UNIT 1 Respiratory Flashcards
Which muscles tense & relax the vocal cords? Which muscles abduct & adduct the vocal cords?
STARE AT THIS PHOTO AND KNOW HOW TO LABEL EVERYTHING
Tense & Relax:
- cricothyroid “cords tense”
- thyroarytenoid “they relax” & vocalis
Abduct & Adduct:
- thyroarytenoid & lateral cricoarytenoid: adduct
- posterior cricoarytenoid: abduct
Which muscles abduct & adduct the vocal cords?
Abduct: posterior cricoarytenoid: “please come apart”
Adduct: lateral cricoarytenoid: “let’s close the airway”
Name 3 nerves involved in sensory innervation of the upper airway:
REVIEW THIS IN DEPTH! Write it out to make it stick!!!
1) Trigeminal (CN V)
V1 (opthalmic): nares & anterior 1/3 of septum
V2 (maxillary): turbinates & septum
V3 (mandibular): anterior 2/3 of tongue
2) Glossopharyngeal (CN IX)
posterior 1/3 of tongue, soft palate, oropharynx, vallecula, anterior of epiglottis- review all of these
3) VAGUS innervates both of these:
- SLN
internal branch: posterior side of epiglottis –> level of vocal cords
external branch: no sensory
- RLN
below vocal cords –> trachea
How does RLN injury affect integrity of the airway?
Where does the right RLN and left RLN loop under?
Which side is more susceptible to injury?
Bilateral:
acute = respiratory distress
chronic = no respiratory distress
Unilateral:
no respiratory distress
RLN innervated by Vagus nerves, the right RLN loops under subclavian artery, and the left RLN loops under the aortic arch. The left RLN is more susceptible to injury
Left side RLN injuries from: PDA ligation, left atrial enlargement (mitral stenosis), aortic arch aneurysm, thoracic tumor
Either side (right or left RLN) injury: pressure from ETT/LMA, thyroid surgery, neck stretching, neck tumor
Stare at this picture and be able to label everything
How does SLN injury affect the integrity of the airway?
Bilateral:
hoarseness but no respiratory distress
Unilateral:
no respiratory distress
Name 3 airway blocks, and ID the key landmarks for each one.
- glosspharyngeal block: palatoglossal arch @ the anterior tonsillar pillar.
- SLN block: greater cornu of hyoid
- Transtracheal block: Cricothyroid membrane, ask pt to take a deep breath and inject 3-5ml of local into tracheal lumen
Where does the adult larynx extend from?
What are the 3 paired & 3 unpaired cartilages of the larynx?
Adult larynx extends from C3-C6 ( serves as airway protection, respiration, phonation)
unpaired: epiglottis, thyroid, cricoid
paired: corniculate, cuniform, arytenoid
What is the treatment for laryngospasm?
100% FiO2 remove noxious stimuluation deepen anesthesia CPAP 15-20cmH2O open airway w/ head extension, chin lift Larson's maneuver succinylcholine I.M. Dose is 4mg/kg for child or adult. For neonates or infants it’s 5mg/kg Children < 5 years, give 0.02mg/kg of atropine to avoid bradycardia when giving Sux
how to reduce risk:
- CPAP 5-10 cm/H2O after extubation
- lidocaine
Describe how the respiratory muscles function during the breathing cycle.
KNOW THIS WELL!
Inspiration:
- diaphragm & external intercostals (tidal breathing)
- accessory: sternocleidomastoid & scalene muscles
Expiration:
usually passive, (TIREO!)
- transverse abdominis
- internal rectus abdominis
- external obliques, secondary role: internal intercostals
A vital capacity of at least 15mL/kg
What is the difference between minute ventilation & alveolar ventilation?
MV = Vt x RR
AV: only measures the fraction of Ve that is available for gas exchanges
AV = (Vt- dead space) x RR
Define the 4 types of dead space.
