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The Cardiovascular System > Physiology > Flashcards

Physiology Flashcards

1
Q

Where does excitation originate in the heart?

A

SA node

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2
Q

Where is the SA node located

A

Upper right atrium (close to SVC entry)

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3
Q

When the heart is controlled by the SA node, it is said to be in what type of rhythm?

A

Sinus rhythm

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4
Q

What is the pacemaker potential due to?

A
  1. Decrease in funny current 2. Background current of potassium influx (Ib) 3. Transient Ca2+ influx
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5
Q

What happens when the pacemaker potential reaches threshold?

A

L-type calcium channels open allowing for calcium influx

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6
Q

What are the 2 main causes of the falling phase in a nodal action potential?

A
  1. Inactivation of L-type Calcium channels 2. Activation of delayed rectifier outward potassium channels
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7
Q

What permits the spread of excitation between myocardial cells?

A

Gap junctions

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8
Q

Where is the AV node located?

A

At the base of the right atrium just above the atrium/ventricular junction

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9
Q

What is the purpose of the AV node?

A

To allow conduction to spread to the ventricles from the atria

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10
Q

What attribute of the AV node allows for heart contraction coordination?

A

It has a low conduction velocity allowing there to be delay between atrial and ventricular contraction

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11
Q

What is the bundle of His?

A

This is a bundle of nerve fibres which carries the impulse from the AV node to the ventricles where the impulse passes upwards via Purkinje fibres in the ventricles

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12
Q

What is the resting potential of a myocardial cell?

A

-90mv

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13
Q

In a myocardial action potential, what is phase 0

A

Rapid depolarisation from -90mv to +20mv due to Na+ influx

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14
Q

In a myocardial action potential, what is phase 4

A

Resting membrane potential is achieved (-90mv)

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15
Q

In a myocardial action potential, what is phase 3

A

Closure of Ca2+ channel influx and K+ efflux begins

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16
Q

In a myocardial action potential, what is phase 2

A

L-type Ca2+ channel influx

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17
Q

In a myocardial action potential, what is phase 1

A

Closure of Na+ channels and transient K+ channels

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18
Q

What is the plateau phase and what causes it?

A

Maintained during phase 2 of a myocardial AP. Due to Ca2+ influx through L-type channels. Maintains peak AP

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19
Q

How does the sympathetic system affect heart rate?

A

Increases

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20
Q

How does the parasympathetic system affect heart rate?

A

Decreases

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21
Q

What is vagal tone?

A

Continuous influence of the vagus nerve on SA node lowering heart rate to normal levels

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22
Q

What is the normal range for heart rate?

A

60-100bpm

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23
Q

What is the term for low heart rate (<60bpm)?

A

Bradycardia

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24
Q

What is the term for high heart rate (>100bpm)?

A

Tachycardia

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25
Q

On which receptors does acetylcholine from the vagus nerve act?

A

Type 2 Muscarinic

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26
Q

What type of drug is atropine and what may it be used for?

A

Competitive acetylcholine inhibitor Treats bradycardia by speeding up heart rate

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27
Q

What three effects does sympathetic stimulation have on the heart?

A
  1. Increase HR 2. Decrease AV node delay 3. Increases contractile force
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28
Q

Noradrenaline from the sympathetic system acts on which receptors in the heart?

A

B1

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29
Q

What is a chronotropic effect?

A

Something which influences heart rate e.g. positive chronotropic increases HR

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30
Q

In an ECG what does the P wave represent?

A

Atrial depolarisation

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31
Q

In an ECG what does the QRS complex represent?

A

Ventricular depolarisation

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32
Q

In an ECG what does the T wave represent?

A

Ventricular repolarisation

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33
Q

In an ECG what does the PR interval represent

A

AV node delay

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34
Q

In an ECG what does the ST segment represent?

A

Ventricular systole

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35
Q

In an ECG what does the TP interval represent?

A

Diastole

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36
Q

How long does the cardiac cycle normally last?

A

0.8s

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37
Q

What 5 events comprise the cardiac cycle?

A
  1. Passive Filling 2. Atrial Contraction 3. Isovolumetric ventricular Contraction 4. Ventricular Ejection 5. Isovolumetric ventricular Relaxation
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38
Q

Describe passive filling

A

Pressure in atria is slightly higher than ventricles allowing for passive filling of ventricles with blood

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39
Q

Passive filling accounts for what percentage of ventricular filling?

