Arrhythmias Flashcards
1
Q
What are the two types of myocytes?
A
Conduction/ contraction
Myocytes can perform both functions but tend to favour one/ other
Most myocytes are contractile
2
Q
Where does the SAN lie?
A
Between superior vena cava and right atrium
Spontaneously depolarises at a quicker rate than other cardiac cells and acts as the pacemaker of the heart
3
Q
At what level does the inferior vena cava pass through the diaphragm?
A
T8
Via the vena caval foramen
The phrenic nerve can also be found running through this foramen
*Image shows inferior vena cava entering right atrium
4
Q
What is shown in the image?
A
Right atrial appendage
5
Q
What is the Vaughan Williams classification?
A
Classification of anti-arrhythmic drugs
Based on the effect the drugs have on the action potential of the cardiac cells
6
Q
Phases of the action potentials of pacemaker cells
A
Phase 4: first upward slope due to opening of Na+ channels
Phase 0: Rapid up-slope due to opening of Ca2+ channels once there is enough Na+ inside cell and membrane is at -40mV
Phase 3: Once membrane potential reaches +10mV K+ channels open and K+ rushes out of cell, bringing it back down to starting point of -60mV
7
Q
Phases of the cardiac myocyte action potential
A
Phase 4: resting potential of -90mV
Phase 0: neighbouring cell triggers opening of Na+ channels and there is a rapid upstroke to +40mV, Slow-type Ca2+ channels also open
At the top of phase 0 Na+ channels close
Phase 1: K+ channels open and allow a small amount of K+ out - bringing membrane potential down
Phase 2: 2 channels (K+ and Ca2+) working in equilibrium in opposite directions hence the plateau
Phase 3: Calcium channels close and K+ continues to exit cell - accounting for repolarisation
8
Q
What is arrhythmia?
A
Deviation from a normal rhythm
Normal being regular and 60-100bpm
With each beat generated from SA node
9
Q
How are arrhythmias broadly classified?
A
Bradyarrhythmia (<60bpm)
Tachyarrhythmia (>100bpm)
10
Q
What are the main mechanisms responsible for tachyarrhythmias?
A
1. Abnormal automaticity: the pacemaker cells become abnormally permeable to Na+ during phase 4 resulting in an increase in the first upslope leading to disorganised firing of the cells
2. Triggered activity: abnormal leakage of + ions into the myocytes leading to a second bump on the myocyte action potential after depolarisation has occurred (= after depolarisations) This can trigger premature action potentials
3. Re-entry: an accessory pathway exists between the upper and lower chambers of the heart which allows the action potential to travel from the ventricles back to the stria causing them to contract before the SA node has fired (AVRT) - think Elliott think simple think one less letter
AVNRT: fast and slow pathways throguh the AV node - the signal from the SA node splits and half goes down the slow pathway, half goes down the fast pathway. The fast pathway signal reaches sooner than the slow pathway signal. The fast signal travels through the ventricles as well as up the slow pathway where it cancels the slow signal. Problems with the slow and fast pathway synchronisation leads to abberant conduction and repetetive firing of the AV node - leading to AV nodal re-entrant tachycardia
11
Q
AVRT vs AVNRT
A
Both cause fast, irregular heart rates (tachyarrhythmias)
AVRT - think Elliott, think simple, think one less letter
AVRT: accessory pathway allows signal from ventricles to travel back to the atria and cause them to contract without firing of the SA node
AVNRT: involves de-synchronisation between fast and slow pathways of AV node - signals loops round AV node and causes ventricles to contract without SA node firing/ atrial contraction - there will not be a P wave before the QRS
12
Q
Class 1 anti-arrhythmic drugs
A
Na+ channel blockers
Prolong phase 0 of AP, reducing the rate of depolarisation on non-nondal myocytes therefore reducing heart rate
Divided into 1A, 1B and 1C
13
Q
Discuss class 1A antiarrhythmics
A
1 Na+, oK+ hun
Block Na+ & K+ channels
1A: block fast Na+ channels responsible for phase 0 of the cardiac myocyte action potential and block some K+ responsible for repolarisation
- Class 1A agents cause a less-steep upstroke + a slower depolarisation (due to blockage of Na+ channels) and a longer effective refractory period (due to blockage of K+ channels, it takes more time before another AP can begin) PROCAINAMIDE, DISOPYRAMIDE
14
Q
Discuss class 1B antiarrhythmic drugs
A
Minimal blockage of fast Na+ channels
Shorterns action potential and shortner effective refractory period
LIDOCAINE
Mainly used for ventricular arrhythmias
15
Q
Discuss class 1C antiarrhythmic drugs
A
1C = powerful - think C think Charlotte think lots of salt blocked
They strongly block Na+ channels and therefore lead to a shallow upslope
Limited effect on the effective refractory period
FLECAINIDE
16
Q
Problem with class 1 anti-arrhythmic drugs?
