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Emergency Medicine > approach to dysrhythmias > Flashcards

approach to dysrhythmias Flashcards

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1
Q

Step 1 or the basics

A

Basics:

ABCs & IV, Oxygen, Cardiac Monitor

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2
Q

step 2 in the 6 step approach

A

Patient Assessment

Stable or Unstable?

  • Interpretation based on a spectrum
  • ALOC, ↓BP, CP, pulmonary edema
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3
Q

step 3

A

–> Regular or Irregular EKG

  • Irregular
  • Issue that happens above the ventricles (atrium/AV node issue)
  • NOT VTach (usually regular)
  • Block AV Node
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4
Q

Step 4

A

fast or slow

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5
Q

step 5

A

indentify complexes

Are P wave present?

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

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6
Q

step 6

A

Complex Distance –> Narrow or Wide?

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7
Q

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

A

PSVT

Atrial flutter

WPW

Narrow complex VT

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8
Q

two types of WPW

A

orthodromic=narrow

orthodromic=wide

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9
Q

AV node can not go faster than

if it does you have to assume there is ___

A

200-220

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

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10
Q

A flutter is what type of issue

A

macrocircuit

  • global re-entry; different foci; circular
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11
Q

WPW is due to

A
  • d/t accessory pathway – P wave buried QRS; Delta wave
    • Drives the rate really high
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12
Q

what are some vagal maneuvers

A
  • Vagal maneuvers –> have them blow on a syringe while they are sitting up and then drop their head back
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13
Q

medication for – Narrow, Regular, No P waves

A
  • AV Nodal blockers: Adenosine (PSVT), CCB,* *ẞ-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
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14
Q

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

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

adenosine feels like DYING

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15
Q

if you give adenosine to somone with A flutter

A

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

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16
Q

Narrow, Irregular, No P waves DDX

A

A-fib

A-flutter w/ variable block

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17
Q

what is the cause of AFIB

A

: increased automaticity within the atria

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18
Q

Tx of A fib -chronic (stable)

A

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
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19
Q

Tx of chornic unstable A fib

A
  • 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
Q

what is dilt and what does it do

A

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

21
Q

New Onset = Rhythm Conversion Tx

A
  • 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
Q

magnesium is a vasodilator or vasoconstrictor

A

vasodilator

23
Q

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

A

Vtach*******

SVT with abberancy (bb block)

antidromic WPW

24
Q

cause of Vtach, SVT with BBblock, and Antidromic WPW

A

circuit re-entry in the ventricles

25
Q

how do you know WPW

A

shortened PR interval with delta wave

26
Q

if your Vtach is unstable

A

cardioversion

27
Q

why would you consider adenosine in a wide regular without p

A

SVT with abberancy

28
Q

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

A
  • Careful when giving adenosine to WPW (conduction can reverse)
29
Q

why do you admit after seeing a pt with VTACH

A

ADMIT

30
Q

Wide, Irregular, No P waves

A
  • A-fib w/ BBB
  • A-fib w/ WPW
  • A-flutter w/ variable block & BBB
  • Polymophic VT = Torsades
31
Q

A-fibb tx

A
  • 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
Q

how does tx for stable SVT work

A

vagal maneuvers

6 rapid push (doesn’t last long)

12

(can do 18)

synchronized cardioversion

33
Q

unstable rapid irregular narrow tx

A

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
Q

chronic A-fib

A
35
Q

6 step approach

A
  1. ABC’s, IV, O2, Monitor
  2. Stable or Unstable
  3. Regular or Irregular
  4. Fast or Slow
36
Q

appraoch to the brady pt (big 3)

A

DRUGS

ISCHEMIA

ELECTROLYTES

37
Q

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

A
  • Block is below AV node
  • Slower rhythm
  • More likely to stop/asystole
  • Not atropine sensitive
38
Q

Brady treatment

A
  • 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
Q

which AV blocks are unstable

A

mobitz type two can move into third degree

and of course third degree

40
Q

electrolyte abnormalities that could lead to pronloged qt

A

Electrolyte abnormalities

hypokalemia

hypocalcemia

hypomagnesmia

Na channel blockers

miscellaneous: elevated ICP, ACS

hypothermia, hereditary

41
Q

what are the considerations with determining prolonged QT

A

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

if QT lengthen due to stretching of T wave=ischemia

42
Q

2 EKG findings for burgadas

A

cove type (Seal)

saddle type

43
Q

treatment is brugada

A

defibb

(ICD)

44
Q

leads to focus on when suspecting cardiomyopathy

A

lateral

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

45
Q

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

A
  • : 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
    *

Emergency Medicine (28 decks)

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