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CHAPTER 27 Hypertensive Emergencies 285
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TABLE 27.6 Therapeutic Agents for Hypertensive Emergency—cont’d
Drug Dosing (Intravenous) Mechanism of Action Adverse Effects/Risks
Nitroglycerin
Onset: 2–5 min
Duration: 5–10 min
Nitroprusside
Onset: within seconds
Duration: 1–3 min
Continuous infusion: start at 5 µg/min.
Increase by 5 µg/min every 3–5 min
to 20 µg/min.
If no response at 20 µg/min, increase
by 10 µg/min every 3–5 min, up to
200 µg/min (many clinicians initiate
with a higher infusion rate).
Continuous infusion: start at 0.5 µg/
kg/min.
Increase in increments of 0.5 µg/kg/
min every 5–10 min; titrate to
desired effect.
Maximum dosage is 10 µg/kg/min IV
for 10 min.
For infusions 4–10 µg/kg/min,
institute a thiosulfate infusion.
Nitroglycerin is converted by
mitochondrial aldehyde
dehydrogenase to nitric oxide, a
potent venodilator. It causes
venous capacitance vessel
dilatation at low doses (5 µg/min)
and arterial dilatation only at very
high doses.
Nitric oxide donor, which reduces
both preload and afterload
Can cause dose-related decreases in
coronary, cerebral, and renal
perfusion.
Avoid in cases of compromised cerebral and renal
perfusion.
Avoid concurrent use (within past 24–48 h) with
phosphodiesterase 5 inhibitors (sildenafil,
tadalafil, or vardenafil).
Methemoglobinemia may occur.
Common side effects: hypotension (especially in
volume-depleted patients), reflex tachycardia,
headache, nausea, vomiting
Avoid in patients with kidney or hepatic failure,
atriovenous shunts, hereditary optic nerve atrophy
(increases nerve ischemia), elevated ICP, or
patients who are pregnant.
Risk of cyanide and thiocyanate toxicity in patients
with reduced renal function or therapy >
24–48 h
or at rates >2 µg/kg/min.
Greater variability in BP response; needs more
titrations than patients receiving nicardipine.
Greater cardiac surgery mortality rates than with
clevidipine.
128
Nitroprusside is recommended only
71
when other agents fail.
Common side effects: hypotension, nausea,
vomiting, cyanide, and thiocyanate toxicity
Other Agents
Dexmedetomidine
Onset: 4–6 min
Duration: 2–4 h
Fenoldopam
Onset: 5–10 min
Duration: 10–15 min
Phentolamine
Onset: 1–2 min
Duration: 10–30 min
Peak effect:
10–20 min
Loading dose: 1 µg/kg over 10 min,
then 0.2–0.7 µg/kg/h (≤24 h)
Continuous infusion: 0.03–0.1 µg/kg/
min
Titrate no more than every 15 min by
0.05–0.1 µg/kg/min.
Fenoldopam is approved for
short-term use in adults (≤
48 h) and
children (≤4 h).
Bolus 2–5 mg every 5–10 min
(normally given IV but also can be
given IM)
Centrally acting α2-adrenergic
agonist that is 8–10 times more
selective to α
-adrenergic
2
receptors than clonidine.
It decreases BP via a decrease in
peripheral vascular resistance.
Peripheral dopaminergic-1 receptor
agonist, which raises intracellular
cyclic AMP and leads to
vasodilation of most arterial beds,
including renal, mesenteric, and
coronary arteries.
148
Competitive α-adrenergic receptor
antagonist α1 > α2 effects
α
leads to relaxation of systemic
1
vasculature, which leads to
activation of the baroreceptor
reflex, norepinephrine release,
which is attenuated by
phentolamine’s effects on
α
-receptors, and a decrease in BP,
2
which is accompanied by a rise,
sometimes dramatic, in heart rate.
Primarily used for light to moderate sedation in ICU
settings; second agent for sympathomimetic
hypertensive emergencies.
133,134
Slight increase in blood pressure at the onset of
infusion, lasting approximately 5–10 min.
Common side effects: hypotension, bradycardia
Avoid in patients with concomitant β-antagonist
use and with elevated intraocular pressure or ICP.
