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CVS 1.2 > cardiac contraction > Flashcards

cardiac contraction Flashcards

1
Q

duration of AP

A

200-500ms

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2
Q

what is the force of contraction proportional to

A

[Ca2+]i

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3
Q

[Ca2+]i during systole

A

~1uM

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4
Q

[Ca2+]i at maximum contraction

A

~10uM

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5
Q

why doesn’t [Ca2+]i usually reach 10uM

A

Normally cell shortening is submaximal

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6
Q

what happens in the depolarisation phase

A

ca signal and cell shortening - when Ica is generated

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7
Q

what happens in the repolarisation phase

A

cell relaxation - when ca2+ signal is reduced.

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8
Q

what is contraction determined by

A

INCREASE in IC Ca2+ levels

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9
Q

what does a higher increase in [Ca2+]i lead to

A

increased force of contraction

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10
Q

how does [Ca2+]i change

A

from 0.1uM to about 10uM

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11
Q

which receptor does calcium active on the sarcoplasmic reticulum

A

Ryanodine / calcium induced calcium release (CICR)

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12
Q

what causes Ca release from SR

A

(AP upstroke) Na+ ions depolarise T tubules, activating VDCCs, allowing Ca2+ influx
Ca binds to RyR /CICR on SR - close association with T tubules
Release of Ca from SR

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13
Q

How does rise in [Ca2+]i cause myosin-actin interactions

A

Originally my-ac binding sites blocked by troponin-tropomyosin complex;
ca2+ displaced troponin-tropomyosin;
binding sites exposed, cross bridge formed;
myosin head flexes to move actin and Z line to sarcomere centre: contraction

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14
Q

what is troponin made up of

A

TnT - binds to tropomysoin
TnI - binds to actin to hold tropomyosin in place
TnC - binds Ca

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15
Q

how does tropomysoin get displaced

A

binding of Ca to TnC subunit, exposing actin binding sites

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16
Q

Other clinical significance of TnI and TnT

A

important plasma markers for cardiac cell death

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17
Q

how does decrease in [Ca2+]i occur

A

(AP downstroke) K+ ions repolarise T tubules - VDCCs close, decrease in Ca influx;
no Ca influx, no CICR; extrusion of Ca from cell (30%) by Na/Ca exchanger

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18
Q

Where does Ca uptake occur in decreased [Ca2+]i

A

into SR via SR Ca2+ATPase (SERCA, 70%) - Ca in SR for next contraction;
uptake of Ca in mitochondria

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19
Q

fancy name for contractility

A

inotropy

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20
Q

drugs used to correct acute or chronic heart failure do what to the heart

A

increase its contractility

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21
Q

how do drugs increase contractility

A

increase [Ca2+]i levels

22
Q

how do heart failure drugs increase contractility/[Ca2+]i levels

A

increase VDCC activity OR

reduce Ca2+ extrusion

23
Q

what classes of drug increase VDCC activity

A

sympathetic mimetic

24
Q

what classes of drug reduce Ca2+ extrusion

A

cardiac glycosidases

25
Q

how does beta 1 adrenoceptor stimulation a contractility increase

A 
NA binds B1 > Gs, AC, inc cAMP
inc PKA, inc Pi'n of VDCCs
inc Ca influx, inc CICR
inc sliding filament mechanism
inc contractility
26
Q

effect of increased PKA on force of contraction

A

increased Ca2+ influx

increased FOC

27
Q

effect of increased PKA

A 
increased open K channels
increased repolarisation
inc SERCA activity
increased Ca uptake
both increase relaxation
28
Q

sympathetic effect on inotropy

A

positive - increased contractility

29
Q

sympathetic effect on chrontropy

A

positive - increased HR

30
Q

Sympathetic effect on dromotropy

A

positive - increased conduction through AV node

31
Q

sympathetic effect on relaxation

A

positive lusitropic effect - increase rate of relaxation, K channels, SERCA

32
Q

what are drugs that have positive inotropic action called

A

inotropes

33
Q

examples of inotropes

A

cardiac glyocsidases

34
Q

how does digoxin work

A

reducing Ca2+ extrusion

35
Q

what does digoxin do

A

increase contractility

36
Q

what is the mechanism of action for digoxin

A

inhibits Na+/K+ ATPase
causing [Na+]i build up
less Ca2+ extrusion by NCX
More Ca uptake by stores, therefore greater CICR

37
Q

what do dobutamine and dopamine act on

A

beta one adrenoceptors - may be used in acute heart failure

38
Q

where does glucagon act

A

acts on Gs coupled receptor - increase cAMP and PKA activity - used in patients with acute heart failure that take B blockers

39
Q

what is amrinone

A

a phosphodiesterase inhibitor (PDE)

40
Q

which PDE is heart specific

A

Type 3/PDE3

41
Q

how does PDE reduce cAMP

A

by converting cAMP to AMP

42
Q

what is the result of PDE’s conversion of cAMP to AMP

A

reduction in cAMP, reduced activity of PKA

43
Q

what is the IC result of PDE inhibition

A

cAMP build up - PKA activated to increase activity of VDCCs and increased Ca2+ - only used in transplant cases

44
Q

what is the link between electrical activity, change in [Ca2+]i, and contraction

A

higher activation of VDCCs
higher Ca2+ influx
stronger force of contraction

45
Q

what causes a rise and a reduction in [Ca2+]i in cardiac myocytes

A

u

46
Q

what is the importance of a submaximal effect of [Ca2+]i in cardiac myocytes - how does this differ to skeletal muscle?

A

n

47
Q

how does a rise in [Ca2+]i produce contraction?

A

fin

48
Q

can you define the differences between inotropy and Starling’s law

A

i

49
Q

Can you describe the effects of the SNS on the heart?

A

sh

50
Q

?

A

ed

CVS 1.2 (4 decks)

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