Cardiovascular Flashcards

1
Q

What is isovolumetric contraction?

A

Ventricular contraction when all valves are closed. This increases ventricular pressure but as all the valves are closed the volume remains the same.

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2
Q

What produces the first heart sound ‘lub’

A

closing of mitral valve

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3
Q

what causes the mitral valve to close

A

when LVp exceeds LAp. Just before ventricular isovolumetric contraction

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4
Q

describe systole

A

Wave of depolarisation arrives, Ca2+ channels open.
LVp>LAp and mitral valve closes.
LVp rises, isovolumetric contraction, LVp> aortic pressure
Aortic valve opens and ejection begins

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5
Q

What produces the second heart sound ‘dub’

A

closing of aortic valve

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6
Q

describe diastole

A

LVp decreases and there is a phase of reduced ejection.
LVp < aortic pressure so aortic valve closes
isovolumetric ventricular relaxation
LVp >LAp so mitral valve closes

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7
Q

systole duration time?

A

0.3s

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8
Q

diastole duration time?

A

0.5s

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9
Q

what is the end systolic volume?

A

the volume of blood remaining in the LV following systole

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10
Q

define preload

A

the volume of blood in the ventricles just before contraction (EDV)

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11
Q

define afterload

A

the pressure which the heart must work against to eject blood in systole

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12
Q

define contractility

A

the inherent strength and vigour of the hearts contraction during systole

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13
Q

define elasticity

A

myocardial ability to recover its original shape after systolic stress

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14
Q

define compliance

A

how easily a chamber of the heart expands when it is filled with blood (C=change in V/change in P)

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15
Q

define diastolic distensibility

A

the pressure required to fill the ventricle to the same diastolic volume

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16
Q

define resistance

A

a force that must be overcome to push blood through the circulatory system

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17
Q

what is the basic principle of starlings law of the heart

A

Increased End Diastolic volume (EDV)= Increased stroke volume (SV)

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18
Q

explain starlings law

A

the greater the EDV, the greater the sarcomeres stretch and the more forceful the contraction

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19
Q

relate to starlings law, what is the effect of an increased venous return

A

EDV will increase so SV Increases so cardiac output increases
Cardiac output= stroke volume x heart rate

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20
Q

stroke volume equation

A

SV=EDV-ESV

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21
Q

cardiac output equation

A

CO=SVxHR

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22
Q

Define cardiac output

A

volume of blood each ventricle pumps out per unit of time

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23
Q

mean arterial pressure equation

A
MAP= DP +1/3 (SP-DP) 
DP= diastolic pressure SP= systolic pressure
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24
Q

pulse pressure equation

A

PP=SP-DP

DP= diastolic pressure SP= systolic pressure

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25
Q

blood pressure equation

A

BP=COx Total peripheral resistance

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26
Q

ohms law?

A

V=IR

So in this case force=change in pressure/ resistance

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27
Q

poiseuille’s equation?

A

Q=r^4
Q= volumetric flow rate
r= pipe radius

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28
Q

the principle vessels for resistance

A

arterioles

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29
Q

what do arterioles respond to

A

Blood pressure changes. local,neural and hormonal factors

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30
Q

name 2 local factors that result in vasoconstriction

A

endothelin, internal blood pressure

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31
Q

name 6 local factors that result in vasodilation

A

hypoxia, nitrous oxide, K+ (accumulate from AP),CO2, H+, adenosine

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32
Q

what neural factors result in vasoconstriction

A

sympathetic nerves that release noradrenaline

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33
Q

what neural factors result in vasodilation

A

parasympathetic innervation

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34
Q

name 3 hormonal factors that result in vasoconstriction

A

angiotensin II, ADH, adrenaline (binds to alpha-adrenergic receptors in smooth muscle

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35
Q

name 2 hormonal factors that result in vasodilation

A

atrial natriuretic peptide, adrenaline (binds to beta2 receptors)

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36
Q

What is myogenic auto-regulation of the blood?

