CARDIOLOGY Flashcards
1
Q
Fetal circulation
Fetal lungs are underdeveloped ?
A
Not used during the intrauterine life.
2
Q
Fetal circulation
Fetal organ involved in gas exchange
A
Placenta
3
Q
Fetal circulation
Placenta consists of (Blood vessels)
A
- Umbilical vein (Carries oxygenated blood from the placenta)
- 2 Arteries (carries deoxygenated blood from fetus to mother)
4
Q
Fetal circulation
The pressure in the LA and RA
A
RA>LA (Lungs are sending little to no blood to the LA)
5
Q
Fetal circulation
Right atrium recieves blood from
A
- Venous blood from fetal systemic circulation
- blood coming from the placenta
6
Q
Fetal circulation
Fetal circulation has… which is not seen in adult circulation
A
- Ductus venosus
- Ductus arteriosus
Foramen ovale
7
Q
Fetal circulation
Foramen ovale is located
A
between the LA and RA
8
Q
Fetal circulation
Ductus arteriosus is connected between
A
the pulmonary artery and the descending aorta
9
Q
Fetal circulation
Fetal hypoxia causes
A
increased production of EPO
10
Q
Cardiac cycle
Systole lasts… of the cardiac cycle
A
2/3
11
Q
Cardiac cycle
Diastole lasts….of the cardiac cycle
A
1/3
12
Q
Cardiac cycle
When the HR increases what happens to the diastole
A
Diastole shortens
13
Q
Cardiac cycle
Mitral and tricuspid valves close during
A
Systole
14
Q
Cardiac cycle
Aortic valve closes… than the pulmonary valve
A
earlier
15
Q
Cardiac cycle
Physiological splitting of the 2nd HS
A
Change in intra- thoracic pressure during inspiration causes the IVC to drain more blood into the RA. More blood leads to delayed closure of the pulmonary valve later than the aortic valve
16
Q
Cardiac cycle
Stroke volume
A
amount of blood pumped during a single contraction
17
Q
Cardiac cycle
Ejection fraction
A
Percentage of blood pumped from each ventricle (~60-70%)
18
Q
Cardiac cycle
Cardiac output
A
Amount of blood pumped out calculated per minute
CO=SVxHR
19
Q
Neonatal circulation
Effect of lungs when the neonate cries soon after birth
A
Lungs expand.resistance to pulmonary blood flow falls and the volume of blood flowing through the lungs increase
20
Q
Neonatal circulation
How does the ductus arteriosus close
A
After birth, aortic pressure will go up and the pulm pressure will go down. Oxygenated blood from aorta will go through the ductus arteriosus. Increased oxygen causes the Ductus to close within 96 hours after birth
21
Q
Neonatal circulation
How does the foramen ovale close
A
- lungs expand after birth
- the resistance to pulmonary blood flow falls
- volume of blood flowing through the lungs increase.
- Blood to LA increase
- LA pressure increase than the RA
- Foramen closes
22
Q
Neonatal circulation
Regurgitation of Mitral and tricuspid valves causes…… murmurs
A
Systolic murmurs
23
Q
Neonatal circulation
Stenosis of mitral and tricuspid valves causes….. murmurs
A
Diastolic Murmurs
24
Q
Neonatal circulation
Regurgitation of aortic and pulmonary valves causes……. Murmurs
A
Diastolic Murmurs
25
# Neonatal circulation
Stenosis of Aortic and pulmonary valves causes…… murmurs
Systolic murmurs
26
# Rheumatic fever
Age group
5-15
27
# Rheumatic fever
MO causing Rheumatic fever
Group A beta- hemolytic streptococcus
28
# Rheumatic fever
Pathophysiology of Rheumatic fever
Abnormal immune response to a preceding infection with group A beta- hemolytic streptococcus
29
# Rheumatic fever
Rheumatic fever diagnostic criteria
Modified Duckett- Jones criteria
30
# Rheumatic fever
Major criteria
* Migratory polyartheritis
* Carditis
* Sydenham chorea
* Erythema marginatum
* Subcutaneous nodules
31
# Rheumatic fever
Minor criteria
* Fever
* Polyarthralgia
* Raised ESR, CRP
* Prolonged P-R interval
* History of Rheumatic fever
32
# Rheumatic fever
Dx of Rheumatic fever
* 2 major OR
* 1 major + 2 minor
+
* supportive evidence of preceding Group A streptococcal infection
33
# Rheumatic fever
Supportive evidence of preceding Strep infection
* markedly rasied ASOT
* Strep Antibodies
* Group A strep throst swab culture
34
# Rheumatic fever
Joints involved in migratory polyarthritis
Large joints such as
* ankles
* Knees
* wrists
35
# Rheumatic fever
Features of migratory polyarthritis
* Tenderness
* Moderate redness and swelling
36
# Rheumatic fever
How long does the arthritis last in one joint and when does it migrate
<1 week in one joint and migrate over 1-2 months
37
# Rheumatic fever
Pancarditis involves
* Endocarditis
* Myocarditis
* Pericarditis
38
# Rheumatic fever
Mumur in endocarditis
Mid- diastolic murmur ( Carey Coomb murmur due to swelling of mitral valve)
39
# Rheumatic fever
Valvular dysfunction is due to
endocarditis
40
# Rheumatic fever
Myocarditis leads to
* Heart failure and death
41
# Rheumatic fever
Pericarditis involves
* Pericardial friction rub
* Effusion
* Tamponade
42
# Rheumatic fever
Late manifestation in Rheumatic fever
Sydenham chorea
43
# Rheumatic fever
Sydenham chorea occurs after
2-6 months after the strep infection
44
# Rheumatic fever
Sydenham chorea consists of
* Involuntary movements
* Emotional lability
* lasts 3-6 months
45
# Rheumatic fever
Erythema marginatum is common. (T/F?)
