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Physiology > Phys Exam 2 > Flashcards

Phys Exam 2 Flashcards

1
Q

what does the cardiovascular system do

A

moves materials entering the body, cell to cell, and moves stuff out of the body

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2
Q

what are examples of a closed loop system

A

systemic/caval system: vena cavas, coronary system, portal systems

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3
Q

what is a pulmonary embolism

A

clot that eventually gets stuck in lung -> no blood to heart = no blood to brain

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4
Q

what is a stroke from

A

clot on arterial side that got into a small enough vessel that gets STUCK

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5
Q

what is a portal system

A

systemic circulation in which blood draining from capillary bed of one structure flows through a larger vessel to supply capillary bed of another structure before returning to heart

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6
Q

what are examples of portal systems

A

hepatic (liver), renal (kidneys), hypothalamic-hypophyseal

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7
Q

average pressure in arteries and veins

A

arteries: 100 mmHg (aorta has highest pressure
veins: 0 mmHg (vein cava has lowest)

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8
Q

what is static pressure influenced by

A
  1. fluid volume (increase in fluid, increase in pressure)
  2. wall compliance (increase in compliance, increase in pressure)

think of tubes connected with common tube on the bottom that is plugged. the water is exerting pressure on the walls of the container -> hydrostatic pressure

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9
Q

hydraulic pressure in influenced by

A

driving force/pressure: pumping force
pressure gradient: must be present for flow
resistance to flow: diameter and total length of vessel AND viscosity of fluid

thing of 4 tubes lined up, connected with one common tube on bottom plugged. once you remove the plug, pressure falls with distance as energy is lost because of friction (this is how our cardiovascular system works)

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10
Q

do arteries or veins have more smooth muscle

A

arteries have much more -> regulates blood flow to tissues

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11
Q

Fluid pressure basics:

what is the driving force in the heart

A

pressure created by the heart muscle contraction -> driving pressure

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12
Q

Fluid pressure basics:
flow is proportional to ______
flow is inversely proportional to _______

A

flow is proportional to CHANGE IN PRESSURE GRADIENT
flow is inversely proportional to RESISTANCE

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13
Q

what happens when we have a higher system pressure gradient in terms of flow and resistance

A

Flow: increases (proportional to pressure gradient)
resistance: decreases (inversely proportional to flow)

increase in flow and decrease in resistance

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14
Q

Fluid pressure basics:

resistance to flow is a function of (3)

A

vessel length
blood viscosity
vessel diameter

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15
Q

Fluid pressure basics:
what is the most significant influence in our bodies when it comes to resistance and flow

A

VESSEL DIAMETER! it is the only thing that can change in our body

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16
Q

what happens to our bp with vasoconstriction

A

increase bp

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17
Q

what happens to our bp with vasodilation

A

decrease bp

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18
Q

what controls vessel diameter

A

changes in volume (dehydration) and wall compliance

this can also affect bp

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19
Q

what happens to our bp is we are very dehydrated

A

can faint bc our bp decreases

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20
Q

what happens to our bp with an increase of plaque in arteries

A

increases bp

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21
Q

what organ regulates blood volume

A

kidney (renal)

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22
Q

what really affects blood flow the most

A

RESISTANCE!!

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23
Q

small change in vessel diameter does what to flow

A

HUGE EFFECT. Going from 1mm to 3mm increases flow from 1 to 81

to the 4th power

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24
Q

what is the volume of blood called

A

flow rate

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25
Q

what is the distance an amount of blood travels called

A

flow velocity

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26
Q

what is the heart mostly composed of

A

myocardium

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27
Q

what are the two types of myocardium and what has only 1%

A

myocardial CONTRACTILE: majority of heart
myocardial AUTO-RHYTHMIC: 1% of heart

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28
Q

what are the cells called that are the pacemakers of the heart

A

myocardial autorhythmic cells

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29
Q

what heart cells have sarcomeres

A

myocardial contractile cells

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30
Q

what are unique features about myocardial autorhythmic cells

A

no sarcomeres
smaller and no driving pressure force
conducting cells -> set rate of beat

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31
Q

what sets the pace of the heart

A

SA node. 70/80 bpm

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32
Q

what is the backup pacemaker cell

A

AV node. 40-60 bpm

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33
Q

what the the backup pacemaker if a “heart block” occurs?

A

bundle of His and Purkinje fibers 20-40 bpm

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34
Q

what is the purpose of 2 way valves

A

ensures one-way flow

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35
Q

what are the AV valves

A

tri and bicuspid

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36
Q

what are the semilunar valves

A

aortic and pulmonary valves

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37
Q

what do papillary muscles and cordae tendinae do

A

prevents blood from shooting back into atrium

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38
Q

do cardiac cells do E-C coupling?

