The hypertensive dental patient

BC Muzyka and M Glick

J Am Dent Assoc 1997;128;1109-1120

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ARTICLE 1

THE
BRIAN

C.

HYPERTENSIVE

MUZYKA,

D.M.D.;

MICHAEL GLICK,

iaries."2
A single elevated blood pressure alone does not constitute a
diagnosis of hypertension.
Currently, an adult is classified
as hypertensive when the mean
value of three or more blood
pressure readings taken at
three or more medical visits reveals a systolic pressure of 140
millimeters of mercury, or mm
Hg, or greater or a diastolic
pressure of 90 mm Hg or
greater. This definition differs
dramatically from the earlier
definition supported by the
JNC-IV in 1988.3 In that report,

PATIENT

The dental team plays an integral role in safeguarding the gen-

eral health of patients. Dental

health care workers should be
able to recognize risk factors associated with hypertension and

counsel patients in an effort to

reduce those that are present. In

addition, dental professionals

should recognize how these risk

factors and associated hypertension affect the provision of dental care. This article reviews recent findings and therapies for

hypertension, evaluates historically accepted but unsupported

anecdotal information on the
dental management of hypertensive patients and proposes

guidelines for the dental management of these patients.

the JNC-IV defined hypertension as a mean diastolic blood

pressure level of 90 mm Hg or
greater, with no regard to a sys-

tolic component, and further

separated hypertension into
three degrees: severe, moderate
and mild.
The newer JNC-V guidelines
attempt to de-emphasize descriptive terms formerly used,
such as severe, moderate and
mild hypertension, because they
lack a sense of emphasis and
urgency; instead, the guidelines
include normal, high normal
and hypertensive descriptive
categories (Box, "Classification
of Adult Blood Pressure ...").
The JNC-V guidelines also include a systolic component in
the definition of hypertension,
which was not recognized in
previous guidelines. Additional
chemotherapeutic agents, such
as a-blockers and oc-, blockers
that may be used as initial
monotherapy, have also been
added to the JNC-V guidelines
(Box, "Antihypertensive
Medications").
Since most causes of hypertension are unknown, the initial
medical workup consists of accurate blood pressure readings, a
complete medical history and a
thorough physical examination.
The goal of this workup is to define the severity of hypertension
JADA, Vol. 128, August 1997 1109

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Ohere have been significant

changes in recent years regarding the definition of hypertension. In 1993 the Fifth Report of
the Joint National Committee
on Detection, Evaluation, and
Treatment of High Blood
Pressure, or JNC-V, released
the most recent guidelines to be
used in evaluating hypertension.' In 1995, the American
Dental Association House of
Delegates amended a directive
to "develop guidelines for dentists on hypertension detection
and further promote the procedure through continuing education for dentists and their auxil-

DENTAL

D.M.D.

-CUNICAL POACTICE

W5g

SDIT'

DENA

SYTOIC
PRESSURE
(mm Hg)

DISOC
PRESSURE
(mm 1Hg)

< 130

< 85

No modification of dental care

130-139

85-89

No modification of dental care

;g; ;

140-159

90-99

160-479

100-109

No modification of,dental-4c,ae, medical

referral, infor m patient t
Selective dental care,* medical referral

180f-209

110-119

CATQRf

Norml

High normal

TREATWENT

Hypertension

jStage I
Stage II

Sta*e

III

Emergent nonstreseful procedixres,t

immediate medical referral/

Stage IV

2 210

2 120

Emergent nonstressful procedures,t

immediate medical referral

Selective dental care may include, but is not limited to, dental prophylaxis, nonsurgical periodontal therapy, restorative procedures and
nonsurgical endodontic therapy.
t Emergent nonstressful procedures may include, but are not Limited to, dental procedures that may help alleviate pain, infection or
masticatory dysfunction. These procedures should have limited physiological and psychological effects. An example of an emergent nonstressful procedure might be a simple incision and drainage of an intraoral fluctuant dental abscess. The medical benefits achieved by
performing emergent nonstressful procedures in stage Ifl and IV hypertensive patients should outweigh the risk of complications
secondary to the patient's hypertensive state.
*

and its associated risk of target

organ damage. The medical history focuses on personal and familial history of hypertension and
other predisposing factors. These
factors may include excessive alcohol intake, history of renal disease, stroke, other cardiovascular
diseases, diabetes, obesity and
smoking. As much as 95 percent
of hypertension has an unknown
etiology and is termed primary,
essential or idiopathic. Many factors are thought to play a role in
primary hypertension, including
heredity, environmental factors,
stress, sympathetic nervous system overactivity and other disease states.
FACTORS ASSOCIATED
WITH INCREASED BLOOD
PRESSURE AND
HYPERTENSION

