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All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Aug 2019. | This topic last updated: Jul 15, 2019.
INTRODUCTION
Preexisting hypertension is the most common medical reason for postponing surgery [1].
Hypertension is well known to be a risk factor for cardiovascular catastrophe, a risk that logically
extends into the perioperative period [2,3]. In a case-control study of 76 patients who died of a
cardiovascular cause within 30 days of elective surgery, a preoperative history of hypertension was
four times more likely than among 76 matched controls [4].
The issues regarding the perioperative management of the patient with hypertension are reviewed
here. Intraoperative management of hypertensive patients is presented elsewhere. (See "Anesthesia
for patients with hypertension".)
Sympathetic activation during the induction of anesthesia can cause the blood pressure to rise by 20
to 30 mmHg and the heart rate to increase by 15 to 20 beats per minute in normotensive individuals
[5]. These responses may be more pronounced in patients with untreated hypertension in whom the
systolic blood pressure can increase by 90 mmHg and the heart rate by 40 beats per minute.
The mean arterial pressure tends to fall as the period of anesthesia progresses due to a variety of
factors, including direct effects of the anesthetic, inhibition of the sympathetic nervous system, and
loss of the baroreceptor reflex control of arterial pressure. These changes can result in episodes of
intraoperative hypotension. Patients with preexisting hypertension are more likely to experience
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intraoperative blood pressure lability (either hypotension or hypertension) [6], which may lead to
myocardial ischemia [7].
Blood pressure and heart rate slowly increase as patients recover from the effects of anesthesia
during the immediate postoperative period. Hypertensive individuals, in particular, may experience
significant increases in these parameters [8].
Preexisting hypertension can induce a variety of cardiovascular responses that potentially increase
the risk of surgery, including diastolic dysfunction from left ventricular hypertrophy, systolic
dysfunction leading to congestive heart failure, renal impairment, and cerebrovascular and coronary
occlusive disease. The level of risk is dependent upon the severity of hypertension.
However, much of the evidence for the impact of preoperative hypertension comes from uncontrolled
studies performed before contemporary (more effective) management was available. Furthermore, it
is still unclear whether postponing surgery to achieve blood pressure control will lead to reduced
cardiac risk [9]. The American College of Cardiology/American Heart Association (ACC/AHA)
guidelines list uncontrolled hypertension as a "minor" risk factor for perioperative cardiovascular
events [10].
Severe hypertension — An early study found that patients with untreated severe hypertension
(mean systolic and diastolic pressures of 211 and 105 mmHg, respectively) had exaggerated
hypotensive responses to the induction of anesthesia and marked hypertensive responses to noxious
stimuli [11]. Patients with well-controlled hypertension responded similarly to normotensive subjects.
Other studies have found that a diastolic pressure over 110 mmHg immediately before surgery is
associated with a number of complications including dysrhythmias, myocardial ischemia and
infarction, neurologic complications, and renal failure [5]. (See "Possible prevention and therapy of
ischemic acute tubular necrosis".)
Mild to moderate hypertension — Patients with less marked hypertension (diastolic pressure less
than 110 mmHg) do not appear to be at increased operative risk. This was illustrated in a study of 676
operations involving a general anesthetic in patients over the age of 40 years [6]. Subjects were
divided into five groups:
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IV), and who had untreated hypertension (group V) (8 and 6 versus 27, 25, and 20 percent,
respectively).
● Patients with inadequately treated or untreated hypertension (groups IV and V) were no more
likely to experience cardiac complications than normotensive patients not taking diuretics (group
I).
● Among patients with a history of hypertension (groups III, IV, and V), multivariate analysis
identified only two independent risk factors for cardiac complications: the preoperative cardiac
risk index score (which does not include hypertension (table 1)); and marked reductions in
intraoperative blood pressure (a decrease to less than 50 percent of preoperative levels or a
decrease of 33 percent or more for more than 10 minutes).
These results suggest that elective surgery in patients with hypertension does not need to be delayed
as long as the diastolic blood pressure is less than 110 mmHg and intraoperative and postoperative
blood pressures are carefully monitored to prevent hypertensive or hypotensive episodes. On the
other hand, when hypertension has caused end-organ disease such as congestive heart failure and
renal insufficiency, the probability of adverse cardiac outcome in the perioperative period increases
significantly [12]. (See "Evaluation of cardiac risk prior to noncardiac surgery".)
