1
Q
Convert one Kpa to mmHg
A
1 Kpa = 7.5 mmHg
2
Q
What is the formula for partial pressure?
A
Concentration of gas x total pressure
3
Q
Ficks law of diffusion states that the amount of gas that moves across a sheet of tissue is proportional to the area of the sheet. Is the thickness inversely proportional or proportional to the thickness
A
inversely proportional to its thickness.
Rate of diffusion ∝ (Surface area * Concentration gradient) / Thickness of membrane
4
Q
Which part of the airways are classified as conductive?
A
Trachea – bronchi (right and left main) – lobar bronchi – segmental bronchi – terminal bronchioles.
After terminal comes respiratory bronchioles (occasional alveoli) -alveolar ducts (lined with alveoli). This are not conductive. Also called the acinus or transitional and respiratory zones
5
Q
What is the acinus?
A
The area distal to the terminal bronchus, aka respiratory bronchioles (occasional alveoli) and alveolar ducts (lined with alveoli).
6
Q
Before diffusion takes over after the terminal bronchioles, what type of flow occurs in the conductive airways?
A
Convection flow
7
Q
What is the name of the circulation that supplies the conducting airways?
A
Bronchial circulation
8
Q
State 4 mechanisms that the body uses to remove inhaled particles.
A
- Filtered in nose
- Moving staircase of mucus in conducting airways (cilia)
- Macrophages in alveoli
- Leucocytes
9
Q
Rate the order of PA, Pa and PV in the different West zones.
A
Zone 1: PA>Pa>Pv
Zone 2: Pa>PA>PV
Zone 3: Pa>Pv>PA
10
Q
Give two examples when the blood flow in West zone 1 can get affected. (West zone 1 doesn’t exist in healthy lung, what can happen to cause a West zone 1?)
A
Severe haemorrhage and raised alveolar pressure (positive pressure ventilation). PA > Pa > Pv
11
Q
What is vital capacity, residual volume and functional residual capacity?
A
- Vital capacity: maximal inspiration and maximal expiration
- Residual volume: air remained in the lung after maximal expiration
- Functional residual capacity: air remained in the lung after normal expiration
12
Q
State two lung volumes that can be measured with a simple spirometer and State three lung volumes that can be measured with gas dilution technique (helium).
A
simple spirometer: Tidal volume, vital capacity
gas dilution: total lung capacity, functional residual volume, residual volume
13
Q
State three lung volumes that can be measured with body plethysmography.
A
Total lung capacity, functional residual capacity, residual volume
Same three lung volumes can also be measured with gas dilution technique
14
Q
State Boyle’s law and with what pulmonary function test can the formula be used to measure total lung capacity, FDR and residual volume.
A
P2V2 = P4 (V2 + deltaV). Also have P1V1= P2V2 for Boyle’s law. Body plethysmography.
15
Q
What is the alveolar ventilation equation?
A
VA = VCO2/PCO2 x K
16
Q
What is the definition of alveolar ventilation?
A
The volume of fresh (non–dead space) gas entering the respiratory zone per minute. It can be determined from the alveolar ventilation equation, that is, the CO2 output divided by the fractional concentration of CO2 in the expired gas. VA= VCO2 /PCO2 x K. The concentration of CO2 (and therefore its partial pressure) in alveolar gas and arterial blood is inversely related to the alveolar ventilation.
17
Q
What two volumes make up tidal volume?
A
Dead space volume + alveolar volume
18
Q
How do you calculate the alveolar ventilation volume?
A
Expired ventilation – anatomical deadspace
(VT-DR) x RR
19
Q
What is the alveolar ventilation equation?
A
VA= VCO2 / Pco2 x K
K=0.863
20
Q
How can alveolar ventilation be increased?
A
Raising tidal volume and/or respiratory frequency.
Increasing tidal volume is often more effective because this reduces the proportion of each breath occupied by the anatomic dead space.
21
Q
The volume of lung that doesn’t eliminate CO2 is also called what type of dead space?
A
Physiological or total dead space = anatomic + alveolar dead space
22
Q
What method is used to measure physiological dead space?
A
Bohr’s method, Vd/Vt= (PACO-PECO)/PACO
23
Q
What part of the lung (in humans) is better ventilated?
A
Lower region
24
Q
How is anatomic dead space measured?
A
Nitrogen concentration following a single inspiration of oxygen. Anatomic dead space is the conducting airways (nose, trachea, bronchi)
25
What nerve supplies the diaphragm?
Phrenic nerve from C3, C4, C5 segments
26
What muscles are used for inspiration?
Diaphragm, external intercostal muscles.
In forced also accessory muscles (scalene, sternomastoids)
27
What muscles are used for expiration?
- Abdominal wall muscles (rectus abdominis, internal and external oblique muscles, transversus abdominis)
- Internal intercostal muscles
28
Is alveolar pressure normally the same as atmospheric pressure, true or false?
True
29
State 5 reasons for reduced compliance and 2 for increased compliance.
Reduced: increase fibrous tissue, alveolar oedema, atelectasis, increased surface tension, increased pulmonary venous pressure
Increased: pulmonary emphysema, asthma attack
30
What law is used to describe the surface tension between liquid molecules in the lung?
LaPlace law. Transmural pressure x radius /2 x wall thickness. Surfactant
31
What cell is responsible for surfactant production?
Type 2 pneumocyte
32
What cell is responsible for gas exchange in the lungs?
Type 1 pneumocyte
33
What is surfactant made of?
Phospholipids and dipalmitoyl phosphatidylcholine (DPPC). DPPC is hydrophobic at one end and hydrophilic at the other end.
34
State 3 advantages of surfactant.
- Low surface tension in the alveoli increases compliance and reduces the work of expanding it with each breath
- Promotes stability of alveoli
- Keeps alveoli dry
35
State consequences of loss of surfactant.
- Low compliance, increased work of breathing
- Areas of atelectasis (loss of stability)
- Alveoli filled with transudate
36
Is this true for the base or the apex of the lung? Large expanding volume, big resting volume, and small change in volume in inspiration.
Apex. The base has small resting volume, large change in volume on inspiration.
37
What formula is used to determine laminar flow?
Poiseuille V= Pnr4/8nl
38
If a radius is halved, what happens to the resistance in laminar flow? And what happens with the resistance if the length is doubled?
Halved radius, resistance increases 16 times. Doubled length, doubled resistance.
Poiseuille V= Pnr4/8nl can be changed to R= 8nl/nr4
39
What is the name of the formula/number used to determine if it is laminar or turbulent flow?
Reynolds number, turbulent if >2000
Re= (D x p x V) / ή
Diameter x density x velocity / viscocity
40
How do you measure (the formula) for airway resistance?
Pressure difference between the alveoli and the mouth divided by flow rate
R= P/F
41
When does driving pressure occur/start?
When the alveolar pressure falls which starts inspiratory flow. Depends on flow rate and resistance in the airways.
Depends on flow rate and resistance in the airways
42
What happens with airway resistance if lung volume is reduced?
Resistance increases
43
What happens with airway resistance if lung volume is increased?
Resistance is decreased
44
What determines flow in dynamic compression of airways?
Alveolar pressure minus pleural pressure (not mouth pressure). Independent of effort.
45
State 4 things that exaggerate flow limited mechanisms during forced expiration.
- Increase in resistance of peripheral airways
- Low lung volume (reduces the driving pressure)
- Reduced recoil pressure (reduces driving pressure) ie emphysema
- Reduced radial traction ie emphysema
46
what test can be performed to distinguish between obstructive and restrictive pulmonary disease
forced expiration test
measures forced expiratory volume and forced vital capacity. Both FEV and FVC reduced (ratio the same) in restrictive diseases like pulmonary fibrosis. FEV is more reduced than the FCV (low FEC/FVC%) in obstructive diseases like COP or bronchial asthma
(Vital capacity: maximal inspiration and maximal expiration)
47
48
In negative pressure ventilation, describe the difference in volume in decreased compliance and increased resistance.
Decreased compliance: rapid but small change in volume. Increased resistance: slow inspiration that’s not completed before expiration starts.
49
What two types of resistance make up the total pulmonary resistance?
Tissue resistance + airway resistance.
50
Work of breathing is dependent on what two major factors?
Pressure x volume.
51
What are the three elements to the respiratory control system?
Central controller, effectors, sensors.
central: pons, medulla, other parts of brain (limbic system, hypothalamus)
effectors: respiratory muscles
sensors: chemoreceptors, lung and other receptors
52
What are the 2 respiratory centers in the pons
apneustic centre
pneumotaxic centre
53
Central chemoreceptors and peripheral chemoreceptors mostly respond to which substance?
central: H+ (CO2 affects it via pH). Does NOT respond to O2.
peripheral: o2, pH, (CO2)
54
State three types of receptors and one type of fiber in the lungs that are sensors for the respiratory control system.
Receptors: pulmonary stretch, irritant, and J.
Fiber: bronchial C fibers.
55
Describe the mechanism of action for arterial hypoxemia becoming the chief stimulus for ventilation in chronic CO2 retention.
normally co2 changes pH in brain and this triggers central chemoreceptors in brain to increase ventilation. In chronic co2 retention, the pH of the extracellular fluid in the brain has returned to normal. The peripheral chemoreceptors are also not stimulated, as the kidneys has compensated for the acidosis. Therefor arterial hypoxemia becomes the main stimulus for ventilation
56
What is the breathing pattern with periods of apnoea of 10-20 sec separated by approx. equal periods of hyperventilation cresecendo decrescendo pattern called?
Cheyne stokes.
57
What does Biot's breathing pattern look like?
Periods of apnea separated by hyperventilation. NO crescendo-decrescendo pattern like in Cheyne stokes.
58
What is the breathing pattern that can be seen in severe metabolic acidosis (DKA)?
Kussmaul.
59
What are the three phases in the respiratory cycle?
Inspiratory,
post inspiratory/expiratory phase 1,
expiratory phase 2.
60
Describe the neuro and muscle activity in the three phases of the respiratory cycle.
- Inspiratory phase: sudden onset of activity of early inspiratory neurons and a ramp increase in inspiratory augmenting neurons, resulting in motor discharge to inspiratory muscles and airway dilators.
- Post inspiratory phase/expiratory phase I: declining motor discharge to inspiratory muscles and passive exhalation.
- Expiratory phase II: no inspiratory muscle activity.
61
What are the key neurotransmitters involved in respiration?
Glutamate, GABA, glycine. Also acetylcholine, monoamines, neuropeptides, Na, K, Ca.
62
What is the central pattern generation involved in respiration?
Collection of neurons that form a pacemaker system in the medulla, mostly concentrated in pre-Bötzinger complex.
63
Gas movement in the alveolar is via passive diffusion. How is inspired gas taken to the terminal bronchioles?
Convective flow.
64
What law is used to describe diffusion?
Fick's law. states that the rate of transfer of a gas through a sheet of tissue is proportional to the tissue area and the difference in gas partial pressure between the two sides, and inversely proportional to the tissue thickness. J= A/t x D x (P1 – P2)
65
In Ficks law, what properties does the diffusion constant depend on?
The properties of the gas (solubility)and the molecular weight. Co2 has 20 times faster diffusion than 02, is due to having higher solubility and therefore changes the D in ficks law.
66
What is the oxygen content equation?
(1.34 x Hb x Sao2/100) + (0.003 x PaO2)
1.34 ml/g at 37 degrees C, Hb g/dl, 0.003 ml/dl, PaO2 mmHg, CaO2 ml/dl.
## Footnote
1.34 ml/g at 37 degrees C, Hb g/dl, 0.003 ml/dl, PaO2 mmHg, CaO2 ml/dl.
67
State the formula for Fick's law.
J= A/t x D x (P1 – P2)
J= amount of substance that will diffuse over time, A= area of tissue gas is diffusing across, t= thickness of tissue gas is diffusing across, D= diffusion measured in length over time, P= gas partial pressure.
## Footnote
J= amount of substance that will diffuse over time, A= area of tissue gas is diffusing across, t= thickness of tissue gas is diffusing across, D= diffusion measured in length over time, P= gas partial pressure.
68
Are NO, CO, and O2 diffusion or perfusion limited?
CO diffusion limited, NO perfusion limited, O2 normally perfusion limited but under certain conditions can be diffusion limited.
CO - No back pressure develops as CO is taken up by haemoglobin. The only limitation would be if there was an issue with diffusion
NO – back pressure develops as NO is not taken up by haemoglobin. The limitation is the blood flow
69
Diffusion is dependent on which properties?
Proportional to the solubility of the gas, inversely proportional to the square root of the molecular weight, proportional to the area, proportional to the difference in partial pressure, inversely proportional to the thickness.
70
What does the single breath method measure?
Diffusion capacity using inhaled carbon monoxide. Normal value 25 ml·min−1·mm Hg−1.
71
What does the formula DL = Vgas/(P1 − P2) define?
Diffusion capacity of the lung (flow of gas / pressure difference).
72
What is cooperative binding in hemoglobin?
Increase in O2 affinity of Hb with each successive O2 binding. Initial state tense and Beta chains far apart. Once first 02 binds, the conformation changes and the B chains comes closer together, makes it easier for the second 02 to bind. Once fourth 02 is bind, is in a relaxed state
73
How does cooperative binding influence the oxygen dissociation curve?
The reason for the sigmoid shape.
74
In what forms is O2 carried in the blood and how is the division in %?
Dissolved (2%), bound to hemoglobin (98%).
75
What does Henry's law state regarding O2?
The amount of O2 dissolved is proportional to the partial pressure. For each mmHg of PO2, there is 0,003 ml O2
76
What are the components of hemoglobin?
Four polypeptide globin subunits, 2 alpha, 2 beta chains. Each globin chain has its own heme group, an iron-containing porphyrin ring with iron in ferrous stage.
77
How many O2 molecules can be bound by one Hb molecule?
4.
78
What is the expected pulse ox reading in a patient with methemoglobinemia and why?
85%. Methaemoglobin absorbs both wavelengths (660 and 940 nm) of light equally well. In the presence of metHb (if more than 30%) the pulse oximeter defaults to a value of 85%
79
What is O2 capacity and what is the normal value?
the maximum amount of 02 that can be combined with Hb/when all the binding sites are occupied by o2. Can be measured by exposing the blood to very high po2 and substracting the dissolved 02. One gram Hb can combine with 1.39 ml O2, normal Hb is 15 g -> 02 capacity is approx. 20,8 ml O2
80
What is O2 saturation and how is it calculated?
The percentage of the available binding sites that have O2 attached. Can be calculated by O2 combined with Hb / O2 capacity x 100. (o2 capacity is 1,39 x 15 g= 20,8 ml o2)
81
How is CO2 transported in the blood?
Dissolved in solution, as bicarbonate (buffered with water as carbonic acid), bound to proteins/hemoglobin (carbamino).
82
What is the chloride shift?
* CO2 buffers with water to form H+ and HCO3-.. HCO3 diffuses out of the RBC, H+ cant. H+ binds to histadine side chains on deoxygenated hemoglobin. Cl ions move into the cell to maintain electron neutrality and keep the process going
83
What is the Hamburger effect?
Same as chloride shift.
84
What is the name of CO2 bound to hemoglobin and roughly what % of the total venous-arterial difference is it?
Carbaminohemoglobin, 30%.
85
State the Henderson-Hasselbalch equation.
pH= 6.1 + log ((HCO3) / (pCO2 x 0.03)).
86
What is the formula for oxygen delivery?
DO2= CO x CaO2.
87
State the 4 groups/reasons for hypoxic hypoxia.
Hypoventilation, diffusion impairment, shunt, VQ inequality.
88
Explain what histocytic hypoxia is and give one example of toxicity than can cause it
toxic substance that interferes with the ability of the tissues to utilize available O2. example is cyanide, which prevents the use of O2 by cytochrome oxidase
89
* Give examples of conditions shifting oxygen dissociation curve to the right
* Increased temp, increased pCo2, increased H conc (acidosis), increased 2,3 diphosphateglycerate conc (2,3 DPG), excersise.
90
How does the co2 dissociation curve differ in appearance to the o2 dissociation curve
Is much steeper and more linear (which explains why the difference between o2 in venous and arterial blood is bigger than the difference between co2 in arterial and venous blood)
91
* What is the bohr effect
what happens to oxygen binding because of CO2 and lower pH. Oxygen affinity for haemoglobin decreases in the presence of CO2 -> increase in pH lead to less oxygen affinity and facilitated release of O2 into tissue (right shift of dissociation curve)
think O2 and hemoglobin
92
What is the Haldane effect and during which toxicity can it occur
* The Haldane effect is a physicochemical phenomenon which describes the increased capacity of blood to carry CO2 under conditions of decreased haemoglobin oxygen saturation -> The less O2 saturation (deoxygenation of blood), the more Co2 can be taken up by haemoglobin
(Co2 and hemoglobin)
Oxygen toxicity: O2 therapy increases oxygenated Hb and reduced the capacity to bind CO2
93
* What is p50 and happens with the p50 when O2 dissociation curve shifts to the right
* the point of the oxygen Hb dissociation curve at which Hb is 50% is saturated with O2. Measured in mmHg. Normal value in humans 27 mmHg. P50 goes up (the Pao2 is higher). Is 36 mmHg in cats. 32 mmHg in dogs, 34 in bovine
94
* In which direction does carbon monoxide shift the oxygen dissociation curve
* left
95
* The 02 diffusing to the tissue from the blood, is it dissolved or bound to hemgoglobin
* dissolved
96
* Explain what hufners constant is and what is the number
* Each gram of fully saturated Hb can bind 1,34 ml of O2
97
* Why is cyanosis not seen in carbon monoxide toxicity
* Cyanosis is only clinically evident when there is at least 5 g/dL of deoxyhaemoglobin, and any Hb that has not bound to carbon monoxide is usually fully saturated with O2.
98
3 specific treatments for cyanide toxicity
* Amyl nitrate (conversion of Hb to metHb which cyanide prefers to bind to)
* Chelation, ex with dicobalt edetase
* Sodium thiosulphate, (converts cyanide to thiocynate)
99
* The sigmoid shape of the oxygen dissociation curve have important clinical consequences, what are they
* C the upper position is flat, a small change in Pao2 will hardly change Sao2. the steep part of the curve means in peripheral tissue where pao2 is low, the steep fall in sa02 means a large quantity of 02 is offloaded for only a small decrease in po2
100
* What symptoms are seen with carbon monoxide toxicity
* a COHb concentration of 15–20% causes mild symptoms – headache and confusion.
* at higher concentrations – weakness, dizziness, nausea and vomiting.
* At COHb >60% – convulsions, coma and death.
101
* Give two mechanism that maintain methemoglobin as normal levels in the body.
* Glutathione/NADPH system: Oxidizing agents within the RBC are reduced by glutathione before they are able to oxidize the haem Fe2+ to Fe3+.
* metHb reductase/NADH system: Any MetHb formed has its Fe3+ ion reduced back to Fe2+ by a protective reduction system involving the enzyme MetHb reductase and NADH.
102
* What is a normal level of metHb
* Less than 1%
103
5 things/groups that cause hypoxemia
Low FiO2, hypoventilation, diffusion impairment, shunt, VQ mismatch/inequality
If ask for 4, leave out low FiO2
104
4 examples of things that can cause hypoventilation
- drugs that depress central drive to respiratory muscles (opioids, barbiturates)
- damage to the chest wall
- paralysis respiratory muscles
- high resistance to breathing (very dense gas at great depth underwater)
105
what equation describes the relationship between alveolar ventilation and pCo2
alveolar ventilation equation
Pco2 = VCo2 / VA x K
VCo2= CO2 production
VA= alveolar ventilation
K= constant
If alveolar ventilation is halved, Co2 is doubles (once steady state been established)
VA= VCO2 /PCO2 x K
106
If alveolar ventilation is halved, how much does co2 change
It doubles. Alveolar gas equation
107
What equation describes the relationship between fall in PO2 and rise in PCO2
Alveolar gas equation
PAO2= PI02 – Paco2/R + F
F can be ignored as small correction factor.
R = 0,8
PA02= 0,21 x (760 mmhg – 47 mmHg) – (PaCo2 / 0.8)
Barometric pressure sea level 760 mmHg, Water vapour pressure 47 mmHg
If PAO2 is decreased, the Pao2 pressure gradient is reduced, leading to a low PaO2
108
If PAO2 is decreased, what happens to the PaO2 pressure gradient and the PaO2
If PAO2 is decreased, the Pao2 pressure gradient is reduced, leading to a low PaO2. Alveolar gas equation
109
Give the shunt equation
Qs /Qt = (CcO2 – CaO2) / (CcO2-CmvO2)
110
How is the Cco2 in the shunt equation calculated
Cco2 is o2 in pulmonary end capillary blood. Is assumed to have Hb saturation of 100% as its just left the alveolus.
First step: calculate PAO2 from alveolar gas equation PAO2= 0,21 x (760 mmhg – 47 mmHg) – (PaCo2 / 0.8).
second step: use PAO2 from alveolar gas equation in oxygen content formula . CcO2= Hb × 1,34 × 100% +(PAO2 × 0,003).
111
Are shunt oxygen responsive
No. can be used as diagnostic test as Po2 doesn’t rise to expected levels despite 100% fi02. PCO2 stays normal as chemoreceptors sense co2 and increase ventilation
112
Shunt perfusion and dead space ventilation, which is low and which is high VQ
Shunt- low VQ (ventilation is affected, perfusion ok)
Dead space - high VQ (ventilation is ok, perfusion is affected)
113
The high end (flat curve) of the dissociation curve has what type of ventilation perfusion ratio
High ratio (increase the O2 concentration of their effluent blood very little)
114
Formula for A a gradient and what is the normal value
A-a (mmHg)= PAO2 – PaO2
PAo2= 0,21 x (760 mmhg – 47 mmHg) – (PaCo2 / 0.8)
0,21 x (760-47)= 150
Normal <15 mmhg
115
What are the 2 major causes of co2 retention (hypercapnia)
Hypoventilation. Ventilation perfusion inequality
116
Forced expiratory volume can be measured to help different between obstructive and restrictive lung disease. Give example of restrictive and obstructive lung disease
Restrictive; weakness inspiratory muscles, reduced compliance (pleural effusion etc)
Obstructive: asthma
117
What methods can be used to measure functional residual capacity
Helium dilution, 100% O2 for several minutes to wash out N2 and using formula V1 × 380 = (V1 × C3) + (V 2 × C2)
118
What methods can be used to measure total lung capacity
Body plethysmography (Boyles law)
119
What method can be used to measure anatomic dead space
Fowlers method
120
* What unit is used for flow rate, driving pressure, inspiratory time
Flow rate usually ml/sec, driving pressure usually cmH2O (or mmHg), millisec
121
* What unit is used for compliance
* ml/cmH2O
122
How is the diffusion capacity for carbon monoxide measured
Single breath method (DL= VCO / PACO)
123
How is total pulmonary blood flow measured
Fick principle and the indicator dilution method
124
How can inequality of ventilation be measured
Single breath method, multiple-breath method
125
Give 1 examples of equation/formula that can be used to measure ventilation-perfusion inequality
Aa gradient
126
What is the formula for alveolar dead space?
Bohr equation Vd/Vt= PiCO2-Paco2 / PiCO2
127
*What is the equation for physiological dead space
Vd/Vt= PaCO2 -PECo2 / PaCo2
128
hat dead spaces make up the physiological dead space
Physiological or total dead space = anatomic + alveolar dead space
129
What is the method used to measure airway resistance?
