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102 PART II ANESTHESIA
Oxyhemoglobin Dissociation Curve
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Saturation
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100%
90%
75%
50%
27 40 60
PaO
2
Figure 8-3. The oxyhemoglobin dissociation curve describes the nonlinear relationship between PaO2 and percentage
saturation of hemoglobin with oxygen (SaO2). In the steep part of the curve (50% region), small changes in PaO2 result
in large changes in SaO2. The converse is true when PaO2 rises above 60 mm Hg. Three regions of the curve have been
marked. (From Edwards RK: Pulse oximetry. In Duke J, editor: Anesthesia secrets, ed 3, Philadelphia, 2006, Mosby.)
36. How long does it take before changes in oxygen saturation are reflected in pulse
oximeter readings?
Approximately 20 seconds. It takes time for O2 delivered to the lung to influence oxygenation at the
fingertip. Pulse oximeter signals are also averaged over different periods. This is mainly to reduce
spurious pulse oximeter readings, such as those caused by patient movement. The trade-off is that
true reductions in pulse oximeter readings are delayed (a patient desaturating faster than the pulse
oximeter indicates). Similarly, once adequate delivery of oxygen is restored, there will be a delay in
recovery of the pulse oximeter readings. The period of signal averaging can often be changed in
commonly used pulse oximeters.
BiBliography
Adamson DT: Oxygenation and ventilation. In Duke J, editor: Anesthesia secrets, ed 2, Philadelphia, 2000, Hanley & Belfus.
Becker D, Rosenberg M: Nitrous oxide and the inhalation anesthetics, Anesth Prog 55(4):124–131, 2008.
Browne MD: Volatile anesthetics. In Duke J, editor: Anesthesia secrets, ed 3, Philadelphia, 2006, Mosby.
Cahalan MK, Lurz FW, Eger 2nd EI, et al.: Narcotics decrease heart rate during inhalation anesthesia, Anesth Analg
66:166–170, 1987.
Christensen LQ, Bonde J, Kampmann JP: Drug interactions with inhalational anaesthetics, Acta Anesthesiol Scand
37:231–244, 1993.
Clark MS, Brunick AL: Handbook of nitrous oxide and oxygen sedation, ed 2, St Louis, 2003, Mosby.
Duke J: Airway management. In Duke J, editor: Anesthesia secrets, ed 3, Philadelphia, 2006, Mosby.
Eger 2nd EI, Saidman LJ: Hazards of nitrous oxide anesthesia in bowel obstruction and pneumothorax, Anesthesiol
26:61–66, 1965.
Gomez R, Guatimosim C: Mechanism of action of volatile anesthetics: involvement of intracellular calcium signaling, Curr
Drug Targets CNS Neurol Disord 2:123–129, April 2003.
Foltz B, Benumof J: Mechanisms of hypoxia and hypercarbia in the perioperative period, Crit Care Clin 3:269–286, 1987.
Haenel JB, Johnson JL: Oxygen monitoring and assessment. In Duke J, editor: Anesthesia secrets, ed 2, Philadelphia,
2000, Hanley & Belfus.
Hayashi Y, Kamibayashi T, Sumikawa K, et al.: Adrenoreceptor mechanism involved in thiopental-epinephrine-induced
arrhythmias in dogs, Am J Physiol 265:H1380–H1385, 1993.
Johnston RR, Eger 2nd EI, Wilson C: A comparative interaction of epinephrine with enflurane, isoflurane, and halothane in
man, Anesth Analg 55:709–712, 1976.
Kamibayashi T, Hayashi Y, Takada K, et al.: Adrenoreceptor mechanism involved in thiopental-induced potentiation of
halothane-epinephrine arrhythmias in dogs, Res Comm Mol Pathol Pharmacol 93:225–234, 1996.
CHAPTER 8 INHALATION ANESTHESIA AND NEUROMUSCULAR BLOCKING AGENTS 103
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Katz RL, Matteo RS, Papper EM: The injection of epinephrine during general anesthesia with halogenated hydrocarbons and
cyclopropane in man. 2. Halothane, Anesthesiol 23:597–600, 1962.
Leichliter C: Awareness during anesthesia. In Duke J, editor: Anesthesia secrets, ed 3, Philadelphia, 2006, Mosby.
Malamed SF: Sedation: a guide to patient management, ed 4, St Louis, 2003, Mosby.
Miller HJ: Chronic obstructive pulmonary disease. In Duke J, editor: Anesthesia secrets, ed 3, Philadelphia, 2006, Mosby.
