valves, right side of heart
Quiz yourself by thinking what should be in
each of the black spaces below before clicking
on it to display the answer.
Help!
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|---|---|---|---|---|---|
| Causes for TS: | Rheumatic heart disease (90%)
Systemic lupus erythmatosus
Carcinoid heart disease
Loeffler’s endocarditis
Metastatic melanoma
Congenital heart disease
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| Causes for TS: | Rheumatic MV disease can have associated TV involvement
Isolated rheumatic TV stenosis almost never occurs
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| M-Mode characteristics of TS | Diminished EF slope
Anterior displacement of posterior leaflet
Thickening of valve leaflets and apparatus
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| Findings associated with TS | RAE
IAS bows to the left from high RA pressure
Dilated IVC
Pulmonary hypertension
Right ventricular hypertrophy
Both of the above can cause diminished EF slope
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| Doppler velocities with TS: | Higher diastolic velocity than normal
Decreased EF slope
Turbulent flow
Prolonged reduction in velocity throughout diastole
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| Doppler velocities with TS: | Increased “a” wave on hepatic vein flow
With TR, TV velocities usually not higher than 0.7 m/sec
With TV stenosis the velocities are > 1.0 m/sec
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| Clinical symptoms in carcinoid heart disease | Results from the presence of carcinoid tumors
Tumors found mostly in GI tract
Produce vasoactive substance that causes endothelial damage to right side of heart
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| symptoms in carcinoid heart disease | Primary tumors can be small
Can involve heart and cause liver mets
Heart affect late in disease progression
½ of patients with carcinoid syndrome have cardiac involvement
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| symptoms in carcinoid heart disease | Facial flushing with stimuli
Abdominal pain
Diarrhea
Renal failure
Hepatic failure
Hepatomegaly in later stages
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| Cardiac signs | Elevated venous pressure
Systolic and diastolic murmurs
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| 2D appearance of carcinoid heart disease: | RVE
Abnormal septal motion indicating RVVO
Thickened TV leaflets that are retracted
Foreshortened chordae
Thickened retracted PV cusps
TV leaflets don’t coapt completely and remain open throughout cardiac cycle
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| Physical findings with TR: | Jugular venous distention with prominent v wave
Jaundice
Thrill (lower left sternal border)
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| Physical findings with TR: | Hyperdynamic RV impulse along left sternal border
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| Color assessment of TR | 1/3 into RA = mild TR
2/3 into RA = moderate TR
Fills RA = severe TR
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| Flow patterns in IVC w/severe TR | Ratio of RA area to jet area
Hepatic vein and IVC flow
Flows into RA during systole
Pressure falls with atrial relaxation
Color flow doppler shows
Retrograde flow in hepatic veins and IVC
Systolic flow reversal
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| Flow patterns in IVC w/severe TR | The reasons for determining severity:
Deciding to repair or replace TV in patients having other cardiac surgeries Determining systolic pulmonary pressures (this is the most common reason)
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| Equations for calculating gradients and RVSP or SPAP: | SPAP = RVSP
RVSP = 4 x (VmaxTR^2) + RAP
Use CW in presence of high velocities or aliasing
Calculate pressure using Bernoulli equation 4V2
Add RA pressure (which is equal to jugular venous pressure) to peak TR gradient
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| Equations for calculating gradients and RVSP or SPAP: | Normal RA pressures range from 10-14 mmHg
Usually just add 10 mmHg
Alternate calculation method
(TV PG x 25%) + TR gradient
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| Normal IVC dimension | 0-5 mmHg
IVC is small (<1.5cm)
Change with respiration or “sniff”
Collapse
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| Normal IVC dimension | 5-10 mmHg
