RVS Part I

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marie78
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303831
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RVS Part I
Updated:
2015-07-13 15:02:53
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Vascular Fl Dynamics Cerebrovascular
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Vascular Exam
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  1. Conservation of Energy Law
    • Energy is never lost only converted fr 1 form to another
    • Bl moves fr HI to LOW
    • Amt of flow depends on Friction & Resistance
  2. Potential & Kinetic Energy
    • Potential= Static Po (resting energy)
    • It is the force exerted on the vessel walls

    Kinetic= Dynamic Po (movement or motion) Velocity (speed+direction) of bl flow

    Total Energy=Potential + Kinetic Energy
  3. Pressure (Po)
    • Force behind fluid flow
    • Force per Unit area
    • Po exists as Static Po or Dynamic Po
  4. Hydrostatic Po
    • Po of fl due to its wt
    • Form of Potential energy (static Po)

    Factors: Density (p), force of gravity (g), Ht (h) of the col. of bl = pgh
  5. Volumetric flow aka Volume Flow Rate (Q)
    Amt or Vol of fl. that moves past a point @ a specific unit of time
  6. Viscosity (n)
    • Thickness of a fl
    • Causes Resistance to flow in motion as well as energy
    • Energy is lost due to (n) & inertia
    • Heat is a factor of (n) = ↑ temp; ↓ (n)
  7. Resistance (R)
    • Force that tends to oppose the flow of bl
    • AKA Impedance (z)
    • Factors: Viscosity(n), Length(L) & Radius(r)

     
  8. Capacitance
    • Change in Fl vol per change in time
    • In the Venous sys: 65% of Bl Vol is w/in the Vns

  9. Compliance
    • Ratio of the change in fl vol to a change in Po
    • ↑ comp = large ↑ in vol for a small ↑ in Po 

    EX: As bl is ejected fr the heart during systole, AO becomes distended to store large Qts of bl
  10. Bernoulli's Principle
    • Velocity=Flow ÷ Area
    • All energy @ one location must equal ALL the energy @ another location
    • Frictional losses is affected by Bernoullis Principle
    • Explains Po & Vel changes @ stenosis
    • @Stenosis, there is ↑ Vel due to DR and ↓ in Po to maintain constant vol of bl flow
    • Flow separation is seen @ the Proximal ICA due to Bulb
  11. Pouseuille's Law
    • Vel & Area are inversely related
    • Determines how much fluid is moving thru the vessel (Quantify)
    • Relationship betw Resistance (R), Pressure, and Volume flow (Q)   

  12. Reynolds number
    • >2000=Turbulence
    • <2000= Laminar flow

  13. Relationships to remember
    • ↑ R = ↓ Q
    • ↑ Po = ↑ Q
    • ↑ R = ↑ Po

    Vol Flow (Q) & Resistance (R) are inversely related
  14. Rigid Tube
    Is a smooth surface that has constant (n) and fl is incompressible flowing @ a steady state

    It consists of Laminar flow where it has lowest vel along the wall & highest in the center

    *Laminar flows in a Rigid tube
  15. Curved Tube
    Vel along the outer/inner radius will change w/ location along a curve. NO Laminar flow exists.

    ↑ flow Vel seen @ outer edge of the vessel
  16. Left Heart
    • Oscillatory flow in the ART tree is initiated w/ every heart beat.
    • Each beat pumps approx 70 ml of bl into the ART sys causing a BP pulse
  17. Stroke Vol (SV)
    • Amt of bl ejected fr the heart on a beat-by-beat basis
    • SV=end diastolic vol (EDV)- end systolic vol (ESV)
  18. Cardiac Output (CO)
    • Vol of bl ejected by the heart per min.
    • CO determines the Qty of bl that enters the ART sys.

    CO = SV x HR

    • -ART Po & Total Peripheral R determine bl vol that leaves it
    • -Peripheral R depends on level of vasoconstriction in (Arterioles, Venules)
  19. Ejection Fraction (EF)
    Gives the % of bl ejected per beat

    EF%= SV/EDV x 100
  20. Pre-Load (PL)
    Refers to the vol of bl in the LT Ventricle (LV) @ the End of diastolic filling

    Conditions that may ↑ PL: Regurgitation, VSD, ASD & FL overload

    • VSD: Ventricular Septal Defects
    • ASD: Atrial Septal Defects
  21. After-Load (AL)
    Resistance against w/c the ventricle must pump. This will cause an ↑ in systolic Po

    Conditions that may ↑ AL: Hypertension, AO Stenosis & pulmonic stenosis
  22. Cardiac Cycle
    • - LV rises rapidly until it exceeds Po → Ascending AO → AO Valve Opens & Bl is ejected & BP ↑ & causes BP in AO to rise (systolic BP)
    • - Elastic walls of the ART expand during systole and store excess bl vol. Large portion of ♡ output (bl vol & energy) creates ea ventricular contraction resulting in ART to be distended (during systole) results in ART 'reservoir'
    • -During Diastole, elastic walls contract & is relaxed, and the stored energy propels fwd→
    • Peripheral R vessels. Stored energy & vol promotes constant flow of bl →  the tissues
  23. Pulsatile Wave
    • -Variations of bl vol & energy occuring w/ ea cardiac cycle
    • -It has a rapid acceleration (systole), a gradual ↓ to the DN (↑ in Po as the AO valve closes) → Cont of ↓ during diastole
    • -During Diastole (in microcirculation) a temp cessation of FWD flow or even diastolic reversal occurs frequently in portions of the ART sys
  24. Peripheral Art system (fr Large art to capillaries)
    • 1. AO  2.Large Art = ↓ R
    • 3. Major art branches
    • 4. Arterioles = ↑ R, ↓ r4 (smaller diam), ↓ P
    • 5. Capillaries = ↑ R,  ↓ P
  25. Arterial (R)
    • (R) is inversely ∞ to the r4
    • Low (R) & High (R)
  26. Low (R)
    • -Seen in Large Art of the body
    • -Continuous flow throughout systole/diastole feeding a DILATED vascular bed
    • -Monophasic flow is due to a Low Peripheral (R)

    EX: ICA, VERT A, RENAL A, SMA (Postprandial)
  27. High (R)
    • -Seen in Small Art such as arterioles & capillaries
    • -Flow is pulsatile w/ lower or absent diastolic flow
    • -Distal (R) produces a flow reversal in diastole
    • -Triphasic & Biphasic flow are high (R)

    EX: ECA & LE ART
  28. Volume Flow (Q) Changes in the Peripheral Art System
    *Effects of vessel diameter: changes in vessel's r4 have the greatest single effect on flow Vol 



    -Organs w/ High Vol needs such as the brainvisceral organs will have LOW (R) vascular beds

    -Organs w/ Low Vol needs such as the scalp will have HIGH (R) vascular beds
  29. Peripheral Venous System
    -Radius of the Vns ↑ in size fr the very small venules to the large vns (SVC & IVC)

    • -VP ↓, AP ↑
    • -(R) of venules is much ↓ than the (R) in arterioles & capillaries but still high in respect to the AO
    • -Fr venules →larges vns→Vena Cava, (R) drops below (R) of the AO in order to keep bl flowing to the RT atrium of the heart
  30. RT & LT HEART (Effects on Peripheral flow patterns)
    • 1.Bl→RA fr IVC, ↓P & TV is closed
    • 2.Bl Vol ↑ (RA), ↑P (RA) exceeds P (RV)
    • 3.Due to ΔP, TV opens, BL→RV
    • 4.Bl Vol ↑ (RV), ↑P (RV)→↑P exceeds ↓P (RA)=Bl to backflow→(RA) & closes TV
    • 5.Po in RV is below Po in PA & PV (betw RV & PA) is closed
    • 6.Po in RV exceeds PA, PV opens & bl flows → PA (Ventricular contraction)
    • 7.↑P (PA) exceeds RV & backflow of bl closes PV & enters the lungs
    • 8.O2 Bl in lungs returns→LA via PV

    • 9.Po in LA exceeds LV, MV is forced to open & BL rapidly enters LV
    • 10.During LV filling, AO valve is closed; LV Po ↑ above the AO, AO valve opens & allows BL to enter AO (VC); AO valve closes when AO Po fr ↑ BL Vol exceeds Po of LV
    • 11.BL is then dispersed to the Peripheral ART beds
  31. RT Sided HEART failure
    • -Congestion of Peripheral Tissues
    • -Edema/Ascites
    • -Liver Congestion
    • a. Impaired Liver Function
    • -GI Tract Congestion
    • a. Anorexia, GI Distress, Wt Loss
  32. LT Sided HEART Failure
    • -↓ CO
    • -Activity Intolerance
    • -Signs of ↓ Tissue Perfusion
    • -Cyanosis & Signs of Hypoxia
    • -Pulmonary Congestion
    • a. Orthopnea
    • b. Cough w/ Frothy Sputum
    • c. Nocturnal Dyspnea
  33. Diffusion (Pulmonary hemodynamics)
    • -Oxygenation of bl in the lungs happen thru diffusion
    • -Occurs fr higher O2 to lower O2 
    • -Alveoli =↑O2 concentration
  34. Vel vs. Cross-Sectional Area
    • -Vel of bl accelerates & decelerates as it goes fr ART to VENOUS sys
    • -Relationship betw Vel & CSA

  35. Po changes in ART system
    • 1. AO→2.Art = ↑Po
    • 3.Arterioles→Cap→Venules→Vns→IVC→♡ = ↓, ↓↓, ↓↓↓ Po
  36. Vasoconstriction
    • -Occurs when there is ↓ in r4= ↑ R & restricted bl flow to an organ.
    • -Occurs w/ body cooling
  37. Vasodilatation
    -Occurs when there is ↑ in r4 = ↓ R & ↑ bl flow to an organ

