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PCCM Fellowship > Pulmonary > Flashcards

Pulmonary Flashcards

1
Q

Define ‘Alveolar Ventilation’

A

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

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2
Q

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

A

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.

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3
Q

Relate V/Q ratios to each West Zone

A

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

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4
Q

What 3 ways are CO2 carried in the blood?

A

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

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5
Q

What 3 ways does the body counteract respiratory acidosis?

A
  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

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6
Q

What is the ‘Alveolar Gas Equation’?

A

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)

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7
Q

What shifts the O2 Hb dissociation curve to the Left?

A

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

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8
Q

What shifts the O2 Hb dissociation curve to the Right?

A

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

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9
Q

What is the Bohr effect?

A

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

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10
Q

What is the Haldane effect?

A

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

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11
Q

Define ‘VO2’

A

Oxygen Consumption

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

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12
Q

Define ‘Arterial Oxygen Content’

A

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)
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13
Q

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

A
  1. Hypoventilation
  2. V/Q mismatch - MCC [ >1 = wasted ventilation]
  3. Shunted blood flow = V/Q approaching zero
  4. Diffusion limitation
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14
Q

Define ‘physiological dead space’

A

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
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15
Q

What is the ‘Bohr equation’

A

Calculating physiological dead space:

Vd / Vt = [PaCO2 − EtCO2] / PaCO2

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16
Q

What is the ‘shunt fraction equation’?

A

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

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17
Q

What is the relationship between PaCO2 and change in pH?

A

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

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18
Q

How do you calculate ‘Base Excess’?

A

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

Based off of the Siggaard-Anderson nomogram

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19
Q

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

A

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)

20
Q

Calculate the A-a gradient

A

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

21
Q

Calculate the Oxygenation Index

A

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

Marker of lung injury = injurious therapies / outcome

22
Q

Calculate the P/F ratio

A

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 #)

23
Q

How does Pulse Oximetry work?

A

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

24
Q

What can give false pulse oximetry readings?

A
  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
25
Q

At what SpO2 is pulse oximetry most accurate?

A

> 70% with confidence limits of 2-4%

Interference with hypoperfusion, vasoconstriction, hypothermia, ambient lighting

26
Q

Describe the 2 types of Capnometry

A
  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
27
Q

How do colorimetric capnometers work?

A

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

28
Q

How closely does EtCO2 approximate PaCO2?

A

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

29
Q

Describe the Capnogram Wave Form

A
  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
30
Q

Describe inaccuracies with transcutaneous CO2 monitors

A

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.

31
Q

Define Arterial Oxygen Content (CaO2)

A

Sum of O2 bound to Hb + O2 dissolved in blood

CaO2 = (Hb x 1.34 x SpO2) + (PaO2 x 0.003)

32
Q

Define DO2, VO2 and O2ER

A 
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
33
Q

Describe the carotid and aortic body response to hypoxemia

A

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
34
Q

Define Shunt vs. Dead Space Ventilation

A

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

35
Q

Types of Capnography

A

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

36
Q

Name 5 pulmonary interactions responsible for the pathophysiology of ARDS

A
  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
37
Q

Name inflammatory and anti-inflammatory mediators of ARDS

A

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
38
Q

Describe the 3 phases of ARDS

A
  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)
39
Q

Name 5 lung protective strategies in ARDS

A
  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

40
Q

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

A

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

41
Q

Define ‘Lung Compliance’

A

Change in lung volume per unit change in transmural pressure gradient (i.e. between the alveolus and pleural space)

Compliance = delta V / delta P

42
Q

What is static vs dynamic compliance?

A

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.
43
Q

Define hysteresis and why does it occur?

A

“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
44
Q

Name factors which influence lung compliance

A
  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
45
Q

Where is the highest resistor in the airways?

A

Segmental bronchi - in series

As you go more distally = more branching = in parallel so lower resistance

46
Q

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

A

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

PCCM Fellowship (18 decks)

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