echo4

Why, Prosthetic Valves

These valves are constructed of artificial material: = pyrolite carbon, silastic and titanium

• Starr Edwards is the most common brand
• A ball within a cage ( held in place by a welded metal cage
• Pressure pushes the ball up and down to open and close the valve
• High profile

Mechanical Valve: Tilting Disc:
• Bjork Shiley – low profile (toilet seat) no longer used
• Lillehei Kaster – low profile
• Medtronic Hal
• Pivoting disc design with no fixed hinges
• Disc rotates freely within the housing and pivots on two struts
Problems:
• Elevated pressure gradients
• Ball variance (high profile)

Heterografts-animal
Homografts-human(autopsy)
Autografts-human(patients use own tissue)

Valved conduits: used to repair some types of congentital heart disease
May be homograft or an artificial material such as Gore-Tex or Dacron
Carpentier Ring: repair AV valves
Flexible ring that is sewn into the annulus to help support the native ring
Resembles calcified mitral annulus

•All prosthetic valves are inherently stenotic
•Thrombus – due to trapped particles on the stents or discs
•Pannus – fibrous ingrowth of tissue leads to stenosis or regurgitation
•Turbulent flow = infective endocarditis = vegetations
•Dehiscence = sutures in the sewing ring loosen , perivalvular leaks
•Abscess formation
•Mechanical failure
•Calcification or degeneration of valve (bioprosthetic)
•Hemolysis – red cells become damaged as they pass through the mechanical valves

Mechanical:
•Children and young adults
•Patients with renal failure, small valve annulus, high re- operative risk, or another reason for anticoagulation
•Aortic root replacement – dissection with severe AI

Bioprosthetic:

•Elderly patients
•Patients in whom chronic anticoagulation is not advised
•Those at risk for thromboembolism

-traua
radiation therapy
collagen diseases
viral diseses
CA
cardiac surgery
-certai drugs

Constrictive pericarditis has great flow in early diastole, whereas tamponade has poor flow throughought the cardiac cycle

False cords
-papillary muscles
-LV trabeculations

-Lamble's Excresence-small fibroelastic protrusion that mimics a vegge
-nodule of arantus

-anticoagulation therapy
-surgical excision depeding on location
-if valve is involved, it can be repaired during surgery.

-most common primary malignant tumor
-usually in Rt atrium
-often have pericardial effusions=tamponade

Myxoma(30% of benign masses)
-appear in atria, ventricles cardiac valves , or the IVC
-moves in and out of atria
-usually attached with a pedicle to the fossa ovalis of the intraatrial septum
-drops through the MV during diastole

-compications related to LVOT obstruction
-thromboembolic event(MI, stroke)

-dyspnea and cyanosis
-peripheral/pulmonary emboli
-CVA-TIA
-angina
-usually over 55yrs old

-yellowish gray tumor found in ventricular walls
-may be multiple
-most common primary cardiac tumor in children
-may present within first year of life and >90% present by age 15
-assoc. w/ tuberous sclerosis
-seen in adults 8.5%

(10% of benign tumors in adults)
-most common valvular tumore
-on the AO and MV in adults
-on the TV in children
-very small(rarely>1cm)
-dense mobile mass with consistancy resebling chordae tendonae

-moderator band
-muscle bundles/trabelulartions
-catheters and pacemaker wire

COMPLICATIONS:
-ventricular arrythmias
-LVOTO
-CHF
-sudden death

TREAMENT:
-surgical removal
-heart transplant in children w/ large LV fibroma

-family hx-dyspnea upon exertion
-orthopnea(dizzyness when stand up quickly)
-acute pulmonary edema
-cough
-hemoptysis(expectoration of blood)
-palpitiations
-tumor plop(highly suspicous of myxoma)

LA-74%
RA-18%
RV-4%
LV-4%
cardiac valves, or IVC

-4%
-bulky tumore, frequently embedded in myocardial wall of the ventricles or IVS
-typically seen during childhood

-joint pain and rash(clubbing of fingers)-complication of myxoma

-heart failure due to obstruction of conduction pathways
-ventricular tachycardia

TREATMENT:
-surgical excision -sometimes impossible to remove

-angiosarcoma(most common)
-rhabdomyosarcoma
-fibrosarcoma
-osteosarcoma
-

-inverse of compliance
-ratio of change in pressure to change in volume

MYXOMA:
-mobile
-sharp borders
-mottles appearnce
-point of attachment
-normal atrial dimensions
-normal AV valve

THROMBUS:
-irregular surface
-layered
-imobile
-broad based
-Dialated LA
-Abnormal AV valve
-near post wall of LA.

