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Physiology & Anatomy Flashcards

1
Q

Name and define the different lung volumes

A
  1. Tidal volume: volume inspired or expired with each normal breath
  2. Inspiratory reserve volume: volume that can be inspired above the tidal volume
  3. Expiratory reserve volume: volume that can be expired after the expiration of tidal volume
  4. Residual volume: volume that remains in the lung after maximum expiration
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2
Q

Which is the only lung volume that cannot be measured by spirometry?

A

Residual volume

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3
Q

Name and describe the different lung capacities

A
  1. Inspiratory capacity: sum of tidal volume and inspiratory reserve volume
  2. Functional residual capacity: sum of expiratory reserve volume and residual volume
  3. Vital capacity: sum of tidal volume. inspiratory reserve volume and expiratory reserve volume
  4. Total lung capacity: sum of all 4 volumes
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4
Q

Describe the anatomy of the conducting airways as well as the respiratory zone

A

Conducting airways (main bronchial tree): No alveoli, no gas exchange, bulk movement of air coming into respi zone
1. Trachea (cartilaginous rings)
2. Mainstem bronchi
3. Lobar bronchi
4. Segmental, subsegmental bronchi
5. Terminal bronchioles

Respiratory zone - Acinus
1. Respiratory bronchioles (transitional zone)
2. Alveolar ducts & alveolar sacs (gas exchange zone)

*Note that gas moves by bulk flow down a pressure gradient in the conducting airways, and then by diffusion in the respiratory zone

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5
Q

What are the 3 types of dead space and the difference between them?

A

Anatomic dead space: conducting airways (fixed volume) - nose, pharynx, trachea, main bronchi, bronchioles

Alveolar dead space: non functional alveoli (mainly in disease)

Physiologic dead space: anatomic + alveolar dead space (= volume of the respiratory system that does not participate in gas exchange)

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6
Q

What is the equation for physiologic dead space?

A

Vd = Vt x [(PACO2 - PECO2)/PACO2]

PACO2 = PCO2 of alveolar gaz
PECO2 = PCO2 of expired air

-> % dead space can be estimated by (PaCO2-ETCO2)/PaCO2

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7
Q

Define minute ventilation and alveolar ventilation

A

Minute ventilation = RR x Vt

Alveolar ventilation = total volume of air entering gas exchange areas each minute = RR x (Vt – Vd (dead space))

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8
Q

What is the forced expiratory volume (FEV1)

A

It is the volume that can be expired in the first second of a forced maximal expiration (normally 80% of forced vital capacity)

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9
Q

How can obstructive and restrictive diseases affect vital capacity?

A

In normal lungs, 80% of the vital capacity is expired in the first second of forced expiration (FEV1).

Obstructive (asthma, COPD): FEV1 and VC are reduced, but FEV1 more that VC.

Restrictive (fibrosis): FEV1 and VC are reduced, but VC more that FEV1.

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10
Q

What are the muscles of inspiration and expiration?

A

Inspiration:
1. Diaphragm (C7, C6, C5)
2. External intercostal muscles and accessory muscles (used in exercise and resp distress)

Expiration:
* normally passive - elastic recoil (3-5% of total energy)
1. Abdominal & internal intercostal muscles (used in exercise or when airway resistance is increased)

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11
Q

Briefly describe the sympathetic vs parasympathetic control of the airways

A

Sympathetic stimulation via circulating catecholamines –> Beta 2 stimulation –> bronchodilator

Parasympathetic stimulation via vagus nerve & acetylcholine –> bronchoconstriction

  • local parasympathetic stimulation - respiratory irritants, pulmonary micro emboli, low pACo2
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12
Q

What is the central controller of automatic breathing and what are the 3 main groups of neurons?

