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FRCPC > Cardiology > Flashcards

Cardiology Flashcards

1
Q

List 4 infectious causes of myocarditis

A 
Enterovirus
Coxsackie virus
Adenovirus
Parvovirus
EBV/CMV
Rickettsia
Diptheria
Hep C
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2
Q

List 3 cardiac defects associated with DiGeorge

A

Conotruncal defects

  • TOF-usually PA, MAPCAs***
  • TA**
  • DORV
  • Subarterial VSD

Branchial arch defects

  • CoA
  • Interrupted aortic arch (type 2B!)***
  • Right aortic arch
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3
Q

List steps in transitional circulation

A
  1. UA closes, UV remains more patent
  2. Cord clamped–>removal of placenta–>ductus venosus closes–>↑SVR
  3. ↓PVR from (1) mechanical expansion of lungs and (2) ↑ in arterial PAO2 (causing ↑ in vasodilation)
  4. PVRoutput from right heart flows through lungs
  5. PDA closure (due to o ↑ arterial PAO2 )
  6. PFO closure (due to ↑ volume of flow returning to left atrium)
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4
Q

In what % of adults does PFO persist?

A

1/3

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5
Q

What is the incidence of CHD i?

A

0.8% of live births

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6
Q

What is the common CHD ?

A

VSD (1/3)

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7
Q

What cardiac lesions cause in utero heart failure (hydrops)?

A

Severe RVOTO
Severe AVVR
Ebstein

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8
Q

List 3 genetic counselling points for CHD

A
  1. 1 affected sib risk increased to 2-6%, 2 sibs 10% (vs. 0.8% in general population)
  2. If 2 1st degree relatives, risk 20-30% in subsequent
  3. Tend to be similar class (conotruncal, atrioventricular septal, Rt obstruction, Lt obstruction)
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9
Q

How do you perform a hyperoxia and what do the results mean?

A

Apply 100% O2 x 15 min, then ABG taken from right radial artery

If Pao2 rises > 150 mm Hg: intracardiac right–left shunt essentially excluded

If PaO2 remains < 50 mmHg, cyanotic CHD vs severe PPHN/lung disease

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10
Q

CXR findings in TGA

A

Egg on a string

Thin mediastinum

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11
Q

CXR findings in TA

A

Wide mediastinum

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12
Q

CXR findings in Ebstein

A

Wall to wall heart

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13
Q

What is the primary defect in TOF?

A

Abnormal infundibular septum, that separates aortic/pulmonary outflow tracts

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14
Q

4 components of TOF

A

(1) RVOTO (pulmonary stenosis + subpulmonic area)
(2) VSD
(3) aorta that overrides ventricular septum
(4) RVH

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15
Q

Which component of TOF determines degree of cyanosis?

A

RVOTO

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16
Q

List 4 treatments for TOF spell and how they work

A

(1) Prone in knee-chest position (increases afterload thus decreasing R to L shunting)
(2) Supplemental O2
(3) Calming and holding
(4) Morphine (treat hyperpnea and decrease systemic catecholamines)
(5) Phenylephrine (increases afterload)
(6) β blockers (to block beta receptors in infundibulum therefore lessening RVOTO)

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17
Q

Describe the murmur in TOF

A

Loud harsh SEM at LUSB, sounding more holosytolic at LLSB

S2 single or soft P2 component

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18
Q

List CXR findings in TOF

A

Normal heart size
“Boot shaped heart” (elevation of apex, concavity of main PA area)
Right-sided AoA
↓ pulmonary vascularity

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19
Q

Repair and treatment of TOF

A

Repair in infancy

Severe RVOTO requires PGE infusion

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20
Q

List 2 long term complications patients with repaired TOF

A

Pulmonary insufficiency

RV dilatation (QRS duration increases)

Ventricular arrhythmias

Increased risk of SCD

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21
Q

Describe the physiology of tricuspid atresia

A

Single ventricle physiology!

All systemic venous return moves from RA to Lt side of heart by ASD

Blood then enters LV and is ejected to systemic circulation (through aorta) and to pulmonary circulation (by Lt–Rt shunt either by a PDA or a VSD)

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22
Q

What is the classic ECG finding in tricuspid atresia

A

Leftward superior axis on ECG, LVH (similar to AVSD)

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23
Q

Murmur in tricuspid atresia

A

Holosystoic murmur LSB

Prominent LV impulse (in most cyanotic CHD there is ↑d RV impulse)

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24
Q

Describe the pathophysiology of Ebstein’s

A

Downward displacement of an abnormal tricuspid valve into the RV

Leaflets adherent to wall

TV is insufficient resulting in TR

Extra volume of desaturated right atrial blood shunted right–left across an ASD or PFO

Due to combo of TR, poorly functioning small RV, and RVOTO from large sail-like TV leaflet, the effective output from Rt heart ↓s; if patent, PDA provides additional pulmonary flow

Due to TR, RA becomes enlarged

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25
Q

What determines the severity of cyanosis in Ebstein?

A
  1. Extent of TV displacement

2. Severity of RVOTO

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26
Q

What murmur is characteristic of Ebsteins?

A

Holosystolic murmur from TR
Gallop rhythm
Multiple clicks at LLSB

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27
Q

What ECG findings are typical of Ebstein’s?

A

RBBB without signs RVH

Associated with WPW

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28
Q

What is the classic CXR finding in Ebstein’s?

