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CVS Flashcards

1
Q

Describe the phases of the blood

A
  1. Cellular component (45%) - red cells, white cells & platelets
  2. Fluid component (55%) - plasma
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2
Q

How many litres of blood do we have?

A

5

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3
Q

What does ‘haematocrit’ refer to?

A

The volume of red blood cells, and therefore haemoglobin, in the blood.
Normal = 0.45

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4
Q

What is haemopoiesis?

A 
The process of production of blood cells and platelets which continues throughout life.
Primitive cells (stem cells) are pluripotent - can differentiate into red blood cells, white blood cells and platelets.
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5
Q

Lifetime of:
RBC =
Platelets =
WBC =

A 
RBC = 120 days
Platelets = 7-10days
WBC = 6hrs
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6
Q

Where are the precursor cells for red blood cells located?

Adults, children, in utero

A

Bone marrow -
In adults, this is in the axial skeleton (skull, ribs, spine, pelvis, long bones)
In children, this is in all bones
In utero this is in the yolk sac, then liver and spleen

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7
Q

What would be suspected if precursor cells for blood cells are found in the blood?

A

sign of leukaemia

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8
Q

How are precursor stem cells stimulated to divide to form blood constituents?

A

Hormonal growth factors stimulate their proliferation and differentiation:
Epo/Erythropoietin - hormone made in kidney = RBC
G-CSF (Granulocyte Colony Stimulating Factor) = WBC
Tpo = platelets

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9
Q

Why do RBCs have a relatively short lifespan?

A

Simple, anucleate with no mitochondria so cannot repair themselves

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10
Q

What are young RBCs known as?

A

reticulocytes

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11
Q

Effect of decreased pH on oxygen dissociation curve?

A

Shifts right

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12
Q

Effect of increased temp on oxygen dissociation curve?

A

Shifts right

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13
Q

Effect of decreased temp on oxygen dissociation curve?

A

shifts left

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14
Q

Effect of increased pH on oxygen dissociation curve?

A

shifts left

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15
Q

What do RBCs consist of?

A

Membrane to enclose haemoglobin (would clog uo kidneys if not enclosed)
Enzymes of glycolysis
Haemoglobin for O2 transport

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16
Q

Role of haemoglobin?

A

Carries O2 from lungs to tissues where it transfers O2 to myoglobin in muscles

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17
Q

Structure of haemoglobin

A

Haemoglobin is formed of 2 alpha and 2 beta chains and 4 haem groups - has an
overall quaternary structure.
Oxygen binds to the Fe 2+ in haem REVERSIBLY

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18
Q

What determines an individual’s blood type?

A

Possession of the gene that results in the synthesis of the A antigen on the surface of RBCs = Type A.
Type A individuals have anti-B antibodies in their plasma. A antigen is co-dominant.
Gene that results in the synthesis of the B antigen on the surface of RBCs = Type B.
Type B individuals have anti-A antibodies in their plasma. B antigen is codominant.
Neither = O type.
Type O individuals have both anti-A and anti-B antibodies in their plasma - anti-erythrocyte antibodies, known as natural antibodies. Type O antigen is recessive.
UNIVERSAL DONOR.
Both = AB
AB individuals have neither anti-A nor anti-B antibodies in their plasma = UNIVERSAL RECIPIENT.
A is more common than B
O is must common
AB is most rare

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19
Q

What does Rhesus positive mean about an individual?

Rhesus negative?

A

Positive possess D antigen.

Negative do not.

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20
Q

What is the normal blood haemoglobin? What is the significance of a score that is lower than this?
Higher?

A

Normal = 12.5-15.5 g/dl

Lower = anaemia.

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

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21
Q

Symptoms of anaemia?

A

Tiredness, lethargy, malaise, reduced exercise tolerance,

shortness of breath on exertion and angina

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22
Q

Signs of anaemia?

A

Palor, pale mucus membranes and palmar creases (pink hands), glossitis
(sore tongue), angular stomatitis ( cracking at corners of mouth), kylonychia (caused
by the iron deficiency - spoon shaped nails)

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23
Q

What are the classifications of anaemia? (5)

A

Iron deficiency, B12/folate deficiency, anaemia of chronic disorder,
haemolysis, bone marrow failure/infiltration

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24
Q

Describe iron deficiency anaemia

A

Lack of iron needed for haemoglobin production - fewer small red cells produced.
MCV<80fl.
Causes:
- bleeding: occult gastrointestinal, menhorragia
Dietary:
most common cause worldwide.

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25
Q

What is the significance of red cell size?

A

Measured as MCV (mean cell volume).
Normal = 82-96fl
Iron deficiency characterised by low haemoglobin and MCV<80fl.
Macrocytosis = MCV> 100fl. Usually caused by B12/deficiency anaemia but can have raised MCV due to liver disease/alcohol/hypothyroidism.

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26
Q

Describe B12 and folate deficiency anaemia

A

Causes macrocytosis.
B12 and folate needed for DNA synthesis - without, RBCs cannot be made in bone marrow so less are released. All dividing cells affected, but bone marrow most active so detected first.
Causes:

B12
Stomach damage: less parietal cells —> less intrinsic factor. B12 binds to Intrinsic factor in the terminal ileum and is then absorbed.
Autoimmune disease called pernicious anaemia causes antibodies again gastric parietal cells to be made - slow onset, as liver has vast store of B12 (can last 4yrs).

Folate:
Malabsorption e.g. coeliac.
Dietary - dont eat enough fruit and veg
Increased need due to haemolysis.

