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Body in Balance Midterm #2 > Control of Ventilation > Flashcards

Control of Ventilation Flashcards

1
Q

peripheral chemoreceptors of ventilation

A
  • located in aortic bodies and carotid bodies
    • near lots of capillaries and blood flow
  • monitor the composition of blood PO2, PCO2, and pH
  • can respond to changes quickly , but not a strong response
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2
Q

central chemoreceptors of ventilation

A
  • located in medulla in extracellular fluid (ECF)
  • most important chemoreceptor for minute-to-minute ventilation
  • monitors pH and pCO2 in ECF; does NOT monitor pO2
    • between the ECF and cerebral blood vessel in the blood-brain barrier which is hard for O2 to cross
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3
Q

lung receptors

A
  • embedded in lung tissue
  • types
    • pulmonary stretch receptors
    • irritant receptors
    • juxtacapillary (J) receptors
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4
Q

Pulmonary Stretch Receptor

A
  • Hering-Breur Reflex: slows down respiratory rate when activated
  • In response to a deep breath we slow down breathing; in shallow breaths (lack of stretch) breathing rate is increased
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5
Q

Irritant Receptors in ventilation

A
  • in lungs, nose, pharynx, larynx, trachea
  • responds to noxious gases, dusts, cigarette smoke, cold air
  • reflex is to cough, hold breath
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6
Q

Juxtacapillary Receptors (J receptors)

A
  • respond to increased interstitial fluid
  • sends signals to increase respiratory rate
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7
Q

Joint/Muscle Receptors in Limbs in ventilation

A
  • movement stimulates increased ventilation in exercise
  • faster response to the demand of exercise than if just depending on chemoreceptors
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8
Q

Gamma System in ventilation

A
  • muscle spindles sense elongation of muscle and can reflexly control strength of contraction
  • in cases where muscles in respiration are not being stretched as much as they should can respond by increasing contractioni of the muscles
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9
Q

diaphragm in ventilation

A

dome-shaped muscle that flattens when contracting which increases volume of thorax space for lungs to expand

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10
Q

external intercostal muscles in ventilation

A

lift ribcage upward and outward to increase thorax volume

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11
Q

accessory muscles in ventilation

A

scalene – lifts first two ribs

sternocleidomastoid – lift sternum, first rib, and clavicle

  • accessory muscles used in deep inspiration
  • can evaluate a patient’s breathing state by seeing if accessory muscles are being used
    • use indicates state respiratory distress
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12
Q

internal intercostasl muscles in ventilation

A

bring ribcage inward and downward to decrease thorax volume

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13
Q

upper airway dilating muscles

A

upper airway naturally wants to collapse during inspiration – by contracting these muscles we conteract this tendency

  • nasal alae: dialte nasal passages
  • genioglossus: protrudes tongue
  • levator and tensor palatine muscles: opens laryngeal aperture
  • posterior cricoarytenoid muscle: opens laryngeal aperture
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14
Q

nerve roots of spinal cord

A

inital segment of nerve as they come off spinal cord; come together to form spinal cord

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15
Q

naming of spinal nerves in relationship to vertebral bodies

A
  • cervical nerve above the vertebra (C1 nerve above C1; ends with C8 below C7)
  • THEN thoracic, lumbar, sacral nerve below the vertebra named after (T1 under T1)
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16
Q

Nerve Roots Supplying Respiratory Muscles

A

diaphragm: C3 - C5
accessory: C1 - C8

intercostal muscles: corresponding nerve root

abdominal muscles of expiration: T7 and below

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17
Q

respiratory centers

A

groups of neurons in brainstem responsible for basic rhythm of expiration; some in medulla and some in pons

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18
Q

cerebral cortex and ventilation

A

can override breathing function of brainstem; examples are when we want to take a deeper breath to blow on something or hold our breath

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19
Q

limbic system and hypothalamus on ventilation

A

can change breathing via emotions, pain, temperature responses

20
Q

purpose of interspersing occasional, involuntary signs into the breathing pattern

A

to increase surfactant

21
Q

physiology of restricted thoracic cage

A
  • increased elastive load
  • feedback from
    • stretch receptors
    • gamma receptors
    • chemoreceptors
22
Q

definition of hyperventilation

A

an increase in ventilation that is excessive for the rate of metabolic carbon dioxide production, resulting in a decreased pCO2 to below the normal range

23
Q

causes of hyperventilation

A
  • Hypoxemia (altitude, disease states)
  • Anxiety
  • Fever
  • Metabolic acidosis
  • Congestive heart failure
  • Drugs (aspirin, progesterone)
  • Pregnancy
24
Q

definition of Cheyne-Stokes Respirations

A

cyclic breathing marked by a gradual increase in the rapidity of respiration followed by a gradual decrease and then total cessation

25
Q

why is there a delay between SaO2 and apnea in cheyn-stokes breathing?