- Anatomic (air confined to the conducting airways)
- Alveolar (alveoli that are ventilated but not perfused)
- Physiologic (Anatomic + Alveolar Vd)
- Apparatus (Vd added by airway equipment)
Provide an example for each type of dead space.
- Apparatus = face mask/HME
- Anatomic = nose/mouth/ trachea/ terminal bronchioles
- Alveolar = Zone 1 alveoli
- Physiologic = anatomic and alveoli
What does the alveolar compliance curve tell you?
alveolar ventilation is a function of alveolar size & it’s position on the alveolar compliance curve.
- best ventilated alveolar are the most compliant (steep slope of curve)
- worst ventilated alveoli are the least compliant (flat portion of the curve)
What does the V/Q ratio represent?
V/Q is the ratio of ventilation to perfusion
- normal MV = 4L/min
- normal CO = 5L/min
- -> normal V/Q = 0.8
dead space V/Q –> infinity
shunt V/Q –> 0
Define the West zones of the lungs
Zone 1
PA>Pa>Pv
dead space (ventilation w/out perfusion)
Normal lung doesn’t have this. The is increased by P.E and hypotension
Zone 2
Pa>PA>Pv
waterfall (normal physiology) more blood flow
Zone 3
Pa>Pv>PA
shunt (perfusion w/out ventilation)
Atelectasis
PA cath tip goes here
Zone 4
Pa>Pist>Pv>PA
pressure in the interstitial space pulmonary edema) impairs ventilation & perfusion
Alveolar gas equation?
PAO2 = FiO2(Pb-PH2O) - (PaCO2/RQ) NEED TO KNOW THIS
tells us that hypoventilation can cause hypercarbia & hypoxemia.
Pb = 760mmHg sea level PH2O = 47mmHg RQ = CO2 elimination/O2 consumption = 200/250 = 0.8 - RQ = 1 --> over feeding - RQ < 0.7 --> starvation
What is the A-a gradient, what is the normal range, and what factors increase it?
It compares partial pressure of O2 inside the alveolus and the partial pressure of O2 in the arterial circulation to diagnose the cause of hypoxemia. Get an ABG to get the PaO2 and use the Alveolar gas equation
- it is normally 5-15mmHg
It is increased by: (VHARD)
- Vasodilators: decreased hypoxic vasoconstriction
- High FiO2
- Aging
- R–>L shunt: Atelectasis, pneumonia, bronchial intubation, Intracardiac defect
- Diffusion limitation: pulmonary fibrosis, emphysema, interstitial lung disease
List the 5 causes of hypoxemia. Which ones are reversed w/ supplemental oxygen?
- Reduced FiO2- (A-a gradient is normal)
- Hypoventilation- (A-a gradient is normal)
- Diffusion Limitation- (A-a gradient is increased)
- V/Q mismatch- (A-a gradient is increased)
- Shunt- (A-a gradient is increased)
1-4: are reversed w/ supplemental oxygen
Define the 5 lung volumes & give reference values for each.
- inspiratory reserve volume (3000mL)
- tidal volume (500mL)
- expiratory reserve volume (1100mL)
- residual volume (1200mL)
- closing volume (variable - approaches RV in healthy young patients)
Define the lung capacities & give reference values for each.
- total lung capacity (5800mL): IRV + TV + ERV + RV
- vital capacity (4500mL): IRV + TV + ERV
- inspiratory capacity (3500mL): ERV + TV
- functional residual capacity (2300mL): RV + ERV
- closing capacity (variable): RV + CC absolute volume of gas contained in the lungs when the small airways close
Vital capacity is 65-75ml/kg
FRC is 35ml/kg
Spirometry can’t measure RV, CC, and CV. It can’t measure TLC and CC FRC cus there’s RV in it. It CAN measure VC
FRC consists of? What factors influence FRC? Name an example of increased FRC?
