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Cardio - mine > Physiology > Flashcards

Physiology Flashcards

1
Q

what does the P wave signify

A

atrial depolarisation

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2
Q

what does the QRS complex signify

A

ventricular depolarisation

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3
Q

what does the T wave signify

A

ventricular repolarisation

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4
Q

what does the PR interval signify

A

AV nodal delay

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5
Q

what does the ST segment signify

A

ventricular systole

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6
Q

what does the TP interval signify

A

diastole

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7
Q

what system mainly influences HR

A

autonomic nervous system

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8
Q

what effect does sympathetic stimulation have on HR

A

increase

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9
Q

what effect does parasympathetic stimulation have on HR

A

decrease

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10
Q

how does sympathetic stimulation increase HR

A

decreases AV nodal delay

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11
Q

what chemical acts upon which cells during cardiac sympathetic stimulation

A

noradrenaline acting on B1 adrenoreceptors

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12
Q

how does parasympathetic stimulation decrease HR

A

vagus nerves exerts a continous influence on SA node (vagal tone)
increases AV nodal delay

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13
Q

what chemical acts upon which cells during cardiac parasympathetic stimulation

A

ACh acting on M2 receptors

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14
Q

what is a competitive inhibitor of ACh

A

atropine

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15
Q

when would atropine be used

A

during bradycardia to increase HR

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16
Q

what is a resting HR

A

60-100bpm

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17
Q

what HR is bradycardia

A

below 60bpm

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18
Q

what Hr is tachycardia

A

above 100bpm

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19
Q

where does the excitation of the heart originate

A

pacemaker cells in the SA node

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20
Q

if the HR is driven by the SA node and is in regular rhythm it is said to be in what

A

sinus rhythm

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21
Q

describe the route of excitation

A

spreads from SA node to AV node via gap junctions
then speeds down the bundle of his
then down the L and R bundle branches to the purkinje fibres

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22
Q

what is the AV node

A

small bundle of specialised cardiac cells

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23
Q

what is the only point of electrical contact between the atria and the ventricles

A

AV node

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24
Q

where is the AV node located

A

at the base of the RA just above the junction of the atria and ventricles

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25
Q

what allows atrial systole to precede ventricular systole, why?

A

the AV node; is has a slow conduction velocity which delays conduction across the AV node

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26
Q

what is atrial systole also know as

A

contraction

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27
Q

outline the structure of cardiac muscle

A

striated fibres contains myofibrils
coupled via gap junctions
desmosome provide mechanical support

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28
Q

describe the structure of myofibrils

A

contain thick filaments (myosin) and thin filaments (actin) arranged into sarcomeres

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29
Q

what is stroke volume (SV)

A

the volume of blood ejected by each ventricle per heart beat

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30
Q

what is stroke volume equal to

A

end diastolic volume - end systolic volume

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31
Q

describe the intrinsic mechanisms that regulate SV

A

changes in the diastolic length of myocardial fibres, this is determined by EDV

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32
Q

what extrinsic mechanisms that regulate SV

A

hormones and nerves

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33
Q

what effect does sympathetic stimulation have on SV

A

increases

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34
Q

what effect does parasympathetic stimulation have on SV

A

no effect due to lack of innervation

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35
Q

what hormones effect SV

A

adrenaline and noradrenaline

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36
Q

what is the effect of adrenaline and noradrenaline on SV

A

increase

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37
Q

what is end diastolic volume (EDV)

A

the volume of blood within each ventricle at the end of diastole

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38
Q

what does EDV determine

A

preload

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39
Q

what is EDV determined by

A

venous return

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40
Q

what is end systolic volume (ESV)

A

the volume of blood in each ventricle at the end of systole

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41
Q

explain how changes to ventricular preload causes changes in SV

A

the more the ventricle is filled during diastole (EDV) the greater the volume of blood ejected during the resulting systolic contraction (SV)

