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ISBM > Spring Exam 4 > Flashcards

Spring Exam 4 Flashcards

1
Q

how does the presence of H20 affect partial pressures

A

H20 decreases partial pressures!

  • as we breath in we humidfy the air
  • water vapor is independent of altitude–> fxn of temp
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2
Q

describe the conducting airways

A
  • Trachea and bronchi (cartilagenous) and bronchiolies (membranous)
  • conduit for air to alveoli, not do engage in gas exchange –> anatomical dead space
  • each branch is a generation
  • made of SmM. (can contract and relax)
  • can hold ~150mL
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3
Q

describe the gas exchange airways

A
  • resp. bronchioles and alveoli
  • where gas exchange occurs
  • LOTS of generation –> LARGE SA
  • can hold 1500-3000mL
  • intimate w/ vasculature
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4
Q

where is air flow resistance greatest in the system?

A

at the front of the airway (lowest at alveoli)

*most resistance is seen where pressure drop is greatest (6th generation- at level of arterioles)

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5
Q

where is mass air flow greatest in the system?

A

greatest at large airways

-velocity decreases in the periphery

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6
Q

normal breathing at any level (subject to change)

A

TV

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7
Q

-the maximal volume of air that can be exhaled from the end-expiratory position

  • volume remaining in the lungs
  • volume of air capable of being expired
A

ERV

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8
Q

volume remaining in lungs after ERV

A

RV

*cannot be measured w/ spirometry

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9
Q

ability to inhale to max inspired volume

A

IRV

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10
Q

sum of all volumes

A

TLC

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11
Q

force VC is the sum of what

A

ERV + TV + IRV

*inhale as deeply as you can and then blow out as fast as you can

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12
Q

volume left in lungs following normal breathing

A

FRC

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13
Q

___ is subject to change but ___ does not change

A

TV is subject to change

RV does not change (unless w/ some pathological conditions)

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14
Q

what muscles are involved w/ inspiration and expiration?

A

inspiration: diaphragm (increase chest dimension), external intercostals (elevate ribs)
expiration: internal intercostals (depress ribs), abdominal ribs (compress abdomen)
* more muscles used in active breathing

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15
Q

describe the lungs at rest

A
  1. pleural space is neg press. (subatmospheric)
  2. elastic outward recoil of chest wall is equal and opposite of elastic inward recoil of lungs
  3. at FRC (recoils balanced)
  4. muscles at rest
  5. no airflow
  6. pressure of gas in alveoli = pressure in airway opening
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16
Q

describe the lungs during inspiration

A
  1. muscles contract due to phrenic n. –> thoracic volume expands
  2. pleural space becomes more neg.
  3. lungs expand–> pressure drops in alveoli (more neg.)
  4. pressure at airway is same and more neg at alveoli –> air moves INWARD w/ gradient (neg. pressure breathing)
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17
Q

describe the lungs during expiration

A
  1. muscles relax
  2. recoil of lung causes alveolar pressure to exceed pressure at airway–> more + pressure in alveoli
  3. air flows OUT due to gradient
    * expiration is passive
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18
Q

what is hysteresis

A

when you take a lung and apply positive pressure to the airway opening (OR negative pressure to the pleural surfaces via expansion of chest wall) you see that the change in volume of the lung is initially very small. As pressures continue to increase, however you will find that the volume will begin to expand more rapidly
*due to surface tension

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19
Q

It develops due to the larger attractant forces between adjacent molecules at the air liquid interface compared with the molecules lower down in the body of fluid.

A

surface tension

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20
Q

how does LaPlace’s law relate to surface tension?

A

pressure w/in an alveoli is directly proportional to the Tension and inversely proportional to the alveoli radius

  • small alveoli= higher tension= more pressure
  • larger alveoli= lower tension= less pressure
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21
Q

what is the purpose of surfactant as it relates to surface tension

A

surfactant coats alveoli and prevents surface tension from getting high enough to allow alveoli to collapse
*makes ST increase w/ radius NOT tension

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22
Q

describe babies first breath

A
  • born they have very small alveoli with very high surface tension–>require a huge pressure to combat that surface tension and open up the alveoli.
  • use substantial inspiratory m. to expand the thoracic cavity and create a large neg. pleural press. around -45–>pulls the alveoli open against its high internal ST and press.–> press. in the alveoli drops and air will rush in and fill alveoli
  • When surfactant is around it will coat the alveoli so that the subsequent inhalations become easier by decreasing surface tension exhibited by alveoli
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23
Q

describe FRC at the end of a normal tidal breath

A

FRC is ~45% of TLC at the end of a normal tidal breath

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24
Q

how do we get the lungs to inflate (increase in volume)

A

apply a POSITIVE pressure at the airway opening

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25
Q

what is the chest walls pressure when it is at 70% TLC?

