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Year 1 - BRS > 6.14 - Control of Heart Function > Flashcards

6.14 - Control of Heart Function Flashcards

1
Q

What can the main anatomical components of the heart be broadly categorised as?

A
  • muscle cells (cardio-myocytes) - can contract and relax in response to electrical stimuli, essential for pumping blood around the body
  • specialised electrical cells - cells that create spontaneous currents and those that transmit currents exist within the heart, essential for supplying blood to the heart - most prominent in controlling heart function
  • vessels - major BVs transport blood in/out of heart, whilst coronary BVs supply blood to the heart
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2
Q

What is the sinoatrial node and where is it?

A
  • pacemaker of the heart: 60-100 bpm
  • junction of crista terminalis - upper wall of right atrium & opening of superior vena cava
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3
Q

What is the atrioventricular node and where is it?

A
  • has pacemaker activity: slow calcium-mediated action potential
  • triangle of Koch at base of right atrium
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4
Q

What are the tracts of the heart?

A
  • internodal tracts - specialised myocytes which connect the SAN and AVN
  • Bundle of His & bundle branches - AVN –> Bundle of His –> branches at intraventricular septum –> Purkinje fibres –> apex
  • Purkinje fibres - specialised conducting fibres
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5
Q

What are the phases of nodal cell action potential?

A
  • nodal AP only has 3 phases (4, 0, 3)
  • phase 4 - pre-potential - Na+ influx through a ‘funny’ channel, nodal cells do not have resting membrane potentials
  • phase 0 - upstroke - due to Ca2+ influx (and Na+ influx)
  • phase 3 - repolarisation - due to K+ efflux
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6
Q

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

A

Caused by different ion currents flowing and different ion channel expression in cell membrane

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7
Q

What is the difference in length of action potential between cardiac myocytes and nerves?

A

Cardiac AP much longer - 200-300ms vs 2-3ms

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8
Q

Why is cardiac action potential so long?

A
  • duration of AP controls duration of contraction of heart
  • long, slow contraction is required to produce an effective pump
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9
Q

What are the phases of a cardiac myocyte action potential?

A
  • 5 phases - 0,1,2,3,4
  • phase 0 - upstroke (Na+ influx)
  • phase 1 - early repolarisation (K+ efflux)
  • phase 2 - plateau (Ca2+ influx)
  • phase 3 - repolarisation (K+ efflux)
  • phase 4 - resting membrane potential
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10
Q

What is the absolute refractory period? (ARP)

A

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

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11
Q

What is relative refractory period? (RRP)

A

Period after ARP where an AP can be elicited but only with larger stimulus strength

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12
Q

Which organ systems are involved in exogenous regulation of heart function?

A
  • brain/CNS - can effect immediate changes through nerve activity or slower changes through hormonal activity
  • kidneys - heart and kidneys share a bi-directional regulatory relationship usually through indirect mechanisms
  • blood vessels - by regulating the amount of blood that goes to and from the heart
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13
Q

What part of the CNS controls the heart?

A

Autonomic nervous system - cardioregulatory centre and vasomotor centres in medulla

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14
Q

How does the parasympathetic NS control heart rate?

A
  • ‘rest and digest’
  • decreases heart rate - decreases slope of phase 4 of SAN cell
  • communicates through vagus nerve to heart
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15
Q

How does the sympathetic NS control heart rate?

A
  • ‘fight or flight’
  • increases heart rate (chronotropy) - increases slope of phase 4 of SAN cell and decrease in time
  • increases force of contraction (inotropy) - increases Ca2+ dynamics
  • communicates through sympathetic nerves to heart
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16
Q

What do parasympathetic nerves consist of and where do they come from?

A
  • arise from cranial and sacral part of spinal cord
  • pre-ganglionic fibres release ACh as NT (nAChR)
  • post-ganglionic fibres also release ACh (muscarinic AChR)
  • PNS important for controlling heart rate
17
Q

What type of receptor on the SA nodal cell receives the post-ganglionic fibre (parasympathetic NS)?

A
  • M2 muscarinic receptor - G-coupled receptor
  • coupled with Gi protein which inhibits adenylyl cyclase which prevents conversion of ATP to protein kinase A
18
Q

What do sympathetic nerves consist of and where do they come from?

A
  • arise from thoracic and lumbar vertebra
  • pre-ganglionic fibres use ACh as NT (nAChR)
  • post-ganglionic fibres use NA as NT
  • synapse onto paravertebral ganglia (sympathetic chain)
  • SNS important for controlling the circulation
19
Q

What type of receptor on the SA nodal cell receives the post-ganglionic fibre (sympathetic NS)?

A
  • beta1-receptor
  • stimulates adenylyl cyclase and increases levels of protein kinase A through second messenger pathway
20
Q

Where is the vasomotor centre (VMC) located?

A

Bilaterally in reticular substance of medulla and lower third of pons

21
Q

What is the vasomotor centre composed of?

A
  • vasoconstrictor (pressor) area
  • vasodilator (depressor) area
  • cardio-regulatory inhibitory area
22
Q

What does the vasomotor centre do?

A
  • transmits impulses distally through spinal cord to almost all blood vessels
  • many higher centres of the brain such as the hypothalamus can exert powerful excitatory or inhibitory effects on the vasomotor centre
  • lateral portions of VMC controls heart activity by influencing heart rate and contractility
  • medial portions of VMC transmits signals via vagus nerve to heart that tend to decrease heart rate
23
Q

Describe the graph showing how heart rate changes due to parasympathetic and sympathetic NS stimulation.

A
  • cut nerves show that the paraNS and symNS are constantly sending out signals to heart - there is basal activity of both nerve types
  • e.g. as sympathetic nerves cut, HR decreases showing there was some sympathetic activity before
24
Q

What does sympathetic innervation to the kidney do?

A
  • increased activity decreases glomerular filtration –> reduced Na+ excretion –> increase in blood volume (also done through aldosterone)
  • change in blood volume detected by venous volume receptors
  • increase in renin secretion –> increased angiotensin-II production –> vasoconstriction and increased blood pressure (detected by arterial baroreceptors)
  • renin secretion also causes aldosterone release which impacts blood volume
25
Q

What part of the kidney do sympathetic nerves innervate?

A

Afferent and efferent arterioles of the glomerulus (and nephron tubule cells)

26
Q

What happens at afferent arterioles of glomerulus due to sympathetic activity?

A
  • primary site of sympathetic activity
  • activation of alpha1-adrenoreceptors by NA causes vasoconstriction –> reduced GFR –> reduced Na+ filtered –> increased blood volume
  • juxtaglomerular cells are the site of synthesis, storage and release of renin
  • beta1-adrenoceptor activation causes renin secretion which increases blood volume
27
Q

What do large pulmonary vessels in cardiopulmonary circuit do?

A
  • they are volume sensors (also atria and right ventricle) - send signals through glossopharyngeal and vagus nerves
  • decrease in filling (due to less blood returning to heart) –> reduced baroreceptor firing –> increased sympathetic NS activity
  • distention (more filling) –> increased baroreceptor firing –> decreased sympathetic NS activity
28
Q

What is part of the arterial circuit?

A
  • aortic arch
  • carotid sinus
  • afferent arterioles of kidneys
29
Q

What does the arterial circuit do?

A
  • pressure sensors - send signals through glossopharyngeal and vagus nerves
  • decrease in pressure –> reduced baroreceptor firing –> increases sympathetic NS activity
  • increase in pressure –> increased baroreceptor firing –> decreased sympathetic NS activity
30
Q

What are the two circulations of the blood?

A
  • pulmonary and systemic
  • right heart –> lungs –> left heart –> body
  • pulmonary to lungs, systemic to body
31
Q

What is venous volume distribution affected by?

A
  • veins and venules contain 61% of blood
  • peripheral venous tone
  • gravity
  • skeletal muscle pump
  • breathing
32
Q

What is central venous pressure and what does it determine?

A
  • mean pressure in the right atrium
  • determines amount of blood flowing back to the heart, which in turn determines stroke volume (using Starling’s Law)
33
Q

What does constriction in veins do?

A
  • reduces compliance and increases venous return
  • increased blood volume / SNS activation of veins / skeletal muscle pump / respiratory movements –> increased venous pressure –> increased venous return –> increased atrial pressure
34
Q

What does constriction in arteries determine?

A
  • blood flow to downstream organs
  • mean arterial blood pressure
  • pattern of blood flow to organs
35
Q

What % of blood are in different components of the circulation?

A
  • pulmonary circulation: 17%
  • heart: 9%
  • veins and venules: 61%
  • arteries: 11%
  • arterioles and capillaries: 7%
36
Q

What are some local mechanisms which regulate blood flow in an organ?

A

Intrinsic to smooth muscle and are endothelium-derived modulators:

  • nitric oxide (NO) - potent vasodilator, which diffuses into vascular smooth muscle cells
  • prostacyclin - vasodilator that also has antiplatelet and anticoagulant effects
  • thromboxane A2 (TXA2) - vasoconstrictor that is also heavily synthesised in platelets
  • endothelins (ET) - vasoconstrictors generated from nucleus of endothelial cells
37
Q

What are some systemic mechanisms which regulate blood flow?

A

These include autonomic NS and circulating hormones and non-endothelium-derived mediators that are extrinsic to smooth muscle:

  • kinins - bind to receptors on endothelial cells and stimulate NO synthesis = vasodilator effects
  • atrial natriuretic peptide (ANP) - secreted from the atria in response to stretch - vasodilator effects to reduce BP
  • vasopressin (ADH) - secreted from pituitary gland, binds to V1 receptors on smooth muscle to cause vasoconstriction
  • noradrenaline/adrenaline - secreted from adrenal gland (& SNS) and cause vasoconstriction
  • angiotensin II - potent vasoconstrictor from the renin-angiotensin-aldosterone axis, also stimulates ADH secretion

Year 1 - BRS (73 decks)

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