Hypertensive Emergencies & ICU

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