The impact of systolic hypertension on operative risk is less clear. One study of patients undergoing
carotid endarterectomy found that a systolic pressure greater than 200 mmHg was associated with an
increased risk of postoperative hypertension and neurologic deficits [13]. Patients with isolated
systolic hypertension are at increased risk for cardiovascular morbidity after coronary artery bypass
surgery [2].
Secondary hypertension — Patients with suspected secondary hypertension should ideally undergo
a diagnostic evaluation prior to elective surgery (see "Evaluation of secondary hypertension").
However, most patients are not at increased perioperative risk as long as the hypertension is not
severe and serum electrolytes and renal function are normal. An important exception is the patient
with pheochromocytoma, in whom operative mortality may be as high as 80 percent in unsuspected
cases [14]. (See "Clinical presentation and diagnosis of pheochromocytoma".)
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● Abruptly discontinuing some medications (eg, beta blockers, clonidine) may be associated with
significant rebound hypertension.
● There are risks associated with severe, uncontrolled hypertension. (See 'Severe hypertension'
above.)
The following is a brief summary of recommendations for the various classes of antihypertensive
drugs.
Diuretics — Patients in whom chronic diuretic therapy has caused hypokalemia may have
potentiation of the effects of muscle relaxants used during anesthesia, as well as predisposition to
cardiac arrhythmias and paralytic ileus [15]. Clinicians should be aware of the potential perioperative
risks associated with diuretics and pay close attention to volume and potassium replacement. (See
"Perioperative medication management", section on 'Diuretics'.)
Calcium channel blockers — Patients receiving calcium channel blockers may have an
increased incidence of postoperative bleeding, probably due to inhibition of platelet aggregation [20].
The multiple benefits of these drugs probably outweigh the small risk of continued therapy.
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Withdrawal syndromes — The centrally acting sympatholytic drugs (eg, clonidine, methyldopa, and
guanfacine) and the beta blockers are associated with acute withdrawal syndromes that can lead to
adverse perioperative events. These drugs should not be abruptly stopped perioperatively.
Centrally acting sympatholytic drugs — The primary clinical manifestation following abrupt
cessation of clonidine therapy is acute, rebound hypertension above the pretreatment level. Rebound
hypertension usually occurs after abrupt cessation of fairly large oral doses (eg, greater than 0.8
mg/day) but has also been noted with transdermal clonidine [21]. Withdrawal symptoms have also
been reported with methyldopa and guanfacine withdrawal but are less likely because of their slower
onset of action [22]. (See "Perioperative medication management", section on 'Alpha 2 agonists' and
"Withdrawal syndromes with antihypertensive drug therapy".)
Beta blockers — Beta blockers reduce intraoperative myocardial ischemia [23]. Thus, in addition
to a rise in blood pressure, beta blocker withdrawal in patients with underlying coronary disease can
lead to accelerated angina, myocardial infarction, or sudden death [24]. (See "Perioperative
medication management", section on 'Beta blockers' and "Withdrawal syndromes with
antihypertensive drug therapy".)
Furthermore, atenolol or bisoprolol given before surgery to patients with, or at high risk for, coronary
heart disease decreases mortality [25,26]. Guidance on the use of perioperative beta blockers for
noncardiac surgery is presented elsewhere. (See "Management of cardiac risk for noncardiac
surgery", section on 'Beta blockers'.)
A history of hypertension preoperatively is the most important risk factor for postoperative
hypertension [27]. Other factors contributing to the development of hypertension were pain (35
percent), excitement on emergence from anesthesia (16 percent), and hypercarbia (15 percent). The
type of surgery may influence the likelihood of developing postoperative hypertension [6].
As illustrated in a study of 1844 patients, hypertension usually begins within 30 minutes of the
completion of surgery and lasts approximately two hours [27]. On the other hand, some patients with
preexisting hypertension may experience normalization of blood pressure as a nonspecific response
to surgery [28]. This response can persist for months, usually followed by a gradual return to
preoperative levels.
Indications for and approach to therapy — Any patient who experiences a marked rise in blood
pressure following surgery (ie, a sustained increase in systolic pressure greater than 180 mmHg not
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due to severe pain) should be treated immediately with intravenous antihypertensive therapy. (See
"Evaluation and treatment of hypertensive emergencies in adults".)
● Therapy should be considered for patients with a sustained systolic blood pressure above 180
mmHg or diastolic blood pressure greater than 110 mmHg, once remedial causes have been
excluded or treated.
