Structural heart disease Flashcards

1
Q

Ductus arteriosus

A

Stops functioning within 1-3days of birth
Closes within first 2-3 weeks
If this fails = patent ductus arteriosus (PDA)

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2
Q

Causes/risk factors of PDA

A

Genetic
Maternal infections - rubella
Prematurity

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3
Q

PDA pathophysiology

A

Link b/ween aorta and pulmonary vessels
Blood: aorta to pulmonary vessels - L to R shunt
Pulmonary hypertension
R sided heart strain
R ventricular hypertrophy
L ventricular hypertrophy, as blood returns to L side of heart after pulmonary vessels

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4
Q

PDA presentation

A

SOB
Difficulty feeding (kids)
Poor weight gain (kids)
Lower respiratory tract infections
Heart failure
Asymptomatic

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5
Q

PDA murmur

A

Normal S1
Continuous crescendo to decrescendo machinery murmur - continues during S2

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6
Q

PDA diagnosis

A

Echo
Doppler flow used to assess left to right shunt

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7
Q

PDA management

A

Monitored till 1 year of age using echos if asymptomatic
Trans-catheter or surgical closure

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8
Q

Atrial septal defect definition

A

Hole in septum between two atria

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9
Q

ASD embryology

A

Walls of atria grow downwards from top of heart
Then fuse together with endocardial cushion in middle - separates the atria
Walls =septum primum and septum secondum
Septum secondum has hole called foramen ovale - normally closes at birth

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10
Q

ASD pathophysiology

A

ASD
Shunt - blood moves from RA to LA (higher pressure in RA)
Blood flows to pulmonary vessels - no cyanosis
R sided overload and heart strain
Right heart failure + pulmonary hypertension
Can lead to Eisenmenger syndrome

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11
Q

Types of ASD

A

Ostium secondum (septum secondum fails to fully close)
Patent foramen ovale (not strictly ASD)
Ostium primum (septum primum fails to fully close - atrioventricular septal defect)

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12
Q

ASD complications

A

Stroke if venous thromboembolism (DVT) - instead of travelling to lungs (PE) it can now travel to brain
AF/atrial flutter
Pulmonary hypertension/right sided heart failure
Eisenmenger syndrome

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13
Q

ASD murmur

A

Mid-systolic
Crescendo-decrescendo
Loudest at upper left sternal border
Fixed split S2 - aortic and pulmonary valves shut at slightly different times - does not change with inspiration/expiration (normal at inspiration)

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14
Q

ASD symptoms

A

SOB
Difficulty feeding
Poor weight gain
Lower respiratory tract infections

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15
Q

ASD managmeent

A

Refer to paeds cardiologist
Transvenous catheter closure via femoral vein
Open heart surgery
Anticoagulants in adults

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16
Q

Ventral septal defect definition

A

Congenital hole in ventricle septum
Entire septum or small hole

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17
Q

VSD associations

A

Down’s and Turner’s syndrome
Can occur in isolation

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18
Q

VSD pathophysiology

A

Blood flows from LV to RV
Remain acyanotic
Right sided overload, right heart vailure and pulmonary hypertension
Can cause Eisenmenber syndrome

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19
Q

VSD presentation

A

Initially symptomless
Poor feeding
Dysponea
Tachypnoea
Failure to thrive

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20
Q

VSD murmur

A

Pan-systolic
Left lower sternal border
3rd/4th ICS
Systolic thrill

21
Q

VSD treatment

A

Paeds cardiologist
Transvenous catheter closure via femoral vein
Open heart surgery
Increased risk of IE - antibiotic prophylaxis

22
Q

Eisenmenger syndrome causes

A

ASD
VSD
PDA

23
Q

Eisenmenger syndrome timeline

A

develops after 1-2 years with large shunts or with small shunts in adulthood
More quickly in pregnancy

24
Q

Eisenmenger syndrome pathophysiology

A

L to R shunt
Pulmonary hypertension
Pulmonary pressure > systemic pressure
R to L shunt
Blood bypasses lungs
Cyanosis

25
Q

Cyanosis

A

Blue discolouration of skin due to low level of O2 sats
Bone marrow responds - produces more RBC and Hb
Polycythaemia (high Hb)
Plethoric complexion
Blood more viscous - blood clots

26
Q

Eisenmenger syndrome signs

A

Pulmonary hypertension:
R ventricular heave - contracts forcefully against pressure
Loud S2
Raised JVP
Peripheral oedema

R-L shunt and hypoxia:
Cyanosis
Clubbing
SOB
Plethoric complextion (red)

