Apex Unit 1 Flashcards Resp
what does thyroarytenoid muscle do?
shorten the cords THEY RELAX
what dos cricothyroid muscle do
elongates the cords CORDS TENSE
what dos posterior cricoarytenoid do?
ABducts
what does Lateral cricoarytenoid do
ADducts
what are 2 attachment point for vocal cords
thyroid cartilage and the arytenoid cartilage
how is cricothyroid ligament innervated from
SLN (external)
whihch muscles depress the larynx
omohyoid, sternohyoid, sternothyroid
which muscles elevate the larynx
stylohyoid geniohyoid mylohyoid thyrohyoid digastric stylopharyngeus
the superior laryngeal nerve innervates the
underside of epiglottis (internal) & cricothyroid muscles (external)
what do the R & L RLN loop under
R - subclavian
L - Aortic arch ( more susceptible to injury)
what are the three branches of trigeminal nerve
V1: ophthalmic
V2: maxillary
V3: Mandibular
what does glossopharyngeal nerve innervate
soft palate, tonsils, posterior 1/3 of tongue, vallecula, afferent limb of GAG
whats does SLN external innervate (sensory)
nothing
what does SLN internal innervate (sensory
posterior side of epiglottis
what does RLN innervate
area under vocal cords - trachea
How does superior laryngeal nerve injury affect the integrity of the airway?
Superior laryngeal nerve injury
Bilateral: Hoarseness / No respiratory distress
Unilateral: No respiratory distress
Name 3 airway blocks, and identify the key landmarks for each one.
Glossopharyngeal nerve block: Palatoglossal arch at the anterior tonsillar pillar
Superior laryngeal nerve block: Greater cornu of hyoid
Transtracheal nerve block: Cricothyroid membrane
What are the 3 paired and 3 unpaired cartilages of the larynx?
unpaired = epiglottis thyroid, cricoid paired = corniculate, arytenoid, cuneform
What is the treatment for laryngospasm
Significant consequences of laryngospasm include hypoxia and negative-pressure pulmonary edema.
Treatment:100% FiO2 Remove noxious stimulation Deepen anesthesia CPAP 15 - 20 cm H2O Open the airway (head extension, chin lift) Larson’s maneuver Succinylcholine
Regarding succinylcholine:
Infants and small children should receive atropine 0.02 mg/kg with succinylcholine.
If no IV access, submental administration will produce the fastest onset.
If no IV access and the patient can’t have succinylcholine, then rocuronium is the only other NMB that can be given IM.
Describe how the respiratory muscles function during the breathing cycle.
Contraction of the inspiratory muscles reduces thoracic pressure and increases thoracic volume. This is an example of Boyle’s law.
Inspiration:
The diaphragm and external intercostals contract during inspiration (tidal breathing).
The diaphragm increases the superior-inferior dimension of the chest.
The external intercostals increase the anterior-posterior diameter.
Accessory muscles include the sternocleidomastoid and scalene muscles.
Exhalation:
Exhalation is usually passive; this process is driven by the recoil of the chest wall.
Active exhalation is carried out by the abdominal musculature (rectus abdominis, transverse abdominis, internal obliques, and external obliques).
The internal intercostals serve a secondary role in active exhalation.
Exhalation becomes an active process when minute ventilation increases or in patients with lung disease, such as COPD.
A forced exhalation is required to cough and clear the airway of secretions.
What is the difference between minute ventilation and alveolar ventilation?
Minute ventilation (Ve) is the amount of air in a single breath multiplied by the number of breaths per minute.
Ve = Vt x RR
Alveolar ventilation (VA) only measures the fraction of Ve that is available for gas exchange. Said another way, it removes anatomic dead space gas from the minute ventilation equation.
VA = (Vt - Anatomic dead space) x RR
VA is directly proportional to CO2 production
VA is indirectly proportional to PaCO2
Define the 4 types of dead space.
Anatomic Vd:
Air confined to the conducting airways
Alveolar Vd:
Alveoli that are ventilated but not perfused
Physiologic Vd:
Anatomic Vd + Alveolar Vd
Apparatus Vd:
Vd added by equipment
Provide an example for each type of dead space.
Anatomic Vd:
Nose/mouth → terminal bronchioles
Alveolar Vd:
Reduced pulmonary blood flow (↓ CO)
Physiologic Vd:
Anything that increases anatomic or alveolar Vd
Apparatus Vd:
Facemask, HME, limb of circle system if incompetent valve present
What does the alveolar compliance curve tell you?