* Body plethysmograph
130
which disease has the longest time constant, ards, copd, pulmonary edema or pneumonia?
COPD
131
What is the formula needed to calculate the airway resistance using body plethysmography
* Boyles law P1V1= P2V2. Change in volume can be measured and then that can be converted into alveolar pressure using Boyles law
132
What method is used to measure closing volume
* Single-breath N2 washout
133
Functional reserve capacity is made up of which volumes
expiratory reserve volume and residual volume
134
* What cant be measured in static lung volumes
Residual volumes, functional residual capacity, total lung capacity
135
What does this formula measure (VT/platau pressure-PEEP)
Static compliance
136
What does this formula measure (peak plateau pressure/flow)
* Resistance
137
What is the 6 minute walk test?
Dog walk for 6 minutes to correlate to “activities of daily living”. Used as exercise induced desaturation may be more common. Follow individual dog over time. measure distance walked and measure pre and post oxygenation and rate
138
What is the Pasteur point?
Critical threshold when mitochondria PO2 is insufficient for aerobic metabolism. 0,15-0,3 kPA
139
Change in volume/change in transpulmonary pressure is the formula for what
* Compliance, is how much pressure it takes to inflate the lung to a specific volume, unit ml/cmH2O
140
* Respiratory compliance is made up of two parts, lung compliance and what more
* Thoracic cage compliance . 1/RC = 1/LC + 1/TCC
141
give 1 example of condition that can increase compliance and 8 examples of conditions that can decrease Increased compliance:
increase: Emphysema, (Advancing age)
Decreased compliance:
* Fluid within alveoli or lung interstitium (oedema)
* Posture
* Pneumonia
* Pulmonary contusions
* Pregnancy
* Ateclectasis
* pulmonary hypertension
* pulmonary fibrosis
* extremes of lung volume
* obesity
142
What is the formula for LaPlace law
P= 2T/r
P transmural pressure, T surface tension, r radius
143
What is the alveolar gas equation
PAO2= 0,21 x (760 mmhg – 47 mmHg) – (PaCo2 / 0.8).
144
What are the 3 main roles of surfactant
* General decrease in alveolar surface tension
* Stabilization of small alveoli
* Prevention of fluid transudation
145
* What cells produce surfactant and what are the two main components
Pneumocytes type II . Phospholipids (DPPC most important) and apolipoproteins
146
Is dynamic or static compliance lower
Dynamic (due to airway resistance)
147
The difference between static and dynamic compliance can be used as an indirect measurement of what
Flow resistance properties of the airways
148
* The lung base and lung apex differ in pressure, volume, compliance, and perfusion. Describe the lung base.
* The lung base has less negative pressure, greater volumes during normal inspiration, is more compliant, and is better perfused
149
What is hysteresis in respiration
when a measurement differs depending on whether the value measured is rising or falling, ex pressure volume loop
150
* What is the pulmonary circulation regarding pressure and resistance, high or low
Low pressure, low resistance. (systemic circulation is high pressure, high resistance)
151
* What is the formula for calculating pulmonary vascular resistance
PVR= 80 x MPAP-PCWP / CO
MPAP mean pulmonary artery pressure, PCWP pulmonary capillary wedge pressure. 80 constant related to the unit conversion
152
What is a normal pulmonary vascular resistance
1/10 of systemic vascular resistance
153
State 3 factors that affect pulmonary artery resistance
Pulmonary artery pressure, lung volumes, HPV (hypoxic pulmonary vasoconstriction)
154
True or false, increased MPAP results in significant reduction in PVR
true
155
* State one gas and one membrane channel that mediate HPV (hypoxic pulmonary vasoconstriction)
* NO (decreased production in hypoxia)
* O2 sensitive K channels (stimulated in hypoxia, leads to depolarization of membrane and opening of Ca channels
156
* Give 4 examples of when HPV can occur (hypoxic pulmonary vasoconstriction
* Fetal circulation, pneumonia, high altitude, upper lobe diversion in cardiogenic pulmonary oedema
157
* Give examples of conditions or agents that can enhance HPV 2 p
hypoxic pulmonary vasoconstriction
* Acidosis, hypercapnia
158
* Give examples of conditions or agents that can reduce HPV 5 p (hypoxic pulmonary vasoconstriction)
* Alkalosis
* Hypocapnia
* Vasodilators (Nitrates, sodium nitroprusside, NO)
* Bronchodilators
* Volatile anaesthetic agents (If MAC >1)
159
* State 3 uses of a pulmonary artery catheter
* Diagnostics (pulmonary hypertension, ards etc)
* Measurement of haemodynamic parameters (ex CO and mixed venous O2 saturation)
* Therapeutic (aspiration or air emboli)
160
* State complications of using a Swan-Ganz catheter/pulmonary artery catheter
* Line infection/nosocomial infection
* Cardiac arrythmias
* Pulmonary infarction
* clot emboli/thrombus
* air emboli
* Pulmonary artery rupture
* Bleeding, hemothorax
* Pneumothorax
* Knotting of the catheter
* death
161
Describe how to place a pulmonary artery catheter
* Pulmonary artery catheter is inserted (usually) in right internal jugular vein. Pressure of the tip is used to identify tips location. Ra approx. 5 mmHg. Once the PAC has been inserted as far as the right ventricle (about 20 cm, pressure approx. 25 mmHg), the balloon is inflated. The tip of the PAC is guided by the flow of blood through the pulmonary valve and into a pulmonary artery, until it wedges in a branch of the pulmonary artery, giving the PCWP.(approx. 10 mmHg)
* Don’t forget to deflate the balloon! Re-inflate when want repeat measure
162
Give reasons for left shift of oxygen dissociation curve
decreased pCO2, decreased H+ (high pH, metabolic alkalosis (bicarbonate administration), Methaemoglobinemia, carboxyhaemoglobin, (some haemoglobin substitutes like oxyglobin), decreased 2,3DPG
163
when the dissociation curve shifts to the right, does the p50 go up or down
p50 goes up
164
what cell produced 2,3DPG
RBC during glycolysis
165
High 2,3 levels binds to B chains of deoxyhemoglobin, stabilizing the configuration and reduced the o2 binding affinity. Less o2 binding pushes curve to the right and there is more offloading. True or false
True
166
Describe the Haldane effect
physicochemical phenomenon which describes the increased capacity of blood to carry CO2 under conditions of decreased haemoglobin oxygen saturation
167
state a toxicity that can cause Haldane effect
oxygen toxicity
168
describe the bohr effect
Oxygen affinity for haemoglobin decreases in the presence of CO2
169
What is the partial pressure of 02 and the spo2 in severe hypoxemia
PaO2 <60 mmHg, Spo2 <90%
170
What is the partial pressure of 02 and the spo2 in life-threatening hypoxemia
PaO2 <30 mmHg, Spo2 <40%
171
Definition of hypoventilation
elevated PaCO2 > 45 mm hg (or elevated end-tidal CO2 (5 mmHg lower than PaCo2), or central venous PCO2 (5 mmHg higher than PaCo2))
172
what are the gases in the alveoli and what are their mmHg 4 p
- o2 105 mmHg
- co2 40 mmHg
- water vapour 50 mmHg
- nitrogen 560 mmHg
755 mmHg in total
173
State 4 mechanisms of venous admixute
Low vq regions
Atelectatis (no vq region)
Diffusion defects
Right to left shunts
174
What is a normal A a gradient
Less than 10-15 mmHg. if over 20 considered decreased oxygenation deficiency (venous admixture). Will increase if inspired oxygen increases.
175
What is the rule of 120
PaCo2 + PaO2 (40 + 80 = 120 mmHg) only when FiO2 room air, 21 % oxygen. If <120 indicated venous admixture
176
P/F ratio of <300 is what in S/F ratio
<315. (P/F of 200 equals S/F 235
177
How do you calculate oxygenation index
OI= MAP x FiO2 x 100/PaO2
MAP mean airway pressure
Low number= better lung function
178
How much deoxygenated haemoglobin needs to be present for cyanosis to be seen
5 g/dl (PCV 15%)
179
Examples where cyanosis can be seen
- FATE
- Right to left shunting (caudal mucous membranes)
o Persistent ductus arteriosus
o Fallots tetraology
- Sulph-hemoglobin
- Methemoglobin
- Anaphylaxis
180
At what mmHg and % should oxygen supplementation be considered
provided whenever a patient’s PaO2 is less than 70 mm Hg or their oxygen saturation (SpO2) is less than 93% on room air.
181
What is the definition of hypoxemia
hypoxemia inadequate oxygenation of arterial blood and is defined as a PaO2 less than 80 mm Hg (at sea level).
182
Describe how to administer transtracheal oxygen
Method 1. Through the needle large bore catheter percutaneously through the skin and tissue into trachea. 3-5 tracheal ring. 50 -150 ml/kg/min
Method 2. Skin incision 3-5 tracheal ring and blunt dissection through sc tissue and sternohyoid muscle. Incision between 4-5 tracheal ring with nr 11 scalpel, groove director inserted and large-bore multifenestrated catheter with a stylette is then inserted into the tracheal lumen along the grooved director. 50 ml/kg/min for 40-60% FiO2
183
Nasal oxygen flow rates, 50, 100, 200, 400 ml/kg/min gives what tracheal fio2 (slightly rounded numbers) saccm table 15.1
50 – 30 %
100 - 37%
200 – 58%
400 – 77%
184
State 3 reasons for oxygen to become diffusion limited gas
Thickening blood gas barrier example lung fibrosis
Exercise at high altitude
Alveolar hypoxia
185
Which west zone results in alveolar dead space and list 2 causes that leads to this zone to occur
Zone 1. Hypovolemia/poor perfusion/severe haemorrhage, mechanical ventilation
186
List 3 disease that can lead to an increase in the difference between anatomical and physiological dead space
Emphysema, ards, pneumonia, PTE (anything that increases alveolar dead space)
187
State two complications of 02 therapy
- Diminished O2 respiratory drive in px dependent on hypoxia driven respiratory drive
- Oxygen toxicity
188
Benefits of high flow oxygen
Heated and humidified (better tolerance for the px, minimise desiccation, mucosal erosion, haemorrhage and impaired local immunity. also decrease airway inflammation, maintain mucocilliary function and improve mucus clearance)
Increased flow demands
Increased functional residual capacity/PEEP
Lighter
Oxygen dilution
Wash out dead space
189
Complications from high flow oxygen therapy
- Pneumothorax (rare, avoid in pre-excising pneumothorax or bullae waiting to rupture)
- Px discomfort (unusual if increases flow rate over 15 min)
- Hypercapnia (breath stacking)
- Aerophagia
- Hyperthermia (most common)
190
What % of cats with FATE have hitherto undiagnosed HCM?
