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CARDIOLOGY Flashcards

1
Q

Fetal circulation

Fetal lungs are underdeveloped ?

A

Not used during the intrauterine life.

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2
Q

Fetal circulation

Fetal organ involved in gas exchange

A

Placenta

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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)
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4
Q

Fetal circulation

The pressure in the LA and RA

A

RA>LA (Lungs are sending little to no blood to the LA)

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5
Q

Fetal circulation

Right atrium recieves blood from

A
  • Venous blood from fetal systemic circulation
  • blood coming from the placenta
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6
Q

Fetal circulation

Fetal circulation has… which is not seen in adult circulation

A
  • Ductus venosus
  • Ductus arteriosus
    Foramen ovale
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7
Q

Fetal circulation

Foramen ovale is located

A

between the LA and RA

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8
Q

Fetal circulation

Ductus arteriosus is connected between

A

the pulmonary artery and the descending aorta

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9
Q

Fetal circulation

Fetal hypoxia causes

A

increased production of EPO

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10
Q

Cardiac cycle

Systole lasts… of the cardiac cycle

A

2/3

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11
Q

Cardiac cycle

Diastole lasts….of the cardiac cycle

A

1/3

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12
Q

Cardiac cycle

When the HR increases what happens to the diastole

A

Diastole shortens

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13
Q

Cardiac cycle

Mitral and tricuspid valves close during

A

Systole

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14
Q

Cardiac cycle

Aortic valve closes… than the pulmonary valve

A

earlier

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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

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16
Q

Cardiac cycle

Stroke volume

A

amount of blood pumped during a single contraction

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17
Q

Cardiac cycle

Ejection fraction

A

Percentage of blood pumped from each ventricle (~60-70%)

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18
Q

Cardiac cycle

Cardiac output

A

Amount of blood pumped out calculated per minute
CO=SVxHR

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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

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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

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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
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22
Q

Neonatal circulation

Regurgitation of Mitral and tricuspid valves causes…… murmurs

A

Systolic murmurs

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23
Q

Neonatal circulation

Stenosis of mitral and tricuspid valves causes….. murmurs

A

Diastolic Murmurs

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24
Q

Neonatal circulation

Regurgitation of aortic and pulmonary valves causes……. Murmurs

A

Diastolic Murmurs

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25
Q

Neonatal circulation

Stenosis of Aortic and pulmonary valves causes…… murmurs

A

Systolic murmurs

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26
Q

Rheumatic fever

Age group

A

5-15

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27
Q

Rheumatic fever

MO causing Rheumatic fever

A

Group A beta- hemolytic streptococcus

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28
Q

Rheumatic fever

Pathophysiology of Rheumatic fever

A

Abnormal immune response to a preceding infection with group A beta- hemolytic streptococcus

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29
Q

Rheumatic fever

Rheumatic fever diagnostic criteria

A

Modified Duckett- Jones criteria

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30
Q

Rheumatic fever

Major criteria

A
  • Migratory polyartheritis
  • Carditis
  • Sydenham chorea
  • Erythema marginatum
  • Subcutaneous nodules
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31
Q

Rheumatic fever

Minor criteria

A
  • Fever
  • Polyarthralgia
  • Raised ESR, CRP
  • Prolonged P-R interval
  • History of Rheumatic fever
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32
Q

Rheumatic fever

Dx of Rheumatic fever

A
  • 2 major OR
  • 1 major + 2 minor
    +
  • supportive evidence of preceding Group A streptococcal infection
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33
Q

Rheumatic fever

Supportive evidence of preceding Strep infection

A
  • markedly rasied ASOT
  • Strep Antibodies
  • Group A strep throst swab culture
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34
Q

Rheumatic fever

Joints involved in migratory polyarthritis

A

Large joints such as
* ankles
* Knees
* wrists

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35
Q

Rheumatic fever

Features of migratory polyarthritis

A
  • Tenderness
  • Moderate redness and swelling
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36
Q

Rheumatic fever

How long does the arthritis last in one joint and when does it migrate

A

<1 week in one joint and migrate over 1-2 months

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37
Q

Rheumatic fever

Pancarditis involves

A
  • Endocarditis
  • Myocarditis
  • Pericarditis
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38
Q

Rheumatic fever

Mumur in endocarditis

A

Mid- diastolic murmur ( Carey Coomb murmur due to swelling of mitral valve)

