Anesthesia and Analgesia

Question 1

A 36 year-old female (ASA 1) loses consciousness prior to IV deep sedation. She is breathing, has a pulse rate of 84, and blood pressure of 63/34. Which of the following is appropriate treatment?
(A) Atropine 2.0 mg IV
(B) Ephedrine 10 mg IV
(C) Epinephrine 0.1 mg IV q. 3–5 min 
(D) Nalaxone 0.4 mg IV

Answer 1

(B) Ephedrine 10 mg IV

COMSSAT: 2019
Explanation:
Source: Becker, et. al. (2007). Management of complications during moderate and deep sedation: Respiratory
and cardiovascular complications. Anesthesia progress, 54 (2), 59-69.

Question 2

Which of the following is correct regarding the use of naloxone for suspected opioid induced respiratory depression?
(A) The appropriate dose is 0.1- 0.4 mg IV q. 3-5 min
(B) It should be titrated in 1 mg increments IV q. 3-5 min until respiratory depression is
reversed
(C) The maximum recommended dose is 1.6 mg IV
(D) It should never be administered to a patient with a current history of opioid dependence

Answer 2

(A) The appropriate dose is 0.1- 0.4 mg IV q. 3-5 min

COMSSAT: 2019
Explanation:
Source: Malamed, S. (3rd ed.). (1995). Sedation: A guide to patient management, (pp. 120). St. Louis, MO: Mosby.

Question 3

On a patient with known asthma, the use of fentanyl for sedation may produce:
(A) direct bronchoconstriction.
(B) reflex bronchoconstriction.
(C) release of vasoactive substances from mast cells.
(D) ventilatory depressant effects.

Answer 3

(D) ventilatory depressant effects.

COMSSAT: 2019
Explanation:
Source: Becker, et. al. (2007). Management of complications during moderate and deep sedation: Respiratory
and cardiovascular complications. Anesthesia progress, 54 (2), 59-69.

Question 4

A submental intubation can be easily accomplished when a patient has been intubated with a:
(A) nasal RAE tube.
(B) wire-reinforced oral tube.
(C) LMA.
(D) standard oral endotracheal tube.

Answer 4

(B) wire-reinforced oral tube.

COMSSAT: 2019
Explanation:
Source: Hamed, H.H. et al. (2008). Submental intubation versus tracheostomy in maxillofacial trauma patients. Journal of oral and maxillofacial surgery, 66, 1404-1409.
Chandu, A., Witherow, H., & Stewart, A. (2008). Submental intubation in orthognathic surgery: initial experience. British journal of oral and maxillofacial surgery, 46, 561-563.

Question 5

Which benzodiazepine has active metabolites that have clinical impact?
(A) Triazolam (Halcion) 
(B) Midazolam (Versed) 
(C) Diazepam (Valium) 
(D) Oxazepam (Serax)

Answer 5

(C) Diazepam (Valium)

COMSSAT: 2019
Explanation:
Source: Malamed, S. (3rd ed.). (1995). Sedation: A guide to patient management, (pp. 120). St. Louis, MO: Mosby.

Question 6

Oral midazolam in children:
(A) has a narrow toxic-therapeutic ratio.
(B) has a long onset of action.
(C) has a recommended dose of 0.5 mg/kg.
(D) is not recommended to be mixed in different carrying vehicles (juice, cola, and syrup) to
alleviate unpalatable taste.

Answer 6

(C) has a recommended dose of 0.5 mg/kg

COMSSAT: 2019
Explanation:
Source: Loeffler, P. (1992). Oral benzodiazepines and conscious sedation: a review. Journal of oral and maxillofacial surgery, 50, 991.
Bergman, S. (1999). Review of its pharmacology and its use in pediatric anesthesia. Anesthesia progress, 46, 10-20.

Question 7

Which medication given concomitantly would most effectively diminish the likelihood of ketamine emergence phenomena?
(A) Fentanyl 
(B) Midazolam 
(C) Atropine
(D) Esmolol

Answer 7

(B) Midazolam

COMSSAT: 2019
Explanation:
Source: Malamed, S. (3rd ed.). (1995). Sedation: A guide to patient management, (pp. 120). St. Louis, MO: Mosby.

Question 8

Propofol:
(A) is a sedative-hypnotic anesthetic agent.
(B) increases intracranial pressure.
(C) increases systemic vascular resistance.
(D) is a barbiturate anesthetic agent.

Answer 8

(A) is a sedative-hypnotic anesthetic agent.

COMSSAT: 2019
Explanation:
Source: Cillo, J.E. & Finn, R. (2006). Hemodynamics in elderly coronary artery disease patients undergoing propofol sedation. Journal of oral and maxillofacial surgery, 64 (9), 1338-1342.
Huettemann, E. et. al. (2006). Effects of propofol vs methohexital on neutrophil function and immune status in critically ill patients. Journal of anesthesia, 20(2), 86-91.

Question 9

The use of intramuscular ketamine:
(A) can cause significant pain on injection. 
(B) has a smooth but slow onset.
(C) does not provide amnesia.
(D) does have analgesic properties.

Answer 9

(D) does have analgesic properties.

COMSSAT: 2019
Explanation:
Source: Malamed, S. (3rd ed.). (1995). Sedation: A guide to patient management, (pp. 120). St. Louis, MO: Mosby.

Question 10

During intravenous sedation with propofol a possible complication is an increased risk of:
(A) tachycardia following sedation. 
(B) hypotension during sedation. 
(C) prolonged sedation.
(D) neutrophil dysfunction.

Answer 10

(B) hypotension during sedation.

COMSSAT: 2019
Explanation:
Source: Yorozu, T., et. al. (2007). Factors influencing intraoperative bradycardia in adult patients. Journal of anesthesia.
Becker, et. al. (2007). Management of complications during moderate and deep sedation: Respiratory
and cardiovascular complications. Anesthesia progress, 54 (2), 59-69.
Cillo, J.E. & Finn, R. (2006). Hemodynamics in elderly coronary artery disease patients undergoing propofol sedation. Journal of oral and maxillofacial surgery, 64 (9), 1338-1342.
Huettemann, E. et. al. (2006). Effects of propofol vs methohexital on neutrophil function and immune status in critically ill patients. Journal of anesthesia, 20(2), 86-91.

Question 11

Which of the following patients would best allow safe induction of an intubation general anesthetic according to current American Society of Anesthesiologists guidelines?
A. 6 month old male having taken 30 ml of formula 5 hours ago
B. 15 year-old male having taken 500 ml cola 2.5 hours ago
C. 46 year-old female having taken 40 ml of fresh squeezed orange juice 3.5 hours ago
D. 65 year-old having eaten peanut butter on toast 6 hours ago.

