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SRNAAnatomy II > Arrhythmias > Flashcards

Arrhythmias Flashcards

1
Q
  • **• Bradycardias

* **• Tachycardias

A

(Bradyarrhythmias)

Tachyarrhythmias

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2
Q

Supraventricular

A

when involving atrium or AV

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3
Q

Ventricular

A

Originate HIS-PURKINJE

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4
Q

**Mechanisms of arrythmias

A
  • Altered impulse formation
  • Altered impulse conduction
  • BOTH
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5
Q

*** Fastest cells preempt all others

A

= “Overdrive Suppression

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6
Q

*****Normally____ node dominates _____
AV and Bundle of HIs ________
Purkinje

A

SA ; 60-100
50-60
30-40

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7
Q

***3 causes of altered impulse formation

A

3 Causes:
• Altered SA rate
• Abnormal automaticity in myocytes
• Triggered activity

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8
Q

**Triggered Activity

A

Abnormal oscillations in membrane voltage

can develop during or after repolarization “afterdepolarizations”

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9
Q

*****TRIGGERED ACTIVITY• Once triggered, they can become

A

selfsustaining tachycardias.

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10
Q

**Triggered activity EARLY (LPDT)

Occur when?

A 
can occur in LONG depolarization
• ex. Conditions that cause PROLONGED QT
• (slowing can cause reversal of ion mvmt.)
• Depolarization initiates tachycardia
TORSADES DE POINTES
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11
Q

**Triggered activity DELAYED (DAD)

A

occur after REPOLARIZATION
**Due to ↑ Ca++ in cell SECONDARY to digitalis intoxication or ↑ catecholamines
• Activates Cl- out channels or Na -Ca exchanger (Na+ in Ca++ out)
• Depolarizes membrane, triggers *V-Tach.

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12
Q

*****Altered Impulse Conduction

A

• Normal conduction pathway does not have blocks

or reentry pathways

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13
Q

***Blocks =

A

bradycardias

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14
Q

***** Reentry pathways =

A

tachycardias

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15
Q

***3 types of Tachycardias

A

Supraventricular
Ventricular
Ventricular Pre-excitation Syndrome

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16
Q

*****Supraventricular tachycardias are

A 
Sinus Tachycardia
– PACs
– SVT
– Multifocal Atrial Tachycardia
A-flutter
– A-fib
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17
Q

*****Ventricular Tachycardias are

A

– PVCs
– V-tach
– V-fib

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18
Q

*****Ventricular Pre-excitation Syndrome

A

– WPW

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19
Q

PACs

  • Arise from_______
  • Felt as _____
A

Arise from ectopic foci in atria

• Felt as “fluttering” or a “heavy” heartbeat

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20
Q

SA node rate

A

60-`100

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21
Q

AV node rate

A

50-60

22
Q

Purkinje fibers

A

30-40

23
Q

Anesthesia consideration for tachycardia

A

Avoidance of vagolytic drugs intraoperatively

ex. Pancuronium

24
Q

PACs anesthesia consideration

A

Avoid excessive sympathetic stimulation
• Treatment only required if they trigger secondary
dysrhythmias

25
Q

SVT rate
Initiated where?
In EKG, p waves are

A

140-250 bpm
at or above AV node
-buried in QRS

26
Q

What is the goal of therapy for a patient with Atrial flutter? what are we avoiding?

A

Ventricular rate control is initial goal of therapy to avoid 1:1
AV conduction

27
Q

• If 1:1 conduction occurs with ventricular rate ≥ 300, is _______most likely mechanism - - consider

A

reentry; procainamide (Class IA)

28
Q

Most important clinical consequence of AF is

A

thromboembolic event causing stroke

29
Q

When 3 or more consecutive PVCs occur

A

Vtach

30
Q

Torsades de Pointes -

A

“twisting of the points”

• A.k.a. Polymorphic VT

31
Q

Tx of torsade

A

Magnesium

32
Q

Vfib

A

Cessation of C.O. & Death without prompt

treatment

33
Q

Survival is highest if defibrillation occurs in

A

3 to 5 minutes of cardiac arrest

34
Q

_____ _______ is only effective treatment

A

Electrical defibrillation

35
Q

After 3 attempts with epi or vaso, administration of.

A

amiodarone, lidocaine (or Mg for TdP) is indicated

36
Q

WPW (On left side of heart =

A

Type A, on right = Type B)

37
Q

For Orthodromic (narrow QRS) : –

A

begin with vagal maneuvers, if unsuccessful, consider

adenosine, verapamil, beta-blockers or amiodarone.

38
Q

For Antidromic (wide QRS): –

A

Treatment is intended to block the accessory pathway – The above drugs may worsen condition – Use procainamide 10 mg/kg IV infused up to 50mg/min. – (procainamide slows accessory pathway)

39
Q

Bradycardia

A 
Sinus Bradycardia 
Escape Rhythms
First degree AV Block
2nd degree AV Block
Thrid Degree AV Block

Atropine 0.5 mg IV q 3-5 min. (to a max of 3 mg) – Note: doses < 0.5 mg can cause further slowing of HR

40
Q

Bradycardia Can occur with or without sedation.

• Can occur any time during neuraxial blockade, but

A

1 hour after anesthetic is

initiated.

41
Q

• Warning Signs prior to arrest for Bradycardia:

A

SOB, nausea, restlessness, light-headedness, tingling fingers, deterioration in mental status

42
Q

First Degree AV Block

•

A

Prolonged PR interval (> 5 small boxes)

43
Q

1st degree AVB tx

A

Check Digoxin levels prior to surgery

• Maintain serum K+ levels in pts. on Digoxin

44
Q

Second Degree AV Block
• Mobitz Type I
– Wenckebach
•

A

Caused by intermittent failure of AV conduction

• Progressive prolongation of PR until a QRS is dropped

45
Q

Mobitz Type II – Sudden

A

QRS drop, more dangerous

46
Q

Type I Vs Type more dangerous type is

A

Type II

47
Q

Does atropine work in type II AVB

A

no

48
Q

Tx of type I is only for symptomatic patient, but treatment of Type II AVB

A 
Cardiac Pacing (transcutaneous or transvenous)
• Atropine does not work
• Pacemaker warranted, even if pt. is asymptomatic
49
Q

This block most common with Acute MI

A

3rd degree AVB

50
Q

3rd AVB there is dissociation of the __________.

A

atria and ventricles

51
Q

Medication that can be used as a chemical pacemaker until pacemaker becomes functional?

A

Isoproterenol

SRNAAnatomy II (16 decks)

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