Respiratory System Flashcards

1
Q

Respiration definition

A

gas movement & gas metabolism

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2
Q

Internal respiration definition

A

intra- cellular metabolic processes (in mitochondria) that use O2 & produce CO2
– “cellular respiration”

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3
Q

External respiration definition

A

events involved in exchange of O2 & CO2 between cells & external environment

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4
Q

4 steps of external respiration

A

1- Ventilation (breathing)
2- Respiratory exchange (at lungs or gills)
3- Circulation
4- Cellular exchange (between blood & cells)

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5
Q

What is gas exchange governed by?

A
partial pressure
(Molecules diffuse down concentration gradients
But gases diffuse down partial pressure gradients)
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6
Q

Partial pressure (PP or P)

A

pressure exerted by a particular gas within a mixture of gases
measured in mm Hg

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7
Q

Total atmospheric pressure

A

sum of partial pressures that each gas in atmosphere contributes
Pressure exerted on objects by atmospheric air can push a column of mercury (Hg) up some amount of mm = total atmospheric pressure
Atmospheric air contains N2 (~79%), O2 (~21%), plus small amounts of CO2, H2O vapor, other gases, & pollutants

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8
Q

Calculating partial pressures

A

Total atmospheric pressure at sea level = 760 mm Hg
21% of that = O2 so PO2 = 160 mm Hg

At elevation, total atmospheric pressure drops = partial pressure of all gases drops = less drive for O2 diffusion into tissues

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9
Q

strategies for increasing gas exchange:

A

Diffusion is slow except over short distances

  1. To maximize gas exchange, epithelial lining of respiratory surface (e.g. lungs) must be very thinAlso want as much surface area as possible for as much diffusion as possible to take place
  2. To increase surface area, respiratory surfaces in vertebrates have specialized folds: invaginations (in-pockets) & evaginations (out-pockets)
    Steeper partial pressure gradient = faster diffusion
  3. Respiratory pigments (e.g. hemoglobin in erythrocytes) bind O2, which means it is no longer freely dissolved & no longer contributing to partial pressure inside the body

Maintains low PO2 inside body, keeping gradient steep & allowing for greater diffusion, plus prevents any backwards diffusion

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10
Q

Respiratory anatomy

A

In vertebrates, water respirers have gills while air respirers have lungs
Each is adapted to specialized needs
Less O2 in water
Potential for desiccation in air

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11
Q

Gills

A

have many evaginations & very thin epithelial cells to increase gas exchange

1 other adaptation: countercurrent blood flow

Blood flows counter to water across gills – causes PP gradient all along gills rather than reaching equilibrium & O2 diffusion stopping

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12
Q

lungs

A

Dry air can cause desiccation (& death) of sensitive epithelial cells in the lungs

Lungs must stay moist & lubricated for protection & easy movement during inhalation & exhalation

Mucus-secreting cells produce an aqueous mucus lubricant: “pulmonary surfactant”

Ciliated cells are lined with tiny hairs that help distribute the mucus

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13
Q

Mammals have a very high metabolic rate affect on lungs

A

had to significantly increase lung surface area

Accomplished this with numerous small alveoli covered by incredibly dense capillaries

Alveoli = small sacs in grape-like clusters where gas exchange in lungs takes place

~300 million in a human!

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14
Q

Anatomy of mammalian lungs

A

Nasal passages  pharynx (throat)  trachea  right & left bronchi  bronchioles  alveoli
The trachea & larger bronchi must be open most or all of the time, so are rigid structures with cartilaginous rings to prevent compression

Smaller bronchioles do not have cartilage – instead have smooth muscle with autonomic innervation & sensitivity to hormones

thus can have altered contraction to regulate amount of air flow

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15
Q

Alveoli

A

have no cartilage or smooth muscle to help them inflate & deflate

Instead rely on on muscles in the thoracic (chest) cavity: diaphragm, external intercostal, abdominal wall, & internal intercostal muscles

these change the volume of the thoracic cavity, causing a corresponding change in lung volume

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16
Q

Mammalian lungs

A

take up most of the thoracic cavity

Each lung is enclosed within the double- walled pleural sac

inside of sac is filled with fluid allowing the layers to slide past each other during respiratory movement

The inside of the pleural sac (where the lungs are) = pleural cavity

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17
Q

Inspiration (inhalation)

