CONTINUING EDUCATION IN MEMORY OF NORMAN TRIEGER, DMD, MD

Anesthetic Management of the Hypertensive Patient: Part I

Russell Yancey, DDS
PGY-2 Resident, New York University–Langone Hospital Dental Anesthesiology Service, Brooklyn, New York

Hypertension is an important health challenge that affects millions of people across the world and is a major risk factor
for cardiovascular disease. It is critical that anesthesia providers have a working knowledge of the systemic
implications of hypertension. This review article will discuss the medical definitions of hypertension, the physiology of
maintaining blood pressure, outpatient treatment of hypertension, anesthetic implications, and the common
medications used by anesthesia providers in the treatment of hypertension. Part I will provide an overview of
hypertension and blood pressure regulation. In addition, drugs affecting predominantly renal control of hypertension,
such as diuretics, angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, and renin-inhibiting agents,
will be discussed. In part II, the remaining major antihypertensive medications will be reviewed as well as anesthetic
implications of managing patients with hypertension.

Key Words: Hypertension; Antihypertensives; Anesthetic; Review.

lood pressure typically fluctuates throughout the

B day, but hypertension, or high blood pressure,
can cause undue stress on the patient’s heart,
CLASSIFICATION AND GUIDELINES

There are 2 types of hypertension: essential hypertension

vasculature, and other organs, leading to a variety of and secondary hypertension. Essential hypertension
health problems. Those health problems include heart accounts for approximately 95% of the cases and
disease and stroke, which are the leading causes of represents a form of hypertension without a clear
death in the United States.1 Almost half of Americans cause.4 However, many health care providers recognize
are identified as having high blood pressure according that a number of factors may contribute to increased
to the recent classification changes of high blood blood pressure, including but not limited to obesity,
insulin resistance, high alcohol intake, high salt intake,
pressure in 2017 by the American Heart Association
aging, sedentary lifestyle, stress, low potassium intake,
and the American College of Cardiology. Only an
and low calcium intake.5 Secondary hypertension has a
estimated 54% of those people have their condition
clear etiology with many causes that may include renal
under control.2 Hundreds of thousands of deaths each disease, hyperthyroidism, obstructive sleep apnea, hy-
year are primarily due to high blood pressure,1 and peraldosteronism, and many others.4
this disease ends up costing patients in the United There are 4 levels of blood pressure, as outlined by the
States $48.6 billion each year.3 American Heart Association/American College of Car-
Because of the growing public health concern that is diology in the updated 2017 guidelines (see Table 1). The
associated with hypertension, it is important that choice and the naming of the categories were based on a
dental providers are knowledgeable about the implica- pragmatic interpretation of blood pressure–related
tions, management, and treatment options available cardiovascular disease risk and benefit of blood pressure
for the hypertensive patient. This article will provide a reduction in clinical trials. Prior to diagnosing a person
contemporary review of the definition, physiology, with hypertension, it is important to use an average
pharmacologic management, and other concerns sur- based on greater than 2 readings obtained on more than
rounding the anesthetic management of the hyperten- 2 occasions to estimate the individual’s blood pressure
sive patient. level.5 The new guidelines also recommend allowing
patients to rest at least 5 minutes prior to taking the
Received April 27, 2018; accepted for publication April 30, 2018. blood pressure readings and taking the blood pressure
Address correspondence to Dr Russell Yancey, 408 77th Street, measurement while the patient is seated, feet on the
Apt C4, Brooklyn, NY 11209; [email protected]. floor, and the arm at the level of the heart with an
Anesth Prog 65:131–138 2018 j DOI 10.2344/anpr-65-02-12 appropriately sized cuff that encircles at least 80% of the
Ó 2018 by the American Dental Society of Anesthesiology arm.5,6

131
132 Anesthetic Management of the Hypertensive Patient Anesth Prog 65:131–138 2018

Table 1. Classification of Hypertension* The sympathetic vasoconstrictor system is important

