3 Layers of Art wall Tunica: Intima=Innermost layer (endothelial cells) Media=Middle layer (thickest) Externa (Adventitia)= Outermost layer Vaso Vasorum Tiny vessels that carry bl to the walls of larger arteries Feed Adventitial layer and some of medial layer Duplex Ultrasonography aka Duplex U/S 2 elements: Gray Scale & Color doppler Both displays are presented on the same screen ("duplex") to facilitate interpretation. Duplex Ultrasonography-Gray Scale 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) Duplex Ultrasonography-Color Doppler 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). Stenosis Criteria 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 LE Art Anatomy Common Terminology to be familiar with 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 LE 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 Plantar Arch 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 What membrane passes superficial to ATA After arising fr the dist Pop A, ATA passes superficial to Interosseous membrane Landmarks for Tibia & Fibula Ant Tibia: ATA & paired ATV's Post Tibia: PTA & paired PTV's Medial to Fibula: Peroneal Art & paired Pero Vns LE Art -EIA 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 LE ART- Internal Iliac Art (IIA) 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 LE ART-CFA 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 LE ART-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 LE ART-SFA 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 LE ART-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 LE ART-ATA 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 LE ART-Tibioperoneal Trunk aka Proximal/Post Tibial Art 2nd branch off distal POP A w/c divides into PTA & Pero Art LE ART-PTA Post to Tibia, behind Medial Malleolus Terminates into medial/lateral Plantar art of the foot Feeds medial aspect of lower leg & foot LE ART-PERO Art Adjacent to the border of Fibula (small bone) Supplies Lateral aspect of leg & foot Courses deep in the post compartment of the leg. LE ART-DPA ATA comes on lateral aspect of ankle and → DPA w/c branches into Deep Plantar Art & part of Plantar arch LE ART Pathway 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 LE ART Disease Diabetes is the major risk factor PPG in leg does NOT diagnose superficial thrombophlebitis Guides to performing U/S guided tx compression of pseudoaneurysm Adequately visible Appropriate position so it can be uniformly & completely compressed Size Location Monitor Ankle Po Limitations in neck compression w/ Thrombosis of the aneurysm Pt currently on bl thinning meds Pt has discomfort; no sedation available Popliteal Entrapment 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 Compartment Syndrome 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 Blue Toe Syndrome 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 Plaque Ulceration Caused by thrombosis, intraplaque hemorrhage, embolization Major risk factors of Atherosclerosis Smoking Hyperlipidimia Family Hx Diabetes Hypertension Sedentary lifestyle Common locations of Atherosclerotic diseases -Aortic Bifurcation -Iliac/Femoral Bifurcation -Tibial Trifurcations -SFA @ the level of the adductor Hiatus (important site in diabetic pts.) LE ART-Chronic Occlusive Disease  Claudication 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 Pseudo Claudication Mimics vascular symptoms Usually orthopedic or neurogenic in origin 3 types of Claudication 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 Intermittent Claudication -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 LE ART-Chronic Occlusive Disease Rest Pain 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 LE ART-Chronic Occlusive Disease Necrosis 3rd Stage---Most Severe Tissue death Revascularization or amputation is usually required Signs & Symptoms of Chronic Art Disease 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 Causes of Chronic Occlusive Disease-ASO Atherosclerosis Obliterans (ASO) Plaque build up on intima leading to hardening of the vessel 99% of Chronic vascular disease=ASO (plaque) Causes of Chronic Occlusive Disease- Buerger's Disease (TAO) 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 Causes of Chronic Occlusive Disease- Takayasu Arteritis aka Pulselessness Disease Inflammation of Tunica Media/Intima Inflammation of AO/AO arch Causes of Chronic Occlusive Disease- Leriche's Arteritis Occlusion in ART of Abd AO Assoc. w/ claudication of LE w/c can cause Male impotency Causes of Chronic Occlusive Disease- Polyarteritis Mult art are swollen/painful Related to trauma/surgery Causes of Chronic Occlusive Disease- Temporal Arteritis Idiopathic of Superficial Temp Art Acute Arterial Occlusion Results from trauma, embolism, thrombus No Collaterals develop w/ Acute Art Occlusion Arterial Ulcers 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 Symptoms of Acute Art Occlusive Disease 6 P's 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 Causes of Acute Occlusion Disease Thrombus Plaque Dissecting Aneurysm Trauma Tumors Entrapment of vessel Hypercoagulability Raynaud's Phenomenon Vasospastic Disorders Abnormal vasospasm of the digital art in hand/feet due to exposure to cold Vasospastic Symptoms 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 LE ART Non-Imaging exam Physical Exam Doppler Waveform Doppler segmental pressures Palpation Auscultation CWD LE ART Non-Imaging exam- Physical Exam 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 LE ART Non-Imaging exam- Palpation Pulses/aneurysms AO CFA POP A DPA PTA/ATA 0-4 (0:No pulse; 4:Aneurysmal/bounding) LE ART Non-Imaging exam- Auscultation Stethoscope