This document provides information on hypertensive emergencies and urgencies, including their classification, evaluation, and management. It defines hypertensive emergencies as severe hypertension with evidence of acute target organ damage, while urgencies involve severe hypertension without organ damage. For emergencies, rapid parenteral treatment is needed to stop organ damage progression while avoiding hypoperfusion. Several parenteral agents are discussed for specific conditions along with their dosing and side effects. The goal is to lower blood pressure gradually to avoid complications. Hypertensive urgencies can often be treated orally as outpatients after initial control.
The presentation covers definitions, identification, Treatment goals, Special situations, Practice points, and cardinal pharmacotherapy. Session presented in NBE learning session
The presentation covers definitions, identification, Treatment goals, Special situations, Practice points, and cardinal pharmacotherapy. Session presented in NBE learning session
This is a comprehensive approach to a hypertensive patient presenting to the emergency department.
Discussing:-
- Hypertensive emergency
- Hypertensive Urgency
- Hypertensive Crisis
- Hypertensive encephalopathy and retinopathy
- Accelerated Hypertension
- Malignant hypertension
Management of hypertensive condition in 2020 according to AHA/ASA guidelines. We will discuss the presentation, clinical assessment, investigations, and management of hypertension along with major randomized controlled trials and guidelines.
Severe hypertension that is a potentially life-threatening condition refers to a hypertensive crisis.
Severe hypertension is further classified into hypertensive emergencies or hypertensive urgencies.
Hypertensive emergency refers to a severe hypertension that is associated with new or progressive end-organ damage. In these clinical situations, blood pressure should be reduced immediately to prevent or minimize organ dysfunction.
Hypertensive urgency refers to severe hypertension without evidence of new or worsening end-organ injury.
A hypertensive emergency is hypertension with acute impairment of one or more
organ systems that can result in irreversible organ damage. Especially:-
Central nervous system
Cardiovascular system
Renal system.
The term hypertensive emergency is primarily used as a specific term for a hypertensive crisis with a diastolic blood pressure greater than or equal to 120mmHg and/or systolic blood pressure greater than or equal to 180mmHg.
Hypertensive emergency differs from hypertensive crisis in that, in the former, there is evidence of acute organ damage.
This is a comprehensive approach to a hypertensive patient presenting to the emergency department.
Discussing:-
- Hypertensive emergency
- Hypertensive Urgency
- Hypertensive Crisis
- Hypertensive encephalopathy and retinopathy
- Accelerated Hypertension
- Malignant hypertension
Management of hypertensive condition in 2020 according to AHA/ASA guidelines. We will discuss the presentation, clinical assessment, investigations, and management of hypertension along with major randomized controlled trials and guidelines.
Severe hypertension that is a potentially life-threatening condition refers to a hypertensive crisis.
Severe hypertension is further classified into hypertensive emergencies or hypertensive urgencies.
Hypertensive emergency refers to a severe hypertension that is associated with new or progressive end-organ damage. In these clinical situations, blood pressure should be reduced immediately to prevent or minimize organ dysfunction.
Hypertensive urgency refers to severe hypertension without evidence of new or worsening end-organ injury.
A hypertensive emergency is hypertension with acute impairment of one or more
organ systems that can result in irreversible organ damage. Especially:-
Central nervous system
Cardiovascular system
Renal system.
The term hypertensive emergency is primarily used as a specific term for a hypertensive crisis with a diastolic blood pressure greater than or equal to 120mmHg and/or systolic blood pressure greater than or equal to 180mmHg.
Hypertensive emergency differs from hypertensive crisis in that, in the former, there is evidence of acute organ damage.
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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
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
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.
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.
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
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,
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?
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
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
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