cardiovascular system Flashcards
(123 cards)
1
Q
pulmonary arteries
A
go to the lungs and chest to oxygenate oxygen deficient blood
2
Q
pulmonary veins
A
go from the heart to the lungs –> oxygen rich
3
Q
systemic arteries
A
oxygenated blood from the heart (aorta) for tissues around the body
4
Q
systemic veins
A
take deoxygenated blood from repairing tissue back to the right atrium
5
Q
why does the right ventricle have a larger diameter
A
due to having a thinner muscle
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
7
Q
systolic
A
contracting
8
Q
diastolic
A
relaxing
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.
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
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
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
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.
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
15
Q
which receptor is responsible for calcium induced calcium release
A
ryanodine receptor
16
Q
difference between cardiac smooth muscle and skeletal muscle
A
calcium induce calcium release
17
Q
what alter Ca2+ release or storage and therefore also affect contractility/relaxation
A
- calcium channel blockers
- Beta blockers (effect A/NA)
- caffeine
18
Q
sympathetic nervous system increases
A
permeability of membrane to Na+ and Ca2+
19
Q
parasympathetic increases
A
permeability of the membrane to K+
20
Q
sympathetic response
A
increase spontaneous depolarisation and educes time to initiate depolarisation
21
Q
parasympathetic response
A
decreases spontaneous depolarisation and increases time to initiate depolarisation
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
23
Q
PACE
A
preload
after load
contractility
‘Eart rare
24
Q
stroke volume
A
SV= EDV-ESV
25
EDV
end diastolic volume - volume of blood just before contraction
26
ESV
end systolic volume- the volume of blood after contraction (left overs)
27
both hypertension and aortic valve stenosis lead to
decreases stroke volume
28
cardiac output
heart rate x stroke volume
29
Preload --> end diastolic volume
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.
30
as the length of the muscle increases
contraction will also increases due to more cross bridges being formed. known as a strength force relationship
31
EDV effects
contractility and thus SV and thus CO
32
an increase in venous return will
1) increase EDV
2) increase stretch of muscle
3) increase cross bridge formation
4) increase force of contraction
5) increase SV and thus CO
33
venous return
Venous return is the rate of blood flow back to the heart. It normally limits cardiac output.
34
afterload/ ESV
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
35
three factors that effect EV:
- preload/edv
| - edv increases contractility and therefore less blood at the end of contraction
36
as after load increase
cardiac output decreases
37
contractility
controlled hormonally by A and NA that is circulating
38
B2
found in lungs
39
quantification of contractility- ejection fraction
ratio of SV to EDV
EF= SV/EDV
normal is between 55 and 75%
40
'eart rate
neuronal and endocrine regulation--> increase HR= positive chrontopic factors (A and NA)
41
atrial reflex
Bainbridge reflex--> adjust heart rate in response to venous retune
--> stretch receptors in right atrium trigger increase in heart rate through increase sympathetic activity.
42
angina
chest pain when blood supply to muscles is restricted
43
common arteries affected by atherosclerosis
LAD
LCX
RCA
can occur at any point only artery
44
left coronary artery
divides into tow branches; circumflex and left anterior descending artery
45
circumflex artery
supplies the blood to the left atrium and the side and back of the left ventricle
46
left anterior descending artery
supplies blood to the front an bottom of the left ventricle and the front of the septum
47
coronary veins
take oxygen poor blood that has already been used by muscles of the heart and returns it to the right atrium
48
right coronary artery
supples blood to the right atrium and right ventricles , bottom portion of the left ventricle and back of the septum
49
three types of capillary
continuous
fenestrated
sinusoidal
50
continuous capillary
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
fenestrated capillaries
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
where are fenestrated capillaries found
Located in specialised space; endocrine (hypothalamus, pituitary, and thyroid) and intestines and glomerulus
53
sinusoidal capillaries
resemble fenestrated capillaries but more 'pores'. allows larger molecules such as plasma proteins to cross--> located in bones, lives and other endocrine rogans
54
where are sinusoidal capillaries found
bones, liver and other endocrine organs
55
structure of arteries
wide lumen, elastic wall maintains pressure
56
arterioles
narrow lame, contractile wall --> controls resistance ultimately pressure of the blood by altering the lumen size
57
capillaries
narrow lumen, thin walls, site of exchange of nutrients, oxygen and metabolic waste
58
venules and veins
wide lumen, compliant walls, low resistance, lod reservoir, contains valves to ensure adequate blood is returned to the heart and prevents blood pooling
59
why do veins contain valves
to ensure adequate blood is returned tot he heart and prevents blood pooling
60
long term control of blood pressure (RAAS)
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
cardiac parasympathetic activity onyl
decreases heart rate
62
cardiac sympathetic activity (2)
1) increase heart rate
| 2) increase stroke volume
63
arterial pressure
after load --> decrease stroke volume
64
filling pressure
preload--> increase in stroke volume
65
hypertension
high blood prssure
66
cardiac and vascular changes accompanying heart failure: cardiac
- decreased stroke volume and cardiac output
- increased End diastolic pressure
- ventricular dilation
- impaired filling
- reduced ejection fraction
67
vascular changes accompanying heart failure
- increased systemic vascular resistance
- decreased arterial pressure
- impaired arterial pressure
- impaired organ functionn
- impaired organ perfusing
- decreased venous compliance
- increased venous pressure
68
B blockers
used to protect against heart attack by lowering blood pressure
69
what ar eb blockers used to treat
angina, hf, heart rhythm disorders
70
how to b blockers work
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
three known B receptors
B1
B2
B3
72
ACE inhibitors
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
main role of ACE inhibitors
lowers the amount of water your body retains, which lowers your blood pressure.
