Cardio test 5

What does the blockade of the hERG channel lead to?

Prolonged QT risk

If there is a long QT interval what medication should be administered to prevent Torsades

Non-dihydropyridine CCBs

What is Torsades

polymorphic ventricular tachycardia

What is 0

What is 1

Opening of Na+ current

what is 2

Opening of Ca2+ channels

what is 3

opening of K+ channels 

what is 4

Membrane at resting potential

Why is it important to weight the risk and benefits of AAD

AAD can exacerbate existing arrhythmias and cause new ones 

What is the main goal of AAD

blunt or prevent abnormal impulses formation and/or abnormal conduction

What is the major MOA of class 1 AAD

Na+ channel inhibition

What is the major MOA of class 2 AAD

Beta blockers

What is the major MOA of class 3 AAD

K+ channel blockers

What is the major MOA of class 4 AAD

Ca 2+ channel blockers

Where do the AAD work at in the graph

• Effective refractory period

• Rate of depolarization/repolarization (slope)

• Resting potential (4)

Quinidine drug class

Class 1A sodium channel blocker

Procainamide drug class

Class 1A sodium channel blocker

Disopyramide drug class

Class 1A sodium channel blocker

Lidocaine drug class

Class 1B sodium channel blocker

Phenytoin drug class

Class 1B sodium channel blocker

Mexiletine drug class

Class 1B sodium channel blocker

Flecainide drug class

Class 1C sodium channel blocker

Propafenone drug class

Class 1C sodium channel blocker

What are the class 2 AAD

Beta blockers

What are the class 3 AAD

K+ channel blockers

Amiodarone Drug class

K+ channel blockers

Dofetilide Drug class

k+ channel blockers

Ibutilide drug class

k+ channel blockers

Sotalol drug class

k+ channel blockers

Diltiazem drug class

CCB

Verapamil drug class

CCB

Class 1A sodium channel MOA

• Open  >inactivated = slow dissociation

• decrease Vmax in phase 0

• Decrease in conduction velocity

• increase duration of AP and ERP

Class 1B sodium channel MOA

• Inactivated > open = rapid dissociation 

• Increase ERP due to depolarization cells due to slowed recovery of Na+ channels from inactivation

Class 1C sodium channel MOA

Open > inactivated = very slow dissociation

decreased Vmax and conduction velocity in AV node

Increased duration of ERP

Quinidine Therapeutic Uses

Supraventricular and ventricular dysrhythmias

Procainamide Therapeutic Uses

Atrial, Supraventricular, and VT dysrhythmia

Disopyramide Therapeutic Uses

VT dysthymia

What medication is preferred for short-term VT dysrhythmia

Amiodarone

Lidocaine Therapeutic Uses

Short-term VT dysrhythmia

Phenytoin Therapeutic Uses

Acute and chronic VT dysrhythmia

Mexilitene Therapeutic Uses

VT dysrhythmia

Flecainide Therapeutic Uses

SPVT and VT dysrhythmia

Propafenone Therapeutic Uses

SPVT and VT dysrhythmia

What cells get effected most by Class 1 AAD

Depolarized cells

Does lidocaine block sodium channels in normal cells 

Nah 

What is only class 1 AAD that does decrease refractory period

Lidocaine

Why would cells be depolarized

Ischemia, metabolic/electrolyte imbalance

What two sodium channel blockers AAD that act on the calcium channels

Disopyramide and Propafenone

What sodium channel blocker AAD act on K+ current

class 1A sodium channel blockers

How do all sodium channel AAD prolong ERP

slowing recovery of Na+ channels from inactivation and thus delaying new AP 

Major site of metabolism of Quinidine and DDI

CYP2D6

Quinidine AEs

Cardiotoxic at higher doses due to anti-cholinergic effect 

• increasing SA automaticity, AV conduction

Quinidine DDI

Macrolide antibiotics

Amiodarone

digoxin

Procainamide metabolism

hepatic acetylation to NAPA- which can block K+ channels

Procainamide AEs

Lupus like syndrome

Procainamide DDI

Macrolide antibiotics

Amiodarone

Disopyramide AEs

Stong negative inotropic effect

• cardiotoxicity at high doses

Disopyramide DDI

CYP2D6 macrolide antibiotics 

Why is lidocaine preferred IV/IM and not oral

rapid hepatic metabolism orally and only 3% shows up in plasma

Lidocaine AEs

Direct CNS effects at high doses

• Seizures 

• Drowsiness

• confusion

Mexiletine administration

Orally

• Low first pass effect

Mexiletine DDIs

• Anti-depressants

• Theophylline

What are the most are the most pro-arrhythmics of the sodium channel blockers 

Class 1C

What drugs can you not use with in pts with MI

flecainide and propafenone

Of the class 3 AAD what medication really increase refractory period

Amiodarone and Dronedarone

what are amiodarone and dronedarone effect on QT interval

Very mush increase

What is the most commonly prescribed medication for post-operate arrhythmia

Amiodarone 

Where are Amiodarone and Dronedarone metabolisms

CYP3A4

What is interesting about the amiodarone and dronedarone half lives

The half life is weeks

Amiodarone DDI

Increase serum lvls of Digoxin, warfarin, and statins

Amiodarone AEs

Bradycardia or heart block

pulmonary fibrosis

corneal deposits

hypothyroidism 

Dronedarone AEs

exacerbation of severe HF

Amiodarone MOA

mixture of all 4 drug classes

Adenosine MoA

Blocks Ca2+ channels

• Slows AV nodal conduction 

• Does the opposite effect of group 3 AAD

Does Esmolol act on Na+ channels?

Yes, acts on depolarized cells

Does Diltiazem act on the sympatholytic system

No

Sotalol MOA

Dual acting class 2 and 3

How does Mg2+ effect arrhythmics

Interacts with Na/K ATPase, weakly blocks Ca2+ channels

• Increases AV conduction

• Useful for long QT

How does K+ effect arrhythmias

Slows AV conduction 

What is the P-wave

Atrial depolarization

• Conduction

What is the QRS complex

Ventricular Depolarization

What is the T wave

Ventricular repolarization

What is the average QT interval

< 440 msec

What increases the atrial stretch

• HTN

• Ischemic heart disease

• Valvular disorders 

• HF

• Pulmonary disease 

• Obesity

What increase Sympathetic system

• Hyperthyroidism

• Alcohol intake

• Sepsis/infection

• Surgery

What are the symptoms of Arterial Fibrillation?

• Palpitations

• Dizziness

• Fatigue

• Dyspnea 

• Weakness

• Decreased exercise tolerance

What are the ways to see Arterial Flutter in EKG 

Absence of P waves

What are the goals of therapy for AF

• Ventricular rate control

• Preventing clots

• Restore sinus rhythm

For acute AFib, what are the severe symptoms

• low BP

• Syncope

• Altered mental status

• Severe chest pain

What are the ways to treat severe symptoms in acute AFib

DCCV or electroshock

What are the minimal symptoms an Acute AFib

rapid ventricular rate

>120-140

What are the ways to treat minimal symptoms for acute AFib

BB, CCB and digoxin

What is the drug of choice for acute Ventricular Rate control in AFib

Beta blockers