Term
SA node
AV node
Bundle of His
Bundle branches
Purkinje fibers
involved in electrical impulse conduction, don't have as many contractile proteins but have a lot of ion channels |
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Definition
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Term
atrial and ventricular myocytes
cardiac myocytes, participate in pumping action
many contractile proteins but not as many ion channels |
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Definition
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Term
| originates in the sinoatrial (SA) node. The impulse is conducted through internodal fibers to the atrioventricular (AV) node and then through the bundle of His, bundle branches, and Purkinje fibers to the ventricular muscle. |
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Definition
| flow of electrical impulse through the heart |
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Term
P wave: atrial depolarization
QRS complex: ventricular depolarization
T wave: ventricular repolarization
PR interval: conduction time through the AV node
QT interval: time between ventricular depolarization and repolarization |
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Definition
| On an EKG, what does the P wave, QRS complex, T wave, PR interval, and QT interval represent? |
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Term
0: ventricular depolarization is caused by sodium influx through the fast sodium channel.
1: the membrane is transiently repolarized as a result of potassium eflux
2: the membrane potential is relatively stable because of the concurrent influx of calcium and efflux of potassium
3: repolarization is caused by continued potassium efflux as calcium influx declines
4: ion balance is returned to normal by the action of the sodium pump (Na/K/ATPase). Ca is removed from the cell by the Na/Ca exchanger and CaATPase |
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Definition
[image]
what does each phase represent? |
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Term
phase 0 (depolarization) is due to Ca influx instead of Na
in nodal tissue there is more abundant Ca channels |
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Definition
Why do the SA node and AV node have a rounder curve?
[image] |
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Term
1) alteration in slope of phase 4: NE stimulates opening of a greater number of pacemaker channels that leads to faster phase 4 depolarization. higher number of contractions in the same period of time
2) alteration in threshold potential: NE stimulates opening of a greater number of Ca channels and thereby shifts threshold potential to more negative potential. increases HR.
3) alteration in maximum diastolic potential: Ach makes the maximum diastolic potential more negative by increasing the probability of K channels opening, reduces the slope of phase 4, shifts threshold potential to more positive potential. decreases heart rate
[image] |
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Definition
| 3 ways heart rate can be regulated |
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Term
coronary ischemia and tissue hypoxia
electrolyte disturbances
overstimulation of the sympathetic nervous system
general anesthetics
drugs the perturb cardiac transmembrane potential |
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Definition
| pathophysiology of arrhythmias, causes |
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Term
altered automaticity is an abnormal impulse formation, it can be caused by any change that decreases the time required for depolarization from the maximal diastolic potential to the threshold potential. increased automaticity occurs if the rate of diastolic repolarization (the slope of phase 4) in the SA node or in latent pacemakers is increased. It also occurs if a shift of the threshold potential occurs to a more negative value or if a shift occurs of the maximum diastolic potential to a more positive value.
phase 4 slope: increased by sympathomimetic drugs and hypokalemia, decreased by Ach
threshold potential: Ca channel blockers make it less negative (takes longer to reach threshold)
maximum diastolic potential: Ach makes it more negative
duration of action potential: K channel blockers increase
[image] |
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Definition
| what can cause altered automaticity? |
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Term
triggered automaticity is an abnormal impulse formation
[image]
absolute refractory period: Na channel is inactivated and cannot be activated again (needs to go through resting phase)
early afterdepolarization or torsade de pointes: distinctive form of polymorphic ventricular tachycardia characterized by a gradual change in the amplitude and twisting of the QRS complexes around the isoelectric line. it is associated with a prolonged QT interval, which may be congenital or acquired. It usually terminates spontaneously but frequently recurs and may degenerate into ventricular fibrillation
drugs that cause EAD: class 1A drugs - quinidine, procainamide, disopyramide. Class III drugs - amiodarone, sotalol, dofetilide, ibutilide
drugs that cause DAD (tachycardia with AV block): digoxin
Drugs that cause DAD (ventricular tachycardia): increased sympathetic tone, myocardial ischemia/reentry |
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Definition
| causes of triggered automaticity |
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Term
| reentry of ventricular tissue - abnormal impulse conduction |
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Definition
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Term
AV node reentry - abnormal impulse conduction
most common electrophysiologic mechanism responsible for paroxysmal supraventricular tachycardia.
reentry occurs when a premature atrial depolarization arrives at the AV node and finds that one pathway (B) is still refractory from the previous depolarization. The other pathway (a) is able to conduct the impulse to the ventricle. Retrograde conduction of the impulse through pathway B leads to reentry of the atrium and results in tachycardia. In the AV node, the unidirectional block results from the B pathway's longer refractory period, which blocks anterograde conduction but permits retrograde conduction after it has recovered its excitability. |
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Definition
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Term
tissue damage by trauma, ischemia, or scarring
drug induced block (*digoxin*, *BB*, *verapamil*)
*conduction block can be manifested clinically as bradycardia* |
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Definition
| causes of conduction block |
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Term
Wolff-Parkinson-White syndrome: abnormal impulse conduction
[image]
atrioventricular re-entrant tachycardia: an accessory atrioventricular connection is present (light blue). A premature atrial impulse blocks the accessory pathway (1) and propagates slowly through the AV node and conducting system. On reaching the accessory pathway (by now no longer refractory), the impulse re-enters the atrium (2), where it can then re-enter the ventricle via the AV node and become self sustaining. |
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Definition
impulses originate at the SA node and preexcite peripheral conduction system and ventricular muscle via bundle of Kent without delay at AV node.
after normal delay at AV node, impulses also arrive at ventricles via normal route to continue depolarization.
P wave is immediately followed by short delta wave, producing slurred upstroke on wide QRS with short or no PR interval |
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Term
AV nodal blocking drugs that terminate this tachycardia (with caution will slow conduction through the AV node): Ca channel blockers, BB, digoxin
drugs that remove atrial premature beats
catheter ablation: removal of Bundle of Kent |
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Definition
| treatment for WPW syndrome |
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Term
sympathomimetic drugs: can increase automaticity of the SA node, AV node, or His-Purkinje fibers and thereby produce tachycarida
digitalis glycosides: sometimes evoke delayed afterpolarizations by increasing Ca influx into cardiac cells, they can also impair AV node conduction and cause AV block
Drugs that cause torsades de pointes: antiarrhythmic drugs (quinidine, sotalol), H1 antagonists (astemizole and terfenadine - removed from market due to cardiac side effects), psychotropic drugs (phenothiazides); these drugs prolong action potential by blocking K efflux |
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Definition
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Term
| disopyramide, procainamide, quinidine |
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Definition
| class 1A antiarrhythmic drugs |
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Term
| lidocaine, mexiletine, phenytoin |
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Definition
| Class 1B antiarrhythmic drugs |
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Term
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Definition
| Class 1C antiarrhythmic drugs |
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Term
| beta blockers: esmolol, metoprolol, propranolol |
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Definition
| Class II antiarrhythmic drugs |
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Term
| amiodarone, sotalol, dofetilide, ibutilide |
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Definition
| Class III antiarrhythmic drugs |
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Term
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Definition
| Class IV antiarrhythmic drugs |
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Term
| adenosine, magnesium sulfate, digoxin |
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Definition
| Class V antiarrhythmic drugs |
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Term
decrease automaticity in SA node: shift threshold to more positive potential, decrease slope of phase 4
decrease likelihood of reentry: decrease conduction velocity, increase refractory period (*1A*)
state dependent ion channel block: most Na channel blockers bind preferentially to the open and inactivated states of Na channel, not to the closed state of the channel (*ischemic tissue: depolarized for a longer period of time*)
[image]
[image]
dissociation rate of ion channel block: [image]
[image] |
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Definition
| mechanism of action of Class 1A antiarrhythmic agents |
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Term
quinidine, procainamide, disopyramide
a moderate block on Na channels
*preferentially bind to open Na channels*
recovery time moderate
decreases phase 0 upstroke velocity, which decreases conduction velocity through the myocardium
*also block K channels, increases refractory period*
prolonged repolarization of both SA nodal cells and ventricular myocytes
all the Class 1A drugs have some degree of anticholinergic effects (significant clinically because it can increase conduction velocity through the AV node) |
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Definition
| mechanism of action of Class 1A antiarrhythmic agents |
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Term
Class 1A antiarrhythmic drug
diarrhea: often responsible for discontinuation of its use
torsade de pointes: can cause syncope secondary to a reduction in CO and blood pressure
thrombocytopenia
cinchonism (higher doses): neurological symptoms including tinnitus, dizziness, and blurred vision
quinidine induced digoxin toxicity: ***increases serum levels of digoxin***
*atrial flutter = 300 bpm with 2:1 AV block, with quinidine = 200 bpm with 1:1 AV conduction, recommendation = use quinidine with BB or verapamil. (quinidine has actions on the AV node, it can permit more impulses to get through to the ventricles, use of BB or verapamil with quinidine will eliminate some of the impulses) |
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Definition
| adverse effects of quinidine |
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Term
Class 1A antiarrhythmic agent
long term use of procainamide often causes a syndrome that resembles *lupus erythematosus*, presents arthralgia and a butterfly rash on the face, but is reversible
this adverse effect is often responsible for discontinuation of the drug |
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Definition
| adverse effects of procainamide |
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Term
Class 1A antiarrhythmic agent
is administered orally to prevent *life threatening sustained ventricular tachycardia* (limited usage?)
is sometimes effective in patient who have not responded to other drugs
disopyramide has electrophysiological effects similar to those of quinidine
because it has greater *negative inotropic* and *anticholinergic* effects than other class 1A agents, is should be used with caution in patients with heart failure and in elderly patients |
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Definition
| mechanism of action of disopyramide |
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Term
lidocaine, mexiletine, phenytoin
preferentially binds to both open and inactivated Na channels (*I>O*)
fast dissociation from Na channels (Na channels recover quickly from Class 1B blockade)
recovery time is rapid
exhibit *use dependent block* - effective for ischemic cells (ischemic cells are usually in the open state) |
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Definition
| mechanism of action of Class 1B antiarrhythmic agents |
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Term
Class 1B antiarrhythmic agents
used most commonly to treat ventricular arrhythmias (***ventricular fibrillation and ventricular tachycardia***) in emergency situations associated with myocardial ischemia
a high serum concentration of lidocaine can cause CNS side effects such as confusion, dizziness, seizure
a drug that inhibits CYP450 enzymes (***cimetidine***) can precipitate lidocaine toxicity |
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Definition
| mechanism of action of lidocaine |
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Term
Class 1B antiarrhythmic agent
an analog of lidocaine metabolite
the primary indication for mexiletine is life threatening *ventricular tachycardia*
major adverse effects include dose related nausea and tremor |
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Definition
| mechanism of action of mexiletine |
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Term
Class 1B antiarrhythmic agent
usually considered an antiepileptic medication
effective in ventricular tachycardia in young children
also used to treat ventricular tachycardia after congenital heart surgery
has been used in the treatment of congenital prolonged QT syndrome when mono therapy with BB has failed
an inducer of hepatic enzymes (CYP450 3A4) |
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Definition
| mechanism of action of phenytoin |
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Term
flecainide, propafenone
preferentially binds to both open and inactivated Na channels (*I=O*)
recovery time prolonged
most potent Na channel blockers
has little or no effect on action potential
suppress premature ventricular contractions
prevent paroxysmal supraventricular tachycardia and atrial fibrillation
marked depressive effects on cardiac function |
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Definition
| mechanism of action of class 1C antiarrhythmic agents |
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Term
Class 1C antiarrhythmic agent
used to treat various atrial and ventricular arrhythmias
flacainide is no longer used to treat ventricular arrhythmias associated with myocardial infarction because it increased the mortality rate (Cardiac Arrhythmia Suppression Trail)
other adverse effects include bronchospasm, leukopenia, thrombocytopenia, seizures. |
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Definition
| mechanism of action of flecainide |
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Term
class 1C antiarrhythmic agent
used to treat various atrial and ventricular arrhythmias
has a potential to cause ventricular arrhythmias and several hematologic abnormalities, including agranulocytosis, anemia, and thrombocytopenia |
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Definition
| mechanism of action of propafenone |
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Term
esmolol, metoprolol, propranolol
decrease automaticity by decreasing the slope of phase 4
decreases the incidence of reentry by slowing electrical conduction at the AV node
the AV node is more sensitive than the SA node to the effects of BB
the most frequently used agents in the treatment of supraventricular and ventricular arrhythmias *precipitated by sympathetic stimulation* |
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Definition
| mechanism of action of Class II antiarrhythmic agents |
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Term
block K channels
prolong action potential duration
decrease the incidence of reentry by increasing the effective refractory period
Class III antiarrhythmic agents increase the likelihood of developingearly afterdepolarization and torsade de pointes |
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Definition
| mechanism of action of Class III antiarrhythmic agents |
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Term
Class III antiarrhythmic agent
also acts as a class I, class II, and class IV antiarrhythmic
alters the lipid membrane in which ion channels and receptors are located
decreases reentry by prolonging the action potential duration
decreases the rate of firing in pacemaker cells as a class I agent
exert class II antiarrhythmic activity by noncompetitively antagonizing B-adrenergic receptors
can cause significant AV nodal block and bradycardia
used to treat atrial fibrillations |
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Definition
| mechanism of action of amiodarone |
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Term
adverse cardiovascular effects: hypotension, AV block, various arrhythmias
other adverse effects: blue-gray skin discoloration, thyroid abnormalities, fatal pulmonary fibrosis
it can also cause corneal deposits, blurred vision, photosensitivity, and GI disturbances
amiodarone inhibits the metabolism of other drugs: digoxin, flecaininde, phenytoin, procainamide, warfarin |
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Definition
| adverse effects and interactions of amiodarone |
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Term
Class III antiarrhythmic agent
used to terminate *atrial fibrillation and atrial flutter*
the major adverse effects of these drugs are torsade de pointes, which may require electric cardioversion |
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Definition
| mechanism of action of ibutilide and dofetilide |
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Term
a mixed class II and class III antiarrhythmic agent
used to treat severe ventricular arrhythmias, especially in patients who cannot tolerate the side effects of amiodarone
also used to prevent recurrent atrial flutter and fibrillation
can cause fatigue and bradycardia
can induce torsade de pointes |
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Definition
| mechanism of action of sotalol |
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Term
block cardiac Ca channels
act preferentially on AV and SA nodal tissues
the major therapeutic actions of class IV antiarrhythmics is to slow the action potential upstroke in AV nodal cells, leading to slowed conduction velocity through the AV node
used to treat re-entrant paroxysmal supraventricular tachycardia that involves the AV node |
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Definition
| mechanism of action of Class IV antiarrhythmic agents |
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