Common disturbances of cardiac rhythm COPY

Question 1

List examples of tachyarrhythmias

Answer 1

• atrial arrhythmias: atrial fibrillation, atrial flutter, supraventricular tachycardias (which itself encompasses many different tachycardias)
• ventricular arrhythmias: monomorphic/polymorphic VT, ventricular fibrillarion, ventricular flutter

Question 2

List examples of bradyarrhythmias

Answer 2

• sinus node disease
• pauses
• AV nodal diseases
• first degree HB
• second degree HB
• third degree HB

Question 3

Describe common presentations of cardiac arrhythmias

Answer 3

Common presentations of cardiac arrhythmias include:

• Palpitations
• Shortness of breath
• Tiredness
• Chest discomfort
• Syncope or presyncope (near-fainting)

Question 4

Define tachyarrhythmias

Answer 4

Heart rate greater than 100 bpm

Question 5

Define bradyarrhythmias

Answer 5

HR < 50 bpm

Question 6

List examples of atrial tachyarrhythmias

Answer 6

• Atrial fibrillation (AF)
• Atrial flutter (AFL)
• Supraventricular tachycardias (SVT)

Question 7

Describe atrial fibrillation

Answer 7

Definition
AF is the most common cardiac arrhythmia characterized by a chaotic heart rhythm, or “disorganised atrial electrical activity and contraction resulting in an irregularly irregular ventricular responses a.k.a fibrillation waves”.

Characteristics
Key points about AF are:
- Absence of P wave on 12-lead ECG
- Lasts for >30 seconds
- AF can be acute, transient, paroxysmal, or chronic
- Patients may be stable or unstable
- Has multiple possible underlying causes
- Prevalence increases with age
- It is a common occurrence post cardiac surgery

Note: no need for 12 lead ECG to diagnose, multiple modalities

Mechanism of AF
AF can be triggered by various factors:

1. Atrial distension as a results of pulmonary hypertension (Pulmonary vein triggers), septal defects and valvular disease e.g. mitral stenosis including infective endocarditis (80%)
2. Non-PV triggers: abnormalities of the conducting system, increased atrial automaticity or irritation i.e. due to alcohol, caffeine, myocarditis, electrolyte derangement
3. Substrate i.e. catecholamine excess or increased sensitivity - which can be sourced exogenously or endogenously

Complications
Complications of atrial fibrillation can be broadly categorised into two types:
- adverse effects on haemodynamics, including loss of atrial systole, decreased diastolic filling time due to tachycardia, and rate-related cardiomyopathy
- atrial thrombus formation: including systemic embolism especially stroke, and pulmonary embolism

Management of AF
The management of AF involves several considerations:

1. Recorded 12-lead ECG to identify atrial fibrillation and associated disease
2. Anticoagulation issues
   
   • Assess Thromboembolic (TE) Risk, treated with warfarin or NOAC
3. Rate and Rhythm control
   
   • AF type symptoms
4. Treatment of underlying disease
   
   • Consider referral
   • Treat with ACEIs, ARBs, CPAP, or others depending on comorbidities or underlying causes

Side notes:
- anticoagulation issues – aka prevent stroke risk. Consider warfarins vs NOAC
- rhythm control is potentially better ^[**]
- when treating, focus on setting rhythm over rate, unless enderly, with comorbidities, no symptoms or minimal symptoms

There are several lines of treatment available for maintenance of sinus rhythm

Note:
- amiodarone and other class III drugs (sotalol at high dose) can have poor side effects including torsades de pointes
- care must be taken when prescribing these

Question 8

Compare and contrast radiofrequency and cryoablation

Answer 8

• both techniques rely on removing the problematic portion of the circuit, either thermally (to scar the tissue) or by freezing
  
  • radioablation has a 80% success rate

Question 9

Describe management of atrial fibrillation

Answer 9

Management of AF
The management of AF involves several considerations:

1. Recorded 12-lead ECG to identify atrial fibrillation and associated disease
2. Anticoagulation issues
   
   • Assess Thromboembolic (TE) Risk, treated with warfarin or NOAC
3. Rate and Rhythm control
   
   • AF type symptoms
4. Treatment of underlying disease
   
   • Consider referral
   • Treat with ACEIs, ARBs, CPAP, or others depending on comorbidities or underlying causes

Side notes:
- anticoagulation issues – aka prevent stroke risk. Consider warfarins vs NOAC
- rhythm control is potentially better ^[**]
- when treating, focus on setting rhythm over rate, unless enderly, with comorbidities, no symptoms or minimal symptoms

There are several lines of treatment available for maintenance of sinus rhythm

Note:
- amiodarone and other class III drugs (sotalol at high dose) can have poor side effects including torsades de pointes
- care must be taken when prescribing these

Radiofrequency vs Cryoablation
This section discusses the comparison between radiofrequency (thermal technique) and cryoablation for the treatment of typical (CTI dependent) flutter.
- both techniques rely on removing the problematic portion of the circuit, either thermally (to scar the tissue) or by freezing
- radioablation has a 80% success rate

Question 10

Describe assessment for anticoagulation

Answer 10

Assessment for anticoagulation in AF includes the following scoring systems:
- CHADS2
- CHA2DS2-VASC

2 risk factors constitutes anti-coagulation risk.
If there is only one risk factor, consider anti-coagulants.
note: sex is not considered an independent risk factors

Question 11

Describe atrial flutter

Answer 11

Definition
Atrial flutter is a narrow complex tachycardia.
It is a “regularly irregular” pattern.

Characteristics
- regular atrial activity at 300 bpm
- loss of isoelectric line
- upright flutter waves in V1 that may resemble P waves
- can be typical (with sawtooth appearance, especially in leads II, III, aVF, tricuspid/mitral isthmus)
- or atypical (CHD, damage)

Mechanism
Atrial flutter is a form of SVT caused by a re-entry circuit within the right atrium.

Typical atrial flutter
- is more common
- it involved the IVC and tricuspid isthmus in the re-entry circuit
- it can be further classified based on whether the direction of the re-entry circuit is anticlockwise or clockwise
- anticlockwise re-entry: commonest form of atrial flutter, produces inverted flutter waves in leads II, III and aVF; and positive flutter waves in V1 that may resemble upright P waves
- clockwise re-entry: opposite pattern to anticlockwise re-entry

Atypical atrial flutter
- often associated with rhythm instability, higher atrial rates, and less amenable to treatment with ablation

Management
Note: atrial flutter and fibrillation are treated the same, for example, beta blockers, calcium channel blockers, amiodarone or sotalol, cardioversion ^[quick, low energy shocks to restore rhythm, synchronised to QRS complex] and radiofrequency ablation (but flutter is more refractory to treatment)

Note 2: similarly, CHAD score is used to assess risk

Question 12

Describe management of atrial flutter

Answer 12

Management
Note: atrial flutter and fibrillation are treated the same, for example, beta blockers, calcium channel blockers, amiodarone or sotalol, cardioversion ^[quick, low energy shocks to restore rhythm, synchronised to QRS complex] and radiofrequency ablation (but flutter is more refractory to treatment)

Note 2: similarly, CHAD score is used to assess risk

Question 13

List the two types of atrial flutter

Answer 13

Typical and atypical

Question 14

List the types of supraventricular tachycardia

Answer 14

SVT encompasses various types of tachycardias:
- AV nodal reentry tachycardia
- AV reentry tachycardia - Wolff-Parkinson-White (WPW) Syndrome
- Atrial flutter
- Atrial Fibrillation
- Atrial Tachycardia
- Sinus Tachycardia and Sinus Node Reentry

Question 15

Describe AVNRT

Answer 15

Definition
- a type of paroxysmal SVT that is te consequence of a re-entry circuit within or adjacent to the AV node
- it is the most common cause of palpitations in patients with structurally normal hearts