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39
Q

Rheumatic fever

Valvular dysfunction is due to

A

endocarditis

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40
Q

Rheumatic fever

Myocarditis leads to

A
  • Heart failure and death
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41
Q

Rheumatic fever

Pericarditis involves

A
  • Pericardial friction rub
  • Effusion
  • Tamponade
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42
Q

Rheumatic fever

Late manifestation in Rheumatic fever

A

Sydenham chorea

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43
Q

Rheumatic fever

Sydenham chorea occurs after

A

2-6 months after the strep infection

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44
Q

Rheumatic fever

Sydenham chorea consists of

A
  • Involuntary movements
  • Emotional lability
  • lasts 3-6 months
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45
Q

Rheumatic fever

Erythema marginatum is common. (T/F?)

A

False

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46
Q

Rheumatic fever

Erythema marginatum is seen on

A

Trunk and limbs

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47
Q

Rheumatic fever

Describe the appearance of erythema marginatum

A

Pink macules spread outwards, causing pink border with fading centre. Borders may unite to give a map-like outline

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48
Q

Rheumatic fever

Subcutaneous nodules are seen mainly on

A

Extensor surfaces

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49
Q

Rheumatic fever

Subcutaneous nodules appearance

A

Painless, pea-sized, hard

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50
Q

Rheumatic fever

Rheumatic fever occurs 2 weeks after a

A

pharyngeal infection

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51
Q

Rheumatic fever

All Rheumatic fever patients have a positive ASOT (T/F?)

A

F (only 80-85%)

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52
Q

Rheumatic fever

Chronic Rheumatic fever mainly affects

A

Mitral stenosis (scarring and fibrosis)

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53
Q

Rheumatic fever

The least common valve affected in Rheumatic fever

A

Pulmonary valve

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54
Q

Rheumatic fever

Mx of an acute Rheumatic fever episode

A
  • Admit
  • Bed rest
  • Aspirin
  • Steroids - if carditis or heart failure
  • Stop steroids- if only arthralgia
  • ABx (Oral penicillin or IM Benzathine penicillin)
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55
Q

Rheumatic fever

Usage of aspirin

A

NSAID. stop inflammation of the joints and the heart

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56
Q

Rheumatic fever

Anti- streptococcal ABx dose

A
  • Oral penicillin 10 days
    OR
  • IM benzathine penicillin single dose
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57
Q

Rheumatic fever

When will the anti streptococcal ABx be given

A

if there’s any evidence of persisting infections

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58
Q

Rheumatic fever

Most effective prophylaxis

A

2 weekly injections of benzathine penicillin or oral penicillin

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59
Q

Rheumatic fever

Issue with oral penicillin prophylaxis

A

poor compliance

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60
Q

Rheumatic fever

substitute to penicillin allergic patients

A

oral erythromycin

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61
Q

Rheumatic fever

Length of prophylaxis of only Rheumatic fever

A

for 5 years or until 21 years of age ( whichever is longer)

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62
Q

Rheumatic fever

Length of prophylaxis of Rheumatic fever + cardits

A

for 10 years or until 25 years of age ( whichever is longer)

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63
Q

Rheumatic fever

Length of prophylaxis of Rheumatic fever with residual heart disease

A

for 10 years or until 40 years of age ( whichever is longer) or even lifelong

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64
Q

Rheumatic fever

Complication of Rheumatic fever

A

chronic valve disease therefore getting infective endocarditis

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65
Q

infective endocarditis

infective endocarditis

A

inflammation of the endocardium due to alpha- hemolytic streptococcus

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66
Q

infective endocarditis

MO

A

Streptococcus viridans

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67
Q

infective endocarditis

Risk factors

A
  • congenital heart disease (except ostium secundum ASD)
  • Patients with prosthetic valves
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68
Q

infective endocarditis

Diagnostic criteria

A

Modified duke criteria

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69
Q

infective endocarditis

Major criteria of duke criteria

A
  • 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
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70
Q

infective endocarditis

Minor criteria of duke criteria

A
  • 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
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71
Q

infective endocarditis

Dx of infective endocarditis

A

2 major criteria/ 1 major+ 3 minor/ 5 minor

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72
Q
A
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73
Q

infective endocarditis

Ix of infective endocarditis

A
  • Blood culture- before ABx
  • Echo
  • ESR, CRP
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74
Q

infective endocarditis

Mx of infective endocarditis

A

IV ABx for 4-6 weeks ( penicillin + gentamicin)

