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Paediatrics > Cardiology > Flashcards

Cardiology Flashcards

1
Q

In what percentage of children can an innocent murmur be heard?

A

25%

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2
Q

What causes innocent murmurs?

A

These are due to the rapid flow and turbulence of blood through the great vessels and normal valves- not a sinister cause.

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3
Q

OSCE style, what causes innocent murmurs?

A

These are heard as in children there is much less space between the heart and the chest, unlike adults, so there are heard louder and there are tight bends and turns in the heart of a child which causes turbulent flow of blood within the vessels (IE MURMUR), as they get older the heart will rest deeper into the chest and the tight bends and turns will even out. IE THEY WILL GROW OUT OF IT. nothing to worry about

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4
Q

What are the three types of innocent murmurs?

A

Venous hum (uncommon), flow murmur and musical murmur.

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5
Q

Describe a venous hum?

A

This is a machinery quality sound and it is heard at the left sternal edge, and is due to the blood flow in the great vessels.

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6
Q

Describe a flow murmur?

A

This is a short systolic murmur, heard at the mid left sternal edge, often heard during acute illness with fever and it disappears when the fever resolves.

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7
Q

RECAP, which type of murmur is often heard during acute illness with fever?

A

Innocent FLOW murmur

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8
Q

Where is a musical murmur heard?

A

Lower left sternal edge

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9
Q

What are the main clinical features of innocent murmurs?

A

They are NEVER diastolic, they are soft systolic ejection murmurs usually heard at the lower sternal edge, the may sound harsh but have NO radiation or thrills, they are often heard with fever and caused by tachycardia causing increased CO. They also CHANGE with position/head tilt.

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10
Q

So to recap, what are the 7 S’s of innocent murmurs?

A

Soft, systolic, short, S1 &S2 are normal, standing and sitting variation, symptomless, special tests normal and STERNAL edge.

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11
Q

What is the most common cause of congenital cyanotic HD?

A

Tetralogy of fallot

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12
Q

What syndrome is TOF associated with?

A

Di George syndrome

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13
Q

What is DiGeorge syndrome?

A

22q11.2 deletion associated with cardiac problems e.g. TOH, hypycalcaemia, immune deficiencies, problems with hearing and growth, renal problems and many more.

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14
Q

What are the 4 features of TOF?

A

RV outflow obstruction (caused by pulmonary artery stenosis), RV hypertrophy (cause by obstruction), a large VSD and overriding aorta with respect to VSD.

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15
Q

What are the consequences of outflow obstruction (pulmonary stenos)?

A

Reduced flow of deoxygenated blood from RA to pulmonary arteries, and also causes hypertrophy due to increased pressure.

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16
Q

What does the RV hypertrophy appear as on an X ray?

A

Boot shaped heart

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17
Q

What is the consequence of the large VSD?

A

In isolation, VSD would cause movement of blood from L to R ventricle due to pressure gradient, However in TOF, RV hypertrophy means the RV may have a higher pressure,causing R to L shunting of blood (deoxygenated blood therefore enters aorta → rest of the
body)
In severe VSD this can cause SO2 to reach <80% causing cyanosis 􃱺 TOF is a cyanotic CHD

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18
Q

What are the clinical features of TOF?

A

Clubbing of children’s fingers and toes, and a loud harsh ejection systolic murmur heard on the L sternal edge.

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19
Q

When is TOF usually diagnosed?

A

20 week scan or within first 2 months of life

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20
Q

What is the management of TOF?

A

Surgical closure of the VSD, reducing the RV outflow obstruction and cyanosed infants may require an artificial shunt to increase pulmonary blood flow.

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21
Q

Describe transposition of the great arteries? TGA

A

The aorta is connected to the right ventricle and the pulmonary artery is connected to the left ventricle (switched).

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22
Q

What does TGA mean for the blood flow?

A

Deoxygenated blood will then pass from the right ventricle to the aorta and then around the body and back to the right atrium.
Oxygenated blood passes from the left ventricle to the pulmonary artery, to the lungs and back to the left atria.
This causes 2 circuits of blood flow

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23
Q

Why does TGA cause no symptoms in utero?

