Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Paediatrics > Cardiology > Flashcards

Cardiology Flashcards

1
Q

In paediatric basic life support, what is the ratio of compressions to breaths?

A

15:2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

In cyanotic congenital heart diseases, what should be given to maintain a patent ductus arteriosus?

A

Prostaglandin E1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

5 T’s of cyanotic congenital heart diseases:

A 
Tetralogy of fallot
Transposition of great vessels (TGA)
Tricuspid atresia
Total anomalous pulmonary venous return
Truncus arteriosus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

When does TGA generally present?

A

within hours to days of the neonate’s birth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Causes of congenital heart defects?

A

Mostly unknown

Down/Edward/Patau/Turner’s

FH > 3X risk

Maternal illness: rubella (PDA, PS), SLE (complete HB), DM (10X risk, if uncontrolled)

Maternal meds: warfarin (PDA, PS), FAS (ASD, VSD, ToF).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are acyanotic heart defects?

A

L>R shunting

ASD, VSD, PDA

Breathless or asymptomatic.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are cyanotic heart defects?

A

R>L

blood can’t get into lungs

R sided problem.

PTA, transposition of great arteries, tricuspid atresia, ToF, total anomalous pulmonary venous connection.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is acrocyanosis?

A

healthy newborn periph cyanosis mouth + extremities. Benign vasomotor changes, vasoconstriction ↑tissue O2 extraction. May persist 24-48hrs.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Complications of congenital heart defects?

A

Can present from mins to days, postnatal, lots of still births have CHD.

Decompensation: engorged neck veins, tachycardia, brady poor sign, weak pulse, acidosis

Eisenmenger: pulmonary HTN, shunt reversal, R>L, cyanosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is Eisenmenger syndrome?

A

describes the reversal of a left-to-right shunt in a congenital heart defect due to pulmonary hypertension.

This occurs when an uncorrected left-to-right leads to remodeling of the pulmonary microvasculature, eventually causing obstruction to pulmonary blood and pulmonary hypertension.

Associated with VSD, ASD, PDA

Features:
original murmur may disappear
cyanosis
clubbing
right ventricular failure
haemoptysis, embolism

Management
- heart lung transplantation is required

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Diagnosis of congenital heart defects?

A

Antenatal: anomaly scan, fetal ECHO

FBC

CXR

4 limb BP

Pre-post ductal SpO2 = O2 R hand (pre) vs foot (post). Any differences i.e. post-ductal SpO2 is low > cyanotic CHD

ECHO, cardiac cath

Cardiac MRI

Nitrogen washout test: hyperoxia test, differentiate cardiac from non-cardiac Infant given 100% O2 for 10 mins after which ABG taken. pO2 of <15 kPa cyanotic congenital heart disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are Ventricular septal defects?

A

most common cause of congenital heart disease.

They close spontaneously in around 50% of cases.

L>R shunt between ventricles, overload of R side, RVH.

Can be acquired following MI, congenital infections, ToF, FAS, Turner’s, Edward’s, Patuau, cri-du-chat + Downs

Small: restrictive, normal pressure between ventricles.

Moderate/large: non-restrictive, no pressure difference between ventricles.

Mostly failure of descending membranous septum coming down from endocardial cushion = normally fuses with ascending muscular

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Features of VSD?

A

Asymptomatic IU

failure to thrive

features of heart failure:
hepatomegaly
tachypnoea
tachycardia
pallor

Small: asymptomatic, loud, harsh pansystolic blowing murmur left sternal edge/ tricuspid

Moderate-large: early HF Eisenmenger. Sweating, poor feeding/ FTT, resp infections. Murmur + systolic thrill + diastolic rumble mitral area. LA/LV dilation. Pul HTN.

Signs of congestive HF (dyspnoea, cough, pul vascular resistance, hepatomegaly, ↑HR/RR pallor). Displaced apex, RV heave > cardiomegaly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Murmur in VSD?

