Respiratory Flashcards
fIf a patient were to develop a tension pneumothorax during HBOT, when does it most likely to happen?
At the decompression phase
Fick’s law and relevance in gas exchange
Vgas = A/T x (P1-P2) x d
Vgas = flow of gas across membranes
A= area of the membrane
T= thickness of the membrane (alveolar thickness <0.3um)
P1-P2 = pressure gradient
d= diffusion coefficient
d=solubility/√MW
True or False: Patient with marked respiratory acidosis can become hypoxemic too.
True
What is the definition of hypoxemia
PaO2 < 80 mmHg
List 4 different kinds of hemoglobins.
Oxygenated hemoglobin
Deoxygenated hemoglobin
Methemoglobin
Carboxyhemoglobin
Sulfhemoglobin
What is the two wavelengths of light on pulse oximeter?
940 nm (infrared)
660 nm (red)
How many percentage of total lung elasticity does tissue elastic forces contribute (to collapse the lung) and how many does fluid-air surface tension forces contribute?
Tissue elastic forces 1/3
Fluid-air surface tension forces 2/3
What cells secrete surfactant?
Type II alveolar epithelial cells (10% of the surface area of the alveoli)
What are the main components of surfactant?
Phospholipid dipalmitoyl phosphatidylcholine
Surfactant apoproteins
Calcium ions
True or False: Alveolar pressure caused by surface tension is directly related to alveolar radius. (Laplace’s law)
False
Alveolar pressure caused by surface tension Is INVERSELY related to alveolar radius → the smaller the alveolar, the greater the alveolar pressure caused by the surface tension
What are the three main components of the work of inspiration?
1) Compliance work/elastic work - work that required to expand the lungs against the lung and chest elastic forces
2) Tissue resistance work - work that required to overcome the viscosity of the lung and chest wall structures
3) Airway resistance work - work that required to overcome airway resistance to movement of air in
Fill out the blank.
What is the remaining of the air after a normal expiration call?
Functional residual capacity
*** NOT RESIDUAL VOLUME
Define anatomic dead space and physiological dead space.
Anatomic dead space: the total volume of the conducting airway (the area where normally gas exchange does not occur)
Physiological dead space: anatomic dead space + alveolar dead space
What is the formula for minute ventilation?
Minute ventilation = tidal volume x respiratory rate
The respiratory system has two circulation. What are they called and where are they?
High-pressure, low-flow circulation
- systemic arterial blood to the trachea, bronchia tree, connecting tissue of the lung
Low-pressure, high-flow circulation
- venous blood that enters the pulmonary arteries and to the alveolar capillary to gas exchange
How does hypoxia affect the systemic vessels and pulmonary vessels?
Systemic vessels - vasodilation
Pulmonary vessels - vasoconstriction
What is the definition of terminal bronchioles?
The smallest airways without alveoli.
What is the definition of respiratory bronchioles?
divided from terminal bronchioles, which have occasional alveoli budding from their walls
What concept does this graph highlight?
Gases move via convection in the large airways then they slow down significantly when they reach terminal and respiratory bronchi and alveoli due to massive increase in cross sectional area and the gases will move via diffusion
Which of the following volume can spirometer measure?
1) Total lung capacity
2) Tidal volume
3) Residual volume
4) Functional residual capacity
2) Tidal volume
What are the two methods to measure FRC?
Helium dilution
This method uses a harmless gas called helium.
You breathe in and out through a tube connected to a machine. The machine has a known amount of helium in it. When you breathe, the helium mixes with the air in your lungs.
The machine measures how much the helium gets diluted as it mixes with the air in your lungs. Because the amount of helium is known, and how much it is diluted is measured, the machine can figure out how much air was already in your lungs (which is the FRC).
Whole body plethysmography
Imagine you’re sitting inside a special airtight box. This box is part of the plethysmograph machine. When you breathe in and out, the amount of air in your lungs changes. This also changes the air pressure inside the box.
As you breathe, sensors in the box measure how much the air pressure changes. By knowing how much the pressure changes, the machine can calculate the amount of air left in your lungs after you’ve breathed out all you can (this is called the Functional Residual Capacity, or FRC).
