37. A 55-year-old woman with a 35 pack-year history of tobacco smoking is undergoing

laryngobronchoscopy utilizing the Sanders jet ventilation technique. The principle

behind apneic oxygenation is

A. Contrasting density of inhaled gases

B. Maintenance of spontaneous ventilation

C. Air entrainment

D. Use of helium–oxygen mixtures

38. During apneic oxygenation via a rigid bronchoscope, anesthetic considerations

include all of the following, except

A. Duration of the procedure is limited by the increase in carbon dioxide

B. Denitrogenation should be performed prior to apnea

C. PaCO2

remains unchanged for the first 15 minutes

D. Functional residual capacity and body weight influence the rate of desaturation

Questions 39 to 43

A 35-year-old male with a toxic multinodular goiter presents for thyroidectomy with radical

neck dissection. He denies any other significant medical history. Review of systems

reveals orthopnea and dysphagia with a recent change in the caliber of his voice.

39. True statements about this patient include all of the following, except

A. A flow–volume loop on spirometry can evaluate tracheal compression

B. The airway may obstruct with sedation

C. The trachea may collapse postoperatively

D. An abnormally low forced expiratory volume in 1 second (FEV1

) would be

diagnostic of an upper airway obstruction

40. To attenuate risk of a “cannot ventilate, cannot intubate” scenario, an awake airway

intubation is discussed. The neural structure that does not need to be blocked in

order to provide adequate airway analgesia for a nasal intubation is

A. Hypoglossal nerve

B. Sphenopalatine ganglion

C. Superior laryngeal nerve

D. Recurrent laryngeal nerve

41. At the conclusion of a complicated 4-hour resection, the patient is extubated and

brought to the recovery room. One hour after extubation, the patient complains of

dyspnea with stridorous respiration. Initial steps include all of the following, except

A. Intravenous administration of calcium

B. Nebulized racemic epinephrine

C. Inspection of the surgical site

D. Direct laryngoscopy

42. If bilateral recurrent laryngeal nerves were unintentionally severed, the likely finding

on direct laryngoscopy would be

A. Paralysis of the cricothyroid muscles

B. Intermediate position of the cords

C. Midline, closed position of the cords

D. Pure adductor vocal cord paralysis

43. Instead, postoperative direct laryngoscopy reveals normal position of the cords at

rest, widely open glottic opening at maximal inspiration, and symmetrically moving

cords during quiet breathing but with weak phonation and inability to speak loudly or

shout. The most likely etiology is

A. Recurrent laryngeal nerve paralysis

B. Superior laryngeal nerve (SLN) paralysis

C. External airway compression

D. Vagus nerve paralysis

Questions 44 to 45

A 27-year-old male arrives to the operating room with laryngotracheal injuries stemming

from a motorcycle collision. He presents with hoarseness and dyspnea while sitting, but is

unable to lie flat due to worsening dyspnea. He is unable to swallow, and is

drooling/spitting moderately blood-stained sputum. His anterior neck is diffusely swollen

and exquisitely tender with notable subcutaneous emphysema. Oxygen saturation is 100%with supplemental oxygen via face mask. Review of imaging reveals a thyroid cartilage

fracture horizontally and crossing the midline.

44. The most appropriate approach to his airway management is

A. Tracheostomy

B. Laryngeal mask airway

C. Nasotracheal intubation

D. Cricothyroidotomy

45. His injury would be consistent with trauma to this zone of his neck:

A. Zone I

B. Zone II

C. Zone III

D. Zone IV

Questions 46 to 47

During thyroidectomy for carcinoma, a 22-year-old patient develops tachycardia to 115

bpm while blood pressure intensifies to 145/100 mm Hg. The inhaled anesthetic is

deepened and minute ventilation is increased. Thirty minutes later, tachycardia and

hypertension persists despite all efforts (Table 16-1).

Table 16-1

46. The appropriate treatment to consider at this time is

A. Propranolol

B. Acetaminophen

C. Iodine

D. Dantrolene

47. Diagnosis of malignant hyperthermia is most commonly confirmed by

A. Caffeine halothane contracture test (CHCT)

B. Urinalysis

C. Arterial blood gas

D. Core temperature >42°C

CHAPTER 16 ANSWERS

1. D. Topically applied drops are quickly absorbed by the mucosal lining of the

nasolacrimal duct as well as by blood vessels in the conjunctival sac with a potential

to produce systemic effects. Absorption is rapid, faster than oral or subcutaneous

administration, but still slower than intravenous.

