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► Med - Anatomy & Physiology > Cardiovascular Principles > Flashcards

Cardiovascular Principles Flashcards

1
Q

What is an electrically controlled muscular pump which sucks and pumps blood?

A

The heart

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2
Q

Where are the electrical signals which control the heart generated?

A

Within the heart itself

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3
Q

What is the term used to describe the hearts capability of beating rhythmically in the absence of external stimuli?

A

Autorhythmicity

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4
Q

Where does excitation of the heart normally originate?

A

In the pacemaker cells in the sino-atrial node

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5
Q

What cluster of cells in the SA node initiate the heart beat?

A

Specialised pacemaker cells

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6
Q

Where is the SA node located?

A

In the right upper atrium, close to where the superior vena cava enters the right atrium

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7
Q

What is a heart controlled by the SA node said to be in?

A

Sinus rhythm

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8
Q

Do cells in the SA node have a stable resting membrane potential?

A

No

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9
Q

What do cells in the SA node exhibit?

A

Spontaneous pacemaker potential

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10
Q

What takes the membrane potential to a threshold to generate action potential in the SA nodal cells?

A

Pace maker potential

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11
Q

What is the threshold of an SA node cell?

A

-40 mV

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12
Q

What is the permeability to K+ in pacemaker cells like between action potentials?

A

Not constant

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13
Q

What is - the slow depolarisation of membrane potential to a threshold?

A

The pacemaker potential

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14
Q

What is the pacemaker potential due to?

A

Decrease in K+ efflux superimposed on a slow Na+ influx (the funny current)

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15
Q

Once the threshold for SA nodal cells has been reached, what is the rising phase of the action potential (i.e. depolarisation) caused by?

A

Activation of voltage-gated calcium channels

Ca influx

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16
Q

In the ionic basis for pacemaker action potential: what causes the falling phase of the action potential (i.e. repolarisation)?

A

Activation of K+ channels, resulting in K+ efflux

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17
Q

How does the SA node excitation spread to teh AV node?

A

By cell-cell conduction

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18
Q

Where does the SA node excitation spread to after the AV node?

A

Bundle of His
Left and right branches
Purkinje fibers

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19
Q

What does cell-cell spread of excitation occur via?

A

Gap junctions

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20
Q

What is a small bundle of cardiac cells?

A

AV node

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21
Q

Where is the AV node located?

A

At the base of the right atrium; just above the junction of atria and ventricles

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22
Q

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

A

AV node

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23
Q

What cells are small in diameter and have slow conduction velocity?

A

AV node cells

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24
Q

How does spread of excitation occur across the atria?

A

Mainly cell-cell conduction, via gap junctions

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25
Q

Where is the conduction in the heart delayed?

A

At the AV node

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26
Q

What does the delay of conduction in the AV node allow?

A

Atrial systole to precede ventricular systole

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27
Q

What allows rapid spread of action potential to the ventricles?

A

Bundle of His and Purkinje fibres

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28
Q

Is the contractle cardiac muscle cell action potential different from the action potential in pacemaker cells?

A

Yes

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29
Q

In ventricular muscle cells what does the resting membrane potential remain at before excited?

A

-90 mV

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30
Q

In ventricular muscle cells: what is the rising phase of action potential (i.e. depolarisation) caused by?

A

Fast Na+ influx

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31
Q

In ventricular muscle cells: what does the fast Na+ influx reverse?

A

The membrane potential to +30

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32
Q

What is known as Phase 0 of action potential in contractile cardiac muscle cells?

A

The depolarisation of action potential by fast Na+ influx, reversing the membrane potential from -90 to +30

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33
Q

What occurs in phase 1 of contractile cardiac muscle cell action potential?

A

Closure of Na+ channels and transient K+ efflux

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34
Q

What occurs in phase 2 of contractile cardiac muscle cells action potential?

A

Mainly Calcium influx

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35
Q

What occurs in phase 3 of contractile cardiac muscle cell action potential?

A

Closure of calcium channels and K+ efflux

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36
Q

What occurs in phase 4 of contractile cardiac muscle cell action potential?

A

Resting membrane potential

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37
Q

What is the phase called of ventricular muscle action potential, where the membrane potential is maintained near the peak of action potential for a few hundred seconds?

A

The plateau phase of action potential

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38
Q

What is a unique characteristic of contractile cardiac muscle cells?

A

The Plateau phase

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39
Q

What is the plateau phase due to?

A

Influx of calcium through voltage gated calcium channels

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40
Q

What causes the falling phase of action potential (i..e. repolarisation) in ventricular muscle action potential?

A

Inactivation of Ca channels and activation of K+ channels, resulting in K+ efflux

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41
Q

What is the heart rate mainly influenced by?

A

The autonomic nervous system

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42
Q

What stimulation increases the heart rate?