False
46
# Rheumatic fever
Erythema marginatum is seen on
Trunk and limbs
47
# Rheumatic fever
Describe the appearance of erythema marginatum
Pink macules spread outwards, causing pink border with fading centre. Borders may unite to give a map-like outline
48
# Rheumatic fever
Subcutaneous nodules are seen mainly on
Extensor surfaces
49
# Rheumatic fever
Subcutaneous nodules appearance
Painless, pea-sized, hard
50
# Rheumatic fever
Rheumatic fever occurs 2 weeks after a
pharyngeal infection
51
# Rheumatic fever
All Rheumatic fever patients have a positive ASOT (T/F?)
F (only 80-85%)
52
# Rheumatic fever
Chronic Rheumatic fever mainly affects
Mitral stenosis (scarring and fibrosis)
53
# Rheumatic fever
The least common valve affected in Rheumatic fever
Pulmonary valve
54
# Rheumatic fever
Mx of an acute Rheumatic fever episode
* Admit
* Bed rest
* Aspirin
* Steroids - if carditis or heart failure
* Stop steroids- if only arthralgia
* ABx (Oral penicillin or IM Benzathine penicillin)
55
# Rheumatic fever
Usage of aspirin
NSAID. stop inflammation of the joints and the heart
56
# Rheumatic fever
Anti- streptococcal ABx dose
* Oral penicillin 10 days
OR
* IM benzathine penicillin single dose
57
# Rheumatic fever
When will the anti streptococcal ABx be given
if there's any evidence of persisting infections
58
# Rheumatic fever
Most effective prophylaxis
2 weekly injections of benzathine penicillin or oral penicillin
59
# Rheumatic fever
Issue with oral penicillin prophylaxis
poor compliance
60
# Rheumatic fever
substitute to penicillin allergic patients
oral erythromycin
61
# Rheumatic fever
Length of prophylaxis of only Rheumatic fever
for 5 years or until 21 years of age ( whichever is longer)
62
# Rheumatic fever
Length of prophylaxis of Rheumatic fever + cardits
for 10 years or until 25 years of age ( whichever is longer)
63
# Rheumatic fever
Length of prophylaxis of Rheumatic fever with residual heart disease
for 10 years or until 40 years of age ( whichever is longer) or even lifelong
64
# Rheumatic fever
Complication of Rheumatic fever
chronic valve disease therefore getting infective endocarditis
65
# infective endocarditis
infective endocarditis
inflammation of the endocardium due to alpha- hemolytic streptococcus
66
# infective endocarditis
MO
Streptococcus viridans
67
# infective endocarditis
Risk factors
* congenital heart disease (except ostium secundum ASD)
* Patients with prosthetic valves
68
# infective endocarditis
Diagnostic criteria
Modified duke criteria
69
# infective endocarditis
Major criteria of duke criteria
* 2 positive blood culture with typical organisms, 2 or more for less typical organism
* Evidence of endocarditis on echo - vegetations on a valve or another site, regurgitation near a prosthesis or abscess
70
# infective endocarditis
Minor criteria of duke criteria
* Predisposing conditions- Rheumatic heart disease
* fever
* Emboli- vascular signs
* Immune complex phenomena ( Glomerulonephritis, arthrits, Rheumatoid factor, osler nodes, roth spots, janeway lesions)
* Single positive blood culture/ serological evidence of infections/ echo signs not meeting the major criteria
* Newly diagnosed clubbing/ splenomegaly
* Splinter hemorrhages, petechiae
* High ESR, CRP
* Non feeding lines or peripheral lines
* Microscopic hematuria
71
# infective endocarditis
Dx of infective endocarditis
2 major criteria/ 1 major+ 3 minor/ 5 minor
72
73
# infective endocarditis
Ix of infective endocarditis
* Blood culture- before ABx
* Echo
* ESR, CRP
74
# infective endocarditis
Mx of infective endocarditis
IV ABx for 4-6 weeks ( penicillin + gentamicin)
75
# infective endocarditis
Main prophylactic step
Good dental hygiene
76
# infective endocarditis
ABx prophylaxis is given on
* dental treatment
* surgery
77
Child with fever and new- onset murmur
Infective endocarditis
78
# infective endocarditis
complications
* Heart failure ( If aortic/ mitral V is involved)
* Myocardial abscess
* Myocarditis
* Life- threatening arrythmia
* systemic emboli ( with CNS Sx)
* Pulmonary emboli ( With VSD, TOF)
79
# infective endocarditis
ADRS of gentamicin
nephrotoxic
Ototoxic
80
# Cyanotic Heart disease
ToF consists of
* Overriding aorta
* Pulmonary stenosis
* Large VSD
* RV hypertrophy
81
# Tetralogy of Fallot
Overriding aorta?
