Physiology of Haemodynamics Flashcards

(36 cards)

1
Q

one cardiac cycle

A
  1. atrial contractions
  2. isovolumic contraction
  3. ventricular ejection
  4. isovolumic relaxation
  5. passive ventricular filling
  6. atrial contraction
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2
Q

between left and right, which has the greatest pressure

A

LEFT

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3
Q

in passive filling is the atria doing any work

A

no, no work is being done by the atria

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4
Q

atrial waves

A

a - atrial contraction
c - AV close and bulge into the atria
v - atria is filling with blood before the AV valves open (max atrial filling pressure)

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5
Q

how and where are the atrial waves measured

A

in the RAuding CVP

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6
Q

two key principles that determine blood flow/cardiac output

A
  1. CO = SV * HR
  2. CO = (MAP - AP)/ R
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7
Q

vessels with the greatest pressure

A
  • large arteries and left ventricle
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8
Q

vessels with the lowest pressure

A

capillaries and venules/veins

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9
Q

radius and resistance relationship

A

inversely proportional

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10
Q

vasocon extrinsic factors

A
  • SNS - a1 from NA
  • angiotensin II - hormone that increases BP
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11
Q

vasocon intrinsic (local) factors - PEMELO

A

Prostaglandin
Endothelin
Myogenic responses
Endothelial factors
Local metabolites
Oxygen

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12
Q

vasodi extrinsic factors

A
  • SNS - B2 from NA
  • PNS - Ach - NO
  • ANP
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13
Q

vasodi intrinsic (local) factors - HELP

A

Histamine
Endothelial factors = NO
Local metabolites = adenosine, carbon monoxide
Prostaglandin

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14
Q

3 dterminants of SV

A
  • preload
  • contractility
  • afterload
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15
Q

preload

A
  • how much the ventricles fill BEFORE they contract
  • it is the EDV
  • exclusive to ventricles
  • associated with VR
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16
Q

5 factors affecting preload

A
  • venous return
  • changes in blood volume
  • diastolic dysfunction
  • decreased filling time - HR >180
  • decreased volume ejected
17
Q

effects of a HR greater than 180

A
  • doesnt give tehe ventricles enough time to fill properly
  • fast filling time = less time to fill = less blood going to the body (SV) less blood going to the lungs for oxygenation
18
Q

does breath holding increase or decrease VR

A

decrease - chest is tight or presurrised

  • it is NOT the same as breathing in please
19
Q

preload in constriction vs dilatation

A
  • constriciton increases VR while dilation decr it - which is weird..
20
Q

contractility

A
  • doesnt have to do with the stretching of the heart - SQUEEZING (pushing blood out)
21
Q

4 things increasing contractility

A
  • SNS- B1 agonist
  • PDEi incr cAMP
    -long acting calcium channels
  • Na-K ATPase pumps or Na-Ca exchange pump
22
Q

4 things decreasing contractility

A
  • oxygen
  • depressants
  • cell death
  • adenosine type 1 receptors
23
Q

a2 modulation of SNS

A
  • inhibits VMC
  • inhibits NA release from presynaptic terminals
24
Q

examples of PDEi

A
  • caffeine
  • milrinone
  • amrinone
25
afterload
- th resistance that the ventricles have to push against - arterial pressure (aortic pressure)
26
increase in after load
decreases stroke volume - if AL is increased it means the resistance is increased so less blood leaves the ventricles and goes to the body.. so decr SV
27
tension formular
pressure x radius / 2x wall thickness
28
increase in tension
- increased oxygen demand - reduced systolic function
29
what factors can increase afterload
- incr resistance to flow which incr p - acute incr in contractility which incr p - incr filling volumes which incr radius - geometric changes in incr r and decr h - incr HR which incr oxygen demand - basically anything that increases pressure
30
SV relationship with AL and PL
AL - inversely proportional PL- directly proportional
31
Apoptosis examples - 6
- activation of SNS - activiation of RAAS - calcium overload - cytokines - decreased oxygen - oxygen free radicals (superoxides)
32
Necrosis examples - 7
- activation of SNS (NE excess) - calcium overload - decreased oxygen - oxygen free radicals - toxins - infectious agents - anticancer and immunosuppressive drugs
33
CHP vs COP
- CHP - out - COP - in
34
oedema (starling's forces)
incr CHP and decr COP
35
systemic venous side
low pressures, allows fluid reabsorption
36
systemic arterial side
high pressures, promotes fluid filtration out