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Pulm > Lec 6 Control of breathing > Flashcards

Lec 6 Control of breathing Flashcards

1
Q

The most important stimulus for ventilatory drive is:
A) Oxygen saturation
B) Pa O2
C) Pa CO2

A

C) PaCO2

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2
Q

At maximal levels of exercise:

A) arterial blood gases show elevated PaCO2

B) arterial blood gases show reduced PaO2

C) arterial blood gases show normal PaCO2 and PaO2

A

C) arterial blood gases show normal PaCO2 and PaO2

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3
Q 
Assuming a reasonable number of hours of sleep, the most common reason to be sleepy during the day is
A) Obstructive Sleep Apnea
B) Central Sleep Apnea
C) Depression
D) Narcolepsy
A

A) Obstructive Sleep Apnea

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4
Q

Normal PaO2?

A

90-100

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5
Q

Normal PaCO2?

A

40

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6
Q

Normal pH?

A

7.4

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7
Q

paCO2 if you

  • hold your breath?
  • fall asleep?
  • exercise?
  • hyperventilate?
A

hold breath: 55

fall asleep: 45

exercise: 40
hyperventilate: 20

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8
Q

What generally happens in respiration?

A
  • brain signals phrenic nerve to send signals to inspiratory [mostly diaphragm] muscles –> causes diaphragm to contract and pull down leading to inspiration
  • expiration is passive
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9
Q

Where are the centers that initiate breathing located?

A

in medulla beneath floor of 4th ventricle

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10
Q

Where is the dorsal respiratory group located? action?

A
  • in nucleus tractus solitarius
  • mostly inspiratory neurons
  • receive afferents from CN9 and CN10
  • main site for driving phrenic nerve
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11
Q

What is the ventral respiratory group? action?

A
  • contains inspiratory and expiratory neurons

- main respiratory pacemaker

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12
Q

What is the apneustic center?

A

in the pons = site of neurons which normally turn off inspiration

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13
Q

What sets normal respiratory rhythm?

step1

A

pre-botzinger complex in the VRG [ventral respiratory group] of medulla

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14
Q

What is the pneumotaxic center?

A

in pons; modulates apneustic center

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15
Q

What are main afferents to central respiratory center?

step1

A

CN 9 (glossopharyngeal) and CN 10 (vagus)

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16
Q

Where are central chemoreceptors? action?

step1

A
  • near surface of medulla
  • on brain side of blood brain barrier
  • stimulated by change in pCO2 [directly measures pCO2/pH of blood interstitial fluid which is influence by arterial CO2]
  • quicker response to respiratory acidosis than metabolic acidosis b/c CO2 can diffuse across BBB and H+ cant
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17
Q

Where are the peripheral chemoreceptors? what stimulates them?

step1

A
  • carotid and aortic bodies = between external/internal carotid branch and on top of aortic arch
  • mostly respond to pO2 < 60
    also respond to
  • high PCO2
  • low pH
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18
Q

What are steps of baroreceptor reflex in hypotension?

step1

A

hypotension –> decrease arterial P –> decrease stretch –> decrease afferent baroreceptor firing –> increase efferent sympathetic and decrease efferent parasympathetic –> vasoconstriction, increase HR, increase contractility, increase BP

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19
Q

Does baroreceptor fire more with hypotension or hypertension?

step1

A

fires more with hypotension

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20
Q

Does signal to increase ventilation in response to chemoreceptors cause greater increase in rate or tidal volume?

A

greater increase in tidal volume

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21
Q

What is the slope of hypercapnic ventilation drive?

A

2 L/min/torr

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22
Q

What happens minute ventilation in person if PCO2 increase from normal 40 to 43?

A

hypercapnic drive = 2 L/min/torr
so if we increase by 3 torr –> increase ventilation rate by 6 L/min

normal = 6 L /min so we can more than double minute ventilation

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23
Q

IF someone who looks comfortable has a PCO2 of 45 what should you think?

A

they must have a chronic pulmonary problem

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24
Q

What is normal minute ventilation?

A

5-6

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25
Q

What happens to hypercapnic drive in response to hypoxemia?

A

in hypoxia hypercapnic drive increases = we are more sensitive to PCO2 when we don’t have enough O2

26
Q

What happens to ventilation drive with hypoxia?

A

very little change in ventilation with decreased PO2 until you reach ~ 60 torr then exponential increase with further hypoxia

27
Q

At what PO2 do you lose consciousness?

A

35 torr

28
Q

What happens if you plot O2 sat vs ventilation rate [rather than PO2 vs ventilation]?

A

relationship is linear

–> increase ventilation wen decrease O2 sat

29
Q

Do peripheral chemoreceptors respond to O2 sat or PO2?

A

PO2

30
Q

What symptoms if you are hypoxic?

A

may be asymptomatic; not uncommon to be hypoxic with little or no dyspnea

31
Q

What are the types of lung receptors?

A
  • stretch receptors = increase firing with inflation of lung
  • J receptors = next to capillaries; respond to inflammation or fluid in interstitium by increasing rate
  • nociceptors = respond to chemicals/smoke/dust to stimulate ventilation by increasing resp frequency
  • chest wall receptors = in muscle of chest wall; feedback to respiratory centers about work of breathing
32
Q

What is the definition of hypoventilation?