A

The brainstem - medulla & pons (can be overridden by cortex for voluntary control)

  1. Medullary respiratory center (reticular formation of the medulla beneath the 4th ventricle)
    - Pre-Botzinger complex (rhythm) = Central Pattern Generator
    - Dorsal respiratory group (inspiration/timing)
    - Ventral respiratory group (expiration)
  2. Apneustic center (lower pons)
    - Coordination of speed of inspiration and exhalation
    - can have excitatory effect, prolonging ramp of inspiration from medulla
  3. Pneumotaxic center (upper pons)
    - inhibition of inspiration –> regulates volume and RR (fine-tuning of resp)
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13
Q

Where are the most important central chemoreceptors for ventilation situated? What do they respond to?

A

Ventral surface of the medulla

  • Respond to changes in pH in the CSF (so indirectly to changes in CO2), and less so to changes in CO2 directly

Do NOT respond to changes in O2

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14
Q

How does brain extracellular fluid composition impact ventilation?

A

Central chemoreceptors respond to changes in brain ECF composition –> increase in H+ stimulates ventilation, decrease in H+ inhibits ventilation

CSF is most important controller of brain ECF composition –> blood CO2 diffuses into CSF, liberating H+

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15
Q

What is the normal CSF pH?

How can CSF pH impact ventilation in the face of chronic disease?

A

7.32

CSF has a lower buffering capacity than blood (less protein), therefore, changes in pH are greater and occur more rapidly. In patients with chronic hypercapnia (or obese patients), when CSF pH is displaced over a prolonged period, compensation with HCO3 occurs more rapidly than in blood (renal compensation over 2-3 days) to (almost) normalize pH –> the central chemoreceptors are no longer stimulated -> leads to abnormally low ventilation in the face of high arterial CO2

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16
Q

Where are the peripheral chemoreceptors located?

A

Carotid body, aortic bodies

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17
Q

Which sensors are responsible for changes in ventilation in response to arterial hypoxemia?

A

Peripheral chemoreceptors
- respond to decrease in PO2 (mainly), pH (carotid bodies only) and increase in CO2 (response is less important than that of the central receptors)

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18
Q

Name lung receptors and their effect on ventilation

A
  1. Pulmonary stretch receptors in airway smooth muscles (slowly adapting)
    –> Inhibit inspiration via vagus nerve (Hering–Breuer reflex) in response to distention of the lungs
  2. Irritant receptors between airway epithelial cells (rapidly adapting) –> bronchoconstriction and hypernea via vagus nerve in response to irritants (cigarette smoke, dust, cold air)
  3. J receptors in the alveolar walls close to the capillaires (juxtacapillary, very quick response)
    –> shallow rapid breathing vs apnea in intense stimulations. Respond to chemicals injected into pulmonary circulation and increased interstitial alveolar volume
  4. Bronchial C fibers in the bronchial circulation (quick response)
    –> Rapid shallow breathing, bronchoconstriction & mucus secretion in response to chemicals injected into the bronchial circulation
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19
Q

How can blood pressure affect ventilation?

A

Through stimulation of the aortic and carotid baroreceptors –> increased BP can cause hypoventilation, decreased BP can cause hyperventilation

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20
Q

True or false: the ventilatory response to CO2 is increased if work of breathing is increased.

A

False. It is reduced with more work of breathing

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21
Q

In normal conditions, hypoxemia has a minimal role in evoking ventilation. In which situations does the hypoxic drive become very important?

A

Patients with severe chronic lung disease and chronic CO2 retention

** If O2 is provided to these patients to relieve hypoxemia, ventilation may significantly decrease

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22
Q

What innervates the different muscles involved in breathing?

A

Diaphragme: phrenic nerves (C7-C6-C5 cervical segments)

Intercostal muscles: intercostal nerves from spinal cord at same level (paralysis does not seriously affect breathing)

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23
Q

What are the 3 major intrathoracic pressures?

