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Ephrem Hassen (CCNP)
 Overview
 Clinical Presentation
 Evaluation and Diagnosis
 Management
 Clinical Relevance
 References
Severe hypertension (hypertensive crisis):
 A confirmed blood pressure ≥ 180 mm Hg systolic and/or ≥ 120 mm Hg diastolic
 May occur in previously undiagnosed or known hypertensive individuals
 May be isolated or sustained
 A clinical spectrum:
Hypertensive urgency:
Asymptomatic, or relative asymptomatic, severe hypertension without end-organ damage
Hypertensive emergency:
Severe hypertension associated with signs of end-organ damage
Resistant hypertension:
Blood pressure that remains uncontrolled despite concurrent use of 3 antihypertensive
agents of different classes:
o Of these agents 1 must be a diuretic (or a diuretic was not tolerated).
o All must be dosed at the maximum allowable (or tolerable) dose.
o Blood pressure that is controlled on maximal doses of ≥ 4 medications belong to this class by
default.
Refractory hypertension:
 Blood pressure that cannot be controlled even with maximally tolerated doses of ≥ 5 drugs
 Must include chlorthalidone
 Must include spironolactone
Secondary hypertension:
Resistant hypertension with an identifiable and potentially treatable etiology, such as:
 Renal artery stenosis (RAS), Primary hyperaldosteronism
 CKD, Obstructive sleep apnea (OSA)
 Pheochromocytoma
 Cushing syndrome, Coarctation of the aorta
 Head trauma
 Blood pressure medication noncompliance
 Suboptimal therapy
 Rebound hypertension
 Emotional disturbance
 Hyperthyroidism
 Extracellular volume expansion:
o High-sodium diet
o Underlying renal insufficiency
o Sodium retention (side effect of vasodilators)
Use of stimulants:
 Cocaine, Methamphetamine
 Caffeine, Nicotine
Medications that cause increased blood pressure:
 NSAIDs
 Sympathomimetics:
o Weight-loss drugs
o Decongestants
o Amphetamines
 Glucocorticoids, Oral contraceptives
 Antidepressants, Calcineurin inhibitors
 Difficult to assess because of inconsistent coding practices among practitioners/institutions
Clinical Presentation
 Regardless of the manifestation of severe hypertension, by definition, the individual will have a
blood pressure ≥ 180 mm Hg systolic and/or ≥ 120 mm Hg diastolic.
Hypertensive urgency
 Blood pressure ≥ 180 mm Hg systolic and/or ≥ 120 mm Hg diastolic
 Asymptomatic or vague/minimal symptoms:
 Headache
 Fatigue
 Flushing
 Blurred vision
Hypertensive emergency
 Blood pressure ≥ 180 mm Hg systolic and/or ≥ 120 mm Hg diastolic with manifestations of target
organ damage
 Potential symptoms:
o Chest pain
o Shortness of breath
o Visual disturbance
o Focal neurologic symptoms
o Altered mental status
o Hematuria
o Anuria
Evidence of myocardial ischemia or MI:
o Diagnostic ECG changes
o Elevated cardiac enzymes
o Acute and/or decompensated heart failure
Evidence of cerebrovascular accident:
o Focal neurologic deficits
o CT/MRI findings indicative of cerebral ischemia and/or bleeding
Evidence of acute/acute-on-chronic renal failure:
o Acute uremia
o Acidosis/alkalosis
o Abnormal electrolytes
Evaluation and Diagnosis
 During the initial assessment of an individual with severe hypertension, it is
imperative to exclude chronic target-organ damage.
 Severe elevations in blood pressure should be quickly confirmed with repeat
measurement.
