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Phase 3a Finals > Paediatric Cardiology > Flashcards

Paediatric Cardiology Flashcards

1
Q

What is an Atrial Septal Defect?

with pathophysiology

A

Defect (hole) in septum (Wall) between 2 atria. connecting right and left atria so blood flows left to right. (pressure in left atrium is higher)

because left to right. pulmonary vessels and lungs get oxygenated so pt doesnt become cyanotic.

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2
Q

comps of atrial septal defect

A

right side overload
right side strain.

right heart failure and pulmonary hypertension

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3
Q

in atrial septal defect, pulmonary hypertension can lead to what complication?

A

Eisenmenger syndrome

pulmonary pressure greater than systemic pressure.

shunt reverse.

right to left shunt

blood bypassess lungs
pt cyanotic!!

others:
stroke - vte
af or atrial flutter
pulmonary htn and right sidesd heart failure

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4
Q

Types of ASD
MC- LC

A

Ostium Secondum - septum secondum fails to fully close - leave hole in wall

Patent Foramen Ovale - foramen ovale fails to close

Ostium Primum - septum primum fails to fully close - hole in wall. = atrioventricular valve defects, make it an atrioventricular septal defect

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5
Q

Features of atrial septal defects

A

congenital heart defect. - found in adulthood.

ejection systolic murmur, fixed splitted of s2
mid systolic crescendo-decrescendo murmur (heard loudest at upper left sternal border)

embolism might pass from venous system to left side of heart causing stroke

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6
Q

features of ostium secondum - asd

A

associated with holt-oram syndrome (tri-phalangeal thumbs)

ecg: RBBB with Right axis deviation

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7
Q

features of ostium primum

A

present earlier than ostium secondum defects

associated with abnormal av valves

ECG: RBBB with left axis deviation, prolonged PR interval

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8
Q

how to pick up on ASD?

A

antenatal scans or newborn examinations.

could be asx.

child/adult may present with : dyspnoea, HF, stroke.

typical sx:
sob
difficulty feeding
poor weight gain
LRTI

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9
Q

How would you manage ASD?

A

if small and asx - watch and wait

surgery: transvenous catheter closure (via femoral vein) or open heart surgery.

Anticoagulant (aspirin,warfarin, NOACs) - reduce risk of clots and stroke in adults.

NOAC: non vit k oral anticoag

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10
Q

give me 4 examples of noac?

A

apixaban
rivaroxaban
dabigatran
edoxaban

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11
Q

What is Ventricular Septal Defect? (give pathophysiology)

A

congenital hole in septum (wall) between 2 ventricles.

can be tiny to entire septum forming 1 ventricle.

more pressure in left so left to right shunt. - acynotic.

leads to right sided overload, rhf, increased flow into pulmonary vessels = pulmonry htn

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12
Q

genetic underlying conditions with VSD

A

downs syndrome
turners syndrome
edwards
patau
cri-du-chat

congenital infections

acquired: post mi

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13
Q

presentation of vsd’s

A

asx initially.
present as late as adulthood.

pick up on antenatal scan or new born baby check hear murmur. 20 week scan.

sx:
poor feeding
dyspnoea
tachypnoea
pallor
failure to thrive

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14
Q

examination findings in vsd

A

pan-systolic murmur more prominently heard at left lower sternal border in 3rd and 4th intercostal space.

poss systolic thrill on palpation.

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15
Q

how would you manage VSD?

A

SMALL VSD with no sx or evidence of pulmonary htn or hf.

surgery: transvenous catheter close via femoral vein or open heart surgery.

med for heart failure: diuretics
nutritional support.

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16
Q

potential complication for VSD and how to manage

give all

A

Infective Endocarditis

abx prophylaxis during surgery to prevent risk of it.

eisenmenger complex - cyanosis and clubbing. heart lung transplant.
aortic regurg: due to poorly supported right coronary cusp resulting in cusp prolapse.
rhf

pulmonary htn - pregnancy is contraindicated with this. 30-50% mortality risk

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17
Q

What is Tetralogy of Fallot?

