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62 Cards in this Set

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What is a normal arterial blood gas value for pH?
7.4
7.4
What is a normal arterial blood gas value for PaO2?
80 mmHg
80 mmHg
What is a normal arterial blood gas value for PaCO2
40 mmHg
40 mmHg
What is a normal arterial blood gas value for Bicarbonate?
24 mEq/L
24 mEq/L
What does the term FiO2 stand for? What does this mean clinically?
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
How can you give a patient 100% Oxygen (FiO2 = 1.0)?
Deliver O2 via face mask + reservoir w/ high flow
What receptors respond to a decrease in PaO2 (<80 mmHg)?
Chemoreceptors in CAROTID BODY
Chemoreceptors in CAROTID BODY
What receptors respond to an increase in PaCO2 (>40 mmHg)?
- Chemoreceptors in BRAIN (70%)
- Chemoreceptors in carotid body (30%)
- Chemoreceptors in BRAIN (70%)
- Chemoreceptors in carotid body (30%)
What happens when a low PaO2 (<80 mmHg) is detected in the carotid body?
↑ Ventilation
→ Improves PaO2 + Blow out CO2
→ Lowers PaCO2
→ Increase in pH
↑ Ventilation
→ Improves PaO2 + Blow out CO2
→ Lowers PaCO2
→ Increase in pH
What happens when a high PaCO2 (>40 mmHg) is detected in the brain and carotid body?
↑ Ventilation
→ Blow out CO2
→ Normalizes PaCO2
→ Normalizes pH (previously decreased d/t excess CO2)
↑ Ventilation
→ Blow out CO2
→ Normalizes PaCO2
→ Normalizes pH (previously decreased d/t excess CO2)
What is the relationship between SaO2 and PO2?
- SaO2 = O2 saturation of Hemoglobin 
- PO2 = O2 pressure in mmHg

- Sigmoidal curve
- At 88% saturation, PO2 is 55 mmHg (normal is 80 mmHg)
- SaO2 = O2 saturation of Hemoglobin
- PO2 = O2 pressure in mmHg

- Sigmoidal curve
- At 88% saturation, PO2 is 55 mmHg (normal is 80 mmHg)
What are the signs and symptoms of hypercapnia (>40 mmHg)?
- Morning headaches
- Confusion
- Lethargy / drowsiness / sleepiness
- Flushed skin
- Rapid breathing
- Tremors (flapping)
What is the role of the Carotid Body chemoreceptors?
* Sense dissolved O2 in blood (PaO2)
* Respond to PaO2 < 75 mmHg