A

SaO2 is being measured with a oximeter on finger; takes time for the blood that experience the apnea to get to the finger

26
Q

what is a loop gain and what’s the equation for it

A

demonstrates how responsive a feedback loop is;

loop gain = corrective response / disturbance

27
Q

What contributes to loop gain?

A
  • Circulatory time (time it takes from blood to get from the thorax to the chemoreceptors) – longer delay between signal and response
  • Neurologic disease – central controllers maybe degenerated
28
Q

how can initiation of sleep trigger cheyne-stokes breathing?

A

when we’re awake, aterial pCO2 is just above a breathing threshold; at the onset of sleep our threshold exceeds the arterial pCO2 level causing decreased ventilation for a moment, and then we adjust to pCO2 above breathing threshold again – this non-pathological phenomenom can trigger some people to enter Cheyne-Stokes breatching if they have high loop gain

29
Q

Why do heart failure patients get CSA?

A
  • Longer circulatory time
  • Stimulation of J receptors while awake (from edema)—increases the apneic threshold (larger difference between wakeful pCO2 and sleeping pCO2)
  • More prone to hypoxia during sleep-onset apnea (due to interstitial edema)
30
Q

changes in ventilation in response to pO2 and pO2 + hypercapnia

A

hypoxemia has a great increase in ventilation but is even more pronounced if there is also hypercapnia; synergistic relationship

31
Q

the three physiological changes that occur in sleep

A
  • increased upper airway resistance
  • decreased chemosensitivity
  • inhibition of skeletal muscles, especially during REM sleep
32
Q

why does airway resistance increase during sleep?

A

upper airway dilator muscles lose tone and airway becomes more narrow

33
Q

how is chemosensitivity affected by sleep?

A

when we are sleeping we are less chemosensitive; rises in pCO2 while we sleep increase ventilation, but not as sharply as when we’d be awake (least change seen in REM)

34
Q

types of apnea

A
  • central apnea
    • period of no ribcage or abdomen movement
  • obstructive apnea
    • during apnea there’s paradoxic motion
  • mixed apnea
    • starts out as central then turns into obstructive
35
Q

most vulnerable location in upper airway to apnea

A

posterior oropharynx

36
Q

factors that promote airway collapse in upper airway

A
  • negative pressure on inspiration
  • extralumenal positive pressure, fat deposition, small mandible
37
Q

factors that can lead to decreased airway patency in upper airway

A
  • less contraction of pharyngeal dilator muscle
  • decreased lung volume –> longitudinal traction
38
Q

if there is any effort demonstrated during apnea what does this indicate?

A

this indicates obstructive apnea instead of central apnea

39
Q

looking at brain electrogram during apnea what pattern might you notice

A

after period of apnea might see state of arousal from brain to compensate – these arousals keep a patient from getting a restful night of sleep

40
Q

increased risk factors for sleep apnea

A
  • Obesity- increased visceral fat
  • Increased size of upper airway soft tissue structures
  • Recessed mandible
  • Increased neck size (> 18”)
  • Nasal airway obstruction
  • Heredity
41
Q

How is obstructive sleep apnea treated?

A
  • CPAP
  • Weight loss
  • avoidance of supine position during sleep (in supine more prone to collapse, tongue falls back)
  • avoidance of sedatives and alcohol
  • Dental appliances (to move the mandible forward)
  • Surgeries (uvulopalatopharyngoplasty/UPPP, tracheostomy)
42
Q

what is a uvulopalatopharyngoplasty (UPPP)

A

srugery to carve out excess tissue in the treat; can be used to help treat sleep apnea

43
Q

best treatment for sleep apnea

A

CPAP (continuous positive airway pressure)

44
Q

what is a tracheostomy and how can it help sleep apnea

A

a surgical procedure which consists of making an incision on the anterior aspect of the neck and opening a direct airway through an incision in the trachea – this can bypass the obstruction in sleep apnea

45
Q

at what point in sleep cycle is apnea most likely to occur?

A

during REM – muscles and the most atonic meaning more likely for airway collapse; body is the least chemosensitive during REM

Body in Balance Midterm #2 (26 decks)

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