A

YES!

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39
Q

are autorythemic cardiac cells spontaneous or non?

A

spontaneous

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40
Q

what ion plays a HUGE role in cardiac AP

A

Ca2+!!!!!

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41
Q

are myocardial contractile forces variable or all or nothing?

A

VARIES!

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42
Q

What determines the force of a myocardial contractile cell generated

A

the force is generated by cardiac cell is proportional to the number of crossbridges that are active AND sarcomere length at the beginning of contraction

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43
Q

what determines the # of crossbridges that are active

A

the amount of Ca2+ available to bind to troponin

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44
Q

what does more stretch and more blood mean in terms of force generated? small or large?

A

the more stretch and more fluid = GREATER FORCE

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45
Q

how are myocardial contractile cells SIMILAR to neurons (2)

A
  1. DEpolarization due to Na+ ENTER
  2. REpolarization due to K+ EXIT
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46
Q

how are myocardial contractile cells DIFFERENT from neurons (1)

A

LOOONG AP due to Ca2+ entry in cell -> prevents tetanus

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47
Q

what is tetanus and what could it do to the heart

A

a continuous tonic spasm of muscle

could result in fainting or be fatal

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48
Q

5 phases of AP of myocardial contractile cells

A
  1. resting membrane potenital
  2. depolarization -> Na+ entry
  3. initial repolarization -> Na+ channels CLOSE
  4. Repolarization Plateau: Ca+ OPEN and FAST K+ CLOSE
  5. Rapid Repolarization: Ca+ CLOSE and SLOW K+ OPEN
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49
Q

do cardiac cells have long or short refractory periods?

A

LONG! lasts almost as long as the muscle twitch

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50
Q

how does lidocaine work

A

blocks fast-voltage gated Na+ channels in the neuronal cell membrane that is responsible for signal propagation.

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51
Q

how do we not feel pain with lidocaine

A

the membrane of the postsyn. neuron will NOT depolarize because there was no AP.

It doesn’t prevent the pain signals going to the brain but rather it doesnt allow pain signals to even be produced

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52
Q

what is the point of epinephrine in lidocaine

A

vasoconstrictor -> prolongs numbing effect

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53
Q

what could happen if a patient was hyper-reactive to lido?

A

because the heart has voltage gated Na+ channels, they could potentially go into cardiac arrest or faint

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54
Q

what cells makes up the conducting system of the heart (SA, AV, Pukinjie, His)

A

myocardial autorhythmic cells! 1% !!

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55
Q

what cells control the heartbeat rhythm and pace

A

myocardial autorhythmic cells

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56
Q

what causes autorhythmic cells to have an unstable membrane potential

A

leaky channels

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57
Q

what is the resting membrane potential called for autorhythmic cells?

A

pacemaker potential -> has an unstable membrane potential

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58
Q

what is the autorhythmic cell’s resting potential called?

A

pacemaker potential phase

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59
Q

what happens during the pacemaker potential phase

A

Na+ flows in through If channels -> as membrane potential slowly rises, If channels CLOSE and one set of SLOW Ca2+ channels open

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60
Q

what happens during the depolarization phase of autorhythmic cells

A

threshold is reached -> AP due to voltage gated FAST Ca2+ channels. TONS OF Ca2+ during this following in!!

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61
Q

what happens during the rapid repolarization phase in autorhythmic cells

A

at peak AP, Ca2+ CLOSE and K+ channels OPEN -> repolarization -> K+ channels close at the end of this phase

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62
Q

what would happen if If channels were blocked

A

heart would stop

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63
Q

how do depolarizations of autorhythmic cell spread to adjacent contracile cells?

A

Gap junctions!! intercalated discs!

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64
Q

rising phase of AP in autorhythmic cells is due to

A

Ca2+ entry

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65
Q

rising phase of AP in contractile cells is due to what

A

Na+ entry

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66
Q

what is the repolarization phase like in contractile cells?

A

EXTENDED plateau due to Ca2+ entry
RAPID phase caused by K+ efflux

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67
Q

what is the repolarization phase like in autorhythmic cells

A

RAPID -> caused by K+ efflux (flowing out)

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68
Q

do heart cells have a hyperpolarization?

A

not normally

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69
Q

what heart cells have a refractory period?