A

Sympathetic

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43
Q

What stimulation decreases the heart rate

A

Parasympathetic

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44
Q

What gives parasympathetic supply to the heart?

A

The vagus nerve

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45
Q

What exerts a continuous influence on the SA node under resting conditions?

A

The vagus nerve

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46
Q

What dominates under resting conditions?

A

The vagal tone

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47
Q

What does the vagal tone do?

A

Slows the intrinsic heart rate from ~100bpm to produce a normal resting heart rate of ~70 bpm.

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48
Q

What is considered to be a normal resting heart rate?

A

60 to 100 bpm

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49
Q

What is a resting heart rate of

A

Bradycardia

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50
Q

What is a resting heart rate of more than 100bpm said to be?

A

Tachycardia

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51
Q

What supplies the SA node and AV node?

A

Vagus nerve

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52
Q

What does vagal stimulation do?

A

Slows the heart rate and increases AV nodal delay

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53
Q

What does parasympathetic neurotransmitter acetyl choline act through?

A

M2 receptor

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54
Q

What is a competitive inhibitor of acetylcholine and what is it used in?

A

Atropine

Used in extreme bradycardia to speed up the heart

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55
Q

What are the 5 effects of vagal stimulation on pacemaker potentials?

A
  1. Cell hyperpolarises
  2. Longer to reach threshold
  3. Slope of pacemaker potential decreases
  4. Frequency of AP decreases
  5. Negative chronotropic effect
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56
Q

What 3 things does the cardiac sympathetic nerve supply?

A
  1. SA node
  2. AV node
  3. Myocardium
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57
Q

What increases the force of contraction?

A

Sympathetic stimulation

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58
Q

What is the sympathetic neurotransmitter and what does it act through?

A

Noradrenaline acting through B1 adrenoceptors

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59
Q

What are the 3 effects of noradrenaline on pacemaker cells?

A
  1. Slope of pacemaker potential increases
  2. Pacemaker potential reaches threshold quicker
  3. Frequency of action potentials increases - positive chronotropic effect
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60
Q

What do the surface electrodes on an ECG detect?

A

Waves of depolarisation and repolarisation moving across the heart and setting up electrical currents

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61
Q

What is ECG lead I?

A

RA - LA

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62
Q

What is ECG lead II?

A

RA - LL

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63
Q

What is ECG lead III?

A

LA - LL

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64
Q

What does the P wave represent?

A

Atrial depolarisation

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65
Q

What does the QRS complex represent?

A

Ventricular depolarisation (masks atrial repolarisation)

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66
Q

What does the T wave represent?

A

Ventricular repolarisation

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67
Q

What does the PR interval represent?

A

Largely AV node delay

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68
Q

What does the ST segment represent?

A

Ventricular systole

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69
Q

What does the TP interval represent?

A

Diastole

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70
Q

What type of fibre pattern does cardiac muscle have?

A

Striated

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71
Q

What is cardiac muscle striation caused by?

A

Regular arrangmenet of contractile protein

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72
Q

What are cardiomyocytes electrically coupled by?

A

Gap junction

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73
Q

What is the term for protein channels which form low resistance electrical communication pathways between meighbouring myocytes?

A

Gap junctions

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74
Q

What do the desmosomes within the intercalated discs of cells provide?

A

Mechanical adhesion between adjacent cardiac cells

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75
Q

How is tension developed by one cardiac myocyte transmitted to the next?

A

By desmosomes

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76
Q

What does each muscle fibre contain many of?

A

Myofibrils (contractile units of muscle)

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77
Q

What do myofibrils have alternating segments of?

A

Thick and thin protein filaments

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78
Q

What causes the lighter appearance in myofibrils and fibers?

A

Actin (thin filament)

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79
Q

What causes the darker appearance in myofibrils and fibers?

A

Myocyin (thick filaments)

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80
Q

Within each myofibril, what are actin and myocin arranged into?

A

Sacromeres

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81
Q

How is muscle tension produced?

A

By sliding of actin filaments on myocin filaments

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82
Q

What does force generation depend on?

A

ATP-dependent interaction between thick (myosin) and thin (actin) filaments

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83
Q

What is required for both contraciton and relaxation?

A

ATP

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84
Q

What is required to switch on cross bridge formation?

A

Calcium ions

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85
Q

In an excited cell state, what has occured between troponin and actin binding site?

A

Binding

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86
Q

Where is calcium released from?

A

The sarcoplasmic reticulum

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87
Q

In cardiac muscle, what is the relase of calcium from SR dependent on?

A

Presence of extra-cellular calcium

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88
Q

In relation to systole, when the action potential has passed - what occurs?

A

Calcium influx ceases, calcium is re-sequestered in SR by calciumATPase and the heart muscle relaxes

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89
Q

When the cardiac muscle fibre is relaxed, why is there no cross-bridge binding?

