Ventricular arrythmias Flashcards

1
Q

Where in the heart does a narrow complex tachycardia vs a wide complex tachycardia occur?

A

Narrow complex tachycardia occurs via the His bundle-Purkinje fiber conduction system whereas a wide complex tachycardia does NOT occur via the conduction system

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2
Q

What is the pathology indicated by the ECG below?

A

Ventricular tachycardia

**Note the wide complex, very regular rhythm**

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3
Q

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)?

A

Ventricular tachycardia

Ventricular fibrillation

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4
Q

Name the subtypes of ventricular tachycardia and ventricular fibrillation (2 for each)

A

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**

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5
Q

Antiarrythmatics can be split into 4 (5 technically) general categories, namely ___

A

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

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6
Q

All Class I antiarrythmatics are ___ (MOA) and can be further split into 3 subgroups.

A

All Class I antiarrythmatics are Na+ channel blockers (MOA) and can be further split into 3 subgroups (Ia, Ib, Ic)

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7
Q

What is the mechanism of Class Ia drugs? How do they impact the action potential?

Which drugs are in Class 1a? (4)

A

Class Ia drugs block K+ as well >> extend AP (prolonged QT interval)

Guinidine, procainimide, disopyramide are Class 1a drugs

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8
Q

Describe the MOA and effects on action potential on Class 1b drugs

Which drugs are in this class? (5 but 2 most commonly used)

A

Class Ib drugs decrease Na+ current (+/- increase K+ current) >> shorten AP

Drugs in this class: Lidocaine, mexilitine (see below for others)

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9
Q

What is the mechanism of action of class Ic drugs and their effect on action potential?

A

Class Ic drugs decrease Na+ current >> no change in AP

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10
Q

Fill in the blanks

A

**see below**

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11
Q

___ is a procainamide metabolite (N-acetyl-procainamide) and a pure K+ channel blocker

A

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*

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12
Q

Which drugs are the class III drugs and what is their MOA?

A

Amiodarone

Sotolol

Dofetilide

Dronedarone (amiodarone-type)

**Class 3 ADDS some blocks to the mix - Class 3 drugs = ADDS; blocks = K+ blockage

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13
Q

What is the acute Rx for wide complex tachycardia?

A

**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

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14
Q

___ 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)

A

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)

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15
Q

What are the side effects of amiodarone? (5, try to name 5)

A

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**

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16
Q

Why does IV amiodarone cause hypotension when given as a bolus for treating ventricular arrhythmias?

A

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)

17
Q

What is one major issue with giving amiodarone (besides all the other side effects)?

A

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

18
Q

What is the chronic treatment for wide complex tachycardia if a pt has structural heart disease vs no structural heart disease?

A

If no structural heart disease: ablation

If structural heart disease/can’t do ablation: Implantable cardioverter defibrillator (ICD) + adjuvant therapy

19
Q

How does an implantable defibrillator work?

A

Basically they shock the heart

(see below for deetz)

20
Q

Two types of VT that occurs in normal hearts are ___

A

Two types of VT that occurs in normal hearts are outflow tract VT and LV VT

21
Q

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

A

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

22
Q

What is a channelopathy? Name 3 channelopathies

A

A channelopathy is a congenital defect in an ion channel

3 channeopathies discussed: Brugada’s syndrome, Long QT syndrome, Idiopathic VF

23
Q

___ most often occurs in SE Asia (asian males) and arises from a defect in Na+ channel (and others) leading to decreased na+ currents

A

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

24
Q

What is the pathology indicated in the ECG below?

A

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 **

25
Q

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?

A

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)

26
Q

Under what physiological conditions (e.g. rest, stress, exercise etc) would people present w/ LQT1, 2 or 3?

A

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)

27
Q

___ is the 2nd leading cause of death (after all cancers combined)

A

Sudden cardiac death is the 2nd leading cause of death (after all cancers combined)

28
Q

Most sudden cardiac death is due to ___

Name 3 other causes of sudden cardiac death

A

Most sudden cardiac death is due to ventricular arrhythmias

3 other causes of sudden cardiac death: bradycardia, Torsades de Pointes, primary ventricular fibrillation

29
Q

Name 3 heart issues ass’d with sudden cardiac death

A

Main ones are coronary artery disease, idiopathic cardiomyopathy and hypertrophic cardiomyopathy

**all other heart issues as well - see below**

30
Q

___are really the only drugs that improve survival in pts with weakened hearts after an MI

A

Beta blockers are really the only drugs that improve survival in pts with weakened hearts after an MI

31
Q

If a pt is tachycardic and is hemodynamically unstable, ___

If a pt is tachycardic and is symptomatic, ___

A

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

32
Q

T/F: All wide complex tachycardias are ventricular techycardia

A

True