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3a Notes AC > Paeds Cardio > Flashcards

Paeds Cardio Flashcards

1
Q

Most common Septal Defect

Ventricular Septal Defects
Epdiemiology

Congenital hole in the septum between the two ventricles.

A
  • 30% of all defect cases
  • Associated with Turner’s and Down’s yndrome
  • They close spontaneously in around 50% of cases.
  • VSDs may be detected in utero during the routine 20 week scan
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2
Q

L->R Shunt

Pathophysiology of VSD

Congenital hole in the septum between the two ventricles

A

Increased pressure in the left ventricle compared to the right, blood typically shunts from left to right. Blood is still flowing into the lungs before entering the rest of the body and therefore patient remains acyanotic. The shunt leads to right side overload, right heart failure and increased pulmonary vessel flow.

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3
Q

Define Paediatric Heart Failure

Caused by: Severe aortic stenosis, interrupted aortic arch, transposition of the great arteries, large patent ductus arteriosus, VSD, Rheumatic fever, cardiomyopathy, Eisenmenger syndrome.

A
  • Cardiac output which is inadequate for the body’s requirements.
  • Cases are due to congenital malformations which usually result in high output cardiac failure
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4
Q

Symptoms Paediatric HF

What tests are performed?

A

– Shortness of breath

– Inability to gain weight/poor growth

– Predisposition to recurrent chest infections

– Hepatomegaly

– Signs of specific cause –> e.g., murmur, cardiomegaly, cyanosis

– Chest X-ray –> may show cardiomegaly

– ECG –> can show ischaemic changes as well as congenital arrythmias

– Echocardiogram –> this is used to diagnose structural disease

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5
Q

Management HF

A

– Treat the underlying cause of the heart failure

– Medical management can be used to reduce afterload of the heart reducing the work the heart has to do

– If unresolving –> consider need for heart transplant

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6
Q

Signs & Symptoms VSD

VSDs that are bigger than aortic valve are Symptomatic otherwise not.

What type of Murmur is there?

A
  • failure to thrive
  • features of heart failure
  • hepatomegaly
  • tachypnoea
  • tachycardia
  • pallor
  • PAN SYSTOLIC MURMUR at Left Sternal Edge

*

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7
Q

Complications VSD

A
  • Infective Endocarditis
  • Extra Blood in RV= Pulmonary HTN
  • If RV pressure exceeds LV then eventually shunts back into LV = cyanotic - Eisenmenger’s Syndrome
  • R Heart Failure
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8
Q

Investigations VSD

A
  • VSDs may be detected in utero during the routine 20 week scan
  • Echocardiography is the diagnostic investigation
  • Chest x-ray may show cardiomegaly, enlarged pulmonary arteries and pulmonary oedema in large VSDs and there may also be ECG changes.
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9
Q

Management VSD

A
  • Small VSDs close spontaneously
  • Larger ones can present with HF so need diuretics, often combined with captopril.
  • Surgical management 3-6m to prevent Eisenmenger’s
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10
Q

Atrial Septal Defect Epidemiology

Patent Foramen Ovale

A
  • Most common defect detected in Adulthood
  • Significant mortality, with 50% of patients being dead at 50 years.
  • RF Maternal Diabetes and Smoking
  • Higher in Women than Men
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11
Q

Two Types

Atrial Septal Defect Pathophysiology

Secundum & Primum

A

Ostium Secundum
* Most Widespread - 70-80%
* Hole between two atria
* Associated with Holt-Oram syndrome
Ostium Primum
* Septum primum fails to close, and this tends to lead to atrioventricular defects

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12
Q

Signs And Symptoms Atrial Septal Defect

What murmur

A

Adulthood
* Arrythmia, Dyspnoea, HF
Childhood
* SOB, Difficulty feeding, failure to thrive.
* EJECTION SYSTOLIC MURMUR Left upper sternal edge
* Fixed splitting of S2

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13
Q

Complications Atrial Septal Defect

A
  • Embolism may pass from venous system to left side of heart causing a stroke
  • Eisenmenger’s Syndrome
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14
Q

Investigations & Management Atrial Septal Defect

A
  • Echo
  • ECG: RBBB
  • Secundum ASD, cardiac catheterisation may be used with insertion of occlusion device.
  • For partial AVSD surgical correction is required.
  • Treatment: 3-5Y
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15
Q

Pathophysiology Patent Ductus Arteriosus

L-R shunt

Ductus Arteriosus connects pulmonary artery to aorta in foetus, allows blood to detour away from the lungs before birth.
closed by maternal prostaglandin pressure after birth.