Choice of drugs — A number of parenteral antihypertensive medications are available for patients
who are unable to take oral medications postoperatively. These are the same drugs used to treat
patients with hypertensive emergencies (table 2) [29]. Without any data from controlled trials to
indicate which is best, the experience of the surgeons, anesthesiologists, and internists who are
caring for the patients should guide the choice. For short-term control of severe postoperative
hypertension (eg, systolic pressure of >180 mmHg), we prefer intravenous labetalol or nicardipine.
In patients with chronic hypertension who were treated with antihypertensive therapy prior to surgery,
we typically resume their usual medications. However, with the exception of beta blockers and
clonidine, it is not necessary for patients who are unable to resume oral medications to continue the
same class of drugs postoperatively. Nevertheless, in many cases, a comparable parenteral
alternative is available:
Goals of therapy — Goal blood pressure in patients treated for postoperative hypertension is similar
to the general population.
In patients treated for postoperative hypertension who did not have preexisting hypertension, we
discontinue antihypertensive therapy once the patient is surgically stable and the blood pressure is at
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goal for at least 24 hours, and we observe them over a period of 48 to 72 hours. Antihypertensive
therapy should be resumed if the blood pressure remains consistently elevated.
Links to society and government-sponsored guidelines from selected countries and regions around
the world are provided separately. (See "Society guideline links: Hypertension in adults".)
● Preexisting hypertension is the most common medical reason for postponing surgery.
Hypertension is well known to be a risk factor for cardiovascular catastrophe, a risk that logically
extends into the perioperative period. (See 'Introduction' above.)
● Sympathetic activation during the induction of anesthesia can cause the blood pressure to rise by
20 to 30 mmHg and the heart rate to increase by 15 to 20 beats per minute in normotensive
individuals. These responses may be more pronounced in patients with untreated hypertension
in whom the systolic blood pressure can increase by 90 mmHg and the heart rate by 40 beats
per minute. The mean arterial pressure tends to fall as the period of anesthesia progresses.
Blood pressure and heart rate then slowly increase as patients recover from the effects of
anesthesia during the immediate postoperative period. Hypertensive individuals, in particular,
may experience significant increases in these parameters. (See 'Blood pressure response during
anesthesia' above.)
● In patients treated for chronic hypertension, oral antihypertensive medications can usually be
continued. In most cases, continuing antihypertensive medications is relatively safe, and
discontinuing some medications (eg, beta blockers, clonidine) may be associated with significant
rebound hypertension. Thus, we typically continue most antihypertensive agents until the time of
surgery, taken with small sips of water on the morning of surgery. However, we usually hold
angiotensin-converting enzyme (ACE) inhibitors and angiotensin II receptor blockers (ARBs) for
a period of 24 hours prior to surgery. Conversely, centrally acting sympatholytic drugs (eg,
clonidine, methyldopa, and guanfacine) and beta blockers are associated with acute withdrawal
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syndromes that can lead to adverse perioperative events; these drugs should not be abruptly
stopped perioperatively. (See 'Management of patients on chronic antihypertensive therapy'
above and 'Safety of antihypertensive drugs preoperatively' above and 'Angiotensin-converting
enzyme inhibitors and angiotensin II receptor blockers' above and 'Withdrawal syndromes'
above.)
● Any patient who experiences a marked rise in blood pressure following surgery (ie, a sustained
increase in systolic pressure to 180 mmHg or greater not due to severe pain) should be treated
immediately with intravenous antihypertensive medication. In other cases, remedial causes of
hypertension such as pain, agitation, hypercarbia, hypoxia, hypervolemia, and bladder distention
should be excluded or treated, and patients on chronic antihypertensive therapy should resume
their usual medications postoperatively. (See 'Management of postoperative hypertension' above
and 'Indications for and approach to therapy' above.)
• For short-term control of severe postoperative hypertension (eg, systolic pressure of >180
mmHg), we prefer intravenous labetalol or nicardipine.
• In patients with chronic hypertension who were treated with antihypertensive drugs prior to
surgery and who do not require immediate parenteral therapy for severe hypertension, we
typically resume their usual oral medications. However, with the exception of beta blockers
and clonidine, it is not necessary for patients who are unable to resume oral medications to
continue the same class of drugs postoperatively.
● Goal blood pressure in patients treated for postoperative hypertension is similar to the general
population. In patients treated for postoperative hypertension who did not have preexisting
hypertension, we discontinue antihypertensive therapy once the patient is surgically stable and
the blood pressure is at goal for at least 24 hours. (See 'Goals of therapy' above.)
REFERENCES
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4. Howell SJ, Sear YM, Yeates D, et al. Hypertension, admission blood pressure and perioperative
cardiovascular risk. Anaesthesia 1996; 51:1000.