Characteristics
- characterized by a fixed, short RP interval mimicking r’ deflection.
Like other SVTs, AVNRT can be categorised based on location and regularity:
- typically ECG shows heart rate between 140 and 280 bpm
- location: AV node
- regularity: regular

• similar to junctional tachycardia

There are several types of AVNRT:
- Slow-fast AVNRT: pseudo- S in II, III and aVF, and pseudo R’ in V1
- Fast-slow AVNRT: P waves between QRS and T
- slow-slow AVNRT: late P waves after QRS, appears as atrial tachycardia

Note: a fast conduction pathway has rapid conduction, but slow refractory period
Note 2: a slow conduction pathway has slow conduction coupled with slow refractory period

Question 16

Describe AVRT

Answer 16

Definition
AVRT is a form of paroxysmal SVT that occurs in patients with accessory pathways. This is usually a result of a re-entry circuit between the AVN and accessory pathways. ECG features depend on whether conduction is orthodromic or antidromic.

Characteristics
- congenital
- present anywhere in heart
- PR interval short, due to fast conduction
- when symptomatic, leads to WPW syndrome
- slurring of QRS leads to **delta wave

Orthodromic AV Reentrant Tachycardia
Anterograde conduction via the AVN, producing a narrow complex rhythm (antidromic, via AP, produces regular wide complex rhythm).

Characteristics
- rate usually 200-300 bpm
- retrograde P waves usually visible, with long RP interval
- narrow QRS
- rate-related ischaemia common

• similar to WPW ^[note: WPW is similar to SVT, using slow AV node], but circuit is transmitted through accessory pathway
• P waves present
• treatment: radiofrequency, ablation, medication

Note: the RP interval can be used to differentiate AVNRT from orthodromic AVRT
- retrograde P waves occur early in AVNRT, so it is usually not seen
- retrograde P waves more visible in orthodromic AVRT with long RP intervals

Treatment
includes urgent DC cardioversion

Question 17

Describe how to determine AV nodal participation in SVT

Answer 17

Determining AV Nodal Participation in SVT
Various methods to determine AV nodal participation in SVT are explained:
- Vagotonic maneuvers (Stimulates AV node to remove the tachycardia)
- Carotid sinus massage
- Valsalva maneuver (blow into an empty syringe)
- Facial ice pack (“diving reflex;” for kids)
- Adenosine (6-12 mg I.V.)
- If SVT terminates, a reentrant mechanism involving the AV node is likely
- If atrial rate unchanged, but ventricular rate slows (Ps > QRSs), SVT is atrial in origin

Question 18

Detail the treatment for narrow QRS tachycardia

Answer 18

This section covers the treatment options for narrow QRS tachycardia based on the specific type:
- PSVT (Paroxysmal Supraventricular Tachycardia)
- Metoprolol
- Diltiazem
- Radiofrequency ablation
- Atrial flutter
- beta blockers, CCBs, amiodarone/sotalol
- Cardioversion
- Anticoagulation according to risk score
- Radiofrequency ablation –high success rate
- Atrial fibrillation
- Rate control or rhythm control if hemodynamically stable
- Cardioversion if unstable
- Anticoagulation according to risk score
- Radiofrequency ablation

Question 19

Provide examples of wide QRS complex tachycardia

Answer 19

In this section, wide QRS complex tachycardia is discussed, and different types are listed:

• Ventricular fibrillation
• Ventricular flutter
• Polymorphic VT (Ventricular Tachycardia) - different shape (for example, TdP)
• Monomorphic VT (Ventricular Tachycardia) - aka same shape

Regular Wide QRS Tachycardia
Various causes of regular wide QRS tachycardia:
- VT
- SVT with aberrancy
- SVT with manifest pre-excitation/anti-dromic AVRT
- Hyperkalemia/drugs
- Paced rhythm

