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
