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A Pediatrics Compendium > Pediatric First Aid: Cardiovascular Disease > Flashcards

Pediatric First Aid: Cardiovascular Disease Flashcards

1
Q

Murmur Grading

Grade I
Grade II
Grade III

Grade IV
Grade V
Grade VI

A 
I = very soft; need very careful auscultation 
II = soft and readily heard, but faint; equal to S1/S2 
III = moderate intensity; louder than S1/S2 
IV = loud murmur; palpable thrill intermittent 
V = loud murmur with palpable thrill 
VI = loud murmur with palpable thrill that can be heard when stethoscope is lifted slightly off chest
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2
Q

What is a Still’s murmur?

What age range is it commonly seen in?

A

benign murmur due to turbulent flow in the left ventricular outflow tract

  • typically seen between 3-6 yo; uncommon < 2 yo

LLSB w/musical or vibratory midsystolic accentuation

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3
Q

How much time does each small box and large box on an ECG correspond to?

A 
Small = 0.04 seconds (1 mm) 
Large = 0.2 seconds (5 mm)
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4
Q

What is the most common cause of bradycardia in children?

A

Hypoxemia

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5
Q

What is the normal QRS axis and which leads do you look at to help determine Axis on an ECG?

A

0 to +90 degrees

  • check leads I and aVF (both should be upright if normal)
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6
Q

How long is a normal P-wave on ECG of an infant vs children?

A 
Infant = \< 0.08 seconds (2 small boxes) 
Children = \< 0.10 seconds (1/2 big box)
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7
Q

What does a Premature Ventricular Contraction look like on ECG?

A

premature and wide QRS without P wave; T wave may be inverted

  • evaluate further if runs of PVS or they occur regularly
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8
Q

In what direction do the T-waves face on an ECG of a patient with Ventricular Tachycardia?

A

OPPOSITE direction of the QRS complex

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9
Q

What is the QRS axis if Leads I and aVF are:

  1. I (+) and aVF (+)
  2. I (-) and aVF (+)
  3. I (+) and aVF (-)
  4. I (-) and aVF (-)
A
  1. normal axis
  2. LEFT axis deviation
  3. RIGHT axis deviation
  4. EXTREME axis deviation (direction based on Q-wave)
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10
Q

What are 3 common pathologies that can result in Right Axis Deviation (RAD)?

A

severe pulmonary stenosis w/right ventricular hypertrophy
pulmonary hypertension
conduction disturbances (RBBB)

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11
Q

Left Axis Deviation with Right Ventricular Hypertrophy (RVH) is highly suggestive of what, especially in children with Down Syndrome?

A

AV canal

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12
Q

Mild LAD with Left Ventricular Hypertrophy (LVH) in a cyanotic infant suggests what condition?

A

Tricuspid Atresia

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13
Q

What is the normal P axis and what leads are commonly used to determine it?

What does a P axis > +90 degrees indicate?

A

Normal deflection: Lead II (+), Lead aVR (-)

> +90 = atrial inversion or misplaced leads

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14
Q

Peaked, pointed T waves occur due to what? (3)

Flattened T waves occur due to what? (2)

A

Peaked = HYPERkalemia, LVH, head injury

Flattened = HYPOkalemia, hypothyroidism

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15
Q

What leads would you look at to determine Right Atrial Enlargement and Left Atrial Enlargement?

How does the P-wave look?

A

RAH = Peaked waves in Leads II and V1

LAH = notched Lead II, deep terminal inversion V1

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16
Q

What is Wolff-Parkinson-White Syndrome?

A

ventricular preexcitation via accessory conduction pathway through Bundle of Kent

  • conducts more rapidly than AV node but takes longer to recover

**DELTA WAVE**

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17
Q

For infants and children, what echo is commonly used to evaluate the coronary arteries?

A

Transthoracic Echocardiogram

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18
Q

Transesophageal Echocardiogram

A

transducer down esophagus for enhanced imaging during cardiac surgery or catherization

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19
Q

2-D Echocardiography

A

cross-sectional images of the heart are seen in order to assess structures

Ex: inflow/outflow tracts, valves, ascending/descending aorta, pulmonary arteries/veins, ventricles, septa

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20
Q

Color-Flow Doppler Echocardiography

What do the red and blue colors indicate?

A

blood flow and direction can be seen via this method

Red = blood flowing TOWARDS from transducer 
Blue = blood flowing AWAY from transducer
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21
Q

Color-Flow Doppler Echocardiography

Difference between M-Mode Echo vs Fetal Echo?

A

M-Mode = info from one scan point is measured over time

  • motion creates depth graph of structures
  • determines chamber/valve dimensions and size

Fetal = prenatal diagnosis of congenital heart disease
- screen > 16 weeks

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22
Q

What is a normal Cardiothoracic ratio (heart size) on CXR and how is it determined?