    -Occurs w/ body heating
  38. Po changes in the Venous Sys
    • -Bl enters venous sys fr capillary bed→small venules→larger Vns that dir bl back to the heart
    • - ↑P in arterioles & ↓P in venules allow flow to occur thru the capillary beds =ΔP
  39. Cardiac Influence
    • -Po fr the RA causes (R) & pulsatility in the venous sys
    • -Commonly seen in the Prox UE Vns (ie Subc Vn & IVC)
    • -Venous pulsatility is damped out & should NOT be seen in  LE vns
  40. Venous capacitance & static filling Po
    • -Vns = High capacitance in the cardiovascular sys
    • -Serve as "Reservoir" to supply high demand of bl vol
    • -Empty Vns=elliptic CSA shape w/c ↑ R
    • -Distended Vns=↓ R
  41. Hydrostatic Po (pgh) in Cardiovascular sys
    • -Related to Ht of the col of bl, density of the fl & gravitational force
    • -Supine= 0 mmHg
    • -Pt standing=lowest @ the head & max @ the ankle level
    • -↑pgh = ↑ transmural po, venous distention distally, edema & ↓ venous ret
  42. Calf muscle pump
    • -Due to the effects of pgh, VR (venous ret)→♡ is an uphill battle
    • -W/o some method of propelling VV, stasis & edema can occur in the LE when standing
    • -Calf muscle pump aids VR fr the LE in a standing position
    • -Consists of: Deep & Superficial Vns of LE, Perforators, contracting muscles, Venous sinusoids, Venous Valves
  43. Calf muscle pump method
    • -Contractions of muscles compress the deep & superficial vns, ↑ VP w/c helps propel bl→♡
    • -Venous valves close as bl moves thru them w/c prevent retrograde flow
    • -Large amt of Venous valves in the LE help diminish effects of pgh
  44. Respiratory related changes
    • -Respiration creates a variable (R) to venous bl flow
    • -Po changes result fr insp/exp as diaphragm distends & contracts
    • -VM changes intra-thoracic & intra-abd Po & (R) & thus change venous flow
  45. Venous (R) & transmural Po
    • -Referenced fr Inside vessel→wall→outside vessel
    • -Vn shape is determined by transmural Po:
    • Low TP=Elliptical or dumb bell shaped;
    • High TP=Vn expands & more rounded
    • - ↓ TP= ↑ (R)
    •   ↑ TP= ↓ (R)
    • -TP in LE vns is ↑ when standing & ↓ when supine
    • -Obstruction to venous outflow in arms/legs can ↑ TP
  46. Venous Hypertension & Edema
    • -It is caused fr venous Po usually due to an obstruction, venous reflux, CHF or ↑ RT sided cardiac overload.  
    • -↑ venous Po can lead to venous congestion & peripheral edema
    • -If venous congestion is present=capillary venous Po↑ causing fl to pass →capillary walls @ an incr rate & edema occurs
  47. ART Hemodynamics
    -Total energy in the circulatory sys=Potential (Po), Kinetic & Gravitational energy
  48. ART Hemodynamics-Potential Energy
    • -aka Pressure energy (BP)
    • -MAIN form of energy present in flowing bl
    • -Po causing distention to the vessel walls created by the pumping of the heart
    • -Hydrostatic & Gravitational Po are both forms of Potential energy
  49. ART Hemodynamics-Kinetic Energy
    • -Ability of bl to do work due to its VELOCITY
    • -Energy of motion
    • -Smaller component of the total energy of bl flow
    • -K ∞ pv2
    • -↑ K=↑ V (in HI Vel state that occurs Distal to stenotic lesions)
    • -↑ K=↑ Q/ ↓ R (ie during Exercise)
  50. ART Hemodynamics-Conservation of energy
    • -States energy is not lost, but converted fr one form to another
    • -Kinetic energy is related to VEL
    • -↑ Kinetic energy= ↑ Vel and vice versa

    -↑ Kinetic energy = ↓ Potential energy
  51. ART Hemodynamics-Energy Gradient
    • -Energy level diff betw 2 points
    • -Bl flows fr HI to LOW 
    • -Po greatest in the ♡ and ↓ as bl travels distally
    • -HI Po ART are connected to LOW Po Vns in capillary beds
    • -Small comm vessels betw ART & Venous sys are: arterioles, capillaries & venules
  52. ART Hemodynamics-Effects on flow
    • -In order for fl to move betw 2 points:
    • 1. Route
    • 2. ΔP (energy or Po gradient) (ie Po diff betw ♡'s LV & tissues of the foot)
    • -Viscosity (thickness of bl) and Inertia (motion)
    • -Flow depends on Friction & R



    Q=Vol flow & (R) are inversely Related
  53. ART Hemodynamics-Effects of CO & Peripheral (R)
    • -CO governs amt of bl that enters the ART sys
    • -ART Po & total peripheral (R) determines vol of bl that leaves it
    • -↑CO=↑BP=↑ΔP
    • -ΔP=QxR (Q & R inversely related)
    • =ΔP will ↑ if the r↑=↓ peripheral (R)
  54. ART Hemodynamics-Resistance (R)
    -Effects of Viscosity (n), friction & inertia on flow
  55. ART Hemodynamics-Viscosity (n)
    • -Property of fl that resists flow
    • -Causes friction betw layers of fl or an ART wall
    • -↑ (n) = ↑ (R)
    • -(n) is related to hematocrit (RBC)
    • -Indir related to Velocity
  56. ART Hemodynamics-Friction
    • -(R) of movement of 1 layer of bl against another layer or the vessel wall
    • -In Laminar flow, vel is highest in the CTR than it is near the walls due to friction, (n) & the Laminar effect
    • -Energy is converted to heat due to friction
    • -EX: Smaller r4 = more friction & less flow

       R ∞ L
  57. ART Hemodynamics-Inertia
    • -Causes bl to resist a change in DIR or Speed
    • -Energy loss is seen in tortuous vessels & @ Bif. 
    • -Whenever bl has to change dir or speed, it goes against Inertia
    • -Once the ♡ ejects bl, it cont to move to the peripheral vessels. The continued pumping action of the ♡ helps to maintain energy needed for flow to cont.
  58. ART Hemodynamics-Autoregulatory
    • -Bl usually flows fr arterioles to the venules @ a constant rate, yet bl thru ea capillary can be quite variable
    • -This process is controlled @ the tissue level
  59. ART Hemodynamics-Sympathetic/Parasympathetic
    • -"Fight or flight response"
    • -Stimulation by nerve & hormonal activity such as:
    • a. Acceleration of bl to muscles & brain
    • b. Constriction of cutaneous bl vessels
    • c. Stimulation of energy production to muscles d. Stimulation of sweat glands
    • e. Dilation of pupils to focus on distance
    • f. ↑ HR
    • g. Dilation of Resp passages
    • -Parasympathetic has the exact opposite effect
  60. Application of Po/Flow relationship
    • -The greater the Po diff, the greater the flow rate
    • -Consider Poiseuille & Resistance equations
    • Q=ΔPℵr4/8nL    ΔP=QxR     R=8Ln/ℵr4
    • -Reynold's # that determines if flow will be laminar, disturbed or turbulent
  61. Application of flow/Po/Vel relationship
    • -Bernoulli's principle explains BP & Vel changes w/ stenosis
    • -Q=V x A or  V=Q/A or r
    • -Vel & Area or Radius are inversely related
    • -In a stenotic vessel, VEL ↑ @ area of stenosis (↑ amt of Kinetic energy) causing ↓ in BP in the stenotic region.
    • -Distal to the stenotic region, VEL ↓ = ↑ BP
  62. STEADY FLOW
    • -Stability where Vel & Dir are maintained
    • -Poiseuille's equation can be applied to analyze energy losses
  63. PULSATILE FLOW
    • -Alterations in the Po of moving bl
    • -Ex in Art flow:
    • -Pulsatility is due to cardiac contraction creating Po wave
    • -Reversal of flow seen during diastole due to peripheral (R) & changing ΔP
  64. Pulsatile Flow in response to Vasoconstriction & Vasodilatation
    • -Vasoconstriction:
    • -Pulsatility of flow in medium & small size ART of limbs ↑, but ↓ in minute ART, arterioles & cap
    • -Vasodilatation:
    • -Pulsatility of flow in med & small size ART of limbs ↓, but ↑ in min ART, arterioles & cap
  65. DOPPLER FLOW PROFILES
    Laminar
    • -Bl cells moving in layers @ diff Vel.
    • -Fastest Vel @ the CTR
    • -Little or no flow @ the vessel wall known as Parabolic flow
  66. DOPPLER FLOW PROFILES
    Plug flow
    • -When bl cell layers move @ a uniform speed and waveform becomes flattened
    • -During systole flow profile becomes uniform
    • -In diastole, flow returns to a parabolic pattern
    • -Plug flow occurs @ the AO root
  67. DOPPLER FLOW PROFILES
    Disturbed or Turbulent flow
    • -When Laminar flow breaks down & bl cells move in random dir.
    • -Occurs w/ high vel where bl flows thru regions of plaque & after a stenosis
    • -Influential factors: Vel of flow & r4 of the vessel
    • -Bruits can be heard caused by vibration in the Art wall
    • -Seen just DIST to vessel narrowing or stenosis where Vel ↓ dropped
  68. Triphasic Waveform
    • -High pulsatility waveforms have tall, narrow, sharp systolic peaks w/ reversed or absent diastolic flow
    • -Frequently seen in ART w/ HI peripheral (R) such as the extremities
    • -Sharp upstroke in Systole, Brief flow reversal (Arteriole R) & brief FWD flow
  69. Biphasic Waveform
    • -Moderate pulsatility have tall, sharp systolic peaks, but mild FWD flow in diastole
    • -EX: ECA, Preprandial SMA
  70. Monophasic Waveform
    • -Low pulsatility have wide, broad systolic peaks & FWD flow in diastole
    • -Is the result of LOW peripheral (R)
    • -EX: ICA, Vert A, Renal & Celiac A
    • **Disease processes can alter (R) & change waveform morphology
  71. Pulse Po Amplitude
    -The diff betw systolic & diastolic Po is affected by cardiac SV, Time of ventricular ejection, Peripheral (R), & stiffness of ART walls
  72. Effects of Stenosis/occlusion on flow characteristics
    • -HDS stenosis=major reduction in Q & Po w/in a vessel.  75%AR=50%DR
    • -HDS stenosis causes ↓ Po across the stenosis & Turbulent flow
  73. Direction of flow, turbulence & disturbed flow
    • -When parallel streamlines of laminar flow are altered fr their straight form
    • -Cross currents or Eddy curr cause multiple vel & disturbances in dir of flow=Turbulent/Disturbed flow
    • -Spectral doppler=Spectral broadening
    • -Critical stenosis=Both Po & Q ↓
    • -↓ Q=V↓ ÷ A/R ↑
  74. Vel Acceleration/deceleration
    • -Pulsatile flow state=Vel ↑ & ↓ cardiac contractility
    • -↓ r4 = ↑ in Vel @ the region of narrowing

