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Zero Paeds > Cardiology > Flashcards

Cardiology Flashcards

1
Q

What are the three foetal shunts and what do they do?

What is the blood supply to the placenta?

A

DUCTUS VENOSUS - connects umbilical vein to IVC allowing bypass of liver.

FORAMEN OVALE - connects RA with LA allowing bypass of RV and pulmonary circulation.

DUCTUS ARTERIOSUS - connects pulmonary artery with aorta allowing bypass of pulmonary circulation.

Placenta:
Receives deoxygenated blood from the internal iliac arteries via the two umbilical arteries.
Transfers blood via the umbilical vein to join either the portal vein and liver, or the IVC (via the ductus venosus).

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2
Q

What happens to foetal circulation at birth?

A

FORAMEN OVALE
Breath –> Decrease pressure in alveoli –> decrease pulmonary vascular resistance –> fall in RA pressure –> LA pressure is greater than RA –> RA pressure closes the atrial septum –> functional closure of foramen ovale –> structural sealing over weeks leads to fossa ovalis.

DUCTUS ARTERIOSUS
prostaglandins keep DA open –> increased blood oxygen at birth decreases prostaglandins –> this causes closure of DA –> DA becomes the ligamentum teres.

DUCTUS VENOSUS
after birth the umbilical cord is clamped –> no flow in umbilical vein. A few days later the DV structurally closes –> DV becomes the ligamentum venosum.

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3
Q

What is an innocent murmur and what are is features?

When would you Ix or refer?

A

aka flow murmurs, common in children and are just fast blood in the heart during systole. Clear innocent is concerning and no Ix.

Features are S:

  • Soft
  • Short
  • Symptomless
  • Situation dependent (quieter on standing or only appears when unwell or feverish)

Features for further Ix and paeds cardio referral:

  • louder than 2/6
  • diastolic murmurs
  • louder on standing
  • other Sx eg failure to thrive, feeding difficulty, cyanosis, SOB

Ix: ECG, CXR, echo

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4
Q

What are your differentials for a pansystolic murmur in a child?

A

Mitral regurg (M area: 5th space, mid clavicular)

Tricuspid regurg (Tri area: 5th space, left sternal border)

Ventricular Septal Defect (left lower sternal border)

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5
Q

What are your differential for an ejection-systolic murmur?

A

Aortic stenosis

Pulmonary stenosis

Hypertrophic obstructive cardiomyopathy (4th inter space on left sternal border)

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6
Q

What is splitting of the second heart sound?

A

INSPIRATON
In breath –> negative intrathoracic pressure –> right heart fills faster as draws venous blood –> increased volume in RV means longer to empty –> pulmonary valve closes slightly later than aortic valve –> heart sound is “split”

(ASD can give a “fixed split” during insp and exp…)

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7
Q

What does ASD sound like? Why?

A

mid-systolic, crescendo-decrescendo:
loudest a upper left sternal border with
“fixed split” 2nd heat sound.

In ASD blood flows from LA to RA thus increasing the volume of blood that the RV has to empty before the pulmonary valve can close giving a split.

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8
Q

What does a PDA sound like?

A

May be silent.
Big PDA may have a normal first HS and then a continuous crescendo-decrescendo “machinery” murmur that may continue and make the 2nd HS difficult to hear.

(blood goes from aorta to PDA to pulmonary artery)

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9
Q

What murmur might you hear in tetralogy of Fallot?

A

ejection systolic murmur in pulmonary area due to:

pulmonary stenosis

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10
Q

What can cause cyanotic heart disease?

A

Deoxygenated blood entering the systemic circulation – blood bypasses the lungs due to a RIGHT to LEFT shunt.

Heart defects causing RIGHT to LEFT:

  • Ventricular septal defect (VSD)
  • Atrial septal defect (ASD)
  • Patent ductus arterioles (PDA)
  • Transposition of the great arteries

VSC, ASD or PDA are not usually cyanotic as pressure on left is usually great than on the right so the shunt goes LEFT to RIGHT. If pulmonary pressure increases then you get a right to left shunt causing cyanosis – this is EISENMENGER SYNDROME.

Transposition will always have cyanosis as right side pumps directly into aorta.

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11
Q

When does the ductus arteriosus close and why might it fail to close?

A

Normally stops functioning within 1-3days of birth and complete closure within 2-3weeks.

Unclear why it doesnt close, risk factors:

  • genetics
  • maternal infection eg rubella
  • prematurity
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12
Q

Pathophysiology changes seen when there is a PDA?

