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Flashcards in approach to dysrhythmias Deck (45):
1

Step 1 or the basics 

Basics:

 

ABCs & IV, Oxygen, Cardiac Monitor

2

step 2 in the 6 step approach 

Patient Assessment

 

Stable or Unstable?

  • Interpretation based on a spectrum
  • ALOC, ↓BP, CP, pulmonary edema

3

step 3 

--> Regular or Irregular EKG 

  • Irregular
  • Issue that happens above the ventricles (atrium/AV node issue)
  • NOT VTach (usually regular)
  • Block AV Node

4

Step 4

fast or slow 

5

step 5

indentify complexes

 

Are P wave present?

 Indicates sinus rhythm/normal axis -->  DO NOT DEFIBRILLATE!

6

step 6

Complex Distance --> Narrow or Wide?

7

what is the ddx of Narrow, Regular, No P waves

PSVT

Atrial flutter

WPW

Narrow complex VT

8

two types of WPW

orthodromic=narrow

orthodromic=wide

 

9

AV node can not go faster than 

 

if it does you have to assume there is ___

200-220 

 

if it goes higher than that it is because there is an accessory pathway 

10

A flutter is what type of issue

macrocircuit 

 

  • global re-entry; different foci; circular

11

WPW is due to 

  • d/t accessory pathway – P wave buried QRS; Delta wave
    • Drives the rate really high

12

what are some vagal maneuvers

  • Vagal maneuvers --> have them blow on a syringe while they are sitting up and then drop their head back

13

medication for – Narrow, Regular, No P waves

  •  AV Nodal blockers: Adenosine (PSVT), CCB, -Blocker
    • Block AV node b/c it is receiving too much stimulation
  •  Cardioversion – synchronized
    • Delivers right after the R complex
    • Used for Vtach or Vfib

14

if someone is unstable with narrow regular no P waves can you consider adenosine 

  • UNSTABLE
  •  Can consider Adenosine but…
  •  Cardioversion start at 50J and 2x every time

adenosine feels like DYING

15

if you give adenosine to somone with A flutter 

works on the AV node for a short period of time. need to use a longer agent 

16

Narrow, Irregular, No P waves DDX

A-fib

A-flutter w/ variable block

17

what is the cause of AFIB 

: increased automaticity within the atria

18

Tx of A fib -chronic (stable)

nodel blocker agent 

  • CBB -->Diltiazem 5-10mg IVP slow. If tolerated can 2x it. Up to 60mg in 30 min
  • Beta Blockers
  • Digoxin ....Old Drug

19

Tx of chornic unstable A fib

  • Rapid Cardioversion: Start high! Sync! b/c chronic A-fib pts are electrically stable??
  • Support Blood Pressure: Pressers b/c if you do not perfuse brain/heart -->ALOC + harder to shock
    • ​this is just a measure so thta you can cardiovert 
  • Slow down heart: drips not IV Push – do not give elderly of CCB/BB
    • Infuse it--> can bottom out BP and lead to cardiac arrest 
    • will have to push higher dose of dilt in a bigger pt
  • Magnesium if drip does not work (caution: vasodilator)
  • Repeat Cardioversion
  • Other considerations: Is it really A-Fib? TREAT UNDERLYING CAUSE 
    • ​sepsis?
    • necrotizing fascitis? 
    • is there something causing low blood pressure 

20

what is dilt and what does it do 

By blocking calcium, diltiazem relaxes and widens blood vessels and can normalize heart rates. Diltiazem injection is used to treat irregular heartbeats

21

New Onset = Rhythm Conversion Tx

  • Clear Hx with in 48 hours
  • No structural heart dz
  • Age not a C/I
    • Caution Elderly - don’t ruse often p/w vague sxs
  • Chemical cardioversion: Procainamide: 1g over 1 hour --> Electrical cardioversion: Biphasic 200J --> D/C home without meds
    • If procainamide doesn’t work, then do electrical cardioversion
  • this all really depends on how connected they are to care (may need to schedule a follow up

22

magnesium is a vasodilator or vasoconstrictor 

vasodilator 

23

Wide, Regular, No P waves (If wide, signal coming from ventricles)-ddx

Vtach*******

SVT with abberancy (bb block)

antidromic WPW

24

cause of Vtach, SVT with BBblock, and Antidromic WPW

circuit re-entry in the ventricles

25

how do you know WPW

shortened PR interval with delta wave

26

if your Vtach is unstable 

cardioversion 

 

27

why would you consider adenosine in a wide regular without p 

SVT with abberancy 

28

why do you want to exercise caution when administering adenosine to a wide irregular no p

  • Careful when giving adenosine to WPW (conduction can reverse)

29

why do you admit after seeing a pt with VTACH 

ADMIT 

30

Wide, Irregular, No P waves

  • A-fib w/ BBB
  • A-fib w/ WPW
  • A-flutter w/ variable block & BBB
  • Polymophic VT = Torsades

31

A-fibb tx

  • A-Fib = Rate control: Be careful If…
  • WPW
    • Regular: Consider Adenosine (can send into overdrive), Electricity 
    • Irregular: No AV nodal blocker--> Yes Electricity (synchronized), Procainamide (anti-arrhythmic)
    • Torsades = Magnesium

32

how does tx for stable SVT work

vagal maneuvers

6 rapid push (doesn't last long)

12

(can do 18)

synchronized cardioversion 

33

unstable rapid irregular narrow tx

rapid high synch cardioversion

can sedate with etomidate +ketamine (less risk of dropping BP but still some)

Elevating BP to decrease irritation on heart increase profusion and improve chances of cardioverting 

 

target diastolic >60mg) 

push dose pressors with phnylephrine 50-299mcgIVP

 

 

34

chronic A-fib 

35

6 step approach

  1. ABC’s, IV, O2, Monitor
  2. Stable or Unstable
  3. Regular or Irregular
  4. Fast or Slow

36

appraoch to the brady pt (big 3)

DRUGS

ISCHEMIA

ELECTROLYTES

37

WHAT DO WE NEED TO THINK ABOUT HWEN LOOKING AT BRADY  (other than big 3)

  • Block is below AV node
  • Slower rhythm
  • More likely to stop/asystole
  • Not atropine sensitive

38

Brady treatment 

  • Algorithm Bradys Are Too Darn Easy 
  • Atropine: start 0.25-0.5mg bolus
  • Transcutaneous Pacing: Sedation (might need transvenous pacer in obese pt)
  • Dopamine: 2-10 mcg/kg per min
  • Epinephrine: 2-10 mcg per min
    • 1ml of crash cart epi (1:10,000) = 100mcg
    • Put 1ml in 100ml of NS = 1mcg per ml 

Pacemaker for all 3rd degree AVB + symptomatic Mobitz Type II

39

which AV blocks are unstable 

mobitz type two can move into third degree

and of course third degree

40

electrolyte abnormalities that could lead to pronloged qt

 

Electrolyte abnormalities 

 

hypokalemia

hypocalcemia 

hypomagnesmia 

Na channel blockers 

miscellaneous: elevated ICP, ACS

hypothermia, hereditary 

41

what are the considerations with determining prolonged QT

if QT lengthening due to stretching of ST segment = hypocalcemia and hypothermia 

 

if QT lengthen due to stretching of T wave=ischemia 

42

2 EKG findings for burgadas

cove type (Seal)

saddle type 

43

treatment is brugada

defibb 

(ICD)

44

leads to focus on when suspecting cardiomyopathy 

lateral 

 

look at Q waves if super sharb and super deep (dagger like) thing hypertrophic cardiomyopathy 

45

41 y/o female no sig past medical hx c/o CP over the past 2 days, no sx now

  • : Wellen’s  → Highly specific to LAD → V2-V3, +/- V4
  • type 1 = deep symmetric T-wave in precordial leads
  • type 2= biphasic T waves in precordial leads
  • needs PCI with proximal LAD lesion 
  •