ECG interpretation - arryhthmias, BBB etc Flashcards
List the main supraventricular arryhthmias
Supraventricular tachycardia:
- Atrial Fibrillation
- Atrial Flutter
- Ectopic atrial tachycardia
Bradycardia:
- Sinus bradycardia
- Sinus pauses
List the main ventricular arryhthmias
- Ventricular ectopics or Premature Ventricular Complexes (PVC)
- Ventricular Tachycardia (VT)
- Ventricular Fibrillation (VF)
- Asystole
List the main AV node arryhthmias
AVN re-entry tachycardia (AVNRT)
AV reciprocating or AV Reentrant tachycardia (AVRT)
AV block:
- 1st degree
- 2nd degree
- 3rd degree
List the clinical causes of arryhthmias
Abnormal anatomy:
- left ventricular hypertrophy
- accessory pathways
- congenital HD
Autonomic nervous system (ANS):
- Sympathetic stimulation: stress, exercise, hyperthyroidism
- Increased vagal tone causing bradycardia
Metabolic:
- Hypoxia: chronic pulmonary disease, pulmonary embolus
- Ischaemic myocardium: acute MI, angina
- Electrolyte imbalances: K+, Ca 2+, Mg2+
Inflammation: viral myocarditis
Drugs: direct electrophysiologic effects or via ANS
Genetic: mutations of genes encoding cardiac ion channels e.g. the congenital long QT syndrome
What are the common symptoms of arryhthmias ?
- Palpitations, ”pounding heart”
- Shortness of breath
- Dizziness
- Loss of consciousness; ”Syncope”
- Faintness: “presyncope”
- Sudden cardiac death
- Angina, heart failure
What are the 1st line investigations to be done on someone presenting with a possible arryhthmia ? (will commonly present with palpatations)
- 12-lead ECG:
- TFT’s - thyrotoxicosis may precipitate atrial fibrillation and other arrhythmias
- Urea and electrolytes: looking for disturbances such as a low potassium
- FBC
- CXR
First-line investigations are often normal in patients complaining of palpitations. The next step is to exclude an episode arrhythmia, what investigations should now be done ?
Most commonly a 24hr Holter ECG is done - patients are asked to keep a diary to record any symptomatic palpitations. This can later be compared to the rhythm strip at the time of the symptoms
Others which may be done include:
- Excercise ECG
- Electrophysiological study
What is the characteristic sign seen on ECG suggestive of WPW syndrome ?
Slurred upstroke (delta wave)
What does an excericse ECG allow you to assess?
- To assess for ischaemia
- Exercise induced arrhythmia
What does echocardiography allow you to assess?
Assess for structural disease of the heart e.g:
- Enlarged atria in AF
- LV dilatation
- Previous MI scar, aneurysm
What is able to be done at the same time of studying the arryhthmia on electrophysiological study ?
Opportunity to treat the arrhythmia by delivering radiofrequency ablation to extra pathway
When analysing the rhythmn of an ECG what are the 6 steps you should analyse?
- Is there electrical activity?
- Is the rhythm regular or irregular?
- What is the HR?
- Are the P-waves present?
- What is the relationship between the P and QRS complexes?
- What is the QRS duration?
How do you determine if there is normal sinus rhythm on an ECG ?
Check there is a p wave for every QRS complex and that the PR interval is < 200ms
How do you determine if an arryhthmia is supraventricular or ventricular in origin ?
- A supraventricular arryhthmia has a narrow QRS complex
- A ventricular arryhthmia has a broad QRS complex (>120ms)
What is shown in this ECG and explain if it is a problem or not
Normal sinus arryhthmia - it is normal and caused by Inspiration reducing vagal tone and increasing HR.
Define what sinus bradycardia is
rate < 60 beats/min (pwaves and QRS complexes normal)
What are the causes of sinus bradycardia ?
