Apex Unit 1 Respiratory Flashcards
Match each intrinsic muscle of the larynx with its action on the vocal cords. Thyroarytenoi Cricothyroid Posterior cricoarytenoid Lateral cricoarytenoid
ABducts
ADducts
Elongates
Shortens
Thyroarytenoid + Shortens
Cricothyroid + Elongates
Posterior cricoarytenoid + ABducts
Lateral cricoarytenoid + ADducts
The superior laryngeal nerve innervates the
Underside of epiglottis
Cricothyroid muscles
Whenever you think about the innervation of the airway, there are 4 nerves that should come to mind:
- Trigeminal n.
- Glossopharyngeal n.
- Superior laryngeal n. (internal & external branch)
- Recurrent laryngeal n.
The question asked about the superior laryngeal nerve.
The SLN internal branch is a sensory nerve. It innervates the posterior side of the epiglottis to the top side of the vocal folds.
The SLN external branch is a motor nerve. It innervates the cricothyroid muscles.
Tensor palatine muscle relaxation will MOST likely cause airway obstruction at which level?
Soft palate
Soft palate: Relaxation of the tensor palatine muscle
Tongue: Relaxation of the genioglossus muscle
Epiglottis: Relaxation of the hyoid muscles
When compared to the trachea, which of the following is increased in the terminal bronchioles?
Cross-sectional area
The tracheobronchial tree is a branching network of airways that includes the trachea, bronchi, and bronchioles. This question asked about the anatomic and physiologic differences between the trachea and the terminal bronchioles.
A division is where an airway divides into two or more smaller airways. There are 23 – 25 divisions (or generations) in humans. At each division, the diameter of the new branches becomes smaller, however the total cross sectional area of all the airways in the division increases. This explains why airflow velocity slows as you move down the tracheobronchial tree.
The trachea contains cartilage (C-shaped rings) and goblet cells (mucus secretion), while the terminal bronchioles have neither.
Anatomic dead space begins in the mouth and ends in the:
Terminal bronchioles
The airway is functionally divided into 3 zones: conducting, respiratory, transitional.
The conducting zone is anatomic dead space. This region extends from the nares and mouth to the terminal bronchioles.
The respiratory zone is where gas exchange occurs. This region extends from the respiratory bronchioles to the alveoli.
What is the primary determinant of carbon dioxide elimination?
Alveolar ventilation
Alveolar ventilation (NOT minute ventilation) determines the rate of removal of carbon dioxide from the body. Let’s examine why…
Minute ventilation = Tidal volume x Respiratory rate
Alveolar ventilation = (Tidal volume – Dead space) x Respiratory rate
The key here is to recognize that dead space doesn’t contribute to gas exchange, so only the fraction of the tidal volume that reaches the respiratory zone contributes to gas exchange.
Which conditions will MOST likely increase the PaCO2 to EtCO2 gradient? (Select 3.)
Hypotension Endotracheal tube Laryngeal mask airway Neck flexion Positive pressure ventilation Atropine
Hypotension
Atropine
Positive pressure ventilation
Conditions that increase dead space tend to increase the volume of the conducting zone or reduce pulmonary blood flow.
Hypotension reduces pulmonary blood flow, which increases alveolar dead space.
Atropine is a bronchodilator, so it increases anatomic dead space by increasing the volume of the conducting zone.
Positive pressure ventilation increases alveolar pressure, which increases ventilation relative to perfusion. This is another way of saying that dead space increases.
Dead space is reduced by anything that reduces the volume of the conducting zone or increases pulmonary blood flow.
Examples include an endotracheal tube, LMA, or neck flexion.
A patient is in the sitting position. When compared to the apex of the lung, which of the following are higher in the base? (Select 2.)
Partial pressure of alveolar carbon dioxide
V/Q ratio
Partial pressure of alveolar oxygen
Blood flow
Partial pressure of alveolar carbon dioxide
Blood flow
The distribution of alveolar ventilation and perfusion is unequal throughout the lung.
The non-dependent region (apex in the sitting position) has a higher PAO2 and a higher V/Q ratio (V > Q).
The dependent region (base in the sitting position) has a higher PACO2 and has a lower V/Q ratio (V < Q).
Identify the statements that represent the MOST accurate understanding of V/Q mismatch. (Select 2.)
Hypoxic pulmonary vasoconstriction minimizes dead space.
Blood passing through underventilated alveoli tends to retain CO2.
The A-a gradient is usually small.
Bronchioles constrict to minimize zone 1.
Bronchioles constrict to minimize zone 1.
Blood passing through underventilated alveoli tends to retain CO2.
What was wrong with the other answers?
V/Q mismatch usually increases (not decreases) the A-a gradient.
Hypoxic pulmonary vasoconstriction minimizes shunt (not dead space).
Variables described by the law of Laplace include all of the following EXCEPT:
radius.
tension.
pressure.
density.
Density
The law of Laplace states that as the radius of a sphere or cylinder becomes larger, the wall tension increases as well.
The variables in this equation include:
Tension Pressure Radius Density is not a variable in the law of Laplace.
Select the correct statements regarding the West zones of the lung. (Select 3.)
In zone 3 pulmonary blood flow is proportional to the arterial-to-venous pressure gradient.
In zone 1 there is no pulmonary blood flow.
In zone 3 alveolar pressure exceeds venous pressure.
In zone 1 alveolar pressure is higher than arterial pressure.
In zone 2 ventilation is greater than perfusion.
In zone 2 venous pressure is higher than alveolar pressure.
In zone 1 there is no pulmonary blood flow.
In zone 1 alveolar pressure is higher than arterial pressure.
In zone 3 pulmonary blood flow is proportional to the arterial-to venous pressure gradient.
Why were the other answers wrong?
In zone 2 ventilation is matched to perfusion (not V > Q).
In zone 2 arterial (not venous) pressure is higher than alveolar pressure.
In zone 3 venous pressure exceeds alveolar pressure (not the other way around).
A patient is breathing room air at sea level. The arterial blood gas reveals a PaO2 of 60 mmHg and a PaCO2 of 70 mmHg. Calculate the patient’s alveolar oxygen concentration.
(Enter your answer in mmHg and round to the nearest whole number)
62 mmHg
The alveolar gas equation tells us the partial pressure of oxygen in the alveolus. Imagine a patient that has a PaO2 of 100 mmHg. How do you know if this is good or bad? The alveolar gas equation provides the context to make this assessment.
Alveolar oxygen = FiO2 x (Pb - PH2O) - (PaCO2 / RQ)
0.21 x ( 760 - 47 ) - (70 / 0.8) = 62.23 ~ 62 mmHg
Causes of an increased A-a gradient include: (Select 2.)
hypoxic mixture.
V/Q mismatch.
hypoventilation.
diffusion limitation.
Diffusion limitation
V/Q mismatch
The A-a gradient is the difference between PAO2 and PaO2.
After we get a blood gas (PaO2) and calculate the alveolar gas equation (PAO2), we can use the A-a gradient to determine the cause of hypoxemia.
There are 5 causes of hypoxemia: hypoxic mixture, hypoventilation, diffusion limitation, V/Q mismatch, and shunt.
The A-a gradient is normal in hypoxic mixture and hypoventilation.
The A-a gradient is increased by diffusion limitation, V/Q mismatch, and shunt.
Which conditions reduce functional residual capacity? (Select 2.)
Pulmonary edema
COPD
Advanced age
Obesity
Pulmonary edema
Obesity
The FRC is the lung volume where the inward elastic recoil of the lungs is balanced by the outward elastic recoil of the chest wall (FRC = RV + ERV).
FRC is reduced by obesity and pulmonary edema.
Patients with COPD and advanced age have an increased FRC. Air trapping increases RV, and this increases FRC.
Closing capacity is the sum of closing volume and:
expiratory reserve volume.
tidal volume.
residual volume.
functional residual capacity.
Residual volume
Closing capacity is the lung volume above residual volume where the small airways begin to collapse during expiration. It is the sum of closing volume and residual volume.
Calculate the patient’s arterial oxygen content from the data set:
Hgb 9 g/dL Heart rate 100 bpm Stroke volume 70 mL SaO2 90% PaO2 60 mmHg
(Enter your answer as mL O2/dL blood and do not round your answer)
10.872 – 11.439
Oxygen content (CaO2) tells us how much oxygen is present in 1 deciliter of blood.
Most oxygen forms a reversible bond with hgb, while the remainder dissolves into the blood according to Henry’s law.
CaO2 = (1.34 x Hgb x SaO2) + (PaO2 x 0.003)
CaO2 = (1.34 x 9 g/dl x 0.90) + (60 x 0.003) = 11.034 mL O2/dL blood
Some books will use 1.32, 1.34, 1.36, or 1.39 as the constant, so we accepted a range of answers.
It’s easy to confuse CaO2 (O2 carrying capacity) and DO2 (O2 delivery). CaO2 equals how much O2 is in the blood, while DO2 equals how much O2 is delivered the tissues per minute.
P50 is reduced by: (Select 3.)
acidosis. hypocarbia. increased 2,3 DPG. carboxyhemoglobin. hgb F. hyperthermia.
Hgb F
Hypocarbia
Carboxyhemoglobin
The oxyhemoglobin dissociation curve plots hemoglobin saturation (SaO2) vs the oxygen tension in the blood (PaO2). P50 is the PaO2 where hemoglobin is 50% saturated with oxygen.
Decreased P50 (left shift):
Hgb has a stronger hold on oxygen.
Examples: Hgb F, hypocarbia, and carboxyhemoglobin
Increased P50 (right shift):
Hgb is more willing to release oxygen.
Examples: acidosis, hyperthermia, and increased 2,3 DPG
Identify the statement that BEST describes aerobic metabolism.
Pyruvic acid is converted to lactate.
1 molecule of glucose converts to 38 molecules ATP.
NADH is the final electron accepter during electron transport.
Electron transport occurs in the cytoplasm.
1 molecule of glucose converts to 38 molecules ATP.
You spend so much time thinking about how to get oxygen to the cells, however knowing the intracellular mechanism is nearly as important. While we won’t cover a semester of biochemistry here (thank goodness) we will provide a brief review of cellular energetics on the next page.
Which ion belongs in the box with the question mark?
hamburger shift
Chloride
CO2 is the by-product of aerobic respiration. It diffuses from the cells into the venous circulation and then diffuses into erythrocytes.
In the presence of carbonic anhydrase (inside the RBC), CO2 and H2O react to form H2CO3. Carbonic acid rapidly dissociates into H+ and HCO3-. The H+ is buffered by hemoglobin, and the HCO3- is transported to the plasma to function as a buffer.
Cl- is transported into the erythrocyte to maintain electroneutrality. This is known as the chloride or Hamburger shift.
The Haldane effect states that in the presence of deoxygenated hemoglobin, the carbon dioxide dissociation curve shifts:
to the right.
to the left.
up.
down.
To the left
The Haldane effect states that at a given PaCO2, deoxygenated hemoglobin can carry more CO2. This allows hemoglobin to load more carbon dioxide at the tissue level and release more CO2 in the lungs.
Deoxygenated hemoglobin causes the CO2 dissociation curve to shift to the left.
Consequences of hypercapnia include: (Select 2.)
increased oxygen carrying capacity.
hypokalemia.
hypoxemia.
increased myocardial oxygen demand.
Hypoxemia
Increased myocardial oxygen demand
Hypercarbia affects nearly all of the systems in the body. Consequences include:
Hypoxemia
Increased myocardial oxygen demand
Hyperkalemia (not hypokalemia)
Decreased oxygen carrying capacity (not increased)
All of this is explained in detail on the next page.
Which conditions increase minute ventilation for a given PaCO2? (Select 3.) Hypoxemia Carotid endarterectomy Respiratory alkalosis Sevoflurane Surgical stimulation Salicylates
Hypoxemia
Salicylates
Surgical stimulation
The CO2 response curve illustrates the minute ventilation for a given PaCO2.
A right shift means that the respiratory center is less sensitive to CO2.
Examples: sevoflurane, s/p carotid endarterectomy
A left shift means that the respiratory center is more sensitive to CO2.