Aorta starts from both RV and LV chambers
82
Most common cyanotic congenital HD
Tetralogy of Fallot
83
# Tetralogy of Fallot
Pathophysiology
1. Aorta starts from both RV and LV
2. This causes the pulmonary artery to stenose due to lack of space
3. Pulmonary stenosis cause RV outflow obstruction.
4.RV outflow obstruction causes RV hypertrophy
84
# Tetralogy of Fallot
Time of onset
around 6 months to show Sx
85
# Tetralogy of Fallot
Hypercyanotic spell
Severe hypoxia causes the child to squat down to relieve Sx. This increases vascular resistance. LV pressure increases and it will increase the pressure a little bit mor than RV. (reversal of R to L shunt in the VSD)
86
# Tetralogy of Fallot
Delayed Dx of a hypercyanotic spell can lead to
* MI
* CVA
* Fatal
87
# Tetralogy of Fallot
Sx of hypercyanotic spell
* Sudden increase of central cyanosis
* Irritable child
* Inconsolable child
* Breathlessness
88
# Tetralogy of Fallot
Late Sx
Clubbing of toes and fingers
89
# Tetralogy of Fallot
Murmur
Loud harsh ejection systolic murmur at the left sternal edge from day 1
90
# Tetralogy of Fallot
Sx of RV hypertrophy
* RV heaving
* Epigastric pulsations
91
# Tetralogy of Fallot - T/F
1. Heart failure is common
2. Hypercyanotic spell is seen in late infancy.
3. VSD and Pulmonary stenosis murmurs can both be heard
4. Hypercyanotic spell can occur during inflammation and infections.
1. F
2. T
3. F (Only pulmonary stenosis)
4. T
92
# Tetralogy of Fallot
why is heart failure rare
For HF to occur there should be an overload of blood to the lungs. Here there is a pulmonary stenosis
93
# Tetralogy of Fallot
VSD murmur is not heard
Not much heard because it is a large defect
94
# Tetralogy of Fallot
The pulmonary stenosis murmur is not heard during a hypercyanotic spell.
Coz there's little to no blood through the pulmonary valve
95
# Tetralogy of Fallot
Dx
* CXR
* ECG
* Echo
96
# Tetralogy of Fallot
CXR findings
* Boot- shaped heart due to RVH
* Pulmonary oligemia (Black lungs)
97
# Tetralogy of Fallot
ECG findings
* RAD
98
# Tetralogy of Fallot
Echo findings
The 4 cardinal features
* Overriding aorta
* Pulmonary stenosis
* Large VSD
* RVH
99
Minimum SpO2 levels
at least 92%
100
# Tetralogy of Fallot
Mx of an acute hypercyanotic spell
* Knee chest position
* Give O2
* IV morphine
* IV/ PO propranolol
* IV fluids
* Bicarbonates
101
# Tetralogy of Fallot
When should you intervene during a hypercyanotic spell
usually they are self- limiting. But if it>15 minutes should intervene
102
# Tetralogy of Fallot
Purpose of knee- chest position
Increase vascular resistance and this will inturn increase the pressure in the LV. If the pressure in LV> RV the reversal of right to left shunt in VSD can reduce cyanosis
103
# Tetralogy of Fallot
purpose of IV morphine during a Mx of an acute hypercyanotic spell
Sedation
Pain relief
Venodilation
104
# Tetralogy of Fallot
Why is venodilation important during Mx of hypercyanotic spell
Reduce the blood entry to RA and in turn reduce the blood volume and pressure in RV.
