Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Paeds FOP/TAS > Cardiology > Flashcards

Cardiology Flashcards

1
Q

What are the x3 shunts present in the antenatal circulation?

A

Ductus Venosus
Ductus Arteriosus
Foramen Ovale

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What circulatory changes occur at birth?

A

1) Ductus Venosus closes as placenta removed

2) Left sided circulation pressure increases which closes the Ductus Ateriosus

3) LA pressure > RA pressure causes the foramen ovale to close

There is an increase in left sided circulation as increased pulmonary return and reduced IVC flow / placenta removed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Incidence of significant cardiac malformations in live births?

A

8 in 1000

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Incidence of cardiac abnormalities in stillborns?

A

1 in 10 / 10%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Incidence of some cardiac abnormality in live births?

A

1-2%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What % of CHD is VSD?

A

30%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What % of CHD is PDA ?

A

12%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What % of CHD is ASD?

A

7%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What % of CHD is TOF?

A

5%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What % of CHD is TGA?

A

5%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What % of CHD is AVSD (complete)

A

2%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What % of CHD is pulmonary stenosis?

A

7%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What % of CHD is aortic stenosis?

A

5%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What % of CHD is coarctation of the aorta?

A

5%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

List some causes of congenital heart disease?

A

Maternal factors:
- Rubella infection
- SLE
- DM
- Enterovirus in 3rd Trimester
- Coxsackie virus in 3rd Trimester

Drugs:
- Warfarin
- Alcohol
- Lithium

Genetic causes:
- Trisomy (13, 18, 21)
- Turner Syndrome (45XO)
- William’s Syndrome (7q11.23 microdeletion)
- Noonan Sx (PTPN 11 mutation)
- Chromosome 22q11.2 deletion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Left to Right shunts (breathless)

A

VSD
ASD
PDA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Right to Left shunts (blue)

A

TOF
TGA
Eisenmenger Sx

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Common Mixing (blue and breathless)

A

Complete AVSD
Tricuspid atresia
Complex CHD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Outflow Obstruction (Well Child)

A

Aortic Stenosis
Pulmonary Stenosis
Adult type CoA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Outflow Obstruction (Sick/Collapsed Neonate)

A

Critical AS
HLHS
CoA
Total anomalous pulmonary venous connection
Interruption of the Aortic Arch

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Incidence of Infective Endocarditis

A

1 in 1000

Increased risk with CHD, prosthetic material in the heart, long term central lines and immunosuppression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Most common organisms in Infective Endocarditis

A

Staph aureus
Coagulase Negative Staph (CoNs)
Strep viridans (alpha-haemolytic strep)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Common organisms causing Infective Endocarditis in diabetic and immunocompromised children

A

HACEK
- Haemophilus
- Actinobacillus
- Cardiobacterium
- Eikenella
- Kingella

The above are fastidious (difficult to culture)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Sequelae of emboli in infective endocarditis

A

Brain
- Strokes
- Intracranial abscess/infection
- Intracranial vasculitis and bleeds

Lung
- Septic pulmonary emboli +/- haemorrhage

Kidney
- Glomerulonephritis

Spleen
- Splenic infarct + splenomegaly

Gut
- Mesenteric infarct

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

List the diagnostic criteria for IE

A

Modified Duke Criteria (2 major, 1 major + 3 minor or 5 minor)

Major criteria:
- x2 positive blood cultures
- Mass/vegetation/paravalvular abscess/new valvular regurgitation/prosthetic valve dehiscence on Echo

Minor criteria:
- Predisposing factors (CHD, IVDU, tattoos)
- Fever >38
- Vascular phenomena (PE, arterial emboli, ICH, conjunctival haemorrhage, Janeway lesions)
- Immunologic phenomena (Roth spots, Osler nodes, Glomerulonephritis, Rf factor positive)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What are Roth spots

A

Also known as Litten spots

Seen in IE;
- white centered retinal haemorrhages

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Criteria for prophylaxis against infective endocarditis?

A

Acquired valvular heart disease (stenosis or regurgitation)

Hypertrophic cardiomyopathy

Prev IE

Structural CHD (including surgically corrected or palliative conditions)

Valve replacements

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

3 stages of surgical correction for HLHS?