Genetics. Most causes of hypertension are multifactorial, and

1110 JADA, Vol. 128, August 1997

current research focuses on

characterization of possible biochemical or physiological markers that may identify individuals

or groups with a predisposition
for hypertension. Population
studies have shown a direct
quantitative relationship between increased arterial pressure and hypertension in firstdegree relatives.4 One study has
shown that people with two or
more first-degree relatives with
hypertension that developed before age 55 years have a 3.8
times increased risk of developing hypertension before age 50
years.5 The specific nature of
these inherited abnormalities
continues to be investigated and
debated, and includes research
into cellular membrane transport systems, renin-aldosteroneangiotensin system and the effects of increased activation of

the sympathetic nervous system.6 Further study is needed to

determine the role of genetically
mediated hypertension.
Researchers have noted a
racial correlation with hypertension, especially among
African-Americans.7 It is largely
believed that lower socioeconomic status and reduced access to health care are partially
responsible for this phenomenon.8-1' Other theories regarding the differences in hypertension prevalence between
whites and African-Americans
have been put forward. AfricanAmericans tend to retain sodium more than other groups,
and consequently experience a
greater rise in blood pressure
when given specific salt
loads.12'1' African-Americans are
noted to have lower plasma
renin levels than other groups,

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consultation

CLINIAL

PHA CIICE

-i

~UCi4A4

OIACINAW0PYIOOIALEFC
.l

i.

1.

%..

Inhibit sodiu adchord transport; decrease ple'asma

and e4xtracliarflidvolumie; decrease cardiacmotu

Potassilu"a-sparinag

Inhibit sodium
n andt Chloride reabsorption
4 bY- increasinmg
potass3iuam eXcretio
P'revent potassiumi -loss either throuigh diirect in]hibitionM Of
secretion! or truhatgnzn lotrn

smooth ~muscle In walls of peripheral arteOrioles;

decrease prheal resitstance and, decrease blood

Dir4~~~ct ~Rele10

preissure

Interfiaere- with

Angiotenskin-convertin
e-nzyme Iinhibitors

Inhibit renin-aldosterone system; interfere with the con'versio,n of aniotezzein -angiotensin JII ~(powexrful vasoconstrictor); remove the direct -vaLsoconstrictingK efct Of ancese in blood pressure
gioten'sin II, casn

Angiotensin I1I receptor

Cause vatsodilattatio; edu-Cie aldosterone anxd anatidiur-etic

hormone levels; in-hibit sodiuam reabsorption

blockers,

mnuscle; decrease peripheral vascula'r resistance

Adr.n.rglc nhibitig

Peripheral'

IMay block stor-age of norepinephrine so less is available

eve
of adrenri
rcuerelease of
norepinephrine, dcepAleting ~the storage supply; dlecrease in
sympathetic tone;,d~crease in peripheral vascula-r
on stimulation

resistance

Central oc-agonists

]Decrease in peripheral resistanice thr-ough depressor

symapathoinhibitory mechanismns; dlecr-ease in symxpathetic
acti-vity with lower norepinephrine; decrease in plasma
renini levels

cz-adrenergic blockers

Block activation of postsynaptic cx-i- receptors (normxially

induces vasoconstriction); decrease ina peripheral
resistance; some agents may also lower blood pressure
through direct arterial di'lation

f3-adrenergic blockers

Inaterfere with symnpathetic vasocon-strictor ner-ve acti-vity;

reduce cardiac output

which causes the renal excretion of sodium to be delayed and

a subsequent elevation in blood
pressure. The higher prevalence
of hypertension in AfricanAmericans most likely reflects
both genetic and environmental
factors.
Environmental factors.
Environmental factors influencing hypertension include high

sodium intake, excessive alcohol

consumption, physical inactivity and tobacco smoking.
Excessive sodium intake induces hypertension through an
increase in fluid volume and cardiac preload, resulting in an increased cardiac output. Large
studies have shown a direct relationship between the level of salt
intake, level of blood pressure

and incidence of hypertension.'4

The long-term daily con.sumption of large amounts of
ethanol has been associated
with blood pressure elevation.'15
The effects of mild or moderate
ethanol consumption on blood
pressure are not fully understood. The response is described