Systolic, Diastolic,
in maintaining proper homeostatic blood pressure via
Category mm Hg mm Hg the vasomotor center. The vasomotor center is located
in the reticular substance of the medulla and in the lower
Optimal blood pressure ,120 and ,80
Elevated 120–129 and ,80 third of the pons and is responsible for providing
Stage 1 hypertension 130–139 or 80–89 sympathetic and parasympathetic outflow to the effec-
Stage 2 hypertension 140 or 90 tor organs. This center transmits sympathetic impulses
Hypertensive urgency/crisis .180 or .120 through the spinal cord and peripheral sympathetic
* Updated in October 2017 according to the American nerves to virtually all arteries, arterioles, and veins in the
College of Cardiology Foundation and the American Heart body as well as parasympathetic impulses through the
Association, Inc. vagus nerve to the heart.9 The postganglionic nerve
fibers of the sympathetic nervous system that terminate
Currently, optimal blood pressure is a systolic in the vasculature functionally produce a level of partial
pressure of less than 120 mm Hg and a diastolic constriction and also have the ability both to dilate and
pressure of less than 80 mm Hg. A patient is considered to constrict adaptively around this level of resting tone.7
to have an elevated blood pressure if they have a systolic Through this powerful influence of sympathetic outflow
reading of 120 to 139 mm Hg and a diastolic reading of from the vasomotor center, the body can regulate
less than 80 mm Hg. The previous reading of 120/80 mm vascular vasoconstriction and heart rate to maintain
Hg is no longer considered ideal and is now categorized normal blood pressure values.
as stage 1 hypertension. Stage 1 hypertension begins The most well-known autonomic nervous system
when the systolic pressure is 130 to 139 mm Hg or the mechanism for regulating arterial pressure is the
diastolic pressure is between 80 and 89 mm Hg. Stage 2 baroreceptor reflex. This reflex is initiated by stretch
hypertension is now apparent when the systolic pressure receptors within the aortic arch and carotid bodies that
is equal to or greater than 140 mm Hg or the diastolic is transmit feedback signals to the central nervous system
equal to or greater than 90 mm Hg. A hypertensive for minute-to-minute regulation of blood pressure. The
urgency or crisis involves a systolic pressure higher than baroreceptors in the carotid sinus near the bifurcation of
180 mm Hg or a diastolic reading higher than 120 mm the common carotid arteries are most sensitive to
Hg and the absence or presence of specific symptoms. decreasing arterial pressures, whereas the baroreceptors
The recommended blood pressure classification system in the aortic arch are most sensitive to increasing arterial
is most valuable in untreated adults as an aid in pressures.8 The baroreceptors respond rapidly to chang-
decisions about prevention or treatment of high blood es in arterial pressure; in fact, the rate of impulse firing
increases within a fraction of a second during each
pressure. However, it is also useful in assessing the
systole and decreases again during diastole.9
success of interventions to reduce blood pressure.5
The baroreceptor reflex signals the nucleus tracts
solitarius in the medullary portion of the brain stem.
These baroreceptor signals inhibit the vasoconstrictor
PHYSIOLOGY OF BLOOD PRESSURE
center in the medulla and excite the vagal center, which
REGULATION
stimulates parasympathetic activity via the glossopha-
ryngeal nerve from the carotid sinus receptors and the
The physiology of blood pressure regulation on a vagus nerve from the receptors in the aortic arch. The
moment-to-moment basis, a daily basis, and a lifetime resultant parasympathetic activity causes predominately
basis consists of a delicate balance of nervous system (1) decreased heart rate and strength of cardiac
and hormonal control mechanisms to maintain arterial contraction and less so (2) vasodilation of veins and
pressure at or near normal. Mean arterial pressure is the arterioles.10 This decreases the blood pressure due to a
steady-state component of blood pressure and is crucial decline in cardiac output and peripheral vascular
as the body regulates proper perfusion pressures to vital resistance. This baroreceptor reflex is also crucial in
organs and also optimizes cardiovascular work. The maintaining relatively constant blood pressures despite
basic scheme by which blood pressure is regulated is positional changes, such as when a person stands up
through a feedback control system consisting of pressure after lying down or other activities that increase blood
sensors and effector mechanisms.7 The most important pressure, such as eating and exercise. A primary purpose
mechanisms for regulating blood pressure are a fast, of the arterial baroreceptor system is to reduce the
neurally mediated baroreceptor mechanism and a minute-by-minute variation in arterial pressure to about
slower, hormonally regulated renin-angiotensin-aldoste- one-third that which would occur if the baroreceptor
rone mechanism.8 system were not present.9
Anesth Prog 65:131–138 2018 Yancey 133

The renin angiotensin aldosterone system is a relatively slow, hormonal mechanism whereby there is a long-term blood pressure
regulation.