IVC is normal (1.5 – 2.5 cm)
Change with respiration or “sniff”
Decrease by > 50%
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| Normal IVC dimension | 10-15 mmHg
IVC is normal (1.5 – 2.5 cm)
Change with respiration or “sniff”
Decrease by < 50%
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| Normal IVC dimension | 15 – 20 mmHg
IVC is dilated (> 2.5 cm)
Change with respiration or “sniff”
Decrease < 50%
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| Normal IVC dimension | >20 mmHg
IVC dilated with dilated hepatic veins
Change with respiration or “sniff” No change
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| Differentials for TV veggies | Myxoma (attach to IAS by stalk)
Vegetations
Move with valve during cardiac cycle
TV endocarditis, Rare
Usually seen with: IV drug use, Alcoholism
Congenital defects (ie VSD)
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| Clinical SBE findings | Temperature > 100 degrees
Murmurs of TR and PI
Positive blood cultures. Usually Staphylococcus aureus
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| 2D SBE finginds | Dense mass
Highly mobile
Shaggy appearance of entire valve
Polypoid structure attached to single leaflet
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| Difference between Physiologic and Pathologic PI: Causes of PI: | (Pathologic)
Pulmonary hypertension
Bacterial endocarditis
Pulmonary valvotomy
Congenital defects
Carcinoid heart disease trauma
It is possible to differentiate between PI from physiologic causes and PI from pathology
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| Causes of PI: | The velocity of PI jet reflects the transpulmonary pressure difference during diastole
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| Causes of PI: | Causes of PI:In a normal patient transpulmonary gradient is small
Gradient approx 9 mmHg
Velocity approx 1.5 m/sec
In pt w. normal PA pressures <18mmHg, PW shows PI that peaks in early diastole and slows in late diastole
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| Higher PA pressure: | Pulmonary HTN pts have higher gradient
Higher PA pressure >25 mmHg the PW velocity profile shows wideband spectrum that is sustained throughout diastole
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| What flying W is: | the mid-systolic closure arrow the flying -W sign is specific for pulmonary hypertension.
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| How to measure RVET AcT: There are several methods: | AcT/RVET ratio
SPAP values
RVOT acceleration time
Pulmonary Doppler flow velocities-
Place sample volume just proximal to PV in the center of RVOT
Measure acceleration time (AcT)
Measure right ventricular ejection time (RVET)
AcT/RVET
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| Acceleration time- | Measured from onset of systolic flow to the peak of the velocity
Normal > 120msec
Mild PHTN 80-100 msec
Moderate PHTN 60-80 msec
Severe PHTN < 60 msec
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| RVET | THIS IS THE TIME FROM THE ONSET TO THE END OF SYSTOLIC FLOW MEASURED FROM
AcT/RVT- Normal ratio .45
Significant pulmonary hypertension ratio is reduced to .25
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| RVVO Common causes | TR
PI
ASD
Partial or total anomalous venous return
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| RVVO Less common causes | VSD w/ LV-RA shunts
Ruptured sinus of Valsalva
Coronary artery fistula w/ communication to RA or ventricle
RVVO Echo signs-
Dilated RV
Flatttened septum or “D” sign on 2D
RV appears more oval than usual crescent shape
RV apex may extend past LV ape
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| RVH- | Occurs with
PV stenosis or obstruction of infundibular( A funnel or funnel-shaped structure or passage) or supravalvular regions
Tetralogy of Fallot
Chronic pulmonary hypertension
Mitral stenosis
Pulmonary emboli
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| RVH- | Eisenmenger’s physiology (reversal of congenital shunt from lt-rt to rt-lt)
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| Normal free wall measurement | Normal free wall measurement is 1.9-2.9mm
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| Normal free wall measurement | May become thickened from infiltrative disease
Amyloidosis (Amyloidosis is a progressive, incurable, metabolic disease characterized by abnormal deposits of protein in one or more organs or body systems.)
