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Peads > Cardiology > Flashcards

Cardiology Flashcards

1
Q

What is the most common cardiological problem / presenting feature in children?

A

A MURMUR

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2
Q

Are most murmurs concerning?

A

Most murmurs are completely innocent (30% of children will have an innocent murmer at some point)

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3
Q

What percentage of children will have an innocent murmur at some point during their childhood?

A

30% of children will have an innocent murmer at some point in their life

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4
Q

What are some features that will make a murmur REASSURING?

A

THE S FACTORS

  • Systolic (commonly ejection systolic) - no diastolic murmur present
  • Soft, blowing murmur
  • aSymptomatic patient
  • Left Sternal edge

***these are all factors that would reassure you to a murmur being innocent

Extra re-assuring factors:

  • Normal heart sounds with no added sounds
  • No parasternal thrill
  • No radiation
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5
Q

What are some causes of innocent murmurs?

A

Mostly the murmurs are idiopathic and we don’t identify a cause. Organic causes include:

  • FEBRILE ILLNESS
  • ANAEMIA

***Any disease process that might mean that the cardiac output is increased could theoretically lead to the development of a murmur

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6
Q

What should you do if you hear a murmur?

A 
Describe:
Site
Character (e.g. harsh, soft, blowing)
Radiation
Intensity
Pitch
Timing

-refer to PAEDIATRIC CARDIOLOGY if parents are concerned or worrying features

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7
Q

How do we investigate murmurs to rule out pathology?

A

Echocardiogram - gold standard
ECG
CXR

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8
Q

What are the four cardinal features of TOF?

A

PROV:

  • Pulmonary stenosis (ejection systolic murmur)
  • RVH (right side has to work harder because of stenosis)
  • Overridng aorta (the aorta sits in front of the VSD-picking up blue blood from right side of heart)
  • VSD (mix of red and blue blood)
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9
Q

How is TOF identified?

A
  • Nowadays usually antenatally or following identification of a murmur in the first 2 months
  • If not there might be severe CYANOSIS in the first few days of life
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10
Q

What symptomatic features of TOF can you see?

A

Severe CYANOSIS and breathlessness and pallor
worsened by: exercise/crying
relieved by: squatting

-Important to be able to identify the cyanotic spells as they may lead to an MI if not treated properly

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11
Q

What signs might you find o/e in TOF?

A
  • Might find soft murmur during tet spell
  • May have clubbing
  • LOUD, HARSH EJECTION SYSTOLIC MURMUR at Left sternal edge
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12
Q

What investigations should you do if suspecting TOF?

A

CXR -uptilted apex (boot shaped-pulmonary artery bay)
ECG-might show RVH in older child
Echo -cardinaly features

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13
Q

How should a tet spell be managed?

A

Usually limited and followed by sleep. If 15mins+:

  • oxygen
  • sedation and pain relief (morphine)
  • IV propanolol - perisperhal vasoconstrictor
  • IV fluids
  • Bicarbonate to correct respiratory acidosis
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14
Q

When will definitive surgery for TOF be offered and what will it involve?

A

-At 6 MONTHS
○ Close the VSD
○Pulmonary valve replacement

A surgery can be offered in the neonatal period as well in severe cyanotic cases - SHUNT between the subclavian and pulmonary arteries to improve blood flow to the lungs

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15
Q

What is transposition of the great arteries (TGA)?

A
  • When the pulmonary artery connects to the LV and the aorta to the RV
  • 2 closed circulations (red>red, blue>blue)
  • INCOMPATIBLE WITH LIFE UNLESS there is a defect that stays open (VSD)
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16
Q

How and when does TGA present?

A
  • Profound cyanosis

- Usually presents around day 2 of life when ductus arteriosus starts to close

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17
Q

What clinical signs might we be able to hear on TGA?

A
  • Second heart sound often loud and single

- Usually no murmur but might be one associated with increased pressure through pulmonary artery (smaller than aorta)

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18
Q

What three investigations should be done for TGA?

A

CXR, Echo (anatomy) and ECG (usually normal)

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19
Q

What will the CXR show in TGA?

A
  • Egg on its side

- There might also be some signs of pulmonary oedema due to the increased pressures through the pulmonary system

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20
Q

What is the initial management for TGA and what is the definitive management?

A
  • Initial management is to preserve blood mixing and so PROSTAGLANDINS are given to keep the ducts arteriosis patent
  • Sometimes a BALLOON ATRIAL SEPTOSOTOMY may be needed - rupture the foramen oval to improve blood mixing
  • The definitive treatment - an operation to switch the arteries then ideally occurs in the second week of life
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21
Q

What are the two types of atrial septal defect?

A

Secundum (80%)

Primum / AVSD (Downs syndrome-involves AV valves)

22
Q

What condition is assosiated with ASD?

A

Fetal alcohol syndrome

Downs syndrome

23
Q

How are atrial septal defects detected clinically?