A

1) Norwood procedure within first week of life

2) Glenn procedure at 3-6 months

3) Fontan procedure at 2-3 years (one ventricle supports both the pulmonary and systemic circulation). IT IS A PALLIATIVE PROCEDURE.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Surgical management for TGA?

A

Typically have a balloon atrial septostomy for stabilisation

Followed by the arterial switch operation (this has replaced the mustard operation)

If a VSD is also present would undergo the Rastelli operation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What type of vasculitis is Kawasaki disease?

A

Medium vessel vasculitis

Predilection for coronary arteries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Management of PDA

A

Trial of paracetamol , ibuprofen or indomethacin (if no contraindications e.g. renal impairment, hepatic impairment)

Duct ligation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

List some duct dependent lesions

A

TGA
HLHS
Pulmonary atresia
Tricuspid atresia
CoA
Pulmonary stenosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What is the most common congenital heart defect?

A

Bicuspid Aortic Valve

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Management of Paediatric SVT

A

1) Ice water to the face
2) Adenosine
3) Synchronised DC cardioversion (1J/kg for first shock followed by 2J/kg)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

At what age do cyanotic spells usually develop in those with TOF?

A

4-6 months of age

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Pathophysiology of hypertrophic cardiomyopathy (HCM)

A

Genetic predisposition (abnormal formation of sarcomeric proteins of the cardiac myocyte)

Hypertrophy reduces the volume of the LV cavity and thus the ability of the LV to fill in diastole.

Reduced LV filling = rising LA pressure, pulmonary oedema and congestive heart failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

x2 types of HCM

A

Obstructive (obstruction caused by the anterior leaflet of the mitral valve)

Non-obstructive (more common)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Pharmacological management of HCM

A

Beta blockers (slow HR and improve LV filling)

CCBs

Diuretics

ACEi (reduces afterload)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Surgical options for HCM

A

Implantable cardioverter defibrillator

LV myomectomy if significant obstruction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Biggest risk associated with HCM/HOCM?

A

High arrhythmia and SCD risk

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What is the most common cause of acquired heart disease in children/adolescents?

A

Rheumatic fever

42
Q

Aetiology of Rheumatic fever?

A

Immunologic reaction that is a delayed sequela of group A beta-haemolytic strep infection of the pharynx (Strep throat or scarlet fever)

Exact pathophysiology unclear, theories include:
- GAS produces enzymes e.g. streptolysin O which may be cytotoxic to cardiac cells
- Immune response fails to differentiate between epitopes of strep pathogen and host tissue

43
Q

List the diagnostic criteria for Rheumatic Fever

A

Duckett-Jones / Modified Jones criteria (2 major or 1 major and 2 minor)

Major criteria:
- Migratory polyarthritis
- Carditis
- Subcutaneous nodules (extensor surfaces or scalp)
- Erythema marginatum (non pruritic, worse with warm water)
- Sydenham’s chorea

Minor criteria:
- Arthralgia
- Fever
- Elevated acute phase reactants (ESR, CRP)
- Prolonged PR interval

Recurrent RF can be diagnosed with 3 minor criteria and evidence of previous group A strep infection

44
Q

In what % of cases is ASOT elevated in Rheumatic Fever?

A

80%

45
Q

Management of Rheumatic Fever

A

Bed rest in the acute phase (1-6 weeks)

Pharmacological:
- Aspirin / Pred
- Penicillin (IM BenPen). Erythromycin if pen allergic.
- ACEi, Digoxin, diuretics to manage heart failure
- Diazepam / AEDs or IVIG for chorea

Surgical:
- Valvular repair or replacement (mitral valve)

46
Q

What is key to think about in the long term management of Rheumatic Fever?

A

High risk of recurrence so may require penicillin prophylaxis (duration/frequency dependent on whether there is cardiac involvement)

Minimum is at least 5 years treatment

47
Q

At what time period does Rheumatic fever occur following an URTI (strep throat or scarlet fever)

A

2-6 weeks

48
Q

Which side of the heart is most commonly affected in IE?

