Physiology/Pathophysiology Flashcards
(147 cards)
1
Q
What cell types comprise the lining of the respiratory tract?
A
- Cuboidal (ciliated pseudostratified columnar) with goblet cells (mucous secreting) line the majority
- In bronchioles, club cells replace goblet cells
- In the alveoli:
- Type I (95% of surface area)=modified squamous epithelium
- Type II (~ 2x as many of these however)=cuboidal, produce surfactant
- Phagocytic alveolar macrophages
2
Q
Define collateral ventilation.
What are 3 possible pathways for collateral ventilation?
A
- Ventilation of alveolar structures through passages that bypass the normal airways; without collateral ventilation, alveoli distal to obstructed airways (in disease) would become atelectatic
- Possible pathways:
- Interalveolar communications through the Pores of Kohn
- Between the bronchioles and the alveoli through the canals of Lambert
- Interbronchiolar communications of Martin
3
Q
Describe the changes in breathing/respiratory pattern that occur with an upper airway obstruction.
A
- During inspiration, airways outside the thorax experience a transmural pressure gradient directed towards the lumen that tends to make them collapse (low pressure within, high pressure outside)
- Patients with upper airway obstruction present with inspiratory dyspnea
- Increasing respiratory effort worsen these conditions, since they augment the pressure gradient and cause a worsening of the collapse
-
Paradoxical abdominal movement (abdominal wall moves in instead of out during inspiration)
- URT obstruction, pleural effusion, reduced pulmonary compliance and diaphragmatic rupture/paralysis
4
Q
Explain the principle responsible for the appearance of expiratory dyspnea with lower airway disease.
A
Durring passive exhalation with healthy lower airways, transmural pressure gradient that tends to collapse the small airways is resisted by the attachment of elastic tissue in the alveolar septa.
When lower airways are diseased, intima thickened by inflammation and the lumen reduced by mucus, the same transmural pressure will end up collapsing these airways.
When severe, leads to air trapping, some degree of active exhalation.
Increased transmural pressure during forced exhalation preciptates small airway collapse and manifests as an expiratory effort.
5
Q
What is Poiseuille’s law?
A
Raw=8nl/πr4
n= viscosity, l=length, r= radius
Indicates that airway resistance is inversely proportional to the 4th power of the radius–airway narrowing profoundly increases airway resistance.
6
Q
Where is the location of greatest pulmonary airway resistance?
A
-
Medium sized bronchi (diameters >2mm)
- One would think that as the airways become smaller, the resistance would increase, however, as the airways branch further and further down, the cross-sectional area of the tracheobronchial tree actually increases…
7
Q
Define pulmonary compliance.
A
- Change in volume divided by change in pressure
- Lungs with high compliance can easily be distended such that a small increase in pressure causes a large increase in volume
- Steep slope on PV curve
-
Less compliant lungs require a large distending pressure to effect a small change in volume
- Shallow slope on PV curve
8
Q
Define hysteresis
A
- At any volume, the pressure on the expiratory curve is less than that of the inspiratory curve
- As tidal volume increases, the difference between the inspiratory/expiratory curve increases
- Occurs because the pressure generated by elastic recoil on expiration is always less than the distending transmural pressure gradient required to inflate the lung
- Hysteresis of the lung as a whole may be due to recruitment of new alveoli or small airways on inspriation and derecruitment/closing on expiration
9
Q
What is the purpose of surfactant and where is it produced?
A
- Surfactant is produced by the type II pneumocytes
- 90% lipid–dipalmitoyl phosphatidylcholine;
- Surface protein B&C: hydrophobic; asociated with lipid film, regulate absorption of lipid to the surface
- Surface proteins A&D: hydrophilic. role in innate antimicrobial defense.
- Lines the alveolar surfaces, lowering the elastic recoil due to surface tension, even at high lung volumes
- Increases the compliance of lungs, decreasing inspiratory work of breathing
- Surface tension of different-sized alveoli unequal; smaller alveoli have lower surface tensions, equalizing alveolar pressures within the lungs
10
Q
Discuss the concept of a lung unit (fast/slow alveoli) and how alterations in compliance and resistance affect the speed with which lung units fill and empty.
A
- The volume with which each lung unit fills depends upon its compliance and resistance
- Lung units with normal/low resistance, but low compliance fill rapidly
- Fast alveoli/short time constant
- Lung units with high resistance, but normal/high compliance fill slowly
- Slow alveoli/long time constant
- Flow applied to different lung units for same amount of time, will result in a difference in volume–units have different time constants!
11
Q
What is the pendelluft effect?
A
- Refers to non-homogeneous filling; fast alveoli will fill quickly and transfer to the slow alveoli, filling over time
- In patients with airway disease/abnormal compliance, can be transient gas movement out of some alveoli and into others as a result of lung units with different time constants, even when flow has ceased at the mouth
- Filling of a lung region with a partially obstructed airway will lag behind the rest of the lung such that it may continue to fill even when the rest of the lung has begun to empty, with gas moving into it from adjoining lung units.
12
Q
Compare static versus dynamic compliance
A
-
Static compliance
- Compliance calculated after an inspiratory hold (inflate to full inspiration, hold so no air can enter/leave, pressure will fall)–estimate of the true compliance of the lung tissue
- Independent of airway effects (resistance)
-
Dynamic compliance
- Calculate without an inspiratory hold--gas is moving–using the pressure measured at peak inspiration, incorporates airway resistance
Static compliance will ALWAYS be higher than dynamic compliance
13
Q
What are the equations for:
Static compliance
Dynamic compliance
A
- Static Compliance: Delta volume/(plateau pressure-PEEP)
- Dynamic Compliance: Delta volume/(peak pressure-PEEP)
14
Q
What is alveolar ventilation?
A
- The volume of fresh gas entering the alveoli per minute
- (VT-VD)/f
- (have to remember how to calculate dead space!)
15
Q
Define minute ventilation.
A
Volume of air breathed per minute
VT x f
16
Q
Define anatomic dead space.
A
The volume of the conducting airways (150ml in people…)
17
Q
Define physiologic dead space.
A
Encompasses anatomic+alveolar dead space
The volume of the lung that does not elimate CO2
**Physiologic and anatomic dead space are almost the same in normal patients, however, the physiologic dead space is increased in many lung diseases (because alveolar dead space is increased**
18
Q
List conditions that can increase anatomic dead space.
A
- Increasing body size
- Increasing age
- Increasing lung volume
- Sitting posture
- Hypoxia (bronchoconstriction)
- Lung disease (emphysema)
- Endotracheal intubation
19
Q
List conditions that can increase physiologic dead space.
