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Hypertension is one of the most common medical problems that affects approximately
1 billion individuals worldwide. Hypertension also results in significant morbidities
despite the availability of antihypertensive medications. Severe hypertension usually
develops in individuals with chronic hypertension but may also occur in individuals
with no previous elevation of blood pressure. Patients with severe hypertension may
present to their primary care physician with relatively mild symptoms or to the
emergency department or intensive care unit (ICU) with life-threatening
complications. Severe hypertension may be the cause of critical illness, complicate
the course of another critical illness, or have little impact on the primary critical
illness. In general, elevations of blood pressure, either acute or chronic, can be
particularly detrimental in a critically ill patient. Some patients can be managed in the
outpatient setting but others require hospitalisation on the general ward, an
intermediate care unit, or the ICU. Appropriate evaluation and management of
patients with severe hypertension is important because inadequate therapy as well as
overaggressive therapy can result in adverse consequences. This module will address
the evaluation and therapy of acute severe hypertension rather than chronic
management of hypertension.
Try to remember the circumstances where you have encountered patients with severe elevation
of blood pressure and whether the patients had chronic hypertension.
References that provide additional information on hypertension in the critically ill are
listed below. Both articles review causes of hypertensive emergencies and the
management of specific clinical conditions associated with severe hypertension. More
information on the use and pharmacology of drugs used to treat severe hypertension is
Chronic or acute increases in blood pressure are a common finding in the general population as we
in critically ill patients. It is important for the physician to determine the accuracy of the blood pressu
measurement and its clinical significance. The impact of an elevated blood pressure may be more
difficult to assess in a critically ill patient due to concomitant diseases and therapeutic interventions
such as mechanical ventilation, or sedation.
Categories of hypertension
The Joint National Committee on Prevention, Detection, Evaluation and Treatment of High Blood
Pressure in the USA classified hypertension in adults aged 18 years and older into stages based on
the severity of blood pressure elevation. This classification may be helpful in the evaluation and
management of patients with chronic hypertension, but is less helpful for acutely ill patients with sev
elevations of blood pressure. It does, however, emphasize the importance of even slight elevations
blood pressure.
Blood Pressure
Systolic (mmHg)
Diastolic (mmHg)
120-139 or
140-159 or
≥160 or
Severe hypertension that is potentially life-threatening is referred to
as a hypertensive crisis. Severe hypertension is further characterised
into hypertensive emergencies or hypertensive urgencies.
Hypertensive emergency refers to severe hypertension that is
associated with new or progressive end-organ damage (primarily
brain, heart and kidney). In these clinical situations, blood pressure
should be reduced immediately (within minutes or a few hours
depending on the clinical circumstances) to prevent or minimise
organ dysfunction (see table below). Hypertensive urgency refers to
severe hypertension without evidence of new or worsening endorgan injury (see table below). Blood pressure can be lowered less
rapidly in these conditions.
Classification of blood
pressure in ambulatory adults
The finding of new or
progressive end-organ injury
is key to distinguishing a
hypertensive emergency from
an urgency
Consider how elevations of blood pressure lead to organ dysfunction. Useful
information may be found in the following reference.
Patients with severe hypertension who are asymptomatic and have no endorgan injury do not require urgent lowering of blood pressure. In most cases,
institution or modification of an antihypertensive regimen is indicated.
Classification of hypertensive
When knowledge of prior end-organ dysfunction is unavailable, differentiating hypertensive
emergencies from urgencies may be difficult. Accelerated hypertension is a term used to describe a
hypertensive urgency characterised by the presence of retinal haemorrhages and exudates without
papilloedema. The term malignant hypertension is best avoided since it has been used in a confusin
manner to describe either pathological, fundoscopic or clinical findings.
Document the number of patients in your ICU over the next several months who
have severe elevations of blood pressure and classify them as hypertensive
emergencies, hypertensive urgencies, or chronic hypertension. Determine whic
type of severe hypertension is most common in your patient population
There is not a specific blood pressure level that differentiates a
hypertensiveemergency from a less urgent situation. The degree of blood
pressure elevation does not necessarily correlate with the severity of end-orga
injury. The rate at which blood pressure rises and the prior level of blood
pressure are more important than the absolute level. Most hypertensive
emergencies are associated with a diastolic blood pressure greater than 120
mmHg, but a previously normotensive patient may experience end-organ injury
with a diastolic blood pressure of 100 to 110 mmHg. Conversely, patients with
chronic elevations of blood pressure may be asymptomatic with diastolic blood
pressures greater than 120 mmHg.
What types of patients are likely to have hypertensive emergencies with lower diastolic blood
Explain what pathophysiological factors play a role in the development of severe hypertension?
Measurement of blood pressure
Since potentially life-threatening conditions due to severe
hypertension are first recognised by an elevated blood pressure, it is
imperative that blood pressure is correctly measured. A standardised
approach with properly calibrated equipment should be utilised when
obtaining a manual blood pressure reading. The patient should be
sitting or supine with the arm at heart level. The width of the bladder
inside the cuff should be 40% of the circumference of the upper arm
and the length should encircle 80% of the arm circumference. A cuff
that is too small or wrapped too loosely on the arm may result in
falsely elevated blood pressure measurements. A stethoscope is
placed over the antecubital fossa and the blood pressure cuff inflated
to a level at which the radial pulse disappears. The first appearance
of repetitive sounds as the pressure is slowly released in the cuff is
the systolic pressure (phase 1) and the disappearance of repetitive
sound signals the diastolic pressure (phase 5).
In circumstances where the sounds are difficult to auscultate, it is
usually possible to obtain a systolic pressure by palpation of the
radial pulse and its disappearance. If severely elevated, blood
pressure should be measured in both upper extremities to assess for
One of the most common
errors in measuring blood
pressure is using a cuff that is
too small for the patient's arm
discrepancies suggesting aortic dissection. The reference below
provides detailed standards for measuring blood pressure accurately
with a sphygmomanometer device.
Automated blood pressure devices using auscultatory or oscillometric techniques are frequently use
to obtain intermittent blood pressure measurements. Oscillometric devices derive the diastolic press
from the systolic pressure and the mean arterial pressure. Although the arm is the preferred site for
cuff, the calf, thigh, or forearm can also be used. The cuff should not be placed on an extremity bein
used for intravenous infusion or that has circulatory compromise. Inflation of the cuff will also
transiently interfere with pulse oximetry readings from the same extremity.
New noninvasive monitoring technologies being developed that measure beat by beat blood pressu
are currently undergoing validation. Further information can be found in the PACT modules
on Haemodynamic monitoring and Health Technology Assessment.
Automatic blood pressure devices are less accurate in clinical situations that
are commonly encountered in the critically ill patient such as shock, mechanica
ventilation and arrhythmias. If an abnormal reading is obtained, the position of
the cuff and the function of the device should be assessed.
The most accurate measurement of blood pressure is obtained by use of an appropriately calibrated
intra-arterial catheter that allows continuous blood pressure measurements. Intra-arterial monitoring
may be indicated for patients with hypertensive emergencies who require use of potent
antihypertensive agents and close monitoring of blood pressure variation.
In your ICU, compare blood pressures obtained by intra-arterial pressure
monitoring and blood pressures obtained in the same patient by a manual or
automated blood pressure device. Note discrepancies of systolic and diastolic
pressures in patients with stable and unstable haemodynamics and in younger
and older patients. Determine if the mean arterial pressures are similar with
different devices.