used to listen for a bruit (mainly after stenosis) heard over an art Bruit is a vibration transmitted to surround tissue. BRUIT 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%) "Vibration/Thrills" may be due to the ff: AVF AVM Cardiac murmur Dissecting Aneurysm Post stenotic turbulence Patent Hemodialysis graft 4 sites auscultated by stethoscope CCA AO Femoral A POP A Absence of Bruit suggests 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 LE ART Non-Imaging exam- CWD Eval plaque, stenosis, narrowing disease Approximate location of plaque/disease Follow up post surgery Less expensive LE ART Non-Imaging exam- CWD limitations 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 LE ART Non-Imaging exam- CWD Method 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 LE ART Non-Imaging exam- CWD Results 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 LE ART Non-Imaging exam- CWD sources of error Improper probe position  Incorrect angle s/b 45-60 Inadequate amt of gel used Excessive Po on end of probe Inadvertent probe motion Reasons for a False + test (abnormal flow pattern but W/O any obstruction) in a CW technique 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 Reasons for a False - test (Normal flow but with venous obstruction present) in a CW technique Partial obstruction Collateralization Paired vns of lower extremity Bi-fed sys (mult. deep vns) LE ART exam-Duplex Method 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 LE ART exam-Duplex Results 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 LE Art-Normal Peak Vel (PV) Waveform characteristics 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   Classifications of a Peripheral Art Stenosis -Waveform Shape -PSV -Spectral Window/Envelope -Look for focal acceleration of Velocities & Distal Turbulence Classifications of an Occlusion -Absence of flow -Proximal flow is High Resistance -Distal flow is Low Resistance w/ Tardus Parvus -Collateral Flow Classifications of a Collateral Flow -Low Vel Monophasic waveforms -Lose Triphasic character -Tardus Parvus appearance -Low Resistance to degree of Ischemia Pulsatility Index PI=Max Vel - Min. Vel                Mean Vel Peak Systolic to peak end diastolic vel divided by Mean vel Pulsatility Index Results 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 Acceleration Time (AT) 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 Acceleration Time (AT) Results 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 Outflow vs. Inflow 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) ABI Compares Brachial systolic BP to the ankle Po to identify lower extremity art disease ABI Method 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 ABI Results >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 LE ART- Doppler Segmental Po (DSP) Taking BP (only systolic components) of the diff segments of the body Part of ABI exam, but helps narrow down area of disease LE ART- Doppler Segmental Po (DSP) Method Supine Bilat BA & ankle Po & calculate ABI Bilat BP of LE w/ help of 4 cuff or 3 cuff technique LE ART- Doppler Segmental Po (DSP) Order 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 LE ART- Doppler Segmental Po (DSP)  4 cuff technique 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 LE ART- Doppler Segmental Po (DSP) 3 cuff technique 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 LE ART- Doppler Segmental Po (DSP) Comparisons of 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 LE ART- Doppler Segmental Po (DSP) Results 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 LE ART- Doppler Segmental Po (DSP) Disadvantages Cant discriminate betw Stenosis/Occlusion Can't pinpoint exact location Difficulty distinguishing betw CFA & EIA disease Ca++ vessels yield falsely elevated bp Toe Brachial Index (TBI) Quantitative info -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 TBI Range 0.6-0.8 (60-80% of ↑ Brachial Po) Toe Po ÷ ↑ Brachial Po TBI rel to Peripheral Art Disease (PAD) ≥ 0.8 = NO Significant PAD 0.2-0.5 = CLAUDICATION <0.2 = REST PAIN LE ART- Plethysmography: PVR (Pulse Vol Recording) or Pneumo (air) Plethysmography -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 LE ART- Plethysmography Amplitude 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 LE ART- 3 Methods of PVR Air Cuff Strain Gauge PPG LE ART- Strain Gauge Uses mercury filled silicon like tube that has electrodes on both ends LE ART- Photoplethysmography (PPG) 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 LE ART- PVR/DSP Test Do DSP Do PVR    First upper & lower thighs    Calves then feet Use table values of DSP LE ART- PVR Waveform Analysis 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 LE ART - Treadmill Testing or Exercise Hyperemic 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 LE ART - Treadmill Testing or Exercise Hyperemic Method 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 LE ART - Treadmill Testing or Exercise Hyperemic Results 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 LE ART- Reactive Hyperemia aka Post Occlusive Reactive Hyperemia (PORH) Uncomfortable exam for pt LE ART- Reactive Hyperemia Alternate Test 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 LE ART- Reactive Hyperemia Method 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 LE ART- Reactive Hyperemia Results 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 LE ART- Cardiac & Claudication Treadmill testing Diff between the 2 testing is speed & elevation UE ART-Anatomy UE ART 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 UE ART-Palmar Arches 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 