Alveolar ventilation is a function of alveolar size and its position on the alveolar compliance curve.
The best ventilated alveoli are the most compliant (steep slope of the curve).
The poorest ventilated alveoli are the least compliant (flat portion of the curve).
perfusion is greatest at lung base due to gravity.
ventilation is best at lung base due to higher alveolar compliance.
What does the V/Q ratio represent?
The V/Q ratio is the ratio of ventilation to perfusion (minute ventilation / cardiac output).
Normal minute ventilation = 4 L/min
Normal cardiac output = 5 L/min
Normal V/Q ratio = 0.8
Dead space and shunt are absolutes. Dead space (No PERFUSION): V/Q = infinity (10/0 = infinity) Shunt (NO VENTILATION): V/Q = 0 (0/10 = 0)
V/Q mismatch occurs when the ratio is disturbed.
If the number is larger than 0.8, then this moves towards dead space.
If the number is smaller than 0.8, then this moves towards shunt.
Define the West zones of the lung.
Zone I
PA > Pa > Pv
Dead space
Ventilation without perfusion
Zone II
Pa > PA > Pv
Waterfall
Normal physiology
Zone III
Pa > Pv > PA
Shunt
Perfusion without ventilation
Zone IV
Pa > Pist > Pv > PA
Pressure in the interstitial space impairs ventilation and perfusion
Recite the alveolar gas equation.
The alveolar gas equation tells us that hypoventilation can cause hypercarbia and hypoxemia. It also explains how supplemental oxygen reverses hypoxemia, but it does nothing to reverse hypercarbia.
PAO2 = FiO2 x (Pb - PH2O) - (PaCO2 / RQ)
Pb = Atmospheric pressure PH2O = 47 mmHg RQ = Respiratory quotient = 0.8
RQ = (CO2 elimination / O2 consumption) = (200 mL / 250 mL)
Alveolar oxygen in the healthy adult patient breathing room air at sea level is ~ 105.98 mmHg.
What is the A-a gradient, and what factors affect it?
The A-a gradient is the difference between alveolar oxygen (PAO2) and arterial oxygen (PaO2).
It helps us diagnose the cause of hypoxemia by quantifying the amount of venous admixture.
It is normally 5 - 15 mmHg.
It is increased by high FiO2, aging, vasodilators, right-to-left shunting, and diffusion limitation.
List the 5 causes of hypoxemia. Which ones are reversed with supplemental oxygen?
normal A-a Gradient - reduced FIO2 & Hypoventilation
Increased A-a Gradient = DIffusion Limitation, VQ mismatch , Shunt
ALL are fixed with supplemental O2 except Shunt bc there is no way for O2 to reach pulmonary capillary .
Define the 5 lung volumes, and give reference values for each.
IRV = 3000 TV = 500 ERV = 1100 RV = 1200 CV = variable
Define the capacities, and give reference values for each.
TLC = 5800 IRV + TV + ERV + RV VC = 4500 IRV + TV + ERV IC = 3500 IRV + TV FRC = 2300 ERV + RV CC = variable RV + CV
What factors influence FRC?
FRC = RV + ERV (35 mL/kg)
Because it contains RV, the FRC can’t be measured by conventional spirometry.
Conditions that reduce FRC have several things in common. They tend to reduce outward lung expansion and or reduce lung compliance. When FRC is reduced, intrapulmonary shunt (zone III) increases. PEEP acts to restore FRC by reducing zone III.
COPD or any condition that causes air trapping increases FRC.
Why can’t spirometry measure FRC?
Because it contains RV, the FRC can’t be measured by conventional spirometry.
What tests can measure FRC?
FRC is measured indirectly by nitrogen washout, helium wash in, or body plethysmography.
What is closing volume, and what increases it?
Closing volume is the point at which dynamic compression of the airways begins. Said another way, it’s the volume above residual volume where the small airways begin to close during expiration.
C OPD L eft ventricular failure O besity S upine position E xtreme age P regnancy
mnemonic: CLOSE-P
State the equation and normal value for oxygen carrying capacity.
O2 Carrying Capacity (CaO2)
How much O2 is carried in the blood
CaO2 = (1.34 x Hgb x SaO2) + (PaO2 x 0.003)
Normal = 20 mL O2/dL
State the equation and normal value for oxygen delivery.