    • V=Q/A (radius)
    • 75%AR=50%DR
  75. Hemodynamic abnormalities depend on:
    • -Length/Diameter of the narrow segment
    • -Roughness of the tissue
    • -Degree of irreg of the narrowing
    • -Rate of flow
    • -AV ΔP
    • -Peripheral R beyond the stenosis
  76. Entrance/Exit effects
    • -Critical Stenosis: ↑R to flow just PROX to the stenosis (Slight ↓ in Vel in systole or diastole may be seen)
    • -In HR systems (ie LE Art flow)=↑ in reverse flow component in late systole
  77. As bl flow enters the stenotic region:
    • -Vel ↑
    • -Often laminar flow is maintained
  78. As bl flow exits the stenotic region:
    • -Vel ↓
    • -Laminar flow disrupted
    • -Turbulence occurs
    • -Reverse flow currents (eddy curr) may develop
  79. Diameter Reduction
    • -When atherosclerotic plaque or thrombus is present, ART lumen diam & Area are reduced
    • -Vessel diam/AR can also occur in large vessels during vasospasm (ie MCA >125 cm/s)
    • -75%AR=50%DR
    • -ART stenosis caused by atherosclerotic plaque is reported in %DR 
    • %D stenosis= 1 - TL ÷ RL x 100
  80. Peripheral (R)
    • -Caused by a ↓ in vessel diameter along the course of the ART tree
    • -DIST Art are smaller than PROX Art
    • -Vasoconstriction & Vasodilation of the arterioles change peripheral (R) & affect bl flow in larger art
    • -Varies from Low to HR vascular beds
    • -Can change from HI→Low and Low→HI due to Ischemia, chemical, emotional & environmental infl.
    • -During exercise, HR vascular bed becomes LR to allow bl to enter muscle grps
    • -Affects Diastolic flow more than systolic flow (HR flow=NO diastolic components) 
    • -LE ART flow (person @ rest)=↑R, ↓Q
    • -During & shortly after exercise=↓R, ↑Q
  81. Collateral effects
    • -In the presence of ART occlusive disease, bl flow may ↑ in branches of the ART sys to compensate for ↓ bl flow in the disease art
    • -Can provide sufficient perfusion to the organ, muscle grp or distal art=bl flow to be normal or near normal
    • -Flow can reverse in art branches to provide bl flow to distal art segment & the affected organ
    • -They evolve in response to ART obstruction.  Small vessels, functioning as collaterals will often enlarge over time
  82. Effects of Exercise
    • -↑ metabolism triggers ANS (autonomic Nervous Sys) to vasodilate the arterioles in the affected vascular beds =LR waveform
    • -↓ (R) and ↑ capacitance=↑ in bl flow to the limbs
    • -If bl vol is sufficient, distal art Po is maintained
    • -If art obst is present, flow vol to extremity is inadequate to perfuse to muscle grps; Po ↓ occurs in the distal art beds
    • -Measuring perfusion parameters b4 & after exercise (ankle Po & ABI) allows assessment of the severity of the disease & effects of collateralization
  83. Effects of Occlusion
    • -Is present when ART segment is totally blocked & NO FLOW passes thru the segment
    • -May be ACUTE or CHRONIC (if Chronic, bl thromboses w/in & DIST to severe stenosis)
    • -NO Doppler signal or color doppler is present w/in the occluded segment
    • -If occluded segment is moving due to "water hammer" effect of pulsatile Po, fD may occur=Low Vel 'to & fro' spectral signal
    • -Blunted doppler signals often seen PROX to the occlusion & HR flow
    • -W/ ICA occlusion, compensatory (incr) flow may be seen in the ipsilateral ECA or in the contralateral ICA
    • -In the ICA it is important to distinguish betw an occlusion & a low-flow or 'trickle' flow w/in the vessel. 
    • -Occluded ICA's not amenable to surg whereas near-total occlusion can undergo endarterecetomy
    • -Appropriate color duplex techniques: ↓ PRF (scale) in both color & spectral doppler & a careful investigation of the region in question
    • -Power Doppler may also be useful in determining existence of flow
  84. Venous Hemodynamics
    -Total energy in the circulatory sys is the sum of potential (Po), kinetic and gravitational energy
  85. Venous Hemodynamics-Hydrostatic (h)Po & Gravitational (g) Po
    • -Both are forms of potential energy
    • -(h) Po can result in Venous distention & pooling of bl in LE
    • -(g) Po is Po exerted fr gravity when pt is erect.  Venous bl must overcome effects of (g) for bl to return to the heart
  86. Venous (R)
    • -Bl enters the venous sys fr capillary beds
    • -Flows→small venules→larger vns→back to ♡
    • -ΔP w/in capillary bed, ↑Po in arterioles & ↓Po in venules allow flow thru capillary beds
  87. Venous (R) Cardiac Infl
    • -Po fr RT Atrium causes R & pulsatility in Venous Sys
    • -Most obvious is PROX UE & IVC due to its close proximity to the heart
    • -Venous Pulsatility is damped out in the LE
  88. Venous (R) Capacitance
    • -↓ TP = ↓ Q= ↑ R (Elliptical cross section shape)
    • -↑ TP = ↑ Q= ↓ R (Distended Vns)
  89. Venous ®
    • -Veins can carry up to 65-70% of our blood volume
    • -TP determines the Vn shape. From the Po w/in (Intravascular/Intraluminal) and external Po (Interstitial Po)
    • -↓ TP = ↓ Q= ↑ R (Elliptical cross section shape)
    • -↑ TP = ↑ Q= ↓ R (Distended Vns)
    • -↑ TP=Standing/ ↓ TP=Supine
    • -Venous Outflow Obst ↑ TP
  90. Venous Hemodynamics ΔP
    • -Diff betw ↑Art Po & ↓ Venous Po creates a ΔP in the capillary beds
    • -Gradient allows flow & perfusion thru capillary beds
    • -Venous Po is Lower than Art Po
  91. Venous Hemodynamics Respiration
    • During...                          Venous outflow fr...
    • Insp=Intra-thoracic Po ↓       UE ↑ / LE ↓  
    • & intra-abd Po ↑