The renin-angiotensin-aldosterone system (RAAS; see Vasopressin, also known as antidiuretic hormone, is the
the Figure) is part of a powerful feedback system for key humoral component of the vasopressinergic system,
long-term control of arterial pressure and volume which has a profound effect on blood pressure control.
homeostasis.11 The RAAS is stimulated by reduced Vasopressin is synthesized in the paraventricular and
cardiac output, decreased renal perfusion, hypovolemia, supraoptic nuclei in the hypothalamus, and the most
and decreased sodium intake. The stimulation of the potent stimuli for vasopressin release are hypertonic
RAAS traditionally begins with angiotensinogen, which conditions, severe hypotension, and hypovolemia.15 The
is generated by the liver and cleaved by renin, released vasopressin receptors that are crucial in blood pressure
from the juxtaglomerular cells in the kidneys, in control are V1 receptors located on vascular smooth
response to hypotension or decreased renal perfusion muscle and produce peripheral vasoconstriction, while
pressure, to form angiotensin I. Angiotensin I is further V2 receptors located in the collecting ducts in the
cleaved by angiotensin-converting enzyme (ACE) pro- kidneys promote water retention.16
duced primarily by the lungs to form the active hormone
Other regulators of blood pressure include another
angiotensin II.12 Angiotensin II is a hormone that acts
hormone, atrial natriuretic peptide, which is released
on a variety of sites to increase blood pressure, primarily
when the atrial stretch receptors are stimulated. This
by binding to specialized receptors that induce vaso-
results in increased natriuresis (increased sodium excre-
constriction. Angiotensin II has other functions as it
tion) with resultant decrease in blood volume. In
increases the neuroanatomic center for thirst, sodium
appetite, and cardiovascular control, making extensive addition, chemoreceptors located in the carotid and
connections with the hypothalamus, limbic system, and aortic bodies are stimulated by low arterial oxygen
brain stem.13 Angiotensin II also stimulates the adrenal concentrations and also play a role in blood pressure
cortex to release aldosterone, which in turn promotes regulation. These chemoreceptors are stimulated when
the retention of sodium and free water within the distal there is diminished blood flow that causes a decrease of
tubules of the kidneys and the excretion of potassium. oxygen and an increase in carbon dioxide and hydrogen
Specifically, angiotensin II binds to angiotensin II (AT ions (lowered serum pH). This chemoreceptor reflex is
type 1) receptors on the blood vessels, resulting in not a powerful arterial pressure controller until the
vasoconstriction as well as constriction in specific pressure falls below 80 mm Hg. 9 Although the
organs, including the heart, adrenal cortex, and brain.14 chemoreceptors indeed play a role in the regulation of
In addition to the humoral control of angiotensin II in blood pressure, they have a much more important role
the RAAS, there are other hormones that are vasoactive in respiratory control. Increased arterial partial pressure
and contribute to the regulation of blood pressure. of carbon dioxide in cerebral ischemia also increases
134 Anesthetic Management of the Hypertensive Patient Anesth Prog 65:131–138 2018

blood pressure, which stimulates sympathetic outflow to Table 2. Factors That May Interfere With Blood Pressure
the heart and blood vessels. Control
Commonly used medications19
 Nonsteroidal anti-inflammatory drugs (NSAIDs)
 Oral contraceptives
TREATMENT RECOMMENDATIONS
 Some antidepressants (eg, tricyclic antidepressants,
serotonin and norepinephrine reuptake inhibitors,
The first treatment recommendation for patients with bupropion, monoamine oxidase inhibitors)
hypertension primarily involves lifestyle modification.  Sympathomimetics (eg, decongestants such as
Weight loss is the most effective of all the non- pseudoephedrine/ephedrine)
 Corticosteroids
pharmacologic measures to prevent and treat hyperten-
Recreational or illicit drugs19
sion,17 although increased physical activity and diet  Alcohol
modification are usually recommended as well. The  Cocaine
first-line pharmacologic treatment for uncomplicated  Amphetamines
stage 1 hypertension is usually a thiazide-type diuretic,  Chewing tobacco

an angiotensin-converting enzyme inhibitor (ACEI), Significant predictors of nonadherence to antihypertensive

