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Boards: Respiratory > Respiratory > Flashcards

Respiratory Flashcards

1
Q

If 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

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

A

True

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3
Q

What is the definition of hypoxemia

A

PaO2 < 80 mmHg

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4
Q

List 4 different kinds of hemoglobins.

A

Oxygenated hemoglobin
Deoxygenated hemoglobin
Methemoglobin
Carboxyhemoglobin
Sulfhemoglobin

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5
Q

What is the two wavelengths of light on pulse oximeter?

A

940 nm (infrared)
660 nm (red)

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6
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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7
Q

What cells secrete surfactant?

A

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

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8
Q

What are the main components of surfactant?

A

Phospholipid dipalmitoyl phosphatidylcholine
Surfactant apoproteins
Calcium ions

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9
Q

True or False: Alveolar pressure caused by surface tension is directly related to alveolar radius.

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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10
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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11
Q

Fill out the blank.

A
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12
Q

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

A

Functional residual capacity

*** NOT RESIDUAL VOLUME

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13
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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14
Q

What is the formula for minute ventilation?

A

Minute ventilation = tidal volume x respiratory rate

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15
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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16
Q

How does hypoxia affect the systemic vessels and pulmonary vessels?

A

Systemic vessels - vasodilation
Pulmonary vessels - vasoconstriction

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17
Q

What is the definition of terminal bronchioles?

A

The smallest airways without alveoli.

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18
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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19
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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20
Q

What are the two methods to measure FRC?

A

Helium dilution
Whole body plethysmography

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21
Q

What does the alveolar ventilation mean?

A

The amount of air that is available for gas exchange

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22
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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23
Q

What is the alveolar ventilation equation?

A
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24
Q

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

A
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25
Q

What is normal physiological dead space percentage?

A

0.2 - 0.35

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26
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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27
Q

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

A

0.75 seconds

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28
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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29
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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30
Q

Which gas is ideal for diffusion capacity measurement. Why?

A

Carbon monoxide
Because the gas is purely diffusion limited

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31
Q

Describe the route oxygen reach RBC in the long.

A

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

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32
Q

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

A

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

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33
Q

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

A

1/10

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34
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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35
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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36
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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37
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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38
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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39
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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40
Q

True or False: Hypoxemia can cause pulmonary vasoconstriction.

A

False

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

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41
Q

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

A

Alveolar PO2 < 70 mmHg

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42
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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43
Q

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

A

Angiotensin I
Bradykinin

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44
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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45
Q

What is the most abundant immunoglobulin in the bronchial secretion?

A

IgA

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46
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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47
Q

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

A
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48
Q

What is normal percentage of pulmonary shunt?

A

2%

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49
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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50
Q

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

A

True

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51
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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52
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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53
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

Because CO2 is more diffusible than O2

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54
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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55
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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56
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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57
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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58
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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59
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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60
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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61
Q

What is the definition of compliance?

A

The volume change per unit pressure change

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62
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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63
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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64
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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65
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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66
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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67
Q

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

A

Medium-sized bronchi

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68
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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69
Q

What is the equate for work of breathing?

A

WOB = pressure x volume

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70
Q

Where does breathing center locate?

A

Brainstem (pons, medulla)

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71
Q

Where is the normal respiratory rhythm generated?

A

Medullary respiratory center, Pre-Botzinger complex

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72
Q

What does apneustic center and pneumotaxic center do?

A

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

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73
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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74
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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75
Q

Where is the central chemoreceptors?

A

Ventral surface of the medulla

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76
Q

What change does the peripheral chemoreceptors detect?

A

Change in PO2, pH and PCO2

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77
Q

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

A

Slow down the respiratory frequency (because the lung needs longer expiration time)

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78
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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79
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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80
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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81
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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82
Q

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

A

Peripheral chemoreceptors

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83
Q

Draw and describe the three bottle system.

A

Pressure for suction: 10-20 cmH2O

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84
Q

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

A

25 - 40%

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85
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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86
Q

What is the landmark to place a nasopharyngeal catheter?

A

From the nose to the mandibular ramus

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87
Q

What is the landmark to place a nasal oxygen catheter?

A

From the nose to the lateral canthus

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88
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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89
Q

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

A

PaO2

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90
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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91
Q

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

A
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92
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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93
Q

What is the relationship between PaCO2 and ETCO2?

A

ETCO2 is about 5mmHg lower than PaCO2

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94
Q

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

A

CVCO2 is about 5mmHg higher than PaCO2

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95
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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96
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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97
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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98
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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99
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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100
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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101
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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102
Q

What is the relationship between PvCO2 and PaCO2?