-Calcified mitral annulus
-cornary sinus
-suture line following transplants
-fossa ovalis
-ridge btw LUPV, and LAA
-Lipomatous hypertrophy of IAS
-pectinate muscles
-TRX sinus

-CHiari network
-Crista terminalis-ridge i post part of RA
-catheters/pacemaker leads
-Fatty material(surrounding TV annulus)
-Lipomatous hypertrophy of IAS
-pectonate muscles
-Eustachian valve

Right:
-TV, and IAS

from 4 chamber view, turn 90 degrees for appendage

Direct source:
-high probablility of stroke=throbus, tumor, vege, aortic atheroma

Indirect source:
-lower probability of causing strok
-dilated cardiomyopathy, ASD, PFO, spontaneous echo contrast

Cephalad=see ascendind AO
90 left=RVOT, pulmonary artery
90 right=SVC, IVC, LA, A< IAS(aka bicaval views)

1st-LA thrombus due to atrial fibrillation
Then:
-acute myocardial infarction,
- ventricular aneurysm,
-rhumatic heart disease and -prosthetic valves

1. repositioning-up and down esophagus
2. rotation-retating from 0-180 degrees
3. turing-moving transducer in a rotational fashion to show medial and lateral
4. angulation-superior to inferior
5. tilt-lateral motion of the tip to image different structures in the same imaging plane

-vege and aortic sclerosis
-valvular strands seen on native as well as prosthetic valves

-thrombus sits on Lt side of LA
-tumors are closer to septum

-thromboembolism is a consequence of a-fib
-most common cardiac rhythm disturbance
-untrated patients w/ a-fib=higher risk of strok=%

-single set of phased array
-64 elements/set transverse imaging
-5mHz
-produces only 2 or the three primary planes(short axis, and 4 chamber)
-not used anymore

-second generation-single set of phased array elements
-64 elements/seg-distal=longitudinal Proximal=transverse
-5-7HHz, or 3-5MHz
-not used anymore

-pulmonary veins

-pt. intolerance
-sore throat
-transient hypoxia
-supraventricular tachycardia
-transient hypertension or hypotension
-blood tinge sputum etc.

-probe buckling
-probe compression of surrounding structures
-probe interference w/ other esophageal or nasogastric devices

-prior esophageal surgery, radiation therapy
-oropharyngeal distortion, servical spondylosis, cervica arthritis(kinky spine)
-severe cardiopulmonary distress
-suspected esophageal varices

-passed into stomach
-probe tip in stomach, superior angulation
-see global LV systolic and diastolic function
-wall thickness and LV diameters
-regional LV function

-obese patient
-evaluate the AO
-LV function
-encocarditis
-sosrce of embolism
-right heart function and prosthetic valves

-image rotated btw 30-45 degrees
-aortic valve-seen very well
-LCA-easily seen
-RCA-NWS

-high esophagus posiitoin to LA
-retation of 120 degrees
-asc. ao well seen
-ant. and post MV leaflets seen
-ant. septum and post LV walls seen.

-evaluation of AO stenosis
-imaging apex
-seeing aortic arch

-esophageal tumors, stenosis, strictures, diverticulum, varicies, perforated viscus, gastric volvus or perforation, GI bleeding
-unwilling patient

-endocardits prophylaxix(of they have a vegge)
-pharyngeal anesthesia-lidocain(10%)spray(freezes tounge and throat)
-drying agent(robinul)
-sedative(demerol)

-cardiovrsion
-antiarrytmic drugs
-anticoagulation therapy

-Basal
-Four chamber
-Transgastric
-Aorta

-atrial septum
-valvular abnormalitites
-pulmonary emboli
-A-fib

-annular array, rotation crystal
-13mm diameter
-sector angle, 15 degrees to 270 degrees
=4-10mHz for 2D
-3.3 MHz for doppler