medications20,21
angiotensin receptor blocker (ARB), or a calcium  Age ,50 y
channel blocker. In stage 2 hypertension, the treatment  Male gender
typically expands to a 2-drug combination, which  Hispanic or African American
 Low family income (,$55,000/y)
usually includes the aforementioned drugs and the
 No health insurance
introduction of b-adrenergic receptor blocking agents  No medical visits within past year
(b-blockers) or a second drug from the stage 1
category.18
The treatment of patients with hypertension is diuretics decrease extracellular fluid volume by decreas-
variable and contingent on other comorbidities, such ing the sodium content in the body. Where sodium goes,
as chronic kidney disease, diabetes mellitus, or heart water follows, and diuretics can be very effective in
failure. The treatment goals and medications are target decreasing intravascular fluid volume to control blood
oriented, and patients have a wide variety of target pressure. There are many types of diuretics that mainly
blood pressures and medication combinations for have a similar goal of inhibiting the tubular sodium
optimal treatment. The American Heart Association reabsorption but have different mechanisms of action at
recommends that for most patients with hypertension, different points in the nephron. Some common diuretics
including patients with stable cardiovascular disease, and their mechanisms and sites of action are outlined in
chronic kidney disease, diabetes mellitus, and age- Table 3.
related issues, the target blood pressure treatment goal Thiazide diuretics inhibit sodium transport in the
is ,130/80 mm Hg.5 distal convoluted tubule and also in part of the cortical
ascending limb of the loop of Henle.14 Loop diuretics
act on the ascending limb of the loop of Henle at the
sodium, potassium, and chloride symporters or mem-
Common Antihypertensive Medications and Their brane transporter proteins and inhibit sodium, potassi-
Anesthetic Implications um, and chloride uptake. Thiazide diuretics have a
longer duration of action than loop diuretics and
A thorough understanding of the common antihyper- therefore are usually more effective for long-term
tensive medications is beneficial to all health care hypertension management. It is important to recognize
providers during the management of these patients. the effects that these diuretics have on calcium and
The major classes of antihypertensive agents include potassium regulation. Thiazide diuretics activate epithe-
diuretics, ACEIs, ARBs, direct renin inhibitors, calcium lial sodium channels (which are inhibited by calcium)
channel blockers, a-adrenergic blockers, b-adrenergic and thereby favor potassium secretion.22 With regard to
blockers, a2-adrenergic agonists, and vasodilators. This calcium levels, thiazide diuretics and loop diuretics have
also includes being familiar with the medications or opposite effects on calcium balance; whereas thiazides
factors that could worsen blood pressure control (Table promote calcium retention, loop diuretics enhance
2). urinary calcium loss. This is possibly one reason why
Diuretics. Diuretics increase the rate of urine volume loop diuretics, which increase distal calcium delivery,
output and clinically act by decreasing renal tubular result in lesser degrees of hypokalemia.22,23
sodium reabsorption, causing natriuresis, which in turn Aldosterone antagonists, specifically spironolactone,
leads to diuresis (increased water excretion).9 Most act on the distal nephron to increase the amounts of
Anesth Prog 65:131–138 2018 Yancey 135

Table 3. Classes of Diuretics and Their Mechanisms and Sites of Action

Class of Diuretic Mechanism of Action Site of Action
Thiazide diuretics (hydrochlorothiazide) Inhibit Naþ and Cl– transport Early distal tubules
Loop diuretics (furosemide) Inhibit Naþ, Kþ, Cl– uptake Loop of Henle
Aldosterone antagonists (spironolactone) Inhibit Naþ reabsorption and Kþ secretion Collecting tubules
Osmotic diuretics (mannitol) Increase osmotic pressure and inhibit H2O Primarily proximal tubules
and solute reabsorption
Carbonic anhydrase inhibitors (acetazolamide) Inhibits carbonic anhydrase, which inhibits Collecting tubules
HCO3– and reduces Naþ reabsorption
Sodium channel blockers (triamterene) Directly inhibit Naþ reabsorption and Kþ Collecting tubules
secretion