Particular focus on risk factors for end-organ vascular events:
 Acute head injury
 Use of stimulant drugs (cocaine, methamphetamine)
 Known myocardial ischemia
 Known cerebrovascular ischemia
 Known arterial deformity:
oAbdominal aortic aneurysm (AAA)
oCerebral aneurysm, Arteriovenous malformation (AVM)
oRecent vascular surgery, RAS (Renal artery stenosis)
Multiple vascular risk factors:
 Age
 Family history
 Smoking
 Diabetes
 Hypertension
 Dyslipidemia
 Obesity
 Sedentary lifestyle
 Obstructive sleep apnea (OSA )
Symptoms of end-organ dysfunction:
 Headache, Fatigue
 Blurred vision, Chest pain
 Shortness of breath
 Nausea/vomiting (increased intracranial pressure)
 Visual disturbance, Focal neurologic symptoms
 Altered mental status
 Acute severe back pain (aortic dissection)
 Hematuria, Anuria
Physical examination
 Blood pressure evaluation:
oStandard blood pressure measurement with a manual sphygmomanometer
at regular intervals is appropriate for low-risk individuals.
oHigher-risk individuals may need continuous monitoring with an automatic
sphygmomanometer with a digital display.
oIndividuals requiring urgent and controlled blood pressure lowering with
IV antihypertensives may benefit from the placement of an intraarterial catheter for
continuous blood pressure monitoring.
Mental status:
o Agitation
o Delirium
o Stupor
o Seizure
o Coma
Focal neurologic findings:
o Visual loss
o Limb paresis/paralysis
o Speech deficit
Ophthalmic exam:
 Hemorrhages
 Exudates
 Papilledema
Signs of cardiac decompensation:
 Jugular venous distention (JVD)
 Palpitations/abnormal rhythm
 New murmur
 New gallop
 Pulmonary rales
 Peripheral edema
Miscellaneous:
• Abdominal bruit (AAA or RAS)
• Carotid or femoral bruit (suggests atherosclerosis)
 Preeclampsia or eclampsia in pregnancy
Diagnostic tests
 ECG
 Urine studies:
• Urinalysis, 24-hour urine collection:
o Protein
o Catecholamines/metanephrines for pheochromocytoma
o Sodium excretion
Blood chemistry:
 Electrolytes
 Serum creatinine
 Cardiac biomarkers
 Serum aldosterone
Imaging for ischemia/vascular compromise
 Chest X-ray:
 Pulmonary edema
 Cardiac enlargement
 Widened mediastinum
CT/MRI brain:
 Cerebral ischemia
 Cerebral hemorrhage
CT chest/abdomen:
 Thoracic aortic dissection
 Abdominal aortic dissection
Rate of reduction for elevated blood pressure
 Target blood pressure should be achieved over a period of hours to days.
 Slower reductions may be needed in older individuals with an increased risk of
cerebral or myocardial ischemia.
 Blood pressure should be slowly reduced to < 160/< 100 mm Hg.
 Mean arterial pressure (MAP) should not be lowered >25%–30% in the 1st few hours.
 Long-term reductions back to previous therapeutic target (i.e., ≤ 130/80 mm Hg)
Outpatient management:
 Outcomes may be poor:
 High rate of loss to follow-up soon after evaluation
 High rate of return to the ED for recurrent uncontrolled hypertension within 3 months
 May be appropriate if:
 No evidence of end-organ damage
 Blood pressure was previously controlled on an antihypertensive regimen.
 Individual or their caregiver is reliable for monitoring blood pressure and ensuring that
medications are taken.
 Move individual to a quiet room: can lead to a fall in systolic pressure of ≥ 10–20 mm Hg
 Determine time course of blood pressure lowering:
• Balance between 2 concerns:
oBlood pressure ↓ too quickly, potential inability for autoregulation to maintain end-
organ tissue perfusion
oBlood pressure ↓ too slowly, potential risk of imminent cardiovascular events
If blood pressure needs to be lowered quickly (hours):
 Includes individuals with high risk:
o Imminent coronary or cerebral ischemia
o Known renal artery stenosis
o Known existing cerebral or aortic aneurysm
 Oral clonidine (rapid-acting)
 Oral captopril (rapid-acting)
 Oral or sublingual nitrates (rapid-acting)
 Oral hydralazine (rapid-acting)
 Consider admitting the individual for observation and blood pressure medication titration.
 Consider discharge home with short-interval follow-up.