A

“Wall to wall heart”

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29
Q

List the cyanotic heart lesions that have decreased pulmonary blood flow

A

(1) Tricuspic atresia
(2) Tricuspid malformation (Ebstein)
(3) TOF
(4) Pulmonary atresia with intact septum

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30
Q

List the cyanotic heart lesions that have increased or normal pulmonary blood flow

A

NOTE: Can results from either

i) Abnormal ventricular-arterial connection (i.e. TGA)
ii) Mixing

(1) TGA
(2) Truncus arteriosus
(3) Single ventricle without pulmonary obstruction
(4) TAPVR

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31
Q

Which lesion classically results in post ductal sats > preductal sats?

A

TGA

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32
Q

What murmur is classic in TGA?

A 
Usually none
Can have holosystolic murmur from VSD
Single S2 (because PV very posterior and can't hear)
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33
Q

What ECG finding is classic in TGA?

A

None

Usually normal :)

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34
Q

What are the CXR findings in TGA?

A

Egg on a string
Narrow mediastinum
Normal to increased pulmonary blood flow

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35
Q

What emergency treatment is required in TGA if PGEs fail?

A

BAS

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36
Q

Where do you pulmonary veins drain in supracardiac and infracardiac TAPVD?

A

Supracardiac-RA, coronary sinus, or SVC

Infracardiac-Below the diaphgram into IVC, often via ductus venosus

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37
Q

Why are infracardiac TAPVDs more likely to be obstructed?

A

Ductus venosus closes after birth and can result in complete obstruction oxygenated pulmonary blood flow back to heart

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38
Q

Why is obstructed TAPVD a surgical emergency?

A

PGEs don’t work!

May make things worse by increasing pulmonary blood flow

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39
Q

What is the classic CXR finding in obstructed TAPVD?

A

Dramatic perihilar pattern of pulmonary edema and a small heart

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40
Q

What is the classic CXR finding in unobstructed/mild TAPVD?

A

Snowman-in supracardiac
Cardiomegaly
PA and RV are prominent
Increased pulmonary venous blood

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41
Q

What is the murmur of truncus arteriosus?

A

Single loud S2
Early systolic ejection click (from truncal valve)
SEM over LSB

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42
Q

How does truncus arteriosus typically present?

A

Usually minimally cyanotic +murmur at birth

Signs of heart failure as PVR drops (few months of age)

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43
Q

What is the ECG finding in truncus arteriosus?

A

BVH

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44
Q

Describe the major hemodynamic abnormalities in HLHS

A
  1. Inadequate systemic circulation
  2. Depending on the size of the atrial-level communication, either pulmonary venous hypertension (restrictive foramen ovale) or pulmonary overcirculation (moderate or large ASD)
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45
Q

What surgery is used for HLHS?

A

Norwood–>Glenn–>Fontan

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46
Q

Which cyanotic heart lesions have a single S2?

A

TGA
Truncus
PA/IVS

TOF
HLHS
Tricuspid atresia

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47
Q

Which cyanotic heart lesions have no murmur?

A

TGA

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48
Q

Which cyanotic heart lesion has diastolic murmur?

A

Truncus

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49
Q

List 4 side effects of PGEs

A 
Apnea
HypoTN
Brady
Fever
↓ plt
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50
Q

What is the most common type of ASD?

A

Secundum* (75%)
Primum (15%)
Sinus venosus (10%)

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51
Q

What associated defect should you always rule out in sinus venosus ASD?

A

Partial anomalous pulmonary venous drainage

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52
Q

What is the murmur of ASD?

A

SEM
Fixed split S2
RV systolic lift
Can have mid-diastolic rumble with increased flow across TV

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53
Q

List indications for ASD repair

A
  1. Symptomatic
  2. RV dilatation
  3. Qp:Qs>=2:1
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54
Q

What type of shunt does PAPVD cause?

A

Left to right

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55
Q

Describe the pathophysiology of AVSD

A

Contiguous atrial and ventricular septal defects with

Abnormal AV valves

May be associated with hypoplasia of one ventricle

Combine AVVR + left to right shunt cause Rt sided volume overload

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56
Q

Murmur of AVSD

A

Similar to ASD (SEM at LSB, wide fixed-split S2)

Additional apical holosytolic murmur from MV insufficiency

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57
Q

What is the classic ECG finding in AVSD***

A

(1) Leftward-superior axis** classic
(2) Q wave leads I and aVL
(3) Biventricular hypertrophy, (4) Tall P waves (rt atrial enlargement)
(5) Rt conduction delay rSR’ (especially after repair)

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58
Q

When should AVSD be repaired and why?

A 
4-6 months
Avoid PHTN (can develop as early as 6-12 months)
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59
Q

When do VSDs become symptomatic typically and why?

A

4-8 weeks

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60
Q

CXR findings in VSD

A

Cardiomegaly
Prominent PA
↑ pulmonary vasculature

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61
Q

List 3 physical exam findings consistent with VSD

A 
Holosytolic murmur over  LLSB (loud, harsh, blowing)
Thrill
Prominence of left precordium
Parasternal lift
Laterally displaced apex
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62
Q

What percentage of small VSDs close spontaneously and by what age?

A

(30-50%) close spontaneously
Usually by 4yo
More likely if muscular than membranous

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63
Q

When are large VSDs typically repaired?

A

4-6 months

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64
Q

In term infant, after how many days is a PDA unlikely to spontaneously close?

A

1 week

In a term infant, usually due to structurally abnormal PDA

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65
Q

List physical findings associated with PDA

A

Continuous murmur LUSB/LLSB (machinery-quality)

Ventricular heave

Prominent apical pulse

Wide pulse pressure

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66
Q

List 3 reasons all PDAs in term infants should be surgically closed

A

Prevent endocarditis
Prevent CHF
Prevent PHTN

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67
Q

What is the most common CHD in Noonan’s?