A

Because the cross-bridge binding site on actin is physically covered by the troponin-tropomyosin complex

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90
Q

What triggers powerstroke and pulls thin filament inward during contraction?

A

Binding of actin and muosin cross bridge

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91
Q

When the muscle fiber is excited, what occurs when calcium binds with troponin?

A

It pulls troponin-tropomyosin complex aside to expose cross-bridge binding site, then cross-bridge binding occurs

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92
Q

What does the long refractory period prevent?

A

Generation of tetanic contracion

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93
Q

What is the refractory period?

A

The period following an action potential in which it is not possible to produce another action potential.

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94
Q

During the plateau phase of ventricular action potential what are the Na channels like?

A

In a depolarised, closed state (i.e. not available for opening)

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95
Q

During the descending phase of action potential, the K+ channels are open - what cant the membrane do?

A

Be depolarised

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96
Q

What ejects the stroke volume?

A

Contraction of ventricular muscle

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97
Q

What is the stroke volume defined as?

A

The volume of blood ejected by each ventricle per heart beat.

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98
Q

What is an equation for stroke volum?

A

EDV - ESV (end diastolic volume - end systolic volume)

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99
Q

What brings about changes in stroke volume?

A

Changes in the diastolic length of myocardial fibers

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100
Q

What is the diastolic length of myocardial dibers determined by?

A

The volume of blood within each ventricle at the end of diastole. This is called end diastolic volume.

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101
Q

What does end diastolic volume determine?

A

Preload

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102
Q

What is the end diastolic volume determined by?

A

Venous return to the heart

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103
Q

What describes the relationship between venous return, end diastolic volume and stroke volume?

A

The Frank-Starling mechanism

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104
Q

What states that “the more the ventricle is filled with blood during diastole (EDV), the greater the volume of ejected blood will be during the resulting systolic contraction (stroke volume)?

A

Frank-Starling Curve

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105
Q

What does stretch also increase?

A

The affinity of troponin for calcium

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106
Q

What is optimal length in cardiac muscle achieved by?

A

Stretching the muscle (Frank-Starling mechanism)

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107
Q

What happens when venous return to the right atrium increases?

A

EDV of right ventricle increases

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108
Q

What does Starling’s law lead to?

A

Increased SV into pulmonmary artery

Increased SV into aorta

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109
Q

Whta does venous return to left atrium from pulmonary vein increase?

A

EDV of left ventricle

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110
Q

What does hte Frank-Starling mechanism partially compensate for?

A

Decreased stroke volume caused by increased afterload

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111
Q

What is afterload?

A

The resistance into which the heart is pumping

The extra load is imposed after the heart has contracted

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112
Q

What condition is there incrwased afterload continuously?

A

Hypertension

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113
Q

What does increased afterload eventually lead to?

A

Ventricular hypertrophy

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114
Q

What does extrinisc control of stroke volume involve?

A

Nerves and hormones

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115
Q

What kind of effect is increasing the force of contraction, and what effect is increasing the heart rate?

A

Positive inotropic

Positive chronotropic

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116
Q

What is the force of contraction effect mediated by?

A

cAMP

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117
Q

During sympathetic stimulation, what happens to the ventricular pressure?

A

Rises

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118
Q

What does the increased rate of pressure change during systole, as a result of peak ventricular pressure rising reduce?

A

Duration of systole

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119
Q

When the peak ventricular pressure rises and the contractility of the heart at a given EDV rises, what happens to the Frank-Starling curve?

A

It is shifted to the left

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120
Q

Where does heart failure shift the FS curve to?

A

The right

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121
Q

What is cardiac output?

A

The volume of blood pumped by each ventricle per minute.

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122
Q

What is the equation for CO?

A

SV x HR

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123
Q

What is the resting CO in a healthy adult normally?

A

5 litres per minute (70 ml SV x 70 bpm = 4900 ml CO)

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124
Q

Do heart valves produce a sound when they shut and open?

A

Only a sound is heard when they shut

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125
Q

What does the orderly depolarisation/repolarisation sequence trigger?

A

A recurring cardiac cycle of atrial and ventricular contractions and relaxations

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126
Q

What does the cardiac cycle refer to?

A

All events that occur from the beginning of one heart beat to the beginning of the next

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127
Q

What is the term for the stage where the heart ventricles are relaxed and fill with blood?

A

Diastole

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128
Q

What stage occurs where the heart ventricles contract and pump blood into the aorta (LV) and pulmonary artery (RV)?

A

Systole

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129
Q

At a heart rate of 75 bpm; how long is ventricular diastole and how long is ventricular systole?

A

Diastole 0.5 sec

Systole 0.3 sec

130
Q

What are the five events that occur during the cardiac cycle?

