Cardiac Flashcards
Right Atrium
Defined by the IVC.
The Crista Terminalis is a frequently tested normal structure (it’s not a clot or a tumor). It is a muscular ridge that runs from the entrance o f the SVC to that o f the inferior vena cava.
Another normal anatomic structure that is frequently shown (usually on IVC gram) is the IVC valve or Eustachian valve. It looks like a little flap in the IVC as it hooks up to the atrium.
When the tissue o f this valve has a more
trabeculatated appearance it is called a Chiari Network.
Coronary Sinus
The main draining vein o f the myocardium. It runs in the AV groove
on the posterior surface o f the heart and enters the right atrium near the tricuspid valve.
Right Ventricle
Defined by the Moderator Band. Has several characteristics that are
useful for distinguishing it (and make good test questions).
The tricuspid papillary muscles insert on the septum (not the case with the mitral valve). There is no fibrous connection between the AV valve / outflow tract.
The pulmonary valve has three cusps, and is separated from the tricuspid valve by a thick muscle known as the crista supraventricularis . This differs from the left ventricular outflow
tract, where the mitral and aortic valves lie side by side.
Left Atrium
overview
The most posterior chamber. When you think about multiple choice
questions regarding the left atrium, think about the various signs of enlargement.
Left Atrium
double density
(direct sign): Superimposed second contour on the right heart, from
enlargement o f the right side o f the left atrium
Left Atrium
splaying of the carina
(indirect sign): Angle over 90 degrees suggests enlargement
Left Atrium
walking man sign
(indirect sign): Posterior displacement o f the left main stem
bronchus on lateral radiograph. This creates an upside down “V ” shape with the
intersection o f the right bronchus (looks like a man walking).
Left Ventricle
The leaflets o f the mitral valve are connected to the papillary muscles
via cord-like tendons called chordae tendinae. The papillary muscles insert into the lateral
and posterior walls as well as the apex o f the left ventricle (not the septum, as is the case on the right).
Echogenic Focus in Left Ventricle
Relatively common sonographic observation seen on pre-natal ultrasound. It is a calcified papillary muscle that usually goes away by the third trimester. So who gives a shit? Well they are associated with an increased incidence of Downs (13%). Don’t get it twisted, having one means nothing other than you should look for other signs of downs (most of the time it’s normal).
Lipomatous Hypertrophy
of the Interatrial Septum:
This has a very classic look o f a
dumbbell (bilobed) appearance of
fat density in the atrial septum,
sparing the fossa ovalis. This
sparing of the fossa ovalis,
creates a dumbbell appearance
{when it doesn’t spare it think
lipoma). It’s associated with
being fat and old. As a point of
trivia it can cause
supraventricular arrhythmia,
although usually does nothing.
Additional even more high-yield
trivia is that it can be hot on
PET because it’s often made of
brown fat.Lipomatous
Hypertrophy of the
Interatrial Septum
quick
common
ft in the atrial sptum, thicker than 2cm
spares the fossa ovalis
can be PET hot
RAre assoiated with arhythmias (usually asymptomatic)
Interatrial septum lipoma
rare
encapsulated
does not spare fossa ovalis
if multiopl = tuberous sclerosis
is usually PET HOT, T1 birght, drops out on fat sat
rarely associated with arrhythmias (usually asymptomatic)
Normal coronaries origin
There are three coronary cusps; right, left, and non-coronary (posterior).
The left main comes off the left cusp, the right main comes off the right cusp.
With regard to what perfuses what, the following are high yield factoids:
- RCA perfuses SA node 60%
* RCA perfuses AV node 90%
Posterior Descending Artery
PDA
RCA 65%-80%
-(*the other 20% have the PDA
supplied by the left coronary)
Conus
Off of RCA
*About 1/2 the time this
is the first branch.
-It supplies the
ventricle outflow tract.
Acute marginal
off the RCA, R forms an acute angle
nodal branc
off the RCA
Left main
LAD, circumfles, diagonals, obtuse marginals
obtuse marginals
supply the lateral margin
The 2 Chamber view
This displays the LV and LA (2 chambers). This is
good for a few things (1) Wall motion / Global LV
function , and (2) Mitral valve issues - regurg, etc.
The anatomy trick would be to have you ID the
coronary sinus on this view.
The 3 Chamber view
Some people will call this an “apical long axis
view.” The major plus to this view is that it lets you
see the left ventricular outflow tract (LVOT), - and is
ideal for look at flow through this area (i.e. aortic
regurg). A way a question could be asked is “what
view is best for aortic regurg? / stenosis?” or “which
of the following views” - and make you pick out the
picture of the 3 chamber. Or just straight ask you -
what is this view?
Dominance
Coronary Dominance is determined by what vessel gives rise to the
posterior descending artery and posterior left ventricular branches (most are right-
85%). You can be “co-dominant” if the posterior descending artery arises from the right
coronary artery and the posterior left ventricular branches arise from the left circumflex
coronary artery.
Malignant Origin
Most Common and Most Serious: LCA from the Right Coronary Sinus, coursing between the Aorta and Pulmonary Artery. This guy can get compressed and
cause sudden cardiac death.
Anomalous right off the left cusp
repair is symtomatic
Anomalous left off the right cusp
Always Repair
Malignant coronary artery with origin from the opposite sinus and an interarterial course is the
second most common cause of sudden cardiac death in young patients (most common is hypertrophic cardiomyopathy).
ALCAPA
Anomalous Left Coronary from the Pulmonary Artery. There are two types:
(a) Infantile type (they die early - CHF & dilated cardiomyopathy), and (b) Adult (still at
risk of sudden death). The multiple choice question is going to be “STEAL SYNDROME”
- which describes a reversed (retrograde) flow in the LCA as pressure decreases in the
pulmonary circulation.
Myocardial Bridging
This is an intramyocardial course of a coronary artery (usually
the LAD). The finding may cause symptoms as the diameter decreases with systole, or may
cause an issue for CABG planning. This can be a source o f ischemia.
Coronary Artery Aneurysm
By definition this is a vessel with a diameter greater
than 1.5x the normal lumen. Most common cause is atherosclerosis. Most common cause
in children is Kawasaki (spontaneously resolves in 50%). They can occur from lots of other
vasculitides as well. Last important cause is iatrogenic (cardiac cath).
Coronary Fistula
Defined as a connection between a coronary artery and cardiac
chamber or great vessels. It’s usually the RCA, with drainage into the right cardiac
chambers. They are associated / result in coronary aneurysm. I f you see big crazy dilation o f the coronaries - think about this.
