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Peds Cardiology > 8. Outpatient Cardiology > Flashcards

8. Outpatient Cardiology Flashcards

1
Q

Supplemental labs for Kawasaki?

A
  1. Albumin <3
  2. Anemia for age
  3. Elevated ALT
  4. Plts >450,000 after 7 days
  5. WBC > 15,000
  6. Urine >10WBC/hpf
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2
Q

What age do you start pharmacotherapy for hypercholesterolemia?

A

8

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3
Q

What is management focus for hypercholesterolemia in children <8?

A

Weight management

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4
Q

Gene for Marfan?

A

Fibrillin 1 (FBN-1)

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5
Q

Besides Marfan, name 3 things associated with FBN-1

A
  1. Shprintzen-Goldberg
  2. Weill-Marchesani
  3. Ectopia lentis
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6
Q

TGFBR1

A

Loeys-Dietz

Familial thoracic aortic aneurysm

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7
Q

COL3A1

A

Ehlers-Danlos

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8
Q

ADAMTS10

A

Weill-Marchesani

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9
Q

ACTA2

A

Familial thoracic aortic aneurysm syndrome

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10
Q

Name meds used for patients with Marfans

A
  1. B-blockers (Marfan + Aortic root dilation)
  2. Losartan
  3. Can use ACEi, other ARBs, CCB in patients with B-blocker intolerance
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11
Q

How many BP to confirm diagnosis of HTN?

A

3

-Good to get ambulatory BP monitoring

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12
Q

What is pre-hypertension?

A

Average systolic or diastolic BP that is >90%, but <95%

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13
Q

What intervention for pre-hypertension?

A

Lifestyle modifications

Repeat BP in 6 months

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14
Q

SEM at RUSB
Blowing decrescendo diastolic murmur
Systolic ejection click apex

A

AR

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15
Q

Patient with AS/AI + a systolic ejection click

A

Bicuspid aortic valve

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16
Q

Why do you see a widened pulse pressure in AI (mod-severe)?

A
  • Increased systolic BP because increased SV that causes distension of peripheral arteries
  • Reduced diastolic BP because regurg into LV leads to rapid fall in pressure
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17
Q

High-pitched, blowing, holosystolic murmur at apex of chest

A

MR

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18
Q

How is rheumatic fever diagnsoed?

A

Jones criteria

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19
Q

Jones criteria?

A

Evidence of group A strep infection &
2 Major
or
1 Major + 2 Minor

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20
Q

Major Jones critera?

A
  1. Migratory arthritis
  2. Carditis/Valvulitis
  3. CNS involvement/Syndenham chorea
  4. Erythema marginatum
  5. Subcutaneous nodules
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21
Q

Minor Jones criteria?

A
  1. Arthralgia
  2. Fever
  3. Elevated ESR/CRP
  4. Prolonged PR interval
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22
Q

What abx for 5 year old with rheumatic fever and PCN allergy?

A

Cephalexin x 10 days

-Also azithromycin x5 days or clindamycin x10 days

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23
Q

What feature of syncope is most concerning?

A

Syncope with exertion

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24
Q

High risk criteria that prompt hospitalization or intensive evaluation following syncope?

A
  • Severe structural or coronary artery disease (HF, low LVEF, previous MI)
  • Clinical/ECG features that suggest arrhythmic syncope: Syncope during exertion or supine, palpitations at time of syncope, family history of SCD, non-sustained VT, bifasicular block (LBBB or RBBB combined with left anterior or left posterior fascicular block) or other intraventricular conduction abnormalities with QRS duration >120ms), inadequate sinus bradycardia (<50bpm) or SA block in absence of negative chronotopric medications or physical training, pre-excited QRS complex, prolonged or short QT interval, RBBB pattern with ST elevation in leads V1-V3 (Brugada), negative T-waves in right precordial leads, epsilon waves and ventricular later potential suggestive of ARVC
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25
Q

Name 2 non-cardiac things to evaluate with syncope

A
  1. Anemia

2. Electrolyte distrubance

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26
Q

Gold standard for diagnosis of myocarditis?