Hypertrophic cardiomyopathy
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| Different types of prosthetic valves: 3 basic types: | Tissue valves or bioprostheses
Homograft valves
Mechanical valves+
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| Different than evaluating native valves: | 1) several types of prosthetic valves have different fluid dynamics & velocities w/ different sizes
2) mechanisms of dysfunction are different from native valve disease
3) artifacts make diagnostic approach difficult
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| BIOPROSTHETIC VALVES | AKA tissue valves
3 biologic leaflets
Traditional stented prosthetic valves are called heterograft or xenograft (which is transferred from animal to human
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| Heterograft- | Leaflets are porcine or bovine
Porcine leaflets is transplanted pig valve mounted on sewing ring
Bovine valve is usu pericardium shaped to mimic normal leaflets
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| Heterograft- | Valve is mounted on a cloth covered ring support that acts like annulus
Raised “stent” at each of 3 commissures
There are many variations
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| FLOW PATTERNS | Trileaflet open to a circular orifice
Flow similar to native valve
Laminar flow with a blunted flow profile
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| FLOW PATTERNS | High % of normally functioning bioprosthetic valves have small amount of regurg
Prosthesis in mitral position
Inflow stream directed anteriorly and medially toward septum (toward apex is normal
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| PORCINE VALVES- | Pigs aortic valve placed on stents
Attached to sewing ring
Most common brands are:
Hancock I & II
Carpentier-Edwards (standard or supraannular)
Intact (aortic
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| STENTLESS PORCINE VALVES- | Low pressure intact porcine valve supported by Dacron cloth instead of rigid stents
Tries to optimize valvular hemodynamics and are easier to implant
2 approved valves:
St. Jude Toronto SPV
Carpentier-Edwards freestyle valves
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| BOVINE PERICARDIUM- | Cow’s pericardium fashioned into trileaflet mounted on stents and sewing ring
These valves are more prone to sudden failure from a tear in one of the leaflets compared to other bioprosthetic valves
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| Most common brands are | Carpentier-Edwards
Ionescu-Shiley (taken off US market)
Mitroflow
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| HOMOGRAFT (ALLOGRAFT)- | Cryopreserved human aortic valve harvested @ autopsy
Usually the AMVL, aortic valve & asc. Ao are taken & trimmed at the time of implantation
No stents are needed
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| HOMOGRAFT (ALLOGRAFT)- | These valves can be used in the aortic or pulmonic position
Rarely seen in AV valve replacement because more support would be needed
Valve failure is usu because of regurg
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| HOMOGRAFT FLUID DYNAMICS- | Similar to native valve
Flow velocities are slightly higher
Valve areas are slightly smaller
This is because the homograft annulus takes up room in the patient’s outflow tract
Homograft conduit is placed between RV and PA
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| AUTO-GRAFT (SELF TO SELF)- | Excision of aortic valve & placement of pulmonic valve & trunk into aortic position w/ reimplantation of coronaries
Those used in mitral position
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| AUTO-GRAFT (SELF TO SELF)- | Made from patient’s own tissue
Can be made from fascia lata
Fibrous membrane that covers and supports the thigh muscle
? Whether these are still in use
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| ADVANTAGES OF BIOPROSTHETIC VALVES | May avoid antocoagulation
Lower pressure gradients
Central flow dynamics
Failure usually occurs slowly
Valve of choice for TV and PV
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| How occluder moves in caged ball valve: BALL & CAGE VAVLE- | Spherical occluder is in metal cage
In mitral position
During diastole ball moves towards the apex
During systole ball moves towards the LA
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| TYPES OF BALL & CAGE- | Starr Edwards is the most common
Smeloff-Cutter
Braunwald-Cutter
Magovern- surgitool
Magover – Cromie
Harken
DeBakey – surgitool
Hufnagel
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| How many orifices in tilting disc and bileaflet pros. Valves: TILTING DISC VALVE- | A single circular disc opens at an angle to the annulus plane.