UE ART Pathology- TOS -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 UE ART Pathology- TOS (2 types) ATOS: Art TOS caused by compression of the Subc Art VTOS: Venous TOS caused by compression or blockage of the Subc Vn UE ART Pathology- TOS Symptoms Neck pain UE pain, weakness or clumsiness Numbness & tingling in shoulder/arm Intermittent pain/weakness during exercise Headache UE ART Pathology- TOS Tests Adison's Test: arm extended 90 Costo clavicular Maneuver Hyper abduction EAST: Elevated Arm Stress Test UE ART Pathology- TOS Steps in testing 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 UE ART Pathology- TOS Results Normal: PVR waveform does not change (DN)and BP remains constant Abnormal: opposite UE ART Pathology- 2 conditions that produce similar symptoms to TOS (Thoracic Outlet Syndrome) Carpel Tunnel Cervical Disk condition UE ART Pathology-Subclavian Steal Syndrome -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. UE ART Pathology-Subclavian Steal Syndrome U/S indications 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 UE ART Pathology-ASO Plaque build-up on intimal layer causing hardening of the vessel Rare condition UE ART Pathology-TAO aka Buerger's Disease Occurs equally in UE/LE Starts distally→Proximally (NO collaterals) Rest pain in both hands/feet UE ART Pathology-Takayasu Arteritis aka Pulselessness Disease Inflammation of Intima/media causes narrowing of the lumen USA: Intimal thickening >0.08 cm PVR waveform abnormal UE Art Pathology-Primary Raynaud's syndrome 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 UE Art Pathology-Primary Raynaud's syndrome Vasospastic -Vasospastic w/c vasoconstriction ↑ and dist resistance ↓ due to arterioles & capillaries dilation -Vasospasm of the arteries reduces blood flow to the fingers and toes UE Art Pathology-Secondary Raynaud's Phenomenon or Raynaud's Phenomenon 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 UE Art Pathology-Raynauds Phenomenon Symptoms -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 - UE Art Pathology- Exam used to distinguish betw 2 types of Raynauds PPG is used to obtain PVR waveforms (DN) Quality of w/c is used to differentiate obstructive vs. vasospastic UE Art Pathology-Peripheral Art Aneurysm Bulge or dilation of vessel diameter Ulnar aneurysms Subclavian/Axillary aneurysm→ fusiform UE Art Examination-DSP Method 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 UE Art Examination-DSP Results 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 UE Art Examination-PVR Results -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 UE Art Examination-FBI ≥0.8 (80% of ↑ Brachial Po) 0.75-1.05 =Normal <0.75 =Abnormal ≤0.29 =Occlusion Finger Po ÷ ↑ Brachial Po UE Art Examination-Duplex Method 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) UE Art Examination-Duplex Method  Obtain ff images: SCA AXILLARY ART BRACHIAL ART RADIAL ART ULNART ART PALMAR ARCHES (optional) Eval for signs & symptoms of Aneurysm such as pseudo-aneurysm or discoloration UE Art Examination-Duplex Results (Normal) Tri-phasic waveform Bi-phasic waveform can be considered normal in pts 65-70 y/o Clear, spectral windows w/ narrow BW UE Art Examination-Duplex Results (Abnormal) 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 UE Art Examination-The Allen Test Used to determine if Radial/Ulnar Art is occluded UE Art Examination-The Allen Test Method 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 UE Art Examination-The Allen Test Result 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 UE Art Examination-The Modified Allen Test 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 UE Art Examination-Limitations to Allen Test Excessive dorsiflexion of hand = false + Extension of hand/fingers= Pallor UE Art Examination-Grafts -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) UE Art Examination-Bypass Grafts  Synthetic -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 UE Art Examination-Bypass Grafts  Autologus 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" UE Art Examination-Bypass Grafts & other treatments Angioplasty and/or stenting, atherectomy, or cryoplasty Grafts provide good inflow, outflow, and adequate conduit of blood flow UE Art Examination-Types of Bypass Grafts Aortobifemoral graft  Axillofemoral femerofemoral graft Femoral-popliteal graft Popliteal-tibial graft Femoral-tibial graft UE Art Examination-Bypass Grafts Pathology Acute -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 UE Art Examination-Bypass Grafts Pathology Chronic -Atherosclerosis -Scar tissue may compress graft & occlude flow -Pseudoaneurysm -Intimal Hyperplasia @ anastamosis site UE Art Examination-Bypass Grafts Testing Method 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 UE Art Examination-Bypass Grafts Normal Results PSV betw 100-200 cm/s w/ organized turbulence Vel tends to be higher in the first 6 mos after placement of graft UE Art Examination-Bypass Grafts Abnormal Results 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 Hemodialysis Grafts Direct connection between high pressure arterial sys and low pressure venous sys There are marked anatomic & hemodynamic changes Hemodialysis Grafts Connection between Art/Vns 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 AVF 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 AVM Present @ birth Not a dir connection between art/vns Hemodialysis Grafts 3 Main Types 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 Hemodialysis Grafts Clinical Indications 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 Hemodialysis Grafts Complications 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) 4 drawbacks in using analog doppler display 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  Diff betw low from high resistant flow patterns 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) Define Vasopressors -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. Vasoconstriction ↑ 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 Vasodilatation ↓ 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 What is Nitroglycerin Transdermal patch? -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. 