Block 2-Reymann (Anti-arrhythmic) Flashcards
1
Q
Classes of drugs
A
- Fast channel blockers (Na+): Quinidine, Lidocaine, Flecainide
- Beta-adrenoceptor blockers (Ca+2): Propranolol, atenolol, esmolol, sotalol
- Inhibitors of repolar (K+): Amiodarone, Bretylium, dofetilide
- CCB: Verapamil & Dilitiazem
- Unclassified: Adenosine, Atropine, Digoxin, & Mg+2
2
Q
Mechanism of Arrhythmias
A
- Main promoting factors:
- Ischemia-Hypoxia (<strong>Delayed Afterdepolar</strong>)
- Acidosis, alkalosis, electrolyte imbalance
- Excessive autonomic input (catecholamine exposure)
- Drug toxicity (Digitalis)-Delayed afterdepolar
- Overstretching of cardiac fibers
- Scarred or functionally impaired tissue
- ALL occur from:
- Disturbances in impulse formation or conduction
- Or combo of both
3
Q
Examples of Arrhythmias
A
- Premature Vent beat = 1 or 2 Depressed QRS out of normal Ekg
- PSVT(parox suprevent tachy) = Equally spaced sinus rhythm Pwaves & QRS peak are close together
- Atrial Fib = NO sinus <u><strong>(IRREG/IRREG BEAT)</strong></u>
- Atrial flutter (AV block/2nd degree) = Depressed P wave w/small QRS peak
- Atrial flutter w/1:1 Av conduction = Pwave connected to QRS
- Monomorphic vent tachy = All QRS wave pointing down
- Torsades de pointed (Bradycardia) = Irregular P wave & QRS w/splits
- Vent fib = Death
4
Q
Therapy of Cardiac Arrhythmias
A
- Eliminate or minimize precipitating factors
- Define type of arrhythmia(suprevent or vent)
- Most ANTI-arrhythmic drugs can cause arrhythmias-Minimize risks of combined DRUG therapy
- Termination of ongoing arrhythmias
- Prevention of recurrent arrhythmias (could LEAD to death)
5
Q
Class 1 (Fast Na+)
A
- Subclasses:
- 1A = prolonged (quinidine, procainamide, disopyramide)
- 1B = Accelerated (lidocaine, mexlietine, tocainide)
- 1C = little effect (Flencainide, Propafenone)
- Mech:
- recovery of Na+ channel is Voltage-dependent
- Na+ channel blocker delays recovery=Prolonged ERP
- Shifts voltage-response relationship
6
Q
Class 1A quinidine PK & PD
A
- Anti-malaria drug & isomer of quinine
- PK:
- Oral , IV & 1/2 life 1 hour
- Hepatic metab, 20% unchanged in renal excretion
- Digitalis interaction
- PD:
- Blockade of Na+ channels in activated site=<u><strong>Reduction in Vmax PHASE 0</strong></u>
- Blockade of K+channels=<u><strong>Prolonged AP</strong></u>
- Antimuscarinergic effect (@ low doses)=<u><strong>Increase in AV-conduction </strong></u>(death)
- Alpha blocker activity @ high conc
7
Q
Class 1A quinidine Use & EKG
A
- Use:
- Treat paroxysmal supravent tachy
- Conversion of Atrial flutter or fib to Sinus rhythm (Second line treatment)
- Need to use prior digitalization=Protective block (3:1)
- Recovery from block is slower & less complete in depolarized cell than in FULLY polarized tissue
- Result: Prolongation of refractory period in depolarize tissue
- Blockade of K+=Prolongation of AP, ERP & reduction of MAX re-entry
- EKG=
- Long QRS <u><strong>(delayed cond in Punkinje & HIS)</strong></u>
- Long QT & alterations in T
- Variable PR <u><strong>(slow AV-conduction)</strong></u>
8
Q
Class 1A quinidine (SE)
A
- SE:
- Paradoxical-Increase in sinus & AV conduction due to ANTI-muscar (atropine)-
- Removal of protective AV-block
- Vent tachy (3:1, 2:1, 1:1 AV)
- Torsades- polymorphic Vent tachy (quinidine syncope)
- Slowing of conduction-QRS prolongation greater than 30-50% indicates toxicity
- Extracardiac effects:
- Antimalarial activity
- Hypotensive due to Alphablocker
- Can cause GI issues
- CNS Tinnitis in high doses
9
Q
Procainamide Class 1A
A
- Protected from enzymatic hydrolysis-LESS CNS effects
- PK:
- Oral & IV (arrythemia & hypotension)
- Hepatic metab, Variable rate of acetylation of NAPA
- PD: LIKE QUINIDINE
- Less muscarinergic than quinidine
- SE: LIKE QUINIDINE
- CNS can lead to psychosis
- Much more hypersensitivity - fever, rashes, arthritis, lupus like (ANA)
- USE:
- same as quinidine
- Sustained Vent arrhythmias w/Acute MIs
10
Q
Lidocaine Class 1B
A
- Amide local anaesthetic
- PK:
- Only IV binds to alpha1acid-glycoprotein
- PD:
- Blockade of activated & inactivated Na channels= MORE prounounced effect on tissues w/long plateus (punkje & vent)
- Little to NO effect on K+ channels-<strong>shortening of APD</strong>
- Main effect on depolarized, <strong>Arrhythmogenic tissue</strong>
- SE:
- Cardiac exacerbation of arrhythmias less than 10%
- CNS tremor, paresthesias in TOXIC lvls coma or convulsions
- Interactions: Agents that interfere w/hepatic perfusion or hepatic microsomal metab
11
Q
Lidocaine Class 1B Uses
A
- Drug of choice in _supression of VENT tachy & Afib _
- Supression of arrhythmia associated w/Depolarization (<u><strong>POST MI & Digitalis Toxicity)</strong></u>
- Rx: IV loading dose 100-200mg
- Monitor plasma lvls
- Not for chronic use POST MI
12
Q
Mexiletine & Phenyioin Class 1B
A
- Mex orally active version of lidocaine
- PK: Oral 1/2 life of 8-20 hours
- PD: same as lidocaine
- SE: happens with frequent dosing
- Neurologic-nausea, tremor, lethargy
- Allergies-rash, fever, Agranulocytosis <u><strong>(Low WBC @ Bone marrow)</strong></u>
- _Phenytoin antiepileptic drug _
- PK: IV 1/2 less than 17 hrs
- PD: same as lidocaine
- _SE: _
- Neurologic-sedation, double vision, vertigo
- Gingival hyperplasia <u><strong>(swollen gums)</strong></u>
13
Q
Flecainide & Propafenone Class 1C
A
- Very SLOW dissociation from Na channel DURING recovery.
- Used in life threatening-refactory arrhythmia ONLY
- Flecainide=Increased Mortality rate in POST-MI pts treated for premature Vent contractions
- Use only oral for atrial arrhythmias
14
Q
Beta-Blockers Class 2
A
- _Anti-arrhythmic properties due Beta-blockade _
- Propranolol <u><strong>(non-selective)</strong></u>
- Atenolol<u><strong> (B1)</strong></u>
- Esmolol<u><strong> (SHORT acting 1/2 life 9min)</strong></u>
- Sotalol <u><strong>(non-selective & K+ channel blocker)</strong></u>
- Cardio effects:
- Depress SA-node = sinus bradycardia
- Depresses auto of punkenje fibers
- Prolongs ERP of AV node
- SUPPRESSES ectopic vent depolar
- (-) ionotrope
15
Q
Beta-Blockers Class 2 (Propranolol)
A
- Cardio SE:
- Hypotension
- Aggravation of CHF
- Asystolia <u><strong>(weakening of contraction/SYSTOLE)</strong></u>
- Extracardiac SE:
- Predisposed Asthma & diabetes
- Peripheral occulsive disease
- Use:
- Decrease risk of sudden death in <u><strong>POST MI</strong></u>
- Control of supravent tachy
- Exercise or stress induced <u><strong>Vent arrhythmias</strong></u>
- Ischemic heart disease <u><strong>(agina)</strong></u>