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cardiovascular > physiology 2 > Flashcards

physiology 2 Flashcards

1
Q

what are the basic leads

A

standard limb leads

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2
Q

what planes to the limb leads work in

A

vertical or frontal plane

coronal plane

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3
Q

what are the 3 standard limb leads

A

I
II
III

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4
Q

what does SLL I record

A

left arm with regard to right arm

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5
Q

what does SLL II record

A

left leg with regard to right arm

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6
Q

what dose SLL III record

A

left leg with regard to left arm

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7
Q

what is transmitted well to the ECG

A

fats events - depolarisation and repolarisation of the action potentials

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8
Q

what is not transmitted well to the ECG

A

slow events - the plateau of the action potential

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9
Q

what causes a upward going blip

A

a move of approaching depolarisation

or a wave of repolarisation going away

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10
Q

what 3 limbs have electrodes on them

A

the left leg

left arm

right arm

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11
Q

what has the positive electrode on it

A

the limb being recorded with regards to another limb

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12
Q

what happens if a wave of depolarisation goes away from the limb being measured

A

a downward blip will occur

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13
Q

what happens when a wave of repolarisation approaches the limb being measured

A

a downward blip will occur

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14
Q

what does the time for QRS tell us

A

time for whole ventricle depolarisation

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15
Q

how ling dose the QRS complex take to complete - abnormal

A

about 0.08 secs

abnormal is greater than 0.12 seconds

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16
Q

what is the PR interval showing

A

time from atrial depolarisation to ventricular depolarisation

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17
Q

how long is the PR interval - why

A

normally = 0.12 - 0.2 seconds

due to wave having to pass through slow AV node

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18
Q

what does the QT interval show

A

the time spent were the whole ventricle is depolarised

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19
Q

what is the normal QT interval

A

about 0.42 seconds at 60bpm

depends on HR

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20
Q

can you see atrial repolarisation - why

A

NO

as the possible signal coincides with the ventricle depolarisation

it gets ‘‘drowned out’’

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21
Q

why is the QRS complex so complex

A

different parts of the ventricle depolarise at different times in different directions:

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22
Q

what causes the Q wave - and the downward blip

A

the interventricular septum depolarising from left to right

away from the left leg = blip down

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23
Q

what causes the R wave - why the upward spike

A

the bulk of the ventricle depolarises

upward blip = goes from endocardial to epicardial surface (inside to out)

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24
Q

what causes the S wave

why the downward blip

A

the upperpart of the intraventricular septum depolarises

it goes from bottom to top

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25
Q

why is the t wave positive

A

as the action potential is longer on the endocardial cells then the epicardial cells - the wave of repolarisation runs the other way (ALMOST LIKE DOWN A CONC GRADIENT)

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26
Q

why is the R wave bigger on SLL 2

A

as the heart is tilted it follows the direction of SLL 2 the best

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27
Q

what would happen if heart rotated

A

you would see a decreased SLL 2 R wave and see either an increase or decrease in the other SLL depending on direction

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28
Q

what would happen during Right/left ventricular atrophy/hypertrophy

A

atrophy wastes away
hypertrophy - builds up

the side that wastes away would be weaker i.e. left atrophy would lead to weaker SLL 1 R wave being smaller

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29
Q

what are Augmented limb leads

A

it leads to two limb leads being combined ang giving an extra direction to the positive electrode

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30
Q

why are they useful

A

give 3 new perspectives

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31
Q

what are the names of the augmented limb leads - where do they lead

A

aVR - right arm
aVL - left arm
aVF - foot (left)

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32
Q

combining SLL and augmented limb leads gives you what

A

6 different vies of the vertical (coronal plane)

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33
Q

. What extra information do the precordial (chest) leads give you

A

look at the same events of the other leads, but in the horizontal (or transverse) plane

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34
Q

where are the precordial (chest) leads laced

A

front of the chest

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35
Q

what are all precordial chest leads

A

positive

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36
Q

what is normal for a precordial chest lead

A

negative blip on 1

by the end is a positive blip on 6

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37
Q

how may precordial leads are there

A

6

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38
Q

what way dose the wave of depolarisation go through the heart in the transverse plane

A

towards the midclavicular line

39
Q

what does the rhythm strip tell us (5)

