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Cardiology Flashcards

1
Q

Why is pressure bigger in * atrium in fetal life?

A

Pressure in RA is bigger bc receives blood from placenta and systemic return

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2
Q

What happens w pressure when taking first breath?

A

Resistance in pulmonary blood flow decrease which makes pressure to left atrium bigger which also close the foramen ovale flap

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3
Q

How long does it take for ductus arteriosus to close?

A

Within few hrs to days

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4
Q

What is the typical presentation of congenital heart disease?

A
  • Shock
  • Cyanosis
  • Murmur
  • Heart failure
  • Antenatal dx
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5
Q

How is antenatal dx of cong. HD

A
  • 18-20wg
  • 70 % requiring surgery first 6 m are detected
  • Risk factors: Down sd, previous child w CHD or mother w CHD
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6
Q

What characterize an innocent murmur?

A

1) aSymptomatic
2) Soft blowing
3) Systolic
4) left Sternal edge
5) normal sounds, no added
6) no parasternal thrill
7) no radiation
- Are often heard w febrile illness or anemia bc of increased CO

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7
Q

What are the symptoms of heart failure?

A
  • Breathlessness, esp w feeding or excertion
  • Sweating
  • Poor feeding
  • Recurrent chest inf
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8
Q

What are the signs of HF?

A
  • Poor weight gain / faltering growth
  • Tachypnea
  • Tachycardia
  • Heart murmur, gallop rhythm
  • Enlarged heart
  • Hepatomegaly
  • Cool peripheries
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9
Q

Signs of RHF

A
  • Are rare in developed countries
  • May be seen w: 1) long standing rheumatic HD 2) Pulm. HT 3) Tricusp regurg 4)Right atrial dilatation
  • Ankle edema, sacral edema, ascites
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10
Q

What is Eisenmenger sd

A

Irreversibly raised pulmonary vascular resistance from chronically raised pulmonary artery pressure and flow

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11
Q

What are the causes of HF in neonates

A
  • Obstructed (duct dependent) systemic circulation
  • 1) Hypoplastic left heart sd 2) Critical aortic valve stenosis 3) Severe coarctation of aorta 4) Interruption of aortic arch
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12
Q

What are the causes of HF in infants

A
  • High pulmonary blod flow

- 1) VSD 2) AVSD 3) Large persistent ductus arteriosus

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13
Q

Cause of HF in older child

A
  • Right or left HF

- 1) Eisenmenger sd (right HF only) 2) Rheumatic HD 3) Cardiomyopathy

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14
Q

What is peripheral cyanosis

A
  • Blue hands and feet
  • May occur when child is cold or unwell
  • other cause is polycythemia
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15
Q

What is central cyanosis

A
  • Seen on the tongue as blue color
  • ass. w. fall in arterial blood oxygen tension
  • seen clinically when Hb exceeds 50 g/L (less pronounced in anemic child)
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16
Q

What is the limit sats

A

more or 94%

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17
Q

What are the causes of cyanosis + resp. distress

A
  • Cardiac disorder
  • Resp disorder: surfactant def., meconium asp., pulm hypoplasia
  • Persistent pulm. HT (failure of vascular resistance to fall)
  • Infection
  • IEM
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18
Q

How to dx cong. HD

A
  • CXR
  • ECG: arrhythmia, superior QRS axis, RV hypertrophy, LV ..
  • Echo + Doppler
  • Pitfalls w ECG: RBBB are mostly normal in children unless ASD, sinus arrhythmia is normal finding
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19
Q

Left to right shunt cong. HD

A
  • Breathless og asymptomatic

- ASD, VSD, PDA

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20
Q

Right to left shunt cong. HD

A
  • Cyanosis

- ToF, TGA

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21
Q

Common mixing cong. HD

A
  • Breathless and blue

- AVDS, complex long. HD

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22
Q

Well children w obstruction

A
  • Asymptomatic

- AS, PS, adult type CoA

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23
Q

Sich neonate w obstruction

A
  • Collapsed w shock

- Coarction, HLHS

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24
Q

What is the most common cong. HD

A

VSD, about 30%

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25
Q

Small VSD

A
  • Smaller than aortic valve, up to 3mm
  • Are asymptomatic
  • loud pansystolig murmur at lower left sternal edge, quiet pulm. sound
  • will close spontaneously
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26
Q

