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Respirology > Pulmonary Physiology (Raf) > Flashcards

Pulmonary Physiology (Raf) Flashcards

1
Q

How much compensation is expected for primary metabolic or respiratory acid/base disorder?

A

(NEJM 2014 article)

If there is a primary metabolic problem, the extent of PaCO2 compensation should be:

  • Acidosis: PaCO2 = 1.5 (HCO3) + 8 (+/- 2)
  • Alkalosis: PaCO2 = (HCO3 - 24)(0.7) + 40 (+/- 2)
  • Lung adapts faster than kidney so the adaptive is completed in 12-36 hours, so there is no differentiation between acute and chronic

If there is a primary respiratory problem, the extent of HCO3 compensation is:
* Acidosis, acute: HCO3 increases by 1, for every 10 point increase in PaCO2 above 40
* Alkalosis, acute: HCO3 decreases by 2, for every 10 point decrease in PaCO2 below 40
* Acidosis or alkalosis, chronic: HCO3 changes by 4-5, for every 10 point change in PacO2 above/below 40
(Memory trick: 1, 2, 4 for acute acidosis, acute alkalosis, chronic for either acidosis/alkalosis)

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2
Q

What is normal tidal volume in an adult and a child?

A

Adult 500 mL

Child: about 10 mL/kg (double check), be we usually ventilate at a lower volume of 5-8 mL/kg

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3
Q

What is normal anatomic dead space volume?

A

150 mL

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4
Q

Describe TAPVR

What is the mechanism of hypoxemia

A
  • No direct connection of pulmonary veins to left atrium
  • Pulmonary veins connect with right sided circulation either above or below diaphragm
  • RA and RV tend to larger, LA and LV tend to be smaller
  • Mixing of oxy with deoxy blood–>shunt
  • Blood goes systemic through a conenction like ASD, PFO or PDA
  • Presentation depends on if obstruction–>pulmonary edema, pulmonary hypertension
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5
Q

What is the main muscle of inspiration? what happens when one side of this muscle is paralyzed?

A
  • Diaphragm

- When one side is paralyzed, that side will paradoxically move up rather than down.

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6
Q

What are some secondary muscles of inspiration?

A
  • External intercostal (inspiration is external, expiration is internal–>opposite letters)
  • Accessory muscles which are not normally involved: scalene (raises first 2 ribs) and sternocleidomastoid (raises sternum)
    (Whole thoracic cage expands in vertical, AP and lateral dimension with inspiration. There is “bucket handle” movement of the ribs.
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7
Q

What muscles are involved in expiration?

A
  • Generally no muscles are involved in expiration, except physical activity, respiratory distress or during infancy
  • Most important ones for active expiration are abdominal: rectus abdominus, external and internal oblique muscles, transversus abdominus
  • Less important: internal intercostals
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8
Q

What is different about FRC in infants?

A

Infants have a low FRC because the chest wall is very compliant and non-stiff. So the point at which elastic recoil is balance with chest wall recoil is at a very low volume. This is actually above below volume, so infants have to breathe above FRC

  • End expiratory lung volume in infants is above FRC
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9
Q

What is different about exhalation in infants?

A
  • Exhalation is ACTIVE and the end expiratory lung volume is above FRC
  • To avoid having the lung collapse down to FRC, they have various breaking maneuvers:
  • short exhalation time (they have a high RR)
  • active diaphragm (post inspiratory movement)
  • glottic adduction
  • When an infant is mechanically ventilated, their ability to use vocal cords to maintain end expiratory lung volume above FRC is affected, also rate is controlled–>need ot have enough PEEP
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10
Q

What are some useful anchor points on oxygen hemoglobin dissociation curve?

A 
PaO2-saturation
30-60
60-90 
28-50  
40-75 (venous blood)
100-97
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11
Q

What is the P50

A

On the oxygen hemoglobin dissociation curve, the saturation that correspond to a PaO2=50

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12
Q

What causes rightward shift of the oxygen-hemoglobin dissociation curve?

