Anti Arrythmics Flashcards by Iseoluwa Ojo

Cardiac arrhythmia

Also known as cardiac ______ or _______, is a group of conditions in which the heartbeat is _______,_____, or _______

dysrhythmia

irregular heartbeat

irregular, too fast, or too slow.

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Cardiac arrhythmia

An abnormality of impulses in terms of _____,_______ , or _______

Usually (symptomatic or asymptomatic?) .

site of origin, rate or conduction.

asymptomatic

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Cardiac arrhythmia

When symptoms are present, these may include palpitations miss heartbeats, light-headedness, syncope, shortness of breath, or chest pain.

T/F

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While most arrhythmias are (serious or not serious?) some predispose a person to complications such as _____ or _______. Others may result in cardiac arrest and death.

Not serious

stroke or heart failure

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There are four main types of arrhythmias: ______,_____,______,_____

extra beats, supraventricular tachycardias, ventricular arrhythmias, and bradyarrhythmias.

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Anti-Arrhythmic agents are drugs clinically used in treating or preventing abnormalities in _______ and _____

Heart rate and rhythm

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Heart rate is the ____________

Normal Heart Rate is ____ to ______

number of heart beat occurring within a minute

60 to 100 bpm

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Heart rhythm is the _____________________

Normal Heart rhythm is regular with _____ contracting before ______

pattern in which the heart beats

atrium; ventricles

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Heart rate and rhythmic are determined by four major properties of the Heart

______
_______
_______
_______

EXCITABILITY
RHYTHMICITY
CONDUCTIVITY
CONTRACTILITY

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MECHANISM

Excitation of SA and AV

Phase 0
_______

Phase 3
_________

Phase 4
____________

Ca2+ Influx

K+ Efflux

Ca2+ influx, Na+ influx , K+efflux

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MECHANISM
Excitation of Atrium and Ventricle

Phase 0- ____

Phase 1-______

Phase 2- _______

Phase 3- _____

Phase 4- _______

Na+ influx

Rapid K+ efflux

Ca2+ influx

K+ efflux

Na+/K+ ATPase( resting membrane potential)

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If the arrhythmia arises from ____,______, or _______ it is called supraventricular arrhythmia

If the arrhythmia arises from the ———- it is called ventricular arrhythmia

atria, SA node, or AV node

ventricles

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Cardiac cell undergo depolarization and repolarisation to form cardiac action potential about ___ times per minute.

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In the atria, purkinje, and ventricles the AP curve consists of ___ phases

In the SA node and AV node, AP curve consists of __ phases

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Pacemaker cells (automatic cells) have ______ membrane potential so they can generate AP _______

unstable

spontaneously

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In Plateau phase of AP generation ,

It’s Due to (fast or slow?) inward current caused by _____channels (__-type _____ channels) opening which also leads to cardiac muscle ———.

Slow ; Ca2+

L; Ca2+

contraction

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In phase 4 of regular AP generation,

Spontaneous _____ to threshold where critical voltage activates ____+ channels. If this phase is steeper, then heart rate ___eases. Involves the spontaneous action of various channel types.

depolarisation; Na

incr

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Mechnisms of Arrhythmogenesis

Divided into 2

_______
_______

Abnormal impulse generation

Abnormal impulse conduction

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Mechnisms of Arrhythmogenesis

Abnormal impulse generation can either be _______ or ———

Automatic rhythms

Triggered rhythms

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Mechnisms of Arrhythmogenesis

Abnormal impulse conduction can either be _______ or ———

Conduction block or re-entry

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Mechnisms of Arrhythmogenesis

Automatic rhythms can either be ________ which means _____ or ——— which means _____

Ectopic focus; AP arises from sites other than SA node

Enhanced normal automaticity; increased AP from SA node

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Mechnisms of Arrhythmogenesis

Triggered rhythms can either be ________ or ———

Delayed afterdepolarization

Early afterdepolarization

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Conduction block is when __________

This is when the impulse is not conducted from the atria to the ventricles

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Mechnisms of Arrhythmogenesis

Conduction block has _____ types

List them

First degree
Second degree
Third degree

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Mechnisms of Arrhythmogenesis Re-entry can either be ——— or _____

Circus movement or reflection

Dihydropiridines works on the _____ while the non- Dihydropiridines works on the _________

Blood vessels, thereby leading to reflex tachycardia Heart gan gan

Arrhythmias Examples under Sinus rhythm ?????

Sinus arrhythmia Sinus tachycardia Sinus bradycardia

Arrhythmias Examples under atrial arrythmia

Paroxysmal Atrial Tachycardia Atrial Flutter Atrial Fibrillation

Arrhythmias Examples under nodal arrhythmia

AV Nodal blocks Nodal re-entrant arrhythmia

Arrhythmias Examples under ventricular arrhythmia

Paroxysmal Ventricular Tachycardia Ventricular Tachycardia Ventricular Fibrillation

Sinus Tachycardia: high sinus rate of ____-___ beats/min, occurs during _____ or other conditions that lead to ______________

100-180; exercise increased SA nodal firing rate

Atrial Tachycardia: a series of __ or more consecutive _______ occurring at a frequency >____/min

3 atrial premature beats 100

Paroxysmal Atrial Tachycardia (PAT): tachycardia which ___________________

begins and ends in acute manner

Atrial Flutter: sinus rate of _____-___beats/min.

250-350

Atrial Fibrillation:_______ atrial depolarizations.

uncoordinated

AV blocks A __________ within the ______ , occasionally in the _______, that impairs impulse conduction from the atria to the ventricles.

conduction block AV node bundle of His

Ventricular Flutter - ventricular depolarizations >____/min.

200

Ventricular Fibrillation -________ ventricular depolarizations

uncoordinated

2 main things used in DIAGNOSIS of arrhythmias ______ ______

Pulse Electrocardiogram (ECG

A Regular irregular Pulse can be caused by ???

Heart block Sinus arrhythmia

An IRegular irregular Pulse can be caused by ???

Atrial arrhythmia Ventricular tachycardia

P wave = _______ QRS wave=———- T wave _________

Atrial depolarization Ventricular depolarization Ventricular repolarization

Describe the following PR interval QRS interval QT interval

Start of P wave to start of QRS wave Start of QRS wave to end of QRS wave Start of QRS wave to end of T wave

Describe the following PR Segment ST segment

End of P wave to start of QRS wave End of QRS wave to start of T wave

End of QRS wave is also knows as ______

J point

COMPLICATIONS caused by heart arrhythmias _____tension ___________ _____ failure _______ shock ______ ______

Hypo Thromboembolism Heart Cardiogenic Cardiac arrest Stroke

Pharmacologic Rationale & Goals The ultimate goal of antiarrhythmic drug therapy: Restore normal ______ and _____ Prevent _______________ from occurring.

sinus rhythm and conduction more serious and possibly lethal arrhythmias

Antiarrhythmic drugs are used to: decrease ________ change the duration of the ___________ suppress _________

conduction velocity effective refractory period (ERP) Abnormal automaticity

With regards to management of atrial fibrillation, Class _____ and _____ are used in _______ control as medical cardioversion agents while Class ____ and _____ are used as ____ control agents.

I and III ; rhythm II and IV ; rate

There are _____ main classes in the Singh Vaughan Williams classification of antiarrhythmic agents

five

Class I agents interfere with the _______ Class II agents are __________agents. Most agents in this class are ______

sodium (Na+) channel. anti-sympathetic nervous system beta blockers.

Class III agents affect __________ Class IV agents affect ———— and the ______ Class V agents work by _________

potassium (K+) efflux. calcium channels ; AV node. other or unknown mechanisms.