A

Left

Unless IVDU then right sided more lesions more common

49
Q

Mortality in IE

A

20% mortality rate!

50
Q

Diagnostic Criteria for IE

A

Modified Duke’s criteria

51
Q

Diagnostic criteria for Rheumatic Fever

A

Modified Jones’ / Duckett Jones criteria

52
Q

Where exactly is the infection in IE?

A

Infection of the endothelium (endothelial surface of cardiac valves)

53
Q

Why is CHD a risk factor for IE?

A

Turbulent blood flow

54
Q

Most common cause of myocarditis in the Western world

A

Viral infections
Coxsackie = most common organism

55
Q

Most common cause of myocarditis in children globally?

A

Chagas disease (Trypanosoma cruzi)

56
Q

Management of Kawasaki disease

A

High dose aspirin and IVIG

57
Q

What are the x2 genetic causes of long QT syndrome?

A

Romano-Ward syndrome
Jervell and Lang-Nielsen syndrome

58
Q

Pathophysiology of long QT syndrome and risk of arrhythmias

A

Defective ion channels (Na/K/Ca) slows the flux of ions in stage 2/3 of the cardiac action potential leaving the myocardium to be depolarised for longer than it should be.
In this state there is a much higher risk of generating abnormal conduction pathways that degenerate into uncoordinated electrical activity, e.g. monomorphic VT / VF / Torsades de Pointes (polymorphic VT)

59
Q

Causes of Long QT syndrome

A

Genetic:
- Romano-Ward syndrome (most common)
- Jervell and Lang-Nielsen syndrome

Acquired:
- Electrolyte imbalances (hypokalaemia, hypocalcaemia, hypomagnasaemia)
- Medications (antipsychotics, antibiotics, antimalarials)
- Cocaine
- HIV
- MI
- Hypothyroidism

60
Q

Inheritance pattern of Romano-Ward syndrome

A

Autosomal dominant

61
Q

Inheritance pattern of Jervell and Lang-Nielsen syndrome

A

Autosomal recessive

62
Q

Which genetic long QT syndrome is associated with sensorineural hearing loss?

A

Jervell and Lang-Nielsen syndrome (affects K channels in the ear as well)

63
Q

Medication of choice to manage long QT syndrome and risks associated with this

A

Beta blockers (propranolol or atenolol) as they reduce the risk of ectopic activity during prolonged repolarisation

Risk it can also further prolong the QT interval

64
Q

Management of long QT syndrome

A

Non-pharmacological:
- Avoid stressful stimuli and heavy exercise
- Close control of electrolytes, particularly post-op

Pharmacological:
- Beta blockers

Surgical
- ICD

65
Q

What is long QT syndrome?

A

A group of conditions causing abnormality of the repolarisation of ventricles (affects ion channels involved in stage 2/3 of the cardiac action potential)

66
Q

Bazett’s formula for calculating QTc

A

QTc = QT / √ (RR)

67
Q

Which is the most common genetic long QT syndrome?

A

Romano-Ward syndrome

68
Q

Types of SVT

A

Atrial tachycardia
- Rare, usually only post-cardiac surgery

Nodal tachycardia (AVN/junctional/AVNRT)
- Abnormal re-entrant pathway within the AVN

AV re-entrant tachycardia (AVRT) (10-20% of SVTs)
- Accessory conduction pathway between atria and ventricles, e.g. WPW syndrome

69
Q

What are the x2 types of WPW syndrome?

A

Orthodromic:
- Conduction flows normally from SAN->AVN-> Ventricle however accessory pathway allows retrograde conduction back up to atria

Antidromic:
- Normal conduction from SAN->AVN however accessory pathway then allows abnormal conduction through ventricles back up to AVN

70
Q

ECG findings in WPW syndrome

A

Delta wave (slur of QRS due to accessory pathway)

Narrow complex tachycardia

Short PR (due to pre-excitation of ventricle due to accessory pathway)

Normal/narrow QRS in Orthodromic
Broad QRS in Antidromic

71
Q

Loud pansystolic murmur lower left sternal edge

A

VSD

Rare but another cause is Tricuspid regurgitation (Ebstein anomaly)

72
Q

1) ESM at right upper sternal edge which radiates to the carotids

2) What other signs may you find

A

1) Aortic Stenosis

2) Suprasternal notch or carotid thrill

73
Q

Systolic murmur at left upper sternal edge with a split S2 (does not vary with respiration)

A

ASD

74
Q

ESM loudest at the left upper sternal edge radiating to the back

A

Pulmonary Stenosis

75
Q

What defects may you find a precordial thrill in?

