3 - Respiration Flashcards

1
Q

What are the three major components of the respiratory center?

A
  1. dorsal respiratory group (dorsal medulla, inspiration)
  2. Ventral respiratory group (ventrolateral medulla, exp)
  3. Pneumotaxic center (superior pons, rate and depth of breathing)
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2
Q

What does the dorsal respiratory group control?

A

inspiration and respiratory rhythm

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3
Q

Most of the neurons in the dorsal respiratory group are located in the _______

A

Nucleus of the tractus solitarius (NTS)

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4
Q

What is the NTS?

A

Nucleus tractus solitarius

Main component of the dorsal resp group

sensory termination of both the vagal and glossopharyngeal nn

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5
Q

Where is the basic rhythm of respiration generated?

A

the dorsal respiratory group

even when it’s completely severed from afferent and efferent nerves, it will still emit inspiratory action potentials!

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6
Q

Instead of sending bursts of inspiratory action potentials, the dorsal group signal is an inspiratory _______

A

ramp

steadily increases and then ceases abruptly

results in inspiration rather than gasping

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7
Q

How does the inspiratory ramp signal change with heavy respiration?

A

Increases the rate of increased signalling (increases the steepness of the ramp)

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8
Q

How is the inspiratory ramp modified to acheive a change in respiration?

A

the limiting point at which the ramp suddenly ceases is lengthened or shortened.

The earlier the ramp ceases, the shorter the duration of inspiration and therefore expiration, and therefore the more breaths that take place per minute

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9
Q

What is the function of the pneumotaxic center?

A

limits duration of inspiration and increases respiratory rate

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10
Q

When the pneumotaxic signal is strong, respiration is _____

A

increased

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11
Q

What is the function of the ventral respiratory group?

A

Overdrive mechanism when high levels of pulmonary ventilation are required

When there are an excess of signals to the dorsal ventral group, they “spill over” into the ventral respiratory group

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12
Q

How does the ventral respiratory group contribute to resting rate and rhythm?

A

It doesn’t. It’s completely inactive during normal quiet respiration

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13
Q

What is the Hering-Breuer Inflation Reflex?

A

Stretch receptors in the muscular walls of the bronchi and bronchioles send messages through the vagus when they’re overstretched

The signal causes a completely switching off of the dorsal group, preventing further inspiration

Mostly prevents against extreme overinflation, not triggered during normal inspiration

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14
Q

What is the effect of oxygen levels on the respiratory centers of the brain?

A

Pretty much no effect on the respiratory centers of the brain

acts almost entirely on peripheral chemoreceptors in the carotid and aorta, which transmits nervous signals to the respiratory center

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15
Q

How do CO2 and H interact with the respiratory center?

A

Indirectly

Changes in CO2 and H trigger the chemosensitive area (near the pneumotaxic center)

the chemosensitive area then excites other portions of the respiratory center

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16
Q

What is the primary stimulus for excitation of the chemosensitive area?

A

Hydrogen, not CO2

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17
Q

If CO2 does not readily cross the blood brain barrier, how is it the primary stimulus of the chemosensitive area?

A

In blood, CO2 is dissociated into carbonic acid, then bicarb and H, which is what the chemosensitive area responds to

Even though CO2 isn’t technically reaching the brain, an increase in the level of CO2 will trigger the chemosensitive area indirectly because of its buffered state

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18
Q

A change in blood [CO2] has a potent _______ effect but a weak _____ effect

A

acute

chronic

Subsides after a couple of days

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19
Q

Do chemoreceptors respond to arterial or venous O2 levels?

A

Arterial

They have a massive arterial supply with almost no O2 extraction, leading to accurate interpretation of PaO2

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20
Q

During hypoxia, which neurotransmitter is released by the carotid body glomus cells to trigger the respiratory center?

A

ATP!

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21
Q

Since CO2, O2, and pH levels remain constant throughout exercise, what stimulates the increased respiratory rate seen during strenuous exercise?

A

When motor impulses leave the brain to stimulate the exercising muscles, they transmit collateral impulses to the respiratory center

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22
Q

When a person begins to exercise, how quickly does respiration increase?

A

Almost immediately, before there are any chemical changes in the blood

In fact, PCO2 decreases below normal initially in anticipation of the increase in serum CO2

23
Q

What are J receptors?

A

stimulated when the pulmonary capillaries become engorged or pulmonary edema occurs

May be responsible for the sensation of dyspnea

24
Q

How does acute brain edema impact respiratory function?

A

depresses the respiratory center

25
Q

What causes Cheyne-Stokes breathing?

A

CO2 and O2 flux causing over-reactions in the respiratory center

26
Q

Why doesn’t Cheyne Stokes breathing occur in everyone?