If blood pressure needs to be lowered slowly (days):
 Previously diagnosed hypertension:
o Previously controlled → resume previous regimen
o Previously suboptimally controlled → increase doses for previous regimen or add a new agent
 If new diagnosis:
 Amlodipine
 Chlorthalidone
 Beta-blockers if the individual has a comorbid indication for beta-blockade (e.g., heart failure)
 ACE inhibitor if the individual has a comorbid indication for ACE inhibition (e.g., diabetes)
 Combination therapy may be considered.
 Consider hospital admission for medication titration.
 Consider discharge home with short-interval follow-up.
Prior to discharge:
 Ensure:
oShort-interval follow-up with appropriate specialist
oPrescription given for any new medications
 Counsel:
oImportance of adherence to blood pressure medication regimen
oImportance of dietary sodium restriction
Admit individual to ICU:
 For intensive monitoring
 For rapid intervention in the event of decompensation.
 For rapidly titratable IV delivery of blood pressure medications
In general, rapid lowering of BP is not advised:
 Risk of ischemia if vascular physiology has habituated to higher BP
 Goal:
o Lower MAP by 10%–20% in the 1st hour and an additional 5%–15% over the next 24 hours.
o Often equates to a goal BP of <180/<120 mm Hg for the 1st hour and <160/<110 mm Hg for the
next 23 hours
 For ischemic stroke, DO NOT initiate BP-lowering measures unless:
oBlood pressure > 185/110 mm Hg if candidate for reperfusion (thrombolytic therapy)
oBlood pressure > 220/120 mm Hg if not candidate for reperfusion
 Acute aortic dissection: Lower systolic BP rapidly to 100–120 mm Hg to decrease
the shearing forces and control the tear.
 Intracerebral hemorrhage: DO initiate rapid systolic blood pressure lowering:
oTarget blood pressure 140 mm Hg if presenting blood pressure is 150–220 mm Hg
oTarget blood pressure 140–160 mm Hg if presenting blood pressure is >220 mm Hg
 Interventional cardiology, Neurology/neurosurgery
 Vascular surgery, Interventional radiology, Nephrology
Therapeutic IV blood pressure agents:
 Beta-blockers:
o Labetalol, Esmolol
 Calcium channel blockers:
o Nicardipine, Clevidipine, Felodipine
 Nitrates:
o Nitroprusside, Nitroglycerine
 Others:
o Phentolamine, Hydralazine
 Intracerebral hemorrhage: IV labetalol or nicardipine (1st-line)
 Acute heart failure (volume overload):
oLoop diuretics
oNitroprusside or nitroglycerin to reduce the afterload
oAVOID medications that reduce contractility (such as beta blockers)
 Acute coronary syndrome:
o Beta blockers
o Nitroglycerin, Clevidipine
o Nicardipine
 Acute aortic dissection:
o Beta blockers (reduces heart rate)
o Nitroprusside
o Clevidipine
 Hypertensive emergency in pregnancy:
o Methyldopa, Labetalol
o Hydralazine
After 8–24 hours of stable blood pressure control:
 Transition to oral agents
 Wean IV agents
 Transition out of ICU
 Discharge planning as above
Counsel about DASH (Dietary Approach to Stop hypertension)
 Eat high fiber fruits: this help you urinate extra fluid in the body
 Limit sodium to 2.4 grams per day, this lower blood pressure
 Eat meat that are not high processed: fish , chicken
 Consume low diary products : low fat cheese, low fat milk
 Limit sweets
 Eat whole wheat rather than white
 Eat food high in omega 3
 No more alcohol, cigarettes has chemical in it that causes high BP
 Avoid high calorie food to prevent building of plaque
 Know the acronyms Diuretic:-
 Daily weight
 Intake
 Urine output
 Response of blood pressure
 Electrolyte in your body
 Take pulses
 Ischemic stroke: sign of mini heart attack
 Complication watch out
Close monitoring:-
 Vital sign: HR, SPO2,RR,especialy BP with both arms (SBP,DBP& MAP frequency should
be close like Q 10,5min or less depends on BP)
 Perform focused examination ,including (but not limited to):
 LOC
 Speech / language
 Attention /ability to follow direction
 Orientation
 Cross strength on all 4 extremities
1. If blood pressure is too low [90/60],hold the medication and inform for
responsible physician
2. If reading is high ,take it twice and compare the number as order
3. If still high try different position sitting ,laying If consistence call for help
4. Preventing hypertensive crises
 Severe headache
 Severe anxiety
 Nose bleeding
 Shortness of breath
Labile (paroxysmal) hypertension:
• Marked elevations in blood pressure that are recurrent, sudden, and transient.