Answer 11

B. 15 year-old male having taken 500 ml cola 2.5 hours ago

COMSSAT: 2009
Rationale:
Perioperative fasting guidelines were revised by the ASA to reflect length of time and
nature of ingested foods correlated to gastric emptying time, and hence risk of
aspiration. Studies suggest that clear liquids (water, soda pop, coffee without creamer,
fruit juice without pulp), regardless of volume ingested, essentially clear the stomach after
two hours in healthy individuals who have no conditions which might delay gastric
emptying, and that clear fluid starvation over 2 hours may be counterproductive with
respect to dehydration and post-anesthetic recovery. Conditions which may delay gastric
emptying may include: gastroparetic conditions (diabetic neuropathy), proliferative
connective tissue disorders, obesity, extreme pain or fear, and opioid use. Non-clear
liquids such as non-human milk products and formula delay gastric empyting similar to
solids. Human milk has an intermediate gastric emptying period, for which a four hour
fast has been recommended. A six hour fast from all “light”solids (i.e., non-meat and
non-fat) and non-clear liquids (except breast milk) has been recommended for otherwise
healthy individuals who have no gastric emptying delaying factors. Fat and meats should
be avoided for at least 8 hours prior to induction of general anesthesia, since these
significantly delay gastric emptying.
The 15 year-old male falls within these ASA guidelines. The 6 month old has taken
formula, not breast milk and must fast 6 hours. The 46 year-old female has fresh
squeezed and hence pulp-laden fruit juice, and also requires a 6 hours fast. The 65
year-old male has had peanut butter, a highly fatty food and must fast for at least 8
hours.
Reference:
American Society of Anesthesiology Taskforce on Preoperative Fasting: Practical
Guidelines
for Preoperative Fasting. Anesthesology, 90:896-905 1999
McGlinch BP: Issues in Ambulatory Anesthesia. In: Faust RJ et al: Anesthesiology
Review
(3rd. Ed.) Churchill Livingstone, Philadelphia, 2002 pp477-479

Question 12

Which of the following decreases the incidence or severity of perioperative pulmonary
aspiration?
A. Post-aspiration left lateral Trendelenberg position
B. Age appropriate for uncuffed endotracheal tube
C. Post-aspiration tracheal lavage
D. Exploratory bronchoscopy

Answer 12

B. Age appropriate for uncuffed endotracheal tube

COMSSAT: 2009
Rationale:
Post-anesthetic pulmonary aspiration occurs in 1:3000-10,000 general anesthetics
administered. Most aspirations are sub-clinical with minor symptoms that resolve
spontaneously. The amount of tracheal and bronchial mucosal damage brought about by
aspiration of gastric contents increases with the amount of aspirate, its acidity, and the
amount of particulate matter present. Certain disorders are associated with a higher risk
of aspiration, including: extreme age, gastrointestinal or upper abdominal procedures,
pregnancy, obesity, GERD, gastric mobility disorders, and recent meal.
While not uncommon in the pediatric population, aspiration in this population is generally
not as serious as in the adult population and has a much lower morbidity and mortality.
Uncuffed endotracheal tubes are generally used in pediatric patients 8 years of age or
younger; so a patient age appropriate for use of an uncuffed tube has a decreased
aspiration risk. Post-aspiration positioning should be in the right lateral Trendelenberg
position, since the left mainstem bronchus leaves the trachea at a more acute angle than
the right and therefore viscous aspirated material is more likely to flow into the left
mainstem in a left decubitus position than would flow in the right mainstem in a right
decubitus. Since tracheobronchial mucosal chemical damage occurs within seconds and
relative neutralization of aspirant occurs within minutes, routine tracheobronchial lavage
for most pulmonary aspiration cases is not indicated. Similarly, exploratory
bronchoscopy is not routinely indicated unless large amounts of particulate matter are
aspirated.
Reference:
Warner MA: Perioperative Pulmonary Aspiration. In: Faust RJ et al: Anesthesiology
Review. Churchill Livingstone, Philadelphia, 2002. pp 564-568
Office Anesthesia Evaluation Manual, 6th ed. American Association of Oral and
Maxillofacial
Surgeons, 2002. pp 32-33

Question 13

You plan office extractions for a 65 year-old female with a history of compensated congestive
heart failure and Parkinson’s disease. Pre-anesthetic vital signs include BP = 135/85, pulse is
100, respirations = 15. She has taken her routine medications including selegiline (selective
irreversible MAO-B inhibitor), digoxin (cardiac glycoside), enalapril (ACE inhibitor), and
potassium. After initiating conscious sedation using nitrous oxide/oxygen, fentanyl and
midazolam, you note the following vital sign changes prior to local anesthetic administration: BP
= 70/40, pulse = 85, respirations = 18. The pulse oximetry reading has dropped to 90. You
note no change after administering 100% oxygen, flumazenil (Romazicon), and naloxone
(Narcan). Which next step would be the most appropriate?
A. Trendelenberg position
B. 750 ml intravenous saline fluid bolus
C. Ephedrine 2.5 mg IV
D. Phenylephrine (neosynephrine) 0.1 mg IV

Answer 13

D. Phenylephrine (neosynephrine) 0.1 mg IV

COMSSAT: 2009

Rationale:
Intraoperative hypotension can present treatment challenges in the medically compromised patient. This patient presents with a history of compensated ischemic congestive heart failure and is on a digitalis glycoside (digitoxin), and an angiotensin converting enzyme inhibitor (enalapril). Her history of congestive heart failure would mitigate against any maneuver that might lead to increased central venous pressures, which may precipitate a new episode of congestion. Therefore, Trendelenberg positioning and a relatively large isotonic intravenous fluid challenge might not be
desired early therapies. Selegiline is a relatively selective monoamine oxidase-B inhibitor, which preferentially decreases the central metabolism of dopamine. It is used in the treatment of
Parkinson’s disease; either to replace carbidopa/levodopa early in the disease course or
to decrease the latter’s dosage and minimize dopaminergic side effects. Older
nonselective MAOI’s depressed the central metabolism of a number of monoamine
neurotransmitters including serotonin, epinephrine, norepinephrine, and dopamine; and
have been used for refractory depression. Relatively MAOI-A selective drugs decrease
the metabolism of the first 3 listed neurotransmitters; so that side effects can include
hypertensive crises and. In low to moderate doses, selegeline activity is approximately
80% MAOI-B and 20% MAOI-A. Selegeline has a fairly frequent incidence of orthostatic
hypotension, which can be exaggerated with the concomitant use of vasodilators such
as nitrous oxide, benzodiazepines, and opioids. The first step in treating intraoperative
hypotension in this case is to terminate the procedure and cautiously reverse the agents
used. Cautious use of low dosages of an alpha selective peripheral vasoconstrictor
would be indicated next to increase blood pressure without increasing cardiac
chronotropy. Low-dose phenylephrine would be a good choice in this situation.
Ephedrine is an indirect alpha- and beta-stimulating agent that should be avoided, since
some MAOI-A inhibition occurs with selegiline. The interaction between indirect acting
sympathomimetic drugs and MAOI occurs because an MAOI increases the amount of
presynaptic transmitter that is available to be released. The central release of monoamine neurotransmitters in the case of MAOI-I inhibition could lead to a
hypertensive crisis. Also, the beta adrenergic effects of ephedrine would potentially
worsen the tachycardia in this patient with a history of ischemic heart disease. Direct
acting sympathathomimetic agents are not contraindicated in combination with MAOIs.
Reference:
Baranov D et al: Neurologic Diseases. In: Fleisher L: Anesthesia and Uncommon
Diseases. WB Saunders, Philadelphia, 2006 pp 261-4
Jedd M: Monoamine Oxidase Inhibitors and Anesthesia. In: Faust R et al:
Anesthesiology Review Churchill Livingstone, Philadelphia 2002 pp 163-4

