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3a paeds > Paeds Cardio > Flashcards

Paeds Cardio Flashcards

1
Q

What is ventricular septal defect

A

most common form of heart defect

congenital hole in the septum (wall) between the two ventricles.
causes left to right shunt

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2
Q

what can severe untreated VSD lead to

A

severe pulmonary htn and early onset heart failure

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3
Q

what can moderate untreated VSD lead to

A

enlarged atria and ventricles can lead to pulmonary HTN and congestive heart failure

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4
Q

What direction does blood shunt in VSD

A

Left to right

increased pressure in left ventricle

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5
Q

how does ventricular septal defect cause pulmonary htn and heart failure

A

increased pressure in LV compared to RV -> blood flows left to right through hole = right side overload right heart failure and increased flow into pulmonary vessels -> causing pulmonary htn

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6
Q

What is Eisenmenger syndrome

A

eventually pulmonary hypertension will cause pulmonary pressure to be greater than the systemic pressure, the shunt reverses and forms a right to left shunt -> blood bypasses the lungs & patient will become cyanotic

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7
Q

what are risk factors of ventricular septal defect

A

premature birth
genetic conditions > Downs Turners Edwards Patau
family history of congenital heart defects

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8
Q

How does ventricular septal defect present?

A

often can by symptomless
tachypnoea
dyspnoea
failure to thrive

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9
Q

How does ventricular septal defect sound on auscultation?

A

pan-systolic murmur more prominently heard at the left lower sternal border in the third and fourth intercostal spaces.

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10
Q

How is VSD investigated?

A

Echo *GS
ECG
XRay - show cardiomegaly

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11
Q

How is VSD treated?

A
  • can close spontaneously
  • Diuretics to relieve pulmonary congestion
  • ACE inhibitors to reduce systemic pressure
  • surgically -> transvenous catheter closure via famoral vein or open heart surgery
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12
Q

What are complications of VSD

A
  • Eisenmengers
  • Endocarditis - antibiotic prophylaxis
  • Heart failure
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13
Q

What is an atrial septal defect

A

a defect (a hole) in the septum (the wall) between the two atria

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14
Q

What direction does blood shunt in ASD

A

Left to Right

higher pressure in left atria
acyanontic

= inc pressure in lungs

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15
Q

Causes of ASD

A
  • Maternal smoking in 1st trimester
  • Family History of CHD
  • Maternal diabetes
  • Maternal rubella
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16
Q

What is the name of the two walls that fuse with endocardial cushion to separate the atria and affected in ASD

A

septum primum and septum secondum

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17
Q

What is a small hole in the septum secondum called

A

foramen ovale

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18
Q

How is patent foraman ovale distinct from ASD

A

patent foramen ovale due to failed fusion

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19
Q

What does prolonged left to right shunt in ASD cause

A

right sided overload and right heart strain.

right sided overload can lead to right heart failure and pulmonary hypertension.

and eventually Eisenmenger syndrome

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20
Q

How does ASD present

A

Shortness of breath
Difficulty feeding
Poor weight gain
Lower respiratory tract infections

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21
Q

How does ASD present on auscultation

A

ejection systolic murmur with a fixed split second heart sound

loudest at the 2nd IC at the upper left sternal border

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22
Q

What is a splitting of the second heart sound

A

closure of the aortic and pulmonary valves at slightly different times

fixed split = does not change on inspiration or expiration

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23
Q

Why does ASD have fixed splitting of S2 heart sound

A

increase in RA and RV volume -> increase flow through pulmonic valve = delayed pulmonic valve closure

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24
Q

What are two types of ASD

A

Ostium secundum (70% of ASDs)
Ostium primum - present earlier usually occurs with other cardiac conditions

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25
Q

How is ASD investiagted

A

XRay - R heart dilation and pulmonary vasularity
ECG
Echo GS

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26
Q

What are complications of ASD

A
  • Stroke from DVT **
  • Atrial fibrillation
  • Pulmonary HTN
  • Eisenmenger’s syndrome
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27
Q

Why is ASD linked to stroke risk

A

systemic venous emboli use ASD to bypass lungs and become systemic arterial emboli

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28
Q

How is ASD managed

A

can close watch and wait to se eif closes on own
surgically - transvenous catheter closure (via the femoral vein) or open heart surgery
anticoagulants to reduce risk of clots and strokes in adults

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29
Q

What is tetralogy of fallot

A
  • Overriding aorta
  • VSD
  • Pulmonary valve stenosis
  • Right ventricular hypertrophy

MC cyanotic congenital heart disease

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30
Q

What causes tetralogy of fallot

A

anterosuperior displacement of the infundibular septum

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31
Q

What is the epidemiology of tetralogy of fallot?