A
- Increasing age
- Decreased pulmonary artery pressure
- IPPV (leads to increased pulmonary vascular resistance, decreased pulmonary blood flow)
- Increasing tidal volume
- Hyperoxic vasodilatation
- Anesthetic gases
- Lung disease (ALI/ARDS, PTE, atelectasis)
20
Q
What is Fick’s law of diffusion?
A
Vgas= (As x D x deltaP)/T
Vgas=volume of gas diffusing per minute
As=membrane surface area (can be altered by changes in pulmonary capillary blood volume, CO, pulmonary artery pressure, changes in lung volume)
D=diffusion coefficient of gas (dependedn on gas and properties of alveolar/capillary membrane)
deltaP=partial pressure difference of gas
T=membrane thickness (can be altered by changes in pulmonary capillary blood volume, CO, pulmonary artery pressure, changes in lung volume)
21
Q
What is the Bohr Equation for Dead Space?
A
VD/VT= (PaCO2-PECO2)/PaCO2
In people, if dead space is >0.6, weaning from the ventilator is considered to be unlikely….
22
Q
Discuss diffusion versus perfusion limited gases.
A
-
Diffusion limited
- Partial pressure of gas in pulmonary capillary blood equilibrates fully with the partial pressure of the gas in the alveoli while the blood is adjacent to the alveolus
- Properties of the barrier and the diffusivity of the gas limit its transfer
- CO–only increasing the available surface area for diffusion will increase its uptake
-
Perfusion limited
- Diffuse extremely rapidly
- Alveolar pressures of these gasess equilibrate completely with mixed venous blood before blood has left the alveolar-capillary unit
- Additional diffusion is only possible once new blood arrives at the alveolus
- **Nitrous oxide; under normal conditions, O2 and CO2 are perfusion limited, but some diffusion limitation may occur under some conditions**
23
Q
List the potential causes for hypoxemia.
Which are the most common?
A
- Low FiO2
- Hypoventilation
- Venous admixture
- Low V/Q regions
- No V/Q regions
- Shunting
- Diffusion impairment
**hypoventilation, V/Q mismatch, shunt**
24
Q
What may lead to diffusion impairment?
Is this O2 responsive or not?
A
- Processes that may thicken the barrier (interstitial/alveolar edema, fibrosis)
- Processes that decrease surface area (low cardiac output, tumors, emphysema)
- Processes that decrease RBC uptake of O2 (anemia, low pulmonary capillary blood volumes)
- In general, is a relatively uncommon cause of hypoxemia; the flat, type I pneumocytes have to be damaged enough that in the healing phase, thick cuboidal type II pneumocytes proliferate.
- Partially O2 responsive
25
What are some causes of **hypoventilation** and how does it **lead to hypoxemia**?
Is it oxygen responsive?
* Drugs (morphine, barbiturates) that depress drive to respiratory muscles, damage to the chest wall, paralysis of respiratory muscles...
* **Always leads to an increase in PCO2; will decrease PO2 unless additional O2 is inspired**
* Quite O2 responsive:
* Adding FiO2 has a substantial benefit on oxygenation even in the face of increased CO2 concentrations--increasing the FiO2 displaces nitrogen and allows more of the total partial pressure in the alveolus to equilibrate
26
How do you calculate the **A-a gradient** and what does it **signify**?
**PAO2-PaO2**
Where PAO2=(PB-PH2O)xFiO2 - (PaCO2/R)==the alveolar air equation!!
* PB=barometric pressure; 760mmHg at sea level
* PH2O=partial pressure of water vapor in air; typically 47mmHg
* FiO2=fractional inspired concentration of O2; 21% on room air
* PaCO2 comes from your blood gas
* R=respiratory quotient; use 0.8
And PaO2 comes from your arterial blood gas.
**Typical A-a gradient is \<10-15mmHg; calculated as a way to signify efficiency of gas exchange**
* Values **greater than this represent decreased oxygenating efficiency=venous admixture**
\*\*At sea level, breathing room air, the alveolar air equation can be shortened to **PAO2=150-PaCO2**\*\*
27
What are the **main capacitance vessels in the lungs**?
The **pulmonary capillaries** (distend markedly with pressure, important for the capacitative effects)
28
Describe **hypoxic pulmonary vasoconstriction**.
Alveolar *hypoxia/atelectasis causes active vasoconstriction in the pulmonary circulation*, s*hunting blood away from hypoxic or poorly ventilated areas of the lung and redirecting it to better ventilated areas.*
Mechanism is not well understood, but is a local respone, with hypoxia acting directly on pulmonary vascular smooth muscle to produce contraction and subsequent vasoconstriction.
Not a very strong response because of the small amounts of smooth muscle in the pulmonary vasculature.
29
Describe the PO2 and PCO2 levels in units with...
Low to no V/Q?--causes of low to no V/Q?
High V/Q?--causes of high V/Q?
* **Low V/Q:** low PO2 and high PCO2
* Low V/Q regions caused by small airway narrowing d/t moderate edema, pneumonia, hemorrhage, etc
* No V/Q regions are full small airway obstructions
* **High V/Q**: high PO2 and low PCO2
* Receives no blood flow but continues to ventilate
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30
Describe the differences in ventilation/perfusion in a given lung unit based upon its position within the lung (i.e top to bottom)...
* There is a very *HIGH V/Q ratio at the top of the lung, where there is minimal blood flow*
* There is a *LOWER V/Q ratio at the bottom of the lung, where there is much higher blood flow*
Ventilation increases slowly from top to bottom of the lung, whereas blood flow increases more rapidly.
31
Describe the **concept of a shunt** and the **3 types of pulmonary shunting** that can occur.
* Shunting refers to *blood that enters the arterial system without going through ventilated areas of the lung.*
* Types:
* **Anatomic** (physiologic vs pathologic): systemic venous blood entering the left ventricle wihout having traversed the pulmonary vasculature.
* *Physiologic*: 1-2% of CO enters the left side of circulation without passing through pulmonary capillaries
* *Pathologic*: right-to-left intracardiac shunts (i.e. tetralogy of Fallot)
* **True shunts/absolute intrapulmonary shunts**
* Mixed venous blood perfuses pulmonary capillaries that are associated with totally unventilated or collapsed alveoli. No gas exchange occurs here as this blood passes through the lung.