A
  • More common in premature babies, born at high altitude or maternal rubella infection in the first trimester
  • Defect in the constrictor mechanism of the duct.
  • Blood flows from the aorta to the pulmonary artery (to the lungs)
  • Following the fall in pulmonary pressure after birth.

eventually causing RHF or Eisenmengers. RISK OF LIFELONG BACTERIAL ENDOCARDITIS

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16
Q

Features Patent Ductus Arteriosus

A

Symptoms: Shortness of breath, Difficulty feeding, Poor weight gain
* Left subclavicular thrill
* Continuous ‘machinery’ murmur
* Large volume, bounding, collapsing pulse
* Wide pulse pressure
* Heaving apex beat

17
Q

Investigations and Management Patent Ductus Arteriosus

A
  • Echo
  • Indomethacin or ibuprofen
    inhibits prostaglandin synthesis, closes the connection in the majority of cases.
  • If associated with another congenital heart defect amenable to surgery then prostaglandin E1 is useful to keep the duct open until after surgical repair
18
Q

Rheumatic Fever Pathophysiology

Start of with tonsilitis

Multisystem autoimmune response to group A streptococcus (GAS) infection.

A
  • Cross-reactive immune response (a form of type II hypersensitivity) thought to be mediated by molecular mimicry when Streptococcus pyogenes infection activates innate immune response.
  • The antibodies against M protein (in S. Pyogenes) cross-react with myosin and the smooth muscle of arteries (Cardiac)
  • Aschoff bodies describes the granulomatous nodules found in rheumatic heart fever

Process usually delayed 2-4 weeks after the initial infection.
Multi-system disorder that affects the joints, heart, skin and nervous system.

19
Q

Signs & Symptoms Rheumatic Fever

A
  • Latent interval of around 2-6 weeks following Tonsilitis: acute febrile illness with polyarthritis and often carditis.
  • Endocarditis,
  • Sydenham chorea,
  • Migratory (Poly) Arthritis (knee, wrists etc)
  • Erythema marginatum (rash on trunk & limbs)
  • Subcutaneous Nodules
20
Q

Complications Rheumatic Fever

A

Rheumatic heart disease. Mitral valve most frequently affected
- Mitral Stenosis

21
Q

Management Rheumatic Fever

A
  • Diagnosis made using jones criteria (other card)
  • Antibiotics: oral penicillin V (prophylactic)
  • Anti-inflammatories: NSAIDs are first-line Naproxen
  • Treatment of any complications that develop e.g. heart failure
22
Q

JONES CRITERIA

Diagnostic Criteria Rheumatic Fever

2 Major symps Vs 1 Major 2 Minor symps

Evidence of recent streptococcal infection
* raised or rising streptococci antibodies,
* positive throat swab
* positive rapid group A streptococcal antigen test

A

Major
* erythema marginatum
* Sydenham’s chorea: this is often a late feature
* polyarthritis
* carditis and valvulitis (eg, pancarditis)
* Subcutaneous Nodules
Minor criteria
* raised ESR or CRP
* pyrexia
* arthralgia (not if arthritis a major criteria)
* prolonged PR interval

23
Q

Infective Endocarditis Pathophysiology

now the most common cause of infective endocarditis

Staph aureus

All children of any age with congenital heart disease are at risk of infective endocarditis.

A
  • Infection of the heart and surrounding vessels.

Triad of
1. endothelial damage
2. platelet adhesion
3. microbial adherence.

Bacteraemia that occurs can adhere to this lesion (damage) and go on to invade underlying tissue.

24
Q

Infective Endocarditis Signs & Symptoms

A
  • Low grade fever
  • Heart Murmur (type varies)
  • Splenomegaly
  • Petechiae
  • Osler’s Nodes
  • Janeway Leisons
  • Splinter haemorrhages on nails
  • Arthralgia

Complications include embolic phenomena – can lead to pulmonary emboli, glomerular nephritis, cerebral emboli, or Roth spots

25
Q

Dukes

Investigations Infective Endocarditis

A

Modified Duke’s criteria used for diagnosis; two major criteria, one major and three minor, or five minor are needed to confirm.
Major criteria:
- Positive blood cultures: typical organisms from 2 separate cultures or microorganisms consistent with IE from persistent blood cultures
- Evidence of endocardial involvement: positive echo findings.
Minor criteria:
- Predisposing risk factors
- Fever >38°C
- Vascular phenomena
- Immunological phenomena – glomerulonephritis, Oslers node, Roth spot, rheumatoid factor positive
- Microbiological evidence that doesn’t meet major criteria
- Echo findings consistent but not meeting major

26
Q

Management Infective Endocarditis

A
  • high-dose penicillin in combination with an aminoglycoside, giving 6 weeks of IV therapy and checking serum levels of antibiotics.
  • Prophylaxis is important – good dental hygiene should be strongly encouraged in children with congenital heart disease.
  • Prophylaxis used in high risk situation
27
Q

Coarctation of Aorta pathophysiology

defect in the vessel media during development.