    • Exp=Intra-thoraci Po ↑          UE ↓ / LE ↑
    • & intra-abd Po ↓
  92. Calf Muscle @ Rest
    • -Venous bl flow is propelled→♡ by residual Po fr the Art tree
    • -Semilunar valves in the deep & superficial sys & calf muscle vns allow bl to proceed in one dir→♡ (antegrade flow)
    • -Valves in perforator vns allow bl to flow fr superficial→deep vns
    • -Competent valves prevent bl from flowing retrograde
    • -Valves are numerous below the knee
    • -IVC & CIV have few or no valves
  93. Calf Muscle-During Exercise
    • -Soleal & gastrocnemius muscle grps in the calf are the primary 'pumps
    • -Soleal→PTV & Pero Vns
    • -Gastrocnemius→POP Vns
    • -During walking, vns w/in these muscle grps are squeezed & bl→upwards toward the ♡ under ↑Po = Venomotor pump
    • -During contraction, Proximal valves open, distal valves & perf valves close
    • -Competent valves allow only FWD flow of bl resulting in ↓ VP and ↑ VR→♡
  94. Calf muscle-During Relaxation
    • -PROX valves close due to Hydrostatic Po
    • -DIST & Perf Valves open to allow empty vns to be filled with bl
    • -Bl is drawn into the deep vns via Perf during relaxation
    • -Intramural Po & Hydrostatic Po ↓=↓ Venous flow to the heart.
    • -Perfusion to the capillaries ↑ due to ↑ Po in Arterioles & Venules
  95. Venous Hemodynamics-Obstruction
    • -Obstruction to venous outflow in the legs/arms can ↑ TP = ↑ Venous (R)
    • -CHF &/or Tricuspid Insufficiency causes vns to distend due to inability to empty all bl of the Rt Atria of the ♡ causing ↑ VP
    • -Shallow breathers or chest breathers will have a Venous flow to be more continuous
  96. Venous Insufficiency
    • -aka Venous incompetence or Valvular insufficiency
    • -Incompetent pump mechanism
    • -3 factors for efficient pump action:
    • 1. Good contracting muscles
    • 2. Competent Valves to prevent retrograde flow
    • 3. Unobstructed Venous Outflow
    • -Incompetent Valves causes ↑TP (aka Venous Hypertension) distally & contributes to venous pooling, edema, & symptoms assoc w/ VI
    • -Incompetent perforator valves allow bl to be forced into the Superficial sys (GSV/LSV) & become dilated & enlarged & varicosities can result
  97. Primary Venous Insufficiency
    Congenital absence of valves or incompetent valve development
  98. Secondary Venous Insufficiency
    -Valve damage secondary to a previous thrombus
  99. Venous Hemodynamics-Cardiac Cycle
    • -Flow w/in vns is due to changing phases of the cardiac cycle usually in the Large Central Vns=IVC, SVC, PV, HV
    • -2 Periods of ↑ Venous flow: 
    • -1st phase=occurs during ventricular systole-↓ in Atrial Po causes the flow in the extra cardiac vns to ↑
    • -2nd phase=occurs after AV valves open & bl rushes →ventricles fr the atria
  100. Effects of Edema
    • -Body tissue contains excessive fl caused fr imbalance of the Transmural Po & osmotic Po
    • -Edema fr venous disease is caused by ↑ Venous bl vol & Po in the limbs
    • -↑ VP, ↓ bl flow in capillary beds & forces fl→interstitial spaces
    • -DVT causes an ↑ in venous intraluminal Po due to obstructed outflow
    • -Can also be caused by lymph fl=lymphedema
    • -Is ↓ by the action of the calf venomotor pump
  101. Chronic Venous Edema can result in:
    • -Chronic impairment to skin perfusion
    • -Stasis dermatitis
    • -Ulcerations
  102. Venous Hemodynamics-Doppler Flow Profiles
    • -Phasic: bl flow that rises & falls in phase w/ respiration
    • -Caused fr an ↑ & ↓ in intra-abd Po
    • -Venous flow is non-pulsatile except in the intra-thoracic UE due to contraction of the RT ♡ causing pulsatile venous flow (ie Jugular, SUBC, & INNOM Vns)
    • -Fl overload that may ↑ CVP (ie CHF) may have pulsatile venous signals. ↑VP=↑(R)
  103. Venous Hemodynamics-Continuous/Non-Phasic
    • -Bl flow that does NOT change w/ respiration
    • -A more continuous, non-phasic flow may be due to:
    • Shallow breathing, Supine position, Arms raised & hands behind their head, Spinal cord injuries, Proximal DVT, Extrinsic venous compression, Vasodilation (due to infection or inflammation)
  104. Calibration & optimization
    • -Used to test the accuracy of any testing device
    • -Duplex: Calibration done thru QA (Quality Assurance) like AIUM Test Obj, Tissue Equivalent Phantom, Doppler Phantom (string), Beam Profile/slice thickness phantom
  105. AC (Alternate Current)
    • -Electricity fr a standard wall plug
    • -Electrical charges ALT dir periodically
    • -Used to generate ART plethysmographic waveforms
    • -Meas. instantaneous changes in limb or cutaneous bl vol
    • -Used in PVR
  106. DC (Direct Current)
    • -Electricity you get fr a battery
    • -Does NOT change dir; creates Constant volt
    • -Used in Venous plethysmographic waveforms, venous capacitance & outflow studies
    • -Detects slower changes in bl content
    • -Used in Venous PPG reflux studies
  107. Units of Measure in Non-Invasive Vascular Testing
    • -PSV & EDV: cm/s or m/s
    • -Systolic Po: Indir Art testing mmHg
    • -Frequency (F): kHz (used in doppler studies) or MHz. 
    • -Distance: mm or cm Used to calculate % DR in Art stenosis
    • -AT or RT: seconds-Time period fr onset to completion of systole on Spectral Doppler waveform
    • -Flow Vol: mL/min
    • -Time: seconds; measures Venous Reflux on Spectral Doppler
    • -Ratios (index): NO units; comparison of 2 values
  108. Ratios (Index)
    • -RI: measurement of vascular (R) w/in an ART segment=Max & Min vel (PSV&EDV)
    • -PI: 3 VEL measurements=Max, Min, Mean Vel
    • -ABI: Ankle & Brachial systolic Po calculated to assess perfusion in the legs
    • -ICA/CCA ratio: Calculates % stenosis
    • -RAR:Vel used to assess RA stenosis
    • -TBI: used in Peripheral ART evaluation
  109. Tissue Mechanics/Po Transmission-
    Venous occlusion by limb positioning
    • -Appropriate pt & limb position for venous duplex imaging & CWD exam:
    • -Pt upper body elevated (15-300) in Reverse Trendelenburg position
    • -Leg being examined slightly bent at the knee & externally rotated
    • -Venous PG outflow studies, pt s/b supine w/ legs elevated above the level of the heart, this ensures min amt of bl vol is in the leg prior to exam & (R) to venous outflow will be ↓ to a minimum
    • -Arms s/b resting on pts side to prevent compression of the Axillary vn
  110. Tissue Mechanics/Po Transmission-
    Superficial venous occlusion by tourniquet
    • -In PPG venous reflux testing, tourniquets are placed to alternately occlude the GSV & LSV to help differentiate Superficial fr Deep vn incompetency
    • -If an abnormal Venous Reflux study becomes normal after retesting w/ a tourniquet, incompetence is likely found in the Superficial Venous System &/or perforators
  111. Tissue Mechanics/Po Transmission-
    Vol Changes by bl inflow/outflow
    • -Limb vol changes during ea cardiac cycle
    • -Can be assessed by ART APG or PVR
    • ( in limb vol during systole or ↓ in limb vol during diastole)
    • -Tourniquet restriction of venous outflow & release of tourniquet is the basis of measuring venous capacitance & outflow
    • -MVC: measurement of the max filling capability of vns w/ an outflow tourniquet applied
    • -MVO: rate of outflow ff the release of a venous tourniquet
  112. Tissue Mechanics/Po Transmission-
    ART occlusion by cuffs
    • -Cuff inflation to suprasystolic Po will stop ART inflow under & Distal to the cuff
    • -Accurate BP determination, cuff bladder s/b 20% wider than limb diameter @ the site of cuff placement
    • -Prolonged ART occlusion by the cuff causes vasodilatation in the distal vascular beds w/c is the basis of Post-occlusive reactive hyperemia testing in lower art exam
  113. Plethysmography
    • -Technique that measures vol changes in a limb or organ
    • -Displacement plethysmography aka Vol PG, APG, Pneumo PG, and most commonly PVR
    • -APG uses pneumatic cuffs placed around the limb & inflated (45-65mmHg) depending on cuff location.  Po cuff is set to 65 +/-5mmHg except in digits & metatarsal cuffs
    • -Limb segment enlarges during Art pulse, Air in cuff is displaced=↑ in cuff Po
    • -The ↑ & ↓ in Po is measured by a Po tx & is recorded as a waveform
