ACUTE SEVERE HYPERTENSION
DR NASIR MOHI UD DIN
DNB RESIDENT
HYPERTENSION
Hypertension is defined as systolic blood
pressure (SBP) of 140 mmHg or greater,
diastolic blood pressure (DBP) of
90 mmHg or greater, or taking antihypertensive
medication.
VI JNC, 1997
SBP-mmHg DBP-mmHg
NORMAL <120 AND<80
PREHYPERTENSION 120-139 or 80-89
STAGE 1 140-159 or 90-99
STAGE 2 >=160 >=100
HYPERTENSION(JNC-7class.)
BLOOD PRESURE MEASURING.
Incidence In India
• 25% of urban population and 10 % of rural
population suffer from hypertension
• 70% of all hypertensive patients are stage I
hypertension
• 12% of all hypertensive suffer from isolated
systolic hypertension
.Evaluation and management of acute severe hypertension
HYPERTENSIVE URGENCY
• Severely elevated arterial BP (SBP >180
and/or DBP >120 mm Hg) with nonspecific
complaints but without evidence of acute
target organ damage
• It has less serious prognosis than
hypertensive emergency in spite of severe
hypertension
• Most of the hypertensive crisis presentations
(75%) are hypertensive urgencies
HYPERTENSIVE EMERGENCY
• severe elevation of arterial BP (systolic >180
mm Hg and/or diastolic 110 to 120 ) and
evidence of acute target organ damage.
• life-threatening (mortality 20 % if untreated)
• requires immediate but careful intervention
• Hypertensive emergency is diagnosed if SBP is
>180 and/or DBP is >120 mm Hg and at least
one of the following clinical situations is
present
Presentation of hypertensive emergencies
• Ischemic stroke: 24%
Pulmonary edema: 22%
• Hypertensive encephalopathy: 16%
• Acute heart failure: 14%
• Acute myocardial infarction: 12%
• Intracerebral hemorrhage: 5%
• Dissecting aortic aneurysm:2%
• Subarachnoid hemorrhage
• Acute renal failure
• Eclampsia (SBP > 170, DBP > 110 mm Hg): 5%
Symptoms of hypertensive emergencies and urgencies
Hypertensive Urgencies Hypertensive Emergencies
Headache 22% Chest Pain 27%
Epistaxis 17% Dyspnea 22%
Somnolence 9% Neurological deficits 21%
Chest Pain 9% Somnolence 10%
Dyspnea 9% Paraesthesia 8%
Neurological deficit 7% Nausea ,Vomiting, Dizziness, Headache,
12%
Auto regulation of cerebral blood flow
• -In normotensive individuals cerebral perfusion
remains constant in spite of fluctuation of mean
arterial pressure (MAP) between 60 and 130mm Hg
• -In hypertensive individuals there is a shift to the
right in the cerebral auto regulation curve: the
cerebral perfusion remains constant at higher
range (between MAP 80 and 160 mm Hg)
.
Pathogenesis
• Following diseases represent the most
common underlying causes of hypertensive
emergencies:
• Essential hypertension: 90%
• Renal hypertension
• Malignant hypertension.
• Phaeochromocytoma
• Pre eclampsia
• Cerebrovascular disease
PHYSICAL
• Use an approach based on organ systems to identify
signs of end-organ damage
-CNS: focal neuro deficits , seizures ,stupor, coma,
papilledema, hemorrhages, exudates, or evidence of
closed-angle glaucoma
-CVS: JVD , lung auscultaion for crackles , peripheral
edema , extra heart sounds, equal and symmetric BP
and pulses bilaterally.
-Check for abdominal masses and bruits.
Work-up
• 1. Short history and physical examination
• 2. Repeated measurement of BP to confirm
severe elevation of BP
• 3. ECG
• 4. Chest X-ray
• 5. Funduscopy
Contd
• 6. Lab: serum elecrtolytes, creatinine, urea,
urinalysis, CBC, troponin and CK-MB if needed
• 7. Abdominal U/S: if dissecting aortic
aneurysm is suspected
• 8. Echocardiography if needed
• 9. CT scan of the brain: if neurological deficit is
present
Treatment strategy
• sometimes immediate treatment is needed before
diagnostic tests are completed or before laboratory
results are available! but top priority:
• Primum nihil nocere (Hippocrates)
First do no harm
An important point to remember in the management
of the patient with any degree of BP elevation is to
“ treat the patient and not the number
Treatment of hypertensive urgencies:
• -immediate therapy: gradual lowering of elevated
BP within 24 hours to avoid the development of
serious complications
• -controlled lowering of elevated BP (reduction of
mean arterial pressure by 25%, aim DBP 100 -110 mm
Hg) to avoid sudden drop of BP and cerebral hypo
perfusion
• -outpatient treatment is possible
ORAL DRUGS
DRUG DOSAGE ADV. EFF.