A

The open foramen ovale and ductus arteriosus in utero allows pathways for oxygenated blood to reach the body.

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24
Q

What happens in TGA after birth (usually day 2)?

A

Closure of these pathways and death as NO oxygenated blood is reaching the organs.

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25
Q

What are the clinical features of TGA?

A

In most babies, there will be another defect so that oxygenated blood can reach the organs, e.g. VSD, PDA or ASD allowing some transportation of oxygen, cyanosis occurs usually day 2 of life, there is a loud 2nd heart sound and a normal ECG.

26
Q

Which heart sound is loud in TGA?

A

SECOND

27
Q

What is the management of TGA?

A

Initially management aims to open the FA and DA, this can be achieved by giving prostaglandin E.
Prostaglandin E1 also known as alprostadil
Prostaglandin E2 also known as dinoprostone
Surgery then to switch arteries position.

28
Q

How is prostaglandin administered?

A

Slow injection through the vein to open the DA.
Alprostadil is used in maintaining a patent ductus arteriosus in newborns. This is primarily useful when the threat of premature closure of the ductus arteriosus exists in an infant with ductal-dependent congenital heart disease, including cyanotic lesions (e.g., hypoplastic left heart syndrome, pulmonary atresia/stenosis, tricuspid atresia/stenosis, transposition of the great arteries) and acyanotic lesions (e.g., coarctation of the aorta, critical aortic stenosis, and interrupted aortic arch).

29
Q

What are the complications of TGA?

A

It can lead to congestive heart failure in later life if undiagnosed (e.g. if there is a large VSD present).

30
Q

What causes ASDs?

A

Incomplete closure of the foramen oval after birth (90%) or a partial AV septal defect (10%).

31
Q

Which way does the blood shunt in ASDs and what does this mean?

A

Left to right shunting meaning there will be oxygenated blood going back into pulmonary circulation.

32
Q

What type of heart defect is an ASD and why?

A

It is an cyanotic heart defect because oxygenated blood is entering the lungs and then the left side of the heart and NO DEOXYGENATED blood is reaching the organs. ASD therefore causes blood with increased O2 sats in the RA and RV and pulmonary artery, causing an increase in blood VOLUME in the right side and this causes DELAYED PULMONARY VALVE CLOSURE- causing a split S2 ejection systolic murmur.

33
Q

Recap, what type of murmur does an ASD cause?

A

Split S2 ejection systolic due to delayed pulmonary valve closure. (so 2nd heart sound = the closure of the pulmonary artery valve so if theres loads of pressure in the right side this is taking the heart 2 goes to try and shut the valve because of the pressure, think of someone trying to close a door with loads of people pushing it back)

34
Q

In what conditions are ASDs seen?

A

FAS, Down’s, TGA.

35
Q

What are the clinical features of an ASD?

A

Usually none, recurrent chest infection??/wheeze, arrhythmias,

36
Q

What is the management for ASDs?

A

Smaller ones may be ok and only require monitoring while bigger ones may require cardiac catheterisation and occlusion device.

37
Q

What are ASD patients at an increased risk of?

A

Paradoxical embolism

38
Q

What is a paradoxical embolism?

A

Passage of a clot from a vein to an artery, CONTEXT: if a normal person gets a DVT then this will enter the blood stream then the right side of heart then lungs and be a pulmonary embolus, BUT in a pt with ASD, the clot will enter the blood stream then the right side of the heart, go through the septal defect, end in the left side of the heart and then go into the systemic system and potentially lodge in the brain.

39
Q

What happens in VSDs?

A

This results from incomplete closure of the upper and lower portions which should fuse together and form the septum.

40
Q

What direction does blood flow move in VSD?

A

It moves from left to right shunting again, causing oxygenated blood to again enter the right ventricle and the lungs.

41
Q

What conditions are VSDs associated with?

A

FAS, Down’s and TGA

42
Q

What are the clinical features of VSDs?

A

Hollow systolic murmur heard in the left sternal border.

43
Q

What happens in long term VSD?