    • -Proper application of cuff is needed to reduce artifacts
    • -PVR waveforms are compared to contralateral limb segments & to ipsilateral adj segments
    • -Same cuffs are used in PVR & segmental Po
  114. PPG
    • -Infrared light emitting diode & a photo-electric sensor
    • -Placed against the skin, PPG transmits infrared light into tissues & light is absorbed & reflected back to the photo sensor by skin bl flow
    • -Diff betw transmitted & reflected light is the basis for the waveform that represents cutaneous bl flow
    • -PPG can be used in AC mode (arterial)=instantaneous changes in bl content. Useful in eval digit perfusion
    • -PPG can also be used in DC mode (Venous)=Overall change in bl content over time. Useful in Venous Reflux studies
  115. Methods of Po Measurements
    • 1. Palpation
    • 2. Auscultation
    • 3. CWD - flow meter
    • 4. Segmental Po measurements
  116. Methods of Po Measurements- Palpatory method
    • -Relies on sensitivity of the fingers for examiner to feel a pulse
    • -Not recommended for routine Po measurements due to its subjectivity
  117. Methods of Po Measurements- Ausculatory Method
    • -Use of a stethoscope to listen for sounds (ie Bruit) to determine peak systolic and end diastolic Po
    • -Bruit sounds are produced when releasing Po in the Po cuff.  At this time intravascular Po exceeds the cuff Po & bl hits into the static bl that is DISTAL to the cuff location=vibration & turbulence
  118. Methods of Po Measurements- CWD
    • -Device used DISTAL to a cuff occlusion to determine @ what Po systolic flow returns
    • -Same procedure as the ausculatory method except the bruit sounds are picked up by a machine
    • -End Diastolic Po can NOT be obtained
  119. Methods of Po Measurements- Segmental Po
    • -Using CWD, Po measurements are taken @ various locations on the extremities to document presence, level & severity of ART occlusive disease
    • -Cuff too narrowOverestimation of Po
    • -Cuff too wideUnderestimation of Po
    • -Cuff width→20% wider than segment diam
    • -Cuff length→ ≥2 x width
  120. Skin Temperature
    • -Vascular testing s/b in a warm room to avoid vasoconstriction brought about by a cold room & cool skin temp w/c can adversely affect test results
    • -Assessment of skin temp is useful in evaluation of Raynaud's syndrome.  It involves Pre & post cold immersion testing of the hand & foot
  121. Transcutaneous Oximetry
    • -aka tcPO2 measure oxygen content in tissues as an indication of perfusion
    • -Measurement depend on the bal betw oxygen supply & oxygen consumption of pt
    • -Measurement of PO2 @ the surface of the skin are usually w/in 1-2% of the true value
    • -It is useful in determining wound healing potential & amputation level
  122. Laser Doppler flowmetry (LDF)
    • -Used in some clinical settings to assess healing potential to an area of skin
    • -Uses monochromatic laser beam dir @ the skin
    • -Movement of RBC's reflect back the light onto a photodetector & calculates vel of bl flow underneath
    • -Helps determine the healing potential of that area
  123. OPG-Gee
    • -Obsolete test used to meas & compare OA Po as an indir indication of significant carotid art stenosis
    • -Suction cups are placed on the LAT portion of anesthesized eyeballs & negative Po is applied.  
    • -PG tracing of ea eye is recorded
  124. CEREBROVASCULAR ANATOMY-AO Arch
    • -Consists of Ascending AO, Transverse Arch, Descending AO
    • -Originates @ the base of the LV of the ♡
    • -3 major branches: 
    • 1. Innominate Art (aka brachiocephalic art): 1st branch on the RT side of the AO arch. Terminates @ the Bif on the RCCA & RSA @ the level of the sternoclavicular joint
    • 2. LCCA: 2nd branch on the LT side of the AO arch. Terminates @ the carotid bif
    • 3. LSA: 3rd branch on the LT side of the AO arch.  Terminates @ the Thoracic outlet
  125. CEREBROVASCULAR ANATOMY-AO Arch Variants
    • -Common origin of the RT brachiocephalic & LCCA
    • -Lt VA origin is dir fr the AO
    • -Common origin of both CCA
  126. CEREBROVASCULAR ANATOMY-Common Carotid System (CCA)
    • -LAT→trachea & Thyroid gland
    • -Bif →ICA & ECA @ the Superior aspect of the thyroid (thryoid cartilage)
    • -RCCA: Originates fr the innominate art. 4th to 6th cervical TRV processes lie Posteriorly. Esophagus, trachea, larynx, pharynx & thyroid are MEDIAL. IJV is LAT. Terminates @ the Carotid Bif→ICA & ECA
    • -LCCA: Longer than RCCA & originates dir off the AO arch. Courses in the same dir as the RCCA. Terminates @ the Carotid Bif→ICA & ECA
  127. CEREBROVASCULAR ANATOMY-Carotid Bifurcation
    • -CCA's ascend in the neck to the border of the thyroid cartilage (C-4) where they divide→ICA & ECA
    • -Contains many receptor endings of the glossopharyngeal nerve
    • -Receptors respond to changes in ART BP & act as a baroreceptor to control intracranial Po
  128. CEREBROVASCULAR ANATOMY-Internal Carotid Artery (ICA)
    • -Originates @ the upper border of the thyroid cartilage where the CCA bif.
    • -Usually located POST & LAT to the ECA
    • -Supplies bl to LR vascular beds; ANT portion of the brain & eyes w/ branches to the forehead & nose
    • -NO extracranial branches
    • -First major branch=Ophthalmic Art @ the level of the carotid siphon
    • -Branches of Ophthalmic Art: Central Retinal Art, Supraorbital Art, Frontal Art. Provides important collateral circulation via anastamosis w/ branches of the ECA=Periorbital circulation
    • -Terminates @ the Circle of Willis→ACA & MCA
  129. CEREBROVASCULAR ANATOMY-Internal Carotid Artery (ICA) 4 major segments
    • -Cervical: Extracranial portion enters the skull via carotid canal
    • -Petrous: Ascends in the carotid canal curving to enter cranial cavity
    • -Cavernous: aka Carotid Siphon due to its "S" shape. Branches=Cavernous, Meningeal, Hypophyseal art
    • -Cerebral: aka Supraclinoid. Distal portion of ICA. Branches=Ophthalmic, MCA, Ant choroid, ACA & PCA
  130. CEREBROVASCULAR ANATOMY-External Carotid Artery (ECA)
    • -Originates @ the upper border of the thyroid cartilage where CCA bif
    • -Usually ANT & MEDIAL to the ICA
    • -Supplies bl to HR vascular beds: face, scalp & neck
    • -8 branches: SALOFPMS
    • -Most important ECA branches vital to collateral circulation are those that comm. w/ OA or VA branches
  131. CEREBROVASCULAR ANATOMY-Vertebral Art (VA)
    • -Arise fr upper & back portion of the PROXIMAL Subc A & enter the skull thru the Foramen magnum
    • -1st & largest branch of the Subc A
    • -Supplies bl to the POST portion of the brain
    • -Asymmetrical in size w/ the LT VA usually Larger than the RT
    • -VA & BA aka Vertebrobasilar circulation
  132. CEREBROVASCULAR ANATOMY-Vertebral Art (VA) Segments
    • -Pre Vert: fr the Subc A→TRV foramen C6
    • -Cervical: fr TRV foramen C6→TRV foramen C1.
    • May anastamose w/ ECA to form collaterals in the presence of VA or Carotid occlusive disease
    • -Horizontal (atlantic): Courses POST & ascends Anteromedial thru dura mater, loops betw atlas & axis b4 entering the skull
    • -Intracranial: fr dura mater thru foramen magnum joins contralateral VA to form BA
  133. Intracranial Circulation-BA
    • -Located @ the base of the skull formed by the confluence of RT & LT VA
    • -Terminates as it branches→RT/LT PCA
    • -Provides bl supply to entire pons, SUP & ANT aspects of the cerebellum
    • -Smaller branches of BA: ANT INF Cerebellar, Internal Auditory, Mult small pontine, SUP cerebellar art
  134. Intracranial Circulation-Circle of Willis
    • -Circle of vessels lying @ the base of the brain
    •  connecting the ANT & POST circulations
    • -Most important source of collateral circulation in the Cerebrovascular sys
    • -3 trunks that together supply ea cerebral hemisphere:
    • 1. ANT: 2 ACA's (w/c are branches of the ICA) connected by the AcoA
    • 2. ANTeroLAT: MCA w/c originate @ the terminal ICAs
    • 3. POST: 2 PCAs (w/c are terminal branches of the BA) connected by the PcoA→the MCAs
  135. Intracranial Circulation-Circle of Willis arteries
    • 1. AcoA
    • 2. ACA (Rt & Lt)
    • 3. Terminal ICA (Rt & Lt)
    • 4. PcoA (Rt & Lt)
    • 5. PCA (Rt & Lt)

