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exam review 3 on hea

valves, right side of heart

Causes for TS: Rheumatic heart disease (90%) Systemic lupus erythmatosus Carcinoid heart disease Loeffler’s endocarditis Metastatic melanoma Congenital heart disease
Causes for TS: Rheumatic MV disease can have associated TV involvement Isolated rheumatic TV stenosis almost never occurs
M-Mode characteristics of TS Diminished EF slope Anterior displacement of posterior leaflet Thickening of valve leaflets and apparatus
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
Doppler velocities with TS: Higher diastolic velocity than normal Decreased EF slope Turbulent flow Prolonged reduction in velocity throughout diastole
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
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
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
symptoms in carcinoid heart disease Facial flushing with stimuli Abdominal pain Diarrhea Renal failure Hepatic failure Hepatomegaly in later stages
Cardiac signs Elevated venous pressure Systolic and diastolic murmurs
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
Physical findings with TR: Jugular venous distention with prominent v wave Jaundice Thrill (lower left sternal border)
Physical findings with TR: Hyperdynamic RV impulse along left sternal border
Color assessment of TR 1/3 into RA = mild TR 2/3 into RA = moderate TR Fills RA = severe TR
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
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)
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
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
Normal IVC dimension 0-5 mmHg IVC is small (<1.5cm) Change with respiration or “sniff” Collapse
Normal IVC dimension 5-10 mmHg IVC is normal (1.5 – 2.5 cm) Change with respiration or “sniff” Decrease by > 50%
Normal IVC dimension 10-15 mmHg IVC is normal (1.5 – 2.5 cm) Change with respiration or “sniff” Decrease by < 50%
Normal IVC dimension 15 – 20 mmHg IVC is dilated (> 2.5 cm) Change with respiration or “sniff” Decrease < 50%
Normal IVC dimension >20 mmHg IVC dilated with dilated hepatic veins Change with respiration or “sniff” No change
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)
Clinical SBE findings Temperature > 100 degrees Murmurs of TR and PI Positive blood cultures. Usually Staphylococcus aureus
2D SBE finginds Dense mass Highly mobile Shaggy appearance of entire valve Polypoid structure attached to single leaflet
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
Causes of PI: The velocity of PI jet reflects the transpulmonary pressure difference during diastole
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
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
What flying W is: the mid-systolic closure arrow the flying -W sign is specific for pulmonary hypertension.
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
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
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
RVVO Common causes TR PI ASD Partial or total anomalous venous return
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
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
RVH- Eisenmenger’s physiology (reversal of congenital shunt from lt-rt to rt-lt)
Normal free wall measurement Normal free wall measurement is 1.9-2.9mm
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
Different types of prosthetic valves: 3 basic types: Tissue valves or bioprostheses Homograft valves Mechanical valves+
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
BIOPROSTHETIC VALVES AKA tissue valves 3 biologic leaflets Traditional stented prosthetic valves are called heterograft or xenograft (which is transferred from animal to human
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
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
FLOW PATTERNS Trileaflet open to a circular orifice Flow similar to native valve Laminar flow with a blunted flow profile
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
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
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
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
Most common brands are Carpentier-Edwards Ionescu-Shiley (taken off US market) Mitroflow
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
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
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
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
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
ADVANTAGES OF BIOPROSTHETIC VALVES May avoid antocoagulation Lower pressure gradients Central flow dynamics Failure usually occurs slowly Valve of choice for TV and PV
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
TYPES OF BALL & CAGE- Starr Edwards is the most common Smeloff-Cutter Braunwald-Cutter Magovern- surgitool Magover – Cromie Harken DeBakey – surgitool Hufnagel
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
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
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
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
BJORK-SHILEY & LILLHEI-KASTER- Design No fixed hinges Disc rotates freely within the housing Disc pivots on two side struts (u-shaped)
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
Other types: Carbomedics Duromedics (Hemex) Gott-Daggett
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
BILEAFLET VALVES- Discs are parallel to annulus plane during systole Discs perpendicular to annulus plane during diastole Blood flow through 3 orifices
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
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
What valve conduits are used for: VALVED CONDUIT- Used to repair congenital heart disease May be homograft May be artificial material Gore-Tex Dacron
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
Complications of prosthetic valves: MECHANISM OF PROSTHETIC VALVE DYSFUNCTION- Falls into 3 categories: Structural failure Thromboembolic complications Endocarditis
COMPLICATIONS OF BIOPROSTHETIC VALVES- Calcification/degeneration Infective endocarditis Perivalvular leak Dehiscence Stenosis Regurg Thrombus
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)
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 +
COMPLICATIONS FOR MECHANICAL VALVES- Thrombus Stenosis (thrombus, pannus ingrowth) Dehiscence Infective endocarditis Hemolysis Mechanical failure (ball/disc/cage variance/strut fracture) Heart-valve mismatch
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)
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
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
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
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
PANNUS INGROWTH: Newly formed vascular tissue around the valve Problems similar to those with thrombi Impair excursion and cause Stenosis Regurgitation Both
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
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
Abnormal position- Poses no problem Flow patterns will be different Doppler may be more difficult to obtain
NORMAL PROSTHETIC REGURG MR jet area of <2cm2 MR jet length <2.5cm AI jet area < 1cm2 AI jet length <1.5cm
SEVERE MV PROSTHETIC REGURG- Increased mitral inflow peak velocity Normal mitral inflow PHT Dense MR CW signal Regurgitant fraction of 55% or higher
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
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-
ACQUIRED ANEURYSMS- Result from : Atherosclerosis (which is the most common) Syphilis Trauma Aortic stenosis Aortic coarctation PDA Infection Aortic arterits
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
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
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
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
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
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
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
Created by: 100001592513232