80%
191
What is the definition (mmHg) of hypoventilation and hyperventilation. Definition of hypercapnia
Hypovent: PaCo2 >40-45 mmHg
Hypervent: PaCo2 < 30-35 mmHg
Hypercapnia: PCo2 in arterial blood greater than 36 mmHg in cat, 42 mmHg dog
192
State 4 types of dead space
Anatomic
Alveolar
Physiologic
Apparatus
193
What makes up the anatomic dead space
upper airway, trachea, lower airways to level of terminal bronchus
194
what is the definition of alveolar dead space
the portion of inspired gas that passes through the anatomic dead space and mixes with gas in the alveoli but does not participate in gas exchange with the pulmonary capillaries
195
definition of minute ventilation
volume of gas EXHALED per minute: tidal volume x RR
196
how can you calculate alveolar ventilation using minute ventilation and dead space volume
alveolar ventilation = minute ventilation expired – dead space volume
197
what method is used to measure alveolar dead space and what method is used for physiological dead space
alveolar: fowlers method
physiological dead space: Bohrs method VD / VT = (PAco2 – PEco2 /PAco2)
198
how do you calculate alveolar ventilation
Alveolar ventilation= Total ventilation from spirometer – dead space from bohr calculation
Bohr equation= VD / VT = (PAco2 – PEco2 /PAco2)
PACo2= (VCO2 /VA) x k
VA= VCO2 /PCO2 x K
199
Causes of increased co2 production with a fixed minute ventilation
thyrotoxicosis, fever, sepsis, malignant hyperthermia, overfeeding, reperfusion injury, exercise
200
differential diagnosis of hypoventilation in categories
- decreased minute ventilation
o central neurological disease
o cervical spinal cord disease
o lower motor neuron/neuromuscular
o chemoreceptor abnormalities
o abnormal respiratory mechanics
o increased airway resistance
- increased dead space ventilation
- increased co2 production with fixed tidal volume
- increased insp co2
201
what is Pickwickian syndrome
obesitas hypoventilation syndrome
202
how does co2 affect vasotone in systemic circulation and in the pulmonary circulation
systemic: vasodilation
pulmonary: vasoconstriction
203
at what mmHg is co2 narcosis seen
>90 mmHg
204
5 places for arterial sampling
femoral, dorsal pedal, coccygeal, sublingual and dorsal auricular arteries
205
what is the difference in mmHg in co2 between arterial and venous sample
venous co2 is normally 3-6 mmHg higher than in arterial. (Arterial higher than etco2 by 2-6 mmHg)
206
state three mechanism that how sudden correction of arterial hypoxemia causes further hypercapnia
- depression of hypoxia-driven chemoreceptors
- relief of hypoxic pulmonary vasoconstriction in poorly ventilated lung regions as local perfusion increases without concomitant increase in ventilation
- significant correction of hypoxemia causes better saturation of haemoglobin so that previously buffered protons on deoxyhemoglobin are released with subsequent generation of new CO2 from stores (Haldane effect)
207
what % of cats with nasopharyngeal disease has nasopharyngeal polyps
28%
208
What % has reoccurrence after traction avulsion of nasopharyngeal polyp
40-50%
209
What % of owners report improvement in their dogs regarding respiratory status and stridor post op for laryngeal paralysis
90%
210
What is a V-gel supraglottic airway devise
useful for mechanical ventilation pressure maintenance up to 16 cm H2O and had less leaking than endotracheal intubation- Less postintubation stridor
211
What are the grades for laryngeal collapse
grade 1 eversion of the laryngeal saccules
grade 2 is medial positioning of the cuneiform processes and aryepiglottic collapse
grade 3 is collapse of the corniculate cartilages.
212
What is the suspected pathophysiology for tracheal collapse
suspect decreased glycosaminoglycan, chondroitin and calcium causes dorsal trachealis flaccidity and loss of rigidity of tracheal cartilages.
The repeated mucosal contact from cyclic collapse results in chronic irritation, inflammation, and the loss of the ciliated columnar epithelial component of the mucociliary escalator.
213
Grades for tracheal collapse
Graded I-IV
- each grade approx. 25% progressive reduction in tracheal diameter
- grade IV also inversion of the ventral tracheal cartilages (IV might be separate disease process and a static form)
214
What are the two forms of tracheal collapse
- traditional chondromalacia with dynamic collapse (also called traditional form)
- static form of airway obstruction (also called malformation form) - cartilage inversion into the tracheal lumen (grade IV/“W” shape to the ventral margin of the trachea). This inversion varies from rigid and noncompressible to soft and easily displaced ventrally out of the airway lumen
215
what are the clinical characteristics of honkers with airway obstruction versus coughers with lower airway disease
honkers: abducted elbows, prolonged inspiration phase of respiration, increased respiratory effort on inspiration, pectus excavatum, sinus arrythmia, external rotation of the costochondral junction creating pointed ventral ribs, extended head/neck/orthopnoea, increased or decreased sounds on cervical/thoracic inlet tracheal auscultation
coughers: increased respiratory effort on expiration, expiratory abdominal push, harsh expiratory lung sounds, herniation of cranial lung lobes, crackles on pulmonary auscultation, overdeveloped abdominal musculature creating heave line, perineal hernia, fecal incontinence from increased abdominal pressure on coughing expiration
saccm table 19.1
216
what % of patients with tracheal collapse has concurrent laryngeal dysfunction
30%
217
what % of patients with cervical tracheal collapse has concurrent bronchial collapse
83%
218
Is radiographs or fluoroscopy better at diagnosis tracheal collapse
Radiographs misdiagnosed the location of tracheal collapse in 44% of dogs and failed to diagnose tracheal collapse in 8% of dogs when compared with fluoroscopy
219
What is the medical management for tracheal collapse and what is the success rate
- cough control, corticosteroid (if inflammation), bronchodilators (if suspicion), harness, avoid heat, stress, excitement, weight loss.
- medical management successful up to a year in 71% of dogs
220
in Conguista article looking at medical vs surgical management of tracheal collapse, what type of tracheal collapse more often required stent placement, what was the mean survival time in the medical management group vs the surgical group
malformation type
Medical 3.7 years. Surgical 5.2 years
221
Definition of feline asthma and chronic bronchitis
- Feline asthma is defined as hyperreactive airways with reversible bronchoconstriction. Type 1 hypersensitivity
- chronic bronchitis is characterized by thickening of the airways and excessive mucus production
222
what type of hypersensitivity reaction is feline asthma
type 1
223
what breed is overrepresented for feline asthma
Siamese
224
What side effect can potassium bromide cause in cats
Cough and respiratory disease
225
What is the name of the cats lung worm
Aelurostrongylus abstrusus
226
What % of eosinophilia is considered abnormal in airway sampling in diagnosing feline asthma
>5%
(BAL fluid normally comprises 70%–75% macrophages and 5%–8% neutrophils, eosinophils, and lymphocytes)
227
What is the ratio to determine bronchiectasis
Pulmonary artery to bronchial lumen ration >2
228
What % of dogs with airway collapse have cranial lung herniation
70%
229
How is bronchomalacia characterised
>50% collapse of airway luminal diameter
230
Treatment for lower airway disease in dogs
- avoid stressors
- avoid warm exercise, use harness
- extended-release theophylline beneficial in reducing cough and respiratory effort by improving expiratory airflow. Caution as vomiting and agitation are side effects, which could trigger exacerbation of disease
- steroids in bronchitis and eosinophilic airway disease. Can worse as cause panting, weight gain, worsening preexisting infections
231
things that can exacerbate lower airway disease in dogs
infection, intubation, cardiac enlargement, CHF, pulmonary hypertension, obesity, aspiration injury
232
definition for pulmonary hypertension in humans
Definition: Abnormally elevated pressure within the pulmonary vasculature
In humans, PH has been defined by a mean pulmonary arterial pressure (PAP) >25 mm Hg at rest measured invasively by right heart catheterization
233
Classification of pulmonary hypertension by ACVIM
- 1.pulmonary arterial hypertension
o Idiopathic, heritable, drugs and toxin, congenital shunts, etc
- 2.secondary to left heart disease
o must have documentation of left heart disease ie mMVD and documentation of unequivocal left artrial enlargement
- 3.secondary to respiratory disease / hypoxia
- 4.pulmonary emboli / pulmonary thrombi / pulmonary thromboembolism
- 5.parasitic disease (dirofilaria, angiostrongylos)
- 6.multifactorial or unclear mechanism
Saccm table 22.3
234
Whats the hemodynamic classification of pulmonary hypertension
- increased pulmonary blood flow (cardiac output)
- increased pulmonary resistance (precapillary pulmonary hypertension)
o group 1, 3, 4, 5, 6
- increased pulmonary pressure (postcapillary pulmonary hypertension)
o group 2
- combination of above
o group 2 and 6
235
what are the key echo findings and mean PAP and PAWP comparing pre and post capillary pulmonary hypertension
pre: no LA enlargement, structural or functional changes of the RV, pulmonary artery, or RA/caudal vena cava. PAP >25 mmHg, PAWP <15 mmHg
post: unequivocal LA enlargement, no/minimal, structural or functional changes of the RV, pulmonary artery, or RA/caudal vena cava. PAP >25 mmHg, PAWP >15 mmHg
236
what clinical findings are strongly associated with pulmonary hypertension and what are possible associated
strongly
- syncope
- resp distress at rest
- activity or exercise terminating in resp distress
- right-sided heart failure
possibly
- tachypnoea at rest
- increased resp effort at rest
- prolonged post exercise or post-activity tachypnoea
- cyanotic or pale mucous membranes
237
what is the Bernoulli equation and what is the cut off for pulmonary hypertension
peak tricuspid regurgitation velocity (TRV) x 4
cut off > 3,4 m/s
238
what are the 3 anatomic sites in echo to assess probability of pulmonary hypertension
ventricles, pulmonary artery, right atrium and caudal vena cava
239
What are the two main pathophysiological types of oedema
High pressure and increased permeability
240
State the starling equation involved in lung filtration
net filtration of fluid from lung microvascular to the interstitium= K (Pmv-Pi) – omega (πmv - πi)
K= filtration coefficient or leakiness of the endothelium to water
Pmv= pulmonary microvascular pressure
Pi= pulmonary interstitial pressure
Omega= protein reflection coefficient
πmv= protein osmotic pressure in the microvascular
πi= interstitial protein osmotic pressure
241
what does the reflection coefficient in starlings equation stand for
relative permeability of membrane to protein (osmotic pressure)
242
state 5 tissue safety factors the body has as protection against oedema
- extravasation of low protein fluid reduces interstitial COP, preserves net CPO gradient
- increased interstitial hydrostatic pressure opposes further extravasation
- increased driving pressure for lymphatic flow
- Na K Atpase pump in alveoli wall pumps Na out causing osmotic gradient
- Aquaporins in type 1 pneumocytes also play role in fluid removal
243
2 reasons for high pressure oedema and 5 reasons for increased permeability oedema
High pressure: Cardiogenic, fluid therapy
Increased permeability: ALS/ARDS, Pneumonia, PTE, ventilator associated lung injury, inhaled toxic insult (ex volatile hydrocarbons)
244
State 3 groups that can cause mixed-cause oedema
Neurogenic, negative pressure, re-expansion
245
4 main causes of neurogenic pulmonary oedema
Head trauma, seizure, electric cord bite, upper airway obstruction
246
What are the main mechanism in blast theory in pulmonary oedema
Neurogenic pulmonary oedema. massive, neuronal, sympathetic activation ie blast theory. Hypothalamic injury cause increased levels of catecholamines cause pulmonary vasoconstriction, increased hydrostatic pressure, toxic damage to cells and increase permeability. spectrum of oedema ranging from purely hydrostatic oedema to high-protein oedema, to finally haemorrhagic oedema. Possible mediators are endothelin 1, norepinephrine, neuropeptide Y, NO, cytokines
247
how does the aetiology of neurogenic pulmonary oedema affect prognosis
- upper airway obstruction, seizures 50% survival (aka worse survival than head trauma, electrocution)
- head trauma, electrocution 79% survival .
- Worse survival rate in px needing MV 17%
248
What is the gold standard method to different cardiogenic and non cardiogenic pulmonary oedema
Capillary wedge pressure , ncpe <18 mmHg
249
Mechanism of action of furosemide
- loop diuretic
- inhibits Na/K/2CL transporter in the thick ascending loop of Henle, inhibiting Na, K, CL reabsorption -> diuresis, natriuresis, and reduced effective circulating blood volume; as well as Na and CL reabsorption in distal renal tubules.
- pulmonary venodilator (which is why some respond without having lung oedema)
- bronchodilator
250
mechanism of action nitroprusside
* works on both arterial and venous smooth muscle, however, it is slightly more active in the veins than the arteries
* Prodrug bioactivation to nitric oxide (NO) in erythrocytes by NO synthase
* NO acts by activating/increasing the activity of guanylate cyclase (GC). GC converts GTP to cGMP which:
o Activates myosin light-chain phosphatases causing smooth muscle relaxation
o Activates calcium-sensitive potassium channels increasing potassium efflux and inhibiting L-type calcium influx channels. This inhibits calcium release from the sarcoplasmic reticulum via Inositol Triphosphate (IP3)
o Net action: relaxation of smooth muscle via NO and decreases available intracellular calcium for further muscle contraction
251
Toxicity that can be seen with nitroprusside and what is tx
Cyanide. O2, B12, amyl nitrate, sodium thiosulphate, edta
252
What % of animals with thoracic injuries have pulmonary contusions
Approx. 50%
253
Pathophysiology behind pulmonary contusions 4p
Mechanical force: first increase in tissue pressure, followed by sudden decrease in pressure cause tearing, oedema and haemorrhage
Spalling effect: shearing or bursting phenomenon at gas-liquid interface, may disrupt alveoli at the point of initial contact with shock waves
Inertial effect: when low density alveolar are ripped from heavier hilar structures as they accelerate at different rated
Implosion effect: from rebound or overexpansion of gas bubbles after a pressure wave pass can lead to tearing of the pulmonary parenchyma from excess distention
Also crushing injury from inward displacement of thoracic wall.
Possible lung laceration
254
Compare CT and radiopgraphs ability to detect pulmonary lesion (contusions)
CT scan enabled detection of 100% of the pulmonary lesions, but initial thoracic radiographs only allowed identification in 37%. In addition, 21% of lesions still not visible radiographically after 6 hours. In this study, CT imaging underestimated the extent of the lesions in only 8% of the animals, whereas thoracic radiography underestimated the extent in 58% of the animals
255
In people, what % contusion volume is predictive of MV
MV: 20% or more. >20%, less than 4 fractured ribs, GCS <14 predicted need of MV in 100% of cases
256
Treatment for pulmonary contusions
- maintain in sternal recumbency
- O2
- Fluids, caution
- Analgesia (consider intercostal nerve block)
- Thoracic physiotherapy (get up and move. No coupage)
- Mechanical ventilation (survival to discharge <50% if ventilation is required)
o Pressure control with PEEP in people
o Dogs >25 kg more likely to survive
- Vitamin C and E combo, surfactant, dexmedetomidine, melatonin, salbutamol: human meds, unknown vet med
257
What is the prognosis for pulmonary contusions
Outcome is related to the severity of pulmonary contusions as well as any coexisting thoracic and extrathoracic lesions. Survival rates of 82%.
approximately 30% of dogs requiring MV for contusions survived to discharge
258
bacterial infections that can cause pulmonary haemorrhage, 3 p
leptospirosis, e coli, streptococcus equi subspecies zooepidemicus
259
factors predispose to or associated with pneumonia
impaired px mobility
upper airway disorder
regurgitation syndromes
other
260
magnitude of aspiration pneumonia after gastric aspirations depends on what. 4p
pH: maximal damage by <1,5 pH, minimal damage pH >2,4 (unless also particular matter)
volume
osmolality
presence of particulate matter in the aspirate
261
risk factors for aspiration pneumonia
- GI disorder
o most common, > 60%
o megaesophaugs leading cause 26%
- neurological 18%
- laryngeal 13%
- recent anaesthesia
- 68% have a single underlying cause
262
Viruses associated with pneumonia in canine infectious respiratory disease
- canine adenovirus type 2
- canine parainfluenza
- canine distemper
- canine respiraorty corona
- canine influenza virus
- canine pneumoviru
- canine herpesvirus
263
clinical signs in canine distemper infection
ocular and nasal discharge, resp distress, vomiting, diarrhea, hyperkeratosis of foot pads, progressive neurological dysfunction
264
what type of bacteria is Bordetella bronchiseptica
gram neg, aerobic coccobacillus
265
what pathogen causes acute haemorrhagic fatal pneumonia in shelter dogs
streptocoocus equi subspecies zooepidemicus
266
foreign bodies in the respiratory tract, where do they get stuck in cats and in dogs and what bacteria is most often cultured
- Pasteruella, streptococcus, nocardia, actonimyces, anaebocis, anaerobes
- Right bronchus in dogs (and accessory, left caudal lung bronchi)
- Trachea or carina in cats
267
What % of cats with pneumonia have no clinical signs
36%
268
What % of dogs with pneumonia have concurrent predisposing disorders
35-57%
269
What % of dogs with pneumonia cough, and cats
Dogs 47%
Cats 8%
270
What % of dogs with pneumonia have abnormal lung sounds
>90%
271
How does radiographic findings correlate with clinical signs in pneumonia
poor although involvement of multiple lobes has been associated with reduced survival.
272
What lobe is most commonly affected in aspiration pneumonia, in inhaled FB
Right middle lobe
273
What % of puppies with pneumonia are tachypnoeic and what % have increased RR
78% tachypnoeic
72% increased RE
274
How does sensitivity and specificity compare between transtracheal wash and transbronchial biopsy/lung aspirates/, BAL for diagnosis of pneumonia
Sensitivity similar, less specific
275
What is the (only?) indication for therapeutic bronchoscopy in dogs
Atelectatis caused by mucus plug
276
What antibiotics penetrate to lung tissue and reach therapeutic levels in bronchial secretions
Chloramphenicol, doxycycline, enrofloxacin, trimethropim-sulfa, clindamycin
Cephalosporin and penicillin thought to penetrate poorly but pulmonary inflammation might allow penetration
Aminoglycosides like amikacin and gentamicin have rapid onset action and are bactericidal but caution in rapidly deteriorating patients with fulminant pneumonia and sepsis that are considered likely to be gram negative bacterial origin
277
What antibiotic is first choice in pneumonia suspected caused by Bordetella and in streptococcus equi subspecies zooepidemicus. And if also evidence of sepsis
Bordetella: doxycycline
Strept: amoxicillin
Sepsis: amoxicillin or clindamycin in combo with enrofloxacin
278
Should antibiotics be given in early stages of aspiration
No tx in early stage of aspiration. only if additional risk factors for pneumonia like antacids or GI obstruction
279
Advantages (3) and disadvantages (4) with bronchodilators in pneumonia
+
o Increase airflow
o Improve ciliary activity
o Increase serous nature of respiratory secretions (mucokinetic properties)
–
o Supress cough reflex
o Enhance spread of exudated within lung
o Increase perfusion of poorly ventilated lung units worsening hypoxemia (V/Q mismatch)
o Anti-inflammatory effect by decreasing mucosal oedema and downregulation cytokine release
- May worsen outcome in two human trials
280
Mechanism of action of methylxanthine
Bronchodilator, Inhibition of phosphodiesterase (PDE) III and IV, the enzyme that degrades cAMP. Increased concentrations of cAMP cause bronchodilation, Increase mucociliary speed, inhibit degranulation mast cells, decrease microvascular permeability and leak. improved skeletal muscle and diaphragmatic contractility
281
What size of the particle is appropriate in nebulisation
0.5-5 um appropriate
<0,5 um may be exhaled, >5-10 um will stay in upper airway
282
Mechanism of action of n-acetylcystein
Breakdown of disulfide bonds in airway mucus (mucolytic) and glutathione precursor
283
When is coupage contraindicated
coagulopathic, frequent regurgitation, pain in chest region, fractious
284
what % dogs with pneumonia respond to antimicrobial therapy and what is the survival rate for aspiration pneumonia.
ab response: 69-88%
asp survival: 77-82%
285
prognostic factors for pneumonia
- Difference in survival depending on number of lung lobes affected radiographically
- No other prognostic factors determined (though acute fulminant hemorrhagic pneumonia in shelter dogs does very poorly)
286
What fluid should be used in an endotracheal wash
0.9% Nacl isotonic to maintain cellularity
287
What is the ab treatment for canne infectious respiratory disease complex
if mucopurulent discharge, fever, lethargy, inappetence but no pneumonia treats with doxycycline 7-10 days. Poss amoxicillin-clavulanic acid if other sec bacterial infection.
If pneumonia and sepsis: enrofloxacin and ab with gram positive and anaerobic spectra
288
What are the 3 major phases in aspiration pneumonia pathophysiology (Ab guidelines Lappin)
One - Direct chemical injury
Two – localised inflammatory cascade
Three – secondary bacterial inflammation
289
Radiographic differential for aspiration pneumonia
infectious bronchopneumonia, pulmonary haemorrhage, neoplasia, lobar collapse or torsion
290
what is the evidence for bronchodilators, saline neubulisation and coupage in tx of aspiration pneumonia
no bronchodilators, only useful in early stages <12-24h for bronchoconstriction. Suggested potential harm in later stages)
saline nebulisation. no evidence for or against. possibly better with hypertonic saline. furosemide nebulisation can result in more comfort in humans
Coupage: no evidence for or against
291
Pathophysiology of ARDS, what are the different overlapping phases (saccm 3, describe other way in seminals)
One – acute exudative. 1-7 days. Neutrophilic influx, oedema, damage to pneumocytes, hyaline membrane
Two – fibroproliferative. 5-10 days. fibrosis
Three – resolution
292
What is the main function of pneumocyte I and II
I - o2 and Co2 exchange
II - surfactant production
293
What is a hyaline membrane in ards
fibrin, cellular debris, red blood cells, rare neutrophils and macrophages
294
what ards phenotypes are there and which has worse prognosis
hypoinflammatory
hyperinflammatory. Worse mortality, higher prevalence of shock and metabolic acidosis
Have different responses to PEEP and fluid management and may require different management strategies (ALVEOLI and FACCT trials)
295
Risk factors for ARDS
direct pulmonary
- Ex aspiration pneumonia, pneumonia, pulmonary contusion, chest trauma, MV
Indirect extrapulmonary
- Ex sepsis, sirs, shock, pancreatitis, trauma, AKI, multiple tranfusions
Additional
- Ex smoke inhalation, lung lobe torsions, tracheal collapse, bee envenomation, adverse drug reactions, paraquat intoxication
infectious process, with pneumonia, aspiration pneumonia, and sepsis accounting for more than 85% of human cases of ARDS
296
compare berlin definition with the definition in vet med regarding timing
timing for ards: berlin within one week. Vet <72 h
297
veterinary definition ards
dorodthy Havemeyer working group. One of each of the first four. Fifth is optional.
* Acute onset respiratory distress (<72 hours) at rest
* Presence of known risk factors
* Presence of pulmonary capillary leak not as a result of heart failure or fluid overload (aka no increased pulmonary capillary pressure).