Who is the ideal patient to g et a coronary CT
There are two main groups o f people
getting these. (1) Low risk or atypical chest pain patients. A negative coronary CT will
help stop a stress test or cath from occurring. Why do a procedure with risks on someone
with GERD? (2) Suspected aberrant coronary anatomy.
What is the ideal heart rate
To reduce motion related artifacts a slow heart rate is
preferred. Most books will tell you under 60 beats per min. Beta blockers are used to
lower the heart rate to achieve this ideal rate.
Are there contraindications to beta blockers
Yup. Patients with severe asthma, heart
block, acute chest pain, or recent snorting o f cocaine - should not be given a beta blocker
Are all heart blocks contraindications to beta blockers
2nd and 3rd Degree are contraindications. A 1st degree block is NOT.
What i f I can V give the beta blocker
Can he still have the scan? Yes, you just can’t use a
prospective gating technique. You’ll have to use retrospective gating.
Prospective gating
“Step and Shoot” - R-R interval * data acquisition triggered by R Wave
Pro: There is reduced radiation b/c the scanner isn’t on the whole time
• Con: No functional imaging
• Trivia: Always axial, not helical
retrospective gating
Scans the whole time, then back calculates
Pro: Can do functional imaging
Con: Higher radiation (use of low pitch - increases dose)
Trivia: this is helical
Other than beta blockers, are any other drugs given fo r coronary CT
Yup. Nitroglycerine is given to dilate the coronaries (so you can see them better).
Are there contraindications to nitroglycerine
Yup. Hypotension (SBP < 100), severe
aortic stenosis, hypertrophic obstructive cardiomyopathy, and Phosphodiesterase (Viagra- Sildenafil, “boner pills”) use.
Velocity-encoded cine MR imaging (VENC), also known as velocity mapping or phase-contrast
imaging, is a technique for
quantifying the velocity of flowing blood.
Aortic Stenosis
This may be congenital (bicuspid) or Acquired (Degenerative or Rheumatic
Heart). Increased afterload can lead to concentric LV hypertrophy. Peak velocity through the valve
can be used to grade the severity. Velocity-encoded cine MR imaging (VENC), which also answers
to the name “velocity mapping” or “phase-contrast imaging”, is an MRI technique for quantifying the
velocity of flowing blood (if anyone would happen to ask). Dilation of ascending aorta is due to jet
phenomenon related to a stenotic valve. Aortic Stenosis comes in three flavors: (a) valvular, (b)
subvalvular, (c) and supravalvular. Valvular is the most common (90%).
When I say “Supra-valvular Aortic Stenosis ’’you say
williams syndtome
When I say “Bicuspid Aortic Valve and Coarctation ” you say
Turner syndrome
Bicuspid Aortic Valve
overview
This is very common, some
sources will say nearly 2% of the general population. As a
result, it becomes the source of significant fuckery with
regard to one particular multiple choice question - “what is
the most common congenital heart disease?” The answer is
probably bicuspid aortic valve, but because it’s often
asymptomatic and not a problem till later in life when it gets
stenotic and causes syncope - 1 think it messes with peoples’
math. How do you handle this question? Well… if they list
bicuspid aortic valve then you have to pick it. If they don’t
list it then the answer is VSD.
Bicuspid Aortic Valve
things to know
• Aortic Stenosis is the most common complication
• Bicuspid aortic valve (even in absence of stenosis) is an
independent risk factor for aortic aneurysm. Severity of
valve dysfunction does not predict aneurysm formation.
• Association with Cystic Medial Necrosis (CMN)
• Association with Turners Syndrome, and Coarctation
• Association with AD Polycystic kidney disease
Aortic Regurgitation
Seen with bicuspid aortic valves, bacterial endocarditis, Marfan’s, aortic
root dilation from HTN, and aortic dissection. How rapid the regurgitation onsets determines the
hemodynamic impact (acute onset doesn’t allow for adaptation). Step 1 question was “Austin Flint
Murmur.”
Mitral Stenosis
Rheumatic heart disease = most
common cause. Could be shown as a CXR with left atrial
enlargement (double density sign, splaying of the carina,
posterior esophageal displacement).
Ortner’s Syndrome
Cardio Vocal Hoarseness
Hoarseness caused by
compression o f the left recurrent
laryngeal nerve by an enlarged
left atrium
Mitral Regurgitation
The most common acute causes are endocarditis or papillary muscle /
chordal rupture post MI. The chronic causes can be primary (myxomatous degeneration) or
secondary (dilated cardiomyopathy leading to mitral annular dilation). Remember the isolated Right
Upper Lobe pulmonary edema is associated with mitral regurgitation
Pulmonary Stenosis
Just like in the Aortic Valve, comes in three flavors: (a) valvular, (b) subvalvular, (c) and supravalvular. Valvular is the most common, and can lead to ventricular hypertrophy. Associated with Noonan Syndrome (male version of turners). “Peripheral Pulmonary Stenosis” is seen with Alagille syndrome (kids with absent bile ducts). Williams can give you supra-valvular aortic stenosis (and pulmonic).
Pulmonary stenosis
williams syndrom
supra=valbular stenosis
Pulmonary stenosis
Noonans syntdrome
valvular stenosis
Pulmonary stenosis
TOF
sub-valvular stenosis
Pulmonary Regurgitation
The classic scenario is actually TOF patient who has been repaired.
TOF repair involves patch repair of the VSD and relief of the RV outlet obstruction. To fix the RV
obstruction the pulmonary valve integrity must be disrupted. Eventual failure of the valve (regurgitation)
is the primary complication of tis procedure.
Pulm regurg repair
Cardiac MRI is used to guide the timing of pulmonary regurg repair. If the valve is repaired before the
RV is severely dilated (150 ml end diastolic volume) the outcomes are good. If the RV reaches a certain
degree of dilation- it typically won’t return to normal and the patient is pretty much fucked.
Tricuspid Regurgitation
Most common form of tricuspid disease, due to the relatively weak
annulus (compared to the mitral). May occur in the
setting of endocarditis (IV drug use), or carcinoid
syndrome (serotonin degrades the valve). The most
common cause in adults is pulmonary arterial
hypertension. A testable pearl is that TR causes RV
dilation (NOT RV Hypertrophy).
valves gamesmanship
Rheumatic heart
disease most commonly involves the mitral
and aortic valves. Anytime there is multivalve
disease, think Rheumatic Fever!
Valves step 1 trivia
Rheumatic heart disease is
an immune modulated response to Group ABeta
hemolytic strep.
