ECG Flashcards
Rhythm
the place where the action potential started
Sinus rhythm - physiology
action potential originates from the SA node, through the atria and to the ventricles via the AV node, bundle of His and Purkinje fibres
Sinus rhythm - ECG
- Normal rate (50-100bpm)
- Regular PQRST pattern
- Constant PR interval
- QRS complex duration < 100ms wide
- Normal P wave morphology
Sinus arrhythmia - Physiology
Heart rate varies due to reflex changes in vagal tone during the different stages of the respiratory cycle
Normal phenomenon, most common in young healthy people
Sinus arrhythmia - ECG
Variation in P-P interval is more than 120ms (3 small boxes) - changes in length normally correspond with the respiratory cycle
P wave has normal morphology and P-R interval is constant
Sinus arrhythmia - ECG
Variation in P-P interval is more than 120ms (3 small boxes) - changes in length correspond with the respiratory cycle
P wave has normal morphology and PR interval is constant
Sinus tachycardia - Physiology
Action potential originates from the SA node, through the atria and to the ventricles via the AV node, bundle of His and Purkinje fibres (happens too fast due to an increased rate of depolarisation in the SA node)
Sinus tachycardia - ECG
Sinus rhythm with a resting rate > 100bpm
P waves can be hidden within preceding T waves
Sinus tachycardia - causes
Exercise, pain, anxiety, sepsis, anaemia, pulmonary embolism (blocked vessel in lungs), cardiac tamponade (space around heart fills with fluid causing pressure on heart), hyperthyroidism, hypoxia (low oxygen levels), hypovolaemia (loss of fluid)
Pharmacological causes… Beta-agonists (adrenaline, salbutamol, isoprenaline), sympathomimetic, antihistamines, tricyclic antidepressants, caffeine.
Inappropriate sinus tachycardia = If patient is symptomatic and these things are ruled out
Sinus tachycardia - treatment
Treat underlying cause, may require beta-blockers or calcium channel blockers to lower heart rate
Can be due to re-entry phenomenon in the SA node (abrupt onset/termination with a rate of 130-140bpm) – vagal manoeuvres may stop it.
Sinus bradycardia - physiology
Action potential originates from the SA node, through the atria and to the ventricles via the AV node, bundle of His and Purkinje fibres (happens too slow)
Sinus bradycardia - ECG
Sinus rhythm with a rate of <60bpm
P-R interval is at least 0.12s
Common to see prominent U waves (a small deflection immediately following the T wave) in the precordial leads
Sinus bradycardia - causes
normal when sleeping and athletes with increased vagal tone
pathological causes - inferior MI, hyperthyroidism, anorexia, hyperkalemia, myocarditis, sick sinus syndrome, hypothermia
drugs - beta-blockers, calcium channel blockers, digoxin, amiodarone, GABA-ergic agents
Beta blockers =
used to slow down heart rate and reduce blood pressure
Propranolol, Bisoprolol
calcium-channel blockers =
used to reduce blood pressure
Verapamil, Diltiazem
Digoxin =
used to control arrythmias
Amiodarone =
anti-arrhythmic medication that slows conduction rate and prolongs refractory period of SA + AV nodes = used to treat VT, VF, AF
Sick sinus syndrome - physiology
dysfunction of the SA node with impairment of its ability to generate impulses (associated with myocardial ischaemia, digoxin toxicity, myocarditis and cardiac surgery) =
Sick sinus syndrome - ECG
Severe sinus bradycardia
Periods of sinoatrial block
Sinus arrest
Junctional or ventricular escape rhythms
Tachycardia-bradycardia syndrome
Paroxysmal atrial flutter and atrial fibrillation.
Tachycardia-bradycardia syndrome =
Common in sick sinus syndrome
Characterised by bursts of atrial tachycardia interspersed with periods of bradycardia
Paroxysmal atrial flutter or fibrillation may also occur
Cardioversion may be needed
Absolute bradycardia:
< 40 bpm
Sinus exit block - physiology
caused by failed propagation of pacemaker impulses beyond the SA node – the SA node depolarises normally but some impulses are blocked before leaving the SA node = intermitted failure of atrial depolarisation
Sinus exit block - ECG
Dropped P waves caused by SA node dysfunction
The pauses are the length of two or more P-P intervals.
Failure of SA pace-making cells causes…
sinus pause/sinus arrest
Failure of SA transitional cells (that transmit the impulse) causes…
SA exit block
Sinus arrest - physiology
Sinus arrest occurs when there is transient cessation of impulse formation at the sinoatrial node
Sinus arrest - ECG
prolonged pause without P wave activity (>3s)
the pause is unrelated to the length of the P-P cycle.
Escape rhythms =
the result of spontaneous activity from another pacemaker in the atria, atrioventricular junction or ventricles, which take over when normal impulse formation in the SA node fails
Escape beats/rhythms - physiology
Groups of pacemaker cells throughout the conducting system are capable of spontaneous depolarisation
The rate of depolarisation decreases from top to bottom: fastest at the sinoatrial node; slowest within the ventricles
Ectopic impulses from subsidiary pacemakers are normally suppressed by more rapid impulses from above
However, if an ectopic focus depolarises early enough (before the arrival of the next sinus impuls) it may produce a premature contraction
Premature contractions (“ectopics”) are classified by their origin — atrial, junctional or ventricular
The rate of spontaneous depolarisation of pacemaker cells decreases down the conducting system:
- SA node (60-100 bpm)
- Atria (< 60 bpm)
- AV node (40-60 bpm)
- Ventricles (20-40 bpm)
Atrial premature beats (atrial ectopics) - physiology
premature beat arising from ectopic pacemaking tissue within the atria
Atrial premature beats (atrial ectopics) - ECG
- Abnormal (non-sinus) P wave
- Normal QRS complex
- Pauses may be present after ectopic
Atrial premature beats (atrial ectopics) - symptoms and treatment
Ectopics are a normal electrophysiological phenomenon not usually requiring treatment
Frequent ectopics may cause palpitations
In patients with underlying predispositions (e.g. left atrial enlargement, ischaemic heart disease, WPW), ectopics may trigger the onset of a re-entry tachyarrhythmia — e.g. Atrial fibrillation, atrial flutter, AVNRT, AVRT
Supraventricular tachycardia =
any tachyarrhythmia arising from the atria or atrioventricular junction (above the Bundle of His)
SVT is classified based onsite of origin (atria or AV node) and regularity (irregular or regular):
Regular atria:
- Sinus tachycardia
- Atrial tachycardia
- Atrial flutter
- Inappropriate sinus tachycardia = elevated rate without a reason
- SA node re-entrant tachycardia
Irregular atria
- AF
- Multifocal atrial tachycardia = A rapid, irregular atrial rhythm arising from multiple ectopic foci within the atria.
Regular atrioventricular
- AV nodal re-entry tachycardia (AVNRT)
- AV re-entry tachycardia (AVRT)
- Junctional tachycardia = arrhythmias arising from the region of the atrioventricular junction as a result of a re-entry mechanism
Atrial flutter - physiology
A form of supraventricular narrow complex tachycardia
Caused by a single re-entry circuit in the right atrium with secondary activation in the left atrium = produces atrial contractions at a rate of 300bpm = looks like F waves
The AV node only lets electrical activity through at certain points = regular ventricle rhythm.
Atrial flutter - ECG
Loss of isoelectric baseline - Jagged pattern (Flutter waves = saw-toothed and best seen in inferior leads and V1)
Regular atrial (~300bpm) and ventricular rhythm (depends on AV conduction ratio - can be 2:1, 3:1, 4:1) – in contrast, AF will be completely irregular
Atrial fibrillation - physiology
P waves are not visible due to abnormal atrial depolarisation = irregular atrial rhythm (300-600bpm)
The AV node is unable to transmit beats as quickly as this, and thus does so intermittently, resulting in an irregular ventricular rhythm.
Atrial fibrillation - causes
o Idiopathic
o Heart failure
o MI
o Hypertension
o valve disease
o Congenital heart disease
Atrial fibrillation - management
- Beta-blockers
- Cardioversion
- Ablation
AF is a potential risk for stroke…
the atria are not contracting properly (because there is no depolarisation) so blood can pool in the atria and cause thrombus formation which can embolise and go to the brain = patients with AF need anti-coagulants to prevent this.
AV nodal (junctional) rhythm - physiology
If rhythm starts at AV node the action potential would spread upwards and downwards to activate the heart = heart would beat in rhythm with AV node.
Because the AV node is at the junction between the atria and ventricles its often described as a junctional rhythm
AV nodal (junctional) rhythm - ECG
rate of 40-60bpm
QRS morphology is typically narrow (< 120ms)
no relationship with P waves or inverted P waves
AV Nodal Re-entry Tachycardia (AVNRT) - physiology
1) A premature atrial contraction arrives while the fast pathway of the AV node is still refractory, and is directed down the slow pathway
2) The refractory in the fast pathway ends, and the ectopic impulse travels retrogradely up the fast pathway
3) The impulse continually cycles around the two pathways
short cycle = fast heart rate
Paroxysmal and occurs in young/healthy patients or those with chronic heart disease
AV Nodal Re-entry Tachycardia (AVNRT) - ECG
Regular tachycardia ~140-280 bpm
Regular narrow QRS complexes (< 120ms)
P wave embedded in the QRS complexes
Pseudo R wave may be seen in V1 or V2
Pseudo S waves may be seen in leads II, III or aVF
If P waves are visible they inverted in leads II, III, aVF.
Widespread ST depression possibly seen (resolves when patient is in sinus)
AV Nodal Re-entry Tachycardia (AVNRT) - ECG
Regular tachycardia ~140-280 bpm
Regular narrow QRS complexes (< 120ms)
P wave embedded in the QRS complexes
Pseudo R wave may be seen in V1 or V2
Pseudo S waves may be seen in leads II, III or aVF
If P waves are visible they inverted in leads II, III, aVF.
Widespread ST depression possibly seen (resolves when patient is in sinus)
AV Nodal Re-entry Tachycardia (AVNRT) - symptoms and treatment
Palpitations
Vagal manoeuvres may cause reversion to sinus rhythm
Adenosine (blocks AV nodal conduction and increases AV nodal refractory period)
Ventricular pre-excitation (Wolff-Parkinson-White syndrome) - physiology
early activation of the ventricles due to impulses bypassing the AV node via an accessory pathway formed during cardiac development (bundle of kent)
Ventricular pre-excitation (Wolff-Parkinson-White syndrome) - ECG
Atrial impulse conducts over the accessory pathway without delay encountered with AV node conduction = transmitted rapidly = short PR interval.
Because the impulse enters non-specialised myocardium, ventricular depolarisation progresses slowly at first, distorting the early part of the R wave (slurringrise) and producing a delta wave + QRS prolongation (>110ms)
This slow depolarisation is then rapidly overtaken by depolarisation propagated by the normal conduction system, and the rest of the QRS complex appears relatively normal.
Right bundle branch block - physiology
When conduction in the right bundle branch is blocked, depolarisation of the right ventricle is delayed.
The left ventricle depolarises normally = early part of the QRS complex appears normal.
The wave of depolarisation then spreads to the right ventricle through non-specialised conducting tissue, with slow depolarisation of the right ventricle = the later part of the QRS complex is abnormal
Right bundle branch block - ECG
- QRS duration ≥ 0.12 s
- A secondary R wave (R’) in V1 or V2
- Wide slurred S wave in leads I, V5, and V6
- Can be associated with ST segment depression and T wave inversion in the right precordial leads
Conditions associated with RBBB:
- Rheumatic heart disease
- Right ventricular hypertrophy
- Myocarditis or cardiomyopathy
- Ischaemic heart disease
- Pulmonary embolus
- Atrial septal defects)
- Atrioventricular conduction is delayed
Left bundle branch blocks - physiology
The left bundle branch is supplied by both the anterior descending artery (branch of the left coronary artery) and the right coronary artery = LBBB is associated with MI
In the normal heart, septal depolarisation proceeds from left to right (producing septal Q waves in left chest leads)
In LBBB
Left bundle branch blocks - ECG
- QRS duration of ≥ 0.12 s
- Broad monophasic R wave in I, V5, V6
- Absence of Q waves in leads V5 and V6
o Displacement of ST segment and T wave in an opposite direction to the dominant deflection of the QRS complex (appropriate discordance)
o Poor R wave progression in the chest leads
o RS complex, rather than monophasic complex, in leads V5 and V6
1st degree AV block - physiology
delay in the conduction of the atrial impulse to the ventricles, usually at the level of the atrioventricular node
1st degree AV block - ECG
Prolongation of the PR interval (> 0.2 s)
1st degree AV block - managment
No specific treatment is indicated.