Question 14

Which of the following muscle relaxants is the best choice for intubation in the atopic patient
with severe gastroesophageal reflux disease?
A. Succinylcholine
B. Mivacurium
C. Atracurium
D. Rocuronium

Answer 14

D. Rocuronium

COMSSAT: 2009

Rationale:
Succinylcholine is a depolarizing muscle relaxant. Due to initial depolarization of skeletal
muscles, a variety of side effects can occur. These include: increased intraocular
pressures, myalgias, increased intracranial pressures, and intragastric pressure
increases. The latter effect is brought about by skeletal abdominal muscle contracture.
The increase in intragastric pressure secondary to succinylcholine can be blocked by
precurarization. Additionally, succinylcholine causes an even greater increase in lower
esophageal pressure, such that the increase in gastric pressure does not routinely result
in aspiration of gastric contents. However, in the patient prone to incompetence of the
gastroesophageal sphincter, increases in intragastric pressures can lead to regurgitation
and aspiration of stomach contents.
Non-depolarizing muscle relaxants avoid these pressure increases. However, the
benzylisoquinolone derivatives (mivacurium, atracurium, cisatracurium, metocurine, and
d-tubocurarine) can cause histamine release, especially in large doses or when injected
quickly. In the atopic patient, who presumably has significant environmental allergy
symptoms, the effects of additional sudden histamine release mediated by atracurium or
mivacurium (with bronchospasm, hypotension, and tachycardia) would best be avoided.
Steroidal non-depolarizing muscle relaxants include rapacuronium, vecuronium,
rocuronium, pancuronium, and pipercuronium. These lack histamine releasing properties
and may be indicated in the atopic patient. Rocuronium has an intermediate onset of
action and duration of effect, and would be a good choice for this patient.
Rapacuronium, having an onset and duration of effect approaching that of
succinylcholine, was initially developed as a substitute for the depolarizing paralytic
agent, especially in the pediatric population who have a higher incidence of bradycardia
with succinylcholine. However, it has been found to have an unacceptably high rate of
severe bronchospastic toxicity, especially if a history of bronchospastic disease is
present; and it’s bronchospastic activity appears to be dose-related. Rapacuronium has
recently been withdrawn from the US market.

Reference:
Christopherson T: Succinylcholine Side Effects. In: Fleisher L: Anesthesia and
Uncommon Diseases. WB Saunders, Philadelphia, 2006 pp 134-6
Stoelting R, Miller R: Basics of Anesthesia, 4th Ed. Churchill Livingstone, Philadelphia
2000 pp 89-106
Rajchert D et al: Rapacuronium and the risk of bronchospasm in pediatric patients.
Anesth Analg 94:483-4 2002

Question 15

Which of the following medications would not require significant dosing adjustments in the
elderly patient?
A. Cisatracurium
B. Alfentanil
C. Desflurane
D. Thiopental

Answer 15

A. Cisatracurium

COMSSAT: 2009

Rationale:
Physiologic changes in the aging process include decreases in perfusion, relative
increase in poorly perfused fatty tissues, slowed redistribution of medications, decreased
pulmonary and cardiac reserve, decreased hepatic and renal blood flow hence
decreased hepatic and renal drug elimination, reduced hepatic microsomal enzyme
activity, and increased central nervous system sensitivity to anesthetic agents.
Atracurium and its cojoiner cisatracurium are nondepolarizing muscle relaxants. Unlike
other benzylisoquinilone muscle relaxants, these two agents have little histamine release
tendency and thereby have no significant cardiovascular effects. Both undergo
spontaneous nonenzymatic degradation at body temperatures (Hoffman elimination) and
also undergo hydrolysis by nonspecific plasma esterases. Because of these factors, plus
the fact that the sensitivity of the neuromuscular junction does not change with age, no
dosage adjustment for cisatracurium is necessary in the aged patient.
The pharmacodynamics of opioids, inhalational anesthetics, and other intravenous
agents are markedly changed with advances in age, generally thought to be due to a
marked increase in CNS sensitivity to such agents, necessitating downward dosing
adjustments in initial administration in the elderly. Pharmacokinetics are less profoundly
altered, but maintenance dosing of intravenous anesthetics should be also adjusted
downward due to a slower redistribution. This slower redistribution is due to decreased
muscle mass (which is generally well perfused and classically is the “first compartment”
of redistribuion), and the increases in poorly perfused adipose tissue leading to delayed
final body drug clearance from the fat reservoir. Contributing to this slow clearance are
the geriatric cardiac, hepatic, and renal changes mentioned previously.
References:
Stoelting R, Miller R: Elderly Patients. In: Stoelting R, Miller R: Basics of Anesthesia
Churchill Livingstone, Philadelphia, 2000 pp 376-85
Sandler N, Swift J: Geriatric Considerations. In: Bennett J, Rosenberg M: Medical
Emergencies in Dentistry. WB Saunders, Philadelphia, 2002 pp 73-6
Keyword: assessment of patient for anesthesia, pharmacology of anesthetic agents,
geriatric patient, neuromuscular blocking agents, pharmacokinetics

Question 16

A patient with a T-4 spinal injury has a 4.5 hour general anesthetic. The patient has no foley
catheter because the intended surgery was to have taken 2 hours. The patient suddenly
becomes hypertensive and bradycardic. The ECG reflects sinus bradycardia in Lead II. Flushing
is evident in the face and mucous membranes. You notice the patient sweating and exhibiting
mydriasis of both pupils. The best explanation for this complex of symptoms is:
A. myocardial infarction.
B. autonomic hyperreflexia.
C. increased intracranial pressure.
D. massive pulmonary embolism.

