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Phase 1 > Cardio > Flashcards

Cardio Flashcards

1
Q

what are the 6 limb leads?

A

in eithovens triangle, 1 is across teh top, 2 is down from the right and 3 is down from the left
then from the centre it goes AVR (right), AVL (left) and AVF (foot)

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2
Q

where are the chest leads placed?

A 
V1: R.of sternum 4th intercostal
space
• V2: L.of sternum 4th intercostal
space
• V4- R. of sternum 5th intercostal
space midclavicular line 
• V3: inbetween V2 and V4
• V5: 5th intercostal space anterior
axillary line
• V6: 5th intercostal space
midaxillary line
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3
Q

what times do the squares on an ecg represent?

A

• One small square represents 40ms one big square 02s

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4
Q

how big should the PR interval be

A

• PR interval should be 3-5 small squares (0.12-0.20s)

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5
Q

what are teh 4 layers of teh heart - inside to outside

A

endocardium, myocardium, epicardium, pericardoum

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6
Q

what trilaminar disk layer does the cardiac system and blood vessles form form

A

mesoderm

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7
Q

what are the 5 lumps if teh heart tibe and what do the form

A
  • Truncus arteriosus - aortic arcches and arteries
    • Bulbus cordis - right ventricle and outflow trats
    • Priitive ventricle - left ventricle
    • Primitive atrium - parts of left and right atrium
    • Sinus venousus - superior vena cava and right artium
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8
Q

what are the layers in a blood vessle

A

• Blood vessels - basement membrrane, endothelium, intima, internal elastic lamina, media, external elastic lamina, adventitia

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9
Q

where is the sight of most resistnace in teh blood vessles

A

The arteroles are the sight of most resistance as the lumen is smaller byt there arent as many as in capillereues they can regulate blood flow by contracing and dilating

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10
Q

what is teh difference between and artyery and an arteriole

A

• Arterioles have 3 or less muscle layers in their media!!!

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11
Q

defien heamocrit

A

the ratio of red blood cellls to total blood volume (45%)

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12
Q

wht is heamophillia

A

Heaophllia - the deficancy of von willibrand clotting factor (8, its an x linked genetic condition

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13
Q

wht is heamophillia

A

Heaophllia - the deficancy of von willibrand clotting factor (8, its an x linked genetic condition

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14
Q

what protien chanis make up heamoglobin

A
  • Heamoglobin has 4 chains, 2 alpha and 2 beta in adults

* 2 alpha and 2 gamma in feotuses

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15
Q

what is pernicius anemia

A

caused by deficiancies of B12

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16
Q

what is macryotic anemia

A

• Deficioencies of iron and folate are macrocytic anemia

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17
Q

what whte blood cells are granulocytes

A

neutrophills, eosinophills, basophills

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18
Q

what WBCs are agranulocytes

A

lymphocytes and monocytes

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19
Q

what is a blood stem cell called and what does it dividie into

A

heamocytoblast

commen myloid progenator, common lymphoid progenator

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20
Q

what does a commen myloid progenator trun into

A

megakaryocyte, erethrocyte, mast cell, myloblast

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21
Q

wat does a myloblast differentiate into

A

basophil, eosinophil, neutrophill, monocyte

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22
Q

what does a commen lympohid progenator divide into

A

natural killer cell and small lymphocyte

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23
Q

what does a samll lympphcyte divide into

A

t and b lymphocytes

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24
Q

what is a monocyte

A

mature cells with kidney bean nucleus that travle around in the blood phagocytosing and tehn settle donw in a tissue tobecome a macrophage in a tissue such as a kupffer cell

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25
Q

what is serum

A

plasma minus clotting factors

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26
Q

where are erethrrocyeted prosuced in teh feotus

A

• Erethrocytes are produces in the liver and spleen in the feotus

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27
Q

what are neutrophills

A

• Neutrophill shave a multilobed nucleus and granulur cytoplasm
• They are phagocytic and engluf and destory the forign macromolecuels
They destroy pathogens using eh respiritory burst and so contain the enzyme myeloperoxidase

