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Physiology > Test 1, Deck 3 > Flashcards

Test 1, Deck 3 Flashcards

1
Q

what is the equation for ejection fraction?

A

EF= EDV-ESV/EDV * 100 (normally 60%)

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2
Q

what is the ejection fraction a clinical index of?

A

left ventricular contractility

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3
Q

systolic heart failure

A 
decreased contractility (depends on activity)
- shifts contractility line down
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4
Q

diastolic heart failure

A

decreased compliance, reduced preload (can’t fill normally because volume creates more pressure)
- shift diastolic pressure-volume curve up

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5
Q

factors that determine preload

A
  • pressure gradient from atria-ventricle
  • time for ventricular filling (hr)
  • ventricular compliance
  • atrial function (kick)
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6
Q

factors that determine contractility

A
  • sympathetic nerve activity
  • drugs (digitalis)
  • disease (infarct)
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7
Q

factors that determine afterload

A
  • aortic pressure (hypertension)
  • ventricular outflow tract resistance (valvular or subaortic stenosis)
  • ventricular size- dilated hearts= larger afterload
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8
Q

venous return

A

rate at which blood returns to the thorax (central venous pool) from the periphery

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9
Q

central venous pool

A

the volume of blood enclosed by the right atrium and great veins (IVC, SVC)

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10
Q

cardiac output and what it equals

A

rate at which blood leaves CVP and is pumped out of the heart; equals venous return

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11
Q

relationship between cardiac output and central venous pressure? which variable is independent? what is this called?

A

as you lower cardiac output (& venous return), the blood backs up in the central venous pool & you get a higher central venous pressure

up CO/VR, down CVP (inverse relationship)

CO is the independent variable

vascular function curve

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12
Q

what is Pmc? what is it a relationship between? what is it normally?

A
  • mean systemic circulatory pressure- the pressure in the venous system that occurs when the heart stops;
  • relationship between volume of blood and the capacity of the system (venous tone)
  • 7 mmHg
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13
Q

what happens when CVP= Pmc?

A

blood flow ceases- have no gradient for return

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14
Q

if you increase cardiac output, what happens?

A

decrease CVP, increase venous return (via pressure gradient)

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15
Q

what happens at negative CVP?

A

large veins collapse

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16
Q

which curve does transfusion shift?

A

vascular function curve

- higher CO for lower pressure

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17
Q

which curve does sympathetic stimulation shift?

A

cardiac function curve

  • increases venous tone which increases venous return
  • higher CO for lower pressure (shifts up and left)
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18
Q

increase venous return by increasing peripheral venous pressure (PVP)

A
  • increased sympathetic venoconstriction
  • increased skeletal leg pump
  • increased blood volume
  • cardiac contraction
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19
Q

increase venous return by decreasing central venous pressure (CVP)

A
  • respiratory pump activity (decreased intrathoracic pressure)
  • cardiac suction (heart going from circular to oblong)
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20
Q

how do valves change venous return?

A

maintain pressure gradient between peripheral and central venous pools

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21
Q

where do you measure CVP (central venous pressure) graphically?

A

intersection of vascular function curve and cardiac function curve

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22
Q

which curve does heart failure shift?

A
  • cardiac function curve
  • shifts down progressively
  • hypervolemia also shifts vascular function curve out
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23
Q

2 main things that shift venous function curve

A

blood volume

venous tone

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24
Q

what happens with hemmorage?

A
  • shifts the venous function curve down;\

- sympathetics boost it back up AND boost the cardiac function curve to give you same CO at reduced CVP

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25
Q

what is Poiseuille’s law?

A

flow= (change in pressure)/(resistance)

OR

flow=(change in pressure * pi * r^4)/ (8Lviscosity)

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26
Q

what is the main way in which flow is regulated?

A

by changing vessel radius (r^4)

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27
Q

what is viscosity; what is the equation; how does it relate to velocity, hematocrit, and radius

A
  • lack of slipperiness
  • viscosity= sheer stress/sheer force (p/v)
  • inverse relationship w/ velocity
  • direct relationship with hematocrit
  • direct relationship with radius due to axial streaming
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28
Q

what is the definition of a non-newtonian fluid?