A
They all have the potential to cause arrhythmia
17
Q
Discuss class 2 anti-arrhythmics
A
Class 2 = beta blockers
Block the effects of adrenaline on the heart - they depress the automaticity of the SA node and slow conduction through the AV node
Decrease HR and decreased contractility
PROPRANOLOL, ATENOLOL
18
Q
Class 3 antiarrhythmic drugs
A
K+ channel blockers
Slower efflux of K+ leaving cell means the absolute refractory period is prolonged and more time is needed before another action potential can occur
AMIODARONE, SOTALOL (which also works as a b-blocker 🙄🤨)
19
Q
Which anti-arrhythmic is given for VT/ VF cardiac arrest in A&E?
A
Amiodarone
Class III agent - given after adrenaline to treat life-threatening arrhythmia
20
Q
Side effects of amiodarone
A
Pulmonary fibrosis
Blue/ grey skin
Liver toxicity
Hyperthyroidism/ hypothyroidism (conatins iodine and is toxic to thyroid gland)
Long half life and lingers for months
21
Q
Which anti-arrhytmics cause prolonged QT syndrome?
A
Class 1A and class 3
They prolong time for repolarisation and therefore prolong time between the depolarisation and repolarisation of the ventricular cells
22
Q
Class 4 antiarrhythmic drugs
A
Block Ca channels particularly in the SA and AV nodes
Decrease sinus rate and reduce conduction through AV node
Reduce contractility of the heart
Decrease atrial rate
VERAPAMIL, DILTIAZEM
23
Q
What is the difference between non-dihydropyridines and hydropyridines?
A
Non-dihydropyridines: work in the heart and cause a negative ionotropic effect
e.g. diltiazem, verapamil
Dihydropyridines: work on the periphery and cause vasodilation
e.g. nifedipine, amlodipine
24
Q
Which drugs are used to treat AF?
A
Beta blockers e.g. propranolol or non-dihydropyridine Ca2+ blockers e.g. verapamil/ diltiazem
NICE doesn’t reccomend one over the other
They cana be used at the same time if monotherapy is ineffective
25
Class 5 antiarrhytmics
**Drugs that don't really fit elsewhere are grouped into class 5**
**DMSAD - doesn't matter, sad because they don't fit**
Digoxin, Magnesium Sulphate, Adenosine
**Digoxin:** Na/K ATPase inhibitor: enhances contractility and stimulates vagus node - which slows the heart rate)
**Magnesium sulfate:** mechanism unclear but when given IV is very good for treateing torsades de pointes and digoxin-induxed arrhythmia
**Adenosine:** works by stimulating adenosine receptors on the SA and AV nodes - slowing conduction time through the AV node. It can also interrupt re-entry pathways through the AV node
26
What is digoxin especially good for?
**Patients with heart failure and AF**
Blocks NA/K ATPase, causes more calcium to enter cell and therefore increases strength of contraction (inotropic)
Digoxin also stimulates the vagus nerve which causes a slower rate of firing of the SA node thus slowing the HR in AF
27
What is adenosine mainly used for?
Supraventricular tachycardia
It is 1st line drug for AVNRT and AVRT
28
Define arrhythmias
Disturbance of electrical activity in the heart
Can be asymptomatic/ symptomatic/ deadly
Often paroxysmal (sudden/ unpredictable) meaning diagnosis can be difficult
Primary causes: the heart itself
Secondary causes: non-cardiac cause
29
Description of arrhythmias after feeling pulse
Regularly irregular: not a steady pattern but a predictable one
Irregularly irregular: no pattern
30
What is bradyarrhythmia?