Avoid in patients with CAD (reflex tachycardia).
May cause hypotension in patients receiving
concomitant β-antagonist therapy.
May cause hypokalemia or anaphylactic reactions in
patients sensitive to sodium metabisulfite.
Associated with hypokalemia (<
3 mEq/L).
Common side effects: headache, dizziness, reflex
tachycardia, excessive hypotension, flushing
Contraindicated in patients with MI or CAD.
Avoid in patients with neurologic hypertensive
emergencies—has been associated with CVA
owing to cerebral artery occlusion.
Common side effects: hypotension, tachycardia,
arrhythmias, angina, headache, nausea, vomiting
ACS, Acute coronary syndrome; BP, blood pressure; CAD, coronary artery disease; CVA, cerebrovascular accident; GFR, glomerular filtration
rate; ICP, intracranial pressure; ICU, intensive care unit; IM, intramuscular; IV, intravenous; MI, myocardial infarction; SLE, systemic lupus
erythematosus.
286 PART IV Noncoronary Diseases: Diagnosis and Management
perfusion
140
Cerebral blood flow
pressure (mm Hg)
https://t.me/medicina_free
both hemispheres and occasionally hemorrhage (Fig. 27.3).
31,59
PRES is a reversible form of hypertensive encephalopathy. In
cases in which neurologic deficits remain, the majority are believed
to be due to intracerebral hemorrhage.
56
The treatment goal of PRES is to reduce the SBP by 10% to
15% within the first hour and by 25% within the first few hours,
with some recommending a target of less than 160/100 mm
59,62
Hg.
Few therapeutic trials of PRES treatment are available;
thus, the choice of antihypertensive agent is left to the discretion
of the treating physician and may include calcium channel
antagonists, labetalol, and fenoldopam.
63–66
Clevidipine, a
dihydropyridine calcium channel blocker, has gained favor due
to its rapid action and ease of titration (see Table 27.5).
)
–1
min
–1
70
(mL 100g
0
060 120
Fig. 27.2 Autoregulation of cerebral blood flow. (From Vaughan
CJ, Delanty N. Hypertensive emergencies. Lancet. 2000;356:
411–417.)
Vasoconstriction
Vasodilation
Mean arterial
hyper
Autoregulation
failure
63,64,67
Cerebral
Subarachnoid Hemorrhage. Subarachnoid hemorrhage (SAH)
is a significant cause of morbidity and carries a mortality rate
as high as 67%. Roughly half of survivors experience persistent
neurologic deficits.68 The classic presentation of SAH involves
an awake patient who describes the “worst headache of my life”
often characterized as reaching maximal intensity within the
first hour of onset (thunderclap headache). Noncontrast head
CT remains the cornerstone for diagnosis of SAH with a negative
predictive value of 99.9% if performed within 6 hours from
symptom onset.69 The sensitivity of CT falls sharply as time
progresses and, to ensure a diagnosis, a lumbar puncture is
required. Xanthochromia or red blood cells in the cerebrospinal
fluid are highly suggestive of an SAH.
Acute BP reduction in the setting of SAH has not been shown
to improve patient morbidity or mortality. There is, however,
general agreement that acute hypertension should be controlled
after aneurysmal SAH and prior to aneurysm obliteration, but
parameters for BP control have not yet been defined. Titratable
infusions are preferred, such as nicardipine, clevidipine, labetalol,
and esmolol.
70–74
The feared delayed complication of aneurysmal SAH, cerebral vasospasm, occurs most frequently 7 to 10 days following
aneurysm rupture. The cascade of events culminating in arterial
narrowing is initiated when oxyhemoglobin comes in contact
with the abluminal side of the vessel.68 To prevent cerebral
artery vasospasm, all patients should receive oral nimodipine,
a dihydropyridine calcium channel blocker, which was originally
developed for the treatment of hypertension. As such, it modestly
decreases BP as well as vasospasm and subsequent cerebral
infarction rates.68 Clinical trials have demonstrated a reduction
Fig. 27.3 Magnetic resonance brain axial fluid-attenuated inversion recovery images showing
radiographic features of posterior reversible encephalopathy syndrome. There is vasogenic edema
resulting in a symmetrical high signal within subcortical white matter of predominately occipital
and parietal lobes. These MRIs were obtained on a 16-year-old, postpartum female who presented
with intractable headache and depressed sensorium.