Pain, anxiety, stress of hospitalisation and cold can result in elevations of bloo
pressure. These factors should be treated or corrected before considering use
of antihypertensive medications.
Clinical assessment of the patient
The history and physical examination should be targeted to detect abnormalities in those organ
systems most affected by elevations of blood pressure, in particular: the neurological, cardiovascula
and renal systems. This evaluation will provide the necessary information to identify the clinical
syndrome associated with the hypertensive crisis (see table
). In many circumstances, however,
definitive diagnosis will require additional laboratory or imaging studies.
Assessing neurological end-organ damage
Neurological symptoms may be subtle or overt. Neurological
involvement is suggested by complaints of headache, nausea,
vomiting, visual disturbances, confusion, lethargy, seizures and focal
neurological deficits. Subtle abnormalities of mental status may
require confirmation from friends or family members. A rapid yet
detailed neurological examination should be undertaken to assess
mental status, the presence of focal motor or sensory deficits, and
presence of cerebellar dysfunction. The examination should include a
thorough inspection of the optic fundi for evidence of cotton wool
exudates or flame-shaped haemorrhages as well as papilloedema.
See the website below for more information.
A fundoscopic examination is
required as part of the
assessment for neurological
end-organ injury
Lumbar puncture, if there is no cerebral oedema present, and toxicologic screens may be further
required. See the PACT module on Altered consciousness for more information on lumbar puncture
Neuroimaging (computed tomography or magnetic resonance imaging, see the PACT module
on Clinical imaging) is mandatory for the diagnosis of acute intracranial events. A non-contrast CT s
should be obtained initially to evaluate for the presence of intraparenchymal or subarachnoid blood.
Typical hypertensive bleeds occur in the basal ganglia/hypothalamic regions and cerebellum (see th
images below). A CT scan may initially be normal in acute thrombotic stroke. A normal CT scan or t
presence of cerebral oedema may be compatible with hypertensive encephalopathy.
CT scans showing
hypertensive bleeds
How is hypertensive encephalopathy diagnosed?
It is crucial to rapidly distinguish hypertensive encephalopathy from other
intracranial catastrophes because immediate blood pressure reduction is
mandatory for hypertensive encephalopathy whereas it may worsen
neurological deficits in stroke and intracranial haemorrhage.
Using neuroimaging, a syndrome of reversible posterior leukoencephalopathy has been recently
described in association with hypertensive encephalopathy and preeclampsia/eclampsia. It is also
associated with immunosuppressive and cytotoxic therapy, erythropoietin use, and other conditions
This syndrome is potentially fully reversible. You can read more about it in the following reference
Assessing cardiovascular end-organ damage
Symptoms suggesting involvement of the cardiovascular system due to severe hypertension include
anginal chest pain, dyspnoea, or severe tearing chest pain associated with acute aortic dissection.
Physical examination may reveal jugular venous distension, a third or fourth heart sound, tachycard
or pulmonary rales. Physical findings that may suggest acute aortic dissection include pulse deficits
the extremities, a new murmur of aortic valve insufficiency, and signs of left pleural effusion.
An electrocardiogram and chest radiograph should be obtained in
patients with severe hypertension who are suspected to have an
acute coronary syndrome, left ventricular dysfunction causing
pulmonary oedema or acute aortic dissection as the end-organ injury.
Myocardial infarction may be apparent from ST-segment elevation on
the electrocardiogram and/or confirmed by elevation of markers of
myocardial injury such as CPK-MB or troponins. See the PACT
module on Acute brain ischaemia.
An electrocardiogram may
reveal evidence of myocardial
ischaemia or infarct
Diagnosis of other acute coronary syndromes may depend on the
clinical history and electrocardiographic findings such as ST-segment
depressions or T-wave inversions. Left ventricular dysfunction
associated with severe hypertension may be due to systolic or
diastolic abnormalities.
What clinical and ancillary test findings may be helpful in distinguishing between systolic and
diastolic dysfunction?
Echocardiography is useful to assess left ventricular function and to identify left ventricular hypertrop
or dilation. Right heart catheterisation may differentiate haemodynamic pulmonary oedema from oth
forms of bilateral pulmonary infiltrates (e.g. acute respiratory distress syndrome, severe bilateral
pneumonia) but it is usually not needed in hypertensive emergencies.
Echocardiography may show normal systolic function during hypertensive
pulmonary oedema, since the majority of episodes are due to exacerbation of
diastolic dysfunction. The clinical study cited below shows that left ventricular
ejection fraction was normal in most patients, and similar during an episode of
hypertensive pulmonary oedema and after treatment, when the blood pressure
has been controlled.
If acute aortic dissection is suspected, a definitive diagnostic test
should be obtained and the choice will depend on availability of
imaging procedures and patient factors. Recommended imaging
studies are aortography, transoesophageal echocardiography (TOE),
computed tomography scans or magnetic resonance imaging.
Additional information on aortic dissection can be found in the review
by Khan and Nair.
If the patient is already in the
ICU on a ventilator and there
is good local expertise with
echocardiography, TOE – if
not contraindicated – can be
diagnostic in dissection of the
thoracic aorta.
It is crucial to distinguish between aortic dissection and myocardial infarction
quickly to avoid delay in proper treatment and to ensure that thrombolytic and
anticoagulant therapy are not given to the patient with a dissection.
Assessing renal end-organ damage
The renal system is difficult to assess by history and physical examination in the setting of severe
hypertension. Patients may present with non-specific symptoms of weakness, pretibial oedema,
oliguria, polyuria, nocturia, or haematuria. Physical examination may rarely pick up the presence of
bladder distension or polycystic kidneys in some individuals.
Laboratory evaluation includes full blood count, measurement of blood urea nitrogen, creatinine, an
electrolytes. The peripheral blood smear may reveal signs of microangiopathic haemolysis
(schistocytes and other fragmented red cells). Urine analysis must be obtained to detect proteinuria
haematuria, and the presence of cellular casts. Renal and urinary tract ultrasound is useful to detec
obstructive acute renal failure. If acute glomerulonephritis is suspected, a renal biopsy should be
performed soon after blood pressure control to confirm diagnosis and initiate appropriate therapy.
See the PACT modules on Oliguria and anuria
and Acute renal failure
There is a higher than expected prevalence of secondary hypertension (such a
renal artery stenosis, acute glomerulonephritis, Cushing's syndrome,
phaeochromocytoma) among patients who present with a hypertensive crisis.
Most authorities recommend screening for secondary causes of hypertension
after initiation of antihypertensive treatment. In the acute setting, however, it is
not useful to request costly laboratory or imaging studies to detect secondary
hypertension. Kidney can be easily seen using an echo.
Other assessments
A urine toxicologic screen may be indicated in some patients with severe
Observe the clinical course of the next patients with drug or toxin-induced
hypertensive crisis. What were the products suspected or identified? How did
their care differ from patients with hypertensive crises due to other causes?
If untreated, hypertensive emergencies are associated with a high mortality and
morbidity, depending on the severity of the associated organ damage. Since the
advent of effective antihypertensive drug therapy, the prognosis of patients with
hypertensive crisis has improved dramatically.
