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1. Hypertensive Crisis
Moderator: Dr. Teshome (MD, Assistant Professor of Internal medicine)
Presenter: Dr. Hussen (R1)
May, 2023
Haramaya University
Department of Medicine

2. Outlines
 Introduction
 Etiology
 Pathophysiology
 Clinical Evaluation
 Management
 Summery

3. Introduction
• Hypertension is one of the leading causes of the global burden of
disease.
• Hypertension doubles the risk of cardiovascular diseases, including
coronary heart disease (CHD), congestive heart failure (CHF), ischemic
and hemorrhagic stroke, renal failure, and peripheral arterial disease
• Overall, approximately 22% of the world's adults are estimated to
have hypertension
• Sub Saharan Africa has the highest prevalence(40%).
• It accounts for loss of 57 million disability adjusted life years (DALYS).

4. Intro…
oThe likelihood of hypertension increases with age, and among individuals
aged ≥60 years, the prevalence is 65.4%
o Probably due to the widespread availability of antihypertensive
therapy, in the United States, there has been a decline in the
numbers of patients presenting with hypertensive crisis.
oApproximately 1% of American hypertensive pts may develop hypertensive
crisis during their lifetime.
oAny primary or secondary hypertension can give rise to a hypertensive
crisis, but the most common cause uncontrolled primary hypertension

5. Intro…
o Epidemiological associations between BP and CV risk are directly
related to the height of the blood pressure, beginning at 115/75 mmHg,
without evidence of a threshold
o Clinically, hypertension may be defined as that level of blood pressure
at which the institution of therapy reduces blood pressure–related
morbidity and mortality
o Hypertension is diagnosed based on the average of two or more
seated blood pressure reading Systolic BP > or = 140 mm Hg and
Diastolic BP > or = 90 mm Hg at least 6 hours apart.

7. Mechanism of hypertension
 Cardiac output and peripheral
resistance are the two
determinants of arterial pressure
 Cardiac output is determined by
stroke volume and heart rate;
stroke volume is related to
myocardial contractility and to the
size of the vascular compartment.
 Peripheral resistance is
determined by functional and
anatomic changes in small arteries
and arterioles

8. Blood Pressure Regulation
• Many neurohormonal, renal, and vascular mechanisms interact to
varying degrees to the mechanism, pathogenesis and progression of the
different hemodynamic forms of hypertension
• 1. Autonomic Nervous system
• With drop in blood pressure sympathetic outflow will increase with the
final effect of raising blood pressure by increasing heart rate, myocardial
contractility and increasing peripheral vasoconstriction
• Change in blood pressure is sensed by baroreceptors in carotid sinus, aortic
sinus and heart muscles
• In the kidney, activation of α1-adrenergic receptors by norepinephrine
increases renal tubular reabsorption of sodium

10. 2. Renin-Angiotensin-Aldosterone system:
• The renin-angiotensin-aldosterone system contributes to the regulation of
arterial pressure primarily via the vasoconstrictor properties of angiotensin
II and the sodium-retaining properties of aldosterone.
• There are three primary stimuli for renin secretion:
• (1) decreased NaCl transport in the distal portion of the thick ascending
limb of the loop of Henle that abuts the corresponding afferent arteriole
(macula densa),
• (2) decreased pressure or stretch within the renal afferent arteriole
(baroreceptor mechanism),
• (3) sympathetic nervous system stimulation of renin-secreting cells via β1
adrenoreceptors

11. RAAS system …
• Aldosterone is a potent mineralocorticoid that increases sodium
reabsorption by amiloride-sensitive epithelial sodium channels (ENaC)
on the apical surface of the principal cells of the renal cortical
collecting duct
• Electric neutrality is maintained by exchanging sodium for potassium
and hydrogen ions
• Consequently, increased aldosterone secretion may result in
hypokalemia and alkalosis

13. 3 .VASCULAR MECHANISMS
• In hypertensive patients, decreased vascular compliance and lumen size
result from vascular fibrosis lead to increased peripheral resistance
• The vascular endothelium synthesizes and releases several vasoactive
substances, including nitric oxide, a potent vasodilator.
• Endothelium-dependent vasodilation is impaired in hypertensive patients
4 .INTRAVASCULAR VOLUME
When NaCl intake exceeds the capacity of the kidney to excrete sodium,
vascular volume may initially expand and cardiac output may increase
• As arterial pressure increases in response to a high NaCl intake, urinary
sodium excretion increases and sodium balance is maintained at the
expense of an increase in arterial pressure

14. Vascular mechanism

15. Hypertensive Crises
 Hypertensive crises are acute severe elevation in blood pressure (
usually > 180/120 mmHg ) that may or may not be associated with
end organ dysfunction
 Based on the degree of end organ damage rather than level of blood
pressure alone it has two categories
Two subsets
 Hypertensive Urgency
 Hypertensive Emergency

16. Hypertensive Urgency
 Hypertensive urgency is suddenly elevated in blood pressure greater
than 180/120 with out end organ dysfunction.
 Usually due to under controlled hypertension.
 No specific symptoms
 Need to be reduced over hours to days not over minutes
 No laboratory evidence of new or worsening target organ damage

17. Hypertensive Emergency
 It is acute severe elevation in blood pressure ( usually >
180/120 mmHg ) associated with impending or progressive
organ dysfunction involving neurological, cardiac or renal
systems.
 Require lowering of blood pressure within minutes to hour to
prevent morbidity ( not necessarily to normal range ).
 The clinical presentation and rapidity of BP rises more
relevant than the actual level of BP.

18. Hypertensive Emergency ...
 ICU admission usually required
 Examples of target organ damage associated hypertensive emergency include;
Hypertensive encephalopathy
Cerebral infarction ( ischemic stroke)
Cerebral hemorrhage ( SAH and ICH )
Pulmonary edema
Acute congestive heart failure
Acute kidney injury
Aortic dissection
Malignant hypertension: Clinical Syndrome associated with severe abrupt rise in BP
(commonly >200/120 mm Hg) , retinopathy ,deteriorating RF with PU, microangiopathic
hemolytic anemia and encephalopathy.

19. Etiology
• Essential hypertension : Inadequate blood pressure control and noncompliance
are common precipitants
• Renal parenchymal disease
• Eclampsia/pre-eclampsia
• Pheochromocytoma
• Anti-hypertensive withdrawal syndromes
• CNS. Guillain Barre Syndrome
• Drug-induced hypertension ( cocaine /amphetam/clonidine withdrawal )
• Idiopathic hypertension rapid unexplained rise in BP
• Post-op hypertension
• Coarctation of aorta

20. Pathophysiology
• The pathophysiology of hypertensive crises is not completely understood.
• With mild-to-moderate elevations in blood pressure, arterial and arteriolar
vasoconstriction initially maintains tissue perfusion while preventing
increased pressure from being transmitted to more distal vessels.
• With severe elevations in blood pressure (i.e., >180/110 mm Hg), this
autoregulation fails, and increased pressure in capillaries leads to
endothelial damage of the vascular wall, causing fibrinoid necrosis and
perivascular edema. Fibrinoid necrosis obliterates the vascular lumen,
resulting in organ damage.

21. Pathophysiology

22. Clinical Assessment
Although we consider hypertensive crisis in all patients who present
with severely elevated blood pressure ( > 180/120 ) ,regardless of
symptoms, quick and focused evaluation is critical in establishing a
diagnosis and initial therapy.
This include by
 History
 Physical examination
 lab test
 Imaging

23. History
A brief and focused history should address the presence of end organ
damage, the circumstances surrounding the hypertension, and any
identifiable etiology
 Medical Hx previous diagnosis and treatment
chronic illness ( CKD )
 Personal Hx smoking
alcohol drinking
 Family Hx DM, cardiac death
 Pregnancy last menstrual period preeclampsia

24. History . . .
 Specific Hx for end organ damage
 CVS ( MI ) ; chest pain ,SOB, cough
 CNS ( stroke ); change in mental status, severe headache, body
weakness, blurring vision
 GUS ( AKI ) ; decreased in urine amount flank pain

25. Physical Examination
The physical examination should focus on the presence of end organ damage and
help with identifying secondary causes of hypertension
Confirm elevated BP Proper position, appropriate cuff size Supine and
standing and both arms
 Fundoscopy finding may suggest retinal exudates, hemorrhages, or papilledema
which show hypertensive encephalopathy.
It is helpful to use an organ system–based approach to identify signs of end-
organ damage.

26. Focused Physical Examination
CNS
Focal neurologic finding
Seizures
Altered mental status
Papilledema, hemorrhages, exudates
Cardiovascular
Evidence of congestive heart failure
pulmonary edema
Murmur
Jugular venous distension
Peripheral edema
Equal and symmetric blood pressure

27. Investigation
Lab studies:
Electrolytes, urea, and creatinine
RBS, CBC ,and urinalysis
Imaging studies
CXR (chest pain or SOB)
Head CT/MRI (abn neurology)
Chest CT/Aortic angio (Aortic dissection)
12-lead ECG
Other Test
Troponin, CK-MB
Toxicology
Urine HCG
Echocardiography

28. Management
• The treatment of hypertensive crises 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.
• At what rate and to what extent should the blood pressure be
lowered depend on types of hypertensive crisis and end organ
damage

29. Management
 Hypertensive Urgency
Gradual lowering of elevated BP with in 24 hours ( reduction of MAP
by not more than 25% and DBP to 100 -110 mmHg ) to avoid sudden
drop of BP and tissue hypo perfusion
Drugs used in these case are Captopril 6.25mg po q6hrs and
Clonidine 0.1-0.2mg hourly, up to max 0.8mg in 24 hrs

30. Management…
Hypertensive emergency
o It requires immediate lowering of BP ,admission and intravenous medication.
o Initial treatment should reduce MAP by not more than 25 % while maintaining
DBP to 100-110mmHg within first few minutes to two hours.
oThere are exceptional to this rule : Aortic dissection
Acute stroke
Preeclampsia
o More aggressive and rapid BP reduction (Acute Pulmonary edema ,Aortic
dissection)
o More slowly for acute cerebrovascular damages with monitoring of neurological
status.

32. Preferred Parenteral Drugs for Selected
Hypertensive Emergencies

33. Usual Intravenous Doses of Antihypertensive Agents Used
in Hypertensive Emergencies

34. Specific Treatment
• The specific management depend on the end organ systems that affected
by the BP
• Hypertensive encephalopathy; defined as acute neurologic syndrome in
the setting of severe hypertension in absence of others cause
• It is due to increased cerebral perfusion from loss of blood brain barrier
integrity, which results in cerebral edema, vasospasm and
microhemorrhage formation.
• Symptoms include severe headache, nausea, vomiting, visual disturbance,
confusion and abnormal body movement.
• Signs include disorientation, lethargic, seizure, focal deficits, papilledema
and retinopathy.

35. Hypertensive encephalopathy
• The most common cause is abrupt BP elevation in a chronic
hypertension. Other conditions that can predispose a patient to
elevated BP and cause the same clinical situation include: AGN,
withdrawal from hypertensive drugs, pheochromocytoma,
preeclampsia and sympathomimetic agents ( cocaine and
amphetamines).
• Resolve with reduction in BP. MAP should be reduced by 20 % to DBP
of 100 to 110mmHg with in first hour. Suitable drugs in management
IV nitroprusside ( DOC ), labetalol, nicardipine and hydralazine.

36. Acute Aortic Dissection
• Separation of the layers within the aortic wall. The blood driven by pulsatile pressure entering tear
in the intima layer results in propagation of dissection . Clinically, patients complain of sudden
onset retrosternal or interscapular chest pain that tearing or ripping type. Diagnosis involve
clinical and imaging
• Anatomic location classified as type A and type B
• Type A- Ascending aorta with or without distal aorta involvement
• Type B- Only the aortic arch or descending aorta
• Type A and life threatening type B are surgical emergency in addition to BP control reduce shear
force on damage aorta
• Rapidly reduce SBP to 100 -120 mmHg or lowest level that is tolerated with in 5 – 10 munites after
achieving HR lower than 60 bpm
• Esmolol and nitroprusside are DOC

37. Myocardial ischemia/infarction
• May be associated with HTN at presentation (usually in a previously
HTN pt).
• High BP exacerbated by pain and agitation.
• IV Nitrates reducing systemic vascular resistance, LV preload,
improves coronary perfusion
• B blockers may contribute to a fall in BP (reduces myocardial O2
consumption)
• BP control mandatory before thrombolysis (BP<180/100 mmHg).

38. Acute Pulmonary Edema/Left
Ventricular Dysfunction
 Oxygen (face mask, INO2, intubation
• Reduction of LV preload and afterload.
• IV nitrate ( nitroglycerin ), loop diuretics.
• Others – urapidil, nicardipine,sodium nitroprusside
•Ischemic stroke
BP elevations can occur in previously hypertensive and in
normotensive pts.
BP declines to pre stroke values within 3-4 days after an
ischemic stroke.
Hypertension often transient, physiologic response which
resolves spontaneously

39. Ischemic stroke….
• Acute treatment of BP elevations is only indicated in limited circumstances
• High BP can cause hemorrhagic transformation of infarct ,cerebral edema.
But, if CPP is low, ischemic penumbra may occur
• Indication for acute treatment include
1. Use of thrombolytic therapy : BP goal before initiating thrombolysis is
less than 185/110 mm Hg
2. Other target-organ damage (e.g., aortic dissection, myocardial
infarction) : The BP goal is reduction with cautious of 15% (10%– 20%) in
the MAP over 24 hours
3. Severe” elevations in BP ( SBP > 220mmHg or DBP >120mmHg ) .

40. Acute Hemorrhagic stroke
• To prevent rebleeding and reduce edema formation
• Reduce SBP to < 180 mmHg over first 24 hrs , if SBP > 220 and Pt with elevated ICP
• Reduce SBP to < 160 mmHg over the first few hrs, if the Pt is stable and SBP 150 -220
• Nimodipine, a dihydropyridine calcium blocker,is effective (antagonist effects on
cerebrovasospasm).
• Preeclampsia : leading cause of maternal and fetal mortality. It defined HTN ( SBP
> 140 mmHg and DBP > 90 mmHg on at least two occasion in 4 hrs apart) and
Proteinuria( 24 hours collection more than 300 mg ) or HTN and end organ dysfunction
with or without proteinuria after 28 wks of gestation or postpartum in previously
normotensive woman

41. Preeclampsia
• Acute severe HTN ( SBP >160 mmHg or DBP >110 mmHg ) and signs/symptoms of end organ
dysfunction show severity.
• For severe acute HTN, MAP should be decreased by 20%–25% over the first few minutes to hours
• Target goal BP is SBP :155-160 mmHg, DBP>105mm Hg.(initiation of Rx)
• The target of < or =160/110 mm Hg over the subsequent hours
• MgSo4 for seizure prophylaxis
• For acute severe BP reduction, it is recommended to use intravenous labetolol or hydralazine, and
for chronic severe HTN methyldopa is drug of choice.
• Avoid sublingual or oral nifedipine.
• Nitroprusside,ACEI – C/I

42. Summery

43. References
• Harrison's principle of internal medicine - 21th Edition
• Up to date
• 2017 ACC/AHA Guideline for the Prevention, Detection, Evaluation,
and Management of High Blood Pressure in Adults
• 2018 ESC/ESH Guidelines for the management of arterial
hypertension
• 2020 ISH Global Hypertension Practice Guidelines
• National NCD guideline