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Peadiatrics > Cardiology > Flashcards

Cardiology Flashcards

1
Q

What are the causes of acquired long QT?

A

Antibiotics - macrolides, bactrim, fluoroquinolones
Antifungals - fluconazole, itraconazole, ketoconazole
Antihistamines (non-sedating)
Antipsychotics - haloperidol, risperidone
Tricyclic antidepressant
Class 1A and III anti-arrhythmics
Diuretics - frusemide
Opiates
HYPOcalcaemia/kalaemia/magnesaemia

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2
Q

What is the cut-off in sec for prolonged QT?

A

> 0.47 sec = highly indicative

>0.44 sec = suggestive

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3
Q

What are the causes of short QT?

A

Digoxin toxicity
Hypercalcaemia

= due to gain-of-function of cardiac potassium channels
Manifests as atrial or ventricular fibrillation, a/w syncope/sudden death.
Has congenital causes

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4
Q

What is the treatment for long QT syndrome?

A
  1. Beta-blocker
    - Propanolol > atenolol/metoprolol
    - Not effective in LQTS type 3
  2. Pacemaker
  3. Implanted cardiac defibrillator
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5
Q

What are the auscultatory findings of ASD?

A
  1. Fixed, wide splitting of S2
  2. Systolic ejection murmur
    (Crescendo-decrescendo, loudest left UPPER sternal border)
  3. +/- Early/mid-diastolic murmur
    (If shunt large as will have increased flow across tricuspid valve; best heard left LOWER sternal)
  4. +/- Apical holosystolic murmur t
    (Tricuspid/mitral regurgitation if ostium primum)
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6
Q

When do you treat ASD?

A
  1. Symptomatic
  2. Asymptomatic with Qp:Qs > 2:1
  3. Right ventricular enlargement

Done >1 year but before enters school as less mortality/morbidity

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7
Q

What are the auscultatory findings of AV septal defect?

A
  1. Low-pitched, mid-diastolic murmur at left lower sternal border (increased pulmonary venous return and diastolic flow across AV valve)
  2. Pulmonary systolic ejection murmur (large pulmonary flow)
  3. +/- Harsh apical holosystolic murmur (mitral regurgitation)
  4. +/- Widely split S2 (if massive pulmonary flow)
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8
Q

What are the auscultatory findings of VSD?

A
  1. Holosystolic
    (Begins before AV valve closure thus obscures S1
    - Intensity depends on size (small = louder); left LOWER sternal border
  2. +/- Mid-diastolic murmur at apex
    (Due to extra flow across mitral valve when pulmonary:systemic flow >2:1)
  3. +/- Prominent S2
    (If pulmonary HTN develops as more forceful pulmonic valve closure during diastole)
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9
Q

What are the auscultatory findings of PDA?

A
  1. Continous, rumbling/machinery-like murmur, increasing in intensity during late systole; BELOW left clavicle

OTHER
1. Bounding pulses
2. Wide pulse pressure
(Both due to pulmonary artery ‘stealing’ blood from aorta during diastole)

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10
Q

What are the auscultatory findings of pulmonary hypertension?

A 
1. Narrowly split or single S2 
(Pulmonic valve closes faster as there is higher pulmonary pressure) 
2. Loud pulmonic S2 component 
3. +/- Diastolic decrescendo murmur 
(Secondary to pulmonary regurgitation)
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11
Q

What are the auscultatory findings of coarctation of the aorta?

A
  1. Systolic murmur to left axilla/back
  2. +/- Continuous murmur over praecordium
    (If collateral vessels develop)

OTHER

  1. Upper and lower limb BP gradient (>10 mmHg)
  2. Diminished extremity pulses
  3. Brachiofemoral delay
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12
Q

When does the ductus arteriosus close?

A

Functional haemodynamic closure within 10-15 hours after birth
(50% close within 24 hours, 90% in 48 hours, virtually all in 72 hours)

Fully closes anatomically by 3 weeks

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13
Q

When does the foramen ovale close?

