Netherlands Journal of Critical Care

Copyright 2011, Nederlandse Vereniging voor Intensive Care. All Rights Reserved.  Received April 2010; accepted September 2010

Review

Perioperative hypertension: 
Diagnosis and Treatment
KM Soto-Ruiz1, WF Peacock2, J Varon3

1 Dorrington Medical Associates, Houston, Texas and School of medicine, Autonomous University of Baja California, Tijuana, Mexico
2 Department of Emergency Medicine, The Cleveland Clinic, Cleveland, United States of America
3 The University of Texas Health Science Center at Houston, and The University of Texas Medical Branch at Galveston. St. Lukes
Episcopal Hospital/Texas Heart Institute, Houston, United States of America

Abstract - With hypertension affecting more people every year, it is commonly encountered in the perioperative setting by
anaesthesiologists, surgeons, intensivists, and internists. The presence of perioperative hypertension poses a risk for patients that can
affect the morbidity and mortality of a surgical procedure. Despite well documented findings of complications that can arise from this
condition, and the beneficial effects of therapeutic management, there are few diagnostic or treatment guidelines. Multiple agents can
be used in the acute setting of perioperative hypertension, however some of the agents currently available are less than ideal. We have
reviewed current and emerging pharmacological agents available.

Keywords - Hypertension, cardiac surgery, surgery, hypertensive crisis, hypertension management, preoperative, perioperative, postoperative

Introduction following terms: hypertension epidemiology, management and

It is estimated that there are currently 73 million people in the complications, preoperative care, perioperative hypertension,
United States with hypertension [1]. Affecting more than 30% postoperative hypertension, postoperative complications, and
of the population over 20 years of age, it is one of the most periprocedural hypertension. In addition, articles were sought
common chronic medical pathologies [2]. Hypertension, seen as in the specific areas of neurosurgical operations complications,
a significant public health problem, is not uniformally distributed cardiac and non-cardiac surgery mortality, and antihypertensive
as it occurs twice as often in African Americans compared therapy/agents. From the results of our search we reviewed 45
with Caucasians [3] and affects men more than women [4]. papers.
From a global perspective, the World Health Organization has
predicted that by 2025 one third of the worlds population will Perioperative hypertension
be hypertensive, and this will be responsible for over 7.1 million Because hypertension is so common, it is frequently detected
deaths per year [5]. in patients about to undergo surgery [8]. The presence of
Hypertension is a major risk factor for adverse cardiovascular preoperative hypertension portends more difficult haemodynamic
outcomes, renal disease, and stroke [5]. Furthermore, it has control during anaesthesia, increased risk of intraoperative and
been established that treating hypertension reduces the risk postoperative cardiovascular events, and challenges with post-
of these conditions developing [6]. Consequently, the Joint procedural blood pressure control [9]. Just the presence alone of
National Committee on Prevention, Detection, Evaluation, hypertension is a risk factor for other cardiovascular diseases that
and Treatment of High Blood Pressure (JNC VII) recommends may contribute to perioperative adverse events [9]. In fact, the
risk factor modification and treatment with antihypertensive National Veterans Administration Surgical Risk study of 83,000
agents in patients with systolic blood pressure (SBP) greater patients found hypertension was the second most common risk
than 140mmHg and/or diastolic blood pressure (DBP) greater factor associated with surgical morbidity [10].
than 90mmHg, regardless of age [7]. While these parameters Perioperative hypertension can occur during the induction
represent a guide for chronic hypertension management, they are of anaesthesia. Intraoperative hypertension is associated with
even more critical in patients undergoing operative interventions acute pain-induced sympathetic stimulation that leads to
where the risks of adverse outcomes are increased. vasoconstriction. In the post anaesthesia period, hypertension
can be associated with pain-induced sympathetic stimulation,
Methods hypothermia, and/or hypoxia. Hypertension may also be the result
We performed a PubMed search to identify suitable articles of intravascular volume overload from excessive intraoperative
to review. A systematic review was performed with the intravenous fluid therapy, and persist 24 to 48 hours until the
fluid has been mobilized from the extravascular space. Blood
Correspondence pressure can also rise due to discontinuation of blood pressure
medications postoperatively [11]. Postoperative hypertension
J Varon has a variable incidence ranging from 4% to 30%, following
E-mail: [email protected] cardiac or non-cardiac surgery [12].

