The deliberate reduction of blood pressure in an attempt to reduce intra-

operative blood loss has generated significant controversy in the 30 years

since its clinical introduction. Numerous series have been reported, but few
have met generally accepted, current criteria for controlled studies. In this
article, the effect of blood pressure reduction on organ perfusion will be
presented together with a review of techniques of achieving hypotension.
A summary of results is included and, based on this data, recommendations
are offered regarding the application and limits of deliberate hypotension.
HEAD & NECK SURGERY 2:185-195 1980

DELIBERATE HYPOTENSION
IN HEAD AND NECK SURGERY
C. F. WARD, MD, DAVID D. ALFERY, MD,
L. J. SAIDMAN, MD, and J. WALDMAN, MD

Deliberate hypotension is the intentional reduc- INDICATIONS

tion of blood pressure below the level that is nor-
mally associated with a surgical plane of anes-
thesia. The introduction of this concept of reducing
intraoperative blood loss is generally attributed
to G a r d n e ~ -who
, ~ ~ reported his results in 1948;
however, as early as 1928 KosteP attributed a
dry surgical field to a reduction in blood pressure.
In the 30 years since Gardner’s report, contro-
versy has continued regarding the definition of,
and the indications for, this technique.
This article reviews the indications, physiol-
ogy, methods, and results associated with delib-
erate hypotension and offers specific recommen-
dations regarding blood pressure reduction during
surgery. This information should allow the reader
t o evaluate the usefulness of deliberate hypoten-
sion and should clarify why the controversy re-
mains unresolved.
From the Department of Anesthesia, School of Medicine, University of
California. San Diego, San Diego. CA
The authors wish to acknowledge with appreciation Harvey Shapiro, MD,
for reviewing the manuscript, and Cathie Drew, Christina Lloyd, and Ann
Wargo for administrative assistance
Address reprint requests to Dr Ward at the Clinical Teaching Facility, T-
001 University of California Medical Center 225 Dickinson S t , San
Diego, CA 92103
Accepted for publication August 8, 1979
0148-64031020310185 $00 OOiO
‘ 1980 Houghton Mifflin Professional Publishers
The intent of deliberate hypotension is to reduce
bleeding and thus facilitate surgery and/or to de-
crease the amount of blood transfused. In certain
surgical procedures, notably middle ear surgery,
the amount of bleeding does not have to be great
to obscure the operative area and jeopardize suc-
cess. In other procedures, a dry field may result
in a more definitive removal of a neoplasm as well
as in less damage to adjacent vital structures.
Finally, trauma and tissue infection are mini-
mized because fewer sutures are required and less
electrocoagulated, devitalized tissue remains in
the wound.
The use of deliberate hypotension may de-
crease the amount of blood that must be trans-
fused. Although routine screening for Australian
antigen and the elimination of paid donors has
reduced the morbidity of blood transfusion, cer-
tain other risks still exist.” The incentive to re-
duce the amount of blood lost is increased when
patients have rare blood types, are difficult to
crossmatch, or refuse tranfusion.
Additional advantages of deliberate hypoten-
sion are: (1)it may reduce the time required to
, ~ ~(2) it may make “im-
perform the ~ p e r a t i o nand
possible” procedures, such as an intracranial
aneurysm clipping, possible.
The decision to employ deliberate hypotension
is a joint understanding between surgeon and
anesthesiologist. The suggestion for its use should

Deliberate Hypotenston HEAD & NECK SURGERY JaniFeb 1980 185

originate well in advance of surgery, and either
party should be able to veto the plan if the patient
is considered a poor risk, if the benefits to be
gained are not sufficient to warrant its use, or if
the anesthesiologist’s experience with the tech-
nique is inadequate. The request for, and decision
to use, a hypotensive technique should rarely-if
ever-be initiated after surgery has begun.
CONTRAINDICATIONS
Contraindications to deliberate hypotension in
most instances are relative and should be weighed
against the possible advantages in each particu-
lar case. For example, the presence of cerebro-
vascular disease does not preclude its use in sur-
gery for an intracranial aneurysm, although it
might be an unwise technique for other less se-
rious procedures (e.g., middle ear surgery) when
there is cerebrovascular disease.
In general, cerebrovascular disease, myocar-
dial ischemia, peripheral vascular disease, severe
renal or hepatic disease, and hypovolemia are rel-
ative contraindications to deliberate hypoten-
s i ~ n . ~In
* , patients
~~ with these disorders, the
technique is limited to those procedures that are
essential to saving life or that are impossible or
futile because of the amount of hemorrhaging ex-
pected. Other relative contraindications include
hypertension, anemia, fever, and diabetes melli-
tus with significant small vessel disease. Finally,
an anesthesiologist’s inexperience with the tech-
nique is the least appreciated and perhaps the
most important contraindication to its use.3*
ORGAN PERFUSION DURING DELIBERATE
HYPOTENSION
The effect of deliberate hypotension upon organ
perfusion depends upon the relationship of blood
pressure to blood flow. Flow is a function of both
mean arterial pressure (MAP) and autoregulation
in the cerebral, myocardial, pulmonary, and renal
beds. However, MAP alone controls hepatic per-
fusion. MAP may be approximated by the follow-
ing formula: MAP = (Systolic Pressure) + 2 (Di-
astolic PressureY3. In this regard, a major failing
in many clinical reports is the presentation of sys-
tolic pressure only, which prevents this conver-
sion. Using the concept of MAP (rather than sys-
tolic pressure), the physiology of the five perfusion
systems must be examined separately to deter-
mine which is the critical “weak link,” i.e., the
system that sets the minimum permissible
pressure.