Question 20

Describe torsade de pointes

Answer 20

Definition
a specific type of polymorphic VT with a prolonged QT interval

Characteristics:
- both PVT and QT prolongation must be present
- it has a characteristic morphology in which the QRS complexes “twist” around the isoelectric line

Cause:
- A prolonged QT reflects prolonged myocyte repolarisation due to ion channel malfunction
- This prolonged repolarisation period also gives rise to early after-depolarisations (EADs)
- EADs may manifest on the ECG as tall U waves; if these reach threshold amplitude they may manifest as premature ventricular contractions (PVCs)
- TdP is initiated when a PVC occurs during the preceding T wave, known as ‘R on T’ phenomenon
- The onset of TdP is often preceded by a sequence of short-long-short R-R intervals, so called “pause dependent” TDP, with longer pauses associated with faster runs of TdP

Factors:
- ischemia
- dyselectrolytemia
- drugs
- LQTS (Long QT Syndrome).

Question 21

Describe ventricular fibrillation

Answer 21

Definition:
Ventricular fibrillation is described as a totally chaotic rapid ventricular rhythm, often precipitated by VT.
It is the most important shockable cardiac arrest rhythm.

Characteristics:
Can be marked by low blood pressure, hypoxia.
- Chaotic irregular deflections of varying amplitude
- No identifiable P waves, QRS complexes, or T waves
- Rate 150 to 500 per minute
- Amplitude decreases with duration (coarse VF –> fine VF)
-
Causes
- Electrical (electrocution, lightning, trauma)
- Ischaemia/hypoxic susceptibility (respiratory arrest)
- Electrolyte abnormality (low K and Mg)
- Altered autonomic and vagal inputs
- Mechanical stimuli (wire or catheter in RV)
- Congenital susceptibility (conduction abnormalities)
- Acquired disorders (ischaemia, hypertrophy, myocarditis, pro-arrhythmic drugs)

Treatment
Immediate treatment: shocking the patient, otherwise death.

Question 22

Describe electrocardiographic differentiation of VT vs SVT with aberrancy

Answer 22

Key points for differentiating between VT and SVT with aberrancy are listed, including:
- clinical history
- AV dissociation
- QRS morphology
- QRS axis
- fusion beat
- capture beat.

Note:
- VT does not invariablt cause haemodynamic collapse
- patients may be conscious and stable
- history of heart disease especially prior MI suggests VT
- JVP cannon waves
- 12 lead EKG if patient is stable, should be obtained

Question 23

Describe management of VT

Answer 23

The management options for ventricular tachycardia include:
- cardioversion
- antiarrhythmic drugs
- intracardiac defibrillator (ICD)
- treatment of the underlying cause (e.g., ischemia)
- radiofrequency ablation.

Question 24

Recall the normal impulse conduction pathway in the heart

Answer 24

• Sinoatrial node
• Atrioventricular (AV) node
• Bundle of His
• Bundle Branches
• Purkinje fibres

Question 25

Describe the signs and symptom basis of bradycardia

Answer 25

Bradycardia can lead to various symptoms due to decreased cardiac output and perfusion. These usually occurs when heart is not pumping enough blood to meet body’s needs. This often happens if rate is very slow, or remains slow for a long period of time. These symptoms include:

• Dizziness or lightheadedness
• Fainting (syncope) or near-fainting
• Tiredness (fatigue)
• Shortness of breath
• Palpitations
• Chest pain (angina)
• Increased difficulty exercising
• Confusion or difficulty concentrating
• Some may not have symptoms

Question 26

Describe the classification of bradyarrhythmias

Answer 26

Bradycardias can be classified into two categories based on the underlying problem:

All of the issues detailed below can be classified under the umbrella term “sick sinus syndrome”
1. Problems with Impulse Formation
- Sinus Arrest
- Sinus Bradycardia
- Chronotropic Incompetence
- Brady/Tachy syndrome

2. Problems with Impulse Conduction
   - Exit Block
   - First Degree AV Block
   - Second Degree AV Block
   - Mobitz Type 1 (Wenckebach)
   - Mobitz Type 2
   - Third Degree AV Block (Complete heart block)
   - Bifascicular/Trifascicular block

Question 27

Describe sinus bradycardia

Answer 27

Definition
Sinus Bradycardia is characterized by a slow depolarization of the sinus node.
It is usually seen as a resting heart rate of less than 60 bpm for adults, or below the reference range for children.

