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ECVECC Board Exam > Respiratory > Flashcards

Respiratory Flashcards

1
Q

fIf a patient were to develop a tension pneumothorax during HBOT, when does it most likely to happen?

A

At the decompression phase

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2
Q

Fick’s law and relevance in gas exchange

A

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

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3
Q

True or False: Patient with marked respiratory acidosis can become hypoxemic too.

A

True

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4
Q

What is the definition of hypoxemia

A

PaO2 < 80 mmHg

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5
Q

List 4 different kinds of hemoglobins.

A

Oxygenated hemoglobin
Deoxygenated hemoglobin
Methemoglobin
Carboxyhemoglobin
Sulfhemoglobin

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6
Q

What is the two wavelengths of light on pulse oximeter?

A

940 nm (infrared)
660 nm (red)

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7
Q

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?

A

Tissue elastic forces 1/3
Fluid-air surface tension forces 2/3

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8
Q

What cells secrete surfactant?

A

Type II alveolar epithelial cells (10% of the surface area of the alveoli)

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9
Q

What are the main components of surfactant?

A

Phospholipid dipalmitoyl phosphatidylcholine
Surfactant apoproteins
Calcium ions

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10
Q

True or False: Alveolar pressure caused by surface tension is directly related to alveolar radius. (Laplace’s law)

A

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

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11
Q

What are the three main components of the work of inspiration?

A

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

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12
Q

Fill out the blank.

A
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13
Q

What is the remaining of the air after a normal expiration call?

A

Functional residual capacity

*** NOT RESIDUAL VOLUME

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14
Q

Define anatomic dead space and physiological dead space.

A

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

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15
Q

What is the formula for minute ventilation?

A

Minute ventilation = tidal volume x respiratory rate

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16
Q

The respiratory system has two circulation. What are they called and where are they?

A

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

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17
Q

How does hypoxia affect the systemic vessels and pulmonary vessels?

A

Systemic vessels - vasodilation
Pulmonary vessels - vasoconstriction

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18
Q

What is the definition of terminal bronchioles?

A

The smallest airways without alveoli.

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19
Q

What is the definition of respiratory bronchioles?

A

divided from terminal bronchioles, which have occasional alveoli budding from their walls

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20
Q

What concept does this graph highlight?

A

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

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21
Q

Which of the following volume can spirometer measure?
1) Total lung capacity
2) Tidal volume
3) Residual volume
4) Functional residual capacity

A

2) Tidal volume

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22
Q

What are the two methods to measure FRC?

A

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).

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23
Q

What does the alveolar ventilation mean?

A

The amount of air that is available for gas exchange

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24
Q

If you want to increase alveolar ventilation, which way is more effective, increasing tidal volume or respiratory frequency?

A

Increase tidal volume, because anatomic dead space is fixed

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25
Q

What is the alveolar ventilation equation?

A
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26
Q

Respiratory laboratory commonly use Bohr’s method to measure physiology dead space. What is the equation?

A
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27
Q

What is normal physiological dead space percentage?

A

0.2 - 0.35

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28
Q

When the patient has pulmonary disease, how will the relationship between anatomic dead space and physiological dead space change?

A

Physiological dead space will be bigger than the anatomic dead space

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29
Q

How long does a red blood cell usually stay in the pulmonary capillary?

A

0.75 seconds

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30
Q

Explain what is diffusion limited and perfusion limited, and name an example for each of them

A

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

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31
Q

Is O2 diffusion limited or perfusion limited? Why?

A

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
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32
Q

Which gas is ideal for diffusion capacity measurement. Why?

A

Carbon monoxide
Because the gas is purely diffusion limited

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33
Q

Describe the route oxygen reach RBC in the lung.

A

Surfactant → alveolar epithelium → alveolar epithelium basement membrane → interstitial space → capillary basement membrane → capillary endothelium → plasma → red blood cell

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34
Q

What is normal systolic, diastolic and mean pulmonary arterial pressure? What about Aorta?

A

Pulmonary artery: 25/8 (15) mmHg
Aorta: 120/80 (100) mmHg

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35
Q

Pulmonary vascular resistance is only ____ that of the systemic circulation. What is the number?

A

1/10

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36
Q

What are the two mechanisms of decreased pulmonary vascular resistance when pulmonary vessels pressure increases?

A

1) Distension
- Predominant when pulmonary pressure is already high

2) Recruitment
- Main mechanism for pulmonary artery
- Open up more closed capillaries

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37
Q

How does the lung volume affect the pulmonary capillary and extra-alveolar vessels resistances?

A

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&raquo_space;> capillary pressure

  • There is a sweet spot when the total resistance is the lowest
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38
Q

True or False: West’s zone 1 does not occur in healthy individual.

A

True

  • It can happen when patient’s hypotensive or alveolar pressure increased significantly
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39
Q

What is West Zone 4? When will you see it?

A

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

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40
Q

What determines the blood flow in West Zone 2 and Zone 3?

A

Zone 2: gradient between alveolar and pulmonary arterial pressure

Zone 3: gradient between pulmonary arterial and pulmonary venous pressure

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41
Q

What determines the blood flow in West Zone 2 and Zone 3?

A

Zone 2: gradient between alveolar and pulmonary arterial pressure

Zone 3: gradient between pulmonary arterial and pulmonary venous pressure

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42
Q

True or False: Hypoxemia can cause pulmonary vasoconstriction.

A

False

Alveolar hypoxia (not blood!) cause vessel wall hypoxia → vasoconstriction

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43
Q

What is the cut-off for alveolar hypoxia induced-vasoconstriction?

A

Alveolar PO2 < 70 mmHg

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44
Q

What is the proposed mechanism of alveolar hypoxia induced-vasoconstriction?

A

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

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45
Q

What are the two substances that ACE can convert/inactivate?

A

Angiotensin I
Bradykinin

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46
Q

List 5 substances that can be inactivated when they enter the pulmonary circulation

A

Bradykinin
Serotonin
Norepinephrine
Leukotriene
Prostaglandin E2 and F2𝜶

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47
Q

What is the most abundant immunoglobulin in the bronchial secretion?

A

IgA

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48
Q

What is the equation for A-a gradient?

A

A-a gradient = PAO2 - PaO2 = [FiO2x(Patm-PH2O) - PaCO2/0.8] - PaO2

Normal: < 10

  • Normal PH2O = 47 mmHg
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49
Q

What is the formula to calculate pulmonary shunt from mixed venous blood?

A

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

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50
Q

What is normal percentage of pulmonary shunt?

A

<5%

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51
Q

True or False: Ventilation and blood flow both increase from top to bottom of the lungs. Blood flow increase more rapidly than ventilation.

A

True

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52
Q

True or False: The ventilaiton perfusion ratio decreases from the top to the bottom of the lung.

A

True

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53
Q

Is the pH higher at the top or the bottom of the lung?

A

Higher at the top of the lung

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54
Q

True or False: The respiratory exchange ratio (CO2 output/O2 uptake) is higher at the apex than at the base.

A

True

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55
Q

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?

A

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.

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56
Q

What is Henry’s Law?

A

The amount of gas dissolved in the liquid/blood is proportional to its partial pressure

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57
Q

Does presence of COHb shift oxygen-hemoglobin dissociation curve to the right or left?

A

Left (increased O2 and hemoglobin binding)

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58
Q

Describe Bohr effect and Haldane effect.

A

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

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59
Q

Which state of hemoglobin has lower affinity to oxygen, the tense state (T-state) or relax state (R-state)?

A

T-state

  • It becomes more relaxed as more and more oxygen binds to the hemoglobin
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60
Q

The CO2-hemoglobin dissociation curve will shift to the left or right as SO2 increases?

A

Shift to the right (higher O2 → decrease hemoglobin affinity to CO2)

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61
Q

What are the four types of tissue hypoxia?

A

1) Hypoxic hypoxia
2) Anemic hypoxia
3) Circulatory hypoxia
4) Histotoxic hypoxia

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62
Q

On the pressure volume curve, the inspiration and expiration are not overlapped. What is it called and why?

A

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.

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63
Q

What is the definition of compliance?

A

The volume change per unit pressure change

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64
Q

What are the 3 main factors determining compliance?

A

1) elasticity of the lungs
2) elasticity of the chest wall
3) surfactant

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65
Q

Elasticity vs compliance

A

Elasticity= ΔP/ΔV
Compliance= ΔV/ΔP

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66
Q

List 2 causes of decreased lung compliance and 2 causes of increased lung compliance.

A

Decreased compliance: lung fibrosis, pulmonary edema, atelectasis

Increased compliance: pulmonary emphysema, normal aging lung

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67
Q

What is specific compliance?

A

Specific compliance = Cstat/FRC

FRC=functional residual capacity

It is a way to normalise compliance to lung volume (or patient size)

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68
Q

List 3 benefits of surfactant.

A

1) Reduce surface tension of the alveoli
2) Decrease work of breathing
3) Keep the lung dry
4) Promote stability of alveoli

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69
Q

Compared to the apex and base of the lungs, which one has better compliance and ventilation?

