Hypertensive Emergencies
Department of Critical Care Medicine King Saud Medical City
Riyadh Saudi Arabia
Muhammad Asim Rana MBBS, MRCP, SF-CCM, EDIC, FCCP
HYPERTENSIVE CRISES
HYPERTENSIVEENCEPHALOPATHY
ACCELERATEDMALIGNANT
HYPERTENSION
HYPERTENSIVEEMERGENCY
HYPERTENSIVEURGENCY
Category Systolic BP (mmHg) DiastolicBP(mmHg)
Blood Pressure
Optimal < 120 and < 80
Normal 120- 129 &/or < 85
High Normal* 130-139 &/or 85-89
Hypertension
Grade 1 (mild) 140-159 &/or 90-99
Grade 2 (moderate) 160-179 &/or 100-109
Grade 3 (severe) ≥ 180 ≥ 109
Isolated Systolic HypertensionGrade 1 140-149 < 90
Grade 2 ≥ 160 < 90
* Equivalent to pre-hypertension
Classification of Blood Pressure
Hypertensive Crisis
Severe elevation in blood pressure that have the potential to cause target organ damage.
Target organs areHeartVasculatureKidneysEyesBrain
These include emergencies
& urgencies
Hypertensive Urgency
without evidence of acute & ongoing target organ damage.
Severe elevation in blood pressure
Hypertensive Emergency
withevidence of acute & ongoing target organ damage.
Severe elevation in blood pressure
Hypertensive EncephalopathyA hypertensive emergency characterized by irritability, headaches & mental status changes caused by significant and often rapid elevation in blood pressure
Accelerated Malignant HypertensionA hypertensive emergency characterized by fundoscopic findings of papilledema (KW gr4) &/or acute retinal haemorrhages & exudates (KW gr3)
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
Severe HypertensionBP > 180/120 mm Hg
History & Examination
HistoryHOPI: Symptoms of End Organ Damage?
PMH:Hx of HTNHx of CNS, Cardiac, Renal diseaseOb/Gyn HxMedications:Anti HTN Rx dose changes, complianceMAO inhibitors, OTC’s, HerbalSocial/Family Hx:Cocaine, Amphetamine, illicit drug abuse Family Hx of Cardiac, Aortic disease
Physical ExaminationVital 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
CNS Cardiac Renal
Mental Status Changes
Chest pain Haematuria
Headaches SOB/DOE ↓ Urine output
Weakness/ Vision changes
Orthopnea
• 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
Urgent Investigations in severe hypertension
Evidence of Acute Ongoing Target Organ Damage
YES NO
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
Stop progression of Target Organ DamageAvoid organ hypoperfusion during treatment
General Goals:
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.
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.
Management Pearls
Hypertensive Encephalopathy
Accelerated malignant hypertension
cardiac
Renal
Catecholamine excess
Aortic Dissection
Pre-eclampsia/Eclampsia
Ischaemic Stroke
Intracerebral haemorrhage
Subarachnoid haemorrhage
Syndrome Specific Hypertension management
Hypertensive Encephalopathy
Autoregulation of CBF fails at critically elevated BP levels leading to cerebral hyperperfusion & edema
Variable symptomsAgitationRestlessnessFatigueHeadachesNausea & vomitingOvert deliriumEncephalopathy
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:LabetalolFenoldopamNicardipine
Accelerated Malignant Hypertension
Symptoms include headaches, nausea & vomiting, vision changesFundoscopic: haemorrhages, exudates, papilledemaMay be accompanied by renal, neurological impairment
Sodium NitroprussideReduce MAP by 20-25% in first hour then to 160/110 over next 5 hours if tolerated
Management Pearls
Cardiac Patient with severe HTN
Unstable anginaMyocardial ischemiaMyocardial infarctionLV failure, acute pulm edema
HistoryChest painSOB/DOEOrthopneaPNDDiaphoresis
Cardiac risk factorsDMHTNSmokingHigh cholestrolAge
Dietary indiscretionRx complianceHx of CAD, CHF
↑HR, ↑RR, ↑JVPS3, S4, displaced apex, ↓SaO2
Crackles, rales, peripheral edema
↑Cardiac enzymes, ↑BNP, Dynamic ST-T changes in ECGCXR showing cardiomegaly, pulm edema
Physical Examination
Diagnostic studies
Management Pearls
NTG IV titrated to symptoms reliefAdd 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 failureAcute glomerulonephritisScleroderma renal crisisRenal artery stenosisRenal transplant rejection
History:Haematuria↓ urine outputRecent URIHx of CRF, Renal transplantHx of meds like ACEI, NSAIDS, Cyclosporin,
Dietary indiscretionRx complianceHx of CAD, CHF
Skin findings of sclerodermaAbdominal bruitsGross haematuria
Urine analysis: RBCs,proteins,casts ↑ creatinine
Physical Examination
Diagnostic studies
Management Pearls
Previous creatinine levels are vital Nicardipine or FenoldopamFenoldopam 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 necessaryScleroderma renal crisis must include ACEI
Catecholamine Excess
Pheochromocytoma Tyramine ingestion with MAOICocaine, amphetaminesRebound HTN
History:Headaches, sweating, palpitationsHx of depression/MAOI use with dietary indiscretionAnti HTN medications: clonidine, beta blockers, compliance?Illicit drug use?
