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Physiology Flashcards

1
Q

What is blood pressure?

A

The outwards/hydrostatic pressure exerted by the blood on the blood vessel walls.

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2
Q

What is (systemic) systolic (arterial) blood pressure?

A

The pressure exerted by the blood on the walls of the aorta and systemic arteries when the heart contracts

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3
Q

What is (systemic) diastolic (arterial) blood pressure?

A

The pressure exerted by the blood on the walls of the aorta and systemic arteries when the heart relaxes.

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4
Q

What is pulse pressure?

A

The difference between systolic and diastolic blood pressures

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5
Q

What is mean arterial blood pressure?

A

The average arterial blood pressure during a single cardiac cycle which involves contraction and relaxation of the heart.

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6
Q

How do you estimate MAP and why?

A

[(2 x diastolic pressure) + systolic pressure] / 3

Because the diastolic portion is twice as long as the systolic portion of the cardiac cycle

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7
Q

What is a normal resting systolic, diastolic value and MAP range?

A

Systolic: <140mmHg
Diastolic: <90mmHg
MAP: 70-105mmHg

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8
Q

What is the normal range for pulse pressure?

A

Between 30-50 mmHg

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9
Q

Why does MAP need to be regulated?

A

To ensure pressure is high enough to perfuse essential organs but not too high to damage the blood vessels or place extra strain on the heart.

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10
Q

Which Korotkoff sounds are used to measure the diastolic and systolic pressures?

A

Diastolic is recorded at the fifth sound

Systolic is recorded at the first sound

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11
Q

What is the role baroreceptor reflex?

A

It is a negative feedback system that acts to minimise changes in MAP including the prevention of postural hypotension.

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12
Q

What happens to the normal heart rate and blood pressure when you suddenly stand up from lying position?

A

Normal heart rate: increases

Normal blood pressure: there is a slight increase in diastolic bp due to the increase in SVR.

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13
Q

Define postural hypotension

A

Low bp resulting from failure of baroreceptor responses to gravitational shifts in blood when moving from horizontal to vertical position.

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14
Q

What are the risk factors for postural hypotension?

A 
Age
Medications
Certain diseases (eg: diabetes)
Reduced intravascular volume
Prolonged bed rest
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15
Q

Which hormones regulate extracellular volume, hence regulating MAP in the long term?

A
  • The Renin-angiotensin-aldosterone system (RAAS)
  • Natriuretic peptides (NPs)
  • Antidiuretic hormone (ADH)
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16
Q

What is the stroke volume?

A

The volume of blood pumped by each ventricle of the heart per heart beat

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17
Q

What effect does parasympathetic stimulation have on the MAP?

A

Decreases the heart rate which decreases the cardiac output which decreases the MAP

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18
Q

What effect does sympathetic stimulation have on the MAP?

A

On the heart:

  • the heart rate is increased
  • the contractile strength of the heart increases which increases the SV
  • both of these increase the CO which increases the MAP.

Arterioles:
- vasoconstriction is increased which increases the SVR which increases the MAP.

Veins:
- venoconstriction is increased which increases the venous return, which increases the SV which increases the CO which increases the MAP

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19
Q

Where are the baroreceptors and how do the signals reach the medulla?

A

Carotid are in the carotid sinus and signal to the medulla via the IXth CN
Aortic are in the aorta and signal to the medulla via the Xth CN

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20
Q

Describe what happens during postural hypotension mentioning the baroreceptor reflex’s role.

A

When a normal person suddenly stands up from lying position:
- the venous return to the heart decreases due to gravity
- the MAP very briefly decreases
- this reduces the rate of firing of baroreceptors
- the vagal tone to the heart decreases and the sympathetic tone to the heart increases (increasing the SV and HR)
- The sympathetic constrictor tone increases which increases the SVR
- the sympathetic constrictor tone to the veins increases the venous return to the heart and SV
THE RESULT Is…rapid correction of the transient fall in MAP: HR, SV and SVR increases

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21
Q

Describe the baroreceptors response to decreased bp.

A

The baroreceptor firing decreases causing:
- decreased vagal activity (no longer slowing HR)
- increases the cardiac sympathetic activity (increasing HR and SV increasing CO)
- increases the sympathetic constrictor tone which causes: vasoconstriction (increasing SVR) PLUS
venoconstriction (increasing SV via venous return so increasing CO)

All of these act to raise BP

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22
Q

What would a positive result for postural hypotension be?

A

A drop in systolic bp of at least 20mmHg

A drop in diastolic bp of at least 10mmHg

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23
Q

What are the symptoms of postural hypotension?

A

Cerebral hypoperfusion: lightheadedness, dizziness, blurred vision, faintness and falls

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24
Q

Describe the baroreceptor’s response to increased bp.

A

The baroreceptor firing increases which:
- increases the vagal activity on the heart (slowing HR, decreasing CO)
- decreases the cardiac sympathetic activity (slows HR, decreasing SV and CO)
- decreases the sympathetic constrictor tone which causes:
venodilation (decreasing SV via venous return, decreasing CO)
vasodilation (decreases SVR)

All of these act to lower BP

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25
Q

What happens if high bp is sustained?