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28
Q

what are basophills

A

• Basophills are for inflimation due to allergic reations

Basophill are the circulation version of mast cells which are stationar in tissue but also release histamine

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29
Q

what are eospnophills

A

Eosinophills are involved in the parasites and allergy mediation/inflamaiton

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30
Q

where do platelets come from

A

tehy are the blebs fromed from megakaryocyte cyosol

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31
Q

where are blood stem cells in an adult

A

teh axial skeleton

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32
Q

what stimulates teh production of megakaryocytes and hence teh production of platelets

A

Thrombropoietin stimulates the production of megakaryocytes, hence platelet production

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33
Q

what are teh three stages for lpatelet release

A

thrombropoeitin is released whihc stimulates megakaryocyte production
Megakaryocytes enter endomitossi where the nda doubles but the cell doent divide
• The blebbing process is when beits break off and makes the platelets

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34
Q

what is teh extrinsiec pathway

A

The extrinsic pathway is activated by the collagen on the outside of the blood vessels which has facotr 3 (also called tissue factor) on it
this cleaves 7 to 7a whihc then cleaves 10 to 10a
the commen cascade then takes over

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35
Q

what is teh intrinsic clotting oathway

A

he intrinsic pathway is activated through exposed endothelial collagen, and the extrinsic pathway is activated through tissue factor released by endothelial cells after external damage
12 is cleaved to 12a, then 11 to 11a then 9 to 9a ten 8 to 8a then 10 to 10 a. teh commen cascade can tehn begin

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36
Q

what is teh commen cascade

A

starts wiith 10 being cleaved into 10a by teh extrinsic or intrinsic factors
10a then turns 5 into 5a whihc turns 2 into 2a and 1 into 1a

37
Q

what are the other names for clotting factor 2, 2a, 1, 1a

A

2- prothrombin
2a- thrombrin
1 - fibrinogen
1a - fibrin

38
Q

how does fibrin end teh clotting cascade

A

it ban being oer teh olatelat plufg and stabalie it

39
Q

what are the three stages when a blood vessle si damaged

A

vasocontriction, platelt plug, clotting cascade

40
Q

what cases vasoconstriction in a blood vessle

A

release of endothelin 1, nihibition of NO and prostacyclin

41
Q

what are teh granules contained within platelets

A

• Peatlets contain 2 tyoes of granules - electorn dense and alpha
• Electron dense ones contain Ca2+, ATP and seratonin
• The alpha ones have platelet growth factor, fibrinogen and von willibrands factor
• The ATP release d=from electron dense granules are energy provision for the plug formation
The alpha dense granules are to help mediate the scaffolding aspect (clotting cascade)

42
Q

how is teh platelet plug formed, including teh receptos used in each stage

A

VWF binds to exposed collgen and acts as a bridge for platelts to bind to using GP1b receptors
platelets then bind to otehr platelets using fibrinogen that is connected to Gp2a/3b receptors

43
Q

what breaks down fibrin

A

the fibrolytic system, plasminogen is converted to plasmin by 7a which can then digest the fibrin

44
Q

what are the ABO antigens made from and can they cross teh placenta?

A

ABO antigens are made from carbohydrates and the antibodues for them (imunogloblin M) cant cross the placenta. It is mae in the spleem

45
Q

ehat are the local factors of vasodilation and vasoconstriction

A

NO, prostacyclin, K+, hypoxia, low pH and O2, bradykinin

endothelin 1

46
Q

what are the hormonal factros for vasodilation and constrictione

A

Ach, ANP

Angiotensin 2, ADH, NAD

47
Q

describe teh action potential of non nondal pathways (in teh myocytes) in teh heart

A

• Resting potential is -90 and then the threshold is at -60
• This then causes an influx of NA+ up to +20 where it tehn start a decrease
• At +20 the gates open and the k+ start to move out
• Then after it gets to 0 the Ca2+ open up which leads to the rate of repolarization being massively slowed down as they diffuse out an the k+ are diffusing in
Then after a while the Ca2+ shut and the K+ continue to influx out which leads to it decreasing in potential again