A

Normal ratio = < 0.6

measure largest width of heart and divide by largest diameter of the chest

**needs good inspiratory effort**

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23
Q

Why are the hearts of patients with Tetralogy of Fallot commonly in the shape of a “boot?”

A

due to hypoplastic main pulmonary artery

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24
Q

Why are the hearts of patients with Transposition of the Great Arteries commonly in the shape of an “egg?”

A

due to narrow superior aspect of cardiac silhouette

  • absence of thymus and irregular relationship of great arteries
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25
Q

What is the name of the shape that can sometimes been seen on CXR of a patient with Total Anomalous Pulmonary Venous Return (TAPVR)?

A

“Snowman” shape

  • left vertical vein, left innominate (brachiocephalic) vein, and dilated SVC create the head
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26
Q

Rheumatic Fever

What is it and how long does it take to show signs?

A

delayed immunologic sequela of previous Group A streptococcal infection of pharynx
- cutaneous infection precursor to glomerulonephritis but not rheumatic fever

  • peaks in children 5-15 yo; follows pharyngitis by 1-5 weeks (average: 3 weeks)
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27
Q

Rheumatic Fever

Typically causing carditis in 50-70% of patients, what 3 valves (in order of dec. frequency) are most commonly affected?

A

Mitral Valve regurgitation
Aortic Valve regurgitation
Tricuspid Valve regurgitation

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28
Q

Rheumatic Fever

What is the most common first symptom of ARF?

Where is it most commonly found and what does it respond to?

A

First Symptom –> Migratory Arthritis

  • large joints >> spine/cranial joints

Tx: aspirin (usually lasts less than a month)

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29
Q

Rheumatic Fever

What is Chorea and when is it typically seen?

A

loss of motor coordination with spontaneous, purposeless movement and motor weakness

  • emotional lability onset before motor symptoms (similar to ADHD or OCD behavior)
  • longest latent period (vs other sxs), presenting 1-8 months post-infection and lasting for months
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30
Q

Rheumatic Fever

Erythema Marginatum looks like what and is most commonly found where on the body of a patient?

A

pink, erythematous, nonpruritic macular rash with clear center

  • evanescent and migratory; disappears when cold/reappears when warm

TRUNK and PROXIMAL EXTREMITIES

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31
Q

Rheumatic Fever

Where are the subcutaneous nodules most commonly found at? (3)

A

BONY PROMINENCES over extensor surfaces (most commonly tendons of hand)

  • also scalp and spine
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32
Q

Rheumatic Fever

What is required to make the diagnosis?

A
  1. 2 Major criteria (JONES)
    - joints (polyarthritis)
    - heart (carditis)
    - nodules (SubQ)
    - Erythema Marginatum
    - Sydenham’s Chorea
  2. 1 Major criteria and 2 minor criteria
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33
Q

Rheumatic Fever

What are 5 minor criteria that can help make the diagnosis of Rheumatic Fever?

A

arthralgia
fever
elevated ESR/CRP
prolonged PR interval
ASO titer (lab evidence of antecedent group A strep infection)

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34
Q

What diagnostic atrial myocardium finding can be found in patients with Rheumatic Fever?

A

Aschoff bodies

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35
Q

Where is Erythema Marginatum NEVER found?

A

the face

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36
Q

Rheumatic Fever

What is the approach to treatment once diagnosed? What medication is used if patient is allergic to first-line option?

A

Aspirin –> reduce fever and arthritis symptoms

Oral PCN V x10 days OR PCN G IM, single dose

**if PCN allergy –> Azithromycin x5 days**

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37
Q

Rheumatic Fever

What are the 3 options for patient prophylaxis?

A
  1. Benzathine penicillin G IM every 3-4 weeks
  2. PCN PO 3x/day
  3. Sulfadiazine PO 1x/day
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38
Q

Endocarditis

What are the two most common organisms that cause infection?

If you get a culture-negative endocarditis, what two organisms should you keep in mind?

A
  1. alpha hemolytic streptococci (70%)
    - S. pneumoniae and S. viridans
  2. Staph Aureus (20%)

culture (-)? = Coxiella burnetii or Bartonella

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39
Q

How does endocarditis develop?

A

due to turbulent blood flow across an abnormal valve or any cardiac defect

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40
Q

Embolic phenomena of Endocarditis

A

roth spots
splinter hemorrhages
Osler nodes
Janeway lesions (less common in children)

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41
Q

4 high risk predisposing conditions that can lead to endocarditis

A

Prosthetic cardiac valves
Previous bacterial endocarditis
CHD
Surgical pulmonary-systemic shunts (correct cyanotic heart disease)

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42
Q

What is Libman-Sacks valve?

