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*LSS Cardiovascular Y1* > CVS Control > Flashcards

CVS Control Flashcards

1
Q

What is the potassium hypothesis?

A

Potassium ions can move over the semi-permeable cell membranes, while chloride ions cannot, diffusing out the cell down their concentration gradient and reaching equilibrium when the positive charge outside the cell begins to repel the efflux of ions, so there is no net movement over the membrane

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2
Q

What is the Goldman–Hodgkin–Katz equation?

A

Takes into account the relative permeabilities of K+, Na+ and Cl- in order to calculate a membrane potential

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3
Q

What is the resting membrane potential dependent on?

A

Depends on the flow of K+ out of the cells, and the [K+] is maintained by the Na+/K+-ATPase pumps

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4
Q

Describe a graph of Membrane potential against time showing changes in permeability:

A
  1. Sodium permeability increases, allowing an Na+ influx
  2. Transient outward current due to brief K+ efflux
  3. Calcium permeability increases, allowing a Ca2+ influx to prolong the AP (CICR)
  4. Potassium permeability slowly increases to partially depolarise, and when potential becomes low enough, IK1 opens significantly to efflux a large amount of K+ and returning cell to RMP
  5. IK1 open to allow flow in diastole to stabilise RMP
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5
Q

Draw an action potential for the ventricle

A
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6
Q

Draw an action potential for an SA node cell

A
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7
Q

What are the differences between action potentials for ventricular and SAN cells?

A
  • SA node is always oscillating
  • SA node has no IK1 current and so no RMP
  • Sodium channels open in SA node diastole to produce small depolarisation, but upstroke provided by calcium influx
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8
Q

Where is the SAN located?

A

Below the epicardial surface at the RA/SVC boundary

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9
Q

What is the role of the SAN?

A

To spontaneously depolarise to allow autorhythmic contraction (start conduction pathway)

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10
Q

What happens to the SAN upon increased sympathetic stimulation?

A

Decreases the length of an SA node AP - Noradrenaline; depolarise and reach threshold more quickly to increase HR

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11
Q

What is the effect of Increased parasympathetic stimulation on the SAN?

A

Increases length of an SA node AP - Acetylcholine; depolarise and reach threshold more slowly to decrease HR

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12
Q

What modulates the intrinsic heart rate?

A
  • Parasympathetic vagus nerve from cardioregulatory/vasomotor centres in the Medulla to slow heart rate
  • Sympathetic innervation increases heart rate (chronotropy) and contractility (inotropy)
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13
Q

Compare cardiac action potentail and nervous action potential:

A

Cardiac much longer than nervous (200-300ms v 2-3ms); duration of AP controls duration of contraction, so longer + slower contraction needed for effective pumping

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14
Q

What is the absolute refractory period?

A

NO action potentials can be initiated regardless of stimulus intensity

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15
Q

What is the relative refractory period?

A

A larger than normal stimulus can produce an action potential

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16
Q

What are refractory periods?

A

Caused by Na+ channel inactivation; recovery in repolarisation (more negative membrane potential = more channels reactivated - allow heart filling

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17
Q

What is the AV node?

A

Specialised cells delay wave of excitation and insulate from superior ventricular myocardium, allowing ventricular filling through separation of atrial/ventricular contraction

18
Q

What are internodal fibres?

A

Rapid conduction tracts to stimulate atrial myocardium

19
Q

What is the bundle of His?

A

Rapid conducting fibres that are slightly insulated - allowing conduction to apex

20
Q

What are ventricular fibres?

A

Allow upward spread from apex, producing ventricular excitation for increased pressure

21
Q

How does a wave of depolarisation carry to other cells?

A

Wave of depolarisation carried to neighbouring cell, and if exceeds threshold will cause an AP, but keeps spreading and diminishing

22
Q

What reduces resistance to APs between cells?

A

Gap junctions reduce resistance between cells to allow current to leak

23
Q

What are connexons?

A

Connexons in the gap junctions join to form tube between cells

24
Q

What is Flow autoregulation?

A

Intrinsic capacity to compensate for changes in perfusion pressure by changing vascular resistance; decreased perfusion pressure would decrease flow, but autoregulation decreases resistance to increase flow

25
Q

What are the three methods of flow autoregulation?

