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FOP/TAS > cardiology > Flashcards

cardiology Flashcards

1
Q

when does heart start contracting in gestation

A

day 22

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2
Q

how does heart develop in fetus

A

develops mainly from mesoderm
formation of primitive heart tube at end of 3rd week

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3
Q

describe fetal cicrulation

A

vascular shunts bypass non functioning organs e.g. lung and liver

  1. foramen ovale - connection between 2 atria
  2. ductus arteriosis - any blood that doesnt pass through foramen ovale, passes through DA
    - shunts 30% of umbilical blood to IVC
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4
Q

vessels made up of…

A
  1. tunica intima - smooth endothelial cells
  2. tunia media - elastic fibres and smooth muscle
  3. tunica adventitia - fibrous layer made of connective tissue
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5
Q

calculate cardiac output

A

stroke volume (volume ejected by each ventricle) x heart rate

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6
Q

factors that increase sinoatrial node (primary pacemaker site)

A
  • increased sympathetic circulation
  • pyrexia
  • hyperthyroid
  • hypokalaemia
  • catecholaemines
  • beta adrenoreceptors
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7
Q

factors that decrease sinoatrial node action

A
  • increased parasympathetic action
  • beta blockers, digoxin
  • hyperkalaemia
  • ischaemia
  • hypoxia
  • Na and Ca channel blockers
  • hypothermia
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8
Q

ECG leads and areas of the heart

A

ANTERIOR = V1-V4
INFERIOR = 2, 3, AVF
LATERAL = 1 , AVL, V5, V6
R atrium = V1 and AVR

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9
Q

ECG changes of L ventricular hypertrophy

A

inverted T wave in V6
increased R wave voltages in leads 1, 2, aVL and AVF
deep S wave in V1

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10
Q

ECG changes of R ventricular hypertrophy

A

increased R wave voltage in aVR and 3, dominant S wave in V5-V6
upright T wave in V1
R axis deviation
HIGH AMPLITUDE V1-V3 QRS complex
dominant R wave in lead V1

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11
Q

most common cause of heart failure under 2 y/o

A

structural heart defects

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12
Q

CXR changes in heart failure

A

cardiomegaly
pleural effusions
fluid in fissures
pulmonary oedema

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13
Q

management of heart failure

A
  1. adequate nutition
  2. fluid restriction
  3. diuretics (furosemide 1mg/kg) - reduce preload
  4. ACE-I - reduce afterload
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14
Q

describe innocent murmurs

A

short systolic murmur
grade 2/6
loudest at L sternal border
child well
murmur changes with position

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15
Q

ASD cause

A

failure of endocardial cushion development

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16
Q

describe the murmur in ASD

A

ejection systolic murmur heard over upper L sternal edge
fixed wide split 2nd heart sound

= due to turbulent flow over pulmonary valve

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17
Q

definition of PDA

A

persistance of ductus arteriosus beyond one month corrected gestation (usually closes day 7)

causes L to R shunt from aorta to pulmonary circulation and causing over circulation of pulmonary blood

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18
Q

how do PDA present

A

symptoms of heart failure and from over congestion of lungs

resp distress
recurrent resp tract infections
feeding issues
faltering growth
asymptomatic murmur - machine like murmur at L sternal edge

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19
Q

management of PDA

A
  1. fluid restriction
  2. high calorie milk
  3. diuretics
  4. ibuprofen/ paracetamol/ indomethacin - pharmacological closure of ductus in preterm by reducing prostaglandins
  5. surgical closure with transcatheter when >6kg

may want to keep PDA open if have cyanotic heart disorder e.g. give prostaglandin E1

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20
Q

describe VSD

A

most common congenital heart defects
causes L -> R shunt
-> cause pulmonary overcirculation and cardiac failure (usually 6-8 weeks old)

magnitude of shunt depends on:
1. size of defect
2. pulmonary vascular resistance
3. pulmonary to aortic flow ratio - est predictor of heart failure