A

more common in males
Rubella
increased maternal age
alcohol consumption in pregnancy
diabetic mother

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32
Q

what kind of shunt is present in tetralogy of fallot

A

Right to Left
blood bypasses lung = cyanosis
decreased RV outflow

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33
Q

What determines the degree of cyanosis in tetralogy of fallot

A

severity of pulmonary stenosis

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34
Q

what causes murmurs

A

turbulent blood

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35
Q

How does Tetralogy of fallot present

A
  • Tet spells (squatting child/knees to chest)
  • Irritability
  • SOB
  • Cyanosis
  • Clubbing
  • Poor feeding
  • Poor weight gain
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36
Q

What are tet spells

A

intermittent symptomatic peroids where R to L shunt becomes worsened precipiating a syanotic episode

when exerting increased CO2 (vasodilator) = systemic vasodilation = reduced vascular reisitance = blood pumped RV to aorta rather than pulmonary vessels

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37
Q

Why do children squat in tet spells

A

Squatting increases the systemic vascular resistance. This encourages blood to enter the pulmonary vessels

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38
Q

How does tetralogy of fallot present on XRay

A

boot shaped heart

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39
Q

How is tetralogy of fallot investiagted

A
  • MRI/Cardiac catheter
  • Echo**
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40
Q

What is heard on auscultation with tetralogy of fallot

A

ejection systolic murmur due to pulmonary stenosis

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41
Q

how are tet spells managed

A

Supplementary oxygen

Beta blockers -> relax the RV and improve flow to the pulmonary vessels.
IV fluids -> increase pre-load
IM Morphine -> decrease respiratory drive and reduce spasm in heart
Sodium bicarbonate -> buffer metabolic acidosis
Phenylephrine infusion -> increase systemic vascular resistance.

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42
Q

What causes tet spells

A

crying
fever
exercise
= exacebation of RV outflow obstruction

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43
Q

how is tetralogy of fallot managed

A
  • Prostaglandin infusion PGE1 to maintain ductus arteriosus if found at birth
  • Beta blockers
  • Morphine to reduce respiratory drive
  • Surgical: repair under bypass 3 months - 4 years but needs ICU post op
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44
Q

What are the complications of tetralogy of fallot

A
  • Pulmonary regurgitation
  • Lifelong follow up
  • heart failure
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45
Q

Why would you want to maintain ductus arteriosus in tertalogy of fallot

A

allows blood to flow from the aorta back to the pulmonary arteries.

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46
Q

What is transposition of great arteries

A

Aorta rises from right ventricle and pulmonary artery from left ventricle

not compatible with life unless shunt is present to allow mixing (eg VSD PDA)

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47
Q

What is the epidemiology of transposition of great arteries

A

diabetic mothers
More common in males
Mum>40
alcohol consumption in pregnancy

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48
Q

What causes transposition of great arteries

A

failure of aorticopulmonary septum to spiral

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49
Q

why will patients with transposition of great arteries present always have cyanosis

A

the right side of the heart pumps blood directly into the aorta and systemic circulation.

50
Q

Why is transposition of great arteries not life threatening in utero

A

gas and nutrient exchange happens in the placenta, therefore it is not necessary for blood to flow to the lungs

51
Q

What direction does blood shunt in transposition of great arteries

A

Right to Left

52
Q

What are the 5 right to left shunt conditions

A

truncus arteriosus
transposition of great vessels
tricuspid atresia
tetralogy of fallot
TAPVR

53
Q

How does transposition of great arteries present

A

Cyanosis at birth if not found on scans

if not detected at birth
respiratory distress, tachycardia, poor feeding, poor weight gain and sweating, death

54
Q

how is transposition of great arteries investigated

A

often diagnosed during pregnancy with antenatal ultrasound scans.

if not detected during pregnancy it will present with cyanosis at or within a few days of birth

55
Q

How is transposition of great arteries heard on auscultation

A
  • Right ventricular heave
  • Loud S2 heart sound
  • Systolic murmur if VSD present
56
Q