A

Endomyocardial biopsy

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27
Q

What % of cases does endomyocardial biopsy yield diagnostic information?

A

10-20%

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28
Q

True or False; Biopsy is a class IIb recommendation in the current ACA/AHA guidelines for treatment of heart failure

A

True

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29
Q

What accounts for the findings of cardiomegaly, LVH and flow murmur in a patient with sickle cell anemia?

A

Chronic anemia (which leads to increased CO causing murmur and enlarged heart)

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30
Q

What ECG findings can you see in patients with sickle cell disease?

A

Prolonged PR interval, non-specific ST changes

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31
Q

What causes cardiac abnormalities in patients with thalassemia major?

A

Iron overload

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32
Q

BP cuff should have a bladder that is at least what % of the arm circumference?

A

80%

Less than this can cause falsely elevated measurements

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33
Q

How should a patient be positioned when taking a BP?

A

Seated with black flat to a firm surface and arm at heart level (if below, can lead to venous congestion and falsely elevated readings)

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34
Q

What are the 5 Korotkoff sounds?

A

1: SBP- First appearance of faint clear tapping sounds that gradually increase and are heard for at least 2 consecutive beats
2: Softening of sounds, can be swishing in nature
3: Sounds become more sharp and crisp again compared to phase 2, but less intense than phase 1
4: Distinct abrupt muffling of sounds, becomes soft and blowing
5: Point at which all sounds disappear- Use this for DBP

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35
Q

Cause of a systolic ejection murmur in isolated ASD?

A

Increased stroke volume across a normal pulmonary valve

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36
Q

Cause of diastolic flow murmur in isolated ASD?

A

Increased volume in RA across tricuspid valve (if Qp:Qs >2:1)

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37
Q

Older patient with isolated ASD, S2 splits with expiration and is prominent…cause?

A

Decreased L-R shunting due to increased PA pressures

Prominent S2 + Paradoxical splitting = High PA pressures

  • Inspiration: RV outflow increases and splitting resolves
  • Expiration: RV outflow decreases and increased PA pressures resulting in faster/louder closure of the pulmonary valve

-If decrease in L-R shunt was from the ASD becoming smaller… you would expect the splitting to be physiologic and the P2 to be of normal intensity

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38
Q

Signs of pulmonary overcirculation in an infant?

A
  1. Poor feeding
  2. Tachypnea
  3. Poor weight gain
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39
Q

1st med to start with pulmonary overcirculation?

A

Lasix 1mg/kg/dose BID

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40
Q

2/6 early systolic murmur best heard between apex and LLSB, low pitched, musical quality, best heard with bell of stethoscope and decreases with Valsalva

A

Stills

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41
Q

Common innocent murmur of childhood

A

Stills

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42
Q

What % of school-age children can you periodically hear a Still’s murmur in?

A

75-85%

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43
Q

Cause of Stills murmur?

A

Unknown…Theories: Physiologic narrowing of LVOT, systolic/diastolic hypermobility of MV chordae, small aortic diameter, presence of LV false tendon, increased aortic flow volume and velocity

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44
Q

What happens to murmur in HCM with Valsalva or standing?

A

Becomes louder (decreased venous return)

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45
Q

What happens to Still’s murmur with Valsalva or standing?

A

Becomes softer (decreased venous return)

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46
Q

Term infant with 2/6 mid-systolic murmur best heard in axilla and back

A

PPS

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47
Q

Which infants ae more likely to have PPS murmur?

A

Premature

Low birthweight

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48
Q

A PPS murmur should disappear in 2/3 of infants by what age?

A

6 weeks

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49
Q

Where is a PPS murmur classically heard?

A

Axilla and back

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50
Q

If you hear a PPS murmur after what age should you evaluate for branch PS?

A

Past 6-9 months

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51
Q

Where do you hear a PS murmur?

A

LUSB

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52
Q

Two defects with continuous murmur?

A
  1. PDA

2. AV fistula

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53
Q

Who needs endocarditis prophylaxis?

