This Presentation talks about Hyprtension, the mode of presentation of hypertensive crisis and the effective management of hypertensive crisis to prevent case fatalities.

1. MEDICINE TUTORIALS
HYPERTENSIVE
EMERGENCIES
ADEBAYO AYOMIDE
600L MBBS
CMUL

2. Outline
• Introduction and Definition of
terms
• Epidemiology
• Risk factors
• pathophysiology
• Classification
• Clinical Presentation
• Symptoms
• Management
• History taking and Examination
• Investigations
• Treatment
• Prognosis and Prevention

3. HYPERTENSION
DEFINITION
Hypertension is defined as having a systolic BP ≥140 mm
Hg and/or diastolic BP ≥90mmhg however the 2017
American College of Cardiology/American Heart
Association Hypertension Guideline,uses a systolic BP
≥130 mm Hg and/or diastolic BP ≥80mmhg.
Blood Pressure
Blood Pressure SBP DBP
Classification mmHg mmHg
Normal <120 and <80
Prehypertension 120–139 or 80–89
Stage 1
Hypertension
140–159 or 90–99
Stage 2
Hypertension
≥160 or ≥100

4. HYPERTENSIVE CRISIS
• According to JNC 7,Hypertensive crisis occurs when systolic BP rises above
180mmHg and or a diastolic BP above 120mmHg.
• However in reality,there is no critical level of BP that defines the presence of
hypertensive crisis. For example,in a previously normotensive patient,crisis can
occur at 100/110 DBP and in a chronically hypertensive patient,very high DBP can
persist without the development of a crisis.
• According to JNC 2003 ,this is also referred to as a severe hypertension.
• Hypertensive crisis can further be classified into Hypertensive Emergency and
Hypertensive Urgency.
• Other colloquial terms used include; malignant hypertension,accelerated
hypertension.

5. MALIGNANT AND ACCELERATED
HYPERTENSION
• Malignant hypertension is a clinical syndrome characterised by marked elevation of
BP,systolic BP [SBP] >180 mm Hg or diastolic BP [DBP] >120 mm Hg,with widespread
acute arteriolar injury ( hypertension induced arteriolitis) in the presence of
fundoscopy findings of hypertensive neuroretinopathy (striate/flame shaped
haemorrhages,cotton wool/soft exudates and papilledema).
• Regardless of how high the BP is ,if there is no evidence of hypertensive
neuroretinopathy,that is not a malignant hypertension.
• Hallmark of malignant hypertension is the presence of fibrinoid necrosis.
• 90% of persons with untreated malignant hypertension will not live past 1-2 years.
• Accelerated Hypertension is similar to malignant hypertension without papilledema.
• Prognosis is same in both conditions. WHO recommends that they can be used as
synonyms of the same disease.

6. EPIDEMIOLOGY
• 1% of all hypertensive patients will have an episode of hypertensive
crisis in their lifetime.
• 3.2% of all patients presenting to the Emergency Department are
cases of hypertensive crisis
• Male to female ratio is 2:1
• 1yr survival rate of adequately treated patients is 90%
• 5yr survival rate of adequately treated patients is 74%
• Occurs more commonly in blacks than whites.

7. RISK FACTORS
• Commonest cause: Chronic hypertension
with acute exacerbation resulting
medication non-compliance.
• Undiagnosed hypertension: 8% of all crisis.
• Emergency surgery in a poorly controlled
hypertensive.
• Systemic illnesses with renal involvement:
SLE, scleroderma, HUS/TTP, cushing’s
disease, pheochromocytoma
• Autonomic hyperactivity in spinal cord or
head injury.
• In a quadriplegic, autonomic hyperreflexia
with stimulation of nerves below the spinal
cord injury.
• Cerebrovascular accident (CVA)
• Extensive burn injury
• Children receiving high dose
cyclosporine for allogenic bone
marrow transplantation.
• Drugs: oral contraceptives, cocaine,
phencyclidine, MOA inhibitors +
tyramine, linezolid, NSAIDS,
amphetamine.
• Pregnancy