How is transposition of great arteries investigated

A

Low SATS
Echo GS
CXR
Metabolic acidosis

57
Q

How does transposition of great arteries appear on XRay

A

egg on a string appearance due to narrowed mediatinum and cardiomegaly

58
Q

How is transposition of great arteries managed

A

prostaglandin (PGE1) to maintain ductus arteriosus.
Balloon septostomy to create an ASD

Surgical correction -> definitive management “arterial switch” before 4 weeks old
emergency septostomy (maintain PDA)

59
Q

What is patent ductus arteriosus

A
  • Persistent connection between the descending aorta and pulmonary artery
  • Normal in utero but usually closes within first 10-15 minutes of life
60
Q

What direction does blood shunt in Patent ductus arteriosus

A

left to right

61
Q

why does Patent ductus arteriosus usually close in first few breathes of life

A

increased pulmonary flow which enhances prostaglandins clearance

62
Q

How is ductus arteriosus maintained

A

PGE synthesis and low O2 tension

63
Q

What are RF for Patent ductus arteriosus

A

Female
Prematurity

64
Q

How does Patent ductus arteriosus present

A
  • Respiratory distress
  • Apnoea
  • Tachypnoea
  • Tachycardia
  • Shortness of breath
  • Difficulty feeding
  • Poor weight gain
  • Lower respiratory tract infections

can remain asymptomatic and present as HF in adulthood

65
Q

how does Patent ductus arteriosus lead to HF

A

L to R shunt causes pulmonary hypertension leading to R sided heart strain as the right ventricle struggles to contract against increased resistance = right ventricular hypertrophy = left ventricular hypertrophy

66
Q

what is the ausculation finding for Patent ductus arteriosus

A

Continuous machinery murmur at the left sternal edge

bounding pulse

67
Q

How is Patent ductus arteriosus investigated

A
  • Echo GS
  • ECG/CXR
68
Q

How is Patent ductus arteriosus managed

A
  • monitor to close up to 1 year if not closed -> Cardiac catheterisation to close or sooner in more severe cases
  • Premature infants: Indomethacin or Ibuprofen inhibits prostaglandin and stimulates closure
69
Q

how is VSD and PDA managed before surgery

A

increase calories, nasogastric feeds
diuretics -> furosomide/spirolactone

70
Q

What is pulmonary valve stenosis

A

pulmonary valve has three leaflets when these become thicken or fused of abnormal create narrow opening btwn R Ventricle and Pulmonary artery

= congenital pulmonary valve stenosis.

71
Q

What conditions is congenital pulmonary valve stenosis associated with

A
  • Tetralogy of Fallot
  • William syndrome
  • Noonan syndrome
  • Congenital rubella syndrome
72
Q

What are symptoms of pulmonary valve stenosis

A

often asymptomatic

can present with symptoms of fatigue on exertion, shortness of breath, dizziness and fainting

73
Q

How does pulmonary valve stenosis present on auscultation (4 findings)

A
  • Ejection systolic murmur heard loudest at the pulmonary area (second intercostal space, left sternal border)
  • Palpable thrill in the pulmonary area
  • Right ventricular heave due to right ventricular hypertrophy
  • Raised JVP with giant a waves
74
Q

What is the gold standard investigation for diagnosing pulmonary stenosis

A

echocardiogram

75
Q

How is asymptomatic pulmonary stenosis progression managed

A

if asymptomatic generally do not require any intervention

“watching and waiting” approach.

76
Q

How is symptomatic pulmonary stenosis progression managed

A

treatment of choice = balloon valvuloplasty via a venous catheter

catheter into femoral vein, through the inferior vena cava and right side of the heart to the pulmonary valve and dilating the valve by inflating a balloon

77
Q

What is coarctation of the aorta

A

congenital condition where there is narrowing of the aortic arch, usually around the ductus arteriosus

78
Q

What genetic condition is Coarctation of the Aorta often associated with

A

Turners syndrome

79
Q

What pressure changes does Coarctation of the Aorta result in

A
  • reduces the pressure of blood flowing to the arteries that are distal to the narrowing.
  • It increases the pressure in areas proximal to the narrowing, such as the heart and the first three branches of the aorta
80
Q

How does Coarctation of the Aorta present in neonate/infancy

A

often only presents as weak femoral pulses.

