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my phase 1 > CVS > Flashcards

CVS Flashcards

1
Q

what are the great vessels of the thorax

A
  • ascending and descending aorta
    • brachiocephalic trunk
    • left common carotid artery
    • left subclavian artery
  • superior vena cava
    • brachiocephalic veins
  • inferior vena cava
  • pulmonary arteries
  • pulmonary veins
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2
Q

what are the main nerves in the thorax

A
  • phrenic nerves
    • passes anterior to the hilum
    • pierces through the diaphragm and innervates from the abdominal side
  • vagus nerves
    • joins up with and passes through the diaphragm via the oesophageal hiatus
    • recurrent laryngeal nerve- branch of the vagus - passes over the arch of the aorta
      • left recurrent laryngeal passes under ligamentum arteriosum then back up to the larynx muscles.
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3
Q

what is the difference between the left and right recurrent laryngeal nerves

A

the left comes down into the thorax while the right doesn’t

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4
Q

root and site of function of the phrenic nerve

A

C3,4,5

innervates the diaphragm - motor and sensory

pierces through the diaphragm to innervate from the abdominal side

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5
Q

what are the branches of the aorta

A
  • brachocephalic trunk → right common carotid and right subclavian
  • left common carotid artery
  • left subclavian artery
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6
Q

name the layers of the heart

A
  1. endocardium
  2. myocardium
  3. pericardium - divided into 3 main layers
    1. epicardium AKA visceral pericardium [part of serous pericardium]
    2. parietal pericardium [part of serous pericardium]
    3. fibrous pericardium
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7
Q

what is the endocardium location, composition and function

A
  • inner most layer of the heart
  • made up of endothelial cells
  • lines the heart chambers and valves
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8
Q

what is the myocardium location, composition and function

A
  • muddle layer of the heart
  • made up of muscle cells - cardiac myocytes
    • striated branching cells with many mitochondria
    • intercalated discs to allow for contraction in syncytium
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9
Q

what is the pericardium, how many layers/subdivisions

A

a double layered sac covering the heart.

  • inner layer = serous pericardium: has simple squamous epithelium
    • visceral serous pericardium [epicardium] lines the outer surface of the heart
    • parietal serous pericardium lines the fibrous pericardium and secretes fluid.
  • outer layer = fibrous pericardium
    • tough connective tissue that anchors the heart to the mediastinum.
  • outside → in = FPSV
    • Fibrous, parietal serous, SPACE, visceral serous
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10
Q

what is the pericardium, how many layers/subdivisions

A

a double layered sac covering the heart.

  • inner layer = serous pericardium: has simple squamous epithelium
    • visceral serous pericardium [epicardium] lines the outer surface of the heart
    • parietal serous pericardium lines the fibrous pericardium and secretes fluid.
  • outer layer = fibrous pericardium
    • tough connective tissue that anchors the heart to the mediastinum.
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11
Q

what is the significance of level T4/T5?

A

sternal angle

point at which the trachea bifurcates

end of the aortic arch and begining of the thoracic aorta.

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12
Q

what surface marking marks the apex of the heart

A

midclavicular line of the 5 intercostal space

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13
Q

where can you hear the aortic valve

A

the 2nd intercostal space at the right sternal margin

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14
Q

where can you hear the pulmonary valve

A

2nd intercostal space of the left sternal margin

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15
Q

where does the right coronary artery originate from

A

the ascending aorta

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16
Q

where is the right coronary artery located

A

on the anterior surface of the heart in the atrioventricular sulcus.

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17
Q

what are the main branches of the right coronary artery?

A

the right marginal artery

posterior interventricular artery - present in 90% of people.

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18
Q

where does the left coronary artery originate from

A

the ascending aorta

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19
Q

what are the main branches of the left coronary artery?

A
  • left anterior descending
  • the left marginal artery / obtuse marginal artery
  • Circumflex artery
  • diagonals
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20
Q

what are the potential sources of blood in the posterior interventricular arterty

A
  • 90% of people have PIV supplied by the right coronary artery
  • 30% of people have the PIV supplied by the circumflex artery
  • 20% of people have TWO PIVs supplied by each
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21
Q

what are the potential sources of blood in the posterior interventricular arterty

A
  • 90% of people have PIV supplied by the right coronary artery
  • 30% of people have the PIV supplied by the circumflex artery
  • 20% of people have TWO PIVs supplied by each
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22
Q

the Posterior interventricular artery supplies …

A

the atrioventricular node recieves blood supply from..

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23
Q

describe the consequence of disease in the PIV

A

as the PIV supplies the AVN, disease could limit O2 supply → electrical blockage in the heart.

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24
Q

the atrioventricular node recieves blood supply from..

A

the Posterior interventricular artery supplies …

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25
Q

how does blood enter the right atrium

A

through the superior vena cava orifice and inferior vena cava orifice

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26
Q

crista terminalis

A

the name of the internal smooth muscular ridge that divides the right atrium?

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27
Q

the name of the internal smooth muscular ridge that divides the right atrium?

A

crista terminalis

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28
Q

what is the fossa ovalis and where is it located

A

This is the remnant of the foramen ovale in the foetal heart, which allows right to left shunting of blood to bypass the lungs.

located in the septum of the heart above the inferior vena cave orifice

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29
Q

what are the 2 parts of the righ atrium, divide by the crista terminalis

A

trabeculated aurecle

smooth walled atria

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30
Q

where is the tricuspid valve located

A

in the right Atrioventricular orifice

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31
Q

how many pulmonary veins are there

A

4

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32
Q

describe the valves of the heart

A
  • right atria → ventricle via tricuspid valve
  • left atria → ventricle via bicuspid valve AKA mitral
    • both of these are operated by chordae tendinae and papillary muscle
    • right has 3 flaps while left has 2
  • aortic semilunar valve
  • pulmonary semilunar valves
    • operated by pressure of the aorta and pulmonary vein exceeding that of the ventricles
    • backflow of blood fills the pouches of the semilunar valves, forcing them shut → 2nd heart sound DUB
      • aorta valve is thicker
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33
Q

how do the tricuspid and bicuspid valves work?

A

when the pressure in the atria exceeds that of the ventricle, they open to allow blood to pass through

The chordae tendineae prevent the prolapse of these valves by becoming tense thus pulling the flaps, holding them in closed position.

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34
Q

describe the muscle walls of the right and left atria

A

pectinate

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35
Q

describe the muscle walls of the right and left ventricles and how do they differ

A

trabeculated

left is thicker than right due to having to pump blood around the body

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36
Q

at what phase of the cardiac cycle do the coronary arteries fill and why

A

during diastole

during systole the coronary arteries are compressed such that no blood flow can occur

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37
Q

describe the conducting system of the heart

A
  1. An excitation signal (an action potential) is created by the sinoatrial (SA) node.
  2. The wave of excitation spreads across the atria, causing them to contract.
  3. Upon reaching the atrioventricular (AV) node, the signal is delayed.
  4. It is then conducted into the bundle of His, down the interventricular septum.
  5. The bundle of His and the Purkinje fibres spread the wave impulses along the ventricles, causing them to contract
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38
Q

what is the SAN and where is it located?

A

the sinoatrial node is a collection of pacemaker cells, located in the upper wall of the right atrium, at the junction where the superior vena cava enters.

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39
Q

where is the AVN located

A

located within the right atrioventricular septum, near the opening of the coronary sinus.

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40
Q

what is the blood supply of the AVN and SAN

A

right coronary artery

PIV specifically for AVN

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41
Q

WHAT MAKES UP THE BORDERS OF THE HEART

A
  • Right border – Right atrium
  • Inferior border – Left ventricle and right ventricle
  • Left border – Left ventricle (and some of the left atrium)
  • Superior border – Right and left atrium and the great vessels
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42
Q

What area does each coronary artery supply

A
  • right coronary artery = right atrium and ventricle
  • LAD = right and left ventricles and interventricular septum
  • obtuse / left marginal artery = left ventricle
  • circumflex = left atrium and ventricle
  • Right marginal = right ventricle and apex
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43
Q

What does the azygos system do and what structures drain into it?

A

The azygos vein transports deoxygenated blood from the posterior walls of the thorax and abdomen into the superior vena cava vein.

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44
Q
  1. What are the names of the three splanchnic nerves? What functions do they serve?
A
  1. greater splanchnic - supplies the foregut: T5-T9
  2. lesser splanchnic - supplies the midgut: T10-T11
  3. least splanchnic - supplies the hindgut: T12
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45
Q

2 If an object is inhaled into the trachea, in which lung would you most expect it to be lodged and why?

A

THE RIGHT

its more vertical and wider

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46
Q

where do the sympathetic nerves attach to the central nervous system

A

spinal cord

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47
Q

what forms the primitive heart tube

A

the endocardial tubes

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48
Q

summarise first breath and the closing of the heart shunts

A
  • •First breaths of life → lungs expand → the alveoli in the lungs are cleared of fluid.
  • An increase in the baby’s BP and a significant reduction in the pulmonary pressures reduces the need for the ductus arteriosus to shunt blood → closure of the shunt.
  • These changes increase the pressure in the left atrium of the heart and decrease the pressure in the right atrium -> foramen ovale closes → newborn circulation.
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49
Q

where and when does the heart develop?

A

¢Heart develops in the cardiogenic region of the mesoderm in 18 days

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50
Q

three main layers of most blood vessel and their composition

A

[lumen]

  • tunica intima
    • inner most layer
    • endothelial cells produce a slick surface for smooth blood flow
    • one cell thick
    • gets nutrients from the lumen
  • tunica media
    • middle layer
    • mostly made of elastin, smooth muscle cells
    • gets nutrients from the lumen
  • tunica adventita / externum
    • outermost layer
    • loosely woven fibres of collagen and elastic
    • protects and reinforces the vessel and serves as an anchor
    • requires it’s own blood supply via vasa vasorum
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51
Q

name 5 types of blood vessel

A
  1. arteries
  2. arterioles
  3. veins
  4. venules
  5. capillaries
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52
Q

difference between arteries and veins

A

arteries have thicker walls and smaller lumens

BUT both have the same components, namely endothelium, smooth muscle elastic tissue and fibrous tissue

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53
Q

how many elastic membranes/ lamina are ther

A

2 - inernal and external

one in the tunica intima and the other between the tunica media and adventitia

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54
Q

where is the vasa vasorum found?

A

adventita

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55
Q

types of arteries

A
  • elastic arteries:
    • lots of elastin in the tunica media and adventitia
    • found close to the heart because
      • allow arteries to expand and recoil
      • absorb pressure
      • form the largest arteries
      • concentric sheets of elastin
  • muscular arteries
    • have thick muscular walls
    • carry blood to organs and tissues, thus are distributing arteries.
    • The media is made up of smooth muscle and has little elastin
  • arterioles
    • smallest arteries
    • site of the most resistance
    • have a thick tunica media
    • dilate and constrict in response to hormones and ANS
      • regulate blood flow to organs
      • allows for thermoregulation
    • having 3 or less muscle layers in the media
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56
Q

how thick are capillaries and why

A

1 cell thick

minimal distance for gas exchange and nutrients exchange/ waste removal

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57
Q

which vessel has the widest lumen and which has the smallest

A

the veins have the widest

arteries are narrow but lumen varies in size with pulse of blood passing through.

capillaries v narrow - wide enough for 1 RBC

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58
Q

which vessels have valves and why

A

the veins, to prevent backflow of blood due to most of the pressure being lost

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59
Q

how does the structure of capillaries fit its function

A
  • no strong walls needed as most BP has been lost
  • thin walls for delivery and removal of products
  • narrow lumen allows RBC to come into close contact with tissues cells thus aiding diffusion of materials
  • WBCs are able to pass through the walls
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60
Q

how does the structure of veins fit its function

A
  • wide lumen offers less resistance to blood flow
  • thinner walls with less muscle as most BP is lost by now
  • valves to prevent backflow due to low BP
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61
Q

how does the structure of arteries fit its function

A
  • strength and elasticity needed to withstand and maintain the high pressure and pulsing of blood and to prevent bursting
  • maintaining the high BP helps to prevent backflow, thus no valves needed
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62
Q

NAME A AND B

A

A= artery

B =vein

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63
Q

where are pericytes found

A

in capillaries and venules

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64
Q

describe a lymphatic vessel

A
  • thin walled vessels
  • similar to capillaries and veins and they have valves
  • they don’t contain blood but contains lymph and may contain lymphocytes
    • lymphocytes mainly found in the blood
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65
Q

what are the 3 main forms of muscle

A
  • Smooth muscle
  • skeletal muscle
  • cardiac muscle
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66
Q

histological characteristics of smooth muscle

A
  • individual fusiform cells with a central nucleus, no striations and is non-branching.
  • Transverse sections appear polygonal
  • longitudinal sections appear spindle shaped
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67
Q

features that allow smooth muscle contraction

A
  1. The cells are joined by electrically coupled gap junctions that permit a stimulus to pass rapidly through the muscle - electrical coupling.
  2. the smooth muscle cells are joined together
  3. They also have a number of surface receptors which allows them to respond to a variety of hormonal stimuli.
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68
Q

what are gap junctions

A
  • 6 connexon proteins that span the cell membranes linking the interiors of adjacent muscle cells.
  • they allow electrical coupling which is crucial for coordinated contraction of smooth muscle.
    • also speeds up contraction as only one signal is needed
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69
Q

Differences between skeletal, cardiac and smooth muscle

A
  • cardiac striations aren’t as clear as skeletal
  • cardiac myocytyes remain as individual cells throughout life therefore each one has a single nucleus positioned centrally
    • smooth muscle also have central nuclei
  • cardiac myocytes branch and connect to neighbours via intercalated discs (specialised intercellular connections)
    • this join individual myocytes mechanically and chemically.
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70
Q

To help decide what type of muscle you’re looking at ask:

A
  1. is the muscle striated? NO = smooth muscle YES —>
  2. where are the Nuclei? EDGE = skeletal CENTRE = cardiac.
  3. double check its cardiac by looking for branching.
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71
Q

Features of the myocardial cells:

A
  1. striated - myofibrils are in register
  2. nuclei are centrally located
  3. single nucleus for each cardiac muscle cell
  4. branching fibres and
  5. intercalated discs - connections between myocytes to form long connecting chains. - only found in cardiac myocytes
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72
Q

intercalated discs contain:

A
  • Gap junctions
  • adhering junctions
  • desmosomes
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73
Q

does the size of a myocyte affect its function

A

yes

the largest myocytes are found in the left ventricle as it has to work the hardest.