8. PATHOPHYSIOLOGY
• Blood Pressure is a product of cardiac output and total peripheral vascular resistance.
• Total peripheral vascular resistance is influenced by neurohumoral and vasoactive
substances.
• During an acute hypertensive episode,there is a failure of autoregulatory function
precipitated by one or more of a host of potential causes. This failure of autoregulation
then leads to increased systemic vascular resistance. In the setting of end-organ damage,
release of inflammatory markers ensues,which ultimately causes endovascular injury
and fibrin necrosis of arterioles. This leads to production of more vasoconstrictors and
the cycle continues
• The renin-angiotensin-aldosterone system also plays a significant role in the cascade of
hypertension,stimulating decreased renal perfusion and lowering tubular sodium
concentration. This in turn stimulates aldosterone to increase blood pressure by
maintaining excess volume through sodium retention and potassium excretion,further
potentiating the cycle of uncontrolled blood pressure.

9. CLASSIFICATION OF
HYPERTENSIVE CRISIS
Hypertensive Emergency is a condition in which
severe hypertension with SBP 180mmHg and DBP
120mmHg is associated acute and rapidly
evolving end-organ damage. It commonly affects
cardiopulmonary and renal system. The most
common damage is Ischemic heart disease.
Hypertensive urgency is a condition in which severe
uncontrolled hypertension with SBP 180mmHg and
DBP 120mmHg is observed in a patient who may have
evidence of previous end-organ damage but in whom
there exists no evidence of ongoing or imminent target
organ dysfunction related to this episode of
hypertension.
Hypertensive
Emergency
Hypertensive
Urgency

10. PRESENTATIONS OF HYPERTENSIVE EMERGENCIES
Neurologic
• Hypertensive
Encephalopathy
• Intracranial
Hemorrhage
• Sub Arachnoid
Hemorrhage
• Acute Ischemic
Stroke
Cardiopulmonary
• Acute Aortic
Dissection
• Acute Coronary
Syndrome
• Acute Heart
Failure/Pulmonary
Edema
Renal
• Acute Renal
Failure
Pregnancy
associated
• Preeclampsia
• Eclampsia
Others
• Peri-operative
hypertension
• Pheochromocytoma
crisis
• Sympathomimetic
crisis

11. SYMPTOMS
• HYPERTENSIVE EMERGENCY
• Chest pain
• Headache
• Blurred vision
• Weight loss
• Dizziness
• Nausea
• Dyspnea
• Fatigue
• Malaise
• Epigastric pain
• Polyuria
• Gross hematuria
• HYPERTENSIVE URGENCY
• Usually asymptomatic
• Mild headache
• No signs or symptoms of acute end-
organ damage.

12. MANAGEMENT
HISTORY
• Presenting symptoms
• Secondary cause of hypertension
• Onset of hypertension
• Duration of hypertension
• Severity of hypertension (baseline BP)
• Medication history: drug therapy, compliance, use of OTCs, illicit
drugs,
• History of previous end organ dysfunctiom: renal, CVA
• Any medical co-morbidities
• LMP in females
• Alcohol use, MAOI + antidepressants/tyramine containing foods
• CVA accident, head trauma, brain tumors

13. MANAGEMENT
PHYSICAL EXAMINATION
Aim: to discover what end- organs are being affected
• BP measurement : done in both arms (r/o aortic dissection) and both
supine and standing positions (r/o volume depletion)
• Fundoscopy: papilledema, flame hemorrhages, cotton wool spots or AV
nicking ( due to ischemic infarction of the nerve bundles of the retina)
• Cardiovascular exam: peripheral pulse ( delay or absence point to aortic
dissection, distended JVP as seen in heart failure and pulmonary edema,
irregular heart rate, rhythm, S3 hrt sound, displaced apical beat, murmur.
• Chest exam: rales, crackles
• Abdominal exam: renal bruit, abdominal masses
• Neurological exam: altered mental status, lateralizing signs, decreased
visuals fields.
• Peripheral edema

