Jacda

1. presenter : dr.bouni
moderator: Dr.samir abdi MD (associate prof HU)

2. Outline of Presentation
oIntroduction
oEpidemiology
oEtiology
oClassification
oClinical Picture
oDiagnosis
oManagement

3. is a life threathing condition
that caused by acute increase of blood pressure usually ≥180/120
mmHg leading end-organ damage.
In the Emergency Department appropriate management of
“Hypertensive Emergencies” is crucial for preventing death or
irreversible disability.
most patients with significantly elevated blood pressure (systolic pressure
≥180 mmHg and/or diastolic pressure ≥120 mmHg) have no acute, end-
organ injury (so called severe asymptomatic hypertension)

4. oDefinition: These are acute, severe elevations in blood pressure that
may or may not be associated with end organ damage or dysfunction.
oBP Values:
oSBP: >180 mmHg
oDBP: >120 mmHg
oThese can be one of two subsets:
oHypertensive Urgency: Severe elevations in Blood pressure without
any evidence of end-organ damage
oHypertensive Emergency: Severe elevations in Blood pressure with
any evidence of end-organ damage

5. The worldwide prevalence of
hypertension is around 31%, exceeding
1.3 billion people Of these, 1% to 2% will
suffer a hypertensive crisis in their
lifetime.
Men may be more likely than
women to suffer a hypertensive
emergency.
Hypertensive emergency is more
common in older patients and in
black people.

6. oThere is no single predisposing factor identified to be
associated with these conditions.
oThe most common ones are:
oPoorly controlled HTN
oReno-vascular disease
oCerebro-Vascular Disease
oLow Socioeconomic status
oSubstance or alcohol abuse
oCigarette smoking
oOral Contraceptive Use

8. o The underlying mechanism is still not
fully understood.
o The transition from mild
hypertension or normo-tension to
a hypertensive crisis usually is
precipitated by an event that leads to
an abrupt increase in blood pressure.
o These may include:
oCessation of hypertensive
medications with potential rebound
effects
oconsumption of illicit drugs
osevere pain
oseveral clinical syndromes
oIn most hypertensive crises, the initial
rise in blood pressure is secondary to
increased systemic vascular resistance.
oThe rise in systemic vascular resistance
is believed to be caused by
humoral vasoconstrictors
o With the increase in blood pressure,
mechanical stress on the arteriolar wall
leads to endothelial damage and fibrinous
necrosis of the arterioles, this in turn leads
to loss of auto-regulatory
mechanisms, ischemia, and acute end-
organ damage, which prompts further
release of vasoconstrictors, thereby
initiating a vicious circle

9. pathophysiology
oIt is also linked to 4 distinct mechanisms:
oVascular damage:
oDue to mechanical stress and vascular damage.
oRAAS Activation:
oCausing vasoconstriction and Expression of inflammatory cytokines
oOxidative stress:
oDue to increase in production of reactive oxygen species
oEndothelial Dysfunction:
oDue to excessive vasoconstriction and coagulation cascade activation

10. Clinical Presentation
Hypertensive Urgency:
oMostly Completely
Asymptomatic
oCan Present with:
• Headaches
• Nausea
• Epistaxis
• Severe Anxiety
oSigns
• Elevated BP
Hypertensive Emergency:
oDepends on the End-Organ Affected:
• Chest Pain
• Acute Myocardial Infraction
• Myocardial IschemiaAngina
• Back Pain
• Thoracic Aortic Dissection
• Dyspnea
• Acute Pulmonary Edema
• Altered Mentation of FND
• Hypertensive Encephalopathy
• Cerebrovascular Event

12. aproach of History
Taking
• Current Sx like headache, blurred
vision, chest pain, back pain,
dyspnea, etc.
• Any associated symptom
• Co-morbid conditions
• Duration of HTN and Medication
Control, Compliance, Abrupt
cessation
• Any Illicit Drug use, Smoking, or
Alcohol consumption
• Any Other medication ex. MOA, SSRI
• Any recent head trauma
• Full and Thorough examination is needed
• Vital Signs Specially BP (both setting and
standing), if peripheral pulses are
reduced take lower limb BP as well
• General: signs of dehydration (natriuresis
occurs in response to rapid BP rise)
• CVS: murmurs (aortic insufficiency or
ischemic MR). S3 gallop, peripheral
edema, raised JVP
• Respiratory: Basal Crackles, Tachypnea
• Neuro: Altered mental status, FND
• Funduscopic: Cotton wool exudates,
Hemorrhage, Papilledema
PHYSICAL EXAM

13. Workup of patients
Work-up should be done to check for
damaged organs and includes:
• Complete blood count
• Urinalysis (Proteinu
• ria and Hematuria)
• Creatinine and BUN
• Cardiac Bio-markers
• Urine Toxicology
• RBS
• Liver Function Test
• Serum Electrolytes
• ECG
• Echocardiogram
• Chest Radiography
• Non-Contrast Head
CT
• Contrast Induced
Chest CT or
Transesophageal
Echo

14. Management
o1st ask yourself these 3 question:
ois there any end organ damage?
oYes: Manage HTN Emergency
oNo: Manage HTN Urgency
oHow Quickly should BP be
reduced?
oWhat is the BP Target during
that time period?
oHow should that Goal be
Achieved?
 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.
 This often results in a target blood pressure
of <180/<120 mmHg for the first hour and
<160/<110 mmHg for the next 23 hours (but
rarely <130/<80 mmHg.

15. Blood Pressure Targets
The ESC and AHA guidelines do
not mention any specific target
for SBP.
A post hoc analysis of the
REALITY-AHF study reported
that patients in the ED whose
SBP was reduced by >25% may
have had a higher mortality rate;
however, this study did not report
any baseline characteristics of the
BP groups that could explain the
difference in mortality and had
several limitations to consider.
Therefore, it is reasonable to target
lowering SBP by 10% to 25% for
patients with hypertension and
ADHF

16. No End Organ Damage - Urgency
oThe cut-off of lowering BP time is
controversial and decision should be taken
considering individual risk factors for
patients.
oHowever, Generally: BP should be reduced
gradually over the period of hours to days,
to avoid causing ischemic injury and tissue
hypo-perfusion to vital organs.
oShort-Term Goal: lower BP to
<160<100mmHg in first few hours provided
that MAP shouldn’t be lowered more then
25% over first 24 hours
oPreviously the preferred agent
was Sublingual or Oral Nefidipine
oThat is no longer recommended
due to propensity to cause Severe
Rebound Hypotension and Organ
Ischemia.
oCurrent preferred agents Include:
oCaptopril
oClonidine
oLabetalol

17. In the case of not requiring rapid BP reduction, BP should be
reduced over the period of days with specific considerations
• Pre-Exisitng Hypertension (Options are:)
• Re-administer previous medication
• Increase the dose of previous medication or add another agent
• Add diuretic and adjust sodium intake for patient
• Un-Treated Hypertension:
• Gradually reduce BP using one of previously mentioned agents.
• Evaluate patient's HTN and start new individualized Anti-HTN
treatment regimen, considering risk factors, duration of
treatment and adverse effects

18. End organ damage - emergency
o Overall Approach: choice of drug,
BP goal, and outcome varies based
on specific emergency faced
o Generally: MAP should be lowered
10-20% in the first hour and
subsequent 5-15% over next 23
hours.
o Time Frame: <180120mmHg over
first hour
o <160110mmHg over
next 23 hours
oExceptions to that rule are certain conditions:
1. Acute Ischemic Stroke: BP isn’t lowered unless
>185110mmHg if ptn is candidate for reperfusion and
>220120mmHg if ptn are not candidates for
reperfusion
2. Acute Aortic Dissection: SBP should be rapidly
lowered to target of 100-120mmHg within 20
minutes to reduce the shearing force of the aorta
3. Intracerebral Hemorrhage: goal of HTN
management in these patient’s is variable and
individualized case dependant
oChoice of medication is dependent on the type of emergency encountered.
oDuring the first 8-24 hours, BP control should be obtained via Parenteral Drugs.
oAfter that period patients should be switched to oral agents with tapering of parenteral agents

19. End organ damage - emergency
oManagement Specific Emergencies should be undertaken as
well as BP Control
oEx:
otPa for Ischemic Stroke Patients
oRevascularization for Acute MI patients
oDialysis for ESRD patients
oManagement Protocol for Acute Heart Failure
oSurgery for Acute Aortic Dissection

20. Acute Ischemic Stroke
For patients receiving
thrombolytics or
mechanicalthrombectomy,
AHA/ASA and ESO
guidelines both recommend
lowering
BP to <185/110 mm Hg prior to
the intervention and
maintaining BP <180/105 mm
Hg for 24 hours post
intervention.
if patients are hypertensive
>220/120 mm Hg, both AHA/ASA
and ESO guidelines state that
lowering BP no more
than 15% is reasonable and likely to be
safe, with
no evidence to suggest that doing so
improves or
worsens outcomes.

21. • RESULTS
• The primary outcome occurred in 855 of 1607 participants (53.2%) in the low-dose group
• and in 817 of 1599 participants (51.1%) in the standard-dose group (odds ratio, 1.09; 95%
• confidence interval [CI], 0.95 to 1.25; the upper boundary exceeded the noninferiority margin
• of 1.14; P = 0.51 for noninferiority). Low-dose alteplase was noninferior in the ordinal
• analysis of modified Rankin scale scores (unadjusted common odds ratio, 1.00; 95% CI,
• 0.89 to 1.13; P = 0.04 for noninferiority). Major symptomatic intracerebral hemorrhage occurred
• in 1.0% of the participants in the low-dose group and in 2.1% of the participants in
• the standard-dose group (P = 0.01); fatal events occurred within 7 days in 0.5% and 1.5%,
• respectively (P = 0.01). Mortality at 90 days did not differ significantly between the two
• groups (8.5% and 10.3%, respectively; P = 0.07).

22. Acute Coronary Syndromes
ACS includes STEMI, NSTEMI,
and unstable angina.
ESC guidelines specify a
normotensive target for NSTEMI
patients, while AHA guidelines
do not comment on any target
BP.
Acute hypertension in patients
with ACS may signify good
cardiac function in response to
significant stress, and is associated
with improved outcomes.
 AHA and ESC STEMI
management guidelines state that
SBP >180 mm Hg and DBP >110
mm Hg are
relativecontraindications to
fibrinolytic therapy,

23. Intracerebral Hemorrhage
Blood Pressure There is debate about how
much BP should be lowered to optimize
outcomes. Both the AHA/ASA and ESO
guidelines recommend immediately lowering
SBP to <140 mm Hg when ICH is recognized,
and maintaining SBP between 130 and 150 mm
Hg, but not <130 mm Hg.(INTERACT-2 and
ATACH-2 trials )
Lowering SBP when ≥180 mm
Hg clearly improves patient
outcomes, potentially reaching a
peak benefit when lowered <140
mm Hg; however, other variables
such as SBP variability and
relative SBP reduction are
important to be cognizant of
when considering BP goals.
 The pooled analysis of ATACH-
2 and INTERACT-2 showed
statistically significant improved
functional recovery when SBP
was reduced 40 to 59 mmHg
below the baseline SBP.

24. Subarachnoid Hemorrhage
Elevated BP is a known risk
factor for re bleeding;
however, there are no good
data to support the benefit of
lowering BP in the acute
phase of SAH.
• AHA/ASA guidelines
recommend lowering SBP to
<160 mm Hg; ESO guidelines
recommend lowering SBP
<180 mm Hg; and the
Neurocritical Care Society
guidelines recommend
treating only extreme
hypertension (MAP >110 mm
Hg).

25. Aortic Dissection
the 2022 ACC/AHA guidelines
recommend reducing the patient’s
heart rate to 60 to 80 beats/min and
then lowering SBP to <120 mm Hg,
also recommends using an IV beta
blocker before lowering the patient’s
BP to prevent any possible reflex
tachycardia
ESC guidelines cite a SBP goal of
<120 mm Hg, with no specific heart
rate

26. Hypertensive Encephalopathy
Hypertensiveencephalopathy is
mostcommonly seen with BP >
220/120 mm Hg.
There are no RCTs to suggest a
specific goal inBp reduction or
which antihypertensive agent to
use.
• The International Society of
Hypertension guidelines recommend
immediately reducing MAP by 20% to
25% using nicardipine or labetalol as
first-line agents.

27. Severe Pre-Eclampsia and Eclampsia
ESC guidelines recommend hospital admission when patients
have a single BP reading ≥170/110 mm Hg;
ACOG defines this as SBP >160 mm Hg or DBP >110 mm Hg,
confirmed by a repeat BP 15 minutes later; or 2 BP readings
≥140/90 mm Hg (and ≤160/110 mm Hg) 4 hours apart, with
thrombocytopenia, impaired liver function, renal insufficiency,
pulmonary edema, new-onset headache unresponsive to
medication

28. Acute Renal Failure
 There is no consensus as to what
degree of acute kidney injury constitutes
acute renal failure, nor whether there is
benefit to rapid BP management.
Reducing SBP or MAP by a
maximum of 25% might be a
reasonable option, if hypertensive
emergency is the suspected cause
of the acute renal failure

33. 1. Observe patient for few hours at
hospital to make Ascertain BP
Stably improving and that patients
remains Asymptomatic
2. Send Home with close monitoring
for one week explaining signs of
end organ damage
3. Over next weeks to months
frequent follow up with dose
adjustment of antihypertensive
drugs should be commenced to
achieve desired pressure goals for
individual patients
1. Since Secondary causes are more
common in HTN emergencies,
patients should be evaluated and
treated for secondary causes if
present
2. Ensure high quality out-patient
follow up and for presenting
problems (ex. Dialysis for patients
with ESRD)
3. Recurrence and 2nd admission rate is
high due to inadequate follow up

34. Prognosis
Without therapy, the prognosis of hypertensive emergencies is poor, with
1-year survival rates of 10% to 20%. However, current antihypertensive
therapy has greatly improved survival, with 5-year survival rates around
70% in patients who receive appropriate treatment.
The presence of acute kidney injury upon diagnosis of hypertensive
emergency increases the mortality rate.

35. •harison principle 2021 edition
•ESC guideline
•ACOG guideline
•uptodate 20th ed