A

contractile cells do. its long due Na+ channel gated not resetting until end of AP

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70
Q

pathway of electrical conduction in heart

A
  1. SA node depolarizes
  2. electrical activity goes to AV node
  3. depolarization spreads slowly across atria (conduction slows through AV node)
  4. depolarization moves rapidly through ventricular conducting system to apex of heart
  5. depolarization wave spreads upward from the apex
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71
Q

what is the internodal pathway

A

pathway from SA -> AV

routes the direction of electrical signals through atria so the heart contracts in a coordinated fashion to pump efficiency from atria -> ventricles (atria contract first -> SA node sets pace)

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72
Q

AV node during conduction:

A

signal from SA reaches AV. AV delays, allowing ventricles to fill before they contract

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73
Q

Bundle of His action in conduction:

A

signal continues down bundle of His, through L and R bundle branches into Purkinjie fibers.

ventricles contract bottom up

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74
Q

what is the purpose of the AV valves (bi/tricuspids) during contraction

A

AV valves stays closed to prevent backflow during contraction

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75
Q

what does an ECG show

A

heart’s electrical activity and sum of many AP

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76
Q

what do the waves show on an ECG in general

A

show depolarization/repolarization of atria and ventricles

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77
Q

what does the P wave represent

A

the atria depolarize then contract

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78
Q

what does the P-R segment represent

A

atria contraction continues. electrical signal travels through AV node and bundle of His -> slows signal down/AV node delay

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79
Q

what does the QRS wave show

A

ventricular contraction begins @ end of Q wave and continues through T wave. atrial repolarization occurs during R wave

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80
Q

what does the T wave show

A

ventricles repolarization

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81
Q

what does the T-P segment show

A

heart is silent- everything is relaxed

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82
Q

EKG segment shows

A

baseline between waves

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83
Q

EKG interval shows

A

combo of wave and segment

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84
Q

mechanical events are slightly ______ behind electrical events

depolarization vs. muscle contraction

A

LAGGED

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85
Q

diastole means

A

relaxed

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86
Q

systole means

A

contraction

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87
Q

MECHANIAL EVENTS
what is happening in the heart at the beginning of cycle

A

R atria filling with blood from vena cavas
L atria filling with blood from pulmonary veins
AV valves open -> ventricles filling

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88
Q

MECHANIAL EVENTS
what happens during #2 -> atrial systole/atria contract

A

completes last 20% of ventricular filling
some blood is forced back into vena cava

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89
Q

MECHANIAL EVENTS
isovolumic ventricular contraction -> first phase of ventricular contraction

what happens

A

AV valves forced closed -> LUB
semilunar valves still closed until pressure inside ventricular becomes greater than pressure in aorta
atrial diastole is going on during this time -> all 4 valves closed (isometric contraction of heart, atria relaxed and blood begins to flow back into atria)

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90
Q

MECHANIAL EVENTS
ventricular ejection events

A

completion of ventricle systole: ventricle contraction pressure becomes high enough to push semilunar valves OPEN and blood ejected to arteries.

blood is pumped into the pulmonary/peripheral systems

atria -> relaxed, continuing to fill with blood

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91
Q

MECHANIAL EVENTS
isovolumic ventricle relaxation events

A

ventricular diastole: ventricular relaxation and pressure drops -> still higher than atrial pressure

arterial blood pressure flows backward pushing semilunar valves shut -> second heart sound DUB

cardiac muscle cells of ventricles are relaxing. AV valves wont open until pressure within ventricles decreases lower than pressure in atria

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92
Q

at what point could you hear blood regurgitating through the semilunar valve back into the left ventricle?

A

isovolumic ventricular relaxation

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93
Q

what is stroke volume

A

amt of blood pumped per contraction/heartbeat “one pump”

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94
Q

what is end diastolic volume

A

max volume of blood in ventricle during mechanical heart cycle (max amt before contraction) EDV

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95
Q

what is end systolic volume ESV

A

the least volume of blood in a ventricle during a mechanical heart cycle (min. amt after contraction)

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96
Q

is there blood left in the ventricular after contraction?

A

yes, safety mech. allows for compensatory change w/ change in vessel capacity

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97
Q

what is stroke volume

A

volume of blood before contraction minus volume of blood after contraction

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98
Q

is stroke volume constant

A

no. exercise and other factors can change it

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99
Q

what is cardiac output

A

volume of blood pumped by 1 ventricle in a given period of TIME (1 min)

indictor of total blood flow in body but DOESNT reflect where the distribution occurs in the various body tissues

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100
Q

what are the 4 determinates of cardiac output

A
  1. heart rate
  2. preload
  3. contractility
  4. afterload

stroke volume = 2,3,4

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101
Q

what happens to blood if one side of the heart begins to fail?