Examples: hypoxemia, salicylates, and surgical stimulation
Respiratory alkalosis is a consequence (not a cause) of a left shift.
What is the pacemaker for normal breathing? Pneumotaxic center Ventral respiratory center Apneustic center Dorsal respiratory center
Dorsal respiratory center
The dorsal respiratory center is the respiratory pacemaker (dorsal = inspiration).
The ventral respiratory center is primarily responsible for expiration (ventral = expiration).
The pneumotaxic center inhibits the DRC (inhibits the pacemaker).
The apneustic center stimulates the DRC (stimulates the pacemaker).
The central chemoreceptor:
is stimulated by pH changes in the cerebrospinal fluid.
is unaffected by bicarbonate in the serum.
is located on the dorsal surface of the medulla.
responds to PaCO2 and PaO2.
Is stimulated by pH changes in the cerebrospinal fluid
The central chemoreceptor is located on the ventral surface of the medulla (not dorsal).
It responds to PaCO2 (not PaO2).
It is stimulated by the pH of the CSF.
Because HCO3- in the plasma does not freely diffuse across the blood-brain-barrier, it does not acutely affect the central chemoreceptor. If serum HCO3- rises, it takes hours or days for the CSF pH to equilibrate.
Select the statements that BEST describe the carotid chemoreceptors. (Select 2.)
They are more sensitive after carotid endarterectomy.
Type I Glomus cells mediate hypoxic ventilatory drive.
Hering’s nerve is part of the afferent limb.
They are more sensitive to SaO2 than PaO2.
Hering’s nerve is part of the afferent limb.
Type I Glomus cells mediate hypoxic ventilatory drive.
While the central chemoreceptor in the medulla primarily responds to PaCO2, the peripheral chemoreceptors in the carotid bodies primarily respond to PaO2 (not SaO2).
Type I Glomus cells are the sensors that transduce PaO2 into an action potential. They mediate the hypoxic ventilatory drive.
This action potential is propagated along the afferent limb, which consists of Hering’s nerve and the glossopharyngeal nerve (CN IX).
Carotid endarterectomy impairs the function of the peripheral chemoreceptors on the same side.
Which reflex prevents alveolar overdistension? Hering-Breuer inflation reflex Pulmonary chemoreflex Hering-Breuer deflation reflex Paradoxical reflex of Head
Hering-Breuer inflation reflex
The Hering-Breuer inflation reflex prevents alveolar overdistension by stopping inhalation when lung volume is too large.
Which agent is MOST likely to increase intrapulmonary shunt?
Propofol
Desflurane
Ketamine
Etomidate
Desflurane
Hypoxic pulmonary vasoconstriction minimizes shunt by diverting pulmonary blood flow away from unventilated alveoli.
Agents that impair HPV increase the shunt fraction and reduce PaO2.
Examples: Halogenated anesthetics (> 1 – 1.5 MAC)
IV anesthetic agents preserve HPV.
Click on the area where the needle is inserted during a right superior laryngeal nerve block.
injected just below the border of the greater cornu of the hyoid bone.
There are 3 key airway blocks:
- Glossopharyngeal
- Superior laryngeal
- Transtracheal
To block the superior laryngeal nerve, local anesthetic is injected just below the border of the greater cornu of the hyoid bone.
1 mL of local anesthetic is injected outside of the thyrohyoid membrane.
2 mL are injected just beneath the thyrohyoid membrane.
Click on the corniculate cartilage.
NOT the arytenoids but same spot!!
You guys have seen this view hundreds of times. Even so, you’ve likely succumbed to one of the most common misteachings in anesthesia. You CANNOT see the arytenoids during laryngoscopy!
What you are actually seeing are the corniculate and cuneiform cartilages. The cuneiforms are lateral to the corniculates.
Click on the region of the skull where Larson’s maneuver is performed.
You may know this concept as the laryngospasm notch. Like it or not, the NCE likes to test your vocabulary.
There are times where you’ll have to know two or more words for the same thing. Believe it or not, we have 5 synonyms for pseudocholinesterase! Don’t worry, we’ll cover that in the neuromuscular blockers tutorial. For now, let’s get back to laryngospasm and Larson’s maneuver.
Chemicals that contribute to increased airway resistance include: (Select 3.) inositol triphosphate. cyclic adenosine monophosphate. vasoactive intestinal peptide. phospholipase C. leukotrienes. nitric oxide.
Inositol triphosphate
Phospholipase C
Leukotrienes
While second messenger systems are covered in the autonomic nervous system tutorial, it’s important to discuss them as they relate to control of airway caliber.
Bronchoconstriction is mediated by the PNS (muscarinic-3 receptor) and the immune response.
Bronchodilation is mediated by circulating catecholamines and the VIP receptor (nitric oxide pathway).
Match each drug with its corresponding drug class. Theophylline Zafirlukast Cromolyn Triamcinolone
Theophylline + Methylxanthine
Zafirlukast + Leukotriene modifier
Cromolyn + Mast cell stabilizer
Triamcinolone + Corticosteroid
Many of you will see questions very similar to this on the NCE. While it’s nearly impossible to learn all of the drugs in all of the classes, we recommend that you memorize at least the most common examples.
Which pulmonary function test is the MOST sensitive indicator of small airway disease?
Forced expiratory volume in 1 second
Diffusion capacity of carbon monoxide
Forced vital capacity
Forced expiratory flow 25-75%
Forced expiratory flow at 25-75% vital capacity
Airway resistance can be measured with dynamic pulmonary function testing. These tests include:
FEV1
FVC
FEV1/FVC ratio
Forced expiratory flow at 25-75% vital capacity
Forced expiratory flow is the average forced expiratory flow during the middle half of the FEV measurement. This test is the most sensitive indicator of small airway disease (obstruction).
Diffusion capacity of CO is a measure of gas transfer and not airway resistance.
All of the following are independent risk factors for postoperative pulmonary complications EXCEPT: asthma. chronic obstructive pulmonary disease. age > 65 years. congestive heart failure.
Asthma
Positive predictors of postoperative pulmonary complications can be divided into patient, procedure, and diagnostic tests.
Patient examples: age > 60, CHF, COPD, and cigarette smoking
Procedure examples: surgical site, procedure lasting > 2.5 hours, and GA
Diagnostic test examples: serum albumin < 3.5 g/dL
Mild/moderate asthma, ABGs, and PFTs have not been shown to be independent predictors of postoperative pulmonary complications.
A patient with severe kyphoscoliosis is expected to have a reduced: (Select 2.)
FEF 25-75%.
FRC.
FEV1.
FEV1/FVC ratio.
FEV1
FRC
Restrictive disease reduces all of the lung volumes. FRC is decreased, although it may remain unchanged relative to the other volume and capacities.
Since TLC is smaller and there is less volume to exhale, the amount of air exhaled in 1 second (FEV1) will be reduced. The FEV1/FVC ratio is usually unchanged.
The FEF 25-75% is sensitive to increase air flow resistance in the medium sized airways. This isn’t a problem for patients with a restrictive lung disease.
A patient with asthma experiences bronchospasm immediately following tracheal intubation. This is MOST likely the result of: decreased sympathetic tone. mast cell degranulation. histamine release. vagal stimulation.
Vagal stimulation
In the textbooks, you’ll usually find that asthma is classified by etiology or severity, but are these systems helpful in the differential diagnosis of asthmatic bronchospasm in the operating room? A more useful framework is to consider the source of bronchospasm as the result of direct PNS stimulation or as a consequence of an immune response (mast cell degranulation).
Although intubation does not cause an immune response, it can activate vagal afferents leading to bronchospasm. This is most likely to occur during a lighter plane of anesthesia.
Airway smooth muscle is not innervated by the SNS, so a reduction in SNS tone can’t precipitate bronchospasm. Instead, airway smooth muscle is rich in beta-2 receptors, which explains how beta-2 agonists (epi, albuterol) cause bronchodilation.
Although some of our induction agents cause histamine release, there are others that don’t. Since the question didn’t specifically state which drugs were administered, you shouldn’t make any assumptions. The stem gives you exactly what you need to answer the question.
Which drug is LEAST likely to be effective in relieving symptoms of acute bronchospasm?
Epinephrine 1 mcg/kg IV
Ketamine 1 mg/kg IV
Hydrocortisone 2 mg/kg IV
Lidocaine 1.5 mg/kg IV
Hydrocortisone 2 mg/kg IV
The key here is “acute” bronchospasm. Hydrocortisone may be given to prevent the requirement for longer term therapy, however it does nothing to reverse the acute phase. Indeed, corticosteroids require several hours to take effect.
Epinephrine, ketamine, and lidocaine are useful in the treatment of acute bronchospasm.
Alpha-1 antitrypsin deficiency: (Select 2.)
can be treated with IgG.
increases the risk of bronchospasm.
causes panlobular emphysema.
is the most common metabolic disease affecting the liver.
Is the most common metabolic disease affecting the liver
Causes panlobular emphysema
Alpha-1 antitrypsin deficiency causes a relative increase in alveolar protease activity. This enzyme degrades pulmonary connective tissue and leads to the development of panlobular emphysema. Cigarette smoking doubles the rate of alveolar destruction.
A deficiency in this enzyme does not increase the risk of bronchospasm.
The only treatment for this condition is liver transplantation.
Identify the MOST appropriate strategy for mechanical ventilation in the patient with COPD.
Tidal volume 10-12 mL/kg
Respiratory rate 7 breaths per minute
FiO2 < 50%.
I:E ratio 1:1
Respiratory rate 7 breaths per minute
COPD is an issue of getting the air out of the lung. Any intervention that increases expiratory time will be useful. A slower respiratory rate accomplishes this goal.
An I:E ratio of 1:1 increases I time at the expense of E time. This increases the risk of dynamic hyperinflation. FiO2 should be adjusted to prevent hypoxemia. Smaller tidal volumes (6-8 mL/kg) are preferred, again to minimize the risk of dynamic hyperinflation.
A patient with COPD is mechanically ventilated. Which interventions will improve this patient’s condition? (Select 2.) rising baseline
Increase inspiratory flow.
Disconnect the circuit.
Decrease respiratory rate.
Increase inspiratory time.
Decrease respiratory rate
Disconnect the circuit
The airway pressure in this waveform clearly depicts dynamic hyperinflation, otherwise known as breath stacking. Patients with COPD have a longer expiratory time constant, and this means they require a longer period of time to exhale fully.
Of the answer choices provided, there are two options that reverse dynamic hyperinflation. By reducing the respiratory rate, the patient will spend more time over the course of a minute in E time. If PEEP becomes dangerously elevated, the definitive treatment for dynamic hyperinflation is to remove the patient from the ventilator.
Increasing inspiratory time is another way of saying reducing expiratory time, so this choice will actually make the patient’s condition worse. The inspiratory flow determines how fast the tidal volume is delivered to the patient. Increasing the inspiratory flow will deliver the preset tidal volume faster, and this does nothing to facilitate expiration.
All of the following are examples of restrictive lung disease EXCEPT: negative pressure pulmonary edema. cystic fibrosis. sarcoidosis. flail chest.
Cystic fibrosis
CF is an autosomal recessive genetic disorder that affects chloride channels. Excessive pulmonary secretions plug the airways and create an obstructive ventilatory defect. Management is similar to COPD and be sure to humidify the airway to minimize the tenacity of secretions. Avoid anticholinergics for the same reason.
Sarcoidosis is a chronic granulomatous disorder that results in the development of granulomas that may progress to fibrosis. Nearly all patients with sarcoidosis have pulmonary involvement, and the disease can also affect the heart, CNS, skin, and eyes. They are often on steroids, so be sure to continue this therapy throughout the perioperative period.
Flail chest results when cracked ribs move inward during inspiration, while the rest of the rib cage moves outward. The flail region then moves outward during expiration. Tidal volumes are reduced during spontaneous ventilation and increases the risk of hypoxemia. Positive pressure ventilation is the best treatment until the ribs can be stabilized.
Negative pressure pulmonary edema increases interstitial lung water. This creates a restrictive defect.
