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CVS > Cardiovascular Control 1 > Flashcards

Cardiovascular Control 1 Flashcards

1
Q

How is resting membrane potential established?

A

membrane more permeable to K ions so diffuse down [] gradient carrying positive charge with them
not permeable to negative charge so incident chamber becomes more positive

electrical gradient opposes concentration gradient and equilibrium reached when they equal

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2
Q

What is used to predict equilibrium potentials?

Example for K (Ek)

A

Nerst equation - depends on flow of ion out of cell

[K] outside = 5mM
[K] inside = 120mM
Ek = -80mV (near RMP of ventricular myocyte)
K[] maintained by Na/K ATPase that pumps K into cell against [] gradient

Ek = RT/ZF ln[K]o/[K]i

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3
Q

What is the resting membrane potential (diastole)?

A

K+ equilibrium potential (Ek)

because at rest (diastole) the membrane is only permeable to K

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4
Q

What is the equilibrium potential for Na? ENa

A 
[Na]o = 140mM
[Na]i = 10mM
ENa = +66mV
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5
Q

When does membrane potential = ENa?

A

during upstroke of action potential

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6
Q

What is the Goldman-Hodgkin-Katz Equation?

A

membrane potential is better described when the relative permeability of all ions is considered simultaneously

E(mv) = 61log Px[x]i + y + z
—————————
Px[X]o + y + z

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7
Q

What can change membrane potential?

A

permeability of membrane to ions

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8
Q

What is RMP for a ventricular myocyte?

A

-90mV
RMP depends on flow of K out of the cell
IK1 flows during diastole to stabilise the RMP - membrane is more negative

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9
Q

Why does depolarisation not reach equilibrium potential of Na in nerve cell?

A

Na+ channels inactivate as potential becomes positive to stop the outflow of Na
K permeability increases so positive charge flows out of the cell to restore membrane potential

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10
Q

What is the absolute refractory period?

A

time where no action potential initiated regardless of stimulus intensity

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11
Q

What is relative refractory period?

A

period after ARP where action potential elicited if stimulus strength is larger than normal

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12
Q

What is the difference between nerve and cardiac AP?

A 
nerve shorter (2-3ms)
cardiac (200-300ms)
duration of the action potential controls the duration of heart contraction so for the heart to be an effective pump it must have a long and slow contraction
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13
Q

What determines cardiac action potential at rest?

A

K+

membrane is largely permeable to K to stabilise membrane potential

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14
Q

What physiological mechanism reduces the risk of arrhythmia in cardiomyocytes?

A

a large stimulus is required to excite the cell

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15
Q

What happens during Phase 0?

A

= UPSTROKE
AP causes a large change in Na permeability of the cardiomyocyte
Influx of Na

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16
Q

What happens during Phase 1?

A

= EARLY REPOLARISATION
Large intracellular Na inactivates Na channels and reduces PNa - Na channels enter ARP
Increase in permeability to K
K leaves the cell causing notch in graph (TO/ transient outward potassium current starts)

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17
Q

What happens during Phase 2?

A

= PLATEAU
Large intracellular Na[] increases PCa early in plateau via LTCC
Influx of Ca triggers CICR release from Ca stored for contraction
Increase Ca intracellular and efflux of K maintains plateau at 0mV to allow prolonged AP

18
Q

What happens during Phase 3?

A

= REPOLARISATION
PCa decreases and PK increases (slow and small)
LTCC inactivated slowly
Repolarisation by normal K channel causes IK1 K channels (other subtype) to open

19
Q

What is the full recovery time?

A

time at which a normal AP is elicited with a normal stimulus

20
Q

What is the significance of refractory periods?

A

Recovery time is caused by Na inactivation
Na channels reactivate as the membrane repolarises
RP is good for the heart to allow it to fill before next stimulus causes a contraction

21
Q

What is the difference in RP between skeletal and cardiac muscle?

A

Skeletal - repolarisation occurs early in contraction phase so restimulation and summation of contraction is possible and a second AP can quickly be stimulated

Cardiac - long RP so you cannot re-excite the muscle until the contraction is already well underway
Muscle cannot be tetanised

22
Q

What is tetanus?