However, serious and avoidable sequelae may occur if blood pressure is reduced
too quickly and/or too much. Hence, the goal of antihypertensive therapy is to
decrease blood pressure while maintaining organ perfusion and avoiding
complications. The intensivist may be involved in making the initial decisions on
management of patients when the hypertensive crisis occurs in the ICU or they
may be called on to continue care that was initiated in the emergency
department, operating suite or other hospital location. Both situations require
prudent choices in management.
The following steps are helpful in addressing critical decisions that need to be
made for patients with severe elevations of blood pressure. They are to be
considered successively.
Should the blood pressure be lowered acutely?
End-organ damage is present. This is a hypertensive
emergency. Admit the patient to an intensive care unit or
other available monitored bed, monitor blood pressure,
and use parenteral agent(s) (see Task 3
and Task
) to lower blood pressure to safer levels (not
necessarily normal levels) within several minutes or hours.
No end-organ damage is present (or unchanged from
baseline). This could be a hypertensive urgency (see
above). Admit the patient to a short-stay unit or the
general ward, monitor blood pressure using non-invasive
devices, and use oral therapy (see Task 3
and Task
) to lower blood pressure to safer levels over several
The most important
management decision is to
determine if the blood
pressure needs to be lowered
hours to 24 hours. The level of care is often dependent on
the nature of coexisting conditions.
Asymptomatic patients with severe hypertension usually
do not require immediate reduction of blood pressure. An
appropriate antihypertensive regimen should be instituted
and adequate follow-up arranged.
Since many potent antihypertensive drugs are available, the challenge is 'when' to
reduce blood pressure rather than 'how'. As for many other medical situations, the
principle, 'first do no harm', is to be applied.
How much should the blood pressure be lowered?
No clinical study has been designed to examine the optimal target blood
pressure for each clinical condition associated with a hypertensive
emergency or urgency. In hypertensive emergencies, a reasonable goal is to
reduce mean arterial blood pressure by 20 to 25% or to reduce diastolic
blood pressure to 100-110 mmHg over minutes to hours. If the patient's
baseline blood pressure is known, that information should also be taken into
account when choosing a target blood pressure. In aortic dissection, the
target blood pressure could be as low as a systolic blood pressure
≤ 110 mmHg.
Blood pressure should be
lowered to a safer, but not
usually a normal level
In most situations, the blood pressure is not lowered to a normal range because
hypoperfusion of vital organs may result. The vascular autoregulatory mechanisms in
individuals with chronic hypertension have adapted to higher levels of blood pressure.
An example is the autoregulation of cerebral blood flow in normotensive individuals
compared to hypertensive patients (see figure below). The autoregulatory curve is
shifted to higher pressures in hypertensive patients. A normal mean arterial blood
pressure in a hypertensive patient may be below the lower limit of their ability to
maintain cerebral blood flow and result in cerebral ischaemia. Similar autoregulation
occurs in the myocardial and renal vasculature.
Which medication should be used to lower blood pressure?
More options are now available to lower blood pressure in hypertensive emergencies and the choice
medication can be individualised depending on patient characteristics and the clinical situation.
Coexisting patient conditions may determine whether some drugs are desirable. The available facili
and personnel may also influence the drug choice especially if frequent monitoring is not available.
course, the pharmacodynamics and pharmacokinetics of antihypertensive drugs play a role in all of
these considerations. The drugs available to treat hypertensive crises are discussed in Task 3
Consider which patient conditions would influence the use of certain parenteral
antihypertensive drugs.
The aim of drug therapy in patients with hypertensive emergencies is
to reduce blood pressure in a controlled, predictable, and safe way.
Depending on the nature of the end-organ damage, a particular
therapeutic strategy may be more or less appropriate. This section
reviews the pharmacology of drugs used to treat hypertensive crises
and Task 4
addresses drug options for specific clinical conditions.
All agents used to treat
hypertensive emergencies
can result in excessive
decreases in blood pressure
The availability of individual drugs will vary from country to country.
What are the ideal characteristics of an agent for treatment of a hypertensive emergency?
Observe in your unit the drug(s) used for specific hypertensive emergencies. Was the
drug choice based on its pharmacodynamic properties, on the haemodynamic profile
of the patient or on the underlying disease?
Treating hypertensive emergencies
Intravenous medications should be chosen for the treatment of true hypertensive emergencies. In
general, a single agent is preferable to using multiple agents.
Pharmacodynamic characteristics of parenteral antihypertensive drugs
i.v. infusion 0.25-10 mcg/kg/min
Immediate 1-2 min
i.v. bolus
3-5 min
3-6 h
Start 10-20 mg up to 80 mg every 10 min
i.v. infusion 0.5-2 mg/min
i.v. infusion 5-300 mcg/min
1-2 min
1-3 min
i.v. infusion 5-15 mg/h
5-10 min
15-40 min
i.v. loading
1-2 min
20-30 min
1 mg/kg for 1 min
i.v. infusion 150-300 mcg/kg/min
i.v. infusion 15-120 mg/h
2 min
2-3 h
i.v. bolus
0.625-1.25 mg every 6 h
10-15 min
6-8 h
i.v. bolus
5-20 mg every 20-60 min
10-30 min
3-6 h
i.v. infusion 0.1-1.6 mcg/kg/min
15 min
30-60 min
i.v. bolus
1-2 min
10-30 min
i.v. infusion 1-16 mg/h
2-4 min
5-15 min
5-10 mg every 10 min
A separate line should be used for the infusion of antihypertensive agents to
avoid flushing the line while giving another medication.
Diazoxide, a potent arteriolar dilator, and trimethaphan camsylate, a ganglionic blocker, are now
obsolete because of frequent adverse effects and the advent of better intravenous agents.
Sodium nitroprusside Nitroprusside is the prototype of a shortacting easy-to-titrate arteriolar and venous vasodilator. It has been
used effectively in all conditions associated with hypertensive
emergencies. The most common adverse effect is arterial
hypotension. Excessive drops in blood pressure can be detected by
intra-arterial monitoring and are managed by reducing the dosage
and administering fluids if needed. Other adverse effects include
reflex tachycardia and cyanide or thiocyanate toxicity.
These drugs are not grouped
by class since there are no
well defined pharmacological
classes among these agents
Explain which clinical conditions may increase the risk of cyanide or thiocyanate toxicity?
Cyanide toxicity is best prevented by avoiding administration of large dosages for prolonged periods
time (e.g. dosages greater than 3 mcg/kg/min for more than 72 hours), especially in patients with re
or hepatic dysfunction. The maximum administration rate of 10 mcg/kg/min should not be maintaine
for more than 10 minutes. In some centres, cyanide levels are monitored and sodium thiosulphate o
hydroxocobalamin are co-administered to prevent or treat cyanide toxicity. Haemodialysis is effectiv
removing thiocyanate.
What are the clinical signs of cyanide and thiocyanate toxicity?
Although sodium nitroprusside has been reported to increase intracranial pressure, the associated f
in systemic vascular resistance seems to offset this effect. Nitroprusside may increase mortality whe
infused in the early hours after acute myocardial infarction. Intrapulmonary shunting may result in a
decrease in oxygenation.