105
# Tetralogy of Fallot
Usage of propranolol in Mx of hypercyanotic spell
* Work as a peripheral vasoconstrictor
* Relieve subpulmonary muscular obstruction
106
# Tetralogy of Fallot
Usage of bicarbs in the Mx of hypercyanotic spell
To prevent the lactic acid buildup which act as a vasodilator. (Vasodilation reduce pressure in the LV) LA is formed during hypoxia because of cyanosis
107
# Tetralogy of Fallot
Long term Mx of Very cyanosed babies
BT shunt
108
# Tetralogy of Fallot
* BT shunt
* Balloon dilatation of the RVOT
artifical tube connecting the subclavian artery and the pulmonary artery
109
# Tetralogy of Fallot
Definitive surgery
at around 6 months (~10kg)
* Close the VSD
* relieve the RVOT obstruction
110
# Tetralogy of Fallot
BT scar location
Under the left scapula on the back
111
commonest cause of cyanosis AT BIRTH/ FEW DAYS AFTER BIRTH
Transposition of great vessels
112
# Transposition of great vessels
Pathophysiology
aorta is connected to the RV and the pulmonary artery is connected to the LV
113
# Transposition of great vessels
Only situation this condition is compatible with life
associated with ASD, VSD or PDA
Having a patent ductus is essential.
114
# Transposition of great vessels
Sx
* Cyanosis within 2 days after birth
* Loud single second heart sound (No physiological splitting if 2nd HS)
115
# Transposition of great vessels
Ix
* CXR- egg on side appearance
* Echo
* ECG- RVH, RAD
116
# Transposition of great vessels
Immediate Mx
Give prostaglandin to keep the ductus open to buy time
117
# Transposition of great vessels
Surgical Mx
* Balloon atrial septostomy
* Arterial switch
118
# Tricuspid atresia
Pathophysiology
* No tricuspid valve
* Blood doesn't enter the RV
* RV is virtually useless
* LV undergoes hypertrophy
119
# Tricuspid atresia
How is Tricuspid atresia compatible with life
If there is
* A ductus
* An ASD+ VSD
120
# Tricuspid atresia
Mx
* BT shunt
* Total correction is not possible
* Palliative surgery - fontan or Glenn operation
121
The cyanotic congenital HD with LAD
Tricuspid atresia
122
# Total anomalous pulomary venous drainage
Subtypes
* Supra- cardiac TAPVD
* Cardiac type TAPVD
* Infra- cardiac TAPVD
123
# TAPVD
Pathophysiology
The pulmonary vein drains into either the IVC, SVC or the Right atrium
124
# TAPVD
Dx
* ECG- RAD
* Echo
* CXR
125
# TAPVD
CXR findings
* Pulmonary plethora ( more blood to lungs)
* Cardiomegaly
* Snowman appearance/ figure of 8 appearance
126
# TAPVD
Mx
Surgical correction of the anatomical abnormality and connect the pulmonary vein to the LA
127
# Truncus arteriosus
Defect in
Spiral septum incompletely seperated into the aorta and pulmonary vein.
Both connected to eachother at the beginning before seperating as individual vessels
128
# Truncus arteriosus
Complications
* cyanosis
* Bi- ventricular failure
129
5yr old child presents with fever >7days, Cold with runny nose, lump on neck, Irritable and with a red colored tongue. What's the most likely diagnosis?
Kawasaki Disease
130
# Kawasaki Disease
Pathophysiology
A systemic Vasculitis.
Due to immune hyperactivity to a variety of triggers in a genetically susceptible host.
131
# Kawasaki Disease
Affects children of what age?
6M to 5Yrs
Peak at the end of the first year
132
# Kawasaki Disease
Most serious complication is
Coronary artery aneurysms
133
# Kawasaki Disease
C/F
Fever for >5days, child will be irritable
+4 of the following features
* Conjunctivitis - Non-purulent
* Mucous membrane changes - Pharngeal injection (Red throat), red, dry and cracked lips, strawberry tongue.
* Unilateral Cervical Lympadenopathy
* Polymorphous rash - rashes of different nature
* Red and oedematus palms and soles/ peeling of finger and toe skin.
There maybe inflammation at the BCG vaccination site (L/Deltoid)
134
# Kawasaki Disease
Ix
FBC - Increased WBC (Neutrophils during 1st week of illness, Increased platelets in 2nd to 3rd weeks (Late feature)) Platelets will be low/N in the 1st week.
Increased ESR and CRP
Echo - May show aneurysms of coronary arteries in prolonged untreated illness.
Hb will drop a bit.
