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Congenital Heart Disease in Congenital Heart Disease in AdultsAdults
BackgroundBackground
8/1000 Live born births 32,000 cases/yr Liveborn prevalence lower than fetal prevalence
– Fetal echo
20% die within first year– 80% of first year survivors reach adulthood– Prevalence 800,000 adults in U.S.
Focus on Adult congenital heart disease
Atrial Septal DefectAtrial Septal Defect
One third of adult patients with CHDF:M=2:1Secundum (75%)Primum 15%Sinus Venosus 10%
ASDASD
ASDASD
ASDASD
ASDASDAssociated AbnormalitiesAssociated Abnormalities
MVPCleft Mitral Leaflet MR (Primum)Anomalous Pulmonary Venous Return
– Sinus Venosus
ASD PhysiologyASD Physiology
Increased flow L-R– High-low pressure
Increased Right sided blood flowDilation of RA, RV and PA
ASD Clinical PresentationASD Clinical Presentation No symptoms until third or fourth decades
of life despite pulmonary to systemic flow (Qp:Qs) of 1.5 or more
Over the years, the increased volume of blood usually causes right ventricular dilatation and failure
Fatigue or dyspnea on exertion Supraventricular arrhythmias Paradoxical embolism, or recurrent
pulmonary infections Death from RV failure or Arrhythmias in 40-
50’s if uncorrected
Physical ExamPhysical Exam
Right ventricular or pulmonary arterial impulse may be palpable.
Wide and fixed splitting of the second heart sound– Increased blood flow in PA
A systolic ejection murmur second left intercostal space (pulmonic)– usually so soft that it is mistaken for an
“innocent”flow murmur. Flow across the atrial septal defect itself
does not produce a murmur.
ASD EKGASD EKG Right-axis deviation Incomplete right bundle-branch block
– R’ > R in V1 Left-axis deviation occurs with ostium primum
defects– 1-deg AVB, “notched s wave II”
A junctional or low atrial rhythm (inverted P waves in the inferior leads) occurs with sinus venosus defects.
Normal sinus rhythm for the first three decades of life, after which atrial arrhythmias may appear.
Secundum EKGSecundum EKG
Primum EKGPrimum EKG
ASD CXRASD CXR
Prominent pulmonary arteries Peripheral pulmonary vascular
pattern– Small pulmonary arteries well visualized in
periphery
RAE/RVE when advanced
ASD CXRASD CXR
ASD EchoASD Echo
RAE/RVEDirect visualization of Primum and
Secundum defectsSinus venosus defects require TEEMicrobubbles to assist with diagnosis
ASD EchoASD Echo
ASD PrimumASD Primum
ASD TreatmentASD Treatment
Qp:Qs 1.5 or more should be closed to prevent right ventricular dysfunction
Not recommended if irreversible pulmonary hypertension
Prophylaxis against infective endocarditis not recommended repaired or unrepaired– Except for first 6 months after closure
Percutaneous ClosurePercutaneous Closure
VSDVSD
VSDVSD
Most common congenital cardiac abnormality in infants and children
M:F=1:1 25-40 percent close spontaneously by 2 y.o. 90 percent of those that eventually close do
so by age10 70% are membranous, 20% muscular 5% just below the aortic valve (undermining
the valve annulus and causing regurgitation),
VSD PhysiologyVSD Physiology
Initially left-to-right shunting predominates
Over time pulmonary vascular resistance increases and left-to-right shunting declines
Eventually the pulmonary vascular resistance exceeds the systemic resistance and right to left shunting begins
VSD ExamVSD Exam
With left-to-right shunting and no pulmonary hypertension– left ventricular impulse is dynamic and
laterally displaced– murmur is holosystolic, loudest at the lower
left sternal border usually accompanied by a palpable thrill
– A short mid-diastolic apical rumble (caused by increased flow through the mitral valve) may be heard
VSD ExamVSD Exam Small, muscular VSD may produce high
frequency systolic ejection murmurs that terminate before the end of systole – High pressure, small defect– defect is occluded by contracting heart muscle.
