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FRACP Exam > Cardiology > Flashcards

Cardiology Flashcards

1
Q

Acute Treatment SVT

A

asymptomatic: usually revert spontaneously

symptomatic: attempt vagal, IV adenosine, CCB

if shocked: synchronised shock

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2
Q

Adenosine

A

receptors: AV nodal tissues, vascular SM

mechanism: activates K+ channels and hyperpolarises cells

use: SVT (slows AV conduction and breaks reentry in AVRNT)

properties: short half life

SE: vasodilations, hypotension, flushing, dyspnoea, chest pain

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3
Q

Allagille’s Cardiac

A

85% peripheral artery stenosis

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4
Q

Anginal therapy

A

mechanisms:

  1. decrease oxygen consumption
  2. increase blood flow

drugs:

  • nitrates: increase NO in vascular SM, increase cGMP and cause relaxation
  • beta 1 receptor blocker: decreased ionotropy/chronotropy
  • calcium channel blocker: coronary artery vasodilator
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5
Q

Antiarrythmics

A

class I: Na channel blockers

class II: beta blockers

class III: K channel blockers

Class IV: calcium channel blockers

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6
Q

Antihypertensive drugs

A

ACEi “prils”

  • mechanism: inhibit conversion angiotension I to angiotensin II with increased bradykinin
  • SE: hyperkalaemia, decrease GFR, crosses placenta, cough, oedema

Angiotension II Receptor Blockers “sartans”

  • mechanism: block activation ARII receptors
  • SE: hyperkalaemia, crosses placenta

Effects:

  • decrease SNS
  • decreased Na/Cl reabsorption
  • decreased ADH secretion
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7
Q

Aortic Arch anomalies

-associated disorders-

A

Marfan’s syndrome: MV prolapse, aortic aneurysm

Ehler-Danlos: aortic root dilatation

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8
Q

Aortic Stenosis

A

incidence: 5% CHD

pathogenesis: failed development 3 leaflets

types: valvular 70%, supra 7%, sub 15%

physiology: high pressure LV with hypertrophy

clinical: chest pain on exertion

ECG: LVH

mumur: systolic right 2nd ICS radiation to neck
treatment: surgical (sub/supra), balloon dilation (valvular)

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9
Q

Atrial Fibrillation

A

incidence: rare in children

pathogenesis: absence of SA stimulus with rapid electral discharges of atria producing fibrillation

RF: large atria, WPW, cardiac surgery

treatment: rate then rhythm control

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10
Q

Atrial flutter

A

pathogenesis: reenterant rhythm from single focus in RA and circles triscuspid annulus

ECG: uniform, HR 250-300, AV node transmits every 2-4 atrial beat

RF: CHD, intra-atrial surgery

treatment: drugs to slow rate

  • non-dihydropyridine CCB: verapamil, diltiazem
  • beta blocker
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11
Q

Atrial Septal Defect

ASD

A

incidence: 10% CHD, F>M

pathogenesis: 50% in association other CHD

types:

  • ostium secundum (70%): site of FO
  • ostium primum (30%): level TM/MV
  • sinus venosus (10%): entry SVC into RA
  • coronary sinus ASD: defect in coronary sinus
  • PFO

clinical: symptomatic if large, RA/RV enlargement

ECG: RAD, RVH

mumur: widely split S2, systolic mumur

treatment:

  • <3mm 100% close spontaneously
  • 3-8mm 80% close by 2 years
  • large closed with device
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12
Q

Atrioventricular Nodal Re-entry Tachycardia

AVNRT

A

incidence: mainly adolescents

pathogenesis: 2 pathways within the AV node

clinical: syncope with exercise/stress

treatment: beta blockers, ablation

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13
Q

Atrioventricular Re-entry Tachycardia

AVRT

A

incidence: 90% SVT in children

clinical: acute onset/cessation at rest or in illness

pathogenesis: normal circuit and accessory pathway

variants

  1. retrograde accessory
  2. bidirectional accessory
  3. antegrade accessory
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14
Q

Atropine

A

mechanism: muscarinic receptor antagonist causing PNS block and increased AV node conduction

use: heart block, bradycardia

SE: dry mouth, constipation, urinary retention

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15
Q

Brugada Syndrome

A

incidence: 3/1000, M>F, asians, presents in 30’s but 2-77yrs

cause: AD, mutation SCN5A gene producing sodium channel causing phase 2 reentry

diagnosis: permanent or transient ECG changes

  • type 1 (20-25%): SCN5A with RBBB, ST elevation V1-V3
  • type 2: GPD1L with <2mm saddleback ST elevation
  • type 3: CACNA1c with type 1/2 ECG changes

clinical: recurrent syncope, arrythmia, sudden death

treatment: quinidine, defibrillation

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16
Q

Calcium Channel Blockers

non-dihydropyridine vs dihydropyridine

A

dihydropyridines (amlodipine, felodipine, nifedipine)

