Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Z YEAR 1 BRS cardiology > Control of Heart Function > Flashcards

Control of Heart Function Flashcards

1
Q

What is the ANS in the heart?

A

Cardio-regulatory centre & vasomotor centres in medulla

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the PNS in the heart?

A
  • ‘Rest & digest’

* decrease heart rate (HR) – decreases the slope of phase 4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the SNS in the heart?

A
  • ‘fight or flight’
  • ­ increase HR (chronotropy) – increases the slope of phase 4
  • ­ increase force of contraction (inotropy) – increases Ca2+ dynamics
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How does the sympathetic nerves in renal system increase blood volume? ?

A
  1. Blood volume: Detected by venous volume receptors
    2, When sympathetic activity increases, this acts on alpha-1 receptors in the afferent arteriole that will cause them to vasoconstrict via their Gq-protein coupled mechanism
  2. This means less glomerular filtrate is created (lowered GFR) due to less blood flow and therefore less sodium enters the filtrate, so less water is lost resulting in increased water remaining in the blood =increased Blood volume
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is another way that the sympathetic nerves in renal system control heart function?

A
  1. Blood pressure: Detected by arterial baroreceptors
  2. When sympathetic activity increases, this acts on Beta-1 adrenoreceptors in the juxtaglomerular apparatus that will cause the release of renin via their Gs-protein coupled receptor.
  3. Renin will go on to activate the renin-angtiontesin-aldosterone system creating ATII that is a potent vasoconstrictor of blood vessels, thereby increasing peripheral resistance and as MBP = CO*TPR there is an increase in BP.
  4. ATII also causes Increase ALD release = Increase Na+ retention and also H2O
    Increase sympathetic activity
    Increase ADH secretion = Increased H2O retention at CD
    -ACE converts ATI to ATII
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

How does the cardiopulmonary circuit affect heart function with baroreceptors?

A

-Large pulmonary vessels
•Volume sensors (also atria & right ventricle): send signals though glossopharyngeal & vagus nerves
-The baroreceptors:
1. stimulatory of the parasympathetic nerve to the heart: decreasing heart rate
2. Reduce SNS actively which which increase HR and vasoconstriction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

How does the arterial circuit affect heart function?

A

-Aortic arch, carotid sinus & afferent arterioles of kidneys are where bbsrorecptors found
•Pressure sensors: send signals though glossopharyngeal & vagus nerves
•Decrease in pressure -> decrease baroreceptor firing -> increase SNS activity
•Increase in pressure -> increase baroreceptor firing -> decrease SNS activity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the parasympathetic ANS?

A

Parasympathetic
‘rest and digest’
•Pre-ganglionic fibres use ACh as neurotransmitter
•PNS post ganglionic NT = ACh
•PNS is important for controlling the heart rate
-Arise from cranial part of spinal cord
-Arise from sacral part of spinal cord

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the sympathetic ANS?

A

‘fight or flight’
•Pre-ganglionic fibres use ACh as their neurotransmitter
•SNS post ganglionic NT = NA
•SNS is important for controlling the circulation
-Sympathetic arising from thoracic vertebra
-Sympathetic arising form lumbar vertebra

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Where is the vasomotor centre?

A

VMC located bilaterally in reticular substance of medulla & lower third of pons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the vasomotor centre composed of?

A
  • Vasoconstrictor (pressor) area
  • Vasodilator (depressor) area
  • Cardio-regulatory inhibitory area
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What does the vasomotor centre do?

A
  • Transmits impulses distally through spinal cord to almost all blood vessels
  • Many higher centers of the brain such as the hypothalamus can exert powerful excitatory or inhibitory effects on the VMC.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What does the lateral portion of VMC do?

A

Lateral portions of VMC controls heart activity by influencing heart rate and contractility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What does the medial portion of the VMC do?

A

Medial portion of VMC transmits signals via vagus nerve to heart that tend to decrease heart rate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is cardiac innervation?

A
  • Symph and para goes to SAN
  • Symph increase activity by beta 1 receptors which are associated with GS linked proteins which activate adenolocyclase and increase activity of cyclic a and B and protein kinase A
  • Cyclic A and B which for molecular regulation of ion channels
  • Para: activates M2 receptors of SAN and are GI linked reduce levels of clcic A and B reduce activity of adenocylase so reduces heart rate and force of contraction
  • If remove one, some tonic underlying activity of systems, but if take off both increase so para more active
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How do the sympathetic nerves affect renal system?