It’s motion is controlled be a central strut or slanted slot in the valve ring
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| TILTING DISC VALVE- | Bjork-Shiley and Medtronic Hall are the most common
Bjork-Shiley is no longer in the US because of strut fracture
Lillehei-Kaster
Hall-Kaster
Wada-Cutter
Omniscience
Omnicarbon
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| FLUID DYNAMICS OF TILTING DISC- Characteristics | Two orifices in the open position
Major orifice and minor orifice
Asymmetric flow profile as blood accelerates along the tilted surface of the open disc
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| FLUID DYNAMICS OF TILTING DISC- Characteristics | Subtle variations are seen in flow pattern depending on:
Sewing ring design
Shape of disk
Convex surface
Concave surface
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| BJORK-SHILEY & LILLHEI-KASTER- Design | No fixed hinges
Disc rotates freely within the housing
Disc pivots on two side struts (u-shaped)
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| BILEAFLET VALVE: | 2 semicircular disks hinge open to form 2 large lateral orifices and a smaller central orifice
St. Jude is the most frequently used mechanical valve. It is the least stenotic mechanical prosthetic valve
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| Other types: | Carbomedics
Duromedics (Hemex)
Gott-Daggett
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| FLOW VELOCITY PROFILE- | Three peaks corresponding to three orifices
Higher velocity in the center of each orifice
Pressure gradient from central smaller orifice is usually much higher than the overall valvular pressure gradient
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| BILEAFLET VALVES- | Discs are parallel to annulus plane during systole
Discs perpendicular to annulus plane during diastole
Blood flow through 3 orifices
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| What Carpentier ring is used for: ANNULOPLASTY RINGS- | Repair of the native valve is usually preferable to replacement
They are flexible rings that:
Are sewn into the annulus position
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| ANNULOPLASTY RINGS- | Helps support the native annulus and attached valve leaflets. They restore size and shape of the valves and Help prevent recurrent dilatation
Resembles calcified annulus in echo
There a number of types but Carpentier-Edwards is the classic type of ring
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| What valve conduits are used for: VALVED CONDUIT- | Used to repair congenital heart disease
May be homograft
May be artificial material
Gore-Tex
Dacron
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| What valve conduits are used for: VALVED CONDUIT- | Conduit may have mechanical or biologic valve
Blood flow through valved conduit is similar to blood flow through a valve implanted in the annulus position
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|
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| Complications of prosthetic valves: MECHANISM OF PROSTHETIC VALVE DYSFUNCTION- Falls into 3 categories: | Structural failure
Thromboembolic complications
Endocarditis
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|
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| COMPLICATIONS OF BIOPROSTHETIC VALVES- | Calcification/degeneration
Infective endocarditis
Perivalvular leak
Dehiscence
Stenosis
Regurg
Thrombus
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| COMPLICATIONS OF BIOPROSTHETIC VALVES- | Valve bed abnormality (psuedoaneurysm (A dilation of an artery with actual disruption of one or more layers of its walls, rather than with expansion of all wall layers. Also called false aneurysm), hematoma)
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| COMPLICATIONS OF BIOPROSTHETIC VALVES- | Ventricular dysfunction
Hemolysis/anemia
Heart valve mismatch
LVOT obstruction
*faliure of bioprosthetic valves (to open or close) usu happens 10 yrs +
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| COMPLICATIONS FOR MECHANICAL VALVES- | Thrombus
Stenosis (thrombus, pannus ingrowth)
Dehiscence
Infective endocarditis
Hemolysis
Mechanical failure (ball/disc/cage variance/strut fracture)
Heart-valve mismatch
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|
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| COMPLICATIONS FOR MECHANICAL VALVES | LVOT obstruction
Valve bed abnormality (pseudoaneurysm, valve ring abscess, fistula, hematoma)
Pannus ingrowth (fibrous ingrowth of tissue can cause regurg or stenosis)
Regurg (central, perivalvular)
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|
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| DISC OR BALL VARIANCE- Changes due to abrasion and deposits of lipids Results in: | Increase in disc size
Distorts contour
Cracking, grooving, or tearing of prosthesis
Decreased disc or ball size
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|
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| DISC OR BALL VARIANCE- | Break loose from cage struts
Severe regurgitation
Increased size or contour distortion
Stick to struts or cage in open position
Severe regurgitation
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|
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| THROMBOEMBOLIC COMPLICATIONS- Causes from flow characteristics | Eddies (. A current, as of water or air, moving contrary to the direction of the main current, especially in a circular motion.)
