Cardiology (Arrhythmia) Flashcards
describe the pathophysiology of heart block
- Heart block describes impaired electrical conduction in the heart.
- The sinoatrial node (SAN) sends impulses to the atrioventricular node (AVN) which then sends impulses down the Bundle of his and via the bundle branches towards the apex of the heart which split into fascicles which supply the myocardium.
types of heart block
1) Sinoatrial node blocks - blocks within the SAN
2) Atrioventricular blocks- blocks within AVN
- 1st degree
- 2nd degree : Mobitz 1 and Mobitz 2
- 3rd degree: complete heart block
3) Hisian block: blocks within bundle of His
4) Bundle branch blocks- within the left and right bundle branches
5) Fasicular/hemiblocks- within the fasicles of the left bundle branch
first degree heart block
abnormally slow conduction through the AV node
- despite slow conduction, every impulse that origiates from the SAN is passed to the ventricles
- leads to PR interval prolongation
On an ECG, a first-degree AV block is defined as a PR interval >0.20 seconds (>5 small squares)
causes of first degree heart block
1) Common in younger, athletic patients due to increased vagal tone
2) Ischaemic heart disease:
* Coronary heart disease
* Myocardial infarction
3) Electrolyte imbalances:
* Hypokalaemia
* Hypomagnesaemia
4) Infection:
* Rheumatic fever
* Infective endocarditis
5) Drugs:
* Digoxin
6) Autoimmune and inflammatory conditions:
* Sarcoidosis
* Systemic lupus erythematosus
* Rheumatoid arthritis
* Systemic sclerosis
second degree heart block
Second-degree atrioventricular (AV) block describes impaired conduction between the atria and ventricles leading to PR interval progression. More specifically, second-degree heart block describes when one or more (but not all) atrial impulses fail to pass to the ventricles.
Second-degree AV block can be divided into two subtypes:
- Mobitz type I (Wenckebach)
- Mobitz type II
Mobitz type I (Wenckebach)
there is a progressive prolongation of the PR interval until a P wave is completely blocked (known as a dropped beat)
- each impulse leads to the prolongation of the refractory period of the AV node
- when an impulse from the atria arrives at the AV node during the rleative refractory periodm it is conducted more slowly
- as the refractory period gets longer with each impulse, an atrial impulse arrives at the AV node during its absolute refractory period and is not conducted
- After this the AV node resets and the cycle repeats
On an ECG, this appears as progressive PR prolongation until a P-wave is dropped, resulting in a P-wave with no QRS complex following it.
causes of mobitz type 1
- Normal variant in people with high vagal tone and no structural heart disease (e.g. athletes)
- Inferior myocardial ischaemia
- Hyperkalaemia
- Some drugs (e.g. beta-blockers, calcium channel blockers, digoxin)
Mobitz type 2
- In a Mobitz type II heart block, the PR interval is constant, however, each P wave is associated with a QRS complex until one P wave arises that does not have a QRS complex.
- There is usually a fixed number of P-waves for every successful QRS complex.
- For example, if there are three P waves for every QRS complex, this is a 3:1 Mobitz II block.
There is a high risk of asystole with Mobitz type 2 heart blocks. This is because dropped beats can happen suddenly and unexpectedly, and progress to third-degree (complete) heart block or asystole, resulting in sudden cardiac death
why are the PR intervals consistency different in Mobitz type 1 vs 2
This occurs because the block is lower down than Mobitz type I, below the AV node.
Mobitz type 2
Mobitz type II blocks are most commonly due to structural heart damage.