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21
Q

describe eisenmengers syndrome

A
  1. L-R shunts (VSD) can cause pulmonary hypertension ( increased pulmonary vascular resistance and R ventricle has increase pressure)
  2. causes shunt to reverse to R -> L
  3. become CYANOSED

usually occurs in early childhood
manage with sildenafil

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22
Q

how do VSD present

A

asymptomatic
pan systolic murmur (louder if smaller) + thrill at L sternal edge
faltering growth
resp distress
recurrent LRTI
reduced exercise tolerance
heart failrue at 6-8 weeks

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23
Q

investigations for VSD

A

ECG - L ventricular hypertrophy or R ventricular hypertrophy
CXR
ECHO **

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24
Q

describe hypoplastic L heart syndrome

A
  1. hypoplasia of L ventricle
  2. atresia or stenosis of aortic valve +/- mitral valve
  3. hypoplasia of ascending aorta and aortic arch

= obstructive CHD

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25
Q

presentation of hypoplastic L heart syndrome

A

collapsed neonate in first few days - 14 days of life (when ductus arteriosus close)
absence of all pulses
unwell looking baby
severe acidosis

maternal obesity can prevent detection antenatally

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26
Q

management of hypoplastic L heart syndrome

A

target sats 75-80%
prostin
avoid pulmonary dilators
surgery
1. norwood procedure - atrial septotomy, first few weeks
2. glenn procedure - few months later
3. fontan procedure - at 2/3 y/o, total cavopulmonary correction

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27
Q

describe coarction of aorta

A

narrowing of the aorta (commonly at insertion of ductus arteriosus)
10% of cardiac defects
85% have bicuspid aortic valve (murmur= ejection click)

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28
Q

presentation of crtical coarction of aorta

A
  • cardiovascular collapse at day 2-7 of life (when ductus arteriosus closes as depends on R-> L shunt) - tachypnoea, poor feeding, sweating, unwell baby
  • weak femoral pulses / not palpable
  • hypertension of upper limbs
  • high risk fo NEC
  • systolic murmur that radiates to the back
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29
Q

investigations for coarction of aorta

A
  1. ECHO **
  2. high lactate
  3. CXR - normally normal, rib notching
  4. ECG - L ventricular hypertrophy (deep S wave in V1, tall R wave V6)
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30
Q

management of coarction of aorta

A
  1. resuscitate
  2. intubate and ventilate
  3. inotropes
  4. IV prostaglandin
  5. surgical - ballooon dilatation of aorta / stent
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31
Q

how does total anomalous pulmonary venous drainage present

A

1st few hours of life
increased work of breathing
high lactate

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32
Q

4 features of tetralogy of fallot

A
  1. ventricular septal defect
  2. overriding aorta
  3. pulmonary stenosis (causes R ventricular outflow obstruction)
  4. right ventricular hypertrophy

associated with R sided aortic arch

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33
Q

what type of congenital heart defect in ToF

A

cyanotic defect : R -> L shunt

right ventricular outflow obstruction due to pulmonary stenosis -> causes R to L shunt across VSD -> deoxygenated blood ejected from aorta -> cyanosis

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34
Q

how does tetralogy of fallot present

A

collapsed cyanotic neonate in first few days of life (most common cyanotic CHD)
ejection systolic and thrill murmur
finger clubbing

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35
Q

describe a ‘tet’ spell in ToF

A

begin at 4-6 months of age (< 1 y/o)
increased pulmonary vascular resistance causes worse shunt across VSD -> worsening cyanosis as more deoxygenated blood circulated around body

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36
Q

how to manage tet spell in ToF

A
  1. squatting / raising knees to chest - increases pulmonary vascular resistance
  2. high flow oxygen - pulmonary vasodilator to increase pulmonary flow
  3. morphine - vasodilator
  4. fluid bolus - increases RV venous return
  5. beta blockers
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37
Q

investigations for tetralogy of fallot

A
  1. ECG - R ventricular hypertrophy
  2. CXR - boot shaped heart
  3. ECHO
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38
Q

management of tetralogy of fallot

A
  1. ventilation
  2. IV prostaglandin
  3. beta blcokers
  4. surgical closure at 4-6 months (COMPLICATION = PERICARDIAL EFFUSION)
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39
Q

