exam 3 part 2 Flashcards

1
Q

contraction

A

systole

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2
Q

atrial systole

A

SL close, AV open
-blood to ventricles

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3
Q

ventricular systole

A

-blood to pulm. trunk and a.a.

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4
Q

phases of ventricular systole

A

-isovolumetric contraction (all valves are closed)
-ventricular ejection (SL open AV close)

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5
Q

when do chambers fill with blood

A

diastole

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6
Q

early ventricular diastole

A

isovolumetric relaxation (all valves are closed)

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7
Q

late ventricular diastole

A

atria and ventri8cles fill passively
-av open SL closed

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8
Q

what affects output?

A

preload and afterload

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9
Q

what determines prelaod

A

-stretching when ventricle diastole, venous return, blood in ventricle post systole

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10
Q

what is aferload?

A

pressure the heart has to generate to pump blood out of heart, main source of afterload is the systemic arterial pressure

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11
Q

what does hr control

A

the frequency at which blood is ejected from the heart

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12
Q

what affects hr

A

-medulla ob, sympathetic and parasypathetic activation at the vardiovascular vasomotor control center, neural reflexes (low bp increases hr bc the arterioles constrict), hormones (epi, ne, thyroid)

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13
Q

friction btwn blood and vessel wall is?

A

vascular resistance

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14
Q

decrease vessel radius

A

increase friction and resistance

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15
Q

what regulates CO in the body

A

cardia centers (parasym and sympathetic nervous systems) and the vasomotor center that regulates vessel diameter `

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16
Q

what responds to bp changes

A

baroreceptor reflexes

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17
Q

where are stretch receptors in walls?

A
  1. carotid sinuses (to brain)
  2. aortic sinuses (monitor systemic circuit)
  3. right atrium (moniter end of systemic circuit)
18
Q

what respond to changes in o2, co2, ph

A

chemorepectors

19
Q

where are peripheral chemoreceptors

A

carotid and aortic bodies

20
Q

where are central chemoreceptors

A

medulla ob.

21
Q

epi and ne from adrenal medulla will increase co and peripheral vasoconstriction when?

A

when sympathetic is activates
-this is short term

22
Q

what are long term endocrine mechanisms?

A

-adh and angiotensin 2

23
Q

adh

A

increase bp bc cause reabsorb water from tubular fluid in collecting duct of nephron

24
Q

angiotensin 2

A

decrease renal bp by adh secretion, thirst, peripheral vasoconstriction

25
atherosclerotic lession types
fatty streaks and fibrous atheromatous plaques
26
yellow, thin, enlarging, have macrophages combines with lipid to form foam cells and visible bc macrophages will ingest and oxidize lipoproteins
fatty streals
27
fatty streaks that proliferate into smooth muscle over time, lumen of artery narrows, macrophages cuae inflammation by releasing stuff
fibronous atheromatous plaque
28
components of atherosclerotic plaques?
-SMCs, macrophages, ECM w collagen, elastic fibers, lipids
29
what is below fibrous caps
central core of lipid laden foam cells and fatty debris
30
most arterial occlusions (stop bf to orga/ tissue) are from?
embolus
31
pistol shot, pallor, poikilotherma, pulselessness, pain. paresthesia, paralysis are?
embolus signs
32
atherosclerotic occlusive disease/ peripheral artery disease?
sudden event stopping bf, common in lower extremeties, claudication (pain w walking like calf pain that is releived w rest), thinning of kin and cold foot and has a weak pulse
33
beurger disease causes
thrombus formation due to inflammatory arterial disease -common in medium sized arteries and hands (mostly leg) -chronic inflammation and thrombosing
34
what cuases raynaud?
vasospasms of arteries and arterioles in fingeres and toes -vasoconstriction in response to stimuli
35
what can raynaud cause?
ischemia due to vasospasms, cold, numbness tingling, pallor and syanosis (pale and purple fingers)
36
where do primary varicose veins originate?
superficial saphenois vein
37
where do secondary varicose veins come from?
impaired bf in deep venous channels -DVT
38
sings of varicose veins?
aching in extremeties, edema after standing
39
impaired unidirectional flow of blood and empyting of deep veins that causes stretching of veins, valve ruptures and thrombosis is?
chronic venous insufficiency
40
etiology of chronic venous insufficiency?
increase venous hydrostatic pressure that worsens with standing, incompetent vaalves in veins and DVT
41