Large VDS

A
  • Same size or bigger than aortic valve
  • 1) HF w dyspnea 2) faltering growth after 1w 3) recurrent chest inf 4) TP, TC 5) enlarged liver 6) soft pan systolic murmur or no murmur, apical mid-diastolic murmur 7) loud pulm. 2.nd sound
  • CXR: cardiomegaly, enlarged pulm. arteries, increased pulm markings/ edema
  • MX: HF drugs ( diuretic w captopril), added calorie input, surgery at 3-6m
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27
Q

What are the types of ASD

A
  • Secundum: 80%, defect in centre of atrial septum, involving foramen ovale
  • Primum (AVSD)/ partial : Interarterial communication btw bottom of atrial septum and AV-valves, abnormal AV-valves (3 leafs and tend to leak)
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28
Q

What are the S&S of ASD

A
  • Symp: none, recurrent chest inf/wheeze, arrhythmias (4th decade)
  • Sign: ejection systolic murmur at upper left sternal edge, fixed widely split second sound,
  • w partial: apical pansystolic murmur from Av valve regurgitation
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29
Q

DX in ASD

A

CXR: cardiomegaly, enlarged puilm. arteries and increased vascular markings
ECG secundum: partial RBBB, right axis deviation( ventricular enlargement)
ECG partial: superior QRS bc middle part (AV node) is diplace, conducts to ventricles superiorly
Echo: mainstay of DX

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30
Q

TX in ASD

A
  • Only significant will require TX (large enough to cause RV dilatation)
  • Seccundum: catheterization w insertion of occlusion device
  • Partial ASD need surgical correction
  • Tx usually at 3-5 yrs to prevent RHF
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31
Q

PDA explaination

A
  • Failed to close 1 m after expected delivery
  • Due to defect in contrictor mechanism of the duct
  • After fall of pulm. resistance the flow goes from aorta to pulm artery
  • In preterm caused by prematurity
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32
Q

Clinical features of PDA

A
  • Continous murmur at left clavicle
  • increased pulse pressure
  • w large duct HF and HT
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33
Q

Dx of PDA

A
  • CXR and ECG are normal

- Echo is 1st line

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34
Q

TX of PDA

A
  • Closure abolish lifelong risk of bact. endocarditis and pulm disease
  • Closed w coil or occlusion device by catheters at 1 yr, sometimes surgical ligation
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35
Q

How is the right to left shunts presentation

A

cyanosis (sats 94% or below) usually in first week of life

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36
Q

How do you determine HD in cyanosed neonate

A

Hyperoxia (nitrogen washout ) test

  1. Placed on 100% O2 for 10min
  2. Right radial arterial partial pressure of O2 from ABG remains low (<15kPa, 113 mmHg) -> dx of cyanotic HD can be made if lung disease & persistent pulm HT are excluded
  3. If PaO2 > 20 kPa -> not cyanotic HD
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37
Q

Mx of cyanosed neonate

A
  1. ABC w artificial ventilation if necessary
  2. Start prostaglandin infusion 5ng/kg per min, most are duct dependent
  3. Observe potential SE: apnea, jitteriness, seizures, flushing, hypotension
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38
Q

Most common cause of cyanotic cong. HD

A

ToF

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39
Q

Clinical features of Tof

A
  1. A large VSD
  2. Overriding of the aorta w respect to the ventricular septum
  3. Subpulmonary stenosis causing right ventricular outflow tract obstruction
  4. Right ventricular hypertrophy
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40
Q

S&S of Tof

A

Symp: Dx antenatally, murmur in 1st 2 m of life
Sign: clubbing of fingers/toes in older child, loud harsh ejection systolic murmur at left sternal edge from day 1

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41
Q

CXR in Tof

A

1) Small heart w boot shape (RV hypertrophy) 2) Right sided aortic arch 3) pulm. artery bay 4) Concavety on the left heart border 5) decreased pulm. markings

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42
Q

ECG in Tof

A

Normal at birth, RV hypertrophy when older

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43
Q

Echo in Tof

A

will demonstrate cardinal features

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44
Q

MX of Tof

A
  • Surgery at 6 m closing VSD and relieving RV obstruction
  • W severe cyanosis -> shunt btw subclavian artery and pulm. artery (Blalock- Taussing shunt) or baloon dilatation of RV outflow
  • Hypercyanotic spells: usually self limiting but if >15 min: sedation and pain relief, IV propanolol, IV volume admin, bicarbonate (acidosis), muscle paralysis and artificial ventilation
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45
Q