A
  1. Intraleural pressure
    - Between visceral and parietal pleura
    - At beginning of insp: - 5mmHg
    - At full insp: -7.5 mmHg
  2. Alveolar pressure
    - Inside the alveoli
    - End of inspiration and end of expiration: 0 mmHg
    - Inspiration: - 1 mmHg
    - Expiration: 1 mmHg
  3. Transpulmonary pressure
    - Difference between alveolar pressure and pleural pressure
    - Measure of the elastic forces of the lungs
    - 4mmHg
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24
Q

What is hysteresis?

A

In the pressure volume relationship, the curve that follows the lung on inspiration is different than on expiration.
Lung volume at any given pressure is larger during deflation than inflation (because of the need to overcome surface tension forces during inspiration)

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25
Define compliance
The volume change per unit of time C = change V / change in P Represented by the slope of a PV loop
26
True or false: the lung is less compliant at higher pressures.
True - shown by flattening of the PV curve slope
27
What are the 2 elastic forces that affect compliance?
- lung tissue (30%) - surface tension of fluid that lines the alveoli (60%) * also affected by chest wall
28
Name 4 things that can reduce compliance and 2 things that can increase compliance
Reduced compliance: - Increased fibrous tissue - Unventilated lung (atelectasis) - Alveolar oedema - Increased pulmonary venous pressure Increased compliance: - Normal aging lung - Emphysema
29
Laplace's law
Pressure = (2 x surface tension) / alveolar radius
30
What is surfactant and what is its role?
- Surface active agent in water - Phospholipid (DPPC = dipalmitoyl phosphatidylcholine) that lowers surface tension of the alveolar lining fluid. - Produced by type II alveolar epithelial cells. - Molecules are hydrophobic at one end and hydrophilic at the other --> align along a surface Role: 1. Provide low surface tension within alveoli --> increase lung compliance + reduces work of breathing 2. Provide stability 3. Keep the alveoli dry (normally when alveoli collapse, suck fluid into the space)
31
What is the major component of surfactant?
DPPC - dipalmitoyl phosphatidylcholine which is synthesized in the lung from fatty acids extracted from blood. Fast turnover so may be depleted if blood flow reduced (ie embolism)
32
What are the 3 forces that must be overcome by the work of breathing?
- Compliance work (elastic forces of lungs and chest wall) - Tissue resistance work (viscosity of tissues as they slide over eachother) - Airway resistance
33
Where is airway resistance at its highest in the lungs?
Medium sized bronchi - low resistance in the very small airways due to high number
34
What is normal O2 consumption of the act of breathing vs during activity?
5%-10% vs 30%
35
True or false: Airway resistance is higher at low lung volumes?
True (At higher lung volumes there is more traction on the airways)
36
Difference between ventilation and respiration
Ventilation: movement of gas in and out of the alveoli Respiration: Total process whereby O2 is is supplied and used by the cells, and Co2 is eliminated
37
What is the Bohr equation?
See picture
38
What are the differences between pulmonary circulation and bronchial circulation?
Pulmonary circulation: - Low pressure, high flow - Arises form R heart - Supplies bronchioles to alveoli - 100% of CO - PA carries deoxygenated blood Bronchial circulation: - High pressure, low flow - Arises from aorta - Supplies bronchi to terminal bronchioles + supporting tissue - 1-3% of CO - Shunt deoxygenated to oxygenated (pulmonary vein)
39
What are the mean pressures in the pulmonary artery, pulmonary capillary and pulmonary vein?
