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PHASE 1 Medicine > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

What are the two components of blood and their proportions?

A

Plasma component- 55%

Cellular component- 45%

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2
Q

What is the plasma component made of?

A

Water (91%)
Proteins (8%)
Other (nutrients, hormones, electrolytes) (1%)

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3
Q

What is in the cellular component of blood?

A

Leukocytes, and platelets (1%)

Erythrocytes (99%)

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4
Q

Which proteins are in the plasma component of blood?

A

Albumin/carrier proteins, coagulation factors, and immunoglobulins (antibodies)

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5
Q

How many litres of blood do we have in our body?

A

5 litres

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6
Q

What does Haematocrit mean?

A

Percentage of RBC in the cellular component of blood

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7
Q

What is a normal Haematocrit?

A

45%

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8
Q

Where are Albumin, most carrier protein and coagulation factors made?

A

Liver

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9
Q

Where are Immunoglobulins made? (antibodies)

A

Made by plasma cells

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10
Q

What are Leukocytes and name the types? (never eat brown monkey lungs)

A

Cells involved in body’s immune system

Neutrophils, Eosinophils, Basophils, Monocytes, Lymphocytes

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11
Q

What is Haemopoesis?

A

The formation of blood cells and platelets, which continues throughout life

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12
Q

Where does Haemopoesis occur in adults?

A

Bone marrow of the axial skeleton

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13
Q

Where does Haemopoesis occur in children?

A

Bone marrow of all bones

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14
Q

Where does Haemopoesis occur in foetus?

A

Yolk sac, then Liver and spleen

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15
Q

What is the lifespan of a RBC?

A

120 days

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16
Q

What are the most primative cells?

A

Stem cells

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17
Q

Feature of a stem cell?

A

Pluripotent- can differentiate into RBC, white blood cell and platelets

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18
Q

Platelet lifetime?

A

7-10 days

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19
Q

White blood cell lifetime

A

6 hours

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20
Q

Features of RBC?

A

Anucleate, biconcave disc, contain Haemoglobin (and a membrane to enclose it) and enzymes of glycolysis

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21
Q

What is the HORMONAL GROWTH FACTOR that stimulates precursor stem cells to proliferate and differentiate into RBC and where is it made? (Erythropoesis)

A

Erythropoetin, hormone made in kidney and liver

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22
Q

What happens if precursor cells are found in blood?

A

Not normal, sign of Leukaemia

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23
Q

What is the HORMONAL GROWTH FACTOR that stimulates precursor stem cells to proliferate and differentiate into WBC? (Myelopoesis)

A

G-CSF (granulocyte colony stimulating factor)

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24
Q

What is the HORMONAL GROWTH FACTOR that stimulates precursor stem cells to proliferate and differentiate into platelets and where is it produced? (Thrombopoesis)

A

Tpo (Thrombopoetin)

Liver and kidneys

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25
Q

What is a Reticulocyte?

A

An immature RBC, not usually found in blood

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26
Q

Why does Haemoglobin need to be closed off in a membrane?

A

Haemoglobin would clog up kidneys

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27
Q

Features of Platelets?

A

Anucleate, discoid, which becomes spiculated with pseudopodia once activated

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28
Q

What is the function of a platelet?

A

To create a clot by forming a platelet plug

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29
Q

Where are platelets derived from?

A

Megakaryocytes in bone marrow

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30
Q

What are the two types of granules in platelets?

A

Alpha and dense

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31
Q

What do Alpha platelets contain?

A

Coagulation factors, fibrinogen and other clotting mediators

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32
Q

What do Dense platelets contain?

A

ADP, and platelet activation mediators

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33
Q

Why do RBC have such a short lifespan?

A

Subject to mechanical stress as they flow through vessels
They are simple cells
With no nucleus and have no mitochondria so cannot repair themselves

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34
Q

What happens to the oxygen disassociation curve when PH is decreased or when temperature is increased?

A

Shift to the right

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35
Q

What happens to the oxygen disassociation curve when PH is increased or when temperature is decreased?

A

Shift to left

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36
Q

What is the role of Haemoglobin?

A

Carry oxygen from lungs to tissues, where it transfers oxygen to myoglobin in muscles

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37
Q

What is the Quaternary structure of haemoglobin?

A

2 alpha chains, 2 beta chain, 4 haem groups (Porphyrin with a central ferrous iron ion- Fe2+ which can reversibly bind with oxygen)

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38
Q

What is Anaemia?

A

Reduction in Haemoglobin in blood

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39
Q

What is a normal Haemoglobin level?

A

12.5-15.5 g/dl

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40
Q

What is Polycthaemeia and causes?

A

High concentration of RBC in blood, so blood is thicker and less able to travel through organs.

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41
Q

Symptoms of Anaemia

A

Tiredness, lethargy, reduced exercise tolerance, shortness of breath on exertion and angina

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42
Q

Signs of Anaemia

A

Palor, pale mucous membranes and pink hands, sore tongue, cracking at corners of mouth, spoon shaped nails

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43
Q

Causes of Anaemia?

A
  • Acute blood loss
  • Production mismatch
  • Increased removal of RBC
  • Deficiencies in iron, folate or vitamin b12
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44
Q

What causes iron deficiency Anaemia?

A
  • Occult Gastrointestinal bleeding
  • Menorrhagia (heavy periods)- in premenopausal women only or those who have repeated childbirths
  • Diet- not getting enough iron in diet
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45
Q

What causes B12 deficiency anaemia?

A
  • IF stomach is damaged, less parietal cells, less intrinsic factor so B12 less absorbed
  • Autoimmune disease called Pernicious Anaemia, create antibodies against Parietal cells so less intrinsic factor produced, so B12 malabsorbtiion.
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46
Q

What causes Folate deficiency Anaemia?

A
  • Malabsoption due to celiac disease
  • Dietary- don’t eat enough fruit or vegetables (where folate is found)
  • Increased need, e.g. due to haemolysis or anything that results in increased cells division
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47
Q

What is Macrocytic anaemia?

A

MCV (mean cell Volume of RBC) is more than 100 fl

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48
Q

How can macrocytosis occur without Anaemia?

A

Raised MCV (mean cell volume), but normal haemoglobin levels due to liver disease, alcohol or hypothyroidism

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49
Q

How is Red cell size measured?

A

MCV (mean cell volume) normal= 82-96 fl

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50
Q

What are vitmin b12 and folate needed for?