-60 degrees from 4 chamber
-ant. and inf walls of LV seen
-can calculate EF using simpsons
-only the anterior leaflet of the mitral valve is seen

-120 degrees from apical four
-difficult to obtain because of lung

-0 degree probe
-probe post to LA
-Lateral and inferior septal walls seen

-inflammation
-pericarditis
-rupture or tear in the pericardial wall
-blunt trauma

-reliable for heart transplant rejection
-myocarditis
-amyloidosis
-causes of cardiomyopathy

-local anesthesia
-done in heart cath
-venous sheath placed in RT IJV
-bioptome is advanced under fluiro or echo in the right ventricular apex
-multiple(3-6) specimens are obtained form different sites

-increased thickenss of the IVS and LVPS due to edema and cellular infiltration
-increased RV wall thickness
-reduced EF
-reduced IVRT(stiffness)
-global enlargement of the LV
-paradoxical septal motion
-PE

-m-mode-record motino of ventricle walls and septum in patiens w/ ventricular pacemaker
-RV pacemakers=eartly post IVS motion immediately after the pacemaker artifact(LBBB)

-Preload = (LVED pressure)
-Afterload = force the ventricle faces when it is contracting in systole = wall stress
I-ntrinsic ventricular contractility – intensity of myocardium in its active state
-Heart Rate

left ventricular ejection time
measurement taken from m-mode of the AO

Measure LVOT diameter – PSLA during systole
D = 2.2 cm
Calculation of LVOT area
LVOT = (2.2)²x .785
= 3.8 cm²
X by VTI(using pw @ aortic annulus)

-flat root, and LA
-poor AO cusp separation

LV pre-ejection period/left ventricular ejection period
LVPEP/LVEP
Normal = < 0.35 =

Stress is defined as the force exerted on an object divided by its cross-sectional area
-often described as Newtons per square meter , N/m² or dynes/cm²

normal=>1200mmHg/27ms
mild-mod dysfunction=800-1200mmhg/27-40ms
severe dysfuntion=,800mmhg/>40ms

Index of myocardial performance
-combines systolic and diastolic parameters
-global function independant of geometry
-(MR or TR)-(LVOT or RVOT)/(MR or TR)
-normal=<0.4
-mild=.4-.5
-mod-.6-.9
-severe->1

Ballon-tipped catheter to create a tear in the wall of the pericardium
Fluid drains through the tear and into the pleural cavity, which can accommodate a larger volume of fluid
Local anethesia

-General anesthesia
-incision in the chest and pericardium to gain access for the drainage tube
-Removal of pericardial sac
-Specimen for the pathologist

-Part of the pericardium is removed
-Done if scarring is present with cardiac tamponade
-Usually performed in severe cases only

formed @ 3-7 wks
starts beating on day 22
circulation starts day 27-29

-heart arises as 2 cords(cardiogenic cords)
-canalize to form 2 heart tubes
-tubes move toward eachother and fuse to form a single heart tube
-bulbus cordis and ventricle grow faster than the other regions, causing the heart tube to bend upon itself and form a bulboventricular loop
-cardiac tube consists of myocardial mantle line w/ a core of cardiac jelly, surrounding an inner endocardium.

Consists of:
-myocardial mantle line
-core of cardiac jelly
-inner endocardium

-Endocardium and cardiuac jellly forms the endocardial cushions
-myocardial mantle becomes muscular wall of heart enriched w/ contractile myocytes

-sinus venosus
-common atria
-common ventricle
-conus cordis
-trucus arteriorsus

common atrial, two horms-left and right from the sinus venosus

truncus and conus
truncus=forms AO and pulm
conus=forms outflow tracts
-moves inferior, anterior, and to the right

-coronary sinus and the oblique vein of left atrium form from the Lt horn
-SVC, IVC, and part of RA form from the RT horn

-day 21-common atrial, two horns, lt and rt form from the sinus venosus
-left horn forms oblique vein of LA, and Coronary sinus
-obliteration of left sinus venosus(lt to rt shunt)
-rt horn-sinus venosus enlarges
-right side sinus venosus becomes rt atrium
-rt atrial-atrial fold-helps direct oxygenated blood across the IAS to fetal circulation(eustachian valve)

-the ventricle expands more rapidly in its lateral aspects and more slowly in its medal portion
-gradually fuses to form a portion of the IAS