A

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)

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70
Q

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.

A

True

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71
Q

True or False: The normal intrapleural pressure is 0.

A

False

-5 cmH2O (because of elastic recoil of the lung)

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72
Q

In the entire pulmonary system, where is the major site of airway resistance from?

A

Medium-sized bronchi

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73
Q

What does 0ABCD, ABCE, and 0AECD represent?

A

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

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74
Q

What is the equate for work of breathing?

A

WOB = pressure x volume

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75
Q

Where does breathing center locate?

A

Brainstem (pons, medulla)

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76
Q

Where is the normal respiratory rhythm generated?

A

Medullary respiratory center, Pre-Botzinger complex

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77
Q

What does apneustic center and pneumotaxic center do?

A

Apneustic center: excite the inspiratory center
Pneumotaxic center: inhibit inspiratory

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78
Q

There are two respiratory group (dorsal and ventral) in the medullary respiratory center. Which controls inspiration and which controls expiration?

A

Inspiration: Dorsal respiratory center
Expiration: Ventral respiratory center

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79
Q

How does PCO2 regulate the respiration?

A

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

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80
Q

Where is the central chemoreceptors?

A

Ventral surface of the medulla

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81
Q

What change does the peripheral chemoreceptors detect?

A

Change in PO2, pH and PCO2

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82
Q

What is the effect when the pulmonary stretch receptors are activated (during lung expansion)?

A

Hering-Breuer reflex
Vagus efferent –> inhibition of DRG and VRG –> stop inflation of the lung (protective mechanism)

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83
Q

Where are the pulmonary stretch receptors and irritant receptors?

A

Pulmonary stretch receptors: within airway smooth muscles
Irritant receptors: between airway epithelial cells

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84
Q

Where are the J receptors (Juxtacapillary receptors) and what is its function?

A

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

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85
Q

True or False: Decreased PO2 can stimulate both central and peripheral chemoreceptors and cause increased ventilation.

A

False

Only peripheral chemoreceptors

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86
Q

Why patients with chronic respiratory disease lose their adequate response to elevated PCO2?

A

Renal compensation → the change in pH is abolished

  • In this case, hypoxemia becomes the main stimulus to ventilate
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87
Q

Does the pH change mainly stimulate the central or peripheral receptors?

A

Peripheral chemoreceptors

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88
Q

Draw and describe the three bottle system.

A

Pressure for suction: 10-20 cmH2O

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89
Q

What is the FiO2 when the flow-by oxygen is provided at 2-3 L/min?

A

25 - 40%

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90
Q

what FiO2 can be provided when the nasal oxygen is provided at 50-150 ml/kg/min?

A

30 - 70%

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91
Q

What is the landmark to place a nasopharyngeal catheter?

A

From the nose to the mandibular ramus

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92
Q

What is the landmark to place a nasal oxygen catheter?

A

From the nose to the lateral canthus

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93
Q

To avoid oxygen toxicity, a FiO2 of higher than 50% should not be administered more than what?

A

24-72 hours

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94
Q

What is the main drive for oxygen diffusion to the tissue, PaO2 or SaO2?

A

PaO2

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95
Q

True or False: The higher the PaO2, the higher the SaO2.

A

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.

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96
Q

What are the correlation of the following PaO2 and SaO2: SaO2 = 100%, 99%, 98%, 95%, 90%.

A
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97
Q

What are the cause of hypoxemia?

A

Low inspired oxygen
Global hypoventilation
Venous admixture
- Low V/Q regions
- Diffusion impairment
- Atelectasis
- Right-to-left shunt
Very low venous oxygen content

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98
Q

What is the relationship between PaCO2 and ETCO2?

A

ETCO2 is about 5mmHg lower than PaCO2

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99
Q

What is the relationship between PaCO2 and CVCO2 (central venous)

A

CVCO2 is about 5mmHg higher than PaCO2

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100
Q

What is the normal gas composition in alveoli at sea level room temperature?

A

N2 560 mmHg
O2 105 mmHg
CO2 40 mmHg
H2O 50 mmHg (47 mmHg)

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101
Q

How do you calculate pO2 from FiO2 and what is the final concentration in the alveoli?

A

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

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102
Q

True or False: Hypoventilation is a cause of hypoxemia in patient’s breathing room air but not in patients breathing enriched oxygen mixtures.

A

True

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103
Q

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)

A

3)

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104
Q

When breathing room air at sea level, what is normal sum of PaO2 and PaCO2?

A

120

PaO2 = 80 mmHg
PaCO2 = 40 mmHg
* If the added value is not 120 → presence of venous admixture

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105
Q

What is one of the big limitations of using P/F ratio to evaluate lung function at room air?

A

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.

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106
Q

How does S/F ratio correlate to P/F ratio

A

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

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107
Q

What are the 3 dead space in the respiratory system?

A

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)

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108
Q

True or False: Physiologic dead space is approximately the same as anatomic dead space when the lung is normal.

A

True

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109
Q

What is the relationship between PvCO2 and PaCO2?

A

PvCO2 is about 3-6 mmHg higher than PaCO2

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110
Q

Why the patient with C3-C5 spinal cord injury may be unable to breath spontaneously?

A

The nerve fibers mediating inspiration converge on the phrenic motor neurons in the ventral horns from C3 to C5.

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111
Q

Define Hering-Breuer inflation reflex.

A

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

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112
Q

True or False: Arterial baroreceptors can affect the breathing.

A

True

A large decrease in arterial blood pressure causes hyperventilation, whereas a large increase in arterial blood pressure causes respiratory depression.

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113
Q

What are the four big categories for the differential of hypercapnea?

A

1) Hypoventilation
2) Increased inspired CO2
3) Increased CO2 production with a fixed minute ventilation
4) Increased dead space ventilation

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114
Q

List 6 clinical consequences of hypercapnoea

A

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

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115
Q

When there is decreased tissue perfusion or decreased cardiac output, how will the PvCO2-PaCO2 gradient change, increase or decrease? Why?

A

Increased

Decrease tissue perfusion → increased tissue CO2 production due to increased H+ production secondary to lactate formation and hydrolysis of ATP

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116
Q

What is the ETCO2-PaCO2 gradient used to evaluation? What does the increased gradient mean?

A

Dead space ventilation
Increased gradient means increased physiological dead space (alveolar dead space?) either increased V/Q or decreased V/Q

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117
Q

What are the three mechanisms for oxygen-induced hypercapnea in patient with chronic hypoventilation and acute hypoxemia?

A

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

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118
Q

List 4 complications of oxygen therapy

A
  1. oxygen toxicity
  2. absorbtion atelectasis (nitrogen washout)
  3. decreased respiratory drive
  4. vasoconstriction
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119
Q

What are the pros and cons of mainstream and sidestream capnography?

A

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

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120
Q

List 4 respiratory stimulants.

A

1) Doxapram
2) Caffeine
3) Progesterone
4) Aminophylline/theophylline

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121
Q

Mechanisms of action of theophylline as bronchodilator

A
  1. non-selective PDEi
  2. Adenosine antagonist
  3. 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.

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122
Q

Why is cyproheptadine useful as a bronchodilator in cats?

A

Blocks serotonin and cats’ airways are particularly sensitive to serotonin

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123
Q

Discuss pathophysiology of tracheal collapse

A

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

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124
Q

Classification of tracheal collapse

A

Grade IV might have a different patophysiology with congenital malformation being most likely vs chondromalacia

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125
Q

During inspiration, which part of the trachea has higher tendency to collapse?

A

Trachea rostral to the thoracic inlet

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126
Q

Tracheal collapse treatment

A

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)

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127
Q

Describe paradoxical laryngeal movement.

A

Inward movement of the arytenoids during inspiration.

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128
Q

In normal dogs, where do most of the airway resistance come from?

A

Nose

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129
Q

What are the anatomic abnormalities of BOAS?

A

Elongated soft palates, stenotic nares, tracheal hypoplasia
Everted laryngeal saccules, tonsillar eversion, laryngeal collapse, chronic GI signs

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130
Q

For cats with middle ear polyps, what is the name of the surgical management? What is the most common complications?

A

Ventral bulla osteotomy (VBO)
Horner’s syndrome (57%, can last for 4 weeks)

Other approach is traction-avulsion but higher rate of recurrence

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131
Q

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.

A

True

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132
Q

How much percentage of trachea can be resected in a mature dog?

A

25-50%

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133
Q

For the intrathoracic tracheal tear repair, which side should the thoracotomy be performed?

A

Right

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134
Q

What is the recommended ET tube cuff pressure?

A

20 - 30 cmH2O

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135
Q

Does asthma cause increased or decreased FRC?

A

Increased (due to air-trapping)

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136
Q

What is the most common parasite causing allergic response in canine lungs?

A

Toxocara canis

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137
Q

What are the two main pathophysiologic forms of pulmonary edema?

A

High-pressure edema
Increased-permeability edema

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138
Q

Describe normal fluid re-absorbtion by type I and type II alveolar cells

A

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

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139
Q

Explain the blast theory in neurogenic pulmonary edema.

A

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.

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140
Q

List 3 proposed mechanisms for reexpansion edema.

A

1) Decreased surfactant production
2) Mechanical force leading to pulmonary parenchyma injury
3) Reperfusion injury

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141
Q

True or False: The most common clinical signs in cats with infectious pneumonia are fever and coughing.

A

False

Cats rarely cough, the most common clinical signs is dyspnea

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142
Q

What is the MOA of NAC in clearing the mucus?

A

breakdown of the disulfide bonds

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143
Q

What is the cutoff of the particles size to be able to enter the alveoli?

A

3 um

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144
Q

Explain the biphasic pathogenesis of aspiration pneumonitis.

A

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)

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145
Q

Why is bronchodilator not recommended in dogs with aspiration pneumonia?

A

It cause inotropic and vasodilation → potentially increase V/Q mismatch

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146
Q

One recent study showed no difference in CXR lesions resolution in dogs with AP receiveing >14 days of antibiotics vs dogs <14d of antibiotics

A

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

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147
Q

In ARDS/ALI, how will the pulmonary compliance change?

A

Decreased compliance Hallmark of ARDS

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148
Q

In human, how many percentage of pulmonary contusion volume predicts the need for mechanical ventilation?

A

> 20%

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149
Q

Patophysiological mechanisms of lung contusions

A
  1. implosion
  2. spalding
  3. inertia

1.hemorrhage
2.inflammation
3.alveolar flooding
4.proliferation
5. resolution

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150
Q

What percentage of dogs with lung contusions develop bacterial pneumonia?

A

1%

pre-emptive antibiotic use not justified

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151
Q

What is the primary reason for PTE-induced hypoxemia?

A

High V/Q mismatch

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152
Q

List 5 changes in hemodynamics & pulmonary gas exchange that can be observed in PTE.

A

1) Right sided pressure overload
2) Hypoxemia (due to dead space ventilation)
3) pulmonary hypertension
4) Decreased cardiac output
5) Hypotension

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153
Q

What is the difference between massive and submassive PTE?

A

Massive PTE = low BP and CV instability

154
Q

Definition of flail chest

A

Injury to 3 or more sequential ribs in which both proximal and distal end are fractured.
Paradoxycal movement of the segment ensues.

155
Q

When you need to put a patient with flail chest on lateral recumbency, which side should be down?

A

The side with the flail chest down

156
Q

What is pseudoflail chest?

A

No fractured ribs, but severe muscle injury of the chest wall resulting in mild paradoxycal pattern

157
Q

Where does the segmental intercostal nerves leave?

A

C6 - T2

158
Q

What is the proposed pathophysiology of acute idiopathic polyradiculoneuritis?

A

Immune-mediated demyelination and degeneration of axons of the ventral roots and spinal nerves

  • Decreased segmental reflexes, normal sensation, hyperesthesia
  • Treatment: supportive care (steroid doesn’t seem to help)
  • usually take 3+ weeks to recover
159
Q

What is the cause of polyradiculoneuritis?

A

Racoon saliva or Campylobacter infection

Hunting dogs are most at risk

160
Q

Which type of botulism toxin is the primary one in dogs?

A

Type C toxin

161
Q

What is the pathophysiology of botulism?

A

Botulinum toxin blocks release of ACh at the pre-synaptic terminal of skeletal muscle and cholinergic autonomic synapsis

  • The toxin cause irreversible enzymatic cleavage of Soluble N-ethylmaleimide-sensitive factor activating protein receptor (SNARE) proteins. SNARE proteins are essential for “docking” synaptic ACh vesicles to pre-synaptic membranes, allowing release of ACh into the synaptic cleft.
162
Q

In patient with botulism or MG, which antibiotic should be avoided and why?

A

Aminoglycoside, because it can prolong or lead to complete NM blockage

MOA: interfere with Ca movements through the Ca channels of the membrane of the nerve-endings → inhibits acetylcholine release at the synaptic cleft

163
Q

Which one is the post-synaptic NM junctional disease?
1) Myasthenia gravis
2) Botulism
3) Tick paralysis
4) Elapid Snake Envenomation

A

1)
* Some 4) are post-synaptic too

164
Q

What is normal pleural space pressure?

A

-5 cmH2O

165
Q

Define tension pneumothorax

A

Air leaks into the thoracic cavity but cannot exit fully (one way valve at the leakage site)

166
Q

When do hypoxemia become the primary drive for ventilation?

A

When PaO2 < 50 mmHg

167
Q

Submersion in ice-cold water (<5°C [41°F]) increases the chances of survival because of the diving reflex. Explain diving reflex.

A

It is a reflex mediated by trigeminal nerve. When the animal’s face touch cold water, the trigeminal nerve will send signal to the CNS and cause bradycardia, hypertension, and preferential shunting of blood to the cerebral and coronary circulations → protect the brain and heart from hypoxia-induced injury

The cold temperature also decreased the metabolic rate.

168
Q

In smoke inhalation, what chemical can cause histotoxic hypoxia?

A

Hydrogen cyanide (HCN)

169
Q

List 3 mechanism of smoke inhalation causing airway obstruction.

A

1) thermal injury causing laryngeal edema
2) bronchoconstriction from irritant gases and Particulate Matter
3) Increased bronchial secretion and edema fluid

170
Q

What is the CO in room air and with 100% oxygen supplementation?

A

Room air: 250 min
100% Oxygen: 26-148 min

171
Q

What is the treatment for cyanide toxicity?

A

Hydroxocobalamin

*Bind to cyanide to form cyanocobalamin (vitamin B12)

172
Q

Fill out A to E.

A

A: Respiratory baseline
B: Expiratory upstroke
C: Alveolar plateau
D: EtCO2
E: Inspiratory downstroke

173
Q

How small should the aerosol particles be to reach the small bronchioles and alveoli?

A

The aerodynamic equivalent diameter (AED) should be < 5 𝜇m

174
Q

There are two types of albuterols on the market - levalbuterol and racemic mixture. Which one is recommended for cats and dogs? Why?

A

levalbuterol
The main components is R-albuterol, which is an effective bronchodialtor. Racemic mixture has both R-albuterol and S-albuterol. The S-albuterol is proinflammatory and can cause bronchoconstriction.

175
Q

What is Bordetella bronchiseptica?

A

Gram negative, obligate aerobic coccobacillus

176
Q

What dose this EtCO2 tell you?

A

Bronchoconstriction/Asthma

177
Q

What does this EtCO2 tell you?

A

Rebreathing

178
Q

What does this EtCO2 tell you?

A

Patient is breathing spontaneously

179
Q

What does this EtCO2 tell you?

A

Cardiac oscillation

180
Q

True or False: HFNO can increase FRC.

A

True

It can provide some degree of PEEP and increase FRC → improve compliance, decrease V/Q mismatch

181
Q

True or False: The alveolar oxygen concentration will be determined by the ratio of oxygen gas flow to minute volume.

A

True

182
Q

What is the initial patient’s flow rate for HFNO?

A

calculate patient’s minute ventilation (estimated tidal volume = 10-15 ml/kg)

183
Q

List 5 benefits of HFNC

A
  1. delivery of high FiO2
  2. provision of continuous positive airway pressure
  3. CO2 washout (elimination of rebreathing of air in the upperwairways)
  4. reduction of upper airways resistance
  5. potential to reduce need for intubation and invasive MV
184
Q

What are ROX and ROX-HR?

A

ROX is RR-Oxygenation index used to predict need to escalate to MV in patients receiving HFNO (in humans SF ratio/RR >4.8 = successful weaning from HFNO)

ROX-HR (ROX/HR x100) improves predictive ability of ROX alone (in humans >6.8 at 10h = significantly lower risk of failure)

185
Q

What cut off for ROX and SF have been shown to predict failure of HFNO at 6h?

A

ROX<3.68 and SF<143 (sens 75% spec 90%)

186
Q

List 4 complications of HFNC

A
  • nasal irritation
  • mild increase in PaCO2 (due to increased resistance to expiration - important to choose prongs that won’t occlude more than 50% diameter of nostrils)
  • aerophagia
  • pneumothorax
187
Q

List 3 main clinical indications for HFNC

A
  • hypoxemic respiratory failure (pneumonia, pulmonary oedema, asthma)
  • post-GA recovery for BOAS
  • CO toxicity (reduced half-life as much as with MV)
188
Q

Initial settings for HFNC

A

100% FiO2
minute ventilation as flow rate
temperature close to patient’s body temperature

189
Q

Under normal condition, what is the proportion of the expired tidal volume is re-breathed?

A

1/3

190
Q

List 10 proposed etiology for laryngeal paralysis.

A

1) Congenital (degeneration neurons in nucleus ambiguous)
2) GOLPP (geriatric acquired form)
3) Neoplasia
4) Trauma
5) Toxin (e.g. organophosphate, lead)
6) Hypothyroidism
7) Iatrogenic (e.g. previous surgery, ventral slot)
8) Immune-mediated
9) Infectious disease
10) SLE

191
Q

How many patients presented with laryngeal paralysis have concurrent proprioceptive deficits? how many have oesophageal dysfunction?

A

33% proprioceptive deficits
69% oesophageal dysfunction

192
Q

Pathophysiology of laryngeal paralysis

A

Damage to recurrent laryngeal nerve innervating the dorsal cricoarytenoideus muscle that abducts arytenoids

193
Q

What is the surgery called for laryngeal paralysis?

A

unilateral arytenoid lateralization

194
Q

Why is crycoarytenoid lateralization considered > thyroarythenoid lateralisation?

A

Achieves wider rima glottis however not associated with difference in long term survival (possible that wider rima glottis = increased risk of aspiration pneumonia)

195
Q

Can bilateral lateralization of arytenoid be performed?

A

Yes, but much higher risk of aspiration pneumonia and shorter survival time

196
Q

What is the most common post-op complication of laryngeal paralysis surgery?

A

Aspiration pneumonia (up to 1/3 of patients) in dogs

In cats laryngeal paralysis is rare and post-op Horner’s syndrome is the most common complication

197
Q

What is the landmark for nasotracheal tube?

A

From the nose to the 5th intercostal space

  • This length should place the tube’s tip just cranial to the tracheal bifurcation.
198
Q

True or False: The diameter of the tracheostomy tube should be the same as the inner diameter of the trachea.

A

False

It should be 1/2-1/3 of the tracheal diameter to minimize iatrogenic tracheal trauma and decrease the incidence of post-intubation stenosis.

199
Q

What is the ideal tracheostomy tube length?

A

6-7 tracheal rings down from the insertion site

200
Q

Describe how to perform a temporary tracheostomy.

A
  1. Collect necessary supplies.
  2. Anesthetize and orotracheally intubate the patient with a cuffed ET tube.
  3. Position the animal in dorsal recumbence with a towel rolled under the neck. Clip and aseptically prepare a large surgical field on the ventral cervical surface.
  4. Perform hand hygiene, and don cap, mask, and sterile gloves.
  5. Isolate the prepared surgical site with a barrier drape.
  6. Make a ventral midline cervical skin incision just caudal to the cricoid cartilage for a distance of approximately 3 to 4cm.
  7. Apply a self-retaining retractor (e.g. Gelpi) to hold open the skin edges and clear just enough subcutaneous tissue to identify the midline
    division of the sternohyoideus muscles.
  8. Using Metzenbaum scissors, bluntly separate the sternohyoideus muscles on the midline, taking care to avoid the thyroidea caudalis vein on the midline between these two muscles. Retract the thyroidea caudalis vein to one side along with one of
    the sternohyoideus muscle.
  9. Reposition the self-retaining retractors on the sternohyoideus muscles to expose the trachea and clear the loose fascia away at the proposed tracheotomy site. Application of a second self-retaining retractor at a right angle to the original retractor to retract the skin in a craniocaudal direction enhances exposure.
  10. Using a scalpel blade, incise the interannular ligament between the 2nd and 3rd tracheal rings. Do not incise the interannular ligament beyond 50% of the tracheal circumference.
  11. Place stay sutures around the second and third tracheal rings, knot the sutures to create large suture loops, and tag the suture strands with mosquito hemostatic forceps.
  12. Use the stay sutures to manipulate the interannular opening while the orotracheal tube is removed. Insert the tracheostomy tube with the obturator in place, and then quickly remove the obturator and replace it with an inner cannula.
  13. Leave the stay sutures in place for postoperative nursing care manipulations.
  14. Secure the tracheostomy tube by attaching umbilical tape to the flange eyelets and tying the tapes behind the neck.
  15. Do not suture the tracheostomy wound unless the incision was made too large. In that case, place a few interrupted sutures in the subcutaneous tissue and/or skin to decrease the size of the wound, taking care not to make the wound too small.
  16. Once the surgical procedure is completed, the area is gently cleaned and left uncovered for easy observation.
201
Q

What are the three phases of ARDS?

A

Exudative
Proliferative
Fibrotic

202
Q

Difference between direct and indirect lung injury

A

Direct lung injury –> epitelial damage first
Indirect lung injury –> endothelial damage first

203
Q

ARDS subphenotypes

A
  • extrapulmonary vs pulmonary causes: extrapulmonary homogeneously diffused damage, so more likely to respond to recruitment strategies
  • hyperinflammatory vs hypoinflammatory: hyperinflammatory more likely to have extra-pulmonary causes and benefit from high PEEP and immunomodulatory drugs
  • radiological phenotypes: focal vs diffuse
204
Q

Describe The Berlin Definition.

A

1) Onset: Within 7 days of the known insult or new or worsening of respiratory signs
2) Chest images: Bilateral opacities (no fully explained by nodules, effusion or lobar collapse)
3) Origin of edema: rule out cardiac failure or fluid overload (by echo)
4) Oxygenation
- Mild: 200 mmHg < PaO2/FiO2 ≤ 300 mmHg with PEEP or CPAP ≥ 5 cmH2O
- Moderate: 100 mmHg < PaO2/FiO2 ≤ 200 mmHg with PEEP or CPAP ≥ 5 cmH2O
- Severe: PaO2/FiO2 ≤ 100 mmHg with PEEP or CPAP ≥ 5 cmH2O

205
Q

Recent Kigali modification

A
  • introduction of S/F ratio instead of P/F
  • POCUS instead of CXR
  • introduce HFNO settings as well as MV

However application of Kigali showed higher false positives vs traditional Berlin definition

206
Q

What is the characteristics of exudative phase of ARDS?

A

Protein-rich edema and eosinophilic hyaline membrane in the alveolar wall

207
Q

List 5 risk factors for ARDS/ALI in veterinary medicine.

A

1) Sepsis
2) Inflammation
3) Infection
4) SIRS
5) Major trauma
- Long bone fractures
- Head injury
- Pulmonary contusion
6) Multiple transfusion
7) Smoke inhalation
8) Near drowning
9) Aspiration of stomach content

  • Neoplasia is not one of them
208
Q

Key ventilation strategies in ARDS

A
  • baby lung
  • open lung
  • protective lung ventilation
  • proning
  • avoiding hyperoxia
  • conservative IVFT
  • other (currently under investigation): pressure release ventilation, recuiting manourver, reduction of driving pressure, reduction of mechanical power, NMB and corticosteroids
209
Q

Corticosteroids in ARDS

A

Current Recommendations:
Early Administration: Corticosteroids may be considered in moderate-to-severe ARDS within the first 7-14 days, particularly in patients not improving with conventional treatment. Dexamethasone is commonly used in such cases.
Late-Phase ARDS: Corticosteroids might be used in the fibroproliferative phase, but this should be done cautiously, weighing the potential benefits against the risks of prolonged corticosteroid therapy.

210
Q

What is lung protective ventilation?

A

Low tidal volume: 4-8 ml/kg
High PEEP
Keep the target plateau pressure < 30 cmH2O

*Permissive hypercapnea

211
Q

Baby lung and open lung concepts

A

The baby lung concept focuses on protecting the small remaining functional lung from overdistension.
The open lung concept focuses on recruiting collapsed lung units to enhance ventilation and oxygenation and reduce ventilator-induced lung injury (VILI) from alveolar collapse and re-opening.

212
Q

What is the most common clinical presentation of ARDS/ALD in veterinary medicine?

A

Refractory hypoxemia

213
Q

Describe the definition of VetARDS/VetALI (5 points).

A
  1. Onset: Acute onset (<72 hours) of respiratory distress at rest
  2. Known risk factors
  3. Evidences of pulmonary capillary leakage without increased capillary hydrostatic pressure (no evidence of cardiogenic edema)
    - bilateral pulmonary infiltrates on TXR
    - bilateral dependent density gradient on CT
    - proteinaceous fluid within the conducting airway
    - increased extravascular lung water
  4. Inefficient gas exchange
    - PaO2/FiO2 ratio WITHOUT PEEP or CPAP
    ≤ 300 mmHg (VetALI)
    ≤ 200 mmHg (VetARDS)
    - Increased A-a gradient
    - Increased dead space ventilation
  5. Evidence of diffuse pulmonary inflammation (optional)
    - TTW/BAL samples show neutrophilia
    - TTW/BAL samples biomarkers show inflammation
    - Molecular imaging (PET)
214
Q

What are the three types of ventilator breaths?

A
  1. Spontaneous
  2. Assisted
  3. Controlled
215
Q

In patients with severe pulmonary disease, does the airway pressure need to be higher or lower on the ventilator setting? What about the volume?

A

Volume: usually benefit from lower volume
Pressure: usually need higher airway pressure (to be able to reach the tidal volume needed)

216
Q

What is the common initial flow rate setting in mechanical ventilation?

A

Flow rate (ml/min) = Tv / I time

10ml/kg/min / 1sec = 0.6ml/kg/min

217
Q

What is an appropriate trigger?

A

flow change of 1-2 L/min
Airway pressure dropped 1-2 cmH2O

218
Q

What is normal minute ventilation in small animals?

A

150-250 ml/kg

219
Q

What are the four main indications for mechanical ventilation?

A
  1. Severe hypoxemia despite oxygen therapy (PaO2 < 60 mmHg)
  2. Severe hypoventilation (PaCO2 > 60 mmHg)
  3. Respiratory fatigue
  4. Severe hemodynamic compromise that is refractory to therapy → goal is to decrease oxygen consumption
220
Q

What are the goals of mechanical ventilation according to ARDS net?

A
  • oxygenation goals with paO2 55-80mmHg with SpO2 88-95%. Achieved by a combination of high PEEP/low FiO2 or low PEEP/high FiO2 (no evidence one approach superior to the other)
  • Pplat <30cmH20. Check Pplat with inspiratory hold of 0.5 sec every 4h and at each change of settings. If Pplat>30cmH20 try to decrease Vt. If breath stacking increase Vt to meet patient’s demand.
  • normal pH. If pH <7.3 increase RR, if no changes increase Vt. If alkalotic reduce RR.
  • keep I:E with I<E
221
Q

What is the equation of motion?

A

It is used to describe the force that drive ventilation

Pmuscle + Pvent = (Tidal volume/compliance) + (resistance x flow)

Pmuscle: pressure generated by the muscle
Pvent: pressure generated by the ventilator
Tidal volume/compliance: elastic load
Resistance x flow: resistant load

222
Q

Which one is volume-control ventilation and which one is pressure-control ventilation?

A

A: Pressure-control
B: Volume-control

  • Pressure-controlled → pressure is the same
  • Volume-controlled → shark fin volume time scalar → flow stops once volume is reached
223
Q

Fill in the blank: All the breaths delivered in assist-control ventilation are ________ in nature.

A

mandatory

224
Q

Name two examples of continuous spontaneous ventilation.

A

CPAP (Continuous positive airway pressure)
PSV (Pressure support ventilation)

225
Q

Describe the difference between assisted breath and supported breath.

A

Assisted breath: patient initiates the breath; machine provide entire inspiratory flow and terminates the cycle

Supported breath: patient initiates the breath and finishes the whole cycle; the machine support the patient with the inspiratory flow

226
Q

List 2 possible complication from fast respiratory rate.

A

1) Auto-PEEP (air stacking)
2) Hypotension (decreased venous return)

227
Q

List 5 adverse effects of PEEP.

A

1) Barotrauma
2) Decreased cardiac output due to decreased venous return
3) Compression of some alveolar capillaries → increased alveolar dead space
4) Increased pulmonary vascular resistance
5) Decreased LV compliance

228
Q

What are the common setting for low and high airway pressure alarm? What are the common DDx for each of them?

A

Low Airway Pressure Alarm
- 5-10 cmH2O lower than peak airway pressure
- Circuit leak

High Airway Pressure Alarm
- 10 cmH2O higher than peak airway pressure
- Pneumothorax, ET tube kink or obstruction, patient-ventilator asynchrony

229
Q

What are the common setting for low and high tidal volume alarm? What are the common DDx for each of them?

A

Low Tidal Volume Alarm
- 15% lower than the patient’s tidal volume
- leak, disconnection of the circuit, drop in compliance

High Tidal Volume Alarm
- 20% higher than the patient’s tidal volume
- Increased in compliance

230
Q

Describe two ways to perform recruitment maneuver.

A
  • Stepwise approach
    Increase PEEP by 2cm H2O every 3-5 minutes. At each increment monitor P/F, PaO2, Cstat and driving pressure (Pplat-PEEP). Keep going until no more improvement in Cstat (driving pressure starts increasing)
  • Sustained inflation
    Put patient on CPAP mode (no mandatory breaths) with a pressure of 30-45cmH20 for 30-40sec
    Kepp patients in A/C mode increase PEEP 20cmH2O and step down by 2cmH2O every 2 min
231
Q

Patient-ventilator asynchrony can be classified into two groups - patient related and equipment related. Name 5 examples for each.

A

Patient-related
- Hypoxemia
- Hypercapnea
- Hyperthermia
- Drug-induced panting
- Inadequate anesthesia depth

Equipment-related
- Circuit/Equipment leak
- Inappropriate trigger setting
- ET tube/circuit kink/obstructed
- Insufficient tidal volume
- Inspiratory time too long/short

232
Q

Fill out the blank. During jet ventilation, distribution of ventilation and tidal volume depend more on ___________. Please fill in lung compliance or airway resistance.

A

Airway resistance

233
Q

What are the indications of jet ventilation.

A

Key of Jet ventilation: tiny Tv and very high RR
- When mechanical ventilation is needed but traditional positive pressure ventilation cannot be delivered (e.g. tracheal/laryngeal surgery, bronchoscopy, bronchial resection, laryngoscopy)
- If ventilation is required in patients with a tracheal lesion secondary to tracheostomy or prolonged intubation

*Jet ventilation still requires intubation, but often with **smaller or more specialized tubes **that are designed to allow for both ventilation and access to the airway.

234
Q

7 mechanisms fo enhanced gas transport in Jet ventilation

A

More homogeneous diffusion of gas in diseased lungs due to:
1. turbulence in large airways = mixing gas
2. direct ventilation of proxymal alveoli
3. radial mixing in medium size bronchi
4. pendelluft
5. laminar flow in small airways
6. asymmetric inspiratory vs expiratory flow (outflow of gas spiralling out vs parabolic flow in)
7. use of pores between alveoli (collateral ventilation)

235
Q

What are 1-4 and a & c?

A

1: pressure used to overcome the circuit and airway
2: pressure used to expand the lung/alveoli
3: pressure throughout the expiratory phase
4: PEEP
a: peak inspiratory pressure (PIP)
c: plateau pressure

236
Q

What is the equation for dynamic and static compliance? Which one is bigger? Why?

A

Dynamic compliance = tidal volume/(PIP-PEEP)
Static compliance = tidal volume/(Pplateau - PEEP)

Dynamic compliance < static compliance

Because dynamic compliance includes the pressure needed to overcome the airway and circuit

237
Q

In this figure, which one indicates increased airway resistance, which one indicates decreased compliance?

A

A: increased airway resistance
B: decreased compliance

238
Q

What can expiratory hold tell us?

A

Whether or not there is intrinsic PEEP (auto-PEEP).

239
Q

List 2 differences of constant flow pattern and decelerating ramp flow pattern (in volume-control mode)

A

1) The PIP for constant flow pattern will be higher
2) The decelerating ramp flow allow fine-tuning of inspiratory time
3) decelerating ramp more comfortable as more physiological and less likely to cause barotrauma

240
Q

This is a flow pattern for VC mode. What is the difference between b, c, d?

A

b: the inspiratory time is too short → flow asynchrony
c: optimal inspiratory time
d: the inspiratory time is too prolonged → increase risk of patient-ventilator dyssynchrony

241
Q

What are the two ways to detect Auto-PEEP?

A

1) Expiratory hold
2) Check the flow scalar → if the expiratory flow does not return to baseline → Auto-PEEP

242
Q

What is dyssynchrony index?

A

Number of dyssynchrony breaths/total breaths

If >10% increased duration of ventilation and increased need for tracheostomy

243
Q

What does the change from purple to blue indicate?

A

Increased circuit/airway resistance
slightly decrease dynamic compliance

244
Q

What does A and B indicates, respectively?

A

A: decreased dynamic compliance
B: increased dynamic compliance

245
Q

What does LIP and UIP indicates, respectively?

A

LIP (lower inflection point): where the lung compliance suddenly increases due to opening of the collapsed conducting duct/alveoli
UIP (higher inflection point): where the lung compliance significantly decreases due to overdistension of alveoli

  • PEEP should be set above LIP
    PIP lower than UIP
246
Q

What does scooping tell us?

A

Increased airway resistance

247
Q

What does this flow-volume loop tell us?

A

Excessive airway secretion

248
Q

Define patient-ventilator dyssynchrony

A

Mismatch between the breaths delivered by the ventilator and the patient’s needs.

Gold standard to detect dyssynchrony would be phrenic neurogram and oesophageal baloon catheter for pressure measurement but in clinical practice relying on waveform analysis

249
Q

What are the 4 phases that patient-ventilator dyssynchrony can happen?

A

1) Initiation/trigger phase
2) Flow delivery phase
3) Breath termination point (cycling)
4) Expiratory phase

250
Q

Trigger asynchrony is the most common form of PVD in human. What are the three types of trigger asynchrony?

A

1) Ineffective triggering
2) Auto-triggering - the ventilator “thinks” the patient is trying to initiate a breath when they are not, leading to unintended breaths
3) Double triggering - two breaths are delivered in quick succession, often because the patient’s effort or demand for air is not fully met by the first breath, leading them to trigger another breath immediately afterward.

251
Q

List 3 causes of double triggering.

A

1) Patient has higher ventilatory demand
2) Tidal volume is too small
3) Inspiratory time is too short or “flow-cycle threshold set too high” (the ventilator is ending the inspiratory phase too early. The ventilator switches to expiration before the patient has finished inhaling)

252
Q

What does premature cycling and delayed cycling mean?

A

Premature cycling: the patient is continuing to make inspiratory efforts at the time the ventilator cycles off

Delayed cycling: the patient initiates active expiratory efforts while the ventilator is continuing to deliver inspiratory flow

253
Q
A

Flow starvation

254
Q
A

Excessive inspiratory flow

255
Q
A

Delayed cycling - the patient is trying to exhale while machine still delivery inspiratory breath

256
Q

Why inhalant anesthetics should not be used for patient on mechanical ventilator?

A

1) It inhibits the hypoxic induced vasoconstriction → make hypoxemia worse
2) irritating to lung parenchyma

257
Q

According to the current meta-analysis in human, does histamine-2 receptor antagonists a routine therapy for patients on mechanical ventilation?

A

No

higher rates of gastric colonization and VAP

258
Q

What are the 6 criteria for patient to be able to enter the spontaneous breathing trial.

A

1) The primary disease has improved and stable
2) PaO2/FiO2 > 150-200 with FiO2 < 0.5
3) PEEP ≤ 5 cmH2O
4) Adequate respiratory drive
5) Hemodynamically stable
6) No evidence of organ failure

259
Q

During the spontaneous breathing trial, does rapid-shallow breathing pattern or slow-deep breathing pattern has better change of weaning off?

A

slow-deep breathing pattern

260
Q

What are the main reasons for weaning failure?

A
  • unresolved primary cause
  • muscle weakness
  • inappropriate recovery from sedation/GA
  • increased WOB
  • CV instability

Re-intubation increases odds of developing VAP by 7.6x

261
Q

What are the 9 criteria for failure of the spontaneous breathing test?

A

1) Tachypnea (RR > 50)
2) PaO2 < 60 mmHg or SpO2 < 90%
3) PaCO2 > 55 mmHg or PvCO2 > 60 mmHg or EtCO2 > 50 mmHg
4) Tidal volume < 7 ml/kg
5) Tachycardia
6) Hypertension
7) Hyperthermia or temp increase > 1C
8) Anxiety
9) Clinical judgement

262
Q

What are the three weaning techniques?

A

Spontaneous breathing trial (with CPAP)
PSV
SIMV

263
Q

Fill in the blank: When the inspiratory pressure is higher than _____ or tidal volume is higher than _____, pathologic change of the respiratory system can be observed.

A

30 cmH2O
40 ml/kg

264
Q

List 5 ventilator-induced lung injury.

A

Volutrauma
Barotrauma
Pneumothorax
Oxygen toxicity
Atelectrauma
Biotrauma

265
Q

What is the main risk factor of developing VAP?

A

Endotracheal intubation

266
Q

What does the VAP refer to?

A

Ventilator-associated pneumonia

Pneumonia that arises more than 48 hours after endotracheal intubation that was not present at the time of intubation.

267
Q

What are the two major pathologic mechanisms of VAP?

A

Biofilm formation within the endotracheal tube
Microaspiration pass the endotracheal tube cuff

Additional factors:
- pulmonary and GI dysbiosis during critical illness
- biotrauma with activation of resident macrophages + recruitment of neutrophils (upregulation of cytokines production)
- impairment of muco-ciliary protection during mechanical ventilation

268
Q

What is the major type of bacteria for VAP?

A

Early (48-96h post ET tube placement) vs late VAP

  • early VAP: antibiotic susceptible Staph and Streptococcus
  • late VAP: antibiotic-resistant Pseudomonas and Acinetobacter
269
Q

For clinical diagnosis of VAP, what are the three criteria (2/3 need to be met)

A

1) Fever
2) Leukocytosis/leukopenia
3) Purulent airway secretions

270
Q

Describe the criteria of VAP based on modified CDC National Healthcare Safety Network definition of pneumonia.

A

Clinical Criteria
1) Presence of ET tube/tracheostomy at least 48 hours prior to the presence of clinical signs
2) Radiologic criteria: consolidation, cavitation, new or progressive and persistent pulmonary infiltrates
3) Systemic criteria: fever, leukocytosis/leukopenia
4) Pulmonary criteria (need 2): purulent airway discharge or increased secretion, worsening of gas exchange, new onset or worsening of coughing, dyspnea or tachypnea, crackles or bronchial breath sounds

Microbiological Evidence

1) Positive Cultures:
Sputum, tracheal aspirate, or bronchoalveolar lavage (BAL) samples showing growth of pathogenic organisms are a key microbiological criterion.
Quantitative cultures: e.g., from BAL (>10⁴ CFU/mL) or tracheal aspirates (>10⁵ CFU/mL).
2) Positive blood cultures from a sterile site (when not attributed to another source) can also support the diagnosis.
3) histopathological evidence

271
Q

4 histologic phases of VAP

A
  1. early bronchiolitis
  2. focal broncopneumonia
  3. confluent bronchopneumonia
  4. lung abscess

These phases usually occur simultaneously in different areas of the lung

272
Q

True or False: To avoid VAP, the ventilator circuits should be change every 3 days.

A

False

Routine changing of the ventilator circuit should not occur unless contamination is noted.

273
Q

Do brachycephalic dogs tend to be hypercoagulable or hypocoagulable?

A

hypercoagulable

Chronic hypoxia → inflammatory state

274
Q

List 3 surgical interventions for BAOS.

A

1) Wedge nasoplasty (rhinoplasty/alarplasty)
2) Soft palate resection (staphylectomy)
3)Everted laryngeal saccules resection (ventriculectomy or sacculectomy)

Turbinectomy if CT findings supportive and if patient not responding to traditional medical and surgical treatment.

Surgical complications are reported to be uncommon with a success rate of up to 94%

275
Q

True or False: Feline herpesvirus-1 is a double-stranded, enveloped DNA virus; Feline calcivirus is a single-stranded non-enveloped RNA virus.

A

True

276
Q

Where does FHV-1 persists in during latent form?

A

Trigeminal ganglia

277
Q

What are the three stages of laryngeal collapse?

A

Stage 1: laryngeal saccule eversion
Stage 2: loss of rigidity and collapse of the cuneiform processes of the arytenyoid cartilages
Stage 3: complete laryngeal collapse characterized by midline collapse of the corniculate processes

278
Q

What is the most common tracheal neoplasia in dogs?

A

Osteochondroma

279
Q

There are two types of sensory nerves for coughing - mechanical receptors and chemoreceptors. Where do they locate?

A

Mechanical receptors (myelinated afferent nerves): larynx, trachea, large bronchi

Chemoreceptors (C-fibers; unmyelinated axon): within all segments of the respiratory tree, including the larynx, carina, terminal bronchioles, and alveoli

280
Q

What is the most common cause for hemoptysis in dogs?

A

Bacterial bronchopneumonia

281
Q

Which bacteria are most commonly isolated in bacterial pneumonia in dogs and cats?

A

gram - : Pasteurella, Bordetella. E.Coli
gram +: Staph, Strep
Mycoplasma

Polymicrobial in 74% of dogs and 38% of cats

282
Q

What is the most common cause of feline bacterial bronchopneumonia?

A

Hematogenous spread

283
Q

Where are airway FB most commonly located in dogs and cats?

A

Dogs: right bronchus
Cats: trachea or carina

284
Q

What is the success rate for endoscopic FB retrieval in dogs and cats respectively? what is an alternative diagnosis in cats?

A

86% in dogs but only 40% in cats
Consider Cuterebra spp. in cats as a differential

285
Q

What are the two most common mycosis in cats?

A

Cryptococcosis
Histoplasmosis

286
Q

Why shouldn’t NAC be used for nebulization?

A

Bronchoconstriction
Epithelial toxicity

287
Q

How high of pulmonary venous pressure is sufficient to produce edema?

A

> 25 mmHg

288
Q

Describe how to perform TTW.

A

1) Patient needs to be > 15kg
2) Patient is restrained in sternal recumbency with nose tipped dorsally
3) The ventral cervical area is clipped and aseptically cleaned
4) Local anesthesia (2 to 5 mg/kg, 2% lidocaine) is instilled intradermally and SC at the intended needle insertion site
5) A stab incision is made through the skin using a #11 blade at that site to facilitate passage of a sterile 14-gauge needle through the cricothyroid ligament.
6) Measure the insertion site to 4th ribs
7) Inserting a sterile 3.5-French red rubber or polypropylene catheter through the needle
8) Inject sterile saline 0.5 to 5 mL/kg per aliquot and aspirate when patient coughs
9) After removal of the catheter and needle from the trachea, the area is covered with a sterile, nonadherent gauze sponge and lightly bandaged

289
Q

How does furosemide reach the NAK2Cl transporters?

A

Furosemide is secreted from the blood into the tubule lumen using an organic ion transporter located in the proximal convoluted tubule.
The efficacy of this process is regulated by renal perfusion, competition by other organic anions, such as NSAIDs, and the degree to which furosemide is bound to albumin in the circulation.

290
Q

List 3 conditions that may interfere with furosemide’s efficacy.

