Resp 03: Respiratory Centers And Chemoreceptors

Front 1

What is a normal arterial blood gas value for pH?

Back 1

7.4

Front 2

What is a normal arterial blood gas value for PaO2?

Back 2

80 mmHg

Front 3

What is a normal arterial blood gas value for PaCO2

Back 3

40 mmHg

Front 4

What is a normal arterial blood gas value for Bicarbonate?

Back 4

24 mEq/L

Front 5

What does the term FiO2 stand for? What does this mean clinically?

Back 5

Fraction of Inspired Oxygen

Room air:
- 20% of air is O2 → FiO2 = 0.2

Oxygen via nasal cannula:
- Increases flow by 1 L/min increments → increases 4%
- 1 LPM: FiO2 = 0.24
- 2LPM: FiO2 = 0.28
- Etc. but increase in FiO2 stops at 10 LPM, so FiO2 limit is 50-60% w/ nasal cannula

Oxygen via face mask w/ high flow:
- FiO2 = 0.8-0.9

Oxygen via face mask + reservoir w/ high flow:
- FiO2 = 1.0

Front 6

How can you give a patient 100% Oxygen (FiO2 = 1.0)?

Back 6

Deliver O2 via face mask + reservoir w/ high flow

Front 7

What receptors respond to a decrease in PaO2 (<80 mmHg)?

Back 7

Chemoreceptors in CAROTID BODY

Front 8

What receptors respond to an increase in PaCO2 (>40 mmHg)?

Back 8

- Chemoreceptors in BRAIN (70%)
- Chemoreceptors in carotid body (30%)

Front 9

What happens when a low PaO2 (<80 mmHg) is detected in the carotid body?

Back 9

↑ Ventilation
→ Improves PaO2 + Blow out CO2
→ Lowers PaCO2
→ Increase in pH

Front 10

What happens when a high PaCO2 (>40 mmHg) is detected in the brain and carotid body?

Back 10

↑ Ventilation
→ Blow out CO2
→ Normalizes PaCO2
→ Normalizes pH (previously decreased d/t excess CO2)

Front 11

What is the relationship between SaO2 and PO2?

Back 11

- SaO2 = O2 saturation of Hemoglobin
- PO2 = O2 pressure in mmHg

- Sigmoidal curve
- At 88% saturation, PO2 is 55 mmHg (normal is 80 mmHg)

Front 12

What are the signs and symptoms of hypercapnia (>40 mmHg)?

Back 12

- Morning headaches
- Confusion
- Lethargy / drowsiness / sleepiness
- Flushed skin
- Rapid breathing
- Tremors (flapping)

Front 13

What is the role of the Carotid Body chemoreceptors?

Back 13

* Sense dissolved O2 in blood (PaO2)
* Respond to PaO2 < 75 mmHg

- Sense ↑ [H+] / elevated PaCO2 (30% of response)

Front 14

What is Oxygen Content?

Back 14

O2 bound to Hb + O2 dissolved in plasma (PaO2)

Front 15

What are Carotid Body chemoreceptors UNABLE to detect?

Back 15

- Not sensitive to changes in Hemoglobin levels or if Hemoglobin has lost its capacity to carry O2
- Therefore, not sensitive to anemia or CO poisoning

*Only detects ↓PaO2 <75 mmHg (and contribute to resposnse to hypercapnia/↑[H+]

Front 16

What is the role of the Central chemoreceptors?

Back 16

- Respond to ↑[H+] / ↑PaCO2
- Responsible for ~70% of increased ventilation in response to hypercapnia

Front 17

What is increased PaCO2 (hypercapnia) responsible for?

Back 17

Main cause of increased Tidal Volume and increased respiratory rate under normal conditions

Front 18

What can cause PaCO2 to rise?

Back 18

- Increasing oxygenation decreases CO2 carrying capacity of Hemoglobin
- Removal of hypoxemic vasconstriction in lungs, shunts blood to areas where CO2 exchange cannot take place
- Removal of hypoxemic respiratory drive

Front 19

What happens if you have bilateral carotid artery resection?

Back 19

* Almost complete loss of ventilatory response to hypoxia (↓PaO2) (may be some chemoreceptors in aortic bodies?)
- Partial loss (30%) of ventilatory response to hypercapnia (↑PaCO2) (causes PaCO2 to rise 2-4 mmHg (or more in COPD)

Front 20

What happens in COPD with CO2 retention?

Back 20

- Theoretically, w/ CO2 retention, the respiratory drive from hypercapnia is diminished
- They must rely on hypoxemic respiratory drive to breathe faster

Front 21

What should you do for a patient w/ COPD and hypoxia?

