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
Q

atherosclerotic lession types

A

fatty streaks and fibrous atheromatous plaques

26
Q

yellow, thin, enlarging, have macrophages combines with lipid to form foam cells and visible bc macrophages will ingest and oxidize lipoproteins

A

fatty streals

27
Q

fatty streaks that proliferate into smooth muscle over time, lumen of artery narrows, macrophages cuae inflammation by releasing stuff

A

fibronous atheromatous plaque

28
Q

components of atherosclerotic plaques?

A

-SMCs, macrophages, ECM w collagen, elastic fibers, lipids

29
Q

what is below fibrous caps

A

central core of lipid laden foam cells and fatty debris

30
Q

most arterial occlusions (stop bf to orga/ tissue) are from?

A

embolus

31
Q

pistol shot, pallor, poikilotherma, pulselessness, pain. paresthesia, paralysis are?

A

embolus signs

32
Q

atherosclerotic occlusive disease/ peripheral artery disease?

A

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
Q

beurger disease causes

A

thrombus formation due to inflammatory arterial disease
-common in medium sized arteries and hands (mostly leg)
-chronic inflammation and thrombosing

34
Q

what cuases raynaud?

A

vasospasms of arteries and arterioles in fingeres and toes
-vasoconstriction in response to stimuli

35
Q

what can raynaud cause?

A

ischemia due to vasospasms, cold, numbness tingling, pallor and syanosis (pale and purple fingers)

36
Q

where do primary varicose veins originate?

A

superficial saphenois vein

37
Q

where do secondary varicose veins come from?

A

impaired bf in deep venous channels
-DVT

38
Q

sings of varicose veins?

A

aching in extremeties, edema after standing

39
Q

impaired unidirectional flow of blood and empyting of deep veins that causes stretching of veins, valve ruptures and thrombosis is?

A

chronic venous insufficiency

40
Q

etiology of chronic venous insufficiency?

A

increase venous hydrostatic pressure that worsens with standing, incompetent vaalves in veins and DVT

41
Q
A