Hypertensive
more frequently than women.9–12
crisis—pathophysiology,
initial evaluation, and
management
Mukesh Singh, MBBS MD MRCP
BACKGROUND
The Joint National Committee on Prevention, Detection,
Evaluation, and Treatment of High Blood Pressure recently
classified hypertension according to the degree of blood pres-
sure elevation. Stage 1 patients have systolic blood pressure
(SBP) of 140–159 mmHg or diastolic blood pressure (DBP) of
90–99 mmHg. Stage 2 patients have SBP of 160–179 mmHg or
DBP of 100–109 mmHg, whereas stage 3 corresponds to SBP of
180 mmHg or greater or DBP of 110 mmHg or greater. Stage 3
hypertension has also been called severe hypertension or ac-
celerated hypertension.1 Although chronic hypertension is an
established risk factor for cardiovascular, cerebrovascular, and
renal disease, acute elevations in BP can result in acute end-
organ damage with significant morbidity. Prompt recognition,
evaluation, and appropriate treatment of these conditions are
crucial to prevent permanent end-organ damage.
Hypertensive crisis refers to a syndrome characterized by
severe acute elevations in blood pressure associated with im-
minent risks to the patient.2,3 Although not specifically ad-
dressed in the JNC-7 report, patients with a SBP > 179 mmHg
or a DBP > 109 mmHg are usually considered to be having a
“hypertensive crisis.” The absolute level of BP itself is less impor-
tant, as acute increases in BP of even modest degree can lead to
critical target organ damage in previously normotensive patients
and those with certain medical conditions like acute myocardial
infarction or aortic dissestion.4
Prior to the introduction of antihypertensive medications,
approximately 7% of hypertensive patients had a hypertensive
emergency.5 Currently, it is estimated that ∼1% of patients with
hypertension will, at some point, develop a hypertensive crisis.6,7
It is a common medical problem and accounts for 27.5% of all
medical emergencies presenting to the emergency department.8
The epidemiology of hypertensive crises is similar to that of
hypertension (i.e. higher among African-Americans and the
Department of Cardiology, Chicago Medical School & Mount Sinai
Hospital.
Correspondence: Dr. Mukesh Singh, 1500 S California Avenue, Chicago,
IL-60608, United States. E-mail: drmukeshsingh@yahoo.com
JICC Vol 1 Issue 1
elderly); however, men are affected approximately two times
Hypertensive urgencies are hypertensive crises associated
with severe elevations in BP without progressive target-organ
dysfunction.11,13–19 The majority of these patients present as
noncompliant or inadequately treated hypertensive individuals,
often with little or no evidence of target-organ damage. Hy-
pertensive emergencies are hypertension crises characterized
by severe elevations in BP > 180/120 mmHg complicated by
evidence of impending or progressive target-organ dysfunction.
They require immediate BP reduction (not necessarily to normal
levels) to prevent or limit target-organ damage.20,21
PATHOPHYSIOLOGY
Acute severe hypertension can develop de novo or can compli-
cate underlying essential or secondary hypertension. The exact
mechanism of hypertensive crisis is not known but the rapidity
of onset suggests a triggering factor superimposed on pre-existing
hypertension.22 Most accepted hypothesis is shown in Figure 1.
Under normal circumstances, the renin-angiotensin-aldosterone
system plays a central role in the regulation of normal BP
homeostasis.23 Overproduction of renin by the kidney stimu-
lates the formation of angiotensin II, a potent vasoconstrictor.
Consequently, both peripheral vascular resistance and BP in-
crease. Hypertensive crisis is thought to be initiated by an
abrupt increase in systemic vascular resistance likely related to
humoral vasoconstrictors.24,25 In the hypertensive crises state,
amplification of renin system activity occurs, leading to vascular
injury, tissue ischemia, and further overproduction of renin-
angiotensin. This vicious cycle contributes to the pathogenesis
of hypertensive crises. The pathophysiologic link between the
Abrupt increase in systemic Humoral
vascular resistance vasoconstrictors
↑ BP
↑ Mechanical stress Endothelial injury
• ↑ Vascular permeability
• Platelet activation
• Activation of
coagulation cascade
• Fibrin deposition
Ischemia
Release of vasoactive
mediators
Figure 1 Pathophysiology of hypertensive crisis.