If pulmonary hypertension develops, RV heave and a pulsation over the pulmonary trunk may be palpated – Murmur and thrill eventually disappear as flow
through the defect decreases Cyanosis and clubbing are late findings
VSD EKGVSD EKG
Small defect-normal Large defect- left atrial and
ventricular enlargementIf pulmonary hypertension occurs
– QRS axis shifts to the right,– right atrial and ventricular
enlargement
VSD CXRVSD CXR
Small defect- normalLarge defect LAE, LVE, “Shunt
Vascularity”Pulmonary hypertension:
– proximal pulmonary arteries enlarged– rapid taperingof the peripheral
pulmonary arteries, and oligemic lung fields “Pruning”
VSD CXRVSD CXR
VSD EchoVSD Echo
Two-dimensional echocardiographyConfirm the presence and locationColor-flow mapping provides
information about the magnitude and direction of shunting
Qp:Qs
VSDVSD
VSD ManagementVSD Management
Small defects (Qp:Qs < 1.5)– No need for surgery– High Risk SBE, Prophylaxis provided
Large defects who survive to adulthood usually have left ventricular failure or pulmonary hypertension/ right ventricular failure– Surgical closure recommended
Once the ratio of pulmonary to systemic vascular resistance > 0.7 risk of surgery is prohibitive
PDAPDA
PDAPDA Connects descending aorta (just distal to the
left subclavian artery) to the left pulmonary artery
In the fetus, it permits pulmonary arterial blood to bypass lungs and enter the descending aorta for oxygenation in the placenta
10 percent of cases of congenital heart disease. – Perinatal hypoxemia – Maternal rubella– Infants born at high altitude or prematurely
PDA ExamPDA Exam
Bounding arterial pulses with widened pulse pressure
Hyperdynamic left ventricular impulse A continuous “machinery” murmur
– Second left anterior intercostal space – Peaks immediately after the second heart sound
(thereby obscuring it)– declines in intensity during diastole.
If pulmonary hypertension develops continuous murmur decreases in duration eventually disappears
PDA CXRPDA CXR
Left atrial and ventricular hypertrophy
Pulmonary plethora, proximal pulmonary arterial dilatation, RVH
Prominent ascending aorta May be visualized as an opacity at
the confluence of the descending aorta and the aortic knob
PDA CXRPDA CXR
PDA ImagingPDA Imaging
With two-dimensional echocardiography the ductus arteriosus can usually be visualized
Doppler studies demonstrate continuous flow in the pulmonary trunk
Quantify the magnitude of shunting
PDA EchoPDA Echo
PDA ManagementPDA Management Small defects
– No need for surgery– High Risk SBE (0.45 % annually after age 20) Prophylaxis
provided – Some recommend closure to prevent SBE
Large defects– Sx during childhood or adulthood: fatigue, dyspnea, or
palpitations– The ductus arteriosus may become aneurysmal and
calcified, which may lead to its rupture – Left ventricular failure from Vol overload– When pulmonary vascular resistance exceeds systemic
vascular resistance, the direction of shunting reverses (Cyanosis)
PDA SurgeryPDA Surgery
1/3 of patients not surgically repaired die of heart failure, pulmonary hypertension, or endarteritis by age 40 2/3 die by age 60
Surgical ligation or percutaneous closure accomplished without cardiopulmonary bypass
Mortality of less than 0.5 percent Once severe pulmonary vascular obstructive
disease develops closure is contraindicated.
CoarctationCoarctation
Coarctation PhysiologyCoarctation Physiology
A diaphragm-like ridge extending into aorta just distal to the left subclavian artery at the ligamentum arteriosum
Less commonly immediately proximal to the left subclavian artery– difference in arterial pressure is noted between the
arms Collateral circulation through the internal
thoracic, intercostal, subclavian, and scapular arteries develops
CoarctationCoarctation
M:F = 4-5:1 Associated abnormalities Gonadal dysgenesis (e.g.,Turner’s
syndrome) Bicuspid aortic valve (30%) Ventricular septal defect Patent ductus arteriosus Mitral stenosis or regurgitation Aneurysms of the circle of Willis
Coarctation PresentationCoarctation Presentation Most adults are asymptomatic Diagnosis is made during physical exam
– Systemic arterial hypertension observed in the arms, with diminished or absent femoral pulses
If symptoms are present, they are usually those of hypertension: headache, epistaxis, dizziness, and palpitations.