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75
Q

infective endocarditis

Main prophylactic step

A

Good dental hygiene

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76
Q

infective endocarditis

ABx prophylaxis is given on

A
  • dental treatment
  • surgery
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77
Q

Child with fever and new- onset murmur

A

Infective endocarditis

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78
Q

infective endocarditis

complications

A
  • Heart failure ( If aortic/ mitral V is involved)
  • Myocardial abscess
  • Myocarditis
  • Life- threatening arrythmia
  • systemic emboli ( with CNS Sx)
  • Pulmonary emboli ( With VSD, TOF)
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79
Q

infective endocarditis

ADRS of gentamicin

A

nephrotoxic
Ototoxic

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80
Q

Cyanotic Heart disease

ToF consists of

A
  • Overriding aorta
  • Pulmonary stenosis
  • Large VSD
  • RV hypertrophy
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81
Q

Tetralogy of Fallot

Overriding aorta?

A

Aorta starts from both RV and LV chambers

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82
Q

Most common cyanotic congenital HD

A

Tetralogy of Fallot

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83
Q

Tetralogy of Fallot

Pathophysiology

A
  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
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84
Q

Tetralogy of Fallot

Time of onset

A

around 6 months to show Sx

85
Q

Tetralogy of Fallot

Hypercyanotic spell

A

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
Q

Tetralogy of Fallot

Delayed Dx of a hypercyanotic spell can lead to

A
  • MI
  • CVA
  • Fatal
87
Q

Tetralogy of Fallot

Sx of hypercyanotic spell

A
  • Sudden increase of central cyanosis
  • Irritable child
  • Inconsolable child
  • Breathlessness
88
Q

Tetralogy of Fallot

Late Sx

A

Clubbing of toes and fingers

89
Q

Tetralogy of Fallot

Murmur

A

Loud harsh ejection systolic murmur at the left sternal edge from day 1

90
Q

Tetralogy of Fallot

Sx of RV hypertrophy

A
  • RV heaving
  • Epigastric pulsations
91
Q

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.
A
  1. F
  2. T
  3. F (Only pulmonary stenosis)
  4. T
92
Q

Tetralogy of Fallot

why is heart failure rare

A

For HF to occur there should be an overload of blood to the lungs. Here there is a pulmonary stenosis

93
Q

Tetralogy of Fallot

VSD murmur is not heard

A

Not much heard because it is a large defect

94
Q

Tetralogy of Fallot

The pulmonary stenosis murmur is not heard during a hypercyanotic spell.

A

Coz there’s little to no blood through the pulmonary valve

95
Q

Tetralogy of Fallot

Dx

A
  • CXR
  • ECG
  • Echo
96
Q

Tetralogy of Fallot

CXR findings

A
  • Boot- shaped heart due to RVH
  • Pulmonary oligemia (Black lungs)
97
Q

Tetralogy of Fallot

ECG findings

98
Q

Tetralogy of Fallot

Echo findings

A

The 4 cardinal features
* Overriding aorta
* Pulmonary stenosis
* Large VSD
* RVH

99
Q

Minimum SpO2 levels

A

at least 92%

100
Q

Tetralogy of Fallot

Mx of an acute hypercyanotic spell

A
  • Knee chest position
  • Give O2
  • IV morphine
  • IV/ PO propranolol
  • IV fluids
  • Bicarbonates
101
Q

Tetralogy of Fallot

When should you intervene during a hypercyanotic spell

A

usually they are self- limiting. But if it>15 minutes should intervene

102
Q

Tetralogy of Fallot

Purpose of knee- chest position

A

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
Q

Tetralogy of Fallot

purpose of IV morphine during a Mx of an acute hypercyanotic spell

A

Sedation
Pain relief
Venodilation

104
Q

Tetralogy of Fallot

Why is venodilation important during Mx of hypercyanotic spell

A

Reduce the blood entry to RA and in turn reduce the blood volume and pressure in RV.

