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PHSL232 Cardiovascular and Respiratory > Cardiovascular Systems 1 > Flashcards

Cardiovascular Systems 1 Flashcards

1
Q

What are the components of the cardiovascular system?

A

The heart
Blood vessels
Blood

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2
Q

What are the types of blood vessels?

A

Arteries
Arterioles
Capillaries
Venules
Veins

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3
Q

Roughly how many L of blood do we have in our body?

A

4-6L of blood

(variation dependant on size of the body)

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4
Q

What are the two circuits of the cardiovascular system?

A

Pulmonary Circuit
Systemic Circuit

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5
Q

What occurs in the capillary beds?

A

Gas exchange

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6
Q

What is the difference between veins and arteries?

A

Arteries carry blood away from the heart, whereas veins carry blood towards the heart.

Arteries carry oxygenated blood and veins carry deoxygenated blood (with the exception of pulmonary blood vessels).

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7
Q

What is pulmonary circulation of the cardiovascular system?

A

Pulmonary circulation transports oxygen-poor blood from the right ventricle to the lungs, where blood picks up a new blood supply. Then it returns the oxygen-rich blood to the left atrium.

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8
Q

What is systemic circulation of the cardiovascular system?

A

Systemic circulation carries oxygenated blood from the left ventricle, through the arteries, to the capillaries in the tissues of the body. From the tissue capillaries, the deoxygenated blood returns through a system of veins to the right atrium of the heart.

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9
Q

What is the difference between the movement of blood in the pulmonary and systemic circuits?

A

Pulmonary circulation moves blood between the heart and the lungs.

Systemic circulation moves blood between the heart and the rest of the body.

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10
Q

Why do we have a cardiovascular system?

A

For adequate supply of oxygen and nutrients.

For the removal of unwanted metabolic by-products (Co2 and H+).

To transport substances and heat around the body.

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11
Q

What is the key purpose of the heart?

A

Acts a pump

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12
Q

What is the heart located within?

A

In the pericardium

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13
Q

What is the pericardium?

A

A protective, fluid-filled sac that surrounds your heart and helps it function properly. Your pericardium also covers the roots of your major blood vessels as they extend from your heart.

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14
Q

What type of cells is the heart made up of?

A

Cardiac muscle cells (myocardium)

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15
Q

What side of the heart is thicker?

A

The left ventricle of the heart is thicker.

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16
Q

What do fibrocartilaginous rings contain?

A

Heart valves

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17
Q

What are the two atrioventricular valves?

A

Mitral valve (left) and tricuspid valve (right)

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18
Q

What are the two semilunar valves?

A

Aortic valve (left ventricular aorta) and the pulmonary valve (right ventricular pulmonary artery).

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19
Q

What causes valves to open and close?

A

Pressure gradient

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20
Q

What direction does blood flow?

A

Unidirectionally - meaning it only flows one direction.

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21
Q

What feature of the heart prevents the backwards flow of blood?

A

Valves

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22
Q

What is the appearance of cardiac muscle and why?

A

Striated in appearance due to its repeating units of sarcomeres.

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23
Q

What joins neighbouring cardiac muscle cells?

A

Gap junctions within intercalated discs.

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24
Q

What influences arterial blood pressure?

A

Cardiac output and peripheral resistance.

Pressure = Flow x Resistance (MAP = CO x TPR)

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25
Q

What is cardiac output?

A

Cardiac output is the volume of blood ejected by either ventricle in 1 min (value per ventricle not total heart).

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26
Q

How do you work out CO?

A

CO = SV (stroke volume) x HR (heart rate)

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27
Q

What are the units for CO?

A

L.min-1

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28
Q

What are the units for SV?

A

L.beat-1

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29
Q

What are the units for HR?

A

Beat.min-1

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30
Q

What is systole?

A

Ventricular contraction

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31
Q

What is diastole?

A

Ventricular relaxation

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32
Q

Roughly how many times does our heart beat a minute?

A

70 beats per minute (therefore 100,800 times a day).

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33
Q

If you miss 5-10 heart beats within a minute what happens?

A

Unconsciousness

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34
Q

What do mechanical events of the heart maintain?

A

Blood pressure and blood flow

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35
Q

What do valvular events of the heart create?

A

Heart sounds

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36
Q

What are the phases of the cardiac cycle?