A

Dysplastic pulmonary valve (leading to stenosis)

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68
Q

List 3 clinical manifestations of severe pulmonary stenosis

A

Right sided HF

  • Hepatomegaly
  • Peripheral edema

Cyanosis (from PFO shunt)

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69
Q

Murmur of pulmonary stenosis

A

SEM at LUSB radiating to lung fields
Split S2 with delayed/soft P2
Pulmonic ejection click (stiff valve)
RV lift

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70
Q

ECG findings in pulmonary stenosis

A

RVH

Right atrial enlargement

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71
Q

CXR findings in pulmonary stenosis

A

Cardiomegaly
Prominent RV, RA
Prominent PA due to poststenotic dilatation
↓ pulmonary vascularity

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72
Q

List 2 conditions associated with peripheral pulmonary stenosis

A

Williams Syndrome

Allagille syndrome

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73
Q

What are the 3 types of aortic stenosis and what conditions are associated with them?

A

Valvar AS-most common!
Subvalvar AS-HOCM
Supravalvar AS-Williams syndrome

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74
Q

Murmur in aortic stenosis

A

SEM at RUSB

Radiating to neck

Early systolic ejection click

S4 with decreased LV compliance

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75
Q

ECG findings in aortic stenosis

A

LVH
LAD
LV strain (inverted t-waves in left leads)

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76
Q

Should patients with moderate/severe aortic stenosis participate in sports?

A

NO

At risk of SCD

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77
Q

Why do you have differential cyanosis with CoA?

A

Blood shunts R–>L through PDA to supply lower extremities, resulting in differential cyanosis (blue LEs)

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78
Q

List physical exam findings consistent with CoA

A

UE>LE pulses
Radial-femoral delay
Lower BP in LE
Systolic murmur LSB

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79
Q

What finding on CXR is pathognomic of CoA?

A

Rib notching

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80
Q

ECG findings in CoA

A

Infants-RVH/BVH

Older children-LVH

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81
Q

What the physiology of ALCAPA?

A

Anomalous Lt Coronary Artery from Pulmonary Artery

As PVR ↓s, perfusion pressure to LCA becomes inadequate

Blood supply to LV myocardium severely compromised

LV dilatation, dysfunction

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82
Q

How does ALCAPA typically present?

A

First few months of life

Recurrent attacks of discomfort, restlessness, irritability, sweating, dyspnea, and pallor

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83
Q

ECG in ALCAPA

A

Q waves and inverted T waves leads I and aVL; left precordial leads (V5 and V6) may have deep Q waves, elevated ST segments, inverted T waves

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84
Q

Explain physiologic split S2

A

On inspiration–>decreased intrathoracic pressure, fills right heart and increases RV ejection time and delayed closure of pulmonary valve

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85
Q

What lesions have fixed split S2

A

RV overload!:

ASD
TAPVD
PS
Ebstein anomaly

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86
Q

What is the murmur of mitral valve prolapse?

A

Mid systolic click

Late systolic murmur at apex

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87
Q

List 5 functional murmurs

A

Still’s murmur
Venous hum
Innocent pulmonic murmur

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88
Q

Describe the features of Still’s murmur

A 
Medium-pitched
Vibratory or musical
Short SEM
LLSB/MSB
Age 3-7 years
Decreases with sitting
Changes with respiration/position
DOES not radiate
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89
Q

Describe the features of innocent pulmonic murmur

A

Heard in supine position
2nd parasternal space
High pitched, blowing

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90
Q

Describe features of venous hum

A 
Early childhood
Turbulence in jugular/venous system 
Heard in anterior neck/upper chest
Subclavicular area
Soft humming sound in systole and diastole – exaggerated or disappears with changing head position or compressing jugular venous system
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91
Q

In a patient with a murmur, list 5 features that suggestive of CHD

A 
Diastolic
Pansystolic
Late systolic
Grade III or higher
Harsh
Loudest at Left upper sternal border
Associated with early or midsystolic click
Abnormal second heart sound
Absent or diminished femoral pulses
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92
Q

List 5 characteristics of innocent murmurs

A 
Murmur intensity grade II or less
Heard at left sternal border
Varies with position (decreases when upright)
Normal second heart sound
No audible clicks
Normal pulses
Normal growth, development, no cyanosis
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93
Q

Which lesions cause ejection clicks

A

Stenosis (Ao/Pulm)
MVP
Dilated aorta/PA (TOF/TA)

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94
Q

How do you diagnose vascular rings?

A

CT and MRA

Old study-barium esophagram

95
Q

What conditions predispose children to myocardial ischemia?

A

Hyperlipidemia
Prior Kawasaki disease with coronary artery aneurysms or stenoses
Substance use
ALCAPA

96
Q

List a differential for chest pain

A

Cardiac disease***

  • LVOTO: Hypertrophic cardiomyopathy, aortic stenosis, coarctation of the aorta
  • Coronary artery anomalies (KD, ALCAPA)
  • Pericarditis
  • Myocarditis
  • Dilated cardiomyopathy
  • Tachyarrhythmias
  • Aortic root dissection
  • Drug induced angina (cocaine, amphetamines, bath salts, marijuana)

Musculoskeletal:

  • Costochondritis
  • Muscle strain
  • Trauma
  • Pleurodynia
  • Slipping rib
  • Precordial catch

Psychogenic conditions:

  • Panic attack
  • Anxiety
  • Somatization

Respiratory conditions:

  • PTX***
  • Pulmonary hypertension ***
  • Acute chest syndrome **
  • Foreign body***
  • Asthma
  • Pneumonia
  • Pleuritis
  • Pulmonary embolism

Gastrointestinal:

  • Esophageal rupture (Boerhaave syndrome) ***
  • Gastroesophageal reflux
  • Esophagitis
  • Esophageal spasm
  • Gastritis
97
Q

What is the characteristic ECG of Pompe disease?