135
# Kawasaki Disease
Rx
Decrease inflammation and prevent thrombosis
* Prompt Rx with IVIg given within the first 10 days lowers the risk of Coronary artery aneurysms. By reducing inflammation.
* Aspirin to reduce the risk of thrombosis.
* If child does not respond to Ig, steroids can be given.
136
# Kawasaki Disease
Complications
CVS signs,
* Gallop rhythm - when child goes into HF
* Myocarditis, pericarditis
* Coronary and peripheral aneurysms
* Sudden death
137
# Kawasaki Disease
How can a dx of myocarditis be made?
Check cardiac enzymes - they will be elevated
Creatine phosphokinase
Echo will show signs of HF - Ejection fraction decreased.
Difficulty in breathing
138
# Kawasaki Disease
Cost of a IVIg vial in SL
Around 50K
139
# Dilated cardiomyopathy
Problem in
A large, poorly contracting heart.
Abnormally relaxed.
Impaired systole
140
# Dilated cardiomyopathy
Causes
* Inherited
* Secondary to metabolic disease or storage disease
* May result from a direct viral infection of the myocardium - Dengue, cox-sackie A
It should be suspected in any child with an enlarged heart and HF who has previously been well
141
# Dilated cardiomyopathy
Dx
Echo
Elevated cardiac enzymes
142
# Dilated cardiomyopathy
Rx
Symptomatic Rx for HF - Oxygen, other drugs like frusemide
Role of steroids and Immunoglobulins is controversial.
Myocarditis usually improves spontaneously, but sometimes children require heart transplantation.
143
Different types of cardiomyopathy
1. Dilated - Abnormally relaxed heart. Impaired systole
2. Hypertrophic - Heart muscle increase in size, not enough space to accomodate blood.
3. Restrictive - Heart does not relax enough, diastole is impaired.
144
# Dilated cardiomyopathy
Is heart transplantation done in SL?
Yes.
Not done in pediatrics yet.
145
# Cyanosis
Definition
Blue discoloration occuring due to deoxygenated Hb in blood >5g/dl
146
# Cyanosis
Types
1. Peripheral - Blueness of the hands, feet and lips. Due to constricted vessels maybe when exposed to cold weather. Or due to being unwell from any cause (Eg: circulatory collpase) or with polycythemia.
2. Central - Seen on the tongue as a slate blue color, is associated with a fall in arterial blood oxygen tension. (Central cyanosis is very significant).
147
# Cyanosis
Visible when
Recognised clinically if the concentration of reduced Hb exceeds 5g/dl.
>5g/dl of total Hb is deoxygenated leads to visible cyanosis to naked eye.
148
# Cyanosis
More prominent/highest chance of getting in a polycythemic patient with 18g/dl of Hb or in an anemic patient with 8g/dl of Hb?
In the polycythemic patient
149
# Cyanosis
Persistent cyanosis in an otherwise well infant is nearly always a sign of?
Structural Heart disease.
150
# Cyanosis
Causes of cyanosis in a newborn infant with respiratory distress (RR>60)
1. Cardiac disorders - Cyanotic congenital heart disease
2. Respiratory diseases - Surfactant defciency, meconium aspiration, pulmonary hypoplasia
3. Persistent Pulmonary HTN of the newborn (PPHN) - Failure of the pulmonary vascular resistance to fall after birth.
4. Infections - Septicemia from Group B strep and other organisms
5. Metabolic disease - Metabolic acidosis and shock
151
# Cyanosis
Test to differentiate between cardiac and respiratory causes
Hyperoxia Test (Nitrogen washout) - High concentration of oxygen will be given to the child and observed whether the cyanosis will disappear.
If it disappears, Its a problem in the lungs.
If not its a Cardiac problem.
152
# Congenital Heart Diseases
Types of acyanotic congenital heart diseases
* VSD - 30%
* PDA - 12%
* ASD - 7%
* Pulmonary stenosis
* Coarctation of aorta
* Aortic stenosis
153
# Congenital Heart Diseases
Most common in children
VSD
154
# Venticular Septal Defect (VSD)
Types
1. Perimembranous - adjacent to the tricuspid valve. More commoner and generally needs surgery.
2. Muscular - Completely surrounded by muscle
155
# Venticular Septal Defect (VSD)
Pathophysiology
* L to R shunt is present.
* When pulmonary vascular resistance falls after about 4 to 6W of birth, Blood flows from LV to RV.
* More blood in pulmonary arteries (Pulmonary plethora), more blood in lungs (Causing Pulmonary edema, breathlessness (due to Impaired gas exchange) and **recurrent infections**)
* More blood drains into LV from pulmonary veins, LV overload and with time results in HF.
