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Phase 1 Med > Cardio > Flashcards

Cardio Flashcards

1
Q

Describe the composition of blood.

A

Plasma - 55%.

Cellular - 45% - RBC: 44%, WBC: 1%.

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2
Q

What is Haematocrit?

A

the volume of red blood cells i.e haemoglobin in the blood, normal
haematocrit is 0.45

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3
Q

What is Haemopoeisis?

A

the process of the production of blood cells and platelets which
continues throughout life

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4
Q

What is the lifespan of an erythrocyte?

A

120 days

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5
Q

What is the lifespan of a platelet

A

7-10 days

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6
Q

What is the lifespan of a white blood cell

A

6 hours

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7
Q

Where are the precursor cells of erythrocytes located?

A

Bone marrow

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8
Q

Where can haemopoiesis occur in

a) Adults
b) Children
c) in Utero

A

a) axial skeleton - skull, ribs, spine, pelvis and long bones
b) all bones
c) yolk sac, then liver and spleen

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9
Q

What hormone is required for erythropoiesis and where is it produced?

A

Erythropoietin - produced in the kidney

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10
Q

What hormone is required for white blood cell production?

A

G-CSF - (granulocyte colony-stimulating factor)

Thrombopoietin

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11
Q

What hormone is required for platelet formation?

A

Thrombopoietin

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12
Q

What causes the oxygen dissociation curve to shift to the left

A

Decreased temp

increased pH

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13
Q

What causes the oxygen dissociation curve to shift to the right

A

Increased temp

decreased pH

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14
Q

What happens when the oxygen dissociation curve shifts to the left

A

Hb has a higher affinity for oxygen - (left locks oxygen)
at lower partial pressures of oxygen
decreased unloading

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15
Q

What happens when the oxygen dissociation curve shifts to the right

A

Hb has a lower affinity for oxygen

Increased unloading to tissues

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16
Q

What are reticulocytes

A

Young (immature) red blood cells

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17
Q

Briefly describe the structure of Hb

A

2 alpha and 2 beta chains
4 haem groups
has a quaternary structure

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18
Q

Which of the ABO blood groups is recessive?

A

O, A and B are co-dominant.

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19
Q

Which blood group do people have that make them universal recipients?

A

AB - have neither anti-A or anti-B antibodies

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20
Q

Which blood groups do people have to make them universal donors?

A

Type O - have both anti-A and anti-B antibodies, but don’t have any ANTIGENS on the surface of RBC

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21
Q

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

A
  1. Test using antibodies.

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

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22
Q

Describe how testing for the presence of antibodies against A or B antigens will determine someone’s blood group?

A

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

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23
Q

What antigens are part of the Rhesus blood group system?

A

C, D and E.

D is the most important

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24
Q

What problems can arise if a pregnant lady is found to be rhesus D negative?

A
  • Mother RhD negative/ baby RhD positive
  • mothers blood exposed to babies blood
  • mother sensitised / production of anti-D antibodies
  • First baby unaffected
  • second baby has RhD positive blood
  • antibodies cross placenta and destroys RBC of baby
  • can lead to Rh disease and anaemia/jaundice
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25
Q

What can be given to rhesus D negative mothers to prevent sensitisation?

A

Anti-D.

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26
Q

Define anaemia

A

reduction in haemoglobin in the blood

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27
Q

What do you call an increased level of Hb and causes?

A

polycythaemia (caused by smoking, lung diseases, inefficient lungs
meaning less O2 is exchanged so more haemoglobin is required etc.)

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28
Q

Why might iron deficiency cause iron-deficiency anaemia?

A

Iron is needed for haemoglobin production, lack of

iron results in the reduced production of small red cells

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29
Q

Why might vitamin B12 and folate deficiency lead to anaemia?

A
  • required for DNA synthesis

- RBC cannot be made in bone marrow

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30
Q

Where is folate found?

A

Vegetables and fruit

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31
Q

what is Haemolysis?

A

Normal or increased cell production but DECREASED LIFE SPAN < 30 DAYS, red
blood cells are destroyed before their 120 day lifespan

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32
Q

What is the lifespan of neutrophils?

A

10 hours

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33
Q

What is the most numerous WBC in the body?

A

Neutrophils

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34
Q

What is the role of neutrophils?

A
  • Phagocytose and kill bacteria

- release cytokines (important in inflammatory response)

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35
Q

Where are platelets made and what are they derived from?