A

NON-bacterial endocarditis associated with Lupus

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43
Q

How is the diagnosis of endocarditis made?

A
  • at least 3 blood cultures over 48 hrs from different sites

(+) Cx, ESR, hematuria, anemia

  • Echo showing vegetations or thrombi
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44
Q

How is endocarditis treated?

A
  • 4-8 weeks of organism-specific IV antibiotics
  • surgery for refractory cases or those with prosthetic valves, fungal endocarditis, or hemodynamic compromise
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45
Q

Endocarditis PPX meds

A
  • needed prior to dental procedures in children with structural heart dz or predisposing conditions

Amoxicillin –> Clindamycin (PCN allergy)

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46
Q

What are Janeway lesions and Osler nodes?

A

J = small, painless, erythematous lesions on palms/soles
- septic emboli causing microabscesses of the dermis

O = red, painful on hands/feet
- immune complex deposition

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47
Q

Myocarditis

What 3 viruses are common causes of disease?

A

Coxsackieviruses
Echoviruses
Adenoviruses

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48
Q

Myocarditis

Non-viral causes of disease

A
  • immune-mediated diseases
  • toxic ingestion (alcohol, amphetamines, anthracyclines, clozapine)
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49
Q

What long-term disease etiology can myocarditis lead to if left untreated?

A

DILATED cardiomyopathy and Heart Failure

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50
Q

Patient is tachycardic and tachypneic, and has a gallop on auscultation. What is the likely disease etiology?

A

Congestive Heart Failure (CHF)

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51
Q

Myocarditis

How is it treated?

A

First - treat underlying cause
- largely supportive (viral disease = rest/activity mod)

  • possibly treat CHF (diuretics, inotropic agents); gamma globulins
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52
Q

Pericarditis

What is the most common cause and what 5 bacteria are commonly implicated?

A

most common: VIRAL

Bacteria: S. aureus, H. flu, N. meningitidis, Strep, TB

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53
Q

Pericarditis

What causes it and what can it lead to long-term?

A
  • caused by inflammation of the pericardium
  • can progress to pericardial effusion/cardiac tamponade if significant fluid accumulates around heart
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54
Q

What is Pulsus Paradoxus and what disease is it classically associated with?

A

decrease in SBP > 10 mmHg on inspiration

  • commonly associated with Pericarditis

**due to reduced venous return because of increased intrathoracic or intracardiac pressure during inspiration**

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55
Q

Child has pericarditis and a salmon-colored rash with joint pain. What should you think of?

A

Juvenile Rheumatoid Arthritis

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56
Q

What is Electrical Alternans and what disease is it classically associated with?

A

QRS alternates between larger and smaller voltages as heart swings with the pericardial effusion

  • commonly associated with Cardiac Tamponade
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57
Q

Pericarditis

How does it classically present on exam? What about Cardiac Tamponade?

A

precordial pain (sudden chest pain that comes and goes) with radiation to the shoulder/neck

  • pericardial friction rub on auscultation

CT: distant heart sounds, tachycardia, pulsus paradoxus, hepatomegaly/venous distension

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58
Q

How is Pericarditis diagnosed?

A

Echocardiograph

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59
Q

What are the 3 most common causes of Congestive Heart Failure in the first 6 months of life?

A

VSD, PDA, and endocardial cushion defects

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60
Q

Pericarditis

How is it treated?

A
  • treat underlying disease process
  • pericardiocentesis indicated if effusion present
  • urgent drainage if signs/symptoms of tamponade
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61
Q

How long does a left-to-right shunt take to start putting significant stress on the left ventricle?

A

6 weeks

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62
Q

Which is better for treating pediatric CHF: salt/fluid restriction or diuretics?

A

Diuretics

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63
Q

Congestive Heart Failure

How do Digitalis and Diuretics help treat patients?

What are some common AFTERload-reducing agents that can help treat CHF?

A

Digitalis - improve ventricular function
- CI’d in complete heart block and HCM

Diuretics - dec. volume overload and pulmonary edema
- loop diuretics (Furosemide) most common

AL agents: ACEi, CCBs, nitroglycerin –> dilate peripheral vasculature and dec. work on heart

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64
Q

Central Cyanosis vs Acrocyanosis

A

CC: mucus membrane, blue-tinged lips

  • ALWAYS pathologic in newborns
  • either cardiac or pulmonary disease
  • > 5 mg/dL of deoxyhemoglobin

A: distal extremities

  • NORMAL in newborns
  • dec. distal perfusion, exposure to cold
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65
Q

What are the 5 T’s and 1 P of Cyanotic Heart Defects?