A

1) Hypoalbuminemia
2) Concurrent use of NSAIDs
3) Poor cardiac output

291
Q

What is Kussmaul breathing?

A

Kussmaul breathing can be seen with severe metabolic acidosis and is defined as an extremely deep, rapid breathing pattern associated with hypocapnia

292
Q

True or False: Animals with neurogenic pulmonary edema due to upper airway obstruction and seizures appear to have worse outcomes compared to NPE secondary to head trauma or electrocution.

A

True

293
Q

Which of the following physiologic changes will not be observed in diving in room temperature water?
1) Diuresis
2) Natriuresis
3) Kaliuresis
4) Increased work of breathing
5) Decreased cardiac output

A

5)

  • Cardiac output increases
294
Q

Does hypothermia increase or decrease antidiuretic hormone production?

A

Decreased → patient becomes polyuric

295
Q

List 5 complications from submersion injury.

A

1) Hypoxemia
2) Aspiration pneumonitis
3) Arrhythmias
4) Metabolic acidosis
5) Neurological signs

296
Q

In patient with submersion injury and hypothermia, when should the active warming stop?

A

Active rewarming should stop when core temperature reaches 37 °C (98.6 F) to prevent rebound pyrexia

297
Q

What does Westermark sign indicate?

A

PTE

  • Areas of relative oligemia (less blood) secondary to decreased caliber of regional pulmonary arteries
298
Q

When pleurodesis is used to treat spontaneous pneumothorax, how many ml of blood is usually used in total?

A

5-10 ml/kg

299
Q

How many ml/kg of pleural effusion in dogs and cats will make them clinical?

A

Dog: 30-60 ml/kg
Cat: 20 ml/kg

300
Q

Describe tracheostomy tube management.

A

1) Nebulization & airway humidification 10-15 min q4-6 hours
- Postural drainage and coupage (percussion) after
2) Clean the skin around the tracheostomy site with diluted chx (0.05%)
3) Check the tube ties
4) Tracheostomy tube suctioning
- Preoxygenation
- The entire suctioning procedure should be completed in less than 15 seconds
- No suction after eating
5) Tracheostomy tube cleaning
- q4-6 hours
- Replace the inner piece
6) Change the entire tracheostomy tube every 24 hours

301
Q

Define “pendelluft.”

A

it is a phenomenon describing the gas movement between lung regions with different compliances and airway resistance.

Pendelluft is often seen when:

Different lung regions have unequal time constants (the product of resistance and compliance).
During the inspiratory phase, one lung region fills with air more quickly, while another fills more slowly due to higher resistance or lower compliance.
Air then moves from the faster-filling region to the slower-filling region, even while the airway pressure is constant.

302
Q

How to calculate driving pressure?

A

Driving pressure = Pplateau - PEEP

303
Q

Where is the air emboli absorbed?

A

Lung

304
Q

Which procedures are more at risk for development of gas emboli?

A
  • venous catheterization above the level of the heart
  • laparoscopic procedure (use CO2 as more likley to be reabsorbed and at a pressure <15mmHg so no gradient to get into vessels)
  • HBO
  • lung biopsies
    -CBP procedures
305
Q

Fill out the blank: In dogs, clinical air embolism occurs in 50% of animals when _____ ml/kg/min of air (consisting of primarily nitrogen, an insoluble gas) is infused

A

0.35

306
Q

What is the solubility of O2 in water?

A

0.003ml/dL/mmHg

Part of the CaO2 equation (PaO2 x 0.003)

307
Q

Define:
- transpulmonary pressure
- transthoracic pressure
- transrespiratory pressure

A
  • transpulmonary pressure = pulmonary pressure - pleural pressure (positive and keeps lung open)
  • transthoracic pressure = intrapleural pressure - atmospheric pressure (negative and opposing elasticy of chest that wants to spring open)
  • transrespiratory pressure = pulmonary - atm pressure
308
Q

Boyles law

A
309
Q

Glomus cell

A

sensory cells in aortic and carotid bodies - sense drop of pO2, actovate Kv channels, open Ca channels, depolarization, neural input or respiratory centers in medulla and pons

310
Q

List extra-pulmonary receptors that can influence respiratory centers

A
  • muscolo-skeletal proprioceptors (tachypnoea during exercise before hypercapnoea)
  • aortic and carotid baroceptors (tachypnoea secondary to drop in BP)
  • pain receptors
  • thermoreceptors (tachypnoea secondary to hyperthermia)
311
Q

List 3 drugs that inhibit central respiration

A
  • anaesthetics
  • opioids
  • benzodiazepines
312
Q

Define dyspnoea

A

Dyspnoea is a subjective unpleasant sensation of perceived inadequate ventilation

313
Q

Describe pathophysiology of dyspnoea

A

Although similar to pain in the subjective perception of real or perceived threat, dyspnoea doesn’t have specific receptor. The sensation is created by several peripheral afferent pathways including upper airways, lower airways (main generators of dyspnoea sensation), chest wall and chemoreceptors. These will be matched with the output generated in the CNS. If there is a mismatch between afferent input and output generation –> NEUROVENTILATORY MISMATCH and dyspnoea perception

314
Q

List 3 forms of dyspnoea

A
  • air hunger (from stretch and chemoreceptors - i.e. J receptors and furosemide)
  • increased WOB (from mechanoreceptors)
  • asthmatic thightness (bronchoconstriction)
315
Q

List 4 therapeutic strategies to tackle dyspnoea sensation

A
  • furosemide (acts on slow adaptive receptors and J receptors)
  • opioids (opioid receptors present in bronchioli and parenchyma)
  • steroids (? possibly helping with reducing inflammatory mediators)
  • chest wall vibration (reduce mechanoreceptor firing - less perception of WOB)
316
Q

Explain chloride shift

A
317
Q

How is CO2 transported in blood?

A

70% HCO3-
20% HHb
10% CO2 disolved in plasma

318
Q

Relating to pulmonary function testing what are the two main pathological patterns?

A
  • restrictive (“small lungs”)
  • obstructive (“big lungs”)
319
Q

What is FEV1 and FVC

A

FEV1: forced expiratory volume (how much air can be expelled from the lungs in 1s)
FVC: forced vital capacity - total amount of air that a patient can forcibly exhale from their lungs after taking the deepest breath possible.

320
Q

Is FEV1/FVC increased or decreased in obstructive vs restrictive pulmonary disease?

A

FEV/FVC decreased in obstructive disease (improves with administration of bronchodilators)
FEV/FVC decreased in restrictive disease

321
Q

Interpret the following flow-volume loops

A

Left is obstructive patter (increased total lung volume) and right is restrictive lung pattern (decreased total lung volume)

322
Q

Define ‘time constant’

A

time constant = compliance x resistance

After 1 time constant, about 63% of lung volume has been inhaled or exhaled.
After 2 time constants, about 86% of lung volume has been inhaled or exhaled.
After 3 time constants, about 95% of lung volume has been inhaled or exhaled.
After 4 time constants, about 98% of lung volume has been inhaled or exhaled.

323
Q

In a normal animal how do you calculate the inspiration and exalation time?

A

Usually ratio I:E is 1:2

so expiration usually calculated as 4xtime constant to ensure complete exhalation

324
Q

Byosynthesis of reactive species

A
325
Q

Ischemia-reperfusion injury

A
326
Q

Best sedation protocols for upper airway exam

A
  1. thiopental has the least impact on laryngeal function
  2. dexmedetomidine alone or in combination with opioids > titration of propofol
  3. ACP+butorphanol

an anticholinergic can be added to reduce secretions

Doxapram test - normal dogs have their larynx “pin open”

327
Q

Criteria for post-capillary PH

A

PAP≧25mmHg and PAWP ≧ 15mmHg

328
Q

why is post-capillary PH often accompanied by pre-capillary PH

A

Back pressure into pulmonary capillaries causes endothelial damage and vascular remodelling inducing pre-capillary PH

329
Q

What is the hallmark sign of combined pre- and post-capillary PH?

A

PAP-PAWP gradient >7mmHg as PAP↑↑↑

330
Q

What is the different in PAP estimation when using TV regurgitation vs PA regurgitation?

A

TV is closed in systole –> PAPs
PA closed in diastole –> PAPm/d

331
Q

What are the 3 main echo sites for diagnosis of PH?

A
  1. Ventricles (flattening IV septum, underfilling LV, RV enlargement and wall thickening)
  2. PA/Ao>1.4 and distensibility <30%
  3. RA and vena cava enlargement
332
Q

Echo probability of PH

A
333
Q

What are the most common clinical signs for PH?

A
  1. tachypnoea/dyspnoea at rest
  2. syncope
  3. split S2
  4. RH failure
  5. exercise intolerance
334
Q

In a recent study dogs with PH due to primary respiratory disease had a poorer prognosis if sPAP was ____
Furthermore the most severely affected patients had PA distensibility < ___ and PA/Ao <___

A

≧ 47mmHg
10%
0.98

335
Q

Pathophysiolog yof pneumonia

A

Respiratory epithelium has PRRs for DAMPs and PAMPs –> nfKB and cytokine production + activation alveolar macrophages –> recruitment of neutrophils and platelet activation
Also concurrent anti-inflammatory response with secretion of IL-10 and phenotype M2

336
Q

Histopathological progression of pneumonia

A
  1. congestion
  2. red hepatization
  3. grey hepatization
  4. resolution (if type I shift to type II + scarring if basal membrane severely damaged)
337
Q

How to choose the best antibiotic for respiratory tract infection?