  • reduce SVR and arterial pressure

non-dihydropyridines (verapamil, diltiazem)

  • myocardium selective
  • decrease oxygen demand and reverse coronary vasospasm
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17
Q

Cardiac Axis

A
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18
Q

Cardiac Glycosides

  • digitalis/digoxin-
A

use: CHF/arrhythmias

mechanisms:

  • digitalis: inhibits Na/K ATPase, increased Nai and slows down Ca efflux causing increased contractility and delayed repolarisation
  • digoxin: as above, slower 1/2 life

ECG: increased PR (“digitalis effect”), ST segment depression, T wave inversion

toxicity: AV block, VT/VF, nausea/diarrhoea, yellow halows

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19
Q

Cardiac muscle contraction

A
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20
Q

Cardiac Muscle Depolarisation

A
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21
Q

Cardiac Tamponade

A

definition: inadequate cardiac output due to pericardial effusion

pathogenesis:

  • acute/subacute accumulation of pericardial fluid causing pressure
  • increased diastolic pressure with decreased pulmonary venous return to LA
  • collapsed RA/RV
  • decreased CO/BP
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22
Q

Cardiomyopathies

A

definition: intrinsic disease of the heart muscle

types:

  1. dilated: idiopathic or secondary to infection/disease/cardiotoxic drugs/familial
  2. hypertrophic: familial with AD inheritance
  3. restrictive: idiopathic or associated with systemic disease
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23
Q

Cardiomyopathy

associated disorders

A

DMD

Fabry disease

Hunter/Hurler’s syndrome

Pompe disease

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24
Q

CHF therapy

A

ASPECTS

Afterload reduction: ACEo, ARBs, BNP, milrinone, nitrates

Sympathetic inhibition: beta blockers, BNP, digoxin

Preload reduction: BNP, diuretics

Enhanced contractility: digoxin

Cardiac remodelling prevention: spironolactone

Timely surgery

Systemic disease treatment

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25
Q

Class Ia antiarrhythmics

Na channel blockers

A

drugs: quinidine, procainamide

mechanism: moderate Na channel blockers

  • non-specifically block K channels and slow repolarisation
  • prolongs depolarisation/repolarisation/QRS/QT
    use: atrial/ventricular arrhythmias

SE: agranulocytosis, thrombocytopaenia, tinnitus, torsades, hypotension, rash

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26
Q

Class Ib antiarrythmics

Fast Na channel blockers

A

drugs: phenytoin, lignocaine

mechanism: block fast Na channel

  • decreased AP/QT duration
  • no effect refractory period

use: VT (ischaemic arrhythmias with fast HR)

SE: bradycardia, HB

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27
Q

Class Ic antiarrythmic

Slow Na channel blocker

A

drugs: flecainide, encainide

mechanism: blocks slow Na channels

  • slow phase 0 depolarisation
  • prolongs QRS

use: suppression of PVC, last resort in normal heart

CI: previous MI/VT

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28
Q

Class II Antiarrhythmic

Beta blocker

A

drug: propranolol, metoprolol, atenolol

mechanism: decrease SNS activity to heart by beta 1 receptor

  • decrease cAMP/depolarisation/repolarissation
  • decreased conduction through AV

use: SVT, CHF

SE: bradycardia, AV block, CHF, impotence, bronchospasm

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29
Q

Class III antiarrhythmic

K channel blocker

A

drugs: amiodarone, sotalol

mechanism: K channel blocker

  • normal QRS, increased QT

use: WPW, VT/AF, unstable VT

SE: torsades, pulmonary fibrosis, photodermatitis, hepatotoxicity, thyroid issues, corneal deposits

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30
Q

Class IV antiarrhythmics

Ca channel blocker

A

drugs: diltiazem, verapamil

use: SVTs

mechanism: decrease SA/AV node automaticity

  • prolong depolarisation/repolarisation
  • increase PR interval

SE: CHF, AV block, flushing, headache, gingival hyperplasia

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31
Q

Classification CHD

A
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32
Q

Classification Congenital Heart Disease

A

Stenotic: AS, PS, CoA

Right to Left: TOF, TGA, TA

Left to Right: ASD, VSD, PDA

Mixing: truncus, TAPVR, HLH

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33
Q

Coarctation of the aorta

A

incidence: 10% CHD, M>F, 70% with bicuspid aortic arch

pathogenesis: constriction aorta at any point

  • 98% below left SCA at origin of ductus arteriosus

clinical: difference pulses UL/LL, femoral-radial delay, LL hypoperfusion, BP high in UL and low in LL