105
Q

Tetralogy of Fallot

Usage of propranolol in Mx of hypercyanotic spell

A
  • Work as a peripheral vasoconstrictor
  • Relieve subpulmonary muscular obstruction
106
Q

Tetralogy of Fallot

Usage of bicarbs in the Mx of hypercyanotic spell

A

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
Q

Tetralogy of Fallot

Long term Mx of Very cyanosed babies

108
Q

Tetralogy of Fallot

  • BT shunt
  • Balloon dilatation of the RVOT
A

artifical tube connecting the subclavian artery and the pulmonary artery

109
Q

Tetralogy of Fallot

Definitive surgery

A

at around 6 months (~10kg)
* Close the VSD
* relieve the RVOT obstruction

110
Q

Tetralogy of Fallot

BT scar location

A

Under the left scapula on the back

111
Q

commonest cause of cyanosis AT BIRTH/ FEW DAYS AFTER BIRTH

A

Transposition of great vessels

112
Q

Transposition of great vessels

Pathophysiology

A

aorta is connected to the RV and the pulmonary artery is connected to the LV

113
Q

Transposition of great vessels

Only situation this condition is compatible with life

A

associated with ASD, VSD or PDA
Having a patent ductus is essential.

114
Q

Transposition of great vessels

Sx

A
  • Cyanosis within 2 days after birth
  • Loud single second heart sound (No physiological splitting if 2nd HS)
115
Q

Transposition of great vessels

Ix

A
  • CXR- egg on side appearance
  • Echo
  • ECG- RVH, RAD
116
Q

Transposition of great vessels

Immediate Mx

A

Give prostaglandin to keep the ductus open to buy time

117
Q

Transposition of great vessels

Surgical Mx

A
  • Balloon atrial septostomy
  • Arterial switch
118
Q

Tricuspid atresia

Pathophysiology

A
  • No tricuspid valve
  • Blood doesn’t enter the RV
  • RV is virtually useless
  • LV undergoes hypertrophy
119
Q

Tricuspid atresia

How is Tricuspid atresia compatible with life

A

If there is
* A ductus
* An ASD+ VSD

120
Q

Tricuspid atresia

Mx

A
  • BT shunt
  • Total correction is not possible
  • Palliative surgery - fontan or Glenn operation
121
Q

The cyanotic congenital HD with LAD

A

Tricuspid atresia

122
Q

Total anomalous pulomary venous drainage

Subtypes

A
  • Supra- cardiac TAPVD
  • Cardiac type TAPVD
  • Infra- cardiac TAPVD
123
Q

TAPVD

Pathophysiology

A

The pulmonary vein drains into either the IVC, SVC or the Right atrium

124
Q

TAPVD

Dx

A
  • ECG- RAD
  • Echo
  • CXR
125
Q

TAPVD

CXR findings

A
  • Pulmonary plethora ( more blood to lungs)
  • Cardiomegaly
  • Snowman appearance/ figure of 8 appearance
126
Q

TAPVD

Mx

A

Surgical correction of the anatomical abnormality and connect the pulmonary vein to the LA

127
Q

Truncus arteriosus

Defect in

A

Spiral septum incompletely seperated into the aorta and pulmonary vein.
Both connected to eachother at the beginning before seperating as individual vessels

128
Q

Truncus arteriosus

Complications

A
  • cyanosis
  • Bi- ventricular failure
129
Q

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?

A

Kawasaki Disease

130
Q

Kawasaki Disease

Pathophysiology

A

A systemic Vasculitis.
Due to immune hyperactivity to a variety of triggers in a genetically susceptible host.

131
Q

Kawasaki Disease

Affects children of what age?

A

6M to 5Yrs
Peak at the end of the first year

132
Q

Kawasaki Disease

Most serious complication is

A

Coronary artery aneurysms

133
Q

Kawasaki Disease

C/F

A

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
Q

Kawasaki Disease

Ix

A

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
Q

Kawasaki Disease

Rx

A

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
Q

Kawasaki Disease

Complications

A

CVS signs,
* Gallop rhythm - when child goes into HF
* Myocarditis, pericarditis
* Coronary and peripheral aneurysms
* Sudden death

137
Q

Kawasaki Disease

How can a dx of myocarditis be made?

A

Check cardiac enzymes - they will be elevated
Creatine phosphokinase
Echo will show signs of HF - Ejection fraction decreased.
Difficulty in breathing

138
Q

Kawasaki Disease

Cost of a IVIg vial in SL

A

Around 50K

139
Q

Dilated cardiomyopathy

Problem in

A

A large, poorly contracting heart.
Abnormally relaxed.
Impaired systole

140
Q

Dilated cardiomyopathy

Causes

A
  • 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
Q

Dilated cardiomyopathy

Dx

A

Echo
Elevated cardiac enzymes

142
Q

Dilated cardiomyopathy

Rx

A

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
Q

Different types of cardiomyopathy

A
  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
Q

Dilated cardiomyopathy

Is heart transplantation done in SL?