A
  1. Myogenic theory: smooth muscle fibres respond to tension in vessel wall, so increased pressure causes contraction, and reduced perfusion causes relaxation
  2. Metabolic theory: as blood flow decreases, metabolites accumulate, causing dilation to increase flow and wash metabolites away
  3. Injury: serotonin release from platelets causes constriction
26
Q

Name the endothelium derived Vasodilators and Vasoconstrictors

A

Vasodilators:

Nitric oxide and Prostacyclin

Vasoconstrictors:

Thromboxane A2 and Endothelins

27
Q

Name the non-endothelium derived Vasodilators and Vasoconstrictors:

A

Vasodilators:

Kinins and ANP (Atrial natriuretic peptide)

Vasoconstrictors:

ADH, (nor)adrenaline and AGTII

28
Q

Describe the following details of the Sympathetic innervation:

  • Role
  • Controls
  • Originates from
  • Length of pre-ganglionic fibres
  • First synapse
  • Length of post-ganglionic fibres
  • Second synapse
A
  • Role
    • Fight/Flight
  • Controls
    • Circulation
  • Originates from
    • Thoracic/Lumbar verterbra
  • Length of pre-ganglionic fibres
    • Short
  • First synapse
    • ACh in a nicotinic receptor
  • Length of post-ganglionic fibres
    • Long
  • Second synapse
    • Noradrenaline release
29
Q

Describe the following details of the Parasympathetic innervation:

  • Role
  • Controls
  • Originates from
  • Length of pre-ganglionic fibres
  • First synapse
  • Length of post-ganglionic fibres
  • Second synapse
A
  • Role
    • Rest/digest
  • Controls
    • Heart rate
  • Originates from
    • Cranial/sacral regions of cord
  • Length of pre-ganglionic fibres
    • Long
  • First synapse
    • ACh in a nicotinic receptor
  • Length of post-ganglionic fibres
    • Short
  • Second synapse
    • ACh in Muscarinic receptor
30
Q

What is the vasomotor centre?

A

Located bilaterally in the reticular substance of the medulla and lower third of the pons; comprised of a vasoconstrictor, vasodilator and cardioregulatory inhibitory area; transmits impulses distally through cord to all blood vessels

31
Q

What do lateral portions of the vasomotor centre do?

A

Control heart activity by influencing HR and contractility

32
Q

What do the medial portions of the vasomotor centre do?

A

Control traffic down the Vagus nerve to change HR

33
Q

What is the effect of noradrenaline on vessels?

A

Binds to Alpha1 receptors to cause vasoconstriction

34
Q

What is the tonic activity of the sympathetic NS?

A

Always some level of SNS activity, so baseline can be decreased for vasodilation or increased for constriction by vasomotor centre’s depressor and pressor regions

35
Q

What is the effect of noradrenaline on the heart?

A

Binds to beta1 receptors on the heart to increase force of contraction and hence larger stroke volume (^cAMP = ^PKA to phosphorylate/activate L-type Ca2+channels/SR release channels = ^Ca2+ influx) - increases contractility

36
Q

How can venous return be controlled?

A

Venous return can be increased by skeletal muscle pumping/respiratory movements, increased blood volume and increase SNS vein activation

37
Q

What are baroreceptors?

A

Specialised cells that can detect blood pressure, whose firing mirrors that of blood pressure

38
Q

Where do Carotid sinus baroreceptors send impulses?

A

Down glossopharyngeal PNS afferent to VMC (Vasomotor centre)

39
Q

Where do aortic arch baroreceptors send impulses?

A

Down Vagus nerve PNS afferent to VMC

40
Q

What happens when the carotid sinus baroreceptors detect increased BP?

(Carotid sinus reflex)

A

Increased blood pressure leads to increased baroreceptor firing and…

Increased vagus nerve (PNS) firing to decrease HR

Decreased SNS cardiac (+) and vasoconstrictor (++) nerve impulses to cause vasodilation and decrease contractility

41
Q

What happens to baroreceptors during haemorrage, and what does this lead to?

A

\/ SV = \/ Baroreceptor firing = …

Reduced PNS/increased SNS firing to increase contractility to increase stroke volume

Increased SNS discharge to veins to increase tone and hence pressure/return

Increased SNS discharge to arterioles to increase vasoconstriction

*LSS Cardiovascular Y1* (9 decks)

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