Bradycardia and Tachycardia Flashcards
tachycardia
- > 100 bpm
- SVT
- VT
SVT
•supra ventiricular tachycardia - critically rely on cardiac structures that are not within the ventricle. While the ventricle may be a critical part of the circuit, there are also other non-ventricular regions (such as the atria or AV node) that must be engaged for SVT to occur
VT
- ventricular tachycardia - relies solely on activity within the ventricle alone
- QRS is very WIDE
- Mostly a reentrant tachycardia that originates within the ventricle
- Monomorphic is most common – each QRS looks the same
- Polymorphic is less common – each QRS looks different
- Most forms are potentially life threatening, occurring in patient with a history of coronary artery disease and heart failure
– Often the tachycardia needs to be terminated emergently
• Some forms occur in normal individuals due to automaticity or triggered activity: this is benign
electrophysiology mechanisms
- automaticity
- triggered activity
- reentry
EP mechanisms - automaticity
- Spontaneous depolarization during phase 4 of the AP, as a result of net inward positive current (calcium)
- Leading to the initiation of a new action potential
- Autonomic nervous system may modulate those currents, changing the rate of impulse formation
- Sinus Node
- AV junction and other subsidiary pacemakers in the ventricle
- Other sites:
– Crista terminalis
– Pulmonary Veins
– AV valves
– Coronary sinus
– Ventricle: right ventricular outflow tract most common
EP mechanisms - triggered activity
• This refers to the “triggering” of an action potential during either
– Phase 3: Early Afterdepolarization (EAD)
OR
– Phase 4: Delayed Afterdepolarization (DAD)
• EADs and DADs are generated by different ionic mechanisms
EP mechanisms - triggered activity - EADs
- Early Afterdepolarizations refer to an AP that is triggered during phase 3 of the previous AP due to altered transit of potassium
- On the electrocardiogram the QT interval is also prolonged
- Causes: drugs, genetic defects
EADs are potentially dangerous as they can trigger Torsades De Pointes
- This is a form of what is called “polymorphic ventricular tachycardia” in the setting of a prolonged QT interval
- Polymorphic means that the QRS is different from one beat to the next
- And can quickly degenerate to ventricular fibrillation (cardiac arrest)
EP mechanisms - triggered activity - DADs
Delayed After depolarizations are triggered AP’s (action potential) that occur during phase 4 of the previous AP, due to an excess of Calcium in the cell.
• Digoxin toxicity is the best known example: poisons Na/K/ATPase, leading to a rise of intracellular Calcium.
– Atrial tachycardia (usually with AV block) and ventricular tachycardia can occur
• Catecholamine excess also raises intracellular calcium, by release from the SR (sarcoplasmic reticulum)
–Some types of monomorphic ventricular tachycardia and premature ventricular complexes (PVCs) arise by this mechanism (DADs)
EP mechanisms - reentry
- A loop or circuit of excitable tissue that critically participates in the tachycardia
- Fundamental Elements:
– Potential for unidirectional block
– Core of inexcitable tissue around which the wavefront propagates
– Presence of an excitable gap of tissue ahead of the wavefront that is ready to be depolarized again
- Unidirectional block (functional or absolute)
– so you rather go down one way than another
- Something you can go around (like a valve)
•3.Excitable gap – tissue ahead of you that’s ready to accept the wavefront
ex: atrial flutter, VT due to prior MI, SVT due to: –AV nodal reentrant tachycardia –AV reentrant tachycardia
SVT subtypes
- Atrial Tachycardia
- AV nodal Reentrant Tachycardia
- AV reentrant Tachycardia (also called atrioventricular reciprocating tachycardia)
- While supraventricular in origin atrial flutter (and atrial fibrillation) are not regarded clinically as forms of SVT
SVT - atrial tachycardia
- Usually due to automaticity, sometimes due to reentry near the sinus node or upper crista terminalis, rarely due to triggered activity (i.e. digoxin toxicity)
- P wave before every QRS
- Treatment: beta blockers, calcium channel blockers, catheter ablation (invasive procedure that cauterizes the tachycardia focus)
