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CVS > Cardiovascular control > Flashcards

Cardiovascular control Flashcards

Look at flow diagrams from lecture

1
Q

Membrane potential components

Equilibrium?

A

Electrical gradient- taking into account all ion charges
Concentration gradient- conc. of that specific molecule
Equilibrium = no further net movement of ions+ difference between gradients= 0

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2
Q

What does the resting membrane potential depend on?

A

Flow of K+ out of cells

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3
Q

Membrane potential at diastole

A

Membrane= only permeable to K+ at rest= potential across it= K+ equilibrium potential

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4
Q

K+ concentration maintained by?

Otherwise what will happen?

A

Na+/ K+ ATPase

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5
Q

What does the membrane change depend on?

A

Relative permeabilities of membrane to various ions

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6
Q

Membrane potential at upstroke of action potential (depolarisation)

A

Only permeable to Na+ so membrane potential= Na+ equilibrium potential
Goes towards Na equilibrium potential but Na channels close after so can’t do that and K+ channels open= back to repolarisation

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7
Q

Cardiac action potential compared to nerves
Duration?
Why?

A

Much longer+ slower- duration control duration of heart contraction
Needed for an effective pump

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8
Q

Refractory period terms+ definitions+ purpose

Caused by?

A

Absolute refractory period= time during which no action potential can be initiated regardless of stimulus intensity- useful to allow atria to fill whilst cardiomyocytes can’t contract
Relative refractory period= period after ARP where action potential can be elicited BUT only with stimulus strength larger than normal
Caused by Na+ channel inactivation- channels recover from inactivation as membrane repolarises (as membrane potential becomes more negative again, increase Na channels available)

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9
Q

Refractory periods compared to skeletal muscle?

A

Tetanus: Repolarisation occurs early in contraction phase= re-stimulation+ summation is possible
Cardiac muscle: long refractory period= not possible to re-excite muscle until contraction occurs= cannot be tetanised

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10
Q

Phases of action potential in ventricular cells

A 
0= Upstroke: similar to nerve cell, influx of Na= depolarisation
1= Early repolarisation: caused by increase in K conductance of membrane
2= Plateau: Ca2+ channels opening up
3= Repolarisation: K+ channels opening up
4= Resting membrane potential: diastole
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11
Q

Phase 0 of action potential depends on?

A

Large increase in permeability to Na+

Also increase in permeability to Ca2+ but not as much

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12
Q

What is required for Calcium Release from intracellular stores?
Why is it important?

A

Ca2+ influx

Essential for contraction

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13
Q

Phase 2 inhibition drug

A

Dihyropyridine calcium channel antagonists (eg. nifedipine)

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14
Q

Iₖ₁: specialised K+ channel action?
Responsible for?
When does it flow?

A

Allows for Phase 2/ Phase 3 happening later because GRADUAL activation of K+ currents that balance, then overcome inward flow of Ca2+
Large K+ current (Iₖ₁) from specialised K+ channel that is inactive when the plateau and only starts to flow once the cells have partially repolarised
Responsible for fully repolarising the cell + stabilise resting membrane potential= decrease risk of arrhythmias because takes large stimulus to excite cells
Flows during diastole

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15
Q

Action potential profiles in heart cause

A

Different ion currents flowing+ different ion channel expression in cell membrane

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16
Q

Intrinsic electric properties of heart
Capable of? Through?
What happens if seperated from nerve supply?
Extrinsic nerve supply function? Where does it come from?

A

Independent spontaneous generation+ coordinated propogation of electrical activity through specialised conduction system that starts with SA node that spontaneously depolarises
Heart can beat independently
Modifies+ controls intrinsic beating established by heart.
Comes from autonomic nervous system

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17
Q 
SA node cell action potentials compared to ventricular cell
Upstroke produced by?
Ca channels?
Diastolic membrane potential?
Repolarisation?
A

Very little Iₖ₁- doesn’t have a stable resting membrane potential
Very little Na+ influx so upstroke produced by Ca2+ influx during CICR= slower upstroke
T type Ca2+ channels- activate more negative potentials than L type in ventricular cells
During diastole Na+ channels open which causes small depolarisation
Pacemaker current If present
Repolarisation= same as in ventricular cells (more gradual though because little Iₖ₁

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18
Q

Increased sympathetic stimulation effect on SA node cells action potential
Neurotransmitter?

A

Noradrenaline
Leads to depolarisation much more quickly
Reaches threshold value more quickly (-40mV)
Increase heart rate

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19
Q

Increased parasympathetic stimulation effect on SA node cells action potential
Neurotransmitter?

A

Acetylcholine
Slower depolarisation
Reaches threshold value slower (-40mV)
Decrease heart rate

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20
Q

Draw shape of action potential for
Ventricular cell
SA node cell
(slide 20, CV control 1)

A

-

21
Q

Structures that modulate intrinsic heart rate
Parasympathetic nerve?
Where do the nerves work?
Sympathetic nerve stimulation nerves (SNS nerves) innervation leads to what?

