Apex- Respiratory Pathophys Flashcards
Chemicals that contribute to increased airway resistance (select 3):
- nitric oxide
- inositol tirphosphate
- vasoactive intestinal peptide
- phospholiapase C
- leukotrienes
- cyclic AMP
- inositol triphosphate
- phospholiapse C
- leukotrienes
Bronchoconstriction is mediated by what 2 things?
What about bronchodilation?
Bronchoconstriction:
1. PNS:
- CNX >ACH > muscarinic-3 receptor (GQ > phospholipase C > IP3 >CA+ release from SR> Myosin light-chain kinase activation> contraction)
2. The immune response:
- Histamine, leukotrienes, mast cells, ect
Bronchodilation:
1. Circulating catecholamines
- Epi, NE > B2 receptor (GS) > activates adenylate cyclase > cAMP (2nd mes) > DECREASED release of CA+ from SR > bronchodilation
2. VIP receptor (nitric oxide pathway)
- Nitric oxide - potent smooth muscle relaxant
- non-cholinergic PNS nerves release VIP (Vasoactive intestinal peptide) onto airway smooth muscle > increase NO > activates cGMP > smooth muscle relaxation and bronchodilation.
What turns off the adenylate cyclase > cAMP > decreased CA+ release from SR > bronchodilation pathway?
How?
PDE III
*deactivates cAMP by converting it to AMP
What cranial nerve supplies parasympathetic innervation to the airway smooth muscle?
With all other things being equal, what part of the airway has the most significant contribution to airflow resistance?
Radius
(R^4)
T/F: there are NO sympathetic nerve endings in the airway smooth muscle
True
Instead, B2 receptors embedded in the airway smooth muscle are activated by catecholamines in the systemic circulation (ok?)
Match the drug with it’s corresponding drug glass
- Theophylline:
- Zafirlukast:
- Cromolyn:
- Triamcinolone:
Corticosteroid, Leukotriene modifier, Methylxanthine, Mast cell stabilizer
- Theophylline: Methylxanthine
- Zafirlukast: Leukotriene modifier
- Cromolyn: Mast Cell stabilizer
- Triamcinolone: Corticosteroid
2 anesthetic agents with bronchodilating properties
volatile anesthetics and ketamine
Pulmonary medications can be broken down into what 3 classes?
- Direct acting Bronchodilators
-
Beta 2 agonists = albuterol, metaproterenol, salmeterol
- B2 stimulation → increased cAMP → decreased CA+
-
Anticholinergics = atropine, glycopyrrolate, ipratropium
- M3 antagonism = decreased IP3 → decreased CA+
- Anti-inflammatories
-
Inhaled corticosteroids: beclomethasone, fluticasone, triamcinolone
- Stimulates intracellular steroid receptors
- Regulates inflammatory protein synthesis
- Stimulates intracellular steroid receptors
-
Cromolyn
- Mast cell stabilizer → decreased release of mediators
-
Leukotriene modifiers: zileuton, montelukast
- Inhibits 5-Lipoxygenase enzyme → decreased leukotriene synthesis
- Methylxanthines
- Theophylline
- Inhibits phosphodiesterase (PDE) (usually turns off cAMP pathway) → increased cAMP → increased release of endogenous catecholamines to stimulate B2
What PFT is the MOST sensitive indicator of small airway disease?
- Forced expiratory volume in 1 second
- Forced expiratory flow 25-75%
- Forced vital capacity
- diffusion capacity of carbon monixide (DLCO)
-Forced expiratory flow 25-75%
The average forced expiratory flow during the middle half of the FEV measurement.
Normal FEV 1
>80% of predicted value
Normal FEV1/FVC ratio value
>75-80% of the predicted value
What does FEV1 measure
the volume of air that can be exhaled after a maximal inhalation over 1 second
(>80% predicted volume)
What does Forced Vital Capacity (FVC) measure?
Normal volumes for males/females
The volume of air that can be exhaled after a maximal inhalation
Male= 4.8 L
Female = 3.7L
(can we just say 3.8 to make it easier?)
What does the FEV1 to FVC ratio compare?
What is it useful for
the volume of air expired in 1 second and the total volume of air expired
useful in diagnosing obstructive vs restrictive disease
Normal = 75-80% of predicted value
< 70% suggests obstructive disease (have a problem getting air out)
normal in restrictive disease (no problem getting air out, but problem getting it in, but the small amount they take in is the same amount they can exhale)
FEV1/FVC of < 70%
obstructive disease
What does Forced Expiratory Flow at 25-75% vital capacity measure?
