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Y1 Cardiovascular > Physiology > Flashcards

Physiology Flashcards

1
Q

What is stroke volume

A

Volume of blood ejected by each ventricle during each heart beat

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2
Q

Equation of stroke volume

A

SV = End diastolic volume - end systolic volume

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3
Q

What is end diastolic volume

A

The volume of blood in each ventricle after diastole, before ventricular systole

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4
Q

What is end systolic volume

A

Volume of blood left in each ventricle after ventricular systole

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5
Q

What is cardiac output

A

Volume of blood pumped out of ventricles per minute

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6
Q

Equation for cardiac output

A

CO = SV x HR

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7
Q

What is Frank Starling’s law

A

the more blood is filled in each ventricle at the end of diastole, the more blood will be ejected during systole

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8
Q

What is preload

A

Diastolic stretch of myocardial fibres

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9
Q

What is afterload

A

The resistance that the heart needs to pump against to pump blood through

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10
Q

How does Frank Starling’s mechanism partially compensate for increase in afterload

A

Increase in afterload causes not all stroke volume pumped out
so increase in EDV for next cardiac cycle
increase in EDV then causes increase in stroke volume

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11
Q

How is venous return related to EDV, preload and SV

A

Increase in venous return stimulates diastolic stretch (increase in preload)
This increases EDV hence increases SV

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12
Q

What is positive chronotropic effect

A

Increase in heart rate

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13
Q

What is positive inotropic effect

A

Increase in force of contraction and contractility

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14
Q

What is positive dromotropic effect

A

Increase conduction velocity through AV node

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15
Q

What is positive lusitropic effect

A

Decrease in duration of systole

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16
Q

Cause of positive lusitropic effect

A

Increase in rate of Ca2+ reuptake into the SR

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17
Q

Causes of positive chronotropic effect

A

Increase in slope of phase 4 (pacemaker potential)

Decrease in threshold

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18
Q

How does slope of pacemaker potential increase

A

Increase in INa and ICa,L - more Na+ and Ca2+ moving in so depolarises and reaches threshold quicker

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19
Q

How does positive inotropic effect occur

A

L type Ca2+ channels open with more probability
Increase in sensitization of contractile proteins to Ca2+
PKA phosphorylates phospholamban which activates SERCA so Ca2+ reuptake into SR is quicker (quicker relaxation -> ready to contract sooner)

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20
Q

Effect of sympathetic stimulation on the heart

A 
\+ chronotropic 
\+ inotropic 
\+ lusitropic 
\+ dromotropic 
increase in automaticity 
increase in activity of Na+/K+ ATPase
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21
Q

What type of cells do sympathetic nerves supply in the heart

A

Nodal cells

Myocardial cells

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22
Q

What type of cells do parasympathetic nerves supply in the heart

A

Nodal cells

Atrial myocardial cells (not ventricles)

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23
Q

Mechanism of parasympathetic stimulation

A
  1. ACh binds to muscarinic receptors (M2) on nodal cells
  2. This activates Gi complex and causes it to dissociate into alpha and beta+gamma subunits
  3. alpha subunit inhibits adenylyl cyclase -> reduce cGMP -> reduce cellular responses
  4. beta+gamma subunit opens GIRKs
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24
Q

What are GIRKs

A

G protein coupled inward rectifier K+ channels

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25
Q

Effects of parasympathetic stimulation on heart

A

Negative chronotropic effect
Negative dromotropic effect
Negative inotropic effect (only in atria)

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26
Q

Describe the phases of nodal action potential

A

Phase 4 (pacemaker potential) - Na+ influx through HCN and Ca2+ influx through voltage gated Ca2+ channels. This causes slow depolarisation of the membrane, reaching threshold (-40mV)

Phase 0 - L type Ca2+ open, causing fast depolarisation

Phase 3 - repolarisation; K+ channels open, L type Ca2+ channels close
HCN channels will open once membrane potential is lower than -50mV

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27
Q

What are HCN channels

A

Allows Na+ influx during phase 4 of nodal action potential

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28
Q

List the ion channels involved in each phase of nodal action potential

A

Phase 4 - HCN and voltage gated Ca2+ channels
Phase 0 - L type Ca2+ channels
Phase 3 - K+ channels

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29
Q

Definition of automaticity

A

Heart being able to beat rhythmically without any external stimuli due to regular, spontaenous generation of electrical activities

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30
Q

How do electrical excitation spread from SA node to AV node

A

Mostly cell to cell conduction

some internodal routes

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31
Q

How do electrical excitation spread from AV node to ventricles

A

Bundle of His -> Purkynje fibres -> cell to cell conduction throughout ventricular myocytes

32
Q

What is cell to cell conduction

A

Electrical excitation spreads between adjacent cells via gap junctions

33
Q

What are gap junctions

A

Low resistance electrical communication pathways

34
Q

What are desmosomes

A

Intercellular cell junctions that provides adhesion between cardiac cells

35
Q

Why does AV node have slower conduction

A

So atrial systole occurs before ventricular systole

36
Q

What is vagal tone

A

Continuous vagal influence on heart rate under normal conditions to produce normal heart rate