CAPTOPRIL
(ACE inhibitor)
6.25-25MG q 6hrs. Hypotension in high renin
states
CLONIDINE
(a2 agonist-
centrally acting)
0.1-0.2 mg PO
initially then 0.1mg
hrly, Upto max
0.8mg in 24hrs.
Sedation, bradycardia , dry
mouth
NIFEDIPINE
(CCB)
10 mg PO
Repeated after 30
mins
Headache, Flushing
edema, dizziness , nausea
Treatment of Hypertensive Emergencies
• a. General guidelines:
-immediate therapy: prompt lowering of
elevated BP within 30 min.to avoid and
limit the risk of serious complications
(cerebral hyper perfusion, perivascular
edema, increased ICP)
Contd
• -controlled lowering of elevated BP to a safer
noncritical level but not to normal range
(reduction of mean arterial pressure by 25%,
• Aim SBP 160-170, aim DBP 100-110mm Hg) to
avoid sudden drop of BP and reduction of
cerebral perfusion and development of brain
infarction.
Medical treatment
• -The medical treatment of hypertensive
emergencies depends on the clinical
presentation
• -No treatment should be started without
clinical evaluation
• -Clinical evaluation should be performed
without delay
DRUGS
• Once the diagnosis of hypertension is made
and end-organ damage confirmed,the BP
should be lowered by about 25% of the mean
arterial pressure.
• There are 2 main classes of drugs:
-Vasodilators
-Adrenergic inhibitors
VASODILATORS
DRUG DOSAGE ADV.EFFE
Nitroprusside
(directly acting
vasodilator)
0.25-10mcg/kg/min Thiocyanate,cyanide
poisoning
Nitroglycerine 0.25 – 5mcg/kg/min
iv infusion
Flushing,headache,methemo
globin
Nicardipine
(CCB)
5mg/hr iv infusion
increased by 1-2 mg
every 15 min upto
15mg/hr
Tachycardia,flushing.avoid-heart
failure
Hydralazine
(DAV)
10-20mg iv bolus Flushing,tachy,avoid-A.diss,MI
Enalapril
(ACE Inhibitor)
10-40mg IM,1.25-
5MG iVq6hr
Hypotension,renal
failure,hyperkalemia
Fenoldopam 0.1-0.3mcg/kg/min Flushing,headache,tachy
DRUG DOSAGE ADV.EFF
Labetalol
(a+b blocker)
20-80mgiv bolus every
10 min,2mg.min iv
infusion
Heart block,ortho
hypotension.avoid-heart
failure,asthma
Esmolol
(b-1 selective
blocker)
200-500 mcg/kg/min for
4min,then 150-
300mcg/kg/min
Hypotension,avoid-heart
failure,asthma
Phentolamine
(a1 blocker)
5-15mg iv Tachycardia,flushing,headache
ADRENERGIC INHIBITORS
Differential
-Steroid use
-Use of over-the-counter or recreational
sympathomimetic drugs
-Pheochromocytoma
-Acute vasculitis
-Serotonin syndrome
-Other CNS pathology
-Coarctation of the aorta
RAPID BP REDUCTION
– Acute myocardial ischemia :IV NTG, b-blockers ,
ACE inhibitors.
• CHF with pulmonary edema :iv NTG, furosemide,
morphine.
• Acute aortic dissection : iv nitroprusside + b-blockers
or iv trimethaphan + b-blockers.
• Hypertensive encephalopathy or sub-arachnoid
hemorrhage :iv nitroprusside , labetalol or
nimodipine .
• MAO- tyramine interactions with acute hypertension
: iv phentolamine.
Specific Treatment
• AORTIC DISSECTION: Immediate reduction. In BP and mainly ,
shear stress(change in BP with change in time) is essential to
limit the extension of damage as surgery is being considered .