A

blood pools in the circulation behind failing side

LV fails -> blood pools in lungs (LA goes to lungs) -> problems in limbs -> swelling of ankles/feet

everything gets backed up!

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102
Q

SA node control is dominated by which branch on NS

A

PNS -> slows/narrows ion channels -> slow HR

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103
Q

tonic control of HR is dominated by what NS

A

PNS

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104
Q

why cant heart transplant patients do exercise?

A

increase HR due to loss of PNS control and decrease in HR response during exercise -> chronotropic incompetence

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105
Q

increase in Na and Ca2+ does what to HR and what NS

A

SNS -> increases HR

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106
Q

increase in Ca2+ and decrease in K+ does what to HR and what NS

A

PNS -> decrease heart rate

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107
Q

what is epinephrine

A

synthetic form of adrenaline
increases HR
relaxes smooth muscle in airways (dilation)
constricts blood vessels -> decreases swelling
SNS

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108
Q

what is cholinergic

A

PNS
form of AcH -> PNS drug
PNS is known as the cholinergic system
slows HR -> vasodilation

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109
Q

what is a chronotropic drug

A

increases of decreases HR

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110
Q

what is chronotropic incompetence

A

the inability of the heart to increase its rate in proportion with increased activity or demand

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111
Q

what controls HR during exercise

A

catecholamines

slow HR at start of exercise then reduced peak HR and a delay return towards resting values after cessation of exercise

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112
Q

what is preload (SV)

A

stretch of myocardial cells in ventricular walls (determined by volume of blood in the ventricle at the beginning of contraction)

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113
Q

what influences the contractility of the heart

A

the stretch of muscle cells, chemical/electrical factors (hormones drugs etc)

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114
Q

what is the Frank-Starling Law

A

increase in SV -> increase in EDV

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115
Q

how is EDV determined via a process

A

venous return

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116
Q

what 3 things affect venous return

A
  1. skeletal muscle pump
  2. respiratory pump
  3. sympathetic innervation of veins
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117
Q

what would venous dilation due to SV

A

reduce it -> reduction in venous return

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118
Q

what is iontropic

A

a chemical that changes the force/speed of contractility

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119
Q

what does a POS. inotropic drug do and examples of them

A

increase/strengthen contractility -> pump MORE blood
increase SV with fewer heart beats (forceful and shorter contractions)
epi. norepi and adrenaline
used for congestive heart failure

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120
Q

what does a NEG. inotropic drug do and examples

A

weaken/decrease contractility -> pump LESS blood
decreases SV with fewer heartbeats
beta-blockers -> vasodilation
used for hypertension, chronic heart failure

121
Q

what is afterload

A

combined load of EDV and arterial resistance during ventricular contraction

122
Q

what factors affect afterload

A

arterial constriction -> vasoconstriction increases BP
BP is an indirect measure of afterload

123
Q

what is ejection fraction

A

percentage of EDV ejected with 1 contraction
amt of blood pumped out of ventricles in 1 heartbeat relative to total amt of blood in ventricle

124
Q

what factors determine cardiac output -3

A

heart rate and SV and afterload

125
Q

does pulmonary BP have higher or lower BP than systemic

A

LOWER! would damage lungs if high

has much lower resistance too

126
Q

where is the site of exchange in the vascular system

A

capillaries

127
Q

what vessel has a lot of elasticity and collagen

A

large arteries

128
Q

capillary microcirculation:
what has HIGH hydrostatic pressure and LOW oncotic pressure

A

capillary side. fluid OUT

129
Q

capillary microcirculation:
what has LOW hydrostatic pressure and HIGH oncotic pressure

A

venule side.
fluid IN

130
Q

capillary microcirculation:
what factors determine direction of water exchange

A

hydrostatic and oncotic pressure

131
Q

capillary microcirculation:
what determines the rate of exchage

A

permeability of the capillary itself

132
Q

how is systemic blood pressure created -3

A
  1. ventricular contraction
  2. elastic recoil in arteries sustains driving force - windkessel effect
  3. blood flow obeys the rules of fluid flow
133
Q

what is the most important factor influencing blood flow

A

RADIUS!!!

134
Q

what is MAP

A

avg pressure in large arteries over a cardiac cycle

135
Q

flow of blood in veins is influenced by -3

A
  1. one-way valves
  2. skeletal muscle/diaphragm
  3. gravity
136
Q

what is MAP proportional to

A

CO x peripheral resistance in arterioles

137
Q

what 4 things influence MAP

A
  1. blood volume
  2. CO
  3. blood flow into/out of arteries
  4. distribution of blood b/w arteries and veins
138
Q

what NS controls the heart

A

PNS and SNS

139
Q

what NS controls vessels?

