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Exam > Cardiology > Flashcards

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
Q

Clinical features TAPVD with venous obstruction

A

Cyanosis and resp distress from birth
Infracardiac- cyanosis will be worse with feeding (oesophageal obstruction)
Loud single S2 and gallop
Signs of CCF

26
Q

Ebstein’s anomaly pathophysiology

- Can be associated with

A

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
Q

Ebstein’s anomaly presentation (mild and severe) and clinical features
- CXR

A

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
Q

PV stenosis types and associations

A

Valvular- Noonan’s
Infundibular- usually assoc with large VSD eg. ToF
Supravalvular- Williams

29
Q

Severity of PS- pressure gradient and ventricular pressures

A

Mild- <35-40mmHg, RV systolic pressure <50% LV
Mod: 40-70, RV 50-75% LV
Severe: >70mmHg or RV >75% LV pressures

30
Q

PS clinical features, OE, ECG, CXR

A

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
Q

ECG criteria for RAH

A

p wave >3mm

32
Q

DDx RAH on ECG (5)

A 
Tricuspid regurg
Pulm HTN
Ebstein's anomaly
Large late ASD
Tricuspid stenosis (rare)
33
Q

ECG criteria LAH

A

> 2.5 small squares long, bifid p wave

>2 small squares in infants

34
Q

DDx LAH on ECG (5)

A 
MR (most common)
Big VSD leading to dilated LA
MS (eg. post rheumatic fever)
Large PDA with shunt
Severe LVH (untreated)
35
Q

DDx LAD on ECG

A

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
Q

RVH on ECG

A

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
Q

LVH on ECG

A

V6 R >5 large squares

V6 ST depression and T waves inversion

38
Q

DDx Q wave in V1 (4)

A

L-TGA
Single ventricle
Severe RVH
Anterior MI

39
Q

DDx cardiac defects that will be symptomatic during fetal life (2)

A

Valve regugitation- TR, ECD, truncus (volume loads the ventricle)
Arrhythmia

40
Q

DDx cardiac defects that cause a critically ill neonate in the first 24 hours (4)

A

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
Q

DDx cardiac defects that present 24 hours to 2 weeks when duct closes (7)

A

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
Q

DDx cardiac defects that present 2-6 weeks once pulmonary vascular resistance falls (7)

A 
VSD with CoA (early failure)
Large VSD
Large PDA
Large AVSD
Truncus
ToF with pulm atresia
Single ventricle with no PS
43
Q

DDx asymptomatic mumur (7)

A 
Functional/benign
ASD
VSD
PS
Mild- mod AS
Small PDA
CoA
44
Q

Fick principle

A

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
Q

Poiseullie equation

A

Used to calculate pulmonary vascular resistance

PVR = mean PA p - LA p / pulmonary blood flow

46
Q

Normal values in cardiac catheterisation

  • PVR
  • Mixed venous sats
  • RA pressure
  • RV pressure
  • Mean PA pressure
  • LA pressure
  • LV pressure
A 
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
Q

Types of SVT (3)

A

Reentrant tachycardia using an accessory pathway eg. AVRT
Reentrant tachycardia without an accessory pathway eg. AVNRT
Ectopic tachycardia eg. JET

48
Q

AVRT

A

Atroventricular reciprocating tachycardia
Involves an accessory pathway
MC SVT in infants
Cause of SVT in WPW

49
Q

AVNRT

A

Atrioventricular node reentry tachycardia
SVT in association with syncope or exercise
Rare in infants

50
Q

Atrial flutter

A

Rare in children with structurally normal hearts- usually precipitated by large stretched atria
Common following cardiac surgery

51
Q

WPW

  • 2 types
  • ECG
A

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
Q

Single second heart sound (4)

A

Pulmonary or aortic atresia or severe stenosis, truncus arteriosus, transposition of the great arteries.

Exam (16 decks)

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