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The Thorax > Cardiac Physiology > Flashcards

Cardiac Physiology Flashcards

1
Q

How does the heart muscle act as a syncytium

A

Single cell formed from a number of fused cells

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2
Q

Contents on myocytes

A

Contain myofibrils which are made up of sarcomeres which are made up of actin (thin) and myosin (thick) filaments

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3
Q

Describe how cross-bridging occurs between actin and myosin heads

A
  • Calcium from SR causes uncovering of active site by binding to troponin
  • Allows myosin head to bind to active site
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4
Q

What is required for the myosin head to detach from the actin filament for the contraction cycle to repeat itself

A

ATP

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5
Q

What is phase 0 of the action potential

A
  • Initial rapid depolarisation

- Rapid increase in sodium permeability

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6
Q

What is phase 1 of the action potential

A
  • Rapid repolarisation
  • Rapid decrease in sodium permeability
  • Small increase in potassium permeability
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7
Q

What is phase 2 of the action potential

A
  • Slow repolarisation
  • Plateau effect due to inward movement of calcium
  • Plateau lasts 200ms
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8
Q

What is phase 3 of the action potential

A
  • Rapid repolarisation

- Increase in potassium permeability and inactivation of slow inward calcium channels

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9
Q

What is phase 4 of the action potential

A
  • Resting membrane potential of the ventricular muscle is about -90mV
  • SAN and conducting system do not have a resting membrane potential as they are constantly depolarising
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10
Q

What does calcium bind to to uncover the active site and activate the actin-myosin complex

A

Troponin C

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11
Q

Length of cardiac action potential

A

200-300ms

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12
Q

What is the most important factor controlling cardiac contractility

A

Calcium:

  • Increased = more force
  • Decreased = less force
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13
Q

Where is the SAN situated

A

Right atrium near entry of SVC

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14
Q

Describe conduction through the atria

A

SAN sends impulse which is transmitted from one atrial myocyte to the next

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15
Q

Where is the AVN situated

A

Within the atrioventricular fibrous ring - it is the only electrical pathway through the ring

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16
Q

Describe conduction distal to the AVN

A
  1. Leaves AVN
  2. Travels down bundle of His
  3. Travels through right and left bundles
  4. Enter Purkinje fibres
  5. Apex of ventricles
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17
Q

Which parts of the heart have the ability to depolarise themselves

A
  • SAN
  • AVN
  • Purkinje fibres
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18
Q

Which cells of the heart have the longest refractory period

A
  • SAN
  • AVN
  • Purkinje fibres
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19
Q

What controls the rate of firing of the heart if the SAN fails

A

AVN - has the next highest firing frequency

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20
Q

Describe phase 4c of the cardiac cycle

A
  • Atrial systole
  • SAN depolarises
  • Atrial muscle contracts
  • Blood flows into ventricles (completing final 15% of filling)
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21
Q

Describe phase 1 of the cardiac cycle

A
  • Isovolumetric contraction of the ventricles
  • AV valve closes
  • Aortic and pulmonary valves are closed
  • Volume of blood remains constant but pressure rises
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22
Q

Describe phase 2a of the cardiac cycle

A
  • Ejection

- Pressure in the ventricles exceeds that in the aorta and pulmonary artery = valves open

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23
Q

Describe phase 2b of the cardiac cycle

A
  • Ejection

- Aortic and pulmonary artery pressures equalise with ventricles

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24
Q

Describe phase 3 of the cardiac cycle

A
  • Diastolic relaxation
  • Isovolumetric relaxation
  • Ventricular pressure falls
  • Aortic and pulmonary valves close
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25
Q

Describe phase 4a of the cardiac cycle

A
  • Filling phase in diastole
  • AV valves re-open
  • Passive ventricular filling
  • Low atrial pressure due to ‘sucking’ effect from ventricles
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26
Q

Describe phase 4b of the cardiac cycle

A
  • Decline in rate of filling as atrial volume increases

- Finally, atrial contraction begins again

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27
Q

What is the textbook ejection fraction

A

60%

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28
Q

What is the average circulating volume

A

4.5L (7% of body weight)

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29
Q

What does the A-wave represent in the JVP

A

Atrial systole

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30
Q

What happens to the A-wave in AF

A

Absent

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31
Q

What causes cannon waves

A

Complete heart block

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32
Q

What causes giant A-waves

A
  • Pulmonary HTN

- Tricuspid and pulmonary stenosis

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33
Q

What does the C-wave represent in the JVP

A
  • Bulging of the tricuspid valve leaflets in right atrium during isovolumetric contraction of the ventricles
  • Synchronous with carotid pulse
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34
Q

What does the V-wave represent in the JVP

A

Rise in atrial pressure before tricuspid valve opens

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35
Q

What does the X-descent represent in the JVP

A

Due to tricuspid valve moving down during ventricular systole

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36
Q

What does the Y-descent represent in the JVP

A
  • Tricuspid valve opening

- Right atrial pressure falls

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37
Q

What is the rate of coronary blood flow

A
  • 250ml/minute at rest

- 1L/minute during exercise

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38
Q

What phase of the cardiac cycle does coronary blood flow occur in

A

Diastole (intramyocardial arteries are compressed during systole)

39
Q

What causes a characteristic notch (incisura) in the aortic/pulmonary pressure tracings

A

Closure of aortic and pulmonary valves

40
Q

What is the average stroke volume

A

70ml (55-100ml)

41
Q

How is CO calculated

42
Q

What is the cardiac index

A

CO per square metre of body surface area

43
Q

What reduces cardiac blood flow

A
  • Pain

- ADH

44
Q

What is Starling’s law

A

The energy of contraction of cardiac muscle fibre is a function of the initial length of the muscle fibre

45
Q

What does Starling’s law mean

A
  • The greater the stretch of the ventricle in diastole, the greater the SV and force of contraction
  • Up to a critical point
46
Q

What 3 things affect stroke volume

A
  1. Contractility
  2. Preload
  3. Afterload
47
Q

List the causes of increased cardiac contractility

A
  • Increased preload
  • Sympathetic stimulation
  • Increased extracellular calcium
  • Catecholamines, thyroxine, glucagons
48
Q

List the causes of reduced cardiac contractility

A
  • Reduced filling (Starling’s law)
  • Hypoxia
  • Hypercapnia
  • Acidosis
  • Ischaemia and cardiac disease
  • Parasympathetic stimulation
  • Electrolyte imbalance
49
Q

What is equivalent to cardiac preload

A

End-diastolic volume

50
Q

What is preload dependent on

A
  • Venous return
  • Atrial systole
  • Myocardial distensibility
51
Q

How is cardiac preload measured

A
  • Central venous pressure

- Pulmonary artery occlusion pressure (PAOP)

52
Q

Define afterload

A

Tension in the ventricular wall during ventricular ejection

53
Q

List the causes of increased afterload

A
  • Raised aortic pressure
  • Aortic stenosis
  • Increased ventricular volume (Laplace law)
  • Raised SVR
54
Q

List the causes of reduced afterload

A

Vasodilators - drugs or metabolites

55
Q

How is cardiac output typically measured

A

Thermodilution and doppler USS

56
Q

Define the Fick Principle

A

The amount of a substance taken up by an organ per unit time is equal to the blood flow multiplied by the difference in concentration of that substance between arterial and mixed venous blood

57
Q

Outline the thermodilution process

A
  • Bolus of ice-cold dextrose is injected into right atrium via proximal lumen of Swan-Ganz
  • Dextrose mixes with blood to cause fall in temp
  • Temp is recorded at catheter tip in distal pulmonary artery
  • Algorithm calculates CO
58
Q

What is the pulse pressure

A

SBP - DBP = 40mmHg on average

59
Q

How is mean arterial pressure calculated

A

MAP = DBP + 1/3rd of pulse pressure = 70mmHg on average

60
Q

Where are baroreceptors for control of BP located

A
  • Aortic arch

- Carotid artery

61
Q

Describe the Bainbridge reflex

A

Increase in HR following rapid transfusion

62
Q

How is systemic vascular resistance calculated

A

SVR = MAP - (mean right atrial pressure / CO)

63
Q

Best method to measure BP

A

Intra-arterial catheter (usually in the radial artery)

64
Q

Normal CVP

65
Q

CVP uses

A
  • Indication of preload

- Useful guide to fluid replacement

66
Q

What is pulmonary artery wedge pressure equivalent to

A

Left atrial pressure

67
Q

Normal PAOP

68
Q

Consequences of raised PAOP

A

Pulmonary oedema

69
Q

Pulse oximeter wavelength range

70
Q

Role of inotropes and what receptor do they usually effect

A
  • Increase force of ventricular contraction

- Beta-effect

71
Q

Role of vasopressors and what receptor do they usually effect

A
  • Constrict blood vessels

- Alpha-effect

72
Q

Role of chronotropes and what receptor do they usually effect

A
  • Increase HR

- Beta-effect

73
Q

Effect of adrenaline

A
  • Inotrope
  • Vasopressor
  • Chronotrope
74
Q

Describe the effect of adrenaline at different doses on vascular tone

A
  • Beta-2 effect at low doses causes vasodilatation in skeletal muscle
  • Alpha-vasoconstrictor at higher doses increases SVR and myocardial oxygen demand
75
Q

Effect of nor-adrenaline

A

Vasopressor (indicated in septic shock when hypotension persists despite adequate volume replacement)

76
Q

Effect of isoprenaline

A
  • Inotrope
  • Chronotrope
    (-Vasodilatation in skeletal muscle)
77
Q

Describe the effects of dopamine on vascular tone at different doses

A
  • Low dose = dilates renal, cerebral, coronary, splanchnic vessels via D1 and D2
  • High dose = causes vasoconstriction through alpha stimulation
78
Q

Which receptors does dobutamine act on

A
  • Beta 1

- Beta 2

79
Q

Uses of Dobutamine

A

1st-line drug in cardiogenic shock

80
Q

Effect of Dobutamine

A
  • Inotrope (Beta 1 effect)

- Vasodilator (Beta 2 effect)

81
Q

Which receptors does adrenaline act on

A
  • Alpha-1
  • Alpha-2
  • Beta-1
  • Beta-2
82
Q

Which receptors does noradrenaline act on

A
  • Alpha-1 (mainly)

- Alpha-2, Beta-1, Beta-2

83
Q

Which receptors does dopamine act on

A
  • D-1
  • D-2
  • Alpha-1
  • Alpha-2
  • Beta-1
84
Q

Effect of Alpha-1 and Alpha-2 receptor binding

A

Vasoconstriction

85
Q

Effect of Beta-1 binding

A

Increased cardiac contractility and HR

86
Q

Effect of Beta-2 binding

A

Vasodilation

87
Q

Effect of D-1 binding

A

Renal and spleen vasodilation

88
Q

Effect of D-2 binding

A

Inhibits noradrenaline release

89
Q

Effect of nitrates

A

Vasodilators reducing preload

90
Q

Effect of nitroprusside

A

Arterial vasodilator with short half-life

91
Q

Effect of hydralazine

A

Arterial vasodilator reduces afterload

92
Q

Mechanism of action of phosphodiesterase inhibitors

A

Decrease the rate of breakdown of cAMP by phosphodiesterase 3

93
Q

Effect of phosphodiesterase inhibitors

A
  • Inotrope

- Vasodilator

The Thorax (5 decks)

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