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Cardiovascular > Physiology > Flashcards

Physiology Flashcards

1
Q

Where are cardiac electrical impulses generated?

A

Within the heart

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2
Q

What is the name given to the term used to describe the way by which the heart can beat without external stimuli?

A

Authorhythmicity

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3
Q

Where does excitation originate?

A

Pacemaker cells found in the sino-atrial node

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4
Q

What is the SA node and where can it be found?

A

A cluster of pacemaker cells that initiates a heart beat. It is located in the upper right atrium close to where the superior vena cava enters the right atrium

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5
Q

What is it called when a heart is controlled by the SA node?

A

Sinus rhythm

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6
Q

What can be said about the resting potential of pacemaker cells?

A

They have no stable resting membrane potential, it drifts until an action potential is reached.

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7
Q

How is an action potential generated in pacemaker cells?

A

The spontaneous pacemaker potential takes the membrane potential to a threshold where an action potential is generated

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8
Q

Why does permeability not remain constant between action potentials?

A
  • decrease in potassium efflux - sodium and potassium influx - transient calcium influx
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9
Q

What is the other name for the sodium/potassium influx?

A

The funny current

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10
Q

Once the threshold is reached what results in the rising phase of the action potential?

A
  • activation of L type calcium channels - calcium influx
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11
Q

What is the falling phase due to?

A
  • inactivation of L type calcium channels - activation of potassium channels leading to potassium efflux
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12
Q

Describe the pathway of impulse

A

SA - AV - Bundle of His - Right/left branches - purkinje fibres

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13
Q

What is the AV node and where can it be found?

A

It is the only point of electrical contact between the atria and ventricles. It is a small bundle of specialised cells found just above the junction of the atria and ventricles.

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14
Q

Why is conduction slow?

A

The cells are small in diameter

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15
Q

How does current flow from cell to cell?

A

Gap junctions

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16
Q

What does the conduction delay allow?

A

Atrial systole to precede ventricular systole

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17
Q

How many stages are there of cardiac myocyte action potential?

A

5 phase 0-4

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18
Q

Describe phase 0

A
  • resting potential remains - 90mV - fast sodium influx causes the potential to become 20mV
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19
Q

What happens in phase 1?

A
  • closure of sodium channels - transient potassium efflux
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20
Q

Give another name for phase 2 and describe what happens

A

plateau phase - calcium influx through L type calcium channels

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21
Q

What happens in phase 3?

A
  • closure of calcium channels - potassium efflux
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22
Q

Describe phase 4

A

resting membrane potential

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23
Q

What is the normal heart rate?

A

60-100bpm

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24
Q

Name HR<60 and HR>60

A

<60 bradycardia >60 tachycardia

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25
Q

What nerve continuously influences the heart and what does it do?

A

Vagus nerve Slows the heart rate from 100bpm to 70 bpm by supplying the SA and AV node

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26
Q

What is the effect of vagal stimulation?

A

decreased heart rate and increased AV nodal delay

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27
Q

What does vagal stimulation do to the action potential graph?

A

Decreases the slope of pacemaker potential so it takes longer to reach the threshold so the frequency of action potentials decreases

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28
Q

State the term used to describe an effect that slows the heart rate

A

Negative chronotopic

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29
Q

Describe the sympathetic innervation of the heart

A

Cardiac sympathetic nerves supply the SA node, AV node and myocardium

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30
Q

What does sympathetic stimulation result in?

A

increased heart rate, decreased AV nodal delay and increased force of contraction

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31
Q

What does sympathetic stimulation do to the action potential graph?

A

increased the slope of pacemaker potential so it reaches threshold faster so the frequency of action potentials increases

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32
Q

State the term used to describe an effect that speeds up the heart rate

A

positive chronotopic

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33
Q

Are cardiac myocytes striated?

A

Yes, due to the regular arrangement of contractile protein

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34
Q

Are there neuromuscular junctions in cardiac cells?

A

No - gap junctions

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35
Q

What is the function of gap junctions?

A

Protein channels that form low resistance electrical communication pathways between neighbouring myocytes. They ensure electrical impulses reach all cardiac myocytes

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36
Q

Other than gap junctions what other junction is there between cells?