A

Diastole: (1) isovolumetric relaxation and (2) ventricular filling.

Systole: (1) isovolumetric contraction and (2) ventricle ejection.

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37
Q

What happens during diastole 1 - isovolumetric relaxation?

A

All valves are closed = no blood flow in or out.

Minimal ventricular volume

Ventricles are relaxing

Atrial pressure is lower than ventricular therefore the atrium fills with blood returning to the heart.

Atrial pressure rises above ventricular pressure and therefore creates a pressure gradient and the AV valve opens passively causing the ventricular filling to begin.

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38
Q

What does isovolumetric mean?

A

Volume of blood staying the same

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39
Q

What occurs during Diastole 2 - ventricular filling?

A

The AV valve is open and the ventricule fills with blood.

It is in this phases that about 90% of the heart filling occurs passively down the pressure gradient.

P wave = trigger for contraction of atrial - this causes the final 10% of filling of the ventricle.

Now that the heart is 100% fill we are at end-diastole volume.

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40
Q

What occurs during systole 1 - isovolumetric contraction?

A

Ventricles are filled and depolarise.

Ventricles contract and ventricular pressure rises.

AV valves close = first heart sound.

All valves are shut therefore there is no blood flow and no change in blood volume.

Isovolumetric contraction

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41
Q

What occurs during systole 2 - ventricle ejection?

A

Ventricles continue to contract and build pressure.

Pressure becomes higher than aortic pressure therefore aortic valves open.

Blood ejects into the aorta

Arterial blood volume and arterial pressure increases.

Depolarisation of ventricles = T wave signalling ventricle to relax and pressure falls below aortic pressure. Therefore aortic semilunar valves close = 2nd heart sound.

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42
Q

What percentage of blood ejection occurs in the first 1/3 of ejection time?

A

2/3

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43
Q

Approx how long does diastole 1 last?

A

0.05s

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44
Q

Approx how long does Diastole 2 last?

A

0.6s

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45
Q

How long does systole 1 approx last?

A

0.05s

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46
Q

How long does systole 2 approx last?

A

0.3s

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47
Q

What is the aortic pressure during diastole?

A

80 mmHg

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48
Q

What is aortic pressure during systole?

A

120 mmHg

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49
Q

What is LV pressure during diastole?

A

80 mmHg

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50
Q

What is LV pressure during systole?

A

120 mmHg

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51
Q

What is a healthy ejection fraction?

A

Between 55 and 60%

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52
Q

What is the third heart sound?

A

Passive ventricular filling in early diastole - tends to only be heard in the young

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53
Q

What is the P wave of an ECG representing?

A

Where atrial depolarisation precedes atrial contraction

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54
Q

What does ECG stand for?

A

Electrocardiogram

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55
Q

What is the QRS complex of an ECG representing?

A

Ventricular depolarisation preceding ventricular contraction

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56
Q

What is the T wave of an ECG representing?

A

Ventricular repolarisation and ventricular relaxation

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57
Q

What percentages of the cardiac cycle are diastole and systole?

A

Diastole approx 2/3
Systole approx 1/3

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58
Q

What part of the cardiac cycle speeds up when our heart rate increases?

A

The entire cardiac cycle gets faster (both diastolic and systolic cycle will get shorter) - However the diastolic phase shortens more so that we now have 1/3 of our cycle in diastole and 2/3 in systole.

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59
Q

Cells have a high permeability to …, low to … and very low to …?

A

Cells have high permeability to potassium (K+), low to sodium (Na+) and very low to calcium (Ca2+).

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60
Q

What is depolarisation?

A

Less negative charge inside the cell compared to outside the cell (generally means that positive charge enters the cell).

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61
Q

What is repolarisation?

A

More negative charge inside the cell compared to outside the cell.

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62
Q

Where does conduction of an AP in the heart begin?

A

In the SA node (sinoatrial node) which is located in the top of the right atrium

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63
Q

What is the peacemaker of the heart?

A

SA node - it gets this name because it determines the frequency of heart beats by initiating AP conduction.

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64
Q

What is the conduction pathway in the heart?

A

Sinoatrial node (SA node) - origin of the AP

Atrioventricular node (AV node)

Bundle of His

Purkinje fibers

Cardiomyocytes

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65
Q

Where is the AV node located?