Rosen MA: Management of anesthesia for the pregnant surgical patient, Anesthesiol 91:1159–1163, 1999.
Stoelting RK, Miller RD: Effects of inhaled anesthetics on ventilation and circulation. In Stoelting RK, Miller RD, editors:
Basics of anesthesia, ed 3, New York, 1994, Churchill Livingstone.
Warnecke DE: Neuromuscular blocking agents. In Duke J, editor: Anesthesia secrets, ed 2, Philadelphia, 2000, Hanley &
Belfus.
Wenker O: Review of currently used inhalation anesthetics: part I, Internet J Anesthesiol 3(2), 1998.
ANESTHESIA FOR
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DIFFICULT PATIENTS
CHAPTER 9
Stuart Lieblich
1. What important physiological changes occur during pregnancy?
• Cardiovascular: An increase in cardiac output of up to +40% is seen by the second trimester.
This is a result of both an increase in heart rate and stroke volume. Blood pressure is normally
decreased due to effects of progesterone on peripheral vascular resistance. During the third
trimester, the uterus can cause compression of both the vena cava and the abdominal aorta,
resulting in postural decrease in venous return and a drop in cardiac output and blood pressure.
Patients during their third trimester should be positioned on the left side with the right hip elevated
with the use of a pillow.
• Pulmonary: There is a decrease in functional residual capacity due to decrease in both expiratory
reserve volume and residual volume that results in lowering of oxygen reserve. Resting minute
ventilation and tidal volume increase by 40% to 50%, which results in hyperventilation and lower
mean arterial CO2 levels.
• Hematological: Hematocrit and hemoglobin levels decrease during pregnancy. By the third trimes-
ter, the hematocrit averages 31% to 33% and hemoglobin 11 g/dl. Several coagulation factors such
as factors VII, VIII, X, and fibrinogen increase during pregnancy. In addition the fibrinolytic activity is
decreased, causing an overall hypercoagulable state during pregnancy.
• GI: There is a decrease in GI motility and delayed gastric emptying as well as compromised gastro-
esophageal sphincter. These changes predispose pregnant patients to reflux and increased risk of
aspiration during deep sedation and general anesthesia.
• Renal: There is an increase in renal blood flow and glomerular filtration rate resulting in faster
clearance of drugs that are cleared by kidneys.
2. When is the fetus most sensitive to teratogenic influences of anesthetic drugs?
Teratogens have either a lethal effect or no effect on the embryo in the first two weeks of intrauterine
life. Organogenesis takes place between the third and eighth week; drug exposure during this period
can produce major developmental abnormalities. After completion of organogenesis teratogen exposure results in only minor morphological abnormalities but can also produce significant physiological
abnormalities and growth retardation.
3. What are the categories in evaluating the severity of obesity?
Body mass index (BMI) has been used to categorize severity of obesity. BMI greater than 25 kg/m2 is
considered overweight, 30 to 39 kg/m2 is considered obese, and anyone with BMI greater than
40 kg/m2 is considered morbidly obese.
4. What is Pickwickian syndrome?
Pickwickian syndrome is also known as obesity hypoventilation syndrome. It is a condition in which
obese patients fail to breathe rapidly enough or deeply enough, resulting in low blood oxygen levels
and high blood carbon dioxide levels.
5. What are the pharmacokinetic differences in the obese population compared to
that in healthy adults?
Obese patients will have reduced total body water volume, increased body fat, and increased renal
clearance because of increased GFR. A hypophilic drug has an increased volume of distribution, which
translates into longer time for drug elimination.
6. What factors make office-based anesthesia more difficult for patients with
Obstructive Sleep Apnea (OSA)?
OSA patients are very sensitive to central nervous system (CNS) depressant drugs, especially
opioids that are routinely used in office-based anesthesia. Peripherally, CNS depressant drugs can
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alter normal phasic negative pressure reflex, which is important in protecting the upper airway
from collapse during inspiration. Centrally, opioids act on the medulla respiratory center to blunt the
response to a hypercapnia challenge. Several studies have also shown that moderate-severe OSA
results in both difficult mask ventilation and difficult tracheal intubation. In addition, OSA is associated with several metabolic and cardiovascular comorbidities such as HTN, MI, strokes, insulin
resistance, and GERD.
For the reasons outlined above, OSA patients are at increased risk of developing respiratory
events, which emphasizes the importance of screening all patients for OSA and identifying suitable
candidates for office-based anesthesia.