J-shaped dose-response relationship, with moderate

as a

JADA, Vol. 128, August 1997 1111

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calcum-depe*ndent conitraction of smooth

Calcium antagnit's

_-CLINICAL PRACTICE-

1112 JADA, Vol. 128, August 1997

Stress. Stress can raise

blood pressure readings acutely
and may contribute to hypertension. Timio and co-workers
showed that blood pressure remained normal among secluded
nuns over a 20-year period,
while it rose with age in women
not living in this order in the
same geographical area.22
Individual responses to stress
rather than the stress itself
may enhance the development
of hypertension. Studies have
suggested that hypertensive patients have a greater intensity

Hypertensive patients

who drnk alcoholic

beverages should be
counseled to limit
consumption to less
than I ox of ethanol
daily, which has been
associated with a significant decrease in
blood pressure.

of anger and hostility together

with a tendency to suppress
their anger.23
The role of psychological stress
in hypertension remains unclear,
however. Its effects are likely to
depend on three factors: the nature of the stressor, its perception
by the person and his or her
physiological susceptibility.24
"White coat" hypertension,
first described in 1940, is a phenomenon in which blood pressure readings are higher at a
clinic or medical office than
they are at home. The etiology
is obscure and patients do not
exhibit abnormal cardiovascular
responses to pressure stimuli;
however, researchers postulate
that the anxiety and tension as-

sociated with a medical visit

may be responsible for the increased blood pressure.25
White coat hypertension has
been considered a relatively benign condition until recently,
when it was shown that these
patients had diastolic left ventricular dysfunction and similar
abnormalities in elasticity, compliance and stiffness of the
large arteries as those seen in
hypertensive patients.26 Clinical
trials may show that cardiovascular morbidity and mortality
may be reduced with antihypertensive treatment in patients
with white coat hypertension.
Nitric oxide. The recent
data regarding nitric oxide, or
NO, as an important regulator
of many biological functions
such as vascular tone, platelet
activation and neurotransmission may explain the pathogenesis of hypertension and hemostatic changes associated with
this disease. Nitric oxide synthase, the isoform of the enzyme
that catalyzes production of NO,
has been identified in peripheral, nonadrenergic, noncholinergic nerves innervating the gastrointestinal tract and blood
vessels.27 Continuous generation
of NO mediates underlying vascular smooth-muscle relaxation,
thereby causing a decrease in
total peripheral resistance and a
decrease in systemic blood pressure. The lack of NO will cause
the opposite effect and hypertension. Endothelial-derived NO
inhibits platelet adhesion and
aggregation and disaggregation
of preformed platelet aggregates,27 and may promote prolonged bleeding.
SECONDARY
HYPERTENSION

Approximately 5 percent of hypertension may be directly re-

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drinkers (1 ounce of ethanol per

day) having lower systolic and
diastolic blood pressures than
abstainers or heavy drinkers.15
Alcohol consumption also
causes resistance to treatment of
hypertension. These effects may
be a result of cell membrane alteration, which possibly inhibits
sodium transport'6 or allows increased amounts of calcium to
enter the cell.'7 Hypertensive patients who drink alcoholic beverages should be counseled to limit
consumption to less than 1 oz of
ethanol daily, which has been
associated with a significant decrease in blood pressure.'8
Physical inactivity has also
been implicated in increased
risk of developing hypertension,
while physical activity has been
shown to lower blood pressure
in hypertensive patients.'9 In
addition, physical activity may
protect against cardiovascular
disease through the prevention
of hypertension.
Tobacco smoking has most recently been implicated in blood
pressure elevation.20 A transient
rise in both systolic and diastolic
pressure may last for 15 to 30
minutes after smoking and may
result from the release of norepinephrine from the adrenergic
nerves. Continual smoking,
however, can result in sustained elevated blood pressure
readings in patients who generally smoke one pack per day or
more. Cigarette smoking alone
is a powerful and independent
risk factor for stroke.2' In combination with hypertension,
cigarette smoking has been
shown to produce a 10- to 20fold increase in risk of stroke
compared with that for normotensive nonsmokers.2'
Cigarette smoking also contributes to the incidence of
other cardiovascular diseases.

