Respiratory Flashcards
What is in the conducting zone of the respiratory tract
Trachea to terminal bronchioles
Anatomical dead space as no gas exchange occurs
What is in the respiratory zone of the respiratory tract
alveolar sacs
cross sectional area is very large
What is the force that moves air from the terminal broncheols to the avleoli
diffusion
Pollutants then get to region as unable to move bast conjuction of respiratory and conducting zone
Does all the tidal volume get to the alveoli
No due to anatomical deadspace
Define total lung capacity
amount (volume) able to breath in during large breath + residual volume
Define residual volume
amount (volume) remaining in the lungs after max exhalation
Define functional residual volume
Volume remaining after a normal breath exhale
What is the best method to calculate alveloar minute ventilation
VCO2/PACO2 x K
- Based that all expired CO2 comes from the alveolar gas
What is the bohr effect in relation to the O2 dissassociation curve
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
What are the axis labels for the O2 disassociation curve
X- PO2
Y- % Hgb saturated
What shifts the O2 diassociation curve to the left and what does that mean
Increase O2 affinity of Hgb (bound more tightly)
Decrease PaCO2, Temp, H+, 23DPG (RBC Metabolism)
What shifts the O2 diassociation curve to the right and what does that mean
Reduced O2 affinity of Hgb
Increase in PaCO2, Temp, H+, 23DPG (RBC metabolism)
Where is the most carbonic anhydrase
RBCs
What are the RBC mechanism for CO2 transport
Dissolved CO2, HCO3-, Carbamino Hgb
How does the solubulity of CO2 compared to O2
CO2 is about 24 times greater than O2.
How does PEEP affect the left side of the heart
Increases afterload
How is the caudal vena cava alter in the abdomen with mechanical ventilation
Increases diameter
Define ARDS
Peracute onset of respiratory distress, severe hypoxemia, bilateral diffuse alveolar infiltrates not causes by left atrial hypertension or hydrostatic pulomonary edema
What are the ARDS P/F ratio cut offs
ARDS = 200 mmHg ALI = 300 mmHg
What is the criteria for ARDS in veterinary medicine
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
What are Known risk factors of ARDs
(SIRS, sepsis, trauma, apsiration, multiple transfusions, adverse drug rx, drowing
What is the henderson-hasselbach equation for bicarb
pH = 6.1 + Log [HCO3- /(0.03 x PCO2)]
pK for bicarb is 6.1
How does hemoglobin effect buffering
More = increased buffering effect
Define base excess
measure of the amount of bicarbonate added to get to a normal pH at a normal temperatures
What is Fick’s Law of gas diffusion
(Area/Thickness)x Diffusion constant x (P1-P2)
Diffusion constant = Solubility/ square root (MW)
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
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
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
What are the causes of hypoxemia
V- V/Q Mismatch F- Low FiO2/ Low PO2 S- Shunt (R-> L) H- Hypoventilation D- Diffusion impairment
What is the mechanism for Hypoventilation to lead to hypoxia
Reduced addition of O2 to lungs therefore PO2 decreases.
Normal PAO2 = 100
What is the alveolar gas equation
PAO2= PiO2 - (PACO2/r)
= 150 - (PaCO2/0.8)
What are differentials for hypoventilation
damage to brainstem/respiratory center; cervical nerve tract damage; obstruction to upper airway. Respiratory muscle damage
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
What is a normal shunt in the body
Bronchial arterial blood— small amount
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
What are the determinates of gas exchange in the lungs
ventilation and blood flow
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.
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.
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
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
What in the Berlin definition is outdated
The requirement for PEEP. As ARDS can be identified in spontaneous breathing people.
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
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
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
What is the pressure volume relationship in the lungs
Non linear. At higher pressure lung becomes stiffer and get less volume change
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
How does the curve change with positive or negative presssure (PV Loop)
The pressure difference at a static compliance will remain equal to volume
Define compliance
Change in volume/ change in pressure
normal 200 ml/cmH20
What will lead to decrease compliance
fibrosis, edema, stiffer lung
What will lead to incrase compliacne
emphysema, age,
What is Lapalace law
P= (4 xtension)/ r
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
What is the pressure in the pleural space
-5 from atmospheric pressure
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
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
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
What mechanism occurs in sever airway disease to decrease resistance
Maintenance of a high lung volume
What is dynamic compression of airway
difference between alveolar and transpulmonary pressure during expiration flow is independent of effort
What is the starling resistor effect
alveolar pressure increases with transmural pressure to flow rate will be constant
Indications for permanent tracheostomy
Laryngeal paralysis/ collapse, neoplasia, trauma, persistent inflammation/edema of upper airway;
Permenant laryngeal dysfuction
What is the SPO2 absorbance wavelengths
Oxygenated hemoglobin 950 nm
Deoxygenated hemoglobin 650 nm
What is the normal P/F ratio
Should be 5 times the FiO2
What are reasons that the A-a gradient may be negative
Previous O2 supplementation, air bubble in sample, lab error, transcription air.