A

Made in the bone marrow and derived from the megakaryocytes

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36
Q

What is the lifespan of platelets?

A

5-10 days

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37
Q

What term is used to describe reduced platelet count?

A

thrombocytopenia (main risk is cerebral bleeding) > 80 =

increased bleeding, > 20 = spontaneous bleeding

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38
Q

What term is used to describe elevated platelet count?

A

thrombocytosis, can lead to arterial & venous thrombosis, leading
to an increased risk of heart attack + stroke

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39
Q

Where are coagulation proteins/enzymes made from and what is needed to make them?

A
  • Produced in the liver
  • The key enzyme is thrombin
  • Vitamin K is needed for coagulation factors 2,7,9 and 10
  • circulate in an inactive form
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40
Q

Why might someone with liver injury experience prolonged bleeding time?

A

Because the liver produces clotting factors.

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41
Q

Give 3 functions of Thrombin.

A
  1. Converts fibrinogen into fibrin.
  2. Activates factor XIII into XIIIa.
  3. Has a positive feedback effect resulting in further thrombin production.
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42
Q

In haemostasis what is prothrombin converted into?

A

Thrombin.

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43
Q

why is blood stay as a fluid in blood vessels?

A

-The proteins of the coagulation cascade and the platelets circulate in an inactive
state
-Proteins and platelets are only activated by tissue factor, which is present on every
single-cell APART from endothelial cells thus when the endothelium is punctured etc.
blood comes into contact with tissue factor and thus starts clotting

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44
Q

What is the coagualtion cascade?

A

Results in the beginning of the coagulation cascade - series of proteolytic enzymes
that circulate in an inactive state being activated (usually by exposure to tissue
factor) in a cascade or waterfall sequence - in order to generate the key enzyme
THROMBIN which cleaves fibrinogen creating fibrin polymerisation i.e a blood
clot

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45
Q

Why might obstructive jaundice cause a prolonged bleeding time?

A

Malabsorption of vitamin K as it is a fat soluble vitamin

Vitamin K is needed to produce clotting factors

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46
Q

When a blood vessels is damaged what is the first response?

A
  • Vasoconstriction due to neural control and release of endothelin-1
  • slows the blood flow in the area
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47
Q

What is exposed when the endothelium is injured

A

Collagen fibres and the attached VWF.

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48
Q

Which receptor do the platelets use to bind to the VWF on the collagen fibres?

A

glycoprotein 1b receptor

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49
Q

What do the platelets release when they bind to the collagen fibres via the VWF?

A

Platelet dense granules via exocytosis

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50
Q

What is released from the platelet dense granules and what do they act on?

A
  • ADP released
  • act on P2Y1 and P2Y12
  • causes platelet activation
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51
Q

Which receptors does thrombin bind to and what does this cause?

A
  • Binds to PAR1 and Par2 receptors
  • Platelet activation
  • further thrombin release (positive feedback)
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52
Q

What happens in platelet activation?

A
  • Increased expression of GP2b/3a receptors
  • they bind to fibrinogen from alpha granules enabling new platelets to adhere to old ones
  • from smooth to spiculated with pseudopodia which increases SA
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53
Q

What do activated platelets synthesise and what does this lead to ?

A
  • Thromboxane A2
  • vasoconstriction
  • platelet activation
    further stimulate release of vesicle contents of other platelets
  • platelet aggregation
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54
Q

What is present in high concentration in platelets which aim to strengthen and compress the platelet plug?

A

actin and myosin

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55
Q

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

A
  • Prostacyclin (inhibits platelet aggregation) and - - - NO (inhibits platelet adhesion).
  • both vasodilators
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56
Q

What is the role of vWF?

A

vWF binds to collagen and platelets bind to vWF via GP 1b receptor

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57
Q

What is the essential component of a blood clot?

A

fibrin

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58
Q

Briefly describe the Fibrinolytic system.

A

Plasminogen is converted into plasmin. Plasmin cuts the fibrin at various places leading to the formation of fragments.

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59
Q

What is the purpose of the fibrinolytic system?

A

It acts to prevent blood clots from growing and becoming problematic.

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60
Q

What is contained within alpha granules of the platelets?

A
  • VWF
  • Thromboxane A2
  • Fibrinogen
  • fibrin stabilising factor
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61
Q

What is contained within dense granules of the platelets?

A
  • ADP
  • Ca2+
  • Serotonin
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62
Q

What is found within the intercalated disks of cardiac muscle?