* If not Rx, with time pulmonary arterial resistance increases to cope up with the increased flow, causing Pulmonary HTN (therefore RV failure.
* Reversal of shunt leading to Eisenmenger's Xd.
* By the time of Eisenmenger's Xd, child will get following features - Cyanosis, Finger Clubbing.
156
# Venticular Septal Defect (VSD)
At birth, there might not be a L to R shunt, why?
At birth, Pulmonary resistance is high.
157
# Venticular Septal Defect (VSD)
There maybe a period of no recurrent infections, Why?
Due to increased pulmonary resistance and decreased pulmonary blood flow. Therefore the lungs will no longer be wet and will not facillitate infections.
158
# Venticular Septal Defect (VSD)
Rx for Eisenmenger Xd
Heart-Lung transplant
(Min. Rs.10Million)
Still might not recover completely.
Organ rejection.
159
# Venticular Septal Defect (VSD)
Murmur during Eisenmenger Xd
Murmur may disappear and come again later.
When RV pressure = LV pressure, murmur can disappear.
160
# Venticular Septal Defect (VSD)
Cut off for small and large VSD
Small VSD - Smaller than the aortic valve in diameter, perhaps upto 3mm.
Large VSD - Defects are the same size or bigger than the aortic valve.
161
# Venticular Septal Defect (VSD)
Sx and Signs of a small VSD
Asymptomatic
Physical signs -
* **Loud pansystolic murmur** at Lower sternal edge (Loud murmur implies smaller defect)
* Normal Pulmonary second sound (P2) since there is no pulmonary HTN
162
# Venticular Septal Defect (VSD)
Sx and signs of a large VSD
Sx -
* HF with breathlessness and failure to thrive
* Recurrent Chest infections - Because lungs get wet due to increased pulmonary blood flow.
Physical Signs -
* Tachypnoea, tachycardia, enlarged tender liver from HF.
* Active precordium - Visible heartbeat
* **Soft pansystolic murmur**
* **Loud pulmonary second sound (P2)** due to pulmonary HTN
163
# Venticular Septal Defect (VSD)
Ix of small defect
Normal Chest X-ray and ECG
Echo - shows the anatomy of the defect
164
# Venticular Septal Defect (VSD)
Ix of large defect
Chest X-ray -
* Cardiomegaly
* Enlarged pulmonary arteries - Pulmonary plethora. White phase (Lungs are normally black on Xray, but here lungs appear white due to increased blood flow and the lungs being wet)
* Increased pulmonary markings
* Pulmonary edema
ECG - Biventricular hypertrophy by 2M of age
Echo - Shows the anatomy of the defect, Hemodynamic effects and Pulmonary HTN
165
# Venticular Septal Defect (VSD)
Mx of small defect
Will close spontaneously - takes upto 6yrs
While VSD is present, Bacterial endocarditis must be prevented by maintaining good dental hygiene.
Follow up 6 monthly to detect if it closes or whether pulmonary HTN develops.
166
# Venticular Septal Defect (VSD)
Mx of Large defect
Drug therapy for HF - Frusemide
Additional calorie input
Surgery is usually needed,
* Mx HF and failure to thrive
* Prevent permenant lung damage from pulmonary HTN and high blood flow
167
# Venticular Septal Defect (VSD)
Complications of large VSD
1. HF
2. Pulmonary HTN
3. Recurrent chest infections
4. Infective Endocarditis
5. Failure to thrive
168
# Atrial Septal Defect (ASD)
Cause
Occurs commonly due to failure of closure of foramen ovale after birth. There are several other reasons as well.
169
# Atrial Septal Defect (ASD)
Types
1. Primum ASD - More dangerous as surgical repair is difficult. Defect of the AV septum and is characterised by,
* An inter-atrial communication between the bottom end of the atrial septum and the AV valves.
* Abnormal AV valves (with a left AV valve which has 3 leaflets and tends to leak - Regurgitant valve)
2. Secondum ASD - Defect in the centre of the atrial septum involving the foramen ovale. 80% of ASDs. Less dangerous.
170
# Atrial Septal Defect (ASD)
C/F, Signs and Sx of both types
C/F - Similar in both
Sx -
* None (Commonly)
* Recurrent chest infections (In large defects)
* Arrythmias
Physical Signs -
* An **ejection systolic murmur** best heard at the upper left sternal edge (Pulmonary Area) - Due to increased blood flow across the Pulmonary Valve, not due to the blood flow through the defect.
* A fixed and widely split second heart sound - due to the Right ventricular stroke volume being equal in both inspiration and expiration (RV blood flow is high in both Inspiration/ Expiration).
* With a primum AtrioVentricular septal defect, an apical pansystolic murmur from AV valve regurgitation.