A

Main barrier is the broncho-alveolar-blood barrier
Best drugs should be lipophylic and small molecular weight.

Index of bronchial [drug]/plasma[drug]

TMPS 100%
Fluoroquinolones 70%
vs penicillin 9% (but with inflammation can still penetrate)
aminoglycosides (38% but used effectivey against Bordetella when nebulised)

338
Q

What type of snake envenomation is most likely to cause respiratory paralysis?

A

Elapids (coral snake).
Two main toxins:
1. phospholypidase: binds and hydrolyses phospholipids of nerve terminals
2. 𝛼-neurotoxin: binds post-synaptic ACh receptors at the NMJ

Clinical signs consistent with progressive LMN defects and ultimately flaccid respiratory paralysis

339
Q

Treatment for snake envenomation and respiratory paralysis

A

Anti-venom (IgG against venom –> immunocomplexes easily phagocytized) - polyvalent best one as no need for specific snake identification

Nerve regeneration after phospholipidase (PLA2) occurs over 3-4 days –> prolonged MV need

72% survival with aggressive treatment (MV + antivenom)

340
Q

Which species of ticks are responsible for paralysis in USA and Australia respectively? What’s the mechanism of action?

A

Australia: Ixodex
USA: Dermatocentor

Pre-synaptic inhibition of Ach in the NMJ

Also toxin can cause ALI/ARDS, myocardial failure

341
Q

Treatment for tick paralysis

A

Antiserum + MV (average duration 4 days - weaning best with pressure support vs SIVM)

Consider tracheostomy due to high incidence of upper airway obstruction (flaccid paralysis upper airways)

342
Q

Prognosis for tick paralysis

A

Gait and respiratory scores

High scores significantly associated with poorer prognosis

75% survival overall (much better if MV started due to hypoventilation rather than hypoxemia)

343
Q

According to the recent literature which complications are most commonly reported with long-term MV?

A
  • VAC 24%: hypothermia, hypotension, arrhythmia, positive fluid balance, oral and corneal lesions
  • VAP 14%
344
Q

what is the % of patients with cardiac conditions weaned off MV vs non-cardiac conditions? which poor prognostic factors were recognised in the two groups?

A

66% cardiac patients vs 35% non-cardiac

development of azotemia in CHF
anaemia in non-cardiac group

345
Q

Up to 71% of dogs with VAP had negative cytology but positive cultures

A

True

346
Q

Definition of refractory hypoxaemia

A

PaO2<60mmHg despite FiO2 0.8-1, PEEP 10-30 cmH20, Pplat >30cmH20

347
Q

When applying recruiter manouver how are responders and non-responders assessed?

A

Very controversial, no clear definition.
Low vs high responders
Also anatomic recruitment (assessed by CT) ≠ functional recruitment (assessed by improved oxygenation)

348
Q

How many consequential ribs can be removed without compromising stability of the chest wall?

A

6

349
Q

Most cats with pyothorax present with an increased rectal temperature

A

False

over 50% of cats with pyothorax present with hypothermia

350
Q

CT in dogs can predict the type of pleural effusion

A

False

CT is the most sensitive method to detect both pneumothorax and pleural effusion.
In humans features of pleural effusion are predictive of type but not in dogs.

351
Q

Classification of effusions

A
352
Q

Criteria for chylothorax diagnosis

A

Triglycerides 3:1 vs serum (or>100mg/dL)
Cholesterol < than in serum
Small lymphocytes cellularity

353
Q

Most common cause of chylothorax

A
  • CHF
  • obstruction of thoracic duct
  • idiopathic
  • lung lobe torsion
  • CVC thrombosis
354
Q

What is the physiological Jv in the pleural space

A

9 cmH2O –> constant flow into pleura to lubricate

355
Q

Chylothorax treatment

A

Mainly surgical with pericardiectomy and thoracic duct ligation

Medical management can be attempted with low fat diet and rutin (increase lymphatic fluid uptake)

356
Q

How many cats develop sepsis from pyothorax?

A

Up to 40%

357
Q

What is the most common clinico-pathological abnormalities in patients with pyothorax?

A

neutrophilia in 93% of dogs and 73% of cats

358
Q

In what percentage of patients with pyothorax blood cultures were found to be positive?

A

Less than 20%

359
Q

Is surgical treatment the recommended approach for both dogs and cats with pyothorax?

A

Dogs are much more likely to require surgical exploration (sternotomy preferred) as dogs not undergoing surgery were 5.4x more likely to fail to resolve pyothorax.
Cats undergoing surgery also more likely to survive, but significantly longer hospitalisation time.

360
Q

What is the rate of recurrence for pyothorax in dogs? what are the main risks factors?

A

14%

Actinomyces, Nocardia and migrating FBs

361
Q

Most common causes of traumatic pneumothorax in dogs and cats

A

47% of dogs involved in RTA and 20% of cats post high-rise fall

362
Q

What modality of ventilation is this?

A

A/C the patient can trigger a breath but all breath delivered are mandatory

363
Q

What modality of ventilation is this?

A

SIMV - patient can trigger breaths and they can be spontaneous or assisted if the fall within the pre-set cycle

364
Q

Which variables are intrinsic of the patient and which are controlled by the ventilators?

A
  • patient: resistance and compliance
  • ventilator: pressure, volume and flow
365
Q

Define:
- trigger variable
- cycle variable
- limit variable

A
  • what triggers the delivery of a breath (time, pressure or flow)
  • what determines the change from inspiration to expiration (time, I:E, RR)
  • parameter that can’t be exceeded during the inspiration phase (it limits but doesn’t terminate the breath≠from cycling variable)
366
Q

What is the VC+?

A

Volume controlled pressure limited

367
Q

What is the difference between functional and fractional Hb saturation?

A

Functional Hb saturation obtained with pulseox and is the ratio between HbO2 and the sum of HbO2 and HHb. It reflects the pulmonary function best.

Fractional Hb saturation is obtained via co-oxymetry and it it the ration of HbO2 and the sum of all Hb (HHb, MetHb, SulfHb, CoHb and HbO2)

368
Q

According to the recent literature nasal capnography is a reliable non-invasive method that correlates well with traditional ETCO2

A

Yes, two studies confirmed good correlation in both healthy and critically ill dogs with and without oxygen supplementation

369
Q

In BAL what is the usual volume of fluid injected? how can you tell if appropriate sample obtained? what’s the difference between the first and the second sample?

A

In medium to large dogs 2x25ml saline vs small dogs and cats 2x10ml.

First sample more representative of airways vs second sample more representative of alveoli.

Sample with foam = presence of surfactant
Cytologically should see large amount of alveolar macrophages.

370
Q

Why is it important to perform quantitative cultures on BAL samples?

A

Airways are not sterile so significant only when CFU>10 (5)
If on abx CFU>10 (3)

371
Q

BRISK score

A

Include:
- breed
- emergency presentation
- BCS
- hyperthermia/hypothermia
- procedures planner
- surgical history

Predictor of negative surgical outcomes:
BRISK>4 high risk
BRISK>3 mediumm to high risk

372
Q

What is the part of the diaphragm usually most likely to rupture after trauma?

A

Muscular part > central tendon or crural portion

Right side also most commonly affected

373
Q

After traumatic event patient presented with diaphragmatic hernia often had other overt injuries

A

False

Only 25%, so don’t discard possibility of hernia despite no other findings on clinical exam
Also 25% completely asymptomatic

374
Q

Which lobes are most likely to be involved in torsions?

A

Right middle and Left cranial

375
Q

What is the classical xray sign for lung lobe torsion?

A

vescicular emphysema

376
Q

which breeds are more predisposed to develop lung lobe torsion?

A

Pugs and large breeds

377
Q

Predisposing factor for lung lobe torsion?

A
  1. pleural disease
  2. aspiration pneumonia
  3. previous surgical manipulation
378
Q

Is chylothorax a possible post-op complication of lung lobe torsion?

A

Yes, due to possible damage of thoracic duct and lymphatics system
Often requires revision surgery

379
Q

Direct causes of ARDS are more common than indirect causes in dogs

A

True
Aspiration and SIRS were the most common

In cats are equally distributed

380
Q

Overall reported fatality rate in ARDS for dogs and cats

A

Dogs 84% and cats 100%

381
Q

Which spinal lesions are more likely to require ventilation? what is the outcome?

A

C2-C5 ventral slot
4.9% of cervical lesion required MV
80% survival with appropriate interventions

382
Q

According to the most recent evidence is which is more beneficial a lower or higher oxygenation target?

A

No difference has been found in multiple trials, cochrane review and meta-analysis

ECVECC Board Exam (24 decks)

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