All of the following reduce the incidence of ventilator-associated pneumonia EXCEPT:
oropharyngeal decontamination.
limiting sedation.
proton pump inhibitors.
minimizing the duration of mechanical ventilation.
Proton pump inhibitors
Methods to reduce the incidence of ventilator associated pneumonia include:
Minimizing the duration of mechanical ventilation
Limiting sedation
Oropharyngeal decontamination
Proton pump inhibitors increase gastric pH, which provides an environment where bacterial pathogens can flourish. Microaspiration introduces these pathogens into the lungs.
What is the first line treatment for this patient? (tension pneumo)
14g angiocath insertion at the 2nd intercostal space midclavicular line
Pericardiocentesis
Cardiopulmonary resuscitation
Chest tube insertion
14g angiocath insertion at the 2nd intercostal space midclavicular line
Emergency treatment of a tension pneumothorax includes insertion of a 14g angiocath into the 2nd intercostal space at the mid-clavicular line or the 4th or 5th intercostal space at the anterior axillary line. This will release the tension and relieve hemodynamic instability, but not the underlying pneumothorax.
Chest tube insertion is the definitive treatment. Pericardiocentesis is a treatment for pericardial tamponade. CPR should not be started based on a CXR alone.
Order the monitors of venous air embolism according to their relative sensitivities.
(1 is most sensitive, and 4 is least sensitive)
TEE
precordial doppler
CVP
ETCO2
TEE + 1
Precordial Doppler + 2
EtCO2 + 3
CVP + 4
A patient with pulmonary hypertension develops tricuspid regurgitation. Which treatments will MOST likely improve this patient’s condition? (Select 3.)
Nitric oxide Nitroglycerine Nitrous oxide Hypothermia PEEP Hyperventilation
Hyperventilation
Nitric oxide
Nitroglycerine
When managing the adult with right heart failure or the infant with bronchopulmonary dysplasia or a right-to-left shunt, you must understand how to manipulate pulmonary vascular resistance.
PVR is reduced by: hyperventilation, nitric oxide, and nitroglycerine.
PVR is increased by: hypoxia, hypercarbia, nitrous oxide, hypothermia, and PEEP.
Carbon monoxide:
poisoning is reversed with methylene blue.
shifts the oxyhemoglobin dissociation curve to the right.
binds to the oxygen binding site on hemoglobin with an affinity 200 times that of oxygen.
production is highest with isoflurane.
Binds to the oxygen binding site on hemoglobin with an affinity 200 times that of oxygen
Carbon monoxide:
Shifts the oxyhemoglobin dissociation curve to the left (not right).
Is produced in soda lime, particularly after desiccation. Production is highest with desflurane (des > iso»_space;>sevo).
Poisoning (increased carboxyhemoglobin) is treated with oxygen therapy.
Methemoglobinemia is treated with methylene blue.
Identify the strongest indications for intubation and mechanical ventilation. (Select 2.) Inspiratory force < 25 cm H2O Respiratory rate 35 breaths per minute PaCO2 > 60 mmHg Vital capacity 25 mL/kg
PaCO2 > 60 mmHg
Inspiratory force < 25 cm H2O
Other indications for tracheal intubation include:
Vital capacity < 15 mL/kg (not < 25)
Respiratory rate > 40 breaths per minute (not > 35)
Keep in mind that no single variable indicates the need for intubation and mechanical ventilation.
Identify the absolute indications for one-lung ventilation. (Select 2.)
Esophageal resection
Bronchopleural fistula
Thoracic aortic aneurysm repair.
Pulmonary infection
Pulmonary infection
Bronchopleural fistula
Indications for one lung ventilation are divided into absolute and relative.
Absolute indications are further broken down into 3 areas:
Isolation to avoid contamination Control of distribution of ventilation Unilateral bronchopulmonary lavage Most indications that improve surgical exposure are relative indications. Examples include esophageal resection and thoracic aortic aneurysm repair.
You placed a left-sided double lumen endotracheal tube and clamped the tracheal lumen. Match the complication of tube position with the region where breath sounds will be heard.
DLT is in too far on left side + Right breath sounds absent
DLT is too far on right side + Left breath sounds absent
DLT tip is in the trachea + Left and right breath sounds heard
Identify the MOST common serious complications of mediastinoscopy. (Select 2.) Pneumothorax Chylothorax Hemorrhage Left recurrent laryngeal nerve injury
Hemorrhage
Pneumothorax
The thorax contains some high value real estate, which explains why there are many complications associated with mediastinoscopy.
The most common serious complications are: #1 Hemorrhage #2 Pneumothorax (usually right side)
The thoracic ducts drain lymph into the subclavian veins. The left duct is much larger than the right duct, which explains why a left-sided injury is more common than a right-sided injury. Chylothorax (chyle or lymphatic fluid in the pleural space) is the result of thoracic duct injury.
The left recurrent laryngeal nerve loops under the aortic arch before ascending the trachea. This explains why the left RLN is more susceptible to injury.
What is this patient’s mandibular protrusion test classification?
(Enter a number)
overbite
Class 3
The mandibular protrusion test assesses the function of the temporomandibular joint. The patient is asked to sublux the jaw, and the position of the lower incisors is compared to the position of the upper incisors.
A class III assessment (like the patient in this question) suggests a more difficult laryngoscopy.
Which muscle abducts the vocal cords? Lateral cricoarytenoid Cricothyroid Aryepiglottic Posterior cricoarytenoid
Posterior cricoarytenoid
The posterior cricoarytenoid is the only muscle that ABducts the vocal cords. You may question the clinical relevance of knowing these sorts of details, however the NBCRNA website has a practice question about the intrinsic laryngeal muscles. That’s a pretty good reason to learn it.
The cricothyroid is the only muscle that tenses (elongates) the vocal cords.
The aryepiglottic closes the laryngeal vestibule, and the lateral cricoarytenoid ADDucts the vocal cords.
The cricothyroid muscle is innervated by the:
external branch of the superior laryngeal nerve.
internal branch of the superior laryngeal nerve.
glossopharyngeal nerve.
recurrent laryngeal nerve.
External branch of the superior laryngeal nerve.
Two branches of the vagus nerve provide innervation to the larynx: the superior laryngeal n. and the recurrent laryngeal n.
The external branch of the SLN innervates the cricothyroid muscle. Remember that this is the only muscle that tenses (elongates) the vocal cords.
The internal branch of the superior laryngeal n. is purely sensory.
The recurrent laryngeal nerve innervates all of the other intrinsic laryngeal muscles.
The glossopharyngeal n. does not innervate the larynx.
Match the nerve to the structure that it innervates. Trigeminal Glossopharyngeal Recurrent laryngeal Superior laryngeal
Trigeminal - Anterior tongue
Glossopharyngeal - Vallecula
Recurrent laryngeal - Trachea
Superior laryngeal - Posterior epiglottis
Knowing the sensory innervation of the airway is the foundation of understanding regional anesthesia for fiberoptic intubation. It will also help identify areas of failed topicalization. From proximal to distal:
Anterior tongue: Trigeminal (V) V3 - mandibular branch
Posterior tongue: Glossopharyngeal (IX)
Soft palate: Glossopharyngeal (IX)
Oropharynx: Glossopharyngeal (IX)
Vallecula: Glossopharyngeal (IX)
Anterior epiglottis: Glossopharyngeal (IX)
Posterior epiglottis: Superior laryngeal internal branch (X)
Laryngeal mucosa to level of vocal cords: Superior laryngeal internal branch (X)
Laryngeal mucosa below level of vocal cords: Recurrent laryngeal (X)
Trachea: Recurrent laryngeal (X)
In preparation for an awake intubation, you anesthetize the upper airway with aerosolized lidocaine. Shortly after you begin the procedure, the patient is unable to tolerate the scope just beyond the epiglottis but before the vocal cords. Which regional technique will increase the patient’s ability to tolerate the rest of the procedure?
2 mL at the tonsillar pillars bilaterally
3 mL at the inferior aspect of the greater cornu of the hyoid bone bilaterally
4 mL at the thyroepiglottic membrane
5 mL at the cricothyroid membrane
3 mL at the inferior aspect of the greater cornu of the hyoid bone bilaterally
There are three nerve blocks that will provide anesthesia for oral fiberoptic intubation: glossopharyngeal, superior laryngeal, and recurrent laryngeal. Once you learn the innervation of the airway, this question becomes much easier.
This patient tolerated the scope in the oropharynx, which is innervated by the glossopharyngeal nerve. Once the scope entered the territory covered by the superior laryngeal internal branch, the patient became uncomfortable. To increase his tolerance for the rest of the procedure, you’ll need to know which block to perform (superior laryngeal n. block) and know how to do it (inject 3 mL at the inferior aspect of the greater cornu of the hyoid bone bilaterally).
This also could’ve been a hotspot question. As you study each question, ask yourself other ways that the question writer might cover the same material.
The glossopharyngeal n. block is performed by injecting 1 - 2 mL at the tonsillar pillars bilaterally.
The transtracheal block is performed by injecting 3 - 5 mL through the cricothyroid membrane.
Which of the following is MOST likely to injure the left RLN while sparing the right RLN?
Parathyroidectomy
External pressure from an endotracheal tube
External pressure from a laryngeal mask airway
Mitral stenosis
Mitral stenosis
The right RLN loops under the right subclavian artery, while the left RLN loops under the aorta. This makes the left RLN more susceptible to injury.
Causes of left RLN (only) injury include:
Mitral stenosis (left atrial enlargement compresses the nerve and may present as hoarseness).
PDA ligation
Aortic arch aneurysm
Thoracic tumor
Causes of left or right RLN injury include: parathyroid or thyroid surgery, external pressure from an LMA or ETT, neck tumor, and neck extension.
For the patient in the sitting position, order the cartilages from superior to inferior.
(One is most superior and four is most inferior)
Epiglottis
Corniculate
Arytenoid
Cricoid
Epiglottis - 1
Corniculate - 2
Arytenoid - 3
Cricoid - 4
This question forces you to see the anatomy with your mind’s eye. Whenever you answer any question, try to visualize what is going on. Maybe an image from this website, a textbook, or something of your own creation. Additionally, you should be able to label these if you are presented with the posterior or sagittal cut of the larynx.
Order from most superior to most inferior in the sitting position: Epiglottis Corniculate Arytenoid Cricoid
How many unpaired cartilages are present in the larynx?
Three
The larynx consists of 9 cartilages (3 paired and 3 unpaired):
Paired cartilages = corniculate, arytenoid, and cuneiform
Unpaired cartilages = epiglottis, thyroid, and cricoid
Where is the adult larynx located?
C2-C4
C3-C6
C4-C7
C5-T1
C3-C6
The adult larynx is located at the C3-C6 vertebrae.
By comparison, the infant larynx is located at C2-C4.
Risk factors for intraoperative laryngospasm include: (Select 3.)
old age. hypercapnia. exposure to second hand smoke. deep anesthesia. gastroesophageal reflux disease. recent upper respiratory tract infection.
Gastroesophageal reflux disease
Exposure to second hand smoke
Recent upper respiratory tract infection
Laryngospasm is the sustained and involuntary contraction of the vocal cord adductors that results in the inability to ventilate. This response often outlasts the stimulus, and may result in complete airway obstruction, negative pressure pulmonary edema, gastric aspiration, cardiac arrest, and death.
Risk factors include:
Age < 1 year (not old age) Hypocapnia (not hypercapnia) Light anesthesia (not deep anesthesia) Saliva or blood in the upper airway Gastroesophageal reflux disease Exposure to second hand smoke Recent upper respiratory tract infection
Match the upper airway dilator muscle to its function.
Tensor palatine - Opens the nasopharynx
Genioglossus - Opens the oropharynx
Hyoid muscles - Open the hypopharynx
The upper airway dilator muscles maintain airway patency. Impairment of these muscles (anesthesia, sedation or OSA) can contribute to airway obstruction.
All of the following are landmarks for Larson's maneuver EXCEPT the: mastoid process. ramus of mandible. mandibular body. skull base.
