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Written exam > Cardiology > Flashcards

Cardiology Flashcards

1
Q

Stages of hypertension?

A

Elevated BP >90th centile
Stage 1 hypertension BP >95th centile
Stage 2 hypertension BP >95th centile +12mmHg

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2
Q

Renal causes of secondary hypertension

A

Peel, GN, HSP, HUS, hydronephrosis, Wilms tumour/other renal tumours, renal trauma, SLE, reflux nephropathy, ureteral obstruction, renal artery stenosis/thrombosis, renal vein thrombosis

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3
Q

Endocrine causes of secondary hypertension

A

DM, hyperthyroidism, Cushing syndrome, hyperparathyroidism, CAH, primary hyperaldosteronism, pheochromocytoma, neuroblastoma

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4
Q

Cardiac causes of secondary hypertension

A

Coarctation of the aorta

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5
Q

Genetic causes of secondary hypertension

A

Neurofibromatosis
Tuberous scslerosis
Williams syndrome
Turner syndrome

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6
Q

Drug-induced causes of secondary hypertension

A

Corticosteroids
Stimulants
Oral contraceptives
Drugs of abuse (cocaine, PCP, nicotine)
Caffeine
Sympathomimetics
Heavy metal poisoning

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7
Q

Other causes of secondary hypertension

A

White coat hypertension
Pre-eclampsia
Autonomic instability
Intracranial mass
Arteriovenous shunt
Liddle syndrome
Hypercalcaemia

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8
Q

LV outflow tract obstruction causes of chest pain

A

Hypertrophic cardiomyopathy
Aortic stenosis
Coarctation of the aorta

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9
Q

Coronary artery anomalies leading to chest pain

A

Kawasaki disease
Abnormal origin of a coronary artery
Myocardial bridge
Hyperlipidaemia causing atherosclerosis

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10
Q

Other causes of chest pain (excluding LV outflow obstruction or coronary artery anomalies)

A

Coronary vasospasm
Pericarditis
Myocarditis
Dilated cardiomyopathy
Arrhythmias
Aortic root dissection
Ruptured sinus of Valsalva aneurysm
Pulmonary hypertension

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11
Q

GI causes of chest pain

A

Reflux
Gastritis
Peptic ulcer disease
Cholecystitis
Pancreatitis

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12
Q

MSK causes of chest pain

A

Costochondritis/Tietze syndrome
Slipped rib syndrome
Precordial catch syndrome
Muscle strain
Trauma

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13
Q

Respiratory causes of chest pain

A

Pneumothorax
Pulmonary embolus
Pneumonia
Acute chest syndrome in sickle cell disease
Asthma
Pleuritis

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14
Q

Other causes of chest pain

A

Skin infections
Breast disease
Psychosomatic pain

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15
Q

Red flags for syncope

A

LOC without prodromal symptoms
Syncope following loud noise/surprise/emotional distress (suspicious for long QT syndrome)
Exercise induced syncope
Syncope when lying flat
Family history of sudden death
Syncope with an abnormal ECG

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16
Q

Type of shunt from PDA?

A

Left to right, acyanotic

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17
Q

Examination findings in PDA?

A

Grade 1-4 continuous murmur, “machinery like”
Left upper sternal border
May have widened pulse pressure and associated bounding pulses

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18
Q

Clinical features of PDA?

A

Small PDAs are asymptomatic
Moderate to large PDAs associated with increased risk of respiratory tract infections, congestive heart failure symptoms/pulmonary oedema (due to increased pulmonary flow)

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19
Q

Risk of PDA in preterm babies?

A

Can cause such significant left to right shunting that there is systemic hypoperfusion, increasing risk of NEC, myocardial ischaemia, renal injury etc

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20
Q

Complications of persisting PDAs?

