Hypertensive Crises in

Adults
Prof.dr. Djoko Santoso, SpPD, K-GH, PhD
Nephrology – Hypertension Division, Internal Medicine
Department Faculty of Medicine, Universitas Airlangga
INTRODUCTION
• Hypertensive crises are acute, severe elevations in blood
pressure that may or may not be associated with target-
organ dysfunction.
• Within the hypertensive crises, hypertensive emergencies
account for only around one-fourth of presentations
compared with hypertensive urgencies, which account for
around three-fourths.
• Despite the low incidence of hypertensive emergencies,
hospitalizations because of hypertensive emergencies
have increased since 2000, possibly because of the
heightened awareness, recognition, and subsequent
diagnosis of hypertensive emergency.
• However, even though more hospitalizations are
secondary to hypertensive emergencies, mortality remains
low, with an in-hospital mortality of around 2.5% and 1- and
10-year survival greater than 90% and 70%, respectively
Hypertensive Emergency
• The term "malignant hypertension" was coined in
1928 because, at that time, patients with this
condition had a prognosis that was similar to
patients with many cancers → the term is now
considered outdated and used primarily by billing
and coding personnel
• Although hypertensive emergencies can lead to
significant morbidity and potentially fatal target-
organ damage, only 1%–3% of patients with
hypertension will have a hypertensive
emergency during their lifetime
DEFINITION
• Hypertensive urgency
• a blood pressure in the "severe" range (ie,
≥180/≥120 mmHg), often a mild headache, but no
signs or symptoms of acute end-organ damage
• relatively asymptomatic or completely
asymptomatic patient
• Hypertensive emergency
• significantly elevated blood pressure have signs or
symptoms of acute, ongoing target-organ damage
• In younger (< 60 years of age) people, the diastolic
pressure is typically ≥120 mmHg, but there is no
specific threshold
HYPERTENSIVE CRISES
Hypertensive Emergencies :
Definition
• A rapid decompensation of vital organ function
secondary to an inappropriately elevated BP
• Require lowering of BP within 1 hour to decrease
morbidity
• Not determined by a BP level, but rather the
imminent compromise of vital organ function
Hypertensive Emergencies
• CNS - Hypertensive encephalopathy
• CVS
• Acute myocardial ischemia
• Acute cardiogenic pulmonary edema
• Acute aortic dissection
• Post-op vascular surgery
• Renal - Acute renal failure
• Eclampsia
• Catechol excess- Pheochromocytoma, Drugs
Hypertensive Emergencies
•High BP WITHOUT acute end-
organ dysfunction IS NOT a
hypertensive emergency
• “Hypertensive Pseudo-emergency”
Acute Target-Organ Damage and Clinical
Manifestations of Hypertensive Emergency
Causes of Sympathetic Over-Activity
• Withdrawal of short-acting antihypertensive agents
(especially clonidine, propranolol, or other beta
blockers)
• Ingestion of sympathomimetic agents (eg, tyramine-
containing foods in patients who take chronic
monoamine oxidase inhibitors, amphetamine-like
compounds, cocaine, etc)
• Pheochromocytoma can also produce severe
hypertension and acute target-organ damage.
• Severe autonomic dysfunction (eg, Guillain-Barré and
multiple system atrophy syndromes or acute spinal
cord injury) is occasionally associated with hypertensive
emergency.
Pathophysiology of Hypertensive
Emergencies
• Rate of change of BP determines
likelihood
• Chronic HTN lowers probability
• adaptive vascular changes protect end-
organs from acute changes in BP
• Previous normotensives (eclampsia,
acute GN) develop signs and symptoms
at lower BP’s
Pathophysiology of Hypertensive
Emergencies
• Endothelial Role in BP Homeostasis
• Secretion of vasodilators (NO,
Prostacyclin)
• Sudden increased vasoreactivity
• norepinephrine, angiotensin II
• activation of renin-angiotensin-
aldosterone
Pathophysiology of Hypertensive
Emergencies
• ? ATII direct cytotoxicity to vessel wall
• ? mechanical stretching
• Inflammatory vasculopathy
• cytokines, endothelial adhesion molecules
• Loss of endothelial function
• permeability
• inhibition of local fibrinolysis
• activation of coagulation cascade
Molecular Pathophysiology of
Hypertensive Emergency
Signs and Symptoms
• Hypertensive Urgency:
• Can be completely asymptomatic
• Some symptoms include:
• Severe headache
• Shortness of breath
• Nosebleeds
• Severe anxiety
• Signs:
• Elevated BP on consecutive readings
HYPERTENSIVE URGENCY:
EVALUATION AND DIAGNOSIS