A

sustained contraction following series of stimuli

23
Q

Which K channel is responsible for fully repolarising the cell?

A

IK1
large current that stabilises the membrane potential to reduce the risk arrhythmia. Gradual activation of K currents (K outward of cell) balances and overcomes Ca influx
activated once the cell is partially repolarised
during RRP

24
Q

How to reduce contraction of smooth muscle to prevent hypertension?

A

Ca influx blocked by dihydropyridine Ca channel antagonists that bind to LTCC and block it
NIFEDIPINE, NITRENDIPINE, NISOLDIPINE

25
Q

How are Ca channel antagonists used in cardiac muscle?

A

block LTCC to reduce rate of upstroke
decrease strength of contraction
decrease HR

26
Q

Why do different parts of the heart have different AP shapes?

A

different ion currents flow
different ion channel expression in the cell membrane
graphs combined produce PQRST wave (depolarisation towards +ve electrode = upwards deflection, away = downwards deflection)
Repolarising effects are the opposite

27
Q

What properties of myocytes allow an intrinsic heart beat?

A

spontaneously generate
propagate electrical activity in coordinated way via specialised conduction system to excite cells from apex upwards
has own intrinsic pacemaker (cells of SAN)

28
Q

Where is the SAN located?

A

where the SVC and IVC meet the right atrium

29
Q

What does intrinsic heart beat mean? What is the heart extrinsic nerve supply?

A

heart beats independently of nerve supply

autonomic extrinsic nerve supply modifies and controls intrinsic beating of the heart

30
Q

What is the action potential of the SAN?

A
  • produce own AP
  • do not have IK1 channels therefore SAN cells do not have a stable MP
  • upstroke caused by Ca influx via LTCC (not Na)
  • also contain TTCC that activate at more negative MP than LTCC
  • Ito current is very small
  • IF/Pacemaker current present
  • repolarisation by gradual inactivation of Ca channel and increase K permeability
31
Q

What do contractile cells do ?

A

depolarise upon stimulation

32
Q

What nervous supply affects SAN?

A

sympathetic/para nerves synapse with SAN cells
transmitter released has different effects on the SAN
affects the rate of SAN firing that is responsible for modulating heart rate

33
Q

How does sympathetic stimulation to SAN work?

A

adrenaline
increase HR (chronotropy)
increase contractility (inotropy)
steeper pacemaker potential so threshold potential reached more quickly

34
Q

How does parasympathetic stimulation to SAN work?

A

acetylcholine
decrease gradient of pacemaker potential so TP reached more slowly
decrease speed of depolarisation to threshold of SAN cell - fire less frequently - HR decreases

35
Q

How does the CNS connect to the SAN?

A

from: regulatory and vasomotor centres in medulla of brain
parasympathetic is via vagus nerve to SAN
sympathetic nerves from centre to SAN/ventricular tissue

36
Q

What is the structure and function of the SAN?

A

below epicardial surface at boundary of SVC and RA

  • cells spontaneously depolarise
  • heart generates own rhythm (autorhythmicity)
  • SAN is a specialised cluster of autorhythmic cells
37
Q

What are internodal fibres?

A

rapid conduction tracts to AVN to stimulate atrial myocardium

38
Q

What is the AVN?

A

specialised cells that delay the wave of excitation and insulate from superior ventricular myocardium

allows ventricles to fill (-100ms)

39
Q

What is the Bundle of His?

A

splits into 2 branch bundles

rapid conduction of insulated excitatory wave

40
Q

What are Purkinje fibres?

A

conduct action potential at 6x velocity of myocardium

propagate impulse across ventricular myocardium

41
Q

Describe the process of impulse propagation?

A

cardiac AP is propagated by the passive spread of current and existence of threshold over which cell can generate own AP

Gap junctions reduce membrane resistance

  • current easily leaks from cell to cell
  • connexins form tubes linking cells (connexons)
  • GJs located at intercalated discs
42
Q

What is responsible for cardiac muscle relaxation?

A

sarcoplasmic ER Ca ATPase pumps Ca from cytoplasm into SR

CVS (16 decks)

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