A

classically a pan-systolic murmur which is louder in smaller defects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Management of VSD?

A

clearly highly specialised

small VSDs which are asymptomatic often close spontaneously are simply require monitoring

moderate to large VSDs usually result in a degree of heart failure in the first few months:
nutritional support
medication for heart failure e.g. diuretics
surgical closure of the defect:
Patch closure
Transcatheter closure: mesh (higher risk)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Complications of VSD?

A

aortic regurgitation
aortic regurgitation is due to a poorly supported right coronary cusp resulting in cusp prolapse

infective endocarditis

Eisenmenger’s complex
due to prolonged pulmonary hypertension from the left-to-right shunt
results in right ventricular hypertrophy and increased right ventricular pressure. This eventually exceeds the left ventricular pressure resulting in reversal of blood flow
this is turn results in cyanosis and clubbing
Eisenmenger’s complex is an indication for a heart-lung transplant

right heart failure

pulmonary hypertension
pregnancy is contraindicated in women with pulmonary hypertension as it carries a 30-50% risk of mortality

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Diagnosis of VSD?

A

CXR: LA enlarged, RVH, cardiomeg, LVH, pul a enlarged, pulmonary plethora.

Echocardiogram: location + size

MRI: if echo doesn’t diagnose

Cardiac cath: echo + MRI didn’t Dx but pul HTN. ↑O2 sats in RV

ECG: LVH, RVH (L/RA enlargement (Katz-Wachtel phenomenon). Ventricular strain

20 wk scan

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are atrial septal defects?

A

most likely congenital heart defect to be found in adulthood.

L>R shunt, blood through pulmonary circuit redundantly

Associated with FAS/ Down’s, F>M

They carry a significant mortality, with 50% of patients being dead at 50 years.

Two types of ASDs are recognised, ostium secundum and ostium primum. Ostium secundum are the most common

Ostium secundum - 70% of ASDs - associated with Holt-Oram syndrome (tri-phalangeal thumbs)
ECG: RBBB with RAD

Ostium primum - present earlier than ostium secundum defects
associated with abnormal AV valves
ECG: RBBB with LAD, prolonged PR interval

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Features of atrial septal defects?

A

ejection systolic murmur, fixed splitting of S2
embolism may pass from venous system to left side of heart causing a stroke

Pul ejection/ systolic murmur, upper sternal edge, crescendo-decrescendo, RV heave

Infants + children: resp infections, FTT

Adults (before 40): palpitations, exercise intolerance, dyspnoea, fatigue, pul HTN, cyanosis, arrhythmia, haemoptysis + chest pain

↑JVP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Murmur in ASD?

A

ejection systolic murmur, fixed splitting of S2 (no change with breathing)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Complications of ASD?

A

Eisenmenger: murmur shortens + splitting disappears

Pul/ tricuspid regurg

Paradoxical emboli from DVT can cause stroke.

Pul HTN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Diagnosis of ASD?

A

CXR: r heart dilation, prominent pul vascularity, small aortic knuckle, pulmonary plethora, progressive atrial enlargement. Cardiomegaly, globular heart.

Transoesophageal echo: size/ location

Right heart cath: ↑O2 sat in: RA, RV + pul a, extra blood delay pul valve closure compared to aortic valve closure.

ECG: RBBB LAD + prolonged PR, or RAD. RVH.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Management of ASD?

A

Observation

Percut surgical closure

Adults: surgery in cases of RV enlargement, paradoxical embolism, R>L shunt

Pts need anticoags.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is Patent Ductus Arteriosus?

A

DA stays open after birth. L>R shunt. Usually closes after 1st breaths, ↑pul flow, enhances prostaglandin clearance.

