APPROACH TO HYPERTENSIVE CRISIS IN EMERGENCY SETTINGS

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1. Jwan Ali AlSofi
APPROACH TO
HYPERTENSIVE
CRISIS
PRESENTED BY :
DR MUHAMMAD AFIQ BIN AB RAHMAN
HOSPITAL DARO
SUPERVISED BY :
DR HADILA
EMERGENCY PHYSICIAN HOSPITAL
SIBU

2. Outline of this lecture:

What is Hypertensive Crisis?
Epidemiology.
Classification of Hypertensive Crisis.
Causes of Hypertensive Crisis
Clinical presentation of Hypertensive Crisis

Managment of Hypertensive Crisis

3. What is Hypertensive
Crisis?
Hypertensive crises refer to clinical situations in which the blood
pressure is elevated and there is either acute (hypertensive emergencies)
or impending end-organ damage* (hypertensive urgencies).
Examples of impending end-organ damage include papilledema, shortness of breath, and
pedal edema.
Historically, hypertensive urgencies have been defined as diastolic blood pressures 120 mm
Hg.
It is important to remember, however, that the absolute blood pressure is not as critical as
the degree and rate of increase from baseline blood pressure in determining what is or is
not a hypertensive urgency.
Untreated or sub-optimally controlled hypertension leads to
increased
cardiovascular, cerebrovascular and renal morbidity/ mortality and
overall
mortality

4. Epidemiology
•Approximately 1% of hypertensive pts. may develop
hypertensive crises during their lifetime.
•Annual incidence of hypertensive emergencies being
1-2 cases/1,00,000 pts.
•Higher rates have been reported in African Americans, low
socioeconomic people, in developing countries.
•Incidence in men 2 times higher than in women
Epidemiology

6. Definitions of hypertensive crisis:-
•Hypertensive emergencies:- are defined as severe
elevations in BP (>180/120 mm Hg) associated with
evidence of new or worsening target organ damage.
•Hypertensive urgencies:- are situations associated with
severe BP elevation (>180/120 mm Hg) in otherwise stable
patients without acute or impending change in target
organ damage or dysfunction.
•Accelerated hypertension (aka malignant hypertension):- A
severe increase in blood pressure to 180/120
 mmHg or
higher (and often over 220/120
 mmHg)
with signs of retinal
haemorrhage and/or papilloedema (grade 3-4). It is usually
associated with new or progressive target organ damage.

7. Definition of HTN-emergency:-

9. •Renovascular Disease
•Pheochromocytoma
1.Non-adherence to anti-HTN medications (most
common)
2.Hyperaldosteronism
3.Anti-hypertensive withdrawal syndromes
4.Head injuries and CNS trauma
5.Post-op hypertension
6.Drug-induced hypertension
Causes of hypertensive emergencies ?

12. •As with hypertensive emergencies ,severe BP
elevations may result from inadequate control or poor
adherence to current antihypertensive drug regimens.
•Another cause for patients reaching hypertensive
urgency is previous inaccurate BP measurements that
underestimate or do not detect increased BP at all
(e.g. poor patient technique for selfmonitoring).
‐
Causes of hypertensive Urgencies ?

13. Causes Hypertensive Urgencies
Drugs:
•Non-Narcotic Analgesics :
- Non-steroidal anti-inflammatory agents including
aspirin
- Selective COX-2 inhibitors
• Sympathomimetic agents:
- Decongestants
- Diet pills
- Cocaine
• Stimulants:
-Methylphenidate, amphetamine.
Causes of hypertensive Urgencies ?

14. Causes Hypertensive Urgencies
•Lifestyle:
- High salt diet, excessive alcohol use.
•Comorbid Conditions:
- Thyroid storm, trauma, renovascular disease, acute
ischemic stroke or adrenal dysfunction
Causes of hypertensive Urgencies ?

15. Clinical Presentation of HC
Emergency
Characterized by severe increase in systolic
and/or diastolic blood pressure associated with
signs or symptoms of acute end-organ
damage.
Usually, SBP > 180 mm Hg - DBP > 120 mm Hg
Requires an immediate BP reduction in few
minutes - hours.
Requires an ICU care & IV drugs
Urgency
•Elevated BP ( usually systolic > 180
mmHg &/or diastolic > 120 mmHg ) but
without evidence of end-organ
damage.
•Usually asymptomatic; severe
headache, shortness of breath,
epistaxis, severe anxiety.
•Adequate treatment of these conditions,
a BP lowering within 24-48 hrs by
administration of oral drugs.
•ICU admission is usually not required
•Controlled by oral medications.

