Ventricular arrythmias Flashcards
Where in the heart does a narrow complex tachycardia vs a wide complex tachycardia occur?
Narrow complex tachycardia occurs via the His bundle-Purkinje fiber conduction system whereas a wide complex tachycardia does NOT occur via the conduction system
What is the pathology indicated by the ECG below?
Ventricular tachycardia
**Note the wide complex, very regular rhythm**
A pt presents with a very high heart rate of 200bpm. You’ve done the work up and determined from a 12 lead ECG that the pt has a wide complex tachycardia. What conditions are on your differential (2)?
Ventricular tachycardia
Ventricular fibrillation
Name the subtypes of ventricular tachycardia and ventricular fibrillation (2 for each)
Ventricular tachycardia - monomorphic VT and polymorphic VT
**Monomorphic VT the most common (if sinus rhythm is regular)
Polymorphic – when rhythm is irregular**
**
Ventricular fibrillation - SVT w/ aberration; SVT w/ WPW syndrome
**SVT w/ aberration – SVT traveling down the ventricles but one of the bundles isn’t working; very rare**
Antiarrythmatics can be split into 4 (5 technically) general categories, namely ___
Antiarrythmatics can be split into 4 general categories, namely:
Class I: Na+ channel blockers
Class II: Beta blockers
Class III: K+ channel blockers
Class IV: Ca2+ channel blockers
Class V: Digoxin
All Class I antiarrythmatics are ___ (MOA) and can be further split into 3 subgroups.
All Class I antiarrythmatics are Na+ channel blockers (MOA) and can be further split into 3 subgroups (Ia, Ib, Ic)
What is the mechanism of Class Ia drugs? How do they impact the action potential?
Which drugs are in Class 1a? (4)
Class Ia drugs block K+ as well >> extend AP (prolonged QT interval)
Guinidine, procainimide, disopyramide are Class 1a drugs
Describe the MOA and effects on action potential on Class 1b drugs
Which drugs are in this class? (5 but 2 most commonly used)
Class Ib drugs decrease Na+ current (+/- increase K+ current) >> shorten AP
Drugs in this class: Lidocaine, mexilitine (see below for others)
What is the mechanism of action of class Ic drugs and their effect on action potential?
Class Ic drugs decrease Na+ current >> no change in AP
Fill in the blanks
**see below**
___ is a procainamide metabolite (N-acetyl-procainamide) and a pure K+ channel blocker
NAPA is a procainamide metabolite (N-acetyl-procainamide) and a pure K+ channel blocker
*Procainamide is actually metabolized to both NAPA and acetyl-procainamide, both of which block K+ channels*
Which drugs are the class III drugs and what is their MOA?
Amiodarone
Sotolol
Dofetilide
Dronedarone (amiodarone-type)
**Class 3 ADDS some blocks to the mix - Class 3 drugs = ADDS; blocks = K+ blockage
What is the acute Rx for wide complex tachycardia?
**if pt is hemodynamically unstable >> shock
if stable: 12 lead ECG first
1st line Rx for acute wide complex tachycardia: IV Amiodarone
Other choice: IV Procainamide
___ has a narrow therapeutic index and is used at decreasing intervals
Magnesium if very useful for ___ (type of ventricular tachycardia)
Beta blockers are given __ (IV/oral) and are useful for ___ (type of VT)
Lidocaine has a very narrow therapeutic index. Use with (1/2) decreasing intervals
Magnesium: very useful for polymorphic VT
Beta blockers: given IV and useful for VT storm (recurrent episodes of VT)
What are the side effects of amiodarone? (5, try to name 5)
Bradycardia
Makes it harder to use a defibrillator
Pneumonitis
Pulmonary fibrosis
Hyper or hypothyroidism (due to high iodine content in drug)
Neuropathy
**think about how the drug works - remember that this drug actualy has properties of all 4 drug classes**
Why does IV amiodarone cause hypotension when given as a bolus for treating ventricular arrhythmias?
IV amiodarone can cause hypotension when given as a bolus (because it’s prepared w/ a detergent – Tween – which is what actually causes the hypotension)
What is one major issue with giving amiodarone (besides all the other side effects)?
Amiodarone has many drug-drug interactions
**partial list of drugs it interacts with:
Digoxin – increases bioavailability
Quinidine – increases concentrations
Warfarin – increases effectiveness
Beta-blockers – worsens bradycardias
Ca channel blockers – worsens bradycardias and hypotension
Dilantin – increases concentration
What is the chronic treatment for wide complex tachycardia if a pt has structural heart disease vs no structural heart disease?
If no structural heart disease: ablation
If structural heart disease/can’t do ablation: Implantable cardioverter defibrillator (ICD) + adjuvant therapy
How does an implantable defibrillator work?
Basically they shock the heart
(see below for deetz)
Two types of VT that occurs in normal hearts are ___
Two types of VT that occurs in normal hearts are outflow tract VT and LV VT
For patients with structural heart disease, the most common case of VT is ___
Other causes include ___ (type of cardiomyopathy), ___(hint: what is dysplasia?) and channelopathies
For patients with structural heart disease, the most common cause of VT is coronary artery disease
Other causes include dilated cardiomyopathy, RV dysplasia, and channelopathies
What is a channelopathy? Name 3 channelopathies
A channelopathy is a congenital defect in an ion channel
3 channeopathies discussed: Brugada’s syndrome, Long QT syndrome, Idiopathic VF
___ most often occurs in SE Asia (asian males) and arises from a defect in Na+ channel (and others) leading to decreased na+ currents
Brugada syndrome most often occurs in SE Asia (asian males) and arises from a defect in Na+ channel (and others) leading to decreased Na+ currents
What is the pathology indicated in the ECG below?
Brugada syndrome
**Note the elevated end of the QRS in leads V1 and V2 followed by the inverted T waves. This is classic.
The arrhythmia seen is polymorphic VT **
What is Long QT syndrome and what cause it?
The main genetic defects in Long QT syndrome are LQT1, 2 and 3. What ion channels are affected in each defect?
Literally a channelopathy in which there’s prolong myocardial depolarization.
Caused by anything that prolongs the QT interval
***
LQT 1 and 2 are defects in K+ channels (2 is HERG channel)
LQT 3 is a defect in a Na+ channel (increased Na+ currents)
Under what physiological conditions (e.g. rest, stress, exercise etc) would people present w/ LQT1, 2 or 3?
LQT1 ass’d with exercise
LQT2 ass’d with emotional stress
LQT3 ass’d with sleep/rest without arousal (so people just died in their sleep)
___ is the 2nd leading cause of death (after all cancers combined)
Sudden cardiac death is the 2nd leading cause of death (after all cancers combined)
Most sudden cardiac death is due to ___
Name 3 other causes of sudden cardiac death
Most sudden cardiac death is due to ventricular arrhythmias
3 other causes of sudden cardiac death: bradycardia, Torsades de Pointes, primary ventricular fibrillation
Name 3 heart issues ass’d with sudden cardiac death
Main ones are coronary artery disease, idiopathic cardiomyopathy and hypertrophic cardiomyopathy
**all other heart issues as well - see below**
___are really the only drugs that improve survival in pts with weakened hearts after an MI
Beta blockers are really the only drugs that improve survival in pts with weakened hearts after an MI
If a pt is tachycardic and is hemodynamically unstable, ___
If a pt is tachycardic and is symptomatic, ___
If a pt is tachycardic and is hemodynamically unstable, SHOCK them (but they need to be unconscious/sedated)
If a pt is tachycardic and is symptomatic, use a pacemaker
T/F: All wide complex tachycardias are ventricular techycardia
True