A

If small, likely asymptomatic
If large, can lead to pulmonary hypertension, which then results in risk of shunt becoming right to left (Eisenmenger’s) with differential cyanosis
A patent PDA which is enough to cause a murmur is associated with a 1% per year risk of bacterial endocarditis

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21
Q

Indications for treatment of PDA

A

Haemodynamic instability
Congestive heart failure
To prevent development of pulmonary hypertension in large PDAs

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22
Q

Medical management of PDA

A

Fluid restriction and diuretics
Indomethason or NSAIDs (contraindicated if bleeding risk)

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23
Q

Surgical management of PDA

A

Catheterisation
Surgical closure (usually just in preterm infants)

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24
Q

Complications of surgical closure of PDA

A

Vocal cord paralysis (due to injury of recurrent laryngeal nerve)/diaphragm paresis (injury to phrenic nerve)
Chylothorax (injury to thoracic duct)
Later-onset scoliosis related to thoracotomy

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25
Q

Overview of ASD

A

13% of CHD
Characterised by location of the defect - includes PFO, premium ASD (15-20%), secundum ASD (70%), sinus venous defect (5-10%) or coronary sinus defect (<1%)
Severe cases result in high LA pressure which can help the PFO close/increases L-R shunting

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26
Q

PFO overview

A

Present in 30% of healthy adults
In utero, placental blood crosses the PFO to bypass the lungs and allows the most oxygenated blood to reach the coronary arteries and the brain

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27
Q

Primum ASD overview

A

Endocardial cushion defect
Comprises the atrial component of AV canal defects

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28
Q

Secundum ASD overview

A

Most common type of ASD (70%)
Defect in the septum primum

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29
Q

Sinuses venous defect

A

5-10% of ASDs
Majority of these occur in conjunction with partial anomalous pulmonary venous return (PAPVR)

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30
Q

Symptoms of ASD

A

Often asymptomatic
Symptoms can include exercise intolerance, dyspnoea or fatigue
May have palpitations due to atrial arrhythmias (flutter and/or AF) related to atrial stretch

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31
Q

ASD examination findings

A

Wide, fixed splitting of S2 due to delayed closure of PV from increased volume in RV
May have ejection systolic murmur at LUSB (due to increased flow across PV) and a diastolic rumble at LLSE (due to increased flow across the tricuspid valve)

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32
Q

Genetic syndromes associated with secundum-type ASDs?

A

Noonan syndrome
Holt-Oram syndrome (TBX5 gene)
Treacher Collins
Thrombocytopenia with absent radius (TAR) syndrome

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33
Q

Natural history of ASDs

A

PFOs generally close spontaneously in the first few weeks of life
Spontaneous closure of secundum defects can occur up to about 8 years of age
In 5-10%, increased pulmonary blood flow leads to pulmonary HTN and Eisenmengers

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34
Q

What is Eisenmenger’s physiology?

A

Elevated PVR causes reversal of atrial shunting (shunt becomes right to left), leading to differential cyanosis (sats normal in the upper body, cyanotic in the lower limbs)

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35
Q

ECG findings in ASD?

A

RSR’ in V1

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36
Q

Treatment of ASD

A

PFO: none unless high risk for paradoxical embolism
Catheter-based closure for some secundum ASDs
Surgical closer if not appropriate for catheter
Surgery is contraindicated in Eisenmenger’s

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37
Q

Cardiac defects associated with Alagille syndrome?

A

Peripheral pulmonary stenosis
Pulmonary valve stenosis

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38
Q

Cardiac defects associated with congenital rubella syndrome?

A

PDA
Peripheral pulmonary stenosis

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39
Q

Cardiac defects associated with Noonan syndrome?

A

Pulmonary stenosis (dystrophic pulmonary valve) 50%
ASD
Cardiomyopathy (hypertrophic 20%)
LVH
Anterior septal hypertrophy

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40
Q

Cardiac defects associated with velocardiofacial syndrome?

A

Conotruncal abnormalities
Aortic arch abnormalities

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41
Q

Cardiac defects associated with Williams syndrome?