Characteristics
Looks exactly like sinus rhythm, with much longer RR intervals.
Causes
Can be pharmacological or non-pharmacological
* Hypothyroidism
* Drugs
* During vomiting or vasovagal syncope
* Increased intracranial pressure
* Hypoxia, hypothermia
* Infections
* Depression
* Jaundice

Can also be physiological – atheletes

Management

If the patient is symptomatic and the rhythm is persistent and irreversible, a pacemaker may be required.

Question 28

Describe sinus pause and arrest

Answer 28

Definition
Sinus Pause/Arrest involves the failure of the sinus node to discharge, resulting in periods of ventricular asystole.
Note arrest = pause greater than 3 seconds

Characteristics
- rate varies, typically slow
- rhythm = irrregular
- PP and RR intervals irregular
- P waves present except for pause
- P: QRS usually 1:1
- PR and QRS intervals of normal width

Mechanism
SAN dysfunction

Management
Pacemaker treatment may be necessary in some cases.

Question 29

Describe exit block

Answer 29

Definition
A consequence of failed propagation of pacemaker impulses beyond SAN.

Characteristics
- some dropped P waves, otherwise present
- rate varies, usually slow
- PP and RR irregular
- P: QRS usually 1:1
- PR and QRS intervals of normal width

Question 30

Describe sinus arrest

Answer 30

Sinus arrest
Definition
* Failure of sinus node discharge
Characteristics
* Absence of atrial depolarization
* Periods of ventricular asystole
* May be episodic as in vaso-vagal syncope, or carotid sinus
hypersensitivity

Management
– May require a pacemaker

Question 31

Describe chronotropic incompetence

Answer 31

Definition
In Chronotropic Incompetence, the heart rate is unable to increase adequately in response to the body’s metabolic demand, leading to limited activity and symptoms.

Cause
Chronotropic incompetence is often caused by SND, and is very common among heart failure patients.
NOTE: beta blcokers can increase chronotropic incompetence

Normal, healthy heart is able to increase peak cardiac output by up to 5x
baseline with exercise
* In chronotropic incompetence, patient may only be able to double cardiac
output over baseline
* An increase in stroke volume only may limit activity and
cause symptoms

Diagnosis
- failure to reach 80% of expected maximum heart rate, adjusted for age

Treatment
As with other bradyarrhythmias. Avoid BBs. Can be addressed with pacemaker

Question 32

Describe brady/tachy syndrome

Answer 32

Definition
Brady/Tachy Syndrome presents with intermittent episodes of slow and fast rates from the SA node or atria, often associated with periods of atrial fibrillation and chronotropic incompetence. Pacing may be indicated.

Characteristics
Brady/Tachy Syndrome
* Intermittent episodes of slow and fast rates from the SA node
or atria
* Brady < 60 bpm
* Tachy > 100 bpm
* Sinus Node Disease
– Patient may also have periods of AF and chronotropic incompetence
– Most common pacing indication

Question 33

Define high vagal tone

Answer 33

High Vagal Tone, usually observed in the young, where the heart rate response is normal during exercise and normal intrinsic heart rate, but can be severe enough to cause syncope, especially in familial forms.

Question 34

Define exit block

Answer 34

Exit Block involves a transient block of impulses from the SA node. Pacing is rare unless symptomatic, irreversible, and persistent. Note sinus wenckeback is possible but rare. Can be first, second or three degree block.

Question 35

Describe first degree AV block

Answer 35

Definition
First-Degree AV Block is characterized by a prolonged PR interval (>200 ms) due to delayed conduction through the AV node. In most cases, it is not an indication for pacing.

