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TN Pédiatrie > 5. Cardiology > Flashcards

5. Cardiology Flashcards

1
Q

Describe: Prenatal circulation (1)

A
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2
Q

Describe heart before birth (2)

A
  • shunting deoxygenated blood
    • ductus arteriosus: connection between pulmonary artery and aorta
  • shunting oxygenated blood
    • foramen ovale: connection between right and left atria
    • ductus venosus: connection between umbilical vein and inferior vena cava
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3
Q

Describe heart before at birth (5)

A
  • with first breath, lungs open up -> pulmonary resistance decreases -> pulmonic blood flow increases
  • separation of low resistance placenta -> systemic circulation becomes a high resistance system -> ductus venosus closure
  • increased pulmonic flow -> increased left atrial pressures -> foramen ovale closure
  • increased oxygen concentration in blood after first breath -> decreased prostaglandins -> ductus arteriosus closure
  • closure of fetal shunts and changes in vascular resistance -> infant circulation assumes normal adult flow
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4
Q

Fetal circulation is designed so that oxygenated blood is preferentially delivered where? (2)

A

to the brain and myocardium

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5
Q

Describe epidemiology: Congenital Heart Disease Cardiology (2)

A
  • 8/1000 live births have congenital heart defect (CHD), which may present as a heart murmur, heart failure, or cyanosis;
  • ventricular septal defect (VSD) is the most common lesion
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6
Q

Describe investigations: Congenital Heart Disease Cardiology (2)

A
  • Echo, ECG, CXR
  • pre and postductal oxygen saturations, 4 limb BPs, hyperoxia test
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7
Q

Compare CYANOTIC VS. ACYANOTIC CONGENITAL HEART DISEASE (3)

A
  • cyanosis: blue mucous membranes, nail beds, and skin secondary to an absolute concentration of deoxygenated hemoglobin of at least 30 g/dL
  • acyanotic heart disease (i.e. L to R shunt, obstruction occurring beyond lungs): blood passes through pulmonic circulation -> oxygenation takes place -> low levels of deoxygenated blood in systemic circulation -> no cyanosis
  • cyanotic heart disease (i.e. R to L shunt): blood bypasses the lungs -> no oxygenation occurs -> high levels of deoxygenated hemoglobin enters the systemic circulation s cyanosis
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8
Q

Name Common congenital heart diseases (figure)

A
  • ASD: atrial septal defect
  • VSD: ventricular septal defect
  • PDA: patent ductus arteriosus
  • TGA: Transposition of the Great Arteries
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9
Q

Name: Characteristic CXR Findings in congenital heart defect (3)

A
  • Boot-shaped heart: tetralogy of Fallot, tricuspid atresia
  • Egg-shaped heart: transposition of great arteries
  • “Snowman” heart: total anomalous pulmonary venous return
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10
Q

Describe: LEFT-TO-RIGHT SHUNT LESIONS (3)

A
  • extra blood is displaced through a communication from the left to the right side of the heart -> increased pulmonary blood flow -> increased pulmonary pressures
  • shunt volume is dependent upon three factors: (1) size of defect, (2) pressure gradient between chambers or vessels, and (3) peripheral outflow resistance
  • untreated shunts can result in pulmonary vascular disease, left ventricular dilatation and dysfunction, right ventricular HTN and RVH, and ultimately R to L shunts
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11
Q

Name 3 types of atrial septal defect

A
  • ostium primum (common in DS, defect located at mitral or tricuspid valves)
  • ostium secundum (most common type, 50-70%, defect located at septum between left and right atria)
  • sinus venosus (defect located at entry of superior vena cava into right atrium)
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12
Q

Describe natural history: Atrial Septal Defect (2)

A
  • 80-100% spontaneous closure rate if atrial septal defect diameter <8 mm
  • if remains patent, CHF and pulmonary HTN can develop in adult life
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13
Q

Describe clinical features Atrial Septal Defect (3)

A
  • history: often asymptomatic in childhood
  • physical exam: grade 2-3/6 pulmonic outflow murmur, widely split, and fixed S2
  • children with large atrial septal defects may have signs of heart failure (tachypnea, FTT, hepatomegaly, pulmonary rales/retractions)
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14
Q

