Ventricular arrythmias Flashcards

(32 cards)

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
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)
26
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)
27
\_\_\_ 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)
28
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
29
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\*\*
30
\_\_\_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
31
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 **pace**maker
32
T/F: All wide complex tachycardias are ventricular techycardia
True