A

Flap fusion complete by age 2 in 70-75% of children

Remaining 25-30% have PFO

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14
Q

What are the auscultatory findings of supravalvular aortic stenosis?

A
  1. Systolic murmur WITHOUT click; heard at base of neck

OTHER
1. BP right arm > 15mmHg left arm
As jet directed into the brachiocephalic artery

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15
Q

What are the CXR findings of coarctation of the aorta?

A
  1. Figure of 3 sign
    (Formed by pre-stenotic dilatation of aortic arch and left subclavian artery, indentation at coarctation site and post-stenotic dilation of descending aorta)
  2. Inferior rib notching
    (Dilated intercostal vessels which form to bypass erode inferior margin of ribs)
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16
Q

What are the auscultatory findings of pulmonary stenosis?

A
  1. Systolic ejection click (varies with respiration) along LEFT UPPER sternal border
  2. Harsh, systolic crescendo-decrescendo murmur; LEFT UPPER sternal border
  3. Radiation to below left clavicle and often to back
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17
Q

What are the ECG findings in right vs. left atrial hypertrophy?

A

P wave -> look at leads II, V1
aVR will be negative
Depolarises in RA first -> LA

RIGHT atrial enlargement = P pulmonale
(‘T’ricuspid) -> ‘T’all, peak P wave
> 2.5mm (inferior leads II, III, aVF)
> 1.5mm V1 and V2

LEFT atrial enlargement (‘M’itral) -> ‘M’-like notched P wave in II (specific sign); and enlarges terminal negative portion of P wave in V1 (sensitive sign)

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18
Q

What are the auscultatory findings of mitral valve stenosis?

A
  1. Apical diastolic murmur
  2. +/- Apical systolic murmur (if mitral insufficiency present)
  3. Loud pulmonic S2
    (From pulmonary hypertension)

ECG
1. LA enlargement
(notched P waves lead II and enlarged negative terminal portion of P wave in V1)
2. RVH (rather than LVH; due to pulmonary HTN)

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19
Q

What effects does the Valsava maneauver have on HOCM vs. AS?

A

Valsalva maneauver -> REDUCES venous return (as increased intrathoracic pressure)
(Note: Squatting INCREASES venous return)

HOCM
Decreased venous return -> decreased LV volume -> increase effect of obstruction -> LOUDER murmur

AS
Decreased venous return -> decreased LV volume -> less flow through AS -> SOFTER murmur

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20
Q

What does the degree of cyanosis in TOF depend on?

A

Degree of right ventricular outflow obstruction

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21
Q

What are the auscultatory findings of hypertrophic cardiomyopathy?

A
  1. Systolic murmur, grade 3-4 crescendo-decrescendo at MIDDLE LEFT to UPPER RIGHT sternal border
  2. Gets louder with Valsalva or rising to erect position
  3. +/- Thrill over praecordium
    (No thrill over suprasternal notch)
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22
Q

What are the auscultatory findings of ToF?

A
  1. Systolic ejection at LEFT UPPER sternal border
  2. +/- Aortic click (in older patients; due to aortic dilation)

If RVOT obstruction severe, very little flow hence murmur can disappear

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23
Q

What condition(s) is ToF associated with?

A

DiGeorge (22q11.2 deletion) - especially if right aortic arch present

Also: T21/18/13, Alagille syndrome, CHARGE

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24
Q

What is the most common cause of sudden death in young athletes?

A

Hypertrophic cardiomyopathy = most common cause in competitive athletes

Aortic stenosis = congenital defect most commonly associated with sudden death in children

Other:
Coronary artery anomalies, commotio cordis (blow to chest -> V.fib), aortic rupture, long QT, WPW, myocarditis

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25
Q

What are the two most common infective causes of myocarditis?