Eliminate pain and reduce systolic BP to 100-120 or lowest
level that permits perfusion . BP reduction should proceed
with reduction in force of LV contraction. Labetalol or
nitroprusside + b-blocker like propranolol agents of choice.
• MI: NTG, b-blockers , ACE inhibitors.
• ACUTE LVF: usually associated with pulmonary edema and
diastolic/systolic dysfunction. IV nitroprusside , NTG agents of
choice . Titrate until BP controlled and signs of heart failure
alleviated.
• RENAL INSUFFICIENCY: is a cause and effect of high BP . Goal
is to prevent further renal damage by maintaining adequate
blood flow . Nitroprusside effective.
Pre-eclampsia/ Eclampsia
• Preeclampsia
– mild = 140/90 with proteinuria
– severe = 160/110, 5 gm protein, Sx
• "Standard" therapy is hydralazine
• Other agents: Nifedipine , labetalol,
methyldopa
• Nitroprusside (risk of fetal CN toxicity)
• Additional measures: MgSO4; Delivery
FOLLOW-UP
• The Joint National Committee on High Blood Pressure has
published a series of recommendations for appropriate
follow-up, assuming no end-organ damage.
-For a systolic BP 140-159 mm Hg/diastolic 90-99 mm Hg,
confirm BP within 2 months.
-For systolic BP 160-179 mm Hg/diastolic 100-109 mm Hg,
evaluate within a month.
- For systolic BP 180-209 mm Hg/diastolic 110-119 mm Hg,
evaluate within a week.
-For systolic BP greater than 210 mm Hg/diastolic greater than
120 mm Hg, evaluate immediately.
Conclusions
• -Hypertensive Emergencies and Urgencies are clinical
presentations associated with severe elevation of BP which
needs to be lowered immediately or gradually to prevent
brain edema and increase in ICP but controlled(aim SBP 160,
aim DBP 110 mm Hg) to avoid sudden drop of BP and
reduction in cerebral perfusion
• -Differential diagnosis should be considered before starting
possible harmful treatment
• -medical treatment should be started according to the
clinical presentation
THANK YOU
FOR
YOUR ATTENTION

HypertenEmerg.ppt

  • 1.
    ACUTE SEVERE HYPERTENSION DRNASIR MOHI UD DIN DNB RESIDENT
  • 2.
    HYPERTENSION Hypertension is definedas systolic blood pressure (SBP) of 140 mmHg or greater, diastolic blood pressure (DBP) of 90 mmHg or greater, or taking antihypertensive medication. VI JNC, 1997
  • 3.
    SBP-mmHg DBP-mmHg NORMAL <120AND<80 PREHYPERTENSION 120-139 or 80-89 STAGE 1 140-159 or 90-99 STAGE 2 >=160 >=100 HYPERTENSION(JNC-7class.)
  • 4.
  • 5.
    Incidence In India •25% of urban population and 10 % of rural population suffer from hypertension • 70% of all hypertensive patients are stage I hypertension • 12% of all hypertensive suffer from isolated systolic hypertension
  • 6.
    .Evaluation and managementof acute severe hypertension
  • 7.
    HYPERTENSIVE URGENCY • Severelyelevated arterial BP (SBP >180 and/or DBP >120 mm Hg) with nonspecific complaints but without evidence of acute target organ damage • It has less serious prognosis than hypertensive emergency in spite of severe hypertension • Most of the hypertensive crisis presentations (75%) are hypertensive urgencies
  • 8.
    HYPERTENSIVE EMERGENCY • severeelevation of arterial BP (systolic >180 mm Hg and/or diastolic 110 to 120 ) and evidence of acute target organ damage. • life-threatening (mortality 20 % if untreated) • requires immediate but careful intervention • Hypertensive emergency is diagnosed if SBP is >180 and/or DBP is >120 mm Hg and at least one of the following clinical situations is present
  • 9.
    Presentation of hypertensiveemergencies • Ischemic stroke: 24% Pulmonary edema: 22% • Hypertensive encephalopathy: 16% • Acute heart failure: 14% • Acute myocardial infarction: 12% • Intracerebral hemorrhage: 5% • Dissecting aortic aneurysm:2% • Subarachnoid hemorrhage • Acute renal failure • Eclampsia (SBP > 170, DBP > 110 mm Hg): 5%
  • 10.