14. 1. E/U/Cr, BUN to r/o renal
impairment
2. Urinalysis: hematuria, proteinuria
3. Microscopic urinalysis: red cell
and red cell casts
4. ECG: if chest pain, to r/o ischemic
changes, LBB block, compare with
old ECGs
5. Cardiac enzymes: to r/o ACS
6. Chest x-ray: if dyspneic, may find
widened mediastinum as in Aortic
D., evidence of pulmonary edema
7. Echo: may find LV dysfunction,
valvular insufficiency
INVESTIGATIONS
8. Chest CT: to confirm Aortic D.
9. Head CT: to r/o stroke
10. FBC, peripheral blood smear:
microangiopathic anemia
11. Toxicology screening: to r/o cocaine,
amphetamine toxicity
12.Pregnancy test
13. Endocrine screening r/o
pheochromocytoma
Other investigation to r/o secondary causes
of HTN

15. PRINCIPLES OF TREATMENT
HYPERTENSIVE URGENCY
• Hypertensive urgency develops over days to weeks hence BP SHOULD
NOT be lowered acutely or could lead to symptomatic hypotension.
• After r/o the presence of end organ damage, treat according to the
recommended guidelines.
• Use rapid onset ORAL antihypertensive for gradual, short-team reduction
over a period of 24-48 hours while patients is being monitored for
hypertension related organ damage. DOC: Clonidine, labetalol, captopril.
• Once the short-term meds have adequately lowered BP, transition to ong
term agents to prevent rebound hypertension and monitor for extra 24 hrs
during transition phase in ER or observational setting.
• Discharge with follow up schedule in 1-2 days.
• Carry out patient education on medication adherence, weight loss, low
salt diet to prevent re occurrence.

16. PRINCIPLES OF TREATMENT
HYPERTENSIVE EMERGENCY
• Treatment must be individualized to patient’s need, treat patient not the numbers.
• All patients must be admitted to hospital emergency preferably ICU for continuous monitoring of BP,
target organ damage and parental drug administration.
• Give medications parentally
• While giving medications, continuously monitor for evidence of hypoperfusion (yawning, nausea,
hyperventilation, chest pain)
• Monitor for resolution of symptoms of organ damage
• Volume expansion may be needed in evidence of volume depletion (ensure no volume overload) with
IV saline which help suppress renin secretion and prevent hypotension with use of vasodilator
therapy.
• For adults with a compelling condition i.e. aortic dissection, severe per-eclampsia, eclampsia,
pheochromocytoma crisis: lower BP to below 140mmHg (120mmHg in aortic D) in the first hour.
• For adults without a compelling condition, lower BP by a max of 25% in the first hour then if clinically
stable, lower to 160/100-110mmHg in 2-6 hrs then to normal in 24-48 hrs.

17. MEDICATIONS USED IN HYPERTENSIVE
EMERGENCIES
B-blockers
• Labetalol
• Esmolol
Vasodilators
• Nitroglycerin
• Sodium
nitroprusside
• Hydralazine
• Phentolamine
Calcium
channel
blockers
• Nicardipine
• Clevidipine
Others
• Fenoldopam
• Enalaprilat

19. BETA-BLOCKERS
Labetalol
• Useful in most emergencies
• Selective alpha-1 and non selective beta blocking properties
and decreases SVR without affecting the Cardiac output.
• Contra-indicated in heart failure, heart block, COPD,
hypertensive crisis following coronary artery bypass surgery.
• Safe in pregnancy
• Preferred in ESD and aortic dissection.
Esmolol
• Cardio selective beta blocker, ultra short acting.
• Decreases heart rate, contractility and cardiac output,
• Very useful in severe post op hypertension.
• Contraindicated in heart failure, COPD, bradycardia.

20. VASODILATORS 1
Sodium nitroprusside
• Commonly used, short-acting and can be titrated minute to minute.
• Potent IV hypotensive agent with rapid onset
• Causes both arteriolar and venous dilation which lowers SVR and
venous return leading to less preload and afterload and decreased
LV wall tension and myocardial O2 demand.
• Preferred in heart failure, aortic dissection, adrenergic crisis and
also hypertensive encephalopathy.
• Metabolized to cyanide which is then converted to thiocyanate by the
liver. Thiocyanate is excreted unchanged by the kidney with a half
life of 1 week in a patient with normal renal function.
• Risk of thiocyanate and rarely cyanide poisoning when used for over
48-72 hours, particularly in persons with renal or liver dysfunction.
Thiocyanate poisoning treated by hydroxycobalamin and thiosulfate
infusion.

21. VASODILATORS 2
Nitroglycerin
• Potent venous dilator but at high doses it dilates arteries too.
• Reduces BP by reducing preload and Cardiac output.
• Eliminated by hepatic mechanism in 1-4 mins. Has low efficacy
hence majorly used as an adjunct with other medication.
• Preferred in acute coronary syndrome and pulmonary edema.
Hydralazine
• Dilates arteries but it has less predictable effects and it raises
the heart rate.
Phentolamine
• Non selective alpha adrenergic blocking agent used to manage
pheochromocytoma in conjunction with beta blocker.

22. CALCIUM CHANNEL BLOCKERS (CCB)
Nicardipine
• 2nd generation dihydropyridine CCB. Strong cerebral and coronary
vasodilator activity.
• Useful in coronary artery disease and systolic heart failure
• Also recommended for ischemic stroke by American Heart
Association.
Clevidipine
• New 3rd generation dihydropyridine CCB. Short acting selective
arterial vasodilator with very little effects on myocardial contractility
or chronotropy.
• Effective in peri operative cardiac surgery complicated by
hypertension however it has a very short half life.
• Contra indicated in patients with soybeans, soy products, eggs
allergy and defective lipid metabolism.

23. OTHERS
Fenoldopam
• Peripheral dopamine 1 receptor agonist which decreases
systemic vascular resistance, increases renal blood flow and
causes natriuresis and aquauresis.
• 6x more potent than dopamine.
• Preferred in acute renal failure. Acute heart failure, pregnancy
• Contra indicated in glaucoma, sulfa allergy
Enalapril
• An angiotensin converting enzyme inhibitor.
• A poor choice .

24. SPECIFIC TREATMENT FOR THE DIFFERENT PRESENTATIONS
CONDITION MEDICATION PRECAUTIONS AIMS
Hypertensive Encephalopathy Labetalol, nicardipine,
fenoldopam
Avoid clonidine, methyldopa,
reserpine can cause CNS
depression
Decrease MAP by 20%
Acute Intracranial
Haemorrhage
Nicardipine, labetalol,
enalapril, hydralazine, esmolol
Monitor ICP with
ventriculostomy, maintain at
60-80mmHg. Do not lower
MAP below 20% in 24 hrs.
If SBP >200mmHg and or
MAP >150mmHg, reduce to
SBP ≤160mmHg, MAP≤
130mmHg
Acute ischemic stroke No specific medication Allow permissive
hypertension to protect
penumbra
If pt can receive thrombolysis,
lower to SBP <180mmHg,
DBP <105mmHg in 24 hrs, if
not only lower if SBP>
220mmHg or DBP
>110mmHg.
Subarachnoid haemorrhage Nicardipine, labetalol,
esmolol, nimodipine
Must be treated Ensure SBP <160mmHg
Aortic dissection Nitroprusside + esmolol Must be swiftly treated, begin
with beta blocker before
vasodilator. If aortic root is
involved, avoid beta blocker
use Calcium channel blocker
instead
Ensure SBP <100-110mmHg
Ensure heart rate btw 60-80
bpm

25. SPECIFIC TREATMENT FOR THE DIFFERENT PRESENTATIONS
CONDITION MEDICATION PRECAUTIONS AIMS
Myocardial infarction Esmolol, nitroglycerin +
thrombolytics and reperfusion
Avoid thrombolytics if
BP>185/100mmHg
Reduce BP by 20-30% of the
baseline till symptoms
resolve or DBP < 100mmHg
Acute heart failure nitroglycerin., ACEI Hydralazine, clonidine Reduce BP < 130/80mmHg
Acute renal failure Fenoldopam, nicardipine General treatment
recommendations
Pheochromocytoma/ cocaine
toxicity
Phentolamine, nitroprusside Beta adrenergic antagonists SBP < 140mmHg in 1 hour
Pre-eclampsia/eclampsia Hydralazine, labetalol, mag
sulphate
BP < 150/100mmHg
Peri operative hypertension Nitroprusside, nitroglycerin,
clevidipine
Lower to 20% of baseline
pressure

26. NEXT STEPS
• Oral antihypertensive agents should be initiated as soon as the patient has been stabilized and is
able to tolerate oral medications,along with gradual tapering off of parenteral agent.,the
cornerstone of initial oral therapy should be an arteriolar vasodilator such as hydralazine,sustained
release nifedipine,or minoxidil.
• Vasodilators may cause reflex tachycardia with increase in cardiac output and blunt the
hypotensive response. Therefore,treatment with β-adrenergic blockers is usually also required.
• Vasodilators also cause renal salt and water retention and hence the tolerance to hypotensive effect
by volume overload. Thus,although diuretics may not be required for the initial management,they
are usually required as a part of the long-term maintenance antihypertensive regimen.
• After BP has been controlled with parenteral therapy and while the infusion is continued,
hydralazine (100 mg) and metoprolol (50 mg) are administered orally. As the oral agents become
effective and BP declines,the parenteral infusion is tapered. Brief interruption of the infusion can
be used to assess the hypotensive response to oral agents.

27. NEXT STEPS
• If after 6 to 8 hours the DBP remains higher than 100 mm Hg,a second dose of hydralazine
(100 mg) should be given. The metoprolol dose is increased as needed to maintain adequate β-
blockade (heart rate,60-80 beats/min).
• If BP is not controlled with hydralazine at a dose of 100 mg twice daily,minoxidil should be
substituted for hydralazine. The starting dose of minoxidil (2.5 mg) is increased by 2.5 mg to 5
mg every 6 to 8 hours until the blood pressure is adequately controlled. The usual effective
dose is 5 to 10 mg twice a day. As the blood pressure is brought under control with oral agents,
the infusion is gradually weaned.
• When the convalescing patient is mobilized,upright BP should be carefully monitored to
avoid orthostatic hypotension.
• A diuretic,usually furosemide at a starting dose of 40 mg twice daily,is added to vasodilator
regimen when it becomes evident that salt and water retention is beginning to occur.
• The goal is to reduce BP below <160/100 by the time of discharge with ultimate goal to reduce
blood pressure <130/80 over next 2-3 months.

28. PREVENTION
PRIMARY PREVENTION
• Health education against substance abuse,
• Prevention of hypertension by exercise, low salt diet, healthy
diet including fruits and veggies.
SECONDARY PREVENTION
• Early diagnosis of hypertension and treatment
• Education on drug compliance
• Adherence to lifestyle modification: DASH diet
TERTIARY PREVENTION
Substance abuse rehab centre
Rehabilitation from MI, CVA

29. SUMMARY
• Evaluate properly to
appropriately classify
patient for accurate
management.
• Treat patients not the
numbers.
• Hypertensive urgency
• No end organ damage
• Lower BP gradually over
hours to days.
• Hypertensive emergency
• Evidence of end organ
damage
• Lower BP less gradually
over minutes to hours.