A

SNS! NOT PNS

140
Q

what vessel has the greatest influence on resistance

A

arterioles (accounts for 60% of total resistance)

141
Q

what influences arteriolar resistance -3

A

local tissues metabolic needs via signaling (exercise)
ANS sympathetic reflexes (paracrine)
hormones

142
Q

active hyperemia

A

increases metabolic activity and increases blood flow (blushing/redness) can be from exercise

143
Q

reactive hypereria

A

vessel occlusion, increase flow

144
Q

adenosine (paracrine)

A

released by cardiomyocytes low on O2

145
Q

histamine (paracrine)

A

vasodilator

146
Q

serotonin (paracrine)

A

vasoconstrictor

147
Q

how do different receptors respond to the SAME NT

A

different receptors will cause different responses!

148
Q

what organs gets the most amount of blood due to their filtering jobs

A

kidney and liver!

149
Q

what is the most observable sign of any type of hyperemmia?

A

blushing/redness

150
Q

does reactive hyperemia do in terms of homeostasis

A

goes AGAINST it

151
Q

what is systemic control

A

hormones influence kidney excretion of ions and H2O

hormones such as atrial natriuretic peptide and angiotension III

152
Q

what is systemic control in terms of NS

A

ANS sympathetic reflexes –> CNS mediated, MAP maintenance and body temp. homeostasis

such as norepine and epine

153
Q

norepine and epine are what

A

types of catecholamines. act as NT and hormones

154
Q

where does norepine come from (NS)

A

ANS -> sympatheic division.

PNS DOES NOT AFFECT VESSELS

155
Q

does PSNS affect vessels?

A

NO! SNS does (autonomic)

156
Q

what does norepinephrine do

A

CONSTRICTION. tonic control of arteriolar diameter

increase in norep = vasoconstriction
decrease in norep = vasodiliation

157
Q

Norepine from from the ANS neurons do what

A

help maintain arteriole wall SM tone

158
Q

Blood flow through individual blood vessels is determined by what

A

vessel’s resistance to flow

159
Q

what happens to the blood pressure proximal and distal to the constriction

A

proximally the pressure INCREASES
distally the pressure DECREASES

160
Q

increase to resistance does what to flow

A

DECREASES
inversely proportional

161
Q

what are baroreceptors sensitive to

A

pressure!

162
Q

what does carotid reflexes detect

A

PRESSURE. sends feedback to medullary cardiovascular control center if there is an increase in P

163
Q

what do carotid chemoreceptores respond to

A

blood O2 levels

164
Q

what does the hypothalamus regulate

A

temp and SNS reponses

165
Q

what does the cerebral cortex regulate

A

emotional responses (blushing)

166
Q

what is vasovagal syncope

A

seeing blood and fainting. CV system overreaction to certain emotional triggers

167
Q

what is syncope and what causes it

A

fainting

no blood to brain
dehydration, SNS dysfunction, heart failure (hypotension)

168
Q

normal BP

A

systolic < 120mmHg
diastolic < 80mmHg

169
Q

why does tachycardia decrease the perfusion of the coronary circulation? EXAM Q!!!

A

bc the amt of tine the ventricles spend in diastole is decreased over the span on a minute

170
Q

air follows the principle of

A

bulk flow

171
Q

what moves air?

A

we use muscles like the diaphragm to create a pressure gradient

NO muscular pump like the CV system!

172
Q

what is external respiration

A

movement of gases b/w the environment and body’s cell

173
Q

what is cellular respiration

A

intracellular rxn of O2 w/ organic molecules

174
Q

main steps of external respiration (4)

A
  1. atmosphere to lung
  2. lung to blood exchange
  3. transport of gases in the blood
  4. blood to tissue exchange –> cellular respiration
175
Q

what are the 2 functional divisions of the pulmonary system

A

conducting zone and respiratory zone

176
Q

what is the conducting zone

A

provides rigid conduits for air to reach the sites of gaseous exchange

nose, pharynx, larynx, trachea, bronchi, bronchioles

warms, humidifies and filters air
gaseous exchange doesn’t take place in this zone

177
Q

does gas exchange take place in conducting or respiratory zone?