Ebstein Anomaly
Seen in children whose moms used Lithium (most cases are actually
sporadic). The tricuspid valve is hypoplastic and the posterior leaf is displaced apically (downward).
The result is enlarged RA , decreased RV (“atrialized”), and tricuspid regurgitation. They have the
massive “box shaped” heart on CXR.
Tricuspid Atresia
Congenital anomaly that occurs with RV hypoplasia. Almost always has an
ASD or PFO. Recognized association with asplenia. Can have a right arch (although you should
think Truncus and TOF first). As a point of confusing trivia; tricuspid atresia usually has pulmonary
stenosis and therefore will have decreased vascularity. If no PS is present, there will be increased
vascularity.
Carcinoid Syndrome
This can result in valvular disease, but only after the tumor has met’d to
the liver. The serotonin actually degrades heart valves, typically both the tricuspid and pulmonic
valves. Left sided valvular disease is super rare since the lungs degrade the vasoactive substances.
When you see left sided disease you should think of two scenarios:
(1) primary bronchial carcinoid, or (2) right-to-lcft shunts.
The most common variant in branching
is the “bovine arch” in which the brachiocephalic artery and left common carotid artery arise from a common origin.
The terminology right arch / left arch is
described based on
the aortic arch’s
relationship to the trachea.
When I say Right Arch with Mirror
Branching
You say congenital heart
There are 5 types of right arches, but only two are worth knowing
(Aberrant Left, and
Mirror Branching^. The trick to tell these
two apart is to look fo r the origin o f the left subclavian.
originating fromt he front of the arch=mirror image (bad one lots of congenital heart)
originating from the back of the arch = aberrant left subclavian
Right Arch with Mirror Branching
Although these are often asymptomatic they
are strongly associated with congenital heart disease. Most commonly they are associated
with TOF. However, they are most closely associated with Truncus. Obviously, this tricky
wording lends itself nicely to a trick question.
f there is a mirror image right arch
then 90% will have TOF (6% Truncus).
I f the person has Truncus, then they have a mirror image right arch
33% (TOF 25%).
Right Arch with Aberrant Left Subclavian
The last branch is the aberrant left subclavian artery. This is a vascular ring
because the ligamentum arteriosum (on the left) completes the “ring’
encircling the trachea.
Left Arch Aberrant Right
Subclavian
The most common arch
anomaly. Although it is usually
asymptomatic it can sometimes be
associated with dysphagia lusoria, as the
RSCA passes posterior to the esophagus. The
last branch is the aberrant right subclavian
artery. The origin of the RSCA may be
dilated = Diverticulum of Kommerell.
Double Aortic Arch
The most common vascular ring. As a point o f trivia, symptoms may begin at birth and include tracheal compression and/or
difficulty swallowing. The right arch is
larger and higher, and the left arch is
smaller and lower. Arches are posterior to the esophagus and anterior to the trachea
(encircling them both).
Subclavian Steal Syndrome/Phenomenon
phenomenon
Stenosis and/or occlusion o f the proximal subclavian with
retrograde flow in the ipsilateral vertebral artery.
Subclavian Steal Syndrome/Phenomenon
syndrome
Stenosis and/or occlusion o f the proximal subclavian artery with
retrograde flow in the ipsilateral vertebral artery AND associated cerebral ischemic
symptoms.
Subclavian Steal Syndrome/Phenomenon
If the level o f stenosis and/or occlusion is proximal to the vertebral artery, reversal o f flow
in the vertebral artery can occur, resulting in the theft o f blood from the posterior
circulation. When the upper limb is exercised, blood is diverted away from the brain to the
arm. Cerebral symptoms (dizziness, syncope, etc…) depend on the integrity o f collateral
intracranial flow (PCOMs).
Subclavian Steal is almost always caused by atherosclerosis (98%), but other very testable
causes include Takayasu Arteritis, Radiation, Preductal Aortic Coarctation, and Blalock-
Taussig Shunt. In an adult they will show atherosclerosis. If they show a teenager / 20 year
old it’s gonna be Takayasu. Case books love to show this as an angiogram, and I think
that’s the most likely way the test will show it. They could also show a CTA or MRA
although I’d say that is less likely.
My thoughts on multiple choice questions regarding congenital heart is that they will come in 3
flavors
(A) Aunt Minnie, (B) Differentials with crappy distractors, and (C) Associations / Trivia.
Congenital heart CXR
egg on a string
transposition
Congenital heart CXR
snow man
TAPVR (supracardiac)
Congenital heart CXR
boot shaped
TOF
Congenital heart CXR
Figure 3
Coarctation
Congenital heart CXR
box shaped
Ebstein
Congenital heart CXR
scimitar sword
PAPVR with hypoplasia
Another classic trick with regard to the
big box heart
non-cardiac causes o f high output failure (Infantile Hemangioendothelioma
and Vein of Galen Malformation).
Cyanotic
right sided arch
TOF or truncus (types 1-3)
Cyanotic left sided arch, massive heart size
Ebsteins or
Pulmonary Atresia without VSD
Non-Cardiac (won’t be cyanotic)
- Infantile Hemangioendothelioma
- Vein of Galen Malformation
cyanotic, left sided arch, normal heart size, increased pulmonary blood flow
- TAPVR (especially type 3)
- D-Transposition
- Truncus (look for R Arch)
- “Tingle Ventricle”
cyanotic, left sided arch, normal heart size, decreased or normal pulmonary blood flow
TOF
Ebsteins
tricuspid atresia
Cyanotic congenital heart ddx
TOF TAPVR Transposition Truncus Tricuspid Atresia
not-cyanotic congenital heart ddx
ASD VSD PDA PAPVR Aortic coarctation (adult type-postductal)
CHF in Newborn
ddx
TAPVR (Infracardiac type “III”) Congenital Aortic or Mitral Stenosis Left Sided Hypoplastic Heart Cor Triatriatum Infantile (pre-ductal) Coarctation
Survival dependent on admixture - Cyanotics
ddx
TAPVR (has PFO) Transposition TOF (has VSD) Tricuspid Atresia (has VSD) Hypoplastic Left
Small heart DDx
Adrenal Insufficiency (Addisons)
Cachectic State
Constrictive Pericarditis
VSD
The most common congenital heart disease. There are several types with
Membranous (just below the aortic valve) being the most common (70%). Outlet subtypes(infundibulum) must be repaired as the right coronary cusp prolapses into the defect. On CXR we are very nonspecific (big heart, increased vasculature, small aortic knob). They
could ask or try and show splaying of the carina (from big left atrium). About 70% of the small ones close spontaneously.
