Arrhythmias Flashcards
- **• Bradycardias
* **• Tachycardias
(Bradyarrhythmias)
Tachyarrhythmias
Supraventricular
when involving atrium or AV
Ventricular
Originate HIS-PURKINJE
**Mechanisms of arrythmias
- Altered impulse formation
- Altered impulse conduction
- BOTH
*** Fastest cells preempt all others
= “Overdrive Suppression
*****Normally____ node dominates _____
AV and Bundle of HIs ________
Purkinje
SA ; 60-100
50-60
30-40
***3 causes of altered impulse formation
3 Causes:
• Altered SA rate
• Abnormal automaticity in myocytes
• Triggered activity
**Triggered Activity
Abnormal oscillations in membrane voltage
can develop during or after repolarization “afterdepolarizations”
*****TRIGGERED ACTIVITY• Once triggered, they can become
selfsustaining tachycardias.
**Triggered activity EARLY (LPDT)
Occur when?
can occur in LONG depolarization • ex. Conditions that cause PROLONGED QT • (slowing can cause reversal of ion mvmt.) • Depolarization initiates tachycardia TORSADES DE POINTES
**Triggered activity DELAYED (DAD)
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.
*****Altered Impulse Conduction
• Normal conduction pathway does not have blocks
or reentry pathways
***Blocks =
bradycardias
***** Reentry pathways =
tachycardias
***3 types of Tachycardias
Supraventricular
Ventricular
Ventricular Pre-excitation Syndrome
*****Supraventricular tachycardias are
Sinus Tachycardia – PACs – SVT – Multifocal Atrial Tachycardia A-flutter – A-fib
*****Ventricular Tachycardias are
– PVCs
– V-tach
– V-fib
*****Ventricular Pre-excitation Syndrome
– WPW
PACs
- Arise from_______
- Felt as _____
Arise from ectopic foci in atria
• Felt as “fluttering” or a “heavy” heartbeat
SA node rate
60-`100
AV node rate
50-60
Purkinje fibers
30-40
Anesthesia consideration for tachycardia
Avoidance of vagolytic drugs intraoperatively
ex. Pancuronium
PACs anesthesia consideration
Avoid excessive sympathetic stimulation
• Treatment only required if they trigger secondary
dysrhythmias
SVT rate
Initiated where?
In EKG, p waves are
140-250 bpm
at or above AV node
-buried in QRS
What is the goal of therapy for a patient with Atrial flutter? what are we avoiding?
Ventricular rate control is initial goal of therapy to avoid 1:1
AV conduction
• If 1:1 conduction occurs with ventricular rate ≥ 300, is _______most likely mechanism - - consider
reentry; procainamide (Class IA)
Most important clinical consequence of AF is
thromboembolic event causing stroke
When 3 or more consecutive PVCs occur
Vtach
Torsades de Pointes -
“twisting of the points”
• A.k.a. Polymorphic VT
Tx of torsade
Magnesium
Vfib
Cessation of C.O. & Death without prompt
treatment
Survival is highest if defibrillation occurs in
3 to 5 minutes of cardiac arrest
_____ _______ is only effective treatment
Electrical defibrillation
After 3 attempts with epi or vaso, administration of.
amiodarone, lidocaine (or Mg for TdP) is indicated
WPW (On left side of heart =
Type A, on right = Type B)
For Orthodromic (narrow QRS) : –
begin with vagal maneuvers, if unsuccessful, consider
adenosine, verapamil, beta-blockers or amiodarone.
For Antidromic (wide QRS): –
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)
Bradycardia
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
Bradycardia Can occur with or without sedation.
• Can occur any time during neuraxial blockade, but
1 hour after anesthetic is
initiated.
• Warning Signs prior to arrest for Bradycardia:
SOB, nausea, restlessness, light-headedness, tingling fingers, deterioration in mental status
First Degree AV Block
•
Prolonged PR interval (> 5 small boxes)
1st degree AVB tx
Check Digoxin levels prior to surgery
• Maintain serum K+ levels in pts. on Digoxin
Second Degree AV Block
• Mobitz Type I
– Wenckebach
•
Caused by intermittent failure of AV conduction
• Progressive prolongation of PR until a QRS is dropped
Mobitz Type II – Sudden
QRS drop, more dangerous
Type I Vs Type more dangerous type is
Type II
Does atropine work in type II AVB
no
Tx of type I is only for symptomatic patient, but treatment of Type II AVB
Cardiac Pacing (transcutaneous or transvenous) • Atropine does not work • Pacemaker warranted, even if pt. is asymptomatic
This block most common with Acute MI
3rd degree AVB
3rd AVB there is dissociation of the __________.
atria and ventricles
Medication that can be used as a chemical pacemaker until pacemaker becomes functional?
Isoproterenol