Describe investigations: Atrial Septal Defect (3)

A
  • ECG: RAD, mild RVH, RBBB (normal ECG does not rule out)
  • CXR: increased pulmonary vasculature, cardiac enlargement (normal ECG does not rule out)
  • Echo: diagnostic
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15
Q

Describe management: Atrial Septal Defect (2)

A
  • elective surgical or catheter closure between 2-5 yr of age, though majority require no surgery
  • size <8 mm will likely spontaneously close
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16
Q

Name most common congenital heart defect

A

Ventricular Septal Defect (30-50%)

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17
Q

Describe: Small Ventricular Septal Defect (4)

A
  • majority
  • clinical feature
    • history: asymptomatic, normal growth, and development
    • physical exam: early systolic to holosystolic murmur, best heard at LLSB, thrill
  • investigations: Echo to confirm diagnosis (ECG and CXR are normal)
  • management: most close spontaneously
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18
Q

Describe: Large Ventricular Septal Defect (4)

A
  • epidemiology: CHF by 2 mo; late secondary pulmonary HTN if left untreated
  • clinical feature
    • history: delayed growth, decreased exercise tolerance, recurrent URTIs or “asthma” episodes
    • physical exam: holosystolic murmur at LLSB, mid-diastolic rumble at apex, size of VSD is inversely related to intensity of murmur, loss of splitting of second heart sound and a loud P2 suggests pulmonary hypertension
  • investigations
    • ECG: LVH, LAH, RVH (normal ECG does not rule out)
    • CXR: increased pulmonary vasculature, cardiomegaly, CHF (normal CXR does not rule out)
    • Echo: diagnostic
  • management: treatment of CHF and surgical closure by 1 yr old, if surgery required
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19
Q

True or false

Moderate-to-Large VSD Size of VSD is inversely related to intensity of murmur

A

True

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20
Q

Describe: Patent Ductus Arteriosus (1)

A
  • patent vessel between descending aorta and left pulmonary artery (normally, functional closure within first 15 h of life, anatomical closure within first days of life)
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21
Q

Describe epidemiology: Patent Ductus Arteriosus (2)

A
  • 5-10% of all congenital heart defects
  • delayed closure of ductus is common in premature infants (1/3 of infants <1750 g); this is different from PDA in term infants
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22
Q

Describe natural history: Patent Ductus Arteriosus (1)

A
  • spontaneous closure common in premature infants, less common in term infants
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23
Q

Describe clinical features: Patent Ductus Arteriosus (2)

A
  • history: asymptomatic, or have apneic or bradycardic spells, poor feeding, accessory muscle use, CHF
  • physical exam: tachycardia, bounding pulses, hyperactive precordium, wide pulse pressure, continuous “machinery” murmur best heard at left infraclavicular area
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24
Q

Describe investigations: Patent Ductus Arteriosus (3)

A
  • ECG: may show left atrial enlargement, LVH, RVH
  • ECHO is diagnostic
  • CXR: may show normal to mildly enlarged heart, increased pulmonary vasculature, prominent pulmonary artery
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25
Q

Describe management: Patent Ductus Arteriosus (2)

A
  • indomethacin (Indocid®): antagonizes prostaglandin E2, which maintains ductus arteriosus patency; only effective in premature infants
  • catheter or surgical closure if PDA causes respiratory compromise, FTT, or persists beyond 3rd mo of life
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26
Q

Define: Coarctation of the Aorta (1)

A
  • narrowing of aorta (almost always at the level of the ductus arteriosus)
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27
Q

Describe epidemiology: Coarctation of the Aorta (1)

A
  • commonly associated with bicuspid aortic valve (50%); Turner syndrome (35%)
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28
Q

Describe clinical features: Coarctation of the Aorta (5)

A
  • history: often asymptomatic
  • physical exam
    • blood pressure discrepancy between upper and lower extremities (increased suspicion/severity if >20 mmHg difference)
    • diminished or delayed femoral pulses relative to brachial (i.e. brachial-femoral delay)
    • possible systolic murmur with late peak at apex, left axilla, and left back
    • if severe, presents with shock in the neonatal period when the ductus arteriosis closes
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29
Q