A
  1. Passive filling
  2. Atrial contraction
  3. Isovolumetric ventricular contraction
  4. Ventricular ejection
  5. Isovolumetric ventricular relaxation
131
Q

During passive filling, what happens to the pressure in the atria and ventricles?

A

Close to 0

132
Q

During passive filling, why do AV valves open?

A

So venous return flows into the ventricles

133
Q

During passive filling, once the AV valve has opened and venous return flowed into the ventricles, what happens to the aortic pressure and valve?

A

Aortic pressure ~80 mmHg and aortic valve is closed

134
Q

During passive filling, similar events happen in the right side of the heart - however what can be said about the pressures (RV and PA)?

A

Much lower

135
Q

How full do ventricles become by passive filling?

A

80% full

136
Q

What occurs between the P-wave and the QRS?

A

Atria contracts

137
Q

What is the EDV in resting normal adults, after atrial contraction?

A

130ml

138
Q

During isovolumetric ventricular contraction, when does ventricular contraction start?

A

After the QRS signals ventricular depolarisation in the ECG

139
Q

During isovolumetric ventricular contraction, what occurs after the ventricular contraction has started?

A

Ventricular pressure rises

140
Q

During isovolumetric ventricular contraction, what happens once the ventricular pressure exceeds atrial pressure?

A

The AV valves shut

141
Q

What produces the first heart sound (LUB)?

A

The AV valve shutting

142
Q

During isovolumetric ventricular contraction, after the first heard sound what is the aortic valve doing?

A

Still shut, so no blood can enter or leave the ventricle

143
Q

What is isovolumetric contraction?

A

The tension rising around a closed volume

144
Q

During ventricular ejection, what occurs when the ventricular pressure exceeds aorta/pulmonary artery pressure?

A

Aortic/pulmonary valve opens

145
Q

During ventricular ejection, once the aortic/pulmonary valves have opened - what occurs?

A

Stroke volume is ejected by each ventricle leaving behind the end systolic volume (ESV)

146
Q

What is the equation for SV (stroke volume), with values added?

A

SV = EDV - ESV
135 - 65
= 70ml

147
Q

During ventricular ejection, once the SV has been ejected what happens to the aortic pressure?

A

Rises

148
Q

What does the T wave in the ECG represent?

A

Ventricular repolarisation

149
Q

What starts to occur during ventricular repolarisation?

A

The ventricles relax and ventricular pressure starts to fall

150
Q

During ventricular ejection, what occurs when the ventricular pressure falls below aortic/pulmonary pressure?

A

Aortic/pulmonary valves shut

151
Q

What produces the second heart sound (DUB)?

A

When the ventricular pressure falls below aortic/pulmonary pressure: aortic and pulmonary valves shut

152
Q

During ventricular ejection, what produces the dicrotic notch in the aortic pressure curve?

A

The valve vibration produces the dicrotic notch

153
Q

What signals the start of isovolumetric ventricular relaxation?

A

Closure of aortic/and pulmonary valves

154
Q

What is “isovolumetric relaxation”?

A

The tension falls around a closed volume

155
Q

During isovolumetric ventricular relaxation, what occurs when the ventricular pressure falls below atrial pressure?

A

AV valve open and the heart starts a new cycle

156
Q

What does the closure of mitral and tricuspid valves cause?

A

First heart sound (S1)

157
Q

What does S1 herald?

A

The beginning of systole

158
Q

What does the closure of aortic and pulmonary valves cause?

A

The second heart sound (S2)

159
Q

What does S2 hearald?

A

The end of systole and beginning of diastole

160
Q

Is S3 diastolic or systolic?

A

S3 is diastolic

161
Q

Where does S4 occur?

A

Just before S1

162
Q

What does JVP occur after?

A

Right atrial pressure waves

163
Q

JVP - what does “a” stand for?

A

Atrial contraction

164
Q

JVP - what does “c” stand for?

A

Bulging of tricuspid valve into atrium during ventricualr contraction

165
Q

JVP - what does “v” stand for?

A

Rise of atrial pressure during atrial filling: release as AV valves open

166
Q

What is the outwards (hydrostatic) pressure exerted by the blood on blood vessel walls?

A

Blood pressure

167
Q

What is the systemic systolic arterial blood pressure?

A

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

168
Q

What should systolic BP not exceed under resting conditions?

A

140 mmHg

169
Q

What is systemic diastolic arterial blood pressure?

A

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

170
Q

What should siastolic arterial blood pressure not exceed under resting conditions?

A

90 mmHg

171
Q

How does blood flow in normal arteries?

A

In a laminar fashion

172
Q

Can you hear laminar blood flow through a stethoscope?

A

No

173
Q

If external pressure (e.g. cuff pressure) exceeding the systolic blood pressure is applied to an artery, what happens to the flow and sound of that artery?

A

The flow in that artery would be blocked and no sound is heard through a stethoscope.

