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Hypertensive Emergencies
Muhammad Asim Rana
MBBS, MRCP, SF-CCM, EDIC, FCCP

Department of Critical Care Medicine
King Saud Medical City
Riyadh Saudi Arabia
Classification of Blood Pressure
Category

Systolic BP (mmHg) DiastolicBP(mmHg)

Blood Pressure
Optimal

< 120 and

< 80

Normal

120- 129 &/or

< 85

High Normal*

130-139 &/or

85-89

Grade 1 (mild)

140-159 &/or

90-99

Grade 2 (moderate)

160-179 &/or

100-109

Hypertension

Grade 3 (severe)

≥ 180

≥ 109

Grade 1

140-149

< 90

Grade 2

≥ 160

< 90

Isolated Systolic
Hypertension

* Equivalent to pre-hypertension
Hypertensive Crisis

Severe elevation in blood pressure that have the
potential to cause target organ damage.
Target organs are
Heart
Vasculature
Kidneys
Eyes
Brain

These include
emergencies
&
urgencies
Hypertensive Urgency
Severe elevation in blood pressure

without
evidence of acute & ongoing target
organ damage.
Hypertensive Emergency
Severe elevation in blood pressure

with
Hypertensive Encephalopathy
evidence of acute & ongoing target
A hypertensive emergency characterized by
organ damage.
Accelerated Malignant Hypertension
irritability, headaches & mental status
A hypertensive by significant and often
changes causedemergency characterized by
fundoscopic findings of pressure
rapid elevation in blood papilledema (KW
gr4) &/or acute retinal haemorrhages &
exudates (KW gr3)
Severe Hypertension
BP > 180/120 mm Hg

Perform targeted, brief and often simultaneous
history & physical examination:
Identify patient characteristics that increase risk
for hypertensive emergency
Identify signs & symptoms of target organ damage
History & Examination
History
HOPI:
Symptoms of End Organ Damage?
CNS

Cardiac

Renal

Mental Status
Changes

Chest pain

Haematuria

Headaches

SOB/DOE

↓ Urine output

Weakness/ Vision
changes

Orthopnea

PMH:
Hx of HTN
Hx of CNS, Cardiac, Renal disease
Ob/Gyn Hx
Medications:
Anti HTN Rx dose changes, compliance
MAO inhibitors, OTC’s, Herbal
Social/Family Hx:
Cocaine, Amphetamine, illicit drug abuse
Family Hx of Cardiac, Aortic disease

Physical Examination
Vital signs:
BP in both arms and
legs,↑HR,↓SaO2
General:
Agitation, Anxiety, Restlessness
Fundoscopic:
Papilledema, Haemorrhage,
Exudates
Cardiovascular:
S3,S4, Diastolic murmur of AR,
Peripheral Edema,
↑JVP, Arterial bruits, Pulse deficit
Pulmonary:
Crackles/rales
Neurological:
Mental Status changes, Focal
neurological deficit
Urgent Investigations in severe hypertension
• Blood glucose
• Sodium, potassium and creatinine (check daily)
• Full blood count
• Plasma renin/aldosterone (for later analysis)
• Urine stick test and microscopy
• Ultrasound of kidneys and urinary tract
• Urinary catecholamine excretion
• Urinary free cortisol excretion if suspected Cushing
syndrome
• Chest X-ray
• ECG
Evidence of Acute Ongoing Target Organ Damage

NO

YES

Evidence of Acute Ongoing Target Organ
Damage
Hypertensive Urgency
Initiate oral hypertensive therapy based on medical
comorbidities and home medications.
Determine level of monitoring required based on clinical
substrate & availability of close outpatients follow-up.

Most patients can be managed as outpatients with goal
of lowering MAP by 20% in 1-2 days with further
reduction to goal ambulatory levels in weeks.
OPD follow-up should be arranged within 48-72 hrs to
encourage compliance & to emphasize need for long
term BP control to lower CV risk.
If the answer of your examination is

YES
Hypertensive Emergency
General Goals:
Stop progression of Target Organ Damage
Avoid organ hypoperfusion during treatment
Points of emphasis:
Parenteral therapy should be initiated immediately

Further diagnostic testing should not delay Rx
ICU admission & intra-arterial BP monitoring is
preferred
Management Pearls
In general, one should aim to lower the BP by no
more than 20% within minutes to an hour.
Over the next 2-6 hours, one should aim for a goal BP of
approximately 160/110 mmHg if initial reduction was well
tolerated.

