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Cardiovascular Control Flashcards

(61 cards)

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1
Q

Which equation is usually used for membrane potential

A

Nernst equation

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2
Q

How is potassium concentration maintained across the membrane

A

sodium potassium ATPase

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3
Q

Which equation is better used for membrane potential and why

A

Goldman-Hodgkin-Katz equation as it takes into account the relative permeabilities of several ions simultaneously

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4
Q

How long is the cardiac action potential

A

200-300ms

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5
Q

Why is the cardiac action potential much longer than that of nerves

A

The potential controls the duration of contraction in the heart and long, slow contraction is required to produce an effective pump

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6
Q

Define the absolute refractory period (ARP)

A

Time during which no action potential can be initiated regardless of stimulus intensity

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7
Q

Define the relative refractory period

A

The period after ARP where an AP can be elicited but only with stimulus strength larger than normal

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8
Q

What causes refractory periods

A

Sodium channel inactivation. As more sodium channels recover from this the membrane depolarises

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9
Q

Why can cardiac muscle not tetanus

A

Long refractory period means it is not possible to re-excite the muscle until contraction is well underway

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10
Q

What are the 5 phases of ventricular AP generation

A 
upstroke
early repolarisation
plateau
repolarisation
resting membrane potential
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11
Q

Describe what occurs during upstroke in the ventricle

A

Large increase in membrane permeability to sodium, so large influx of sodium

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12
Q

Describe what occurs during early repolarisation in the ventricle

A

increase in channels that give rise to a transient outward current (PTO) which is carried by potassium ions
Very brief opening of potassium channels for efflux and repolarisation

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13
Q

Describe what occurs during plateau in the ventricle

A

calcium channels open -> calcium influx
stimulated further influx of calcium from the sarcoplasmic reticulum
Prolonged due to inwards movement of calcium and outwards movement of potassium

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14
Q

Describe what occurs during repolarisation in the ventricle

A

slow increase in potassium efflux

IK1 (channel) opens up largely to restore resting potential

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15
Q

Why do different parts of the heart have different action potential shapes

A

different ion currents flowing and different ion channel expression in the cell membrane

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16
Q 
Draw the different action potential shapes for the following:
SA node
Atrial myocardium
Atrioventricular node
Bundle of His
Endocardium
Myocardium
Epicardium
A

-

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17
Q

What is the role of the autonomic nervous system in heart contraction

A

modification and control of the intrinsic beating established by the SA node pacemaker cells

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18
Q

How does SA node’s resting potential differ to others

A

There is no resting potential as some ion channels are missing so it is always oscillating

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19
Q

How does upstroke in the SA node differ to that of other cells

A

upstroke is produced by calcium influx and there is no IK1

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20
Q

What is the difference between T-type and L-type calcium channels

A

T-type activated at more -ve potentials and let more calcium in

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21
Q

Where are L-type calcium channels found

A

Smooth muscle

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22
Q

How does the SNS affect the pacemaker

A

Increased sympathetic stimulation decreases the time taken for depolarisation (acetyl choline)
Heart rate increases

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23
Q

How does the PNS affect the pacemaker

A

Parasympathetic increases the time taken for depolarisation (noradrenaline)
Slows heart rate