37
Q

Normal heart rate range

A

60 - 100bpm

38
Q

Type of beta adrenoceptors in nodal and myocardial cells

A

beta 1

39
Q

Type of muscarinic receptor in nodal cells

A

M2

40
Q

Describe the phases of action potential in myocardial cells

A

Phase 4
- voltage gated Na+ and L type Ca2+ channels are closed
- NCXR transports 3Na+ in for 1 Ca2+ out
- K+ channels are open, allowing K+ efflux
Phase 0
- nodal action potential reaches the myocyte to trigger this
- fast depolarisation
- K+ channels close
- voltage gated Na+ channels open
Phase 1
- early repolarisation
- Na+ channels close
- L type Ca2+ channels begin to open
- transient K+ channels open
Phase 2
- plateau phase
- efflux of K+ via rectifier channel = influx of Ca2+
Phase 3
- repolarisation
- L type Ca2+ channel close while K+ remains open

41
Q

Phases that represent the refractory period of action potential of myocardial cells

A

phase 1 to 3

Na+ channels cannot open during this period

42
Q

Why do myocardial cells have long refractory period

A

to prevent tetanic contractions

43
Q

When do myocardial cells contract

A

Phase 1 to 2

When L type Ca2+ channels are open, it causes CICR from SR

44
Q

Why do myocardial cells stop contraction in phase 3

A

1) L type Ca2+ channels close so no CICR
2) Ca2+ actively transported back into SR
3) Ca2+ actively transported out of the cell via NCXR using 3Na+ gradient
= no intracellular Ca2+

45
Q

How does Ca2+ cause smooth muscle constriction

A
  1. Ca2+ binds to CaM to form Ca2+ - CaM
  2. Ca2+ - CaM activates myosin LCK
  3. myosin LCK phosphorylates myosin LC into myosin LC + phosphate
  4. myosin LC + phosphate causes muscle contraction
46
Q

Equation for ejection fraction

A

Stroke volume / end diastolic volume

47
Q

How do non polar lipids travel in blood

A

In lipoproteins

48
Q

Examples of non polar lipids

A

Cholesterol
Triacylglyceride
Esters

49
Q

Examples of lipoproteins

A

Chylomicron
VLDL
HDL
LDL

50
Q

What does the outer layer of lipoproteins contain

A

Cholesterol
Apoprotein
Phospholipids

51
Q

Function of apoprotein

A

Signaling molecules recognized by the liver receptors, allow lipoproteins to bind

52
Q

What apoproteins do HDL have

A

apoA-I and apoA-II

53
Q

What apoproteins does VLDL have

A

apoB-100

54
Q

apoB-48 is the aporpotein of

A

chylomicron

55
Q

What is the feature of chylomicron

A

Highest proportion of TAGs

56
Q

What does the core of apoproteins contain

A

cholesteryl ester

triacylglycerols

57
Q

What is the feature of VLDL

A

Highest proportion of cholesterol

58
Q

What are lipids used for

A

Energy source
Membrane biogenesis
Precursors for hormones and signaling molecules

59
Q

Where are chylomicrons and VLDL metabolised

A

Muscle cells and adipocytes

60
Q

Where are chylomicrons made

A

Enterocytes

61
Q

Where are VLDL made

A

hepatocytes

62
Q

Formation of TAGs and cholesteryl ester

A

1) pancreatic lipase hydrolyses TAG into monoglycerides and fatty acids
2) Monoglycerides and fatty acids diffuse into enterocytes by simple diffusion
3) cholesterol from diet enters enterocytes via NPC1L-1
4) Monoglycerides and fatty acids are resynthesized to TAG in SER
5) cholesterol is esterified into cholesteryl ester with a free fatty acid

63
Q

Where is cholesterol obtained

A

Diet

Formed by liver using HMG-CoA reductase

64
Q

Where does the formation of chylomicrons occur

A

RER

65
Q

Formation of chylomicron

A

1) apoB-48 is moved into RER by MTP
2) TAG and phospholipid added to apoB-48 to form primordial chylomicron
3) more TAG added by MTP
4) cholesteryl ester also added, chylomicron formed

66
Q

How are chylomicrons released

A

1) chylomicron move from RER to golgi apparatus
2) apoA-I is added to chylomicron
3) chylomicron is then released into lymphatic system by exocytosis

67
Q

How does the content of lymphatic system drain into systemic circulation

A

By thoracic duct draining into subclavian vein

68
Q

Metabolism of chylomicrons and VLDL

A

1) ApoC-II from HDL is added to VLDL and chylomicrons
2) VLDL and chylomicrons bind to lipoprotein lipase
3) lipoprotein lipase hydrolyzes the TAGs in core
4) TAGs depleted, forming chylomicron and VLDL remnants

69
Q

Feature of chylomicron and VLDL remnants

A

They are enriched with cholesteryl ester due to depletion of TAG

70
Q

Formation of LDL

A

1) apoC-II is transferred back to HDL in exchange for apoE
2) remnants are transported back to liver to be further metabolised by hepatic lipase
3) all chylomicron and 50% of VLDL are cleared
4) the remaining 50% of VLDL lose more TAG and more enriched with cholesteryl ester
5) eventually, VLDL loses apoE and forms LDL

71
Q

Where are remnants of chylomicron and VLDL metabolised

A

Liver

72
Q

Where does LDL clearance occur

A

liver

73
Q

How are LDL cleared

A

1) LDL binds to LDL receptors on cells hence moved in by endocytosis
2) forms lysosome
3) LDL receptors are recycled back onto surface
4) cholesteryl ester in LDL hydrolysed in lysosome
5) cholesterol is released

74
Q

Effects of release of cholesterol

A

Inhibits HMG CoA reductase = stops synthesis of cholesterol

Downregulates LDL receptors

75
Q

Uses of cholesterol

A

To form bile

Stored as cholesteryl ester

76
Q

What is the normal stroke volume

A

50-100ml

Y1 Cardiovascular (6 decks)

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