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Platelet and Bleeding Disorders > Week 8 > Flashcards

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
Q

dyspnea and obstructive lung disease

A

Not a problem of elastane/compliance but rather increased resistance.
increased physiologic dead space
anxiety–hyperinflation
hyperinflation puts diaphragm at mechanical disadvantage

26
Q

hyperventilation

A

an increase in ventilation that is excessive for rate of metabolic carbon dioxide production, resulting in decreased PCO2

27
Q

Causes of hyperventilation

A

hypoxemia, anxiety, fever, metabolic acidosis, CHF, aspirin, progesterone, pregnancy

28
Q

Cheyne Stokes

A

cyclic breathing marked by gradual increase in rapidity, followed by gradual decrease and total cessation

29
Q

Loop gain

A

corrective response/disturbance. smaller is better

30
Q

Contributors to loop gain

A 
circulatory time (time it takes from blood to get from the thorax to the chemoreceptors)
neurologic disease
31
Q

unstable breathing at sleep onset: CO2-apnea threshold

A
  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
Q

HF and CSA

A
  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
Q

Physiologic changes in sleep

A
  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
Q

Chemosenstiivy and CO2 in regular sleep

A

lower ventilation and higher PaCO2
Lowest/highest in REM
In REM, PCO2 can increase and barely increases ventilation (because less chemrsensitivity)

35
Q

Central apnea

A

No rib cage or abdominal activity-no respiratory effort

36
Q

Obstructive apnea

A

apnea because airway is occluded

Abdomen and RC are trying to breathe (see muscle activity)

37
Q

mixed apnea

A

start as central and develop obstructive

38
Q

Obstructive apnea and soft tissue

A

completely collapsed on itself-loss of tone dilating muscles so no air gets through

39
Q

Posterior Oropharynx

A

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
Q

Arousal follows apnea

A

brief, 3s increase in amplitude/frequency of waves on EEG

41
Q

RF for apnea

A

obesity, increase size of upper airway soft tissue, recessed mandible, increased neck >18 in, nasal airway obstruction, heredity

42
Q

Obstructive sleep apnea Tx:

A

CPAP, weight loss, avoid supine, avoid alcohol, dental appliances, uvulopalatopharyngoplasty (carve out excess tissue), tracheostomy

43
Q

CPAP

A

generating air pressure to sten open airway, very effective

Platelet and Bleeding Disorders (4 decks)

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