CLINICAL

EFFECTS OF
HYPERTENSION

Adequate arterial pressure is

required so sufficient amounts
of blood, and the oxygen and
nutrients it carries, may perfuse through capillaries and
into tissues to supply the
metabolic needs for the maintenance of life. However, continuously high arterial resistance
results in increased workload
on the heart, which may lead to
left ventricular hypertrophy
and congestive heart failure.

Angina pectoris, a precordial or

radiating tight pain to the
shoulder, arm or jaw, due to excessive myocardial oxygen demands, may also occur.
Long-standing hypertension
can cause both retinal and central nervous system changes.
Retinal changes may be observed directly; increasing hypertension severity is associated with retinal hemorrhage.
Papilledema, a condition causing venous congestion and
edema of the optic disk secondary to increased intracranial
pressure, may also occur and
produces blurry vision and
blindness at a late stage.
Neurological symptoms associated with hypertension include
dizziness, lightheadedness, tinnitus and occipital headaches,
especially in the morning.
Prolonged untreated hypertension can also lead to renal insufficiency caused by atherosclerotic lesions.
Patients may not readily detect the gradual onset of symptoms or long-standing symptoms; therefore, if the clinician
suspects long-standing untreated hypertension, a thorough review of systems is indicated.
MEDICAL TREATMENT
OF THE HYPERTENSIVE
PATIENT

Once a diagnosis of hypertension has been made and further

medical workup has evaluated
targeted organ damage, the disease must be medically managed. Therapy is instituted essentially to reduce the chance of
target organ damage occurring.
Initial treatment of high normal
to stage II hypertension involves patient education and
lifestyle modifications to reduce
contributing factors, such as
obesity, physical inactivity, ex-

cessive ethanol use and excessive sodium intake (Box,

"Factors Associated With High
Blood Pressure Reduction or
Protection"). Once valid attempts at lifestyle modifications
have failed, practitioners turn
to pharmacological agents to
treat hypertension (Box,
"Antihypertensive Medications").
The goal for pharmacologically controlled hypertension is to
reduce blood pressure readings
by at least 10 percent in patients with stage I and stage II
hypertension.33 There is little
difference in efficacy between
the currently available drugs.34
Individual responses to treatment do vary and all patients
should be re-evaluated regularly to determine the effectiveness of their drug therapy. This
re-evaluation includes home
blood pressure monitoring and
a review of side effects associated with the antihypertensive
medication. In treating hypertensive patients, practitioners
should lower blood pressure
gradually to allow maintenance
of blood flow to the vital organs
while preventing ischemia.3536
According to the 1988 JNC-IV
guidelines, medical treatment of
hypertensive patients used a
stepped-care approach in which
initial therapy included a diuretic, ,B-adrenergic blocking
agent, angiotensin-converting
enzyme, or ACE, inhibitor or
calcium antagonists. If control
was not achieved within a 3month period, the drug dosage
was increased and/or another
drug from a different class was
added to the treatment regimen.
If control was still not achieved
after another 3 months or less, a
third drug could be added or a
second drug could be substituted. This treatment strategy was
rather effective in reducing
JADA, Vol. 128, August 1997 1113

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lated to a specific cause.

Treating the disease in these
patients differs from that for essential hypertension and focuses on the underlying disease
factor.
Causes of secondary hypertension include renovascular
stenosis, pheochromocytoma,
coarctation of the aorta and
mineralocorticoid excess.
Mineralocorticoid excess also
causes hypertension through
stimulation of excessive aldosterone release. Aldosterone is
involved in increased plasma
volume and sodium retention,
which causes hypertension.28
Estrogen-containing oral contraceptives have also been associated with hypertension.29
Estrogen stimulates angiotensinogen, which is converted to angiotensin I and angiotensin II, which further
stimulate secretion of aldosterone.30-32
Pregnancy has been associated with hypertension, and hypertension occurs in more than
5 percent of pregnancies. The
causes of gestational hypertension are not completely known
but may be related to a progressive increase in plasma and extracellular fluid volume with an
increase in cardiac output.

RACIICE

-CLINICAL PRACIICE

od pressure, especially in; peoip -1

Reduct*ionof
per P
o xe b
c
dea weigh enhnce
gI
if
antiKypar te:;ivedrugsS;
;;0EX y

4se4svalcho intake may incre od peuea

caue rei

to ahpertensive terapy

Avoid tobacco

blood pressure levels, but it did

have certain shortcomings.
The stepped-care approach did
not realize that hypertension resistant to treatment with one
type of drug may be treated effectively with a different drug class
before combined therapy is instituted. The stepped-care approach
also failed to realize certain longterm complications of drug therapy, such as decreased insulin
sensitivity and an increase in
plasma lipids in patients.
The current medical recommendations for treating hypertension are less structured and
use information from many
large antihypertension treatment trials. For example, recent
trials have shown that low-dose
diuretic treatment37 and use of
,-blockers can reduce the incidence of coronary complications
and cerebrovascular incidents.38
Other studies have shown that
,Bblockers were most effective
in lowering blood pressure in
white patients younger than
age 40 years, while calcium an1114 JADA, Vol. 128, August 1997

Tobacco use increases the risk of stroke and contributes to

cardiovascular disease

tagonists were more effective in

lowering blood pressure in
African-Americans than were
ACE inhibitors or n-blockers."
The current recommendations of JNC-V incorporate the
data from these types of trials
into more individualized treatment regimens. Recently, the
U.S. Food and Drug Administration approved a new class
of antihypertensive agents-angiotensin II receptor (type 1)
blockers. These new agents are
not included in any of the JNC
guidelines. Losartan potassium,
the new agent, works through
blocking angiotensin II receptors in the vascular smooth
muscle, brain and adrenal
glands, resulting in vasodilatation, natriuresis and diuresis.4'
There are no known dental-related implications associated
with this agent.4'
ANTIHYPERTENSIVE
MEDICATIONS

Medications used in the treatment of hypertension can have

untoward side effects that may

influence the provision of dental
care. Practitioners should be familiar with the mechanism of
action of these medications as
well as the potential complications and interactions arising
from their use (Tables 1 and 2).
Gingival overgrowth has been
reported in patients receiving
calcium channel antagonists.
This condition is classically described as multilobulated enlargement of the buccal and lingual gingiva, most often noted
in the anterior region, and reported to occur within 1 to several months of initiation of drug

therapy.4'
Histologically, there is a proliferation of fibroblasts, and a
nonspecific chronic infiltration
and modification of the endothelium have been noted in this hyperplastic connective tissue.4"
Similar findings have been
noted in patients prescribed
phenytoin and cyclosporine,
sodium valproate and phenobarbital.4'45 A reduction in the

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Moderate lervel of physical fitness may enhance weit loss

and reduce risk of cardio-vascular disease

CLINICAL PRACTICE
TABLE I

|111,1!I

lEll""11g.1K11111g E,l1.
9It]|1Xl1|111#!X1111
:=r=~~~~~~~~~~~~~~~~~4ksmfli"
OFtAML IEIFIFIUG

AJO I II.Y?..?I U

UYW5W. WI5DI.iI.7 I..FU4

Central oc-agonists

alterationt-

A:ngiotensin-converting

Taste

Calcitim chainnel antagoniists

Gingival overgrowth

enzyme iihibitors

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free cystolic calcium in T-lymphocytes and fibroblasts caused

by the interference of certain
hypotensive agents such as calcium channel antagonists and
other agents such as phenytoin
and cyclosporine has been postulated by some authors46 to
alter the homeostasis of collagen and result in enlarged gingivae.
Gingival surgery remains the
best treatment for extensive
gingival overgrowth caused by
calcium channel antagonists. A
change in drug treatment may
be desirable, especially if the
gingival overgrowth recurs.47
Excellent oral hygiene practices
and frequent periodontal appointments may lessen the occurrence of the overgrowth.48

sponta

ANTI HYPERTENSIVE
MEDICATIONS AND
NSAIDS

TABLE

Nonsteroidal anti-inflammatory
drugs, or NSAIDs, have become
some of the most frequently
prescribed medications.49 Of the
nearly 50 million patients in the
United States receiving antihypertensive therapy,50 possibly 12
million concomitantly use
NSAIDs on a long-term basis.5
It is estimated that a total of
more than 20 million medically
treated hypertensive patients in
the United States receive
NSAID therapy on either a
long- or a short-term basis,51including use for odontogenic
pain.
NSAIDs attenuate the antihypertensive actions of diuretics,12 53-blockers, 5 ACE inhibitors,55 central agonists,56
vasodilators5457 and a-blockers.5
In a meta-analysis of 50 trials
studying the relationship between NSAID use and blood
pressure, the authors noted a
mean arterial pressure increase

of 5 mm Hg.58 This small sustained increase in arterial pressure is clinically relevant. A 5 to

