Alterations in Blood Pressure Flashcards

1
Q

circulation route of blood

A

from the body>right atrium>right ventricle>lungs>left atrium>left ventricle>pumps blood to the body

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2
Q

arterial blood pressure

A

made by the force of the left ventricle contraction to open the aortic valve

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3
Q

preload

A

blood in the ventricles at the end of diastole (filling)-amount of blood returned to the heart

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4
Q

preload is increased from

A

hypervolemia, regurgitation of the valves, heart failure

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5
Q

afterload

A

the resistance the left ventricle combats to open aorta/circulate blood
-increased afterload means increased cardiac work

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6
Q

afterload is increased from

A

hypertensin, vasoconstriction

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7
Q

cause of hypertension

A

from flow: increased fluid and pressure
from resistance: increased resistance and pressure but decreased diameter
-all can cause stretching of the endothelial cells

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8
Q

cardiac output equals

A

CO=SVxHR

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9
Q

systemic vascular resistance (SVR)

A

radius of arteries, degree of vessel compliance

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10
Q

blood pressure equals

A

BP=COxSVR

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11
Q

systolic BP

A

peak pressure during systole, controlled by stroke volume

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12
Q

diastolic BP

A

lowest pressure during diastole, controlled by SVR

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13
Q

pulse pressure equals

A

SBP-DBP

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14
Q

mean arterial pressure

A

average pressure in the circulatory system through the cardiac cycle
-65 is healthy, under is abnormal

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15
Q

ANS regulation of BP (short term regulation)

A

carotid/aortic baroreceptors respond to drops in BP>vasomoter center activates SNS>PNS is inhibited>increased BP from heart rate and SVR

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16
Q

long term regulation of BP

A

baroreceptors sense changes in pressure>a1 receptors in arterioles and b1 receptors in the heart activated
-ADH secretion from osmolarity and aldosterone from RAAS affect the fluid balance (angiotensin II increases SVR/causes vasoconstriction to increase BP)
-natriuretic peptides
-involves HR, SV, SVR

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17
Q

RAAS and blood pressure

A

kidneys secrete renin from decreased perfusion>creates angiotensin I>converted to angiotensin II in the lungs>arteriole constriction and aldosterone secretion>Na+, H20 retention>increased blood volume>increased vascular resistance>increased BV, SVR cause hypertension

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18
Q

hypertension

A

high blood pressure
-damaged endothelial tissue risks atherosclerotic vascular disease and vascular rupture
-increases morbidity with heart disease, kidney disease, PVD, stroke
-primarily asymptomatic

19
Q

hypotension

A

low blood pressure-tissues don’t get enough nutrients, oxygen, and removal of waste

20
Q

normal blood pressure

21
Q

elevated blood pressure

A

120-129/80

22
Q

stage 1 hypertension

A

130-139/80-89

23
Q

stage 2 hypertension

24
Q

primary hypertension

A

idiopathic disorder-no known causes but related risks
-most common form of hypertension
-treatment is usually lifestyle changes, drug therapy is a last resort

25
ACE inhibitors
decreases vascular resistance without increasing heart rate, cardiac output, or cardiac contractibility
26
secondary hypertension
from a pathologic condition or from medications/chemicals -usually in infants and preschool children
27
vessel damage from hypertension
increased arterial pressure damages the endothelium>angiotensin causes endothelial wall contraction>plasma leaks into endothelial space>vessel wall necrosis
28
organ damage from hypertension
from atherosclerosis in the coronary, renal and cerebral arteries -increases the risk of stroke, angina, MI, heart failure, renal failure, retinopathy
29
hypertensive emergecy
spiked systolic and/or diastolic blood pressure with organ damage >180/>120
30
hypertensive urgency
spiked systolic and/or diastolic blood pressure without organ damage >180/>120
31
orthostatic hypotension
drop in systolic (>20) and diastolic (>10) BP when sitting up -failure of the short-term control mechanism -can have an excessive increase in heart rate (20-30 BPM) -dizziness/blurred vision/fainting -risk factor for stroke, cognitive impairment and death -associated with heart disease
32
orthostatic hypotension associations
existing pathologies, vasovagal reactions, cardiac volume depletion, dysrhythmias, drug therapy, alcohol, heat exhaustion, arterial stiffness
33
orthostatic hypotension treatment
slow positional changing, avoiding heat, avoiding large meals, squatting/bending forward, compression socks
34
t/f: a stroke can be transient, reversible, progressive, or complete
true
35
ischemic strokes
interruptions of blood flow in a cerebral vessel (ex: thrombi, embuli) -most common stroke -location of stroke is important (area of brain, vessels involved, R/L side) -duration/lack of O2 is important to see damage -symptoms are sudden and severe
36
hemorrhagic strokes
bleeding into brain tissue from blood vessel ruptures -can be from: hypertension, aneurysms, arteriovenous malformations, head injuries, blood disorder -hypertension is the MOST common cause -high mortality rate -headaches from ICP
37
cerebral aneurysms
symptoms: headache, stiff neck, vasospasm treatment: neurosurgery complications: vasospasms
38
arteriovenous malformation (AVM)
malformations where blood goes into the venous system without capillaries -causes HIGH venous pressure -AVM compresses structures or ruptures them -treatment: surgical removal, radiation, embolization to close AVM
39
transient ischemic attacks (TIAs)
quick episodes of ischemia -doesn't cause neurological damage but puts you at high risk for stroke -usually from thrombi, sometimes emboli -symptoms: sudden headache, vomiting, loss of neurologic function -full recovery within a day
40
ischemic penumbra
evolving strokes -an area around a core of dead or dying cells getting low blood flow from an occlusion -associated with embolic strokes
41
stroke symptoms
hemorrhagic: sudden severe headache -loss of vision, aphasia, confusion, numbness/weakness in the face/arms/legs/side of the body, trouble walking and balancing
42
stroke treatment
depends on the stroke-ischemic or hemorrhagic -limiting the size of infarction, supporting body functions, rehab
43
speech impediment with ischemic stroke
left area damage (brocas area, wernickes area): aphasia, impaired speech and language