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27
Q

Describe haemolytic anaemia

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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28
Q

Describe e.gs of congenital causes of anaemia

A
  • Membrane issues e.g SPHEROCYTOSIS - blood cells are spherical so
    get stuck in vessels easily. Dominant condition but variable penetrance.
  • Enzyme issues e.g PYRUVATE KINASE DEFICIENCY
  • Haemoglobin issues e.g. SICKLE CELL ANAEMIA (defect in beta globin chain in
    haemoglobin) - whereby red blood cells are sickle shaped thus get trapped in vessels
    easily, and THALASSAEMIA - mutation in haemoglobin chains, beta is more common
    in india + Pakistan whereas alpha is more common in east e.g. Thailand
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29
Q

Examples of acquired anaemia?

A

autoimmune - immune system attacks own blood cells, can be triggered by a blood transfusion due to presence of foreign antibodies.
mechanical - fragmentation of RBCs by mechanical heart valve/intravascular thrombosis
pregnancy - haemolytic disease of the foetus and newborn.

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30
Q

Describe haemolytic disease of the foetus and newborn

A
  • mother has rhesus negative blood and baby has rhesus positive. When mother’s blood is exposed to babies blood in pregnancy, she recognises foreign rhesus positive blood and begins making antibodies against it. First baby is unaffected due to time it takes to produce antibodies - however mother is sensitised to rhesus positive.
    If second baby has rhesus positive, when blood is exposed antibodies are produced immediately and begin destroying baby’s RBCs resulting in homeless of foetus/ newborn leading to anaemia and jaundice.
    Antibodies can cross to baby via placenta - this is known as rhesus disease.
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31
Q

What are the types of white blood cells?

A

neutrophils

lymphocytes - B cells and T cells

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32
Q

Describe neutrophils

A

Most numerous WBCs. Lifespan 10hrs.
Phagocytose and kill bacteria.
Release chemotaxins to signal more WBCs to come to site, and cytokines for inflammatory response.
Lack of/compromised function results in recurrent bacterial infections

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33
Q

Describe B lymphocyes

A

Made in Bone marrow, stored in secondary lymphoid organs.

Differentiate into plasma cells and produce immunoglobins when stimulated by exposure to foreign antigens.

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34
Q

Describe T lymphocytes

A

Made in bone marrow, mature in Thymus.
Some are helper cells (CD4, help B cells in antibody generation, responsible for cell edited immunity), some are cytotoxic cells (CD8)

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35
Q

Define acute leukemia

A

proliferation of primitive precursor cells usually found in bone marrow. Proliferation without differentiate.
Replaces normal bone marrow cells, resulting in anaemia, neutropenia(infections), thrombocytopenia(bleeding).
Detected by presence of primitive white precursor cells in the blood.

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36
Q

How do acute myeloblastic leukaemia, acute lymphocytic leukaemia and high grade lymphoma differ?

A

AML: malignant proliferation of the precursor myeloblasts (unipotent stem cells) in the bone marrow. Primarily affects adults. 50% survive 5 years.
ALL: malignant proliferation of the lymphoblast precursor cells in the bone marrow. Primarily affects children - 80% cured.
High grade lymphoma: lymphocytes in lymph nodes become malignant. Classified as Hodgkins/Non-Hodgkins, spreads to liver, spleen , bone marrow and blood from lymph nodes.

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37
Q

Describe platelets:

A

Small cytoplasmic anucleate cells that block up holes in blood vessels. Made in bone marrow from megakaryocytes.
Spherical, enucleate - cannot repair itself.
Lifespan 5-10 days.

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38
Q

Significance of reduced/uncreased platelet count?

A

Normal number = 140-400x10^9/l

Reduced: thrombocytopenia. Risk of cerebral bleeding. Count >80 = increased bleeding, >20 = spontaneous bleeding.

High numbers = thrombocytosis, can lead to arterial and venous thrombosis, leading to an increased risk of heart attack and stroke.

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39
Q

Describe the coagulation proteins present in the blood.

A 
Coagulation proteins (enzymes)- produced in the liver. Key enzyme is thrombin (makes 'plug'). 
Vitamin K is essential for correct synthesis of coagulation factors 2, 7, 9 and 10. They circulate in inactive form. Convert soluble fibrinogen into insoluble fibrin polymer.
Overactivity = thrombosis
Failure = bleeding
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40
Q

What proteins are present in the blood?

A

Coagulation proteins.

Plasma proteins (soluble, in plasma)

  • albumin is most numerous.
  • carrier proteins for nutrients/hormones
  • immuniglobins
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41
Q

Brief roles of albumin

A

Produced in liver.
Maintenance of oncotic pressure.
Lack of results in oedema.
Carries fatty acids, steroids, thyroid hormones.

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42
Q

What are immunoglobins?

A 
Antibodies produced by plasma cells.
Several classes:
IgG = most important
IgM = precursor to all
IgA, IgE = produced in response to non-self protein antigens
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43
Q

What is haemostats?

A

The arrest of bleeding.

Involves physiological processes of blood coagulation and the contraction of damaged blood vessels.

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44
Q

Why is blood usually fluid inside blood vessels?

A

Proteins of the coagulation cascade and the platelets circulate in an inactive state.
Correct balance is vital to life. (risk thrombosis vs. bleeding)

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45
Q

What activates the proteins and platelets of the coagulation cascade?

A

activated by tissue factor, present on all cells apart from endothelial cells - when endothelium is punctured, blood comes into contact with tissue factor and starts clotting.

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46
Q

How does the coagulation cascade eventually create blood clotting?

Why is the fact that it has multiple steps important?

A

Cascade to generate the key enzyme thrombin which cleaves fibrinogen to create fibrin polymerisation - blood clot.
Multiple steps allow for biological amplification and allows for regulation - not an all or nothing response so can be graduated depending on the severity of the challenge.

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47
Q

What is the role of platelets in the coagulation cascade?

A

Responsible for primary haemostasis - adhere to damaged endothelium and aggregate to form a platelet plug, buying time for coagulation cascade

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48
Q

Briefly describe key features of the coagulation cascade:

A
  1. Platelets aggregate and form plug in damaged epithelium - primary haemostasis - due to exposure of collagen fibres.

However, fibrin needed to mesh them together.
2. Extrinsic pathway - contact of sub endothelial cells with blood activates tissue factor (3), which is located on the outer plasma membrane of tissue cells. It activates factor 7 which activates factor 10.
This pathway starts the ball rolling - initiates thrombin’s positive feedback mechanisms on the intrinsic pathway independently of factor 12-(starting point of intrinsic pathway).

Factor 10 triggers formation of thrombin from inactive prothrombin that is circulating in the blood. Thrombin converts inactive fibrinogen to active fibrin strands.
Thrombin also activates factors 5, 7, 8, 11 and 13, allowing the intrinsic pathway to produce more thrombin.

Intrinsic pathway: 12–>11–>9+8—>10+5 —> thrombin(2)—>fibrin(1)

Thrombin;s activation of factor 13 provides cross links for the fibrin strands, strengthening the mesh holding down the platelet plug.

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49
Q

Describe the disease haemophilia.

Brief epidemiology of 3 types.

A

Recessive X-linked bleeding disorder caused by not enough clotting factors in the blood leading to slow clotting time or long prothrombin time (PTT). Only affects males - females are carriers.
A and B = bleed into muscles and joints.
VWD = muco-cutaneous.
A - deficiency in factor 8. Rare, 1 in 10000. Treat with factor 8.
B- deficiency in factor 9. Treat with factor 9. More rare, 1 in 50000.
Von Willebrands disease - incidence up to 1% (common.) Affects males and females - autosomal dominant. Mild bleeding disorder, deficiency in factor 11.

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50
Q

Describe Von Willebrands disease

A

Autosomal dominant inheritance.
Lack of Von Willebrands Factor (VWF) - factor 11.
Required for platelets to bind to damaged blood vessels - lack leads to muco-cutaneous bleeding (bleeding in skin and mucous membranes).
Common - incidence 1%.
Usually mild - often unrecognised and undiagnosed.

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51
Q

Common causes of acquired bleeding disorders?

Vitamin K importance.

A

Most common = anti-platelet/anti-coagulation medication.
Other:
liver disease -
Vit. K deficiency-
Drugs (aspirin, heparin, warfarin-inhibits vitK, steroids )
DIC - disseminated intravascular coagulation caused by sepsis/obstetric/malignancy

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52
Q

Liver disease as a cause of acquired bleeding disorders

A

Liver is site of synthesis of coagulation factors and fibrinogen. Damage caused mainly by alcohol.

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53
Q

Vitamin K deficiency

A

needed for correct synthesis of coag factors 2, 7, 9, 10 (‘1972’). Deficiency caused by malabsorption e.g. in obstructive jaundice. Long PTT. Treat with IV vitamin K. Without vitamin K coag factors are still produced but do not work.

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54
Q

Disseminated Intravascular coagulation

A

Breakdown of haemostatic balance leads to simultaneous bleeding and microvascular thrombosis.
Causes: sepsis, obstetric, malignancy.
Activation of coagulation cascade occurs inside blood vessels, thrombin converts fibrinogen to fibrin leading to formation of microvascular thrombosis’ - platelet plugs - everywhere.
Formation of these uses up clotting factors and platelets leading to a deficiency so bleeding occurs.
Treatment - treat underlying cause, stop generation of intravascular thrombin, transfuse new platelets.

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55
Q

First response to blood vessel damage

A

Vasoconstriction due to neural control and release of endothelia-1 by endothelial cells.
This temporarily slows blood flow to affected area and presses opposed endothelial surfaces together inducing stickiness.
This is only permanent as a stand alone response in smallest vessels of the microcirculation.

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56
Q

2 interdependent processes following vasoconstriction in response to blood vessel damage.

A

1, formation of a platelet plug

2. blood coagulation

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57
Q

Describe in more detail the formation of a platelet plug

A
  1. Platelets aggregate and form plug in damaged epithelium - primary haemostasis - due to exposure of collagen fibres. VWF (factor 11) is adhered to collagen, and platelets adhere to the factor via a receptor on the platelet membrane called glycoprotein 1b factor.

This triggers the platelet to exocytose platelet dense granules which release ADP which causes platelet amplification.
Thrombin induces platelet activation (increases its surface area by making in spiky) and further thrombin release, in positive feedback.

Platelet activation increases expression of glycoprotein receptors on the platelets which bind to fibrinogen allowing new platelets to adhere to the old one.

Platelet adhesion rapidly induces them to synthesise THROMBOXANE A2 (causes
vasoconstriction & platelet activation) which is then released into the extracellular
fluid and acts locally to further stimulate platelet aggregation

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58
Q

How does the platelet plug stay in the right positition in the damages epithelium, e.g. doesn’t expand away on either side?

A

Normal undamaged endothelium on either side synthesised and releases prostacyclin (aka prostaglandin I2)which inhibits platelet aggregation.
Normal endothelium also releases nitric oxide which is a vasodilator and inhibitor of platelet adhesion, activation and aggregation.

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59
Q

What is blood coagulation?

A

transformation of blood into a solid gel called a
clot or thrombus which consists mainly of a protein polymer called fibrin.
- Clotting occurs locally around the platelet plug and is the dominant haemostatic
defence - its function is to support & reinforce the platelet plug and to solidify
blood that remains in the wound channel

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60
Q

Important indirect roles of the liver in blood clotting

A

Site of production for many plasma clotting factors.
Produces bile salts essential for absorption of lipid-soluble vitamin K, required to produce prothrombin and several other clotting factors.

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61
Q

What is the fibrinolytic system?

A

Fibrin clots are a temporary fix until permanent repair of blood vessel occurs.
Plasminogen is converted into plasmin by activators, which goes on to break down fibrin.