Mandibular body
Larson’s maneuver is another name for stimulating the laryngospasm notch. Application of postcondylar pressure stimulates a sigh and effectively breaks laryngospasm.
Landmarks for Larson’s maneuver include:
Posterior: Mastoid process
Superior: Skull base
Anterior: Ramus of mandible
Also, don’t confuse Larson’s maneuver with Muller’s maneuver. Muller’s maneuver is inhaling against a closed glottis. It’s the opposite of the Valsalva maneuver - exhaling against a closed glottis.
Which type of pneumocyte produces surfactant?
Two
There are three types of pneumocytes (alveolar cells):
Type 1: Cells where gas exchange occurs ~80 percent of the alveolar surface
Type 2: Produce surfactant and can divide to produce type 1 cells
Type 3: Macrophages that fight lung infection
What is the MOST common etiology of hypoxemia in the postanesthesia recovery area?
Left-to-right shunt
Ventilation/perfusion mismatch
Hypoxic mixture
Diffusion limitation
Ventilation/perfusion mismatch
A ventilation/perfusion mismatch (specifically atelectasis) is the most common cause of postoperative hypoxemia.
As FRC becomes smaller (the result of anesthesia and surgery), there is less radial traction to hold the airways open. The ultimate result is atelectasis, right-to-left shunt, V/Q mismatch, and hypoxemia.
Treatment includes humidified oxygen, mobility, and pulmonary toilet (coughing, deep breathing, incentive spirometry).
Intrapleural pressure becomes positive during: end-inspiration. maximum inspiration. forced exhalation. end-expiration.
Forced exhalation
Breathing is a process that creates cyclic pressure changes inside the thorax. This mechanism exchanges fresh gas in the upper airway with alveolar gas in the distal airway, saturating hemoglobin with oxygen and eliminating carbon dioxide from the blood.
For air movement to occur, the airways must remain patent. Transpulmonary pressure is the pressure inside the airway (it keeps the airway open).
Transpulmonary pressure = alveolar pressure - intrapleural pressure
Intrathoracic pressure and intrapulmonary pressure are other names for transpulmonary pressure.
During tidal breathing:
Transpulmonary pressure is always positive (keeps airway open).
Intrapleural pressure is always negative (keeps lungs inflated).
Alveolar pressure becomes slightly negative during inspiration and slightly positive during expiration.
Aside from pathologic states, such as pneumothorax, the only time that intrapleural becomes positive is during a forced expiration.
Which muscle(s) provide the MOST significant contribution to forced exhalation?
Rectus abdominis
Sternocleidomastoids
Internal intercostals
Diaphragm
Rectus abdominis
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. 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.
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.
Knowing this should help you better understand why upper abdominal surgery increases the risk of post-operative pulmonary complications.
Click on the region of the alveolar compliance curve where ventilation is the greatest.
Alveolar ventilation is a function of alveolar size and its position on its compliance curve (Alveolar compliance = Alveolar volume / Alveolar Pressure).
The best ventilated alveoli are the most compliant.
They exchange more gas, because their volumes change more throughout the respiratory cycle.
These alveoli reside at the steep slope of the curve.
The least ventilated alveoli are the least compliant.
They exchange less gas, because their volumes change very little throughout the respiratory cycle.
These alveoli reside near the top of the curve.
Which letter corresponds with the region where dead space is the greatest?
A B C D perfusion ventialtion plot that makes X
Dead space is ventilation without perfusion and shunt is perfusion without ventilation.
The graph examines the V/Q relationship in the entire lung.
Point C marks where ventilation and perfusion are equally matched.
Point D marks the region where ventilation is greater than perfusion; dead space is increased here.
Points A and B mark where perfusion exceeds ventilation; shunt is increased here.
Compared to spontaneous ventilation, what happens to the Vd/Vt ratio when a patient is placed on a mechanical ventilator?
It increases
It decreases
It remains the same
There is not enough information to answer this question.
It increases
Vd/Vt describes the fraction of the tidal volume that is lost to dead space. Said another way, this gas is not involved in alveolar gas exchange.
In the spontaneous ventilating patient, we can assume that the Vd = 2 mL/kg and Vt = 6 mL/kg. For easy math, we’ll call Vd 150 mL and Vt 450 mL.
Vd/Vt = 150 mL / 450 mL = 0.33 = 33%
Mechanical ventilation increases alveolar pressure, and this increases ventilation relative to perfusion. This explains why Vd/Vt increases to 0.5 or 50 percent. Said another way, mechanical ventilation increases West zone one.
A patient’s PaCO2 has increased while her EtCO2 has decreased. All of the following are likely to contribute to this phenomenon EXCEPT:
increasing the tubing length of the circle system.
amniotic fluid embolism.
hypotension.
chronic obstructive pulmonary disease.
Increasing the tubing length of the circle system
This question asked about an increased PaCO2-EtCO2 gradient. This is another way of asking what increases dead space ventilation or West zone one.
The most common cause of increased dead space under general anesthesia is a reduction in cardiac output.
COPD and pulmonary embolism increase dead space. Other causes include anticholinergics, mechanical ventilation, neck extension, adding a heat and moisture exchanger between the y-piece and the endotracheal tube, and an incompetent unidirectional valve.
Remember that dead space begins at the y-piece. Increasing the length of the inspiratory or expiratory limb of the anesthesia circuit does NOT affect dead space. The only time that the limbs contribute to increased Vd is when one (or both) of the unidirectional valves is incompetent.
What is the consequence of adding a heat and moisture exchanger between the endotracheal tube and the y-piece. Assume that minute ventilation is held constant. (Select 2.)
PaCO2 decreases
PaCO2 increases
PaO2 decreases
PaO2 remains unchanged
PaCO2 increases
PaO2 decreases
Adding an HME in-between the endotracheal tube and the y-piece increases apparatus dead space. If ventilation is held constant, the PaCO2 rises.
An increased PaCO2 increases the alveolar concentration of CO2. Remember the alveolar gas equation? One of the many teaching points from this equation is that an increased PaCO2 causes the alveolar partial pressure of O2 to decrease. If this doesn’t ring a bell, be sure to go back and read this in the Respiratory II: Physiology Tutorial.
All of the following variables are required to calculate the partial pressure of alveolar oxygen EXCEPT:
PaCO2.
PaO2.
barometric pressure.
respiratory quotient.
PaO2
The alveolar gas equation is among the most important calculations in anesthesia. Chances are you’ll see this concept tested in some way on the NCE. Here’s the equation.
PAO2 = FiO2 x (Pb - PH2O) - (PaCO2 / RQ)
PAO2 = partial pressure of O2 inside the alveolus FiO2 = fraction of inspired oxygen Pb = barometric pressure PH2O = humidity of inspired gas (assume this is 47 mmHg) PaCO2 = partial pressure of CO2 in the blood RQ = respiratory quotient (CO2 production / O2 consumption = 0.8)
All of the following venous systems contribute to anatomic shunt EXCEPT the:
Thebesian veins.
bronchiolar veins.
pleural veins.
internal thoracic veins.
Internal thoracic veins (internal mammary veins)
Anatomic shunt (venous admixture) describes any venous blood that empties directly into the left side of the heart. Since this blood bypasses the lungs, it never has the opportunity to saturate with oxygen. Indeed, anatomic shunt explains why there is always an A-a gradient.
There are three causes of anatomic shunt: 1. Venous blood that empties into the left atrium: Thebesian veins (drains left heart) Bronchiolar veins (drains bronchial circulation) Pleural veins (drains bronchial circulation)
- Right-to-left shunt due to an intracardiac lesion.
- AV malformations that develop as a consequence of liver disease.
Venous admixture increases when:
inspiratory reserve volume increases.
inspiratory reserve volume decreases.
expiratory reserve volume increases.
expiratory reserve volume decreases.
Expiratory reserve volume decreases
Don’t you just love it when a question ties a bunch of concepts together?
Whenever you see shunt or venous admixture, you should think about FRC. Since FRC is the sum of residual volume and expiratory reserve volume, a reduction in ERV leads to a reduction in FRC. A smaller FRC decreases the amount of pulmonary blood that comes into contact with oxygenated alveoli per unit time. This increases the venous admixture (shunt).
In the clinical environment, a smaller FRC explains the faster rate of arterial desaturation during apnea as well as an increased A-a gradient.
Residual volume contributes to what percentage of total lung capacity?
10%
15%
20%
25%
20 percent
The residual volume is the volume of gas that remains in the lungs after a full exhalation.
In the healthy 70 kg adult, the residual volume = 1200 mL and the total lung capacity = 5800 mL.
You were asked how RV contributes to the overall percentage of the TLC (1200 mL / 5800 mL = 20%).
You must be able to calculate each of the four lung volumes and four lung capacities, and this requires knowing the normal value for each one.
Match each lung capacity to its respective components.
Total Lung volume = IRV + TV + ERV + RV
Vital capacity = IRV + TV + ERV
Inspiratory capacity = IRV + TV
Functional residual capacity = ERV + RV
The end-tidal CO2 is 5 percent. Convert this to mmHg.
Assume you are at sea level, and enter your answer as a whole number
38 mmHg
Don’t be intimidated by calculation questions! This one is easy once you understand the concept.
Dalton’s law of partial pressures says that the sum of the partial pressures of each gas in a mixture equals the total partial pressure of the mixture.
P total = P1 + P2 + P3…
The atmospheric pressure at sea level is 760 mmHg, so this is the total partial pressure. All you have to do is calculate 5 percent of this number.
Atmospheric pressure = 760 mmHg
End-tidal CO2 = 5 percent
So, what is five percent of 760 mmHg? The correct answer is 38 mmHg.
You could also use this same calculation (or use algebraic substitution depending on the variables provided in the stem) if you were asked to calculate the partial pressure or vol% of an anesthetic gas in a container.
How much oxygen is consumed by a 70 kg healthy adult at rest?
(Enter your answer as mL/100g/min)
0.357 mL/100g/min (we also accepted 0.350)
The NCE might ask about normal oxygen consumption as mL/min, mL/kg/min, or mL/100g/min.
- VO2 as mL/min:
The classic answer for a 70 kg adult is 250 mL/min.
The classic answer on a per weight basis is 3.5 mL/kg/min.
Commit both of these to memory. - VO2 as mL/kg/min:
If you chose to use 250 mL/min, then simply divide 250 mL/min by the patient’s weight (250 mL/min divided 70 kg = 3.57 mL/kg/min).
Alternatively, you could’ve used 3.5 mL/kg/min, since this is the number we told you to memorize. - VO2 as mL/100g/min:
You’ll need to change kg to 100g.
3.57 mL/kg/min = 0.357 mL/100g/min
Or … 3.5 mL/kg/min = 0.350 mL/100g/min
EMLA cream toxicity: (Select 2.)
increases P50.
decreases P50.
shifts the oxyhemoglobin dissociation curve to the left.
shifts the oxyhemoglobin dissociation curve to the right.
Decreases P50
Shifts the oxyhemoglobin dissociation curve to the left
You’ll see plenty of questions that require you to apply knowledge from several different subject areas. This is a perfect example.
EMLA cream contains prilocaine.
Prilocaine is metabolized to o-toluidine.
O-toluidine causes methemoglobinemia.
Methemoglobin decreases P50 (shifts the oxyhemoglobin dissociation curve to the left).
As an aside, methemoglobinemia is treated with IV methylene blue 1-2 mg/kg.
By the time you’ve completed APEX, this type of thinking will become second nature for you.
Match each concept with its definition.
The Bohr effect describes how changes in acid (PCO2 or H+) alter the carrying capacity of O2 in the blood. It explains why hemoglobin releases O2 at the tissue level and binds O2 in the lungs. Remember bOHr = Oxygen + Hgb.
The Haldane effect describes how changes in PO2 in the blood alter the carrying capacity of CO2 in the blood. It explains why venous blood can carry more CO2 than arterial blood.
The Hamburger phenomenon describes how Cl- is exchanged for HCO3- to maintain electroneutrality when the erythrocyte acts as a buffer.
Which phenomenon is responsible for tachypnea that accompanies pulmonary embolism?
J receptor stimulation
Dive reflex
Paradoxical reflex of Head
Hering-Breuer inflation reflex
J receptor stimulation
J receptor stimulation causes tachypnea. These receptors are activated by pulmonary embolism or during pulmonary vascular congestion, such as CHF.
The Hering-Breuer inflation reflex stops inspiration when the lungs become hyperinflated.
The paradoxical reflex of head causes a newborn baby to take her first breath.
The dive reflex causes apnea, bradycardia, and vasoconstriction when the face is submerged in cold water.
Select the statement that BEST describes hypoxic pulmonary vasoconstriction.
Nitroprusside increases venous admixture.
Low PaO2 causes pulmonary vasoconstriction.
1.5 MAC desflurane stimulates pulmonary vasoconstriction.
It achieves maximum effect after two hours.
Nitroprusside increases venous admixture
Hypoxic pulmonary vasoconstriction minimizes shunt by reducing blood flow through poorly ventilated alveoli. 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 minutes.
Anything that inhibits HPV increases shunt. Examples include: Halogenated anesthetics > 1-1.5 MAC Phosphodiesterase inhibitors Dobutamine Vasodilators IV anesthetics do not inhibit HPV.
Anesthesia-induced atelectasis is BEST reversed by:
increasing peak airway pressure to 30 cm H2O for 8 seconds.
increasing peak airway pressure to 40 cm H2O for 8 seconds.
using a tidal volume of 6 mL/kg and positive end-expiratory pressure of 5 cm H2O.
using a tidal volume of 6 mL/kg and positive end-expiratory pressure of 10 cm H2O.
Increasing peak airway pressure to 40 cm H2O for eight seconds
Alveolar recruitment maneuvers (ARMs) are the best way to reverse anesthesia-induced atelectasis. Indeed, increasing peak airway pressure to 30 cm H2O is required for initial reopening, and increasing the PIP to 40 cm H2O for eight seconds appears to reverse anesthesia-induced atelectasis almost completely
The application of PEEP reverses atelectasis, but only partially. PEEP should be applied after an ARM in an effort to prevent open airways from collapsing again. Mixing air with oxygen also helps to prevent atelectasis.
Which diagnostic indicator is MOST indicative of a severe asthma attack?
MMEF = 40% PaO2 = 65 mmHg FEV1 = 30% PaCO2 = 45 mmHg
FEV1 = 30%
Spirometry: There are two key measures that quantify the severity of expiratory airflow obstruction:
1. FEV1 = The volume of air that can be expired in 1 second.
Normal = > 80%
Severe = < 35%
- MMEF = Best test of airflow in the medium size airways.
Normal = > 75%
Severe = < 30%
Blood Gases: The PaO2 and PaCO2 change in predictable ways during a severe asthmatic attack.
The most common ABG findings during an asthmatic attack are hypocarbia and respiratory alkalosis. CO2 retention usually begins when FEV1 < 25%; this is a sign of impending respiratory failure!
Bronchospasm can cause hypoxemia due to V/Q mismatch, but this typically doesn’t occur until the FEV1 < 50%.
All of the following are appropriate in the setting of acute bronchospasm EXCEPT:
hydrocortisone.
sevoflurane.
montelukast
albuterol.
Montelukast
Albuterol is a beta-2 agonist with bronchodilator properties. It is a first-line agent in the setting of acute bronchospasm.
Sevoflurane improves bronchospasm in two ways: 1) It has a direct bronchodilator effect, and 2) It deepens the level of anesthesia. If the patient’s bronchospasm is so severe that you are absolutely unable to ventilate, you’ll need to use an IV agent.
Here’s where it gets tricky … There are two key points to understand:
Montelukast is NOT used in the treatment for acute bronchospasm.
Hydrocortisone IS administered during acute bronchospasm, however it does NOT treat acute symptoms - instead it’s given to prevent symptoms down the road.
Although there are some investigations examining the use of montelukast for acute bronchospasm, you will not find this agent in the protocols available in the textbooks.
All of the following are associated with a reduction in the carbon monoxide diffusion capacity of the lung EXCEPT:
sarcoidosis.
emphysema.
asthma.
pulmonary edema.
Asthma
You do NOT have to memorize every test for every disease process. Instead, just understand the test and understand the disease, and you’ll be able to reason your way through the question.
The diffusing capacity for carbon monoxide (DLCO) is used to assess how well the lung can exchange gas. This test measures the partial pressure difference between the inspired and expired CO after a known quantity of CO has been inhaled (CO inspired - CO expired = amount of CO that entered the blood).
The normal value for DLCO is 17-25 mL/CO/min/mmHg. Lower values correlate with a significant reduction in diffusing capacity.
Using Fick’s law of diffusion, the DLCO tells us two key characteristics about the alveolocapillary interface:
Surface area (decreased by emphysema)
Thickness (increased by fibrosis and pulmonary edema)
Asthma affects airway diameter, but not the alveolocapillary interface itself. This would affect tests of pulmonary mechanics (FEV1, MMF, etc), but not tests of gas exchange (DLCO).
When compared to emphysema, which of the following MOST accurately describe chronic bronchitis? (Select 3.)
Higher risk of cor pulmonale
Decreased diffusing capacity
Decreased airway diameter
Loss of elastic recoil
Polycythemia
Normal PaCO2
Decreased airway diameter
Polycythemia
Higher risk of cor pulmonale
You must be able to compare chronic bronchitis with emphysema.
Pathophysiology:
Chronic bronchitis is caused by inflammation and mucus production that reduce airway diameter.
Emphysema is caused by a reduction in the surface area of the alveolocapillary interface and loss of elastic recoil.
Blood Gases:
The patient with chronic bronchitis is polycythemic; an increased RBC mass compensates for a chronically low PaO2. They tend to retain CO2. We call them “blue bloaters.”
The patient with emphysema generally has a normal (or slightly reduced) PaO2. The PaCO2 is usually normal or decreased (as a result of hyperventilation). We call them “pink puffers.”
Cor Pulmonale:
This complication is more common with chronic bronchitis, generally as a result of pulmonary hypertension.
Chronic alveolar hypoxia causes pulmonary vasoconstriction, and this increases pulmonary vascular resistance. In consequence, the workload of the right ventricle increases, leading to RV hypertrophy (right axis deviation) and ultimately RV failure.
Anesthetic considerations for the patient with cor pulmonale include avoidance of all of the following EXCEPT:
hypoventilation.
hypothermia.
dexmedetomidine.
nitrous oxide.
Dexmedetomidine
Cor pulmonale is always the result of pulmonary hypertension. An increased PVR increases the workload of the right heart, and this leads to RV hypertrophy and ultimately RV failure. Therefore, anesthetic management specifically avoids anything that increases PVR.
Anesthetic goals for the patient with pulmonary hypertension includes the avoidance of:
Hypoxia Acidosis Hypercarbia Hypothermia Nitrous oxide Vasoconstrictors Conditions that increase SNS tone Ketamine (maybe) Other IV anesthetic agents are safe to use. Because dexmedetomidine doesn't cause respiratory depression, it won't cause hypercarbia. This makes it an attractive drug in this patient population.
Regional anesthesia is safe, unless a high sensory level is required during neuraxial blockade. A decreased SVR in the setting of a fixed PVR can lead to profound hypotension.
A patient with cor pulmonale due to COPD presents for an inguinal hernia repair. All of the following signs are consistent with cor pulmonale EXCEPT:
hepatomegaly.
lower extremity edema.
increased pulmonary artery occlusion pressure.
pulmonary hypertension
Increased pulmonary artery occlusion pressure
Cor pulmonale is right-sided heart failure that results from pulmonary hypertension (increased PAP and normal PAOP). This creates a back pressure on the venous circulation that leads to:
Jugular venous distension Hepatomegaly Lower extremity edema An increased PAOP is consistent with LV (not RV) failure.
All of the following are expected to increase in the patient experiencing a massive pulmonary embolism during surgery EXCEPT:
heart rate.
dead space.
right ventricular stroke work.
end-tidal carbon dioxide.
End-tidal carbon dioxide
Pulmonary embolism prevents blood in the affected vessels from reaching the alveoli. Said another way, these alveoli are ventilated and not perfused, so they become dead space.
Because end-tidal gas is a mixture of gas from perfused alveoli and alveoli lacking perfusion, it is diluted and the EtCO2 decreases. By extension, the PaCO2 to EtCO2 gradient increases.
Large emboli can plug the main pulmonary arterial vessels, and this can increase PVR and right ventricular work. In extreme cases, this can progress to RV failure and tricuspid regurgitation.
Tachycardia and tachypnea are common findings in the patient with PE.
Which of the following is indicated immediately after nonparticulate pulmonary aspiration?
Bronchoscopy
Clindamycin
Hydrocortisone
Positive end-expiratory pressure
Positive end-expiratory pressure
This risk of aspiration pneumonitis is increased in patients with Mendelson syndrome. This is characterized by a gastric volume > 25 mL and gastric pH < 2.5.
Here is the pathophysiology and treatment for the patient who has aspirated gastric contents.
Immediately After Aspiration:
Because chemical injury to the lung tissue occurs immediately after the insult, there is no need for deep tracheal suctioning or bronchoscopy. Suctioning the mouth and pharynx for particulate matter is useful.
Minutes After Aspiration:
Atelectasis increases pulmonary shunt. Indeed, hypoxemia is the hallmark sign of aspiration pneumonitis. In fact, it is often the first sign. PEEP is indicated to reduce shunt.
Hours After Aspiration
The inflammatory response takes hold within hours. Macrophages release cytokines and tumor necrosis factor-alpha. Neutrophils release proteases and oxygen free radicals. Collectively these chemicals lead to non-cardiogenic pulmonary edema.
Lidocaine reduces free radical production, inhibits neutrophil chemotaxis, minimizes reperfusion injury, and improves outcomes in patients with aspiration pneumonitis.
Steroids are of questionable benefit.
A Day After Aspiration:
Necrosis of alveolar cells occurs within 24 hours.
Two Days After Aspiration:
Antibiotics are only indicated if fever or an increased WBC count persist for more than 48 hours.
Choose the BEST mechanical ventilation strategy for the patient with severe pulmonary edema.
Tidal volume 6 mL/kg and respiratory rate = 8 breaths/min
Tidal volume 6 mL/kg and respiratory rate = 16 breaths/min
Tidal volume 10 mL/kg and respiratory rate = 8 breaths/min
Tidal volume 10 mL/kg and respiratory rate = 16 breaths/min
Tidal volume 6 mL/kg and respiratory rate = 16 breaths/min
As a general rule, restrictive lung disease is associated with a reduction in all lung volumes and decreased lung compliance. Expiratory flow rates remain normal.
The best ventilatory strategy for restrictive lung disease aims to minimize the risk of barotrauma. This is best accomplished with a smaller tidal volume (6 mL/kg IBW) and faster respiratory rate (14-18 breaths/min). Maintaining peak inspiratory pressure < 30 cm H2O also minimizes the risk of barotrauma.
A patient breathing ambient air has an A-a gradient of 100. Which conditions BEST explain this finding? (Select 2.)
Pulmonary edema
Pneumonia
Opioid overdose
High altitude
Pulmonary edema
Pneumonia
There are five causes of hypoxemia. For each of these, you must know how the A-a gradient is affected, if the condition responds to supplemental oxygen, and be able to identify examples. 1. High altitude A-a gradiant = normal O2 helpful = yes Example = low barometric pressure 2. Hypoventilation A-a gradient = normal O2 helpful = yes Example = low PAO2, opioid overdose 3. Diffusion defect A-a gradient = increased O2 helpful = yes Example = pulmonary fibrosis 4. V/Q mismatch A-a gradient = increased O2 helpful = yes Example = dead space, shunt
- Right to left shunt
A-a gradient = increased
O2 helpful = no (if shunt > ~ 30%)
Example = VSD, Tetralogy of Fallot, VSD, Eisenmenger syndrome
Identify the BEST example of acute intrinsic restrictive lung disease. Amiodarone induced pulmonary fibrosis Negative pressure pulmonary edema Ankylosing spondylitis Pregnancy
Negative pressure pulmonary edema
Restrictive lung diseases can be divided into categories:
Acute intrinsic: negative pressure pulmonary edema
Chronic intrinsic: Amiodarone induced pulmonary fibrosis
Disease of chest wall/mediastinum: Ankylosing spondylitis
Other/increased intraabdominal pressure: Pregnancy
All of the following are absolute indications for one lung ventilation EXCEPT:
control of distribution of ventilation.
esophageal resection.
unilateral bronchopulmonary lavage.
isolation of one lung to prevent contamination.