171
# Atrial Septal Defect (ASD)
Ix
1. Echo - Diagnostic
2. CXR - Cardiomegaly, enlarged pulmonary arteries and increased pulmonary vascular markings. Similar to VSD.
3. ECG -
In Primum ASD: A superior QRS axis. RBBB. Left axis deviation/ Superior axis deviation.
In Secondum ASD: Partial RBBB, Right axis deviation due to RV hypertrophy.
172
# Atrial Septal Defect (ASD)
Mx
Primum ASD - Surgical correction (Open) done at 3-5yrs of age.
Secondum ASD - Cardiac catheterisation with insertion of an occlusion device if the defect is large. Device closure.
ASD generally don't close spontaneously.
173
Features of Right ventricular hypertrophy
Epigastric Pulsation
Right ventricular heave
174
Why is there a splitting of S2 in ASD but not in VSD?
In ASD, Blood flow through pulmonary valve is slow.
In VSD, Blood flow through pulmonary valve is fast.
175
What is the Aortic pressure and Pulmonary pressure?
Aortic - 120/80
Pulmonary - 25/8
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# Patent Ductus Arteriosus (PDA)
Pathophysiology
Ductus arteriosus connects the pulmonary artery to the descending aorta. In term infants, it normally closes within **96hrs** after birth.
In persistent ductus arteriosus it has failed to close by 1M due to a defect in the constrictor mechanism of the duct. Common in pre-term babies.
Blood flow in a PDA is from the aorta to the pulmonary artery (Left to right), following the fall of pulmonary vascular resistance after birth.
There is no cyanosis.
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# Patent Ductus Arteriosus (PDA)
Sx and Signs
Sx - Not common. But when the duct is large there will be increased pulmonary blood flow with HF and Pulmonary HTN, wet lungs, recurrent infections (Mechanism similar to VSD).
Signs -
* **Continous machine like murmur ** beneath the L/Clavicle.
* Collapsing or bounding pulse (due to increased pulse pressure). High volume pulse.
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# Patent Ductus Arteriosus (PDA)
Why is the murmur continuous?
Murmur continues into diastole because the pressure in the pulmonary artery is lower than that in the aorta throughout the cardiac cycle.
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# Patent Ductus Arteriosus (PDA)
Ix
Echo - Dx
CXR and ECG - Usually normal, but if the PDA is large, features similar to VSD such as cardiomegaly.
180
# Patent Ductus Arteriosus (PDA)
Mx
Indomethazine - a NSAID (Prostaglandin Inhibitor)
Closure with a coil or occlusion device introduced via a cardiac catheter at about 1yr of age - Coil embolization (To prevent pulmonary HTN, bacterial endocarditis, etc.)
Occasionally surgical ligation is required - suturing ductus srterious via open heart surgery.
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# Patent Ductus Arteriosus (PDA)
In what condition is the ductus arterious maintained patent? How?
In cyanotic heart diseases.
By means of prostaglandins.
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# Patent Ductus Arteriosus (PDA)
Can eisenmenger Xd occur?
Theoretically possible.
Rare
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What is the commonest cause of collapse due to L/ventricular outflow obstruction?
Coarctation of Aorta (COA)
184
# Coarctation of Aorta (COA)
Pathophysiology
Due to ductus arteriosus tissue encircling aorta just at the point of insertion of the duct. So when the duct closes after birth, the aorta also constricts, causing severe obstruction to the L/ventricular outflow.
i.e.
If ductal closure at birth is not smooth, it will drag aorta down with it causing constriction.
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# Coarctation of Aorta (COA)
It is an example of duct dependant circulation. T/F?
T
186
# Coarctation of Aorta (COA)
C/F
Neonates usually present with acute circulatory collapse at 2 to 4 days of age when the duct closes.
Physical signs -
* A sick baby, with severe HF - Difficulty in breathing, head sweating, tender hepatomegaly.
* Absent or weak femoral pulses.
* Severe metabolic acidosis - Decreased tissue oxygenation causing lactic acid formation.
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# Coarctation of Aorta (COA)
Dx
Echo
Radio-femoral delay
Upper Limb HTN
Lower Limb low BP
CXR- LVH, figure of 3 appearance
188
# Coarctation of Aorta (COA)
Mx
1. First Resuscitate (ABC)
2. Prostaglandin should be commenced at the earliest opportunity to keep the ductus arteriosus patent - Beneficial in pre-ductal COA
3. Referral for cardiac surgery as soon as possible.
Baloon aortic dialation by paediatric cardiologist.
Cut constriction & end-to-end anastomosis done by cardio-thoracic surgeon.
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# Coarctation of Aorta (COA)
Adult type C/F
* Not duct dependant
* Gradually becomes more severe over many years.