A

The baroreceptors are re-set and will only fire again if there is an acute change in MAP above the new higher steady state level

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26
Q

How can MAP be controlled in the long term?

A

Through the use of effector hormones regulating the blood plasma volume which in turn regulates the MAP.
This is all controlled by controlling the extracellular fluid volume.

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27
Q

What is the extracellular fluid made up of?

A

plasma volume and interstitial fluid volume (this is the fluid that bathes the cells and acts as the medium between blood and body cells.

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28
Q

How is the fluid in the body split up?

A

2/3rds is intracellular fluid

1/3 is extracellular fluid

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29
Q

What are the two main factors that affect extracellular fluid volume and how do our bodies control these factors?

A
  1. Water excess or deficit
  2. Na+ excess or deficit
    These are controlled by hormones which act as effectors to regulate the extracellular fluid volume (including plasma volume) by regulating the water and salt balance in our bodies where water input=water output
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30
Q

Describe the role of the Renin-Angiotensin-Aldosterone system.

A

It regulates the plasma volume and SVR and hence regulates the MAP

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31
Q

Describe how the Renin-Angiotensin-Aldosterone system works?

A
  1. Renin is released from the kidneys and stimulates the formation of angiotensin I in the blood from angiotensinogen (which is produced by the liver)
  2. Angiotensin I is converted to angiotensin II by angiotensin converting enzyme (ACE - which is mainly produced by pulmonary vascular endothelium)
  3. Angiotensin II:
    - stimulates the release of aldosterone from the adrenal cortex
    AND
    - causes systemic vasoconstriction which increases the SVR
    AND
    - stimulates thirst and ADH release whic h contributes to increasing plasma volume that was brought about by aldosterone
  4. Aldosterone (steroid hormone) acts on the kidneys to increase sodium and water retention which increases the plasma volume.
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32
Q

Describe how Natriuretic peptides work in regulating MAP.

A

Peptide hormones are synthesised by the heart (also brain and other organs).
They are release in response to cardiac distension or neurohormonal stimuli.
They cause:
-excretion of salt and water in the kidneys which reduces the blood volume and blood pressure.
- decrease in renin release which decreases bp
- act as vasodilators which decreases SVR and bp

33
Q

What is the role of natriuretic peptides?

A

To provide a counter-regulatory system for the renin-angiotensin-aldosterone system

34
Q

Describe the main 2 types of natriuretic peptides released by the heart.

A

Atrial natriuretic peptide (ANP):
- is a 28 amino acid peptode synthesised and stored by atrial muscle cells
- released in response to atrial distension
Brain-type natriuretic peptide (BNP):
- a 32 amino acid peptide
- synthesised by heart ventricules, brain and other organs.

35
Q

Why do we meausre serum BNP and the N-terminal piece of pro-BNP?

A

If the patients has suspected heart failure

36
Q

What is the antidiuretic hormone (ADH)?

A

ADH = a peptide hormone derived from a prehormone precursor synthesised by the hypothalamus and stored in the posterior pituitary

37
Q

What is the antidiruetic hormone’s secretion stimulated by?

A

Reduced extracellular fluid volume
OR…
Increased plasma osmolarity - main stimulus

38
Q

What does plasma osmolarity indicate and what is it monitored by?

A

Plasma osmorality indicates relative solute to water balance.
It is monitored by osmoreceptors which are mainly in the brain close to the hypothalamus.

39
Q

Describe what the antidiuretic hormone does.

A

ADH acts in the kidney tubules to increase the reabsorption of water (to conserve water by creating concentrate urine)
This increases extracellular and plasma volume and therefore increases CO and bp.
It also causes vasoconstriction which increases SVR and bp (this effect is small, but is important in hypovolaemic shock - haemorrhage

40
Q

What is the heart driven by?

A

The SA node acts as the pacemaker for the heart. When this occurs the heart is in sinus rhythm.

41
Q

Where in the heart does excitation normally originate?

A

In the pacemaker cells in the SA node, located in the upper right atrium.

42
Q

How is the cardiac excitation (action potential) normally generated?

A

The cells in the SA node have no stable resting membrane potential so generate regular spontaneous pacemaker potentials as they are always slowly drifting towards depolarisation.
This will hit threshold generating an action potential.
Resulting in regular spontaneous action potentials.

43
Q

How does the cardiac excitation normally spread across the heart?

A

An action potential is generated in the SA node that is then conducted to the AV node where there is a slight delay before the signal is conducted to the bundle of his, down the septum separating the ventricles and into the Purkinje fibres that curve up around the bottom of the ventricles and up the sides.

44
Q

What influences the heart rate?

A

Mainly by the autonomic nervous system.

45
Q

Describe the ionic basis for the pacemaker potential.

A

It is due to:

  • decrease in K+ efflux
  • Na+ influx, the funny current
  • Transient Ca2+ influx
46
Q

Describe the ionic mechanisms resulting in the phases of ventricular muscle action potential.