A

Peripheral pulmonary stenosis

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42
Q

Cardiac defects associated with fatal alcohol syndrome?

A

Septal defects

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43
Q

Cardiac defects associated with fatal hydantoin (phenytoin) syndrome?

A

VSD
ASD
PDA
Coarctation of the aorta

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44
Q

Incidence of congenital heart disease?

A

0.8% in the normal population
1-4% in a pregnancy after the birth of a child with CHD (or if a parent is affected)

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45
Q

What is the strongest stimulus for postnatal closure of the ductus arterioles?

A

Increased systemic oxygen stimulation
Functional closure usually occurs by 15 hours of life

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46
Q

Cardiac defects associated with 22q11?

A

Conotruncal heart defects - Tetralogy of Fallot, interrupted aortic arch, VSDs, truncus arteriosus and PDA

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47
Q

Cardiac defects associated with Down syndrome?

A

Endocardial cushion defect (AV canal)
VSD

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48
Q

Cardiac defects associated with Turner syndrome?

A

Bicuspid aortic valve
Aortic root dilatation
CoA
AS
ASD
Anomalous pulmonary venous drainage

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49
Q

Cardiac defects associated with VACTERL?

A

VSD

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50
Q

Which embryologic structures do the right and left ventricles arise from?

A

Bulbus cordis - right ventricle
Primitive ventricle - left ventricle

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51
Q

Ion movement abnormalities seen in LQT1 and LQT2?

A

Prolonged potassium efflux

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52
Q

Ion movement abnormalities seen in LQT3?

A

Prolonged sodium influx - due to SCN5A mutation

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53
Q

Which long QT subtypes are associated with prolonged potassium efflux?

A

LQT1
LQT2
LQT5

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54
Q

Acquired causes of a prolonged QT?

A

Electrolyte abnormalities (hypocalcaemia, hypokalaemia and hypomagnesaemia)
Myocarditis
Drugs

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55
Q

Which event in the cardiac cycle is represented by the third heart sound?

A

Rapid ventricular filling
- occurs in any condition that causes left ventricular volume overload or dilatation

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56
Q

Calculation for cardiac output

A

Cardiac output = (oxygen consumption ml/min) / (Arterial sats - venous sats)

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57
Q

Cause of wide splitting of S2?

A

ASD
PS
Epstein anomaly
TAPVR
RBBB

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58
Q

Causes of single S2?

A

think about the position of aortic/pulmonary arteries and the function of the aortic/pulmonary valves
Pulmonary or aortic atresia
Severe stenosis
Truncus arteriosus
TGA

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59
Q

Which cardiac structure is most likely to be affected in chronic rheumatic heart disease?

A

Mitral valve (70%)
Aortic valve next most affected (25%)

60
Q

Newborn with sats 88%, single S2, soft ESM?

A

Truncus arteriosus
- single S2 due to single semi-lunar valve
- ESM due to increased flow across the valve
- may have bounding pulses due to run off to the pulmonary vascular bed during diastole

61
Q

Calculating PVR?

A

PVR = (mean PA pressure - mean LA pressure) / Qp
= value in woods units

62
Q

Woods units cut off for pulmonary hypertension?

A

Pulmonary hypertension >3 woods units

63
Q

Overview of Brugada syndrome

A

Uncommon cause of SCD/syncope
Caused by genetic defect in myocardial sodium channels predisposing patients to ventricular tachyarrhythmias (may be triggered by fevers)
ECG findings: ‘coved’ ST elevation in V1-2, pseudo RBBB

64
Q

Overview of WPW

A

Caused by accessory pathway between atria and ventricles allowing impulses to bypass the AV node
ECG findings: short PR, prolonged QRS complexes with delta wave

65
Q

Clinical differences between LQT1 and LQT2

A

LQT1: more common (35%), arrhythmia triggered by exercise or emotional events
LQT2: second most common (25%), arrhythmia triggered by sleep/rest

66
Q

ECG showing tachycardia, irregularly irregular, narrow QRS, abnormal p waves?