The parenteral agents used should be chosen
based on the specific hypertensive syndromes
Begin to plan oral regimen based on medical
comorbidities & home medications.
Management Pearls
Start weaning parenteral agents and
institute appropriate oral therapy once
BP is controlled for 24-48 hours &
autoregulation is reestablished.

After acute Rx has begun, consider
initiating workup of secondary causes
hypertension in appropriate patients.
Syndrome Specific Hypertension management

Hypertensive Encephalopathy

Aortic Dissection

Accelerated malignant hypertension
Pre-eclampsia/Eclampsia

Ischaemic Stroke

cardiac
Renal
Catecholamine excess

Intracerebral haemorrhage
Subarachnoid haemorrhage
Hypertensive Encephalopathy
Autoregulation of CBF fails at critically elevated BP
levels leading to cerebral hyperperfusion & edema
Variable symptoms
Agitation
Restlessness
Fatigue
Headaches
Nausea &
vomiting
Overt delirium
Encephalopathy

CT Brain is indicated in all patients
MS changes & neurological deficits
Management Pearls
Reduce MAP no more than 20-25% in minutes
to an hour then to 160/110 over next 5 hours
if tolerated

Sodium nitroprusside is traditionally used
Other options are:
Labetalol
Fenoldopam
Nicardipine
Accelerated Malignant Hypertension
Symptoms include headaches, nausea & vomiting,
vision changes
Fundoscopic: haemorrhages, exudates, papilledema
May be accompanied by renal, neurological
impairment
Management Pearls

Sodium Nitroprusside
Reduce MAP by 20-25% in first hour then to 160/110
over next 5 hours if tolerated
Cardiac Patient with severe HTN
Unstable angina
Myocardial ischemia
Myocardial infarction
LV failure, acute pulm edema

Dietary indiscretion
Rx compliance
Hx of CAD, CHF

History
Chest pain
SOB/DOE
Orthopnea
PND
Diaphoresis
Cardiac risk factors
DM
HTN
Smoking
High cholestrol
Age
Physical Examination
↑HR, ↑RR, ↑JVP
S3, S4, displaced apex, ↓SaO2
Crackles, rales, peripheral edema

Diagnostic studies
↑Cardiac enzymes, ↑BNP,
Dynamic ST-T changes in ECG
CXR showing cardiomegaly, pulm edema
Management Pearls

NTG IV titrated to symptoms relief
Add beta blockers to all except
acute LV failure
(hold until compensated/euvolumic)

Add loop diuretics if in pulmonary edema
ACEI should be initiated unless contraindicated
Renal patient with severe HTN
Acute renal failure
Acute glomerulonephritis
Scleroderma renal crisis
Renal artery stenosis
Renal transplant rejection

Dietary indiscretion
Rx compliance
Hx of CAD, CHF

History:
Haematuria
↓ urine output
Recent URI
Hx of CRF,
Renal
transplant
Hx of meds like
ACEI, NSAIDS,
Cyclosporin,
Physical Examination
Skin findings of scleroderma
Abdominal bruits
Gross haematuria

Diagnostic studies
Urine analysis: RBCs,proteins,casts
↑ creatinine
Management Pearls

Previous creatinine levels are vital
Nicardipine or Fenoldopam
Fenoldopam to SNP:
improves natriuresis, diuresis and CrCl
(SNP- renal- caution cyanide toxicity)

Goals:↓MAP by 10-20% in one hour then
another 10% in next 5 hours

Haemodialysis if necessary
Scleroderma renal crisis must include ACEI
Catecholamine Excess
Pheochromocytoma
Tyramine ingestion with MAOI
Cocaine, amphetamines
Rebound HTN

Dietary indiscretion
Rx compliance
Drugs Hx is vital

History:
Headaches, sweating,
palpitations
Hx of
depression/MAOI use
with dietary
indiscretion
Anti HTN medications:
clonidine, beta
blockers, compliance?
Illicit drug use?
Physical Examination
↑HR
Hyperhydrosis
Restless, agitated, anxious
Café-au-lait spots, port wine stains, neurofibromas

Diagnostic studies
Urine/serum toxicology
Serum catecholamine
Urinary metanephrines
Management Pearls
Pheo/MAOI/Cocaine: α blocker (phentolamine)
+/- β blocker (after α blocker started)