A

An intrinsic mechanism in smooth muscle blood vessels. If BP increases, the vessel constricts. This is important in regulating blood flow

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37
Q

Myogenic auto regulation of blood flow: what is the response to an increase in BP

A

Vasoconstriction and so blood flow decreases in blood vessels

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38
Q

Myogenic auto regulation of blood flow: what is the response to decrease in BP

A

Vasodilation so blood flow in blood vessels increases

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39
Q

What is hyperaemia

A

An increased blood flow to tissues

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40
Q

What is the cause of active hyperaemia

A

When blood flow increases due to an increase in metabolic activity.
Increased metabolic activity= decreased O2 and increased metabolites= arteriolar dilation = increased blood flow

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41
Q

What is the cause of reactive hyperaemia

A

When blood flow increases following occlusion of arterial flow

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42
Q

Describe excitation-contraction coupling

A
  1. Na+ depolarises membrane
  2. A small amount of Ca2+ is released from T tubules.
  3. Ca2+ channels open in sarcoplasmic reticulum
  4. Ca2+ flows into Cytosol. Cytosolic Ca2+ conc is raised
  5. Ca2+ binds to troponin C which pulls troop myosin and exposes the myosin binding site on actin
  6. Cross bridge cycling begins
  7. After depolarisation, Ca2+ is returned to sarcoplasmic reticulum. K+ outflow= repolarisation
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43
Q

What effect does myocardial contraction have on A band of sarcomere

A

No effect, it stays same length

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44
Q

What effect does myocardial contraction have on I-band and H-Zone of sarcomere

A

They get shorter

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45
Q

Describe actin (thin filament)

A

A globular protein, single polypeptide. It polymerises other actin monomers to form double stranded helix. Together they form F actin

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46
Q

Describe myosin (thick filament)

A

2 heavy polypeptide chains and 4 light chains. The myosin heads have 2 binding sites; one for actin and one for ATP

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47
Q

Describe tropomyosin

A

An elongated molecule made of 2 helical peptide chains

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48
Q

Function of troponin I

A

Together with tropomyosin, inhibits actin and myosin binding

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49
Q

Function of troponin T

A

Binds to tropomyosin

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50
Q

Function of troponin C

A

Has a high affinity for Ca2+. Troponin C drives away troponin I and so allows cross bridge formation

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51
Q

Name 3 effectors in circulation control

A
  1. Blood vessels- vasoconstrict/dilate and effect TPR
  2. Heart- can affect rate or contractility
  3. Kidneys- regulates blood volume and fluid balance
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52
Q

Where are baroreceptors located

A

Aortic arch and carotid sinus

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53
Q

What activates baroreceptors

A

They contain stretch receptors that respond to pressure

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54
Q

Are atrial baroreceptors involves in short-term or long term regulation of BP

A

Short term (Cardiopulmonary =long term)

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55
Q

Where are central chemoreceptors located

A

Medulla oblangata

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56
Q

What do central chemoreceptors respond to

A

Changes in pH (H+)
Increased PaCO2 increases H+ so decreases pH
Increased PaCO2 results in Vasodilation

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57
Q

What is the ligamentum teres a remnant of

A

The umbilical vein

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58
Q

What is the ligamentum venosus a remnant of

A

The ductus venosus

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59
Q

Briefly describe foetal circulation

A

Maternal circulation- umbilical vein (oxygenated blood) - ductus venosus - Inferior vena cava- RA- LA/RV- aorta- umbilical artery (deoxygenated blood)- maternal circulation

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60
Q

What layer of the trilaminar disc forms the cardiovascular system

A

The mesoderm

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61
Q

What does the first heart field produce

A

The left ventricle (LV)

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62
Q

What does the second heart field produce

A

The right ventricle, atria and outflow tracts

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63
Q

What are the 3 stages of heart formation

A
  1. Formation of primitive heart tube
  2. Cardiac looping
  3. Cardiac septation
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64
Q

Describe the formation of primitive heart tube

A

2 endocardial tubes form (day19)

The tubes fuse together and heart hearts (day22)

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65
Q

Describe what happens in cardiac looping

A

Nodes secrete nodal, this circulates to the left due to ciliary movement. Nodal causes a cascade of transcription factors that transduce looping

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66
Q

What happens in cardia septation

A

Endocardial cushions form. Fuse at midline to from atrioventricular septum.muscular ridge in the floor of primitive ventricle migrates to endocardial cushions forming interventricular septum

