Pulmonary

Question 1

Define ‘Alveolar Ventilation’

Answer 1

Volume of fresh gas each minute that reaches the alveoli and takes part in gas exchange
- Most important factor in determining PaO2

Question 2

What is ‘Fick’s first law of diffusion’?

Answer 2

Amount of gas diffusing through membrane is directly proportional to surface area available for diffusion, but inversely proportional to the distance it has to diffuse.

Question 3

Relate V/Q ratios to each West Zone

Answer 3

V/Q is highest at lung apex and lower towards base
Zone 1 - PA > Pa > Pv (least amount of blood flow)
Zone 2 - Pa > PA > Pv
Zone 3 - Pa > Pv > PA

A - alveolar; a - arterial; v - venous

Question 4

What 3 ways are CO2 carried in the blood?

Answer 4

5-10% dissolved in blood
5-20% bound to carbamino compounds
Majority exists as H2CO3 [CO2 + H2O ↔ H2CO3 ↔ H+ + HCO3-]

Question 5

What 3 ways does the body counteract respiratory acidosis?

Answer 5

1. Brainstem and carotid body receptors increase minute ventilation
2. Deoxygenated Hb molecules bind H+ and CO2 to form carbaminoHb (buffers pH)
3. Kidneys increase NH4+ excretion (eliminates H+ ions) and Cl- while retaining HCO3- and Na+

Buffer: HCO3 increases by 4mEq/L for every 10mmHg increase in PaCO2

Question 6

What is the ‘Alveolar Gas Equation’?

Answer 6

PAO2 = PiO2 - (PaCO2 / RQ)

PiO2 = (PBarom - PH20) x 0.21 = (760 - 47) x 0.21 = 150mmHg
PaCO2 used bc CO2 is so readily diffusable
RQ = 0.8 (Ratio of CO2 excretion : O2 consumption)

Question 7

What shifts the O2 Hb dissociation curve to the Left?

Answer 7

Decrease in: H+, 2,3 DPG, Temperature, PCO2, HbF

Increase in Hb affinity for O2 = lower P50 - lower PaO2 where 50% of Hb is saturated to O2

Question 8

What shifts the O2 Hb dissociation curve to the Right?

Answer 8

Increase in: H+, 2,3 DPG, Temperature, PCO2

(Decrease in Hb affinity for O2) = higher P50 - higher PaO2 where 50% of Hb is saturated to O2

Note: 2,3 DPG occurs in the presence of hypoxemia. Acid concentration declines with time in stored PRBCs, potentially degrading ability of Tx to release O2 to tissues

Question 9

What is the Bohr effect?

Answer 9

Property of Hb whereby its affinity for O2 changes depending on [H+] or CO2

Inc in either = decreased affinity of Hb for O2, vice versa = alveolar offload to blood or tissues

Question 10

What is the Haldane effect?

Answer 10

Property of Hb whereby deO2 blood has an increased ability to carry CO2, and oxygenated blood has a decreased affinity for H+ and CO2

Question 11

Define ‘VO2’

Answer 11

Oxygen Consumption

Reverse Fick equation: VO2 = (CaO2 - CvO2) x CO x10dL/L

Question 12

Define ‘Arterial Oxygen Content’

Answer 12

CaO2 (mL O2 / dL) = (1.34 x Hb x SaO2) + (0.003 x PaO2)

1. 34 = amount of O2 in ml that a fully saturated g of Hb can carry
2. 003 = solubility coefficient of O2 (of O2 mls in dL of blood for each mmHg partial pressure)

Question 13

What abnormalities of pulmonary gas exchange contribute to arterial hypoxemia? (4)

Answer 13

1. Hypoventilation
2. V/Q mismatch - MCC [ >1 = wasted ventilation]
3. Shunted blood flow = V/Q approaching zero
4. Diffusion limitation

Question 14

Define ‘physiological dead space’

Answer 14

Anatomical + Alveolar dead space

Anatomical = conducting airways (nasopharynx, trachea, subsegmental bronchi, terminal bronchioles) where ~25% of each tidal volume is lost
Alveolar = alveoli not participating in gas exchange due to inadequate perfusion

Question 15

What is the ‘Bohr equation’

Answer 15

Calculating physiological dead space:

Vd / Vt = [PaCO2 − EtCO2] / PaCO2

Question 16

What is the ‘shunt fraction equation’?

Answer 16

Qs /QT = (CcO2 - CaO2) / (CcO2 - CvO2)
Under normal conditions, the percentage of intrapulmonary shunt is less than 10%
If >30%, supplemental O2 won’t help bc shunted blood not coming into contact with enough of high alveolar O2 content

Question 17

What is the relationship between PaCO2 and change in pH?

Answer 17

For every 10mmHg acute change in PaCO2, there is an inverse change of 0.08 pH units

Question 18

How do you calculate ‘Base Excess’?

Answer 18

Approx. Base Excess = -1.2 x ( 24 − measured bicarb)

Based off of the Siggaard-Anderson nomogram

Question 19

What is the relationship between base excess and change in pH?

Answer 19

For every change of 10 mEq/L in base excess, there should be a 0.15 pH unit change
(a pH change of 0.01 = base excess change by 2/3)

Question 20

Calculate the A-a gradient

Answer 20

A - a gradient = PAO2 - PaO2
= [ PiO2 - (PaCO2 / RQ)]−PaO2
= { [ ( PBar - PH2O ) x FiO2 ] - ( PaCO2 / RQ ) } - PaO2

Question 21

Calculate the Oxygenation Index

Answer 21

[ ( MAP x FiO2 ) x 100 ] / PaO2 ; if >40 = consider ECMO

Marker of lung injury = injurious therapies / outcome

Question 22

Calculate the P/F ratio

Answer 22

PaO2 / FiO2
ARDS: < 300 mild, < 200 moderate, < 100 severe
Useful to be used in non-intubated patients, but misleading if using NIPPV (inc MAP will improve #)

Question 23

How does Pulse Oximetry work?

Answer 23

1 - Pulsation of arterial blood attenuates (gradually decreases) light passing through tissues
2 - Degree of attenuation is based on composition of arterial blood

Visible red absorption (660 nm) = oxyHb - changes in this light range reflect oxygenation = algorithms can estimate arterial blood oxygen saturation
Near-infrared (900–940 nm) = deoxyHb - absorption of light here is relatively constant over a wide range of O2 sats

Light absorption of tissues, venous/capillary blood doesn’t change = can be subtracted from total light absorption leaving only absorption of arterial blood

Question 24

What can give false pulse oximetry readings?

Answer 24

1. CarboxyHb - similar light absorption as oxyHb at 660nm = pulse ox over estimates true O2 sat of Hb (also w/ hemolysis bc ++carboxyHb formed)
2. MetHb - pulse ox decreases to ~85%, but bc metHb adsorbs light equally well at 660 and 940 nm, it will overestimate SpO2
3. HbSS alters light absorption, rightward shift of oxyHb curve = SpO2 reading for any give PaO2

Question 25

At what SpO2 is pulse oximetry most accurate?

Answer 25

>70% with confidence limits of 2-4% Interference with hypoperfusion, vasoconstriction, hypothermia, ambient lighting

Question 26

Describe the 2 types of Capnometry

Answer 26

1. Mainstream - in-line with ETT, Infrared light adsorbance detects CO2 - breath to breath 2. Sidestream - use in non-intubated pts - aspirates gas as patient ventilates - may decrease minute ventilation

Question 27

How do colorimetric capnometers work?

Answer 27

CO2 produces H+ ions --> change in pH = colour change Beware if pt drank carbonated beverage, received vigorous BMV, ETT above VC, or in cardiac arrest where there is no lung perfusion

Question 28

How closely does EtCO2 approximate PaCO2?

Answer 28

EtCO2 ~2-5mmHg lower than PaCO2 bc anatomical deadspace ventilation and VQ mismatch in West Zone 1 Alterations in VQ = inaccuracies --> Inc V:Q (PE, LCOS) = underestimation PaCO2 Dec V:Q with pulmonary shunts (atelectasis, mucous plugs) = less underestimation

Question 29

Describe the Capnogram Wave Form

Answer 29

1. Inspiratory baseline - atmospheric air has little CO2 = value of zero 2. Rapid rise in CO2 - Expiration begins and clears anatomic deadspace --> alveolar air rich in CO2 rises 3. Highest value = EtCO2, where CO2 level stabilizes and flattens 4. Inspiration and CO2-free air washes out sensor = level plummets to zero * wider capnogram upslope = slower CO2 removal and inc airway resistance

Question 30

Describe inaccuracies with transcutaneous CO2 monitors

Answer 30

Inaccurate when skin not optimally perfused - edema, acidosis, shock or hypothermia Works by warming skin to promote hyperperfusion = allowing monitors to electrochemically detect O2 and CO2 levels.

Question 31

Define Arterial Oxygen Content (CaO2)

Answer 31

Sum of O2 bound to Hb + O2 dissolved in blood | CaO2 = (Hb x 1.34 x SpO2) + (PaO2 x 0.003)