A

Desmosomes - provide mechanical adhesion between adjacent cardiac cells. Ensure tension is transmitted from one cell to the next

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37
Q

What is another name for cardiac muscle cells?

A

muscle fibres

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38
Q

Describe myofibrils

A

contractile units of muscle, they have alternating segments of thick and thin protein filaments

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39
Q

What causes the thick/thin appearance? What do these proteins form?

A

actin - thin/light myosin - thick/darker Forming sarcomeres

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40
Q

What does muscle contraction depend on?

A

ATP and calcium

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41
Q

Describe muscle in the relaxed state in terms of actin and myosin

A

no cross bring binding because binding site is covered by troponin

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42
Q

Describe muscle contraction

A

binding of calcium to troponin means the binding site is exposed and myosin can bind. This triggers a power stroke that pulls actin forward.

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43
Q

What is the refractory period?

A

the period following an action potential in which it is not possible to generate another action potential

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44
Q

How does the refractory period occur?

A

Sodium channels are closed Potassium channels are open Therefore the membrane cannot be depolarised

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45
Q

What is the benefit of the refractory period?

A

It protects the heart and prevents tetanic contractions

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46
Q

Define stroke volume

A

the volume of blood ejected by each ventricle per heart beat

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47
Q

How can stroke volume be calculated?

A

SV = EDV - ESV

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48
Q

Describe the intrinsic control of stroke volume

A

Diastolic stretch is determined by the volume of blood in each ventricle at the end of diastole. EDV is determined by venous return.

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49
Q

What does the Frank Starling curve show?

A

the more the ventricle is filled with blood (higher EDV) the higher the stroke volume

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50
Q

As well as stroke volume what else does stretch increase?

A

Affinity of calcium for troponin, the optimal length is achieved by stretching unlike skeletal muscle which can be overstretched

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51
Q

Define preload and afterload

A

preload - initial stretching prior to contraction afterload - pressure required to eject blood

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52
Q

What happens if afterload increases?

A

The heart is unable to eject full stroke volume so EDV increases. Force of contraction increases and eventually ventricular mass too.

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53
Q

Name two types of extrinsic control of stroke volume

A
  • Nerves - Hormones
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54
Q

What nerve supply influences stroke volume?

A

sympathetic fibres with noradrenaline

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55
Q

Describe the effect of noradrenaline

A

increases the force of contraction known as a positive inotropic effect

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56
Q

How is force of contraction increased?

A
  • Increased calcium influx - Increased ventricular pressure - Increased rate of pressure change - Decreased duration of systole - Decreased duration of diastole
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57
Q

What hormones control stroke volume?

A

adrenaline & noradrenaline released from adrenal medulla have inotropic and chronotropic effects

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58
Q

Define cardiac output

A

volume of blood pumped by each ventricle per minute

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59
Q

How can cardiac output be calculated what is the usual value?

A

CO = SV x HR Usually about 5L (70x70)

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60
Q

Define blood pressure

A

The outwards pressure exerted by the blood on the vessel walls

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61
Q

Define 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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62
Q

What should systolic BP be less than?

A

140mmHg

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63
Q

Define 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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64
Q

Give the values required for a diagnosis of hypertension

A

clinic BP >140/90 day time BP >135/85

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65
Q

What is pulse pressure?

A

The difference between systolic and diastolic normally between 30mmHg and 50mmHg

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66
Q

For a BP of 120/80 give examples of korotkoff sounds

A
  1. At 120 the first sound will be heart as systolic exceed the cuff 2/3 intermittent sound will be heart as the BP is turbulent but exceeds the cuff 4. The sound becomes muffled 5. No sound - diastolic
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67
Q

What drives the blood around the systemic circulation?

A

A pressure gradient between the aorta and the right atrium MAP - CVP

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68
Q

Define mean arterial pressure

A

the average arterial blood pressure during a single cardiac cycle

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69
Q

How can MAP be calculated?

A

MAP = 2diastolic+systolic/3 MAP = DBP+1/3 pulse pressure MAP= SVxHRxSVR

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70
Q

What is the normal range for MAP?

