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Physiology Flashcards

1
Q

What is autorythmicity?

A

Autorhythmicity means that the heart can beat rhythmically in the absence of external stimuli

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2
Q

Where does excitation the heart originate?

A

Excitation of the heart originates in the pacemaker cells of the sinoatrial node

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3
Q

Where is the SA node located and what does it do?

A

The SA node is located in the upper right atrium and it initiates the heartbeat

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4
Q

What does sinus rhythm mean?

A

A heart controlled by the sinoatrial node is said to be in sinus rhythm

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5
Q

What is the resting potential of SA cells?

A

The SA cells have no stable resting membrane potential

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6
Q

What do SA cells generate?

A

These cells generate regular spontaneous pacemaker potentials

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7
Q

What happens when threshold is reached in the SA cells?

A

When threshold is reached there will be regular spontaneous action potentials

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8
Q

What happens to the permeability of K+ channels during SA cells action potentials?

A

The permeability of potassium does not remain constant between action potentials

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9
Q

What does the pacemaker potential of SA cells depend on?

A
  • decrease in K+ efflux
  • Na and K+ influx (funny current)
  • transient Ca2+ influx
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10
Q

What causes the rising phase of the action potential in SA cells?

A

L-type Ca2+ channels opening resulting in Ca2+ influx

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11
Q

What causes the falling phase of the action potential in the SA cells?

A

Inactivation of L-type Ca2+ channels and activation of K+ channels resulting in K+ efflux

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12
Q

How does the excitation spread from the SA node to the ventricular muscle cells?

A

SA node to AV node by cell-to cell conduction
Delay allows atria to finish contracting before ventricles do
Down bundle of His via right and left branches down to Purkinje fibres
Cell-to-cell current flow is via gap junctions

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13
Q

What is the only electrical point of contact between the atria and the ventricles?

A

AV node

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14
Q

Where is the AV node located?

A

at the base of the right atrium

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15
Q

What are the features of AV node cells?

A

they are small in diameter and have slow conduction velocity

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16
Q

What is the conduction across atria?

A

cell-to-cell conduction via gap junctions

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17
Q

What is the conduction from SA to AV node?

A

via gap junctions but some internodal pathways

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18
Q

Where is conduction delayed?

A

AV node

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19
Q

What is the conduction in the ventricular muscle cells?

A

cell-to-cell conduction

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20
Q

What is the resting membrane potential of the ventricular myocytes?

A

-90mV

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21
Q

What s the rising phase of the action potential in the ventricular myocytes caused by?

A

The rising phase of the action potential is caused by fast Na+ influx which rapidly reverses the membrane potential to +20mV

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22
Q

What is phase 0 of ventricular myocytes?

A

fast Na+ influx

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23
Q

What is the phase 1 of fast ventricular mycocytes?

A

Closure of Na+ channels and transient K+ efflux

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24
Q

What is the phase 2 of ventricular myocytes?

A

Mainly Ca2+ influx

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25
Q

What is the phase 3 of ventricular myocytes?

A

Closure of Ca2+ channels and K+ efflux

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26
Q

What is the phase 4 of ventricular myocytes?

A

Resting membrane potential

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27
Q

What is the plateau phase of ventricular myocytes and what is it due to?

A

The plateau phase is where the membrane potential is maintained near the peak of action potential which is unique to contractile muscle cells
The plateau phase is mainly due to influx of Ca2+ through L-type Ca2+ channels

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28
Q

What is the falling phase of the ventricular myocytes caused by?

A

The falling phase of action potential is caused by inactivation of Ca2+ channels and activation of K+ channels resulting in K+ efflux

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29
Q

What is a normal, slow and fast heart rate?

A

Normal is 60-100, less than 60 is bradycardia, greater than 100 is tachycardia

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30
Q

What is heart rate influenced by?

A

Heart rate is influenced by the autonomic nervous system
Sympathetic increases HR
Parasympathetic decreases HR

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31
Q

What tone dominates at rest?

A

The vagus nerve (parasympathetic) exerts a continuous influence on SA node so vagal tone dominates at rest

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32
Q

What does vagal tone do to the heart rate?

A

Vagal tone slows intrinsic HR from 100 to 70

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33
Q

What does vagal nerve supply and what does it cause?

A

Vagus nerve supplies SA and AV node, vagal stimulation slows heart rate and increases AV nodal delay

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34
Q

What is the neurotransmitter for vagal tone?

A

Neurotransmitter is acetylcholine acting through muscarinic M2 receptors

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35
Q

What is a common competitive inhibitor of acetlyl choline used in extreme bradycardia?

A

atropine

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36
Q

What does vagal stimulation do on a graph?

A
  • decreases the slope of the pacemaker potential
  • decreases the frequency of AP
  • there is a negative chronotropic effect
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37
Q

Where is sympathetic supply to?

A

Sympathetic supply is to SA node, AV node and myocardium

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38
Q

What does sympathetic stimulation do?

A

Sympathetic stimulation increases heart rate, decreases AV nodal delay and increases force of contraction

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39
Q

What is the sympathetic neurotransmitter?

A

Neurotransmitter is noradrenaline acting through beta 1 adrenoceptors

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40
Q

What is the influence of noradrenaline on a graph?

A

Noradrenaline increases the slope of pacemaker potential, increases the rate of firing of AP so there is a positive chronotropic effect

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41
Q

What does an ECG show?

A

ECGs are a record of depolarisation and repolarisation cycle of cardiac muscle obtained from the skin surface

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42
Q

What do the letters P-T stand for on the ECG wave?

A 
QRS complex is ventricular depolarisation (don’t see atrial repolarisation)
T wave is ventricular repolarisation 
PR interval is AV node delay
ST segment is ventricular systole
TP interval is diastole
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43
Q

What is the cardiac cycle?

A

The cardiac cycle is all the events from the beginning of one beat to the beginning of the next beat

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44
Q

What is diastole?

A

Diastole is when the heart ventricles are relaxed and fill with blood

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45
Q

What is systole?

A

Systole is the when the heart ventricles contract and pump blood into the aorta and the pulmonary artery

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46
Q

How long is systole and diastole?

A

diastole is 0.5s

systole is 0.3s

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47
Q

What is the passive filling stage?

A
  • Pressure in the atria and ventricles is very close to 0
  • The AV valves open so venous return flows into the ventricles
  • Pressures on the right side of the heart is lower than the left. The ventricles become 80% full by passive filling.
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48
Q

What is the atrial contraction stage?

A
  • The P wave in the ECG signals atrial depolarisation. - The atria contracts between the P wave and the QRS.
  • Atrial contraction completes the EDV.
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49
Q

What is the isovolumetric ventricular contraction stage?

A
  • Ventricular contraction starts after the QRS in the ECG
  • Ventricular pressure rises when the ventricular pressure exceeds the atrial pressure the AV valves shut - First LUB sound as the mitral valve closes
  • Tension rises around the closed volume so the ventricular pressure rises steeply
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50
Q

What is the ventricular ejection stage?

A
  • Ventricular pressure exceeds the aorta pressure the semilunar valve opens but this is silent
  • Stroke volume is ejected by each ventricle leaving behind the ESV
  • SV = EDV - ESV
  • Aortic pressure rises
  • T-wave in the ECG signals repolarisation and the ventricles relax and the pressure starts to fall
  • Ventricular pressure falls below the aortic pressure the valves shut which produced the second heart sound which is a DUB
  • Valve vibration produces the dicrotic notch in the aortic pressure curve
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51
Q

What is the isovolumetric ventricular relaxation stage?

A
  • Closure of the aortic valve is the start of the isovolumetric ventricular relaxation
  • Ventricle is again a closed box as the AV is shut
  • Tension falls and when it falls below the atrial pressure, the AV valves open and the heart starts a new cycle
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52
Q

What are the phases of the cardiac cycle?

A
  • passive filling
  • atrial contraction
  • isovolumetric ventricular contraction
  • ventricular ejection
  • isovolumetric ventricular relaxation
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53
Q

What is the S1 sound?

A

S1 is the closure of the mitral and tricuspid valves and is the beginning of systole LUB

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54
Q

What is the S2 sound?

A

S2 is the closure of the semilunar valves and is the beginning of diastole DUB

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55
Q

Why does the arterial pressure not drop during ventricular diastole?

A

The arterial pressure does not fall to zero during diastole because the vessels can stretch and recoil to maintain the arterial pressure

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56
Q

When does JVP occur?

A

JVP occurs after right atrial pressure waves

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57
Q

What are the stages of JVP wave?

A

A is atrial contraction
C is bulging of tricuspid valve into atrium during ventricular contraction
V is rise of atrial pressure during atrial filling, release as AV valves open

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58
Q

What type of muscle is cardiac muscle?

A

striated which iis caused by regular arrangement of contractile proteins

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59
Q

What joins cardiac myocytes?

A

no neuromuscular junctions but the cardiac myocytes are coupled by gap junctions

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60
Q

What do gap junctions between cardiac myocytes do?

A

gap junctions have low resistance electrical communication between neighbouring myocytes and they ensure that any electrical excitation reaches all the myocytes (all-or-none law)

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61
Q

What do desmosomes do between myocytes?

A

Desmosomes provide mechanical adhesion and ensure tension developed is transmitted between cells

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62
Q

How is muscle tension produced?

A

Muscle tension is produced by the sliding of actin filaments on myosin filaments

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63
Q

What is the production muscle tension dependent on?

A

dependent on ATP and the presence of calcium ions

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64
Q

What covers the myosin binding site on acting at rest?

A

Myosin binding site on actin is covered by tropomyosin, when there is calcium ions the troponin and tropomyosin will leave the binding site to allow myosin to bind

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65
Q

What is the release of calcium ions from the sarcoplasmic reticulum dependent on?

A

The release of calcium ions from the sarcoplasmic reticulum is dependent on the presence of extracellular calcium ions

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66
Q

What happens ionically during the plateau phase of ventricular muscle action?

A

The plateau phase of ventricular muscle action potential involves calcium ion influx through L-type calcium ion channels

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67
Q

What is CICR and when does it occur?

A

CICR is calcium-induced calcium release from the sarcoplasmic reticulum during muscle contraction

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68
Q

How is ventricular diastole achieved?

A

When the action potential has passed the calcium ions go back into the sarcoplasmic reticulum

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69
Q

What does the long refractory period prevent?

A

The long refractory period prevents generation of tetanic contraction

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70
Q

What is the refractory period?

A

The refractory period follows an action potential and it is not possible to produce another action potential during this time

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71
Q

What state are the Na+ channels in during the plateau phase of a ventricular action potential?

A

During the plateau phase of a ventricular action potential, the Na+ channels are closed

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72
Q

What state are the K+ channels in during the descending part of the ventricular action potential?

A

During the descending part of the action potential the K+ channels are open so the membrane can’t be depolarised

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73
Q

What does stroke volume mean?

A

The stroke volume is the volume of blood ejected by each ventricle per heartbeat

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74
Q

What is stoke volume regulated by?

A

The stroke volume is regulated by intrinsic and extrinsic mechanisms

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75
Q

What are the intrinsic mechanisms that control SV?

A

within the heart itself

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76
Q

What are the extrinsic mechanisms that control SV?

A

nervous and hormonal control

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77
Q

What is intrinsic control brought about by?

A

diastolic length or diastolic stretch of myocardial fibres

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78
Q

What is the diastolic length of myocardial fibres determined by?

A

volume of blood within each ventricle (EDV)

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79
Q

What is EDV determined by?

A

venous return to the heart

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80
Q

What does stroke volume equal?

A

end diastolic volume- end systolic volume

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81
Q

What is Starling’s law of the heart?

A

the more the ventricle is filled with blood (EDV), the greater the volume of blood ejected during the resultant contraction (SV)

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82
Q

What increases the affinity of troponin for calcium ions?

A

stretch

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83
Q

Is cardiac muscle at optimal length at rest?

A

no, it must stretch to reach optimal length

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84
Q

What happens when venous return to the right atrium increases?

A

the EDV of the right ventricle will increase and so there will be increased SV in the pulmonary artery by staling’s law

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85
Q

What is after load?

A

Afterload means the resistance into which the heart is pumping
The extra load is imposed after the heart has contracted

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86
Q

What happens when after load increases?

A

the heart is first unable to eject full SV so EDV increases and force of contraction increases by Starling’s law
If increased afterload continues to exist then the ventricular mass will increase (hypertrophy) to overcome the resistance

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87
Q

What does extrinsic control involve?

A

Extrinsic control involves nerves and hormones

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88
Q

What is ventricular muscle supplied by? and what is the neurotransmitter?

A

sympathetic muscle fibres

noradrenaline

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89
Q

What does sympathetic stimulation of the heart lead to?

A

increased force of contraction which is a positive inotropic effect and so increases the left ventricular pressure and the rate of development of contraction
(also causes positive chronotropic effect)

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90
Q

How does sympathetic stimulation lead to the peak ventricular pressure rising?

A

there will be a greater influx of calcium ions so force of contraction increases which is cAMP mediated so the peak ventricular pressure rises

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91
Q

If the rate of ventricular pressure change rises what will then happen?

A

duration of systole is reduced

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92
Q

If the rate of ventricular relaxation increases what will happen?

A

reduces the rate of diastole

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93
Q

What does sympathetic stimulation do to the frank-starling curve? and why?

A

Frank-Starling curve is shifted to the left by sympathetic stimulation because contractility of the heart at a given EDV rises

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94
Q

What does vagal stimulation mainly affect?

A

vagal stimulation has a major influence on rate but not on force of contraction as there is very little vagal innervation of the ventricles

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95
Q

What effect do adrenaline and noradrenaline have?

A

Adrenaline and noradrenaline released from adrenal medulla have inotropic and chronotropic effect

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96
Q

What is meant by the term cardiac output?

A

Cardiac output is the volume of blood pumped by each ventricle per minute

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97
Q

What is the equation for CO?

A

CO = SV * HR

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98
Q

What is blood pressure?

A

Blood pressure is the outwards pressure exerted by the blood on the blood vessel walls

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99
Q

What is systolic blood pressure?

A

Systolic is the pressure exerted by the blood of the walls of the aorta and systemic arteries when the heart contracts

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100
Q

What should systolic BP not exceed at rest?

A

140 mmHg

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101
Q

What is diastolic BP?

A

Diastolic is the pressure exerted on the walls of the aorta and systemic arteries when the heart relaxes

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102
Q

What should diastolic BP not exceed at rest?

A

90 mmHg

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103
Q

What is pulse pressure?

A

difference between systolic and diastolic blood pressures

104
Q

What is the normal range for pulse pressure?

A

30-50

105
Q

What is mean arterial blood -pressure?

A

the average arterial blood pressure during a single cardiac cycle

106
Q

What is the pressure gradient (between aorta and right atrium)?

A

mean arterial pressure - central venous pressure

107
Q

How do you estimate MAP?

A

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

108
Q

What is the normal range for MAP?

A

about 70-105 mmHg

109
Q

What is the minimum MAP needed and what happens if this is not reached?

A

60 mmHG minimum is needed and without this, the brain, heart and kidneys will not e adequately perfused

110
Q

When is the first Korotkoff sound heard?

A

peak systolic

111
Q

When is there now no Korotkoff sounds?

A

minimum diastolic

112
Q

Why can’t MAP be too high?

A

damage of blood vessels or place extra strain on the heart

113
Q

What is systemic vascular resistance?

A

the sum of resistance of all vasculature in the systemic circulation

114
Q

What are the main resistance vessels?

A

arterioles

115
Q

What does parasympathetic impulse do in the heart?

A

decreased HR –> decreased CO –> decreased MAP

116
Q

What does sympathetic impulse do in the heart?

A

increased HR and contractile strength/ SV –> increased CO –> increased MAP

117
Q

What does sympathetic impulse do in the arterioles?

A

increased vasoconstriction –> increased SVR –> increased MAP

118
Q

What does sympathetic impulse do in the veins?

A

increased vasoconstriction –> increased venous return –> increased SV –> increased CO –> increased MAP

119
Q

Where do baroreceptors send impulses?

A

control centre in the medulla

120
Q

What do baroreceptors activate?

A

effectors in the heart (HR and SV) and blood vessels (SVR)

121
Q

What does negative feedback act to do?

A

minimise disturbance to the MAP

122
Q

Where are the baroreceptors?

A

carotid sinus (9th cranial nerve) and aortic arch (10th cranial nerve)

123
Q

What is baroreceptor reflex important in?

A

moment-to-moment regulation of arterial blood pressure including prevention of postural changes

124
Q

What happens when someone stands after lying flat?

A
  • venous return to heart decreases due to gravity
  • MAP decreases
  • reduced rate of firing baroreceptors
  • vagal tone decreases and sympathetic tone to the heart increases
  • increased HR and SV
  • increased sympathetic constrictor tone
  • increased SVR, mainly in arterioles
  • increased sympathetic tone to veins increases VR to heart and stroke volume
  • rapid correction of the fall in MAP so HR increases, SV increases and SVR increases.
125
Q

What is postural hypotension?

A

postural hypotension results from failure of baroreceptor responses to gravitational shifts in blood when moving from horizontal to vertical position

126
Q

What are the risk factors of postural hypotension?

A
  • age
  • medications
  • certain diseases
  • reduced intravascular volume
  • prolonged bed rest.
127
Q

What is a positive result for postural hypotension?

A

within 3 minutes if standing from lying in a drop in systolic of at least 20 mmHg or a drop in diastolic of at least 10 mmHg

128
Q

What are the symptoms of postural hypotension?

A

cerebral hypo-perfusion: dizziness, blurred vision, faintness and falls

129
Q

What happens to baroreceptor if there are chronic changes in BP?

A

firing decreases if high BP sustained, they reset so they will only fire again if there are acute changes in MAP above the new higher steady state

130
Q

How is long-term changes in blood pressure death with?

A

control in blood volume

131
Q

How much of the body fluid is outside of the cell?

A

1/3rd

132
Q

Where is the fluid outside the cell located?

A
  • plasma volume

- interstitial fluid volume which is a go-between the blood and the body and bathes the cells

133
Q

What is done to correct a fall in plasma volume?

A

fluid is shifted from the interstitial compartment to the plasma compartment

134
Q

If you control extra cellular fluid volume what are you indirectly controlling?

A

blood volume and MAP

135
Q

What are the two main factors that affect extracellular fluid volume?

A
  • water excess or deficit

- Na+ excess or deficit

136
Q

What do hormones do to the extracellular fluid volume?

A

regulate the water and salt balance in our bodies

137
Q

What is the RAAS?

A

the renin-angiotensin-aldosterone system

138
Q

What does the RAAS do?

A

regulation of plasma volume and SVR and hence the regulation of MAP

139
Q

What are the three components of RAAS?

A

renin, angiotensin and aldosterone

140
Q

What is the process of RAAS from renin to aldosterone?

A
  • renin is released from the kidneys and stimulates the formation of angiotensin 1 from angiotensinogen (produced by liver)
  • angiotensin 1 is converted to angiotensin 2 by angiotensin converting enzyme ACE (produced in the pulmonary vascular endothelium)
  • angiotensin 2 stimulates the release of aldosterone from the adrenal cortex and causes systemic vasoconstriction (which increases SVR and BP) and stimulates thirst and ADH release (increases plasma volume and BP)
141
Q

What does aldosterone do?

A

acts on the kidneys to increase sodium and water retention so increases plasma volume and blood pressure

142
Q

What is the RAAS regulated by?

A

mechanisms that stimulate renin release from juxtaglomerular apparatus in the kidneys so:

  • renal artery hypotension caused by systemic hypotension
  • stimulation of renal sympathetic nerves
  • decreased Na+ concentration in renal tubular fluid
143
Q

What are natriuretic peptides?

A

natriuretic peptide hormones are synthesized by the heart and released in response to cardiac distension or neurohormonal stimuli

144
Q

What do natriuretic peptides cause?

A
  • excretion of salt and water in the kidneys and reduce blood volume and blood pressure
  • decreased renin release so decrease in blood pressure
  • vasodilation to decrease SVR and blood pressure
  • provide counter-regulatory system for the RAAS
145
Q

What are the two types of NPs?

A
  • Atrial Natriuretic peptide

- Brain-type Natriuretic peptide

146
Q

What is ANP?

A

atrial natriuretic peptide is a 28 amino acid peptide synthesised and stored by atrial muscle cells (myocytes)

147
Q

When is ANP released?

A

in response to atrial distension

148
Q

What is BNP?

A

brain-type natriuretic peptide is synthesised by the ventricles, brain and other organs and is a 32 amino acid peptide

149
Q

How is BNP formed?

A

BNP is first made as prepro-BNP which is then cleaved to pro-BNP and finally BNP

150
Q

What types of BNP can be measured in patients with suspected heart failure?

A

serum BNP and the N-terminal piece of pro-BNP

151
Q

What is another name for ADH?

A

Vasopressin

152
Q

What is ADH?

A

a peptide hormone derived from a pre-hormone precursor synthesised by the hypothalamus and stored in the posterior pituitary

153
Q

What stimulates secretion of ADH?

A

reduced extracellular fluid volume and increased extracellular fluid osmolality

154
Q

What does plasma osmolality indicate?

A

relative solute-water balance and is monitored by osmoreceptors mainly near to the hypothalamus

155
Q

Where and how does ADH act?

A

acts in the kidney tubules to increase reabsorption of water which conserves it

156
Q

What is the result of increased ADH?

A

increases extracellular and plasma volume and hence CO and BP and stimulates vasoconstriction

157
Q

When is the vasoconstriction caused by ADH most important?

A

in hypovolemic shock

158
Q

What does the pumping of the heart produce?

A

cardiac output

159
Q

Which are the capacitance vessels and what does this mean?

A

veins are the capacitance vessels because they contain most of the blood volume under resting conditions, venous return must provide the heart with sufficient blood to pump

160
Q

If HR, SV and SVR are regulated, then what is also regulated?

A

MAP

161
Q

What is HR regulated by?

A

the autonomic nervous system

162
Q

What is SV affected by?

A

preload, myocardial contractility and afterload

163
Q

What is SVR regulated by?