What does the alveolar ventilation mean?
The amount of air that is available for gas exchange
If you want to increase alveolar ventilation, which way is more effective, increasing tidal volume or respiratory frequency?
Increase tidal volume, because anatomic dead space is fixed
What is the alveolar ventilation equation?
Respiratory laboratory commonly use Bohr’s method to measure physiology dead space. What is the equation?
What is normal physiological dead space percentage?
0.2 - 0.35
When the patient has pulmonary disease, how will the relationship between anatomic dead space and physiological dead space change?
Physiological dead space will be bigger than the anatomic dead space
How long does a red blood cell usually stay in the pulmonary capillary?
0.75 seconds
Explain what is diffusion limited and perfusion limited, and name an example for each of them
Diffusion limited
- The gas that enter the capillary can be rapidly picked up/bind to the red blood cells due to high affinity → minimal change in partial pressure → minimal back pressure to slow it down → the rate of diffusion depends on the property of the blood gas barrier
- Example: CO
Perfusion limited
- The gas that enter the capillary is barely bound to RBCs due to very low affinity → partial pressure rapidly increase → the faster the blood flow is, the more gas that can enter the capillary
- Example: N2O
Is O2 diffusion limited or perfusion limited? Why?
A combination of both
Under normal resting condition, O2 is already partially saturated in the blood due to mixed venous blood. O2 usually reach fully saturated state when the RBC is at 1/3 way of the capillary → perfusion limited
- If the patient’s blood gas barrier is abnormal and the oxygen cannot reach fully saturated state when the RBC is at the end of the capillary → perfusion limited + diffusion limited
Which gas is ideal for diffusion capacity measurement. Why?
Carbon monoxide
Because the gas is purely diffusion limited
Describe the route oxygen reach RBC in the lung.
Surfactant → alveolar epithelium → alveolar epithelium basement membrane → interstitial space → capillary basement membrane → capillary endothelium → plasma → red blood cell
What is normal systolic, diastolic and mean pulmonary arterial pressure? What about Aorta?
Pulmonary artery: 25/8 (15) mmHg
Aorta: 120/80 (100) mmHg
Pulmonary vascular resistance is only ____ that of the systemic circulation. What is the number?
1/10
What are the two mechanisms of decreased pulmonary vascular resistance when pulmonary vessels pressure increases?
1) Distension
- Predominant when pulmonary pressure is already high
2) Recruitment
- Main mechanism for pulmonary artery
- Open up more closed capillaries
How does the lung volume affect the pulmonary capillary and extra-alveolar vessels resistances?
When the lung volume is very small
- Extra-alveolar vessels become narrow/collapse (pull from the parenchyma «< vascular smooth muscle tone) → increased resistance
- Pulmonary capillary remains open
When the lung volume is very big
- Extra-alveolar vessels are pulled open by the lung parenchyma → decreased resistance
- Pulmonary capillary are collapsed because alveolar pressure»_space;> capillary pressure
- There is a sweet spot when the total resistance is the lowest
True or False: West’s zone 1 does not occur in healthy individual.
True
- It can happen when patient’s hypotensive or alveolar pressure increased significantly
What is West Zone 4? When will you see it?
When the interstitial pressure is higher than alveolar pressure and pulmonary venous pressure (but no pulmonary arterial pressure)
Pa > Pinterstitial > Pv > PA
Pulmonary edema at the base of the lung
What determines the blood flow in West Zone 2 and Zone 3?
Zone 2: gradient between alveolar and pulmonary arterial pressure
Zone 3: gradient between pulmonary arterial and pulmonary venous pressure
What determines the blood flow in West Zone 2 and Zone 3?
Zone 2: gradient between alveolar and pulmonary arterial pressure
Zone 3: gradient between pulmonary arterial and pulmonary venous pressure
True or False: Hypoxemia can cause pulmonary vasoconstriction.
False
Alveolar hypoxia (not blood!) cause vessel wall hypoxia → vasoconstriction
What is the cut-off for alveolar hypoxia induced-vasoconstriction?
Alveolar PO2 < 70 mmHg
What is the proposed mechanism of alveolar hypoxia induced-vasoconstriction?