Also BZD’s useful in cocaine intoxication.
Rebound HTN: Typically from clonidine or β blocker
withdrawl so reinstituting a single dose of withdrawn med
usually sufficient to abate crisis
If above stategies yield little response,

alternative therapies:

Sodium nitroprusside & labetalol
Aortic Dissection
Management Pearls
Minimize shear stress
Decrease dP/dt
Goal: MAP 60-75 mmHg HR 60-70 bpm
Beta blockers +/- SNP
Preeclampsia/Eclampsia
Management Pearls
Definitive Rx: Delivery
Hydralazine, labetalol, methyldopa
IV MgSO4
I.V. 4-5 g infusion; followed by a 1-2 g/hour
continuous infusion; or may follow with I.M. doses of
4-5 g in each buttock every 4 hours; maximum: 40
g/24 hour
Intracerebral Haemorrhage

MAP={SBP+2ХDBP}/3

Lower MAP by ~15%
with IV hydralazine,
labetalol, nicardipine

Risk of EOD?

Lower BP cautiously

NO Rx
Sodium of Emphasis
Points nitroprusside
•Potent arterial and venous dilator with rapid onset &
DOSE
offset of effect.
Initial 0.2 -0.50 mcg/kg/min continuous infusion
•Preferred agent for most HTN emergencies
Maintainance: Titrate
Onset/Duration to goal BP upto 8-10in aortic dissection
•Use with beta blockers if used
mcg/kg/mint
•Administer continuous IV under monitoring
Onset : Seconds
•Caution in Renal and Hepatic patients
Duration: 2-3 minutes after infusion is
Adverse Effects
•Signs of toxicity: met acidosis, tremors, seizures, nausea &
stopped
vomiting
Thyocyanate & Cyanide poisoning
•Avoid prolonged Vomiting
Nausea use
•Thyocyanate levels more than 10 mg% should be avoided
Hypotension
Points of Emphasis
Labetalol

DOSE

•Combined alpha & beta adrenergic blocker
Bolus: 20 mg x 1, then 20-80 mg q 10 min
•Can be given as IV300 mg or IV infusion
Onset/Duration dose boluses
Maximum
•Excessive BP drops are unusual
Infusion: 0.5-2 mg/min
•Useful inOnset : 5-10 min
most hypertensive emergencies except
Adverse Effects
Duration: 3-6 hrs after Failure stopped
Congestive Heartinfusion is & severe asthma
•Commonly used agent along with hydralazine in
Bradycardia, HF, HB,
HTN in pregnancy Bronchospasm
Nausea, Vomiting, Flushing
Points of Emphasis
Nitroglycerine

DOSE

•Similar to SNP, but causes mostly venodialatation
& modestly arteriolar dialatation effects at higher
Initial: 5mcg/min
Onset/Duration
Maintenance: titrate q 3-5 min upto
doses
100mcg/minute
•Most useful in: 2-5 min
Onset emergencies complicated by
Duration: 5-15 minutes after infusion is
cardiac compromise like MI, LVF & Pulmonary
Adverse Effects
stopped
Edema
•Also indicated in Rx of post-op HTN in CABG
Tolerance, Headaches, Nausea,
•Tolerance will develop with prolonged use
Hypotension, methemoglobinemia
Points of Emphasis
Hydralazine

DOSE

•Direct arteriolar vasodilator with no significant
Bolus 10-20 mg q 30 minutes until goal BP
Onset/Duration
venous effect
acheived
•Caution in patients with CAD & Aortic dissection!
Onset : 10-30 min
•Avoid in patients with high ICP
Duration: 2-4
Adverse Effects hours
•BP lowering response is less predictable than with
other agents
Hypotension, Tachycardia, Flushing
Points of Emphasis
Fenoldopam

DOSE

•Selective peripheral dopamine-1 receptor agonist
Initial: 0.5 mcg/kg/min
Onset/Duration
Maintenance: titrate q 15 min, upto
causing primarily arterial vasodilation with rapid
0.6mcg/kg/min
onset & relatively short offset of effect
Onset : 3-5 min
•Shown to improvemins perfusion, so useful in
renal
Duration: 30
Adverse Effects
patients with renal impairment
•Contraindicated in patients with glaucoma
Headache, Tachycardia, Flushing
Lets’ Review
Treatment of HTN emergencies
has a simple goal

