Unit 3: Pulmonary Physiology Pt 4 Flashcards

1
Q

What stimulates our first breath after birth?

A
  • cooling of skin

- slightly asphyxiated state (elevated CO2)

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2
Q

What is the negative pleural pressure necessary to open alveoli on first breath?

A

40-60 cm H2O

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3
Q

What are the circulatory changes at birth?

A
  • placenta disconnects
  • TPR increases
  • Pulmonic resistance decreases
  • closure of Foramen ovale (atria)
  • closure of ductus arteriosis (great vessels)
  • closure of ductus venosus (bypass liver)
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4
Q

As one ascends to higher altitude, how is the barometric pressure change?

A

it decreases

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5
Q

T/F. The fractional concentration of O2 doesn’t change with altitude.

A

true

but the partial pressure will due to the total pressure getting smaller

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6
Q

What is the equation to calculate the PO2 based on barometric pressure?

A

PO2 = (.21)(barometric P)

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7
Q

At 63,000 ft what is the barometric pressure? What happens to blood?

A

bP = 47 mmHg and blood “boils”

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8
Q

What does an unacclimatized person suffer from that occurs from ascending to great heights?

A

deterioration of nervous system function

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9
Q

What are the acute effects of ascending to great heights primarily due to? What are the symptoms?

A

hypoxia

  • sleepiness
  • false sense of well being
  • impaired judgement
  • clumsiness
  • blunted pain perception
  • decrease visual acuity
  • tremors
  • twitching
  • seizures
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10
Q

What will Acute Mountain Sickness cause/two effects it has? How quick does it onset?

A
  • cerebral edema –> hypoxia –> stimulates local vasodilation
  • pulmonary edema –> hypoxia–> stimulates local vasoconstriction (more stress)

onset hours - 2 days

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11
Q

Hypoxia to systemic tissues will promote________, while hypoxia to pulmonary tissues will promote _______.

A

vasodilation

vasoconstriction

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12
Q

What will hypoxia stimulate immediately when an individual is exposed to low PO2 at high altitude?

A

arterial Peripheral Chemoreceptors

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13
Q

What will the immediate stimulation of arterial Peripheral Chemoreceptors due to hypoxia at high altitude cause?

A

increased ventilation —> which decreases CO2–> which limits increase in ventilation as pH is increasing —->

= respiratory alkalosis

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14
Q

Due to low PO2 at high altitude, what effect does the increase in blood pH have on ventilation? Therefore, what is it opposing?

A

is inhibitory to ventilation and opposes the stimulatory effects of hypoxia on Peripheral Chemoreceptors

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15
Q

After several days of exposure to low PO2 at high altitude, what happens to ventilation?

A

ventilation increases 5x, as inhibition fades–> thought to be due to:

  • excretion of HCO3- by kidneys offsetting the decrease CO2 —> and therefore decrease pH back toward normal
  • -> now hypoxic stimulation of peripheral chemoreceptors is NO longer opposed by alkalosis and ventilation can increase many fold
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16
Q

What occurs with Chronic Mountain Sickness?

A
  • red cells mass (Hct) increases
  • increase in pulmonary arterial BP
  • enlarged right ventricle
  • decrease total peripheral resistance
  • congestive heart failure
  • death if person is not removed to lower altitude
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17
Q

What occurs when someone undergoes Acclimatization to a high altitude?

A
  • great increase in pulmonary ventilation
  • increase RBC (Hct)
  • increase diffusing capacity of lungs
  • increase tissue vascularity (increase capillary density)
  • increase ability of tissues to use O2
  • increased synthesis of 2,3-DPG (shifts oxy-hemoglobin dissoc. curve to RIGHT
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18
Q

How will the Acclimatization of someone in higher altitude shift the oxy-hemoglobin dissociation curve? What part of the body is this an advantage to? disadvantage to?

A

shifts it to the right favors dissociation and:

  • advantages –> tissues
  • disadvantages –> lung

(so oxygen disassociates more off hemoglobin)

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19
Q

When one is born into living at a higher altitude, “Natural Acclimatization”, when does this occur for them, and what happens?

A

begins at infancy and chest to body ratio increases

  • high ratio of ventilatory capacity to body mass
  • increased size of right ventricle
  • shift in oxy-hemoglobin dissociation curve
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20
Q

As people descend beneath the sea, to keep the lungs from collapsing air must be supplied at high pressures, which exposes pulmonary capillary blood to extremely high alveolar gas pressures–> what is this called?

A

Hyperbarism

these high pressures can be lethal

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21
Q

What effect will a high partial pressure of N2 cause?

A

causes narcosis in about an hour of being submerged

(state of stupor, drowsiness, or unconsciousness)

similar to alcohol intoxication

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22
Q

What effect will a high partial pressure of O2 cause?

A

Oxygen Toxicity

  • seizures followed by coma w/in 30-60 mins (likely lethal to divers)
  • above a critical alveolar PO2 (> 2 atms PO2) –> free radical damage
23
Q

How can oxygen toxicity be prevented?

A

if one never exceeds the established maximum depth of a given breathing gas

24
Q

What effect does a high partial pressure of CO2 cause?