Answer 16

B. autonomic hyperreflexia.

COMSSAT: 2009

Rationale:
Autonomic hyperreflexia is a syndrome of massive, disinhibited reflex sympathetic
discharge in response to cutaneous or visceral stimulation below the level of the spinal
cord lesion. Myocardial infarction may manifest under anesthesia as hypotension and by
changes on the ECG; lead V5 being the most sensitive in detecting ischemia. Lead II will
detect ischemia in the RCA distribution. New Q waves and ST segment changes are
suggestive of M.I. Elevated intracranial pressure may lead to the Cushing reflex which is
hypertension and bradycardia, but only when the ICP approaches systemic arterial
pressure. A massive pulmonary embolism will show tachycardia, hypotension,
hypoxemia and right axis deviation on ECG.
Reference:
Amzallag m: Autonomic hyperreflexia. Int Anesthesiol Clin 31: 87, 1993
Hambly PR, Martin B: Anesthesia for chronic spinal cod lesions. Anesthesia 53: 273,
1998

Question 17

Which of the following drugs should be avoided for induction of general anesthesia in the severe
coronary artery disease patient?
A. Propofol
B. Fentanyl
C. Sevoflurane
D. Ketamine

Answer 17

D. Ketamine

COMSSAT: 2009

Rationale:
Ketamine is contraindicated in the CAD patient due to its resultant tachycardia and
hypertension. This will increase the demand for oxygen upon the heart muscle. Propofol
has minimal effects upon oxygen demand by the heart. It will produce a decrease in
arterial blood pressure and decrease in CO. Opiates will reduce both HR and BP. Most
opiates will reduce sympathetic tone and enhance parasympathetic tone. Inhalational
agents may show a beneficial effect against ischemia in humans.
Reference:
Warltier Dc, Pagel PS, Kersten JR: Approaches to the prevention of perioperative
myocardial ischemia. Anesthesiology 92: 253, 2000
Allen RB: Ischemic Heart Disease and Myocardial Infarction. Anesthesia Secrets, 2nd
Edition, Philadelphia, PA, Hanley & Belfus Inc 2000, pg 189-192.

Question 18

You are extracting teeth on a morbidly obese man who is a heavy smoker and has obstructive
sleep apnea. The patient receives 100 mcg of fentanyl and 5 mg of midazolam prior to local
anesthetic injection. After a few minutes you note that the patient’s ventilation has decreased
and he appears clinically cyanotic. However, the pulse oximeter reads 96% (SpO2). What is the
most likely explanation for this phenomenon?
A. Motion artifact due to patient movement
B. High levels of carboxyhemoglobin
C. Elevated hemoglobin and hematocrit
D. Supplemental oxygen by nasal cannula

Answer 18

B. High levels of carboxyhemoglobin

COMSSAT: 2009

Rationale:
Heavy smokers may have high levels of carboxyhemoglobin. Oxygenation is
overestimated in the presence of significant levels of carboxyhemoglobin. This occurs
because the pulse oximeter sees carboxyhemoglobin as oxyhemoglobin.
Contemporary pulse oximeters average signals over different periods of time. This
reduces the effect of noise (motion) upon the reading. An obese patient may have
elevated levels of hemoglobin and hematocrit associated with sleep apnea. This occurs
under periods of chronic hypoxemia. This would not elevate the SpO2.
Reference:
Barker SJ, Tremper KK: The effect of carbon monoxide inhalation on pulse oximetry and
transcutaneous PO2 . Anesthesiology 73:573, 1990
Buckley RG, Aks SE, Eshom JL, et al: The pulse oximetry gap in carbon monoxide
intoxication. Ann Emerg Med 24:252, 1994

Question 19

An 18 year-old healthy male patient in your office was given 10 mg of midazolam, 50 mcg of
fentanyl and 30 mg of propofol during a long extraction case. The patient has prolonged
emergence from anesthesia and decreased ventilations. The pulse oximeter reads 89%
oxygenation on 4 L nasal cannula oxygen. The patient is administered flumazenil 0.2 mg and
naloxone 0.2 mg. His mental status and ventilations improve. Forty minutes later in your
recovery room he appears drowsy and is non-responsive to commands. The pulse oximeter
reads 91%. Shallow unobstructed respirations are approximately 12 per minute. How should
you proceed?
A. Administer flumazenil
B. Administer supplemental oxygen
C. Support the patient’s airway
D. Administer naloxone

Answer 19

A. Administer flumazenil

COMSSAT: 2009

Rationale:
Resedation is a potential problem given the short half-life of reversal agents. Flumazenil’s
onset is 1 – 2 minutes, its peak effect is 2 – 10 minutes, and its duration of effect is 45 –
90 minutes. Naloxone’s onset is 1 – 2 minutes, its peak effect is 5 – 15 minutes and its
duration of effect is 60 – 240 minutes. The patient was given a large dose of
benzodiazepine. In this situation, it is likely that the benzodiazepine was more likely
contributory to the initial depressed ventilations and prolonged emergence despite both
naloxone and flumazenil being administered by the practitioner. Another dose of
Flumazenil is the appropriate treatment. The maximum total dose is 3 mg. This patient is
able to maintain an unobstructed airway and has spontaneous ventilations. Supporting
the patient’s airway is not necessary as he is not demonstrating obstruction.
Administering supplemental oxygen may increase the level of oxygen saturation,
however, will not correct the depressed level of consciousness.
Reference:
Weinbrum A, Geller E: The respiratory effects of reversing Midazolam sedation with
Flumazenil in the presence or absence of narcotics. Acta Anesthesiol Scand Suppl
92:65, discussion 78, 1990.
Klotz U, Kanto J: Pharmacokinetics and clinical use of Flumazenil. Clin Pharmacokinet
14:1, 1988

Question 20

The OMS team is treating an orbital floor blow-out fracture in a 47 year-old man who has a
history of hypertension and is a smoker. During elevation of the orbital contents the patient is
noted to become hypotensive (SBP = 65) and bradycardic (45). The most appropriate initial
pharmacologic treatment for this clinical situation is?
A. Ephedrine 20 mg IV
B. Transcutaneous pacing
C. Epinephrine 1.0 mg IV
D. Atropine 0.5 mg IV

Answer 20

D. Atropine 0.5 mg IV

COMSSAT: 2009

Rationale:
It is evident that the patient has experienced an oculocardiac reflex. Atropine remains the
first-line drug for acute symptomatic bradycardia. The recommended dose is 0.5 mg
every 3-5 minutes to a maximum of 3 mg. Scopolamine is an anticholinergic agent.
However, it is not used in treating symptomatic bradycardia. Transcutaneous pacing is
indicated for the treatment of symptomatic bradycardia if the patient fails to respond to
atropine. Epinephrine is used to treat symptomatic bradycardia as a second-line drug in
an infusion of 2-10 mcg/min. Ephedrine is a sympathomimetic amine which may be used
to treat the hypotensive patient. However, considering the most likely etiology of the
hypoetension and bradycardia it would be an inappropriate agent.
Reference:
Advanced Cardiovascular Life Support – Provider Manual, Field JM editor, American
Heart Association, 2006
2005 American Heart Association Guidelines for Cardiopulmonary Resuscitation and
Emergency Cardiovascular Care: Management of symptomatic bradycardia and
tachycardia. Circulation 2005;112:IV-67-IV-77.

