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Cardiology Flashcards

1
Q

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

A

15:2

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2
Q

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

A

Prostaglandin E1

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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
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4
Q

When does TGA generally present?

A

within hours to days of the neonate’s birth

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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).

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6
Q

What are acyanotic heart defects?

A

L>R shunting

ASD, VSD, PDA

Breathless or asymptomatic.

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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.

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8
Q

What is acrocyanosis?

A

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

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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.

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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

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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

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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

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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

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14
Q

Murmur in VSD?

A

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

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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)

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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

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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

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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

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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

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20
Q

Murmur in ASD?

A

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

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21
Q

Complications of ASD?

A

Eisenmenger: murmur shortens + splitting disappears

Pul/ tricuspid regurg

Paradoxical emboli from DVT can cause stroke.

Pul HTN

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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.

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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.

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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
Features of PDA?
``` left subclavicular thrill continuous 'machinery' murmur large volume, bounding, collapsing pulse wide pulse pressure heaving apex beat ```
26
Management of PDA?
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
Diagnosis of PDA?
Echo: dilated LA +LV CXR: normal, cardiomegaly ECG: LVH, LA enlargement
28
What is coarctation of the aorta?
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
Features of coarctation of the aorta?
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
Complications of coarctation of the aorta?
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
Diagnosis/investigations of coarctation of the aorta?
Angiography: visualise narrowing CXR: rib notching, 3 sign. Cardiomegaly. ECHO: visualise location, size, blood turbulence ECG: LVH, RVH, RA enlargement
32
Management of coarctation of the aorta?
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
What is truncus arteriosus?
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
Features of trunks arteriosus?
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
Murmur of coarctation of the aorta?
mid systolic murmur, maximal over back
36
Murmur of truncus arteriosus?
Loud systolic murmur along left sternal border, ↑flow across mitral Diastolic flow murmur at apex when pul blood ↑
37
Diagnosis/investigations of truncus arteriosus?
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
Management of truncus arteriosus?
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
What is transposition of the great arteries?
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
Features of transposition of the great arteries?
``` 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
Management of transposition of the great arteries?
maintenance of the ductus arteriosus with prostaglandins surgical correction is the definite treatment.
42
Difference between D-TGA and L-TGA?
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
Diagnosis/ investigations of TGA?
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
Management of TGA?
Prostaglandin E: ST, keeps DA open Balloon atrial septostomy: hole created in septum Surgically switch vessels
45
What is tricuspid atresia?
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
Features of tricuspid atresia?
``` Tire easy esp during feeds Cyanosis Difficulty breathing Slow growth + weight gains HF ```
47
Murmur of tricuspid atresia?
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
Investigations and management of tricuspid atresia?
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
What is tetralogy of Fallot?
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
Features of Tetralogy of Fallot?
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
Investigations for TOF?
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
Management of TOF?
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
Murmur of TOF?
ejection systolic murmur due to pulmonary stenosis (the VSD doesn't usually cause a murmur)
54
What is Total anomalous pulmonary venous congestion?
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
What is Epstein anomaly?
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
Features of Epstein anomaly?
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
Investigations and management of Epstein anomaly?
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
RF for pulmonary stenosis in children?
Noonans

Paediatrics (11 decks)

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