A

Likely atrial tachycardia

67
Q

Most common cause of congenital heart block?

A

Autoimmune CHB (90%)
- usually due to maternal autoantibodies to Ro (SSA) or La (SSB)
- most mothers are asymptomatic
- risk factor is poor antenatal care

68
Q

Baby with tachypnoea, poor feeding, sats of 75% in the right hand and 85% on the left?

A

TGA
- reverse differential cyanosis may be seen in TGA with PDA

69
Q

Causes of a long QT?

A

CNS cause/head injury
Hypokalaemia
Hypocalcaemia
Hypomagnesaemia
Adrenal insufficiency
Hypothermia
Erythromycin, quinidine, cisapride
Phaeochromocytoma
Romano-Ward syndrome
Jervell-Lange-Nielson syndrome

70
Q

Normal QTc?

A

Upper limit of normal is 0.45 seconds (up to 6 months), and 0.44 seconds in older children

71
Q

Calculating corrected QT?

A

QT / (square root of RR interval)

72
Q

Most common complication following end-to-end anastomosis to repair coarctation of the aorta?

A

Systemic hypertension (particularly when diagnosed in older children)

73
Q

Concave ST elevation and PR depression throughout most limb leads and precordial leads, with reciprocal ST depression and PR elevation in aVR?

A

Pericarditis

74
Q

Calculating Qp:Qs ratio?

A

= (Aorta sats - mixed venous O2 sats) / (PV sats - PA sats)

75
Q

ECG clues for corrected TGA?

A

Q waves over right precordium (due to reverse septal depolarisation) with absent Q waves over the lateral precordium (in the absence of other criteria for RVH)

76
Q

Soft ESM at left sternal edge, single loud second heart sound, cyanotic?

A

Repaired TGA
- single loud S2 due to anterior position of the aortic valve following repair

77
Q

Single loud S2 due to abnormal position of arteries?

A

Abnormal position of aortic/pulmonary arteries:
- truncus arteriosus
- tricuspid atresia
- hypoplastic LH syndrome
- TGA
- L-TGA
- Tetralogy of Fallot

78
Q

Single loud S2 due to abnormal valves?

A

Abnormal aortic/pulmonary valves:
- severe aortic or pulmonary stenosis
- pulmonary atresia
- Eisenmenger syndrome
- large VSD

79
Q

Findings on auscultation in an infant with tetralogy of Fallot DURING a cyanotic spell?

A

Ejection systolic murmur becomes softer (less blood flow crossing the pulmonary valve)

80
Q

Findings in hypercyanotic episodes?

A

Paroxysms of tachypnoea
Prolonged crying
Intense cyanosis
Reduced intensity of ejection systolic murmur

81
Q

Clinical findings in pulmonary overcirculation (mixed-circulation)

A

Persistent saturations >90%
Tachypnoea (may be effortless/with effort)
Tachycardia
Lactic acidosis
Plethoric lung fields on CXR
Normal pulses (may have cool peripheries)

82
Q

Warm peripheries with bounding pulses?

A

High cardiac output to the systemic circulation, may be seen in sepsis

83
Q

Degree of L to R shunting in moderate-large VSDs is expected to increase over the first 3-4 weeks of life due to what physiological event?

A

Reduced pulmonary vascular resistance
- increased shunting leads to symptoms/signs of heart failure (tachypnoea, tachycardia, WOB, pallor and FTT)
- are at risk of developing pulmonary hypertension over time

84
Q

Overview of Eisenmenger’s syndrome?

A

Reversal of longstanding L to R shunt, to become R to L shunt (occurs due to development of pulmonary hypertensive vascular disease)
Surgical repair is contraindicated at this stage.

85
Q

ECG findings of pre-excitation in WPW?