• Labile hypertension is linked to sympathetic hyperstimulation, though the link is poorly understood.
• Treatment is with adrenergic blocking agents (i.e., beta-blockers, alpha-blockers).
Secondary hypertension:
Resistant hypertension with an identifiable and potentially treatable etiology. Includes
• RAS, primary hyperaldosteronism,
• CKD, OSA, pheochromocytoma, Cushing syndrome, coarctation of the aorta.
Treatment depends on the specific cause.
Head trauma:
 Complex cascade of neurohormonal factors resulting from a traumatic brain injury can
cause severe hypertension.
 This cascade likely represents compensatory mechanisms to maintain cerebral perfusion in
the setting of increased intracranial pressure.
 The balance between maintenance of cerebral perfusion and prevention of cerebrovascular
events makes treatment of elevated blood pressure with head trauma controversial.
Hypertensive encephalopathy:
• Dramatic change in the level of consciousness, cognition, or personality in the setting of
severe hypertension and attributable to cerebral edema.
• Management includes aggressive but careful lowering of the blood pressure and immediate
neurologic/neurosurgical consultation to avoid or minimize cerebrovascular events and/or
permanent brain damage.
Hypertensive retinopathy:
• Characterized by retinal hemorrhages, exudates, and papilledema in the setting of severe hypertension.
• Management consists of aggressive but careful lowering of the blood pressure and immediate
ophthalmologic consultation to avoid or minimize vision loss.
Hypertensive heart disease:
 Cardiomyopathy is directly attributable to the physiologic compensations the myocardium must
make to maintain cardiac output in the face of chronically elevated afterload and may result in:
oSystolic dysfunction,
oDiastolic dysfunction,
oValvular dysfunction,
oIncreased arrhythmogenic potential, and
oMyocardial ischemia (even with normal coronary arteries).
 Management consists of blood pressure optimization and prevention of heart failure,
arrhythmia, and ischemia
Hypertensive nephropathy:
• Progressive nephrosclerosis involving the renal vasculature, glomeruli, and tubule-
interstitial elements in the setting of uncontrolled hypertension.
• The long-term result is progressive loss of kidney function ultimately manifesting as end-
stage renal disease that may require hemodialysis.
Obstetric hypertensive
 Gestational hypertension, preeclampsia, eclampsia, and HELLP syndrome are the obstetric
complications of pregnancy that can pose health risks to the mother and fetus.
 Management includes control of blood pressure and delivery of the fetus.
 Defined as a blood pressure (BP) of ≥130/80 mm Hg.
 Significantly elevated BP (≥ 180 mm Hg systolic and/or ≥ 120 mm Hg diastolic) carries
a substantial risk of morbidity and mortality.
 Despite the prolonged presence of hypertension, there may be no signs or symptoms of
end-organ damage (e.g., brain, eyes, heart, kidneys) until function becomes
decompensated or severely impaired.
Individuals may present with clinical symptoms such as:
 Chest pain due to MI or focal neurologic changes associated with a cerebral infarction
or intracranial hemorrhage.
 Diagnosis is made using serial blood pressure measurements and testing for end-organ
damage.
 Management includes lowering the blood pressure and treating specific organ damage.
 Varon, J., Elliot, W. (2020). Management of severe asymptomatic hypertension (hypertensive
urgencies) in adults. UpToDate. Retrieved July 10, 2021,
from https://www.uptodate.com/contents/management-of-severe-asymptomatic-hypertension-
hypertensive-urgencies-in-adults
 Varon, J., Elliot, W. (2021). Evaluation and treatment of hypertensive emergencies in adults.
UpToDate. Retrieved July 10, 2021, from https://www.uptodate.com/contents/evaluation-and-
treatment-of-hypertensive-emergencies-in-adults
 Townsend, R. (2020). Definition, risk factors, and evaluation of resistant hypertension. UpToDate.