3 types of high resistant pulsatile signals 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 Organic (fixed) Obstructive disease Has abnormal: Doppler Art signals Systolic segmental Po PPG tracings Functional (Intermittent) obstructive disease Has normal: Doppler Art signals Systolic segmental Po &/or PPG tracings Abnormal findings after cold stimulation Transcutaneous Oximetry (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 2 Limitations of TcP02 Inability to keep electrode on surface of skin It can NOT be applied to non-intact skin (ie ulceration) "Step" in setup process of TcP02 Manual Calibration prior to obtaining a reading at any portion of the extremity ABDOMINAL- AO 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 Major branches of ABD 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 4 Visceral Art branches (ABD-AO) 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 2 main branches of the Celiac Art Hepatic/Splenic Art (both have low resistance) "Seagull" sign: Hepatic Art/Splenic Art/Celiac Trunk Aortic Pathology-Ectasia 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 Aortic Pathology-Atherosclerosis 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 Aortic Pathology- Coarctation of AO Narrowing of AO due congenital or external compression & may affect Abd AO/Thoracic AO Assoc w/ hypertension & symptoms of LE ischemia & claudication Aortic Pathology- Aneurysm -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) Aortic Pathology- AAA -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 Aortic Pathology- AAA Test -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 Most frequent complication of Aortic aneurysm & peripheral art aneurysm 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 Aortic Pathology-Marfan Syndrome 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 ABDOMINAL AO Duplex Exam 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.  ABDOMINAL AO Duplex Method 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 Evaluation of Abdominal AO 50% DR = 100% ↑ in PSV across adj segments -Prestenotic to stenotic PSV ratio >4:1 = >75%DR -PSV >400 cm/s= >75% DR ABDOMINAL-Renals 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 Renal Image in B-mode Kidneys perform two essential functions: 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 What two methods are used in u/s evaluation of renal artery stenosis? 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. Renal Doppler waveform analysis, what should the acceleration time be? -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. Renal Duplex 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 RAR formula 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 PR (Parenchymal Resistance Ratio) RI (Resistive Index) 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) Normal Renal Parenchyma echogenicity Hypoechoic to the liver or same echogenecity Renovascular Hypertension (HTN) -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. Renovascular HTN - Clinical Indications HTN (new onset or uncontrollable) Follow-up post PTA/stenting  Follow-up bypass grafting Follow-up renal allograft Renovascular HTN - Clinical Exam 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. Renal Art Occlusion or Infarction 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 Renal Art Stenosis Image Renal Art Stenosis May be caused by plaque or fibromuscular hyperplasia or Renal hypertension Renal Stenosis treatments Bypass graft Angioplasty:ballooning of art wall Stent Renal Vein Thrombosis Can cause obstruction to the drainage Renal Art Aneurysm Infra (BELOW) renal aneurysms Renal Transplants 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 Causes of ↑ Resistance in a Renal Art Transplant Acute Rejection Renal Vn thrombosis Infection Tubular necrosis AVF perinephric fluid accumulations & hydronephrosis Stenosis in RENAL transplants usually occur @ Connection sites Distal donor art Recepient art Signs of Acute Rejection in Renal Transplants Abnormal texture of kidney w/ ↑ cortical echogenecity Abnormal size >13cm Hypoechoic area w/in the kidney (signs of failure) Signs of Chronic Rejection in Renal Transplants Smaller size kidney <9cm ↑ in RI (Resistive Index) Normal/Abnormal measurements of Kidney transplants Normal Arcuate Art Resistance: 0.6-0.8 cm Abnormal: >0.9 cm Normal PSV: ≤180 cm/s Abnormal: >180 cm/s indicates Stenosis Abdominal- Mesenteric Ischemia 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 Normal Results in Mesenteric Ischemia Pre-prandial→ High Resistance w/ RI= 0.75 Post prandial→Low Resistance w/ RI= 0.6 PSV <275 cm/s Abnormal Results in Mesenteric Ischemia 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 Celiac Axis Compression Syndrome (CACS) 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 ABDOMINAL-Portal System 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 ABDOMINAL- Portal Hypertension -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 Portal Hypertension-Varices Enlarged coronary vn Subcapsular varices Esophageal varices Hemorrhoids Patent Umbilical Vn (Caput Medussa) Splenic Varices (Pleural Effusion) Generalized Ascites Portal Hypertension-Cirrhosis -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. Portal Hypertension-Pre Hepatic causes Any ↑ in portal bl flow caused by: PV thrombosis Splenic V thrombosis Compression of PV due to lymph node Pancreatitis Splenomegaly Portal Vn Thrombosis in PTH (USA) Absence of flow on color doppler Dilated PV w/ internal echoes Make sure vel scale ↓ to detect slow flow Causes of Portal Vn Thrombosis Can be caused by: Inflammatory process, Portal Hypertension, Post Surgicalcomplications, Pregnancy, Contraceptives, Smoking, Tumors, Idiopathic (dont know) Portal Hypertension-Intra Hepatic causes ↓ in capacity of liver to transmit bl to IVC causes incl: Fatty liver Cirrhosis of the liver Parasitic infections called Shistosomiasis METS Portal Hypertension-Post Hepatic causes Budd Chiari Syndrome-Obst of HV Cardiac abnormalities Tumor in IVC (clot or compression) Budd Chiari Syndrome in PTH (USA) Non-visualization of flow in HV or IVC Echogenic intraluminal thrombus Flat continuous flow in PROX HV Portal Hypertension- Treatment 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 TIPS Evaluation-Normal 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 TIPS Evaluation-Abnormal 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 Portal Hypertension-USA Post surgical complications in a Liver Transplant -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 HV in USA-NORMAL Dark walls Hepatofugal flow (away) Phasic, Bi-dir/pulsatile flow due to pulsations from the heart Same flow is seen in IVC Hepatic Veins Evaluation-Abnormal 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) Portal Vn USA-NORMAL Echogenic walls Hepatopetal flow (towards) Phasic w/ respiration consistent w/ Splenic & mesenteric vns Size is up to <1.3 cm or <13 mm Portal Vein Evaluation-Abnormal MPV size >1.3 cm Hepatofugal flow Patent umbilical vn/Ligamentum Teres (LT) Tumor/bl clot w/in the vessel Hepatic Arteries Evaluation Normal: Low Resistance, pulsatile flow Abnormal: ↓ flow or absent flow after liver transplant indicates obstruction of HA AO  AO: Never touches the liver Has thicker/ stronger medial layer Triphasic, pulsatile/ high vel plug flow Tapers inferiorly IVC Wraps around the left lobe of liver Thinner walls Steady flow that changes w/ respiration Gets bigger in diameter closer to the heart Arteries used for mapping 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 Internal Mammary 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 Observations in Preoperative Vein mapping 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) Veins often used in mapping 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 Angiogrpahic studies (filling defect) 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 Complications after angiographic procedure Puncture site hematoma Pseudoaneurysm Local Art occlusion Neurologic complications 2 endovascular procedures Angioplasty (PTA) STENT ANGIOPLASTY (PTA) procedure -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) Angioplasty Site Stenosis Criteria STENT Procedure (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 Peripheral Stent Criteria Extracranial & Intracranial Segments of ICA EXTRA: Cervical INTRA: Petrous, Cavernous Siphon (Carotid Siphon), Supraclinoid → ICA terminates into ACA/MCA Branches of Ophthalmic Art Central Retinal Art Supra Orbital Art Frontal Art Major branch of ICA 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 Branches of ECA 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) Vascular bed supply of ICA/ECA 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 ICA characteristics in B-Mode & Doppler flow 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 ECA characteristics in B-Mode & Doppler flow B-mode:  More medial Usually smaller Branches evident Doppler flow: More pulsatile flow High-resistance signal (↓ flow in diastole) Oscillates w/ Temp art tapping Factors that may cause poor visualization of ECA on duplex imaging 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 Holenhurst Plaque -Bright yellow spot w/in an Art Branch in Ophthalmologic exam -Pts have a 75% risk of TIA w/ this incident Origin & termination of Vert Art 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 2 Circulatory systems for the brain 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 Circle of Willis 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 Describe Hemispheric or Lateralizing symptoms 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. Vessels of Ant Circulation Intracranial: ACA & MCA Extracranial: CCA, ECA, ICA Symptoms of Ant Circulation insufficiency in Cerebrovascular Unilateral effects on the body Hemiparesis: 1 sided weakness Hemiparesthesia: prickling or tingling of the skin Aphasia Behavior changes Peripheral vision loss Amaurosis Fugaux Symptoms presented with a diseased ICA 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 Amaurosis Fugax Temp partial or total blindness "shade coming down over the involved eye" Affects the same or ipsilateral side of the lesion Aphasia/Dysphasia 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 Symptoms assoc w/ a lesion in Middle Cerebral art Aphasia More severe hemiparesis or hemiplegia (one-side) of face & arm than of the leg Behavioral changes Homonymous Hemianopia Disrupts vision in 1/2 the visual field of both eyes Obstruction of MCA branch Symptoms assoc. with Lesion in the Ant Cerebral Art (ACA) Severe leg hemiparesis or hemiplegia Incontinence & loss of coordination Vessels of Post Circulation Intracranial: PCA & Basilar Art Extracranial: Vert Art Symptoms of Post Circulation insufficiency in Cerebrovascular 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 Symptoms assoc w/bl flow alterations to Post circulation or Vertebrobasilar system 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 RIND Reversible Ischmeic Neurologic Deficit  Completely resolves after 24 hrs Opposite of RIND is CVA 2 main classifications of Cerebrovascular disease 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 Cerebrovascular disease-TIA Warning signs 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 Cerebrovascular disease-CVA 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. 