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62
Q

How are cardiac cells joined?

A

By desmosomes called intercalated discs. These also have gap junctions within them.

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63
Q

Describe the thick filament of myofibrils

A

Myosin forms the majority of the thick filament.
Composed of 2 large polypeptide heavy chains and 4 smaller light chains, combining to form a molecule with 2 globular heads made of light and heavy chains and a long tail of intertwined heavy chains.

Each globular head has 2 binding sites - one for ATP, one for attaching to the thin filament.
Attached to the myosin head is an inorganic phosphate molecule and ADP.
ATP binding site also serves as an ATPase that hydrolyses the bound ATP to provide energy for contraction.

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64
Q

Describe the thin filament in myofibrils

A

Actin forms majority of thin filament.
Also troponin and tropomyosin, important for regulating contraction.
Actin is a globular protein consisting of a single polypeptide which polymerises with another actin monomers to form a double-stranded helix known as F-actin.
Each actin molecule has a binding site for myosin.
Tropomyosin occupies the grooves between the 2 actin strands and overlies the myosin binding sites.
Troponin protein changes shape when Ca2+ binds to it, pushing the tropomyosin aside and exposing the myosin binding sites on actin enabling contraction to occur.

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65
Q

A band of sarcomere

A

Whole length of thick filament.

Has some overlapping thin filament.

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66
Q

I band of sarcomere

A

region occupied only by thin filaments, z disc forms midline

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67
Q

Z line of sarcomere

A

define the limits of one sarcomere. Contains actin, tropomyosin, troponin.

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68
Q

H zone of sarcomere

A

area occupied by myosin only

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69
Q

M line of sarcomere

A

In the centre of the H zone.

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

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70
Q

What are titins?

A

Elastic protein filaments that extend from the Z line to the M line, linked to the M line proteins and the thick filaments. Act to maintain alignment of the thick filaments in the middle of each sarcomere.

71
Q

Describe the process of a cardiac action potential

A
  • sarcolemma more permeable to K+ at resting potential than to Na+, maintained by Na/K/ATPase pumps (3Na+ out for every 2K+in)
  • action potential arrives, opening Na+ voltage-gated channels - cell depolarises opening even more channels (pos. feedback)
  • Ca2+ channels also triggered to open - but much slower
  • at +52mV Na+ channels close, and K+ channels open - K+ outflow, partially repolarising the cell.
  • Meanwhile Ca2+ channels open at T-tubules and Ca2+ flows in. K+ channels close.
  • flow of calcium ions in balances flow of K+ ions out, keeping membrane depolarised at plateau value of 0mV
  • eventually calcium channels close and K+ channels reopen, depolarising the membrane back to negative values.

stages:

    • rapid depolarisation due to Na+ inflow
  2. Partial repolarisation due to K+ outflow, Na+ inflow stops
  3. Plateau - Ca2+ slow inflow
  4. Repolarisation - K+ outflow, Ca2+ inflow stops
  5. Pacemaker potential - Na+ inflow, slowing of K+ outflow
72
Q

How is excitation contraction coupling carried out in cardiac muscle?

A
  • Action potential –> influx Ca2+ via L-type Ca2+ channels on T-tubules
  • Leads to not only depolarisation but a small increase in cytosolic Ca2+ conc.
  • The Ca2+ that influx bund to receptors on sarcoplasmic reticulum, causing it to release many Ca2+ ions into cell cytoplasm
  • Ca2+ binds to binding site on troponin on actin
  • troponin changes shape, displacing tropomyosin, exposing myosin binding sites
  • myosin head forms cross-bridge, binding to the actin filament by dropping an inorganic phosphate - ADP remains attached
  • myosin head drops ADP to contract and pull actin filament over myosin filament = POWER STROKE
  • ATP binds to myosin head, detaching it from actin and returning it to its starting position
  • ATPase present in myosin hydrolyses the ATP –> ADP+Pi ready for next contraction provided myosin binding sites remain open.
    Contraction stops when cytosolic Ca2+ cmc is restored to resting value by pumps in the sarcoplasmic reticulum and sarcolemma
73
Q

What is the cause of rigour mortis?

A

ATP is required for the myosin head to detach from the actin - when the person is dead, there is no ATP meaning the myosin head does not detach - resulting in stiffness of the skeletal muscles

74
Q

Compare duration of contraction in skeletal vs cardiac muscle

A

Cardiac contraction up to 15 longer in duration due to slow (L-type) Ca2+ channels

75
Q

Compare the refractory period in skeletal muscle contraction vs. cardiac muscle contraction

A

The refractory period is the period of time after an action potential where
second impulse CANNOT cause a second contraction - exists in cardiac muscle.
This is to prevent excessively frequent contraction and to allow adequate filling time.

76
Q

What is the blood supply of myocardial cells?

A

Supplied by coronary arteries.

77
Q

Entrance/exit of coronary arteries

A

Originate at the base of the aorta behind the aortic valve cusps. Most drain into a single vein - the coronary sinus - which empties into the right atrium.

78
Q

How is heartbeat coordinated? - electrical conduction in the heart

A

1% cardiac cells constitute the conducting system of the heart and are in electrical contact with the cardiac myocytes via gap junctions.
Initial depolarisation arises in the SAN, a group of conducting-system cells.
The action potential spreads throughout the atria, causing a wave of contraction.
Impulse reaches the AVN (brief delay, 0.1s, allows complete emptying of atria).
Impulse spreads down Bundle of His and Purkinje fibres.
Purkinje fibres trigger ventricular contraction.

79
Q

where is the SAN located?

A

right atrium near the entrance of the superior vena cava at the junction of the crista terminalis

80
Q

What is the resting membrane potential of cells of the SAN? why is this significant?

A

-55 to -60mV - this is closer to the threshold of depolarisation, thus it depolarises first.
It has slow Na+ inflow leading to this membrane potential, a feature not found anywhere else in the body.

81
Q

How does the SAN achieve action potential?

A

It does not have a steady resting potential, instead undergoing slow depolarisation (this is known as the pacemaker potential) - which brings the membrane potential to a threshold triggering an action potential.
This allows automaticity.

82
Q

How is the ‘pacemaker potential’ set up?

A

By 3 ion channel mechanisms:
1. Progressive reduction in K+ permeability The K+ channels that opened during the repolarisation phase of the previous action potential gradually
close as the membrane returns to negative potential
2. 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 channels conduct mainly an inward Na+ current. Called F-type channels.
3. The third channel is a Ca2+ channel that opens VERY BRIEFLY but contributes to an
inward current of Ca2+ which acts as an important final depolarising boost to the pacemaker potential. Transient opening gives them their name of T-type Ca2+ channels

83
Q

How do the SA and AV nodes differ?

A

Despite similar shape, pacemaker currents in the SA node bring them to threshold more rapidly meaning SAN initiates action potentials and determines pace of heart.

84
Q

What is the sequence of action after pacemaker mechanisms have brought a nodal cell to threshold, bringing the wave of excitation to the AVN?

A

Action potential occurs.
Depolarisation brought about by Ca2+ influx through L-type Ca2+ channels (slower depolarisation than Na+ channels).
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 - rapid enough for both atria to contract simultaneously.
Internodal pathways carry action potential rapidly from SAN to AVN.

85
Q

Where is the AVN located?

A

At the base of the right atrium.

86
Q

What cells does the AVN consist of?

A

Modified cardiac cells that have lost contractile capability but conduct
action potentials with LOW RESISTANCE.

87
Q

Pathway of action potential following excitation of the AVN

A

Progresses down the inter ventricular septum down a pathway of conducting fibres called the Bundle of His. Surrounding connecting tissue is non conducting.
Divides into right and left bundle branches at the apex of the heart, and enter the walls of both ventricles.
These fibres make contact with Purkinje fibers, large-diameter conducting
cells that make contact with ventricular myocardial cells, spreading the impulse throughout the ventricles.

88
Q

Innervation of the heart

A

Parasympathetic stimulation:
• Fibers are transmitted via the vagus nerve (CN10)
• Controlled by acetylcholine which bind to muscarinic receptors

  • Sympathetic stimulation:
    • Sympathetic postganglionic fibers innervate the entire heart
    • Controlled by adrenaline & noradrenaline
89
Q

Effect of parasympathetic stimulation on the heart?

A

Acetylcholine decreases heart rate (negatively chronotropic)
Decreases force of contraction (negatively inotropic)
Descreases CO by up to 50%

90
Q

Effect of sympathetic stimulation on the heart

A

Adrenaline and noradrenaline:

  • increase heart rate (positively chronotropic)
  • increase force of contraction (positively inotropic)
  • increase CO by up to 200%
91
Q

What does ECG measure?

A

The currents generated in the EXTRACELLULAR FLUID by the changes occurring
simultaneously in many cardiac cells.

92
Q

P wave of ECG

A

atrial depolarisation, seen in every lead except aVR

93
Q

significance of the PR interval on an ECG

A

time taken for atria to depolarise and electrical activation to reach AV node

94
Q

QRS complex of ECG

A

ventricular depolarisation

95
Q

What is the ST segment on an ECG?

A

interval between depolarisation and repolarisation

96
Q

What does the T wave on an ECG represent?

A

ventricular repolarisation

97
Q

Define:
tachycardia
bradycardia
dextrocardia

A 
tachy = increased heart rate
brady = decreased heart rate
dextrocardia = heart on right side of chest
98
Q

What does an ECG look like during:

  1. Acute anterolateral myocardial infarction
  2. Acute inferior MI
A
  1. ST segments are raised in anterior (V3
    - V4) and lateral (V5-V6) leads.
  2. ST segments are raids in inferior (II, III, aVF) leads
99
Q

Why is atrial depolarisation not evident on an ECG?

A

occurs at the same time as the QRS complex so it hidden

100
Q

Duration of systole?

A

0.3s

101
Q

Describe systole

A
  • isovolumetric contraction of the ventricles (pressure increases but volume remains the same as the valves are closed)
  • once ventricular pressure > pressure in aorta and pulmonary trunk, aortic and pulmonary valves open and maximal ejection of blood from ventricles into arteries occurs.(don’t empty completely)
102
Q

Duration of diastole?

A

0.5s

103
Q

Describe diastole

A
  • period of reduced ejection
  • ventricles relax, decreasing pressure and aortic&pulmonary valves close. Mitral valves are also closed so ventricular vol. stays the same —- isovolumetric ventricular relaxation.
  • venous return from superior and inferior vena cava and pulmonary vein mean pressure in atria is slightly higher than in ventricles, enough to open mitral valves - rapid left ventricle filling occurs down pressure gradient. (80%ventricular filling before atrial contraction)
  • slow ventricular filling as diastasis (pressure equalisation in atria and ventricles) is reached - little to no net movement of blood. At this point AVN delays stimuli from SAN to allow full filling.
  • atrial booster: atria contract, increasing pressure forcing remaining blood into ventricles
104
Q

Where is the left ventricle palpated?

A

In the 5th left intercostal space and mid-clavicular line. Responsible for the apex beat.

105
Q

What is stroke volume

A

The volume of blood ejected from each ventricle during systole

106
Q

What is cardiac output?

A

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

107
Q

What is total peripheral resistance?

A

The total resistance to flow in systemic blood vessels

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

108
Q

What is the preload?

effect of vein dilation on 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).

109
Q

What is meant by the term afterload?

Effect of artery dilation on after load?