* **Shunt-like states**:
* *Collections of alveolar-capillary units with low V/Q ratios that act to lower the arterial O2 content* because blood draining these units has a lower PO2 than blood from units with a high V/Q ratio
* **Hypoxemia associated with shunting responds poorly to added inspired O2 (if 100% O2 is inspired, the arterial PO2 will not rise to the expected level)**
32
How do you **calculate the shunt fraction**?
How do you interpret the values?
**QS/QT= (CCO2-CaO2)/(CCO2-CvO2)**
Where:
* QS=shunt flow
* QT=total cardiac output
* CcO2=calculated pulmonary capillary blood O2 content
* CaO2=arterial oxygen content
* CvO2=mixed venous oxygen content
Doesn't necessarily indicate how the deviation away from normal oxygenation occurred, rather, it calculates what fraction of the CO would have to be "shunted" away from the gas exchange surfaces in order to account for the documented hypoxemia.
Venous admixture is usually \<5%; **values \>10% considered to be increased** and may increase to \>50% in severe diffuse lung disease
33
What is the formula for calculating **arterial oxygen content**?
**CaO2=(1.34 x [Hgb] x SaO2) +(0.003 x PaO2)**
34
What is the **Bohr effect**?
*Increases in the carbon dioxide partial pressure of blood or decreases in blood pH result in a lower affinity of hemoglobin for oxygen*
(The effect pH and pCO2 have on HGb/O2 affinity)
35
Draw the oxyhemoglobin desaturation curve; what are the useful "**anchor points**", and what **causes a right or left shift (and what do these "shifts" mean?**)
* **Anchor Points**: PO2 40=SO2 75%, PO2 100, SO2 97%
* **Right Shift**:
* Increase in temperature
* Increase in PCO2
* Increase in H+ (and thus a decrease in pH)
* Increase in 2,3-DPG (end product of RBC metabolism, will occur in chronic hypoxia)
* **Left Shift:**
* Decrease in temperature
* Decrease in PCO2
* Decrease in H+ (and thus an increase in pH)
* Decrease in 2,3 DPG
* Presence of CO (has 240x the affinity for Hgb than O2; interferes with the unloading of O2)
\*May help to remember that an exercising muscle is acidic, hypercarbic, and hot and it benefits from increased unloading of O2 from its capillaries!\*\*
A right shift means a reduced affinity of Hgb for O2--\>more uloading of O2 at a given PO2 in a tissue capillary!!!!
36
Define the **Haldane effect**.
Describes the **effect of oxygen on CO2 transport**
Deoxygenated blood can carry increasing amounts of CO2, whereas oxygenated blood has a reduced CO2 capacity
37
38
Which lung volumes **cannot** **be measured with a spirometer**?
*Total lung capacity,* *functional residual capacity* and *residual volume*
39
Define **tidal volume**
Lung volume representing the normal volume of air displaced between normal inhalation and exhalation
(ml/kg)
"normal breathing/filling of lungs"
40
Define **vital capacity**.
The greatest volume of air that can be expelled from the lungs after taking the deepest possible breath
"max inhalation followed by max exhalation--\>the exhaled volume"
41
Define **residual volume**
lung volume representing the **amount of air left in the lungs after a forced exhalation**; this volume cannot be measured, only calculated
42
Define **functional residual capacity**.
The **volume of air present in the lungs at the end of passive expiration (normal expiration)**
43
Define **inspiratory reserve volume**.
additional **air that can be forcibly inhaled after the inspiration of a normal tidal volume**
44
Define **expiratory reserve volume**.
the **additional amount of air that can be expired from the lungs by determined effort after normal expiration**
45
Define **inspiratory capacity**.
sum of the **expiratory reserve volume, tidal volume, and inspiratory reserve volume**. The inspiratory capacity (IC) is the *amount of air that can be inhaled after the end of a normal expiration*
46
Define **hypoxia** versus **hypoxemia** (and severe hypoxemia).
* **Hypoxia**: decrease in the *level of oxygen supply to the tisues*
* **Hypoxemia**: inadequate oxygenation of *arterial blood*; defined as *PaO2 \<80mmHg of SaO2 (SpO2) of \<95%*
* **Severe** hypoxemia is *PaO2 \<60, SpO2 of \<90%*
47
When is **supplemental oxygen administration indicated**?
* When **SaO2 is \<93% on room air or if PaO2 is \<70mmHg**
48
What is the equation for oxygen delivery (DO2)?
**DO2= Q x CaO2**
Where Q is cardiac output and CaO2 is the arterial oxygen content (remember how to calculate!)
49
What FiO2 is provided via:
1. Flow-By oxygen at 2-3L/min (nasal prongs similar)
2. A tight fitting facemask with flow rates of 8-12L/min
3. Oxygen hood (after flooding at 1-2L/min); flow rates of 0.5-1L/min
4. Oxygen cage
5. Nasal/nasopharyngeal catheters with 50-150ml/kg/min flow rate (patient discomfort likely above 100ml/kg/min)
6. Transtracheal oxygen at 50ml/kg/min
1. 25-40%
2. 50-60% (rebreathing is highly possible; awake patient probably won't tolerate!)
3. 30%-40%
4. 40-50%
5. 30-70%
6. 40-60%
50
Describe how **hyperbaric oxygen** functions.
* Provides *100% oxygen under supra-atmospheric pressures (\>760mmHg) to increase the percent of dissolved oxygen in the patient's bloodstream by 10-20%*
* Dissolved oxygen can *readily diffuse into damaged tissues that may not have adequate oxygen supply*
* Recommended for treatment of severe soft tissue injuries
51
What possible risk may be associated with **administration of supplemental oxygen to a chronically hypercapnic patient**?
* **Depression of the hypoxic respiratory drive** and can result in severe hypoventialation and respiratory failure
* The hypoxic drive for ventilation is important in these patients--they have chronically increased CO2 levels, and therefore, a diminished central/peripheral O2 response. Arterial hypoxemia in these patients is the principle stimulus for ventilation.
52
Describe the **5 phases of pulmonary oxygen toxicity.**
How long can an FiO2 of 50% be administered to avoid oxygen toxicity?