A

Cardioregulatory centre+ Vasomotor centres in medulla
Parasympathetic nerve= Vagus
Vagus+ SNS nerves both act on SA node, SNS nerves work on ventricles too
Increased chonotropy (heart rate)+ ionotropy (contractility)

22
Q

SA node location?

A

Just below epicardial surface at boundary between RA and superior+ inferior vena cava

23
Q

Cardiac conduction system

Pathway of impulse

A
  1. SA node- cluster of autorhythmic cells
  2. Internodal fibres- rapid conduction tracts to stimulate atrial myocardium
  3. Atrioventricular node- delay wave of excitation+ insulate from superior ventricular myocardium- allows ventricular filling through seperation of atrial/ ventricular contraction
  4. Bundle of His- rapid conduction cells to transport insulated wave of excitation
  5. Ventricular fibres- propogate impulse across ventricular myocardium
    Impulse carried on over atria , then down bundle of his to apex then travels up along base
24
Q

Impulse propogation due to?

What reduces membrane resistance? Where do they form? What are they made of?

A

Combination of passive spread of current (either Na or Ca)+ existence of threshold which once reached, causes cell to generate its own action potential (no TV reached= no conduction)
Gap junctions= allow current to easily leak between cells + also allows for intercellular communication.
Form at intercalated discs
Made of connexons made of connexin joining to form tube

25
Q

What mainly causes relaxation of cardiac muscle?

A

Sarcoplasmic- endoplasmic reticulum Ca2+ ATPase pumps Ca2+ from cytoplasm into SR

26
Q

How long does SA action potential usually take for depolarisation?

A

400ms

Adrenaline= less time taken

27
Q

What is venous volume distribution affected by?

A

Peripheral venous tone (how constricted veins are)
Gravity (blood often pools in veins)
Skeletal muscle pump
Breathing

28
Q

What determines amount of blood flowing back to heart?

A

Central venous pressure (mean pressure in RA)

29
Q

What determines stroke volume?
Extrinsic
Intrinsic

A

Extrinsic:
Increased SNS efferents to heart= increase stroke volume
Increase plasma adrenaline= increase stroke volumex`

Intrinsinc:
Increased respiratory movements= decreased intrathoracic pressure which assists Increase EDV
Increase venous return= increase atrial pressure= increase EDV
Increase EDV= Increase stroke volume (Frank-Starling relationship)

30
Q

What does venous constriction lead to?

A

Decreased compliance+ venous return

31
Q

What does arterial constriction determine?

A

Blood flow downstream organs
Mean arterial pressure
Pattern of blood flow to organs

32
Q

Systemic mechanisms

Smooth muscle relation?

A

Extrinsic to smooth muscle, e.g. circulating hormones, ANS

33
Q 
Local mechanisms regulating blood flow
Smooth muscle relation?
Imp for?
Compensates for?
Action?
Myogenic theory?
Metabolic theory?
(Don't know underlying reasons, both might be happening)
Influenced by?
A

Intrinsic to smooth muscle
Imp for reflex local blood flow regulation within an organ
Compensates for changes in perfusion pressure by changing vascular resistance (decrease perfusion pressure would decrease flow and there would be passive constriction but increase vascular resistance compensates for that)
Myogenic theory: Smooth muscle fibres respond to tension in vessel wall (increase pressure= contraction of fibres, involves stretch sensitive Ca channels)
Metabolic theory: As blood flow decreases, metabolites accumulate+ vessels dialate, subsequent increased flow washes metabolites away)
Influenced by O2, K, CO2, Metabolites, Osmolarity, H+

34
Q

Local hormones (another local mechanism)
Vasodilator/ Vasoconstrictor?
Produced from?
Action?

A

Nitric oxide- vasodilator produced from arginine, diffuses into vascular smooth muscle cells

Prostacyclin- cardioprotective vasodilator made from prostaglandin precursor (PGH₂)+ also has antiplatelet+ anticoagulant effects

Thromboxane A₂- vasoconstrictor made from prostaglandin precursor (PGH₂)+ heavily synthesised in platelets (amplify platelet activation)

Endothelins- vasoconstrictors produced nucleus of endothelial cells- has some vasodilator effects

35
Q

Circulating hormones
Vasodilator/ Vasoconstrictor?
Produced from?
Action?

A

Kinins- vasodilator effects, bind to receptors on endothelial cells+ stimulate nitric oxide synthesis

Atrial naturiuretic peptide (ANP)- vasoldilator effects, secreted from atria in response to stretch, reduce BP

Vasopressin (ADH)- vasoconstriction effects, secreted from posterior pituitary gland in response to high blood osmolarity, binds to V1 receptors on smooth muscle= vasoconstriction

Noradrenaline/ Adrenaline- vasoconstriction effects, secreted from adrenal gland

Angiotensin II- vasoconstrictor, product from renin-angiotensin system, also stimulates ADH secretion+ SNS activity

36
Q

Importance of SNS

A

Controls circulation

37
Q

Importance of PNS

A

Controls heart rate

38
Q

PNS Pre-ganglionic fibres neurotransmitter
Neurone length?
Point of synapse?
PNS post-ganglionic neurotransmitter
Neurone length?
How is PNS innervated? (2 methods, 1 has 2 locations)
Increased parasympathetic stimulation leads to?