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KM Soto-Ruiz, WF Peacock, J Varon

Preoperative hypertension episodes occur in the first 20 minutes of the postoperative

At least 25% of patients undergoing non-cardiac surgery will period, although its resolution can require up to 3 hours [19-22].
have hypertension before undergoing their procedure. This If left untreated, postoperative hypertension increases the risk
has important outcome implications as high blood pressure is of myocardial ischaemia, myocardial infarction, cerebrovascular
associated with complications such as myocardial ischaemia. accidents, and bleeding [11].
Preoperative hypertension is frequently a hypertensive urgency APH is characterized by peripheral vasoconstriction,
- not an emergency - as it doesnt involve end organ damage catecholamine release and reduced baroreceptor sensitivity
and there is usually enough time to reduce the blood pressure [23]. Some of the complications associated with APH are,
[13]. It has been suggested that a DBP of 110mmHg or above myocardial ischaemia, myocardial infarction, cardiac arrhythmia,
is considered a preoperative marker of perioperative cardiac congestive heart failure, pulmonary oedema, cerebral ischaemia,
complications in patients with chronic hypertension [8,11]. In a hemorrhagic stroke and encephalopathy; it also increases the
study by Forrest et al., preoperative hypertension was associated risk of bleeding from the surgical site [5].
with perioperative bradycardia, tachycardia, and hypertension Myocardial ischaemia most commonly occurs in the
[14], and Browner et al found a 3.8 times increase on postoperative postoperative setting and may present hours to days after the
death when compared to normotensive patients [15]. surgical procedure. Several factors may increase the risk of
When hypertension is detected, a work up for secondary causes myocardial ischaemia, and include oxygenation problems,
of hypertension should be done. Even though pheochromocytoma altered thrombotic potential, tachycardia, and postoperative
is rare, if present, it can produce serious complications during hypertension that increases myocardial oxygen demand.
a procedure. Long-term excess catecholamine stimulation can Postoperative hypertension can also cause pulmonary oedema
produce vasoconstriction and hypovolaemia that can potentially in patients with preexisting left ventricular systolic cardiac
complicate management [9]. dysfunction [9].
Clonidine withdrawal syndrome can simulate the hypertensive Rose et al., found that patients that presented with
crisis of pheochromocytoma. This can be misdiagnosed intraoperative hypertension, excessive pain, and inadequate
as symptoms usually present 18 to 24 hours after sudden ventilation had a higher risk of developing APH, and also noted
discontinuation of clonidine. When detected, clonidine that these patients had more critical care admissions and a higher
withdrawal symptoms can be corrected simply by administering risk of mortality [24]. Additionally, a unique cause of hypertension
intramuscular clonidine or treating with labetalol and methyldopa may occur after surgical repair of coarctation of the aorta in two
[11]. ways: an early component during the first 36 hours of systolic
hypertension, and a late component of systolic and/or diastolic
Intraoperative hypertension hypertension that persists beyond postoperative day two. If it
Intraoperative acute blood pressure elevations of over 20% persists beyond day two, there is an increased risk of developing
during surgery are considered a hypertensive emergency, postcoarctectomy syndrome, characterized by abdominal pain
and chronic hypertensive patients are more likely to have and associated mesenteric arteritis [25, 26].
labile haemodynamics during a procedure. Even small blood
pressure elevations during surgery can result in increased risk Management
of post-operative mortality and renal failure, especially during Before starting antihypertensive pharmacological treatment,
cardiovascular procedures. Hypertensive events occur more other reversible causes of postoperative hypertension should be
commonly in patients undergoing surgery of the carotids, addressed. These include pain, hypoxia, hypercarbia, agitation,
followed by abdominal aorta, peripheral vascular procedures, bladder distension and hypervolaemia [18]. Appropriate analgesia
intraperitoneal, and intrathoracic surgery [8]. Patients undergoing and sedation should be considered a prerequisite to the initiation
cardiac surgery represent a unique pathophysiologic cohort of antihypertensive therapy [27]. If a patient is hypertensive and
in perioperative hypertensive management. Hypertension in unable to take oral agents, parenteral therapy should be used
this group is characterized by peripheral vasoconstriction and [18], this makes drugs such as clonidine less attractive, as they
reduced baroreceptor sensitivity. [16] Because of pre-existing are available only in oral or transdermal presentation and this
underlying pathology, elevated blood pressure and heart rate makes titration a challenge. Volume status should be assessed as
can place a patient with preexisting left ventricle dysfunction intravascular volume depletion can increase sympathetic activity
or coronary artery disease at risk for developing myocardial and vasoconstriction, thus contributing to hypertension [5]
ischemia or heart failure [17]. When hypertension is present, the distinction between an
emergency and an urgency is useful. Hypertensive emergencies
Acute postoperative hypertension (APH) are defined by the coexistence of end organ damage, and a
Postoperative hypertension is more common in preoperative parenteral antihypertensive agent is usually necessary. In the
hypertensive patients, and in those undergoing vascular acute setting, the goal of blood pressure management should
procedures[18]. It has been defined as an SBP of above 190 be a 25% decrease in systolic BP. It is believed the immediate
mmHg and/or DBP of 100 mmHg on two consecutive readings therapeutic goal should be to reduce DBP by 10% to 15% or
after surgical intervention [11]. Postoperative hypertension to 110 mmHg in 30 to 60 minutes [11]. Some of the therapeutic