Describe prognosis: Coarctation of the Aorta (1)

A
  • can be complicated by HTN; if associated with other lesions (e.g. patent ductus arteriosus, ventricular septal defect) can lead to CHF
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30
Q

Describe management: Coarctation of the Aorta (2)

A
  • give prostaglandins to keep ductus arteriosus patent for stabilization and perform surgical correction in neonates
  • for older infants and children balloon arterioplasty may be an alternative to surgical correction
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31
Q

Name 4 types: Aortic Stenosis

A
  • valvular (75%)
  • subvalvular (20%)
  • supravalvular
  • idiopathic hypertrophic subaortic stenosis (5%)
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32
Q

Describe: Aortic Stenosis

  • clinical feature
  • investigations
  • management
A
  • clinical feature
    • history: often asymptomatic, but may be associated with CHF, exertional chest pain, syncope, or sudden death
    • physical exam: SEM at RUSB with aortic ejection click at the apex (only for valvular stenosis)
  • investigations: echo for diagnosis
  • management: valvular stenosis is usually treated with balloon valvuloplasty, patients with subvalvular or supravalvular stenosis require surgical repair, exercise restriction required
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33
Q

Name 3 types: Pulmonary Stenosis

A
  • : valvular (90%), subvalvular, or supravalvular
34
Q

Definition of critical pulmonary stenosis (1)

A

inadequate pulmonary blood flow, dependent on ductus for oxygenation, progressive hypoxia and cyanosis

35
Q

Describe natural history: Pulmonary Stenosis (2)

A
  • may be part of other congenital heart lesions (e.g. Tetralogy of Fallot)
  • or in association with syndromes (e.g. congenital rubella, Noonan syndrome)
36
Q

Describe clinical features: Pulmonary Stenosis (2)

A
  • history: spectrum from asymptomatic to CHF
  • physical exam: wide split S2 on expiration, systolic ejection murmur at LUSB, pulmonary ejection click (for valvular lesions)
37
Q

Describe investigations: Pulmonary Stenosis (3)

A
  • ECG findings: RVH
  • CXR: post-stenotic dilation of the main pulmonary artery (due to high velocity jet past stenotic valve)
  • Echo: diagnostic
38
Q

Describe management: Pulmonary Stenosis (1)

A

surgical repair if critically ill or if symptomatic in older infants/children

39
Q

Describe: Cyanotic Congenital Heart Disease (4)

A
  • systemic venous return re-enters systemic circulation directly
  • most prominent feature is cyanosis (O2 sat <75%)
  • hyperoxic test differentiates between cardiac and other causes of cyanosis
    • obtain preductal, right radial ABG in room air, then repeat after the child inspires 100% O2
    • if PaO2 improves to > mmHg, cyanosis less likely cardiac in origin
  • pre-ductal and post-ductal pulse oximetry
    • >5% difference suggests R to L shunt
40
Q

Describe epidemiology: Tetralogy of Fallot (1)

A

10% of all CHD, most common cyanotic heart defect diagnosed beyond infancy with peak incidence at 2-4 mo of age

41
Q

Describe pathophysiology: Tetralogy of Fallot (3)

A
  • embryological defect due to anterior and superior deviation of the outlet septum leading to: ventricular septal defect, right ventricular outflow tract obstruction RVOTO (i.e. pulmonary stenosis ± subpulmonary valve stenosis), over-riding aorta, and right ventricular hypertrophy RVH
  • infants may initially have a L -> R shunt (therefore no cyanosis); however, RVOTO is progressive, leading to increasing R -> L shunting with hypoxemia and cyanosis
  • degree of RVOTO determines the direction and degree of shunt and, therefore, the extent of clinical cyanosis and degree of RVH
42
Q

Describe clinical features: Tetralogy of Fallot (4)

A
  • history: hypoxic “tet” spells
    • during exertional states (crying, exercise) the increasing pulmonary vascular resistance and decrease in systemic resistance causes an increase in right-to-left shunting
    • clinical features include paroxysms of rapid and deep breathing, irritability and crying, increasing cyanosis, decreased intensity of murmur (decreased flow across right ventricular outflow tract obstruction RVOTO), patient squatting for relief (increased peripheral resistance, decreased R to L shunting)
    • if severe, can lead to decreased level of consciousness, seizures, death
  • physical exam
    • single loud S2 due to severe pulmonary stenosis (i.e. RVOTO), systolic ejection murmur at left sternal border LSB
43
Q

Describe investigations: Tetralogy of Fallot (3)

A
  • ECG: RAD, RVH
  • CXR: boot-shaped heart, decreased pulmonary vasculature, right aortic arch (in 20%)
  • Echo: diagnostic
44
Q

Describe the management of spells: Tetralogy of Fallot (3)

A

O2, knee-chest position, fluid bolus, morphine sulfate, propranolol

45
Q

Describe the treatment: Tetralogy of Fallot (3)

A
  • surgical repair at 4-6 mo of age; earlier if marked cyanosis or “tet” spells
46
Q

Name: Causes of Cyanotic Heart Disease (5)

A

5T’s

  • Truncus arteriosus
  • Transposition of the great vessels
  • Tricuspid atresia
  • Tetralogy of Fallot
  • Total anomalous pulmonary venous return
47
Q

Describe epidemiology: Transposition of the Great Arteries (TGA) (1)

A

3-5% of all congenital cardiac lesions, most common cyanotic CHD in neonates

48
Q

Describe pathophysiology: Transposition of the Great Arteries (TGA) (4)

A
  • parallel pulmonary and systemic circulations
    • systemic: body -> RA -> RV -> aorta -> body
    • pulmonary: lungs -> LA -> LV -> pulmonary artery -> lungs
    • survival is dependent on mixing through patent ductus arteriosus, atrial septal defect, or ventricular septal defect
49
Q

Describe physical exam: Transposition of the Great Arteries (TGA) (3)

A
  • neonates: ductus arteriosus closure causes rapidly progressive severe hypoxemia unresponsive to oxygen therapy, acidosis, and death
  • ventricular septal defect present: cyanosis is not prominent; CHF within first weeks of life
  • ventricular septal defect absent: no murmur
50
Q

Describe investigations: Transposition of the Great Arteries (TGA) (3)

A
  • ECG: RAD, RVH, or may be normal
  • CXR: egg-shaped heart with narrow mediastinum (“egg on a string”)
  • Echo: diagnostic
51
Q

Describe management: Transposition of the Great Arteries (TGA) (2)

A
  • symptomatic neonates: prostaglandin E1 infusion to keep ductus open until balloon atrial septostomy
  • surgical repair: arterial switch performed in the first two weeks in those without a VSD while LV muscle is still strong
52
Q

Describe epidemiology: Total Anomalous Pulmonary Venous Return (1)

A
  • 1-2% of CHD
53
Q

Describe pathophysiology: Total Anomalous Pulmonary Venous Return (4)

A
  • all pulmonary veins drain into right-sided circulation (systemic veins, RA)
  • no direct oxygenated pulmonary venous return to left atrium
  • often associated with obstruction at connection sites
  • atrial septal defect must be present for oxygenated blood to shunt into the LA and systemic circulation
54
Q

Describe management: Total Anomalous Pulmonary Venous Return (1)

A
  • surgical repair in all cases and required urgently for severe cyanosis
55
Q

Describe: Ebstein’s Anomaly (3)

A
  • Septal and posterior leaflets of tricuspid valve are malformed and displaced into the RV
  • Potential for RV dysfunction, tricuspid stenosis, tricuspid regurgitation, or functional pulmonary atresia if RV unable to open pulmonic valves
  • Accessory conduction pathways (e.g. WPW) are often present
56
Q

Describe etiology: Ebstein’s Anomaly (1)

A
  • Unknown, associated with maternal lithium and benzodiazepine use in 1st trimester
57
Q

Describe tx: Ebstein’s Anomaly (2)

A
  • Newborns: consider closure of tricuspid valve + aortopulmonary shunt, or transplantation
  • Older children: tricuspid valve repair or valve replacement + atrial septal defect (ASD) closure
58
Q

Describe: Truncus Arteriosus (pathophysiology and management) (4)

