week 6-L1 control of heart function Flashcards

(43 cards)

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
how to regulate blood flow
local and systemic mechanism
26
local mechanism of blood flow regulation
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
systemic mechanism of blood flow regulation
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
what increases atrial pressure?
blood volume, respiratory movements, SNS activation of veins and skeletal muscle pumps- increase venous pressure that in turn increase venous return
29
cardiac action potential features
longer action potential for longer slower contraction for more efficient pumping 5 phases ranging 0-4
30
Name the 5 phases of cardiac action potential
``` 0- upstroke 1- early repolarisation 2- plateau 3- repolarisation 4- resting membrane potential ```
31
absolute refractory period
time lag during which no AP can be initiated independent of the stimulus intensity- phase 1 and 2
32
relative refractory period
period where an AP can be initiated follow ARP but required high stimulus intensity
33
what defines resting membrane potential
K+ influx
34
what defines upstroke
large increase in membrane to Na+
35
what defines contraction
Calcium influx which release calcium form intracellular store- L-type VGCC during plates phase
36
what defines the 100-200ms cardiac AP
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
what is the role of Ik
large and flows during diastole to stabilise the resting membrane potential
38
features of pacemaker (SAN) AP
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
SNS effect on cardiac AP graph
chronotropy- cAMP activates If causing increase slope of phase 4 SAN inotropy- increase calcium dynamics in myocytes
40
B1 receptor activation in renal afferent arterioles will have which initial effect?
secretion of renin
41
which receptor transmits signal from pre to post ganglionic nerves in the SNS?
nicotinic Ach receptor
42
when is the afferent nerve activity in the baroreceptor at its highest
high systolic blood pressure and pulse pressure
43
what effect will activation of renal alpha 1 receptor eventually have on the heart?
increased chronotropy and inotropy