• Exclude acute, ongoing, target-organ

damage, which would indicate a diagnosis of
hypertensive emergency rather than severe
asymptomatic hypertension
• Should be swiftly confirmed with repeated
measurement utilizing proper technique
Signs and Symptoms Continued
• Hypertensive Emergencies
• Symptoms:
• nausea, vomiting (cerebral edema)
• Chest Pain
• SOB
• Blurry vision
• Confusion
• Loss of consciousness
Signs and Symptoms Continued
• Signs:
• Retinal hemorrhages, exudates, or
papilledema
• Renal involvement (malignant
nephrosclerosis) with AKI, proteinuria,
hematuria
• Cerebral edema → seizures and coma
• Pulmonary Edema
• Myocardial Infarction
• Hemorrhagic Stroke, lacunar infarcts
HYPERTENSIVE EMERGENCY:
EVALUATION AND DIAGNOSIS

• The history and physical examination in patients

presenting with a severely elevated blood pressure
(or an acute rise in blood pressure over a previously
normal baseline, even if the presenting pressure
is <180/120 mmHg)
• Relevant sign and symptoms
• Evaluate the presence of target-organ damage:
Electrocardiography, Conventional chest
radiography, Urinalysis, Serum electrolytes and
serum creatinine, Cardiac biomarkers, CT/ MRI
TREATMENT
• Overall approach to therapy — Optimal therapy,
including the choice of agent and the blood pressure
goal, varies according to the specific hypertensive
emergency
• Generally unwise to lower the blood pressure too
quickly or too much as ischemic damage can occur in
vascular beds that have become habituated with the
higher level of blood pressure (ie, autoregulation).
• For most hypertensive emergencies, mean arterial
pressure should be reduced gradually by approximately
10 to 20 percent in the first hour and by a further 5 to
15 percent over the next 23 hours.
• The optimal management of patients with severe
asymptomatic hypertension is unclear.
The major exceptions to gradual
blood pressure lowering
• The acute phase of an ischemic stroke – The blood
pressure is usually not lowered unless it is
≥185/110 mmHg in patients who are candidates for
reperfusion therapy or ≥220/120 mmHg in patients
who are not candidates for reperfusion
(thrombolytic) therapy
• Acute aortic dissection – The systolic blood
pressure should be rapidly lowered to a target of
100 to 120 mmHg (to be attained in 20 minutes) to
reduce aortic shearing forces
• Intracerebral hemorrhage
Neurologic emergencies
• Ischemic stroke – Patients with acute ischemic stroke-in-
evolution are most often not given antihypertensive drugs
during the initial three days of hospitalization unless they
are candidates for tissue plasminogen activator
• Hemorrhagic stroke – Management of blood pressure in
patients with spontaneous intracerebral hemorrhage and
subarachnoid hemorrhage is complicated by competing risks
(eg, reducing cerebral perfusion) and benefits (eg, reducing
further bleeding)
• Head trauma – Head trauma with increased intracranial
pressure can produce severe elevations in blood pressure
• Hypertensive encephalopathy -- In contrast to stroke and
head trauma, the signs and symptoms of hypertensive
encephalopathy (eg, headache, confusion, nausea,
vomiting) usually abate after the blood pressure is lowered
Cardiac emergencies
• Acute heart failure – Patients with acute left
ventricular dysfunction and pulmonary edema should
usually receive loop diuretics.
• Acute coronary syndrome – Severe hypertension
associated with an acute coronary syndrome
(including acute myocardial infarction) is appropriately
treated with intravenous nitroglycerin, nicardipine (to
reduce myocardial oxygen consumption, to reduce the
underlying coronary ischemia, and to improve
prognosis)
Vascular emergencies
• Acute aortic dissection – Patients with acute aortic
dissection are treated to rapidly reduce the blood
pressure to a goal systolic of 100 to 120 mmHg
• Severe hypertension in patients with recent
vascular surgery – Severe elevations of blood
pressure can threaten suture lines
Renal emergencies
• May occasionally cause acute injury to the kidneys
(acute hypertensive nephrosclerosis, formerly
called "malignant nephrosclerosis") →
characterized by hematuria (usually microscopic
hematuria, which is found in approximately 75
percent of patients with hypertensive emergencies)
and an elevated serum creatinine
Treatment goal decision-algorithm in
hypertensive crisis
Treatment Options
• Hypertensive Urgency:
• Goal: Reduce BP to <160/100 over several hours
to day
• Elderly at high risk of ischemia from rapid reduction
of BP, therefore slower reduction in BP in this patient
population
• Previously treated hypertension:
• Increase dose of existing med or add another med
• Reinstitution of med in non-compliant patients
Treatment Continued
• Hypertensive Emergency:
• Goal: Lower Diastolic BP to approximately 100-
105 over 2-6 hours; max initial fall not to exceed
25%
• More aggressive decrease can lead to ischemic
stroke and myocardial ischemia
• If focal neurological symptoms present → obtain
MRI to r/o acute stroke (rapid BP correction
contraindicated)
• Parenteral antihypertensive (IV Drip)
recommended over oral agents in hypertensive
emergency
Parenteral drugs for treatment of
hypertensive emergencies in adults
• Nitrates → Nitrovasodilators such
as nitroprusside and nitroglycerin provide nitric oxide
that induces vasodilatation (of both arterioles and
veins) via generation of cyclic GMP, which then
activates calcium-sensitive potassium channels in the
cell membrane
• Calcium channel blockers → clevidipine, nicardipine
• Dopamine-1 agonist → fenoldopam
• Adrenergic-blocking agents → labetalol, esmolol
• Other agents → hydralazine, enalaprilat, phentolamine
Treatment
• Recommended parenteral antihypertensive agents
(IV drip) for Hypertensive Emergencies and
admission to ICU
• Nitroprusside (cautious about cyanide toxicity),
Nicardipine, and Labetalol.
• Once BP controlled, switch to oral anti-
hypertensives and follow-up closely
BP Treatment Goals for
Hypertensive Emergency
Categories of BP in Adults*
BP Category SBP DBP

Normal <120 mm Hg and <80 mm Hg

Elevated 120–129 mm and <80 mm Hg

Hg
Hypertension
Stage 1 130–139 mm or 80–89 mm Hg
Hg
Stage 2 ≥140 mm Hg or ≥90 mm Hg

*Individuals with SBP and DBP in 2 categories should be

designated to the higher BP category.
BP indicates blood pressure (based on an average of ≥2
careful readings obtained on ≥2 occasions, as detailed in
DBP, diastolic blood pressure; and SBP systolic blood
pressure.
Hypertensive Crises: Emergencies and Urgencies (ACC & AHA, 2017)

COR LOE Recommendations for Hypertensive Crises and Emergencies

In adults with a hypertensive emergency, admission to an intensive
care unit is recommended for continuous monitoring of BP and
I B-NR target organ damage and for parenteral administration of an
appropriate agent.

For adults with a compelling condition (i.e., aortic dissection,

severe preeclampsia or eclampsia, or pheochromocytoma
I C-EO crisis), SBP should be reduced to less than 140 mm Hg during
the first hour and to less than 120 mm Hg in aortic dissection.

For adults without a compelling condition, SBP should be

reduced by no more than 25% within the first hour; then, if
I C-EO stable, to 160/100 mm Hg within the next 2 to 6 hours; and
then cautiously to normal during the following 24 to 48 hours.
Diagnosis and Management of a Hypertensive Crisis (ACC & AHA, 2017)
SBP >180 mm Hg and/or
DBP >120 mm Hg

Target organ damage new/

progressive/worsening

Yes No

Hypertensive
Markedly elevated BP
emergency

Admit to ICU
(Class I) Reinstitute/intensify oral
antihypertensive drug therapy
and arrange follow-up

Conditions:
• Aortic dissection
• Severe preeclampsia or eclampsia
• Pheochromocytoma crisis

Yes No

Reduce SBP to <140 mm Hg Reduce BP by max 25% over first h†, then
during first h* and to <120 mm Hg to 160/100–110 mm Hg over next 2–6 h,
in aortic dissection† then to normal over next 24–48 h
(Class I) (Class I)
Thank You