A

Prominent P waves
Short P-R interval
Massive QRS voltages

98
Q

List 4 causes of hypertrophic cardiomopathy

A

Familial or sporadic HCM

IEM (Mitochondrial disorders, GSD, Pompe, MPS, hemochromatosis)

Genetic syndromes (Noonan, Beckwith Widemann, swyer’s syndrome, LEOPARD syndrome, friedrich’s ataxia)

Infant of a diabetic mother

99
Q

Describe the pathophysiology of HOCM

A

Cardiac myofibrils and myofilaments demonstrate disarray and myocardial fibrosis

Increased LV wall thickness

Asymmetric septal hypertrophy

Systolic function preserved, diastolic dysfunction

Systolic anterior motion of MV

Resting or provocable outflow tract gradient

100
Q

Physical exam findings in HOCM

A

Forceful LV apical impulse

Systolic ejection murmur
Increased intensity with:
i) Upright posture (from a squatting, sitting, or supine position)
ii)Valsalva maneuver

Decrease intensity with:

  • Standing to a sitting or squatting position
  • Handgrip
  • Passive elevation of the legs.
101
Q

What ECG findings are consistent with HOCM?

A

LVH

ST segment and T-wave abnormalities

Intraventricular conduction delays

102
Q

List 3 management strategies for HOCM

A

Avoidance of competitive sports
Beta blockers (reduce outflow tract obstruction)
ICD if risk factors for SCD
Screening of first degree relatives + genetic testing

103
Q

List etiologies of dilated cardiomyopathy

A

Familial or sporadic DCM

Viral myocarditis

Muscular dystrophies

IEM (fatty acid oxidation disorders, carnitine abnormalities, mitochondrial disorders, organic acidemia)

Genetic syndromes (alstrom syndrome, barth syndrome)

Drugs (anthracyclines)

Ischemic (rare)

104
Q

What is the inheritance pattern of DCM?

A

Familial-Autosomal dominant
DMD/Beckers-X-linked
Mitochondrial myopathies-mitochondrial or AR

105
Q

Workup for DCM

A

CBC, renal and LFT, CPK, cardiac troponin I, lactate, plasma amino acids,urine organic acids, and an acylcarnitine profile

Genetic and enzymatic testing may be useful

Consider screening of 1st-degree family members with echo and ECG

106
Q

List cardiac findings in Marfan’s

A

Dilation of aortic root (50% of children, 60-80% of adults

Mitral valve prolapse (40-50%)

VT/SVT

Prolonged QT

Aortic aneurysm/dissection

Dilated cardiomyopathy

107
Q

Management of hypertrophic cardiomyopathy in IDM?

A

Symptomatic infants typically recover after 2-3 weeks of supportive care

Echocardiographic findings resolve within 6 to 12 months

If symptomatic-can try propanolol

108
Q

What is the most common cardiac lesion in IDM?

109
Q

What is pulsus alternans and what is it associated with?

A

Beat to beat alternation in pulse size and intensity

Associated with left sided heart failure

110
Q

What is pulsus bisferiens and what is it associated with?

A

Double beating pulse with two systolic beats

Associated with aortic insufficiency, HOCM, high cardiac output states

111
Q

What is pulsus paradoxus and what is it associated with?

A

Exaggerated decline in BP during inspiration (>10 mmHg), resulting from increase in negative thoracic pressure

On inspiration, RV EDV increases, septum bows out and decreases LV preload

Associated with tamponade, constrictive pericarditis, severe lung disease

112
Q

What is pulsus bigeminus and what is it associated with?

A

Two heartbeats close together followed by a longer pause.

The second pulse is weaker than the first

Alternating QRS

Associated with digitalis toxicity, HOCM

113
Q

List 3 physical findings consistent with pericarditis

A 
Muffled heart sounds
Narrow pulse pressure
JVD
Pulsus paradoxus
Pericardial friction rub
114
Q

List 10 causes of PHTN

A 
Idiopathic
Familial
Connective tissue disorder
PVOD
Pulmonary capillary hemangiomatosis
PPHN
Left sided heart disease 
Lung disease (ILD, CLD, OSA,)
Chronic thrombotic/embolic disease
Sarcoidosis
Histiocytosis X
115
Q

What is the definitive diagnostic test for PHTN?

A

Catheterization

-Should show pulmonary arterial HTN and NORMAL pulmonary capillary wedge pressure

116
Q

List 5 causes of CHF that present at birth

A 
Anemia
Acidosis
Hypoxia
Hypoglycemia
Hypocalcemia
Sepsis
117
Q

List 5 causes of CHF that present in first month

A 
HLHS
Aortic stenosis
Coarctation
VSD (4-8 weeks depending on size and fall in PVR)
Anomalous left coronary (ALCAPA)
118
Q

List 5 causes of CHF that present as child

A 
Myocarditis
Cardiomyopathy (dilated or hypertrophic)
Tachyarrhythmia
Severe anemia
Rheumatic fever
119
Q

List 5 important aspects in management of CHF

A

1) Ensure adequate nutrition
- NG feeds
- Aggressive reflux management
2) Diuretics
3) Afterload reduction
- Useful in HF secondary to cardiomyopathy, mitral, aortic insufficiency left-to-right shunts
4) Fluid/salt restriction