A

Truncus Arteriosus
Transposition of the Great Arteries
Tricuspid Atresia
Tetralogy of Fallot
Total Anomalous Venous Pulmonary Return (TAPVR)

Pulmonary Atresia

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66
Q

What is the most common form of cyanotic CHD in the postinfancy period?

A

Tetralogy of Fallot

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67
Q

What 4 anomalies constitute Tetralogy of Fallot?

A

Right Ventricular Outflow Obstruction (RVOTO)
- aka “Pulmonary Stenosis”
VSD
Overriding Aorta
Right Ventricular Hypertrophy (RVH)

68
Q

What dictates the degree of shunting in ToF? What’s the difference between minimal, mild, and severe obstruction?

A

severity of RVOT obstruction dictates shunting

Minimal - inc. flow with PVR dec; eventual CHF

Mild - hemodynamic balance pressure between ventricles equal = NO SHUNTING (“pink tet”)

Severe - blood cannot exit through RVOT, pulmonary blood flow dec. –> cyanosis

69
Q

What is Conotruncal Facies seen in DiGeorge Syndrome and ToF?

A

hypertelorism (wide-set eyes)
lateral displacement of inner canthi
flat nasal bridge
narrow palpebral fissures
ear anomalies

70
Q

How does squatting help children with ToF?

A

desaturated blood gets trapped in LEs and SVR increases

RVOT remains fixed but squatting decreases R –> L shunting, increase pulmonary blood flow, and inc. arterial saturation

71
Q

Why is there a single S2 sound in ToF?

A

Pulmonary Stenosis

72
Q

What is a “Tet Spell”? What age is it most commonly observed at?

A

most common: 2-6 months of age
- morning or after nap (low SVR)

Precipitating factors: stress, drugs that dec. SVR, hot baths, fever, exercise

  • inc. CO with fixed RVOTO = inc. R–>L shunting with inc. cyanosis
73
Q

How is ToF diagnosed? (4)

A
  • CXR
  • “boot-shaped” heart
  • dec. pulmonary vascular markings
  • right aortic arch (25%)
74
Q

What shunt is commonly used to treat ToF with severe pulmonary stenosis?

A

Blalock-Taussig shunt

  • increases pulmonary blood flow by grafting the Subclavian or Carotid artery to the pulmonary artery
75
Q

What four things must be repaired in order to completely resolve ToF?

A
  1. VSD closure
  2. relief of RVOTO
  3. ligation of shunts
  4. ASD/PFO closure
76
Q

Without repair of ToF, what is the mortality rate at 3, 20, and 30 years?

A

3 years = 50% mortality

20 years = 90% mortality

30 years = 95% mortality

77
Q

What is the most common cyanotic heart lesion in the newborn period?

A

Transposition of the Great Arteries

78
Q

How does Transposition of the Great Arteries develop?

What is ESSENTIAL for survival of these patients?

A

primitive heart loops to the LEFT instead of the RIGHT

aorta originates from RV and pulmonary trunk originates from LV

(Aorta is Anterior, Pulmonary trunk is Posterior)

there MUST be a mixing lesion SOMEWHERE (i.e VSD/ASD/PDA)

79
Q

How does TGA (Transposition of the Great Arteries) present?

How does it appear on CXR?

A

CHF in the first week (PDA alone is not sufficient enough to allow adequate mixing in extrauterine environment)

CXR: “egg-shaped” heart with narrow mediastinum and cardiomegaly with increased pulmonary markings

80
Q

How is TGA with IVS (intact ventricular septum) treated vs TGA with VSD?

A

IVS? - “ductal dependant” = needs PGE to keep PDA open

  • early balloon atrial septostomy (allows blood mixing)
  • Arterial Switch procedure definitive

VSD? - PA band to control inc. pulmonary blood flow

  • Arterial Switch procedure definitive

**Arterial Switch = reattach great arteries to their appropriate ventricles**

81
Q

What syndrome is Truncus Arteriosus associated with?

A

DiGeorge Syndrome

82
Q

What is the most common congenital heart lesions in children?

A

Bicuspid Aortic Valve

83
Q

What is the difference between a Type I, II, and III Truncus Arteriosis?

A

Type I - short common pulmonary trunk from right side of common trunk, just above truncal valve

Type II - pulmonary arteries arise directly from ascending aorta, from posterior surface

Type III - similar to Type II; PAs arise more laterally and distant from semilunar valves

84
Q

How does Truncus Arteriosus present clinically?

A

CHF/cyanosis in the first week

  • initially L–>R shunting
  • 2nd heart sound prominent and single due to single semilunar valve
  • strong, bounding peripheral pulses
  • often, systolic ejection click
85
Q

How is Truncus Arteriosus treated?

