Cardiology Flashcards

1
Q

Eisenmenger Syndrome

A

Increased pulmonary pressures leads to reversal of L-R shunt, causing R-L shunt and cyanosis.

Can occur with many different underlying defects including PDA, ASD, and VSD.

Onset typically 2nd-3rd decade

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2
Q

Management of Tet Spell

A

Increase SVR
- squatting
- bring knees to chest

Decrease PVR
- calm child
- O2

Slow HR to allow RV filling
- beta blocker
- morphine

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3
Q

4 components of Tetralogy of Fallot

A
  1. RVOT
  2. VSD
  3. Overriding aorta (dextroposition of aortas with overriding of the ventricular septum)
  4. RVH
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4
Q

Genetic conditions associated with TOF

A

DiGeorge syndrome
Trisomy 21, 13 and 18
Alagille Syndrome
CHARGE syndrome

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5
Q

What is transposition of great arteries

A

Aorta connected to RV and pulmonary artery connected to LV

Most mixing occurs through PFO, then PDA, and 50% will also have a VSD

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6
Q

Presentation of TGA

A

Early severe cyanosis

OR

If also have a VSD, will present with HF and cyanosis at 3-4wks

Single, loud S2
Egg shaped heart on CXR
Persistently positive T waves in V1

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7
Q

Congenital heart lesions with LAD?

A
  • Ostium primum ASD
  • Complete AV canal defect
  • Tricuspid atresia
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8
Q

Types of TAPVR

A
  1. Supracardiac (50%): pulmonary venous blood drains into left vertical vein -> L innominate vein -> SVC
  2. Infracardiac (~23%): pulmonary venous blood drains via a descending vein below the diaphragm -> ductus venosus -> IVC. This type is most likely to have severe obstruction to pulmonary venous return
  3. Cardiac (~20%): connects to RA (usually via the coronary sinus)
  4. Mixed type
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9
Q

Features of obstructed TAPVD

A

Profound cyanosis
Shock
Respiratory distress

Get elevated PA pressure and reduced systemic output

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10
Q

Features of RA isomerism

A

Bilateral “right-sidedness”

  • Bilateral Right atria and right lungs (3-lobes)
  • Horizontal liver with equal-sized lobes
  • Bilateral morphologic RA, each with an SA node
  • Asplenia
  • Bowel malrotations common
  • Complex CHD common (90%) - complex cyanotic CHD and anomalous pulmonary venous return
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11
Q

Features of LA isomerism

A

Bilateral “left-sidedness”

  • 2-30 equal-sized spleens (polysplenia) which often function abnormally
  • Bilateral left atria and left lungs (2 lobes each)
  • Central transverse liver
  • Risk of bowel malrotation
  • CHD (50%) - simple acyanotic + abnormal rhythms (including complete heart block)
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12
Q

Situs inversus

A

Mirror image configuration include arrangement of GIT
- 3 lobed lung on L, 2 lobes on R
- Liver on L
- The atria are switched
- Risk of primary ciliary dyskinesia (25%), no increased risk of cardiac anomalies

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13
Q

CXR findings in CoA

A
  • Cardiomegaly
  • ‘3’ or ‘reverse E’ (notching of aortic isthmus in L superior mediastinum)
  • Rib notching due to erosion from large collaterals
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14
Q

What is Ebstein anomaly

A

Rare anomaly, associated with maternal lithium use

Leaflets of tricuspid valve are displaced downwards to RV wall, forming a large RA.
Will see RA enlargement on ECG and CXR with wall-to-wall enlargement

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15
Q

Aortic stenosis murmur

A

Systolic ejection murmur at RUSE with radiation to the neck
Suprasternal thrill with more severe stenosis
Can have ejection click at apex

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16
Q

HCM Murmur

A

Harsh, systolic crescendo-decrescendo murmur heard best at LLSE
May also have S3 and S4

Quieter with squatting (increased venous return)
Louder with Valsalva (reduced venous return)
ie opposite to AS

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17
Q

Pulmonary artery sling

A

Left PA arises from Right PA and runs between the trachea and oesophagus, leaving an ANTERIOR indentation on the oesophagus

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18
Q

Double aortic arch

A

Persistence of both R and L 4th embryonic arches

Encircling of trachea and oesophagus, with indentation of the R and L sides of the trachea and oesophagus

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19
Q

Right aortic arch

A

Common with TOF and TA

Usually only symptomatic if there is an aberrant L subclavian artery which the ductus arteriosus can arise from and create a ring

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20
Q

Most common cardiac cause of cyanosis in first 24hrs?

