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Human Phys > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

how does Ca increase in cardiovascular system

A
  • SR less developed than in skeletal
  • T-tubule network more developed - as AP spreads channels on cell membr open allowing influx of extracellular Ca - interacts w/ ryano receptors on SR - more Ca influx wia CICR
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2
Q

repolarization of cardiac tissue

A

channels close - Ca pumped into extracellular matrix and SR

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3
Q

resting potential of contractile myocardium

A

-85 to -95 mv

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4
Q

depolarization of contractile myocardium caused by

A
  1. fast Na+ channels
  2. slow channels (L-channels, Ca)
    cause “plateau effect” of AP
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5
Q

importance of Plateau effect in myocardium

A

prevents summation of twitches (duration of AP = duration of twitch)

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6
Q

repolarization of contractile myocardium

A

caused by closing of slow channels and opening of K+ channels

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7
Q

pacemaker cells

A

capable of spontaneous and rhythmic depolarization

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8
Q

resting potential at SA node

A

-55 mV

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9
Q

how does electrical excitation at SA node spread

A

gap junctions
electrical resistance lower than rest of membrane

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10
Q

why are heart contractions staggered

A

ventricles need to fill before they can contract to make the most efficient pump

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11
Q

what causes delay in atrial/ventricular contraction

A

delay in spread of electrical activity from atria to ventricle via the AV node to AV bundle to bundle of His to purkinje fibers

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12
Q

AV node

A

conducting cells at base of right atrium that crosses fibrous tissue

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13
Q

How does heart incr CO

A
  1. intrinsic regulation (ex. change in SV)
  2. regulation by autonomic NS and hormones (HR and SV)
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13
Q

cardiac output (Q) or (CO)

A

amt of blood ejected by each ventricle per min
CO = HR x SR

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14
Q

chronotropic vs ionotropic

A

chronotropic - factors affecting speed of HR
ionotropic - factors affecting force of HR (SV)

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15
Q

chronotropic factors

A

parasymp input decr HR
symp input incr HR
neural input affect AP conduction thru AV junction

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16
Q

inotropic factors

A

ACh, NE
E increases contractility
Starlings law

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17
Q

Starling’s Law

A

as end diastolic volume increase so does SV
force incr bc of change in length of sarcomeres and elastic recoil

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18
Q

blood flow determining factors

A
  1. pressure diff between 2 ends of vessel
  2. resistance to blood flow (diameter of vessel, length, viscosity)
19
Q

BF

A

diff in pressure / resistance

20
Q

basic principles of controlling BF

A
  1. to tissue - controlled in relation to tissue needs
  2. CO regulated by sum total of local tissue flow - as EDV incr so does CO
  3. arterial pressure can be regulated independently of local BF or CO control
21
Q

as A pressure decrease

A

restore by contstricting arterioles and contracting large veins

22
Q

vascular system order

A

arteries - arterioles - capillaries - venules - veins
pressure progressively decr

23
Q

Arteries

A

transport blood under high pressure to tissues
- strong elastic walls
- large w low resistance
- incr pressure vessels (changes during cardiac cycle)

24
Q

pulse pressure

A

difference between systolic and diastolic pressure

25
Q

MAP

A

considered average pressure during cardiac cycle
MAP = DP + 1/3PP

26
Q

Arterioles

A

small branches of arterial system
- strong muscular walls
- act as control valves
- high pressure vessels
- resistance to BF regulated by smooth muscle

27
Q

Arterial smooth muscle control

A

Local - decr O2, incr CO2, incr H+ cause vasodilation and decr resistance
Extrinsic Neural - symp NS cause vasodilation/constriction
Extrinsic Hormonal - E can cause either vasoconstriction/dilation

28
Q

Capillaries

A

allows exchange of gasses, nutrients, and metabolic byproducts between blood and tissue
- thin walls, not elastic, no smooth muscle
- small diameter
- walls very permeable
- flow rate lower = higher transit time
- substance pass via simple diffusion

29
Q

Venules

A

diameters greater than those of caps and arts
- walls thinner and weaker than arteriole
- pressure much less so they can significantly contract

30
Q

Veins

A

return blood to heart
- low resistnance due to incr diameter and compliance of walls - avg pressure around 10 mm Hg
- walls have little smooth muscle

31
Q

how do veins regulate pressure and return to heart

A

smooth muscle innervated by symp NS, venous (muscle) pump

32
Q

rate of venus return and CO

A

as total BF demand inc so mus venus return

33
Q

blood make-up

A

plasma - liquid component
55% total vol
erythrocytes - rbcs
45% total vol
“buffy coat” - leukocytes, platelets

34
Q

Albumins

A

most abundant plasma protein
formed in liver
binding/carrier proteins

35
Q

globulins

A

clotting, enzymes, antibodies

36
Q

fibrinogen

A

blood clotting

37
Q

Leukocytes (WBCs)

A

immune response
- monocytes, neutrophils, macrophages, lymphocytes

38
Q

Platelets

A

cell fragments involved in clotting

39
Q

Erythrocytes (RBCs)

A

transport O2 from lungs to tissue
- H ct = 45% in males 42% in females
- small and easily deformed
- biconcave disk

40
Q

Hb

A

carries O2
4 subunits
Fe-containing heme and polypeptide chain

41
Q

Growth and formation of RBC

A
  1. stem cells in bone marrow
  2. diff into proerythroblasts
  3. continue to dif - produce Hb, shrink nucleus and extrude, lose other organelles
  4. leave marrow and enter circulation
42
Q

regulation of RBC formation

A

tissue oxygenation
- EPO levels in kidneys

43
Q

RBC lifespan

A

apprx 120 days
- cell becomes fragile and ruptures during passage thru capillaries (spleen) - Fe carried by transferrin to bone marrow where stored as ferritin

44
Q

Anemia

A

inadequate O2 carrying capacity bc
1. low Hct
2. low Hb content of RBC
3. combination

Human Phys (8 decks)

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