A

surgery BEFORE significant pulmonary vascular disease (3-4 months of age)

  • VSD surgically closed (valve on LV side)
  • pulmonary arteries freed from truncus and attached to valved conduit = new pulmonary trunk (RASTELLI procedure)
86
Q

What 4 conditions make up Hypoplastic Left Heart Syndrome (HLHS)?

A
  1. aortic valve hypoplasia, stenosis, atresia (with or without mitral valve involvement)
  2. hypoplasia of ascending aorta
  3. LV hypoplasia or agenesis
  4. mitral valve stenosis or atresia

**result? = single RV providing blood to pulmonary system, the systemic circulation (PDA), and coronary system via retrograde flow across PDA**

87
Q

How does HLHS differ in utero vs at birth?

A

In utero = all systemic flow is DUCT DEPENDENT

  • pulm resistance > systemic resistance
  • normal perfusion pressure maintained with R–>L shunt through PDA and pulmonary resistance

Birth = PDA closes and SVR > PVR

  • PDA closes = dec. CO and systemic perfusion = METABOLIC ACIDOSIS
  • PDA dependent until intervention is undertaken
88
Q

What is the second most common congenital heart defect, presenting in the first week of life (and most common cause of death from CHD in the first month)?

A

Hypoplastic Left Heart Syndrome

89
Q

How is Hypoplastic Left Heart Syndrome diagnosed? (2)

A

CXR: cardiomegaly with globular-shaped heart; inc. pulmonary vascular markings, pulmonary edema

Echo: DIAGNOSTIC; typically detected in utero

90
Q

How does Hypoplastic Left Heart Syndrome present?

A
  • pulses ranging from normal to absent (depending on ductal patency)
  • hyperdynamic RV impulse
  • single S2 of INCREASING intensity
  • nonspecific LSB murmur
  • skin with grayish pallor
91
Q

What is the 3 stage surgical treatment of Hypoplastic Left Heart Syndrome?

A
  1. Norwood - pulmonary trunk reconstructs hypoplastic aorta, and RV becomes functional LV
    - pulmonary arteries connected but separated from heart
    - subclavian arteries used to establish blood flow to pulmonary arteries
  2. Glenn - superior vena cava connected to right Pulmonary Artery, restoring partial venous return to lungs
  3. Fontan - inferior vena cava anastomosed to PAs, resulting in complete venous diversion from systemic circulation to the lungs
92
Q

What is a Subendocardial Cushion Defect and what 3 conditions does it cause?

A

abnormal development of AV canal (endocardial cushion)

  • VSD
  • ostium primum ASD
  • clefts in the mitral and tricuspid valves
93
Q

What 3 conditions are Subendocardial Cushion Defects associated with?

A
  1. Down Syndrome (30%)
  2. asplenia
  3. polysplenia syndromes
94
Q

What does the ECG of a patient with Subendocardial Cushion Defects look like? (3)

A

Superior QRS axis with RVH

RBBB and LVH

prolonged PR interval

95
Q

What is the most common congenital heart disease recognized in adults?

A

ASD

96
Q

What is the difference between Secundum, Primum, and Sinus Venous ASD defects?

A

Secundum - most common (50-70%) = CENTRAL portion of atrial septum

Primum - (30%) = atrial LOWER margin and associated with mitral/tricuspid valves

Sinus Venous - (10%) = UPPER portion of atrial septum and often extends into superior vena cava

97
Q

Why is widely split and fixed S2 a common feature of ASDs?

A

right-sided volume overload causes delayed closing of pulmonic valves

murmurs more likely to occur as patient ages

98
Q

When do symptoms of CHF and pulmonary HTN occur in adults with ASD?

A

CHF - second decade

Pulmonary HTN - third decade

99
Q

How are ASDs treated?

A
  • nearly 90% close spontaneously, and 100% will lose if < 3 mm
  • ASDs > 8 mm are unlikely to close spontaneously (use surgical or catheter closure = clamshell or umbrella device)
100
Q

What causes the closure of Foramen Ovale?

A

increasing Left Atrial pressure causes the septae to press against each other

101
Q

What is the most common congenital heart disorder?

A

VSD

102
Q

How often does VSD occur out of 1000 live births?

A

2

103
Q

How often does spontaneous closure occur in VSDs?

A

30-50% of the time

104
Q

How is VSD treated (if not closed)?

A

intervention based on development of CHF, pulmonary HTN, and growth failure

Initially: diuretics and digitalis

Medical therapy fails? = SURGERY

**don’t forget endocarditis prophylaxis**

105
Q

How long does it typically take a PDA murmur to disappear in a newborn infant?

A

12 hours

106
Q

What is the process by which the PDA closes? What pulmonary vascular pressure is required?