A

When you want to unload oxygen–eg. sepsis (or think of an exercising muscle):
fever, low pH, high CO2, increased 2,3 DPG (which happens with chronic hypoxia, including chronic lung diseases). There is also high DPG in anemia–>anemia will cause rightward shift
The opposite of these factors causes leftward shift

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13
Q

What does CO do to oxygen-hemoglobin dissociation curve?

A
  • Leftward shift
  • CO has a very high affinity for Hb. So CO occupies most of the binding sites and the unoccupied binding sites bind O2 and have a very affinity so hard to unload oxygen
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14
Q

What does fetal hemoglobin and sickle cell do to oxygen-hemoglobin dissociation curve?

A

Fetal hemoglobin: left shift

Sickle cell: right shift

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15
Q

What does methhemoglobin do? How does it affect oxygen-hemoglobin dissociation curve?

A

In methhemoglobin, Fe2+ on heme is changed to Fe3+, which irreversibly binds oxygen

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16
Q

How does 100% oxygen treat pneumothorax?

A

100% oxygen into alveoli–>high oxygen content in blood–>create a gradient for nitrogen (which is the main gas in the entrapped air) to diffuse
pneumothorax resolve faster

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17
Q

How is large pneumothorax defined?

A

> 3 cm from apex to lung

>2 cm to lateral edge

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18
Q

Which is most effective for increasing oxygen delivery (DO2):

  • fiO2
  • transfusion
  • cardiac output
A

cardiac output

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19
Q

Will transfusion increase % saturation?

A

No, but it will increase oxygen content of the blood

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20
Q

What is normal cardiac output?

A

5.5 L/min

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21
Q

What is the problem with methemoglobin?

A

The problem with methemoglobin: it has a significant affinity oxygen, but similarly is not able to release oxygen so blood can be oxygenated with minimal oxygen delivery (oxygen dissociation curve shifted to the left)

  • Congenital: generally better tolerated and patients usually asymptomatic. They have cyanosis, just because of how methemoglobin absorbs light. They have a functional anemia and there compensatory erythrocytosis.
  • Acquired: often drug triggered or environment related. These patients can be very sick and die, despite being given supplemental oxygen
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22
Q

Persistent saturation of 85% despite giving supplemental oxygen

A

Methhemoglobin and pulse ox: methemoglobin absorbs light at the two ends of the spectrum detected by the routine pulse ox, so it confuses the assessment of oxy versus deoxy blood. Having a significant amount of methemoglobin will lead to a persistent saturation of 85%, even if supplemental oxygen is given.

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23
Q

How to test for methemoglobin

A
  • Blood gas analyzer:
  • The blood gas analyzer will detect methhemoglobin by it’s absorbance at 630 nm, but other agents with similar absorbance level such as sulfhemoglobin, methylene blue and certain will interfere and cause a falsely elevated value
  • Co-oximeter (multiple wave length oximetry):
  • Absorbance is measured at a fixed wave length of 630 nm
  • Similar to the blood gas analyzer, other substances with a similar absorbance frequency will cause false elevation
  • Specialized testing (direct assay):
  • A reaction with cyanide (the Evelyn-Malloy method) can be used to directly measure methohemogloin, but this is a pretty specialized test and only done by speciality laboratories like Mayo Clinic
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24
Q

What is the difference between arterial/arterolized and venous PCO2?

A

6 mmHg (as per Kendig)

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25
Q

Alternate to regular pulse oximetry for patients with CO poisoning or metHb suspceted?

A

Co-oximeter

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26
Q

What is mixed venous blood and typical PvO2 and saturations?

A

Mixed venous blood—this is technically from pulmonary artery, but it’s often measured from central line. —>PvO2=40, saturation 73% (or could say 75% as per other sources)

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27
Q

Which cytokines are involved in asthma, allergy, IgE, eosinophilia?

A

IL4, IL5, IL13

IL4 is important for Th0–>Th2

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28
Q

Which cytokine promotes differentiation of Th0 cell to Th2 cell?

A

IL-4

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29
Q

What kind of cytokines does Th2 cell make?

A

IL4, 5, 13

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30
Q

What is the predominant type of airway inflammation in pediatric asthma?