A

Pressure in aorta is higher –> blood moves to pulmonary arteries –> pulmonary hypertension –> right heart strain –> RV hypertrophy
Also increased blood returning from pulmonary vessels to LV –> LV hypertrophy

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13
Q

Presentation of PDA?

A

Small PDA may be asymptomatic until adulthood –> sign of heart failure.

Newborn:

  • MURMUR
  • difficulty feeding
  • poor weight gain
  • lower respiratory tract infections
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14
Q

What murmur is heard in a PDA?

Diagnosis?

A

Small PDA may have no sounds.
Bigger:
“continuous crescendo-decrescendo machinery” murmur that may continue during HS 2 making it hard to hear.

DX:
with echocardiogram –> doppler flow shows left to right shunt. Observe changes to heart (hypertrophies to RV and or LV)

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15
Q

Management of PDA?

A

Monitor with echos until 1 year.
After 1 year it is unlikely to spontaneously close and TRANS-CATHETER or SURGICAL CLOSURE.

Earlier if symptomatic or HF.

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16
Q

How does the atrial septum develop?

A

Atria are connected, then two walls grow down from the top and fuse with the endocardial cushion in the middle of the heart.
The two walls are the septum primum and the septum secondum.

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17
Q

How does an ASD form and how does the foramen ovale form?

A

If septum secondum and septum primum have a defect then you end up with an ASD.

The foramen ovale is in the septum secondum and closes at birth.

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18
Q

What happens to blood when there is an ASD? What does this cause?

A

LA to RA shunt as pressure in LA is higher.
Plenty of oxygenation via lungs so not cyanotic.

Right side get overloaded –> pulmonary hypertension…

Eventually pulmonary hypertension leads to EISENMENGER SYNDROME where pulmonary pressure > systemic –> shunt reverse to right to left, blood bypasses lungs and patient becomes CYANOTIC

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19
Q

What are the types of ASD?

A

Common to least common:

  • OSTIUM SECONDUM; septum secondum fails to fully close, leaving a hole in the wall
  • PFO (technically not an ASD)
  • OSTIUM PRIMUM where the septum primum fails to fully close, leaving a hole and leads to ATRIOVENTRICULAR VALVE defects making it and atrioventricular septal defect (AVSD).
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20
Q

Complications of ASD?

A
  • stroke with a VTE
  • AF and AFib
  • pulmonary HTN and right HF
  • Eisenmenger syndrome and cyanosis

(stroke can be with DVT than embolises and instead of lungs can cross and then go to brain - in lifelong asymptomatic ASD)

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21
Q

Murmur in ASD?

A

“mid-systolic, crescendo-decrescendo” murmur loudest at upper left sternal border with FIXED SPLIT HS2 (Ao and pulm valves close separately, more load in RV… normal in inspiration)

22
Q

Presentation of ASD?

A

Often found in antenatal scan or newborn exams.

Childhood Sx:

  • SOB, feeding difficulty, less weight gain
  • lower respiratory tract infections

Asymptomatic until adulthood may have:
- dyspnoea, HF, stroke

Link between migraines with aura and PFO

23
Q

Management of ASD?

A

Surg:
transvenous catheter closure or open heart surgery.

Anticoagulants for stroke / clots in adults:
- aspirin, warfarin, NOACs

24
Q

VSDs can occur in isolation, but what are they also associated with?

A

Down’s syndrome

Turner’s syndrome

25
Q

Pathophysiology when there is a VSD?

A

LV blood into RV
Blood goes to lungs

–> pulmonary HTN –> right to left shunting –> cyanotic = Eisenmenger Syndrome

26
Q

Presentation of VSD?

Murmur heard?

A
  • Often symptomless and patients can present as late as adulthood.
  • Antenatal scans
  • murmur during baby check

Sx:

  • poor feeding
  • dyspnoea
  • tachypnoea
  • failure to thrive

“pan-systolic heard more at the left lower sternal border 3rd and 4th spaces”, may have a systolic thrill.

(Ddx for pan systolic murmurs: VSD, mitral regurg, tricus regurg)

27
Q

Treatment of VSD?

A

May close over time so if no Sx you can watch.

Surg: transvenous catheter via femoral vein or open heart surgery.

Increased risk of INFECTIVE ENDOCARDITIS in VSD, surgery is given prophylactic Abx.

28
Q

What is Eisenmenger Syndrome and three causes?

A

When blood flows from right to left heart and bypasses the lungs.

  • ASD
  • VSD
  • PDA

Can develop quickly if a large shunt, or slowly in adulthood if a small shunt. Quick in pregnancy so when with hole in the heart need checking.