TGA explain

A
  • Aorta connected to RV
  • Pulm artery connected to LV (discordant ventriculo- arterial connection)
  • Blue blood returned to body
  • Pink blood returned to lung
  • Two parallell circuits which are incompatible w life
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46
Q

ass anomalies w TGA

A

VSD, ASD, PDA

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47
Q

Clinical features of TGA

A
  • Cyanosis if predominant sx, profound. Presents on 2nd day w ductus closure. Less severe w ass anomalies
  • 2nd heart sound is loud and single
  • Usually no murmur, bur may be systolic murmur from increased flow or stenosis within LV
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48
Q

Dx of TGA

A
  • CXR: narrow upper mediastinum w “egg on side”, increased pulm vascular markings (increased flow)
  • ECG: usually normal
  • Echo: essential for DX
49
Q

MX of TGA

A
  • Maintain patency og of ductus w PG infusion
  • Balloon atrial septostomy (through ovale and tears septum)
  • Surgery in first few days, transected and switched + transfer of coronary arteries
50
Q

AVSD explain

A
  • Most commonly in Down
  • Defect in the middle of the heart w a single five leaflet valve btw atria and ventricles
  • Stretch across entire AV junction, tends to leak
51
Q

Clinical features of AVSD

A
  • Presentation on antenatal US
  • Cyanosis at birth or HF at 2w-3w
  • Always superior axis on ECG
  • Mx is tx of HF and surgical repair at 3-6 m
52
Q

Maternal Rubella inf cause

A

Peripheral pulm stenosis, PDA

53
Q

Maternal SLE cause

A

Complete heart block (anti-Ro and anti-La antibody)

54
Q

Maternal DM cause

A

Increased overall incidence of cardiac abnormality

55
Q

Maternal warfarin tx

A

Pulm valve stenosis, PDA

56
Q

Fetal alcohol sd

A

ASD, VSD, ToF

57
Q

Down sd

A

AVSD, VSD (30%)

58
Q

Edward sd

A

Complex

59
Q

Patau

A

Complex

60
Q

Turner

A

Aortic valve stenosis, coarctation of aorta

61
Q

Chr 22q11 (diGeorge)

A

Aortic arch anomalies, ToF, common arterial trunk (80%)

62
Q

Williams

A

Supravalvular aortic stenosis, peripheral pulm artery stenosis

63
Q

Noonan (PTPN11)

A

Hypertrophic cardiomyopathy, ASD, pulm valve stenosis

64
Q

Complex cong. HD

A
  • Tricuspid atresia (most common)
  • Mitral atresia
  • Double inlet LV
  • common arterial trunk (truncus arteriosus)
65
Q

Presenting in complex

A

Depends on whether cyanosis of HF is more predominant

66
Q

Tricuspid atresia

A
  • Only LV is effective

- Right is small and nonfunctioning

67
Q

Clinical tricuspid atresia

A
  • Common mixing of systemic and pulm. venous return
  • cyanosis in newborn if duct dependent
  • well child at birth then become cyanosed and breathes
68
Q

Mx tricuspid atresia

A
  • Early palliation
  • Blalock- Taussing shunt intervention ( subclavian and pulm arteries) w severe cyanosis
  • Pulm artery banding operation, decrease blood flow if breathless
  • Not possible w complete corrective surgery ( Glenn or hemi- Fontan operation, connecting SVC w pulm artery after 6 m, Fontan IVC to pulm artery at 3-5y)
69
Q

Outflow obstruction in the well child

A

AS, PS, adult type CoA

70
Q

AS explain

A
  • Valve leaflets are partly fused together (1-3)
  • Restrictive exit from LV
  • Often ass w mitral valve stenosis and CoA (should be excluded)
71
Q

AS Sx

A
  • Asymptomatic murmur
  • Decrease exercise tolerance
  • Chest pain on exertion
  • Syncope
  • Critical stenosis: ductdependent -> severe HF and shock
  • Small volume slow rising pulses
  • Carotid thrill (always)
  • Ejection systolic murmur at upper right sternal edge, radiating to neck
  • Delayed and soft aortic second sound
  • Apical ejection click
72
Q

AS dx

A
  • CXR: normal or prominent LV w poststenotic dilatation of ascending aorta
  • ECG: may be LV hypertrophy
  • Echo
73
Q

Mx AS

A
  • Regular clinical and echo assessment
  • Child w sx on exercise or pressure gradient is > 64mmHg across aortic valve -> balloon valvotomy
  • Most will need valve replacement eventually
74
Q