- Physiological i.e., athlete
- Drugs (B-Blocker)
- Ischaemia : common in inferior STEMIs
What is the treatment of sinus bradycardia ?
- If asymptomatic & rate >40bpm then no treatment, but stop causative factors e.g. drugs.
- If symptomatic or rate is <40bpm 1st line = IV atropine
- 2nd line = temoprary cardiac pacing required if haemodynamic compromise: hypotension, CHF, angina, collapse
Define a sinus tachycardia
HR > 100 beats/min (note the p wave and QRS are both normal)
What are the causes of sinus tachycardia ?
- Physiological (Anxiety, fever, hypotension, anaemia, excerise, stimulants e.g. caffeine, nicotine etc)
- Inappropriate (drugs, etc)
What is the treartment of sinus tachycardias ?
Treat underlying cause /lifestyle changes +/- Beta-blockers
What are the 3 types of AF?
- Paroxysmal - lasts < 48hrs, often recurrent
- Persistent - lasts > 48hrs but is able to be cardioverted back to normal sinus rhythm (unlikely to spontaneously revert to NSR)
- Permanent (chronic) - Inability of pharmacologic or non-pharmacologic methods to restore NSR
What are the 3 ways in which AF may be terminated and reverted back to normal sinus rhythm (NSR)?
- Pharmacologic cardioversion with anti-arrhythmic drugs (30% effective)
- Electrical Cardioversion (90% effective) by direct current (DCCV)
- Spontaneous reversion to sinus rhythm
List the possible causes of AF
- Hypertension
- Congestive heart failure
- Sick sinus syndrome - ‘tachy brady syndrome’
- Coronary heart disease
- Obesity
- Thyroid disease
- Familial
- Cardiac Valve disease
- Alcohol abuse
- Congenital heart disease
- Cardiac surgery
- COPD, Pneumonia,
- Septicaemia,
- Pericarditis, tumors
- Vagal cause – high endurance athletess
Define what idopathic (lone) AF is
This is AF in the absence of any heart disease and no evidence of ventricular dysfunction ==> diagnosis of exclusion
What are the symptoms of AF ?
- Palpitations
- Pre-syncope (dizziness)
- Syncope
- Chest pain
- Dyspnea
- Sweatiness
- Fatigue
Basically the same as any other arryhthmia
What ECG features are characterisitic of atrial fibrillation ?
- Irregularly irregular QRS complexes (distance between them)
- Absent p waves
What ECG abnormality is shown ?
AF
What are the 2 different approaches for the management of AF ?
- Rhythm control - aim is to maintain SR
- OR Rate control - aim is to accept AF but control ventricular rate
Anti-coagulation for both approaches if high risk for thromboembolism
What is the treatment of new onset AF with haemodynamic instability ?
1st line = emergency electrical cardioversion (do not delay this to achieve anticoagulation)
What is the preferred treatment of AF if the onset is > 48hrs or is uncertain and they are haemodynamically stable?
Rate control
When is rate control not the preferred treatment method of AF ?
If there is co-existent heart failure, first onset AF or where there is an obvious reversible cause of the AF (do rhythm control here)
What is the stepwise options for rate control of AF ?
- 1st line = standard Beta-blocker (but not sotalol) or a rate-limiting CCB (diltiazem or verapamil)
- 2nd line = combination of any of the following 3; Beta-blocker (but not sotalol), diltiazem or digoxin
- 3rd line = Rhythm control
Why is digoxin not a 1st line option for rate control of AF?
Because it is less effective at controlling rate in exercise and ==> better for very sedentry people
What are the 2 ways in which rhythm control of AF is achieved
- Pharmacological cardioversion
- Electrical cardioversion (DC)
Prior to doing rhythm control in patients other than those previously mentioned needing emergency DC cardioversion, what needs to be ensured prior to cardioversion ?
That the patient has either been anticoagulated or their symptom onset was < 48hrs prior to attempting cardioversion
What is the stepwise options for rhythm control ?
- 1st line in patients where AF present > 48hrs = electrical cardioversion
- 2nd line = pharmacological cardioversion with flecainide or amiodarone
What should electrical cardioversion not be attempted before (unless emergency)
Until ≥ 3 wks of anticoagulation or a transoesophageal echo is done to exclude a left atrial thrombus (if this is done then can immediately heparinise & cardiovert)
Following cardioversion what may be required to maintain NSR ?
- 1st line = standard beta-blocker
- 2nd line = amiodarone or flecainide mainly (or sotalol)
When should amiodarone or flecainide be used over oneanother ?
- Amiodarone used if patient has structural heart disease
- Flecainide if they dont have it
If an AF patient is at high risk of cardioversion failure, what should they take prior ?
Amiodarone or sotalol for ≥ 4wks
Following cardioversion of someone with AF what should be given for at least ≥ 4wks ?
Anticoagulation & then decision to continue based on the standard AF risk assessment
The treatment of atrial flutter has the same principles as AF (rate vs rhythm control) however atrial flutter does not respond as well to drug treatment as AF.
When is rate control usually used in atrial flutter treatment then ?
As an interium measure prior to restoration of NSR
What are the stepwise options for rate control of atrial flutter?
- 1st line = beta-blocker (but not sotalol) or CCB (diltiazem or verapamil)
- 2nd line = may add digoxin, it can be useful for those in heart failure
Rhythm control is preferred as the treatment of atrial flutter, what is the stepwise options ?
- 1st line for when rapid conversion to NSR needed i.e. when associated with haemodyanmic compromise = electrical cardioversion (usually DC)
- 1st line for recurrent atrial flutter = catheter ablation
If electrical cardioversion not done as emergency then need to follow same guidelines on anticoagulating or doing a TOE prior same as in AF
Pharma cardioversion has limited effect
What should all patients with AF be assessed for risk of and how ?
- Risk of stroke (thrombus) & ==> the need for anticoagulation
- Done using the CHA2DS2-VASc score (note this needs to be weighed against risk of bleeding using the HASBLED score)
A CHA2DS2-VASc score of what required anticoagulation ?
What should patients with AF or atrial flutter requiring anticoagulation be offered?
A choice between warfarin or NOAG unless valvular AF then warfarin preferred
What are the characterisitic features on ECG of atrial flutter ?
- A regular narrow complx tachycardia
- Sawtooth baseline
- Rate is a division of 300 (usually 150, but can be 100, 75 etc)
- Best seen in V1 or lead II
What ECG abnormality is shown here ?
Atrial flutter
What are the characterisitc features of junctional rhythms?
- Regular rhythm
- No p waves prior to QRS complex, instead they are seen following the ARS complex in the ST segment and are inverted
- Narrow QRS complex unless co-exisitent L or RBBB
- May have a normal, bradycardic or tachycardic rate
What are SVT’s usually caused by?
- AV nodal re-entrant tachycardia (AVNRT)
- AV reciprocating tachycardia / AV reentrant tachycaria (via an accessory pathway) (AVRT) i.e. Wolf-parkison white
- Ectopic atrial tachycardia (EAT)
What are the characterisitc features of an SVT?
- Regular and tachycardic
- Often no clear p waves
- Narrow ARS complex (<120)
What ECG abnormality is shown ?
SVT
What is the acute management of an SVT ?
- 1st line = Valsalva manoeuvre, carotid masage (used to increase vagal tone) if haemodyanmically stable
- 2nd line = IV adenosine or verapamil if asthmatic
- 3rd line = Electrical cardioversion
In whom should verapamil be avoided in ?
Those on/recently treated with beta blockers
What is the chronic management of SVT?
Either Electrophysiologic study and Radiofrequency ablation or drugs:
- Electrophysiologic study and Radiofrequency ablation 1st line for young symptomatic people
- Drugs include beta-blockers (atenolol, soltalol) and anti-arrhythmic drugs (diltiazem, verapamil, propanefenone)
What are the characterisitc ECG features of supraventricular ectopics ?
- Sinus rhythm (p, ARS and T waves all present) but every 3rd beat (3,6,9 etc) a p-wave comes early
- This early p wave results in varying PR and RR intervals but the abrnomality is regular
What ECG abnormality is shown ?
supraventricular ectopic
What are the main ventricular arryhthmias ?
- Ventricular premature complexes
- Ventricular tachycardia (monomorphic)
- Polymorphic ventricular tachycardia
- Ventricular escape rhythm
- Ventricular fibrillation
What are the 2 types of ventricular premature complexes ?
- Bigeminy
- Trigeminy
What is the characterisitc appearance of a bigeminy ventricular premature complex?
- 1 sinus beat (i.e. p, ARS and T wave) coupled with 1 ventricular premature complex (VPC)
Recall QRS complex represents ventricular contraction so think the VPC is a premature QRS complex essentially
What is the characterisitc appearance of a trigeminy ventricular premature complex?
1 sinus beat coupled with 2 VPC’s
What ECG abnormality is shown ?
You can see both bigeminy and trigeminy VPC’s
What are the 2 main types of ventricular tachycardias?
Monomorphic and polymorphic
What do most patients with ventricular tachycardia have causing the arryhthmia and what are some of the other rarer causes ?
Most patients have significant heart disease:
- Coronary artery disease
- A previous myocardial infarction
Rare causes:
- Cardiomyopathy
- Inherited/ Familial arrhythmia syndromes
- Long QT, Brugada syndrome
What are the characteristic features on ECG of a monomorphic ventricular tachycardia ?
Regular borad complex tachycardia
What may a monomorphic ventricular tachycardia be associated with ?
- Haemodyanmic compromise
- It is always abrnormal and must be acted upon
What are the characteristic features of polymorphic ventricular tachycardia on ECG ?
- Broad complx tachycardia - looks like the forth rail bridge
- An uncommon subtype is torsade de pointes (gradual change in amplitude and twisting of QRS complexes around the isoelectric line)
What is the treatment of ventricular tachycardia in patients who are haemodyanmically stable ?
- 1st line = amiodarone (flecainide, propafenone or lidocaine are less effective but sometimes used)
- 2nd line = electrical cardioversion
What is the treatment of ventricular tachycardias in patients whom are not haemodyanmically stable or pulseless ?
(e.g. systolic BP < 90 mmHg, chest pain, heart failure, syncope)
DC cardioversion (electrical)
What is the long-term treatment of ventricular tachycardia ?
- electrophysiological study (EPS) and ablation OR
- implant able cardioverter-defibrillator (ICD) - this is particularly indicated in patients with significantly impaired LV function
What drug in particular should not be used in the treatment of ventricular tachycardias ?
Verapamil
What are the characteristic ECG features of ventricular fibrillation ?
- Irregular random basline
- No clear discernable waveform
What is ventricular fibrillation always associated with ?
Loss of conciousness
What is the treatment of ventricular fibrillation ?
Defibrillation and cardiopulmonary resuscitation
What are capture beats ?
occur when the sinoatrial node transiently ‘captures’ the ventricles, in the midst of AV dissociation, to produce an early narrow QRS complex
What are fusion beats?
occur when a sinus and ventricular beat coincides to produce a hybrid complex.
The hallmark of a rhythm that originates in the ventricles is a broad QRS complex, but what can complicate this ?
Abbernacy which is when
- L and RBBB can complicate this as they both cause broad ARS complexes.
- This can therefore make it difficult to discern between a supraventricular rhythm with bundle branch block e.g. atrial flutter with LBBB from VT
What are some useful ways to differentiate between supraventricular rhythms with aberracny and ventricular rhythms ?
A good predictor of supraventricular + aberrancy is if the person had pre-exisiting bundle branch block
A good predictor of ventricular rhythm is if the person has pre-existing coronary disease or capture and fusion beats
Define what heart block is
- This is where there is a block in the conduction between the atria and ventricles
- Not to be confused with bundle branch block
What is heart block due to ?
AV node dysfunction, caused by:
- Drugs
- ischaemia
- Age
What is the characteristic ECG appearance of 1st degree heart block?
The PR interval is prolonged > 0.2 seconds
What ECG abnormality is shown?
1st degree heart block
What is the treatment of 1st degree heart block?
None but observe as they may develop a greater degree of heart block
What are the 2 types of 2nd degree heart block and they’re characteristic ECG appearance ?
- Type 1/Mobitz I = there is progressive prolongation of the PR interval with an eventual missed beat (p wave not followed by QRS complex)
- Type 2/Mobitz II = constant prolonged PR interval but the P wave is not followed by a QRS complex every 2:1 or 3:1
What ECG abnormality is shown ?
Mobitz I
What ECG abnormality is shown ?
Mobitz II
Does 2nd degree heart block need treatment ?
- Mobitz I does not unless there is haemodynamic compromise or collapse (if so tx is same as mobitz II)
- Mobitz II need a permanent pacemaker due to risk of 3rd degree heart block/ asystole
What is the characteristic ECG appearance of 3rd degree heart block?
- Also known as complete heart block
- There is no relationship between the p waves and ARS complexes - ‘the p waves march through’
What treatment is required for 3rd degree heart block?
Ventricular pacing - pacemaker
List the main arryhthmias associated with cardiac arrests
- Ventricular tachycardia
- Ventricular fibrillation
- Complete AV block (3rd degree heart block)
- Pulsless electrical activity
- Terminal rhythm sequence
What is required in the event of cardiac arrest with defibrillation?
Prompt defibrillation
In the event of circulatory collapse with 3rd degree heart block what needs to be done ?
IV atropine and isoprenaline may be indicated until trans-venous pacing wire can be done
What is meant by pulsless electrical activity and what tx is required ?
- Refers to cardiac arrest in which the electrocardiogram shows a heart rhythm that should produce a pulse, but does not.
- Requires prompt CPR and identification of a reversible cause
What is meant by a terminal rhythm sequence ?
This is where if a ventricular arryhthmia is left untreated it can deteriorate from ventricular tachycardia to ventricular fibrillation and then to asystole
Define what ventricular hypertrophy is
This is thickening of the ventricle walls. It is more common in the left ventricle, but can occur in the right or both.
What are the 2 types of ventricular hypertrophy and their causes ?
- Physiological/athletes heart - it is a normal response to healthy exercise or pregnancy
- Pathological - it is the response to stress or disease such as HTN, MI, heart failure or neurohormones
List the framingham criteria for LVH
- R wave in aVL > 11mm, R in V4-6 > 25mm
- S wave in V1-3 > 25mm
- S wave in V1 or V2 + R wave in V5 or 6 > 35mm
- R wave in I + S wave in III > 25mm
What ECG abnormality is shown ?
LVH
What ECG abnormality is shown ?
LVH
Define what is meant by bundle branch block
This is where there is a delay in conduction in either of the bundle branches
What does the left branch of the bundle of his further split up into ?
Into the anterior and posterior hemi-bundles
What are the 2 main types of bundle branch block (BBB)?
Left and right BBB (because the bundle of his splits up into 2)
In BBB what does the QRS complex duration need to be ?
>0.12s (i.e. broad complex)
What is partial/incomplete bundle branch block?
This is where the pattern of bundle branch block (either R or L type) is present but the QRS complex is not > 0.12s
What leads do you check for BBB?
V1-6
How do you remember what is RBBB and what is LBBB?
WiLLiaM MaRRoW
- in LBBB there is a ‘W’ in V1 and a ‘M’ in V6
- in RBBB there is a ‘M’ in V1 and a ‘W’ in V6
Which bundle branch block type can you not reliably diagnose an MI in without using specific criteria ?
LBBB
What are the causes of RBBB?
- normal variant - more common with increasing age
- right ventricular hypertrophy
- chronically increased right ventricular pressure - e.g. cor pulmonale
- pulmonary embolism
- myocardial infarction
- atrial septal defect (ostium secundum)
- cardiomyopathy or myocarditis
What are the causes of LBBB?
Usually indicative of heart disease:
- ischaemic heart disease
- hypertension
- aortic stenosis
- cardiomyopathy
What ECG abnormality is shown?
RBBB
What ECG abnormality is shown ?
LBBB
What are the criteria of left anterior hemiblock (LAHB)?
- Left axis deviation
- rS complexes in the inferior leads (II, III and aVF)
What are the criteria of left posterior hemiblock (LPHB)?
- Right axis deviation
- rS pattern in lead I
- qR pattern in lead III
What are the 2 types of fasicular block and their criteria ?
Bifasciular and trifasciular block
What are the criteria for bifasicular block?
2 of:
- PR interval > 0.2s
- Left axis deviation (Left anterior hemiblock)
- RBBB
What are the criteria for trifasicular block?
- PR interval > 0.2s
- Left axid deviation (left anterior hemiblock)
- RBBB or alternating RBBB & LBBB
What are the different stages of ECG changes of hyperkalaemia ?
Note - VF can also occur
What are the characteristic ECG changes seen in hypo and hyper calcaemia (they are not the same)
- The ECG hallmark of hypocalcemia is prolongation of the QTc interval because of lengthening of the ST segment, which is directly proportional to the degree of hypocalcemia
- The exact opposite holds true for hypercalcemia i.e. shorening of the QTc interval
Interpret the following ECG
- Normal axis
- Dx = AF at a rate of 90-100bpm
Interpret the following ECG
Note - pt has know dilated cardiomyopathy
- Sawtooth waves seen characterisitic of atrial flutter
- Rate not reg so element of AV block
Dx = atrial flutter + variable block (this fits with known dilated cardiomyopathy as these pt’s are more prone to dysarrhythmias)
Interpret the following ECG
- No P-waves present & Narrow QRS complex tachycardia (rate about 150) ==> thinking SVT or atrial flutter
- Also had evidence of LVH could be physical fitness
Specifically an AV-nodal re-entrant tachycardia because notching in the T-wave esp seen in V6 which is characterisitic of this
Note - the notching is a retrograde P-wave because of dysarrhytmia in the AV node causing conduction back up into the atria, whilst also allowing conduction down into the ventricles hence a P-wave in the T-wave
Interpret the following ECG
- Broad QRS complexes, no obvious P-waves
- Regular rate
Dx = Classic of monomorphic VT (normally caused by CAD/previous ischaemia and scarring so pt’s usually have a background history of this)
Interpret the following ECG
Dx = ventricular fibrillation
Interpret the following ECG
- ST segment elevation in V2-5
- Reciprocal changes (ST depression) seen in lead II, III & aVF
- Pre-exisiting RBBB
Dx = STEMI in anteroseptal leads
Note - Reciprocal change is a very important ECG finding, not only supporting the diagnosis of STEMI but also indicating a high-risk patient. Reciprocal change is defined as ST-segment depression occurring on an ECG which also has ST-segment elevation in at least 2 leads in a single anatomic segment.
Interpret the following ECG
2nd degree Mobitz type I
Interpret the following ECG
2nd degree Mobitz type II
Interpret the following ECG
Complete heart block
Interpret the following ECG
- Congenital (hereditary) long QT syndrome. The ECG demonstrates sinus rhythm with a very prolonged QT interval of 0.6 second.
- Note the broad T waves with notching (or possibly U waves) in the precordial leads. This characteristic may identify patients with long QT syndrome at increased risk for torsade de pointes and syncope and sudden death.