A
  • ductus arteriosus primarily closes in response to ductal PO2 > 50 mmHg
  • PDA closes within the first 15 hours of life with complete closure by 3 weeks of life (Ligamentum Arteriosum)
107
Q

What is the most common complication of PDA in late childhood?

A

Infective Endocarditis

  • subacute bacterial endocarditis more common in small PDAs vs large PDAs
108
Q

If Eisenmonger Syndrome develops in a patient with PDA, what kind of cyanosis would be seen?

A

cyanosis restricted to the LOWER extremities as oxygen poor blood mixes into aorta distal to subclavian arteries

109
Q

What is an occasional complication of surgical ligation of PDAs?

A

recurrent LARYNGEAL nerve injury = HOARSENESS

110
Q

What are 6 common PDA-dependent congenital heart abnormalities?

A
  1. Tetralogy of Fallot
  2. Tricuspid Atresia
  3. TAPVR with obstruction
  4. severe Aortic Coarctation
  5. Pulmonic Atresia
  6. Hypoplastic Left Heart Syndrome
111
Q

CHD presenting in the first 2-3 weeks of life is usually due to what?

A

Ductal-DEPENDANT lesions

112
Q

PGE1 administration

What dosage is used to reopen the ducts and to maintain ductal patency?

A

0.5-1.0 mg/kg/min = reopen ductus
0.01 mcg/kg/min = maintain ductal patency

113
Q

What are the most common symptoms associated with PGE1 administration?

A

Apnea - endotracheal intubation prior to transport

fever, hypotension (vasodilator), and seizures

114
Q

Name 5 congenital valvular defects

A
  1. Tricuspid Atresia
  2. Pulmonary Atresia
  3. Aortic Insufficiency
  4. Mitral Stenosis
  5. Mitral Valve Prolapse
115
Q

Tricuspid Atresia

Signs/Symptoms, Diagnosis, and Treatment

A

S/S = LV impulse displaced laterally

Dx: ECG = LVH, prominent LV forces (dec. RV voltages)

Tx: PGE1 (ductal patency), surgical intervention (modified Blalock-Taussig), Glenn then Fontan

116
Q

Pulmonary Atresia (with intact ventricular septum; IVS)

How does it present?

A

cyanosis within hours of birth (PDA closing)

hypotension, tachycardia, acidosis

single S2 with holosystolic murmur (tricuspid regurgitation)

117
Q

Pulmonary Atresia (with intact ventricular septum; IVS)

How is it diagnosed and treated?

A

Dx: ECG = dec. RV forces and occasional RVH, CXR = normal-enlarged RV with dec. pulmonary vascular markings

Tx: PGE1 (ductal patency), BAS (sometimes; balloon atrial septostomy), reconstruction of RVOT (transannular patch or pulmonary valvotomy), ASD left open

118
Q

How many congenitally stenoic aortic valves are bicuspid?

A

85%

119
Q

What kind of pain do older children with Aortic Stenosis complain of?

A

chest or stomach (epigastric) pain

120
Q

What kind of sounds can be auscultated on a patient with Aortic Stenosis?

A
  1. crescendo-decrescendo systolic murmur
  2. systolic ejection click

**severe Dz = paradoxical S2 splitting that narrows with inspiration**

121
Q

What treatment is available for Aortic Stenosis? When is Valvotomy typically indicated?

A

Tx: surgical/interventional balloon, valvotomy, valve replacement

  • valvotomy is most common intervention; indicated if catheterization gradient is > 50 mmHg
  • valve replacement typically deferred until patient completes growth
122
Q

How is Aortic Insufficiency diagnosed?

A

CXR showing LV enlargement and dilation of ascending aorta

123
Q

How is Aortic Insufficiency treated?

A

surgery or balloon valvuloplasty to treat stenosis may WORSEN the insufficency

  • only definitive therapy is aortic valve replacement
124
Q

Signs and Symptoms of Aortic Insufficiency

A
  • diastolic, decrescendo murmur at LUSB
  • chest pain and CHF are ominous signs (presentation with symptoms indicates advanced disease)
125
Q

Listening at the apex of the heart, what is the difference in etiology between an opening snap and a mid-systolic “click”?

A

Snap = mitral STENOSIS

Click = mitral PROLAPSE

126
Q

What syndrome is Coarctation of the Aorta associated with?

A

Turner Syndrome

127
Q

While rare in children, what is mitral stenosis typically a sequale of, especially if vaccination status is unknown?

A

Acute Rheumatic Fever

128
Q

What is the most common symptom of Mitral Stenosis and what can be seen on CXR?

