Cardiac by Astu CHD

COLLEGE OF MEDICINE AND HEALTHSCIENCE
DEPARTMENTOF ANESTHESIA
Common congenital heart disease and their anesthetic implications
By: Astemamagn A. (BSc, MSc)

Jan, 2023
Arba Minch Ethiopia
1 By Astemamagn 26/11/2023
Outline
 Introduction
 General principles and perioperative considerations
 Some specific cardiac lesions
Lt – Rt shunt lesions ( ASD, VSD & PDA)
Outflow obstruction lesions ( PS, AS, CoA)
The incidence of types of CHD
Condition Incidence
VSD /Ventricular septal defect 32%
PDA/ Patent arterial duct 12%
PS /Pulmonary stenosis 8%
CoA /Coarctation of the aorta 6%
ASD /Atrial septal defect 6%
TOF /Tetralogy of Fallot 6%
AS Aortic stenosis 5%
TGA /Transposition of the great arteries 5%
HLHS /Hypoplastic left heart syndrome 3%
AVSD/ Atrioventricular septal defects 2%
Circulatory Changes at birth
 The LA pressure is low
 The RA pressure is higher than LA
( receives all sys VR)
 The flap valve of foramen ovale is
held open
 Blood across the atrial septum to
LA
 With the 1st breath, resistance to

pulm BF falls and volume of blood
returning to RA falls
 Changes in pressure difference
cause flap valve of FO to be closed.
The ductus arteriosus will
normally close within first
few hrs. or days
 Some babies with CH
lesion rely on BF through
the duct.
 Clinical condition
deteriorate dramatically
when duct closed (1-2
6 By Astemamagn
days) 26/11/2023
Epidemiology
 CHD occurs in 8 per 1000 infants .
 About 1 in 10 stillborn infants have a cardiac anomaly.
 About 10-15% have complex lesions with more than 1 cardiac abnormality.
 About 10-15 % also have non-cardiac abnormality.
 CHD is the most common group of structural malformations in
children.
Classification CHD
Acyanotic Cyanotic
Left-to-right Outflow  Tetralogy of Fallot

shunt obstruction  transposition of
the great arteries
 Ventricular Septal  Pulmonary  Atrioventricular
Defect (VSD) Stenosis septal defect
 Persistent Ductus  Aortic
Arteriosus (PDA) Stenosis
 Atrial Septal Defect  Coarctation of
(ASD) aorta
8 By Bahiru D. 11/26/2023
General Etiology
Chromosomal
Maternal disorders Maternal drugs
abnormality
Rubella infection Warfarin therapy Down’s syndrome
(30-35%) (5%) (30%)
PDA, peripheral PDA, pulmonary Atrioventricular
pulmonary valve stenosis septal defect, VSD
stenosis Fetal alcohol Edward’s and Patau’s
SLE (35%) syndrome (25%) syndrome (60-80%)
Complete heart ASD, VSD, Complex
block tetralogy of Fallot Turner’s syndrome
DM (2%) (15%)
Aortic valve stenosis,
coarctation of the
aorta
9 By Bahiru D. 11/26/2023
Recognizing Cardiac Disease in Children
Goals
 To treat cardiac failure prior to surgery (VSD, AVSD)
 To recognize a condition that may be associated with acute
decompensation during surgery (hyper cyanotic episode in tetralogy of

fallot, loss of cardiac output in aortic stenosis, coarctation,
cardiomyopathy)
10
Preoperative consideration
Category of Pediatric CHD patients presenting for Non-cardiac surgery.
1. Before the lesion is diagnosed  These pts
 Present with unexpected complication with cyanosis, arrhythmias, or
ventricular dysfunction.
 Rx consists- resus, termination of surgery & consultation.
2. After diagnosis before intervention.

 Have cardiac workup & are under the care of cardiologist
11
Patients who had previous palliative surgery
a. ToF with Blalock-Taussig shunt Degree of invasive

monitoring depend on
b. Atrial septostomy for TGA degree of symptoms.
4. Patients in whom total correction has been done but they may have residual
defects requiring certain pre-cautions.
5. Inoperable cardiac lesions – hypoplastic Lt heart syndrome…this pts are @
high risk of M & Mo…full invasive monitoring is needed even for minimally
invasive procedures.
12
Preoperative cont…
1. History
 Pregnancy – maternal ds, drug and alcohol intake
 Birth history – history of prematurity associated with PDA, birth asphyxia