A

elevated PCO2

33
Q

What is can’t do vs won’t do hypoventilation?

A

can’t do = decreased pulmonary function from bad lungs or muscle

won’t do = decreased ventilatory drive from drugs/meds, sleep related, or ondine’s curse

34
Q

What are the 3 stages of non-rem sleep?

A

stage 1 = light sleep, easily arousable
stage 2 = deeper sleep, about 50% of the time
stage 3 = slow wave or delta sleep = most refreshing

35
Q

What kind of sleep decreases most with age?

A

stage 3 sleep

36
Q

What is cheyne-stokes respiration?

A

specific pattern of periodic breathing seen mostly in sleep

respiration waxes/wanes with period of apnea betwen cycles

seen with neurologic disease or CHF

its a feedback control problem related to circulation time = like delayed thermostat

37
Q

What is REM sleep?

A
  • brain is active, muscles nearly paralyzed including respiratory muscles
  • most cardiac and respiratory instability
38
Q

What happens to PCO2 in sleep?

A

rises 2-6 torr

39
Q

What is breathing like in stage 3 [slow wave] sleep?

A
  • very regular breathing and HR

body on autopilot

40
Q

What happens to breathing in REM sleep

A
  • decrease in ventilatory drive
  • greater dependence on diaphragmatic function
  • decreased muscle tone

–> if you are dependent on muscle tone you will get problems here; if you die in your sleep most likely REM

41
Q

What is obstructive sleep apnea?

A
  • sleep apnea cause by diminished diameter of airway
  • decreased muscular activity + supine posture creates obstruction
    you keep trying to breath but you cant

have really loud snoring

42
Q

What is sleep apnea?

A

repeated cessation of breathing for > 10 seconds during sleep 5 or more times / hr

43
Q

Who most commonly gets obstructive sleep apnea?

A
  • obese

- those with family hisotry

44
Q

Is obstructive or central sleep apnea more common?

A

obstructive

45
Q

What causes central sleep apnea?

A

obesity or ondines curse

46
Q

What is ondine’s curse?

A
  • congenital central hypoventilation syndrome
  • due to defect in PHOX2b gene
  • causes central sleep apnea
47
Q

What is mild vs moderate vs severe sleep apnea?

A 
mild = 5-15 times /hr sleep stop breathing
moderate = 15-30 times / hr
severe = > 30 times / hr
48
Q

Sleep apnea puts you at risk for what diseases?

step1

A
  • coronary artery disease
  • stroke
  • CHF
  • systemic/pulp HTN
  • arrhythmias [AFib/flutter]
  • sudden death
49
Q

What are signs/symptoms of sleep apnea?

A
  • snoring

- daytime sleepiness

50
Q

How does exercise change ox cunsumption?

A
  • increases ox consumption
  • increases minute ventilation
  • arterial blood gases unchanges
51
Q

What is respiratory system response to exercise?

step1

A
  • increase CO2 production
  • increase O2 consumption
  • increase ventilation to meat O2 demand
  • increase pulm blood flow to increase CO
  • decrease pH during strenuous exercise
  • no change PaO2 and PaCO2 but increase in venous CO2 and decrease venous O2
52
Q

What happens to O2/CO2 in arteries in exercise? what about in veins?

step1

A
  • no change PaO2 and PaCO2

- increase in venous CO2 and decrease venous O2

53
Q

What is fick principle equation?

A

Qt [CO] = VO2 / (CaO2 - CvO2)

= ox consumption / (arterial O2 - venous O2)

54
Q

What is the equation for CaO2 oxygen content?

step1

A

CaO2 = 1.34 * Hb * SaO2 + 0.003 * PaO2

SaO2 = usually closet to 1
PaO2 = usually 100
55
Q

How does minute ventilation change in exercise?

A

Ve = Vt * frequency

  • increase tidal volume and frequency
56
Q

What is the anaerobic threshold?

A

threshold of exercise [oxygen uptake] after which you start building up lactate = function of how good your heart is [not your lungs]

usually about 40% of your max oxygen uptake

57
Q

How do you increase muscle oxygen extraction in exercise?

A
  • shunt blood from other organs [at rest muscles = 20% of CO; in max exercise 80%]
  • increase CO
58
Q

What is limiting factor on exercise?

A

mostly limited by CO not by lungs

59
Q

What happens to O2 hemoglobin dissociation curve in exercise?

A

shifts to the right –> hemoglobin decrease affinity; increase P50

60
Q

What are the risk factors for obstructive sleep apnea?

A
  • obesity
  • crowded upper airway
  • male
  • advanced age
  • family history
  • drugs and meds
  • HTN and AFib
61
Q

What is obesity hypoventilation syndrome?

A
  • morbid obesity (BMI > 30) –> hypoventilation –> decrease PaO2 and increase PaCO2 during waking hours

hypoventilation during sleep without much apnea; particularly occurs in REM sleep

62
Q

What is treatment for sleep apnea?

A

CPAP, surgery, weight loss

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