4 characteristic features

when it presents

A

most common cause of cyanotic congenital heart disease.

presents at around 1-2 months
may not be picked up until 6 months old.

vsd
rv hypertrophy
rv outflow tract obstruction - pulmonary stenosis
overriding aorta

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18
Q

how can pulmonary hypertension cause eisenmenger syndrome

A

pulmonary htn increase the pulmonary pressure so much it means its more than systemic.

blood flows from right to left instead.

blood bypasses lungs and become cyanotic.

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19
Q

Pathophysiology of tetralogy of fallot?

A

VORP - causes right to left cardiac shunt: blood bypasses lungs

ventricular septal defect - blood shunts between ventricles. oxygenated and deox. deox more into left than ox into right.

overriding aorta: aorta further right than normal. RV sends deox blood into it.

RV hypertrophy: due to added resistance of LV, deox blood shunted to left rather than other way.

pulmonary stenosis - rv outflow obstruction makes it harder for deox blood to reach lungs

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20
Q

Risk factors of tetralogy of fallot

A

rubella infection
diabetic mother
increased age of mother - over 40
alcohol consumption in pregnancy

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21
Q

how would you investigate for tetralogy of fallot?

A

echocardiogram. - itll produce colour pics to show direction of blood flow. - doppler flow studies.

cxr - boot shaped heart. due to rv thickening.

right sided aortic arch - 25% pts.

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22
Q

presentation of tetralogy of falor

A

antenatal scan.

ejection systolic murmur by pulmonary stenosis on newborn baby check.

severe caseS: hf before 1 yr old.

older kid - sx of hf

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23
Q

signs and symptoms of tetralogy of fallot

A

cyanosis
clubbing
poor feeding
poor weight gain
ejection systolic murmur heard loudest in pulmonary area - second intercostal space, left sternal border

TET SPELLS - hypercyanotic.

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24
Q

What are tet spells and how would you treat?

A

when right to left shunt is temporarily worse for you get cyanotic episode.

when pulmonary vascular resistance increase or systemic resistance decreases.

ex: child exerting himself - produce co2 which is vasodilator cause systemic vasodilation and therefore systemic vascular resistance.

blood follows path of least resistance so goes from rv to aorta rather than pulmonary vessels, bypass lungs.

precipated by waking physical exertion or crying.
child will be irritable cyanotic and sob.

severe spells: reduced gcs, seizures and potentially death.

tx:
older kid: squat. increases systemic vascular resistance, encourage blood to enter pulmonary vessels
young: position knees to chest.

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25
Q

what medical management could you give to tet spell?

A

supplementary oxygen - hypoxic?

beta blocker: relax rv and improve pulmonary vessel blood flow.

iv fluids - increase preload

morphine: decrease respiratory drive, more effective breathing

sodium bicarbonate: buffer any met acidosis

phenylephrine infusion: increase systemic vascular resistance.

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26
Q

how would you manage tetralogy of fallot

prognosis

A

neonate: prostaglandin infusion to maintain the ductus arteriosus. allows blood to flow from aorta back to pulmonary arteries.

total surgical repair by open heart surgery - definitive. - mortality of surgery 5%

depends on severity - poor without tx. with corrective surgery 90% will live to adulthood.

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27
Q

in cyanosis , beta blockers help how? - ToF

A

reduce infundibular spasm

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28
Q

What is transposition of the great arteries?

A

where attachments of aorta and pulmonary trunk to the heart are swapped (transposed)

rv pumps blood to aorta.
lv pumps blood into pulmonary vessels.

2 seperate circulations that dont mix - one through systemic system and right side of heart and the other through pulmonary system and left side of heart.

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29
Q

3 conditions transposition of great arteries is asociated to?

A

vsd
coarctation of aort
pulmonary stenosis

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30
Q

why is transposition of great arteries not an issue until birth?

A

gas and nutrient exchange happens in placenta - dont need blood to flow to lungs.

after birth, no connection between 2 systems. - baby cyanosed.

survival depends on shunt between both circulations systemic and pulmonary to allow blood to flow through body to get oxygenated in lungs.

shunt accours in PDA, ASD,VSD

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31
Q

when is transposition of great arteries diagnosed?