    Symptoms of hypertensiveemergencies and urgencies Hypertensive Urgencies Hypertensive Emergencies Headache 22% Chest Pain 27% Epistaxis 17% Dyspnea 22% Somnolence 9% Neurological deficits 21% Chest Pain 9% Somnolence 10% Dyspnea 9% Paraesthesia 8% Neurological deficit 7% Nausea ,Vomiting, Dizziness, Headache, 12%
  • 11.
    Auto regulation ofcerebral blood flow • -In normotensive individuals cerebral perfusion remains constant in spite of fluctuation of mean arterial pressure (MAP) between 60 and 130mm Hg • -In hypertensive individuals there is a shift to the right in the cerebral auto regulation curve: the cerebral perfusion remains constant at higher range (between MAP 80 and 160 mm Hg)
  • 12.
  • 13.
    Pathogenesis • Following diseasesrepresent the most common underlying causes of hypertensive emergencies: • Essential hypertension: 90% • Renal hypertension • Malignant hypertension. • Phaeochromocytoma • Pre eclampsia • Cerebrovascular disease
  • 14.
    PHYSICAL • Use anapproach based on organ systems to identify signs of end-organ damage -CNS: focal neuro deficits , seizures ,stupor, coma, papilledema, hemorrhages, exudates, or evidence of closed-angle glaucoma -CVS: JVD , lung auscultaion for crackles , peripheral edema , extra heart sounds, equal and symmetric BP and pulses bilaterally. -Check for abdominal masses and bruits.
  • 15.
    Work-up • 1. Shorthistory and physical examination • 2. Repeated measurement of BP to confirm severe elevation of BP • 3. ECG • 4. Chest X-ray • 5. Funduscopy
  • 16.
    Contd • 6. Lab:serum elecrtolytes, creatinine, urea, urinalysis, CBC, troponin and CK-MB if needed • 7. Abdominal U/S: if dissecting aortic aneurysm is suspected • 8. Echocardiography if needed • 9. CT scan of the brain: if neurological deficit is present
  • 17.
    Treatment strategy • sometimesimmediate treatment is needed before diagnostic tests are completed or before laboratory results are available! but top priority: • Primum nihil nocere (Hippocrates) First do no harm An important point to remember in the management of the patient with any degree of BP elevation is to “ treat the patient and not the number
  • 18.
    Treatment of hypertensiveurgencies: • -immediate therapy: gradual lowering of elevated BP within 24 hours to avoid the development of serious complications • -controlled lowering of elevated BP (reduction of mean arterial pressure by 25%, aim DBP 100 -110 mm Hg) to avoid sudden drop of BP and cerebral hypo perfusion • -outpatient treatment is possible
  • 19.
    ORAL DRUGS DRUG DOSAGEADV. EFF. CAPTOPRIL (ACE inhibitor) 6.25-25MG q 6hrs. Hypotension in high renin states CLONIDINE (a2 agonist- centrally acting) 0.1-0.2 mg PO initially then 0.1mg hrly, Upto max 0.8mg in 24hrs. Sedation, bradycardia , dry mouth NIFEDIPINE (CCB) 10 mg PO Repeated after 30 mins Headache, Flushing edema, dizziness , nausea
  • 20.
    Treatment of HypertensiveEmergencies • a. General guidelines: -immediate therapy: prompt lowering of elevated BP within 30 min.to avoid and limit the risk of serious complications (cerebral hyper perfusion, perivascular edema, increased ICP)
  • 21.
    Contd • -controlled loweringof elevated BP to a safer noncritical level but not to normal range (reduction of mean arterial pressure by 25%, • Aim SBP 160-170, aim DBP 100-110mm Hg) to avoid sudden drop of BP and reduction of cerebral perfusion and development of brain infarction.
  • 22.
    Medical treatment • -Themedical treatment of hypertensive emergencies depends on the clinical presentation • -No treatment should be started without clinical evaluation • -Clinical evaluation should be performed without delay
  • 23.
    DRUGS • Once thediagnosis of hypertension is made and end-organ damage confirmed,the BP should be lowered by about 25% of the mean arterial pressure. • There are 2 main classes of drugs: -Vasodilators -Adrenergic inhibitors
  • 24.