A

Delta waves (indicates ventricles are receiving an early electrical signal)
- upsloping/hump at the beginning of QRS (where the Q wave should be)

86
Q

Pre-excitation in WPW increases risk of what?

A

Re-entrant SVT

87
Q

Murmur associated with Williams syndrome?

A

Systolic murmur - supravalvular aortic stenosis (most commonly), can also develop PA stenosis

88
Q

What proportion of pulmonary arterial blood flow is directed through the ductus arteriosus?

A

90%

89
Q

Treatment of SVT?

A
  1. Vagal manouvres
  2. IV adenosine (0.1mg/kg, increase to 0.2mg/kg and 0.3mg/kg as needed)
  3. If unstable: synchronised DC shock (0.5J/kg first)
90
Q

Overview of supracristal VSD?

A

5% of VSDs
Located anterior to and directly below to pulmonary valve in the outlet septum, superior to the crust supraventricularis

91
Q

Clinical manifestations of supracristal VSD?

A

Wide range of symptoms: trivial aortic regurgitation and small L to R shunts in asymptomatic children, or massive cardiomegaly in symptomatic adolescents

92
Q

Complication of supracristal VSD?

A

Prolapse of aortic valve into the defect and aortic insufficiency, which can eventually occur in 50-90% of patients

93
Q

Overview of the formation of the heart tube?

A

Primitive heart tube forms during 3rd week of embryogenesis through convergence of the bilateral endocardial tubes, formed from the mesodermal germ cell layer.
The heart tube forms through five distinct regions, which after cardiac looping go on to form the major structures of the heart

94
Q

Truncus arteriosus becomes?

A

Aorta and pulmonary artery

95
Q

Bulbus cords becomes?

A

Right ventricle and outflow tracts of the right and left ventricle

96
Q

Primordial ventricle becomes?

A

Left ventricle

97
Q

Primordial atrium becomes?

A

Right and left auricles and the left atrium

98
Q

Sinus venosus becomes?

A

Right atrium, vena cavae and coronary sinus

99
Q

5 regions of the heart tube?

A

Truncus arteriosus
Bulbus cordis
Primordial ventricle
Primordial atrium
Sinus venosus

100
Q

Role of beta blockers in Tet spell?

A

Reduce dynamic muscular stenosis of the RVOT, thereby reducing R to L shunting

101
Q

Pathophysiology of a Tet spell?

A

Increased PVR increases R to L shunting
Classic sign: reduced intensity of the murmur due to less blood crossing the pulmonary valve
Precipitants include crying, fever, defaecation, feeding and waking from naps

102
Q

Newborn with continuous murmur present at delivery, asymptomatic, normal saturations?

A

Coronary artery fistula

103
Q

Overview of coronary artery fistulae?

A

90% terminate into the right heart
Symptoms depend on where fistula occurs and where the additional blood ends up
Continuous murmur (like PDA but lower on the sternal border), and often peaks in mid to late diastole
Less commonly, can present with angina, cardiac failure, endocarditis or arrhythmias

104
Q

Baby with cyanosis, single S2, systolic murmur loudest at the LLSE?

A

Pulmonary atresia (usually with a VSD)

105
Q

“To and fro” systolic and diastolic murmur?

A

Characteristic of ToF with absent pulmonary valve
- murmur in pulmonary region, short pause between components
- present with respiratory distress, variable cyanosis, single S2 and murmur

106
Q

Overview of antenatal finding of echogenic foci?

A

Usually normal variant
Seen in 20% of 2nd-3rd trimester scans
May be associated with slightly increased risk of T21
Most cases self resolve by birth, the remainder mostly resolve by the age of 5

107
Q

Complication of double inlet left ventricle (single ventricle)?

A

If pulmonary blood flow reduced: cyanosis
If pulmonary blood flow not reduced: excessive pulmonary flow resulting in CCF

108
Q

Management of double inlet left ventricle?

