Respiratory Flashcards

(152 cards)

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
What is Fick's Law of gas diffusion
(Area/Thickness)x Diffusion constant x (P1-P2) Diffusion constant = Solubility/ square root (MW)
26
What is the difference between perfusion limited and diffusion limited gas exchange
Perfusion limited = No difference in end capillary partial pressure of gas for alveolar capillary partital pressure Diffusion If there is a difference
27
What is the limiting factor of O2, CO2, and N20 gas exchange
CO2- diffusion N20 and O2 are perfusion limited If there is pathology to blood gas barrier O2 can be diffusion limited
28
What does diffusion of the blood gas barrier depend on
distance in capillary, rate of reaction of hemoglobin with O2, resistance to diffusion Volume of blood
29
What are the causes of hypoxemia
``` V- V/Q Mismatch F- Low FiO2/ Low PO2 S- Shunt (R-> L) H- Hypoventilation D- Diffusion impairment ```
30
What is the mechanism for Hypoventilation to lead to hypoxia
Reduced addition of O2 to lungs therefore PO2 decreases. | Normal PAO2 = 100
31
What is the alveolar gas equation
PAO2= PiO2 - (PACO2/r) | = 150 - (PaCO2/0.8)
32
What are differentials for hypoventilation
damage to brainstem/respiratory center; cervical nerve tract damage; obstruction to upper airway. Respiratory muscle damage
33
What are underlying causes of diffusion impairment
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
34
What is a normal shunt in the body
Bronchial arterial blood--- small amount
35
What is the alveolar PO2 with a shunt
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
36
What are the determinates of gas exchange in the lungs
ventilation and blood flow
37
What occurs with increasing and decreasing V/Q assuming no diffusion impairement
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.
38
Can an area of High V/Q compenasate for an area of low V/Q
No. The normal lung attempts to get close but is not able to.
39
What are the stages of V/Q mismatch
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
40
How do you calculate and assess the A-a gradient
PAO2-PaO2 = [150-(PaCO2/0.8)] - PaO2 Normal < 15 mmHg > 20 mmHg V/Q mismatch
41
What in the Berlin definition is outdated
The requirement for PEEP. As ARDS can be identified in spontaneous breathing people.
42
How can neuromuscular blockade aid with mechanical ventilation
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
43
What muscles are involved in inspiration
Active process Diaphragm- shortens on contraction and moves ribs out; also leads to increase in ab pressure which forces ribs out external intercostals
44
What muscles are involved in expiration
Passive Abodminal most- pushes ab contents in then pushes the diaphragm up make thoracic cavity smaller Internal IC muscles
45
What is the pressure volume relationship in the lungs
Non linear. At higher pressure lung becomes stiffer and get less volume change
46
Define historesis
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
47
How does the curve change with positive or negative presssure (PV Loop)
The pressure difference at a static compliance will remain equal to volume
48
Define compliance
Change in volume/ change in pressure | normal 200 ml/cmH20
49
What will lead to decrease compliance
fibrosis, edema, stiffer lung
50
What will lead to incrase compliacne
emphysema, age,
51
What is Lapalace law
P= (4 xtension)/ r
52
How does surfacant change the lung, list 3 benifits
produced by Type II alveolar epithelial cells Reduces surface tension of the lungs increase compliance, increase stability, and decrease tendency alveoli edema
53
What is the pressure in the pleural space
-5 from atmospheric pressure
54
In laminar flow how does the radius alter resistance
inversely proportional to the 4th power of the radius. | If decrease by 1/2 will have increase by 16 fold in resistance
55
How do small airways contribute to air flow resitence
They do not considered silent zone. | Due to the significant area of all the airways together it is not able to be detected
56
How does airway resistance change as volume increases
Decreases. Extra-alveoli vessels and parenchymal pulled open by radial expansion of the lungs. Tensions increase as lung expands
57
What mechanism occurs in sever airway disease to decrease resistance
Maintenance of a high lung volume
58
What is dynamic compression of airway
difference between alveolar and transpulmonary pressure during expiration flow is independent of effort
59
What is the starling resistor effect
alveolar pressure increases with transmural pressure to flow rate will be constant
60
Indications for permanent tracheostomy
Laryngeal paralysis/ collapse, neoplasia, trauma, persistent inflammation/edema of upper airway; Permenant laryngeal dysfuction
61
What is the SPO2 absorbance wavelengths
Oxygenated hemoglobin 950 nm | Deoxygenated hemoglobin 650 nm
62
What is the normal P/F ratio
Should be 5 times the FiO2
63
What are reasons that the A-a gradient may be negative
Previous O2 supplementation, air bubble in sample, lab error, transcription air.