A

The base of the right atrium

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66
Q

What is functional syncytium?

A

A functional syncytium refers to a group of cells that function as a single unit while still maintaining their individual cellular role.

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67
Q

Is the heart a functional syncytium?

A

Yes. As all cells are attached through gap junctions every AP in the heart propagates through all cells = all or nothing contraction.

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68
Q

Approximately how many AP does the SA node generate per minute?

A

100

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69
Q

Approximately what speed are AP conducted through the atrium?

A

0.5 ms-1

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70
Q

Where in the heart is AP conduction slowest?

A

AV node (0.05ms-1)

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71
Q

What does the delay in conduction at the AV node allow for?

A

The delay permits full depolarisation and contraction of the atria before depolarisation and contaction of the ventricles.

In other words it means that the entire heart doesn’t contract at the same time and thus allows for the “top up period”.

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72
Q

Where is AP propagation the fastest?

A

Bundle of His, Bundle Branches and Purkinje Fibers: at approximately 5.0 ms-1

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73
Q

Approximately what speed does an AP spread in ventricular myocardium?

A

0.5 ms-1

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74
Q

What do purkinje fibres allow for?

A

Synchronous depolarisation and contraction of all ventricular regions (due to wide spread branching)

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75
Q

What cells are the “leaders” in the heart?

A

Pacemaker cells - SA node - origin of AP

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76
Q

What are “followers” in the heart?

A

Ventricular cells - Cardiomyocytes - (they are followers because they do nothing until an AP to reaches them)

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77
Q

How many phases do pacemaker cells have?

A

3

Phases 4, 0 and 3

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78
Q

How many phases do ventricular cells have?

A

5

Phases: 4, 0, 1, 2 and 3

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79
Q

What is phase 4 of pacemaker cells?

A

At RMP (-60/-70 mV)

BUT unstable due to “funny Na+ channels” that allow a slow influx of Na+

In the late phase T-type Ca2+ channels (TTCC) allow an influx of Ca2+ aswell making the cell more positively charged and reach threshold

80
Q

At what voltage does pacemaker cells reach threshold in Phase 4?

A

-50/-40 mV

81
Q

What is phase 0 of pacemaker cells?

A

Upstroke

L-type or voltage operated Ca2+ channels (LTCC) open allowing an influx of Ca2+.

82
Q

What is phase 3 of AP in pacemaker cells?

A

repolarisation - slow K+ efflux

83
Q

What is the RMP for pacemaker cells?

A

-60/-70 mV

84
Q

What is the RMP for ventricular cells?

A

-90 mV

85
Q

What is phase 4 of an AP in ventricular cells?

A

Stable at RMP of -90mV
K+ influx

86
Q

What is phase 0 of AP in ventricular cells?

A

Upstroke - fast depolarisation due to the opening of fast Na+ channels. The influx of Na+ causes threshold to be reached (-65 mV).

87
Q

What is threshold for an AP in ventricular cells?

A

-65 mV

88
Q

What is phase 1 of AP in ventricular cells?

A

Early repolarisation - fast Na+ channels close and the influx stops - small K+ efflux.

89
Q

What is Phase 2 of AP in ventricular cells?

A

Cardiac Ca2+ plateau - sustained depolarisation.

LTCC open and Ca2+ influx counterbalance a K+ efflux

90
Q

What is phase 3 of ventricular cell AP?

A

Late repolarisation

Inactivation of Ca2+ channels and activation of K+ efflux causing fast repolarisation.

91
Q

Are pacemaker cells or ventricular cells stable?

A

Ventricular

92
Q

Why are pacemaker cells unstable?

A

due to funny nA+ channels and TTCC

93
Q

What do APs in the heart depend on?

A

Function and localisation

94
Q

What is an ECG?

A

A recording of potential changes at the skin surface that result from depolarisation and repolarisation of heart muscle

95
Q

Where are the three recording electrodes on an ECG?

A

Left Arm - LA
Right Arm - RA
Left Leg - LL

96
Q

How are ECG recordings made?

A

Between 2 electrodes - the ECG represents the difference between 2 electrodes called bipolar leads.

97
Q

What is Lead 1 in an ECG?

A

The potential difference between LA and RA.