120
Q

Cardiac lesions associated with T21

A

VSD*** most common
AVSD
ASD

121
Q

Cardiac lesions associated with T13/T18

A

T13-ASD, VSD, PDA, valvar disease, CoA

T18-VSD, polyvalvar disease

122
Q

Cardiac lesions associated with Turner syndrome

A

Bicuspid AoV
Coarct
AS

123
Q

Cardiac lesions associated with Fragile X

A

Mitral valve prolapse

Ao root dilatation

124
Q

Cardiac lesions associated with DiGeorge

A

Interrupted aortic arch

Truncus arteriosus

125
Q

Cardiac lesions associated with CHARGE

A 
ASD
VSD
AVSD
PDA
TOF
126
Q

Cardiac lesions associated with Alagille

A

Peripheral pulmonic stenosis

127
Q

Cardiac lesions associated with Williams

A

Supravalvular aortic stenosis

PPBS

128
Q

Cardiac lesions associated with FASD

129
Q

Cardiac lesions associated with Holt Oram

A

ASD (60%), VSD (30%), arrhythmia

130
Q

Cardiac lesions associated with Ellis-van Creveld

131
Q

Cardiac lesions associated with VACTERL

A

ASD
VSD
PDA
TOF

132
Q

Cardiac lesions associated with PHACES

A

VSD
PDA
Coarctation
Arterial aneurysms

133
Q

Cardiac lesions associated with Noonans

A

Pulmonic stenosis
ASD
Cardiomyopathy

134
Q

What are the 3 most common bacteria causing infective endocarditis

A
  1. Alpha hemolytic Strep (Strep viridans) (after dental procedures)
  2. S. aureus (more common in kids without CHD)
  3. Enterococci (GI/GU manipulation)
  4. Pseudomonas (IV drug users)
  5. Serratia (IV drug users)
  6. CONS (indwelling line)
  7. Fungal (after open heart sx)
135
Q

Physical exam features of IE

A

New murmur

Splenomegaly

Petechiae

Osler nodes(tender pea-sized intradermal nodules in the pads of the fingers and toes)

Janeway lesions(painless small erythematous or hemorrhagic lesions on the palms and soles)

Splinter hemorrhages(linear lesions beneath the nails)

Roth spots

New clubbing

136
Q

Duke Criteria for IE

A

2 major criteria, 1 major and 3 minor, or 5 minor criteria suggest definite endocarditis

Major criteria:

(1) Positive blood cultures (2 separate cultures for a usual pathogen, ≥2 for less typical pathogens)
(2) Evidence of endocarditis on echo (cardiac mass on a valve or other site, regurgitant flow near a prosthesis, abscess, partial dehiscence of prosthetic valves, or new valve regurgitant flow)

Minor criteria:

(1) Predisposing conditions
(2) Fever
(3) Embolic-vascular signs
(4) Immune complex phenomena (glomerulonephritis, arthritis, rheumatoid factor, Osler nodes, Roth spots)
(5) Single positive blood culture or serologic evidence of infection
(6) Echo signs not meeting the major criteria

137
Q

List complications of endocarditis

A

CHF
Myocardial abscesses
Emboli (often with CNS manifestations)

Pulmonary emboli may occur in children with VSD or TOF

Mycotic aneurysms

Obstruction of a valve secondary to large vegetations

Acquired VSD

Heart block

Others:
Meningitis
Osteomyelitis
Arthritis
Renal abscess
Purulent pericarditis
Immune complex-mediated glomerulonephritis
138
Q

Empiric therapy for endocarditis

A

Vanco +gent

139
Q

Duration of treatment for endocarditis

140
Q

Which groups have the highest probability of adverse outcomes from IE (and thus should receive prophylaxis)? (CPS)

A
  1. Prosthetic cardiac valve or prosthetic material used for valve repair
  2. Previous IE
  3. Congenital heart disease (CHD)
    a. Unrepaired cyanotic CHD, including palliative shunts and conduits
    b. Completely repaired CHD with prosthetic material or device (both surgical and cath) during the first six months after the procedure
    c. Repaired CHD with residual defects at the site or adjacent to the site of a prosthetic patch or prosthetic device (which inhibit endothelialization)
  4. Cardiac transplant recipients who develop cardiac valvulopathy
  5. Rheumatic heart disease if prosthetic valves or prosthetic material used in valve repair
141
Q

Which procedures require endocarditis prophylaxis? (CPS)

A
  1. Dental procedures that involve the manipulation of gingival tissue, the periapical region of teeth or perforation of the oral mucosa-including CLEANING
  2. Invasive procedures of the respiratory tract that involves incision or biopsy of the respiratory mucosa, e.g.T&A
142
Q

What antibiotic should be used for endocarditis prophylaxis and how many doses?

A

Single dose
Amoxicillin/Ampicillin

Pen allergic-keflex, clinda, azithro

143
Q

What was the reasons for revising guidelines on cardiac prophylaxis?

A

Infections were more likely from exposures from everyday life and not that much more from dental procedures

144
Q

What are the most common patterns of valve involvement in rheumatic heart disease?

A

MR>AR>MS>AS

145
Q

What is a bacterial cause of myocarditis that has been eliminated by vaccination?

A

Diptheria (AV block, bundle branch block, or ventricular ectopy)

146
Q

ECG findings in pericarditis

A

Low QRS voltage
Diffuse ST segment elevation
PR segment depression
T wave inversion (later)

147
Q

List causes of pericarditis

A 
Viral (Enteroviruses, influenza, adenovirus, RSV, parvovirus)
Bacterial (pneumococcal, Hib)
TB
JIA
SLE
Hypothyroidism
CKD
Malignancy
148
Q

What is the cause of constrictive pericarditis?

A

Recurrent or chronic pericarditis
Cardiac surgery
Radiation to the mediastinum

149
Q

What is the definition of hypertension?