A

the pressure the left ventricle must overcome to eject blood during
contraction. Dilate arteries = decrease in afterload

110
Q

What is meant by 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

111
Q

what does the elasticity of the heart refer to?

A

myocardial ability to recover normal shape after systolic stress

112
Q

what is diastolic dispensibility?

A

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

113
Q

what is cardiac compliance?

A

how easily the heart chamber expands when filled with blood volume

114
Q

What does Starling’s law state?

A

That the force of contraction is proportional to the end diastolic length of cardiac muscle fibre - the more the ventricle fills the harder it contracts.

115
Q

Describe the sequence of events through which increased venous return leads to increased stroke volume and force of contractions (starling’s law)

A

increased venous return –> increased end diastolic volume –> increased preload –> increased sarcomere stretch –> increased force of contraction = increased stroke vol. and force of contractions

116
Q

What is the effect of standing on blood pressure and why?

A

Starling’s law -
Venous return decreases due to gravity, so cardiac output decreases, causing a drop in blood pressure.
This stimulates baroreceptors to increase blood pressure.

117
Q

How is blood flow maintained constant by the vascular system?

A

Intrinsic autoregulation - Arterioles vasoconstrict/vasodilate in response to changes in resistance to maintain constant blood flow
Myogenic autoregulation - when blood flow increases, stretching vascular smooth muscle, the muscle automatically constricts. When smooth muscle isn’t getting stretched as much due to low blood pressure, the muscle dilates in response to increase blood flow.

118
Q

What is hyperemia?

A

increase in blood flow

119
Q

What is the difference between active hyperemia compared with reactive hyperemia?

A

Active - increase in blood flow when metabolic activity is increased

Reactive - extreme form of autoregulation whereby a profound transient increase in blood flow occurs in response to complete occlusion of an organ or tissue’s blood supply

120
Q

What are the three heart sounds?

A
  1. Soft, low pitched ‘lub’ = closure of atrioventricular/mitral valves
  2. Louder ‘dub’ = closure of aortic and pulmonary valves
  3. Sounds of blood rushing into the left ventricle
121
Q

What is mean systemic arterial pressure (MAP)?

Equation?

A

average blood pressure in the arteries during the cardiac cycle.
Neural control aims to mainting constant MAP.

Equal to diastolic pressure + 1/3pulse pressure

pulse pressure = systolic pressure - diastolic pressure

122
Q

Effectors involved in circulation control/maintenance of constant MAP?

A

blood vessels, heart, kidneys

123
Q

Role of medullary cardiovascular centre in control of circulation?

A

Central chemoreceptors in the medulla respond to a decrease in pH due to CO2 diffusing across the blood-brain barrier to reduce the pH of the CSF.
Pressor region in the medulla - Sympathetic, responsible for raising blood pressure.
Also in the medulla within the medullary cardiovascular centre is the depressor region, a parasympathetic region responsible for lowering blood pressure.

124
Q

How does the Pressor region act to control circulation?

What route does it take

A

Pressor region –> SYmpathetic -> medulla –> spinal cord –> synapses at T1-L2 –> heart
Increases blood pressure by increasing vasoconstriction, cardiac output and contractility.

125
Q

How does the depressor region act to control blood pressure?

Route?

A

Parasympathetic control - decreases blood pressure by inhibiting the pressor region.
Depressor region –> medulla –> vagus nerve –> heart

126
Q

How are changes in blood pressure detected?

  • location of receptors
A

Central chemoreceptors in the medulla respond to decreased pH caused by increased blood CO2 levels in the CSF.
Cardiopulmonary baroreceptors located in the atria, ventricles and pulmonary artery detect stretch.

127
Q

How to cardiopulmonary baroreceptors act to change blood pressure?

A

Cardiopulmonary baroreceptors bring about a decrease in blood pressure when stimulated, by promoting vasodilation and fluid loss. They control long term blood pressure.
In response to high blood pressure, they bring about:
- inhibition of the pressor region of the medulla
- inhibition of the Renin-angiotensin aldosterone system, preventing angiotensin 2 from causing vasoconstriction and aldosterone from stimulating increase Na+ and H2O reabsorption, both of which would increase blood pressure.
- inhibition of vasopressin/ADH release

128
Q

Describe peripheral control of circulation in response to increased blood pressure - key component?

A

Total peripheral resistance is mainly dependent on arteriole resistance, as they are the principal site of resistance to vascular flow.
Therefore arterioles respond to blood pressure:
- muscle of arteriole contracts, increasing resistance to flow and decreasing the blood flow to decrease blood pressure
They also respond to local factors:
- endothelin-1 released by endothelium cells results in potent vasoconstriction
- myogenic auto regulation whereby arteriole smooth muscle contracts automatically in response to stretch
Hormonal factors:
angiotensin 2, vasopressin, adrenaline

129
Q

What are examples of arteriole vasodilators acting to increase local blood flow?

A
  • hypoxia: causes accumulation of vasodilator metabolites which will dilate vessels
  • increased CO2
  • decreased pH
  • Bradykinin
  • Nitric oxide/prostaglandin I2 released by endothelial cells (potent)
  • increased K+
  • tissue breakdown products e.g. lactic acid

Hormonal factors:
- Atrial Natriuretic Peptide, adrenaline

130
Q

Is adrenaline a vasodilator or a vasoconstrictor?

A

Can be either depending on which receptors are present

131
Q

Where are peripheral chemoreceptors located?

How are they stimulated?

A

In the aortic arch and carotid sinus (base of internal carotid artery - at the division between internal and external carotid).
Stimulated by a fall in PaO2 and a rise in PaCO2 leading to a fall in pH.

132
Q

What are arterial baroreceptors?

Where are they found and what route do they take to decrease blood pressure?

A

Arterial stretch receptors.
One found in the aortic arch –> vagus –> medulla: decreased sympathetic stimulation and increased parasympathetic –> decreased blood pressure.