Esophageal resection
Isolation of one lung to prevent infection:
Massive pulmonary hemorrhage
Infection
Control of distribution of ventilation:
Bronchopleural fistula
Surgical opening of a major airway
Large unilateral lung cyst or fistula
Unilateral bronchopulmonary lavage:
Pulmonary alveolar proteinosis
Surgical exposure can be of high or low priority, but it is always a relative indication for one lung ventilation. Esophageal resection is a low priority procedure.
The site of injury in the patient with flail chest moves: (Select 2.)
inward during inspiration.
inward during expiration.
outward during inspiration.
outward during expiration.
Inward during inspiration
Outward during expiration
Flail chest is a consequence of 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 and lungs expand.
Flail chest: The injured ribs move inward and collapses affected region.
Expiration (Positive Intrathoracic Pressure)
Normal: The chest wall moves inward and lungs empty.
Flail chest: The injured ribs move outward and affected region doesn’t empty.Since part of the lung isn’t moving normally, it doesn’t participate in gas exchange. Consequences include alveolar collapse, hypoxemia, hypoventilation, and hypercarbia.
Treatment includes reducing pain with an epidural catheter or intercostal nerve blocks. Remember, this area is highly vascular and that the rate of local anesthetic uptake into the systemic circulation is high.
Which I:E ratio is MOST appropriate for a patient with severe chronic obstructive pulmonary disease?
1: 1
1: 2
1: 3
2: 1
1:3
The patient with severe COPD experiences gas trapping (increased alveolar time constant). Therefore, your ventilatory strategy must allow ample time for exhalation to occur.
Increasing the expiratory time minimizes air trapping and dynamic hyperinflation. If you are using volume cycled ventilation, know that this comes at the cost of a higher peak inspiratory pressure (you have less time to get the same volume of gas into the patient).
Match each drug with its mechanism of action.
Montelukast + Leukotriene antagonist
Theophylline + Phosphodiesterase inhibitor
Cromolyn + Mast cell stabilizer
Ipratropium + Anticholinergic
A patient in the PACU exhibits signs of recurarization despite reversal with neostigmine and glycopyrrolate. Which of the following conditions will further impair reversal?
Hyperkalemia
Hypercalcemia
Hypoalbuminemia
Hypoventilation
Hypoventilation
Acidosis impairs the ability of the body’s enzymatic systems to function properly. This is exemplified by the presence of respiratory acidosis and reversal of neuromuscular blockers.
Anticholinesterases inhibit acetylcholinesterase, which increases the concentration of Ach in the synaptic cleft at the neuromuscular junction. It is the ratio of Ach and NMB at the neuromuscular junction that determines the quality of the reversal.
An inadequate reversal leads to respiratory muscle weakness, hypoventilation, and respiratory acidosis. This potentiates the NMB and reduces the efficacy of the anticholinesterase, creating a self-perpetuating cycle of increasing respiratory muscle weakness.
Don’t forget that the benzylisoquinolines are metabolized by Hofmann elimination (cisatracurium 100% and atracurium 33%). This reaction is slowed in the patient with respiratory acidosis, thereby prolonging the duration of action for these drugs.
Respiratory acidosis can also cause myocardial depression.
As an aside, you’ll find a question very similar to this on the 2015 version of the National Certification Examination Handbook. You would be wise to analyze the questions in that document.
A patient is scheduled for a thoracotomy and right upper lobe resection. Which of the following preoperative findings is the BEST predictor of an increased risk of postoperative pulmonary complications?
PaCO2 = 43 mmHg
DLCO = 47% predicted
FEV1 = 62% predicted
VO2 max = 8 mL O2/kg/min
VO2 max = 8 mL O2/kg/min
Assessment of respiratory reserve can be divided into 3 key areas: respiratory mechanics, gas exchange, and cardiopulmonary reserve.
1. Respiratory Mechanics: The ability to move gas in and out of the lungs FEV1 < 40% (best measurement) 2. Gas Exchange: The ability to transfer O2 and CO2 across the alveolocapillary interface DLCO < 40% predicted (best measurement) PaO2 < 60 mmHg PaCO2 > 45 mmHg 3. Cardiorespiratory Interaction:
The ability of the lungs and heart to work together to maintain PaO2 and PaCO2
VO2 max < 15 mL O2/kg/min (best measurement)
Unable to climb 1 flight of stairs
SpO2 decreases > 4% during exercise
Of all of the tests mentioned above, the single best predictor of postoperative pulmonary complications is VO2 max.
In addition to lung function, hypoalbuminemia (<3.6 g/dL) is also a predictor of PPC.
You may think that this list is too specific to memorize, but trust us when we say that it’s not!
A patient is scheduled for a VATS with lung resection. Click on the alveolar compliance curve that BEST illustrates what happens after he is anesthetized and placed in the lateral decubitus position.
When the anesthetized patient is placed in the lateral decubitus position:
The nondependent lung moves from the flat (noncompliant) region of the curve to an area of better compliance. Ventilation is best here, because the lung is on a favorable position of the curve.
A patient is undergoing thoracotomy in the lateral decubitus position with one-lung ventilation. The SpO2 has decreased to 86%, and it has not improved with CPAP on the non-dependent lung. Which of the following maneuvers should be attempted next?
Resume two-lung ventilation.
Increase tidal volume.
Ask the surgeon to clamp the pulmonary artery of the non-dependent lung.
Apply positive end-expiratory pressure to the dependent lung.
Apply positive end-expiratory pressure to the dependent lung
Hypoxemia during OLV is the result of intrapulmonary shunt. The most important predictor of PaO2 during OLV is the PaO2 during two-lung ventilation.
Strategies for reversing hypoxemia during OLV:
Increase FiO2 to 100%
Check the DLT position with a fiberoptic bronchoscope.
Apply CPAP 10 cm H2O to the non-dependent lung (this can impede visualization during VATS).
Apply PEEP 5-10 cm H2O to the dependent lung.
Ligate or clamp the pulmonary artery of the non-dependent lung (not always possible).
Resume two-lung ventilation.
As an aside, insufflating oxygen at 5 L/min into the non-dependent lung can be a very effective method to increase PaO2 without obscuring surgical visualization.
A patient is scheduled for a left pneumonectomy. Crystalloid administration should be less than:
3 liters in 12 hours.
3 liters in 24 hours.
5 liters in 12 hours.
5 liters in 24 hours.
Three liters in 24 hours
During OLV, the dependent lung must perform all of the gas exchange functions. Excessive crystalloid administration increases hydrostatic pressure, which increases interstitial lung water and impairs gas exchange.
In the patient scheduled for pneumonectomy, the dependence on a single lung continues into the postoperative period as well. For this reason, it’s best to limit crystalloid to replacement of volume deficits and maintenance requirements (no third space). It’s recommended to limit crystalloids to < 3L in the first 24 hours.
A patient requires mediastinoscopy with tracheal lymph node biopsy. Where is the MOST appropriate place to insert an arterial line to monitor for vascular compression from the mediastinoscope?
Right arm
Right leg
Left arm
Left leg
Right arm
Mediastinoscopy is performed to diagnose and stage lung cancer. The most common approach involves a small incision made at the midline of the lower neck at the suprasternal notch. The scope is placed anterior to the trachea and posterior to the innominate artery artery and thoracic aorta. Because this region is rich in high value real estate, there are a number of serious complications that can result:
Thoracic aorta (hemorrhage and reflex bradycardia)
Innominate artery (decreased carotid blood flow and cerebral blood flow)
Tracheal (airway obstruction)
Vena cava (hemorrhage)
Lung (tension pneumothorax)
Thoracic duct (chylothorax)
Phrenic and recurrent laryngeal nerve (paresis)
The right common carotid and right subclavian arteries branch off the innominate artery. Compression of the innominate artery impairs perfusion of the brain as well as the right upper extremity. For this reason, you must continuously monitor the pulse in the right upper extremity while the mediastinoscope is inside the patient. This can be accomplished with an arterial line, SpO2 probe, or even your finger.
A blood pressure cuff is placed on the left arm to monitor systemic blood pressure in the event of innominate compression.
Another name for the innominate artery is the brachiocephalic artery.
What is the NPO policy for the following liquids? Use the ASA Practice Guidelines for Preoperative Fasting and the Use of Pharmacologic Agents to Reduce the Risk of Pulmonary Aspiration to answer this question.
Apple juice = 2 hours
Breast milk = 4 hours
Cow’s milk = 6 hours
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
Miller states that ingestion of fried and fatty foods “may” require eight hours or more.
Ingestion of clear liquids two hours before surgery reduces gastric volume and increases gastric pH. Both of these reduce the risk of Mendelson syndrome.
What is this patient’s Mallampati classification?
Enter your answer as a number
Three
The Mallampati score is used to assess the size of the tongue relative to the volume of the mouth. The more space the tongue occupies, the less space there is to work
To perform the exam, the patient should sit upright, extend the neck, open the mouth as wide as possible, and stick out the tongue. The patient should not phonate.
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
By itself, the MMT is a poor predictor of difficult airway, however its predictive power increases substantially as it is combined with additional airway tests.
Predictors of difficult mask ventilation include: (Select 3.) Age 50 years History of snoring Edentulousness Mallampati II Presence of a beard BMI 25 kg/m2
Edentulousness
History of snoring
Presence of a beard
You must know the independent risk factors that predict difficult mask ventilation. The mnemonic “BONES” should help:
Beard (odds ratio = 3.18) Obese (odds ratio = 2.75) No teeth (odds ratio = 2.28) Elderly (odds ratio = 2.26) Snoring (odds ratio = 1.84)
Which characteristics predict difficulty with laryngoscopy? (Select 3.) Arched palate Prognathism Long upper incisors. Long neck Mandibular protrusion test class three Cormack-Lehane class four
Arched palate
Long upper incisors
Mandibular protrusion test class three
Predictors of difficult laryngoscopy include:
Small mouth opening
Prominent overbite / retrognathic jaw (short jaw)
Inability to bite upper lip with lower teeth (mandibular protrusion test class three)
Long incisors
Mallampati class three or four
High, arched palate
Short, thick neck
Short thyromental distance
Reduced cervical mobility
The Cormack-Lehane grading system is used to measure the view you obtain during laryngoscopy. A class four means that you cannot see the epiglottis or any of the glottic structures. This IS a difficult airway and NOT a predictor of a difficult airway!
All of the following are appropriate landmarks for sizing an oropharyngeal airway EXCEPT the:
tip of the nose.
corner of the patient’s mouth.
angle of mandible.
earlobe.
Tip of the nose
How to size an oropharyngeal airway:
Measure the distance between the corner of the patient’s mouth and the earlobe or the angle of the mandible.
An incorrectly sized OPA can worsen airway obstruction.
A nasopharyngeal airway should be avoided in all of the following circumstances EXCEPT:
coagulopathy.
previous transsphenoidal hypophysectomy.
light anesthesia.
basilar skull fracture.
Light anesthesia
The lightly anesthetized patient is more tolerant of a nasopharyngeal airway than he is of an oropharyngeal airway. In fact, an oropharyngeal airway in a lightly anesthetized patient can precipitate laryngospasm.
Contraindications to an NPA include:
Coagulopathy (risk of epistaxis) Basilar skull fracture LeFort II or III fracture Nasal fracture CSF rhinorrhea Previous transsphenoidal hypophysectomy Previous Caldwell-Luc procedure
To ensure the best chance for successful tracheal intubation, which axes should be aligned? (Select 3.)