    *MCA anatomically does NOT lie w/in the Circle of Willis
  136. Intracranial Circulation-Collateral Pathways of Circle of Willis
    • 1. Crossover collateral via the AcoA
    • 2. POST→ANT circulation collateral via the PcoA
  137. Intracranial Circulation: Intracranial - Extracranial anastamoses
    • 1. Connection betw terminal branches of ICA→ECA:
    • -Supraorbital A (ICA)→Superficial Temp A (ECA)
    • -Frontal A (ICA)→Superficial Temp A (ECA)
    • -Nasal A (ICA)→Facial A (ECA)
    • 2. Conn via Occipital branch of ECA & atlantic portion of VA
    • 3. ECAs conn across the midline
    • 4. Cervical branches of Subc A→branches of the VA & occipital branch of the ECA
  138. Common Congenital Anomalies-Circle of Willis
    • < 20% of the population has an intact Circle of Willis
    • -Absence or hypoplasia of 1 or both Comm A
    • -Abnormal origin of PCA fr 1 or both ICAs
    • -Absence or hypoplasia of PROX segments of ACA betw ICA & AcoA
  139. Common Congenital Anomalies-AO arch
    • -Sharing or close assoc betw origin of Innominate A & LtCCA
    • -Abnormal origin of the LtVA→AO arch betw LCCA & Subc A
    • -Rt Subc A has an unusual origin on the AO arch
    • -Agenesis of the ICAs
  140. Risk Factors in Cerebrovascular Disease (Controllable)
    • 1. Diabetes
    • 2. Hyperlipidimia
    • 3. Hypertension (HTN)
    • 4. Smoking
  141. Risk Factors in Cerebrovascular Disease-DIABETES (Controllable)
    • -Hardening of ART wall structure & loss of wall elasticiy (medial calcinosis)
    • -Medial Wall Ca++
    • -Frequency of Occlusive Disease→Low in Aortoiliac region, similar in fempop region, higher in distal pop & tibial vessels
  142. Risk Factors in Cerebrovascular Disease-HYPERLIPIDIMIA & HTN (Controllable)
    • -Hyperlipidimia:
    • -↑ saturation of lipid fats in bl leads to development & progression of Atheromatous plaque
    • -HTN: High BP
    • -Causes ↑ in intraluminal ART wall stress
    • -↑ incidence of coronary atherosclerosis 
    • -Aggravates arteriosclerosis & is a cause of cerebral hemorrhage
  143. Risk Factors in Cerebrovascular Disease-Smoking (Controllable)
    • -Strong risk factor in development of atherosclerosis:
    • 1. Recurr vasoconstriction of arterioles & capillaries
    • 2. ↑ BP
    • 3. ↑ cardiac O2 demand
    • 4. ↑ platelet aggregation
    • 5. ↑ cholesterol levels
  144. Risk Factors in Cerebrovascular Disease- Uncontrollable
    • -Aging (older pts)
    • -Family Hx
    • -Gender (Males)
  145. Mechanisms of Disease in Cerebrovascular
    • 1. Atherosclerosis, ASO
    • 2. Aneurysm
    • 3. Thrombolic events
    • 4. Carotid Body Tumor (CBT)
    • 5. Fibromuscular dysplasia (FMD)
    • 6. Subc (Vert) Steal
    • 7. Neointimal Hyperplasia
  146. Mechanisms of Disease in Cerebrovascular-Atherosclerosis, ASO
    • -A form of arteriosclerosis that causes thickening, hardening & loss of elasticity of ART walls
    • -Plaque causes endothelial inj fr: Lipids, complex carbs, Bl, fibrous tissue, Ca+ deposits, smooth muscle cells, collagen, fibrin, platelets
    • -Plaque protrudes→ART lumen & become altered by hemorrhage, cell necrosis or ulceration=Distal embolization or thrombosis
    • -Common causes of Cerebral Ischemia: Hypoperfusion & Embolization fr atherosclerotic plaque
    • -Common sites: Branches, Bif & origins of vessels
  147. Mechanisms of Disease in Cerebrovascular-Types of Atherosclerotic Plaque
    • 1. Fatty Streak: homogenous, low-level echoes fr a thin layer found on the intima of the art
    • 2. Fibrous plaque: homogenous, low→med level echoes fr accumulations of lipid deposits, collagen & elastic fibers
    • 3. Complicated lesion: heterogeneous, bright echoes w/ shadowing fr fibrous plaque. Fr deposits of more collagen, Ca+ & cellular debris
    • 4. Ulcerative lesion: fr deterioration of smooth fibrous plaque. May result in DIST embolization assoc w/ intraplaque hemorrhage. Seen as eddies of color w/in the plaque
  148. Mechanisms of Disease in Cerebrovascular-Aneurysm
    • -Abnormal dilatation of an ART=by a weakening in the ART wall structure due to congenital defect, trauma, atherosclerosis or infection
    • -Rarely occur in cervical CCA
    • -Types of Aneurysms: True (Fusiform, Saccular→Berry), Dissection, Pseudo
  149. Mechanisms of Disease in Cerebrovascular-True Aneurysm
    • -Involves all 3 layers of the Art wall
    • 1. Fusiform: Uniform dilatation of Art wall commonly found in the ABD AO
    • 2. Saccular: focal out-pouching on 1 side of an Art that does NOT involve the entire vessel circumference
    • -Berry Aneurysm: small saccular aneurysm primarily affects intracranial cerebral vessels. Rupture will cause extensive hemorrhage (subarachnoid hemorrhage)
  150. Mechanisms of Disease in Cerebrovascular-Dissecting Aneurysm (ART)
    • -When bl tears thru the intima & enters media wall=longitudinal splitting of the ART wall
    • -Can occur spontaneously or caused by trauma
    • -Spontaneous dissection incl: Hypertension, Marfan's syndrome, FMD, Syphillis
    • -Seen as a mobile or fixed echogenic flap
    • -Commonly located: AO, CCA & PROX ICA
    • -Sx: Acute, severe localized headache, neck pain
  151. Mechanisms of Disease in Cerebrovascular-Psedoaneurysm
    • -HI Po leakage of Bl out of an ART → surrounding tissue
    • -Common cause: ART puncture during catheterization or angiographic procedures; trauma & graft blow-out
  152. Mechanisms of Disease in Cerebrovascular-Thromboembolic Events
    • -Bl clot or foreign substance travels in Bl stream of an ART & lodges in a DIST vessel of smaller diameter=BLOCKAGE
    • -Embolism may be SOLID, LIQUID or GAS
    • -Occurs in adv stage of coagulation process; causes stenosis or complete occlusion of the ART where it lodges
  153. Mechanisms of Disease in Cerebrovascular-CBT
    • -Highly vascular tumor (paraganglioma/chemodectoma) located w/in the adventitia of the Carotid Bif (Betw ICA/ECA)
    • -Causes External compression of ICA
    • -May be BILAT
    • -Sx: Neck pain, Dizziness, Palpable neck mass, Hoarseness, Dysphasia, Syncope
  154. Mechanisms of Disease in Cerebrovascular-FMD
    • -Abnormal growth of the media wall layer fr an overgrowth of collagen=Mult Art stenoses
    • -Non-atherosclerotic disease occuring mostly in young females
    • -Found in Carotid & Renal Art
    • -Bead-like (string of pearls) appearance on angiography
  155. Mechanisms of Disease in Cerebrovascular-Subclavian (Vert) steal
    • -Stenosis or occlusion of the PROX Subc A ( or Innominate Art on the RT)=in Reversal of flow in the IPSILATERAL VA
    • -Brachial Art ΔP  of 20 mmHg or > usually on the side of the disease
    • -Result in neurological sx w/in the POST hemisphere (Subc steal syndrome) when significant, concomitant ICA disease exist
    • -Usually asymptomatic
  156. Mechanisms of Disease in Cerebrovascular-Neointimal Hyperplasia
    • -A rapid ↑ & growth of intimal cells that occurs Post-endarterectomy
    • -In Vn bypass grafts wall thickening may occur=diffuse or local narrowing @ surgical sites or w/in the graft
    • -Intimal Hyperplasia is absent or minimal in synthetic material grafts
    • -Located in: Surgical sites for carotid endarterectomy & venous anastamosis & outflow vn in hemodialysis access grafts
  157. Mechanisms of Disease in Cerebrovascular-Reversed Robin Hood Syndrome
    • -Steal syndrome compensates bl flow to vessels DIST to a high grade or occlusive lesion by attracting or stealing flow fr normal flow vol vessels as flow will take the path of least (R)
    • -Creates collateralization & maintains flow to the brain
    • -Occurs when changes in cerebral hemodynamics such as hypercapnia, creates a 'steal' fr low flow of ischemic areas
    • -Assessed thru TCD interrogation
    • -Clinical assoc: Acute thromboembolic occlusion, Sleep apnea, Daytime sleepiness, Hypoventilation
  158. Cerebrovascular-Types of Stroke
    • 1. Hemorrhagic: Bleeding w/in the brain causing damage to nearby brain tissue. Common Cause: Hypertension=Po on ART walls or aneurysm
    • 2. Ischemic: Interruption of bl supply to the brain causing ↓ O2 → brain 
    • Common cause:Bl clot or emboli
    • Atherosclerosis is most common factor
    • 3. Lacunar: Nonatherothrombotic obstruction of small perf ART that supply deep cortical structures in the brain.
    • Occurs in elderly pts w/ diabetes or poorly controlled Hypertension
  159. Cerebrovascular-Signs & Sx (Transient)
    • -TIA: appears suddenly & last fr few mins→24 hrs; sx may be repetitive
    • -Resolves w/in 24 hrs-pt goes back to normal
    • -Sx: 1. Amaurosis Fugax (monocular blindness)
    • a. Hollenhurst plaque: bright yellow spot due to cholesterol deposit in the eye. Pt are @ high risk of TIA or CVA.
    • 2. Dysphasia or Aphasia of comm: inability or partial ability to speak
    • 3. Contralateral Hemiparesis: Muscle weakness on opposite side of body fr w/c brain has the deficit
    • 4. Behavioral disturbances
  160. Cerebrovascular-Signs & Sx (RIND)
    • -Reversible (resolving) Ischemic Neurological Deficit: Sx last for >24 hrs; pt goes back to normal after
    • -Sx: Amaurosis Fugax, Dysphasia or Aphasia, Contralateral hemiparesis, Behavioral disturbances
  161. Cerebrovascular-Signs & Sx (POST Circulation Insufficiency)
    • -Bilateral effects on the body
    • -Bilat Paresthesia
    • -Bilat Paresis
    • -Vertigo (loss of bal)
    • -Diplopia (double vision)
    • -Drop attackAtaxia (loss of muscle coord)
    • -Dysphagia (difficulty swallowing)
    • -Horner Syndrome (Ptosis) drooping of upper eyelid
  162. Cerebrovascular-Signs & Sx (ANT Circulation Insufficiency)
    • -Unilateral effects on the body
    • -Hemiparesis: 1 sided weakness
    • -Hemiparesthesia: prickling or tingling of the skin
    • -Aphasia
    • -Behavior changes
    • -Peripheral vision loss
    • -Amaurosis Fugaux
  163. 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
  164. 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
  165. Symptoms assoc. with Lesion in the Ant Cerebral Art (ACA)
    • -Severe leg hemiparesis or hemiplegia
    • -Incontinence & loss of coordination
  166. Symptoms assoc w/bl flow alterations to Vertebrobasilar system or POST circulation
    • -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
  167. Cerebrovascular Accident (CVA)
    • -Complete Stroke: persistent, permanent neurological deficit
    • -Sx: Dysphasia, aphasia, Hemiparesis, Misc neurological deficits, DEATH
    • -Classification of a stroke: 
    • -ACUTE: sudden onset of sx
    • -STROKE IN EVOLUTION: Sx come & go
    • -COMPLETE: Permanent deficit; Stable
  168. Physical Examination
    • -Palpation of pulses
    • -Ausculation for Bruits
    • -Bilat Brachial Systolic Po measurements
  169. Physical Examination-Palpation of pulses
    • -Take Bilat palpation of easily accessible art for evidence of diminished or absent pulses, then compare→contralateral side
    • -Diminished or absent pulse=stenosis or occlusion @ or PROX to the pulse site
    • -Eval for pulse strength in the ff locations: 1. CCA (low in the neck) A pulsatile mass in the PROX neck is usually a tortuous CCA
    • 2. Superficial Temp Art,
    • 3. Brachial or Radial Art
    • AO, CFA, POP A, DPA, PTA/ATA
  170. Physical Examination-Auscultation for Bruits
    • -Bruit is a sound detected by stethoscope caused by or related to Post stenotic turbulence, AV Fistula, or Cardiac murmur
    • -S/b performed Bilaterally on: 
    • -CCA (low→mid neck)
    • -Carotid Bif (mid→dist neck)
    • -Subc A
    • -Brachial A (can indicate Subc or Axillary A disease)
    • -AO, Femoral A, POP A
  171. Physical Examination-Bilat Brachial Systolic Po measurements
    • -Comparison of bilat Brachial BP can indicate presence of Subc A occlusive disease
    • -ΔP of 20 mmHg or greater=Subc stenosis or occlusion on the ↓ Po side
  172. Cerebrovascular-Non Invasive Test Procedures (Duplex sonography)
    • -Combines Hi F real time imaging w/ doppler flow analysis. 
    • -Sonographic image used to define anatomy or bl vessels
    • -Doppler determines bl flow velocity info @ specific locations
  173. Cerebrovascular-Non Invasive Test Procedures (Duplex sonography) Capabilities
    • -IDs extracranial carotid disease & qtfy degree of stenosis incl atheroscloretic plaque, aneurysms, masses, thrombi & dissections
    • -Detects: abnormal flow patterns, Vert, Subc & Innominate Art stenosis or occlusion
    • -Identifies: total carotid occlusion, surface characteristics of plaque
  174. Cerebrovascular-Non Invasive Test Procedures (Duplex sonography) Limitations
    • -Operator dependent
    • -May under/over estimate severity of disease
    • -Size or contour of pts neck
    • -Pt unable to hold still
    • -Pt w/ difficulty breathing
    • -Recent neck surgery
    • -Depth or course of vessel
    • -Acoustic shadowing for Ca++ may cause limited visualization
  175. Cerebrovascular-Non Invasive Test Procedures (Duplex sonography) Patient Positioning & Instrumentation
    • -Supine or comfortable reclining
    • -Neck slightly hyperextended w/ head rotated away fr side being examined
    • -thin pillow under head & shoulds allows for pt comfort
    • -10 MHz, 7.5 MHz or 5 MHz flat linear tx
    • -Use the highest F for adequate penetration
    • -HI doppler F=sensitive to low flow
    • -LOW doppler F=Large PRF (scale) & reduces aliasing
  176. Cerebrovascular-Non Invasive Test Procedures (Duplex sonography) Examination Protocol
    • -Obtain Bilat Brachial Systolic BP
    • -TRV & Long images: CCA, ICA & ECA
    • -Vessels are ID: by their size, location, visualized branches, & characteristic Doppler signals
    • -Eval for presence, location & severity of plaque
    • -Ea vessel is routinely & thoroughly studied w/ Doppler
    • -Color flow Doppler can help ID any disordered flow
  177. Cerebrovascular-Non Invasive Test Procedures (Duplex sonography) 2D TRV & Long Imaging
    • -Assess CCA from base of neck→bif
    • -ICA & ECA ID @ Bif
    • -Eval Prox ECA
    • -Eval Prox, Mid, Dist ICA
    • -Bulb & ICA s/b imaged fr Anterolateral, LAT, PosteroLat approach
    • -Note any pathologies incl location & severity of plaque
    • -Use color Doppler to ID flow
  178. Cerebrovascular-Non Invasive Test Procedures (Duplex sonography) Spectral Doppler Imaging
    • -PW Doppler s/b obtain for Systolic Vel measurements in Long axis, PROX CCA, BIF, DIST ICA, ECA, Assess VA @ origin & mid locations
    • -Spectral Waveforms obtained @ ff:
    • -Prox, mid, dist CCA
    • -Prox bulb, mid, dist ICA
    • -Prox ECA (tt)
    • -VA origin
    • -Mid cervical VA
    • -Subc A (not for BP diff of >20mmHg)