2 where left and right common carotid divide - the carotid sinus. Carotid sinus –> sinus nerve –> glossopharyngeal –> medulla: decreased sympathetic stimulation and increased parasympathetic –> decreased blood pressure.

133
Q

Structure of arteries - from lumen

A

Squamous epithelium
Basement membrane
Intima: endothelial cells, small amount of collagen
- adventitia: mainly collagenous. loose fibrous connective tissue connective tissue
- internal elastic lamina
- media: thick payer connective tissue - smooth muscle, fibroblasts, collagen, elastin
- external elastic lamina
- adventitia: loose fibrous connective tissue, mostly fibroblasts and collagen, some smooth muscle cells

134
Q

Compare elastic arteries with muscular arteries and arterioles

A

Elastic - found near the heart (aorta, pulmonary arteries). Media contains abundant concentric sheets of elastin. Very large lumen.

Muscular - most abundant
Media contains concentric layers of smooth muscle, very little elastin

Arterioles - arteries with 3 or fewer muscle layers in media. Up to 100micrometrs in diameter.
Poorly defined elastic lamina, thin adventitia and normal intima.

135
Q

Structure of capillaries

A

Endothelial cells bound to a basement membrane with co-existing pericytes.
May be fenestrated to allow transfer of materials.
Pericytes control cell diameter.

136
Q

Structure of venules and veins

A

Vein - larger lumen, endothelium, basement membrane, intimate, internal elastic lamina, media thinner than arteries, adventitia.
no external elastic lamina.
Some have valves.
Venues surrounded by contractile parasites which are replaced by smooth muscle media as venules–>veins

137
Q

Route of pulmonary circulation

A

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

138
Q

Route of 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.
Left ventricle –> aorta –> Microcirculation: arterioles->capillaries->venules—> inferior and superior vena cava –> right atrium

139
Q

Describe the developments that take place in the 3rd week of embryonic development

A

Gastrulation - embryoblast develops into trilaminar disc/gastrula.
Cells migrate from the primitive streak to form a mesoderm in between the epiblasts (which become ectoderm layer) and hypoblasts (which are now known as endoderm layer).

140
Q

What will the ectoderm germ layer develop into?

A
  • gives rise to structures that are in contact with the outside of the body:
    CNS;
    PNS;
    sensory epithelium of the nose, ear and eye;
    epidermis of the skin hair and nails;
    Pituitary, mammary and sweat glands;
    Enamel of teeth
141
Q

What will the mesoderm layer of the trilaminar disc develop into?

A

Described as 3 parts…

  1. Paraxial plate mesoderm, immediately lateral to notochord:
    - gives rise to somites, which give rise to the supporting tissue of the body: myotome(muscle tissue), sclerotome(cartilage and bone), dermatome(dermis of skin).
  2. 3 parts
    a) Intermediate plate mesoderm: between paraxial and lateral plate mesoderm:
    - generates the urogenital system (kidneys, gonads, respective duct systems)
    b) Lateral plate mesoderm: found at the periphery of the embryo, splits into 2 layers:
    i. somatic/parietal: future body wall
    ii. splanchnic/visceral: circulatory system, connective tissue for glands, muscle connective tissue and peritoneal components of the wall of the gut.
  3. Endoderm:
    - epithelial lining of GI tract, resp. tract and urinary bladder
    - parenchyma of the thyroid gland, parathyroid glands, liver&pancreas
    - epithelial lining of the tympanic cavity and auditory tube
142
Q

From which cells of the trilaminar disc is the cardiovascular system derived from?

A
  • mesoderm: blood, heart, smooth muscles, endothelium

- some contribution from cardiac neural crest cells of the ectoderm

143
Q

Describe the processes of heart development that take place during the 3rd week of embryonic development

A

Formation of the primitive heart tube
- cells form a horseshoe shaped region called the cariogenic region, composed of 1st heart field (future LV) and 2nd heart field(outflow tract, RV, atria).
Day 19 - 2 endocardial tubes form
Day 21- as the embryo undergoes lateral folding, 2 endocardial tubes fuse to form a single heart tube

144
Q

What happens during heart formation after the formation of the primitive heart tube?

A

It grows and developed bulges:

  • aortic sac
  • bulbus cordis
  • primitive ventricle
  • primitive atrium
  • sinus venosus
145
Q

What will the bulbs cordis of the primitive heart tube eventually form?

A

Proximal 1/3: gives rise to muscular RV
Truncus cordis/arteriosus(upper part of bulbus cordis): proximal aorta and pulmonary trunk
Conus cordis(lower part of bulbs cordis): smooth outflow portion of RV and LV

146
Q

What will the primitive/primordial ventricle of the developing heart tube eventually form?

A

LV

147
Q

What will the primitive/primordial atrium of the developing heart tube eventually form?

A

Anterior part of RA
Entire LA
Left and right auricles

148
Q

What will the sinus venosus of the developing heart tube eventually form?

A

Part of RA, vena cava and coronary sinus

149
Q

What will the aortic sac of the developing heart tube eventually form?

A

aorta and pulmonary artery

150
Q

By what day does the heart begin to beat?

A

22

151
Q

Describe the progress of the developing heart tube from day 23

A

Folding:
- bulbus cordis moves inferiorly, anteriorly and to the embryo’s right
- primitive ventricle moves to the embryos left side
- primitive atrium and sinus venous move superiorly and posteriorly, resulting in the sinus venous being posterior to the primitive atrium.
At this stage there is one common atrium and one common ventricle.

152
Q

How is blood shunted right to left in week 4 of the developing foetus?

