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Physiology Flashcards

1
Q

What is P50?

A

● P50 is the PO2 at which 50% of the hemoglobin present in the blood is in the deoxyhemoglobin state and 50% is in the oxyhemoglobin state.
● (At a temperature of 37C, a pH of 7.4 and PCO2 of 40mmHg, normal human blood has a P50 or 26 or 27mmHg. If the oxyhemoglobin dissociation curve is shifted to the right, the P50 increases. If it is shifted to the left, the P50 decreases).

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2
Q

What factors cause rightward shift of oxygen hemoglobin dissociation curve?

A

c. Increased temperature
d. Reduced pH
e. Increased 2,3 DPG
f. Increased PCO2

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3
Q

what is the shunt equation and what assumptions to use the shunt equation?

A

Qs/Qt = blood flow through shunt/total cardiac output = CcO2 - CaO2 /CcO2 - Cv02
Concept: end capillary oxygen content (ideal) - arterial oxygen content /total cardiac output
Ideally: CcO2 = CaO2 (that being said, there is physiologic shunt)
Oxygen content = 1.39 x Hb x % saturation + 0.003PaO2

Assumptions:

  • CcO2: saturation is 99%, Hb is measured Hb
  • CaO2: these values of PaO2 and % saturation are actually measured
  • CvO2 (mixed venous): assume a saturation of 75% and PaO2=45

Shunt is venous admixture–how much venous blood is mixed with the arterial blood. (The blood that shunt is basically venous blood)

If the patient is on 100% oxygen, then the equation can be reduced to 1-SaO2/1-SvO2

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4
Q

What is normal shunt fraction and why does physiologic shunt exist?

A

Normal: 2-5%

  • But, the normal lung has physiologic shunt because:
    • Bronchial circulation: blood going to lungs via bronchial circulation and it oxygenates the lung itself, but then it doesn’t go through the lung to get more oxygen and so it’s deoxy blood when it goes through pulmonary veins
    • Thesbian veins: coronary vein blood (deoxy blood) that is dumped directly into left ventricle
    • Capillary shunt: if unventilated alveoli or if blood directly passes from arterial to venous through anastomoses and bypasses capillaries
    • Because there is a normal shunt, PAO2 is not the same as PaO2
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5
Q

How do you clinically sort out if someone has a shunt?

A

Hyperoxia test: give 100% oxygen x 10 minutes. Measure preductal PaO2 before and after. If PaO2 increases by >150 mmHg, then it’s likely a pulmonary reason for low saturations. If minimal increase, then it’s likely a shunt. To avoid doing a blood gas, a “poor” man’s version is monitoring >10% increase in oxygen saturation, though this is less reliable.
Also do an echo to look for intracardiac shunt

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6
Q

What conditions cause elevated DLCO?

A

asthma, obesity, pulmonary hemorrhage

  • polycythemia
  • mild left heart failure
  • exercise

I think the theory for obesity: ventilation is heterogeneous so the same holds true for blood flow, so in areas of blood flow–>there is a higher concentration of hemoglobin

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7
Q

What PFT abnormalities are associated with obesity?

A
  • reduced ERV, FRC - this happens early on in obesity
  • reduced FVC, reduced FEV1 (proportionately reduced) - signs of restriction with progression of obesity
  • reduced TLC
  • normal or elevated FEV1/FVC (although increased risk of asthma with obesity since the extra fat is proinflammatory)
  • reduced MIP/MEP
  • increased DLCO
    (because FRC is lower, then it will be closer to closing volume. FRC is even lower in the supine position)

Physiologic features:

  • decreased lung compliance, since lower FRC means more unfavorable position on compliance
  • hypercapneic respiratory failure
  • increased work of breathing since lower lung compliance and the respiratory muscles are in a less favorable position
  • abnormalities in ventilation distribution
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8
Q

What is normal MIP/MEP?

A

Normal is 80-120
<60 is associated with symptomatic respiratory impairment
<20 - will require mechanical ventilation

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9
Q

With diving, what is the change in partial pressure for every 10 metres dived?

A

10 metres of depth corresponds to 1 atm = 760 mmHg

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10
Q

Contraindications for diving, as based on BTS?

A
  • 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
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11
Q

Recommendations for asthma patients re: diving?