A
  • Desmosomes

- Gap junctions

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63
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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64
Q

Describe actin (thin filament).

A

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

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65
Q

Describe tropomyosin and its position

A

elongated molecule that occupies the grooves between the two actin
strands, overlies MYOSIN binding sites on actin

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66
Q

What is the function of troponin I?

A

Troponin I, together with tropomyosin, inhibits actin and myosin binding.

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67
Q

What is the function of troponin T?

A

Troponin T binds to tropomyosin.

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68
Q

What is the function of troponin C?

A

Troponin C has a high affinity for Ca2+. TnC drives away TnI and so allows cross bridge formation.

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69
Q

What effect does myocardial contraction have on the I-band and H-zone of a sarcomere?

A

They get shorter.

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70
Q

What effect does myocardial contraction have on the A-band of a sarcomere?

A

No effect, it stays the same length

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71
Q

What is in the A-band?

A

occupied by thick filaments and a few thin filaments

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72
Q

What is in the I - band?

A
  • only thin filaments

- extends from the z-lines

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73
Q

What is in the H-zone?

A

only thick filaments (myosin)

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74
Q

What is titin and what is its function in a sarcomere?

A
  • elastic protein filaments
  • extends from Z-line to M-line
  • titin linked to M-line though myosin
  • maintains alignment of the thick filaments of each sarcomere
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75
Q

What is the sarcoplasmic reticulum?

A

membrane network that surrounds the contractile

proteins. Releases Ca2+ when Ca2+ binds to it ryanodine receptor

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76
Q

Describe excitation-contraction coupling.

A
  1. Na+ depolarises membrane.
  2. A small amount of Ca2+ is released from T tubules.
  3. Ca2+ channels in sarcoplasmic reticulum open.
  4. Ca2+ flows into cytosol. Cytosolic Ca2+ conc raised.
  5. Ca2+ binds to troponin C, this pulls tropomyosin and exposes the myosin binding site on actin.
  6. Cross bridge cycling begins.
  7. After depolarisation, Ca2+ is returned to SR. K+ outflow = repolarisation.
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77
Q

When an action potential arrives sodium channels open, which other channel starts to open slowly at this stage?

A

L-type Ca2+ channels

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78
Q

What occurs at phase 0 of an action potential?

A
  • rapid depolarisation
  • Na+ channels open and L-type Ca2+ channels start to open
  • Rapid Na+ inflow
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79
Q

What occurs at phase 1 of an action potential?

A
  • Partial repolarisation
  • Na+ channels close
  • voltage gated K+ channels open
  • outflow of K+
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80
Q

What occurs at phase 2 of an action potential?

A
  • Plateau
  • Calcium slow inflow
  • matched by potassium outflow
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81
Q

What occurs at phase 3 of an action potential?

A
  • repolarisation
    L-type calcium channels close
  • Ca2+ inflow stops
  • K+ outflow remains
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82
Q

What occurs at phase 4 of an action potential?

A
  • Pacemaker potential
  • Na+ inflow
  • Slowing of potassium outflow
  • Na+/K+ ATPase
    3Na+ out and 2K+ in
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83
Q

What is the function of the refractory period?

A
  1. It prevents excessively frequent contractions.

2. It allows time for the atria to fill.

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84
Q

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

A

Fast Na+ and Ca2+ channels.

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85
Q

Which group of arteries supplies the myocardial cells?

A

Coronary arteries

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86
Q

Which vein do the coronary arteries drain into and where does the vein empty?

A
  • Coronary sinus

- Drains in the right atrium

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87
Q

Why is the O2 saturation in coronary venous blood very low?

A

O2 extraction by the heart muscle is very high.

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88
Q

Where is the coronary sinus found?

A

Between the LA and LV - left atrio-ventricular sulcus.

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89
Q

Where is the SAN located?

A

In the RA under the crista terminalis.

90
Q

What is the resting potential of the SA node?

A
  • 55 to -66mv
  • closer to threshold of depolarisation
  • hence depolarises first
91
Q

Name the three ion channels that contribute to the pacemaker potential and briefly explain their role

A
  • K+ channel - Channels that opened during the repolarisation phase of previous action potential gradually close due to return of negative potential
  • F-type Na+ channels - funny as they open at negative potentials
  • T- type Ca2+ channels - open briefly important in final depolarisation push
92
Q

Where is the AV node located?

