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Integrated clinical studies > cardiovascular system > Flashcards

cardiovascular system Flashcards

1
Q

pulmonary arteries

A

go to the lungs and chest to oxygenate oxygen deficient blood

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2
Q

pulmonary veins

A

go from the heart to the lungs –> oxygen rich

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3
Q

systemic arteries

A

oxygenated blood from the heart (aorta) for tissues around the body

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4
Q

systemic veins

A

take deoxygenated blood from repairing tissue back to the right atrium

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5
Q

why does the right ventricle have a larger diameter

A

due to having a thinner muscle

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6
Q

the left ventricle pumps with

A

4-6 times more pressure due to a 3:1 ratio in muscle mass between the left and right ventricles

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7
Q

systolic

A

contracting

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8
Q

diastolic

A

relaxing

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9
Q

steps of conducting system (contraction of the heart)

A

1) SAN activity and atrial activation begins
2) stimulus spreads across the atrial surfaces and reaches the AVN
3) there is a 100msec delay at the AVN, to allow the atria to fill
4) impulse travels along the interventriuclar septum (bundle of HIS) within the AV bundle branches to the Purkinje fibres and via moderator bands, to the papillary muscle of the right ventricle
5) the impulse is distributed by Purkinje fibre and relayed throughout the ventricular myocardium. Atrial contraction is completed and ventricular contraction begins.

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10
Q

SAN action potential

A

1) decrease in K+ permeability along with an increase in Na+ permeability (If current)
2) T-type (transient) Ca2_ channels open
3) threshold reached–> l type Ca2+ channels open (AP)
4) K+ channels open causing an efflux of K+
5) resting potential achieved

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11
Q

cardiac muscle action potential

A

1) rapid rise in Na+ permeability (voltage gated Na+)
2) slower rise in Ca2+ permeability and decrease in K+ permabilit. @nd smaller wave increases Na+ permeability
3) decrease in permeability in Ca2+ and an increase in K+ permeability

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12
Q

conductance of a cardiac action potinetal

A

intercalated discs: interconnect cardiac muscle cells and secured by desmosomes. Linked by gap junctions (propagate AP).

loca changes in currents–> passive depolarisation of adjacent muscle cells (voltage gated ion channels) through gap junctions

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13
Q

excitation contraction coupling

A

physiological process of converting an electrical stimulus to a mechanical response. It is the link between the AP generated in the sarcolemma and the start of muscle contraction.

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14
Q

excitation-contraction coupling process

A

1) impulse arrives at T-tubule, deep into the muscle
2) Ca2+ enter via L-type Ca+ channel
3) some of the ca2+ goes straight to the sarcomere and cause conformation change and contraction
4) other ca2+ will forma receptor complex with ryanodine (RyRs) and this causes Ca2+ induced Ca2+ release
5) this ca2+ will now go to the sarcomere

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15
Q

which receptor is responsible for calcium induced calcium release

A

ryanodine receptor

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16
Q

difference between cardiac smooth muscle and skeletal muscle

A

calcium induce calcium release

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17
Q

what alter Ca2+ release or storage and therefore also affect contractility/relaxation

A
  • calcium channel blockers
  • Beta blockers (effect A/NA)
  • caffeine
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18
Q

sympathetic nervous system increases

A

permeability of membrane to Na+ and Ca2+

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19
Q

parasympathetic increases

A

permeability of the membrane to K+

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20
Q

sympathetic response

A

increase spontaneous depolarisation and educes time to initiate depolarisation

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21
Q

parasympathetic response

A

decreases spontaneous depolarisation and increases time to initiate depolarisation

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22
Q

B1 blockade leads to

A
  • reduced contractility via reduction in the conc of cAMP
  • reduced HR-similar effect to parasympathetic input
  • reduced Ca2+ entry via camp-dpeendnet pK activity
  • decrease in L type channel activity
  • reduced renin secretion via selective B1 inhibition at GJ cell
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23
Q

PACE

A

preload
after load
contractility
‘Eart rare

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24
Q

stroke volume

A

SV= EDV-ESV

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25
Q

EDV

A

end diastolic volume - volume of blood just before contraction

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26
Q

ESV

A

end systolic volume- the volume of blood after contraction (left overs)

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27
Q

both hypertension and aortic valve stenosis lead to

A

decreases stroke volume

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28
Q

cardiac output

A

heart rate x stroke volume

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29
Q

Preload –> end diastolic volume

A

increases in EDV leads to increases in myocardial performance. Because as EDV increases, the starting myocardial muscle length also increases. This leads to more cross bridge formation and therefore there will be a more powerful contraction.