A

Enterovirus (coxsackie B)

Adenovirus

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26
Q

How do you treat atrial fibrillation/flutter in WPW?

A

IV procainamide

For cardioversion if haemodynamic instability

NEVER treat with digxoin and digoxin: although increases AV refractory period, it DECREASES refractory period in accessory pathway -> V-fib

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27
Q

Why is IV verapamil contraindicated in infants (<1 year)?

A

Haemodynamic collapse with hypotension and bradycardia

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28
Q

What is the difference between class 1a, 1b and 1c antiarrhythmics?

A

1a - lengthens action potential (right shift); i.e. depresses phase 0, prolongs repolarisation
Examples: procainamide, quinidine

1b - shortens action potential (left shift); i.e. depresses phase 0 selectively in abnormal/ischaemic tissue, shortens repolarisation
Examples: lignocaine, phenytoin

Ic - does not affect action potential (no shift); i.e. markedly depresses phase 0, minimal effect on repolarisation
Examples: flecainide

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29
Q

Which class of antiarrhythmic drug prolonged QT?

A

Class III (K+ channel blockers)

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30
Q

What are the contraindications for verapamil use in children?

A 
Infants < 1 year age 
A-fib occurring in WPW
A-flutter 
Wide complex tachycardias 
Beta blockers (relative contraindication) as both negative chrono/inotropes
31
Q

There is an increased risk of which congenital heart disease in maternal PKU?

A

Coarctation of the aorta

32
Q

What cardiac defects are seen in fetal alcohol syndrome?

A 
Septal defects (VSD, ASD) 
Conotruncal defects (ToF, aberrant great vessels)
33
Q

What congenital heart conditions demonstrate left axis deviation?

A

Ostium primum
Complete AV defect (endocardial cushion defect)
Tricuspid atresia

34
Q

In which condition do you see reverse differential cyanosis?

A

d-TGA with right-to-left shunt secondary to pulmonary hypertension

The R->L shunting into the descending aorta is more saturated than ascending

35
Q

What is normal progression of T wave (in lead V1) in children as they age?

A 
V1 LEAD (looks at RIGHT side) 
Birth -> 7 days = positive T wave (right-predominance)
7 days -> 9-10 years old = negative T wave 
> 9-10 years old = positive/negative T wave
36
Q

What changes do you see in hyper/hypokalaemia?

A

HYPERkalaemia

  1. Defective ventricle repolarisation = peaked T wave
  2. Atrial paralysis = wide, flat P wave; prolonged PR -> eventual P wave disappearance
  3. Conduction defect = wide QRS, RBBB/LBBB; high AV block; sinus brady -> sine wave progression
  4. Cardiac arrest = asystole/V fib
HYPOkalaemia 
1. Flat T wave/TWI 
2. Increased P wave amplitude 
3. Prolonged PR
4. U wave (V2-V3) -> increased tendency for torsades 
(Also seen in digitalis, amiodarone) 
5. ST depression
37
Q

What are causes of ST elevation/depression?

A

ST ELEVATION

  1. Pericarditis/myocarditis
  2. Intracerebral haemorrhage
  3. Cocaine abuse
  4. LBBB; LVH
  5. Hypothermia

ST DEPRESSION

  1. HYPOkalaemia
  2. Subendocardial ischaemia
  3. LVH with strain
  4. Digitalis
  5. RVH
38
Q

What does positive T wave in V1 after age 7 days mean?

A

Right VENTricular hypertrophy

T wave = ventricular REpolarisation
Normally positive all leads except V1, aVR (as left-dominance)

In newborn -> right dominant; so T wave in V1 (looking at right) is positive. If remain positive, indicates RVH (as left dominance should take over)

39
Q

What are the ECG changes for LVH?