BA
CHAPTER 27 Hypertensive Emergencies 287
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in mortality by 74% and marked improvements in neurologic
disability in patients receiving nimodipine prophylaxis.75
Clazosentan, an investigational endothelin receptor antagonist
that can be given intravenously, also decreases the incidence of
vasospasm and has similar BP lowering effects as nimodipine
but its effects on morbidity and long-term disability remain
unclear.76 Nonsteroidal antiinflammatory drugs (NSAIDs) have
shown some promise in patients with aneurysmal SAH, with
reduced mortality rates, shorter duration of intensive care unit
and total hospital stays, as well as better functional outcomes
in patients treated with NSAIDs compared to controls.77 If
seizure prophylaxis is initiated, use caution with intravenous
phenytoin and benzodiazepines, as these can further lower BP (see
Table 28.5).
Intracerebral Hemorrhage. Intracerebral hemorrhage (ICH)
affects more than 1 million people worldwide annually and is
the least treatable of all stroke syndromes.78 Elevated BP is
extremely common in acute ICH, likely owing to a confluence
of factors—including stress, pain, increased intracranial pressure,
and premorbid hypertension.79 Current evidence indicates that
early intensive BP lowering is safe and feasible and that surviving
patients show modestly better functional recovery.79Although
the largest trial to date, the second Intensive Blood Pressure
Reduction in Acute Cerebral Hemorrhage Trial (INTERACT II),
demonstrated no statistically significant difference in the primary
outcome of death or disability among patients randomized to
an SBP target of less than 140 mm Hg compared to standard
treatment (SBP <180 mm Hg), functional improvements among
subgroups were noted.80 For ICH patients presenting with SBP
greater than 140 mm Hg, the American Heart Association (AHA)
recommends consideration of antihypertensive therapy for
improving functional outcome (Fig. 27.4).79 Antihypertensive
therapy should be individualized, with consideration of pharmacologic profile, potential side effects, and cost. Nicardipine
and labetalol have consistently been demonstrated to be safe
and effective in this population (see Table 27.5).
81–85
Ischemic Cerebrovascular Accident. The acute hypertensive
response in the setting of ischemic stroke is poorly understood.
Because it occurs in patients with transient ischemic attack as
well as stroke patients, the Cushing reflex is likely not responsible,
except in cases of massive cerebral infarction.86 Up to 80% of
patients with acute ischemic stroke are hypertensive on presentation.87 The elevated BP usually spontaneously resolves and, 10
days after the event, approximately two-thirds of patients are
normotensive. In some, the response reflects poorly treated or
long-standing hypertension. In others, it appears to be due to
other transient and stroke-specific mechanisms, including anxiety
surrounding the event or an abnormal autonomic response
No
SBP ≥150 mm Hg without
contraindication to BP
treatment
Yes
Consider antihypertensives
If GCS ≤8, evidence of herniation
or significant intraventricular
hemorrhage or hydrocephalus, THEN
Systolic BP > 220 mm Hg?
No
No antihypertensive
therapy
Yes
Consider aggressive BP reduction
with continuous intravenous
infusion and frequent monitoring
Acute lowering of SBP to
140 mm Hg is safe
and can improve
functional outcome
Consider need for ICP monitoring
to maintain cerebral perfusion
pressure of 50 to 70 mm Hg
Fig. 27.4 Blood pressure management algorithm for patients with intracerebral hemorrhage.
GCS, Glasgow Coma Scale; ICP, intracranial pressure. (Modified from Hemphill JC 3rd, Greenberg
SM, Anderson CS, et al. Guidelines for the management of spontaneous intracerebral hemorrhage:
a guideline for healthcare professionals from the American Heart Association/American Stroke
Association. Stroke. 2015;46[7]:2032–2060.)
288 PART IV Noncoronary Diseases: Diagnosis and Management
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induced by the ischemic insult and direct injury to areas of the
brain involved in cardiovascular regulation.
86,88
Hypertension
during acute ischemic stroke is an independent indicator of poor
neurologic prognosis.
