Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
122 Cards in this Set
- Front
- Back
|
how can the build up of toxic metabolites during an MI lead to an arrhythmia?
|
it leads to abnormal ion concentrations due to membrane leaks; ultimately ischemic tissue is depolarized with less negative diastolic membrane potential which facilitates generation of spontaneous ectopic impulses and slows conduction
|
|
|
what is the principle current during phase 4 and what does it determine?
|
potassium current; determines the resting membrane potential of the myocyte
|
|
|
what results in the rapid upstroke of phase 0?
|
Na+ influx
|
|
|
what is responsible for the partial repolarization during phase 1?
|
transient outward potassium current
|
|
|
what results in the plateau of phase 2?
|
slow Ca++ influx and relatively low K+ efflux
|
|
|
what results in the rapid repolarization of phase 3?
|
K+ efflux
|
|
|
what causes the slow depolarization of phase 4 in pacemaker cells?
|
pacemaker currents through slow Na+ channels
Ca++ and K+ currents also contribute |
|
|
what causes the upstroke of the AP in phase 0 in pacemaker cells
|
slow inward Ca++ currents
|
|
|
what is responsible for the repolarization of phase 3?
|
inactivation of calcium channels and K+ efflux through potassium channels
|
|
|
what does the effective refractory period comprise in the myocyte?
|
phase 0, 1, 2, and the initial part of phase 3
|
|
|
What is the P wave?
|
how long atrial depolarization takes
|
|
|
what is the PR interval?
|
how long it takes an action potential to travel through the atria to the AV node
|
|
|
what is the QRS duration?
|
how long it takes for the wave of depolarization to spread through the ventricles
|
|
|
what is the QT interval
|
how long it took the action potential to depolarize and repolarize the ventricles
|
|
|
which segment of the EKG will shorten with increased HR?
|
QT interval
|
|
|
What is a 1st degree AV conduction block?
|
when the normal delay between atrial and ventricular depolarization is lengthened. The AV node still conducts all impulses but does so slower than normal
|
|
|
EKG in 1st degree AV block
|
P wave:QRS complex ratio is preserved
|
|
|
what is a 2nd degree AV conduction block?
|
intermittent failure of AV conduction resulting in some P waves not being followed by a QRS complex
|
|
|
what is a 3rd degree AV conduction block?
|
complete failure of conduction between atria and ventricles
|
|
|
EKG in a 3rd degree AV block
|
no relationship between P waves and QRS complex
|
|
|
3 requirements of reentry
|
1) a closed conduction loop
2) a region of unidirectional block 3) sufficiently slow conduction of action potentials around the loop |
|
|
two step process of drug therapy for atrial flutter/fibrillation
|
1) slow ventricular rate with drugs that increase the AV block (beta blockers, calcium channel blockers, digoxin)
2) restore the sinus rhythm with drugs that slow conduction or prolong the refractory period of the atrial myocardium (class IA, IC, III); these drugs may be administered chronically to prevent recurrences |
|
|
What is the rapid treatment for AVNRT?
|
IV adenosine to impair AV nodal conduction
|
|
|
What does AVNRT stand for?
|
AV nodal reentrant tachycardia
|
|
|
what is the treatment for patients with frequent AVNRT symptoms?
|
oral beta blockers, calcium channel blockers, digoxin
|
|
|
3 drugs that are contraindicated in WPW and why
|
digitalis, calcium channel blockers, and beta blockers
these drugs block the AV node which precipitates conduction through the accessory pathway |
|
|
drug therapy in WPW
|
Na channel blockers (class IA, IC, III) which can slow conduction and prolong the refractory period of the accessory pathway as well as the AV node
|
|
|
treatment of sinus bradycardia
|
treat with IV anti-cholinergics (atropoine) or beta-adrenergic agonists to transiently increase HR
|
|
|
definition of sick sinus syndrome
|
intrinsic SA node dysfunction that causes period of inappropriate bradycardia which can be followed by SVTs in elderly patients
|
|
|
treatment of sick sinus syndrome
|
requires a combination of antiarrhythmic drugs to suppress the tachyarrythmias plus a permanent pacemake to prevent bradycardia
|
|
|
definition of escape rhythms
|
arise when the SA node is impaired and the AV node or bundle of his has to take over
|
|
|
what is junctional escape rhythm?
|
40-60bpm
beats arise from the AV node or proximal bundle of his; QRS complexes are not preceded by P waves |
|
|
what is ventricular escape rhythm?
|
30-40bpm
ventricles are no depolarized by the normal, rapid, simultaneous conduction over the right and left bundle branches but from a more distal point in the conduction system; wide QRS complexes |
|
|
definition of a triggered rhythm
|
depolarization-dependent automaticity
under certain conditions, an AP can trigger abnormal depolarization that results in extra heart beats or rapid arrhythmias |
|
|
APs in triggered rhythms
|
stimulated by a preceeding action potential
the first AP leads to oscillations of membrane voltage known as after depolarizations |
|
|
what causes EAD?
|
an in crease in the frequency or abortive action potential before normal repolarization is completed, i.e. when ventricular AP duration is prolonged
may be inherited or due to drug therapy |
|
|
what causes EAD in phase 2
|
augmented opening of calcium channels
|
|
|
what causes EAD in phase 3
|
opening of sodium channels
|
|
|
why is EAD bad?
|
eventually the outward K current restores the Vm to resting membrane potential, but if the EAD is large enough it can trigger a "run" in extrasystoles (ventricular beats) that can devolve into a torsades and lethal Vfib
|
|
|
torsades
|
caused by a prolonged QT interval and can degenerate into Vfib
|
|
|
what is a DAD
|
an abnormal depolarization that occurs during phase 4, after repolarization is completed but before another action potential would normally occur
|
|
|
what causes a DAD
|
elevated cytosolic calcium overloads the SR leading to spontaneous Ca release during repolarization
Ca is then released from the cell through the 3Na/Ca exchanger resulting in a net depolarizing current |
|
|
MOA of class I drugs
|
sodium channel blockers
decrease phase 0 upstroke velocity which in turn decreases conduction velocity in ventricular myocytes; in pacemaker cells, the threshold is increased which thus decreases the phase 4 slope and the rate of firing |
|
|
what are class I drugs used to treat?
|
arrhythmias that result in tachycardia
|
|
|
MOA of Class IA
|
prolongs AP duration thus prolonging repolarization and increasing the ERF
|
|
|
How can the exacerbating effects of hyperkalemia on IA drugs be reversed?
|
sodium lactate IV
increase the sodium current by increasing ionic gradient; reduces drug receptor binding by alkalinizing the tissue |
|
|
what type of drug is Quinidine?
|
Class IA
|
|
|
MOA of quinidine
|
derived from cinchona bark
anticholinergic properties allow it to augment conduction at the AV node which then antagonizes and directly suppresses it; usually want to combine with beta blockers |
|
|
route of administration of Quinidine
|
usually orally
|
|
|
where is qunidine metabolized?
|
in the liver; thus reduce dose in hepatic patients
|
|
|
side effects of quinidine (5)
|
digoxin toxicity (quinidine reduces the clearance of digoxin)
nausea, diarrhea Cinchonism (deafness, tinnitus, blurred vision) Quinidine syncope (due to ventricular arrythmias associated with a prolonged QT interval - can precipitate torsades) thrombocytopenic purpura |
|
|
what type of drug is procainamide?
|
Class IA
|
|
|
MOA of procainimide
|
anticholinergic properties at the AV node but does not prolong the AP duration like quinidine (thus does not precipitate torsades)
|
|
|
route of procainimide administration
|
given orally, well absorbed
|
|
|
where is procainimide metabolized
|
50% is excreted unchanged in the urine, the rest is acetylated in the liver
thus adjust dosage in renal patients |
|
|
side effects of procainimide (5)
|
high incidence with chronic use
lupus like symptoms (reversible) hypotension depression hallucination psychosis |
|
|
what type of drug is dispyramide?
|
class IA
|
|
|
what is dispyramide used to treat?
|
reserved for treatment of ventricular arrhythmias due to quinidine or procainamide
|
|
|
MOA of dispyramide
|
prolongs the QT interval thus contraindicated in long QT syndrome
|
|
|
side effects of dispyramide (5)
|
pronounced antimuscarinic effects:
dry mouth blurred vision urine retention precipitates glaucoma can worsen heart block and adversely affect sinus node activity |
|
|
MOA of class IB drugs
|
mild Na+ channel block which shortens AP duration
preferentially blocks the Na channels that are open or in active configuration thus precipitating repolarization and shortetning the AP rate of dissociation from sodium channel is fast so it does not affect normal conduction |
|
|
what type of drug is lidocaine?