A

at the base of the right atrium

93
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. There is a brief delay to ensure the 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.
94
Q

Briefly describe the cardiac action potential in 5 steps.

A
  1. Na+ channels open; influx of Na+ into cell; depolarisation.
  2. When the Na+ channels close, a small number of K+ leave the cell resulting in partial repolarisation.
  3. Ca2+ channels open and there is Ca2+ inflow. K+ channels are also open and there is K+ outflow. This results in the plateau period.
  4. Ca2+ channels close and K+ channels remain open. K+ leaves the cell resulting in repolarisation.
  5. Maintaining the resting potential (approx -90mV). Na+ inflow, K+ outflow.
95
Q

Which nerve supplies parasympathetic innervation to the heart?

A

Vagus nerve ( CN10)

96
Q

Which neurotransmitter is released from the vagus nerve and what type of receptor does it bind to?

A
  • Ach

- Muscarinic receptor

97
Q

What affect does parasympathetic innervation have on the heart?

A
  • Decreases heart rate (negatively chronotropic)
    • Decreases force of contraction (negatively inotropic)
    • Decreases cardiac output (by up to 50%)
    • Decreased parasympathetic stimulation will result in an increased heart rate
98
Q

Which nerves provide sympathetic innervation to the heart and which neurotransmitter is used?

A
  • Sympathetic postganglionic fibres

- adrenaline & noradrenaline

99
Q

What affect does sympathetic innervation have on the heart?

A

• Increases heart rate (positively chronotropic)
• Increases force of contraction (positively inotropic)
• Increases cardiac output (by up to 200%)
• Decreased sympathetic stimulation will result in decreased heart rate & force of
contraction and a decrease in cardiac output by up to 30%

100
Q

What does the P wave on an ECG represent and duration?

A
  • Atrial depolarisation

- duration lasts between 0.08- 0.01s

101
Q

What does the QRS complex show on an ECG and duration?

A
  • Ventricular depolarisation

- 0.06-0.1 s

102
Q

What does the T wave on an ECG represent?

A

Ventricular repolarisation.

103
Q

ECG: where would you place lead 1?

A

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

104
Q

ECG: where would you place lead 2?

A

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

105
Q

ECG: where would you place lead 3?

A

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

106
Q

ECG: where would you place lead aVR?

A

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

107
Q

ECG: where would you place lead aVF?

A

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

108
Q

ECG: where would you place lead aVL?

A

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

109
Q

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

A

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

110
Q

ECG chest leads: In which intercostal space would you place V3-V6.

A

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

111
Q

ECG: Name the leads that correspond to the lateral surface of the heart

A
  • Lead 1
  • aVL
  • V5
  • V6
112
Q

ECG: Name the leads that correspond to the septum on the heart

A
  • V1
113
Q

ECG: Name the leads that correspond to the anterior surface of the heart

A
  • V2
  • V3
  • V4
114
Q

ECG: Name the leads that correspond to the inferior surface of the heart

A
  • Lead 2
  • Lead 3
  • aVF
115
Q

atrial depolarisation is seen in every lead apart from one, which one?

A
  • aVR
116
Q

describe the PR interval

A

Time taken for atria to depolarise and electrical activation to get
through AV node

117
Q

Describe the ST segment

A
  • interval between depolarisation & repolarisation
118
Q

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

A

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

119
Q

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

A

Lead aVR.

120
Q

How long is the AV node delay?

A

0.12-0.2 seconds

121
Q

State how long diastole and systole last for

A

Systole: 0.3 seconds
Diastole: 0.5 seconds

122
Q

Describe the events that occur in systole

A
  • Wave of depolarisation arrives, Ca2+ channels open
  • LVp>LAp and the mitral valve closes.
  • isovolumic contraction
  • all valves are closed at this point
  • LVp > aortic/pulmonary pressure
  • valves open, maximal ejection
  • Ventricles do not completely empty
123
Q

Describe the events of diastole

A
  • LVp decreases and there is a phase of reduced ejection
  • LVp is less than aortic pressure and the aortic valve closes
  • isovolumetric ventricular relaxation
  • LAp >LVp due to venous return
  • Mitral valve opens
  • 80% ventricular filling ( passive)
  • atrial booster/ atria contract and ventricles filled
  • LVp > LAp and mitral valve closes.
124
Q

What causes the mitral valve to close?

