2. Recent classification recommends hypertension be defined as systolic blood pressure
≥130 mmHg or diastolic blood pressure ≥80 mmHg(average of two or more seated
blood pressure readings during each of two or more outpatient visits).
Primary or Essential hypertension tends to be familial and is likely to be the
consequence of an interaction between environmental and genetic factors.
Secondary hypertension, a specific mechanism for the blood pressure elevation is
often more apparent.
Resistant hypertension refers to patients with blood pressures persistently >140/90
mmHg despite taking three or more antihypertensive agents, including a diuretic.
3.
4. Hypertensive crisis: A generic term for severe elevations in blood pressure (systolic
blood pressure ≥180 mmHg or diastolic blood pressure ≥120 mmHg) that have the
potential to cause target organ (heart, vasculature, kidneys, eyes, and brain) damage.
This includes both hypertensive emergency and hypertensive urgency.
Hypertensive urgency: A severe elevation in BP without evidence of acute
and ongoing target organ damage (TOD).
Hypertensive emergency: A severe elevation in BP with evidence of acute,
ongoing TOD.
Hypertensive encephalopathy: A specific hypertensive emergency
characterized by irritability, headaches, and mental status changes caused by
significant and often, rapid elevations in BP.
5. • Accelerated malignant hypertension: A specific hypertensive emergency that is
associated with an abrupt increase of blood pressure in a patient with underlying
hypertension or related to the sudden onset of hypertension in a previously normotensive
individual.
• Pathologically, the syndrome is associated with diffuse necrotizing vasculitis, arteriolar
thrombi, and fibrin deposition in arteriolar walls. Fibrinoid necrosis has been observed in
arterioles of kidney, brain, retina, and other organs.
• Clinically, the syndrome is recognized by
progressive retinopathy (arteriolar spasm, hemorrhages,exudates and papilledema).
deteriorating renal function with proteinuria.
microangiopathic hemolytic anemia.
encephalopathy.
6.
7. Pathophysiology
of Hypertensive
Emergencies
Failure of normal
autoregulatory
function
Leads to sharp
increase in systemic
vascular resistance.
Endovascular injury
with arteriole
necrosis.
Ischemia, platelet
deposition and
release of vasoactive
substance.
Further loss of
autoregulatory
mechanism
Exposes organs to
increased pressure.
8. • In hypertensive individuals, the upper
and lower limits of autoregulation
of cerebral blood flow are shifted to
higher levels of arterial pressure, and
rapid lowering of blood pressure
to below the lower limit of
autoregulation may precipitate
cerebral ischemia or infarction because
of decreased cerebral blood flow. Renal
and coronary blood flows also may
decrease with overly aggressive acute
therapy.
9.
10.
11. A general goal could be lowering BP in a controlled manner with a systolic
BP reduction of no more than 25% within the first hour, followed by a
gradual reduction to 160/100 mmHg within the next two to six hours,
before cautiously reducing the BP to normal over the next 24 to 48 h .
However, exceptions are not rare, such as aortic dissection, pre-
eclampsia, or pheochromocytoma, which require rapid BP reduction,
while others require less aggressive approaches, such as ischemic stroke.
12. HYPERTENSIVE ENCEPHALOPATHY
In the case of rapid elevation of BP, the autoregulatory response is incapable of preventing
cerebral hyperperfusion, causing increased intracranial pressure, damage of the blood–
brain barrier, and fluid extravasation into the brain tissue, especially in the posterior
regions, where BP oscillations are less effectively managed because of lowered
sympathetic innervation.
If no ischemia or hemorrhage is present, clinical and radiological findings
gradually disappear once the BP is controlled.
A syndrome of posterior reversible encephalopathy can be described in
the presence of acute onset headache, seizures, altered consciousness,
and visual disturbance occurring in the context of increased BP.
13. • The initial management should be aimed at lowering the mean arterial BP by 20-25% in
minutes to 1 hour, then to 160/110 over next 5 hours if tolerated.
• A further decrease in mean arterial BP increases the risk of cerebral hypoperfusion.
• Nicardipine or labetalol are preferred because they can be administered continuously,
therefore avoiding major BP fluctuations, which in the set of altered autoregulation can
disrupt the normal blood flow .
• It is, however, contraindicated to administer nitroglycerine in hypertensive
encephalopathy because of its venous vasodilatory effect and the potential to increase
intracranial pressure, thus worsening cerebral oedema.
• Nitroprusside can be used as it is a more balanced arterial and venous vasodilator and
acts mainly on the systemic rather than the cerebral vascular resistance.
• If not properly treated, hypertensive encephalopathy and posterior reversible
encephalopathy syndrome can evolve to cerebral hemorrhage, coma, and death.
14. • Magnetic resonance image
showing occipital bilateral
hyperintense images on T2
and fluid-attenuated inversion
recovery sparing the calcarine
and paramedian occipital lobe
structures.
15. INTRACRANIAL
HEMORRHAGE
• Based on the available data, current guidelines
have concluded that in patients presenting with
hyperacute intracerebral hematoma (symptoms
less than 6 h), lowering BP to less than 140
mmHg (but not lower than 110 mmHg) is
advisable as it can lead to a reduction in
hematoma expansion. Nonetheless, the
magnitude of BP reduction should not be larger
than 90 mmHg.
• Treatment should be started with an intravenous
rapid acting, easily titratable drug, such as
clevidipine, labetalol, nicardipine, or urapidil.
• For instance, in a multicenter comparison of
outcomes, nicardipine compared with
nitroprusside infusion during the first 24 h after
intracranial hemorrhage is associated with
reduced risk of in-hospital mortality without any
increase in hospitalization cost or length of stay
16.
17. SUBARACHNOID
HEMORRHAGE
• The most common etiology of SAH is rupture of an
intracranial aneurysm.
• Risk factors for aneurysmal rupture include hypertension,
cigarette smoking, heavy alcohol use, polycystic kidney
disease, and a history of aneurysms/SAH in first-degree
relatives.
• Patients with SAH usually present with sudden severe
headache that reaches maximum intensity within seconds
(i.e., thunderclap headache), associated with syncope or
persistent alteration in level of consciousness.
Meningismus develops often over hours.
• The diagnosis is confirmed by noncontrast computed
tomography (CT) of the head that has almost perfect (99%)
sensitivity if performed within 24 hours of symptom onset.
• Those presenting in a delayed fashion (i.e., headache for
>24 hours) or with negative CT despite clinical suspicion
should undergo lumbar puncture to evaluate for red blood
cells and xanthochromia (the yellow discoloration of
centrifuged CSF seen with blood breakdown).
18. • Early treatment of the ruptured aneurysm is critical to
prevent rebleeding and may be accomplished by
surgical clipping (with craniotomy) or endovascular
approach with coiling.
• Blood pressure should be controlled to prevent
further bleeding; mean arterial pressure (MAP)
should be kept below 110 mm Hg and/or systolic
blood pressure below 140 mm Hg.
• Short acting antihypertensives (e.g., labetalol,
nicardipine), analgesics, and sedatives are preferred.
• Administration of antifibrinolytic agents such as
tranexamic acid (1g IV q 4 to 6 hours, prior to
aneurysm treatment) has been shown to reduce the
risk of rebleeding
• All patients should receive nimodipine, a calcium
channel antagonist that has demonstrated efficacy in
improving neurological outcome(at a dose of 60 mg
every 4 hours enterally, continued for 21 days). The
dose may be halved and given q 2h if blood pressure
drops after each dose.
19. ECLAMPSIA
AND SEVERE
PRE-ECLAMPSIA
• Hypertension is defined at blood pressure ≥140 systolic or ≥90
diastolic on two occasions at least 4 hours apart in a woman
with previously normal blood pressure. Severely elevated
blood pressure ≥160 systolic or ≥110 diastolic confirmed
within a few minutes is also diagnostic.
• Proteinuria is defined at urinary excretion of 300 mg of protein
in a 24-hour urine collection, alternatively a protein/creatinine
(mg/dL) ratio of at least 0.3 is an acceptable equivalent.
• The proposed mechanisms that render pregnant women at
increased risk of ischemic/thrombotic stroke are endothelial
dysfunction, abnormal cerebral autoregulation resulting in
higher perfusion pressures, hemoconcentration due to third
spacing of intravascular fluids and activation of coagulation
cascade with microthrombi formation.1 The most common
obstetric etiologies of both ischemic and hemorrhagic stroke
are pre-eclampsia, eclampsia and HELLP syndrome
20. • Medical therapy relies on intravenous labetalol, intravenous nicardipine, or
immediate release nifedipine associated with magnesium sulphate for prevention of
seizures and convulsions.
• Monitoring of fetal heart rate is mandatory to avoid bradycardia due to the use of β-
blocker therapy.
• In a recent meta-analysis, it was demonstrated that oral nifedipine can be considered as
a first-line antihypertensive agent for reducing the risk of persistent high BP
in pregnancy compared to intravenous hydralazine or labetalol, with no differences in
the incidences of adverse effects, maternal or fetal outcomes, or maternal hypotension.