(FEF25-75%)
how does it measure in obstructive vs restrictive disease?
Normal Value
AKA
Measures airflow in the middle of FEV
- reduced with obstructive disease (prob getting air out)
- normal with restrictive disease (no prob getting air out)
normal = 100 +/- 25% predicted value (whatever the hell that means)
AKA- Mid-Maximal Expiratory Flow Rate (MMEF)
What does the Maximum Voluntary Ventilation (MMV) Measure?
The maximum volume of air that can be inhaled and exhaled over the course of 1 minute
- Male = 140-180
- Female = 80-120
What is the best test of endurance?
Maximum Voluntary Ventilation (MMV)
max volume of air that can be inhaled and exhaled over the course of 1 minute
What does DLCO (diffusing capacity) measure?
How is it measured?
What law?
Normal Value?
the ability of the alveolocapillary membrane to exchange gas
- CO ususally used to measure this
- Ficks law
- normal value 17-25ml/min/mmHg
How does restrictive disease affect the FEV1/FVCC ratio?
It’s usually normal
What do flow-volume loops allow us to differentiate between?
obstructive and restrictive respiratory diseases
What’s ABC&D
A- Exhalation
B- Inhalation
C- Total Lung capacity
D- Residual volume
All of the following are independent ris kfactors for postop pulmonay complications EXCEPT:
- Age >65yo
- COPD
- CHF
- Asthma
Asthma
What 3 things alone are not shown to be indepedent predictors of postop pulm complications?
- Asthma
- PFTs/ABGs
- Obestiy
What are the 4 C’s and 4 S’s of risk of postop pulmonary complications?
Class 3 ASA
Cigg smoking
CHF
COPD
Sixty or older
Serum albumin <3.5 (malnutrition)
Surgery duration > 2.5 hours
Surgical site: uppder abd/thorax/peripheral vascular
Serum albumin less than what puts patient at risk for postop pulmnary complications?
< 3.5g/dL
How long should patients stop smoking before surgery?
6 weeks
What is the t 1/2 life of carbon monoxide?
4-6 hours
After you stop smoking, how long until P50 returns to normal?
12 hours
(reduction in carboxyhemoglobin > improved P50 [but does not reduce risk of postop pulm complications])
2 ways to reverse anesthesia-induced atelectasis
1. ARMs
*PIP to 40cm H20 for 8 seconds
2. Use the lowest FiO2 the patient will tolerate
(high FiO2 contributes to absorption atelectasis)
What blood test indicates a higher risk of postop pulmonary complications?
Serum Albumin < 3.5
A patient with severe kyphoscoliosis is expected to have a reduced: select 2:
- FEV1/FVC ratio
- FRC
- FEF 25%-75%
- FEV1
-FRC & FEV1
- restrictive lung disease - all volumes are decreased
- since TLC is smaller , there is less volume to exhale , so the FEV1/FVC ratio is usually unchanged (they can get out what they bring in) but the FEV1 will be decreased bc they are taking in decreased volumes
- the FEF 25-75% is sensitive to increased air flow resistance in the small airways; not a problem for those with restrictive lung disease
How does obstructive disease affect the following:
FEV1, FEV, FEV1/FVC ratio
FEV1 & FEV - normal or decreased
FEV1/FVC ratio always decreased (they cant get out what they brought in)
How are the following affected with restrictive disease:
FEV1, FVC, FEV1/FVC ratio
FEV1 and FVC are decreased (taking in and expiring small volumes bc they cant get air in)
FEV1/FVC ratio is NORMAL (they can exhale everything they take in)
T/F- Obstructive disease is characterised by small airway obstruction
True
Small airway obstruction & increased resistance to expiratory flow
Problem = getting air out
How is compliance in someone with restricitive disease?
decreased
Identify each
Blue = obstructive (icream cone, left shift)
- Someone took a bite of my icecream cone (COPD)
Red = fixed (rock)
- Someone smashed my icecream cone; it needs to be fixed
Green = Normal
Purple = Restrictive (narrow, shift right)
- On a restrictive diet, you’ll have to eat a smaller ice cream cone
What kind of obstructions do these loops represent
1. Extrathoracic
- pt inhales, airway colllapses, reduces flow being inhaled
- pt exhales and pushes the obstruction open; flow out is normal
- Inspiratory limb is flat in an Extrathoracic obstruction
2. Intrathoracic
- pt inhales, pulls open the obstruction; flow going in = normal
- pt exhales, airway collapses; flow going out = reduced
- Expiratory limb is flat in the Intrathoracic obstruction
A patient with astham expereinces bronchospasm immediately following tracheal intubation. This is most likely the result of:
- mast cell degranulation
- decreased sympathetic tone
- histamine release
- vagal stimulation
Vagal Stimulation
- Bronchospasm can be due to direct PNS stimulation OR consequence of an immune response (mast cell degranulation)
- intubation does not cause an immune response; however, it can activate vagal afferents leading to bronchospasm
What is defined by an acute, resversible airway obstruction that is accompanied by chronic airway inflammation and bronchial hyperreactivity?
Asthma
What is the greatest risk factor for developing asthma?
Atopy
-the condition of being “hyper-allergic”
What’s to be noted about FEV1, FEV1/FVC ratio, and FEF25-75% in the astmatic?
They are all reduced but will improve following bronchodilator therapy (asthma = reversible)
What is the most common ABG finding in the asthmatic and why?
What would suggest impending respiratory failure?
Resp. Alkalosis with hypocarbia
Hypercarbia would suggest impending respiratory failure due to air trapping and respiratory muscle fatigue
5 Histamine releasing agents that should be avoided in the asthmatic patient (mneumonic)
MMAST
Morphine
Meperidine
Atracurium
Sux
Thiopental
(mast cells implicated in immune response)
What might an EKG show during a severe asthma attack?
Right ventricular strain with right axis devation due to the increased pulm vasc resistance increasing the workload of the right heart
T/F: during an asthma attack, tachypnea and hyperventilation are the result of hypoxemia
FALSE
-result of neural reflexes
(whatever the hell that means)
PFTs are not predictive of postop pulm complications. What is the exception to this?
lung reduction surgery
T/F - a flow volume loop where the inspiratory or expiratory portion of the loop is flat suggests that wheezing is cuased by asthma.
FALSE
-suggesting wheezing is a reslt of uppper airway obstruction (tracheal stenosis or foregin body)
What will an asthma CXR show
hyperinflated lungs with diaphragmatic flattening
How should you adjust vent settings for an asthamatic
-limit inspiratory time, prolong expiratory time
& tolerate moderate permissive hypercapnia
What does stimulation of presynaptic H2 receptors result in?
decreased histamine release
(H2 blockers [famotidine and ranitidine] can allow for unopposed H1 stimulation which can produce bronchospasm) - risk is very low though but hey, why not know it
What’s the problem with giving a beta-2 agonist to an asthmatic pregnant patient?
beta-2 agonists relax the uterus which can slow the progression of labor and lead to post-delivery bleeding .
What drug used to stop uterine bleeding in the OR can cause bronchoconstriction in asthmatics?
By what mechanism?
Carboprost (Hemabate)
-it mimics the action of F2 alpha prostaglandin …. great
Would you want to keep asthmatics on the drier side or hydrated side in terms of giving IV fluids
hydrated side to reduce the viscosity of airway secretions
What 4 things would indicate intraop bronchospasm
- Wheezing
- Decreased breath sounds
- Increased PIPs (increased plats)
- increased alpha angle on ETCO2
Treatment for acute bronchospasm: 6 key steps + 2 more
1. 100% FIO2
2. Deepen anesthetic (crank up gas and give propofol)
3. Albuterol
4. Ipratropium
5. Epi 1mcg/kg IV
6. Hydrocortisone 2-4mg/kg IV
- Aminophylline
- Helium-oxygen gas mixture
Alpha-1 antitrypsin deficiency: (select 2):
- increases risk of bronchospasm
- caues panlobular emphysema
- can be treated with IgG
- is the most common metabolic disease affecting the liver
- increases risk of bronchospasm
-caues panlobular emphysema
-can be treated with IgG
-is the most common metabolic disease affecting the liver
Treatment for Alpha-1 antitrypsin deficiency
liver transplant
What is alpha-1 antitrypsin deficency casue an increase in?
alveolar protease activity > an enzyme that degrades pulmonary connective tissue and leads to the development of panlobular emphysema.
How can you minimize the risk of oxygen-induced hypercapnia in the patient with severe COPD?