A

Yes.
Not done in pediatrics yet.

145
Q

Cyanosis

Definition

A

Blue discoloration occuring due to deoxygenated Hb in blood >5g/dl

146
Q

Cyanosis

Types

A
  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
Q

Cyanosis

Visible when

A

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
Q

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?

A

In the polycythemic patient

149
Q

Cyanosis

Persistent cyanosis in an otherwise well infant is nearly always a sign of?

A

Structural Heart disease.

150
Q

Cyanosis

Causes of cyanosis in a newborn infant with respiratory distress (RR>60)

A
  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
Q

Cyanosis

Test to differentiate between cardiac and respiratory causes

A

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
Q

Congenital Heart Diseases

Types of acyanotic congenital heart diseases

A
  • VSD - 30%
  • PDA - 12%
  • ASD - 7%
  • Pulmonary stenosis
  • Coarctation of aorta
  • Aortic stenosis
153
Q

Congenital Heart Diseases

Most common in children

154
Q

Venticular Septal Defect (VSD)

Types

A
  1. Perimembranous - adjacent to the tricuspid valve. More commoner and generally needs surgery.
  2. Muscular - Completely surrounded by muscle
155
Q

Venticular Septal Defect (VSD)

Pathophysiology

A
  • 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
Q

Venticular Septal Defect (VSD)

At birth, there might not be a L to R shunt, why?

A

At birth, Pulmonary resistance is high.

157
Q

Venticular Septal Defect (VSD)

There maybe a period of no recurrent infections, Why?

A

Due to increased pulmonary resistance and decreased pulmonary blood flow. Therefore the lungs will no longer be wet and will not facillitate infections.

158
Q

Venticular Septal Defect (VSD)

Rx for Eisenmenger Xd

A

Heart-Lung transplant
(Min. Rs.10Million)
Still might not recover completely.
Organ rejection.

159
Q

Venticular Septal Defect (VSD)

Murmur during Eisenmenger Xd

A

Murmur may disappear and come again later.
When RV pressure = LV pressure, murmur can disappear.

160
Q

Venticular Septal Defect (VSD)

Cut off for small and large VSD

A

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
Q

Venticular Septal Defect (VSD)

Sx and Signs of a small VSD

A

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
Q

Venticular Septal Defect (VSD)

Sx and signs of a large VSD

A

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
Q

Venticular Septal Defect (VSD)

Ix of small defect

A

Normal Chest X-ray and ECG
Echo - shows the anatomy of the defect

164
Q

Venticular Septal Defect (VSD)

Ix of large defect

A

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
Q

Venticular Septal Defect (VSD)

Mx of small defect

A

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
Q

Venticular Septal Defect (VSD)

Mx of Large defect

A

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
Q

Venticular Septal Defect (VSD)

Complications of large VSD

A
  1. HF
  2. Pulmonary HTN
  3. Recurrent chest infections
  4. Infective Endocarditis
  5. Failure to thrive
168
Q

Atrial Septal Defect (ASD)

Cause

A

Occurs commonly due to failure of closure of foramen ovale after birth. There are several other reasons as well.

169
Q

Atrial Septal Defect (ASD)

Types

A
  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
Q

Atrial Septal Defect (ASD)

C/F, Signs and Sx of both types

A

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
Q

Atrial Septal Defect (ASD)

Ix

A
  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
Q

Atrial Septal Defect (ASD)

Mx

A

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
Q

Features of Right ventricular hypertrophy

A

Epigastric Pulsation
Right ventricular heave

174
Q

Why is there a splitting of S2 in ASD but not in VSD?

A

In ASD, Blood flow through pulmonary valve is slow.
In VSD, Blood flow through pulmonary valve is fast.

175
Q

What is the Aortic pressure and Pulmonary pressure?

A

Aortic - 120/80
Pulmonary - 25/8

176
Q

Patent Ductus Arteriosus (PDA)

Pathophysiology

A

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.

177
Q

Patent Ductus Arteriosus (PDA)

Sx and Signs

A

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.