74
blood pressure
blood pressure= cardiac output (HR x SV) X total peripheral rsistance
75
TPR
total peripheral resistance
76
total peripheral resistance
total resistance of blood in the systemic circuit
77
in the SAN L type channels open when
Na+ influx via what is known as the IF current as well as K+ efflux via voltage gated K+ channels
78
what effect does the parasympathetic nerve have on the SA node?
decreases in firing rate due to an increase in K+ permeability and decrease in Na+ permeability
79
which response would increase blood pressure the most by increases CO?
increased sympathetic innervation of venous muscle
80
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
baroreceptors will decrease their firing rate along afferent nerves, initiating an increase in sympathetic activity to the heart and vascular smooth muscle
81
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:
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
systolic blood pressure
pressure created in the arteries by the contraction of the left ventricle
83
diastolic blood pressure
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
parts of the cardiovascular system
heart, lungs, arteries and veins
85
resting heart rate
60 to 100bm
86
blood pressure between
90/60 mmHg nd 120/80 mmHg
87
tricuspid valve
prevents back flow into the right atrium and has three flap like cusps
88
bicuspid
prevents back flow into the left atrium
89
aortic valve
between left ventricle and the aorta
90
pulmonary valve
located between the right ventricle and pulmonary artery
91
atria
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
ventricle muscle
trabecular carnage
93
ventricle
- 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
longer the tube
the higher the resistance , the tiger the blood pressure, the stronger the face of contraction applies
95
cardiac muscle
striated, single nucleated.
96
4 layers of the heart
pericardium
epicardium
myocardium
endocardum
97
pericardium
double walled sac that surround the heart. the space between the linings is called the pericardiac cavity
98
epicardium
layer of the pericardium closely aligned to the heart wall--> also known as the visceral layer the sorts pericardium
99
myocardium
muscles ar earrnaged in spiral and circular bundles--> muscle contracts and the chambers constrict and blood is expelled out of the chmabed
100
endocaridum
thin, slick sheet of connective tissue located on the inner surface of the myocardium --> continuous with blood vessels
101
systole
contracting
102
diastole
relaxation
103
three stages of cardiac cycle
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
myogenic
contracts by itself due tot he SAN, which is a cluster of cells found in the right atria.
105
nerves supplied to the heart can only change
rate of heart beat and cannot initiate muscle contraction
106
cardiac output
amount of blood pumped by the heart per minute
107
stroke volume
amount of blood the heart pumps per beat
108
Transmission of action potential from SAN
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
on the ECG what is P
atrial depolarisation
110
on the ECG what is R
ventricular depolarisation
111
on the ECG what is T
ventricular repolarisation
112
if blood rate drops too much
organs will not receive accurate perfusion
113
if blood rate rises too much
damage inner lining of blood vessels and lead to heart disease or strokes
114
baroreceptors
special receptors that detached changes in blood pressure with the walls of the aorta and carotid
115
if bp is too high
¬ 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
if blood pressure is too low
¬ 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
if carbon dioxide levels are high
¬ 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
if levels of carbon dioxide are low
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
layers of the heart
pericardium is the outermost layer and made out of three layers: (fibrous pericardium, parietal pericardium, epicardium).
epicardium
myocardium
endocardium
120
epicardium
outer most later of the heart wall, inner most layer of the pericardium
121
myocardium
middle layer, muscle layer --> responsible for contracting and pumping blood
122
endocardium
thin, innermost layer of tissue.
Makes direct contact with blood
123
what anchors the heart in place
the pericardium
