1. Hypertensive emergencies involve uncontrolled high blood pressure leading to target organ dysfunction. Rapid blood pressure reduction within 1 hour is needed to prevent morbidity. 2. The document discusses classifications of hypertensive crises and emergencies. It also covers epidemiology, etiology, pathophysiology, clinical features, investigations, and general treatment goals for hypertensive emergencies. 3. Specific conditions like aortic dissection, ischemic stroke, and hemorrhagic stroke are exceptions to general treatment goals, with their own target blood pressure and heart rate ranges for management.

1. MANAGEMENT OF HYPERTENSIVE
EMERGENCIES
DR. REBECCA ENEJO
MEDICAL OFFICER
A/E Dept.,
FMCL

2. OUTLINE
•Introduction
•Classification
•Epidemiology
•Etiology/risk factors
•Pathophysiology
•Clinical features
•Management
•Follow up
•Prognosis
•Prevention
•Recommendation
•Conclusion

3. INTRODUCTION
Hypertensive emergencies encompass a spectrum
of clinical presentations in which uncontrolled blood
pressures (BPs) lead to progressive or impending
target-organ dysfunction.
A rapid decompensation of target organ function
secondary to an inappropriately elevated BP
Largely Require lowering of BP within 1 hour to
decrease morbidity

4. CLASSIFICATION
•HYPERTENSIVE CRISES are acute, severe elevations in
blood pressure that may or may not be associated
with target-organ dysfunction.
•HYPERTENSIVE EMERGENCIES, a subset of
hypertensive crises, are characterized by acute, severe
elevations in blood pressure, often greater than
180/110 mm Hg (typically with systolic blood pressure
[SBP] greater than 200 mm Hg and/or diastolic blood
pressure [DBP] greater than 120 mm Hg) associated
with the presence or impendence of target-organ
dysfunction

5. •HYPERTENSIVE URGENCIES are characterized by a
similar acute elevation in blood pressure but are not
associated with target-organ dysfunction.
•ACCELERATED HYPERTENSION is associated with group
3 Keith-Wagener-Barker retinopathy, which is
characterized by the presence of exudate and
hemorrhages.
•MALIGNANT HYPERTENSION is associated with group
4 Keith-Wagener-Barker retinopathy, which is
characterized by the presence of papilledema,
heralding neurologic impairment from an elevated
intracranial pressure (ICP)
CLASSIFICATION

6. CLASSIFICATION OF HTN (ESH/ESC
GUIDELINES.)
•Normal BP <130 and <85
•High-normal BP 130–139 and/or 85–89
•Grade 1 hypertension 140–159 and/or 90–99
•Grade 2 hypertension 160-179 and/or 100-109
•Grade 3 systolic ≥180mmhg and /or ≥110
Average of two or more readings taken at each of
two or more visits.

7. EPIDEMIOLOGY
•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.
•In the US: More than 60 million Americans, about 25-
30% of the population, have hypertension. Of these
individuals, 70% have mild disease, 20% moderate, and
10% severe hypertension (diastolic BP [DBP] >110 mm
Hg). Approximately 1-2% develop a hypertensive
emergency with end-organ damage.

8. EPIDEMIOLOGY ctd.
•Mortality/Morbidity: Morbidity and mortality
depend on the extent of end-organ damage on
presentation and the degree to which BP is
controlled subsequently. BP control may prevent
progression to end-organ impairment.
•Race: African Americans have a higher incidence of
hypertensive emergencies than Caucasians.

9. ETIOLOGY/ RISK FACTORS
•higher grades of obesity,
•presence of hypertensive or coronary heart disease,
•collagen vascular disease (e.g., systemic lupus
erythematosus)
•higher number of antihypertensive medications,
•nonadherence to antihypertensive medications
•intoxications (e.g., cocaine, amphetamines,
phencyclidine hydrochloride, stimulant diet
supplements),
•pheochromocytoma, (increased catecholamines)
•pregnancy,

10. PATHOPHYSIOLOGY
•Recent investigations into the pathophysiology of
hypertensive crises have failed to clarify the exact
mechanisms involved.
•Normally, autoregulatory changes in vascular resistance
through the autocrine/paracrine system occur in response
to the production of endogenous vasoconstrictors (e.g.,
catecholamines) or endogenous vasodilators (e.g., nitric
oxide)

11. PATHOPHYSIOLOGY
•During a hypertensive emergency, acute elevation in blood
pressure overwhelms the autoregulation of the endothelial
control of vascular tone, leading to mechanical vascular
wall stress with subsequent endothelial damage and
vascular permeability. This permeability leads to the
leakage of plasma into the vascular wall, resulting in
activation of platelets, initiation of the coagulation
cascade, deposition of fibrin, and recruitment of
inflammatory mediators.
•This inappropriate vasoconstriction and microvascular
thrombosis leads to hypoperfusion and end-organ
ischemia with subsequent target-organ dysfunction.