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30
Q

as the length of the muscle increases

A

contraction will also increases due to more cross bridges being formed. known as a strength force relationship

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31
Q

EDV effects

A

contractility and thus SV and thus CO

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32
Q

an increase in venous return will

A

1) increase EDV
2) increase stretch of muscle
3) increase cross bridge formation
4) increase force of contraction
5) increase SV and thus CO

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33
Q

venous return

A

Venous return is the rate of blood flow back to the heart. It normally limits cardiac output.

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34
Q

afterload/ ESV

A

the pressure in which the heart has to pump against. Higher the pressure in the aorta–> the more force required by the heart.

As afterload increases, cardiac output decreases

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35
Q

three factors that effect EV:

A
  • preload/edv

- edv increases contractility and therefore less blood at the end of contraction

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36
Q

as after load increase

A

cardiac output decreases

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37
Q

contractility

A

controlled hormonally by A and NA that is circulating

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38
Q

B2

A

found in lungs

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39
Q

quantification of contractility- ejection fraction

A

ratio of SV to EDV
EF= SV/EDV

normal is between 55 and 75%

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40
Q

‘eart rate

A

neuronal and endocrine regulation–> increase HR= positive chrontopic factors (A and NA)

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41
Q

atrial reflex

A

Bainbridge reflex–> adjust heart rate in response to venous retune
–> stretch receptors in right atrium trigger increase in heart rate through increase sympathetic activity.

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42
Q

angina

A

chest pain when blood supply to muscles is restricted

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43
Q

common arteries affected by atherosclerosis

A

LAD
LCX
RCA

can occur at any point only artery

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44
Q

left coronary artery

A

divides into tow branches; circumflex and left anterior descending artery

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45
Q

circumflex artery

A

supplies the blood to the left atrium and the side and back of the left ventricle

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46
Q

left anterior descending artery

A

supplies blood to the front an bottom of the left ventricle and the front of the septum

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47
Q

coronary veins

A

take oxygen poor blood that has already been used by muscles of the heart and returns it to the right atrium

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48
Q

right coronary artery

A

supples blood to the right atrium and right ventricles , bottom portion of the left ventricle and back of the septum

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49
Q

three types of capillary

A

continuous
fenestrated
sinusoidal

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50
Q

continuous capillary

A

supplies most of the body and allows small solutes and h2o to. adaptations include in BBB where gap junctions between endothelial cells prevent movement between the blood and interstitial space

51
Q

fenestrated capillaries

A

contain pores- allows much greater movement between blood and interstitial space, including that of small peptides.Located in specialised space; endocrine (hypothalamus, pituitary, and thyroid) and intestines and glomerulus

52
Q

where are fenestrated capillaries found

A

Located in specialised space; endocrine (hypothalamus, pituitary, and thyroid) and intestines and glomerulus

53
Q

sinusoidal capillaries

A

resemble fenestrated capillaries but more ‘pores’. allows larger molecules such as plasma proteins to cross–> located in bones, lives and other endocrine rogans

54
Q

where are sinusoidal capillaries found

A

bones, liver and other endocrine organs

55
Q

structure of arteries

A

wide lumen, elastic wall maintains pressure

56
Q

arterioles

A

narrow lame, contractile wall –> controls resistance ultimately pressure of the blood by altering the lumen size

57
Q

capillaries

A

narrow lumen, thin walls, site of exchange of nutrients, oxygen and metabolic waste

58
Q

venules and veins

A

wide lumen, compliant walls, low resistance, lod reservoir, contains valves to ensure adequate blood is returned to the heart and prevents blood pooling

59
Q

why do veins contain valves

A

to ensure adequate blood is returned tot he heart and prevents blood pooling

60
Q

long term control of blood pressure (RAAS)

A

1) rescued flow to juxtaglomerular cells detected
2) renin secreted from kidneys in response
3) converting angitensinogen to angiotensin 1
4) ACE causes angiotensin 1 to become angiotensin 2
5) ang2 causes vasoconstriction (increased TPR) and stimulated aldosterone relates from adrenal glands on kidney
6) aldosterone stimulates water and sodium reabsorption, increasing blood volume and therefore blood pressure

61
Q

cardiac parasympathetic activity onyl

A

decreases heart rate

62
Q

cardiac sympathetic activity (2)

