The document discusses the management of hypertensive emergencies, emphasizing the need for immediate blood pressure reduction and the use of specific intravenous medications. It outlines the epidemiology, causes, and clinical guidance for effective treatment, while highlighting the lack of randomized trials to establish definitive management strategies. Future research directions and the potential role of novel therapeutic agents are also mentioned, alongside the critical importance of public awareness regarding hypertension.

1. Management of
Hypertension Emergencies
Dr. Nagula Praveen
MD, DM (Cardiology)
Associate Professor
Osmania Medical College, Hyderabad

2. Agenda
 Introduction
 Epidemiology
 Confirm “true” severe hypertension
 Management
 Guidelines
 Future
 Is it time to retire the diagnosis Hypertensive emergency
 Take home message

3. Introduction
 Pharmacological approach - first proposed by Gifford (1959).1
 Seen in all types of hypertension patients [chronic (mostly), short-duration and
newly discovered].
 Risk of complications more common in the latter.
 Poor prognosis
 Evidence of impending or progressive end-organ damage.
 While acute organ damage is the sine qua non in many scenarios there is a
“chicken and egg” conundrum.
 Older and less specific terminology - malignant hypertension, accelerated
hypertension should no longer be used.
Gifford RW. Treatment of Hypertensive Emergencies, including the use of Sodium Nitroprusside. Mayo Clin Proc 1959;34(16):387.

4. Epidemiology
 Hypertension affects  1.3 billion people globally (only 20% have adequate
control).1
 Acute severe HTN accounts for 0.6 -2% of ER visits.2
 However, 1/3 of patients have HTN emergencies.
 The mean age of presentation is 55 years vs 62 years.3
 Seen in men more than in women (52.5% vs 47.5%).
 Complications are more common in females.
 Black patients account for the highest proportion of admissions.4
1. World Health Organization. Hypertension. 2023. https://www.who.int/news-room/fact-sheets/detail/hypertension.
2. Janke AT et al. Trends in the incidence of hypertensive emergencies in US emergency departments from 2006 to 2013. J Am Heart Assoc 2016;5:e004511.
3. Francis-Morel G et al. Gender disparities in hypertensive emergency admissions: a national retrospective cohort study. Cureus 2023;15:e40287.
4. Waldron FA et al. Prevalence and risk factors for hypertensive crisis in a predominantly African American inner-city community. Blood Press 2019;28:114-23.

5. Common causes
 Inhospital mortality remained quite high among all patients.
Siddiqi TJ, et al doi: 10.1161/JAHA.122.029355.
0
5
10
15
20
25
30 28.1
24.1
14.6
10.8
8
6.9 6.1
1.8
Percentage

6. Rossi et al. Management of hypertensive emergencies: a practical approach. Blood Pressure, 30(4), 208–219.

7. Strandgaard S. Cerebral blood flow in hypertension. Acta Med Scand Suppl 1983;678:11-25.
CBF = CPP/CVR
CPP = MAP – ICP
MAP = DP + 1/3 (PP)

8. Confirm true “severe”
hypertension

9.  Proper measurement of blood pressure.
 Appropriate sized and positioned cuff.
 Sitting and relaxed
 Adequate analgesia.
 In aortic dissection - invasive monitoring
 Appropriately sized cuffs – titration of
drugs
Unger T, Borghi C, Charchar F, et al. 2020 International Society of Hypertension Global Hypertension Practice Guidelines.
Hypertension 2020;75:1334-57. doi:10.1161/HYPERTENSIONAHA.120.15026

10. Clinical examination
 A focused neurological exam is precious.
 Headache (in nearly 25% of patients, alone does not indicate HTN emergency).
 Focal neurological deficits point to ICH/Stroke
 Visual symptoms, visual acuity
 Fundoscopic exam – severity of hypertensive retinopathy.
 Arteriole tortuosity, AV nipping - mild retinopathy, chronic findings.
 New flame haemorrhages, cotton-wool spots, or microaneurysms - acute
injury, moderate or grade 3 retinopathy.
 Papilledema - severe retinopathy, immediate lowering of blood pressure.
 Next common - cardiovascular symptoms.
Heath I. Hypertensive urgency- Is this a useful diagnosis? JAMA Intern Med 2016;176:988-9. doi:10.1001/jamainternmed.2016.1498.
Downie LE et al. Hypertensive retinopathy: comparing the Keith-Wagener-Barker to a simplified classification. J Hypertens