A
  • foetus pulmonary circulation is not fully functional - and alveoli are filled with fluid, leading to hypoxic pulmonary vasoconstriction.
  • This creates increased vascular resistance in the pulmonary arterial circulation, and increases pressure in right side of heart.
  • therefore the pressure in RA>LA - so blood entering the RA is shunted to LA.
  • at the end of the 4th week, a crescent-shaped tissue called the septum primum starts to grow towards endocardial cushions. The diminishing gap between the two is called the foramen primum - shunts blood RA->LA.
153
Q

Describe the formation of the foramen ovale

A
  • As the septum primum begins to disappear, a second crescent shaped ridge of tissues called the septum secundum grows towards the endocardial cushions - more thick and muscular - finishes growing by end of 6th week.
  • it contains a permanent opening on its posterior-interior surface, called the foramen ovale.
154
Q

what forms the valve of the foramen ovale?

what is the path of blood at this point?

A

As the foramen secundum enlarges, the upper part of the septum primum degenerates, leaving the lower part - this forms a flap covering the foramen ovale.
Blood flow:
- blood enters RA
- blood flows through foramen ovale, pushing valve of foramen ovale to the left
- enters LA

155
Q

How does the interatrial septum change when a baby is born and takes its first breath?

A

Lungs and pulmonary arterial circulation become fully functional, resistance decreases so pressure in right side of heart drops.
pressure RA

156
Q

Following the folding of the primitive heart tube, after which the heart comprises one common atrium and one common ventricle, describe the division of the atrioventricular canal

A
  • common atrium and ventricle are connected by an internal opening called the atrioventricular canal: blood enters the atrium, passes through the canal and exits via the trunks arteriosus.
  • masses of tissue called endocardial cushions grow from the sides of the canal to partition it into 2 separate openings - it is repositioned to the right side of the hear
  • superior and inferior endocardial cushions fuse, forming 2 separate openings: R and L atrioventricular canals
  • blood now flows from atrium (still 1 common, before formation of interatrial septum), through both atrioventricular openings into the ventricle and up through the trunks arteriosus
157
Q

describe the formation of the inter ventricular septum

A

end of 4th week:

  • muscular ventricular septum grows from floor of ventricle - divides left and right
  • an opening still remains between this septum and the fused endocardial cushion, called the inter ventricular foramen
158
Q

describe the division of the truncus arteriosus into the aorta and pulmonary trunk.

A

end of 5th week:

  • 2 ridges of tissue appear on the sides of the truncus arteriosus, called the conotruncal ridges
  • they grow towards each other and make a spiral shaped septum called the aorticopulmonary septum - divides truncus arteriosus into the aorta and pulmonary trunk
  • as the conotruncal ridges grow and fuse to form the aorticopulmonary septum they also grow inferiorly to the ventricles
  • the aorticopulmonary septum will rise with the endocardial cushion and the ventricular septum
159
Q

Sequence of events leading to the closing off of the inter ventricular foramen.

A
  • week 8: aorticopulmonary septum, endocardial cushions and muscular ventricular septum fuse and form the membranous ventricular septum, which closes off the inter ventricular foramen.
160
Q

How does the division of the truncus arteriosus into the aorta and pulmonary trunk change blood flow through the heart?

A

Blood flow through the heart:
blood enters RV through the right atrioventricular opening, leaves via the newly developed pulmonary trunk.
Blood enters the LV through the left atrioventricular opening and leaves via the newly developed aorta.
Previously blood left common atrium via trunks arteriosus.

161
Q

Aortic arch vessels: what will the 1st arch develop into?

A

LEFT: regress into part of maxillary artery

162
Q

Aortic arch vessels: what will the 2nd arch develop into?

A

LEFT: leaguers into stapedial artery

163
Q

Aortic arch vessels: what will the 3rd arch develop into?

A

Left: left/right common, internal&external carotid arteries

164
Q

Aortic arch vessels: what will the 4th arch develop into?

A

LEFT: part of aortic arch
Right: part of R subclavian artery

165
Q

Aortic arch vessels: what will the 5th arch develop into?

A

no 5th arch

166
Q

Aortic arch vessels: what will the 6th arch develop into?

A

Pulmonary trunk -
LEFT:left pulmonary artery and ductus arteriosus (becomes ligament arteriosum)
RIGHT: right pulmonary artery

167
Q

How does blood flow after leaving the truncus arteriosus in embryological heart?

A

truncus arteriosus –> aortic sac –> aortic arches (left and right) –> respective left and right dorsal aorta, fuse more caudally to form dorsal aorta.
The arches form large vessels.

168
Q

What does the dorsal aorta become?

A

Right: part of the R subclavian artery
Left: arch of aorta and descending aorta

169
Q

What is the ligament teres in adults?

A

Remnant of the umbilical vein

170
Q

What is the ligamentum venosus on adults?

A

Remnant of the ductus venous, a branch from the umbilical vein which allows connection with the inferior vena cava, thus bypassing the liver

171
Q

Describe foetal circulation?

A
  • oxygenated blood from the placenta enters foetus via the umbilical vein
  • is bypasses the liver via the ductus venous and combines with deoxygenated blood in the inferior vena cava
  • oxygenated blood from the superior vena cava also joins, empty into the right atrium
  • RA pressure>LA pressure, blood shunted via foramen ovale
  • blood moves directly to aorta via the ductus arteriosus
  • deoxygenated blood returns to placenta via the umbilical arteries originating from the internal iliac near the bladder
172
Q

what is the ductus arteriosus?

A

connects pulmonary artery and aorta

173
Q

what anatomical take place in postnatal circulation?

A
  • increased alveolar O2 pressure causes vasodilation of pulmonary vessels and increased LA pressure - foramen ovale closes, becoming fossa ovalis.
  • umbilical vein constricts spontaneously, becomes ligament teres
  • umbilical arteries change to the medial umbilical ligaments
  • ductus arteriosus constricts to become the ligament arteriosum
  • ductus venosus constricts, will become the ligament venosum

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