A

heart rate

is there a P wave before QRS

is PR to short/long

is QRS to wide

is QT to long

40
Q

what is the calibrating pulse

A

0.2sec - l large square - 5mm

41
Q

what speed should the rhythm strip go

A

run at 25mm/second

42
Q

how is HR measured

A

could the R waves in 30 large squares (= 6 seconds) and multiply by 10

43
Q

what is the term for below 60

A

bradycardia

44
Q

what is the term for above 100

A

tachycardia

45
Q

what is STEMI used for

A

hear attack classification

STEMI is worse than NSTEMI

46
Q

what is a STEMI

A

ST elevated myocardial infarction

47
Q

what is a NSTEMI

A

non-ST elevated myocardial infarction

48
Q

what happens in a STEM

A

the ST segment is raised up high and this is very prominent on a ECG

49
Q

what dose myocardial infarction mean

A 
myo = muscle 
cardial = cardiac 
infarction = death of tissue (necrosis) due to obstruction of blood
50
Q

what is diastole

A

diastole occurs when the heart relaxes after contraction

51
Q

what is systole

A

Systole occurs when the heart contracts to pump blood out

52
Q

what are the 5 phases of the cardiac cycle

A

late diastole

atryial systole

isovolumic ventricular contraction

ventricular ejection

isovolumetric ventriculare relaxiation

53
Q

what is the fancy name for listening to heart sounds

A

phonocardiogram

54
Q

what generates the LUB sound

A

mirtal (bicuspid) and tricuspid valves closing

55
Q

what generates the DUB sound

A

aortic and pulmonary vales closing

56
Q

what sound indicates an abnormality or further investigation

A

a murmur = hissing, ssshhhh sound

57
Q

when would you hear a murmur between the LUB and DUB

A

Stenosis of either Stenosis of either atrioventricular valves

OR

incontenance/ regurgitaion of the mitral and tricuspid valves

58
Q

what would give arise to a constat murmur sound

A

a spetal defect

59
Q

what would give arise to a murmur after the DUB and before the LUB

A

incontanace or regurgitation therough the Stenosis of either atrioventricular valves

or

stenosis of the mitral and/ or tricuspid valves

60
Q

what causes the dicotic notch

A

the elastic energy of the ventricle

61
Q

how long is systole roughly compared to diastole

A

1/3 systole

2/3 diastole

62
Q

what is isometric contraction

A

the contraction of the ventricle that doesnt open the aortic valve due to the

63
Q

what is at the start and then the end of the isometric contraction phase

A

mitral valve closes

aortic valve opens

64
Q

after the aortic valve opens what is this phase called

A

the rapid ejection phase

65
Q

what happens after the rapid ejection phase - why

A

the slower ejection phase

its slower as the pressure built up by the blood vol/isometric contraction has subsided

66
Q

what does the aortic valve open

A

as the pressure in the ventricle is grater than in the aorta

67
Q

what is the difference between systolic and diastolic called

A

pulse pressure

68
Q

what does the 3rd heart sound relate to

A

rapid filling phase

69
Q

when would you hear a healthy 3rd heart sound

A

in someone young/ or who has a healthy heart - with good elasticity

70
Q

what is stroke volume

A

the difference between end systolic volume and end diastolic volume `

71
Q

what is the ESV roughly

A

60ml

72
Q

what happens when HR increases

A

it shortens diastole

73
Q

when does preload start to get effected by HR

A

at about 120bpm

reduces slow filling phase - encroaching on rapid filling phase

74
Q

what does the sympathetic nervous system release

A

noradrenaline

and circulating adrenaline from the adrenal medulla

75
Q

what does noradrenaline/ adrenaline act on

A

the beta 1 receptors on sinoatrial node

76
Q

what does the sympathetic nervous system do

A

increase the slope of the pace maker potential - get closer to the threshold

77
Q

what does the parasympathetic nervous system release

A

vagus releases

acetylcholine

78
Q

what does ACh act on

A

the muscarinic receptors on sinoatrial node

79
Q

what does the parsympathetic do

A

hyperpolarises cells and decreases the slope of pacemaker potential

80
Q

what is starlings law

A

the energy of contraction is proportional to the initla length of the cardiac muscle volume

81
Q

what is preload affected by

A

end diastolic volume

82
Q

what are the dominos after increased venous return

A

increased diastolic volume

therefore increasing the stroke volume

83
Q

what are the dominos after decreased venous return

A

decreased end diastolic volume

and decreasing the stroke volume

84
Q

what is afterload

A

the load against which the muscle tries to contract

85
Q

what does TPR

A

total peripheral resistance

86
Q

what happens if total peripheral resistance increases

A

aortic pressure will increase

ventricle will have to work harder - less energy for ejecting blood (stroke volume)

87
Q

what happens to stimulated beta 1 receptors on the myocytes

A

increase contractility
ionotropic effect

stronger but shorter contraction

move the graph up
more stroke volume for the same diastolic volume

88
Q

does parasympathetic NS effect stroke volume

A

no

valgus does not innervate ventricular muscle

89
Q

how can cardiac out put increase by 4-6 times

A

increased HR
increased contractily
increased venous return
TPR falls

90
Q

what causes increased venous return

A

venoconstriction

skeletal/respiratory pumps

91
Q

cardiac out put =

A

stroke volume x heart rate

92
Q

what is hypercalcemia - pathological response

A

more calcium - shifts curve up

93
Q

ischemia does what to ‘‘the curve’’

A

shifts it down

94
Q

what is the ejection fraction

A

the stroke volume/EDV

the stuff squirted out/stuff left in

cardiovascular (26 decks)

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