Week 8 Flashcards

1
Q

central chemoreceptors

A

Very sensitive to pH (CO2 crosses blood brain barrier easily and converts to H+), located in ECF of brain (medulla)
most influential
respond to pH and PCO2 NOT O2

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2
Q

Peripheral chemoreceptors

A

located in carotid and aortic bodies, respond faster but less powerful than central. Respond to PO2 in addition to PCO2 and pH

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3
Q

Lung Receptors (pulmonary stretch)

A

when stretched, they slow down RR (reflex to pause after deep breath)

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4
Q

Lung Receptors (irritant receptors)

A

respond to noxious gases, dust, smoke etc (cough)

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5
Q

Lung receptors (Juxtacapillary J Receptors)

A

respond to increased interstitial fluid (if capillaries are engorged with fluid) send signal to breathe faster

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6
Q

Other Receptors (irritants in nose, pharynx, larynx, trachea)

A

similar to irritants in lung

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7
Q

Other Receptors (joint/muscle receptors in limbs)

A

stimulate ventilation during exercise

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8
Q

Other Receptors (Gamma system)

A

muscle spindles sense how long muscle is and tells how much to contract

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9
Q

Upper airway dilating muscles

A

nasal alas: dilates nasal passages
genioglosus: protrudes tongue
elevator and tensor palatine: elevate/stabilize soft palate
posterior cricoarytenoid muscle: open laryngeal aperture

contracture dilates air passage

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10
Q

C1-C7 come out where

A

above corresponding vertebral body

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11
Q

Innervation of diaphragm

A

C345

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12
Q

Innervation of accessory muscles

A

C1-C8

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13
Q

Innervation of intercostal musscles

A

corresponding nerve root

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14
Q

Innervation of abdominal muscles

A

T7 and below

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15
Q

Phrenic nerve runs between

A

subclavian artery and vein

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16
Q

Spinal cord injury at T7

A

lose abdominal muscles, less strong expiration

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17
Q

spinal cord injury at T6

A

lose abs, and intercostals-still breathe in but expiration is always passive, never forceful

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18
Q

spinal cord injury at T2

A

everything lost, entirely dependent on ventilator

19
Q

Respiratory centers

A

pons and medulla

20
Q

Cerebral cortex in respiration

A

can override function of brainstem within limits

can hold breath, take large breath, hyperventilate

21
Q

limbic system and hypothalamus

A

emotions, pain, temperature all affect breathign

22
Q

Ventilatory control system, conflicting signals

A

At high altitudes, low PaO2, sensed by peripheral chemoreceptors-send signals to respiratory centers to increase breathing and PO2. As consequence, PCO2 decreases (alkalosis). Now central control gets two signals-to breathe more to increase PO2 and to breathe less to decrease pH

23
Q

synergy between hypoxia and hypercarbia

A

in setting of high PCO2, a small amount of hypoxemia (decrease in PO2) causes a larger increase in ventilation

24
Q

Dyspnea and restricted thoracic cage

A

hyperkyphosis: increased elastic load (decreased compliance), get feedback from stretch, gamma, chemoR, lower tidal volume for same decrease in Pip. likely to develop pneumonia

25
dyspnea and obstructive lung disease
Not a problem of elastane/compliance but rather increased resistance. increased physiologic dead space anxiety--hyperinflation hyperinflation puts diaphragm at mechanical disadvantage
26
hyperventilation
an increase in ventilation that is excessive for rate of metabolic carbon dioxide production, resulting in decreased PCO2
27
Causes of hyperventilation
hypoxemia, anxiety, fever, metabolic acidosis, CHF, aspirin, progesterone, pregnancy
28
Cheyne Stokes
cyclic breathing marked by gradual increase in rapidity, followed by gradual decrease and total cessation
29
Loop gain
corrective response/disturbance. smaller is better
30
Contributors to loop gain
``` circulatory time (time it takes from blood to get from the thorax to the chemoreceptors) neurologic disease ```
31
unstable breathing at sleep onset: CO2-apnea threshold
1. stimulating effect of wakefulness, disappears 2. threshold to stimulate breathing of PaCO2 increases 3. ventilation stops right before falling asleep (til PaCO2 gets to above new threshold)
32
HF and CSA
1. longer circulatory time 2. stimulation of J receptors (increases apneic threshold --larger diff between wakeuful PCO2 and sleeping PCO2 3. more prone to hypoxia during sleep onset apnea
33
Physiologic changes in sleep
1. increased upper airway resistance (more narrow bc cave in from lack of tone) 2. decreased chemosenstiivty 3. inhibition of skeletal muscles (esp REM)
34
Chemosenstiivy and CO2 in regular sleep
lower ventilation and higher PaCO2 Lowest/highest in REM In REM, PCO2 can increase and barely increases ventilation (because less chemrsensitivity)
35
Central apnea
No rib cage or abdominal activity-no respiratory effort
36
Obstructive apnea
apnea because airway is occluded | Abdomen and RC are trying to breathe (see muscle activity)
37
mixed apnea
start as central and develop obstructive
38
Obstructive apnea and soft tissue
completely collapsed on itself-loss of tone dilating muscles so no air gets through
39
Posterior Oropharynx
most vulnerable region of airway 1. obesity--extraluminal positive pressure 2. mandible further back-less space for airway 3. full abdomen--push up on airways--lose longitudinal traction and decrease airway patency
40
Arousal follows apnea
brief, 3s increase in amplitude/frequency of waves on EEG
41
RF for apnea
obesity, increase size of upper airway soft tissue, recessed mandible, increased neck >18 in, nasal airway obstruction, heredity
42
Obstructive sleep apnea Tx:
CPAP, weight loss, avoid supine, avoid alcohol, dental appliances, uvulopalatopharyngoplasty (carve out excess tissue), tracheostomy
43
CPAP
generating air pressure to sten open airway, very effective