Anti-arrhythmic drug Class I - Fast Channel Blockers Ia - _______,______,______ Ib - ________,_____,________ , Tocaininde Ic - ______ ,_______ ,________, Indecainide, Moricizine

Quinidine, Disopyramide, Procainamide Lidocaine, Phenytoin, Mexilitine Ecainide, Flecainide, Propafenone,

Anti-arrhythmic drug Class II - ________ Propanolol, Acebutolol, Atenolol, Betaxolol, Bisoprolol, Esmolol, Labetalol, Metoprolol, Nadolol, Oxprenolol, Penbutolol, Pindolol, Sotalol, Timolol

Beta Blockers

Anti-arrhythmic drug Class III _______,_______,_____

Bretylium, Amiodarone, Sotalol

Anti-arrhythmic drug Class IV - Calcium Channel Blockers ______,_______

Verapamil, Diltiazem

Anti-arrhythmic drug Unclassified - ______,______ ,_____

Digoxin, Adenosine, Mg

Anti arrhythmic mech of action Class 1 : are Na+ channel blockers _________ effect (Positive or negative ?) inotropic action

Local anaesthetic Negative

Anti arrhythmic mech of action Class 1( A ): it ______ duration of __________ and _______ Have ____ channel blocking effect _________ & hypotensive effects.

prolongs action potential & refractory period. K+ ; Antimuscarinic

Anti arrhythmic mech of action Class I(B): ______ the duration of _______

Shorten action potential & refractory period

Anti arrhythmic mech of action – Class1(C) : ______ on the duration of ______

No effect action or refractory period.

Anti arrhythmic mech of action Class III: K+ channel blockers, ________ duration of action potential and refractory period.

Prolong

Class 1(A) Quinidine: ______ plant It ____ open & inactivated_____ channel Block _____ channel

Cinchona Block; sodium potassium

Quinidine _______ inotropic effect ___________ effect

Negative Antimuscarinic

Quinidine – Prolong _____________ on the ECG

Q-T interval

Quinidine Well absorbed _____ (Low or High?) bound to plasma protein

orally High

Quinidine Metabolized in the ____ Excreted via _____ with 20% unchanged

liver Kidney

Quinidine Has ____ blocking and ______ properties Drug interaction with ____

K+ antimuscarinic Digoxin

Adverse effects of quinidine 1- Cardiac effects A) Due to _____ effect ,in A.Flutter or A.fibrillation, may precipitate _________

antimuscarinic ventricular tachycardia

Adverse effects 1- Cardiac effects Syncope _________

Torsade de pointes

Adverse effects 1- Cardiac effects Cardiac stand still (____) in patients with ______ syndrome .

asystole sick sinus

Torsades de Pointes is a type of very fast heart rhythm (tachycardia) that starts in ___________

your heart's lower chambers (ventricles).

Extracardiac adverse effects of quinidine ___tension ______ (headache, dizziness,tinnitus, deafness ) _________ reactions (hepatitis, thrombocytopenia) GIT, diarrhea,nausea,vomiting

Hypo Cinchonism Hypersensitivity

Quinidine ___eases the plasma level of digoxin by : a)_____________ b)______________

incr displacement from tissue binding sites decreasing digoxin renal clearance

Procainamide - Actions Suppresses automaticity by: •decreasing the rate and amplitude of __________ •prolongs __________ •reduces the ___________ •suppresses ______ activity in the atria and ventricles

phase 4 diastolic depolarization action potential duration speed of impulse conduction fibrillatory

Procainamide - Actions ____ dependant ______ activity

Dose anticholinergic

Procainamide - Actions _____ Inotrope •more pronounced in ischemic myocardium _________ in high doses •vasodilatation of peripheral vasculature

Negative Hypotension

Procainamide is Metabolized to _______

N-acetyl Procainamide (NAPA)

Torsade de pointes is an adverse effect or indication of procainamide and quinidine?

Adverse effects for quinidine Contraindication for procainamide

PROCAINAMIDE Given through ________ routes _________ is safer than _____

IV, IM and Oral Continous infusion bolus

PROCAINAMIDE Excreted via ______ Has —————- properties

Kidney anticholinergic

Procainamide - Administration QRS widens by ______ % QT interval ______ Total of 17 mg/kg has been administered

> 50 prolongation

Procainamide - Adverse Effects Myocardial ________ prolonged QRS, QT, AV conduction, VF and Torsade de pointes _________ High doses or rapidly administered _______ angioedema, bronchoconstriction, vascular collapse, febrile episodes, respiratory arrest

Depression Hypotension Hypersensitivity

Lidocaine - Actions Class ___ antiarrhythmic blocks ________ channels

IB fast sodium

Lidocaine - Actions decreases slope of phase ____ decreased automaticity in the ______ action potential duration and effective refractory period of His-purkinje is ______eased

4 His-purkinje system incr

Lidocaine - Actions Acts preferentially on _____ tissue ________ the duration of A.P.& R.P. Effective in _______ arrhythmias.

ischemic Shorten ventricular

Lidocaine Causes ______ effect on AV conduction (Depresses or Elevates?) v-fib threshold

little or no Elevates

Lidocaine (Supresses or elevates ?) ventricular ectopy _____ effect on autonomic nervous system, myocardial contractility and peripheral vascular tone

Suppresses negligible

LIGNOCAINE Given ____ only Well absorbed _____ (High or Low?) first pass effect by Liver

IV orally High

LIGNOCAINE Half life is 2 hours Excreted via ______ Also used as a ________

Kidney Local anesthetic

_______ is the First drug of choice in treatment of ventricular arrhythmias

Lidocaine

Mexiletine Effective _____ Half-life (8-20hrs ). Used in chronic treatment of ______ arrhythmias.

orally ventricular

Mexiletine Effective in relieving chronic pain due to _________ and ______ Adverse effects - _______ side effects

diabetic neuropathy& nerve injury. Neurologic

Class1(c)- Flecainide _____ effect on the duration of A.P.& R.P. Approved for _______________ arrhythmias.

No refractory ventricular

Class1(c)- Flecainide Pro or Anti arrhythmic?

Pro

Class1(c) -Propafenone Has a weak ________ effect.

β-blocking

Class1(c) -Propafenone Used to maintain sinus rhythm in patients with _______ arrhythmias including AF.

supraventricular

Class1(c) -Propafenone Adverse effects : ________________, constipation .

Metallic taste

Compare between class IA, IB , and CI drugs as regards effect on Nat channel & ERP • Sodium-channel blockade: _____ >___ >____ • Increasing the ERP:___>___>___ (lowered)

IC; IA; IB IA; IC; IB

Specific ADVERSE EFFECTS of class 1 drugs Quinidine: _______,_____ reaction , G.I disturbance, ______ toxicity Procainamide: _______ Lignocaine: _______ effect

Cinchonism; Hypersensitivity; Digoxin Hypersensitivity Neurological

Specific ADVERSE EFFECTS of class 1 drugs Mexiletine: ______ effect Propafenone :______,_______

Neurological Metallic taste, Constipation

INDICATIONS for class 1 drugs _______ _______ ________

Atrial flutter Atrial fibrillation Ventricular arrhythmia

Esmolol - Very (short or long?) acting used for ______ and ——— arrhythmias

Short intraoperative & acute

Esmolol ______ half life of ______

ultra-short 9 minutes

Beta Blockers - Contraindicated • in > _____ degree heart block •_______ or _______ •Caution with _______

first CHF or cardiogenic shock calcium channel blockers

MECHANISM OF ACTION of beta blockers Binds and blocks Beta adrenergic receptors on the heart Inhibit PHASE ____ at _____

4; SA node

Class 2 drugs Decreased slope of ___________ Prolonged ________

phase 4 depolarization repolarization

Class 3- Amiodarone cardiac effects ______ channel blocking _______ channel blocking ______ channel blocking ____________ blocking

Sodium Potassium Calcium β- adrenoceptor

Class 3- Amiodarone Extracardiac effect Peripheral _______

vasodilation

Pharmacokinetics of amiodarone Given ______ (Slow or Fast?) onset of action (Short or Long?) half-life(_____).

orally Slow Long; 13-103 hrs

Pharmacokinetics of amiodarone Is highly lipo______ , is concentrated in many tissues. Eliminated by ______ mostly as (active or inactive ?) metabolites.

philic liver Active

Clinical uses of amiodarone Recurrent & refractory ventricular & supraventricular arrhythmias . Arrhythmias associated with ________. In maintaining sinus rhythm in patients with AF.

Wolff Parkinson syndrome

Adverse effects of amiodarone __________ discoloration & ______ . Corneal microdeposits leading ____,_____,_______ pulmonary ______

Gray- blue skin; photodermatitis corneal opacity ,optic neuritis, blindness fibrosis

Adverse effects of amiodarone hypo or hyperthyroidism Nausea & constipation Hepatic impairment _______ effects A-V block & bradycardia

neurological ISEOLUWA, just look at it, you are tired

Drug interactions of amiodarone __________ leading to _____ ______ leading to ____ toxicity _________ has an additive effect

Oral anticoagulant; bleeding Digoxin; digoxin β- blockers

Bretylium - Actions Class ____ ______ effects

3 Biphasic

Bretylium - Actions Class 3 Biphasic effects _________ effects last 20 minutes Then ____________ 45 to 60 minutes after administration

Norepinephrine release Blocks release of norepinephrine

Bretylium - Actions Class 3 Affects phase ____ (_____) prolongs refractoriness - (pro or anti?) fibrillatory

3; repolarization Anti

Sotalol Is used for the treatment of : _____________ arrhythmias. To maintain sinus rhythm in patients with _________.

Life- threatening ventricular atrial fibrillation

_______ is used For treatment of supra & ventricular arrhythmias in pediatric age group.

Sotalol

Specific ADVERSE EFFECTS of Amiodarone _______ discoloration _______ disorder _______ dysfunction

Gray-blue skin Corneal Thyroid

INDICATIONS of class 3 drugs??

All arrhythmias

Class IV Calcium channel blockers e.g. Verapamil, Diltiazem Their main site of action is ______ and ________ Effective only in _____ arrhythmias

A.V.N & S.A.N. atrial

Class IV Calcium channel blockers Second drugs of choice for the treatment of ______________

paroxysmal supraventricular tachycardia

Calcium channel blockers are effective in Wolff Parkinson White syndrome T/F

F Not effective in Wolff Parkinson White syndrome

Class IV Adverse effect Negative inotropic effect causes heart failure, AV block T/F

MECHANISM OF ACTION of class 4 drugs Binds and Blocks Calcium channels on the heart Inhibit •_________ •PHASE __ at ______ and _____

All PHASE 4 0 SA and AV node

Adenosine - Actions Negative Chronotropic effects on ___________ Blockade of the ______

SA and AV node AV node

Adenosine - Binds to specific __________ coupled adenosine receptors (____) leading to opening of ____ channel and hence ______.

G protein - A1&A2; K+ hyperpolarization

adenosine leads to a ____eased influx of calcium

Decr

Adenosine - Pharmacokinetics Very (slow or rapid?) onset of action . (Short or Long?) half- life (______) Given as a rapid _____ injection

Rapid Short; seconds IV Bolus

Adenosine - Pharmacokinetics For the acute termination of _____________ tachycardia ( paroxysmal attack) First choice.

re-entrant supraventricular

Drug Interactions of adenosine Less effective with adenosine receptor blockers (_______ or ________) More effective with uptake inhibitors as __________

Caffeine or theophylline dipyridamole

MECHANISM OF ACTION of Adenosine Inhibits PHASE ___ at ___________

0 SA and AV node

INDICATIONS of Adenosine _________________ tachycardia

Paroxysmal supraventricular

MECHANISM OF ACTION of Magnesium Direct: ________________ Indirect: _____________

Binds and blocks Na+, K+ ATPase pump Binds and blocks Calcium channel

MECHANISM OF ACTION of Magnesium Inhibits PHASE _______

4, 3 and 0

ADVERSE EFFECT of Magnesium _______ ____

Hypermagnesemia Hyperkalemia

_______ can be used to treat Torsade de pointes

Magnesium

Anti Arrythmics Flashcards

(139 cards)