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CPR Exam 1 > Systemic Circulation and Hemodynamics - Dr. Rogers > Flashcards

Systemic Circulation and Hemodynamics - Dr. Rogers Flashcards

1
Q

Arteries with P

A

stress volume : high flow and pressure = BP

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2
Q

Arterioles

A

moderate P, SM walls

change resistance of blood

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3
Q

Capillaries

A

LARGE CROSS SECTION area, exchange site

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4
Q

Veins

A

Low P, large V, contract to move blood to arterial side = increase BP

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5
Q

greatest cross section area

A

capillaries

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6
Q

greatest blood V

A

Veins

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7
Q

blood flow =

A

Q= Pressure gradient (delta P)/Resistance (R)

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8
Q

Poiseullies law

A

resistance through tube calculation

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9
Q

R =

A

(8nl)/ (pi r^4)
n = viscosity
r= radius
l = length

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10
Q

if P stays the same how does R decrease

A

increase r of tube

+ increase flow rate to keep P the same

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11
Q

How to find viscosity

A 
Hematocrit =  (RBC: plasma) ratio
increased hematocrit (high RBC) ----> lower BF
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12
Q

R of 8 tubes in series

A

you add the R for each = TOTAL R

*increases total R

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13
Q

R of 8 tubes in parallel

A

this lowers the TOTAL R

* capillaries are like this

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14
Q

another thing Q = to

over all heart function

A

Q= CO = (A P - V P) / TPR

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15
Q

greatest control of BF

A

TPR in arterioles

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16
Q

what increases and decreases TPR

A

Increase : increase sympathetic N to arterioles = vasoconstriction
Decrease : decrease sympatetic N to arterioles = vasodilation

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17
Q

how to calculate V of blood in BVs

A

V = Q/CSA

CSA: cross sectional area of vessle

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18
Q

highest and lowest V is found

A

highest : As

lowest : capillaries

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19
Q

3 things that make BF more likely to be turbulent

A
  1. high V
  2. large CSA
  3. low Viscosity
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20
Q

what is Reynolds Number

A

N= pdv/n
p - density
d- diameter
*if N > 2000 = laminar –> TURBULENT transition

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21
Q

what does turbulence cause

A

bruits sounds + lesions = arteriosclerosis

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22
Q

compliance

A

delta V/ delta P

* shows vascular capacitance

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23
Q

highest compliance

lowest complience

A

highest : veins

lowest : arteries

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24
Q

what condition can cause decrease in compliance

A

arterosclerosis, causes artery to be unable to distend (systole) and recoil (diastole) as much

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25
Q

reason Veins have compliance and what can this lead to is not functioning right

A

they have SM flexible walls
if the SM constrict (decrease v, same P) = lowers compliance = more blood pushes to arteries
= INCREASE BP

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26
Q

where is the biggest pressure drop in the circulation

A

arterioles

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27
Q

before the largest P drop in the circulation, what keeps the P high

A

Aorta, Large As, Small As all have high P due to Aorta having so much pulsatile action

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28
Q

Lowest BP

Highest BP

A

DIASTOLE : 80mmHg

SYSTOLE : 120mmHg

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29
Q

Pulse Pressure

A

SBP-DBP = 40mmHg

proportional to SV

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30
Q

How to calculate the Mean Arterial Pressure (MAP)

A

1/3 (SBP) + 2/3(DBP)
(DBP) + 1/3(pulse Pressure)
80-40/3 = 93.3mmHg

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31
Q

Dichroctic Notch

A

when aortic valve closes

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32
Q

compliance in the practical setting

A

SV/ Pulse Pressure

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33
Q

compliance and Pulse Pressure relationship

A

as compliance increases the pulse pressure decreases

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34
Q

increases R on compliance

A

decrease in R, lowers P, which increases Compliance

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35
Q

what happens in Arteriosclerosis

A

increase SPB, PP, and MAP

STAYS SAME : DBP

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36
Q

What happens in Aortic Stenosis

A

decrease SBP, PP, MAP

STAYS SAME : DBP

37
Q

what does increasing TPR do

A

Increase in DBP, SBP, MAP

STAYS SAME : PP

38
Q

3 things about Venous Pressure

A
  1. Low P
  2. Large V
  3. High Compliance
39
Q

Venocontriction of veins causes
compliance
radius

A

decrease compliance
small change in r (no large R change)
= increased flow back to heart

40
Q

Venous Pressure waves (3 of them)

A

A wave
C wave
V wave
* part of jugular pressure

41
Q

A wave

A

mid P wave to R wave )when A contracts

42
Q

C wave

A

Ventricular Contraction: (has the bulding of the AV valve up into A

43
Q

V wave

A

after Ventricles contracted and the AV valves are closed = blood flows into Atrium and stays there
when the valves open the V wave is gone

44
Q

3 parts of microcirculation

A
  1. Arterioles : extensive SM
  2. Metarterioles : less SM connecting Arterioles and Venules
  3. Capillaries: Branches from the Metarterioles, have precapillary sphincters
45
Q

where are capillaries the largest in exchange and the smallest in exchange

A

LARGEST : Liver and GI

SMALLEST : Brain

46
Q

vesicular transport across capillaries when needed are called

A

caveolae

47
Q

Vasomotion

A

the metareterioles and precapilllary sphincters constrict in an oscillating way (every few sec) = oscillating BF
* REGULATED BY O2 LEVELS