Back 21

- Correct hypoxia to a level that supplies enough O2 to the brain (O2 sats >88% sufficient = PaO2 of 55mmHg)
- Do not hold O2 just because CO2 will go up, O2 is essential for life
- DO NOT GIVE EXTRA O2 just to make saturations increase to 100%; this does not improve O2 content of blood

Front 22

What causes the rise in PaCO2 in COPD?

Back 22

- Loss of hypoxemic drive (responsible for 10-20% of level of PaCO2)
- Increasing O2 flow to these patients causes O2 to displace sites on Hb, preventing CO2 from leaving blood (30-40%)
- Ventilation perfusion mismatch (40-50%)

Front 23

What O2 pressure and saturation should you target?

Back 23

PaO2: 55 mmHg
O2 Sat: 88%

If you try to go higher than this you can increase PaCO2; 88% saturation is high enough because this corresponds to the horizontal part of the hemoglobin dissociation curve

Front 24

How do O2 and CO2 affect partial pressures?

Back 24

O2 and CO2 bound to hemoglobin do not contribute to partial pressures, only the free O2 and CO2 contribute to PaO2 and PaCO2

Front 25

Where are the pulmonary receptors?

Back 25

- In lung parenchyma (via vagus)
- In chest wall

Front 26

What kind of receptors are found in the lung parenchyma?

Back 26

- Slowly adapting receptors
- Rapidly adapting receptors
- Juxtacapillary receptors

Front 27

What are the features of the slowly adapting receptors?

Back 27

- Found in lung parenchyma (airway smooth muscle)
- Detects increases in lung volume --> sends signal via vagus to inhibit further inspiration = Hering-Breuer Reflex
- Ultimately, prevents over-inflation of lungs

Front 28

What are the features of the rapidly adapting receptors?

Back 28

- Found in lung parenchyma (carina)
- Irritant receptors - very sensitive to chemical stimuli
- Communicate via vagus nerve

Front 29

What are the features of the juxtacapillary receptors?

Back 29

- Found in lung parenchyma (next to capillaries)
- Innervated by vagus

Front 30

What kind of pulmonary receptors are found in the chest wall?

Back 30

- Muscle Spindles
- Tendon Organs

Front 31

What happens in Pickwickian Syndrome?

Back 31

- Obesity Hyperventilation Syndrome
- Depressed hypercapnic and hypoxic drive
- They have lower tidal volume when compared to person of same height and weight who does not have elevated PO2

Front 32

Case: 24 yo female w/ chronic iron deficiency anemia is admitted for a blood transfusion. Her hemoglobin is 4.0 g/dL. She has no respiratory distress. The resident orders an ABG.
What is the expected pH? paO2? paCO2?

Back 32

All should be normal:
- pH: 7.4
- PaO2: 100 mmHg
- PaCO2: 40 mmHg

Front 33

How can neuromuscular disease affect respiration?

Back 33

Can cause respiratory failure d/t muscle weakness (of the inspiratory and expiratory muscles)

Front 34

What change in vital capacity and maximum inspiratory force indicates the start of respiratory failure?

Back 34

- Vital capacity falls to <55% of predicted value
- Maximum inspiratory force falls to <30% of predicted value

Front 35

What are the different patterns of breathing?

Back 35

- Normal
- Kussmaul's respirations
- Cheyne-Stokes respirations
- Biot's breathing
- Apneustic respirations

Front 36

What kind of breathing is this?

Back 36

Normal

Front 37

What kind of breathing is this? Characteristics?

Back 37

Kussmaul's Respirations:
- Consistently deep and rapid respirations
- Severe metabolic acidosis (eg, diabetic ketoacidosis)

Front 38

What kind of breathing is this? Characteristics?

Back 38

Cheyne-Stokes Respirations:
- Tidal volume starts shallow
- Gets progressively deeper (crescendo)
- Then gets progressively shallower (decrescendo)
- Caused by heart failure, strokes, traumatic brain injuries, brain tumors, or first-time high altitude sickness

Front 39

What kind of breathing is this?

Back 39

Biot's Breathing:
- Periods or clusters of rapid respirations of near equal depth or VT
- Followed by regular periods of apnea
- Caused by damage to medulla oblongata (stroke (CVA), trauma, uncal or tentorial herniation)

Front 40

What kind of breathing is this? Characteristics?

Back 40

Apneustic Respirations:
- Prolonged inspiratory phase
- Followed by a prolonged expiratory phase
- Caused by damage to upper part of pons

Front 41

Which kind of respirations are associated with severe metabolic acidosis?

Back 41

Kussmaul's Respirations:
- Consistently deep and rapid respirations

Front 42

Which kind of respirations are caused by heart failure, strokes, traumatic brain injuries, brain tumors, and first-time high altitude sickness?