Tachypnoea and increased work of breathing
Poor feeding
Grey and floppy baby
Acidoic

81
Q

How can Coarctation of the Aorta be investigated and what are findings

A

four limb blood pressure:

  • high blood pressure in the limbs supplied from arteries that come before the narrowing
  • lower blood pressure in limbs that come after the narrowing.
82
Q

What additional signs may develop over time due to Coarctation of the Aorta

A
  • Left ventricular heave due to left ventricular hypertrophy
  • Underdeveloped left arm where there is reduced flow to the left subclavian artery
  • Underdevelopment of the legs
83
Q

What murmur is associated with Coarctation of the Aorta

A

systolic murmur heard below the left clavicle (left infraclavicular area) and below the left scapula.

84
Q

How is Coarctation of the Aorta managed

A

mild = leave til adulthood
severe = emergency surgery after birth
surgical = balloon valvoplasty or surgical repair

85
Q

What medication is used to keep ductus arteriosus open while waiting for surgery in CoA

A

Prostaglandin E1 eg alprostadil

allows some blood flow flow through the ductus arteriosus into the systemic circulation

86
Q

What is infective endocarditis

A

infection of the endothelium (the inner surface) of the heart

MC affects heart valves

87
Q

What are RF for infective endocarditis

A
  • Intravenous drug use
  • Structural heart pathology (see below)
  • Chronic kidney disease (particularly on dialysis)
  • Immunocompromised (e.g., cancer, HIV or immunosuppressive medications)
  • History of infective endocarditis
88
Q

What structural pathology can increase risk of infective endocarditis

A
  • Valvular heart disease
  • Congenital heart disease
  • Hypertrophic cardiomyopathy
  • Prosthetic heart valves
  • Implantable cardiac devices (e.g., pacemakers)
89
Q

What is the MC infective cause of infective endocarditis

A

Staphylococcus aureus.

90
Q

What are two other causes of infective endocarditis

A
  • Streptococcus viridans
  • Staphylococcus epidermidis
91
Q

how does infective endocarditis present

A

Fever
Fatigue
Night sweats
Muscle aches
Anorexia (loss of appetite)

92
Q

What are key examination findings for infective endocarditis

A
  • New or “changing” heart murmur
  • Splinter haemorrhages (thin red-brown lines along the fingernails)
  • Petechiae (small non-blanching red/brown spots) on the trunk, limbs, oral mucosa or conjunctiva
  • Janeway lesions (painless red flat macules on the palms of the hands and soles of the feet)
  • Osler’s nodes (tender red/purple nodules on the pads of the fingers and toes)
  • Roth spots (haemorrhages on the retina seen during fundoscopy)
  • Splenomegaly (in longstanding disease)
  • Finger clubbing (in longstanding disease)
93
Q

How is infective endocarditis investigated

A

Blood cultures are essential before starting antibiotic

Three blood culture samples are recommended, usually separated by at least 6 hours and taken from different sites.

94
Q

What is the imagining investigation of choice for infective endocarditis

A

Echocardiography

Transoesophageal echocardiography (TOE) is more sensitive and specific than transthoracic echocardiograph

Vegetations (an abnormal mass or collection) may be seen on the valves.

95
Q

What is imaging investigation of choice w patients with prosthetic heart valves

A
  • 18F-FDG PET/CT
  • SPECT-CT
96
Q

What criteria is used to diagnose infective endocarditis

A

Modified Duke Criteria

One major plus three minor criteria
Five minor criteria

97
Q

What are major criteria for Modified Duke criteria infective endocarditis

A
  • Persistently positive blood cultures (typical bacteria on multiple cultures)
  • Specific imaging findings (e.g., a vegetation seen on the echocardiogram)
98
Q

What are minor criteria for Modified Duke criteria infective endocarditis

A
  • Predisposition (e.g., IV drug use or heart valve pathology)
  • Fever above 38°C
  • Vascular phenomena (e.g., splenic infarction, intracranial haemorrhage and Janeway lesions)
  • Immunological phenomena (e.g., Osler’s nodes, Roth spots and glomerulonephritis)
  • Microbiological phenomena (e.g., positive cultures not qualifying as a major criterion)
99
Q

How is infective endocarditis managed

A

Intravenous broad-spectrum antibiotics (e.g., amoxicillin and optional gentamicin)

4 weeks for with native heart valves
6 weeks for patients with prosthetic heart valves

100
Q

When is surgical management required for infective endocarditis

A

Heart failure relating to valve pathology
Large vegetations or abscesses
Infections not responding to antibiotics

101
Q

What are key complications of infective endocarditis

A
  • Heart valve damage, causing regurgitation
  • Heart failure
  • Infective and non-infective emboli (causing abscesses, strokes and splenic infarction)
  • Glomerulonephritis, causing renal impairment
102
Q

Is there prophylaxis for infective endocarditis

A

Antibiotics are not routinely recommended for dental and non-dental procedures as prophylaxis of infective endocarditis.