A

80%

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40
Q

Describe how atrial contraction contributes to ventricular filling

A

The final 20% of ventricular filling is achieved by atrial conraction

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41
Q

Describe isovolumetric ventricular contraction

A

Ventricular pressure rises past atrial pressure upon contraction cause AV valves to close. Semilunar valves remain close so pressure builds around a closed volume

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42
Q

Describe ventricular ejection

A

Ventricular pressure exceeds aortic/pulmonary valve pressure causing ejection of stroke volume

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43
Q

What is the end systolic volume?

A

This is the amount of blood left behind in the ventricles after contraction

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44
Q

How is stroke volume calculated?

A

SV = EDV - ESV

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45
Q

When do the semilunar valves close?

A

When ventricular pressure falls after contraction?

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46
Q

What causes the first hearts sound?

A

Closing of AV valves during isovolumetric ventricular contraction

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47
Q

What causes the second heart sound?

A

Closing of semilunar valves after ventricular ejection

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48
Q

What causes the dicrotic notch in the pressure curve?

A

Valve vibration

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49
Q

What does isovolumetric ventricular relaxation involve?

A

The closing of aortic and pulmonary valves

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50
Q

What causes the third heart sound (S3)?

A

Occurs after 2nd heart sound - due to acceleration and deceleration of blood into the ventricles - can signify cardiac disease

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51
Q

What causes the fourth heart sound (S4)?

A

Occurs shortly before the first heart sound - due to rapid blood flow into less compliant ventricles (usually left) causing turbulence

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52
Q

Where are the S3 and S4 heart sounds best heard?

A

Apex

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53
Q

Where is the aortic area?

A

2nd intercostal space Right parasternal

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54
Q

Where is the pulmonary area?

A

2nd intercostal space Left parasternal

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55
Q

Where is the tricuspid area?

A

4th intercostal space Left parasternal

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56
Q

Where is the mitral area?

A

5th intercostal space Left parasternal

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57
Q

For which two reasons does arterial pressure never fall to zero?

A
  1. Contraction of arterial muscle 2. Retraction of elastic fibres
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58
Q

What is blood pressure?

A

Hydrostatic (outward) pressure exerted on vessels by blood flow

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59
Q

What is the upper limit of blood pressure before treatment?

A

140/90mmHg

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60
Q

What is the term used to describe blood flowing without turbulence?

A

Laminar blood flow

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61
Q

What are Korotkoff sounds?

A

There are 5 and they are heard when blood pressure is taken

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62
Q

At which Korotkoff sound is diastolic pressure measured and why?

A

5

At sound 5, the change is more easily heard as any sound heard changes to silence

Technically the fourth Korotkoff sound is where diastolic pressure occurs

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63
Q

What drives blood circulation?

A

The pressure gradient between aorta and right atrium

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64
Q

How is mean arterial blood pressure (MABP) calculated? (3)

A
  1. MABP = (2 x diastolic + systolic)/3
  2. MAP = 1/3 (systolic – diastolic) + diastolic
  3. MABP = CO x TPR
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65
Q

What is the pulse pressure?

A

This is the difference between systolic and diastolic pressure

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66
Q

What is the range for MABP?

A

70 - 105mmHg

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67
Q

What is the minimum requirement of MABP to perfuse organs?

A

60mmHg

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68
Q

What can happen is MABP is too high?

A

Damage to organs, vessels and extra strain is placed on the heart

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69
Q

What is TPR?

A

Total peripheral resistance

The sum of all the resistances in systemic and peripheral circulations

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70
Q

What are the main resistance vessels and what eveidence is there for this?

A

Arterioles

The blood pressure drops the most after entering these vessels

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71
Q

What effect does parasympathetic stimualtion have on the cardiovascular system?

A
  1. Decreases heart rate
  2. Decreases cardiac output
  3. Decreases MABP
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72
Q

What effects does sympathetic stimulation have on the cardiovascular system?

A
  1. Increase heart rate
  2. Increase contractile strength
  3. Increase cardiac output (increased stroke volume)
  4. Increase MABP
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73
Q

What are baroreceptors?

A

Pressure receptors

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74
Q

Where is the control centre located for baroreceptors?

A

The medulla

75
Q

What are the effectors for the baroreceptors?

A

The heart and blood vessles

76
Q

Where are the two groups of baroreceptors located?

A
  1. Aortic arch
  2. Carotid sinus (bifurcation)
77
Q

Which cranial nerves allow signals to be sent from baroreceptors to the brain?

A

9 and 10

(IX and X)

(Glossopharyngeal and Vagus)

78
Q

How do blood vessles “react” to increased carotid sinus afferent nerve fibre firing?

A

Vasodilate

79
Q

How do blood vessles “react” to cardiac vagal nerve efferent nerve fibres?

A

Vasodilation

80
Q

Explain the process baroreceptors go through when a person stands up quickly after lying down

A
  1. Venous return decreased due to a drop in blood pressure
  2. Firing rate of baroreceptors decreases
  3. Vagal tone of the heart decreases as the sympathetic system increases heart arte and stroke volume to attempt a blood pressure increase
  4. Sympathetic constrictor tone increases TPR which increases venous return and stroke volume correcting the low MABP and increasing it
81
Q

What happens to the baroreceptor response when blood pressure is maintained over a long period of time?

A

The baroreceptor response is designed tor respond to acute changes.

The response sets a new baseline value to an acute change, if this change is mainatined it will become the new “normal”

82
Q

How is MABP controlled long term?

A

Blood volume

83
Q

Total body fluid is made up of which two components?

A
  1. Extracellualr volume
  2. Intracellular volume
84
Q

What two components make up extracellular fluid volume?

A
  1. Plasma volume
  2. Interstitial fluid volume
85
Q

What happens in order to balance a fall in plasma volume?

A

Compensatory mechanisms shift fluid from the interstitial fluid volume

86
Q

Blood volume and MABP are controlled by mechanisms regarding ____________ _____ ______

A

Extracellular Fluid Volume

(ECFV)

87
Q

Which two main factors affect ECFV?

A
  1. Water excess or deficit
  2. Na+ excess or deficit
88
Q

Which three systems are involves in regulating ECFV?

A
  1. Renin Angiotensin Aldosterone system
  2. Atrial Naturiuretic Peptide
  3. Antidiuretic Hormone (Vasopressin)
89
Q

How does the RAAS regulate MABP?

A

By regulating TPR and plasma volume

90
Q

Where is renin produced and what is its function?

A

Kidneys (juxtaglomerular apparatus)

Stimulates formation of angiotensin I in the blood from angiotensinogen (from liver)

91
Q

What happens to angiotensin I?

A

It is converted to angiotensin II by angiotensin converting enzyme (ACE, produced in pulmonary vascualr endothelium)

92
Q

What does angiotensin II stimulate?

A
  1. Release of aldosterone from adrenal cortex
  2. Causes systemic vasoconstriction increasing TPR
  3. Stimulates thirst and ADH release (contributes to increasing plasma volume)
93
Q

What does aldosterone do?

A

Acts on kidneys to increase sodium and water retention to increase plasma volume and hence MABP

94
Q

What can stimulate renin release form the juxtaglomerular apparatus in the kidneys?

A
  1. Renal artery hypotension
  2. Stimulation of renal sympathetic nerves
  3. Decreased [Na+] in renal tubuar fluid (sensed my macra densa)
95
Q

What are the macra densa?

A

Can detect [Na+] in renal tubular fluid

Specialised renal tubules composed of extraglomerular mesangial and granular cells (which release renin)

96
Q

What is atrial natriuretic peptide (ANP) and when is it released?

A

Atrial myocytes synthesise a 28-amino acid peptide (ANP)

Released in response to atrial distension (stretch) in hypervolaemic states

97
Q

What does ANP do?

A

Causes release of water and Na+ in urine.

The system reduces MABP and causes vasodilatation and reduced renin release.

This is a counter regulatory mechanism for RAAS

98
Q

What is ADH?

A

Anti-diuretic hormone (vasopressin)

A peptide hormone

99
Q

Where is ADH produced?

A

Precursor formed in hypothalamus and stored in posterior pituitary

100
Q

What will stimulate ADH secretion?

A

Reduced ECFV or increased extracellular fluid osmolarity

101
Q

What monitors plasma osmolarity?

A

Osmoreceptors

102
Q

How does ADH function?

A

Acts on kidney tubules to increase water reabsorption allowing for increased blood volume and MABP.

It will stimulate vasoconstriction to increase TPR and MABP

103
Q

What is shock?

A

An abnormality of the circulating system resulting in inadequate tissue perfusion

104
Q

What is the pathway for shock?

A
  1. Inadequate tissue perfusion
  2. Inadequate tissue oxygenation
  3. Anaerobic metabolism
  4. Waste product build up
  5. Cellular failure and death
105
Q

Which two factors are essential for there to be adequate tissue perfusion?

A

Adequate cardiac output and blood pressure

106
Q

Which three factors can affect the stroke volume?

A
  1. Preload
  2. Myocardial contractility
  3. Afterload
107
Q

What is the preload?

A

The preload is the amount of blood in the ventricles before systole - it is the EDV

108
Q

What is afterload?

A

This is the amount of blood left in the ventrciles after systole - provides resistance for contracting heart muscle during the next contraction

109
Q

Why does hypovolaemic shock occur?

A

Loss in blood volume

110
Q

Why does hypovolaemic shock lead to inadequate tissue perfusion?

A
  1. Loss in blood volume
  2. Venous return/EDV reduced
  3. Stroke/cardiac volume reduced
  4. Blood pressure lowered
  5. Inadequate tissue perfusion
111
Q

In response to hypovolaemic shock, which way does the Frank-Starling curve shift and why?

A

To the right

Decreased EDV (sub-optimal fibre length) hence stroke volume is reduced

112
Q

What is cardiogenic shock?

A

Occurs when the heart cannot pump enough blood around the body due to decreased cardiac contractility

113
Q

How does cardiogenic shock lead to inadequate tissue perfusion?

A
  1. Decreased contractility
  2. Decreased stroke volume
  3. Decreased cardiac output
  4. Reduced blood pressure
  5. Inadequate tissue perfusion
114
Q

How does cardiogenic shock affect the Frank-Starling curve?

A

Shifts very far to the right - more than heart failure alone

115
Q

What is obstructive shock?

A

Due to increased intrathoracic pressure which decreases venous return

(e.g. pneumothorax)

116
Q

Why does tissue perfusion become inaqequate in obstructive shock?

A
  1. Decreased venous return and EDV
  2. Decreased stroke volume
  3. Decreased cardiac output
  4. Reduced blood pressure
  5. Decreased tissue perfusion
117
Q

What does neurogenic shock involve?

A

Loss of sympathetic tone causing massive vasodilatation

118
Q

Why does neurogenic shock lead to a lack in tissue perfusion?

A
  1. Massive vasodilatation
  2. Reduced venous return and EDV
  3. Reduced stroke volume
  4. Reduced cardiac output and blood pressure
  5. Inadequate tissue perfusion
119
Q

What is vasoactive shock?

A

The release of vasoactive mediators causing massive vasodilatation and increased capillary permeability

120
Q

Why is capillary permeability a relevant factor to vasoactive shock?

A

This can lead to a decreased blood volume and cause hypovolaemic shock

121
Q

How does vasoactive shock lead to inadequate tissue perfusion?

A
  1. Massive vasodilatation
  2. Decreased venous return and EDV
  3. Decreased stroke volume and cardiac output
  4. Lowered blood pressure
  5. Inadequate tissue perfusion
122
Q

How should shock be treated?

A
  1. ABCDE approach
  2. High flow oxygen - makes most of tissue perfusion that does occur
  3. Increase blood volume
  4. Use of positive inotropes e.g. adrenaline for anaphylaxis
  5. In septic shock, vasopressors can be used to cause mass vasoconstriction and increase MABP
123
Q

What are the two main causes of hypovolaemic shock?

A
  1. Haemorrhage (trauma, surgery etc.)
  2. Vomiting, diarrhoea, excessive sweating (decreases ECFV)
124
Q

How is haemorrhagic shock characterised?

A

Tachycardia - baroreceptor reflex

Small volume pulse - cardiac output is lowered

125
Q

What is the myogenic (Bayliss) effect?

A

This involves the control of vessel dilatation/constriction to ensure blood flow remains constant when there is fluctuating blood pressure

It prevents damage to areas such as the brain

126
Q

What are the first vessels to arise from the aorta?