A

When LVp exceeds LAp. Just before ventricular isovolumetric contraction.

125
Q

What is isovolumetric contraction?

A

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

126
Q

What produces the first heart sound?

A

Closing of the mitral valve.

127
Q

What produces the second heart sound?

A

Closing of the aortic valve.

128
Q

What is end-systolic volume?

A

The volume of blood remaining in the LV following systole.

129
Q

Define preload.

A
  • The volume of blood in the ventricles just before contraction (EDV).
  • stretches myocytes
  • dilating veins increases preload
130
Q

Define afterload.

A
  • The pressure against which the heart must work to eject blood in systole.
  • dilate arteries = decreased afterload
131
Q

Define contractility.

A

The inherent strength and vigour of the heart’s contraction during systole.

132
Q

Define elasticity.

A

Myocardial ability to recover its original shape after systolic stress.

133
Q

Define compliance.

A

how easily the heart chamber expands when filled with blood volume

134
Q

Define diastolic distensibility.

A

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

135
Q

Define resistance.

A

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

136
Q

Describe starlings law

A

Force of contrition is proportional to the end-diastolic length of
cardiac muscle fibre - the more ventricle fills the harder it contracts

137
Q

What is the basic principle of Starling’s law of the heart?

A

Increased EDV = increased SV.

138
Q

With relation to Starling’s law, what is the effect of an increased venous return?

A
  • increased EDV
  • increased preload
  • increased sarcomere stretch
  • increased force of contraction
  • increased stroke volume and force of contractions
  • increased CO (CO= SVxHR)
139
Q

What is myogenic auto-regulation of blood flow?

A
  • An intrinsic mechanism in smooth muscle blood vessels.
  • If BP increases the vessel (arteriole) constricts.
  • If smooth muscle into getting stretched as low BP the muscles relax in the arteriole
  • This is important in
    regulating blood flow.
140
Q

Myogenic auto-regulation of blood flow: What is the response to an increase in BP?

A

Increased BP will result in vasoconstriction and so blood flow decreases.

141
Q

Myogenic auto-regulation of blood flow: What is the response to a decrease in BP?

A

Decreased BP will result in vasodilation and so blood flow increases.

142
Q

What is hyperaemia?

A

An increased blood flow to tissues.

143
Q

Give the equation for mean arterial pressure.

A

MAP = DP + 1/3(SP-DP).

SP - systolic pressure, DP - diastolic pressure

144
Q

Name 3 effectors in circulation control.

A
  1. Blood vessels - vasoconstrict/dilate and affect TPR.
  2. The heart - can affect rate or contractility.
  3. Kidneys - regulates blood volume and fluid balance.
145
Q

Which region in the brain is responsible for raising blood pressure?

A
  • Pressor region in medulla

- sympathetic

146
Q

How does the pressor region in the medulla increase BP?

A
  • increased vasoconstriction
  • increased heart rate
  • increased stroke volume due to more forceful contractions
  • hence increased CO ( CO= SVxHR)
  • increased contractility
147
Q

Which region in the brain is responsible for lowering blood pressure?

A
  • Depressor region in the medulla

- parasympathetic via the vagus nerve

148
Q

How does the depressor region in the medulla lower BP?

A
  • inhibits the pressor region
149
Q

Where are central chemoreceptors located?

A

In the medulla oblangata.

150
Q

What do central chemoreceptors respond to?

A

Changes in pH/(H+).
Increased PaCO2 increases H+ and so decreases pH.
Increased PaCO2 results in vasodilation.

151
Q

Where are the cardiopulmonary baroreceptors found?

A
  • Atria
  • ventricles
  • pulmonary artery
152
Q

What happens when the cardiopulmonary baroreceptors are stimulated

A
  • high blood pressure leads to the inhibition of the pressor region/ vasoconstrictor centre in the medulla - leading to a fall in blood pressure
  • decrease in
    blood pressure by promoting vasodilation & fluid loss
  • Also inhibits the Renin-angiotensin & aldosterone system
  • inhibits vasopressin/ADH
153
Q

What are the principal vessels of resistance?

A

Arterioles.

154
Q

What do arterioles respond to?

A

Blood pressure changes. Local, neural and hormonal factors.

155
Q

Name 2 local factors that result in vasoconstriction.

A
  • Endothelin

- internal BP - increase internal BP results in myogenic contraction, diameter normalised

156
Q

Name 5 local factors that result in vasodilation.

