4. Physiology II - Conducting System Flashcards

1
Q

what BEGINS the CARDIAC CYCLE (at end of diastole) what causes ATRIA to CONTRACT after passive filling

A

SINO-ATRIAL NODE FIRES (DEPOLARISES)

spreads wave of depolarisation through right atrium and to left atrium

-> ATRIA CONTRACT
(15% ventricular filling)

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2
Q

what happens as the CONDUCTION / wave of DEPOLARISATION PASSES through the AV NODE

A

DELAYS it - slows down before reaching Bundle of His, Bundle Branches, Purkinje Fibres

allows time for atria to move blood out through valves before the ventricles contract (so atria and ventricles don’t contract simultaneously)

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3
Q

how are IMPULSES in SYSTOLE (ventricular contraction)

A

RAPID TRANSMISSION through VENTRICLES

  • COORDINATED VENTRICULAR CONTRACTION
    (radially, longitudinally and twisting motion)
    SPECIFIC ACTIVATION SEQUENCE to OPTIMISE EJECTON of blood

(bundle branch block is dangerous)

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4
Q

in what direction are VENTRICULAR CONTRACTIONS to OPTIMISE ejection of blood

A

RADIALLY (side to side)
LONGITUDINALLY (from apex to base)
and TWISTING MOTION

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5
Q

what is POLARISATION

A

a DIFFERENCE in CHARGE between sides of a MEMBRANE

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6
Q

if something is POLARISED what does it mean

A

INSIDE MORE NEGATIVE

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7
Q

if something is DEPOLARISED what does it mean

A

INSIDE MORE POSITIVE

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8
Q

what is VOLTAGE

A

the DIFFERENCE in POSITIVE CHARGES from one side of a membrane to the other

(-80mV in myocytes, resting)

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9
Q

what is a CURRENT

A

the FLOW of CHARGED PARTICLES ACROSS a MEMBRANE

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10
Q

how are CARDIAC MYOCYTES at REST (resting potential)

A

POLARISED (inside Negative)
at - 80mV

due to K+ EFFLUX (out of cells)

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11
Q

how do CURRENTS PASS BETWEEN MYOCYTES (excite each other)

A

via GAP JUNCTIONS

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12
Q

when can MYOCYTES REGAIN EXCITABILITY

A

ONLY when FULLY REPOLARISED

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13
Q

what is REFRACTORY PERIOD

A

period of TIME during which a second STIMULUS will FAIL to GENERATE a 2ND ACTION POTENTIAL in a myocyte

  • as cannot generate 2nd action potential unless fully repolarised
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14
Q

how do PARTICLES travel into cells (by what gradients)

A

DOWN ELECTRO-CHEMICAL GRADIENT

  • CHEMICAL gradient
  • ELECTRICAL gradient for CHARGED particles
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15
Q

What is a REVERSAL POTENTIAL

A

when ELECTROCHEMICAL GRADIENT is BALANCED

(inward and outward forces are equal / eventually reach equilibrium)

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16
Q

name of the EQUATION that PREDICTS WHERE the REVERSAL POTENTIAL will lie / where the ELECTROCHEMICAL GRADIENT WILL BALANCE

A

NERNST EQUATION

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17
Q

what CHANNELS should we OPEN if we want to make MEMBRANE REVERSAL POTENTIAL LOWER / MORE NEGATIVE, as they have really negative reversal potential

A

K+ CHANNELS

(-95mV reversal potential)

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18
Q

what CHANNELS should we OPEN if we want to make MEMBRANE REVERSAL POTENTIAL HIGHER / MORE POSITIVE, as they have high reversal potential

A

Na+ CHANNELS

(+55mV reversal potential)

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19
Q

types of ION CHANNELS in cardiomyocytes

A

VOLTAGE GATED
- activation gate opens when membrane potential becomes more positive
- are TIME DEPENDENT

LIGAND GATED
by chemical (ie Ach) or mechanical (stretch)

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20
Q

what channel uses ATP in cardiomyocytes

A

NA/K PUMP

3 Na+ OUT
2 K+ IN

(restore balance)
(electrogenic, creates current)

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21
Q

what TRANSPORTER is used in cardiomyocytes

A

NA/CA EXCHANGER

1 Ca2+ OUT (CALCIUM EFFLUX)
exchanged for
3 Na+ IN

  • PASSIVE, no ATP

can also work in reverse for Calcium Influx

  • electrogenic, creates current
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22
Q

what is the RESTING POTENTIAL and how is this GENERATED

A

-80 mV

  • K+ EFFLUS as K+ CHANNELS OPEN in resting state
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23
Q

stages of an ACTION POTENTIAL GENERATION that make the SPIKE AND DOME MORPHOLOGY

A
  1. RAPID Na+ INFLUX as Na+ channels OPEN
    (exceeds threshold)
  2. K+ CHANNELS OPEN, K+ EFFLUX
  3. Ca2+ CHANNELS OPEN, Ca2+ INFLUX (makes plateau as balances K+ efflux)
  4. Ca2+ CHANNELS CLOSE
  5. REPOLARISATION (flat)
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24
Q

ACTION POTENTIAL CREATED by the FLOW of which ION(S)

A

-

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25
Q

CHANNELS used to CREATE ACTION POTENTIALS

A
  • Na+ CHANNEL (Na+ in)
  • K+ CHANNEL (K+ out)
  • Ca2+ CHANNEL (Ca2+ in)
  • NA/K ATPase (Na+ out, K+ in)
  • NA/Ca EXCHANGER (Na+ in, Ca2+ out)
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26
Q

how does Na+ TRAVEL when Na+ CHANNEL is OPEN

A

IN

27
Q

how does K+ TRAVEL when K+ CHANNEL is OPEN

A

OUT

28
Q

how does Ca2+ TRAVEL when Ca2+ CHANNEL is OPEN

A

IN

29
Q

how does Na+ TRAVEL through NA/K PUMP

A

OUT (3)

30
Q

how does K+ TRAVEL through NA/K PUMP

A

IN (2)

31
Q

how does Na+ TRAVEL through NA/CA EXCHANGER

A

IN

32
Q

how does Na+ TRAVEL through NA/CA EXCHANGER

A

IN (3)

33
Q

how does CA2+ TRAVEL through NA/K PUMP

A

OUT (1)

34
Q

INFLUX of …. leads to MYOCYTE CONTRACTION

A

CALCIUM

35
Q

what happens in PHASE 0 of CARDIOMYOCYTE ACTION POTENTIAL in SPIKE AND DOME MORPHOLOGY

A

RAPID UPSTROKE

(Na+ influx)

36
Q

what happens in PHASE 1 of CARDIOMYOCYTE ACTION POTENTIAL in SPIKE AND DOME MORPHOLOGY

A

INITIAL REPOLARISATION

(K+ efflux)

37
Q

what happens in PHASE 2 of CARDIOMYOCYTE ACTION POTENTIAL in SPIKE AND DOME MORPHOLOGY

A

PLATEAU

(Ca+ influx and K+ efflux BALANCE)

38
Q

what happens in PHASE 3 of CARDIOMYOCYTE ACTION POTENTIAL in SPIKE AND DOME MORPHOLOGY

A

FINAL REPOLARISATION

(K+ efflux)

39
Q

what happens in PHASE 4 of CARDIOMYOCYTE ACTION POTENTIAL in SPIKE AND DOME MORPHOLOGY

A

STRONGLY POLARISED

almost FLAT RESTING POTENTIAL

40
Q

how are ACTION POTENTIALS from ATRIAL MYOCYTES

A

SHORTER DURATION

lower plateau

41
Q

the SINO-ATRIAL NODE (SAN) ACTION POTENTIAL is adapted to FUNCTION as a …

A

PACEMAKER

42
Q

how is PHASE 0 of SAN ACTION POTENTIAL

A

SLOW UPSTROKE

  • less steep
43
Q

how is PHASE 4 of SAN POTENTIAL

A

LESS POLARISED (moderately)

UPSLOPING RESTING POTENTIAL, NOT FLAT

  • SLOWLY DEPOLARISING
44
Q

CARDIAC CONDUCTION is LARGELY CONTROLLED by … TONE

A

AUTONOMIC TONE

45
Q

impact of SYMPATHETIC TONE on HEART RATE (chronotropy), SPEED of conduction (dromotropy) and FORCE of contraction (inotropy)

A

INCREASES HEART RATE, CONDUCTION SPEED, FORCE

46
Q

impact of PARASYMPATHETIC TONE on HEART RATE (chronotropy), SPEED of conduction (dromotropy) and FORCE of contraction (inotropy)

A

DECREASES HEART RATE, CONDUCTION SPEED, FORCE

47
Q

what NERVE STIMULATION SLOWS HEART RATE

A

VAGAL NERVE stimulation

48
Q

DRUG that can SLOW HEART RATE by BLOCKING SYMPATHETIC TONE

(increase RR intervals - time between systoles)

A

BETA BLOCKERS ie PROPANOLOL

49
Q

DRUG that can INCREASE HEART RATE by BLOCKING PARASYMPATHETIC TONE

(decreases RR intervals - time between systoles)

A

ATROPINE

50
Q

PROPANOLOL BLOCKS…

A

SYMPATHETIC TONE and thus SLOWS HEART RATE

51
Q

HEART RATE is MODULATED by VARYING the SLOPE of … of the SAN ACTION POTENTIAL

A

PHASE 4

52
Q

what happens if you STEEPEN the SLOPE of PHASE 4 of the SAN ACTION POTENTIAL

A

INCREASES HEART RATE

(next action potential comes sooner)

53
Q

what happens if you FLATTEN the SLOPE of PHASE 4 of the SAN ACTION POTENTIAL

A

DECREASE HEART RATE

(next action potential comes later)

54
Q

… TONE STEEPENS the SAN PHASE 4

A

SYMPATHETIC TONE

(increases heart rate)

55
Q

…. TONE FLATTENS the SAN PHASE 4

A

PARASYMPATHETIC

(slows heart rate)

56
Q

in ECG what does the P WAVE show

A

ATRIAL DEPOLARISATION

57
Q

in ECG what does the QRS COMPLEX WAVE show

A

VENTRICLE DEPOLARISATION

58
Q

in ECG what does the T WAVE show

A

VENTRICULAR REPOLARISATION

59
Q

in PHARMACOLOGY which IONS HOMEOSTASIS are used to treat ABNORMAL HEART RHYTHMS - ANTIARRYTHMICS

A

SODIUM (eg Flecainide)
CALCIUM (eg Verapamil)

60
Q

what can also be used that influence Na+ Channels

A

LOCAL ANEASTHETICS eg Lidocaine

61
Q

Ca+ Channel blockers can also be used to control..

A

BLOOD PRESSURE

in ANTIHYPERTENSIVES eg Amlodipine

62
Q

HIGH SERUM POTASSIUM (HYPERKALAEMIA) has what effect on the HEART
(caused be renal failure or drugs ie ACE inhibitors)e

A
  • SLOWED CONDUCTION
  • HEART BLOCK (block in AV node)
63
Q

LOW SERUM POTASSIUM (HYPOKALAEMIA) has what effect on the HEART
(caused by GI loss, drugs ie diuretics)

A

INCREASED incidence of TACHYARRHYTHMIAS
- RAPID HEART RHYTHMS