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67
Q

What does sinus venosus form

A

The coronary sinus and RA

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68
Q

What does primitive atrium form

A

Right and left atriums

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69
Q

What does primitive ventricle form

A

Most of left ventricle

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70
Q

What does bulbus Cordis form

A

Part of the ventricles

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71
Q

What does the truncus arteriosus form

A

Aorta and pulmonary trunk

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72
Q

What do the first and second aortic valves come from

A

Minor vessels in the head

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73
Q

What does the 3rd aortic arch form

A

Common carotid arteries

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74
Q

What does the left and right 4th aortic arch form

A
Left = aorta 
Right = right subclavian artery
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75
Q

What does the 5th aortic arch form

A

There is no 5th arch lol

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76
Q

What does the the left and right 6th aortic arch form

A
Left = left pulmonary artery and ductus arteriosus 
Right = right pulmonary artery
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77
Q

What does the 7th segmental aortic arch form

A

Left and right subclavian arteries

78
Q

What does the dorsal aortae form

A
Left= descending aorta 
Right= part of subclavian artery
79
Q

What are chronotropic effects

A

These change the heart rate eg positive chronotropic= increased heart rate

80
Q

What are inotropic effects

A

Alter the force of muscular contractions

81
Q

What affect does parasympathetic stimulation have on heart rate

A

Decrease heart rate (negative chronotropic)

Therefore cardiac output decreases

82
Q

What affect does sympathetic stimulation have on force of contraction

A

Increases force ( positive inotropic)

83
Q

What pump maintains the negative testing potential of a membrane

A

Sodium potassium pump

Na+/K+ pump

84
Q

Purpose of Nernst equation

A

Determines membrane potential

85
Q

What is Nernst equation

A

E=60log(conc outside/conc inside)

86
Q

What membrane channels are responsible for the plateau period in the cardiac Action Potential

A

Voltage gated Ca2+ ‘slow’ channels

87
Q

Briefly describe the cardiac action potential in 5 steps

A
  1. Na+ channels open; influx of Na+ into cell; depolarisation
  2. When Na+ channels close a small number of K+ leave the cell resulting in partial repolarisation
  3. Ca2+ channels open and there is a Ca2+ inflow. K+ channels are also open so there is a K+ outflow. This results in the plateau period.
  4. Ca2+ channels close and K+ channels remain open. K+ leaves cell resulting in repolarisation
  5. Maintaining the resting potential (approx -90mV) Na+ inflow, K+ outflow
88
Q

Where is SAN located?

A

Right atrium under cristae terminalis

89
Q

Briefly describe the electrical conduction pathway in the heart

A
  1. The SAN generates an electrical impulse
  2. This generates a wave of contraction in the atria
  3. Impulse reaches AVN
  4. Their is a brief delay to make sure atria have fully emptied
  5. The impulse then rapidly spreads down the Bundle of His and Purkinje Fibres
  6. The purkinje fibres then trigger coordinated ventricular contraction
90
Q

Why is there rapid conduction in the bundle of his and purkinje fibres?

A
  1. The fibres have a large diameter

2. There is high permeability at the gap junctions

91
Q

What is the function of the refractory period

A
  1. Prevents excessive frequent contractions

2. It allows time for the atria to fill

92
Q

What does the P wave on an ECG represent and what’s the duration

A

Atrial depolarisation. Duration less than 0.12s

93
Q

What does the QRS complex on an ECG represent? And it’s duration

A

Ventricular depolarisation. Duration 0.08-0.1s

94
Q

What does the T wave on an ECG represent

A

Ventricular repolarisation

95
Q

What might an elevated ST segment be associated with on an ECG

A

Myocardial infarction. (STEMI- ST elevated myocardial infarction)

96
Q

ECG: where would you place lead 1

A

Right arm (-ve) to left arm (+ve)

97
Q

ECG: where would you place lead 2

A

Right arm (-ve) to left leg (+ve)

98
Q

ECG: where would you place lead 3

A

Left arm (-ve) to left leg (+ve)

99
Q

What is einthovens triangle

A

An imaginary formation of the 3 limb leads in a triangle shape

100
Q

ECG: where would you place lead aVR

A

Left arm and left leg (-ve) to right arm (+ve)

101
Q

ECG: where would you place lead aVF

A

Right arm and left arm (-ve) to left leg (+ve)

102
Q

ECG : where would you place lead aVL

A

Right arm and left leg (-ve) to left arm (+ve)

103
Q

ECG chest leads : in which intercostal space would you place V1 and V2

A

The 4th intercostal space. V1 is on right of the sternum and V2 in left.