|
Class IB
|
|
|
what is lidocaine used for?
|
used to suppress ventricular arrhythmias in hospitalized patients
drug of choice to terminate digitalis induced arrhythmias and arrhythmias in the ER after amiodaorne |
|
|
how is lidocaine administered
|
IV
rapid distribution means it must be given as a continuous infusion |
|
|
what type of drug is mexilitine?
|
class IB
|
|
|
what is mexilitine used for?
|
similar to lidocaine, used to suppress ventricular arrhythmias but can be given orally
|
|
|
what can make mexiliitine more effective?
|
co-administration with beta-blockers; allows for dose reduction in each drug
|
|
|
where is mexilitine metabolized?
|
90% in the liver, so lower the dosage in liver patients
|
|
|
What type of side effects are common in mexilitine?
|
CNS side effects
|
|
|
Class IB drugs (2)
|
lidocaine
mexilitine |
|
|
class IA drugs (3)
|
quinidine
procainamide dispyramide |
|
|
Class IC MOA
|
slows phase 0 and conduction velocity in atria, ventricles, and purkinje fibers; significantly prolongs the refractory period within the AV node and accessory tracts
|
|
|
what are class IC drugs used to treat?
|
both atrial fibrillation and paroxysmal SVT
reserved for refractory ventricular tachycardias that tend to progress to Vfib because these drug are very proarrhythmic |
|
|
side effects of class IC drugs (4)
|
very proarrhythmic (increased mortality in patients with underlying pathologies; should not be given as a prophylactic in MI survivors)
negative ionotropic effect can aggravate CHF CNS effects (dizziness, blurred vision, headached, nausea) however, beneficial and reasonable safe to treat SVTs in patients with normal hearts |
|
|
Class IC drugs(4)
|
flecainide
encainide propafenone moricizine |
|
|
what type of drug is flecainide?
|
class IC
|
|
|
what type of drug is encainide?
|
class IC
|
|
|
what type of drug is propafenone?
|
class IC
|
|
|
what type of drug is moricizine?
|
class IC
|
|
|
Class II drugs MOA
|
beta blockers
decrease phase 4 slope in pacemaker cells results in a decreased rate of firing and automaticity; prolongation of AV node repolarization increases ERF and reduces reentry |
|
|
Use of class II drugs
|
suppresses tachyarrhythmias induced by excessive sympathetic activation
frequently used to slow ventricular rate in atrial flutter and fibrillation by impairing conduction and increasing refractories of AV node terminates AV nodal reentrant SVT terminates ventricular arrhythmias related to prolonged QT interval |
|
|
Class II drugs are a first line treatment for...
|
suppressing arrythmias in patients with a previous MI
|
|
|
side effects of class II drugs (5)
|
excessive bradycardia
bronchospasms (careful in asthma patients; switch to beta 1 selective) depression fatigue masks the symptoms of hypoglycemia |
|
|
what type of drug is esmolol?
|
class II
|
|
|
what type of drug is propranolol?
|
class II
|
|
|
what type of drug is metorprolol?
|
class II
|
|
|
what is esmolol used for?
|
very short acting beta blocker given via IV; used exclusively in acute arrhythmias
|
|
|
class II drugs (3)
|
esmolol
propranolol metropolol |
|
|
MOA of class III drugs
|
potassium channel blockers
increases ERF which decreaes reentry |
|
|
What type of drug is amiodarone?
|
class III
|
|
|
MOA of amiodarone
|
decreases conduction velocity which decreases reentry
decreases rate of firing which decreasing automaticity decreases sinus node firing rate , automaticity, interrupts reentrant circuits prolongs PR, QRS, and QT interval powerful antiarrhythmic |
|
|
what is amiodarone a first line treatment for?
|
emergency treatment of ventricular arrhythmias during cardiac resuscitation
more effective than lidocaine |
|
|
administration of amiodarone
|
when given orally, it is absorbed slowly through the GI tract
can be given IV in emergent situations |
|
|
Clinical relevance of 1/2 life of amiodarone
|
highly lipophilic; extensively sequestered in tissues
long and variable 1/2 life (25-60 days) means effects may last for weeks or months after the drug is discontinued |
|
|
excretion of amiodarone
|
via biliary tract, lacrimal glands, and skin
thus can be given to patients with reduced renal function |
|
|
side effects of amiodarone (6)
|
thyroid abnormalities because it contains iodine and is structurally similar to thyroxine
photo-sensitive skin rashes slate-grey/bluish skin pulmonary fibrosis (onset is slow but irreversible) corneal micro deposits GI side effects Thus, regular EKG, thyroid and liver function tests, chest radiographs, and PFTs are a must with chronic therapy |
|
|
contraindications of amiodarone
|
do not combine with other drugs that prolong the QT interval or other antiarrhythmics
|
|
|
what type of drug is sotolol
|
class III
|
|
|
MOA of sotolol
|
also non-selective beat blocker
like amiodarone it can prolong the QT interval but lacks other side effects of amiodarone |
|
|
side effects of sotolol
|
dyspnea
dizziness torsades |
|
|
excretion of sotolol
|
renal; careful with renal patients
|
|
|
what type of drug is ibutilide?
|
class III
|
|
|
what type of drug is dofetilide?
|
class III
|
|
|
what type of drug is bretylium?
|
class IIII
|
|
|
Class III drugs (5)
|
amiodarone
sotolol ibutilide dofetilide bretylium |
|
|
Class IV drugs MOA
|
calcium channel blockers
slows conduction in the AV node and phase 4 depolarization reduces spontaneous depolarization PR interval increased contractility is decreased most potent in tissues in which AP depends on calcium currents |
|
|
clincal uses of class IV drugs
|
slowing of HR
slows transmission of rapid atrial impulses to ventricles (thus used in atrial flutter and fibrillation) terminates AV nodal reentrant arrhythmias |
|
|
side effects of class IV drugs (4)
|
limited use in ischemic hearts because of its negative ionotropic effects
causes AV block when given in large doses or in patients with partial block peripheral vasodilation and reflex tachycardia at high doses adverse cardiac effects are exacerbated when taken along with beta blockers |
|
|
what type of drug is verapamil?
|
class IV
|
|
|
what type of drug is diltiazem?
|
class IV
|
|
|
class IV drugs (2)
|
verapamil
diltiazem |
|
|
MOA of adenosine
|
agonists at A1 adenosine receptors in SA node, AV node, and atria which leads to opening of K channels and hyperpolarization, thereby decreasing automaticity
also inhibits adenylate cyclase and subsequently reduces active protein kinases which decrease pacemaker and Ca currents. this results in decreased automaticity and conduction through the AV node |
|
|
clinical use of adenosine
|
drug of choice to terminate acute SVTs, especially in AVNRT
|
|
|
advantages of adenosine (3)
|
lower toxicity than class IV
not orally active but effective in IV ultra-short acting and can be administered several times without side effects |
|
|
side effects of adenosine (4)
|
flushing
hypotension chest pain dyspnea |
|
|
digitalis MOA
|
creates a positive ionotrpoic effect
|
|
|
drugs to treat atrial flutter (2-3)
|
propranolol (class II)
verapamil (class IV) digoxin (sometimes) |
|
|
drugs to treat Afib (3)
|
propranolol (class II)
amiodarone (class III) beta blockers are the drug of choice because they decrease HR and promote conversion to sinus rhythm anticoagulants are used to reduce the risk of stroke |
|
|
drugs to treat AV nodal reentry (2-3)
|
proprnolol (class II) - slows conduction through AV node
verapamil (class IV) - slows conduction through AV node digoxin (sometimes) |
|
|
drugs to treat acute SVT (1-2)
|
adenosine
verapamil (sometimes) |
|
|
drugs to treat acute ventricular tachycardia (common cause of death in MI patients because CO is impaired) (2)
|
lidocaine (class I)
amiodarone (class III) |
|
|
drugs to treat Vfib in patients not responding to cardioversion (2-3)
|
amiodarone (class III)
epinephrine lidocaine (sometimes) |
