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Cardio 1 > Clinical Arrhythmias > Flashcards

Clinical Arrhythmias Flashcards

1
Q

Arrhythmias can arise from problems in the

A

SA node
Atrial cells - most COMMON
AN junction
Ventricular cells

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2
Q

Pathways

A

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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3
Q

Dec automaticity

A

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

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4
Q

increased automaticity

A

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

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5
Q

Fts of increased automaticty

A

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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6
Q

Reentrant circuit

A

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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7
Q

Fts. of reentrant circuits

A

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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8
Q

AVNRT vs AVRT

A

AVNRT - entire circuit housed in the AV node

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

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9
Q

A fib

A

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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10
Q

SA node poblems

A

Fire too slow - sinus brady

Fire too fast - sinus tachy

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11
Q

Sinus bradycardia

A

SA node depolarizing slower than normal, impulse is conducted normally

Rate <60 BPM

Regular

QRS is narrow

Clear P-waves

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12
Q

SInus tachy

A

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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13
Q

Sinus arrhythmia EKG

A

Presence of sinus P waves

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

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14
Q

Atrial cell problems

A

PACs
Atrial tachycardia
Multifocal tachycardia

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15
Q

PACs

A

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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16
Q

Multifocal atrial tachycarida

A

Discrete P waves with at 3 different morphologies

Atrial rate >100 BOM

PP, PR, and RR intervals all vary

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17
Q

A fib and a flutter problems

A

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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18
Q

A fib

A

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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19
Q

A flutter

A

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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20
Q

Afib risk factors

A

Obstructive sleep apnea is a big one

21
Q

AVNRT

A

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

22
Q

EKG finding in AVNRT vs sinus tachy

A

Pseudo R’ in V1 during tachycardia

23
Q

AVRT

A

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

24
Q

Preexcitation

A

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

25
Q

Orthodromic and antidromic AVRTs

A

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

26
Q

Short RP
Long RP
P buriend in QRS

A

AVRT, AT, slow-slow AVNRT

AT, atypical ANRNT, PJRT

Typicaly AVNRT, AT

27
Q

Vagal maneuvers/adensoine

A

Block the AV node

AVNRT, AVRT, Junctional, some atrial tachycardia

AV nodal independent rhythms will block QRS and can see underlying atrial rhythm better

28
Q

Vagal maneuver and adenosine risks and logistical issues

A

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

29
Q

Bigeminla rhythms

A

Each sinus beat followed by a premature contraction

COuplet rhythm

Benign

30
Q

Vent tachycardia

A

No P waves and wide WRS

Re-entrant pathway looping in a ventricle

Can sometimes generate neoguh CO to produce a pulse

31
Q

Vent fibrillation

A

Ventricular cells are excitable and depolarizing randomly

Rapid drop and cardiac output

Totally abnormal

32
Q

Narrow vs. wide

A

Narrow - AV node or higher

Wide - probably in the ventricles

33
Q

Wide complex tachycardia in pt that has structurally abnormal heart

A

IS VT UNTIL PROVEN OTHERWISE

34
Q

Sick sinus syndrome

A

Sx sinus bradycardia

Tachy-brady

Sinus pause or sinus arrest

35
Q

Tachy-brady

A

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

36
Q

1st degree AV block

A

Every P wae conducts but it is delayed

Common but pathologic

Level of block is AV node and benign

37
Q

Mobitz type 1

A

Progressive PR prolongation before a dropped beat

Common and can be physiologic…benign

38
Q

Mobitz type 2

A

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

39
Q

2:1 block

A

Every other beat is dropped so can’t tell

Exercise increases HR (type 2)

40
Q

3rd degree block

A

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

41
Q

Pacemaker malfunction

A

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)

42
Q

Risks of tachyarrhythmias

A

Bypass natural checkpoints for rate control

Prolonged can lead to cardiomyopathy

Some people sx

Disorganized atrial rhythms are at higher risk of thrombus formation

43
Q

Afib/flutter managmenet

A

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

44
Q

Catheters for Afib and flutter

A

Afib - success lower nad higher risk

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

45
Q

Cardioveriosn and stroke risk

A

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

46
Q

VT/VF

A

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

47
Q

Bradyarrhythmias to tx

A

High grade AV block or sick sinus

48
Q

How to tx brady

A

Stop offending agents

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

49
Q

LT management of brady

A

Pacemaker placement

Cardio 1 (30 decks)

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