associated with persistent circulation (PPHN)
 Cardiac symptoms
 Cyanosis – blue discoloration of tongue, lips and may be confirmed by
pulse oximeter
 Hypercyanotic ‘spell’ – classic symptom of TOF
13
 Respiratory symptoms – breathlessness due to inc. pul blood flow in
children with cardiac failure. This presents as slow feeding, breathlessness,

cold clammy sweatiness and poor weight gain.
 Funny turns and chest pain – unusual presentation for cardiac disease in
children, much more commonly associated with simple faints, or
neurological ds such as epilepsy.
14
 Sudden collapse may be due to arrhythmias, and collapse with exercise is a
very worrying sign in a child with significant left ventricular outflow tract
obstruction such as aortic stenosis.
 Most chest pain in children is due to musculoskeletal problems, especially in
older children.
 Chest pain due to angina is rare.
 Poor weight gain – common in conditions causing HF or associated with inc.
pul blood flow such as VSD.
15
General inquiry….
 Other symptoms suggestive of complex congenital disorders such as Down’s
syndrome, a family Hx of cardiac ds, or symptoms suggestive of acquired
heart ds such as rheumatic fever or endocarditis.
16
2. Examination
Inspection
 Dysmorphic features
 Signs of Poor weight gain
 Signs of breathlessness ( Inc. RR, IC/SC recession, nasal flaring & grunting)
 Central cyanosis – color of tongue
 Long standing cyanosis - ‘clubbing’ of the nails, hands and feet.
 Children who have long standing cyanosis develop compensatory

polycythemia and possibly complications such as cerebral
thromboembolism.
17
 The jugular venous pulse is very difficult to see in children < 5 years – the
liver size gives a much better estimate of venous pressure.
Palpation
 Pulse ( rate, rhythm, volume & character)
 Absent femoral pulse – seen in coarctation
18
 Suprasternal ‘thrill’ – felt in AS or other causes of aortic arch anomaly
 Liver size – abnormal increase may indicate Inc. Rt atrial pressure 20 to HF
 Dependent peripheral edema – late sign but may be felt by palpation over
the sacrum.
19
Percussion
 To estimate liver size, & presence of ascites ( rarely due to cardiac failure in
children)
Auscultation
 Cardiac murmurs
20
Cardiac murmurs in children
Type of murmur X’tics & best heard @ Possible pathology
Ejection systolic • Upper right sternal edge +/- carotid thrill Aortic stenosis
murmur
• Upper left sternal edge, no thrill Pul. stenosis or ASD
• Long harsh murmur with cyanosis TOF
Pansystolic murmur • Lower Lt sternal edge +/- thrill VSD
Ejection
• Apex MR
Diastolic murmurs systolic
• Lower left sternal edge, sitting forward, AR (endocarditis)
(unusual in children) collapsing pulses
murmur
Continuous murmur • Left infraclavicular region PDA
(machinery murmur)
Innocent murmurs • Soft, systolic, asymptomatic, best heard @ Lt Heard in 10% of

(still’s murmur) sternal edge, no radiation & softer when normal children.
standing
21 By Bahiru D. 11/26/2023
FBC/CBC
 Polycythemia very common  w/c leads to blood viscosity & leads to
thrombosis and infarction in cerebral, renal and pul. Region.

 Coagulation profile ( Plt, PT & aPTT)
 ECG – ventricular strain, hypertrophy
 ECHO - gold standard to confirm dx
22
 Cardiac catheterization
 To measure the pulmonary vascular resistance, or
 Investigate the anatomy of the pulmonary vessels.
 CXR - for heart position (Dextrocardia) and size, atelectasis, acute

respiratory infection, vascular markings and elevated hemi diaphragm.
23
Left-to-right shunts
VSD
24
Left-to-right shunts
Ventricular Septal Defects (VSD)
 There is a defect anywhere in the ventricular septum, usually

perimembranous (adjacent to the tricuspid valve) or muscular (completely
surrounded by muscle)
 Location of the VSD – prognostic and repair approach
 The amount of flow crossing a VSD depends on the size of defect and the
By Astemamagn
pulmonary vascular resistance.
25 26/11/2023
 At birth, the pulmonary vascular resistance is normally elevated, thus,
even large VSDs are not symptomatic at birth.

 Over the first 6-8 weeks of life, pulmonary vascular resistance normally
decreases.
 More blood flows through the lung and into the left atrium. However, in
VSD, the amount of shunt increases, and symptoms may start to

develop.
 The size of the VSD affects the clinical presentation.
Pathophysiology
 VSD permits a left-to-right shunt to occur at the ventricular level with 3
adverse hemodynamic consequences:
1. left ventricular (LV) volume overload,

2. Increased pulmonary blood flow,
3. Compromise of systemic cardiac output
Pathophysiology
 In time, as PVR increases, irreversible histologic changes may occur
within the pulmonary vascular bed
 Untreated, a reversal of the flow occurs, leading to a right-to-left shunt with

the development of increasing cyanosis (Eisenmenger complex)
Small VSDs
 Smaller than the aortic valve in diameter (3mm)
Clinical features
Symptoms
Asymptomatic
Physical signs
 Thrills at lower sternal edge
Loud pansystolic murmur at lower left sternal edge
29 Quiet pulmonary second sound (P2)

By Astemamagn 26/11/2023
Cont.
 Investigations
 Chest X-ray - normal
 ECG - normal
 Echocardiography
 Demonstrates the precise anatomy of the defect. Assessment of
haemodynamic effect using Doppler echocardiography.
Large VSds
 Defects are the same size or bigger than the aortic valve.
 Clinical features
 Symptoms
 Heart failure with breathlessness and failure to thrive after 1 week old
 Recurrent chest infections
 Physical signs
 Prominence of the left precordium
 Soft pansystolic murmur
 Apical mid-diastolic murmur at the apex
 Loud pulmonary second sound (P2)
31
 Tachypnea, tachycardia and enlarged liver from heart failure .
Investigations
 Chest X-ray
 Cardiomegaly
 Enlarged pulmonary arteries
 Pulmonary vascular markings
 Pulmonary edema
 ECG
 Biventricular hypertrophy by 2 months of age and signs of pulmonary
HPT  right ventricular enlargement and hypertrophy
 Demonstrates the anatomy defect, hemodynamic effects and severity of
32 pulmonary HPT.
Enlarged pulm arteries
Increased pulm cardiomegal

markings y
Mx of anesthesia
 Abc prophylaxis
 Induction of anesthesia depends on the extent of ventricular dysfunction.
 Good LV function  use inhalational induction
 Poor LV function  Etomidate/ketamine/opioid is better choice.
 Acute and persistent increases in systemic vascular resistance or

decrease in pulmonary vascular resistance are unwanted b/c these
changes can increase the magnitude of LR intracardiac shunt at the
ventricular level.
 So VAA (dec. SVR) and PPV (inc. pul VR) are well tolerated
Complications
 Eisenmenger complex
 Secondary aortic insufficiency
 Aortic regurgitation
 RV outflow tract obstruction
 Sub aortic obstruction
 Infective endocarditis
Atrial Septal Defects (ASD)
 Due to failure of Septal growth or excessive reabsorption of tissue
 Represent about 6 - 10% of CHD
 Classification:
 Secundum ASD (80%)
 Defects occur from either excessive resorption of septum primum or
from deficient growth of septum secundum
 Primum ASD or partial atrioventricular Septal defect
 Incomplete fusion of septum Primum with the endocardial cushion.
 An inter-atrial communication between the bottom end of the atrial
septum and the atrioventricular(AV) valves.

 Abnormal AV valves, with a left AV valve having 3 leaflets and tends to
leak (regurgitant valve).

 Sinus venosus defect (least common)
 Associated with anomalous pulmonary venous return

Pathophysiology: Atrial Septal Defects (ASD)
 Shunting across an atrial septal defect is left to right
 The degree of this shunting is dependent on;
- The size of the defect

- The relative compliance of the right and left ventricles.
- The relative vascular resistance in the pulmonary and systemic
circulations.
 Resistance in the pulmonary vascular bed is commonly normal in children
with ASD, and increase in volume load is usually well tolerated

 However, altered ventricular compliance with age can result in an
increased left-to-right shunt contributing to symptoms
 The chronic significant left-to-right shunt can alter the pulmonary
vascular resistance leading to pulmonary arterial hypertension, even

reversal of shunt and Eisenmenger syndrome.
SIGNS AND SYMPTOMS
 Initially no symptoms, no physical finding.
 May remain undetected for years.
 Small ASD no closure of ASD required.
 Large ASD, ratio causes dyspnea on exertion, supraventricular
arrhythmias, RHF, paradoxical embolism and recurrent pulmonary

infections.
 A systolic ejection murmur is present in 2nd left intercostal space .
Ix modalities: Atrial Septal Defects
(ASD)
 Chest X-ray
 Cardiomegaly
 enlarged pulmonary arteries
 increased pulmonary vascular markings
 Documents type, size and direction of shunt
 The mainstay of diagnostic investigations
 41 By Astemamagn 26/11/2023
 ECG
 provide strong diagnostic clue
 secundum ASD – right axis deviation and right ventricular
hypertrophy
 partial AVSD – left axis deviation
Mx of anesthesia: Atrial Septal Defects (ASD)
 ASD associated with a left-to-right intracardiac shunt has only minor
implications for the management of anesthesia.

 In the absence of CHF, no significant alteration in intravenous or volatile
anesthetic response.
 Avoid increase in SVR because it will increase magnitude of shunt.
 Decrease in SVR due to volatile anesthetics will decrease magnitude of shunt.
 IPPV will increase PVR that will also decrease the shunt.
Mx of anesthesia: Atrial Septal Defects (ASD)
 Avoid air entrance in circulation.
 Give prophylactic antibiotics against infective endocarditis if valvular
abnormality is present.
 Transient SVT and AV conduction defect may occur in early post operative
period after surgical repair of ASD.
Patent Ductus Arteriosus
PDA…
 The ductus arteriosus allows blood to flow from the pulmonary artery to
the aorta during fetal life. This changes to the opposite after birth.
 In term infants, it normally closes shortly after birth.
 Failure of the normal closure of it by a month post term is due to a
defect in the constrictor mechanism of the duct.
 In preterm infants, the PDA is not from CHD but due to prematurity.
Pathophysiology
 Higher aortic pressure,  blood shunts left to right through the ductus
 The magnitude of the excess pulmonary blood flow depends on:
The larger the internal diameter of the narrowest portion of the ductus
arteriosus, the larger the left-to-right shunt.

If the ductus arteriosus is restrictive, then the length of the narrowed area
also affects the magnitude of the shunt.
Patho…
 If the systemic vascular resistance is high and/or the pulmonary vascular
resistance is low, the flow through the ductus arteriosus is potentially large
 If the PDA is large, pulmonary artery pressure may be elevated to systemic
levels during both systole and diastole
 Extremely high risk for the development of pulmonary vascular disease if
48 left unoperated.
Signs & symptoms
 Depends on the size of PDA
 small – asymptomatic
 Moderate to larger shunts – symptoms of CHF or even Pul. HTN
 Physical findings
 Continuous machinery murmur beneath the left clavicle
 Widened pulse pressure  collapsing or bounding pulse
 Larger shunts  mid-diastolic murmur at the apex
Ix modalities
 Features indistinguishable from VSD
 ECG and CXR show LVH.
 Echocardiography with Doppler studies confirms the diagnosis.
ANESTHETIC MANAGEMENT
 Antibiotic prophylaxis against infective endocarditis.
 Anesthesia with volatile anesthetic and IPPV is useful.
 Arterial BP monitoring is helpful.
 Ligation of PDA is often associated with hypertension in post operative

period.
Acyanotic
Outflow obstruction
Outflow obstruction
 Pulmonary stenosis – 8%
 Aortic stenosis – 5 %
 Coarctation of the aorta – 6%
Pulmonary stenosis
 Narrowing of the pulmonary valve
opening that increases resistance to

blood flow from the right ventricle to the
pulmonary arteries.
Pulmonary stenosis
Site: Valvar (most), supravalvar, or subvalvar

The valve may have only two or one leaflets
The leaflets that are partially fused together
Three leaflets, but thick and partly or
completely stuck together
Narrowing of the valve
Pulmonary stenosis
Pulmonary valve is mildly to

moderately narrowed
The right ventricle pump harder

and at a higher pressure to propel
blood through the valve
Right ventricular hypertrophy
severe stenosis in a
neonate
Right ventricle cannot eject sufficient volume of
blood flow into the pulmonary artery
Right ventricular pressure becomes extremely high
Lead to right-to-left shunting through a

patent foramen ovale/atrial Septal
defect
Right-to-left shunt
cyanosis
57
Clinical features: Pulmonary stenosis
 Severity depend on degree of stenosis
 Most asymptomatic (mild)
 Moderate – Severe :
 Exertional dyspnoea, easily fatigability, rapid breathing, shortness of
breath, chest pain (angina), cyanosis