PS explain

A

Pulm leaflets are partly fused together, give restrictive exit from RV

75
Q

PS clinical

A
  • Most are asymptomatic
  • Dx is clinical
  • Ejection systolic murmur best heard at upper left sternal edge
  • When severe prominent RV impulse
76
Q

PS dx

A
  • CXR: normal or post stenotic dilatation of pulm artery

- ECG: RV hypertrophy

77
Q

PS mx

A

When pressure gradient across pulm. valve >64 mmHg it is transcatheter baloon dilatation (ToC)

78
Q

Adult type CoA

A
  • Is uncommon, not duct dependent and increase gradually in severity
79
Q

Adult type CoA clinical

A
  • Asymptomatic
  • Systemic HT in right arm
  • Ejection systolic murmur at upper sternal edge
  • Collaterals heard w continuous murmur at the back
  • Radio-femoral delay
80
Q

dx adult type coa

A
  • CXR: rib notching, due to development of large collateral intercostal arteries running under the ribs. 3-sign w visible notch in descending aorta
  • ECG: LV hypertrophy
81
Q

mx adult type coa

A
  • When severe stent may be placed w catheter

- sometimes surgical repair is required

82
Q

outflow obstruction in the sick infant

A
  • CoA
  • Interruption of aortic arch
  • Hypoplastic left heart sd
83
Q

CoA

A
  • Arterial duct tissue encircling aorta just at the point of insertion of the duct
  • When duct closes, aorta constricts causing severe obstruction to LV outflow
  • Most common cause of collapse due to left outflow obstruction
  • Normal 1st day, collapse 2nd day, severe HF, absent femoral pulse, severe metabolic acidosis
  • DX: CXR cardiomegaly from HF, ecg normal
  • MX surgical
84
Q

Interruption of aortic arch

A
  • Uncommon, w no connection btw proximal aorta and distal arterial duct
  • CO is dependent on R-L shunt via duct
  • VSD usually present
  • Present w shock in neonatal period
  • MX correction w closure of VSD within first few days
  • Ass w DiGeorge
85
Q

Hypoplastic left heart sd

A
  • Underdevelopment of entire left side
  • Mitral is small/atreic, LV is diminutive and usually aortic valve atresia, usually CoA
  • Detected antenatally, sickest of all neonates w duct dependent disease, profound acidosis, absence of all peripheral pulses
  • Mx w Norwood preocedure, hybrid ( catheted + surgery), Glenn or Hemi- Fontan at 6 m ant Fontan at 3y
86
Q

SVT

A
  • Most common childhood arrhythmia
  • HR 200-300
  • Can cause poor cardiac output and pulm edema
87
Q

Presentation of SVT

A
  • Sx of HF in neonate/infant
  • Can cause hydrops fetalis and intrauterine death
  • rarely a structural heart problem
88
Q

dx SVT

A

ECG: 1) Narrow complex TC of 250-300 bpm 2) myocardial ischemia if HF is severe 3) In sinus, short PR interval 4) In WPW: short PR + delta wave

89
Q

mx SVT

A
  1. Circulartory and resp support, correct acidosis and PPV
  2. Vagal stimulation a) carotid massage b) cold ice pack to face (successful in 80%)
  3. IV adenosine (ToC)
  4. Electrical cardioversion w synchronized direct current shock (0,5-2 J/kg bw)
90
Q

Congenital complete heart block

why?

A
  • Related to presence of anti Ro or anti La Ab´s in maternal serum (manifest or latent CTD)
  • Subsequent pregnancies often affected
  • Prevent development of electrical conduction system , atrophy and fibrosis of AV node
91
Q

congenital complete heart block may cause

A
  1. fetal hydrops 2. death in utero 3. HF in neonatal period
92
Q

Sx congenital complete heart block

A
  • Most are symptom free for many years

- Few w pre syncope or syncope

93
Q

mx cong. complete heart block

A

Insertion of endocardial pacemaker

94
Q

Long QT sd

A

Sudden loss of consciousness during exercise, stress or emotion, usually late in childhood. May be mistaken for epilepsy

95
Q

Sudden death from VT

A

Ass w erythromycin tx, electrolyte disorders and head injury

96
Q

Channelopathies

A

Gene mutation , Na, K, Ca, anyone w FH of sudden death or history of syncope on exertion (J-wave sd, CPVT, Brugada sd)

97
Q

Afib, flutter, ectopic atrial TC, ventricular TC, Vfib

A

Are rare in children. Most often seen after surgery for complex congenital heart disease

98
Q

Syncope

A

Transient LOC, ass loss of postural tone w spontaneous recovery. Caused by transient impairment of brain oxygen delivery, generally due to impaired cerebral perfusion.

