Cardiovascular Flashcards

(45 cards)

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
pulse pressure
difference between systolic and diastolic pressure
25
MAP
considered average pressure during cardiac cycle MAP = DP + 1/3PP
26
Arterioles
small branches of arterial system - strong muscular walls - act as control valves - high pressure vessels - resistance to BF regulated by smooth muscle
27
Arterial smooth muscle control
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
Capillaries
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
Venules
diameters greater than those of caps and arts - walls thinner and weaker than arteriole - pressure much less so they can significantly contract
30
Veins
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
how do veins regulate pressure and return to heart
smooth muscle innervated by symp NS, venous (muscle) pump
32
rate of venus return and CO
as total BF demand inc so mus venus return
33
blood make-up
plasma - liquid component 55% total vol erythrocytes - rbcs 45% total vol "buffy coat" - leukocytes, platelets
34
Albumins
most abundant plasma protein formed in liver binding/carrier proteins
35
globulins
clotting, enzymes, antibodies
36
fibrinogen
blood clotting
37
Leukocytes (WBCs)
immune response - monocytes, neutrophils, macrophages, lymphocytes
38
Platelets
cell fragments involved in clotting
39
Erythrocytes (RBCs)
transport O2 from lungs to tissue - H ct = 45% in males 42% in females - small and easily deformed - biconcave disk
40
Hb
carries O2 4 subunits Fe-containing heme and polypeptide chain
41
Growth and formation of RBC
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
regulation of RBC formation
tissue oxygenation - EPO levels in kidneys
43
RBC lifespan
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
Anemia
inadequate O2 carrying capacity bc 1. low Hct 2. low Hb content of RBC 3. combination