2 most common causes for CVA Atheromatous plaque Thromboembolic diseases Atherosclerosis 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 Atheromatous plaque 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 Thromboembolic diseases 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 Venous Thromboembolism (VTE) Is a general term w/c refers to mainly 2 conditions: DVT and its potentially fatal acute complication, pulmonary embolism (PE). Arterial Embolism 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. Types of Non-atherosclerotic disease evaluated by carotid duplex exam Aneurysm Dissection Fibromuscular Dysplasia (FMD) Carotid Body Tumor (CBT) Neointimal Hyperplasia Carotid Dissection Causes tearing injury to AO/Art (ie Car accident) Causes RT side weakness & aphasia Arterial Dissection 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 Pseudo aneurysm in Art Dissection 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.” Art-to-art thromboembolism 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 FMD 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 CBT Highly vascular Develops above carotid bif betw ICA & ECA  Usually fed by ECA Neointimal Hyperplasia Intimal thickening fr overproduction of smooth muscle cells Usually seen in vascular injury/reconstruction (post carotid endarterectomy) Waveform characteristics of a diseased Proximal ICA 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 Characteristics of flow patterns 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 Factors that may produce ↑ flow other than a stenosis (overestimation) ↑ Cardiac output Tortuosity of the vessel Collateralizing for ipsi/contra lateral disease Inappropriate doppler angle (ie >600) Factors that may be inconsistent betw Doppler & B-mode finding Low cardiac output ↑ flow vel NOT detected Long, smooth plaque formation Stenosis @ area of dilatation (ie carotid bulb) Inappropriate doppler angle Diff types of art wall irreg in B-mode imaging Fatty streaks Fibrous (soft) plaque Complex plaque Ca++ Thrombus Surface characteristics Fatty streaks Hypoechoic & homogenous (low-level echoes of similar appearance) Fibrous plaque Low, medium & high level echoes that have heterogeneous (non-uniform) appearance Ca++ Bright, highly reflective echoes Acoustic shadowing fr Ca+ deposit Thrombus Same echogenicity as flowing bl Bl clot Hematoma aka Bruise Occlusion Blockage *Occluded vessels do NOT produce a Bruit Stenosis Narrowing of a vessel Stenosis profile characteristics 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 Stenosis criteria table Tardus Parvus characteristics 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 Aliasing 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) TCD Study characteristics 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 Purpose of TCD (non-imaging) 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. Common indications for performance of a TCD? 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. Guidelines for ID of TCD 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 3 Pathways for Intracranial collateralization Cross-over External-to-internal  Post-to-Ant Cross-over collateralization Antegrade flow is evident in ACA.   Flow is crossing over from the contralateral ACA via a patent Ant Comm Art ACA: Ant Cerebral Art External-to-Internal collateralization 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 Post-to-Ant collateralization ↑ flow vel found in PCA Ant circulation is via Post Comm Art PCA: Post Cerebral Art Diagnosis of Vasospasm fr a subarachnoid hemorrhage 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 Innominate Art Occlusion ↓ Po on the Rt side Angina Chest pain, sometimes w/ radiation to jaw & or arm Temporal Arteritis 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 Diagnosis of Temporal Arteritis -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 Diameter Reduction formula DR=[1- d÷D] x 100 d=Residual Lumen D=True Lumen 50%DR = 75%AR MRA method -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 CT Method 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 Treatment options to Pts w/ disease of Extracranial carotid art Categories are:  Medical Surgical Endovascular Medical treatment to pts w/ disease of Extracranial carotid art Life style modifications such as: Stop smoking, Wt control & low cholesterol diet Aspirin may be prescribed to ↓ thrombolic activity Surgical treatment to pts w/ disease of Extracranial carotid art -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. Endovascular treatment to pts w/ disease of Extracranial carotid art Stenting continues to be an emerging technology w/ extensive clinical investigation continuing Bl flow from Deep vns of the toes to the RT atrium 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 Deep Vns include: CFV SFV DFV POP VN Paired ATV's Paired PTV's Paired Peroneal Vns Lower Extremity Anatomy 2 main Superficial Vns of the lower extremities 1. Small Saphenous Vn 2. Great Saphenous Vn (GSV) Small Saphenous Vn 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 Great Saphenous Vn (GSV) -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. Perforators -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 Important Perforators in the leg Hunters → Medial aspect of leg Dobbs → Above the knee Boyds → Behind the knee Cockett's → Calf (1,2,3) LSV has lateral perf branches 3 major perforating Vns in the lower extremity 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) Causes of Incompetent 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. Venous sinuses of lower extremities (Soleal Sinus) -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 Calf Muscle Pump 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 ♥) What is an effective calf muscle pump consist of? 