Exam 1 lecture 3 Flashcards

1
Q

Phase 4 of ventricular action potentials

A

resting potential. membrane is permeable t potassium through leak channels, outward flow of potassium ions generate the Ik2p current. Inward rectifer outward potassium current Iir. Em approx. for potassium (-96mv)

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2
Q

Phase 0

A

rapid opening of voltage gated sodium channels and inward sodium current, driving membrane potential in direction of sodium (+52)

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3
Q

Phase 1

A

closing of voltage gated sodium channels, coupled with voltage gated transient outward potassium current (Ito). Pulls membrane potential back to resting

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4
Q

Phase 2

A

Plateau, reduced outward potassium current (Ik1 or Iir) coupled with an inward calcium current (Ica (l)) through L type voltage gated calcium channels

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5
Q

Phase 3

A

repolarization. closure of L-type calcium channels, an increase in outward potassium current (Ik1), and rapid and slow voltage-gated delayed outward rectifier potassium current (Iks and Ikr). Delay in reporlarization allows for calcium channels to reactivate

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6
Q

why is delayed outward rectifier Ikr for potassium important for repolarization

A

hERG forms the major portion of voltage gated ion channel protein involved in Ikr. mutations can delay cardiac repolarization. In ECG, effect is LONG QT INTERVAL, or congenital long QT syndrome

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7
Q

what can congenital long QT syndrome cause

A

serious ventricular tachycardia and ventricular fibrillation

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8
Q

What else can cause congenital long QT syndrome

A

mutations in sodium and calcium channels

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9
Q

drugs that block hERG cause

A

acquired long QT syndrome, antiarrhythmics, anti-psychotic agents and antibiotics

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10
Q

inward rectifier

A

channels close as the cell depolarizes, (ooposite potassium channels which close when cell depolarizes). This is why rectifier current is reduced at plateau phase of cardiac action potential and increases again as cell repolarizes

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11
Q

directions of rectifier current

A

downward deflections are inward currents and upward deflections are outward currents

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12
Q

effective refractory period

A

during plateau phase, arrival of second depolarizing impulse has no effect

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13
Q

what follows effective refractory period?

A

relative refractory period: when sodium channels in membrane are unable to open when voltage is changed (when other are reset and ready to respond)

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14
Q

why dont cardiac muscle experience tetanus like the muscles do?

A

because the effective refractory period last quite a long time

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15
Q

when does calcium enter myocardial cells,

A

phase 2, during the plateau phase, triggers a release of more calcium from SR-> calcium concentration int he sarcoplasm increases-> calcium binds troponin which causes conformational change in tropomyosin, allowing mysoin to bind actin

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16
Q

what increases inward trigger calcium current

A

by catecholamines acting via beta-1 adrenegic receptors and cAMP/protein kinase-> leads to phosphorylation of L-type calcium channels

17
Q

why does triger calcuim lead to

A

increased cardiac inotropic state because more trigger calcium enters the myocyte, more is released from the SR

18
Q

what blocks catecholamines

A

beta-blockers (bind beta adrenergic)

19
Q

what do all cardiac cells have the capability of doing?

A

rhythmically and spontaneously depolarizing and repolarizing

20
Q

override supression

A

normally SA node fires before the slower pacemaker can fire and so its depolarizes them before they can spontaneously depolarize

21
Q

escape rhythm

A

another pacemaker taking over a defective SA node, fires at slower rate

22
Q

ectopic focus

A

certain conditions in which there can be an isolated spontaneous depolarization of a cell or group of cells in another region of the heart, ventricular or atrial myocardium, area is referred to as eptopic focus

23
Q

what is funny current

A

prepotential or pacemaker potential is represented by a slow depolarization of the cell, caused by If “funny current” carried mainly by sodium. ( basically sodium leaking into the cell)

24
Q

how does parasympathetic affect pacemaker frequency

A

decreases heart rate, Ach (muscarinic receptors) causes potassium permeability of SA nod cells to increase. repolarization Em is dirve closer to Ek and rate of prepontential formation is reduced-> takes longer for prepotential to reach firing threshold-> heart is slowed

25
Q

how does sympathetic affect pacemaker frequency

A

stimulate increase heart rate. NE (beta 1 adrenegeric) causes potassium channels that are opened at the last phase of AP to close more rapidly, reducing the time taken for prepotential to reach firing threshold-> heart rate is accelerated.

26
Q

annulous fibrosis

A

electrical depolarization can only reach the ventricles by passing through the AV node-> electrically insulated from each other by fibrous 4 ringed skeleton of heart

27
Q

why is there a delay in the AV node

A

allows time for atria to contract before ventricular contraction begins

28
Q

P wave

A

depolarization of atria, indicates SA node function

29
Q

P-R internval

A

indicative of time it takes for impulse to pass through the AV node into the ventricles (atrioventricular time) normal is .12-.2 seconds
( increases in AV block)

30
Q

QRS

A

depolarization of the ventricles, normally .12 seconds. indicates the duration of the ventricular depolarization-> Q wave may be exaggerated following myocardial infarction

31
Q

T wave

A

progressive repolarization of ventricles, after which they are ready to be stimulated again
(inverted or peaked in myocardial infarction or hyperkalemia)

32
Q

S-T segment

A

when elevated above baseline, indicates the possibility of myocardial infarction, depression below baseline may indicate myocardial ischemia

33
Q

Q-T interval

A

varies with heart rate: abnormally prolonged in long QT syndrome. Rule of thumb: for heart rates between 65-90 is that QT is normal if half preceding R-R interval

34
Q

U wave

A

if present-> follows T wave, notable in hyperkalemia, digoxin, quindine and other conditions

35
Q

J point

A

junction between QRS and ST segment

36
Q

one complete ECG wave

A

PQRSTP