Occasionally, diminished blood flow to the legs causes claudication
May present with heart failure or aortic dissection Women with coarctation are at high risk for aortic
dissection during pregnancy
Coarctation Physical ExamCoarctation Physical Exam Systolic arterial pressure higher in the arms than
in the legs The femoral arterial pulses are weak and delayed A systolic thrill in the suprasternal notch A systolic ejection click (due to a bicuspid aortic
valve) A harsh systolic ejection murmur along the left
sternal border and in the back, particularly over the coarctation
A systolic murmur, caused by flow through collateral vessels, may be heard in the back
Coarctation CXRCoarctation CXR
Increased collateral flow through the intercostal arteries causes notching of the posterior third of the third through eighth ribs– Usually symmetric.
Notching is not seen in the anterior ribs – Anterior intercostal arteries are not located in costal
grooves The coarctation may be visible as an
indentation of the aorta with prestenotic and poststenotic dilatation of the aorta, producing the “reversed E” or “3” sign
CoarctationCoarctation
Coarctation ImagingCoarctation Imaging
The coarctation may be visualized echocardiographically
Doppler examination can estimate transcoarctation pressure gradient.
Computed tomography, magnetic resonance imaging, and contrast aortography– Location and length of the coarctation – Visualization of the collateral circulation– Measurement of Gradient on Cath
Coarct EchoCoarct Echo
Coarctation ComplicationsCoarctation Complications
Hypertension Left ventricular failure (2/3 of pts > 40 yo) Aortic dissection Premature coronary artery disease Infective endocarditis Cerebrovascular accidents (due to the
rupture of an intracerebral aneurysm) If uncorrected 3/4 die by the age of 50,
and 90% by the age of 60
Coarctation RepairCoarctation Repair
Repair considered for transcoarctation pressure gradient of more than 30 mm Hg
Balloon dilatation is a therapeutic alternative– Higher incidence of subsequent aortic aneurysm
and recurrent coarctation than surgical repair Postoperative complications include residual
or recurrent hypertension, recurrent coarctation, and the possible sequelae of a bicuspid aortic valve
Age at Time of RepairAge at Time of Repair
Surgery during childhood: – 90 percent are normotensive 5 years
later, 50 percent are normotensive 20 years later
– 89 percent of patients are alive 15 years later and 83 percent are alive 25 years later
Surgery after age 40: – Half have persistent hypertension– 15-year survival is only 50 percent
Bicuspid AoVBicuspid AoV
Aortic StenosisAortic Stenosis Supravalvular and Infravalvular Stenoses typically
present in childhood Bicuspid aortic valve 2 to 3 percent adult population. M:F=4:1 20% have associated cardiovascular abnormality
such as patent ductus arteriosus or aortic coarctation. Not stenotic at birth, subject to abnormal
hemodynamic stress, leads to thickening and calcification of the leaflets
Abnormality of the medial layer of the aorta above the Valve predisposes to dilatation of the aortic root
Aortic Stenosis PresentationAortic Stenosis Presentation
The classic symptoms are angina pectoris, syncope and heart failure
Adults with aortic stenosis who are asymptomatic have a normal life expectancy; they should receive antibiotic prophylaxis
Once symptoms appear, survival is limited: the median survival– five years after angina develops– three years after syncope occurs– two years after heart failure appears
Aortic Stenosis Physical ExamAortic Stenosis Physical Exam Carotid upstroke delayed and diminished
(parvus et tardus) The aortic component of S2 diminished or
inaudible Fourth heart sound is present A harsh systolic crescendo–decrescendo
murmur is audible over the aortic area and often radiates to the neck
As the aortic stenosis worsens, the murmur peaks progressively later in systole
Aortic Stenosis Work UpAortic Stenosis Work Up
Left ventricular hypertrophy is usually evident on EKG
Unless the left ventricle dilates, CXR demonstrates a normal cardiac silhouette
TTE with Doppler permits assessment of the severity of the stenosis and of left ventricular systolic function.
Cardiac catheterization is performed to determine the severity of aortic stenosis and to determine concomitant coronary artery disease.
Aortic Stenosis TreatmentAortic Stenosis Treatment
If mild, only SBE prophylaxisIf symptomatic, valve replacement
necessaryValve replacement prior to development of
LV dysfxn– Nl LV fxn– LVH will regress
Pulmonic StenosisPulmonic Stenosis
10 to 12 percent of congenital heart disease in adults.
Valvular in 90 percent of patients, remainder supravalvular or subvalvular
Supravalvular pulmonary stenosis in pulmonary trunk or branches– Often coexists with other congenital cardiac abnormalities
(valvular pulmonary stenosis, ASD, VSD, PDA, tetralogy of Fallot or Williams syndrome)
Subvalvular pulmonary stenosis caused by narrowing of the right ventricular infundibulum usually occurs in ventricular septal defect.