Describe transposition of great arteries

A

aorta and pulmonary artery arise from opposite ventricles
incompatible with life if not corrected as no mixing between pulmonary and systemic circulations -> CYANOSIS

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40
Q

presentation of transposition of great arteries

A

CYANOSIS on day 1-5 life (usually first 24 hours) when ductus arteriosus closes

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41
Q

investigations for transposition of great arteries

A

CXR - egg on side , congested lung fields
ECHO

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42
Q

management of transposition of great arteries

A
  1. IV prostaglandin to keep ductus arteriosus open
  2. arterial switch procedure (high risk of MI) - if has VSD, Rastelli operation performed
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43
Q

presentation of myocarditis

A

prior flu like symptoms/ viral gastroenteritis e.g. coxsackie, adenovirus
resting tachycardia ***
fever
—-> heart failure and arrhythmias

44
Q

presentation of pericarditis

A

chest pain relieved by sitting forwards
grafting rub
post measles complication

45
Q

management of pericarditis

A
  1. ECG - widespread concave ST elevation and PR depression
  2. NSAIDs
46
Q

risk factors for infective endocarditis

A
  1. structural / congenital heart disease (turbulent jet of blood)
  2. prosthetic valve
  3. immunosuppression
  4. previous IE
  5. long term venous catheters
47
Q

bacterial causes of infective endocarditis

A
  1. staph epidermidis - most common in prosthetic valves
  2. staph aureus
  3. kingella
  4. strep
48
Q

describe mechanism of infective endocarditis

A

microbes colonize cardiac endothelium -> vegetations on valves -> valve regurgitation or stenosis

infection of endothelial surface of the heart, mainly mitral valves

49
Q

presentation of infective endocarditis

A

fever
malaise
new murmur
hepatosplenomegaly

50
Q

signs of infective endocarditis

A
  1. janeway lesions -> micro abscess formation from septic emboli, lesions on palms or soles
  2. oslers node -> immune complex deposition , painful nodes on dorsum of hands
  3. splinter haemorrhages -> micro embolic necrosis
  4. roth spots -> retinal haemorrhages
  5. clubbing
  6. septic emboli -> osteomyelitis
51
Q

management of infective endocarditis

A
  1. blood cultures x 3 before starting abx
  2. ECHO
  3. ECG
  4. IV antibiotics for 4-6 weeks +/- surgical excision of vegetations
52
Q

criteria for IE

A

DUKES CRITERIA

53
Q

cause of rheumatic fever

A

group A streptococcus / after strep throat

most common acquired heart disease

54
Q

criteria / presentation of rheumatic fevers

A

MAJOR CRITERIA
C- carditis - 50-60%, tachycardia, pansystolic murmur from mitral regurg
A - arthritis - 75% large joints
S - subcutaneous nodules
E - erythema marginatum - macular lesion with pale centre
S - sydenhams chorea - 10-15%, involuntary movement of hands and legs

MINOR CRITERIA
F - fever
R - raised ESR/CRP
A - arthralgia
P - prolonged PR interval
P- previous RF

55
Q

diagnosis of rheumatic fever

A

DUCKETT JONES CRITERIA : 2 major or 1 major and 2 minor criteria

throat cultures/ ASOT titres

56
Q

management of rheumatic fever

A

penicillin
aspirin for carditis

57
Q

cardiac defects in DiGeorge syndrome

A

ToF
interrupted aortic arch
VSD

58
Q

2 types of SVT

A
  1. AV re-entry tachycardia (AVRT) - most common in children <8 y/o, re-enterant loop due to accessory conduction pathway e.g. WPW
  2. AV nodal re-entry tachycardia (AVNRT) - most common >8 y/o, 15%, re-enterant circuit through the AV node causing rapid conduction and ventricular beats
59
Q

presentation of SVT

A

HR 200-300 bpm
palpitations
syncope
chest pain
episodic, resolves spontaneously

60
Q

ECG of SVT

A

no p waves
HR 200-300 bpm
QRS normal or narrow
fixed RR interval
regular
sudden onset