Pulmonary artery: 15 mmHg (systolic 25, diastolic 8) Pulmonary capillary: 8mmHg Pulmonary vein: 2mmHg
40
What are the mediators of pulmonary circulation vasoconstriction and vasodilation?
Vasoconstriction: - Histamine - Serotonin - Norepinephrine - (Hypoxia) Vasodilation: - Acetylcholine - Isoproterenol - NO
41
Describe hypoxic pulmonary vasoconstriction
Contraction of smooth muscles in the walls of small arterials in hypoxic regions. Stimulus response curve is not linear. Significant vasoconstriction generally when pAO2 < 70 mmHg Exact mechanism unknown, but increase in cytoplasmic Ca+ concentration = major trigger for smooth muscle contraction. - NO activates cGMP, which inhibits Ca+ channels, preventing intracellular Ca+. NO synthase inhibitors augment hypoxic vasoconstriction - Endothelin-1
42
What are treatment options for hypoxic pulmonary vasoconstriction?
- Oxygen - Vasodilators - Sildenafil - Calcium channel blockers - Inhaled nitric oxide
43
Other than hypoxia, what else can cause a change in pulmonary vascular resistance?
- Increased arterial pressure --> reduced PVR (recruitment and distention of capillaries) - Very high and very low lung volumes --> Increased PVR (effect on alveolar and extra-alveolar vessels) - Vasoconstrictors: serotonine, histamine. Thromboxane A2, endothelin - Vasodilators: NO, phosphodiesterase inhibitors, calcium channel blockers,PGI1
44
What are the 3 zones of the lung in humans and what drives the uneven blood flow between these zones
Uneven distribution of blood flow because of gravity 1. Zone 1 (only in cases of low blood pressure) - apex of the lung --> no flow because alveolar pressure > arterial pressure 2. Zone 2 - mid-heart to apex --> blood flow is determined by difference between alveolar and arterial pressure (Pa > pA > Pv) 3. Zone 3 - base of the lungs --> blood flow is determined by difference between arterial and venous pressure (Pa > pv > PA) * Note that alveolar pressure remains static in all zones
45
Appart from gravity, name other determinants of uneven blood flow in the lungs
- Peripheral vs central regions - Complex and random nature of capillary arrangements - Areas of intrinsic higher resistance -
46
What are the components of hemoglobin?
- Globin subunits (2 alpha and 2 beta polypeptide chains, each have a heme) - Central atom of heme is Fe2+ (Ferrous)​ - O2 binds to Fe2+ in heme - RBCs contain several hundred thousand Hgb molecules ​
47
What is methemoglobin
Hemoglobin where the ferrous iron Fe2+ has been replaced by ferric iron Fe3+ in the heme - cannot bind O2 (+ shifts the dissociation of other hemes to the left so retain O2)
48
What role does PaO2 have in oxygen delivery and give a clinical example to this relevance
Disolved O2 (PaO2) has a minimal impact of total oxygen content of the blood - as seen in the DO2 equation. --> Patients with low PaO2 but high Hb may have better CaO2 than patients with high PaO2 but anemic --> Providing O2 to anemic animals will have minimal impact on O2 content
49
What is hemoglobin p50?
Represents the binding affinity of Hgb to O2 - PaO2 where 50% of Hgb is saturated with O2 (27-31 mmHg in dogs, 34-36 mmHg in cats) Higher p50 = less affinity of Hb to O2 (needs more PaO2 to reach 50%) --> O2-Hgb shifted to the right
50
What is positive cooperativity in hemoglobin
The affinity of Hb for O2 increases each time Hb binds an O2 (ie. the 4th O2 molecule is bound much more easily to the hemoglobin than the 1st one)
51
What shifts O2-Hgb dissociation curve to the right = higher p50 = less Hgb binding affinity to O2?
- Increased temp - Acidosis - 2,3-DPG - Increased CO2 -> increased O2 delivery to tissues
52
What are the 3 ways CO2 is transported in the blood?
1. Disolved (10%) 2. As HCO3 (70%) - HCO3 + H+ --> H2CO3 --> H2O + CO2 3. Carbaminohemoglobin (20%)
53
What is the chloride shift?