An inappropriately low HR \<60bpm
Sinus bradycardia is an appropriately low rhythm seen in athletes/ during sleep
31
What are the classic symptoms of bradyarrhythmias?
Symptoms often not present until HR \<45bpm
- Palpitations
- Light-headedness
- Dizziness
- Fatigue
- SOB
- Chest pain
- Syncope (Stokes-Adams attacks)
- Cardiogenic shock and hypotension: late stage + life threatening
32
Outline some non-cardiac causes of bradycardia and bradyarrhythmias
- Sleep and athletic training
- Drugs: beta blockers, calcium blockers, amiodarone
- Metabolic: hypothyroidism, hypothermia
- Electrolyte disturbance: hyperkalaemia, hyponatremia, hypercalcaemia, hypomangesaemia
Others: raised ICP, obstructive sleep apnoea
33
What is sick-sinus syndrome?
**Sinus node fails to pace the heart appropriately**
Leads to:
Sinus pauses: cessation in electrical activity
Sinus tachycardia
Sinus bradycardia
Atrial tachycardia
Chronitropic incompetence: heart does increase rate in respond to exercise
Atrial fibrillation
Brady-tachy syndrome (
34
Brady-tachy syndrome suggests what specific disease?
Sick sinus syndrome
35
What causes sick sinus syndrome?
Mainly due to idiopathic fibrosis of the sinus node
MI, cardiomyopathy, myocarditis
Sarcoidosis, amyloidosis, haemachromatosis
36
How is brady-tachy syndrome managed?
Pacing for bradyarrhythmia, drugs for tachyarrhythmia
37
Types of bradyarrhythmia
Sick sinus syndrome
Heart block:
- 1st degree
- 2nd degree : Mobitz 1&2
- 3rd degree
38
Normal ECG intervals
39
What is heart block?
Impaired conduction between the atria and ventricles
Caracterised into 1st, 2nd and 3rd degree
40
Where does geart block occur?
Can occur anywhere in the conduction system
AV node/ bundle of His = AV block
Block lower down = bundle branch block
41
Discuss 1st degree heart block
**Prolongation of the PR interval \>0.2seconds**
**0.2seconds = 1 large box**
Considered more of a delay rather than a block because every atrial impulse eventually reaches the ventricles
ECG change: prolonged PR interval \>0.2seconds
Husband comes home late every day ⌚️
42
Discuss 2nd degree heart block
**_Mobitz type 1_**
Longer and longer PR prolongation until a P wave fails to conduct - leading to a P wave that is not followed by a QRS
Only requires treatment if it is symptomatic, few cases progress to complete block
Husband comes home later and later until one night he doesn't come home 🤨 🐍
**_Mobitz type 2_**
Regularly \>1 P wave before every QRS e.g. 2:1 or 3:1
More likely to progress to complete heart block and is therefore often treated
Often symptomatic
Husband is home every now and again 😡
43
How is Mobitz type 2 managed?
Pacemaker
44
Discuss 3rd degree heart block
There is no association between atrial and ventricular actiivty
P waves = regular
QRS complexes = regular
But they are not associated at all
QRS rate is driven by spontaneous escape rhythm
Occasionally the atria and ventricles contract at the same time: atria contract but tricuspid vavle is closed - blood shoots back up jugular vein and **causes canon waves**
Serious and requires pacemaker
Husband and wife live separate lives 🧔🏻 ❌ 👩🏻🦱
45
Investigations for heart block
**Bedside:** 12-lead ECG
**Bloods:**
Troponin if thinking MI
U&E: derrangement can cause heart block
Calcium: derrangement can cause heart block
Thyroid function tests: hypothyroidism can cause heart block
If patient on digoxin, can check serum levels as this can cause heart block
46
How does digoxin cause heart block?
Digoxin enhances Vagus nerve activity, which slows conduction over the AV node.
Digoxin also has a direct effect on AV conduction, by slowing it.
This causes prolongation of the PR interval, which is considered a normal finding, unless severely prolonged.
Second- and third-degree AV block is evidence of intoxication
47
What causes a curved ST segment depression?