Oxygen Delivery (DO2) How much O2 is delivered to the tissues
DO2 = CaO2 x Cardiac output x 10
Normal = 1,000 mL O2/min
Discuss the factors that alter the oxyhemoglobin dissociation curve.
Right Shift = inc. Temp, CO2, H+, dec pH, inc 23DPG
Left Shift = HGB MET, HGB F, HGBCO,
Left = latch onto
right = release decreased affinity for O2
How is carbon dioxide transported in the blood?
Carbon dioxide is the primary by-product of aerobic metabolism. Venous blood transports it to the lungs, where it’s excreted into the atmosphere.
Mechanisms of CO2 Transport:
Bicarbonate = 70%
Bound to hemoglobin = 23%
Dissolved in the plasma = 7%
The reaction that converts CO2 to HCO3- requires the enzyme carbonic anhydrase.
c.a.
H2O + CO2 H2CO3 H+ + HCO3-
When the RBC releases HCO3- into the plasma, Cl- is transported into the RBC to maintain electroneutrality. This is called the Hamburger shift (chloride shift).
Describe the Bohr effect.
The Bohr effect describes O2 carriage.
It says that ↑ CO2 and ↓ pH cause the erythrocyte to release O2.
Conceptually, it’s the cell’s way of asking hemoglobin to release oxygen to support aerobic metabolism. ( think exercising)
Describe the Haldane effect.
The Haldane describes CO2 carriage.
It says that ↑ O2 causes the erythrocyte to release CO2 (occurs in the lungs).
Said another way, the Haldane effect states that deoxygenated Hgb is able to carry more CO2 (occurs in venous blood).
List the 3 primary causes of hypercapnia, and provide examples of each.
Increased CO2 Production, - sepsis, burns, overfeeding,
Decreased CO2 Elimination - ARDS, deadspace, COPD< drug overdose
Rebreathing - bad one way valve, exhausted soda lime
Describe the 4 areas in the respiratory center.
Pontine Respiratory Centers: Pneumotaxic center (upper pons): Inhibits the DRC Apneustic center (lower pons): Stimulates the DRC
Medullary Respiratory Centers:
Dorsal respiratory center: Active during inspiration (respiratory pacemaker)
Ventral respiratory center: Active during expiration
Contrast the location and function of the central and peripheral chemoreceptors.
Central Chemoreceptor:
Located in the medulla
Responds to the H+ concentration in the CSF
The H+ in the CSF is a function of the PaCO2 of the blood (remember, the PaCO2 is the primary stimulus to breathe)
Peripheral Chemoreceptors:
Located in the carotid bodies: Nerves of Hering → Glossopharyngeal n. (CN IX)
Located in the aortic arch: Vagus n. (CN X)
They respond to ↓O2, ↑CO2, and ↑H+
Which reflex prevents overinflation of the lungs?
Hering-Breuer inflation reflex
What is hypoxic pulmonary vasoconstriction?
Hypoxic pulmonary vasoconstriction minimizes shunt by reducing blood flow through poorly ventilated alveoli (think atelectasis or OLV).
A low alveolar PO2 (not arterial PO2) is the trigger that activates HPV. The effect begins almost immediately and reaches its full effect after 15 min.
What things impair HPV, and what is the consequence of this?
Anything that inhibits HPV increases shunt (perfusion without ventilation).
Examples include: Halogenated anesthetics > 1-1.5 MAC Phosphodiesterase inhibitors Dobutamine Vasodilators
IV anesthetics do NOT inhibit HPV.
What does the diffusing capacity for carbon monoxide tell us?
The diffusing capacity for carbon monoxide (DLCO) is used to assess how well the lung can exchange gas.
Normal = 17 - 25 mL/CO/min/mmHg
Using Fick’s law of diffusion, the DLCO tells us 2 key characteristics about the alveolar-capillary interface:
Surface area (↓ by emphysema) Thickness (↑ by pulmonary fibrosis and pulmonary edema)
Therefore, DLCO is reduced by anything that reduces alveolar surface area and/or increases the thickness of the alveolar-capillary interface.
How is tobacco smoke harmful?
Smoking increases SNS tone, sputum production, carboxyhemoglobin concentration, and the risk of infection.
Describe the short and intermediate term benefits of smoking cessation.
Short term effects:
Short term cessation does NOT reduce the risk of postoperative pulmonary complications, but short term benefits include:
SNS stimulating effects of nicotine dissipate after 20 – 30 minutes
P50 returns to near normal in 12 hours (CaO2 improves)
Intermediate term effects: The return of normal pulmonary function requires at least 6 weeks. This includes: Airway function Mucociliary clearance Sputum production Pulmonary immune function
Hepatic enzyme induction subsides after 6 weeks.
Compare and contrast pulmonary function tests in obstructive vs restrictive lung disease.
restrictive = everything decreased except normal fev1/fvc ratio & FEF 25-75%
Obstructive all normal except decreased Fev1/fvc ratio & FEF 25-75%
Discuss the following pulmonary flow-volume loops: normal, obstructive, restrictive, and fixed obstruction.
Normal:
Upside down ice cream cone
Obstructive:
Normal inspiration with expiratory obstruction.
Restrictive:
Shape is similar to normal loop, but the restrictive loop is smaller and right shifted.
Fixed Obstruction:
Inspiration and expiration are affected.
An extrathoracic obstruction is abnormal during inspiration and normal during expiration.
An intrathoracic obstruction is normal during inspiration and abnormal during expiration.
Give an example of a disease that produces the following pulmonary flow-volume loops: obstructive, restrictive, and fixed obstruction.
Obstructive:
COPD
Restrictive:
Pulmonary fibrosis
Fixed Obstruction:
Tracheal stenosis
What is the treatment for acute bronchospasm?
100% FiO2
Deepen anesthetic (volatile agent, propofol, lidocaine, ketamine)
Inhaled beta-2 agonist (albuterol)
Inhaled anticholinergic (ipratropium)
Epinephrine 1 mcg/kg IV
Hydrocortisone 2-4 mg/kg IV (takes several hours to take effect)
Aminophylline
Helium-oxygen (Heliox) reduces airway resistance (↓’s Reynold’s number)
*Montelukast is not used in the treatment of acute bronchospasm
What is alpha-1 antitrypsin deficiency?
Alveolar elastase is a naturally occurring enzyme that breaks down pulmonary connective tissue. This enzyme is kept in check by alpha-1 antitrypsin (produced in the liver).
When there’s a deficiency of alpha-1 antitrypsin, alveolar elastase is free to wreak havoc on pulmonary connective tissue. This ultimately leads to panlobular emphysema.
Liver transplant is the definitive treatment for alpha-1 antitrypsin deficiency.
Describe the goals and strategies for mechanical ventilation in the patient with COPD.
The goal is to prevent barotrauma and reduce air trapping. This is accomplished by:
Low tidal volume (6-8 mL/kg IBW)
Increased expiratory time to minimize air trapping
Slow inspiratory flow rate optimizes V/Q matching
Low levels of PEEP are ok, so long as air trapping does not occur
Define restrictive lung disease.
Restrictive lung disease is characterized by:
Impaired lung expansion
Decreased lung volumes
Normal pulmonary flow rates
Give examples of intrinsic lung diseases (acute and chronic).
Intrinsic Lung Disease (affects lung parenchyma):
Acute: aspiration, negative pressure pulmonary edema
Chronic: pulmonary fibrosis, sarcoidosis
Give examples of extrinsic lung diseases (acute and chronic).
Extrinsic Lung Disease (affects areas around the lungs):
Chest wall / mediastinum: kyphoscoliosis, flail chest, neuromuscular disorders, mediastinal mass
Increased intraabdominal pressure: pregnancy, obesity, ascites
List the risk factors for aspiration pneumonitis.
trauma emergency surgery pregnancy GI Obstruction GERD PUD Hiatal Hernia Ascites Difficult airway management Cricoid Pressure Impaired airway reflex Head injury seizures Residual NMBA blockade
Describe the pharmacologic prophylaxis of aspiration pneumonitis.
antacids: soidum citrate, sodium bicarb, magnesium trisilate
H2 antagonists: rantidine, cimetidine, famotidine
GI stimulants: metoclopramide
PPI: omeprazole, lansoprazole, pantroprazole
antiemetics: droperidol, ondansetron
dont use routinely if not risk for aspiration, don’t give anticholinergics to reduce aspiration risk
What is Mendelson’s syndrome?
Mendelson’s syndrome is a chemical aspiration pneumonitis that was first described in OB patients receiving inhalation anesthesia. Risk factors include:
Gastric pH < 2.5
Gastric volume > 25 mL (0.4 mL/kg)
Describe the treatment of aspiration.
Tilt the head downward or to the side (first action).
Upper airway suction to remove particulate matter.
Lower airway suction is only useful for removing particulate matter. It doesn’t help the chemical burn from gastric acid.
Secure the airway to support oxygenation.
PEEP to reduce shunt.
Bronchodilators to reduce wheezing.
Lidocaine to reduce the neutrophil response.
Steroids probably don’t help.
Antibiotics are only indicated if the patient develops a fever or an increased WBC count > 48 hours
Discuss the pathophysiology and treatment of flail chest.
Flail chest is a 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 (Negative Intrathoracic Pressure)
Normal: The chest wall moves outward & lungs expand.
Flail chest: The injured ribs move inward & collapses affected region.
Expiration (Positive Intrathoracic Pressure)
Normal: The chest wall moves inward & lungs empty.
Flail chest: The injured ribs move outward & affected region doesn’t empty.
Treatment = epidural catheter or intercostal nerve blocks (higher risk of LA toxicity).
Define pulmonary hypertension, and discuss the goals of anesthetic management.
Pulmonary hypertension is defined as a mean PAP > 25 mmHg.
Causes: COPD, left-sided heart disease, connective tissue disorders
Goals: Optimize PVR
The patient with cor pulmonale (right-heart failure) is also sensitive to increased PVR, so keep these same principles in mind.
want to decrease PVR (see photo), NTG, Sildenafil, Prostaglandins, CCB, ACEI
Discuss the pathophysiology of carbon monoxide poisoning.
Carbon monoxide reduces the oxygen carrying capacity of blood (left shift). It binds to the oxygen binding site on hemoglobin with an affinity 200x that of oxygen. Oxidative phosphorylation is impaired and metabolic acidosis results.
CO is measured with a co-oximeter (not pulse oximeter)
Patients take on a cherry red appearance (not cyanosis)
SNS stimulation may be confused with light anesthesia or pain
If soda lime is desiccated, then volatile anesthetics can produce CO (Des > Iso»_space;> Sevo)
Discuss the treatment of carbon monoxide poisoning.
100% FiO2 until CoHgb is less than 5% or for 6 hours
Hyperbaric oxygen if CoHgb >25% or the patient is symptomatic
List the absolute and relative indications to one-lung ventilation.
absolute: infection, massive hmeorrhage, bronchpleural fistula, large unilateral cyst/bulla, pulmonary alveolar proteinsos
relative: thoracic aortic aneurysm, pneumonectomy, thoracoscopy, upper lobectomy, pulmonary edema s/p CABG, severe hypoxemia r/t lung disease
Discuss how anesthesia in the lateral decubitus position affects the V/Q relationship.
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 (effect of gravity).
A reduction of alveolar volume contributes to atelectasis.
The net effect is that ventilation is better in the nondependent lung and perfusion is better in the dependent lung. This creates V/Q mismatch and increases the risk of hypoxemia during OLV.
Discuss the management of hypoxemia during one-lung ventilation.
100% FiO2
Confirm DLT position with bronchoscope (poor position is the most common DLT complication)
CPAP 10 cm H2O to non-dependent (non-ventilated) lung
PEEP 5 - 10 cm H2O to dependent (ventilated) lung
Alveolar recruitment maneuver
Clamp pulmonary artery to the non-dependent (non-ventilated) lung
Resume two-lung ventilation
*If hypoxemia is severe, then it’s prudent to resume two lung ventilation promptly.
What is mediastinoscopy, and why is it performed?
Mediastinoscopy is performed to obtain biopsy of the paratracheal lymph nodes at the level of the carina. This helps the surgeon stage the tumor prior to lung resection.
What are the potential complications of mediastinoscopy? What is the most common
Innominate artery compression compromises the circulation to the right upper extremity and the right side of the circle of Willis.
Place an a-line or pulse oximeter on the right upper extremity to monitor for innominate compression.
hemorrhage from vascular injury most common
pneumo 2nd most common
Describe the Mallampati score.
The Mallampati exam assesses the oropharyngeal space. Said another way, it helps us quantify size of the tongue relative to the volume in the mouth.