* Bilateral/diffuse infiltrates on chest rads
* Bilateral dependent density on CT
* Proteinaceous fluid within conductive airways
* Increased extracellular lung water
* Evidence of inefficient gas exchange
* Hypoxaemia without PEEP or CPAP and known fio2
* P/F ratio (300 ali, 200 ards)
* Increased Aa gradient
* Venous admixture (noncardiac shunt)
* Increased dead space ventilation
* Evidence of diffuse pulmonary inflammation
* Transtracheal wash/BAL neutrophilic
* Transtracheal wash/BAL biomarkers of inflammation
* Molecular imaging (PET)
* An arterial blood gas sample with PaO2/FiO2 of <200 consistent with ARDS and 200–300 consistent with ALI
298
What are the two main features with lung protective ventilation
tidal volumes of <6 ml/kg and plateau pressures <30 mmHg
299
what pao2 is recommended in MV of human ards px
pao2 55-80 mmHg
300
should you use higher or lower PEEP in an MV ards px
higher. Normally 5 mmHg, in ards 10-15 mmHg
301
Give one example of a nmda receptor agonist and one antagonist
Agonist glutamine
Antagonist ketamine
302
What is the baby lung concept in ventilation and ards
two distinct lung regions, one healthy that is harmed by MV and one causing the issues/not useful. The oedema and atelectasis mean less proportion of the lung can participate in the gas exchange ie less volume required for expansion, “baby lung”. Overdistension can lead to release of inflammatory mediators (ie MODS -> Use tidal low volume (normal 10-15 ml/kg, in ards 6 ml/kg)
303
does glucocorticoids have a place in ards tx
limited benefits, possible in early moderate to severe ARDS (under 14 days)
304
what tx are recommended in tx ards in humans
lung protective ventilation
prone positioning
high PEEP (if moderate to severe)
ecmo (if severe)
conservative fluid strategy
nmblockers maybe
steroids maybe if early
(Gorman seminal)
305
What % of dogs with ards require MV
Dogs 50%
Cats 80%
306
What is virchows triad
Hypercoagulability, blood statis, endothelial damage
307
Predisposing factors for PTE
- Vascular endothelium:
o Neoplasia
o Sepsis
o indwelling catheter
o pancreatitis
o other inflammatory conditions, SIRS
o (amyloids)
- Procoagulable state:
o PLN (ATE)
o Hyperadrenocorticism
o Dirofilaria
o Surgery
o IMHA (VTE)
- Vascular stasis:
o cardiac disease (DCM)
o trauma with crush injury
o neoplasia
majority had IC catheters, 50% had glucorticoids, >1/3 had had cytotoxic agents, 21% had had recent sx, 10% had blood transfusion
308
pathophysiology of PTE
initial high vq mismatch (low perfusion) due to mechanical obstruction and reactive constrictions -> cause redistribution of blood and low v/q mismatch (more perfusion, no increase ventilation) areas (hypoxic pulmonary vasoconstriction) and pulmonary oedema. Physiological shunting also contribute to reduced arterial o2 content
this leads to increased pressure in right ventricle (increased afterload), reduced preload to left ventricle and reduced cardiac output
309
clinical signs in PTE
acute onset hypoxia, tachypnoea, dyspnoea, lethargy, altered neuro state (1/3 of dogs), cough, syncope, haemoptysis, crackles, wheezes, right sided heart murmur, poor perfusion
symptoms often worse for the first 2-3 h due to compensatory reactions in the lung (vasoconstriction)
right sided heart failure signs (ascites, pleural effusion) if chronically elevated pulmonary arterial pressure
310
what is your first suspicion in a px that’s on glucocorticoids, that acutely developed severe respiratory signs and normal radiographs
PTE
311
Describe the radiographic findings in a dog with PTE
radiographs (pleural effusions, loss of definition of pulmonary artery, unstructured interstitial to alveolar infiltrates (if lots of small PTE) (most often caudodorsal) with indistinct borders (unlike neoplastic or infectious infiltrates), cardiomegaly, hyperlucent lung regions (regional oligemia) (if massive PTE), enlargement of main pulmonary artery). can be normal, does not exclude PTE (25% have no changes)
312
what is McConnells sign
akinesia of the right midventricular wall, seen in PTE
313
what does the PESI and sPESI score look at and how is predictive of morality in what disease process
- The pulmonary embolism severity index (PESI) and Simplified PESI (sPESI)
- patient demographics, comorbidities, and baseline physical examination parameters
- if not increased predict a low risk of mortality within 30 days
- Patients with an elevated PESI or sPESI are further classified as intermediate (submassive PTE) or high risk (massive PTE), based on evidence of right ventricular dysfunction, increased cardiac troponin concentration, or hemodynamic instability (cardiac arrest, cardiogenic shock, or persistent hypotension due to PTE)
314
Treatment for PTE
Underlying disease, oxygenation and support normal function, prevent further clots, potentially thrombolysis
Anticoagulant: Start in all with confirmed, and start in those with high probability before diagnostic results. Minimum 3 months. Venous thrombi: Low molecular weight heparin or direct Xa inhibitor preferred
Thrombolytic agents: Streptokinase, tissue plasminogen activator (tpa). Generally, only recommended if can be given locally via pulmonary artery catheter (depends on how desperate), surgical pulmonary embolectomy, interventional techniques
315
Treatment in massive thrombus (PTE) with shock and hypotension
1. maintain adequate BP
a. use vasopressors (norepinephrine/noradrenaline)
b. use inotropes if required for myocardial failure
c. control arrythmias
d. fluids contraindicated (will decrease coronary perfusion pressure)
2. support oxygenation
a. non-invasively first (nasal cannula, cage, high flow)
b. if have to; rapid, hemodynamically neutral induction (opioid + benzodiazepine +/- paralytic agent)
c. minimize impact on pulmonary vasculature (low PEEP, low pressure, low frequency if possible)
d. be ready for px coding
3. decrease pulmonary vascular resistance
a. treat reflex vasoconstriction (oxygen, sildenafil)
b. anticoagulant (unfractionated heparin bolus + CRI)
c. thrombolysis (recombinant tissue plasminogen activator, tPA)
316
mechanism of action of tpa in PTE treatment
binds to fibrin in thrombus -> converts entrapped plasminogen to plasmin -> initiated local fibrinolysis. Risk bleeding, death. Only use if high risk of death without it.
317
What muscle is most important for inspiration and what nerve innervates it
Diaphragm, phrenic nerve
318
Which muscles are used in active inspiration
diaphragm, external intercostal, scalene, sternomastoids
319
what is the most common congenital chest wall disease/anatomic defect
pectus excavatum
320
What is the Ribscore, would you use in in dogs
point based scoring system in rib fractures, based on radiographs. Predict pneumonia, respiratory failure, need for tracheostomy. Not validated in vet med. Not predictor of outcome in recent study on dogs with traumatic rib fractures
321
What score was a strong predictor of outcome in canine patients with traumatic rib fractures in a recent study according to saccm 3
Animal trauma triage score
322
What does the ATT predict
The lower the ATT score, the higher the probability of survival at seven days posttrauma
With each point increase in ATT associated with a 2.3–2.6 times decrease in likelihood of survival
Score of ≥7 have a <50% survival to discharge
323
What % of rib fractures are from vehicular accidents and what % from canine bite injuries
Vehicle: 56%
Bite: 44%
324
Describe a flail chest
three or more rib fractures in series, in which both the dorsal and ventral aspect of the ribs are fractured. This segment can then affect respiratory mechanics, as the flail portion will paradoxically move inward during inspiration and outward during exhalation
325
What is a pseudo flail chest
same movement as “true” fail chest but no or few rib fractures but torn intercostal muscles
326
Medical management of flail chest
Pain control, placement of px in lateral recumbency with flail segment down, chest wrap
327
Damage in what area of the spine can cause respiratory failure due to failure of diaphragmatic contractions
Cervical nerve roots 4-7 (cervical nerve roots exit above the named veterbral body so C3-C6, vetemcrit says C4-6)
328
Give an example of a snake with neurotoxin that can cause respiratory paralysis, and where do they live
Elapid snakes
southern United States, Australia, Central and South America, the Middle East, Asia, and Africa.
329
What types of toxins does the elapid snakes have (4 p)
neurotoxin, hemolytic toxin, hemostatis/bleeding causing toxin, cytotoxins
330
What advise do you give to an owner that phones telling you their dog has been bitten by a coral snake
Restrict activity. Immediate vet examination. Mouth to mouth if collapsed (hypoxia sec to resp paralysis most common cause of acute death)
331
What is the mechanism of action of elapid neurotoxin
Presynaptic or Postsynaptic neuromuscular blockade or a combo, LMN
- Presynaptic (phospholipase A2 group): prevents release of acetylcholine by structural changes of nerve terminal. Can be irreversible bound and unresponsive to antivenom after about 24 h-days, if quick tx might be able to reverse
- Postsynaptic: western hemisphere of elapids. Antagonist at acetylcholine receptor. Not irreversible binding.
332
What preparalytic signs can be seen in elapid snake envenomation
vomiting, nausea, hypersalivation, urination and defecation, and/or collapse. These signs may rapidly progress (<30 minutes) to a nonpainful paralytic state
333
What is the primary treatment for tick paralysis and in what country can more aggressive tx including MV be warranted
Remove the tick. Australia. Has the tick Ixodes holocyclus
334
What is the mechanism of action of the holocyclotoxin in tick paralysis
o interference with the release of acetylcholine at the neuromuscular junction by blocking Ca2+ influx presynaptically
o acts on both motor and sensory neurons to cause inhibition of depolarization in the distal segments of motor neurons
335
What is the most common acute polyneuropathy in dogs and what can cause it
* Acute idiopathic polyradiculoneuritis
* Exposure to racoons (reaction to their saliva), recent vaccinations, possible coinfection with cambylobacter is a risk factor. Is an immunmediated reaction with an iimunmediated attack on proteins in ventral nerve root and motor nerves causing neuronal demyelination and degeneration of axons
336
Which botulinum toxin is most commonly seen in dogs
* Type C
337
What is the mechanism of action for botulinum toxin
Preformed toxin, most often ingested. In the alkaline environment of the GI tract, inactive progenitor toxin is activated. Toxin is absorbed from GI tract by endocytosis, enters lymphatic system and blood stream. The toxins heavy chains binds to the presynaptic peripheral nerve terminals and is internalised via endosomes. The toxin modifies SNARE proteins required for exocytosis of acetylcholine at the neuromuscular junction -> neuromuscular flaccid paralysis, generalised lower motor neurone disease and parasympathetic dysfunction
Botulinum toxin A cleaves synaptosomol–associated protein (SNAP-25)
Botulinum toxin B, D, F, G cleaves synaptobrevin
Botulinum C cleaves SNAP-25 and syntaxin
338
What is the average intrapleural pressure
* -5 cm H2O
339
Give 3 examples of pocus findings that can be seen in pneumothorax
Glide sign, curtain sign, double curtain sign
340
What can a double curtain sign indicate on pocus
Pneumothorax, Diaphragmatic hernia
341
Which has the highest sensitivity for pneumothorax and pleural effusion out of CT, rads and pocus (saccm 3)
* CT
342
Causes of pure transudate, modified transufate, exudate, asepitic exudate
* Pure: hypoalbuminemia (most common), CHF cats, right sided CHF dogs, lymphatic obstruction
* Modified: heart failure, neoplasia, vasculitis, lung lobe torsion, diaphragmatic hernia
* Exudate: Infection, neoplasia, foreign body, chronic chylous, immune complex
* Aseptic exudate: pneumonia, abscess, sepsis, pancreatitis, necrosis of intracavitary neoplasia
343
Protein and total nucleated cell count in pure transudate, modified transudate, exudate
Pure transudate: tp <2,5 g/dl. Cell count <1000 cells/ul
Modified: tp >2,5 g/dl, cells 1000-5000
Exudate: tp >2,5 g/dl, cells >5000
344
Aetiology for pyothorax in dogs
migrating foreign bodies, penetrating and blunt thoracic trauma, hematogenous and lymphatic spread, esophageal perforation, parasitic migration, discospondylitis, osteomyelitis, parapneumonic spread, ruptured lung abscesses, and iatrogenic
345
Aetiology for pyothorax in cats
parapneumonic spread of aspirated oropharyngeal flora, from thoracic wounds, foreign body migration, parasitic migration
346
What are the criteria for removal of thoracostomy tube in pyothorax
clinical improvement, a decrease in fluid production to <2 ml/kg/day, and resolution of infection on cytology
347
When is sx indicated in pyothorax cases
indicated in patients with loculated fluid, lung or pleural abscesses, suspected neoplasia, perforated esophagus, penetrating thoracic injury, or those that fail medical therapy
348
Whats the reoccurance rate in pyothorax cases
Reported recurrence rates range from 0%–14%.
349
How often (%) is the underlying cause found for pyothorax in dog and in cat
* Underlying cause found in 35-67% of cases in cats
* Definite aetiology in dogs found in 4-22% of cases in dogs
350
Common organisms causing pyothorax in dogs and cats
Nocardia, streptococcus, corynebacterium, e coli, Pasteurella, actinomyces, staph, fusobacterium, clostridium, cryptococcus, candida
351
What cell type is seen in cytology of chylous effusion
small lymphocytes. Neutrophils and macrophages can develop over time
352
What chemistry values can be run to confirm chylous effusion and how do you interpret them
* triglycerides conc higher in effusion than serum >3.1
* triglyceride concentration in effusion > 100 mg/dl
* cholesterol equal or lower than in serum.
353
Roughly what % of chylothorax are idiopathic
50%
354
What breed is more predisposed to chylothorax
Afghans
355
Is traumatic chylothorax an indication for surgery
No, most are self limiting within 10 days
356
What surgical procedures are most successful for idiopathic chylothorax and what are the success rates (dogs and for cats)
thoracic duct ligation + subphrenic pericardiectomy. dogs are 60%–100% and 80% in cats
357
Give one example of drug used for medical management of idiopathic chylothorax and its mechanism
* Rutin: benzopyrone nutraceutical that is theorized to increase lymphatic fluid uptake, reduce blood vessel permeability, and increase macrophage phagocytosis of protein in lymph)
* Octreotide: somatostatin analogue, study in 5 dogs 40% efficacy, saccm 3 says other study says not effective)
358
How is hemothorax diagnosed
diagnosed when the packed cell volume of pleural effusion is at least 25% that of peripheral blood (saccm 3)
(saccm 2 definition: pleural space effusion with a HTC >10% of peripheral blood PCV)
359
Roughly how much pleural effusion is needed before ventilation is impaired
30-60 ml/kg in dogs, 20 ml/kg in cats before
360
Most common cause of spontaneous haemothorax when normal coagulation in dogs
* neoplasia
361
What is the protein count typically of a FIP effusion and what is the sensitivity and specificity for FIP.
What cell count is normally seen.
What other analysis can be done on the effusion to help the diagnosis
effusion total protein concentration of >3.5 g/dl had a sensitivity of 87.1% and a specificity of 60%, 94% positive predictive value, 100% negative predictive value. low cell count (<5000)
Cytology: viscous, straw-coloured, clear to cloudy, nondegenerate neutrophils predominating.
a1-acid glycoprotein concentration, Rivalta test, Reverse transcriptase PCR for feline coronavirus
362
How is bilothorax and urothrorax diagnosed
Bilirubin effusion to serum ratio >1:1
Creatinine >1:1
363
How is pneumothorax categorised (4p)
Traumatic, iatrogenic, spontaneous (primary, secondary), infectious OR open, closed, tension
364
What % of dogs following vehicular trauma have pneumothorax
47%
365
What is a tension pneumothorax
the site of air leakage creates a one-way valve during inspiration and results in a rapidly increasing pleural pressure that exceeds atmospheric pressure, often leading to cardiopulmonary arrest)
366
Most common cause of spontaneous pneumothorax in dogs and in cats
Bulla in dogs, airway disease in cats
367
What dog breed is overrepresented in primary spontaneous pneumothorax
* Siberian husky (middle-aged, large-breed, deep-chested dogs)
368
When should thoracic drain placement be considered in a pneumothorax
* patients with tension pneumothorax
* pneumothorax that develops during positive pressure ventilation
* those requiring more than two thoracocenteses within 24 hours
* when negative pressure cannot be achieved
369
should exploratory sx be considered in spontaneous pneumothorax in dogs and justify your answer
Yes, higher survival rate and decreased recurrence. (medical management more successful in cats)
370
Initial treatment for a penetrating injury causing an open pneumotothorax
the site of penetration should be covered by a sterile occlusive bandage and thoracocentesis performed immediately, and surgical intervention should not be delayed.
371
Indications for immediate surgery in diaphragmatic hernia
immediate surgery: herniated stomach, strangulated bowel or organ, inability to oxygenate after medical intervention, ruptured viscera
372
when has re-expansion pulmonary oedema been seen in vet med
after thoracocentesis, pectus excavatum repair, and diaphragmatic hernia repair
373
State 6 non-respiratory causes of respiratory distress
Non respiratory causes of decreased oxygen delivery (anaemia, low cardiac output)
Metabolic derangements (metabolic acidosis, hyperthyroidism, hypoglycaemia)
Drugs (bicarbonate, opioids)
Hyperthermia
Behavioural
Brain disease
374
Name of respiration centers/groups in the brainstem 3 p
* respiratory, pneumotaxic, and apneustic centers
* Respiratory dorsal and ventral group in the medulla, and the pneumotaxic and apneustic in the pons
375
Central chemoreceptors are more sensitive to Co2 or O2?
* CO2
376
The peripheral chemoreceptors that respond to changs in Pao2, Paco2 and pH are located where
Carotid and aortic bodies
377
What are the receptors in the lungs that can affect ventilation, P, J, R or L?
* J receptors
378
what % of hyperthyroid cats have panting as clinical sign
* 25%
379
What does peripheral and central thermoreceptors sense and where is the information transmitted
Changes in ambient or body temperature, transmitted to the hypothalamus
380
What are the 4 main mechanisms of thermoregulation
Radiation, convection, evaporation, conduction
381
Changes in pH is sensed by which chemoreceptors, peripheral or central
* Peripheral
382
Describe Kussmaul respiration and when it occurs
a respirator pattern characterized by deep and laboured breathing, is seen with severe acidosis in people
383
Explain 2 mechanism behind anaemia causing increased respiratory rate
* Decreased arterial oxygen content (primarily a decrease in PaO2) is sensed by the peripheral chemoreceptors (glomus type I cells) in the aortic and carotid bodies; this causes an increase in firing of the glossopharyngeal nerve, which stimulates neurons in the medulla to increase the respiratory rate
* change in pH associated with tissue hypoxia and hyperlactatemia, which is sensed primarily by the carotid body chemoreceptors -> increase in ventilation
* Hypovolemia may also contribute
384
Describe biots respiration, cheynes stokes ventilation
* Biots respiration, apnea alternating with periods of quick, shallow inspirations. differed from Cheyne-stokes as not crescendo-decrescendo
* Cheyne-stokes respiration: quick respiration in crescendo-decrescendo pattern alternating with periods of apnea of 10-20 sec
385
Relative contraindications to thoracocentesis?
pleural disease that cant be treated by thoraocentesis; pneumomediastinum, diaphragmatic hernia without fluid accumulation, and pleural masses. Coagulopathy (unless significant respiratory distress)
386
what arteries in the ventral thorax should be avoided in thoracocentesis 1 p
Internal thoracic arteries
387
388
5 techniques for drainage of pleural effusion
butterfly needle. hypodermic needle with a saline-filled hub. over-the-needle iv catheter. Thoracostomy tube. Large volume via passive gravity-based drainage
389
What possible complications are there in thoracocentesis and which 2 are most common in people?
Pneumothorax and arterial laceration most common in humans
Hypotension and re-expansion pulmonary oedema if chronic.
Vagal event.
Formation of hematoma or seroma at puncture site
390
Describe active suction drainage using the three bottle suction apparatus and what suction pressure is needed
Three-bottle suction apparatus. Active drainage. The three bottle system has a collection bottle, a water trap, and suction-control bottle. It allows the suction level to be regulated by changing the water depth in bottle 3. There is a water seal (central bottle) so that suction can be turned off without worry that air will leak back into the pleural space, achieved by submerging the tubing entering the second bottle in 2 to 3 cm of water. The exudates in bottle 1 can be evaluated and emptied independently. The water trap (central chamber bottle 2) will bubble if air is evacuated from the pleural space. Continuous suction requires water seal between suction pump and chest tube. Suction pressure of 10-20 cmH20 used, achieved by filling the third chamber with water to 10-20 cm
391
What is the physiology behind paradoxical breathing
* During normal lung expansion pulmonary stretch receptors in the lung are activated and this stretch has a negative feedback effect on external intercostal muscle activity limiting expansion of the thoracic cavity and lung inflation. This is a normal protective mechanism to prevent overdistension of the lungs
* With pleural space disease there is less of a change in pleural space pressure (due to presence of space occupying fluid/viscera) and therefore less pressure gradient for air flow and lung expansion is reduced. This reduces the amount of negative feedback on the external intercostal muscles resulting in prolonged external intercostal muscle activity.
* This uninhibited expansion of the chest wall overrides the effect of diaphragm contraction on the abdominal contents and instead pulls the abdominal contents in resulting in a sunken abdomen as the ribs elevate. Giving the appearance of the abdomen moving in as the chest moves out
392
Give examples of antitussive drugs that cause direct depression on the cough center in medulla oblongata
Butophanol (K receptor agonist), codeine (mu receptor agonist)
393
Mechanism of action of butorphanol (receptor activity)
K receptor agonist, mu receptor antagonist (competitive)
394
Mechanism of action of b adrenergic bronchodilators
B2 agonist – increased adenyl cyclase – increases cAMP – decreased Ca conc and activated PKA – inactivates MLK and activates myosin light chain phosphatase (MLCP) - relaxation bronchial smooth muscle. Also open calcium activated K channels – hyperpolarization
Stabilizes mast cells via inhibition release of inflammatory mediators. Very little effect on neutrophils and eosinophils
Increased mucociliary clearance
395
State 2 short acting B2 agonists and 3 long acting b2 specific drugs
Short: adrenalin, isoproterenol
Long acting: terbutaline, metaprosterenol, albuterol
396
Give 3 examples of metylxanthines
Theobromine, caffeine, theophylline (pentoxyfyllin)
397
Mechanism of action of metylxanthines
Inhibit phosphodiesterase type 3 and 4 ->increased cAMP -> increased inhibition of inflammatory mediator release from mast cells, increased antiinflammatory effects, relaxation bronchial smooth muscle
Antagonism of adenosine receptors -> antagonism of bronchoconstriction
Diminishes activity of eosinophils
398
Why can anticholinergic drugs be useful in asthmatic individuals
Inhibit vagal-mediated cholinergic smooth muscle tone in respiratory tract. Asthmatic individuals have excessive stimulation of cholinergic receptors
399
What is the mechanism in with glucocorticoids exacerbate the risk of CHF
due to increase in plasma glucose, volume expansion and increase in plasma volume
400
mechanism of action of acetyl cystine
o mucolytic effect is caused by an interaction of the exposed sulfhydral groups on the compound with disulfide bonds on mucoprotein - breakdown respiratory mucus, reduce the viscosity of mucus, and enhance the clearance.
o may also increase the levels of glutathione, which is a scavenger of oxygen-derived free radicals.
401
Mechanism of action of doxapram
direct stimulation of the medullary respiratory center and activation of the aortic and carotid body chemoreceptors to improve sensitivity to carbon dioxide
402
inhaled medication efficacy can be affected by
px cooperation, breed, age, underlying disease process, type of medication, type of mask, type of nebulizer
type of medication include: molecular weight, pH, electrical charge, solubility, stability
403
mass medium diameter determines what
used to determine particle size to reach lower airways in nebulizing. determines the particle size (um) above and below which 50% of the mass of the particle is contained
404
what diameter of aerosolized particles are deposited where. >20, 10-30, 5-25. 0,5-5 um (saccm table 169.1)
>20 nasopharynx
10-30 trachea
5-25 bronchi
0,5-5 peripheral airways
405
State delivery system for aerosolized particles
jet nebulizers
ultrasonic and mesh nebulisers
metered dose inhaler (MDI)
406
is n-acetylcysteine recommended as aerosol in bronchial disease
no
407
when can aerosol gentamicin be considered and what are the advantages
Bordetella bronchiseptica
attach to the tracheal cilia and difficult to reach with systemic antibiotics
aerosol minimal systemic absorption, does not affect renal parameters
408
what can be administered to reduce the risk of BAL induced bronchoconstriction in cats
aerosol treatment with ipratropium bromide (anticholinergic) + salbutamol (B2 agonist)
409
state the equation of motion
Pvent + Pmuscles = elastance x volume + resistance x flow
410
Resistance equation
Driving pressure/flow
411
What is the definition of compliance
change in lung volume for a given change pressure. Measure distensibility of the lungs
High compliance: large increase in volume for a small pressure change
Low compliance: requires large pressure change to create a small increase in volume
412
How do you calculate dynamic and static compliance
dynamic compliance: tidal volume/(PIP-PEEP).
static compliance: tidal volume/(Pplat-PEEP)
413
which is the lowest, dynamic or static compliance
dynamic compliance is lower due to the resistance that occurs during gas movement.
414
What is driving pressure
The pressure it takes to extend the alveoli for each breath
Pplat-PEEP
(PIP to Pplat is the resistance I think)
415
Difference supported and assisted breath
Px trigger both breaths. In assisted, the breath is then controlled by vent. In supported a set insp flow is given but the px terminated the breath (cycle).
416
Describe SIMV
Synchronized intermittent mandatory ventilation (SIMV)
The ventilator has a window of time in which it will deliver a mandatory breath. If the patient triggers a breath during this period, it will be assisted (px trigger and then controlled by vent) appropriately. If no breath is triggered by the end of this time period, a mandatory breath will be given. Between these mandatory breaths, the patient can breathe spontaneously as often or as few times as desired (unassisted, “normal” breath)
Minimum rate and minute ventilation controlled, maximum rate and maximum minute ventilation
not controlled
417
What is the difference between assisted ventilation and assist control
Controlled ventilation: all breaths mandatory and controlled by machine
Assist/control: px triggers, all breath delivered are mandatory
418
Ventilator breath types, vent or px controls initiation (trigger), inspiratory flow, termination (cyckle) in mandatory, assisted, spontaneous, supported ventilation
Mandatory: trigger, flow, cycle all by ventilator
Assisted: patient trigger. Flow and cycle by ventilator
Spontaneous: trigger, flow, cycle all by patient
Supported: patient trigger, ventilator flow, patient cycle
419
What does control, cycle, trigger, limit variable in MV signify
control: pressure, volume or flow
Cycle: determines termination of inspiratory flow (when to change from insp to exp), time most common but can be pressure, volume or flow as well
Trigger: what initiates inspiration. Can be time if vent controlled. Pressure, flow or volume if px controlled
Limit: parameter the breath cannot exceed, max volume or pressure
420
What is an example of a baseline variable/expiratory control variable in MV
PEEP
421
If inspiratory time exceed expiraty time in MV, what can that cause
Breath stacking/intrinsic PEEP/auto PEEP
422
If there isn’t a PEEP setting on the machine, how can you amend the machine to achieve it
Two options:
- adding a tube to the exhalation port of the ventilator and attach the tube to the PEEP valve
- submerge the end of the tube in the desired depth of water (depth in cm = cm H2O pressure)
423
PEEP + set inspiratory pressure make up what in MV
Peak inspiratory pressure (PIP)
424
Benefits and disadvantages of PEEP
benefits
- recruiting previously collapsed alveoli
- preventing further alveoli collapse
- reducing ventilator-induced lung injury
- counter balance of hydrostatic forces leading to pulmonary oedema (shift fluid back from alveoli and interstitial place back into circulation)
disadvantages
- reduced venous return (as increased pressure in chest cavity), reduced CO and increased afterload.
- Reduced CO due to increased pulmonary vascular resistance
- Barotrauma
- Auto PEEP (progressive air accumulation, due to incomplete exp of air before insp.)
- Alveolar over distention, will collapse surrounding capillaries and reduce O2
425
Dead space vs shunt, which is which
Dead space: wasted ventilation, is ventilated but not perfused
Shunt: venous admixture, not ventilated, is perfused, ex oedema
426
Suggested ventilator settings in healthy lungs and in lung disease
Fio2 100%, 100%
Tidal volume ml/kg 10-12, 6-8
RR 10-20, 15-30
Pressure above peep cmH20 8-10, 10-15
PEEP cm H2O 0-5, 5-8
Insp flow l/min 40-60, 40-60
Insp time sec 0.8-1, 0.8-1
Rise time sec 0,1-0.3. 0,1-0,3
Insp tp exp ration 1:2, 1:1-1:2
Insp trigger 1-2 cmH2o or 1-2 m/min, 1-2 cmH2o or 1-2 m/min
427
What is rise time in MV
time in which airway pressure increases from baseline to peak pressure. Faster rise time indicated in px with rapid RR. Careful in animals with small ET tubes due to increased resistance to flow
428
Indications for MV
- Severe hypoxia despite oxygen supplementation
- Severe hypoventilation despite therapy
- Excessive respiratory effort with impending respiratory fatigue or failure
- Severe hemodynamic compromise refractory to therapy
429
Complications with MV
- Cardiovascular compromise
- Ventilator-induced lung injury (Volutrauma, barotrauma)
Ventilator-associated pneumonia
- Pneumothorax
430
What % dog MV for parenchymal disease was successfully weaned, how many left hospital
What % dog MV for intracranial or neuromuscularl disease was successfully weaned, how many left hospital
What % dog MV for aspiration pneumonia was successfully weaned
What % dog MV for ARDS was successfully weaned
What % dog MV for tick paralysis survived
What % dog MV for CHF survived
parenchymal disease 30%, 20%
intracranial or neuromuscular 50%, 40%
aspiration pneumonia 50%
ARDS 8%
tick paralysis 64%
CHF 63%
431
Does brachycephalic breeds do worse on MV than other dogs? Does cats do worse than dogs
Bracy same as other dogs, cats worse than dogs
432
Gold standard for diagnosis patient ventilator asynchrony
Gold standard for diagnosis: phrenic neurogram, oesophageal ballon catheter
(Non invasive diagnosis: wave form analysis)
433
What are the general settings for lung protective ventilation
Low tidal volume 4-6 ml/kg
Limited plateau pressure <30 cm H2O (some evidence high PEEP/low Fio2 better than low PEEP/high FiO2, but current recommendation low tidal volumes and limited peak and plateau pressure best)
434
What is the definition of refractory hypoxemia
Patients that remain hypoxemic despite mechanical ventilation with 100% oxygen and lung protective strategies
435
Risk of recruitment manouvers
overdistention, volutrauma, barotrauma, and hemodynamic compromise.
436
What does the manouver expiratory hold check for
Intrinsic/auto PEEP
437
What scaler can be used to diagnose auto PEEP without doing an expiratory hold
Descending flow pattern. The flow will fail to return to baseline before the next breath begins
Saccm figure 35.9
438
How can lower infliction point and upper infliction point be used to adjust your MV settings
LIP: increase PEPP to a value greater or equal to LIP. Avoid atelecttrauma.
UIP: keep PIP below UIP. Avoid volutrauma
439
state types of patient ventilator asynchrony
- trigger asynchrony
- flow asynchrony
- termination or cycling asynchrony
- expiratory asynchrony
440
reasons for patient ventilator asynchrony due to issues in initiation of inspiration
ineffective triggering:
- patient-generated decrease in airway pressure with a simultaneous increase in airflow without triggering a machine breath. Most often sue to inappropriate settings. Can also be auto PEEP, significant muscle weakness/fatigue, reduced respiratory drive, or an excessively deep level of anesthesia. easiest to identify on flow scaler
auto triggering:
- breath is delivered by the ventilator because of a change in airway pressure or flow not caused by patient effort. due to wrong settings or circuit leaks, fluid/secretions within the circuit, or cardiac oscillations.
double triggering:
- two delivered breaths separated by an expiratory time less than half the mean expiratory time. due to exceptionally high ventilatory demand of the patient, low tidal volumes, an I-time that is too short, or a flow-cycle threshold set too high
441
describe how to tell if your pulmonary artery catheter is in the correct place
look at pressure waveforms whilst introducing the ballon tipped catheter into the pulmonary artery
right atrium 3-5 mmhg
right ventricle 3-25
pulmonary artery 25-10
pulmonary artery occlusion 10sih
chambers 22.3 or drobatz figure 12.3
442
Indications for MV
Pao2 <50 mmHg with Fio2 of > 0,5
Paco2 >50 mmhg with pH <7.25
Increased RR/RE
Increased work of breathing
(acvecc talk)
443
Contraindications for permissive hypercapnia 4p
Increased intracranial pressure
High intrathoracic pressures
Hemodynamic instability
Myocardial irritability/dysfunction
444
What is the normal difference between Paco2 and etc02 and what is the reason
etco2Co2 s underestimated by 2-6 mmHg compared to Pa02. The difference is alveolar dead space. Due to alveoli being ventilated but not perfused making them alveoli dead space. The dead space has the same gas mix as inspired gas. This inspired gas mix mixes with expired gas and dilutes the co2
445
normal spontaneous tidal volume
7-9 ml/kg (acvecc MV lecture)
446
The term “control” in MV refers to what
Remains constant despite changes in compliance and resistance (volume or pressure control)
447
What does time trigger mode of ventilation mean
Inspiration begins when a preset time has elapsed
448
A breath in which the ventilator determines the start or end of inspiration, is it spontaneous, assisted, supported or mandatory
Mandatory
449
The variable that terminates inspiration and causes expiratory time to begin is the trigger, cycle, limit or control variable
Cycle
450
A PIP that is set by the clinical and remains constant despite changes in the px resistance and compliance is consisted with pressure or volume control ventilation
Pressure control ventilation
451
A peak airway pressure that varies depending on ventilator settings, mode, compliance, and resistance is consistent with pressure or volume control ventilation
Volume control
452
What is the cycle variable in pressure support ventilation
Pressure (cycle variable terminated inspiration and cause expiration to start)
453
your px is on a mode in which minimum rate, sensitivity level, and volume control are set. The px can breath faster than the set rate, but the preset volume will be delivered with each breath (mandatory and spontaneous), what mode is your px on, cpap, pressure support, simv or assist/control
assist/control
(not simv because the spontaneous breaths are not always assisted)
454
A px is on volume control-SIMV with PEEP, the clinician adds pressure support. what is the purpose of adding pressure support in this scenario? Is it Improve oxygenation, decrease WOB, prevent auto-PEEP or to protect against lung injury?
Decrease work of breathing
455
The baseline pressure is raised above atmospheric pressure in which if the following modes. PEEP, pressure control, pressure support, volume control
PEEP
456
Which of the following is thought to be the most detrimental in a ventilated px… fio2 or peak pressure >30 cm H20
Peak pressure >30
457
Decreased cardiac output is a potential detrimental effect of PEEP. Which mechanism is thought to be responsible. Is it increased intraabdominal pressure, increased left ventricle afterload, increased pulmonary vascular resistance or decreased transpulmonary pressure?
increased pulmonary vascular resistance
458
on a capnogram, how does bronchoconstriction affect the alpha and beta angel
sloped alveolar plateau, increased alpha angle but normal beta angle (shark fin)
a _____b
/ l
/ l
x
flashcards
Decks in class (25)
# Cards
-
Anaesthesia and Analgesia0
-
Cardiovascular0
-
CPR0
-
Electrolyte and Acid-Base0
-
Endocrine185
-
Extracorporeal0
-
Fluid therapy0
-
Haematology, Coagulation, Hemolymphatics147
-
Infectious, Inflammation299
-
Intraabdominal0
-
Neurology175
-
Nutrition0
-
Pharmacology, Antimicrobial0
-
Renal/Urinary1
-
Reproductive0
-
Respiratory458
-
Sepsis, SIRS, MODS, Shock0
-
Transfusion Medicine82
-
Trauma, Environmental, Misc0
-
Ventilation, mechanical0
-
Monitoring0
-
Procedures0
-
Dermatology42
-
ophthalmology19
-
Musculoskeletal15
