1. Describe the autonomic nervous system.
The autonomic nervous system (ANS) is a network of nerves and ganglia that controls involuntary
physiologic actions and maintains internal homeostasis and stress responses. The ANS
innervates structures within the cardiovascular, pulmonary, endocrine, exocrine, gastrointestinal,
genitourinary, and central nervous systems (CNS) and influences metabolism and thermal
regulation. The ANS is divided into two parts: the sympathetic (SNS) and parasympathetic (PNS)
nervous system. When stimulated, the effects of the SNS are widespread across the body. In
contrast, PNS stimulation tends to produce localized, discrete effects. The SNS and PNS generally
have opposing effects on end-organs, with either the SNS or the PNS exhibiting a dominant
tone at rest and without exogenous stimulating events (Table 1-1). In general the function of the
PNS is homeostatic, whereas stimulation of the SNS prepares the organism for some stressful
event (this is often called the fight-or-flight response).
KEY POINTS: AUTONOMIC NERVOUS SYSTEM
1. Patients should take b-blockers on the day of surgery and continue them perioperatively.
Because the receptors are up-regulated, withdrawal may precipitate hypertension,
tachycardia, and myocardial ischemia.
2. Clonidine should also be continued perioperatively because of concerns for rebound
hypertension.
3. Indirect-acting sympthomimetics (e.g., ephedrine) depend on norepinephrine release to be
effective. Norepinephrine-depleted states will not respond to ephedrine administration.
4. Under most circumstances peri-induction hypotension responds best to intravenous fluid
administration and the use of direct-acting sympathomimetics such as phenylephrine.
5. Orthostatic hypotension is common after surgery and may be caused by the use of any or all
anesthetic agents and lying supine for extended periods. It is necessary to be cognizant of this
potential problem when elevating a patient’s head after surgery or even when moving the patient
fromthe operating roomtable to a chair (e.g., procedures requiring only sedation and monitoring).
2. Review the anatomy of the sympathetic nervous system.
Preganglionic sympathetic neurons originate from the intermediolateral columns of the
thoracolumbar spinal cord. These myelinated fibers exit via the ventral root of the spinal nerve
and synapse with postganglionic fibers in paravertebral sympathetic ganglia, unpaired
prevertebral ganglia, or a terminal ganglion. Preganglionic neurons may ascend or descend the
sympathetic chain before synapsing. Preganglionic neurons stimulate nicotinic cholinergic
postganglionic neurons by releasing acetylcholine. Postganglionic adrenergic neurons synapse
at targeted end-organs and release norepinephrine (Figure 1-1).
3. Elaborate on the location and names of the sympathetic ganglia. Practically
speaking, what is the importance of knowing the name and location of these
ganglia?
Easily identifiable paravertebral ganglia are found in the cervical region (including the stellate
ganglion) and along thoracic, lumbar, and pelvic sympathetic trunks. Prevertebral ganglia
are named in relation to major branches of the aorta and include the celiac, superior and inferior
mesenteric, and renal ganglia. Terminal ganglia are located close to the organs that they serve. The
practical significance of knowing the location of some of these ganglia is that local anesthetics can
be injected in the region of these structures to ameliorate sympathetically mediated pain.
4. Describe the postganglionic adrenergic receptors of the sympathetic nervous
system and the effects of stimulating these receptors.
There are a1, a2, b1, and b2 adrenergic receptors. The A1, A2, and B2 receptors are
postsynaptic and are stimulated by the neurotransmitter norepinephrine. The A2 receptors are
presynaptic, and stimulation inhibits release of norepinephrine, reducing overall the autonomic
response. Molecular pharmacologists have further subdivided these receptors, but this is
beyond the scope of this discussion. Dopamine stimulates postganglionic dopaminergic
receptors, classified as DA1 and DA2. The response to receptor activation in different sites is
described in Table 1-2.
5. Review the anatomy and function of the parasympathetic nervous system.
Preganglionic parasympathetic neurons originate from cranial nerves III, VII, IX, and X and
sacral segments 2-4. Preganglionic parasympathetic neurons synapse with postganglionic
neurons close to the targeted end-organ, creating a more discrete physiologic effect. Both
preganglionic and postganglionic parasympathetic neurons release acetylcholine; these
cholinergic receptors are subclassified as either nicotinic or muscarinic. The response to
cholinergic stimulation is summarized in Table 1-3.