A

Sx: Dyspnea

CXR: interstital edema (pulmonary venous congestion)

**hemoptysis can also be seen due to small bronchial vessel rupture**

129
Q

How is Mitral Stenosis treated? (2)

A
  1. balloon valvuloplasty
  2. surgery (commissurotomy/valve replacement)
130
Q

What heart disease do nearly all patients with Marfan syndrome have?

A

Mitral Valve Prolapse

131
Q

What is Mitral Valve Prolapse caused by and how is it commonly treated?

A

caused by thick and redundant valve leaflets that bulge into the mitral annulus

Tx: symptomatic (BB for chest pain)

132
Q

How long does Failure to Thrive, Respiratory Distress, and CHF take to develop in a child with Coarctation of the Aorta?

What develops as the lower extremity receives insufficient blood supply?

A

2-3 months

acidosis may develop as lower extremity receives significantly less blood supply than upper extremity

133
Q

In a symptomatic child with CoA, where is the murmur most commonly heard?

A

Left back

134
Q

What CXR finding can help diagnose Coarctation of the Aorta?

A

“3 Sign” and dilated ascending aorta that displaces the SVC to the right

“3 Sign” –> made at section that is narrowed

135
Q

How is Coarctation of the Aorta treated?

A

Initial Tx: resection of coarctation with end-to-end anastomosis

Allograft augmentation can also be considered

Catheter balloon dilation can be used BUT has higher rate or restenosis and inc. risk of aortic aneurysms

136
Q

What is Ebstein’s Anomaly? (3 parts)

A
  1. tricuspid valve displaced APICALLY in RV
  2. valve leaflets redundant and plastered against ventricular wall = functional tricuspid atresia
  3. RA frequently LARGEST structure
137
Q

Without intervention, what is the outlook for patient’s with Ebstein’s Anomaly?

A

CHF in first 6 months with nearly 50% mortality rate

138
Q

How does Ebstein’s Anomaly present?

A

normal growth/development are possible, but older pts complain of dyspnea, cyanosis, and palpitations

widely split S1, fixed split S2, variable S3/S4

holosystolic LSB murmur

opening snap and cyanosis (R–>L shunt)

139
Q

What is seen on CXR and ECG for a patient with Ebstein’s Anomaly?

What imaging is diagnostic for this disease?

A

CXR = cardiomegaly (“balloon-shaped”) w/”wall-to-wall” heart in severely affected children

ECG = right-axis deviation, RA enlargement, RBBB (WPW in 20% due to accessory pathways developing due to increased surface area)

ECHO is DIAGNOSTIC

140
Q

How is Ebstein’s Anomaly treated?

A

Glenn procedure = inc. pulmonary blood flow (passive venous flow to pulmonary artery)

possible aortopulmonary shunt (severely affected)

tricuspid valve replacement/reconstruction

right atrial reduction surgery

ablation of accessory pathways

141
Q

What is Totaly Anomalous Pulmonary Venous Return (TAPVR)?

A

pulmonary veins bring blood from lungs to the right atrium instead of the left atrium

NO CONNECTION exists between the pulmonary veins and left atrium and all PV’s drain to a common vein

142
Q

Where does the Common Vein in TAPVR most common drain to in order of most common to least? (4)

A
  1. Right SVC (50%)
  2. Coronary sinus or Right atrium (20%)
  3. Portal vein or IVC (20%)
  4. combination of above types (10%)
143
Q

What is the most important thing to insure survival in a patient with TAPVR?

A

ASD

144
Q

What is the difference between TAPVR with Obstruction vs TAPVR without Obstruction?

A

Obstruction = inc. pulmonary artery pressure (pulmonary edema) due to PVR in response to excessive volume being pumped into lungs from RV

No Obstruction = free communication between right atrium and left atrium (large R–>L shunt)

145
Q

How does TAPVR with Obstruction present and how is it treated?

A

inc. pulmonary pressure = inc. RV and eventually RA pressures (R–> shunt and cyanosis)

early/severe respiratory distress and cyanosis, no murmur, hepatomegaly

CXR = normal-size heart/pulmonary edema (ECHO diagnostic)

Tx: BAS or immediate corrective surgery

146
Q

How does TAPVR without Obstruction present and how is it treated?

A

presents later in life, with mild FTT, recurrent pulmonary infections, tachypnea, right heart failure, and rarely cyanosis

CXR = cardiomegaly, large PAs, inc. pulmonary vascular markings (“snowman” or “figure 8” sign) infants > 4 months old

Tx: surgical movement of pulmonary veins to left atrium

147
Q

What is Hypertrophic Obstructive Cardiomyopathy and how is inherited?

A

asymmetrical septal hypertrophy or idiopathic hypertrophic subaortic stenosis (IHSS) is most common

Inheritance = AutoDom (60%) or sporadic (40%)

148
Q

What is the incidence of Sudden Death in pts with HOCM?

