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4th Yr - CMS 1 > Cardiovascular 1 > Flashcards

Cardiovascular 1 Flashcards

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Introductory Sommelier Exam (CMS) flashcards
1
Q

What are the 2 circulatory systems?

A

Pulmonary and systemic

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2
Q

What is the role of the pulmonary system?

A

supplies lungs with deoxygenated blood via pulmonary arteries

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3
Q

What is the role of the lungs?

A

oxygenates blood and removes CO2

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4
Q

What is the role of the pulmonary vein?

A

Receives oxygenated blood from left side of heart

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5
Q

What is the role of the left Side of the heart?

A

pumps oxygenated blood into aorta and around body via several parallel circuits

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6
Q

Where does deoxygenated blood from the body go to?

A

returns to right side of heart via vena cava

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7
Q

List all the types of vessels?

A
  • Arteries
  • Arterioles
  • Capillaries
  • Venules
  • Veins
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8
Q

List the structures of artery wall

A
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9
Q

what do the arteries do?

A

carry blood form the heart and they’re thick walled and elastic

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10
Q

what can we feel when feeling the pulse?

A

you can feel the stretching of the vessel wall with each heart contraction

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11
Q

what happens when the arteries relax between each beat ?

A

can cause the stored blood to continue to flow between each heart beat

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12
Q

Describe the capillaries ?

A
  • highly branched
  • thin walled
  • increase SA of gas electrolyte exchange between tissues and blood
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13
Q

what do w have between the capillaries ?

A

arterioles (baby arteries)

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14
Q

role of arterioles ?

A

can constrict or dilate to control blood flow to a specific tissue

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15
Q

where does blood flow from capillaries ?

A

venules and then to the thin walled, highly compliant veins (pressure gradient)

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16
Q

what is the pressure like once blood reaches the veins ?

A

very low ( the heart doesn’t suck blood towards it as this would collapse the thin walled veins )

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17
Q

what do veins have that prevent back flow?

A

valves

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18
Q

What are the 4 things that can contribute to blood flow back to the heart via venous return?

A

1) intermittent contraction of skeletal muscles eg. leg muscles
2) increases and decreases in thoracic pressure when we breath
3) the diaphragm compressing the abdominal veins with each breath
4) increase in blood in veins as we get closer to heart as more blood has returned from the tissue via the venues

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19
Q

heart anatomy

A
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20
Q

List the different valves?

A
  • tricuspid
  • mitral
  • pulmonary
  • aortic
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21
Q

what are the atrioventricular valves ?

A
  • tricuspid
  • mitral
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22
Q

where do the anterioventricular valves sit between?

A

between an atrium and an ventricle

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23
Q

where does the tricuspid valve sit between?

A

between RA and RV

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24
Q

where does the mitral valve sit between?

A

between LA and LV

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25
Q

Where does the pulmonary valve sit between?

A

pulmonary artery and RV

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26
Q

where does the aortic valve sit between ?

A

Aorta and LV

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27
Q

What specialised structures do valves have to stop backwards blood flow?

A

little papillary muscles that contract to prevent valves opening in wrong direction

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28
Q

what is systole?

A

heart contraction

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29
Q

what is diastole?

A

heart relaxation

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30
Q

what happens during diastole? (3)

A
  • AV valves are open ( tricuspid and mitral)
  • aortic/ pulmonary valves closed
  • blood flows from atria to ventricles
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31
Q

what happens during systole? (7)

A

1) atria contract which pushes last bits of blood into the ventricles from the atria
2) this causes higher pressure in ventricles than the atria and therefore closes T and M valves
3) papillary muscles contract to prevent these valves closing too far or opening in other direction
4) atria refill with blood from VC and PV
5) ventricles contract which further increases ventricular pressure and pushes aortic and pulmonary valve open
6) once pressure in arteries increase enough and pressure is higher than in ventricles this pushes aortic and pulmonary valves closed again and ventricles relax
7) the pressure in ventricles thus become lower than the atrial pressure which pushes the AV valve open = now in diastole

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32
Q

simplified version of systole

A
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33
Q

what is the Frank Starling Mechanism?

A
  • heart adapts such that it can always pump the blood that is returned to it by the venous onwards
  • the greater it is stretched, the stronger it contracts (upto a point due to intrinsic properties of the cardiac muscle cells and the overlap of myosin and actin)
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34
Q

what controls the relaxation and contractions of the heart muscle to cause diastole and systole?

A

electrical activity that spreads between muscle cells

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35
Q

where does electrical conductivity start?

A

SAN (in the RA)

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36
Q

what happens In the SAN?

A

the cells have an intrinsic timer that causes ion permeability

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37
Q

what does ion permeability cause in SAN?