Question 21

The patient you are treating is a spinal cord injured dialysis patient with end stage renal disease
(ESRD). He exhibits a serum potassium of 5.1. Which of the following muscle relaxants is the
agent of choice with this patient?
A. Rocuronium
B. Vecuronium
C. Atracurium
D. Succinylcholine

Answer 21

C. Atracurium

COMSSAT: 2009

Rationale:
The administration of succinylcholine in patients with renal failure or spinal cord lesions
can lead to an exaggerated hyperkalemia response. This may result in adverse cardiac
events. This phenomenon occurs from the proliferation of post-synaptic acetylcholine
receptors beyond the neuromuscular junction. This results in an increase in serum
potassium upon depolarization by succinylcholine administration.
Renal excretion of the nondepolarizing muscle relaxants, atracurium, rocuronium,
mivacurium is approximately 10%, vecuronium approximately 15% with the other
nondepolarizing muscle relaxants being more dependent on renal excretion. Of the
nondepolarizing agents atracurium is the preferred agent because it undergoes
spontaneous Hofmann degradation and ester hydrolysis. A larger initial dose of the water
soluble atracurium is required to produce rapid paralysis in patients with altered body
water composition. Less frequent and smaller doses will be required to maintain paralysis
in the patients with ESRD.
Reference:
Hunter JM, Jones RS, Utting JE: Use of the muscle relaxant atracurium in anephric
patients. J R Soc Med 75:336-340, 1982
Thapa S, Brull, SJ: Succinylcholine-Induced hyperkalemia in

Question 22

Which of the following best supports the discontinuation of pyridostigmine (Mestinon
cholinesterase inhibitor) during the anesthetic management of the patient with myasthenia
gravis?
A. Continuation would increase risk of cholinergic crisis
B. Continuation would increase risk of respiratory muscle weakness
C. Discontinuation decreases sensitivity to respiratory depression associated with opioids
D. Continuation results in resistance to succinylcholine and shortened duration

Answer 22

A. Continuation would increase risk of cholinergic crisis

COMSSAT: 2009

Rationale:
Myathenia gravis is an autoimmune disease of the motor endplate. These patients have
a 70 -80% reduction in the number of acetylcholine motor-endplate receptors.
Approximately 25% of these receptors are required for functional neuromuscular
transmission.
Anticholinesterase therapy is the primary pharmacologic treatment of patients with MG.
The goal of the administration of an anticholinesterase agent is to increase the amount of
acetylcholine. The increase in acetylcholine overcomes the reduction in acetylcholine
receptors with a resultant increase in neuromuscular function. The anticholinesterase
agents generally used in the management of MG are edrophonium, pyridostigmine,
neostigmine and ambedonium. These agents do not cross the blood brain barrier.
Pyridostigmine is the most commonly prescribed agent because of its 3 – 6 hour duration
and the fewer muscarinic side effects. Administration of excessive amounts of
anticholinesterase agents can result in cholinergic crisis. Cholinergic crisis is manifested
by bradycardia, hypotension, increased secretions, lacrimation, wheezing, muscle
weakness, nausea and vomiting, and constricted pupils.
There are several points to consider in the anesthetic management of a patient with MG.
(1) Respiratory function should be assessed preoperatively through pulmonary function
tests. Opioids must be used sparingly to avoid further compromising a patient with
diminished respiratory reserve. (2) There is differing opinions pertaining to the
continuation of the patient’s anticholinesterase agent. If the patient continues their
anticholinesterase there is the potential for various drug interactions including
prolongation of the succinylcholine, and antagonism of the nondepolarizing
neuromuscular blocking agent. Continuation of the anticholinesterase has the potential
risk of resulting in cholinergic crisis. The benefit of stopping the anticholinesterase agent
is the avoidance of a cholinergic crisis post-operatively. Additionally, the withholding of
the anticholinesterase agent results in muscle weakness and a reduction or elimination of
the need for neuromuscular blockade. If neuromuscular blockade is required the MG
patient demonstrates a resistance to succinylcholine and a prolongation of its effects; and
an increased sensitivity to nondepolarazing agents. The latter is a result of the
diminished neuromuscular receptors in a patient with MG.
`
Reference:
Barak A: Anesthesia and myasthenia gravis. Can J Anaesth 39:476-486;1992
Abel M: Myasthenia gravis in Clinical Cases in Anesthesia. Ed Reed AP & Yudkowitz FS.
Elsevier 2005 pages 137 – 142

Question 23

Which of the following patterns is characteristic of a response to nerve stimulation produced by
a depolarizing neuromuscular agents?
A. A lack of fade in response to train of four (TOF)
B. Increase in post-tetanic stimulation
C. Tetanus is associated with fade in muscle response
D. Fourth twitch of TOF disappears with 60-70% receptor occupancy

Answer 23

A. A lack of fade in response to train of four (TOF)

COMSSAT: 2009

Rationale:
A nerve stimulator delivers a set electrical impulse either as a single stimulus, a tetanic
stimulation, or a series of 4 impulses (TOF – train of four). Clinically the TOF and the
tetanic stimulation provide the greatest clinical information.
The train of four delivers 4 impulses at a set frequency. The practitioner assesses the
ratio of the amplitude of the fourth twitch to that of the first twitch. In a patient who has
received a non-depolarizing neuromuscular blocking agent the twitches disappear in
reverse order (1st twitch 90-95% receptor occupancy, 2nd twitch 85-90% receptor
occupancy, 3rd twitch 80-85% receptor occupancy, 4th twitch 75-80% receptor
occupancy). A lack of observable fade on a train of four is used clinically to assess for
recovery from a neuromuscular blockade. In a patient who has received a depolarizing
agent the TOF is uniformly decreased.
Tetanic stimulation is an impulse that is administered at a frequency of 50 Hz. A fade in
muscle response or “tetanic fade” occurs secondary to a non-depolarizing muscle
relaxant. A lack of tetanic fade occurs with a depolarizing agent. A tetanic fade or loss of
contraction associated with the tetanic stimulation indicates a phase 2 neuromuscular
blockade, which may be associated with prolonged exposure to succinylcholine. A
tetanic stimulation causes the release of acetylcholine. This can cause a post-tetanic
facilitation associated with non-depolarizing agents.
Reference:
Donati F, & Bevan DR: Neuormuscular blocking agents. In Clinical Anesthesia Editors
Barash PG, Cullen BF, Stoelting RK. 5th ed. Lippincott, Williams & Wilkins. Pg 440 – 444
Torda TA: Monitoring neuromuscular transmission. Anaesth Intensive Care 30:123;2002
Duke J: Muscle relaxants and monitoring of relaxant activity. InAnesthesia Secrets 3rd ed.
Mosby Elsevier. Page 88 - 96