A

Adults : BP ≥140/90 mmHg

Prehypertension: SBP or DBP between 90th – 95thpercentile

Children: SBP and/or DBP ≥95th percentile for age, sex, and height on ≥3 occasions

Stage 1 HTN: BP between 95th - 99th percentile plus 5 mmHg

Stage 2 HTN: BP >99th percentile plus 5 mmHg

150
Q

List risk factors for primary HTN

A

Overweight
Male
Black, Hispanic
Family hx of HTN

151
Q

List causes of secondary HTN

A

Renal

  • Renovascular (fibromuscular dysplasia, UAC)
  • Glomerulonephritis
  • PCKD
  • CKD

Cardiac
-Coarctation

Endocrine

  • Pheochromocytoma
  • Neuroblastoma
  • Cushing’s syndrome
  • Hypercalcemia
  • Thyroid disorder

Drugs

  • Steroids
  • OCP
  • Tacrolimus
  • Cyclosporine
152
Q

Definition of hypertensive emergency

A

Severe HTN
+
End organ damage (seizures/encephalopathy, heart failure, renal dysfunction, papilledema/retinal hemorrhage/exudates)

153
Q

List 4 signs of target end organ damage in chronic HTN

A

LVH (40% with subclinical HTN)
Retinopathy
Microalbuminuria
Carotid intima-media thickness

154
Q

Workup of HTN

A
  1. Confirm
    - If repeated measurements >90th percentile, confirm with 24H ambulatory blood pressure monitoring
    - If BP >95th%ile confirmed, investigate for secondary causes
2. Etiology:
4-limp BP
Echocardiogram
CBC, retic
Urinanalysis, lytes, BUN/Cr
Ca
Renal U/S + doppler
Urine tox

3 Screen for end organ damage

  • Echo
  • UA
  • Eye exam
  1. Screen for comorbidities
    - Fasting lipids and BG
    - Sleep history
155
Q

List the indications for pharmacologic management of HTN

A 
Symptomatic HTN
Secondary HTN
Target organ damage (incl LVH!)
Diabetes (types 1 and 2)
Persistent HTN despite nonpharmacologic measures
156
Q

What drug classes can be used for hypertension management in children?

A

ACE-I, ARBs, β-blockers, Ca-channel blockers, and diuretics

157
Q

What is the goal of HTN management?

A

Goal should be to reduce BP to <95th percentile

If pt withCKD, diabetes, or target organ damage, goal should be to reduce BP to <90th%le

158
Q

What antihypertensives should be used in patients with migraines?

A

β-Blockers or Ca-channel blockers

159
Q

What antihypertensives should be used in diabetics with proteinuria or proteinuric renal disease?

160
Q

What antihypertensives should be used in hypertensive emergency?

A

IV Labetalol
IV Nicardipine
IV SNP (can cause CN toxicity)

161
Q

How quickly should you decrease BP in hypertensive emergency?

A

No more than 25% in first 8 hours

162
Q

When should you restrict physical activity (high static sports) in a patient with HTN?

A

Stage 2 HTN

LVH

163
Q

Proper BP measurement

A

Right arm (pre ductal; left can be falsely low in coarctation)

Appropriate width cuff (bladder cover 80% of upper arm)

Bladder length should encircle arm completely

Seated and resting quietly x 5 minutes

164
Q

List the late complications of Fontan

A

PLE
Plastic bronchitis
Arryhtmias (sinus node dysfunction, aflutter, SVT)
Thromboembolism
Baffle obstruction causing superior or inferior vena cava syndrome
Liver cirrhosis

165
Q

Right atrial enlargement on ECG

A

Peaked p wave in lead II and V1(>2.5mm)

166
Q

Left atrial enlargement on ECG

A

P wave in lead II is bifid and >120 ms OR negative p in V1 (>1mm wide and deep)

167
Q

RVH on ECG

A

R in V1 and/or S in V6 more than upper limit of normal range for age
RAD

168
Q

LVH on ECG

A

S in V1 and/or R in V6 more than upper limit of normal range for age
LAD

169
Q

RBBB on ECG

A

RSR’ in V1

Slurred S in V6

170
Q

LBBB on ECG

A

RSR’ in V6

Slurred S in V1

171
Q

ECG findings in Hyperkalemia

A

Peaked T waves
Flat P waves
Widening of QRS

172
Q

ECG findings in hypokalemia

A

Flat T wave
ST depression
Prominent U wave

173
Q

What electrolyte abnormalities can cause prolonged QTc?

A

Hypocalcemia
Hypomagnesemia
Hypokalemia

174
Q

What are the 4 requirements for sinus rhythm?

A

Regular rate and rhythm for age
P wave before every QRS complex
Normal axis
Upright P in lead II

175
Q

What features would be concerning in a patient with PVCs?

A

Multiform/multifocal

Associated with underlying heart disease

History of syncope or fhx of sudden death

Precipitated by or increased with activity

Multiform or couplets

Runs of PVCs with symptoms

176
Q

List 5 causes of sinus bradycardia

A 
Athletes
Increased vagal stimulation
Increased ICP
Hypothyroidism
Electrolyte disturbance (low K)
Drug effect
177
Q

What rate is consistent with a junctional rhythm?

178
Q

What type of second degree heart block is more likely to progress to complete heart block?

A

Mobitz Type 2 (PR Interval is constant with abrupt failure of conduction of P wave)

179
Q

Cause of Second degree AV block Mobitz I (Wenkebach)

A

Advanced vagal tone

Seen often in athletes

180
Q

Causes of second degree AV block Mobitz 2

A

Aging degeneration of conduction system

Medications that block AV node (digoxin, betablockers, CCBs)

181
Q

List causes of complete heart block

A

Congenital:

  • Anti-ro/la antibodies
  • cc-TGA, atrial isomerism
  • Long QT

Acquired:
• Cardiac surgery
• Infectious: Rheumatic fever, myocarditis, Chagas disease

182
Q

When is ventricular pacing indicated in CHB?