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Perioperative hypertension: Diagnosis and Treatment

options for parenteral blood pressure management are described kg/min. Because it is manufactured in a lipid emulsion, it is
below (See Table 1): recommended that the infusion set up be changed every four
hours to prevent the possibility of bacterial contamination.
Clevidipine Furthermore, the maximal 24 hour dosage should not exceed
Clevidipine is a third generation dihydropyridine calcium channel 2.5g/kg [28], and clevidipine should not be given to patients with
blocker. Metabolized by red blood cell (RBC) esterases, it has a soy or egg allergies
half-life of 1-2 minutes which is not altered by renal or hepatic A comparative effectiveness trial of clevidipine versus
failure. An arterially selective vasodilator, clevidipine reduces nitroglycerin, nicardipine, and nitroprusside has been performed
afterload without affecting cardiac filling pressures and is not [28]. The Evaluation of CLevidipine In the Perioperative
reported to cause reflex tachycardia. A direct coronary vasodilator, Treatment of Hypertension Assessing Safety Events (Eclipse)
clevidipine increases coronary blood flow while increasing trial prospectively evaluated outcomes in1512 cardiac surgical
stroke volume and cardiac output. Clevidipine protects against patients that required treatment for APH. In this analysis, the
ischaemia/reperfusion injury, and maintains splanchnic blood clevidipine cohort was found to have a significantly lower mortality
flow and renal function [5]. rate as compared to the nitroprusside group. Clevidipine was also
A clevidipine infusion is started at a rate of 0.4g/kg/min, found to achieve goal SBP more effectively than nitroglycerin or
titrating by doubling increments every 90 seconds up to 3.2g/ nitroprusside.