  • poor feeding, respiratory distress, CHF, acidosis

CXR: notching of inferior border of ribs by enlarged collaterals

ECG: RVH, cardiomegaly, pulmonary oedema

treatment: end to end anastomosis

prognosis: HTN, CVD, re-coarctation, stroke, aneurysm, endocarditis

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34
Q

Complete endocardial cushion defect

AVSD

A

incidence: 2% CHD, 70% with T21

pathogenesis: failured fushion of upper/lower endocardial cushions with primum ASD/inlet VSD

associations other CHD: TOF, DORV, TGA

clinical:

  • shunts left to right with AV regurgitation
  • hyperactive precordium, systolic thrill/mumur, mid diastolic rumble
  • CHF

ECG: LAD, prolonged PR, RVH, LVH

CXR: cardiomegally, increase pulmonary markings

treatment: surgery at 2-4 months with patch closure

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35
Q

Complete Heart Block

A

acquired: post cardiac surgery, post myocarditis, drugs, rheumatic fever, cardiac tumour

congenital: AI 70% (neonatal lupus), gene mutation, complex structural disease (TGA)

clinical: cardiomegally, CCF

examination: prominent peripheral pulse, systolic mumur left sternal edge, variable 1st heart sound

ECG: prolonged QRS duration with slow ventricular rate as pacemaker is below the bundle of his

treatment: indication for pacemaker

  • CCF, long QT, bradycardia, wide QRS, exercise intolerance
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36
Q

Congenital rubella

-cardiac issues-

A

35% cardiac anomalies

  • PDA, PA stenosis, ASD, VSD
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37
Q

Coronary artery fistula

A

incidence: most common CA anomaly (50%)

pathogenesis: R>>L, most terminate right side of heart (40% RV, 30% TA, 20% PA)

types:

  1. branching tributary: from CA along normal distribution 7%
  2. abnormal CA system with aberant termination >90%

clinical: usually asymptomatic

  • CHF if left to right shunt is large

management: ligation

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38
Q

Cyanotic Heart Diseases

A
  1. Tetralogy of fallot
  2. Transposition of the great arteries
  3. Tricuspid atresia
  4. Truncus arteriosus
  5. TAPVD
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39
Q

DiGeorge syndrome

-cardiac issues-

A

TOF

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40
Q

Diuretics

A

thiazide

mechanism: inhibit NaCl reabsorption in DT

SE: hypokalaemia, hyponatraemia, acidosis, hyperglycaemia, hypercalcaemia

loop diuretics (frusemide)

mechanism: inhibit NaK2Cl transported in thick ascending LOH producing PG

SE: nephritis, ototoxicity, hypokalaemia, hypocalcaemia, alkalosis, increased uric acid

K-sparing diuretics (spironolactone, amiloride)

mechanism: aldosterone receptor antagonist OR Na channel blocker

  • decreased reabsorption of Na and influx of K

side effect: gynaecomastia, hyperkalaemia

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41
Q

Double outlet right ventricle

A

pathogenesis: aorta and PA both originate RV

  • blood shunts across VSD to reach great arteries
  • PA circulation under high pressure

subtypes:

  1. sub-aortic VSD
  2. sub-pulmonary VSD
  3. doubly commited VSD
  4. non-commited VSD
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42
Q

Ebstein’s anomaly

A

incidence: <1% CHD

pathogenesis:

  • downward displacement of TV into RV causing RV hypoplasia
  • TV regurg due to dilated/hypertrophic RA
  • decreased CO
  • required interatrial communication in ALL cases

clinical: cyanosis, dyspnoea, HUGE cardiomegally, CHF, HM, SVT

mumur: TR mumur, wide split S2

ECG: RAH, RBBB, 1st degree block, WPW in 20%

CXR: balloon shaped heart, decreased pulmonary markings

treatment: TV repair and fontan procedure

prognosis: 19% die neonatally, 30% before 10 yrs

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43
Q

Eisenmenger syndrome

A

pathogenesis: left to right cardiac shunt with subsequent pulmonary HTN

  • eventual reversal of shunt causes cyanosis

associations: ASD, VSD, PDA

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44
Q

Fetal circulation

A

drainage

SVC: drains upper body including brain (15%CO)

IVC: drains lower body/placenta (70%CO)

cardiac circulation

  • most SVC and 2/3 IVC goes to RA to RV to PA
  • 10% to lungs and 90% to PDA

outflow

  • 55% of CO goes to placenta (low resistance)
45
Q

Fick’s principle

A

amount of oxygen consumed by body is equal to the AV difference in oxygen content x blood flow (CO)

ie.

CO= oxygen consumption/AV difference

= oxygen consumption/(saturation difference % x oxygen content)

46
Q

Heart block

A

1st degree: prolonged PR

2nd degree:

  • type 1: progressive prolongation PR until QRS dropped
  • type 2: prolonged PR with intermittent QRS dropped

3rd degree: no relationship A/V activity

47
Q

HOCM

A

incidence: 0.2%

genetics: AD, 12 genes encoding sarcomere proteins

pathogenesis: disorganised LV architecture

  • septal/LV hypertrophy causing dynamic outflow obstruction (30%) and abnormal electrical activity

clinical: syncope, chest pain, palpatations, dyspnoea

examination: LV impulse/lift, systolic mumur, S3/S4, MR mid-diastolic rumble

ECG: deep narrow Q waves in lateral/inferior leads, LAH with p wave changes

CXR: cardiomegally

treatment: medications (beta blockers, CCB), myectomy, ventricular pacing

prognosis: survival 10yrs w/o surgery 61%, with 83%

48
Q

Hyperlipidaemia drugs

A

statins (rosuvastatin/atrovastatin/simvastatin)

mechanism: HMG-CoA reductase inhibitor, increased production LDL receptors

SE: myositis, increased LFTs, photosensitivity

fibrates (gemfibrozil/fenofibrate)

mechanism: upregulation lipoprotein lipase and increased clearance TG lipoprotein

SE: myositis, ATN, increased LFTs, cholelithiasis

Niacin:

mechanism: lipolysis inhibition/TG synthesis in adipose tissue

SE: flushing, hyper glycaemia, hyperuricaemia

resins (cholecystyramine, colestipol, colesevalam)

mechanism: bile acid sequesterant preventing intestinal absorption

SE: GI upset, malabsorption, pruritis

Ezetimibe

mechanism: selective inhibitor of dietary cholesterol in small bowel

49
Q

Hypoplastic Left Heart Syndrome

A

incidence: 1% CHD, 40% neonatal cardiac deaths

RFs: Turner’s, T13, T18, Jacobsen’s syndrome

pathogenesis: LV and aorta are hypoplastic and unable to support circulation
- RV supplies both pulmonary and systemic circulation
- survival depends on PDA/ASD or mixing

clinical: ill early, cyanosis, resp distress, CCF, HM

examination: NO mumur, single S2, weak pulses, low CO

ECG: RAH/RVH

CXR: pulmonary oedema, right sided cardiomegally

management: PGE1 infusion, surgery

surgery: 1st Norwood (RV to PA), 2nd 3-6 months bidirectional Glenn (SVC to right PA), 3rd 18-30 months Fontann (IVC to PA)

50
Q

Indications intervention Aortic Stenosis

A

refer:

  • chest pain, SOB, syncope
  • asymptomatic but LVH on ECG or ECHO gradient >50mmHg

intervention:

  • symptoms or LVH strain or cathether gradient >50mmHg
51
Q

Indications VSD intervention

A

1. CHF

2. FTT

3. Aortic regurgitation into VSD

4. Qp/Qs > 2

52
Q

Interrupted aortic arch

A

pathogenesis: part of aorta absent causing obstruction blood flow to lower body

clinical: symptoms post PDA closure

treatment: PGE1, end to end anastomosis

53
Q

Junctional ectopic tachycardia

A

pathogenesis: abnormal automaticity AV node

  • junctional rate>sinus rate and AV dissociation occurs

causes: cardiac surgery, congenital

ECG: narrow QRS, p waves not seen

treatment: difficult

54
Q

Left atrial hypertrophy

-causes-

A
  1. mitral valve disease
  2. cardiomyopathy
  3. large PDA/VSD
55
Q

Long QT syndrome

A

pathogenesis: prolongation myocardial repolarisation causing refractory areas of myocardium with reentry and VT

causes

congenital (50%): defective ion channels

romano-ward syndrome (AD): syncope with exercise/stress

  • KCN/SCN genes coding Na/K channel

jervell and lange-nielson syndrome (AR): bilateral SNHL, syncope with exercise/stress