A

in pregnancy with antenatal uss.

if not detectedL will present with cyanosis at birth or within a few days. a patent ductus arteriosus or vsd can initially compensate by allowing blood to mix between systemic circulation and lungs but in after a few weeks of life will get respiratory distress, tachycardia, poor feeding , poor weight gain and sweating

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32
Q

how would you manage transposition of great arteries?

A

if VSD, allows some mixing of blood between 2 system and gives time for definitive tx.

prostaglandin infusion - used to main ductus arteriosus. allows blood from aorta to flow to pulmonary arteries for oxygenation

balloon septostomy - involves inserting a catheter into the foramen ovale via umbilicus - inflating a balloon to create a large atrial septal defect. - allows blood returning from lungs (on left side) to flow to the right side of the heart and out through aorta to the body.

open heart surgery - definitive. cardiopulmonary bypass machine to do arterial switch. if present asd/vsd corrected same time

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33
Q

clinical features of transposition of great arteries

A

cyanosis
tachypnoea
loud single s2
prominent right ventricular impulse

egg on side appearance : cxr

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34
Q

what is a ductus arteriosus?

reason for patent

sx

A

fetal blood vessel connecting pulmonary artery to aorta bypassing lungs.

should stop within 1-3 days of birth and close.
if it doesnt closed its called patent ductus arteriosus.

poss genetic
maternal infections like rubella. prematurity - rf

asx
poss adulthood signs of hf

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35
Q

presentation of patent ductus arteriosus

A

new born examination if murmur heard.

sob
difficulty feeding
poor weight gain
lrti

small pda : no abnormal heart sounds

significant pda: normal 1st heart sound with continuous crescendo-decrescendo “machinery” murmur that might continue during 2nd heart sound. makes 2nd heart sound hard to hear.

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36
Q

how would you diagnose pda?

A

echocardiogram
doppler flow student during echo - assess size and characteristics of left to right shunt.

youll see hypertrophy of rv , lv or borth

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37
Q

how would you manage pda?

A

monitor until 1 using echo.

after 1 it wont close spontaneously: trans-catheter or surgical closure.

indomethacin or ibuprofen - give to neonate. inhibits prostaglandin synthesis- closes connection in most cases.

if another congenital heart defect too, then give prostaglandin e1 to keep duct open until after surgery.

38
Q

Pathophysiology of PDA

A

pressure in aorta higher than that in pulmonary vessels.
blood flows from aorta into pulmonary artery.

left to right shunt

increase pressure in pulmonary vessels = htn.
right side heart strain, increased resistance. = rv hypertrophy.

increased blood flowing through pulmonary vessels return to left side = lv hypertrophy.

39
Q

who is pda more common in ?

A

premature babies,
born at high altitudes
maternal rubella infection in 1st trimester

40
Q

features of pda

A

left subclavicular thrill
continous “machinery” murmur - upper left sternal edge
large volume, bounding, collapsing pulse
wide pulse pressure
heaving apex beat

41
Q

acyanotic types of congenital heart disease

A

vsd - mc
asd
pda
coarctation of aorta
aortic valve stenosis

42
Q

what is pulmonary atresia?

A

pulmonary valve dont form properly.
blood cant reach lungs
requires alternative pathway to lungs.

43
Q

3 cyanotic causes of congenital heart disease

A

ToF
TGA
tricuspid atresia

44
Q

initial mx for suspected cyanotic congenital heart disease

A

supportive care

prostaglandin e1: alprostadil

maintains PDA in ductal dependent congenital heart defect.

act as holding measure until definite diagnosis is made and surgical correction performed.

45
Q

what is acrocyanosis?

A

seen in healthy newborns

cyanosis around mouth and extremeties - hands and feet.

diff from other causes of peripheral cyanosis.

occurs immediately after birth in healthy infants.

last 24-48 hrs

46
Q

when is central cyanosis recognised clinically in neonatal period?

A

when conc of reduced haemoglobin in blood exceeds 5g/dl

47
Q

what is the nitrogen washout test used for?