Digoxin toxicity
48
Management of bradyarrhythmia
Asymptomatic: often treated conservatively unless type 3
Symptomatic: pacemaker
Emergency treatment: transcutaneous pacing or IV atropine
49
Which drug is said to cause a feeling of impending doom?
Adenosine: causes complete AV block to terminate supraventricular tachycardias (AVRT, AVNRT
Idea is that it stops 2 hearts: that of the patient and that of the doctor...
50
How is bradyarrhythmia managed?
If symptomatic or type 3/ complete heart block: pacemaker
51
What is bundle branch block?
A block in conduction in the right/ left bundle branches
This causes a wide, biphasic QRS \>0.12seconds (120ms or 3 small boxes)
The shape of the QRS depicts where the block is
52
Right bundle branch block
Produces a late activation of the right ventricle because the right ventricle is activated by secondary conduction vs the left ventricle
53
ECG change in RBBB
**QRS is broad**
Deep S wave in lead I and V6
Tall, late R wave in V1
VI change is said to look like an M (**R**abbit ears in **R**ight chest lead V1)
V6 change is said to look like a W
54
Causes of RBBB
Often benign and can be found in normal hearts
Important to look for a cause: anything that causes strain on right side of heart
- PE
- Pulmonary HTN
- RV hypertrophy
- Cor pulmonale
- Inferior MI
55
Heart sound in RBBB?
S2 is split
56
Discuss LBBB
Delay in contraction of left ventricle due to conduction failure in left bundle branch
ECG: Deep S wave in V1 - 'W'
Tall, late R wave in lead I, aVL, V5 and V6 - 'M'
57
Can LBBB be normal?
NOOOOO - never occurs in normal hearts
It is a poor prognostic sign and needs investigating
New LBBB in a patient with chest pain - think MI
58
Causes of LBBB
- HTN
- Aortic stensosis: causes LV hypertrophy and damage to left bundle branches
- Coronary artery disease
59
What are tachyarrhythmias?
Abnormal heart rhythms \>100bpm
60
How are tachyarrhythmias categorised?
**Narrow complex: QRS \<120ms/ 3 small squares**
- AKA supraventricular tachycardias, they reflect organised & efficient electrical activity originating above the AV node
**Broad complex: QRS \>120ms/ 3 small squares**
- Reflect disorganised and delayed electrical activity usually originating in the ventricles - more unstable than narrow complex tachycardias
61
What is a supraventricular tachycardia?
Fast heart rates that arise from the atria or AV node
Can occur in healthy or diseased hearts
62
Discuss sinus tachycardia
Persistent increase in HR unrelated to level of physical/ emotional distress
Acute causes: exercise, emotion, pain, fever, infection, acute HF, acute PE, hypovolaemia, drugs
Chronic causes: pregnancy, anaemia, hyperthyroidism, atrial tachycardia associated with COPD
Management: treat the cause, beta blockers, ivabradine
63
Causes of narrow complex tachycardia?
**Supra-ventricular tachycardia**
- Sinus tachycardia
- Atrial flutter
- Atrial fibrillation
- AVRT
- AVNRT
64
What % of the population have a supraventricular tachycardia?
0.2%
65
What is atrial tachycardia?
A rapid, regular rhythm arising from a discrete area in the atria
AKA focal atrial tachycardia
Due to a hyper-excitable focus in the atria that fires at a faster rate than the SA node meaning it takens control from the SA node
ECG: regular SVT (narrow complex tachycardia) with abnormal P wave morphology e.g. very upright or inverted P waves
\*Can be difficult to diagnose by ECG alone
66
What is multi-focal atrial tachycardia?
Same mechanism as atrial tachycardia but many foci for abnormal activity
ECG: an SVT with 3 different-looking P waves
Typically seen in COPD where the right side of the heart is dilated
67
Which SVT is classically associated with COPD?