6. What are catecholamines? Which catecholamines occur naturally? Which are
synthetic?
Catecholamines are hydroxy-substituted phenylethylamines and stimulate adrenergic nerve
endings. Norepinephrine, epinephrine, and dopamine are naturally occurring catecholamines,
whereas dobutamine and isoproterenol are synthetic catecholamines.
7. Review the synthesis of dopamine, norepinephrine, and epinephrine.
The amino acid tyrosine is actively transported into the adrenergic presynaptic nerve terminal
cytoplasm, where it is converted to dopamine by two enzymatic reactions: hydroxylation of
tyrosine by tyrosine hydroxylase to dopamine and decarboxylation of dopamine by aromatic
8. How is norepinephrine metabolized?
Norepinephrine is removed from the synaptic junction by reuptake into the presynaptic nerve
terminal and metabolic breakdown. Reuptake is the most important mechanism and allows reuse
of the neurotransmitter. The enzyme monoamine oxidase (MAO) metabolizes norepinephrine
within the neuronal cytoplasm; both MAO and catecholamine O–methyltransferase (COMT)
metabolize the neurotransmitter at extraneuronal sites. The important metabolites are
3-methoxy-4-hydroxymandelic acid, metanephrine, and normetanephrine.
9. Describe the synthesis and degradation of acetylcholine.
The cholinergic neurotransmitter acetylcholine (ACh) is synthesized within presynaptic neuronal
mitochondria by esterification of acetyl coenzyme A and choline by the enzyme choline
acetyltransferase; it is stored in synaptic vesicles until release. After release, ACh is principally
metabolized by acetylcholinesterase, a membrane-bound enzyme located in the synaptic
junction. Acetylcholinesterase is also located in other nonneuronal tissues such as erythrocytes.
10. What are sympathomimetics?
Sympathomimetics are synthetic drugs with vasopressor and chronotropic effects similar to
those of catecholamines. They are commonly used in the operating room to reverse the
circulatory depressant effects of anesthetic agents by increasing blood pressure and heart rate;
they also temporize the effects of hypovolemia while fluids are administered. They are effective
during both general and regional anesthesia.
11. Review the sympathomimetics commonly used in the perioperative
environment.
Direct-acting sympathomimetics are agonists at the targeted receptor, whereas indirect-acting
sympathomimetics stimulate release of norepinephrine. Sympathomimetics may be mixed in
their actions, having both direct and indirect effects. Practically speaking, phenylephrine (direct
acting) and ephedrine (mostly indirect acting) are the sympathomimetics commonly used
perioperatively. Also, epinephrine, dopamine, and norepinephrine may be used perioperatively
and most often by infusion since their effects on blood pressure, heart rate, and myocardial
oxygen consumption can be profound. Dopamine is discussed in Chapter 15.
12. Discuss the effects of phenylephrine and review common doses of this
medication.
Phenylephrine stimulates primarily A1 receptors, resulting in increased systemic vascular
resistance and blood pressure. Larger doses stimulate A2 receptors. Reflex bradycardia may
be a response to increasing systemic vascular resistance. Usual intravenous doses of
phenylephrine range between 50 and 200 mcg. Phenylephrine may also be administered by
infusion at 10 to 20 mcg/min.
13. Discuss the effects of ephedrine and review common doses of this medication.
Give some examples of medications that contraindicate the use of ephedrine
and why.
Ephedrine produces norepinephrine release, stimulating mostly A1 and B1 receptors; the effects
resemble those of epinephrine although they are less intense. Increases in systolic blood
pressure, diastolic blood pressure, heart rate, and cardiac output are noted. Usual intravenous
doses of ephedrine are between 5 and 25 mg. Repeated doses demonstrate diminishing
response known as tachyphylaxis, possibly because of exhaustion of norepinephrine supplies or
receptor blockade. Similarly, an inadequate response to ephedrine may be the result of already
depleted norepinephrine stores. Ephedrine should not be used when the patient is taking drugs
that prevent reuptake of norepinephrine because of the risk of severe hypertension. Examples
include tricyclic antidepressants, monoamine oxidase inhibitors, and acute cocaine intoxication.
Chronic cocaine users may be catecholamine depleted and may not respond to ephedrine.
14. What are the indications for using b-adrenergic antagonists?
b-Adrenergic antagonists, commonly called b-blockers, are antagonists at b1- and
b2- receptors. b-blockers are mainstays in antihypertensive, antianginal, and antiarrhythmic
therapy. Perioperative b-blockade is essential in patients with coronary artery disease,
and atenolol has been shown to reduce death after myocardial infarction.