4
Optimal management of BP in ischemic stroke remains
unclear. Aggressive lowering of BP may reduce cerebral perfusion pressure, aggravating brain ischemia and threatening the
vulnerable ischemic penumbra. Conversely, very high BP may
worsen cerebral edema and increase the risk for hemorrhagic
transformation.
88,89
Furthermore, there is evidence that controlling
hypertension immediately poststroke confers no benefit on shortterm mortality or morbidity.90 Current guidelines recommend
against lowering the BP unless BP elevations are extremely high
(SBP >220 mm Hg or DBP >120 mm Hg) or if the patient is
eligible for thrombolysis.4 Both US and European guidelines
recommend BP reduction if thrombolysis is planned (goal
<185/110 mm Hg).
4,91
Observational studies have demonstrated
a strong association between postthrombolysis hypertension and
poor outcome, prompting strong recommendations for careful
BP management in patients treated with tissue plasminogen
activator (tPA).
92
For the treatment of ischemic stroke, labetalol and nicardipine
are the recommended agents. However, the route and degree of
BP reduction depend on whether the patient is a candidate for
reperfusion therapy (Table 27.5).
4,90,93
Acute Renal Insufficiency
Patients with acute renal insufficiency may present with peripheral
edema, oliguria, loss of appetite, nausea and vomiting, orthostatic
changes, or confusion. However, some patients have few or no
specific symptoms. A patient with severely elevated BP with either
new hematuria (microscopic or gross) or a decline in renal
function is experiencing a hypertensive emergency. Physicians
should inquire about past kidney and urologic issues, including
renovascular disease, renal parenchymal disease, autoimmune
diseases (for possible vasculitis), renal artery stenosis and anatomic
abnormalities, such as horseshoe kidney, solitary kidney, and
prior renal transplantation.
the use of diuretics, nephrotoxic drugs, and sympathomimetic
agents. In renal transplant patients, stenosis of the graft site and
the use of cyclosporine, steroids, and other immunosuppressants
can predispose patients to a hypertensive emergency.97 Excessive
renin secretion by the native kidney may also precipitate a
hypertensive crisis.
Evaluation of these patients includes a basic chemistry panel
to reveal electrolyte abnormalities, the degree of creatinine elevation, and the patient’s bicarbonate level. Current values should
be compared to prior values to see if the decline in renal function
34
is acute.
A bedside, postvoid residual sonogram may identify
bladder outlet obstruction, in which case a urinary bladder
catheter should be placed. This should be followed by a renal
sonogram to evaluate kidney size and higher urinary tract
obstructions because obstruction of the urinary tract at any level
can raise BP.98 BP management in renal hypertensive emergency
patients includes fenoldopam, nicardipine, and clevidipine, as
they reduce systemic vascular resistance while preserving renal
blood flow.
99–102
In patients presenting with severe hypertension
94–96
Patients should be asked about
owing to renal vasculitis, such as scleroderma renal crisis and
Takayasu arteritis, enalaprilat has been shown to work well and
preserve renal function.
103,104
Preeclampsia or Eclampsia
Hypertensive disorders of pregnancy, including preeclampsia
and eclampsia, complicate up to 10% of pregnancies worldwide
and account for up to 80,000 maternal and 500,000 perinatal
deaths annually.
liver enzymes, low platelets) is considered to be a variant of
preeclampsia and presents within the same time period. The
three are not separate entities but rather related diseases along
a continuum.
From 1987 to 2004, the incidence of preeclampsia in the
United States increased 25%.
prevalence of obesity (a strong risk factor for preeclampsia),
changes in the diagnostic criteria, or earlier symptom identifica-
108,109
tion.
(typically ≥160/110 mm Hg) in patients who have progressed
beyond the 20th week of gestation. Current diagnostic criteria
for the diagnosis no longer require the presence of proteinuria
and instead incorporate other features of target organ damage
(Fig. 27.5).
Risk factors for the development of preeclampsia and eclampsia
include maternal age 30 years or greater, high body mass index,
nulliparity, absence of antenatal care, chronic hypertension,
gestational diabetes, cardiac or renal disease, pyelonephritis or
urinary tract infection, and severe anemia.
complain of headache, visual changes, and nausea or vomiting.
Since preeclampsia can rapidly become fulminant, health care
providers need to remain vigilant when mild disease has been
diagnosed.
this indicates progression to eclampsia. Eclamptic patients can
present from 20 weeks of gestation to 8 weeks postpartum.
The cause of preeclampsia is unclear; however, leading hypotheses summarize the syndrome as a failed interaction between
two genetically different organisms.
of the trophoblast and incomplete vascular remodeling result
in ischemia-reperfusion injury, oxidative stress, and a systemic
inflammatory response.
decreased release of nitric oxide and prostacyclin, causing more
vasoconstriction, BP elevation, and eventually end-organ damage
(Fig. 27.6).
Definitive treatment of preeclampsia and eclampsia is delivery.
However, there are risks with this approach: for preeclamptic
women remote from term (<34 weeks), there is evidence that
expectant management confers perinatal benefit with a minimum
of additional maternal risk.
weeks gestation with nonsevere hypertensive disorders, immediate delivery resulted in only minimal improvement in maternal
outcome and it was at the expense of significant increases in
neonatal morbidity and neonatal health care costs.
For preeclamptic women with severe hypertension (≥160/
110 mm Hg) or elevated BP with target-organ damage, antihypertensive therapy is recommended with labetalol, hydralazine, and
oral nifedipine considered first-line agents (see Table 27.5).
Patients with severe preeclampsia or eclampsia should be given
105,106
HELLP syndrome (hemolysis, elevated
107
This may be due to the increased
Preeclampsia is characterized by severe hypertension
6,107
110
Patients often
111
When seizures occur in the setting of elevated BP,
112
111
Impaired placentation
113
Endothelial dysfunction results with
114
115
In a study of women of 34 to 37
116,117
6,107,118
CHAPTER 27 Hypertensive Emergencies 289
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SBP ≥140 mm Hg and/or DBP ≥90 mm Hg after 20 weeks' gestation
in a woman with previously normal blood pressure
SBP ≥160 mm Hg or DBP ≥110 mm Hg
OR
PLUS
Proteinuria
≥300 mg per 24-hour urine collection
(or extrapolated from timed collection)
Protein/creatinine ratio ≥0.3
Dipstick∗ reading of 1+
Fig. 27.5 Diagnostic criteria for preeclampsia. *Use only if other methods are not available. Cr,
Creatinine; DBP, diastolic blood pressure; LFTs, liver function tests; SBP, systolic blood pressure.
(Modified from Hypertension, Pregnancy-Induced—Practice Guideline. ACOG Task Force on
Hypertension in Pregnancy. 2013;1–100. http://www.acog.org/Resources-And-Publications/Task-
Force-and-Work-Group-Reports/Hypertension-in-Pregnancy.)
intravenous magnesium sulfate for seizure prophylaxis and
treatment.
107
or
or
Perioperative Hypertension. Hypertensive emergencies typically
occur in perioperative patients with preexisting hypertension who
are either untreated or inadequately treated.
119
The mechanism
of action for elevated BP in perioperative patients is thought
to be multifactorial, including cessation of antihypertensive
medications (often the previous day), sympathetic activation
during induction of anesthesia and endotracheal intubation,
loss of vasodilation as anesthetic agents are weaned and further
sympathetic discharge, especially in patients with postoperative pain.
120,121
Management of these patients can be difficult
owing to hemodynamic instability that may occur during the
operative state: sudden changes in BP may be owing to release
of catecholamines, rapid intravascular volume shifts, blunted
baroreceptor response, renin-angiotensin activation, and reperfusion injury.
122–124
The proinflammatory and hypercoagulable state
of operative patients further contributes to vascular injury, platelet
activation, and endothelial dysfunction.
119
Complications include
bleeding from surgical sites, cardiovascular events (myocardial
ischemia and infarction and cardiac arrest), stroke, and death.
These complications are significant, as bleeding, MI, and cerebral
ischemia owing to acute hypertension occur in 5% to 35% of
perioperative patients and carry a fourfold higher mortality
119,125,126
risk.
While it is generally accepted that preoperative and
operative hypertension are predictive of poor postoperative outcomes, there is increasing evidence that postoperative hypertension
may also lead to adverse events, including increased mortality,
longer length of hospital stay, and higher incidence of renal
dysfunction.