A

For DNA synthesis, so with a deficiency RBC cannot be made in bone marrow and less are released.
deficiency will affect all dividing cells, but bone marrow most active so is affected first

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51
Q

What is Haemolysis?

A

Normal/increased cell production but decreased lifespan <30 days

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52
Q

Two types of haemolysis?

A

Congenital (present from birth)

Acquired

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53
Q

Describe some types of Congenital haemolysis?

A
  • Membrane issues. e.g. spherocytosis- blood cells are spherical, but they get stuck in vessels easily (less flexible and broken down faster)
  • Haemoglobin issues- e.g. sickle cell (defect in beta globin chain, sickle shaped, get trapped, broken down faster
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54
Q

Describe some types of Acquired Haemolysis?

A
  • Autoimmune- immune system attacks own RBC (e.e.g triggered due to blood transfusion)
  • Mechanical- Fragmentation of RBC due to mechanical heart valve
  • Pregnancy- Haemolytic disease of foetus and newborn (Rhesus)
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55
Q

Describe what is Rhesus disease?

A
  • Mother has Rhesus negative blood and baby has rhesus positive blood.
  • Mothers immune system, recognises foreign Rhesus positive blood, and produces antibodies.
  • Baby might not be affected as it takes time for antibodies to be produced.
  • But if mother has second baby with rhesus positive blood antibodies produced immediately (cross to baby via placenta) and begins destroying babies RBC.
  • Causing Anaemia and Jaundice
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56
Q

What is the most numerous white cell?

A

Neutrophils

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57
Q

What do Neutrophils do?

A

Phagocytose and kill bacteria.

Release chemotaxins and cytokines?

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58
Q

What do Chemotaxins do in Neutrophils?

A

Signal more WBC to come to sight

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59
Q

What do Cytokines do in Neutrophils?

A

Important in inflammatory response

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60
Q

What happens if there is a lack in number or function of Neutrophils?

A

Recurrent bacterial infections

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61
Q

What are the two types of lymphocytes?

A

B & T lymphocytes

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62
Q

What do B lymphocytes do?

A

Differentiate into plasma cells, and produce immunoglobulins when stimulated by exposure of foreign antigen

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63
Q

Where do B lymphocytes mature?

A

In bone marrow

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64
Q

What do T lymphocytes do?

A

Some are helper T cells (CD4), responsible for cell mediated immunity, some are cytotoxic cells (CD8)

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65
Q

What is Acute Leukemia?

A

Prolifration of primative precursor cells, without differentiation.
Results in anaemia, thrombocytopenia (excessive bleeding), and nautropenia (infections as white cells aren’t being differentiated)

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66
Q

What is Prothrombin time?

A

Bleeding time

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67
Q

What is Thrombocytopenia?

A

Reduced numbers of platelets.

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68
Q

What is Thrombocytosis?

A

High number of platelets.

Can lead to arterial and venous thrombosis, leading to an increased risk of heart attack and stroke

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69
Q

Which coagulation factors needs vitamin K for correct synthesis?

A

1972

10,9,7,2

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70
Q

What do coagulation factors do?

A

Circulate in inactive form, need to activate to form thrombin which converts soluble fibrinogen into insoluble fibrin polymer, to make blood clot

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71
Q

Which protein in the blood maintains oncotic pressure, carries FA, steroids and thyroid hormones?

A

Albumin, most numerous protein in plasma

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72
Q

What do carrier proteins carry?

A

Nutrients, hormones

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73
Q

What are Immunoglobulins?

A

Antibodies produced by plasma cells (differentiated B cells)

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74
Q

What is Haemostasis?

A

Arrest of bleeding, blood coagulation and contraction of damaged blood vessels

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75
Q

How is blood fluid, inside blood vessels?

A

Proteins of coagulation cascade and platelets circulate in an inactive state.
They’re activated by tissue factor which is present on every cell apart from endothelial cell

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76
Q

What is the coagulation cascade?

A

Coagulation factors circulation inactive, are activated by tissure factor in cascade sequence, in order to generate key enzyme thrombin which converts fibrinogen into fibrin

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77
Q

In the coagulation cascade, there are multiple complex steps, what do these allow for?

A

Allow for biological amplification and regulation.

Can be graduated in response to severity of challenge

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78
Q

What do Platelets do?

A

Responsible for primary haemostasis, bleeding time, adhere to damaged endothelium and aggregate to form platelet plug that blocks hole in vessel

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79
Q

What is Haemophilia?

A

Recessive X linked disorder
Severe bleeding disorder into muscles and joints.
Not enough clotting factors in blood= slow clotting time, long Prothrombin time.
Only affects males, females are carries

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80
Q

What is Von Willebrands disease?

A

Lack of VWF, which is needed for platelets to bind to damaged blood vessels.
Mild bleeding disorder.
muco-cutaneous bleeding
Autosomal dominant inheritance.

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81
Q

Why does liver disease affect prothrombin time?

A

Site of synthesis of coagulation factors and fibrinogen

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82
Q

What do Heparin and Warfarin do?

A

Oral anticoagulant

Inhibit Vitamin K, affecting coagulation cascade

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83
Q

What causes Polycthemia?

A

Caused by:

  • smoking, lung disease, inefficient lungs so less 02 is exchanged so more Haemoglobin is required.
  • RBC count is normal, but plasma fluid is reduced due to overweight, smoking, drinking, diuretics
  • change to JAK2 gene which causes bone marrow cells to produce too many RBC
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84
Q

Why is iron needed in blood?

A

To produce haemoglobin

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85
Q

Which coagulation factor deficiency causes Haemophilia A and B?

A 
A= deficiency in CF 8
B= deficiency in CF9
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86
Q

What are the types of Immunoglobulins

A 
IgG- most important 
IgM- all start off as this)
IgA
IgE
final two- produced in response to non-self protein antigens
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87
Q

How is vitamin B12 absorbed into the body?

A

To be absorbed in the terminal ileum, B12 must bind to intrinsic factor produced in gastric parietal cells in stomach.

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88
Q

How many blood groups are there, and what are they?

A

4

A, B, AB, O

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89
Q

Which antibodies and antigens do type A individuals have?

A

A antigen on RBC surface

Anti-B antibodies in plasma

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90
Q

Which antibodies do type B individuals have?

A

B antigen on RBC surface

Anti- A antibodies in plasma

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91
Q

Which antibodies and antigens do type AB individuals have?