5. Wolfsthal SD. Is blood pressure control necessary before surgery? Med Clin North Am 1993;
77:349.
6. Goldman L, Caldera DL. Risks of general anesthesia and elective operation in the hypertensive
patient. Anesthesiology 1979; 50:285.
9. Casadei B, Abuzeid H. Is there a strong rationale for deferring elective surgery in patients with
poorly controlled hypertension? J Hypertens 2005; 23:19.
10. Eagle KA, Berger PB, Calkins H, et al. ACC/AHA guideline update for perioperative
cardiovascular evaluation for noncardiac surgery---executive summary a report of the American
College of Cardiology/American Heart Association Task Force on Practice Guidelines
(Committee to Update the 1996 Guidelines on Perioperative Cardiovascular Evaluation for
Noncardiac Surgery). Circulation 2002; 105:1257.
12. Goldman L, Caldera DL, Nussbaum SR, et al. Multifactorial index of cardiac risk in noncardiac
surgical procedures. N Engl J Med 1977; 297:845.
13. Towne JB, Bernhard VM. The relationship of postoperative hypertension to complications
following carotid endarterectomy. Surgery 1980; 88:575.
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15. Cygan R, Waitzkin H. Stopping and restarting medications in the perioperative period. J Gen
Intern Med 1987; 2:270.
18. Colson P, Saussine M, Séguin JR, et al. Hemodynamic effects of anesthesia in patients
chronically treated with angiotensin-converting enzyme inhibitors. Anesth Analg 1992; 74:805.
19. Ryckwaert F, Colson P. Hemodynamic effects of anesthesia in patients with ischemic heart
failure chronically treated with angiotensin-converting enzyme inhibitors. Anesth Analg 1997;
84:945.
20. Zuccalá G, Pahor M, Landi F, et al. Use of calcium antagonists and need for perioperative
transfusion in older patients with hip fracture: observational study. BMJ 1997; 314:643.
21. Metz S, Klein C, Morton N. Rebound hypertension after discontinuation of transdermal clonidine
therapy. Am J Med 1987; 82:17.
22. Ram CV, Holland OB, Fairchild C, Gomez-Sanchez CE. Withdrawal syndrome following
cessation of guanabenz therapy. J Clin Pharmacol 1979; 19:148.
23. Stone JG, Foëx P, Sear JW, et al. Myocardial ischemia in untreated hypertensive patients: effect
of a single small oral dose of a beta-adrenergic blocking agent. Anesthesiology 1988; 68:495.
24. Psaty BM, Koepsell TD, Wagner EH, et al. The relative risk of incident coronary heart disease
associated with recently stopping the use of beta-blockers. JAMA 1990; 263:1653.
25. Mangano DT, Layug EL, Wallace A, Tateo I. Effect of atenolol on mortality and cardiovascular
morbidity after noncardiac surgery. Multicenter Study of Perioperative Ischemia Research
Group. N Engl J Med 1996; 335:1713.
26. Poldermans D, Boersma E, Bax JJ, et al. The effect of bisoprolol on perioperative mortality and
myocardial infarction in high-risk patients undergoing vascular surgery. Dutch
Echocardiographic Cardiac Risk Evaluation Applying Stress Echocardiography Study Group. N
Engl J Med 1999; 341:1789.
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27. Gal TJ, Cooperman LH. Hypertension in the immediate postoperative period. Br J Anaesth
1975; 47:70.
28. Kaplan NM. Treatment of hypertension: Drug therapy. In: Kaplan's Clinical Hypertension, 9th ed,
Lippincott, Williams & Wilkins, Baltimore 2006. p.290.
29. Chobanian AV, Bakris GL, Black HR, et al. Seventh report of the Joint National Committee on
Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. Hypertension 2003;
42:1206.
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GRAPHICS
History of ischemic heart disease (history of myocardial infarction or a positive exercise test, current complaint of
chest pain considered to be secondary to myocardial ischemia, use of nitrate therapy, or ECG with pathological Q
waves; do not count prior coronary revascularization procedure unless one of the other criteria for ischemic heart
disease is present)
Rate of cardiac death, nonfatal myocardial infarction, and nonfatal cardiac arrest
according to the number of predictors [2]
No risk factors – 0.4% (95% CI: 0.1-0.8)
One risk factor – 1.0% (95% CI: 0.5-1.4)
Two risk factors – 2.4% (95% CI: 1.3-3.5)
Three or more risk factors – 5.4% (95% CI: 2.8-7.9)
Rate of myocardial infarction, pulmonary edema, ventricular fibrillation, primary cardiac
arrest, and complete heart block [1]
No risk factors – 0.5% (95% CI: 0.2-1.1)
One risk factor – 1.3% (95% CI: 0.7-2.1)
Two risk factors – 3.6% (95% CI: 2.1-5.6)
Three or more risk factors – 9.1% (95% CI: 5.5-13.8)
ECG: electrocardiogram.