    *If an area of stenosis is seen, Vel s/b obtained in Pre, @, Post Stenosis
  179. Cerebrovascular-Non Invasive Test Procedures & Technical Considerations for Spectral Doppler
    • -Doppler 0 =45 & 600 
    • -SV s/b kept as small as possible. ↑ gate size when assessing for 'trickle flow' or occlusion
    • -SV s/b in CTR alleviating spectral broadening fr slow flow
    • -Color flow Doppler s/b used as an aid in ID stenotic regions but should NOT be used as a replacement for Spectral Doppler (Vel)
    • -Fresh thrombus may be difficult w/ B-MODE; complete interrogation is necessary 

    -B-MODE=accurate to classify <50% DR 

    -Spectral Doppler=accurate for >50% DR 
  180. Cerebrovascular-Non Invasive Test Procedures (Duplex sonography) 2D Interpretation
    • -Normal: Smooth vessel walls w/ anechoic lumen & NO visible plaque
    • -Abnormal:
    • 1. ID surface characteristics: smooth, irreg or ulcerative
    • 2. ID & characterize areas of plaque formation: fatty streaks, Fibrous plaque, Complex/complicated, Ca++
    • 3. Stenosis: show in both planes SAG/TRV
    • 4. Occlusion: Complete filling (echoes can range fr anechoic→highly echogenic). Doppler findings are essential to diagnose this.
  181. Cerebrovascular-Non Invasive Test Procedures (Duplex sonography) Measurements
    • -Diameter vs. Area
    • -%DR = 1-RL ÷ TL x 100
    • -%DR= [1 -RL ÷TL]2 X 100
    • -50%DR=75%AR only in circumferentially shaped stenosis
    • -Intimal Medial Thickness (IMT) used as marker for cardiovascular risk. Meas. Long that is void of plaque
    • -Aneurysm size=2x the size is aneurysmal
  182. Cerebrovascular-Non Invasive Test Procedures (Duplex sonography) Abnormal Characteristics
    • -ICA/CCA ratios are used in conj w/ elevated PSV & end EDV to determine % of stenosis
    • -Assist in ID of a HDS Stenosis that falls outside of PSV or EDV values such as Low Cardiac Output, HTN, Mult lesions or contralateral occlusion
  183. Cerebrovascular-Non Invasive Test Procedures (Duplex sonography) Abnormal Characteristics-Technique
    • -ICA Peak Vel ÷ CCA Peak Vel
    • -Obtain DIST CCA PSV 2 cm prior to Bif
    • -Obtain Highes Peak Vel in the ICA
    • *If ICA is tortuous it could overestimate PSV
  184. Cerebrovascular-Non Invasive Test Procedures (Duplex sonography) COLOR Doppler Interpretation
    • -Determines the presence/absence of flow, dir of flow, turbulence or aliasing
    • -Aliasing is an artifact that occurs when PRF or scale is too low for the existing VEL
    • -Turbulence is a mixture of shades or REDS & BLUES; Can be seen in Bif or Post stenosis
  185. Ways to eliminate Aliasing
    • -Incr Scale (↑ PRF)
    • -Decr F
    • -Lower baseline
    • -Switch to CW
    • -Change view to decr vessel depth (SV)
  186. Cerebrovascular-Non Invasive Test Procedures (Duplex sonography) SPECTRAL Doppler Interpretation -NORMAL-
  187. 1. Narrow band of F during systole w/ clean spectral window
    • 2. PSV: >125 cm/s
    • 3. ECA: HR waveform; DN seen
    • 4. ICA: LR waveform; NO DN seen
    • 5. CCA: Combination of both ECA & ICA waveforms
    • 6. VA: Similar to ICA (LR waveform)
  188. Cerebrovascular-Non Invasive Test Procedures (Duplex sonography) SPECTRAL Doppler Interpretation -ABNORMAL-
    • -Wider band of F during systole w/ a 'filling in' of spectral window
    • -Stenosis profile becomes evident PROX & DIST to area of stenosis
    • -Absence of Doppler signal=Occlusion
    • -Vel below 6 cm/s may NOT be detectable w/ PW or Color Doppler due to wall filters='trickle flow'
    • -Focal Vel accel over plaque w/ ↑ PSV/EDV
    • -POST Stenotic Turbulence present
    • -ICA/CCA ratios
    • -VA (Bi-dir or retrograde flow=abnormal & may suggest Subc steal syndrome)
    • -Low CO=Bilat damped waveform in carotids
  189. Cerebrovascular-Non Invasive Test Procedures (Duplex sonography) SPECTRAL Doppler Interpretation -ABNORMAL ICA/CCA RATIOS-
    • -ICA/CCA ratios used in conjunction w/ ↑PSV & EDV to determine % of Stenosis
    • -IDs HDS stenosis outside of PSV/EDV values due to ↓ CO, Hypertension, Mult lesions or contralateral occlusion
    • -ICA ÷ CCA Peak Vel
    • -Obtain Dist CCA PSV 2 cm b4 BIF
    • -Obtain Highest ICA PSV (If ICA tortuous=overestimation)
  190. SRU Carotid Consensus Criteria
  191. Cerebrovascular-Non Invasive Test Procedures (Duplex sonography) Pitfalls of measurements
    • -Vel measurement varies betw U/S sys
    • -Improper angle placement=inaccurate vel measurements
    • -Inconsistency of Doppler angles used fr 1 exam to the next
    • -False + : Inability to detect 'trickle flow'
    • -False - : When ECA or one of its branches is ID as ICA in presence of ICA occlusion
  192. Cerebrovascular-Non Invasive Test Procedures (Duplex sonography) Clinical Trials
    • -Endarterectomy vs. Medical treatment to reduce risk of stroke
    • -NASCET: (N. American Symptomatic Carotid Endarterectomy) Symptomatic pts w/ ≥70% DR ICA Stenosis
    • -ACAS: (Asymptomatic Carotid Atherosclerosis Study) Asymptomatic pts w/ ≥60%DR ICA Stenosis
  193. Cerebrovascular-Non Invasive Test Procedures (Intraoperative Duplex Sonography)
    -Used w/ sterile technique to ID abnormalities during carotid endarterectomy & Post carotid endarterectomy to check patency
  194. Cerebrovascular-Non Invasive Test Procedures (TCD/TCI examination) Capabilities
    • -TCD & TCI are indicated to detect ff IC circulatory conditions:
    • 1. Stenosis >65% in major basal IC vessels
    • 2. Vasopasm (MCA)
    • 3. AVM
    • 4. Suspected brain death
    • 5. Pediatric vasculopathies
    • 6. Collateral flow (Most important is Cross-fill via AcoA)
  195. Cerebrovascular-Non Invasive Test Procedures (TCD/TCI examination) Limitations
    • -Probe angle
    • -Anatomic Variants
    • -Recent eye surg may make TO difficult
    • -Inability to penetrate Temp bone adequately
    • -Operator error in ID vessels
    • -Pt cooperation
  196. Cerebrovascular-Non Invasive Test Procedures (TCD/TCI examination) Pt Positioning
    • -Comfortable, supine position for TO & TT approach
    • -Lying on side or sitting for Transoccipital approach
  197. Cerebrovascular-Non Invasive Test Procedures (TCD/TCI examination) Instrumentation & Tx F
    • -TCD: Blind non-imaging uses a low F
    • 1.5-2.5 MHz PW, range-gated Doppler
    • -TCI: Imaging of IC vessels & spectral Doppler using a low F of 2-2.5 MHz Phased array sector 
    • TCI has a larger 'footprint' than TCD thus ↓ Doppler sensitivity & ↑ technical failure rate
  198. Cerebrovascular-Non Invasive Test Procedures 
    (TCD) Exam protocol
    • -3 windows:
    • 1. Transorbital (TO) eval OA & Carotid Siphon
    • 2. TT: eval ACA, MCA, PCA, PcoA, & Terminal ICA
    • 3. Transoccipital (Transforaminal or Suboccipital) eval BA & IC segments of VA
  199. Cerebrovascular-Non Invasive Test Procedures TCD Paramater for vessel ID
    • -Depth of SV
    • -Dir of flow @ specific depths
    • -Vel measurements of various vessels
    • -Probe position
    • -Dir of U/S beam
    • -Response of CCA oscillations & compressions
    • -0 degree Doppler angle
    • *Doppler waveforms fr IC vessels are similar to ICA (LR waveform)
  200. Guidelines for ID of TCD
    • V       W        D        Dir     Vel          Angle                                                            
    •                  (mm)           (cm/s)
    • MCA   TT    30-60   Ante   55±12     Ant/Sup
    • TICA  TT     55-65    BI     39±9       same
    • ACA   TT     60-80   Retro  50±11    same
    • PCA   TT     60-70   Ante   39±10     Post
    • Siphon  TO  60-80  Varies  47±14    varies
    • Opht     TO  40-60  Ante    21±5     Medial
    • VA    TF   60-90   Retro   38±10   R/L midline
    • BA    TF   80-120  same  41±10     Midline
  201. Cerebrovascular-Non Invasive Test Procedures (TCD) Abnormal spectral Doppler characteristics
    • -↑ F or V seen in: Localized stenosis, Vasospasms & AVM
    • -↓ Pulsatility seen in: Significant stenosis, Occlusion
    • -Retrograde flow in cerebral vessel indicates collateral or compensatory flow for disease
  202. Cerebrovascular-Non Invasive Test Procedures (TCD) Measurements
    -MCA/ICA ratio criteria for MCA vasospasm