A

vascular smooth muscles

164
Q

What does contraction of vascular smooth muscles cause?

A

vasoconstriction and increased SVR and MAP

165
Q

What does relaxation of vascular smooth muscles cause?

A

vasodilation and decreased SVR and MAP

166
Q

What two mechanisms control vascular smooth muscles?

A

extrinsic and intrinsic mechanisms

167
Q

What is resistance to blood flow directly proportional to?

A

blood viscosity and length of blood vessel

168
Q

What is resistance to blood flow controlled by?

A

vascular smooth muscles through changes to the radius of the arterioles

169
Q

What does the extrinsic control of vascular smooth muscle involve?

A

nerves and hormones

170
Q

What is the neurotransmitter for the vascular smooth muscles for extrinsic control?

A

noradrenaline acting on alpha receptors

171
Q

What is vasomotor tone?

A

partial constriction of vascular smooth muscle at rest

172
Q

What is vasomotor tone caused by?

A

tonic discharge of sympathetic nerves resulting in continuous release of noradrenaline

173
Q

What does increased sympathetic discharge do to vasomotor tone?

A

increase vasomotor tone resulting in vasoconstriction

174
Q

What does decreased sympathetic discharge do to vasomotor tone?

A

decrease vasomotor tone resulting in vasodilation

175
Q

Is there parasympathetic innervation of arterial smooth muscles?

A

no

176
Q

What happens when adrenaline acts on alpha receptors?

A

vasoconstriction

177
Q

What happens when adrenaline acts on beta 2 receptors?

A

vasodilation

178
Q

Where are alpha receptors for vasoconstriction predominant?

A

skin, gut and kidney arterioles

179
Q

Where are beta 2 receptors for vasodilation predominant?

A

cardiac and skeletal muscle arterioles

180
Q

What does angiotensin do to vessels and what is this important in?

A

vasoconstriction (important in intermediate control of blood pressure)

181
Q

What does ADH do to vessels and what is this important in?

A

vasoconstriction (important in intermediate control of blood pressure)

182
Q

Which overrides which- intrinsic or extrinsic control mechanisms for vascular smooth muscle contraction?

A

intrinsic overrides extrinsic

183
Q

What are the two branches of extrinsic control mechanisms on vascular smooth muscle?

A

chemical and physical factors

184
Q

What does relaxation of arteriolar smooth muscles result in?

A

vasodilation and metabolic hyperaemia

185
Q

What local metabolic changes cause relaxation of arteriolar smooth muscles?

A
  • decreased local PO2
  • increased local PCO2
  • increased local [H+]
  • increased extra-cellular [K=]
  • increased osmolality of ECF
  • increased adenosine release
186
Q

What are some local humeral agents that cause relaxation of arteriolar smooth muscles resulting in vasodilation?

A

histamine, bradykinin and nitric oxide

187
Q

Where is NO continuously released from?

A

the vascular endothelium from L-arginine through enzymatic action of nitric oxide synthase

188
Q

What does NO cause in the vessels?

A

vasodilation and maintenance of vascular health

activates formation of cGMP that serves as a second messenger for signalling smooth muscle relaxation

189
Q

What are examples of local humoral agents that cause vasoconstriction?

A

serotonin, thromboxane A2, leukotrienes and endothelin

190
Q

What is endothelin?

A

a vasoconstrictor released from endothelial cells

191
Q

What do cold and hot conditions do to the vessels?

A

cold is vasoconstriction and hot is vasodilation

192
Q

If MAP rises what will the vessels do?

A

constrict to limit flow

193
Q

If MAP falls what will the vessels do and what is this important in?

A

dilate to increase flow (important in brain and kidneys)

194
Q

What does dilation of the arterioles do to the arteries?

A

causes sheer stress in the arteries upstream to make them dilate which increases blood flow to metabolically active tissues

195
Q

What can endothelium damage be caused by?

A

high blood pressure, high cholesterol, diabetes and smoking

196
Q

What are the features of endothelial produced vasodilators?

A

anti-thrombotic, anti-inflammatory and anti-oxidant

197
Q

What are the features of endothelial produces vasoconstrictors?

A

pro-thrombotic, pro-inflammatory and pro-oxidant

198
Q

What is autoregulation of blood flow?

A

autoregulation of blood flow is the maintenance of a steady blood flow to an organ despite changes in perfusion pressure

199
Q

What are some factors that increase venous return?

A
  • increased venomotor tone - increased skeletal muscle pump
  • increased blood volume
  • increased respiratory pump
  • increased atrial pressure leading to increased EDV leading to increased stroke volume.
200
Q

What is venomotor tone?