Multi-focal atrial tachycardia (MAT)
68
Classification of atrial tachycardias
1. Sinus tachy: regular tachycardia with regular and uniform P waves before every QRS
2. Focal atrial tachycardia: recurrent, regular tachy, HR 100-250bpm. P waves are visible before every QRS but they are abnormal
3. AVNRT: P waves may be visible but usually follow the QRS
4. AVRT
5. Multi-focal atrial tachycardia: irregular tachycardia, P waves before every QRS and at least 3 different P wave morphologies when looking at a single lead
6. Atrial flutter: atrial activity is regular and ~300bpm, rate is usually ~150 bpm because every 2nd contraction propogates to ventricles
7. Atrial fibrillation: irregular tachycardia with a beat-beat variation in heart rate
69
How is atrial flutter sawtooth appearance sometimes more easily seen?
Turn the ECG upside down...
70
ECG showing a regular SVT with P waves that have an unusual axis e.g. inverted?
Think focal atrial tachycardia
71
ECG showing regular SVT with P waves before every QRS but the P waves all appear different?
Multifocal atrial tachycardia
72
What are re-entrant tachycardias?
Occur when electrical activity conducts through abnormal circuits which loop back on themselves to form a re-entry loop which is self stimulating
Often occurs around a circuit of scar tissue
Key features: seen in youn patients, tend to be short-lasting, rarely life-threatening but are often symptomatic
73
Types of re-entrant tachycardias
Atrioventricular nodal re-entry tachycardia (AVNRT)
Atrioventricular re-entry tachycardia
74
Discuss AVNRT
Most common SVT - 80%
* *AV node has 2 tracks;*
* Fast conducting track=long refractory period; P wave normally conducted through this pathway.
* Slow conducting track=short refractory period.
* If have an ectopic immediately after a normal P wave it will conduct through slow tract (as fast is still refractory).
* By time has reached bottom of slow-track, fast will have recovered so it travels back up the fast track, which then re-stimulates the slow-track
75
ECG in AVNRT
Typical appearance = absent P waves and tachycardia
Normal QRS with rhythm of 140-240bpm
Atria and ventricles depolarise almost simultaneously so P waves are hidden in the QRS or seen immediately before/ after QRS
\*P waves can sometimes be seen within the QRS as a pseudo R wave
76
Difference between atrial tachycardia and other SVT?
Atrial tachycardia is defined as a supraventricular tachycardia (SVT) that does not require the atrioventricular (AV) junction, accessory pathways, or ventricular tissue for its initiation and maintenance
77
What is the classic presenting rhythm in patients with digoxin toxicity?
Focal AT
78
Which type of patient is AVNRT classically seen in?
75% of cases are in women
Can occur in young patients as well as those who are older with heart disease
79
Investigations for AVNRT
Patient often presents with palpitations
**ECG:** tachycardia with normal and regular QRS complex + either
a) no P wave
b) P wave immediately before QRS
c) P wave immediately after QRS
**Bloods:** U&E to look for electrolyte causes
**Echo:** look for any structural damage
80
Typical clinical presentation of AVNRT in A&E
Middle aged or older female
Pounding sensation in neck, palpitations, lightheadedness, syncope, SOB
Canon A waves - referred to as 'frog sign' because the JVP with buldge like a frog's neck 🐸
81
How are AVNRT and AVRT managed?
**_Medical: if patient haemodynamically stable_**
Valsalva manoeuvre: ask patient to push down/ bear down as if having a poo while glottis is closed
Dive reflex: ice-cold cloth to face
Carotid sinus massage: 5-10 seconds
**_Pharmacological:_**
- Adenosine: rapid bolus, works in 80-95%
**_If patient is haemodynamically unstable emergency cardioversion is needed_**
**_Long term management_**
Beta blockers, verapamil, diltiazem, ablation therapy (1st line in WPW)
82
Why does polyuria occur in patients with AVNRT and AVRT
Increased levels of atrial-natriuretic peptide - typically occurs once the episode is over
83
Appearance of ECG in AVRT
P waves clearly seen between QRS and T wave - Impulse travels back up and causes atrial contraction after ventricular contraction
84
On which side of the heart are accessory pathways found?
Left
Called the bundle of Kent in WPW
85
Which SVT is esecially common in women?
AVNRT
86
Good way to try and manage AVNRT/ AVRT in children?
Get them to blow into a syringe
87
What would cause a new normall-narrow complex tachycardia to be broad?
Pre-existing BBB
88
What is Wolf-Parkinson White?