Pulmonary Stenosis Pulmonary Stenosis PhysiologyPhysiology
Typically is an isolated abnormality, may occur with VSD
Valve leaflets usually are thin and pliant; all three valve cusps are present
Commissures are fused– Valve is dome-shaped with a small central orifice – 10-15 percent have dysplastic thickened leaflets
2/3 of patients with Noonan’s syndrome have pulmonary stenosis due to valve dysplasia.
Pulmonic Stenosis DefinitionPulmonic Stenosis Definition Mild if the valve area >1.0 cm, transvalvular
gradient < 50 mm Hg, or peak right ventricular systolic pressure is <75 mm Hg
Moderate if the valve area is 0.5 to 1.0 cm, the transvalvular gradient is 50 to 80 mm Hg, or the right ventricular systolic pressure is 75 to 100 mm Hg.
Severe pulmonary stenosis is characterized by a valve area of less than 0.5 cm, a transvalvular gradient of > 80 mm Hg, or a right ventricular systolic pressure of more than 100 mm Hg
Pulmonic Stenosis Pulmonic Stenosis PresentationPresentation
If mild, usually Asx When the stenosis is severe, dyspnea on
exertion or fatigability may occur Less often may have chest pain or syncope with
exertion Eventually, right ventricular failure may develop,
with peripheral edema and abdominal swelling If the foramen ovale patent, shunting of blood
from the right to the left causing cyanosis and clubbing
Pulmonic Stenosis Physical Pulmonic Stenosis Physical ExamExam
With moderate or severe pulmonary stenosis: A right ventricular impulse at the left sternal border Thrill at the second left intercostal space Harsh crescendo–decrescendo systolic murmur
increases with inspiration at left sternal border If the valve is pliable, an ejection click often
precedes the murmur As the stenosis becomes more severe, the systolic
murmur peaks later in systole
Pumonic Stenosis CXRPumonic Stenosis CXR
Post-stenotic dilatation of the main pulmonary artery
Diminished pulmonary vascular markings
The cardiac silhouette is usually normal– An enlarged cardiac silhouette may be
seen if the patient has right ventricular failure or tricuspid regurgitation.
Pulmonic Stenosis EchoPulmonic Stenosis Echo
Right ventricular hypertrophy and paradoxical septal motion during
Site of obstruction can be visualized in most patients.
With the use of Doppler flow studies, the severity of stenosis can usually be assessed
Pulmonic Stenosis EchoPulmonic Stenosis Echo
Pulmonic Stenosis, TreatmentPulmonic Stenosis, Treatment
If mild only SBE Prophylaxis Survival 94 percent 20 years after diagnosis Severe stenosis should be relieved Moderate pulmonary stenosis have an
excellent prognosis with either medical or interventional therapy– Interventional therapy is usually recommended,
since most patients with moderate pulmonary stenosis eventually progress
Balloon ValvuloplastyBalloon Valvuloplasty
The procedure of choice High success rate provided the valve is
mobile and pliant Long-term results are excellent Secondary hypertrophic subpulmonary
stenosis regresses after successful intervention
Valve replacement is required if the leaflets are dysplastic or calcified or if marked regurgitation is present
Tetrology of FallotTetrology of FallotMost common cyanotic heart defect after
infancyOveriding aortaObstruction of RVOTRVHVSDAssociated with L-PA stenosis (40%), R
sided aortic Arch (25%), ASD (10%), Coronary Anomalies (10%)
Tetralogy of FallotTetralogy of Fallot
Tetralogy of FallotTetralogy of Fallot
Equal pressure in R and L ventriclesR-L shunting due to elevated RV pressures
from RVOT obstructionChanges in SV resistance affect shunting
– Increased SVR decreases R-L shunting
Tetralogy of FallotTetralogy of FallotPresentationPresentation
Cyanotic spells beginning in first year of life– Tachypnea, cyanosis– Can progress to LOC, Seizures, CVA, Death
Adults– Dyspnea and limited exercise tolerance– Complications of chronic cyanosis-
erythrocytosis, hyperviscosity, abnormalities of hemostasis, cerebral abscesses or stroke, and endocarditis.
