Cardio Flashcards

1
Q

Describe the foetal circulation.

A
  • oxygenated bloods from placenta is carried via umbilical vein into IVC
  • oxygenated blood arrives at RA and flows through foramen ovale into LA then to LV –> aorta and body
  • portion of blood makes it to RV and is pumped to pulmonary artery which moves to aorta via ductus arteriosus (high pressure in collapsed lung)
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2
Q

what could go wrong to cause congenital heart defects?

A
  • Genes like trisomy 21, cardiomyopathy genes
  • Environment factors such as teratogens like alcohol, smoking, warfarin and lithium
  • Maternal disorders like rubella
  • Maternal diabetes
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3
Q

what are the foetal shunts available?

A
  • Foramen ovale : from foetally higher pressure RA to LA via atrial septum with intention of bypassing the lungs
  • Ductus arteriosus : shunt from pulmonary artery into aorta to bypass lungs in systole
  • Ductus venosus : umbilical vein into IVC (bypassing liver?)
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4
Q

what cause the foetal shunts to close?

A
  • with initial breaths and increase in volume of blood to lungs and resistance in pulmonary circulation the LA pressure rises
  • RA pressure falls due to exclusion of placental circulation and this change in pressure causes foramen ovale flap to shut - septum primum against septum secundum
  • ductus arteriosus closes within first few hours to days
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5
Q

what might be the initial presentation of a congenital heart defect?

A
  • antenatal cardiac USS detects 50-60%
  • cyanosis at birth
  • detection of murmur
  • HF
  • shock when foramen ovale shuts causing obstruction
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6
Q

how do you differentiate between an innocent murmur and a pathological one?

A
  • aSymptomatic
  • Soft blowing murmur
  • Systolic murmur only
  • left Sternal edge
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7
Q

how does HF present in a baby?

A
  • breathlessness
  • sweating
  • poor feeding
  • recurrent chest infections
  • poor weight gain, tachypnoea, tachycardia, murmur etc
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7
Q

what are some examples of acyanotic heart defects?

A
  • VSD
  • ASD
  • PDA
  • coarctation of aorta
  • aortic valve stenosis
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8
Q

what are some classic features of an acyanotic heart lesion?

A
  • L -> R shunting with mixing
  • increased pulmonary blood flow risking pulmonary HTN and Eisenmenger
  • lesions above nipple ejection systolic murmur
  • lesions below nipple pan systolic murmur
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9
Q

What are some examples of cyanotic congenital heart disease?

A
  • TOF
  • TGA
  • tricuspid atresia
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10
Q

what is an ASD?

A

left to right shunt from LA into RA down pressure gradient
- acyanotic
- may lead to right sided strain and Eisenmenger
- types: ostium secondum, primum and patent foramen ovale

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11
Q

what might you find on examination for ASD?

A
  • Ejection systolic murmur heard loudest at the upper-left sternal border
  • Widely fixed splitting of the second heart sound
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12
Q

how might ASD present?

A

*asymptomatic, recurrent infections
- may present at 4-5y
- 40+ with arrhythmias and dyspnoea

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13
Q

how might you investigate acyanotic congenital heart defects?

A
  • pulse oximetry
  • Echo
  • CXR: cardiomegaly and pulmonary oedema?
  • ECG: may show hypertrophy
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14
Q

how is an ASD managed?

A
  • 7-8mm may spontaneously close so w&w
  • large defects require percutaneous catheter closure via femoral vein
  • tx at about 3-5y to prevent RHF and arrhythmias
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15
Q

what is a VSD?

A

VSD means left to right shunt from LV into RV down pressure gradient through a defect in septum
*most common CHD
*associated with Down’s and Turner’s

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16
Q

how might VSD present?

A

Small – may be asymptomatic, normal growth
Moderate – poor feeding, failure to thrive (FTT), short of breath (SOB)
Large – poor feeding, FTT (falls below centiles), SOB, sweaty and pale with feeds

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17
Q

what might you find on examination for VSD?

A

Pan-systolic murmur heard loudest at the lower left sternal border (LLSB)
- may palpate systolic thrill
- loud P2 shows pulmonary HTN

18
Q

how is VSD managed?

A
  • <5mm may close spontanously
  • moderate: diuretic therapy with (furosemide+spironolactone) and high caloric feeds (infantrini)
  • large: moderate mx, optimise weight gain, surgery before 12m to present PPHN –> transvenous catheter closure
19
Q

how might a PDA present on examination?

A

Symptoms usually present 3-5 days after birth when the duct begins to close
- bounding pulses and wide pulse pressure
- continuous machinery murmur at upper-left sternal border and thrill

20
Q

how is PDA managed?

A
  • preterm may close spontaneously
  • medical: indomethacin, ibuprofen to neonate
  • surgical: catheter closure or PDA ligation when weight 5kg
21
Q

why might it be not so wise to close a PDA in certain situations?

A

if associated with another heart defect amenable to surgery then prostaglandin E1 given to keep duct open until after repair - alprostadil

*to prevent obstruction

22
Q

what are the 4 abnormalities found in a patient with a TOF?