A

respiratory zone

178
Q

what is the respiratory zone

A

site of gaseous exchange!

respiratory bronchioles, alveolar ducts and alveoli

179
Q

what are the sites of the conducting zone

A

nose, pharynx, larynx, trachea, bronchi, bronchioles

180
Q

what are the sites of the respiratory zone

A

respiratory bronchioles, alveolar ducts and alveoli

181
Q

what is involved in quite inspiration

A

diaphragm

182
Q

what is involved in quite expiration

A

NO muslces

183
Q

what muscles are used during inspiration during exercise

A

accessory ms, diaphragm, external intercostal, scalene, SCM

184
Q

what muscles are used during expiration during exercise

A

abdominal ms, internal intercostal

185
Q

what happens to thoracic volume and air pressure during inspiration

A

thoracic volume INCREASES
air pressure DECREASES

186
Q

is expiration a passive or active phenomenon

A

passive!

muscles of expiration are only needed during forced breathing and NOT quite

187
Q

how can you strengthen your abs and obliques

A

blowing balloons

188
Q

what are the branching structures of airways that supply air

A

in the lungs -> trachea, brochi, and bronchioles

189
Q

what are the functional units of the respiratory system where the exchange of respiratory gases occur

A

alveoli

190
Q

is air exchange 100% ?

A

no! not everything makes it to the alveoli!

191
Q

where does the exchange of respiratory gases occur

A

alveoli

192
Q

where does the blood-air barrier exist in gas exchange

A

in the lungs -> alveoli

193
Q

where does pulmonary gas exchange occur

A

across the fused basement membrane of the type I pneumocytes and endothelim

194
Q

what is the point of the fused BM in the type I pneumo and endothelium

A

prevents air bubbles from forming in the blood and from blood entering the alveoli

195
Q

what epi is the trachea lined with

A

PSCC with goblet cells

196
Q

what is mucus secreted by in the airway

A

goblet cells and seromucus cells

197
Q

how does saline play a role in the airway

A

epi cells secrete saline -> lowers mucous viscosity and allow cilia to push mucus towards the pharynx (from the trachea)

198
Q

where does cilia move mucous towards from the trachea

A

pharynx!

199
Q

what is Dalton’s Law

A

total P of a mixture of gases in the sum of the P of the individual gases

200
Q

what is a partial P

A

P of an indivudal gas in a mixture

201
Q

what does the presence of water vapor do gas

A

it dilutes the contribution of other gases

humidity makes it hard to breathe since the O2 has been diluted with H2O

202
Q

what is Boyle’s Law

A

increase V, decrease P

203
Q

during fetal development, what grows faster than the lungs

A

the thoracic cage and parietal pleura -> neg. pleural cavity P

204
Q

what maintains the sub-atmosphere intrapleural P

A

2 opposing forces -> elastic recoil of the lung creating an inward P and the chest wall pulling outward

205
Q

what does the pleural fluid serve as

A

a lubricant so lungs can move freely in chest wall

206
Q

what allows for chest expansion

A

parietal (outside) and visceral (inside) pleura

(these two together create the pleural cavity)

207
Q

during inspriation, what ms contract

A

diaphragm, external intercostal, scalene

208
Q

what happens during inspriation

A

increase in thoracic volume and decrease in air pressure and air moves into lungs

diaphragm contracts and flattens

209
Q

what happens during expiration

A

inspriatory muscles RELAX –> decrease in thoracic volume and increase in air pressure –> outward movement of air = expiration

210
Q

are expiratory muscles involved during quite expiration

A

NO!

211
Q

T/F: inspiration is the expansion of the lungs

A

FALSE! it is drawing of air into lungs

212
Q

T/F: expiration is NOT the contraction of the lungs

A

True! it is releasing air from lungs

213
Q

what are the 4 pressure changes during quiet breathing

A
  1. inspiration
  2. expiration
  3. alveolar pressure
  4. intrapleural pressure
214
Q

is expiration or inspriation take longer

A

expiration

215
Q

what is residual volume (lungs)

A

amt of air leftover after exhaling. never really changes. always have leftovers

216
Q

what is tidal volume

A

amt of air that moves in/out lungs w/ each cycle

217
Q

what is inspiratory reserve volume

A

forced inspiration. more than normal

218
Q

what is expiratory reserve volume

A

forced expiratory. more than normal

219
Q

what is total lung capacity

A

amt of air lungs can hold (abt 6 liters)

220
Q

what is pneumothorax

A

a collapsed lung that cannot function normally

221
Q

what happens when you get stabbed in the lung

A

when air/fluid enters space b/w parietal and visceral linings -> lung collapses due to subatmo. and atmo pressure equalizing