Inhibition of voltage-gated K+ channel → Decrease the efficiency of Na/K-ATPase → increase intracellular Na → more Na to exchange for Ca (Na/Ca channel) → Increase Ca inflow → vasoconstriction
What are the two substances that ACE can convert/inactivate?
Angiotensin I
Bradykinin
List 5 substances that can be inactivated when they enter the pulmonary circulation
Bradykinin
Serotonin
Norepinephrine
Leukotriene
Prostaglandin E2 and F2𝜶
What is the most abundant immunoglobulin in the bronchial secretion?
IgA
What is the equation for A-a gradient?
A-a gradient = PAO2 - PaO2 = [FiO2x(Patm-PH2O) - PaCO2/0.8] - PaO2
Normal: < 10
- Normal PH2O = 47 mmHg
What is the formula to calculate pulmonary shunt from mixed venous blood?
This formula should only be used at 100% O2 to eliminate hypoventilation, low FiO2 and low V/Q mismatch as causes of hypoxaemia and leaving only physiologic or anatomic shunts as differentials
What is normal percentage of pulmonary shunt?
<5%
True or False: Ventilation and blood flow both increase from top to bottom of the lungs. Blood flow increase more rapidly than ventilation.
True
True or False: The ventilaiton perfusion ratio decreases from the top to the bottom of the lung.
True
Is the pH higher at the top or the bottom of the lung?
Higher at the top of the lung
True or False: The respiratory exchange ratio (CO2 output/O2 uptake) is higher at the apex than at the base.
True
Why the increased minute ventilation to a lung with V-Q inequality is usually effective at reducing the Paco2, but much less effective at increasing arterial Pao2?
The sigmoid shape (specifically, the plateau) of the oxygen-haemoglobin dissociation curve gives rise to a phenomenon whereby it is impossible to compensate for low V/Q areas. As blood travelling through well-ventilated regions of the lung (high V/Q) is already maximally oxygenated (i.e. lays along on the plateau), there is no way you can get any better oxygenation by increasing ventilation. In contrast, because the CO2 dissociation relationship is more linear, increasing ventilation of the already well-ventilated regions will still continue to improve the CO2 clearance from those regions.
What is Henry’s Law?
The amount of gas dissolved in the liquid/blood is proportional to its partial pressure
Does presence of COHb shift oxygen-hemoglobin dissociation curve to the right or left?
Left (increased O2 and hemoglobin binding)
Describe Bohr effect and Haldane effect.
Bohr effect: at the peripheral tissue, the increased partial pressure of CO2 and H+ decrease the affinity of hemoglobin affinity to O2 → facilitates unloading of O2
Haldane effect: at the lung, the increased partial pressure of O2 decrease the affinity of hemoglobin affinity to CO2 → facilitates unloading of CO2
* Deoxygenated hemoglobins have higher affinity to CO2
Which state of hemoglobin has lower affinity to oxygen, the tense state (T-state) or relax state (R-state)?
T-state
- It becomes more relaxed as more and more oxygen binds to the hemoglobin
The CO2-hemoglobin dissociation curve will shift to the left or right as SO2 increases?
Shift to the right (higher O2 → decrease hemoglobin affinity to CO2)
What are the four types of tissue hypoxia?
1) Hypoxic hypoxia
2) Anemic hypoxia
3) Circulatory hypoxia
4) Histotoxic hypoxia
On the pressure volume curve, the inspiration and expiration are not overlapped. What is it called and why?
Hysteresis
pressure required for inspiration is greater than the pressure required for expiration because of the surface tension and surfactant, as well as the alveolar recruitment and elastic property of the lung.
What is the definition of compliance?
The volume change per unit pressure change
What are the 3 main factors determining compliance?
1) elasticity of the lungs
2) elasticity of the chest wall
3) surfactant
Elasticity vs compliance
Elasticity= ΔP/ΔV
Compliance= ΔV/ΔP
List 2 causes of decreased lung compliance and 2 causes of increased lung compliance.
Decreased compliance: lung fibrosis, pulmonary edema, atelectasis
Increased compliance: pulmonary emphysema, normal aging lung
What is specific compliance?
Specific compliance = Cstat/FRC
FRC=functional residual capacity
It is a way to normalise compliance to lung volume (or patient size)
List 3 benefits of surfactant.
1) Reduce surface tension of the alveoli
2) Decrease work of breathing
3) Keep the lung dry
4) Promote stability of alveoli
Compared to the apex and base of the lungs, which one has better compliance and ventilation?
Base of the lungs
Because the resting volume is smaller and the change of volume during inspiration is bigger (expanding pressure is smaller at the base due to smaller transmural pressure due to the weight of the lung)
True or False: Functional residual capacity (FRC) is the equilibrium volume when the elastic recoil of the lung is balanced by the normal tendency for the chest wall to spring out.
True
True or False: The normal intrapleural pressure is 0.
False
-5 cmH2O (because of elastic recoil of the lung)
In the entire pulmonary system, where is the major site of airway resistance from?
Medium-sized bronchi
What does 0ABCD, ABCE, and 0AECD represent?
0ABCD represents work of breathing
ABCE represents the work to overcome the airway and tissue resistance
0AECD represents the work to overcome the elastic force
What is the equate for work of breathing?
WOB = pressure x volume
Where does breathing center locate?
Brainstem (pons, medulla)
Where is the normal respiratory rhythm generated?
Medullary respiratory center, Pre-Botzinger complex
What does apneustic center and pneumotaxic center do?
Apneustic center: excite the inspiratory center
Pneumotaxic center: inhibit inspiratory
There are two respiratory group (dorsal and ventral) in the medullary respiratory center. Which controls inspiration and which controls expiration?
Inspiration: Dorsal respiratory center
Expiration: Ventral respiratory center
How does PCO2 regulate the respiration?
By changing the pH of CSF
Blood Pco2 rises ➜ CO2 diffuses into the CSF from the cerebral blood vessels ➜ liberates H+ ions that stimulate the chemoreceptors ➜ hyperventilation ➜ blood Pco2 reduces and therefore in the CSF
Where is the central chemoreceptors?
Ventral surface of the medulla
What change does the peripheral chemoreceptors detect?
Change in PO2, pH and PCO2
What is the effect when the pulmonary stretch receptors are activated (during lung expansion)?
Hering-Breuer reflex
Vagus efferent –> inhibition of DRG and VRG –> stop inflation of the lung (protective mechanism)
Where are the pulmonary stretch receptors and irritant receptors?
Pulmonary stretch receptors: within airway smooth muscles
Irritant receptors: between airway epithelial cells
Where are the J receptors (Juxtacapillary receptors) and what is its function?
In the alveolar walls (close to the capillary)
When the pulmonary capillaries are enlarged or there is increased interstitial fluid in the alveolar wall → J receptors are stimulated → signals are transmitted through **non-myelinated C fibers **→ increased respiratory rate
True or False: Decreased PO2 can stimulate both central and peripheral chemoreceptors and cause increased ventilation.
False
Only peripheral chemoreceptors
Why patients with chronic respiratory disease lose their adequate response to elevated PCO2?
Renal compensation → the change in pH is abolished
- In this case, hypoxemia becomes the main stimulus to ventilate
Does the pH change mainly stimulate the central or peripheral receptors?
Peripheral chemoreceptors
Draw and describe the three bottle system.
Pressure for suction: 10-20 cmH2O
What is the FiO2 when the flow-by oxygen is provided at 2-3 L/min?
25 - 40%
what FiO2 can be provided when the nasal oxygen is provided at 50-150 ml/kg/min?
30 - 70%
What is the landmark to place a nasopharyngeal catheter?
From the nose to the mandibular ramus
What is the landmark to place a nasal oxygen catheter?
From the nose to the lateral canthus
To avoid oxygen toxicity, a FiO2 of higher than 50% should not be administered more than what?
24-72 hours
What is the main drive for oxygen diffusion to the tissue, PaO2 or SaO2?
PaO2
True or False: The higher the PaO2, the higher the SaO2.
False
When the PaO2 is below 100 mmHg, the statement is true, but when the PaO2 is above 100 mmHg, the SaO2 will always show as 100% no matter how high PaO2 is.