7. What screening tool can you use to detect patients with high risk of OSA?
The STOP-BANG questionnaire should be used to screen for patients that are considered to be at risk
for OSA before anesthesia. This includes all middle-aged obese men and postmenopausal women. The
total score received on the questionnaire is related directly to the severity of OSA. A score of 4 or more
answered “yes” questions indicates a high risk for OSA. A score of 5 to 8 is predictive of moderatesevere OSA. A score of 3 or less predicts a low risk for OSA.
S = Snoring
T = Tiredness
O = Observed apnea
P = Pressure (HTN)
B = BMI >35 kg/m
A = Age >50 years
N = Neck circumference >40 cm
G = Male gender
8. What physical findings are consistent with obstructive sleep apnea?
1. BMI greater than 35 (95th percentile for age and gender)
2. Neck circumference greater than 17 inches (men) or 16 inches (women)
3. Craniofacial abnormalities affecting airway
4. Anatomic nasal obstruction
5. Tonsils nearly touching or touching in the midline
9. What general considerations should be taken into account in sedating patients
with obstructive sleep apnea?
For most dentoalveolar surgeries, local anesthesia, with or without minimal sedation, should be
considered. If minimal sedation is used, ventilation should be continuously monitored by capnography
due to increased risk of undetected airway obstruction in these patients. Patients should be placed in
a sitting position and an independent head holder should maintain neck extension. Reversal agents
should be immediately available to rescue from deeper levels of anesthesia. A nasopharyngeal airway
can be helpful in maintaining a patient’s SpO2 above 90%. Lastly, one should strongly consider
general anesthesia with a secure airway in an operating room over office-based anesthesia without a
secure airway for patients with moderate-severe OSA.
10. What general consideration should be taken into account in postoperative management of patients with obstructive sleep apnea?
The supine position should be avoided and patients should sleep upright while taking opioids. Nono-
pioid medications such as NSAIDs should be considered for pain management. Nasal CPAP should be
used strictly, especially while taking opioids. Patients should be kept in close contact during the first
postoperative week to monitor pain levels and opioid use.
11. List some of the important anatomical abnormalities seen in Trisomy 21 syndrome
patients. What anesthetic consideration should be taken into account in managing these patients?
Some of the concerning abnormalities seen in Down syndrome patients include a short neck, irregular
dentition, mental retardation, hypotonia, and a large tongue. Additionally, congenital heart disease
(particularly ventricular septal defect) is seen in 40% of these patients. Due to the mentioned anatomical differences, these patients often have difficult airways. Neck flexion during laryngoscopy and
intubation may result in atlantooccipital dislocation due to congenital laxity of these ligaments. Special
consideration must be taken to avoid air bubbles in the intravenous line because of possible right-toleft shunts (paradoxical air embolus).
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12. What is cerebral palsy?
Cerebral palsy (CP) is a nonprogressive motor and posture disorder of cerebral or cerebellar origin.
The primary impairment involves significant deficits in motor planning and control (patient can be
spastic, dyskinetic, or ataxic). Although the disorder is nonprogressive, clinical manifestations often
change over time as the functional expression of the underlying brain is modified by normal brain
development and maturation.
13. What are the anesthetic concerns for cerebral palsy patients?
Muscle spasticity and limb contractures can make airway management, intravenous access, and
surgical positioning difficult. Medical findings, such as seizure disorder, GI reflux, scoliosis, and multiple
history of pulmonary infections are commonly found in this population. CP patients may also have
impaired pharyngeal function, which leads to pooling of oral secretions and increasing risk of aspiration.
If muscle relaxant is needed, a nondepolarizing skeletal muscle relaxant is preferred to prevent hyperkalemic episodes; however, a higher dose of depolarizing agent may be needed due to drug resistance.
14. What are the special considerations in the perioperative assessment of alcoholabusing patients?
Chronic alcohol-abusing patients can have multiorgan diseases. Alcohol-induced cardiac disease
should be evaluated with preoperative 12-lead ECG. These patients are also less sensitive to endogenous or parenteral catecholamine. Electrolyte imbalance (hypokalemia), hypoglycemia, anemia, and
coagulopathy should also be evaluated. Hypervolemia is also a major concern for a long operating
procedure, but less so in the outpatient setting.
15. What is the mechanism of action for marijuana and its physiological effects?
The active substances in marijuana are tetrahydrocannabinol and cannabinoids, which stimulate canna-
binoid receptors to produce euphoric, analgesic, anxiolytic, and sedative effects. Low-dose marijuana can
stimulate the sympathetic nervous system, which leads to hypertension and tachycardia. High-dose marijuana inhibits the sympathetic system, which results in bradycardia and hypotension. Marijuana smokers
also have similar pulmonary effects to tobacco users (airway irritation and increased CO-Hb level).