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 ↓ Postphlebetic Syndrome Chronic Venous Insufficiency Unilat LE swelling, aching & a sense of heaviness Usually from a previous DVT *Prolonged return to pre-exercise Ischemic Ulcers Commonly occur on the dorsum of the foot Baker's Cyst Contains synovial fluid from the knee joint Deep Veins of Upper extremity fr fingers to the RT Atrium 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 Upper Extremity Venous Anatomy Superficial Venous Sys of Upper Extremity 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 Veins you encounter fr the Lat aspect of the forearm 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 Veins you encounter fr the Medial aspect of the forearm Basilic Vn Brachial Vns w/ Cephalic Vn most Lateral Venae Comitantes 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 Deep Vns begin & end @ the ff landmarks 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 Central Veins refer to which vessels? 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 Differences in the Venous system from Art sys 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 What are Veins? -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. What are Venous 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 Upper Extremity Vns w/ OR w/o valves W/o Valves: Innominate Vns Sup Vena Cava (SVC) W/Valves: Jugular Vn Cephalic & Basilic Vns Lower Extremity Vns w/o valves Soleal Sinuses EIV: contains valves 25% of the time CIV IIV IVC Lower Extremity Vns w/ valves 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 What affects structure of Vn wall Venous Vol Venous Resistance Venous Po Venous Vol -Thin walled collapsible nature of the veins affect venous volume  Low vol = dumbbell shape High vol = Circular shape Venous Resistance & Compliance Flattened shape allows ↑ flow resistance than circular shape Compliance: Ability of vns to accomodate large shifts in vol w/ limited changes in venous Po Venous Pressure The shape of the vn determines transmural pressure (distension pressure)    Low bl vol=low Po High vol=High Po Factors that influence Venous Return in Hydrostatic 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 5 major factor influencing Venous Return 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 Venous Dysfunction -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. Inspiration -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 Expiration -Thoracic Po ↑ (CVP ↑ & Venous Return ↓) -Abd Po ↓ -Bl fr legs ↑ in flow → IVC -Bl fr arms ↓/stops due to high Po in that region Valsalva Maneuver -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 Valsalva Maneuver-Normal Result -Diminishes Venous bl flow everywhere in the body   As pt releases the breath & stops bearing down, there s/b a brief ↑ in flow Valsalva Maneuver-Abnormal Result 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 In CWD reflux texting, NORMAL result is: -Cessation of flow w/ proximal compression, resuming on release -Augmentation w/proximal compression or on release of distal compression=insufficiency Reflux study results -If color flow display lights up blue w/ calf compression then red for 2-3 seconds on release=Venous Reflux Anatomical explanation for a deep vein thrombus (DVT)? 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 May Thurner Syndrome -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. DVT's common signs & symptoms -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 Differential diagnoses of DVT 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 Superficial Thrombophlebitis 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 Types of skin changes in venous disease -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) Cellulitis (skin change in venous disease) Infection of dermal tissue causing abscess on skin Red, warm tissue commonly seen on the shin/foot Edema/Pitting Edema (skin change in venous disease) -↑ 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) Lymphedema-Venous Pathology Chronic Condition Painless, swelling due to obstruction in the lymphatic system Brownish discoloration (skin change in venous disease) Evident in the medial surface of lower leg-to-ankle area (gaiter zone) Whiteness (pallor) (skin change in venous disease) fr arterial spasm secondary to extensive, acute ilio-femoral thrombosis called Phlegmasia alba dolens Bluish discoloration (cyanosis) (skin change in venous disease) fr severely reduced venous obstruction called Phlegmasia Cerulea Dolens 3 Risk Factors of Virchow's Triad in DVT Trauma to the vessel aka endothelial damage Venous stasis Hypercoagulability Examples of Trauma to a vessel in Virchow's Triad Could be intrinsic (ie drugs, indwelling catheter) or extrinsic (ie following a fall, Paget-Schroetter Syndrome) Examples of Venous stasis in Virchow's Triad 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 