A

Eosinophilic

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31
Q

Why is IL-5 important for eosinophils?

A

promotes eosinophil production from bone marrow precursor, movement out of bone marrow, recruitment to airway, growth and survival

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32
Q

How do inhaled steroids work for asthma?

A
  • promote eosinophil apoptosis

- block the survival effect of IL5

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33
Q

What do mast cells release?

A
  • histamine

- leukotriene

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34
Q

What cytokine do mast cells release?

A

IL13

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35
Q

Which cytokine is low in patients with sever asthma (who tend to not be responsive to steroid therapy)

A

IL10 (this is an anti-inflammatory cytokine, which is produced by regulatory T cells)

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36
Q

Which cytokine promotes Th0 to become Th1?

A

IL-12

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37
Q

What does the Th1 inflammatory do? What cytokines are produced by Th1 cells

A
  • Infection + cell mediated immunity

- Ctyokines: IL-2, Interferon gamma, TNF alpha

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38
Q

What is pulmonary vascular resistance compared to systemic?

A

1/10 of systemic and furthermore, recruitment and distension enable a further drop in pulmonary resistance. (so by the time a patient develops PH, they have exhausted these mechanisms)

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39
Q

With airway closure, do airways at bottom or top of lung close first?

A

Bottom of lung since the airways are less open to start with

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40
Q

How does lung volume affect blood vessel and airway resistance? Be able to draw a graph of lung volume versus resistance

A

At high lung volume, low resistance of extra-alveolar vessels and high resistance of intra-alveolar vessels. (opposite for low lung volume). Total vascular resistance is lowest at FRC. (recall diagram of U shaped curve)
At high lung volume, low airway resistance
At low lung volume, high airway resistance

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41
Q

Which chemokine for attraction of eosinohpils to airway?

A

CCL5 (important for leaving circulation)

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42
Q

What is the trigger and threshold for hypoxic pulmonary vasoconstriction? Why is this response important?

A
  • Trigger: PAO2 (alveolar)
  • Threshold: PAO2 of <70 mmHg as per west (50-60 in Kendig’s)
  • minimizes VQ mismatch
43
Q

What are the components of surfactant?

A
  • Phospholipids is 80%, with the most common being phosphatidyl choline
  • Neutral lipids (8%), with cholesterol being the most common
  • Proteins (8%), like A, B, C, D
44
Q

What is static compliance versus dynamic compliance?

A

Static compliance = change in volume/change in pressure in the absence of flow. It consists of lung compliance and chest wall compliance.
Dynamic compliance = change in volume/change in pressure in the presence of flow. Consists of: lung compliance, chest wall compliance, airway resistance (and therefore frequency)

45
Q

Why does dynamic compliance depend on the frequency?

A

As frequency increases, there is less time for alveolar units with a slow time constant (due to increased airway resistance) to fill and so they can’t contribute volume to the compliance equation. In obstructive disease, there is low dynamic compliance and so the ratio of dynamic compliance/static compliance decreases as frequency increases.
For normal airways, the ratio stays at 1:1 regardless of breath frequency

46
Q

What is Laplace’s law?

A 
P = 2T/r
Pressure ot inflate a lung unit 
T = surface tension 
r = radius 
Key point: surface tension varies depending on size of alveoli. Smaller alveoli have lower surface tension. Bigger alveoli have higher surface tension. this inverse relationship between radius and surface tension prevents significant pressure differences between the lung (that would make it unstable)
47
Q

What is the difference between measuring lung volume via body pleth versus gas dilution?

A
  • Body pleth measures the TOTAL volume of gas in the lung, included gas trapped behind closed airway (Eg. obstructive lung disease) or pneumothorax
  • For a healthy subject, there wouldn’t be a significant difference in lung volume between the two methods
48
Q

How does gas dilution measure lung volume?

A

C1V1 = C2V2

49
Q

How does body pleth measure lung volume?

A

P1V1=P2V2 on both the body and the box

50
Q

Why would a biPAP patient have ventilatory asynchrony?

A
  • Inspiratory flow inadequate to trigger machine, eg. neuromuscular disease
  • Mask leak, which can lead to either autotriggering or ineffective inspiratory effort
51
Q

What are the theorized benefits of high flow?