6 mm Hg increase in diastolic
blood pressure over an extended
time may be associated with a
67 percent increase in total occurrence of stroke and a 15 percent increase in coronary heart
disease in normotensive and hy-

pertensive patients.59
Standard anti-inflammatory
dosages were evaluated in this
meta-analysis, which also found
that NSAIDs did not appear to
increase salt and water retention but may cause effects
through increased peripheral
vascular resistance and cardiac
function.58
JADA, Vol. 128, August 1997 1115

-CLINICAL PAACTIIE
It may be prudent for practitioners to recommend shortterm NSAID therapy or other
analgesic agents for patients
using n-blockers, vasodilators,
diuretics, a-blockers, central aagonists or ACE inhibitors.
DENTAL TREATMENT
OF THE HYPERTENSIVE
PATIENT

1116 JADA, Vol. 128, August 1997

ITwng patients with

Iwellcontrolled hypertension genlly
poses little difmulty
for the dental team
and involves minimal
deviaton from normal
ent care protocols.
Local anesthetics containing epinephrine. Clinical
studies on epinephrine-containing local anesthetic solutions
have consistently shown negligible influences on blood pressure in hypertensive patients.
Numerous studies in young
healthy patients with no known
history of cardiovascular disease show that injection of local
anesthetic with epinephrine is
associated with an increased
plasma epinephrine level but no
corresponding significant hemodynamic effect.6768
Davenport and co-workers67
evaluated epinephrine effects
on elderly patients with stable
cardiovascular disease who underwent periodontal surgery
and found elevated plasma

epinephrine levels after injection of a local anesthetic. These

elevated levels again failed to
produce a significant change in
heart rate or mean arterial
blood pressure.
Schechter and co-workers69
described the physiological effects of direct intravenous epinephrine infusion into 39 adult
patients being evaluated for
chest pain. A total amount of
0.105 milligrams of epinephrine
infused during a 5-minute period produced minimal cardiovascular effects. This is equivalent
to 5.8 cartridges of dental anesthetic solution containing epinephrine at a concentration of
1:100,000 (that is, 0.018 mg of
epinephrine per cartridge of
anesthetic solution).
Schechter and co-workers
found a mean increase in systolic
blood pressure of 36 mm Hg, a
mean decrease in diastolic blood
pressure of 7.0 mm Hg and a
mean heart rate increase of 13.9
beats per minute. All physiological changes returned to normal
levels within 15 minutes of
epinephrine administration.
Subsequent testing found that
23 of these patients (59 percent)
had significant coronary artery

disease."'
Epinephrine is included in
the anesthetic solution to delay
systemic absorption, which increases the duration and profoundness of anesthesia. The
preponderance of data in regard
to epinephrine-containing local
anesthetics shows that blood
pressure and heart rate are
minimally affected by the typically low doses and short-term
use of the drug in dentistry.
Furthermore, the exogenous
epinephrine contained in anesthetic solution may actually
help prevent the release of excessive endogenous epineph-

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Dentists should inform patients

that hypertension may have serious health consequences and
necessitate changes in their
dental treatment.2 Dental care
should focus on the actions, interactions and adverse effects of
antihypertensive medications
and the prevention of hypertensive crisis. Treating patients
with well-controlled hypertension generally poses little difficulty for the dental team and
involves minimal deviation
from normal patient care protocols.
Preprocedural monitoring of
blood pressure is recommended
for all patients and is especially
important for those with a diagnosis of hypertension. Dental
practitioners who find large
variation from normal blood
pressure ranges should report
the results to the primary
health care practitioner, and
ask the patient if he or she is
complying with the treatment
protocol. Dental practitioners
should measure blood pressure
at every visit for known hypertensive patients and at least
once per year for all other patients without cardiovascular
risk factors.
Patients who are using antihypertensive medications, particularly diuretics and agents
that are anticholinergic or have
anticholinergic effects, are at
increased risk of developing
root caries.60'61 This may be a re-

sult of decreased salivation,

which occurs secondary to administration of these medications. We strongly recommend
that practitioners educate patients about the importance of
improving oral hygiene; increased frequency of recall examinations may also be advisable.62 Additionally, the use of
sodium fluoride,63 1 percent
chlorhexidine gel64'65 or chlorhexidine fluoride mouthrinses66
may be advisable for patients
who have extensive caries and
diminished salivary gland function.