FRC = RV + ERV (35mL/kg)
conditions that reduce FRC tend to reduce outward lung expansion and/or reduce lung compliance –> zone III (shunt) increases. PEEP restores FRC by reducing zone III
- position changes
- increased intraabdominal pressure/contents
- anesthesia/NMB
- surgical displacement
COPD or any condition that causes air trapping increases FRC
Why can’t spirometry measure FRC?
Spirometry can’t measure residual volume so this includes (FRC and TLC). It also can’t measure closing capacity and closing volume
Which 3 tests can measure FRC?
1) nitrogen washout
2) helium wash in
3) body plethysmography
What is closing volume & what increases it?
Volume above residual volume where the small airways begin to close during expiration.
CLOSEP:
- COPD
- LVF
- Obesity
- Supine position
- Extreme age
- Pregnancy
State the equation and normal value for oxygen carrying capacity
CaO2 = SaO2Hgb1.34 + PaO2*0.003
normal = 20mL O2/dL
State the equation and normal value for oxygen delivery
DO2 = CaO2 x CO x 10
normal = 1000mL O2/min
Discuss the factors that alter oxyhemoglobin dissociation curve
Left shift (love, increased affinity, decreased offloading to the tissues)
Right shift (release, decreased affinity, increased offloading to the tissues)
What 3 ways is CO2 transported in the blood? Which one is 70%?
1) bicarbonate 70%!!!!
2) bound to Hgb by aminos 23%
3) dissolved in plasma 7%
CO2 to = HCO3- requires carbonic anhydrase & release of HCO3- from RBC to plasma, this causes Cl- shift out of the RBC (aka Hamburger shift)
Describe the Bohr effect
Bohr effect describes: O2 carriage
increased CO2 & decreased pH = RBC releases O2
Describe the Haldane effect
Haldane effect describes CO2 carriage
Increased O2 causes RBC to release CO2 (lungs)
(Where as Bohr effect describes O2 carriage and releases O2)
List the 3 primary causes of hypercapnia and provide examples of each
- increased CO2 production:
- sepsis
- overfeeding
- malignant hyperthermia
- shivering
- seizures
- thyroid storm
- burns - decreased CO2 elimination:
- a/w obstruction
- increased Vd
-increased Vd/Vt
- ARDS
- COPD
- respiratory depression
- drug OD
- inadequate NMB reversal - rebreathing: incompetent one-way valve, exhausted soda lime
Describe the 4 areas in the respiratory center
Medullary Respiratory Centers:
- Dorsal respiratory center: active during inspiration (respiratory pacemaker)
- Ventral respiratory center: active during expiration
Pontine Respiratory Centers:
- Pneumotaxic center: inhibits the DRC
- Apneuristic center: stimulates DRC
Contrast the location & function of the central & peripheral chemoreceptors.
Central:
- located in the medulla
- responds to the pH [H+] in the CSF
- CO2 diffuses freely in the BB and is hydrated with H2O (there’s no carbonic anhydrase involvement like in a RBC) = H+ and HCO3. The CSF responds to the H+. Increased H+ causes increase in Minute Ventilation and vice versa
Peripheral:
- located in the carotid bodies, nerves of Hering CN IX (9) glossopharyngeal
- located in the aortic arch CN X (10) vagus
- responds to decreased O2, increased CO2, and increased H+
- Monitors PaO2 < 60mmhg. When it’s lower than this it closes the O2 sensitive K+ channels in the type 1 glomus cells
Which reflex prevents overinflation of the lungs?
Hering-Breuer inflation reflex
What is hypoxic pulmonary vasoconstriction?
- It minimizes shunt by reducing blood flow through poorly ventilated alveoli… seen in one lung ventilation
- a low PAO2 (NOT arterial) is the trigger that activates HPV! LOW PAO2!!! Pay attention to multiple choice questions
- effect begins immediately & takes 15mins for full effect
What (4) things impair HPV?