Tracheal Mandibular Oral Sternal Pharyngeal Laryngeal
Oral
Pharyngeal
Laryngeal
Head elevation and head extension aim to align the oral, pharyngeal, and laryngeal axes. This offers the greatest chance for successful laryngoscopy and intubation.
Problems with other positions:
Head in the neutral position does not align any of these axis.
Head elevated on a pad with head in the neutral position only aligns the PA and LA.
Head on the bed with head extension only aligns the PA and LA.
What is the MOST reliable sign of endotracheal intubation?
Mist inside the endotracheal tube
Bilateral breath sounds
Endotracheal tube visualized between the vocal cords
Chest rise and fall
Endotracheal tube visualized between the vocal cords
You were probably hoping to see (+) EtCO2 for three consecutive breaths, huh? Remember, your job is the identify the best answer choice of those provided in the question - these may not always align with your expectations.
According to Hagberg, the two most reliable signs of endotracheal intubation are:
Visualizing the ETT between the vocal cords.
Fiberoptic visualization of the tracheal rings with a fiberoptic bronchoscope.
Notice that both of these provide direct, visual proof of successful intubation.
We know what you’re thinking - what about the presence of carbon dioxide on the capnograph?
While (+) EtCO2 for three breaths is reliable most of the time, there a few circumstances that will yield a false-negative result. These situations include cardiac arrest, severe bronchospasm, complete ETT obstruction (kinking or plugging), and equipment malfunction.
Bilateral breath sounds, chest rise and fall, and mist in the endotracheal tube are less reliable than the presence of CO2 on the capnograph or the methods of direct visualization described above.
Connect the correct pairings.
Oral ETT in women = 21 cm
Oral ETT in men = 23 cm
Nasal ETT in women = 25 cm
Nasal ETT in men = 27 cm
Which of the following neck positions is associated with the GREATEST chance of endobronchial intubation?
Neutral
Flexion
Extension
Neck position does not influence the position of the endotracheal tube in the trachea.
Flexion
We’re going to make this really easy to remember; the tube goes where the nose goes.
Flexion moves the tip towards the carina (~ 2 cm).
Extension moves the tip away from the carina (~ 2 cm).
Lateral rotation of the head moves the tip away the carina (~ 0.7 cm).
Another thing to keep in mind is the position of the bed. The steep Trendelenburg position causes the abdominal contents to shift towards the chest, reduce thoracic volume, and cause endobronchial intubation.
Which nerve innervates the region where the tip of the Macintosh blade should be placed during laryngoscopy?
Glossopharyngeal
Superior laryngeal
Recurrent laryngeal
Trigeminal
Glossopharyngeal
During laryngoscopy with the Macintosh blade, the tip of the blade is placed in the vallecula. You should be able to identify this on a hotspot-type question as well.
Airway innervation from proximal to distal:
Anterior tongue: Trigeminal (V) V3 - mandibular branch
Posterior tongue: Glossopharyngeal (IX)
Soft palate: Glossopharyngeal (IX)
Oropharynx: Glossopharyngeal (IX)
Vallecula: Glossopharyngeal (IX)
Anterior epiglottis: Glossopharyngeal (IX)
Posterior epiglottis: Superior laryngeal internal branch (X)
Vocal cords: Superior laryngeal internal branch (X) and recurrent laryngeal (X)
Trachea: Recurrent laryngeal (X)
The cuff pressure for an LMA Classic should NOT exceed:
Enter your answer in cm H2O
60 cm H2O
While the maximum cuff pressure for an endotracheal tube is 25 cm H2O, the maximum cuff pressure for an LMA is 60 cm H2O (target pressure 40 - 60 cm H2O).
Excessive cuff pressure (LMA or ETT) can cause nerve injury and is associated with a higher incidence of sore throat
Cuff pressures should be measured periodically throughout the anesthetic, particularly if nitrous oxide is used.
The adequacy of the seal created by an LMA classic is most dependent on: (Select 2.) cuff pressure. correct placement. cuff volume. appropriate sizing.
Correct placement and appropriate sizing
The LMA Classic is a small mask that covers the laryngeal inlet. It is inflated to permit positive pressure ventilation up to 20 cm H2O.
The integrity of the seal is more dependent on correct placement and appropriate sizing and less dependent on cuff volume or pressure.
The LMA cuff pressure should never exceed 60 cm H2O. If the pressure is this high and you are unable to generate an adequate seal, then the LMA may be improperly positioned, the patient is inadequately anesthetized, and/or there is a partial or complete laryngospasm.
Remember that nitrous oxide diffuses into the cuff, and this will increase cuff pressure (Boyle’s law). You must periodically measure cuff pressure with a monometer when N2O is used.
What is the BEST size LMA Classic for a seven year old that weighs 54 lbs.
2.5
This is a two part question; convert the weight to kg then answer the question
- 54 / 2.2 = 24.5 kg
- LMA-Classic size = 2.5
Patient Size = LMA-Classic Size < 5 kg = 1 5 - 10 kg = 1.5 10 - 20 kg = 2 20 - 30 kg = 2.5 30 - 50 kg = 3 50 - 70 kg = 4 70 - 100 kg = 5 > 100 kg = 6
What is the LARGEST size endotracheal tube that can be passed through a LMA Classic size two?
4.5
While some may say that the largest size endotracheal tube that passes through an LMA is the “one that fits,” we argue that knowing this information helps you get it right the first time and it may even get you points on boards.
LMA-Class Size / Largest ETT that fits: 1 = 3.5 1.5 = 4.0 2 = 4.5 2.5 = 5.0 3 = 6.0 cuffed 4 = 6.0 cuffed 5 = 7.0 cuffed 6 = 7.0 cuffed
All of the following factors increase the risk of complications when an LMA is used EXCEPT:
an undersized LMA.
nitrous oxide.
lateral decubitus position.
cuff pressure = 50 cm H2O.
Cuff pressure = 50 cm H2O
Complications of LMA use include:
Nerve injury: recurrent laryngeal, hypoglossal, lingual
Pharyngeal necrosis
Trauma to the uvula
Sore throat
Conditions that can increase the risk of complications include:
LMA is too small
Nitrous oxide (if cuff pressure isn’t monitored throughout the procedure)
Non-supine positions
Which airway management technique activates the sympathetic nervous system the LEAST?
Laryngeal mask airway
Combitube
Direct vision laryngoscopy
Fiberoptic intubation
Laryngeal mask airway
We all know that direct vision laryngoscopy is an intensely stimulating procedure that can lead to increased catecholamines, tachycardia, hypertension, dysrhythmias, bronchorrhea and bronchospasm. Interestingly, combitube placement may be even more stimulating.
The tendency of airway device placement to activate the SNS (from most activation to least activation):
Combitube
DVL
Fiberoptic intubation
LMA
Following placement of the device in the image, the distal balloon is MOST likely to occlude the:
mainstem bronchus.
hypopharynx.
esophagus.
trachea.
Esophagus
The Combitube is a supraglottic, double lumen device that is blindly placed in the hypopharynx. The proximal balloon occludes the hypopharynx, while the distal balloon occludes the esophagus.
If the tip is placed in the esophagus (this is common), the lungs can be ventilated through the lumen between the distal and proximal balloons.
It is uncommon that the tip is positioned in the trachea, but if you get lucky, the distal lumen can be used for ventilation.
Pathology at or below the larynx may render this device useless. Esophageal rupture has been reported. Cricoid pressure should be released (not maintained) when placing the Combitube.
What is the next best step during an intubation with a lighted stylet?
Pass the endotracheal tube off of the lighted stylet.
Turn off the light.
Advance the lighted stylet three inches.
Withdraw and reposition the lighted stylet.
Pass the endotracheal tube off of the lighted stylet
The trachea is anterior to the esophagus. Placement of the lighted stylet into the trachea results in a “well-defined circumscribed glow” below the thyroid prominence. This is what you saw in the image. If the lighted stylet was in the esophagus, you would observe a “more diffuse transillumination of the neck without the circumscribed glow.”
Benefits of the lighted stylet:
Useful for the anterior airway.
Useful with small mouth opening.
Requires very little manipulation of the neck.
Less stimulating than direct vision laryngoscopy.
Less sore throat than direct vision laryngoscopy.
We want you to notice the difference between:
Esophageal placement = diffuse transillumination of the neck without the circumscribed glow
Tracheal placement = well defined circumscribed glow just below the thyroid prominence
Compared to using the Trachlight in the adult population, all of the following are true for its use in children EXCEPT:
it should be bent at a less acute angle.
there is a higher incidence of false positive results.
transillumination will occur sooner.
the bend should be closer to the tip.
It should be bent at a less acute angle
This question requires you to draw on your knowledge of the pediatric airway to answer it correctly.
When using the Trachlight in the adult, it should be bent to a 90 degree angle. When using this device in children, the angle should be 60-80 degrees (more acute angle) to better accommodate a more cephalad glottic opening.
Since the pediatric airway is smaller, the Trachlight should be bent closer to the tip. For the same reason, you should expect that transillumination will occur sooner.
Because of the thinner neck in the child, the circumferential glow will be more prominent. It’s possible that there are more false positive results (you think the tip is in the tracheal when it is really in the esophagus).
What is an absolute contraindication to cricothyroidotomy?
Facial trauma
Neck burn injury
Unstable cervical spine
Age less than six years
Age less than six years old
The only absolute contraindication to cricothyroidotomy is young age (Hagberg says age < 10 years). Children have pliable and mobile laryngeal and cricoid cartilages, and this can make cricothyroidotomy incredibly challenging. In this age group, percutaneous transtracheal ventilation is the surgical airway technique of choice.
Cricothyroidotomy is useful when facial trauma impairs conventional airway management methods.
An unstable c-spine is ok, so long as cervical spine immobilization is employed.
A neck burn injury can make landmark identification more difficult, however it is not a contraindication.
Hagberg notes that some people argue that laryngeal fracture and transection should be considered absolute contraindications, but there is some disagreement on this.
In the patient with an unstable cervical spine, which of the following techniques is associated with the LEAST amount of cervical motion? (Select 2.)
Direct vision laryngoscopy
Blind nasal intubation
Bullard laryngoscopy
Fiberoptic bronchoscopy
Fiberoptic bronchoscopy and blind nasal intubation
Based on cineradiography data, fiberoptic bronchoscopy and blind nasal intubation are associated with less cervical motion than other intubation techniques. Of the two, FOB is favored with c-spine injury due to a lower risk of trauma and a higher success rate.
It should be noted that these techniques are not necessarily associated with a lower incidence of neurologic deficits.
A patient with which condition is the BEST candidate for retrograde intubation?
Pretracheal abscess
Tracheal stenosis
Cervical spine injury
Morbid obesity
Cervical spine injury
Retrograde intubation involves puncturing the cricothyroid membrane and passing a wire between the vocal cords and out of the mouth. Next, an endotracheal tube is loaded over the wire and advanced into the trachea.
Most of the reported cases of retrograde intubation described its use in patients with cervical spine injuries.
Contraindications to retrograde intubation:
A neck flexion deformity can make this procedure challenging if not impossible.
Obesity or the presence of a goiter may prevent you from accurately identifying the cricothyroid membrane.
Coagulopathy increases the risk of bleeding into the airway following needle puncture.
Placing a needle through a pretracheal abscess can cause a respiratory infection.
What are the next steps after the tip of the double lumen endotracheal tube is placed between the vocal cords?
(One is the first step and four is the last step)
1 = Remove the stylet 2 = Rotate the DLT 90 degrees 3 = Advance the DLT into the bronchus 4 = Confirm placement with fiberoptic bronchoscope
After the tip is placed between the vocal cords, you should:
Remove the stylet to avoid mucosal damage.
Rotate the DLT 90 degrees in the direction of the bronchus to be intubated.
Advance the tube to 29 cm in males and 27 cm in females at the teeth. Stop if you encounter resistance.
Fill the tracheal cuff with 5-10 mL of air and the bronchial cuff with 1-2 mL of air. Be aware that the bronchial balloon is a low volume and high pressure cuff - keep it deflated when you don’t need lung separation.
Auscultation is not the most reliable method of determining correct placement. Confirm placement with a fiberoptic bronchoscope.