CLINICAL

pressure is associated with the

hours surrounding awakening
that peaks by midmorning,7",7
afternoon appointments for hypertensive patients are desirable. Fluctuation of blood pressure associated with a diurnal
rhythm is less likely to occur
during afternoon sessions.
Orthostatic hypotension.
Dental health care providers are
also concerned with preventing
orthostatic hypotension.
Orthostatic hypotension is defined as a decline in blood pressure that occurs on moving from
a recumbent to a standing position, and may be associated with
dizziness and syncope as a result of cerebral hypoperfusion.
Nonautonomic causes of orthostatic hypotension may include
use of certain antihypertensive
medications, particularly those
that affect sympathetic activity
of intravascular volume.
Antihypertensive agents may
produce orthostatic hypotension
by reducing sympathetic outflow or peripheral vasodilatory
actions, and include centrally
acting x-2-adrenergic agonists
(methyldopa, clonidine), postganglionic adrenergic inhibitors
(guanethidine) and a-1-adrenergic antagonists (prazosin and
terazosin).
Depletion of intravascular
volume by excessive diuresis
may also result in orthostatic
hypotension.74 In the dental setting, supportive measures are
usually adequate to manage orthostatic hypotension. Patients
who may be prone to this problem should avoid rapid postural
changes. Care should be taken
when patients are returned
from the supine position, and
patients should remain seated
for a short period to allow adequate cerebral perfusion to
occur.

Oral bleeding. The relationship between elevated blood

pressure and oral bleeding is
unclear. Although anecdotal evidence suggests that elevated
blood pressure causes increased
bleeding tendencies, there are
few documented cases. One case
of oral hemorrhage 8 days after
periodontal surgery in a hypertensive, nonpharmacologically
compliant patient was brought
under control with hypotensive
agents.7' The relationship between epistaxis and elevated
blood pressure is also unclear.
Researchers are divided into
those who believe that nasal
bleeding is a symptom of elevated blood pressure and those
who believe that bleeding is the
result of local factors such as
trauma.76-79
In hypertension, the arterial

system is exposed to increased

pressure flow but the complications are mainly thrombotic
rather than hemorrhagic. Miller
and colleagues recently noted
that angiotensin II, a potent
vasoconstrictor, is also a potent
intra-arterial procoagulant8'
and that hypertensive patients
are hypercoagulable.8' Such an
intravascular prothrombotic
state may contribute to the development of atheromatous lesions, especially since endothelial dysfunction may also be
present.8' The effects of endothelial-derived NO may promote prolonged bleeding
through inhibition of platelet
adhesion and aggregation and
disaggregation of preformed
platelet aggregates.27
The mechanisms of rheological abnormalities in hypertensive
patients are unclear; however,
there is clear evidence that whole
blood and plasma viscosity is increased in patients with hypertension.82 Further study of the reJADA, Vol. 128, August 1997 1117

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rine. Less-than-profound anesthesia has been associated with

increased release of endogenous
epinephrine. The benefits of the
small doses of epinephrine used
in dentistry, when administered
properly, far outweigh the cardiovascular disadvantages.
Patients with stage I to stage
II well-controlled hypertension
who use antihypertensive medications tolerate regular doses of
local anesthetic that contain
epinephrine. Dentists should
use an aspirating injection
method and avoid intraligamentary and intrabony injections.
They should avoid using anesthetic solutions with vasoconstrictors in patients with uncontrolled hypertension, and
elective dental procedures are
contraindicated.7' Furthermore,
using an epinephrine-impregnated retraction cord in this patient population is absolutely
contraindicated. There are reports in the literature of vasopressors and nonselective ,blocker interactions possibly
precipitating a hypertensive
episode.6' Consequently, dental
practitioners should avoid administering local anesthetics
with vasopressors in patients
using nonselective f-blockers
when possible.
Dental anxiety. The dental
team should strive to produce
an anxiety-free atmosphere for
all dental patients, but particularly for hypertensive patients.
Anxiety and psychosocial stressors have been linked to increases in blood pressure.7'
Dental practitioners may find it
beneficial to premedicate this
anxious population with an anxiolytic agent the evening before
and the morning of the dental
appointment68; nitrous oxide, if
available, may also prove beneficial. Since an increase in blood