Question 24

A 37 year-old female presents for emergent surgery. She has been recently diagnosed with
Graves’ disease but has yet to start any treatment. She also has hypertension and arthritis. Her
only medication is Lasix (furosemide), which she takes sporadically. What would be the most
appropriate medication to administer pre-operatively to avoid anesthetic complications in this
emergent situation?
A. Propylthiouracil
B. Decadron
C. Iodide
D. Propranolol

Answer 24

D. Propranolol

COMSSAT: 2009

Rationale:
Graves disease is a hyperthyroid state that typically occurs in females between the ages
of 20 – 40 years of age. The stress of surgery can cause a life threatening exacerbation
of this state called thyroid storm. Thyroid storm is a hypermetabolic condition that
presents with hypertension, dysrhythmias including tachycardia, myocardial ischemia,
and hyperthermia.
A patient who is hyperthyroid must be treated prior to being taken to surgery. For
elective cases this is frequently done with antithyroid medications such as
propylthiouracil or methimazole. Propylthiouracil inhibits iodination and coupling reactions
in the thyroid gland inhibiting the synthesis of thyroid hormones and inhibiting the
peripheral conversion of T4 to T3. It takes 6 – 8 weeks of treatment for a patient to
become euthyroid.
Iodide containing solutions, such as potassium iodide or Lugol’s solution, may also be
administered. These agents inhibit T3 and T4 release for a period of time from days to
weeks. Iodide is usually administered with either antithyroid drugs or 􀀀-adrenergic
antagonists and preoperative preparation can take ideally from 7 to 14 days.
􀀀-adrenergic antagonists are effective in attenuating sympathetic activity. Propranolol
does not inhibit hormone synthesis but does prevent the conversion of T4 to T3. The
administration of a 􀀀-blocker does prevent sympathetic activity such as hypertension and
dysrhythmias. Corticosteroids, such as decadron, can also be used in the management
of thyrotoxicosis because they reduce thyroid hormone secretion and peripheral
conversion of T4 to T3
The administration of a 􀀀-adrenergic antagonist is the preferred agent in the
management of an acute situation requiring emergent surgery.
Reference:
Miller, RD. Miller’s Anesthesia, 6th edition. Elsevier, 2005, pg 1045-1047.

Question 25

A 22 year-old 50 kg female presents for the extraction of 4 wisdom teeth. Pre-operative vital
signs are BP 115/75 and HR 64 regular. Anesthetic induction was achieved with midazolam 3.5
mg, fentanyl 50 mcg, ketamine 50 mg and propofol 50 mg. Lidocaine 144 mg with epinephrine
0.072 mg was administered. The patient’s heart rate increases to 95 after the ketamine and
local anesthesia with epinephrine. Fifteen minutes after the conclusion of the procedure and a
total of 45 minutes from the time the patient received the last anesthetic agent, the patient is
slightly confused, complaining of palpitations, and feeling warm. The patient’s blood pressure is
150/60, heart rate is 145 and irregular, respiratory rate is 22 and end-tidal CO2 via nasal cannula
sampling is 43. What is the most appropriate diagnosis and treatment?
A. Increased heart rate most likely secondary to combination of ketamine and epinephrine.
In a healthy individual would observe for another 30 minutes.
B. Increased heart rate most likely secondary to combination of ketamine and epinephrine
and possible postoperative pain. The persistent elevation in heart rate warrants
pharmacologic intervention.
C. Tachycardia, and hypercapnea must alert the practitioner to consider a diagnosis of
malignant hyperthermia and initiate dantrolene therapy.
D. The clinical presentation is that of a hypermetabolic state. Would consider a diagnosis of
hyperthyroidism and initially manage with esmolol 20 – 30 mgs.

Answer 25

D. The clinical presentation is that of a hypermetabolic state. Would consider a diagnosis of
hyperthyroidism and initially manage with esmolol 20 – 30 mgs.

COMSSAT: 2009

Rationale:
Signs of hyperthyroidism include (1) sinus tachycardia, (2) warm, moist skin, (3) systolic
hypertension with widened pulse (although with severe tachycardia and decompensation
can become hypotensive), (4) atrial fibrillation (10% incidence). Initial treatment includes
intravenous fluids to replace intravascular volume, acetaminophen for hyperthermia and
beta-adrenergic blockade.
The sympathomimetic effect of ketamine results in an increase in heart rate (􀀀20%) and
an increase in blood pressure. These effects are seen within minutes of the drugs
intravenous administration and persist for approximately 20 minutes. In this scenario the
increased heart rate and blood pressure should not have persisted for the duration
described. The pulse pressure is also widened more consistent with hyperthyroidism.
The most sensitive indicator of malignant hyperthermia is hypercapnea and one of the
early manifestations is tachycardia. Other early clinical manifestations of MH include
muscle rigidity and tachypnea. Later clinical findings include increased temperature, and
skin mottling. In the clinical scenario presented the patient was not administered an agent
associated with the induction of MH. MH can be considered in the differential, however,
should not be primary.
Reference:
Van Tassel & Schulman. Malignant Hyperthermia in Complications in Anesthesiology. 2nd
edition ed Atlee pg 654-656
Gronert, Pessah, Muldoon et al. Malignant Hyperthermia Miller’s Anesthesia 6th edition.
ed Miller RD Elsevier pg 1169-1186
Reves JG, Glass PSA, et al: Intravenous nonopioid anesthetics. In Miller RD (ed): Miller’s
Anesthesia, 6th ed Churchill Livingston, 2005 pg 317-378
Prielipp RC, Roberts PR: Hyperthyrodism: Thyroid Storm. In Atlee JL (ed). Complications
in Anesthesia. 2nd edition Elsevier 2007 pg 454-456

Question 26

A 27 year-old female with a previously unknown medical history arrives in the PACU after repair
of a facial laceration under general anesthesia. She has not had a significant blood loss.
Shortly after arrival, she is noted to have a heart rate of 150, a temperature of 39o C, a
respiratory rate of 30, oxygen saturation of 99 %, and a blood pressure of 92/65. A blood gas
reveals a pH of 7.4, PaO2 of 80, PaCO2 of 38, and a bicarbonate of 24. She is agitated and
confused. What is the most likely diagnosis?
A. Thyrotoxicosis
B. Malignant Hyperthermia
C. Pheochromocytoma
D. Postoperative pain