104
Q

ECG chest leads: in which intercostal dove would you place V3-V6

A

The 5th intercostal space. V3 is left of the sternum, V4 is in the midclavicular line, V5 is left of V4 and V6 is under the left arm

105
Q

What are the average systolic and diastolic pressures of the pulmonary circulation

A

25 and 10mmHg

106
Q

What are the average systolic and diastolic pressures of the systemic circulation

A

120 and 80mmHg

107
Q

Why might someone with liver injury experience prolonged bleeding time

A

Because the liver produces clotting factors

108
Q

What is exposed if you damage the endothelium vessel

A

Underlying connective tissue and collagen

109
Q

What is the role of von willebrands factor

A

Binds to collagen. Platelets also bind to the von willebrands factors

110
Q

What happens in platelet activation?

A

Platelet changes shape: smooth to spiculated
This increases its surface area.
New platelets adhere to old ones = platelet aggregation
This forms a platelet plug

111
Q

What do activated platelets synthesise

A

Thromboxane A2

112
Q

What is the function of thromboxane A2 (TXA2)?

A

Leads to further platelet aggregation

113
Q

What are the platelet receptors for fibrinogen

A

Glycoprotein IIb/IIIa. Fibrinogen forms ‘bridges’ between platelets.

114
Q

What does an undamaged endothelium release In order to prevent platelet activation in undamaged areas

A

Prostacyclin (inhibits platelet aggregation)

And Nitric Oxide (NO)(inhibits platelet adhesion)

115
Q

What are platelets made from and where are they made

A

Made from megakaryocytes in the bone marrow

116
Q

In haemostatsis what is prothrombin converted to

A

Thrombin

117
Q

Give 3 functions of thrombin

A
  1. Converts fibrinogen to fibrin
  2. Activates factor XIII to XIIIa
  3. Has a positive feedback effect resulting in further thrombin production
118
Q

What is the essential component of a blood clot

A

Fibrin

119
Q

Briefly describe the fibrinolytic system

A

Plasminogen is converted to plasmin.

Plasmin cuts the fibrin at various places leading to the formation of fragments

120
Q

What is the purpose of the fibrinolytic system

A

It acts to prevent blood clots from growing and becoming problematic

121
Q

What is the structure of haemoglobin

A

2 alpha and 2 beta chains. 4 haem groups

122
Q

Describe the composition of blood

A

Plasma - 55%

Cellular - 45% —> RBC: 44% and WBC: 1%

123
Q

Does blood flow to the heart occur during diastole or systole

A

Diastole

124
Q

What is diastole and systole

A

Diastole - relaxing and refilling of heart with blood

Systole - contraction and pumping of blood

125
Q

What does left coronary artery divide into

A

Left anterior descending and the circumflex

126
Q

Why is O2 saturation in coronary and venous blood very low

A

O2 extraction by the heart muscle is very high

127
Q

What surface of the heart does the right coronary artery supply

A

The inferior surface of the heart (underside)

128
Q

What is release upon cell activation and contains a high conc of a molecule that’s acts as an agonist of the platelet P2Y12 receptor

A

Platelet dense granules

129
Q

What valve prevents high pressures developing in the jugular veins during ventricular systole

A

The tricuspid valve

130
Q

What is the normal duration of PR interval

A

0.12-0.2 secs

131
Q

What ECG lead yield complexes that are normally inverted compared to the anterior and inferior leads?