As CO2 is converted to HCO3- in the red cell, HCO3- enters the plasma in exchange for Cl-
54
What is the Bohr effect?
Effect of CO2 on the affinity of Hgb for O2 – When PvCO2 levels increase (at the level of the tissues), O2 is displaced from Hgb, increasing download of O2 to the cells When PvCO2 levels decreases (at the level of the lungs), curve shifts to the left --> increased quantity of O2 binding to Hgb
55
What is the Haldane effect?
The effect of changes in oxyhemoglobin (O2) saturation on the affinity of Hgb for CO2​ (deoxyHb can bind more CO2 than oxyHb) - In the tissues --> enhanced ability of Hgb to bind to CO2 as it becomes deoxygenated​ - In the lungs --> binding of O2 with hemoglobin tends to displace CO2 from the blood *Also true for transport of CO2 as HCO3- (not bound to hemoglobin): deoxygenated blood has increased O2 carrying capacity because de-oxygenated Hb is a better proton acceptor
56
Between the Bohr effect and the Haldane effect, which has the most important impact on the transport of its respective molecule?
The Haldane effect for CO2 transport
57
What is the respiratory exchange ratio?
R = rate of CO2 output / rate of oxygen uptake Normal : 0.7-0.8
58
What is 2,3-DPG?
2,3-diphosphoglyceric acid End product of red cell metabolism and assists in unloading of O2 to peripheral tissues. Increased in chronic hypoxia, high altitude, chronic lung disease Can be depleted in stored pRBC --> unloading of O2 is impaired (curve shifted to the left)
59
What enzyme participates in the CO2 / HCO3 reaction in the red cell?
Carbonic anhydrase
60
Henry's law
Partial pressure = concentration of dissolved gas / solubility coefficient ** More soluble = lower partial pressure CO2 is 20X more soluble than O2 and diffuses 20 times as rapidly as O2 for a given pressure diff
61
Fick's law
Factors that affect rate of diffusion of gaz through the respiratory membrane Diffusion rate is proportional to: - Surface area - Partial pressure gradient - Diffusion coefficient of the gas (gas solubility/MW) Diffusion rate is inversly proportional to: - Thickness - MW of the gas
62
Which gases are perfusion limited and which are diffusion limited?
Diffusion limited: - CO - O2 in abnormal conditions (exercise, thickened blood-gas barrier, alveolar hypoxia) - CO2 in very abnormal conditions (thickened blood-gas barrier - but more soluble than O2) Perfusion limited: - NO - O2 in normal conditions - CO2 in normal conditions
63
What are the 5 mechanisms of hypoxemia? Which ones can be reversed with O2 supplementation?
1. Hypoventilation -->responds to O2 2. Low FiO2 --> responds to O2 3. V/Q mismatch --> Low V/Q will respond, 0 V/Q does NOT respond 4. Diffusion limitation --> responds to O2 5. Shunt --> does NOT respond to O2
64
What is the normal anatomical shunt fraction?
2-3% of CO from 1. Bronchial circulation - arises form aorta and drains into pulmonary veins 2. Thebesian vessels - coronary venous blood that drains into left ventricle
65
True or false: in pathological shunt and in V/Q mismatch, hypoxemia is present, but PaCO2 does not rise.
True: chemoreceptors sens elevation in PCO2 of shunted blood and increase ventilation to normalize CO2
66
Of the 5 causes of hypoxemia, which ones have a normal A-a gradient?
- Low FiO2 - Hypoventilation
67
Of the 5 causes of hypoxemia, which ones have an abnormal A-a gradient?
- Diffusion impairment - Shunt - V/Q mismatch
68
True or false? Incerasing ventilation in patients with V/Q mismatch will improve CO2 and O2 to the same degree?
False - ventilation is much more effective at decreasing CO2 than it is at increasing O2 --> ue to their different dissociation curves (CO2 is steeper)
69
Amongst the 5 cases of hypoxemia, which are the 2 main mechanisms for hypercapnia?
- Hypoventilation - High V/Q
