Hypertensive Emergencies & ICU
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Transcript of Hypertensive Emergencies & ICU
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Hypertensive Emergencies
Department of Critical Care Medicine King Saud Medical City
Riyadh Saudi Arabia
Muhammad Asim Rana MBBS, MRCP, SF-CCM, EDIC, FCCP
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HYPERTENSIVE CRISES
HYPERTENSIVEENCEPHALOPATHY
ACCELERATEDMALIGNANT
HYPERTENSION
HYPERTENSIVEEMERGENCY
HYPERTENSIVEURGENCY
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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
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Hypertensive Crisis
Severe elevation in blood pressure that have the potential to cause target organ damage.
Target organs areHeartVasculatureKidneysEyesBrain
These include emergencies
& urgencies
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Hypertensive Urgency
without evidence of acute & ongoing target organ damage.
Severe elevation in blood pressure
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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)
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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
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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
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• 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
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Evidence of Acute Ongoing Target Organ Damage
YES NO
Evidence of Acute Ongoing Target Organ Damage
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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.
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If the answer of your examination is
YES
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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
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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.
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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
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Hypertensive Encephalopathy
Accelerated malignant hypertension
cardiac
Renal
Catecholamine excess
Aortic Dissection
Pre-eclampsia/Eclampsia
Ischaemic Stroke
Intracerebral haemorrhage
Subarachnoid haemorrhage
Syndrome Specific Hypertension management
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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
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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
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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
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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
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↑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
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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
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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
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Skin findings of sclerodermaAbdominal bruitsGross haematuria
Urine analysis: RBCs,proteins,casts ↑ creatinine
Physical Examination
Diagnostic studies
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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
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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
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↑HR Hyperhydrosis Restless, agitated, anxiousCafé-au-lait spots, port wine stains, neurofibromas
Urine/serum toxicologySerum catecholamineUrinary metanephrines
Physical Examination
Diagnostic studies
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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
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Minimize shear stressDecrease dP/dtGoal: MAP 60-75 mmHg HR 60-70 bpmBeta blockers +/- SNP
Aortic Dissection
Management Pearls
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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
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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
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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
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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
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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
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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
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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
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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
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I think its enough
Thanks a lot for your patiance