178
Q

Patent Ductus Arteriosus (PDA)

Why is the murmur continuous?

A

Murmur continues into diastole because the pressure in the pulmonary artery is lower than that in the aorta throughout the cardiac cycle.

179
Q

Patent Ductus Arteriosus (PDA)

Ix

A

Echo - Dx
CXR and ECG - Usually normal, but if the PDA is large, features similar to VSD such as cardiomegaly.

180
Q

Patent Ductus Arteriosus (PDA)

Mx

A

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.

181
Q

Patent Ductus Arteriosus (PDA)

In what condition is the ductus arterious maintained patent? How?

A

In cyanotic heart diseases.
By means of prostaglandins.

182
Q

Patent Ductus Arteriosus (PDA)

Can eisenmenger Xd occur?

A

Theoretically possible.
Rare

183
Q

What is the commonest cause of collapse due to L/ventricular outflow obstruction?

A

Coarctation of Aorta (COA)

184
Q

Coarctation of Aorta (COA)

Pathophysiology

A

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.

185
Q

Coarctation of Aorta (COA)

It is an example of duct dependant circulation. T/F?

186
Q

Coarctation of Aorta (COA)

C/F

A

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.

187
Q

Coarctation of Aorta (COA)

Dx

A

Echo
Radio-femoral delay
Upper Limb HTN
Lower Limb low BP
CXR- LVH, figure of 3 appearance

188
Q

Coarctation of Aorta (COA)

Mx

A
  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.
189
Q

Coarctation of Aorta (COA)

Adult type C/F

A
  • 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)
190
Q

Examples of outflow obstruction in a well looking child

A

Adult type COA
Aortic stenosis
Pulmonary stenosis

191
Q

Coarctation of Aorta (COA)

Collateral blood vessels

A

Intercoastal arteries
Inferior epigastric artery

192
Q

Coarctation of Aorta (COA)

Ix of adult type

A
  • 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
Q

Coarctation of Aorta (COA)

Mx of adult type

A

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.

194
Q

Pulmonary Stenosis

C/F

A
  • 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
Q

Pulmonary Stenosis

Ix

A

Echo
ECG - Right axis deviation
X-ray - Right ventricular hypertrophy

196
Q

Pulmonary Stenosis

Mx

A

Baloon dilation of pulmonary valve
Surgical correction

197
Q

Pulmonary Stenosis

Does it cause cyanosis?

A

Generally does not cause cyanosis, but if blood flow to lungs is severely obstructed (Very severe pulmonary stenosis), can lead to cyanosis.

198
Q

Aortic stenosis

C/F

A
  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.
199
Q

Aortic stenosis

Dx

A

Echo
ECG - Left axis deviation, evidence of L/ventricular hypertrophy.
X-ray - Cardiomegaly, L/Ventricular hypertrophy

200
Q

Aortic stenosis

Mx

A

Baloon dialation of AV or surgical correction

201
Q

Congenital Heart Disorders

Maternal disorders and associated cardiac abnormalities

A
  • Rubella infection - Pulmonary stenosis, PDA
  • SLE - Complete heart block
  • DM - Overall incidence of cardiac abnormalities. cardiac septal hypertrophy (settles with time)
202
Q

Congenital Heart Disorders

Maternal drugs and associated cardiac abnormalities

A
  • Warfarin therapy - Pulmonary stenosis, PDA
  • Fetal alcohol Xd - ASD, VSD, TOF
203
Q

Congenital Heart Disorders

Chromosomal abnormalities and associated cardiac abnormalities

A
  • 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
Q

Congenital Heart Disorders

Non-cardiac abnormalities

A

VACTERL
* Vertebral anomalies
* Anal anomalies
* Cardiac anomalies
* Tracheo-esophageal anomalies
* Renal anomalies
* Limb anomalies

205
Q

Heart Murmurs

Innocent murmurs hallmarks

A
  • 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
Q

Heart murmurs

Causes of Innocent murmurs

A

Due to increased cardiac output
* Anemia
* Pregnancy
* Fever
* Thyrotoxicosis

207
Q

Heart Murmurs

Venous hum C/F

A
  • 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
Q

Heart Murmurs

Mx of functional murmurs

A
  • Reassurance is needed and correct underlying pathology if present. Eg: Anemia

PAEDIATRICS (15 decks)

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