MV and TV

-Four mesenchymal swellings appear(30-40 days):
-2 endocardial cushions
-2 lateral cushions

2 endocardial cushions:
-form the septal leaflet of MV, a portion of inflow perimembranous IVS

2 lateral cushions:
-form anterior and posterior TV leaflets, and posterior leaflets of the MV

-the tuvercles on the main truncus

-4th weeks-six sets of symmetrically paired aortic arches form
-arches system loses its symmetry as it changes into the adult arterial system
-3rd set becomes the common and internal carotid artery bilaterally
-left 4th arch becomes the aorta
-6th arch becomes the right and left pulmonary arteries
-others obliterate

-O2 blood from placenta is returned fromthe IVC and shunted across the atrial septum
-SVC is directed through the RA and into RV
-patent ductus arteriosus causes blood from RV to enter ductus and passes to the aorta for return to the placenta
-only a small amount of blood enters the lungs

-3 weeks-5-6 part primitive cardiac tube
-four weeks-cardiac loop begins
-six-8 weeks-all 4 chambers are complete

-Lt & Rt atrial lie at caudal end outside pericardium
-Ventricles in the middle
-Aortic Arches – lie cephalad and outside pericardium

-Placenta
-Presence of shunt pathways-foramen ovale and patent ductus arterious
-Low levels of pulmonary flow

3rd week – horseshoe shaped region = cardiogenic region
Day 19 – 2 endocardial tubes form = will form primitive tube
Day 21 – embryo undergoes lateral folding – 2 tubes = 1 single tube
Day 22 – heart begins to beat

forms the anterior parts of right & left atrium – primative atrium & sinus venosus moves superior & posterior

-atrial fold-helps direct oxygenated IVC blood across the IAS

-annulus(1.4-2.6)
-sinus of valsalva-(2.1-3.5)
-sinotubular juction(1.7-3.4cm)
-ascending aorta(2.1-3.4cm)

-bicuspid valve
-supravalvular stenosis
-subvalvular(discreet subaortic stenosis)
-coparctation of the aorta
-marfan's syndrome

-similar to marfans, but w/ a dialated abdominal AO

Simple: focal thickening < 5mm-no evidence of disruption of the intimal surface
Complex: disruption and irregularity of the intimal surface w/ overlying shaggy material exceeding 5mm

pre-ductal-above ductus arteriosus
Post-ductal-common in adults-below ductus arteriosus
Juxaductal-@ ductus arteriosus level

CONGENITAL:
-windsock appearance
-protrudes from AO sinus into adj. cardiac structes
-if aneurysm isn't fenestrated, doppler flow is unremarkable
-if fenestrations are present, doppler is high velocity and turbulent from the high pressure AO to low pressure adj. chamber.

CONGENITAL:
-windsock appearance
-protrudes from AO sinus into adj. cardiac structes
-if aneurysm isn't fenestrated, doppler flow is unremarkable
-if fenestrations are present, doppler is high velocity and turbulent from the high pressure AO to low pressure adj. chamber.

-dyspnea on exertion(most common)
-congestive heart failure(end stage)
-low BP
-angina pectoralis
-right heart failure

-thickened AV leaflets
-elliptical"football" shaped opening
-systolic doming
-eccentric diastolic closure
-LVH or LV enlargement
-LA enlargement
-poststenotic dialation of AO root

-bicuspid AO valve(80-85%)
-Patent ductus arteriosis(50%)
-VSD's(35-40%)
-valvular aortic stenosis(15%)
-subaortic stenosis(15%)
-turner's syndrome

-bicuspid AO valve(80-85%)
-Patent ductus arteriosis(50%)
-VSD's(35-40%)
-valvular aortic stenosis(15%)
-subaortic stenosis(15%)
-turner's syndrome

-dialation of the aortic sinus of valsalva(rare)
-may be congenital or aquired(acute infections, or inflammatory process)
-RCC most commonly effected(90%)

-malignant systemic hypertension
-congestive heart failure
-aortic aneurysm

aka discreat sub aortic stenosis or subvalvular stenosis:
-Fibromuscular(tunnel)
-Membranous(collar)

ACQUIRED
-less irregular shape(endocarditits more spherical)