What are the correlation of the following PaO2 and SaO2: SaO2 = 100%, 99%, 98%, 95%, 90%.
What are the cause of hypoxemia?
Low inspired oxygen
Global hypoventilation
Venous admixture
- Low V/Q regions
- Diffusion impairment
- Atelectasis
- Right-to-left shunt
Very low venous oxygen content
What is the relationship between PaCO2 and ETCO2?
ETCO2 is about 5mmHg lower than PaCO2
What is the relationship between PaCO2 and CVCO2 (central venous)
CVCO2 is about 5mmHg higher than PaCO2
What is the normal gas composition in alveoli at sea level room temperature?
N2 560 mmHg
O2 105 mmHg
CO2 40 mmHg
H2O 50 mmHg (47 mmHg)
How do you calculate pO2 from FiO2 and what is the final concentration in the alveoli?
pO2 in the atmosphere:
FiO2xPatm = 760x0.21 = 160 mmHg
However 47mmHg is due to pH2)
FiO2 x (760-47) = 150mmHg (pO2 inspired)
By the time O2 reaches alveoli there’s dilution with other gases (i.e. CO2) = 100mmHg
True or False: Hypoventilation is a cause of hypoxemia in patient’s breathing room air but not in patients breathing enriched oxygen mixtures.
True
Theoretically, which V/Q condition will decrease PaO2?
1) Ventilated but unperfused lung units (e.g. PTE)
2) High V/Q (e.g. hypovolemia)
3) No ventilated but perfused lung areas (e.g. physiological shunt)
3)
When breathing room air at sea level, what is normal sum of PaO2 and PaCO2?
120
PaO2 = 80 mmHg
PaCO2 = 40 mmHg
* If the added value is not 120 → presence of venous admixture
What is one of the big limitations of using P/F ratio to evaluate lung function at room air?
The P/F ratio can be very misleading when used at 21% inspired oxygen concentrations if PaCO2 values are elevated. PaCO2 values have been ignored in this calculation, but when breathing room air, changes in PaCO2 can have a significant impact on PaO2.
How does S/F ratio correlate to P/F ratio
less invasive and good correlation found in dogs undergoing surgery and GA, however consider limitation in pulseox measurements.
S/F < 315 = P/F <300
S/F < 235 = P/F <200
What are the 3 dead space in the respiratory system?
Anatomic: upper airway, trachea
Alveolar
Physiologic: anatomic + alveolar dead space
Apparatus: dead space resulting from devices placed between the ET tube and the Y-piece of the breathing circuit (e.g. the ET tube that is too long)
True or False: Physiologic dead space is approximately the same as anatomic dead space when the lung is normal.
True
What is the relationship between PvCO2 and PaCO2?
PvCO2 is about 3-6 mmHg higher than PaCO2
Why the patient with C3-C5 spinal cord injury may be unable to breath spontaneously?
The nerve fibers mediating inspiration converge on the phrenic motor neurons in the ventral horns from C3 to C5.
Define Hering-Breuer inflation reflex.
When the alveolar is inflated, the pulmonary stretch receptors will be stimulated and send signals through vagus nerve to the apneustic center in lower pons → slowing of respiratory frequency by increasing expiratory time
True or False: Arterial baroreceptors can affect the breathing.
True
A large decrease in arterial blood pressure causes hyperventilation, whereas a large increase in arterial blood pressure causes respiratory depression.
What are the four big categories for the differential of hypercapnea?
1) Hypoventilation
2) Increased inspired CO2
3) Increased CO2 production with a fixed minute ventilation
4) Increased dead space ventilation
List 6 clinical consequences of hypercapnoea
1) respiratory acidosis leading to decreased myocardial contractility and decreased vascular tone
2) tachyarrhythmias
3) pulmonary vasoconstriction
4) increased ICP
5) AKI due to afferent arteriole vasoconstriction
6) right shift of Hb curve
When there is decreased tissue perfusion or decreased cardiac output, how will the PvCO2-PaCO2 gradient change, increase or decrease? Why?
