Successfully reported this slideshow.
We use your LinkedIn profile and activity data to personalize ads and to show you more relevant ads. You can change your ad preferences anytime.

Hypertensive Emergencies & ICU


Published on

Hypertensive Emergencies their diagnosis and management described in a very simple way.

Published in: Education, Health & Medicine
  • Be the first to comment

Hypertensive Emergencies & ICU

  1. 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. 2. 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
  3. 3. 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
  4. 4. Hypertensive Urgency Severe elevation in blood pressure without evidence of acute & ongoing target organ damage.
  5. 5. 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)
  6. 6. 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
  7. 7. 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
  8. 8. 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
  9. 9. Evidence of Acute Ongoing Target Organ Damage NO YES Evidence of Acute Ongoing Target Organ Damage
  10. 10. 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.
  11. 11. If the answer of your examination is YES
  12. 12. 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
  13. 13. 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.
  14. 14. 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.
  15. 15. Syndrome Specific Hypertension management Hypertensive Encephalopathy Aortic Dissection Accelerated malignant hypertension Pre-eclampsia/Eclampsia Ischaemic Stroke cardiac Renal Catecholamine excess Intracerebral haemorrhage Subarachnoid haemorrhage
  16. 16. 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
  17. 17. 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
  18. 18. 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
  19. 19. 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
  20. 20. 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
  21. 21. 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
  22. 22. 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,
  23. 23. Physical Examination Skin findings of scleroderma Abdominal bruits Gross haematuria Diagnostic studies Urine analysis: RBCs,proteins,casts ↑ creatinine
  24. 24. 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
  25. 25. 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?
  26. 26. Physical Examination ↑HR Hyperhydrosis Restless, agitated, anxious Café-au-lait spots, port wine stains, neurofibromas Diagnostic studies Urine/serum toxicology Serum catecholamine Urinary metanephrines
  27. 27. 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
  28. 28. Aortic Dissection Management Pearls Minimize shear stress Decrease dP/dt Goal: MAP 60-75 mmHg HR 60-70 bpm Beta blockers +/- SNP
  29. 29. 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
  30. 30. Intracerebral Haemorrhage MAP={SBP+2ХDBP}/3 Lower MAP by ~15% with IV hydralazine, labetalol, nicardipine Risk of EOD? Lower BP cautiously NO Rx
  31. 31. 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
  32. 32. 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
  33. 33. 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
  34. 34. 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
  35. 35. 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
  36. 36. 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
  37. 37. I think its enough