Cardiac Arrhythmias-Mechanisms Flashcards
What are tachyarrhythmias? What are the mechanisms? How are they classified?
Heart rate>100bpm for 3 or more beats
mechanisms: enhanced automaticity, reentry and triggered activity
classified according to origin: supraventricular or ventricular
There are 6 tachyarrhythmias. What are they?
sinus tachycardia
atrial tachycardia
atrial flutter
atrial fibrilation
AV-Nodal Reentrant Tachycardia (AVNRT)
AV-Reentrant tachycardia (AVRT)
Define the 4 mechanisms of enhanced automaticity:
Enhanced Automaticity:
Abnormal Automaticity
Triggered Activity:
Reentry:
- Enhanced Automaticity: increased rate of impulse formation in tissue normally capable of pacemaker activity
- Abnormal Automaticity: impulse formation in tissue not normally capable of pacemaker activity
- Triggered Activity: single or repetitive cellular activity following a prior action potential EAD, DAD
- Reentry: two distinct paths, slowed conduction, unidirectional block
What is the origin of sinus tachycardia? what is the rate? what do the p and qrs look like? what does it result from? is it pathologic?
- origin SA node (supraventricular), rate>100bpm
- p and qrs are normal
- results from increased sympathetic or decreased vagal tone
- may be appropriate during exercise, fever, anemia, hypoxia, hypotyroidism or hypovolemia. May also be Inappropriate
What are atrial premature beats?where is their origin? what is the p wave like? Do we treat?
PAC-premature atrial contractions (beat that come in earlier than you would expect)
- automaticity or reentry in an atrial focus outside of the SA node
- may cause palpitations
- produce early p-wave with abnormal shape, dissimilar to sinus rhythm p wave
- depending on refractoriness may be conducted to ventricle or non conducted (blocked)
- if symptomatic beta bockers can treat but usually are benign
What is atrial tachycardia? What is the p wave like? Do we treat?
(a lot of PACs all together)
- Narrow tachcardia >100bpm
- the p-wave axis or morphology is different, and the QRS is usually the same as sinus rhythm (often inverted)
- BC these tachycardias do not involve the AV node, vagal maneuvers or AV nodal blockers are usually ineffective at terminating the tachycardia (adenosine)
What is multifocal Atrial tachycardia? What causes it?
Irregular, narrow tachycardia (>100bpm) wtih multiple (at least 3) different p-wave morphologies
this rhthm is likely caused by either abnormal automaticity in several foci within the atria or triggered activity and occurs most often in the setting of severe pulmonary disease
**precursor to atrial fibrilation, organized activity coming from multiple sites
What is atrial flutter? What causes it? WHat is the common form? What are the 2 types?
- rapid regular atrial activation
- caused by reentry over a large fixed circuit
- common form: circuit is atrial tissue along tricuspid valve annulus
- counterclockwise: circuit produces right atrial depolarization up the septum, across the roof and down the RA free wall, then along the floor of RA between tricuspid valve and inferior vena cava “Cacal tricuspid isthmus (CTI): producing saw tooth pattern (inverted p-waves)
- clockwise flutter: same circuit, opposite direction
What ratio is the conduction of AV conduciton usually during atrial flutter? What is important to rememebr about drugs that slow atrial flutter circuit? What are the symptoms? what are the predisposing factors?
- AV cnonduction is variable can be 1:1 but more commonly more flutter waves than QRS complexes (2:1)
- Drugs that slow atrial flutter circuit (flecainide) may promote 1:1 AV condution, paradoxically increasing ventricular rate
- may be asymptomatic or associated with palpitations, dyspnea, weakness, and stroke from atrial thrombus (loss atrial contractility d/t rapid A rates)
- predisposing factors: prior heart surgery, coronary disease, cardiomyopathy
Treatment for atrial flutter
- rate control: B blockers, Ca channel blockers, digoxin
-
rhythm control:
- duration> 48hrs necessitates transesopageal echo to rule out left atrial thrombus or 3 weeks anticoagulation prior to conversion. Anticoagulation continued post cardioeversion at least 4 weeks (delays recovery mechanical atrial function)
- electrical cardioeversion
- pace termination
- catheter ablation of tricuspid caval isthmus, curative 95, thus preferred
- antiarrhythmic drug therapy (class I, III agents) for sinus rhythm maintenance, occasional chemically convert, mostly effective
What is Atrial Fibrilation? describe the P waves
- Chaotic rapid rhythm with atrial rates> 400 discharges/min. No distinct P waves, Most of P waves find AV node refractory, only some of the depolarizations are conducted to ventricle, resulting in “irregularly irregula: rhythm
- Mechanism: triggered by rapid firing from atrial foci often localized to atrial muscle extending into pulmonary veins.sustained by multiple wandering reentrant circuits wthin the atria; promoted by enlarged atrium (Multiple wavelet hypothesis, Focal mechanism with fibrillatory conduction)
- Predisposing factors: ETOH, CHF, valvular disease, enlarged atria hypertenson, coronary disease, pulmonary disease, sleep apnea, hyperthyroidism, cardiothoracic surgery
Treatment for A fib
Rate control: ensure appropriate venticular rate control
Rhythm control: assess the need for, the proper timing of, and the appropriate method for the restoration of sinus rhythm
anticoagulation: assess the need for and the appropriate drugs for anticoagulation to prevent embolic stroke
What are the 2 distinct pathways that frequently exist within the AV node?
Fast pathway (conducts fast, slow to recover)
Slow pathway (conducts slo, fast to recover)
What are the requirements for SVT?
- Two pathways with closed circuit of connection
- Unidirectional block in one pathway
- Slow conduction over one pathway
What is SVT: AV Nodal Reentrant Tachycardia? (AVNRT) Which pathway is uaully antegrade and which is retrograde? Whod does it present it? What are the symptoms? Acute vs chronic treatment?
- most common form paroxysmal SVT
- reentry utilizing 2 AV nodal pathways, fast (rapid conducting and long refractory period) and slow (slow conduction and short refractory period)
- relies on slow conduction in one patway and transient block in the other
- conduction antegrade from A to V occurs via slow pathway and retrograde limb of circuit is over fast pathway
- presents in young adults
- symptoms: palpitations, dizziness, chest pain, dyspnea
- acute treatment at temrination: valsalva maneuvers, adenosine, beta blockers, calcium channel blockers
- chronic treatment: observation, AV nodal blockade, catheter ablation targeting “slow” pathway of AV node and infrequently Class I, III antiarrhythmic drugs
What is Wolff-Parkinson White (WPW)
- considered AVRT
- conduction over AP beats AVN, short PR
- slurred QRS (Delta wave) due to slow ventricular activation by pathway other than HPS and fusion activation of ventricle by 2 wavefronts, proceeding over AP and HPS
What are Atrioventricular reentrant Tachycardias (AVRT)
reentry utilizing bypass tract or accessory oathway
accessory pathway is an abnormal band of muscle cells crossing the AV groove to connect atrium and ventricle
prevalence: 1 in 1500 people
may conduct antegrade (atrium to ventricle), retrograde (ventricle to atrium) or bidirectionally
if tract conducts only retrograde can promote supraventricular tachycardia but is termed “concealed”
tract conducts antegrade produces finding on ECG termed Wolff-Parkinson-WHite or ventricular pre-excitation syndrome
WHat are the 2 kinds of AVRT and what are the differences amung them?
- orthodromic:
- A to V via AV node
- V to A via Kent (accessory)
- no delta wave in orthodromic tachycardia (narrow QRS) as antegrade depolarization of ventricles occurs exclusively over AV node
- Antedromic
- A to V via kent
- V to A via AV node
- Maximum delta wave in antidromic tachycardia (wide QRS) as antegrade depolarization of ventricles occurs exclusively over accessory pathay
What is pre-excited atrial fib?
A to V via both AV node and AP
variable preexcitation depending on rate
How do we treat WPW?
because digoxin. beta blockers and calcium channel blockers may actually shorten the refractory period of accessory pathways, effectiely speeding conduction, these drugs should not be used in WPW patients presenting with wide complex or pre-excited tachycardias
intravenous amiodarone or procainamide may be used. sow accessory pathway conduction
actue therapy may require cardioaversion if hemodynamically unstable
definitive therapy with catheter ablation of accessory pathway is preferred in symptomatic and high risk patients
what things cause a narrow QRS vs wide?
- narrow (<120ms)
- native conduction via the his-purkinje system
- wide (>120ms)
- ventricular origin
- abberancy
- bundle branch block
- RBBB
- LBBB
- Pre-excitation (WPW)
- bundle branch block