Labetalol hydrochloride Labetalol is a non-selective β-adrenergic blocker with associated α-block
activity, in a 7 to 1 ratio in intravenous formulation. It reduces systemic vascular resistance with mild
reduction in heart rate and maintains cardiac output. Labetalol can be given intravenously (bolus or
infusion) or orally. It is useful in most hypertensive emergencies, especially those associated with hi
levels of circulating catecholamines. It is also effective in preeclampsia/eclampsia, by decreasing bl
pressure while maintaining placental perfusion. As a β-blocker, labetalol is contraindicated in patien
with active obstructive pulmonary diseases or second or third degree heart block, and should be use
with caution in patients with decompensated systolic heart failure. Side effects are minor and includ
nausea, vomiting, paresthesias and headache.
Nitroglycerin Nitroglycerin is a venous and coronary artery dilator although higher doses can also
dilate systemic arteries. Intravenous nitroglycerin is ideally indicated in hypertensive patients with ac
coronary syndromes and has also been used for perioperative hypertension. Side effects include
headache, nausea, bradycardia, hypotension, and rarely methaemoglobinaemia. Prolonged use ma
induce tachyphylaxis.
Nicardipine hydrochloride Nicardipine is a dihydropyridine calcium channel antagonist with system
and coronary artery vasodilating effects. It can be administered intravenously for hypertensive
emergencies and has minimal or no negative inotropic effects or atrioventricular conduction effects.
Nicardipine is widely used for control of perioperative hypertension, and is also effective and safe in
other forms of severe hypertension including preeclampsia/eclampsia. Lower doses may be
appropriate in older patients or patients with liver disease who may have decreased hepatic
metabolism. Side effects include headache, flushing, hypotension, nausea, vomiting and tachycardi
(although there is usually minimal, if any, increase in heart rate in adult patients).
Esmolol hydrochloride Esmolol is a short-acting cardioselective β-adrenergic blocker that is mainl
used to control perioperative hypertension and tachycardia. It has no vasodilatory effects and lower
blood pressure by decreasing heart rate and myocardial contractility. Side effects and contraindicati
are those of β-blockers. If it is the only agent used and concurrent longer acting drugs are not initiat
a prolonged infusion of esmolol, especially in high dose, is a relatively expensive means of blood
pressure control.
Phentolamine mesylate Phentolamine is a peripheral α-adrenergic blocker indicated for the
management of hypertensive emergencies associated with catecholamine excess such as
phaeochromocytoma, monoamine oxidase inhibitor interaction, antihypertensive withdrawal syndrom
and cocaine abuse. This agent may cause tachycardia, hypotension, headache, vomiting, flushing a
Catecholamine storm is uncommon and can be effectively controlled by other
agents such as labetalol, nitroprusside, or reinstitution of the previous
antihypertensive regimen (especially clonidine).
In the ICU patient, typically
with unresponsive,
intermittent (bursts of)
hypertension, one should
suspect the potential
presence of
pheochromocytoma, consider
phentolamine, or alternative
vasodilator, treatment acutely
and be prompted to
investigate formally for
Urapidil Urapidil is a peripheral α1-adrenergic blocker with additional central 5-hydroxytryptamin A1
receptor agonist activity that has been found to be effective in severe hypertension, including
perioperative hypertension. Its main advantage is that reflex tachycardia does not occur as a result
reduced sympathetic outflow. It is not available in the USA. A test dose of 40-50 mg in an adult is
useful and may discriminate whether urapidil will be effective in lowering blood pressure.
Enalaprilat Enalaprilat is the intravenous formulation and the active metabolite of the orally active
angiotensin-converting enzyme inhibitor enalapril. It reduces blood pressure by dilating arterial and
venous vessels. The long duration of action, variable response and limited experience do not make
agent an ideal drug for hypertensive emergencies. Moreover, angiotensin-converting enzyme inhibi
are contraindicated during pregnancy, in patients with renal impairment especially with stenosis of
renal arteries as the cause of hypertension. Adverse effects are hypotension (especially in sodium o
volume-depleted patients), angio-oedema, renal dysfunction and hyperkalaemia.
Hydralazine hydrochloride Hydralazine is a direct arteriolar dilator that may be given intravenously
and orally. It is more difficult to manage than other intravenous agents because of the variable
magnitude and duration of response. Its remaining parenteral indication is preeclampsia and eclamp
because it improves placental blood flow. Even for this indication, labetalol and calcium antagonists
seem preferable because maternal and perinatal side effects are less common. Since hydralazine
increases heart rate, cardiac output and myocardial oxygen consumption, it should not be used in
patients with myocardial ischaemia or aortic dissection.
Fenoldopam mesylate Fenoldopam is a short-acting peripheral postsynaptic dopamine-1-receptor
agonist approved for inhospital, short-term management of severe hypertension. Its antihypertensiv
action is due to a combination of arterial vasodilatation, renal vasodilatation and natriuresis. It has n
toxic metabolites. Fenoldopam and nitroprusside are equally effective in the treatment of severe
hypertension, so that fenoldopam may be an alternative to nitroprusside. Fenoldopam may be
particularly useful in severely hypertensive patients with impaired renal function or congestive heart
failure. Adverse effects include headache, flushing, hypotension, dose-related tachycardia, decreas
serum potassium and increased intraocular pressure. It is not available in the European community.
learn more about this drug, read the following review article.
Clevidipine Clevidipine is a short-acting intravenous dihydropyridine calcium channel antagonist
recently approved for treatment of severe hypertension in the USA. This agent is an arteriolar
vasodilator resulting in decreased blood pressure with little change in heart rate or cardiac output.
Favourable characteristics include rapid hydrolysis by blood and tissue esterases to an inactive
metabolite, a short duration of effect (1-3 min), and metabolism unaffected by renal or hepatic functi
Intrapulmonary shunt fraction is increased and associated with a decrease in PaO2. Clinical trials
reported in the references below suggest that clevidipine may be an option for blood pressure contr
the perioperative period. Hypotension and reflex tachycardia have been described.
What is the intravascular volume status of patients with hypertensive crises?
Treating hypertensive urgencies
Hypertensive urgencies do not require acute lowering of blood pressure. In most
cases, oral medication appropriate for the chronic underlying disease processes
can be initiated. There is no evidence to suggest that immediate lowering of
blood pressure improves any outcome measure but considerable adverse effects
can be precipitated by inappropriate rapid reductions in blood pressure. The
decision to treat the blood pressure with an oral agent in the hospital or to
institute a therapeutic regimen as an outpatient should take into consideration
comorbid conditions, the potential for progression to a hypertensive emergency,
and the ability to obtain timely follow-up. Most patients with hypertensive
urgencies will not require intensive care.
Oral agents for hypertensive urgencies
Labetalol See
. Oral labetalol has been used effectively to lower blood
pressure in non-emergency conditions. This drug may be particularly helpful in
patients with tachycardia.
Clonidine Clonidine is a central α2-adrenergic agonist that decreases
sympathetic outflow, and hence systemic vascular resistance and heart rate. It is
an alternative to oral β-blockers or labetalol if contraindications to these agents
are present. It is available as a parenteral agent in Europe. Administration of
clonidine is particularly helpful in patients with severe hypertension due to
discontinuation of chronic clonidine therapy or withdrawal states. Side effects are
dry mouth, bradycardia and orthostatic hypotension. Sedation may occur that can
interfere with neurological evaluation in patients with cerebral disease.
Captopril Captopril, an angiotensin-converting enzyme (ACE) inhibitor, has been
used successfully in hypertensive urgencies. Other ACE inhibitors have also
been administered with similar efficacy. Adverse effects are first-dose
hypotension in patients with sodium or volume depletion or acute renal failure in
patients with bilateral renal artery stenosis. Therefore, captopril should not be
used when renal artery stenoses are suspected.
Nifedipine Oral, sublingual or bite-and-swallow fast-acting nifedipine has been
widely used to rapidly reduce blood pressure in acute hypertension in the past.
However, the inability to control the rate or magnitude of decrease in blood
pressure has been associated with serious adverse effects, including death,
making this agent unacceptable for this purpose. In hypertensive urgencies tha
require immediate oral antihypertensive treatment, an adequate dose of a longacting agent should be provided. The following position paper gives welldocumented arguments against the use of short-acting nifedipine.
Hypertensive emergencies encompass a wide variety of clinical
conditions and several drugs are now available for use in these
situations. The clinician should take into account the specific
aetiology of the severe hypertension, co-existing patient conditions,
and the pharmacology of agents when selecting a drug for use.
The antihypertensive drug
should be tailored to the
patient's needs and
underlying disease
Hypertensive encephalopathy
In hypertensive encephalopathy, the lowering of blood pressure is therapeutic as
well as diagnostic. If the mental status does not improve within a few hours of
lowering the blood pressure, other diagnoses should be considered. Historically,
nitroprusside has been the most commonly used agent in this clinical situation.
Alternative drugs that are easy to administer include labetalol and fenoldopam.
Nitroglycerin and nicardipine may also be effective but clinical experience in
hypertensive encephalopathy is limited. Drugs that cause sedation such as
clonidine should not be used in order to avoid confusion with the neurological
Acute intracranial events
Little prospective evidence exists for lowering the blood pressure or the extent of
blood pressure reduction in the setting of traumatic injury, intracranial
haemorrhage and thrombotic stroke. It is often difficult to determine if elevated
blood pressure caused the intracranial injury or the primary intracranial injury
caused the elevated blood pressure. Severe elevations of blood pressure may
cause further damage leading to increased or new haemorrhage, extension of
infarct, or cerebral oedema. However, injured areas may lose the ability to
autoregulate cerebral blood flow and become dependent on blood pressure for
collateral flow. Lowering the blood pressure could lead to inadequate cerebral
perfusion and further ischaemia. Elevated blood pressure in the setting of an
acute intracranial injury is often transient so a period of observation may be
warranted. If moderate hypertension is present, an oral agent can be instituted
with control of blood pressure achieved over several days. Severe sustained
hypertension should be treated with a parenteral medication that can be easily
A recent pilot study referenced below found that acute lowering of blood pressure
in patients with thrombotic or haemorrhagic stroke was safe and may potentially
improve mortality. This trial suggests that further evaluation in larger studies is
warranted. Several clinical trials of intensive blood pressure control in
intracerebral haemorrhage may provide more specific guidance in the future. You
can read more about the Antihypertensive Treatment in Acute Cerebral
Hemorrhage (ATACH) study and the Second Intensive Blood Pressure Reduction
in Acute Cerebral Hemorrhage (INTERACT2) study at the following websites:
During the acute phase of stroke, the increase in blood pressure is regarded as
a compensatory mechanism to maintain cerebral perfusion pressure in face of
an increased intracranial pressure (cerebral perfusion pressure = mean arterial
pressure minus intracranial pressure). Therefore, antihypertensive treatment
should be initiated only if blood pressure is markedly elevated:
Recommended thresholds for antihypertensive therapy in stroke
Recommended approach to hypertension in acute ischaemic stroke
Threshold for lowering BP
Eligible for thrombolysis or other acute
reperfusion intervention
Systolic BP >185 mmHg or diastolic BP >110 mmHg (I
BP does not decline, do not administer thrombolytic)
During or after treatment with thrombolysis Systolic BP >180 mmHg or diastolic BP >105 mmHg
or other acute reperfusion intervention
No thrombolysis or acute reperfusion
Systolic BP >220 mmHg or diastolic BP>120 mmHg
(Lower BP by ~15% in first 24 h)
BP = blood pressure.
Suggested guidelines for treating elevated blood pressure in spontaneous intracranial
Systolic BP>200 mmHg or mean
BP>150 mmHg
Consider aggressive reduction of BP with IV infusion
Systolic BP>180 mmHg or mean
BP>130 mmHg with suspicion or
evidence of elevated ICP
Consider ICP monitoring and reducing BP with intermittent
or continuous IV medications to maintain cerebral
perfusion pressure >60-80 mmHg
Systolic BP>180 mmHg or mean
BP>130 mmHg without suspicion or
evidence of elevated ICP
Consider modest reduction of BP (target mean BP 110 or
BP 160/90 mmHg) with intermittent or continuous IV
Mean BP = Diastolic BP + 1/3 (Systolic BP − Diastolic BP). BP = blood pressure.
ICP = intracranial pressure.
These consensus recommendations are found in the following guidelines. Further
information on stroke can be found in the PACT module on Acute brain
Drugs that may be considered include labetalol, nicardipine, nitroprusside, and
nitroglycerin. Fenoldopam has not been systematically evaluated in intracranial
injury. The effects of these agents on autoregulation, intracranial pressure, and
cerebral blood flow must be considered. If the neurological status deteriorates
while blood pressure is being lowered, therapy should be altered to allow the
blood pressure to increase.
Both high and low blood pressure have been found to be independent
prognostic factors for poor outcome in acute stroke in the following report.
Direct vasodilators such as nitroprusside and nitroglycerin may increase cerebral
blood volume and intracranial pressure while decreasing mean arterial pressure.
These effects may compromise cerebral perfusion, particularly in patients with
increased intracranial pressure. If the patient's baseline neurological examination
makes observation of further deterioration difficult or if neurological examinations
cannot be performed frequently, drugs other than direct vasodilators are more
appropriate. Labetalol does not appear to increase intracranial pressure and
requires less intensive monitoring. Nicardipine causes cerebral vasodilatation and
associated increased intracranial pressure and offers little advantage over direct
vasodilators. A further discussion of the pharmacologic effects of these agents in
intracranial injury can be found in the following reference.
In the setting of subarachnoid haemorrhage, it may be prudent to treat severe
hypertension until the aneurysm is effectively managed. Nimodipine is routinely
used in this clinical situation and its effects on blood pressure must be considered
before instituting any additional antihypertensive agents. Some centres use the
maintenance or induction of hypertension to treat or prevent cerebral vasospasm
in patients with subarachnoid haemorrhage.
You can see further images of intracerebral haemorrhages in Task 1
. You
can also find some further information about subarachnoid haemorrhage in the
PACT module on Acute brain ischaemia
and on Traumatic brain injury
CT scan of basal ganglia bleeding
Acute coronary syndromes
Sustained hypertension in patients with myocardial ischaemia should be treated
to reduce myocardial oxygen demand. Despite an initial elevation of blood
pressure in many patients, the blood pressure usually decreases without specific
antihypertensive therapy within the first six hours of admission. The first priority in
patients with myocardial ischaemia is to relieve pain with traditional medications
such as nitroglycerin and morphine. An intravenous beta-blocker is also
administered as part of standard care in most patients. If further interventions are
needed for severe sustained hypertension, intravenous nitroglycerin in higher
doses would address blood pressure as well as coronary vasodilatation.
Labetalol is an alternative agent that benefits the patient for the β-blocking effects
as well as the vasodilatation. Although nitroprusside has been used in this clinical
setting, concerns have been raised about coronary artery steal resulting in
decreased collateral flow to ischaemic areas and it is no longer used for this
Mild to moderate hypertension (less than 160/100 mmHg) can usually be treated
with oral β-blockers and angiotensin-converting enzyme inhibitors. Both classes
of drugs are routinely used in myocardial ischaemia to improve outcomes. Pure
vasodilator agents such diazoxide and hydralazine should be avoided because of
reflex tachycardia that could increase myocardial oxygen demand.
Acute left ventricular dysfunction
The clinician should consider whether the patient with pulmonary oedema
secondary to acute left ventricular dysfunction has systolic or diastolic
dysfunction. Systolic dysfunction with low cardiac output and dilated
ventricles can be associated with hypertension resulting from
catecholamine-induced peripheral vasoconstriction. Often, there is only a
mild to moderate increase in the diastolic blood pressure. Additional clues
include the lack of hypertensive retinopathy and the presence of marked
cardiomegaly on chest radiograph. Hypertensive emergencies associated
with diastolic dysfunction are more common. In these situations, the
hypertrophied left ventricle has decreased compliance due to the acute
elevation of blood pressure that results in inadequate diastolic filling.
Elevations of diastolic blood pressure are often greater with diastolic
dysfunction. Other clinical clues that suggest diastolic dysfunction are the
presence of significant hypertensive retinopathy and left ventricular
hypertrophy on electrocardiogram. Differentiation of the clinical situations
may be difficult.
Hypertensive emergencies
with pulmonary oedema are
most commonly due to left
ventricular diastolic
Nitroprusside would be effective in systolic or diastolic dysfunction. If ischaemia is
thought to play a role in the ventricular dysfunction, nitroglycerin may be an
appropriate agent. Labetalol is an excellent drug to treat diastolic dysfunction in this
setting and the decrease in heart rate facilitates left ventricular filling. Alternatives
include fenoldopam and nicardipine. Intravenous diuretics may be considered in the
patient with systolic dysfunction and evidence of volume overload (pulmonary rales,
jugular venous distension, and peripheral oedema). Diuretics should be avoided
initially in the setting of diastolic dysfunction in order to avoid excessive reduction of
left ventricular filling pressures. Adequate preload is needed to optimise filling of the
hypertrophied, non-compliant left ventricle.
To view pathology specimens of dilated cardiomyopathy and left ventricular
hypertrophy, click on image numbers 106 and 113 under systemic
pathology/cardiovascular pathology/cardiomyopathies on the following website.
Acute aortic dissection
MRI showing a type A acute
aortic dissection
Aortic dissection may occur either in the ascending aorta (proximal, type A), which requires surgery
or in the descending aorta (distal, type B), which can initially be treated medically. The immediate
goal in acute aortic dissection is to lower the blood pressure and reduce the shear force (from
ejection of ventricular blood) on the aorta until definitive surgical or medical therapy can be instituted
The blood pressure should be reduced to the lowest level that relieves pain and allows adequate
organ perfusion. Usually, the goal is a systolic blood pressure of 100 to 110 mmHg. Therapy include
a β-blocker usually associated with an easy-to-titrate vasodilator. A vasodilator should never be use
alone, since it may worsen the shear force. Labetalol is a single agent that provides β-blockade and
vasodilatation in this setting. Trimethaphan is rarely used because of adverse effects but it may be
needed in patients who cannot tolerate β-blockers.
Excess catecholamine states
The treatment of choice for severe hypertension due to increased levels of
catecholamines depends on the aetiology if known. Drug-induced hypertension
due to cocaine and other illicit sympathomimetic agents is often transient and
responds to sedation with benzodiazepines. If blood pressure elevations are
severe and sustained, labetalol may be used. Alternative agents include
nitroprusside and fenoldopam. Severe alcohol withdrawal associated with
hypertension will also respond to benzodiazepines. Phentolamine has been the
treatment of choice for phaeochromocytoma but other drugs such as labetalol
and nitroprusside are also effective. In phaeochromocytoma, an α-blocker should
always be used before a β-blocking agent. Intravascular volume should be
optimised to attenuate vasoconstriction due to salt and water excretion.
Explain what foods can precipitate severe hypertension through interaction with monoamine
oxidase inhibitors?
Severe preeclampsia/eclampsia
Preeclampsia is diagnosed on the basis of pregnancy-induced hypertension
(>140 mmHg systolic or >90 mmHg diastolic blood pressure, confirmed by two
separate measurements, occurring after 20 weeks gestation in a woman who
was normotensive before 20 weeks gestation) and proteinuria (500 mg/l protein
in a random specimen or an excretion of 300 mg per 24 h). Peripheral oedema is
often associated.
The treatment of severe preeclampsia/eclampsia includes consideration of
delivery of the fetus, seizure prophylaxis with magnesium sulphate, blood
pressure control, and supportive measures. In this setting, the diastolic blood
pressure should be reduced to 90 to 100 mmHg. However, precipitous drops in
blood pressure should be avoided to prevent compromise of placental circulation.
Hydralazine, labetalol, and nicardipine are commonly used and preserve
myometrial blood flow. Nifedipine has also been used safely in this setting. In the
pregnant patient, nitroprusside and angiotensin-converting enzyme inhibitors
should be avoided due to adverse fetal effects. Additional information on the
management of hypertension in pregnancy and severe preeclampsia/eclampsia
can be found in the following references.
Perioperative hypertension
A preoperative history of hypertension and the type of surgery
influence the incidence of perioperative hypertension. The decision to
treat hypertension in the perioperative setting requires an
assessment of the risk of myocardial ischaemia, haemorrhage, and
disruption of vascular integrity. As previously mentioned, the impact
of pain, anxiety and hypothermia on blood pressure must be
addressed. The effects of analgesics, anaesthetic agents and shifts
in intravascular volume on blood pressure must be taken into account
before initiating additional therapy. Postoperative hypertension is
usually self-limited (2-6 h) so short-acting titratable agents are
preferred. Nitroprusside and nitroglycerin have been routinely used in
the postoperative period. Additional agents that have been used
effectively include labetalol, esmolol, nicardipine, urapidil,
fenoldopam and clevidipine.
Although nitroglycerin and
nitroprusside are commonly
used, the choice of agent will
be decided by the clinical
circumstance, the experience
of the clinician and local
custom. Consider intravenous
clonidine in difficult situations
where supplementary
analgesia and control of
hypertension and agitation
are required.
In postoperative hypertension, the clinician must assess for precipitating
factorssuch as pain, anxiety, altered blood gases (hypoxaemia, hypercapnia,
acidosis), hypervolaemia, bladder distention, and hypothermia. These factors
should be corrected before considering antihypertensive drug therapy.
The resident was called to see a patient with hypertension the evening after a
urological operation. On arrival, obvious dyspnoea and cyanosis were noted. Physica
examination showed dullness to percussion and no air entry in the right lung. Chest
radiograph revealed a massive right pleural effusion and malposition of the right
jugular catheter. Arterial blood gases showed hypoxaemia and respiratory acidosis.
Hypertension and respiratory failure resolved after pleural drainage and removal of th
jugular catheter.
Which types of surgery are most likely to be associated with perioperative hypertension?
Severe hypertension must be rapidly and appropriately evaluated to assess its
clinical significance and to determine if treatment should be immediately
instituted. An organised approach using the following questions can guide the
clinician in decision-making.
Should the blood pressure be lowered?
Should the blood pressure be lowered acutely?
How much should the blood pressure be lowered?
Which medication should be used to lower the blood pressure?
Hypertensive emergencies and hypertensive urgencies should be identified and
an individualised plan developed that includes a goal for blood pressure reduction
and selection of the best parenteral drug for the patient's clinical situation.
In the Patient Challenges, you are given information about patients with acute
care problems. As a case develops, you are asked to interpret the nature of the
problems or make management decisions. You are presented with questions and
materials designed to raise learning issues relevant to the subject. The learning
issues link to the relevant sections in the Tasks.
Two cases are presented here, a 62-year-old woman with diabetes and chronic
hypertension, and a 68-year-old-man admitted to the emergency department for
acute respiratory failure.
Case 1
A 62-year-old woman with diabetes and chronic hypertension underwent
elective coronary artery revascularisation for progressive unstable angina. She is
known to have renal insufficiency with a creatinine of 210 µmol/l (2.4 mg/dl). Her
medication prior to surgery included enalapril, hydrochlorothiazide, metformin,
glyburide, atenolol, isosorbide dinitrate, and aspirin. The patient had taken her
antihypertensive medications at 5.00 am, and her surgery was completed at 3.00
pm. General anaesthesia consisted of midazolam, fentanyl, vecuronium, and
isoflurane. She is transferred to the ICU with heart rate 95 beats/min, respiratory
rate 14 beats/min (on mechanical ventilation), blood pressure 140/88 mmHg by
intra-arterial monitor, and temperature 36 °C. Thirty minutes later, the patient is
noted to be agitated with blood pressure 168/94 mmHg and heart rate 104
Pressure monitoring by intra-arterial catheter provides the most accurate
measurement of blood pressure.
Case 1 Screen 2
Is this patient experiencing a hypertensive emergency or hypertensive urgency? Give reasons fo
your answer.
Learning issues
Evaluation of the hypertensive patient
Definitions of hypertensive crises
Perioperative hypertension
What evaluations would be helpful to determine the significance of the elevated blood pressure?
Learning issues
Assessment of end-organ injury
The operative record should be reviewed for blood loss, fluid balance, and
administered medications.
Case 1 Screen 3
The patient's lung examination is clear except for decreased breath sounds in the
bases and no cardiac gallop is appreciated. Blood loss in the operating room was
500 ml and fluid balance was +2200 ml. Urine output in the previous hour was 60
ml. Blood pressure during surgery was well controlled with systolic pressures
ranging from 110-120 mmHg. An electrocardiogram shows inverted T-waves in
the inferior leads that were changed from the preoperative electrocardiogram.
Her blood pressure remains at 158/96 mmHg.
What additional factors must be considered before administering medication to lower blood
Learning issues
Perioperative hypertension
Case 1 Screen 4
The patient is medicated with morphine 4 mg intravenously and lorazepam 1 mg
intravenously. There is no evidence of excessive blood loss, hypoxia,
hypercapnia or acidosis. Despite control of the agitation, the blood pressure
remains elevated at 160/94 mmHg and the heart rate is 100-110 beats/min.
Should a medication be administered to lower the blood pressure? Why?
What medication characteristics are desirable when considering treatment of this patient's blood
Learning issues
Pharmacotherapy of hypertensive crises
Treatment of specific clinical conditions
Case 1 Screen 5
What options are there to lower this patient's blood pressure?
Learning issues
Initial treatment
The effects of one agent on the blood pressure should be assessed before
initiating another medication that affects blood pressure in order to prevent
excessive decreases.
Esmolol is administered as a continuous infusion to decrease the heart rate to
60-70 beats/min. The blood pressure subsequently is 150/90 mmHg. A
nitroglycerin infusion is titrated to 50 micrograms/min with a reduction in blood
pressure to 120/74 mmHg.
Case 1 Screen 6
What is the optimum blood pressure for this patient?
Four hours after nitroglycerin is initiated, the blood pressure decreases to 100/60
mmHg. Then, the nitroglycerin infusion is gradually decreased to allow the
systolic blood pressure to rise to 110-120 mmHg. Within 30 minutes, the
nitroglycerin infusion is discontinued. Analgesics are administered as needed and
the patient is successfully extubated that evening. A follow-up electrocardiogram
shows resolution of the inferior ischaemic changes. The following morning, oral
antihypertensives are administered with reinstitution of β-blocker therapy.
Case 2
A 68-year-old man is admitted to the emergency department for acute
respiratory failure. He had experienced a similar episode two months ago,
which came on abruptly and resolved rapidly. He has a history of long-standing,
poorly controlled systemic hypertension, and revascularisation for femoralpopliteal artery disease. He is taking a diuretic (chlorthalidone 25 mg daily), a βblocker (atenolol 100 mg daily), a calcium antagonist (amlodipine 5 mg daily),
and an antiplatelet agent (aspirin 75 mg daily), but admits poor compliance. The
patient is cyanotic, pulse rate is 100 beats/min and systemic arterial pressure is
224/118 mmHg. Pulmonary rales are heard but there is no jugular venous
distension or peripheral oedema of the lower extremities. Electrocardiogram
shows left ventricular hypertrophy, an ischaemic pattern, but no evidence of an
acute event. Serum creatinine is 140 µmol/l (1.6 mg/dl).
Case 2 Screen 2
Is this a hypertensive emergency or hypertensive urgency? Why?
Learning issues
Evaluation of the hypertensive patient
Cardiovascular end-organ damage
Poor compliance to antihypertensive therapy and secondary hypertension are
common causes of difficult blood pressure control.
Together with antihypertensive treatment, other measures should be taken.
What immediate actions should be taken?
Learning issues
Emergency measures
Case 2 Screen 3
Pulse oximetry confirms severe arterial desaturation. The patient receives oxygen
and an injection of nitroglycerin, and he is immediately transferred to your
intensive care unit where continuous positive airway pressure is applied using a
face mask. Blood pressure decreases to 196/112 mmHg.
The application of continuous positive airway pressure may by itself reduce
blood pressure, by improving arterial PO 2, which decreases sympathetic
stimulation, and by increasing intrathoracic pressure, which reduces venous
How much should the blood pressure be lowered?
Learning issues
Initial treatment
Case 2 Screen 4
Explain what would be the appropriate antihypertensive drug therapy for this patient?
Learning issues
Pharmacotherapy of hypertensive crises
Management of specific conditions
In patients with left ventricular hypertrophy and diastolic dysfunction,
overzealous reduction of filling pressures may compromise left ventricular
volume, and hence cardiac output. Echocardiography or right heart
catheterisation may help to evaluate filling of the left ventricle.
Nitroglycerin and morphine are administered intravenously. Nitroglycerin is
titrated so that blood pressure gradually decreases to 156/98 mmHg within the
next 6 hours. Echocardiography shows left ventricular hypertrophy and normal
systolic function.
Many episodes of pulmonary oedema are due to exacerbation of diastolic
dysfunction in hypertensive patients, who usually have left ventricular
Learning issues
Acute left ventricular dysfunction
For how long should intravenous therapy administered?
Case 2 Screen 5
Arterial oxygenation improves rapidly, positive airway pressure is discontinued,
and intravenous antihypertensives are shifted to orally administered agents
(chlorthalidone, atenolol, amlodipine). Blood pressure remains around 150/90
mmHg and the patient is discharged from the intensive care unit to a general
ward the day after admission.
You could recommend further evaluation.
What are your recommendations for the further management of this patient and why?
Learning issues
Secondary hypertension
Further evaluation includes a magnetic resonance angiogram that shows bilateral
atherosclerotic renal artery stenosis. After angioplasty and stenting of the
affected arteries, blood pressure normalises on chlorthalidone and atenolol
therapy, and the patient subsequently remains free of pulmonary oedema for four
On reflection
On reflection, many effective agents exist for the treatment of hypertensive crises, so that it is almo
always possible to decrease blood pressure. The challenge is to reduce blood pressure without
compromising organ perfusion. Unfortunately, no trial has definitively identified optimal blood pressu
targets or rates of blood pressure lowering in hypertensive emergencies and urgencies. Clinical
judgment and knowledge of the underlying pathophysiological process and autoregulation
mechanisms will help the physician to avoid the adverse effects of antihypertensive therapy.
Q1. Which of the following statements are correct regarding management of severe
hypertension in a patient with a thrombotic stroke?
A. Lowering the blood pressure may result in worsening of the
neurological deficits
B. Antihypertensive agents should only be initiated if
thrombolytics are to be administered
C. A period of observation of a severely elevated blood pressure
may be appropriate before considering use of an
antihypertensive agent
D. Labetalol increases intracranial pressure and should be
Q2. A hypertensive patient presents to the emergency department with a suspected
broken ankle. His blood pressure is 180/108 mmHg. Which of the following
interventions should be done?
A. Control the pain and ask for radiograph of the ankle
B. Give nifedipine 5 mg sublingually
C. Insert an intravenous line to be prepared for intravenous
antihypertensive treatment as this is a hypertensive emergency
D. Emphasize to the patient that he has to take his usual
antihypertensive medications every day
Q3. A 68-year-old hypertensive patient presents with acute crushing chest & interscapular pain. BP 172/100 mmHg. ECG and troponin levels do not suggest
myocardial ischaemia. Which are indicated?
A. Consider an intra-arterial catheter to monitor blood pressure
and its response to therapy
B. Give a fibrinolytic agent
C. Reduce blood pressure progressively, first using an
intravenous beta-blocker
D. Administer intravenous hydralazine
Q4. Which of the following intravenous drugs can be used to
control blood pressure in a patient with preeclampsia and
severe hypertension?
A. Enalaprilat
B. Labetalol
C. Hydralazine
D. Nicardipine
Q5. Identify which of the following is a hypertensive emergency requiring
intravenous therapy
A. BP of 175/110 mmHg associated with acute pulmonary
B. BP of 185/105 mmHg associated with headache
C. BP of 185/105 mmHg associated with an acute coronary
D. BP over 220/120 mmHg in a patient with acute ischaemic
Q6. In an ischaemic stroke, guidelines for therapy are
A. BP should be controlled to less than 220/120 mmHg if
thrombolysis not indicated
B. Aim of BP control therapy should be a 15% reduction
(approx) in 24 hours
C. BP should be controlled to less than 185/110 mmHg if
thrombolysis indicated
D. BP should be controlled to less than 180/105 mmHg after
Q7. A hypertensive emergency is characterised by
A. A diastolic BP > 130 mmHg
B. A systolic BP > 250 mmHg
C. Worsening signs and symptoms of end-organ damage
D. Mean arterial BP > 180 mmHg
Q8. Worsening of end-organ damage is a feared complication to
any hypertensive crisis; the following are a list of often
encountered end-organ damage in this context:
A. Hypertensive encephalopathy
B. Hypertensive retinopathy
C. Acute coronary syndromes
D. Acute polyneuropathy
Hypertension Type A Q9
Which of the following is correct in regard
to intravenous antihypertensive agents?
A. Nitroglycerin is contraindicated in patients with renal
B. Since labetalol combines α and β-blocking properties, it
can be used safely in patients with chronic obstructive
pulmonary disease
C. Nicardipine is an agent of choice to control blood
pressure after coronary artery bypass surgery
D. Enalaprilat is an agent of choice for hypertensive
E. Cyanide levels should be monitored systematically
during nitroprusside infusion
Hypertension Type A Q10
A 76-year-old male is admitted to the ICU
for recovery after lung volume reduction
surgery for severe emphysema. He is alert
and his BP is 168/96 mmHg. All of the
following are appropriate EXCEPT?
Assess for pain
Start an antihypertensive treatment with a β-blocker
C. Reassess the patient later since there is no end-organ
D. Fundoscopic examination is not indicated for the
transient, postoperative, acute hypertensive episode
E. Recommend the consultation of a hypertensive specialist
once the patient is transferred to the ward if the blood
pressure remains high
Hypertension Type A Q11
Which of the following patients requires immediate lowering of
blood pressure with a parenteral antihypertensive drug?
A. A patient with chronic hypertension undergoing upper
endoscopy whose medications were held; blood pressure
188/110 mmHg
B. An agitated cocaine abuser; blood pressure 180/120
C. A patient with heart failure, dyspnoea, and rales; blood
pressure 170/116 mmHg
D. A chronic alcoholic with vomiting and tremulousness;
blood pressure 160/102 mmHg
E. A patient in pain in the recovery room following repair of
an aortic aneurysm; blood pressure 150/100 mmHg
Hypertension Type A Q12
Which of the following is correct in regard
to measurement of blood pressure in severe
A. Automated oscillometric monitors are adequate for
blood pressure measurement in the critically ill patient
B. A blood pressure cuff that is too small for the patient
may result in a falsely decreased blood pressure
C. Hypothermia causes hypotension; it does not increase
blood pressure
D. Intra-arterial pressure monitoring provides the most
accurate blood pressure measurement
E. A blood pressure cuff that is wrapped too loosely on the
arm may result in a falsely low blood pressure
Hypertension Type A Q13
In a hypertensive emergency patient (BP
200/110 mm Hg, HR 100/min) associated
with acute coronary syndrome, the following
are appropriate therapies EXCEPT
IV cannulation, oxygen and IV morphine
Intravenous beta blockade e.g. by esmolol infusion
Intravenous titration of metoprolol 2-3mg boluses
Labetalol by infusion
Nifedipine by chewable capsule
Hypertension Type A Q14
An acute hypertensive episode (190/110
mmHg), in a known hypertensive patient, is
associated with acute congestive heart
failure (HR 95/min). All of the following are
A. Is a medical emergency requiring IV antihypertensive
B. Is a medical urgency requiring oral antihypertensive
Could be appropriately treated with a labetalol infusion
D. Requires caution with diuretics in case of diastolic
Is most likely due to diastolic dysfunction
Hypertension Type A Q15
The following medications are frequently
used to lower arterial BP in an emergency
hypertensive crisis, EXCEPT
Esmolol hydrochloride