A

a fluid whose viscosity changes based on sheer stress (pressure) and force (velocity)

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29
Q

as a vessel diameter gets smaller, hematocrit _________ because of ________

A

decreases; plasma skimming

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30
Q

laminar vs turbulent blood flow

A

laminar- parallel concentric layers

turbulent- disorderly patterns (murmurs, endothelial damage, thrombi); leads to Krotokoff sounds

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31
Q

what is the reynold’s # and its equation?

A
  • propensity for turbulent blood flow

- R#= (densitydiametervelocity)/(viscosity)

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32
Q

what is Bernouilli’s principle and its equation?

A

in CONSTANT FLOW system (aka there are no escape routes), total energy remains constant

total energy = potential energy + (1/2)*(density *velocity^2)

aka if blood is going faster, will have decreased lateral pressure on the walls

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33
Q

what is the laplace relationship and its equation?

A
  • the force ripping the balloon apart

- wall tension= (pressure * radius)/wall thickness

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34
Q

what happens with an aneurysm?

A

decreased velocity
increased pressure
increased radius
decreased wall thickness

ALL increase wall tension

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35
Q

example of low wall tension

A

capillaries in feet- have small radius, can resist a lot of force

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36
Q

what allows arterioles and precapillary sphincters to control vessel diameter and blood flow?

A
  • a high wall thickness/radius ratio; this provides low wall tension (laplace)
  • also have low volume-high pressure- low compliance- high resistance
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37
Q

cross sectional area and the velocity of blood flow

A

total cross sectional area is inversely related to the velocity of blood flow

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38
Q

what holds 60% of blood volume

A

veins (larger cross sectional area than arteries)

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39
Q

series vs parallel resistance

A
  • series- add them up (think vessles- aorta to large arteries to capillaries to arterioles, etc.)
  • parallel- less than an individual- (think organs- open more up, have less resistance)); inverse- 1/r1 + 1/r2 etc
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40
Q

what is pulse pressure and where does pulse pressure become greater?

A
  • systolic-diastolic pressure
  • further you go away from the heart- greatest in ankle
  • large in arteries
41
Q

what is mean arterial pressure?
what is MAP determined by?
what happens to it throughout the circulatory system?

A
  • avg pressure in the aorta and proximal arterial system during one cardiac cycle
  • diastolic pressure + 1/3 PP
  • declines- driving force- greatest in aorta?
42
Q

3 layers (‘tunica’) of arterial wall

A
  • intima: connective tissue, endothelials, IEL
  • media: smooth muscle & EEL
  • adventitia- connective tissue w/ vasa vasorum, innervation
43
Q

relationship between compliance and pressure

A

higher compliance (e.g. elastin), lower pressure

44
Q

wall thickness/diameter ratio tells you what

A

greater ratio, better control of the system- greatest in arterioles, provides lots of resistance

45
Q

where are continuous capillaries found?

A

muscle, connective tisues

46
Q

where are fenestrated capillaries found?

A

kidney, intestines

47
Q

where are discontinuous/sinusoidal capillaries found?

A

liver, bone marrow, spleen

48
Q

what is the ‘windkessel’/hydraulic filtering?

A

when the aortic valve closes, the recoil of the aorta wall recoiling (was pushed out by systolic pressure) sends a second wave of pressure throughout the system, maintaining diastolic pressure

49
Q

relationship between compliance and pulse pressure

A

low compliance- high pulse pressure- high afterload- high O2 consumption

50
Q

what is pressure pulse?

A

the wave of energy that passes through the aorta at 5 m/sec and increases to 10-15 m/sec in arteries- velocity increases as compliance decreases

51
Q

what are some specific determinants of mean arterial pressure?

A
  • cardiac output (hr * sv)
  • peripheral resistance
    (& baroreceptor, exercise, disease)
  • blood volume
  • arterial compliance
52
Q

primary determinants of systolic & diastolic pressure?