A

the sinus node creates a depolarisation that spreads across the atria to the AVN

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38
Q

what is the annulus fibrosis?

A

a non conductive fibrous tissue found In the AVN

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39
Q

what does the depolarisation need in order to progress to the ventricles

A

needs to pass through AVN due to non conductive fibrous tissue called annulus fibrosis

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40
Q

what does the AVN do?

A

slows the spread of current and then propagates it between the ventricles via the bundle of his and then to the purkinje fibres

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41
Q

where is the bundle of his located?

A

between the ventricles

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42
Q

what happens when the atria are depolarised ?

A

they contract

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43
Q

why is the delay in the AVN important ?

A

allows for the contraction of the atria to have time to fill the ventricles before they in turn are depolarised contract and push blood around the body

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44
Q

how do we measure the flow of current around the heart?

A

ECG by using electrodes

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45
Q

what do electrodes do?

A

detects the direction and amount of current flowing thru the heart

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46
Q

what is a 12 lead ECG?

A

provides 12 (planes of direction) directional views of electricity across the heart

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47
Q

what is special about the 12 lead ECG?

A
  • provides 3D model of heart
  • we can see rate of electrical activity and abnormalities in the direction of the electrical flow or timing of the conduction
48
Q

what does the first small P bump on an ECG show ?

A

atrial activity and contraction

49
Q

what does the second spike (QRS) show?

A

ventricular depolarisation and contraction

50
Q

what does the T wave show?

A

the cells are depolarising getting them ready for the next repolarisation and contraction

51
Q

ECG diagram

A

P QRS T

52
Q

What is a normal heart rate?

A

60-100 bpm

53
Q

what do we call a heart rate more than 100 bpm?

A

tachycardia

54
Q

what do we call a heart rate slower than 60 bpm?

A

bradycardia

55
Q

what is heart rate set by?

A
  • sinus node = with keeps generating impulses due to ion permeability
  • sympathetic = fight or flight
  • parasympathetic = relax
56
Q

what is the role of PNS at rest?

A

provide a baseline inhibition of the heart rate preventing it form getting to fast

57
Q

how does the PNS prevent heart rate going too fast?

A

via the vagus nerve which inputs to SA and AVN so we slow heart rate (which is created at sinus node) and we slow the transmission to the ventricles at AVN

58
Q

what causes an increase in heart rate?

A

a reduction in parasympathetic inhibition of heart rate and we increase sympathetic stimulation

59
Q

what does the sympathetic nervous system do?

A
  • releases noradrenaline which acts on beta adernogic receptors which increases rate of firing of the SAN
  • increases the rare at which impulses are transmitted through the heart
  • increases the force of heart contraction
60
Q

how else can the heart rate increase?

A

in response to increased venous return this keeps the system balanced

61
Q

when does the heart rate slow down ?

A
  • reduce sympathetic stimulation and increased parasympathetic inhibition
62
Q

what happens if the SAN is slowed to a stop? what is it called?

A
  • cells in ventricles can generate their own depolarisation (but very slow eg. 15 to 40 bpm)
  • escape rhythm
63
Q

cardiac output = ______ + ________ ?

A

heart rate X stroke vol

64
Q

what is cardiac output?

A

the vol of blood that the heart pumps around the body per unit of time

65
Q

why does CO need to be constant?

A

tissue needs baseline amount of oxygen and nutrients

66
Q

when does CO not become constant?

A

when we need to alter the distribution depending on usage eg. increase metabolism such as exercise or physiological stress

67
Q

how much blood can the heart pump out?

A

as much blood as it receives from the veins

68
Q

the blood that is receiving back from the veins is called what?

A

venous return

69
Q

what are venous reservoirs ?

A

change the circulating vol in the body (not changing the amount of blood in the body but changing how much of it actively circulating around the tissues )

70
Q

how do we increase CO?

A
  • increase venous return:
    by constricting blood vessels in splanchnic circulation (spleen and GIT)
71
Q

what happens when blood vessels in splanchnic circulation are constricted?

A

we squeeze that blood into the circulation which can be redistributed elsewhere where needed therefore increases circulating volume

72
Q

how else can we increase CO?

A
  • increase venous return:
    changes in thoracic pressure by breathing and compressive action of diagrpram on abdominal vessels can increase venous return by increasing respiratory rate
73
Q

________ X _________ = blood pressure

A

cardiac output and total peripheral resistance

74
Q

what is blood pressure ?

A

the measurement of the amount of push caused by heart contractions to push blood around the body

75
Q

total peripheral resistance?

A

how difficult it is to pump blood around body due to diameter of blood vessels

76
Q

do smaller or larger vessels cause higher peripheral resistance?