sodium and water to be excreted while potassium is decreased blood pressures from normal, orthostatic
retained.14 Aldosterone antagonists provide competitive heart rate and blood pressure changes from positional
blockade of epithelial aldosterone receptors in the distal changes, urine specific gravity, and decreased urinary
tubule and collecting duct.24 Osmotic diuretics such as flow rates and output.26 The early reduction in blood
mannitol decrease water reabsorption by increasing the pressure with thiazide use is due to a reduction in blood
osmotic pressure of tubular fluid and are primarily used volume, and chronic thiazide treatment results in blood
in the operating room and critical care settings.9 pressure control through reduced vascular resistance
Carbonic anhydrase inhibitors, as the name implies, despite return of fluid to pretreatment levels.14 Thiazide
inhibit the enzyme carbonic anhydrase, which decreases diuretics may aggravate glucose control, especially in
the reabsorption of bicarbonate and therefore reduces combination with b-blockers.24 Although modest in-
sodium reabsorption, resulting in diuresis. Acetozola- creases in blood glucose are reported, this is an
mide, the classic carbonic anhydrase inhibitor used in uncommon presentation in the outpatient setting unless
altitude sickness, treatment of glaucoma, and control of the patient has a history of uncontrolled blood glucose
edema in congestive heart failure, is seldom used for levels. In addition, thiazide diuretics appear to prolong
long-term treatment of hypertension. Sodium channel neuromuscular blockade with nondepolarizing neuro-
blockers, such as triamterene, which has decreased in muscular blockers. Diuretics may be continued in the
use recently, act directly on the sodium channels of the perioperative period but can be discontinued if there is
collecting tubules and block sodium reabsorption to reason to suspect volume depletion or hypokalemia.27 In
create their diuretic effects. This is similar to aldosterone addition, diuretic-induced volume depletion on a
antagonists, but instead of acting indirectly through biochemical level is due to the loss of sodium from the
aldosterone, these diuretics directly block the entry of body. Diuretics, along with other hypertension medica-
sodium in the sodium channels located in the collecting tions, may induce a hyponatremic state, which leads to
tubules. The latter 2 agents are termed potassium-sparing decreased extracellular fluid osmotic pressure. This
diuretics and can be combined with thiazide diuretics to results in a shift of fluid into the cells and therefore
minimize hypokalemia. causes a hypovolemic state.28 Many long-term hyper-
Anesthetic Implications. Because thiazide and loop tensive patients therefore have a masked state of
diuretics are not potassium sparing, an adverse effect is hypovolemia. Prudent volume augmentation in ambu-
hypokalemia with metabolic acidosis. In contrast to this, latory settings with a crystalloid solution prior to the
the potassium-sparing agents may produce hyperkale- induction of anesthesia may help with masked hypovo-
mia. Because of this, it is important to monitor serum lemia.
potassium levels after administration of these diuretics. ACEIs. ACEIs block the conversion of angiotensin I
In an outpatient setting, 1-time potassium lab values are to angiotensin II in the renin-angiotensin system.
practical. The measurement of a 24-hour urinary Blocking angiotensin II formation is a key antihyper-
potassium excretion is appropriate for patients who tensive strategy since angiotensin II promotes vasocon-
are at high risk, for example, those patients with striction as well as salt and water retention by
congestive heart failure.25 stimulating aldosterone secretion by the adrenal gland
Diuretics can cause dehydration. The volume status of and thus sodium reabsorption by the proximal tubule.29
a patient can be difficult to assess in the outpatient and Furthermore, ACEIs promote the accumulation of
ambulatory setting without laboratory values, yet bradykinin in or at the vessel wall.30 Bradykinin is a
indirect measures of volume status may include an powerful vasodilator that increases capillary permeabil-
observation of mucous membranes, quality of periph- ity, possibly leading to angioedema (0.3%-0.6%), which
eral pulses, increasing resting heart rate accompanied by can involve the glottic or laryngeal regions.31 In
136 Anesthetic Management of the Hypertensive Patient Anesth Prog 65:131–138 2018

addition, there is a bradykinin-evoked sensitization of fective in the bradykinin-mediated angioedema, as seen

