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17 Cards in this Set

  • Front
  • Back
where is the rhythm generator/controller?
in the medulla
Central chemoreceptors
- specialized cells in ventrolateral medulla that respond to pH of CSF
- rapidly stimulates central controller to increase output and increase ventilation
- response decreased w/ drugs and increased w/ hypoxemia
peripheral chemoreceptors respond to?
receptors in lungs/airways
slowly adapt to respond to lung volume
Hering-Breuer reflex
↑ lung inflation inhibits inspiration, but not activated until large volume
Unmyelinated C-fibers
– in airways, they respond to noxious stim (irritant R’s), can -> cough
– in the parenchama, respond to chemical/mechanical stim in interstitium (J-fibers), -> tachypnea
diving reflex
– face in water inhibits insp
- chest wall receptors may alter muscle output to given stimulus from controller
COPD and obesity / hypoventilation syndrome
increased work of breathing may result in inadequate V (inc PaCO2, dec PaO2) despite high “drive”
main causes of hypoxemia
- ↓ drive
– can be neural (Spinal cord injury, polio, ALS)
- Weak muscles
- Increased work of breathing (Stiff lungs or chest wall)
- airway resistance (emphysema, severe asthma)
other causes of hypoxemia
- bad central controller, drugs, alcohol, disease/injury, severe hypoxemia
– Sleep to some extent
- can be from ↑ CC (Drugs, meningitis, stroke)
– cortical (pain, fear, anxiety)
- Periph. chemoreceptors (hypoxemia at altitude)
- Periph & Central receptors (metabolic acidosis)
- Lung/airway receptors (fibrosis, inhaled irritants) can ↑ CC input
Exercise in Normals
- Ventilation ↑ in proportion to ↑ production of CO2
– PaCO2 and pH remain constant until heavy exertion
– PaO2 does not fall so feedback from changes in arterial blood gases is NOT the cause of the ↑ in ventilation, and dyspnea is not caused by hypoxemia
Normal sleep
- no wakefulness stimulus (RAS) on CC -> small ↑ in PaCO2 & variable ↓ PaO2
- increased UAR and decrease in load compensation
central apnea
- resp drive falls below phrenic threshold, diaphragmatic resp effort ceases and a “central” apnea occurs
- rare if no narcotics or Arnold-Chiari malformation
Obstructive Sleep Apnea
- hypoglossal to UA is before phrenic to diaphram
- If UA dilating signal is delayed or weak, (-) P in pharynx during insp -> collapse
- possible b/c Hypoglossal has a higher PCO2 threshold than the phrenic
Anesthesia & Alcohol on OSA
- they depress both phrenic and hypoglossal activity, but the hypoglossal is affected more
- Tx is CPAP via mask is to mainain upper airway
Cheyne-Stokes Respiration
- Oscillatory pattern w/ recurrent central apneas and then gradual ­inc in rate and depth often w/ brief arousal
- associated w/ CHF w/ prolonged circulation time
- low O2 and CO2
- Signal reaches CC late, so PaCO2 rises more than noraml