Examples of Hypercoagulability in Virchow's Triad 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. Most frequent complication of DVT Chronic Venous insufficiency-typical rusty brown color at ankles & calves Chronic Venous Insufficiency -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 Most life threatening complication of a DVT Pulmonary embolism 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). Types of Tests used for PE -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 Common physical findings in 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 How does Chronic Venous insufficiency secondary to Valvular Incompetence lead to formation of venous stasis ulcers? -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 Venous Stasis Ulcers 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 -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. Primary Varicose Veins -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 Secondary Varicose Veins -Pain during walking -Secondary varicose veins are those due to obstruction and valvular incompetence of the deep veins.  -This is the more serious form. PPG Technique & diagnostic criteria in venous insufficiency -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 Type of modalities for IPG, SPG & Air Plethysmography -They are all capacitance/outflow modalities and utilizes a scoring grid to plot them -All used in detecting significant DVT Capabilities & limitations of APG in diagnosing Venous disease -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) How does PPG monitor flow in either Venous or Arterial systems 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 DC (Direct Current) equipment 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 AC (Alternating Current) equipment 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  Venous flow using Air-plethysmography (APG) 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 3 measurements obtained using APG 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 UE Vns-Duplex Exam 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 LE Vns-Duplex Exam 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 LE Vns-Duplex Exam SAGGITAL 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 LE Vns-Duplex Exam PW 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 CWD Venous assessment 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) Sonographic finding with Venous compression -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 Object of Venous study 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 What is a Venous thrombectomy? -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. Risk factors that Incr complications following venous thrombectomy >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 IF pulsatile flow is seen in Vns 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 Guidelines to determine Acute DVT -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 Guidelines to determine Chronic DVT -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 Venogram or Contrast Venography -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 Describe Ascending venography -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 Descending Venography -Is performed to diagnose Valvular Insufficiency -Identifies specific Valvular Incompetence -Venous puncture site is @ the CFV Limitations to Venography 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 Venography of the UE -Assesses blockage, lesions, or thrombosis in the veins of the neck and axillary (armpit) region Thrombocytopenia ↓ in platelets Causes bleeding complication (hematoma) in pts w/ heparin treatment Medications that are usually prescribed to pts w/ acute DVT 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) What invasive treatments are available to pts w/ acute DVT? Placement of IVC interruption device to prevent PE (pulmonary embolism) Iliofemoral thrombectomy may also be considered for impending limb loss What is an Anticoagulant? -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. How does Vitamin K influence anticoagulants? -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. What is a Diuretic? -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. Abdominal Venous duplex evaluates the ff: 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 Quality assurance values Sensitivity Specificity +Predictive value - Predictive value Accuracy Sensitivity (QA val) Ability of a test to detect disease when it is present Divide # of true + noninvasive studies by # of all false - = # of + gold standard studies Specificity (QA val) 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 + Predictive Val (QA val) 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 - Predictive Val (QA val) 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 Accuracy (QA val) 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 Define True +, False +, True -, False - 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 Steps to take in calculating QA test 1. Compare noninvasive results w/ gold standard What is Statistics? 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. What is Statistics "mode"? 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.  What is Statistical median of a group? 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 Vagal Stimulation of the heart will? ↓ 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, Kinetic Energy, Potential Energy, Hydrostatic Po, Viscosity, Stasis 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 Respiratory Acidosis/Alkalosis 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)