airway sensory nerves, coupled with an accumulation of with ACEIs. Some newer agents, such as bradykinin
kinins, substance P, and prostaglandins, which may receptor antagonists such as icatibant or kallikrein
contribute to the pathogenesis of the common and inhibitors (eg, ecallantide), may provide novel alterna-
bothersome ACEI cough.32,33 This ACEI cough can tives for the treatment of ACEI-induced angioede-
occur in up to 10% of patients and is the most common ma.37,38
adverse effect of ACEIs. The treatment of choice is to ARBs. ARBs, otherwise known as angiotensin II
discontinue the ACEI.32 receptor antagonists, whose generic names all end in -
There are 3 classes of ACEIs that differ in potency, sartan, block angiotensin II from binding to the
bioavailability, half-life, and route of elimination. Class angiotensin II (AT type 1) receptor on vascular smooth
I ACEIs, such as captopril, have the shortest half-life (6– muscle cells. This blockade results in a decrease in
12 hours vs 24 hours) and contain a problematic peripheral vasoconstriction, thereby decreasing systemic
sulfhydryl (not sulfonamide) group that can cause a vascular resistance and arterial blood pressure and
skin rash, loss of taste, neutropenia, and proteinuria.14 increasing angiotensin II and normal bradykinin plasma
Class II ACEIs, such as enalapril, are prodrugs that are levels.39
converted to active drugs by the liver. Enalaprilat is a Anesthetic Implications. ARBs have no effect on
parenteral form that can be administered to patients on bradykinin metabolism; therefore, their use is associated
ACEIs during the perioperative period. Lisinopril is the with significantly reduced incidence of cough and
only class III ACEI and is not a prodrug, but it is water angioedema as compared with ACEIs. Because of this
soluble and excreted unchanged by the kidneys without decreased incidence of angioedema, some patients are
hepatic metabolism.14 shifted toward ARB therapy from ACEI therapy.
Anesthetic Implications. Because of an increased risk However, it is important to note that there is still a
of refractory hypotension, ACEIs are typically held on small angioedema risk involved. The current thinking
the day of surgery if general anesthesia or some type of among many anesthesiologists is that, similar to ACEIs,
deep sedation is planned, particularly during induction ARBs should be withheld on the day of surgery to avoid
of general anesthesia. Coriat and colleagues34 found that refractory hypotension during induction of general
ACEIs were associated with hypotension in 100% of anesthesia. Heightened awareness of the possible refrac-
patients during induction versus approximately 20% in tory hypotension that can occur with ACEIs and ARBs
whom ACEIs were withheld on the morning of the and recognition of the need to treat with an adequate
surgical procedure. If the patient did take their usual dose of vasopressin, epinephrine, or norepinephrine are
dose of ACEI on the day of surgery, some sources required.40 In addition to the refractory hypotension
suggest administering an intravenous bolus of 250 mL to that can occur during induction, there have been
1 L of crystalloid solution prior to the induction of incidents of rebound hypertension following the discon-
general anesthesia to decrease the severity of hypoten- tinuation of ARBs. The risks and benefits of continuing
sion.35 If traditional vasopressor options such as or withholding ARBs should be taken into consider-
phenylephrine or ephedrine have been used without ation during any medication adjustment in the periop-
the desired clinical response for the treatment of erative period.
hypotension, then further treatment options include Direct Renin Inhibitors. The direct renin inhibitor
vasopressin, epinephrine, and norepinephrine. ACEIs aliskiren binds to the S3bp binding site of renin and
may generally be continued during the perioperative inhibits the RAAS by blocking the conversion of
period if moderate sedation is planned. angiotensinogen to angiotensin I.14 This is a relatively
As mentioned above, angioedema is a known adverse new drug that received approval from the US Food and
effect of ACEIs. It is important to make the distinction Drug Administration in 2007. Because it does not
between the histamine-mediated edema that is often significantly affect the cytochrome P450 system, it has
associated with urticaria or anaphylaxis and the been associated with few drug interactions.41
bradykinin-mediated angioedema that is associated with Anesthetic Implications. It is well known that ACEIs
ACEI use.30 Although the incidence of ACEI angioede- and ARBs are associated with refractory hypotension
ma is low, Banerji et al36 reported that 30% of during induction of general anesthesia, and it can be
angioedema cases that presented to the emergency assumed that direct renin inhibitors, which act earlier on
department were due to ACEIs. Discontinuation of the same pathway and produce similar if not more
the ACEI, maintaining airway patency, and supportive exaggerated downstream effects, would have similar
therapies are the mainstay of treatment.35 Corticoste- anesthetic implications.42 If the standard treatment for
roids and antihistamines are typically given to rule out postinduction hypotension, such as a fluid bolus,
histamine-mediated angioedema and are usually inef- ephedrine, or phenylephrine administrations, is ineffec-
Anesth Prog 65:131–138 2018 Yancey 137