A

usually not a problem as depth does not increase the alveolar PCO2

can increase in certain types of diving gear:

  • problems can occur when alveolar PCO2 > 80 mmHg
    • depression of respiratory centers
    • respiratory acidosis
    • lethargy
    • narcosis
    • anesthesia
25
Q

The high partial pressure of what gas will most likely cause narcosis in about an hour of being submerged?

A

High Partial pressure of N2

26
Q

As a person breaths air under high pressure for an extended period of time, what happens to the amount of N2 in the body fluids?

A

increases as higher N2 levels equilibrate with levels in tissues

27
Q

Can N2 be metabolized by the body? Expand on that.

A

No; will remain dissolved in tissues until N2 pressure in lungs decreases as person ascends back to sea level

28
Q

How long does it take for gas pressures of N2 in all body tissues to equilibrate with alveolar P-N2?

A

several hours

29
Q

Why can it be a potential problem is a person is submerged at a deep level for several hours?

A

b/c blood does not flow rapidly enough and N2 doesn’t diffuse rapidly enough to cause instantaneous equilibration

  • N2 dissolved in H2O equilibrates < 1 hour
  • N2 dissolved in fat equilibrates in several hours
30
Q
What is the volume of N2 dissolved in the body at these feet below sea level?
0
33
100
200
300
A
0 ft -- 1 L
33 ft -- 2 L
100 ft -- 4 L
200 ft -- 7 L
300 ft -- 10 L
31
Q

What is it called when nitrogen bubbles out of fluids after sudden decompression and may block blood vessels?

A

Decompression Sickness

aka “Bends”

32
Q

What are the signs and symptoms of Decompression Sickness, aka “Bends”?

A
  • pain in joints, muscles of arms/legs (85-90%)
  • NS symptims; dizziness, paralysis, unconsciousness (5-10%)
  • Pulmonary capillaries blocked; “the chokes” (2%)
33
Q

What organ ranks second as an organ of body metabolism? What is first?

A

the lung ranks second behind the liver

34
Q

What is one advantage the lung has over the liver when it comes to being an organ of metabolism?

A

all blood passes through the lungs with every complete cycle

35
Q

How much air does the average adult inhale per day?

A

10,000 L air/day

36
Q

What is the thickness of the respiratory membrane? What is the surface area?

A

.5 microns b/w air and blood

surface area of 50-100 sq. meters

37
Q

What are some things in the 10,000 L of are we inhale each day?

A
  • Inert dust
  • Particulate matter (plant and animal)
  • Gases (fossil fuel combustion)
  • Infectious agents (viruses and bacteria)
38
Q

What are three defense mechanisms of the pulmonary system?

A
  1. protect tracheobronchial tree and alveoli from injury
  2. prevent accumulation of secretions (cough/sneeze)
  3. repair
39
Q

What is associated with an increased incidence of bacterial infections in the pulmonary system?

A

chronic alcohol

40
Q

What is associated with an increased incidence of chronic bronchitis and emphysema?

A

cigarette smoke

41
Q

What is associated with increased incidence of hyperactive airways or interstitial pulmonary fibrosis?

A

occupational irritants

42
Q

What are three ways the nasal passages protect airways and alveolar structures from inhaled foreign materials?

A
  1. filter–> long hairs (vibrassae) in nose filters out larger particles
  2. Moisten –> mucous coating nasal mucous membranes traps particles
  3. Warm air–> nasal turbinates are high vascularized and act as radiators to warm air
43
Q

What CN does coughing utilize primarily?

A

CN X

44
Q

What area is the cough ineffective at clearing? Why?**

A

ineffective at clearing smaller airways due to large total cross-sectional area

cannot generate sufficient velocity

45
Q

What is the process of coughing?

A
  1. 2.5 L of air rapidly inspired
  2. epiglottis closes and vocal chords close tightly
  3. muscles of expiration contract forcefully which causes pressure in lungs to rise to 100 mmHg
  4. epiglottis and vocal chords open widely which results in explosive outpouring of air to clear larger airways (speeds of 75-100 mph)
46
Q

What can the velocity of air escaping from the mouth and nose from sneezing and coughing get up to?

A

75-100 mph

47
Q

What CN is associated with sneezing? What occurs?

A

irritation sends signal over CN V to medulla

similar to cough, but in addition the uvula is depressed so large amounts of air pass rapidly through nose to clear nasal passages

48
Q

What clears the smaller airways in the lung?**

A

mucociliary elevator

49
Q

What produces the mucous in the respiratory tract?

A

goblet cells in epithelium and small submucosal galnds

50
Q

How is the mucous moved up in the Mucociliary elevator?

A

ciliated epithelium that lines the respiratory tract down to the terminal bronchiolses moves mucous to pharynx

51
Q

How many times does the Mucociliary elevator beat per minute? How fast does the mucous flow?

A

1000x

1 cm/min

52
Q

What are the two innate immune responses in the lung?

A
  1. Alveolar macrophages (Dust Cells)

2. Complement System

53
Q

What are the antibodie associated with the mucosa of the lung?

A

IgG –> lower respiratory tract
IgA –> dominate in upper respiratory tract
IgE –> predominantly a mucosal Ab