99
Q

Syncope is common in…

A

Adolescents! Is usually being, but are rarely due to cardiac disease and may be life threatening

100
Q

Neurally mediated syncope

A
  • In response to 1) Standing up to quickly (orthostatic) 2) sight of blood or needles 3) sudden unexpected pain
  • Usually prodrome of dizziness, lightheadedness, abnormal vision, nausea, sweating, pallor
  • A maladaptive drop in BP ( a minority get decreased HR and asystole)
101
Q

Cardiac syncope

A
  • Arrhythmic: heart block, SVT, VT
  • Ass w long QT sd or structural like AS, hypertrophic cardiomyopathies
  • Features: 1) sx w exercise 2) FH of sudden unexplained deth 3) Palpitations
102
Q

Mx of syncope

A
  • Check BP
  • Signs of cardiac disease: murmur, femoral pulses, Marfans sd
  • 12 lead ECG -> corrected QT interval
103
Q

Rheumatic fever explain

A
  • Rare in developed world, bur remains the most important cause of heart disease in children worldwide
  • Short-lived multi system autoimmune response to a preceding inf. w group A strep beta hemolytic Strep
  • Progress to chronic rheumatic HD in 80%
104
Q

Age group Rheumatic fever

A

5-15 yrs

105
Q

Clinical features in rheumatic hd

A
  • Latent interval of 2-6 w
  • Following skin/ pharyngeal inf
    – mild fever
  • malaise
    major
  • polyarthritis
  • carditis: 1)endo/2)myo/3)pericardium, tamponade, murmur, friction rub, valvular dysfunction, HF, death
  • sydenham chorea: 2-6m after strep
  • erythema marginatum on trunk and limbs
  • subcutaneous nodules: painless, hard on extensor surface
    minor:
  • fever
  • polyarthralgia
  • increased acute phase reactants
  • prolonged PR interval
106
Q

Chronic rheumatic hd

A
  • most common long term damage is from scarring and forbrosis of valve tissue (mitral stenosis)
  • may occur in 2nd decade
  • aortic, tricuspid and pulm valve may also occur
107
Q

mx of rheumatic hd

A
  • Acute phase: bed rest and anti-inflammatory agents
  • active myocarditis: limitation of exercise
  • aspirin for joint/heart, if not effective use steroids
  • HF: diuretics and ACEis
  • Pericardial effusion: pericardiaocentesis
  • ABs if persisting inf
108
Q

Infective endocarditis risk

A

All children w cong. HD are at risk of inf. endocarditis. Risk is highest when there is a turbulent jet of blood or prosthetic device (VSD, CoA, PDA)

109
Q

Clinical features of inf. endocardtitis

A
  • Fever
  • Anemia and pallor
  • Splinter hemorrhage in nailbed
  • Clubbing (late)
  • Necrotic skin lesions
  • Splenomegaly
  • CNS signs of cerebral infarction
  • Retinal infarctions
  • Arthritis and arthralgia
  • Hematuria (microscopic )
110
Q

Dx of endocarditis

A
  • blood culture: strep viridian’s
  • echo: may confirm DX if vegetations (consist of fibrin and plot and infecting organisms
  • increased acute phase reactants
111
Q

mx of endocarditis

A
  • Penicillin and aminoglycosides in 6 w IV

- w prosthetic valve: surgical removal may be required

112
Q

prevention of endocarditis

A
  1. good dental hygiene

2. avoidance of body piercings and tatoos

113
Q

Dilated cardiomyopathy may be caused by

A

1) Inherited 2) secondary to metabolic disease 3) viral infection

114
Q

what jones criteria are required for rheumatic fever dx

A
  • 2 major,

- or one major + 2 minor + supportive evidence og bacteria (ASO titer/ positive rapid strep test/ culture)

115
Q

when should myocarditis/cardiomyopathy be suspected

A

In any child w enlarged heart and HF who was previously well

116
Q

dx of myocarditits/ cardiomyopathy

A

Echo

117
Q

Mx of cardiomyopathy/myocarditits

A
  • Symptomatic w diuretics
  • ACEis
  • Usually improves spontaneously
  • Some require transplant
118
Q

Hypertrophic/restrictive cardiomyopathy in children

A

Are rare, usually related to systemic disease- eg. Hurler. Pompe and Noonan.

Pediatrics (4 decks)

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