A

systolic- cardiac output

diastolic- peripheral resistance

53
Q

if you decrease compliance, what happens to pulse pressure?

A

decrease compliance, increase pulse pressure

54
Q

increase resistance, what happens to pulse pressure?

A

increase diastolic pressure (and some systolic)

55
Q

what regulates peripheral arterial resistance?

A

changes in the arteriolar radius (viscosity would, but doesn’t change)

56
Q

two types of ways to change arteriolar radius?

A

local- myogenic, endotheial, metabolites

global (extrinsic)- baroreceptor, hormonal, sympathetics (aka not specific)

57
Q

which is the main player of the autonomic nervous system in regulating mean arterial pressure?

A

sympathetics- acts on heart, veins, arterioles
(increases HR, contractility, veno/vasoconstiction)
- increasing CO increases BP

58
Q

changes that occur during exercise

A
  • cardiac output rises (increase in contractility and hence stroke volume) BUT when HR reaches max, SV decreases
  • systolic pressure rises (increase in SV)
  • peripheral resistance decreases (skeletal capillaries open up)
  • enhanced O2 extraction
  • increases venous return (muscle and respiratory pump, venoconstriction)
  • pulse pressure widens
  • MAP increases- more time in systole
59
Q

structures of microcirculation

A

precapillary resistors (arterioles, metarterioles, sphincters), exchange vessels, and venules

60
Q

characteristics of capillary blood flow

A
  • slow
  • intermittent, not uniform/1 direction
  • follows pressure gradients
61
Q

what is a Rouleaux formation?

A
  • stacks of RBCs

- blood cells squeezing through capillaries at an angle, touching allows for good gas exchange

62
Q

pressure gradients in capillaries

A

hydrostatic- 32 to 15

osmotic- 25

63
Q

what is the main force that holds things in? what is the most clinically relevant protein and what does it attract?

A
  • plasma osmotic (oncotic) pressure

- albumin- attracts sodium (and water back into blood); produced by liver

64
Q

what determines capillary hydrostatic pressure?

A

pre and post capillary resistance to arterial and venous flow

65
Q

what happens when you decrease the pre/post capillary resistance ratio?

A
  • decrease pre resistance- more water flowing in OR
  • increase post resistance- less water able to flow out
  • OVERALL increase capillary hydrostatic pressure
66
Q

when hydrostatic pressure is greater than osmotic pressure, you get

A

filtration

67
Q

examples of vasodilators

A

prostacyclins, EDRF, NO, adenosine, H+, CO2, K+

68
Q

examples of vasoconstrictors

A

endothelin (ET)

69
Q

important structural features of lymphatic system

A
  • unidirectional flow of plasma & protein
  • valved, thin walls
  • non-fenestrated, no smooth muscles
  • return to subclavian veins
70
Q

factors governing lymph flow

A
  • amount of filtration
  • skeletal muscle activity
  • valves
71
Q

specific causes of edema

A
  • reduction in plasma protein (albumin- liver failure), renal disease
  • increase cap. hydrostatic pressure (congestive heart failure)
  • increased permeability of membrane (burns)
  • lymphatic obstruction (surgery)
72
Q

what is edema?

A

excess fluid accumulation in interstitial space

73
Q

which has a greater influence on hydrostatic pressure- arterial or venous pressure?

A
  • venous; excessive arterial pressure is normally dissipated by resistance
74
Q

what is resting sympathetic tone and what is it due to

A
  • vascular constriction under resting conditions (basal tone) plus a small level sympathetic nerve activity due to being awake
  • due to tonically released norepinephrine
75
Q

active vs passive mechanisms

A
  • can be sympathetic or parasympathetic
  • active- change in resistance away from basal arterial tone
  • passive- change in resistance towards basal tone
76
Q

two types of inputs

A

sympathetic adrenergic- increases resistance

sympathetic cholinergic- decreases resistance

77
Q

which type of sympathetic fibers cause active vasodilation?

