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Board Review 2020 > Respiratory > Flashcards

Respiratory Flashcards

1
Q

What is in the conducting zone of the respiratory tract

A

Trachea to terminal bronchioles

Anatomical dead space as no gas exchange occurs

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2
Q

What is in the respiratory zone of the respiratory tract

A

alveolar sacs

cross sectional area is very large

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3
Q

What is the force that moves air from the terminal broncheols to the avleoli

A

diffusion

Pollutants then get to region as unable to move bast conjuction of respiratory and conducting zone

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4
Q

Does all the tidal volume get to the alveoli

A

No due to anatomical deadspace

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5
Q

Define total lung capacity

A

amount (volume) able to breath in during large breath + residual volume

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6
Q

Define residual volume

A

amount (volume) remaining in the lungs after max exhalation

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7
Q

Define functional residual volume

A

Volume remaining after a normal breath exhale

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8
Q

What is the best method to calculate alveloar minute ventilation

A

VCO2/PACO2 x K

- Based that all expired CO2 comes from the alveolar gas

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9
Q

What is the bohr effect in relation to the O2 dissassociation curve

A

If have 1/3 hemoglobin bound with CO will shift O2 dissociation to the left therefore O2 is bound tigher and not available to periphery

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10
Q

What are the axis labels for the O2 disassociation curve

A

X- PO2

Y- % Hgb saturated

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11
Q

What shifts the O2 diassociation curve to the left and what does that mean

A

Increase O2 affinity of Hgb (bound more tightly)

Decrease PaCO2, Temp, H+, 23DPG (RBC Metabolism)

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12
Q

What shifts the O2 diassociation curve to the right and what does that mean

A

Reduced O2 affinity of Hgb

Increase in PaCO2, Temp, H+, 23DPG (RBC metabolism)

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13
Q

Where is the most carbonic anhydrase

A

RBCs

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14
Q

What are the RBC mechanism for CO2 transport

A

Dissolved CO2, HCO3-, Carbamino Hgb

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15
Q

How does the solubulity of CO2 compared to O2

A

CO2 is about 24 times greater than O2.

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16
Q

How does PEEP affect the left side of the heart

A

Increases afterload

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17
Q

How is the caudal vena cava alter in the abdomen with mechanical ventilation

A

Increases diameter

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18
Q

Define ARDS

A

Peracute onset of respiratory distress, severe hypoxemia, bilateral diffuse alveolar infiltrates not causes by left atrial hypertension or hydrostatic pulomonary edema

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19
Q

What are the ARDS P/F ratio cut offs

A 
ARDS = 200 mmHg
ALI = 300 mmHg
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20
Q

What is the criteria for ARDS in veterinary medicine

A

First 4 are requried

1) acute onset <72 hrs of tachypnea and labored breathing
2) Known risk factor
3) evidence of pulmonary capillary leak without increased pulmonary capillary pressure
4) Evidence of inefficient gas exchange without PEEP or CPAP (P/F ratio, Increased Aa gradient, decreased SmvO2)
5) evidence of diffuse pulmonary inflammation

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21
Q

What are Known risk factors of ARDs

A

(SIRS, sepsis, trauma, apsiration, multiple transfusions, adverse drug rx, drowing

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22
Q

What is the henderson-hasselbach equation for bicarb

A

pH = 6.1 + Log [HCO3- /(0.03 x PCO2)]

pK for bicarb is 6.1

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23
Q

How does hemoglobin effect buffering

A

More = increased buffering effect

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24
Q

Define base excess

A

measure of the amount of bicarbonate added to get to a normal pH at a normal temperatures

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25
Q

What is Fick’s Law of gas diffusion

A

(Area/Thickness)x Diffusion constant x (P1-P2)

Diffusion constant = Solubility/ square root (MW)

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26
Q

What is the difference between perfusion limited and diffusion limited gas exchange

A

Perfusion limited = No difference in end capillary partial pressure of gas for alveolar capillary partital pressure
Diffusion If there is a difference

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27
Q

What is the limiting factor of O2, CO2, and N20 gas exchange

A

CO2- diffusion
N20 and O2 are perfusion limited

If there is pathology to blood gas barrier O2 can be diffusion limited

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28
Q

What does diffusion of the blood gas barrier depend on

A

distance in capillary, rate of reaction of hemoglobin with O2, resistance to diffusion
Volume of blood

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29
Q

What are the causes of hypoxemia

A 
V- V/Q Mismatch
F- Low FiO2/ Low PO2 
S- Shunt (R-> L)
H- Hypoventilation
D- Diffusion impairment
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30
Q

What is the mechanism for Hypoventilation to lead to hypoxia

A

Reduced addition of O2 to lungs therefore PO2 decreases.

Normal PAO2 = 100

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31
Q

What is the alveolar gas equation

A

PAO2= PiO2 - (PACO2/r)

= 150 - (PaCO2/0.8)

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32
Q

What are differentials for hypoventilation

A

damage to brainstem/respiratory center; cervical nerve tract damage; obstruction to upper airway. Respiratory muscle damage

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33
Q

What are underlying causes of diffusion impairment

A

Abnormal thickened blood gas barrier
Pulmonary fibrosis
Alttitude- due to decreased parital pressure so will be working on the steep part of the dissociation curve

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34
Q

What is a normal shunt in the body

A

Bronchial arterial blood— small amount

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35
Q

What is the alveolar PO2 with a shunt

A

No improvement with increasing FiO2
Because the alveolar PO2 is already increased at the end capillary but not able to see as reduced when adding the shunted blood back in

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36
Q

What are the determinates of gas exchange in the lungs

A

ventilation and blood flow

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37
Q

What occurs with increasing and decreasing V/Q assuming no diffusion impairement

A

Decreasing V/Q - airway obstruction - alveolar gas will be same as mixed venous gas
Increasing V/Q - capillary obstruction. reach infinity and will get alveolar gas.

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38
Q

Can an area of High V/Q compenasate for an area of low V/Q

A

No. The normal lung attempts to get close but is not able to.

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39
Q

What are the stages of V/Q mismatch

A

0) normal to uneven V/Q
1) Transition: Decrease VO2 and VCO2 leads to decreased Pa O2 and increase PaCO2
2) Steady state: Normal VO2, VCO2 leads to Decreased PaO2 and Increased PaCO2
3) Increase in alveoli ventilation leads to Normal VO2, VCO2 with decreased PaO2 and Normal PaCO2

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40
Q

How do you calculate and assess the A-a gradient

A

PAO2-PaO2 = [150-(PaCO2/0.8)] - PaO2
Normal < 15 mmHg
> 20 mmHg V/Q mismatch

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41
Q

What in the Berlin definition is outdated

A

The requirement for PEEP. As ARDS can be identified in spontaneous breathing people.

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42
Q

How can neuromuscular blockade aid with mechanical ventilation

A

decrease work of breathing, reduce ventilator patient dysynchrony, improve oxygenation, may decrease mortality in severely hypoxemic
Risks deep sedation and residual paralysis
Use early- limit for 24 hrs

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43
Q

What muscles are involved in inspiration

A

Active process
Diaphragm- shortens on contraction and moves ribs out; also leads to increase in ab pressure which forces ribs out
external intercostals

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44
Q

What muscles are involved in expiration

A

Passive
Abodminal most- pushes ab contents in then pushes the diaphragm up make thoracic cavity smaller
Internal IC muscles

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45
Q

What is the pressure volume relationship in the lungs

A

Non linear. At higher pressure lung becomes stiffer and get less volume change

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46
Q

Define historesis

A

The path for inspiration for pressure volume relationship is not the same as expiration (lags behind)
Result of surface tension forces of the air liquid interface in the alveoli

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47
Q

How does the curve change with positive or negative presssure (PV Loop)

A

The pressure difference at a static compliance will remain equal to volume

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48
Q

Define compliance

A

Change in volume/ change in pressure

normal 200 ml/cmH20

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49
Q

What will lead to decrease compliance

A

fibrosis, edema, stiffer lung

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50
Q

What will lead to incrase compliacne

A

emphysema, age,

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51
Q

What is Lapalace law

A

P= (4 xtension)/ r

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52
Q

How does surfacant change the lung, list 3 benifits

A

produced by Type II alveolar epithelial cells
Reduces surface tension of the lungs
increase compliance, increase stability, and decrease tendency alveoli edema

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53
Q

What is the pressure in the pleural space

A

-5 from atmospheric pressure

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54
Q

In laminar flow how does the radius alter resistance

A

inversely proportional to the 4th power of the radius.