Remember the mnemonic: PUSH
Class I: Pillars, Uvula, Soft palate, Hard palate
Class II: __ Uvula, Soft palate, Hard palate
Class III: __ __ Soft palate, Hard palate
Class IV: __ __ __ Hard palate
Describe the inter-incisor gap. What is normal?
The patient’s ability to open the mouth directly affects your ability to align the oral, pharyngeal, and laryngeal axes. A small inter-incisor gap creates a more acute angle between the oral and glottic openings, increasing the difficulty of intubation.
Normal = 2-3 finger breaths or 4 cm
What is the thyromental distance, and what values suggest an increased risk of difficult intubation?
The thyromental distance helps us estimate the size of the submandibular space.
With the neck extended and mouth closed, you can measure the distance from the tip of the thyroid cartilage to the tip of the mentum. Laryngoscopy may be more difficult if the TMD is less than 6 cm (3 finger-breadths) or greater than 9 cm.
measured from tip of thyroid cartilage to tip of the mentum
What is the mandibular protrusion test, and what values suggest an increased risk of difficult intubation?
The MPT assesses the function of the temporomandibular joint. The patient is asked to sublux the jaw, and the position of the lower incisors it compared to the position of the upper incisors.
Class I: Patient can move LI past UI and bite the vermilion of the lip (where the lip meets the facial skin).
Class II: Patient can move LI in line with UI.
Class III: Patient cannot move LI past UI (increased risk of difficult intubation).
What conditions impair atlanto-occipital joint mobility?
Degenerative joint disease Rheumatic arthritis Ankylosing spondylitis Trauma Surgical fixation Klippel-Feil Down syndrome
Describe the Cormack and Lehanne score.
The Cormack and Lehane grading system helps us measure the view we obtain during direct vision laryngoscopy. Obviously you can’t make this determination before performing laryngoscopy.
List 5 risk factors for difficult mask ventilation.
Beard Obese (most books say BMI > 26 kg/m2) No teeth Elderly (age > 55 years) Snoring
Mnemonic: BONES
List 10 risk factors for difficult tracheal intubation.
Small mouth opening Palate is narrow with high arch Long upper incisors Inter-incisor distance < 3 cm Mallampati class 3 or 4 Mandibular protrusion test class 3 Poor compliance of submandibular space Thyromental distance < 6 cm (<3 fingerbreadths) or > 9 cm Neck is thick and short Poor AO joint mobility (can’t touch chin to chest and/or can’t extend the neck)
List 6 risk factors for difficult supraglottic device placement.
Limited mouth opening
Upper airway obstruction (prevents passage of device into pharynx)
Altered pharyngeal anatomy (prevents seal)
Poor airway compliance (requires excessive PIP)
Increased airway resistance (requires excessive PIP)
Lower airway obstruction
List 5 risk factors for difficult invasive airway placement.
Abnormal neck anatomy (tumor, hematoma, abscess, hx of radiation)
Obesity (can’t ID cricothyroid membrane)
Short neck (can’t ID cricothyroid membrane)
Limited access to cricothyroid membrane (halo, neck flexion deformity)
Laryngeal trauma
What is angioedema?
Angioedema is the 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?
Angiotensin converting inhibitors
Treatment = Epinephrine, antihistamines, steroids (just like anaphylaxis)
Hereditary angioedema (C1 esterase deficiency) Treatment = C1 esterase concentrate or FFP (not epinephrine, antihistamines, or steroids)
What is Ludwig’s angina?
Ludwig’s angina is a bacterial infection characterized by a rapidly progressing cellulitis in the floor of the mouth. Inflammation and edema compress the submandibular, submaxillary, and sublingual spaces.
The most significant concern is posterior displacement of the tongue resulting in complete, supraglottic airway obstruction.
What is the best way to secure the airway in the patient with Ludwig’s angina?
The best way to secure the airway is with the patient awake:
Awake nasal intubation
Awake tracheostomy
Describe the Practice Guidelines for Preoperative Fasting and Use of Pharmacologic Agents to Reduce the Risk of Pulmonary Aspiration.
The Practice Guidelines for Preoperative Fasting and Use of Pharmacologic Agents to Reduce the Risk of Pulmonary Aspiration have been updated since their original publication in 1999. Here are the most current recommendations:
2 hours = Clear liquids
4 hours = Breast milk
6 hours = Nonhuman milk, infant formula, solid food
8 hours = Fried or fatty foods
Ingestion of clear liquids 2 hours before surgery reduces gastric volume and increases gastric pH.