16. What are the withdrawal signs and symptoms of chronic opioid users?
Agitation, hypotension, tachycardia, lacrimation, and diarrhea are the typical withdrawal signs and symp-
toms found in chronic opioid users. Naloxone and mixed agonist-antagonist agents (buprenorphine) are
relatively contraindicated in this patient population as they can precipitate withdrawal symptoms.
17. What is the management strategy of the chronic opioid user, who is currently
on mixed agonist-antagonist agents (buprenorphine), when required to undergo
surgery?
Buprenorphine is a mixed agonist-antagonist opioid receptor modulator that is used to treat opioid addic-
tion in high dosage. A patient who is on this medication and undergoes major surgery should discontinue
the medication one to three days preoperatively to prevent its antagonist effect against postoperative opioid
medication. Low-dose opioid may be needed to prevent withdrawal symptoms during this time. Postoperatively, buprenorphine can be resumed once acute pain is no longer an issue. For a minor procedure,
patients should continue buprenorphine until the morning of surgery to prevent withdrawal symptoms.
18. What are the anatomical differences between a pediatric and adult airway?
A pediatric patient has a larger tongue size, floppier omega-shaped epiglottis, and funnel-shaped larynx.
The narrowest point of the airway is lower in the subglottic region. Patients in this group also have
decreased compliance in the upper airway, which makes them more prone to collapse. They also have
decreased total lung capacity and faster respiratory and metabolic rates.
19. How is an endotracheal tube (ET) of appropriate size chosen?
Age/4 + 4 = mm of diameter for ET tube. Patient variation does exist; a half size above and a half size
below the estimated size should be available. The leak around the tube should be <30 cc, H2O, and
the ET should be placed to a depth of approximately three times its internal diameter.
20. What is the appropriate size laryngeal mask airway for pediatric patient?
The laryngeal mask airway should be based on the patient’s age and weight (Table 9-1).
21. What is malignant hyperthermia (MH)?
A hypermetabolic state involving skeletal muscle that is precipitated by certain anesthetic agents in
genetically susceptible individuals.
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Table 9-1. Laryngeal Mask Airways for Children
SIZE OF CHILD LARYNGEAL MASK SIZE
Neonates up to 5 kg 1
Infants 5-10 kg 1.5
Children 10-20 kg 2
Children 20-30 kg 2.5
Children/small adults >30 kg 3
Children/adults >70 kg 4
Children/adults >80 kg 5
22. Which patients are at risk of developing MH?
Patients at risk of developing MH include those with:
• A diagnosis of MH (see question 6)
• A first-degree relative with a diagnosis of MH
• An elevated resting creatine kinase (CK) and family with suspected MH tendency
• Central core disease
• Musculoskeletal disease associated with MH (see question 23)
23. With which muscle diseases has MH been associated?
• Dystrophinopathy
• Myotonia
• Phosphorylase deficiency
• King-Denborough and Barnes myopathies
• Minicore disease
24. How are susceptible patients diagnosed?
The diagnosis of MH in susceptible patients is made by the muscle contracture test. Muscle fibers from
MH-positive patients produce an exaggerated response to electrical stimulation when exposed to halothane and caffeine. When a muscle contracture test is not possible, muscle biopsy may be performed.
Characteristic findings on muscle biopsy include variable muscle fiber size, increased number of
internalized nuclei, and the presence of “moth-eaten” fibers. These findings are nonspecific and cannot
be used alone to establish diagnosis. Patients with MH also may have elevated baseline CK levels.
25. Which anesthetic drugs are known to trigger MH?
Inhalation anesthetics:
• Halothane
• Desflurane
• Enflurane
• Sevoflurane
• Isoflurane
Depolarizing neuromuscular blockade agents:
• Succinylcholine
• Decamethonium
• Suxamethonium
26. What are the three early presenting signs and symptoms of MH during an anesthetic procedure?
1. Early masseter contracture following administration of succinylcholine
2. An unexplained rise in end-tidal CO2 following induction of anesthesia
3. An unexplained tachycardia following induction of anesthesia
27. What is the initial management of an acute attack of MH in the adult patient?
1. Discontinue the anesthetic agent.
2. Hyperventilate with 100% oxygen.
3. Administer dantrolene sodium intravenously until heart rate and end-tidal CO2 decrease.
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4. Begin infusion of iced intravenous (IV) fluids (avoid lactated Ringer’s).
5. Cool patient with iced saline lavage of stomach, bladder, and rectum; cooling blankets; and ice
packs.