A

•Sympathetic nerve fibres innervate afferent & efferent arterioles of the glomerulus (& nephron tubule cells)
-MORE EFFECT ON afferent then efferent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

How do the sympathetic nerves affect afferent arterioles?

A
  1. •Primary site of sympathetic activity relase of noradrenaline act on:
    •a1-adrenoceptor -> vasoconstriction
    • decrease in glomerular filtration rate -> decrease Na+ filtered
  2. •Juxtaglomerular cells are the site of synthesis, storage & release of renin
    •beta 1-adrenoceptor -> renin secretion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are the two circulations?

A

•Two circulations: pulmonary (17%) and systemic
-Heart (9%) Veins and venues (61%), arterieoles and capillaries (7%), arteries (11%)
•Right heart -> lungs -> left heart -> body

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is venous volume distribution affected by?

A

peripheral venous tone, gravity, skeletal muscle pump & breathing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What does central venous pressure determine?

A

•Central venous pressure (mean pressure in the right atrium) determines amount of blood flowing back to heart

21
Q

What does the amount of blood flowing back to the hear determine?

A

stroke volume (using Starling’s Law of the Heart)

22
Q

In veins what does contraction reduce?

A

compliance and venous return

23
Q

In arterioles what does contraction determine?

A

a) Blood flow to downstream organs
b) Mean arterial blood pressure
c) The pattern of blood flow to organs

24
Q

What are the local mechanisms for regulating blood flow?

A
  • Intrinsic to the smooth muscle (or closely associated)

* Important for reflex local blood flow regulation within an organ

25
Q

What are the endothelium derived mediators (local mechanisms)? What do they do?

A
  • Nitric oxide (NO): potent vasodilator, which diffuses into vascular smooth muscle cells.
  • Prostacylin: vasodilator that also has antiplatelet & anticoagulant effects
  • Thromboxane A2 (TXA2): vasoconstrictor that is also heavily synthesised in platelets
  • Endothelins (ET): vasoconstrictors generated from nucleus of endothelial cells
26
Q

What are systemic ways to regulate blood flow?

A
  • Extrinsic to the smooth muscle

* These include the autonomic nervous system & circulating hormones

27
Q

What are the non-endothelium derived mediators (systemic mechanisms)? What do they do?

A
  • Kinins: bind to receptors on endothelial cells & 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); causes vasoconstriction
  • Angiotensin II: potent vasoconstrictor from the renin-angiotensin-aldosterone axis. Also stimulates ADH secretion
28
Q

What impacts atrial pressure?

A
  • Increase SNS activation of veins
  • Increase Skeletal muscle pump
  • Increase Respiratory movements
  • Increase blood volume
    1. Increase Venous pressure
    2. Increase Venous return
    3. Increase atrial pressure
29
Q

What is the Sinoatrial Node?

A
  • Pacemaker of the heart: 60-100 bpm

* Junction of crista terminalis; upper wall of right atrium & opening of superior vena cava

30
Q

What is the Atrioventricular (AV) node?

A
  • Has pacemaker activity: slow calcium mediated action potential
  • Triangle of Koch at base of right atrium
31
Q

What are the bindles of His and bundle branches?

A

•Specialised myocytes. AV node: His bundle -> branches at intraventricular septum -> apex
Purkinje fibres
•Specialised conducting fibres

32
Q

What is the cardiac action potential?

A
  • Compared with nerves the cardiac action potential (AP) is very long (200-300 ms vs. 2-3 ms)
  • Duration of AP controls duration of contraction of heart
  • Long, slow contraction is required to produce an effective pump
33
Q

How many cardiac action potential phases are there?

A

5 phases number 0-4

34
Q

What is the Absolute refractory period (ARP)?

A

time during which no AP can be initiated regardless of stimulus intensity

35
Q

What is the Relative refractory period (RRP)?

A

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

36
Q

What are the different phases of cardiac action potential?

A
  1. Phase 0: Upstroke
  2. Phase 1: Early depolarisation
  3. Phase 2: Plateau
  4. Phase 3: depolarisation
  5. Phase 4: Resting membrane potential
37
Q

Describe the first phases of the action potential

A
  • Resting membrane potential determined by K+ efflux
  • Upstroke determined by large increase in membrane to Na+ permeability
  • Ca2+ influx required to trigger Ca2+ release from intracellular stores – essential for contraction
  • Ca2+ current (ICa) activates rapidly (within a few milliseconds) but the upstroke is more dependent on INa
38
Q

Describe the last phases of the action potential

A
  • Gradual activation of K+ currents (K+ moving outward) that balance, then overcome, inward flow of Ca2+
  • Large K+ current (IK1) that is inactive during the plateau starts to flow once the cells have partially repolarised
  • IK1 is responsible for fully repolarising the cell
  • IK1 is large and flows during diastole. It stabilises the resting membrane potential
39
Q

Are there different action potential profiles?