A

Both A and B antigens
Neither anti- A or B antibodies
UNIVERSAL RECIPIENT

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92
Q

Which antibodies and antigens do Type O individuals have, and what is the benefit?

A

No A or B antigens on surface of RBC
Both, Anti-A and Anti- B antibodies in plasma
UNIVERSAL DONOR, so can give to someone in emergency

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93
Q

What happens if someone with Type A blood was transfused with Type B blood?

A

Anti B antibodies in the recipients blood would attack the transfused blood.
Anti A antibodies in donor blood would attack recipients blood, but little consequence as it becomes diluted in plasma so ineffective

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94
Q

What does Rhesus positive mean?

A

D antigen is present (and vice versa for Rhesus negative)

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95
Q

What is the normal number of platelets in the blood?

A

140-400 x10<9/L

96
Q

If you have reduced numbers of platelets, (THROMBOCYTOPENIA) you get increased bleeding at __ and spontaneous bleeding at __

A
  1. > 80

2. >20

97
Q

Why is increased no. of platelets dangerous? Thrombocytosis

A

Leads to arterial and venous thrombosis, increasing risk of heart attack or stroke

98
Q

Are plasma proteins soluble or insoluble?

A

Soluble

99
Q

What does a lack of Albumin result in ?

A

Oedema

100
Q

Acquired bleeding disorders causes?

A
  • Antiplatelets/anticoagulation medication
  • Liver disease
  • Vitamin K deficiency
  • Drugs
101
Q

How do steroids cause bleeding?

A

Thin tissues and cause bruising and bleeding

102
Q

What does Aspirin do to cause bleeding?

A

Affects platelet function

103
Q

What is Disseminated intravascular coagulation?

A

Simultaneous bleeding and microvascular thrombosis

104
Q

Causes of Disseminated intravascular coagulation?

A
  • Sepsis
  • Obstretic (anything goin wrong with pregnancies, death of foetus etc…)
  • Malignancy
105
Q

How does Disseminated intravascular coagulation occur?

A

Coagulation cascade is activated in blood vessels.
Thrombin is produced turning fibrinogen into fibrin, forming platelet plugs everywhere.
This uses up clotting factors and platelets, causing a deficiency.

106
Q

How do platelets adhere to collagen fibres?

A

It adheres to the Von willebrand factor which is attached to collagen via a receptor on the platelet membrane called Glycoprotein 1b receptor

107
Q

What is the first response when a blood vessel is damaged?

A

Constrict (due to neural control)

Release of endothelin-1 (released by endothelia cells)

108
Q

What does constriction of a blood vessel and release of endothelia-1 cells

A

Temporarily slows blood flow in affected area.
Opposed ends of endothelial surfaces press together, and contact induces a stickiness capable of keeping them glued together

109
Q

What does the stopping of blood depend on?

A

Formation of a platelet plug and blood coagulation which involves platelets

110
Q

When platelets bind to the collagen fibre wall what does it trigger the platelets to release?

A

The contents of their secretory vesicles via exocytosis

Platelet dense granules

111
Q

What happens when a vessel is injured?

A

Endothelium is disrupted and collagen fibres are exposed

112
Q

When are platelet dense granules released?

A

On cell activation and when platelets bind to the collagen fibre wall

113
Q

What do platelet dense granules release?

A

ADP

114
Q

What does the ADP from platelet dense granules do?

A

Acts on the P2Y1 and P2Y12

causing platelet amplification

115
Q

Where does thrombin bind and what does it cause?

A

PAR1 and PAR4 receptors
Induced platelet activation and further thrombin release
Positive feedback

116
Q

What is platelet activation?

A

Platelets change shape from a smooth discoid shape to more spiculated with pseudopodia.
This increases surface area

117
Q

What is platelet aggregation?

A

Platelet activation causes an increase in the expression of glycoprotein llb/lla receptors on platelets which bind to fibrinogen.
New platelets bind to old ones
Positive feedback mechanism

118
Q

What does platelet adhesion cause?

A

Rapid inducing of Thromboxane A2 synthesis

Which releases into the extracellular fluid

119
Q

What does Thromboxane cause?

A

Vasoconstriction and platelet activation

Acts locally to further stimulate platelet aggregation and therelease of there secretory vesicle contents

120
Q

What does a platelet plug do?

A

Completely seal small breaks in vessels.

121
Q

How do platelets contract (leading to the compression and strengthening of the platelet plug)?

A

High concentration of actin and myosin

122
Q

How does the contraction of the vascular smooth muscle in a damaged vessel at the same time platelet activation/aggregation and plug formation affect blood flow?

A

Decreasing blood flow to the area and pressure within the damaged vessel

123
Q

What causes vasoconstriction?

A

Thromboxane released due to platelet adhesion and by chemicals contained in the platelets secretory vesicles.

124
Q

Why doesn’t the Platelet plug expand away from damaged endothelium?

A

The undamaged side synthesises and releases prostacyclin (also known as prostaglandin I2 vasodilator)
which is a profound inhibitor of platelet aggregation
And releases nitric oxide, (which is a vasodilator) and an inhibitor of platelet adhesion, activation and aggregation.

125
Q

What is blood clotting/coagulation?

A

Transformation of blood into a solid gel/clot consisting of protein polymer fibrin

126
Q

Where does clotting occur and what is its function?

A

Clots occur locally around the platelet plug to support and reinforce the platelet plug and and solidify the blood that remains in the wound channel

127
Q

The coagulation cascade can be divided into two parallel pathways. What are they?

A

Extrinsic (an cellular element outside the blood is needed) and the Intrinsic (everything necessary for it is within the blood)

128
Q

Intrinsic pathway of the coagulation cascade

A

Factor 12 converts into Factor 12a due to exposed collagen fibres
Which catalyses the activation of factor 11 into 11a
which activates 9 into 9a, which converts 10 into 19a (with the help of factor 13)
Factor 10a converts prothrombin into thrombin, which converts fibrinogen into fibrin.

129
Q

What is the first plasma protein in the intrinsic pathway called and how is it activated

A 
Factor XII (12)
activated into Factor XIIa when it comes into contact with exposed collagen fibres underlying the damaged endothelium
(Known as contact activation)
130
Q

What does Factor XIIa (12) cause?

A

Catalyses the activation of factor XI (11)to factor XIa

131
Q

What does Factor XIa (11) cause?

A

Catalyses the activation of factor IX (9) to Factor IXa

132
Q

What does factor IXa (9) catalyse the activation of, (with the help of factor VIIIa)

A

Factor X (10) into Xa

133
Q

In Haemophilia, which factor is there a lack of?

essential for clotting

A

Factor VIII (13)

134
Q

What is the enzyme factor Xa (10) responsible for?