A
  • 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
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12
Q

Investigations prior to diving, as based on BTS?

A
  • If history of current respiratory symptoms, prior lung disease or chest trauma—>need an evaluation before diving—>spirometry and CXR
  • If no respiratory concerns, then don’t need routine evaluation, but may benefit from physical exam, spirometry, but don’t need CXR
  • If anything is abnormal on evaluation (like abnormal spirometry or CXR)—>not recommended to dive
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13
Q

Central and peripheral chemoreceptor location and what they respond to?

A

Central chemoreceptor: responds to PCO2 by responding to changes in pH of the CSF. Located largely on ventral surface of medulla, but also newly discovered locations like cerebellum.

Peripheral chemoreceptor: responds to PO2, PCO2 and pH. Located in carotid body and aortic arch. Carotid body receptors are the most important

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14
Q

What is the mechanism of nitric oxide?

A

The conversion of L-arginine to L-citrulline is done by NO synthetase and also results in production of NO (endogenous NO).
- Both endogeneous NO and exogenous NO stimulate soluble guanylate cyclse to promote conversion of GTP–>cGMP, which then causes a decrease in smooth muscle tone and decreases intracellular calcium

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15
Q

What is the mechanism of action of sildenafil and tadalafil?

A
  • They are PDE5 inhibitors
  • PDE5 is an enzyme which breaks down cGMP
  • so this part of the NO pathway for vasodilation
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16
Q

Mechanism of action of riociguat?

A

Guanylate cycllase stimulator (similar to NO)

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17
Q

Side effects of nitric oxide?

A
  • Hemodynamic instability: pulmonary edema if there is pulmonary vein obstruction, decreased systemic blood pressure
  • Rebound pulmonary hypertension (even in patients whose pulmonary hypertension doesn’t benefit from NO)
  • ## Methemoglobinemia: higher risk with doses above 20-40 ppm
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18
Q

Which cytokines are involved in the Th1 pathway? Th2 pathway?

A

Th1 pathway: IL-12 promotes differentiation of Th0 into Th1 cell, IL2, INF gamma, TNF alpha promote cell mediated immunity
Th2 pathway: IL4 promotes differentiation of Th0 into Th2 cell. IL4, 5 and 13 contribute to allergy, eosinophilia, IgE production, airway hyper-responsiveness.

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19
Q

Why doesn’t atelectasis always cause hypoxemia?

A

Hypoxic pulmonary vasoconstriction

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20
Q

What is the difference between SpO2 and SaO2? How does an oximeter work?

A

SpO2 is the measured pulse oximetry. Traditional oximeter has 2 wavelengths of light (660 nm and 940 nm).
HbO2 absorbs at 660 nm
Normal Hb absorbs at 940
HbO2/Hb + HbO2

SaO2 is the calculated saturation on a blood gas, based on PaO2

○ The oximeter measurements are timed with arterial pulse so you get an arterial oxygen saturation

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21
Q

Limitations of oximetry?

A

○ Does NOT detect COHb or methemologlobin or dyshemoglobin
○ Perfusion
○ Technical issues: skin pigmentation, nail polish, motion artifact

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22
Q

What is the difference between type 1 and type 2 respiratory failure?

A

Hypoxemic respiratory failure (type I) is characterized by an arterial oxygen tension (PaO2) lower than 60 mm Hg with a normal or low arterial carbon dioxide tension (PaCO2). This is the most common form of respiratory failure, and it can be associated with virtually all acute diseases of the lung, which generally involve fluid filling or collapse of alveolar units. Some examples of type I respiratory failure are cardiogenic or noncardiogenic pulmonary edema, pneumonia, and pulmonary hemorrhage.
Hypercapnic respiratory failure (type II) is characterized by a PaCO2 higher than 50 mm Hg. Hypoxemia is common in patients with hypercapnic respiratory failure who are breathing room air. The pH depends on the level of bicarbonate, which, in turn, is dependent on the duration of hypercapnia. Common etiologies include drug overdose, neuromuscular disease, chest wall abnormalities, and severe airway disorders (eg, asthma and chronic obstructive pulmonary disease [COPD]).

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23
Q

What are the factors that affect residual volume in a healthy person?

A
  • Chest wall recoil: stiff chest wall such as with kyphoscoliosis then there is a higher residual volume
  • Expiratory muscle strength: neuromuscular disease than high RV
  • Elastic recoil: fibrotic lung disease then high elastic recoil and low residual volume. Emphysema then low elastic recoil and high residual volume.
  • Airway resistance
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24
Q

What are the changes in lung and chest wall mechanics with obesity?

A
  • Chest wall is less compliant
  • Lung is less compliant
  • Lower FRC–>decreased airway calibre–>increased resistive
  • Less compliance–>increased elastic work of breathing
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25
Q

What is the relationship between compliance and elastic recoil?

A

inverse relationship

  • as compliance increases, elastic recoil decreases (eg. emphysema–>inflating a thin grocery bag which doesn’t store much potential energy)
  • as compliance decreases, elastic recoil increases (eg. fibrotic lung)
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26
Q

What is the reason for sigh breaths and yawning?

A
  • A chance to exhale more CO2

- With normal breathing, we inhale more O2 than we do exhale CO2 in typical tidal breathing

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27
Q

Why does dead space ventilation exist in the first place? Why not build a lung with no dead space?

A
  • Having airways will decrease resistance

- Balance between decreasing resistance and minimizing dead space

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28
Q

What is the effect of exercise on dead space?

A
  • Exercise leads to capillary recruitment–>less alveolar dead space, no change in anatomic dead space, but overall physiologic dead space decreases
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29
Q

How does lying down (from upright position) affect dead space?

A
  • More blood flow to all parts of lung since lose the effects of gravity–>less alveolar dead space
  • Apparently, there is also less anatomic dead space (not sure why)
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30
Q

What is reynold’s number and what are some clinical applications?

A
  • this describes if flow is turbulent versus laminar
  • as the number increases, then the flow is more turbulent
  • 2(radius)(density)(velocity)/viscosity
  • radius–>bigger airways have more turbulent flow
  • density–>low density gas like helium has more laminar flow (I think this is the idea behind heliox)
  • velocity–>if you slow down the velocity of gas with pursed lip breathing then there is more laminar flow. With exercise, there would faster velocity and more turbulent flow. (I wonder if VCD exercises would also decrease flow and turbulence)
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31
Q

What is the general anatomic organization of airways?

A
  • Trachea
  • Mainstem bronchi
  • The next level of bronchi (Eg. right upper lobe bronchus)
  • The segmental level bronchi
  • By the 4th generation, you are at the level of bronchioles, which don’t have cartilage
  • Generation 4-16: bronchioles with no cartilage
  • Generation 16: terminal bronchiole
  • There are exchange units after level of terminal bronchiole (respiratory bronchiole, alveolar ducts, alveolar sacs)
  • Everything distal to a terminal bronchiole is called an acinus, and it’s a gas exchange unit
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32
Q

At what level of airway, does the greatest resistance exist?

A
  • Generation 5-7
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33
Q

At which lung volumes is there decreased lung compliance?

A
  • at the extremes so high lung volume and low lung volume
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34
Q

at high lung volume, what happens with elastic and resistive work of breathing?

A
  • Less resistance so less resistive work of breathing

- Less compliance so increased elastic work of breathing

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35
Q

Which lung pressure can be measured as a surrogate for work of breathing? What affects work of breathing?

A
  • Ppl (intrapleural pressure) is a surrogate for work of breathing
  • Increased work of breathing if:
  • Increased flow, such as with exercise
  • Increased resistance
  • Increased lung elastic recoil
  • With increased resistance and elastic recoil, there has to be a more negative Ppl to generate flow
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36
Q

How do patients with “stiff lung” breathe?

A
  • lower tidal volume, higher respiratory rate
  • lower tidal volume will decrease elastic work of breathing
  • even though patients need to breathe faster, there is still overall less work of breathing
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37
Q

What is the role of oxygen therapy in most pulmonary diseases?

A

Many pulmonary diseases result in hypoxemia (whether it’s acute VQ mismatch from pneumonia or asthma or impaired diffusion from ILD). Giving oxygen will increase the pressure gradient for diffusion of oxygen, to prevent hypoxemia. Oxygen will not solve the underlying problem.

There may be a very slight triggering of the respiratory drive by hypoxemia, but I don’t think that’s the main reason for tachypnea in these diseases. I think it’s more so the changes in lung compliance and resistance that result in increased work of breathing. (Oxygen will not treat work of breathing or tachypnea).