6. Draw blood for serum electrolytes, arterial blood gases, prothrombin time (PT), partial thrombo-
plastin time (PTT), and myoglobin studies.
7. Monitor vital signs, electrocardiogram (ECG), end-tidal CO2, blood gases, temperature, and urine
output.
8. Treat metabolic acidosis with sodium bicarbonate.
9. Treat arrhythmias with antiarrhythmic drugs (avoid calcium channel blockers).
10. Treat hyperkalemia with glucose and insulin.
11. Maintain urinary output of greater than 2 mL/kg/hr with hydration and diuretics (furosemide or
mannitol).
28. What is dantrolene sodium, and how does it work?
Dantrolene sodium is a hydantoin-derivative muscle relaxant that exerts its muscle relaxant effect by
interfering with excitation-contraction coupling in the muscle fiber. Dantrolene sodium is used in the
treatment of MH because it blocks calcium release from the sarcoplasmic reticulum calcium channels.
29. What is the recommended dose of dantrolene sodium for treatment of MH?
• 2 to 3 mg/kg IV every 5 minutes up to a total dose of 10 mg/kg.
• 1 mg/kg IV every 6 hours for 24 to 48 hours in recovery.
• Then oral dantrolene for an additional 24 hours.
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PerioPerative Care
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FLUID AND ELECTROLYTES
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Alia Koch
1. What is the distribution of water in the human body?
Total body water (TWB) in men is 60% of body weight and in women comprises 50% of body weight.
The water is then split between intracellular fluid (ICF) and extracellular fluid (ECF). ICF is two-thirds
of TWB, and ECF is one-third of TBW. The ECF is then further divided with one-third resting in the
intravascular space and two-thirds in the interstitial fluid.
2. What is the TBW, ECF volume (ECFV), and blood volume in a 70-kg man?
TBW: 6 × 70 = 42 L
ECFV: 42 L × 1/3 = 14 L
Intravascular fluid (blood volume): 14 L × 1/3 = 4.66 L
3. What are the major extracellular and intracellular cations?
The major extracellular cation is sodium, and it is responsible for most of the osmotic force that
maintains the size of the ECFV. The concentration is usually kept within a narrow range (135 to
145 mEq/L). Potassium is the major intracellular cation. The intracellular concentration is about
130 to 140 mEq/L, and the extracellular concentration is 3.5 to 5.0 mEq/L. A stable plasma
concentration is essential for normal cellular function, cardiac rhythm, and proper neuromuscular
transmission.
4. How is TBW maintained?
Total body water is maintained through numerous systemic systems including the hypothalamic
center, antidiuretic hormone (ADH), and the renin-angiotensin-aldosterone system. The hypothalamic thirst center is stimulated when the plasma becomes hypertonic. The hypothalamus secretes
vasopressin (ADH), stimulating more water reabsorption. ADH is also secreted in the renin system.
Low perfusion of the kidney stimulates renin secretion, which stimulates production of angiotensin 1.
Angiotensin 1 is converted to angiotensin 2 in the lungs. Angiotensin 2 stimulates ADH release from
the pituitary, leading to an increase in sodium and water reabsorption.
5. What is the water exchange process in a normal person?
An average adult takes in approximately 2.5 L of water in one day, with approximately 1.5 L from
drinking. The remaining 1 L is extracted from food. Water is excreted through the kidneys (500 to
1500 cc/day), stool (250 cc/day), and insensible losses (600 cc/day).
6. What is normal urine output in an adult patient?
One cc/kg/hr is considered normal urine output. However, the patient’s systemic issues may play a
role in volume status and may affect urine output. For example, patients with sepsis will have higher
insensible losses; patients with liver failure will have more third spacing of fluid.
7. How is maintenance fluid calculated?
The 4/2/1 rule is used with 4 cc/kg for the first 10 kg, 2 cc/kg for the next 10 kg, and 1 cc/kg for every
kg over 20 kg. As mentioned before, the patient’s total health needs to be considered and additional
fluid is necessary in those patients with fevers, sepsis, or burns. Decreased fluid infusion should be
considered in those patients with edematous states, hypothyroidism, and renal failure.
8. What is body osmolality?
Osmolality is the ratio of solutes to water in body compartments. The main solutes include sodium,
glucose, and urea.
Calculated osmolality = 2[Na+] + [glucose]/18 + [BUN]/2.8
When the measured osmolality is greater than the calculated osmolality, an osmolar gap is calculated.
When the gap is greater than 10, extra solutes such as ethylene glycol, methanol, and ethanol may be
found.
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