186 Deliberate Hypotension
Cerebral Circulation. The discussion of this subject
is somewhat extensive, for we feel that perfusion
to the brain is the critical factor that limits MAP
reduction. This statement is based on two lines of
reasoning: (1) complete cerebral function is inor-
dinately difficult to estimate intraoperatively,
even with an electroencephalogram (EEG), thus
rendering the assessment of circulatory adequacy
speculative, and (2) even minimal derangements
in postoperative function of this organ are
unacceptable.
Through the mechanism of autoregulation,
normal cerebral blood flow (CBF) is maintained
constant at 45-50 m1/100g/min through a MAP
range of 50-150 torr, provided that arterial pres-
sures change gradually40 (fig. 1). The absolute
value for CBF below which cerebral ischemic hy-
poxia occurs is not known, but several studies
have allowed some estimate to be made. Sundt
et a1 measured CBF with Xenon133 and
simultaneously-recorded electroencephalograms
(EEG) during carotid endarterectomy with halo-
thane anesthesia and normocapnia. They found
no EEG changes indicative of ischemia if CBF
was above 25 m1/100g/min.60~6s If this flow rate is
taken as a critical limit, i t is possible to estimate
a critical perfusion pressure below which is-
chemia might occur in conscious humans (fig. 1).
However, several factors under the control of the
anesthesiologist modify the calculation. Volatile
anesthetics (halothane, e d u r a n e ) shift the entire
autoregulation curve to the leftlo and modify the
shape of the curve in a dose-dependent manner
(fig. 2). Hypercarbia increases overall CBF,’O while
hypocarbia plus thiopental decrease it.52
A final difficulty arises in the discussion of the
control of CBF when overall flow is contrasted to
regional flow. In regions of marginal flow, local
factors such as hypoxia or acidosis may predom-
inate, which may cause maximal dilation of ves-
sels in the area. Since the skull limits the volume
of blood that can be accomodated, events that in-
crease blood flow to areas of normal perfusion
may displace flow that previously went to areas
of marginal perfusion. Because of this uncer-
tainty of regional blood flow distribution, and an
inability to evaluate the impact of these factors,
a safety factor is inserted into the determination
of critical pressures. Assuming the use of a hal-
othane or enflurane anesthetic, an attendant shift
in CBF autoregulation, and an essentially normal
PaCO,, it should be safe to gradually lower
the MAP to 50 torr with no significant decrease
in CBF. Any further reduction in MAP requires
HEAD & NECK SURGERY JaniFeb 1980
 125
n
.
E
I
15
-E
\
-
25
Figure 1 , Cerebral blood flow (CBF) versus mean arterial pressure (MAP). Dashed line represents
minimum acceptable CBF versus MAP. Solid line remesents MAP of 50 torr, demonstrating no
reduction in CBF.
EEG monitoring to provide some estimate of ad-
equate perfusion. The minimum MAP of 50 torr
usually corresponds to a systolic pressure of 65-
70 torr.
The preceding discussion refers to the adult
patient; much less is known about the control of
CBF in the child. Extrapolation of laboratory data
in the fetal and the newborn coupled
with a normally lower MAP and an absence of
vascular disease in the child, all support the con-
cept that a MAP of 50 torr is acceptable.
The hypertensive patient deserves special
comment, since it has been shown that this pa-
tient population has an autoregulation curve that
is shifted higher a t both ends, proportional to the
elevation in resting MAP.66Theoretical safe lim-
its of hypotension may be calculated based on this
shifted curve. Also, a recent study has shown that
the risk of precipitating infarcts by hypotension
Deliberate Hypotension
I I I 1 I
75 125 115
MAP (torr)
is not increased in hypertensive patient^.^? How-
ever, these patients do present an increased risk-
even when a n elevated MAP is accounted for-
and hypertension therefore poses a relative con-
traindication to deliberate hypoten~ion.'~
Myocardial Circulation. Myocardial oxygen de-
mand is determined mainly by ventricular wall
tension, cardiac rate, and contractile perfor-
mance. Coronary blood flow is dependent upon
mean aortic blood pressure and coronary vascular
resistance.6 Control of coronary blood flow is au-
toregulated predominantly by means of altera-
tions in coronary vascular resistance that are
made t o meet myocardial oxygen demand. The
coronary circulation differs from the cerebral cir-
culation in that, as arterial pressure and cardiac
output fall, there is reduction in myocardial oxy-
gen consumption. However, patients with coro-
HEAD & NECK SURGERY JaniFeb 1980 187
 UPPER
LIMIT 8
HIGH DOSE
88
8
8-

I
8
8
I MODERATE DOSE
8
i 0-
8
8
0
/
8
/
U 8
8 0 iOW DOSE
m H8
0 0
/
0 I# 0 / /' I CONSCIOUS

50 150
MAP (torr)
F/gure 2 Cerebral blood flow (CBF) and volatile anesthetrcs Diagramatic presentation of the leftward
sh/ft of autoregulat/on with dose-dependent rnod/f/cat/onof the curve

nary artery disease may have some areas of the
myocardium that are entirely dependent upon
pressure t o supply adequate blood flow. Hypoten-
sion in these patients is accompanied by signifi-
cant risk of intraoperative myocardial i n f a r ~ t i o n . ~ ~tension. The probable mechanism involves a ven-
The electrocardiogram (ECG) provides a con-
stant, albeit imperfect, monitor of the adequacy
of coronary flow during deliberate hypotension.
Several studies have documented that transient,
nonspecific ST-segment and T-wave changes oc-
cur in patients with no known coronary artery
diseases while they are undergoing deliberate hy-
potension, but that there are no serious sequel-
ae;57*61*72
however, these changes may indicate that
the demandflow relationship has become unfa-
vorable. The appearance of definite ECG changes
indicative of ischemia suggests the need to reev-
aluate the indication for producing hypotension,
and it probably should be discontinued.