Tetralogy of FallotTetralogy of FallotPhysical ExamPhysical Exam
Cyanosis and digital clubbing– Severity determined by the degree of RVOT
obstruction RV lift is palpable A Systolic ejection murmur caused by
turbulent flow across the RVOT (thrill may be may be palpable)– Intensity and duration inversely proportional to
severity of obstruction- flow shunted across VSD– a soft, short murmur suggests severe obstruction
Second heart sound is single, since its pulmonary component is inaudible
An aortic ejection click (due to a dilated, overriding aorta) may be heard
Tetralogy of FallotTetralogy of Fallot
EKG- right-axis deviation and right ventricular hypertrophy.
CXR- heart size is normal or small– lung markings are diminished. – “bootshaped,” heart– upturned right ventricular apex and
concave main pulmonary arterial segment.
– A right sided aortic arch may be present.
Tetrology of FallotTetrology of FallotCXRCXR
Tetralogy EKG Tetralogy EKG
Tetralogy of FallotTetralogy of FallotEchoEcho
Establishes diagnosisDetermines severity of RVOT obstructionFlow across VSDCardiac Cath
– Pressures, gradients, shunting, O2 sat, VSD– Origins of coronary arteries
Also seen by MRI or CTA
Tetralogy EchoTetralogy Echo
Tetralogy of FallotTetralogy of Fallot
Without surgical intervention, most patients die in childhood
Survival rate- 66 percent at 1 year of age, 40 percent at 3 years, 11 percent at 20 years, 6 percent at 30 years, and 3 percent at 40 years
Tetralogy of FallotTetralogy of FallotSurgical correctionSurgical correction
Relieves sx and improves survival Waterston: a side-to-side anastomosis of the
ascending aorta and the right pulmonary artery Potts: side-to-side anastomosis of the
descending aorta to the left pulmonary artery Blalock–Taussig: end-to-side anastomosis of
the subclavian artery to the pulmonary artery.– Long-term complications- pulmonary hypertension,
left ventricular volume overload, and distortionof the pulmonary arterial branches.
Blalock-TausigBlalock-Tausig
WaterstonWaterston
Tetralogy of FallotTetralogy of FallotSurgical correctionSurgical correction
Complete surgical correction– Closure of VSD– Relief of RVOT obstruction
Mortality 3% in children, 2.5-8% in AdultsRate of survival 32 years after
surgery 86% with repair vs. 96% in age-matched controls
Tetralogy of FallotTetralogy of FallotPost Surgical ComplicationsPost Surgical Complications
Ventricular arrhythmias detected with Holter monitoring in 40 to 50 percent
Moderate or severe pulmonary regurgitation
Systolic and diastolic ventricular dysfunction
Atrial fibrillation or flutter are common
Tetralogy of FallotTetralogy of FallotPost Surgical ComplicationsPost Surgical Complications
Pulmonary regurgitation may develop as a consequence of surgical repair of the RVOT– Can result in RVE and RV dysfunction– May require repair or replacement of the
pulmonary valve RVOT aneurysm may occur at site of repair
– Rupture has been reported Recurrent obstruction of RVOT may occur 10-20% have residual VSD CHB may occur AI is common but usually mild
EbsteinEbstein’’s Anomalys Anomaly
Downward displacement of septal leaflet of Tricuspid valve– Sometime posterior leaflet as well
“Atrialized Ventricle”Tricuspid regurg common80% have ASD or PFO
– Can result in R-L shunting
EbsteinEbstein’’s Anomalys Anomaly
EbsteinEbstein’’ss
EbsteinEbstein’’s Anomalys Anomaly Severity of defect depends upon degree of valvular
displacement Presentation ranges from severe HF in neonate to
incidental discovery in adults Neonates with severe disease have cyanosis, heart failure,
murmur noted in the first days of life– Worsens after the ductus arteriosus closes
Older children with Ebstein’s anomaly often come to medical attention because of an incidental murmur
Adolescents and adults present with a supraventricular arrhythmia.
EbsteinEbstein’’s Anomalys AnomalyPhysical ExamPhysical Exam
Severity of cyanosis depends on the magnitude of right-to-left shunting
Tricuspid regurgitation is usually present at the left lower sternal border.
Hepatomegaly from passive hepatic congestion due to elevated right atrial pressure may be present.
