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RCR1 Physiology > Circulation > Flashcards

Circulation Flashcards

0
Q

What is recruitment?

A

More capillaries open

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1
Q

What happens to pulmonary vascular resistance when pulmonary vascular pressure rises?

A

Resistance falls

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2
Q

What is distension?

A

Capillaries widen

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3
Q

How are capillaries used to control VQ mismatch?

A

Capillaries to underventilated alveoli can constrict, forcing the blood to flow elsewhere.

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4
Q

What is a pulmonary embolus?

A

An obstruction to the pulmonary arterial system. Usually a thrombus.

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5
Q

What is blood pressure?

A

Blood pressure = cardiac output x peripheral resistance

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6
Q

What may cause pulmonary hypertension?

A

High cardiac output

High pulmonary vascular resistance

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7
Q

What increases vascular resistance?

A

Vasoconstriction
Obstruction
Damaged vascular bed

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8
Q

What does the p wave represent on an ECG?

A

Atrial systole

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9
Q

What does the QRS complex show?

A

Ventricular systole

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10
Q

What does the t wave represent?

A

Ventricular repolarisation

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11
Q

What is an isovolumic contraction?

A

Ventricular pressure rises but the volume is constant.

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12
Q

What is isovolumic relaxation?

A

The ventricular pressure decreases but the volume is constant.

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13
Q

What is S1?

A

AV valves closing

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14
Q

What is S2?

A

Semilunar valves closing

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15
Q

What is S3?

A

Rapid ventricular filling

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16
Q

What is S4?

A

Atrial systole

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17
Q

Why are capillaries good for diffusion?

A

Large cross sectional area so they are low velocity.

Thin walls.

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18
Q

What is Darcy’s law?

A

Blood flow = MABP/TPR

Same as saying that Arterial BP = CO x TPR

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19
Q

What causes resistance to blood flow?

A

Vessel radius

Viscosity

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20
Q

What determines viscosity?

A

Haematocrit - proportion of blood that is RBCs

Plasma protein concentration and type

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21
Q

What is turbulence?

A

Stenotic vessels cause blood to flow in a disorganised way (not laminar flow)

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22
Q

What determines vascular tone?

A 
Intrinsic regulation (stretch and chemicals)
Extrinsic regulation (hormones and nerves)
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23
Q

How does NO cause vasodilation?

A

Ca2+ causes NO Synthase to produce NO which activates Guanylyl cyclase. GC causes GTP to be converted into cGMP which phosphorylates Myosin, causing the vascular muscle to relax.

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24
Q

What is the vascular response to an increase of metabolic rate in a tissue?

A

Increased metabolism leads to an increase of metabolites which causes a local vasodilation and increased blood flow to remove the excess metabolites.

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25
Q

Does sympathetic activity cause vasoconstriction or vasodilation?

A

Vasoconstriction

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26
Q

Does sympathetic activity increase or decrease peripheral resistance?

A

Increase

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27
Q

What is the effect of parasympathetic activity on vascular tone?

A

Causes vasodilation

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28
Q

What are baroreceptors?

A

Receptors which detect the blood pressure depending on the stretch of the vessel walls

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29
Q

Where are baroreceptors found?

A

Aortic arch and carotid sinuses

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30
Q

What is dynamic sensitivity?

A

Rate of pressure rise

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31
Q

What is static sensitivity?

A

Magnitude of pressure

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32
Q

What would be the autonomic result of an increase in BP?

A

Increase parasympathetic and decrease sympathetic.
This causes vasodilation and a decrease in HR and CO.
MABP falls

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33
Q

What determines the rate of diffusion?

A

Rate of diffusion = permeability x SA x concentration gradient

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34
Q

What is hydrostatic pressure?

A

Where fluid moves from an area of high pressure to an area of low pressure

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35
Q

What is colloid oncotic pressure? (Osmotic pressure)

A

Movement of fluid from an area of low [protein] to an area of high [protein]

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36
Q

When does oedema occur?

A

When the capillary filtration rate is faster than the lymphatic drainage

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37
Q

Describe Cardiac muscle.

A

Striated, multinucleate, branched, intercalated discs, Myogenic activity

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38
Q

Can recruitment alter strength of contraction in the heart?

A

No, all fibres in the heart contract together anyway.

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39
Q

Does the frequency of action potentials control heart rate?

A

Not really, the heart has an automatic rhythmic control system (SAN)

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40
Q

What ion increases the strength of a contraction in the heart?

A

Ca2+

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41
Q

What types of drugs increase the intracellular concentration of Calcium ions?