2. D. Intraocular pressure (IOP) is a reflection of the eye’s ability to form and drain

aqueous humor. The posterior chamber’s ciliary body is the major producer of

aqueous humor. Obstruction of the drainage system, whether it is at the canal of

Schlemm, the trabecular network, or the episcleral venous system, will elevate IOP.

Tear ducts do not contribute to the drainage of aqueous humor.

3. B. Normally, IOP of the eye varies between 10 and 22 mm Hg, and is generally

considered abnormal when >25 mm Hg. This pressure is not static, as it can vary by

1 to 2 mm Hg with each cardiac contraction. Diurnal variations of up to 5 mm Hg

also exist, with a higher pressure noted upon awakening.

4. D. Hypoventilation (↑PaCO2

) along with hypoxemia (↓PaO2

) will result in

increased IOP, whereas hyperventilation (↓PaCO2

) will serve to minimize choroidal

blood flow to decrease IOP. Hyperoxemia (↑PaO2

) does not affect IOP significantly.

5. B. Inhaled and injected anesthetics (with the exception of ketamine) along with

opioids tend to lower IOP. Nondepolarizing muscle relaxants will decrease IOP,

presumably via their relaxant effects on extraocular muscles. Hypoventilation

(↑PaCO2

) results in respiratory acidosis, which will increase IOP (Table 16-2).

Table 16-2 Factors Affecting Intraocular Pressure (IOP)

Increased IOP

• Hypertension (sympathetic stimulation) as occurs during laryngoscopy and

intubation

• Acidosis

• Hypoxia

• Increased central venous pressure (coughing, valsalva maneuver)

Decreased IOP

• Hypotension

• Inhalational anesthetics (volatile and nitrous oxide)

• Opioids

• Nondepolarizing muscle relaxants

Table 16-3 Signs of Malignant Hyperthermia

Early Late

Increased EtCO2 Hyperthermia

Tachycardia Elevated creatine phosphokinase

Skeletal muscle spasm/rigidity Myoglobinuria

Tachypnea Cyanosis

Sweating Disseminated intravascular coagulation

Acidosis—respiratory and metabolic Cardiac arrest

6. C. The use of succinylcholine for eye surgery is controversial. Succinylcholine

can increase IOP by about 5 to 10 mm Hg for about 5 to 10 minutes after intravenous

administration (longer duration of ↑IOP following intramuscular administration).

Pretreatment with nondepolarizing muscle relaxants, lidocaine, or β-blockers may

reduce the ocular hypertensive response to minimize increases in IOP. The increase

in IOP after succinylcholine persists whether or not the extraocular muscles are

intact, suggesting that cycloplegic effects, rather than physical contraction, are

responsible for IOP elevation.

7. B. Ketamine may cause nystagmus and blepharospasm and may not be suitable

for ophthalmic surgery. Studies with respect to the effect of ketamine on intraocular

pressure (IOP) have shown conflicting results, but it appears more likely to increase,

as opposed to decrease, ocular pressures. This may depend on whether ketamine is

administered through the IM or IV route. Ketamine is not known to affect pupil size.

Myoclonus is commonly associated with etomidate and likely should also be

avoided when IOP control is essential.

8. A. Topical ophthalmic medications undergo sufficient and prompt absorption to

produce systemic effects and may cause adverse cross-reactions to medications used

in routine anesthesia care. Acetazolamide drops, due to its action as a carbonic

anhydrase inhibitor, can induce a hypokalemic metabolic acidosis. Topical

echothiophate iodine, an irreversible cholinesterase inhibitor, can reduce plasma

cholinesterase activity, prolonging the duration of action of succinylcholine and

mivacurium. Absorption of timolol, a nonselective β-adrenergic blocker has been

associated with atropine-resistant bradycardia, hypotension, and bronchospasm

during general anesthesia. Hyperchloremic acidosis is largely related to large volume

resuscitation with normal saline.

