cardiology: ecg Flashcards
(371 cards)
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
2
Q
what is the tetrad in tetralogy of fallot
A
1) rvh
2) ps
3) overriding aorta
4) vsd
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
4
Q
2 key characteristics of SA node
A
1) automaticity
2) intrinsic rate
5
Q
avn does not allow 1:1 conduction beyond ___
A
150
6
Q
position of v1 lead
A
4th intercostal space to the right of sternum
7
Q
position of v2 lead
A
4th intercostal space to the left of sternum
8
Q
position of v4 lead
A
5th intercostal space mid clavicular line
9
Q
position of v3 lead
A
directly between v2 and v4
10
Q
position of v5 lead
A
level with v4 at left anterior axillary line
11
Q
position of v6 lead
A
level with v5 at left midaxillary line
12
Q
bipolar lead I
A
RA & LA
13
Q
bipolar lead II
A
RA & LL
14
Q
bipolar lead III
A
LA & LL
15
Q
augmented unipolar lead aVR
A
RA
16
Q
augmented unipolar lead aVL
A
LA
17
Q
augmented unipolar lead aVF
A
LL
18
Q
what surface/region/coronary artery of the heart do leads I, II, aVL look at?
A
left lateral surface
LV
LCx
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
20
Q
what surface/region/coronary artery of the heart do leads V1, V2 look at?
A
anteroseptal region
mainly LV
LAD
21
Q
what surface/region/coronary artery of the heart do leads V3, V4 look at?
A
IV septum and LV
LV
LCx
22
Q
what surface/region/coronary artery of the heart do leads V5, V6 look at?
A
anterior/lateral wall of LV
LV
LCx
23
Q
what surface/region/coronary artery of the heart does lead avR look at?
A
lateral surface
24
Q
what surface/region/coronary artery of the heart does lead avR look at?
A
lateral surface
25
physiological significance of P wave
depolarisation of atria in response to SA node triggering
26
physiological significance of PR interval
delay of AV node to allow filling of ventricles
27
physiological significance of QRS complex
depolarisation of ventricles
28
physiological significance of ST segment
beginning of ventricle repolarisation (should be flat)
29
physiological significance of T wave
ventricular repolarisation
30
what does size of QRS complex represent?
muscle mass
31
approach to interpreting ecg
1) check normal features first (speed, scale)
| 2) 7+2 step plan
32
what does each large square on ecg represent?
200ms (0.2s)
33
what does each small square on ecg represent?
40ms (0.04s)
34
what is the scale of an ecg?
10mm/mV
35
what are the 7 +2 steps of an ecg?
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
36
maximum height of P waves in sinus rhythm in leads II and/or III
2.5mm
37
what is considered tachycardia?
>100bpm
38
what is considered narrow complex tachycardia?
QRS < 120ms
| >100bpm
39
types of REGULAR narrow complex tachycardia
1) sinus tachycardia
2) atrial tachycardia
3) atrial flutter with fixed conduction
4) SVT: AV nodal re-entry tachycardia (AVNRT), orthodromic AVRT, junctional tachycardia
40
causes of sinus tachycardia
- 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
41
what is considered wide complex tachycardia?
QRS > 120ms
42
what criteria describes the features of VT?
brugada criteria
43
features of VT based on brugada criteria
- 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
44
features of AVNRT
- regular, 180-250/min
- P in QRS complex (resulting in RsR' in V1)
- young patients and paroxysmal
- treatment: valsalva/carotid massage/adenosine
45
what type of wide complex tachycardia is torsades de pointes?
polymorphic ventricular tachycardia
46
how does torsades de pointes usually present?
pulseless in cardiac arrest
47
treatment for torsades de pointes?
IV MgSO4 1g x 1-2 doses
48
usual demographic for VT
older patient with previous MI
49
reference range for bradycardia
<60bpm
50
reference range for 1st degree heart block
PR interval > 200ms (>1 large square/>5 small squares)
51
types of second degree heart block
1) mobitz I (wenckebach phenomenon)
| 2) mobitz II
52
describe mobitz I heart block
progressive PR interval prolongation culminating in non-conducted P wave (usually benign)
53
usual wenckebach pattern of P:QRS
3: 2
4: 3
5: 4
54
cause of mobitz I heart block
reversible conduction block at AV node
- drugs; bb, ccb, digoxin, amiodarone
- increased vagal tone in athletes
- MI
- myocarditis
- post cardiac surgery
55
describe mobitz II heart block
intermittent non-conducted P waves without progressive prolongation of PR interval
56
cause of mobitz II heart block
failure of conduction at level of his-purkinje system
57
mobitz II is more likely than mobitz I to be associated with _____ , _____ and progression to ____ ?
haemodynamic compromise
severe bradycardia
3rd degree heart block
58
describe 3rd degree heart block
no relationship between p wave and qrs complex (absence of AV conduction)
59
typical presentation of 3rd degree heart block
severe bradycardia with av dissociation (independent atrial and ventricular rates)
60
method to calculate HR on ecg
300/number of large squares between 2 consecutive R waves
OR
no. of QRS complexes in rhythm strip x 6
61
normal PR interval
120-200ms (3-5 squares)
62
conduction interval in WPW syndrome
PR interval <120ms + delta wave
63
PR interval <120ms without delta wave
lown-ganong-levine syndrome
64
normal QTc interval
<420ms in men
| <450ms in women
65
formula for calculation of QTc
bezett's formula
66
what is bezett's formula?
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
67
reference range for prolonged QTc
>450ms
68
causes of prolonged QTc
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
69
inheritance pattern of romano-ward syndrome
AD
70
inheritance pattern of jervell and lange-nielsen
AR
| a/w congenital deafness
71
drugs which cause prolonged QTc interval
1) antipsychotics
2) type IA, IC and III anti arrhythmics
3) tricyclic antidepressants
4) antihistamines
5) others: chloroquines, hydroxychloroquine, quinine, macrolides (erythromycin, clarithromycin)
72
reference range for shortened QTc
<350ms
73
causes of shortened QTc
1) hypercalemia
2) congenital short QT syndrome (K+ channel defect - AD)
3) digoxin effect
74
normal cardiac axis
-30deg to +90deg
75
causes of left axis deviation (lead I +ve and AVF -ve)
- may be normal in short and fat individuals
- LVH
- RV infarct
- L anterior hemiblock
76
causes of right axis deviation (lead I -ve and AVF +ve)
- 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
77
normal PR interval
0.12-0.2s
78
describe p wave in p pulmonale
peaked, tall P wave
79
height in p wave on inferior leads (II, III, aVF) in p pulmonale
>2.5mm
80
height of p wave in V1 and V2 in p pulmonale
>1.5mm
81
causes of p pulmonale
1) cor pulmonale
2) tricuspid stenosis
3) congenital heart disease (pulmonary stenosis, ToF, primary pulmonary HTN)
82
causes of absent p wave
1) AF
| 2) junctional/ventricular rhythm
83
describe p wave in p mitrale
bifid, broad
84
what does p mitrale indicate
LA enlargement
85
what does p pulmonale indicate
RA enlargement
86
p mitrale is a precursor to ____
AF
87
appearance of p wave in lead II in p mitrale
bifid p wave >40ms between both peaks
| total p wave duration >110ms
88
appearance of p wave in lead V1 in p mitrale
biphasic p wave with terminal negative portion >40ms
| terminal negative portion > 1mm deep
89
causes of p mitrale
1) mitral stenosis (classical)
2) mitral regurgitation
3) systemic HTN
4) aortic stenosis
5) HOCM
90
causes of p wave inversion
ectopic atrial rhythm e.g. MAT
91
normal duration of QRS complex
≤ 120ms (3 small squares)
92
causes of pathologic Q waves in V1/V2
old STEMI
93
what is the index for voltage criteria of LVH?
sokolow-lyon-index
94
what is the voltage criteria for LVH according to the sokolow-lyon index?
R in V5/V6 + S in V1 > 35mm
95
normal R wave progression
R increases V1-V5
| R>S beyond V3
96
types of abnormal R wave progression
1) no R wave
2) exaggerated R wave progression
3) reversed R wave progression
4) small R waves with little progression
97
what does absence of R wave indicate
evolved/old anterolateral STEMI (+ Q waves)
98
what does exaggerated R wave progression indicate
LVH
99
what does reversed R wave progression indicate
RVH
100
what does small R waves with little progression indicate
pericardial effusion
101
5 causes of large R waves in V1
1) dextrocardia
2) RVH
3) posterior AMI
4) type A WPW
5) RBBB
102
causes of microvoltages (<5mm) of QRS complex
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)
103
causes of widened QRS complexes (>3 small squares)
1) BBB
2) pre excitation (WPW)
3) ventricular extrasystoles/VT
4) complete heart block
104
causes of ST elevation (>1mm)
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
105
features of pericarditis on ecg
1) globally raised ST segments
2) saddle shaped ST elevations
3) PR depression in all leads
4) PR elevation in aVR
106
appearance of T waves in hyperkalemia
tall tented T waves
107
cause of brugada syndrome
mutation in na+ channel
108
what factors unmask/augment brugada syndrome?
- fever
- ischemia
- drugs
- hypokalemia
- hypothermia
- post cardioversion
109
drugs which unmask/augment brugada syndrome
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
110
who is the most perfect girl in the world?
chlochlo!
111
types of brugada syndrome ecg patterns
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
112
describe type 1 brugada's syndrome
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
113
describe brugada's sign
coved ST segment elevation >2mm in >1 of V1-V3 + negative T wave
114
describe type 2 brugada syndrome
>2mm of saddleback shaped st elevation
115
describe type 3 brugada syndrome
morphology of either type 1 or 2 but with <2mm of ST segment elevation
116
causes of ST depression (≥1mm)
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
117
causes of peaked T wave
1) hyperkalemia
2) hypermagnesemia
3) hyperacute T wave in STEMI (less tented, broad base)
4) normal grusin type II variant
118
causes of flat and prolonged T wave
hypokalemia
119
physiological causes of T wave inversion
- normal in children
| - normal in V1 in males, V1-V2 in females
120
pathological causes of T wave inversion
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
121
pathological causes of u waves
hypokalemia
| hypomagnesemia
122
ecg features of RBBB
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
123
mode of depolarisation of RV in RBBB
cell to cell conduction
124
causes of RBBB
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
125
ecg features of LBBB
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)
126
causes of LBBB
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
127
name of scoring system for acute coronary system in LBBB
smith- modified sgarbossa's criteria
128
describe smith-modified sgarbossa's criteria
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)
129
conduction system supplied by RCA
- SAN, AVN, bundle of his
| - variable twig to posterior fascicle of LBB
130
conduction system supplied by LCA
- RBB and anterior fascicle of LBB
- variable twig to posterior fascicle of LBB
- anterior STEMI: RBBB + left posterior hemiblock
131
ecg features in left anterior hemiblock
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
132
pathophysiology of left anterior hemiblock
- usually due to previous ischemic insult
| - delayed activation of anterior portion of LV due to blocked/delayed transmission in anterior fascicle
133
ecg features of left posterior hemiblock
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
134
types of combined blocks
1) bifascicular block
| 2) trifascicular block
135
describe bifascicular blocks
RBBB + left anterior/posterior hemiblock
| - RBBB + left axis deviation
136
desecribe trifascicular blocks
RBBB + LAFB + 1st degree heart block
| - high risk of entering complete heart block
137
types of ectopic beats
1) escape beats
| 2) premature beat
138
describe escape beats
- failure of SAN to discharge (dysfunctional SAN) > beat later than expected
- pause BEFORE ectopic beat (sinus arrest)
139
describe premature beats
- ectopic pacemaker discharges before SAN > beat earlier than expected
- pause AFTER ectopic beat
- normal SAN
140
define escape rhythm
ectopic pacemaker continues pacemaking function to maintain CO
141
types of escape rhythms
1) atrial escape rhythm
2) junctional escape rhythm
3) ventricular escape rhythm
142
HR in atrial escape rhythm
normal; 60-80bpm
143
HR in junctional escape rhythm
40-60 bpm
| regular
144
HR in ventricular escape rhythm
20-40bpm
| regular
145
morphology of atrial escape rhythm
indistinguishable from sinus rhythm
146
morphology of junctional escape rhythm
1) no P waves
| 2) narrow QRS
147
consequences of junctional escape rhythm
usually tolerated
148
management of junctional escape rhythm
treat underlying cause
149
morphology of ventricular escape rhythm
1) no p wave
2) big, broad QRS complex
3) T wave inversion
150
consequences of ventricular escape rhythm
1) symptomatic (hypotension, chest tightness, dizziness, syncope)
2) cardiogenic shock
151
management of ventricular escape rhythm
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
morphology of atrial premature beat
1) abnormal P waves
| 2) normal narrow QRS complex
153
morphology of junctional premature beat
1) NO P waves/abnormal P wave with PR <120ms
| 2) normal narrow QRS complex
154
morphology of ventricular premature beat
1) NO P waves
2) wide bizarre QRS
3) T wave opposite polarity
155
differential diagnosis of atrial premature beat
1) sinus arrhythmia
- p waves identical
2) MAT
- > 3 different P wave morphologies
- no sinus rhythm
156
differential diagnosis of junctional premature beat
AF
157
causes of atrial and junctional premature beat
1) idiopathic
2) ischemia
3) electrolyte abnormalities
158
causes of ventricular premature beat
1) idiopathic
2) ischemia
3) electrolyte abnormalities
4) trauma (>6 PVCs/min definite pathological)
159
treatment of atrial premature beat
1) no treatment needed
| 2) treat underlying cause
160
treatment of junctional premature beat
treat underlying cause
161
treatment of ventricular premature beat
1) treat underlying cause
2) antiarrhythmatics
3) unstable: cardioversion
162
describe trigeminy rhythm of PVC
2 sinus beats followed by 1 PVC
163
ecg features of PVCs
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
name the grading system for PVCs
lown's grading
165
purpose of lown's grading
determine if PVCs need to be treated
166
characteristics of lown I ectopics
uniform, unifocal, infrequent (<30/hr)
167
management for lown I ectopics
treat STEMI
168
characteristics of lown II ectopics
uniform, unifocal, frequent (>30/hr)
169
management for lown II ectopics
none necessary
170
characteristics of lown III
multiform, multifocal
171
management of lown III
treat hypertension/AS
172
characteristics of lown IV A
PVCs in couplets (2)
173
treatment of lown IV A
treat STEMI
174
characteristics of lown IV B
PVCs in salvos (≥3)
175
number of PVCs for VT
≥5
176
treatment of lown IV B
treat STEMI AND VT (amiodarone)
177
characteristics of lown V
R on T: PVC starts before preceding T wave ends
178
management of lown V
admit & monitor even if NIL symptoms
| high risk of developing into VT/VF (irritating heart during repolarisation)
179
clinical features of digoxin toxicity
GIT: n/v, anorexia, diarrhoea
visual: blurred vision, yellow/green discolouration, halos
CVS: palpitations, syncope, dyspnoea
CNS: confusion, dizziness, delirium, fatigue
180
ecg features of digoxin toxicity
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
cause of increased automaticity in digoxin toxictiy
increased intracellular calcium
182
cause of decreased AV conduction
increased vagal effect at AV node
183
approach to etiology of palpitations
1) cardiac causes
| 2) non cardiac causes
184
cardiac causes of palpitations
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
non cardiac causes of palpitations
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
causes of IRREGULAR narrow complex tachycardia
1) atrial flutter with variable conduction
2) atrial fibrillation
3) multifocal atrial tachycardia
187
causes of REGULAR broad complex tachycardia
1) monomorphic VT
2) antidromic AVRT
3) any regular narrow complex tachycardia with BBB or pre-excitation (e.g. SVT with aberrancy)
188
causes of IRREGULAR broad complex tachycardia
1) polymorphic VT
| 2) any irregular narrow complex tachycardia with BBB or pre-excitation (e.g. WPW with A fib)
189
general pathophysiology of narrow complex tachycardia
1) automatic firing of foci
| 2) re-entry
190
ecg pattern in atrial flutter
saw tooth pattern (multiple p waves)
191
types of atrial flutter
1) cavotriscupid isthmus dependent flutter
- re entry circuit within RA
2) CTI independent flutter (atypical AFL)
- re entry circuit within RA or LA
192
types of CTI dependent flutter
1) typical (counterclockwise) flutter (majority)
| 2) reverse typical AFL
193
long term treatment of typical AF
CTI ablation
| anticoagulation
194
long term treatment of atypical AF
beta blocker
| anticoagulation
195
what scoring system used for AF stroke risk (in deciding use of anticoagulation)?
CHA₂DS₂-VASc Score
196
types of atrial fibrillation
1) paroxysmal (≤ 48h)
2) persistent (> 7d or requires cardioversion)
3) long standing persistent (> 1y)
4) permanent (accepted)
197
etiology of afib
1) valvular afib
- moderate to severe MS
- mechanical heart valve
3) others (non valvular afib) - 90%!
198
complications of afib
1) CCF
| 2) thromboembolism
199
complications of treatment
1) overanticoagulation
| 2) underanticoagulation
200
describe permanent AF
1) CV failed OR
| 2) persistent afib where joint decision made by patient and clinician to no longer pursue rhythm control strategy
201
extracellular matrix alterations in afib
1) interstitial and replacement fibrosis
2) inflammatory changes
3) amyloid deposition
202
myocyte alterations in afib
1) apoptosis
2) necrosis
3) hypertrophy
4) dedifferentiation
5) gap junction
203
changes to heart in afib
1) extracellular matrix alterations
2) myocyte alterations
3) microvascular changes
4) endocardial remodelling (endomyocardial fibrosis)
204
general classification of causes of afib
1) cardiac
2) non cardiac
3) lone afib
205
cardiac causes of afib
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
non cardiac causes of afib
1) sepsis
2) respiratory (COPD/PE/pneumo)
3) endocrine (hyperthyroidism, DM, hypoglycemia)
4) electrolyte (hyperkalemia)
5) alcohol (holiday heart syndrome)
207
describe lone afib
patients with paroxysmal, persistent, longstanding persistent, or permanent AF who have no structural heart disease or attributable non-cardiac causes
208
clinical features of afib
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
symptoms of afib
1) palpitations/tachycardia
2) fatigue/weakness
3) dizziness
4) reduced exercise capacity
more severe:
5) dyspnea
6) angina
7) syncope (infrequent)
210
name of clinical scoring system for AF
european heart rhythm association (EHRA) score
211
describe EHRA I
no symptoms
212
describe EHRA II
mild symptoms
| normal daily activity NOT affected
213
describe EHRA III
severe symptoms
| normal daily activity AFFECTED
214
describe EHRA IV
disabling symptoms
| normal daily activities discontinued
215
how would you split your investigations for afib?
1) cardiac
| 2) non cardiac
216
what cardiac investigations would you order for afib?
1) ECG
2) 2D echo
3) holter monitoring or event recorders
4) exercise testing
217
what non cardiac investigations would you order for afib?
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
ecg changes to make diagnosis of afib
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
2D echocardiogram changes in afib
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
rationale for holter monitoring/event recorders for afib
- identify arrhythmia if it is intermittent
- assess overall ventricular response rate (esp if rate control strategy chosen)
- look for pauses
221
function of exercise therapy for afib
to evaluate CAD (class I antiarrhythmics contraindicated in CAD)
222
summarise the treatment for afib according to AHA/ACC/HRS guidelines
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
oral anticoagulation options for afib/atrial flutter
1) vit k antagonist: warfarin
2) DOAC
- factor Xa inhibitors: apixaban, rivaroxaban, edoxaban
- direct thrombin inhibitors (DTI): dabigatran
224
name 3 factor Xa inhibitors
apixaban, rivaroxaban and edoxaban
225
name a direct thrombin inhibitor
dabigatran
226
name 2 scoring systems used in guiding anticoagulation therapy
1) CHA2DS2-VASc score
| 2) HAS-BLED score
227
risk factors in CHA2DS2-VASc score
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
CHA2DS2-VASc score cut off to begin OAC
male: ≥2
female: ≥3
229
are DOAC or VKA preferred for anticoagulation therapy?
DOAC
230
why are DOAC preferred in anticoagulation therapy over VKA?
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
what therapy can be offered if patients have CI to OAC?
antiplatelet therapy
232
CHA2DS2-VASc score cut off to CONSIDER OAC
male: 1
female: 2
233
anticoagulation treatment for valvular AF patient
all to be treated with warfarin regardless of CHA2DS2-VASc score
234
is CHA2DS2-VASc score used for non valvular AF?
NO
235
rationale for HAS-BLED score
prediction of risk of bleeding in patients on anticoagulation for AF
236
describe HAS-BLED score
```
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
reference rate for ESRF
CrCl <15ml/min (whether on dialysis or not)
238
categories of patients with afib and CKD
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
OAC for patients with afib + ESRF
warfarin or apixaban (but still not approved by TTSH cvm or renal)
240
OAC for patients with afib
serum Cr ≥ 1.5mg/dL: apixaban
CrCl 15-30mL/min: dabigatran
CrCl 15-50mL/min: edoxaban
CrCl <50mL/min: rivaroxaban
241
lab monitoring for patients on warfarin
initiation: weekly INR
stable: monthly INR
242
lab monitoring for patients on DOAC
before initiation: RF & LFT + annual reevaluation
243
what procedure can be done for patients who have CI to LT anticoagulation?
left atrial appendage occlusion (percutaneous or surgical)
244
in general is rate or rhythm controlled preferred?
rate control
245
when is rhythm control preferred over rate control?
1) pre excited afib
| 2) afib during pregnancy
246
when is rhythm control considered a safe alternative to rate control in symptomatic patients?
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
methods of rate control therapy
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
contraindications of beta blockers in afib
afib complicated by
- haemodynamic instability (cardiogenic shock)
- acute decompensating HF (ADHF)
- severe bronchospasm (if non severe: can opt for b1 selective BB)
249
contraindications of non-dihydropyridine CCB
afib complicated by
- haemodynamic instability (cardiogenic shock)
- ADHF
- EF < 40%
250
why is digoxin esp good in IMMOBILE patients?
exercise induces sympathetic activation > inhibits efficacy of digoxin
digoxin works by increasing vagal tone
251
risk of amiodarone
pharmacological cardioversion (only use amiodarone as rate control agent in ACUTE setting)
252
most important consideration prior to commencing rhythm control in AF >48h
ensure no LA thrombus!
253
methods of rhythm control
1) electrical cardioversion (DCCV)
2) pharmacological cardioversion (class Ic, III antiarrhythmics)
3) catheter ablation
254
examples of drugs used in pharmacological cardioversion
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
contraindication of class I antiarrhythmics in pharamacological cardioversion
patients with IHD/structural heart disease > use class III antiarrhythmics (amiodarone)
256
lab monitoring for pharmacological cardioversion
1) ecg
2) RF
3) LFT
257
drugs used for bridging regimen prior to interruption of warfarin (for initiation of certain procedures to treat the underlying cause of afib)
unfractionated heparin (IV UFH) or low molecular weight heparin (SC clexane)
258
drugs used after procedures/when newly initiating OAC
UFH or LMWH
259
why is UFH/LMWH used as a bridging regimen when initiating warfarin treatment in patients with afib?
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
reversal agent for DABIGATRAN in the event of life threatening/uncontrolled bleeding or urgent procedure
iDArucizumab
261
reversal agents for apiXAban, rivaroXAban and edoXAban (factor Xa inhibitors) in the event of life threatening/uncontrolled bleeding or urgent procedure
andeXAnet alfa
262
define wolff parkinson white syndrome
congenital pre-excitation syndrome characterised by combination of presence of congenital accessory pathway and episodes of tachyarrhythmia
263
what congenital heart disease is WPW most commonly associated with?
ebstein's anomaly
264
WPW is a cause of _____ _____ _____
sudden cardiac arrest
265
describe the pathophysiology of WPW syndrome
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
clinical features of WPW synrome
1) asymptomatic
2) symptomatic
- palpitations: episodes of AF, AVRT
- cardiogenic syncope
267
most common arrhythmia a/w WPW syndrome?
afib
268
what investigations to order for WPW syndrome?
12 lead ecg
269
ecg changes in WPW syndrome
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
ecg changes in type A WPW syndrome
positive delta wave in all precordial leads with R/S > 1 in V1
271
ecg changes in type B WPW syndrome
negative delta waves in leads V1 and V2
272
management for WPW syndrome
- 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
is orthodromic AVRT a narrow or broad complex tachycardia?
narrow complex
| indistinguishable from AVNRT
274
management of orthodromic AVRT
as per AVNRT
275
is antidromic AVRT a narrow or broad complex tachycardia?
broad complex (appearing like VT)
276
management of antidromic AVRT
1) IV procainamide
2) synchronised cardioversion
3) AICD once an arrhythmia develops
277
definition of ventricular tachycardia
regular broad complex tachycardia originating from a ventricular focus with at least 5 consecutive ventricular ectopic beats
278
types of ventricular tachycardia
1) sustained VT: >30s or requiring intervention due to haemodynamic compromise
2) non sustained VT
- ≥3 consecutive ventricular complexes terminating spontaneously in <30s
279
what are the 3 mechanisms for initiation and propagation of ventricular tachycardia
1) re-entry (commonest mechanism)
2) triggered activity
3) abnormal activity
280
describe the re-entry mechanism for ventricular tachycardia
- 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
describe triggered activity as a mechanism for VT
early or late after depolarisations (e.g torsades de pointes, digoxin toxicity)
282
describe abnormal activity as a mechanism for VT
accelerated abnormal impulse generated from a region of ventricular cells
283
differential diagnosis for regular broad complex tachycardia
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
clinical features suggestive of VT
1) age >35
2) structural heart disease/cardiomyopathy
3) ischaemic heart disease/previous AMI
4) CCF
5) family history of sudden cardiac death
285
what does family history of sudden cardiac death suggest?
- HOCM
- congenital long QT syndrome
- brugada syndrome
- arrhythmogenic right ventricular dysplasia
286
ecg features suggestive of VT (slight variation from brugada's criteria)
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
types of VT
1) monomorphic VT
2) polymorphic VT
3) bidirectional VT
288
causes of monomorphic VT
1) ischemic heart disease
2) dilated cardiomyopathy
3) hypertrophic cardiomyopathy
4) chagas disease: american trypanosomiasis
289
describe ecg of torsades de pointes
- QRS complexes twisting around isoelectric line
- PVT
- QT prolongation
290
causes of bidirectional VT
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
presentation of ventricular fibrillation
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
causes of ventricular fibrillation
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
differential diagnosis of ventricular fibrillation
1) ventricular flutter
2) PEA
3) asystole
294
ecg features of ventricular flutter
1) continous sine wave
2) no identifiable p waves, qrs complexes or t waves
3) >200bpm
295
management of ventricular flutter
defibrillate if pulseless
296
differential diagnosis for fine ventricular fibrillation
asystole
297
define cardiac arrest
cessation of effective cardiac activity as confirmed by absence of signs of circulation
298
define return of spontaneous circulation
1) palpable pulse (SBP ≥ 60mmHg)
| 2) effective waveform for at least 30s
299
define sustained ROSC (i.e. survived the event)
ROSC ≥ 20min
300
define end of event
- death is declared OR
- spontaneous circulation restored and sustained for ≥ 20min OR
- 20min after extracorporeal circulation has been established
301
define survival to hospital discharge
point at which patient is discharged from hospital's acute care unit regardless of neurological status
302
describe the chain of survival
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
time interval for administration of epinephrine in ACLS
3-5mins
304
dosage of epinephrine in ACLS protocol
1mg
305
dosage of amiodarone in ACLS protocol
1st dose: 300mg
| 2nd dose: 150mg
306
describe the initial management for cardiac arrest
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
minimum acceptable compression depth for CPR
5cm
308
minimum acceptable compression rate for CPR
100/min
309
describe good quality ventilation in CPR
1) tidal volumes 400-600ml
2) 1s/breath
3) compression: ventilation ratio = 30:2
310
how is CPR effectiveness monitored?
waveform capnography (EtCO2)
311
describe steps in secondary ABCD
1) airway
2) breathing
- pre-intubation: 30:1
- post-intubation: 10:1 uninterrupted
3) circulation
4) drugs
312
methods of confirming ETT placement
1) 5 point auscultation
2) bilateral chest expansion
3) tube misting and demisting
4) EtCO2 (N: 35-40mmHg)
313
EtCO2 in cardiac arrest
<10mmHg
314
EtCO2 in good quality CPR
10-20mmHg (better quality CPR > higher EtCO2)
315
drugs administered in secondary ABCD for VF/pulseless VT
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
drugs administered in secondary ABCD for asystole/PEA
1) IV adrenaline 1mg
- given every 2 cycles of CPR (3-5min)
2) NaHCO3
- hyperkalemia/TCA overdose
317
methods to confirm asystole
1) check connection of lead and cables
2) select different leads
3) increase gain (identify fine VF)
318
potentially reversible causes of cardiac arrest
5H:
- Hypovolemia
- Hypoxia
- H+: acidosis
- Hyper/Hypokalemia
- Hypothermia
5Ts:
- tamponade (cardiac)
- thrombosis (coronary)
- thrombosis (pulmonary)
- tension pneumothorax
- tablets (drug OD)
319
describe the post ROSC bundle
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
describe investigations to be done post ROSC
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
describe monitoring post ROSC
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
initial management of tachydysrhythmias
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
signs of clinical instability
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
wide QRS tachycardia is ___ until proven otherwise
VT
325
describe the algorithm for wide complex tachycardia
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
describe management post cardioconversion of WCT
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
management of stable MONOmorphic VT
- 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
management of stable POLYmorphic VT if QTc prolonged
- IV MgSO4 1-2g
- stop drugs prolonging QTc
- overdrive pacing (may precipitate VF: have DCCV available)
329
indications of overdrive pacing
1) failure of drug therapy
2) recurrent arrhythmia
3) contraindication to cardioversion (digoxin toxicity)
4) aid to differentiate VT from SVT
330
management of stable POLYmorphic VT if QTc normal
- treat ischemia
| - control electrolytes
331
management of stable SVT with aberrancy
adenosine 6mg rapid push then 12mg rapid push
332
what is the half life of adenosine
7s
333
avoid ___ if there is a possibility of VT
verapamil (irreversible block to AV node: asystolic arrest)
334
management of UNSTABLE WCT
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
describe the algorithm for REGULAR narrow complex tachycardia
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
describe management of STABLE SVT
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
physiological basis of valsalva maneouvres
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
what position is patient in during carotid sinus massage
trendenlenburg position
339
what would you explain to the patient during administration of IV adenosine for chemical cardioversion?
1) transient chest discomfort
2) nausea
3) flushing
340
steps in administration of IV adenosine for chemical cardioversion
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
describe the management of UNSTABLE SVT
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
describe the algorithm for irregular narrow complex tachycardia
1) initial management
2) establish irregular NCT with pulse AF
3) unstable vs stable
- unstable: synchronised cardioversion
- stable: rate/rhythm control
343
management of STABLE irregular narrow complex tachycardia
1) rate control
| 2) rhythm control
344
describe rate control in STABLE irregular narrow complex tachycardia
- 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
describe rhythm control in STABLE irregular narrow complex tachycardia
- check coagulation status
- TEE to identify atrial thrombi
- IV amiodarone 150mg over 20min and repeat once if needed
346
management of UNSTABLE irregular narrow complex tachyardia
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
what is the classification for antiarrhythmic drugs
vaughan williams classification
348
describe class Ia agents according to the vaughan williams classification
Na+ channel blockade, prolongs repolarisation
| - e.g. procainamide, quinidine, disopyramide
349
describe class II agents according to the vaughan williams classification
beta blockers: indirect Ca channel blockade by attenuating adrenergic activation
- e.g. propranolol, esmolol, metoprolol
350
describe class III agents according to the vaughan williams classification
potassium channel blockers: widen action potential by blocking potassium K+ efflux
- e.g. amiodarone, sotalol, ibutilide
351
describe class IV agents according to the vaughan williams classification
```
non dihydropyridine (cardioselective) CCB
- e.g. verpamil, diltiazem
```
352
describe class V agents according to the vaughan williams classification
work via unknown mechanisms
| e.g. adenosine, digoxine, MgSO4
353
describe class Ib agents according to vaughan williams classification
Na+ channel blockade, shortened repolarisation
| - e.g. lidocaine, mexiletine, phenytoin, tocainide
354
describe class Ic agents according to vaughan williams classification
Na+ channel blockade, repolarisation unchanged
| - e.g. encainide, flecainide, propafenone
355
causes of sinus bradycardia
- athletes
- physiological response to sleep
- vagotonic procedures
- hypothyroidism
- raised ICP: cushing's reflex
- drugs: BB, CCB, digoxin
- sick sinus synrome
- glaucoma: oculocardiac reflex
356
describe cushing's reflex
physiological nervous system response to acute elevations of intracranial pressure (ICP), resulting in Cushing’s triad
357
describe cushing's triad
1) widened pulse pressure
2) bradycardia
3) irregular respiration
358
causes of 1st degree heart block
- 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
define a high grade AV block
when 2 or more P waves not conducted
360
causes of mobitz II second degree heart block
- 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
definitive management of mobitz II second degree heart block
insertion of permanent pacemaker
362
what level of blockage is indicated by a narrow QRS complex in 3rd degree heart block
block at the level of AV node
| - HR usually 40-60min
363
what level of blockage is indicated by a broad QRS complex in 3rd degree heart block
infranodal block
| - HR usually <40/min
364
causes of 3rd degree/complete heart block
- 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
define UNSTABLE bradycardia
- bradycardia +
- <90/60mmHg
- symptomatic (breathlessness, ams, clinical features of shock, heart failure)
366
define STABLE bradycardia
bradycardia +
- >90/60mmHg
- NO symptoms
367
general management for unstable bradycardia
drugs or pacing
368
general management for stable bradycardia
monitor (no further treatment required)
369
drugs for the management of unstable bradycardia
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
should you treat 3rd degree heart blocks + ventricular escape beats with lignocaine?
NO
| - may induce asystolic arrest!
371
indications for transcutaneous pacing
1) failure of pharmacological agents
2) infranodal blocks with broad QRS complexes
3) transplanted hearts