PDA
The PDA normally closes around 24 hours after birth (functionally), and
anatomically around 1 month. A PDA should make you say three things (1) Prematurity, (2) Maternal Rubella, (3) Cyanotic Heart Disease. CXR is nonspecific (big heart, increased pulmonary vasculature, large aortic arch “ductus bump”). You can close it or keep
it open with meds.
ASD
Several types with the Secundum being the most common (50-70%). The larger
subtype is the Primum, (results from an endocardial cushion defect), is more likely to be symptomatic. Only Secundums may close without treatment (Primum, AV Canal, Sinus Venosus will not). Primums are not amendable to device closure because of proximity to AV valve tissue. On CXR, if it’s small it will show nothing, if it’s large it will be super
nonspecific (big heart, increased vasculature, and small aortic knob). It’s more common in female.
When I say hand/thumb defects + ASD, you say
Holt Oram
When I say ostium primum ASD (or endocardial cushion defect), you say
Downs
When 1 say Sinus Venosus ASD, you say
PAPVR
AV Canal
Also referred to as an endocardial cushion defect. They happen secondary to deficient development o f a portion o f the atrial septum, a portion o f the inter-ventricular septum, and the AV valves. Strong association with Downs. You can’t use closure devices on these dudes either. Surgical approach and management is complex and beyond the scope o f this text.
AV Canal
trivia
Of all the congenital heart stuff with Downs patients - AV Canal is the most common
Unroofed Coronary Sinus:
overview
This is a rare ASD which occurs secondary to a fenestrated (as in the cartoon) or totally unroofed coronary sinus. The most important clinical is that you can get paradoxical emboli and chronic right heart volume overload.
Unroofed Coronary Sinus:
trivia
STRONG association with a persistent left SVC
Holes in the roof of the coronary sinus allow for
two way flow
PAPVR
Partial anomalous pulmonary venous return, is defined as one (or more) of the four pulmonary veins draining into the right atrium. It is often of mild or no
physiologic consequence. It is often associated with ASDs (secondum and sinus venosus types).
When I say Right Sided PAPVR,
you say
Sinus venosus ASD
When I say Right Sided PAPVR + Pulmonary Hypoplasia, you say
Scimitar Syndrome
Sinus Venosus association
PAPVR
Ostium Secundum association
most common
ostium primum association
downs
TAPVR
overview
cyanotic heart disease characterized by all of the pulmonary venous system draining to
the right side of the heart. A large PFO or less commonly ASD is required for survival (this is a high
yield and testable point). There are 3 types, but only two are likely to be tested (cardiac type II just
doesn’t have good testable features). All 3 types will cause increased pulmonary vasculature, but type
3 is famous for a full on pulmonary edema look in the newborn.
TAPVR
type 1
Supracardiac:
0 Most Common Type
0 Veins drain above the heart, gives a snowman appearance.
TAPVR
Type 2
Cardiac
O Second Most Common Type
TAPVR
Type 3
Infracardiac
O Veins drain below the diaphragm (hepatic veins or IVC)
O Obstruction on the way through the diaphragm is common and causes a full on
pulmonary edema look
TAPVR
Key points
- Supracardiac Type = Snowman
- Infracardiac Type = Pulmonary Edema in Newborn
- Large PFO (or ASD) needed to survive
- Asplenia - 50% of asplenia patients have congenital heart disease. Of those nearly 100% have TAPVR, (85% have additional endocardial cushion defects).
Transposition
This is the most common cause o f cyanosis during the first 24 hours. It
is seen most commonly in infants o f diabetic mothers. The basic idea is that the aorta arises from the right ventricle and the pulmonary trunk from the left ventricle (ventricularterial discordance).
Just like TAPVR survival depends on an ASD, VSD, or PDA (most commonly VSD). There are two flavors: D & L. The D type only has a PDA connecting the two systems. Where as the L type is “Lucky” enough to be compatible with Life.
Transposition
whic one is hte right ventricle
You have to find the moderator band (that defines the RV)
D-Transposition
ltrivia
Classic radiographic appearance is the “egg on a string”. Occurs from discordance between the ventricles and the vessels. The intra-atrial baffle (Mustard or Senning procedure) is performed to fix them
D-Transposition
overview
in D-Transposition, the ductus may be the only connection
between the two systems, which would otherwise be
separate (and not compatible with life)
D-Transposition
connections
Aorta > Systemic > RA > RV > Aorta
PA > Lungs > LA > LV > PA
PDA connects the two
L-Transposition
tribia
The L type is “Lucky” enough to be congenitally corrected. This occurs from a “double discordance” where the atrium hooks up with the wrong ventricle and the ventricle hooks up with the wrong vessel.
L-Transposition
overview
In L-Transposition of the great vessels - there is an
inversion of the ventricles, leading to a “congenital
correction. ” No PDA is needed.
L-Transposition
connections
Aorta > systemic > RA > LV > PA > lungs > LA > RV > Aorta
A corrected D-transposition has a very
characteristic appearance, lending itself to an
Aunt Minnie-type question.
The PA is draped overtop the Aorta, which occurs after a surgeon has performed the “LeCompte Maneuver” — sounds French so must be high yield.
Corrected D Transposition
via Jatene Arterial Switch
Tetralogy of Fallot (TOF):
The most common cyanotic heart disease. Describes 4
major findings; (1) VSD, (2) RVOT Obstruction - often from valvular obstruction, (3)
Overriding Aorta, (4) RV hypertrophy (develops after birth). The degree of severity in
symptoms is related to how bad the RVOT obstruction is. If it’s mild you might even have a
“pink tet” that presents in early adulthood. This is called a pentalogy o f Fallot if there is an
ASD. Very likely to have a right arch.
Tetralogy of Fallot (TOF):
treatment
Surgically it’s usually fixed with primary repair. The various shunt procedures (Blalock-
Taussig being the most famous) are only done if the kid is inoperable or to bridge until
primary repair.
Tetralogy of Fallot (TOF):
trivia
The most common complication following surgery is pulmonary regurgitation.
Truncus Arteriosus
Cyanotic anomaly where there is a single trunk supplying both
the pulmonary and systemic circulation, not a separate aorta and pulmonary trunk. It almost
always has a VSD, and is closely associated with a right arch. Associated with CATCH-22
genetics (DiGeorge Syndrome).