A

4-6%

149
Q

What affects the murmur in patients with HOCM and what is seen on ECG/ECHO?

A

Murmur = systolic ejection murmur best heard with maneuvers that DECREASE PRELOAD (valsalva/squatting) –> dec. preload decreases ventricular volume = hypertrophic septum comes closer to aortic outflow tract = inc. turbulence

**murmur DECREASES with INCREASED preload –> larger ventricular volume expands outflow tract causing less turbulent flow**

ECG: LVH, LA enlargement, large Q wave (septal hypertrophy)

Echo: asymmetrical septal hypertrophy, outflow obstruction

150
Q

What does a large Q wave indicate on ECG?

A

septal hypertrophy

151
Q

How is Hypertrophic Obstructive Cardiomyopathy treated? (3)

A
  1. moderate physical activity restriction
  2. BB or CCB to improve filling
  3. endocarditis prophylaxis
152
Q

Henoch-Schonlein Purpura is caused by what?

What 3 areas does it commonly affect?

When does it most often occur?

A

immune-mediated vasculitis affecting GI tract, joints, and kidneys with characteristic rash

occurs most often in WINTER months, following Group A strep URI

153
Q

How does Henoch-Scholein Purpura affect the GI tract and kidneys?

How is it treated?

A

GI = vomiting, upper/lower GI bleeding, gut wall hematoma cause intussussception

Renal = glomerulonephritis with RBC casts –> acute renal failure (1-2%); more commonly chronic proteinuria

Tx: supportive with full recovery in 4-6 weeks

154
Q

What is Kawasaki Disease and who does it most commonly affect?

A

acute vasculitis of MEDIUM-sized arteries of unknown etiology

mostly affects infants and children (>80% under 4 yo), Asians, males

**most common in Winter and Spring**

155
Q

What is Kawasaki Disease also known as?

A

Mucocutaneous Lymph Node Syndrome

156
Q

What is the most common acquired heart disease in children?

A

Kawasaki Disease

157
Q

Diagnostic Critera for Kawasaki Disease

Fever for > 5 days + 4 of the following 5 things

A
  1. bilateral conjunctivitis (no exudate)
  2. mucocutaneous lesions (“strawberry tongue”, dry/cracked red lips, diffuse erythema of oral cavity)
  3. erythema/edema of hands/feets
  4. polymorphic rash (truncal)
  5. cervical lymphadenopathy (>1.5 cm diameter); usually unilateral
158
Q

What is the dosage for IVIG and ASA in children with Kawasaki Disease?

A

IVIG = usually 1 dose, 2g/kg over 10-12 hrs (dec. coronary artery dilation by >90%)

ASA = high-dose (80-100 mg/kg/day QID) until 48-72 hrs after defervescence

159
Q

Difference in ASA use if coronary artery abnormalities present vs not being present?

A

(+) coronary artery abnormalities = continue indefinitly in consultation with pediatric cardiologist (reduced after afebril for 48 hrs)

(-) coronary artery abnormalities = low-dose ASA (3-5 mg/kg/day daily) for 6-8 weeks, or until platelet/ESR normal

160
Q

What is Polyarteritis Nodosa?

A

necrotizing inflammation of SMALL/MEDIUM muscular arteries

involves renal/visceral vessels and spares pulmonary circuation

161
Q

How does Polyarteritis Nodosa present and how is it diagnosed?

A

Sxs: prolonged fever, WL, malaise, subQ nodules on extremities; Livedo reticularis; waxes and wanes; distal gangrene (severe)

Dx: no Dx tests; p-ANCA (+), thrombocytosis/leukocytosis/proteinuria/hematuria; medium-sized vessel aneurysms; Echo of coronary artery aneurysms is DIAGNOSTIC with other clinical evidence

162
Q

How is Polyarteritis Nodosa treated? (2)

A
  1. corticosteroids suppress clinical manifestations
  2. Cyclophosphamide/Azathioprine induces remission
163
Q

What is Takayasu’s Arteritis?

A

“aortoarteritis” –> large vessel vasculitis of unknown cause involving aorta, aorta’s branches, and pulmonary vasculature

lesions are segmental and obliterative; aneurysmal and saccular dilations occur

**thoracoabdominal aorta predominant site in children**

164
Q

Who does Takayasu’s Arteritis most commonly affect?

A

females age 4-45 yo

165
Q

What physical exam finding might help you determine a patient has Takayasu’s Arteritis?

How is this diease treated?

A

check peripheral pulses = “pulseless disease” due to absent, decreased, or unequal peripheral arterial pulses

Tx: corticosteroids to induce remission

166
Q
A

A Pediatrics Compendium (47 decks)

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