However, it is still considered on a case-by-case basis in those at particularly high risk.

103
Q

What is Rheumatic Fever

A

autoimmune condition triggered by streptococcus bacteria. It is caused by antibodies created against the streptococcus bacteria that also target tissues in the body.

T2 hypersensitivity

Multi system disorder

104
Q

What is the infective cause of Rheumatic Fever

A

group A beta-haemolytic streptococcal, typically streptococcus pyogenes causing tonsillitis.

105
Q

what is the pathophysiology of Rheumatic Fever

A

the immune system creates antibodies to fight the infection. These antibodies not only target the bacteria, but also match antigens on the cells of the person’s body, for example the muscle cells in the myocardium in the heart.

106
Q

What type of hypersensitivity reaction is Rheumatic Fever

A

type 2 hypersensitivity reaction

cross-reactive immune response

the immune system begins attacking cells throughout the body

107
Q

When does Rheumatic Fever present

A

occurs 2 – 4 weeks following a streptococcal infection, such as tonsillitis

Fever
Joint pain
Rash
Shortness of breath
Chorea
Nodules

108
Q

How does Rheumatic Fever affect joints

A

migratory arthritis affecting the large joints, with hot, swollen, painful joints.

migratory because different joints become inflamed and improve at different times, giving the appearance that the arthritis is moving from one joint to the next.

109
Q

How does Rheumatic Fever affect the heart

A

Carditis, or inflammation throughout the heart, with pericarditis, myocarditis and endocarditis

110
Q

What are the two key skin findings of Rheumatic Fever

A

Subcutaneous nodules
Erythema marginatum rash

111
Q

what does Carditis lead to

A

Tachycardia or bradycardia
Murmurs from valvular heart disease, typically mitral valve disease
Pericardial rub on auscultation
Heart failure

112
Q

how does Rheumatic Fever affect the nervous system

A

Chorea

113
Q

What is Chorea

A

irregular, uncontrolled and rapid movements of the limbs.

This is also known as Sydenham chorea

114
Q

What investigations can support a diagnosis of Rheumatic Fever

A

Throat swab for bacterial culture
Anti-streptococcal antibodies titres peak 3-6 weeks
Echocardiogram, ECG and chest xray can assess the heart involvement

115
Q

What criteria is used to diagnose Rheumatic Fever

A

Jones criteria

116
Q

What antibodies are present in Rheumatic Fever

A

Anti-streptococcal antibodies (ASO)

Indicate a recent streptococcus infection

Rise over 2 – 4 weeks
Peak around 3 – 6 weeks
Gradually falls over 3 – 12 months

117
Q

What is the jones criteria for Rheumatic Fever

A

evidence of recent streptococcal infection, plus:

Two major criteria OR
One major criteria plus two minor criteria

118
Q

What are major Jones criteria

A

J – Joint arthritis
O – Organ inflammation, such as carditis
N – Nodules
E – Erythema marginatum rash
S – Sydenham chorea

119
Q

What are minor Jones criteria

A
  • Fever
  • ECG Changes (prolonged PR interval) without carditis
  • Arthralgia without arthritis
  • Raised inflammatory markers (CRP and ESR)

FEAR

120
Q

how is Rheumatic Fever managed

A

Tonsillitis caused by streptococcus should be treated with phenoxymethylpenicillin (penicillin V) for 10 days.

pen allergy = erythromycin or azithromycin

  • NSAIDs (e.g. ibuprofen) are helpful for inflammation and fever joint pain
  • Aspirin and steroids are used to treat carditis
  • diuretics ACE-i, B-B for severity of carditis
  • Monitoring and management of complications
121
Q

What are complications of Rheumatic Fever

A

Recurrence of rheumatic fever
Valvular heart disease, most notably mitral stenosis
Chronic heart failure

3a paeds (12 decks)

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