A
  1. Different parts of the heart have different action potential shapes
  2. Caused by different ion currents flowing and different ion channel expression in cell membrane
40
Q

What is the sinoatrial node-pacemaker (action potential)?

A
  • SA node AP only has phase 0, 3 & 4
  • No early repolarisation or plateau phase
  • Resting membrane potential becomes ‘pre-potential’ due to T-type Ca2+ channels & ‘funny’ current (If)
41
Q

What does the sympathetic nervous system do for the heart?

A
  • ‘fight or flight’
  • ­ INCREASE HR (chronotropy) – increases the slope of phase 4 in SA node
  • cAMP activates If
  • ­ INCREASE force of contraction (inotropy) – increases Ca2+ dynamics in myocytes:
  • ­ INCREASE Ca2+ influx
  • ­ INCREASE Ca2+ uptake into intracellular stores
  • ­ INCREASE Ca2+ release from intracellular stores
42
Q

What does the parasympathetic system ganglions do in the brain for the heart?

A
  1. Long pre-ganglionic from the spinal cord synapse with post-ganglionic via a nicotinic receptor that utilises ACh
  2. Short post-ganglionic will synapse with the target organ again using ACh but on muscarinic receptors
43
Q

What happens when blood volume is high?

A
  1. increased SV so increased CO
  2. Therefore increased BP, so to decrease BP, the baroreceptors increase in firing thereby increasing PNS activation so cause vasodilation and lowered HR => decreased BP
  3. Decreased SNS means less renin so less vasoconstriction and decreased blood volume.
44
Q

What happens when blood volume is low?

A
  1. there is decreased filling (SV) off the heart and so decreased CO (CO=HRSV) so BP is low (BP=COTPR) so to maintain CO we need to increased TPR
  2. Hence the baroreceptors come into play so baroreceptors decrease in firing therefore decrease PNS activation and increased SNS so there is an increase in HR and vasoconstriction and venoconstriction causing increased TPR so overall increased BP, CO and in turn increased BV via the kidney as on the previous slide.
45
Q

What happens in the sympathetic ganglion system in the brain?

A
  1. Short pre-ganglionic from the thoracolumbar spine use ACh as the transmitter to the post-ganglionic fibres via nicotinic receptors that lie in the sympathetic chain
  2. Long post-ganglionic fibres use Noradrenaline on the beta or alpha (adrenergic) receptors depending on the organ.
46
Q

What happens with the sympathetic system in the brain for control of heart function?

A
  1. Except the adrenal medulla receives direct NA
  2. Beta and alpha receptors are Gs coupled protein receptors so cause an increase in cAMP levels therefore increased PKA so increased L-type channel opening and increased Ca2+ influx therefore increased force of contraction and rate in the heart
    3/ Also increases Ca2+ store uptake
47
Q

What happens with the parasympathetic system in the brain for control of heart function?

A

M2-receptors are Gi-protein linked causing inhibition of Adenylyl cyclase therefore decreased cAMP so decreased opening of L-type channels therefore less Ca2+ influx and less forceful contraction and lower rate.

48
Q

What are the local hormone by endothelial cells?

A
  1. Nitric Oxide – Vasodilator via SM effects
  2. Prostacyclin – Vasodilator + anti-platelet +anti-coagulant
  3. Thromboxane A2 – Vasoconstrictor (made in platelets as well)
  4. Endothelins – Vasoconstrictor (from nuclei)
49
Q

What are the systemic hormones?

A
  1. Kinins - Vasodilator that circulate in blood +stimulate NO
  2. Atrial natriuretic peptide (ANP) - Vasodilator release from atria when they are stretched = lowered BP
  3. Vasopressin (ADH) – Vasoconstriction via binding V1-R on SM
  4. NA/A from SNS – Vasoconstriction
  5. ATII from RAAS – Vasoconstriction, SNS activation, ADH release and ALD release

Z YEAR 1 BRS cardiology (10 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions