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CSC1005 - Integrated Human Physiology > Cardiac Structure and Function > Flashcards

Cardiac Structure and Function Flashcards

1
Q

What are the two major circulations of the cardiovascular system?

A
  • Pulmonary circulation

- Systemic circulation

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2
Q

What re the three distinct layers of the heart?

A
  • Epicardium
  • Myocardium
  • Endocardium
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3
Q

Is the epicardium in the outer, middle or the inner layer?

A

Outer

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4
Q

Is the myocardium in the outer, middle or the inner layer?

A

Middle

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5
Q

Is the endocardium in the outer, middle or the inner layer?

A

Inner

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6
Q

Describe the epicardium:

A
  • Outer layer

- Connective tissue (areolar)

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7
Q

Describe the myocardium:

A
  • Middle layer

- Cardiomyocytes and connective tissue

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8
Q

Describe the endocardium:

A
  • Inner layer

- Thin layer of connective tissue and endothelium

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9
Q

What are the clinical importance of pericarditis?

A
  • Multiple causes (infections, cancer and trauma autoimmune)

- Overall effect: accumulation of fluid effusion - restricts ventricular filling

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10
Q

What is the pericardium?

A
  • Parietal and visceral (epicardium)

- Cavity contains pericardial fluid

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11
Q

What is the purpose of pericardial fluid?

A

Lubrication

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12
Q

What is the muscle mass ration between the left and right side of the heart?

A

3:1

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13
Q

What is the goal blood pressure?

A

120/80

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14
Q

What is another name for cardiomyocytes?

A

autorhythmic cells

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15
Q

What are the different types of specialised cardiomyocytes?

A
  • SA
  • AV
  • bundle of His
  • Purkinji fibres
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16
Q

What is the primary pacemaker?

A

SA

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17
Q

What do pacemakers do?

A

To initiate cardio cycle and provide conduction system to coordinate cells contraction throughout the heart

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18
Q

What is excitation-contraction coupling?

A

Causing of excitatory phase to a contraction phase within in the hear

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19
Q

What are Purkinje fibres?

A

Specialised conducting fibres composed of electrically excitable cells

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20
Q

What are sarcomere?

A

Complicated unit of striated muscle tissue

-Repeating unit between two Z lines

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21
Q

What are sarcolemma?

A

cell membrane if started muscle fibre cells

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22
Q

What are T-tubules?

A

Extension of the cell membrane that penetrate into the centre of skeletal and cardiac muscle cells

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23
Q

What is similar in cardiomyocytes?

A
  • Have no sarcomere so no contraction

- Creates action potential

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24
Q

What does L in L-type calcium channel stand for?

A

Long-lasting referring to length of activation

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25
Q

Describe exception-contraction coupling:

A
  • SA node begins action potential as primary pacemaker
  • Goes through atria (non-conductive tissue to prevent excitation into ventricle)
  • AV nose picks up excitation via inter nodal pathway
  • AV sends signal down bundle of His
  • Leads to Purkinje fibres (linked to cardiomyocytes in ventricle tissue)
  • Causes action potential at cardiomyocytes
  • Action potential running down sarcolemma
  • L-type Ca2+ channels open as action potential changes voltage
  • Ca2+ ions in the extracellular fluid and space go through the channels
  • Increase in Ca2+ side cytosol
  • T-tubules and sarcoplasmic reitculum are at close association so an influx in Ca2+ enters cytosol causes Ca2+ binding to ryanodine receptors of SR
  • Increase in Ca2+ in cytosol will bind to tropic to cause muscle contraction
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26
Q

What is calcium induced calcium release process?

A

T-tubules and sarcoplasmic reitculum are at close association so an influx in Ca2+ enters cytosol causes Ca2+ binding to ryanodine receptors of SR

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27
Q

What alters contractility and relaxation of muscles?

A

Concentration of Ca2+

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28
Q

Frank a 56yr old male is currently being prescribed verapamil, a
CCB, to treat his angina. Which of the following best explains its
negative inotropic (contractile) effect.