List the 4 types of oropharyngeal airways. Which are best suited for fiberoptic intubation?
geudel
berman
williams FOB, Blind orotracheal intubation
Ovassapian - FOB
When is the best time to use an Eschmann introducer?
The Eschmann introducer is best used when a grade 3 view is obtained during laryngoscopy (grade 2 is the next best time). The likelihood of successful intubation is unacceptably low when a grade 4 view is obtained.
AKA intubating stylet, gum elastic bougie
When is a nasopharyngeal airway contraindicated?
Cribriform plate injury (risk of brain injury): LeFort II or III fracture Basilar skull fracture CSF rhinorrhea Raccoon eyes Periorbital edema
Coagulopathy (risk of epistaxis)
Previous transsphenoidal hypophysectomy
Previous Caldwell-Luc procedure
Nasal fracture
*Caution during pregnancy (risk of epistaxis)
Contrast the maximum recommended cuff pressures for an endotracheal tube vs LMA.
ETT < 25 cm H2O
LMA < 60 cm H2O
Contrast the maximum recommended peak inspiratory pressures for an LMA-Unique vs LMA-Proseal vs LMA-Supreme.
LMA-Unique < 20 cm H2O
LMA-ProSeal < 30 cm H2O
LMA-Supreme < 30 cm H2O
What is the largest size endotracheal tube that can be passed through each LMA size?
LMA 1 = ETT 3.5 LMA 2 = ETT 4.5 LMA 3 = ETT 6 LMA 4 = ETT 6 LMA 5 = ETT 7
List 6 indications for the Bullard laryngoscope.
The Bullard laryngoscope is a rigid, fiberoptic device used for indirect laryngoscopy.
Indications: Small mouth opening (minimum = 7 mm) Impaired cervical spine mobility Short, thick neck Teacher Collins syndrome Pierre-Robin syndrome
The tip is disposable. Don’t forget to recover it after you’ve intubated the patient!
Describe the proper placement of the lighted stylet.
When the patient is supine, the trachea is anterior to the esophagus. Therefore, we can look at the quality of the light shining through the neck to determine if the tip of the device is located in the trachea or esophagus.
When the lighted stylet is in the trachea, the light has to travel through less tissue, so you’ll observe a well-defined circumscribed glow below the thyroid prominence.
When the lighted stylet is in the esophagus, the light has to travel through more tissue, so you’ll observe a more diffuse transillumination of the neck without the circumscribed glow.
List 5 indications for the use of a bronchial blocker.
Bronchial blockers are indicated for patients requiring lung separation who:
Are children < 8 years of age (smallest DLT = 26F for 8 - 10 years old).
Require nasotracheal intubation.
Have a tracheostomy.
Have a single lumen ETT in place.
Require intubation after surgery, and you want to avoid changing the DLT to a single-lumen ETT at the end of the case.
How can the lumen of the bronchial blocker be used during OLV?
It can be used to:
Insufflate oxygen into the non-ventilated lung
Suction air from the non-ventilated lung (improves surgical exposure)
It can NOT be used to:
Ventilate
Suction blood, pus, or secretions from the non-ventilated lung
List 2 indications for retrograde intubation.
Unstable cervical spine (most common use of RI)
Upper airway bleeding (can’t visualize glottis)
Since RI requires time (~ 5-7 minutes for experienced practitioners), it is best used when intubation has failed but ventilation is still possible.
Compare and contrast the benefits of awake extubation.
awake pros = airway reflex remain intact, ability to maintain airway patency, decreased risk of aspiration
cons = increased CV & SNS stimulation, increased coughing, increased intracranial pressure, increased intra-ocular pressure, increased intrabdominal pressure
Deep extubation pros & cons
pros = decreased CV & SNS stimulation, decreased coughing
CONS = airway reflexes are ineffective, increased risk of airway osbstruction, increased risk of aspiration
When is the best time to use an airway exchange catheter, and what can you do with it?
The airway exchange catheter is a long, thin, flexible, hollow tube that maintains direct access to the airway following tracheal extubation. It is the most common device used to manage extubation of the difficult airway.
What else can you do with an AEC?
EtCO2 measurement Jet ventilation (via Luer-lock adapter) Oxygen insufflation (via 15 mm adapter)