If there are symptoms of dizziness or syncope cardiac monitoring should be considered to identify higher degrees of block.
2nd degree AV block =
Atrioventricular conduction is intermittently blocked = some P waves are not followed by a QRS complex
There are 3 types:
- Mobitz I Wenckebach
- Mobitz II
- 2:1 AV block
Mobitz type I block (Wenckebach) - physiology
Block at the level of the atrioventricular node
Produces intermittent failure of transmission of the atrial impulse to the ventricles
Mobitz type I block (Wenckebach) - ECG
The initial PR interval is normal but progressively lengthens with each successive beat until eventually atrioventricular transmission is blocked completely and the P wave is not followed by a QRS complex (dropped)
The PR interval then returns to normal, and the cycle repeats
Mobitz type II block - physiology
Intermittent failure of AV conduction, normally at the level of the bundle branches
Mobitz type II block - ECG
Occasionally a P wave is not followed by a QRS complex (dropped)
The PR interval is constant (may be prolonged)
Associated with wide QRS complexes
2:1 AV block - physiology
Every alternate beat from the atria is not being conducted through the AV node
2:1 AV block - ECG
2 P waves for every QRS complex
3rd degree (complete) AV block - physiology
Complete failure of conduction between the atria and ventricles, with complete independence of atrial and ventricular contractions.
Will need a pacemaker
3rd degree (complete) AV block - ECG
The P waves bear no relation to the QRS complexes and usually proceed at a faster rate
ECG shows complete AV dissociation (independent atrial and ventricular rates)
Severe bradycardia due to absence of AV conduction
No supraventricular impulses conduct to the ventricles - perfusing rhythm is maintained by junctional or ventricular escape rhythm… or patient may display ventricular standstill leading to syncope (if self-terminating) or sudden cardiac death (if prolonged).
Ventricular escape beats - ECG
A ventricular rhythm with a rate of 20-40 bpm.
Broad QRS complexes (> 120ms, may have a LBBB or RBBB morphology).
No P wave
Ventricular premature beats (ventricular ectopics) - physiology
Ectopic firing of a focus within the ventricles bypasses the His-Purkinje system and depolarises the ventricles directly
This disrupts the normal sequence of cardiac activation, leading to asynchronous activation of the two ventricles
Ventricular premature beats (ventricular ectopics) - ECG
Broad QRS complex (≥ 120ms) with abnormal morphology
Premature — i.e. occurs earlier than would be expected for the next sinus impulse
Discordant ST segment and T wave changes.
Usually followed by a full compensatory pause
Ventricular tachycardia - cause
Result from direct damage to the myocardium secondary to ischaemia or cardiomyopathy, or from the effects of myocarditis or drugs.
Monomorphic ventricular tachycardia usually occurs after myocardial infarction and is a sign of extensive myocardial damage.
Ventricular tachycardia - physiology
initiated by re-entry circuits that occurs in the zone of ischaemia or fibrosis surrounding damaged myocardium.
often precipitate cardiac arrest, and they are common immediately after arrest.
Polymorphic ventricular tachycardia requires immediate direct current cardioversion.
Ventricular tachycardia - ECG
the morphology of the QRS complex is bizarre, and the duration of the complex is prolonged (> 0.12s)
The QRS complex often has a right or left bundle branch morphology
In VT the rate is normally 120-300 bpm.
The rhythm is almost regular
The atrial rate is usually slower than the ventricular rate
Torsades de pointes =
twisting of points
a type of polymorphic ventricular tachycardia in which the cardiac axis rotates over a sequence of 5-20 beats, changing from one direction to another and back again = the QRS amplitude varies
Sustained VT =
lasts longer than 20s
Ventricular fibrillation - pathology
Individual myocardial cells contract in an uncoordinated, rapid fashion.
Fibrillation is maintained by the continuous re-entry of waves of activation.
Activation is initially rapid but slows as the myocardium becomes increasingly ischaemic.
Can lead to sudden death – will need defibrillation
Ventricular fibrillation - ECG
Rapid irregular deflections of varying amplitude and morphology and no visible QRS complexes
The deflection rate varies (150-500bpm)
Although the atria may continue to beat, no P waves are visible
Coarse VF =
Initially, ventricular fibrillation tends to be high amplitude
Fine VF =
later ventricular fibrillation degenerates to low amplitude
Causes of VF:
- Myocardial ischaemia/infarction
- Cardiomyopathy
- Acidosis
- Electrocution
- Drugs (quinidine, digoxin, antidepressants)
- Electrolyte disturbance (hypokalaemia)
Asystole =
Asystole implies the absence of any cardiac electrical activity. It results from a failure of impulse formation in the pacemaker tissue or from a failure of propagation to the ventricles. Ventricular and atrial asystole usually coexist.
Venticular standstill = Atrial activity may continue for a short time after ventricular activity has stopped and the electrocardiogram shows a flat line interrupted by only P waves
Conduction abnormalities that can cause ventricular standstill include…
complete AV block and the occurrence of alternating left and right bundle branch block
Ventricular standstill - physiology + ECG + treatment
SA node functioning = P waves present
No ventricular response due to advanced AV block (complete heart block without an escape rhythm) = no contraction
No cardiac output = patient is in full arrest
Can be paroxysmal or prolonged
Treatment = resuscitation measures such as CPR, medications, and defibrillation
Reasons for needing a pacemaker:
- Sick sinus syndrome
- Complete heart block
- Mobitz-type II heart block
- Atrial tachycardia and heart block
- Asystole
- Carotid sinus hypersensitivity
AAI pacing
Used in patients with underlying sinus node dysfunction but intact cardiac conduction.
Sense atrial activity and inhibit pacing if the patient’s heart rate remains above the pre-set target.
At lower rates the pacer stimulates the atrium.
VVI pacing
Used in patients without useful atrial function, including those with chronic atrial fibrillation or flutter and those with silent atria.
Tracks only ventricular activity and paces the ventricle if a QRS complex is not sensed within a predefined interval
Dual chamber pacing (DDD)
an atrial impulse is generated if the patient’s natural atrial activity fails to occur within a pre-set time period after the last atrial or ventricular event.
An atrial event (paced or sensed) begins the atrioventricular interval. If a spontaneous QRS complex does not occur during the programmed atrioventricular interval, a ventricular stimulus is generated.
The ventricular stimulus, or sensed QRS complex, initiates a refractory period of the atrial amplifier known as the post-ventricular atrial refractory period.
The combination of the atrioventricular interval and the post-ventricular atrial refractory period form the total atrial refractory period. The total atrial refractory period is important because it determines the upper rate limit of the pacemaker
Mobitz type I (wenckebach) - QRS compelex
Narrow as block is at level of AV node
Mobitz type 2 - QRS compelex
Broad as block is at level of bundle of his/bundle branches
1st degree AV block - PR interval is…
Longer than 0.2s (1 large square)
Flutter: ventricle rhythm =
Regular
AF: ventricular rhythm =
Irregular
VF compared to VT
VF = loads of focuses and multiple waves of activation in all directions
VT = specific point of focus (polymorphic - two to more specific origins)
AF =
Result of multiple wavelets of depolarisation moving around the atria chaotically, rarely completing a re-entrant circuit
Junctions rhythm
Narrow QRS complex
P waves can be before, within or after QRS
Rate of 40-60bpm
Difference between atrial and ventricular ectopic beat:
Atrial had non-sinus p wave + normal QRS
Ventricular has no p wave + wide QRS
Mediation given to patient with high VE burden =
Beta blockers
Why is VT life threatening?
Increased HR - no proper ventricular contraction - reduced cardiac output
VT =
Regular
RAPID Ventricular rate
Wide QRS
VF =
Chaotic ventricular activity
Ventricular standstill =
Blocked/non conductive p waves
Absence of ventricular activity
No escape rhythm
Difference between complete AV block and ventricular standstill?
Complete AV block - has escape rhythm (there is atrial and ventricular activity, just uncoordinated)
Ventricular standstill - no escape rhythm (there is atrial activity but no ventricular activity)
Regular narrow complex tachycardia =
SVT (cannot distinguish which one)
Lateral STEMI -
Left circumflex and LAD occlusion
Anterior stemi =
Lad occlusion
Inferior STEMI =
Right coronary artery
Ventricular ectopics -
Broad
Doesn’t effect RR interval
No compensatory pause
Doesn’t effect cardiac cycle
When inverted P wave is present in II…
If PR interval is normal = atrial rhythm
If PR is short = junctions rhythm