12. PATHOPHYSIOLOGY CONT’D
NORMAL
AUTOREGULATION
RISE IN BP
ARTERIAL AND
ARTERIOLAR
CONSTRICTION
Normal flow.
RISE IN BP
FAILURE OF
VASOCONSTRICTION
ENDOTHELIAL DAMAGE
(due to shear stress on the
wall)
AUTOREGULATION
FAILURE

13. PATHOPHYSIOLOGY CONT’D
• Acute rise in BP Failure of vasoconstriction Endothelial
by autoregulatio damage
FIBRINOID Activates coagn and Depsn. Of proteins/
NECROSIS inflammation fibrinogen in vessel
wall

15. CLINICAL FEATURES
The CNS is affected as the elevated BP overwhelms the
normal cerebral autoregulation. Under normal
circumstances, with an increase in BP, cerebral arterioles
vasoconstrict and cerebral blood flow (CBF) remains
constant. During a hypertensive emergency, the elevated
BP overwhelms arteriolar control over vasoconstriction and
autoregulation of CBF. This results in transudate leak across
capillaries and continued arteriolar damage. Subsequent
fibrinoid necrosis causes normal autoregulatory
mechanisms to fail, leading to several neurologic target
organ damage.

16. CLINICAL FEATURES
Neurologic end-organ damage due to uncontrolled BP
may include
•hypertensive encephalopathy: Severe BP elevation
associated with lethargy, seizures, visual disturbances,
altered level of consciousness in the absence of other
explanations.
•cerebral vascular accident(Ischaemic or hemorrhagic)
Confusion, disorientation or memory loss, Numbness,
weakness in an arm, leg or the face, especially on one
side, Abnormal or slurred speech, Loss of balance,
coordination or the ability to walk

17. CLINICAL FEATURES
•CARDIOVASCULAR SYSTEM
•The cardiovascular system is affected as increased
cardiac workload leads to cardiac dysfunction; this
can be accompanied by pulmonary edema, or
myocardial infarction, acute left ventricular failure.

18. CLINICAL FEATURES
Cardiovascular end-organ damage may include
•myocardial ischemia/infarction, Chest pain (early
morning hours), altered mental status Anxiety,
Lightheadedness, with or without syncope, Nausea +-
vomiting, Profuse sweating, tachycardia, fever, RR
•acute left ventricular dysfunction, dyspnea, orthopnea,
PND, edema, fatigue

19. CLINICAL FEATURES
• acute pulmonary edema, sudden onset of extreme
breathlessness, anxiety, feelings of drowning, profuse
sweating
• aortic dissection. chest pain radiating to the back,
unequal palpable pulses accompanied by a blood pressure
difference of 15 mm Hg or greater between both arms.

20. CLINICAL FEATURES
•RENAL SYSTEM
•The renal system is impaired when high BP leads to
arteriosclerosis, fibrinoid necrosis, and an overall
impairment of renal protective autoregulation
mechanisms. This may manifest as worsening renal
function, hematuria, red blood cell (RBC) cast
formation, and/or proteinuria.

21. CLINICAL FEATURES
renal and other systems:
• acute renal failure/insufficiency, Lethargy, Weakness,
Edema, anorexia,
• retinopathy,-Malignant hypertension: Severe BP
elevation (commonly >200/120 mm Hg) associated with
advanced bilateral retinopathy (papilledema).
• microangiopathic hemolytic anemia (Hypertensive
thrombotic microangiopathy) Severe BP elevation
associated with widespread hemolytic anaemia and
thrombocytopenia in the absence of other causes and
improvement with BP-lowering therapy.
• eclampsia

22. HISTORY
circumstances surrounding hypertension &
etiology :
-Medications: esp. hypertensive drugs/their
compliance, illicit drugs, concomitant drug use, etc
-Duration of hypertension if known
-Duration of current symptoms
-Date of LMP
-Other medical problems: prior hypertension,
thyrotoxicosis, renal, dm