Congen rubella, premature babies, cytopathic damage to BVs, ischaemia to organs, prematurity, perinatal distress, hypoxia, born at high altitude, warfarin.

generally classed as ‘acyanotic’. However, uncorrected can eventually result in late cyanosis in the lower extremities, termed differential cyanosis

connection between the pulmonary trunk and descending aorta

25
Q

Features of PDA?

A 
left subclavicular thrill
continuous 'machinery' murmur
large volume, bounding, collapsing pulse
wide pulse pressure
heaving apex beat
26
Q

Management of PDA?

A

indomethacin or ibuprofen
given to the neonate
inhibits prostaglandin synthesis
closes the connection in the majority of cases

if associated with another congenital heart defect amenable to surgery then prostaglandin E1 is useful to keep the duct open until after surgical repair

Sx management: digoxin, furosemide

Surgery: closure, surgical ligation, cardiac catheterisation + coil.

27
Q

Diagnosis of PDA?

A

Echo: dilated LA +LV

CXR: normal, cardiomegaly

ECG: LVH, LA enlargement

28
Q

What is coarctation of the aorta?

A

describes a congenital narrowing of the descending aorta.

common at site of insertion of DA, distal to L subclavian a

↑blood flow in aortic branches before coarctation (upper extremities in head). ↓blood flow + pressure in lower extremities, kidneys activate RAAS, 2° HTN

more common in males (despite association with Turner’s syndrome)

Associations
Turner's syndrome
bicuspid aortic valve
berry aneurysms
neurofibromatosis
29
Q

Features of coarctation of the aorta?

A

infancy: heart failure

PDA: gradual onset, infantile HF
DA closure: normal at birth, circulatory collapse at 2 days of life.

adult: hypertension

radio-femoral delay

mid systolic murmur, maximal over back

apical click from the aortic valve

notching of the inferior border of the ribs (due to collateral vessels) is not seen in young children

CP, cold extremities, claudication on exertion

30
Q

Complications of coarctation of the aorta?

A

Aortic dissection

Berry aneurysm

HF

IE

Underdevelopment of limbs

DiGeorge: completely occluded, interruption of aortic arch, shock in neonatal period.

FTT/ poor feeding

2° HTN

Polycythaemia

31
Q

Diagnosis/investigations of coarctation of the aorta?

A

Angiography: visualise narrowing

CXR: rib notching, 3 sign. Cardiomegaly.

ECHO: visualise location, size, blood turbulence

ECG: LVH, RVH, RA enlargement

32
Q

Management of coarctation of the aorta?

A

Prostaglandin E: keep DA open. Alprostadil

Surgery: resection, end to end anastomosis, bypass graft across area of coarctation, stent/ surgery by 5

Patch aortoplasty, balloon angioplasty with stend, balloon dilation.

33
Q

What is truncus arteriosus?

A

occurs when the blood vessel coming out of the heart in the developing baby fails to separate completely during development, leaving a connection between the aorta and pulmonary artery.

fails to divide into aorta/ pul a.

Single giant artery branching off from R+LV, oxygenated + deoxygenated blood mix > systemic circulation, cyanosis

DiGeorge syndrome, 22q11.2 deletion syndrome.

XS blood shunted to pul circuit, pul pressure < systemic circuit, fluid overload, HF.

RF: smoking, XS alcohol, teratogens, gestational DM, viral illness (rubella).

34
Q

Features of trunks arteriosus?

A

Difficulty breathing

Pounding heart, weak pulse
impaired growth

Lethargy

Physical exertion: dizziness, fatigue, palpitations, dyspnoea

Loud systolic murmur along left sternal border, ↑flow across mitral

Diastolic flow murmur at apex when pul blood ↑

Cardiomegaly 
Pulmonary HTN, lung damage 
Resp problems 
Arrhythmia 
Valve regurg 
Poor feeding/ FTT,
35
Q

Murmur of coarctation of the aorta?

A

mid systolic murmur, maximal over back

36
Q

Murmur of truncus arteriosus?