It is rarely seen in patients without structural heart disease. Its causes include:
- Anterior myocardial infarction
- Myocardial fibrosis/sclerosis
- Amyloidosis
- Haemochromatosis
- Rheumatic fever
- Autoimmune disorders (e.g. systemic lupus erythematosus, systemic sclerosis)
- Hyperkalaemia
- Some drugs (e.g. beta-blockers, calcium channel blockers, digoxin, adenosine, amiodarone)
2:1 block
A 2:1 block describes the presence of two P waves for each QRS complex. Because Mobitz type I blocks occur in regular cycles, there is always a fixed number of P waves to QRS complexes. In general, in the P:QRS ratio, Mobitz type I blocks have one more P wave than QRS complex (e.g. 5 P waves and 4 QRS complexes per cycle are a 5:4 Mobitz Type I block). Mobitz type II blocks generally have a fixed ratio of P:QRS complexes and are generally X:1 (e.g. 3:1, 4:1, 5:1). Ratios of 3:1 and above are known as ‘high-grade AV blocks’. With 2:1 blocks, it is difficult to tell whether it is due to a Mobitz type I or type II block.
third degree heart block
COMPLETE HEART BLOCK
- no impulses from the SAN are conducted to the ventricles
- SAN continues sneding impulses and ventricles activate via escape rhythms
- leads to bradycardia (45-50bpm) and haemodynamic instability
On an ECG, there is no association between the P waves and QRS complexes. There may be a regular P-P interval and regular R-R interval, but the P-R interval may vary.
There is a high risk of asystole with third-degree heart blocks.
causes of a third-degree heart block
are the same as Mobitz I and II, such as:
- Inferior myocardial infarction
- Drugs (beta-blockers, calcium channel blockers, amiodarone, adenosine, digoxin)
bundle branch block
The left and right bundle branches emerge from the bundle of His in the heart. They transmit impulses from the bundle of His to the Purkinje fibres. The bundle branches are found along the interventricular septum and each bundle branch depolarises their respective ventricles. The interventricular septum itself is depolarised by the left bundle branch and is depolarised from left to right. The ventricles contract simultaneously.
left bundle branch block pathophysiology
Left bundle branch block (LBBB) describes slowed or absent conduction through the left bundle branch. This leads to delayed depolarisation of the left ventricle. This results in the left ventricle being depolarised via the right bundle branch, whose impulses travel through the right ventricle, and then to the left ventricle via the septum.
causes of new LBBB
ALWAYS PATHOLOGICAL
- MI
- Aortic stenosis
- HTN
- Cardiomyopathy
findings of LBBB on ECG
- Prolonged, positive R waves in the left ventricular leads (I, V5-6)
* These are usually negative, but since depolarisation is happening in the opposite direction, - Secondary R waves in the left ventricular leads (I, V5-6) giving “M-shaped” R waves
* This is due to delayed activation between the right ventricle and left ventricle - QRS prolongation
* Due to delayed conduction as the left ventricle now needs to be depolarised via the right ventricle through a slower and less efficient pathway
Right bundle branch block (LBBB)
describes slowed or absent conduction through the right bundle branch. This leads to delayed depolarisation of the right ventricle. This results in the right ventricle being depolarised via the left bundle branch, whose impulses travel through the left ventricle first, then to the right ventricle via a slower and less efficient pathway.
findings of RBBB
- Secondary R waves in the right ventricular leads (V1 and V2) giving “M-shaped” R waves
* This is due to delayed activation between the left ventricle and right ventricle - QRS prolongation
* Due to delayed conduction as the right ventricle now needs to be depolarised via the left ventricle through a slower and less efficient pathway - Wide, slurred S waves in leads I and V6
causes of RBBB
- RBBB can be a normal variant
- Ischaemic heart disease
- Pulmonary disorders (e.g. COPD)
- Right ventricular hypertrophy
- Pulmonary embolism
what does bifascicular block mean?