High shear stress
Usually seen on valve housing not disc, ball, or leaflet
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|
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| THROMBUS- | Clot from housing can continue to valve surface causing valve thrombosis
Normal function is altered
May fail to open or stick
Functional obstruction occurs quickly and heart can’t adapt as it does in native stenosis
Severe regurg results
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|
||||
| PANNUS INGROWTH: | Newly formed vascular tissue around the valve
Problems similar to those with thrombi
Impair excursion and cause
Stenosis
Regurgitation
Both
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|
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| PSEUDO-PROSTHETIC DYSFUNCTION: | Cardiac dysfunction due to:
Implant too small for pt
Implant too large and prosthesis obstructs outflow
Ball and cage mitral can obstruct LVOT if too large
Poor cardiac output
Abnormal EKG can mimic dysfunction
A-fib
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|
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| INCIDENTAL FINDINGS- | Spontaneous contrast
Not from slow flow
Clot formation incidence does not increase
Flow seen from microcavitation downstream from impact of occluder to sewing ring
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|
||||
| Abnormal position- | Poses no problem
Flow patterns will be different
Doppler may be more difficult to obtain
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|
||||
| NORMAL PROSTHETIC REGURG | MR jet area of <2cm2
MR jet length <2.5cm
AI jet area < 1cm2
AI jet length <1.5cm
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|
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| SEVERE MV PROSTHETIC REGURG- | Increased mitral inflow peak velocity
Normal mitral inflow PHT
Dense MR CW signal
Regurgitant fraction of 55% or higher
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|
||||
| SEVERE AO PROSTHETIC REGURG- | PHT of regurg 250m/sec or lower
Restrictive mitral inflow pattern
Holodiastolic reversals in the descending thoracic aorta
Regurgitant fraction of 55% or higher
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|
||||
| Types of Aneurysms: ANEURYSMS | When dilation is severe it is classified as an anerysm
Localized areas of abnormal dilation of a blood vessel wall (usu. an artery)
There are several types-
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|
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| ACQUIRED ANEURYSMS- Result from : | Atherosclerosis (which is the most common)
Syphilis
Trauma
Aortic stenosis
Aortic coarctation
PDA
Infection
Aortic arterits
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|
||||
| Saccular- | Weakening of the vessel wall at one point
Results in a pouch-like expansion and a small neck
🗑
|
||||
| Fusiform- | Involves the entire circumference of the vessel
Dilataion is uniform
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|
||||
| SINUS OF VALSALVA ANEURYSM- | Dilatation of the aortic sinus of Valsalva
Rare anomaly
May be acquired or congenital
May present ruptured or unruptured
Symptoms depend on whether the aneurysm has ruptured or not
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|
||||
| ATHEROSLCEROTIC ANEURYSM | Most common
25% are thoracic, the rest are abdominal aneurysms
🗑
|
||||
| THORACIC AO ANEURYSM: | Most common sites
Aortic arch
Descending aorta
🗑
|
||||
| ATHEROSCLEROTIC PROCESS- | Weakening of AO wall
Medial degeneration
Localized vessel dilatation
🗑
|
||||
| HYPERTENSION- | Causes disease of the aorta
Undermines strength of AO wall
Eventual expansion to aneurysm
🗑
|
||||
| SYMPTOMS OF ANEURYSMS | Related to size and location
Occurs when the aneurysms are large enough to impinge on adjacent structures
🗑
|
||||
| Compression of : | Lt mainstem bronchus
Recurrent laryngeal nerve
Esophagus
🗑
|
||||
| SYMPTOMS | Wheezing
Cough
Dyspnea
Hemoptysis
Hoarseness
dysphagia
🗑
|
||||
| Layers of the Aorta: | Tunica intima
Tunica adventitia
Tunica media
🗑
|
||||
| Tunica media | Most important