A

sympathetic cholinergics (release Ach as opposed to Ne)

78
Q

what are alpha-1 receptors?

A
  • adrenergic receptors
  • on vascular smooth muscles
  • cause vasoconstriction
  • not on coronary/cerebral vessels (never want to constrict flow to the brain or the heart)
79
Q

what are beta-2 receptors?

A
  • adrenergic receptors
  • on heart, are secondary receptors that stimulate heart rate and contractility
  • on smooth muscles, cause vasodilation
80
Q

baroreceptors- anatomy

A

located on carotid sinus (MOST BLOOD FLOW IN BODY) & aortic arch (structures with LESS vascular smooth muscle)

81
Q

baroreceptors- mechanism

A
  • are mechanoreceptors (respond to stretch)
  • fire more frequently by an increase in arterial pressure (vice-verse for decrease)
  • join 9&10 to medulla
  • decrease in stretch/firing= increases sympathetics and inhibits parasympathetics
82
Q

ways sympathetics/PS change via baroreceptor

A

1) peripheral vasoconstriction (sympathetics)
2) increase in heart rate (s and ps)
3) increase in contractility (s)

83
Q

baroreceptors respond to changes/absolute pressure and are more responsive to phasic/constant pressure

A

changes & phasic

84
Q

what are chemoreceptors activated by?

A

low arterial PO2**, high arterial PCO2 (shifts curve up), and high H+

85
Q

at a low CO2 concentration, receptors are ___ sensitive to a drop in O2

A

less

86
Q

what do chemoreceptors stimulate?

A

vasoconstriction (sympathetics)
bradycardia (parasympathetics) BUT this is overruled by respiratory system which promotes tachycardia (stretch receptors in the lungs inhibit vagal nerve activity)

87
Q

what is the hormonal control of the circulator system? over what time frame and circumstances does it take place?

A
  • renin-angiotensin-aldosterone

- dehydration or heart failure over weeks

88
Q

RAA pathway

A
  • increase in fluid volume
  • low arterial pressure (baroreceptors)
  • renin is released from JGA kidney cells in afferent arterioles
  • renin converts angiotensinogen to angitensin 1
  • ACE enzymes in lungs & kidneys convert 1 to 2
  • result in vasoconstriction of renal vessels
  • stimulates aldosterone release which pulls Na back into blood from kidneys
  • acts on hypothalamus to stimulate thirst and ADH
89
Q

local mechanisms responsible for vascular resistance

A

autoregulation (myogeneic, metabolic)
endothelial
mechanical

90
Q

what is autoregulation? what are the two primary mechanisms?

A
  • when an abrupt increase in flow caused by an increase in arterial pressure is counteracted by an increase in resistance to maintain constant flow
  • myogenic (smooth muscle contracts in response to stretch)
  • metabolic (production of adenosine, H+, Co2= VASODILATORS)
91
Q

auto-regulation among different organs

A

strong- heart, brain, kidney, skeletal muscle
weak- splanchnic
little- skin, lungs

92
Q

what is it called when you see a decreases in diameter in response to an increase in pressure with or without the endothelium

A

autoregulation

93
Q

what is it called when you see an increase in diameter in response to an increase in pressure gradient, but only with endothelium; what it is due to

A

endothelial-mediated mechanism (exercise);

due to increase in sheer stress of blood, result of increase in EDRF

94
Q

what is active hyperemia?

A

increased blood flow caused by increased tissue activity (skeletal and cardiac muscle)

95
Q

what is reactive hyperemia?

A

overshoot of blood flow in response to a metabolic debt created by a temporary occlusion

96
Q

how does mechanical activity regulate blood flow?

A

increase in tissue pressure (think during a bicep curl) compresses small vessels and alters blood flow

97
Q

where does mechanical activity regulate blood flow

A

muscle contraction, alveolar pressure, tumors, aortic stenosis

98
Q

what is shock a primary reaction to?

A

cardiovascular system is unable to supply enough blood to the body; LOW BLOOD PRESSURE

Physiology (22 decks)

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