Control of Ventilation

Question 1

peripheral chemoreceptors of ventilation

Answer 1

• 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

Question 2

central chemoreceptors of ventilation

Answer 2

• 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

Question 3

lung receptors

Answer 3

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

Question 4

Pulmonary Stretch Receptor

Answer 4

• 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

Question 5

Irritant Receptors in ventilation

Answer 5

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

Question 6

Juxtacapillary Receptors (J receptors)

Answer 6

• respond to increased interstitial fluid
• sends signals to increase respiratory rate

Question 7

Joint/Muscle Receptors in Limbs in ventilation

Answer 7

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

Question 8

Gamma System in ventilation

Answer 8

• 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

Question 9

diaphragm in ventilation

Answer 9

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

Question 10

external intercostal muscles in ventilation

Answer 10

lift ribcage upward and outward to increase thorax volume

Question 11

accessory muscles in ventilation

Answer 11

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

Question 12

internal intercostasl muscles in ventilation

Answer 12

bring ribcage inward and downward to decrease thorax volume

Question 13

upper airway dilating muscles

Answer 13

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

Question 14

nerve roots of spinal cord

Answer 14

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

Question 15

naming of spinal nerves in relationship to vertebral bodies

Answer 15

• 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)

Question 16

Nerve Roots Supplying Respiratory Muscles

Answer 16

diaphragm: C3 - C5
accessory: C1 - C8

intercostal muscles: corresponding nerve root

abdominal muscles of expiration: T7 and below

Question 17

respiratory centers

Answer 17

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

Question 18

cerebral cortex and ventilation

Answer 18

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

Question 19

limbic system and hypothalamus on ventilation

Answer 19

can change breathing via emotions, pain, temperature responses

Question 20

purpose of interspersing occasional, involuntary signs into the breathing pattern

Answer 20

to increase surfactant

Question 21

physiology of restricted thoracic cage

Answer 21

• increased elastive load
• feedback from
  
  • stretch receptors
  • gamma receptors
  • chemoreceptors

Question 22

definition of hyperventilation

Answer 22

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

Question 23

causes of hyperventilation

Answer 23

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

Question 24

definition of Cheyne-Stokes Respirations

Answer 24

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

Question 25

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

Answer 25

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

Question 26

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

Answer 26

demonstrates how responsive a feedback loop is; loop gain = corrective response / disturbance

Question 27

What contributes to loop gain?

Answer 27

* 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

Question 28

how can initiation of sleep trigger cheyne-stokes breathing?

Answer 28

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

Question 29

Why do heart failure patients get CSA?

Answer 29

* 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)

Question 30

changes in ventilation in response to pO2 and pO2 + hypercapnia

Answer 30

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

Question 31

the three physiological changes that occur in sleep

Answer 31

* increased upper airway resistance * decreased chemosensitivity * inhibition of skeletal muscles, especially during REM sleep

Question 32

why does airway resistance increase during sleep?

Answer 32

upper airway dilator muscles lose tone and airway becomes more narrow

Question 33

how is chemosensitivity affected by sleep?

Answer 33

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)

Question 34

types of apnea

Answer 34

* 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

Question 35

most vulnerable location in upper airway to apnea

Answer 35

posterior oropharynx

Question 36

factors that promote airway collapse in upper airway

Answer 36

* negative pressure on inspiration * extralumenal positive pressure, fat deposition, small mandible

Question 37

factors that can lead to decreased airway patency in upper airway

Answer 37

* less contraction of pharyngeal dilator muscle * decreased lung volume --\> longitudinal traction

Question 38

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

Answer 38

this indicates obstructive apnea instead of central apnea

Question 39

looking at brain electrogram during apnea what pattern might you notice

Answer 39

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

Question 40

increased risk factors for sleep apnea

Answer 40

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

Question 41

How is obstructive sleep apnea treated?

Answer 41

* 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)

Question 42

what is a uvulopalatopharyngoplasty (UPPP)

Answer 42

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

Question 43

best treatment for sleep apnea

Answer 43

CPAP (continuous positive airway pressure)

Question 44

what is a tracheostomy and how can it help sleep apnea

Answer 44

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

Question 45

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

Answer 45

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