Composes 80% of aortic wall
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|
||||
| AO WALL ELASTICITY- Does 2 things: | Damping (storing) of force generated by ventricle in systole
Expulsion of stored energy in diastole
Wide surges in arterial pressure are avoided this way
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|
||||
| Where do we see coarctations: | Aortic isthmus-
Just distal to left subclavian where arch and descending ao join
Coarctation commonly occurs here
Vulnerable to traumatic injury here
Ao is fixed to thorax @ this point
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|
||||
| OBSTRUCTIVE LESIONS SUPRAVALVULAR AO STENOSIS- | Congenital narrowing of the ascending ao just distal to insertion of coronary arteries
Least common site for congenital aortic stenosis
Very rare
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|
||||
| OBSTRUCTIVE LESIONS SUPRAVALVULAR AO STENOSIS- | Two features usu accompany these anomalies:Dilatation of the coronary arteries sometimes with ostial obstruction
Thickening and fibrosis of the aortic valve cusps usu with some AI
🗑
|
||||
| SUPRAVALVULAR AO STENOSIS- | 3 types
“hour-glass” shaped
Fibrous membrane with narrow opening
Diffuse narrowing (hypoplasia) of the descending ao
🗑
|
||||
| SUPRAVALVULAR AO STENOSIS | Fibromuscular thickening producing and hourglass-shaped narrowing
Just above aortic sinuses
🗑
|
||||
| Most common type | Cusps may be thickened
There is some degree of associated PA stenosis
Supravalvular or peripheral
Associated with Williams syndrome
🗑
|
||||
| Williams syndrome Features of this syndrome include: | Supravalvular aortic stenosis
Elfin facies
Mental retardation
And occasionally peripheral pulmonic stenosis
🗑
|
||||
| DISCRETE FIBROUS MEMBRANE- | Seen in a normal sized aorta
Usually located near the sinotubular junction
🗑
|
||||
| HYPOPLASIA OF ASC AORTA: | Often involves the origins of the brachiocephalic arteries
Also called “strand” stenosis
Associated with hypoplastic left heart syndrome
🗑
|
||||
| COARCTATION- | Localized narrowing of the desc aorta near origin of ductus arteriosus
Usu just distal to origin of the left subclavian
Is associated with other congenital heart defects :
Bicuspid ao valve
MV malformations
🗑
|
||||
| SUBVALVULAR OBSTRUCTION- Two types: | Discrete form
Tunnel type of subaortic obstruction
🗑
|
||||
| DISCRETE (MEMBRANOUS)SUBAORTIC OBSTRUCTION- | Results from a thin, fibrous membrane or ridge that forms a crescent barrier w/in LVOT just below AoV
Membrane usu extends from anterior septum to anterior MV leaflet
Echo appearance is thin linear echo in LVOT perpendicular to IVS
🗑
|
||||
| Average Ao diameter: ABDOMINAL AORTA | Begins at the diaphragm
Average diameter is 2cm
How intimal flap moves in dissection:
Flap moves towards true lumen in diastole
🗑
|
||||
| AORTIC DISSECTION | Catastrophic event initiated by a sudden tear in the intima
A column of blood enters the aortic wall and destroys the media while stripping the intima from the adventitia
They are classified by location using the DeBakey or Stanford classification
🗑
|
||||
| AO DISSECTION Location | Stanford classification
Type A - Ascending ao
Type B – All dissections that do not include ascending ao
More common in men
🗑
|
||||
| AO DISSECTION II Location | DeBakey classification
Type 1 – Ascending, transverse & descending ao involved (70%)
Type 2 – Ascending ao involved but stops prox to brachiocephalic (5%)
Type 3 – Descending ao and may extend into abd ao (25%)
🗑
|
||||
| AO DISSECTION- Can be caused by: | HTN
Atherosclerosis
Marfan’s
Aging
Pregnancy
Trauma
🗑
|
||||
| AO DISSECTION- Can be caused by: | Iatrogenic injury
Inflammatory diseases
Cocaine use
Renal disease
Strenuous physical exercise
🗑
|
||||
| Findings assoc with Marfan’s syndrome: | A hereditary condition of connective tissue, bones, muscles, ligaments and skeletal structures
🗑
|
||||
| ECHO FINDINGS W/MARFAN’S | Prox ao dilatation
Multivalvular prolapse
LA compression
AI, MR
Ao dissection (most common)
LVVO pattern
LV dilatation w/ hyperkinesis
🗑
|
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