A

stimulation of venous smooth muscles with sympathetic nerve fibres to gibe venous constriction

201
Q

What does increased venomotor tone do?

A

increases venous return, SV and MAP

202
Q

What does increased vasomotor tone do?

A

increased SVR and MAP

203
Q

What is respiratory pump?

A

During inspiration intra-thoracic pressure decreases and intra-abdominal pressure increases
This increases pressure gradient for venous return and moves blood from the veins to the heart
Increasing rate and depth of breathing increases venous return to the heart

204
Q

What is skeletal muscle pump?

A

large veins in limbs lie between skeletal muscles, contraction of muscles pushes blood towards heart and muscle activity increases venous return to the heart

205
Q

What is the acute response to exercise?

A
  • sympathetic activity increases so HR and SV increase so CO increases
  • sympathetic vasomotor nerves reduce flow to kidneys and gut so vasoconstriction
  • vasodilation in skeletal muscle and cardiac muscle so metabolic hyperaemia overcomes vasomotor drive- blood flow to these increases which increases systolic BP
206
Q

What effects does metabolic hyperaemia have?

A

decreases SVR and decreases diastolic BP which increases pulse pressure

207
Q

How does sympathetic stimulation increase HR?

A

increases SA node firing, decreases AV node delay and increases force if contraction

208
Q

What is the effect of sympathetic stimulation on pacemaker cells?

A
  • slope of pacemaker potential increases
  • pacemaker potential reaches threshold quicker
  • positive chronotropic effect (frequency of action potentials increases)
209
Q

What is the effect of sympathetic stimulation on ventricular contraction?

A

the contractility of the heart at a given EDV rises and the frank-starling curve is shifted to the left

210
Q

What is the chronic response to exercise?

A
  • reduction in sympathetic tone and noradrenaline levels
  • increased parasympathetic tone to the heart
  • cardiac remodelling
  • reduction in plasma renin levels
  • improved endothelial function so increase in vasodilators and decrease in vasoconstrictors
  • decrease in arterial stiffening
211
Q

What does regular aerobic exercise do?

A

reduces blood pressure

212
Q

What is shock?

A

an abnormality of the circulatory system resulting in inadequate tissue perfusion and oxygenation

213
Q

What does shock lead to?

A
  • inadequate tissue perfusion
  • inadequate tissue oxygenation
  • anaerobic metabolism
  • accumulation of metabolic waste products
  • cellular failure
214
Q

What does adequate tissue perfusion depend on?

A
  • adequate blood pressure

- adequate cardiac output

215
Q

What are the different types of shock with examples?

A
  • Hypovolaemic: haemorrhagic, non-hemorrhagic
  • Cardiogenic eg acute MI
  • Obstructive eg cardiac tamponade, tension pneumothorax, PE, severe aortic stenosis
  • Distributive: neurogenic eg spinal cord injury, vasoactive eg septic shock, anaphylactic shock
216
Q

What is hypovolaemic shock?

A
  • a loss of blood volume
  • decreased venous return
  • decreased end diastolic volume
  • decreased stroke volume
  • decreased CO and BP
  • inadequate tissue perfusion
217
Q

What is cariogenic shock?

A

sustained hypotension caused by decreased cardiac contractility

218
Q

What is the process of cariogenic shock?

A
  • decreased cardiac contractility
  • decreased SV
  • decreased CO and BP
  • inadequate tissue perfusion
219
Q

What will cariogenic shock do to the Frank-Starling curve?

A

massive downwards drop

220
Q

What is the process of obstructive shock?

A
  • increased intrathoracic pressure
  • decreased venous return
  • decreased end diastolic volume
  • decreased SV
  • decreased CO and BP
  • inadequate tissue perfusion
221
Q

What is the process of neurogenic distributive shock?

A
  • loss of sympathetic tone to blood vessels and heart
  • massive venous and arterial vasodilation
  • decreased HR
  • decreased SVR and venous return
  • decreased CO and BP
  • inadequate tissue perfusion
222
Q

What is the process of vasoactive distributive shock?

A
  • release of vasoactive mediators
  • massive venous and arterial vasodilation
  • increased capillary permeability
  • decreased venous return
  • decreased SVR
  • decreased CO and BP
  • inadequate tissue perfusion
223
Q

What is the management of shock?

A

ABCDE
high flow oxygen
volume replacement (not cardiogenic)
call for help

224
Q

What do you give for cariogenic shock?

A

inotropes

225
Q

What do you give for septic shock?

A

vasopressors

226
Q

What are the causes of hypovolemic shock?

A
  • haemorrhage→ decrease blood volume→ decreased CO→ circulatory shock
  • Vomiting, diarrhoea, excessive sweating→ decreased ECFV→ decreased blood volume→ decreased CO→ circulatory shock
227
Q

How long can compensatory mechanisms maintain blood pressure?

A

until more than 30% of blood volume is lost

228
Q

How will the body react to shock?

A

increase HR and decrease SV

229
Q

Where does most coronary venous blood drain to?

A

via the coronary sinus into the right atrium

230
Q

What are the features of the coronary circulation?

A
  • high capillary density
  • high basal blood flow
  • high oxygen extraction so O2 can only be supplied by increasing coronary blood flow which is controlled by intrinsic and extrinsic mechanisms
231
Q

How is coronary blood flow regulated by intrinsic mechanisms?

A
  • decreased O2 causes coronary arteriole vasodilation
  • metabolic hyperaemia matches flow to demand
  • adenosine (from ATP) is a vasodilator
232
Q

How is coronary blood flow regulated by extrinsic mechanisms?

A
  • sympathetic vasoconstrictors (that usually exist) are overcome by metabolic hyperaemia (increased HR and SV)
  • therefore, sympathetic stimulation= coronary vasodilation
  • adrenaline actives beta2 so vasodilation
233
Q

When does peak left coronary blood flow occur?

A

during diastole because the aortic pressure is high enough to deliver blood flow

234
Q

What does increasing the heart rate do to coronary flow of the heart?

A

coronary flow is decreased so there can still be ischemia even if there isn’t atherosclerosis

235
Q

What is the brain supplied by?

A

internal carotids and vertebral arteries

236
Q

How does the circle of Willis ensure the brain has adequate oxygen?

A

basilar and carotid arteries anastomose to form the circle of willis which means that cerebral perfusion is maintained despite obstruction of one carotid artery

237
Q

What is autoregulation of blood flow?

A

guards against cerebral blood flow changes despite pressure changes (MAP of 60-160mmHg)

238
Q

Does sympathetic stimulation affect cerebral blood flow?

A

barely

239
Q

What happens if MABP rises in the brain?

A

vessels constrict to limit blood flow

240
Q

What happens if MABP falls in the brain?

A

the vessels dilate to maintain blood flow

241
Q

What is the change in MABP that the brain can counteract?

A

down until 60

up until 160

242
Q

What does an MABP of 50 or less result in?

A

confusion, fainting and brain damage

243
Q

What does increased PCO2 do in the brain?

A

cerebral vasodilation and decreased causes vasoconstriction

244
Q

What is normal intracranial pressure?

A

8-13 mmHg

245
Q

What does central perfusion pressure equal?

A

MAP minus intracranial pressure

246
Q

What effect does increasing intracranial pressure have?

A

decreases cerebral perfusion pressure and the cerebral blood flow

247
Q

What substances move across the blood brain barrier and how?

A

very permeable to oxygen and carbon dioxide and glucose crosses this by facilitated diffusion using carrier molecules to fulfill the obligatory requirement of the brain for glucose

248
Q

What is the blood brain barrier impermeable to and why is this good?

A

impermeable to hydrophilic substances which protects the brain neurons from fluctuating levels of ions in the blood

249
Q

What is the blood pressure in the pulmonary tissue?

A

20-25 over 6-12

pulmonary resistance is low

250
Q

Why is there low pressures in the pulmonary circulation?

A

Absorptive forces exceeds filtration so protects against pulmonary oedema

251
Q

What does hypoxia in the lung cause?

A

vasoconstriction of pulmonary arterioles (opposite to systemic arterioles so that it helps the blood be diverted from the poorly ventilated areas of the lung)

252
Q

Why is resting blood flow in the skeletal muscle tissue low?

A

sympathetic vasomotor tone

253
Q

What happens to muscle blood flow during exercise?

A

local metabolic hyperaemia overcomes sympathetic vasoconstrictor activity, circulating adrenaline causes vasodilation and increased CO during exercise increases skeletal muscle blood flow

254
Q

What is skeletal muscle pump?

A

large veins lie between skeletal muscles
contraction of muscles aids venous return
one-way valves allow blood to move forward towards the heart

255
Q

What does skeletal muscle pump reduce?

A

postural hypotension

256
Q

What is varicose veins?

A

blood pooling in the lower veins

257
Q

Why doesn’t varicose veins affect CO?

A

chronic compensatory mechanisms increase the blood volume

My Cardiovascular (13 decks)

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