What is the calculation for PiO2
FiO2 x (atmospheric pressure - water pressure) Generally at at room air sea level it is .21 x (713)
What is the 120 rule
On room air PaCO2 + PaO2 > 120
If less decreased pulmonary function
What is the oxygen saturation ratio
The ratio of full O2 hemoglobin to the total hemoglobin in the blood capable of binding O2
What is the oxygen delivery
DO2= CaO2 x CO CaO2= Hgb x SaO2x1.34 + (.003 x PaO2)
How is central venous oxygen saturation written
ScvO2
At the level of the right atrium or central vein
What affects oxygen consumption in tissues
metabolic rate, non nutrient flow w/ low metabolic exchange, base O2 extraction
What is normal SmvO2
75% with PO2 40 mmHg
What is normal O2 consumption
- 5 ml/kg/min at rest
81. 6 ml/kg/min at heavy excerise
What is the oxygen extraction ration
VO2/DO2
What reduces the oxygen extraction ration
Increased demand: exercise, seizures, inflammation, hyperthermia
Decreased supply: hypovolemia, anemia, lung disease, cardiac dysfunction
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
How does fever affect clinical supiscion of pyothorax in cats
does not… <50% had a fever
What are the recommended abx for pyothorax
Dogs: Potentiated penicillin and fluorquinolone
Cats: potentiated penicillin alone may be enough
What is Boyle’s law
P1V1 = P2V2
Volume and pressure of gas increase proportionaly
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.
What are benifits of HBOT
Intravascular and tissue gas bubble reduction
Improved oxygenation, vasoconstriciton
increased antimicrobial activity
modulate inflammation and immune system
What are contraindications to HBOT therapy
pneumothorax
What are complications of HBOT therapy
O2 toxicity (cataracts, myopia)
Barotrauma, seizures, decompression sickness, reactive O2 species generation
Remove metal collars
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
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
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
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
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
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
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
What is the increased in breathing in metabolic acidosis mediated by
Carotid body
What is the hering breuer reflex
inflated lungs will hinbit further inspiration
Reflex that prevents further expansion
Negative feedback
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
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
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
What is VO2 max
The point were above will get energy from anerobic metabolism
How does venetilation correlate with O2 consumption during exercise
Will increase linerally until a break point
Point where lactate increased rapidly in the periphery
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
How does altitude affect the diassocation curve
at high and respiratory alkalosis- to the left
at moderate shift to right
What is the goal of a recruitment maneuver
Transpulmonary pressure (distending lung pressure) is increased transiently in an effort to open (recurit) collapsed alveoli
What are adverse effects of a recruitment maneuver
hyemodynamic compromise
alveolar overdistension
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
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
Define tidal volume
Volume of a single breath
Define total minute ventilation
Tidal volume x RR
Define platueau pressure
Airway pressure measured at end of inspiratory pause
What are the three independent variables in mechanical ventilation determined by the machine
Pressure, volume, flow
In mechanical ventilation what variabiles are determined by the patient/circuit
Compliance and resistance
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
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
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
In mechanical ventilation/breathing how is complicanc
change in volume/ change in pressure
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
Flow rate in mechanical ventilation
40-80 ml/min; generally faster inspiratory time
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
What is the general PIP setting
Peak inspiratory pressure
Normal 5-15 cmH2o
ARDS may increase to > 30
Barotrauma results if excessive
What are the changes of lung protective ventilation strategies
Lower tidal volumes, higher peep
Limited plateau pressures
Higher PaCO2 considered permissive in people
What are adverse effects of lung protective ventilation strategies
Increased ICP, acidemia, PEEP associated cardiovascular compromise
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
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
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
What anesthetic agent is not recommended for mechanical ventilation
Etomidate due to adrenal suppression and hemolytic effect of propylene glycol
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
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)
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
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
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
What are causes of low airway pressure alarm with mechanical venitlation
Leak, disconnect from circuit
What are causes of high airway pressure alarm with mechanical ventilation
Decrease pulmonary compliance (pneumothorax, endobronchial intubation)
Obstruction in circuit
Patient ventilator assynchronry
What are causes of low tidal volume alarm with mechanical ventilation
Leaks, decrease in compliance, increase in resistance, inadequate preset pressure
What are causes of high tidal volume alarm with mechanical ventilation
Patient initiating inspiration
Increase in compliance
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
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
On your blood gas in a patient mechanically ventilated what might you see with a pneumothorax
rapid increase in PaCo2 and decrease in PaO2
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
What are the four types of trauma with mechanical ventialtion
Barotrauma, volutrauma, atelectrauma and biotrauma
What is barotrauma in MV
Higher airway pressure
What is volutramua in MV
High tidal volume, overdistension
What is atelectrauma in MV
shear and strain of alveoli opening and closing
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
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
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
What does the pressure vs volume loop tell you about
compliance
What does the flow vs volume loop tell you about in mechanical ventilation
Resistance
How does a change in compliance shift the loop
PV loop
Decreased compliance down and to the right
Increased up and to the left
Which loops/scalars to evaluate with pressure control mechanical ventilation
Volume scalar
Flow scalar
PV Loop
What loops/scalars to evaluate with volume control mechanical ventilation
pressure scalar- PIP and plateau pressure
Flow scalar
PV loop
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%
What are the 5 phases of O2 toxicity
initiated inflammation destruction proliferation scaring
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
What occurs in the inflammation phase of O2 toxicity
Massive release of inflammatory mediators result in increase tissue permeability and development of pulmonary edema
What occurs in the destruction phase of O2 toxicity
severe local destruction from the inflammation
Phase with highest mortality
What occurs in the proliferation phase of O2 toxicity
Type II pneumocytes and monocytes increase
What occurs in the scaring phase of O2 toxicity
collagen deposition and interstitial fibrosis