Anything that inhibits HPV, aka increases shunt (perfusion w/out ventilation)
1) halogenated anesthetics >1-1.5MAC
2) PDE inhibitors
3) dobutamine
4) vasodilators
IV anesthetics DO NOT inhibit HPV
What does the diffusing capacity for CO (DLCO) tell us? Normal range?
Using Fick’s law of diffusion, the DLCO tells us:
- surface area (decreased w/ emphysema)
- thickness (increased by pulmonary fibrosis & edema)
It tells us how well the lung can exchange gas.
Normal = 17-25mL/CO/min/mmHg
How is tobacco smoke harmful?
- increases SNS tone
- sputum production
- carboxyhemoglobin concentration
- risk of infection
Describe the short & intermediate term benefits of smoking cessation.
Immediate short term benefits (doesn’t reduce risk of postop pulmonary complications)
- SNS stimulation dissipates after 20-30mins
- P50 returns to near normal in 12hrs, CaO2 improves
Intermediate term effects- return of normal pulmonary function requires at least 6 weeks
- improved airway function, mucociliary clearance, sputum production, & pulmonary immune function
- CYP450 induction subsides after 6 weeks
Compare & contrast PFTs in obstructive vs. restrictive lung disease. Name an example of each:
Restrictive:
- Decrease in all lung volumes: FRC, RV, TLC, FEV 1 and FVC & FEV1
- normal FEV1/FVC ratio
- normal FEF25-75
- example is obesity
Obstructive:
- decreased FEV1/FVC & FEF25-75
- may have normal other values
- example is COPD
Discuss the following pulmonary flow-volume loops: normal, obstructive, restrictive, and fixed obstruction
normal = upside down ice cream cone
obstructive = normal inspiration w/ expiratory obstruction (negative exponential slope)
restrictive = shape similar to normal loop but smaller & shifted to the R
fixed obstructive = inspiration & expiration are affected.
Give an example of a disease the produces the following pulmonary flow-volume loops: obstructive, restrictive, and fixed obstruction
obstructive = COPD, asthma
restrictive = pulmonary fibrosis and obesity
(reduced lung volumes, reduced FVC and FEV1, but with normal FEV1 ratio and normal FEF25-75)
fixed obstruction = tracheal stenosis
What is the treatment for acute bronchospasm?
- 100% FiO2 - deepen anesthetic (IA, propofol, lidocaine, ketamine) - inhaled B2 agonist (albuterol) - inhaled anticholinergic (ipratropium), they’re bronchodilators! - epi 1mcg/kg IV - hydrocortisone 2-4mg/kg (takes several hours) - **aminophylline** - heliox to reduce airway resistnace
What is alpha-1 antitrypsin deficiency? What is the definitive treatment?
alpha-1 antitrypsin is produced in the liver. This deficiency is seen in COPD!!
alpha-1antitrypsin helps break down alveolar elastase enzyme. This alveolar elastase enzyme is like Drano in the lungs and destroys lung tissue.
With alpha-1antitrypsin deficiency, the alveolar elastase builds up and starts destroying more lung tissue = panlobular emphysema
It’s the MOST common metabolic disease affecting the liver
Liver transplant is the definitive treatment
Describe the goals & strategies for mechanical ventilation in the patient w/ COPD.
prevent barotrauma & reduce air trapping:
- low Tv 6-8mL/kg
- increased expiratory time
- slow inspiratory flow rate to optimize V/Q matching, like 7bpm! SLOW THEIR RR!!!