15. Review the mechanism of action for b1-antagonists and side effects.
b1-Blockade produces negative inotropic and chronotropic effects, decreasing cardiac
output and myocardial oxygen requirements. b1-Blockers also inhibit renin secretion and
lipolysis. Since volatile anesthetics also depress contractility, intraoperative hypotension is a risk.
b-Blockers can produce atrioventricular block. Abrupt withdrawal of these medications is not
recommended because of up-regulation of the receptors; myocardial ischemia and hypertension
may occur. b-Blockade decreases the signs of hypoglycemia; thus it must be used with caution
in insulin-dependent patients with diabetes. b-Blockers may be cardioselective, with relatively
selective B1 antagonist properties, or noncardioselective. Some b-Blockers have membranestabilizing
(antiarrhythmic effects); some have sympathomimetic effects and are the drugs of
choice in patients with left ventricular failure or bradycardia. b-Blockers interfere with the
transmembrane movement of potassium; thus potassium should be infused with caution.
Because of their benefits in ischemic heart disease and the risk of rebound, b-blockers should be
taken on the day of surgery.
16. Review the effects of b2-antagonism.
b2-Blockade produces bronchoconstriction and peripheral vasoconstriction and inhibits insulin
release and glycogenolysis. Selective b1-blockers should be used in patients with chronic
or reactive airway disease and peripheral vascular disease because of respective concerns for
bronchial or vascular constriction.
14 CHAPTER 1 AUTONOMIC NERVOUS SYSTEM
17. How might complications of b-blockade be treated intraoperatively?
Bradycardia and heart block may respond to atropine; refractory cases may require the
b2-agonism of dobutamine or isoproterenol. Interestingly, calcium chloride may also be
effective, although the mechanism is not understood. In all cases expect to use larger than
normal doses.
18. Describe the pharmacology of a-adrenergic antagonists.
a1-Blockade results in vasodilation; therefore a-blockers are used in the treatment of
hypertension. However, nonselective a-blockers may be associated with reflex tachycardia.
Thus, selective a1-blockers are primarily used as antihypertensives. Prazosin is the
prototypical selective a1-blocker, whereas phentolamine and phenoxybenzamine are examples
of nonselective a-blockers. Interestingly, labetalol, a nonselective b-blocker, also has selective
a1-blocking properties and is a potent antihypertensive.
19. Review a2-agonists and their role in anesthesia.
When stimulated, a2-receptors within the CNS decrease sympathetic output.
Subsequently, cardiac output, systemic vascular resistance, and blood pressure decrease.
Clonidine is an a2-agonist used in the management of hypertension. It also has significant
sedative qualities. It decreases the anesthetic requirements of inhaled and intravenous
anesthetics. It has also been used intrathecally in the hopes of decreasing postprocedural pain,
but unacceptable hypotension is common after intrathecal administration, limiting its usefulness.
Clonidine should be continued perioperatively because of concerns for rebound hypertension.
20. Discuss muscarinic antagonists and their properties.
Muscarinic antagonists, also known as anticholinergics, block muscarinic cholinergic
receptors, producing mydriasis and bronchodilation, increasing heart rate, and inhibiting
secretions. Centrally acting muscarinic antagonists (all nonionized, tertiary amines with the ability
to cross the blood-brain barrier) may produce delirium. Commonly used muscarinic antagonists
include atropine, scopolamine, glycopyrrolate, and ipratropium bromide. Administering
muscarinic antagonists is a must when the effect of muscle relaxants is antagonized by
acetylcholinesterase inhibitors, lest profound bradycardia, heart block, and asystole ensue.
Glycopyrrolate is a quaternary ammonium compound, cannot cross the blood-brain barrier, and
therefore lacks CNS activity. When inhaled, ipratropium bromide produces bronchodilation.
21. What is the significance of autonomic dysfunction? How might you tell if a
patient has autonomic dysfunction?
Patients with autonomic dysfunction tend to have severe hypotension intraoperatively.