A

cyanosis

diff cardiac/non cardiac cause.

give infant 100% ox for 10 mins after which abg taken.

po2 of less than 15kpa tells you cyanotic congenital heart disease

48
Q

how does an innocent (flow) murmur sound/

A

soft
short
systolic
symptomless (no thrill, added sounds, cyanosis,sob)
situational(quieter when standing, only when unwell)

49
Q

when are pan systolic murmurs heard?

A

mitral regurgitation- mitral 5th intercosta, mid clavicular
tricuspid regurg - tricuspid(5th intercostal, left sternal edge)

vsd - left lower sternal border

50
Q

features of a murmur that suggest bad murmur

A

louder than2/6
diastolic
louder standing

sx(failure to thrive, feeding difficulty, cyanosis, sob)

51
Q

where are the ejection systolic murmurs heard

A

aortic stenosis - aortic - 2nd intercostal, right sternal edge

pulmonary stenosis - pulmonary - 2dn intercostal left sternal edge

hypertrophic obstructive cardiomyopathy - 4th intercostal left sternal edge- just above tricuspid

52
Q

What is BnP ?
causes of raised bnp?
effects of bnp

A

b-type natriuretic peptide - hormone produced by mainly lv myocardium in response to strain

any cause of lv dysfunction like mi or valvular disease.

reduced excretion in pts with ckd.

vasodilator
diuretic and natriuretic
suppresss both sympathetic tone and RAAS system.

53
Q

factors that reduce bnp levels

A

tx with acei, angiotensin-2 receptor blocks and diuretics, beta blockers, aldosterone antagonists

obesity

54
Q

clinical uses of bnp

A

if low conc of bnp (under 100pg/ml - hf unlikley.

bnp good marker for chornic heart failure.

effective tx lowers it.

55
Q

what is considered high, raised and normal level for:
BNP
NTproBNP

A

High: over 400 pg/ml (116 pmol/l)
over 2000 pg/ml (236 pmol/litre)

Raised: 100 -400 pg/ml (29-116 pmol/l)
400- 2000 pg/ml (47-236)

Normal : <100 pg/ml (29 pmol/l)
over 400 pg/ml (47)

56
Q

factors that increase bnp levels

A

lv hypertrophy
ischaemia
tachycardia
rv overload
sepsis
copd
dm
over 70
liver cirrhosis

hypoxemia - including pulmonary embolism

57
Q

classifying chronic heart failure

A

NYHA - new york heart association

class 1
no sx
no limitation - ordinary physical exercise doesnt cause undue fatigue, dyspnoea or palpitations

class 2:
- mild sx
- slight limitation of physical activity: comfortable at rest but ordinary activity = fatigue, palpitations or dyspnoea

class 3 :
- moderate sx
- marked limitation of physical activity: comfortable at rest but less than ordinary activity results in sx

class 4:
- severe sx
- unable to carry out any physical activity without discomfort : hf sx present even at rest with increased discomfort with any physical activity.

58
Q

Types of Heart Failure

A

Ejection Fraction: reduced is less than 35-40%. left ventriclular ejection fraction measured

reduced ejection fraction - systolic dysfunction (impaired myocardial contraction during systole)
preserved ejection fraction (diastolic dysfunction , impaired ventricular filling during diastole)

59
Q

what is heart failure?

A

clinical syndrome where heart in unable to pump enough blood to meet metabolic needs of the body.

60
Q

how do you check for ejection fraction? hf

A

echocardiography

61
Q

give examples of systolic dysfunction

give examples of diastolic dysfunction

A

ihd, dilated cardiomyopathy, myocarditis, arrhythmias

hypertrophic obstructive cardiomyopathy, restrictive cardiomyopathy, cardiac tamponade, constrictive pericarditis.