  • KCNQ1/KCNE1 genes encoding K channels

acquired

  • antiA (Arrhythmics): amiodarone, sotalol, quinidine
  • antiB (AB): erythromycin, clarithromycin, azithromycin, bactrim
  • antiC (psyChotics): haloperidol, risperidonse, chlorpromazine
  • antiD (Depressant): TCA
  • LowEL kiw Ca/K/Mg/thyroid
  • AntiF (fungal): fluconazol
  • AntiH (Histamine)
  • neurological/nutritional/cardiac

clinical: syncope 26%, seizures 10%, palpatations, arrhythmias, cardiac arrest

diagnosis: Schwarz score

treatment: if score <4 or QT>0.47

prognosis: SCD in 50% untreated

56
Q

Longterm treatment SVT

A

1st line: beta blockers +/- digoxin

DON’T USE DIGOXIN/VERAPAMIL WPW

2nd line: flecainide (structurally normal), amiodarone (neonates), sotalol, ablation

57
Q

Magnesium

A

mechanism: prevents influx Ca and prevents early depolarisation

use: torsades

58
Q

Management TOF

A

early: PGE1

late: surgery in 1st year if life

  • initial shunt procedure: Blalock-Taussig with right SCA linked to PA
  • patch closure of VSD
  • enlargement RVOT
59
Q

Maternal conditions

associated CHD

A

diabetes mellitus: TGA 5%

rubella: PDA, PA stenosis, ASD, VSD

alcohol: septal defects 30%

phenylketonuria: TOF 25-50%

SLE: CHB 40%

lithium: TV defect 20%

60
Q

Multifocal atrial tachycardia

A

definition: >3 ectopic p waves with varying PR intervals

incidence: <1yr, usually resolves by 3 years

associations: Noonan’s, hypertrophic CM

61
Q

Myocarditis

A

pathogenesis: cell mediated immunologic reaction causing myocardial inflammation and necrosis leading to fibrosis/dilation/cardiomyopathy

causes

viral: coxsackie B, adenovirus, CMV, echovirus, EBV, Hep C, herpes, HIV, influenza, measles, mump, rubella, varicella

bacterial: mycoplasma, staph

toxins: cocaine, EtOH, diptheria

immune: rheumatic fever, kawasaki, SLE, thyrotoxicosis, IBD

clinical: fever, chest pain, palpatations, syncope, shock

ECG: low voltage QRS, ST-T changes, PR/QT prolongation, arrythmias

XR: cardiomegally

bloods: troponin, CK, viral serology

prognosis: 75% mortality in neonates

treatment: CHF drugs, IVIg

62
Q

Non-cardiac syncope

A

behavioural: breath holding spells

metabolic/endocrine: DM, DI, adrenal insufficiency

neurological: seizures, vertobasilar migraine

psychiatric: conversion

vasovagal: diagnosis of exclusion

63
Q

Noonan’s

cardiac issues

A

pulmonary stenosis 65%

  • also associated with hypertrophic cardiomyopathy
64
Q

Pacemaker AP

A
65
Q

Patent Ductus Arteriosus

PDA

A

incidence: 5-10% CHD, F>M

pathogenesis: failure of DA to close in early weeks of life

  • large PDA causes increased pulmonary pressure

clinical: tachypnoea, CO2 retention, apnoeas, CHF

examination: bounding pulses, wide PP, palpable thrill

mumur: continuous machine like

ECG: LVH

CXR: increased pulmonary vascular markings, cardiomegally

treatment:

  • medical: PGE1 inhibitors, diuretics
  • surgical: <2mm coil/plug, >2mm surgical
66
Q

Pericarditis

A

pathogenesis: inflammation of parietal and visceral surfaces of the pericardium

causes

  • viral: coxsackie, echovirus, mumps, influenza, epstein-barr, CMV
  • bacterial: staph aureus, strep pneumo, pneumococcus, meningococcus, HiB, TB

other: fungal, collagen vascular disease, metabolic, neoplasm

CXR: cardiomegally

ECG: tachycardia, elevated ST, reduced QRS

treatment: pericardiocentesis, anti-inflammatory medications

67
Q

Peripheral pulmonary hypertension

A

incidence: 1/1500

diagnosis: PA>25mmHg

pathogenesis

pulmonary vasoconstriction: hypoxia

increased pulmonary SM hypertrophy: chronic asphyxia, maternal PGE inhibitors

decreased area vascular bed: diaphragmatic hernia, pulmonary hypoplasia, fibrosis, inflammation

other: excess endothelin, deficit NO/prostacyclin

ECG: normal

CXR: cardiomegally

treatment: reverse cause, 100% oxygen, inhaled NO

68
Q

Peripheral vascular resistance

A

PVR: (mean PA pressure-mean LA pressure)/Flow

69
Q

Persistent Truncus Arteriosus

A

pathogenesis: single origin of PA and aorta from the heart

  • large VSD always present
  • blood from both ventricles passes across VSD to single trunk
  • lung exposed to high pressure circulation

associations: Di George, maternal DM

treatment: surgery (<6m) closure VSD and conduit to connect RV to PA

70
Q

Premature atrial contractions

A

incidence: common in childhood

pathogenesis: premature beat arising from an ectopic focus within the atria

ECG: may have normal, prolonged or absent QRS

  • premature p wave may be superimposed on t wave
  • p waves usually different axis
  • long pause after premature atrial contraction
71
Q

Premature ventricular contractions

A

definition: premature, widened bizarre QRS complexes not preceded by p wave

types

  • bigeminy: 1 PVC for each QRS
  • trigeminy: 1 PVC for 2 normal QRS

pathological: 2 or more PVCs in a row, multiform PVCs, increased PVCs with exercise, R on T phenomenon, underlying heart disease

treatment: none, lidocaine, procainamide

72
Q

Pulmonary atresia with intact VS

A

pathogenesis: PA valves fused and triscupid valves are hypoplastic so blood shunts via FO to LA and entire volume flows into LV to the aorta

clinical: cyanosis, respiratory distress

examination: single S2, harsh systolic mumur

ECG: LAD, tall p waves

treatment: PGE1, surgery (pulmonary valvotomy, A-P shunt)

73
Q

Pulmonary Shunt Fraction

A

Qp:Qs= (SatA-SatSVC)/(SatPV-SatPA)

74
Q

Pulmonary stenosis

A

incidence: 10% CHD

pathogenesis:

  • valvular PS: PV thickened with small orifice and hypoplastic RV
  • isolated infundibular PS: rare, associated large VSD
  • supravalvular PS: 3% CHD, stenosis of single or multiple branches PA, associated PV stenosis/VSD/TOF

associations: rubella, William’s, Noonan’s, Allagille, Ehler-Danlos, Silver-Russell

clinical: SOB, tachypnoea, poor feeding, cyanosis

examination: split S2, ejection click, RV thrill, ESM left 2nd ICS

ECG: RVH

CXR: normal

treatment: PGE1, surgery (balloon valvuloplasty, valvotomy)

75
Q

Pulsus paradoxus

A

definition: drop BP>10mmHg during inspiration

pathogenesis: inspiration causes negative thoracic pressure and increased venous return

  • increased pulmonary blood capacity decreasing left sided return
76
Q

Restrictive cardiomyopathy

A

incidence: rare

causes:

  • infiltration: amyloidosis, sarcoidosis
  • non-infiltrative: idiopathic, familial
  • storage diseases: haemochromatosis, Fabry
  • endomyocardial disease
    pathogenesis: massive atrial dilatation

clinical: dyspnoea, respiratory illness, syncope, hepatomegally

examination: S4

ECG: atrial enlargement

77
Q

Right Atrial Hypertrophy

A

causes:

  1. tricuspid atresia
  2. hypoplastic right heart
  3. ebstein’s anomaly
  4. pulmonary atresia
78
Q

Schwartz long QT diagnostic criteria

A
79
Q

Sick sinus syndrome

A

pathogenesis: dysfunction of SA node secondary to dysgenesis of SA node and surround atrial myocardium

incidence: older people

clinical: fatigue, lightheadedness, palpitations

ECG: bradycardia with sinus pauses and sinus arrest

treatment: PACEMAKER

80
Q

Single S2

A

cause: loss of A2 or P2

differentials: severe AS/PS, severe AR, absent pulmonary valve, TOF, Ebstein’s anomaly, pericardial effusion

81
Q

Sinus arrhythmias

A

phase sinus arrhythmia: impulse discharge related to respiration

  • increases with inspiration, decreases with expiration

sinus bradycardia: fitness, anorexia, beta blockers, high vagal tone, sleep, hypothyroidism

extrasystoles: isolated extrasystoles unsignificant

82
Q

Spontaneous Bacterial Endocarditis

A

risk factors

  1. Multiple interventions ie. CVC
  2. Immunocompromised
  3. Unrepaired cyanotic heart defect
  4. Prosthetic material

investigations: 3 blood cultures in 48 hours prior ot AB

prophylaxis: PO amoxycillin 1 hr prior to procedure or IV if with anaesthetic

83
Q

Sudden cardiac death

A

CAD (30%): abberant origin left coronary artery, acquired (Kawasaki, atherosclerosis), coronary arteritis

primary arrythmia (22%): WPW, long QT, brugada, torsades, myopathies, pre-excitation syndromes, CHB

cardiomyopathies (20%): dilated, hypertrophic, restrictive, myocarditis, arrythmogenic RV cardiomyopathy

CHD (15%): HLHS, TGA, TOF

other: obstructive lesions, tumours, Marfan’s, pulmonary HTN, sarcoidosis, aortic dissection

84
Q

SVT

A

incidence: commonest cause tachycardia in children

pathogenesis: all forms of tachycardia except VT

3 types:

  1. reenterant tachycardia with accessory p/w
  2. reenterant tachycardia w/o accessory p/w
  3. ectopic or automatic tachycardias

diagnosis: HR>220, p waves present and related to QRS

treatment: vagal manouvers, medications (adenosine, digoxin, CCB, beta blockers), cardioversion

85
Q

Sympatholytics

A

beta blockers:

  • mechanism: decreased renin release, decreased AII and blocks B1
  • SE: asthma, bradycardia, AV block, CHF, impotence, sedation

clonidine/methyldopa:

  • mechanism: central alpha 2 agonist, decreases NE release
  • SE: sedation, dry mouth, rebound HTN

prazosin:

  • mechanism: alpha 1 blocker
  • SE: orthostatic hypotension
86
Q

Syncope

-pathological signs-

A
  • associated stress/exercise
  • whilst supine
  • in water
  • palpitation prior
  • family hx death before 30yrs
  • odd history
87
Q

Systemic vascular resistance

A

SVR= (mean aortic pressure-mean RA pressure)/flow

88
Q

Tet (hyperpcyanotic) spells

A

incidence: TOF patients 2-4 months

pathogenesis:

  • triggered decreased systemic vascular resistance
  • increased R to L shunt
  • decreased pulmonary blood flow

examination: cyanosis, no mumur, LOC

treatment: knee-chest position to increased venous return, oxygen, morphine, propranolol for prevention

89
Q

Total Anomylous Pulmonary Venous Return

TAPVR

A

definition: pulmonary veins return to the venous system with hypoplasia of the left heart causing mixing of systemic and pulmonary blood

  • all have ASD or incompatible

pathogenesis: abnormal development pulmonary veins week 3 gestation

types:

  1. supracardiac 50%
  2. cardiac (usually RAD) 20%
  3. infracardiac (portal vein, ductus venosus, hepatic vein, IVC) 20%
  4. mixed 10%

clinical: poor growth

examination: mild cyanosis, hyperactive RV impulse, S2 widely split, ESM in pulmonary area, mid diastolic mumur TV

ECG: RVH

CXR: cardiomegally ‘snowman’, increased pulmonary markings

management: medications (PGE1), surgery (balloon atrial septostomy, return of PA to LA)

prognosis: 60% dead by 1yr if untreated

90
Q

Transposition of the Great Arteries

TGA

A

incidence: 5% CHD but most common cyanotic lesion in newborn period

pathogenesis: aorta arises RV, PA arises left ventricle

  • 50% have mixing defect: 40% VSD, 50% PFO/PDA

clinical: early cyanosis

examination: palpable left/right ventricular impulses, loud/single S2, pansystolic mumur (VSD)

ECG: RAD, RVH, Q waves in V1

CXR: egg on string, increased pulmonary vascularity

treatment: PGE1 infusion, surgery (enlarged FO via balloon septostomy, arterial switch operation at week 2)

91
Q

Tricuspid Atresia

A

incidence: 1-3% CHD

definition: absent connection between right atrium and ventricle with hypoplastic right ventricle

  • blood diverted from RA to LA via ASD/FO
  • then from LV to RV

clinical: cyanosis, poor feeding, TET spells

examination: single S2, increased LV impulse, mumur, CHF, clubbing

ECG: LAD, LVH

CXR: cardiomegally, decreased pulmonary markings

treatment: early (PGE1, Blalock-Taussig procedure), late 2yrs (Fontan operation connecting SVC to PA with VSD patch)

prognosis: LVH causes cardiomyopathy

92
Q

Tricuspid Stenosis

A

incidence: rare

clinical: mid diastolic mumur, right heart failure

ECG: left axis deviation, RAH, peaked p waves

93
Q

Trisomy 21

cardiac issues

A

50% have cardiac anomalies

  • AVSD 40%
  • AVSD>VSD>ASD>PDA
  • TOF
94
Q

Truncus Arteriosus

A

incidence: 1% CHD

definition: single arterial trunk from the heart with a large VSD below the truncal valve

pathogenesis: failure of separation of the truncus at 3-4 weeks gestation

clinical: cyanosis, CHF, bounding pulses

examination: systolic ejection click and mumur, single S2

treatment: surgery (VSD closure, conduit between arteries)