Condition where an accessory pathway (bundle of Kent) results in ventricular pre-excitation
Signal from pathway and AVN combine to contract ventricles - on ECG pre-excitation is seen as a delat wave and a PR interval \<120ms with a QRS \>110ms
Usually benign but can lead to other arrhythmias and is often symptomatic so treated
89
Clinical features of SVTs
Palpitations: flitter in chest, fast beat, start and stop suddenly, commonly terminated by Valsalva manoeuvre
\*Many patients with palpitations are due to extrasystole (both atrial and ventricular extrasystoles are common)\*
- If palptations occur immediately after/ during exercise they need referring to cardio, also if the palpitations are associated with pain/ syncope
- Dyspnoea, fatigue, polyuria due to increased ANP, raised JVP
90
What are extrasystoles?
AKA ectopic beats, contractions that occur out fo the normal rhythm when there is electrical discharge from somewhere in the heart other than the SAN
Common
Atrial extrasystoles: seen in \>60% adults
Ventricular extrasystoles: 40-75% adults, common in structural heart disease (nost common type of arrhythmia after MI
91
Risk factors for extrasystoles
HTN
Heart disease
Electrolyte disturbance
Alcohol
Drugs
Stress
Infection
Hyperthyroidism
Caffeinr
92
Presentation of patient with extrasystole
Palpitations = main symptom
- Worse at rest, dissapear with exercise - if they get worse with exercise this is a worrying feature
- Syncope, atypical chest pain, fatigue, chronic cough
93
History taking for extrasystoles
- Onset, duration, associated symptoms and recovery
- Other cardiac symptoms: chest pain, breathlessness, syncope or pre-syncope
- Exertional syncope = alarming
- FHX: cardiac death/ disease
- CHD risk factors
94
Investigations for extrasystoles
12-lead ECG resting/ ambulatory/ holter (24hr ECG)
FBC, TFTs
U&Es
Echo
95
ECG finding in atrial extrasystole
Premature P waves which look different to normal P wave
96
Ventricular extrasystole ECG
Wide, abnormally shaped QRS complexes
If they occur at every 2nd or third beat they are called bigeminy/ reigeminy respectively
97
In the context of extra systole, which patients need referring
Urgent symptoms: chest pain, SOB, LOC
Syncope/ pre-syncope
Significant ECG abnormality
Significant cardiac disease
FHx
Troublesome symptoms
98
Managament of extrasystole
Low risk with no symptoms/ cardiac problems: reassure
Medication: beta blockers, catheter ablation of ectopic focus
Lifestyle: avoid caffeine
99
What is atrial flutter?
A type of atrial tachycardia due to a macro re-entrant curcuit where the atria contract at a very high rate (typically ~300bpm)
Many patients with flutter have associated atrial fibrillation
Typical flutter: origin is in right atrium, classic saw-tooth pattern and rates of 240-350 bpm
Atypical flutter: origin is in right or left atrium, ECG is variable and rates may be faster than those seen in typical flutter
100
Epidemiology of atrial flutter
2nd most common arrhythmia after AF
Commonly associated with AF
Increases with age
80% cases in men
Systemic thromboembolism less likely to occur in atrial flutter than AF
101
Aetiology of atrial flutter
Age is most common risk factor
- Structural anomalies: left-atrial dilatation = strongest predictor for developing flutter
- CHD, atrial dilatation, cardiac surgery/ ablation, obesity, alcohol, COPD, cardiomyopathy, myxoma, pericarditis, sick sinus syndrome, obstructive sleep apnoea, very high-intensity sport
102
Presentation of atrial flutter
Varies, can be an incidental ECG finding, can be found after patient has had a stroke
Palpitations, fatigue, dyspnoea, pre syncope
Syncope
TIA/ stroke
Pulse: can be regular/ irregular, AV conduction usually 2:1 so ventircular rate is 150bpm - if. AV conduction is 1:1 this can cause haemodynamic collapse
Associated with symptoms of underlying disease e.g. alcoholism, thyrotoxicosis
103
Where is the saw-tooth pattern of atrial flutter best seen?
