Dysrhythmias Flashcards
1
Q
stable or unstable
A
- Interpretation based on a spectrum
- ALOC, ↓BP, CP, pulmonary edema
-This is not a dichotomous decision. If someone is able to talk to you, they are perfusing enough to get o2 to the brain – they are STABLE even if their BP is 80
2
Q
regular or irregular rhythm?
A
- Irregular
- Above the ventricles
- NOT VT
- Block AV Node
3
Q
are P-waves present?
A
If there are P waves present, it is unlikely that it is a tachydysrythmia
4
Q
Narrow or wide complex?
A
Narrow
- Above the ventricles
- Block the AV- Node
- Not VT
- Duration (<0.12 (adults), < 0.08 (children))
- If it is narrow, its from the atrium. If its wide its from the ventricles
- If you have narrow complex you need to block the av node
5
Q
Group A: narrow, regular, no p-waves
A
- PSVT
- Atrial Flutter
- WPW (orthodromic)
- Narrow complex VT (very rare)
-Cause: electrical circuit movement
- Narrow complex VT resolves by shock etc. its not picked up very often
- Orthodromic – narrow – starts in atrium
- Antidromic – wide – starts in ventricle
- WPW – accessory pathway
- The AV node cannot go faster than 220! If it goes higher than that, there is an accessory pathway
- A flutter = microcircuit issue
6
Q
Treatment for group A dysrhythmias
A
STABLE
- Vagal maneuvers
- AV Nodal blockers: Adenosine, CCB, ẞ-Blocker
- Cardioversion
UNSTABLE
- Can consider Adenosine but…
- Cardioversion start at 50J and 2x every time
- You need to block the AV node
- If you use medication and it doesn’t work, you use synchronized cardioversion
- Unstable: you CAN push adenosine
- What does adenosine feel like? FEELS LIKE DYING!! You need to prime the patients so theyre ready for this
7
Q
Group B dysrhythmias: narrow, irregular, no Ps
A
- A-fib
- A-Flutter with variable block
-Cause: increased automaticity
- Anyone in group A (SVT, Aflutter) – AV NODE ISSUE
- Adenosine is FAST! Lasts for a few seconds and goes away – if you give adenosine to someone with aflutter, it will NOT CURE Aflutter
- For Aflutter, you need a longer acting agent
-Increased automaticity – fireworks going off in the atrium all the time
8
Q
Group B treatment
A
- it depends:
- chronic: rate control
- new onset: rhythm control
You will see a chronic pt if they have palpitations
9
Q
Group B treatment: Chronic - stable vs unstable
A
Stable patient
- Stabilize Atrium by blocking AV node
- CCB
- ẞ-blocker
- Digoxin…old drug
- Diltiazem 5-10mg IVP slow. If tolerated can 2x it. (Up to 60mg in 30min)
Unstable
- Rapid Cardioversion: Start high! Sync!
- Support Blood Pressure: Pressers – you need to ensure perfusion of brain and heart – success rate of conversion with low blood pressure is LOW
- If the diastolic pressure is low, you will NOT convert these patients because their heart is irritable! You need to get the BP up!
- Slow down heart: drips not IV Push
- If you push, you may bottom out the BP and cause cardiac arrest
- But, if the person is bigger, you may need to push since the drip wont do anything
- Magnesium – vasodilator
- Repeat Cardioversion
- Other considerations: Is it really A-Fib?
-For elderly, TREAT UNDERLYING CAUSE FIRST!
10
Q
Group B tx: new onset
A
- Rhythm Conversion: Ottawa Aggressive Protocol for A-fib
- Clear Hx with in 48 hours
- No structural heart dz
- Age not a contraindication
- Caveat in elderly don’t rush often p/w vague sx’s
- New onset – you want to get them back into sinus rhythm
- AGE IS NOT A DETERMINING FACTOR!
- If you have a patient with longstanding Afib, the risk of converting them is STROKE!
-Chemical cardioversion: Procainamide 1g over 1 hour ↓ -Electrical cardioversion: Biphasic 200J ↓ -D/C home without meds
11
Q
Group C: wide, regular, no Ps
A
- VT
- SVT with aberrancy (BBB)
- Antidromic WPW
- Cause: circuit re-entry in the ventricles
- WIDE and REGULAR – VTACH!!!!!!
- WPW – shortened PR interval with delta wave
- You CARDIOVERT for unstable people!!
12
Q
Group C tx: stable vs unstable
A
STABLE
- Consider Adenosine
- Cardioversion: 100J
- Antiarrythmic Infusion: Procainamide, Amiodarone, Magnesium
UNSTABLE
- CARDIOVERT
- ACLS
-Why consider adenosine? SVT with abberancy - adenosine in this patient that is stable is like pressing a restart button on the heart
13
Q
AV node
A
- AV node cant go faster than 200-220! This is 300 so its WPW
- CALL CARDIOLOGY!! In the ED, think about in this group whether they are stable or unstable. If you convert, do they go home or get admitted? ADMITTED
- Vtach can turn to Vfib!!