A

Converts prothrombin to thrombin

135
Q

What does Thrombin do?

A

Converts soluble fibrinogen into insoluble fibrin

136
Q

What does fibrin do?

A

Secures the blood clot and builds it up

137
Q

What does the extrinsic pathway being with?

A

A protein called TISSUE FACTOR, located on the outer plasma membrane of various tissue cells, (Outside the endothelium)

138
Q

What does the extrinsic pathway begin with?

A

A protein called TISSUE FACTOR, located on the outer plasma membrane of various tissue cells, (Outside the endothelium)

139
Q

What does the tissue factor do when the endothelial lining is disrupted?

A

Tissue factor binds to factor VII (7) which becomes activated to factor VIIa

The complex of tissue factor and factor 7a catalyse reaction of factor 10 into factor 10a

Also, the complex catalyses the activation of factor IX, which can help activate even more factor X via intrinsic pathway

140
Q

What are the two ways the clotting cascade can be initiated?

A

Activation of factor XII

and generation of the tissue factor- factor VIIa complex

141
Q

Which factors does Thrombin help to activate?

A

Factors 11 and 13 in the intrinsic factor

Factor 5, with factor 5a serves as a cofactor for factor Xa

142
Q

What is the usual way of initiating clotting (extrinsic or intrinsic)?

A

Extrinsic with the tissue factor

Intrinsic factor plays little role

143
Q

What is thrombin initially generated by?

A

Extrinsic pathway

144
Q

Is the amount of thrombin produced initially by the extrinsic pathway adequate to sustain coagulation?

A

No, it is too little!
But it can trigger Thrombin’s positive feedback mechanisms on the intrinsic pathway.
(Activation of factor 10,13, and 9 and platelets)
this pathway generates large amounts of thrombin for adequate coagulation

145
Q

What does the liver produce?

A

Plasma clotting factors

Bile salts

146
Q

Why are bile salts important in blood clotting?

A

Bile salts are needed for the absorbtion of lipid-soluble substance vitamin K.
Liver needs vitamin K to produce prothrombin and several other clotting factors

147
Q

How is a fibrin blood clot broken down?

A

Plasminogen is converted, by plasminogen activators, into plasmin which breaks fibrin down

148
Q

Why do we need more plasma in the blood that RBC?

A

Keeps cells fully suspended in fluid, easy to pump round, less chance of clotting

149
Q

Cardiac muscle

A

Found only in the heart
combines properties of both skeletal and smooth muscle

Has a striated appearance (like skeletal) due to regularly repeating sarcomeres composed of myosin-containing thick filaments interdigitating with thin filaments that contain actin

Individual cardiac muscle cells are relatively small and generally contain a single nucleus

Adjacent cells are joined end to end at structures called intercalated discs- within which are desmosomes that hold the cells together and to which the myofibrils are attached. Also found within intercalated disks are gap junctions

Cardiac muscle cells are arranged in layers around the blood-filled chambers of the heart

150
Q

Ultrastucture of the myocardial cell

A

Contractile proteins (actin & myosin) are arranged in a regular array of thick (myosin) and thin (actin) filaments - known as myofibrils

151
Q

Myosin?

A

Forms majority of thick filament

composed of two large polypeptide heavy chains and 4 smaller light chains

These polypeptides combine to form a molecule that consists of two globular heads (containing heavy and light chains) and a long tail formed by the two intertwined heavy chains

The tail of each molecule lies along the axis of the thick filament and two globular heads extend out to the sides forming cross-bridges, which make contact with the thin filament and exert force during muscle contraction

Each globular head contains two binding sites, one for attaching to the thin filament and one for ATP.
Attached to the myosin head is an inorganic phosphate molecule (Pi) and ADP.

The ATP binding site also serves as an enzyme - an ATPase that hydrolyses the
bound ATP, harnessing its energy for contraction

152
Q

Actin?

A

Forms majority of thin filament

The thin filament is composed mainly of actin, but also of troponin & tropomyosin
(play important roles in regulating contraction)

Actin is a globular protein composed of a single polypeptide (a monomer) thatpolymerises with other actin monomers to form a polymer made up of two
INTERTWINED, helical chains. These chains make up the core of the thin filament.

Each actin molecule contains a binding site for myosin

153
Q

What is tropomyosin?

A

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

154
Q

What is troponin?

A

Protein that changes shape when Ca2+ binds to it, when it does it
changes shape in doing so pushes the tropomyosin EXPOSING myosin binding
sites on actin enabling contraction to occur

155
Q

What is the A band in a sarcomere?

A

The region of the sarcomere occupied by thick and a few overlapping thin
filaments - overall there are twice as many thin as thick filaments in the region of
filament overlap

156
Q

What is the I band in a sacromere?

A 
Occupied only
by thin filaments that
extend to the centre of
the sarcomere from the
Z-lines - two successive Z lines defines the limits of one sarcomere.

It also contains tropomyosin and troponin (located on
the actin filament)

157
Q

What is the H zone in a sacromere?

A

Contains only thick filaments (myosin)

158
Q

What is the M line in a sarcomere?

A

In the centre of the
H-zone, comprised entirely of thick filament myosin.

Corresponds to proteins that link together the central region of adjacent thick filaments

159
Q

What is titin?

A

Elastic protein filaments, extend from the Z-line to the M-line, linked to both
the M-line proteins and the thick filaments.

Both the M-line linkage between the thick filaments and the Titin filaments act to maintain the alignment of the thick filaments in the middle of each sarcomere

160
Q

What are the bands of one of the sarcomere?

A

2 half I-bands, 1 A-band, 1 H-zone, 1 M-line and 2 Z-lines

161
Q

Sarcoplasmic reticulum?

A

Membrane network that surrounds the contractile protiens. Releases Ca2+ when Ca2+ binds to it ryanodine receptor

162
Q

How is the resting cardiac myoctye membrane (sarcolemma) maintained?

A

Membrane is more permeable to K+ (since K+ channels are open meaning K+ is leaving the cell)

Na+/k+ ATPase pumps (pumping 3Na+ ions out for every 2K+ ions pumped in)

Resting potential is closer to K+ equilibrium potential (-90mV) than to the Na+ equilibrium potential (+60mV)

163
Q

What happens when an action potential arrives?

A

Na+ voltage gated Na+ channels are opened, and Na+ entry depolarises the cell, triggering more Na+ channels to open- positive feedback effect

164
Q

What happens when a potential in cell is positive?

A

When potential in cell is positive (+52mV) then voltage gated Na+ channels close, at the same time voltage gated K+ channels open= partially repolarising the cell

165
Q

What happens during partial re polarisation?

A

Outflow of K+, Ca2+ voltage gated channels finally open at T-Tubules which are in part of the sarcolemma (myocyte membrane), resulting in the inflow of Ca2+ into the cell, since these channels remain open for a long duration of time they are often referred to as L-type Ca2+ channels (L=long lasting), these channels are modified versions of the dihydropyridine (DHP) receptors that function as voltage sensors in excitation-contraction coupling of skeletal muscles

166
Q

How is the cell kept polarised?

A

The flow of Ca2+ ions into the cell just balances the flow of K+ ions out of the cell and keeps the membrane depolarised at the plateau level of roughly 0mV (K+ channels open at the start also close-maintaining depolarisation)

167
Q

Why does repolarisation occur?

A

Eventual closure of L-type Ca2+ channels and the reopening of the K+ channels (the ones open at the start)- similar to the ones in neurons and skeletal muscle;

they open in response to depolarisation (after a delay) and close once K+ current has depolarised the membrane back to negative values

168
Q

Quick summary of Cardiac action potential

A

0- Rapid depolarisation; Na+ inflow

1- Partial repolarisation; K+ outflow, Inflow of Na+ stops

2- Plateau, Ca2+ slow inflow

3- Repolarisation, K+ outflow, inflow of Ca2+ stops

4- Pacemaker potential; Na+ inflow, slowing of K+ outflow

169
Q

Excitation contraction coupling in cardiac muscle

A

When AP is generated, influx of Ca2+ via the T-tubules via L-type Ca2+ voltage gated channels.

Not only does this Ca2+ influx aid depolarisation but it also causes a small increase in cytosolic Ca2+ concentration

Small amount of Ca2+ ions that influx (too small to be able to initiate muscle contraction) bind to ryanodine receptors on the sarcoplasmic reticulum- this binding causes the sarcoplasmic reticulum to release many Ca2+ ions into the cytoplasm of the cell- initiating cardiac muscle contraction- the start of the CROSS-BRIDGE cycle

170
Q

Excitation contraction coupling in cardiac muscle

A

When AP is generated, influx of Ca2+ via the T-tubules via L-type Ca2+ voltage gated channels.

Not only does this Ca2+ influx aid depolarisation but it also causes a small increase in cytosolic Ca2+ concentration

Small amount of Ca2+ ions that influx (too small to be able to initiate muscle contraction) bind to ryanodine receptors on the sarcoplasmic reticulum- this binding causes the sarcoplasmic reticulum to release many Ca2+ ions into the cytoplasm of the cell- initiating cardiac muscle contraction- the start of the CROSS-BRIDGE cycle

Ca2+ binds to the Ca2+ binding site on troponin protein on actin filament

This causes troponin to change shape and thus displace the tropomyosin protein on the actin filament exposing the myosin binding sites

The myosin head on the myosin filament then binds to the actin filament via the myosin binding site, the inorganic phosphate i dropped in order for the myosin head to bind to the actin, the ADP still remains attached to the head- this is known as cross-bridge formation

The myosin head then drops the ADP to contract and pull the actin filament OVER the myosin filament - thereby decreasing the Z lines resulting in muscle
contraction - this is know as the power stroke

ATP then binds to the myosin head, detaching the head from the actin filament, and moving the head to its start position

The ATPase in the myosin head then hydrolyses the ATP into ADP & Pi ready for
the next contraction IF THE MYOSIN BINDING SITES REMAIN OPEN

NOTE: ATP is required for the myosin head to detach from the actin - in rigour
mortis when the person is dead, there is no ATP meaning the myosin head DOES NOT detach - resulting in stiffness of the skeletal muscles

Contraction stops when cytosolic Ca2+ concentration is restored to its original extremely low resting value by primary active Ca2+ - ATPase pumps in the sarcoplasmic reticulum & sarcolemma AND Na+/Ca2+ counter-transporters in the sarcolemma.

The amount of Ca2+ returned to the extracellular fluid & sarcoplasmic reticulum EXACTLY MATCHES the amounts that entered the cytosol during excitation

171
Q

How does cardiac contraction differ to skeletal muscle?

A

Contraction lasts longer than in skeletal muscle- up to 15 times longer in duration; this is due to the slow calcium channels

The refractory period is the period of time after an action potential where second impulse cannot cause a second contraction of cardiac muscle:

To prevent excessive frequent contraction

Allow adequate filling time

172
Q

Blood supply of myocardial cells

A

Coronary arteries exit behind aortic valve cusps in the very first part of the aorta

Most of the coronary arteries drain into a single vein called coronary sinus, which empties into the right atrium

173
Q

Propagation of action potential and heartbeat coordination

A

1% of cardiac cells done contract, but are specialised called the conducting system

They are in electrical contact with the cardiac myocytes via gap junctions

The conducting system initiates the heartbeat and helps spread the action potential rapidly throughout the heart

Gap junctions interconnect myocardial cells and allow AP to spread from one cell to another. The AP spreads over cell membranes.

Positive charge from Na+ affects adjacent cells, resulting in depolarisation the newly depolarised cells can cause further depolarisation and the gap junctions enable ions to travel directly to other cells.

The initial excitation of one cardiac cell allows eventually results in the excitation of all cardiac cells

This initial depolarisation normally arises in a small group of conducting-system cells called the sinoatrial node (SAN)- Located in the right atrium near the entrance of the superior vena cava, the action potential then spreads from the SA node thorguhout the atria and then into and throughout the ventricles

174
Q

Sinoatrial node

A

Normally determines the rate the heart beats at - the number of times the heart
contracts per minute

Resting membrane potential of -55 to -60 mV - this is closer to the threshold of depolarisation thus it depolarises first, it is closer to the depolarisation threshold due to its slow Na+ inflow not found anywhere else in the body

175
Q

Action potentials

A

The SA node does not have a steady resting potential, instead it undergoes SLOW DEPOLARISATION - this is known as the pacemaker potential; it brings the membrane potential to a threshold, at which point an action potential occurs

Three ion channel mechanisms contribute tot he pacemaker potential

The first is the progressive reduction in K+ permeability. the K+ channels that opened during repolarisation phase of the previous action potential gradually close due to the membranes return to negative potentials