A

70-105mmHg At least 60mmHg is required to perfuse the coronary arteries, brain and kidneys.

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71
Q

Define systemic vascular resistance

A

The sum of resistance of all vasculature in the systemic circulation

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72
Q

What are the main resistance vessels?

A

arterioles

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73
Q

What are the two types of baroreceptor? Where are they found?

A

carotid and aortic found in their respective arteries

74
Q

What is the control centre and effectors for baroreceptor signals?

A

control centre - medulla effectors - heart and blood vessels

75
Q

How are the baroreceptors transmitted?

A

aortic - vagus nerve - 10th cranial nerve carotid - glossopharyngeal nerve - 9th cranial nerve

76
Q

What disease do baroreceptors prevent?

A

postural hypotension

77
Q

Describe postural hypotension is overcome

A

when someone stands up the venous return to the hearts decreases so MAP decreases and baroreceptor firing decreases. This decreases vagal tone but increases sympathetic tone. HR and SV increase, sympathetic constrictor tone increases so SVR increases and venous return increases

78
Q

What is postural hypotension?

A

Failure of baroreceptors responses to gravitational shifts in blood

79
Q

What are the risk factors for postural hypotension?

A
  • Age - Medications - Certain diseases - Reduced intravascular volume - prolonged bed rest
80
Q

What is a positive result for postural hypotension?

A

Standing up from lying down within 3 mins a drop of; systolic BP of at least 20mmHg (with or without symptoms) diastolic BP of at least 10mmHg with symptoms

81
Q

What are the symptoms of postural hypotension?

A
  • light head - dizzy - falls - faints - blurred vision
82
Q

What happens to baroreceptor control if abnormal blood pressure is sustained?

A

It will reset to the new level and only fire when there is an acute change in MAP

83
Q

Can baroreceptors supply information about steady state BP?

A

No

84
Q

What regulates long term MAP?

A

Hormones that regulate plasma volume

85
Q

What is total body fluid made up of?

A

intracellular fluid (2/3) + extracellular fluid (1/3)

86
Q

Name the two components of extracellular fluid volume

A

plasma volume - in the vessels interstitial volume - bathes the cells acts as the go between blood and vessels

87
Q

What can be said about the plasma and interstitial?

A

They are at equilibrium so if plasma fluid falls, fluid from the interstitial compartment will move into the plasma

88
Q

Name two factors that affect extracellular fluid volume

A
  • water excess or deficit - sodium excess or deficit
89
Q

How are the factors affecting extracellular fluid controlled?

A

By hormones

90
Q

What three classes of hormones control blood pressure?

A

Renin-Angiotensin- Aldosterone Natriuretic Peptides Antidiuretic Hormone (ADH)

91
Q

Describe the function of renin

A

It is released by granular cells in the kidneys and stimulates the formation of angiotensin I in the blood from angiotensin produced in the liver. Angiotensin I is converted to angiotensin II by angiotensin converting enzyme (ACE) which is mainly produced in the pulmonary vascular endothelium

92
Q

Describe the function of angiotensin II

A
  • stimulates the release of aldosterone from the adrenal cortex - causes sympathetic vasoconstriction (increases SVR and BP) - stimulates thirst and ADH release to increase plasma volume and BP
93
Q

Where is aldosterone produced?

A

Adrenal Cortex

94
Q

What is the function of aldosterone?

A

Steroid hormone that acts on the kidneys to increase sodium and water reabsorption to increase plasma volume and blood pressure

95
Q

What is the rate limiting step in RAAS?

A

renin secretion

96
Q

Name three stimuli that regulate renin secretion

A
  • renal artery hypotension cause by sympathetic hypotension
  • stimulation of renal sympathetic nerves
  • decreased sodium in the renal tubular fluid - sensed by macula densa
97
Q

Where are natriuretic peptides synthesised? When are they released?

A

The heart, brain and other organs, they are released in response to cardiac distension and neurohormonal stimuli.

98
Q

What do natriuretic peptides cause?