STOP
The complexity of management ofagent
The choiceprogression lies in:
The of the parenteral
The careful balance between BP control &
That have a rapid onset of action & a short
Target Organ Damage
organ hypoperfusion
half life, like ON-OFF or light switch
properties
I think its enough

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Hypertensive Emergencies & ICU

  • 1. Hypertensive Emergencies Muhammad Asim Rana MBBS, MRCP, SF-CCM, EDIC, FCCP Department of Critical Care Medicine King Saud Medical City Riyadh Saudi Arabia
  • 2.
  • 3. Classification of Blood Pressure Category Systolic BP (mmHg) DiastolicBP(mmHg) Blood Pressure Optimal < 120 and < 80 Normal 120- 129 &/or < 85 High Normal* 130-139 &/or 85-89 Grade 1 (mild) 140-159 &/or 90-99 Grade 2 (moderate) 160-179 &/or 100-109 Hypertension Grade 3 (severe) ≥ 180 ≥ 109 Grade 1 140-149 < 90 Grade 2 ≥ 160 < 90 Isolated Systolic Hypertension * Equivalent to pre-hypertension
  • 4. Hypertensive Crisis Severe elevation in blood pressure that have the potential to cause target organ damage. Target organs are Heart Vasculature Kidneys Eyes Brain These include emergencies & urgencies
  • 5. Hypertensive Urgency Severe elevation in blood pressure without evidence of acute & ongoing target organ damage.
  • 6. Hypertensive Emergency Severe elevation in blood pressure with Hypertensive Encephalopathy evidence of acute & ongoing target A hypertensive emergency characterized by organ damage. Accelerated Malignant Hypertension irritability, headaches & mental status A hypertensive by significant and often changes causedemergency characterized by fundoscopic findings of pressure rapid elevation in blood papilledema (KW gr4) &/or acute retinal haemorrhages & exudates (KW gr3)
  • 7. Severe Hypertension BP > 180/120 mm Hg Perform targeted, brief and often simultaneous history & physical examination: Identify patient characteristics that increase risk for hypertensive emergency Identify signs & symptoms of target organ damage
  • 8. History & Examination History HOPI: Symptoms of End Organ Damage? CNS Cardiac Renal Mental Status Changes Chest pain Haematuria Headaches SOB/DOE ↓ Urine output Weakness/ Vision changes Orthopnea PMH: Hx of HTN Hx of CNS, Cardiac, Renal disease Ob/Gyn Hx Medications: Anti HTN Rx dose changes, compliance MAO inhibitors, OTC’s, Herbal Social/Family Hx: Cocaine, Amphetamine, illicit drug abuse Family Hx of Cardiac, Aortic disease Physical Examination Vital signs: BP in both arms and legs,↑HR,↓SaO2 General: Agitation, Anxiety, Restlessness Fundoscopic: Papilledema, Haemorrhage, Exudates Cardiovascular: S3,S4, Diastolic murmur of AR, Peripheral Edema, ↑JVP, Arterial bruits, Pulse deficit Pulmonary: Crackles/rales Neurological: Mental Status changes, Focal neurological deficit
  • 9. Urgent Investigations in severe hypertension • Blood glucose • Sodium, potassium and creatinine (check daily) • Full blood count • Plasma renin/aldosterone (for later analysis) • Urine stick test and microscopy • Ultrasound of kidneys and urinary tract • Urinary catecholamine excretion • Urinary free cortisol excretion if suspected Cushing syndrome • Chest X-ray • ECG
  • 10. Evidence of Acute Ongoing Target Organ Damage NO YES Evidence of Acute Ongoing Target Organ Damage
  • 11. Hypertensive Urgency Initiate oral hypertensive therapy based on medical comorbidities and home medications. Determine level of monitoring required based on clinical substrate & availability of close outpatients follow-up. Most patients can be managed as outpatients with goal of lowering MAP by 20% in 1-2 days with further reduction to goal ambulatory levels in weeks. OPD follow-up should be arranged within 48-72 hrs to encourage compliance & to emphasize need for long term BP control to lower CV risk.
  • 12. If the answer of your examination is YES
  • 13. Hypertensive Emergency General Goals: Stop progression of Target Organ Damage Avoid organ hypoperfusion during treatment Points of emphasis: Parenteral therapy should be initiated immediately Further diagnostic testing should not delay Rx ICU admission & intra-arterial BP monitoring is preferred
