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Sheff Phase 4 > Cardio > Flashcards

Cardio Flashcards

1
Q

3 Causes of LBBB

A 
hypertension,
 aortic stenosis,
 acute MI,
 coronary artery disease 
 primary conducting system disease,
infection
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2
Q

Primary heart block findings

A

fixed prolonged PR interval (>200 ms)

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3
Q

Seen in LAD

A

Lead I has the most positive deflection

Leads II and III are negative

[Seen in conduction defects]

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4
Q

RAD?

A

Lead III has the most positive deflection

Lead I should be negative

[This is commonly seen in individuals with right ventricular hypertrophy]

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5
Q

PR interval length?

A

120-200ms [3-5 small squares]

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6
Q

2nd degree heart block type 1 findings?

A

PR interval slowly increases then there is a dropped QRS

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7
Q

2nd degree type 2 heart block findings

A

PR interval is fixed but there are dropped beats

[Make sure you clarify that by the frequency of dropped beats e.g 2:1, 3:1, 4:1]

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8
Q

3rd degree heart block

A

P waves and QRS complexes are completely unrelated

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9
Q

Where do the pathologies causing heart block types occur?

A

1: between the SA node and the AV node (i.e. within the atrium)

2: Mobitz I (Wenckebach) – occurs IN the AV node.
[This is the only piece of conductive tissue in the heart which exhibits the ability to conduct at different speeds]
Mobitz II – occurs AFTER the AV node in the bundle of His or Purkinje fibres

3:Occurs anywhere from the AV node down

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10
Q

2 reasons for a shortened PR?

Seen in the pathological cause on ECG?

A

SA node location can vary / people have small atria

Accessory pathway
Slurred upstroke o= delta wave

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11
Q

2 reasons for a shortened PR?

Seen in the pathological cause on ECG?

A

SA node location can vary / people have small atria

Accessory pathway
Slurred upstroke o= delta wave

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12
Q

What is a narrow / broad QRS

A

NARROW (< 0.12 seconds)

BROAD (> 0.12 seconds)

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13
Q

Why do you get broad QRSs

A

BBB
Ventricular ectopic

Conduction system defects

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14
Q

What should be seen in Anterior chest lead R waves?

A

R wave pregression

small in V1 to large in V6

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15
Q

What is the J pount

A

where S wave joins ST

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16
Q

When is ST elevaiton significant ?

A

greater than 1 mm (1 small square) in 2 or more limb leads

or >2mm in 2 or more chest leads.

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17
Q

When is ST depression significant

A

≥ 0.5 mm in ≥ 2 leads

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18
Q

2 times you get tall T waves

A

Hyperkalaemia (“Tall tented T waves”)

Hyperacute STEMI

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19
Q

Where are T waves normally inverted

A

V1

lead 3

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20
Q

3 causes of T wave inversion

A

Ischaemia
Bundle branch blocks (V4 – 6 in LBBB and V1 – V3 in RBBB)
Pulmonary embolism
Left ventricular hypertrophy (in the lateral leads)
Hypertrophic cardiomyopathy (widespread)
General illness

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21
Q

Biphasic T wave seen in ?

A

Ischaemia and hypokalaemia

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22
Q

When might you see U waves/

A

electrolyte imbalances
hypothermia

antiarrhythmic therapy (such as digoxin, procainamide or amiodarone).

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23
Q

RBBB where is the RsR wave?

A

v6 [2 peaks]

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24
Q

Drugs for rate control of AF

A

β-blockers and calcium-channel antagonists.

[Digoxin]

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25
Q

Prescribe with AF rate control

A

anticoagulation eg Warfarin

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26
Q

name 3 ways/drugs for rhythm control

A

amiodarone, flecainide, dronedarone

and/or DC cardioversion and/or ablation therapy

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27
Q

Name 2 causes of raised troponin T

A

a. Cardiac ischaemia
b. Cardiac arrhythmia
c. Pneumonia
d. Pulmonary embolism.

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28
Q

Drugs used for HTN that can cause heart block

A

beta-blockers and

the non-dihydropyridine calcium-channel antagonists, EG verapamil

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29
Q

3rd-degree heart block - what drug might you use? more permanent fix?

A

Atropine

transcutaneous pacing via a defibrillator

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30
Q

2nd degree heart block causes? name 3

Mx if no reversible cause found?

A

ischaemic heart disease, sarcoidosis, Lyme
disease, thyroid disease, strong parasympathetic response,
drugs such as digoxin and verapamil.

Pacemaker

31
Q

Treatment options for SVT

A 
Vagal manoeuvres (blowing hard against closed lips, cold
water splashed into face, carotid massage)

adenosine

BB/CCB/ flecanide/amiodarone (not digoxin)

direct current (DC)
cardioversion.
32
Q

What medication is contraindicated in WPW ?

Mx of WPW

A

Digoxin – this drug will slow AV (atrioventricular)
node conduction exclusively and therefore encourage conduction along the accessory
pathway.

accessory pathway ablation

33
Q

Which leads meaure inferior?

A

II, III, aVF

34
Q

Which leads are lateral

A

I, aVL, v5, v6

35
Q

Inferior STEMI - what is likely artery? What else does it supply?
2 other Comps?

A

Right coronary artery
AV node -> complete heart block

Other comps:
ventricular arrhythmia, reduced left ventricular
function leading to acute left ventricular failure,
right ventricular failure, ischaemic ventricular septal defect
acute mitral regurgitation due to papillary muscle
rupture.

36
Q

Why might you get a ‘cannon wave’ raised JVP in compete heart block?

A

RA contacts against closed tricusid valve [due to heart block]
->blood shoots up jugular vein

37
Q

Mx of severe AS

A

TAVI -transcatheter valve implant
Open valve repair
[Balloon valvuloplasty - usually for palliative / awaiting definitive treatment]

38
Q

2 reasons for a shortened PR?

Seen in the pathological cause on ECG?

A

SA node location can vary / people have small atria

Accessory pathway
Slurred upstroke o= delta wave

39
Q

What is a narrow / broad QRS

A

NARROW (< 0.12 seconds)

BROAD (> 0.12 seconds)

40
Q

Why do you get broad QRSs

A

BBB
Ventricular ectopic

Conduction system defects

41
Q

What should be seen in Anterior chest lead R waves?

A

R wave pregression

small in V1 to large in V6

42
Q

What is the J pount

A

where S wave joins ST

43
Q

When is ST elevaiton significant ?

A

greater than 1 mm (1 small square) in 2 or more limb leads

or >2mm in 2 or more chest leads.

44
Q

When is ST depression significant

A

≥ 0.5 mm in ≥ 2 leads

45
Q

2 times you get tall T waves

A

Hyperkalaemia (“Tall tented T waves”)

Hyperacute STEMI

46
Q

Where are T waves normally inverted

A

V1

lead 3

47
Q

3 causes of T wave inversion

A

Ischaemia
Bundle branch blocks (V4 – 6 in LBBB and V1 – V3 in RBBB)
Pulmonary embolism
Left ventricular hypertrophy (in the lateral leads)
Hypertrophic cardiomyopathy (widespread)
General illness

48
Q

Biphasic T wave seen in ?

A

Ischaemia and hypokalaemia

49
Q

When might you see U waves/

A

electrolyte imbalances
hypothermia

antiarrhythmic therapy (such as digoxin, procainamide or amiodarone).

50
Q

RBBB where is the RsR wave?

A

v6 [2 peaks]

51
Q

Drugs for rate control of AF

A

β-blockers and calcium-channel antagonists.

[Digoxin]

52
Q

Prescribe with AF rate control

A

anticoagulation eg Warfarin

53
Q

name 3 ways/drugs for rhythm control

A

amiodarone, flecainide, dronedarone

and/or DC cardioversion and/or ablation therapy

54
Q

Name 2 causes of raised troponin T

A

a. Cardiac ischaemia
b. Cardiac arrhythmia
c. Pneumonia
d. Pulmonary embolism.

55
Q

Drugs used for HTN that can cause heart block

A

beta-blockers and

the non-dihydropyridine calcium-channel antagonists, EG verapamil

56
Q

3rd-degree heart block - what drug might you use? more permanent fix?

A

Atropine

transcutaneous pacing via a defibrillator

57
Q

2nd degree heart block causes? name 3

Mx if no reversible cause found?

A

ischaemic heart disease, sarcoidosis, Lyme
disease, thyroid disease, strong parasympathetic response,
drugs such as digoxin and verapamil.

Pacemaker

58
Q

Treatment options for SVT

A 
Vagal manoeuvres (blowing hard against closed lips, cold
water splashed into face, carotid massage)

adenosine

BB/CCB/ flecanide/amiodarone (not digoxin)

direct current (DC)
cardioversion.
59
Q

What medication is contraindicated in WPW ?

Mx of WPW

A

Digoxin – this drug will slow AV (atrioventricular)
node conduction exclusively and therefore encourage conduction along the accessory
pathway.

accessory pathway ablation

60
Q

Which leads meaure inferior?

A

II, III, aVF

61
Q

Which leads are lateral

A

I, aVL, v5, v6

62
Q

Inferior STEMI - what is likely artery? What else does it supply?
2 other Comps?

A

Right coronary artery
AV node -> complete heart block

Other comps:
ventricular arrhythmia, reduced left ventricular
function leading to acute left ventricular failure,
right ventricular failure, ischaemic ventricular septal defect
acute mitral regurgitation due to papillary muscle
rupture.

63
Q

Why might you get a ‘cannon wave’ raised JVP in compete heart block?

A

RA contacts against closed tricusid valve [due to heart block]
->blood shoots up jugular vein

64
Q

Mx of severe AS

A

TAVI -transcatheter valve implant
Open valve repair
[Balloon valvuloplasty - usually for palliative / awaiting definitive treatment]

65
Q

Pt comes in with central crushing chest pain…Hx HTN

XR shows mediastinal widening …. what is it?

A

Aortic dissection

66
Q

Type A vs B dissection? Mx?

A

type A
(involves ascending aorta/arch proximal to the origin of the left subclavian artery)
REQUIRES SURGERY

type B
(where the dissection involves the aorta distal to the left subclavian artery origin).
Can be managed conservatively

67
Q

In VT what is usual Mx option?

What if they are stable?

A

DC cardiovert

correct electrolytes, amiodarone, beta-blockers
[this is uncommon]

68
Q

3 most common bugs for IE

A

a. Staphylococcus aureus
b. Streptococcus viridans
c. Enterococcus spp.

69
Q

PE ECG findings

A

S wave in lead I
Q wave in lead III,
Inverted T wave in lead III.

70
Q

Becks triad

A

Muffled heart sounds with hypotension + raised JVP

71
Q

Atrial flutter Mx

A

DC cardiovert

radiofrequency ablation - for long term

72
Q

Name 3 causes of pericarditis

A

a. Viral – in particular coxsackie, cytomegalovirus, herpes virus and HIV
b. Immune conditions, such as systemic lupus erythematosus
c. Myocardial infarction (MI) (Dressler’s syndrome – usually occurring 2 weeks
post-MI)
d. Trauma to the heart
e. Uraemia
f. Malignancy (as a paraneoplastic phenomenon)

73
Q

Pericarditis - what positions make it better/worse

A

The worsening of pain when lying down,

alleviated on sitting forward

Sheff Phase 4 (26 decks)

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