9. B. In the presence of N2O, air bubbles will increase in size as N2O is 35 times

more soluble compared to molecular nitrogen (the major component of air), allowing

it to diffuse into an air bubble more rapidly than nitrogen is absorbed out of the

bubble. If the bubble expands after the incision is closed, intraocular pressure will

rise. This complication can be avoided by discontinuing N2O at least 15 minutes

prior to the bubble injection, as the washout of N2O from the lungs is 90% complete

within 10 minutes. Additionally, repeat general anesthesia with N2O should be

avoided until the bubble is fully absorbed, which for air can take up to 5 days.

10. A. SF6

is an inert gas that is much less soluble than nitrogen (the major component

of air) in blood and, therefore, will have a longer duration of action (10 days)

compared to an air bubble. Bubble size doubles within 24 hours after injection of

SF6 because nitrogen from inhaled air will enter more rapidly into the bubble than

sulfur can diffuse out of it. This slow bubble expansion usually does not

pathologically affect IOP. However, inspired N2O, which is 117 times more

diffusible than hexafluoride (compared to 35 times more than nitrogen), will rapidly

enter the SF6 bubble such that IOP will rise significantly within 30 minutes after the

eye is closed. As with air, repeat general anesthesia with N2O should be avoided

until the SF6 bubble is fully resorbed.

11. C. Although still quite rare, an increased incidence of malignant hyperthermia

(MH) has been reported in patients with strabismus (underlying myopathy) such that

a high index of suspicion should be maintained. EtCO2

is considered the earliest

indicator of a hypermetabolic state with unexpected increases in CO2 despite

constant minute ventilation. Avoiding known triggers can negate the risk of inducing

MH, such that succinylcholine is not recommended during strabismus surgery

involving infants and children.

12. A. Trigeminovagal reflex: the afferent limb of the oculocardiac reflex is via the

trigeminal nerve (CN V), primarily through the ophthalmic division (V1). The

impulse travels along the long and short ciliary nerves (LCN and SCN) to synapse on

the ciliary ganglion. The impulse then continues through the trigeminal ganglion

arriving at the sensory nucleus of the trigeminal nerve. The convergence between the

afferent and efferent limbs is at the motor nucleus of the vagus nerve (CN X) of the

brain stem. From here, the efferent limb is via the vagus nerve, which eventually

synapses on the sinoatrial node of the heart, resulting in an abrupt bradycardia (Fig

16-1).

Figure 16-1.

13. C. The oculocardiac reflex (OCR) occurs frequently during strabismus surgery. It

can occur following traction of the extrinsic eye muscles, or placement of pressure on

the globe. The OCR is most commonly manifested as bradycardia, which regresses

almost immediately after the stimulus is removed. Bigeminy, ectopy, nodal rhythms,

atrioventricular block, and cardiac arrest have also occurred. Traction on any of the

extraocular muscles can evoke this reflex, but it appears that manipulation of the

medial rectus muscle is the most consistent trigger. Though the prophylactic use of

an anticholinergic (atropine or glycopyrrolate) before the potential evoking stimulus

may be recommended, the most effective treatment is the removal of the stimulus.

14. D. The incidence of nausea and vomiting following strabismus surgery can be high,

ranging anywhere from 48% to 85%. Minimizing the use of opioids, substituting

propofol for inhaled anesthetics, along with the prophylactic use of antiemetics can

reduce nausea and vomiting after surgery. Deep extubation has no impact on

postoperative nausea and vomiting, and may place patient at risk for aspiration.

15. B. The afferent limb of the oculocardiac reflex (OCR) is the trigeminal nerve such

that pressures on the globe, conjunctiva, or orbital structures and traction on the

extraocular muscles are potential triggers. This reflex occurs even with an empty

globe. Hypercarbia and hypoxemia are factors believed to augment the incidence and

severity of the reflex. This reflex is noted to fatigue with repeated stimulation and is

not suppressed by general anesthesia.

16. D. The afferent limb of the oculocardiac reflex is the trigeminal nerve such that

triggers include pressure on the globe, conjunctiva, or orbital structures as well as

traction of the extraocular muscles. The vagus nerve is the efferent limb with

connections to the sinoatrial node triggering a reflex bradycardia. The optic nerve is

not involved in this reflex activity.

17. C. Anticholinergics (e.g., glycopyrrolate) may include mydriasis of the pupils,

leading to an increase in intraocular pressure. Unlike atropine, however,

glycopyrrolate is completely ionized at physiologic pH; thus, the occurrence of CNSrelated side effects is lower, as it has difficulty crossing the blood–brain barrier.