Titrate the FiO2 to maintain SaO2 between 88-92%
-Why would you see hypercarbia in a COPD patient receiving O2 therapy? and don’t say because o2 decreases their hypoxic drive to breathe
(How many times have you given o2 to a COPD patient and they stop breathing? never. )
- What does happen is O2 is a very potent pulmonary vasodilator, so if you give them oxygen your going to inhibit their HPV and worsen VQ matching
- your going to have blood going to non-ventilated alveoli which will increase CO2 bc it cant be dropped off at these non-ventilated alveoli to be exhaled
2. Haldane effect- hemoglobin that’s not bound to oxygen will bind hydrogen ions ; so when you give supplemental o2, the hgb kicks off the hydrogen ions and picks up the o2; the excess H+ ions will bind bicarbonate and produce more CO2
How is chronic bronchitis defined?
Cough + sputum production for more than 3 months for 2 consecutive years
What spirometry test is diagnositic of COPD
An FEV1/FVC ratio of < 70% after bronchodilator therapy
If oxygen therapy can cause hypercapneia in the COPD patient, what is the best practice in treating hypoxia?
O2 titrated to maintain a sat of 88-92%
Identify the MOST appropriate stategy for mechanical ventilation in the patient with COPD
- I:E ratio of 1:1
- Fio2 < 50%
- RR 7bpm
- TV 10-12ml/kg
RR 7bpm
Vent setting benificial to COPD:
I:E ratio:
Inspiratory flow:
FiO2:
RR:
TV:
PEEP? - why or why not
I:E ratio: increased (1:2.5-3 to allow more air to be exhaled)
Inspiratory flow: slow (improve VQ matching)
FiO2: adjusted to maintain SpO2 88-92% (avoid oxygen induced hypercapnia)
RR: slow- allows for increased expiratory times between breaths
TV: small (6-8ml/kg) to minimize risk of hyperinflation and PEEP to keep the small airways open instead of collapsing
neuraxial anesthesia should not be considered for COPD patients if a sensory blockade > ____ is required
T6
What block should be avoided in the COPD patient and why
interscalene block bc it causes paralysis of the ipsilateral hemidiaphagm
T/F: all halogenated agents are bronchodilators
True (sevo and iso are better than des)
The COPD patient should receive a volatile agent with a (high/low) blood:gas solubility.
Why?
low
to minimize postop resp depression- fast on fast off.
A patient with COPD is mechanically ventilated. Which interventions will improve this condition? What is this condition?
- increase I-time
- Decrease RR
- Disconnect the circuit
- Increase inspiratory flow
- Decrease RR
- Disconnect the circuit
*Breath stacking (AKA dynamic hyperinflation)
Increasing inspiratory time is another way of saying
reducing expiratory time
What does inspiratory flow determine
How fast the tidal volume is delivered to the patient
All of the following are examples of restrictive lung disease EXCEPT:
- sarcoidosis
- cystic fibrosis
- negative pressure pulmonary edema
- flail chest
Cystic Fibrosis
It’s an autosomal recessive genetic disorder than affects chloride channels.
-Excessive pulmonary secretions plug the airways and create an obstructive ventilatory defectl
What is diagnostic of restrictive lung disease?
FEV1 and FVC <70% with a normal FEV1/FVC ratio
Ventilatory strategies for the restrictive lung disease patient:
TV:
RR:
PIP:
I:E ratio:
TV: 6ml/kg IBW
RR: faster, 14-18BPM
PIP: < 30cm H20 (significant risk of barotrauma)
I:E ratio: 1:1 (increase inspiratory time by decreasing expiratory time; less time expiring = more time to inhale)
Your patient has restrictive lung disease, what is one of your main concerns-re:induction
that they have decreased FRC and will desat fast on you on induction
All of the following reduce the incidence of ventilator-associated pneumona EXCEPT:
- oropharyngeal decontamination
- minimizing duration of mechanical ventilation
- limited sedation
- proton pump inhibitors
- PPIs
- they increased gastric pH which provides an enviornment for bacteria to flourish; microaspiration can introduce these bacteria into the lungs
When does aspiration most commonly occur?
During induction and intubation or within 5 minutes of extubation.
Risk fators for mendelson’s syndrome and what is it?
Gastic pH < 2.5
gastric volume > 25mls (0.4ml/kg)
-it’s a chemical aspiration pneumonitis
Do patients who aspirate have to be admitted overnight?
No, but they must be observed for 2 hours after aspiration event and can be discharged home only if there is no:
- new cough/wheeze
- cxr evidence of injury
- SpO2 decrease > 10% of preop values on RA
- A-a gradient > 300mHg
Hallmark sign of aspriation pneumonitis
Hypoxemia
When are antibiotics indicated after an aspiration event?
only if the patient develops a fever or increased WBC count > 48 hours
2 most common culprits of VAP
Pseudomonas aeruginosa and S. aureus
What is the first-line treatment for this patient?
A. Chest tube insertion
B. 14g angiocath insertion at 2nd intercostal space, midclavicular line
C. pericardiocentesis
D. Cardiopulmonary resusitation
B. 14g angiocath insertion at 2nd intercostal space, midclavicular line
(emergency treatement for tension PTX)
-chest tube insertion is definitive treatment as all the angiocath does is release the tension and improve hemodynamic instability - does not relieve the underlying ptx
A chest ultrasound that reveals lack of lung sliding and the absence of comet tails indicates what
tension PTX
other place you can shove a 14g angiocath other than 2nd intercostal space mid-clavicular line
4th-5th intercostal space at the anterior axillary line
Treatment of flail chest
pain reducing measures (epidural or intercostal nerve blocks)
-some patients may require mechanical ventilation and surgical fixation
With an open pneumothorax, does the lung collapse on inspiration or expiration
inspiration
tx = occlusive dressing that does not let air in but allows air to escape, o2, chest tube , possibly intubation
Which 3 blocks are associated with a risk for PTX?
Supraclavicular, interscalene, intercostal
Blood:gas partition coefficient of nitrous oxide vs nitrogen. Importance?
Nitrous oxide = 0.47
nitrogen = 0.014.
*Nitrous oxide is 34x more soluble in blood than nitrogen
75% Nitrous oxide can double the size of a PTX in ____minutes.
10
The thoracic duct empties lymph into where?
The left subclavian vien
Key characteristic of flail chest
paradoxical movement of the chest wall at the site of rib fractures
What happens with the non-injured vs injured ribs during inspiration and exhalation for flail chest
okay so inspiration = negative intrathoracic pressure, injured ribs get sucked in and normal ribs expand out as per usual (mediastinum shifts to contralateral side)
expiration = postive intrathoracic pressure; injured ribs move outward due to the postive pressure; normal ribs move inward as per usual (mediastinum shifts to ipsilateral side)
[think mediastimum follows injured ribs]
Order the monitors of VAE accordign to their relative sensitivities (1 = most sensitive, 4 = least sensitive):
transesophageal echocardiography, precordial doppler, ETCO2, CVP
#1 = TEE
2- precordial doppler
3 - EtCO2
4 - CVP
What does the presence of a mill wheel murmer on precordial doppler indicate?
VAE
What would you see hemodynamically for VAE? (4)
- End tidal would drop off (air embolus blocking blood from getting to alveoli for CO2 to be exhaled)
- Hypotension (blood cant get through the lungs > LV > systemic = decreased CO)
- tachycardia to try and get more volume through
- hypoxia- no blood can get through to pick up o2
Treatment for VAE: (4)
- 100% FIO2
- Flood surgical field
- D/C insufllation if applicable
- Durant maneuver (left lateral decub position)
What is the durant maneuver and when should it be utlized?
left lateral decub position ; VAE
A patient with pulmonary HTN develops TR, which treatments MOST likely will improve the patient’s condition? (Select 3)
- Hypothermia
- Nitric Oxide
- Nitroglycerine
- Nitrous Oxide
- PEEP
- Hyperventilation
Hyperventilation (Blow off CO2)
Nitric Oxide
Nitroglycerine
What 3 things is PVR reduced by?
- hyperventilation
- Nitric oxide
- Nitroglycerine
What 5 things is PVR increased by?
Hypoxia
Hypercarbia/Acidosis
Hypothermia
Nitrous oxide
PEEP
Pulmonary artery hypertension is defined as a mean PAP > _____mmHg
mean PAP > 25mmHg
Formula for PVR
+ normal values
(mean PAP - PAOP)
/ *80
CO
150-250 dynes/sec/cm^5
Why should you treat hypotension aggressively in the patient with pulmonary hypertension
Because CO is relatively fixed and dependent on preload
increase PVR = less amount of blood able to get to left heart to be expelled
Why is epidural favored over spinal for someone with pulm htn
bc they are preload dependent and a slow sympathectomy is best
Drug of choice to reduce preload in the pregnant mother with pulmonary htn having contractions
(contractions > increased preload > may worsen PAH and RV function)
Nitroglycerine
Increase or decrease PVR:
CCBs
decrease
(less calcium in vascular smooth muscle = dilation)
Increase or decrease PVR:
hypothermia
increases PVR
=cold = clamp down
Increase or decrease PVR:
PEEP
Increases PVR
(don’t shove easter PEEPs in the pulmonary vasculature)
Carbon Monoxide:
A. Shifts the oxyhemoglobin dissociation curve to the right
B. Production is highest with isoflurane
C. Binds to the oxygen binding site on hemoglobin with an affinity 200x that of oxygen
D. Poisioning is reversed with methylene blue
C. Binds to the oxygen binding site on hemoglobin with an affinity 200x that of oxygen
what 3 populations are at risk for carboxyhemoglobinemia
- burn victims
- smokers
- those exposed to desiccated soda lime
What is required for the diagnosis of carboxyhemolobinemia?