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42
Q

how are the SV of the L & R ventricles matched

A

if venous return to the RA increases the EDV of the RA increases leading to an increased SV to the pulmonary artery. As a result venous return to the LA from the pulmonary vein increases causing to a increased EDV of the LV increasing SV to the aorta

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43
Q

what is afterload

A

the resistance into which the heart is pumping

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44
Q

what is the effect of prolonged increases afterload

A

ventricular hypertrophy

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45
Q

what is cardiac output (CO)

A

the volume of blood pumped by each ventricle per minute

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46
Q

what is cardiac output equal to

47
Q

how does sympathetic stimulation affect ventricular contraction

A

increases force of contraction

reduces duration of systole and diastole

48
Q

how does parasympathetic stimulation affect ventricular contraction

A

little effect due to lack of innervation

49
Q

what is BP

A

the outward pressure exerted by the blood on blood vessel walls

50
Q

what is systolic BP

A

the outward pressure exerted by the blood on blood vessel walls of the aorta and systemic arteries when the heart CONTRACTS

51
Q

what is diastolic BP

A

the outward pressure exerted by the blood on blood vessel walls of the aorta and systemic arteries when the heart when the heart RELAXES

52
Q

what is normal systolic BP

53
Q

what is normal Diastolic BP

54
Q

what is normal BP

55
Q

what is pulse pressure

A

difference between the systolic and diastolic BP

56
Q

what is normal pulse pressure

57
Q

what is mean arterial BP (MAP)

A

average arterial BP during a single cardiac cycle

58
Q

what is the normal range for MAP

59
Q

what is the minimum MAP needed to perfuse vital organs

60
Q

how do you calculate MAP

A

diastolic + (1/3 x pulse pressure)

[(2x diastolic) + systolic]/3

61
Q

what is MAP equal to

A

MAP = CO x SVR so:

MAP = HR x HR x SVR

62
Q

What are the main resistance vessels

A

arterioles

63
Q

why are baroreceptors only involved in SHORT TERM regulation

A

sustained high BP will “re-set” baroreceptors

64
Q

what effect does parasympathetic stimulation have on MAP

65
Q

what effect does sympathetic stimulation have on MAP

66
Q

where are baroreceptors located

A

carotid bifurcation

aortic arch

67
Q

how does the baroreceptors signal the medulla

A

carotid bifurcation = IXth CN

aortic arch = Xth CN

68
Q

where do the signals from the baroreceptors go

69
Q

describe the baroreceptor response when the BP decreases

A

rate of firing will decrease

medulla send signals to increase sympathetic tone and decrease vagal tone (increase HR and SV)

sympathetic constrictor tone is increased (increase SVR)

MAP INCREASES

70
Q

describe the baroreceptor response when the BP increases

A

rate of firing will increase

medulla send signals to decrease sympathetic tone and increase vagal tone (decrease HR and SV)

sympathetic constrictor tone is decreased (decrease SVR)

MAP DECREASES

71
Q

what is postural hypotension

A

failure of baroreceptor responses to gravitational shifts in gravity

72
Q

what happens to HR and BP when you suddenly stand up

A

venous return decreases due to gravity = decrease BP

baroreceptor firing decreases

medulla send signals to increase sympathetic tone and decrease vagal tone (increase HR and SV)

sympathetic constrictor tone is increased (increase SVR)

rapid correction of transient fall in MAP

73
Q

what is the main driving force for blood flow

74
Q

what does the 1st korotkoff sound signal

A

peak systolic

75
Q

what does the 4th korotkoff sound signal

A

minimum diastolic

76
Q

what does the 5th korotkoff sound signal

A

diastolic (recorded)