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74
Q

histological description of the endocardium

A

single layer of simple squamous endothelial cells.

75
Q

the valves of the heart are made up of 3 main layers

A
  • fibrosa - dense fibrous connective tissue
  • Spongiosa - loose fibrous connective tissue
  • Ventricularis - looser layer of collagen and elastin.
76
Q

what is haematopoeisis

A
  • Formation of blood cellular components, derived from haematopoietic stem cells.
77
Q

why can stem cells differentiate into any RBCs, white blood cells (leukocytes) or platelets.

A

they are pluripotent

78
Q

where are precursors cells found:

  1. -in adults
  2. -in kids
  3. -in utero
A
  1. axial skeleton bone marrow [not the limbs]
  2. all bones in kids
  3. yolk sac, spleen and liver in utero
79
Q

what is erythropoiesis, where does it happen and what factor regulates it

A
  • production of RBCs
  • in the bone marrow
  • erythropoietin = hormone that controls RBC production
    • made in the kidneys
    • low level constant release, but release ⇡ in hypoxia
80
Q

what is thrombopoiesis,

where does it happen and

what factor regulates it

A
  • production of platelets
  • in the bone marrow
  • Thrombopoietin = hormone that controls the production of thrombocytes [platelets]
    • causes increased production of megakaryocytes which platelets bud off from
81
Q

what is myelopoiesis, where does it happen and what factor regulates it

A
  • production of granulocyte WBCs
  • bone marrrow
  • GM_CSF = granulocyte-macrophage colony stimulating factor = hormone that stimulates the myeloid WBCs only
82
Q

how are RBCs removed from the body

A

by the spleen and liver

by blood loss

83
Q

RBC lifespan

A

120 days

destroyed as they have no nucleus for self maintainance

84
Q

what is contained in an RBC

A
  • Hb
  • Fe
  • glycolytic enzymes
85
Q

what is haemoglobin

A
  • 2 alpha and beta polypeptide chains.
  • each chain has a heme group holding an Fe
    • Fe revesibly binds O2
86
Q

types of haemoglobin

A
  • Hb A = 2 α chains and 2 β chains (97% of adult population)
  • Foetal haemoglobin (HbF): 2α, 2𝛄
  • HbA2: 2α, 2𝛅
87
Q

factors affecting O2 binding

A
  • DPG, pH and temperature and CO
88
Q

2 main groups of leukocytes

A

granulocytes - innate immune response

lymphocytes - adaptive immune response

89
Q

types of granulocytes

A
  • Neutrophil - most abundant WBC, phagocytic and release chemo- and cytokines to induce inflammation•
  • Monocytes – mature in to either macrophages or dendritic cells. Both antigen presenting•
  • Basophils – mature in to mast cells. Will express surface IgE and release histamine. Role in allergies and immunity•
  • Eosinophils – particular role in fighting parasitic infections but also a wide range of regulatory functions
90
Q

types of lymphocytes

A

T and B cells / lymphocytes

91
Q

maturation location and function of T and B cells

A
  • T cells mature in the thymus
    • CD8 cytotoxic
    • CD4 helper
  • Bcells mature in the bone marrow
    • generation of antibodies
92
Q

where do platelets originate from and where are they produced

A

megakaryocytes

bone marrow

93
Q

platelet lifespan

A
  • Lifespan = 7-10 days
94
Q

RBCs and platelets have a nucleus T/F

A

FALSE

95
Q

platelets travel in the blood in their inactive form T/F

A
  • TRUE
  • Platelets circulate in an inactive state until they find a damaged vessel etc.
96
Q

What is thrombosis

A

clotting inside a vessel

97
Q

what is Haemostasis

A

Haemostasis is your body’s natural reaction to an injury that stops bleeding and repairs the damage

2 phases: primary and secondary

98
Q

difference between primary and secondary phases of haemostasis

A

phase 1 = platelet plug formation

phase 2 = coagulation - stabilising the plug

99
Q

how many pathways in the coagulation pathway

A

3:

  1. intrinsic: triggered by surface contact with collagen
  2. extrinsic: triggered by endothelial damage
  3. common
100
Q

what is plasma

A

the fluid component of blood

transports water, salt, glucose and proteins

101
Q

what proteins are carried in plasma

A
  • albumin - produced in the liver
  • carrier proteins
  • coagulation proteins
  • immunoglobulins [antibodies]
102
Q

why is albumin important in the plasma

A
  • determines oncotic pressure
  • keeps intravascular fluid within the vessels
  • lack of albumin →oedema
103
Q

what is blood serum

A
  • Blood serum = blood plasma without the clotting components
104
Q

5 main steps of platelet plug formation

A
  1. endothelial injury
  2. exposure
  3. adhesion
  4. activation
  5. aggregation
105
Q

what is platelet adhesion

A

platelets adhering to exposed collagen from the damaged endothelium via Von Willebrand Factor and GPIIb/iia

106
Q

what trigger platelet activation

A

the binding of platelets to collagen → release of thromboxane A2

107
Q

what are the effects of platelet activation

A
  1. change of platelet shape from smooth discoid → spiculated + pseudopodia
    1. Increases surface areaIncreases possibility of cell-cell interactions
108
Q

difference between low and high dose aspirin

A
  • low dose only inhibits COX1 →
    • less thromboxane A2 → less aggregation and activation of platelets
  • high dose inhibits COX1 and COX2 →
    • inhibition of the conversion of arachidonic acid → PG → prostacyclin, needed for platelet activation
    • therefore, high dose aspirin acts on both pathways
109
Q

what are the 2 main antigen systems found on RBCs

A
  1. ABO
  2. Rhesus
110
Q

how many ABO blood groups? decribe them

A

4

  • Group A
    • has anti-B antibodies
  • Group B
    • has anti-A antibodies
  • Group AB
    • universal acceptor
    • no antibodies
  • Group O
    • no antigens
    • has anti-A and anti-B antibodies
111
Q

what are ABO antigens made of

A

carbohydrates

112
Q

which immunoglobulin makes up anti A and anti-B antibodies. significance?

A

IgM predominantly

doesn’t cross the placenta

113
Q

which immunoglobulin makes up anti-D antibodies. significance?

A

IgG predominantly

Does cross the placenta → foetal anaemia

114
Q

how many antigens involved in the Rhesus system

A

3

  • C, D, E
  • D/d is most important as it can cause an immune response
    • presence of D antigen denoted by + or -
    • a D- person may not always have anti-D antigens allowing them to receivie ONE D+ blood transfusion
    • otherwise a D- pt can’t receive a D+ transfusion
115
Q

where are the anti- A,b,D antigens carried in the blood

A

within the plasma

116
Q

a D- mum and D+ foetus. how is rhesus disease prevented

A

antiD immunoglobulin injection to prevent the mother form being sensitised

117
Q

alternatives to blood transfusions

A
  • treat anaemia pre-op
  • stop anti-platelets and anti-coags prior to transfusion to avoid bleeding
  • operative erythropoietin to stimulate RBC production
  • plasma
  • cryoprecipitate - frozen blood rich in fibrinogen
  • albumin
  • platelets
  • fresh frozen plasma - contains clotting factors and coagulation proteins
118
Q

how does the mV x time graphs for pacemaker cells differ to normal cells or cardiac myocytes

A
  • they only have pases 0, 3 and 4, not 1 and 2
  • uses Ca++ for depolarisation rather than Na+
119
Q

how is the SAN activated

A

it’s not activated by any other cell, it is in an automatic, constant cycle

120
Q

describe the steps of a pacemaker action pd

A
  1. phase 4: spontaneous depolarisation due to slow influx of Na+, changes the potential from -60–40mv
  2. phase 0: Depolarisation. At -40mv voltage gated channels open allowing Ca2+ ion in → further depolarisation to +20mv
  3. Phase 3: Repolarisation. at +20mv the K+ channels open allowing K+ ions out → loss of positive charge and repolarisation
  4. Phase 4: Hyperpolarisation. once -60mV is reached the NA+ channels reopen → depolarisation again and the cycle continues

NaCaK for order of ions

121
Q

how do the pacemaker voltage time graphs differ

A

they are mostly similar but SAN is faster and stronger than AVN and purkinje

122
Q

describe the steps of a cardiac myocyte action pd

A
  1. Phase 0: Rapid depolarisation
    • resting pd= -90mV. depolarisation caused by influx of Na+ → +20mv
  2. Phase 1: Partial repolarisation
    • Na+ influx stops and K+ effluxes
  3. Phase 2: plateau phase
    • charges balance due K+ efflux and Ca2+ influx.
  4. Phase 3: repolarisation
    • K+ efflux
    • Ca2+ Na+ influx stops
  5. Phase 4: resting potential
    • K+ efflux
123
Q

what causes cardiac mycocyte contraction

A

influx of Ca2+ causes the actin-myosin filament contraction

124
Q

effect of sympathetic stimulation on the heart

A
  • Increases heart rate (positively chronotropic)
  • Increases force of contraction (positively inotropic)
  • Increases cardiac output
125
Q

effect of parasympathetic stimulation on the heart

A
  • Decreases heart rate (negatively chronotropic)
  • Decreases force of contraction (negatively inotropic)
  • Decreases cardiac output
126
Q

sympathetic stimulation is controlled by

A

Adrenaline and noradrenaline + type 1 beta adrenoreceptors

  • Increases adenylyl cyclase → increased cAMP
127
Q

parasympathetic stimulation is controlled by

A

ACh and M2 receptors

– inhibit adenyl cyclase → reduced cAMP

128
Q

differences between electrical activation of myocardial cell and skeletal muscle cells

A
129
Q

what is conduction velocity and what factors influence it

A
  • speed of depolarisation
  • ion movement in and out of the cell
  • number of gap junctions
130
Q

which fibres have the fastest and slowest conduction velocities

A
  • purkinje fibres are the fastest - for strong ejection
  • AVN is slowest - for time delay to allow ventricle filling
131
Q

what is a refractory period

A

the time in which the cell cannot depolarise again

132
Q

name 2 types of refractory periods

A

absolute - no stimulus can generate an action pd

relative - a large stimulus can generate an action pd and it can be conducted

133
Q

what happens at each stage of the ecg pathway

A
  • P wave
  • atria fills with blood → SA node firiing → atrial contraction
    • atrial systole occurs partway through the P wave
    • P-R = atrial systole / ventricle diastole
    • P-Q segment = time it takes for signal to pass from SAN → AVN
  • QRS complex
  • represents firing of AVN and depolarisation of the ventricles
  • R-S = isovolumetric contraction
    • AV valves are shut and semilunar valves are shut BUT the ventricle has started contracting
  • ST segment
  • represents the plateau in myocardial action pd = Ca2+ influx → contraction
  • Thus ST segment = ventricular contraction - systole
  • T wave
  • ventricular repolarisation and diastole
  • end of T wave represents isovolumetric relaxation
134
Q

describe myosin

A
  • 2 large heavy filaments with 4 smaller chains
  • 2 globular heads that join onto actin
  • ATPase in the myosin heads
135
Q

describe actin

A
  • double stranded protein - 2 monomers polymerised to form a helical structure
  • has a myosin binding site, covered by tropomyosin and held in place by troponin.
    • tropomyosin is found in the groove between the 2 actin filaments
136
Q

what is troponin

A
  • a protein that holds tropomyosin in place on actin and is involved in myocyte contraction
  • it has 3 subunits
    1. TNI - inhibitory to prevent in actin and myosin interaction
    2. TnT tropomyosin binding
    3. TnC calcium binding
137
Q

describe a sarcomere

A

Thick filament- myosin

Thin filament- actin along with tropomyosin and troponin

H zone- region of sarcomere that only has thick filament

I band- contain thin filament and binds to Z disc

A band- large portion of sarcomere, overlap between thick and thin filament

M line- proteins that connect central points of thick filament

C zone- crosslinks thick filament and titin

Z disc- anchoring point of thin actin filaments

Titin- responsible for the elasticity of muscle. Allows muscles to recoil to its normal form. Prevents muscle fibre from being overstretched.

138
Q

what is Ohm’s Law - relate it to the heart

A

Voltage =current x resistance

V=IR

flow [current] = pressure gradient [voltage] / resistance

139
Q

DESCRIBE THE SLIDING FILAMENT THEORY

A
  1. myosin filament attaches to the actin filaments myosin binding site via the myosin head, forming the cross bridge
  2. the angle of the myosin head changes to pull the actin filament inwards = power stroke
    • this causes the release of ADP and Pi
  3. ATP attaches to the myosin head causing it to detach and reset back to its original position and join onto another myosin binding site further along the actin filament.
    • Calcium binding to troponin on the actin filament allows the myosin head to bind by removing the inhibitory unit of troponin.
140
Q

what causes the first and second heart sounds

A
  1. Mitral valve shutting
  2. aortic valve shutting
141
Q

6 steps of the cardiac cycle

A
  1. atrial depolarisation and contraction
    • SA node fires → depolarisation of the atrial myocytes → contraction.
    • this increases the atrial pressure → further ventricular filling
    • as atrial contraction ends, the atrial pressure falls below that of the ventricles → closure of the AV valves
      • closure of mitral valve = 1st heart sound
  2. isovolumetric contraction
    • both valves are shut
    • the AVN received the signal for depolarisation and passed it onto the bundle of his and purkinje fibres→ depolarisation and contraction of the ventricular myocytes.
    • this increases the pressure within the ventricle
  3. rapid ejection
    • once the pressure within the ventricle exceeds that of the aorta and pulmonary artery the semilunar valves open → rapid ejection.
  4. reduced ejection
    • as ventricular contraction ends, the force of ejection is reduced due to a decrease in ventricular pressure.
  5. isovolumetric relaxation
    • once the pressure of the ventricles falls below that of the aorta and pulmonary artery, the semilunar valves shut
      • closure of the aortic valve = 2nd heart sound.
    • both vessels are shut, hence isovolumetric relaxation
  6. ventricular filling
    • diastole begins and the pressure within the ventricle falls below that of the atria → opening of the AV valves and passive ventricular filling.
142
Q