    • Mean MCA    MCA/ICA    Degree of Vasospasm
    • V (cm/s)         Ratio
    • <120              <3           normal→mild <25%
    • 120-200          3-6          Moderate 25-50%
    • >200              >6          Severe spasm >50%

    • PI=PSV-EDV ÷ MV
    • Normal PI for MCA, ACA & PCA=0.5 - 1.1
    • Very LOW PI w/ ↑ PSV & EDV = AVM
  203. Cerebrovascular-Non Invasive Test Procedures (TCD) Pitfalls of measurement
    • -Lack of flow signal can occur due to inadequate Temporal window
    • -Misinterpret of collaterals or AVM as stenosis
    • -IC lesions can displace Cerebral Art
    • -Physiologic variables w/in Circle of Willis
    • -Misdiagnosis of Vasospasm as stenosis
    • -Difficulty to diagnose disease in VA & BA
  204. Cerebrovascular-Non Invasive Test Procedures (TCD) Intraoperative monitoring
    • -TCD used during surg to monitor cerebral bl flow
    • -Microembolic signals (MES) aka HITS=HI Ampl 'spikes' on a waveform
    • -Auditor spikes alert physician to microemboli
  205. Cerebrovascular-Non Invasive Test Procedures (Periorbital Doppler)
    • -Supine w/ head resting on pillow, eyes gently closed
    • -Use 8-10 MHz CW tx to ID & record flow in the vessels Bilat for dir of flow:
    • 1. Frontal A=inner canthus of the eye
    • 2. Supraorbital A=Under the eyebrow
    • -Do Compression maneuvers on Superficial Temp, facial & infraorbital A while monitoring signals of Frontal or Supraorbital A
    • -Do Carotid Compressions; avoid compressing on Bif or stimulating the Carotid sinus
  206. Cerebrovascular-Non Invasive Test Procedures (Periorbital Doppler)-Normal Interpretation-
    • -Antegrade flow (toward the probe) in all vessels even during compression
    • -During compression, AMP signal should ↑ or remain unchanged
    • -Compression of ipsilat CCA should ↓, obliterated or reversed periorbital signals
    • -Abnormal will result in the opposite effects
  207. Cerebrovascular-Correlative &/or Prior Imaging
    (Arteriography)
    • -Conventional arteriography: 
    • 1. Selective carotid inj of contrast
    • 2. Two view Arch studies
    • 3. Extra/Intracranial views obtained
    • 4. Add'l views may be necessary
  208. Cerebrovascular-Correlative &/or Prior Imaging (Digital Subtraction Arteriography) DSA
    • -Technique for digital storage, subtraction of fluoroscopically generated x-ray images
    • -Allows use of smaller concentrations of contrast material than in conventional studies
  209. Cerebrovascular-Correlative &/or Prior Imaging Arteriography (Interpretation)
    • -Compares RL diameter @ the lesion to normal vessel lumen DIST to the lesion=%DR
    • -Vessels are studies for evidence of Ulceration or other disease
  210. Cerebrovascular-Correlative &/or Prior Imaging Arteriography (Limitations)
    • -Invasive & exposes pt → ionizing radiation
    • -Operator dependent can lead→erroneous meas of stenosis
    • -Cannot outline extent of vessel boundary when disease is present, esp in carotid bulb
    • -Meas. hold true for lesions that are uniform & circumferential NOT for atherosclerotic plaque
    • -"Trickle angiography" s/b used to see "string sign" of a very small RL
    • -Hard to diagnose ulcerations
    • -Not used in pts allergic to contrast agents & impaired Renal function
  211. Cerebrovascular-Correlative &/or Prior Imaging (CTA & MRA)
    • -LESS Invasive than conventional arteriography
    • -CTA offer Higher Resolution than MRA
    • -Both use IV contrast inj & only provide anatomic formation
    • -Used as correlative for Pt management & surgical planning if applicable
  212. Cerebrovascular-Treatment & Follow up (MEDICAL & PHARMACOLOGICAL)
    • -Initial Treatment:
    • -Control or ↓ risk factors incl obesity, HI cholesterol, Hypertension & tobacco use
    • -Lifestyle modification
    • -Dietary changes
    • -↑ amt of Exercise
    • -Stop smoking
    • -PHARMACOLOGICAL:
    • -Hypertensive meds
    • -Cholesterol lowering drugs
    • -Antiplatelet meds (ie Aspirin) ↓ risk of coagulation & thrombus formation
  213. Cerebrovascular-Treatment & Follow up (ENDOVASCULAR)
    • -PTA: Percutaneous Transluminal Angioplasty
    • -A balloon tipped cathether placed in area of stenosis. Balloon is inflated & plaque is compressed against the wall INCR lumen size
    • -STENT: Self-expanding/Deployed w/balloon catheter. Used in combination w/ angioplasty procedure
  214. Cerebrovascular-Treatment & Follow up (Eval after Stent placement)
    • -PSV of <150 cm/s=Normal
    • -A 2:1 ratio can be applied. If PSV across the stent is 2 or more times > the Pre-stent Vel=Restenosis
    • -Vel used w/ Gray Scale imaging show rapid ↑ of intima, thrombus or plaque formation for best assessment
    • -HR waveforms PROX to stent or in CCA=Occlusion or Pre-occlusive disease
  215. Cerebrovascular-Treatment & Follow up (SURGICAL)
    • -Endarterectomy: Removal of EC carotid plaque & thrombus
    • -Bypass Graft: Used for CCA (Subc→ICA), Innominate (AO→Subc) & Subc A occlusion (Contralateral→Ipsilateral Subc)
  216. Cerebrovascular-Treatment & Follow up (Acute Thrombolytic Therapy)
    -Tissue plasminogen activators (tPA): promotes thrombolysis (breakdown of bl clot) in acute stroke & acute ART occlusion

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