3- cardiac arrhythmias Flashcards
where are the anatomical conduction system parts of the heart?
- SA node in upper RA
- AV node
- His bundles in between atria & ventricles
- bundle branches down between ventricles
- purkinje fibres spreading out around muscles
what are names of arrhythmias generally based on?
- anatomical side or chamber of origin e.g. atrial or ventricular
- Mechanism or pathway eg ‘fibrillation’, or ‘ re-entry tachycardia’
- tachycardia - anything more than 100 bpm and bradycardia is anything less than 6o bpm
- Can occurs as single beats (ectopy) or continuously (persistent/sustained) or repeated episodes of limited duration (paroxysmal or non-sustained)
what is supraventricular?
non-specific term used to describe arrhythmias whose origin is above ventricle
where do supraventricular arrhythmias originate from?
originate from above the ventricle, i.e., sinoatrial node, atria, AV node or His bundle
what is appearance of supraventricular arrhythmias on ECG?
- atrial depolarization is visible by rapid P-waves (for atrial fibrillation)
- ventricular depolarisation is visible by narrow QRS complex - indicating that the electrical impulses are conducted through normal conduction pathway (unless there’s a block in His-purkinje fibres)
where does ventricular tachycardia arrhythmia originate from?
ventricular myocardium (common) or fascicles (bundle branches) of the conducting system (uncommon)
what does ventricular tachycardia look like on ECG?
a wide QRS as the arrhythmia path is outside the fast conducting His-Purkinje system, and therefore conducts slower, resulting in a longer depolarization time
what is ventricular tachycardia?
an arrhythmia characterized by a rapid and regular or irregular heartbeat originating from the ventricles (myocardium or bundle branches) of the heart
what are common types of atrial tachycardia?
- atrial fibrillation (irregular heart rhythm characterized by chaotic and rapid electrical activity in the atri)
- atrial flutter (regular heart rhythm characterized by a rapid and organized electrical activity in the atria)
- ectopic atrial tachycardia (arrhythmia characterized by abnormally fast heartbeats originating in the atria)
what are common types of bradycardia?
- sinus bradycardia (abnormally slow heart rate originating from the sinus node)
- sinus pauses
what are sinus pauses?
- Sinus pauses, also known as sinus arrest, occur when there is a temporary interruption in the normal activity of the sinus node.
- During a sinus pause, there is a brief period where the sinus node fails to generate an electrical impulse, resulting in a pause in the heart’s rhythm
what is atrial flutter?
- Atrial flutter is characterized by a regular and organized atrial rhythm.
- The atria contract at a rapid and regular rate
- the ventricular response can be regular or irregular, depending on the conduction through the atrioventricular (AV) node.
why does atrial flutter occur?
often occurs due to re-entry circuits within the atria, where electrical signals circulate in a loop
what does ectopic mean?
an abnormal heart rhythm that originates from a location other than the heart’s normal pacemaker, the sinoatrial (SA) node
what are types of ventricular arrhythmias?
- ectopic or premature ventricular complexes (a beat occurs before expected timing of next normal heartbeat - originate from outside normal conduction pathway)
- ventricular tachycardia (fast, regular & sustained)
- ventricular fibrillation (fast, chaotic, irregular beats - ventricles quiver)
- asystole (absence of electrical activity in the heart, form of cardiac arrest)
what happens in ectopic ventricular arrhythmia?
ectopic ventricular arrhythmia = abnormal site of electrical activity in ventricles is firing at faster rate than SA node
- ectopic ventricular focus = region in ventricles that generates electrical impulse
- when ectopic ventricular focus firing at faster rate than SA node, it overtakes & surpassess the normal heart rate set by SA node →electrical impulses generated by ectopic focus is dominant source controlling heart rhythm
- when SA node initiates normal electrical impulse and it encounters other electrical impulses, there’s a conflict
- the faster firing ectopic focus can suppress the normal pacemaker activity of SA node →heart rhythm dominated by impulses originating from ectopic ventricular focus →arrhythmia where ventricles contract at different rate
what does ventricular tachycardia look like on ECG?
- in VT, QRS complex may have different appearance due to abnormal origin of electrical impulse
- SA node could still be firing →this means that intermittently there could be normal electrical impulses and sometimes they can escape down purkinje fibres and generate impulse that bypasses the abnormal ventricular rhythm
- when SA node escapes down purkinje fibres, the QRS complex on ECG is normal
*this is sign of ventricular tachycardia = intermittent normal QRS
what is atrioventricular node arrhythmia?
AV node arrhythmia can be complete or partial block of electrical impulses between atria & ventricles
(AV node = specialized group of cells in heart that is the only connection between atria & ventricles)
*AV arrhythmia allows some beats and not others = intermittent
what does ECG look like for AV arrythmia?
- In the arrhythmia we see prolongation of conduction - this means that normal passage of electrical signals from atria →ventricles takes longer
- PR interval may initially appear normal but if prolongation excessive then first degree AV block
what is PR interval on ECG?
represents time taken for electrical impulse to travel from atria through AV node into ventricles
what are the different degrees of AVN block?
- First degree AVN block = slow conduction (long PR interval)
- Second degree = intermittent, PR interval may be varying
- Complete or third degree= complete non-conduction
what happens when people have accessory pathway?
leads to 2 types of re-entrant tachycardias:
1. micro-circuit = involves short circuit within AV node
2. macr-circuit = abnormal circuit involving both accessory pathway & AV node, it’s located far away from AV node
what are causes of arrythmias?
- abnormal anatomy that allow re-entrant circuits (accessory pathways, congenital heart defects)
- autonomic nervous system (sympathetic stimulation like stress, exercise, hyperthyroidism and increased vagal tone increasing bradycardia)
- metabolic
what are metabolic causes of arrhythmia?
- hypoxia: chronic pulmonary disease, pulmonary embolus
- ischaemic myocardium; acute MI, angina
- electrolyte imbalances: K+, Ca2+, Mg2+
- inflammation: viral myocarditis
- drugs: direct electrophysiologic effects or via ANS
- genetic: mutations of genes encoding cardiac ion channels e.g. congenital long QT syndrome
what can lead to ectopic beats occurring?
- ectopic beats can occur due to altered automaticity (change in normal rhythm of the heart) e.g. ischaemia, increase in catecholamines
- ectopic beats can also occur from triggered activity, e.g. digoxin, long QT syndrome
what does re-entry mean?
re-entrant circuit = an abnormal electrical pathway within the heart that allows an electrical impulse to circulate continuously, leading to an arrhythmia
- re-entry requires more than 1 conduction pathway, each with different speed of conduction (depolarisation) and recovery of excitability (refractoriness)
what are examples of re-entry arrythmias?
- atrioventricular nodal re-entry tachycardia (AVNRT)
- atrioventricular re-entry tachycardia (AVRT) which is associated with an accessory pathway tachycardia e.g.Wolf Parkinson White syndrome
- myocardial scar from previous myocardial infarction
- congenital heart disease.
what are the 2 main categories for mechanisms responsible for cardiac arrythmias?
(1) enhanced or abnormal impulse formation (ie, focal activity)
(2) conduction disturbances (ie, reentry)
what happens when enhanced automaticity occurs in the SA node?
it can lead sinus tachycardia = an increase in heart rate
- This can be physiological, due to increased sympathetic tone during exercise, or pathophysiological, due to hypovolemia, ischemia, or electrolyte disturbances.
what is enhanced automaticity of pacemaker cells?
increased ability of pacemaker cells to generate spontaneous electrical impulses
what are the 3 main mechanisms that cause enhanced automaticity?
- an increased rate of phase 4 (resting phase) depolarization
- a negative shift in the threshold potential (meaning less stimulus required to reach threshold)
- a positive shift in the maximum diastolic potential (means membrane potential starts at a higher level making it easier to reach threshold and initiate APs)
what can increase phase 4 slope and what does that do?
phase 4 = resting membrane potential
- increasing phase 4 slope = Increasing the rate of spontaneous depolarization which increases the heart rate
increase slope by:
- Hyperthermia (elevated temp)
- Hypoxia (deficiency in O2 in tissues)
- Hypercapnia (increased CO2 level in blood)
- Myocardial stretch (stretching or enlargement of heart muscle)
- Sympathetic nervous system
what can decrease phase 4 slope and what does that do?
phase 4 = resting membrane potential.
decreasing phase 4 slope = decreasing rate of depolarisation which slows heart rate
decreases phase 4 slope:
- Hypothermia (decreased temp)
- Hyperkalaemia (elevated potassium levels in blood)
- parasympathetic nervous system
what are afterdepolarizations?
afterdepolarizations are premature depolarisations that occur in the terminal phase of the AP
2 types:
1. during phase 2 or 3 = early after depolarisation, EAD
2. after AP in phase 4 = delayed afterdepolarization, DAD
what is circus re-entry?
Re-entry can occur in the presence of an obstacle (tissue that disrupts normal propagation like scar, structural abnormality etc), obstacle creates pathway around itself allowing AP to travel in circular loop (circus re-entry) and result in a resulting in a self-perpetuating circuit
when does re-entry occur? (in terms of electrical signals)
Re-entry occurs when an action potential fails to extinguish itself (continues to circulate in heart tissue) and reactivates a region that has recovered from refractoriness (period when heart cell can’t respond to another stimulus) and this leads to a self sustaining where a circuit is established that allows the electrical signal to continuously circulate, creating a loop which can lead to arrhythmias
what are requirements for re-entry?
- More than one conduction pathway, these pathways must be connected and provide a circuit through which an impulse can circle.
- The pathways have different speed of conduction (depolarization) and recovery of excitability (refractoriness), such that an area can be blocked (unidirectional block).
- Central blocking by a core of tissue that is completely blocked and allows the impulse to loop around in the surrounding excitable tissue.
- Block can be caused by structural abnormalities: accessory pathways, scar from myocardial infarction, congenital heart disease, or functional i.e. conditions that depress conduction velocity or shorten refractory period promote functional block, e.g. ischaemia, drugs
what does arrhythmia propagation (how abnormal heartbeat spreads through heart) require?
*what is needed for abnormal heartbeat to spread through heart?
triggers & substrates
- Triggers e.g., EADs (early after depolarisation) and DADs (delayed after depolarisation) which can produce ectopic beats
- Substrate = electrophysiological abnormalities predisposing to re-entry, including increased heterogeneity of conduction or repolarization
*Triggers can produce abnormal heartbeats, and substrates set the stage for these abnormal beats to spread in the heart