LA is positive and RA is negative

98
Q

What is Lead 2 in an ECG?

A

The potential difference between LL and RA.

LL is positive and RA is negative

99
Q

What is Lead 3 in an ECG?

A

The potential difference between LL and LA.

LL is positive and LA is negative

100
Q

What is Einthoven Triangle?

A

Standard Limb Leads 1, 2 and 3 (forms a triangle)

101
Q

What does P wave in an ECG represent?

A

SA cells depolarise

Right and Left atria depolarising towards AV node

Depolarisation towards positive electrode and thus positive deflection

102
Q

What does the T wave in an ECG represent?

A

Repolarisation of ventricles from outside to inside away from the detecting electrode causing a positive deflection

(Ventricular relaxation)

103
Q

What is the large positive deflection on an ECG?

A

R - of the QRS complex

104
Q

What does the term aV refer to?

A

Augmented voltage measured

105
Q

How many leads are involved in augmented limb leads?

A

6

106
Q

What plane of the heart is examined from chest leads?

A

Horizontal plan

107
Q

What type of ECG is a powerful clinical diagnostic tool?

A

12 lead recording

108
Q

Excitation-contraction coupling links action potentials, through calcium transient with what?

A

Sarcomere contraction

109
Q

What happens when Ca2+ enters cardiac muscle cells?

A

Cell membrane depolarisation and the threshold of LTCC is reached causing them to open

110
Q

What enters when LTCC open?

A

Ca2+

111
Q

Where is Ca2+ released from?

A

Intracellular stores in the SR

112
Q

What receptor is activated by entry of Ca2+ in muscle?

A

RyR

113
Q

What percentage of Ca2+ is released from the LTCC and from the RyR2-SR during excitation-contraction coupling?

A

25% from LTCC
75% from RyR2-SR

114
Q

What is the cycle that occurs for contraction of cardiac muscle?

A

Cross Bridge Cycling

115
Q

Explain the process of cross bridge cycling in cardiac muscle:

A

Ca2+ binds to troponin C in troponin complex

Displacement of Troponin-tropomysin allows for the interaction of Actin-Myosin to form a cross-bridge

When actin and myosin bind ADP and Pi are released and the myosin head flips (power stroke) and actin moves towards the centre of sarcomere causing the sarcomere to shorten

ATP then binds causing the cross-bridge to detach

116
Q

What are the three domains of the troponin complex?

A

TnC-Troponin C (Ca2+ binding domain)

TnI-Troponin I (inhibitory domain)

TnT-Troponin T (tropomyosin binding domain)

117
Q

If Ca2+ remains in high quantity what happens to the cross-bridge cycle?

A

It continues

118
Q

What is the sliding filament theory?

A

Myosin is pulling actin towards centre of the sarcomere

Actin filaments slide along adjacent myosin filaments by cycling of cross-bridges with myosin

119
Q

What lines come closer together when a cell shortens producing force and tension?

A

Z lines

120
Q

What makes contraction more forceful?

A

An increase in the number of cross bridges (not an increase in more contracting cardiomyocytes).

121
Q

What causes the end of cross bridge cycling contraction?

A

The influx of Ca2+ ceasing due to SR no longer being stimulated to release Ca2+ due to cytosolic Ca2+ being rapidly reduced

122
Q

What are the three different mechanism to reduce intracellular Ca2+?

A

SERCA

Sodium-Calcium Exchanger (NCX)

Ca2+ ATP-ase

123
Q

Is the SERCA pump ATP dependant?

A

Yes

124
Q

What does the SERCA pump do?

A

Pumps cytoplasmic Ca2+ back into the SR

125
Q

What is SERCA pump activity regulated by?

A

Phospholamban (PLB)

126
Q

What does PLB protein phosporylation stimulate?

A

Ca2+ uptake by the SERCA pump

127
Q

What is the Sodium-calcium exchanger (NCX) driven by?

A

Na+ gradient (which comes from the Na+/K+-ATPase)

128
Q

What are the relative percentages of the ventricle relaxation due to Ca2+ uptake achieved by SERCA, NCX and Ca2+ATPase?

A

SERCA 75%
NCX 24%
Ca2+ATP-ase 1%

129
Q

What is the Ca2+ ATP-ase?