A

Right and left carotid arteries

127
Q

Where does coronary venous blood primarily drain?

A

Coronary sinus

128
Q

In the coronary circulation, what are the two main areas for occulusion?

A
  1. Left carotid
  2. Left anterior descending
129
Q

The coronary circulations have many special adaptions. List 4

A
  1. High capillary density
  2. High basal flow
  3. High oxygen extraction (75% vs normal 25%)
  4. Intrinsic and extrinsic control mechanisms for blood flow
130
Q

Decribe 3 intrinsic mechanisms that confer special adaptions to the coronary circulation

A
  1. Decreased PO2 causes vasodilatation
  2. Metabolic hyperaemia (increased blood flow) ensure blood flow meets demand
  3. Adenosine (from ATP) is a potent vasodilator
131
Q

Noradrenaline acts on which type of receptors in coronary arterioles?

A

Alpha 1

132
Q

The vasoconstricting effect of the sympathetic system is avoided by opposing factors that promote vasodilatation, what are these factors?

A
  1. Increased CO (due to increased HR/SV)
  2. Increased adenosine due to cardiac work
  3. Decreased PO2 due to increased work
  4. Increased metabolites (K, PCO2, H) due to increased metabolism
  5. Increased circulating adrenaline
133
Q

Why does the majority of blood flow in the coronary arteries occur during diastole?

A

The arteries are compressed during systole

134
Q

The brain is supplied by which two artery types?

A
  1. Carotid arteries
  2. Vertebral arteries
135
Q

How is a constant blood flow to the brain maintained?

A

The circle of Willis

Created via the anastomosis of carotid and basilar arteries allowing cerbral blood flow to be mainatined even if half the circle is occluded

136
Q

A stoke can be caused by a _______ but also __________.

A

Thrombosis

Haemorrhage

137
Q

Special adaptions of the cerebral circulation include?

A
  1. Autoregulation - Bayliss effect
  2. Direct sympathetic stimulation has little effect
  3. The brain does not participate in baroreceptor reflexes
138
Q

Increased PCO2 in the brain causes what?

A

Cerebral vasodilatation

139
Q

Decreased cerebral PCO2 causes what?

A

Cerebral vasoconstriction

140
Q

Why does hyperventilation cause fainting?

A

PCO2 is reduced so cerebral vasoconstriction occurs

This limits blood flow to the brain

141
Q

The process by which (sympathetic) vasoconstrictor effects is termed what?

A

Functional symptholysis

142
Q

How is cerebral perfusion pressure calculated?

A

CPP = MABP - ICP

(ICP = intracranial pressure)

143
Q

How can intracranial pressur be increased?

A

Haemorrhage, tumour, and other factors introducing more material into the confined cranial space

144
Q

What forms the blood brain barrier?

A

The tight intercellular junctions formed between cerebral capillaries

145
Q

The blood brain barrier allows ______ _______ and ______ to cross but not ___________ substances

A

Carbon dioxide and oxygen

Hydrophilic subtances

146
Q

How does glucose pass the BBB?

A

Via specific carrier molecules

147
Q

How is the pulmonary circulation resistant to oedema?

A

Absorptive forces exceed filtrative forces

148
Q

How is skeletal blood flow increased during exercise when the sympathetic system induces vasoconstriction?

A
  • Local metabolic hyperaemia overcomes the sympathetic vasoconstrictor activity
  • Circulating adrenaline acts on B2 adrenergic receptors
  • Increased cardiac output contributes to increased muscular blood flow
149
Q

Describe the action of the skeletal muscle pump

A
  • Large veins lie between skeletal muscle
  • The contraction of skeletal muscle aids blood flow
  • Valves present backflow of blood
150
Q

What causes varicose veins?

A

The failure of venous valves leading to the pooling of blood in the lower limbs

151
Q

What are:

a) The major capacitance vessels
b) the major resistance vessels

A

a) Veins
b) Arterioles

152
Q

Which factors can affect the stroke volume?

A
  • Pre-load
  • Myocardial contractility
  • Afterload
153
Q

Total peripheral resistance is mostly controlled by what?

A

Vascualr smooth muscle in walls of arterioles

154
Q

Resistance to blood flow is directly proportional to what?