174
Q

If external pressure is kept between systolic and diastolic pressure, what happens to the flow?

A

It becomes turbulent whenever blood pressure exceeds cuff pressure

175
Q

When is the first Korotkoff sound heard?

A

At peak systolic pressure

176
Q

When is the 2 - 3 Korotkoff sounds heard?

A

As blood pressure due to turbulent spurts of flow cyclically exceeds cuff pressure

177
Q

When is the 4th Korotkoff sound heard?

A

The last sound is heard at minimum/diastolic pressure (muffled/muted sound)

178
Q

Which Korotkoff sound is this - no sound is heard thereafter because of uninterurupted, smooth, laminar flow?

A

5th

179
Q

When is diastolic pressure recorded?

A

At the 5th Korotkoff sound (point at which sound disappears) - more reproducible

180
Q

The RA pressure is close to 0, so what is the main driving force for blood?

A

MAP

181
Q

What - between the aorta and right atrium - drives the blood around the systemic circulation?

A

A pressure gradient

182
Q

What does MAP - Central venous (right atrial) pressure =?

A

Pressure gradient

183
Q

What is MAP?

A

The average arterial blood pressure during a single cardiac cycle

184
Q

Formula for estimating MAP?

A

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

185
Q

What is the second method of estimating MAP?

A

MAP = DBP +1/3 (difference between SBP and DPB)

186
Q

What is normal range of MAP?

A

70 - 105 mm Hg

187
Q

What does CO x TPR =?

A

MAP

188
Q

What is the volume of blood pumped by each ventricle of the heart per minute?

A

co

189
Q

What does SV x HR =?

A

CO

190
Q

What is the volume of blood pumped by each ventricle per heart beat?

A

Stroke volume

191
Q

What is total peripheral resistance?

A

The sum of resistance of all peripheral vasculature in the systemic circulation

192
Q

What are the major resistance vessels?

A

Arterioles

193
Q

What does parasympathetic stimulation do to MAP?

A

Lowers it

194
Q

What does sympathetic stimulation do to arterioles, TPR and MAP?

A

Increases vasoconstriction
Increases TPR
Increases MAP

195
Q

What does sympathetic stimulation do to veins?

A 
Increases vasoconstriction
Increases venous return
Increases SV
Increases CO
Increases MAP
196
Q

What gives short-term regulation of MAP?

A

The baroreceptor reflex

197
Q

Where are the two groups of baroreceptors located?

A
  1. Aortic arch

2. Carotid sinus

198
Q

How do the carotid baroreceptors signal to the medulla?

A

Via the IXth CN

199
Q

How do the aortic baroreceptors signal to the medulla?

A

Via the Xth CN

200
Q

When MAP is low, what happens to carotid sinus afferent nerve fibres firing, cardiac vagal efferent nerve fibres activity, cardiac sympathetic efferent nerve fibres activity and sympathetic vasoconstrictor nerve fibres activity?

A

Carotid sinus afferent nerve fibres firing - decrease
Cardiac vagal efferent nerve fibres activity - decrease
Cardiac sympathetic efferent nerve fibres activity - increase
Sympathetic vasoconstrictor nerve fibres activity - increase

201
Q

What happens to the venous return to the heart when a normal person stands up suddenly?

A

Decreases - effect of gravity

202
Q

When the venous return to the heart decreases what happens to the MAP?

A

Transient decrease

203
Q

When there is a transient decrease in MAP, what happens to rate of firing of baroreceptors?

A

Decrease

204
Q

When the rate of firing of baroreceptors is reduced, what happens to the vagal tone and sympathetic tone, and what results does this give?

A

Vagal tone to heart decreases
Sympathetic tone to heart increases
This increases the HR and SV

205
Q

What does sympathetic constrictor tone to the veins increase?

A

The venous return to the heart and the stroke volume

206
Q

What does postural hypotension result from?

A

Failure of baroreceptor responses to gravitational shifts in blood, when moving from horizontal to vertical position.

207
Q

What only responds to actue changes in blood pressure?

A

Baroreceptors

208
Q

What happens to the baroreceptor firing when high blood pressure is sustained?

A

Decreased

209
Q

What can baroreceptors not supply information about?

A

Prevailing steady state blood pressure

210
Q

What can be controlled by controlling the extracellular fluid volume?

A

Blood volume and MAP

211
Q

How much body weight in a 70kg man is water?

A

60% (42 L)

212
Q

What does total body fluid = ?

A

Intracellular fluid (2/3rd) + extracellular fluid (1/3rd of total)

213
Q

What does ECF Volume (ECFV) = ?

A

Plasma volume (PV) + interstitial fluid volume (IFV)

214
Q

What fluid bathes the cells and acts as the go-between the blood and body cells?

A

ECFV

215
Q

If plasma volume falls, what does the compensatory mechanism do?