61
Q

describe sinus arrhythmias

A

normal variation in HR
increases during inspiration and decreases in expiration

62
Q

diagnosis of SVT

A
  1. 24 hour holter monitor
  2. ECHO
  3. EP studies
63
Q

management of SVT with shock

A

synchronised DC shock 1J/KG - sync to R wave (ventricular depolarisation)

64
Q

management of SVT if haemodynamically stable

A
  1. vagal manouvres e.g. ice dunk, valsava, carotid massage
  2. IV adenosine 0.1mg/kg (3mg -> 6mg -> 12mg every 1-2 minutes) through large proximal vein, short half life

if haemoodynamically unstable -> synchronised shock 1J/kg

65
Q

mechanism of adenosine

A

blocks conduction through AV node and terminates arrhythmia

A1 receptor and inhibits adenyl cyclase and reduces cAMP

66
Q

management of long term SVT

A
  1. beta blockers - prevention
  2. radiofrequency ablation
67
Q

describe wolff parkinson white syndrome

A

accessory pathway (bundle of kent) and gap in myocardial cells to allow conduction through atria and ventricles

ventricles activated before the usual pathway with AVN

AVRT SVT - orthodromic

68
Q

presentation of wolff parkinson white

A

AVRT SVT
babies - resp distress, sweaty, pale, poor feeding
children - chest pain, syncope, palpitations

69
Q

ECG changes in wolff parkinson white

A

delta wave - slurred QRS upstroke
widened QRS
shortened PR interval

70
Q

management of wolff parkinson white syndrome

A
  1. beta blockers
  2. amiodarone *** - give amiodarone when present in tachycardia (dont give adenosine)
  3. calcium channel blockers
  4. radiofrequency ablation - curatuve
71
Q

dangerous arrhythmia in WPW

A

atrial fibrillation in WPW causes broad complex tachycardia irregular
—-> can lead to VF

do not give adenosine or digoxin as can worsen and lead to VF

72
Q

definition of prolonged QT interval

A

> 480 ms in lead 2

73
Q

congenital causes of prolonged qt interval

A

congenital channelopathy most common cause of prolonged QTc
mutations in myocyte potassium channels **

  1. LQTS type 1 - defect in KCNQ1 gene, slows potassium channels
    - jervell and lange nielsen syndrome (congenital sensorineural deafness, AR)
    - romano ward syndrome (AD)
  2. LQTS type 2 - slows cardiac potassium ion channels and causes flatter T waves
  3. LQT3 - affects sodium channels , causes peaked T wave
74
Q

acquired causes of prolonged qt interval

A

hypokalaemia
hypocalcaemia
hypomagnesaemia
medications (azithromycin, olanzapine, quetiapine)
cocaine
HIV
MI
hypothermia

75
Q

presentation of QT interval

A

seizures
sudden syncope
cardiac arrest

76
Q

investigations for QT syndrome

A
  1. ECG
  2. family screening
  3. holter monitor
  4. ECHO
  5. exercise test
77
Q

describe hypertrophic cardiomyopathy

A

25% 1st degree relatives have features of HCM on ECHO

defect in deta cardiac myosin heavy chain
if mild hypertrophy -> mutation in trop T

78
Q

presentation of hypertrophic cardiomyopathy

A

dizziness
fatigue
sudden cardiac death
palpitations
angina
syncope
apex beat displaced
murmur - mid to late systolic impulse,heard when squatting to standing, dynamic murmur

79
Q

management of hypertrophic cardiomyopathy

A
  1. avoid heavy exercise
  2. regular screening
  3. ACE -i - reduce afterload
  4. beta blockers - improve LV filling
80
Q

risk factors for PDA

A

females
trisomy 21
prematurity - most common CHD in preterm babies
rubella
infants born at high altitude

81
Q

when does ductus arteriosus close

A

24-72 hour of age (due to falling prostaglandin level)