Second, pacemaker cells have a unique set of channels that, unlike most voltage gated channels, open when the membrane potential is at NEGATIVE values - these non-specific cation (positive ions) conduct mainly an inward Na+ current, since
this is not normal these channels are referred to as “funny” and are thus called F-type channels

The third channel is a Ca2+ channel; that opens very briefly but contributes to an in ward current of Ca2+ which acts as an important final depolarising boost to the pacemaker potential. Since the channel is only opened briefly it can be called transient so these channels are known as T- type Ca2+ channels

Although the SA node and AV node action potential are similar in shape, the
pacemaker currents in the SA node bring them to threshold more rapidly than the AV node, which explains why the SA node normally initiates action potentials &
determines the pace of the heart

Once the pacemaker mechanisms have brought a nodal cell to threshold, an action potential occurs. The depolarising phase is not caused by Na+ but instead by Ca2+ influx through L-type Ca2+ channels. These Ca2+ currents depolarise the membrane more slowly than voltage-gated Na+ channels, and one result of this is that action potential propagate more slowly along nodal cells than in other cardiac cells. This explains the slow transmission of cardiac excitation through the AV node

Thus the pacemaker potential provides the SA node with automaticity - the ability for spontaneous, rhythmic self-excitation

The action potential initiated at the SA node spreads through the myocardium,
passing from cell to cell by way of gap junctions

Depolarisation first spreads through the muscle cells of the atria - with conduction
being rapid enough that the right & left atria contract simultaneously

The spread of the action potential to the ventricles involves a different conducting system called the atrioventricular node (AVN) - the action potential is conducted relatively rapidly from the SA node to the AV node through the internodal pathways

176
Q

Atrioventricular node

A

Located at the base of the right atrium - transmits cardiac impulse from atria to ventricles

Consists of modified cardiac cells that have
lost contractile capability but conduct action potentials with LOW RESISTANCE

Elongated structure with an important feature; the propagation of action potentials through the AV node is RELATIVELY SLOW
(requiring approximately 0.1 secs) - this is IMPORTANT since it enables the atria to
EMPTY BLOOD into the ventricles, enables atrial contraction to be completed before
ventricular excitation occurs

After the AV node has been excited, the action potential progresses down the interventricular septum - this pathway of conducting fibres is called the bundle of His

The AV node and the bundle of His constitute the ONLY electrical connection between
the atria and ventricles - except from THIS PATHWAY the atria are completely isolated from the ventricles by a layer of nonconducting connective tissue

Within the interventricular septum, the bundle of His divides into right & left bundle branches, conducting fibers that separate at the bottom (apex) of the heart and enter the walls of both ventricles

These fibers in turn make contact with Purkinje fibers, large-diameter conducting cells that rapidly distribute the impulse throughout much of the ventricles

Finally the Purkinje fibres make contact with ventricular myocardial cells - which spread the action potential through the rest of the ventricles

The conduction from the AV node to the ventricles is RAPID to enable coordinate ventricular contraction

177
Q

Parasympathetic stimulation of the heart (rest and digest)

A

Fibers are transmitted via the vagus nerve (CN10)

Controlled by acetylcholine which bind to muscarinic receptors

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

178
Q

Sympathetic stimulation of the heart (fight or flight)

A

Sympathetic postganglionic fibers innervate the entire heart

Controlled by adrenaline & noradrenaline

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%

179
Q

What is the ECG?

A

NOT a DIRECT RECORD of the changes in membrane potential across
individual cardiac muscle cells. But instead it is a measure of the currents
generated in the EXTRACELLULAR FLUID by the changes occurring
simultaneously in many cardiac cells

180
Q

Normal traces of ECG

A

P wave: atrial depolarisation - seen in every lead apart from aVR

PR interval: time taken for atria to depolarise and electrical activation to get
through AV node

QRS complex: ventricular depolarisation, still called QRS even if Q and/or S are
missing depending on what lead you are looking at

ST segment - interval between depolarisation & repolarisation

T wave: ventricular repolarisation

181
Q

Definition of Tachycardia?

A

Increased heart rate

182
Q

Definition of Bradycardia?

A

Decreased heart rate

183
Q

Definition of Dextrocardia?

A

Heart on the right side of chest instead of left

184
Q

What is an acute anterolateral myocardial infarction?

A

ST segments are raised in anterior (V3

- V4) and lateral (V5-V6) leads

185
Q

What is an acute inferior MI

A

ST segments are raids in inferior (II, III, aVF) leads

186
Q

Why isn’t atrial repolarisation evident usually on an ECG?

A

Occurs at same time as QRS complex so is hidden

187
Q

How do electrical impulses in heart move?

A

Electrical impulses in the heart move in 3 dimensions

ECG only measure voltage in 1 dimension

If an impulse is towards the electrode it looks big

If an impulse is away from the electrode it looks small or even negative

If impulse from the atria is smaller since the atria are smaller than the ventricles thus less myocytes

188
Q

Lead positions of ECG

A

Standard limb leads (I, II & III) form a triangle between electrodes on the wrists
and left leg (right leg is a ground electrode) - the negative poles are REFERENCE electrodes and the positive poles are
RECORDING electrodes

Augmented leads (aVR, aVL &amp; aVF) bisect the angles of the triangle by combining two electrodes as reference e.g. for lead aVL,
the right wrist &amp; foot are combined as the negative pole, thus creating a reference point along the line between them, pointing
toward the recording electrode on the left wrist

The precordial leads (V1 - V6) - recording electrodes placed on the chest

When reading an ECG, the graph shows changes in voltage over time, each small
square across represents 40ms & each big square across represents 0.2s

In a normal ECG the p waves are POSITIVE in EVERY LEAD (apart from the aVR)

T waves are POSITIVE in EVERY LEAD (apart from the aVR & sometimes the V1 and V2 depending on trace)

189
Q

What is systole?

A

Systole: ventricular contraction & blood ejection - 0.3 seconds:

  1. Isovolumetric (iso- equal/unchanging) contraction of the ventricles (increase in
    pressure but volume remain the same since valves remain closed) - isovolumetric
    contraction + relaxation is the only time when all valves of the heart are closed
  2. Once the pressure in the ventricles exceeds that in the aorta & pulmonary trunk
    the aortic & pulmonary valves open and maximal ejection from ventricles into
    the arteries occurs - ventricles DO NOT COMPLETELY EMPTY during
    contraction
190
Q

What is diastole?