- low PEEP is ok as long as air trapping doesn’t occur
- avoid regional blocks involving > T6
- if there’s hyperdynamic inflation (breath stacking): decrease RR, disconnect circuit, decrease inspiratory flow
Define restrictive lung disease
characterized by:
- impaired lung expansion
- decreased lung volumes
- normal pulmonary flow rates
Give examples of intrinsic lung diseases (acute & chronic)
Acute: aspiration, negative pressure pulmonary edema
Chronic: pulmonary fibrosis, sarcoidosis
Give examples of extrinsic lung diseases (acute & chronic)
Chest wall/mediastinum: kyphoscoliosis, flail chest, NM disorders, mediastinal mass
Increased intraabdominal pressure: pregnancy, obesity, ascites
List the risk factors for aspiration pneumonitis.
trauma emergency surgery pregnancy GI obstruction GERD peptic ulcer disease hiatal hernia ascites difficult airway management cricoid pressure impaired airway reflexes head injury seizures residual NM blockade
Describe the pharmacologic prophylaxis of aspiration pneumonitis.
antacids: sodium citrate, sodium bicarbonate, magnesium trisilicate
H2 antagonists: ranitidine, cimetidine, famotidine
GI stimulants: metoclopramide
PPI: omeprazole, lansoprazole, pantoprazole
antiemetics: droperidol, ondansetron
routine use of these agents for prophylaxis isn’t recommended
What is Mendelson’s syndrome?
chemical aspiration pneumonitis
risk factors:
- gastric pH <2.5
- gastric volume >25mL (0.4mL/kg)
Describe the treatment of aspiration.
tilt head downward or to the side (first action)
- upper airway suction
- lower airway suction is only useful for removing particulate matter (not helpful for acidic burn)
- secure airway
- PEEP to reduce shunt
- bronchodilators to reduce wheezing
- lidocaine to reduce neutrophil response
- steroids probably don’t help
- Abx only if WBC or fever >48hrs
Discuss the pathophysiology and treatment of flail chest.
Consequence of blunt chest trauma with multiple rib fractures. The key characteristic is paradoxical movement of the chest wall at the site of the fractures
Inspiration: injured ribs move inward & collapse affected region
Expiration: injured ribs move outward & affected region doesn’t empty
Treatment: epidural catheter or intercostal nerve blocks
Discuss pulmonary HTN, and discuss goals of anesthetic management.
mean PAP>25mmHg
causes: COPD, L heart disease, connective tissue disorders
goals: optimize PVR
- increase PaO2
- hypocarbia
- alkalosis
- decreased intrathoracic pressure (prevent coughing, normal lung volumes, spontaneous ventilation)
- drugs: inhaled NO, NTG, phosphodiesterase inhibitors, PGs, CCB, ACEI
Discuss the pathophysiology of CO poisoning
- reduces O2 carrying capacity of the blood (L shift)
-
CO binds O2 binding site of HgB w/ 200x affinity of O2
–> oxidative phosphorylation & metabolic acidosis - Co-oximeter NOT pulse ox measures CO
-
cherry red appearance
-if soda lime is desiccated then volatile anesthetics can produce CO (Des > Iso > Sevo) Des produces CO the most
Discuss the treatment of CO poisoning
100% FiO2 x6hrs
hyperbaric oxygen if COHgb >25% or if the patient is symptomatic
List the absolute & relative indications for OLV
Absolute indications:
- Isolation of one lung to avoid contamination
- Control of Distribution of ventilation
- Unilateral bronchopulmonary lavage
Relative:
- surgical exposure
- pulmonary edema s/p CABG
- severe hypoxemia r/t lung disease
Discuss how anesthesia in the Lateral Dependent position affects the VQ relationship.
So think of this like blood flow
Nondependent lung:
- moves from flatter region (less compliant) to an area of better compliance (slope)
- ventilation is optimal in this lung
Dependent lung:
- moves from the slope to the lower, flatter area of the curve (less compliant)
- perfusion is best in this lung (gravity)
- reduction of alveolar volume contributes to atelectasis
net effect: ventilation is better in nondependent lung & perfusion is better in dependent lung. This creates VQ mismatch & increases the risk of hypoxemia during OLV
Discuss the management of hypoxemia during OLV
100% FiO2
confirm DLT position w/ bronchoscope
CPAP 10cmH2O to nonventilated lung
PEEP 5-10 to ventilated lung
alveolar recruitment maneuver
clamp pulmonary artery to non-ventilated lung
resume two-lung ventilation
What is mediastinoscopy, and why is it performed, any complications? Absolute contraindications?
performed to obtain biopsy of the paratracheal lymph nodes at the level of the carina. Helps to stage the tumor prior to lung resection
Complications #1 hemorrhage it’s near thoracic aorta, #2 pneumo
Absolute contraindications: previous mediastinoscopy due to scarring
know how to label the arteries on this!!!
