Control of Ventilation Flashcards
peripheral chemoreceptors of ventilation
- 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
central chemoreceptors of ventilation
- 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
lung receptors
- embedded in lung tissue
- types
- pulmonary stretch receptors
- irritant receptors
- juxtacapillary (J) receptors
Pulmonary Stretch Receptor
- 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
Irritant Receptors in ventilation
- in lungs, nose, pharynx, larynx, trachea
- responds to noxious gases, dusts, cigarette smoke, cold air
- reflex is to cough, hold breath
Juxtacapillary Receptors (J receptors)
- respond to increased interstitial fluid
- sends signals to increase respiratory rate
Joint/Muscle Receptors in Limbs in ventilation
- movement stimulates increased ventilation in exercise
- faster response to the demand of exercise than if just depending on chemoreceptors
Gamma System in ventilation
- 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
diaphragm in ventilation
dome-shaped muscle that flattens when contracting which increases volume of thorax space for lungs to expand
external intercostal muscles in ventilation
lift ribcage upward and outward to increase thorax volume
accessory muscles in ventilation
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
internal intercostasl muscles in ventilation
bring ribcage inward and downward to decrease thorax volume
upper airway dilating muscles
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
nerve roots of spinal cord
inital segment of nerve as they come off spinal cord; come together to form spinal cord
naming of spinal nerves in relationship to vertebral bodies
- 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)
Nerve Roots Supplying Respiratory Muscles
diaphragm: C3 - C5
accessory: C1 - C8
intercostal muscles: corresponding nerve root
abdominal muscles of expiration: T7 and below
respiratory centers
groups of neurons in brainstem responsible for basic rhythm of expiration; some in medulla and some in pons
cerebral cortex and ventilation
can override breathing function of brainstem; examples are when we want to take a deeper breath to blow on something or hold our breath
limbic system and hypothalamus on ventilation
can change breathing via emotions, pain, temperature responses
purpose of interspersing occasional, involuntary signs into the breathing pattern
to increase surfactant
physiology of restricted thoracic cage
- increased elastive load
- feedback from
- stretch receptors
- gamma receptors
- chemoreceptors
definition of hyperventilation
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
causes of hyperventilation
- Hypoxemia (altitude, disease states)
- Anxiety
- Fever
- Metabolic acidosis
- Congestive heart failure
- Drugs (aspirin, progesterone)
- Pregnancy
definition of Cheyne-Stokes Respirations
cyclic breathing marked by a gradual increase in the rapidity of respiration followed by a gradual decrease and then total cessation
why is there a delay between SaO2 and apnea in cheyn-stokes breathing?
SaO2 is being measured with a oximeter on finger; takes time for the blood that experience the apnea to get to the finger
what is a loop gain and what’s the equation for it
demonstrates how responsive a feedback loop is;
loop gain = corrective response / disturbance
What contributes to loop gain?
- 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
how can initiation of sleep trigger cheyne-stokes breathing?
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
Why do heart failure patients get CSA?
- 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)
changes in ventilation in response to pO2 and pO2 + hypercapnia
hypoxemia has a great increase in ventilation but is even more pronounced if there is also hypercapnia; synergistic relationship
the three physiological changes that occur in sleep
- increased upper airway resistance
- decreased chemosensitivity
- inhibition of skeletal muscles, especially during REM sleep
why does airway resistance increase during sleep?
upper airway dilator muscles lose tone and airway becomes more narrow
how is chemosensitivity affected by sleep?
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)
types of apnea
- 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
most vulnerable location in upper airway to apnea
posterior oropharynx
factors that promote airway collapse in upper airway
- negative pressure on inspiration
- extralumenal positive pressure, fat deposition, small mandible
factors that can lead to decreased airway patency in upper airway
- less contraction of pharyngeal dilator muscle
- decreased lung volume –> longitudinal traction
if there is any effort demonstrated during apnea what does this indicate?
this indicates obstructive apnea instead of central apnea
looking at brain electrogram during apnea what pattern might you notice
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
increased risk factors for sleep apnea
- Obesity- increased visceral fat
- Increased size of upper airway soft tissue structures
- Recessed mandible
- Increased neck size (> 18”)
- Nasal airway obstruction
- Heredity
How is obstructive sleep apnea treated?
- 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)
what is a uvulopalatopharyngoplasty (UPPP)
srugery to carve out excess tissue in the treat; can be used to help treat sleep apnea
best treatment for sleep apnea
CPAP (continuous positive airway pressure)
what is a tracheostomy and how can it help sleep apnea
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
at what point in sleep cycle is apnea most likely to occur?
during REM – muscles and the most atonic meaning more likely for airway collapse; body is the least chemosensitive during REM
