Cardiovascular System Flashcards

(85 cards)

1
Q

apex of heart

A

bottom of heart
contractions spread from here then upwards

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2
Q

lub dub

A

lub-AV valves closing
dub-aortic and pulmonary valves closing

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3
Q

heart arrhythmias

A

irregular heart contractions

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4
Q

cardiomyocytes

A

cardiac muscle cells
-contractile and nodal

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5
Q

contractile cells

A

pumps blood through heart
-communicate between 2 cells using gap junctions
-ions from gap junction go to other cells then causes depolarization

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6
Q

nodal/conducting cells

A

spread electrical activity/AP through heart
self-excitable >make own AP
APs have no stabl RMP, reach threshold by Na and Ca moving in cell

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7
Q

intercalated discs

A

connects cardiomyocytes
locked together by desmosomes (protein)
have gap junctions

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8
Q

gap junctions

A

allows Na, Ca and other small molecules together to allow communication
-on intercalated discs

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9
Q

SA node

A

sinoatrial node
in upper right atrium
pacemaker determines heart rate
receives input from PSNS and SNS

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10
Q

intrinsic rate

A

100 AP/min
1 AP every 0.6s

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11
Q

Steps pace maker potential

A

1) positive charge/graded potential is created by Na and Ca entering cell using their own ion channels (Ca and Na in, K out)
2)Depol- caused by opening Ca channels at threshold
-Ca moves down concentration gradient
3)repol- K leaves cell through K channels
more negative

no hyperpolarization

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12
Q

what happens when SA node fails

A

AV node acts as pacemaker b/c it is the 2nd fastest AP creation

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13
Q

bradycardia

A

too low HR
dizzy, faint

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14
Q

HR lower than 100 bpm *

A

-PSNS
ACh binds to receptors muscarinic receptors on SA node cells
-when ACh binds to muscarinic R, decrease Ca and Na permeability (slower coming in), increase K permeability
-longer time to reach AP threshold, slower HR

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15
Q

HR increasing *

A

-SNS
adrenergic receptors bind with (nor)epinphrine
AP threshold hit fast which increases HR
increase Na and Ca permeability

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16
Q

ECG

A

electrocardiogram
-electrical activity in heart

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17
Q

p wave

A

result of depolarization of atria

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18
Q

QRS wave

A

result of depolarization of ventricles
larger than P wave b/c ventricles have a larger mass

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19
Q

T wave

A

result of repolarization of ventricles

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20
Q

atria repolarization

A

at same time as QRS wave
so small, masked by ventricles depolarization

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21
Q

systole

A

period when cardiomyocytes are contracting

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22
Q

diastole

A

period when cardiomyocytes are relaxing

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23
Q

cardiac cycle *

A

isovolumetric ventricular systole
ventricular systole
isovolumetric ventricular diastole
late ventricular diastole
atrial systole