A

1) increase heart rate

2) increase stroke volume

63
Q

arterial pressure

A

after load –> decrease stroke volume

64
Q

filling pressure

A

preload–> increase in stroke volume

65
Q

hypertension

A

high blood prssure

66
Q

cardiac and vascular changes accompanying heart failure: cardiac

A
  • decreased stroke volume and cardiac output
  • increased End diastolic pressure
  • ventricular dilation
  • impaired filling
  • reduced ejection fraction
67
Q

vascular changes accompanying heart failure

A
  • increased systemic vascular resistance
  • decreased arterial pressure
  • impaired arterial pressure
  • impaired organ functionn
  • impaired organ perfusing
  • decreased venous compliance
  • increased venous pressure
68
Q

B blockers

A

used to protect against heart attack by lowering blood pressure

69
Q

what ar eb blockers used to treat

A

angina, hf, heart rhythm disorders

70
Q

how to b blockers work

A

competitive antagonists that block receptor sites for adrenaline and noradrenaline on adrenergic b receptors of the sympathetic nervous system.

–> some block all types of B-adrengeric receptors and others are selective for one of the three know beta receptors

71
Q

three known B receptors

A

B1
B2
B3

72
Q

ACE inhibitors

A

angiotensin converting enzyme inhibitors are drugs that block the bodies production of angiotensin 2. Angiotensin 2 is a hormone that circulates in the blood and has many effects on the cardiovascular system–> constricting blood vessels. BY reducing the amount in your body, blood vessels are able to relax and widen, making it easier for blood flow through.

73
Q

main role of ACE inhibitors

A

lowers the amount of water your body retains, which lowers your blood pressure.

74
Q

blood pressure

A

blood pressure= cardiac output (HR x SV) X total peripheral rsistance

75
Q

TPR

A

total peripheral resistance

76
Q

total peripheral resistance

A

total resistance of blood in the systemic circuit

77
Q

in the SAN L type channels open when

A

Na+ influx via what is known as the IF current as well as K+ efflux via voltage gated K+ channels

78
Q

what effect does the parasympathetic nerve have on the SA node?

A

decreases in firing rate due to an increase in K+ permeability and decrease in Na+ permeability

79
Q

which response would increase blood pressure the most by increases CO?

A

increased sympathetic innervation of venous muscle

80
Q

when you stand up from a sitting position, your blood pressure initially drops as gravity has its effect on the bod. what immediate response will your autonomic NS make to restore your blood pressure back to normal

A

baroreceptors will decrease their firing rate along afferent nerves, initiating an increase in sympathetic activity to the heart and vascular smooth muscle

81
Q

ACE inhibitors are used to treat hypertension by blocking the vasoactive effect of angiotensin 2.. Angiotensin 2 is released as part of the renin angiotensin aldosterone system. Which of the following statements are relating to the RAAS is true:

A

Renin is released from juxtaglomerular cells in response to a detected fall in NaCL within the distal convoluted tubule. The RAAS aims to increase blood volume in part by stimulating the sensation of thirst.

82
Q

systolic blood pressure

A

pressure created in the arteries by the contraction of the left ventricle

83
Q

diastolic blood pressure

A

once the left ventricle has fully contracted it begins to relax and refill with blood from the left atria. the pressure in the arteries falls whilst the ventricle reflls

84
Q

parts of the cardiovascular system

A

heart, lungs, arteries and veins

85
Q

resting heart rate

A

60 to 100bm

86
Q

blood pressure between

A

90/60 mmHg nd 120/80 mmHg

87
Q

tricuspid valve

A

prevents back flow into the right atrium and has three flap like cusps

88
Q

bicuspid

A

prevents back flow into the left atrium

89
Q

aortic valve

A

between left ventricle and the aorta

90
Q

pulmonary valve

A

located between the right ventricle and pulmonary artery

91
Q

atria

A

Function: receive blood returning to the heart and push it into the ventricles

  • right atrium: low O2- supplied by inferior and superior vena cava and cornonary sinus.
  • left atrium: high oxygen-pulmonary veins
  • SAN found in atria
92
Q

ventricle muscle

A

trabecular carnage

93
Q

ventricle

A
  • L. ventricle is anterior and pumps blood into the systemic circuit. It is the larger ventricle and therefore longer meaning higher resistance so it needs to create higher pressure- therefore more muscle mass
  • R. Ventricle is posterior and pumps blood into the pulmonary trunk and the pulmonary circuit. Shorter distance means lower resistance means lower pressure means lower muscle mass. The high pressure would damage the lungs.
94
Q

longer the tube

A

the higher the resistance , the tiger the blood pressure, the stronger the face of contraction applies

95
Q

cardiac muscle

A

striated, single nucleated.