-underdeveloped aorta-hypoplastic left heart syndrome

-underdeveloped aorta-hypoplastic left heart syndrome

-amnormal thickening of the medial layer of th eaorta

-measurements for continuity equation
-assess AO regurge
-MR, RV assessment
-Measurements for diastolic dysfunction

chronic hypertension

-atherosclerosis
-syphillis
-cystic medial nechrosis
-blunt or penetration chest injury
-infective endocarditis
-marfan's(involves all 3 sinuses w/ round smooth patter of root dialation)

ype 1=dissection throughout the AO
type 2=dissection confined to asc. ao
type 3=dissection confined to desc. ao
(2 + 3 =1)

-eccentric diastolic closure
-thickened AV leaflets
-LVH
-LV dialation(significant regrurge)
-LA dialation

-hemorrhage limited to the medial layer of the aortic wall w/out a internal disruption
-just as bad as an AO dissection
-marker for co-existing coronary artery diseaseand stroke

associated w/ supravalvular aortic stenosis

Ao=early closure of the AV
LVH due to LV pressure overload

Type A=dissection of Asc. ao
Type B=dissection of desc. AO

-determined by the position of the atria because they bear the most consistant relation to the situs of the viscera
-situs solitus=normal or usual
-situs inversus=right to left orientation of unpaired viscera is inverted

step one-position of the apex
step two-situs of the atrium
step three-AV relationship
step four-relationship of the great vessels

-drains coronary sinus, IVC, and SVC
-larger appendage than LA
-could drain some or all of PV(anomolous)

-triangular external shape
-thick muscle bundles(course trabeculation)(especially @ apex)
-pap muscles attach to the IVS
-moderator band seprates the RVOT from the rest of the ventricle
-trileaflet valve

S=solitus(normal visceral and atrial position)
D=normal d-looping of ventricles resulting in AV concordance
S=normal relationship btw great arteries(MPA, and AO)

1. Holes or defects: at atrial, ventricular or arterial levels
2.Underdevelopment/Absence/Atresia/Hypoplasia of any structure
3. Narrowing: sub - valve, at valve, supravalvular
4. Wrong connections: discorcondance, transposition, inversion, anomalous connection

-Transposition=RV opens into the Ao and LV opens into the PA
-Double outlet RV=both great arteries originate fromt he RV
-Double outlet LV-both great arteries originate fromt he LV
-Trunkus arteriosus-single great artery

-morphologic LA is on the same side as the gastric bubble
-morphologic RA is on the same side as the liver

-situs solitus=normal or usual
-situs inversus=right to left orientation of unpaired viscera is inverted

chambers
valves
great arteries

-MV is always attached to the LV
-TV is always attached to the RV
-exeption: patients w/ AB canal malformations

-conical shaped
-smoother internal suface w/ fine trabeculation
-2 clearly defined pap muscles
-bileaflet(bicuspid valve)

-ASH, concentric LVC, apical hypertrophy, mid ventricular hypertrophy
-SAM-may creat LVOTO
-b-notch of MV-increased LVEP
-mid systolic closure of the arotic valve due to a sudden decrease in cardiac output

inferior wall; true aneurysms in apex

-AO regurge-due to increase in LV pressures; underestimates the severity of stenosis
-restrictive diastolic dysfunction also underestimates the severity of stenosis because the slope is very sharp to begin with.

M-mode=no a
doppler=exaggerated A

90% of the time w/ mitral stenosis

usually congenital causes

-ASD
-WPW-wolf parkinson white

-systolic BP
-peak velocity of VSD or PDA

-bicuspid AO valve
-coarctation

-Desc. ao is bigger, and outside the heart
-coronary sinus is smaller, and inside the heart

-anomolous pulmonary venous return into coronary sinus

LA

Jantene and mustard procedure
Jantene=great artery switch
Mustard=atrial switch

close to svc

bicuspid AV
ASD's
Ao stenosis(more in males)
Co-arctation of the aorta
VSD's

-level of AV valves
-usually involves MV (cleft)
-usually associated w/ partial endocardial cushing defect
-20% of all ASD's

-level of entrance of SVC or IVC into RA
-exists in SVC's inflow portion
-associated w/ anomolous drainage of the right pulmonary vein
-diff vis(try tee)

