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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
what medical management could you give to tet spell?
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.
26
how would you manage tetralogy of fallot prognosis
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.
27
in cyanosis , beta blockers help how? - ToF
reduce infundibular spasm
28
What is transposition of the great arteries?
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.
29
3 conditions transposition of great arteries is asociated to?
vsd coarctation of aort pulmonary stenosis
30
why is transposition of great arteries not an issue until birth?
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
31
when is transposition of great arteries diagnosed?
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
32
how would you manage transposition of great arteries?
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
33
clinical features of transposition of great arteries
cyanosis tachypnoea loud single s2 prominent right ventricular impulse egg on side appearance : cxr
34
what is a ductus arteriosus? reason for patent sx
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
35
presentation of patent ductus arteriosus
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.
36
how would you diagnose pda?
echocardiogram doppler flow student during echo - assess size and characteristics of left to right shunt. youll see hypertrophy of rv , lv or borth
37
how would you manage pda?
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
Pathophysiology of PDA
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
who is pda more common in ?
premature babies, born at high altitudes maternal rubella infection in 1st trimester
40
features of pda
left subclavicular thrill continous "machinery" murmur - upper left sternal edge large volume, bounding, collapsing pulse wide pulse pressure heaving apex beat
41
acyanotic types of congenital heart disease
vsd - mc asd pda coarctation of aorta aortic valve stenosis
42
what is pulmonary atresia?
pulmonary valve dont form properly. blood cant reach lungs requires alternative pathway to lungs.
43
3 cyanotic causes of congenital heart disease
ToF TGA tricuspid atresia
44
initial mx for suspected cyanotic congenital heart disease
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
what is acrocyanosis?
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
when is central cyanosis recognised clinically in neonatal period?
when conc of reduced haemoglobin in blood exceeds 5g/dl
47
what is the nitrogen washout test used for?
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
how does an innocent (flow) murmur sound/
soft short systolic symptomless (no thrill, added sounds, cyanosis,sob) situational(quieter when standing, only when unwell)
49
when are pan systolic murmurs heard?
mitral regurgitation- mitral 5th intercosta, mid clavicular tricuspid regurg - tricuspid(5th intercostal, left sternal edge) vsd - left lower sternal border
50
features of a murmur that suggest bad murmur
louder than2/6 diastolic louder standing sx(failure to thrive, feeding difficulty, cyanosis, sob)
51
where are the ejection systolic murmurs heard
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
What is BnP ? causes of raised bnp? effects of bnp
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
factors that reduce bnp levels
tx with acei, angiotensin-2 receptor blocks and diuretics, beta blockers, aldosterone antagonists obesity
54
clinical uses of bnp
if low conc of bnp (under 100pg/ml - hf unlikley. bnp good marker for chornic heart failure. effective tx lowers it.
55
what is considered high, raised and normal level for: BNP NTproBNP
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
factors that increase bnp levels
lv hypertrophy ischaemia tachycardia rv overload sepsis copd dm over 70 liver cirrhosis hypoxemia - including pulmonary embolism
57
classifying chronic heart failure
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
Types of Heart Failure
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
what is heart failure?
clinical syndrome where heart in unable to pump enough blood to meet metabolic needs of the body.
60
how do you check for ejection fraction? hf
echocardiography
61
give examples of systolic dysfunction give examples of diastolic dysfunction
ihd, dilated cardiomyopathy, myocarditis, arrhythmias hypertrophic obstructive cardiomyopathy, restrictive cardiomyopathy, cardiac tamponade, constrictive pericarditis.
62
categorising hf by time
acute - acute exacerbation of chronic heart failure. most urgent sx are often due to lv failure= pulmonary oedema chronic : chronic duhhh
63
categorising hf by left or right
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
left ventricular failure typically results in?
pulmonary oedema dyspnoea orthopnoea paroxysmal nocturnal dyspnoea bibasal fine crackles
65
right ventricular failure typically results in?
peripheral oedema - ankle/sacral oedema raised jugular venous pressure hepatomegaly weight gain due to fluid retention anorexia - cardiac cachexia
66
what is high output heart failure give some causes
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
What is de-novo heart failure? caused by what?
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
what is decompensated heart failure?
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
patients with heart failure can be broadly characterised into 1 of 4 groups what are they?
with our without hypoperfusion with or without fluid congestion
70
symptoms of heart failure acute signs of heart failure acute
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
diagnostic work up of acute hf patients?
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
features of chronic heart failure
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
Heart failure acute management
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
how to treat hypotension in acute heart failure pt? under 75mmHg/cardiogenic shock
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
what regular medication can be continued in hf acute tx? when would you stop beta blocker
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
tx for chronic heart failure
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
which 2 chronic heart failure tx can cause hyperkalaemia?
ace inhibitors aldosterone antagonists
78
what vaccinations could you give for chronic heart failure pts?
annual influencza one-off pneumococcal vaccine - if asplenia, splenic dysfunction or ckd give booster every 5 years. otherwise adults need just one dose.
79
What is Rheumatic Fever?
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
Pathophsyiology of Rheumatic Fever
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
presentation of rheumatic fever
2-4 weeks after strept infection like tonsillitis fever joint pain rash sob chorea nodules
82
what joint involvement in rheumatic fever
migratory arthritis affects large joints with hot swollen painful joints. migratory- diff joints inflamed and improve at different times.
83
what heart involvement in rheumatic fever
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
skin involvement in rheumatic feave
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
nervous system involvement in rheumatic fever
chorea - irregular uncontrolled rapid movements of limbs. sydenham chorea.
86
how would you assess for rheumatic fever?
throat swab- bacterial culture ASO antibody titre echocardiogram, ecg, cxr. use jones criteria
87
diagnostic criteria for rheumatic fever
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
What can be found histologically on the hearts of people with rheumatic fever
Aschoff bodies (granulomatous bodies)
89
What murmurs in rheumatic fever?
Acute - Mitral and aortic regurgitations Chronic - Mitral stenosis
90
how to manage rheumatic fever?
phenoxymethylpenicillin for 10 days. nsaid - joint pain aspirin/steroids- carditis prophylactic abx - prevent further strep infections.
91
What is the modified duke criteria?
infective endocarditis

Phase 3a Finals (26 decks)

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