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38
Q

Why is it necessary that the pulmonary circulation be a low pressure system?

A
  • Very thin alveolar capillary layer–>high pressure will cause rupture of capillaries
  • pulmonary circulation is a low pressure, high capaciance system
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39
Q

What are typical pressures in systemic circulation versus pulmonary circulation?

A
  • Systemic: aortic = 100 mmHg, vena cava = 2 mmg Hg

- Pulmonary: artery = 15 mmHg, vein = 8 mmHg

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40
Q

What is the effect of gravity on ventilation and perfusion of the lung?

A

Dependent locations of the lung have better ventilation and better perfusion. (You want ventilation and perfusion to be matched as best as possible).

  • Although the top of the lung is actually more distended at baseline, the bottom of the lung receives more ventilation since it’s at a more favorable portion of the compliance curve
  • Perfusion: better perfusion at the bottom (makes sense because of gravity)
  • West zones of perfusion:
  • At the top: Palveolar (surrounding pressure) > Parterial (minimal perfusion. This is not usually the case, but is relevant when there is PEEP)
  • Middle zone: pressure gradient depends on Palveolar - Psurrounding (there is development of an equal pressure point)
  • Lower zone: flow depends on Parterial - Pvenous
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41
Q

How does ventilation perfusion relationship compare at bottom and top of lung?

A

Bottom: better perfusion than ventilation (V/Q<1)
Top: better ventilation than perfusion (V/Q>1)

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42
Q

How does compliance vary between bottom and top of lung?

A
  • Bottom of the lung is less distended and more compliant and that’s why there is better ventilation of the bottom of the lung
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43
Q

Normal PaO2?

Normal PvO2?

A

Normal PaO2 is 80-100 mmHg

Normal PvO2 is 40 mmHg

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44
Q

What is the respiratory exchange ratio?

A
  • ratio of CO2 production relative to oxygen consumption

- 0.8 (not a perfect 1:1 relationship; I think this is the reason for sigh breath and yawning)

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45
Q

What causes an elevated A-a gradient?

A
  • basically, all the mechanisms of hypoxemia, except for hypoventilation
  • V/Q mismatch
  • shunt
  • diffusion
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46
Q

Why is exercise a sensitive time for detecting pulmonary hypertension problems and ILD problems?

A
  • With exercise, there is less time available for diffusion of oxygen as a RBC moves along a blood vessel (since there is a much higher cardiac output)
  • In ILD, diffusion is slower because of a thicker interstitium so more likely to have desaturation
  • There is normal recruitment and distension of capillaries during exercise to increase surface for diffusion, but this is not possible pulmonary hypertension
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47
Q

What is the difference between SpO2 versus SaO2?

A

SpO2 is the saturation as measured using a pulse oximeter. This is an estimate of the SaO2, which is measured using a blood gas.

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48
Q

Type 1 versus type 2 respiratory failure?

A

ypoxemic respiratory failure (type I) is characterized by an arterial oxygen tension (PaO2) lower than 60 mm Hg with a normal or low arterial carbon dioxide tension (PaCO2). This is the most common form of respiratory failure, and it can be associated with virtually all acute diseases of the lung, which generally involve fluid filling or collapse of alveolar units. Some examples of type I respiratory failure are cardiogenic or noncardiogenic pulmonary edema, pneumonia, and pulmonary hemorrhage.

Hypercapnic respiratory failure (type II) is characterized by a PaCO2 higher than 50 mm Hg. Hypoxemia is common in patients with hypercapnic respiratory failure who are breathing room air. The pH depends on the level of bicarbonate, which, in turn, is dependent on the duration of hypercapnia. Common etiologies include drug overdose, neuromuscular disease, chest wall abnormalities, and severe airway disorders (eg, asthma and chronic obstructive pulmonary disease [COPD]).

Respiratory failure may be further classified as either acute or chronic. Although acute respiratory failure is characterized by life-threatening derangements in arterial blood gases and acid-base status, the manifestations of chronic respiratory failure are less dramatic and may not be as readily apparent.

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49
Q

Which cytokines are important for eosinophil activation once recruited to the lung?

A

IL5

GMCSF

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50
Q

Where are the central and peripheral chemoreceptors located? What do they respond to?