14
Q
Group D: wide, irregular, no Ps
A
- A-fib with BBB
- A-fib with WPW
- A-flutter with variable block and BBB
- Polymophic VT = Torsades
15
Q
treatment of group D dysrhythmias
A
STABLE
- A-Fib = Rate control: Be carful If…
- WPW
- Regular: Consider *Adenosine (some people don’t like this because it can send them into overdrive), electricity
- Irregular: No AV nodal blocker, Electricity, Procainamide
- Torsades = Magnesium
UNSTABLE
- Defibrillate
- ACLS
- Orthrodromic- Narrow
- Antidromic – Wide treat as VT Cardioversion
- A-Fib with WPW- very hard, if in doubt reg or irreg okay to cardiovert 120-200J Biphasic and 200J, meds likely started in the Unit
- WHEN ITS IRREGULAR YOU DEFIBRILLATE
16
Q
Supraventricular tachycardia tx
A
- Stable
- Vagal maneuvers
- Block AV-node
Adenosine 6mg IVP can mix with 15ml of NS rapid push ↓ Double dose 12mg Rapid IVP ↓ Can Go Up to 18mg Rapid IVP ↓ Synchronized Cardioversion
17
Q
treatment of chronic A-fib
A
Unstable
- Rapid cardioversion: Pads anterior and posterior
- Start high 360J, Sync
- Sedation (Etomidate + Ketamine)
- Elevate BP
- Push dose pressers (PDP) Phenylephrine 50-200mcg IVP temporizing measure
- Target diastolic > 60mm Hg
Slow down the heart
- Diltiazem:
- NO IVP!
- Loading Drip 50 mg mix into 50mL NS (Gtts at 2.5mg per minute)
- Amiodarone
- 150mg over 5-10 min
- Okay to use PDP to maintain BP PRN
Other meds to use:
-Magnesium: 1-2gm IV drip
Repeat Cardioversion
- PUT ON PADS!!
- What does sedation do to BP? Drops it! Ketamine is one of the only sedatives that does not drop BP
- Etomidate has a better safety profile but can still drop BP
- If you elevate BP, youre more likely to convert them
All antiarrhytmics can be proarrythmics!!
Don’t use CCBs in heart failure!!!
18
Q
Treatment of Vtach
A
SHOCK
- PT yells and is awake
- what do you want to know
19
Q
Solution to tachyarythmias
A
-WHEN IN DOUBT, ELECTRICITY
20
Q
how to approach bradycardia
A
- ABC’s, IV, O2, Monitor
- Stable vs. Unstable
- Wide or Narrow
- How slow?
21
Q
Wide or narrow complex brady
A
Wide
- Block is below AV node
- Slower
- More likely to stop
- Not atropine sensitive
Narrow
- More stable
- Faster
- Atropine sensitive
22
Q
brady big 3
A
- electrolytes
- ischemia
- drugs
23
Q
1st degree AVB
A
- PR > 0.20 sec (1 box)
- Usually benign
- Normal in 5% of population
- Usually narrow
TREATMENT
-Refer back to primary doctor - you dont really do much for this patient
24
Q
2nd degree type 1 AV block - Wenckebach
A
PR gets progressively longer then drops a QRS complex
Narrow complex
At level of AV node
Stable and Transient
25
2nd degree type 2 AV block
PR interval consistent, Drops QRS complex
Below AV Node
Likely go into 3rd degree or asystole
26
3rd degree AVB
- narrow complex - AV node
- wide complex - Associated more with asystole
- PR interval is randomly changing
- No associating QRS to a P-Wave
- Great imitator of other AVB
27
treatment of 3rd degree AV blocK
- Atropine: start 0.25-0.5mg bolus
- Transcutaneous Pacing: Sedation
- 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
- BRADY Are Too Darn Easy
- You know the transcutaneous pacing is capturing by just feeling pulse and if its regular, youre good
-Pacemaker for all 3rd degree AVB and symptomatic Mobitz Type II
28
Other abnormal EKG rhythm
Prolong QT syndrome
-Lead to Ventricular dysrhythmia = Torsades
Brugada syndrome/HOCM
-Associated with sudden death
Wellen’s Syndrome
-High Risk for extensive anterior MI and death
29
ddx of prolong QT
- Hypokalemia
- Hypocalcemia
- Hypomagnesmia
- Na Channel Blockers
- Miscellaneous: Elevated ICP, ACS, Hypothermia, hereditary
30
Consideration of QT intervals
- If QT lengthen due to stretching of ST segment = Hypocalcemia and Hypothermia
- If QT lengthen due to to stretching of T-wave = Ischemia
- If you have prolonged QT because T wave is getting really big, THAT IS ISCHEMIA!!
31
Brugada Syndrome
- RBBB or incomplete RBBB with ST elevation in V1-V2
- Two morphology
- Saddle type
- Cove Type (more specific)
- Healthy with structurally normal hearts
- Syncope or Near Syncope
- Mortality 10% per year
- Sudden VT or polymorph VT, spontaneously convert = syncope and if not they die!
- 50% genetic mutation in Na channel
32
HOCM
- Deep Q-waves in Lateral Leads
- Structural heart dz = Left ventricle
- Treatment: Surgery or medical management
- Not ischemic Q-wave these are 1 box wide.
- HOCM narrow!
33
Wellen's
- Proximal LAD lesion
- ST Changes are absent
- Two Morphologies
- Type 1: Deep symmetric T-Wave in precordial leads
- Type 2: Biphasic T-Waves in precordial leads
- WELLENS type 2 (for having 2 waves – biphasic) – if you do a trop on this person it will NOT be positive but if you stress them, they will die! – this person has a proximal LAD lesion
- WELLENS type 1 (deep t wave)
34
treatment of wellen's
-PCI/Cath is the best management
- Medical management = not effective
- 75% develop AMI within weeks
-Stress test = precipitate MI