A

Shifts fluid from the intestitial compertment to the plasma compartment

216
Q

What are the two main factors affecting extracellular fluid volume?

A
  1. Water excess or deficit

2. Na+ excess or deficit

217
Q

How do hormones act as effectors to regulate the extracellular fluid volume (including PV)?

A

By regulating the water and salt balance in our bodies

218
Q

Name three hormones which regulate extracellular fluid volume?

A
  1. The Renin-Angiotensin-Aldosterone system (RAAS)
  2. Atrial Natriuretic Peptide (ANP)
  3. Antidiuretic Hormone (Arginine Vasopressin) - ADH
219
Q

What system plays an important role in the regulation of plasma volume and TPR and hence the regulation of MAP?

A

The Renin-Angiotensin-Aldosterone System

220
Q

What are the three components of the Renin-Angiotensin-Aldosterone System?

A
  1. Renin
  2. Angiotensin
  3. Aldosterone
221
Q

Where is renin released from and what does it stimulate?

A

Renin is released from the kidneys and stimulates the formation of angiotensin I in the blood from angiotensinogen (produced by the liver)

222
Q

What converts Angiotensin I to angiotensin II?

A

Angiotensin converting enzyme (ACE)

223
Q

Where is angiotensin converting enzyme (ACE) produced?

A

By pulmonary vascular endothelium

224
Q

What does Angiotensin II stimulate the release of?

A

Aldosterone from the adrenal cortex

225
Q

What two things does aldosterone from the adrenal cortex cause?

A
  1. Systemic vasoconstriction - increases TPR

2. Stimulates thirst and ADH release (contributes to plasma volume mainly brought about by aldosterone)

226
Q

What type of hormone is aldosterone?

A

A steroid hormone

227
Q

What results from aldosterone acting on the kidneys?

A

Increase in sodium and water retention which increases plasma volume

228
Q

When plasma volume decreases, and then BP decreases - what does the kidney release?

A

Renin

229
Q

Once renin has been released from the kidney, what does it convert?

A

Angiotensinogen from liver to angiotensin I

230
Q

Once angiotensin I has converted to angiotensin II by ACE, where does angiotensin II stimulate and cause the release of?

A

Adrenal cortex

Release aldosterone which increases PV + BP, increases sodium and water reabsoprtion in kidneys

231
Q

Give three effects of angiotensin II, other than stimulating the adrenal cortex?

A
  1. Vasoconstriction (increased TPR & BP)
  2. Increased ADH release (increased PV & BP)
  3. Increased thirst
232
Q

What is the rate limiting step for RAAS?

A

Renin secretion

233
Q

Where exactly in the kidney is renin released from?

A

Juxtaglomerular apparatus - from GRANULAR CELLS

234
Q

What are the three mechanisms which regulate RAAS by stimulating renin release?

A
  1. Renal artery hypotension - caused by systemic hypotension
  2. Stimulaton of renal sympathetic nerves
  3. Decreased [Na+] in renal tubular fluid
235
Q

What senses the decreased [Na+] in renal tubular fluid?

A

Macula densa (specialised cells of kidney tubules)

236
Q

What three components is the juxtaglomerular apparatus made from?

A
  1. Macula densa
  2. Extraglomerular mesangial cells
  3. Granular cells
237
Q

What is Atrial Netriuretic Peptide (ANP) and what is it composed of/stored by?

A

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

238
Q

What is ANP released in response to?

A

Atrial distension (hypervolaemic states)

239
Q

How does the release of ANP reduce blood volume and blood pressure?

A

By causing excretion of salt and water in the kidneys

240
Q

What does ANP act as to reduce blood pressure?

A

Vasodilator

241
Q

What does ANP do to renin release?

A

Decreases renin release

242
Q

What acts as a counter-regulatory mechanism for the Renin-Angiotensin-Aldosterone System (RAAS)?

A

Atrial Netriuretic Peptide (ANP)

243
Q

What is ADH also called?

A

Vasopressin

244
Q

What is a peptide hormone derived from a prehormone precursor synthesised by the hypothalamus and stored in the posterior pituitary?

A

ADH

245
Q

Where is ADH synthesised and stored?

A

Synthesised by the hypothalamus and stored in the posterior pituitary

246
Q

What two things stimulates secretion of ADH?

A
  1. Reduced extracellular fluid volume

2. Increased extracellular fluid osmolarity

247
Q

What is the normal osmolarity of extracellular fluid?

A

280 milli-osmoles/l

248
Q

What monitors plasma osmorality?

A

Osmoreceptors mainly in the brain in close proximity to the hypothalamius

249
Q

What does increased plasma osmolality stimulate?

A

The release of ADH

250
Q

What does ADH act on to increase the reabsorption of water? (i.e. concentrate urine (antidiuresis)?

A

Kidney tubules

251
Q

When ADH acts in the kidney tubules to increase the reabsorption of water - what would this also increase?