36
 Hypertensive crisis—pathophysiology, initial evaluation, and management
Table 1 Initial evaluation and management of hypertensive crisis.
A) Hypertensive urgency
• BP usually > 180/110 mmHg
• Presents with headache, dyspnea, edema
• Observe for 4–6 hours, oral agents for BP control and follow-up evaluation within 24 hours
B) Hypertensive emergency
• BP usually > 220/140 mmHg
• Presents with dyspnea, chest pain, dysarthria, focal neurological signs, altered sensorium, pulmonary edema, encephalopathy, stroke, renal failure
• Admit to ICU, investigate for associated condition, and start parenteral antihypertensive therapy
renin system and hypertensive crises has been established by
demonstrating that this process can be arrested when the renin-
angiotensin system is interrupted either pharmacologically
(i.e., angiotensin converting enzyme [ACE] inhibitor, beta-blocker,
or type 1 angiotensin receptor antagonist) or by removal of an
ischemic kidney.23,26,27 Other factors induced by excess renin-
angiotensin include pro-inflammatory cytokines and vascular
cell adhesion molecules, which may contribute to the vascular
sequelae and target organ damage.28–30
EVALUATION AND INITIAL MANAGEMENT
Patients with hypertensive emergency usually present for eval-
uation as a result of a new symptom complex related to their
elevated BP. Patient triage and physician evaluation should
proceed expeditiously to prevent ongoing end organ damage. A
focused medical history that includes the use of any prescribed
or over-the-counter medications should be obtained. If the pa-
tient is known to have hypertension, their hypertensive history,
previous control, current antihypertensive medications with
dosing, compliance, and time from last dose are important facts
to know as subsequent treatment decisions are made. Also use
of recreational drugs (amphetamines, cocaine, and phencyclidine)
should be considered. Confirmation of the blood pressure
should be obtained in both arms by a physician using a BP cuff
of appropriate size. Patients with long-standing hypertension
may tolerate SBP > 200 mmHg or DBP > 150 mmHg without de-
veloping clinical signs or symptoms of end organ damage;
however, in postoperative or pregnancy patients a much lower
but more rapidly progressive increase in blood pressure may
result in end organ damage. The physical examination should
attempt to identify evidence of end organ damage by assessing
pulses in all extremities, auscultating the lungs for evidence of
pulmonary edema, the heart for murmurs or gallops, the renal
arteries for bruits, and performing a focused neurologic and
fundoscopic examination. Headache and altered levels of con-
sciousness are the usual manifestations of hypertensive enceph-
alopathy.31,32 Focal neurological findings, especially lateralizing
signs, are uncommon in hypertensive encephalopathy, being
more suggestive of a cerebrovascular accident. Subarachnoid
hemorrhage should be considered in patients with a sudden
onset of a severe headache.
JICC Vol 1 Issue 1
Initial objective evaluation should include a metabolic panel
to assess electrolytes, creatinine, and blood urea nitrogen; a
complete blood count (and smear if microangiopathic hemolytic
anemia is suspected); a urinalysis to look for proteinuria or mi-
croscopic hematuria; and an electrocardiogram to assess for car-
diac ischemia.33 Supportive radiographic studies such as a chest
radiograph in a patient with dyspnea or chest pain or a head
computed tomography scan in a patient with neurologic symp-
toms should be obtained in the appropriate clinical scenario. In
patients presenting with pulmonary edema it is important to ob-
tain an echocardiogram to distinguish between diastolic dysfunc-
tion, transient systolic dysfunction, or mitral regurgitation.34
Hypertensive crises share all the pathophysiologic mecha-
nisms and target organ complications (MI, stroke, renal failure)
similar to patients with milder forms of high BP and, thus, to-
gether can be viewed as part of the spectrum of hypertensive
diseases. BP is reduced, in the hypertensive crises and in the
chronic forms of hypertension, by the same drugs that interrupt
relevant pathophysiologic mechanisms. An algorithm for initial
management of hypertensive crisis is given in Table 1.
The majority of patients in whom severe hypertension
(SBP > 160 mmHg, DBP > 100 mmHg) is identified on initial eval-
uation will not have evidence of end organ damage and thus
have hypertensive urgency. As no acute end organ damage is
present, these patients may present for evaluation of another
complaint, and the elevated blood pressure may represent an
acute recognition of chronic hypertension. In these patients,
utilizing oral medications to lower the blood pressure gradually
over 24–48 hours is the best approach to management.35–37 In
fact, rapid reduction of blood pressure may be associated with
significant morbidity in hypertensive urgency because of a
rightward shift in the pressure/flow auto-regulatory curve in
critical arterial beds (cerebral, coronary, and renal).38 Rapid
correction of severely elevated blood pressure below the au-
toregulatory range of these vascular beds can result in a marked
reduction in perfusion causing ischemia and infarction.39–42
Therefore, although the blood pressure must be reduced in these
patients, it must be lowered in a slow and controlled fashion to
prevent this impaired autoregulatory hypoperfusion problem.
Patients with a hypertensive emergency should be managed in
an intensive care unit with close monitoring and are best man-
aged with a continuous infusion of a short-acting, titratable anti-
hypertensive agent. Because of unpredictable pharmacodynamics,
37
 sh Singh

Table 2 Hypertensive emergencies.

A) Aortic dissection
• Beta blocker and nitroprusside
• Reduce to systolic BP < 120 mmHg over few minutes
B) Myocardial infarction
• Nitroglycerine
• Titrate to improvement of ischemic symptoms
C) Pulmonary edema
• Nitroglycerine
• 10–15% reduction leads to improvement in symptoms
D) Hypertensive encephalopathy
• Fenoldopam/nicardipine/nitroprusside
• 25% reduction over 2–3 hours
A) Acute stroke
• Do not attempt to reduce BP unless > 200/110 mmHg
• Keep BP > 180/100 mmHg
• For stroke after thrombolysis aim to keep BP < 180/105 mmHg for first 24 hours and then target < 140/90 mmHg
F) Subarachnoid hemorrhage
• Nimodipine
• 25% reduction over 2–3 hours
G) Acute renal failure
• Fenoldopam
• Up to 25% reduction over 1–12 hours
H) Eclampsia/Pre-eclampsia
• Magnesium sulfate and hydralazine or methyldopa
• Target diastolic BP < 90 mmHg
I) Clonidine withdrawal
• Reinstitute clonidine
J) Cocaine induced hypertensive crisis
• Clonidine

the sublingual and intramuscular route should be avoided.
For those patients with the most severe clinical manifestations
or with the most labile blood pressure, intra-arterial blood pres-
sure monitoring may be prudent. Although there are no con-
crete guidelines as to the degree of desired blood pressure
reduction, a reasonable goal for most hypertensive emergen-
cies is to lower the DBP to 100 mmHg (or to reduce the mean
arterial pressure by 20–25%) over a period of minutes
to hours.43 A list of conditions associated with hypertensive
emergency and the durgs of choice is given in Table 2.
CONCLUSION
Hypertensive crisis represents a serious medical condition with
the potential for permanent end organ damage and significant
morbidity and mortality. No data currently exists to show im-
mediate benefit from acutely lowering BP in asymptomatic pa-
tients with severe hypertension, but data do suggest that an
aggressive approach may be harmful. However, recognition of
elevated BP with evidence of end organ damage should prompt
initiation of timely and appropriate antihypertensive regimens
to prevent on-going end organ damage. There are multiple
therapeutic options for hypertensive emergencies; and, the type
of emergency and the individual patient are the most important
factors in the decision. ♦
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