77
Q

what does the LONG TERM control of BP involve

78
Q

what 2 factors must be controlled to control ECF volume

79
Q

what must be controlled to control MAP and BP

A

ECF volume

80
Q

which 3 hormones effect MAP

A 
renin angiotensin aldosterone system (RAAS)
Natriuretic peptide (NP)
antidiuretic hormone (ADH)
81
Q

what is the rate limiting step in RAAS

A

renin secretion

82
Q

what does the RAAS system regulate

A

plasma volume and SVR

83
Q

where is renin released from

84
Q

what does renin do

A

stimulate formation of angiotensin 1 in the blood from angiotensinogen

85
Q

where is angiotensionogen located

86
Q

what is angiotensionogen converted to

A

angiotensin 1

87
Q

what converts angiotensionogen to angiotensin 1

88
Q

what is angiotensin 1 converted to

A

angiotensin 2

89
Q

what converts angiotensin 1 to angiotensin 2

A

angiotensin converting enzyme (ACE)

90
Q

where is angiotensin converting enzyme (ACE) located

A

pulmonary vascular endothelium

91
Q

what does angiotensin 2 do (4)

A

stimulates release of aldosterone from adrenal cortex
causes systemic vasoconstriction = Increased SVR & BP
stimulates thirst
stimulates ADH release

92
Q

what stimulates the release of aldosterone

A

angiotensin 2

93
Q

where is aldosterone released from

A

adrenal cortex

94
Q

what does aldosterone act on

95
Q

what does aldosterone do

A

increases Na+ and water retention to increase plasma volume = increased BP

96
Q

what is aldosterone

A

steroid hormone

97
Q

what is renin secretion controlled by

A

renal artery hypotension
stimulation of renal sympathetic nerves
decreased [Na+] in renal tubular fluid

98
Q

what is the cardiac cycle

A

all events that occur from the beginning of one heart beat to the beginning of the next

99
Q

what happens during diastole

A

the heart ventricles are relaxed and fill with blood

100
Q

what happens during systole

A

the heart ventricles contract and pump blood into the aorta (LV) and the pulmonary artery (RV)

101
Q

what are the 5 different phases of the cardiac cycle

A
  1. passive filling
  2. atrial contraction
  3. isovolumetric contraction
  4. ventricular ejection
  5. isovolumetric relaxation
102
Q

what happens during passive filling

A

pressure in atria and ventricles are close to 0

AV valves open and venous return flows into the ventricles

Ventricles become 80% full by passive filling

103
Q

what happens during atrial contraction

A

P-wave signals atrial depolarization

The atria contracts between the P-wave and the QRS complex

Atrial contraction completes the end diastolic volume (EDV) = 130ml

104
Q

what happens during isovolumetric contraction

A

starts after the QRS complex

ventricular pressure rises, once the pressure exceeds the atrial pressure the AV valves shut producing the 1st heart sound (LUB)

the aortic valve is still shut so no blood can enter or leave the ventricles and the ventricular pressure rises very steeply

tension rises around the enclosed volume – ‘isovolumetric contraction’

105
Q

what happens during ventricular ejection

A

when the ventricular pressure exceeds aorta/pulmonary artery pressure the aortic and pulmonary valves open

SV is ejected by each ventricle leaving behind the end systolic volume (ESV)

Aortic pressure rises

The T-wave signals ventricular repolarization

The ventricles relax and the ventricular pressure starts to fall

When the ventricular pressure falls below the aortic/pulmonary pressure the aortic and pulmonary valves shut producing the 2nd heart sound (DUB)

106
Q

what produces the dicrotic notch

A

valve vibration during ventricular ejection

107
Q

what happens during isovolumetric relaxation

A

closure of aortic and pulmonary valves signals the start of isovolumetric ventricular relaxation

the tension falls around the enclosed volume – ‘isovolumetric relaxation’

when the ventricular pressure falls below atrial pressure the AV valves open and a new heart cycle begins

108
Q

what causes normal heart sounds

A

shutting of valves

109
Q

what causes the 1st heart sound

A

closure of the mitral and tricuspid valves

110
Q

what does the 1st heart sound signify

A

beginning of systole

111
Q

what causes the 2nd heart sound

A

closure of the aortic and pulmonary valves

112
Q

what does the 2nd heart sound signify

A

end of systole

beginning of diastole

113
Q

how is pressure maintained in blood vessels during ventricular diastole

A

vessels contract from being stretched during systole

Cardio - mine (15 decks)

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