96
Q

4 layers of the heart

A

pericardium
epicardium
myocardium
endocardum

97
Q

pericardium

A

double walled sac that surround the heart. the space between the linings is called the pericardiac cavity

98
Q

epicardium

A

layer of the pericardium closely aligned to the heart wall–> also known as the visceral layer the sorts pericardium

99
Q

myocardium

A

muscles ar earrnaged in spiral and circular bundles–> muscle contracts and the chambers constrict and blood is expelled out of the chmabed

100
Q

endocaridum

A

thin, slick sheet of connective tissue located on the inner surface of the myocardium –> continuous with blood vessels

101
Q

systole

A

contracting

102
Q

diastole

A

relaxation

103
Q

three stages of cardiac cycle

A

cardiac diastole (all chambers are relaxed and filling passively. Bicuspid and tricuspid valves are open. Atrial systole. Atria contract leading to ventricular filling. Ventricular systole –> blood is ejected into both he pulmonary artery and aorta.

104
Q

myogenic

A

contracts by itself due tot he SAN, which is a cluster of cells found in the right atria.

105
Q

nerves supplied to the heart can only change

A

rate of heart beat and cannot initiate muscle contraction

106
Q

cardiac output

A

amount of blood pumped by the heart per minute

107
Q

stroke volume

A

amount of blood the heart pumps per beat

108
Q

Transmission of action potential from SAN

A

1) SAN is a natural pace maker and relates electrical stimuli at a regular rate.
2) electrical stimulus from SAN will diffuse across the atria and once it has reach the AVN there will be a brief delay so that that the atria empty
3) once empty valves will close
4) electrical stimulus will pass through the AVN and bundle of HIS into the Purkinje fibres –> causes ventricles to contract

109
Q

on the ECG what is P

A

atrial depolarisation

110
Q

on the ECG what is R

A

ventricular depolarisation

111
Q

on the ECG what is T

A

ventricular repolarisation

112
Q

if blood rate drops too much

A

organs will not receive accurate perfusion

113
Q

if blood rate rises too much

A

damage inner lining of blood vessels and lead to heart disease or strokes

114
Q

baroreceptors

A

special receptors that detached changes in blood pressure with the walls of the aorta and carotid

115
Q

if bp is too high

A

¬ then the parasympathetic system is stimulated. This will decrease the heart rate. Therefore, stroke volume is also decreased and this decreases cardiac output and therefore blood pressure. Furthermore, the cardio regulatory center will decrease sympathetic input to blood vessels- causing vasodilation, which decreases total peripheral resistance and decreases blood pressure.

116
Q

if blood pressure is too low

A

¬ a decrease in blood pressure causes a decrease in AP send to the cardio regulatory center of the medulla. To raise blood pressure the sympathetic nerve is stimulated causing the SAN to be stimulated. Therefore, heart rate will increase. The heart muscle is also stimulated to pump with more force. Therefore, if both heart rate and stroke volume are increases than cardiac output will also be increased and blood pressure will rise. Second this increases sympathetic input to blood vessels (short term), which stimulate smooth muscle to contract, causing vasoconstriction, which increases total peripheral resistance and increases blood pressure.

117
Q

if carbon dioxide levels are high

A

¬ therefore the tissues need more oxygen for respiration: chemoreceptors in the aorta and carotid artery will register the change in pH. An impulse will be sent to the brain where the sympathetic nervous system will respond and be stimulated. The sympathetic nervous system will cause an increase in heart rate. This will increase cardiac output so more oxygen can be delivered to respiring tissue.

118
Q

if levels of carbon dioxide are low

A

tissues are at rest and need less oxygen for respiration. Chemoreceptors will detect the change in pH and stimulate the parasympathetic NS. This will cause a decrease in heart rate, reducing cardiac output and therefore the amount of blood being supplied to tissues.

119
Q

layers of the heart

A

pericardium is the outermost layer and made out of three layers: (fibrous pericardium, parietal pericardium, epicardium).

epicardium

myocardium

endocardium

120
Q

epicardium

A

outer most later of the heart wall, inner most layer of the pericardium

121
Q

myocardium

A

middle layer, muscle layer –> responsible for contracting and pumping blood

122
Q

endocardium

A

thin, innermost layer of tissue.

Makes direct contact with blood

123
Q

what anchors the heart in place

A

the pericardium

Integrated clinical studies (23 decks)

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