A

0 cm H20

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26
Q

when is the pressure neg. and positive in the chest wall??

A

we exist ~ 40% TLC therefore anything less than 70% is neg pressure. and when we are above 70% the lungs are pressing on the chest wall outward creating positive pressure

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27
Q

what is FRC? (functional residual capacity)

A

the point when the outward recoil of the chest wall equals the inward recoil of the lungs
*at the end of normal tidal expiration

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28
Q

describe the forces when lungs are at RV

A

~12% TLC

  • small inward force from lungs
  • LARGE outward force from chest wall (wants to get to 70% TLC)
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29
Q

describe the forces when lungs are at FRC

A

~45% TLC

  • equal inward and outward forces
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30
Q

describe the forces when lungs are at ~70% TLC

A
  • no force from chest wall

- strong inward force from lungs (“wanting to get back to FRC)

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31
Q

what is a pneumothorax

A

breaching the integrity of the pleural space allowing atmospheric air into the pleural space

  • lungs recoil in
  • chest wall recoils outward
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32
Q

what happens to resistance as we move from TLC to RV?

A

resistance to flow (Raw) increases

*the relationship is hyperbolic–> R is slow to occur at first but rises quickly as you near RV

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33
Q

when is the resistance to flow the least?

A

when airways are inflated at TLC

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34
Q

what is FCV

A

amount of air exhaled from TLC to RV

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35
Q

The volume of air that can forcibly be blown out in one second after full inspiration. –> R to flow to get air out in the large airways

A

FEV1

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36
Q

A ratio of the volume of air expired in the first second over the total air expired during the spirometry test.

A

FEV1/FCV

*Average values vary but are between 80-120%. Predicted values can be calculated online and age, sex, height, weight, ethnicity all factor in.

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37
Q

This is the force of expiratory flow from 75% to 25% of TLC. In other words it looks at flow rate across 50% span of our TLC

A

FEF 25-75

*As the volume diminishes, resistance increases in the lung so the flow rate will slow.

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38
Q

asthma, chronic bronchitis, emphysema, and COPD are examples of what type of airway disease

A

obstructive

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39
Q

pulmonary fibrosis is what type of airway disease

A

restrictive

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40
Q

what is an obstructive airway disease and describe its impact on lung values

A
  • problem getting air OUT of lungs (increase compliance)
  • increase RV, and TLC
  • decreased peak flow
  • decreased FEV, FCV and low/normal FEV:FVC (less than 80%)
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41
Q

what is an restrictive airway disease and describe its impact on lung values

A
  • problem getting air INTO lungs (decreased compliance)
  • decreased TLC and peak flow
  • decreased FEV, FVC, and high FEV:FVC (greater than 80%)
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42
Q
  • pO2 of ambient air = __
  • pO2 of inspired air = __
  • pO2 of air at lungs = __
  • pO2 in tissues = ___
A
  • ambient air pO2= 160mmHg
  • pO2= 150mmHg (adjusted for water)
  • pO2 at lungs= 102 (due to ASD)
  • pO2 in tissue = 40 (drop off O2 for metabolic use)
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43
Q

why is the pO2 different between alveoli/blood interface?

A

diminished due to reducing factors such as shunting and diffusion
PalvO2= 100mmHg
PaO2= 95mmHg

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44
Q

why is alevolar air different from inspired air?

A

ADS!

(compare minute ventilation (6L/min) with alveolar ventilation (4.5L/min))

  • not all air entering the lungs end up in the alveoli due to ADS
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45
Q

alevolar ventilation is all about what?

A

CO2!!
**It is INVERSELY related to pCO2

NOT O2!!