A co-oximeter
…whatever the fuck that is
T/F: oxygen administration is the treatment for carboxyhemoglobinemia
True
hyperbaric o2 therapy may also be required
When soda lime is desiccated, the risk of carbon monoxide formation is greatest with which volatile anesthetic?
Des > Iso >>> Sevo
Oxygen therapy should be continued until CoHgb is < ___% for ____hrs.
<5% for 6 hours
Hyperbaric oxygen is indicated if CoHgb exceeds ____% or if the patient is symptomamtic
>25%
Sodalime is hydrated to ____ - _____ %
13-15%
What are the strongest indications for intubation and mechanical ventilation?/ (Select 2)
- PaCO2 > 60mmHg
- Vital capacity 25ml/kg
- Inspiratory force <25cm H20
- RR 35BMP
- PaCO2 > 60
- Inspiratory force <25cm H20
*vital capacity <15ml/kg
*RR >40bpm
*keep in mind that no single variable indicates the need for intubation and mechanical ventilation
Drugs that can be given via ETT (+mneumoic)
NAVEL
Narcan
Atropine
Vasopressin
Epi
Lidocaine
3 absolute indications for one-lung ventilation
- Bronchopleural fistula
- Pulmonary infection
- massive hemorrhage
What are the 3 best predictors of postop pulmonary complications for patietns undergoing pulmonary surgery?
Instances a right-sided tube would be used
left main bronchus is distorted (tumor/TAA)
Ideal DLT sizing for males vs females
female = 35-37F
male = 39-41F
double lumen tube should not be used for children under what age?
So what would you do?
kids under 8
-bronchial blocker or single lumen tube into the main bronchus
If VO2 max is not available preop for lung surgery, what can you do?
Ask the patient if they can climb 2 flights of steps without stopping
if no, pt is at risk
Insertion depth for a DLT; males vs females
females = 27cm
males = 29cm
(think females 37tube @ 27cm; males 39tube @ 29cm)
You placed a left-sided DLT and clamped the tracheal lumen. Match the complication of tube position with the region where breath sounds will be heard
- DLT in too far:
- DLT tip in trachea:
- DLT too far in on right side:
with
-Right breath sounds absent, left and right breath sounds heart, left breath sounds absent
-DLT in too far on left side: Right breath sounds absent
-DLT tip in trachea: Left and Right breath sounds heard
-DLT too far in on right side: Left breath sounds absent
In the anesthetized lateral decub position, where is alveolar ventilation vs perfusion better?
How does this compare to the awake lateral decub position patient?
aleveolar ventilation better in nondependent lung
persuion better in dependent lung
In the awake lateral decub patient; VQ matching is preserved
- Not preserved with GA on board bc GA reduces lung volumes and diaphragmatic excursion is better on the dependent side
1 lung ventilation, Ideal:
Vent mode:
TV:
RR:
FiO2:
*What are you going to do before starting OLV?
Vent mode: PC with ideal PIP < 20cm H20 above PEEP
TV: 6mL/kg of IBW
RR: 12-15 to maintain PaCO2 35-45 (permissive hypercanpia ok as long as pt isnt sensitive to a rise in PVR)
*Do an ARM before starting OLV
Why would it be important to do serial ABGs after starting OLV?
Bc once the SpO2 reaches 100%, then the PaO2 could be either 100 or 500mmHg and you wont know without an ABG
What poses a higher risk of hypoxemia during OLV, ventilating the right or left lung only and why?
ventilating the left lung only bc the right lung is bigger
What is the most common complication of the DLT?
poor positioning
5 steps in treating hypoxia during OLV
what if these fail?