A
  • excretion of salt and water in the kidneys to reduce blood volume and pressure
  • decrease in renin release to decrease blood pressure
  • vasodilation to decrease SVR They are a counter
  • regulatory system to RAA
99
Q

What are the two types of natriuretic peptide?

A

atrial & brain type

100
Q

Describe atrial natriuretic peptide

A

28 amino acid peptide synthesised and stored by atrial muscle cells. ANP is released in response to atrial distension (hypovolaemic states)

101
Q

Describe brain type natriuretic peptide

A

first synthesised as prepro BNP then cleaved to pro BNP (108 amino acids) and finally BNP (32 amino acids)

102
Q

What can be measured in patients with suspected heart failure?

A

serum BNP and N terminal piece of pro BNP

103
Q

Where does ADH come from?

A

A pre hormone precursor synthesised by the hypothalamus and stored in the posterior pituitary.

104
Q

How is secretion of ADH stimulated?

A
  • reduced extracellular volume - increased extracellular fluid osmolality - increased plasma osmolality
105
Q

What does plasma osmolality indicate and how is it monitored?

A

solute - water balance monitored by osmoreceptors mainly in the brain close to the hypothalamus

106
Q

What does ADH do?

A
  • Acts in the kidney tubules to increase reabsorption of water - this increases extracellular &; plasma volume
  • which increases cardiac output and blood pressure
  • It also acts on blood vessels to cause vasoconstriction and increase SVR and BP
107
Q

When is the vasoconstriction by ADH important?

A

patients in hypovolaemic shock

108
Q

What is the main site of SVR?

A

Arterioles

109
Q

What does contraction cause?

A

Vasoconstriction that increases SVR and increases MAP

110
Q

What does relaxation cause?

A

Vasodilatation that decreases SVR and decreases MAP

111
Q

Describe the relationship of resistance

A

It is proportional to blood viscosity and length of vessel It is inversely proportional to the radius of the blood vessel to the power of four

112
Q

What does extrinsic control involve?

A

Nerves and hormones

113
Q

Describe the nerve supply to vascular smooth muscle

A

sympathetic nerves cause partial constriction at rest vasomotor tone

114
Q

What causes vasomotor tone?

A

Tonic discharge of sympathetic nerves results in continuous release of noradrenaline

115
Q

What is the effect of increased discharge?

A

increased vasomotor tone and vasoconstriction

116
Q

What is the effect of decreased discharge?

A

decrease vasomotor tone and vasodilatation

117
Q

Name the main hormone involved in extrinsic control

A

Adrenaline from the adrenal medulla causes organ specific responses

118
Q

Describe the effect on alpha receptors

A

vasoconstriction, receptors in the skin gut & kidney arterioles

119
Q

Describe the effect on beta 2 receptors

A

vasodilatation, receptors in cardiac and skeletal muscle

120
Q

What other hormones are involved in extrinsic control?

A
  • angiotensin II causes vasoconstriction - antidiuretic hormone causes vasoconstriction
121
Q

How does intrinsic control work?

A

Matches the blood flow of different tissues to their metabolic needs

122
Q

State the two components of intrinsic control

A
  • chemical - physical
123
Q

Describe chemical control

A

local metabolic & humoral changes within an organ influence the contraction of arteriolar smooth muscle

124
Q

Name five metabolic changes that can lead to vasodilatation and relaxation

A
  • decreased pO2
  • increased local CO2
  • increased local [H+]
  • increased extracellular potassium
  • increased osmolality of ECF Adenosine release
125
Q

What are humoral responses to?

A
  • histamine - bradykinin - nitric oxide All cause vasodilatation
126
Q

Where is nitric oxide produced?

A

Vascular endothelium from amino acid L arginine through the enzyme nitric oxide synthase (NOS)

127
Q

What is the impact of stress on NO release?

A

Increased flow causes calcium release & activation of NOS

128
Q

What can also induce NO formation?

A

chemical stimuli

129
Q

Where does NO diffuses from and to?