A

Loud systolic murmur along left sternal border, ↑flow across mitral

Diastolic flow murmur at apex when pul blood ↑

37
Q

Diagnosis/investigations of truncus arteriosus?

A

X-ray: heart size, lung abnormalities, XS fluid in lungs

ECHO: single large vessel from L+RV, abnormal valves Abnormal blood movement, volume of blood to lungs.

Newborn pulse ox: ↓O2 sats, diagnose before Sx develop

ECG: atrial enlargement (notching of P waves/ P mitrale), ventricular hypertrophy, abnormal T waves, right axis deviation.

38
Q

Management of truncus arteriosus?

A

Diuretics

Inotropic agents: digoxin

Abx during dental/ other surgical procedures

Limit intense physical activity, lifelong monitoring

Surgery: vary depending on anatomy, close hole between R/LV separate large vessel into pul a + aorta.

39
Q

What is transposition of the great arteries?

A

Cyanotic

It is caused by the failure of the aorticopulmonary septum to spiral during septation.

Basic anatomical changes
aorta leaves the right ventricle
pulmonary trunk leaves the left ventricle

2 small circuits of blood flow rather than 1 large. After birth, FO + DA close, no exchange between 2 circuits, cyanosis, death

Children of diabetic mothers are at an increased risk of TGA. Also rubella, poor nutrition, alcohol, >40

40
Q

Features of transposition of the great arteries?

A 
cyanosis
tachypnoea
loud single S2
prominent right ventricular impulse
'egg-on-side' appearance on chest x-ray

CV collapse at day 2-3 when duct closes

L-TGA - asymptomatic

41
Q

Management of transposition of the great arteries?

A

maintenance of the ductus arteriosus with prostaglandins

surgical correction is the definite treatment.

42
Q

Difference between D-TGA and L-TGA?

A

D-TGA, which presents with cyanosis early in life, and L-TGA, which on the other hand, may permit survival to adulthood without being diagnosed in childhood

d-TGA: complete (dextro = aorta on R)
I-TGA: congen corrected (levo = aorta on left). Ventricles + valves switched. Great vessels normal orientation, connected to wrong ventricle.

43
Q

Diagnosis/ investigations of TGA?

A

Echo: eval heart function, structure

CXR: heart > egg on side, egg on string appearance, lung congestion, cardiomegaly

Angiogram: pre-surgery

ECG: R heart strain, RVH, axis deviation

44
Q

Management of TGA?

A

Prostaglandin E: ST, keeps DA open

Balloon atrial septostomy: hole created in septum

Surgically switch vessels

45
Q

What is tricuspid atresia?

A

a birth defect of the heart where the valve that controls blood flow from the right upper chamber of the heart to the right lower chamber of the heart doesn’t form at all

Cyanotic.

Tricuspid valve replaced by wall. ↓blood flow from RA to RV. Valve isn’t formed.

R heart small + underdeveloped.

Blood flows RA>LA through hole in wall, ASD, patent FO. Blood to lungs via DA, may also have VSD so LV>RV + pul a.

RF: rubella, alcohol, smoking, DM, parent with CHD, isotretinoin, bipolar/ antiseizure meds. Down’s.

46
Q

Features of tricuspid atresia?

A 
Tire easy esp during feeds
Cyanosis 
Difficulty breathing 
Slow growth + weight gains 
HF
47
Q

Murmur of tricuspid atresia?

A

A holosystolic murmur that may have a crescendo and decrescendo quality is present, signifying blood flow through the ventricular septal defect. A continuous murmur may be present.

48
Q

Investigations and management of tricuspid atresia?

A

USS during gestation
ECHO: absence of tricuspid valve, irregular blood flow

Prostaglandin keep DA open
Atrial septosomy
Shunting: bypass from main BV leading out of heart to pul a,
Pul a band placement: large VSD, too much blood flowing to lungs, band ↓flow
Glenn procedure: 3-6mnths, connect SVC to pul a, blood flow directly to lungs, ↓workload on LV.
Fontan procedure: 2-5 y/o, path from IVC to pul a.

49
Q

What is tetralogy of Fallot?

A

the most common cause of cyanotic congenital heart disease - however, at birth transposition of the great arteries is the more common lesion as patients with TOF generally present at around 1-2 months

typically presents at around 1-2 months, although may not be picked up until the baby is 6 months old

a result of anterior malalignment of the aorticopulmonary septum. The four characteristic features are:
ventricular septal defect (VSD)
right ventricular hypertrophy
right ventricular outflow tract obstruction, pulmonary stenosis
overriding aorta

The severity of the right ventricular outflow tract obstruction determines the degree of cyanosis and clinical severity

Alcohol, maternal >40y/o, poor nutrition, viral illness eg rubella in pregnancy, down’s, DiGeorge syndrome, FH of ToF

50
Q

Features of Tetralogy of Fallot?

A

cyanosis

unrepaired TOF infants may develop episodic hypercyanotic ‘tet’ spells due to near occlusion of the right ventricular outflow tract

features of tet spells include tachypnoea and severe cyanosis that may occasionally result in loss of consciousness
they typically occur when an infant is upset, is in pain or has a fever

causes a right-to-left shunt

ejection systolic murmur due to pulmonary stenosis (the VSD doesn’t usually cause a murmur)

a right-sided aortic arch is seen in 25% of patients

51
Q

Investigations for TOF?

A

chest x-ray shows a ‘boot-shaped’ heart

ECG shows right ventricular hypertrophy, RA enlargement, RBBB

Echo: pre/postnatal, degree of stenosis

Cardiac CT + MRI: info for planning surgery.

Compensatory polycythaemia

52
Q

Management of TOF?

A

Prostaglandin E1

Tet spell: squat, bring knees to chest, kinks femoral a ↓cyanosis, ↑vascular resistance + systemic pressure, LV > RV, reverse shunt L>R, resolve cyanosis.

Surgery: VSD patch closure, 1st yr of life, RV outflow tract enlarged

O2, morphine to sedate child, relax pul outflow

BB

Phenylepinephrine

53
Q

Murmur of TOF?

A

ejection systolic murmur due to pulmonary stenosis (the VSD doesn’t usually cause a murmur)

54
Q

What is Total anomalous pulmonary venous congestion?

A

Both large veins (VC + pul vein) connect to RA, mixing of blood.
Need ASD for survival

In a baby with TAPVR, oxygen-rich blood does not return from the lungs to the left atrium. Instead, the oxygen-rich blood returns to the right side of the heart.

Features - cyanosis

CXR - snowman appearance

55
Q

What is Epstein anomaly?

A

In this condition, your tricuspid valve is in the wrong position and the valve’s flaps (leaflets) are malformed.

Blood may leak back through valve

Tricuspid valve set lower in R side, bigger RA + smaller RV.

Poor flow from RA>RV>pul a

Patent FO/ASD in 80%, R>L shunt + cyanosis

RF: lithium, WPW

56
Q

Features of Epstein anomaly?

A

Gallop rhythm

Cyanosis

SOB, tachypnoea

Poor feeding

Hepatomegaly

TR: pansystolic murmur, worse on inspiration

Widely split S1 + S2

Sx appear 48hrs as DA closes,

DA: blood aorta > pul a, to get oxygenated minimising cyanosis

HF
Cardiac arrest, collapse

57
Q

Investigations and management of Epstein anomaly?

A

Prominent ‘a’ wave in distended JVP

ECG: arrhythmias, RAH, RBBB, LAD

CXR: cardiomegaly, RA enlargement, box in chest

ECHO

Treat arrhythmia + HF medically

Prophylactic Abx, prevent IE

Definitive Tx = surgery

58
Q

RF for pulmonary stenosis in children?

A

Noonans

Paediatrics (11 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions