Arrhythmias: Action potential, ECG, and antiarrhythmics Flashcards
What is automaticity, what is excitability, conductivity
Ability of a cell to initiate an electrical impulse, ability of cell to respond to electrical stimuli, ability of cells to receive and transmit an electrical impulse between adjacent cells
What is ectopy, what is the normal conduction system
Situation in which an electrical impulse is generated outside of the normal conduction system, SA node
What is the normal heart rate produced by SA node, how does the electrical current travel
60-100 bpm, current disseminates down left and right atria and move to the AV node, entering the ventricle system and then transmitted through the Bundle of HIS, spreads among the bundle branches until reaching the Purjinke Fibers causing contracting
What are other sources of automaticity, what BPM do they produce
AV node: 40-60 bpm, Bundle branches: 40-60 bpm, Purkinje Fibers: 20-40 bpm
What is affected by parasympathetic nodal conduction, what drives the conduction
The vagal tone (SA node, AV node, and Atrial response)/ catecholamines, acetylcholine, Calcium channel activity
What is affected by sympathetic nodal conduction, what drives the conduction
Mycotes/ catecholamines, Sodium channels, Potassium channels, calcium channel activity
What controls the rate of the SA node, what is it
The funny current: slow inward depolarizing Sodium inward currents
What are the three phases of SA node conduction, what, brief summary of each phase
Phase 4: Spontaneous depolarization to threshold, Phase 0: Depolarization throughout the cell due to the action potential
Phase 3: Repolarization of the cell
What occurs during phase 4 for the SA node
The funny current causes the cell to depolarize, once the cell hits -50mV T-type calcium channels aid in depolarizng the cell, once the cell hits -40mV L-type calcium channels open driving depolarization of the cell until action potential occurs
What causes depolarization throughout the cell
L-type calcium channels as the T-type calcium channels and funny currents start to close
What causes repolarization during Phase 3, what dominates ion movement and provides automatcity
Potassium channels open and potassium efflux until the cell is back to -60mV to which the potassium channels close, the funny current
What are the phases in cardiac myocyte action potentials
Phase 4: Slow depolarization from potassium leaks and small rush of sodium and calcium ions due to gap junctions
Phase 0: Rapid depolarization due to sodium ion influx
Phase 1: Brief repolarization due to sodium channels closing and potassium channels AND calcium channels open
Phase 2: Plataeu contraction due to balanced potassium efflux and calcium influx
Phase 3: Repolarizastion due to calcium channels closing and potassium channels staying open long enough for the cell to reach resting potential. Once the cell hits resting potential potassium channels close
What is the P-wave, QRS-Wave (upper limit ms), T-wave, RR-interval
P-wave: atrium depolarization, ventricular muscle depolarization (120 ms), ventricular repolarization, Time between R-R peaks for the QRS complexes
What is the PR interval, what should the ms be if it is normal, what does it mean if it is higher than the normal range
Delay through the AV node, 200 mv or less , 1st degree AV block
What is the QT interval, what effects it, what is the equation for QTc
Start of ventricular contraction to ventricular end of relaxation, potassium efflux, QTc (sec)= QT (sec)/√RR (sec)
What is considered prolonged QTc in men, women
Greater than 470, greater than 480
T/F: If the wave ends on the right side of midway point of an RR interval it is normal while on the left side means a possible arrhythymia
False: if the T wave ends before the halfway point then it is normal but if the T wave is to the right side of the midpoint between the RR-interval then it is prolonged
What are the three ways the arrhythmias can occur
Increased automaticity, Triggered activity, re-entry
What is the physiological change seen in increased automaticity, where can it occur, how can this lead to arrhythymias
Increased phase 4 slope increasing the heart rate, SA node and other tissues,the rate of spontaneous impulse generation exceeds that of the SA node
What are characteristics of increased automaticity, medications that possibly cause, conditions that possibly cause
Initiating beat is identical to subsequent beats/ digoxin and catecholamines/ Hypoxia, cardiac dilation, hypokalemia
What are the mechanisms to decrease automaticity what medication classes are given to achieve these effects
Decrease the slope of phase 4 (beta-blockers)/ elevate threshold potential (sodium and calcium channel blockers)/ increase maximum diastolic potential (adenosine and acetylcholine)/ increase action potential duration (potassium channel blockers)
What is the physiological change seen in triggered events, what are the two types of triggered depolarizations
