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Cardiology Flashcards

1
Q

When do NICE say an angiogram should be performed following a STEMI?

A

< 12 hours or <120 mins of when fibrinolysis could have been given

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2
Q

What drug therapy does NICE recommend if undergoing medical management only of STEMI (3)

A
  1. Aspirin
  2. Ticagrelor (clopidogrel or only aspirin if increased bleeding risk)
  3. LMWH
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3
Q

What drug therapy dose NICE recommend in a STEMI going to cath lab?

A
  1. Aspirin
  2. Prasugrel (if on anticoagulant then clopidogrel)
  3. UFH
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4
Q

What does NICE recommend for STEMI being thrombolysed?

A
  1. Aspirin
  2. LMWH/UFH at same time as:
  3. Fibronlysis
  4. Ticagrelor (unless increased bleeding risk, then clopidogrel)
  5. ECG 60-90mins later and if not improved transfer PCI
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5
Q

What treatment does NICE recommend for NSTEMI?

A
  1. Aspirin
  2. LMWH (unless cath lab)
  3. Ticagrelor unless high bleeding risk then clopidogrel or cath lab (prasugrel)
  4. GRACE risk score then decide angiogram < 72 hours or considering ischaemia testing (low risk = <3%)
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6
Q

What are Scarbossa’s Criteria and which bits are the most and least sensitve?

A
  1. Concordant STE >1mm in 1 or more leads (most sensitive) (5 points)
  2. Concordant ST depression >1mm V1-3 (3 points)
  3. Discordant ST elevation >5mm (2 points)

3 or more needed

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7
Q

What are the signs on an ECG of RV infarct? (2)

A

STE VI suggest RV involvemnet
STE V4R highly specific

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8
Q

What part type of MI is right ventricular infarct usually a part of?
What is managed differently about RV infarct?

A

Inferior
Very pre-load sensitive, may need fluid and nitrates can lead to hypotension

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9
Q

What defines a pathological Q wave? (4)

A
  1. > 40ms (1mm) wide
  2. > 2mm deep
  3. > 25% depth QRS
  4. any in V1-3
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10
Q

Causes of acute heart failure:
CHAMPIT

A

C - acute Coronary Syndrome
H - ypertensive emergency
A - rrhythmia
M - echanical cause
P - E
I - infections (myocarditis)
T - amponade

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11
Q

What are first line agents to rate control AF according to NICE? (3)

A
  1. Beta blocker
  2. CCB
  3. Digoxin if very sedentary
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12
Q

What does NICE recommend if 1st line treatment not managing rate for AF?

A

Add second agent e.g beta blocker/CCB/ digoxin

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13
Q

When is flecainide c/i?

A

IHD/structural heart disease

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14
Q

What is first line agent for long term rhythm control according to NICE?

A

Beta blocker

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15
Q

What medical cardioversion does NICE recommend in AF if CCF/LVF?

A

Amioderone

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16
Q

What rate controlling agent does NICE recommend avoiding in AF with decompensated CCF?

A

CCB

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17
Q

Which group should avoid ACEinh and ARBs in particular?

A

Pregnancy

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18
Q

How do you calculate rate on an ecg? (3)

A
  1. 300 divided by no. of large squares between R waves
  2. 1500 divided by number of small squares between R waves
  3. Number of R waves in rhythm strip x 6
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19
Q

What are u waves?

A

Small deflection after the T wave

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20
Q

What are prominent u waves? (2)

A
  1. > 1-2mm
  2. > 25% height of T wave
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21
Q

What are the causes of U - waves (5)

A
  1. Low K+
  2. Low Ca2+
  3. Low Mg2+
  4. Bradycardia
  5. Increased ICP
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22
Q

What are inverted u-waves specific for?

A

CAD - particularly in context of chest pain

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23
Q

What is an AVNRT?

A

AV nodal re-entrant tachycardia.
Functional re-entry circuit within the AV node
‘Classic’ SVT

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24
Q

What helps distinguish AVNRT for orthodromic AVRT on ECG?

A

AVNRT -Pseudo R’ waves V1/2.
P waves either buried in QRS or partially seen in terminal part of QRS leading to pseudo R’ waves

AVRT - retrograde P waves occur later, usually notch in T wave

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25
Q

What is AVRT

A

AV re-entry tachycardia
Pre-excitation

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26
Q

What is orthodromic AVRT?

A

Antegrade pathway with AV node therefore looks very similar or AVNRT

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27
Q

What is antidromic AVRT?

A

Antegrade pathway via accessory pathway therefore widened QRS and looks like VT

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28
Q

How do we treat orthodromic AVRT?

A

Adenosine

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29
Q

How do we treat antidromic AVRT?

A

Procainamide (adenosine blocks AV node and always a chance of precipitating AF, if this was conducted via AP would lead to arrest)

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30
Q

What ECG changes are found in WPW? (4)

A
  1. PR <120ms
  2. Delta waves
  3. QRS >110ms
  4. Discordant ST/T wave changes
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31
Q

What is a type A WPW pattern? (3)

A
  1. Dominant R wave V1
  2. TWI VI-3
  3. Left sided
32
Q

What is a type B WPW pattern? (3)

A
  1. Dominant S wave V1
  2. Tall R waves and TWI inversion V4-6 - pseudo LVH pattern
  3. Right sided
33
Q

What is left anterior fascicular block? (3)

A
  1. LAD
  2. qR complex I, aVL
  3. rS complex II,III,aVF
34
Q

What is left posterior fascicular block? (3)

A
  1. RAD
  2. rS complex I, aVL
  3. qR complex II,III,aVF
35
Q

What is bifascicular block?

A

RBBB + either LAFB or LPFB

36
Q

When does bifasciular block need invesitgating?

A

Pre-syncope/syncope
Has 1-4% progression to CHB per year

37
Q

What is true trifascicular blocl

A

3 degree Hb + RBBB + LAFB/LAFP

38
Q

What do some people describe as trifascicular block and what is its risk of becoming CHB?

A
  1. First degree HB + RBBB + LAFB/LPFB
  2. 1-4% - same as bifascicular block
39
Q

What is an epsilon wave?

A

Small deflection and end of QRS complex
ARVD - 50% have epsilon waves

40
Q

What is the name of the leads that are used to increase the sensitivity of epsilon waves?

A

Fontaine leads

41
Q

What 3 features in electrical alterans?

A
  1. Tachycardia
  2. Low voltage QRS
  3. Consecutive normally conducted QRS that vary in height
42
Q

In what condition is eletrical alterans found?

A

Massive pericardial effusion

43
Q

What is Mobitz type I

A

Wenckebach

44
Q

What is Mobitz type II

A

Intermittently non-conducted p-waves

45
Q

What is Wellens syndome?

A

Clinical syndrome characterised by bipashic or deep T wave inversion V2-3 and a history of recent chest pain, now resolved. Strongly suggestive of critical LAD stenosis

46
Q

What is Brugada sign?

A

Coved ST elevation >2mm in more than one of V1-3 followed by a negative T wave

Only sign that is potentially diagnostic

47
Q

Aside from ECG changes, what are the clinical criteria for Brugada? (6)

A

One of:
1. Document VT/VF
2. FHx: SCD < 45 years
3. Coved type ECGs in family members
4. Inducible VT with programmed electrical stimulation
5. Syncope
6. Noctural agonal respiration

48
Q

What does pre-excited AF look like on ECG?

A

Wide complex, irreg/irreg tachycardia with variable QRS morphology + fast (>200bpm)

Can look like AF with BBB (but this is slower) torsade des pointes (but without the twisting morphology)

49
Q

What is the treatment for stable pre-excited AF?

A

IV Procainamide

50
Q

What drugs should not be given in pre-excited AF?

A

Any AV nodal blocking drugs - VF + arrest

51
Q

What is different between Torsades de Pointes and polymorphic VT?
1.ECG
2. Cause
3. Tx

A
  1. TdP ECG ‘twisting’ around isoelectric line
  2. Caused specifically by QT prolongation
  3. Magnesium
52
Q

What does the Right Ventricular Outflow Tract Tachycardia (RVOT) ECG look like? (2)

A
  1. LBBB pattern
  2. RAD

NB QRS usually <140ms unlike VT

53
Q

What part of the history can be useful in distinguishing RVOT from other causes of VT?

A

Usually no hx of IHD/structural heart disease + relatively young/well patients

54
Q

How can RVOT be treated?

A

If confident of diagnosis treat as SVT (adenosine, beta blocker, calcium anatagonist)

55
Q

What can help differentiate RVOT and VT?

A

The degree of QRS widening:

QRS 110-140 in RVOT
VT it’s usually > 140
This can make it look like SVT

+ VT less likely to have LBBB morphology

56
Q

What is a simple clue that suggests AF with aberrancy/pre-excitation over polymorphic VT?

A

Polymorphic VT not sustained and usually leads to VF and arrest

57
Q

In which types of MI should we be careful/avoid GTN?

A

Inferior STEMI, particularly with evidence of RV infarction

58
Q

Which STEMIs can lead to second and third degree HB and what percentage of these do so?

A

Inferior
20%

59
Q

In NSTEMIs following aspirin what is the second medication that NICE say should be given immediately after?

60
Q

What are the ECG features of AVRD (5)

A
  1. T wave inversion in right precordial leads V1-3, in absence of RBBB (85% of patients)
  2. Epsilon wave (most specific)
  3. Localised QRS widening in V1-3 (> 110ms)
  4. Ventricular ectopy of LBBB morphology, with frequent PVCs
  5. Paroxysmal episodes of ventricular tachycardia (VT) with LBBB morphology (RVOT tachycardia)
61
Q

What are Lewis leads?

A

Lead placements that allows better visualisation of p waves

62
Q

What leads have inverted T waves normally and what is a normal variant?

A
  1. aVR and V1
  2. III
63
Q

What are the ECG changes in the 3 types of Brugada?

A

Type 1 - coved STE over 2mm in V1-3 with TWI
Type 2 - over 2mm ‘saddleback’ STE, no TWI
Type 3 - morphology of either 1 or 2 but < 2mm STE

64
Q

Which is the only ECG type of Brugada that is potentially diagnostic?

65
Q

What areas to the following supply?
1. RCA
2. LAD
3. LCx

A
  1. RA, RV, SA node and AV node (90% patients)
  2. Septum and anterior LV
  3. LA and post-lat LV
66
Q

What thrombolytic agents are preferred pre-hospital? (2)

A

Tenecteplase and reteplase

67
Q

What is the dose of tenecteplase and when should it be given?

A

30-50mg over 10 mins and within 6 hours of symptoms

68
Q

When should tenectaplase be avoided (aside from usual c/i)

A

Hx of gentamicin anaphx (containts trace gentamicin)

69
Q

What are the common side effects of tenecteplase? (5)

A
  1. Anaphx
  2. Hypotension
  3. Cardiac arrest
  4. IC haemorrhage
  5. Pulmonary oedema
70
Q

What are the pacemaker codes (anti-bradycardia PPM)

A

First letter = chamber paced
0 - no chamber paced
V - ventricle
A - atria
D - dual

Second letter = chamber sensed
0 = No chamber sensed
V = ventricle
A = atria
D = Dual

Third letter = response to senses rhythm
0 - no response
T - triggered
I - Inhibted
D - dual (triggered and inhibited)

71
Q

What is the Bezold-Jarisch reflex?

A

Cardioinhibitory reflex of:
- bradycardia
- hypotension
- apneoas

  • Caused by stretch receptors in left ventricle stimulated when poorly filled LV.
  • triggers vagus nerve and inhibits vasopressin
  • thought to be protective reflex seen in acute MIs and associated with coronary
    vasospasm
  • seen in posterior/inf MIs and triggers coronary vasodilation
72
Q

In what MI do you sometimes get bradycardia/hypotension/apnoeas and why?

A

Inferior or posterior

Due to Bezold-Jarisch Reflex

73
Q

What is ventricular standstill/ p wave asystole?

A

Very high AV block leads to complete loss of QRS and mechanical activity e.g. just p waves on ECG

Will lead to collapse is short duration or arrest if prolonged

74
Q

What is the managment for pwave asystole/ ventricular standstill?

A

If not in arrest, pacing

FIMC (17 decks)

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