Coarctation
adult and infantile subtypes
strong association with turners syndrome (15-20%)
bicuspid aortic valve is the most common associated defect (80%)
they have more berry aneurysms
rib notching most often involves 4th-8th ribs. It does not involve the 1st and 2nd bc they are fed by the costocervical trunk
Coarctation of the aorta
infantile
presents with heart failure within the first week of life
preductal (befor the left subclavian A)
aortic arch = hypoplastic
coarctatino of the aorta
adult
lef claudication BP differnces between arms and legs
postductal (distal to left subclavian A)
aortic arch- normal diameter
collateral formation is more likely
Hypoplastic Left Heart:
Left ventricle and aorta are hypoplastic. They present with
pulmonary edema. Must have an ASD or large PFO. They also typically have a large PDA
to put blood in their arch. Strongly associated with aortic coarctation and endocardial
fibroelastosis.
Cor Triatriatum Sinistrum
This is a very rare situation where you have an abnormal pulmonary vein draining into
the left atrium (sinistrum meaning left) with an unnecessary fibromuscular membrane
that causes a sub division o f the left atrium. This creates the appearance of a tri-atrium
heart. This can be a cause o f unexplained pulmonary hypertension in the peds setting.
Basically it acts like mitral stenosis, and can cause pulmonary edema. The outcomes are
often bad (fatal within two years), depending on surgical intervention and associatedbadness.
Is c h e m i c H e a r t
stunned myocardium
After an Acute Injury (ischemia or reperfusion injury), dysfunction
o f myocardium persists even after restoration of blood flow (can last days to weeks). A
perfusion study will be normal, but the contractility is crap.
Is c h e m i c H e a r t
hibernating myocardium
This is a more chronic process, and the result o f severe CAD
causing chronic hypoperfusion. You will have areas of decreased perfusion and
decreased contractility even when resting. Don’t get it twisted, this is not an infarct.
On an FDG PET, this tissue will take up tracer more intensely than normal
myocardium, and will also demonstrate redistribution of thallium. This is reversible
with revascularization.
Is c h e m i c H e a r t
scar
This is dead myocardium. It will not squeeze normally, so you’ll have abnormal wall motion. It’s not a zombie. It will NOT come back to life with revascularization.
Stunned myocardium imaging findings
wall motion abnormal
normal perfusion (thallium or sestamibi)
associated with acute MI
Hibernating myocardium imaging findings
wall motion abnormal
abnormal fixed perfusion
will redistribute with delayed thallium and will take up FDG
associated with chronic grade CAD
Infact/scar miaging findings
wall motion abnormal
abnormal fixed perfusion
will no redistribute with delayed thallium, will not take up FDG
Associated with chronic prior MI
Infact/scar miaging findings
wall motion abnormal
abnormal fixed perfusion
will no redistribute with delayed thallium, will not take up FDG
Associated with chronic prior MI
Diastolic Dysfunction =
echocardiography
systolic dysfunction =
cardiac mri
Cardiac MRI Probable Contraindications
ICDs / Pacemakers
Cochlear Implants
Intracranial Shrapnel
**Cardiac Stents are usually safe
CArdiac MR Delayed imaging
It works for two reasons: (1) Increased volume of contrast material
distribution in acute myocardial infarction (and inflammatory conditions) (2) Scarred
myocardium washes out more slowly. It is done using an inversion recovery technique to
null normal myocardium, followed by a gradient echo. T1 shortening from the Gd looks bright
(“Bright is Dead”).
Cardiac why stress imaging is done
Because coronary arteries can auto-regulate, a stenosis
of 85% can be asymptomatic in a resting state. So demand is increased (by exercise or drugs)
making a 45% stenosis significant. An inotropic stress agent (dobutamine) is used for wall
motion, and a vasodilator (adenosine) is used for perfusion analysis
Cardiac MR typical sequences
5 cine 10 morphology then contrast and adenosine 15 stress perfusion 25 mis (velocity encoding, coronary MRA etc) 30 REst perfusion 35 delay 40 delayed enhancement
MRI in acute MI
Cardiac MRI can be done in the first 24 hours post MI (if the patient is
stable). Late gadolinium enhancement will reflect size and distribution of necrosis.
Characteristic pattern is a zone of enhancement that extends from the subendocardium
toward the epicardium in a vascular distribution. Microvascular obstruction will present as
islands of dark signal in the enhanced tissue (as described above), and this represents an acute
and subacute finding . Microvascular obstruction is NOT seen in chronic disease as these
areas will all turn to scar eventually.
MRI imaging findings in acute mi
In the acute setting (1 week) injured myocardium will have increased T2 signal, which can be
used to estimate the area at risk (T2 Bright - Enhanced = Salvageable Tissue).
THIS vs THAT: Acute vs Chronic Ml
- Both have delayed enhancement
- If the infarct was transmural and chronic you may have thinned myocardium
- Acute will have normal thickness (chronic can too but shouldn’t for the purposes of MC tests.
- T2 signal from edema may be increased in the acute setting. Chronic is T2 Dark (scar)
- You won’t see Microvascular Obstruction in Chronic
How do you diagnose
Myocardial Infarction with
Contrast Enhanced MR?
(1) Delayed Enhancement
follows a vascular
distribution,
(2) The enhancement
extends from the
endocardium to the
epicardium
Microvascular Obstruction
Islands of dark tissue in an ocean of late Gd enhancement. These
indicate microvascular obliteration in the setting of an
acute infarct. The Gd is unable to get to these regions
even after the restoration o f epicardial blood flow.
Microvascular obstruction is a poor prognostic finding,
associated with lack of functional recovery.
Microvascular Obstruction
key point
It’s NOT seen in chronic infarct.
Microvascular Obstruction
trivia
Microvascular obstruction is best seen on first pass imaging (25 seconds)
Ventricular Aneurysm
This is rare (5%), but
can occur as the result o f Ml. The question is always
true vs false:
Ventricular Aneurysm
True
True: Mouth is wider than body. Myocardium is intact. Usually anterior-lateral wall.
Ventricular Aneurysm
False
Mouth is narrow compared to body.
Myocardium is NOT intact (pericardial
adhesions contain the rupture). Usually
posterior-lateral wall. Higher risk of rupture.
Ventricular Aneurysm
location
False Aneurysms are Usually Posterior Lateral
True Aneurysms are Usually Anterior Lateral
MRI cardiac tissue viability
You can grade this based on % o f transmural thickness involved in the infarct.
• <25%: likely to improve with PCI
• 25-50%: may improve
• 50-100%: unlikely to recover function
MRI cardiac tissue viability
imaging
Segmental imaging (imaging over multiple heart beats) T1 post contrast (10-15 min delay) inversion recovery gradient echo
What is the timing on the bad sequelae of an Ml?
