Cardiovascular Flashcards

(179 cards)

1
Q

arteries function

A

low resistance tubes that conduct blood to organs
undergo little pressure
pressure reservoirs for maintaining blood flow to organs during ventricle relaxation

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2
Q

arterioles function

A

major sites of resistance
pattern blood flow to organs
control blood flow and pressure

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3
Q

capillaries function

A

site of nutrient, metabolic end product, and fluid exchange between blood and tissue

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4
Q

venules function

A

site of nutrient, metabolic end product, and fluid exchange between blood and tissue, ensure blood returns to heart

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5
Q

veins function

A

low resistance, conduct blood back to heart

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6
Q

Blood make up

A

Plasma (55%), erythrocytes, luekocytes, platelets

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7
Q

What is function of circulatory system

A

carries nutrients, wastes, chemical signals, and heat

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8
Q

why is diffusion inefficient

A

too slow to support large bodies

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9
Q

types of circulation circuits

A

pulmonary and systemic

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10
Q

pulmonary circulation

A

carries blood between heart and lungs

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11
Q

systemic circulation

A

carries blood between heart and rest of body

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12
Q

If hematocrit increases

A

viscosity of blood increases

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13
Q

Which blood vessel contributes the most resistance to flow

A

arterioles then capillaries

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14
Q

What are types on local control (intrinsic) that allows tissues to control their own blood flow

A

myogenic, paracrine substances, hyperemia

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15
Q

describe myogenic control

A

by smooth muscle of arterioles

increases blood pressure - > increase stretch-> Ca2+ channels open -> vessel constricts so flow remains same

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16
Q

paracrine vasoconstrictors

A

paracrine substances alter smooth muscle activity
serotonin
endothelin

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17
Q

serotonin

A

vasoconstrictor secreted by platelets

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18
Q

endothelin

A

vasoconstrictor secreted by vascular endothelieum

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19
Q

paracrine vasodilators

A

bradykinin
histamine
adenosine

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20
Q

adenosine

A

vasodilator hormone secreted by cells in low O2 conditions

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21
Q

hyperemia

A

locally mediated increases in blood flow

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22
Q

active hyperemia

A

increase in tissue metabolism -> release of vasodilators into extracellular fluid-> decrease resistance-> blood flow increase -> O2 and nutrient supply to tissue increase

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23
Q

reactive hypermia

A

occlusion -> blood flow decrease -> vasodilators accumulate-> arterioles dilate -> occlusion removed _> resistance decrease-> blood flow increase

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24
Q

systemic control (EXTRINSIC) vasoconstriction

A

delivered by neurons
serotonin
vasopressin
angiotensin II

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25
systemic control (EXTRINSIC) vasoconstriction
Beta-2 epinephrine ACT ANP VIPs
26
norepinephrine
systemic control released by sympathetic neuron | moderate amount - intermediate diameter
27
increase in norepinephrine
vasoconstriction
28
decrease in norepinephrine
vasodilation
29
hepatic portal vein
drains blood from gastointestinal tract and speeds into capillary beds in liver blood is rich in nutrients from food not a true vein because it does not conduct blood back to heart
30
\what causes an aneurysm
artherosclerosis- accumulation of calcium and fatty materials on blood vessel wall that weakens it based on law of Laplace an increase in r increases T, and r thus T continues to increase
31
steps to artherosclerosis
1. fatty streak cholesterol accumulate 2. fibrous plaque accumulates around accumulating cholesterol 3. calcified scar tissue forms
32
how does a heart stay in place
pericardial attachments and great vessels
33
ligamentum arteriosum
small ligament attached to outer surface of pulmonary artery with no function (remnant of fetal ductus arteriosus)
34
blood going to the upper heart arrives from
superior vena cava(head and upper limbs) inferior vena cava (trunk and lower limbs) coronary sinus (from myocardium)
35
coverings of heart outer- in
fibrous pericardium | serous pericardium - visceral pericardium pericardial cavity - parietal pericardium
36
heart wall outer-in
epicardium myocardium endocardium
37
where does right atrium receive blood
inferior vena cava, superior vena cava, coronary sinus
38
fossa ovalis
remnant of fetal foramen ovale in right atrium
39
where does left atrium receive blood
pulmonary veins
40
interatrial septum
separates left and right
41
trabeculae carnae
thick-wall with an irregular inner surface that covers ventricles
42
interventricular septum
separates left and right ventricls
43
Valves
Tricuspid mitral semilunar - pulmonary Aortic
44
tricuspid valve
between right atrium and right ventricle
45
mitral valve (bicuspid)
between left atrium and left ventricle
46
chordae tendinae
connect cusps of AV valves to papillary muscle of ventricles, preventing cusps from swinging back into atria during systole
47
papillary muscle
muscular columns located on inner surface of ventricles
48
pulmonary SL valve
lies within pulmonary trunk
49
aortic SL valve
within aorta
50
regurgitation
backflow of blood across closed valve
51
mitral regurgitation occurs
during systole
52
aortic regurgitation occurs
during diastol
53
stenosis
obstruction of forward flow across an opened valve
54
mitral stenosis occurs
during diastole
55
aortic stenosis occurs
during systole
56
S1 heart sound
onset of ventricular contraction
57
S2 heart sound
closure of semilunar valves
58
S3 heart sound
ventricular gallop
59
S4 heart sound
atrial gallop
60
valvular theory
says sounds caused by vibration of heart valves during closure
61
cardiohemic theory
vibration of entire cardiohemic system causes heart sounds
62
sarcomere
functional unit of cardiomyocyte
63
intercalated discs
connects branched fibers of myocardium
64
how are cells held together during contraction
desmosomes
65
L-type Ca channels
how Ca2+ enters cell
66
ranodine receptors
Ca2+ binds to on sarcoplasmic reticulum to trigger release of Ca2+
67
terminal cisternae
where Ca2+ is released from sarcoplasmic reticulum
68
steps of excitation-contraction coupling
1. action potential enters 2. Ca2+ enters through voltage -gated Ca2+ channels 3. bind to ryanodine receptors 4. Ca2+ released from terminal cisternae of sarcoplasmic reticulum 4. Ca2+ binds to troponin, causing tropomyosin to move and expose myosin binding sites - actin 5. myosin head binds to actin and causes cross-bridge movement and a reduction in sarcomere length 6. Ca2+ taken in by SR via SERCA Pump 7. removal of Ca2+, myosin unbinds from actin (Requires ATP), sarcomere resumes original length
69
membrane potential
0. opening of Na+ channels , rapid depolarization 1. opening of K+ channels efflux, repolarize 2. opening of Ca2+ channels, influx, plateau 3. opening K+ channels and closing of Ca 2+, repolarization 4. resting potential Ca 2+ removed with Ca2+ ATP pump and Na+/Ca2+ exchanger Na+removed and K+ returned with NaK pump
70
ERP effective refractory period
time when action potential can't be initiated
71
sinoatrial node
in right atrium is the pacemaker group of cardiomyocytes 65 bpm pace of heart
72
F-type channels
Na2+ leak in through at negative membrane potentials and close as membrane depolarizes; beginning of pacemaker potential
73
pacemaker potential generation
4. myogenic slow depolarization from -60 to -40 mV, Na2+ in through F-type channels that start to close as threshold potential is approached, increase of Ca2+ through T- type channels 0. Rapid opening of Ca2+ channels, rapid depolarization 3. Repolarization, opening of K+ channels, release K_, close Ca2+ channels
74
atrioventricular node
secondary pacemaker | autorhythmic at 55bpm
75
Travel of contraction in heart
1. SA node 2. AV node 3. Bundle of His | 4. Purkinje fibers
76
nervous system role in heart contraction: sympathetic stimulation
increase in firing rate-> increase slope of spontaneous depolarization, lower threshold for action potential
77
nervous system role in heart contraction: parasympathetic stimulation
decrease in firing rate ->decrease in slope of spontaneous depolarization, increase threshold for action potential
78
How does an ECG obtain its signal
electrodes placed to Einthoven's triangle and leads or potentials is recorded between two given electrodes
79
P-wave
impulse spreads from SA node to AV node | atrial depolarization and atrial systole
80
QRS- complex
represents ventricular depolarization | aligns with ventricular systole and atrial diastole
81
Q wave
first area of ventricular muscle activated from left to right
82
R-wave
both ventricles activated
83
S-wave
a few small areas of ventricles activated
84
T-wave
ventricles recover ventricular repolarization ventricle diastole
85
bradycardia/ brachycardia
heart rate
86
Sinus brachycardia
rate = 40-59 bpm
87
Tachycardia
heart rate >100 bpm
88
sinus tachcardia
101-160 bpm | caused by heart failure, stress or increased temperature
89
Paroxysmal atrial tachycardia
short period of rapid and regular heartbeats
90
ventricular tachycardia
one continuous, irregular wave looks like ugly sin wave
91
sinus arrhythmia
rate fluctuates between 45-100bpm
92
sinus arrest
period of no heart beat
93
Atrial flutter
multiple P waves before QRS complex, 250-350 bpm
94
Atrial fibrilation
can't distinguish between P and T waves
95
Ventricular fibrilation
continuous irregular wave with small amplitude
96
AV block
Q wave appears absent
97
premature atrial contractions
palpitations, irregular PR rhytms, irregular P wave
98
Asystole
flatline
99
Ischemia
reduction of blood flow, results in large dip in ST segment of ECG
100
Hypoxia
reduction of oxygen supply due to ischemia
101
angina pectoris
severe pain accompanied by ischemia, relieved by nitroglycerin
102
myocardial infarction diagnosis
heart attack diagnosed by high levels of creatine phosphate and lactate dehydrogenase
103
cause of myocardial infarction
thrombus (stationary clot) embolus(moving clot) in coronary artery
104
cardiac output
volume pumped by left ventricle in one minute
105
calculation of Mean arterial pressure
MAP=CO*TPR(total peripheral resistance)
106
calculation of CO
CO= stroke volume x heart rate
107
stroke volume calculation
end diastolic volume-end systolic volume
108
Stroke volume
amount of blood ejected in one heart beat
109
calculation of total peripheral resistance
change in pressure across entire systemic circulation/ flow
110
factors affecting stroke volume: end diastolic volume
1. venous return 2. preload 3. blood volume 4. force-stretch relationship
111
factors affecting stroke volume: end systolic volume
1. contractility | 2. after-load
112
affecting edv: definition of venous return and how to increase it
volume of blood returning to heart skeletal muscle pump: skeletal muscles compress veins, force blood toward heart respiratory pump: pressure gradient from breathing pulls blood to right atrium
113
affecting edv: Pre-load definition
amount that the contractile myocardial fibers in ventricles are stretched
114
Frank-starling law of the heart
stroke volume increases if volume of blood that returns to it increases
115
affecting edv: force-stretch relationship
cardiac muscle stretch increases the force corresponding increases
116
affecting ESV: how to increase contractility
send inotropic agents: sympathetic signals -epinephrine and norepinephrine, or digitalis
117
epinephrine and norepinephrine binding to beta 1 receptors
binds to beta -1 receptors then causes rapid contraction which causes more force generated and causes rapid relaxation which causes a shorter duration of contraction
118
Digitalis
lowers Na+/K+ ATPase activity-> lower na+-Ca2+ exchange, elevates Ca2+ concentration -> stronger graded contraction
119
affecting ESV: afterload
back pressure exerted by blood in large arteries leaving the heart which must be overcome before ventricular ejection can occur
120
how is heart rate increased
sympathetic stimulation: epinephrine and norepinephrine | parasympathetic inhibition: reduction of neurotransmitter acetylcholine
121
factors affecting Total peripheral resistance
1. friction- viscosity, total blood vessel length, radius | 2. arteriolar radius- vasoconstrictos and vasodilators
122
Vasoconstrictors: Neuronal controls
sympathetic nerves stimulate alpha-adrenergenic receptors for norepinephrine and epinephrine
123
Vasoconstrictors:Hormonal controls
epinephrine and norepinephrine, angiotensin II, vasopressin
124
Vasoconstrictors:local controls
internal blood pressure increase, O2 increase, Co2 decrease, cold environment, hemodynamic forces increase
125
Vasodilators: Neuronal controls
sympathetic nerves stimulate beta-adrenergenic receptors for epinephrine neurons that release Nitric Oxide
126
Vasodilators:Hormonal controls
epinephrine- on beta-adrenergenic receptors | atrial natriuretic peptide
127
Vasodilators :local controls
decrease in O2, increase in K_, CO2, and H_, osmolarity, adenosine, NO, hemodynamic forces decrease
128
Blood flow: Local control
active hyperemia, flow autoregulation
129
Blood flow: Local control: Active hyperemia
increase metabolic activity of organ, decrease O2 and increase metabolites in organ's interstitial fluid, arteriolar dilation , increase blood flow
130
Blood flow: Local control: autoregulation
1. decrease in arteriolar pressure in organ, decrease in pressure in organ, decrease O2 increase metabolites and decrease vessel wall stretch, arteriolar dilation, blood flow increase
131
systolic blood pressure
arterial blood pressure during systole | normal : less than 120 mmHg
132
diastolic blood pressure
arterial blood pressure during diastole | Normal: less than 80 mmHg
133
shygmomanometer
blood pressure cuff, | listen to Korotkoff sounds created by pulsatile blood flow between 80 and 120 mmHg applied
134
brain regulating blood pressure
1. carotid and aortic baroreceptors sense change 2. 2. afferent nerves to medullary cardiovascular control center 3. efferent nerves from control center affect SA node 3. effect HR and SV0> CO and TPR -> BP
135
drugs that treat hypertension
``` diuretics beta-andrenergenic receptor blockers calcium channel blockers angiotensin converting enzyme inhibitors drugs that antagonize sympathetic nervous system ```
136
peripheral feedback system
theory how body controls change in blood pressure | metabolic activity-> arteriolar dilation-> reflex pressure response
137
types of capillaries
continuous, fenestrated, and discontinuous
138
intercellular clefts
assist the exchange between blood of capillaries and interstitial fluid
139
types of capillary exchange
diffusion vesicular transport bulk flow - filtration and absorption
140
net filtration pressure, net fluid enters
``` hydrostatic pressure (inside capillary) - colloid osmotic pressure lymphatic vessels ```
141
how is oxygen delivered from capillaries
convection
142
vasomotion
spontaneous change in tone of blood vessels | opening and closing of capiliaries
143
precapillary sphincters
cut off capillaries
144
roles of endothelial cell in circulation
1. barrier between blood vessels and rest of blood 2. secretion of vasoactive substances 3. exchange of materials between blood and surrounding through vesicular transport 4. formation of platlet plugs
145
hemorrhage causes
reduction in SV->reduction in CO-> reduction in MAP
146
hemorrhage response
HR increases -> CO TPR increases -> MAP autotransfusion mechanism: increase in absorption and decrease in filtration to protect blood volume
147
ultrafiltration
capillary losing fluid, when inward pressure dominates | at the arterial end
148
reabsorption
capillary absorbing fluid, outward pressure dominates, venous end
149
what is blood
connective tissue whose cells are suspended in plasma 45% formed elements 55% plasma
150
erythrocytes
red blood cells, hematocrit
151
hematopoietic stem cells
in bone marrow of adults give rise to eythrocytes
152
hemocytoblast
primitive cell that all blood cells come prom
153
eythropoiesis
production of red blood cells within red bone marrow
154
erythropoietin
hormone produced by cells in kidney and liver that control production of red blood cells
155
dietary factors affecting eythropoiesis
B12, folic acid, iron | intrinsic factor which allows b12 absorption
156
anemia
lack of proper dietary nutrients needed to produce red blood cells
157
destruction of RBCs
1. break into globin and heme -> heme into iron and biliverdin-> transferrin transports iron to tissue and liver for synthesis of new hemoglobin -> 80% of iron chills there as ferritin globin broken into amino acids iron and biliverdin not used becomes bile
158
types of leukocytes (white blood cells): granulocytes
neutrophils, eosinophils, basophils
159
types of leukocytes (white blood cells): agranulocytes
monocytes and lymphocytes
160
neutrophils
WBC most abundant granulocyte phagocytes for foreign particles
161
eosinophils
granulocyte | responsible for allergic reaction
162
Basophil
granulocyte release heparin - inhibits blood clotting histamine: vasodilator may develop into mast cells
163
Monocyte
agranulocyte phagocytosis in blood=phagocyte intissue = macrophage
164
lymphocytes
important for Immune system T-cells attack cells directly B-cells produce antibodies that act against specific foreign substance
165
leukopenia
low WBC count
166
Leukocytosis
high WBC count
167
myeloid luekemia
bone marrow produces too many immature granulocytes, crowds out other blood cells
168
lymphoid leukemia
lymphocytes are cancerous
169
thrombocytes
platelets | fragments of megacaryocytes which helps repair damaged blood vessels and forms a platelet plug
170
Kwashiorkor
disease of blood plasma | resulting from switch from breast milk to food deficient in nutrients
171
hemostatis and its steps
stoppage of bleeding from blood vessel 1. blood vessel spasm 2. platelet plug formation- platelets release serotonin causing vasoconstriction 3, blood coagulation - extrinsic: platelet contacts damaged tissue intrinsic: blood contacts foreign substance
172
fibrinolytic system
provides checks and balances so that blood clotting stayss
173
substances released by fibrinolytic system to check blood clots
Tissue plasminogen activator, heparin, warfarin
174
thrombus
abnormal clot
175
embolus
floating clot
176
embolism
embolus lodged in small vessel
177
what determines blood type
antigen present on cell membrane of RVC
178
what happens if RBC's antigen and plasma antibody are the same
hemolysis (bursting) and agglutination (clumping)
179
erythroblastosis fetalis and treatment
Rh negative woman conceive Rh positive baby and develops Rh antibodies Conceives another Rh positive baby and antibodies attack fetal RBCs RhoGam- destroys anti-Rh antibodies