A

-Prosthetic valves: Bioprosthetic/homograft
-Prosthetic material used for cardiac valve repair
-Prior IE
-Unrepaired cyanotic CHD: Includes palliative shunts and conduits
-First 6 months after repair of CHD with prosthetic material or device (surgery or catheter based)
Repaired CHD with residual defects at the site or adjacent to the site of the prosthetic device
-Valvulopathy (substantial leaflet pathology and regurg) in a transplanted heart

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54
Q

What types of procedures require SBE prophylaxis?

A
  • Dental (manipulation of gingival tissue or periapical region of teeth, or perforation of oral mucosa)
  • Skin procedures
  • Musculoskeletal procedures
  • Only respiratory if there is incision/biopsy of respiratory tract mucosa
  • Only GI/GU if there is active infection
  • No for C-section or vaginal delivery unless there is infection (chorioamionitis)
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55
Q

What bacteria are responsible for the most IE?

A

Gram + Cocci (viridans group strep)

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56
Q

What is 1st line therapy for SBE prophylaxis?

A

Amoxicillin

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57
Q

What are SBE prophylaxis alternatives for someone allergic to PCN?

A
  1. Cephalexin
  2. Clindamycin
  3. Azithromycin
  4. Clarithromycin
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58
Q

What is the greatest RF for development of cardiotoxicity in children who have undergone chemotherapy?

A

Total accumulated anthracycline dose

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59
Q

What are the 3 phases of anthracycline-related cardiotoxicity?

A
  1. Acute
  2. Early onset chronic progressive cardiomyopathy
  3. Late onset toxicity
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60
Q

Describe acute phase toxicity for anthracycline related cardiotoxicity

A
  • Within 1 week of infusion (higher doses can cause cardiac dysfunction immediately)
  • Often transient
  • Wide range of findings (minor ECG abnormalities, sinus tachycardia to severe ventricular dysfunction and fulminant heart failure)
  • Occurs in 1% of peds patients
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61
Q

When does early onset chronic progressive cardiomyopathy occur in anthracycline related cardiotoxicity?

A

Within 1 year

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62
Q

What % of patients develop early onset chronic progressive cardiomyopathy in anthracycline related cardiotoxicity?

A

2% of patients

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63
Q

Describe findings in early onset chronic progressive cardiomyopathy in anthracycline related cardiotoxicity?

A

Non-transient depression in myocardial function that’s due to damage or death of myocytes

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64
Q

When does late onset toxicity occur in anthracycline related cardiotoxicity?

A

At least 1 year after treatment

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65
Q

Within 6 years of treatment, 65% of kids who got what dose of anthracycline have some abnormality of cardiac structure or function?

A

228-550

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66
Q

What is the risk of clinical HF 15-20 years following chemotherapy with anthracyclines?

A

4-5%

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67
Q

True or False: Children with PAH are more likely to initially present with syncope or near-syncopal episodes than with right heart failure

A

True

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68
Q

Most likely presenting symptoms of PAH in children?

A

Dyspnea
Fatigue
Syncope
Near-syncope

*Kids are unlikely to present with right heart failure as an initial finding

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69
Q

Who has lower mortality: People who develop PAH from unrepaired CHD or people with idiopathic/hereditary PAH?

A

PAH from unrepaired CHD

*Takes fore time for secondary PAH to develop

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70
Q

Patients with what other condition are at risk for coronary complications due to hyperlipidemia?

A

DM

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71
Q

What is goal LDL in children?

72
Q

When should you begin a statin in children?

A

> 10 years if LDL is >160 after lifestyle changes

73
Q

Adolescent with unrepaired VSD. Exam with parasternal lift over xiphoid area, 3/6 harsh holosystolic murmur coincident with S1 heart at RLSB, single, loud, palpable S2, no diastolic murmur, SpO2 85%. What is exam consistent with?

A
  • Pulmonary vascular disease
  • Murmur is from TR

*If murmur was pulmonary flow, expect it along LUSB and ejection murmur

74
Q

Gene + for type 1 LQTS with QTc 490msec, asymptomatic. What are recommended activity restrictions?

A

IA activities

75
Q

Gene + for type 1 LQTS with normal QTc, asymptomatic. What are recommended activity restrictions?

A

No data to restrict from competitive activities

  • Risk of SCD isn’t 0
  • Should probably avoid swimming due to association of LQTS and swimming
76
Q

Patients with an ICD are restricted to what activities?

77
Q

What is considered Long QT in males and females?

A

Males: > 470msec
Females: >480msec

78
Q

Double-chamber RV is associated with a VSD in what % of patients?

79
Q

When does double chamber RV typically present?

A

Older children and adults (acquired lesion)

80
Q

What causes double chamber RV to develop?

A
  • Narrowing of RVOT develops in patients with membranous VSDs due to hypertrophy of muscle in RV infundibulum
  • When anomalous bands of muscle divide the RV cavity into 2 chambers
81
Q

Initial evaluation for suspected neurocardiogenic syncope in a teenager?

A
  • H&P

- Then ECG

82
Q

Most common cause of chest pain in children?

83
Q

List types of chest wall pain in children

A
  • Costochondritis
  • Tietze syndrome
  • Idiopathic chest wall pain,
  • Precordial catch syndrome
  • Slipping rib syndrome
  • Hypersensitive xiphoid syndrome
  • Trauma/muscle strain
  • Sickle cell disease
84
Q

List less common causes of chest pain in children

A
  1. Asthma
  2. Infection
  3. Pericarditis
  4. GI
  5. Pneumothorax
85
Q

List the least common causes of chest pain in children

A
  1. HCM
  2. Aortic stenosis
  3. Pericarditis
  4. Arrhythmias
  5. Coronary insufficiency
  6. Dissecting aortic aneurysm
  7. MVP
86
Q

What are the most common causes of coronary insufficiency in children?

A
  1. Kawasaki disease
  2. Williams syndrome
  3. Anomalous origin of the coronary arteries
  4. Coronary AV/coronary cameral fistulae
87
Q

What is the definition of pulsus paradoxus?

A

Exaggeration of the normal BP variation during the inspiratory phase of respiration (systolic pressure declines as one inhales and increases as one exhales)

88
Q

Pulsus paradoxus is a hallmark of what?

A

Cardiac tamponade

89
Q

Besides cardiac tamponade, pulsus paradoxus can be seen in what other conditions?

A
  1. Pericarditis
  2. Chronic sleep apnea
  3. Croup
  4. Obstructive lung disease (asthma/COPD)
90
Q

What are the cardio-pulmonary interactions during normal inspiration?

A
  • Inspiration results in negative intrathoracic pressures
  • Causes an increase in systemic venous return to the right heart and increases the capacity of the pulmonary vascular bed to a greater degree
  • This leads to a decrease in left sided output even though there is increased systemic venous return to the right
91
Q

Why does the SBP have an exaggerated decline during inspiration in tamponade physiology?

A
  • RV filling causes restriction to LV filling
  • During inspiration, the decreased LV filling coupled with increased capacity of the pulmonary vascular bed results in a greater reduction in systemic output and a greater decline in systolic pressure (>10mmHg)
92
Q

How do you measure pulsus paradoxus?

A
  • Listen for difference between first Korotkoff sound (intermittent and heard only in exhalation) and second Korotkoff sound (constant sound not dependent on respiratory cycle) with slow deflation of BP cuff
  • Can also use an arterial line
93
Q

What causes a high pitched early diastolic decrescendo murmur best heart with diaphragm of stethoscope at left midsternal border with radiation to apex which accentuates with leaning forward and exhaling?

94
Q

What causes a low-pitched early diastolic murmur heard at the left mid-sternal border or left upper sternal border radiating down the left sternal border?

95
Q

What can cause a PI murmur to be high pitched?

A

If pulmonary HTN is present

96
Q

Significant PI can lead to what type of murmur?

A

To-Fro

*Increased flow across PV

97
Q

What causes a low-pitched mid to late diastolic murmur best heard with the bell of the stethoscope?

A

TS/MS

  • Mid diastolic from early diastolic filling across a narrow/thickened AV valve
  • Late diastolic with atrial contraction
98
Q

What causes a high-pitched holosystolic murmur at the apex with radiation to the back, left axilla or clavicle?