A
  • Peripheral chemoreceptors are located in the carotid body and aortic arch. They primarily response to PaO2 (but they do also contribute to CO2 response)
  • Central chemoreceptors are located in the medullla, in a group of neurons called the retrotrapezoid nucleus. They respond to pH
  • The drives from central and peripheral chemoreceptors are additive
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51
Q

Where is the central respiratory control centre located and what groups of neurons are part of it?

A
  • Major control centre (which is the pacemaker for breathing) is in medulla and pons
  • Main groups of neurons:
  • Pre-Botzinger complex which is for inspiratory rhythm generation
  • Parafacial respiratory group, which for expiratory musculature control (so exhalation is usually passive from a work of breathing perspective, but surpisingly not from a control of breathing perspective)
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52
Q

How does vital capacity change from upright to supine position? what happens in patients with neuromuscular disease?

A
  • Supine position: vital capacity decrease, TLC decreases. there is no longer the depnedent effect of gravity on diaphragm and abdominal contents to increase lung volume
  • When unilateral diaphragmatic paralysis is present, the forced vital capacity (FVC) is usually decreased to values in the range of 70 to 80 percent of predicted, a less pronounced reduction than seen with bilateral disease. The FVC may decrease further by 15 to 25 percent in the supine position.
  • > 10% decrease in vital capacity is associated with diaphragm weakness
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53
Q

What are different types of vital capacity measurements?

A
  • FVC
  • SVC
  • position: supine versus upright
  • after lung volume recruitment –>maximum insufflation capacity
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54
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
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55
Q

Need to copy rest of pulmonary physiology cards

A

Pending

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56
Q

Define hysteresis and what contributes to it

A
  • lung is less compliant on inspiration than expiration
  • contributor:
  • changes in surfactant activity. on inflation, surfactant is less concentrated so there is more unopposed surface tension
  • stress relaxation, which is a general property of an elastic body
  • recruitment of alveoli
  • most important: changes in surfactant activity
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57
Q

List the components of the starling equation?

A
  • capillary filtration coefficient
  • capillary hydrostatic pressure
  • interstitial hydrostatic presssure
  • reflection coefficient
  • plasma oncotic pressure
  • interstitial oncotic pressure
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58
Q

Causes of decreased DLCO?

A
  • anemia
  • pulmonary vascular disease
  • interstitial disease
  • valsalve maneuver
  • emphsema
  • increased carboxyhemoglobin
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59
Q

Mechanisms for pulmonary edema in someone with cardiac disease?

A
  • Venous obstruction (pulmonary venous hypertension): PVOD, pulmonary vein stenosis, left ventricular dysfunction, TGA, hypoplastic left heart
  • Decreased lymphatic: lymphangiectasia, superior venocaval syndrome, single ventricle physiology, tricuspid valve stenosis, failing RV, RV outflow obstruction (I think all the RV stuff is because fluid would back up into SVC)
  • Left to right heart shunt: ASD, VSD, PDA, partial anomalous pulmonary venous connection, systemic arteriovenous malformation, aortopulmonary connection including surgical shunt
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60
Q

complications with fontan circulation?

A
  • abrupt increase in systemic venous pressure post operatively, so not uncommon to have chylothorax
  • long term: failing fontan:
    Failing Fontan:
  • Increased systemic venous pressure:
  • This makes it hard for thoracic duct to empty into venous circulation
  • Increased hepatic and extra hepatic lymphatic production
  • Overwhelm resoprtive capacity of lymphatics
  • Consequence: lymphatic congestion, chylothorax, chylous ascites, lymphangiectasia
    Other complications:
  • Plastic bronchitis—retrograde flow from thoracic duct to parenchyma
  • Protein losing enteropathy

Risk of systolic and diastolic dysfunction

  • progressive increase in systemic and pulmonary vascular resistance
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61
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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62
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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63
Q

What is normal anatomic dead space volume?

A

150 mL

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64
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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65
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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66
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.
67
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
68
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
69
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
70
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
71
Q

What is the P50

A

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

72
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

73
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
74
Q

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

A

Fetal hemoglobin: left shift

Sickle cell: right shift

75
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

76
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

77
Q

How is large pneumothorax defined?