70
At high altitudes, hypoxemia stimulates peripheral chemoreceptors --> hyperventilation --> respiratory alkalosis. What drug can be used to treat this alkalosis?
Acetazolamide (carbonic anhydrase inhibitor)
71
Name a few drugs that can cause respiratory depression and some that can cause respiratory stimulation
Respiratory depression: - General anesthetic agents - Benzodiazepines - Opiods Respiratory stimulation - Doxapram - Theophylline - Caffeine - Progesterone
72
In which zone of the lungs is compliance the highest (in a standing human)? In which zone is VQ the highest
Compliance is highest in zone 3 (= the base) due to gravitational effects (intrapleural pressure is less negative so resting volume is higher so lungs inflate less on inspiration) VQ is still higher in zone 1 (apex) because blood flow is decreased in zone 1 (and more affected by gravitational effects than ventilation)
73
Define dead space. What is normal dead space for a dog?
Dead space = the portion of tidal volume that does not contribute to gas exchange ~ 6 mL/kg (vs human is 2 mL/kg)
74
What is the diameter of pulmonary capillaries
7-10 um (pretty much the diameter of a RBC)
75
How long does a RBC spend in pulmonary capillaries? How long does it take for Hb to be saturated in O2?
RBC spends 0.75 sec in capillary and Hb is saturated in 1/3 of that
76
How does pulmonary vascular resistance changes with lung volume
- Alveolar vessels are exposed to alveolar pressure -> their resistance increases when lung volume increases - Extra-alveolar vessels are pulled open by the radial traction of surrounding parenchyma -> their resistance decreases when lung volume increases
77
What is the O2 capacity
It is the maximum amount of O2 that Hb could bind if all the binding sites were occupied by O2 Should be 1.39 mL O2 per g of Hb (but in practice 1.34 because of the presence of CO)
78
Why does an increase in ventilation will decrease pCO2 but minimally affect pO2 in VQ mismatch
The CO2 dissociation curve is steeper than the O2 dissociation curve (for levels of PO2 found in the lungs which is the flat upper portion of the curve) -> minimal changes in alveolar PCO2 will affect blood CO2 concentration but not blood O2 concentration
79
Fill the table (PAO2, PACO2, PaO2, PaCO2, CaO2, SaO2, PvO2, CvO2 for hypoventilation / diffusion impairment / shunt / VQ mismatch / anemia / CO poisoning / cyanide poisoning)
See picture
80
What determines if a flow is laminar or turbulent
Reynolds number, which is proportional to velocity, density, radius, and inversely proportional to viscosity Turbulence likely when Reynolds number > 2000 in straight tubes
81
What if the formula for airway resistance
(Pressure at the mouth - alveolar pressure) / air flow rate
82
Name bronchoconstrictors and bronchodilators
Bronchoconstrictors: - Histamine - Acetylcholine (parasympathetic activity) Bronchodilators: - Epinephrine +/- norepinephrine - Isoproterenol - Salbutamol, terbutaline - Theophylline
83
What are the 2 types of resistance that need to be overcome with work of breathing
- Tissue resistance (20%) - Airway resistance (80%) -> total is "pulmonary resistance"
84
What are the sensors involved in regulation of breathing
1. Chemoreceptors: - Central chemoreceptors (near medulla) - Peripheral chemoreceptors (carotid bodies and aortic bodies) 2. Lung receptors: - Pulmonary stretch receptors - Irritant receptors - J receptors - Bronchial C fibers 3. Others - Nose and upper airway receptors - Joint and muscle receptors - Gamma system (stretch receptors in intercostal muscles and diaphragm) - Arterial baroreceptors - Pain and temperature receptors
85
Which chemoreceptors have the strongest response to a change in CO2? Which respond the fastest?