16. Clinical Presentation of HC
Emergency
•Rarely develop in patients without a
previous history of hypertension
•occur in patients with pheochromocytoma
or renal vascular disease
•CNS:-
•Cerebral infarctions,
•HTN Encephalopathy
•intracranial or subarachnoid hemorrhage.
•Heart:-
•acute heart failure (HF) and pulmonary
oedema
•acute myocardial infarction,
•unstable angina.
•Acute dissection,
•Eclampsia .
Urgency
•Not all patient present with same
symptoms
•90% of patients had a history of
hypertension
•Headache (42%) and dizziness
(30%).
•visual changes,
•chest discomfort,
•nausea,
• epistaxis,
•Fatigue
•psychomotor agitation.

17. ACUTE
PROGRESSIVE
END-ORGAN
DAMAGE

18. • Single organ damage in approximately 83%.
• Two organ damage found in 14%,multiorgan damage
in 3 % pts.
Most common clinical presentations :
- cerebral infarction (24%)
- pulmonary oedema (22%)
- HTN encephalopathy (16%)
- Cong. HF (12%)
•Less common presentations –
-IC hemorrhage,
-Aortic dissection
-Eclampsia
Acute End-organ Damage
(Complication of HC).

20. Hypertensive retinopathy:-
Acute/severe
hypertensive
retinopathy

21. Hypertensive retinopathy:-
Retinal hemmorhages (grade 3)-
ACCELERATED HT
Papilloedema (grade 4)-
MALIGNANT HT

22. Hypertensive Encephalopathy
•Is a
 presentation of hypertensive emergency 
•Our brains are under tight control. With severe rises in BP,
autoregulation fails and leads to cerebral edema.
•Hypertensive encephalopathy is defined as the presence of
signs or symptoms of cerebral edema secondary to severe
and/or sudden rises in BP. It’s characterized by:
 
•Severe Hypertension with 1+ of:
 
1.Seizures
2.Lethargy
 
3.Cortical Blindness
4.Coma
•It is a
 
diagnosis of exclusion

24. Of note, there is little evidence to
suggest that headache alone is a sign
of a hypertensive emergency,
however, in combination with visual
changes, lethargy, seizures or altered
mental status it may be an indication
of hypertensive encephalopathy.

25. MALIGNANT HYPERTENSION
- Is a HYPERTENSIVE
EMERGENCY!!!
- Leading to an acute end organ
damage
- Less than 1% of hypertensive
patients develop the malignant
phase
- Avarage age of diagnosis is 40
- Men>women

26. APPROACH TO
HYPERTENSIVE
CRISIS

27. •The treatment of hypertensive crisis must balance
preventing further end-organ damage while
maintaining tissue perfusion.
•The initial goal for blood pressure reduction is not to
obtain a normal blood pressure.
•Rapid and aggressive reductions in blood pressure can
actually induce cerebral, myocardial, or renal
ischemia or infarction if the blood pressure falls below
the range at which tissue perfusion can be maintained
by autoregulation.
MANAGEMENT
History Examination Assessment Treatment

28. •Duration and degree of pre existing hypertension
•Details of antihypertensive therapy
•Compliance with medications
•Use of the over counter drugs
•History of recent operations.
History Examination Assessment Treatment
HISTORY

29. EXAMINATION

30. CLINICAL SYMPTOMS
C.V:
•palpitations
,
•arrhythmias
,
•chest pain,
•dyspnea,
•pul. Edema.
BRAIN:
•headaches,
•nausea,
vomiting,
•blindness,
•seizures,
•coma
KIDNEY:
•oliguria,
•hematuria,
•proteinuria,
•electrolyte
imbalance,
•uremia,
•azothemia
EYE:
•flashes,
•scotoma
GENERAL:
•sweating,
•pallor,
•flushes,
•tinnitus,
•epitaxis,
•fear of
death

31. Lab tests & investigations may be required:-
-FBC,
-ECG,
-urinalysis,
-renal function
-Echo.
-consider head imaging if neurological symptoms
are present
ASSESMENT with INVESTIGATION

32. TREATMENT OF
HYPERTENSIVE CRISIS

33. Severe hypertension is defined as persistent elevated SBP >180 mmHg and/or
DBP >110 mmHg.
These patients may present with:
i. incidental finding in an asymptomatic non-previously diagnosed patient
ii. treated hypertension on follow-up who are asymptomatic
iii. patients with symptoms which may include:
non-specific symptoms like headache, dizziness, lethargy.
 symptoms and signs of acute target organ damage/complication. These include
acute heart failure, acute coronary syndromes, acute renal failure, dissecting
aneurysm, subarachnoid haemorrhage, hypertensive encephalopathy and
preeclampsia/eclampsia.

35. 6.1.1 Hypertensive Urgency
Hypertensive urgency is defined as severe increase in BP which is
not associated with acute end organ damage/complication.
Blood pressure measurement should be repeated after 30 minutes
of bed rest.
Initial treatment should aim for about 25% reduction in BP over 24
hours but not lower than 160/100 mmHg.

36. 6.1.1 Hypertensive Urgency (cont.)
Therapeutic strategies for previously undiagnosed patients include
(Figure 6-A: Flowchart in management of hypertensive urgency):
1. Rest in quiet room for at least 2 hours.
2. Initiate oral anti-hypertensive agents if BP remains >180/110
mmHg .
3. Hypertensive urgency discharge plan (Figure 6-B).

41. 6.1.2 Hypertensive Emergency
Hypertensive emergency is defined as severe elevation of blood
pressure associated with new or progressive end organ
damage/complication such as:
 acute heart failure, dissecting aneurysm, acute coronary
syndromes, hypertensive encephalopathy, acute renal failure,
subarachnoid haemorrhage and/or intracranial haemorrhage.
These may occur in patients with BP <180/110 mmHg,
particularly if the BP has risen rapidly.

42. 6.1.2 Hypertensive Emergency (cont.)
These patients:
• should be admitted for immediate intervention and monitoring.
• need to be reduce their BP rapidly based on clinical scenarios
This is best achieved with parenteral drugs. (Table 6-D)
should have their BP reduced by 10%-25% within certain minutes to
hours but not lower than 160/90 mmHg.

44. Optimal drugs to treat a dissection are those
that decrease not only mean arterial blood
pressure, but also the rate at which blood
pressure increases .This is usually achieved by
the combination of nitroprusside and an
intravenous beta-blocker such as esmolol or
labetalol. Nitroprusside should not be given
alone.
Intravenous parenteral vasodilators, such as
nitroglycerin, are effective. Beta-blockers are
also beneficial in hypertensive patients with
acute coronary syndromes. One
should be careful in using nitroglycerin and
beta-blockers in those patients with posterior
wall or right ventricle ischemia (e.g.,
inferior myocardial infarction), as these
patients are preload and volume dependent.
Drugs that increase cardiac work (hydralazine)
should be avoided

45. Choices of therapy include fenoldopam,
nicardipine, and beta-blockers.
The use of nitroprusside should be limited to a
brief period (i.e., <24 hours), because its toxic
metabolite, thiocyanate, can
accumulate.
Theoretically, beta-blockers, nicardipine,
labetalol, and enalaprilat are ideal choices since
they have little effect on intracranial pressure.
Nitroprusside and nitroglycerin should be
avoided, because
they cause cerebral venodilation.
pregnant women with severe hypertension
(preeclampsia,
eclampsia), intravenous hydralazine is the
treatment of choice because it increases uterine
blood flow. Beta-blockers and
nicardipine can also be used if hydralazine is
contraindicated
Intravenous clevidipine,
nicardipine, phentolamine

46. alpha- and beta-adrenergic
blocker with a rapid
onset (5 minutes). It does not
directly affect cerebral blood
flow. The main side effects of
labetalol include hypotension,
heart block, and bronchospasm.
Nitroglycerin a venodilator is
perhaps most effective in acute
coronary syndromes and in
those with hypertension
following coronary bypass
surgery
arterial vasodilator that causes
unpredictable
hypotension and reflex
tachycardia. It has prolonged
effects and
should be primarily limited to
pregnant women, because it
increases uterine blood flow.

47. a cardioselective beta-blocker
with a short half-life (9
minutes) and a relatively short
duration of action (30
minutes. The main potential
side effects are
hypotension and
bronchospasm
Drug of choice for aortic
dissection
dihydropyridine calcium channel
blocker that is
as effective as nitroprusside in lowering
blood pressure. It may potentially have
favorable effects in patients with
cardiac and cerebral ischemia by
relaxing coronary smooth muscle and
increasing vasodilatation

48. f
an arteriolar and venous dilator
that has an
immediate onset (seconds) and
disappears within minutes.
This toxic risk is increased in
patients with underlying renal
insufficiency and with use for
more than 24–48 hours
potential risk in cases of cardiac
ischemia that nitroprusside
causes “coronary steal,”
shunting blood away from
ischemic areas. Thus,
nitroprusside should be avoided
if possible in patients with
cardiac ischemia.
Avoided in pregnant women,
because it is teratogenic.