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24
Q

Where are the cardioregulatory centre and vasomotor centres found

A

Medulla

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25
Where is the SA node found
Below the epicardial surface at the boundary between the right atrium and superior vena cava
26
What does auto rhythmicity refer to
Spontaneous depolarisation allow the heart to generate its own rhythm
27
Describe the conduction pathway of the heart starting from the SA node
1. SA node spontaneously depolarise and deliver excitations 2. Excitation moves across internal fibres to stimulate atrial myocardium 3. conduction is delayed at the AV cells to allow maximal filling of ventricles 4. Excitation rapidly passes through the bundle of His (insulated) 5. Spreads through the apex of the base to produce ventricular excitation
28
Describe impulse propagation in heart cells
threshold must be generated in the neighbouring cell for impulses to propagate
29
What are gap junctions useful for in heart cells
Allows a lower resistance pathway between heart cells for easier conduction (connexons)
30
How is flow primarily altered
Vessel radius
31
What is the equation for resistance
F=P/R or R=8Ln/𝛑r^4
32
Define autoregulation
Intrinsic capacity to compensate for changes in perfusion pressure by changing vascular resistance
33
What are the 3 types of local autoregulation
Myogenic theory Metabolic theory Injury
34
Describe myogenic theory auto regulation
Myogenic theory = smooth muscle fibres responds to tension in the vessel wall and stretch sensitive channels may be involved
35
Describe metabolic theory autoregulation
Metabolic theory = as blood flow decreases, metabolites accumulate and the vessels dilate so increased flow washes the metabolites away
36
Describe injury auto regulation
Serotonin release from platelets cause constriction
37
Give 2 examples of systemic mechanisms of autoregulation
Circulating hormones e.g. catecholamines | autonomic nervous system
38
Give 2 examples of local autoregulatory hormones
Nitric Oxide Prostacyclin Thromboxane A2 Endothelins
39
Give 2 examples of circulating autroregulatory hormones
``` Kinins Atrial natriuretic peptide (ANP) Noradrenaline/adrenaline Angiotensin II Vasopressin ```
40
What thromboxane A2
Vasoconstrictor local hormone that is synthesised in platelets
41
What is the effect of noradrenaline/adrenaline
Vasoconstriction
42
What is angiotensin II as a auto regulatory hormone
Circulating vasoconstrictor product from the renin-angiotensin-aldosterone axis Stimulates SNS activity and ADH secretion
43
What is vasopressin as a auto regulatory hormone
Circulating Secreted for the posterior pituitary in response to high blood osmolality Binds to V1 receptors on smooth muscle to cause constriction
44
Describe the the nervous systems arising from the cranial part and sacral part of the spinal cord
PNS, shorter post-ganglion Both release ACh 1. nicotinic receptor 2 muscarinic receptor
45
Describe the the nervous systems arising from the thoracic and lumbar vertebra
SNS, longer post-ganglion ACh release then Noradrenaline release Nicotinic receptor in the paravertebral ganglia/sympathetic chain
46
Which nerves are the blood vessels innervated by
Sympathetic system (except the capillaries and precapillary sphincters metarterioles)
47
Which organs are heavily innervated
Kidneys Gur SPleen Skin
48
Which organs are poorly innervated
Skeletal muscle | Brain
49
Where is the vasomotor centre located
Bilaterally in the reticular substance of the medulla and lower third of the pons
50
What is the vasomotor centre composed of
Vasoconstrictor (pressor) Vasodilator (depressor) Cardioregulatory inhibitory area
51
What can control the vasomotor centre
Hypothalamus
52
How does the SNS alter vessel diameter
All blood vessels relieve sympathetic post-ganglionic innervation and as noradrenaline binds to the 𝛼1 receptor, there is either an increase or decrease activity
53
How is the force of contraction increased
1. Noradrenaline binds to the β1 receptor 2. Increase in cAMP 3. Increase in protein kinase A 4. Phosphorylation of L-type calcium channels, SR calcium release channel and calcium ATPase 5. Increase influx of calcium Increase calcium binds to the myofilaments to increase force of contraction
54
How is stroke volume controlled
Extrinsic - increase sympathetic efferents to heart or release adrenaline Intrinsic - increase venous return to increase diastolic volume and stretch
55
What contributes to increase in end diastolic volume
SNS efferents increase Increase in venous return -> increase in atrial pressure Increase in respiratory movements -> thoracic pressure decreases
56
Describe the response when pressure decreases
1. Recognition by the baroreceptors 2. Cardiovascular control centre sends signals to the autonomic nervous system 3. increase in SNS angiotensin II and ADH, decrease in PNS 4. Constriction of the vessels to increase blood pressure 5. Heart rate increases on SNS stimulation
57
Where are the baroreceptors located
Aortic arch and carotid bodies
58
Through where are afferent impulses sent from the baroreceptors
down the glossopharyngeal nerve from carotid arteries (SNS) | Down the vagus nerve from the aortic arch (PNS)
59
How does firing rate change with sympathetic and parasympathetic stimulation
SNS - mechanoreceptors in the aortic arch change firing rate | PNS - mechanoreceptors in the carotid sinus change firing rate
60
How are the blood vessels innervated
Innervation by ONLY SNS efferents while capillaries receive no innervation
61
Describe the response when pressure increases
1. Recognition by the baroreceptors 2. Cardiovascular control centre sends signals to the autonomic nervous system 3. Decrease in SNS angiotensin II and ADH, Increase in PNS 4. Dilation of the vessels to decrease blood pressure with decreased SNS stimulation 5. Heart rate decreases with PNS stimulation

Cardiovascular System (13 decks)

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