29
Q

Examination findings in Eisenmenger Syndrome?

A

Pulmonary HTN:

  • RV heave; forceful contraction against lung pressure
  • loud P2; due to forceful shutting of pulmonary valve
  • raised JVP
  • peripheral oedema

Underlying septal defect:

  • ASD: mid-systolic, crescendo-decrescendo murmur loudest at upper left sternal border
  • VSD: pan-systolic loudest at left lower sternal border
  • PDA: continuous crescendo-decrescendo machinery murmur
  • arrhythmias

R to L shunt and chronic hypoxia:

  • cyanosis
  • clubbing
  • dyspnoea
  • plethoric complexion (red due to polycythaemia)
  • polycythmaemia means theres is a tendency to clot
30
Q

Prognosis of Eisenmenger Syndrome?

A

Reduce life expectancy by 20 years.

  • heart failure
  • infection
  • thromboembolism
  • haemorrhage
  • 50% mortality in pregnancy
31
Q

Management of Eisenmenger Syndrome?

A

Ideally manage defect before Eisenmenger develops.
Can’t be reversed.
Definitive is HEART-LUNG transplant.

Medical Mx:

  • O2
  • SILDENAFIL for pulmonary HTN
  • treat arrhythmias
  • treat polycythaemia with venesection
  • anticoagulate to prevent thrombosis
  • prophylactic Abx for infective endocarditis
32
Q

What abnormality happens in coarctation of the aorta and what is it associated with?

A

CoA is congenital narrowing of the Ao arch usually near the ductus arteriosus.

–> decreased pressure after the narrowing and increased pressure in heart and first 2 vessels of the aorta.

Particularly associated with Turner’s syndrome.

33
Q

Presentation of CoA?

A

NEONATE:

  • maybe only weak femoral pulses.
  • four-limb BP = high BP in some limbs and low in ones supplied after the narrowing.
  • systolic murmur in left infraclavicular area and below left scapula

INFANCY:
- tachypnoea, poor feeding, grey and floppy baby

OVERTIME:

  • LV heave due to LV hypertrophy
  • underdeveloped left arm due to reduced blood flow
  • underdeveloped legs
34
Q

Management of CoA?

A

Severity varies from critical to Sx-free in adulthood.

Critical:
- PROSTAGLANDIN E to keep ductus arteriosus open to allow some blood into systemic distal to narrowing. Then surgery to correct.

35
Q

What happens structurally in Congenital Aortic Valve Stenosis?

A

Born with narrow Ao valve, varying severity.
Ao valve has 3 leaflets called sinuses of Valsalva.
Patients with Ao stenosis may have 1,2,3 or 4 leaflets.

36
Q

Presentation of Congenital Aortic Valve Stenosis?

Key signs?

A

May be asymptomatic with an incidental murmur found.

More significant stenosis will give fatigue, SOB, dizziness, syncope. Worse on exertion.

Severe would give HF within months.

SIGNS:

  • “ejection systolic murmur in Ao area, crescendo-decrescendo and radiates to carotids”
  • ejection click
  • palpable thrill during systole
  • slow rising pulse and narrow pulse pressure
37
Q

Management of Congenital Aortic Valve Stenosis?

Complications?

A

Dx with echocardiagram.
Tends to be progressive and worsen over time.

Monitor condition with: ECG, echo, exercise testing
May need to reduce physical activity.

Treat:

  • percutaneous balloon aortic valvoplasty
  • surgical aortic valvotomy
  • valve replacement

Complications:

  • LV outflow obstruction
  • HF
  • ventricular arrhythmia
  • bacterial endocarditis
  • sudden death, often on exertion
38
Q

What happens in congenital pulmonary valve stenosis and what is this abnormality associated with?

A

Usually has 3 leaflets, they can fuse of thicken.

Associated:

  • Tetralogy of Fallot
  • William Syndrome
  • Congenital Rubella syndrome
39
Q

How does congenital pulmonary valve stenosis present?

Key signs?

A

Often asymptomatic and murmur is incidental finding during routine baby checks.
Significant stenosis can present as fatigue on exertion, SOB, dizziness, fainting.

SIGNS:

  • ejection systolic murmur loudest in pulmonary area
  • palpable thrill in pulm area
  • RV heave due to RV hypertrophy
  • raised JVP and giant A waves
40
Q

Management of congenital pulmonary valve stenosis?

A

Dx with echo

Mild does not need intervention, watchful waiting.

Sx then can do balloon valvoplasty via venous catheter.
Could do open heart surgery.

41
Q

What is present in Tetralogy of Fallot?

