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Cardiology Flashcards

1
Q

Indications for SBE prophylaxis (6)

A
  1. Prosthetic valve/material
  2. Previous IE
  3. Unrepaired cyanotic heart disease
  4. 1st 6 months post repaired congenital heart disease
  5. Repaired CHD with residual defects at the site/adjacent to the site of prosthetic patch/device
  6. Cardiac transplant recipients who develop valvulopathy
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2
Q

Drugs used for SBE prophylaxis

A

PO amoxil, or IM/IV amp/cef

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3
Q

Class Ia antiarrhythmics

A

Inhibits Na fast channel, prolongs repolarisation
Used mainly for tachyarrhythmias
Eg. Quinidine, procainamie, dispyramide

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4
Q

Class Ib antiarrhythmics

A

Inhibits Ns fast channel, shortens repolarisation
Mainly used for ventricular arrhythmias
Lidocaine, mexiletine, phenytoin

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5
Q

Class Ic antiarrhythmics

A

Inhibits Na channel
Used mainly for tachyarrhythmias
Eg. Flecainide, propafenone

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6
Q

Class II antiarrhythmics

A

Beta blockers, mainly used for SVT and long QT

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7
Q

Class III antiarrhythmics

A

Prolong repolarisation

Amiodarone- used for VF, JET, SVT

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8
Q

Class IV antiarrhythmics

A

Ca channel blockers eg. verapamil

Good for SVT if not caused by WPW

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9
Q

Criteria for further Ix/suppressive therapy for PVCs

A 
2 or more in a row
Multiform PVCs
Increased ectopic activity with exercise
R-on-T phenomenon 
Extreme frequency >20% of bears
Presence of underlying heart disease or prev surgery
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10
Q

Features of SVT on ECG

A

Narrow complex
Abnormal P-wave axis (normal = positive on I and aVF)
HR relatively unvarying

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11
Q

SVT associated with syncope

A

AVNRT

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12
Q

Treatment of atrial flutter

A

Cardioversion, maintenance with digoxin or propanolol

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13
Q

Treatment of AF

A

Ca channel blockers

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14
Q

LQTS1

A

KCNQ1 gene
MC genetic cause
Triggered by exercise/stress
Defect in potassium channel

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15
Q

LQTS2

A

KCNH2 gene
Second MC genetic cause
Potassium channel

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16
Q

LQTS3

A 
SCN5A gene
Highly lethal
Triggered by sleep
Na channel mutation
No response to beta blockers- needs ICD
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17
Q

Jervell-Lange-Neilsen syndrome

A

Congenital LQTS
Associated with hearing loss
Triggered by exercise, emotion

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18
Q

Cardiac defects T21

A 
40-50%
AVSD 60%
ASD, VSD, PDA 30%
TOF 10%
Higher risk of pulmonary hypertension, early Eisenmenger syndrome
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19
Q

Truncus arteriosus clinical features

  • Time of presentation
  • Progression
  • OE
  • ECG
  • CXR
A

Presents with cyanosis immediately after birth
Progresses to CHF in days to weeks- clinical improvement if pulmonary vascular obstructive disease develops

Bounding peripheral pulses, wide pulse pressure, hyperactiev praecordium, lateral apex beat
Systolic click ULSE
Single S2
VSD murmur
Mitral flow murmur if PBF increased
Early diastolic murmur = truncal regurg

Normal QRS axis
BVH 70%
Occasional LAH

Cardiomegaly, increased pulm vascular markings
Can have R aortic arch

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20
Q

Types of truncus arteriosus and implications for pulmonary blood flow

A

Type 1: Ao and PA off trunk = increased
Type 2: PAs split off Ao = normal
Type 3: PAs split off trunk = normal
Type 4: “pseudotruncus” = PAs split of Ao after the branching arteries = TOF with pulmonary atresia and aortic collaterals = decreased PBF

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21
Q

Main features of truncus arteriosus (3)

Other associations: (4)

A

Single arterial trunk supplying pulmonary, systemic and coronary circulation
Large perimembranous infundibular VSD below truncus
Truncal valve often incompetent (worsens with time)
= bilateral ventricular hypertrophy, occasional LAH

Often coronary artery abnormalities
Interrupted aortic arch (type 4A) 13%
R aortic arch 30%
22q11 33%

22
Q

Types of TAPVD

A
  1. Supracardiac- common pulmonary vein (CPV) drains to SVC
  2. Cardiac- drains to coronary sinus or direct to RA
  3. Infracardiac (much more common in boys)- CPV drains to portal vein, hepatic vein, IVC. CPV penetrates diaphragm through oesophageal hiatus
  4. Mixed
23
Q

TAPVD pathophysiology, CXR

A

RV hypertrophy, small L heart
R-L shunt through PFO or ASD

Can develop pulmonary HTN secondary to obstruction of the pulmonary venous return- increased resistance due to length of the vessels, in infracardiac can have resistance caused by hepatic sinusoids

With obstruction = early presentation with cyanosis and decreased CO
Lesser degrees of obstruction lead to later presentation with mild cyanosis and CCF

CXR: Snowman sign (supracardiac)

24
Q

Clinical features TAPVD without venous obstruction

A

CHF, frequent LRTI
Mild cyanosis
Quadruple/quintuple rhythym
CXR: cardiomegaly with increased vascular markings