PRAGTIIE

-C[INICA[ PRACTICE

1118 JADA, Vol. 128, August 1997

(within 1 hour) in blood pressure and must be evaluated by

a physician to prevent catastrophic central nervous system,
cardiac and renal injury. These
patients should be treated with
intravenous drugs and must be
monitored continuously.83 A reasonable goal for most hypertensive emergencies is to lower the
diastolic blood pressure to 100
to 110 mm Hg.36
Screening patients. Dental
heath care workers should
screen their patients for elevated blood pressures. However, elevated blood pressure alone
does not constitute a diagnosis
of hypertension. Dentists need
to be familiar with the risk factors associated with hypertension to counsel their patients.
Since hypertension is a common
finding among the adult population in the United States, dental practitioners should have
sufficient knowledge to provide
comprehensive oral care. A diagnosis of hypertension may require changes in how dental
care is provided, but rarely is
the dental procedure itself affected. We recommend that
long-term NSAID use be avoided and dental appointments be
scheduled for afternoons.
Furthermore, dental practitioners should
| keep in mind
that hypoten-

ur.

wuzyka

s an as-

sistant professor of
Oral Diagnosis,
Medicine and
Radiology, Loulsiana
State Universlty
Medical Center,
School of Dentistry,
1 100 Florida Ave.,
New Orieans, La.
70119.2799. Address
reprint requests to
Dr. Muzyka.

Dr. Glck Is director,

Programs for

Medically Complex
Patients, Department
of Oral

Medicine,

University of

Punnsyivania, School
of Dental

Modicine,

Philadelphia.

sive medications may be accompanied by adverse effects.84'85

CONCLUSION

Dental practitioners should not

provide elective dental care to a
hypertensive patient with a 20
percent increase in known baseline blood pressure values or to
patients in whom stage III or
stage IV hypertension may be
present until they consult with
the primary physician. All patients with elevated blood pressures should be counseled and
referred for medical workup, especially if they are not being followed up by a physician. All patients with blood pressures that
are consistent with stage III or
stage IV hypertension should be
referred immediately to a physician to prevent catastrophic occurrences. a
1. Joint National Committee on Detection,
Evaluation and Treatment of High Blood
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Evaluation, and Treatment of High Blood
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2. 1995 Transactions. Oct 7-11, 1995, Las
Vegas: American Dental Association Annual
Session. Chicago: Americal Dental
Association; 1995:610-3.
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Evaluation and Treatment of High Blood
Pressure. The 1988 report of the Joint
National Committee on Detection,
Evaluation, and Treatment of High Blood
Pressure. Arch Intern Med 1988;148:1023-38.
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al. Current knowledge regarding the genetics
of human hypertension. J Hypertens

1989;7(Supplement):s8-s13.
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lationship between increased

blood pressure and bleeding tendencies is warranted.
Only 24 percent of hypertensive
Americans have blood pressures
below 140 mm Hg systolic and 90
mm Hg diastolic.72 Approximately
55 to 60 percent of known, medically treated hypertensive patients have uncontrolled conditions. Although no standard
exists that outlines the effects
of increased blood pressure on
dental treatment, we believe it
is prudent for dental practitioners to defer nonemergent dental
care in hypertensive patients
with a known baseline blood
pressure elevation of 20 percent
over normal levels until they
consult with the primary health
care provider.
Physician referrals. In patients with stage III or IV hypertension, all dental treatment
should be limited to emergent
care, preferably including the
use of antibiotics and oral analgesics, until the dentist consults
further with the physician (Box,
"Classification of Adult Blood
Pressure..."). Furthermore, dental practitioners should immediately refer patients with such
elevated blood pressures to a
physician because they may be
subject to a hypertensive crisis
(defined as a diastolic blood
pressure above 120 mm Hg).
Although hypertensive crises
occur in less than 1 percent of
the hypertensive population,
they are seen among patients
who do not comply with medical
therapy or who are receiving inadequate medical treatment.36
Hypertensive crises are considered emergencies in the presence of end-organ damage or urgent in the absence of endorgan damage. Patients with
hypertensive emergencies require an immediate reduction

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