1. verify 100% O2
2. check position of tube
3. rule out physiologic causes such as:
- decreased CO (reduced amount of blood able to go pick up oxygen)
- bronchospasm (O2 unable to get to alveoli > blood),
- mucus plug (same),
- PTX of dependent lung
4. Apply CPAP to the non-dependent lung
- start at 2cm H2o (up to 10)
- Reduces shunt flow to the non-depedent lung
- Can either use the CPAP device to provicde itnermittent PPV (talk to surgeon first) OR, insufflate oxygen to the non-dependent lung by passing a suction catheter through the DLT lumen on the non-depedent side (won’t cause lung inflation)
5. Apply PEEP to the depedent lung:
- 5-10cm H20
- This may improve FRC or worsen shunt by directing more blood flow to the non-dependent lung so pay attention
- consider doing ARM before applying PEEP to ventilated lung
If none of these work:
- intermittently reinflate with non-depedent lung (communicate with surgeon)
- surgeon can clamp the pulmonary artery if doing a pneumonectomy to reduce shunt flow to the non-dependent lung
- think about drugs that inhibit HPV (can you decrease your inhalational agent or convert to tiva?)
With OLV, how does applying CPAP to the nondepedent lung improve oxygenation?
By reducing shunt flow (blood no air); your providing air, will improve VQ matching.
Unlike a DLT, the bronchial blocker CANNOT: (select 3):
- insufflate oxygen itno the isolated lung
- ventilate the isolated lung
- provide lung separation in the patient requiring naasotracheal intubation
- prevent contamination from contralateral lung infection
- provide lung separation in children
- suction secretions from the isolated lung
- prevent contamination from contralateral lung infection
- ventilate the isolated lung
- suction secretions from the isolated lung
T/F: a bronchial blocker cannot provde lung seperation for hte patient requiring nasotracheal intubation
FALSE- it can (DLT’s cannot- think you cant shove that big ass tube up someones nose)
T/F: both the DLT and the bronchial blocker allow you to insufflate oxygen into the isolated lung
True
*but remember the bronchial blocker cannot provide ventilation nor suction secretions from the isolated lung
Advantage of a bronchial blocker
Since it is plased through a single lumen ETT, the patient wont need to be reintubated with a single lumen ETT if they require postop ventilation
When you put a bronchial blocker in, which lung is ventilated and which side is not (lung same side vs opposite side of blocker)
same side of blocker = not ventilated
opposite side of blocker = ventilated
just think the blocker BLOCKS ventilation (goes through the Single lumen ETT- placement can be guided by fiberoptic
T/F - the lumen of the bronchial blocker can be used to suction blood, pus, or secretions from the non-ventilated lung
False- it is very narrow, so it can only suction (and/or insufflate) air
What is the smallest sizes DLT and who would you use that for?
26F
kids 8-10yo
(no DLT < 8yo, just no DLT small enough)
How would you provide one-lung ventilation to someone with a trach?
throw a bronchial blocker down there
Main issue with bronchial blockers
it’s a high pressure balloon so it can easily slip into the trachea which can lead to contamination from the other lung or even block ventilation of both lungs
What is the MOST common serious complications of mediastinoscopy (select 2):
- Chylothorax
- Pneumothorax
- Left RLN injury
- Hemorrhage
PTX (usually right side- bigger) & Hemorrhage
What is mediastinoscopy used for?
to diagnose and stage lung CA
Absolute contraindication to mediastinoscopy
Previosu mediastinoscopy (due to scarring)
Why do you have to be strategic with placing monitors for a mediastinoscopy?
Bc it can compress the innominate artery and impair cerebral perfusion (right side of the circle of willis)
- pulseox (or a-line) should go in the RUE; if the scope compresses the innominate artery (which feeds the right subclavian > ax and right ICA), the waveform will dampen or dissapear
- BP cuff on LUE to measure BP
(Pro tip- POX on RUE , A-line on left so you dont lose your BP measurement if that happens)
What 2 things should you have availalbe due to severe hemorrhage being a risk of mediastinoscopy?
- large bore IV access (lower extremity)
- If bleeding occurs, fluid and blood given in the upper extremity will past through the vascular injury and enter the mediastinum.
- Large bore IV in a lower extremity avoids this problem (doen’t it eventually need to go through the heart though lol - maybe im just missing something)
- PRBCs available
What syndrome is oat-cell carcinoma associated with?