95
Q

Turner’s Cardiac

A

left heart lesions

  • aortic stenosis 10%
  • biscuspid aortic valves
  • coarctations
  • dilated aortic arch
96
Q

Vascular Ring

A

incidence: 1-3% all CHD

definition: congenital anomaly of aortic arch with abnormal formation of aorta/surrounding vessels

  • complete encircling of the trachea and oesophagus
  • incomplete: PA sling (trache + eso), innominate artery compression (trache), abberant right subclavian artery (eso)

associations: VSD, TOF, coarctation, PDA, cleft palate, CHARGE, subglottic stenosis

clinical: stridor, wheeze, dysphagia, feeding issues

diagnosis: CXR, barium swallow, bronchoscopy, MRI/CT

97
Q

Vasoactive Factors

A

endothelin-1: released endothelium

  • endothelin A: vasocontriction
  • endothelin B: stimulates NO release

prostacyclin (PG12)

  • released endothelium from COW p/w causing vasodilation

PGH2

  • precursor prostcyclin, thromboxane, PGEs

thromboxane A2

  • released platelets and causes vasocontriction and platelet aggregation
98
Q

Velocardial facial syndrome

-cardiac issues-

A

right sided cardiac issues

  • truncus arteriosus, TOF, pulmonary atresia
99
Q

Ventricular Fibrillation

A

definition: uncoordinated contraction ventriles

cause: underlying cardiac disease/damage

clinical: significantly decreased CO

ECG: non-distinct QRS/T waves, irregular undulations

treatment: cardioversion

100
Q

Ventricular Septal Defect

VSD

A

incidence: 15% CHD

types:

  1. perimembranous 70%: membranous septum under aortic arch
  2. outlet 7%: rim formed by aortic/pulmonary annulus
  3. inlet 8%: AV canal
  4. trabecular 10%: muscular

clinical: pulmonary HTN, CHF

examination: systolic mumur, systolic thrill, loud P2, enlarged left heart, increased pulmonary flow

ECG: LVH

treatment: 1/3 close spontaneously, surgery if Qp:Qs 2:1, pulmonary HTN

prognosis: RBBB 10%, CHB 2%

101
Q

Ventricular Tachycardia

A

definition: >3 premature ventricular beats sustained for >30 secs with HR 120-240

pathogenesis: AV dissociation

clinical: impaired CO

treatment: lidocaine, amiodarone, procainamide, propranolol, cardioversion

102
Q

William’s Cardiac

A

supravalvular AS

PA stenosis

103
Q

Wolf-Parkinson White Syndrome

A

incidence: 1/1000

pathogenesis: pre-excitation via accessory pathway (Bundle of Kent) formed during cardiac development

  • can conduct retrograde/antegrade or both

clinical: SVT

ECG: delta wave, long QRS, ST/T wave changes

treatment: flecainide, procainamide, radioablation

AVOID: AV nodal blockers (adenosine, diltiazem, verapamil, beta blockers, amiodarone)

104
Q

LEFT TO RIGHT SHUNT

A

causes:

  • VSD (LAH/LVH)
  • ASD (RAH/RVH)
  • PDA (LAH/LVH)
  • PAPVD (partial anomalous pulmonary venous return) (RAH/RVH/PAH)
105
Q

LEFT CARDIAC OBSTRUCTIVE LESIONS

A

1. coarctation

2. aortic stenosis (supra/valvular/subvalvular)

3. LV restriction

4. mitral stenosis (supra/valvular/subvalvular)

5. Cor triatriatum

6. PV stenosis

106
Q

Scimitar syndrome

A

definition: pulmonary hypoplasia and PAPVR on right side

CXR: small lung with inspilateral mediastinal shift and tubular structure on right heart border

107
Q

Long QT

A
108
Q

Long QT

A
109
Q

Fontan procedure

A

procedure: right atrum connected to the pulmonary artery directly

  • pulmonary resistance must be low

prognosis: associated atrial flutter in 50% by 18yrs

FRACP Exam (23 decks)

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