A
  • With the high flow–>exceed minute ventilation requirement, eliminate inspiration of room air and ilution of fiO2–>washout anatomic dead space
  • some positive nasopharyngeal and intrathoracic pressure at flow rate of 2 L/kg/min
  • reduce upper and lower airway resistance
  • reduces RR and work of breathing
52
Q

How do you initiate high flow?

A
  • Flow rate starting at 1-2 L/kg/min–>titrate based on work of breathing
  • FiO2 starting at 50% –>titrate for saturations
53
Q

Patients to be caution on with high flow?

A
  • Patient already very sick - eg. high PaCO2, severe tachypnea, failure to improve after first few hours of high flow
  • nasal obstruction, epistaxis, severe upper airway obstruction
  • rare cases of air leak such as pnemo
  • in hypovolemic patients–>can be sensitive to increased intrathoracic pressure and increased PA afterload
54
Q

What is a bronchial breath sound and mechanism?

A
  • High frequency relative to normal breath sounds
  • Normally heart at C7 to T3, but they can be pathologically present when there is airspace disease and alveoli can’t do their normal function of filtering out frequency sounds
  • Other signs of alveolar disease (eg. consolidation): whispering petroliloquoy (increased loudness of whispering), egophany
  • compared to normal breath sounds, the I:E ratio is 1:2 versus 3:1, pause between inspiration and expiration
55
Q

Draw the compliance graph, showing static compliance, dynamic compliance and airway resistance?

A
  • Graph of transpulmonary pressure versus volume
  • Dynamic compliance: hysteresis curve
  • Static compliance: straight line
  • Resistance = the difference between the 2 curves
56
Q

What does 1% or 2% lidocaine during bronchoscopy correspond to? What is the maximum dose of lidocaine? complications of too much lidocaine?

A

1% = 10 mg/mL
2% = 20 mg/mL
Maximum dose is 4 mg/kg
S/E: seizures from lidocaine toxicity

57
Q

What are the complications of bronchoscopy?

A

Complications of bronchoscopy:

  • Death is very uncommon, though at least 1 death in a paediatric patient has been reported
  • Not obtaining the right answer or therapeutic result (procedure failure)
  • Greater risk of traumatizing mucosa with rigid than flexible bronchoscopy since the rigid has a larger diameter and is more rigid
  • Mechanical complications:
    • Due to direct trauma to the airway, such as pneumothorax, mucosal oedema, hemorrhage. This is more likely with forceps or trans bronchial biopsy
    • Epistaxis is a risk if trans-nasal approach in patients with thrombocytopenia
    • (Orotracheal will avoid contamination of lower airway specimens with upper airway bacteria in patients who are immunocompromised)—>good to see that Kendig’s directly endorses this
    • What is the mechanism for pneumothorax in the absence of trans bronchial biopsy?
      • When ventilating through an ETT with flexible scope in place: easy to get air in around the tube on inspiration, but on expiration it’s hard to get the air out (since exhalation is passive)
      • Increased intrapulmonary pressure—>decreased pulmonary perfusion or pneumothorax
  • Physiologic complications:
    • The scope obstructs the airway to some extent—>hypoxia, hypercapnia
    • Inadequate sedation/anaesthesia—>cardiac arrhythmia
    • Not enough topical anaesthesia (this is often applied by the bronchoscopist at carina or cords)—>laryngospasm or bronchospasm
    • Lidocaine toxicity—>seizures
  • Bacteriologic:
    • Infection in one part of lung could be spread to another part
    • Risk of bacterial endocarditis in some patients—>but give antibiotic prophylaxis AFTER BAL sample is obtained
    • Risk of infection to bronchoscopy team, eg. in patient with cavitary TB—>administer treatment first, before bronchoscopy, to reduce risk
  • Cognitive risks:
    • failure to obtain useful information
    • failure to make the right diagnosis
    • failure to do a bronchoscopy when it’s the only way of obtaining information
    • helpful to record bronchoscopy to review, revise diagnosis, teaching, research
58
Q

Normal cell counts in BAL and threshold for defining abnormal?