A
  1. Pulmonary artery banding (to protect pulmonary vasculature from over circulation)
  2. Fontan procedure at 3-4 years of age (definitive repair)
    Option of Damus-Kaye-Stansel or Norwood-type procedure (PA to aorta anastomosis) to fix the obstruction to systemic blood flow, if required
109
Q

When do T waves in V1 become upright?

A

Should never be positive before 6 years of age, may remain negative to adolescence
Upright T waves indicate RVH or strain

110
Q

ECG changes in pulmonary valve stenosis?

A

Right axis deviation and RVH mostly

111
Q

ECG changes in PDA?

A

Usually no ECG changes (as not usually clinically significant)
Could have LVH, sometimes biventricular hypertrophy

112
Q

ECG changes in subaortic stenosis?

A

LVH with prominent Q waves in precordial leads

113
Q

Role of the septum primum?

A

Acts as a valve over the foramen ovale
Allows blood to flow from R to L in utero, after birth, pressure in the left heart increases and the septum primum ‘closes’ over the foramen ovale

114
Q

What is the fossa ovalis?

A

Refers to the depression in the intertribal septum (does NOT suggest patency)

115
Q

Direction of septum primum development?

A

At 4 weeks, a ridge forms in the roof of the atria, and develops into the septum primum which grows towards the endocardial cushions

116
Q

Partial AVSD

A

Refers to defects that have an intertribal connection, but lack inter ventricular communication

117
Q

Intermediate AVSD

A

Variably defined, commonly refers to defects in the intertribal portion, a small interventricular defect with a common AV valve annulus containing two AV valves

118
Q

Complete AVSD

A

Refers to presence of defects at both levels, as well as a common AV valve

119
Q

Clinical presentation of AVSD

A

Depends on degree of left to right shunting, and the degree of AV valve regurgitation.
In the neonatal period, PVR is high which limits the degree of left to right shunting, however this increases with age as PVR and RV compliance decreases > results in pulmonary vascular engorgement and symptoms of CCF

120
Q

Medical treatment of CCF

A

Indicated when symptomatic
Involves a combination of captopril (for afterload reduction), frusemide (reduces pulmonary congestion) and digoxin (inotropic and deactivating effects)

121
Q

Surgical treatment of CCF due to AVSD?

A

Patch closure of septal defects as well as valvular repair
Usually performed in first 6 months of life

122
Q

ECG findings in pericarditis

A

Sinus tachycardia with widespread ST elevation

123
Q

Clinical presentation of pericarditis

A

Chest pain and fever
History of viral prodrome and heart failure symptoms may also be present
ECG: widespread ST elevation and PR depression
May have raised troponin

124
Q

ECG findings of PE?

A

Right ventricular strain pattern: S1Q3T3 may be seen, however sinus tachycardia is the most common ECG finding

125
Q

Clinical presentation of myocarditis

A

Variable presentation
May include chest pain, arrhythmia and signs/symptoms of heart failure
History of viral prodrome
ECG changes are generally present but are non-specific (include ST and T wave changes, abnormal axis and reduced voltage)
Elevated cardiac biomarkers are usually seen

126
Q

ECG findings in dilated cardiomyopathy

A

ECG is usually abnormal but non-specific, changes include LVH or biventricular hypertrophy

127
Q

Formation of secundum ASDs?

A

Most common type of ASD
Due to defect in the foramen ovale membrane, in which the osmium secundum is excessively large, or there is inadequate formation of the septum secundum
Associated with anomalous pulmonary venous return in 10%
ESM loud at LUSE, with fixed splitting of S2
Magnitude of L to R shunt is most influenced by the relative right and left ventricular compliances, with the right having the most dominant effect

128
Q

Secondary prevention of rheumatic fever?

A

IM penicillin

129
Q

Term infant with cyanosis since birth, ECG shows LVH/LAD/possible delta waves, cardiomegaly and enlarged RA on CXR?