Evaluation of changes in orthostatic blood pressure and heart rate is a quick and effective way
of assessing autonomic dysfunction. If the autonomic nervous system is intact, an increase in
heart rate of 15 beats/min and an increase of 10 mm Hg in diastolic blood pressure are
expected when changing position from supine to sitting. Autonomic dysfunction is suggested
whenever there is a loss of heart rate variability, whatever the circumstances. Autonomic
dysfunction includes vasomotor, bladder, bowel, and sexual dysfunction. Other signs include
blurred vision, reduced or excessive sweating, dry or excessively moist eyes and mouth, cold
or discolored extremities, incontinence or incomplete voiding, diarrhea or constipation, and
impotence. Although there are many causes, it should be noted that people with diabetes and
chronic alcoholics are patient groups well known to demonstrate autonomic dysfunction.
22. What is a pheochromocytoma, and what are its associated symptoms? How is
pheochromocytoma diagnosed?
Pheochromocytoma is a catecholamine-secreting tumor of chromaffin tissue, producing
either norepinephrine or epinephrine. Most are intra-adrenal, but some are extra-adrenal (within the
bladder wall is common), and about 10%are malignant. Signs and symptomsinclude paroxysms of
CHAPTER 1 AUTONOMIC NERVOUS SYSTEM 15
hypertension, syncope, headache, palpitations, flushing, and sweating. Pheochromocytoma is
confirmed by detecting elevated levels of plasma and urinary catecholamines and their metabolites,
including vanillylmandelic acid, normetanephrine, and metanephrine.
23. Review the preanesthetic and intraoperative management of
pheochromocytoma patients.
These patients are markedly volume depleted and at risk for severe hypertensive crises. It is
absolutely essential that before surgery, a-blockade and rehydration should first be instituted.
The a1-antagonist phenoxybenzamine is commonly administered orally. b-Blockers are
often administered once a-blockade is achieved and should never be given first because
unopposed a1-vasoconstriction results in severe, refractory hypertension. Labetalol may be the
b-blocker of choice since it also has a-blocking properties.
Intraoperatively intra-arterial monitoring is required since fluctuations in blood pressure
may be extreme. Manipulation of the tumor may result in hypertension. Intraoperative
hypertension is managed by infusing the a-blocker phentolamine or vasodilator nitroprusside.
Once the tumor is removed, hypotension is a risk, and fluid administration and administration
of the a-agonist phenylephrine may be necessary. Central venous pressure monitoring will
assist with volume management.
The autonomic nervous system (ANS) is a network of nerves and ganglia that controls involuntary
physiologic actions and maintains internal homeostasis and stress responses. The ANS
innervates structures within the cardiovascular, pulmonary, endocrine, exocrine, gastrointestinal,
genitourinary, and central nervous systems (CNS) and influences metabolism and thermal
regulation. The ANS is divided into two parts: the sympathetic (SNS) and parasympathetic (PNS)
nervous system. When stimulated, the effects of the SNS are widespread across the body. In
contrast, PNS stimulation tends to produce localized, discrete effects. The SNS and PNS generally
have opposing effects on end-organs, with either the SNS or the PNS exhibiting a dominant
tone at rest and without exogenous stimulating events (Table 1-1). In general the function of the
PNS is homeostatic, whereas stimulation of the SNS prepares the organism for some stressful
event (this is often called the fight-or-flight response).
KEY POINTS: AUTONOMIC NERVOUS SYSTEM
1. Patients should take b-blockers on the day of surgery and continue them perioperatively.
Because the receptors are up-regulated, withdrawal may precipitate hypertension,
tachycardia, and myocardial ischemia.
2. Clonidine should also be continued perioperatively because of concerns for rebound
hypertension.
3. Indirect-acting sympthomimetics (e.g., ephedrine) depend on norepinephrine release to be
effective. Norepinephrine-depleted states will not respond to ephedrine administration.
4. Under most circumstances peri-induction hypotension responds best to intravenous fluid
administration and the use of direct-acting sympathomimetics such as phenylephrine.
5. Orthostatic hypotension is common after surgery and may be caused by the use of any or all
anesthetic agents and lying supine for extended periods. It is necessary to be cognizant of this
potential problem when elevating a patient’s head after surgery or even when moving the patient
fromthe operating roomtable to a chair (e.g., procedures requiring only sedation and monitoring).