EbsteinEbstein’’s Anomalys AnomalyEKGEKG
Tall and Broad p-wavesRBBB1st degree AVB20% have ventricular pre-excitation
EbsteinEbstein’’s Anomalys AnomalyEKGEKG
EbsteinEbstein’’s Anomalys AnomalyCXRCXR
Normal in mild casesCardiomegally from RAEPulmonary markings decreased in severe
cases– Marked R-L shunting across ASD
EbsteinEbstein’’s Anomalys AnomalyTreatmentTreatment
Focuses on preventing and treating complications
SBE prophylaxisCHFRx of SVT
– RFA for accessory pathwayFontan procedure in severe cases
FontanFontan
EbsteinEbstein’’s Anomalys Anomaly
Tricuspid SurgeryRepair or replacementClosure of ASD/PFOPatient with severe sx despite medical RxCardiac enlargement
Transposition of the Great Transposition of the Great VesselsVessels
Aorta from RV, PA from LVComplete separation of pulmonic and
arterial saturationRequires communication between the
circuits for survivial– PDA, VSD, ASD or PFO
D-Transposition of the Great D-Transposition of the Great VesselsVessels
Transposition EchoTransposition Echo
Transposition of the Great Transposition of the Great Vessels Physical ExamVessels Physical Exam
Findings are nonspecific. Infants have cyanosis and tachypnea. The second heart sound is single and loud
(due to the anterior position of the aorta). In patients with mild cyanosis, a holosystolic
murmur caused by a ventricular septal defect may be heard.
A soft systolic ejection murmur (due to pulmonary stenosis, ejection into the anteriorly located aorta, or both) may be audible.
Transposition of the Great Transposition of the Great Vessels EKGVessels EKG
RADRVH- RV is systemic ventricleLVH- if VSD, PDA, Pulmonic Stenosis
present
Transposition of the Great Transposition of the Great Vessels CXRVessels CXR
Increased pulmonary vascularityEgg Shaped with a narrow stalk
Transposition CXRTransposition CXR
Transposition of the Great Transposition of the Great VesselsVessels
Mortality 90% by 6 months if uncorrectedInfusion of prostaglandin E (to
maintain or restore patency of the ductus arteriosus),
Creation of an atrial septal defect by means of balloon atrial septostomy (the Rashkind procedure).
Oxygen- to decrease PVR, increase pulmonary blood flow
Transposition of the Great Transposition of the Great Vessels-SurgeryVessels-Surgery
Atrial Switch- (Mustard)– Atrial septum excised and baffle created– Shunts blood to LV
RV continues to function as systemic ventricle– RV failure, SCD
Leakage of the atrial baffle (often clinically inconsequential)
Obstruction of the baffle (often insidious and frequently asymptomatic)
Sinus-node dysfunction Atrial arrhythmias, particularly atrial flutter
Atrial SwitchAtrial Switch
Arterial SwitchArterial Switch
Transposition of the Great Transposition of the Great Vessels-SurgeryVessels-Surgery
The atrial-switch operation has been replaced by the arterial-switch operation
Pulmonary artery and ascending aorta are transected above the semilunar valves
Coronary arteries switched, so that the aorta is connected to the neoaortic valve (formerly the pulmonary valve) arising from the left ventricle, and the pulmonary artery is connected.
This operation can be performed in neonates and is associated with a low operative mortality and an excellent long-term outcome.
Physiologic RepairPhysiologic Repair
Tetralogy of Fallot (TOF)
Senning's or Mustard's operation for transposition of the great arteries
Fontan operation for the single ventricle.
Approach to ManagementApproach to Management
Timetable of Congential Heart Timetable of Congential Heart SurgerySurgery
Congenital Heart Disease in Congenital Heart Disease in Adults Part IIAdults Part II
Cyanotic Heart DiseaseCyanotic Heart Disease
M.Ferguson CAPT, USN
NNMC
Palliative interventions increase or decrease pulmonary blood flow while allowing a mixed circulation and cyanosis to persist
Physiologic repair total or near total anatomic, physiologic, or both anatomic and physiologic separation of the pulmonary and systemic circulations.
Palliative OperationsPalliative Operations
Palliative OperationsPalliative Operations
Systemic arterial-to-pulmonary artery shunts – improvement in saturation levels – high levels of pulmonary blood flow– direct exposure of the pulmonary vascular bed to the
high pressures of the systemic circulation– long-term complications include pulmonary
hypertension, pulmonary artery stenosis, and volume overload of the ventricle receiving pulmonary venous return.
Cyanotic ConditionsCyanotic Conditions
Arterial O2 desaturation due to shutning of venous blood into arterial circulation (R-L)
Magnitude of shunting determines severity of desaturation