-rare
-seen w/ unroofed coronary sinus
-creates a lt to rt shunt from LA to conornary sinus, then to RA
-assoc w/ persistant LT sup. vena cava connecting to the LA

-50% are assymptomatic depending on amount of lt to rt shunt, and pulmonary resistance
-dyspnea, palpitations, and atrial arrhythmias
-increased shunting leads to PHTN and rt heart failure
-Qp/Qs>2:1
-systolic ejection murmur due to delayed emptying of the RV

-congestive heart failure
-pulmonary hypertension
-eisenmenger's syndrome(causes increased pressures on the rt, and results in a rt to left shunt)
-atrial arrythmias
-cerebrovascular accident(paradoxical embolization)
-infective endocarditis(rare)

-enlarge rt side
-RVVO-paradoxical septal motion, flattened IVS(d-shaped in systole and diastole
-pulmonary artery enlargement-no a-dip; flying w
-t-artifact(increased echogenicity @ the edge of the IAS )
-Cleft MV(w/ primum ASD)
-MVP(secundum ASD)

-secundum=MVP, and atrial septal aneurysm
-primum=cleft MV
-sinus venosus=anomolies pulmonary veins
-coronary sinus=peristant lt SVC

-outlet-btw ao and pulmonary-more common in asian population
-membranous-where inlet, outlet, and muscular come together(80%)
-inlet(basal septum)-lies post to TV, btw TV and MV(can involve ECD)
-muscular-least significant
-malalignment(tetrology of fallot(trunkus)

-Lt to Rt shunt until PA pressure rises and equals or exceeds systemic pressure(eisenmengers)
-shunt may be bidirectional, or rt to left(cyanosis)
-systolic murmur
-dyspnea, CHF, endocarditis

-CHF
-endocarditis

-LA and LV enlargement
-LVVO
-Tricuspid valve systolic flutter
-pulmonic valve systolic flutter
-Dialated PA-increased flow going to lungs directly
-RVH-pulmonary hypertension

-primum ASd, and inlet VSD

-outlet, not membranous

-low cardiac output or RV failure causes a decrease in speed of transit of microbubbles
-TR-microbubbles from RA to RV then back to RA and IVC and hepativ veins in systole
-shunts-depends on kind of shunt

-chest pain(initial symptom 25% of the time)
-exertional dyspnea
-palpitations
-CHF
-infectiveendocarditits
-PHTN
-eisenmenger's

-pulm hypertension
-eisenmongers
-CHF

-always on the lateral wall of the lt pulmonary artery
-PSSA may provide direct visulaization
-lA and LV enlargement w/ normal LV function
-LVVO
-dialated PA-pulm hypertension
-d-shaped LV in extreme cases

-LA and LV enlargement
-LVVO
-LA/AO ratio>1.4:1
-pulm hypertension-flying w, and no a-dip

-sample volume placed in PA-turbulence w/ aliasing
-PR-RVOT
-evaluate desc. AO for retrograde flow
-PA pressure(RVSP)=systemic BP
-Qp/Qs=remember to invert the numbers because pulmonic is not systemic

reverse numbers because pulmonic is now sytemic:
Qp=aortic flow
Qs=pulmonic flow

1. infants=rt to lt shunt=desaturated blood enters the sytemic system below the subclavian artery
2. O2 saturation in the upper extremities will be higher than the lower extremities(cyanosis in lower body of infants)
3. CHF in premature babies-rare in full term infants
4. drug can be given indomethacin-causes constriction of the ductus(used w/ premature infants.

aka endocardial cushion defect:
-paradoxical septal motion
-RV enlargement
-Abnormal MV-e-point may closs ventricular septum
-Thick ant. leaflet

-MV and Tv regurge
-identify shunts
-Qp/Qs
-RVSP

-LV doesnt develop dueto Mitral and aortic atresia
-IVS is intact
-blood flow in RT side is normal
-w/out PDA, this defect is lethal

-Bar of tisue in mitral position
-thin slit like LV
-thred like aorta w/ diameter <4mm
-Small LV-poor contractility and brigh walls

-color flow in asc. ao-show retrograde flow from aortic arch to aortic root
-4chamber-no flow into LV from LA
-large lt to rt shunt across the IAS