Question 32

Define DO2, VO2 and O2ER

Answer 32

``` DO2 = supply of oxygen per unit time to a tissue/organ/body DO2 = CaO2 x CO ``` VO2 = Utilization of O2 per unit time by tissue/organ/body ``` O2ER = Fraction of O2 delivered in blood that is actually utilized/consumed by tissue/organ/body O2ER = (CaO2 - CvO2) / CaO2; normal value 0.2-0.3 meaning there's an excess capacity of O2 ```

Question 33

Describe the carotid and aortic body response to hypoxemia

Answer 33

Nerve chemical receptors triggered by PaO2 <60mmHg/SpO2 93%. Signals sent to vasomotor centre of: 1. Brainstem = inc sympathetic tone = inc HR, inc contractility, inc preload by venous constriction = inc CO to inc O2 delivery 2. Respiratory area of medulla = inc minute ventilation, higher PAO2 --> inc arterial O2 content as a result of inc in O2 sat and PaO2

Question 34

Define Shunt vs. Dead Space Ventilation

Answer 34

Shunt perfusion = V/Q <0.8 - Blood adequately gets to alveolus, but not being oxygenated Dead space ventilation = V/Q >0.8 Perfusion not adequate for adequate ventilation

Question 35

Types of Capnography

Answer 35

Mainstream (inline) vs. Sidestream (non ventilated pts) Time-based (EtCO2) Volume-based (volumetric): Looks at total vvolume of gas expired, not only torr amount of CO2

Question 36

Name 5 pulmonary interactions responsible for the pathophysiology of ARDS

Answer 36

1. Starling's Hypothesis: Jv = K(Pc-Pi) - theta(Pic - Pii) 2. Alveolar Surface Tension (Laplace): P = 2T/R - Constant would be 4 if both inner + outer surface of alveolus were in contact with air 3. Lung Compliance: delta V / delta P - Pressure-volume curve less steep than healthy lung 4. Functional Residual Capacity - Volume of gas remaining in lung after normal expiration is reduced in ARDS 5. Intrapulmonary Shunt - Total intrapulm shunt (obstruction of alveolus) won't respond to 100% O2. Must focus on recruiting alveoli instead

Question 37

Name inflammatory and anti-inflammatory mediators of ARDS

Answer 37

Inflamm: - (main mediators) TNF-alpha and IL-1beta released by macrophages --> activates cytokines, ROS, adhesion molecules - IL-6 induces pyrexia (linked to severity) - TGF-beta mediates late tissue fibrosis - PLT-activating factor (PAF) increases vascular permeability Anti-inflamm: - IL-10 - GM-CSF: host defense of lung

Question 38

Describe the 3 phases of ARDS

Answer 38

1. Acute Exudative Phase (7d) - Barrier injury, surfactant deficiency, pulm edema, neutrophil activation, start of hyaline membrane formation 2. Subacute Proliferative Phase (day 7-10) - Fibroblast prolif, hyperplasia type 2 pneumocytes, hyaline membrane organization (steroids may be helpful here) 3. Fibrosis w/ or w/o Recovery (1-3 weeks)

Question 39

Name 5 lung protective strategies in ARDS

Answer 39

1. High PEEP 2. Minimize FiO2 <0.6 3. TV 4-6cc/kg 4. Permissive hypercapnea with pH>7.25 5. Plateau pressure <30cmH2O Other: Conservative fluid management, Tx underlying cause, ?Prone, consider APRV/HFOV/ECMO

Question 40

What are the major groups of respiration for (1) inspiration, (2) expiration and (3) upper airway?

Answer 40

(1) diaphragm (2) lateral intercostals and abdominal muscles (3) bulbar muscles

Question 41

Define 'Lung Compliance'

Answer 41

Change in lung volume per unit change in transmural pressure gradient (i.e. between the alveolus and pleural space) Compliance = delta V / delta P

Question 42

What is static vs dynamic compliance?

Answer 42

Static compliance is change in volume divided by change in pressure, measured in the absence of gas flow. {1/Crs = 1/Cl + 1/Ccw (respiratory system, lung, chest wall)} Dynamic compliance is change in volume divided by change in pressure, measured in the presence of gas flow. - -Dynamic compliance is always lower than static compliance - bc it incorporates airflow resistance + chest wall and lung pressure - -Dynamic compliance decreases with increasing airflow (turbulence) and a faster respiratory cycle.

Question 43

Define hysteresis and why does it occur?

Answer 43

"The energy applied to the lung in inspiration is not recovered in expiration. The property of dissipating energy receives the name of hysteresis." OR "Lung volume at any given pressure during inhalation is less than the lung volume at any given pressure during exhalation" 1. Recruitment and de-recruitment - well inflated alveoli are elastic and require little energy to inflate further 2. Effect of alveolar surface tension - open alveoli = in surface tension and less compliant = deflation curve has lower compliance 3. Stress relaxation - lung stretches, consumes energy, then wastes it on changing shape of collage and elastin fibres instead of storing it for release 4. Gas absorption during measurement

Question 44

Name factors which influence lung compliance

Answer 44

1. Lung volume (affected by PEEP, dynamic hyperinflation, etc) 2. Lung elastic recoil (affected by age and disease states, eg. emphysema reduces it) 3. Chest wall compliance (affected by chest injuries, burns, surgery, eg. open chest) 4. Pulmonary blood volume (a congested lug is less compliant) 5. Dynamic lung compliance is also affected by the respiratory rate 6. Lung surfactant increases lung compliance 7. Posture

Question 45

Where is the highest resistor in the airways?

Answer 45

Segmental bronchi - in series | As you go more distally = more branching = in parallel so lower resistance

Question 46

What is the relationship between pressure and flow if flow is turbulent?

Answer 46

Turbulent flow is non-linear (pressure related to flow rate squared) Laminar flow relationship between pressure and flow is linear with a constant resistance --Laminar flow = pressure related to flow