A

Positive Ionotropic drugs

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42
Q

List 3 ways of increasing intracellular calcium ion concentration.

A
  1. Ca2+ enters from the outside of the cell
  2. Intracellular stores allow ‘quick release’
  3. Calcium induced calcium release
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43
Q

How can you decrease intracellular calcium concentration?

A
  1. Active Na+/Ca2+ exchange on cell membrane

2. Active uptake to Sarcoplasmic reticulum

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44
Q

How do calcium ions cause cardiac muscle contraction?

A

Ca2+ binds to Troponin-c which causes Tropomyosin to move out of the Myosin binding site. Actin-Myosin cross bridges form. Actin filament moves along Myosin and the Myosin head disengages, Repeat!

45
Q

In a Cardiac Action potential, which ions are responsible for each stage?

A

Depolarisation - Na+ influx.Partial Repolarisation - K+ efflux
Plateau - Ca2+ influx
Repolarisation - K+ efflux
Pacemaker depolarisation - Na+ channels reactivation

46
Q

What is the purpose of the plateau phase of the action potential?

A

Prevents tetanic contraction to maintain rhythmic contraction

47
Q

How do beta agonists work as Positive Ionotropic drugs?

A

Speed up Ca2+ uptake to cellular stores, making it more availible

48
Q

How do Glycosides work as Ionotropic drugs?

A

Inhibits Na+/K+ ATPase, increasing intracellular Na+, which causes a decrease in Na+/Ca2+ exchange. This allows the Ca2+ intracellular concentration to increase

49
Q

Name 2 examples of Negative Ionotropic drugs.

A

Ca2+ channel blockers

Beta blockers

50
Q

What is Preload?

A

The stretching of cardiac myocytes prior to contraction (due to venous return)

51
Q

What increases preload?

A
  1. Gravity - inc. preload
  2. Thoracic pump
  3. Muscle pump
  4. Co-localisation
  5. Blood volume
  6. Venomotor tone
52
Q

How does the muscle pump increase preload?

A

Veins are compressed by surrounding muscles which increases venous return

53
Q

What is Co-loacalisation?

A

Pulsating arteries massage veins, thus increasing venous return

54
Q

What is the equation for Cardiac Output?

A

Cardiac output = Heart rate x Stroke Volume

55
Q

What limits the cardiac output?

A

Venous return

56
Q

How is Cardiac Output measured?

A

By looking at the volume of oxygen taken in, the O2 saturation of both arterial and venous blood and the Hb concentration. This calculates the lung blood flow which is equal to the cardiac output.

57
Q

What is a possible impact of a fast heart rate on the coronary blood supply?

A

It may decrease as blood only flows in the coronary arteries during diastole. In severe cases, this may lead to ischaemia.

58
Q

Is the SNS or the PNS mostly in charge of heart rate under normal conditions?

A

PNS

59
Q

What is starlings law?

A

The stroke volume is dependent upon the stretch of the ventricular muscle fibres.

Stretching the fibres (from increased preload) increases the force with which the mucle contracts.

61
Q

What is decompensation?

A

When the muscle is stretched too much, cross bridge formation is reduced and so the force of contraction decreases.

62
Q

What is contractility?

A

The force of contraction caused by Calcium ions.

63
Q

What is heart failure?

A

An inability to maintain a sufficient Cardiac output at a normal filling pressure (preload).

64
Q

What is Dynamic/Isotonic exercise?

A

Rhythmic contraction of muscles (aerobic)

65
Q

What does dynamic/Isotonic exercise do to the muscle length?

A

It shortens it.

66
Q

What is static/Isometric exercise?

A

Continued muscle tension (e.g. weight lifting).

No muscle shortening.

67
Q

What muscle types are there?

A

Slow twitch and fast twitch

68
Q

What are slow twitch muscle fibres?

A

Dependent upon Oxidative Phosphorylation.
Good blood supply
Lots of mitochondria
Mostly used for posture.

69
Q

What are fast twitch muscle fibres?

A

Dependent upon Creatine Phosphate to regenerate ATP.
Lots of Glycolytic enzymes
Used in explosive exercise!

70
Q

How do you measure the intensity of exercise?

A

By O2 uptake

71
Q

What is oxygen debt?

A

The O2 which is used up readily before Cardiopulmonary adaptations start shortly after exercise begins.

72
Q

How does Oxygen debt occur?

A

ATP and Creatine Phosphate are depleated and lactic acid builds up.

73
Q

How is O2 debt repaid?