222
Q

T/F: a normal lung is both complaint and elastic

A

TRUE

223
Q

what is compliance and equation

A

ability to stretch

change in V / change in P

224
Q

what is elastance and equation

A

ability to recoil

= 1/complaince

225
Q

what does restrictive lung disease mean

A

lungs cant fully EXPAND/INHALE (Decrease in V)

226
Q

examples of restrictive lung diseases

A

fibrotic lung diseases, scoliosis, obesity, inadequate surfactant production

227
Q

what does obstructive lung disease mean

A

lungs cant EXHALE normally (increase in residual V)

228
Q

examples of obstructive lung diseases

A

COPD, emphysema, and asthma

229
Q

what do we use to test for lung diseases

A

spirometry. do forced expiratory volume in 1 second

230
Q

an infant that lacks surfactant has what type of lung disease

A

restrictive.

decreases inspiratory reserve V

231
Q

obstructive lung disease treatment

A

pursed-lip breathing

232
Q

surfactant increases/reduces surface tension

A

REDUCES

233
Q

what happens if there is no surfactant

A

the alveoli will collaspe

234
Q

smaller alveoli produce more/less surfactant than larger ones

A

MORE -> P is inversely proportional to radius

235
Q

what is in surfactant

A

surface active agents

proteins and phospholipids -> disrupt cohesive forces b/w H2O molecules

236
Q

what cells secrete surfactant

A

type II pneumocytes cells

237
Q

what is the one factor that changes in our system

A

RADIUS! inversely proportional to resistance

238
Q

what is alveolar dead space

A

volume of air inhaled that does not take part in gas exchange

inspired air at the end of each inspiration in the anatomic dead space is exhaled unchanged bc it remains in the conducting airways

239
Q

slower breathing means what it terms of O2 exchange

A

MORE O2 exchange and O2 moving through system

240
Q

eupnea is

A

normal quiet breathing

241
Q

hyperpnea is

A

increased respiratory rate and/or V in response to increased metabolism

242
Q

hyperventilation is

A

increased respiratory rate and/or V without increased metabolism

243
Q

hypoventilation is

A

decreased alveolar ventilation

244
Q

tachypnea is

A

rapid breathing -> usually increased respiratory rate with decreased depth

245
Q

dyspnea is

A

difficulty breathing

246
Q

apnea

A

cessation of breathing

247
Q

what is hyperventilation

A

fast breathing unaccompanied by increased metabolic demands of your body

increase O2 and decrease in CO2 partial pressure

248
Q

what is hypoventilation

A

super slow breathing

decrease in P O2, increase in P CO2

249
Q

blood flowing past an under ventilated alveoli does/does not get oxygenated

A

does NOT!

leads to constriction of arterioles so that the blood is diverted to a better ventilated alveoli

250
Q

changes in bronchiole diameter is mediated by what

A

levels of CO@ in the exhaled air passing through them

251
Q

is pO2 lower in arterial blood or alveoli’s

A

arterial blood pO2 is lower than alveolis

O2 moves down conc. gradient

252
Q

tissue pCO2 is lower/higher than that of blood

A

lower! CO2 moves down conc. gradient

253
Q

in the venous blood, pCO2 is higher/lower than alveoli’s

A

HIGHER

CO2 moves down conc. gradient -> exhaled out

254
Q

breathing super slow does what in terms of rate of exchagne

A

you get a higher rate of exchange

255
Q

is the pH in arterial or venous higher

A

higher in arterial

arterial 7.4
venous 7.37 (little more acidic)

256
Q

what is hypoxic hypoxia

A

low arterial pO2 (high altitude)

257
Q

what is anemic hypoxia

A

decreases amt of O2 bound to hemoglobin (blood loss)

258
Q

what is ischemic hypoxia

A

reduced blood flow (heart failure)

259
Q

what is histotoxic hypoxia

A

failure to use O2 bc of poison (cyanide)

260
Q

what does the total oxygen content of arterial blood depend on

A

amt of O2 dissolved in plasma and bound to Hb

261
Q

how does O2 enter the plasma

A

diffuses across alveolar epi cells and capillary endothelial cells

262
Q

what affects diffusion

A

gas solubility

263
Q

is CO2 or O2 more soluble in liquid

A

CO2 is 20x more soluble in liquid than O2

harder for O2 to go into bloodstream since it’s MUCH easier for CO2

264
Q

Hb + O2 =

A

HbO2 -> oxyhemoglobin

265
Q

what are 2 characteristics of Hb-O2 binding

A

its reversible and co-operative! (one binds, they all do)

266
Q

total blood O2 content =

A

dissolved O2 + O2 bound to Hb

267
Q

more than 98% of O2 in blood is bound to

A

Hb in RBC

less than 2% is dissolved in plasma

268
Q

what does O2 diffuse through to attach to a RBC

A

alveolar, BM, capillary endothelium, cell membrane of RBC

269
Q

can cells survive without hemoglobin?