1. **Initiation Phase**
1. O2 derived free radicals (superoxide anion, perioxide, hydroxyl radicals) cause direct damage to pulmonary epithelial cells as cellular antioxidant stores become damaged
2. Occurs within 24-72 hours of exposure to 100% O2
2. **Inflammatory Phase**
1. Massive release of inflammatory mediators leading to increased tissue permeability and development of pulmonary edema
3. **Destruction Phase**
1. Severe local destruction occurs, most associated with patient mortality
2. Accumulation of platelets and neutrophils in pulmonary tissue
4. **Proliferation Phase**
1. If patient survives, type II pneumocytes/monocytes proliferate
5. **Fibrosis Phase**
1. Collagen deposition and interstitial fibrosis; can result in permanent pulmonary damage
Administer an *FiO2 of 50% for no longer than 24-72 hours* (difficult to do without mechanical ventilation :) )
53
Describe **3 important clinical implications of the relationship of SO2/PO2 on the oxyhemoglobin dissociation curve.**
1. **Small changes in SpO2 represent large changes in PO2** on the sigmoidal curve
1. Difference between normoxemia, hypoxemia, and severe hypoxemia minimal
2. **Severe hypoxemia is defined at a level when the hemoglobin is still 90% saturated**
1. PO2 is the driving force for O2 diffusion down to the mitochondria
2. SO2 is the reservoir that prevents the rapid decrease in PO2 that would otherwise occur when O2 diffuses out of the blood
3. **Saturation measurements cannot detect the difference between a PaO2 of 100 and 500**
1. Important when monitoring/tracking patients receiving supplemental oxygen
54
* Give an example of a disease process that would lead to l**ow V/Q regions** (V/Q mismatching). Would this be **responsive/non-responsive to oxygen therapy**?
* Progression of this disease process may lead to **atelectasis**, which would represent which type of **venous admixture/cause for hypoxemia**? Would this be responsive/non-responsive to oxygen therapy?
* **Moderate to severe diffuse lung disease**--\>edema, pneumonia, hemorrhage. Responsive to oxygen therapy
* Atelectasis is a representation of **NO v/q units** (airway collapse, but they are perfused); typically **not responsive to oxygen therapy**, requires PPV to open the airways up. Has been referred to as a "physiologic shunt"
55
What effect would the presence of a **PTE** (an example of *ventilated, but unperfused lung units*) have on the net **PaO2**?
**No impact on the net PaO2-**-essentially there will be alveolar dead space ventilation, with no blood flow to or from these regions
56
Describe how **pulmonary injury may progress to development of a diffusion impairment** (which is an uncommon cause of hypoxemia)
* Results due to a **thickened respiratory membrane.**
* With pulmonary injury, fluid leak will ultimately build up enough pressure that they break into airways causing 1) airway narrowing (low V/Q) and then small airway and alveolar collapse (no V/Q), without a diffusion defect.
* In order for a diffusion defect to occur, *flat type I alveolar pneumocytes must be damaged (inhalation/inflammatory injury)*
* In the healing process, *thick cubiodal type II pneumocytes proliferate across the surface of the gas exchange membrane*
* \*\*ARDS, O2 toxicity!\*\*
* *Substantial diffusion defect until the type II pneumocytes ultimately mature to type I pneumocytes*
57
Describe the **"120 rule"** when estimating lung function.
* If a patient is breathing 21% oxygen at sea level, the **PaCO2+PaO2 should equal 120mmHg (normal PaCO2 of 40, minimum PaO2 of 80)**
* If the value is **less than 120, suggests the presence of venous admixture**; the **greater the discrepancy, the worse the lung function**
* \*\*\*Only appropriate at sea level and on room air!!!\*\*\*
58
Describe how to interpret the **PF ratio (PaO2:FiO2)**
* Best to use if the patient is receiving **supplemental oxygen** (use *A-a gradient or 120 rule if on room air*)--on room air, elevated PaCO2 levels will have an impact on the PF ratio
* **Normal** values for **PF \>400mmHg**
* **\<300mmHg=severe defects in gas exchange**
* **\<200mmHg=ARDS suspected**
59
Define **minute ventilation**. How do you **calculate** it?
* **Total ventilation; total volume of gas inhaled/exhaled per minute**
VT x f
60
**Dead space ventilation** consists of the **portion of tidal volume/minute that doesn't participate in gas exchange.**
Describe the **4 categories of dead space**.
1. **Anatomic** dead space: volume of gas filling upper airway, trachea, lower airways to the level of the terminal bronchioles
2. **Alveolar** dead space: portion of inspired gas that passes through the anatomic dead space and mixes with gas in that alveoli, but does not participate in gas exchange with the pulmonary capillaries
3. **Physiologic** dead space: *anatomic + alveolar dead space*. In a normal lung, essentially the same as anatomic dead space, however, with lung disease, the amount of alveolar dead space is likely to increase, therefore the physiologic dead space will as well.
4. **Apparatus** dead space: breathing device/circuit
61
**Venous CO2** levels are typically....
**3-6mmHg higher** than corresponding arterial value during steady state conditions
62
Which **main groups of neurons located in the medulla and pons** are responsible for the **control of breathing**?
* Medullary respiratory center
* Apneustic center
* Pneumotaxic center
63
Describe the division of the neurons in the **medullary respiratory center** and w**hat actions each group is responsible for**
* **Dorsal Group**
* In region of nucleus tractus solitarius
* Responsible for **inspiration**; thought to have **intrinsic, periodic firing**
* **Ventral Group**
* Comprises 4 **nuclei** (nucleus retroambiguus, para-ambiguus, nucleus retrofacialis, pre-Botzinger complex)
* Controls **voluntary forced exhalation**, acts to **increase the force of inspiration**
64
What is the role of the **apneustic center**?
* **Coordination of the speed of inhalation and exhalation.**
* Sends stimulatory impulses to the inspiratory area that activate and **prolong inspiration**
65
What is the role of the **pneumotaxic center**?
* Sends i**nhibitory impulses to the inspiratory center, terminating inspiration**
* **Regulates the inspiratory volume** and **respiratory rate**
* Involved in the fine-tuning of breathing
66
Which s**egment of the spinal cord** contains the nerve fibers mediating **respiration**?
**Phrenic** motor neurons in the ventral horns from **C3-C5**
**External intercostal motor neurons** throughout the thoracic spinal cord
67
Describe the role of the **central chemoreceptors.**
* **Responsible for ~85% of respiratory response to CO2**
* PCO2 value in CSF/venous blood ~10mmHg higher than that of arterial blood
* CO2 readily penetrates BBB, forms carbonic acid, and dissociates into H+ and HCO3
* **H+ concentration in brain interstitium and CSF directly parallels changes in arterial PCO2**
* **CO2 level in blood regulates ventilation primarily through effect on the pH of the CSF**
* \*Increases in CSF H+ result in proportional increases in ventilation
68
Describe the role of the **peripheral chemoreceptors**.
* Located in carotid body and aortic arch
* *Carotid body receptors primarly responsible for ventilation*
* **Respond to decrease in blood pH and PaO2, increasing PCO2 and hypoperfusion with an increased drive for ventilation**
* Exclusively responsible for the **increase in ventilation secondary to hypoxemia**
* Response to arterial PCO2 is less important than that of the central chemoreceptors
* BUT have a more rapid response and may be more important in adjusting ventilation in response to acute changes in PCO2
69
Describe **3 groups of lung receptors** and their actions.
* **Pulmonary stretch receptors**
* Respond to excessive stretching of the lung during large inspirations
* Main effect is slowing of respiratory frequency by increasing expiratory time--\>**"Hering-Breuer inflation reflex**"
* **Irritant receptors**
* Stimluated by noxious gases, cold, ihanled dusts
* Main effect is bronchoconstriction, increased respiratory rate
* **Juxtacapillary "J" receptors**
* Respond readily to chemicals in the pulmonary circulation, distention of the pulmonary capillary walls, accumulation of interstitial fluid
* Triggering leads to rapid, shallow breathing; excessive stimulation may lead to apnea
* Likely play a role in *dyspnea associated with heart failure, interstitial lung disease*
70
Describe the **four categories of abnormalities that may lead to hypercapnia** (\>36mmHg in a cat, \>42mmHg in a dog)
1. Hypoventilation
2. Increased dead space ventilation
3. Increased CO2 production with a fixed minute ventilation
4. Increased inspired CO2
Hypoventilation, increased dead space ventilation are the most common!
71
What are the **neurologic sequelae of hypercapnea**?
**Cerebral blood flow is increased** in response to elevated PCO2 as a result of **vasodilation** of *cerebral blood vessels* and *increased systemic blood pressure.*
This increase in cerebral blood flow leads to an **increase in ICP** and accompanying clinical signs.
72
Describe how sudden **correction of arterial hypoxemia** may cause a **worsened hypercapnia** in a **patient** with **chronic hypoventilation** and the development of an acute hypoxemia (3 proposed mechanisms).
1. *Depression of formerly hypoxic-driven peripheral chemoreceptors* causing worsened hypoventilation
2. *Relief of hypoxic pulmonary vasoconstriction in poorly ventilated lung regions* that further *reduces the ability of these units to eliminate CO2* as *local perfusion increases without concomitant increase in ventilation*
3. Significant correction of hypoxemia causes *better saturation of hemoglobin* so that previously buffered protons on deoxyhemoglobin are released with subsequent generation of new CO2 from the stores (i.e. *Haldane effect*)
## Footnote
**\*\*Give low flow oxygen to increase PO2 to ~60mmHg and SO2 to 90%--don't correct higher!!!\*\***
73
Why do patients with **upper airway disease** tend to have **loud breathing** and **increased inspiratory time**?
**Prolonged expiration** and **expiratory dyspnea**?
* Inspiratory noise/distress result from c*ollapse of the upper airway rostral to the thoracic trachea because generation of negative intrathoracic pressures on inspiration collapse the weakened airway structure into the lumen; prolongs the inspiratory phase and creates noise*.
* *Increased intrapleural pressure on expiration collapses the upper airway* caudal to the thoracic inlet (intrathoracic trachea/mainstem bronchi) resulting in *prolonged expiration and expiratory dyspnea.*
74
Define **paradoxical laryngeal motion**
**Inward movement of the arytenoids secondary to negative pressure** generated upon **inspiration**.
75
What are the primary anatomic components of **brachycephalic syndrome**?
Secondary complications (that may develop from increased resistance to airflow)?
* Primary components
* *Stenotic nares*
* *Elongated soft palate*
* *Tracheal hypoplasia*
* *Everted laryngeal saccules*
* Secondary components
* +/- nasopharyngeal turbinates
* Tonsillar eversion
* Laryngeal/tracheal collapse
* Chronic GI signs
76
What is the most important aspect of surgical intervention for brachycephalic airway syndrome?
Widening stenotic nares (since 80% of resistance of airflow is through nose)
77
List two possible causes for tracheal collapse.
* Dorsal trachealis flaccidity
* Loss of rigidity of tracheal cartilates from decreased GAG, chondroitin, and Ca content
78
The mucociliary apparatus in dogs with tracheal collapse is presumed to be compromised and may predispose them to bacterial pneumonia.
What are the most commonly isolated bacterial spp from these dogs?
* Pseudomonas
* Pasteurella
* Ecoli
* Staph
79
Tracheal collapse is graded I-IV, which are equivalent to what percentages of occlusion of the lumen?
25%, 50%, 75%, 100%
80
List **three potential complications of upper airway obstruction** (aside from hypoxemia/hypercarbia and respiratory distress...)
Hyperthermia
Non-cardiogenic pulmonary edema
Aspiration pneumonia
81
Which **type of ET tube cuff** is more likely to cause **tracheal trauma**?
**Low volume, high pressure cuffs**
82
How much of the trachea can be safely resected?
20% in a young dog, 25-50% in a mature dog
\*\*"Split" cartilage technique has been shown to be more successful\*\*
83
What is the **ideal ET tube cuff pressure to maintain a seal** without compromising tracheal integrity?
**20-30mmHg**
84
Which diseases may be appropriately classified as allergic airway disease?
Canine allergic bronchitis (eosinophilic bronchopneumopathy)
Parasitic larval migration
Pulmonary infiltrates with eosinophils (PIE)
Feline asthma
85
Allergic airway disease in small animals typically causes which three changes?
1. Increased numbers of eosinophils in the airways
2. Hyperinflation of the lungs
3. Thickening of the bronchi/bronchioles
86
What is the most common migratory parasite to cause an allergic response in the canine lungs?
Toxocara canis
Elicit a type I hypersensitivity reaction in the lungs that leads to bronchoconstriction/inflammation within the airways and lung parenchyma
87
What are the **2 main pathophysiologic forms of pulmonary edema**?
**Common causes** of each?
1. **High pressure edema** (caused by increased pulmonary capillary hydrostatic pressure)=cardiogenic with CHF
2. **Increased permeability edema** (caused by damage of the microvascular barrier and alveolar epithelium)=ALI/ARDs, PTE, VALI, inhaled insult (smoke inhalation)
88
**What is Starling's formula**?
89
List **tissue safety factors** **protecting against development of pulmonary edema**.
1. In normal tissues, *extravasation of low-protein fluid causes a fall in interstitial COP, resulting in preservation of the net COP gradient,* protecting against further fluid extravasation
2. I*ncreased interstitial hydrostatic pressure* which *opposes further extravasation*
3. *Increased driving pressure for lymphatic flow*
90
What is the **MAIN factor preventing development of pulmonary edema**?
**Increased lymphatic flow**
91
What is the **main determinant** of **fluid extravasation** and **pulmonary edema development**?
**Hydrostatic pressure**
92
Describe how **high-pressure edema** forms.
* *High pulmonary capillary pressures cause fluid extravasation that eventually overwhelms lymphatic removal*
* Fluid initially flows towars the peribronchovascular interstitium, finally spilling into the airspaces at the junction of the alveolar/airway epithelia
93
Describe how **increased permeability edema** forms
* Occurs following **injury to the microvascular barrier** (or alveolar epithelium), allowing leakage of high protein fluid
* Because of the *increased permeability* (which *reduces the reflection coefficient in Starling's formula*), the *protective fall in interstitial COP is diminished*
* Hydrostatic pressure then becomes the main determinant of edema formation
* **Interstitial fluid accumulation can then occur at lower hydrostatic pressures and can accumulate rapidly**
* In severe injury, with both endothelial/epithelial injury, there is a direct connection between the alveoli and the intravascular space, which allows for flooding
94
How is pulmonary edema fluid cleared?
* Largely via the **bronchial circulation** (likely bc most fluid accumulates in the peribronchovascular areas)
* **Rate of edema clearance depends on fluid type-**-pure water absorbed rapidly, higher protein fluids take longer (hours to days)
95
Briefly describe the **"blast" theory** as it pertains to neurogenic pulmonary edema
* Seen acutely after an acute neurologic event (seizures, head trauma, electric cord bite)
* **_Massive neuronal sympathetic activity_ results in a series of events causing both hydrostatic and increased permeability edema.**
* Initially **hydrostatic pressure edema occurs,** but at very **high pulmonary hydrostatic pressures, endothelial cell injury and vascular leak** result in RBC/protein leakage into the alveouls.
96
Describe the "**permeability defect" theory** as it pertains to neurogenic pulmonary edema
* NPE can occur in the absence of changes in systemic vascular pressure (increases)
* **Stimulated sympathetic nerve fibers of the pulmonary microvasculature can increase the size/number of endothelial pores, resulting in a direct increase in pulmonary vascular permeability and high protein edema**
* **Endothelin I** has been speculated to be a possible mediator , along with **norepi** and **neuropeptide Y**
97
Describe the development of **negative pressure (noncardiogenic) pulmonary edema**
* Occurs after an upper airway obstruction
* **Extreme subatmospheric intrathoracic pressures generated that cause pulmonary vascular pressure overload, an increase in vascular return, and preload.**
* Thought to be exacerbated by sympathetic stimulation associated with hypoxia causing an increase in afterload.
* Both **hydrostatic pressure edema and resultant microvascular damage can occur**
* **Endothelial cell injury** and **vascular leak** can cause **permeability edema**
98
What is **re-expansion edema**?
* *Reported after acute re-expansion of chronically collapsed lung lobes*
* Suggeted mechanisms include decreased surfactant in collapsed lung tissue, negative interstitial pressure, mechanical disruption of pulmonary parenchyma, oxygen free radical formation, reperfusion injury
99
Where is the radiographic pattern for cardiogenic edema located\>
Non-cardiogenic (of any cause)?
* Peri-hilar
* Dorsocaudal (if cranioventral, more suggestive of aspiration pneumonia...)
100
Define pneumonia
Inflammation of the lung parenchyma
101
List characteristic radiographic changes supportive of pneumonia.
* Alveolar opacification:
* Air bronchograms
* Silhouetting of lung(s) with the heart
* Consolidation (with or without interstitial patterns)
102
What are common bacterial isolates from dogs with infectious pneumonia?
Pasteurella, EColi, Staph, Strep
103
What are some advantages of **bronchodilator therapy** in an animal with pneumonia?
Disadvantages?
* **Advantages**
* Increasing airflow
* Improved mucokinetics
* Improving ciliary activity; increasing serous nature of respiratory secretions
* **Disadvantages**
* May suppress cough reflex, worsen VQ mismatch, allow exudates within affected portion of the lung to spread to unaffected areas.
104
Define aspiration pneumonitis versus aspiration pneumonia.
* **Aspiration pneumonitis:** acute lung injury caused by inhalation of chemical irritants (most commonly gastric contents)
* **Aspiration pneumonia**: pulmonary bacterial infection that develops after aspiration
105
What **4 factors contribute to the magnitude of lung injury seen after aspiration**?
1. **pH**
1. *Severe damage* seen with *aspiration of fluid pH \<1.5, minimal damage if pH \>2.4 unless containing particulate matter*
2. **Volume**
3. **Osmolality**
4. Presence of **particulate material**
106
Describe the **pathogenesis of acid-induced lung injury.**
* Initially the *direct caustic effects of the aspirate damage bronchial and alveolar epithelium*
* Stimulates *tracheobronchial substance P neurons* which induces tachykinin release
* Results in **neurogenic inflammation, bronchoconstriction, vasodilation, increased vascular permeability**
* Occurs within 1-2 hours after aspiration
* 4-6 hours after aspiration--\>l*arge increases in pulmonary capillary permeability and protein extravasation*
* Chemotactic mediators are released, attracting neutrophils to the lung
107
What is the **Berlin definition for diagnosis of ARDS**?
108
What is the most **consistent histologic pattern** associated with **ARDS**?
Diffuse alveolar damage (DAD)
109
What are the **three stages of lung injury** associated with ARDS?
1. **Exudative phase (days 0-6)**
1. Characterized by a protein-rich edema and the presence of eosinophilic hyaline membranes in the walls of the alveolar ducts
2. **Proliferative phase (days 4-10)**
1. Decrease in edema and hyaline membranes, increase in interstitial fibrosis
3. **Fibrotic phase (day 8 onward)**
1. Pronounced fibrosis that may ultimately obliterate areas of the lungs
110
What are the **primary factors contributing to the arterial hypoxemia observed in ALI/ARDS**?
* Low PAO2
* VQ mismatch
* Shunting
\*\*Diffusion limitation is rarely a _major_ contributor to hypoxemia in people with ARDS\*\*
111
Treatment of ARDS is largely supportive in nature, however, what is the **basic current ventilation guideline for management**?
* Lung protective ventilation--\>low tidal volumes, appropriate PEEP
* Limiting fluid balance to prevent overhydration
112
What is the **hallmark finding on a PV curve for a patient with ARDS**?
**Lowered compliance**
113
What **4 mechanisms** are described as important in **development of pulmonary contusions** (secondary to acute compression/subsequent expansion leadint to transmission of mechanical forces/energy to pulmonary parenchyma)?
