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phase iii internal medicine > cardiology: ecg > Flashcards

cardiology: ecg Flashcards

1
Q

purpose of performing ecg

A

1) physiologic parameters
2) coronary blood supply
3) conduction system
4) electrolyte abnormalities
5) structural problems
6) infection/inflammation
7) drugs (SE/toxicity)
8) extra cardiac disease (respi/thyroid)
9) physiological response (fever, fear, anxiety, hypovolemic shock, vasovagal syncope)
10) trauma

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2
Q

what is the tetrad in tetralogy of fallot

A

1) rvh
2) ps
3) overriding aorta
4) vsd

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3
Q

draw and label components of ecg

A

1) PR interval
2) PR segment
3) QRS interval
4) ST interval
5) ST segment
6) QT interval
7) RR interval

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4
Q

2 key characteristics of SA node

A

1) automaticity

2) intrinsic rate

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5
Q

avn does not allow 1:1 conduction beyond ___

A

150

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6
Q

position of v1 lead

A

4th intercostal space to the right of sternum

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7
Q

position of v2 lead

A

4th intercostal space to the left of sternum

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8
Q

position of v4 lead

A

5th intercostal space mid clavicular line

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9
Q

position of v3 lead

A

directly between v2 and v4

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10
Q

position of v5 lead

A

level with v4 at left anterior axillary line

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11
Q

position of v6 lead

A

level with v5 at left midaxillary line

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12
Q

bipolar lead I

A

RA & LA

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13
Q

bipolar lead II

A

RA & LL

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14
Q

bipolar lead III

A

LA & LL

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15
Q

augmented unipolar lead aVR

A

RA

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16
Q

augmented unipolar lead aVL

A

LA

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17
Q

augmented unipolar lead aVF

A

LL

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18
Q

what surface/region/coronary artery of the heart do leads I, II, aVL look at?

A

left lateral surface
LV
LCx

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19
Q

what surface/region/coronary artery of the heart do leads II, III, aVF look at?

A

inferior surface
mainly RV (some LV)
RCA

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20
Q

what surface/region/coronary artery of the heart do leads V1, V2 look at?

A

anteroseptal region
mainly LV
LAD

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21
Q

what surface/region/coronary artery of the heart do leads V3, V4 look at?

A

IV septum and LV
LV
LCx

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22
Q

what surface/region/coronary artery of the heart do leads V5, V6 look at?

A

anterior/lateral wall of LV
LV
LCx

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23
Q

what surface/region/coronary artery of the heart does lead avR look at?

A

lateral surface

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24
Q

what surface/region/coronary artery of the heart does lead avR look at?

A

lateral surface

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25
Q

physiological significance of P wave

A

depolarisation of atria in response to SA node triggering

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26
Q

physiological significance of PR interval

A

delay of AV node to allow filling of ventricles

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27
Q

physiological significance of QRS complex

A

depolarisation of ventricles

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28
Q

physiological significance of ST segment

A

beginning of ventricle repolarisation (should be flat)

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29
Q

physiological significance of T wave

A

ventricular repolarisation

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30
Q

what does size of QRS complex represent?

A

muscle mass

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31
Q

approach to interpreting ecg

A

1) check normal features first (speed, scale)

2) 7+2 step plan

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32
Q

what does each large square on ecg represent?

A

200ms (0.2s)

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33
Q

what does each small square on ecg represent?

A

40ms (0.04s)

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34
Q

what is the scale of an ecg?

A

10mm/mV

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35
Q

what are the 7 +2 steps of an ecg?

A

7 steps:

1) rhythm
2) rate
3) conduction interval
4) heart axis
5) p wave
6) qrs complex
7) st segment

+2 steps:

1) compare with previous ecg
2) conclusion

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36
Q

maximum height of P waves in sinus rhythm in leads II and/or III

A

2.5mm

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37
Q

what is considered tachycardia?

A

> 100bpm

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38
Q

what is considered narrow complex tachycardia?

A

QRS < 120ms

>100bpm

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39
Q

types of REGULAR narrow complex tachycardia

A

1) sinus tachycardia
2) atrial tachycardia
3) atrial flutter with fixed conduction
4) SVT: AV nodal re-entry tachycardia (AVNRT), orthodromic AVRT, junctional tachycardia

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40
Q

causes of sinus tachycardia

A
  • fever
  • pain
  • sepsis
  • hypovolemia/haemorrhage
  • drugs: adrenaline, atropine, antihistamines, b agonists, sympathomimetics, GTN
  • endocrine: thyrotoxicosis
  • serious life threatening conditions: myocarditis, pulmonary embolism, CCF, ectopic pregnancy
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41
Q

what is considered wide complex tachycardia?

A

QRS > 120ms

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42
Q

what criteria describes the features of VT?

A

brugada criteria

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43
Q

features of VT based on brugada criteria

A
  • fusion beats
  • absence of RS complex in precordial leads
  • concordance in precordial leads (all QRS upwards or downwards)
  • RS interval > 100ms
  • AV dissociation
  • atypical LBBB
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44
Q

features of AVNRT

A
  • regular, 180-250/min
  • P in QRS complex (resulting in RsR’ in V1)
  • young patients and paroxysmal
  • treatment: valsalva/carotid massage/adenosine
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45
Q

what type of wide complex tachycardia is torsades de pointes?

A

polymorphic ventricular tachycardia

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46
Q

how does torsades de pointes usually present?

A

pulseless in cardiac arrest

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47
Q

treatment for torsades de pointes?

A

IV MgSO4 1g x 1-2 doses

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48
Q

usual demographic for VT

A

older patient with previous MI

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49
Q

reference range for bradycardia

A

<60bpm

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50
Q

reference range for 1st degree heart block

A

PR interval > 200ms (>1 large square/>5 small squares)

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51
Q

types of second degree heart block

A

1) mobitz I (wenckebach phenomenon)

2) mobitz II

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52
Q

describe mobitz I heart block

A

progressive PR interval prolongation culminating in non-conducted P wave (usually benign)

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53
Q

usual wenckebach pattern of P:QRS

A

3: 2
4: 3
5: 4

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54
Q

cause of mobitz I heart block

A

reversible conduction block at AV node

  • drugs; bb, ccb, digoxin, amiodarone
  • increased vagal tone in athletes
  • MI
  • myocarditis
  • post cardiac surgery
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55
Q

describe mobitz II heart block

A

intermittent non-conducted P waves without progressive prolongation of PR interval

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56
Q

cause of mobitz II heart block

A

failure of conduction at level of his-purkinje system

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57
Q

mobitz II is more likely than mobitz I to be associated with _____ , _____ and progression to ____ ?

A

haemodynamic compromise
severe bradycardia
3rd degree heart block

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58
Q

describe 3rd degree heart block

A

no relationship between p wave and qrs complex (absence of AV conduction)

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59
Q

typical presentation of 3rd degree heart block

A

severe bradycardia with av dissociation (independent atrial and ventricular rates)

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60
Q

method to calculate HR on ecg

A

300/number of large squares between 2 consecutive R waves

OR

no. of QRS complexes in rhythm strip x 6

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61
Q

normal PR interval

A

120-200ms (3-5 squares)

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62
Q

conduction interval in WPW syndrome

A

PR interval <120ms + delta wave

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63
Q

PR interval <120ms without delta wave

A

lown-ganong-levine syndrome

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64
Q

normal QTc interval

A

<420ms in men

<450ms in women

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65
Q

formula for calculation of QTc

A

bezett’s formula

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66
Q

what is bezett’s formula?

A

QTc = QT interval/ (RR)^1/2

QTc: corrected QT interval
QT interval: Q wave to end of T wave
RR: time from 2 consecutive RR waves

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67
Q

reference range for prolonged QTc

A

> 450ms

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68
Q

causes of prolonged QTc

A

1) electrolyte imbalances (hypokalemia/calcemia/magnesemia)
2) hypothermia
3) raised ICP
4) post MI
5) congenital long QT syndromes (romano-ward syndrome, jervell and lange nielsen)
6) drugs

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69
Q

inheritance pattern of romano-ward syndrome

A

AD

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70
Q

inheritance pattern of jervell and lange-nielsen

A

AR

a/w congenital deafness

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71
Q

drugs which cause prolonged QTc interval

A

1) antipsychotics
2) type IA, IC and III anti arrhythmics
3) tricyclic antidepressants
4) antihistamines
5) others: chloroquines, hydroxychloroquine, quinine, macrolides (erythromycin, clarithromycin)

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72
Q

reference range for shortened QTc

A

<350ms

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73
Q

causes of shortened QTc

A

1) hypercalemia
2) congenital short QT syndrome (K+ channel defect - AD)
3) digoxin effect

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74
Q

normal cardiac axis

A

-30deg to +90deg

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75
Q

causes of left axis deviation (lead I +ve and AVF -ve)

A
  • may be normal in short and fat individuals
  • LVH
  • RV infarct
  • L anterior hemiblock
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76
Q

causes of right axis deviation (lead I -ve and AVF +ve)

A
  • may be normal in tall and thin individuals
  • RVH
  • congenital diseases involving R heart
  • LV infarct
  • L posterior hemiblock (rare)
  • dextrocardia
  • reversal of arm leads
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77
Q

normal PR interval

A

0.12-0.2s

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78
Q

describe p wave in p pulmonale

A

peaked, tall P wave

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79
Q

height in p wave on inferior leads (II, III, aVF) in p pulmonale

A

> 2.5mm

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80
Q

height of p wave in V1 and V2 in p pulmonale

A

> 1.5mm

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81
Q

causes of p pulmonale

A

1) cor pulmonale
2) tricuspid stenosis
3) congenital heart disease (pulmonary stenosis, ToF, primary pulmonary HTN)

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82
Q

causes of absent p wave

A

1) AF

2) junctional/ventricular rhythm

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83
Q

describe p wave in p mitrale

A

bifid, broad

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84
Q

what does p mitrale indicate

A

LA enlargement

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85
Q

what does p pulmonale indicate

A

RA enlargement

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86
Q

p mitrale is a precursor to ____

A

AF

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87
Q

appearance of p wave in lead II in p mitrale

A

bifid p wave >40ms between both peaks

total p wave duration >110ms

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88
Q

appearance of p wave in lead V1 in p mitrale

A

biphasic p wave with terminal negative portion >40ms

terminal negative portion > 1mm deep

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89
Q

causes of p mitrale

A

1) mitral stenosis (classical)
2) mitral regurgitation
3) systemic HTN
4) aortic stenosis
5) HOCM

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90
Q

causes of p wave inversion

A

ectopic atrial rhythm e.g. MAT

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91
Q

normal duration of QRS complex

A

≤ 120ms (3 small squares)

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92
Q

causes of pathologic Q waves in V1/V2

A

old STEMI

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93
Q

what is the index for voltage criteria of LVH?

A

sokolow-lyon-index

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94
Q

what is the voltage criteria for LVH according to the sokolow-lyon index?

A

R in V5/V6 + S in V1 > 35mm

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95
Q

normal R wave progression

A

R increases V1-V5

R>S beyond V3

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96
Q

types of abnormal R wave progression

A

1) no R wave
2) exaggerated R wave progression
3) reversed R wave progression
4) small R waves with little progression

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97
Q

what does absence of R wave indicate

A

evolved/old anterolateral STEMI (+ Q waves)

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98
Q

what does exaggerated R wave progression indicate

A

LVH

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99
Q

what does reversed R wave progression indicate

A

RVH

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100
Q

what does small R waves with little progression indicate

A

pericardial effusion

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101
Q

5 causes of large R waves in V1

A

1) dextrocardia
2) RVH
3) posterior AMI
4) type A WPW
5) RBBB

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102
Q

causes of microvoltages (<5mm) of QRS complex

A

1) cardiac tamponade/pericardial effusion/pericarditis
2) hypothyroidism
3) pleural effusion/pneumothorax
4) cardiomyopathy (e.g. amyloidosis)
5) COPD (hyperinflated chest + leads located far away from heart)
6) obesity (thick chest wall + leads located far away from heart)

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103
Q

causes of widened QRS complexes (>3 small squares)

A

1) BBB
2) pre excitation (WPW)
3) ventricular extrasystoles/VT
4) complete heart block

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104
Q

causes of ST elevation (>1mm)

A

1) AMI (STEMI)
2) coronary vasospasm (printzmetal’s angina)
3) pericarditis
4) benign early repolarisation
5) hyperkalemia
6) LBBB
7) LVH
8) ventricular aneurysm
9) ventricular paced rhythm
10) raised ICP
11) brugada syndrome

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105
Q

features of pericarditis on ecg

A

1) globally raised ST segments
2) saddle shaped ST elevations
3) PR depression in all leads
4) PR elevation in aVR

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106
Q

appearance of T waves in hyperkalemia

A

tall tented T waves

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107
Q

cause of brugada syndrome

A

mutation in na+ channel

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108
Q

what factors unmask/augment brugada syndrome?

A
  • fever
  • ischemia
  • drugs
  • hypokalemia
  • hypothermia
  • post cardioversion
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109
Q

drugs which unmask/augment brugada syndrome

A

1) na+ channel blockers (e.g. flecainide, propafenone
2) ca2+ channel blockers
3) alpha agonists
4) beta blockers
5) nitrates
6) cholinergics
7) alcohol/cocaine

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110
Q

who is the most perfect girl in the world?

A

chlochlo!

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111
Q

types of brugada syndrome ecg patterns

A

1) type 1: coved type ST segment elevation
2) type 2: saddleback type ST segment elevation
3) type 3: saddleback type st segment elevation <1mm

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112
Q

describe type 1 brugada’s syndrome

A

1) brugada’s sign +
2) one of the following:
- documented VF or polymorphic VT
- F/H of sudden cardiac death at <45yo
- coved type ECGs in family members
- inducibility of VT with programmed electrical stimulation
- syncope
- nocturnal agonal respiration

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113
Q

describe brugada’s sign

A

coved ST segment elevation >2mm in >1 of V1-V3 + negative T wave

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114
Q

describe type 2 brugada syndrome

A

> 2mm of saddleback shaped st elevation

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115
Q

describe type 3 brugada syndrome

A

morphology of either type 1 or 2 but with <2mm of ST segment elevation

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116
Q

causes of ST depression (≥1mm)

A

1) ischemia/unstable angina
2) NSTEMI
3) digoxin (reverse tick sign)
4) reciprocal changes in STEMI
5) posterior MI (leads V1-V3)
6) hypokalemia
7) supraventricular tachycardia
8) RBBB
9) RVH
10) LBBB
11) LVH
12) ventricular paced rhythm

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117
Q

causes of peaked T wave

A

1) hyperkalemia
2) hypermagnesemia
3) hyperacute T wave in STEMI (less tented, broad base)
4) normal grusin type II variant

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118
Q

causes of flat and prolonged T wave

A

hypokalemia

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119
Q

physiological causes of T wave inversion

A
  • normal in children

- normal in V1 in males, V1-V2 in females

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120
Q

pathological causes of T wave inversion

A

1) subendocardial ischemia
2) LVH
3) PE (V1-V3)
4) electrolyte imbalances
5) bundle branch block
6) ventricular hypertrophy (‘strain’ patterns)
7) hypertrophic cardiomyopathy
8) raised ICP

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121
Q

pathological causes of u waves

A

hypokalemia

hypomagnesemia

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122
Q

ecg features of RBBB

A

1) typical RSR’ pattern (m shaped QRS) in V1-3 (right rabbit ear taller)
2) wide slurred s wave in lateral leads (I, aVL, V5-6)
3) broad QRS > 120ms
4) axis deviation to either side
5) limb leads have non specific triphasic pattern
6) ST depression and T inversion

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123
Q

mode of depolarisation of RV in RBBB

A

cell to cell conduction

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124
Q

causes of RBBB

A

1) may be normal

2) acquired
- right ventricular hypertrophy/cor pulmonale
- pulmonary embolus
- ischaemic heart disease
- rheumatic heart disease
- myocarditis or cardiomyopathy
- degenerative disease of conduction system

3) congenital
- congenital heart disease (e.g. ASD)
- ebstein’s anomaly

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125
Q

ecg features of LBBB

A

1) triphasic pattern in lateral leads V5-6
2) dominant s wave in V1
3) QRS duration of >120ms
4) broad monophasic R wave in lateral leads (I, aVL, V5-6)
5) absence of Q waves in lateral leads (I, V5-6; small waves allowed in aVL)
6) prolonged R wave peak time >60ms in left precordial leads (V5-6)

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126
Q

causes of LBBB

A

1) aortic stenosis
2) ischaemic heart diseaes
3) hypertension
4) dilated cardiomyopathy
5) anterior MI
6) primary degenerative disease (fibrosis) of conducting system (e.g. Lenegre disease)
7) hyperkalemia
8) digoxin toxicity

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127
Q

name of scoring system for acute coronary system in LBBB

A

smith- modified sgarbossa’s criteria

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128
Q

describe smith-modified sgarbossa’s criteria

A

1) concordant ST elevation ≥1mm in ≥ 1 lead
2) concordant ST depression ≥1mm in ≥1 lead of V1-V3
3) proportionally excessive discordant STE in ≥ 1 lead anywhere with ≥ 1mm STE (as defined by ≥25% of the depth of the preceding S wave)

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129
Q

conduction system supplied by RCA

A
  • SAN, AVN, bundle of his

- variable twig to posterior fascicle of LBB

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130
Q

conduction system supplied by LCA

A
  • RBB and anterior fascicle of LBB
  • variable twig to posterior fascicle of LBB
  • anterior STEMI: RBBB + left posterior hemiblock
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131
Q

ecg features in left anterior hemiblock

A

1) left axis deviation of at least -45
2) rS complexes in inferior leads II, III, aVF
3) qR complexes in lead I and aVL

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132
Q

pathophysiology of left anterior hemiblock

A
  • usually due to previous ischemic insult

- delayed activation of anterior portion of LV due to blocked/delayed transmission in anterior fascicle

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133
Q

ecg features of left posterior hemiblock

A

1) R axis deviation 90-180 degrees
2) normal QRS complex
3) presence of qR complex in inferior leads II, III, aVF
4) rS complex in lead I

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134
Q

types of combined blocks

A

1) bifascicular block

2) trifascicular block

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135
Q

describe bifascicular blocks

A

RBBB + left anterior/posterior hemiblock

- RBBB + left axis deviation

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136
Q

desecribe trifascicular blocks

A

RBBB + LAFB + 1st degree heart block

- high risk of entering complete heart block

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137
Q

types of ectopic beats

A

1) escape beats

2) premature beat

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138
Q

describe escape beats

A
  • failure of SAN to discharge (dysfunctional SAN) > beat later than expected
  • pause BEFORE ectopic beat (sinus arrest)
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139
Q

describe premature beats

A
  • ectopic pacemaker discharges before SAN > beat earlier than expected
  • pause AFTER ectopic beat
  • normal SAN
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140
Q

define escape rhythm

A

ectopic pacemaker continues pacemaking function to maintain CO

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141
Q

types of escape rhythms

A

1) atrial escape rhythm
2) junctional escape rhythm
3) ventricular escape rhythm

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142
Q

HR in atrial escape rhythm

A

normal; 60-80bpm

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143
Q

HR in junctional escape rhythm

A

40-60 bpm

regular

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144
Q

HR in ventricular escape rhythm

A

20-40bpm

regular

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145
Q

morphology of atrial escape rhythm

A

indistinguishable from sinus rhythm

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146
Q

morphology of junctional escape rhythm

A

1) no P waves

2) narrow QRS

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147
Q

consequences of junctional escape rhythm

A

usually tolerated

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148
Q

management of junctional escape rhythm

A

treat underlying cause

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149
Q

morphology of ventricular escape rhythm

A

1) no p wave
2) big, broad QRS complex
3) T wave inversion

150
Q

consequences of ventricular escape rhythm

A

1) symptomatic (hypotension, chest tightness, dizziness, syncope)
2) cardiogenic shock

151
Q

management of ventricular escape rhythm

A

1) treat underlying cause
2) atropine, inotropes
3) pacemaker
4) check K+

*AVOID antiarrhythmatics e.g. lignocaine, amiodarone (can cause asystole by suppressing ectopic focus > CO drops to 0)

152
Q

morphology of atrial premature beat

A

1) abnormal P waves

2) normal narrow QRS complex

153
Q

morphology of junctional premature beat

A

1) NO P waves/abnormal P wave with PR <120ms

2) normal narrow QRS complex

154
Q

morphology of ventricular premature beat

A

1) NO P waves
2) wide bizarre QRS
3) T wave opposite polarity

155
Q

differential diagnosis of atrial premature beat

A

1) sinus arrhythmia
- p waves identical

2) MAT
- > 3 different P wave morphologies
- no sinus rhythm

156
Q

differential diagnosis of junctional premature beat

A

AF

157
Q

causes of atrial and junctional premature beat

A

1) idiopathic
2) ischemia
3) electrolyte abnormalities

158
Q

causes of ventricular premature beat

A

1) idiopathic
2) ischemia
3) electrolyte abnormalities
4) trauma (>6 PVCs/min definite pathological)

159
Q

treatment of atrial premature beat

A

1) no treatment needed

2) treat underlying cause

160
Q

treatment of junctional premature beat

A

treat underlying cause

161
Q

treatment of ventricular premature beat

A

1) treat underlying cause
2) antiarrhythmatics
3) unstable: cardioversion

162
Q

describe trigeminy rhythm of PVC

A

2 sinus beats followed by 1 PVC

163
Q

ecg features of PVCs

A

1) broad QRS complex (≥120ms) with abnormal morphology
2) premature
3) discordant ST segment and T wave changes
4) usually followed by compensatory pause
5) retrograde capture of atria (+/-)

164
Q

name the grading system for PVCs

A

lown’s grading

165
Q

purpose of lown’s grading

A

determine if PVCs need to be treated

166
Q

characteristics of lown I ectopics

A

uniform, unifocal, infrequent (<30/hr)

167
Q

management for lown I ectopics

A

treat STEMI

168
Q

characteristics of lown II ectopics

A

uniform, unifocal, frequent (>30/hr)

169
Q

management for lown II ectopics

A

none necessary

170
Q

characteristics of lown III

A

multiform, multifocal

171
Q

management of lown III

A

treat hypertension/AS

172
Q

characteristics of lown IV A

A

PVCs in couplets (2)

173
Q

treatment of lown IV A

A

treat STEMI

174
Q

characteristics of lown IV B

A

PVCs in salvos (≥3)

175
Q

number of PVCs for VT

A

≥5

176
Q

treatment of lown IV B

A

treat STEMI AND VT (amiodarone)

177
Q

characteristics of lown V

A

R on T: PVC starts before preceding T wave ends

178
Q

management of lown V

A

admit & monitor even if NIL symptoms

high risk of developing into VT/VF (irritating heart during repolarisation)

179
Q

clinical features of digoxin toxicity

A

GIT: n/v, anorexia, diarrhoea
visual: blurred vision, yellow/green discolouration, halos
CVS: palpitations, syncope, dyspnoea
CNS: confusion, dizziness, delirium, fatigue

180
Q

ecg features of digoxin toxicity

A

1) multitude of dysrhythmias
- SVT (increased automaticity) with slow ventricular response (AV block)

2) reverse tick sign (NOT indicative of toxicity)
3) downsloping ST depression with characteristic sagging appearance
4) flattened, inverted or biphasic T waves
5) shortened QT interval

181
Q

cause of increased automaticity in digoxin toxictiy

A

increased intracellular calcium

182
Q

cause of decreased AV conduction

A

increased vagal effect at AV node

183
Q

approach to etiology of palpitations

A

1) cardiac causes

2) non cardiac causes

184
Q

cardiac causes of palpitations

A

1) arrhythmias (AF/SVT/ectopic beats/VT/others - WPW, long QT syndrome, brugada syndrome, heart block)
2) valvular problems (AR, MVP)
3) shunts (intra/extra cardiac)

185
Q

non cardiac causes of palpitations

A

1) high o/p states (pregnancy, anemia)
2) endocrine (hypoglycemia, thyrotoxicosis, pheochromocytoma)
3) hypovolemia (dehydration, shock)
4) drugs (beta agonist, sudden cessation of beta blockers, vasodilators, anticholinergics)
5) lifestyle (recreational drugs, caffeine, nicotine)
6) psychosomatic (anxiety, panic disorder)

186
Q

causes of IRREGULAR narrow complex tachycardia

A

1) atrial flutter with variable conduction
2) atrial fibrillation
3) multifocal atrial tachycardia

187
Q

causes of REGULAR broad complex tachycardia

A

1) monomorphic VT
2) antidromic AVRT
3) any regular narrow complex tachycardia with BBB or pre-excitation (e.g. SVT with aberrancy)

188
Q

causes of IRREGULAR broad complex tachycardia

A

1) polymorphic VT

2) any irregular narrow complex tachycardia with BBB or pre-excitation (e.g. WPW with A fib)

189
Q

general pathophysiology of narrow complex tachycardia

A

1) automatic firing of foci

2) re-entry

190
Q

ecg pattern in atrial flutter

A

saw tooth pattern (multiple p waves)

191
Q

types of atrial flutter

A

1) cavotriscupid isthmus dependent flutter
- re entry circuit within RA
2) CTI independent flutter (atypical AFL)
- re entry circuit within RA or LA

192
Q

types of CTI dependent flutter

A

1) typical (counterclockwise) flutter (majority)

2) reverse typical AFL

193
Q

long term treatment of typical AF

A

CTI ablation

anticoagulation

194
Q

long term treatment of atypical AF

A

beta blocker

anticoagulation

195
Q

what scoring system used for AF stroke risk (in deciding use of anticoagulation)?

A

CHA₂DS₂-VASc Score

196
Q

types of atrial fibrillation

A

1) paroxysmal (≤ 48h)
2) persistent (> 7d or requires cardioversion)
3) long standing persistent (> 1y)
4) permanent (accepted)

197
Q

etiology of afib

A

1) valvular afib
- moderate to severe MS
- mechanical heart valve
3) others (non valvular afib) - 90%!

198
Q

complications of afib

A

1) CCF

2) thromboembolism

199
Q

complications of treatment

A

1) overanticoagulation

2) underanticoagulation

200
Q

describe permanent AF

A

1) CV failed OR

2) persistent afib where joint decision made by patient and clinician to no longer pursue rhythm control strategy

201
Q

extracellular matrix alterations in afib

A

1) interstitial and replacement fibrosis
2) inflammatory changes
3) amyloid deposition

202
Q

myocyte alterations in afib

A

1) apoptosis
2) necrosis
3) hypertrophy
4) dedifferentiation
5) gap junction

203
Q

changes to heart in afib

A

1) extracellular matrix alterations
2) myocyte alterations
3) microvascular changes
4) endocardial remodelling (endomyocardial fibrosis)

204
Q

general classification of causes of afib

A

1) cardiac
2) non cardiac
3) lone afib

205
Q

cardiac causes of afib

A

1) valvular (term no longer in use)
2) non valvular
(i) HTN
(ii) CCF
(iii) coronary artery disease (IHD or post AMI)
(iv) valves: MR (more infrequently: AS)
3) miscellaneous
- post CABG
- cardiomyopathy
- percarditis/myocarditis
- sick sinus syndrome (sinus node dysfunction
- ASD
- cardiac tumor

206
Q

non cardiac causes of afib

A

1) sepsis
2) respiratory (COPD/PE/pneumo)
3) endocrine (hyperthyroidism, DM, hypoglycemia)
4) electrolyte (hyperkalemia)
5) alcohol (holiday heart syndrome)

207
Q

describe lone afib

A

patients with paroxysmal, persistent, longstanding persistent, or permanent AF who have no structural heart disease or attributable non-cardiac causes

208
Q

clinical features of afib

A

1) asymptomatic
2) symptomatic
3) symptoms of embolic event (stroke)
4) insidious onset of RHF (peripheral edema, ascites)
5) precipitating causes: exercise, emotion, alcohol

209
Q

symptoms of afib

A

1) palpitations/tachycardia
2) fatigue/weakness
3) dizziness
4) reduced exercise capacity

more severe:

5) dyspnea
6) angina
7) syncope (infrequent)

210
Q

name of clinical scoring system for AF

A

european heart rhythm association (EHRA) score

211
Q

describe EHRA I

A

no symptoms

212
Q

describe EHRA II

A

mild symptoms

normal daily activity NOT affected

213
Q

describe EHRA III

A

severe symptoms

normal daily activity AFFECTED

214
Q

describe EHRA IV

A

disabling symptoms

normal daily activities discontinued

215
Q

how would you split your investigations for afib?

A

1) cardiac

2) non cardiac

216
Q

what cardiac investigations would you order for afib?

A

1) ECG
2) 2D echo
3) holter monitoring or event recorders
4) exercise testing

217
Q

what non cardiac investigations would you order for afib?

A

1) TSH and T4 (to be done in all patients with first episode of AF/increase in AF freq)
2) fasting glucose
3) UECr
4) FBC
5) lung function test

218
Q

ecg changes to make diagnosis of afib

A

1) absent p waves
2) irregularly irregular narrow complex rhythm
3) chaotic irregular baseline (fibrillatory waves)
4) ashman phenomenon: wide QRS complexes with RBBB morphology that follow short RR interval preceded by long RR interval

5) look for etiology: LVH (HTN), LAH p mitrale (MS), Q waves (CAD)
6) QT interval (risk of antiarrhythmic therapy)
7) electrical heart disease like pre-excitation or infranodal conduction disease (BBB)

219
Q

2D echocardiogram changes in afib

A

TTE

  • size of RA and LA
  • size and function of RV and LV
  • peak RV pressure
  • ejection fraction
  • etiology: valvular heart disease, LVH, pericardial disease, cardiomyopathy

TEE:
- thrombi in left atrium/left atrial appendage (need to anticoagulate before pharmacologic or electrical CV)

220
Q

rationale for holter monitoring/event recorders for afib

A
  • identify arrhythmia if it is intermittent
  • assess overall ventricular response rate (esp if rate control strategy chosen)
  • look for pauses
221
Q

function of exercise therapy for afib

A

to evaluate CAD (class I antiarrhythmics contraindicated in CAD)

222
Q

summarise the treatment for afib according to AHA/ACC/HRS guidelines

A

1) afib: record 12 lead ecg
2) anticoagulation issues: assess TE risk
3) achieve rate and rhythm control
4) treatment of underlying disease (upstream therapy) + referral

223
Q

oral anticoagulation options for afib/atrial flutter

A

1) vit k antagonist: warfarin
2) DOAC
- factor Xa inhibitors: apixaban, rivaroxaban, edoxaban
- direct thrombin inhibitors (DTI): dabigatran

224
Q

name 3 factor Xa inhibitors

A

apixaban, rivaroxaban and edoxaban

225
Q

name a direct thrombin inhibitor

A

dabigatran

226
Q

name 2 scoring systems used in guiding anticoagulation therapy

A

1) CHA2DS2-VASc score

2) HAS-BLED score

227
Q

risk factors in CHA2DS2-VASc score

A

1) congestive heart failure/LV dysfunction
2) hypertension
3) age ≥ 75 (2)
4) diabetes mellitus
5) stroke/tia/thromboembolism (2)
6) vascular disease
7) age 65 to 74
8) sex category

total score: 9

228
Q

CHA2DS2-VASc score cut off to begin OAC

A

male: ≥2
female: ≥3

229
Q

are DOAC or VKA preferred for anticoagulation therapy?

A

DOAC

230
Q

why are DOAC preferred in anticoagulation therapy over VKA?

A

DOACs are at least non inferior (and superior in some trials) to VKA for preventing stroke and systemic embolism + a/w lower risks of serious bleeding

231
Q

what therapy can be offered if patients have CI to OAC?

A

antiplatelet therapy

232
Q

CHA2DS2-VASc score cut off to CONSIDER OAC

A

male: 1
female: 2

233
Q

anticoagulation treatment for valvular AF patient

A

all to be treated with warfarin regardless of CHA2DS2-VASc score

234
Q

is CHA2DS2-VASc score used for non valvular AF?

A

NO

235
Q

rationale for HAS-BLED score

A

prediction of risk of bleeding in patients on anticoagulation for AF

236
Q

describe HAS-BLED score

A 
H: htn
A: abnormal renal and liver function (1 point each)
S: stroke
B: bleeding
L: labile (unstable/high) INRs
E: elderly (>65)
D: drugs or alcohol (1 point each)

max: 9 points

237
Q

reference rate for ESRF

A

CrCl <15ml/min (whether on dialysis or not)

238
Q

categories of patients with afib and CKD

A

1) afib + ESRF

2) afib + moderate to severe CKD (serum Cr ≥ 1.5mg/dL, CrCl 15-30mL/min, CrCl <50mL/min or CrCl 15-50mL/min)

239
Q

OAC for patients with afib + ESRF

A

warfarin or apixaban (but still not approved by TTSH cvm or renal)

240
Q

OAC for patients with afib

A

serum Cr ≥ 1.5mg/dL: apixaban
CrCl 15-30mL/min: dabigatran
CrCl 15-50mL/min: edoxaban
CrCl <50mL/min: rivaroxaban

241
Q

lab monitoring for patients on warfarin

A

initiation: weekly INR
stable: monthly INR

242
Q

lab monitoring for patients on DOAC

A

before initiation: RF & LFT + annual reevaluation

243
Q

what procedure can be done for patients who have CI to LT anticoagulation?

A

left atrial appendage occlusion (percutaneous or surgical)

244
Q

in general is rate or rhythm controlled preferred?

A

rate control

245
Q

when is rhythm control preferred over rate control?

A

1) pre excited afib

2) afib during pregnancy

246
Q

when is rhythm control considered a safe alternative to rate control in symptomatic patients?

A

1) new onset symptoms/new onset afib <48h
2) age <65
3) no LV dysfunction
4) no mitral valve disease
5) no prior TE event
6) already adequately anticoagulated

247
Q

methods of rate control therapy

A

1) AV nodal blocking agents
- beta blockers
- non dihydropyridine CCB: verapamil, diltiazem
- digoxin
- amiodarone
2) AV nodal ablation and permanent pacemaker insertion (ablate and pace)

248
Q

contraindications of beta blockers in afib

A

afib complicated by

  • haemodynamic instability (cardiogenic shock)
  • acute decompensating HF (ADHF)
  • severe bronchospasm (if non severe: can opt for b1 selective BB)
249
Q

contraindications of non-dihydropyridine CCB

A

afib complicated by

  • haemodynamic instability (cardiogenic shock)
  • ADHF
  • EF < 40%
250
Q

why is digoxin esp good in IMMOBILE patients?

A

exercise induces sympathetic activation > inhibits efficacy of digoxin

digoxin works by increasing vagal tone

251
Q

risk of amiodarone

A

pharmacological cardioversion (only use amiodarone as rate control agent in ACUTE setting)

252
Q

most important consideration prior to commencing rhythm control in AF >48h

A

ensure no LA thrombus!

253
Q

methods of rhythm control

A

1) electrical cardioversion (DCCV)
2) pharmacological cardioversion (class Ic, III antiarrhythmics)
3) catheter ablation

254
Q

examples of drugs used in pharmacological cardioversion

A

1) IV amiodarone (class III)
- last resort: alot of adverse effects (risk of QT prolongation)
- for critically ill or severe LV systolic dysfunction

2) ibutilide (class III)
- risk of QT prolongation

3) flecainide, propafenone (class Ic)

255
Q

contraindication of class I antiarrhythmics in pharamacological cardioversion

A

patients with IHD/structural heart disease > use class III antiarrhythmics (amiodarone)

256
Q

lab monitoring for pharmacological cardioversion

A

1) ecg
2) RF
3) LFT

257
Q

drugs used for bridging regimen prior to interruption of warfarin (for initiation of certain procedures to treat the underlying cause of afib)

A

unfractionated heparin (IV UFH) or low molecular weight heparin (SC clexane)

258
Q

drugs used after procedures/when newly initiating OAC

A

UFH or LMWH

259
Q

why is UFH/LMWH used as a bridging regimen when initiating warfarin treatment in patients with afib?

A

initiation of warfarin > decrease in vit K dependent anticoagulant protein C &S (persistent levels of vit K dependent procoagulation FII and FX due to longer half lives) > transient hypercoagulable state

heparin potentiates anticoagulation effect of antithrombin > protect patient against increased risk of thrombosis

260
Q

reversal agent for DABIGATRAN in the event of life threatening/uncontrolled bleeding or urgent procedure

A

iDArucizumab

261
Q

reversal agents for apiXAban, rivaroXAban and edoXAban (factor Xa inhibitors) in the event of life threatening/uncontrolled bleeding or urgent procedure

A

andeXAnet alfa

262
Q

define wolff parkinson white syndrome

A

congenital pre-excitation syndrome characterised by combination of presence of congenital accessory pathway and episodes of tachyarrhythmia

263
Q

what congenital heart disease is WPW most commonly associated with?

A

ebstein’s anomaly

264
Q

WPW is a cause of _____ _____ _____

A

sudden cardiac arrest

265
Q

describe the pathophysiology of WPW syndrome

A

1) presence of accessory conduction pathway: bundle of kent
2) abnormality allows bypassing of AV node > early electrical activation of ventricles > early ventricular depolarisation > delta waves on ecg
3) impulses may be conducted anterograde or retrograde or in both directions
4) tachyarrhythmias arise from the formation of re-entry circuit involving the accessory pathway: AVRT

266
Q

clinical features of WPW synrome

A

1) asymptomatic
2) symptomatic
- palpitations: episodes of AF, AVRT
- cardiogenic syncope

267
Q

most common arrhythmia a/w WPW syndrome?

A

afib

268
Q

what investigations to order for WPW syndrome?

A

12 lead ecg

269
Q

ecg changes in WPW syndrome

A

1) shortened PR interval (<120ms)
2) delta waves
3) widened QRS complex >110ms
4) ST segment and T wave discordant changes (opp direction to major component of QRS complex)
5) pseudo infarction pattern in up to 70% of patients
- negatively deflected delta waves in inferior/anterior leads
- prominent R wave in V1-3 (mimicking posterior infarction)

270
Q

ecg changes in type A WPW syndrome

A

positive delta wave in all precordial leads with R/S > 1 in V1

271
Q

ecg changes in type B WPW syndrome

A

negative delta waves in leads V1 and V2

272
Q

management for WPW syndrome

A
  • avoid AV nodal blockers (digoxin, beta blockers > precipitate VF)

1) acute management
- antidromic AVRT: IV procainamide
- orthodromic AVRT: IV amiodarone
- electrical cardioversion

2) definitive management
- ablation of accessory conduction pathway

273
Q

is orthodromic AVRT a narrow or broad complex tachycardia?

A

narrow complex

indistinguishable from AVNRT

274
Q

management of orthodromic AVRT

A

as per AVNRT

275
Q

is antidromic AVRT a narrow or broad complex tachycardia?

A

broad complex (appearing like VT)

276
Q

management of antidromic AVRT

A

1) IV procainamide
2) synchronised cardioversion
3) AICD once an arrhythmia develops

277
Q

definition of ventricular tachycardia

A

regular broad complex tachycardia originating from a ventricular focus with at least 5 consecutive ventricular ectopic beats

278
Q

types of ventricular tachycardia

A

1) sustained VT: >30s or requiring intervention due to haemodynamic compromise

2) non sustained VT
- ≥3 consecutive ventricular complexes terminating spontaneously in <30s

279
Q

what are the 3 mechanisms for initiation and propagation of ventricular tachycardia

A

1) re-entry (commonest mechanism)
2) triggered activity
3) abnormal activity

280
Q

describe the re-entry mechanism for ventricular tachycardia

A
  • two distinct conduction pathways with a conduction block in one pathway and region of slow conduction in the other
  • arises due to abnormal myocardial scarring from previous AMI
281
Q

describe triggered activity as a mechanism for VT

A

early or late after depolarisations (e.g torsades de pointes, digoxin toxicity)

282
Q

describe abnormal activity as a mechanism for VT

A

accelerated abnormal impulse generated from a region of ventricular cells

283
Q

differential diagnosis for regular broad complex tachycardia

A

1) antidromic AVRT
2) any regular narrow complex tachycardia with BBB or pre-excitation (e.g. SVT with aberrancy)
3) pacemaker mediated tachycardia
4) metabolic derangements (e.g. hyperkalemia)
5) poisoning with sodium channel blocking agents (e.g. TCA)

284
Q

clinical features suggestive of VT

A

1) age >35
2) structural heart disease/cardiomyopathy
3) ischaemic heart disease/previous AMI
4) CCF
5) family history of sudden cardiac death

285
Q

what does family history of sudden cardiac death suggest?

A
  • HOCM
  • congenital long QT syndrome
  • brugada syndrome
  • arrhythmogenic right ventricular dysplasia
286
Q

ecg features suggestive of VT (slight variation from brugada’s criteria)

A

1) very broad complexes >160ms (<120ms favours SVT)
2) absence of typical RBBB or LBBB morphology
3) extreme axis deviation
4) AV dissociation
5) captured beats
6) fusion beats
7) positive or negative concordance throughout chest leads
8) brugada’s sign: distance from onset of QRS complex to nadir of S wave > 100ms
9) josephson’s sign: notching near nadir of the S wave
10) RSR’ complexes with taller left rabbit ear (most specific finding!)

287
Q

types of VT

A

1) monomorphic VT
2) polymorphic VT
3) bidirectional VT

288
Q

causes of monomorphic VT

A

1) ischemic heart disease
2) dilated cardiomyopathy
3) hypertrophic cardiomyopathy
4) chagas disease: american trypanosomiasis

289
Q

describe ecg of torsades de pointes

A
  • QRS complexes twisting around isoelectric line
  • PVT
  • QT prolongation
290
Q

causes of bidirectional VT

A

1) myocardial ischaemia (most common)
2) drugs: prolonged QTc (e.g. digoxin toxicity)
3) congenital long QT syndrome (romano-ward, jervell and lange-nielsen)
4) electrolyte derangements: hypokalemia, hypomagnesemia

291
Q

presentation of ventricular fibrillation

A

1) clinical: cardiac arrest, pulseless
2) ecg:
- completely disorganised irregular rhythm
- no discernable p wave, QRS complex or t waves
- 150 to 500 bpm
- amplitude decreases with duration (coarse VF > fine VF)

292
Q

causes of ventricular fibrillation

A

1) ischaemia: AMI
2) electrolyte abnormalities: hyperK+
3) cardiomyopathy (dilated/hypertrophic/restrictive)
4) acquired/congenital long QTc
5) brugada syndrome
6) drugs (e.g. verapamil in patients with AF + WPW)
7) environmental (electric shock/drowning/hypothermia)
8) pulmonary embolism
9) cardiac tamponade
10) blunt trauma (commotio cordis)

293
Q

differential diagnosis of ventricular fibrillation

A

1) ventricular flutter
2) PEA
3) asystole

294
Q

ecg features of ventricular flutter

A

1) continous sine wave
2) no identifiable p waves, qrs complexes or t waves
3) >200bpm

295
Q

management of ventricular flutter

A

defibrillate if pulseless

296
Q

differential diagnosis for fine ventricular fibrillation

A

asystole

297
Q

define cardiac arrest

A

cessation of effective cardiac activity as confirmed by absence of signs of circulation

298
Q

define return of spontaneous circulation

A

1) palpable pulse (SBP ≥ 60mmHg)

2) effective waveform for at least 30s

299
Q

define sustained ROSC (i.e. survived the event)

A

ROSC ≥ 20min

300
Q

define end of event

A
  • death is declared OR
  • spontaneous circulation restored and sustained for ≥ 20min OR
  • 20min after extracorporeal circulation has been established
301
Q

define survival to hospital discharge

A

point at which patient is discharged from hospital’s acute care unit regardless of neurological status

302
Q

describe the chain of survival

A

1) early access (recognition and activation of emergency response system)
2) early CPR
3) early defibrillation
4) basic and advanced emergency medical services
5) early advanced care and post resuscitation management

303
Q

time interval for administration of epinephrine in ACLS

A

3-5mins

304
Q

dosage of epinephrine in ACLS protocol

A

1mg

305
Q

dosage of amiodarone in ACLS protocol

A

1st dose: 300mg

2nd dose: 150mg

306
Q

describe the initial management for cardiac arrest

A

1) BCLS
- check responsiveness
- code blue, get defibrillator
- primary ABC (head tilt chin lift, jaw thrust, FB)
- good quality CPR
- defibrillate: biphasic 150J

2) monitor CPR effectiveness
3) secondary ABCD

307
Q

minimum acceptable compression depth for CPR

A

5cm

308
Q

minimum acceptable compression rate for CPR

A

100/min

309
Q

describe good quality ventilation in CPR

A

1) tidal volumes 400-600ml
2) 1s/breath
3) compression: ventilation ratio = 30:2

310
Q

how is CPR effectiveness monitored?

A

waveform capnography (EtCO2)

311
Q

describe steps in secondary ABCD

A

1) airway

2) breathing
- pre-intubation: 30:1
- post-intubation: 10:1 uninterrupted

3) circulation
4) drugs

312
Q

methods of confirming ETT placement

A

1) 5 point auscultation
2) bilateral chest expansion
3) tube misting and demisting
4) EtCO2 (N: 35-40mmHg)

313
Q

EtCO2 in cardiac arrest

A

<10mmHg

314
Q

EtCO2 in good quality CPR

A

10-20mmHg (better quality CPR > higher EtCO2)

315
Q

drugs administered in secondary ABCD for VF/pulseless VT

A

1) IV adrenaline 1mg
- dilute 1ml 1:1000 adrenaline in 9ml NS
- given every 2 cycles of CPR (3-5min)

2) IV amiodarone
- for refractory/recurrent VF/VT

3) IV MgSO4 1-2g
- Torsades de Pointes suspected

4) NaHCO3
- hyperkalemia/TCA overdose

316
Q

drugs administered in secondary ABCD for asystole/PEA

A

1) IV adrenaline 1mg
- given every 2 cycles of CPR (3-5min)

2) NaHCO3
- hyperkalemia/TCA overdose

317
Q

methods to confirm asystole

A

1) check connection of lead and cables
2) select different leads
3) increase gain (identify fine VF)

318
Q

potentially reversible causes of cardiac arrest

A

5H:

  • Hypovolemia
  • Hypoxia
  • H+: acidosis
  • Hyper/Hypokalemia
  • Hypothermia

5Ts:

  • tamponade (cardiac)
  • thrombosis (coronary)
  • thrombosis (pulmonary)
  • tension pneumothorax
  • tablets (drug OD)
319
Q

describe the post ROSC bundle

A

1) insert definitive airway if not done so

2) maintain SpO2 94-98%
- hypoxaemia: reperfusion injury
- ≥99%: free radical formation from excess oxygen

3) maintain normocapnia (PaCO2 35-45mmHg)
4) target MAP >65mmHg
5) early PCI after ROSC
6) induce hypothermia to 32-34°C
7) glycemic control b/w 6-10mmol/L
8) neurological assessment after 72h (prognostication)

320
Q

describe investigations to be done post ROSC

A

1) 12 lead ecg
2) cxr
3) fbc
4) u/e/cr
5) glucose
6) cardiac enzymes
7) abg
8) lactate
9) 2D echocardiogram
10) ct/mri

321
Q

describe monitoring post ROSC

A

1) continuous ecg monitoring
2) BP
3) pulse oximetry
4) capnography
5) temperature
6) urine o/p
7) CVP/swan-ganz catheter
8) ScVO2
9) EEG

322
Q

initial management of tachydysrhythmias

A

1) ABCD
2) supplemental O2
3) secure IV access
4) determine if tachycardia is wide vs narrow complex
5) full monitoring: 12 lead ecg (except in cardiac arrest)
6) determine if patient stable or unstable

323
Q

signs of clinical instability

A

1) chest pain
2) breathlessness
3) AMS
4) SBP >90mmHg
5) clinical features of shock
6) clinical features of heart failure
- APO
- agitated
- severe chest pain

324
Q

wide QRS tachycardia is ___ until proven otherwise

A

VT

325
Q

describe the algorithm for wide complex tachycardia

A

1) initial management
2) establish WCT with pulse

3) unstable (<90/60mmHg; symptomatic) vs stable (>90/60mmHg; no symptoms)

  • unstable: synchronised cardioversion
  • stable: drugs
326
Q

describe management post cardioconversion of WCT

A

1) IV amiodarone 1mg/min x 6h, then 0.5mg/min x 18h OR IV lignocaine 1-2mg/min x24h

2) monitor ABCs, vital signs, 12 lead ECG
3) transfer as appropriate

327
Q

management of stable MONOmorphic VT

A
  • IV amiodarone 150mg over 10 mins repeated once OR IV 1% lignocaine 1-1.5mg/kg over 10mins, repeat dose 50-75mg after 3-5min
  • synchronised cardioversion if still VT after 2 doses
328
Q

management of stable POLYmorphic VT if QTc prolonged

A
  • IV MgSO4 1-2g
  • stop drugs prolonging QTc
  • overdrive pacing (may precipitate VF: have DCCV available)
329
Q

indications of overdrive pacing

A

1) failure of drug therapy
2) recurrent arrhythmia
3) contraindication to cardioversion (digoxin toxicity)
4) aid to differentiate VT from SVT

330
Q

management of stable POLYmorphic VT if QTc normal

A
  • treat ischemia

- control electrolytes

331
Q

management of stable SVT with aberrancy

A

adenosine 6mg rapid push then 12mg rapid push

332
Q

what is the half life of adenosine

A

7s

333
Q

avoid ___ if there is a possibility of VT

A

verapamil (irreversible block to AV node: asystolic arrest)

334
Q

management of UNSTABLE WCT

A

1) sedation + analgesia
- IV midazolam 1-2mg + morphine 1-2mg + metoclopramide 10mg
- if haemodynamically unstable: etomidate + fentanyl

2) synchronised cardioversion
- start at 100J then escalate

335
Q

describe the algorithm for REGULAR narrow complex tachycardia

A

1) initial management
2) establish regular NCT with pulse (SVT)
3) unstable (<90/60mmHg, symptomatic) vs stable (>90/60mmHg, no symptoms)
- unstable: synchronised cardioversion
- stable: vagal manoeuvre, drugs

336
Q

describe management of STABLE SVT

A

1) non pharmalogical methods

a. valsalva maneouvres
- supine
- blow into tube leading to manometer/blow into 20ml syringe to push plunger out/blow against closed glottis
- maintain for 30s

b. carotid sinus massage
- DO NOT perform in elderly (risk of arteriosclerotic disease and stroke)
- DO NOT perform bilaterally
- digital pressure backwards and medially in circular motions for no more than 5-10s

2) pharmacological methods (chemical cardioversion)
- IV adenosine (AV nodal blocking agent) OR IV diltiazem (2.5mg/min up to 50mg) OR IV verapamil (constant infusion of 1mg/min up to max of 20mg)

337
Q

physiological basis of valsalva maneouvres

A

1) initial
a. increased intrathoracic pressure
b. reduced venous return
c. initial increase of HR

2) subsequent (upon release of strain)
- overshoot response of BP
- triggers reflex bradycardia
- conversion occurs during this time

338
Q

what position is patient in during carotid sinus massage

A

trendenlenburg position

339
Q

what would you explain to the patient during administration of IV adenosine for chemical cardioversion?

A

1) transient chest discomfort
2) nausea
3) flushing

340
Q

steps in administration of IV adenosine for chemical cardioversion

A

1) explain to patient
2) record ecg lead during procedure
3) large bore cannula in antecubital fossa
4) prepare 3 way plug
5) rapid bolus of 6mg followed by 20mg NS flush + elevation of arm
6) repeat 12mg bolus x2 if required after 1-2min

note: perform in area with defibrillator > may cause VF

341
Q

describe the management of UNSTABLE SVT

A

AS IN UNSTABLE WCT except for beginning J

1) sedation + analgesia
- IV midazolam 1-2mg + morphine 1-2mg + metoclopramide 10mg
- if haemodynamically unstable: etomidate + fentanyl

2) synchronised cardioversion
- start at 50J then escalate

342
Q

describe the algorithm for irregular narrow complex tachycardia

A

1) initial management
2) establish irregular NCT with pulse AF
3) unstable vs stable
- unstable: synchronised cardioversion
- stable: rate/rhythm control

343
Q

management of STABLE irregular narrow complex tachycardia

A

1) rate control

2) rhythm control

344
Q

describe rate control in STABLE irregular narrow complex tachycardia

A
  • IV diltiazem: 2.5mg/min up to 50mg
  • IV verapamil: constant infusion of 1mg/min up to max 20mg
  • IV digoxin 0.5mg
  • IV amiodarone (AVOID AVN BLOCKING AGENTS IN WPW WITH AF): 150-300mg IV over 30 min followed by 900g over 24h
  • IV procainamide 20mg/min in AF with WPW
345
Q

describe rhythm control in STABLE irregular narrow complex tachycardia

A
  • check coagulation status
  • TEE to identify atrial thrombi
  • IV amiodarone 150mg over 20min and repeat once if needed
346
Q

management of UNSTABLE irregular narrow complex tachyardia

A

AS PER UNSTABLE SVT

1) sedation + analgesia
- IV midazolam 1-2mg + morphine 1-2mg + metoclopramide 10mg
- if haemodynamically unstable: etomidate + fentanyl

2) synchronised cardioversion
- start at 50J then escalate

347
Q

what is the classification for antiarrhythmic drugs

A

vaughan williams classification

348
Q

describe class Ia agents according to the vaughan williams classification

A

Na+ channel blockade, prolongs repolarisation

- e.g. procainamide, quinidine, disopyramide

349
Q

describe class II agents according to the vaughan williams classification

A

beta blockers: indirect Ca channel blockade by attenuating adrenergic activation
- e.g. propranolol, esmolol, metoprolol

350
Q

describe class III agents according to the vaughan williams classification

A

potassium channel blockers: widen action potential by blocking potassium K+ efflux
- e.g. amiodarone, sotalol, ibutilide

351
Q

describe class IV agents according to the vaughan williams classification

A 
non dihydropyridine (cardioselective) CCB
- e.g. verpamil, diltiazem
352
Q

describe class V agents according to the vaughan williams classification

A

work via unknown mechanisms

e.g. adenosine, digoxine, MgSO4

353
Q

describe class Ib agents according to vaughan williams classification

A

Na+ channel blockade, shortened repolarisation

- e.g. lidocaine, mexiletine, phenytoin, tocainide

354
Q

describe class Ic agents according to vaughan williams classification

A

Na+ channel blockade, repolarisation unchanged

- e.g. encainide, flecainide, propafenone

355
Q

causes of sinus bradycardia

A
  • athletes
  • physiological response to sleep
  • vagotonic procedures
  • hypothyroidism
  • raised ICP: cushing’s reflex
  • drugs: BB, CCB, digoxin
  • sick sinus synrome
  • glaucoma: oculocardiac reflex
356
Q

describe cushing’s reflex

A

physiological nervous system response to acute elevations of intracranial pressure (ICP), resulting in Cushing’s triad

357
Q

describe cushing’s triad

A

1) widened pulse pressure
2) bradycardia
3) irregular respiration

358
Q

causes of 1st degree heart block

A
  • increased vagal tone/athletic training
  • inferior MI
  • mitral valve surgery
  • myocarditis (e.g. lyme disease)
  • electrolyte disturbances (e.g. hyperkalemia)
  • AV nodal blocking drugs
  • normal variant
359
Q

define a high grade AV block

A

when 2 or more P waves not conducted

360
Q

causes of mobitz II second degree heart block

A
  • drugs: bb, cbb, digoxin, amiodarone
  • anterior MI: septal infact
  • lenegre’s/lev’s disease: idiopathic fibrosis of conducting system
  • cardiac surgery close to septum (e.g. mitral valve repair)
  • inflammatory condictions: rheumatic fever, myocarditis, lyme disease
  • autoimmune: SLE, systemic sclerosis
  • infiltrative myocardial disease: amyloidosis, haemochromatosis, sarcoidosis
  • hyperkalemia
361
Q

definitive management of mobitz II second degree heart block

A

insertion of permanent pacemaker

362
Q

what level of blockage is indicated by a narrow QRS complex in 3rd degree heart block

A

block at the level of AV node

- HR usually 40-60min

363
Q

what level of blockage is indicated by a broad QRS complex in 3rd degree heart block

A

infranodal block

- HR usually <40/min

364
Q

causes of 3rd degree/complete heart block

A
  • inferior MI (usually transient complete HB)
  • AV nodal blocking drugs: CCB, BB, digoxin
  • idiopathic degeneration of conducing system (lenegre’s or lev’s disease)
  • fibrosis around bundle of His
365
Q

define UNSTABLE bradycardia

A
  • bradycardia +
  • <90/60mmHg
  • symptomatic (breathlessness, ams, clinical features of shock, heart failure)
366
Q

define STABLE bradycardia

A

bradycardia +

  • > 90/60mmHg
  • NO symptoms
367
Q

general management for unstable bradycardia

A

drugs or pacing

368
Q

general management for stable bradycardia

A

monitor (no further treatment required)

369
Q

drugs for the management of unstable bradycardia

A

FIRST LINE
- IV atropine (does not affect infranodal blocks)

SECOND LINE

  • IV dopamine
  • IV adrenaline

move on to transcutaneous pacing if drug therapy fails

370
Q

should you treat 3rd degree heart blocks + ventricular escape beats with lignocaine?

A

NO

- may induce asystolic arrest!

371
Q

indications for transcutaneous pacing

A

1) failure of pharmacological agents
2) infranodal blocks with broad QRS complexes
3) transplanted hearts

phase iii internal medicine (1 decks)

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