A

A cell membrane ATP-dependent pump for Ca2+ uptake (causing relaxation)

130
Q

Why does tetanus of heart muscle not normally occur?

A

Tetanus of heart muscle contraction does not occur because summation of contractions is not possible.

131
Q

How long is the absolute refractory period of heart muscle?

A

250ms

132
Q

How long is the relative refractory period of heart muscle?

A

300ms

133
Q

What do the refractory periods of heart muscle prevent?

A

Re-excitatuon during the contraction period and circuitous recycling of AP.

134
Q

For aerobic metabolism what is the hearts preferred source of energy?

A

Fatty acid and glucose

135
Q

What is the name of the condition the body is put into when it runs out of ATP?

A

Metabolism rigor mortis

136
Q

What processes are driven by ATP?

A

Ca2+-uptake in SR

Deattachment of Actin-myosin cross bridge

Ca2+-extrusion by Ca2+ ATPase

Na+-K+ ATPase pump

Primary active transport

137
Q

What is the most important control of heart rate?

A

Extrinsic controls (parasympathetic and sympathetic control) - intrinsic control of HR is very limited.

138
Q

What is the treppe effect (also known as at the Bowditch effect)?

A

Describes the positive relationship between stimulation frequency and contraction force. As heart rate increases, the force of myocardial contraction increases due to more Ca²⁺ being available within the muscle cells per unit of time.

139
Q

What is the hall-mark of heart failure?

A

Negative force-frequency relationship.

In heart failure, the relationship between force and frequency can become negative, meaning that as the heart rate increases, the force of contraction may decrease. This is a hallmark of failing myocardial function.

140
Q

What does an increase in preload produce?

A

Larger stroke volumes

141
Q

What is the frank-starling law of the heart?

A

MORE IN MORE OUT.
The more you fill the more you squirk.

States that the heart has an intrinsic ability to adjust its force of contraction and stroke volume in response to changes in venous return or blood filling.

E.g.; increased venous return = increase preload = increase in end-diastolic volume = ventricle is more filled with blood. Consequently, ventricle is stretched = increased sarcomere length = increase contraction = larger stroke volume.

142
Q

The heart regulates ventricular output in response to what?

A

In response to ventricular filling

143
Q

What is the units for volume?

A

ml

144
Q

Is ESV or EDV larger?

A

EDV

145
Q

If the left-ventricle is enlarged due to greater EDV what effect does this have on ESV?

A

none?

146
Q

Why does force increase with length?

A

Increased Ca2+ sensitivity of the myofilaments due to better overlap of myosin and actin (Nothing to do with the amount of Ca2+).

147
Q

What is the largest protein in the body?

A

Titin - found in sarcomere between Z line and M line.

148
Q

What does Titin do?

A

Pulls actin and myosin filaments closer together

149
Q

What is lattice spacing?

A

Actin and Myosin myofilament spacing

150
Q

What is ATT?

A

The Actin-Troponin-Tropomyosin complex

151
Q

What is after-load?

A

After-load represents how hard the heart has to work to push blood out (the resistance it has to overcome to eject blood).

After-load is a measure of the tension/stress developed in the ventricular wall to open the aortic valve. Therefore related to aortic pressure and wall stress.

152
Q

What happens if you increase afterload?

A

Increase pressure

Increase ESV, decrease SV and EF, unchanged EDV

153
Q

What is contractility?

A

Measure of how effective the heart is as a pump (how strong the squeeze is - stronger the squeeze the more blood that is pumped out)

154
Q

What its inotropy?

A

The heart muscle ability to contract (same as contractility)

155
Q

What changes the hearts contractility?

A

Hormones or nervous changes

156
Q

What is meant by ‘autonomic control’?

A

Changes that occur automatically/unconsciously

157
Q

What hormone is released in the sympathetic autonomic control of the heart?

A

Noradrenaline

158
Q

What hormone is released in the parasympathetic autonomic control of the heart?

A

Acetylcholine

159
Q

Does noradrenaline or acetylcholine change EDV?

A

No - just change the function

160
Q

What are the four F of autonomic control?

A

Fight, Flight, Feeding, Fucking (mating)

161
Q

What are the sympathetic fibres involved in heart rate?

A

Cardiac nerves

162
Q

What are the parasympathetic fibres involved in heart rate?