64
What is the calculation for PiO2
``` FiO2 x (atmospheric pressure - water pressure) Generally at at room air sea level it is .21 x (713) ```
65
What is the 120 rule
On room air PaCO2 + PaO2 > 120 | If less decreased pulmonary function
66
What is the oxygen saturation ratio
The ratio of full O2 hemoglobin to the total hemoglobin in the blood capable of binding O2
67
What is the oxygen delivery
``` DO2= CaO2 x CO CaO2= Hgb x SaO2x1.34 + (.003 x PaO2) ```
68
How is central venous oxygen saturation written
ScvO2 | At the level of the right atrium or central vein
69
What affects oxygen consumption in tissues
metabolic rate, non nutrient flow w/ low metabolic exchange, base O2 extraction
70
What is normal SmvO2
75% with PO2 40 mmHg
71
What is normal O2 consumption
3. 5 ml/kg/min at rest | 81. 6 ml/kg/min at heavy excerise
72
What is the oxygen extraction ration
VO2/DO2
73
What reduces the oxygen extraction ration
Increased demand: exercise, seizures, inflammation, hyperthermia Decreased supply: hypovolemia, anemia, lung disease, cardiac dysfunction
74
What are the starling forces in the pleural space
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
How does fever affect clinical supiscion of pyothorax in cats
does not... <50% had a fever
76
What are the recommended abx for pyothorax
Dogs: Potentiated penicillin and fluorquinolone Cats: potentiated penicillin alone may be enough
77
What is Boyle's law
P1V1 = P2V2 | Volume and pressure of gas increase proportionaly
78
How does HBOT affect dissolved O2
Increase from 1 ATA to 2-2.5 leads to increase of 3 fold in O2 disolved at room air.
79
What are benifits of HBOT
Intravascular and tissue gas bubble reduction Improved oxygenation, vasoconstriciton increased antimicrobial activity modulate inflammation and immune system
80
What are contraindications to HBOT therapy
pneumothorax
81
What are complications of HBOT therapy
O2 toxicity (cataracts, myopia) Barotrauma, seizures, decompression sickness, reactive O2 species generation Remove metal collars
82
What are factors in the work of breathing
Pressure x volume and resistance | If no airway resistence then work of breathing would simply be determined by compliance
83
What are the central controls of breathing
``` 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
How doe the central receptor of breathing works
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
How does CO2 change the CSF pH
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
How can prolonged hypoventaltion lead to restoration of CSF pH
The chorid plexus will restore CSF pH back to normal then will not see as much increased ventilation
87
What are the peripheral receptors for breathing
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
Why is there not an increased in respiratory rate with carbon monoxoide
decrease in dissolved 02, but normal 02 content therefore teh carotid won't be stimulated
89
What is the increased in breathing in metabolic acidosis mediated by
Carotid body
90
What is the hering breuer reflex
inflated lungs will hinbit further inspiration Reflex that prevents further expansion Negative feedback
91
How do J-receptors in the lung alter breathing
Juxta-capillary receptors in teh alveolar wall clos toe capillarys Rapid shallow breathing Pulmonary edema and interstitial lung disease
92
What is responsibel for the breath rate over a 24 hr period
Level of CO2 | Response reduced due to sleep, increased age, training, increased work of breathing
93
What occurs if chronic condition breathing drive is due to low PAO2
Give supplemental O2 will increrase PAO2 so drive to breath will actually decrease
94
What is VO2 max
The point were above will get energy from anerobic metabolism
95
How does venetilation correlate with O2 consumption during exercise
Will increase linerally until a break point | Point where lactate increased rapidly in the periphery
96
What is the FICK O2 consumption equation
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
How does altitude affect the diassocation curve
at high and respiratory alkalosis- to the left | at moderate shift to right
98
What is the goal of a recruitment maneuver
Transpulmonary pressure (distending lung pressure) is increased transiently in an effort to open (recurit) collapsed alveoli
99
What are adverse effects of a recruitment maneuver
hyemodynamic compromise | alveolar overdistension
100
Describe a recruitment maneuver
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
What are the indications for mechanical ventilation
PaO2 < 60 mmHg (80 in some references) with supplemental O2 PaCO2 > 60 mmHg (PvCO2 ~ 4 mmHg > PaCO2) Increased work of breathing
102
Define tidal volume
Volume of a single breath
103
Define total minute ventilation
Tidal volume x RR
104
Define platueau pressure
Airway pressure measured at end of inspiratory pause
105
What are the three independent variables in mechanical ventilation determined by the machine
Pressure, volume, flow
106
In mechanical ventilation what variabiles are determined by the patient/circuit
Compliance and resistance
107
What are the ventilator breath types
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
What are 4 different types of breath patterns in mechanical ventilation
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
What are control variables in mechanical ventilation
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
In mechanical ventilation/breathing how is complicanc
change in volume/ change in pressure
111
What are the phase variables in mechanical ventilation
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
Flow rate in mechanical ventilation