Dressier Syndrome (effusion) 4-6 weeks
Papillary Muscle Rupture 2-7 Days
Ventricular Pseudoaneurysm 3-7 Days
Ventricular Aneurysm Months - Requires remodeling and thinning.
Myocardial Rupture Within 3 Days (50% o f the time)
Dilated Cardiomyopathy
Defined as dilatation with an end diastolic diameter greater than
55mm, with a decreased EF. Can be idiopathic, ischemic, or from a whole list of other random
crap (Alcohol, Doxorubicin, Cvclosporine. Chagas, etc…)- The ischemic variety may show
subendocardial enhancement. The idiopathic variety will show either no enhancement or linear
mid-myocardial enhancement. There is often an association with mitral regurgitation due to
dilation of the mitral ring.
Restrictive Cardiomyopathy
overview
Basically anything that causes a decrease in diastolic
function. Can be the result of myocardium replaced by fibrotic tissue (endocardial fibroelastosis),
infiltration of the myocardium (Amyloidosis), or damage by iron (hemochromatosis). The most
common cause is actually amyloid.
Restrictive Cardiomyopathy
amyloidosis
Deposits in the myocardium causes abnormal
diastolic function with biatrial enlargement, concentric
thickening of the left ventricle and reduced systolic function of
usually both ventricles. Seen in 50% of cases of systemic
amyloid. Has a terrible prognosis. You can sometimes see late
Gd enhancement over the entire subendocardial circumference.
Amyloid Classic Scenario: A long Tl is needed (like 350
milliseconds, nonnal would be like 200). Tl will be so long that the blood pool may be
darker than the myocardium. Buzzword “difficult to suppress myocardium”.
Restrictive Cardiomyopathy
eosinophilic cardiomyopathy
Loeffler
Bilateral Ventricular thrombus is the classic phrase
/ buzzword. You will need a long Tl to show the thrombus.
restrictive =
myocardial process
constrictive =
pericardial process
Constrictive Pericarditis
Historically this used to be TB or Viral. Now the most
common cause is iatrogenic secondary to CABG or radiation. On CT the pericardium is too thick
(> 0.4 cm), and if it’s calcified that is diagnostic. Calcification is usually largest over the AV
groove. “Sigmoidization” is seen on SSFP cine imaging: The ventricular septum moves toward the
left ventricle in a wavy pattern during early diastole (“Diastolic Bounce”). This “bounce” will be
most pronounced during inspiration - indicating ventricular interdependence.
THIS vs THAT: Constrictive VS Restrictive
Cardiomyopathy
- Pericardium is usually thickened in constrictive
* Diastolic septal bounce is seen in constrictive (Sigmoidization of the septum).
Myocarditis quick imaging
-Mid Wall Late Gd Enhancement
Myocarditis
Inflammation of the heart can come from lots of causes (often viral i.e. Coxsackie virus). The late Gd enhancement
follows a non-vascular distribution preferring the lateral free wall. The pattern will be epicardial or mid wall (NOT subendocardial).
Sarcoidosis
Cardiac involvement is seen in 5% of Sarcoidosis cases, and is associated with an
increased risk of death. Signal in both T2 and early Gd (as well as late Gd) will be increased. Late Gd
pattern may be middle and epicardial in a non-coronary distribution. Focal wall thickening from
edema can mimic hypertrophic cardiomyopathy. It often involves the septum. The RV and
papillaries are RARELY affected.
Takotsubo Cardiomyopathy
A takotsubo is a Japanese Octopus trap, which looks like a pot
with a narrow mouth and large round base. The octopus will go into the pot, but then can’t turn around
and get out (sorta like medical school). A condition with Chest pain and EKG changes seen in post
menopausal women after they either break up with their boyfriend , win the lottery, or some other
stressful event has been described with the shape of the ventricle looking like a takotsubo. There is
transient akinesia or dyskinesia of the left ventricular apex without coronary stenosis.
Ballooning of the left ventricular apex is a buzzword. No delayed enhancement.
Cardiac MRI - Late Gadolinium Enhancement (LGE):
overview
Both diseased and nonnal myocardium will take up gadolinium / enhance - but it depends on when you
image. Early (1-3 mins) you will see normal tissue drink up contrast. Late (5-20 mins) contrast washes out
o f the normal tissue and is retained by pathology (lots o f different pathologies). The patterns that you see is
helpful for making the diagnosis (picking the answer on multiple choice).
Cardiac MRI - Late Gadolinium Enhancement (LGE):
ischemic
Enhancement starts subendocardially and spreads transmurally toward the epicardial surface -
in a distribution corresponding to a known coronary artery territory
Cardiac MRI - Late Gadolinium Enhancement (LGE):
non ischemic
Enhancement is often located in the mid-wall o f the ventricle - patchy or multifocal in
distribution (not corresponding to a known coronary artery territory)
Cardiac MRI - Late Gadolinium Enhancement (LGE):
subendocardial
infarct
Cardiac MRI - Late Gadolinium Enhancement (LGE):
transmural
infarct
Cardiac MRI - Late Gadolinium Enhancement (LGE):
subendocardial circumferential
amyloidosis can also be transmural
Cardiac MRI - Late Gadolinium Enhancement (LGE):
midwall focal nodules
hcm
Cardiac MRI - Late Gadolinium Enhancement (LGE):
midwall IV septum
myocarditis, idiopathic dilated CM
Cardiac MRI - Late Gadolinium Enhancement (LGE):
midwall left lateral ventricle wall
myocarditis, sarcoidosis
Cardiac MRI - Late Gadolinium Enhancement (LGE):
epicardial
Myocarditis, Sarcoidosis
Arrhythmogenic Right Ventricular
Cardiomyopathy (ARVC):
Characterized by fibrofatty degeneration of the RV
leading to arrhythmia and sudden death. Features
include dilated RV with reduced function and fibrofatty
replacement of the myocardium, and normal LV.
People use this major/minor criteria system that includes
a bunch of EKG changes that no radiologist could
possibly understand (if they are stupid enough to ask just
say left bundle branch block). Watch out for the use of
fat sat to demonstrate the fat in the RV wall.
ARVC imaging findings
dilated RV with fat in the wall
HCM
Abnormal hypertrophy (from disarray of myofibrils) of the myocardium that compromises diastole. There are multiple types but the one they are going to show is asymmetric hypertrophy of the intraventricular septum. The condition is a cause of sudden death. There is a subgroup which is associated with LVOT obstruction (“hypertrophic obstructive cardiomyopathy”). Venturi forces may pull the anterior leaflet of the mitral valve into the LVOT (SAM - Systolic Anterior Motion of the Mitral Valve). Patchy midwall delayed enhancement of the hypertrophied muscle may be seen, as is an independent risk factor for sudden death.