A

This differs greatly from the pacemaker cells.
The resting potential is -90mV until the cell is excited.
Phase 0 (depolarisation) is due to fast Na+ influx, resulting in a new membrane potential of +20mV.
Phase 1 due to closure of Na+ channels and transient K+ efflux
Phase 2 due mainly to Ca2+ influx.
Phase 3 due to closure of Ca2+ channels and K+ efflux.

47
Q

How do the cardiac conducting cells allow the current to flow?

A

Through gap junctions

48
Q

What is special about the AV node?

A

It is the only point of electrical contact between the atria and ventricles

49
Q

Why is conduction delayed in the AV node?

A

To allow the systole of the atria to be completed before ventricular systole begins.

50
Q

What does sympathetic stimulation do to the heart rate?

A

increases it

51
Q

What does parasympathetic stimulation of the heart cause?

A

A decrease in heart rate

52
Q

How is the heart rate maintained at a resting heart rate?

A

By the continuous influence of vagal tone (parasympathetic) on the SA node.

53
Q

What is bradycardia?

A

A resting heart rate of less than 60bpm

54
Q

What is tachycardia?

A

A resting heart rate of more than 100bpm

55
Q

Which nerve supplies the SA and AV node

A

the vagal nerve

56
Q

What does vagal stimulation do to the heart?

A

Decreases the heart rate by increasing the AV node delay by decreasing the slope of the pacemaker potential

57
Q

What is the neurotransmitter of the vagus nerve and what does it act on?

A

Acetyl choline acting through muscarinic M2 receptors

58
Q

What is atropine used for and how does it work?

A

To increase the heart rate in extreme brachycardia by acting as a competitive inhibitor of acetylcholine.

59
Q

What is a negative chronotropic effect?

A

Something that can slow the heart rate

60
Q

What is a positive chronotropic effect?

A

Something that will increase the heart rate

61
Q

Describe where the sympathetic cardiac nerves supply and what effect their stimulation has upon the heart.

A

Supplies the SA and AV node as well as the myocardium.
Sympathetic stimulation increases the HR, by decreasing AV nodal delay.
It also increases the force of contraction.

62
Q

What is the neurotransmitter for cardiac sympathetic nerves and where do they act on?

A

Noradrenaline acting through beta-1 adrenoceptors.

63
Q

Describe the effect of noradrenaline on pacemaker cells in terms of the pacemaker potential.

A

It increases the slope of the pacemaker potential.
Causing it to reach threshold more quickly.
Resulting in an increased frequency of action potentials causing a positive chromotropic effect.

64
Q

Resistance to blood flow is ____ proportional to blood viscocity and the length of the blood vessel and ___ proportional to the radius of the blood vessel to the power of ___.

A

directly
indirectly
power of 4

R a n.L/r4

65
Q

What is resistance to blood flow mainly due to?

A

vascular smooth muscle either contracting or relaxing

66
Q

what is the vasomotor tone? (inc cause)

A

vascular smooth muscle being partially constricted at rest due to tonic discharge of sympathetic nerves causing continuous release of noradrenaline

67
Q

what does an increase and decrease in vasomotor tone cause?

A

increase: vasoconstriction (increased symp discharge)
decrease: vasodilation (decreased symp discharge)

68
Q

what is the effect of parasympathetics on arterial smooth muscle?

A

it has no significant effect, except in clitoris and penis (symp innervation would just increase or decrease)

69
Q

Adrenaline acts on alpha receptors (found in __1__ arterioles) to cause __2__ and acts on beta-2 receptors (found in __3__ arterioles) to cause_4__

A

Adrenaline acts on alpha receptors (found in 1[skin, gut and kidney] arterioles) to cause 2[vasoconstriction] and acts on beta-2 receptors (found in 3[cardiac and skeletal muscle] arterioles) to cause 4[vasodilation]

70
Q

why does adrenaline cause vasoconstriction in some arterioles and vasodilation in others?

A

to strategically redistribute blood, eg: during exercise

71
Q

What does ADH/vasopressin cause?

A

vasoconstriction

72
Q

name 3 hormones which cause vascular smooth muscle relaxation (vasodilation)

A

histamine, bradykinin, NO

73
Q

name 4 hormones which cause vascular smooth muscle contraction (vasoconstriction)

A

serotonin, thromboxane A2, leukotrienes and endothelin

74
Q

what is the myogenic response to stretch?

A

Used to keep cerebral flow constant over a wide range of MAP.

if MAP rises, resistance vessels will automatically constrict to limit flow, if MAP falls, will automatically dilate to increase flow

75
Q

Venous smooth muscle is supplied by which part of the ANS?

A

sympathetic

76
Q

What does increased venomotor tone cause? (constriction of venules)

A

venoconstriction which increases venous return, SV and MAP

77
Q

what does increased vasomotor tone cause? (constriction of arterioles)

A

vasoconstriction which increases SVR which increases MAP

78
Q

How does inspiration increase venous return?

A

decreases intrathoracic pressure (ribs etc expand so air can flow in), increases intra-abdo pressure (diaphragm pushed down) which increases the pressure gradient (higher in abdo, lower in thorax) for venous return creating a suction effect to the heart

79
Q

what is hydrostatic pressure?

A

pressure exerted by a fluid at equilibrium, is due to gravity

Cardio (8 decks)

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