99
Q

Most common cause of SCD in athletes?

100
Q

List causes of SCD in the young

A
  1. HCM
  2. Prolonged QT
  3. Arrhythmogenic RV dysplasia
  4. Anomalous origin of the RCA from left sinus of Valsalva
  5. Anomalous origin of the LCA from right sinus of Valsalva
101
Q

In ALCAPA what associated defect can protect from LV dysfunction?

A

Large PDA with L-R shunt

102
Q

Pathophysiology of ALCAPA?

A
  • After birth, PA pressures fall below systemic pressures and PA contains desaturated blood, LV perfusion compromised
  • Collateral flow is initially low
  • LV demand for O2 isn’t met so the LV myocardial vessels dilate to reduce resistance and increase flow
  • When coronary vascular reserve is exhausted you develop Myocardial ischemia
  • In response, collateral vessels form and enlarge between normal right and the abnormal left coronary arteries
103
Q

Describe coronary steal in ALCAPA

A
  • LCA to the low pressure PA, -Blood tends to flow to the PA rather than high-resistance myocardial vessels
  • Results in a L-R shunt (not significant in terms of CO, but can be critical in terms of coronary flow
104
Q

What types of lesions can help with coronary steal in ALCAPA?

A
  • Any that increases the pressure in PA

- Pulm HTN (VSD or PDA), there may be adequate PA pressure to drive LV perfusion and prevent LV ischemia

105
Q

List metabolic disorders which can cause restrictive cardiomyopathy

A
  • Hurler syndrome
  • Gaucher disease
  • Fabry disease
  • Glycogen storage diseases that can be lysosomal disorders or cytoplasmic enzyme deficiencies

*Amyloidosis causes RCM, but almost never seen in children

106
Q

What type of cardiomyopathy does thiamin deficiency, muscular dystrophy and collagen vascular disease cause?

107
Q

What is the most important factor in determining prognosis and natural history in rheumatic carditis and RHD?

A

Severity of the initial carditis and rheumatic fever recurrence

108
Q

Which valve pathology in rheumatic carditis has the most favorable prognosis?

A

Acute MR (v. acute AR)

  • In part because AR usually occurs in combination with MR
  • Isolated AR occurs in 5% of patients with acute rheumatic carditis
  • AR + MR occurs in 15-20%
109
Q

In which gender does acute rheumatic carditis resolve more frequently?

110
Q

More severe cardiac involvement in rheumatic heart disease is seen in patients who present before what age?

111
Q

What is the most common clinical finding in a 7 year old patient with an anomalous RCA from left sinus?

A

No symptoms

*If symptoms, can have syncope, CP, palpitations, death

112
Q

True or False: Anomalous RCA from left sinus has risk of sudden death

A

True, but incidence unknown

113
Q

Kids with a large, unrepaired ASD can participate in what type of sports?

A

1A

*After ASD repair or 6 months after device closure they can play unrestricted

114
Q

What are ECG changes associated with an athletic heart?

A
  • Sinus bradycardia
  • 1st degree AV block
  • Incomplete RBBB
  • Early repolarization
  • Isolated QRS voltage criteria for LVH
115
Q

What % of patients with SLE have a cardiovascular complication at some point in their life?

116
Q

What is the most frequent clinically apparent cardiac complication in SLE?

A

Pericarditis (25%)

117
Q

Pericardial effusion can be seen in what % of patients with SLE?

118
Q

What is the % of clinically evident myocarditis seen in SLE?

A

<25%

*But necropsy studies show myocarditis in up to 40% of SLE cases

119
Q

What can result from lupud myocarditis?

A
  • Heart failure
  • Arrhythmia
  • May contribute to development of cardiomyopathy
120
Q

Libman-sacks endocarditis is found in what % of SLE patients?

121
Q

What valve is most commonly affected by Libman-Sacks endocarditis?

A

Mitral

-Can also occur on tricuspid or aortic valve

122
Q

What causes angina in SLE?

