Lecture 6: Breathing control and sleep apnea Flashcards

1
Q

Dyspnea is the sensation of…

A

A high ventilatory drive

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2
Q

What cell group controls inspiration?

A

Dorsal respiratory group (brainstem)

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3
Q

What does the Pre-Botzinger complex due?

A

Respiratory pace maker

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4
Q

Two broad groups that control ventilatory drive

A

Chemoreceptors and lung receptors

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5
Q

Central chemoreceptors respond to…Where is it?

A

CO2 (measure of low pH) –> breath out; brain side of BBB in medulla

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6
Q

Carotid body and aortic body are termed what kind of chemoreceptors and what do they respond to?

A

Peripheral; O2

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7
Q

What do we do in response to an elevated CO2? What is this called (________ drive)?

A

Increase minute ventilation RAPIDLY; hypercapnic drive

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8
Q

Describe the hypoxic drive

A

Non-linear, small, often no drive untill close to LOC (35 torr)

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9
Q

Is the hypoxic drive clinically relevant?

A

Not really, people can be very hypoxic with little dyspnea

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10
Q

Four types of lung receptors…what do these cause?

A

Stretch (stress in airways), J receptors (stretch in blood vessels), nociceptors (inhale nasty things), chest wall; lead to shortness of breath w/ normal lung gases

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11
Q

Drowsy EEG (awake, drowsy)

A

Alpha waves

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12
Q

Stage 1 EEG

A

Theta waves

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13
Q

Stage 2 EEG

A

Sleep spindles, K complexes (half your night here)

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14
Q

Stage 3 EEG

A

Delta waves (20-25% your night here)

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15
Q

REM sleep

A

Low voltage, like awake

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16
Q

What happens to your CO2 on transition to sleep?

A

Rises (2-6 torr)

17
Q

What happens to breathing in REM?

A

Decreased ventilatory drive, dependence on diaphragmatic function, decreased muscle tone (including breathing muscles)

18
Q

Definition of obstructive sleep apnea and symptoms

A

Respiratory pauses for at least 10 sec, 5+ times per hour of sleep; snoring and sleepiness

19
Q

What is obstructive sleep apnea a risk for?

A

MI, stroke, CHF

20
Q

Causes of ventilatory drive (central) sleep apnea (5)

A

Morbid obesity, Ondine’s Curse (congenital central hypoventilation syndrome), medications (narcotics), brain problem, heart failure

21
Q

Gene of central congenital hypoventilation

A

PHOX2b gene

22
Q

During obstructive sleep apnea, are you trying to breath? Then what’s happening

A

Yes! Upper airways muscles normally contract to keep airway open but sleep –> decreased muscular activity

23
Q

What do we call respiratory pattern in central sleep apnea

A

Cheyne-Stokes Respiration = periodic breathing

24
Q

What happens to our arterial blood gases at end of max exercise?

A

No change

25
Q

Exercise means…

A

Increasing O2 consumption (15 x resting)

26
Q

Equation for O2 consumption…how can we increase this?

A

VO2 = Qt (cardiac output) (CaO2 - CvO2); raise Qt, increase CaO2, reduce CvO2

27
Q

Can we increase CaO2?

A

Not really, only by increasing hemoglobin or arterial oxygen content (but we’re already close to 100%)

28
Q

What do we primarily due during exercise? (3)

A
  1. Increase minute ventilation via respiratory and tidal volume; 2. Improve V/Q matching (zone 1) via increased blood flow; 3. Increase muscle O2 extraction (shunt blood away from other places)
29
Q

What happens to blood pH during exercise?

A

Decreases due to increased CO2 production from lactate metabolism (anaerobic threshold = point when we make lactate, creating CO2, which means we have to breath more)

30
Q

During exercise, how do we increase CO?

A

Acutely –> heart rate, over time –> stroke volume