 may develop as the child gets older.
Pulmonary stenosis
 Physical sign: heart murmur
 Sys ejection murmur best heard at 2nd IS (P2) which radiates to the back
 Thrill may present
 In severe: impulse at the left sternal border(RVH)
 Often associated with click sound
Ix: Pulmonary stenosis
Chest X-ray ECG
 Normal or post-stenotic dilation of the  Shows evidence of right ventricular

pulmonary artery hypertrophy
Mx of anesthesia: Pulmonary stenosis
 Design anesthesia to avoid increases in Rt ventricular O 2 requirements.
 So excessive increases in HR and myocardial contractility are undesirable.
Aortic stenosis
 A narrowing of the valve that opens
to allow blood to flow from the left

ventricle into the aorta and then to
the body
Aortic stenosis
 Valvular, subvalvular or supravulvalar –
5%
 Failure of :
 development of the three leaflets
 Resorption of tissue around the valve
Pathophysiology: Aortic stenosis
Narrowed aortic valve
The LV must pump under very high pressures
Left ventricular hypertrophy

 Mild stenosis: usually well tolerated, with minimal
hypertrophy and normal LV function.
 Severe hypertrophy and valvar obstruction: myocardial
ischemia & limited CO, reduced coronary perfusion, with
increased myocardial oxygen consumption.
 Fibrosis may occur in areas of the myocardium damaged by

ischemia.
Clinical feature: Aortic stenosis
 Depend on degree of stenosis

 Mild to moderate : asymptomatic
 Severe:
 Easy fatigability, exertional chest pain, syncope
 In infant with severe stenosis can survive only if:
 PDA permits flow to the aorta and coronary arteries
Physical signs Aortic stenosis
 Small volume, slow rising pulse
 Sys ejection murmur at Rt 2nd IS and radiating to neck
 Apical ejection click
 Thrill at RUS border/suprasternal notch/carotid
 Congenital bicuspid aortic valve:
 Prone to calcific degeneration in middle age
 Increased risk of infective endocarditis
 66  BySingle
Astemamagn cuspid AV : commonly ass’td with early sudden death 26/11/2023
Ix: Aortic stenosis
 ECG and CXR
 Mild: both normal
 Moderate – severe:
 CXR: LVH, post stenotic dilation of ascending or aortic knob
 ECG : LVH
Mx of anesthesia: Aortic stenosis
 Prophylaxis for infective endocarditis
 Intravenous induction drug that does not decrease systemic vascular
resistance.
 An opioid induction may be useful if left ventricular function is
compromised.
 Maintain normal sinus rhythm
 Avoid bradycardia or tachycardia
 Avoid hypotension
 Optimize intravascular fluid volume to maintain venous return and left
68
ventricular filling
Coarctation of the aorta
 A narrowing of the aorta, usually
just before the point where the

ductus arteriosus joins the aorta.
Coarctation of the aorta
 2X more common in males

 25% of patients with Turner’s Syndrome
have coarctation of aorta
 Associated Defects:
 Bicuspid aortic valve (most common
associated defect seen in 50%)
 VSD
 ASD
Pathophysiology: Coarctation of the aorta
 Afterload on the left ventricle (LV), which

results in increased wall stress
 LV hypertrophy
 Acute increased in afterload lead to rapid development of CHF and
shock.
 LV afterload may gradually increase, allowing children with less
severe coarctation to develop arterial collateral vessels that
partially bypass the aortic obstruction.
The aorta narrows
Reduces blood flow to the lower

half of the body
The BP is lower than normal

in the legs and tends to be
higher than normal in the
arms
HTN
Clinical manifestation: Coarctation of the
aorta
 Depends on the severity of CoA

 Mild - Asymptomatic
 In older children:
 Leg discomfort with exercise
 Headache
 Epistaxis
 Infant severe CoA:
 Dependent on a PDA to provide flow to descending aorta
 If PDA closed: respiratory distress, shock
73
Physical sign: Coarctation of the aorta
 Systemic HTN in the arm

 Diminished lower extremities pulses
 Radio-femoral delay:
 blood bypassing the obstruction via collateral vessels in the chest wall
 Ejection sys murmur
Ix: Coarctation of the aorta
 CXR :
 rib notching with large collaterals
 ECG:
 LVH
CHEST XRAY
Coarctation of the Aorta
Red : rib notching caused by the dilated intercostal arteries.