A

In LVH -> QRS moves left and POSTERIORLY
Left = increase R wave and decreases S wave (in left leads, V6)
Posterior shift = decrease R wave and increases S wave (in right lead, V1)

LV strain = the LEFT side is strained; ECG changes occur in LEFT leads (V6)

  1. ST depression
  2. TWI
40
Q

What are the ECG changes for RVH?

A

Term infant: right ventricle wall > left ventricle wall

  1. Right axis deviation
  2. Increased R voltage (V1) or deep S wave (V6)
  3. ST-segment depression/TWI (V1) - indicate RV stress/HTN
  4. rsR in V1-V2
  5. ‘QR’ pattern in V1 at any age (see below)

RVH IN NEWBORN

  1. ‘Pure’ R wave, R >25mm or QR pattern in right chest leads
  2. +ve T wave in V1 after 1 week of age
41
Q

What is used for maintenance therapy for SVT?

A

FIRST-LINE

  1. Beta-blockers
  2. Digoxin/CCB - digoxin may be effective in infant; contraindicated if accessory pathway present

SECOND-LINE
If resistant -> Flecainide, amiodarone, sotalol, propagenone

CURATIVE
1. Radiofrequency catheter ablation/cryoablation

42
Q

Why are digoxin and CCB contraindicated in patients with accessory pathways?

A

BOTH may increase the rate of antegrade conduction of impulses through bypass tract -> V fib

e.g. If patient has WPW (accessory) and A-fib/flutter, giving digoxin will cause rapid atrial impulses down accessory -> V fib

43
Q

What is the MoA of digoxin and verapamil?

A

BOTH decrease refractory period in ACCESSORY pathways -> contra. in A-fib/flutter with WPW

Digoxin MoA = direct suppression of AV node; increases effective refractory period; decreases conduction velocity; positive inotropic effect

Verapamil MoA = inhibits calcium ions from entering slow channels of SM and myocardium during depolarisation -> slows automaticity and AV node conduction (also coronary artery SM relaxation/dilation)

44
Q

What anomaly is WPW associated with?

A

Ebstein anomaly of tricuspid valve

45
Q

What is the treatment for atrial flutter?

A

SYNCHRONISED electrical cardioversion = most effective

If unstable -> shock

For nonemergent cardioversion: (slows AV conduction)

  1. IV diltiazem
  2. Beta-blocker
  3. Digoxin

OTHER
Ibulitide, procainamide, flecainide, sotalol, amiodarone

46
Q

What is the treatment for atrial fibrillation?

A

To treat RVR:

  1. Digoxin (first-line)
  2. CBB (diltiazem, verapamil)
  3. Beta blockers

Maintenance (after RVR resolved)
1. Dofelitide, quinidine, pracainamide, flecainide, disopyramide, propafenone, sotalol

47
Q

When do you anticoagulate a patient with atrial fibrillation?

A

3 weeks BEFORE and 6 months AFTER cardioversion

Patient needs to be STABLE; if not -> immediate electrical cardioversion

48
Q

What are the causes of ventricular tachycardia?

A 
Myocarditis 
Cardiomyopathy 
Long QT
Electrolyte (e.g. hyperkalaemia) 
Ingestions (e.g. digoxin) 
Post-op CHD
49
Q

How do you treat ventricular tachycardia?

A

VT >30 sec usually indicates underlying organic heart disease

UNSTABLE
1. Synchronised electrical cardioversion

STABLE

  1. IV amiodarone (as per PALS)
  2. IV lidocaine

LONG-TERM (need cardio consult)

  1. Beta blockers, procainamide, flecainide, sotalol
  2. Radiofrequency ablation, AICD
50
Q

What is the treatment for acute torsades de pointes?

A

IV magnesium sulfate

51
Q

What are the two phenotypical syndromes of CONGENITAL long QT?

A

Romano-Ward syndrome

  • Autosomal DOMINANT
  • More common than Jervell
  • No deafness

Jervell and Lange-Nielsen syndrome

  • Autosomal RECESSIVE
  • Sensorineural deafness
52
Q

What are the indications for pacemaker in COMPLETE heart block?