A
  • pathophysiology
    • single great vessel gives rise to the aorta, pulmonary, and coronary arteries
    • truncal valve overlies a large VSD
    • potential for coronary ischemia with fall in pulmonary vascular resistance
  • management: surgical repair within first 6 wk of life
59
Q

Describe epidemiology: Hypoplastic Left Heart Syndrome (1)

A
  • 1-3% of CHD; most common cause of death from CHD in first mo of life
60
Q

Describe pathophysiology: Hypoplastic Left Heart Syndrome (2)

A
  • LV hypoplasia may include atretic or stenotic mitral and/or aortic valve, small ascending aorta, and coarctation of the aorta with resultant systemic hypoperfusion
  • systemic circulation is dependent on ductus patency; upon closure of the ductus, infant presents with circulatory shock and metabolic acidosis
61
Q

Describe management: Hypoplastic Left Heart Syndrome (3)

A
  • intubate and correct metabolic acidosis
  • IV infusion of prostaglandin E1 to keep ductus open
  • surgical palliation (overall survival 50% to late childhood) or heart transplant
62
Q

Name: 4 Features of Hypoplastic Left Heart Syndrome

A
  • Hypoplastic LV
  • Narrow mitral/aortic valves
  • Small ascending aorta
  • Coarctation of the aorta
63
Q

Name etiologies: Congestive Heart Failure (6)

A
  • CHD
  • cardiomyopathy (primary or secondary)
  • high output circulatory states (e.g. anemia, AVMs, cor pulmonale, hyperthyroidism)
  • non-cardiac (e.g. sepsis, renal failure)
  • pressure overload (e.g. aortic stenosis/co-arctation, pulmonary stenosis, HTN)
  • volume overload (e.g. L to R shunt, valve insufficiency)
64
Q

Describe clinical features: Congestive Heart Failure (4)

A
  • infant: weak cry, irritability, feeding difficulties, early fatigability, diaphoresis while sleeping or eating, respiratory distress, lethargy, FTT
  • child: decreased exercise tolerance, fatigue, decreased appetite, respiratory distress, frequent URTIs or “asthma” episodes
  • orthopnea, paroxysmal nocturnal dyspnea, pedal/dependent edema are all uncommon in children
  • physical findings: 4 key features (tachycardia, tachypnea, cardiomegaly, hepatomegaly). Also FTT, alterations in peripheral pulses, four limb blood pressures (in some CHDs), dysmorphic features associated with congenital syndromes
65
Q

Describe investigations: Congestive Heart Failure (4)

A
  • CXR: cardiomegaly, pulmonary venous congestion
  • ECG: sinus tachycardia, signs of underlying cause (heart block, atrial enlargement, hypertrophy, ischemia/infarct)
  • echo: structural and functional assessment
  • blood work: CBC, electrolytes, BUN, Cr, LFTs
66
Q

Describe management: Congestive Heart Failure (3)

A
  • general: sitting up, O2, sodium and water restriction, increased caloric intake
  • pharmacologic: diuretics, afterload reduction (e.g. ACEI), β-blockers; digoxin rarely used
  • curative: correction of underlying cause
67
Q

Name types of: Dysrhythmias (6)

A

can be transient or permanent, congenital (structurally normal or abnormal), or acquired (toxin, infection, infarction)

  • Sinus Arrhythmia
  • Sinus Tachycardia
  • Premature Atrial Contractions
  • Premature Ventricular Contractions
  • Supraventricular Tachycardia
  • Complete Heart Block
68
Q

Describe: Sinus Arrhythmia (4)

A
  • rate of impulses arising from sinus node is elevated (>150 bpm in infants, >100 bpm in older children)
  • characterized by: beat-to-beat heart rate variability with changes in activity, P waves present/normal, PR constant, QRS narrow
  • etiology: HTN, fever, anxiety, sepsis, anemia/hypoxia, pain, PE, drugs, etc.
  • differentiate from supraventricular tachycardia by slowing the sinus rate (vagal massage, β-blockers) to identify sinus P waves
69
Q

Describe: Premature Atrial Contractions (1)

A
  • may be normal variant or can be caused by electrolyte disturbances, hyperthyroidism, cardiac surgery, digitalis toxicity
70
Q

Describe: Premature Ventricular Contractions (3)