A

Vagus nerve

163
Q

What happens when the sympathetic system is stimulated (represented on graph)?

A

Increased slope of pre-potential and less negative membrane potential

164
Q

What is a fast heart rate called?

A

Tachycardia

165
Q

What happens when the parasympathetic system is stimulated (represented on graph)?

A

Reduced slope of pre-potential and More negative membrane potential

166
Q

What is a slow heart rate called?

A

Bradycardia

167
Q

During parasympathetic stimulation what receptors does ACh bind to?

A

M2 muscarinic receptors

168
Q

What is activated during parasympathetic stimulation?

A

ACh-senstive K+ channel

169
Q

What is activated during sympathetic stimulation?

A

PKA (protein kinase A)

170
Q

What are factors affecting heart rate called?

A

Chronotropic factors

171
Q

Does sympathetic or parasympathetic activity decrease heart rate?

A

Parasympathetic

172
Q

Without parasympathetic control what would HR approximately be?

A

110 bpm

173
Q

What are factors affecting duration of contraction and relaxation called?

A

Lusitropic factors

174
Q

What are factors affecting contractility called?

A

Inotropic factors

175
Q

How does the sympathetic system stimulate contraction?

A

More and faster Ca2+ release
Faster cross-bridge cycling
More and faster Ca2+ uptake
Stronger and faster contraction
Faster relaxation

176
Q

During sympathetic stimulation of contraction what does NA (noreadrenaline) bind to?

A

b1-adrenoceptor

177
Q

What effect does TnI have on TnC during sympathetic stimulation for contraction?

A

TnI limits interaction of Ca2+ with TnC which decreases Ca2+ sensitivity

178
Q

What happens to the duration of twitch as a result of increased heart rate by noradrenaline?

A

It shortens

179
Q

What does chronotropic mean?

A

Rhythmic excitation

180
Q

What is meant by dromotropic?

A

Conduction speed

181
Q

What is the effect of positive inotropic?

A

Increase in contractility

182
Q

What are the short term regulators (hormones) for extrinsic control?

A

Catecholamines (adrenaline, noradrenaline and dopamine)

Glycosides (digoxins and digitalis)

183
Q

What are the long term regulators (hormones) for extrinsic control?

A

Angiotensin 2 (AT1 in heart)
Endothelin (ET1 in heart)
Thyroid hormone (T3)

184
Q

What are the two glycosides involved in extrinsic control of the heart?

A

Digoxins and digitalis

185
Q

What is the negative inotropic effect?

A

Decrease in contractility

186
Q

What does ACh bind to causing a negative inotropic effect?

A

M2-receptors

187
Q

What do beta-blockers do?

A

Reduce cAmp
Reduce PKA activity
Reduce activity of LTCC, RyR, SERCA
Increase Ca2+ sensitivity of TnC
Reduces need for ATP - less stress on the heart

188
Q

How do beta blockers reduce the stress on the heart?

A

Because they reduce the need for ATP

189
Q

What is preload?

A

How much the heart fills up - related to the initial stretching of the cardiac muscle fibres (sarcomas) before contraction as the more they stretch the more room for greater volume of blood.

Preload is directly relation to Frank-starlings theory - more in, more out.

190
Q

What is the relationship between EDV and preload?

A

Increasing EDV (the volume of blood in the ventricles at the end of diastole e.g., ventricular filling) is directly related to increase in preload.

191
Q

What is the effect of an increase preload on SV, ESV and EF?

A

SV increased
EF increase
ESV unchanged

192
Q

What is the effect of an increased after load on SV, EF and EDV?

A

SV decreased
EF decreased
EDV unchanged

193
Q

If contractility is increased what is the effect on SV, EF and ESV?

A

SV increased
EF increased
ESV decreased

194
Q

What is ESV?

A

ESV (End-Systolic Volume) is the amount of blood left in the ventricle after the heart has contracted (systole) and pumped blood out. It represents the volume of blood remaining in the heart at the end of each heartbeat.

In simpler terms: ESV is the “leftover” blood in the heart after it has squeezed as much blood as it can.

195
Q

How do you work out SV?

A

EDV - ESV = SV

196
Q

How do you work out EF?

A

EF = (SV / EDV) x 1000

PHSL232 Cardiovascular and Respiratory (12 decks)

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