A

Extracellular and plasma volume and hence cardiac output and blood pressure

252
Q

What does ADH also act on to cause vasoconstriction?

A

Blood vessels

253
Q

What effect is small but becomes important in hypovolaemic shock (e.g. haemorrhage)?

A

ADH causing vasoconstriction, increasing TPR and BP

254
Q

What does long term regulation of MAP involve control of?

A

Blood volume by hormones

255
Q

What regulates ECF (including PV) volume and osmolality to deal with fluid loads/deficits?

A

ADH

256
Q

What regulates total body Na+ and with it ECF volume in the longer term?

A

Aldosterone

257
Q

What are the capacitance vessels?

A

Veins

258
Q

What is resistance to blood flow directly proportional to and inversely proportional to?

A

Directly proportional to blood viscosity and length of blood vessel
Inversely proportional to the radius of blood vessel to the power 4

259
Q

How is the resistance to blood flow mainly controlled?

A

By vascular smooth muscles through changes in the radius of arterioles

260
Q

What does extrnisc control of vascular smooth muscle involve?

A

Hormones and nerves

261
Q

What nerves are vascular smooth muscles supplied by and what is the neurotransmitter?

A

Sympathetic nerves

Noradrenaline acting on alpha receptors

262
Q

What is the term for vascular smooth muscles partially constricted at rest?

A

Vasomotor tone

263
Q

What is the vasomotor tone caused by?

A

Tonic discharge of sympathetic nerves resulting in continuous release of noradrenaline.

264
Q

Where is there the only parasympathetic innervation of arterial smooth muscle?

A

Penis and clitoris

265
Q

Where is adrenaline from?

A

The adrenal medulla

266
Q

What does adrenaline act on to cause vasoconstriction?

A

Alpha receptors

267
Q

What does adrenaline act on to cause vasodilation?

A

Beta receptors

268
Q

Where are alpha receptors predominantly found?

A

Skin, gut, kidney arterioles

269
Q

What receptors are predominantly found in cardiac and skeletal muscle?

A

Beta receptors

270
Q

What does angiotensin II do to vascular smooth muscles?

A

Vasoconstriction

271
Q

What does ADH do to vascular smooth muscles?

A

Causes vasoconstriction

272
Q

What can over-ride extrinsic mechanisms of control of vascular smooth muscle?

A

Intrinisc mechanisms like chemical and physical factors

273
Q

What do local metabolic changes within an organ influence?

A

The contraction of arterial smooth muscles

274
Q

What causes vasodilatation in relation to PO2, PCO2, [H+], [K+], ECF and ATP?

A 
Decreased local PO2
Increased local PCO2
Increased local [H+] - decreased pH
Increased extra-cellular [K+]
Increased osmolality of ECF
Adenosine release from ATP
275
Q

What are local chemicals released within an organ called?

A

Local humoral agents

276
Q

What can be released in response to tissue injury or inflammation?

A

Local humoral agents

277
Q

What 4 humoral agents, when released cause vasodilatation?

A
  1. Histamine
  2. Prostaglandins
  3. Bradykinin
  4. Nitric oxide (NO) - this is continuously released by endothelial cells of arteries and arterioles
278
Q

What produces nitric oxide?

A

Vascular endothelium from the amino acid L-arginine through enzymatic action of nitric oxide synthase (NOS)

279
Q

Name a potent vasdilator which is important in the regulation of blood flow and maintenance of vascular health?

A

Nitric Oxide

280
Q

What does shear stress on vascular endothelium, as a result of increased flow cause?

A

Release of calcium in vascular endothelial cells and the subsequent activation of NOS i.e. flow dependent NO formation.

281
Q

What can also induce NO formation?

A

Chemical stimuli

282
Q

How do chemical stimuli induce NO formation?

A

Receptor stimulated NO formation - many vasoactive substances act through stimulation of NO formation.

283
Q

NO diffuses from the vascular endothelium into “where”, to activate the formation of “what”, that serves as “what”?

A

NO diffuses from the vascualr endothelium into the adjacent smooth muscle cells where it activates the formation of cGMP that serves as a second messenger for signalling smooth muscle relaxation.

284
Q

What converts L-arginine to nitric oxide in the endothelium?

A

eNOS

285
Q

Give 4 local humoral agents that the release of causes vasoconstriction?

A
  1. Serotonin
  2. Thromboxane A2
  3. Leukotrienes
  4. Endothelin
286
Q

What is a potent vasoconstrictor released from endothelial cells. Its production is stimulatsed by angiotensin II and vasopressin?

A

Endothelin

287
Q

What does the cold cause to vascular smooth muscle?

A

Vasoconstriction

288
Q

In relation to myogenic response to stretch: what happens when MAP rises?