A

Normal:

  • 80-90% marcophages
  • 5-10% lymphocytes
  • 0-1% eosinophils
  • <5% neutrophils

Defining abnormal:

  • > 3% neutrophils–>neutrophilia
  • > 15% lymphoytes
  • > 1% eosinophils
59
Q

What disease cause relatively high lymphocyte count on BAL?

A
  • Hypersensitivty
  • Sarcoid
  • Mycobacterial infection
60
Q

For patient with respiratory disease, what investigations are required prior to diving?

A

Physical exam, spirometry, CXR

- Exercise challenge and bid PEF if asthmatic

61
Q

Contraindications for diving in patients with respiratory disease?

A
  • Contraindications to diving:
    • Blebs or cysts
    • Cystic fibrosis
    • Fibrotic lung disease
    • Spontaneous pneumothorax without having had bilateral pleurodesis + normal lung function and thoracic CT post
    • Traumatic pneumo is ok if healed, normal spirometry and CT scan
    • Active sarcoid
    • Active TB
  • Contraindications for asthmatic patient to dive if not:
    • Free of asthma symptoms
    • Asthma not triggered by cold, emotion or exercise
    • Normal spirometry
    • Negative exercise challenge (<15% drop in FEV1 at end of test)
    • At the time of the dive:
    • Can’t required relievers in 48 hours leading up to dive
    • Need to do BID monitoring of PEF. If >10% drop from baseline leading up to dive or >20% diurnal variation, then not advised to dive
62
Q

Findings on CPET for patient with obesity (but not deconditioned)?

A
  • VO2 max low for total body weight, but normal for ideal body weight
  • Normal O2 pulse
  • Early peaking of HR (more steep slope)
  • Reduced or normal anaerobic threshold
  • Normal breathing reserve, but can have expiratory flow limitation (pseudo asthma) since they breathe close to residual volume at rest
  • Normal gas exchange
63
Q

Findings on CPET for patient with deconditioning?

A
  • VO2 max is low
  • Low O2 pulse
  • Normal HR max
  • Low anaerobic threshold
  • Normal breathing reserve
  • Normal gas exchange
64
Q

What is the lung clearance index?

A
  • Derived from the multiple breath washout test
  • Number of lung turnovers required for the end-tidal tracer gas concentration to reach 40% of it’s original concentration
  • Higher LCI is bad –>means more heterogeneity/inhomogeneity
  • Two gases: N2 or SF6
65
Q

What are advantages of LCI?

A
  • More sensitive marker of small airway obstruction and is especially useful for early CF, where the distal airways are more obstructed and spirometry is normal
    Advantages: technique is harmless, easy for patients to perform and reproducible, even in infants and small children. Being non-invasive, it is repeatable on multiple occasions, increasing its longitudinal applicability.
66
Q

Difference between oxygen concentrator versus cylinder?

A
  • Concentrator manufactures oxygen by concentrating air, so smaller, more portable, don’t need to refill, but do need to have good power source, back up battery/generator, and access to oxygen cylinders
  • Cylinder is literally oxygen
67
Q

For what type of oxygen delivery flow rate should humidification be provided?

A

> 1 L

68
Q

For infant with BPD, what is the ideal method of oxygen delivery?

A

either concentrator or cylinder. For flow rate <1 L, consider use of a low flow meter.
If low flow at <0.3 L/min for a short duration, then consider use of cylinder

69
Q

Which patients have high closing volume?

A
  • Elderly since there is low elastic recoil and so low intrapleural pressure to start off with
  • Infants since they have a low residual volume (high elastic recoil, low chest wall recoil)
  • High airway resistance
70
Q

Draw and label a graph of the fowler method which shows N2 washout so as to measure dead space and closing volume.

A

(Regional Differences in Ventilation and Closing Volume - Exam)

71
Q

What is the normal A-a gradient

A

0.3 (age) +4

72
Q

What is differential cyanosis?

Causes of differential cyanosis?