A

smaller

77
Q

what is minimum of the TPR can be?

A
78
Q

why is there a minimum for TPR?

A

Due to the friction that the blood cells generate against the vessel walls = w cannot remove friction from the system

79
Q

how can we increase TPR?

A
  • by constricting arterioles and the veins
80
Q

how can we increase BP?

A
  • increase heart rate and stroke vol ie CO
  • constricting arterioles to non essential peripheral tissues therefore increasing TPR and constriction in veins to increase venous return
81
Q

what is all the constriction of arterioles and veins under the control of?

A

SNS

82
Q

what are baroreceptors?

A

pressure receptors in blood vessels

83
Q

how do baroreceptors detect pressure

A

stretching of vessels

84
Q

what happens when baroreceptors detect increase stretch in vessels?

A

sendS signals to PNS

85
Q

what happens when then there is high BP?

A
  • PNS causes reduction in heart rate
  • dilation in arterioles and veins
86
Q

what is the long term BP control system?

A

renin angiotensin system

87
Q

what will a persistently low BP lead to?

A
  • arterial constriction
  • a reduction In blood flow to kidneys
88
Q

what happens when there is a reduced blood flow to the kidneys when there’s

A
  • there will be a reduction in the amount of sodium and water excretion
  • also triggers renin
89
Q

what is the role of renin in RAS?

A

converts angiotensin to angiotensin 1

90
Q

what is the role of angiotensin 1 ?

A

travels in blood around body and further converts to angiotensin 2 via angiotensin converting enzyme (ACE)

91
Q

where does angiotensin 2 produced in ?

A

lungs

92
Q

what is the role of angiotensin 2?

A

travels back around body, triggers adrenal glands to release aldosterone

93
Q

what is the role of aldosterone?

A
  • causes vasoconstriction and Na and water reabsorption which leads to increase circulating vol and therefore increase BP
94
Q

what do we need to remember about a high BP?

A

high bp doesn’t mean that all tissues are receiving equally increasing blood supply

95
Q

what is local auto regulation?

A
  • a system we have that sends blood where it is required
96
Q

give an eg of local auto reg?

A

a tissue that works rlly heard creates more vasodilating products like CO2 and will use up O2 near the tissue and O2 is a vasoconstrictor therefore will lead to vasodilation and increase blood flow to the tissue that’s working hard

97
Q

overview of the renin angiotensin system?

A
98
Q

what is a cardiac arrest?

A

heart stops pumping but not the electrical activity

99
Q

what is CPR?

A

cardiopulmonary resuscitation

100
Q

what do chest compressions do?

A
  • serves as a heart pump
  • we are creating pressure in chambers of the heart to push blood onwards
101
Q

what happens when we recoil during compressions?

A
  • give heart time to refill
    -allows negative pressure in thorax
  • sucks blood towards heart and allows venous return
  • we also maintain cerebral perfusion to prevent brain damage
102
Q

what is a downside of compressions

A

we increase positive thoracic pressure which will increase pressure to head via neck which will lead to rise in intracranial pressure

103
Q

what does intracranial pressure cause?

A

compresses on vessels and reduces brain perfusion

104
Q

what happens when we do fast compressions?

A

heart doesn’t have time to fully fill between each compression therefore dropping stroke volume

105
Q

what item do we also use during CPR?

A

bag valve

106
Q

what is the use of a bag valve?

A
  • ventilates pt which inflates lungs to allow O2 absorption and CO2 removal
  • also opens up blood vessels in lungs
107
Q

what happens when the pressure causes inflation of lungs ?

A

squeezes on the pulmonary vein to return blood towards left side of heart therefore increasing left ventricular stroke volume

108
Q

what happens when there is too little ventilation?

A

reduced O2 delivery and waste gas removal

109
Q

what happens when there is too much ventilation?

A

increase thoracic pressure too high which reduces venous return to right side of heart so blood blood returning from system that needs oxygenating is reduced and reduced cerebral perfusion

110
Q

what is the 30:2 ratio?

A

30 compressions and 2 breaths

111
Q

why is reduced thoracic pressure due to coughing beneficial?

A

can keep someone conscious when they’re in a certain arhythmia as it increases venous return and cardiac output

111
Q

what is AED?

A

automatic external defibrillator

112
Q

what does an AED do?

A

delivers a shock to the heart (SAN) which stops any ongoing abnormal electrical activity by giving it chance to restart

113
Q

what condition would we use AED for for eg?

A

ventricular fibrillation

114
Q

what is important to note about cardiac arrests?

A

not all are shockable, depends if there is electrical activity going in heart that could be preventing heart rhythm

115
Q
A

4th Yr - CMS 1 (27 decks)

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