Pulmonary Circulation and Gas Exchange. De-
creased arterial oxygen tensions and increased
alveolar-arterial oxygen gradients have been ob-
served during anesthesia with deliberate hypo-
tilatiodperfusion mismatch in the lungs" as well
as an increase in physiologic dead space.3 Pul-
monary shunting is generally ~ n c h a n g e d As-
.~~
sumption of the head-up position and the use.of
agents that blunt hypoxic pulmonary vasocon-
striction (such as sodium nitroprusside-SNP)
further aggravate these En-
riched oxygen mixtures should be administered,
and controlled ventilation may be required when
deliberate hypotension is produced. Arterial blood
gases should be monitored; this is particularly a
course of action that should be taken with those
patients who are known to have a history of
preexisting pulmonary disease.

188 Deli berate Hypotension HEAD & NECK SURGERY JarVFeb 1980
Renal Circulation. The autoregulation that nor-
mally controls blood flow to the kidneys is abol-
ished during general anesthesia, and a decrease
in the renal blood flow and in the glomerular fil-
tration rate occurs as the result of even moderate
decreases in arterial pressures.3gUrine flow may
cease when systolic pressure falls to 70 torr
because the effective filtration pressure is lost.
The kidneys, however, are protected from paren-
chymal damage during deliberate hypotension
because the normal stratification of renal blood
flow is maintained and because there is no intra-
renal shunting.24 A series of patients who were
anesthetized with halothane and made pro-
foundly hypotensive (MAP of 40 torr) suffered no
apparent renal damage, despite cessation of urine
flow for periods in excess of one
Hepatic Circulation. As arterial pressure falls, there
is a reduction in hepatic blood f l o ~ . ~Addition-
~.'~
ally, anesthetic agents and techniques such as
halothane or subarachnoid and epidural blocks
may further diminish hepatic blood f l o ~ . ~Re- ,'~
gardless of this phenomenon, deliberate hypoten-
sion seems to be well tolerated by the liver, and
there are no reports showing morbidity or mor-
tality from hepatic hypoperfusion during delib-
erate hypoten~ion.'~
MONITORING
There are identifiable patient reponses that should
be monitored during deliberate hypotension, by
means of a t least:
Electrocardiogram
Temperature
Precordial or esophageal stethoscope
Blood pressure via oscillotonometer, ultrasound
pulse detection or arterial catheter
Other measurements are optional but may be ap-
propiate in certain cases:
Electronically determined mean arterial pressure
Trend recording on paper
Central venous pressure
Pulmonary artery catheter
Electroencephalogram
Right atrial catheter
Precordial Doppler monitor for air emboli
Urine output
The Riva-Rocca method is adequate for use
with Korotkoff sounds a t normal blood pressure.
However, it is inadequate for measuring very low
pressure3*and must be replaced by either a more
reliable indirect method (such as ultrasound pulse
Deliberate Hypotension
detections3or os~illotonometry~~) or preferably by
direct arterial pressure measurement. The latter
allows beat-to-beat observation of pressure, elec-
tronically determined MAP, trend-recording on
paper, and the availability of samples for testing
blood gases, hematocrit, and electrolytes. The
choice of technique for measuring blood pressure
will depend on the degree and duration of hypo-
tension desired. While a Doppler pulse monitor
would prove sufficient for a short period of hypo-
tension, direct arterial measurement is prefera-
ble for lengthy procedures.
The use of more intensive monitoring must
depend on the preoperative condition of the pa-
tient and the anticipated extent of the surgery. A
central venous-pressure catheter is considered es-
sential by many anesthetists, especially during
head and neck surgery, while a pulmonary arte-
rial catheter may be required in selected patients.
The addition of either of these monitors allows
the cardiac output to be measured via dye injec-
tion or thermal dilution, and potent hypotensive
agents such as sodium nitroprusside may be ad-
ministered directly into the central circulation.
EEG monitoring provides useful information con-
cerning general cerebral perfusion, but it is not
in common clinical use in most hospitals.
If the operative site is elevated 5-10 cm above
heart level, then precautions against air emboli-
zation are advisable. These include the insertion
of a right atrial catheter and the detection of in-
tracardiac gas via ultrasound. The ECG should be
continuously examined, particularly for those
leads most likely to reveal ischemia.35Finally, as
in other anesthetics the temperature, respiration,
and urine output (if appropriate) should be mon-
itored.
POSITION OF THE PATIENT
A hypotensive technique may reduce peripheral
circulation, and the blood flow may cease alto-
gether to areas overlying weight-bearing, boney
prominences. For this reason, a n additional sup-
portive pad should be placed beneath the patient,
with special attention paid to the occiput, scapu-
lae, sacrum, elbows, and heels. Damage to the
skin overlying these areas is probably a function
of both the duration and the degree of hypoten-
sion, and has not been reported as a complication
of deliberate hypotension per se. Also, pressure
must be kept off the orbits-especially if patients
are in the prone position-to avoid compromising
the retinal blood flow.
HEAD & NECK SURGERY JaniFeb 1980 189
METHODS
Arteriotomy and hypovolemia, which are the
methods Gardner initially used to produce delib-
erate hypotension, lead to intense vasoconstric-
tion and tissue hypoxia. This approach has long
since been abandoned for other methods, which
include:
Epidural or subarachnoid blocks
Volatile anesthetic agents
Enflurane
Halothane
Ganglionic blocking drugs
Pentolinium
Trimethaphan
Vasodilating agents
Sodium nitroprusside
Intravenous nitroglycerin
Additional drugs and methods
Chlorpromazine
Diazoxide
Propranolol
Atrial pacing
D-tubocurarine
Adjunctive techniques
Controlled mechanical ventilation
Positive and expiratory pressure
High subarachnoid or epidural block was ap-
plied in 1948 by Griffiths and Gillies to produce
widespread sympathectomy and hypotension, and
it constituted the first physiologic approach to the
production of deliberate h y p o t e n ~ i o nA
. ~ major
~ reports of sodium nitroprusside for control of blood
advantage is the ease of administering the block.