AV Nodal reentry tachycardia (AVNRT)
Circuit entirely within the AV Node which contains two pathways:
- Slow pathway
- Fast pathway
Treatment: beta blocker, Ca channel blocker, catheter ablation of the slow pathway
AV reentry tachycardia (AVRT)
Reentrant tachycardia involving 4 critical components:
– Atrium
– AV node
– Ventricle
– bypass tract
– a separate electrical connection across the mitral or tricuspid valve
bypass tract
- Bypass tracts are extra conducting tissue that connect the atrium and ventricle, separate from the AV node and His bundle
- Most only conduct retrograde (from ventricle to atrium)
- If they conduct antegrade (forward direction) as well there will be a “delta wave” on the ECG, this represents “preexcitation” of the ventricle and this is commonly referred to as a WolffParkinson-White (WPW) ECG
Example of Monomorphic Ventricular Tachycardia: QRS is wide
pacemakers
• Pacemakers – devices that pace to treat bradycardias
ICD (implantable cardioverter defibrillator)
• Defibrillators (ICD)– devices that can BOTH pace and deliver therapy to treat tachycardia by giving a shock
Biventricular ICD
- Three wires: Atrium, RV defib and LV (via coronary sinus – projects posteriorly)
- For patients with heart failure (LVEF <35%) and with LBBB
- corrects dissynchrony
bradycardia - 1st degree AV block
• First degree AV block
– Refers to a PR interval > 200ms
– Remember PR interval reflects the time to get through both the AV node and the His Bundle, and for which is predominantly due to the AV node
– Can be due to medications
bradycardia - 2nd degree AV block
• Second degree AV block
– Refers to the fact that not all P waves lead to QRS’s
- Mobitz I - Wenkebach
- Mobitz II
bradycardia - Mobitz I
• Mobitz I: Wenckebach:
– Site of block is the AV node
– Can be due to medications
– Gradual PR interval lengthening until a dropped beat
– Commonly but not always this block is in the AV node and therefore responsive to autonomic tone and medications (beta blockers, calcium channel blockers and digoxin being the most common offenders)
- PR interval gradually lengthens, while R-R shortens
- Until a P wave blocks and does not conduct to the ventricle (no QRS after the P wave)
bradycardia - Mobitz II
• Mobitz II
– PR interval constant until a P wave is not conducted
– Usually the PR interval is normal or only slightly prolonged
– Essentially always the site of block is in the His-Purkinje system (His bundle or below)
– Often, but not always, there are signs of other conduction disease such as bundle branch block
– Not responsive to autonomic tone or medications
- PR interval constant
- Usually signs of other conduction disease, bundle branch block
- Treatment: PACEMAKER
bradycardia - 2:1 AV block
- This is a form of 2nd degree AV block
- Where every other P wave is conducted to give a QRS • So you can’t tell Mobitz I from Mobitz II!
- (Is this normal sinus rhythm? Yes.)
bradycardia - 3rd degree AV block
• Generally synonymous with Complete Heart Block (CHB)
– AV dissociation (atrial activity is unrelated to ventricular activity)
PLUS
– No P waves no matter where they occur in the cardiac cycle are able to conduct to the ventricle
– Usually this implies an atrial rate faster than the ventricular rate
– Refers to the fact that no P waves lead to QRS’s (along with a few other concepts)
– The ventricular rate arises from an escape mechanism that is below the level of block
- Often wide, as it is from the ventricle itself
- Escape rhythm is usually very slow
– Level of block is usually at or below the His, therefore not responsive to medications
– Treatment: PACEMAKER
bradycardia - LBBB
- QRS > 120ms and negative in V1
- Broad monophasic R wave in I, V5 and V6, usually notched or slurred
- Absence of Q waves in leads I, V5 and V6
- ST segment and T wave is usually directed opposite to the major deflection of the QRS
- With left bundle branch block, activation goes down the right bundle, then proceeds slowly across the left ventricle
- Result is that activation of the left ventricle is delayed
- Lateral wall will contract after the septum
– this is referred to as “dyssynchrony”
• Consequence for patients with heart failure
bradycardia - RBBB
- QRS > 120ms; positive in V1
- Wide S wave in leads I, V5 and V6 (slurred look)