II, III and aVF - usually shows atrial rates of 240-340bpm
104
Investigations for atrial flutter
ECG: no isoelectric baseline, saw tooth waves between the QRS complexes, variable AV conduction e.g. 2:1, 3:1 etc
Look for causes: CXR, TFTs, ESR, renal function and LFTs
Echo
105
Management of atrial flutter
**If haemodynamically unstable:** direct current cardioversion (DCCV)
**Acute, haemodynamically stable:** B-blocker/ Ca2+ blocker - often not as effective as with other SVTs, anticoagulate with a NOAC, cardioversion is 2nd line - patient must have been anti-coagulated for at least 3 weeks
**Recurrent flutter:** catheter ablation
Ongoing: antithrombotics, same as AF
106
What is atrial fibrillation?
Most common sustained arrhythmia characterised by irregularly irregular atrial pulse and loss of association between cardiac apex beat and radial pulse
Conducts rapidly to the ventricles resulting in an irregular ventricular rate
High risk of thromboembolic disease and stroke due to poor atrial contractions leading to blood stagnation
107
Classification of atrial fibrillation
- Paroxysmal: lasts \<7 days
- Persisten: lasts \>7 days
- Long-standing: lasts \>1yr
- Permanent: lasts \>7 days and can't be cardioverted
108
Epidemiology of AF
Most common sustained cardiac arrhythmia with increasing prevalence
3% of adults aged 20+
10% those aged 80+
Greater prevalence in those who are older and have conditions such as HTN, HF, CAD, valvular heart disease, obesity, DM, CKD
More common in men
109
Aetiology of AF
Triggering event: any condition resulting in raised atrial pressure, increased atrial mass, atrial fibrosis, infiltration or inflammation
HTN is most common cause
HF is 2nd most common cause
IHD, valvular disease, hypothyroidism, hyperthyroidism, alcohol, caffeinem pneumonia, PE
110
Foci that cause AF are often located where?
Pulmonary veins - the myocardial tissue of the left atrial wall extends in to the pulmonary venous walls
111
Presentation of patient with AF
30% cases AF is an incidental finding
Breathless
Palpitations
Dizziness
Chest discomfort
Stroke/ TIA
112
Signs of AF
S1 is variable in intensity
Irregularly irregular pulse
**ECG:** no clear P waves, fine oscillations of the baseline, rapid and irregular QRS - described as a worn out saw
113
Investigations for AF
**ECG:** in all who have an irregular pulse, where symptomatic or not
- This can either be a 12 lead, ambulatory, holter or event recorder
**- Bloods:** TFTs, CXR, echo
**- Coagulation screen** if considering patient for anti-coagulants
**Echo** to exclude structural heart disease
114
Management of atrial fibrillation
**Haemodynamic instability:** direct current cardioversion (DCCV)
**Acute but haemodynamically stable:**
Offer rate/ rhythm control if started \<48hrs ago: DCCV or pharmacological cardioversion (with amiodarone/ felecainide or only amiodarone for those with structural heart disease)
Offer rate control (metoprolol, verapamil, diltiazem) if started \>48hrs ago: **if patients with an unknown duration of AF are considered for long-term rhythm control, do not do this until they have been on an anti-coagulant for 3 weeks minimum**
**Anti-coagulation if AF is new:** offer heparin at initial presentation and continue until full assessment and anti-thrombotic therapy started
**Anti-coagulation if AF diagnosis confirmed:** offer oral anti-coagulant if there is high risk of AF recurrence or sinus rhythm isn't restored within 48hrs of onset
115
Which type of AF on ECG is particularly dangerous?
Pre-excited AF
Occurs when an accessory pathway conduction the atrial fibrillation to the ventricles - this can quickly degrade into ventricular fibrillation
\*Important not to give patients with pre-excited AF drugs that block the AV node because this increases conduction through the accessory pathway\*
116
Difference between AF and other SVTs?
AF has an irregularly irregular rhythm
117
What is a delta wave?
Slurring of the QRS upstroke - occurs because the action potential from the SAN is able to conduct very quickly to the ventricles via the accessory pathway (usually the AV node slows it down)
This results in a short PR interval
Seen in WPW
118
When is WPW espeically life threatening?