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46
Q

The greater alveolar ventilation, the ___ the partial pressure of CO2 in alveoli. AND ___ we breath–> the ___ PCO2 will be.
-The PP in arterial blood will be represented in the lungs too

A

Lower

SLOWER

Higher

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47
Q

what is transit time?

A

the amount of time the cap. blood has to equilibriate with alveolar
-Cardiac Output dictates the TT

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48
Q

what dictates the TT

A

Cardiac output

  • increase CO= increase blood flow= short TT
  • decreased CO= slow blood flow= long TT
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49
Q

describe the TT in normal rest vs. exercise state

A

rest: ~0.6 sec. (long TT)
Exercise: ~0.25 sec. (short TT) *max equilibrium still reached

-O2 equilibrium is reached at ~0.2 sec

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50
Q

how does our system combat with a shorten TT w/ exercise?

A

exercise = increased CO= increased RR thus ventiliating the lungs more to combat short TT

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51
Q

how does pulmonary edema or infection affect TT?

A

increase the distance of diffusion–> increased TT needed to get good diffusion of O2 and equilibrate alveolar/capillary interface

*Ficks Law= net flux of a substance is a direct fxn of the area of diffusion

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52
Q

what is the VQ ratio?

A
  • a measurement used to assess the efficiency and adequacy of the matching two variables. It is the ratio of air reaching the alveoli to the amount of blood reaching alveoli.
  • The V/Q values vary depending on the position in the lung so we usually look at the whole lung to determine this ratio and the normal value is usually 0.8
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53
Q

describe the perfusion and ventilation of the lung

A
  • greater at the base of the lung for both due to gravity

- ventilation is also influenced by position

54
Q

what effects the amount of O2?

A
  1. amount of gas dissolved. Po2
  2. amount of Hgb and its saturation
  3. amount of met-Hgb
55
Q

what is the VQ ratio of blood in an anatomical shunt?

A

0 –> blood never interacts w/ alveoli so it is never reoxygenated

56
Q

Why is the PaO2 less than the PAO2?

A

due to differences in V, Q, and VQ ratio
-in apex: high VQ ratio–> blood coming from this area (though small) will be highly oxygenated

-in base: low VQ ratio–> blood coming from this area will be less oxygenated

57
Q

The 4 most common causes of hypoxemia are

A

1-Ventilation/Perfusion mismatch is the most common
2-Diffusion issue like pulmonary edema
3- Shunting like septal defect
4-Hypoventilation (mushroom lady)

58
Q
  • portion of CO that bypasses the lung
  • intracardiac right to left shunt
  • lung vasculature that doesn’t interface with alveoli
A

Anatomic shunt

59
Q
  • perfusion that passes through an alveolar interface with no gas exchange
  • collapsed alveoli
  • pus-filled or edematous alveoli
A

Alveolar shunt

60
Q
  • due to very low V/Q ratios of some lung units
  • essentially no gas exchange
  • venous admixture (wasted blood flow)
  • clinically the most common cause is atelectasis
  • Mucus, edema, tumor, foreign body
A

Physiologic shunt

61
Q

describe the alveolar gas w/ no ventilation

A

takes on the characteristic of plasma motoring pass alveolar

  • low VQ ratio
  • high pCO2 and low pO2
62
Q

describe the alveolar gas w/ no perfusion

A

takes on the characterstics of inspired air

  • high VQ ratio
  • low pCO2 and high pO2
63
Q

Arterial O2 content is a fxn of what

A

VQ inequalities throughout the lung

64
Q

what happens with the content with ok perfusion and low ventilation?

A

decrease content

65
Q

what happens with the content with ok ventilation and low perfusion?

A

increase content

66
Q

liquid is a fxn of what?

A
  1. partial pressure of the gas

2. solubility coeficient

67
Q

describe Henry’s Law

A
  • the relationship btwn pp of a gas and the concentration we see in the plasma
  • increase in pp= increase in concentration
  • NOT all gases are very soluble in liquid so while the pp will equilibriate across the alveolar/cap. interface, the actual amount of [gas] physically dissolved is a fxn of the solubility coefficient
68
Q

where is the O2 in the blood?

how much is where?

A
  • 1.4% is dissolved in O2
  • 98.6% is bound w/ Hgb

*once O2 is bound to Hgb, it no longer can contribute to the partial pressure of O2

69
Q

how much O2 is dissolved in arterial and venous blood?