A

Fast - rephosphorylation of ADP and Creatine

Slow - lactate is converted back to Glucose/Glycogen

Very slow - Increased metabolic rate after exercise

74
Q

What Cardiovascular changes occur during exercise?

A

Increased HR
Increased SV
Increased Arterial BP
Decreased Peripheral resistance

75
Q

Why does peripheral resistance decrease during exercise?

A

Resistance is dependent upon vascular tone.

Increased metabolism leads to increased vasodilation which decreases the resistance.

76
Q

During exercise, where is more of the CO directed to?

A

Heart, muscle, skin (to a certain extent)

77
Q

What happens to the proportion of the CO going to the brain during exercise?

A

It remains the same as before!

78
Q

What respiratory changes are there during exercise?

A

Increased respiratory rate

Increased tidal volume

79
Q

Do ABGs change during exercise?

A

No

80
Q

What triggers cardiopulmonary changes in exercise?

A

Central control of locomotor areas of the brain increase HR and Respiratory rate!

Barorecpetors detect ‘stretch’ to maintain a good BP.

81
Q

What is the limiting factor of the pathway of O2 during exercise?

A

O2 delivery by cardiovascular system

82
Q

What happens to muscles when they are trained?

A

Hypertrophy.
More myofibrils
More mitochondrial enzymes
More ATP, Phosphocreatine and Glycogen

83
Q

What happens to the CVS as a result of training?

A

Bradycardia
Cardiac remodelling
Decreased blood pressure
Increased Myoglobin and BPG

84
Q

What happens to the respiratory system as a result of training?

A

Decreased ventilation rate at the same level of exercise.

85
Q

What is VO2max?

A

The functional capacity of the CVS and pulmonary system.

86
Q

What does the Renin-Angiotensin system do?

A

Regulates blood pressure and blood volume.

87
Q

What is Angiotensin 1 formed from?

A

Angiotensinogen

88
Q

What enzyme helps convert Angiotensinogen into Angiotensin 1?

A

Renin

89
Q

What is Angiotensinogen?

A

A physiologically inactive protein, produced and secreted continuously by the liver.

90
Q

What enzyme helps convert Ang1 to Ang2?

A

Angiotensin converting Enzyme (ACE)

91
Q

What product can be formed from Ang2?

A

Aldosterone

92
Q

What does Ang2 do?

A

Vasoconstriction (short term control)

Produces Aldosterone.

93
Q

What does Aldosterone do?

A

Promotes salt and water retention. (Long term BP control)

94
Q

Where is Renin secreted from?

A

The juxtoglomerulus apparatus in the kidney

95
Q

How often is ACE secreted?

A

Continuously secreted in the same quantity.

96
Q

Aside from converting Ang1 into Ang2, what does ACE do?

A

Breaks down Bradykinin.

97
Q

What affect does Bradykinin have on vascular tone?

A

It causes vasodilation

98
Q

Where is Aldosterone released from?

A

The adrenal cortex.

99
Q

What is the regulatory control of the Renin-Angiotensin system?

A

Renin (under sympathetic control)

100
Q

Where does Renin originate from?

A

The kidneys

101
Q

When is Renin released?

A

Low BP (SNS via Baroreceptor reflex and via Intrarenal stretch receptors)

Low blood volume

Altered Na+ handling

102
Q

What controls whether the Renin-Angiotensin system is on or off?

A

Renin

103
Q

Where does Ang 2 mostly bind?

A

AT1 receptors

104
Q

What happens when AT1 receptors are activated?

A

Vasoconstriction and inc BP
Promotes cell division and growth
Profibrotic

105
Q

What happens when Ang 2 binds to AT2 receptors?

A

Vasodilation and decreased BP

Anti-mitogenic

106
Q

How does AT1 activation cause vasoconstriction?

A

Works directly on smooth muscle. Increases sympathetic activity by increasing NA release but blocking it’s re-uptake back into the pre-synaptic knob.

107
Q

When AT1 is activated, Aldosterone is released. What are the affects of Aldosterone?

A

Salt and water retention.

Increased ADH secretion and thirst.

108
Q

How does AT2 cause vasodilation?

A

NO release

Increases Bradykinin levels

109
Q

What equation represents MABP?

A

MABP = CO x TPR

110
Q

Why would you want to block the Renin-Angiotensin system?

A

Reduce BP or Heart failure.

111
Q

What drugs can be used to block RAS?

A

Beta blockers
Renin Inhibitors
ACE inhibitors
AT1 antagonists

112
Q

How do beta blockers block RAS?

A

Reduces Sympathetic production of Renin.

RCR1 Physiology (5 decks)

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