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The Thorax > Cardiac Physiology > Flashcards

Cardiac Physiology Flashcards

(93 cards)

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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
Describe phase 4a of the cardiac cycle
- Filling phase in diastole - AV valves re-open - Passive ventricular filling - Low atrial pressure due to 'sucking' effect from ventricles
26
Describe phase 4b of the cardiac cycle
- Decline in rate of filling as atrial volume increases | - Finally, atrial contraction begins again
27
What is the textbook ejection fraction
60%
28
What is the average circulating volume
4.5L (7% of body weight)
29
What does the A-wave represent in the JVP
Atrial systole
30
What happens to the A-wave in AF
Absent
31
What causes cannon waves
Complete heart block
32
What causes giant A-waves
- Pulmonary HTN | - Tricuspid and pulmonary stenosis
33
What does the C-wave represent in the JVP
- Bulging of the tricuspid valve leaflets in right atrium during isovolumetric contraction of the ventricles - Synchronous with carotid pulse
34
What does the V-wave represent in the JVP
Rise in atrial pressure before tricuspid valve opens
35
What does the X-descent represent in the JVP
Due to tricuspid valve moving down during ventricular systole
36
What does the Y-descent represent in the JVP
- Tricuspid valve opening | - Right atrial pressure falls
37
What is the rate of coronary blood flow
- 250ml/minute at rest | - 1L/minute during exercise
38
What phase of the cardiac cycle does coronary blood flow occur in
Diastole (intramyocardial arteries are compressed during systole)
39
What causes a characteristic notch (incisura) in the aortic/pulmonary pressure tracings
Closure of aortic and pulmonary valves
40
What is the average stroke volume
70ml (55-100ml)
41
How is CO calculated
SV x HR
42
What is the cardiac index
CO per square metre of body surface area
43
What reduces cardiac blood flow
- Pain | - ADH
44
What is Starling's law
The energy of contraction of cardiac muscle fibre is a function of the initial length of the muscle fibre
45
What does Starling's law mean
- The greater the stretch of the ventricle in diastole, the greater the SV and force of contraction - Up to a critical point
46
What 3 things affect stroke volume
1. Contractility 2. Preload 3. Afterload
47
List the causes of increased cardiac contractility
- Increased preload - Sympathetic stimulation - Increased extracellular calcium - Catecholamines, thyroxine, glucagons
48
List the causes of reduced cardiac contractility
- Reduced filling (Starling's law) - Hypoxia - Hypercapnia - Acidosis - Ischaemia and cardiac disease - Parasympathetic stimulation - Electrolyte imbalance
49
What is equivalent to cardiac preload
End-diastolic volume
50
What is preload dependent on
- Venous return - Atrial systole - Myocardial distensibility
51
How is cardiac preload measured
- Central venous pressure | - Pulmonary artery occlusion pressure (PAOP)
52
Define afterload
Tension in the ventricular wall during ventricular ejection
53
List the causes of increased afterload
- Raised aortic pressure - Aortic stenosis - Increased ventricular volume (Laplace law) - Raised SVR
54
List the causes of reduced afterload
Vasodilators - drugs or metabolites
55
How is cardiac output typically measured
Thermodilution and doppler USS
56
Define the Fick Principle
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
Outline the thermodilution process
- 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
What is the pulse pressure
SBP - DBP = 40mmHg on average
59
How is mean arterial pressure calculated
MAP = DBP + 1/3rd of pulse pressure = 70mmHg on average
60
Where are baroreceptors for control of BP located
- Aortic arch | - Carotid artery
61
Describe the Bainbridge reflex
Increase in HR following rapid transfusion
62
How is systemic vascular resistance calculated
SVR = MAP - (mean right atrial pressure / CO)
63
Best method to measure BP
Intra-arterial catheter (usually in the radial artery)
64
Normal CVP
5-12mmHg
65
CVP uses
- Indication of preload | - Useful guide to fluid replacement
66
What is pulmonary artery wedge pressure equivalent to
Left atrial pressure
67
Normal PAOP
6-12mmHg
68
Consequences of raised PAOP
Pulmonary oedema
69
Pulse oximeter wavelength range
660-940Nm
70
Role of inotropes and what receptor do they usually effect
- Increase force of ventricular contraction | - Beta-effect
71
Role of vasopressors and what receptor do they usually effect
- Constrict blood vessels | - Alpha-effect
72
Role of chronotropes and what receptor do they usually effect
- Increase HR | - Beta-effect
73
Effect of adrenaline
- Inotrope - Vasopressor - Chronotrope
74
Describe the effect of adrenaline at different doses on vascular tone
- Beta-2 effect at low doses causes vasodilatation in skeletal muscle - Alpha-vasoconstrictor at higher doses increases SVR and myocardial oxygen demand
75
Effect of nor-adrenaline
Vasopressor (indicated in septic shock when hypotension persists despite adequate volume replacement)
76
Effect of isoprenaline
- Inotrope - Chronotrope (-Vasodilatation in skeletal muscle)
77
Describe the effects of dopamine on vascular tone at different doses
- Low dose = dilates renal, cerebral, coronary, splanchnic vessels via D1 and D2 - High dose = causes vasoconstriction through alpha stimulation
78
Which receptors does dobutamine act on
- Beta 1 | - Beta 2
79
Uses of Dobutamine
1st-line drug in cardiogenic shock
80
Effect of Dobutamine
- Inotrope (Beta 1 effect) | - Vasodilator (Beta 2 effect)
81
Which receptors does adrenaline act on
- Alpha-1 - Alpha-2 - Beta-1 - Beta-2
82
Which receptors does noradrenaline act on
- Alpha-1 (mainly) | - Alpha-2, Beta-1, Beta-2
83
Which receptors does dopamine act on
- D-1 - D-2 - Alpha-1 - Alpha-2 - Beta-1
84
Effect of Alpha-1 and Alpha-2 receptor binding
Vasoconstriction
85
Effect of Beta-1 binding
Increased cardiac contractility and HR
86
Effect of Beta-2 binding
Vasodilation
87
Effect of D-1 binding
Renal and spleen vasodilation
88
Effect of D-2 binding
Inhibits noradrenaline release
89
Effect of nitrates
Vasodilators reducing preload
90
Effect of nitroprusside
Arterial vasodilator with short half-life
91
Effect of hydralazine
Arterial vasodilator reduces afterload
92
Mechanism of action of phosphodiesterase inhibitors
Decrease the rate of breakdown of cAMP by phosphodiesterase 3
93
Effect of phosphodiesterase inhibitors
- Inotrope | - Vasodilator

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