Back 42

Cheyne-Stokes Respirations:
- Tidal volume starts shallow
- Gets progressively deeper (crescendo)
- Then gets progressively shallower (decrescendo)

Front 43

What are the pre-requisites for Cheyne-Stokes Respirations?

Back 43

- Increased gain
- Increased circulation time
- Changing state of alertness

Front 44

Which kind of respirations are caused by damage to the upper part of the pons?

Back 44

Apneustic Respirations
- Prolonged inspiratory phase
- Followed by a prolonged expiratory phase
- Caused by damage to upper part of pons

Front 45

Which kind of respirations are caused by damage to medulla oblongata such as a stroke (CVA), trauma, or an uncal or tentorial herniation)?

Back 45

Biot's Breathing:
- Periods or clusters of rapid respirations of near equal depth or VT
- Followed by regular periods of apnea

Front 46

What are chemoreceptor neurons?

Back 46

- Neurons whose discharge rate is altered by changes in PO2 or PCO2 in their environment
- Respiratory chemoreceptors are neurons that alter breathing

Front 47

What is the location of O2 chemoreceptors?

Back 47

Carotid Body (also slightly activated by hypercapnia)

Front 48

What innervates the carotid body?

Back 48

- Sensory fibers originating from the petrosal ganglion
- Fibers travel through the carotid sinus nerve (a branch of CN IX)

Front 49

Where is carotid body activity processed?

Back 49

- Initially processed in the Nucleus Tractus Solitarius (NTS) which projects to multiple sites in brainstem
- Carotid sensory mechanism is within glomus cells

Front 50

What happens in the carotid sensory mechanism?

Back 50

- Occurs in glomus cells
- Changes in conductance of K+ channels
- Changes in intracellular Ca2+ → liberates hormones like serotonin and/or ACh → diffuse to nerve endings → initiate changes in discharge frequency

Front 51

How do PaO2 and PaCO2 interact in the carotid chemoreceptors? What is their impact on impulse frequency in the carotid sinus nerve?

Back 51

- As PaO2 ↓, impulse frequency ↑ (non-linear relationship)
- As PaCO2 ↑, impulse frequency ↑ (linear relationship)

Front 52

What is the effect of surgically denervating the carotid chemoreceptors on resting PaCO2 and CO2 sensitivity?

Back 52

- Results in transient hypoventilation and attenuation of CO2 sensitivity
- After 5 days, recovery from initial effects begins

- Graph: PaCO2 increases initially (carotid chemoreceptors responsible for 1/3 response to hypercapnia), and at 5 days starts to recover to return levels to normal

Front 53

What is the relationship between PaCO2 and ventilation rate? Effect of stimulation of carotid body?

Back 53

- As PaCO2 increases, so does ventilatory rate
- With CB stimulation, there was a greater increase in RR / change in PaCO2
- With CB inhibition, there was almost no change in RR / change in PaCO2

Front 54

What does this graph tell us?

Back 54

Ventilatory intracranial chemoreflex is directly related to the level of carotid chemoreceptor activity

- With CB stimulation, there was a greater increase in RR / change in PaCO2
- With CB inhibition, there was almost no change in RR / change in PaCO2

Front 55

What are the sites of the respiratory chemoreceptors (affect breathing)?

Back 55

- Pre-Bötzinger Complex
- Retrotrapezoidal Nucleus
- Lateral Parapyramidal Area
- Nucleus Tractus Solitarius

Front 56

What are the respiratory control functions?

Back 56

- Rhythm generator
- Pattern generator
- Pre-motor neurons and motor neurons

Front 57

What are the sites of non-respiratory chemoreceptors (affect other physiologic functions)? Functions?

Back 57

- Locus Ceruleus (arousal)
- Pontine Raphe (arousal, anxiety, CV)
- Medullary Raphe (CV, metabolic)
- Fastigial Nucleus (?)
- Medial Parapyramidal Area (CV, metabolic)

Front 58

The dogma says that the primary drive for breathing is from what? Why?

Back 58

CO2 chemoreceptors
- Small changes in PaCO2 have much larger effect on breathing than small changes in PaO2

Front 59

What is the major fast-acting neurotransmitter? Function?

Back 59

Glutamate - excitatory to post-synaptic neurons and leads to depolarization

Front 60

What is the action of neuromodulators (as opposed to neurotransmitters)

Back 60

- Bind to post-synaptic receptors to change the membrane potential to increase or decrease the possibility of eliciting discharge
- Some act as ionotropic receptors and others act as G-protein coupled receptors that initiate a cascade of events that change the excitability of the neurons

Front 61

What are the major excitatory neuromodulators?

Back 61

- Serotonin
- ACh
- Substance P
- NE
- Orexin

Front 62

What are the major inhibitory neuromodulators?

Back 62

- GABA
- Glycine