RBBB and blockage of one of the fascicles of the left bundle branch
Trifascicular block:
Bifascicular block and third-degree heart block
tachycardia defined as
≥100 bpm
how can tachycardias be classified
- QRS morphology
- Rhthm regularity
types of tachycardia
- Regular narrow QRS tachycardia:
- Sinus tachycardia
- Postural orthostatic tachycardia syndrome
- Atrial flutter
Other supraventricular tachycardias:
- Atrioventricular (AV) nodal re-entrant tachycardia (AVNRT)
- AV reciprocating tachycardia (AVRT)
- Irregular narrow QRS tachycardia:
- Atrial fibrillation
- Regular broad QRS tachycardia:
- Ventricular tachycardia
- Irregular broad QRS tachycardia:
- Atrial fibrillation with bundle branch block
- Polymorphic ventricular tachycardia (including torsades de pointes)
Paroxysmal Supraventricular Tachycardia
describes arrhythmias that originate at or above the atrioventricular node (AVN) characterised by a narrow complex (QRS duration <120 ms or <3 small squares) tachycardia (heart rate >100 bpm).
causes of SVT
Re-entrant tachycardias– due to accessory pathways resulting in re-entry:
* Atrioventricular nodal re-entry tachycardia (AVNRT)
* Atrioventricular re-entrant tachycardia (AVRT): Wolff-Parkinson-White syndrome
* Macro-re-entrant atrial tachycardia (e.g. atrial flutter)
Automatic tachycardias:
* Focal atrial tachycardia
* Focal junctional tachycardia
presentation of SVT
Palpitations
Chest pain
Shortness of breath
Anxiety
Haemodynamic instability (tachycardia and hypotension)
Acute heart failure
investigations for SVT
ECG
* Shows a narrow complex, regular tachycardia
* P waves may be absent
* Delta waves suggest the presence of Wolff-Parkinson-White syndrome
Holter monitoring:
* If an ECG misses an episode of SVT
managment of supraventricular tachycardia depends on
if there is life threatening features present:
- Shock
- Syncope
- Myocardial ischaemia
- Heart failure
general management of SVT patients
Assess all patients with an ABCDE approach:
- Give oxygen if oxygen saturations are <94%
- Obtain IV access
- Monitor ECG, blood pressure, and oxygen saturations, and record a 12-lead ECG
- Identify and treat reversible causes (e.g. electrolyte abnormalities, hypovolaemia)
SVT management: Evidence of life-threatening features
Evidence of life-threatening features present
First line
* Give a synchronised DC shock and repeat up to 3 attempts
* If the patient is conscious, give sedation or anaesthesia
Second line
* If unsuccessful: give amiodarone 300 mg over 10-20 minutes and repeat synchronised DC shock
SVT management: No evidence of life-threatening features present
First line
Vagal manoeuvres:
- Valsalva manoeuvre – blow into an empty plastic syringe
- Carotid sinus massage – preferably in younger patients due to the risk of stroke from emboli
Second line
- IV adenosine as a rapid bolus if not asthmatic:
- Give 6 mg first, then 12 mg if unsuccessful, then 18 mg if unsuccessful
- Use continuous ECG monitoring
- Adenosine is contraindicated in asthma, use verapamil instead
Third line
- If ineffective: synchronised DC shock up to three attempts
Give sedation or anaesthesia if conscious
when is adenosine contraindicated
Adenosine is contraindicated in asthma, use verapamil instead
long term management of SVT
Long-term management depends on the underlying cause. This may involve radiofrequency catheter ablation or drug management (such as beta-blockers or calcium channel blockers).
Atrial fibrillation (AF)
- is the most common arrhythmia.
- It is a type of supraventricular arrhythmia leading to uncoordinated electrical conduction and ineffective atrial contraction.
ECG findings AF
An ECG shows:
- An irregularly irregular pulse
- Absence of P waves
complications of untreated AF
- Stroke – stagnation of blood can lead to the formation of a thrombus, which can embolise and lead to a stroke
- Heart failure – due to reduced cardiac output and increased workload on the heart
AF classification
Paroxysmal AF:
* Episodes lasting >30 seconds but <7 days (often <48 hours) which are self-terminating and recurrent
Persistent AF:
* Episodes lasting >7 days or <7 days but requiring pharmacological or electrical cardioversion. The 7-day threshold is used because AF is unlikely to spontaneously terminate after this time.