48
Q

describe the action potential of of teh nodes in teh heart

A

The SAN has a resting potential of- 60 and has a threshold of -40 which will cause all of the channels to flood openand the voltage gated ion channels open and the Ca2+ flood in
Then at +20 it start starts ot repolarize againi by the K+ channelsopening and flooding out and then the whole cycle stratrs again, this si scontinuous and also spontanious

49
Q

what causes the myocytes to contract

A

the ca2+ flodding in

50
Q

whihc phase is phase 0 in the myocyte caridac cycle

A

hase 0 is the rapid depolerisation

51
Q

how does teh SAN keep continious contractions going

A

SAN has a resting potential of -60 and once it has contracted it hyperpolerises. This causes the Hyperpolarization-activated, cyclic nucleotide-gated (HCN) ion channels t oopen and start a notehr contraciotn immidiatly

52
Q

what does positive ionotrophic mean and positive chronotrophic

A

Increased force of contraction, increased numbers of contractions

53
Q

how long does it take for contraction to happen

A

Conduction happens in 220ms

54
Q

what are the three refreacoty periods

A
  • Absolute refractory - no stimulus will generate AP
    • Effective refractory period - large stimulus, generate an AP but is too weak to conduct
    • Relative refractory period- secon stimulus has tobe bigger thha the last
55
Q

what is excitability

A

Excitability - ability of myocardial cells to depolerise in response to an incoming current

56
Q

what is hyperaemia and what are the three types

A

• Hyperemia is when your blood adjusts to support different tissues throughout your body. It can be caused by a variety of conditions. There are three types of hyperemia: reactive, active and passive. reactive hyperemia is when you occlude blood flow and when you release t the blood fluches in . Passive hyperemia is usually caused by disease and is more serious. Active hypereamia - dilation in response to extra oxygen needed (ie whne excercising)

57
Q

what is excitation contraction coupling

A

Excitation–contraction coupling is the connection between the electrical action potential and the mechanical muscle contraction.

58
Q

whihc bands in a muscle change length

A

H and I

59
Q

what are all of the bands in teh sarcomere

A

z - end of teh alphabet and sarcomere
M - midline
I band - this letter, only thin filament
H zone - thick letter, only thick filaments
A - hybrind of I and h, both thick and thin secion, its all of teh myosic uincluding teh bit tha pverlaps wit the actin

60
Q

what does titin do

A

responsoble for elasticity of muscles, allow muscls to recoil to the morm and prevent them from being overstrethed

61
Q

what is the makeup of acitn and myosin

A

• Myosin is made up of 2 heavy chains and 4 lighter chains
• There are heads and the heads have ATPase on the ends of tehm
• Acdsin is a globular protien tha is polymerised with other monomers to form a helical structure
•

62
Q

what are the three subunits of troponin

A

• Troponin has 3 subunits - TNI, TNT and TNC
• TNI - Inhibits tyeh actin and myosin binding
• TNT - binds to the TROPOMYOSIN
TnC - calcium binding - calcium binding

63
Q

what occuldes teh myosin bindng sight

A

Actin has a myosin binding sight which is partially coverd by tropomyosin which is moved out of the way by troponin protine when it comes into contact with Ca2+
• Action potential pass doesn the t tubles to the sarcoplasmic reticulum which releases Ca2+
• This then binds with troponins TNC which moves the TNI out of the way

64
Q

what does teh T complex show?

A

repolerisation of teh venticles

65
Q

what is isovolumetric contraction

A

Isovolmetric contraction - when the ventricles contract and the oressure increass but the valves remain shut just causing and increase of pressure but m=no movement

66
Q

what is diastasis

A

diastasis is the middle stage of diastole during the cycle of a heartbeat, where the initial passive filling of the heart’s ventricles has slowed, but before the atria contract to complete the active filling
Diastasis is LV pressure= L arterial pressure, filling temporarily
stops.