A
  • large VSD
  • pulmonary stenosis
  • hypertrophy of RV
  • overriding aorta (over VSD not LV)
23
Q

what are some RF for TOF?

A

Males
1degree family history of CHD
Teratogens like Alcohol (fetal alcohol syndrome)
Warfarin (fetal warfarin syndrome)
Trimethadione
genetics

24
Q

when would TOF present?

A

mild: asymptomatic, continues to progress to cyanosis
moderate: first few weeks (post PDA closure), prone to recurrent chest infections, failure to thrive
extreme: may have pulmonary atresia, hence PDA dependent

25
Q

How would TOF present?

A
  • cyanotic spells due to RV outflow tract obstruction
  • murmur caused by pulmonary stenosis: crescendo-decrescendo with harsh ejection systolic over L sternal edge
  • cyanosis, poor feeding, sweating during feeds
  • tet spells: neonate going blue when feeding
  • CHF signs
26
Q

how might you investigate TOF?

A

ECG: RVH, R axis deviation
bloods for genetic syndromes
CXR: boot shaped heart for RVH, reduced lung markings
ECHO: gold standard
cardiac catheter? delineate lesion

27
Q

How is TOF managed?

A
  • severe cyanosis: prostaglandin infusion to maintain patency of PDA until correction
  • tet spells management
  • HF: digoxin, loop diuretics
  • endocarditis prophylaxis
  • surgical: Blalock-Taussig shunt to mimic PDA,

*lifelong followup with exercise tolerance, ECG etc

28
Q

how are tet spells managed?

A

*Knee to chest position to increase systemic vascular resistance and promote blood flow into the pulmonary circulation

Oxygen
Morphine
B-blockers

29
Q

what is transposition of the great arteries?

A

aorta arises from the RV and pulmonary artery from the LV, resulting in deoxygenated blood from the RV being circulated around the body

RF: diabetic mothers

29
Q

how does TGA present?

A

*when PDA closes at day 3-5

  • signs of CCF like tachypnoea, tachycardia, failure to gain weight
  • cyanosis
  • poor feeding
  • murmur: systolic murmur if VSD, loud single S2
30
Q

How is TGA managed?

A
  • emergency: prostaglandin infusion, correct metabolic acidosis, atrial balloon septostomy
  • definitive: atrial switch by age 4w

*pregnancy complications for patients later

31
Q

how does aortic stenosis present?

A

*born with narrow aortic valve which restricts blood from LV into aorta

  • ejection systolic murmur loudest in aortic area, crescendo-decrescendo radiating to carotids
  • slow rising pulse and narrow pulse pressure
32
Q

how is aortic stenosis managed?

A
  • precutaneous balloon aortic valvoplasty
  • surgical aortic valvotomy
  • valve replacement
33
Q

what is pulmonary stenosis and what is it associated with?

A

usually consists of 3 leaflets that open and close and let blood out into pulmonary artery and prevent back flow into RV

when leaflets abnormally fuse or thicken there is a narrowing between the RV and PA causing a restricted exit of blood

  • associated with TOF, Williams syndrome, Noonan syndrome and congenital rubella
34
Q

how might pulmonary stenosis present?

A
  • ejection systolic murmur loudest at pulmonary area
  • palpable thrill over pulmonary area
  • RV heave due to RVH
  • raised JVP
35
Q

how is pulmonary stenosis managed?

A
  • mild may not require intervention hence watch and wait
  • symptomatic or significantly stenosed
    • balloon valvuloplasty via venous catheter
36
Q

what is hypoplastic left heart?

A
  • abnormal development of left sided cardiac structures which results in obstruction to blood flow from LV - mitral valve, left ventricle, aortic valve, the ascending aorta, and aortic arch
  • survival depends on two key factors
    • patent ductus arteriosus
    • non-restrictive atrial septal defect to ensure adequate mixing
37
Q

how does a hypoplastic left heart present?

A
  • initially healthy until duct closes
  • with PDA closing systemic perfusion decreases
    • hypoxaemia, acidosis, shock
  • cardiogenic shock if duct restricted from birth - due to ischaemia to myocardium
38
Q

how is hypoplastic left heart managed?

A
  • initial - prostaglandin infusion, diuretics, intubation and ventilation, urgent balloon atrial septostomy to ensure mixing
  • definitive - surgical
    • norwood procedure, glenn, fontan
39
Q

what is coarctation of the aorta?

A

congenital narrowing narrowing of aortic arch, usually around the ductus arteriosus
*when duct closes aorta also constricts causing obstruction to LV outflow
*associated with Turner’s

40
Q

how might you detect coarctation of aorta?

A
  • weak femoral pulses : four limb blood pressure to reveal high BP in limbs supplied from arteries that come before narrowing and lower BP after
  • ejection systolic murmur
  • grey floppy baby
  • underdeveloped L arm?
41
Q

how is coarctation managed?

A
  • mild may be symptom free until adulthood without requiring surgical input
  • urgent - prostaglandin E to keep DA open while waiting for surgery, allows some flow into systemic distal to co-arctation
  • surgery - correct narrowing and ligate DA