Also the risk of a venous embolism is most likely to occur during spontaneous ventilation
What are the potential complications of mediastinoscopy. What is most common?
hemorrhage & pneumothorax are most common
others:
- impaired cerebral perfusion
- dysrhythmias
- air embolism
- chylothorax
- hoarseness and/or VC paralysis
describe the mallampati score
assesses teh oropharyngeal space, helps quantify the size of the tongue relative to the volume in the mouth
I: pillars, uvula, soft palate, hard palate
II: uvula, soft palate, hard palate
III: soft palate, hard palate
IV: hard palate
describe the interincisor gap. What is normal?
ability to open the mouth directly affects ability to align the oral, pharyngeal, and laryngeal axes. A small interincisor gap creates a more acute angle b/n the oral & glottic openings, increasing the difficulty of intubation
normal = 2-3FB or 4cm
what is the thyromental distance & what values suggest an increased risk of difficult intubation?
helps estimate the size of the submandibular space
w/ neck extended & mouth closed, you can measure the distance from the tip of the thyroid cartilage to the tip of the mentum.
DL may be more difficult if the TMD is <6cm (3FB) or greater than 9cm
What is the mandibular protrusion test and what values suggest an increased risk of difficult intubation?
assesses the function of the TMJ.
Pt is asked to sublux the jaw, and the position of the lower incisors is compared to the position of the upper incisors
Class I: LI past UI & bite the vermilion of the lip
Class II: LI in line w/ UI
Class III: LI cannot move past UI (increased risk of difficult intubation)
What conditions impair atlanto-occipital joint mobility?
DJD RA ankylosing spondylitis trauma surgical fixation Klippel-Feil Down syndrome
Describe the Cormack & Lehanne score
helps measure the view we obtain during DVL
Grade I: full view
Grade II: partial cords, arytenoids
Grade III: epiglottis
Grade IV: soft tissue
5 risk factors for difficult mask ventilation
BONES beard obese (usually BMI>26) no teeth elderly (age >55) snoring
list 10 risk factors for difficult tracheal intubation
small mouth opening narrow palate w/ high arch long upper incisors interincisor distance <3cm MP class 3 or 4 mandibular protrusion class 3 poor compliance of submandibular spce TM distance <6cm or >9cm neck is thick & short poor AO joint mobility
list 6 risk factors for difficult supraglottic device placement
limited mouth opening upper airway obstruction altered pharyngeal anatomy poor airway compliance increased airway resistance lower airway obstruction
list 5 risk factors for difficult invasive airway placement
abnormal neck anatomy obesity short neck limited access to CT membrane laryngeal trauma
what is angioedema?
result of increased vascular permeability that can lead to swelling of the face, tongue and airway: airway obstruction is an extreme concern
what are two common causes of angioedema? what is the treatment for each?
ACEI:
treat = epi, antihistamines, steroids (just like anaphylaxis)
Hereditary angioedema (C1 esterase deficiency):
treat = C1 esterase concentrate or FFP (NOT epi, antihistamines, or steroids)
What is Ludwig’s angina?
bacterial infection characterized by a rapidly progressing cellulitis in the floor of the mouth. Inflammation & edema compress the submandibular, submaxillary, and sublingual spaces.
the most significant concern is posterior displacement of the tongue resulting in complete, supraglottic airway obstruction