Eaton- Lambert Syndrome
*Sensitive to BOTH sux and non-depolarizers
-think nany eaton is so extra, shes sensitive to EVERYTHING (both NMBs)
Mediastinoscopy:
Incision:
Scope anterior to:
Scope posterior to:
Incision: suprasternal notch
Scope anterior to: trachea
Scope posterior to: innominate and thoracic aorta
What things would you want to look at preop before mediastinoscopy? (2)
airway imaging on CT
evidence of cerbrovascular disease or hx stroke
Best choice if a patient needs to be reintubated after trachea resection
flexible fiberoptic bc the neck must be maintained in a flexed position for several days after surgery to reduce tension on the tracheal anastomosis while it heals
What are the MOST important strategies for managing mechanical ventilation in the patient with acute redspiratory distress sysndrome (Select 2):
- low tidal volume
- reducing plateu pressure
- high-frequency oscillatory ventilation
- permissive hypocapnia
- low tidal volume (4-6ml/kg IBW)
- ARDS doesn’t affect alveoli in the same way (some become very stiff while others maintain normal compliance)
- If you give a poositive pressure breath; the TV will follows the path of least resistance:
- stiff alveoli (poor compliance)- will only minimally fill if at all
- normal alveoli- will fill way too much as they will get the extra TV unable to go to the stiff alveoli
- Can cause volutrauma and barotrauma, which stimulates release of inflammatory mediators, worsening inflammation in the lungs
-reducing plateu pressure
- <30cm H20
- If this isn’t being achieved, reduce TV to 4ml/kg IBW
What is the most common pulmonary etiology of ARDS vs most comon extra-pulmonary etilogy
pulmonary etilogoy = PNA
extra-pulmonary = Sepsis
4 key pathophysiolologic features of ARDS
- protein-rich pulmonary edema
- loss of surfactant
- Hyaline membrane formation
- potential for long-term lung injury
Time of onset of ARDS
within 1 week of initial insult or new/worsening resp symptoms
how will ARDS present on CXR or CT?
Bilateral opacities
-not fully explained by effusions, lobar/lung collapse, or nodules
ARDS is caused by inflammation injury (mediated by neutrophils and platelets) that leads to what
diffuse alveolar destruction
Hallmark of ARDS
hypoxemia despite increased supplemental O2
What vent mode would be best for somone with ARDS?
Pressure control will goals of keeping lower tidal volumes
Goal RR for ARDs patient
6-35
-titrate to a target pH of 7.3-7.45
(dynamic hyperinflation is a risk when using a high RR)
[i think thats autopeep/breath stacking]
oxygen goal for ARDS patients
Target a PaO2 of 55-80
or
SpO2 88-95%
Why should FiO2 be reduced to 50% whenever possible?
because a high concentration of inspired oxygen (likely over 50%) causes oxidatative stress to the lung
Max Fio2 delivered for a regular nasal cannula
40%
PEEP strategies for ARDs patients
Increase PEEP to allow for lowest FiO2
What is the most approrpiate sized DLT for a woman who is 5’2”?
35F
(62” x 2.54 = 157.5cm)
<160 = 35, >160 = 37
How to convert someones height to cm
inches x 2.54
What is the definitive treatment for hypoxemia during OLV in the lateral decub position?
- Resume 2 lung ventilation
- Pulm artery ligation
- Apply CPAP to the non-dependent lung
- Apply PEEP to the dependent lung
Resume 2-lung ventilation
Anesthetic considerations for hte patient with pulmonary HTN secondary to lung disease (select 2):
- permissive hypercapnia
- volume loading before anesthetic induction
- continuing the patient’s sildenafil preoperatively
- treating right heart failure with inhaled nitric oxide
-continuing the patient’s sildenafil preoperatively
-treating right heart failure with inhaled nitric oxide
(fluid therapy should be careful, CO is relatively fixed and pts can be sensitive to inadequate preload but you cant overload them either)
Which variable is reduced by dynamic hyperinflation?
A. Inspiratory capacity
B. Expiratory reserve volume
C. Tidal Volume
D. FRC
A. Inspiratory capacity
- Dynamic hyperinflation = breath stacking = autopeep
- pt’s fully cant exhale delivered tidal volume, FRC rises, IC decreases
What are the primary mechanisms by which carboxyhemoglobinemia produces metabolic acidosis (Select 2):
- Impaired krebs cycle
- decreased CaO2
- left shifted oxyhgb dissociation curve
- accelerated o2 consumption
-decreased CaO2:
- CO2 binds to o2 binding site on the hgb with 200x afinity than o2
- This displaced o2 from hgb and reduces CaO2
-left shifted oxyhgb dissociation curve
- Less O2 is released at the tissue level
*The net result is an impairment of oxidative phyosphorlation, reducing ATP production > metabolic acidosis
