Clinical Arrhythmias Flashcards by Garrett Oberst

Arrhythmias can arise from problems in the

SA node
Atrial cells - most COMMON
AN junction
Ventricular cells

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Pathways

Reentry circuits

Atlered impulse conduction —– reentry —-Tachyaarhythmis

Altered impulse to conduction block to brady

Altered impulse formation —- enahnced automaticity —–tachys

Altered impulse formation—-dec automaticity —- bradys

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Dec automaticity

Sinus bradycardia - seen mostly in younger people because they really don’t need it

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increased automaticity

Sinus tachycardia
Atrial tachycardia - biphasic P wave
Jxnl tachycardia - inverted P wave

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Fts of increased automaticty

Warm up and cool down phase

Temp measures will not abort rhythm but modify temporarily

Inc adrenergic tone will inc automaticity

Most go away on own

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Reentrant circuit

Think atrial flutter

Circuit keeps spinning and every now and then depolarize AV Node and conduct to ventircles

Impulse loops and reslts in self-perpetuating impulse formation

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Fts. of reentrant circuits

ABrupt onset and termination

P wave of the first beat of arrhythmia is diff from reminaing beats of arrythmia

Temp measures will sometimes abort

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AVNRT vs AVRT

AVNRT - entire circuit housed in the AV node

AVRT - one limb in AV node and one limb in accessory

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A fib

Multiple micro reentrt wavelets

Wandering small areas of activation which generate chaotic impulses

Collideing wavelets can generate new foci of activation

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SA node poblems

Fire too slow - sinus brady

Fire too fast - sinus tachy

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Sinus bradycardia

SA node depolarizing slower than normal, impulse is conducted normally

Rate <60 BPM

Regular

QRS is narrow

Clear P-waves

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SInus tachy

Over 100 BMP

SA node is depolarizing faster than normla…conducted normally

Response to physical or psychological stress, not primary arrhythmia

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Sinus arrhythmia EKG

Presence of sinus P waves

Variation of PP interval which cannot be attributed to either SA nodal block or PACs

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Atrial cell problems

PACs
Atrial tachycardia
Multifocal tachycardia

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PACs

Originate in atria so contour of P wave, pR interval and timing are different than a normally generated pulse from SA node

QRS norml

Excitation of atrial cell forms an impulse that is then conducted normally through AV node and ventricles

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Multifocal atrial tachycarida

Discrete P waves with at 3 different morphologies

Atrial rate >100 BOM

PP, PR, and RR intervals all vary

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A fib and a flutter problems

Fire continuously from multiple foci or fire continuously due to multiple micro re-entrant wavelets - A fib

Fire continously due to looping re-entrant circuit - atrial flutter

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A fib

No organized atrial depolarization so no normal P waves

Atrial activity is chaotic

Due to multiple re-entrant wavelets ocnducted bt R and L atria

Totally unpredictable

AV node allows some impuluses to pass through at variable intervals

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A flutter

No P waves…instead flutter waves in a sawtooch battern

Only some impulses conduct thruog the AV node

Irreglular

Reentrat pathway in RA usually with every 2nd or 4th inpulse gneerating a QRS

In presence of 2:1 AV block, flutter waves may not be apparent but may be brought out be admin of adenosine

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Afib risk factors

Obstructive sleep apnea is a big one

AVNRT

Reentrant rhythm can be generated where the AV Node serves as both arms of reentrant circuit

Typical - antegrade down the slow pathway then retrograde through the fast

Atypical - antegrade flow down the fast pathway then retrograde through the slow

EKG finding in AVNRT vs sinus tachy

Pseudo R’ in V1 during tachycardia

AVRT

Reentrant rhythm can be generated whrre hte AV node serves as one arm of the reentrant circuit and the accessory pathway as the other

Can occur in pts with WPW

Preexcitation

Condition characterized by accessory pathway

WPW is most common in which direct AV connection allows the ventricles to begin depolarizaiton while standard AP is still travleing through the AV node

ECG - short PR, QRS prolongation…delta wave

Orthodromic and antidromic AVRTs

Ortho- narrow complex tachy in which wave travels down AV node and retrograde up accessory Anti - wide complex tachy in which wave of depolarization travrls down accessory and retrograde up the AV node

Short RP Long RP P buriend in QRS

AVRT, AT, slow-slow AVNRT AT, atypical ANRNT, PJRT Typicaly AVNRT, AT

Vagal maneuvers/adensoine

Block the AV node AVNRT, AVRT, Junctional, some atrial tachycardia AV nodal independent rhythms will block QRS and can see underlying atrial rhythm better

Vagal maneuver and adenosine risks and logistical issues

Basically cause CHB If they have accessory, can kick to accessory path exclusively Always have zoll pads on Very short T1/2 Need proximal IV with large saline flush immediately

Bigeminla rhythms

Each sinus beat followed by a premature contraction COuplet rhythm Benign

Vent tachycardia

No P waves and wide WRS Re-entrant pathway looping in a ventricle Can sometimes generate neoguh CO to produce a pulse

Vent fibrillation

Ventricular cells are excitable and depolarizing randomly Rapid drop and cardiac output Totally abnormal

Narrow vs. wide

Narrow - AV node or higher Wide - probably in the ventricles

Wide complex tachycardia in pt that has structurally abnormal heart

IS VT UNTIL PROVEN OTHERWISE

Sick sinus syndrome

Sx sinus bradycardia Tachy-brady Sinus pause or sinus arrest

Tachy-brady

Abrupt termination of atrial flutter with variable AV block followed by sinus arrest with jxn escape beat

1st degree AV block

Every P wae conducts but it is delayed Common but pathologic Level of block is AV node and benign

Mobitz type 1

Progressive PR prolongation before a dropped beat Common and can be physiologic...benign

Mobitz type 2

Fixed PR interval with dropped beats PR does not have ot be prolonged Uncommon and always pathologic Level of block is BELOW the AV node before the bundle branches High rate of progression to complete heart block

2:1 block

Every other beat is dropped so can't tell Exercise increases HR (type 2)

3rd degree block

No association between Ps and QRS complexes Need to define what ventricular rhythm is Level below the AV node Unstable QRS complex regular with random P waves Need urgent attention

Pacemaker malfunction

Failure to capture - see spikes when you should, just no P wae or QRS complex Failure to sense - see pacemaker spikes when you should NOT (regardless of QRS complex)

Risks of tachyarrhythmias

Bypass natural checkpoints for rate control Prolonged can lead to cardiomyopathy Some people sx Disorganized atrial rhythms are at higher risk of thrombus formation

Afib/flutter managmenet

Not stable - DCCV +/- AC If tachy, try to slow down No sx - rate control and assess stroke risk Sx - potentially rhythm control and assess stroke risk

Catheters for Afib and flutter

Afib - success lower nad higher risk FLutter - success rate higher, risk lower, sometimes 1st line intervention

Cardioveriosn and stroke risk

Regardless of cardioversion, stroke risk hgih for first 4 weeks...need AC If in rhythm for less than 48 hours or have been on therapuetic systemic AC for 1 mo prior, then just cardiovert

VT/VF

Hx of structural HD is biggest predicotr of WCT Correct reversible etiologies USually are defibrillating sustained VT/VF Beta blockers are effective anti-arrhythmics Assess for structural HD with echo or CMR

Bradyarrhythmias to tx

High grade AV block or sick sinus

How to tx brady

Stop offending agents Minimize vagal stimulaiton - atropine, dopamine/doubtamine/epi, transcutaneous/transvenous pacing

LT management of brady

Pacemaker placement