A

Surgical heart block > 7 days

Congenital heart block:
1. Symptomatic
OR
1. HR < 55 (without congenital heart disease)
OR
1. HR < 70 (with congenital heart disease)

53
Q

What is the incidence of congenital heart disease in children of affected parents?

A

Normal population incidence = 0.8%

Increases to 2-6% after the birth of a child with CHD or if a parent is affected

If mother has aortic stenosis, 10-15% chance child affected

54
Q

What congenital heart defects are associated with 22q11 deletion (DiGeorge locus) and how do you test?

A

FISH test

Truncus arteriosus
Interrupted aortic arch
Pulmonary atresia with VSD
Tetralogy of Fallot

55
Q

What percentage of CHD are due to CHROMOSOMAL abnormalities?

A

5%

T21 -> AV canal defect (endocardial cushion); VSD
Turner syndrome -> coarctation of aorta
William syndrome (sporadic; can be AD) -> supravalvular aortic stenosis
T13/18 -> VSD
Cri-du-chat (5p minus syndrome) -> VSD

56
Q

What percentage of CHD are due to SINGLE MUTANT genes?

A

3%

DOMINANT INHERITANCE
Noonan syndrome -> pulmonary stenosis; hypertrophic cardiomyopathy
Marfan syndrome -> aortic root dilatation/dissection
William syndrome -> supravalvular AS
Holt-Oram syndrome (abnormal upper limbs) -> ASD/VSD

RECESSIVE INHERITANCE
Ellis-van Crevald (dwarfism, polydactyly, fingernail abnormality) -> ASD
Pompe -> cardiomyopathy

57
Q

What types of CHD are due to ENVIRONMENTAL factors?

A 
TOXINS 
Lithium -> Ebstein anomaly (10%) 
Ethanol -> ASD/VSD (25%) 
Anticonvulsants -> PS, AS, ToF
Retinoic acid -> transposition

INFECTIONS
Rubella -> PDA, peripheral pulmonary stenosis
Coxsackie B -> neonatal myocarditis

58
Q

What types of CHD are seen due to MATERNAL factors?

A

Diabetes -> hypertophic cardiomyopathy (septal), transposition
Lupus -> heart block
PKU -> complex CHD, VSD/ASD

59
Q

What TWO congenital heart disease is commonly associated with LEFT axis deviation?

A

AV canal defect
(endocardial cushion defect); both complete and partial (i.e. ostium primum ASD) - acyanotic

Tricuspid atresia - cyanotic

60
Q

How do you differentiate between primum and secundum ASD?

A

Presence of ‘superior’ QRS axis or left anterior hemiblock in primum-type ASD

61
Q

Which is the only vascular ring that runs in between the oesophagus and trachea?

A

Pulmonary sling

Left pulmonary artery arises distally off right pulmonary artery

Barium swallow reveals classic ANTERIOR indentation of the oesophagus (other forms of vascular rings typically result in posterior indentation)

62
Q

Describe erythema marginatum

A

Seen in rheumatic fever

Nonpruritic, erythematous, serpiginous, macular lesions
Red border with pale centres
Most prominent on trunk and extremities
Tend to predominate during episodes of increased temperature or gentle skin warming

63
Q

When is infective endocarditis prophylaxis required?

A

PROCEDURE

  1. Dental procedure
  2. Respiratory tract
  3. Infected skin, skin structure/musculature
    (4. GI or GU)

CONDITIONS
1. Prosthetic heart valves
2. Prosthetic material used for cardiac valve repair
3. Prior IE history
4. Unrepaired congenital cyanotic heart disease
5. REPAIRED congenital heart disease with:
a) Residual shunts/regurgitation
OR
b) Catheter-based intervention during first 6 months after procedure
6. Valve regurgitation from abnormal valve in transplanted heart

64
Q

What antibiotic regimen is used in IE prophylaxis?