Answer 26

A. Thyrotoxicosis

COMSSAT: 2009

Rationale:
Thyrotoxicosis is associated with tachycardia, hyperpyrexia, altered sensorium, and
hypotension. Patients are normally not acidotic. Malignant hyperthermia is unlikely since
patient is not acidotic. MH would also be associated with muscle rigidity.
Pheochromocytoma is not likely as this patient is hypotensive, not hypertensive as would
be expected in pheochromocytoma. Although pain could cause tachycardia and
tachypnea, it should also cause hypertension. This patient has not had significant blood
loss so it is unlikely that her hypotension is due to hypovolemic shock.
Reference:
Miller, RD. Miller’s Anesthesia, 6th edition. Elsevier, 2005, pg 1045-1047.
Morgan GE, Mikhail MS, Murray MJ. Clinical Anesthesiology, 4th edition. Lange Medical
Books, 2006, pgs 807-808, 1016-1017.
Keyword: Complications of anesthesia, Anesthetic technique, thyroid disease,
hypermetabolic state, thyrotoxicosis

Question 27

A 26 year-old , 60 kg female has just opened her eyes after a 35 minute procedure. The patient
was initially sedated with midazolam 3.5 mg and fentanyl 100 mcg. The patient was then
administered atropine 0.4 mg, ketamine 30 mg, and propofol 60 mg. A continuous infusion of
propofol was maintained for the duration of the surgery at 6 mg/kg/hr. The total propofol dose
for the bolus and infusion was 375 mg. The patient maintained a patent airway with
spontaneous ventilations during the procedure. The patient’s vital signs during recovery were
BP 110/65 and HR 72 regular. Approximately 5 minutes after the procedure the patient had
what appeared to be a brief self limiting seizure. The patient had another seizure 5 minutes
later. An EEG was normal. Which of the following scenarios is most consistent with this event?
A. Myoclonic activity associated with opioid compounded by hypoxia
B. Emergence reaction associated with ketamine
C. Dysphoric reaction associated with atropine(tertiary amine)
D. Idiopathic reaction associated with propofol; etiology unknown

Answer 27

D. Idiopathic reaction associated with propofol; etiology unknown

COMSSAT: 2009

Rationale:
Most anesthetic medications have both pro- and anticonvulsant neuroexcitatory effects.
For example, propofol has greter anticonvulsant effect on ECT than other anesthetics.
However, propofol has neuroexcitatory effects that range from mild involuntary myoclonic
limb movements to grand mal seizure – like activity. These neuroexcitatory events may
occur with induction, emergence or during recovery from the anesthetic. They may occur
in patients with and without prior history of neurologic disease. EEG’s done on patients
have not been consistent with seizures. This is the most likely differential for the
described scenario.
Myoclonus, sometimes resembling seizures, but without EEG evidence of seizure
activity, has been observed with high dose opioids. In clinical practice, opioid induced
muscle rigidity and myoclonus are most often observed on induction of anesthesia, but
have been observed postoperatively.
Tertiary amines cross the blood brain barrier and can cause central anticholinergic
syndrome. Central manifestations of anticholinergic overdose include disorientation,
agitation, hallucinations, ataxia and seizures. Peripheral manifestations of
anticholinergic overdose include tachycardia, mydriasis, facial flushing, hyperpyrexia,
urinary retention and decreased sweating. Treatment of central anticholinergic
syndrome is with physostigmine.
Reference:
Walder B, Tramer MR, Seeck: Seizure – like phenomenon of propofol: A systematic
review. Neurology 58:1327-1332;2002

Question 28

A 56 year-old male was admitted at after sustaining a fractured mandible. The patient
undergoes general anesthesia for open reduction of a mandible fracture 15 hours later. He has
a history of hypertension, cigarette smoking, daily alcohol consumption, and cocaine use. He
last used cocaine two days ago. While awakening in the recovery room, he becomes
progressively more confused, tremulous, and agitated. The patient does not complain of pain.
Monitoring shows heart rate – 115; BP 180/98; RR – 22; oxygen saturation – 92%; ECG – sinus
tachycardia. Which medication would you administer initially to manage this situation?
A. Morphine sulfate
B. Labetalol (Trandate)
C. Haloperidol (Haldol)
D. Lorazepam (Ativan)

Answer 28

D. Lorazepam (Ativan)

COMSSAT: 2009

Rationale:
After surgery, possible causes of delirium include cerebral hypoperfusion, hypotension,
hypoxia, anemia, hyperthermia, fluid and electrolyte abnormalities, acid-base
disturbances, inadequate analgesia, anticholinergic syndrome, and benzodiazepine,
opioid or alcohol withdrawal. Alcohol withdrawal is certainly likely, especially if this
patient has been npo prior to surgery in addition to having limited alcohol intake because
of his injury.
Alcohol withdrawal presents as combativeness, tremors, disorientation, hallucinations
and convulsions. Onset of alcohol withdrawal is usually 10 – 30 hours after cessation of
alcohol consumption. The syndrome of alcohol withdrawal may occur under anesthesia.
Delirium tremens develops after prolonged abstinence.
If the patient is suspected to have alcohol withdrawal, then a benzodiazepine is most
effective. Lorazepam is probably the most popular choice because it is fast-acting, mildly
sedating, and has no active metabolites. Morphine sulfate would be a good choice if his
agitation was due to poor analgesia; however, he reported minimal pain. Haloperidol is a
butyrophenone with antipsychotic effects that are usually effective for control of
postoperative delirium.
The signs and symptoms of cocaine intoxication include: tachycardia, hypertension
hallucinations, convulsions, cerebrovascular accident, headache, and chest pain.
Treatment of cocaine intoxication includes the use of 􀀀-adrenergic antagonists (e.g.
labetalol or esmolol), nitrates and calcium channel blockers. The half life of cocaine is
approximately ½ to 1 ½ hours. It is unlikely that this patient is manifesting signs of acute
cocaine intoxication. Signs and symptoms of cocaine withdrawal include agitation,
anxiety, myalgias and tremors.
Reference:
Cavaliere F, D’Ambrosio F, Volpe C, Masieri S: Postoperative delirium. Current Drug
Targets 2005, 6, 807-814.
Meagher DJ: Delirium: Optimising management. BMJ 2001, 322, 144-149.
Karre S, Duke J: Alcohol and substance abuse in Anesthesia Secrets ed. Duke J 3rd
edition Elsevier pages 317-322
Keyword: complications of anesthesia, assessment of patient for anesthesia, alcohol
intoxication, hypertension, tachycardia, cocaine intoxication, alcohol withdrawal

Question 29

A healthy 22 year-old female who is 5 foot 2 inches, 170 pounds presents for extraction of 1
tooth. Oxygen at 4 liters/minute is administered via nasal cannula. Five minutes after oxygen
administration is initiated the patient is induced with propofol 140 mgs. The patient becomes
apneic. Pulse oximeter reads 100%. The surgeon proceeds with extracting the tooth and does
not take immediate intervention to provide airway support and positive pressure ventilation.
Which of the following either justifies or counters the surgeon’s actions?
A. Preoxygenation with the 36% oxygen mixture for 5 minutes will maintain the oxygen
saturation at or above 90% for at least 3 minutes in this individual
B. The surgeon should initiate positive pressure ventilation as obese patients desaturate
approximately twice as rapidly as individuals with lean body mass.
C. Preoxygenation with an FiO2 of 0.36 will produce a PAO2 of 160 mm Hg which does not
provide ample reserve for the surgeon to complete a 30 second procedure
D. The administration of propofol will not result in prolonged apnea and continuous
insufflation of oxygen will sustain an oxyhemoglobin saturation > 90%.