Noncompaction
Left ventricular noncompaction is an uncommon congenital cardiomyopathy that is the result of loosely packed myocardium. The left ventricle has a spongy appearance with increased trabeculations and deep intertrabecular recesses.
As you might expect, these guys get heart failure at a young age. Diagnosis is based of a ratio of
non compacted end-diastolic myocardium to compacted end-diastolic myocardium of more
than 2.3:1.
noncompaction imaging findings
spongy LV with no myocardial thickening
Muscular Dystrophy
Becker (mild one) and Duchenne (severe one) are X-linked
neuromuscular conditions. They have biventricular replacement of myocardium with connective
tissue and fat (delayed Gd enhancement in the midwall). They often have dilated cardiomyopathy.
Just think kid with dilated heart and midwall enhancement.
Cardiac mets
Thirty times more common than a primary malignancy. The pericardium is the
most common site affected (by far). The most common manifestation is a pericardial
effusion (second most common is a pericardial lymph node). Melanoma may involve the
myocardium.
Cardiac mets trivia
Most common met to the heart is lung cancer (pericardium and epicardium)
Angiosarcoma
Most common primary malignant tumor of the heart in adults. They
like the RA and tend to involve the pericardium. They often cause right sided failure and/or
tamponade. They are bulky and heterogenous. Buzzword is “sun-ray” appearance which
describes enhancement appearance of the diffuse subtype as it grows along the perivascular
spaces associated with the epicardial vessels.
THIS vs THAT:
Tumor vs Thrombus
Cardiac MRI is the way to tell.
• Tumor will enhance
• Thrombus will NOT enhance.
Left Atrial Myxoma
Most common primary
cardiac tumor in adults (rare in children). They are
associated with MEN syndromes, and Blue Nevi
(Carney Complex). They are most often attached to the
interatrial septum. They may be calcified. They may
prolapse through the mitral valve. They will enhance
with Gd (important discriminator from a thrombus).
Rhabdomyoma
Most common fetal cardiac tumor. It is a hamartoma. They prefer the
left ventricle. Associated with tuberous sclerosis. Most tumors will regress spontaneously
(those NOT associated with TS are actually less likely to regress).
Fibroma
Second most common cardiac tumor in childhood. They like the IV septum,
and are dark / dark on T1/T2. They enhance very brightly on perfusion and late Gd.
Fibroelastoma
Most common neoplasm to involve the cardiac valves (80% aortic or
mitral). They are highly mobile on SSFP Cine. Systemic emboli are common (especially if
they are on the left side).
Myxoma facts
Most common primary cardiac tumor (adult)
Adult (30-60) with distal emboli and fainting spells.
Younger people are likely syndromic (Carney Complex)
Arise from the intra-atrial se p tum , usually growing into the left atrium
About 1/4 have calcification
“Ball with stalk attached to the interatrial
septum ” Dynamic imaging will show mobility / prolapse of the “ball” .
Fibroelastoma facts
2nd most common primary cardiac tumor (adult)
Adult (50-60) - usually an incidental finding.
If they are symptomatic its from emboli (stroke / TIA)
Involves the cardiac valves - aortic is most common — usually the aortic side o f the aortic cusp.
Most are small less than 1cm.
Discriminator: Vegetations tend to involve the valve free edges. Fibroelastoma does NOT do that.
Rhabdomyoma facts
Most common primary cardiac tumor (infants)
Infant with tuberous sclerosis
Favor the ventricular myocardium
They tend to be multiple
Discriminator: Fibroma is T2 dark
Rhabdomyoma is T2 Bright
- Fibroma is the 2nd most common tumor in this age group
Angiosarcoma facts
The most common primary MALIGNANT tumor
Favors the right atrium
Pericardial thickening = invasion
Large heterogenous mass
Metastatic disease facts
Much more common than Primary tumors
Lung cancer is the most common.
Melanoma goes to the heart with the greatest percentage (but prevalence is less than lung)
Favors the pericardium
Pericardial nodularity and effusion
Cardiac thrombus facts
Most common intra-cardiac “mass”
Favors the left atrial appendage (A-Fib),
Left Ventricular Apex (post MI)
Discriminator: Thrombus won’t enhance. Tumors will.
PERICARDIUM
oveview
The pericardium is composed of two layers (visceral and parietal), with about 50cc of fluid
normally between the layers
Pericardial Effusion
Basically more than 50cc between the pericardial layers. This can be from lots and lots of causes
- renal failure (uremia) is probably the most common. For the purpose of multiple choice tests
you should think about Lupus, and Dressier Syndrome (inflammatory effusion post Ml).
Pericardial effusion CXR
On CXR they could show this 3 ways: (1) Normal Heart on Comparison, Now Really Big Heart (2) Giant Water Bottle Heart, (3) Lateral CXR with two lucent lines (epicardial and pericardial fat) and a central opaque line (pericardial fluid) - the so called “oreo cookie sign.”
Cardiac Tamponade
Pericardial effusion can cause elevated pressure in the pericardium
and result in compromised filling of the cardiac chambers (atria first, then ventricles). This can
occur with as little as lOOcc of fluid, as the rate of accumulation is the key factor (chronic slow
filling gives the pericardium a chance to stretch). The question is likely related to short-axis
imaging during deep inspiration showing flattening or inversion of the intraventricular
septum toward the LV, a consequence of augmented RV filing. Another indirect sign that can be
shown on CT is reflux of contrast into the IVC and azygos system.
Pericardial Cysts
Totally benign incidental finding. Usually seen on the right
cardiophrcnic sulcus. They do not communicate with the pericardium. Rarely they can get
infected or hemorrhage. This would be most easily shown as an ROI measuring water density
along the right cardiophrenic sulcus.
Congenital I Acquired Absence:
Even though you can have total absence of the
pericardium - the most common situation is partial absence of the pericardium over the left
atrium and adjacent pulmonary artery. When the left pericardium is absent the heart shifts
towards the left. They could show you a CT or MRI with the heart contacting the left chest wall,
and want you to infer partial absence. Another piece of trivia is that cardiac herniation and
volvulus can occur in patients who undergo extrapleural pneumonectomy (herniation can only
occur if the lung has also been removed).