48
Q

vasomotion and O2 levels

high and low

A

high O2 : constriction more often

low O2 : the sphincters remain open more

49
Q

Starling Equation shows what

A
  1. H2O moving into capillaries (- direction) = ABSORPTION

2. H2O moving out of capillaries (+ direction) = FILTRATION

50
Q

4 forces in capillary exchange

A
  1. C = intravascular P
  2. i = Extravascular (interstitial) P = Pif
  3. P = Hydrostatic P
  4. (pi) = Osmotic (oncotic) P
51
Q

what causes absorption into capillaries

which Ps

A
  1. Interstitial Fluid P *
  2. Plasma Colloid P*
  3. osmotic (oncotic) P*
52
Q

what causes filtration into capillaries

which Ps

A
  1. Interstitial fluid colloid osmotic P*
  2. Capillary P *
  3. Intravascular P (hydrostatic intravascular P)*
53
Q

location of absorption and reabsorption

A

ABSORPTION : arteriolar end

REABSORPTION : venous end

54
Q

Capillary Hydrostatic Pressure

A

Pc
capillary forces fluid OUT
highest at arteriolar end

55
Q

Capillary Osmotic Pressure

A

(pi)p or (pi)c = colloid osmotic P

Plasma proteins, NA, K in capillaries force fluid INTO capillaries

56
Q

Interstitial Hydrostatic Fluid Pressure

A

Pif =
- : force fluid OUT from capillaries
+ : force fluid INTO capillaries

57
Q

Interstitial Osmotic Pressure

A

(pi)if = force fluid OUT from capillaries

58
Q

equation for net capillary exchange

A

Kf = [(Pc-Pi) - (pic - pii)]

* if + that means net FILTRATION

59
Q

capillaries cant reabsorb what

A

proteins

60
Q

what do lymph carry and what moves substances for them

A

fluid, proteins, chylomicrons (lipids)

Muscle contractions

61
Q

what alters Pc

A

elevated Venous Pressure (heart failure) = increase

62
Q

what alters Pi

A

restricted lymph flow = increased

63
Q

what alters pic

A

reduced albumin (starvation, liver failure) = decrease

64
Q

what alters pii

A

restricted lymph flow or inflammation = i think decrease

65
Q

Acute Control of BF happens how

A

fast changes in local vasodilation and vasoconstriction

66
Q

when does O2 availability decrease to tissues

A

high altitudes
pneumonia
CO poisoning
Cyanide poisoning

67
Q

Autoregulation of BF happens when and how

A

during changes in arterial pressure (metabolically or myogenically)
* fast increase in Arterial P = immediate increased BF
= returns back to normal within minutes

68
Q

Metabolic theory for autoregulation

A

increased Arterial P = too much O2 and nutrients delivered to tissues = hyperemia

69
Q

Myogenic theory for autoregulation

A

increased Arterial P = SM stretch in vessel= causes it to constrict = reduce BF back to normal
*no H or N needed

70
Q

Vasodilator theory

A

low O2 increases vasodilators

71
Q

vasodilators

A

adenosine, CO2, adenosine phosphate, histamine (from mast cells), K+, H+
Bradykinin (also increase permeability) made from Kallikrein

72
Q

O2 demand theory

A

not enough O2 = vasodilation of precapillary sphincter in SM

73
Q

Metabolic Control

A
  1. reactive hyperemia : tissue supply blocked for 2min

2. Active hyperemia : tissue metabolic rate increased high for 2min

74
Q

vasoconstrictors (4)

A
  1. N + H = NE and E
    * mostly NE
  2. Angiotensin 2 : increase TPR, decrease NA+ and H2O excretion = increase BP (+ vasoconstrictor)
  3. Vasopressin (ADH)
  4. Serotonin : from tissue damage or hemostasis
75
Q

ions control BF how for Ca+2

A

ICM CA+ = vasocontriction

76
Q

ions control BF how for K+

A

vasodilation

77
Q

ions control BF how for Mg+ —-I SM contractions =

A

Mg+ —-I SM contractions = vasodilator

78
Q

ions control BF how for H+

A

vasodilation

79
Q

ions control BF how for acetate and citrate

A

vasodilation

80
Q

ions control BF how for CO2

A

some vasodilation (MOST IN BRAIN)

81
Q

SYMPATHETIC EFFECT ON:

  1. small a and arterioles
  2. Large vessels
  3. Heart
A
  1. increase TPR = decrease BF
  2. decrease the Blood volume to push blood forward to the heart
  3. increase HR and Contractility
82
Q

Coronary BF happens when

A

during repolarization of the ventricle—-> diastole*

controlled by adenosine + hypoxia, metabolic

83
Q

Cerebral Blood Flow happens when
autoregulated
injury
BP below 50mmHg

A

under metabolic, PCO2, H+
as BP increases, it vasocontricts (HOWEVER FLOW STAYS THE SAME* when autoregulated
vasodilation + edema
vasoconstriction

84
Q

pulmonary circulation

A

higher RV and pulmonary A
MAP 15mmHg
* keep arterial P low

85
Q

At rest: blood flow is Skeletal muscle does what and is controlled by

A

controlled by central receptors + baroreceptors (NE and a-adrenergic)

86
Q

During Exercise: blood flow is Skeletal muscle does what and is controlled by

A

CO increases, TPR decreases = dilation of BVs
Muscle BV dilation also done by : ATP, adenosine, NO, K+, lactate and Epi–> B-adrenergic R
*hyperemia can happen after

87
Q

rise is body temperature does what to BV flow

A

a-1-adrenergic R induced causing constriction which is inhibited by SYMPATHETIC ACTIVATION
= vasodilation and movement of vessels closer to skin

88
Q

trauma to skin releases what causing what triple response

A

HISTAMINE

  1. red line
  2. red flare
  3. red wheal (edema)

CPR Exam 1 (20 decks)

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