Characteristics
- Delay between impulse generation and transmission to the atrium.
- Generally asymptomatic

Causes
- Increased vagal tone
- Athletic training
- Inferior MI
- Mitral valve surgery
- Myocarditis (e.g. Lyme disease)
- Electrolyte disturbances (e.g. Hyperkalaemia)
- AV nodal blocking drugs (beta-blockers, calcium channel blockers, digoxin, amiodarone)
- May be a normal variant

Treatment
Nothing specific required

Note: Some consider this a normal variant (not an arrhythmia)

Question 36

Describe second degree block

Answer 36

Definition
Second-Degree AV Block, known as Mobitz I , or Wenckeback shows a progressive prolongation of the PR interval until there is a failure to conduct, resulting in a dropped ventricular beat. It is usually not an indication for pacing.

Characteristics
- usually 1:1 ratio
- PP remains relatively constant
- mostly asymptomatic
- Progressive prolongation of the PR interval culminating in a non-conducted P wave:
- PR interval is longest immediately before dropped beat
- PR interval is shortest immediately after dropped beat

Question 37

Describe second degree II block

Answer 37

Defintiion
Second Degree AV Block, known as Mobitz II, involves regularly dropped ventricular beats, indicating a high-grade block and is often an indication for pacing.

Characteristics
- no progressive prolongation of PR interval - remains constant
– 2:1 block (2 P-waves for every 1 QRS complex) aka The RR interval surrounding the dropped beat(s) is an exact multiple of the preceding RR interval (e.g. double the preceding RR interval for a single dropped beat, triple for two dropped beats, etc)
– Atrial rate = 75 bpm, Ventricular rate = 42 bpm

Cause
- Mobitz II is usually due to failure of conduction at the level of the His-Purkinje system (i.e. below the AV node)
- While Mobitz I is usually due to a functional suppression of AV conduction (e.g. due to drugs, reversible ischaemia), Mobitz II is more likely to be due to_structural_damage to the conducting system (e.g. infarction, fibrosis, necrosis)

Question 38

Describe third degree block

Answer 38

Note: Advanced AV Block simply refers to variable block, and is not COMPLETE heart block

Definition:
In third-degree AV block, there is no impulse conduction from the atria to the ventricles, resulting in complete atrioventricular disassociation. The atrial rate is indicated as 130 bpm, while the ventricular rate is 37 bpm. In most cases, complete heart block leads to a wide QRS, as the ventricular rate is idioventricular.
Characteristics:
- severe bradycardia

Causes
The causes are the same as for Mobitz I and Mobitz II second degree heart block.The most important aetiologies are:

• Inferior myocardial infarction
• AV-nodal blocking drugs (e.g. calcium-channel blockers, beta-blockers, digoxin)
• Idiopathic degeneration of the conducting system (Lenegre’s or Lev’s disease), causing true trifascicular block

Question 39

Describe fascicular block

Answer 39

Fascicular blocks are conduction disturbances that affect the right or left bundle branches and can be further classified into the following types:

1. Right Bundle Branch Block and Left Posterior Hemiblock
2. Right Bundle Branch Block and Left Anterior Hemiblock
3. Complete Left Bundle Branch Block

Question 40

Describe right bundle branch block

Answer 40

Characteristics
- QRS duration > 120ms
- RSR’ pattern in V1-3 (“M-shaped” QRS complex) - i.e. MARROW
- Sometimes rather than an RSR’ pattern in V1, there may be a broad monophasic R wave or a qR complex.
- Wide, slurred S wave in lateral leads (I, aVL, V5-6)

Causes of Right Bundle Branch Block
- Right ventricular hypertrophy / cor pulmonale
- Pulmonary embolus
- Ischaemic heart disease
- Rheumatic heart disease
- Congenital heart disease (e.g. atrial septal defect)
- Myocarditis
- Cardiomyopathy
- Lenègre-Lev disease: primary degenerative disease (fibrosis) of the conducting system