40-80 ml/min; generally faster inspiratory time
113
What are negative consequences of PEEP
``` decrease compliance increase alveolar dead space increase pulmonary vascular resistance Decrease left ventricle compliance Impaired venous return during expiration ```
114
What is the general PIP setting
Peak inspiratory pressure Normal 5-15 cmH2o ARDS may increase to > 30 Barotrauma results if excessive
115
What are the changes of lung protective ventilation strategies
Lower tidal volumes, higher peep Limited plateau pressures Higher PaCO2 considered permissive in people
116
What are adverse effects of lung protective ventilation strategies
Increased ICP, acidemia, PEEP associated cardiovascular compromise
117
What is the overall goal of lung protective ventilation strategies
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
Write out a lung protective ventilator settings
``` 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
What are initial settings for mechanical ventilation with normal lungs
``` 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
What anesthetic agent is not recommended for mechanical ventilation
Etomidate due to adrenal suppression and hemolytic effect of propylene glycol
121
What are goals to acheive when optimizing mechanical ventilation
Maintain art blood gas PaO2 80-120 mmHg PaCO2 35-50 Least aggressive ventilator settings possible avoid ventilator complications
122
What are potential cause of hypercapneia with mechanical ventilation
Pneumothorax, bronchoconstriction, obstruction, increased deadspace, incorrectly assempled circuite inadequate tidal volume or respirate increased pulmonary dead space (PTE)
123
What corrections are made with the ventilaor for hypercapnia
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
What are potential causes of hypoxia during mechanical ventilation
Loss of O2 supply; machine circuit malfunction; deterioration of the underlying pulmonary disease Development of new pulmonary disease
125
What corrections are made to the ventilator settings if hypoxemia is noted
If r/o disease as causes | Increase flow rate, inspiratory time, decrease RR; increase FiO2 or PEEP
126
What are causes of low airway pressure alarm with mechanical venitlation
Leak, disconnect from circuit
127
What are causes of high airway pressure alarm with mechanical ventilation
Decrease pulmonary compliance (pneumothorax, endobronchial intubation) Obstruction in circuit Patient ventilator assynchronry
128
What are causes of low tidal volume alarm with mechanical ventilation
Leaks, decrease in compliance, increase in resistance, inadequate preset pressure
129
What are causes of high tidal volume alarm with mechanical ventilation
Patient initiating inspiration | Increase in compliance
130
In a crashing ventilator patient what should be evaluated
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
What are cuases of patient ventilator asynchrony
breathing against the machine, hypoxemia, and hypercapnia - Pneumothroax Full bladder/colon hyperthemia, inadeuate ventilator settings or depth of anasethesia
132
On your blood gas in a patient mechanically ventilated what might you see with a pneumothorax
rapid increase in PaCo2 and decrease in PaO2
133
Name 4 complications of mechanical ventilation
CV compromise- impaired intrathoracic blood flow with CV instability or aggressive vent settings Ventilator induced lung injury Ventilator induced pneumonia Pneumothroax
134
What are the four types of trauma with mechanical ventialtion
Barotrauma, volutrauma, atelectrauma and biotrauma
135
What is barotrauma in MV
Higher airway pressure
136
What is volutramua in MV
High tidal volume, overdistension
137
What is atelectrauma in MV
shear and strain of alveoli opening and closing
138
What is biotrauma in MV
Damage from release of pro-inflammatory cytokines and immune mediated injury that occurs when lung is exposed to physiologic stress strain
139
When do you wean from mechanical ventilation
``` 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
What is the difference of sclar vs loops in evaluating mechanical ventilation
scalar are parameter vs time (x axis) | Loop is two parameters against each other
141
What does the pressure vs volume loop tell you about
compliance
142
What does the flow vs volume loop tell you about in mechanical ventilation
Resistance
143
How does a change in compliance shift the loop
PV loop Decreased compliance down and to the right Increased up and to the left
144
Which loops/scalars to evaluate with pressure control mechanical ventilation
Volume scalar Flow scalar PV Loop
145
What loops/scalars to evaluate with volume control mechanical ventilation
pressure scalar- PIP and plateau pressure Flow scalar PV loop
146
What is the mechanism of O2 toxicity
Above normal partial pressure O2 oxidative damage to epithelial cells leading to collapse of alveoli 24 hrs at 100% or longer at > 50%
147
What are the 5 phases of O2 toxicity
initiated inflammation destruction proliferation scaring
148
What occurs in the initiation phase of O2 toxicity
Oxygen derived free radicals (superoxide anion, peroxide, hydroxyl radicals) cause direct damage to pulmonary epithelial cells
149
What occurs in the inflammation phase of O2 toxicity
Massive release of inflammatory mediators result in increase tissue permeability and development of pulmonary edema
150
What occurs in the destruction phase of O2 toxicity
severe local destruction from the inflammation | Phase with highest mortality
151
What occurs in the proliferation phase of O2 toxicity
Type II pneumocytes and monocytes increase
152
What occurs in the scaring phase of O2 toxicity
collagen deposition and interstitial fibrosis