clinical aspects arrhythmias

Question 1

Tachyarrhythmias

Answer 1

heart rate>100 bpm for 3 or more beats

MEchanisms- enhanced automaticitym reentry and triggered activity

Origine above the ventricle (supraventricular), origin within ventricular (ventricular)

Question 2

Tachycardia mechanisms

Answer 2

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 (EADs, delayed DADs)

Reentry- 2 distinct paths slowed conduction, unidirectional clock

Question 3

Sinus tachycardia

Answer 3

origin in SA node, rate- >100 bpms
P and qrs normal in appearance, increased sympathetic tone or decreased vagal tone

CAn be appropriate or inappropriate

Question 4

Atrial premature beats

Answer 4

automaticity or reentry in atrial focus outside SA node, may cause palpitation, produce early p wave with abnormal shape, dissimilar to sinus rythm P wave, Depending on AV node refractoriness, can be conducted to ventricular or non conducted blocked
if symptomatic beta blockers to treat

Question 5

Atrial tachycardia

Answer 5

narrow tachycardia >100 BPM
The p wave axis or morphology is different, and the QRS is usually the same as sinus rythm

because these tachycardias dont involve the AV node, vagal maneuvers or AV nodal blockers are usually ineffective at terminating the tachycardia(adenosine)

Multifocal atrial tachycardia: irregular narrow tachycardia (>100 BPM) with multiple (3 different P wave morphologies)

This rhythm 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 and hypoxemia

Question 6

Atrial flutter

Answer 6

rapid regular atrial activation produced by reentry over a large fixed circuit

Common form- circuit is atrial tissue along tricuspid valve annulus, couterclockwise typical flutter, circuit produces right atrial depolarization up the septim, accross the roof and down the RA free wall then along the floor of RA between tricuspid valve, and inferior vena cava…sawtooth pattern

Av conduction is variable can be 1:1 but more commonly more flutter waves than QRS complexes, drugs that slow atrial flutter circuit may promote 1:1 AV conduction paradoxically increasing ventricular rate

May be asymptomatic or assocaited with palpitations, dyspnea weakness and stroke from atrial thrombus- prior hrt surgery coronary disease, cardiomyopathy

Question 7

atrial flutter treatment

Answer 7

rate control-beta blockers CA channel blockers, digoxin

rhythm control: > 48 hours transesophageal echo to rule out left atrial thrombus or 3 weeks anticoags
Electrical cardioversion, pace termination, catheter ablation, antiarrhythmics

Question 8

Atrial fibrillation

Answer 8

chaotic rapid rhythm >400 discharges/min. No distinct P waves, most P waves find aV node refractory, only some depolarizations are conducted to ventricles–irregularly irregular rhythm

Mechanism: triggered by rapid firing from atrial foci often localized to atrial muscle extending into pulmonary veins

AF is sustained by multiple wandering reentry circuits within the atria, minimum number of cicuits required number of circuits required for AF thus AF promoted by enlarged atrium

Predisposing factors: ETOH, CHF, valvular disease, enlarged atria, HTN, coronary disease, pulm disease sleep apnea, Hyperthyroidism, CT surgery

Question 9

3 part approach to treatment of atrial fibrillation

Answer 9

Rate control: ensure appropriate ventricular rate control

Rhythm control: asses the need for the proper timing of and the appropriate method for the restoration of sinus rhythm

Anticoagulation: assess the need for and appropriate drug for anticoagulation to prevent embolic stroke

Question 10

Dual AV Node pathways

Answer 10

frequently 2 distinct paths exist within the AV node
Fast pathway: conducts fast, slow to recover
Slow pathway conducts slow, fast to recover

Question 11

SVT Mechanism

Answer 11

2 pathways with closed circuit of connection
Unidirectional block in one pathway
slow conduction over one pathway

Question 12

AV nodal Reentrant tachycardia

Answer 12

Most common form paroxysmal Svt

Reentry utilizing 2 AV nodal paths (fast, rapid conduction and long refractory period) and (slow conduction and short refractory period)

Relies on transient unidirectional block in one pathway and relatively slow conduction in the other

Relies on transient unidirectional block in one pathway and retrograde limb of reentry circuit is over fast pathway

presents in young adults, palps, dizziness, chest pain, dyspnia
Treatment: adenosine, beta block, CCBs
Chronic treatment: observation, AV nodal blockade catheter ablation targeting path of AV node and infrequently class 1 and 3 anitarrhythmics

Question 13

WPW

Answer 13

delta wave: conduction over AP beats AVN, short PR
Slurred QRS due to slow ventricular activation by pathway other than HPS and fusion activation of ventricle by 2 wavefronts, proceeding over AP and hPS

Question 14

Atrioventricular Reentrant Tachycardias

Answer 14

AVRT- bypass tract or accessory path,