A

Hypoxia, NO, K+ (accumulate from AP), CO2, H+, adenosine.

157
Q

What neural factors result in vasoconstriction?

A

Sympathetic nerves release noradrenaline.

158
Q

What neural factors result in vasodilation?

A

Parasympathetic innervation.

159
Q

Name 3 hormonal factors that result in vasoconstriction.

A

Angiotensin 2, ADH, Adrenaline (binds to alpha-adrenergic receptors in smooth muscle).

160
Q

Name 2 hormonal factors that result in vasodilation.

A

Atrial natriuretic peptide, Adrenaline (binds to beta2 receptors).

161
Q

What activates baroreceptors?

A

Baroreceptors contain stretch receptors that respond to pressure.

162
Q

Where are peripheral chemoreceptors found?

A
  • aortic arch & carotid sinus
163
Q

What stimulates the peripheral chemoreceptors

A

a fall in PaO2 & a rise in

PaCO2 & a fall in pH causing blood pressure to increase

164
Q

Describe how the aortic arch can work to decrease BP?

A
  • afferent signals sent via the vagus nerve to the medulla
  • Decreased sympathetic (pressor) and increased parasympathetic (depressor)
  • decrease in blood pressure
165
Q

Describe how the carotid sinus work to decrease BP

A
  • Carotid sinus
  • to glossopharyngeal afferent
  • to the medulla
  • Decreased sympathetic (pressor) and increased parasympathetic (depressor)
  • decrease in blood pressure
166
Q

Give the equation for stroke volume.

A

SV=EDV-ESV.

167
Q

Give the equation for cardiac output.

A

CO=SVxHR.

168
Q

Define cardiac output.

A

The volume of blood each ventricle pumps per unit time.

169
Q

Give the equation for pulse pressure.

A

PP=SP-DP.

170
Q

Give the equation for blood pressure.

A

BP=COxTPR.

171
Q

What is Poiseuille’s equation?

A

Flow = radius to the power of 4

172
Q

What is Ohm’s law?

A

Flow = Pressure gradient/Resistance

173
Q

Why does an increase in LVEDV 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 and so LVEDV increases.

174
Q

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

A

LV EDP.

175
Q

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

A

Mean aortic pressure.

Less blood is being pumped into the aorta

176
Q

What is stenosis?

A

Narrowing.

177
Q

Which pressure is most likely to increase in mitral valve stenosis?

A

Left atrial end-systolic pressure.

178
Q

What does it mean if a heart valve is incompetent?

A

It is regurgitant.

179
Q

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

A

Left ventricular end-diastolic pressure.

180
Q

Pulmonary oedema is a sign of what?

A

Left heart failure.

181
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 afterload.

182
Q

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

A

Biventricular failure.

183
Q

Diastole: what is diastasis?

A

When LVp = LAp. Net movement of blood is zero. This is the time between ventricular suction and atrial contraction.

184
Q

Describe the arterial baroreceptor reflex in response to an increase in blood pressure.

A
  • Increased parasympathetic outflow to the heart means contractility and heart rate are reduced and so cardiac output is reduced: CO=HRxSV.
  • Decreased sympathetic outflow to the arterioles results in vasodilation and so TPR is reduced.
  • BP=COxTPR and so blood pressure is lowered.
185
Q

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

A
  • Increased sympathetic outflow to the heart means contractility and heart rate are increased and so cardiac output is increased: CO=HRxSV.
  • Increased sympathetic outflow to the arterioles results in vasoconstriction and so TPR is increased.
  • BP=COxTPR and so blood pressure is increased.
186
Q

What phase of the cardiac action potential coincides with diastole?

A

Phase 4.

187
Q

Define ischaemia.

A

A decrease in blood flow to a tissue.

188
Q

Define infarction.

A

No blood flow to a tissue - tissue death.

189
Q

Explain the formation of fluid exudate in inflammation.

A

Chemical mediators cause vasodilation of vessels and an increase in permeability.

190
Q

What are the roles of lymphatics in acute inflammation?

A

Lymphatics drain exudate and carry antigens.

191
Q

What occurs in gastrulation?

A
  • mass movement of cells to form a trilaminar disk
192
Q

when does gastrulation occur

A

in the third-week post fertilisation

193
Q

What does the ecotderm devlop into?

A
  • PNS
  • CNS
  • Sweat glands
  • Posterior pituitary
  • Skin
  • Hair
  • Nails
  • enamel of teeth
  • lens of eyes
  • sensory epithelium of nose, ear and eye
194
Q

What does the endoderm form?