If decrease by 1/2 will have increase by 16 fold in resistance

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55
Q

How do small airways contribute to air flow resitence

A

They do not considered silent zone.

Due to the significant area of all the airways together it is not able to be detected

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56
Q

How does airway resistance change as volume increases

A

Decreases. Extra-alveoli vessels and parenchymal pulled open by radial expansion of the lungs. Tensions increase as lung expands

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57
Q

What mechanism occurs in sever airway disease to decrease resistance

A

Maintenance of a high lung volume

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58
Q

What is dynamic compression of airway

A

difference between alveolar and transpulmonary pressure during expiration flow is independent of effort

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59
Q

What is the starling resistor effect

A

alveolar pressure increases with transmural pressure to flow rate will be constant

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60
Q

Indications for permanent tracheostomy

A

Laryngeal paralysis/ collapse, neoplasia, trauma, persistent inflammation/edema of upper airway;
Permenant laryngeal dysfuction

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61
Q

What is the SPO2 absorbance wavelengths

A

Oxygenated hemoglobin 950 nm

Deoxygenated hemoglobin 650 nm

62
Q

What is the normal P/F ratio

A

Should be 5 times the FiO2

63
Q

What are reasons that the A-a gradient may be negative

A

Previous O2 supplementation, air bubble in sample, lab error, transcription air.

64
Q

What is the calculation for PiO2

A 
FiO2 x (atmospheric pressure - water pressure)
Generally at at room air  sea level it is .21 x (713)
65
Q

What is the 120 rule

A

On room air PaCO2 + PaO2 > 120

If less decreased pulmonary function

66
Q

What is the oxygen saturation ratio

A

The ratio of full O2 hemoglobin to the total hemoglobin in the blood capable of binding O2

67
Q

What is the oxygen delivery

A 
DO2= CaO2 x CO
CaO2= Hgb x SaO2x1.34 + (.003 x PaO2)
68
Q

How is central venous oxygen saturation written

A

ScvO2

At the level of the right atrium or central vein

69
Q

What affects oxygen consumption in tissues

A

metabolic rate, non nutrient flow w/ low metabolic exchange, base O2 extraction

70
Q

What is normal SmvO2

A

75% with PO2 40 mmHg

71
Q

What is normal O2 consumption

A
  1. 5 ml/kg/min at rest

81. 6 ml/kg/min at heavy excerise

72
Q

What is the oxygen extraction ration

A

VO2/DO2

73
Q

What reduces the oxygen extraction ration

A

Increased demand: exercise, seizures, inflammation, hyperthermia
Decreased supply: hypovolemia, anemia, lung disease, cardiac dysfunction

74
Q

What are the starling forces in the pleural space

A

Use starling equation and replace hydrostatic pressure with pleural space
Increased capillary hydrostatic pressure or decrease in colloid osmotic pressure leads to increase in fluid production in pleural space

75
Q

How does fever affect clinical supiscion of pyothorax in cats

A

does not… <50% had a fever

76
Q

What are the recommended abx for pyothorax

A

Dogs: Potentiated penicillin and fluorquinolone
Cats: potentiated penicillin alone may be enough

77
Q

What is Boyle’s law

A

P1V1 = P2V2

Volume and pressure of gas increase proportionaly

78
Q

How does HBOT affect dissolved O2

A

Increase from 1 ATA to 2-2.5 leads to increase of 3 fold in O2 disolved at room air.

79
Q

What are benifits of HBOT

A

Intravascular and tissue gas bubble reduction
Improved oxygenation, vasoconstriciton
increased antimicrobial activity
modulate inflammation and immune system

80
Q

What are contraindications to HBOT therapy

A

pneumothorax

81
Q

What are complications of HBOT therapy

A

O2 toxicity (cataracts, myopia)
Barotrauma, seizures, decompression sickness, reactive O2 species generation
Remove metal collars

82
Q

What are factors in the work of breathing

A

Pressure x volume and resistance

If no airway resistence then work of breathing would simply be determined by compliance

83
Q

What are the central controls of breathing

A 
Medulla: dorsal- inspiration, ventral expiration, Pre-botzinger- pattern generator
Pons: apneustic center- excitatory
Pneumotaxic center- inhibitory
Cortex: excerise voluntary control
Limbic system-hypothalmaous- emothional
84
Q

How doe the central receptor of breathing works

A

Ventral part of medulla; Chemoreceptor senses pH changes in the CSF (normal 7.32)
Increased PaCo2 will cause decrease pH (increase H+) in the CSF

85
Q

How does CO2 change the CSF pH

A

H+ and HCO3- can’t move across BBB but CO2 can.
Increase in CO2 will decrease pH.
Buffering ability is less in CSF for a given change in PCO2 will have a large change in pH in the CSF compared to blood

86
Q

How can prolonged hypoventaltion lead to restoration of CSF pH

A

The chorid plexus will restore CSF pH back to normal then will not see as much increased ventilation

87
Q

What are the peripheral receptors for breathing

A

Carotid body via glossypharyngeal (9)
Aortic body via Vagaus (10)
Senses PaO2 changes… high blood flow responds to arterial PO2
Less response to PCO2 (1/5 of central) and pH

88
Q

Why is there not an increased in respiratory rate with carbon monoxoide

A

decrease in dissolved 02, but normal 02 content therefore teh carotid won’t be stimulated

89
Q

What is the increased in breathing in metabolic acidosis mediated by

A

Carotid body

90
Q

What is the hering breuer reflex

A

inflated lungs will hinbit further inspiration
Reflex that prevents further expansion
Negative feedback

91
Q

How do J-receptors in the lung alter breathing

A

Juxta-capillary receptors in teh alveolar wall clos toe capillarys
Rapid shallow breathing
Pulmonary edema and interstitial lung disease

92
Q

What is responsibel for the breath rate over a 24 hr period

A

Level of CO2

Response reduced due to sleep, increased age, training, increased work of breathing

93
Q

What occurs if chronic condition breathing drive is due to low PAO2

A

Give supplemental O2 will increrase PAO2 so drive to breath will actually decrease

94
Q

What is VO2 max

A

The point were above will get energy from anerobic metabolism

95
Q

How does venetilation correlate with O2 consumption during exercise

A

Will increase linerally until a break point

Point where lactate increased rapidly in the periphery

96
Q

What is the FICK O2 consumption equation

A

VO2= Co (CaO2-CmvO2)
Points out why if you increase your ventilation you don’t have to increase your CO as much. The body will accept a lower mixed venoous O2 but will not accept it in the alvoelar

97
Q

How does altitude affect the diassocation curve

A

at high and respiratory alkalosis- to the left

at moderate shift to right

98
Q

What is the goal of a recruitment maneuver

A

Transpulmonary pressure (distending lung pressure) is increased transiently in an effort to open (recurit) collapsed alveoli

99
Q

What are adverse effects of a recruitment maneuver

A

hyemodynamic compromise

alveolar overdistension

100
Q

Describe a recruitment maneuver

A

Must e hemodynamically stable and then increased FiO2 to 100%
1) CPAP at 35-50 cmH20 for 20-40 seconds
2) Pressure control with PEEP. Pressure above PEEP of 20 cmH20 for 1-3 minutes
Post patient must be on adequate peep to maintain

101
Q

What are the indications for mechanical ventilation

A

PaO2 < 60 mmHg (80 in some references) with supplemental O2
PaCO2 > 60 mmHg (PvCO2 ~ 4 mmHg > PaCO2)
Increased work of breathing

102
Q

Define tidal volume

A

Volume of a single breath

103
Q

Define total minute ventilation

A

Tidal volume x RR

104
Q

Define platueau pressure

A

Airway pressure measured at end of inspiratory pause

105
Q

What are the three independent variables in mechanical ventilation determined by the machine

A

Pressure, volume, flow

106
Q

In mechanical ventilation what variabiles are determined by the patient/circuit

A

Compliance and resistance

107
Q

What are the ventilator breath types

A

Madatory- Ventilato controls inhaltation, termination and flow
Spontaneous- Patient controls inhalation, termination and flow
Supported- Pt controls inhalation and termination; venti controls flow
Assisted- patient controls inhalation Vent controls termination and flow

108
Q

What are 4 different types of breath patterns in mechanical ventilation

A

Continuous positive ariway pressure (CPAP) constant level of positive pressure throughout cycle
Continuous mandatory vent: Machine controls all variables
Assisted control: If patient breaths will assist if doesnt breath in certain time will take over
Synchronied intermittent mandatory (SIMV) Will help pt take breath but will not assist breath too frequently

109
Q

What are control variables in mechanical ventilation

A

Volume: Flow and tidal are fixed breath ends at set volume. Peak airway pressure will depend on tidal volume chosen and compliance
Pressure: maintain constant airway pressure. Breath ends at set time. Tidal volume will depend on airway pressure and compliance

110
Q

In mechanical ventilation/breathing how is complicanc

A

change in volume/ change in pressure

111
Q

What are the phase variables in mechanical ventilation

A

Trigger: parameter that initiated breath (time, change in airway pressure, gas flow)
Cycle variable: parameter which inspiration is terminated Often time set by I:E
Limit: parameter which breath can not exceed during inspiration
Baseline variables- controlled during exhalation: PEEP

112
Q

Flow rate in mechanical ventilation

A

40-80 ml/min; generally faster inspiratory time

113
Q

What are negative consequences of PEEP

A 
decrease compliance
increase alveolar dead space
increase pulmonary vascular resistance
Decrease left ventricle compliance
Impaired venous return during expiration
114
Q

What is the general PIP setting

A

Peak inspiratory pressure
Normal 5-15 cmH2o
ARDS may increase to > 30
Barotrauma results if excessive

115
Q

What are the changes of lung protective ventilation strategies

A

Lower tidal volumes, higher peep
Limited plateau pressures
Higher PaCO2 considered permissive in people

116
Q

What are adverse effects of lung protective ventilation strategies

A

Increased ICP, acidemia, PEEP associated cardiovascular compromise

117
Q

What is the overall goal of lung protective ventilation strategies

A

Recruitment of alveoli prevent cyclic opening and closing of alveoli between breaths decreased potential for volutrauma and barotrauma of normal alveoli
Decrease release of inflammatory mediators

118
Q

Write out a lung protective ventilator settings

A 
FiO2 100% 
Tidal Volume 6-9 ml/kg
Inspiratory time 1 sec
RR 15-30 bpm
Pressure above PEEP 10-15 cmH2O
Inspiratory flow 40-60 L/min
I:E 1:2
Minute ventilation 100-250 ml/kg
PEEP 5 cmH2O
Inspiratory trigger 1-2 cm H2O
119
Q

What are initial settings for mechanical ventilation with normal lungs

A 
FiO2 100% 
Tidal Volume 8-12 ml/kg
Inspiratory time 1 sec
RR 12  bpm
Pressure above PEEP 8-10 cmH2O
Inspiratory flow 40-60 L/min
I:E 1:2
Minute ventilation 150-250 ml/kg
PEEP 5 cmH2O
Inspiratory trigger 1-2 cm H2O
120
Q

What anesthetic agent is not recommended for mechanical ventilation

A

Etomidate due to adrenal suppression and hemolytic effect of propylene glycol

121
Q

What are goals to acheive when optimizing mechanical ventilation

A

Maintain art blood gas PaO2 80-120 mmHg
PaCO2 35-50
Least aggressive ventilator settings possible
avoid ventilator complications

122
Q

What are potential cause of hypercapneia with mechanical ventilation

A

Pneumothorax, bronchoconstriction, obstruction, increased deadspace, incorrectly assempled circuite
inadequate tidal volume or respirate
increased pulmonary dead space (PTE)

123
Q

What corrections are made with the ventilaor for hypercapnia

A

If normal breath sounds, rule out obstruction/pronchoconstriction
Inadequate alveolar minute ventilation (RR x tidal volume)- deadspace volume
Adust increase RR, decrease inspiratory time, or increase flow rate

124
Q

What are potential causes of hypoxia during mechanical ventilation

A

Loss of O2 supply; machine circuit malfunction; deterioration of the underlying pulmonary disease
Development of new pulmonary disease

125
Q

What corrections are made to the ventilator settings if hypoxemia is noted

A

If r/o disease as causes

Increase flow rate, inspiratory time, decrease RR; increase FiO2 or PEEP

126
Q

What are causes of low airway pressure alarm with mechanical venitlation

A

Leak, disconnect from circuit

127
Q

What are causes of high airway pressure alarm with mechanical ventilation

A

Decrease pulmonary compliance (pneumothorax, endobronchial intubation)
Obstruction in circuit
Patient ventilator assynchronry

128
Q

What are causes of low tidal volume alarm with mechanical ventilation

A

Leaks, decrease in compliance, increase in resistance, inadequate preset pressure

129
Q

What are causes of high tidal volume alarm with mechanical ventilation

A

Patient initiating inspiration

Increase in compliance

130
Q

In a crashing ventilator patient what should be evaluated

A

DOPE
Displacement- Tube, breath sounds, tidal volume expired vs prescribed
Obstruction: Suction airway, cosnider bronchodilators
Pneumothorax, PEEP, Pain: analyze wave form
Equipment failure: Disconnect and give manual breaths

131
Q

What are cuases of patient ventilator asynchrony

A

breathing against the machine, hypoxemia, and hypercapnia
- Pneumothroax
Full bladder/colon
hyperthemia,
inadeuate ventilator settings or depth of anasethesia

132
Q

On your blood gas in a patient mechanically ventilated what might you see with a pneumothorax

A

rapid increase in PaCo2 and decrease in PaO2

133
Q

Name 4 complications of mechanical ventilation

A

CV compromise- impaired intrathoracic blood flow with CV instability or aggressive vent settings
Ventilator induced lung injury
Ventilator induced pneumonia
Pneumothroax

134
Q

What are the four types of trauma with mechanical ventialtion

A

Barotrauma, volutrauma, atelectrauma and biotrauma

135
Q

What is barotrauma in MV

A

Higher airway pressure

136
Q

What is volutramua in MV

A

High tidal volume, overdistension

137
Q

What is atelectrauma in MV

A

shear and strain of alveoli opening and closing

138
Q

What is biotrauma in MV

A

Damage from release of pro-inflammatory cytokines and immune mediated injury that occurs when lung is exposed to physiologic stress strain

139
Q

When do you wean from mechanical ventilation

A 
Improvement in primary disease
P/F ration 250-300 with FiO2 < 0.5
PEEP < 5 cmH20
Adequate respiratory drive
Hemodynamic stability
abscence of major organ failure
140
Q

What is the difference of sclar vs loops in evaluating mechanical ventilation

A

scalar are parameter vs time (x axis)

Loop is two parameters against each other

141
Q

What does the pressure vs volume loop tell you about

A

compliance

142
Q

What does the flow vs volume loop tell you about in mechanical ventilation

A

Resistance

143
Q

How does a change in compliance shift the loop

A

PV loop
Decreased compliance down and to the right
Increased up and to the left

144
Q

Which loops/scalars to evaluate with pressure control mechanical ventilation

A

Volume scalar
Flow scalar
PV Loop

145
Q

What loops/scalars to evaluate with volume control mechanical ventilation

A

pressure scalar- PIP and plateau pressure
Flow scalar
PV loop

146
Q

What is the mechanism of O2 toxicity

A

Above normal partial pressure O2 oxidative damage to epithelial cells leading to collapse of alveoli 24 hrs at 100% or longer at > 50%

147
Q

What are the 5 phases of O2 toxicity

A

initiated inflammation destruction proliferation scaring

148
Q

What occurs in the initiation phase of O2 toxicity

A

Oxygen derived free radicals (superoxide anion, peroxide, hydroxyl radicals) cause direct damage to pulmonary epithelial cells

149
Q

What occurs in the inflammation phase of O2 toxicity

A

Massive release of inflammatory mediators result in increase tissue permeability and development of pulmonary edema

150
Q

What occurs in the destruction phase of O2 toxicity

A

severe local destruction from the inflammation

Phase with highest mortality

151
Q

What occurs in the proliferation phase of O2 toxicity

A

Type II pneumocytes and monocytes increase

152
Q

What occurs in the scaring phase of O2 toxicity

A

collagen deposition and interstitial fibrosis

Board Review 2020 (37 decks)

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