A

TGA

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21
Q

ECG features of VSD

A

LVH if moderate defect
Biventricular hypertrophy if large defect

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22
Q

Murmur of VSD

A

Harsh holosystolic heard best at LLSE

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23
Q

Stimulus for closure of PDA

A

Increased O2 tension and decreased prostaglandin after birth

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24
Q

Murmur of PDA

A

Continuous “rumbling” murmur heard throughout systole and diastole. Heard best below L clavicle

Will also have wide pulse pressure and bounding pulses

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25
Q

Fixed split S2 suggests which congenital cardiac pathology?

A

ASD

(increased blood volume into RV -> delayed closure of pulmonary valve)

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26
Q

Murmur in ASD?

A

Murmur occurs due to increased flow across RVOT and pulm valve
= systolic ejection crescendo-decrescendo

Can also get an early or mid diastolic murmur due to increased flow across tricuspid valve

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27
Q

Narrowly split or single S2?

A

Pulmonary hypertension

Single loud S2 can also occur with TGA, HLHS, Truncus arteriosis

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28
Q

Medications which reduce PVR?

A
  • Phosphodiesterase 5 (PDE5) inhibitors eg Sildenafil
  • Endothelin receptor antagonists eg bosanten
  • Prostacyclin (PGI2)
  • Nitric oxide
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29
Q

Pulmonary stenosis murmur

A

Systolic ejection click followed by a harsh systolic crescendo-decrescendo murmur heard best at LUSE and radiations to below L clavicle

30
Q

ECG changes in PS

A
  • RAE (tall p waves)
  • RAD
  • RVH with very tall R waves in V1 and V2
31
Q

“Egg on a string” CXR

A

TGA

32
Q

Immediate management of TGA

A

Prostaglandin to keep the duct open
Balloon atrial septostomy to create an ASD
Later (by 2-3wks), arterial switch surgery

33
Q

Snowman or figure 8 on CXR

A

TAPVD

34
Q

ECG features of aortic stenosis

A
  • LVH
  • LV strain (ST depression in left lateral leads)
35
Q

How common are bicuspid aortic valves?

A

1-2% of the population! May develop stenosis over months- decades

36
Q

Most common cardiac defect seen in Williams Syndrome

A

Supravalvular AS
- narrowing just above the level of the coronary arteries

37
Q

Wall-to-wall heart on CXR

A

Ebstein anomaly
- downwards displacement of the valve leaflets of the triscupid valve -> large RA, TR, PS or functional atresia
- associated with maternal lithium use

38
Q

Management of HCM

A

Beta blockers
Restriction from competitive activity
Some need ICD
CCB +/- amiodarone used in some patients

39
Q

ECG features of HCM

A
  • LVH, prominent septal Q waves, abnormal depolarisation or strain (negative T waves in V6)
40
Q

What is ALCAPA?

A

Anomalous origin of the L Coronary Artery from the Pulmonary Artery
- instead of coming off the aortic sinus, the L coronary artery comes off the Pulm Artery
- After birth, when PA pressure falls, blood can flow from RCA to LCA through collaterals (mini R-L shunt) and back to lungs rather than to myocardium -> anterolateral ischaemia

41
Q

ECG features of ALCAPA

A

Anterolateral ischaemia
- deep Q waves in I, aVL, V5, V6; poor R wave progression in praecordial elads
- ST and T waves changes can occur

42
Q

Which type of vascular ring causes anterior indentation of the oesophagus?

A

Anomalous L pulmonary artery aka pulmonary sling

43
Q

Which type of vascular ring causes indentation on both sides of the oesophagus and trachea?

A

Double aortic arch

44
Q

Jones criteria for RF?