25
Clinical features TAPVD with venous obstruction
Cyanosis and resp distress from birth Infracardiac- cyanosis will be worse with feeding (oesophageal obstruction) Loud single S2 and gallop Signs of CCF
26
Ebstein's anomaly pathophysiology | - Can be associated with
Inferior displacement of the septal and posterior leaflets of the tricuspid valve = large RA, functional hypoplasia of the RV, tricuspid regurg. PFO or ASD always present Can be associated with redundant valve tissue = RVOT obstruction Often associated with WPW
27
Ebstein's anomaly presentation (mild and severe) and clinical features - CXR
Mild: Dyspnoea, fatigue, palpations on exertion, SVT Severe: cyanosis and CHF early life- improves once PVR falls Triple or quadruple rhythm Widely split S2 TR murmur Hepatomegaly CXR: extreme cardiomegaly esp RA
28
PV stenosis types and associations
Valvular- Noonan's Infundibular- usually assoc with large VSD eg. ToF Supravalvular- Williams
29
Severity of PS- pressure gradient and ventricular pressures
Mild- <35-40mmHg, RV systolic pressure <50% LV Mod: 40-70, RV 50-75% LV Severe: >70mmHg or RV >75% LV pressures
30
PS clinical features, OE, ECG, CXR
Mild- asymptomatic Mod- exertional dyspnoea, easy fatiguability Severe- CCF, exertional CP Critical- neonate with cyanosis and tachypnoea from significant R -> L shunt ESM over pulm area, can transmit to back Systolic ejection click in valvar PS Can have split S2 due to RVH R axis deviation + RVH R wave in V1 >20 = systemic pressures in RV CXR: normal heart size, can have prominent main PA segment (post stenotic dilatation), can have decreased pulmonary vascular markings in severe PS
31
ECG criteria for RAH
p wave >3mm
32
DDx RAH on ECG (5)
``` Tricuspid regurg Pulm HTN Ebstein's anomaly Large late ASD Tricuspid stenosis (rare) ```
33
ECG criteria LAH
>2.5 small squares long, bifid p wave | >2 small squares in infants
34
DDx LAH on ECG (5)
``` MR (most common) Big VSD leading to dilated LA MS (eg. post rheumatic fever) Large PDA with shunt Severe LVH (untreated) ```
35
DDx LAD on ECG
LVH esp with volume overload (eg. big VSD) LBBB (broad QRS) L anterior hemiblock - "superior axis" with narrow QRS - Tricuspid atresia - AVSD or ostium primum - Congenitally corrected TGA
36
RVH on ECG
V1 R >4 large squares (5 in neonates) V6 S >7 small squares Upright T waves V1 from 4 days to 4-5 years V1 with T wave inversion, ST depression, small q waves = severe RVH (strain pattern)
37
LVH on ECG
V6 R >5 large squares | V6 ST depression and T waves inversion
38
DDx Q wave in V1 (4)
L-TGA Single ventricle Severe RVH Anterior MI
39
DDx cardiac defects that will be symptomatic during fetal life (2)
Valve regugitation- TR, ECD, truncus (volume loads the ventricle) Arrhythmia
40
DDx cardiac defects that cause a critically ill neonate in the first 24 hours (4)
Valve regurgitation esp Ebstein's, absent pulmonary valve syndrome- may be born in failure Obstructed TAPVD "Early" duct dependent presentation Resp distress from severe pulmonary hypoplasia secondary to a cardiac issue eg. Ebstein's, pulmonary atresia
41
DDx cardiac defects that present 24 hours to 2 weeks when duct closes (7)
Duct dependent for pulmonary blood flow (RVOT): - Pulm atresia with VSD - Severe ToF - Critical PS Duct dependent for systemic blood flow (LVOT): - CoA - Severe AS - Hypoplastic L heart Duct dependent for mixing - D- TGA
42
DDx cardiac defects that present 2-6 weeks once pulmonary vascular resistance falls (7)
``` VSD with CoA (early failure) Large VSD Large PDA Large AVSD Truncus ToF with pulm atresia Single ventricle with no PS ```
43
DDx asymptomatic mumur (7)
``` Functional/benign ASD VSD PS Mild- mod AS Small PDA CoA ```
44
Fick principle
Used to measure cardiac output Qp/Qs = (Aosat-MVsat)/(PVsat-PAsat) Qp = pulmonary blood flow Qs = systemic blood flow Aosat = sats in aorta MV sat = mixed venous dats
45
Poiseullie equation
Used to calculate pulmonary vascular resistance PVR = mean PA p - LA p / pulmonary blood flow
46
Normal values in cardiac catheterisation - PVR - Mixed venous sats - RA pressure - RV pressure - Mean PA pressure - LA pressure - LV pressure
``` PVR: <2 normal, 2-4 mild, 4-6 mod MIxed venous sats ~75% RA pressure 5 (<10) RV pressure 25/5 Mean PA pressure 15 (little variation) LA pressure 5-7 (<10) LV = systemic BP ```
47
Types of SVT (3)
Reentrant tachycardia using an accessory pathway eg. AVRT Reentrant tachycardia without an accessory pathway eg. AVNRT Ectopic tachycardia eg. JET
48
AVRT
Atroventricular reciprocating tachycardia Involves an accessory pathway MC SVT in infants Cause of SVT in WPW
49
AVNRT
Atrioventricular node reentry tachycardia SVT in association with syncope or exercise Rare in infants
50
Atrial flutter
Rare in children with structurally normal hearts- usually precipitated by large stretched atria Common following cardiac surgery
51
WPW - 2 types - ECG
AVRT using a bidirectional accessory pathway Orthodromic = normal QRS Antidromic = wide QRS, potential for AF and more serious arrhythmias eg. VF Short PR interval, delat wave
52
Single second heart sound (4)
Pulmonary or aortic atresia or severe stenosis, truncus arteriosus, transposition of the great arteries.

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