82
Q

most common congenital heart defect

A

bicuspid aortic valve

83
Q

cause of cardiomyopathy in chemotherapy

A

doxorubicin toxicity

inhibits DNA replication and transcription
causes dilated cardiomyopathy + congestive heart failure

84
Q

describe holt oram syndrome

A

ASD
hypoplastic thumbs
absent radiii ( radial ray defects)
autosomal dominant

85
Q

structures passed with umbilical venous catheter

A
  1. umbilical vein
  2. taks blood to liver
  3. bifurcates and provides blood into portal circulation via portal vein
  4. blood neters ductus venosus
  5. enters iVC
  6. UVC tip sits at junction of R atrium and IVC
86
Q

murmur in pulmonary stenosis

A

ejection systolic
upper L sternal edge and radiates to back
thrill
click after 1st heart sound (in valvular PS)

87
Q

role of umbilical vein

A

delivers oxygenated blood from placenta to fetus

87
Q

how does ductus arteriosus stay open in fetus

A

low oxygen tension
prostaglandin E2 production from placenta

88
Q

role of umbilical arteries

A

deoxygentaed blood travels back to placenta via 2 x umbilical arteries (arise from internal iliac artery)

89
Q

role of foramen ovale

A

oxygenated blood that arrives in IVC crosses foramen ovale from R atrium to L atrium to then supply the upper body

90
Q

describe fetal haemoglobin

A

HbF = 2 x alpha chains + 2 x gamma chains
start to produce adult Hb in 3rd trimester
by birth, 80% HbF and 20% HbA

HbF has higher affinity for oxygen than adult haemoglobin (oxyhaemoglobin dissociation curve shifts to left due to LOW 2,3 DPG in HbF)

91
Q

describe the 2nd heart sound

A

caused by closure of aortic and pulmonary valves
splitting increased with ASD - independent of inspiration
louder in pulmonary hypertension

92
Q

describe murmur in VSD

A

pansystolic
louder = smaller defect
quieter = larger defect

gallop rhythm/ 3rd heart sound, R ventricular heave, displaced apex beat = heart failure

93
Q

what is the PR interval

A

time between onset of p wave (atrial depolarisation) and onset of QRS complex (ventricular depolarisation)

= conduction through the AV node

94
Q

describe ventricular repolarisation

A

outward flow of potassium
inward flow of sodium and calcium

= t wave on ECG

95
Q

presentation of congenital rubella

A

cardiac defects - PDA (30%), pulmonary artery stenosis, pulmonary arterial hyperplasia
cataract, retinopathy, iris hypoplasia
deafness
microcephaly, IUGR

96
Q

duct dependent pulmonary blood flow

A

critical pulmonary stenosis
pulmonary atresia
tricuspid atresia

97
Q

ductal dependent systemic blood flow

A

coarction of the aorta
hypoplastic L heart syndrome
interrupted aortic arch

98
Q

side effect of prostaglandin E1 and E2

A

HYPOTENSION
flushing
bradycardia (18%)
apnoeas (12%)

causes vasodilation and keeps duct open

99
Q

ECHO changes in VSD

A

dilatation of L atrium and L ventricle

100
Q

types of VSD

A
  1. inlet muscular septal defect (8%) -
  2. outlet or sub pulmonary muscular septal defects (5-7%)
  3. trabecular muscular septal defect (5-20%)
  4. perimembranous septal defects (70-80%)

defects likely to resolve spontaneously: small and moderate apical muscular trabecular or perimembranous
inlet and outlet defects less likely to close

101
Q

cardiac defect in marfans

A
  • aortic regurgitation + aortic dissection due to aortic root dilatation
  • mitral regurgitation / mitral valve prolapse
102
Q

defibrillation in cardiac arrest

A

unsynchronised 4J/KG

103
Q

defibrillation in VT with a pulse

A

synchronised :
1. 1J/KG for first shock
2. 2J/KG for 2nd shock

104
Q

Murmur in aortic stenosis

A

ejection systolic murmur - harsh, loud
loudest at R sternal edge
systolic thrill palpable in suprasternal notch

FOP/TAS (12 decks)

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