A
  • Extramural and intramural coronary arteritis
  • Accelerated atherosclerosis
  • Embolism
  • Thrombosis
  • Spasm
  • Any combination
123
Q

ASDs found in infants between what size have a 80-90% chance of closing on their own?

A

3-5mm

*Chance of closing decreases with age

124
Q

CoA patients have an increased incidence of what neurological problem?

A

Intracranial aneurysm

  • 10% incidence which is 5x higher than general population
  • Typically happens in adulthood
  • Screening with head imaging is controversial
125
Q

True or False: Intracranial aneurysms can still occur after CoA repair?

126
Q

True or False: Intracranial aneurysms seen with CoA aren’t always associated with HTN?

A

True

*Uncontrolled HTN may be a RF though

127
Q

Describe neurodevelopmental outcomes in CHD

A
  • Lower IQ scores
  • Inferior achievement testing
  • Worse gross/fine motor function
  • Weakness with visual-spatial skills
128
Q

True or False: Children with cyanotic lesions have similar neurodevelopmental outcomes compared to children with acyanotic lesions?

A

False- Children with cyanotic lesions more affected

-Degree of cyanosis associated with greater decline in cognitive function

129
Q

What sub-population in CHD is at highest risk of adverse developmental outcomes?

A

Single ventricles

*Children with simple repaired lesions like ASD often have normal developmental outcomes

130
Q

What dosing of ASA is used during acute phase Kawasaki?

A
  • High dose: 30-100mg/kg/day divided QID

- Anti-inflammatory effect

131
Q

When can you switch to low dose ASA in Kawasaki?

A

Once fever absent for 48 hours

132
Q

What is low-dose ASA dosing and what effect is it used for?

A

3-5mg/kg/day

Anti-platelet

133
Q

If Kawasaki echo without coronary abnormalities, when is low-dose ASA continued through?

A

Until lab markers of acute inflammation (Plts/CRP) return to normal

134
Q

What to consider with LAD on ECG?

A
  1. WPW: LAD + Preexcitation
  2. Primum ASD
  3. Tricuspid atresia
  4. AV canal
135
Q

What ECG findings are most likely to be seen in HCM?

A

LVH (versus LAD)

136
Q

What medication would be used for AVNRT that is a Na Channel blocker?

A

Flecainide

137
Q

What happens to flecainide levels once a baby stops breastfeeding or stops getting formula?

A

Levels increase… need to worry about toxicity

138
Q

Name 2 findings of flecainide toxicity

A
  1. PR prolongation

2. Possible signs of heart failure

139
Q

What is a rare embryonic arteriovenous shunt (1:25,000 live births)?

A

Vein of Galen malformation

140
Q

What gender is a Vein of Galen malformation more common in?

141
Q

What is seen on intracardiac anatomy in a Vein of Galen malformation?

A

Normal
Sinus venosus ASD
CoA

142
Q

Describe the fetal presentation of Vein of Galen malformation

A

Mild heart failure to fetal hydrops

*Commonly diagnosed after birth with rapid deterioration and heart failure (large shunt)

143
Q

What is the primary clinical concern in a Vein of Galen malformation?

A

High-output heart failure

*Hemorrhage is uncommon

144
Q

How might smaller shunts due to Vein of Galen malformation present?

A
  • Not in newborn period
  • Macrocephaly
  • Prominent facial veins
145
Q

What is the initial assessment modality for a Vein of Galen malformation?

A
  • CUS

- Then MRI or CT

146
Q

What is the treatment for a Vein of Galen malformation?

A

Transcatheter chemical embolization

*Morbidity and mortality remain high

147
Q

What age range should all children first get a non-fasting lipid profile?

148
Q

What are indications to do cholesterol screening in a 2-8 year old?

A
  • Parent, grandparent, aunt/uncle or sibling had MI, angina, stroke, CABG/stent/angioplasty <55 years in males and <65 years in females
  • Parent with TC >240 or known dyslipidemia
  • Child with DM, HTN, BMI >95, or smoker
  • Child with moderate or high risk medical condition
  • High risk: DM type 1 or 2, CKD/ESRD/Post-renal transplant, post orthotopic heart transplant, Kawasaki disease with current aneurysms
  • Mod risk: Kawasaki disease with regressed coronary aneurysms, chronic inflammatory disease (SLE, JIA), HIV, Nephrotic syndrome
149
Q

When do small VSDs (supracristal/subarterial/conal septal/infundibular) need repair?

