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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
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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
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33
Q

What is left anterior fascicular block? (3)

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

What is left posterior fascicular block? (3)

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

What is bifascicular block?

A

RBBB + either LAFB or LPFB

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36
Q

When does bifasciular block need invesitgating?

A

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

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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

75
Q

How do you know where the reciprocal changes should be on an ECG?

A

PAILS

Posterior
Anterior
Inferio
Lateral
Septal

76
Q

Crudely, how do LVADs work?

A

Drains blood from LV and ejects it into aorta

77
Q

What is the only LVAD system implanted in the UK?

A

Heartmate 3

78
Q

If an LVAD fails, what are the 2 issues?

A
  1. Dysfunctional LV may be unable to generate CO to sustain life
  2. No valves so if fail will be retrograde blood flow during diastole, making perfusion worse
79
Q

What/who can assist you when dealing with LVAD patients? (3)

A
  1. Most patients will have PSP (patient specific protocol)
  2. LVAD centre
  3. Family member will be trained well in how to use
80
Q

What should be done to check if an LVAD is working?

A
  1. Should be loud alarm from external controller
  2. Stethoscope over heart if not - should be humming
  3. Pulse unreliable
81
Q

Describe the LVAD troubleshooting algorithm? (6)

A
  1. Expose controller, power source and driveline
  2. Ensure driveline is firmly attached to controller
  3. Ensure that all connections between the controller and a working power source (charged battery or mains power) are secure
  4. Assess battery charge by pressing charge indicator button on battery. Replace with charged battery or mains power adaptor.
  5. Change controller - detatch driveline from old controller and connect with charged battery.
  6. Consider cable fracture - quickly but gently manipulate driveline to try to restore broken connection
82
Q

Following a patient becoming unresponsive/not breathing what should be done first?

A
  1. Don’t start CPR
  2. Ventilate if needed
  3. Trouble shoot LVAD - this is by far the most effective way to restore circulation
83
Q

Following the troubleshooting LVAD algorithm, if patient still not breathing/responsive what should be done? (3)

A
  1. ALS
  2. AP pads if delivering shock
  3. Contact LVAD centre
84
Q

If a patient with an LVAD is conscious but in VF/VT what should be done?

A

Urgent transfer to LVAD centre for sedation and cardioversion

85
Q

What are the expected circulatory parameters in someone with an LVAD? (4)

A
  1. CRT 2-3 secs
  2. No cyanosis/pallor
  3. Mean BP 60-90mmHg
  4. LVAD flow rate (where displayed) > 3L/min
86
Q

How should BP be measured in patient with LVAD?

A

Oximetry and NIBP unreliable

Arterial line - mean BP 60-90mmHg

87
Q

If a patient with an LVAD is felt to have impaired circulation, what should be attempted?

A

Straight leg raise +/- IVI

88
Q

Describe Wellens syndrome

A
  1. Biphasic or deeply inverted T-waves (V2-3)

plus

history of recent (and usually resolved) chest pain.

89
Q

What does Wellens syndrome represent?

A

Highly specific for critical stenosis of the left anterior descending (LAD) artery.

90
Q

What is the likely cause of a U wave on the ECG of a patient taking furosemide?

A

Hypokalaemia

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