- Sense ↑ [H+] / elevated PaCO2 (30% of response)
What is Oxygen Content?
O2 bound to Hb + O2 dissolved in plasma (PaO2)
What are Carotid Body chemoreceptors UNABLE to detect?
- 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+]
What is the role of the Central chemoreceptors?
- Respond to ↑[H+] / ↑PaCO2
- Responsible for ~70% of increased ventilation in response to hypercapnia
What is increased PaCO2 (hypercapnia) responsible for?
Main cause of increased Tidal Volume and increased respiratory rate under normal conditions
What can cause PaCO2 to rise?
- 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
What happens if you have bilateral carotid artery resection?
* 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)
What happens in COPD with CO2 retention?
- Theoretically, w/ CO2 retention, the respiratory drive from hypercapnia is diminished
- They must rely on hypoxemic respiratory drive to breathe faster
- Theoretically, w/ CO2 retention, the respiratory drive from hypercapnia is diminished
- They must rely on hypoxemic respiratory drive to breathe faster
What should you do for a patient w/ COPD and hypoxia?
- 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
What causes the rise in PaCO2 in COPD?
- 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%)
What O2 pressure and saturation should you target?
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
How do O2 and CO2 affect partial pressures?
O2 and CO2 bound to hemoglobin do not contribute to partial pressures, only the free O2 and CO2 contribute to PaO2 and PaCO2
Where are the pulmonary receptors?
- In lung parenchyma (via vagus)
- In chest wall
What kind of receptors are found in the lung parenchyma?
- Slowly adapting receptors
- Rapidly adapting receptors
- Juxtacapillary receptors
What are the features of the slowly adapting receptors?
- 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
What are the features of the rapidly adapting receptors?
- Found in lung parenchyma (carina)
- Irritant receptors - very sensitive to chemical stimuli
- Communicate via vagus nerve
What are the features of the juxtacapillary receptors?
- Found in lung parenchyma (next to capillaries)
- Innervated by vagus
What kind of pulmonary receptors are found in the chest wall?
- Muscle Spindles
- Tendon Organs
What happens in Pickwickian Syndrome?
- 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
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?
All should be normal:
- pH: 7.4
- PaO2: 100 mmHg
- PaCO2: 40 mmHg
How can neuromuscular disease affect respiration?
Can cause respiratory failure d/t muscle weakness (of the inspiratory and expiratory muscles)
What change in vital capacity and maximum inspiratory force indicates the start of respiratory failure?
- Vital capacity falls to <55% of predicted value
- Maximum inspiratory force falls to <30% of predicted value
What are the different patterns of breathing?
- Normal
- Kussmaul's respirations
- Cheyne-Stokes respirations
- Biot's breathing
- Apneustic respirations
- Normal
- Kussmaul's respirations
- Cheyne-Stokes respirations
- Biot's breathing
- Apneustic respirations
What kind of breathing is this?
What kind of breathing is this?
Normal
Normal
What kind of breathing is this? Characteristics?
What kind of breathing is this? Characteristics?
Kussmaul's Respirations:
- Consistently deep and rapid respirations
- Severe metabolic acidosis (eg, diabetic ketoacidosis)
Kussmaul's Respirations:
- Consistently deep and rapid respirations
- Severe metabolic acidosis (eg, diabetic ketoacidosis)
What kind of breathing is this? Characteristics?
What kind of breathing is this? Characteristics?
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 ...
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
What kind of breathing is this?
What kind of breathing is this?
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)
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)
What kind of breathing is this? Characteristics?
What kind of breathing is this? Characteristics?
Apneustic Respirations:
- Prolonged inspiratory phase 
- Followed by a prolonged expiratory phase
- Caused by damage to upper part of pons
Apneustic Respirations:
- Prolonged inspiratory phase
- Followed by a prolonged expiratory phase
- Caused by damage to upper part of pons
Which kind of respirations are associated with severe metabolic acidosis?
Kussmaul's Respirations:
- Consistently deep and rapid respirations
Kussmaul's Respirations:
- Consistently deep and rapid respirations
Which kind of respirations are caused by heart failure, strokes, traumatic brain injuries, brain tumors, and first-time high altitude sickness?
Cheyne-Stokes Respirations:
- Tidal volume starts shallow
- Gets progressively deeper (crescendo)
- Then gets progressively shallower (decrescendo)
Cheyne-Stokes Respirations:
- Tidal volume starts shallow
- Gets progressively deeper (crescendo)
- Then gets progressively shallower (decrescendo)
What are the pre-requisites for Cheyne-Stokes Respirations?
- Increased gain
- Increased circulation time
- Changing state of alertness
- Increased gain
- Increased circulation time
- Changing state of alertness
Which kind of respirations are caused by damage to the upper part of the pons?
Apneustic Respirations
- Prolonged inspiratory phase 
- Followed by a prolonged expiratory phase
- Caused by damage to upper part of pons
Apneustic Respirations
- Prolonged inspiratory phase
- Followed by a prolonged expiratory phase
- Caused by damage to upper part of pons
Which kind of respirations are caused by damage to medulla oblongata such as a stroke (CVA), trauma, or an uncal or tentorial herniation)?
Biot's Breathing:
- Periods or clusters of rapid respirations of near equal depth or VT
- Followed by regular periods of apnea
Biot's Breathing:
- Periods or clusters of rapid respirations of near equal depth or VT
- Followed by regular periods of apnea
What are chemoreceptor neurons?
- Neurons whose discharge rate is altered by changes in PO2 or PCO2 in their environment
- Respiratory chemoreceptors are neurons that alter breathing
What is the location of O2 chemoreceptors?
Carotid Body (also slightly activated by hypercapnia)
What innervates the carotid body?
- Sensory fibers originating from the petrosal ganglion
- Fibers travel through the carotid sinus nerve (a branch of CN IX)
Where is carotid body activity processed?
- Initially processed in the Nucleus Tractus Solitarius (NTS) which projects to multiple sites in brainstem
- Carotid sensory mechanism is within glomus cells
What happens in the carotid sensory mechanism?
- 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
How do PaO2 and PaCO2 interact in the carotid chemoreceptors? What is their impact on impulse frequency in the carotid sinus nerve?
- As PaO2 ↓, impulse frequency ↑ (non-linear relationship)
- As PaCO2 ↑, impulse frequency ↑ (linear relationship)
- As PaO2 ↓, impulse frequency ↑ (non-linear relationship)
- As PaCO2 ↑, impulse frequency ↑ (linear relationship)
What is the effect of surgically denervating the carotid chemoreceptors on resting PaCO2 and CO2 sensitivity?
- 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 da...
- 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
What is the relationship between PaCO2 and ventilation rate? Effect of stimulation of carotid body?
- 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
- 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
What does this graph tell us?
What does this graph tell us?
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...
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
What are the sites of the respiratory chemoreceptors (affect breathing)?
- Pre-Bötzinger Complex
- Retrotrapezoidal Nucleus
- Lateral Parapyramidal Area
- Nucleus Tractus Solitarius
- Pre-Bötzinger Complex
- Retrotrapezoidal Nucleus
- Lateral Parapyramidal Area
- Nucleus Tractus Solitarius
What are the respiratory control functions?
- Rhythm generator
- Pattern generator
- Pre-motor neurons and motor neurons
- Rhythm generator
- Pattern generator
- Pre-motor neurons and motor neurons
What are the sites of non-respiratory chemoreceptors (affect other physiologic functions)? Functions?
- Locus Ceruleus (arousal)
- Pontine Raphe (arousal, anxiety, CV)
- Medullary Raphe (CV, metabolic)
- Fastigial Nucleus (?)
- Medial Parapyramidal Area (CV, metabolic)
- Locus Ceruleus (arousal)
- Pontine Raphe (arousal, anxiety, CV)
- Medullary Raphe (CV, metabolic)
- Fastigial Nucleus (?)
- Medial Parapyramidal Area (CV, metabolic)
The dogma says that the primary drive for breathing is from what? Why?
CO2 chemoreceptors
- Small changes in PaCO2 have much larger effect on breathing than small changes in PaO2
What is the major fast-acting neurotransmitter? Function?
Glutamate - excitatory to post-synaptic neurons and leads to depolarization
What is the action of neuromodulators (as opposed to neurotransmitters)
- 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
What are the major excitatory neuromodulators?
- Serotonin
- ACh
- Substance P
- NE
- Orexin
What are the major inhibitory neuromodulators?
- GABA
- Glycine