A

breath in
When relaxed, the diaphragm muscle is in a dome shape, protruding into thoracic cavity
Upon contraction, diaphragm moves downward, thereby enlarging area in thoracic cavity & causing inward air flow
Contraction of the external intercostal muscles also enlarges the thoracic cavity by expanding ribs & sternum outward, allowing inward air flow

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18
Q

Passive expiration (exhalation) = breath out

A

As inspiratory muscles relax back into thoracic cavity & lungs exhibit elastic recoil, air is passively pushed out of lungs, with gases diffusing down their PP gradients

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19
Q

While expiration occurs passively during quiet breathing, it is possible to actively push air out too

A

moves air out more completely & rapidly, especially useful for quick breathing during exercise

when contracted, abdominal wall muscles push the diaphragm even further into the thoracic cavity

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20
Q

Internal intercostal muscles

A

have opposite effect of external intercostal muscles, causing ribs to flatten

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21
Q

Airways normally offer very little resistance

A

Allows adequate air flow even when pressure gradients are very small (1 or 2 mm Hg)

Various respiratory diseases can narrow airways, increasing resistance & thus decreasing airflow

e.g. COPD = chronic obstructive pulmonary disease, a group of lung diseases including chronic emphysema, bronchitis, & asthma

22
Q

Lung volumes can be measured by:

A

a spirometer

fits over mouth & measures volume of air breathed in & out  generates a spirogram

this shows the various volumes & capacities of the lungs

23
Q

Total lung capacity (TLC)

A

the maximum amount of air lungs can hold

~5.7L in humans, though affected by build, age, lung health, & disease

However, not all of TLC can be exchanged

24
Q

residual volume(RV)

A

air that cannot be expelled

25
Q

Tidal volume (TV)

A

amount of air moving into or out of the lungs during any one breathing cycle

At rest, human TV = ~2.2L at end of expiration to ~2.7L at end of inspiration

26
Q

Functional residual capacity (FRC)

A

volume of air left in lungs after passive expiration – during quiet breathing, lungs are not close to max expiration or inspiration

27
Q

inspiratory reserve volume (IRV)

A

After normal inspiration it is possible to breathe in additional air

28
Q

expiratory reserve volume (ERV)

A

After normal expiration it is possible to exhale additional air from the lungs

29
Q

vital capacity (VC):

A

3 values (TV, IRV, & ERV) added represent it
amount of air we can control through inhalation & exhalation
usually ~3-5L in vol.

30
Q

Pulmonary ventilation

A

the volume of air breathed in & out in 1 minute
PV= TV x Respiratory Rate
Increasing TV or rate increases pulm. ventilation

However: more advantageous to increase TV rather than rate because of anatomic dead space – the area where air is not available for gas exchange at alveoli (can’t get past conducting airways like bronchi)

Thus a better measure of gas exchange = alveolar ventilation, where dead space is accounted for

31
Q

Obstructive lung disease

A

any problem that doesn’t allow air to move smoothly from alveoli out through trachea (or vice versa) when breathing
e.g. COPD, & smoking cigarettes also permanently damages alveoli, leading to lung obstruction
Spirometry data can be helpful in diagnosing obstructive & restrictive lung diseases

32
Q

Restrictive lung disease

A

normal airflow but decreased lung volumes

e.g. due to pulmonary fibrosis, asbestos poisoning, respiratory distress syndrome, & pneumonia

obesity can also cause decreased lung volumes because of increased pressure on the chest wall

33
Q

forced expired volume in one second (FEV1)

A

FEV1 = the volume expired in the first second of maximal expiration after a full inspiration – is a measure of how quickly the lungs can be emptied

In healthy adults the FEV1/FVC ratio = ~80%

Decreased by obstructive lung disease, damage, or naturally with age (~70% or less)

34
Q

Oxygen is dissolved in blood:

A

as free gas, though very little because O2 is poorly soluble in warm fluids (only 1-5%)

bound to respiratory pigments in erythrocytes, like hemoglobin

35
Q

The vast majority of O2 in blood is carried in circulation by:

A

hemoglobin

ensures enough O2 gets to tissues

also remember: bound O2 doesn’t contribute to PP, so helps keep PP gradient steep

36
Q

hemoglobin (Hb)

A

Main respiratory pigment in vertebrates Hemoglobin contains iron (Fe) molecules & forms a loose, easily reversible combo between Fe & O2

Hb unbound = deoxyhemoglobin, or “reduced”

HbO2 = oxyhemoglobin

37
Q

So why does Hb combine with O2 in the lungs but release O2 at the tissues?

A

1st: Hb & O2 binding increases when the PP of O2 is high &decreases when low
2nd: HbO2 tends to dissociate under several conditions that occur at tissues (but not lungs) & are especially increased at tissues working hard
Increased PCO2
Increased acidity (e.g. lactic acid)
Increased temp
Increased free phosphates inside erythrocytes (affects lungs too – produced during RBC metabolism)

38
Q

So how is CO2 transported in the blood?

A

1- As freely dissolved gas
CO2 more soluble than O2, but still only ~5-10% of CO2 in blood is dissolved

2- Bound to hemoglobin
~25% of CO2 in blood is carried bound to Hb (HbCO2)
only in mammals – fish have altered Hb which can’t bind CO2

3- As bicarbonate (HCO3-)
CO2 is converted into HCO3

39
Q

HCO3- is the most important means of CO2 transport because

A

HCO3- is more soluble in the blood than CO2 – thus easier to transport than free gas

HCO3- cannot diffuse through membranes on its own – thus more controllable than free gas

40
Q

HCO3- / Cl- antiport carrier passively facilitates diffusion across erythrocyte membrane

A

Allows plasma to “soak up” CO2, preventing buildup in RBCs

exchange with Cl- (“chloride shift”) prevents change in electrical gradient across membrane

41
Q

Back at lungs, transport moves in opposite direction

A

Causes restoration of Cl- gradients

HCO3- reaction takes place in reverse to allow release of CO2 from blood to lungs as free gas

42
Q

We’ve now seen that Hb can bind to O2, CO2, & H+ - so how does it choose which one & where?

A

Remember: high PO2 at lungs encourages binding (HbO2), & conditions at tissues (low O2, high CO2, high acidity, etc.) encourage dissociation

As HbO2 unbinds, the affinity of Hb for CO2 & H+ increases  called the “Haldene effect”

Results in HbH+ & HbCO2

Dissociate at lungs & cycle starts again

43
Q

Carbon monoxide (CO)

A

can also bind to Hb

CO2, O2, & H+ all readily dissociate from Hb

CO binds to Hb preferentially (more than O2) & does NOT readily dissociate

not enough O2 to tissues, CO poisoning

44
Q

Hypoxia

A

insufficient O2

45
Q

Hypercapnia

A

excess CO2 in blood
caused by excess CO2 in environment or hypoventilation
Hypercapnia–>  elevated carbonic acid production–>  excess H+ –> respiratory acidosis

46
Q

Hypocapnia

A

low CO2 in blood
caused by hyperventilation
Hypocapnia –> drop in carbonic acid production–>  less H+ than usual –> respiratory alkalosis

47
Q

Why are changes in CO2 dangerous?

A

Changes in blood CO2 affect acid-base balance

    CO2 + H2O    H2CO3    H+ + HCO3- 

Remember the importance of homeostasis, including of pH: low (acidic) or high (basic) pH = denaturation of proteins & irreversible cell damage

48
Q

bronchodilation

A

Sympathetic stimulation

during exercise or other times when O2 needs increase

49
Q

bronchoconstriction

A

Parasympathetic stimulation

when quiet & relaxed

50
Q

Like arterioles, the smooth muscle on bronchioles is sensitive to local CO2 levels

A

High CO2 levels act directly on the smooth muscle, causing relaxation / dilation, while low CO2 levels cause contraction / constriction

51
Q

Like blood flow, air flow is detected by peripheral chemoreceptors in the aorta & carotid artery

A

Chemoreceptors detect low O2, high CO2, & high H+

send info to respiratory center of the brain (in medulla)

However, these are only weakly stimulated – main regulators of ventilation are central chemoreceptors

52
Q

Central chemoreceptors (in the brain) detect CO2 (weakly) & H+ (strongly), sending signals to the respiratory center to adjust ventilation

A

H+ cannot cross BBB on its own, but is produced in the brain when the bicarbonate reaction takes place