• When the opportunity of switching to oral treatment arises, first choice drugs are
methyldopa and long-acting nifedipine. Angiotensin converting enzyme inhibitors,
angiotensin receptor blockers, direct renin-inhibitors, and sodium nitroprusside are
contraindicated because of their teratogenic effects, and diuretics should be avoided
because they reduce the placental blood flow
21. ACUTE
ISCHEMIC
STROKE
• Patients with suspected ischemic stroke who are
eligible for thrombolysis must benefit from a
rapid BP reduction to less than 185/100 mmHg
and further maintenance for at least 24 h to
reduce the risk of intracranial hemorrhage.
• However, the systolic BP should not be reduced
to a value less than 130–140 mmHg in the first 72
h, while keeping it under 180 mmHg .
• Intravenous nicardipine, labetalol, and clevidipine
have been approved as initial agents in recent
stroke guidelines.
• Nitroprusside can be considered if the target BP
is not reached by the former agents or if the
diastolic BP is greater than 140 mmHg.
22. • Management of hypertension in patients
following successful mechanical
thrombectomy is still an area of study, current
literature suggesting better outcomes when
systolic BP is less than 160 mmHg, or even
140 mmHg.
• For patients not eligible for thrombolysis or
thrombectomy, maintaining higher BP is
advised, even as high as 220/120 mmHg to
maintain cerebral perfusion with potentially
reversible ischemia.
• In the first 24 h, a reduction of less than 15%
can be considered safe and reasonable to
pursue. Over the next 24 to 48 h, the blood
pressure needs to be gradually lowered .
Patients presenting with transient ischemic
attack should be treated likewise.
23. ACUTE AORTIC
SYNDROME
• Medical therapy consists of controlling chest pain and
administering the “anti-impulse therapy” represented by
the rapid lowering of systolic BP to 100 to 120 mmHg with
a concomitant reduction of heart rate to lower than 60
beats per minute.
• This therapy is required to decrease the aortic wall shear
stress and to minimize the tendency for the dissection to
propagate, as well as decreasing the development of
complications (rupture, aneurysmal degeneration).
• Intravenous β-blockers are the drugs of choice in this
situation. Intravenous labetalol, which is a non-selective β-
blocker with α- and β-adrenergic blocking effects, can be
used for rapid BP reduction . Esmolol, which has a shorter
half-life, may be favored in aortic dissection as it allows for
rapid correction if hypotension develops.
• If a significant contraindication to β-blockade is present,
calcium channel blockers are a suitable alternative.
• Nitroprusside or nitroglycerin administered intravenously
can be used if the target BP remains elevated but with
additional or after β-blockade to prevent reflex tachycardia.
Hydralazine is contraindicated.
24.
25. ACUTE CORONARY SYNDROME
• Treatment of acute, ongoing, myocardial ischemia associated with
severe BP elevations should be aimed at decreasing LV (left
ventricle) preload and afterload while maintaining a low heart rate
to provide adequate diastolic filling time and decrease myocardial
oxygen demand.
• These can be achieved with the administration of intravenous
nitroglycerin up-titrated for controlling the angina while rapidly
lowering the systolic BP to less than 140 mmHg associated with
intravenous β-blockers, usually esmolol or labetalol, which lower
the cardiac output and myocardial oxygen consumption, while
reducing the rate of nitroglycerin-induced reflex tachycardia. If β-
blockers are contraindicated, diltiazem or verapamil are a
reasonable alternative.
• Nitroprusside, Hydralazine because of its unfavorable effect on the
distribution of myocardial blood flow during ischemia are to be
avoided.
26. • The selective α1 blocker urapidil is a good alternative for the management of
hypertension in patients with acute coronary syndromes. In patients with ST elevation,
myocardial infarction and percutaneous revascularization, urapidil improved coronary
flow, myocardial perfusion, and LV function, were beneficial effects that were associated
with an increased production of nitric oxide
• Patients with acute coronary syndromes commonly receive anti-platelet medication,
which increases the risk for cerebral hemorrhage in the presence of elevated BP, thus
adequate control of BP values is a mandatory step. Nonetheless, during acute ischemia, a
diastolic BP of less than 60 mmHg needs to be avoided as this could lower myocardial
perfusion and aggravate the ongoing physiopathologic process.
27. ACUTE CARDIOGENIC PULMONARY EDEMA
• These patients require careful management with the immediate
goals of reducing the afterload, improving the LV ejection fraction,
and resolving the lung congestion.
• Therefore, the optimal treatment is the administration of
intravenous loop diuretic (furosemide) associated with
nitroprusside or nitroglycerine up titrated to the highest tolerated
dose for decreasing both cardiac preload and afterload.
• A mineralocorticoid receptor antagonist can be combined with the
loop diuretic to prevent hypokalemia.
• Non-invasive positive-pressure ventilation can also improve
hemodynamics by reducing venous return .
• β-blockers, which reduce cardiac contractility is contraindicated in
this acute situation.
• The BP should be lowered by about 20 to 25% within minutes to 1
h, then gradually to 160/100 mmHg within the next 2 to 6 h, and
finally returned cautiously to normal over the next 24 to 48 h.
28.
29. THROMBOTIC
MICROANGIOPATHY AND
ACUTE RENAL FAILURE
• Thrombotic microangiopathy (TMA) results from
hypertensive endothelial injury, which triggers platelets
activation, thrombi formation, micro vessels obliteration,
and disseminated intravascular coagulation.
• The first-line pharmacological treatment is with labetalol
and nicardipine; alternatively, nitroprusside and urapidil can
be used as a safe and effective treatment.
• The cornerstone of treatment is the complete blocking of
the renin-angiotensin system (RAS).
• These patients can be treated with oral medication without
delay, especially RAS blockers.
• Acute renal failure, Acute glomerulonephritis, Scleroderma
renal crisis, Renal artery stenosis, Renal transplant rejection.
30. Physical exam:
• Skin findings of scleroderma.
• Abdominal bruits.
• Gross hematuria.
Diagnostic studies:
• Serum creatinine, U/A: RBCs, protein, casts.
Management pearls:
• HTN may be result or cause of acute renal impairment.
• SNP: Cautiously given in renal impairment (cyanide toxicity).
Goals:
• LMAP by 10-20% within minutes to 1 hour, then another 10% over next 5 hours, Hemodialysis if
necessary.
• Scleroderma renal crisis: Must include ACE-I.
31. PHEOCHROMOCYTOMA/PARAGANGLIOMA
• An undetected PPGL can have a variety of clinical presentations, including
acute heart failure, acute coronary syndrome, aortic dissection, stroke, or
eclampsia as first manifestation of the disease.
• Both plasma and urine tests of free normetanephrine and metanephrine are
used for the screening of pheochromocytoma.
• α 1 blocking agents, either Phentolamine or doxazosin, usually followed by a β
blocker, is the first choice for achieving control of BP. The order should be as
stated above, to avoid enhanced α1-mediated vasoconstriction.
• Labetalol is the only β blocker, which also has an α1 blocking effect when
administered intravenously, that can be used without prior α1 blockade for the
treatment of hypertensive emergencies.
32. ACUTE PERIOPERATIVE AND POSTOPERATIVE
HYPERTENSION
• Adrenergic stimulation, postoperative pain, anxiety, and fluctuating intravascular volume can build
up towards a perioperative Hypertensive emergency.
• If BP tends to rise above 180/110 mmHg, intensive treatment or delay of surgery is advised to avoid
the risk of perioperative or postoperative hypertensive emergency, but every decision needs to be
evaluated individually on a case-by-case basis.
• As for the treatment agents, the utility of intravenous clevidipine, nitroglycerin, esmolol, or
nicardipine is recognized. Clevidipine has been reported as the drug of choice for treating acute
postoperative hypertension because of its rapid onset and short duration of action, with limited
induced variations outside the desired BP and lack of renal or hepatic metabolism.
• Esmolol plays an important role in the perioperative setting in cardiac surgery as it can substantially
decrease the high burden of supraventricular and ventricular arrhythmias in the aftermath of
surgery, with an unclear influence on mortality, acute myocardial infarction, stroke, congestive heart
failure, hypotension, and bradycardia.
33.
34.
35.
36.
37.
38.
39.
40. PREVENTIVE STRATEGIES
• Salt restriction (<5 g per day);
• Reduction of alcohol consumption (less than 14 units per week for men, and less than 8
units per week for women). One unit is equivalent to 10ml or 8grams of pure alcohol.
• Weight reduction (body-mass index about 20–25 kg/m2 and waist circumference values
<94 cm in men and <80 cm in women).
• DASH DIET: a healthy balanced diet with a high intake of vegetables, fruits, fish, and
unsaturated fatty acids and a low intake of red meat and saturated fatty acids.
• Constant physical activity (at least 30 min of moderate dynamic exercise on at least 5 to 7
days per week).
• Cessation of smoking
• Medication adherence