Repetitive mini membrane depolarizations occurring after depolarization but before phase 4/ delayed after depolarization (DAD) and early depolarization (EAD)
How does DAD occur, EAD
Calcium overload either in the cytoplasm or SR resulting in a DAD after an action potential possibly causing a second beat if threshold is reached/ cardiac repolarization is delayed causing prolonged action potentials
T/F:Delayed after-depolarizations are associated with fast heart beats while Early after-depolarizations are associated with slow heart beats
True
What are medications that can cause afterdepolarizations, what are causes strictly associated with DAD, casues associated with EAD
Procainamdie, quinidine, digoxin toxicity/ myocardial ischemia, adrenergic stress, digitalis intoxication, CPVT, catecholamines/ Hypokalemia and class 1a anti-arrhythmic drugs or anything that blacks potassium channels
What are ways to prevent DADs and the medication class that do so
Reduce calcium influx into the cell while decreasing SR load and spontaneous calcium release from SR (calcium channel blockers )/ elevate the threshold required to create the abnormal stroke (sodium channel blockers)
What are way to prevent EADs
shorten the action potential duration with isoproterneol, magnesium WITHOUT normalinzing repolarization or QT
What is the common causes of arrhythymias, what needs to be present for it to occur
reentry/ Two impulse pathways, prolonged refractory in one of the paths, slowed conduction in the other pathway
What are the two types of rerentry, what is the difference between the two
Functionally defined reentry and anatomically-defined reentry/ Heterogeneity in refractoriness among regions of the heart cause anatomically defined while scarring results in tissues having varied conduction velocities thereby promoting multiple pathways of conduction
T/F: Anatomically defined reentry is fixed and is futher caused by CAD, left-ventricular dysfunction or MI while functionally defined reentry is associated with atrial ventricular nodal reentry (AVNRT)
False: Anatomically defined reentry is fixed and is associated with (AVNRT) while functionally defined reentry is caused by conditions such as CAD, left-ventricular dysfunction and MI
What are drug classes that manage anatomical reentry by increasing refractory period AND decrease conduction velocity, what manages but ONLY INCREASES refractory period, what manages but ONLY DECREASES conduction velocity
Potassium channel blcokers, adenosine, calcium channel blockers/ Potassium channel blockers/ sodium channel blockers
What types of arrhythymias can be caused by reentry, triggered events, and increased automaticity
Atrial fibrillation and ventricular tachycardia
T/F: Atrial flutter is only caused by reentry
True
T/F: The VW classification system for the class 1 AADs is sub-stratified based on how tightly the drugs hold onto the sodium channels in phase 0
True
What is the MOA of class 1a AADs,
Sodium is help onto, thereby decreasing the conduction velocity (slope of phase 0), Potassium efflux in phase 3 is slowed thereby prolonging repolariztion (refractory period and lengthening the action potentials)
What is the MOA of class 1b AADs, when are they only used
Sodium is held very briefly possibly shortening the refractory period, Vtach only and otherwise rapidly driven tissues
What is the MOA of class 1c AADs, what is required for them to be used
Sodium is held onto very tightly significantly decreasing the conduction velocity, normal sinus rthym
What are the class 1a AADs, how do they effect an ECG
Quinidine, Disopyramide , Procainamide (IV)/ Increase QRS and QT interval
What are the class 1b AADs, class 1c AADs
Mexiletine (PO) and Lidocaine (IV), decrease QT/ Propafenone and Flecanide, increase PR interval and QRS
What antiarrythmic binds to sodium channels when it is in an inactivated state, ischemic tissue and faster rates
Lidocaine
What AADs are metabolized by CYP3A4
quinidine, disopyramide, lidocaine, and propafenone
What AADs are metabolized by CYP2D6, which of these is also metabolized by CYP1A2 as well
mexiletine, flecainide, propafenone/ mexiletine
What AADs are eliminated renally
NAPA (procainamide active metabolite), 50% of flecainide
If someone has moderate to severe liver disease what AAD should be reduced by 20%-30%
Propafenone
What drug interactions should be cautioned when using flecainide, why
Cimetidine increase levels, flecanide increase digoxin
What drug interactions should be cautioned when using propafenone, why
warfarin and grapefruit juice increase propafenone levels
What are side effects associated with using 1a and 1c AADs
bradycardia, heart block, hypotension
Which 1a cannot be used in heart failure patients
Disopyramide
T/F: If a patient has an atrial flutter an AV blocking agent (beta-blocker/non-DHP CCBs) is used in conjunction with 1a or 1c agents
True
T/F: 1c against are not used in post-MI or HF patients
True
What type of arrhythmia causes Torsade de pointes
Reentry and Triggered activity