A

Symptomatic

Ventricular pauses ≥3 seconds

Resting HR <40 beats/min

183
Q

What monitoring and treatment is required for mother’s with anti-Ro/anti-La antibodies

A

Regular fetal echos from 16 weeks GA until delivery

Can give IVIg or steroids to mom’s (mixed evidence)

184
Q

What is the ventricular rate in complete heart block?

185
Q

What are two things newborns with CHB are at risk for in the future?

A

Arrhythmia

Sudden Death

186
Q

With atrial fibrillation and atrial flutter, how high can the atrial rate get?

187
Q

What are the two main mechanisms of SVT?

A

AVNRT

  • More common after 2 years of age
  • 2 conducting pathways in the AV Node (fast and slow)

AVRT

  • More common in infants
  • Extra-nodal accessory pathway (e.g. WPW)
188
Q

List clues that tachycardia is due to SVT

A 
Absent/retrograde P wave
No HR variation
QRS narrow
HR>180 in children
HR>220 in infants
189
Q

Management of SVT

A
  1. Vagal maneuvers (ice to face, valsava, blow into straw, bear down)
  2. Adenosine
    - 0.1 mg/kg, then 0.2 mg/kg
  3. Synchronized cardioversion (if unstable)
  4. Consider amiodarone
190
Q

ECG findings in WPW

A

Delta wave
Wide QRS
Short PR

191
Q

What two structural abnormalities of heart can be associated with WPW?

A

Ebstein anomaly

Congenital corrected TGA

192
Q

List causes of ventricular tachycardia

A 
Myocarditis
Cardiomyopathy
Myocardial Infarction
Cardiac Tumours
Long QT Syndrome
WPW Syndrome
Congenital Heart Disease
Mitral Valve Prolapse
Trauma
Metabolic: hyoxia, acidosis, hypocalcemia, hypoglycemia, hypo/hyperkalemia
Toxins
193
Q

Treatment for torsades

194
Q

Definitive treatment of WPW

A

Catheter ablation of accessory pathway

195
Q

Causes of syncope

A 
Vasovagal
Breathholding spell
Orthostatic hypotension
Hypoglycemia
Cardiac
•	Long QT Syndrome
•	SVT
•	Pre-excitation Syndrome (WPW)
•	V Tach
•	Hypertrophic and Dilated Cardiomyopathy
•	Vavular defects
•	Pulmonary HTN
•	Myocarditis
196
Q

List syncope mimics

A 
Seizures
Migraine syndromes
Hyperventilation
Conversion Disorders
Narcolepsy
197
Q

What features of syncope on history would be suggestive of a cardiac etiology?

A

During exertion
Triggered by startle or loud noise-long QT
No prodrome
Palpitations
Chest pain
Family history of SCD, arrythmia
Hx of CHD/acquired heart disease or arrythmia

198
Q

What features should you look for on ECG in a patient with syncope?

A 
QT interval
Delta wave/pre-excitation
Epsilon wave
Brugada
Heart block
199
Q

What are the two clinical phenotypes of congenital long QT syndrome and how are they inherited?

A
  1. Romano Ward Syndrome – AD, purely cardiac phenotype
  2. Jervell and Lange-Nielsen Syndrome – AR, associated with congenital sensorineural deafness and a more severe clinical course
200
Q

Components of Long QT syndrome score

A 
1. ECG findings (in the absence of medications or disorders known to affect these features)
o	QTc (= QT/√RR)
≥480 msec: 3 points
460 to 470 msec: 2 points
>450 to 460 msec (in males): 1 point
o	QTc at fourth minute of recovery from exercise stress test ≥480 ms: 1 point
o	Torsades de pointes: 2 points
o	T-wave alternans: 1 point
o	Notched T wave in three leads: 1 point
o	Resting heart rate below second percentile for age (restricted to children): 0.5 point
  1. Clinical findings
    o Syncope
    With stress: 2 points
    Without stress: 1 point
  2. Family history (The same family member cannot be counted in both of these criteria)
    o Family members with LQTS: 1 point
    o Unexplained sudden cardiac death in immediate family members <30 years of age: 0.5 point
201
Q

Diagnostic work up for long QT syndrome

A

ECG
Exercise test
Genetic testing

202
Q

Treatment for Long QT syndrome

A

Beta blockers

In those that don’t respond, ICD

203
Q

Which type of Long QT syndrome does not respond to beta blockers?

A

LQT3

Needs ICD!

204
Q

QT prolonging drugs

A

Antibiotics—macrolides (erythromycin, clarithromycin, telithromycin, azithromycin), clindamycin, septra

Antifungal agents—fluconazole, itraconazole, ketoconazole

Antiprotozoal agents—pentamidine isethionate

Antihistamines—Diphenhydramine

Antidepressants—tricyclics such as imipramine (Tofranil), amitriptyline (Elavil),desipramine (Norpramin), and doxepin (Sinequan)

Antipsychotics—haloperidol, risperidone, phenothiazines such as thioridazine(Mellaril) and chlorpromazine (Thorazine), carbamezipine

Antiarrhythmic agents – Procainamide, amiodarone, sotalol, flecainide

Lipid-lowering agents—probucol

Antianginals—bepridil

Diuretics (through K+ loss)—furosemide (Lasix), ethacrynic acid (bumetanide[Bumex])

Oral hypoglycemic agents—glibenclamide, glyburide

Organophosphate insecticides

Promotility agents—cisapride

Vasodilators—prenylamine

Caffeine

205
Q

ECG findings in Brugada syndrome

A

Coved-ST elevation in right precordial leads and RBBB

206
Q

What is the pathophysiology of Catecholaminergic Polymorphic Ventricular Tachycardia ?

