the cardiac pressure and volume cycle Flashcards

1
Q

explain the special aspects of the cerebral circulation? 3

A
  • brain maintains all vital functions
  • constancy of flow and pressure
  • circle of Willis= arteries on the brains inferior surface organised into a circle, this means there is a redundancy of blood supply, so if one bridge of the circle is blocked, it can be supplied through another
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2
Q

what are the special aspects of renal circulation? 4

A
  • 20-25% of cardiac output when body is a rest
  • kidneys only form a 0.5% of body weight
  • portal system where glomerular capillaries join to peritubular capillaries
  • makes both ACE and renin, which have endocrine functions, control blood volume and respond to renal blood pressure
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3
Q

what are the special aspects of skeletal muscle circulation? 5

A
  • androgenic input leads to vasodilation
  • can use 80% of cardiac output during strenuous exercise
  • 40% of adult body mass
  • major site of peripheral resistance
  • muscle pump augments venous return
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4
Q

what are the special aspects of skin circulation? 4

A
  • role in thermoregulation- perfusion can increase 100x
  • arteriovenous anastomoses have a primary role in thermoregulation
  • sweat glands have a role in thermoregulation, and produce plasma ultrafiltrate
  • response to trauma= red reaction, flare, wheal
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5
Q

what are the events in the cardiac cycle? 4

A
  • ventricular filling
  • isovolumic ventricular contraction
  • ejection
  • isovolumic ventricular relaxation
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6
Q

what does isovolumic mean?

A

the volume of the ventricle doesn’t actually change

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7
Q

where do the ECG waves come in relation to the ventricular pressure changes?

A
  • precede them
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8
Q

what is the isovolumic ventricular contraction affected by?

A

preload

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9
Q

what is the ejection affected by?

A

afterload

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10
Q

what is the isovolumetric ventricular relaxation affected by?

A

afterload

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11
Q

what happens to the cardiac cycle during mitral stenosis? 2

A
  • decreased preload

- decreased afterload

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12
Q

what happens to the cardiac cycle during aortic stenosis?

A
  • increased afterload
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13
Q

what happens to the cardiac cycle during mitral regurgitation?

A
  • increased preload

- decreased afterload

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14
Q

what happens to the cardiac cycle during aortic regurgitation?

A
  • increased preload
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15
Q

what is the general rule for a systolic murmur? 2

A
  • fluid leaves the ventricle

- AV regurgitation or SL (semilunar) stenosis

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16
Q

what is the general rule for a diastolic murmur? 2

A
  • fluid enters the ventricle

- AV stenosis, Sl regurgitation

17
Q

name 2 types of K+ channels? 3

A
  • delayed rectifier K+ channels = open when the membrane depolarises, but all gating takes place without a delay
  • inward rectifier K+ channels= open when Vm goes below -60mV, clamps the membrane firmly at rest
18
Q

explain the initial depolarisation of an AP? 2

A
  • inward rectifier K channels open, K flows out

something causes the cell to become less negative

19
Q

explain the positive feedback of depolarisation? 4

A
  • causes a few Na+ channels to open
  • the additional current of Na+ leads to more depolarisation
  • positive feedback loop
  • once the voltage goes above the threshold (-50mV) the cell is committed to an AP
20
Q

explain repolarisation? 4

A
  • voltage becomes less positive on the inside of the cell
  • delayer NA+ channel inactivation
  • Delayed rectifier K+ channels open
  • this causes the membrane to be less positive and more negative inside
21
Q

explain the refractory period? 3

A
  • period of time when the neuron is incapable of retaining an AP
  • occurs mostly during hyperpolarization
  • if a functional description
22
Q

explain hyperpolarisation? 2

A
  • at the end of an AP, the voltage inside temporarily goes more negative than at rest followed by a return to the resting membrane potential
  • when the voltage goes below -60mV, the inwards rectifier K channels open again and stay open until the next depolarisation
23
Q

describe the phases of the ventricular myocyte action potential? 5

A
  • phase 0= depolarisation: Na+ gates open in response to a wave of excitation from the pacemaker
  • phase 1= transient outward current: tiny amount of K+ leaves the cell
  • phase 2=plateau phase: inflow of Ca2+ just about balances outflow of K+
  • phase 3= rapid repolarization phase: Vm falls as K+ leaves the cell
  • phase 4= back to resting potential
24
Q

compare neuron, skeletal muscle and cardiac action potentials? 3

A
  • neurons= 1ms, always the same
  • skeletal= AP completed before contraction begins, short refractory period means that repeated AP can cause tetany
  • cardiac= much longer, up to 500ms, varies in duration and size, long refractory period so no tetany
25
Q

describe the plateau phase? 3

A
  • dynamic equilibrium of Ca2+ in and K+ out
  • decreased Vm leads to decreased ca2+ current, not as much decrease for K+
  • as there is a decrease in Ca2+ current, positive feedback causes repolarization by K+
26
Q

what determines the ECG recording?

A
  • the cardiac AP varies in timing and shape in different regions of the heart
27
Q

describe the shape and timing of cardiac action potentials? 5

A
  • SA node= pacemaker
  • AV node and bundle of His= potential pacemakers in case of atrioventricular conduction failure
  • QT interval aligns with ventricular AP
  • QRS= ventricular depression
  • T= ventricular repolarization
28
Q

describe the ionic basis for an action potential in ventricular myocytes? 4

A
  • at rest, the inward rectifier K+ channel has an outward current which stabilizes the membrane (phase 4)
  • the rapid rising phase of the action potential is, exactly as in the nerve and skeletal muscle, due to a transient increase in inward Na current (with positive feedback- phase 0)
  • depolarisation also leads to transient opening of time and voltage dependent CA2+ channels (phase 2)
  • the total K+ conductance decreases rather than increases upon depolarisation
29
Q

explain AP in the SA node and the AV node? 4

A
  • at rest it spontaneously depolarises, not stable at rest because there is no inward rectifier
  • the upstroke of the AP is due to a transient increase in inward CA2+, not due to NA+. nodal upstroke is slower than ventricular myocytes
  • the K+ conductance increases shortly after depolarisation which initiates repolarization
  • duration of nodal AP is around 300ms
30
Q

explain the automaticity of the SA node? 3

A
  • the SA cells are autorhythmic, so resting potential is unstable and close to the threshold
  • cells independently beat at 100bpm, which can be increased by symp activity and decreased by parasymp
  • SA node is normally the pacemaker as it has the fastest rate
31
Q

explain pacemaker potential? 4

A
  • in myocytes of the SA node, AV node and conduction system only
  • voltage drifts positive between nodal beats instead of resting potential because the cells lack inward rectifiers
  • the slope of the PP determines the rate of this firing
  • also called the diastolic potential
32
Q

explain the If (funny current)?5

A
  • If makes the SA node cells spontaneously active
  • driven by HCN channel (responsible for Na+ in and K+ out)
  • increases upon hyperpolarization rather than depolarisation
  • leads to ent inward current, a lot of Na+ inwards
  • depolarises cell towards mV
33
Q

explain blocking ion channels of the cardiac AP? 3

A
  • only block a % of channels otherwise you would kill the patient
  • Na+ channel block leads to a decrease in conduction velocity, changing the organisation fo firing in different regions of the heart, preventing arrhythmias, does not prevent depolarization of decrease HR
  • Ca2+ channel block can decrease the heart rate and contractile force