E1: AntiARRhythMICS Flashcards
What are the three sources of a cardiac arrhythmia?
disease, injury, or DRUGS
normal contractions at a faster rate
Tachycardia
all areas may not follow normally (can affect atria or ventricles);
flutters
uncoordinated contractions
fibrillations
normal contractions at a slower rate
bradycardia
complete _______ = His Purkinje system cut in half; therefore atria and ventricles work independently
HEART BLOCK
5 transmembrane phases! Plateau where net influx of Ca+ through Ca+ channels is slightly more than the efflux of K+ channels
Phase 2
5 transmembrane phases! early, partial repolarization through the efflux of K+ ions
Phase 1
5 transmembrane phases! restoration of ionic concentrations via the Na+K+ and the Na+Ca+ exchange pump = resting membrane potential is reestablished (-90 mV)
Phase 4
5 transmembrane phases! predominant efflux of K+ ions
Phase 3
5 transmembrane phases! influx of Na+ ions through fast channels to generate the upstroke (depolarization)
Phase 0
5 transmembrane phases! absolute (effective) refractory period = Phases ___,___,___, & most of ____.
0,1,2,most of 3
5 transmembrane phases! Middle of phase 3 to beginning of phase 4 =
relative refractory period
synonymous with DEPOLARIZAITON…a mechanism that PROTECTS the heart from all other ectopic impulses
ABSOLUTE refractory period
The time when only a strong stimulus can cause depolarization…Occurs when repolarization is almost complete
Relative Refractory period
All cells are repolarized and ready to respond in a normal fashion
Nonrefractory phase
In the __________ period all fast Na+-channels are voltage-inactivated and closed, which prevents sustained tetanus.
absolute refractory
What are the 3 areas of the heart with pacemaker activity?
SA node, AV node, Purkinje Fibers
What drives automaticity?
Spontaneous opening and closing of K+ channels.
The further away from _______ that the cell is maintained, the harder it will be to get the cell to depolarize
resting and threshold membrane potentials
Effective Refractory Period (absolute refractory period) in cells in _______ areas is longer than in _______ cells
pacemaker…myocardial
Myocardial cells repolarize quickly and have to wait for the pacemakers to repolarize before firing again
Myocardial….pacemakers
*different arrhythmias require that the _________ be lengthened or shortened
Effective/Absolute Resting Potential
Yes, I am going to do this to you. GET SOME! What are the 5 indications for Antiarrhythmias? WHATS THE MOST COMMON????
1.Paroxysmal ATRIAL tachycardia, 2.Paroxysmal VENTRICULAR tachycardia, 3.Atrial fibrillation (A FIB IS MOST COMMON), 4.Ventricular ectopic arrhythmias, 5.Digoxin-induced arrhythmias…GOOD JOB DAWG!
What are the 4 Contraindications for Antiarrhythmics?
- Complete A-V heart block 2.Congestive heart failure 3. Hypotension 4.Known hypersensitivity to the drug
IA: Na+ channel blocker (_______): Blocks conduction; ______ duration of AP
medium…. prolongs
IB: Na+ channel blocker (____): Blocks conduction; _______ ERP; _______ the AP
fast… decreases…shortens
IC: Na+ channel blocker (_____): Blocks conduction; _____ effect on ERP; _____ conduction without affecting the ____
slow….little…slows…AP
II: Beta blocker: ________ SA node automaticity; reduces _______ activity
Decreases…SYMpathetic
III: K+ channel blocker: ______ the AP; prolongs phase ___ repolarization
Prolongs…3
IV: Ca+ channel blocker: Slows conduction velocity at the ______; ______ firing rate of SA and AV nodes
AV node… decreases
What are the 3 methods of Class I Na+ blocking antiarrythmic drugs?
1.Decrease Excitability 2.Decrease conduction velocity 3.Prolong effective refractory period
Class IA: slow ______, prolong ____, increase _____
conduction, AP, ERP
Class IA: _______ = toxic; can produce fatal arrhythmias
– Made from bark of CINCHONA tree = overdose leads to cinchonism
QIUN-iD-ine
Class IA: _________ after cardioversion to maintain normal rhythm
Prophylaxis
Class IA: Site of action: _______
Atrial tissues
Class IA: ________-Derivative of the local anesthetic _______…Many adverse effects = reversible _____-like
syndrome in 25% of patients
Procain-amide…..procaine…LUPUS-like
Class IA: Used for treatment of VENTRICULAR arrhythmias, as an ALTERNATIVE to quinine and procainamide
DIS-o-pyramide (NorPACE)
Class IB: decrease duration of AP by ________/________ repolarization (ERP) = ________ rate so overcome ventricular ectopic foci…WHAT IS THE DRUG OF CHOICE? (Treats _______ arrythmias)
shortening/decreasing….speeds up…LIDOCAINE…(treats ventricular arrythmias)
Which Class IB drug would I give during an MI?
LIDOCAINE
Where do Class IB’s act?
the ventricles!
Class IB drug: anticonvulsant/antiarrhythmic….Prolongs ERP and suppresses ventricular pacemaker automaticity; shortens action potential in the heart… **remember this drug causes gingival hyperplasia
Phenytion (Dilantin)
Which Class IB drug? Structurally related to lidocaine….Serious ventricular arrhythmias; suppression of PVCs
mex-il-et-ine (mexico! woo!)
Which class IB drug? Suppression of life-threatening ventricular arrhythmias
TO-cain-ide
Class Ic-MARKED conduction _______…site of action=_____
slowing!…ventricles
What are the names of these Class IC badasses? Approved only for use of refractory ventricular arrhythmias (life-threatening)…Serious safety concerns: Cause arrhythmias because of profound effect on Na+ channels in healthy heart tissue as well…think Tamborine Rhythm!
FLE-CAIN-ide (TAMBocor)…PRO-paf-en-one(RYTHMol)
Approved only for use of refractory ventricular arrhythmias (life-threatening)
Class IC Antiarrythmias
Beta Blockers are ALSO considered Class ____ antiarrythmics!
II
What channel type do Class III antiarrythmics block? What effect does this have on the AP? On the heart in general?
Potassium Channel Blockers! Prolongs the AP (longer Ref Period)..Slows Heart
What are our two examples of Class III antiarrythmics? (one Dr. S made us say out loud and together)
- AMI-O-DaR-ONE 2.Sot-A-LOL(nonselective beta blocker)
Which drug has IODINE and therefore long term use causes BLUE SKIN & thyroid disease?
AMI-O-DaR-ONE….do, dare,dedi,datum-to give iodine=”io-dar” :) LATIN!!!
Class IV Antiarrythmics are Ca2+ channel blockers have a ________ CHRONOtropic effect and a ________ INOtropic effect on the heart.
negative…negative
WHAT IS THE DRUG OF CHOICE FOR CARDIAC ARRYTMIAS???? What is a side effect? Think real hard about what type of drug it is…
VERA-PAM-IL..ca2+ blocker-GINGIVAL HYPERPLASIA!
What is a good Diagnostic drug for arrhythmias? (Class IV)
Adenosine
This CROSSOVER drug is indicated for A-fib, flutter, & congestive heart failure….(a class IV antiarrythmic)
DIG-OX-IN
DigOXin-Increases ERP
– ______ conduction velocity
– _______ inotropic effect…Which one helps with congestive heart failure?
Decreases… Positive (more force)(helps with congestive heart failure)
Treating the Tom BradyArrythmias: what brady drug can also be used to SLOW DOWN salivation for a dental procedure?!
AtroPine!
Treating the Tom BradyArrythmias: What tis the name of the BETA (1&2) AGONIST that is synthetic Epinephrine?
Iso-Pro-Ter-On-oL
What two minerals can we use to treat Ectopic Pacemakers?
Potassium & Magnesium (Mg) haha
What is a good sign of CinChonism? (a side affect of the Class 1A antiarrythmic Quinidine)
TINNITUS!
Drug Interactions with Antiarrhythmics: The vagal blocking effects of antiarrhythmic drugs and anticholinergics (e.g. atropine) can act synergistically and lead to _______
tachycardia
Drug Interactions with Antiarrhythmics: Therapeutic effects of antiarrhythmics are increased by _______ (and reduced in hypokalemia)
potassium
Saliva-inhibiting drugs should not be administered to a patient who is prone to arrhythmias, as they may cause _______…e.g. _______
tachycardia….atropine
Lidocaine solutions used to treat arrhythmias are not the same as dental anesthetics that contain lidocaine = no epinephrine and different _______ = not interchangeable
buffering
Gingival hyperplasia may be seen with _______ drugs… Dr. Taylor St. Vincent clinic..
Ca+channel blocker
