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Physiology > Electrophysiology of the Heart > Flashcards

Electrophysiology of the Heart Flashcards

Lecture 18

1
Q

What is coupled with heart muscle contraction?

A

generation of action potentials in cells

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2
Q

What are the 2 main types of cells of the heart?

A

Conducting cells and contractile cells

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3
Q

Where are conducting cells found?

A

In SA/AV nodes, atrial internodal tracts, Bundle of His, Purkinje system.

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4
Q

2 properties of all cardiac cells

A

automaticity (generate own AP) and rhythmicity (generate APs in regular, repetitive manner

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5
Q

Gap junctions between cardiomyocytes

A

Allow the heart to behave as one big cell; cells are coupled electrically through gap junctions

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6
Q

What voltage-gated channels open when an AP occurs?

A

Sodium, calcium, and potassium

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7
Q

SA node

A

source of initial electrical impulse

pacemaker (60-100 AP/min)

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8
Q

Overdrive suppression

A

The SA node’s ability to keep other conducting cells from spontaneously firing

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9
Q

Where does the AP of the SA node spread to cause the atria to contract?

A

internodal/interarterial fibers

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10
Q

P wave in EKG

A

depolarization of the atria

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11
Q

What blocks from electrical impulse flow from the SA nodes into the ventricles?

A

Annulus fibrosus

-E.I. can only get into ventricles through the AV node

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12
Q

What is the result of the small lag time between the conduction of the AP from the atrium to the ventricles due to the only point of conduction being the AV node to the ventricles?

A

Maximum atrial contraction helps fill the ventricles to the maximum; AV node conduction is slowest which helps the ventricles fill

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13
Q

Pathway of action potential conduction from AV node

A

SA node–> AV node–> Bundle of His–> Purkinje fibers

this correlates with the QRS complex in the EKG

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14
Q

QRS complex

A

AV node–> Bundle of His–> Purkinje fibers

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15
Q

T wave

A

ventricular repolarization

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16
Q

Slowest conduction velocities

A

AV node

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17
Q

Fastest conduction velocities

A

Purkinje fibers

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18
Q

Order of conduction velocities

A

SA/AV node < Atrial pathway/Ventricular cardiomyocytes < Purkinje fibers

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19
Q

What does an EKG record?

A

Electrical extracellular signals produced by AP in cardiac myocytes.

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20
Q

P wave

A

-sequential depolarization of R/L atria and atrial muscle action potential

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21
Q

What things are not seen on an EKG?

A

SA node depolarization/repolarization, AV node depolarization/repolarization

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22
Q

QRS complex

A

R/L ventricular depolarization/AP

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23
Q

ST wave

A

isoelectric, plateau of ventricular AP to rapid ejection phase; myocardium maintain contraction to expel blood

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24
Q

QT interval

A

duration of ventricular depolarization and repolarization

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25
Q

QT interval is inversely proportional to what?

A

HR; can be altered by drugs that alter repolarization

26
Q

What happens if ventricular repolarization is delayed?

A

QT interval is prolonged

27
Q

What health issue is delayed ventricular repolarization associated with?

A

Ventricular arrhythmias

28
Q

Delayed repolarization results in?

A

Ventricular arrhythmias

29
Q

Slow AP response

A

SA/AV nodes

30
Q

Fast AP response

A

normal atrium/ventricular cardiomyocytes and Purkinje fibers

31
Q

Phase 0 FR

A

fast upstroke
voltage-gated Na+ channels open
influx of Na+ into cell

32
Q

Phase 1 FR

A

partial repolarization
inactivation of Na+ channels
rapid opening/closing of K+
K+ leaves the cell

33
Q

Phase 2 FR

A

plateau phase
voltage-sensitive Ca2+ channels open, influx of Ca2+
counterbalanced by slow efflux of K+ through VG-K+ channels

34
Q

What is unique about voltage-gated Ca2+ channels?

A

slower opening/closing kinetics

35
Q

Phase 3 FR

A 
repolarization
inactivation of Ca2+ channels
efflux of K+ via VG channels
repolarization of cell membrane
Na/K ATPase corrects Na/K levels
36
Q

Phase 4 FR

A

cardiomyocytes at rest, resting membrane potential

background Na+ influx and K+ efflux through leak K+ channels

37
Q

What comes before Phase 0 FR?

A

suprathreshold stimulus from a pacemaker cell

resting membrane potential is abruptly changed

38
Q

Activation gate of Na+ channel

A

closed at resting membrane potential, opens with depolarization

39
Q

Inactivation gate of Na+ channel

A

open at rest, closed during depolarization

40
Q

During what phases are Ca2+ channels open?

A

Phase 0 and 2

41
Q

What is the contribution of Ca2+ during phase 0?

A

It makes the AP upstroke steeper and velocity faster

42
Q

AP leads to Calcium influx, which in turn causes…

A

cardiac muscle contraction

43
Q

Steps of Ca release

A

Depolarization–> Ca2+ channels open–> influx of Ca2+–> Ca2+ binds troponin C–> troponin C interacts with tropomyosin–> exposed actin/myosin binding sites–> cross-bridge cycling–> CONTRACTION

44
Q

Where does the Ca2+ come from that interacts with troponin C?

A

It comes from the sarcoplasmic reticulum

extracellular calcium is used for Calcium-induced Calcium release

45
Q

What enhances myocardial contraction?

A

catecholamines bind B-adrenergic receptors

inhibiting Na/K ATPase

46
Q

B-adrenergic activation

A

increased Ca2+ influx of L-type VG-Ca2+ channels

47
Q

Inhibition of Na/K/ATPase

A

increased Na+ leads to the decrease of the Na/Ca transporter, more calcium in the cell

48
Q

Plateau phase

A

as long as K+ efflux is balanced by Ca2+ influx

49
Q

What happens if K+ efflux exceeds Ca2+ influx during Phase 2?

A

plateau duration is short and final repolarization happens early

50
Q

Effective refractory period

A

cell will not respond to any stimuli

51
Q

Relative refractory period

A

some Na+ channels are excitable and can generate a smaller AP

52
Q

Diastolic depolarization

A

decreasing K+ efflux because VGK+ channels are inactivated–> increasing Na+ influx through HCN; results in further depolarization–> Calcium release from SR–> increase in Ca2+ leads to increase NCX–> at -50 mV, Ltype Ca2+ channels open–> increased Ca2+ influx leads to CICR–> K+ VG channels open, repolarization–> SR refills with Ca2+

53
Q

Differences in fast/slow response

A

Slow response has:

  • unstable phase 4
  • slower upstroke in phase 0
  • no phase 1 or 2 (no early repolarization/plateau)
54
Q

Sympathetic nervous system effect on HR

A

increased HR

55
Q

SNS pathway to increased HR

A
  • Norepinephrine/epinephrine binds B1 adrenergic receptors in SA/AV nodal cells
  • Adenylyl cyclase activated
  • increased cAMP
  • cAMP phosphorylates protein kinase
  • PK phosphorylates HCN/VG-Ca2+ channels
  • leads to increased Na influx through HCN/increased Ca2+ influx through VG-Ca2+ channels
  • steepens phase 4 of pacemaker potential
56
Q

Parasympathetic nervous system effect on HR

A

decreased HR

57
Q

PNS pathway to reduced HR

A
  • acetylcholine binds M2 cholinergic receptors
  • inhibits adenylyl cyclase
  • less cAMP
  • less Na+ influx through HCN/less Ca2+ influx through VG-Ca2+ channels
  • reduces steepness of phase 4
58
Q

2 types of effects of SNS activation of B1-adrenergic receptors?

A

Inotropic effect

Lusitropic effect

59
Q

Inotropic effect

A

increased cardiac contractility

increase Ca2+ influx= increase CICR

60
Q

Lusitrophic effect

A

faster atrial/ventricular relaxation
cAMP/PKA phosphorylate phospholamban which increases SRCa2+ ATPase, which pumps Ca2+ back into SR.
Ca2+ removed more quickly

61
Q

What does PKA do to Troponin during Lusitropic effect?

A

It phosphorylates Troponin I, destabilizing actin-myosin cross-bridging

Physiology (3 decks)

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