HYPERTENSIVE CRISES

8/26/08

Romulo E. Colindres, M.D.

The Clinical Syndromes of

Severe Hypertension
Hypertensive crises: acute endorgan dysfunction
Benign hypertension with
chronic end-organ dysfunction
Severe uncomplicated
hypertension

Severe Hypertension:
Definitions
Hypertensive Emergency: Very high BP with
acute end-organ damage or a clinical setting that
could be immediately life-threatening therefore
need to lower BP in a matter of minutes with
parenteral drugs in an ICU
Hypertensive Urgency: Very high BP without
acute end-organ damage or only retinal changes,
therefore BP can be lowered in hours to days,
preferably slowly, sometimes in an outpatient
setting

Hypertensive Crisis Criteria

Level of blood pressure
and/or
rapidity of increase
Life-threatening involvement of CNS or
cardiovascular system
and/or
a clinical setting deemed dangerous

The Clinical Syndromes of

Severe Hypertension
HYPERTENSIVE CRISES
_Malignant hypertension
_Hypertensive encephalopathy
_Benign hypertension with acute dysfunction of
neurologic or cardiovascular system
_Catecholamine excess states
_Preoperative and postoperative hypertension
_Preeclampsia and eclampsia
_Scleroderma renal crisis, acute
glomerulonephritis

Malignant or Accelerated Hypertension:

Essential Diagnostic Features
Elevation of blood pressure, usually
severe and fixed, occurring over days to
weeks
Grade III or IV hypertensive retinopathy
Renal abnormalities: proteinuria,
microscopic hematuria, renal
dysfunction
Progressive decline of kidney function

Neuroretinitis in Optic Fundi of

Subject with Malignant
Hypertension
1
4

3
2

Malignant or Accelerated Hypertension:

Commonly Associated Manifestations
Subjective

Headaches
Visual symptoms
Malaise, fatigue
Weight loss
Dyspnea
Abdominal
discomfort
Neurologic
symptoms

Objective
Retinopathy
hypokalemia
Hyperaldosteronism
Microangiopathic
hemolytic anemia
Heart failure
Hematuria
proteinuria

Br Med J 1959; 2:969

Etiologies of Malignant Hypertension

Primary or essential malignant
hypertension
Secondary malignant hypertension
Acute glomerulonephritis
Renovascular hypertension
Chronic kidney diseases

Etiologies of Malignant Hypertension

All causes of hypertension can evolve to
malignant hypertension with the exception of
coarctation of the aorta
Malignant hypertension has been reported with
primary aldosteronism, Cushings syndrome and
pheochromocytoma but very infrequently
Primary or essential hypertension is the most
common etiology overall, particularly among
persons of African descent.
Primary or essential hypertension as a cause of
malignant hypertension is less common among
caucasians and children

MS03-11829

Malignant Hypertension:Epidemiology
In the U.S. the number of hospital admissions with
malignant hypertension as primary diagnosis increased
from about 16,000 to 32,000 between 1982 and 1993
In a multiracial population in England the incidence rate
was not changed from 1970 to 1993
More common in males(2:1), blacks (4-6:1), smokers
(R.R.5:1)
Younger subjects: 57% are 30-50 years old, very rare after
age 65
In one series only 14% of patients had had hypertension for
more than 10 years

Malignant
Hypertension:Treatment
Goal of therapy is to decrease blood
pressure to diastolic BP of 100-105 mm Hg
in a matter of hours with maximal initial
fall in BP no greater than 25%
Oral therapy can be used if only retinal
changes are present
Initial parenteral therapy indicated if
cardiovascular, neurologic, renal or other
visceral involvement present

Parenteral Therapy in
Malignant Hypertension

Neurologic syndromes
Acute pulmonary edema
Acute myocardial infarction
Rapidly failing vision
Rapid deterioration of kidney
function
Abdominal emergency

Malignant Hypertension:
Prognosis
If treated optimally survival at 4 years is
90%, or higher if treated at an early stage
Prognosis worse if there is acute kidney
injury or if there is delayed diagnosis
Patients can recover life-sustaining kidney
function even if they need acute dialysis
Complications: ESKD, loss of vision
Causes of death: cerebral hemorrhage,
heart failure, abdominal catastrophe

Common Neurologic Syndromes

Associated with Hypertension

Thromboembolic stroke
Transient ischemic attack
Cerebral hemorrhage
Hypertensive encephalopathy
(posterior reversible encephalopathy
syndrome)
Subarachnoid hemorrhage

Hypertensive Encephalopathy
Acute neurologic syndrome characterized by:
Marked, usually sudden blood pressure
Headache
Nausea and vomiting
Visual complaints
Altered mental status
+/- papilledema or retinal exudates and hemorrhages
+/- transient neurological deficits
Head MRI: subcortical/cortical edema mainly in
posterior location; no infarction or hemorrhage
Dramatic improvement with blood pressure

Cerebral Blood Flow

Autoregulation in Hypertension

Breakthrough Theory of
Hypertensive Encephalopathy
Blood Pressure
Failure of Autoregulation

Forced Vasodilatation
(Sausage String Pattern)

Endothelial
Permeability

Hyperperfusion
Capillary Hydrostatic
Pressure

CEREBRAL EDEMA
Hypertensive Encephalopathy
(Headache, Nausea, Vomiting,
Altered Mental Status, Convulsions)
Nolan CR. Malignant Hypertension and Other Hypertensive Crises. In: Diseases of the Kidney and Urinary Tract, 7 th Ed., RW
Schrier, Ed. Lippincott Williams & Wilkins,, Philadelphia, 2001.

Guidelines for Treatment of

Hypertension with Neurologic
Syndromes
Consensus rather than evidence-based
Characteristics of a thrombotic stroke determine approach:
If risk of a watershed stroke and no collateral circulation BP
should be maintained high because of risk of cerebral
ischemia. If good collateral circulation and patient stable
new guidelines (2007) suggest therapy can be started
within 24 hours
BP increases with thrombotic stroke due largely to the
Cushing reflex to maintain cerebral perfusion. BP falls in
about 10 days
The only neurologic syndrome that improves with lowering
of BP is hypertensive encephalopathy

Guidelines for Treatment of

Hypertension with Neurologic
Syndromes
Consensus rather than evidence-based
Good control of BP is needed for thrombolytic therapy
Lowering BP with intracranial hemorrhage decreases new
bleeding with little risk of ischemia
There is a risk of cerebral ischemia with lowering of BP in
subarachnoid hemorrhage. Local vasodilatation with
nimodipine indicated.
The antihypertensive drugs of choice in the past have been
nitroprusside and labetalol but the former may be
associated with increased intracranial pressure and the
latter may lower BP excessively
Treat hypotension: volume repletion, pressors?

Guidelines for Treatment of Hypertension

with Neurologic Syndromes
Thromboembolic stroke
Withhold antihypertensive therapy for 10 days
unless BP > 220/120 mm Hg, or when other
condition is present ( CAD, CHF, aortic dissection)
If necessary lower BP by 15% over 24 hours
Before thrombolysis BP <185/110
After thrombolytic therapy < 180/105 mm Hg
I.V. nicardipine is now the drug of choice in many
centers because of ease of administration and no
increase in intracranial pressure; with nitroprusside
BP can be better regulated although there is a risk
of increased intracranial pressure

Guidelines for Treatment of Hypertension

with Neurologic Syndromes
Hypertensive encephalopathy
Lower BP gradually until usual BP is achieved
TIA
If BP below average, increase. Do not lower BP below
average. Conservative management of high BP.
Intracranial hemorrhage
Maintain mean BP between 90 and 130 mm Hg and CPP at
70mm HG, especially with secondary ICH and during the
first 6 hours
Subarachnoid hemorrhage
Treat only severely elevated BP. Nimodipine 60 mg po q4 hr
within 4 days for local vasodilatation

Hypertension and Stroke: Primary

and Secondary prevention
Preferred agents are thiazide diuretics alone or in
combination with other drugs, ACEI, DCCBs and
ARBs. Target BP not defined <130/80?
ACEIs alone are not effective and BBs have not
been as effective as other drugs. Non-DCCBs
less proven. ARBs effective in limited trials
In patients with recent ischemic stroke whose
SBP is >220 mm Hg or DBP 120-140, cautious
reduction of BP by about 10-15% recommended
SBP > 185 mm Hg or DBP >110 mm Hg are
contraindications to thrombolytic therapy within
the first 3 hours of an ischemic stroke

Hypertensive Crises: Acute

Increase in Sympathetic Activity
Drugs: cocaine, amphetamines,
phencyclidine,phenylpropanolamine
Withdrawl of Sympathetic Blocker
Pheochromocytoma
Autonomic Dysfunction: Guillain Barre
syndrome, post-spinal cord injury
MAO (monoamine oxidase) inhibitorTyramine interaction

Hypertensive Crises:
Cardiologic Causes
Acute Aortic Dissection: Must lower MAP and the
maximal rate of rise of the pressure (dp/dt). First
Beta blockade and then nitroprusside to achieve
a low SBP 100-120mm Hg
Acute Pulmonary Edema: Nitroprusside or
nitroglycerin with a loop diuretic. Try to achieve
BP of 130/80 if possible. Avoid hydralazine and
Beta-blockers
Angina Pectoris or Acute MI: Nitroglycerin; can
add labetalol. Avoid drugs that increase cardiac
work (hydralazine)

Hypertensive Crisis
Principles of Management
Beware of pseudo emergencies
More complications now reported from overzealous
treatment than from under-treatment in hospitalized
patients
Use oral drugs unless there is a true hypertensive
emergency or if oral drugs cannot be taken
Achieving a normal blood pressure is not necessary
except in rare circumstances (aortic dissection)
Accept high blood pressure in patients with certain
neurologic conditions; follow such patients with the
neurologist
If oral therapy is chosen, avoid intermittent IV/SL or
transcutaneous medication

Agents Used for IV Drug Therapy

of Hypertensive Emergencies

Nitroprusside: generally preferred agent except in acute coronary

syndromes, pregnancy, stage 4-5 CKD, states of high ICP
Nicardipine: CNS disease
Nitroglycerin: use in acute coronary syndromes alone or combined with
metoprolol or labetalol
Labetalol: adjunctive therapy with nitroprusside or nitroglycerin; use
alone in less intensely monitored situations or treatment of postoperative
hypertension
Enalaprilat: use for scleroderma crisis or as adjunctive therapy in some
high renin states
Hydralazine: treatment of preeclampsia, eclampsia
Fenoldopam: same as for nitroprusside; use in postop or post procedure
hypertension in closely monitored situations
Esmolol: use in case of need for immediate, short acting beta blocker
effect; use for supraventricular tachycardia

Severe Hypertension
BP > 180/120

Encephalopathy
Progressing target organ damage

YES

NO

(HT Emergency)

New onset
(HT Urgency)

Admit to ICU
Baseline lab

Parenteral Rx

Baseline lab

Oral Rx

Prior similar experience;

Negative workup
(Uncontrolled HT)

Reinstitute oral Rx

Follow closely

Workup for
identifiable causes:
Renovascular HT
Kaplan NM. Hypertensive Crises. In: Kaplans Clinical Hypertension, 8th Ed. W. Neal, Ed. Lippincott Williams &
Wilkins, Philadelphia, 2002

Lowering BP in Acute Phase of a

Stroke may be Harmful
13th (2004) European Stroke Conf.
Philip Bath (University of Nottingham,
UK) reported vasoactive drugs, -Bs
and CCBs, were associated with an
increased risk of death (OR 1.23; 95% CI
1.05-1.43) or dependency. (metaanalysis (?) of 26 trials, 4,146 patients)
(also reported in Cerebrovasc Dis
2004;17(Suppl 5):116.)