Management
- can be asymptomatic
- re-synchronisation is indicated in patients with CHF and RBBB ^[as per StatPearls]

Question 41

Describe LBBB

Answer 41

Characteristics

• QRS duration > 120ms
• Dominant S wave in V1
• Broad monophasic R wave in lateral leads (I, aVL, V5-6) – WILLO (m)
• Absence of Q waves in lateral leads
• Prolonged R wave peak time > 60ms in leads V5-6
  Note: associated changes include left axis deviation, poor R wave progression

Question 42

Describe bifascicular block

Answer 42

Definition
Bifascicular block involves conduction delay below the atrioventricular node in two of the three fascicles

Characteristics

Clinically, bifascicular block presents with one of two ECG patterns:
- Right bundle branch block (RBBB) with left anterior fascicular block (LAFB), manifested as left axis deviation (LAD)
- RBBB and left posterior fascicular block (LPFB), manifested as right axis deviation (RAD) in the absence of other causes

Causes of Bifascicular Block

Causes are similar to those of RBBB and LAFB/LPFB:
- Ischaemic heart disease (40-60% cases)
- Structural heart disease (50-80% association)
- Aortic stenosis
- Anterior MI (occurs in 5-7% of acute AMI)
- Lenègre-Lev disease
- Congenital heart disease
- Hyperkalaemia (resolves with treatment)

Question 43

Describe trifascicular block

Answer 43

Trifascicular block is characterized by complete block in the right bundle branch and complete or incomplete block in both divisions of the left bundle branch. Identification of trifascicular block usually requires electrophysiological study (EPS).

Main Causes

Causes are similiar to those of bifascicular block, related to degeneration or conduction impairment in fascicles below the AV node:

• Ischaemic heart disease (40-60%)
• Structural heart disease (50-80% association)
• Aortic stenosis
• Anterior MI
• Lenègre-Lev disease
• Congenital heart disease
• Hyperkalaemia (resolves with treatment)
• Digoxin toxicity

Question 44

Describe treatment of bradycardias

Answer 44

Management
* Drug
* Electrolyte Imbalance
* Hypothyroidism
* Post MI
* PPM Implantation

Question 45

Describe the classification of recommendations

Answer 45

Classification of recommendations and level of evidence
The classification of recommendations and level of evidence provide guidelines on the benefit and risk of procedures and treatments:

• Class I: Procedure/ Treatment SHOULD be performed/administered (Benefit&raquo_space;> Risk).
• Class IIa: Procedure/Treatment is REASONABLE to perform/administer (Benefit&raquo_space; Risk).
• Class IIb: Additional studies with focused objectives needed; Additional registry data would be helpful.
• Class III: Procedure/Treatment should NOT be performed/administered since it is NOT HELPFUL and may be HARMFUL (Risk ≥ Benefit).

The Level of Evidence is categorized into three levels (A, B, C) based on the strength of data derived from clinical trials or studies e.g. level A data derived from multiple RCTs or meta-analyses, with multiple populations evaluated.

Question 46

List common pacing indications

Answer 46

The American Heart Association (AHA) and American College of Cardiology (ACC) have defined indications for pacing based on the underlying arrhythmia. Common indications for pacemaker implantation include:

• Symptomatic bradycardia
• Sinus Node Disease (SND), or Sick Sinus Syndrome
• Complete Heart Block
• Chronotropic Incompetence

Note: Low-grade blocks, such as Mobitz I and first-degree AV block, are usually excluded from pacemaker indications.

Question 47

Distinguish between pericarditis and inferior STEMI

Answer 47

Pericarditis can cause localised ST elevation but there should be no reciprocal ST depression (except in AVR and V1). STEMI, like pericarditis, can also cause concave up ST elevation. Only STEMI causes convex up or horizontal ST elevation. ST elevation greater in III than II strongly suggests a STEMI.