A

> 3-5% saturation difference or >20 mm Hg PaO2 difference between pre (right arm) and post ductal (any leg).
Causes:
- PPHN
- obstructive left sided disease like HLHS, coarctation, interrupted aortic arch

73
Q

Effects of obesity on PFT?

A
  • decreased FRC
  • decreased ERV (expiratory reserve volume) since FRC is decreased, but normal residual volume
  • In mild obesity, the spirometry is normal, but as BMI increases you will then see restriction with decreased FEV1, decreased FVC. They are proportionately decreased so FEV1/FVC ratio is stable.
  • With severe to morbid obesity, there is airflow obstruction. Lower lung volumes may result in earlier airway closure.
  • Key point: when the lung is restriction, the lung is at less favourable location on compliance curvemore work of breathing
74
Q

If a patient has a pneumothorax, when can they fly?

A

They can fly 7 days post CXR showing radiologic resolution. 2 week delay post normal CXR for patients with CF.
(Patients with pre-existing lung disease who have a secondary pneumothorax with pleurodesis–>increased risk of recurrent pneumothorax for at least 1 year (maybe longer).

75
Q

Why are young children not able to achieve plateau on spirometry?

A
  • High elastic recoil
  • Relatively large airways for lung volume
  • (Inadequate coaching)
  • restrictive lung disease, regardless of age, will result in high elastic recoil
76
Q

Blood gas sample, sitting on the counter for 1/2 hour, what values are altered on the blood gas?

A

Falsely low PaO2 (since gas diffusion through syringe and consumption of oxygen by leukocytes).
Sample needs to be put on ice and analyzed within 15 minutes

77
Q

Blood gas sample with too much heparin?

A

Falsely low PacO2 and low pH

78
Q

Blood gas sample with air bubbles?

A

If air bubbles are >1-2% of volume, then high PaO2, low PaCO2 (so the sample will look better than it is)

79
Q

What is the starling equation?

A

Qf = Kf[(Pc − Pis) − σ(πpl − πis)]

where Qf = net flow of fluid
Kf = capillary filtration coefficient; this describes the permeability characteristics of the membrane to fluids and the surface area of the alveolar-capillary barrier
Pc = capillary hydrostatic pressure
Pis = hydrostatic pressure of the interstitial fluid
σ = reflection coefficient; this describes the ability of the membrane to prevent extravasation of solute particles such as plasma proteins
πpl = colloid osmotic (oncotic) pressure of the plasma
πis = colloid osmotic pressure of the interstitial fluid

80
Q

In terms of CO2 and O2 control, what do peripheral and central chemoreceptors respond to and where are they located?

A

Central - responds to CO2, located in brainstem

Peripheral - responds to CO2 and O2, located in carotid body and aortic body (aortic arch)

81
Q

What are the benefits of high flow?

A

From CPS statement:
- Higher flow rate enables delivery of higher concentration of oxygen since it exceeds minute ventilation requirement. Since the gas is heated and humidified, the higher flow rate is better tolerated
- Positive intranasal and intrathoracic pressure during exhalation when a higher gas flow of 2 L/kg/min is used
- Reduces upper and lower airway resistance
- Washout of anatomic dead space reduces work of breathing
Other:
- humidification prevents airway dessication and secretion removal

82
Q

Causes of acute flaccid paralysis?

A
  • Guillan barre
  • polio
  • Enterovirus D68
  • botulism, myasthenia gravis
  • mechanisms of causing lung disease: hypoventilation, aspiration, secondary infection, guillian barre can cause autonomic neuropathy–>cardiac failure–>pulmonary edema
83
Q

Atelectasis or airway obstruction, but no hypoxemia. Mechanism?

A

Hypoxic pulmonary vasoconstriction to minimize shunt.

VQ mismatch is the main cause of hypoxemia in acute respiratory disease

84
Q

What is the mechanism of pulmonary hypertension that develops in chronic respiratory disease?

A

Hypoxic pulmonary vasoconstriction

85
Q

What other factors modulate hypoxic pulmonary vasoconstriction (HPV)?