2. Review the anatomy of the sympathetic nervous system.
Preganglionic sympathetic neurons originate from the intermediolateral columns of the
thoracolumbar spinal cord. These myelinated fibers exit via the ventral root of the spinal nerve
and synapse with postganglionic fibers in paravertebral sympathetic ganglia, unpaired
prevertebral ganglia, or a terminal ganglion. Preganglionic neurons may ascend or descend the
sympathetic chain before synapsing. Preganglionic neurons stimulate nicotinic cholinergic
postganglionic neurons by releasing acetylcholine. Postganglionic adrenergic neurons synapse
at targeted end-organs and release norepinephrine (Figure 1-1).
3. Elaborate on the location and names of the sympathetic ganglia. Practically
speaking, what is the importance of knowing the name and location of these
ganglia?
Easily identifiable paravertebral ganglia are found in the cervical region (including the stellate
ganglion) and along thoracic, lumbar, and pelvic sympathetic trunks. Prevertebral ganglia
are named in relation to major branches of the aorta and include the celiac, superior and inferior
mesenteric, and renal ganglia. Terminal ganglia are located close to the organs that they serve. The
practical significance of knowing the location of some of these ganglia is that local anesthetics can
be injected in the region of these structures to ameliorate sympathetically mediated pain.
4. Describe the postganglionic adrenergic receptors of the sympathetic nervous
system and the effects of stimulating these receptors.
There are a1, a2, b1, and b2 adrenergic receptors. The A1, A2, and B2 receptors are
postsynaptic and are stimulated by the neurotransmitter norepinephrine. The A2 receptors are
presynaptic, and stimulation inhibits release of norepinephrine, reducing overall the autonomic
response. Molecular pharmacologists have further subdivided these receptors, but this is
beyond the scope of this discussion. Dopamine stimulates postganglionic dopaminergic
receptors, classified as DA1 and DA2. The response to receptor activation in different sites is
described in Table 1-2.
5. Review the anatomy and function of the parasympathetic nervous system.
Preganglionic parasympathetic neurons originate from cranial nerves III, VII, IX, and X and
sacral segments 2-4. Preganglionic parasympathetic neurons synapse with postganglionic
neurons close to the targeted end-organ, creating a more discrete physiologic effect. Both
preganglionic and postganglionic parasympathetic neurons release acetylcholine; these
cholinergic receptors are subclassified as either nicotinic or muscarinic. The response to
cholinergic stimulation is summarized in Table 1-3.
6. What are catecholamines? Which catecholamines occur naturally? Which are
synthetic?
Catecholamines are hydroxy-substituted phenylethylamines and stimulate adrenergic nerve
endings. Norepinephrine, epinephrine, and dopamine are naturally occurring catecholamines,
whereas dobutamine and isoproterenol are synthetic catecholamines.
7. Review the synthesis of dopamine, norepinephrine, and epinephrine.
The amino acid tyrosine is actively transported into the adrenergic presynaptic nerve terminal
cytoplasm, where it is converted to dopamine by two enzymatic reactions: hydroxylation of
tyrosine by tyrosine hydroxylase to dopamine and decarboxylation of dopamine by aromatic
8. How is norepinephrine metabolized?
Norepinephrine is removed from the synaptic junction by reuptake into the presynaptic nerve
terminal and metabolic breakdown. Reuptake is the most important mechanism and allows reuse
of the neurotransmitter. The enzyme monoamine oxidase (MAO) metabolizes norepinephrine
within the neuronal cytoplasm; both MAO and catecholamine O–methyltransferase (COMT)
metabolize the neurotransmitter at extraneuronal sites. The important metabolites are
3-methoxy-4-hydroxymandelic acid, metanephrine, and normetanephrine.
9. Describe the synthesis and degradation of acetylcholine.
The cholinergic neurotransmitter acetylcholine (ACh) is synthesized within presynaptic neuronal
mitochondria by esterification of acetyl coenzyme A and choline by the enzyme choline
acetyltransferase; it is stored in synaptic vesicles until release. After release, ACh is principally
metabolized by acetylcholinesterase, a membrane-bound enzyme located in the synaptic
junction. Acetylcholinesterase is also located in other nonneuronal tissues such as erythrocytes.
10. What are sympathomimetics?
Sympathomimetics are synthetic drugs with vasopressor and chronotropic effects similar to
those of catecholamines. They are commonly used in the operating room to reverse the
circulatory depressant effects of anesthetic agents by increasing blood pressure and heart rate;
they also temporize the effects of hypovolemia while fluids are administered. They are effective
during both general and regional anesthesia.
11. Review the sympathomimetics commonly used in the perioperative
environment.