67
Q

define preload and afterload

A
  • Preload is the initial stretching of the cardiac myocytes (muscle cells) prior to contraction. It is related to ventricular filling.
    • Afterload is the force or load against which the heart has to contract to eject the blood
68
Q

what is starlings law

A

• Starlnigs law - the greater the preload the greater the force of contraction and the greater the stroke volume

69
Q

wat is teh equation for cardiac output

A

Cardiac coutput= stroke volume x heart rate

70
Q

contractility

A

• Contractility - ability to increase the contraction to achive higher pressure, independent of the preload put in

71
Q

compliance

A

• Compliance - how easily a chamber of the heart or the lumen of a blood vessel expands when it is filled with a volume of blood

72
Q

define systolic and distolic pressure

A

• Systolic pressure - maximum arterial pressure during contraction of the left ventricle fo the heart
Diastolic pressure - minimum arterial pressure during diasotle of the left ventricle

73
Q

what is teh equation for blood pressure

A

cardiac output x total peripheral resistance

74
Q

what is teh equation fro pulse pressure

A

systolic - diastolic pressure

75
Q

what is the quation fro mena arterial pressure

A

diastolic pressure + 1/3 pulse pressure

76
Q

what is teh stroke volume

A

end diastolic volum - end systolic volume

77
Q

what is poisuelles equation and wha does it mean

A

flow = radius of teh blood vessle to the power of 4 - thsi means if it gets smaller theres mucg more resistance for the blood

78
Q

what is ohms law

A

flow = pressure gradient/resistance

79
Q

what is teh flow in capilleries dicatated by

A

The flow in capilleries is determined by the pre capillery shpincter and arteriol resistance

80
Q

how is teh blood helped to returned to teh heart in teh veins

A

Unidirectional flow is aided by smooth muscle in lymph vessles, skeletal muscles and also the respiritory pump

81
Q

how does teh respiritory pump work

A

• Respiratory pump- inhalation, pushing down of diaphragm leads to increased abdominal pressure and decreased thoracic
pressure so pressure difference enables venous return

82
Q

how do chemoreceptors controll heart rate

A

• Chemoreceptors are involved in the controll of breathing and decrease the parasympathetic outflow to the heart
• Centra are most sensitive to CO2 and ph, less so to O2
• Increased firing leads to sympathetic outflow
Lead to vasoconstriction hwihc increases total peripheral blood pressure

83
Q

where are baroreceptors located and how can they change the heart rate

A

• Baroreceptors are present in the carotid sinus and aortic arch,
• The afferent nrerves used are the glossopharyngeal to the medulla
• The efferetn tha causes the changes are the sympathetic and vagus
The arterial baroreceptors are located in the arterioles and lead to the short term regulation of blood pressure though vasoconstriction

84
Q

what are periphearl receptors

A
  • Peripheral are in the commen carotid and aortic arch
    • They are very sensitibe to changes in P02
    • But also sentitvie to pH and CO2
85
Q

what are teh centra receptors

A

• Centra are most sensitive to CO2 and ph, less so to O2
• Increased firing leads to sympathetic outflow
Lead to vasoconstriction hwihc increases total peripheral blood pressure

86
Q

what are cardiopulmpnary barreceptors

A

• Cardiopulmonary baroreceptors - in the atria, ventricles and pulmonary artery, when they are stimulated they work on the more long term control, this leads to a decreased release of angiotensin, aldosterone and ADH which overall decreases blood pressure
Chemoreceptor

87
Q

what are the 4 key ways to change blood pressure

A

The key ways to change blood pressure are vasoconstriction/ dilation, heart rate and contractility, kidney fluid balanc

88
Q

what is a bundle block on an ECG

A

Right/left bundle branch block - one of the sides of the septum Purkinje fibres are slowed down, this causes a wide QRS complex

Phase 1 (11 decks)

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