo2=30 alkalosis (hyperventilation)