tive, then an infusion of vasopressin (0.03–1 U/min) or 18. Nguyen Q, Dominguez J, Nguyen L, Gullapalli N.
methylene blue (2 mg/kg over 20 minutes) can be given Hypertension management: an update. Am Health Drug
with documented success.43 Aliskiren has also been Benefits. 2010;3:47–56.
associated with an increased incidence of nonfatal 19. Basile JN, Bloch MJ. Identifying and managing factors
that interfere with or worsen blood pressure control. Postgrad
stroke, renal complications, and hyperkalemia.14
Med. 2010;122:35–48.
20. Bautista LE. Predictors of persistence with antihyper-
tensive therapy: results from the NHANES. Am J Hypertens.
REFERENCES 2008;21:183–188.
21. Shaya FT, Du D, Gbarayor CM, Frech-Tamas F, Lau
1. Centers for Disease Control and Prevention, National H, Weir MR. Predictors of compliance with antihypertensive
Center for Health Statistics. Underlying cause of death 1999- therapy in a high-risk medicaid population. J Natl Med Assoc.
2013. CDC WONDER Online Database, released 2015. 2009;101:34–39.
Available at: http://wonder.cdc.gov/ucd-icd10.html. Accessed 22. Ellison DH, Loffing J. Thiazide effects and adverse
August 11, 2017. effects: insights from molecular genetics. Hypertension. 2009;
2. Farley TA, Dalal MA, Mostashari F, Frieden TR. 54:196–202.
Deaths preventable in the U.S. by improvements in use of 23. Hoenderop JG, Nilius B, Bindels RJ. Molecular
clinical preventive services. Am J Prev Med. 2010;38:600–609. mechanism of active Ca2þ reabsorption in the distal nephron.
3. Benjamin EJ, Blaha MJ, Chiuve SE, et al. Heart disease Annu Rev Physiol. 2002;64:529–549.
and stroke statistics—2017 update: a report from the 24. Stoelting RK, Flood P, Rathmell JP, et al. Stoelting’s
American Heart Association. Circulation. 2017;135:e146–e603. Handbook of Pharmacology and Physiology in Anesthetic
4. Berg SM, Bittner EA, Zhao KH. Anesthesia Review: Practice. Philadelphia, PA: Lippincott Williams & Wilkins;
Blasting the Boards. Philadelphia, PA: Lippincott Williams & 2014.
Wilkins; 2016. 25. Cohn JN, Kowey PR, Whelton PK, Prisant LM. New
5. Whelton P, Carey R, Aronow W, et al. ACC/AHA guidelines for potassium replacement in clinical practice. A
guideline for the prevention, detection, evaluation, and contemporary review by the National Council on Potassium in
management of high blood pressure in adults [published Clinical Practice. Arch Intern Med. 2000;160:2429–2436.
online November 13, 2017]. Hypertension. 26. Butterworth J, Mackey DC, Wasnick J. Morgan and
6. Hogan J, Radhakrishnan J. The assessment and Mikhail’s Clinical Anesthesiology. 5th ed. New York, NY:
importance of hypertension in the dental setting. Dent Clin McGraw Hill Professional; 2013.
North Am. 2012;56:731–745. 27. Miller RD. Miller’s Anesthesia. Philadelphia, PA: Saun-
7. Raff H. Physiology Secrets. Philadelphia, PA: Elsevier ders; 2015.
Health Sciences; 2003. 28. Thibodeau GA, Patton KT. Anatomy and Physiology. St
8. Costanzo LS. Physiology. Philadelphia, PA: Elsevier; Louis, MO: Mosby; 2003.
2017. 29. Levens NR, Peach MJ, Carey RM. Role of the
9. Guyton AC, Hall JE. Textbook of Medical Physiology. intrarenal renin-angiotensin system in the control of renal
Philadelphia, PA: Saunders Medical; 2016. function. Circ Res. 1981;48(2):157–167.
10. Hall JE. Pocket Companion to Guyton and Hall Textbook 30. Hecker M, Blaukat A, Bara AT, Müller-Esterl W, Busse
of Medical Physiology. Philadelphia, PA: Saunders; 2011. R. ACE inhibitor potentiation of bradykinin-induced veno-
11. Hall JE. Control of blood pressure by the renin- constriction. Br J Pharmacol. 1997;121:1475–1481.
angiotensin-aldosterone system. Clin Cardiol. 1991;14(8 suppl 31. Podymow T, Joseph G. Preconception and pregnancy
4):IV6–21. management of women with diabetic nephropathy on angio-
12. Barash P, Cullen BF, Stoelting RK et al. Clinical tensin converting enzyme inhibitors. Clin Nephrol. 2015;83(2):
Anesthesia. 7th ed. Philadelphia, PA: Lippincott Williams & 73–79.
Wilkins; 2013. 32. Fox AJ, Lalloo UG, Belvisi MG, Bernareggi M, Chung
13. Fitzsimons JT. Angiotensin, thirst, and sodium appetite. KF, Barnes PJ. Bradykinin-evoked sensitization of airway
Physiol Rev. 1998;78:583–686. sensory nerves: a mechanism for ACE-inhibitor cough. Nat
14. Murray MJ, Rose SH, Wedel DJ, et al. Faust’s Med. 1996;2:814–817.
Anesthesiology Review. Philadelphia, PA: Elsevier Health 33. Overlack A. ACE inhibitor-induced cough and bron-
Sciences; 2014. chospasm: incidence, mechanisms and management. Drug Saf.
15. Ohbuchi T, Haam J, Tasker JG. Regulation of neuronal 1996;15:72–78.
activity in hypothalamic vasopressin neurons. Interdiscip Inf 34. Coriat P, Richer C, Douraki T, et al. Influence of
Sci. 2015;21:225–234. chronic angiotensin-converting enzyme inhibition on anesthet-
16. Vincent JL, Su F. Physiology and pathophysiology of ic induction. Anesthesiology. 1994;81:299–307.
the vasopressinergic system. Best Pract Res Clin Anaesthesiol. 35. Vasekar M, Craig TJ. ACE inhibitor-induced angioede-
2008;22:243–252. ma. Curr Allergy Asthma Rep. 2012;12:72–78.
17. Oza R, Garcellano M. Nonpharmacologic management 36. Banerji A, Clark S, Blanda M, Lovecchio F, Snyder B,
of hypertension: what works? Am Fam Physician. 2015;91:772– Camargo CA. Multicenter study of patients with angiotensin-
776. converting enzyme inhibitor-induced angioedema who present
138 Anesthetic Management of the Hypertensive Patient Anesth Prog 65:131–138 2018

