# RVS Part I

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 Author: marie78 ID: 303831 Filename: RVS Part I Updated: 2015-07-13 15:02:53 Tags: Vascular Fl Dynamics Cerebrovascular Folders: Description: Vascular Exam Show Answers:

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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
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
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
• -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
• -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
• -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

• 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)
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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