A
  • arterial: 0.3ml O2/dL at a pp 100mmHg
  • venous: 0.12ml O2/dL at a pp 40mmHg
  • O2 solubility coefficient is 0.024
70
Q

Hgb Oxgen is a function of what?

A
  1. Hgb concentration in the system
  2. amount of O2 capable of binding (functional binding capacity)
  3. Saturation of Hgb w/ O2 in arterial blood

*Iron must be in ferrous (Fe2+) form for Hgb to reversibly bind to O2

71
Q

how can you get a normal pulse ox in an anemic patient?

A

a pulseox is not sensitive to the overall [Hgb] therefor an anemic patient has low Hgb (10) and their Hgb is 100% saturated at a low pp bc they dont have much Hgb to begin w/ so it is readily oxygenated

*pulseox only tells you about hte paO2

72
Q

why is a pulseox of 90% bad?

A

due to the sigmoidal dissociation relationship btwn O2 and Hgb at 90% pulseox, that means the pp of O2 is 60mmHg which suggest ineffective gas exchange

**suggests problem w/ ventilation

73
Q

what factors affect Hgbs affinity for O2?

A
  1. oxygenation (each bindind increases affinity)
  2. 2, 3 BPG (increase in BPG= decreased affinity)
  3. pH (decrease in pH=increase [H+]= decreased affinity)
  4. temp (increased temp= decreased affinity)
  5. pCO2 (increased pCO2= decreased affinity)
74
Q

what is a tissue extraction ration?

A

Tissue extraction compares the amount of oxygen removed from the blood during a pass through a particular organ
*avg value = 0.3

75
Q

describe the ER in the kidney, heart, and exercising muscle

A
  • Kidney =10% (seems small but it recieves MASSIVE blood supply)
  • Heart= 60-65% (high metabolic needs, lack of flow can lead to very fast cell death)
  • Exercising- greater than 90% (pO2 can drop dramatically)
76
Q

what are the forms of CO2 in blood?

A
  1. dissolved in plasma - 5% (increases linerally w/ increase pCO2 –> Henrys law)
  2. carbamino compounds- 5%
  3. HCO3- formation - 90%
77
Q

what is the chloride shift?

A

when CO2 levels increase, RBCs move HCO3- out of RBC into plasma in exchange for uptake of Cl-
-HCO3- and Hgb can then act as buffers in the plasma (bohr effect)

78
Q

describe the Haldane effect?

A

oxygen shifts the CO2 dissociation curve to the left

  • presence of O2 decreases the affinity of Hgb for CO2
  • at PaO2 100mmHg- curve is down and right
  • at PaO2 40mmHg- curve is up and left
79
Q

describe the CO2 dissociation curve

A
  • total CO2 content depends on summation of the 3 forms of CO2 components
  • total CO2 content in blood is a hyperbolic fxn of pCO2
80
Q

In tissue:
low pO2 facilitates ___
high pO2 faciliitates ___

A
  • low pO2 facilitates CO2 loading (reverse Haldane)

- high pO2 faciliates O2 unloading (Bohr effect)

81
Q

in Lungs:
low pO2 facilitates ___
high pO2 faciliitates ___

A
  • low pO2 facilitates O2 unloading (reverse Bohr effect)

- high pO2 faciliates CO2 unloading (Haldane)

82
Q

how does changing levels of CO2 in the blood affect bicarb, pH, and pCO2?

A
  • increase [CO2]= increase [pCO2]= increase [HCO3-]= decrease pH
  • decrease [CO2]= decrease [pCO2]= decrease [HCO3-]= increase pH
83
Q

how does carbon monoxide affect Hgb?

A
  • it has a HUGE affinity for Hgb (carboxy-hemoglobin) 300X greater than its affinity for oxygen
  • CO is a POWERFUL competitive inhibitor of oxygen binding

**when CO is bound to Hgb, we see an increase in Hgb affinity for oxygen, so Hgb has a hard time distributing O2 even if it can bind to a spot on Hgb that CO is not occupying

84
Q

what drives the frequency and depth of breathing?

A

the nervous system

  • Inspiration: external intercostals fire (synchronized w/ phrenic nerve-diaphragm)
  • expiration: internal intercostals fire
85
Q

where are central chemoreceptors and what do they detect?