A
  • common in adolescents
  • benign if single, uniform, disappear with exercise, and no associated structural lesions
  • if not benign, may degenerate into more severe dysrhythmias
71
Q

Describe: Supraventricular Tachycardia (3)

A
  • abnormally rapid heart rhythm originating above the ventricles – most frequent sustained dysrhythmia in children
  • no beat-to-beat HR variability, >220 bpm (infants) or >180 bpm (children), P waves absent/abnormal, PR indeterminable, QRS usually narrow
  • pre-excitation syndromes (subset of SVT): WPW syndrome, congenital defect
72
Q

Describe: Complete Heart Block (4)

A
  • congenital heart block can be caused by maternal anti-Ro or anti-La (e.g. mother with SLE)
  • often diagnosed in utero (may lead to development of fetal hydrops)
  • clinical symptoms related to level of block (the lower the block, the slower the heart rate and greater the symptoms of inadequate cardiac output)
  • symptomatic patients need a pacemaker
73
Q

Name: Pediatric ECG findings that may be normal (4)

A
  • HR >100 bpm
  • Shorter PR and QT intervals and QRS duration
  • Inferior and lateral small Q waves
  • RV larger than LV in neonates, so normal to have:
    • right axis deviation RAD
    • Large precordial R waves
    • Upright T waves
    • Inverted T waves in the anterior precordial leads from early infancy to teen years
74
Q

Describe: Heart Murmurs (3)

A
  • 50-80% of children have audible heart murmurs at some point in their childhood
  • most childhood murmurs are functional (e.g. “innocent”) without associated structural abnormalities and have normal ECG and radiologic findings
  • in general, murmurs can become audible or accentuated in high output states (e.g. fever, anemia)
75
Q

Differentiate innocent and pathological heart murmurs

  • History and Physical
  • Timing
  • Grade/Quality
  • Splitting
  • Extra sounds/Clicks
  • Change of position
A
76
Q

Name: Five Innocent Heart Murmurs

A
  • Peripheral Pulmonic Stenosis
  • Still’s Murmur
  • Venous Hum
  • Pulmonary Ejection
  • Supraclavicular Arterial Bruit
77
Q

Describe: Peripheral Pulmonic Stenosis

  • Etiology
  • Location
  • Description
  • Age
  • DDX
A
  • Etiology: Flow into pulmonary branch arteries from main, larger, artery
  • Location: Left upper sternal border
  • Description: Neonates, low-pitched, radiates to axilla and back
  • Age: Neonates, usually disappears by 3-6 mo
  • DDX:
    • patent ductus arteriosus PDA
    • Pulmonary stenosis
78
Q

Describe: Still’s Murmur

  • Etiology
  • Location
  • Description
  • Age
  • DDX
A
  • Etiology: Flow across the pulmonic valve leaflets
  • Location: Left lower sternal border
  • Description: High-pitched, vibratory, LLSB or apex, SEM
  • Age: 3-6 yr
  • DDX:
    • Subaortic stenosis
    • Small VSD
79
Q

Describe: Venous Hum

  • Etiology
  • Location
  • Description
  • Age
  • DDX
A
  • Etiology: Altered flow in veins
  • Location: Infraclavicular (R>L)
  • Description: Infraclavicular hum, continuous, R>L
  • Age: 3-6 yr
  • DDX: patent ductus arteriosus PDA
80
Q

Describe: Pulmonary Ejection

  • Etiology
  • Location
  • Description
  • Age
  • DDX
A
  • Etiology: Flow through the pulmonic valve
  • Location: Left upper sternal border
  • Description: Soft, blowing, LUSB, systolic ejection murmur
  • Age: 8-14 yr
  • DDX:
    • atrial septal defect ASD
    • Pulmonary stenosis
81
Q

Describe: Supraclavicular Arterial Bruit

  • Etiology
  • Location
  • Description
  • Age
  • DDX
A
  • Etiology: Turbulent flow in the carotid arteries
  • Location: Supraclavicular
  • Description: Low intensity, above clavicles
  • Age: Any age
  • DDX:
    • Aortic stenosis
    • Bicuspid aortic valve

TN Pédiatrie (14 decks)

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