A

Increased blood flow to the right side of the heart causes increased BP and therefore PULMONARY HYPERTENSION.

44
Q

What does the pulmonary hypertension in VSD cause?

A

This causes an increase in pressure in the right side of the heart which causes a CHANGE in the direction of blood flow resulting in a right to left V shunt, allowing deoxygenated blood to enter the systemic circulation and making this a CYANOTIC condition.

45
Q

What is the management of VSDs?

A

30-50% will close without any intervention, making them uncommon in adulthood.
Large ones will have an inc risk of pulmonary HTN etc and must be surgically occluded.

46
Q

What is the purpose of the DA?

A

In utero it passes oxygenated blood from the right ventricle to the pulmonary artery to the ascending aorta.

47
Q

What happens to the DA after birth?

A

Due to a huge fall in prostaglandin E and resistance changes in the lungs, it then becomes a remnant (ligamentum arteriosum).

48
Q

What is failure of the DA to close 1 month post-partum?

A

PDA

49
Q

NB:

A

In infancy/ childhood, there is a shunting of oxygenated blood from aorta → pulmonary artery
due to pressure gradient
• However in to adulthood the increased blood volume in pulmonary system over a long time
may cause pulmonary hypertension. This can cause a shift in pressure gradient (higher pressures in the pulmonary artery), causing deoxygenated blood to move from pulmonary artery → aorta (causing cyanotic heart disease)

50
Q

Are PDA related to any conditions normally?

A

Usually an isolate defect in 90% of cases, 10% are due to other causes e.g. congenital rubella syndrome.

51
Q

What are the clinical features of a PDA?

A

CONTINUOUS murmur (systole and diastole) heard below the left clavicle.

52
Q

What type of pulse is heard with a PDA?

A

Collapsing or bounding pulse (bounding = when CO is high and peripheral resistance is low)

53
Q

Why is closure of the PDA strongly recommended?

A

To prevent risk of bacterial endocarditis and pulmonary vascular disease.

54
Q

What changes in circulation occur at birth?

A

In the fetus, only 15% of the right ventricle blood enters the lungs, and the rest passes through the DA to the descending aorta (the ductus is as large as the aorta). After birth the ductus closes within 10-15h and the pulmonary artery pressure falls over the first 3 days of life

55
Q

What happens in coarctation of the aorta?

A 
The coarctation (narrowing) of the aorta occurs AFTER the aortic arch that supplies the upper extremities and BEFORE the PDA.
During normal neonatal circulation the DA closes after birth, however in coarctation the DA stays open and becomes the PDA.
This is because the narrowing of the aorta makes it difficult for blood to pass through and reach the lower extremities, creating lower pressure then usual in the aorta POST-COARCTATION. 
So the blood moves from the right atrium to the right ventricle to the pulmonary artery and instead of bypassing the PDA and going to the lungs, the coarctation creates an area of lower pressure in the aorta, causing deoxygenated blood to be redirected here instead, this means a lot of deoxygenated blood is reaching the lower extremities- lower extremity cyanosis.
56
Q

Which condition is highly associated with COA?

A

Turners and can also be an isolated malformation.

57
Q

What are the clinical features of COA?

A

Severe heart failure, lower extremity cyanosis (present at birth), reduced absent femoral pulses, severe metabolic acidosis

58
Q

NB:

A

Without surgical correction, coarctation is not compatible with neonatal life. Therefore it is
important to check for femoral pulses.

59
Q

Which murmur occurs with COA?

A

Systolic murmur, heard loudest over the aortic valve.

60
Q

What happens in acyanotic heart defects?

A

Blood is shunted from the left side of the heart to the right due to a hole in the septum.

61
Q

Name the three causes of cyanotic heart defects?

A

tetralogy of Fallot
transposition of the great arteries (TGA)
tricuspid atresia

62
Q

Name the acyanotic heart defects?

A 
ventricular septal defects (VSD) - most common, accounts for 30%
atrial septal defect (ASD)
patent ductus arteriosus (PDA)
coarctation of the aorta
aortic valve stenosis

Paediatrics (23 decks)

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