A

vascular endothelium into the adjacent smooth muscle cells where it activates the formation of cGMP that signals smooth muscle relaxation

130
Q

Name four chemical signals that cause vasoconstriction

A
  • serotonin - thromboxane A2 - leukotrienes - endothelin
131
Q

What do endothelial products control?

A
  • thrombus - inflammation - oxidation
132
Q

Name three physical components of intrinsic control

A
  • temperature -myogenic response to stress -sheer stress
133
Q

Explain how temperature influences resistance

A

cold causes vasoconstriction warmth causes vasodilatation

134
Q

How does myogenic response to stress influence resistance?

A

MAP rises, resistance vessels constrict MAP falls resistance vessels dilate

135
Q

What is the effect of dilated arterioles?

A

Causes stress in the arteries upstream making them dilate, increasing flow to metabolically active tissues

136
Q

State four factors that increase venous return

A
  • venomotor tone - skeletal muscle pump - respiratory pump - blood volume
137
Q

What does increase in venous return lead to?

A

increase in atrial pressure, increase EDV and increase stroke volume

138
Q

Describe venomotor tone

A

Veins contain most of the blood volume at rest. Smooth muscle is supplied with sympathetic fibres and stimulation gives venous constriction

139
Q

What does an increased venomotor tone result in?

A

increased venous return, SV and MAP

140
Q

Describe the respiratory pump

A

when intra-thoracic pressure decreases, intra-abdominal pressure increases creating a suction effect that moves towards the heart

141
Q

Describe the skeletal pump

A

contraction aids venous return, one way venous valves allow blood to move towards the heart. Muscle activity increases venous return.

142
Q

How does sympathetic innervation effect the body in the acute response to exercise?

A
  • Increases heart rate and stroke volume
  • Reduces flow to the kidneys and gut by vasoconstriction
  • Metabolic hyperaemia overcomes vasomotor drive causing vasodilatation, blood flow increases in proportion to metabolic activity
  • Cardiac output increases SBP
  • hyperaemia decreases SVR and SBP
143
Q

What is the main chronic response to exercise?

A

Reduced blood pressure

144
Q

Define shock

A

an abnormality of circulatory system resulting in inadequate tissue perfusion & oxygenation

145
Q

How does shock result in cellular failure?

A

inadequate tissue perfusion→ inadequate tissue oxygenation → anaerobic metabolism → accumulation of metabolic waste products → cellular failure

146
Q

What does adequate tissue perfusion depend on?

A
  • adequate blood pressure
  • adequate cardiac output
147
Q

Ultimately what does cardiac output depend on?

A

MAP = CO x SR

CO = SV x HR

Stroke volume

  • preload (venous return)
  • myocardial contractility
  • afterload
148
Q

Name five types of shock

A
  • hypovolaemic
  • cardiogenic
  • neurogenic
  • obstructive
  • vasoactive
149
Q

Describe hypovolaemic shock

A

loss of blood volume → decreased blood volume → decreased venous return → decreased EDV → decreased stroke volume → dereased cardiac output → inadequate tissue perfusion

150
Q

Define cardiogenic shock and give an example

A

sustained hypotension caused by decreased cardiac contractility

e.g. myocardial infarction due to damage to the pump

151
Q

Describe cardiogenic shock

A

decreased cardial contractility → decreased stroke volume → decreased cardiac output & BP → inadequate tissue perfusion

152
Q

Give an example and describe obstructive shock

A

e.g. pneumothorax

increased intra-thoracic pressure → decreased venous return → decreased EDV → decreased stroke volume → decreased cardiac output & BP → inadequate tissue perfusion

153
Q

Describe neurogenic shock

A

loss of sympathetic tone to blood vessels & heart →venous and arterial vasodilatation → decreased heart rate → decreased venous return & SVR → decreased cardiac output & BP → inadequate tissue perfusion

154
Q

Describe vasoactive shock

A

release of vasoactive mediators → venous & arterial vasodilatation → increased capillary permeability & leakage of fluid → decreased venous return & SVR → decreased cardiac output & BP → inadequate tissue perfusion

155
Q

What are the four key steps in treatment of shock?

A
  • ABCDE
  • high flow oxygen
  • volume replacement
  • call for help early
156
Q

What treatment can be used when the specific type of shock is known?