References:
1. Lee TH, Marcantonio ER, Mangione CM, et al. Derivation and prospective validation of a simple index for prediction of
cardiac risk of major noncardiac surgery. Circulation 1999; 100:1043.
2. Devereaux PJ, Goldman L, Cook DJ, et al. Perioperative cardiac events in patients undergoing noncardiac surgery: A
review of the magnitude of the problem, the pathophysiology of the events, and methods to estimate and communicate
risk. CMAJ 2005; 173:627.
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Onset of Duration of
Adverse
Drug Dose range action action Role Δ
effects ¶
(minutes) (minutes)
Vasodilators
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Adrenergic inhibitors
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to 80 mg IV bronchospasm, myocardial
bolus every 10 dizziness, nausea, ischemia,
minutes heart block hypertensive
(maximum 300 encephalopathy,
mg) pregnancy, and
or postoperative
0.5 to 2 hypertension.
mg/minute as Avoid use in acute
IV loading decompensated
infusion heart failure.
following an Use cautiously in
initial 20 mg IV obstructive or
bolus reactive airway.
(maximum 300
mg)
IV: intravenous injection; AMI: acute myocardial infarction; IM: intramuscular injection; ACS: acute coronary syndrome; CAD:
coronary artery disease; CVA: cerebrovascular accident.
* The treatment of acute aortic syndromes (eg, acute aortic dissection, aortic intramural hematoma) requires specific
medication management to minimize disease extension and is presented separately. Refer to UpToDate topics discussing acute
aortic syndromes and acute aortic dissection.
¶ Hypotension may occur with all agents.
Δ IV short-acting agents for treatment of hypertensive emergency should be administered immediately by clinicians who are
trained and experienced in their titration using continuous noninvasive electronic monitoring of blood pressure, heart rate, and
cardiac rhythm. Patients should be admitted to an intensive care unit as rapidly as possible. A combination of IV agents is
often selected depending upon the acute indication. Refer to appropriate UpToDate clinical topic for suggested combinations.
◊ Initial fenoldopam doses in range of 0.01 to 0.3 mcg/kg per minute have been described.
References:
1. Marik PE, Varon J. Hypertensive crises: Challenges and management. Chest 2007; 131:1949.
2. Chobanian AV, Bakris GL, Black HR, et al. Seventh report of the Joint National Committee on Prevention, Detection,
Evaluation, and Treatment of High Blood Pressure. Hypertension 2003; 42:1206.
3. Varon J. Treatment of acute severe hypertension: Current and newer agents. Drugs 2008; 68:283.
NOTE: Recommendations for parenteral treatment of hypertensive emergencies were not given in either the JNC 8 guideline
(James PA, Oparil S, Carter BL, et al. 2014 Evidence-based guideline for the management of high blood pressure in adults:
Report from the panel members appointed to the Eighth Joint National Committee [JNC 8]. JAMA 2014; 311:507) or the Joint
ASH/ISH guidelines (Weber MA, Schiffrin EL, White WB, et al. Clinical practice guidelines for the management of hypertension
in the community: A statement by the American Society of Hypertension and the International Society of Hypertension
[ASH/ISH]. J Hypertens 2014; 32:3).
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Contributor Disclosures
John D Bisognano, MD, PhD Nothing to disclose Mark D Aronson, MD Nothing to disclose George L Bakris,
MD Grant/Research/Clinical Trial Support: Bayer [Diabetes (Finerenone)]; Janssen [Diabetic nephropathy clinical
trials (Canagliflozin)]; Vascular Dynamics [Resistant hypertension trial (Carotid stent)]. Consultant/Advisory
Boards: AstraZeneca [Diabetes (Dapagliflozin)]; Bayer [Diabetes (Finerenone)]; Relypsa [Hyperkalemia
(Patiromer)]; Merck [Diabetes (Many on global advisory, sitagliptin, ertugliflozin)]. Lisa Kunins, MD Nothing to
disclose John P Forman, MD, MSc Nothing to disclose
Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these are
addressed by vetting through a multi-level review process, and through requirements for references to be
provided to support the content. Appropriately referenced content is required of all authors and must conform to
UpToDate standards of evidence.
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