Associated with Turner’s but common in M

A
  • Narrowing of the aortic arch usually around the ductus arteriosus
  • Reduces the pressure of the blood flowing distal to the narrowing; increases the pressure in areas proximal to the narrowing
  • Severity varies
28
Q

Coarctation of Aorta Signs And Symptoms

Coarctation of the aorta describes a congenital narrowing of the descending aorta.

A

Infancy
- A sick baby with severe heart failure
- Absent femoral pulses
- Severe metabolic acidosis
- LV Heave
* radio-femoral delay
* mid systolic murmur, maximal over back

29
Q

Coarctation of Aorta Investigations

Coarctation of the aorta describes a congenital narrowing of the descending aorta.

A
  • four limb blood pressure will reveal high blood pressure in the limbs supplied from arteries that come before the narrowing and lower blood pressure in those that come after the narrowing.
  • Cardiomegaly on X ray
30
Q

Coarctation of Aorta Management

A
  • In mild cases the patient can live symptom free until adulthood without need for surgical input.
  • In severe cases, resuscitation is needed for a sick baby. Prostaglandin E used to keep the ductus arteriosus open while waiting for surgery, which allows some blood flow through the ductus arteriosus into systemic circulation distal to the coarctation.
31
Q

Diabetic Mothers at greater risk

Tranposition of The Great Arteries (TOTGA)
Pathophysiology

R to L shunt (kinda)

Cyanotic congenital heart disease. It is caused by the failure of the aorticopulmonary septum to spiral during septation.

A
  • Condition where the attachments of aorta and pulmonary trunk are swapped
  • right ventricle pumps into the aorta and left ventricle pumps in pulmonary trunk
  • No mixing but this in incompatible with life
32
Q

Life threatening

Tranposition of The Great Arteries Signs & Symptoms

A
  • Cyanosis is the predominant symptom
  • tachypnoea
  • loud single S2
  • prominent right ventricular impulse
  • ‘egg-on-side’ appearance on chest x-ray

Presentation usually on day 2 of life if not detected antenatally, when duct closure leads to reduction in blood mixing.

33
Q

Tranposition of The Great Arteries Management

A
  • Maintenance of the ductus arteriosus with prostaglandins
  • surgical correction is the definite treatment.
  • Balloon atrial septostomy (open foramen ovale to allow mixing) and then arterial switch procedure.
34
Q

most common cause of cyanotic congenital heart disease

Tetralogy of Fallot pathophysiology

22q11 microdeletion syndrome and Down’s syndrome linked

typically presents at around 1-2 months, although may not be picked up until the baby is 6 months old

A
  1. Ventricular septal defect (VSD)
  2. Right ventricular hypertrophy
  3. Right ventricular outflow tract obstruction,pulmonary stenosis
  4. overriding aorta

Due to VSD and pulmonary stenosis, there is shunting of blood from right to left and therefore arterial desaturation and cyanosis results.

35
Q

Tetralogy of Fallot Signs & Symptoms

Most cases are picked up on antenatal scans;

A
  • Cyanosis with hypercyanotic ‘tet’ spells (Loss of conscioussness/cyanosed precipitated by crying/excercise)
  • Right-to-left shunt
  • Ejection Systolic Murmur due to stenosis
  • Right aortic arch
  • Xray: boot.

* others: clubbing, poor feeding, poor weight gain.

Untreated, predisposes to:
- Cerebral thrombosis and ischaemia
- Brain abscess
- Bacterial endocarditis
- Congestive cardiac failure

36
Q

Tetralogy of Fallot Management

Chest x-ray may show relatively small heart and may be decreased pulmonary vascular markings.

A
  • Surgical repair is often undertaken in two parts
  • Cyanotic episodes may be helped by beta-blockers to reduce infundibular spasm

Tet spells may be self limiting; if prolonged prompt treatment with:
- Placing child in knee-to-chest position – increase systemic resistance
- Oxygen administration – reduce hypoxia
- Insert IV line and administer adrenaline (increase systemic resistance), morphine (decrease respiratory drive, giving more effective breathing) and propranolol (peripheral vasoconstrictor)
- IV fluids may be given to increase pre-load, increasing volume of blood to pulmonary vessels.
- Prolonged attacks may require sodium bicarbonate to correct acidosis
- Referral to cardiac centre

3a Notes AC (20 decks)

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