  • 14. Management Pearls In general, one should aim to lower the BP by no more than 20% within minutes to an hour. Over the next 2-6 hours, one should aim for a goal BP of approximately 160/110 mmHg if initial reduction was well tolerated. The parenteral agents used should be chosen based on the specific hypertensive syndromes Begin to plan oral regimen based on medical comorbidities & home medications.
  • 15. Management Pearls Start weaning parenteral agents and institute appropriate oral therapy once BP is controlled for 24-48 hours & autoregulation is reestablished. After acute Rx has begun, consider initiating workup of secondary causes hypertension in appropriate patients.
  • 16. Syndrome Specific Hypertension management Hypertensive Encephalopathy Aortic Dissection Accelerated malignant hypertension Pre-eclampsia/Eclampsia Ischaemic Stroke cardiac Renal Catecholamine excess Intracerebral haemorrhage Subarachnoid haemorrhage
  • 17. Hypertensive Encephalopathy Autoregulation of CBF fails at critically elevated BP levels leading to cerebral hyperperfusion & edema Variable symptoms Agitation Restlessness Fatigue Headaches Nausea & vomiting Overt delirium Encephalopathy CT Brain is indicated in all patients MS changes & neurological deficits
  • 18. Management Pearls Reduce MAP no more than 20-25% in minutes to an hour then to 160/110 over next 5 hours if tolerated Sodium nitroprusside is traditionally used Other options are: Labetalol Fenoldopam Nicardipine
  • 19. Accelerated Malignant Hypertension Symptoms include headaches, nausea & vomiting, vision changes Fundoscopic: haemorrhages, exudates, papilledema May be accompanied by renal, neurological impairment Management Pearls Sodium Nitroprusside Reduce MAP by 20-25% in first hour then to 160/110 over next 5 hours if tolerated
  • 20. Cardiac Patient with severe HTN Unstable angina Myocardial ischemia Myocardial infarction LV failure, acute pulm edema Dietary indiscretion Rx compliance Hx of CAD, CHF History Chest pain SOB/DOE Orthopnea PND Diaphoresis Cardiac risk factors DM HTN Smoking High cholestrol Age
  • 21. Physical Examination ↑HR, ↑RR, ↑JVP S3, S4, displaced apex, ↓SaO2 Crackles, rales, peripheral edema Diagnostic studies ↑Cardiac enzymes, ↑BNP, Dynamic ST-T changes in ECG CXR showing cardiomegaly, pulm edema
  • 22. Management Pearls NTG IV titrated to symptoms relief Add beta blockers to all except acute LV failure (hold until compensated/euvolumic) Add loop diuretics if in pulmonary edema ACEI should be initiated unless contraindicated
  • 23. Renal patient with severe HTN Acute renal failure Acute glomerulonephritis Scleroderma renal crisis Renal artery stenosis Renal transplant rejection Dietary indiscretion Rx compliance Hx of CAD, CHF History: Haematuria ↓ urine output Recent URI Hx of CRF, Renal transplant Hx of meds like ACEI, NSAIDS, Cyclosporin,
  • 24. Physical Examination Skin findings of scleroderma Abdominal bruits Gross haematuria Diagnostic studies Urine analysis: RBCs,proteins,casts ↑ creatinine
  • 25. Management Pearls Previous creatinine levels are vital Nicardipine or Fenoldopam Fenoldopam to SNP: improves natriuresis, diuresis and CrCl (SNP- renal- caution cyanide toxicity) Goals:↓MAP by 10-20% in one hour then another 10% in next 5 hours Haemodialysis if necessary Scleroderma renal crisis must include ACEI
  • 26. Catecholamine Excess Pheochromocytoma Tyramine ingestion with MAOI Cocaine, amphetamines Rebound HTN Dietary indiscretion Rx compliance Drugs Hx is vital History: Headaches, sweating, palpitations Hx of depression/MAOI use with dietary indiscretion Anti HTN medications: clonidine, beta blockers, compliance? Illicit drug use?
  • 27. Physical Examination ↑HR Hyperhydrosis Restless, agitated, anxious Café-au-lait spots, port wine stains, neurofibromas Diagnostic studies Urine/serum toxicology Serum catecholamine Urinary metanephrines