Permanent AF:
* AF that fails to terminate with cardioversion,
* AF that relapses within 24 hours, or
* longstanding AF (usually >1 year) in which cardioversion has not been indicated or attempted (also known as accepted permanent AF).
causes of acute AF
- Coronary artery disease
- Hypertension
- Heart failure
- Valvular disease
- Diabetes mellitus
- Thyrotoxicosis
- COPD
- Obstructive sleep apnoea
- Heavy alcohol intake
- Degeneration from another tachyarrhythmia:
- Atrial flutter
- Atrioventricular nodal re-entrant tachycardia
- Wolff-Parkinson-White syndrome
causes of chronic AF
Cardiac:
- Hypertension
- Coronary artery disease
- Myocardial infarction
- Congestive heart failure
- Rheumatic fever
- Atrial/ventricular dilation or hypertrophy
- Congenital heart disease
- Pericarditis
- Myocarditis
Non-cardiac:
- Thyrotoxicosis
- Alcohol abuse
- Caffeine abuse
- Pulmonary hypertension
- Sepsis
presentation of AF
- Palpitations
- Breathlessness
- Chest pain or tightness
- Anxiety
- Dizziness
- Syncope
- Fatigue
- Stroke or transient ischaemic attack
Haemdynamic instability
- Acute HF
- Cardiogenic shock
- Sycope
- Cardiac chest pain
- SoB
investigations Atrial fibrillation
ECG:
* Diagnoses AF and shows an irregularly irregular rhythm with absent P waves
Holter (ambulatory ECG) monitoring:
* If the ECG fails to show AF and paroxysmal AF is suspected
FBC
- anaemia
- infection
UEs
- electroyle imbalances
TFT
- thryotoxicosis
Echocardiography
- Underlying heart disease
- CHA2DS2-VASc
aim of treating atrial fibrillation
- rate control
- rhythm control
- anticoagulation
Rate control
Rate control reduces the heart rate at rest and on exertion. This reduces the severity of symptoms, but does not terminate AF:
1st-line:
- monotherapy with a beta-blocker (except sotalol) or rate-limiting calcium channel blockers (CCBs, verapamil or diltiazem)
- For instance, people with asthma cannot take beta-blockers, therefore rate-limiting are more appropriate
2nd-line: digoxin
- Considered in patients who do no or very little exercise or if first-line options are ineffective/contraindicated
- Digoxin is less effective with exertion
Rhythm control
Rhythm control aims to restore normal sinus rhythm. This can be done via:
Direct current (DC) cardioversion:
* Using electrical stimulation to restore sinus rhythm
* Pharmacological cardioversion or beta-blockers can be used to maintain sinus rhythm
Pharmacological cardioversion:
* If no structural heart disease present: amiodarone or flecainide
* If structural heart disease present: amiodarone
* Flecainide is contraindicated in those with structural or ischaemic heart disease
rule of rhythm control in Atrial fib
Rhythm control is performed if patients have had a short duration of sym
Anticoagulation in AF
All patients with AF, including those not currently in AF, should have the need for anticoagulation considered due to the risk of stroke. NICE recommends using the CHA2DS2VASc score
The CHA2DS2-VASc score
is used to assess the risk of stroke in any patient with AF.
Management is guided by the score:
0 – no treatment
1:
* If male: consider treatment
* If female: no treatment (being female gives a score of 1 on its own)
2 or more – offer anticoagulation
CHA2DS2-VASc score: If the score suggests no anticoagulation is needed
If the score suggests no anticoagulation is needed, a transthoracic echocardiogram must be performed. If there are signs of valvular/structural heart disease, patients should be anticoagulated regardless of the CHA2DS2-VASc score.
which scoring system is used to assess the risk of bleeding
ORBIT score
The ORBIT score
The ORBIT score is used to assess the risk of bleeds in patients being considered for anticoagulation. NICE recommends that we do not withhold anticoagulation solely on the basis of a person’s age or fall risk. The ORBIT score alone should not exclude anticoagulant treatment. The bleeding risk can vary and requires regular re-assessment.