Table 1. Therapeutic options in the management of perioperative hypertension

Drug Dose Time of action Contraindications/Adverse

effects

Clevidipine Infusion rate started at a rate of 0.4 g/kg/ Half-life of one minute, duration Cannot be given in patient with egg or
min, titrating by doubling increments every 90 of action 5-15 mins soy allergy.
seconds up to 3.2 g/kg/min, up to a maximum Infusion set up should be changed
of 2.5g/kg/24hours every 4 hours
Nicardipine 5mg/hr, increasing 2.5mg/hr every 5 minutes up Onset of action is 5 to 15 Increased half-life may results in
to a maximum of 15mg/hr minutes, duration of action is 4 prolonged action by 24 hours of use
to 6 hours
Nitroglycerin Starting dose is 5 g/kg/min, it can be titrated onset of action is 2 to 5 minutes, Hypotension and reflex tachycardia.
at 5 g /kg/min every 3-5mins, after dose duration of action is 3 to 5 Tachyphylaxis onset within 4 hours.
exceeds 20 g /kg/min, it can be incremented minutes Methemoglobinemia with prolonged
at 20 g /kg/min infusion
Nitroprusside 0.25 to 0.5mg/kg/min titrated every 1-2 minutes Onset of action is seconds, the Decreases renal blood flow and
duration of action is 1-2 minutes, function.
and plasma half-life is 3 to 4 Decreases cerebral blood flow but
minutes increases intracranial pressure.
Coronary steal
Prolonged infusion may result in
cyanide toxicity
Hydralazine IV bolus: 10-20 mg repeated every 1-4 hours Onset of action is 5 to 25 mins, Reflex tachycardia in ischaemic heart
as needed. drop in BP can last up to 12 disease may result in iatrogenic MI
IV Infusion: loading dose of 0.1 mg/kg, followed hours. Circulating half-life is 3 Avoid in patients with dissecting
by a continuous infusion of 1.5-5 mcg/kg/min hours aneurysms.
It can increase intracranial pressure
Fenoldopam Starting dose is 0.1 g/kg/min, titrated by Onset of action 5 mins, maximal Tachycardia
increments of 0.05-0.1 g/kg/min, up to a response at 15 mins. Elimination Increase intraocular pressure
maximum of 1.6 g/kg/min half-life is 5 mins, duration of
action is 30-60 mins.
Labetalol Loading dose 20mg followed by 20-80mg every Onset of action is 2-5 mins, it Should not be used in patients with
10mins. After initial dose, a 1-2mg/min infusion reaches a peak at 5-15 minutes acute heart failure, bradycardia, heart
titrated until desired effect has been achieved and lasts up to 4 hours, its block >1st degree, bronchospasm
elimination half-life is 5.5 hours
Esmolol 500-1000 g /kg Onset of 60 seconds and a short Anaemia can prolong its half-life.
loading dose in 1 min, followed by infusion duration of action of 10 to 20 Should not use with acute heart failure,
starting at 50 g/kg/min and increasing up to minutes bradycardia, heart block >1st degree,
300 g/kg/min PRN bronchospasm
Enalaprilat 1.25mg in over 5 min every 6 hours titrated Onset of action 15 minutes, peak Variable response, slow onset of action,
by increments of 1.25mg at 12-24 hours to a effect in an hour, duration of difficult to titrate to effect
maximum of 5mg every 6 hours action is 6 hours

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KM Soto-Ruiz, WF Peacock, J Varon