Anesthetic agents, whether inhaled or injected, reduce IOP, with the possible

exception of ketamine. Nondepolarizing neuromuscular-blocking agents produce a

slight decrease, while depolarizing relaxants increase IOP. Hyperventilation will

cause vasoconstriction with decrease in choroidal blood flow and intraocular

pressures.

18. C. Nerves blocked are those within the optic cone (annulus of Zinn), which include

optic (CN II), oculomotor (CN III), and the abducens (CN VI). The trochlear nerve

(CN IV) is not affected, since it is located outside of this muscle cone.

19. B. The trochlear nerve (CN IV) remains intact following a retrobulbar block, since

it is located outside of the muscle cone. The trochlear nerve innervates the superior

oblique muscle; thus, rotational movement of the eye remains intact.

20. D. Common complications attributed to a retrobulbar block include retrobulbar

hemorrhage with possible central artery occlusion, oculocardiac reflex, puncture of

the posterior globe, penetration of the optic nerve, and inadvertent intrathecal

injection. Horner syndrome is not commonly seen following retrobulbar blocks;

instead, it results from an interruption of the sympathetic nerve supply to the

head/face, resulting in a triad of miosis, ptosis, and anhidrosis.

21. A. Blockade of the orbicularis oculi muscle, which is a sphincter muscle around

the eye, can further provide adequate surgical conditions for any ocular procedure

with consequent inability to squeeze the lids shut. This can be achieved by blockade

of the facial nerve (CN VII).

22. A. There is 1% to 3% risk of complications with retrobulbar block, ranging from

mild to severe. Possible complications include accidental subarachnoid injection,

which can cause a “total spinal” leading to apnea, unconsciousness, and

cardiorespiratory collapse.

23. C. Eye injuries commonly occur as a result of trauma, which frequently means

providing emergent general anesthesia for patients with full stomachs. It is important

to avoid any sudden increases in intraocular pressure (IOP) that may cause extrusion

of the ocular contents. Although awake tracheal intubation provides the greatest

margin of safety to prevent aspiration, it may in fact promote increase in IOP with

inadequate orotracheal anesthesia. Placement of a retrobulbar block is not advised as

inadvertent globe puncture may lead to extrusion of orbital contents. For most cases,

rapid-sequence or modified rapid-sequence induction is utilized. The choice of

succinylcholine offers the advantage of rapid onset of muscle relaxation, but may

acutely cause elevation in IOP. Alternatively, the use of a large dose of

nondepolarizing neuromuscular-blocking agent will reduce IOP and facilitate tracheal

intubation as long as adequate blockade is confirmed prior to laryngoscopy.

24. A. Hyperventilation, hypotension, and hypothermia decrease IOP, whereas arterial

hypoxemia and hypoventilation elevate IOP. External pressure can also be generated

by venous congestion of orbital veins, which is accentuated during a valsalva,

coughing, and vomiting. Additionally, most inhaled and injected anesthetics (with the

exception of ketamine) can also serve to reduce IOP.

25. C. The oculocardiac reflex best explains this cardiovascular presentation during

ophthalmologic surgeries. First-line therapy is always to remove the stimulus, which

is mediated via trigeminal afferents.

26. B. Hypertensive episodes during anesthesia should be tackled logically. Common

causes are light anesthesia, hypoxia, and hypercarbia. In this case, excessive

systemic uptake of the phenylephrine precipitated severe hypertension. Elevated

diastolic pressures with ECG pathology necessitate immediate action to prevent

further cardiovascular decline. Administration of sodium nitroprusside is beneficial

to quickly reduce the blood pressure and decrease cardiac afterload.

27. D. Corneal abrasions produce a foreign body sensation with associated tearing,

conjunctivitis, and photophobia. This pain is made worse by blinking. Protection

against this occurrence includes application of nonionic petroleum-based ophthalmic

ointment to the eye, securely taping the eyelids shut during anesthesia, and

discouraging patients from rubbing their eye on emergence. Abrasions can be

diagnosed by fluorescein staining, and treatment options include saline flushes,

antibiotic ointment, and patching the eye.

28. A. Laryngospasm can complicate any routine airway management and is especially

prevalent around the time of extubation. It often occurs during stage 2—“excitement

stage”—of general anesthesia in combination with an airway irritant such as blood,