A

> 3 cm from apex to lung

>2 cm to lateral edge

78
Q

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

  • fiO2
  • transfusion
  • cardiac output
A

cardiac output

79
Q

Will transfusion increase % saturation?

A

No, but it will increase oxygen content of the blood

80
Q

What is normal cardiac output?

A

5.5 L/min

81
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
82
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.

83
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
84
Q

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

A

6 mmHg (as per Kendig)

85
Q

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

A

Co-oximeter

86
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)

87
Q

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

A

IL4, IL5, IL13

IL4 is important for Th0–>Th2

88
Q

Which cytokine promotes differentiation of Th0 cell to Th2 cell?

A

IL-4

89
Q

What kind of cytokines does Th2 cell make?

A

IL4, 5, 13

90
Q

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

A

Eosinophilic

91
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

92
Q

How do inhaled steroids work for asthma?

A
  • promote eosinophil apoptosis

- block the survival effect of IL5

93
Q

What do mast cells release?

A
  • histamine

- leukotriene

94
Q

What cytokine do mast cells release?

A

IL13

95
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)

96
Q

Which cytokine promotes Th0 to become Th1?

A

IL-12

97
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

98
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)

99
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

100
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

101
Q

Which chemokine for attraction of eosinohpils to airway?

A

CCL5 (important for leaving circulation)

102
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
103
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
104
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)

105
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

106
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)
107
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
108
Q

How does gas dilution measure lung volume?

A

C1V1 = C2V2

109
Q

How does body pleth measure lung volume?

A

P1V1=P2V2 on both the body and the box

110
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
111
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
112
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
113
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
114
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 and distinct pause between inspiration and expiration
    (hollow, high pitched)
    normally, speech sounds and bronchial breath sounds are filtered, but this is not the case with airspace disease
115
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
116
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

117
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
118
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
119
Q

What disease cause relatively high lymphocyte count on BAL?

A
  • Hypersensitivty
  • Sarcoid
  • Mycobacterial infection
120
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

121
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
122
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
123
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
124
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 1/40 of it’s original concentration
  • Higher LCI is bad –>means more heterogeneity/inhomogeneity
  • Two gases: N2 or SF6
  • Cumulative expired volume/FRC
  • LCI is <7 lung turnovers in children
125
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.
126
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
127
Q

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

A

> 1 L

128
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

129
Q

Which patients have high closing volume?

A
  • Elderly since there is low elastic recoil and so low intrapleural pressure to start off with (minimal traction on airway to keep them open)
  • Infants since they have a low residual volume (high elastic recoil, low chest wall recoil)
  • High airway resistance (if the airway is narrow, it will close sooner)
130
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)

131
Q

What is the normal A-a gradient

A

0.3 (age) +4

132
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

133
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
134
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).

135
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
136
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

137
Q

Blood gas sample with too much heparin?

A

Falsely low PacO2 and low pH (looks like metabolic acidosis with respiratory compensation)

138
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)

139
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

140
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)

141
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

142
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
143
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

144
Q

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

A

Hypoxic pulmonary vasoconstriction

145
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)

146
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
147
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
148
Q

How to diagnose CO poisoning?

A

History + elevate CO hemoglobin (as quantified based on co-oximetry) - you need to do co-oximetry of the blood gas sample

149
Q

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

A

> =5%

150
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)

151
Q

Normal CO for non-smoker and smoker?

A

Non-smoker: 3%

Smoker: 10-15%

152
Q

What is the formula for DLCO?

A

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

153
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)

154
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)

155
Q

Mueller maneuver’s effect on DLCO?

A

Increased DLCO since there is increased pulmonary capillary blood volume

Maneuver : forced expiration, then inhalation, the maneuver is used to figure out the cause of OSA

156
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.

157
Q

What is normal oxygen content in the blood?

A

17-20 mL/dL of oxygen

158
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)

159
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)

160
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

161
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

162
Q

What conditions cause increased DLCO?

A
  • asthma

- complete the rest of this answer

163
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
  • closing volume is higher and might exceed FRC
  • lower muscle strength leads to higher residual volume
  • decreased DLCO due to surface area and pulmonary capillary blood volume
  • stiffening of the chest wall–>less compliant
  • because of higher closing volume, even at FRC the patient may be ventilating just the top of the lung, perfusion needs to match these changes
  • basically aging sucks

Resp Exam (16 decks)

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