-segmental approach
-short axis-ao leftward ant, and sup. to PV
-A-4=abnormal inf. TV in the lt sided morphologic rt ventricle
-malalignment of IAS and IVS
-RV enlarged-decreased sytolic function
-VSD
-LVOT and RVOT obstruction

-Increased volume of blood to the pulmonary arteries & pulmonary veins, LA, LV = volume overload =
-LV contractility increased =
Atrial septum bows to right =
-CONGESTIVE HEART FAILURE

-size of the channel
-the pulmonary vascular resistance
-the presence and degree of left ventricular dysfunction

down syndrome

-single overriding great vessel
-large VSD
-complex abnormal semilunar valve
-truncal insufficinecy or stenosis when present
-

-cyanosis
-right heart failure
-a-fib
-erythocytosis(increase in red blood cells)
-stroke
-renal function reduced

-thin membrane visulaized in LA
-membrane moves toward MV in diastole, and away in systole
-dialated LA and RA
-normal LV
-dialated RV

-obstruction of blood flow from RV to main pulmonary artery during systole
-decreased incidence due to decreased incidence of maternal rubella

-Mv and TV shown on same m-mode
-delayed closure of TV>80seconds
-increased excursion w/ round off appearance of anterior leaflet of the TV
-RVVO
-small LV
-premature PV opening

1. total anomolous venous return
2. partial anomolous venous return
3. cor triatriatum

1. subaortic, where the VSD lies directly below the AV
2. subpulmonic where the VSD lies directly below the PV
3. doubly committed where the VSD is large and eqully committed to each vessel
4. remote where the VSD is at a distance from either great vessel

-congenital(most common)
-carcinoid
-rhumatic(rare)

1. 2 great vessels arising from the morphologic RV
2. VSD though which blood in LV must pass to reach the ao.
3. no fibrous continuity btw either AV or semilunar valves(often pulmonary or subpulmonary stenosis)

--a cyanotic herat defect consisting of:
-VSD
-dextroposition of the AO
-pulmonary hypertension
-RVH

-rare
-membrane dividing the LA into upper and lower chambers
-this is because the membrane from fusion of the comon pulmonary veins and the LA didn't regress
-pulmonary veins drain the upper chamber
-lower chamber communicates w/ the MV
-supravalvular mitral stenosis

-IVS-truncus discontinuity w/ override
-one large vessel w/ complex valve(truncal valves are usually markedly abnorml)

-Dialated RV
-echogenic line visulalized in the LA
-small to normal LV
-paradoxical septal motion

-infundibular(RVOT)
-valvular(most common)
-supra valvular

-dialated coronary sinus(PSLX), or TV annulus, or SVC(whichever recieves the anomolous venous return)
-dialated RA and RV
-Small LA and LV
-ASD
-Pulmonary venous channel separate from LA(common vein)

-sample entire RVOT-stenosis can be anywhere
-tubulent flow
-increased velocity>1m/sec
-color will help w/ direction of flow, ASD, and VSD

-wether the pulmonary artery configuartion allows adequate pulmonary blood flow

-aka supracardiac-more comon
-not through abdomen
-SVC
-behind the heart then the coronary sinus
-directly into RA

-reduced E-F slope of MV
-fluttering of post mitral valve leaflet

-ASD
-VSD
-PDA
-these defects are good beacause there has to be shunts to get the blood to the body.

1. obstruction of pulmonary blood flow w/ prox. rt to lt shunting
2. lg volume venous mixtures

TOF-obstruction is at the pulmonary artery and RV infundibular levels and shunting is through a VSD

Eisenmengers-obstruction@ pulmonary artery level and shunting @ great artery, ventricular or atrial level

Ebsteins-obstruction@ RV body
Shunting across interatrial communication causes desaturation

tricuspid atresia-obstruction@ TV orifice
Shunting @ atrial level

Type 1: pulmonary artery arises from the truncus
Type 2: rt and lt pulmonary arteries arise close together, but independantly from the truncus(adjacent to one another)
Type 3: rt and lt pulmonary arteries arise independently from opposite sides of the truncus
Type 4: absence of pulmonary arteies(no longer form a truncus, type of pulmonary atresia)

-persistant truncus-mixture occurs @ respective levels, lowering the O2 satureation

-TAPVR-02 pulmanary venous blood enters a common venous trunk which drains into the RA