A

Abx BEFORE procedure (never after)

Amoxicillin PO 1 hour prior
(Ampicillin IV 30 min before if cannot tolerate PO)
OR
Clindamycin/cephalexin/azithromycin if allergic

65
Q

What are the side effects of ACEI?

A 
Cough (adults > children) 
HYPERkalaemia 
Elevated creatinine 
Angiooedema (rare)
Leukopenia, anaemia (rare)
66
Q

Which major manifestation of rheumatic fever occurs latest?

A

Chorea

1-8 months after GAS infection

Irregular, usually unilateral, rapid and jerky hand and foot movements, pronation and spooning of hands upon hand extension, facial grimacing with difficulty with fine motor movements.

Milkmaids grip characteristic.

Behavioural changes common - moody, emotionally labile; sudden deterioration in handwriting

67
Q

How do you use maneuvers to differentiate murmurs?

A

DECREASE venous return = Valsalva/squat-> STAND

INCREASE venous return = Passive straight-leg raise/squat

HCM
Any decrease in venous return (less blood to LV) increases murmur (think LV more collapsed, thus obstruction increased)

AS
In AS, decrease venous return (less blood to LV) decreases murmur (opposite to HCM).
Increased SVR decreases murmur
*Decrease in murmur intensity with Valsalva maneuver would be found in setting of most systolic murmurs (AS, PS, MR, TR, VSD without HTN)

MVP
Increased prolapse occurs with decreased ventricular volume (i.e. decreased venous return from Valsalva, squat-to-stand) makes click earlier, with longer/louder murmur
Maneuvers that increase LV volume reduce murmur intensity and move and murmur (and click) later
Increased SVR moves click later

68
Q

What characteristic ECG changes are seen with Brugada syndrome?

A

ST elevation V1-V3 with RBBB

Autosomal dominant
A sodium channelopathy (reduction of sodium inflow, thereby reducing normal AP); risk for ventricular arrhythmia and sudden death

Only treatment = implantable defibrillator

69
Q

What cyanotic condition is worsened with PGE1?

A

Infradiaphragmatic form of TAPVR (as most likely to have severe obstruction to pulmonary venous return)

70
Q

What maneuvers are used in ToF?

A

Decrease in PVR or increase in SVR IMRPOVES cyanosis:
(calming a child, knees to chest)

Cyanosis caused by R->L shunt, thus:

(1) Decrease PVR -> blood directed to lungs away from shunt
(2) Increase in SVR -> increase pressure in left ventricle -> harder for blood to shunt across VSD

71
Q

What ECG changes do you see in pericarditis vs. myocarditis?

A

Pericarditis -> PR depression
Myocarditis -> low voltage QRS

PERICARDITIS
ST elevation (most leads)
T wave flattening/inversion
PR depression (V5-6)

MYOCARDITIS
ST segment and P wave changes
Low voltage QRS pattern

72
Q

What is the most common SYMPTOMATIC vascular ring?

A

Double aortic arch

= Encircling of trachea and oesophagus, resulting in compression

*Note: most COMMON aortic arch abnormality = aberrant right subclavian artery

73
Q

What are the major side effects of antiarrhythmic drugs?

A

CLASS 1a
Procainamide - prolong QT and QRS, blood dyscrasia (agranulocytosis, neutropenia, thrombocytopenia), drug-induced lupus
Quinidine - prolong QRS and QT, hearing loss, psychosis

CLASS 1b
Lidocaine - seizures

CLASS II
Beta-blockers - aggravate asthma

Class III
Amiodarone - corneal deposit, hyper/hypothyroidism, pulmonary fibrosis, gray skin, hepatic toxicity, sun sensitivity

OTHER
Digoxin - arrhythmias

74
Q

Which is more common in children, RBBB or LBBB?

A

RBBB

Normally seen after heart surgery

Peadiatrics (13 decks)

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