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
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
3
Q
How long does it take for ductus arteriosus to close?
A
Within few hrs to days
4
Q
What is the typical presentation of congenital heart disease?
A
- Shock
- Cyanosis
- Murmur
- Heart failure
- Antenatal dx
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
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
7
Q
What are the symptoms of heart failure?
A
- Breathlessness, esp w feeding or excertion
- Sweating
- Poor feeding
- Recurrent chest inf
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
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
10
Q
What is Eisenmenger sd
A
Irreversibly raised pulmonary vascular resistance from chronically raised pulmonary artery pressure and flow
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
12
Q
What are the causes of HF in infants
A
- High pulmonary blod flow
- 1) VSD 2) AVSD 3) Large persistent ductus arteriosus
13
Q
Cause of HF in older child
A
- Right or left HF
- 1) Eisenmenger sd (right HF only) 2) Rheumatic HD 3) Cardiomyopathy
14
Q
What is peripheral cyanosis
A
- Blue hands and feet
- May occur when child is cold or unwell
- other cause is polycythemia
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)
16
Q
What is the limit sats
A
more or 94%
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
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
19
Q
Left to right shunt cong. HD
A
- Breathless og asymptomatic
- ASD, VSD, PDA
20
Q
Right to left shunt cong. HD
A
- Cyanosis
- ToF, TGA
21
Q
Common mixing cong. HD
A
- Breathless and blue
- AVDS, complex long. HD
22
Q
Well children w obstruction
A
- Asymptomatic
- AS, PS, adult type CoA
23
Q
Sich neonate w obstruction
A
- Collapsed w shock
- Coarction, HLHS
24
Q
What is the most common cong. HD
A
VSD, about 30%
25
Small VSD
- Smaller than aortic valve, up to 3mm
- Are asymptomatic
- loud pansystolig murmur at lower left sternal edge, quiet pulm. sound
- will close spontaneously
26
Large VDS
- 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
27
What are the types of ASD
- 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)
28
What are the S&S of ASD
- 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
29
DX in ASD
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
30
TX in ASD
- 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
31
PDA explaination
- 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
32
Clinical features of PDA
- Continous murmur at left clavicle
- increased pulse pressure
- w large duct HF and HT
33
Dx of PDA
- CXR and ECG are normal
| - Echo is 1st line
34
TX of PDA
- Closure abolish lifelong risk of bact. endocarditis and pulm disease
- Closed w coil or occlusion device by catheters at 1 yr, sometimes surgical ligation
35
How is the right to left shunts presentation
cyanosis (sats 94% or below) usually in first week of life
36
How do you determine HD in cyanosed neonate
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
37
Mx of cyanosed neonate
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
38
Most common cause of cyanotic cong. HD
ToF
39
Clinical features of Tof
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
40
S&S of Tof
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
41
CXR in Tof
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
42
ECG in Tof
Normal at birth, RV hypertrophy when older
43
Echo in Tof
will demonstrate cardinal features
44
MX of Tof
- 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
45
TGA explain
- 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
46
ass anomalies w TGA
VSD, ASD, PDA
47
Clinical features of TGA
- 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
48
Dx of TGA
- CXR: narrow upper mediastinum w "egg on side", increased pulm vascular markings (increased flow)
- ECG: usually normal
- Echo: essential for DX
49
MX of TGA
- 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
AVSD explain
- 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
Clinical features of AVSD
- 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
Maternal Rubella inf cause
Peripheral pulm stenosis, PDA
53
Maternal SLE cause
Complete heart block (anti-Ro and anti-La antibody)
54
Maternal DM cause
Increased overall incidence of cardiac abnormality
55
Maternal warfarin tx
Pulm valve stenosis, PDA
56
Fetal alcohol sd
ASD, VSD, ToF
57
Down sd
AVSD, VSD (30%)
58
Edward sd
Complex
59
Patau
Complex
60
Turner
Aortic valve stenosis, coarctation of aorta
61
Chr 22q11 (diGeorge)
Aortic arch anomalies, ToF, common arterial trunk (80%)
62
Williams
Supravalvular aortic stenosis, peripheral pulm artery stenosis
63
Noonan (PTPN11)
Hypertrophic cardiomyopathy, ASD, pulm valve stenosis
64
Complex cong. HD
- Tricuspid atresia (most common)
- Mitral atresia
- Double inlet LV
- common arterial trunk (truncus arteriosus)
65
Presenting in complex
Depends on whether cyanosis of HF is more predominant
66
Tricuspid atresia
- Only LV is effective
| - Right is small and nonfunctioning
67
Clinical tricuspid atresia
- Common mixing of systemic and pulm. venous return
- cyanosis in newborn if duct dependent
- well child at birth then become cyanosed and breathes
68
Mx tricuspid atresia
- 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
Outflow obstruction in the well child
AS, PS, adult type CoA
70
AS explain
- Valve leaflets are partly fused together (1-3)
- Restrictive exit from LV
- Often ass w mitral valve stenosis and CoA (should be excluded)
71
AS Sx
- 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
AS dx
- CXR: normal or prominent LV w poststenotic dilatation of ascending aorta
- ECG: may be LV hypertrophy
- Echo
73
Mx AS
- 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
PS explain
Pulm leaflets are partly fused together, give restrictive exit from RV
75
PS clinical
- Most are asymptomatic
- Dx is clinical
- Ejection systolic murmur best heard at upper left sternal edge
- When severe prominent RV impulse
76
PS dx
- CXR: normal or post stenotic dilatation of pulm artery
| - ECG: RV hypertrophy
77
PS mx
When pressure gradient across pulm. valve >64 mmHg it is transcatheter baloon dilatation (ToC)
78
Adult type CoA
- Is uncommon, not duct dependent and increase gradually in severity
79
Adult type CoA clinical
- 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
dx adult type coa
- 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
mx adult type coa
- When severe stent may be placed w catheter
| - sometimes surgical repair is required
82
outflow obstruction in the sick infant
- CoA
- Interruption of aortic arch
- Hypoplastic left heart sd
83
CoA
- 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
Interruption of aortic arch
- 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
Hypoplastic left heart sd
- 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
SVT
- Most common childhood arrhythmia
- HR 200-300
- Can cause poor cardiac output and pulm edema
87
Presentation of SVT
- Sx of HF in neonate/infant
- Can cause hydrops fetalis and intrauterine death
- rarely a structural heart problem
88
dx SVT
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
mx SVT
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
Congenital complete heart block
| why?
- 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
congenital complete heart block may cause
1. fetal hydrops 2. death in utero 3. HF in neonatal period
92
Sx congenital complete heart block
- Most are symptom free for many years
| - Few w pre syncope or syncope
93
mx cong. complete heart block
Insertion of endocardial pacemaker
94
Long QT sd
Sudden loss of consciousness during exercise, stress or emotion, usually late in childhood. May be mistaken for epilepsy
95
Sudden death from VT
Ass w erythromycin tx, electrolyte disorders and head injury
96
Channelopathies
Gene mutation , Na, K, Ca, anyone w FH of sudden death or history of syncope on exertion (J-wave sd, CPVT, Brugada sd)
97
Afib, flutter, ectopic atrial TC, ventricular TC, Vfib
Are rare in children. Most often seen after surgery for complex congenital heart disease
98
Syncope
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
Syncope is common in...
Adolescents! Is usually being, but are rarely due to cardiac disease and may be life threatening
100
Neurally mediated syncope
- 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
Cardiac syncope
- 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
Mx of syncope
- Check BP
- Signs of cardiac disease: murmur, femoral pulses, Marfans sd
- 12 lead ECG -> corrected QT interval
103
Rheumatic fever explain
- 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
Age group Rheumatic fever
5-15 yrs
105
Clinical features in rheumatic hd
- 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
Chronic rheumatic hd
- 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
mx of rheumatic hd
- 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
Infective endocarditis risk
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
Clinical features of inf. endocardtitis
- 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
Dx of endocarditis
- blood culture: strep viridian's
- echo: may confirm DX if vegetations (consist of fibrin and plot and infecting organisms
- increased acute phase reactants
111
mx of endocarditis
- Penicillin and aminoglycosides in 6 w IV
| - w prosthetic valve: surgical removal may be required
112
prevention of endocarditis
1. good dental hygiene
| 2. avoidance of body piercings and tatoos
113
Dilated cardiomyopathy may be caused by
1) Inherited 2) secondary to metabolic disease 3) viral infection
114
what jones criteria are required for rheumatic fever dx
- 2 major,
| - or one major + 2 minor + supportive evidence og bacteria (ASO titer/ positive rapid strep test/ culture)
115
when should myocarditis/cardiomyopathy be suspected
In any child w enlarged heart and HF who was previously well
116
dx of myocarditits/ cardiomyopathy
Echo
117
Mx of cardiomyopathy/myocarditits
- Symptomatic w diuretics
- ACEis
- Usually improves spontaneously
- Some require transplant
118
Hypertrophic/restrictive cardiomyopathy in children
Are rare, usually related to systemic disease- eg. Hurler. Pompe and Noonan.