A 
ACh
Long
Further away from spinal cord (closer to target organ)
ACh
Short
1. Barorecepors- mechanoreceptors in aortic arch change firing rate in response to changing pressure+ send signal to VMC by vagus nerve/ mechanoreceptors in carotic sinus do same thing+ send signal to VMC by glossopharyngeal nerve 
2. increased blood pressure
Decreased heart rate
39
Q 
SNS Pre-ganglionic fibres neurotransmitter
Neurone length?
Point of synapse?
SNS post-ganglionic neurotransmitter
Neurone length?
Neurotransmitter binds to?
What do SNS fibres innervate?
Decreased sympathetic stimulation of heart leads to?
A

ACh
Short
Closer to spinal cord in sympathetic chain
NA
Long
α1 adrenoceptors= smooth muscle contraction+ vasoconstriction, or β1 receptor in ventricular cells
Heart+ all vessels except capillaries+ pre-capillary sphincters+ some metarterioles
Elsewhere= variable (heavily innervated= kidneys, gut, spleen, skin, poorly innervated= skeletal muscle, brain)
Decreased heart rate+ vasodilation

40
Q 
Vasomotor centre
Location?
Composed of?
How does it transmit impulses?
What can influence the VMC?
Lateral portions of VMC function?
Medial portion of VMC function?
A

Bilaterally in reticular substance of medulla oblongata+ lower third of pons
Vasoconstrictor area (pressor) , Vasodilator area (depressor), Cardioregulatory inhibitory area
Distally through spinal cord to almost all blood vessels
Higher centres of brain e.g. hypothalamus can produce exitatory/ inhibitory effects on VMC
Lateral portions control heart activity by influencing heart rate+ contractility
Medial portions transmit signals via vagus nerve to heart- tends to decrease heart rate

41
Q

Nervous control of vessel diameter

A

Vasomotor Centre- depressor+ pressor

SNS innervation, generally not PNS to vessels

42
Q

Cardiac innervation normally

A

Always some level of parasympathetic innervation because when you cut it heart rate increases

43
Q

Controlling force of contraction

A
  1. Noradrenaline binds to β1 receptor on ventricular cell (instead of α1 which is only on smooth muscle)
  2. Increased cAMP
  3. INcrease PKa (Protein Kinase A)
  4. PKA phosphorylates different Ca channels
  5. Ca2+ influx increased+ delivered to myofilaments
  6. Ca2+ uptake to intracellular stores increased
  7. Ca2+ release from intracellular stores increased
44
Q

Feedback- BP example

A

Target BP⇌Cardiovascular control centre →
either decreased SNS, Increased PNS, decreased Ang II, decreased ADH for decreased heart rate
or increased SNS, decreased PNS, increased Ang II, increased ADH for increased heart rate
→ new BP→ baroreceptor→Cardiovascular control centre

45
Q

Baroreceptor activity
Respond to what?
Carotid sinus baroreceptors respond to what pressure range?
Reflex is most sensitive at what pressure range?

A

Changes in arterial pressure
60 to 180mmHg
90-100mmHg (greatest change in impulse rate/unit change in pressure)
(Sigmoid curve)

46
Q

What happens when increased baroreceptor activity

A

Increased afferent nerve stimulation= increased PNS nerve stimulation to heart+ simultaneously inhibits sympathetic nerves to heart, arterioles, veins through inhibitory interneuron which is the connection between afferent nerve+ SNS nerves
SNS nerves inhibited= decreased SNS activity= slows HR+ vessels vasodilate too

47
Q

Carotid sinus nerve activity in response to blood pressure

A

Increase blood pressure= sensed by baroreceptors= increased stimulation of carotid sinus nerve= increased signals sent to VMC= 3 things:

  1. Increased stimulation of vagus nerve to SA node
  2. Decreased stimulation of sympathetic cardiac nerves in ventricular myocardium
  3. Decreased sympathetic vasoconstrictor nerves (controls venous return) in resistance vessels+ capacitance vessels
48
Q

What leads to increased atrial pressure?

A

Increased blood volume/ Increased SNS activation of veins/ Increased skeletal muscle pump/ increased respiratory movements
Lead to increased venous pressure
Lead to increased venous return
Lead to increased atrial pressure= Increased cardiac output

49
Q

Haemorrhage effect on everything

A 
Decreased blood volume
Decreased venous pressure
Decreased venous return
Decreased atrial pressure
Decreased end diastolic volume
Decreased systolic volume
Decreased cardiac output
Decreased blood pressure
Baroreceptor feedback
Increased SNS discharge to veins
Increased venous constriction
Increased venous pressure

CVS (10 decks)

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