A

Ebstein anomaly - extreme cardiomegaly and WPW on ECG

130
Q

Duration of secondary prophylaxis for acute rheumatic fever?

A

IM benzene every 28 days for 10 years or until 21 years old (whichever is longer)
If severe, may need for 40 years or lifelong

131
Q

Findings in vasovagal syncope?

A

BP, HR and SVR are all low
Underlying mechanism is unclear, but thought to involve inappropriate response to reduced LV filling

132
Q

Overview of pulmonary artery sling?

A

Occurs when the left PA arises from the right PA, and the aberrant left PA then passes between the trachea and oesophagus on its way to entering the left lung
- results in posterior compression of the trachea and anterior compression of the oesophagus

133
Q

Benefit of inhaled NO over IV administration?

A

Results in the direct vasodilation of pulmonary arteries, and action is limited to aerated areas of the lungs, i.e. selective vasodilation (directs blood flow from poorly ventilated areas to better ventilated areas)

134
Q

Mechanism of action of inhaled nitric oxide?

A

Upregulation of cyclic guanosine monophosphate (cGMP)
Binds to Hb and is inactivated instantly in the blood to nitosylhaemoglobins and methaemoglobin
Half life is 3-6 seconds

135
Q

Pressure changes in persistent pulmonary hypertension of the newborn?

A

Pulmonary artery pressure equals systemic pressure
Pulmonary resistance is increased due to pulmonary HTN; therefore pulmonary blood flow is lower than systemic (due to the increased resistance)

136
Q

DDx for widely split S2?

A

Volume overload e.g. ASD, PAPVR
Pressure overload e.g. PS
Electrical delay e.g. RBBB
Early aortic closure e.g. MR
Occasionally seen in normal children

137
Q

Cardiac defect associated with Alagille syndrome?

A

Peripheral pulmonary stenosis (most common)
Can have ToF, septal defects, coarctation of the aorta
(Alagille due to JAG1 or NOTCH2 mutations)

138
Q

Cardiac defect associated with Williams syndrome?

A

Supravalvular aortic stenosis (70%)
Pulmonary valve stenosis
(Williams due to microdeletion in 7q11.23 - elastin gene)

139
Q

Cardiac defects associated with VACTERL association?

A

Usually VSD
Can also have ASD, hypoplastic left heart, TGA, and ToF

140
Q

Electrolyte movement in phase 2 of the action potential in cardiac contractile cells?

A

Efflux of potassium, influx of calcium and sodium via ion channels located in the cell membrane

141
Q

Steps of HLHS surgical management

A
  1. Norwood
  2. Glenn
  3. Fontan
142
Q

Overview of Norwood procedure?

A

Done at 1 week of life, reconstruct the aortic arch using the PA and connect to the RV which can then supply systemic circulation
Pulmonary blood flow classically is established via a BT shunt between the innominate artery and PA, however variations of this can occur

143
Q

Overview of Glenn procedure?

A

At 3-6 months of life
Occurs when the patient outgrows the BT shunt (reflected by progressive cyanosis)
BT shunt is removed and SVT is connected to the PA, providing systemic venous return to the PA

144
Q

Overview of Fontan procedure?

A

Usually slightly older children
Involves connecting the IVC to the PA so the entire systemic venous return flows to the PA, thereby completely relieving cyanosis

145
Q

Primary intervention in newborn with hypoplastic left heart?

A

Prostaglandin infusion
- maintaining the ductus arteriosus using a prostaglandin infusion is essential as this is the only significant source of systemic blood flow
May need balloon atrial septostomy
Following this, a Norwood procedure would be scheduled at around 1 week of life

146
Q

Third heart sound is due to?

A

Rapid ventricular filling

147
Q

Mechanism of cardiomegaly in children with a large PDA?

A

Increased pulmonary blood flow and increased blood returning to the left heart, therefore volume overload of the left ventricle

Written exam (21 decks)

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