  • 28. Management Pearls Pheo/MAOI/Cocaine: α blocker (phentolamine) +/- β blocker (after α blocker started) Also BZD’s useful in cocaine intoxication. Rebound HTN: Typically from clonidine or β blocker withdrawl so reinstituting a single dose of withdrawn med usually sufficient to abate crisis If above stategies yield little response, alternative therapies: Sodium nitroprusside & labetalol
  • 29. Aortic Dissection Management Pearls Minimize shear stress Decrease dP/dt Goal: MAP 60-75 mmHg HR 60-70 bpm Beta blockers +/- SNP
  • 30. Preeclampsia/Eclampsia Management Pearls Definitive Rx: Delivery Hydralazine, labetalol, methyldopa IV MgSO4 I.V. 4-5 g infusion; followed by a 1-2 g/hour continuous infusion; or may follow with I.M. doses of 4-5 g in each buttock every 4 hours; maximum: 40 g/24 hour
  • 31. Intracerebral Haemorrhage MAP={SBP+2ХDBP}/3 Lower MAP by ~15% with IV hydralazine, labetalol, nicardipine Risk of EOD? Lower BP cautiously NO Rx
  • 32. Sodium of Emphasis Points nitroprusside •Potent arterial and venous dilator with rapid onset & DOSE offset of effect. Initial 0.2 -0.50 mcg/kg/min continuous infusion •Preferred agent for most HTN emergencies Maintainance: Titrate Onset/Duration to goal BP upto 8-10in aortic dissection •Use with beta blockers if used mcg/kg/mint •Administer continuous IV under monitoring Onset : Seconds •Caution in Renal and Hepatic patients Duration: 2-3 minutes after infusion is Adverse Effects •Signs of toxicity: met acidosis, tremors, seizures, nausea & stopped vomiting Thyocyanate & Cyanide poisoning •Avoid prolonged Vomiting Nausea use •Thyocyanate levels more than 10 mg% should be avoided Hypotension
  • 33. Points of Emphasis Labetalol DOSE •Combined alpha & beta adrenergic blocker Bolus: 20 mg x 1, then 20-80 mg q 10 min •Can be given as IV300 mg or IV infusion Onset/Duration dose boluses Maximum •Excessive BP drops are unusual Infusion: 0.5-2 mg/min •Useful inOnset : 5-10 min most hypertensive emergencies except Adverse Effects Duration: 3-6 hrs after Failure stopped Congestive Heartinfusion is & severe asthma •Commonly used agent along with hydralazine in Bradycardia, HF, HB, HTN in pregnancy Bronchospasm Nausea, Vomiting, Flushing
  • 34. Points of Emphasis Nitroglycerine DOSE •Similar to SNP, but causes mostly venodialatation & modestly arteriolar dialatation effects at higher Initial: 5mcg/min Onset/Duration Maintenance: titrate q 3-5 min upto doses 100mcg/minute •Most useful in: 2-5 min Onset emergencies complicated by Duration: 5-15 minutes after infusion is cardiac compromise like MI, LVF & Pulmonary Adverse Effects stopped Edema •Also indicated in Rx of post-op HTN in CABG Tolerance, Headaches, Nausea, •Tolerance will develop with prolonged use Hypotension, methemoglobinemia
  • 35. Points of Emphasis Hydralazine DOSE •Direct arteriolar vasodilator with no significant Bolus 10-20 mg q 30 minutes until goal BP Onset/Duration venous effect acheived •Caution in patients with CAD & Aortic dissection! Onset : 10-30 min •Avoid in patients with high ICP Duration: 2-4 Adverse Effects hours •BP lowering response is less predictable than with other agents Hypotension, Tachycardia, Flushing
  • 36. Points of Emphasis Fenoldopam DOSE •Selective peripheral dopamine-1 receptor agonist Initial: 0.5 mcg/kg/min Onset/Duration Maintenance: titrate q 15 min, upto causing primarily arterial vasodilation with rapid 0.6mcg/kg/min onset & relatively short offset of effect Onset : 3-5 min •Shown to improvemins perfusion, so useful in renal Duration: 30 Adverse Effects patients with renal impairment •Contraindicated in patients with glaucoma Headache, Tachycardia, Flushing
  • 37. Lets’ Review Treatment of HTN emergencies has a simple goal STOP The complexity of management ofagent The choiceprogression lies in: The of the parenteral The careful balance between BP control & That have a rapid onset of action & a short Target Organ Damage organ hypoperfusion half life, like ON-OFF or light switch properties
  • 38. I think its enough