The disadvantages are: first, the difficulty of al-
tering blood pressure once hypotension is estab-
lished; second, the difficulty in accurately con-
trolling duration of hypotension; and finally, the
inability to rapidly terminate the hypotension
when necessary.
Pharmocologic Techniques. High concentrations of
potent inhalational agents (halothane or enflur-
ane) produce a dose-dependent fall in blood pres-
sure. The reduction of pressure is produced pri-
marily by myocardial depression, which is accom-
panied by a fall in cardiac and a variable
reduction in peripheral r e s i ~ t a n c e . ~Interest-
’~~
ingly, after more than an hour of halothane anes-
thesia, blood pressure and cardiac output tend to
return to the patient’s awake values, and this re-
quires increased concentrations of anesthetic to
maintain hyp0ten~ion.l~ Although the simplicity
of inhalation anesthesia is initially attractive,
the frequent requirement to “over-anesthetize,”
190 Deliberate Hypotension
together with a reduction in cardiac output and
the inability to reverse hypotension rapidly, make
the technique somewhat t r e a c h e r o u ~ .While
~~
these agents are useful in providing the anes-
thetic necessary for the performance of surgery,
they should be supplemented with other phar-
macologic techniques to produce deliberate hy-
potension. Halothane is contraindicated in pa-
tients with active hepatocellular disease.8 En-
flurane is relatively contraindicated in patients
with significant renal disease4nand, because of
EEG effects, we feel it should be withheld from
patients with seizure disorders.
Adrenergic blockade with such agents as
phentolamine, dibenzyline, and guanethidine has
enjoyed popularity in the past but has been sup-
planted by newer agents. Ganglionic blockade
achieved popularity in the 1950s and continues
in limited clinical use today. Initially, several
drugs including h e x a m e t h ~ n i u mand
~ ~ pentoli-
niumZ1were used, but currently only trimetha-
phan remains available. Trimethaphan is a short
acting drug, which is administered by continuous
intravenous infusion of a dilute Tach-
yphylaxis occurs and blood pressure may not fall
below 80 torr, despite increased dosage.44When
this situation is encountered, an alternative tech-
nique is indicated.
Direct vasodilation, without myocardial de-
pression, has many theoretical advantages in the
production of deliberate hypotension. The initial
pressure served to satisfy practically every re-
quirement for safe hypotension. The drug is ex-
tremely evanescent in its action: hypotension is
produced within 90 seconds and recovery occurs
in a matter of minutes. The hypotensive effect is
caused by a direct relaxation of vascular smooth
muscle, without cardiac depression or direct auto-
nomic effects.44
Initially, the only reported difficulty with SNP
was a minimal increase in transpulmonary shunt:
but this was followed by a case report of apparent
resistance to the drug, requiring increased dos-
age, resulting in acidosis and death.15 Since this
report, the phenomenon of resistance has been
found to be associated with cyanide (CN-) accu-
mulation and CN- induces tissue hy-
poxia by blocking oxygen uptake at the level of
the cytochrome oxidase system, leading to meta-
bolic acidosis. Clinical manifestations of this aci-
dosis are tachycardia and hypertension, leading
to cardiovascular
Experiments in laboratory animals have led
HEAD & NECK SURGERY JanIFeb 1980
to the recommendation that the maximum acute
dose of SNP should not exceed 1.0-1.5 mg/kg.71
The total dosage anticipated is calculated early
in the operation on the basis of the patient's drug
requirement and the surgeon's estimate of the
time of hypotension needed. If the calculated dose
exceeds 1.5mg/kg, an alternate hypotensive tech-
nique is indicated. In addition, arterial blood gas
and acid-base determinations are required during
SNP-induced hypotension. The development of
metabolic acidosis or an increasing drug require-
ment dictates the need to discontinue use of the
drug.
SNP is contraindicated in patients with Le-
ber's hereditary optic atrophy, tobacco amblyopia,
severe renal or liver disease, malnutrition, vita-
min B,, deficiency, and hypothyroidism.28It should
be used cautiously in patients with moderate pul-
monary disease.'
Intravenous nitroglycerine (TNG) is currently
under investigation for use in producing hypoten-
sion during anesthesia.'j4TNG produces a smooth
reduction in blood pressure and offers cardiac pro-
tection by dilating coronary arteries and opening
up collateral coronary flow." In one study that
compared deliberate hypotension using TNG or
SNP for surgery for total hip replacement, there
was less reduction in diastolic and mean pres-
sures, at comparable systolic pressures, with
TNG.25This finding was associated with transient
ECG changes in the SNP group but not the TNG
group. Furthermore, the author felt that pres-
sures were more easily controlled with TNG.
Further studies are necesssary to evaluate intra-
venous TNG, but the outlook is promising-
especially in view of the long use of the drug with
minimal evidence of toxicity.
There are several drugs and methods which
have also been used to aid in producing hypoten-
sion during anesthesia. Chlorpromazine has been
used intravenously to lower blood pressure; its
effect is reversible by means of large doses of cal-
cium Diazoxide is used most often to
treat hypertensive crises, but it has also been
used to produce hypotension during anesthesia.28
Tachycardia frequently results when ganglionic
blocking agents are utilized, and propranolol has
been used to reduce the heart rate in this situa-
t i ~ nConversely,
. ~ ~ atrial pacing to heart rates of
175 beatdmin has been used to produce controlled
hypotension during surgery.I6 As heart rate in-
creased, the cardiac output and blood pressure
were reduced because of a reduction in stroke vol-
ume. This method is obviously impractical for or-
Deli berate Hypotension
dinary use. D-tubocurarine, a neuromuscular
blocking agent, may produce a fall in blood pres-
sure through ganglionic blockade and histamine
release. Thiopental, because it reduces brain oxy-
gen consumption, may be used to provide a fur-
ther margin of safety against cerebral ischemia
during a n e s t h e ~ i a . ~ ' * ~ ~ , ' j ~
Adjunctive Techniques. Two nonpharmacologic
techniques-alteration of posture and controlled
mechanical ventilation-are usually used to sup-
plement the hypotension produced by use of the
above agents. A head-up posture during head and
neck surgery both lowers blood pressure at the
site of the operation and reduces venous bleeding.
Blood pressure is lowered proportionally in the
cerebral circulation as well, and a 2 torriinch (0.8
torricm) above-the-measurement site compensa-
tion must be made for vertical displacement.*OIf
direct pressure is measured, the elevation of the
transducer to patient eye level compensates for
any change in positioning.
Intermittent positive pressure ventilation
(IPPV) reduces blood pressure by raising intra-
thoracic pressure and decreasing venous return. l 3
Application of positive end-expiratory pressure
will further lower blood pressure and may be used
as a fine adjustment to the level of hypotension
obtained.
POSTOPERATIVE CARE
Postoperatively, care of patients made hypo-
tensive intraoperatively must be continued in
the same meticulous fashion. The residual ef-
fect of any hypotensive agent must be fully
accounted for when delineating patient position,
activity, fluid requirements, monitoring, and oxy-
gen supplementation. If the blood pressure re-
mains reduced in the postoperative period, then
measurement techniques for vascular pressure
must be specified. Finally, all personnel involved
in postoperative care must be familiar with un-
usual effects of the drugs employed, such as pup-
illary dilation from ganglionic blockade with
trimethaphan.
RESULTS
There have been 30 years of clinical experience
with deliberate hypotension. Therefore, one should
be able to review numerous articles that present
detailed descriptions of technique-with match-
ing control groups and adequate patient follow-
up-to demonstrate the advantages and disad-
vantages of deliberate hypotension in head and
HEAD & NECK SURGERY Jan/Feb 1980 191
neck surgery. Unfortunately, this is not the case.
If one accepts the initial goals outlined in this re-
view, then an "ideal" study can be constructed
with which to compare the current clinical expe-
rience. The ideal must first define hypotension
and then maintain this definition throughout.
Criteria for the assessment of patient risk and the
selection must be included, and a control group
of patients must be similarly assessed. Reasons
for patient rejection from the hypotension group
should be clarified. Preoperative evaluation, pre-
medication, monitoring, and positioning all re-
quire specific delineation, while anesthetic and
hypotensive techniques must be controlled. Intra-
operative and postoperative complications should
be compared, and patient follow-up must be ade-
quate t o evaluate the quality of the procedure.
Finally, the surgeodanesthesiologist team should
be the same for both groups of patients to elimi-
nate technical variation. Accepting this, all cur-
rent literature is inadequate. Table l follows and
displays a broad review of this literature, with
the deficiencies and the strengths of each paper
noted. Several features are noteworthy: (1)over
43,000 cases are presented, (2) approximately 40
of these cases present enough data to determine
mean pressure, (3) the majority of reports have no
or poor (i.e., nonrandomized) control groups, and
(4)only one study is prospective. The last point
specifically refers to the 1978 study by Thompson
et alG9of deliberate hypotension for total hip ar-
throplasty; this is the only controlled, prospective
study in 30 years to prove an advantage of the
technique of deliberate hypotension for a selected
procedure. The sole deficiency of this paper is the
small number of patients studied.

-
Table 1. Review of the literature on deliberate hypotension
Investigator No of Region of P or Pressures Techniques
(yr published) patients surgery Ra reported used Comments
Hug he^^^ 10 Headandneck R Systolic/ Gang block Methods of monitoring not reported MAP
(1951) diastolic calculable, > 50 torr throughout
Hampton et aI3O 21,125 Variable R Systolic Multiple Questionnaire distributed by mail with 48%
(1953) return Mortality of 1 459
Hampton et aI3' 6,805 Variable R Systolic Multiple Similar to those of Hampton 30
(1953)
Little43 Unknown Variable R Systolic/ Gang block Essentially anecdotal with no real data.
(1 955) diastolic Introduction of trimethaphan.
Anderson' 44 Variable R None Gang block Inadequate data; no control group. First
(1955) sizeable series in children.
Royster et alse 34 Head and neck R Systolic Gang block Inadequate data, Shows reduction in blood
(1956) loss, not operative time.
M~lndoe~~ 4,500 Variable R None Gang block Inadequate data; no control group. Mortality of
(1 956) 1:900; overwhelming positive bias.
EnderDyZ2 9,107 Variable R None Gang block Inadequate data; no control group. Mortality of
(1961) 1:1000; overwhelming positive bias.
Holme~~~ 138 Middle ear R None Gang block Inadequate data; no control group; no results.
(1961) Emphasis on patient position.
Linacre4' 1,000 Pelvis R Systolic Gang block Inadequate data; poor control group.
(1961) (range) Reasonable discussion.
Charnberlin et a19 50 Head and neck R None Gang block Inadequate data; poor control group. Use of
( 1963) EEG and systemic heparinization; reduced
blood loss and operative time.
Loewy et 24 Head and neck R None Unknown Inadequate data; poor control group. Use of
(1 963) mild hypothermia, mention of "fitness" of
patient's postoperative condition.
Eckenhoff et all8 44 Head and neck R Unknown Inadequate data; poor control group.