Yellow : the aortic knob
Blue : the actual coarctation
Green : the post-stenotic dilation of the descending aorta.
Mx of anesthesia: Coarctation of the aorta
 Consider :-
 The adequacy of perfusion to the lower portion of the body during cross-
clamping of the aorta.
 The propensity for systemic hypertension during cross-clamping of the
aorta if repair is considered.
 The risk of neurologic sequelae due to ischemia of the spinal cord.
 Continuous monitoring of systemic blood pressure above and below the
coarctation is achieved by placing a catheter in the right radial artery and
a femoral artery.
7 By Astemamagn 26/11/2023
 MAP in the lower extremities should be at least 40 mm hg to ensure
adequate blood flow to the kidneys and spinal cord.
 If systemic hypertension persists, continuous intravenous infusions of
nitroprusside should be considered.
 The disadvantages of lowering the systemic blood pressure to normal

levels are excessively decreased perfusion pressure in the lower part of
the body and inadequate blood flow to the kidneys and spinal cord.
 Patients with known coarctation of the aorta should be given prophylactic

antibiotics prior to surgical procedures.
Summery
 Understand pathophysiology of defects.

 In left-to-right shunts avoid increase SVR, in fact decrease in SVR and
increase in PVR are desirable.
BUT
 These are fatal in right-to-left shunts.
 So in right-to-left shunts avoid decrease in SVR and increase in PVR.
THANK YOU !

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COLLEGE OF MEDICINE AND HEALTHSCIENCE

Common congenital heart disease and their anesthetic implications

By: Astemamagn A. (BSc, MSc)

 General principles and perioperative considerations

 Some specific cardiac lesions

Lt – Rt shunt lesions ( ASD, VSD & PDA)

Outflow obstruction lesions ( PS, AS, CoA)

 With the 1st breath, resistance to

 About 10-15 % also have non-cardiac abnormality.

 CHD is the most common group of structural malformations in

Left-to-right Outflow  Tetralogy of Fallot

 To recognize a condition that may be associated with acute

decompensation during surgery (hyper cyanotic episode in tetralogy of

2. After diagnosis before intervention.

a. ToF with Blalock-Taussig shunt Degree of invasive

 Pregnancy – maternal ds, drug and alcohol intake

 Birth history – history of prematurity associated with PDA, birth asphyxia

 Cyanosis – blue discoloration of tongue, lips and may be confirmed by

children with cardiac failure. This presents as slow feeding, breathlessness,

 Children who have long standing cyanosis develop compensatory

 Absent femoral pulse – seen in coarctation

 Liver size – abnormal increase may indicate Inc. Rt atrial pressure 20 to HF

• Long harsh murmur with cyanosis TOF

Pansystolic murmur • Lower Lt sternal edge +/- thrill VSD

Innocent murmurs • Soft, systolic, asymptomatic, best heard @ Lt Heard in 10% of

thrombosis and infarction in cerebral, renal and pul. Region.

 ECG – ventricular strain, hypertrophy

 ECHO - gold standard to confirm dx

 To measure the pulmonary vascular resistance, or

 Investigate the anatomy of the pulmonary vessels.

 CXR - for heart position (Dextrocardia) and size, atelectasis, acute

Ventricular Septal Defects (VSD)

 There is a defect anywhere in the ventricular septum, usually

 Location of the VSD – prognostic and repair approach

even large VSDs are not symptomatic at birth.

VSD, the amount of shunt increases, and symptoms may start to

1. left ventricular (LV) volume overload,

 Untreated, a reversal of the flow occurs, leading to a right-to-left shunt with

 Thrills at lower sternal edge

Loud pansystolic murmur at lower left sternal edge

29 Quiet pulmonary second sound (P2)

Increased pulm cardiomegal

 Acute and persistent increases in systemic vascular resistance or

 Secondary aortic insufficiency

 RV outflow tract obstruction

 Sub aortic obstruction

 Due to failure of Septal growth or excessive reabsorption of tissue

 Represent about 6 - 10% of CHD

 Secundum ASD (80%)

 Defects occur from either excessive resorption of septum primum or

from deficient growth of septum secundum

 Incomplete fusion of septum Primum with the endocardial cushion.

 An inter-atrial communication between the bottom end of the atrial

septum and the atrioventricular(AV) valves.

leak (regurgitant valve).

 Associated with anomalous pulmonary venous return

 Shunting across an atrial septal defect is left to right

 The degree of this shunting is dependent on;

- The size of the defect

with ASD, and increase in volume load is usually well tolerated

 However, altered ventricular compliance with age can result in an

increased left-to-right shunt contributing to symptoms

 The chronic significant left-to-right shunt can alter the pulmonary