Which technique is the gold standard for managing the difficult airway?
Flexible fiberoptic bronchoscope with patient awake and spontaneous ventilation
Video laryngoscope with patient asleep and spontaneous ventilation
Flexible fiberoptic bronchoscope with patient asleep and spontaneous ventilation
Video laryngoscope with patient asleep and controlled ventilation
Flexible fiberoptic bronchoscope with patient awake and spontaneous ventilation
Flexible fiberoptic bronchoscopy in the awake, spontaneously ventilating patient is the gold standard for managing the difficult airway. There is nothing else to say about this.
An airway fire has occurred. What are the next steps?
Step 1 = Remove the endotracheal tube
Step 2 = Stop flow of all airway gases
Step 3 = Pour saline into the airway
Step 4 = Re-establish ventilation
You will find debate as to whether you should remove the endotracheal tube or turn off the oxygen as the first step. In reality, you’re doing many steps simultaneously, however on the NCE there is a specific order of steps.
Miller cites the ASA Operating Room Fire Guidelines. We made sure to reconcile this text with the guidelines.
Fire is present: 1. Remove the endotracheal tube. 2. Stop flow of all airway gases. 3. Remove other flammable material from the airway. 4. Pour saline into the airway. 5. If fire not extinguished on first attempt, use a CO2 fire extinguisher. Fire is controlled:
- Re-establish ventilation by mask. Avoid supplemental O2 or N2O.
- Check ETT for damage - fragments may remain in the airway.
- Bronchoscopy to assess the injury and retained ETT fragments.
Click on the tonsillar pillars
By measuring the size of the tongue relative to the volume of the mouth, the Mallampati exam helps us predict the difficulty of endotracheal intubation.
To perform the exam, the patient should: Sit upright Extend the neck Open the mouth as wide as possible Stick out the tongue NOT phonate
This patient has a class I airway, because you can visualize the tonsillar pillars.
Only the epiglottis can be visualized during direct vision laryngoscopy. What is this patient’s Cormack and Lehane score?
(Enter a number)
3
The Cormack and Lehane grading system helps us measure the view we obtain during direct vision laryngoscopy.
Be sure to understand what you can and cannot see with each score.
Identify the BEST predictors of difficult mask ventilation. (Select 3.)
Small mouth opening Presence of a beard Edentulousness High, arched palate Old age Mallampati class III
Old age
Edentulousness
Presence of a beard
You must know the independent risk factors for difficult mask ventilation. The mnemonic “BONES” should help:
Beard Obese (most books say BMI > 26 kg/m2) No teeth Elderly (age > 55 years) Snoring
The distractors are predictors of difficult endotracheal intubation - not mask ventilation.
Which congenital conditions are associated with cervical spine anomalies? (Select 2.)
Treacher Collins
Klippel-Feil
Pierre Robin
Goldenhar
Goldenhar
Klippel-Feil
You must know the congenital conditions that are associated with cervical spine anomalies. Examples include:
Goldenhar
Klippel-Feil
Trisomy 21
What is the optimal position for tracheal intubation?
Cervical flexion only.
Atlanto-occipital joint extension only.
Cervical flexion and atlanto-occipital joint extension.
Cervical extension and atlanto-occipital joint flexion.
Cervical flexion and atlanto-occipital joint extension
The sniffing position maximizes the probability of successful tracheal intubation by aligning the oral, pharyngeal, and laryngeal axes.
It consists of 2 key elements:
Cervical flexion: Moves the chin to the chest
Atlanto-occipital joint extension: Extends the head on the neck
Contraindications to the use of a nasopharyngeal airway include: (Select 2.)
coagulopathy.
Le Fort II fracture.
Pierre Robin syndrome.
dental trauma.
Coagulopathy
Le Fort II fracture
The turbinates are highly vascular structures. Instrumenting the nose places the patient at risk for epistaxis, which can complicate airway management. Coagulopathy makes this more likely.
Le Fort II and III fractures can disrupt the cribriform plate, creating a direct line of communication between the nasal and cranial cavities. Placing a nasal airway, nasal ETT, or NGT could be catastrophic. Signs of cribriform plate injury include “raccoon eyes,” periorbital edema, and/or CSF leak in the nose or ears.
Which intervention demonstrates the MOST accurate understanding of inflating the cuff on the endotracheal tube?
Assess the pressure inside the pilot balloon with your fingers.
Add 10 mL air to the pilot balloon.
Attach a syringe to the pilot balloon to create a minimal occlusive pressure.
Attach a manometer to the pilot balloon.
Attach a monometer to the pilot balloon
Inflating the ETT cuff creates a seal that permits positive pressure ventilation and protects the lungs from aspiration of gastric contents.
Tracheal ischemia can occur if the cuff pressure exceeds tracheal mucosal perfusion pressure. For this reason, the cuff pressure should be less than 25 cm H2O.
Attaching a manometer to the pilot balloon is the best way to determine the pressure inside the cuff.
Click on the region of the LMA that rests against the cricopharyngeus muscle.
Distal end → Upper esophageal sphincter (cricopharyngeus muscle)
Sides → Pyriform sinuses
Proximal end → Base of the tongue
Match each LMA with its unique feature.
LMA ProSeal + Gastric drain
LMA Fastrach + Designed for tracheal intubation
LMA Flexible + Wire-reinforced airway tube
All of the following are contraindications to a laryngeal mask airway EXCEPT:
hiatal hernia.
tracheal tumor.
asthma.
gastroparesis.
Asthma
You need to know when you can use a particular device and when you can’t (or shouldn’t).
Compared to an endotracheal tube, an LMA produces considerably less airway irritation making it a suitable choice in the asthmatic patient.
Although the LMA shields the larynx from oropharyngeal secretions, it does NOT provide a secure airway. Therefore, it is contraindicated in any patient with a full stomach (gastroparesis or hiatal hernia).
An LMA is also contraindicated if there is an airway obstruction at or below the level of the glottis (tracheal tumor).
Identify the contraindications to the device in the image. (Select 3.)
Intact gag reflex Full stomach Zenker’s diverticulum Klippel-Feil Prolonged used Obesity
Intact gag reflex
Prolonged use
Zenker’s diverticulum
The Combitube is a supraglottic, double lumen device that is blindly placed in the hypopharynx. Contraindications to its use include:
Intact gag reflex
Prolonged use (> 2 - 3 hours) due to risk or ischemia from oropharyngeal balloon
Esophageal disease (Zenker’s diverticulum)
Ingestion of caustic substances
Do not use a size 37-F in someone < 4 ft
Do not use a size 41-F in someone < 6 ft
It provides a secure airway, so it is a useful alternative in the patient with a full stomach. Additionally, placement does not require neck extension, so it’s useful in the patient with Klippel-Feil syndrome.
Regarding the operation of the flexible fiberoptic bronchoscope: (Select 2.)
mask ventilation is impossible while the scope is in place.
the non-dominant hand controls the lever.
pushing the lever down points the tip up.
the oral, pharyngeal, and laryngeal axes must align.
Pushing the lever down, points the tip up
The non-dominant hand controls the lever
Flexible fiberoptic bronchoscopy in the awake, spontaneously ventilating patient is the gold standard for managing the difficult airway.
One of the downsides of FOB under general anesthesia is loss of pharyngeal tone and upper airway obstruction. If the patient requires PPV, then a special adapter can be placed between the mask and the y-piece. This will allow you to provide positive pressure ventilation while the FOB is in the patient’s airway.
The dominant hand holds the cord. The non-dominant hand holds the scope near the proximal end, where the thumb controls the lever.
Pushing the lever down, points the tip up.
Pushing the lever up, points the tip down.
Rotating the scope left or right allows you to control the scope in the horizontal plane.
Identify the statements that BEST describe the device in the image. (Select 2.)
It requires a minimum mouth opening 7 millimeters.
It is useful in the patient with Pierre-Robin syndrome.
There are no disposable components.
The oral, pharyngeal, and laryngeal axes must align.
It requires a minimum mouth opening 7 millimeters
It is useful in the patient with Pierre Robin syndrome
The Bullard laryngoscope is a rigid, fiberoptic device used for indirect laryngoscopy. For this reason, the oral, pharyngeal, and laryngeal axes do not have to align.
It is useful in the patient with:
Small mandible (Pierre-Robin syndrome)
Limited mouth opening (requires at least 7 mm)
Limited cervical mobility
There is a disposable tip extender that is useful for tall patients. It snaps in place before laryngoscopy and it must be removed and discarded after laryngoscopy.
Click on the laryngoscopic view where the Eschmann introducer provides the MOST significant benefit.
Remember the Cormack and Lehane grading system?
The Eschmann introducer provides the most significant benefit when you obtain a grade III view during laryngoscopy.
Before moving on, what are some other names for the Eschmann introducer?
Indications for the lighted stylet include: (Select 3.)
mandibular hypoplasia. a can't ventilate and can't intubate scenario. microstomia. severe oropharyngeal bleeding. super morbid obesity. epiglottitis.
Microstomia
Mandibular hypoplasia
Severe oropharyngeal bleeding
The lighted stylet is a blind technique that transilluminates the anterior neck to facilitate endotracheal intubation.
Like other indirect intubation methods (FOB and Bullard), the lighted stylet is useful in the patient with microstomia (small mouth) and/or mandibular hypoplasia.
Unlike the FOB and Bullard that use a camera to visualize the larynx, the lighted stylet is a blind technique. Therefore, it is also useful in the patient with severe oropharyngeal bleeding that would otherwise obscure a camera.
The lighted stylet is not useful in the following situations:
Super morbid obesity (excess neck tissue impairs transillumination)
Epiglottitis (the lighted stylet can injure the epiglottis and worsen airwayobstruction)
A can’t ventilate and can’t intubate scenario (and LMA or invasive airway is a better choice)
Unlike a double lumen endotracheal tube, the bronchial blocker cannot: (Select 3.)
suction secretions from the isolated lung.
prevent contamination from contralateral lung infection.
ventilate the isolated lung.
provide lung separation in children.
provide lung separation in the patient requiring nasotracheal intubation.
insufflate oxygen into the isolated lung.
Prevent contamination from contralateral lung infection
Provide ventilation of the isolated lung
Be used to suction secretions from the isolated lung
The bronchial blocker is an alternative to the double lumen endotracheal tube. You must understand the similarities and differences between both.
Unlike the DLT, the bronchial blocker cannot:
Prevent contamination from contralateral lung infection.
Provide ventilation to the isolated lung.
Be used to suction secretions from the isolated lung.
Unlike the bronchial blocker, the DLT cannot:
Provide lung separation in children < 8 - 10 years old.
Provide lung separation for the patient requiring nasotracheal intubation.
Both the DLT and bronchial blocker allow you to insufflate oxygen into the isolated lung.
Click on the area where the wire is inserted during retrograde intubation.
Just like cricothyroidotomy, retrograde intubation requires you to penetrate the cricothyroid membrane.
Match each percutaneous airway technique with its absolute contraindication.
Transtracheal jet ventilation + Upper airway obstruction
Cricothyroidotomy + Patient age less than 6 years
Tracheostomy + No absolute contraindication
Deep extubation provides the MOST significant benefit in the patient with: (Select 2.)
obstructive sleep apnea.
asthma.
coronary artery disease.
Parkinson’s disease.
Asthma
Coronary artery disease
Pros of deep extubation include:
Decreased CV and SNS stimulation (desirable with CAD)
Decreased coughing and airway irritation (desirable with asthma)
Cons of deep extubation include:
Ineffective airway reflexes
Increased risk of airway obstruction (caution with obstructive sleep apnea)
Increased risk of aspiration (caution with Parkinson’s disease)
What is the BEST technique to manage the patient at high risk of failed extubation?
Airway exchange catheter
Nasal airway
Shikani stylet
Eschmann introducer
Airway exchange catheter
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.
A nasal airway may be helpful in the patient at risk for failed extubation, but it is not the best choice presented in the question.
The Shikani stylet is a cross between a lighted stylet and a FOB. It is used for intubation.
The Eschmann introducer is also used during intubation.