A

in pons and medulla
-sense change in local pH only!
(drive by increased CO2)

-increase CO2 diffuses across blood brain barrier into CSF
CO2+ H2O–> H2CO3–> H+ and HCO3-
-

86
Q

where are the peripheral chemoreceptors and what do they detect?

A

in carotid body/glomus and aortic body/glomus

-sense CO2

87
Q

what is the Hering Breurer Reflex?

A

prevents over inflation of lungs

  • stretch reflex upon inspiration–> when TV doubles–> triggers expiratory activity
  • triggered by mechanoreceptors
88
Q

what happens to CO2 when ventilation increases?

A

decrease CO2

89
Q

describe situations where there is reduced CO2 sensitivities (most reduction to least)

A
  • deep anesthesia
  • narcotics, COPD
  • Sleep
  • awake/normal

*increased sensitivity in metabolic acidosis

90
Q

describe the pulmonary pressure

A
  • pressure generated from RV
  • lower pressure than systemic pressure (1/5th)
  • peak systolic = 25mmHg, MAP 14
  • pressure continues to drop as it reaches the capillaries
91
Q

how do the starling forces differ in the pulmonary capillaries compared to systemic cap?

A
  1. K is larger (more permeable)
  2. HPcap is much less
  3. oncotic p. in ISF is greater
  4. HP ISF is negative
92
Q

how do the alveoli stay dry?

A
  • high oncotic pressure in ISF in lungs drives water out of alevoli
  • negative pressure in HP ISF allows evaporation of water across alveoli
93
Q

what happens to the lungs starling forces in CHF?

A

build up on HP in vasculature will cause and increase in fluid in the lungs

  • this decreases ISF oncotic pressure
  • leads to hypoxic state/rales/SOB
94
Q

describe the effect of a hypercapnic situation both systemically and in pulmonary system

A

systemic: vasodilation of vessels
pulmonary: vasoconstriction

95
Q

what substances vasoconstrict vasculature in lungs?

A

Epi, NE, angio II, histamine, endothelians

-used to increase resistance and therefore decrease blood flow/perfusion

96
Q

what substances vasodilate vasculature in lungs?

A

bradykinin, ACh, isoproterenol, low Epi

  • ACh dilates via NO release
  • bradykinin does opposite of angio II
97
Q

how do local gases affect vasoconstriction of vasculature in lungs?

A

hypoxia, hypercapnia, and acidosis cause vasoconstriction

*suggests low ventilation therefore shunt blood elsewhere by increasing resistance

98
Q

4 main processes of the GI tract

A
  • Motility
  • Digestion
  • Secretory activity
  • Absorption
99
Q

2 plexuses of the GI system

A
  1. myenteric

2. submucosal

100
Q

during digestion, the GI tract can use up to how much of the cardiac output?

A

30%

*requires a lot of O2

101
Q

what type of receptors serve a mean of providing input to the enteric NS for the GI system?

A
  • mechanoreceptors

- chemoreceptors

102
Q

what are goblet cell?

A

cells in the intestinal glands that produce mucous, which acts as lubricant and protectant from mechanical and chemical influences

103
Q

what are paneth cells

A

cells in the intestinal glands that produce lysosomes, phospholipase A2, and defensins, which are responsible for bactericidal activity

104
Q

how often is GI epithelium renewed?

A

fully renewed 1x per week

-a main source of iron loss in the system

105
Q

each vili contains what?

A
  • vascular, lymphatic, and smooth muscle presence

* each one has a single lymphatic lacteal and a single lymphatic capillary for drainage

106
Q

what are the epithelial cells of the GI tract?

A
  • absorptive cells that are metabolically very active w/ a wide variety of passive and active processes moving molecules from the lumen to inside the cells
  • have an unstirred layer above these cells to allow molecules to transport and diffuse
107
Q

what is motility

A

muscular activity that serves to mix intestinal contents and propel contents aborally–accomplished through coordinated muscular activity that is initiated within the enteric nervous system (but can be modulated by the ANS).