Retrieved July 10, 2021, from https://www.uptodate.com/contents/definition-risk-factors-and-
evaluation-of-resistant-hypertension

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Hypertensive Crisis.pptx

  • 2.  Overview  Clinical Presentation  Evaluation and Diagnosis  Management  Clinical Relevance  References
  • 3. Severe hypertension (hypertensive crisis):  A confirmed blood pressure ≥ 180 mm Hg systolic and/or ≥ 120 mm Hg diastolic  May occur in previously undiagnosed or known hypertensive individuals  May be isolated or sustained  A clinical spectrum: Hypertensive urgency: Asymptomatic, or relative asymptomatic, severe hypertension without end-organ damage Hypertensive emergency: Severe hypertension associated with signs of end-organ damage
  • 4. Resistant hypertension: Blood pressure that remains uncontrolled despite concurrent use of 3 antihypertensive agents of different classes: o Of these agents 1 must be a diuretic (or a diuretic was not tolerated). o All must be dosed at the maximum allowable (or tolerable) dose. o Blood pressure that is controlled on maximal doses of ≥ 4 medications belong to this class by default.
  • 5. Refractory hypertension:  Blood pressure that cannot be controlled even with maximally tolerated doses of ≥ 5 drugs  Must include chlorthalidone  Must include spironolactone Secondary hypertension: Resistant hypertension with an identifiable and potentially treatable etiology, such as:  Renal artery stenosis (RAS), Primary hyperaldosteronism  CKD, Obstructive sleep apnea (OSA)  Pheochromocytoma  Cushing syndrome, Coarctation of the aorta
  • 6.  Head trauma  Blood pressure medication noncompliance  Suboptimal therapy  Rebound hypertension  Emotional disturbance  Hyperthyroidism  Extracellular volume expansion: o High-sodium diet o Underlying renal insufficiency o Sodium retention (side effect of vasodilators)
  • 7. Use of stimulants:  Cocaine, Methamphetamine  Caffeine, Nicotine Medications that cause increased blood pressure:  NSAIDs  Sympathomimetics: o Weight-loss drugs o Decongestants o Amphetamines  Glucocorticoids, Oral contraceptives  Antidepressants, Calcineurin inhibitors
  • 8.  Difficult to assess because of inconsistent coding practices among practitioners/institutions Clinical Presentation  Regardless of the manifestation of severe hypertension, by definition, the individual will have a blood pressure ≥ 180 mm Hg systolic and/or ≥ 120 mm Hg diastolic. Hypertensive urgency  Blood pressure ≥ 180 mm Hg systolic and/or ≥ 120 mm Hg diastolic  Asymptomatic or vague/minimal symptoms:  Headache  Fatigue  Flushing  Blurred vision
  • 9. Hypertensive emergency  Blood pressure ≥ 180 mm Hg systolic and/or ≥ 120 mm Hg diastolic with manifestations of target organ damage  Potential symptoms: o Chest pain o Shortness of breath o Visual disturbance o Focal neurologic symptoms o Altered mental status o Hematuria o Anuria
  • 10. Evidence of myocardial ischemia or MI: o Diagnostic ECG changes o Elevated cardiac enzymes o Acute and/or decompensated heart failure Evidence of cerebrovascular accident: o Focal neurologic deficits o CT/MRI findings indicative of cerebral ischemia and/or bleeding Evidence of acute/acute-on-chronic renal failure: o Acute uremia o Acidosis/alkalosis o Abnormal electrolytes
  • 11.
  • 12.
  • 13. Evaluation and Diagnosis  During the initial assessment of an individual with severe hypertension, it is imperative to exclude chronic target-organ damage.  Severe elevations in blood pressure should be quickly confirmed with repeat measurement.
  • 14. Particular focus on risk factors for end-organ vascular events:  Acute head injury  Use of stimulant drugs (cocaine, methamphetamine)  Known myocardial ischemia  Known cerebrovascular ischemia  Known arterial deformity: oAbdominal aortic aneurysm (AAA) oCerebral aneurysm, Arteriovenous malformation (AVM) oRecent vascular surgery, RAS (Renal artery stenosis)
  • 15. Multiple vascular risk factors:  Age  Family history  Smoking  Diabetes  Hypertension  Dyslipidemia  Obesity  Sedentary lifestyle  Obstructive sleep apnea (OSA )
  • 16. Symptoms of end-organ dysfunction:  Headache, Fatigue  Blurred vision, Chest pain  Shortness of breath  Nausea/vomiting (increased intracranial pressure)  Visual disturbance, Focal neurologic symptoms  Altered mental status  Acute severe back pain (aortic dissection)  Hematuria, Anuria
  • 17. Physical examination  Blood pressure evaluation: oStandard blood pressure measurement with a manual sphygmomanometer at regular intervals is appropriate for low-risk individuals. oHigher-risk individuals may need continuous monitoring with an automatic sphygmomanometer with a digital display. oIndividuals requiring urgent and controlled blood pressure lowering with IV antihypertensives may benefit from the placement of an intraarterial catheter for continuous blood pressure monitoring.
  • 18. Mental status: o Agitation o Delirium o Stupor o Seizure o Coma Focal neurologic findings: o Visual loss o Limb paresis/paralysis o Speech deficit
  • 19. Ophthalmic exam:  Hemorrhages  Exudates  Papilledema Signs of cardiac decompensation:  Jugular venous distention (JVD)  Palpitations/abnormal rhythm  New murmur  New gallop  Pulmonary rales  Peripheral edema
  • 20. Miscellaneous: • Abdominal bruit (AAA or RAS) • Carotid or femoral bruit (suggests atherosclerosis)  Preeclampsia or eclampsia in pregnancy Diagnostic tests  ECG  Urine studies: • Urinalysis, 24-hour urine collection: o Protein o Catecholamines/metanephrines for pheochromocytoma o Sodium excretion
  • 21. Blood chemistry:  Electrolytes  Serum creatinine  Cardiac biomarkers  Serum aldosterone Imaging for ischemia/vascular compromise  Chest X-ray:  Pulmonary edema  Cardiac enlargement  Widened mediastinum
  • 22. CT/MRI brain:  Cerebral ischemia  Cerebral hemorrhage CT chest/abdomen:  Thoracic aortic dissection  Abdominal aortic dissection
  • 23. Rate of reduction for elevated blood pressure  Target blood pressure should be achieved over a period of hours to days.  Slower reductions may be needed in older individuals with an increased risk of cerebral or myocardial ischemia.
  • 24.  Blood pressure should be slowly reduced to < 160/< 100 mm Hg.  Mean arterial pressure (MAP) should not be lowered >25%–30% in the 1st few hours.  Long-term reductions back to previous therapeutic target (i.e., ≤ 130/80 mm Hg)
  • 25. Outpatient management:  Outcomes may be poor:  High rate of loss to follow-up soon after evaluation  High rate of return to the ED for recurrent uncontrolled hypertension within 3 months  May be appropriate if:  No evidence of end-organ damage  Blood pressure was previously controlled on an antihypertensive regimen.  Individual or their caregiver is reliable for monitoring blood pressure and ensuring that medications are taken.
  • 26.  Move individual to a quiet room: can lead to a fall in systolic pressure of ≥ 10–20 mm Hg  Determine time course of blood pressure lowering: • Balance between 2 concerns: oBlood pressure ↓ too quickly, potential inability for autoregulation to maintain end- organ tissue perfusion oBlood pressure ↓ too slowly, potential risk of imminent cardiovascular events
  • 27. If blood pressure needs to be lowered quickly (hours):  Includes individuals with high risk: o Imminent coronary or cerebral ischemia o Known renal artery stenosis o Known existing cerebral or aortic aneurysm  Oral clonidine (rapid-acting)  Oral captopril (rapid-acting)  Oral or sublingual nitrates (rapid-acting)  Oral hydralazine (rapid-acting)  Consider admitting the individual for observation and blood pressure medication titration.  Consider discharge home with short-interval follow-up.
  • 28. If blood pressure needs to be lowered slowly (days):  Previously diagnosed hypertension: o Previously controlled → resume previous regimen o Previously suboptimally controlled → increase doses for previous regimen or add a new agent  If new diagnosis:  Amlodipine  Chlorthalidone  Beta-blockers if the individual has a comorbid indication for beta-blockade (e.g., heart failure)  ACE inhibitor if the individual has a comorbid indication for ACE inhibition (e.g., diabetes)  Combination therapy may be considered.  Consider hospital admission for medication titration.  Consider discharge home with short-interval follow-up.
  • 29. Prior to discharge:  Ensure: oShort-interval follow-up with appropriate specialist oPrescription given for any new medications  Counsel: oImportance of adherence to blood pressure medication regimen oImportance of dietary sodium restriction
  • 30. Admit individual to ICU:  For intensive monitoring  For rapid intervention in the event of decompensation.  For rapidly titratable IV delivery of blood pressure medications In general, rapid lowering of BP is not advised:  Risk of ischemia if vascular physiology has habituated to higher BP  Goal: o Lower MAP by 10%–20% in the 1st hour and an additional 5%–15% over the next 24 hours. o Often equates to a goal BP of <180/<120 mm Hg for the 1st hour and <160/<110 mm Hg for the next 23 hours
  • 31.  For ischemic stroke, DO NOT initiate BP-lowering measures unless: oBlood pressure > 185/110 mm Hg if candidate for reperfusion (thrombolytic therapy) oBlood pressure > 220/120 mm Hg if not candidate for reperfusion  Acute aortic dissection: Lower systolic BP rapidly to 100–120 mm Hg to decrease the shearing forces and control the tear.  Intracerebral hemorrhage: DO initiate rapid systolic blood pressure lowering: oTarget blood pressure 140 mm Hg if presenting blood pressure is 150–220 mm Hg oTarget blood pressure 140–160 mm Hg if presenting blood pressure is >220 mm Hg
  • 32.  Interventional cardiology, Neurology/neurosurgery  Vascular surgery, Interventional radiology, Nephrology Therapeutic IV blood pressure agents:  Beta-blockers: o Labetalol, Esmolol  Calcium channel blockers: o Nicardipine, Clevidipine, Felodipine  Nitrates: o Nitroprusside, Nitroglycerine  Others: o Phentolamine, Hydralazine
  • 33.  Intracerebral hemorrhage: IV labetalol or nicardipine (1st-line)  Acute heart failure (volume overload): oLoop diuretics oNitroprusside or nitroglycerin to reduce the afterload oAVOID medications that reduce contractility (such as beta blockers)
  • 34.  Acute coronary syndrome: o Beta blockers o Nitroglycerin, Clevidipine o Nicardipine  Acute aortic dissection: o Beta blockers (reduces heart rate) o Nitroprusside o Clevidipine  Hypertensive emergency in pregnancy: o Methyldopa, Labetalol o Hydralazine
  • 35. After 8–24 hours of stable blood pressure control:  Transition to oral agents  Wean IV agents  Transition out of ICU  Discharge planning as above
  • 36. Counsel about DASH (Dietary Approach to Stop hypertension)  Eat high fiber fruits: this help you urinate extra fluid in the body  Limit sodium to 2.4 grams per day, this lower blood pressure  Eat meat that are not high processed: fish , chicken  Consume low diary products : low fat cheese, low fat milk  Limit sweets  Eat whole wheat rather than white  Eat food high in omega 3
  • 37.  No more alcohol, cigarettes has chemical in it that causes high BP  Avoid high calorie food to prevent building of plaque  Know the acronyms Diuretic:-  Daily weight  Intake  Urine output  Response of blood pressure  Electrolyte in your body  Take pulses  Ischemic stroke: sign of mini heart attack  Complication watch out
  • 38. Close monitoring:-  Vital sign: HR, SPO2,RR,especialy BP with both arms (SBP,DBP& MAP frequency should be close like Q 10,5min or less depends on BP)  Perform focused examination ,including (but not limited to):  LOC  Speech / language  Attention /ability to follow direction  Orientation  Cross strength on all 4 extremities
  • 39. 1. If blood pressure is too low [90/60],hold the medication and inform for responsible physician 2. If reading is high ,take it twice and compare the number as order 3. If still high try different position sitting ,laying If consistence call for help 4. Preventing hypertensive crises  Severe headache  Severe anxiety  Nose bleeding  Shortness of breath
  • 40. Labile (paroxysmal) hypertension: • Marked elevations in blood pressure that are recurrent, sudden, and transient. • Labile hypertension is linked to sympathetic hyperstimulation, though the link is poorly understood. • Treatment is with adrenergic blocking agents (i.e., beta-blockers, alpha-blockers). Secondary hypertension: Resistant hypertension with an identifiable and potentially treatable etiology. Includes • RAS, primary hyperaldosteronism, • CKD, OSA, pheochromocytoma, Cushing syndrome, coarctation of the aorta. Treatment depends on the specific cause.
  • 41. Head trauma:  Complex cascade of neurohormonal factors resulting from a traumatic brain injury can cause severe hypertension.  This cascade likely represents compensatory mechanisms to maintain cerebral perfusion in the setting of increased intracranial pressure.  The balance between maintenance of cerebral perfusion and prevention of cerebrovascular events makes treatment of elevated blood pressure with head trauma controversial.
  • 42. Hypertensive encephalopathy: • Dramatic change in the level of consciousness, cognition, or personality in the setting of severe hypertension and attributable to cerebral edema. • Management includes aggressive but careful lowering of the blood pressure and immediate neurologic/neurosurgical consultation to avoid or minimize cerebrovascular events and/or permanent brain damage. Hypertensive retinopathy: • Characterized by retinal hemorrhages, exudates, and papilledema in the setting of severe hypertension. • Management consists of aggressive but careful lowering of the blood pressure and immediate ophthalmologic consultation to avoid or minimize vision loss.
  • 43. Hypertensive heart disease:  Cardiomyopathy is directly attributable to the physiologic compensations the myocardium must make to maintain cardiac output in the face of chronically elevated afterload and may result in: oSystolic dysfunction, oDiastolic dysfunction, oValvular dysfunction, oIncreased arrhythmogenic potential, and oMyocardial ischemia (even with normal coronary arteries).  Management consists of blood pressure optimization and prevention of heart failure, arrhythmia, and ischemia
  • 44. Hypertensive nephropathy: • Progressive nephrosclerosis involving the renal vasculature, glomeruli, and tubule- interstitial elements in the setting of uncontrolled hypertension. • The long-term result is progressive loss of kidney function ultimately manifesting as end- stage renal disease that may require hemodialysis. Obstetric hypertensive  Gestational hypertension, preeclampsia, eclampsia, and HELLP syndrome are the obstetric complications of pregnancy that can pose health risks to the mother and fetus.  Management includes control of blood pressure and delivery of the fetus.
  • 45.  Defined as a blood pressure (BP) of ≥130/80 mm Hg.  Significantly elevated BP (≥ 180 mm Hg systolic and/or ≥ 120 mm Hg diastolic) carries a substantial risk of morbidity and mortality.  Despite the prolonged presence of hypertension, there may be no signs or symptoms of end-organ damage (e.g., brain, eyes, heart, kidneys) until function becomes decompensated or severely impaired.
  • 46. Individuals may present with clinical symptoms such as:  Chest pain due to MI or focal neurologic changes associated with a cerebral infarction or intracranial hemorrhage.  Diagnosis is made using serial blood pressure measurements and testing for end-organ damage.  Management includes lowering the blood pressure and treating specific organ damage.
  • 47.  Varon, J., Elliot, W. (2020). Management of severe asymptomatic hypertension (hypertensive urgencies) in adults. UpToDate. Retrieved July 10, 2021, from https://www.uptodate.com/contents/management-of-severe-asymptomatic-hypertension- hypertensive-urgencies-in-adults  Varon, J., Elliot, W. (2021). Evaluation and treatment of hypertensive emergencies in adults. UpToDate. Retrieved July 10, 2021, from https://www.uptodate.com/contents/evaluation-and- treatment-of-hypertensive-emergencies-in-adults  Townsend, R. (2020). Definition, risk factors, and evaluation of resistant hypertension. UpToDate. Retrieved July 10, 2021, from https://www.uptodate.com/contents/definition-risk-factors-and- evaluation-of-resistant-hypertension