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24
Q

isovolumetric ventricular systole *

A

ventricles start contracting, blood isn’t being pumped out of heart

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25
ventricular systole *
ventricles are contracting blood moves out of heart and into aorta or pulmonary artery
26
isovolumetric ventricular diastole *
ventricles start relaxing and not filled with blood
27
late ventricular diastole *
ventricles are relaxing and start filling with blood from atria
28
atrial systole *
atria contracting and blood moving in ventricles
29
isovolumetric ventricular systole graph *
ECG: QRS> started at atrial contraction Volume: no change Valves: closed Pressure: increase ventricular P
30
ventricular systole graph *
ECG: no new -QRS Volume: decrease ventricular volume Valves: aortic open, AV closed Pressure: vent P > aortic P
31
isovolumetric ventricular diastole graph *
ECG: T wave in phase 2 Volume: no change Valves: closed Pressure: lower vent p, higher aortic p
32
late ventricular diastole graph *
ECG: no new-T Volume: increase ventricular volume Valves: AV open, aortic closed Pressure: higher atria P, lower vent P
33
atrial systole graph *
ECG: p wave Volume: increase ventricular volume Valves: AV open, aortic closed Pressure: lower vent p, higher atrial p
34
ESV *
end systolic volume amount of blood in ventricle at end of systole after ventricle contract -decrease ESV means more effective heart
35
EDV *
end diastolic volume amount of blood in ventricle before ventricular contraction
36
SV *
stroke volume amount of blood ejected by ventricle with each heart beat SV= EDV-ESV influence cardiac output
37
cardiac output *
amount of blood the heart pumps each minute =HRxSR at rest 5-6L/min in L
38
how to adjust SV *
ANS innervation preload on heart/EDV
39
how to increase excitation contraction coupling
more Ca in cytoplasm, stronger contraction
40
preload *
load on heart prior to contraction -blood that has filled ventricle=EDV larger EDV/fuller heart, more stretch
41
Frank Starling's Law of the heart *
more EDV= more SV this protects heart from over filling then bursting
42
total blood volume + % based on systems
4-6L 15% of blood between pulmonary circuit and heart 85% of blood in systemic circuit
43
general blood vessel structure
have 3 tunics except capillaries > tunic externa, media, interna
44
tunica externa *
outermost layer -composed of connective tissue > protection and maintains structure -has neurons of SNS to communicate with tunica media
45
tunica media *
middle layer -has smooth muscle to contract or relax >changes diameter -elastin>elastin fiber, allows for stretch -collagen -different amount of contains for different vessels
46
tunica interna *
innermost layer -has endothelial cell> special cells that line blood vessels -important for vessel function
47
arteries *
distribution vessel alot of elastin to stretch during vent. diastole -pulsatile pressure
48
pulsatile pressure
the difference between systolic and diastolic blood pressure
49
arterioles *
-resistance vessels thick walls -greatest resistance -higher muscle than elastin -large drop in pressure -smooth muscle innervated by SNS
50
capillaries *
-only single layer of endothelial -exchanges vessels
51
venules
low blood pressure
52
veins *
-capacitance vessels -large diameter, thin walls -low P -uses valves in lumen -some smooth muscle + elastin for stretch and increase diameter -innervated by ANS
53
valves in veins
prevent back flow -have cusps that fill with blood
54
venous return *
-amount of blood returned to heart -SNS cause small contraction, decrease diameter and more blood goes back to heart -increases EDV, SV, cardiac output
55
varicose veins
-enlarged, twisted veins -common in legs and feet -occur from malfunctioning vein valves causing blood to pool + veins to swell, increasing P
56
importance of blood flow regulation
to increase blood flow to active tissues maintain blood supply to vital organs maintain BP maintain temp
57
what affects blood resistance **
-lumen radius (^r, smaller resistance) -viscosity (^, ^resist) -length of blood vessels (lined with endothelial cells increase friction> ^resist)
58
blood pressure equation *
pressure gradient x radius to the power of 4
59
transcellular transport
substance enters and then exits endothelial cell and epithelial cell
60
paracellular transport *
-bulk flow -substance can move between endothelial cells lining capillaries through intercellular clefts
61
intercellular clefts
have proteins called tight junctions between them -vary in size and leakiness of cleft
62
continuous capillaries
most abundant -varies in permeable -intercellular clefts
63
fenestrated capillaries
found in kidneys and intestines -intercellular clefts -more bulk flow than continuous capillaries
64
sinusoidal capillaries
found in liver and spleen
65
edema
excessive filtration causing swelling
66
3 major regulatory systems for controlling flow
local regulation, humoral regulation, neural regulation
67
local regulation *
-intrinsic mechanism -changes condition inside tissues most tissues
68
types of local regulation *
myogenic theory and metabolic theory
69
extrinsic mechanism
signal to change blood flow comes from outside the tissue
70
intrinsic mechanism
stimulus to change blood flow comes from within the tissues that need it
71
myogenic theory *
-muscles contracts or relaxes to control blood flow
72
metabolic theory *
metabolic needs -increase co2, H, adenosine, temp, decrease o2 to increases blood flow by increase radius and vasodilation
73
vasodilator metabolites
co2, H, adenosine
74
humoral regulation *
-substance that are travelling in blood through tissues -substances change radius of BV, usually by binding to receptors -extrinsic mechanism
75
vasoconstrictors *
-increase bp -epinephrine when bind to alpha adrenergic receptors -angiotensin 2 -ADH
76
Vasodilators *
-decrease BP -histamine- released by inflammatory cells -ANP epinephrine > beta adrenergic receptors
77
neural regulation *
neurons from SNS innervate smooth muscle cells in tunica media of ex. norepinephrine -extrinsic
78
what nervous system innervates blood vessels *
SNS
79
MAP *
average BP in arteries during one cardiac cycle
80
MAP equation *
MAP =CO x TPR or =DP + 1/3 (SP -DP)
81
baroreceptors *
-regulates MAP -stretches when change in BP, send signals to medulla oblongata to adjust HR
82
steps of baroreceptor reflex SNS * | not sup import
-baroreceptors stretch and detect change in BP -sends sensory info to cardiovascular center in medulla oblongata -the SNS info is sent out to SA node to change heart's pace by increasing slope of pacemaker potential and change ventricular myocytes -increase SV by increase contractility increase HR (SA node), TPR then increase MAP
83
steps of baroreceptor reflex PSNS * | not sup import
-baroreceptors stretch and detect change in BP -sends sensory info to cardiovascular center in medulla oblongata -then info goes to SA not to blood vessel -decrease HR, SV (contractility), SNS activation (decrease TPR) therefore decrease MAP
84
conducting system: AP conduction
1)SA node 2) atrial cardiomyocytes 3)signals go to AV node 4)atrioventricular bundle 5)bundle branches 6)subendocardial branches- 7)ventricular cardiomyocytes
85
When vasoconstriction occurs, what happens to blood pressure in the sites before and after that constriction?
Increase below, decrease p after