Dietary indiscretionRx complianceDrugs Hx is vital
↑HR Hyperhydrosis Restless, agitated, anxiousCafé-au-lait spots, port wine stains, neurofibromas
Urine/serum toxicologySerum catecholamineUrinary metanephrines
Physical Examination
Diagnostic studies
Management PearlsPheo/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 crisisIf above stategies yield little response, alternative therapies:
Sodium nitroprusside & labetalol
Minimize shear stressDecrease dP/dtGoal: MAP 60-75 mmHg HR 60-70 bpmBeta blockers +/- SNP
Aortic Dissection
Management Pearls
Definitive Rx: DeliveryHydralazine, labetalol, methyldopa
Preeclampsia/Eclampsia
Management Pearls
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
MAP={SBP+2ХDBP}/3
Risk of EOD?
Lower BP cautiously NO Rx
Lower MAP by ~15% with IV hydralazine, labetalol, nicardipine
<130mmHg >130mmHg
YESNO
Intracerebral Haemorrhage
Sodium nitroprusside
Initial 0.2 -0.50 mcg/kg/min continuous infusionMaintainance: Titrate to goal BP upto 8-10 mcg/kg/mint
Onset : SecondsDuration: 2-3 minutes after infusion is
stopped
Onset/Duration
Thyocyanate & Cyanide poisoningNausea Vomiting
Hypotension
DOSE
Adverse Effects
Points of Emphasis
•Potent arterial and venous dilator with rapid onset & offset of effect.•Preferred agent for most HTN emergencies•Use with beta blockers if used in aortic dissection•Administer continuous IV under monitoring•Caution in Renal and Hepatic patients•Signs of toxicity: met acidosis, tremors, seizures, nausea & vomiting•Avoid prolonged use•Thyocyanate levels more than 10 mg% should be avoided
Labetalol
Bolus: 20 mg x 1, then 20-80 mg q 10 minMaximum dose 300 mgInfusion: 0.5-2 mg/min
Onset : 5-10 minDuration: 3-6 hrs after infusion is stopped
Onset/Duration
Bradycardia, HF, HB, BronchospasmNausea, Vomiting, Flushing
DOSE
Adverse Effects
Points of Emphasis
•Combined alpha & beta adrenergic blocker•Can be given as IV boluses or IV infusion •Excessive BP drops are unusual•Useful in most hypertensive emergencies except Congestive Heart Failure & severe asthma•Commonly used agent along with hydralazine in HTN in pregnancy
Nitroglycerine
Initial: 5mcg/minMaintenance: titrate q 3-5 min upto
100mcg/minute Onset : 2-5 min
Duration: 5-15 minutes after infusion is stopped
Onset/Duration
Tolerance, Headaches, Nausea, Hypotension, methemoglobinemia
DOSE
Adverse Effects
Points of Emphasis
•Similar to SNP, but causes mostly venodialatation & modestly arteriolar dialatation effects at higher doses•Most useful in emergencies complicated by cardiac compromise like MI, LVF & Pulmonary Edema•Also indicated in Rx of post-op HTN in CABG•Tolerance will develop with prolonged use
Hydralazine
Bolus 10-20 mg q 30 minutes until goal BP acheived
Onset : 10-30 minDuration: 2-4 hours
Onset/Duration
Hypotension, Tachycardia, Flushing
DOSE
Adverse Effects
Points of Emphasis
•Direct arteriolar vasodilator with no significant venous effect•Caution in patients with CAD & Aortic dissection!•Avoid in patients with high ICP•BP lowering response is less predictable than with other agents
Fenoldopam
Initial: 0.5 mcg/kg/minMaintenance: titrate q 15 min, upto
0.6mcg/kg/min
Onset : 3-5 minDuration: 30 mins
Onset/Duration
Headache, Tachycardia, Flushing
DOSE
Adverse Effects
Points of Emphasis
•Selective peripheral dopamine-1 receptor agonist causing primarily arterial vasodilation with rapid onset & relatively short offset of effect•Shown to improve renal perfusion, so useful in patients with renal impairment•Contraindicated in patients with glaucoma
Lets’ Review
STOP The progression of Target Organ Damage
Treatment of HTN emergencies has a simple goal
The complexity of management lies in:The careful balance between BP control & organ hypoperfusion
The choice of the parenteral agentThat have a rapid onset of action & a short half life, like ON-OFF or light switch properties
I think its enough
Thanks a lot for your patiance