Cardiac physiology Flashcards

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1
Q

what is this and what is it used for

A

the nerst equation used to determine the Ex for a particular ion

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2
Q

what is the RMP of a cardiac myocyte

A

-90mV

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3
Q

what are two factors that generate RMP

A

unequal distribution of ions (Gibbs donnan)

relative permeability of ions (conductance)

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4
Q

how is RMP maintained

A

Na/K pump keeps and restores membrane to RMP

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5
Q

what is the difference in duration of AP between cardiac myocytes and pacemaker cells

A

cardiac myocytes are fast, pacemaker cells are slow

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6
Q

what current is at work in Phase 4 of a cardiac myocyte AP

A

IKir

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7
Q

what current is at work in Phase 0 of a cardiac myocyte AP

A

INa

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8
Q

what current is at work in Phase 1 of a cardiac myocyte AP

A

Ito (IKv1.4)

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9
Q

what current is at work in Phase 2 of a cardiac myocyte AP

A

ICaL

IKv1.4

IKv1.1

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10
Q

what current is at work in Phase 3 of a cardiac myocyte AP

A

IKv1.1

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11
Q

what are the 5 phases of a cardiac myocyte AP

A

Phase 4 (resting)

Phase 0 (upstroke)

Phase 1 (Early Repolarization)

Phase 2 (Plateau)

Phase 3 (final repolarization)

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12
Q

describe the process that produces Phase 2 (plateau)

A

L type calcium channels open at threshold (-50mV)

calcium enters the cell

creates a slow inward current

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13
Q

the movement of what two ions is balanced during phase 2

A

potassium intitally decreases in conductance, then increases as the AP transitions to phase 3

calcium increases in conductance then slowly decreases

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14
Q

what are the two advantages of the plateau period for cardiac function

A

maintenance of force generation (long contraction)

creation of a long absolute refractory period (allows for filling)

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15
Q

what happens when calcium is released from the sarcoplasmic reticulum in cardiac myocytes

A

calcium enters the L type calcium channel

it binds with ryanodine receptors on the SR

calcium induces calcium release from the SR

calcium binds to troponin C on tropomyson

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16
Q

ryanodine receptors

A

receptors on the SR of muscle cells that are triggered by calcium to release calcium into the cytoplasm

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17
Q

what is SERCA

what does it do

A

sarco/endoplasmic reticulum calcium ATPase

pulls calcium from the cytoplasm at the expense of ATP while the muscle is at rest

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18
Q

what causes the absolute refractory period

A

the closing of Na inactivation gates

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19
Q

what is different during relative and absolute refractory periods

A

during the relative refractory period some Na inactivation gates are open a second AP is possible

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20
Q

what is the supranormal period?

when does it occur?

A

a period where cells can be restimulated and threshold is lower than normal

only during phase 4

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21
Q

heart cells are particularly vulnerable to arrhythmias at what point in the cardiac cycle

A

the phase 4 supranormal period

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22
Q

how long does the absolute refractory period last in a cardiac myocyte AP

what are three advantages of this

A

almost as long as the twitch does

  1. no summation of APs
  2. no tetanus
  3. allows for filling
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23
Q

tetradotoxin

A

a volrage gated channel blocker derived from the venom of a puffer fish

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24
Q

what are three general symptoms of tetrotoxin poisoning

A

GI distress

CNS

Cardiovascular

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25
Q

three GI symptoms caused by tetrotoxin

A

nausea, vomitting, cramping

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26
Q

three CNS symptoms caused by tetrotoxin

A

muscle weakness

numbness

coma

27
Q

three cardiovascular symptoms caused by tetrotoxin

A

decreased cardiac output

hypotension

bradycardia

28
Q

automaticity

A

the ability of cardiac pacemaker cells to produce their own APs

29
Q

two locations of nodal cells in the heart

A

SA node (right atria)

AV node (inferior posterior section of the intratrial septum)

30
Q

what are the three phases of a pacemaker cell

A

Phase 4 (slow depolarization)

Phase 0 (upstroke)

Phase 3 (repolarization)

31
Q

how are cardiac pacemaker cells able to produce a slow depolarization

A

they have an unstable resting membrane potential

32
Q

what currents are at work in Phase 4 of a pacemaker cell

A

IF

ICaT

IKv1.1

33
Q

what current is at work in phase 0 of a pacemaker cell

A

ICaL

34
Q

what current is at work in phase 3 of a pacemaker cell

A

IKv1.1

35
Q

what are two factors that determine the fire frequency of pacemaker cells

A

the rate of depolarization in phase 4

the maxium pacemaker potential

36
Q

what causes a change in slope during phase 4 of a pacemaker AP

what will happen in each instance?

A

sympathetic/parasympathetic nerve stimulation

sym: slope increases and causes higher firing frequency
para: slope decreases = lower firing frequency

37
Q

how does the maximum of the pacemaker potential effect firing rate

A

the more negative the pacemaker potential is, the slower the firing rate will be

38
Q

describe the pathway of sympathetic stimulation on pacemaker cells up to PKA

A

Norepinephrine is release from the adrenal medulla

NE binds to beta 2 adrenergic receptor

B2 receptor releases G protein

alpha subunit activates adenylate cyclase

adenylate cyclase releases protein kinase A

39
Q

what are the functions of protein kinase A in pacemaker cells

A

increasing Na conductance to allow If

phosphorylation of T-type calcium channels to increase Ca conductance and allow ICat

40
Q

what is the end result of sympathetic stimulation of cardiac pacemaker cells

A

increase of Ca and Na influx which will increase the rate of depolarization, slope, and heart rate

41
Q

describe the pathway of parasympathetic stimulation on HR (up to G protein release)

A

acetylcholine binds to muscarinic receptors

M receptors release G protein

G protein subunits beta and gamma induce intracellular response

42
Q

describe the effect of G protein subunit ßy (parasympathetic) on heart rate

A

G protein subunit ßy binds to KAch channels

potassium influx increases

membrane is hyper polarized

pacemaker potential is more negative

43
Q

describe the effect of G protein subunit Gαi on pacemaker cells

A

cAMP is decreased, causing a decrease in PKA

If, ICaL, IKv1.1 all decrease

slope/rate of depolarization are decreased

44
Q

what is the end result of parasympathetic stimulation on pacemaker cells

A

decreased pacemaker potential and rate of depolarization, leading to a slower HR

45
Q

which part of the autonomic nervous system dominates HR variability

A

parasympathetic

46
Q

how does tonic stimulation apply to pacemaker cells

A

the parasympathetic nervous system displays tonicity by constantly having a inhibitory effect on heartrate

47
Q

how do SNS and PsNS differ in terms of onset of effect after stimulus and decay of effect when the stimulus is with drawn

A

SNS: slow onset, slow decay

PsNS: fast onset, fast decay

48
Q

which pacemaker node in the heart produces impulses at the highest frequency

A

the SA node

49
Q

describe the path of an action potential through the heart

A

SA node

internodal pathways

AV node

bundle of His

bundle branches

purkinje fibers

50
Q

what is the function of the AV node

A

delays ventricular excitiation to ensure filling

51
Q

how long is an AP delayed at the AV node

A

0.1 second

52
Q

what part of the cardiac conduction system has the slow conduction velocity?

the fastest?

A

the AV node

purkinje fibers

53
Q

what is the function of the bundle of his, bundle branches, and purkinje fibers

A

ventricular excitation

54
Q

T/F the slowest functional pacemaker dominates the heart

A

fast, the fastest pacemaker does

55
Q

what is the firing rate range of the SA node?

AV node?

A

60-120

40

56
Q

what would happen to HR if the SA node were nonfunctional due to injury

A

the AV node would take over and produce a HR around 40bpm

57
Q

what would happen if the AV node were knocked out but the SA was still firing

A

the SA node AP would not be able to reach the purkinje fibers so the fibers would produce a HR of around 30

58
Q

what would happen if the purkinje fibers began to fire at a rate of 140bpm even with a functional SA and AV node

A

the whole heart will be driven by the faster rate

59
Q

what three factors determine the conduction velocity of pacemaker APs

A

diameter of fibers (decrease viscosity)

number of gap junctions (increase conductance)

rate of slow depolarization (increased slope)

60
Q

why does the AV node have the lowest conduction velocity

A

small cell diameter and few gap junctions

61
Q

why do the purkinje fibers have the highest conduction velocity

A

large diameter and many gap junctions

62
Q

what is the physiological and clinical significance of delayed AV conduction

A

optimal ventricalr filling during atrial contraction

63
Q

why does the AV node make the heart vulnerable

A

damage to the AV node will cause a loss of conduction to the ventricles