A

NO!

4x more O2 available than is needed by cells at rest.

270
Q

what is the primary factor that determines the % of available Hb binding sites that are occupied by O2

A

plasma P O2

271
Q

what is percent saturation of hemoglobin

A

plasma p O2 is the primary factor that determines the % of available hemoglobin binding sites are occupied by O2

272
Q

what are. the3 determinates of arterial pO2

A
  1. gas composition of inspired air
  2. alveolar ventilation rate
  3. efficiency of gas exchange b/w alveoli and blood
273
Q

how does altitude sickness occur

A

decrease in barometric P and decrease in pO2 = O2 is more dispersed in air. NO pressure gradient for it to travel down

274
Q

a right shift on the graph for O2-Hb binding means

A

decrease Hb affinity for O2 -> O2 actively unloads

275
Q

a left shift on the graph for O2-Hb binding means

A

increase Hb affinity for O2 -> reluctant to release O2

276
Q

CO2 reacts with H2O to form

A

carbonic acid

277
Q

what is the Bohr Effect

A

increase in CO2 in plasma -> lower blood pH

hemo releases O2 (occurs with exercise)

278
Q

what does a decrease in CO2 do to blood pH

A

increases blood pH (more basic)

hemo picks up or retains O2 (wont release O2)

279
Q

increasing temp does what to the affinity of Hb for O2

A

DECREASES affinity of Hb for O2

280
Q

a decrease in 2,3-BPG does what to the affinity of Hb for O2

A

INCREASES affinity of Hb for O2

chronic hypoxia and anemia both increase 2,3-BPG production

281
Q

low P in fetus does what to O2 affinity

A

increases O2 affinity

low pO2 environment

282
Q

3 ways CO2 is transported

A

7% dissolved in plasma
23% bound to Hb
70% converted to bicarb ion (most CO2 is transported as bicarb -> buffer)

283
Q

Does the diaphragm fire sponetaneously?

A

NO! requires neural control

284
Q

what controls the diaphragm

A

control is based on monitoring of O2, CO2, H+ levels in arterial blood and extracellular fluid

285
Q

ventilation is based on what

A

chemoreceptor and mechanoreceptor linked reflexes (neg. feedback loops) modulated by brainstem neurons

286
Q

respiratory neurons in the medulla nucleus tractus solitarius control what

A

inspiratory (dorsal respiratory group) and expiratory (ventral respiratory group) ms

287
Q

what do neurons in the pons do

A

integrate sensory info and interact w/ medullary neurons to influence ventilation

288
Q

what is found in the dorsal respiratory group and where is it

A

nucleus tractus solitarius

IN MEDULLA

289
Q

in the pons, the pontine respiratory group do what

A

they recieve sensory info from DRG -> influences the initiation and termination of respiration

290
Q

what do the pons do

A

coordinate a smooth respiratory rhythm and influence ventilation

291
Q

what primarily regulates ventilation

A

CO2

levels of respiratory gases are sensed by central and peripheral chemoreceptors which are associated with arterial circulation

292
Q

where are peripheral chemoreceptors

A

located outside CNS in carotid/aortic bodies -> ALWAYS exposed to arterial blood

293
Q

where do peripheral chemoreceptors sense changes in

A

CO2, O2, and pH

carotid/aortic O2 sensors release NT when pO2 in lowered

294
Q

CO2 crosses BBB to react with water to form

A

H2CO3 -> H+ and HCO3-

295
Q

H+ and HCO3- have a potent direct stimulatory effect on what kind of chemoreceptor?

A

CNS!

296
Q

do pH changes in plasma influence the CNS chemoreceptors directly?

A

NO!

CO2 enters the CSF easily, H+ ions cross very slowly

297
Q

is pCO2 remains high for several days, what do the CNS chemorec. do

A

adapt to it by increasing the concentration of HCO3- that buffer the H+

298
Q

what are irritant receptors?

A

receptors in the airway that are stimulated by irritants that enter airway (coughing and bronchoCONSTRICTION)

299
Q

what are stretch receptors? how do they get activated?

A

receptors in the lung that signal brainstem to terminate inspiration (Hering-Breuer inflation reflux).

activated by increase in tidal volume

Physiology (4 decks)

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