A

Normally actions and reactions to the chemoreceptors are highly damped because there are large amounts of O2 and CO2 dissolved in the blood, so fluctuations are slight

27
Q

When does Cheyne Stokes breathing occur?

A
  1. Severe cardiac failure (delayed delivery and removal of blood from the alveoli leads to large swings in the level of CO2 and O2 at the level of the chemoreceptors)
  2. Damage to the respiratory center (causes an increased negative feedback gain). brain damage turns off respiratory drive for a few seconds, then an extra-instense increase in CO2 turns it back on with a vengeance
28
Q

Two types of constrictive lung disease

A

fibrotic (TB, silicosis)

disease that constrict the rib cage (kyphosis, scoliosis, fibrotic pleurisy)

29
Q

In airway obstruction disease, which is more difficult: expiration or inspiration?

Why?

A

Expiration

The airway is already predisposed to close, and when you add the positive pressure in the chest that causes expiration, it puts even more pressure on the structures to close off

Conversely, when the rib cage expands it pulls the airway open, making it relatively easy to get air in

30
Q

What is the FEV1?

A

Forced expiratory volume during the first second. The percentage of the FVC that is expired in the first second (FEV1) is indicative of obstruction.

In normal lungs, 80% of air is expelled in the first second

In airway obstructions, it takes a long time for the same amount of air to escape.

31
Q

Pulmonary emphysema is the result of chronic _________

A

obstruction of the smaller airways

caused by chronic infection and ciliary damage which leads to excess mucus and inflammatory edema

32
Q

How does emphysema impact individual alveoli?

A

Entraps air inside them

causes destruction of as much as 50-80% of the alveolar walls

33
Q

Why do emphysema patients have increased CO2 levels?

A

loss of alveolar walls decreases the diffusing capacity of the lung

34
Q

Why do emphysema patients have abnormal V/Q ratios?

A

some parts of the lung are better ventilated than others

Can get a very high V/Q (phsyiologic shunt) in some areas, and an extremely low V/Q (phsyiologic dead space) in others

35
Q

Why is emphysema associated with pHTN?

A

Loss of the alveolar walls also causes loss of capillaries, so there’s the same amount of blood traveling through fewer capillaries

causes pHTN and eventual Cor Pulmonale

36
Q

What is pneumonia?

A

Any inflammatory condition of the lungs that fills alveoli with fluid and blood cells

37
Q

What is the number one cause of pneumonia?

A

Pneumococci bacteria

38
Q

What does it mean when areas of the lung become “consolidated”?

A

They’re filled with fluid and cellular debris

39
Q

What kind of V/Q ratio will you see in a patient with pneumonia?

A

Decreased

40
Q

What are the two causes of atelectasis?

A

Airway Obstruction

Lack of surfactant

41
Q

What is the usual cause of asthma?

A

Contractile hypersensitivity to particles in the air

42
Q

In most young people, asthmas is caused by ________

In most old people, it’s caused by _______

A

Allergic hypersensitivity (usually plant pollen)

nonallergenic irritants (smog, cigarette smoke)

43
Q

In patients with allergic asthma, the antibodies are attached to:

A

mast cells in the lung instertitium

44
Q

When pollen reacts with a mast cell in the lung insterstitium, what substances are released?

A

Histamine

Slow-reacting substance of anaphylaxis

Eosinophili chemotactic factor

bradykinin

45
Q

When an allergic reaction occurs in an asthmatic patient, what is the result in the lungs?

A

Localized edema and thick secretions

Bronchiolar smooth muscle spasms

Overall: increase airway resistance

46
Q

What lung metrics will decrease during an asthma attack?

Which ones will increase?

A

Maximum expiratory rate, timed expiratory volume

functional residual capacity, residual volume

47
Q

The tubercle bacilli causes what reaction in the tissue of the lungs?

A

invasion the tissue by macrophages

“walling off” of the lesion by fibrous tissue to from the so-called tubercle

Eventually causes thickening of the respiratory membrane

48
Q

What happens to tissues during cyanide poisoning?

A

Cytochrome oxidase is blocked and the tissue cannot utilize oxygen

49
Q

What happens in beriberi?

A

several steps in O2 utilization are compromised because of vitamin B deficiency

50
Q

Cyanosis occurs with the arterial blood contains:

A

more than 5g/dL of deoxygenated hemoglobin

51
Q

Who is more likely to get cyanotic: a patient with anemia, or a patient with polycythemia

A

Polycythemia

52
Q

Mild to moderate hypercapnea cause increased respiratory rate. At what point does it cause respiratory depression?

A

120-150 mmHg

causes a vicious cycle

53
Q

What is dyspnea

A

mental anguish associated the inability to ventilate enough to satisfy the demand for air

54
Q
A