to the emergency department. Ann Allergy Asthma Immunol. 40. Nabbi R, Woehlck HJ, Riess ML. Refractory hypoten-
2008;100:327–332. sion during general anesthesia despite preoperative discontin-
37. Lock RJ, Gompels MM. C1-inhibitor deficiencies uation of an angiotensin receptor blocker. F1000Res. 2013;2:
(hereditary angioedema): where are we with therapies? Curr 12.
Allergy Asthma Rep. 2007;7:264–269. 41. Sanoski CA. Aliskiren: an oral direct renin inhibitor for
38. Schneider L, Lumry W, Vegh A, Williams AH, the treatment of hypertension. Pharmacotherapy. 2009;29:193–
Schmalbach T. Critical role of kallikrein in hereditary
212.
angioedema pathogenesis: a clinical trial of ecallantide, a
novel kallikrein inhibitor. J Allergy Clin Immunol. 2007;120: 42. Palmer EI, Oken A. Aliskiren: a new harbinger of
416–422. hypotension? Open J Anesthesiol. 2013;3:102–103.
39. LECOM Education System. NSAIDS and ACE-Inhibi- 43. Thoma A. Pathophysiology and management of angio-
tors: LECOM Education System. 2017. Available at: https:// tensin-converting enzyme inhibitor-associated refractory hy-
lecom.edu/nsaids-and-ace-inhibitors/. Accessed August 11, potension during the perioperative period. AANA J. 2013;81:
2017. 133–140.

CONTINUING EDUCATION QUESTIONS

This continuing education (CE) program is designed for dentists who desire to advance their understanding of pain
and anxiety control in clinical practice. After reading the designated article, the participant should be able to evaluate
and utilize the information appropriately in providing patient care.
The American Dental Society of Anesthesiology (ADSA) is accredited by the American Dental Association and
Academy of General Dentistry to sponsor CE for dentists and will award CE credit for each article completed. You
must answer 3 of the 4 questions correctly to receive credit.
Submit your answers online at www.adsahome.org. Click on ‘‘On Demand CE.’’
CE questions must be completed within 3 months and prior to the next issue.

1. All of the following are levels of hypertension 3. Which of the following blood pressure regulation
according to the new American Heart Association/ mechanisms provides moment-to-moment control of
the American College of Cardiology hypertension blood pressure?
guidelines published in October 2017, except:
A. Autonomic nervous system
A. Elevated B. Baroreceptor reflex
B. Prehypertension C. Renin-angiotensin-aldosterone system
C. Stage 1 D. Vasopressinergic system
D. Stage 2
2. Angiotensin-converting enzyme inhibitors (ACEIs) 4. Which of the following medications is generally NOT
promote the accumulation of which substance that a common first-line outpatient treatment for hyper-
can lead to airway angioedema? tension?
A. Aldosterone A. ACEIs
B. Bradykinin B. Angiotensin receptor antagonists
C. Norepinephrine C. b-blockers
D. Renin D. Diuretics