27
Q

Eisenmenger mortality

A

Reduce life expectancy of 20 years
Heart failure
Infection
Thromboembolism
Haemmorrhage
Increased in pregnancy

28
Q

Eisenmenger management

A

Heart-lung transplant is only definitive treatment
Oxygen to manage symptoms
Sildenafil - pulmonary hypertension
Tx arrhythmias
Tx of polycythaemia with venesection
Anticoagulation
Prophylactic antibiotics

29
Q

Coarctation of aorta pathophysiology

A

Narrowing of aortic arch, usually around ductus arteriosus
Linked with Turner’s syndrome
Reduced pressure of blood distal to narrowing
Increased pressure of blood proximal to narrowing (in heart and first three branches of aorta)

30
Q

Coarctation of aorta presentation

A

High blood pressure in limbs supplied from proximal arteries
Low blood pressure in limbs supplied from distal arteries
Systolic murmur in left infraclavicular area and left scapula
Tachypnoea
SOB
Poor feeding
Grey/floppy baby
Left ventricular heave (hypertrophy)
Underdeveloped left arm / legs
Weak femoral pulses

31
Q

Coarctation of aorta management

A

Prostaglandin E - keep ductus arteriosus open while waiting for surgery
Surgery to correct coarctation + ligate DA

32
Q

Tetralogy of Fallot pathologies

A

VSD
Overriding aorta (entrance is further to right than normal - above VSD)
Pulmonary valve stenosis
RV hypertrophy

33
Q

ToF pathophysiology

A

Deoxygenated blood enters aorta from RHS
- VSD allows mixing of blood
- Aorta in direction of travel of blood from RHS
- resistance of blood through pulmonary valve (stenosis)
R to L shunt - cyanosis
Increased strain of RV - R ventricular hypertrophy

34
Q

ToF risk factors

A

Rubella
Increased age of mother
Alcohol consumption in pregnancy
Diabetic mother

35
Q

ToF investigations

A

Echo
Doppler flow studies
CXR - boot shaped heart due to RV hypertrophy

36
Q

ToF presentation

A

Ejection systolic murmur esp in pulmonary area
Cyanosis
Clubbing
Poor feeding
Poor weight gain
Tet spells

37
Q

Tet spells pathophysiology

A

Intermittent symptomatic periods
R to L shunt worsened
Pulmonary vascular resistance increases / systematic resistance decreases
Physical exertion - generate CO2 - vasodilation - reduces systematic vascular resistance - increases R to L shunt

38
Q

Tet spell presentation

A

Precipitated by waking, physical exertion or crying
Irritable, cyanotic and SOB
Reduced consciousness, seizures and death

39
Q

Tet spell treatment

A

Squat/position with knees to chest - increase systemic resistance
Oxygen
Beta blockers - relax right ventricle
Iv fluids - increase preload
Morphine - decrease respiratory drive
Sodium bicarbonate - buffer metabolic acidosis
Phenylephrine infusion - increase systemic resistance

40
Q

ToF management

A

Prostaglandin infusion in neonates - maintain ductus arteriosus
Total surgical repair by open heart surgery

41
Q

Ebstein anomaly pathophysiology

A

Tricuspid valve set lower in RHS
Bigger RA and smaller RV
Poor flow to RV and pulmonary vessels
Associated with R to L shunt across ASD
Cyanosis
Associated with Wolff-Parkinson-White syndrome

42
Q

Ebstein anomaly presentation

A

Heart failure
Gallop rhythm (S3 and S4)
Cyanosis
SOB
Tachypnoea
Poor feeding
Collapse / cardiac arrest
If ASD - presents after ductus arteriosus closes

43
Q

Ebstein anomaly diagnosis

A

Echo

44
Q

Ebstein anomaly management

A

Tx arrhythmias and heart failure
Prophylactic antibiotics
Surgical correction

45
Q

Transposition of great arteries pathophysiology

A

Aorta and pulmonary trunk are swapped
Two separate circulations that don’t mix
Pregnancy - placenta does work for lungs
Life threatening at birth
Cyanosis
Need shunt to survive - PDA, ASD, VSD

46
Q

Transposition of great arteries associated conditions

A

VSD
Coarctation of aorta
Pulmonary stenosis

47
Q

Transposition of great arteries presentation

A

Cyanosis
Respiratory distress
Tachycardia
Poor feeding
Poor weight gain
Sweating

48
Q

Transposition of great arteries managment

A

Prostaglandin infusion when neonate
Balloon septostomy - catheter into foramen ovale via umbillicus - create ASD
Open heart surgery - cardiopulmonary bypass machine performs arterial switch