(1 965) Decreased blood loss, mention of "fitness"
of patient's postoperative condition.
Ma~Rae~~ Unknown Middle ear R None Nitroprusside No data. Early mention of nitroprusside
(1971)
Salem et alss 137 Variable R Systolic Gang block, Inadequate data, no control group no results
(1974) propanolol Excellent discussion
KerP 700 Middle ear R Systolic Gang block Inadequate data, no control group Pressures
(1977) propanolol reduced to 30-45 torr in head-up position
Thompson et a P 30 Hip P Mean Nitroprusside Small numbers Superb protocol with definite
(1 978) (50 torr) or halothane reduction in blood loss and time
*P = prospective study, R = retrospective study

192 Deliberate Hypotension HEAD 8, NECK SURGERY JaniFeb 1980

 From the above reports, can any meaningful
conclusions be drawn? It does appear safe to say
that the combination of proper positioning and
blood pressure reduction will reduce blood loss in
head and neck surgery, when compared to nor-
motensive patients undergoing similar proce-
dures. Within the previous statement, it should
be noted that body position is not mentioned in
the normotensive group, for this comparison has
yet to be made. There are no studies in which
blood pressure is the sole variable; therefore, the
“safe” statement above is rendered suspect. How-
ever, the majority of papers allude to a similarity
of body position, and we are inclined to agree with
the statement. A second, frequently mentioned
advantage of deliberate hypotension is shorter
surgery time, and there is some evidence to sup-
port this69(although it has not been an invaria-
ble finding). Other advantages that have been
mentioned are quicker postoperative recovery,
better patient well-being, and superior surgical
results; while all of these are obviously worth-
while, there are no data on which to propose that
deliberate hypotension provides these results.
COMPLICATIONS
In 1975, L i n d ~ previewed
~~ the complications as-
sociated with deliberate hypotension. Based on
the previous discussion of results, the problem
encountered in such a review can be anticipated.
Due to the lack of MAP data, no statistically valid
estimation of the incidence of any complication
can be made. Furthermore, because of a general
lack of control groups, such an estimate would be
of little worth by itself. However, the following
statements can be made:
1. No morbidity or mortality from deliberate hy-
potension has been .recorded secondary to pul-
monary or hepatic dysfunction.
2. Although urine output may cease, the highest
incidence of oliguridanemia reported in the
literature is 0.41%, and most series report no
renal complications.
3. Three isolated cases of retinal artery throm-
bosis have been reported.
4. The incidence of myocardial infarction is ap-
parently less than 1%, although nonspecific
ECG changes have been seen in up to 38% of
previously healthy patients made hypotensive
to no less than 50 torr MAP. (It is worth noting
here that several of the large series did not
monitor the ECG.)
5 . Postoperative reactionary hemorrhage is not
a significant problem.
6 . Cerebral complications extend from postoper-
Deliberate Hypotension
ative confusion and somnolence to overt in-
farction. (This last catastrophe has been “re-
ported” t o occur in 0.7% to 13% of cases.
If the review of complications examines only those
cases in which appropriate patients were selected,
adequate monitoring was used, and MAP was 50
torr or greater, then the nonspecific ECG changes
previously mentioned represent the only compli-
cation. However, recent literature demonstrates
an increasing index of suspicion regarding my-
ocardial ischemia, with the introduction of precor-
dial ECG leads revealing changes not apparent
in limb leads.53The obvious corollary to routine
monitoring with the EEG can be made, possibly
revealing occult cerebral ischemia during hypo-
tension as frequently. For the time being, how-
ever, this remains speculative.
SUMMARY AND RECOMMENDATIONS
Until such time as the criteria set forth above are
met by a sufficiently large, prospective, controlled
study, the controversy over the production of de-
liberate hypotension during anestheia, which
began 30 years ago, will continue. Based on cur-
rent data, a cost-benefit analysis reduces to (1)a
hepatitis risk of 1%per unit of whole blood,12(2)
the economiclphysiologic cost of prolonged sur-
gery, and (3) the unspecified morbidity of delib-
erate hypotension. Surgery of the head and neck
lends itself to surgical field hypotension because
of the ease with which a gravitational differential
can be developed. Therefore, if a patient has no
preexisting condition that contraindicates delib-
erate hypotension, if the surgeon feels it would
benefit the patient or the results, and if the anes-
thesiologist is comfortable in its use, we recom-
mend the elective reduction of blood pressure be-
low that level associated with surgical anesthesia
to reduce blood loss and expedite dissection.
Adequate monitoring is essential, and all other
measures to reduce blood loss should be instituted
before commencing blood pressure reduction. The
pressure should be reduced gradually to that point
where the field is dry. However, in no case should
it be reduced to less than 50 torr MAP (measured
at the patient’s eye level) unless further reduction
is required by a life-threatening situation. The
reduction in pressure can be accomplished using
any one of several methods and agents, but the
actual method or agent used is probably of sec-
ondary importance-provided that all other de-
mands are met regarding the patient selection,
the mutual understanding between surgeon and
anesthesiologist, and the standards of intraoper-
ative and postoperative care.
HEAD & NECK SURGERY Jan/Feb 1980 193
REFERENCES
1. Anderson SM: Controlled hypotension in pediatric.sur-
gery. B r Med J 2:103-104, 1955.
2. Arkin DB, Wahrenbrock EAHypoxemia following nitro-
prusside administration. In A S A Abstracts of Scientific
Papers Chicago, American Society of Anesthesiologists,
1975, pp 161-162.
3. Askrog VF, Pender JW, Eckenhoff JE: Changes in phys-
iological dead space during deliberate hypotension. Anes-
thesiology 45:508-515, 1976.
4. Benumof JL: Anesthesiology editorial: Hypoxic pulmo-
nary vasoconstriction and sodium nitroprusside infusion.
Anesthesiology 50:481- 483, 1979.
5. Berger PE, Culhan JA, Fitz CB, e t al: Slowing of hepatic
blood flow by halothane: angiographic manifestations.
Radiology 118:303-306, 1976.
6. Braunwald E: Control of myocardial oxygen consumption.
A m JCardiol 27:416-432, 1971.
7. Calverley RK, Smith NT, Jones CW, et al: Ventilatory
and cardiovascular effects of enflurane anesthesia during
spontaneous ventilation in man. Anesth Analg (Cleve)
57:610-618, 1978.
8. Carney FM, VanDyke RA: Halothane hepatitis: a critical
review. Anesth Analg (Cleve) 51:135-160, 1972.
9. Chamberlin JA, Mannheimer WH, Keats AS: Hypo-
tensive anesthesia in radical surgery of the head and
neck. Plast Reconstr Surg 31:316-322, 1963.
10. Christensen MS, Hoedt-Rasmussen K, Lassen NA: Cere-
bral vasodilation by halothane anesthesia and hypercap-
nea in man. B R JAnaesth 39:927- 934, 1977.
11. Cohn PF, Maddox DE, Holman BL, e t al: Effect of sublin-
gually administered nitroglycerin on regional myocardial
blood flow in patients with coronary artery disease. A m
J Cardiol 39:672-678, 1977.
12. Conrad ME, Knodell RA, Bradley EL, e t al: Risk factors
in transmission of non-A non-B posttransfusion. Truns-
fusion 17:579-585, 1977.
13. Conway CM: Haemodynamic effects of pulmonary venti-
lation. B r J Anaesth 47:761- 766, 1975.
14. Cullen DJ, Eger EI, Stevens WC, e t al: Clinical signs of
anesthesia. Anesthesiology 3621- 36, 1972.
15. Davies DW, Kadar D, Steward DJ, et al: A sudden death
associated with the use of sodium nitroprusside for in-
duction of hypotension during anesthesia. Can Anaesth
SOCJ 22:547- 551, 1975.
16. Dimant S, Piper CA, Murphy TO. Pacemaker-controlled
hypotension in surgery. Surgery 62:663-669, 1967.
17. Eckenhoff JE, Enderby GEH, Larson A, e t al: Pulmonary
gas exchange duringdeliberate hypotension. B r J Anaesth
35750-758, 1963.
18. Eckenhoff JE, Rich JC: Clinical experiences with delib-
erate hypotension. Anesth Analg (Cleve) 45:21- 27, 1966.
19. Enderby GEH: Controlled hypotension and postural is-
chemia to reduce bleeding in surgery. Lancet i:663-666,
1951.
20. Enderby GEH: Postural ischaemia and blood pressure
Lancet i:185-187, 1954.
21. Enderby GEH: Pentolinium tartrate in controlled hypo-
tension. Lancet ii:1097- 1098, 1954.
22. Enderby GEH: Hypotensive anaesthesia in plastic sur-
gery. B r JPlast Surg 14:41- 43, 1961.
23. Enderby GEH: Guest editorial: Some observations on the
practice of deliberate hypotension. B r J Anarsth 47:743-
744, 1975.
24 Engelman RM, Buy HH, Smith SJ, et al: The effect of
hypotensive anesthesia on renal hemodynamics. J Surg
Res 18:293-300, 1975.
25. Fahmy NR: Nitroglycerin as a hypotensive drug during
general anesthesia. Anesthesiology 49:17- 20, 1978.
26 Fahmy NR, Selwyn AS, Pate1 D, et al: Pulmonary vaso-
motor tone during general anesthesia and deliberate hy-
194 Deliberate Hypotension
potension in man. Anesthesiology 453-13, 1976.
27. Gardner W J The control of bleeding during operation by
induced hypotension. J A M A 132572-574, 1946.
28. Geevarghese K P Induced hypotension and its application
in neurological surgery. Int Anesthesiol Clin 15:195-229,
1977.
29. Griffiths HWC, Gillies J: Thoracolumbar splanchnicec-
tomy and sympathectomy: anesthetic procedure. Anes-
thesia 3:134-146, 1948.
30. Hampton LJ, Little DM: Results of a questionnaire con-
cerning controlled hypotension in anesthesia. Lancet
i:1299-1300, 1953.
31. Hampton LJ, Little DM: Complications associated with
the use of controlled hypotension in anesthesia. Arch
Surg 67:549-556, 1953.
32 Holmes F: Bloodless operating field in middle ear surgery.
J Laryngol Otol 75:248-258, 1961.
33. Hughes G Use of pentamethonium and posture to reduce
bleeding in fenestration operations. Lancet i:666-667,
1951.
34 Jordan WS, Graves CL, Boyd WA, e t al: Cardiovascular
effects of three technics for inducing hypotension during
anesthesia. Anesth Analg (Cleve) 50:1059-1068, 1971.
35 Kaplan J: Electrocardiographic monitoring. In Kaplan
J (Editor): Cardiac Anesthesia. New York, Grune & Strat-
ton, 1979, pp 117- 166.
36 Kerr A R Anaesthesia with profound hypotension for mid-
dle ear surgery. Br JAnaesth, 49:447-452, 1977.
37 Koster H: Spinal anesthesia; with special reference to its
use in surgery of the head, neck and thorax. A M J Surg
28554-570, 1928.
38. Larson A G Deliberate hypotension. Anesthesiology 25:
682-706, 1964.
39. Larson CP, Mazze RI, Cooperman LH, et al: Effects of an-
esthetics on cerebral, renal, and splanchnic circulations:
recent developments. Anesthesiology 41:169- 181, 1974.
40. Lassen NA, Tweed W A Control of the cerebral circulation
in health and disease. Circ Res 34:749-760, 1974.
41. Linacre JL: Induced hypotension in gynaecological sur-
gery. B r JAnaesth 33:45-50, 1961.
42. Lindop M J Complications and morbidity of controlled
hypotension. B r J Anaesth 47:799-802, 1975.
43. Little DM: Induced hypotension during anesthesia and
surgery. Anesthesiology 16:320-332, 1955.
44. Little DM, Hampton LJ, Grossbrentz DC: The use of Ar-
fonad in modification of the technique of controlled hy-
potension. Surgery 35:857- 866, 1954.
45. Loewy A, Skolnik EM, Sadove MS: Hypothermia and hy-
potension in head and neck surgery. Arch Otolaryngol
77:277-280, 1963.
46. MacRae WR: Anaesthesia for middle ear surgery. Proc R
Soc Med 64:1223-1228, 1971.
47. Manney FM J r , Ebert PA, Sabiston DC Jr: Postoperative
myocardial infarction: a study of predisposing factors, di-
agnosis, and mortality in a high risk group of surgical
patients. A n n Surg 172:497- 503, 1970.
48. Mazze RI, Calverley RK, Smith NT: Inorganic fluoride
nephrotoxicity. Anesthesiology 46:265-271, 1977.
49. McIndoe A: Hypotensive anesthesia in surgery. Plast Re-
constr Surg 17:l- 8, 1956.
50 Michenfelder JD: Cyanide release from sodium nitro-
prusside in the dog. Anesthesiology 46:196-201, 1977.
51 Michenfelder JD, Milde JH, Sundt TM: Cerebral protec-
tion by barbiturate anesthesia. Arch Neurol 33:345-350,
1976.
52. Pierce EC, Lambertson CJ, Deutch S, et al: Cerebral cir-
culation metabolism during thiopental anesthesia and
hyperventilation in man. J Clin Znvest 41:1664-1671,
1962.
53. Poppers PJ, Epstein RM, Donham R T Automatic ultra-
HEAD & NECK SURGERY JaniFeb 1980
 sound monitoring of blood pressure during induced hy-
potension. Anesthesiology 35:431- 435, 1971.
54. Prys-Roberts C, Lloyd JW, Fisher A, et al: Deliberate pro-
found hypotension induced with halothane: studies of
hemodynamics and pulmonary gas exchange. Br J Anaesth
46:105-116, 1974.
55. Purves MJ, James IM: Observations on the control of cer-
ebral blood flow in the sheep fetus and newborn lamb. Cwc
Res 25:651- 667, 1965.
56. Randall LO, Peterson WG, Lehman G The ganglionic
blocking action of thiophanium derivatives. J Pharmacol
Exp Ther 97:48-57, 1949.
57. Rollason WN, Cumming ARR. The electrocardiogram in
hypotensive anesthesia. Anaesthesia 2:319-335, 1956.
58. Royster HP, Ditzler JW: The use of controlled hypotension
and operations on the head and neck.Plast Reconstr Surg
17:9-16, 1956.
59. Salem MR, Wong AY, Bennett EJ, et al: Deliberate hy-
potension in infants and children. Anesth Analg (Cleve)
53:975-981, 1974.
60. Sharbrough FW, Messick JM, Sundt TM: Correlation of
continuous electroencephalograms during carotid endar-
terectomy stroke. J Neurosurg 41:310-320, 1974.
61. Simpson P, Bellamy D, Cole P Electrocardiographic stud-
ies during hypotensive anesthesia using sodium nitro-
prusside. Anaesthesia 31:1172-1178, 1976.
62. Smith AL, Hoff JT, Nielsen SL, e t al: Barbiturate protec-
tion in acute focal cerebral ischemia. Stroke 5:l- 7, 1974.
63. Smith RP, Kruszyna H: Nitroprusside produces cyanide
poisoning via a reaction with hemoglobin. J Pharmacol
Deliberate Hypotension
Exp Ther 191:557- 563, 1974.
64. Stetson JB: Intravenous nitroglycerin: a review. Int Anes-
thesiol Clin 15:261- 298, 1977.
65. Stone JG, Khambatta HJ, Matteo RS: Pulmonary shunt-
ing during anesthesia with deliberate hypotension. Anes-
thesiology 45:508-515, 1976.
66. Strandgaard S, Olesen J , Skinhof E, e t al: Autoregulation
of brain circulation in severe arterial hypertension. Br
Med J 1:507- 510, 1973.
67. Strunin L: Organ perfusion during controlled hypoten-
sion. Br JAnaesth. 47:793-798, 1975.
68. Sundt TM, Sharbrough FW, Anderson RE, et al: Cerebral
blood flow measurements and electroencephalograms dur-
ing carotid endarterectomy. J Neurosurg 41:310-320,
1974.
69. Thompson GE, Miller RD, Stevens WC, et al: Hypotensive
anesthesia for total hip arthroplasty. Anesthesiology 48:91-
96, 1978.
70. Tinker JH, Cucchiara RF: Use of sodium nitroprusside
during anesthesia and surgery. Znt Anesthesia1 Clin 15:89-
112, 1977.
71. Tinker JH, Michenfelder JD: Sodium nitroprusside: phar-
macology, toxicology, and therapeutics. Anesthesiology
45:340-351, 1976.
72. Torvik A, Skullerud K: How often are brain infarcts caused
by hypotensive episodes? Stroke 7:255-257, 1976.
73. Wildsmith JAW, Drummond GB, McRae W R Blood-gas
changes during induced hypotension with sodium nitro-
prusside. Br JAnaesth 47:1205-1210, 1975.
HEAD & NECK SURGERY Jan/Feb 1980 195