Congenital I Acquired Absence:
trivia
The left atrial appendage is the most at risk to become strangulated.
Palliative Surgery for the Hypoplastic Left Heart
Surgery for Hypoplasts
is not curative, and is instead designed to extend the life (prolong the suffering) of the child.
It is done in a 3 stage process, to protect the lungs and avoid right heart overload:
(1) Norwood or Sano - within days o f birth
(2) Glenn - at 3- 6 months
(3) Fontan at 1 Zi to 5 years
(1 a ) Norwood
The goal of the surgery is to create an unobstructed outflow tract from
the systemic ventricle. So the tiny native aorta is anastomosed to the pulmonary trunk, and
the arch is augmentented with a graft (or by other methods). The ASD is enlarged to create
non restrictive atrial flow. A Blalock-Taussig Shunt (see below) is used between the right
Subclavian and right PA. The ductus is removed as well to prevent over shunting to the lungs
Apparently, when this goes bad it’s usually from issues related to damage o f the coronary
arteries or over shunting of blood to the lungs (causing pulmonary edema). As a point of
trivia, sometimes the thymus is partially removed to get access.
(1 b) Sano
Same as the Norwood, but instead of using a Blalock-Taussig shunt a conduit is
made connecting the right ventricle to the pulmonary artery. The disadvantage of the BT Shunt
is that it undergoes a steal phenomenon (diverted to low pressure pulmonary system).
(2a) Classic Glenn
Shunt between the SVC and right
pulmonary artery (end-to-end), with the additional step of sewing
the proximal end of the Right PA closed with the goal of reducing
right ventricular work, by diverting all venous return straight to the
lung (right lung).
(2b) Bi-Directional Glenn:
Shunt between the SVC and the
right pulmonary artery (end-to-side). The RPA is left open, letting
blood flow to both lungs. This procedure can be used to address
right sided heart problems in general, and is also step two in the
palliative hypoplastic series. If it’s being used as step two the
previously placed Blalock-Taussig Shunt or Sano shunt will come
down as the Glenn will be doing its job of putting blood in the
lungs
(3) Fontan Operation
Used for Hypoplastic Hearts. The old
school Fontan consisted of a classic Glenn (SVC to RPA), closure of the
ASD, and then placing a shunt between the Right atrium to the Left PA.
The idea is to let blood return from systemic circulation to the lungs by
passive flow (no pump), and turn the right ventricle (the only one the kid
has) into a functional left ventricle. There arc numerous complications
including right atriomegaly with resulting arrhythmias, and plastic
bronchitis (they cough up “casts of the bronchus” that look like plastic).
Glenn =
vein to artery (SVC to pulmonary artery)
Blalock taussig =
subclavian artery to pulmonary artery
Classic Blalock-Taussig Shunt
Originally
developed for use with TOF. Shunt is created
between the Subclavian artery and the pulmonary
artery. It is constructed on the opposite side of the
arch. It’s apparently technically difficult and often
distorts the anatomy of the pulmonary artery.
Modified Blalock-Taussig Shunt
This is a gortex
shunt between the Subclavian artery and pulmonary artery,
and is performed on the SAME SIDE as the arch. It’s easier
to do than the original.
Pulmonary Artery Banding
Done to reduce pulmonary
artery pressure (goal is 1/3 of systemic pressure). Most common
indication is CHF in infancy with anticipated delayed repair. The
single ventricle is the most common lesion requiring banding
Atrial Switch
Mustard and Senning procedures are used to
correct transposition of the great arteries by creating a baffle within
the atria in order to switch back the blood flow at the level of inflow.
The result is the right ventricle becomes the systemic
ventricle, and the left ventricle pumps to the lungs. This is usually
done in the first year o f life.
Atrial switch
senning
Baffle is created from the right atrial wall and
atrial septal tissue WITHOUT use o f extrinsic material
atrial switch mustard
nvolves the resection of the atrial septum and
creation of a baffle using pericardium (or synthetic material).
Rastelli Operation
This is the most commonly
used operation for transposition, pulmonary outflow
obstruction, and VSD. The procedure involves the
placement of a baffle within the right ventricle
diverting flow from the VSD to the aorta (essentially
using the VSD as part of the LVOT). The pulmonary
valve is oversewn and the conduit is inserted between
the RV and the PA. The primary advantage of this
procedure is the left ventricle becomes the systemic
ventricle. The primary limitation of this procedure is
that the child will be committed to multiple additional surgeries
because the conduit wears out and must be replaced.
Jatene Procedure
This is another arterial switch method that
involves transection of the aorta and pulmonary arteries about the
valve sinuses , including the removal of the coronaries. The great
arteries are switched and the coronaries are sewn into the new aorta
(formerly the PA). Apparently this (Lecompte Maneuver) is very
technically difficult, but the advantage is there is no conduit to go
bad, and the LV is the systemic ventricle.
Ross Procedure
Performed for Diseased Aortic Valves in Children. Replaces the aortic
valve with the patient’s pulmonary valve and replaces the pulmonary valve with a
cryopreserved pulmonary valve homograft. Follow-up studies have shown interval growth of
the aortic valve graft in children and infants.
Bentall Procedure
Operation involving composite graft
replacement of the aortic valve, aortic root and
ascending aorta, with re-implantation of the
coronary arteries into the graft. This operation
is used to treat combined aortic valve and
ascending aorta disease, including lesions
associated with Marfan syndrome.
Orthotopic Heart Transplant
All o f the heart is removed, except the circular
part of the left atrium (the part with the pulmonary veins). The donor heart is trimmed
to fit to the left atrium.
Heterotopic Heart Transplant
The recipient heart remains in place, and the donor heart is added on top. This basically creates a double heart. The advantages of this are (1) it gives the native heart a chance to recover , and (2) gives you a backup if the donor is rejected.
Glenn summary
Vein to Artery
(SVC to Pulmonary Artery)
Primary Purpose: Take
systemic blood directly to the
pulmonary circulation (it
bypasses the right heart).
Most Testable Complications:
- SVC Syndrome
- PA Aneurysms
Blalock Taussig summary
Artery to Artery
(Subclavian A rtery to Pulmonary
Artery)
Primary Purpose: Increase
pulmonary blood flow
Most Testable Complications:
-Stenosis at the shunt’s
pulmonary insertion site
Fontan summary
It’s complicated with multiple
versions - steps are unlikely to
be tested
Primary Purpose: Bypass the
right ventricle / direct systemic
circulation into the PAs.
Most Testable Complications:
-Enlarged Right Artium
causing arrhythmia
-Plastic Bronchitis