what are the physiological and clinical durations of systole and diastole

A
  • physiologically
  • systole is both isovolumic contraction and ejection•
  • Diastole starts before A2 then isovolumic relaxation. After you get the filling process.
  • Clinically/cardiology
  • Systole is between 1st and 2nd HS M1-A2
  • In cardiology it is A2-M1.
143
Q

what is starling’s law and why does it occur

A

Starling’s law states that the more the heart chambers fill, the stronger the ventricular contraction, and the greater the stroke volume

  • This occurs because as the heart muscle fills and stretches, it creates more regions of overlap for actin-myosin cross-bridges to form, allowing for a greater force of contraction
144
Q

what is cardiac output?

A

the amount of blood pumped by each ventricle in 1 minute

CO= heart rate x stroke volume

145
Q

what factors affect heart rate

A

age

fitness level

autonomic innervation

hormones

146
Q

what factors affect stroke volume

A

preload [EDV]

afterload [resistance]

contactility

duration of contraction

147
Q

what is preload and what factors affect it

A

the degree of ventricular stretch at the end of diastole - a volume

venous blood pressure and rate of venous return

148
Q

what is afterload and what factors affect it

A

the pressure which the ventricles must overcome to eject blood

i.e. systemic pressure and pulmonary pressure

149
Q

what is pulse pressure

A

PP = systolic pressure - diastolic pressure

150
Q

stroke volume eqn

A

SV = EDV-ESV

151
Q

describe artery circulatory dynamics

A
  • elastic
  • low resistance channels
  • cushion systole
  • maintain blood flow at a high pressure
152
Q

describe arteriole circulatory dynamics

A
  • the main site of resistance to blood flow
    • therefore total peripheral resistance = total arterial resistance
  • major role in determining arterial pressure
  • major role in distributing blood to organs and tissues
  • affected by local, neural and hormonal factors
153
Q

what is TPR

A

total peripheral resistance is arterial resistance

  • determined by the radius of the arterioles which is controlled by vascular smooth muscle
  • VSM Contracts [vasocontraction] = ↓Radius = ↑Resistance ↓Flow
  • VSM Relaxes [vasodilation] = ↑Radius = ↓Resistance ↑Flow
  • • VSM never completely relaxed = myogenic tone
154
Q

describe capillary circulatory dynamics

A
  • Large area = slow flow which allows time for nutrient/waste exchange
  • Interstitial fluids/ plasma determines the ECF distribution
  • Flow is determined by :-
    • Arteriolar resistance
    • number of open Pre-capillary sphincters
155
Q

describe vein circulatory dynamics

A
  • low resistance
  • skeletal muscle contraction squeezes the veins and helps push blood back to the heart
  • respiratory pump aids blood return
  • valves to prevent backflow
156
Q

describe lymphatic circulatory dynamics

A
  • carry excess fluid and protein filtered from capillaries
  • Return of fluid to cardiovascular system through the thoracic duct- subclavian vein
  • Unidirectional flow aided by:
    • smooth muscles in lymph vessels
    • skeletal muscle
    • respiratory pump.
157
Q

what factor affects the starling mechanism

A

venous return

  • venous return impacts EDV which affects SV and thus CO.
  • CO = Sv x HR
  • the greater venous return is the greater EDV is and vice versa
  • Due to Length-Tension (L-T) relationship of muscle:
    • ↑EDV = ↑Stretch = ↑Force of contraction
158
Q

what is blood pressure

A

the pressure of blood against the arteries

159
Q

how is BP controlled

A
  1. autoregulation of smooth muscle
  2. local mediators
  3. central neural control
  4. humoral mediators
  5. baroreceptors
160
Q

describe myocyte autoregulation

A
  • as blood passes through the vessel, the vascular smooth muscle stretches. The VSM reponds automatically by contracting back to a normal diameter
  • this is an intrinsic ability of an organ
  • it maintains constant bloodflow to key organs despite perfusion pressure changes
    • brain, kidneys and heart have v good myocyte autoreg
    • skin has poor autoreg
    • splanchnic, and skeletal muscle have moderat autoreg
161
Q

blood volume regulation involves

A
  • RAAS
  • ADH
  • kidneys and adrenal glands
162
Q

name hormonal factors that affect blood flow

A
  • Vasodilators
  • epinephrine in the muscle
  • atrial natriuretic peptide
  • vasoconstrictors
  • epinephrine in the skin
  • angiotensin 2
  • vasopressin [ADH]
163
Q

difference between intrinsic and extrinsic control

A
  • intrinsic is a mechanism within the organ
  • extrinsic = mechanisms dependent on hormonal or nervous input or external input.
164
Q

name local humoral factors that control the blood vessels

A
  • vasoconstrictors
  • Endothelin 1
  • myogenic contraction - autoreg
  • vasodilators
  • hypoxia
  • NO
  • bradykinin
  • PGs
  • tissue breakdown products
  • •K+, CO2, H+
165
Q

role of the endothelium in blood flow control

A

the endothelium is key for control of circulation as it produces:

  • Nitric oxide NO = potent vasodilator
  • PGs = potent vasodilator
  • Endothelin-1 =potent vasoconstrictor
166
Q

what are baroreceptors AND where are they found

A
  • pressure sensing receptors that detect changes in blood pressure
  • primary are found in the
    • aortic arch - aortic bodies
    • bifurcation of the carotid arteries - carotid bodies
  • secondary are found in
    • myocardium
    • vein and arteries
    • pulmonary vessels
167
Q

how do baroreceptors communicate their info

A
  • via cranial nerves to the medulla
    • afferent nerve = glossopharyngeal CN9
    • efferent nerve = vagus CN10
  • the barorecpetors fire signals at a rate proportional to the MAP and pulse pressure
    • changes from the normal blood pressure → response via changes to para/sympathetic stimulation
168
Q

how would baroreceptors cause a response to ⇡BP

A

↑BP ⇒ ↑Firing via CN9 ⇒ ↑PNS [CN10]/↓SNS ⇒ ↓CO ↓TPR = ↓BP

PNS = parasympathetic nervous stimulation

169
Q

function of arterial baroreceptors

A
  • key role in short term regulation of BP e.g.
    • respond to exercise or blood loss
  • long term role in resetting new level of normal BP
    • if the arterial BP remains elevated for a few days, the arterial baroreceptors will reset the baseline level to this level → hypertension.
170
Q

where are cardiopulmonary baroreceptors found and what is their function

A
  • atria, ventricles and pulmonary arteries
  • ANP from the atria responds to stretch
    • when secreted it ↓ stimulation vasoconstriction centre in the medulla → ↓BP by reducing blood volume via fluid loss
      • ↓ angiotensin
      • ↓ADH
      • ↓aldosterone
171
Q

describe the neural control loop in hypotension

A
  • baroreceptors detect a drop in pressure
  • fire fewer signal to the medulla via CN9
  • medulla increases sympathetic stimulation via spinal cord and decreases parasympathetic stimulation via CN10
  • this increases the heart rate and the stroke volume and decreases the blood vessel diameter
172
Q

what are the main neural influences on the medulla

A
  • baroreceptors
  • chemoreceptors
  • changes in blood oxygen and CO2
  • skin
  • hypothalamus
  • cerebral cortex
173
Q

where are the chemosensitive regions

A
  • Central:
    • in the medulla
  • Peripheral:
    • carotid bodies and aortic bodies
174
Q

what do the central chemosensitive regions detect and how do they respond

A

detect levels of CO2 and pH

  • ↑PaCO2 = vasoconstriction, ↑peripheral resistance, ↑BP
  • ↓PaCO2 = ↓medullary tonic activity, ↓BP
  • Similar changes with ↑ and ↓ pH
  • PaO2 less effect on medulla:
    • moderate ↓PaO2 = vasoconstriction;
    • Severe ↓ = general depression
175
Q

what are the key central effectors following detection of BP change?

A
  • blood vessels: vasodilation, vasoconstriction
  • heart: rate and contractility
  • Kidney: fluid balance
176
Q

short term BP changes are regulated by

A

baroreceptors

–e.g.↑BP ⇒ ↑Firing ⇒ ↑PNS/↓SNS ⇒ ↓CO/TPR = ↓BP

177
Q

longer term BP changes are regulated by

A

adjusting the blood volume

–Na+, H20, Renin-Angiotensin-Aldosterone and ADH

178
Q

how long does each interval last on an ECG

A

PR interval = 120-200ms

QRS complex = <100ms

QT interval = 440ms men and 460ms women

179
Q

Which embryological structure gives rise to the aortic root

A

Truncus arteriosus

180
Q

what substance exerts a local effect on blood vessels resulting in vasoconstriction?

A

endothelin-1

181
Q

blood pressure eqn

A

blood pressure = cardiac output x total peripheral resistance

182
Q

State two effects that stimulating arterial baroreceptors has on systemic blood pressure.

A
  • Decreased sympathetic nervous system stimulation,
  • decreased arteriolar vasoconstriction,
  • decreased blood pressure
183
Q

The visceral pericardium is made up of which cells?

A

mesothelium

184
Q

how long does systole and diastole last

A

Systole 0.3 sec

Diastole 0.5sec

my phase 1 (11 decks)

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