-Transposition of great arteries-ao arises from RV and receives desaturated systemic blood directly

1. normal-aorta posterior to PA
2. aorta to the right of PA w/ valves @ the same level(side by side)
3. aorta to the right and ant. to PA(transposed)
-aorta to the left and anterior to PA

-VSD's
-AV septal defects
-Trunkus arteriosus
-TV atresia
-Single ventricle anatomy

-have sufficient releif of aortic or pulmonary valve obstruction
-commssures of the native valves are incised such that the function of the valve is normal
-usually regurge is seen post op

-done to replace a malformed aortic valve using a patients pulmonic valve
-a valve replacement is then done on the pulmonic valve from a deceased human donor
-autograft

-blalock-Taussig
-potts
-waterston

-anastamosis of the descending ao to left pulmonary artery

-ascending ao to rt pulmonary artery

-tricuspid atresia
-connection of the SVC to an undivided pulmonary artery
-temporary surgical procedure for hearts w/ only one usable ventricle

-Done for tricuspid atresia
-separates the RA from the rest of the heart via a gore tex baffle
-SVC and IVC blood flows into the RA
-RA appendage is sewn to distal portion of the PA, providing desaturated venous blood flow to the pulmonary artery

1. older child-the area of narrowing is excised and two ends are reattached
2. younger child-can be quite narrow, so the subclavian artery is ligated and divided(subclavian flap procedure0
3. balloon dialation angiography

-arterial switch: transposition of the great arteries
-Atrial septum is excised w/ atrial baffle:
-systemic venous return to MV and LV
-pulmonary venous return is baffled to V and RV
-used for d-transposition of the great arteries

-double outlet right ventricle
-pulmonic atresia and VSD
-truncus

-done on the first day of life
-small AO and dialated PA are combined to form one large vessel
-coronary arteries commoff one great vessel
-branch pulmonary arteries are disconnected from the main pulmonary artery
-a shunt is created btw the desc. ao and the pulmonary arteries. (BT shunt)

aka stage 2 norwood procedure:
-hemi-fontan procedure
-SVC is transected and each end is sewn into the right pulmonary artery(bidirectional glenn)
-ligation of BT shunt

-IVC and SVC are baffled away from the RA
-systemic venous return doesn't enter the RA, but goes directly into the pulmonary arteries

-pulmonary venous return enters the LA and crosses the atrial septum
-passes from RA to RV through to TV and is pumped out the new AO

endocardial fibroelastosis:
-hypertrophy of the wall of the LV and conversion of the endocardium into a thick fibroelastic coat, resiulting is a stiff heart(restrictive)

Glycogen storage disesase:
-severe thickening of the IVC, free wall, and post LV wall
-tumor like appearance of the pap muscles
-small LV cavity
-poor global LV systolic function

-LVH
-diastolic dysfunction
-later systolic dysfunction
-MAC
-Mild AO thickening
-Dialation of the Asc. AO-AI

-since in the 3rd trimester, there is an increase in the volume of blood by 50%, there will be a mild increased in chamber dimensions due to an increase in SV
-Altered MV coaptation, TR
-Small pericardial effusions
-Pseudo wall motino abnormalities due to the enlarged UT pressing on the heart
-benign arrythmias

-elderly patients
-hypertension or diabetes=coronary artery disease
-calcification of mitral annulus
-LVH
-small pericardial effusion
-

-non infectous endocarditus(libman-sacks vegetation)-more common on MV, not mobile
-inflammatory component results in leaflet deformity and regurge
-coronary vasculitis=global dysfunction which can mimic cardiomyopathy
-acute pericarditis(PE)

-slowly pregressive disorder of the nervous sytem and muscles
-inability to coordinate voluntary muscle movement
-premature death of nerve cells
-presents usually btw 5-20

-dialated cardiomyopathy
-posterior wall abnormalities
-arrythmias

-due to eosinophilic leukenia
-obliteration of the lt or rt ventricular apex by laminar thrombus
-see thrombus in the apex when the walls are moving good.

-high output state=ventricular dialation=dialated cardiomyopathy
-microinfarction and ventricular dysfunction
-may also develop arterial hypertension

-endocardidits
-pericardidits
-pulmonary hypertension
-dialated cardiomyopathy
-

MVP
MR