A

Lead aVR

132
Q

Is there a point in the cardiac cycle when both atrial and ventricular diastole occur together

A

Yes: when the ventricles and replacing and the atria are filling ( before atrial contraction)

133
Q

Why does an increase in LVEDV (left ventricle end diastolic volume)signify heart failure

A

Heart failure is the inability to pump blood out of the heart. There is blood remaining at the end of systole. The blood therefore accumulates so LVEDV increases

134
Q

Which pressure is most likely to increase in left sided heart failure

A

LV EDP

Left ventricular end diastolic pressure

135
Q

Which pressure is most likely to decrease in left sided heart failure

A

Mean aortic pressure ( less blood being pumped to aorta)

136
Q

What is stenosis

A

Narrowing

137
Q

Which pressure is most likely to increase in mitral valve stenosis

A

Left atrial end systolic pressure

138
Q

What does it means if a heart valve is incompetent

A

It is regurgitant

139
Q

Which pressure is most likely to increase when the aortic valve is incompetent

A

Left ventricular end diastolic pressure

140
Q

Pulmonary oedema is a sign of what

A

Left heart failure

141
Q

What can severe pulmonary hypertension cause

A

Right heart failure

The heart has to pump harder to get blood into the pulmonary circulation due to an increased after load

142
Q

Shortness of breath and severe peripheral oedema and ascites after heart attack can indicate what

A

Biventricular failure

143
Q

What is ascites

A

Accumulation of fluid in the peritoneal cavity and can cause abdominal swelling

144
Q

What does the PR interval represent and how long is it

A

The slow conduction between the AVN and the His-Purkinje system.
It’s 0.12-0.2 secs long

145
Q

Diastole: what is diastasis

A

When left ventricle pressure = right atrial pressure. Net movement of blood is 0. This is the time between ventricular suction and atrial contraction

146
Q

What branch does the right coronary artery give off as it reached the inferior border of the heart

A

Right marginal branch

147
Q

What artery does the RCA anastomose with on the diaphragmatic surface of the heart

A

The circumflex artery

148
Q

What does the left anterior descending anastomose with on the diaphragmatic surface of the heart

A

The posterior inter-ventricular branch of the right coronary artery

149
Q

Where is the coronary sinus found

A

Between the left atrium and left ventricle

The left atrioventricular sulcus

150
Q

What does the coronary sinus drain into

A

The right atrium

151
Q

What artery arises from the RCA in 90% of hearts, the circumflex in 30% and in 20% arises from both the RCA and circumflex

A

The posterior inter-ventricular branch

152
Q

What equation explains why small changes in the diameter of a flood vessel have a great effect on the resistance to flow fluid through that vessel

A

Poiseuilles equation

Q=r^4

153
Q

What is the role of fibrinogen in platelet aggregation.

A

It forms cross links between aggregating platelets

154
Q

Give 2 reasons why liver is important for clotting

A
  1. The liver produces many clotting factors
  2. The liver produces bile salts that are needed for vitamin K absorption. vitamin K is needed for clotting factor production.
155
Q

When are the platelet receptors for fibrinogen exposed

A

During platelet activation

156
Q

Which of the ABO blood groups is recessive

A

A and B are co-dominant

157
Q

Why is the O blood group a universal donor

A

It has no A or B antigens

158
Q

What are the 2 ways of determining someone’s ABO blood group

A
  1. Test using antibodies

2. Test for the presence of antibodies using A or B antigens

159
Q

Describe how testing for the presence of antibodies against A and B antigens will determine their blood group

A

The presence of antibodies in the blood will indicate that this person does not have these antigens on their RBCs. For example, if a persons blood contains antibodies against B antigens then they can’t be AB or B blood groups

160
Q

Describe how testing using antibodies determines someone’s blood group

A

If the antibodies bind it indicates the presence of a specific antigen. For example, if antibodies against the B antigens bind to the patients RBC then the person must either be AB or B blood group

161
Q

What antigens are part of the Rhesus blood group system

A

C,D and E

D is the most important

162
Q

What problems arise if a pregnant lady is found to be Rhesus D negative

A

If exposed to D RBCs the lady will have antibodies against the D antigen. The antibodies can cross the placenta and cause haemolysis of the babies RBCs. This can result in in-utero death.