    VASODILATORS DRUG DOSAGE ADV.EFFE Nitroprusside (directlyacting vasodilator) 0.25-10mcg/kg/min Thiocyanate,cyanide poisoning Nitroglycerine 0.25 – 5mcg/kg/min iv infusion Flushing,headache,methemo globin Nicardipine (CCB) 5mg/hr iv infusion increased by 1-2 mg every 15 min upto 15mg/hr Tachycardia,flushing.avoid-heart failure Hydralazine (DAV) 10-20mg iv bolus Flushing,tachy,avoid-A.diss,MI Enalapril (ACE Inhibitor) 10-40mg IM,1.25- 5MG iVq6hr Hypotension,renal failure,hyperkalemia Fenoldopam 0.1-0.3mcg/kg/min Flushing,headache,tachy
  • 25.
    DRUG DOSAGE ADV.EFF Labetalol (a+bblocker) 20-80mgiv bolus every 10 min,2mg.min iv infusion Heart block,ortho hypotension.avoid-heart failure,asthma Esmolol (b-1 selective blocker) 200-500 mcg/kg/min for 4min,then 150- 300mcg/kg/min Hypotension,avoid-heart failure,asthma Phentolamine (a1 blocker) 5-15mg iv Tachycardia,flushing,headache ADRENERGIC INHIBITORS
  • 26.
    Differential -Steroid use -Use ofover-the-counter or recreational sympathomimetic drugs -Pheochromocytoma -Acute vasculitis -Serotonin syndrome -Other CNS pathology -Coarctation of the aorta
  • 27.
    RAPID BP REDUCTION –Acute myocardial ischemia :IV NTG, b-blockers , ACE inhibitors. • CHF with pulmonary edema :iv NTG, furosemide, morphine. • Acute aortic dissection : iv nitroprusside + b-blockers or iv trimethaphan + b-blockers. • Hypertensive encephalopathy or sub-arachnoid hemorrhage :iv nitroprusside , labetalol or nimodipine . • MAO- tyramine interactions with acute hypertension : iv phentolamine.
  • 28.
    Specific Treatment • AORTICDISSECTION: Immediate reduction. In BP and mainly , shear stress(change in BP with change in time) is essential to limit the extension of damage as surgery is being considered . Eliminate pain and reduce systolic BP to 100-120 or lowest level that permits perfusion . BP reduction should proceed with reduction in force of LV contraction. Labetalol or nitroprusside + b-blocker like propranolol agents of choice. • MI: NTG, b-blockers , ACE inhibitors. • ACUTE LVF: usually associated with pulmonary edema and diastolic/systolic dysfunction. IV nitroprusside , NTG agents of choice . Titrate until BP controlled and signs of heart failure alleviated. • RENAL INSUFFICIENCY: is a cause and effect of high BP . Goal is to prevent further renal damage by maintaining adequate blood flow . Nitroprusside effective.
  • 29.
    Pre-eclampsia/ Eclampsia • Preeclampsia –mild = 140/90 with proteinuria – severe = 160/110, 5 gm protein, Sx • "Standard" therapy is hydralazine • Other agents: Nifedipine , labetalol, methyldopa • Nitroprusside (risk of fetal CN toxicity) • Additional measures: MgSO4; Delivery
  • 30.
    FOLLOW-UP • The JointNational Committee on High Blood Pressure has published a series of recommendations for appropriate follow-up, assuming no end-organ damage. -For a systolic BP 140-159 mm Hg/diastolic 90-99 mm Hg, confirm BP within 2 months. -For systolic BP 160-179 mm Hg/diastolic 100-109 mm Hg, evaluate within a month. - For systolic BP 180-209 mm Hg/diastolic 110-119 mm Hg, evaluate within a week. -For systolic BP greater than 210 mm Hg/diastolic greater than 120 mm Hg, evaluate immediately.
  • 31.
    Conclusions • -Hypertensive Emergenciesand Urgencies are clinical presentations associated with severe elevation of BP which needs to be lowered immediately or gradually to prevent brain edema and increase in ICP but controlled(aim SBP 160, aim DBP 110 mm Hg) to avoid sudden drop of BP and reduction in cerebral perfusion • -Differential diagnosis should be considered before starting possible harmful treatment • -medical treatment should be started according to the clinical presentation
  • 32.