1. "**Spalling effect"**
1. Shearing/bursting phenomenon that occurs at gas/liquid interfaces and may disrupt the alveolus at the point of initial contact with shock waves
2. "**Inertial effect"**
1. Low desnity alveolar tissue stripped from heavier hilar tissue as they accelerate at different rates, resulting in mechanical tearing/laceration of the lungs
3. "**Implosion effect**"
1. Results from rebound/overexpansion of gas bubbles after a pressure wave passes; can lead to tearing of pulmonary parenchyma from excess distention
4. **Damage from displacement of fractured ribs**
\*\*Subsequent hemorrhage leads to bronchospasm and alveolar collapse as a result of decreased surfactant production\*\*
114
Approximately what percentage of dogs requiring IPPV for management of pulmonary contusions survive to discharge?
30%
115
**PTE** results most commonly from....
Formation of **clot material in the right side of the heart** or at a **distant site in the venous system** that breaks free and lodges in the pulmonary vasculature.
116
The **key pathophysiologic responses to PTE** include...
* **Alterations in hemodynamics** as a result of increased pulmonary vascular resistance
* Abnormalities in **gas exchange**
* Altered **ventilatory control**
* Derangements in **pulmonary mechanics**
117
Describe the response that occurs with vascular obstruction from embolization.
* Results in *mechanical obstruction of the vasculature* and r*eactive vasoconstriction* because of the release of vasoactive mediators
* Leads to a r*eduction in the cross-sectional area of the pulmonary circulatory bed, increases in vascular resistance*, and in moderate to severe cases, *increases in pulmonary arterial pressure*.
118
What is the Starling's formula as it applies to the pleural space?
119
Physiologic fluid flux in the pleural space is governed by...
* Starling's forces
* Degree of mesothelial and endothelial permeability
* Lymphatic drainage
120
What are the fluid **triglyceride** and **cholesterol** levels in comparison to those of the serum in a pet with a **chylothorax**?
* Triglyceride
* Higher in fluid than serum
* Cholesterol
* Equal to or less than in fluid than serum
121
What **volume of pleural effusion is necessary to impair ventilation** in dogs? Cats? (assuming normal lung function prior)
* Dogs: 30-60ml/kg
* Cats: 20ml/kg
122
Define tension pneumothorax.
Site of air leakage creates a *one-way valve during inspiration, resulting in a rapidly increasing pleural pressure that exceeds atmospheric pressure*.
123
What are the **Light's criteria for diagnosis of an empyema**?
Evaluation of **protein, lactate, glucose in the fluid.**
An *effusion glucose of \<3.3mmol/L (60mg/dL), a lactate of \>1000 U/L (1000u/dL) and a pH of \<7.2 is suggestive of an empyema*.
Have been evaluated in classification of *feline pleural effusion*, with the lactate and pleural fluid/serum TP ratio found to be most sensitive and specific markers to classify fluid as transudate versus exudate.
124
What would be an appropriate empiric antimicrobial protocol for a dog with pyothorax? A cat?
* Dog
* Potentiated penicillin and a fluoroquinolone for increased gram negative coverage
* Amikacin shouldn't be used as it has poor penetration into the thoracic space
* Cat
* Monotherapy with a penicillin
* Enterobacteriacea are infrequently isolated, therefor monotherapy is likely to be appropriate
125
What are listed as indications for thoracostomy tube placement in humans for treatment of empyema?
* If fluid is obviously purulent on aspiration
* Positive fluid culture results
* Pleural fluid pH \<7.2
* Loculations are present on radiographs/ultarsound
* Poor clinical progress with antimicrobial therapy alone
126
What are *indications for removal* of a thoracostomy tube in a patient being treated for pyothorax?
* clinical patient improvement
* Decrease in pleural fluid volume to less than 2ml/kg/d (per tube)
* Resolution of infection on cytlogic evaluation of aspirated fluid (absence of microorganisms and decreased numbers of neutrophils with a less degenerative appearance)
* Radiologic evidence of successful pleural fluid drainage
127
What are some proposed benefits of pleural lavage in patients being treated for pyothorax?
* Reduction of pleural fluid viscosity
* Facilitation of fluid drainage
* Prevention of thoracostomy tube obstruction
* Dilution/reduction of bacteria and inflammatory mediators
* Debridement of pleural cavity with breakdown of adhesions
\*\*In a study evaluating outcome in dogs treated for pyothorax, pleural lavage was associated with higher short and long term survival rates when compared to dogs treated without lavage (Boothe, JAVMA 2010)\*\*
128
What are some **criteria indicating that surgical intervention is warranted** in patients currently being medically treated for **pyothorax**?
* "Failure" of medical therapy
* Persistance of pleural effusion or infection despite appropriate antimicrobial therapy and chest tube drainage
* Absence of clinical improvement after 3-7 days
129
What is the reported prognosis/survival rate for dogs with pyothorax? Cats?
Risk factors for recurrent disease?
* Dogs
* 83% (range 29-100%)
* Cats
* 62%; cats who survive beyond the first 24 hours of hospitalization generally have a good prognosis
* Recurrance rates range from 0-15%
* Associated with a poor prognosis
* Infection with nocardia/actinomyces
* Inhalation/migration of plant material
130
What is the most common cause of pyothorax in the dog?
In the cat?
* Dog:
* Foreign body/grass awn migration
* Cat
* Parapneumonic spread
131
Define dyspnea
"The subjective experience of breathing discomfort that originates from interactions between various physiological, psychological, social and environmental factors"
132
What are the **5 _upper airway receptor_ types**?
1. Pressure
2. Drive
3. Cold
4. Irritant
5. C-fibers
\*\*The role of the upper airway receptors in the origin of dyspneic sensations is thought to be limited\*\*
133
List the **5 types of lower airway (tracheobronchial) receptors** and their main actions.
1. **Slowly adapting receptors (SARs)**
1. Stimulated by inflation of the lung; a*ctivation leads to shortening of inspiration, prolongation of expiration, reflex bronchodilation*
2. Agents that *increase SAR firing have been shown to alleviate some of the sensation of dyspnea*
2. **Rapidly adapting receptors (RARs)**
1. *Faster adaptation rate;* stimulation will lead to p*rolongation of inspiration and shortening of expiration, reflex bronchoconstrication*
2. Agents that *decrease RAR firing* have been shown to help in dyspnea
3. **C-fibers**
1. Thought to contribute to *neurogenic pulmonary inflammation*
2. Stimulation leads to *bronchoconstriction, mucous secretion, hypotension, bradycardia and laryngospasm*
3. Respiratory response to activation includes apnea and rapid, shallow breathing patterns
4. **Neuroepithelial bodies (NEB)**
1. Thought to serve as hypoxia sensors
5. **A-ð nociceptors**
1. Role in perception of dyspnea is not well known
134
Describe the three categories of dyspnea.
1. **Air Hunger**
1. "Uncomfortable urge to breathe"
2. Thought to arise from altered ventilatory chemical loads (hypoxemia, hypercapnea)
3. Input from pulmonary stretch receptors and chemoreceptors appear to be important in development of sensation
2. **Increased Work/Effort**
1. Unpleasant sensation that arise when greater than usual respiratory muscle activity is required to maintain ventilation.
2. Thought to raise due to increased mechanical loads
3. Signals from c-fibers and muscle mechanoreceptors appear to be most important
3. **Asthmatic Tightness**
1. Thought to result as a result of bronchoconstriction; primarily reported in asthmatics
2. May also be secondary to hyperinflation, although little supporting evidence
135
Describe how **furosemide may function in alleviation of dyspnea.**
* Inhaled furosemide has been shown to protect against bronchoconstriction and inhibition of the cough reflex.
* **Thought to increase SAR signals and decrease RAR output**
* MOA not well known, but thought that it *may increase local sodium ion concentrations in the airways following aerosol delivery*
* Increased local Na concentration may increase Na influx, thought to increase pulmonary stretch receptor capability
136
What are some proposed mechanisms of the role of corticosteroids in the alleviation of dyspnea?
* Not well known
* May reduce airway inflammation, restore epithelial structure, and CNS effects
137
What are the **four phases of the capnogram?**
1. Flat baseline segment; gas typically CO2 free
2. Period of expiration where CO2 containing alveolar gas begins to be exhaled in a mixture of gas from the dead space
3. Plateau; PCO2 is almost as constant as alveolar gas
4. Rapid downstroke corresponding to inspiration
138
What are the causes of these abnormal capnograms?
139
What are the **forms of hemoglobin**?
* **Oxyhemoglobin**
* When oxygen is bound to the heme group (for transport through the bloodstream)
* **Deoxyhemoglobin**
* Hemoglobin without oxygen bound to it
\*\*Oxy+deoxyhemoglobin are the functional hemoglobins\*\*
* **Dyshemoglobins**
* Hemoglobins that are incapable of binding oxygen
* **Methemoglobin**
* Develops when the iron of the heme grop is oxidized from the ferrous form to the ferric form
* **Carboxyhemoglobin**
* Created when hemoglobin binds to CO rather than oxygen
* Hemoglobin has an affinity for CO of \>200x its affinity for oxygen; CO binding to hemoglobin prevents O2 binding and carriage
* **Sulfhemoglobin**
* Rare form; formed when hemoglobin reacts with sulfide in the presence of huemoglobin
140
Compare **functional versus fractional hemoglobin saturation.**
* **Functional** hemoglobin saturation
* Percentage of *total functional hemoglobin that is saturated; takes into account oxy and deoxyhemoglobin*
* Standard pulse oximeters report the functional hemoglobin saturation
* **Fractional** hemoglobin saturation
* Refers to the *ratio of oxyhemoglobin to ALL hemoglobin species present, including methemoglobin and carboxyhemoglobin*.
* *CO-oximeters can report fractional SO2*
* Best to use if abnormal amounts of dyshemoglobin are present; this will accurately reflect the blood oxygen content at the dyshemoglobinemia's effect on the patient
141
How does a **pulse oximeter estimate the oxyhemoglobin percentage**?
* Uses 2 wavelengths of light
* **Red at 660nm and infrared at 990nm**
* As light is introduced into the tissues, each type of hemoglobin absorbs a different wavelength of light
* **Oximeter uses the differential light absorption of deoxyhemoglobin and oxyhemoglobin to calculate the arterial blood's functional hemoglobin saturation.**
\*\*The presence of **methemoglobin** usually causes falsely **depressed** SpO2 values and **carboxyhemoglobin** usually causes falsely **elevated** SpO2 values\*\*
142
How does a **co-oximeter work**? Benchtop versus pulse co-oximetry?
* **Benchtop**
* Measures **hemoglobin oxygen saturation in a blood sample** rather than through tissue; uses different wavelengths of light to measure the fractions of all relevant species of hemoglobin
* Uses conductimetry to estimate the samples hematocrit and then reports the concentration of each species as a percentage of tHB
* **Pulse co-oximeter**
* *Uses wavelengths of light absorbed by carboxyhemoglobin and methemoglobin; functions similarly to pulse oximeter in this aspect*
143
What factors contribute to the pathology seen with smoke inhalation?
* **Carbon monoxide**
* Primary cause of immediate death from smoke inhalation
* Affinity 200-300 times greater for HgB; shifts oxygen-HgB dissociation curve to the left, decreasing offloading of O2 to the tissues
* **Hydrogen cyanide**
* Common in fires with wool, silk, synthetics
* Interferes with O2 utilization by cellular cytochrome oxidase; causes histotoxic hypoxia
* **Thermal injury**
* Direct injury deeper than the larynx is uncommon as heat is dissipated effectively by the thermal regulatory system of the nasal/oropharyngeal areas
* Mucosal edema, erosions, ulceration
* Laryngeal edema of biggest concern
* Steam has much greater heat capacity than dry air, likely to produce more extensive injury
* **Irritant gases, inhaled superheated particulate matter**
* Particulate matter acts as a vehicle by which the irritant noxious gases can be carried deep into the respiratory tract
144
What are some **consequences of smoke inhalation**?
* **Reduced lung compliance**
* Loss of the surfactant layer
* Pulmonary edema; may occur within minutes secondary to increased permeability
* ALI, ARDS...
* **Airway damage/obstruction**
* Mucociliary apparatus significantly impaired
* Progressive mucosal edema accompanied by mucosal sloughing over several hours
* **Bacterial pneumonia**
* Impairment of alveolar macrophage function; stagnant luminal contents create a milieu conducive to bacterial colonization
* Typically occurs as a secondary entity following therapeutic interventions (ET tube placement, trach)
* **Neurologic signs**
* May be delayed up to 2-6 days
145
ETCO2 is **how many mmHg higher/lower** than PaCO2?
**2-6mmHg LOWER**
146
What is the half life of CO on room air?
On 100% O2?
* ~250minutes
* ~26-148min
147
What is the formula to estimate the % of dead space ventilation?
% dead space ~~[(PaCO2-ETCO2)/PaCO2] x 100