163
Q

What can be given to Rhesus D negative mothers to prevent sensitisation

A

Anti-D

164
Q

Describe the arterial baroreceptor reflex in response to increase blood pressure

A
  • Increase parasympathetic outflow to the heart means contractility and heart rate are reduced so cardiac output is reduced: CO=HRxSV
  • Decreased sympathetic outflow to the arterioles results in vasodilation and so the total peripheral resistance (TPR) is reduced
  • BP=COxTPR and so blood pressure is lowered
165
Q

Describe the arterial baroreceptor reflex in response to decrease in blood pressure

A
  • Increased sympathetic outflow to the heart means contractility and heart rate are increased so cardiac output is increased : CO=HRxSV
  • Increased sympathetic outflow to the arterioles results in vasoconstriction and so the total peripheral resistance (TPR) is increased
  • BP=COxTPR and so blood pressure is increased
166
Q

What phase of the cardiac action potential coincides with diastole

A

Phase 4

167
Q

What part of the ECG does the plateau phase of the cardiac action potential coincide with

A

QT interval

168
Q

Give 4 factors that affect the gating of ion channels

A

Voltage, drugs, hormones, temperature

169
Q

What is Virchows triad

A

Describes 3 categories thought to contribute to thrombosis.

  1. Stasis of blood flow
  2. Endothelial injury
  3. Increased coagulation ability
170
Q

Define ischaemia

A

A decrease in blood flow to the tissue

171
Q

Define infarction

A

No blood flow to the tissue - tissue death

172
Q

Explain the formation of fluid exudate in inflammation

A

Chemical mediators cause vasodilation of vessels and an increase in permeability

173
Q

What are the roles of lymphatics in acute inflammation

A

Drain exudate and carry antigens

174
Q

What happens in phase 4 of the cardiac action potential

A

Pace maker potential- na+ inflow and slowing of K+ outflow. Slow depolarisation begins= innate contractility

175
Q

Where is Ca2+ released from in excitation contraction coupling

A

The T tubules and sarcoplasmic reticulum

176
Q

What is the resting potential of SA node

A

-55 to -60mV

177
Q

How to central chemoreceptors respond to an increase in PaCO2

A

Vasoconstriction

178
Q

Why do central chemoreceptors stimulate vasoconstriction in resin to an increase in PaCO2

A

They act to counter the affect of CO2 as a vasodilator and so maintain blood flow to tissues

179
Q

What reaction does adenyl Cyclase catalyse

A

The conversion of ATP to cAMP

180
Q

How do muscarinic M2 receptors cause a decrease in cAMP

A

They inhibits adenyl cyclase

181
Q

What 2 channels are closed during the refractory period in the cardiac action potential

A

Fast Na+ and Ca2+ channels

182
Q

What is the normal duration of the PR interval in ms

A

120-200ms

183
Q

What would an absent P wave on an ECG be a sign of

A

Atrial fibrillation

184
Q

What is the heart supplied by

A

Left and right coronary arteries

185
Q

Blow flow to the myocardium occurs when

A

Mainly during diastole

186
Q

ECG: what represents atrial systole

A

PR interval

187
Q

ECG:What assesses the electrical activity whir in the lateral myocardial territory

A

Leads I,aVL, V5 and V6

188
Q

ECG:Yields completed that are normally inverted compared to anterior and inferior leads

A

Lead aVR

189
Q

ECG:Assesses electrical activity within the inferior myocardial territory

A

Leads II,III and aVF

190
Q

Haematocrit:what is it, how do you calculate it?, what is the percentages of the 2 components it’s made up of?

A

Volume percentage of red blood cells in blood
Haematocrit= ratio of RBC volume - total blood volume

45% is erythrocytes
55% is plasma
<1% is WBC

191
Q

RBC: how long do they live?, organelles?, where are they made?, stimulated by?, production process name?

A

120 days, Anucleate & no mitochondria ( glycolysis enzymes convert glucose to pyruvate, liver pyruvate to lactate), made in bone marrow, stimulated by erythropoietin (made in liver and kidney)! RBC production process called erythropoesis

192
Q

Describe RBC shape and structure

A

7.5um in diameter so can just about fit through capillaries
Biconcave disc for large SA
Thin plasma membrane
4 globin chains - 2 alpha & 2 gamma