Select one:
A. Decreased Ca2+ induced Ca2+ release
B. Inhibition of ryanodine receptors on the SR
C. Decrease efflux of Ca2+ via Na+/Ca2+ exchange pumps
D. Decreased extracellular Ca2+ influx via inhibition of T-types channels

A

A

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29
Q

Describe Sinoatrial Node Action Potential:

A
  • Phase 4: pacemaker potential occurs at end of one action potential
  • Phase 0: depolarisation
  • Phase 3: repolarisation
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30
Q

Describe phase 4: pacemaker potential occurs at end of one action potential

A
  • Slow depolarisation of pacemaker cells

- Pacemaker achieved by activation of hyperolarisation of HCN channels where Na+ enters cell

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31
Q

When are HCN activated?

A

When membrane potential is

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32
Q

Describe phase 0 depolarisation:

A
  • HCN channels bring membrane potential to -40mV
  • Influx of Ca2+ production fast rate depolarisation
  • HCN channels inactivate
  • Peak of action potential, Ca2+ channels inactive and K+ active
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33
Q

Describe phase 3 repolarisation:

A
  • Efflux of K+ ions out of cell
  • Repolarisation of cell
  • HCN channels activate, enabling another action potential
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34
Q

Describe myocyte action potential:

A

Phase 0: depolarisation (influx of Na+ into cell, rapid depolarisation)
Phase 1: Sodium currents stop (K+ slowly flows out of cells, depolarisation stops, repolarisation starts)
Phase 3: Ca2+ currents move into cells (balance of K+ ions moving out, charge balance between cells, pleitu created)
Phase 4: K+ reaches equilibrium between inside so Na2+ and Na+ balances K+ leading to resting potential

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35
Q

Where does myocyte action potential receive the action potential from?

A

Pacemaker cells causing them to contract enabling spread of action potential

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36
Q

What are intercalated discs?

A

-Interconnect cardiac muscle cells

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37
Q

What are intercalated discs secured by?

A

Desmosomes

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38
Q

What are intercalated discs linked by?

A

Gap junctions

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39
Q

What propagate actions potentials?

A

Gap junctions

40
Q

Where are SA nodes located?

A

Inwall of right atrium

41
Q

Where are AV nodes located?

A

Base of right atrium

42
Q

Where are the bundles of His?

A

Divides right and left bundle branches travelling through septum

43
Q

Where are the purkinje fibres?

A

Spread throughout ventricles

44
Q

Where are gap junctions?

A

Occur between adjunct cardiomyocytes

45
Q

What are cardiomyocytes linked by?

A

Intercalated discs

46
Q

Describe excitation propagation:

A
  • Action potential from auto rhythmic cells excite first cardiomyocyte
  • Propagation along sarcolemma (membrane of muscle cell)
  • Na2+ influx from outside cells into the cell
  • Transfers into adjacent cell where voltage-gated channels along membrane along action potential
47
Q

What motion is excitation propagation?

A

Peristaltic motion

48
Q

What is the pathway of electrical conduction?

A

Sinoatrial node (SA) -> Atrial internal fibres -> atrioventricular node (AV) -> bundle of His -> Purkinje fibres -> ventricular myocytes

49
Q

Which myocardial has the slowest conduction speed?

A

AV node

50
Q

Which myocardial has the fastest conduction speed?

A

Purkinje fibres

51
Q

What does velocity depend on in action potential?

A
  • Amount of ions going into cell during action potential

- Interconnectedness of myocardial conduction cells

52
Q

How does interconnectedness of myocardial conduction cells affect velocity?

A

-More gap junctions - more interconnect cells - less resistance to ion flow between cells

53
Q

How does the amount of ions going into cell during action potential affect velocity?

A

More ion - faster depolarisation - faster speed

54
Q

What is refectory period?

A

Time in which myocardial cell cannot be depolarised

55
Q

What is absolute refectory period?

A

No stimulus, no matter its size can dgpolise cell

56
Q

What is effective refectory period?

A

Large stimulus can generate action potential

-Too weak to be conducted

57
Q

What is relative refectory period?

A

Large stimulus can generate action potential

-Big enough to conducted

58
Q

What is excitability?

A

Ability of myocardial cells to depolarise in response to incoming depolarising current

59
Q

What are the mechanisms of cardiac contraction?

A

Preload
Afterload
Contractility
Heart Rate

60
Q

What is the acronym?

A

PACE

61
Q

What is the equation for cardiac output?

A

Heart rate x stroke volume

62
Q

What is the unit for cardiac output?

A

mL/min

63
Q

What is the unit for heart rate?

A

Beat/min

64
Q

What is the unit for stroke volume?

A

mL/beat

65
Q

What is the equation for stroke volume?

A

End diastolic volume (EDV) - End systolic volume (ESV)

66
Q

What is EDV?

A

Volume of blood just before contraction

67
Q

What is ESV?

A

Volume of blood after contraction

68
Q

Is there still blood in the ventricle after contraction?

A

Yes

69
Q

What is related to EDV?

A

Preload

70
Q

What does increase in EDV do?

A

Increases in myocardial performance/contractility

71
Q

How does EDV increase myocardial contractility?

A

Increase myocardial muscles
Increase cross bridge formation
Increase in contractility

72
Q

What is the relation of EDV, preload and contractility relationship known as?

A

Length force relationship

73
Q

If preload/EDV increases the venous return what does it do to stroke volume and cardiac output?

A

Increase SV and CO

74
Q

What are the physical factors which affect preload?

A

more optimum myofilament overlapping
Decreasing in lattice spacing
Increase probability of interaction between adjacent components

75
Q

What are the activating factors which affect preload?

A

Increase in Ca2+ release and sensitivity

76
Q

What are the three factors which affect ESV?

A
  • Preload/EDV
  • Contractility
  • Afterload
77
Q

How does afterload affect ESV?

A
  • Heart pumps against pressure
  • Higher pressure in the aorta the more force required by the heart
  • So increase in afterload decrease in cardiac output
78
Q

What is the clinical importance of afterload?

A

Hypertension and aortic valve stenosis both lead to decrease in stroke volume

79
Q

How does contractility affect ESV?

A

Increase blood pumped out of heart

80
Q

What type of receptor is B1 adrenergic receptor?

A

G-coupled protein receptor

81
Q

What hormones control contractility?

A

Adrenaline and noradrenalin

82
Q

How is contractility controlled?

A
  • Noradrenalin or adrenaline bind to B1 adrenergic receptor
  • Activation of adenlye cyclase from the production of cyclic AMP
  • Cyclic dependent on kinases A
  • Increase in Ca2+ with sarcomere reticulum and cell
  • Increase contractility
83
Q

What is the clinical perspective of ejection faction?

A

Quantifying of contractility by injection factions and ratio of stroke volume and end diastolic volume

84
Q

What is the equation of ejection fraction?

A

SV/EDV

85
Q

What is ejection fractions expressed as?

A

Percentage

86
Q

What is the normal ejection fraction in resting condition?

A

55-75%

87
Q

What do neuronal and endocrine regulation do?

A

Affect heart rate

88
Q

How do you increase heart rate relating to neuronal and endocrine regulation?

A

Positive chronotropic factors

e.g noradrenalin and adrenaline

89
Q

How do you decrease heart rate relating to neuronal and endocrine regulation?

A

Negative chronotropic factors

e.g Acetylcholine

90
Q

What does the martial reflex effect?

A

Adjusts heart rate in responses to venous return

Stretch receptors in right atrium tigger increase in heart rate through increase sympathetic activity

91
Q

What doe the sympathetic do to there permeability of membrane to Na+?

A

Increase permeability

92
Q

What doe the parasympathetic do to there permeability of membrane to Na+?

A

Decrease permeability

93
Q

How does sympathetic increase permeability of membrane to Na+?

A
  • Increase spontaneous depolarisation

- Reduce time to initiate depolarisation

94
Q

How does parasympathetic decrease permeability of membrane to Na+?

A
  • Decrease spontaneous depolarisation

- Increase time to initiate depolarisation

95
Q

Frank is also on bisoprolol, a selective β1-antagonist. Which of
the following is INCORRECT with regard to explaining its
predominant affect on reducing CO.

Select one:
A. Reduced heart rate
B. Reduced cardiac contractility 
C. Reduced renin release
D. Reduced arterial tone
A

D

96
Q

What does B1 blockade lead to?

A
  • Reduced contractility-via reduction in CAMP
  • Reduced heart rate
  • Reduced Ca2+ entry via CAMP-dependent PK activity
  • Reduced renin recreation via selective B1 inhibition at GJ cells

CSC1005 - Integrated Human Physiology (18 decks)

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