A
  • inotropes in cardiogenic shock
  • immediate chest drain in pneumothorax
  • adrenaline for anaphylactic shock
  • vasopressors in septic shock
157
Q

What is the most common type of shock?

A

Hypovolaemic

158
Q

Give two causes of hypovolaemic shock

A
  1. Haemorrhage (trauma, surgery, GI)
  2. Vomitting, diarrohoea, excessive sweating (decreases ECF)
159
Q

How long can compensatory mechanisms control blood pressure for?

A

Until blood lost is >30%

160
Q

What will haemorragic shock do to the body?

A

Increased heart rate via baroreceptors - tachycardia

Decreased stroke volume - small volume pulse

Increased SVR via baroreceptors - cool peripheries

All of which lead to decreased MAP if >30% blood lost

161
Q

What special adaptations are present in the coronary circulation?

A
  • High capillary density
  • High basal blood flow
  • High oxygen extraction (75%)
162
Q

What is the result of a high oxygen extraction?

A

Extra oxygen cannot be supplied by increasing extraction

163
Q

How is the coronary circulation intrinsically controlled?

A
  • Decrease pO2 causes vasodilatation
  • Metabolic hyperaemia matches flow to demand
  • Adenosine causes vasodilatation
164
Q

How is the coronary circulation extrinsically controlled?

A

Coronary arterioles are supplied by sympathetic vasoconstrictor nerves but over-ridden by metabolic hyperaemia as a result of increased heart rate & stroke volume.

Sympathetic stimulation results in vasodilation by adrenaline activating beta 2 adrenoceptors

165
Q

When does most coronary blood flow and perfusion occur?

A

During diastole because the subendocardial vessels from the LCA are not compressed

166
Q

What arteries supply the brain?

A

Internal carotid & vertebral arteries

167
Q

Why does it need a secure supply of oxygen?

A

Grey matter is very sensitive to hypoxia, consciousness is lost after a few seconds of ischaemia

168
Q

How soon does irreversible damage to the brain occur during hypoxia?

A

within 3 mins

169
Q

What is the special adaptation of the cerebral circulation regarding the arteries?

A

Basilar & carotid arteries anastomos to form the circle of willis this mean that if one caroitd artery gets obstructed the brain can still receive a blood supply

170
Q

What is the special adaptation of the cerebral circulation regarding blood pressure?

A

If MAP increases vessels constrict to limit blood flow

If MAP decreases vessels dilate to maintain blood flow

171
Q

What happens if MAP falls below 50mmHg?

A
  • confusion
  • fainting
  • brain damage
172
Q

What does the skull consist of?

A

80% Brain

12% Blood

8% Cerebrospinal fluid

173
Q

What are the normal values of intracranial pressure?

A

8-13mmHg

174
Q

What is the effect of increasing ICP?

A

Decreases cerebral perfusion pressure & blood flow

175
Q

Describe the blood brain barrier

A

Capillaries have very tight intercellular junctions which are highly permeable to oxygen & carbon dioxide. Glucose crosses by facilitated diffusion but in order to protect brain neurons it is impermeable to hydrophilic substances

176
Q

What is the normal range for pulmonary blood pressure?

A

20-25/6-12mmHg

177
Q

What are the special adaptation of the pulmonary circulation?

A
  • Low capillary pressure
  • Absorptive forces exceed filtration to protect against oedema
  • Vasoconstriction in response to hypoxia means blood will be diverted to poorly ventilated lung
178
Q

What percent of body mass is skeletal muscle?

A

40%

179
Q

What is the cause for the low blood flow to skeletal muscle?

A

sympathetic vasomotor tone

180
Q

What happens in response to exercise?

A

Metabolic hyperaemia overcomes sympathetic vasomotor tone and circulating adrenaline causes vasodilation

181
Q

How do muscles aid venous return?

A

Large veins lie between skeletal muscles and one-way venous valves allow blood to move towards the heart

182
Q

What happens if the valves become incompetent?

A

Blood will poll in the lower limb veins as varicose veins

Cardiovascular (19 decks)

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