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BRS > week 6-L1 control of heart function > Flashcards

week 6-L1 control of heart function Flashcards

1
Q

what control the heart function?

A

CNS, blood vessel and kidneys

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2
Q

how CNS control of the heart

A

parasympathetic and sympathetic controls by ANS

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3
Q

CNS what does parasympathetic system do?

A

rest and digest therefore

decrease HR and slope of phase 4

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4
Q

CNS what does sympathetic system do?

A

increase HR and slope of phase 4

increase force of contraction and calcium dynamics

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5
Q

chronotropy

A

increase in heart rate

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6
Q

inotropy

A

increase in contraction force of ventricles from increase calcium dynamics

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7
Q

KIDNEY control of the heart

A

sympathetic innervation only- absence of parasympathetic innervation in the kidney

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8
Q

KIDNEY sympathetic control on heart

A

decrease glomerular filtration- decrease Na excretion

cause increase in blood volume and BP

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9
Q

KIDNEY blood volume regulation

A

detected by venous volume receptors

increase renin secretion- increasing angiotensin II production causing vasoconstriction- blood pressure increase

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10
Q

KIDNEY how is blood pressure detected?

A

arterial baroreceptors

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11
Q

BLOOD VESSEL cardiopulmonary circuit

A

volume sensors in atria and ventricles sending signals through the glossopharyngeal and vagus nerves

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12
Q

BLOOD VESSEL decrease in filling

A

detected by reduction in baroreceptors firing to increase SNS activity

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13
Q

BLOOD VESSEL distention

A

detected by increase in baroreceptors firing to increase the PNS activity and reduce SNS activity

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14
Q

features of PNS

A

pre and post ganglionic fibres release Ach as neurotransmitter and control heart rate

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15
Q

features on SNS

A

pre ganglionic fibres release Ach but post ganglionic fibres release noradrenaline
SNS important in controlling circulation

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16
Q

describe the mechanism SNS

A

beta-1 receptors activation cause Gs stimulation
AC activated converting ATP to cAMP to PKA
increase the HR and BP

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17
Q

describe the mechanism of PNS

A

M2 receptors cause the Gi stimulation that inhibits the conversion of ATP to PKA
reduction in HR and BP

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18
Q

what happens if SNS cut off

A

HR falls below normal

19
Q

what happens if PNS cuts off

A

HR rise above normal

20
Q

what does cut off CNS or PNS show

A

that both systems work together to maintain normal HR

21
Q

renal system sympathetic fibre innervation

A

afferent and efferent arterioles

22
Q

renal afferent arterioles effect of SNS

A

primary site of SNS activity
alpha 1 adrenoceptor causes vasoconstriction
decrease in glomerular filtration rate causes decrease in Na filtered
Juxtaglomerular cells site of renin synthesis, storage and release- beta 1 adrenoceptor stimulation cause renin secretion

23
Q

designs of circulatory circulation and why

A

more blood % in vein and venues and less in arteries

increase preload and decrease after-load

24
Q

constriction of veins and arteries

A

veins- causes reduction in compliance (ability to stretch0 and venous return decreasing preload
arteries- causes increase in after load as blood pressure increases

25
Q

how to regulate blood flow

A

local and systemic mechanism

26
Q

local mechanism of blood flow regulation

A

intrinsic smooth muscles or endothelial-derived mediators
vasodilators- nitric oxide on smooth muscles and prostacyclin anti platelet and anticoagulant effect
vasoconstrictors-thromboxane A2 heavily synthesised in platelets and endothelins from endothelial nucleus

27
Q

systemic mechanism of blood flow regulation

A

extrinsic to smooth muscles and non derived endothelial mediators
vasodilators- kinins bind to receptor on endothelial cells and stimulate no synthesis and atrial natriuretic peptide response to stretch to reduce BP
vasoconstrictors- vasopressin binds to V1 receptors on smooth muscles, noradrenaline and angiotensin II stimulate ADH secretion

28
Q

what increases atrial pressure?

A

blood volume, respiratory movements, SNS activation of veins and skeletal muscle pumps- increase venous pressure that in turn increase venous return

29
Q

cardiac action potential features

A

longer action potential for longer slower contraction for more efficient pumping
5 phases ranging 0-4

30
Q

Name the 5 phases of cardiac action potential

A 
0- upstroke
1- early repolarisation
2- plateau
3- repolarisation
4- resting membrane potential
31
Q

absolute refractory period

A

time lag during which no AP can be initiated independent of the stimulus intensity- phase 1 and 2

32
Q

relative refractory period

A

period where an AP can be initiated follow ARP but required high stimulus intensity

33
Q

what defines resting membrane potential

A

K+ influx

34
Q

what defines upstroke

A

large increase in membrane to Na+

35
Q

what defines contraction

A

Calcium influx which release calcium form intracellular store- L-type VGCC during plates phase

36
Q

what defines the 100-200ms cardiac AP

A

gradual activation of K+ currents outwards balancing and overcoming calcium flow
NB large Ik inactive during plateau but increase once cells partially repolarised
Ik responsible for full repolarisation

37
Q

what is the role of Ik

A

large and flows during diastole to stabilise the resting membrane potential

38
Q

features of pacemaker (SAN) AP

A

presence of only phases 0,3,4

resting membrane potential become prepotential- can initiate another AP due to L-type VGCC and funny current

39
Q

SNS effect on cardiac AP graph

A

chronotropy- cAMP activates If causing increase slope of phase 4 SAN
inotropy- increase calcium dynamics in myocytes

40
Q

B1 receptor activation in renal afferent arterioles will have which initial effect?

A

secretion of renin

41
Q

which receptor transmits signal from pre to post ganglionic nerves in the SNS?

A

nicotinic Ach receptor

42
Q

when is the afferent nerve activity in the baroreceptor at its highest

A

high systolic blood pressure and pulse pressure

43
Q

what effect will activation of renal alpha 1 receptor eventually have on the heart?

A

increased chronotropy and inotropy

BRS (28 decks)

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