Increased
Decrease tissue perfusion → increased tissue CO2 production due to increased H+ production secondary to lactate formation and hydrolysis of ATP
What is the ETCO2-PaCO2 gradient used to evaluation? What does the increased gradient mean?
Dead space ventilation
Increased gradient means increased physiological dead space (alveolar dead space?) either increased V/Q or decreased V/Q
What are the three mechanisms for oxygen-induced hypercapnea in patient with chronic hypoventilation and acute hypoxemia?
1) depress the hypoxemic-driven peripheral chemoreceptor stimulation → depress respiratory drive → worsening of hypoventilation
2) reverse the hypoxemic-induced pulmonary vasoconstriction → worsening the V/Q ratio (increased perfusion without concomitant increased ventilation → worsening of hypercapnea
3) When the hypoxemia is corrected, the increased partial pressure of O2 will decrease the affinity of Hb to CO2 → release more CO2 from the Hb → worsening of hypercapnea
List 4 complications of oxygen therapy
- oxygen toxicity
- absorbtion atelectasis (nitrogen washout)
- decreased respiratory drive
- vasoconstriction
What are the pros and cons of mainstream and sidestream capnography?
Mainstream
- Pros: near real-time waveform
- Cons: device is bulky, increase apparatus dead space
Sidestream
- Pros: less bulky, less dead space, more comfortable
- Cons: delayed waveform, dilutional effect from other gas
List 4 respiratory stimulants.
1) Doxapram
2) Caffeine
3) Progesterone
4) Aminophylline/theophylline
Mechanisms of action of theophylline as bronchodilator
- non-selective PDEi
- Adenosine antagonist
- interferes with Ca++ mobilisation
Less potent as a bronchodilator than beta2 agonists, but it has shown to have effects on strengthening the respiratory muscles –> important in MV patients
Theophylline can only be given orally but aminophylline can ge given IV.
Why is cyproheptadine useful as a bronchodilator in cats?
Blocks serotonin and cats’ airways are particularly sensitive to serotonin
Discuss pathophysiology of tracheal collapse
flaccidity of dorsal trachealis muscle + chondromalacia of tracheal rings (decrease synthesis of glycosaminoglycan, chondroitin and Ca++) –> collapse during respiration –> repeated mucosal contact –> severe inflammation –> failure of muco-ciliary escalator + metaplasia –> coughing as only mechanism for airway clearance
Classification of tracheal collapse
Grade IV might have a different patophysiology with congenital malformation being most likely vs chondromalacia
During inspiration, which part of the trachea has higher tendency to collapse?
Trachea rostral to the thoracic inlet
Tracheal collapse treatment
Up to 70% dogs can be managed medically with rest and steroids for up to 12 months
Extraluminal rings (75% success rate, risk of nerve and vascular damage with subsequent necrosis)
Tracheal stenting (chose diameter +10-20% of current one, need fluoroscopy + endoscopy, risk of granuloma, fracture and migration)
Describe paradoxical laryngeal movement.
Inward movement of the arytenoids during inspiration.
In normal dogs, where do most of the airway resistance come from?
Nose
What are the anatomic abnormalities of BOAS?
Elongated soft palates, stenotic nares, tracheal hypoplasia
Everted laryngeal saccules, tonsillar eversion, laryngeal collapse, chronic GI signs
For cats with middle ear polyps, what is the name of the surgical management? What is the most common complications?
Ventral bulla osteotomy (VBO)
Horner’s syndrome (57%, can last for 4 weeks)
Other approach is traction-avulsion but higher rate of recurrence
True or False: The split cartilage anastomosis technique results in better alignment and apposition of the tracheal ends and less long- term luminal stenosis than the annular ligament and cartilage technique.
True
How much percentage of trachea can be resected in a mature dog?
25-50%
For the intrathoracic tracheal tear repair, which side should the thoracotomy be performed?
Right
What is the recommended ET tube cuff pressure?
20 - 30 cmH2O
Does asthma cause increased or decreased FRC?
Increased (due to air-trapping)
What is the most common parasite causing allergic response in canine lungs?
Toxocara canis
What are the two main pathophysiologic forms of pulmonary edema?
High-pressure edema
Increased-permeability edema
Describe normal fluid re-absorbtion by type I and type II alveolar cells
Normally ongoing fluid reabsorbition due to:
- Na/K ATPase creates gradient for Na reabsorbtion by ENaC channel on alveolar side
- Cl- follows due to electroneutrality via Cl- channels
- K brought in by Na/K expelled on alveolar side by ROMK
During inflammatory states ROS can damage ion channels and alter fluid balance –> non-cardiogenic pulmonary oedema
Beta agonist by increasing CAMP and Na/K activity –> increased ENac intake of Na and quicker oedema reabsorbtion
Explain the blast theory in neurogenic pulmonary edema.
The result of two mechanisms: high hydrostatic pressure + pulmonary endothelial injury due to sympathetic surge
After a massive, neuronal event, the sympathetic nerve system is activated and it can cause high-pressure edema due to increased capillary hydrostatic pressure. The high hydrostatic pressure & sympathetic nerve system activation also cause the barotrauma to the capillary endothelium, which leads to the formation of increased-permeability edema.
List 3 proposed mechanisms for reexpansion edema.
1) Decreased surfactant production
2) Mechanical force leading to pulmonary parenchyma injury
3) Reperfusion injury
True or False: The most common clinical signs in cats with infectious pneumonia are fever and coughing.
False
Cats rarely cough, the most common clinical signs is dyspnea
What is the MOA of NAC in clearing the mucus?
breakdown of the disulfide bonds
What is the cutoff of the particles size to be able to enter the alveoli?
3 um
Explain the biphasic pathogenesis of aspiration pneumonitis.
Phase I - airway response
1-2 hours after aspiration
Initial insult is caused by direct chemical irritation → damage of bronchial epithelium and alveolar endothelium → the acid aspirate also stimulates tracheobronchial substance P–immunoreactive neurons → induces tachykinin neuropeptide release → neurogenic inflammation, bronchoconstriction, vasodilation, increased vascular permeability
Phase II - lung inflammation
4-6 hours after aspiration
Inflammatory mediator cascades producing neutrophil chemotaxis (IL-8, TNF-α,17 and macrophage inflammatory proteins), sequestration, and subsequent increased permeability edema, hypoxic vasoconstriction (pulmonary hypertension)
Why is bronchodilator not recommended in dogs with aspiration pneumonia?
It cause inotropic and vasodilation → potentially increase V/Q mismatch
One recent study showed no difference in CXR lesions resolution in dogs with AP receiveing >14 days of antibiotics vs dogs <14d of antibiotics
True
Also CRP showed normalization much earlier than changes on XRAYs
Dogs can safely have ab treatment discontinued after normalisation of CRp (70% less than 1 week total duration)
POCUS and CXRs are useful for diagnosis but not follow up as after 1 week lesion persisted in 88% of CXR and 71% of POCUS despite CRP normalisation
One recent study comparing 2 vs 4 weeks antibiotic treatment in canine pneumonia (AP and community acquired) found…
No difference in outcome –> 4 weeks likely unnecessary
Clinical resolution occurs much earlier than radiographic resolution –> no longer recommended to base the length of treatment on serial CXR
In ARDS/ALI, how will the pulmonary compliance change?
Decreased compliance Hallmark of ARDS
In human, how many percentage of pulmonary contusion volume predicts the need for mechanical ventilation?
> 20%
Patophysiological mechanisms of lung contusions
- implosion
- spalding
- inertia
1.hemorrhage
2.inflammation
3.alveolar flooding
4.proliferation
5. resolution
What percentage of dogs with lung contusions develop bacterial pneumonia?
1%
pre-emptive antibiotic use not justified
What is the primary reason for PTE-induced hypoxemia?
High V/Q mismatch
List 5 changes in hemodynamics & pulmonary gas exchange that can be observed in PTE.
1) Right sided pressure overload
2) Hypoxemia (due to dead space ventilation)
3) pulmonary hypertension
4) Decreased cardiac output
5) Hypotension
What is the difference between massive and submassive PTE?
Massive PTE = low BP and CV instability
Definition of flail chest
Injury to 3 or more sequential ribs in which both proximal and distal end are fractured.
Paradoxycal movement of the segment ensues.