Direct-acting sympathomimetics are agonists at the targeted receptor, whereas indirect-acting
sympathomimetics stimulate release of norepinephrine. Sympathomimetics may be mixed in
their actions, having both direct and indirect effects. Practically speaking, phenylephrine (direct
acting) and ephedrine (mostly indirect acting) are the sympathomimetics commonly used
perioperatively. Also, epinephrine, dopamine, and norepinephrine may be used perioperatively
and most often by infusion since their effects on blood pressure, heart rate, and myocardial
oxygen consumption can be profound. Dopamine is discussed in Chapter 15.
12. Discuss the effects of phenylephrine and review common doses of this
medication.
Phenylephrine stimulates primarily A1 receptors, resulting in increased systemic vascular
resistance and blood pressure. Larger doses stimulate A2 receptors. Reflex bradycardia may
be a response to increasing systemic vascular resistance. Usual intravenous doses of
phenylephrine range between 50 and 200 mcg. Phenylephrine may also be administered by
infusion at 10 to 20 mcg/min.
13. Discuss the effects of ephedrine and review common doses of this medication.
Give some examples of medications that contraindicate the use of ephedrine
and why.
Ephedrine produces norepinephrine release, stimulating mostly A1 and B1 receptors; the effects
resemble those of epinephrine although they are less intense. Increases in systolic blood
pressure, diastolic blood pressure, heart rate, and cardiac output are noted. Usual intravenous
doses of ephedrine are between 5 and 25 mg. Repeated doses demonstrate diminishing
response known as tachyphylaxis, possibly because of exhaustion of norepinephrine supplies or
receptor blockade. Similarly, an inadequate response to ephedrine may be the result of already
depleted norepinephrine stores. Ephedrine should not be used when the patient is taking drugs
that prevent reuptake of norepinephrine because of the risk of severe hypertension. Examples
include tricyclic antidepressants, monoamine oxidase inhibitors, and acute cocaine intoxication.
Chronic cocaine users may be catecholamine depleted and may not respond to ephedrine.
14. What are the indications for using b-adrenergic antagonists?
b-Adrenergic antagonists, commonly called b-blockers, are antagonists at b1- and
b2- receptors. b-blockers are mainstays in antihypertensive, antianginal, and antiarrhythmic
therapy. Perioperative b-blockade is essential in patients with coronary artery disease,
and atenolol has been shown to reduce death after myocardial infarction.
15. Review the mechanism of action for b1-antagonists and side effects.
b1-Blockade produces negative inotropic and chronotropic effects, decreasing cardiac
output and myocardial oxygen requirements. b1-Blockers also inhibit renin secretion and
lipolysis. Since volatile anesthetics also depress contractility, intraoperative hypotension is a risk.
b-Blockers can produce atrioventricular block. Abrupt withdrawal of these medications is not
recommended because of up-regulation of the receptors; myocardial ischemia and hypertension
may occur. b-Blockade decreases the signs of hypoglycemia; thus it must be used with caution
in insulin-dependent patients with diabetes. b-Blockers may be cardioselective, with relatively
selective B1 antagonist properties, or noncardioselective. Some b-Blockers have membranestabilizing
(antiarrhythmic effects); some have sympathomimetic effects and are the drugs of
choice in patients with left ventricular failure or bradycardia. b-Blockers interfere with the
transmembrane movement of potassium; thus potassium should be infused with caution.
Because of their benefits in ischemic heart disease and the risk of rebound, b-blockers should be
taken on the day of surgery.
16. Review the effects of b2-antagonism.
b2-Blockade produces bronchoconstriction and peripheral vasoconstriction and inhibits insulin
release and glycogenolysis. Selective b1-blockers should be used in patients with chronic
or reactive airway disease and peripheral vascular disease because of respective concerns for
bronchial or vascular constriction.
14 CHAPTER 1 AUTONOMIC NERVOUS SYSTEM
17. How might complications of b-blockade be treated intraoperatively?
Bradycardia and heart block may respond to atropine; refractory cases may require the
b2-agonism of dobutamine or isoproterenol. Interestingly, calcium chloride may also be
effective, although the mechanism is not understood. In all cases expect to use larger than
normal doses.
18. Describe the pharmacology of a-adrenergic antagonists.
a1-Blockade results in vasodilation; therefore a-blockers are used in the treatment of
hypertension. However, nonselective a-blockers may be associated with reflex tachycardia.
