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CVS II > Contractility > Flashcards

Contractility Flashcards

1
Q

What controls SV?

A

preload, HR, contractility, afterload

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2
Q

How does preload control SV?

A

Stretching of heart at rest, increases SV due to Starling’s law

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3
Q

How does HR control SV?

A

Sympathetic + parasympathetic nerves

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4
Q

How does contractility control SV?

A

Strength of contraction at given resting load, due to sympathetic nerves + A increasing [Ca2+ ]

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5
Q

How does afterload control SV?

A

Opposes ejection, reduces SV due to Laplaces law

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6
Q

What does the electrical graph show?

A
  • electrical stimulation, depolarisation
  • brief increase in Ca2+ signal inside cell
  • stays elevated
  • cell shortening (contraction)
  • down repolarisation
  • reduced Ca2+ signal –> relax
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7
Q

What’s the diff between preload vs contractility?

A

preload is what’s the stretch of RESTING cardiac tissue

contractility is strength of contraction at any given stretch due to sympathetic

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8
Q

What’s the force of contraction proportional to?

A

rise in (intracellular) Ca2+

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9
Q

What’s the diastolic, normal + max systolic [Ca2+]?

A

100Nm
1μM
10μm

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10
Q

What’s the inotropic effect?

A

Increase in contractility due to rise in [Ca2+]

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11
Q

Why doesn’t the cardiac muscle do all or nothing?

A

enables change in SV by changing contractility

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12
Q

Why is normal cell shortening sub-maximal?

A

resting enough for proper ejection but can do more when exercise

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13
Q

How does electrical excitability contract cardiac myocytes?

A
  • atrial/ventricular AP
  • plateu phase - opening vgcc
  • Ca2+ influx 2μM to 100nM
  • Ca2+ acts as ligand at ligand gated receptor on sarcoplasmic reticulum (Ca2+ store)
  • Ca2+ binds to RyR (ligand gated ion channel on sarcoplasmic reticulm surface) CICR
  • Ca2+ out of store to cytosol
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14
Q

What 2 ways cause Ca2+ rise from 0.1μM to 10μM in cell?

A

Ca2+ influx from AP

CICR

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15
Q

What are T tubules?

A

invaginations of membrane
contains Na+ channels + vgcc inside
underneath it is SR, actin + myosin

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16
Q

Why does Ca2+ rise so quickly?

A

contricted v in subsarcolemic space

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17
Q

Describe the rise in Ca2+ in sub-cellular?

A
  • AP (Na+) depolarises T-tubules
  • vgcc activated, local Ca2+ influx
  • Ca2+ binds to RyR on SR
  • release of Ca2+ from SR (CICR)
  • Ca2+ to troponin, displacement of tropomyosin/troponin complex, exposing active sites
  • myosin heads bind to active sites
  • myosin head ATPase activity release energy (ATP to ADP)
  • slide filaments - contraction
18
Q

How does rise in Ca2+ produce actin-myosin interaction?

A
  • Ca2+ binds to TnC
  • displaces tropomyosin/TnI so binding sites exposed + actin-myosin cross-bridge formed
  • myosin head flexes moving actin + Z line towards sarcomere centre
  • contraction – ATPase activity
19
Q

How does troponin indicate cardiac cell death/MI?

A

TnI + TnT released from cell into plasma

20
Q

Function of TnT?

A

binds to Tropomyosin

21
Q

Function of TnI?

A

binds to actin filaments to hold tropomyosin in place

22
Q

Function of TnC?

A

binds Ca2+

23
Q

Describe decrease in Ca2+ in sub-cellular?

A
  • AP (K+) repolarises T-tubules
  • closes vgcc, no Ca2+ influx, no CICR
  • extrusion of Ca2+ (30%) by Na+/Ca2+ exchanger on membrane (NCX)
  • Ca2+ uptake into SR via SR Ca2+-ATPase (SERCA, 70%) – recycled for next contraction
  • uptake of Ca2+ in mitochondria
  • myosin head ATPase activity release energy (ATP to ADP)
  • chambers relaxed - fill w blood
24
Q

How does the Na+/Ca2+ exchanger on membrane (NCX) work?

A

1 Ca2+ out for 3 Na+ in

25
Q

Why’s cardiac muscle suscpetible for drop in O2/metabolite?

A

SR has Ca2+-ATPase (SERCA) uses ATP to move Ca2+ from cytosol to SR for relaxation + CICR

26
Q

Diff between Inotropy vs Starling’s law?

A

Inotropy : same resting p/v, extrinsic control – due to rise in [Ca2+]
Starling’s law : increased resting p/v + energy of contraction, intrinsic stretch

Both increase SV in diff ways but inotropy increases it more

27
Q

What does NA do?

A

Acts on β1 adrenoceptors on myocytes to increase contractility

28
Q

How does stimulation of β1 adrenoceptors increase contractility?

A

-NA binds to β1 (Gs) - activate adenyl cyclase producing cAMP from ATP
-cAMP -> PKA
-PKA phophorylates vgcc on membrane + RyR on SR:
vgcc opens often, more Ca2+ influx
RyR more active, greater CICR
-GREATER RISE IN Ca2+ —> contractility

29
Q

How does stimulation of β1 adrenoceptors induce relaxation?

A
  • NA binds to β1 adrenoceptor (Gs) - activate adenyl cyclase producing cAMP from ATP
  • cAMP -> PKA
  • PKA phosphorylates K+ channels on membrane
  • K+ channels switched on
  • K+ efflux
  • cell repolarises quicker so switches off vgcc quicker
  • PKA stimulates SERCA
  • more Ca2+ reuptake
  • DECREASE IN Ca2+ —> relaxation
30
Q

How does sympathetic stimulation relate to cardiac AP?

A

↑depolarisation, repolarisation, HR, conduction

31
Q

Why does next AP come quicker with sympathetic stimulation?

A

↑HR as sympathetics affect SAN

32
Q

How does sympathetic stimulation relate to contraction-relaxation?

A

↑force of contraction, relaxation, Ca2+ store

33
Q

How’s the diastolic time maintained with sympathetics?

A

shortening AP + contraction time

34
Q

Why does the diastolic time need to be maintained?

A
  • chambers fill w blood

- maintain coronary perfusion

35
Q

Define positive inotropic effect

A

↑ contractility

Due to vgcc/Ca2+ influx + RyR/CICR

36
Q

Define positive chronotropic effect

A

↑ HR

Due to pacemaker potential freq at SAN

37
Q

Define positive dromotropic effect

A

↑ conduction at AVN + between cardiac muscle cells

38
Q

Define positive lusitropic effect

A

↑ rate of relaxation

Due to more K channels + SERCA, less vgcc

39
Q

What are negative inotropic agents?

A

High external [K+]
Increased [H+]
Low O2 levels

40
Q

What’s the effect of hyperkalaemia?

A
  • high external K+ from 3.5-5 mM to 7-8mM
  • depolarises membrane potential in cardiac tissue
  • Na+ channels become inactivated conc
  • reduces onset time/amplitude/shorter AP
  • heart in refractory mode
  • heart failure
41
Q

What’s the effect of low pH?

A
  • H+ compete for Ca2+ on Tc binding sites
  • no actin-myosin interaction
  • no contraction
42
Q

What’s the effect of hypoxia?

A
  • no oxidative phosphorylaton so anerobic
  • lactic acid –> local acidosis
  • depolarises membrane potential so smaller/shorter AP -poor contraction

CVS II (19 decks)

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