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LSS Cadiovascular System > conducting system > Flashcards

conducting system Flashcards

cellular electrical activity: explain membrane potential and changes in ionic permeability; draw action potentials for the ventricle and sino-atrial node; explain the role of the sino-atrial node and importance of refractory periods

1
Q

what is the potassium hypothesis of membrane potential

A

K+ can move over semi-permeable cell membranes and Cl- cannot, so K+ diffuse out of the cell down their K+ gradient and reach equilibrium when positive charge outside the cells repels the efflux of K+, resulting in no net movement over the membrane

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2
Q

when is membrane potential equilibrium achieved

A

when electrical gradient exactly balances chemical gradient

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3
Q

define driving force

A

difference between electrical gradient and chemical gradient (at equilibrium, driving force is 0mV)

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4
Q

what does membrane potential depend on most

A

efflux of K+

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5
Q

what is the equation used to predict what the potential difference will be across semi-permeable membrane

A

Nernst

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6
Q

if the membrane is uniquely permeable to K+ at diastole (resting membrane potential), what is the potential difference across the membrane equal to

A

K+ equilibrium potential

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7
Q

how is [K+] in the cell restored after depolarisation

A

Na+/K+-ATPase pumps

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8
Q

what changes membrane potential in the heart, causing different action potential profiles

A

relative permeabilities of membrane to various ions (different cell types in heart express different ion currents flowing and different ion channel expression in membrane)

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9
Q

if the membrane is uniquely permable to Na+ at upstroke of action potential, what is the potential difference across the membrane equal to

A

Na+ equilibrium potential

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10
Q

why is Goldman-Hodgkin-Katz equation used

A

takes into account relative permeabilities of several ions simultaneously

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11
Q

diagram to show change in membrane potential over time

A

benjis

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12
Q

what happens in phase 0 (upstroke)

A

reaches threshold potential so hugely increased permeability to Na+ due to open channels so Na+ influx; more dependent on Na+ influx than Ca2+ influx; membrane potential depolarised from -70mV to +40mV

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13
Q

what happens in phase 1 (early repolarisation)

A

transient outward current due to brief K+ efflux

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14
Q

what do phases 1 and 2 occur simultaneously with and what channel does it enter through

A

Ca2+ influx through L-type channels

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15
Q

what does Ca2+ influx promote

A

release of further internal Ca2+ (binds to SR Ca2+ release channel), prolonging action potential

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16
Q

what does Ca2+ trigger

A

contraction

17
Q

what happens in phase 2 (plateau)

A

K+ efflux is electrically balanced with Ca2+ influx due to gradual activation of K+ currents

18
Q

what happens in phase 3 (repolarisation)

A

K+ permeability slowly increases to partially repolarise, and when potential becomes low enough (overcome influx of Ca2+, and the Ca2+ channels slowly close (Ca2+ ATPase starts to pump Ca2+ back into SR), IK1 opens significantly to efflux large amount of K+, returning cell to resting membrane potential

19
Q

what happens in phase 4 (resting membrane potential)

A

IK1 open to allow flow during diastole, stabilising resting membrane potential

20
Q

ventricle and SAN action potential differences

A

SAN keeps oscilating, SAN has no IK1 current so no resting membrane potential, Na+ channels open in SAN diastole to produce small dissociation, but upstroke provided by Ca2+ influx

21
Q

what Ca2+ channels are activated in SAN

A

T-type

22
Q

what is the significance of T-type Ca2+ channels being present in the SAN

A

activate at more negative potentials than L-type, so require smaller depolarisation

23
Q

how is repolarisation brought about in the SAN

A

inactivation of Ca2+ channels so reduced Ca2+ influx

24
Q

where is the SAN located

A

below epicardial surface at right atria/superior vena cava boundary

25
Q

structure of SAN

A

group of specialised cells

26
Q

role of SAN

A

spontaneously depolarise to allow autorhythmic contraction, starting conduction pathway, by nerves synapsing to it

27
Q

which nervous system is the extrinic nerve supply of the heart

A

autonomic nervous system

28
Q

what does the autonomic nervous system do to the heart

A

modulate pacemaker activity and control intrinsic beating established by heart

29
Q

what nervous systems control heart rate and what neurotransmitters do each secrete

A

sympathetic (noradrenaline) and parasympathetic (acetylcholine) nervous system, which synapse with SAN cells

30
Q

effect on heart rate and contractility of increasing sympathetic stimulation

A

membrane depolarises and reaches threshold potential more quickly, increasing heart rate (positive chronotropy) and contracilitiy (positive inotropy)

31
Q

effect on heart rate of increasing parasympathetic stimulation

A

membrane depolarises and reaches threshold potential more slowly, decreasing heart rate

32
Q

what nerves modulate intrinsic heart rate

A

vagus nerve (parasympathetic nerve), accelerans nerve (sympathetic nerve)

33
Q

where are the cardioregulatory and vasomotor centres from where the vagus nerve begins

A

medulla

34
Q

what is the duration of cardiac action potential and purpose

A

200-300ms (very long), allowing it to be an effective pump

35
Q

define absolute refractory period

A

time during which no action potential can be inititated regardless of stimulus intensity

36
Q

define relative refractory period

A

period after absolute refractory period where an action potential can be elicited, but only with stimulus strength larger than normal (leading to reduced risk of arrhythmias in specialised IK1)

37
Q

what are refractory periods caused by

A

Na+ channel inactivation

38
Q

when do Na+ channels recover from inactivation

A

during membrane repolarisation (more negative membrane potential = more channels reactivated to allow heart filling)

39
Q

why don’t tetanic (summation) contractions occur in cardiac muscle

A

long refractory period so not possible to re-excite muscle until process of contraction well underway

LSS Cadiovascular System (40 decks)

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