A
  1. Qp:Qs >2
  2. Increase AI
  3. Left heart volume overload
  4. Reversible pulmonary vascular resistance
  5. History of IE
150
Q

Most common indication for reoperation after repair of complete AVSD?

151
Q

Late LVOT obstruction due to subaortic stenosis is more common in patients with what type of AVSD?

152
Q

Describe neurodevelopmental problems in CHD

A
  • IQ is typically low-normal (86-90)
  • Important delays are seen in motor skills, visual-motor integration and executive function
  • High incidence of behavioral problems including ADHD (>15% have behavioral problems)
  • 1/3 receive special education services
153
Q

What are lower full-scale IQ, verbal and math scores associated with in patients with CHD?

A

-Longer hospital length of stay at time of initial surgery

154
Q

True or False: There is no difference in neurodevelopmental outcomes in HLHS with regard to type of approach (Transplant v. staged repair)?

155
Q

What 2 metabolic parameters have neurodevelopmental injury been associated with?

A
  1. Hypoglycemia

2. Hypoxia

156
Q

What mutations are found in <30% of clinically diagnosed Brugada syndrome patients?

157
Q

Which gender is Brugada more common in?

A

Men

  • Also more arrhythmic events with this in men
  • Higher testosterone levels thought to play a role
158
Q

How is Brugada inherited?

159
Q

When do symptoms from Brugada commonly occur?

A
  • Rest
  • Sleep
  • Febrile state
  • Vagotonic conditions

*Rarely during exercise

160
Q

True or False: ICD is indicated in an asymptomatic Brugada patients with drug-induced type 1 ECG with a family history of sudden cardiac death

161
Q

True or False: Marfan Syndrome can be diagnosed based on +FHx and dilated aortic root

A

True

<20 years, Z-score > or equal to 3 for Ao Root

162
Q

How often should you image patients with newly diagnosed Marfan?

A
  • Echo every 6 months

- MRI/CT if evidence of descending aortic dilation, type B dissection or after repair of ascending aortic aneurysm

163
Q

What medication should be started at diagnosis of Marfan or in presence of significant aortic dilation?

A

B-blocker (or Losartan)

164
Q

What happens to the mid-systolic click of MVP with standing, squatting, decreased LV contractility and increased afterload?

A
  • Standing: Closer to S1
  • Squatting: Closer to S2 (increases preload and delays prolapse)
  • Decreased LV contractility: Closer to S2
  • Increased afterload: Closer to S2
165
Q

JAG1

166
Q

Bile duct paucity, CHD (ToF, peripheral PS), skeletal (butterfly vertebrae) and ocular abnormalities, abnormal facies (broad forehead, deep-set eyes, small/pointed chin)

167
Q

Palate abnormalities, hypocalcemia, immunodeficiency, speech/learning disabilities, renal anomalies, psychiatric problems, distinct facial features?

168
Q

FBN1

169
Q

Incidence of HCM?

170
Q

True or False: In patients with HCM, the hypertrophy is usually present at birth

171
Q

What can be an initial manifestation of HCM before LVH becomes evident?

A

ECG changes

172
Q

True or False: In HCM, there are disorganized myocytes present in non-hypertrophied areas of the LV

173
Q

Factors that favor HCM over athletes heart?

A
  1. Unusual patterns of LV hypertrophy
  2. LV cavity <45mm
  3. Abnormal LV filling
  4. Female
  5. FHx HCM
174
Q

Factors that favor athletes heart over HCM?

A
  1. LV cavity >55mm
  2. Decreased thickness with deconditioning
  3. VO2 Max >45mL/kg/min or >110% predicted
175
Q

Factors that can be seen in HCM and athletes heart?

A
  1. LAE
  2. Bizarre ECG patterns
  3. LV wall thickness 13-15mm

Peds Cardiology (20 decks)

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