A
  • Often ASx (sometimes chest infections, or arrhythmias in later life)
  • Detected when a murmur is heard on routine examination (think about mum)
24
Q

What will the murmur with a ASD sound like?

A
  • Ejection systolic and at the upper left sternal edge (due to increased blood flow across the pulmonary valve due to L-R shunt-all the red blood taking another trip to lungs)
  • Fixed and widely split second heart sound (increased volume in right side
25
Q

What condition are AVSDs commonly associated with?

A

Down Syndrome

26
Q

How do we managed ASDs?

A
  • Secundum ASDs can be treated with cardiac catheterisation

- For primum AVSDs surgical intervention is often needed Usually treated around 3-5yo

27
Q

What is the most common congenital cardiac defect?

A

VSDs - 30% of all cases of cardiac abnormalities

28
Q

How do we describe VSDs?

A

According to their size (Small or large)

Small <3mm, large >3mm

29
Q

What are some of the clinical features and clinical signs of VSDs?

A
  • Loud panysystolic murmur at LLSE (keep pans in bottom cupboard)
  • Small will be asymptomatic, large will have symptoms
30
Q

Do small or large VSDs produce louder murmurs?

A

Small - more resistance

31
Q

How do we investigate VSDs?

A

CXR, Echo and ECG

CXR and ECG both normal

32
Q

How do we managed small VSDs?

A

Watch and wait - usually they will close spontaneously but arrange regular follow up

33
Q

How will large VSDs present clinically?

A
  • Acute breathlessness due to pulmonary oedema (increase blood flow to right hand side -backflow to lungs
  • Failure to thrive after 1 week old
  • Recurrent chest infections
34
Q

What are some clinical signs in large VSDs?

A

Tachypnoea, tachycardia, enlarged liver due to heart failure

35
Q

What murmur will be heard in large VSDs?

A

A very soft one or no murmur at all

36
Q

What will a chest radiograph/ECG/echo show in large VSDs?

A

CXR shows heart failure
○ Cardiomegaly
○ Enlarged pulmonary arteries
○ Increased pulmonary vascular markings
○ Pulmonary oedema
-ECG will show biventricular hypertrophy by 2 months, -ECHO will show anatomy

37
Q

How should large VSDs be managed?

A

Drug therapy for heart failure - DIURETICS AND CAPTOPRIL (ACE-i used in HF)

38
Q

What is a potential complication of large VSDs?

A

Persistent L-R shunt could lead to EISENMENGER SYNDROME which is a R-L shunt (cyanosis)

39
Q

When is corrective surgery offered in large VSDs?

A

3-6 months to prevent eisenmenger and risk of endocarditis

40
Q

What structures does the ductus arteriosus connect in the foetus?

A

The pulmonary artery to the aorta to bypass pulmonary circulations (pulmonary circulations very high pressure in the unborn baby)

41
Q

What changes happen at birth that lead to the closure of the DA?

A

The baby takes its first breath and pulmonary vascular resistance plummets and the direction of the shunt changes enabling it to close

42
Q

How long does the DA have to remain patent for before we class it as pathological?

A

1 month (corrected gestational age - so prems have longer)

43
Q

How are children with PDAs usually identified?

A

With PERSISTANT murmurs under the L clavicle (heard in both systole and diastole)
-MACHINE-HUM MURMUR

44
Q

What happens to the pulse in children with PDA?

A

Becomes collapsing or bounding due to increase in pulse pressure

45
Q

How is PDA managed? What complications could there be if it is not treated?

A

Coil or occlusion device via cardiac catheterisation at around 1 year of age

Lifelong risk of infective endocarditis if it is not corrected. Also risk of pulmonary hypertension and cyanosis (increased pressure in RHS)

46
Q

What is stills murmur?

A

-Still’s murmur is a low-pitched sound heard at the lower left sternal edge (benign)

47
Q

What do you think might cause a murmur that can be heard just below clavicles?

A
  • Venous hums can be heard just below clavicles

- Due to the turbulent blood flow in the great veins returning to the heart (benign)

48
Q

What paediatric cardio conditions present with cyanosis (right to left shunt)?

A

Cyanosis occurs in:

  • Tetrology of Fallot (most common cause of cyanosis)
  • Transposition of great arteries
49
Q

TofF vs. transposition of arteries?

A
  • TGA occurs early after birth as it is duct dependent
  • Whereas TOF occurs around 1-2 months as the VSD is left to right until the RV hypertrophy increases sufficiently to overcome left ventricular pressures (causing a right to left shunt)
50
Q

In paediatric coarctation of the aorta, where is the narrowing?

A

-paediatric coarctation/narrowing of the aorta occurs after aortic arch but PRE ductus arteriosis.

51
Q

Who is more likely to get coarctation of aorta?

How will neonates with CoA present?

A
  • Turners syndrome increased risk of coarctation of the aorta
  • Neonates will have lower extremity discoloration-really important to detect (otehrwise might die in neonatal period)
  • radio femoral delay

Peads (29 decks)

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