127
BP control in perioperative patients is complex and depends
on the condition being managed operatively, whether the patient
has preexisting hypertension or was previously normotensive,
Severe Features
OR
Thrombocytopenia, platelets <100,000/µL
Renal insufficiency (Cr >1.1 mg/dL) or 2×/normal
New-onset cerebral or visual disturbances
(any of the following)
Elevation in LFTs to 2×/normal
Pulmonary edema
and what target organs are being affected or are at risk.
goals must be individualized and tailored to these factors while
taking into consideration patient comorbidities, analgesia or
anxiolytic requirements, the need for fluid resuscitation, and
the potential for hemodynamic instability.
The greatest experience in BP control has been in cardiac
and vascular surgery patients. After coronary artery bypass graft
(CABG) surgery or carotid endarterectomy, bleeding from vascular
anastomoses is a significant concern. Perioperative BP control
is associated with increased mortality in cardiac surgery patients.
In a recent study of cardiac surgery patients, clevidipine was
compared to nitroglycerin, sodium nitroprusside, and nicardipine.
The composite safety endpoint of 30-day death, MI, stroke, or
renal dysfunction did not differ among treatment groups.
Clevidipine, however, was more effective than nitroglycerin or
sodium nitroprusside in maintaining BP control and there was
a trend for lower mortality in the clevidipine group.
meta-analysis comparing clevidipine to other antihypertensive
agents for the management of BP in the perioperative setting,
similar results were found: clevidipine was more effective in
maintaining BP within prespecified ranges and demonstrated a
reduction in treatment failure rates when compared to other
agents. There was also no difference in adverse events.
129
agents that have been used with success in cardiovascular surgical
patients include nicardipine and labetalol (see Table 27.5).
A unique consideration for BP control is following carotid
endarterectomy or carotid artery stent procedures. These patients
frequently suffer from labile BPs that can last for days. Possible
causes include the disruption of the baroreceptor reflex from
trauma or damage to the carotid sinus or vagus nerve during
surgery. Hypertension in this period can lead to hyperperfusion
syndrome, in which resolution of the stenosis leads to hyperperfusion distal to the site. This syndrome is commonly seen in patients
with high-grade carotid artery stenosis, especially with bilateral
119
BP
128
In a
Other
119,130
290 PART IV Noncoronary Diseases: Diagnosis and Management
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Poor endometrium and inner
myometrium preparation
Impaired trophoblast invasion of
myometrium arteries
Poor spiral artery adaptation
Stage 1
Ischemia-reperfusion injury
Placental oxidative and
endoplasmic reticulum stress
Released components from the
intervillous space into the systemic
maternal circulation
Enhanced maternal intravascular
systemic inflammatory response
Generalized endothelial
dysfunction and leukocyte,
complement, and clotting activation
Decreased intravascular volume and
increased vascular reactivity
Fig. 27.6 Two-stage pathogenesis of preeclampsia. The first
stage begins with poor preparatory remodeling and spiral artery
adaptation, while the second stage is associated with exaggerated
endothelial activation and a generalized inflammatory state.
(Modified from Steegers EA, von Dadelszen P, Duvekot JJ, et al.
Pre-eclampsia. Lancet. 2010;376[9741]:631–644.)
disease, presumably because of a maximal dilation of the arteries
distal to the stenosis to maintain perfusion in a situation in
which autoregulatory mechanisms are lost. These patients present
with a range of neurologic complaints, including headache,
seizure, intracranial hemorrhage, altered mental status, and focal
neurologic changes.
131
Intensive management of BP, with intra-
venous β-antagonists or nitrates titrated to resolution of
symptoms, has been shown to decrease the incidence of
Stage 2
hyperperfusion syndrome and intracerebral hemorrhage from
29% to 4%.
132
Management of other perioperative hypertensive emergencies—
such as myocardial ischemia, aortic dissection, left ventricular
failure, and stroke—can be found in Table 27.5.
Hyperadrenergic States
Sympathomimetic Agents. Sympathomimetic drugs—such as
cocaine, amphetamines, phencyclidine hydrochloride (PCP), and
lysergic acid diethylamide (LSD)—can precipitate a hypertensive
emergency.
documented in patients with illicit use and patients suffering
from iatrogenic complications due to epistaxis treatment or when
cocaine is used as a topical anesthetic for laryngoscopy.
Cocaine blocks the presynaptic reuptake of norepinephrine and
dopamine, releases norepinephrine from sympathetic nerve terminals, and stimulates adrenal gland catecholamine release. Patients
present with agitation, tachycardia, hypertension, mydriasis, and
hyperthermia. Other agents that can precipitate a hypertensive
emergency include dietary supplements such as Ephedra sinica,
also known as ma-huang. This supplement contains ephedrine,
a chemical that stimulates the nervous and endocrine systems to
generate an acute rise in BP and has been temporally associated
with stroke, MI, and sudden death.
U.S. Food and Drug Association in 2006, it can still be obtained
outside the United States and via Internet sources.
receiving monoamine oxidase inhibitor therapy who consume
tyramine-containing foods may develop a hyperadrenergic
state and resultant hypertensive crisis.
tachycardia, elevated BP, diaphoresis, chest pain, and—depending
on the agent—mental status changes. Licorice can also cause
acute elevations in BP and complications may include PRES. The
active agent, glycyrrhic acid, inhibits 11β-hydroxysteroid dehydrogenase, causing mineralocorticoid excess. Most commercial
preparations do not have enough of this compound to cause
adverse effects, but some “original” or “old time” formulations
may and, if consumed in large amounts, can lead to hypertensive
crisis.
Patients with monoamine oxidase inhibitor toxicity often
benefit from intravenous benzodiazepine. Phentolamine, nitroglycerin, and calcium channel blockers may also be used. These
patients should be closely monitored, as the hypertensive phase
is often followed by a hypotensive phase. Therapeutic options
for these patients are presented in Table 27.5.
Abrupt Cessation of Antihypertensive Drugs. An acute cat-
echolaminergic syndrome may occur with abrupt discontinuation
of oral or transdermal clonidine. This “rebound hypertension”
often yields BP elevations higher than pretreatment levels and is
exacerbated by concomitant β-blocker therapy due to unopposed
α-mediated vasoconstriction.
noted with acute cessation of β-antagonists, but to a lesser degree
than with clonidine withdrawal.
increased sympathetic activity related to adrenergic receptor upregulation during the period of sympathetic blockade.
with underlying coronary artery disease are at risk of myocardial
ischemia and death with abrupt cessation of β-blockers.
142
44,133–136
Cocaine hypertensive emergencies have been
139
Although banned by the
141
Patients present with
143,144
145
Elevations in BP have also been
146
This is thought to be owing to
140
Patients
147
Patients
137,138
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In both settings, reinstitution of the original agent is preferred
and will typically have the greatest effect on BP. In patients with
rebound hypertensive emergency owing to abrupt clonidine
withdrawal, BP may be difficult to control unless clonidine is
reinstituted. Clonidine may be given orally at the patient’s normal
dose or, if unknown, 0.1 to 0.2 mg initially. A reduction in BP
will occur within 30 to 60 minutes and peak at 2 to 4 hours.
148
Less ideal is the use of a clonidine patch for patients who are
unable to take oral medications. Here, the onset of action may
be delayed by 2 to 3 days and titration is challenging. For
maximum absorption, apply the patch to the chest or upper
148
arm.
If additional BP control is needed, labetalol may be added.
Pheochromocytoma and Paraganglioma. Tumors arising from
chromaffin cells of the adrenal medulla and the sympathetic
ganglia are referred to as pheochromocytomas and paragangliomas
(extra-adrenal pheochromocytomas), respectively. Both secrete
catecholamines, have similar presentations, and are managed in
a comparable fashion. The main difference between them is the
risk for malignancy. Pheochromocytoma is rare, occurring in less
than 0.2% of patients with hypertension; between 5% and 20%
of tumors are malignant. Patients may experience life-threatening
hypertension, particularly in times of stress, that is, acute trauma,
surgery, infection, or pregnancy.
149
There have been several
reports of pheochromocytoma patients presenting with ACS,
prompting the term “the great imitator”; the diagnosis should be
considered, especially in patients with normal coronary arteries
on angiography.
150,151
Symptoms and signs of pheochromocytoma
include headache, alternating periods of normal and elevated
BP, tachycardia, and flushed skin, punctuated by asymptomatic
periods. Patient evaluation includes measurement of 24-hour
urinary fractionated catecholamines and metanephrines in patients
with a low suspicion of pheochromocytoma. In patients for whom
there is a higher suspicion of a catecholamine-secreting tumor,
free plasma metanephrines (drawn supine with an indwelling
cannula for 30 minutes) is the best screening test owing to its
high sensitivity (99%). This is also considered the best test for
high-risk children, given its relative ease of collection compared
to a 24-hour urine collection.
152
Elevated metanephrines should
prompt a search for the catecholamine-secreting mass, with CT as
the initial diagnostic test. In patients for whom metastatic disease
is suspected, MRI is preferred. Iodine
123
metaiodobenzylguanidine
(MIBG) scintigraphy can be done if suspicion is high but no
tumor is found with CT or MRI. MIBG is a compound that
resembles norepinephrine and is taken up by adrenergic tissue.
An MIBG scan is also helpful in identifying multiple tumors
when the CT or MRI is positive.
152
In patients with pheochromocytoma and a hypertensive
emergency, intravenous phentolamine, a nonselective α-receptor
blocker, is recommended (or intramuscular if venous access
is impaired).
may be needed to control reflex tachycardia.
153
A short-acting β-antagonist, such as esmolol,
153,154
Definitive
treatment is open surgical resection for large or invasive pheochromocytomas and for most paragangliomas and laparoscopic
resection of isolated adrenal gland masses or small, noninvasive
paragangliomas.
152
In the preoperative setting, patients who are hypertensive but
not in crisis may be managed and prepared for resection with
oral phenoxybenzamine, a long-acting (irreversible), nonselective,
α-receptor blocker for 7 to 14 days to allow adequate time to
normalize heart rate and BP.
152
Phenoxybenzamine forms a
permanent bond with α-receptors, preventing the binding of
adrenaline and noradrenaline. The α1-receptor blockade in the
walls of blood vessels leads to vasodilatation and a decrease in
BP. Since this is a nonselective α-receptor blocker, it also blocks
α2-receptors, which can lead to a reflex tachycardia. Even with
this pretreatment, patients will often require additional BP control
perioperatively with additional agents.
Autonomic Dysfunction. Autonomic dysfunction due to acute
spinal cord or head trauma, intracerebral hemorrhage, or
abnormalities such as spina bifida may also present as a hypertensive emergency. Autonomic dysreflexia is well documented
in chronic spinal cord patients, but it can also occur in the acute
phase (<1 month after spinal cord injury).
155
Typically, this occurs
in patients with injuries above T6, where exaggerated sympathetic
responses to noxious stimuli below the level of the injury lead
to diffuse vasoconstriction and hypertension. The parasympathetic
response results in bradycardia and vasodilation above the level
of the lesion and patients may complain of headache, flushing,
and diaphoresis. This response, however, is insufficient to reduce
elevated BP and may cascade into hypertensive emergency and
even cardiac arrest. Spinal cord injuries below T6 do not produce
this complication, because intact splanchnic innervation allows
for compensatory dilatation of the splanchnic vascular bed.
Immediate interventions include sitting the patient upright and
addressing causative factors—such as somatic pain (bed sores,
fracture pain), fecal impaction, and abdominal distension (often
due to incomplete bladder emptying)—before initiating pharmaceutical therapy.
labetalol, and nicardipine.
155
Agents for BP control include nitroglycerin,
157
Several cases of paroxysmal autonomic instability with dystonia (PAID) with BP control refractory
to the aforementioned agents were successfully managed with
dexmedetomidine, a central acting α2 agonist.
158,159
For additional guidance with pharmaceutical management
of hypertensive emergencies, see Table 27.6.
Acknowledgment
We acknowledge the contributions of Drs. Eduardo Pimenta,
David A. Calhoun, and Suzanne Oparil, authors of this chapter
in the previous edition.
The full reference list for this chapter is available at
ExpertConsult.com.
156
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