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module 103 - theme 3 > cardiac pressure-volume cycle > Flashcards

cardiac pressure-volume cycle Flashcards

1
Q

what is the circle of Willis?

A
  • arteries on brains inferior surface organised into a circle
  • redundancy of blood supply
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2
Q

what capillaries are in the portal system?

A

glomerular capillaries to peritubular capillaries

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3
Q

what proportion of body weight is made from the kidneys?

A

0.5%

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4
Q

what does ACE and renin do?

A
  • endocrine functions
  • controlling blood volume
  • responding to renal blood pressure
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5
Q

what does the skeletal muscle pump do?

A

augments venous return

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6
Q

what does adrenergic input lead to?

A

vasodilation

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7
Q

how does skin circulation have a role in thermo-regulation?

A

perfusion can increase 100x

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8
Q

how does skin circulation affect arterio-venous anastomoses?

A

primary role in thermoregulation

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9
Q

how does skin circulation affect sweat glands?

A

role in thermoregulation and plasma ultrafiltrate

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10
Q

how does skin circulation affect the response to trauma?

A

red reaction, flare, wheal

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11
Q

what are the 4 sequential events of the cardiac cycle?

A
  • ventricular filling
  • isovolumic ventricular contraction
  • ejection
  • isovolumic ventricular relaxation
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12
Q

what are the 2 valve sounds for S1 and S2?

A
  • S1: AV valves close, normally loudest

- S2: semi lunar valves close, systole occurs between S1 and S2, duration: systole < diastole

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13
Q

what is a systolic murmur?

A

fluid leaves ventricle, AV regulation of SL stenosis

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14
Q

what is a diastolic murmur?

A

fluid enters ventricles, AV stenosis or SL regurgitation

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15
Q

what causes myocytes to contract?

A
  • sliding filament model
  • thin filaments (actin) and thick filaments (myosin)
  • consumes ATP
  • trigger is increase in free calcium
  • initiated by increase in voltage: the cardiac action potential
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16
Q

what happens when an ion channel in the membrane opens?

A

causes a current flow

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17
Q

what are delayed rectifier K+ channels?

A

open when membrane depolarised but all gating takes place with a delay

18
Q

what are inward rectifier K+ channels?

A

open when Vm goes below -60mV and its function is to clamp the membrane firmly at rest

19
Q

what happens in initial depolarisation?

A
  • the cell starts at rest (-70mV)
  • inward rectifier K+ channels are open, K+ flowing out is the dominant current
  • resting membrane potential is near
  • something causes the cell to become less negative
  • depolarisation: inside the cell the voltage becomes less negative
  • could be a nearly cell depolarising
  • could be synaptic transmission where a neurotransmitter open ligand-gated channel
20
Q

what happens with positive feedback of depolarisation?

A
  • the initial depolarisation causes a few of the Na+ channels to open
  • Na+ permeability increases, Na+ current flows through channels into cell
  • the additional current of Na+ going into the cell leads to more depolarisation: positive feedback loop
  • when the voltage goes above the threshold voltage (-50mV) the cell is committed to an AP
  • the positive feedback of increased Na+ channel conductance and increased voltage continues until the membrane becomes quite positive
21
Q

what is repolarisation?

A

voltage becomes less positive (or negative) inside the cell

22
Q

what happens in repolarisation?

A
  • due to the passage of time, 2 delayed-action events occur: Na+ channel inactivation leads to decreased Na+ current going in
  • delayed rectifier K+ channels open leads to increased K+ going out
  • these cause the membrane to be less positive and more negative inside
23
Q

what happens in the refractory period?

A
  • period of time during which neuron is incapable of reinstating an AP
  • the amount of time it takes for neurons membrane to be ready for a second stimulus once it returns to its resting state following an excitation
  • refractory period occurs mostly after hyperpolarisation
24
Q

what is after-hyperpolarisation (AHP)?

A

at the end of an AP the voltage inside temporarily goes slightly more negative than at rest, followed by a return to the testing membrane potential

25
Q

what happens during after-hyperpolarisation?

A

the increase in K+ permeability and decrease in Na+ permeability leads to the membrane potential moving closer to Ek

26
Q

how big is a neural action potential?

A

approx 1ms, always the same size

27
Q

how big is a cardiac action potential?

A

up to 500ms, varies in size and duration, long refractory period, no tetany

28
Q

what are action potentials like in skeletal muscle?

A

action potentials completed before contraction begins, short refractory period means that repeated action potentials leads to tetany

29
Q

what is the plateau phase?

A
  • dynamic equilibrium: Ca2+ current in, K+ current out
  • decreased Vm leads to decreased Ca2+ current
  • so decreased Ca2+ current leads to positive feedback
30
Q

what is the SA node?

A

heart pacemaker

31
Q

what are the AV node and bundle of His?

A

potential pacemakers in case of atrio-ventricular conduction failure

32
Q

what do QRS an T peaks show?

A 
QRS = ventricular depolarisation
T = ventricular repolarisaiton
33
Q

how do ventricular myocytes work?

A

1) at rest, the inward rectifier K+ channel leads to the outward current stabilising membrane
2) the rapid upstoke of the action potential is exactly as in nerve and skeletal muscle due to a transient increased in inward Na current
3) depolarisation also leads to transient opening of time and voltage dependent Ca channels
4) the total K conductance decreases rather than increases upon depolarisation
5) repolarisation is greatly delayed due to 2 and 3

34
Q

what happens with action potentials in the SA node and AV node?

A
  • at rest spontaneously depolarises: not stable at rest because there is no inward rectifier
  • the upstroke of the action potential is due to transient increase in inward Ca: not Na, Ca current, nodal upstroke is slower than in ventricular myocytes
  • the K conductance increases shortly after depolarisation: initiates repolarisation
  • duration nodal AP (phases 0 + 3) = approx 300ms
35
Q

what does it mean that sinoatrial node cells are autorhythmic?

A

resting potential is unstable, resting potential is close to threshold

36
Q

what cells and where is the pacemaker potential found?

A

in the myocytes of SA node, AV node and conduction system only

37
Q

what determines the rate of firing (diastolic potential)?

A

slope of pacemaker potential

38
Q

when does If increase?

A

upon hyperpolarisation rather than depolarisation

39
Q

what happens when the If leads to a net inward current?

A
  • leads to a lot of Na+ current inward and a tiny K+ current outward
  • depolarises cell towards 0mV
40
Q

why does drug therapy only block a percentage of the ion channels you target?

A

if you blocked them all the patient would die

41
Q

what happens when the Na+ block leading to decreased conduction in velocity?

A
  • the changes of the organisation of firing in different regions of the heart
  • this can prevent (or sometimes cause) arrhythmias
  • it does not prevent depolarisation or affect HR
  • calcium channel block can lead to decreased heart rate and decreased contractile force

module 103 - theme 3 (17 decks)

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