A
  1. Polyarthritis (migratory)
  2. Carditis
  3. Syndenhams chorea
  4. Subcutaneous nodules
  5. Erythema marginatum

Need evidence of recent or concurrent GAS infection + 2major or 1 major + 2minor

45
Q

Most common valve pathology in Acute rheumatic fever?

A

Mitral regurgitation

(2nd = aortic regurgitation)

46
Q

Pericardial friction rub is pathognmonic for…

A

Pericarditis

47
Q

Muffled heart sounds suggests…

A

Pericardial effusion

48
Q

What is pulsus paradoxes and what causes it?

A

Larger change in BP with inspiration that occurs with cardiac tamponade
(usually drops 4-10mmHg with inspiration, with pulsus paradoxus it drops >10-15mmHg)

49
Q

Beck triad for cardiac tamponade

A
  • Rising JVP
  • Quiet, muffled heart sounds
  • Dropping systolic BPs
50
Q

Which drugs are contraindicated in WPW?

A

Digoxin
Verapamil

51
Q

Which CHD commonly causes Wolff Parkinson White?

A

Ebstein anomaly

52
Q

Triggers in congenital long QT syndrome types 1, 2 and 3?

A

Type 1= exercise, commonly swimming
Type 2= arousal eg. loud noises, emotions
Type 3= rest/sleeping

53
Q

Most common type of congenital long QT syndrome and its genetic mutation?

A

Type 1 congenital Long QT syndrome, caused by KCNQ1 gene mutation (~35%)

Type 2 (KCNH2) ~30%
Type 3 (SCN5a) ~10%

54
Q

Management of congenital long QT syndrome?

A

Avoid contraindicated medications
Avoid excessive exertion + no swimming (type 1)
Beta blockers - nadolol or propranolol
Some may need ICD for secondary prevention

55
Q

Defect in the gene for the cardiac ryanodine receptor (RyR2) channel can lead to what condition?

A

Catecholaminergic Polymorphic VT (CPVT)
This channel is particularly sensitive to adrenaline

56
Q

Loss of function in the SCN5A gene encoding cardiac action potential sodium channel?

A

Brugada syndrome

(Congenital Long QT 3 caused by gain of function mutation in same gene)

57
Q

Most common cardiac defect in Alagille syndrome?

A

Branch/ peripheral pulmonary stenosis

58
Q

Acyanotic congenital heart diseases with increased pulmonary blood flow and LVH or combined ventricular hypertrophy?

A

VSD
PDA
AVSD

59
Q

Acyanotic congenital heart diseases with increased pulmonary blood flow and RV hypertrophy?

A

ASD
partial anomalous pulmonary venous drainage

60
Q

Acyanotic heart disease with normal pulmonary blood flow and LVH?

A

Aortic stenosis
Mitral regurgitation
Aortic regurgitation
CoArctation of the aorta

61
Q

Acyanotic heart disease with normal pulmonary blood flow and RVH?

A

Pulmonary stenosis
Coarctation of the aorta in infants
Mitral stenosis

62
Q

Most common ECG finding in acute rheumatic fever?

A

Prolonged PR interval

63
Q

Acyanotic heart defects which can cause LVH/ LAE on ECG and CXR

A
  • PDA
  • VSD

(unlike ASD which usually causes RVH/RAE)

64
Q

Neonate with cyanosis with LAD, LVH on ECG?

A

Tricuspid atresia

(TAPVD, TOF and TGA cause RAD and RVH)

65
Q

What causes S3?

A

Rapid (passive) ventricular filling - deceleration of blood moving from LA to LV

Low frequency brief vibration heard early in diastole

66
Q

What causes S4?

A

S4 is heard during atrial contraction, just before S1 and is due to “stiff” ventricles (LVH or reduced ventricular compliance)

67
Q

Most common type of SVT in infants?

A

AV re-entrant tachycardia (orthodromic more common than antidromic)

68
Q

Management of atrial flutter?

A

Synchronised DC cardioversion
or
Oesophageal overdrive pacing

(don’t give flecainide as can convert to 1:1 conduction)

69
Q

ECG differences between orthodromic and antidromic AVRT?

A

Orthodromic will have narrow QRS complex, and usually retrograde p waves

Antidromic will have wide QRS complex

70
Q
A