A
  1. Blood viscocity
  2. Blood vessel length
155
Q

Resistance to blood flow is inversely proportional to what?

A

The radius of blood vessels

156
Q

Vascualr smooth muscle is innervated by sympathetic nerve fibres. This utilises which neurotransmitter and which receptor?

A

Normadrenaline on alpha receptors

157
Q

What is vasomtor tone and what causes it?

A

The state of vascular smooth mucle always being contracted

This is due to tonic discharge of noradrenaline

158
Q

Where are two regions of the body where the parasympathetic system has influence over blood vessels?

A
  1. Penis
  2. Clitoris
159
Q

Adrenaline has what effect when it binds to beta 2 receptors?

A

Vasodilatation

(of skeletal muscle and cardiac arterioles)

160
Q

Angiotensin II can have what effect on arteries?

A

Vasoconstriction

161
Q

Intrinsic mechanisms of vascular smooth muscle include which two factors?

A
  1. Chemical factors
  2. Physical factors

These allow for matching between blood flow and metabolic need

162
Q

Intrinsic controls are able to _________ the extrinsic controls for vascular smooth muscle contraction

A

Override

163
Q

Give three examples of humoral agents which can cause vasodilatation

A
  1. Histamine
  2. Bradykinin
  3. Nitric oxide
164
Q

How is nitric oxide produced?

A

Produced by vascular endothelium from L-arginine by action of nitric oxide synthase

165
Q

When will nitric oxide be released?

A
  • It is always released by tonic discharge
  • Endothelial stress
  • Receptor activation
166
Q

How does nitric oxide exert its effect?

A

Diffuse into smooth muscle cells and activate cGMP - a secondary messenger

This allows for smooth muscle relaxation

167
Q

Give 4 examples of humoral agents which can stimulate contraction of smooth muscle?

A
  1. Serotonin
  2. Thromboxane A2
  3. Leukotrienes
  4. Endothelin
168
Q

Of the two, endothelial vasoconstrictors or vasodilators, which one contributes to vascular health and which does the opposite promoting thrombosis, inflammation and oxidation?

A

Vasodilators - vascular health

Vasoconstrictors - negative impact on vascular health

169
Q

Name a physical factor responsible for the intrinsic control of vascular smooth muscle contraction

A

Temperature

170
Q

What does the myogenic response allow for?

A

Blood flow to remain relatively constant for a range of mean arterial blood pressures

171
Q

How does increased atrial pressure impact stroke volume?

A

Increases stroke volume

EDV increases leaving to a lerger stoke volume

172
Q

Name factors which aid venous return

A
  • Skeletal muscle pump
  • Respiratory pump
  • Increased blood volume
  • Increased atrial pressure
  • Increased venomotor tone
173
Q

Why does pulse pressure increase during exercise?

A

Increased CO increases systolic BP

Metabolic hyperaemia decreases TPR and DBP

174
Q

What happens to the Frank-Starling curve during exercise?

A

It shift to the left

Ventricular pressure, SV and EDV rise

175
Q

Which vessels regulate blood flow to the capillary bed?

A

Terminal arterioles

176
Q

List chronic cardiovascular responses to exercise

A
  • Reduced BP
  • Reduced sympathetic tone and noradrenaline levels
  • Increased parasympathetic control to the heart
  • Cardiac remodelling
  • Reduction in plasma renin levels
  • Improved endothelial function
  • Arterial stiffening
177
Q

What is NFP?

A

Net filtration pressure

This is the overall pressure gradient either in or out of a vessel

178
Q

Where is NFP postive and negative?

A

Postitive - near beginning of capillaries - this allows for offloading

Negative - near end of capillaries - allows for onloading

179
Q

Overall fitration ________ reabsorption

A

Exceeds

180
Q

Since filtration exceeds reabsorption, what happens to the extra fluid?

A

It is returned to circulation via the lymphatic system as lymph

181
Q

Which tissue type is more resistant to oedema than other tissues and why?

A

Pulmonary tissue

The pressure system is lower than systemic circulation

182
Q

Heart failure causes the Frank-Starling curve to shift to the what?

A

Right

183
Q

What may be present in lung bases as a result of pulmonary oedema?

A

Crepitations

184
Q

What will an Xray show of pulmonary oedema?

A

Haziness around perihilar region

The Cardiovascular System (24 decks)

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