23. HISTORY
 symptomatic approach:
-CNS: headaches, confusion and mental status
changes.
eye: blurred vision,
-CVS: symptoms of CHF,
-Renal: hematuria, oliguria, symptoms of renal
failure
- chest: dyspnea, feeling of doom, chest pain

24. PHYSICAL EXAMINATION
•General examination
•Vital signs RR, HR, O2 Saturation, bp
-CNS: focal neuro deficits, seizures, coma, GCS
- Eye - Fundoscopy: papilledema, hemorrhages,
exudates, visual acuity
-CVS: peripheral edema, extra heart sounds, signs of
heart failure
- Chest: lung auscultaion for crackles,

25. INVESTIGATIONS
General
•Spo2
•FBC
•Urinalysis: hematuria, proteinuria, RBCs.
•E/U/Cr
•Serum glucose
•Liver function tests

26. INVESTIGATIONS
Specific:
•Retina: Fundoscopy
•CVS: Chest radiograph, Chest CT, aortic angiogram,
ECG, cardiac enzymes
•CNS: Head CT, Cerebral angiography, Magnetic
Resonance Imaging (MRI), Magnetic Resonance
Angiogram (MRA)
•Pregnancy: urine or serum PT,
•MI -- cardiac troponin, lipid profile

27. INVESTIGATIONS
•PE: pulse oximetry, arterial blood gases, chest
radiograph, ECG
•Hypertensive thrombotic microangiopathy: blood
film analysis, markers of hemolysis like
unconjugated bilirubin.
•Abdominal scan for masses

28. TREATMENT
•TREATMENT GOALS: Treatment goals for hypertensive
crises depend on classification (e.g., emergency vs.
urgency) and presenting condition.
•Some presenting conditions have unique treatment goals,
including time to goal, additional treatment parameters,
and treatment modalities, to achieve set goals. These
conditions are considered exceptions to the general
treatment principles of hypertensive crisis and in most
recent guidelines termed “compelling conditions”.

29. •Hypertensive urgency often requires initiating,
reinitiating, modifying, or titrating ORAL THERAPY
and usually does not require ICU or hospital
admission.
•The treatment target for hypertensive urgency is a
gradual blood pressure reduction over 24–48 hours.
The more common error with the treatment of
hypertensive urgency is overaggressive correction
because no benefit, but potential harm, may be
associated with too rapid a decrease in blood
pressure
TX OF HTNSIVE URGENCY

30. •In the treatment of hypertensive emergency,
patients who would fall into the general treatment
goals should be identified, as should those who
would have exceptions to the general treatment
goals (compelling conditions).
• For patients without exceptions, the general goal of
therapy is to reduce the mean arterial pressure
(MAP = DBP + 1/3 PP) by 25% over the first hour of
therapy.
TX OF HTNSIVE EMERGENCY

31. TX OF HTNSIVE EMERGENCY
•Greater reductions (by more than 25%) have been
associated with the induction of cerebral ischemia.
In addition, if neurologic deterioration is noted
during the initial 25% MAP reduction (or during
subsequent lowering), therapy should be
discontinued. After the first hour, a more gradual
blood pressure reduction is recommended

32. •For individual populations that qualify for
exceptions to the general treatment goals
(compelling conditions), their treatment varies.
These include patients with
•1. aortic dissection
•2. acute iscahemic stroke
•3. acute hemorrhagic stroke
•4. Pregnancy-associated severe hypertension
(preeclampsia/eclampsia and hypertensive
emergency in the pregnant patient).

33. General Treatment Goals for
Hypertensive Emergency
Goal Time BP Target SBP DBP
First hour Reduce MAP by 25% maintain goal DBP ≥ 100 mm Hg
Hours 2–6 SBP 160 mm Hg and/or DBP 100–110 mm Hg
Hours 6–24 Maintain goal for hours 2–6 during first
24 hr
Maintain goal for hours 2–6
during first 24 hr
24–48 hr Outpatient BP goals according to the
2017 Guidelines for Management of
High Blood Pressure in Adults
Outpatient BP goals according
to the 2017 Guidelines for
Management of High Blood
Pressure in Adults

35. ACUTE AORTIC DISSECTION
•Acute Aortic Dissection. is related to shear stress (a
principle related to blood flow velocity and rate),
the treatment goal for aortic dissection is 2-fold:
blood pressure and heart rate control.
•The goal heart rate during acute management of
aortic dissection is less than 60 beats/minute
within minutes of presentation. The goal blood
pressure after achieving adequate heart rate control
is SBP less than 120 mm Hg and/or as low as
clinically tolerated (i.e., lowest blood pressure that
maintains end- organ perfusion), esmolol, SNP

36. ACUTE ISCHAEMIC STROKE
•Hypertension associated with ischemic stroke is often
considered an adaptive response to maintain cerebral
perfusion pressure (CPP) to the brain Because ischemic
strokes can be associated with increases in ICP, acute
treatment of MAP elevations is only indicated in limited
circumstances.

37. ACUTE ISCHAEMIC STROKE
•Currently, the guidelines recommend acute treatment in
three instances:
•(1) use of thrombolytic therapy,
•(2) other target-organ damage (e.g., aortic dissection,
myocardial infarction), or
•(3) “severe” elevations in blood pressure (SBP greater
than 220 mm Hg and/ or DBP greater than 120 mm Hg).

38. ACUTE ISCHAEMIC STROKE
•use of thrombolytic therapy,
•If thrombolytic therapy is warranted, the blood
pressure goal before initiating thrombolysis is less
than 185/110 mm Hg.
•After commencement, and throughout thrombolysis,
and for the next 24 hours after thrombolysis, that
goal changes slightly to a goal blood pressure less
than 180/105 mm Hg.
•This blood pressure control has been associated with
fewer intracerebral hemorrhages (ICHs) associated
with intravenous thrombolysis .

39. ACUTE ISCHAEMIC STROKE
•other target-organ damage and “severe”
elevations in blood pressure
•The goal is a more modest reduction of 15% (10%–
20%) in the MAP over 24 hours, allowing for
maintenance of CPP while avoiding the
complications of cerebral edema exacerbation and
hemorrhagic transformation.
•nicardipine and labetalol are appropriate first-line
agents.

40. ACUTE HEMORRHAGIC STROKE
•Similar to ischemic stroke, acute hemorrhagic
strokes can increase ICP, potentially compromising
CPP. Because of this risk, acute hypertension in this
setting may again be adaptive.
•In hyperacute (less than 3 hours) and Acute (less
than 4.5 hours) treatment of patients with ICH but
without ICP elevations, a target SBP goal of less
than 160 mm Hg over the first few hours is
relatively safe and may confer benefit regarding
functional recovery, if achieved.

41. •In addition, in patients with “severe” elevations in
blood pressure (e.g., SBP greater than 220 mm Hg),
patients with large hematomas, or those with
known elevations in ICP, and more than 6hrs, it is
unclear whether aggressive treatment targets are
safe because these patients were excluded from all
recent studies on aggressive, rapid blood pressure
lowering.
•In this patient subgroup with ICH (those excluded
from recent studies), the guidelines recommend a
more modest reduction to SBP less than 180 mm Hg
or MAP less than 130 mm Hg over the first 24 hours
ACUTE HEMORRHAGIC STROKE

42. TREATMENT OF HYPERTENSIVE
EMERGENCY
•Given the diverse presentations of hypertensive
emergency, it is challenging to label one medication as
the drug of choice as type of medication often depends
on a risk- benefit analysis of each agent considering the
•(1) affected target organ on presentation,
•(2) pharmacokinetics (PK) and pharmacodynamics (PD)
of the medications available, and
•(3) hemodynamic, adverse effect, and BPV profile of the
medication options.

43. TREATMENT OF HYPERTENSIVE
EMERGENCY
•Preferable traits of medications used to treat
hypertensive emergencies include
•intravenous administration,
•ability to be titrated to desired effect allowing for a
“smooth” reduction of blood pressure,
•short duration of activity, and
•minimal adverse effect profile.
•cost

44. DRUGS
•Sodium nitroprusside: is a potent arterial and
venous vasodilator. Two effects of concern with
sodium nitroprusside are “coronary steal” and
increases in ICP.
•Sodium nitroprusside may result in preferential
vasodilation due to coronary steal, leading to
reduced coronary perfusion pressure and thus
should be avoided in patients presenting with
myocardial infarction as their target-organ damage.
•potential accumulation of toxic metabolites like
cyanide molecule is a concern.

45. DRUGS
•The CCBs: the dihydropyridine intravenous agents
nicardipine and clevidipine and the non-
dihydropyridine agents diltiazem and verapamil.
•A. The dihydropyridine agents are peripherally
selective L-type CCBs that exert their antihypertensive
effects by inhibiting calcium influx through calcium
channels along the vascular smooth muscle. This
inhibition prevents smooth muscle contractility, leading
to vasodilation and reduction in systemic blood
pressure.

46. DRUGS
•B. non-dihydropyridine agents have preferential
effects in the heart in the order of the conduction
systems and contractile myocardial cells in addition
to their peripheral effects.
•These agents do not affect ICP and may be
considered preferential for patients with acute
stroke as the target-organ damage on presentation
of hypertensive emergency

47. DRUGS
•Nicardipine is metabolized in the liver so there may
be more pronounced adverse effect in patients
being treated for hypertensive emergency who have
chronic liver disease
•CCBs are cheaper than sodium nitroprusside.

48. DRUGS
Nitroglycerin is primarily a venous vasodilator and
can reduce relative venous return and subsequently
myocardial preload and there is no “coronary steal”
effect but It causes tachyphylaxis (over the first 24-
48hrs) requiring frequent escalations in dosing to
maintain hemodynamic effects.

49. DRUGS
•β-Antagonists (i.e., β-blockers) e.g. esmolol and
metoprolol
•Esmolol has rapid onset, organ-independent
metabolism and short duration of action.
•Metoprolol has β-selectivity similar to esmolol, but
given its slower onset, intravenous push
administration, and longer duration of activity,
metoprolol has less titratability and can lead to
extended, overaggressive, unintentional correction,
placing patients at risk of induced ischemic
complications.

50. DRUGS
•α1- and β-antagonist e.g. labetalol.
•Labetalol exerts its effects more through the β-
antagonist properties. Often given by continuous
infusion, and intravenous bolus administration but
preferably as a continuous infusion.

51. DRUGS
Hydralazine is a peripheral arterial vasodilator best
known in this clinical setting for its safety in
pregnancy

52. DRUGS.
•Enalaprilat is an intravenous angiotensin-
converting enzyme (ACE) inhibitor.
•its usefulness in hypertensive emergency is minimal
and must be avoided in pregnant patients, its use
may be associated with deterioration of renal
function, especially in states of poor renal perfusion
that potentially occur in hypertensive emergency,
warranting avoidance or great caution with renal
impairment.

53. DRUGS.
•α1 and α2 receptor antagonist e.g. phentolamine
leads to direct vasodilation.
•In general, phentolamine is reserved for
catecholamine-excess presentations of hypertensive
emergency (e.g., cocaine induced,
pheochromocytoma, amphetamine induced).

54. DRUGS
•fenoldopam
•A peripheral dopamine – 1 receptor blocker
•Exerts its antihypertensive effect by combined
natriuretic and vasodilatory effect (esp. intrarenal
arteries)
•Agent of choice in hypertensive emergencies
associated with renal dysfuntion
•Adv effect hypotension, hypokalemia

57. PROGNOSIS:
The 1-year mortality incidence of hypertensive
emergencies is more than 79%, and the median
survival is 10.4 months if these persons are not
treated with antihypertensive drug therapy.
The prognosis has improved dramatically over the
period of a few decades and with
optimal treatment the five-year survival rate is
>90%.

58. PREVENTION
•Regular BP check
•Adherence to prescribed medication
•Avoidance of polypharmacy
•Avoid excess salt intake
•Exercise and weight loss
•Regular medical check up for known hypertensives

59. SUMMARY

60. CONCLUSION
•Hypertensive emergencies are serious medical
conditions that require prompt and accurate
diagnosis and treatment.
•IV Clevidipine is the new drug approved for
hypertensive emergencies however , Iv nicardipine
and iv labetalol are also preferred for most
emergency situations.

61. RECOMMENDATION
•Routine fundoscopy

62. REFERENCES
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National Committee on prevention, detection, evaluation, and
treatment of high blood pressure.
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hypertension-MOD: a modern definition for an old but still dangerous
emergency. J Hum Hypertens. 2016 Aug. 30 (8):463-6. [Medline].
• Figueroa SA, Zhao W, Aiyagari V. Emergency and critical care
management of acute ischaemic stroke. CNS Drugs 2015;29:17-28.
• Scott T. Benken, Pharm.D., BCPS-AQ, Cardiology Critical Care Self-
Assessment Program (CCSAP), 2018 Book 1 medical issues in the ICU
• Vol. 75, No. 6 , 2020 International Society of Hypertension Global
Hypertension practice guidelines.
• Medscape: management of hypertensive emergencies

63. • Thank you