A

Diastole: ventricular relaxation & blood filling - 0.5 seconds:

  1. Reduced ejection
  2. Ventricles begin to relax and aortic and pulmonary valves close - at this time the atrioventricular valves are closed thus no blood is entering or leaving the
    ventricles - ventricular volume is not changing known as isovolumetric ventricular relaxation (decrease in pressure but volume remains the same)
  3. Rapid left ventricle filling and ventricle suction - since blood in the atria is slightly
    pressurised due to the venous return from the superior + inferior vena cava & pulmonary vein, pressure is enough to open mitral (or bicuspid left) and tricuspid valves (right), also since there is a lower pressure in the ventricles blood just rushes in down the pressure gradient (effectively sucked in) - this is responsible for 80% of ventricular filling before atrial contraction
  4. Slow ventricular filling - since blood keeps flowing into atria from the veins,
    pressure between the atrium and ventricle are equalising thus slowing filling this pressure equalisation is known as DIASTASIS - where there is little to no net movement of blood, at this point the AV node is delaying the stimuli from the SAN to allow full ventricular filling
  5. Atrial booster- pressure suddenly increases due to atrial contraction, enables
    ventricles to be actively filled - squeezing remaining blood from atria into ventricles
191
Q

For a normal heart, what is the typical heart rate

A

For a normal heart with a typical heart rate of 72 beats/min, each cardiac cycle lasts 0.8 seconds, with 0.3 sec in systole & 0.5 sec in diastole

192
Q

Where is the left ventricle palpated and which beat is it responsible for?

A

Palpated in the 5th left intercostal space and mid-clavicular line,
responsible for the apex beat

193
Q

Stroke volume definition

A

The volume of blood ejected from each ventricle during systole

194
Q

Cardiac output definition

A

The volume of blood each ventricle pumps as a function of time (liters per minute)

195
Q

Total peripheral resistance definition

A

The total resistance to flow in systemic blood vessels

from beginning of aorta to vena cava - arterioles provide the most resistance

196
Q

What is preload?

A

The volume of blood in the left ventricle which stretches the cardiac
myocytes before left ventricular contraction - how much blood is in the ventricles before it pumps (end-diastolic volume). When veins dilate it results in a decrease in preload (since by dilating veins the venous return decreases).

197
Q

What is afterload?

A

The pressure the left ventricle must overcome to eject blood during
contraction - dilate arteries = decrease in afterload

198
Q

What is the definition of contractility?

A

Force of contraction and the change in fibre length - how hard the heart pumps. When muscle contracts myofibrils stay the same length but the sarcomere shortens - force of heart contraction that is independent of sarcomere
length

199
Q

What is the definition of elasticity?

A

Myocardial ability to recover normal shape after systolic stress

200
Q

What is the definition of diastolic dispensibility?

A

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

201
Q

What is the definition of compliance?

A

How easily the heart chamber expands when filled with blood volume

202
Q

What is the definition of 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

203
Q

When is the cardiac muscle not at optimal length?

A

At rest the cardiac muscle is not at optimal length. Below optimal length means the force of contraction is decreased - inefficient

204
Q

What does an increased venous return lead to?

A

increased venous return leads to an ↑ end diastolic volume
↑ preload
↑ sarcomere stretch
↑ force of contraction
Therefore, ↑ stroke volume and force of contractions

205
Q

When standing what happens to venous return?

A

Standing decreases venous return due to gravity thus, cardiac output decreases,
which causes a drop in blood pressure, stimulating baroreceptors to increase
blood pressure

206
Q

What is intrinsic autoregulation?

A

When the arterioles either vasoconstrict or vasodilate in response to changes in resistance seemingly automatically - with the aim of maintaining constant blood flow

207
Q

What is myogenic autoregulation?

A

When blood flow is increased and stretches vascular smooth muscle the muscle automatically constricts until the diameter is normalised
or slightly reduced.

Furthermore when the smooth muscle isn’t getting stretched as
much due to low blood pressure, the muscle relaxes and dilates in response.

208
Q

What is hyperemia?

A

Increase in blood flow

209
Q

What is active hyperemia?

A

Increase in blood flow when metabolic activity is increased

210
Q

What is reactive hyperemia?

A

When an organ or tissue has had its blood supply completely occluded a profound transient increase in its blood flow occurs if blood flow is reestablish- extreme form of autoregulation

211
Q

What are the three heart sounds?

A

There are three heart sounds:

One is a soft, low pitched lub, associated with the closure of the atrioventricular
valves

The second is, a louder dub is associated with the closure of the aortic &
pulmonary valves

The third is the sounds of blood rushing into the left ventricle

212
Q

What is the main goal of control of circulation

A

Key component is central neural control

Maintain mean systemic arterial pressure (MAP)- the average blood pressure in the arteries during the cardiac cycle

213
Q

What is Mean systemic arterial pressure (MAP)?

A

MAP is equal to the diastolic pressure (DP) plus one-third of the pulse pressure
(systolic pressure (SP) - DP)

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

214
Q

Effectors of control of circulation?

A

Blood vessels
Heart
Kidney

215
Q

The medullary cardiovascular centre

A

Located in the medulla, within this there is a region called the pressor region (region for raising blood pressure)- it is sympathetic

Pressor region increases blood pressure by ↑ vasoconstriction, ↑ cardiac
output (by ↑ heart rate and stroke volume (more forceful contraction)) and ↑
contractility

Pressor region > sympathetic route > medulla > spinal cord > synapses at T1-L2
> Heart

Also located in the medulla, within the medullary cardiovascular center is a region called the Depressor region (region responsible for lowering blood pressure) - it is parasympathetic

The depressor region decreases blood pressure by inhibiting the pressor region

Depressor region > medulla > vagus nerve > heart

216
Q

What do central chemoreceptors in the medulla do?

A

Respond mainly to a decrease in pH (due

to CO2 diffusing across the blood brain barrier thereby reducing the pH of the CSF

217
Q

Where are cardiopulmonary baroreceptors located and what do they do?

A

Located in the atria, ventricles & pulmonary artery

When stimulated i.e high blood pressure leads to the inhibition of the pressor
region/ vasoconstrictor centre in the medulla - leading to a fall in blood pressure

Also inhibits the Renin-angiotensin & aldosterone system - since angiotensin II stimulates vasoconstriction which will increase blood pressure, also aldosterone
stimulates more Na+ and thus H2O reabsorption thereby increasing blood volume and thus pressure

Also inhibits vasopressin/ADH - since it too stimulates more water reabsorption

Thus when stimulated the cardiopulmonary baroreceptors bring about a decrease in blood pressure by promoting vasodilation & fluid loss

218
Q

Peripheral control of circulation?