Anticoagulant drugs used in AF
The following drugs are used if anticoagulation is indicated in a patient with AF:
1st-line: direct oral anticoagulants (DOACs):
- Apixaban, rivaroxaban, edoxaban, dabigatran
2nd-line: warfarin if a DOAC is not tolerated or contraindicated
Aspirin is not used in reducing the risk of stroke in patients with AF.
management: AF with haemodynamic instability
- ABCDE approach
- Immediate direct current (DC) cardioversion
management of stroke caused by AF
- ABCDE approach
- If a stroke occurs, patients are given aspirin for 2 weeks (the same as standard management of stroke) followed by anticoagulation with a direct oral anticoagulant (DOAC) or warfarin as soon as possible.
management: acute AF, onset <48 hours
- Rhythm control can be used straight away since an emboli is unlikely to have formed in under 48 hours
Options for rhythm control:
- DC Cardiovesion: if haemodynamically unstable e.g. shock
- Pharmacological : if haemodynamically stable
- Long term anticoagulation
Oral anticoagulation is given if the CHA2DS2-VASc score indicates it or there are risk factors for AF recurrence (e.g. failed cardioversion, structural heart disease, prolonged AF, or previous occurrences)
option for pharmacological cardioversion
- If no structural/ischaemic heart disease: flecainide or amiodarone
- If structural/ischaemic heart disease present: amiodarone
management of Acute AF, onset >48 hours or unknown
If patients present acutely with AF and its onset is >48 hours, immediate rate control is offered followed by delayed rhythm control
1. Rate control and a minimum of 3 weeks anticoagulation first:
- This is to reduce the risk of clots dislodging and causing a stroke following cardioversion
- A transoesophageal echocardiogram can be performed to exclude a left atrial appendage thrombus. If a thrombus is ruled out, then patients can be given heparin and cardioverted immediately, followed by giving oral anticoagulation if the CHA2DS2-VASc score indicates it or there are risk factors for AF recurrence (e.g. failed cardioversion, structural heart disease, prolonged AF, or previous occurrences)
- Followed by delayed rhythm control:
* Electrical cardioversion is preferred in this scenario rather than pharmacological cardioversion
- Consider amiodarone starting 4 weeks before and up to 12 months after electrical cardioversion
- Followed by anticoagulation:
- This is continued for at least 4 weeks until decisions about long-term anticoagulation are made.
- Oral anticoagulation is given if the CHA2DS2-VASc score indicates it or there are risk factors for AF recurrence (e.g. failed cardioversion, structural heart disease, prolonged AF, or previous occurrences)
if drug treatment is unsuccessful in treating AF
Catheter ablation
If drug treatment is unsuccessful, unsuitable, or not tolerated in AF, catheter ablation may be considered. Ablation may control rhythm but does not decrease stroke risk. Therefore, anticoagulation must still be given as per the CHA2DS2-VASc score.
Patient Advice for AF
- Patients should undertake regular exercise but avoid excessive endurance exercise e.g. marathons, especially if they are >50 years old
- Patients should lose weight/stop smoking where appropriate as this reduces their risk of developing cardiovascular disease
- Patients should reduce alcohol intake as this can contribute to arrhythmia
Complications of AF
Stroke
Heart failure
Myocardial infarction
Atrial flutter (AFL)
Presentation of atrial flutter
- Palpitations
- Breathlessness
- Chest pain or tightness
- Anxiety
- Dizziness
- Syncope
- Fatigue
- Haemodynamic instability
ECG for atrial flutter
Diagnoses AFL and shows flutter waves which are a sawtooth pattern most prominent in leads II, III, and aVF