A

Resistance to vessels automatically constricts to limit flow

289
Q

What does sheer stress do to vascular smooth muscles?

A

Dilatation of arterioles causes sheer stress in the arteries upstream to make them dilate. This increases blood flow to metabolically active tissues.

290
Q

Where do large veins in limbs lie between?

A

Skeletal muscles

291
Q

What does contraction of muscles aid?

A

Venous return

292
Q

What structures allow blood to move forward towards the heart?

A

One-way venous valves

293
Q

What kind of response does exercise cause?

A

Acute CVS responses

294
Q

During exercise what happens to sympathetic nerve activity?

A

Increases

295
Q

When sympathetic nerve activity increases during exercise, what happens to HR, SV and CO?

A

All increase

296
Q

What does sympathetic vasomotor nerves reducing flow to kidneys and gut - vasoconstriction occur in?

A

Exercise

297
Q

During excersise, in skeletal and cardiac muscle, what does metabolic hyperaemia overcome?

A

Vasomotor drive - vasodilatation

298
Q

What does increase in CO do to systolic BP?

What does metabolic hyperaemia do to TPR and DBP?

A

Increases systolic BP

Decreases TPR and decreases DBP (i.e. the pulse pressure increases)

299
Q

What does regular aerobic exercise help reduce?

A

Blood pressure

300
Q

What are these responses due to: reduction in sympathetic tone and NA levels, increased parasympathetic tone to heart, cardiac remodelling, reduction in plasma renin levels, improved endothelial function (increase vasodilators, decrease vasoconstrictors) and decrease arterial stiffening?

A

Chronic cardiovascular responses to regular exercise

301
Q

What is shock?

A

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

302
Q

What are the 4 stages in shock that lead to cellular failure?

A
  1. Inadequate tissue perfusion
  2. Inadequate tissue oxygenation
  3. Anaerobic metabolism
  4. Accumulation of metabolic waste products
303
Q

What two factors does adequate tissue perfusion depend on?

A
  1. Adequate blood pressure

2. Adequate cardiac output

304
Q

What initiates hypovolaemic shock?

A

Loss of blood volume

305
Q

What are the 5 steps in hypovolaemic shock that lead to inadequate tissue perfusion?

A
  1. Decreased blood volume
  2. Decreased venous return
  3. Decreased End Diastolic Volume
  4. Decreased stroke volume
  5. Decreased cardiac output and decreased blood pressure
306
Q

What is the term for sustained hypotension caused by decreased cardiac contracility?

A

Cardiogenic shock

307
Q

What are the 3 steps in cardiogenic shock that lead to inadequate tissue perfusion?

A
  1. Decreased cardiac contracility
  2. Decreased stroke volume
  3. Decreased cardiac output and decreased blood pressure
308
Q

What type of shock is a tension pneumothorax?

A

Obstructive shock

309
Q

What are the 5 steps in obstrutive shock, that lead to inadequate tissue perfusion?

A
  1. Increased intra-thoracic pressure
  2. Decreased venous return
  3. Decreased End Diastolic Volume
  4. Decreased cardiac output and decreased blood pressure
  5. Inadequate tissue perfusion
310
Q

Give the 4 steps that occur in neurogenic shock to cause inadequate tissue perfusion?

A
  1. Loss of sympathetic tone
  2. Massive venous and arterial vasodilatation
  3. Decreased venous return and decreased TPR
  4. Decreased CO and decreased BP
311
Q

What are the 4 steps in vasoactive shock that leads to inadequate tissue perfusion?

A
  1. Release of vasoactive mediators
  2. Massive venous and arterial dilatation - also increased capillary permeability
  3. Decreased venous return and decreased TPR
  4. Decreased CO and BP
312
Q

What is the immediate treatment for anaphylactic shock?

A

Adrenaline

313
Q

What is used to treat septic shock?

A

Vassopressors

314
Q

What is used for tension pneumothorax shock?

A

Immediate chest drain

315
Q

What is used to treat cardiogenic shock?

A

Inotropes

316
Q

What are the two main causes of hypovolaemic shock, that lead to decreased blood volume?

A
  1. Haemorrhage

2. Vomiting, diarrhoea, excessive sweating = decreased ECFV

317
Q

How much blood has to be lost before compensatory mechanisms can not longer maintain blood pressure?

A

> 30%

318
Q

In class I, II, III and IV of shock - what is the blood loss?

A

I : up to 750mL
II : 750 - 1500
III : 1500 - 2000
IV : >2000

319
Q

What are the pulse rate values for shock classes I, II, III, and IV?

A

I :

320
Q

What two classes of shock are the blood pressures normal in?

A

Class one and two

321
Q

What are the respiratory rate values for all the classes of haemorrhagice shock?

A

I : 14-20
II : 20-30
III : 30-40
IV : >35

► Med - Anatomy & Physiology (130 decks)

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