62
Q

categorising hf by time

A

acute - acute exacerbation of chronic heart failure. most urgent sx are often due to lv failure= pulmonary oedema

chronic : chronic duhhh

63
Q

categorising hf by left or right

A

both preserved ef and reduced ef develop left-sided heart failure.
due to increased lv afterload (arterial htn or aortic stenosis) or increased lv preload (Aortic regurg means backflow to lv)

right sided hf : either increased rv afterload (pulmonary htn) or increased rv preload(tricuspid regurg)

64
Q

left ventricular failure typically results in?

A

pulmonary oedema

dyspnoea
orthopnoea
paroxysmal nocturnal dyspnoea
bibasal fine crackles

65
Q

right ventricular failure typically results in?

A

peripheral oedema - ankle/sacral oedema

raised jugular venous pressure
hepatomegaly
weight gain due to fluid retention
anorexia - cardiac cachexia

66
Q

what is high output heart failure

give some causes

A

normal heart cant pump enough blood to meet metabolic needs of the body.

anaemia
ateriovenous malformation
paget’s disease
pregnancy
throtoxicosis
thiamine def (wet beri-beri)

67
Q

What is de-novo heart failure?

caused by what?

A

acute heart failure without a past history of heart failure.

caused by increased cardiac filling pressures and myocardial dysfunction usually as a result of ischaemia.

causes reduced cardiac output and therefore hypoperfusion.

in turn causes pulmonary oedema.

less common causes:
viral myopathy
toxins
valve dysfunction

68
Q

what is decompensated heart failure?

A

most cases of acute heart failure.

causes:
acs
hypertensive crisis
acute arrhythmia
valvular disease

general pre-existing cardiomyopathy.

presenting features:
signs of fluid congestion
weigth gain
orthopnoea
breathlessness

69
Q

patients with heart failure can be broadly characterised into 1 of 4 groups what are they?

A

with our without hypoperfusion

with or without fluid congestion

70
Q

symptoms of heart failure acute

signs of heart failure acute

A

breathlessness, reduced exercise tolerance, oedema, fatigue

cyanosis, tachycardia, elevated jugular venous pressure, displaced apex beat, chest signs: bibasal crackles poss wheeze too, s3 heart sound (left side hf)

90% of ahf will have normal/increased bp

71
Q

diagnostic work up of acute hf patients?

A

bloods - look for underlying abnormality like anaemia, abnormal electrolytes or infection

cxr: pulmonary venous congestion, interstitial oedema, cardiomegaly

echocardiogram:
- for pts with new-onset hf and for pts with known hf with suspected change in cardiac function
- if cardiogenic shock or suspected valvular problems
- may identify post-mi comps

bnp : raised levels (over 100 mg/l) - myocardial damage and supportive of a diagnosis

72
Q

features of chronic heart failure

A

dyspnoea
cough: worse at night - pink/frothy sputum

orthopnoea
paroxysmal nocturnal dyspnoea
wheeze (cardiac wheeze)
weight loss - cardiac cachexia : 15% pts. - may be hidden by weight gained secondary to oedema

bibasal crackles on examination

signs of right sided heart failure: raised jvp, ankle oedema and hepatomegaly

73
Q

Heart failure acute management

A

iv loop diuretic - furosemide or bumetanide

ox - keep 94-98%

vasodilator: dont give nitrates to all pts. only in concomitant mi, severe htn or regurgitant aortic/mitral valve disease. - SIDE EFFECT IS HYPOTENSION

if resp failure: CPAP

74
Q

how to treat hypotension in acute heart failure pt?
under 75mmHg/cardiogenic shock

A

some tx like loop diuretics and nitrates may exacerbate hypotension

inotropic agent - dobutamine - if severe lv dysfunction with potentially reversible cardiogenic shock

vasopressor agent : norepinephrine - if insufficient response to inotropes and evidence of end-organ hypoperfusion

mechanical circulatory assistance : intra-aortic balloon counterpulsation or ventricular assist devices.

75
Q

what regular medication can be continued in hf acute tx?

when would you stop beta blocker

A

beta bloickers/ ace inhibitors.

only stopped beta-blocker if pt has hr less than 50 bpm, 2nd or 3rd degre av block or shock

76
Q

tx for chronic heart failure

A

1st line: ace-inhibitor + beta-blocker - start 1 drug at a time.
bb: bisoprolol, carvedilol, nebivolol
( these 2 dont have an effect on mortality with preserved ef)

2nd line: aldosterone antagonist: spironolactone and eplerenone.

if reduced ejection fraction can give sglt-2 inhibitor :2 line - canagliflozin, dapagliflozin, empagliflozin - reduce glucose reabsorption and increase urinary glucose excretion.

3rd line:
ivabradine - if sinus rhythm over 75/min and lv fraction less than 35%

sacubitril-valsartan - iuf lv fraction under 35%. for hfreduced ef sx on acei or arb. start after acei/arb washout period

digoxin : improve sx due to inotropic effects. if coexistent af give.

hydralazine with nitrate : afrocarribeans

cardiac resynchronisation therpay : widened qrs (lbbb) complex on ecg

or implantable cardioverter defibrillatory : monitors heart and applies defib shock to cardiovert pt back to sinus rhythm if arrhythmia identified.

77
Q

which 2 chronic heart failure tx can cause hyperkalaemia?

A

ace inhibitors

aldosterone antagonists

78
Q

what vaccinations could you give for chronic heart failure pts?

A

annual influencza

one-off pneumococcal vaccine - if asplenia, splenic dysfunction or ckd give booster every 5 years.

otherwise adults need just one dose.

79
Q

What is Rheumatic Fever?

A

Type 2 hypersensitivity to a recent strep pyogenes infection (strep throat - 2-4 weeks after).

Rare in west, causing joint pain and carditis. Repeat exposure can cause fibrosis of valves, causing regurgitations

80
Q

Pathophsyiology of Rheumatic Fever

A

caused by group a beta-haemolytic streptococcal , typically streptococcus pyogenes causing tonsilitis.

immune system makes antibodies to fight infection.

these antibodies target bacteria and antigens on cells of persons body eg myocardium in heart.

type 2 hypersensitivity.

81
Q

presentation of rheumatic fever

A

2-4 weeks after strept infection like tonsillitis

fever
joint pain
rash
sob
chorea
nodules

82
Q

what joint involvement in rheumatic fever

A

migratory arthritis affects large joints with hot swollen painful joints.

migratory- diff joints inflamed and improve at different times.

83
Q

what heart involvement in rheumatic fever

A

carditis with pericarditis, myocarditis and endocarditis leading to :

tachy/b rady
murmurs from valvular heart diseasE: mitral valve disease

pericardial rub on auscultation
hf

84
Q

skin involvement in rheumatic feave

A

subcutaneous nodules

erythema marginatum rash - pink rings of varying sizes on torso and proximal limbs

firm painless nodules over extensor surfaces of joints ie elbows.

85
Q

nervous system involvement in rheumatic fever

A

chorea - irregular uncontrolled rapid movements of limbs.

sydenham chorea.

86
Q

how would you assess for rheumatic fever?

A

throat swab- bacterial culture

ASO antibody titre

echocardiogram, ecg, cxr.

use jones criteria

87
Q

diagnostic criteria for rheumatic fever

A

Revised Jones criteria (JONES-FEAR)

Evidence of recent infection (group A antigen test, positive throat culture, strep antibodies (ASO antibody titre)) + 2 major signs or 1 major 2 minor.

Joint arthritis
Organ inflammation (carditis+murmur)
Nodules under skin (firm, painless)
Erythema marginatum (red splodgy rash all over)
Sydenham’s chorea
Fever
ECG (prolonged PR)
Athralgia without arthritis
Raised ESR/CRP

88
Q

What can be found histologically on the hearts of people with rheumatic fever

A

Aschoff bodies (granulomatous bodies)

89
Q

What murmurs in rheumatic fever?

A

Acute - Mitral and aortic regurgitations
Chronic - Mitral stenosis

90
Q

how to manage rheumatic fever?

A

phenoxymethylpenicillin for 10 days.

nsaid - joint pain
aspirin/steroids- carditis
prophylactic abx - prevent further strep infections.

91
Q

What is the modified duke criteria?

A

infective endocarditis

Phase 3a Finals (25 decks)

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