Peripheral chemoreceptors respond faster but only account for 20% of the ventilatory response (central chemoreceptors do 80%)
86
What factors influence ventilatory response to CO2 changes
- PO2: hypoxemia markedly increases ventilatory response to CO2 (lower threshold and steeper curve) - Age (decreases response) - Drugs eg. opioids (decrease response) - Sleep (decreases response) - Chronic hypercapnia (decreases response)
87
What is PAO2 / PACO2 in a normal / non-ventilated / non-perfused alveolus? What is PO2 / PCO2 in the corresponding capillary?
See picture
88
What is the time constant and what are its determinants? What disease causes a long time constant?
It is the time point at which 63% of the lung is deflated in expiration or inflated in inspiration (4-5 time constants are required to have complete inhalation / exhalation). It is resistance * compliance COPD causes a long time constant
89
Name excitatory and inhibitory neurotransmitters present in the central pattern generator = Pre-Botzinger complex
Excitatory: glutamate Inhibitory: GABA and glycine
90
What degree of hypoxemia is required to cause significant hyperventilation
PaO2 < 50-60 mHg (if CO2 is elevated, ventilation will increase earlier with hypoxemia)
91
What is the composition of alveolar gas (in a normally perfused and ventilated alveolus, at equilibrium)
- PAO2 100 mmHg - PACO2 40 mmHg - PAH2O 47 mmHg - PAN2 560 mmHg
92
Describe the anatomy of the larynx
- Arytenoid cartilage -> corniculate tubercle, cuneiform tubercle - Epiglottis - Vocal folds (laryngeal saccules are just before the vocal folds, not visible if not everted) - Cricoid cartilage
93
Name defenses of the respiratory system against pathogens
- Mucociliary apparatus (mechanical action + enzymes + IgA) - Cough reflex - Phagocytic dendritic cells in the mucosa - Anatomic barriers (nose)
94
What does alveolar drainage rely on
Na transporters at the apical membrane of alveolar epithelial cells, with Na/K ATPase at the basolateral membrane -> reabsorption of Na from alveoli into interstitium Cl follows through cystic fibrosis channels Water follows through aquaporins / paracellular route
95
What is the most accurate way to estimate venous admixture?
Shunt calculation: Qs/Qt = (CcO2-CaO2) / (AcO2 -CvO2) Qs = shunt fraction Qt = cardiac output Qs/Qt = venous admixture expressed as a percent of CO CcO2 = O2 content of end-capillary blood CvO2 = O2 content of mixed venous blood
96
What is the PO2 for an SO2 of 50% / 75% / 90% / 95% / 97% / 100%
- SO2 50% -> PO2 26.6 mmHg (p50) - SO2 75% -> PO2 40 mmHg (same as mixed venous blood) - SO2 90% -> PO2 60 mmHg - SO2 95% -> PO2 80 mmHg - SO2 97% -> PO2 100 mHg - SO2 100% -> PO2 > 100 mmHg
97
What are the wavelengths used by pulse oximeters
- Red: 660 nm - Infrared: 940 nm
98
What is the A-a gradient, how is it calculated, what is a normal value?
- A-a gradient is the difference between alveolar and arterial O2 - Abnormal gradient is the hallmark of poor O2 exchange - Can only be used when on room air at sea level - Normal value < 10mmHg A-a gradient = PAO2 - PaO2 PAO2 = [FiO2 x (Pb-Pwater vapor) - (PACO2/R)] = [0.21 x (760-47) - (PACO2/R)] = 150 - (PACO2/R) A-a gradient = [150 - (PACO2/R)] = PaO2 * R = respiratory coefficient - normal 0.8
99
What is the PaCO2 + PaO2 added value
PaCO2 + PaO2 should be around 120 mmHg. If a patient is hypoxemic with PaCO2 + PaO2 lower than 120, it indicates that the hypoxemia is not only due to hypoventilation (some type of venous admixture). Only true at FiO2 21% at sea level!
100
What is the oxygenation index
OI = 100 * (MaP * FIO2)/PaO2 Where MaP = mean airway pressure Lower number indicates better lung function Can use oxygen saturation index where PaO2 is replaced by SpO2

Respiratory (5 decks)

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