A

VSD
Pulmonary stenosis

76
Q

PSM at the apex

A

Mitral regurgitation

77
Q

When would an ejection click be heard?

A

Valvular AS or PS

NO ejection click if sub or supra-valvular

78
Q

Most common form of SVT in children >8 years old

A

AVNRT

79
Q

Most common form of SVT in children <8 years old

A

AVRT (e.g. WPW Sx)

80
Q

When would you treat aortic stenosis?

A

Gradient across the valve >60mmHg

Treatment usually involves balloon valvuloplasty or surgical valvuloplasty. Avoid valve replacement in children.

81
Q

Types of ASD

A

Ostium secundum (most common)
Ostium primum / partial AVSD
Sinus venosus

82
Q

Continuous murmur in infraclavicular region with collapsing pulse

A

Persistent arterial duct

83
Q

Continuous murmur in infraclavicular region with lateral thoracotomy

A

BT shunt

84
Q

Diastolic murmur at left sternal edge/apex

A

Aortic regurgitation

85
Q

ESM at upper left sternal edge + median sternotomy scar

A

TOF repaired

86
Q

Long harsh systolic murmur and cyanosis

A

TOF

87
Q

Where is the defect in Secundum ASD

A

Defect in the centre of the atrial septum involving the fossa ovalis

88
Q

Where is the defect in Primum ASD

A

Partial AVSD - defect in the lower atrial septum involving the left AV valve which has 3 leaflets and tends to leak

89
Q

Mx of TOF

A

Elective repair 6-9 mths old
May have BT shunt as neonate if severely cyanosed

90
Q

Boot shaped heart on XR

A

TOF
Pulmonary atresia

91
Q

Egg on side on XR

A

TGA

92
Q

Snowman in a snowstorm or cottage loaf appearance on XR

A

Total anomalous pulmonary venous connection

93
Q

When to repair an ASD?

A

Pulmonary-to-systemic-flow ratio > 2:1

94
Q

Most common cause of cyanotic heart disease in the neonatal period?

A

TGA

95
Q

Systolic murmur in the second left intercostal space and prominent precordial motion (tripple ripple) with a late second systolic impulse

A

HOCM

96
Q

Features of Still’s / Innocent mumur

A

Soft
Systolic
Short
Sternal edge (loudest at)
Supine position (heard in)
Symptomless

97
Q

What does a prominent left precordium suggest?

A

The right ventricle was dilated during childhood, e.g. due to pulmonary hypertension

98
Q

Incidence of PDA in pre-term babies?

A

20-60%

The ductus may also remain open for many weeks

99
Q

In which condition would you see a reduction in the intensity of the murmur as cyanosis worsens?

A

TOF - this is because during a tet spell there is increased right sided outflow obstruction / reduced pulmonary blood flow

100
Q

Pathophysiology of a Tet spell

A

Increase in right sided pressure which causes a right to left shunt and increased cyanosis due to more deoxygenated blood entering the systemic circulation

Can be caused by:
- Reduced O2 Sats (pulmonary hypoxic vasoconstriction) e.g due to crying
- Decrease in systemic vascular resistance (playing, hypovolaemia)
- Tachycardia (distress)

This deoxygenation causes:
- Hyperpnea due to stimulation of resp centre (increased adrenergic tone and catecholamines)
- Catecholamines cause increased contractility which increases outflow obstruction

101
Q

Management of a Tet spell

A

Aim to increase systemic pressure / left sided pressure and reduce pulmonary pressure

Increase systemic pressure:
- Squat
- Raise legs / bring knees to chest
- IVI
- Vasopressors

Reduce pulmonary pressure
- O2 to reduce hypoxic vasoconstriction

Reduce RR
- Morphine

Paeds FOP/TAS (12 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions