Arrhythmias Creator: Cameron McCloskey Flashcards
(119 cards)
1
Q
What should be the only pathway for electrical activity to pass between the atria and ventricles?
A
AV node
2
Q
What is an arrhythmia?
A
An irregular heart beat
- o Abnormal electrical activity in the heart:
- Rate Rhythm sequence of conduction origin of conduction)
- o Easiest way to define is by abnormalities in rate As set by SA node: 60-100 bpm (normal heart rate) >100 bpm: tachyarrhythmia • ≥300 bpm: fibrillation <60 bpm: bradyarrhythmia
3
Q
What are the two main classes of arrhythmia?
A
- Supraventricular (SVT)
- Ventricular (VT)
- see N.N
These classifications are based on the origin of the arrhythmia
4
Q
What does “supraventricular” confer about the location of the arryhtmia’s origin?
A
It is above the ventricles and within the atria, SA node, AV node or His origin
5
Q
Name 3 tachycardic SVT arrhythmias
A
- Atrial fibrillation
- Atrial flutter
- Ectopic atrial tachycardia
- More specific
- Atrial - e.g AF, A flutter
- Sinus - SA firing too fast
- Paroxysmal SVT Atrioventricular nodal reentrant tachycardia: o reentry circuit in AV node at fast rates or through accessory pathway
6
Q
Name 2 bradycardic SVT arrhythmias
A
- Sinus bradycardia
- Sinus pauses
7
Q
What are AV node arryhthmias due to?
A
Re-entrant rhythms
e.g. AVN re-entrant tachycardia (SVT arrhythmia)
8
Q
Where and why do ventricular arrhythmias arise?
A
Arise in ventricles due to ectopic beats from latent pacemakers
9
Q
What is supraventricular paroxysmal tachycardia?
A
A re-entrant tacycardia
This comes and goes spontaneously
10
Q
Wolf-Parkinson-White syndrome involves which type of arrhythmia?
A
Paroxysmal supraventicular tachycardia
11
Q
What are the three types of venticular arrythmias?
A
- Ventricular tachycardia
- Ventricular fibrillation
- Asystole - the heart fails to beat
12
Q
What are ectopic beats
A
Beats arising from outwith the SA node
13
Q
Which factors may promote tachycardia and ectopic beats? 5
A
- Hyperthermia
- Hypoxia
- Hypercapnia
- Cardiac dilatation
- Hypokalaemia (prolongs repolarisation)
14
Q
Which factors may induce bradycardia and heart block? (2)
A
- Hypothermia
- Hyperkalaemia
- Physiological
- Pathologica
- Drugs
- ↓ metabolic activity
- Electrolyte imbalance
- High ICP
15
Q
What are afterdepolarisations?
A
Depolarisations occurring, for various reasons, within phase 2 of the myocitic action potential
They may induce a second heart beat
16
Q
Afterdepolarisations are associated with use of which drug and why?
A
Digoxin
It leads to a calcium overload in cells making contractions easier
17
Q
Deficiency of which element will potentiall lead to afterdepolarisations and why?
A
Potassium
Hypokalaemia leads to afterdepolarisations because a lack of potassium makes it difficult for cells to depolarize. Rather, it is because potassium plays a critical role in maintaining the resting membrane potential of cardiac myocytes.
18
Q
What is the name of the accessory pathway utilised in WPW syndrome?
A
The bundle of Kent
19
Q
How is sinus tachycardia treated?
A
Beta blockers
20
Q
What is micro re-entry?
A
This is when the AV nodal re-entrant tachycardia circuit uses the circuit within the AVN
21
Q
Micro re-entry is most common in which type of person?
A
Young woman
22
Q
Acutely, how are SVT arrhythmias treated?
A
Increase vagal tone via:
- Valsalva manouvre
- Carotid sinus massage
23
Q
How are SVTs treated long term to slow the conduction in the AVN?
A
- Adenosine
- Verapamil
24
Q
Problematic accessory tracts are treated by what?
A
Radiofrequency abalation
25
What is first degree AV block?
There is no block
The PR interval is increased
There is no treatment
26
What are the two types of second degree heart block?
1. Mobitz type I
2. Mobitz type II
27
Describe Mobitz type I
PR interval gradually increases until a QRS comple does not occur
The cycle then resets
28
Describe Mobitz type II
The is pathological and usually involves a ratio of P waves to QRS complexes since only some P waves can get through
Common ratios are 2:1 and 3:1
29
What is third degree heart block?
No potentials from the SA node will make it through the AV node so there is no coordination between atrial and ventricular coordination
30
What is the treatment for third degree heart block?
Ventricular pacing
31
How do ventricular arrythmias present on ECG?
Wide QRS
32
How can ventricular tachycardia often be identified on ECG?
* Wide QRS
* No P waves (present, yet not visible)
* Large T wave opposite to QRS deflection
This is for monomorphic VT which involves just one circuit so all the beats are the same
33
What is polymorphic VT and how does it present on ECG?
This happens all over the ventricles so there are numerous circuits leading to completely irregular patterns
34
Give an example of polymorphic VT
Torsades de Pointes
35
How can VT be treated acutely, and why is this treatment useful?
DC and synchronised cardioversion
36
When a VT is unstable, how is it treated?
Direct current cardioversion (DCCV)
37
If VT is stable, how is it treated?
Anti-arrhythmic drugs
38
How is VT treated long term?
* Re-vascularisation to correct ischaemia
* No anti-arrhythmic drugs as these worsen outcomes long-term
* Cardioverter defibrillation use if life threatening
* VT catheter ablation
* Beta blockers
39
What is ventricular fibrillation?
Ventricular activity is chaotic and leads to the heart losing its ability to function as a pump
40
How is ventricular fibrillation treated?
* Defibrillation
* CPR
41
What is the most serious potential consequence of atrial fibrillation?
Stroke
42
Which 3 main categories can atrial fibrillation be classified under?
1. Paroxysmal - episodes terminate spontaneously last \< 48 hours
2. Persistent - episodes are not self terminating - last \> 48 hours
3. Permanent - continuous AF which cannot be cardioverted, or attempts to do so may be inappropriate
The first detected episode of AF is often also described as a form
43
What are the symptoms of AF?
* Palpitations
* Dyspnoea
* Chest pain
* Pre-syncope (dizziness) or syncope
* Fatigue
44
What are the sign(s) for AF?
An irregularly irregular pulse
45
What is used for diagnosis of AF and why?
ECG
Other conditions can give an irreguarly irregular pulse such as ventricular ectopics
46
What are the two components of AF management?
1. Rate/rhythm control
2. Reducing stroke risk (anticoagulation)
47
How do rate and rhythm control vary?
1. Rate - accepts there will be an irregular pulse, yet aims to slow down the pulse
2. Rhythm - attempts to return the patient to normal sinus rhythm (cardioversion)
48
Which two methods can be used for cardioversion?
1. Drugs
2. Synchronised DC electrical shocks
49
What is used for first line in AF to control the rate?
Either:
* Beta blocker
* Rate limiting calcium channel blocker (diltiazem)
50
Assuming first line rate control treatment fails for AF, what is second line?
Combination therapy using any 2 of the following drugs:
1. Beta blocker
2. Diltiazem
3. Digoxin
51
What is a normal rate for atrial fibrillation?
Can be \>300bpm
52
In theory, in atrial fibrillation, the ventricular contraction rate should match the atrial rate since there is nothing wrong with the conduction pathway in this sense.
Why is it that this doesn't happen when atrial contraction rates get very high?
The AV node cannot conduct impulses at this rate and this is the rate limiting factor for ventricular contraction
53
Why is it dangerous when patients switch from AF to sinus rhythm?
There is high risk of an embolism being pushed out the atria when they contract properly
This can lead to stroke
54
Before attempting cardioversion, what must be confirmed about the patient's disease or pharmacological status?
They have had symptoms for less than 48 hours
or
Have been anticoagulated prior to cardioversion
This is to avoid the risks of stoke via embolism release
55
What is the scoring strategy used to determine the most appropriate anticoagulation strategy depending on the patient's risk of stroke?
CHA2DS2-VASc
56
Which invasive procedure can allow for sinus rhythm in AF to be restored?
Catheter abalation of atrial focus
| (or surgery)
57
What treatment is given, or considered, when a patient has the following CHA2DS2-VASc scores:
a) 0
b) 1 (female)
c) 1 (male)
d) 2
a) None
b) None
c) Consider anticoagulation
d) Offer anticoagulation rather than consider
58
What are the components of CHA2DS2-VASc?
C - Congestive heart failure (points = 1)
H - Hypertension (points = 1)
A2 - Age \>= 75 (points = 2); age 65-74 (points = 1)
D - Diabetes (points = 1)
S2 - Prior stroke or TIA (points = 2)
V - Vascular disease (points = 1)
S - Sex - female (points = 1)
59
If AF has an onself of \<48 hours how may a patient be cardioverted?
Electrical - DC cardioversion
Pharmacologically - Amiodarone (structure heart disease), flecainide or amiodarone (without structural disease)
60
If it is confirmed the onset of AF was under 48 hours, what should be done after cardioversion in such patients?
Nothing
Further anticoagulants are unnecessary
(they are already anticoagulated by heparin for example, before cardioversion)
61
If the patient has had AF for \>48 hours what should be done before cardioversion?
The patient must be anticoagulated for at least 3 weeks beforehand
62
If the patient has had AF for \>48 hours what cardioversion technique is recommended?
Electrical cardioversion
Patients should then be anticoagulated for at least 4 weeks
63
What is the main drug used for pharmaclogical cardioversion of atrial fibrillation?
Amiodarone
(or flecainide, if no evidence of structural heart disease)
64
Following a stroke or TIA, what is the anticoagulant of choice?
Warfarin
65
In acute stroke patients, why is anticoagulation therapy delayed?
Risk of haemorrhage
66
When would digoxin be the preffered agen to control rate in patients with AF?
If the patient has coexistent heart failure
(otherwise, beta blocker or calcium channel blockers are used)
67
Which agents can maintain sinus rhythm in patients with a history of AF?
* Amiodarone
* Flecainide
* Sotalol
68
What is lone AF?
AF in the absence of underlying heart disease
Possibly genetic
69
What is the gold standard for terminating AF via cardioversion?
Electrical cardioversion
This is more effective than the pharmacological option
70
In AF, where is the ectopic focus commonly located?
Ostia of pulmonary veins
71
Where does ventricular tachycardia originate?
Ventricular ectopic focus
72
What are the two main types of VT?
Monomorphic VT - Mostly caused by MI (all waves are the same on ECG)
Polymorphic VT - all waves on ECG are different as there are many areas producing ectopic beats
73
Give a common example of polymorphic VT
Torsades de pointes
74
How is VT managed if the patient has low systolic BP (\<90mmHg), chest pain, heart failure or heart rate \>150bpm?
Immediate cardioversion
75
If antiarrhythmic drugs fail for VT management what must be used?
Electrical cardioversion
Syncronised DC shocks
76
Which drugs will be used in VT?2
* Amiodarone
* Lidocaine
77
Which drug is strictly not used to treat VT?
Verapamil
78
If drug therapy fails what can de done for patients with VT?
* Implantable cardioverter-defibrillator (ICD) - particularly useful for patients with LV dysfunction
* EPS - electrophysiological study
79
Name some drugs that can induce a long QT interval
* Amiodarone
* Sotalol
* Class 1a antiarrhythmic drugs
80
What are some causes for a long QT interval?
* Hypokalaemia
* Hypocalcaemia
* Acute MI
* Myocarditis
81
Which sign on an ECG is distinctive of Torsades de pointes?
Long QT interval
| (may also deteriorate into VF)
82
How is long QT interval treated?
Magnesium sulphate (IV)
83
What causes Wolff-Parkinson-White syndrome?
Accessory pathway (bundle of Kent) between atria and ventricles
(can be left or right sided)
84
Which type of arrhythmia is associated with WPW syndrome?
Atrioventricular re-entry tachycardia (AVRT)
85
What are possible ECG features for WPW syndrome?
* Short PR
* Delta waves
* Left/right axis deviation depending on side of accessory pathway
86
How is type A (left sided - by far the most common) differentiated with type B (right sided) WPW syndrome?
There is a dominant R wave in V1 in type A that is not present in type B
87
What is the management for WPW syndrome?
Radiofrequency ablation of the accessory pathway
Sotalol, amiodarone or flecainide
88
When treating WPW syndrome, which drug should be avoided if there is coexistent AF?
Sotalol
(may increase transmission through accessory pathway by prolonging AV refractory period)
89
What are cannon A waves and where are they seen?
Visible pulsations in the JVP
90
What causes cannon A waves?
Particular associated with third degree heart block, when atria and ventricles contract simultaneously
A large pressure is pushed against the AV valves which radiated back up the jugular vein
This is also associated with pulmonary hypertension
91
What defines first degree heart block?
Lengthened PR interval
| (PR \> 0.2 seconds)
92
1. The ECG in ventricular tachycardia usually shows broad complex tachycardia true/ false
2. A.ST segment depression in the ECG is diagnostic of acute myocardial infarction
1. true
2. false
* Hypercalamia causes early depolarisation phase 0 and early repolarisation pahse 4
* myocardium ischemia means more K+ efflux
* NO O2 NO ATP thus more K+ efflux changing the isoelectric point mV
* ST depression caussed by **_sub_** endocardial ischemia
* ST elevation caused by transmural Ischemia MI
*
93
•Ventricular tachycardia can be treated by ICD Ture / False
True
94
heart rate is regular in first heart block true / false
true
95
Diltaiazem can be used to treat arterial fibrillation True? false
True
96
treatment of acute bradycardia with adverse features
Atropine 500mcg IV
97
factors influence bradycardia
Mobitz type II block
Board QRS
recent asystole
Ventricular pause more than 3s
98
other drugs to increase the heart rate
**isoprenaline, adrenaline, aminophylline, dopamine, glucag**o
99
future management of acute bradycardia
transvenous pacing/ **permanent pacemaker insertion**
100
causes of first degree heart block
athletes
acut inferior MI
hyperkalaemia
Digoxin
101
causes of Mobitz I
MI apex area
beta blockers Ca2+ blockers digoxin
myocarditis
102
management of Mobitz type I
if symptoms raised with bradycardia Atropine is mostly used
103
definitive management of third degree heart block
permanent pacemaker
104
**Management of narrow complex tachycardias**
**(DC) cardioversion** is indicated.
105
next step of **Management of narrow complex tachycardias**
determine if its regular or irregular
* regular (SVT) vagal manoeuvres if it falils then adenosine
* Irregular mostly AF thus
1. if Paroxysmal is typically managed with **rhythm control** **.**
2. **if P**ersistent is typically managed with r**ate control**
106
When does CABG have a survival advantage over PCI (in terms of patient profile)?
CABG has a mortality advantage over patients who: are over 65 years old, have diabetes, or who have anatomically complex 3 vessel disease (with or without left main stem stenosis).
107
Causes of acute bradycardia
* Sinus/AV nodal disease
* Drug induced such as beta blockers, calcium channel blockers
* Electrolyte abnormalities
* **_Hypothyroidism_**
108
Clinical features of Acute bradycardia
* Dizziness
* Syncope
* Tiredness
109
What is the 2nd line management of bradycardia with adverse features?
* Transcutaneous pacing OR
* Isoprenaline 5 micrograms per minute, OR adrenaline 2-10 micrograms per minute OR aminophylline or dopamine OR glucagon
110
nitial management of acute bradycardia
* DR ABCDE, ECG monitoring and any reversible causes should be identified and treated.
* If there are any adverse features (shock, syncope, myocardial ischaemia or heart failure) then atropine 500 mcg IV is given
111
What is the management of beta-blocker overdose?
Glucagon
112
Causes of acute myocarditis
* Coxsackie - most common virus
113
Acute myocarditis Question: Signs
Examination findings are non-specific. Signs of heart failure may be evident (along with S3 and S4 gallops). If pericarditis is associated, auscultation can reveal a pericardial friction rub.
114
Acute myocarditis Question: Diagnosis
* ECG - non-specific ST segment and T wave changes (which may be regional, depending on degree and location of myocardial involvement), along with ectopic beats and arrhythmias if present
* Troponin - markedly elevated.
* Echocardiogram can reveal ventricular dysfunction if present, in the form of diastolic dysfunction or regional wall motion abnormalities.
* Cardiac MRI findings can help confirm the diagnosis of myocarditis by showing the presence and extent of inflammation.
* Endomyocardial biopsy via cardiac catheterisation is the gold standard diagnostic tool, but is associated with its own risks as it is an invasive test.
115
VENTRICULAR TACHYCARDIA
• Impulses originate at ventricular pacemaker
• Wide ventricular complexes, WIDER QRS \>0.14 s
• Sequela: May lead to ventricular fibrillation, asystole, and
sudden death.
116
What is the first line of management for VT ?
BOTH A & B
Drug of choices are both a & b. The next line of management is
cardioversion/defibrillation. Long term management would be
administration of Radiofrequency ablation of abnormal tissue or
implantation of Automatic Implantable Cardiac Defibrillator. Look
for underlying myocardial infarction as well and conduct the
appropriate laboratory work-up.
117
a. CONSIDER TORSADES DE POINTES
Typical reading of TDP which has the notable IRREGULAR
rhythm
o This is due to big causes of EADs
o Hypokalemia, hypomagnesemia, hypocalcemia
o Offending drugs (ABCDE)
1st degree heart block:
o Should have P-waves every after QRS and PR-interval is
prolonged
This is NOT how atrial fibrillation looks like:
o Should have the characteristic waves “squiggly lines”
o NO Visible P-waves every QRS
118
Which pathway or underlying mechanism of AVNRT does
fast conduction going to the bundle of His \> bundle branches
B. BETA PATHWAY
Recall. See Table 5.
Beta pathway
Fast conduction going to the bundle of His \> bundle
branches \> ventricles
↓
circles around to go up to the beta pathway, while the
alpha pathway cancels it going down
↓
AV depolarization stops
↓
long refractory period = slower repolarization
↓
Note: due to slow repolarization, next firing goes down
the alpha pathway
119
If found to have a 3rd degree heat block, how do you
administer treatment?
Treat underlying inferior wall myocardial infarction
through PCI.
b. Administer Ca chloride to stabilize cardiac membranes
in cases of hyperkalemia.
c. Add HCO3 to address the acidosis.