11. Biomarkers
 Brain natriuretic peptide (BNP) or NT-BNP
 High sensitivity troponin
 Rules out myocardial damage, important prognostic information
 Lactate dehydrogenase (LDH) - reflects thrombotic microangiopathy,
 Value >190U/L - hypertensive emergency.
 CRP
 Plasminogen activator inhibitor-1,
 D-Dimer,
 Urinary albumin creatinine ratios,
 Their clinical utility is not established.
Talle MA et al. The role of cardiac biomarkers in the diagnosis of hypertensive emergency. Diagnostics (Basel) 2023;13:1605.
El Maraghi S et al. B-type natriuretic peptide in hypertensive crises: Diagnostic use in hypertensive urgencies and emergencies. Egypt J Crit Care Med 2013;1:61-7.
Wang TJ et al. Multiple biomarkers and the risk of incident hypertension. Hypertension 2007;49:432-8.

12. Imaging
 MRI – greater sensitivity for vasogenic edema
 Parieto-occipital pattern.
 Radiological classification of PRES
 hyperintense lesions in T2- T2-weighted or
fluid-attenuated inversion recovery (FLAIR)
sequences.
 microhemorrhages (2/3rd
of HE patients)
 In uncertainty - encephalopathy vs stroke.
Fischer M, doi:10.1007/s00415-016-8377-
8

13. Management
How
much to
reduce
MAP?
What is
the organ
at
damage?
Three
prongs
Drug of
Choice

14. http://dx.doi.org/10.1136/bmj 2023 077205
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15. Hemorrhagic Stroke and
Sub Arachnoid Hemorrhage

16. Hemorrhagic stroke
 This category has the best evidence for BP management.
Goal SBP
<130 mm Hg
SBP - 140 mm Hg Higher targets
(180mm Hg) if initial
SBP > 220 mm Hg.
Risk of
hypoperfusion injury
with intensive BP
reduction
Drugs of choice –
Short-acting CCBs
Clevidipine,
Nicardipine (easily
available)
Whelton PK et al. Circulation 2018;138:e426-83.
van den Born BH et al. doi:10.1093/ehjcvp/pvy032

17. Aneurysmal SAH
 Severe elevation in BP is less common.
 Target SBP <160 mm Hg (based on low-quality data).
 DOC- Nicardipine.
Hoh BL, Ko NU,
doi:10.1161/STR.0000000000000436

18. Ischemic stroke Ischemic stroke
No Reperfusion
therapy
BP <220/120
mm Hg
Not needed
BP > 220/120
mm Hg
Indicated
Nicardipine
Intermittent IV
Labetalol
Reperfusion
therapy
Target SBP
<180
DBP < 110
Maintain for 24
hours after
reperfusion
therapy
Liu L CATIS-2 Investigators doi:10.1136/bmj-2023-
076448
Powers WJ doi:10.1161/STR.0000000000000158
Mistry EA. doi:10.1001/jama.2023.14330

19. Cardiac Emergencies
Acute MI
Cardiogenic pulmonary edema (BP> 180/110mm Hg)

20.  Pulmonary edema is more common than MI (type 2 MI)
 Diagnosis - a rise and fall in cardiac troponin > 99th
percentile reference range.
 Indeterminant elevations - not indicative of a type 2 MI, do not indicate a
hypertensive emergency.
 Chronic elevations common in patients with acute severe HTN - do not
require immediate BP lowering.
Increased afterload
Increased
Myocardial demand
and strain
Worsening
Ischemia
Increased
hydrostatic pressure
Pulmonary edema
Type II MI
Thygesen K, doi:10.1161/CIR.0000000000000617

21. Mild to moderate MAP
reduction , relief of
symptoms (15-25%)
• TARGET
Nitroglycerin
relieve chest pain and MAP
• DRUG OF CHOICE
• Preload reduction
• Venodilation
• Afterload reduction at high doses
• Limited data on effectiveness of higher doses
BB - ↓tachycardia and
myocardial oxygen demand
• NEXT CHOICE
Esomolol and
IV Labetalol – 2nd
line agents
Nicardipine or
Clevidipine - if
BB are C/I
Rapid relief with NTG and
loop diuretic
Levy P, doi:10.1016/j.annemergmed.2007.02.022

22. Hypertension in Pregnancy

24. Aortic disease
Aortic Dissection and Acute Aortic syndrome

25.  MAP to be reduced by >25% reduction (only category).
 Immediate risk of extension of the dissection and mortality.
 Risk of cerebral hypoperfusion – in patients with a right shift of Cerebral
autoregulatory limits.
 In 112 patients with Type B Aortic Dissection (Retrospective study) - the rate
of cerebrovascular injury rose substantially with reductions in the MAP >
25%.
Al Adas Z, doi:10.1016/j.jvs.2018.01.056

26. Target
SBP - <120 mm Hg,
HR <60/min
B blockade +
CCBs as first-line therapy
Esmolol + Nicardipine/
Clevidipine
Nitroprusside
previously 1st
line agent
Reflex tachycardia, cyanide toxicity

27. HTN Encephalopathy

28.  It is a clinical diagnosis.
 Alteration in mental status (beyond the limit of cerebral autoregulation).
 Symptoms - seizures, headache, lethargy, and visual disturbances.
 BP >220/110mm Hg to exceed autoregulatory limits.
 Lower range – young adults, no history of chronic hypertension.
 Concomitant findings - acute hypertensive retinopathy and microangiopathic
hemolytic anaemia.
 Patterns on MRI are those with PRES(posterior reversible encephalopathy
syndrome.
 Reversible with treatment.

29. Treatment
 Immediate reduction of BP to restore cerebral autoregulation.
Reduce MAP by 20-25% (1st
hour of care).
No high-quality studies
Maintain target MAP over the next 2-6 hrs Well
tolerated
If MAP falls > 25% – fluids to be given
(Pressure natriuresis)
If decreased MAP is tolerated, a gradual reduction
(BP of 160/100 mm Hg) over the next 48 hours.
Nicardipine
Ease of titration and
effective
Clevidipine
Labetalol
doi:10.1016/j.jacc.2017.11.006

30. Uncommon causes
Pheochromocytoma
Drug-induced hypertension
Little data exists for the reduction of BP
Moderate reduction of MAP 20-25% is reasonable

31. First Line – Alpha-blockers, CCBs
Phentolamine – rapid onset, alpha activity
Phenoxybenzamine – before
resection (not in acute management)
Nicardipine – in combination with phentolamine or
standalone agent
Labetalol – C/I low risk of paradoxical
hypertension
Pheochromocytoma
 Paroxysmal elevations in
BP are common.
 Classic triad (episodic
headache, diaphoresis, and
tachycardia) - less common.
 Difficult to diagnose as it is
confounded in an
emergency.
 A high index of suspicion
is needed.
Garg MK, doi:10.4103/2230-8210.86976
doi:10.1111/j.1365-2044.2005.04156.x

32. Sympathomimetic drugs
 In Amphetamine, methamphetamine, and cocaine overdose, benzodiazepines
1st choice (clinical symptoms and BP reduction).
 Phentolamine (α blocker - BP control).
 Nicardipine 2nd
choice.
 Selective B1 blockers are contraindicated.
 Labetalol ( a non-selective BB and AB) – is safe and effective.
Kulkarni S et al. doi:10.1038/s41371-022-00776-9

33. SUMMARY OF THREE PRONGS IN MANAGEMENT OF HTN EMERGENCY
http://dx.doi.org/10.1136/bmj 2023 077205
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34. BRAKH

35. http://dx.doi.org/10.1136/bmj 2023 077205
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36. Guidelines

37.  The British and Irish Hypertension Society – focus on HTN emergencies
 Others – broad view of HTN management
 Common for all – 20-25% immediate reduction (in an hour) followed by a
more gradual reduction.
 No signs of acute organ injury – no need for ED evaluation

38. Future

39. Emerging
options
Imaging
Endothelial injury
Autoregulatory failure
The need in ER ????
Real time assessment of CBF,
CPP – personalised approach
Transcranial Doppler
Near infrared spectroscopy –
perioperative monitoring
during major cardiac surgery –
in future ?
Biomarkers
Proinflammatory state
Endothelial damage
Patients at risk of HTN emergency
1.Matrix metalloproteinases -
degradation of ECM
2.Thrombomodulin
Expression-surface of vascular
endothelial cells -  in vascular
damage
3.Endocan – marker of leukocyte
adhesion – endothelial damage in
hypertension
Therapeutics
Blood pressure variability
Neurologic HTN emergencies
Post hoc analysis showed worst CV
outcomes
Both in acute as well as sub acute
Ideal therapeutic agent ?
Preventive measures
Public education and awareness
Initiation of therapy
Strategies to improve adherence
Increased use of HBPM
Novel patient centered strategies
Team based care in remote areas
(health workers, pharmacists)
http://dx.doi.org/10.1136/bmj‑2023‑077205aria

40. Management strategies to prevent HTN emergency in
patients at risk
Drugs
Long acting
aldosterone synthase
inhibitors
Baxdrostat
Lorundostat
(reduction in SBP
upto 14 mm Hg)
RNA
interference agents
Zilebesiran
Hepatic angiotensinogen
synthesis
Efficacy with single injection
Percutaneous
Renal Denervation
Positive trials in
recent times
http://dx.doi.org/10.1136/ bmj 2023 077205
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41. Is it time to retire the diagnosis
“Hypertensive Emergency”?

42. HTN
Emergency
HTN
urgency
High BP in ER has worse outcomes
Emergency – Acute management of BP – benefit of decrease in CV outcomes ???
Urgency – High blood pressure – oral treatment?
When no benefit of acute management on short-term CV outcomes – why differentiate
both? NO CLINICAL TRIALS
Long term benefits would depend on the management after discharge – oral drugs
Chicken and egg conundrum
Reverse causality
DOI: 10.1161/JAHA.122.028494

43. Misguided importance to high BP in ER care
High BP
Acute
pulmonary
edema
High
BP
Acute pulmonary
edema
DOI: 10.1161/JAHA.122.028494

44. Absence of clinical trials with CV outcomes in
patients with hypertensive emergencies
Evolution of fatal outcomes, severe complications to be reduced by treatment
Strategies should be tested in RCTs (different criteria to be used for definition)
It is a syndrome not a single entity
The simple decision to treat or not to treat is naturally different in patients with stroke,
acute LV failure and angina
There is no common denominator to justify a similar BP lowering strategy.
DOI: 10.1161/JAHA.122.028494

45. Take Home Message
 Hypertensive emergency is a major global public health problem.
 Immediate attention toward careful BP reduction (MAP 20-25%) in an hour with IV
antihypertensive medications is indicated to reduce morbidity.
 Short-acting IV drugs are used.
 In the absence of an emergency, and BP >180/110 mm Hg, optimising management with
oral agents on OP basis is needed
 Most of the patients present again to the ER with uncontrolled hypertension after a
diagnosis of hypertension emergency.
 Given the lack of randomised trials to guide the management of hypertensive
emergencies, there remains a large unmet need for further research in these areas.
 Aldosterone synthase inhibitors, RNA interference agents may provide better control
of BP in long run thereby reducing occurrence of HTN emergency.

46. Thank you
“ Hypertension is a silent killer, but awareness can be a lifesaver".