When it occurs in addition with AF
If medication is sued that temporarily blocks the AV node - the ectopic foci continue firing but the fibrillation is sent down the accessory pathway leading to ventricular fibrillation
119
What are the AV node-blocking agents?
**A**denosine, **A**miodarone
**B**eta-blockers
**C**alcium channel blockers
**D**igoxin
ABCD
120
What is ventricular tachycardia?
**Broad complex** (\>120ms or 3 small squares) tachycardia originating from a ventricular focus
Defined as \>=3 successive ventricular beats occurring at \>100bpm
Dangerous as can lead to VF, cardiac arrest and death 🫀
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What is Torsades de Pointe?
Polymorphic VT in which the QRS complexes appear to twist around an imaginary baseline
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Broad complex tachycardia with an irregularly irregular rhythm?
Think about AF with bundle branch block
\*\*Ventricular tachycardia is regular
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Aetiology of VT
Monomorphic VT resulting from an abnormal re-entry circuit often caused by scarring e.g. due to sichaemic heart disease. cardiomyopathy, myocarditis, long QT syndrome
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What are the shockable rhythms?
Heart rhythms associated with cardiac arresr are divided into 2 groups
**Shockable:** VF, pulseless VT
**Non shockable:** asystole (flat line) and pulseless electrical activity (electrical activity of the heart is not accompanied by a palpable or effective pulse
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Classification of VT
Pulsed (palpable pulse) or pulseless
Non-sustained \<30s or sustained \>30s
Monomorphic: QRS always same
Polymorphic: QRS appearance frequently changes
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Key characteristics of sustained VT
\>30 seconds
Often results in syncope, pre-syncope, hypotension, cardiogenic shoch and cardiac arrest
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Management of VT
**Haemodynamically unstable**
* DCCV (3 attempts).
* Amiodarone.
**Haemodynamically stable**
* If cause identifiable
* Lidocaine and procainamide are other options.
* Amiodarone 1st line.
* If medication fails then DCCV.
* Can attempt radiofrequency catheter ablation to certain pt.
* If pt. has high risk of recurrence then give implantable defibrillator.
All patients with Torsades de Pointes require urgent DCCV
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What % of broad complex tachycardias are caused by VT?
85%
The remainder are SVT with BBB
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Which features suggest VT rather than SVT with BBB?
Very broad QRS \>160ms
Extreme axis -90 to -180 degrees
- Capture beats: where a SAN beat captures the ventricles and produces a normal looking beat
Bizarre QRS morphology
AV dissociation
\*Treat as VT until proven otherwise
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You see an ECG with broad complex tachycardia - what is it?
VT until proven otherwise
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What are ICDs?
Implantable cardioverter defibrillators
Used for secondary prevention in patients with VT/ VF causing syncope or cardiac arrest
Used for primary prevention in patients with high-risk conditions e.g. severe heart failure
- They do not prevent VT but they restore sinus rhythm when it occurs
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What is VF?
Myocardium devoid of any coordinated electrical or mechanical activity and cardiac output ceases 🫀❌
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Management of VF
VF always results in cardiac arrest so alays requires DCCV to prevent asystole and death
Long term treatment = ICD
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What is Brugada syndrome?
Inherited AD channelopathy that occasionally presents with sudden cardiac death due to VT/ VF
More common in males in SE Asia
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How is Brugada syndrome diagnosed?
presence of:
- VT/ VF
- FHx of sudden cardiac death
- Family members with Brugada syndrome
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ECG findings Brugada syndrome
ST elevation in V1-V3, without ischemia
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Management of Brugada syndrome
ICD
Avoid drugs that can cause the arrhythmia: anti-arrhythmics, psychotropics and anaesthetic agents
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What is the CHA2DS2-VASC score?
Annual stroke risk in patients with AF
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What is the HASBLED score?
Estimates the risk of bleeding in patients on warfarin
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Medication used for tate control in AF
Beta blockers
Calcium channel blockers
Digoxin (reserved for more sedentary patients because it doesn't allow the heart rate to rise with exercise)
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What are the priorities when treating AF?
Reduce stroke risk
Control HR
Control symptoms
- Restoring sinus rhythm has not been shown to improve prognosis
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Which arrhythmia is commonly seen in systemic illness and following surgery?
AF