A

PvCO2 is about 3-6 mmHg higher than PaCO2

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103
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.

104
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

105
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.

106
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

107
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

108
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

109
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

110
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

111
Q

List 4 respiratory stimulants.

A

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

112
Q

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

A

Trachea rostral to the thoracic inlet

113
Q

Describe paradoxical laryngeal movement.

A

Inward movement of the arytenoids during inspiration.

114
Q

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

A

Nose

115
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

116
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)
Vestibular signs (~50%, can last for 4 weeks)

117
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

118
Q

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

A

25-50%

119
Q

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

A

Right

120
Q

What is the recommended ET tube cuff pressure?

A

20 - 30 cmH2O

121
Q

Does asthma cause increased or decreased FRC?

A

Increased (due to air-trapping)

122
Q

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

A

Toxocara canis

123
Q

What are the two main pathophysiologic forms of pulmonary edema?

A

High-pressure edema
Increased-permeability edema

124
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.

125
Q

List 3 proposed mechanisms for reexpansion edema.

A

1) Decreased surfactant production
2) Mechanical force leading to pulmonary parenchyma injury
3) Reperfusion injury
4)

126
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

127
Q

What is the MOA of NAC in clearing the mucus?

A

breakdown of the disulfide bonds

128
Q

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

A

3 um

129
Q

Explain the biphasic pathogenesis of aspiration pneumonitis.

A

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

4-6 hours after aspiration
Inflammatory mediator cascades producing neutrophil chemotaxis (IL-8, TNF-α,17 and macrophage inflammatory protein 2), sequestration, and subsequent increased permeability edema

130
Q

Why is bronchodilator not recommended in dogs with aspiration pneumonia?

A

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

131
Q

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

A

Decreased compliance Hallmark of ARDS

132
Q

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

A

> 20%

133
Q

What is the primary reason for PTE-induced hypoxemia?

A

High V/Q mismatch

134
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

135
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

136
Q

Where does the segmental intercostal nerves leave?

A

C6 - T2

137
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, hyperesthetic
  • Treatment: supportive care (steroid doesn’t seem to help)
  • usually take 3+ weeks to recover
138
Q

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

A

Type C toxin

139
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.
140
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

141
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

142
Q

What is normal pleural space pressure?

A

-5 cmH2O

143
Q

Define tension pneumothorax

A

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

144
Q

When do hypoxemia become the primary drive for ventilation?

A

When PaO2 < 50 mmHg

145
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.

146
Q

In smoke inhalation, what chemical can cause histotoxic hypoxia?

A

Hydrogen cyanide (HCN)

147
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

148
Q

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

A

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

149
Q

What is the treatment for cyanide toxicity?

A

Hydroxocobalamin

*Bind to cyanide to form cyanocobalamin (vitamin B12)

150
Q

Fill out A to E.

A

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

151
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

152
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.

153
Q

What is Bordetella bronchiseptica?

A

Gram negative, obligate aerobic coccobacillus

154
Q

What dose this EtCO2 tell you?

A

Bronchoconstriction/Asthma

155
Q

What does this EtCO2 tell you?

A

Rebreathing

156
Q

What does this EtCO2 tell you?

A

Patient is breathing spontaneously

157
Q

What does this EtCO2 tell you?

A

Cardiac oscillation

158
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

159
Q

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

A

True

160
Q

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

A

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

161
Q

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

A

1/3

162
Q

List 10 proposed etiology for laryngeal paralysis.

A

1) Congenital
2) GOLPP
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

163
Q

What is the surgery called for laryngeal paralysis?

A

unilateral arytenoid lateralization

164
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.
165
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.

166
Q

What is the ideal tracheostomy tube length?

A

6-7 tracheal rings down from the insertion site

167
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 muscles.
  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.
168
Q

What are the three phases of ARDS?

A

Exudative
Proliferative
Fibrotic

169
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

170
Q

What is the characteristics of exudative phase of ARDS?

A

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

171
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
172
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

173
Q

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

A

Refractory hopoxemia

174
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)
175
Q

What are the three types of ventilator breaths?

A
  1. Spontaneous
  2. Assisted
  3. Controlled
176
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)

177
Q

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

A

40-60 L/min

178
Q

What is an appropriate trigger?

A

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

179
Q

What is normal minute ventilation in small animals?

A

150-250 ml/kg

180
Q

What are the three 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
181
Q

What is the goal of mechanical ventilation?

A

Maintain normal arterial blood gas
PaCO2 35-50 mmHg
PaO2 80-120 mmHg

182
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

183
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
184
Q

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

A

mandatory

185
Q

Name two examples of continuous spontaneous ventilation.

A

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

186
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

187
Q

List 2 possible complication from fast respiratory rate.

A

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

188
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

189
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

190
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

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

191
Q

Describe two ways to perform recruitment maneuver.

A

1) CPAP at 35-50 cmH2O for 20-40 secs
2) Pressure-supported ventilation with PEEP at 20 cmH2O and pressure above PEEP at 20 cmH2O for 1-3 minutes

192
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

193
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

194
Q

What are the indications of jet ventilation.

A
  • When mechanical ventilation is needed but traditional positive pressure ventilation cannot be delivered (e.g. tracheal/laryngeal surgery, bronchoscopy, bronchial resection, laryngoscopy)
  • Respiratory failure with circulatory shock
  • If ventilation is required in patients with a tracheal lesion secondary to tracheostomy or prolonged intubation
195
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

196
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

197
Q

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

A

A: increased airway resistance
B: decreased compliance

198
Q

What can expiratory hold tell us?

A

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

199
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

200
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

201
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

202
Q

What does the change from purple to blue indicate?

A

Increased circuit/airway resistance
slightly decrease dynamic compliance

203
Q

What does A and B indicates, respectively?

A

A: decreased dynamic compliance
B: increased dynamic compliance

204
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
205
Q

What does scooping tell us?

A

Increased airway resistance

206
Q

What does this flow-volume loop tell us?

A

Excessive airway secretion

207
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
4) Expiratory phase

208
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
3) Double triggering

209
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
4) flow-cycle threshold set too high

210
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

211
Q

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

A

It inhibits the hypoxic induced vasoconstriction → make hypoxemia worse

212
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

213
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

214
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

215
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

216
Q

What are the three weaning techniques?

A

Spontaneous breathing trial (with CPAP)
PSV
SIMV

217
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

218
Q

List 5 ventilator-induced lung injury.

A

Volutrauma
Barotrauma
Pneumothorax
Oxygen toxicity
Atelectrauma
Biotrauma

219
Q

What is the main risk factor of developing VAP?

A

Endotracheal intubation

220
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.

221
Q

What are the two major pathologic mechanisms of VAP?

A

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

222
Q

What is the major type of bacteria for VAP?

A

Aerobic bacteria

223
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

224
Q

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

A

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

225
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.

226
Q

Do brachycephalic dogs tend to be hypercoagulable or hypocoagulable?

A

hypercoagulable

Chronic hypoxia → inflammatory state

227
Q

List 3 surgical interventions for BAOS.

A

1) Wedge nasoplasty (rhinoplasty)
2) Soft palate resection (staphylectomy)
3)E verted laryngeal saccules resection (ventriculectomy or sacculectomy)

228
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

229
Q

Where does FHV-1 persists in during latent form?

A

Trigeminal ganglia

230
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

231
Q

What is the most common tracheal neoplasia in dogs?

A

Osteochondroma

232
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

233
Q

What is the most common cause for hemoptysis in dogs?

A

Bacterial bronchopneumonia

234
Q

What is the most common cause of feline bacterial bronchopneumonia?

A

Hematogenous spread

235
Q

Where are the most common airway FB in dogs and cats?

A

Dogs: right bronchus
Cats: trachea or carina

236
Q

What are the two most common mycosis in cats?

A

Cryptococcosis
Histoplasmosis

237
Q

Why shouldn’t NAC be used for nebulization?

A

Bronchoconstriction
Epithelial toxicity

238
Q

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

A

> 25 mmHg

239
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

240
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.

241
Q

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

A

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

242
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

243
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

244
Q

What are 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
245
Q

Does hypothermia increase or decrease antidiuretic hormone production?

A

Decreased → patient becomes polyuric

246
Q

List 5 complications from submersion injury.

A

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

247
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

248
Q

What does Westermark sign indicate?

A

PTE

  • Areas of relative oligemia secondary to decreased caliber of regional pulmonary arteries
249
Q

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

A

5-10 ml/kg

250
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

251
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

252
Q

Define “pendelluft.”

A

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

253
Q

How to calculate driving pressure?

A

Driving pressure = Pplateau - PEEP

254
Q

Where is the air emboli absorbed?

A

Lung

255
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

Boards: Respiratory (27 decks)

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