What does this cause?

A
  • VSD
  • overriding aorta (gets more deoxy blood from RV)
  • pulmonary valve stenosis
  • RV hypertrophy

Leads to:

  • cyanosis from right to left shunting
  • RV hypertrophy
42
Q

Risk factors for Tetralogy of Fallot?

A
  • Rubella infection
  • increased age of mother (over 40)
  • alcohol in pregnancy
  • diabetic mother
43
Q

Presentation of Tetralogy of Fallot?

A
  • Most cases are picked up in antenatal scans.
  • Ejection systolic murmur from pulmonary stenosis at baby check.
  • Severe will have HF within one year.
  • X-ray: “BOOT SHAPED heart” due do RV hypertrophy.
  • milder may develop signs and Sx.

SIGNS and Sx:

  • cyanosis
  • clubbing
  • poor feeding and weight gain
  • ejection systolic murmur in pulm area
  • “TET SPELLS”
44
Q

What happens in a “tet spell”?

A

Intermittent sympomatic periods when right to left shunt is worsened giving a cyanotic episode.

Happens when pulmonary vascular resistance increases or systemic resistance decreases eg when walking, exerting or crying.

Child becomes irritable, cyanotic and SOB. Can lead to reduced consciousness, seizures and even death.

45
Q

Treatment of a “tet spell”?

A

Young children learn to bring knees to chest, older children may squat or handstand –> increased systemic vasc resistance –> more blood to lungs

Medical should have experienced paediatrician, can be life threatening:

  • O2 as hypoxia can be fatal
  • beta blockers van relax RV and improve flow to pulm vessels
  • IV FLUIDS can increase preload and amount of blood flowing to lungs
  • MORPHINE can decrease respiratory rate = more effective breathing
  • Sodium Bicarb can buffer metabolic acidosis
  • PHENYLEPHRINE infusion can increase systemic vascular resistance
46
Q

Management and prognosis of Tetralogy of Fallot?

A

Neonates:
- prostaglandin infusion can maintain ductus arteriosus, allowing blood flow back to the pulmonary arteries

  • total surgical repair by open heart surgery is the only definitive treatment, mortality 5%

Prognosis depends on severity, 90% will live into adulthood.

47
Q

What has happened in Ebstein’s Anomaly?

A

Triscuspid valve is set lower in the heart (closer to apex). This gives big RA and small RV.

–> poor flow to pulm vessels

Associated with:

  • right to left shunt from an ASD
  • Wolff-Parkinson-White syndrome
48
Q

Presenting features and Ix finding in Ebstein’s Anomaly?

Management?

A
  • evidence of HF (oedema)
  • GALLOP rhythm on auscultation from 3rd and 4 Heart Sounds.
  • cyanosis
  • SOB
  • poor feeding
  • collapse or arrest

Symptoms when there is an ASD present a few days after birth when ASD closes. This means blood cannot flow through DA to get oxygenated.

Ix:

  • ECG: arrhythmias, RA enlargement, RBBB, left axis deviation

CXR:

  • cardiomegaly
  • RA enlargement

Management:

  • treat arrhythmias and HF
  • prophylactic ABx for IE
  • surg correction
49
Q

What happens in Transposition of the Great Arteries?

During pregnancy and birth?

A

Attachements for the aorta and pulmonary trunk are swapped.
–> RV pumps blood into aorta
–> LV pumps into pulmonary vessels

This gives two separate circulations that dont mix:

  • systemic system and right heart
  • pulmonary system and left heart

Associated with:

  • VSD
  • CoA
  • pulmonary stenosis

Pregnancy the foetus develops normally (gas and nutrient exchange at placenta)
After birth the condition is immediately life threatening if no connection between systemic and pulm circulation.

–> Immediate survival depends on a shunt between pulm and syst circulation:

  • PDA
  • ASD
  • VSD
50
Q

Presentation of TGA?

A

Usually Dx at antenatal US scans. (monitor and plan for delivery)

Not prior detection:
- cyanosis at or within a few days of birth

PDA or VSD can initially compensate but within a few weeks:

  • resp distress
  • tachycardia
  • poor feeding and weight gain
  • sweating
51
Q

Management of TGA?

A

When VSD this allows blood mixing and time for definitive treatment.

Prostaglandin can maintain ductus arteriosus allowing blood to pulmonary arteries.

Balloon septostomy –> catheter into foramen ovale via the umbilicus –> create a large ASD

Open heart surgery is definitive. Cardiopulmonary bypass machine is used to perform an “arterial switch” procedure within a few days of birth. (And correct any VSD or ASD).

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