108
Q

what is segementation

A
  • most frequent type of contractile activity in the GI tract
  • due to isolated, closely spaced contractions of CIRCULAR SmM. (random in freq. and pressure change)
  • Serves to mix chyme (to facilitate absorption)
109
Q

what is peristalsis

A
  • Successive contractions of circular smooth muscle.
  • stimulated by local distention which triggers the contraction/relaxation reflex.
  • gives ups a 1-4cm movement per contraction
  • not very propelsive
110
Q

what organs contribute to the volume secretion in the GI tract? and how much volume total?

A
  • salivary glands*
  • stomach*
  • pancrease*
  • duodenum
  • liver
  • colon

~8-10L per day!

111
Q

describe the content of GI secretions?

A
  • all have an aqueous base
  • isosmotic w/ respect to plasma
  • contains enzymes, buffers, and emulsifiers
  • avg. 8-10L/day (a lot is reabsorbed)
  • most have bicarb and neutral pH to allow enzymes to fxn
112
Q

describe the digestion process in the GI tract

A
  • accomplished through the activity of enzymes, which are produced in the mouth, stomach and in the small intestine.
  • The purpose of breakdown using enzymes is to produce molecular forms suitable for absorption.
  • Digestion is unregulated
113
Q

describe the absorption process in the GI tract

A
  • occurs in the stomach, SI and LI (but to different degrees)
  • passive and active processes responsible
  • we absorb/reabsorb 99% of volume secreted/ingested (only 100ml per day leave the system in stool)
114
Q

describe the intrinsic electrical activity in the GI tract

A
  • slow waves initiated by automaticity (~3/min)
  • generated at orad region and propagate to pyloric region getting larger as it goes (more neg)
  • gets large enough at bottom to generate AP (unstable RMP)
115
Q

the strength of the GI contraction is proportional to what

A

the extent of depolarization

116
Q

what are ACh’s influences on the GI tract

A
  • impacts level of membrane depolariazation

- stimulates secretion and SmM. contraction

117
Q

what are NE effects on GI contractions?

A

increases the RMP (more neg)–> hyperpolarized–> slows motility

118
Q

how is GI fxn regulated (pace setters)?

A
  1. Neural influences
    - enertic NS
    - ANS
  2. Hormonal influenecs
    - GI HR
    - epi
    - Active Vit. D3, T3/T4, aldosterone
119
Q

what is atropine

A

a muscarinic receptor blocker= anti-diarrheal

120
Q

what hormones are part of the secretin family and what are their main roles?

A

AKA incretins

  • secretin
  • GIP
  • GLP
  • VIP
  • Glucagon

*all increase insulin release

121
Q

what are the main roles of gastrin

A

+ HCL secretion via parietal cells

+ mucosal growth

122
Q

what are the main roles of CCK

A 
\+ pancreatic HCO3 secretion
\+ pancreatic enzyme secretion
\+ gallbladder SmM contraction
\+ pancreatic growth
- gastric emptying
123
Q

what are the main roles of secretin

A

+ pancreatic and bile secretion of HCO3
+ pancreatic growth
- HCl secretion
- motility

124
Q

what are the main roles of GIP

A

+ insulin release

125
Q

what are the main roles of motilin

A

+ gastric and intestinal motility

126
Q

what are 5 main chemical/neural stimulators for GI HR release

A
  1. proteins, fats, carbs- direct +
  2. free [H+]- HUGE stimulator for secretin
  3. increase pH- inhibits gastrin
  4. distention- stimulates gastrin
  5. nervous impulses- stimulate gastrin and motilin
127
Q

Which processes are subject to regulation?

  • Motility
  • Secretion
  • Digestion
  • Absorption
A
  • Motility

- Secretion

128
Q

where does absorption occur

A

stomach, SI and LI

129
Q

where does the digestion of carbs and fats begin?

A

the mouth!

130
Q

describe saliva

A
  • product of 3 glands (parotid, submandibular, sublingual)
  • hypo-osmotic, alkaline solution that moistens and lubricates food
  • ~2L/day
131
Q

describe the actions of ghrelin

A
  1. stimulates GH release from AP
  2. stimulates hunger, food intake, and weight
  3. primes stomach for food (increase prior to meal)
  4. increase HCl secretion and gastric motility
  5. increases CO and reduces SVR (increases BF to gut)
132
Q

what do acinar cells produce and release?

A
  1. amylase- released in active form
  2. lipase- “ “
  3. trypsin- activated via enterokinase in duodenum

ISBM (8 decks)

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