A

The total peripheral resistance is MAINLY dependent on arteriole resistance, this is because ARTERIOLES ARE THE PRINCIPAL SITE OF RESISTANCE TO
VASCULAR FLOW

Arterioles
Local factors
Hormonal factors
Peripheral chemoreceptors
Arterial baroreceptors
219
Q

How do arterioles do peripheral control of circulation?

A

Respond to blood pressure- when the muscle of the arteriole contracts the radius decreases causing the resistance to flow to increase thus causing blood flow to decrease and vice versa

220
Q

What is the Local factors that control the peripheral circulation?

A

Vasoconstrictors (smooth vascular muscle constricts):
* Endothelin-1 (ET-1) released by endothelium cells results in vasoconstriction [potent]

  • Increase in internal blood pressure, resulting in myogenic contraction (when
    smooth muscle is stretched there will be automatic contraction until diameter is
    normalised or slightly reduced) due to the blood pressure increase - this is
    autoregulation

Vasodilators (smooth vascular muscle relaxes):
*Hypoxia- When 02 supply decreases, there will be an accumulation of vasodilator metabolites which will dilate vessels to increase blood flow.

  • Increased C02
  • Decreased Ph
  • Bradykinin
  • Nitric Oxide: released by endothelial cells- triggers vasodilation [POTENT]
  • Increased K+
  • H+
  • Tissue breakdown products e.g. lactic acid
  • Prostacyclin/prostaglandin 12 (PG12)- Released by endothelial cells- triggers vasodilation [POTENT]
221
Q

What are the hormonal factors that control circulation?

A

Vasoconstrictors: Angiotensin II, Vasopressin and adrenaline

Vasodilators: Atrial Natriuretic Peptide, adrenaline (sometimes refered to as epinephrine, can be both vasodilator and vasoconstrictor depending on which receptors are present

222
Q

What are peripheral chemoreceptors?

A

In the aortic arch and carotid sinus (base of internal carotid artery- at the division between the internal and external carotid), stimulated by a fall in PaO2 and a rise in PaCo2 AND a fall in PH causing blood pressure to increase

223
Q

What are arterial baroreceptors?

A

These are stretch receptors that respond to pressure:

One found in the aortic arch: aortic arch > vagus > medulla: ↓ sympathetic & ↑
parasympathetic = ↓ in blood pressure

Two found where the left and right common carotid divide into two smaller arteries
(internal & external carotid) - this portion of the artery is known as the CAROTID
SINUS (found at the base of the internal carotid): carotid sinus > sinus nerve >
glossopharyngeal > medulla: ↓ sympathetic & ↑ parasympathetic = ↓ in blood
pressure

Baroreceptors cause some inhibition of the Renin-angiotensin & aldosterone system,
and are involved in short term blood pressure control

Cardiopulmonary baroreceptors (in atria, ventricles &amp; pulmonary artery) control
long term blood pressure
224
Q

Equation for cardiac output

A

Cardiac Output (CO) = Heart Rate (HR) x Stroke Volume (SR) [typically 5 L/min]

225
Q

Equation for blood pressure?

A

Blood Pressure = CO x Total Peripheral Resistance (TPR)

226
Q

Equation for pulse pressure

A

Pulse pressure (PP) = Systolic - Diastolic pressure

227
Q

Equation for mean arterial pressure (MAP)

A

Mean Arterial Pressure (MAP) = Diastolic pressure + 1/3 PP

228
Q

Equation for stroke volume

A

Stroke Volume = End Diastolic Volume (EDV) - End Systolic Volume (ESV)

229
Q

Equation for Poiseuille’s equation: Flow

A

Poiseuille’s equation: Flow = radius to the power of 4

230
Q

Equation for Ohms law: Flow

A

Pressure gradient/resistance

231
Q

Arteries

A

Contain mainly elastic, collagen & smooth muscle

The intima is composed of an inner surface lining of endothelial cells & a very small amount of collagen

The adventitia shows mainly collagenous connective tissue

There are two elastic laminae, one at the interface of the intima and media and the other on the outer edge of the media

232
Q

Arterioles

A

May have an obvious media & adventitia

Smaller arterioles show only a few medial cells with a poorly defined elastic lamina

A thin adventitia & normal intima also exist

233
Q

Endothelium

A

Single layer or spindle/pavement cells with tight adhesions between adjacent cells

Little cytoplasm and intra-cellular organelles - but gap/adheren junctions are
prominent

They may be fenestrated (have pores in them for rapid diffusion) in the liver, kidney
glomeruli & endocrine tissues

In some areas they may be very thin (lung) to enable rapid fluid & gas transfer

234
Q

Capillaries?

A

Tubes of endothelial cells (one cell thick wall - for
rapid diffusion) bound to a basement membrane
with co-existing pericytes

Pericytes have muscle fibres and may regulate
blood flow

235
Q

Venules and veins

A

Show variable thickness

Veins generally have collagen and little muscle & elastic with the wall & a single internal elastic lamina

Veins contain valves for one way flow to the heart - prevent back flow

Some veins are surrounded by skeletal muscle which contracts to increase vein
pressure and ensure blood flows back to the heart

236
Q

Pulmonary circulation

A

Pulmonary circulation: Blood leaves the right ventricle via a single large artery, the pulmonary trunk, which divides into the two pulmonary arteries, one supplying the
right and one supply the left lung.

In the lungs the arteries continue to branch and
connect to arterioles, leading to capillaries that unite into venules and then veins.

The blood leaves the lungs via four pulmonary veins, which empty into the left
atrium

237
Q

Systemic circulation

A

Blood leaves the left ventricle via single large artery, the
aorta. The arteries of the systemic circulation branch off the aorta, dividing into
progressively smaller vessels.

The smallest arteries branch into arterioles, which
branch into roughly 10 billion very small vessels, the capillaries, which unite to form larger-diameter vessels known as venules.

The arterioles, capillaries & venules are collectively referred to as the MICROCIRCULATION.

The venules then unite to
form larger vessels, veins. The veins from the various peripheral organs and tissues
unite to produce two large veins, the inferior and superior vena cava which drain into the right atrium

PHASE 1 Medicine (5 decks)

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