A

pH: low pH–>increased vasoconstriction. High pH–>decreased vasoconstriction
Hypercapnea increases pulmonary vascular resistance. (The effect of pH is independent of PCO2)
Low temperature decreases pulmonary vascular resistance. Hyperthermia increases HPV
Age: high HPV at birth and during infancy, but then response declines
Iron: increased HPV if low iron (so especially important to ensure that infant with BPD and pH has normal iron)

86
Q

When is pulse oximetry not accurate?

A
  • all saturations <70% are NOT accurate
  • abnormal Hb such as HbS, COHb, methemolglobin
  • non-pulsatile flow - eg. poor perfusion, VAD
87
Q

How does CO cause problems?

A
  • CO has 240 times the affinity for Heme as oxygen does–>limit oxygen binding
  • Causes leftward shift of oxygen hemoglobin dissociation curve–>bound oxygen can’t be unloaded
  • Also affects tissue utilization of oxygen
88
Q

How to diagnose CO poisoning?

A

History + elevate CO hemoglobin (as quantified based on co-oximetry)

89
Q

What extent of variability in FEV1 and FVC within a day is considered significant?

A

> =5%

90
Q

What extent of varaibility in FEV1/FVC within a week is considered significant?

A

> =11-12% (makes sense since 10% is considered significant for CF patient and 12% is significant for BD response)

91
Q

Normal CO for non-smoker and smoker?

A

Non-smoker: 3%

Smoker: 10-15%

92
Q

What is the formula for DLCO?

A

(VA) (pulmonary capillary blood volume) Hb)/ (alveolar capillary thickeness x COHb)

93
Q

If DLCO is corrected for Va, which conditions will then have a normal DLCO?

A

Conditions where there is restriction, but normal lung parenchyma, such as obesity and neuromuscular disease. (all other conditions would NOT have a normal DLCO when applying this correction)

94
Q

What is the effect of pulmonary hemorrhage on DLCO?

A

If there is active bleeding, then DLCO increases. Presence of Hb in the alveoli will take up CO, thus increasing it’s diffusion.

(For other types of hemorrhage or if remote pulmonary hemorrhage with low Hb–>lower DLCO)

95
Q

Mueller maneuver’s effect on DLCO?

A

Increased DLCO since there is increased pulmonary capillary blood volume

96
Q

Difference between chemokine and cytoking?

A

Cytokine is a general term used for all signaling molecules while chemokines are specific cytokines that functions by attracting cells to sites of infection/inflammation.

97
Q

What is normal oxygen content in the blood?

A

17-20 mL/dL of oxygen

98
Q

In an upright lung, which part of the lung receives more ventilation and why?

A

Bottom of the lung (more dependent portion) receives a greater proportion of ventilation. Due to gravity, the intrapleural pressure is more negative at top of lung and less negative at bottom of lung. Alveoli at top of lung are more distended and have a greater baseline volume than alveoli at bottom of lung. Alveoli at bottom of lung are on a more favorable portion of the compliance curve.

This same principle re: difference between dependent and non-dependent region holds true regardless of lung position (Eg. upright versus decubitus)

99
Q

Two situations when rigid bronch is preferred

A

i. Foreign body removal
ii. Assessment of posterior trachea (e.g., tracheoesophageal fistula) and larynx (e.g,. laryngeal cleft)

100
Q

Limitations of rigid bronch ?

A

i. Limited ability to access more distal areas of the lung, and those requiring a flexible curve to reach, e.g., right upper lobe
ii. Limited ability to obtain bronchoalveolar lavage specimens

101
Q

What is fick’s law for diffusion and what are the factors that affect diffusion?

A

Surface area x diffusion coefficient x P1-P2 divided by thickness of diffusion barrier

Diffusion coefficient depends on solubility and molecular weight

102
Q

What conditions cause increased DLCO?

A
  • asthma

- complete the rest of this answer

103
Q

What is the effect of aging on lung compliance, elastic recoil and chest wall compliance?

A
  • With aging, the lung is more compliant, but there is lower elastic recoil. (the lung is easier to inflate, but there is less stored potential energy). This would be similar to emphysema
  • Since there is decreased static recoil, there is increased FRC
  • stiffening of the chest wall–>less compliant

Respirology (28 decks)

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