Basic Electrophysiology Flashcards

1
Q

normal extra-cellular ion concentrations

A

HIGH sodium, chloride, & calcium concentrations outside the cell
LOW potassium concentration outside the cell

Na+: 145 mM
K+: 5 mM
Cl-: 120 mM
Ca++: 2 mM

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2
Q

normal intra-cellular ion concentrations

A

LOW sodium, chloride, & calcium concentrations inside the cell
HIGH potassium concentration inside the cell

Na+: 15 mM
K+: 150 mM
Cl-: 5 mM
Ca++: 10^-7 mM

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3
Q

importance of the cardiac action potential & its phases

A

*foundational to the formation of various components of the ECG
*allows insight into the mechanisms of clinical arrhythmias

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4
Q

propagation of cardiac electrical activation - overview

A

SA node (sinus node) → atria → AV node → bundle of His → right and left bundle branches → Purkinje fibers → ventricles

note: the left bundle branch divides into left anterior and posterior fascicles

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5
Q

cardiac conduction system - overview

A

*specialized myocardial cells
*critical jobs:
-initiation of the heart beat (by the sinus node)
-coordinated contraction of the atria
-pause between atrial contraction and ventricular contraction to allow for atrial emptying (AV node responsible for the pause; allows time for blood to flow from atria to ventricles)
-coordinated ventricular contraction (starting with papillary muscles)

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6
Q

sinus node (SA node) - general principles

A

*pacemaking activity at the sinus node
*this region has to have some “automaticity” to start things off (automaticity = the tissue fires off on its own at a specific rate or a certain number of beats/min)
*this requires that the action potential of the SA node is different from that of atrial or ventricular myocardium

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7
Q

action potential of the sinus (SA) node

A

*“slow response” tissue action potential (“pacemaker action potential”)
*ion carrying current during upstroke: Ca2+-dependent
*conduction: SLOW conduction (decremental)
*recovery from inactivation: TIME-dependent
*has its own automaticity

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8
Q

phases of the pacemaker action potential in the SA and AV nodes (detailed)

A

*phase 0: UPSTROKE- opening of voltage-gated Ca2+ channels; fast voltage-gated Na+ channels are permanently inactivated because of the less negative resting potential of these cells; results in a slow conduction velocity, which is used by the AV node to prolong transmission from the atria to ventricles

*phase 3: REPOLARIZATION - inactivation of the Ca2+ channels and increased activation of K+ channels → increased K+ efflux

*phase 4: SLOW SPONTANEOUS DIASTOLIC DEPOLARIZATION due to If (“funny current”);
-If channels responsible for a slow, mixed Na+ inward/K+ outward current
-slope of phase 4 determines the HR
-accounts for automaticity of SA and AV nodes

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9
Q

factors that INCREASE automaticity

A

*catecholamines
*digitalis
*hypokalemia
*ischemia
*stretch

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10
Q

factors that DECREASE automaticity

A

*acetylcholine
*beta blockers
*calcium channel blockers
*hyperkalemia

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11
Q

AV node - general principles

A

*the bridge between the atrium and ventricle
*shares properties of automaticity with the sinus node
*has decremental properties (the faster you challenge, the slower the conduction)
*AV node transit time is represented by the PR interval on ECG

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12
Q

phases of the ventricular cardiac action potential (detailed)

A

*phase 4: resting state (some cells → pacemaker activity)
*phase 0: RAPID UPSTROKE & DEPOLARIZATION: rapid inward Na+ current when threshold is reached; important determinant of impulse conduction velocity
*phase 1: INITIAL REPOLARIZATION - rapid early repolarization; inactivation of voltage-gated Na+ channels; voltage-gated K+ channels begin to open (transiently outward K+ current)
*phase 2: PLATEAU PHASE - balance between Ca2+ influx and K+ efflux; Ca2+ influx triggers contraction
*phase 3: RAPID/TERMINAL REPOLARIZATION - massive K+ efflux due to opening of slow voltage-gated K+ channels and closing of Ca2+ channels

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13
Q

action potentials of the atria & ventricles

A

*“fast response” tissues
*ion carrying current during upstroke: Na+-channel dependent
*conduction: FAST conduction (“all or none”)
*recovery from inactivation: VOLTAGE-dependent

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14
Q

ventricular cardiac action potential phases (simple)

A

*phase 4: resting state
*phase 0: DEPOLARIZATION due to Na+ influx
*phase 1: early REPOLARIZATION due to K+ efflux
*phase 2: PLATEAU due to balance between Ca2+ influx & K+ efflux
*phase 3: terminal REPOLARIZATION due to continued K+ efflux with closing of Ca2+ channels

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15
Q

pacemaker action potential phases - simple

A

*phase 0: UPSTROKE due to Ca2+ influx
*phase 3: REPOLARIZATION due to K+ efflux & closing of Ca2+ channels
*phase 4: slow DEPOLARIAZATION due to funny current channels (mixed Na+ inward/K+ outward current)

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16
Q

ventricular cardiac action potential: phase 0

A

*opening of voltage-gated Na+ channels
*SODIUM moves INTO the cell, causing depolarization

17
Q

ventricular cardiac action potential: phase 1

A

*initial/early repolarization of the cell
*voltage-gated Na+ channels close
*voltage-gated K+ channels begin to open
*POTASSIUM moves OUT OF the cell, causing initial repolarization

18
Q

ventricular cardiac action potential: phase 2

A

*plateau phase
*voltage-gated Ca2+ channels open
*voltage-gated K+ channels remain open
*balance between INFLUX OF CALCIUM and EFFLUX OF POTASSIUM
*influx of calcium triggers Ca2+ release from the sarcoplasmic reticulum and causes MYOCYTE CONTRACTION

19
Q

ventricular cardiac action potential: phase 3

A

*rapid repolarization of the cell
*voltage-gated Ca2+ channels close
*slow delayed-rectified K+ channels open
*MASSIVE EFFLUX of POTASSIUM causes repolarization

20
Q

ventricular cardiac action potential: phase 4

A

*resting potential (around -85 mV)
*high permeability through K+ channels

21
Q

QTc prolongation - action potential correlation

A

*problems with the potassium channels cause QTc prolongation (repolarization not occurring fast enough due to problems getting K+ out of the cell)

22
Q

widened QRS interval - action potential correlation

A

*problems with the sodium channels cause QRS widening (depolarization not occurring or not occurring fast enough due to decreased influx of Na+)

23
Q

prolonged PR interval - action potential correlation

A

*AV node problems (sluggish conductance through the AV node)

24
Q

conduction velocity

A

*refers to the speed of impulse propagation through cardiac tissues
*more rapid along cells end-to-end than perpendicular to that (anisotropic)
*more rapid in fast response tissue (Na+-dependent; atria & ventricles) than slow response tissue (Ca2+-dependent; SA & nodes)
*in fast response tissue, conduction velocity is a reflection of Na+ current magnitude, which is strongly dependent on membrane potential

25
Q

how do cells communicate with each other in the heart?

A

*through GAP JUNCTIONS
*different properties of the gap junctions result in various properties

26
Q

refractoriness

A

*the concept that tissues are inexcitable for a period of time after they are activated
*the length of time from the prior activations that a cell remains inexcitable is termed the refractory period

*for slow response tissues (AV and SA nodes), the refractory period is TIME-DEPENDENT
*for fast response tissues (atria and ventricles), the refractory period is VOLTAGE-DEPENDENT (how quickly the cell can repolarize)

27
Q

re-entrant arrhythmia

A

*there is an anatomical circuit in the heart that the tachycardia is spinning around
*in order to support a tachycardia, you need:
-a circuit
-an area of slow conduction
-unidirectional block

28
Q

re-entry arrythmia in atrial flutter

A

*circuit = tricuspid annulus
*area of slow conduction = cavotricuspid sinus
*unidirectional conduction block = can be created at the CTI with premature atrial beats