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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 SVA entry)

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3
Q

When the heart is controlled by the SA node, init is said to be in what time 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 (lb)
  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 Ca2+ 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 nose?

A

To allow conduction to spread to the ventricles from the atria

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10
Q

What attributes of the AV node allows for heart contraction and coordination?

A

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

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11
Q

What is the bundle if 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 cells?

A

-90mV

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13
Q

In a myocardial action potential, what is phase 0?

A

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

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14
Q

In a myocardial action potential, what is a 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 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 brachycardia 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. Increase 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 the atria is slightly higher than ventricles allowing for passive filling of the 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 contraction

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41
Q

Describe isovolumetric ventricular contraction

A

Ventricular pressure rises past atrial pressure upon contraction causing the AV valves to close. Semilunar valves remain closed 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 heart sound?

A

Closing of the 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 notching 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 the 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

52
Q

Where are the S3 and S4 heart sounds best heard?

53
Q

Where is the aortic area?

A

2nd intercostal space right parasternal

54
Q

Where is the pulmonary area?

A

2nd intercostal space left parasternal

55
Q

Where is the tricuspid area?

A

4th intercostal space left parasternal

56
Q

Where is the mitral area?

A

5th intercostal space left parasternal

57
Q

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

A
  1. Contractile of arterial muscle

2. Retraction of elastic fibres

58
Q

What is blood pressure?

A

Hydrostatic (outward) pressure exerted on vessels by blood flow

59
Q

What is the upper limit of blood pressure before treatment?

A

140/90 mmHg

60
Q

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

A

Laminar blood flow

61
Q

What are Korotkoff sounds?

A 
There are 5 and they are heard when blood pressure is taken
phase 0- silence
phase 1- Tapping sound
phase 2 - soft swishing sound
phase 3- crisp sound
phase 4 - blowing sound
phase 5 - silence
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

63
Q

What drives blood circulation ?

A

The pressure gradient between aorta and right atrium

64
Q

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

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

What is pulse pressure?

A

This is the difference between systolic and diastolic pressure

66
Q

What is the range for MABP?

A

70- 105 mmHg

67
Q

What is the minimum requirements of MABP to perfuse organs?

68
Q

What can happen if MABP is too high?

A

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

69
Q

What is TPR?

A

Total peripheral resistance

The sum of all the resistance is systemic and peripheral circulations

70
Q

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

A

Arterioles

The blood pressure drops the most after entering these vessels

71
Q

What effect does parasympathetic stimulation have on the cardiovascular system?

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

What effect does sympathetic stimulation have on the cardiovascular system?

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

What are baroreceptors ?

A

Pressure receptors

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 vessels

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 vessels “react” to increased carotid sinus afferent nerve fibre firing?

A

Vasodilate

79
Q

How do blood vessels “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 duet o a drop in blood pressure
  2. Firing rate of baroreceptors decreases
  3. Vagal tone of the heart decreases as the sympathetic system increases heart rate and stroke volume to attempt a blood pressure increases
  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 for response to acute changes
The response sets a new baseline value to an acute change, if this change is maintained 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. Extracellular 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 full 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 involved 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 vascular 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 kidney 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 hypertension

2. Stimulation of renal sympathetic nerves]3. Decreased (Na+) in renal tubular fluid (sensed my macradensa)

95
Q

What are the macra densa?

A 
Can detect (Na+) in renal tubular fluid
Specialised renal tulles 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 vasodilation and reduced renin release
This is counter regulatory mechanisms 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 plasm osmolarity?

A

Osmoreceptors

102
Q

How does ADH function?

A

Acts on kidney tulles 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 preload?

A

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

108
Q

What is after load?

A

This is the amount of blood left in the ventricles 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 is 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 duet o decreases 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 inadequate 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 vasodilation

118
Q

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

A
  1. Massive vasodilation
  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 vasodilation 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 vasodilation
  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. Increased 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 increases 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 haemorrhage 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 dilation/ contraction to ensure blood flow remains constant where 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

Left and right coronary arteries

Cardiovascular (11 decks)

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