A
  • Epithelial lining of the GI tract, respiratory tract and urinary bladder
  • parenchyma of the thyroid gland parathyroid and liver and pancreas
  • epithelial lining of the tympanic cavity and auditory tube
195
Q

Name the three different components of the mesoderm?

A
  • Paraxial plate mesoderm
  • intermediate plate mesoderm
  • lateral plate mesoderm
196
Q

What does the paraxial plate mesoderm form?

A
  • Somites which give rise to:
    A. Myotome (muscle tissue)
    B. Sclerotome (cartilage and bone)
    C. Dermatome (dermis of the skin)
197
Q

What does the intermediate plate mesoderm form?

A

Urogenital system

  • gonads and respective duct systems
  • kidneys
198
Q

What does the lateral plate mesoderm form?

A

Two layers
1. Somatic (parietal) layer: forms the future body wall
2. Splanchnic (visceral) layer forms:
- Circulatory system
- Connective tissue for the glands
- Muscle, connective tissue and peritoneal components of the
way of the gut

199
Q

What are the 3 stages of heart formation?

A
  1. Formation of primitive heart tube.
  2. Cardiac looping.
  3. Cardiac septation.
200
Q

Describe what happens in the formation of the primitive heart tube.

A
  • By day 19 (third week), two endocardial tubes form. These tubes will fuse
    to form a single, primitive heart tube
  • Day 21: As the embryo undergoes lateral folding, the two endocardial
    tubes have fused to form a single heart tube
201
Q

What is formed from the first Heartfield in the cardiogenic region?

A

Left ventricle

202
Q

What is formed from the second Heartfield in the cardiogenic region?

A
  • Atria
  • Smooth outflow tracts
  • Right ventricle
203
Q

From which germ layer(s) is the cardiovascular system formed?

A
  • Mesoderm

- some contribution from cardiac neural crest cells in the ectoderm

204
Q

Name the five bulges that form in the heart tube

A
  • Truncus arteriosus
  • bulbus cordis
  • primitive ventricle
  • primitive atrium
  • sinus venosus
205
Q

What forms from the truncus arteriosus?

A
  • ascending aorta

- pulmonary trunk

206
Q

What forms from the bulbus cordis?

A
  • Smooth outflow tracts of the left and right ventricles
207
Q

What forms from the primitive ventricle?

A

majority of ventricles

208
Q

What forms from the primitive atrium?

A
  • Both auricular appendages
  • Entire L atrium
  • anterior part of R atrium
209
Q

What forms from the sinus venosus?

A
  • Smooth part of R atrium
  • Coronary sinus
  • Vena Cavae
210
Q

from which day does the heart begin to beat

A

day 22

211
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.

212
Q

Describe what happens in cardiac septation.

A

Endocardial cushions form. Fuse at mid-line to form atrio-ventricular septum. Muscular ridge in the floor of the primitive ventricle migrates to endocardial cushions forming interventricular septum.

213
Q

What does the 1st aortic arch form?

A

Maxillary artery

214
Q

What does the 2nd aortic arch form?

A

Stapedial artery

215
Q

What does the 3rd aortic arch form?

A

Common carotid arteries/ part of internal carotid

216
Q

What does the 4th aortic arch form

A

Left - arch of aorta

right - subclavian

217
Q

What does the 5th aortic arch form?

A

there is no fifth aortic arch

218
Q

What does the 6th aortic arch form?

A

Right - pulomonary trunk

left - ducts arteriosus

219
Q

Briefly describe foetal circulation.

A
  • oxygenated blood from placenta to foetus through umbilical vein
  • bypasses the liver - ductus venosus and into IVC
  • RAp>LAp blood is shunted through foramen ovale
  • most blood moves directly to the aorta via ductus arteriosus
  • deoxygenated blood return to placenta via umbilical arteries near the bladder
220
Q

Describe what occurs in postnatal circulation

A
  • first breath vasodialtion of pulmonary vessels
  • umbilical vein constricts into ligamentum trees
  • umbilical arteries constrict to form medial umbilical ligaments
  • 10-15 hours after birth ductus arteriosus constricts to become the ligamentum arteriosum
  • foramen ovale closes- fossa ovalis
  • ductus venosum constrcits - ligamentum venosum

Phase 1 Med (7 decks)

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