A
  • Type 1 is autosomal dominant associated with a mutation in the ryanodine receptor gene RYR2 at 1q42.1
  • Type 2 is autosomal recessive and related to a mutation in the calsequestrin 2 gene CASQ2 at 1p13.3
207
Q

How do you diagnose CPVT?

A

Polymorphic VT on exercise test

208
Q

What situations trigger VT in CPVT?

A

Usually after arousal/emotional experiences (catecholamine release)

209
Q

What is the most common type of long QT syndrome?

A

Romano Ward

210
Q

Criteria for classic Kawasaki Disease

A

5 days of fever+ 4/5 of:

  • B/L non-exudative bulbar conjunctival injection
  • Oral/Mucosal Changes: strawberry tongue, dry/cracked lips, injection of mucosa/pharynx
  • Polymorphous exanthema (anything but vesicular)
  • Cervical LAD with nod >1.5cm: nonsuppurative, usually unilateral
  • Extremity Changes: palmar/plantar erythema or edema
211
Q

List cardiac manifestations of KD other than coronary aneurysms

A

Myocarditis
Pericarditis
Mitral regurgitation

212
Q

What percentage of untreated patients with KD develop coronary aneurysms and when?

A

Coronary artery aneurysms develop in up to 25% of untreated patients in the second to third week of illness

Rarely before day 10

213
Q

When should screening echos be done in KD?

A 
At diagnosis
2-3 weeks
If normal:
Repeat at 6-8 weeks
Repeat at 1 year with lipid profile
214
Q

List risk factors for aneurysms in KD

A

Age younger than one year or older than nine years

Male sex

Fever ≥14 days

Not treated (with IVIG)

Serum sodium concentration <135 mEq/L

Hematocrit <35 percent

White blood cell count >12,000/mm3

215
Q

With timely treatment, what is the risk of coronary aneurysms in KD?

216
Q

What is the prognosis of coronary aneurysms in KD?

A

50% of coronary aneurysms regress in 1 to 2 years

Giant aneurysms unlikely to resolve

217
Q

What is the prognosis of mitral insufficiency in rheumatic heart disease?

A

Spontaneous improvement usually occurs with time

218
Q

When does mitral stenosis typically appear in rheumatic heart disease?

A

Usually takes 10 yr or more for the lesion to become fully established

219
Q

What is the prognosis of aortic insufficiency in rheumatic heart disease?

A

Unlike MI, AI does not regress

220
Q

Cardiac lesions associated with trisomy 22p (cat eye)

A

TAPVD
TOF
VSD

221
Q

What constitutes a positive hyperoxic test?

A

PaO2 <150 after 10 minutes of 100% O2

222
Q

What are the 3 types of duct dependent lesions?

A

Duct dependent pulmonary circulation
Duct dependent systemic circulation
Duct dependent mixing (TGA)

223
Q

List acyanotic heart lesions with normal pulmonary blood flow

A

Pulmonary stenosis
CoA
AS
Mitral stenosis/regurg

224
Q

ECG findings in ASD

A

RAD

Primum-LAD (like AVSD)

225
Q

Complications of ASD

A 
PHTN
CVA/emboli
Atrial fibrillation
Dyspnea
Recurrent infections
226
Q

Do patients with T21 have increased risk of developing PHTN with same cardiac lesion as a health kid?

227
Q

Treatment of TOF spell

A

Quiet, calm environment
Knee to chest/squatting (increase venous return)
O2 (pulmonary vasodilation)
Fluid
Morphine (treat hyperpnea and systemic catecholamines)
Phenylephrine (increase SVR)
Propanolol

228
Q

3 unique things about TAPVD

A
  1. Presents with cyanosis
    severe respiratory distress
  2. PGEs don’t work
  3. No medical therapy works; need surgery right away!
229
Q

Treatment of rheumatic fever

A
  1. PenG x 10 days OR IM penicillin x 1 dose
  2. ASA
  3. Prednisone for severe carditis
230
Q

What is the classic presentation of Brugada syndrome?

A

Unexplained nocturnal death

231
Q

ECG changes in digitalis toxicity

A 
PVCs
Bradycardia
Atrial tachyarrhythmias with AV block
Ventricular bigeminy, junctional rhythms
Bidirectional ventricular tachycardia

Chronic digoxin use:

  • T wave changes (flattening or inversion)
  • QT interval shortening
  • Scooped ST segments with ST depression in the lateral leads
  • Increased amplitude of the U waves
232
Q

Surgical indications for endocarditis

A

Increase in vegegatation size after 4 weeks of antibiotics

Persistent vegetation after systemic embolization

Valvular dysfunction (perforation, rupture, AI/MI causing heart failure)

New heart block

233
Q

What are the guidelines for secondary prophylaxis in rheumatic fever for the following groups:

i) Without carditis
ii) With carditis, no valvular disease
iii) With carditis, persistent valvular disease

A

Without Carditis→ 5 years or until 21 years of age, whichever is longer

With Carditis, but no valvular disease → 10 years or until 21 years of age, whichever is longer

With Carditis, persistent valvular disease → 10 years or until 40 years of age, whichever is longer, sometimes lifelong prophalaxis

234
Q

List 3 options for antiobiotic prophylaxis for ARF

A
  1. IM Benzathine PenG every 4 weeks
  2. Pen V oral daily
  3. Sulfadiazine daily

FRCPC (27 decks)

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