Answer 29

B. The surgeon should initiate positive pressure ventilation as obese patients desaturate
approximately twice as rapidly as individuals with lean body mass.

COMSSAT: 2009

Rationale:
Preoxygenation is the process of administering oxygen to a patient prior to inducing
anesthesia. The intent is to replace the volume of nitrogen in the lungs with oxygen
(denitrogenation). PAO2 is calculated using the formula PAO2 = FiO2 (PB-PH2O) –
PaCO2/RQ where PB = 760, and PaCO2/RQ = 40/0.8. Preoxygenation provides a
reservoir of oxygen occupying the functional residual capacity that can diffuse into the
alveolar capillaries and provide oxygen during periods of hypoventilation and apnea.
Preoxygenation with 100% oxygen for 5 minutes can provide up to 10 minutes of oxygen
reserve to a healthy individual during periods of apnea and normal oxygen utilization. In
one study comparing healthy individuals of ideal weight to obese individuals who were
preoxygenated with 100% oxygen, the obese individuals desaturated to an oxygen
saturation < 90% approximately twice as fast as the nonobese individuals (2.7 minutes
compared to 6 minutes). In another study a nonobese patient breathing room air will
desaturate to an oxygen saturation < 90% in about 2 minutes.
Achievement of a general anesthetic depth solely with propofol will be more predictable
in its recovery. However, the apneic patient, especially the obese patient, cannot rely on
recovery from the propofol bolus and resumption of ventilation to maintain oxygenation.
Apneic oxygenation is a technique that is dependent on pharyngeal insufflation of
oxygen. This technique is dependent on more oxygen diffusing out of the alveoli into the
capillaries than carbon dioxide diffusing into from the capillaries into the alveoli. This
decrease in intrathoracic pressure relative to atmospheric pressure facilitates oxygen
delivery. Carbon dioxide is not removed from the alveoli limiting the duration of this
oxygenation technique. Apneic oxygenation is dependent on a patent airway. It is most
likely that a bolus of propofol that produces apnea also compromises airway patency.
Reference:Rosenblatt WH. Airway management. In Clinical Anesthesia ed Barash P, Cullen BF,
Stoelting RK 5th ed. Lippincott, Williams, & Wilkins pages 599 – 600
Baraka AS, Taha SK, Aouad MT, et al: Preoxygenation: Comparison of maximal
breathing and tidal volume breathing techniques. Anesthesiology 91:612;1999
Keyword: airway management, apnea, preoxygenation, apneic oxygenation, obese
patient

Question 30

A 68 year-old male with a history of emphysema is anesthetized for management of a panfacial
fracture. Intraoperative medications administered include sevoflurane, propofol, succinylcholine,
and morphine. The patient is orally intubated with difficulty. Two hours into the surgery the
anesthesiologist comments that the patient has been developing increased airway pressures.
Auscultation of the chest is difficult with distant sounds. Oxygen saturation is 90%. The patient
is also noted to be hypotensive despite fluid replacement for the blood loss. Which of the
following interventions should be considered?
A. Reposition the endotracheal tube
B. Needle decompression of the chest
C. Administer four puffs of albuterol
D. Administer phenylephrine

Answer 30

B. Needle decompression of the chest

COMSSAT: 2009

Rationale:
As a patient with emphysema subjected to positive pressure ventilation, he is at risk of
pulmonary bullae rupture resulting in a tension pneumothorax. A tension pneumonthorax
is suspected when peak airway pressures increase, accompanied by hypotension,
hypoxemia, decreased breath sounds, and decreased tidal volume on the side of the
pneumothorax. Needle decompression in the second intercostal space in the midclavicular
line will relieve the tension aspect of the pneumothorax and can be life saving.
Difficult intubation could also create a false passage and contribute to a pneuomothorax.
If the endotracheal tube had been placed too deep, this may account for decreased
breath sounds and hypoxemia, but hypotension would not be likely. Albuterol would be
helpful if bronchoconstriction was present, but this is a pneumothorax.
Reference:
Morgan GE, Mikhail MS, Murray MJ. Clinical Anesthesiology, 4th edition. Lange Medical
Books, 2006, pg 578.
Stoelting RK, Dierdorf SF. Anesthesia and Co-Existing Disease, 4th edition. Churchill
Livingstone, 2002, pg 179, 186.
Keyword: complications of anesthesia, emphysema, tension pneumothorax, traumatic
intubation

Question 31

What action would you take in regards to the ventilation of an intubated anesthetized patient
who is in bronchospasm?
A. Increase expiratory time by decreasing ventilator rate
B. Decrease inspiratory flow rates to decrease inspiratory time
C. Apply PEEP (positive end expiratory pressure)
D. Increase minute volume

Answer 31

A. Increase expiratory time by decreasing ventilator rate

COMSSAT: 2009

Rationale:
The objective in managing a patient who is having a bronchospastic episode is to
minimize lung hyperinflation. Lung hyperinflation occurs when there is diminished
expiratory flow which results in gas trapping in the alveoli and small airways. Lung
hyperinflation can be prevented by increasing the expiratory to inspiratory ratio.
A slow breathing rate should be used to allow for adequate ventilation and adequate time
for exhalation. This should be coupled with an increase in inspiratory flow rate which will
decrease inspiratory time. PEEP should not be used because it impairs exhalation and
increases the likelihood of distal air trapping. A decrease in minute ventilation (tidal
volumes less than 10 mg/kg) will allow controlled hypoventilation and should be used
also to allow for adequate ventilation and exhalation.
Reference:
Morgan GE, Mikhail MS, Murray MJ. Clinical Anesthesiology, 4th edition. Lange Medical
Books, 2006, pg 576.
Stoelting RK, Dierdorf SF. Anesthesia and Co-Existing Disease, 4th edition. Churchill
Livingstone, 2002, pg 203
Packer M. reactive airway disease. In Anesthesia Secrets. Ed Duke J 3rd edition,
Mosby/Elsevier pg 261
Keyword: airway management, complications of anesthesia, mechanical ventilation,
bronchospasm