Action Potential, Basic EP Concepts, & Antiarrhythmics Flashcards

(44 cards)

1
Q

Polarization

A

Difference in charge between sides of a membrane

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2
Q

Polarized cell

A

Intracellular side is more negative

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3
Q

Depolarized cell

A

Intracellular side is more positive

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4
Q

Influx

A

Flow into the cells

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5
Q

Efflux

A

Flow out of the cell

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6
Q

Excitability

A

A response to a stimulus out of proportion to the strength of that stimulus

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7
Q

Current

A

The flow of charged particles across a membrane

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8
Q

Voltage

A

Difference in positive charges from one side of a membrane to the other
-example: -80mV means fewer positive charges on the inside of the cell

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9
Q

Sodium

A

-Predominates extracellulary
-Equilibrium potential +60 mV
-Reversal potential is around +55 mV

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10
Q

Potassium

A

-Predominates intracellularly
-Equilibrium potential -90mV
-Reversal potential is around -95mV

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11
Q

Gap junction

A

Low resistance intercellular connections that allows depolarization of neighboring cells

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12
Q

Ion

A

An atom or molecule with a net electric charge due to the loss or gain of one or more electrons

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13
Q

Anion

A

Negatively charged ion

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14
Q

Cation

A

Positively charged ion

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15
Q

Nernst Equation

A

Calculates the equilibrium potential for a specific ion across a membrane based on its concentration inside vs outside the cell

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16
Q

Calcium

A

Equilibrium potential +120 mV

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17
Q

Chloride

A

Equilibrium potential -70 mV

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18
Q

Wedensky effect

A

-When a large suprathreshold stimulus causes a following stimulus which would normally be subthreshold to result in the initiation of an action potential
-Can lead to inaccurately low threshold testing results

19
Q

Action potential phase 0

A

Depolarization

-Na+ channels open
-Abrupt influx of extracellular Na+ ions into the myocyte
-Causes membrane potential to go from -90mV to +20mV

20
Q

Action potential phase 1

A

Initial/brief repolarization

QRS complex

-Change in polarity initiates closure of Na+ channels and opens K+ channels
-K+ ions already in the cell begin to leak out through a newly opened channel, initiation the cell transition back to a negative state

21
Q

Action potential phase 2

A

Plateau

ST segment

-Ca++ channels open
-Ca++ channels open at same membrane potential as K+ channels, but their activation is slower (K+ is 1ms, CA++ is 10-20 ms)
-The counterbalance between the slow inward Ca++ and fast outward K+ mediates the plateau phase

22
Q

Action potential phase 3

A

Repolarization

T wave

-Ca++ channels close
-K+ channels open, allowing potassium to flow out of the cell, becoming more negative
-Cell is vulnerable to depolarization during this phase

23
Q

Action potential phase 4

A

Quiescent period

After T wave, before P wave

-Normal distribution of Na+ and K+ is restored
-Sodium potassium pump helps to maintain the resting membrane potential by actively transporting Na+ ions out of the cell and K+ ions into the cell
-Return to resting membrane potential, which is almost flat
-Cell is repolarized (strongly polarized), ready for depolarization again
-Heart rate is controlled by varying the slope of the phase 4 action potential

24
Q

Absolute refractory period

A

-Period of time in which the action potential of the cell cannot be depolarized regardless of the strength of the stimulus
-Occurs during the depolarization phase and initial part of repolarization phase
-Primarily due to inactivation of voltage gated sodium channels
-Even if very strong stimulus is applied, no new action potential can be generated because sodium channels are blocked

25
Effective refractory period
Longest coupling interval that fails to capture myocardial tissue or fails to conduct an electrical impulse
26
Relative refractory period
Period where it’s possible for the neuron to produce another action potential but it requires a much greater stimulus to reach the threshold
27
SA node
Resting potential: -40 to -60 mV Action potential amplitude: 60 to 70 mV
28
AV node
Resting potential: -60 to -70 mV Action potential amplitude: 70 to 80 mV
29
Purkinje fibers
Resting potential: -90 to -95 mV Action potential amplitude: 120 mV
30
Ventricular muscle
Resting potential: -80 to -90 mV Action potential amplitude: 110 to 120 mV
31
Class 1a antiarrhythmics
Sodium channel blockers - moderate degree of sodium channel blocking Meds: Quinidine, procainamide, disopyramide Pacing threshold: increase Defibrillation threshold: increase EKG changes: increase QRS, increase QT
32
Class 1b antiarrhythmics
Sodium channel blockers - weak degree of sodium channel blocking Meds: Lidocaine, mexiletine Pacing threshold: no change Defibrillation threshold: increase EKG changes: decrease QT
33
Class 1c antiarrhythmics
Sodium channel blockers - strong degree of sodium channel blocking Meds: Flecainide, propafenone Pacing threshold: increase Defibrillation threshold: increase EKG changes: increase QRS (QT), prolong PR
34
Class II antiarrhythmics
Beta blockers Pacing threshold: no effect or increase Defibrillation threshold: no effect
35
Class III antiarrhythmics
Potassium channel blockers Meds: sotalol, Tikosyn, amiodarone, dronaderone Pacing threshold: —Sotalol/Tikosyn: no effect —Amiodarone/dronaderone: increase Defibrillation threshold: —Sotalol/Tikosyn: decrease —Amiodarone/dronaderone: increase EKG changes: Prolong QT
36
Class IV antiarrhythmics
Calcium channel blockers Pacing threshold: increase Defibrillation threshold: no effect
37
Use dependence
Increased drug effect at higher heart rates Occurs with class 1 antiarrhythmics Example of why we get exercise stress test for people on flecainide
38
Revere use dependence
-Greatest lengthening of the action potential duration occurs at slow heart rates, with a shortening of the action potential duration with shorter cycle lengths -Short-long-short intervals may result in a prolongation of the APD following the long R-R interval, leading to instability of repolarization. -Can result in a significant risk of QT prolongation, TdP and VF Occurs with class III antiarrhythmics
39
Volume of distribution
The theoretical volume into which a drug is distributed to maintain the plasma concentration at steady state IV only drugs have a smaller volume of distribution Amiodarone will have a VD greater than the circulating blood volume because it is highly lipophillic VD is decreased in heart failure, shock → drug toxicity
40
First pass metabolism
Concentration is significantly reduced by the time the drug reaches systemic circulation after one pass through the portal vein/liver This accounts for IV only or requirement for high oral dose compared to its IV dose Examples: lidocaine, propranolol
41
Chronotropy
Heart rate
42
Dromotropy
Speed of conduction
43
Inotropy
Force of contraction
44
Starting antiarrhythmics for ICD patients
-Need to increase the VT detection cycle by 30-50 ms so VT doesn’t slow below the cutoff rate and remain undetected