* Asymptomatic
* Systemic HTN in the R/Arm - COA after subclavian artery
* **Ejection systolic murmur** at upper sternal edge radiating to back - Aortic direction.
* Collaterals heard with continuous murmur at the back.
* Radio-femoral delay. This is due to blood bypassing the obstruction via collateral vessels in the chest wall and hence the pulse in the legs is delayed.
* Femoral pulses are weaker.
* Discrepancy in BP in UL and LL (UL Bp>LL BP)
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Examples of outflow obstruction in a well looking child
Adult type COA
Aortic stenosis
Pulmonary stenosis
191
# Coarctation of Aorta (COA)
Collateral blood vessels
Intercoastal arteries
Inferior epigastric artery
192
# Coarctation of Aorta (COA)
Ix of adult type
* Chest radiograph - in small babies, will be normal.
Rib notching - due to development of large collateral intercostal arteries running under the ribs posteriorly to bypass the obstruction.
Figure of 3 sign with visible notch in the descending aorta at site of coarctation.
* ECG
L/Ventricular hypertrophy due to LV overload - Tall R waves in V5, V6. Deep S waves in V1, V2.
* Echo
193
# Coarctation of Aorta (COA)
Mx of adult type
When the condition becomes severe, as assessed by echo, a stent may be inserted at cardiac catheter, baloon dialation can also be done.
Sometimes surgical repair is required.
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# Pulmonary Stenosis
C/F
* **Ejection systolic murmur** at pulmonary area, will radiate to the back and sometimes to the neck as well.
* Soft 2nd heart sound - due to decreased blood flow through Pulmonary artery.
* Associated with Noonan's Xd.
195
# Pulmonary Stenosis
Ix
Echo
ECG - Right axis deviation
X-ray - Right ventricular hypertrophy
196
# Pulmonary Stenosis
Mx
Baloon dilation of pulmonary valve
Surgical correction
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# Pulmonary Stenosis
Does it cause cyanosis?
Generally does not cause cyanosis, but if blood flow to lungs is severely obstructed (Very severe pulmonary stenosis), can lead to cyanosis.
198
# Aortic stenosis
C/F
1. **Ejection systolic murmur** at aortic area, will radiate to the neck (carotid artery)
2. Weak pulse volume
3. Aortic component of 2nd heart sound will be soft (A2)
4. BP normal unless very severe stenosis.
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# Aortic stenosis
Dx
Echo
ECG - Left axis deviation, evidence of L/ventricular hypertrophy.
X-ray - Cardiomegaly, L/Ventricular hypertrophy
200
# Aortic stenosis
Mx
Baloon dialation of AV or surgical correction
201
# Congenital Heart Disorders
Maternal disorders and associated cardiac abnormalities
* Rubella infection - Pulmonary stenosis, PDA
* SLE - Complete heart block
* DM - Overall incidence of cardiac abnormalities. cardiac septal hypertrophy (settles with time)
202
# Congenital Heart Disorders
Maternal drugs and associated cardiac abnormalities
* Warfarin therapy - Pulmonary stenosis, PDA
* Fetal alcohol Xd - ASD, VSD, TOF
203
# Congenital Heart Disorders
Chromosomal abnormalities and associated cardiac abnormalities
* Down's Xd (trisomy 21) - AVSD, VSD, MV, Tricuspid valve
* Edward Xd (trisomy 18) - Complex heart disease
* Patau Xd (trisomy 13) - Complex heart disease
* Turner Xd - COA, Aortic stenosis
* Noonan Xd - Pulmonary stenosis, HOCM
* Marfan Xd - AR, MR
* Holt-oram Xd - ASD
204
# Congenital Heart Disorders
Non-cardiac abnormalities
VACTERL
* Vertebral anomalies
* Anal anomalies
* Cardiac anomalies
* Tracheo-esophageal anomalies
* Renal anomalies
* Limb anomalies
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# Heart Murmurs
Innocent murmurs hallmarks
* Asymptomatic
* A systolic murmur
* At pulmonary area or L/ upper sternal edge
* Normal heart sounds
* No parasternal thrill
* No radiation
* Changes with position
* Soft blowing murmur
206
# Heart murmurs
Causes of Innocent murmurs
Due to increased cardiac output
* Anemia
* Pregnancy
* Fever
* Thyrotoxicosis
207
# Heart Murmurs
Venous hum C/F
* Continous, low-pitched rumble
* Heard beneath either clavicle
* Due to turbulent blood flow in head and neck veins
* Dissapears on lying flat or by compression of jugular veins
208
# Heart Murmurs
Mx of functional murmurs
* Reassurance is needed and correct underlying pathology if present. Eg: Anemia
