Common disturbances of cardiac rhythm COPY Flashcards
List examples of tachyarrhythmias
- atrial arrhythmias: atrial fibrillation, atrial flutter, supraventricular tachycardias (which itself encompasses many different tachycardias)
- ventricular arrhythmias: monomorphic/polymorphic VT, ventricular fibrillarion, ventricular flutter
List examples of bradyarrhythmias
- sinus node disease
- pauses
- AV nodal diseases
- first degree HB
- second degree HB
- third degree HB
Describe common presentations of cardiac arrhythmias
Common presentations of cardiac arrhythmias include:
- Palpitations
- Shortness of breath
- Tiredness
- Chest discomfort
- Syncope or presyncope (near-fainting)
Define tachyarrhythmias
Heart rate greater than 100 bpm
Define bradyarrhythmias
HR < 50 bpm
List examples of atrial tachyarrhythmias
- Atrial fibrillation (AF)
- Atrial flutter (AFL)
- Supraventricular tachycardias (SVT)
Describe atrial fibrillation
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:
- Atrial distension as a results of pulmonary hypertension (Pulmonary vein triggers), septal defects and valvular disease e.g. mitral stenosis including infective endocarditis (80%)
- Non-PV triggers: abnormalities of the conducting system, increased atrial automaticity or irritation i.e. due to alcohol, caffeine, myocarditis, electrolyte derangement
- 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:
- Recorded 12-lead ECG to identify atrial fibrillation and associated disease
- Anticoagulation issues
- Assess Thromboembolic (TE) Risk, treated with warfarin or NOAC
- Rate and Rhythm control
- AF type symptoms
- 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
Compare and contrast radiofrequency and cryoablation
- 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
Describe management of atrial fibrillation
Management of AF
The management of AF involves several considerations:
- Recorded 12-lead ECG to identify atrial fibrillation and associated disease
- Anticoagulation issues
- Assess Thromboembolic (TE) Risk, treated with warfarin or NOAC
- Rate and Rhythm control
- AF type symptoms
- 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
Describe assessment for anticoagulation
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
Describe atrial flutter
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
Describe management of atrial flutter
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
List the two types of atrial flutter
Typical and atypical
List the types of supraventricular tachycardia
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
Describe AVNRT
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
Describe AVRT
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
Describe how to determine AV nodal participation in SVT
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
Detail the treatment for narrow QRS tachycardia
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
Provide examples of wide QRS complex tachycardia
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
Describe torsade de pointes
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).
Describe ventricular fibrillation
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.
Describe electrocardiographic differentiation of VT vs SVT with aberrancy
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
Describe management of VT
The management options for ventricular tachycardia include:
- cardioversion
- antiarrhythmic drugs
- intracardiac defibrillator (ICD)
- treatment of the underlying cause (e.g., ischemia)
- radiofrequency ablation.
Recall the normal impulse conduction pathway in the heart
- Sinoatrial node
- Atrioventricular (AV) node
- Bundle of His
- Bundle Branches
- Purkinje fibres
Describe the signs and symptom basis of bradycardia
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
Describe the classification of bradyarrhythmias
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
-
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
Describe sinus bradycardia
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.
Describe sinus pause and arrest
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.
Describe exit block
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
Describe sinus arrest
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
Describe chronotropic incompetence
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
Describe brady/tachy syndrome
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
Define high vagal tone
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.
Define exit block
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.
Describe first degree AV block
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)
Describe second degree block
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
Describe second degree II block
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)
Describe third degree block
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
Describe fascicular block
Fascicular blocks are conduction disturbances that affect the right or left bundle branches and can be further classified into the following types:
- Right Bundle Branch Block and Left Posterior Hemiblock
- Right Bundle Branch Block and Left Anterior Hemiblock
- Complete Left Bundle Branch Block
Describe right bundle branch block
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]
Describe LBBB
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
Describe bifascicular block
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)
Describe trifascicular block
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
Describe treatment of bradycardias
Management
* Drug
* Electrolyte Imbalance
* Hypothyroidism
* Post MI
* PPM Implantation
Describe the classification of recommendations
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»_space;> Risk).
- Class IIa: Procedure/Treatment is REASONABLE to perform/administer (Benefit»_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.
List common pacing indications
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.
Distinguish between pericarditis and inferior STEMI
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.