Nicardipine complication promptly by termination of the infusion, and

Nicardipine is a second generation dihydropyridine calcium potentially administering a fluid bolus, should this occur.
channel blocker. It has high arterial vascular selectivity, with The vasodilatory effect of nitroprusside can negatively impact
strong coronary and cerebral vasodilator activity that results in end organ function. Because it decreases renal blood flow, this
increased, as well as preserved coronary and cerebral blood flow renal function can be impaired. Furthermore, while decreasing
[11]. Its onset of action is 5 to 15 minutes, and it has a four to cerebral blood flow, its use results in increased intracranial
six hour duration of action. Nicardipines dosing is independent pressure, therefore it should be avoided in patients undergoing
of weight. Its initial infusion rate is 5mg/hr, and this can be craniotomies, or in those in whom increased intracranial pressure
increased by 2.5mg/hr, every five minutes, up to a maximum of could be potentially harmful. Finally, the use of nitroprusside
15mg/hr. Blood pressure control is usually achieved within 10 to in patients with recent MI has been associated with increased
15 minutes, and few adjustments are needed to maintain control mortality, hypothesized due to a reduction in regional blood flow
[5]. Nicardipine initially has a short duration of effect, however, it (coronary steal). Ultimately, its use should also be avoided in
has the disadvantage of an increasing half-life during the next 24 these populations [5].
hours that may result in a prolonged duration of action. Nitroprusside contains a significant amount of cyanide that
is released non-enzymatically in a dose-dependant fashion
Nitroglycerin within the blood stream. It has been shown that the infusion of
Nitroglycerin is a potent venodilator that does not cause arterial as little as 4g/kg/min over 2-3 hours, can lead to toxic levels of
vasodilation until higher doses are reached. Its recommended cyanide. Nitroprusside can also cause toxicity with the release of
starting dose is 5g/kg/min, then titrated upward at 5g/kg/min nitric oxide generated by the formation of hydroxyl radical and
every three to five minutes. After the initial dose has exceeded peroxynitrite; this leads to lipid peroxidation [5].
20g/kg/min, dosage can be increased by 20g/kg/min Because of its potentially toxic effects, nitroprusside is only
increments. Some clinical scenarios may require more rapid up recommended for use when no other agent is available, and only
titration, such as acute pulmonary oedema, although this should if the patient has normal renal and hepatic function. Even in these
be done with caution and very close monitoring. Even though there settings, the use of nitroprusside should be limited to as short a
are no dosing limits, the risk of iatrogenic hypotension increases time as possible, and the dose should not exceed 2g/kg/min [5].
at doses higher than 200 g/kg/min. The onset of action of
nitroglycerin is two to five minutes, and it has a duration of action Hydralazine
of three to five minutes. Tachyphylaxis which begins as early as A direct-acting arteriolar vasodilator, hydralazine demonstrates
four hours after IV initiation, limits its utility as a long-term blood greater blood pressure lowering effect on diastolic, rather than
pressure management agent. Finally, excessively prolonged use systolic pressure. Hydralazine increases renal blood flow, which
has also been associated with methemoglobinaemia [29]. may provide some theoretical advantage for patients with
The hypotensive effect of nitroglycerin is achieved by a impaired renal function. Regardless of whether administered
reduction in preload and cardiac output. Therefore, it is not intravenously or intramuscularly, its onset of action is 5 to 25
recommended for use in volume-depleted patients, or in those minutes, with a maximum effect generally within 10 to 80 minutes
in whom cardiac output is preload dependent. Hypotension after administration. Hydralazines metabolism is dependent on
(i.e., overshoot of titration) and reflex tachycardia are common hepatic acetylation and inactivation, which results in its prolonged
effects of nitroglycerin, and this could be exacerbated by volume effect. Although its circulating half-life is only three hours, it has
depletion. a much longer effect on blood pressure. Once given, hydralazine
Nitroglycerin is recommended only as adjunct therapy for can result in a drop in blood pressure that can last as long as 12
patients with acute coronary syndromes, or in the setting of acute hours. Ultimately, hydralazine is not considered an ideal agent for
pulmonary oedema. In other conditions it is not recommended hypertensive crises due to its difficult titration.
as a single primary blood pressure control agent due to its Hydralazine reduces peripheral vascular resistance, but can
unpredictability to reduce blood pressure and the early onset of trigger reflex tachycardia. Because tachycardia in the setting
tachyphylaxis. of hypertension results in a subsequent increase in myocardial
oxygen demand, hydralazine is not an ideal agent in patients
Nitroprusside with potential ischaemic heart disease. Furthermore, hydralazine
Nitroprusside is an arterial and venous vasodilator and thus should also be avoided in patients with dissecting aneurysms
decreases both preload and afterload. It has onset of action due to its potential for a reflex increase in cardiac output and
measured in seconds, a duration of action of 1-2 minutes, myocardial contractility.
and its plasma half-life is 3-4 minutes. It is given at an initial One population in whom hydralazine is preferred for use in
dose of 0.25 to 0.5 g/kg/min and titrated every 1-2 minutes. blood pressure control is during pregnancy. While it has long been
Because of its significant hypotensive effects, nitroprusside the drug of choice for preeclampsia, a population with little risk of
use is commonly associated with precipitous blood pressure harm due to reflex tachycardia and increased myocardial oxygen
decreases (overshooting the desired blood pressure titration demand, a recent meta-analysis has suggested that its use is
target). The clinician should be vigilant to address this iatrogenic associated with an increase in materno-fetal complications [30].

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Finally, hydralazine has also been reported to increase cardiac output and heart rate [11]. Its hypotensive effect is
intracranial pressure [31]. Thus it should be avoided in patients achieved by decreasing heart rate and myocardial contractility,
in whom potentially increased intracranial pressures would be thereby reducing arterial pressure and it has no vasodilatory
contraindicated. effect.
Esmolol is administered as a 500-1000g/kg loading dose
Fenoldopam over one minute, followed by a continuous infusion starting at
Fenoldopam is a dopamine-1 receptor agonist that mediates 50g/kg/min and increasing up to 300g/kg/min as necessary.
vasodilation by its effect on peripheral dopamine-1 receptors. It has an onset of 60 seconds and a short duration of action
Quickly metabolized by conjugation in the liver, without the of only 10 to 20 minutes. Because of its RBC dependent
participation of cytochrome P-450 enzymes, fenoldopam metabolism, any condition associated with anaemia may result in
mediates renal arterial vasodilation and activates dopamine a prolonged half-life and longer duration of hypotensive effects.
receptors in the proximal and distal tubules. The net renal effects The American College of Cardiology/ American Heart Association
are to inhibit sodium reabsorption, thus promoting diuresis and guidelines state esmolol is contraindicated in patients already
natriuresis [5]. on -blockers, those with bradycardia, or in the setting of acute
After administration of fenoldopam, the onset of effect is within decompensated heart failure as it has the potential to excessively
5 minutes, and maximal response is achieved by 15 minutes. The impair myocardial function.
elimination half-life is 5 minutes and its duration of action is from
30 to 60 minutes. The starting dose is 0.1g/kg/min, titrated by Enalaprilat
increments of 0.05-0.1g/kg/min, up to a maximum of 1.6g/ An IV ACE inhibitor, enalaprilat is effective treating hypertension in
kg/min. While fenoldopam reduces blood pressure, it often patients with congestive heart failure and essential hypertension.
causes reflex tachycardia and can increase intraocular pressure. It has also been found to prevent worsening renal function
Therefore, fenoldopam should be avoided in patients at risk of in patients with diabetic and non-diabetic nephropathy. For
myocardial ischaemia, intraocular or intracranial hypertension perioperative use, it has been specifically reported to be effective
[11]. in patients undergoing craniotomies [32].
Enalaprilat is generally administered IV with a starting dose
Labetalol of 1.25 mg over five minutes and repeated every six hours as
Labetalol is a combined selective 1- and non-selective needed. It can be titrated in increments of 1.25 mg at 12 to 24
-adrenergic blocker, that is given as a bolus or a continuous hour intervals, to a maximum of 5 mg every six hours.
infusion. Metabolized by the liver to form an inactive glucuronide The use of enalaprilat has several advantages. It can be
conjugate, it has an onset of action within 2 to 5 minutes, reaches administered as a bolus instead of a continuous infusion, it has
peak effects at 5 to 15 minutes, has an elimination half-life of 5.5 no effect on intracranial pressure, and it doesnt produce reflex
hours, and has a duration of action of up to four hours. These tachycardia. Disadvantages to its use are that it has a delayed
characteristics make it difficult to titrate labetalol as a continuous onset of action of 15 minutes, requires one hour to reach peak
infusion. It is recommended that labetalol be administered by a effect, and its six hour duration of action is excessively long in the
20 mg loading dose, followed by additional 20 to 80 mg boluses potentially unstable patient. These disadvantages limit enalaprilat
at 10 minutes intervals. After the initial loading dose, labetalol use in hypertensive emergencies as a slow onset and delayed
may also be given as an infusion of 1 mg to 2 mg per minute, time to peak effect make titration to a precise blood pressure
titrated until the desired effect has been achieved. challenging [11]. Despite these concerns, enalaprilat has been
Labetalol reduces systemic vascular resistance without used to achieve postoperative blood pressure control when
affecting peripheral blood flow. Furthermore, cerebral, renal, combined with a faster acting drug that is easier to titrate, such
and coronary blood flow are also maintained, as well as cardiac as labetalol or nicardipine [5].
output, but heart rate may decrease due to its -blocking effects.
Labetalol has been found to be safe and effective for treating Conclusions
APH after vascular, cardiac, general, and intracranial surgical Acute postoperative hypertension is common after cardiac and
procedures, where a response rate of 85-100% has been non-cardiac surgery and frequently requires pharmacological
reported [5]. Labetalol should not be used in patients with severe treatment. The goal of treatment should be to protect organ
sinus bradycardia, asthma, and heart blocks greater than first function, decrease complications, and improve the outcomes.
degree [11]. As there are no guidelines for management and no definitive
treatment exists, emphasis must be to individualize therapy
Esmolol based on the patients risk factors and coexisting morbidities, the
Esmolol is an ultra-short acting cardioselective -adrenergic clinicians experience, and the clinical setting.
blocking agent. It is metabolized via rapid hydrolysis of ester With the implementation of antihypertensive therapy, patients
linkages by RBC esterases, and thus has the advantage of should be closely monitored to reduce the risk of iatrogenic end
being unaffected by renal or hepatic dysfunction. Esmolol is organ hypoperfusion. The ideal pharmacological agent should
recommended for use in hypertensive patients with increased have an immediate onset of action, a short to intermediate

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duration of action, be easily and predictably titratable, have recommended in very specific circumstances, and attention
documented efficacy in treating perioperative hypertension, must be paid to their possible adverse effects. Nicardipine and
and should be proven safe. Nitroprusside should only be used clevidipine are currently the agents recommended for the majority
when no other agents are available. Enalaprilat and nitroglycerin of perioperative cases requiring hypertensive management as
are recommended for combined therapy, but not as single their efficacy has been well documented and they are proven to
agents. Labetalol, esmolol, hydralazine, and fenoldopam are be safe.

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