Thus, selective a1-blockers are primarily used as antihypertensives. Prazosin is the
prototypical selective a1-blocker, whereas phentolamine and phenoxybenzamine are examples
of nonselective a-blockers. Interestingly, labetalol, a nonselective b-blocker, also has selective
a1-blocking properties and is a potent antihypertensive.
19. Review a2-agonists and their role in anesthesia.
When stimulated, a2-receptors within the CNS decrease sympathetic output.
Subsequently, cardiac output, systemic vascular resistance, and blood pressure decrease.
Clonidine is an a2-agonist used in the management of hypertension. It also has significant
sedative qualities. It decreases the anesthetic requirements of inhaled and intravenous
anesthetics. It has also been used intrathecally in the hopes of decreasing postprocedural pain,
but unacceptable hypotension is common after intrathecal administration, limiting its usefulness.
Clonidine should be continued perioperatively because of concerns for rebound hypertension.
20. Discuss muscarinic antagonists and their properties.
Muscarinic antagonists, also known as anticholinergics, block muscarinic cholinergic
receptors, producing mydriasis and bronchodilation, increasing heart rate, and inhibiting
secretions. Centrally acting muscarinic antagonists (all nonionized, tertiary amines with the ability
to cross the blood-brain barrier) may produce delirium. Commonly used muscarinic antagonists
include atropine, scopolamine, glycopyrrolate, and ipratropium bromide. Administering
muscarinic antagonists is a must when the effect of muscle relaxants is antagonized by
acetylcholinesterase inhibitors, lest profound bradycardia, heart block, and asystole ensue.
Glycopyrrolate is a quaternary ammonium compound, cannot cross the blood-brain barrier, and
therefore lacks CNS activity. When inhaled, ipratropium bromide produces bronchodilation.
21. What is the significance of autonomic dysfunction? How might you tell if a
patient has autonomic dysfunction?
Patients with autonomic dysfunction tend to have severe hypotension intraoperatively.
Evaluation of changes in orthostatic blood pressure and heart rate is a quick and effective way
of assessing autonomic dysfunction. If the autonomic nervous system is intact, an increase in
heart rate of 15 beats/min and an increase of 10 mm Hg in diastolic blood pressure are
expected when changing position from supine to sitting. Autonomic dysfunction is suggested
whenever there is a loss of heart rate variability, whatever the circumstances. Autonomic
dysfunction includes vasomotor, bladder, bowel, and sexual dysfunction. Other signs include
blurred vision, reduced or excessive sweating, dry or excessively moist eyes and mouth, cold
or discolored extremities, incontinence or incomplete voiding, diarrhea or constipation, and
impotence. Although there are many causes, it should be noted that people with diabetes and
chronic alcoholics are patient groups well known to demonstrate autonomic dysfunction.
22. What is a pheochromocytoma, and what are its associated symptoms? How is
pheochromocytoma diagnosed?
Pheochromocytoma is a catecholamine-secreting tumor of chromaffin tissue, producing
either norepinephrine or epinephrine. Most are intra-adrenal, but some are extra-adrenal (within the
bladder wall is common), and about 10%are malignant. Signs and symptomsinclude paroxysms of
CHAPTER 1 AUTONOMIC NERVOUS SYSTEM 15
hypertension, syncope, headache, palpitations, flushing, and sweating. Pheochromocytoma is
confirmed by detecting elevated levels of plasma and urinary catecholamines and their metabolites,
including vanillylmandelic acid, normetanephrine, and metanephrine.
23. Review the preanesthetic and intraoperative management of
pheochromocytoma patients.
These patients are markedly volume depleted and at risk for severe hypertensive crises. It is
absolutely essential that before surgery, a-blockade and rehydration should first be instituted.
The a1-antagonist phenoxybenzamine is commonly administered orally. b-Blockers are
often administered once a-blockade is achieved and should never be given first because
unopposed a1-vasoconstriction results in severe, refractory hypertension. Labetalol may be the
b-blocker of choice since it also has a-blocking properties.
Intraoperatively intra-arterial monitoring is required since fluctuations in blood pressure
may be extreme. Manipulation of the tumor may result in hypertension. Intraoperative
hypertension is managed by infusing the a-blocker phentolamine or vasodilator nitroprusside.
Once the tumor is removed, hypotension is a risk, and fluid administration and administration
of the a-agonist phenylephrine may be necessary. Central venous pressure monitoring will
assist with volume management.
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