Hypertensive emergency: Difference between revisions
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''High blood pressure without symptoms is NOT hypertensive emergency (see [[asymptomatic hypertension]])'' | |||
* | ==Background== | ||
*Definition: end-organ damage due to hypertension | |||
** | **Blood pressure is generally >180/120 (usually > 220/130), but presence of end-organ damage defines disease (not absolute blood pressure number) | ||
**1%-6% of all ED patients will present with severe hypertension, but less than half of those will have target organ damage<ref>Chobanian AV, Bakris GL, Black HR, et al. Seventh report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. Hypertension. 2003;42(6):1206-1252. doi:10.1161/01.HYP.0000107251.49515.c2</ref> | |||
==Etiology== | ===Etiology=== | ||
*Idiopathic | |||
*[[Sympathomimetic]] drug use | |||
*[[Preeclampsia]] | |||
*Acute [[glomerulonephritis]] | |||
* | ===Prehospital=== | ||
* | *Prehospital BP measurements should be considered reliable<ref>Cienki JJ, DeLuca LA. Agreement between emergency medical services and expert blood pressure measurements. J. Emerg Med. 2012;43(1):64-68.</ref> | ||
* | *Acute lowering of BP is not typically recommended | ||
* Acute | *Focus on ABCs (assess need for [[intubation]] or [[BiPAP|respiratory support]]) | ||
*Provide care of treatable etiologies | |||
**[[CHF]] | |||
**[[Respiratory failure]] from [[pulmonary edema]] | |||
**Acute pain | |||
== | ==Clinical Features== | ||
'''End-Organ Dysfunction<ref>Levy PD. Hypertensive Emergencies — On the Cutting Edge. EMCREG - International. 2011. 19-26.</ref>''' | |||
*[[Acute kidney injury]] | |||
**Often with microscopic hematuria | |||
*[[Pulmonary edema]] | |||
*Type-II [[myocardial infarction]] | |||
*[[Hypertensive encephalopathy]] | |||
**Visual disturbances | |||
**[[Seizure]] | |||
**Delirium | |||
==Differential Diagnosis== | |||
{{Hypertension DDX}} | |||
==Evaluation== | |||
| Drug | ===Workup=== | ||
| Dose | ''Consider any of the following based on the patient's clinical presentation''<ref>2013 Practice guidelines for the management of arterial hypertension of the European Society of Hypertension (ESH) and the European Society of Cardiology (ESC): ESH/ESC Task Force for the Management of Arterial Hypertension. J Hypertens. 2013;31(10):1925-1938.</ref> | ||
| Mechanism | *CBC with peripheral smear- assess for microangiopathic hemolytic anemia | ||
| Pros | *Chem 8 - assess renal failure and possible secondary causes | ||
| Cons | *[[Troponin|Cardiac enzymes]] | ||
| Notes | *[[Urinalysis]] - Assess renal failure, glomerulonephritis, preeclampsia | ||
*[[ECG]] - [[LVH]], [[myocardial ischemia|ischemia]] | |||
*[[Ultrasound]] - evaluate for aortic dissection, bladder outlet obstruction, or depressed myocardial function | |||
*[[Fundoscopic Exam]] - evaluate for hypertensive retinopathy or papilledema | |||
*[[CXR]] - evaluate for pulmonary edema or dissection | |||
*[[CT head]] - in hypertensive encephalopathy, may not show acute hemorrhage or other acute pathology | |||
**Hypertensive encephalopathy is thought to be secondary to alteration in cerebral auto-regulation leading to [[posterior reversible encephalopathy syndrome]] (now called reversible posterior leukoencephalopathy). Most patients will show changes on MRI, although this is not necessarily indicated in the emergency department. | |||
===Diagnosis=== | |||
*Must have evidence of end-organ dysfunction | |||
**''High blood pressure without symptoms is NOT hypertensive emergency (see [[asymptomatic hypertension]])'' | |||
**''Symptoms such as headache, epistaxis and dizziness are not evidence of acute end-organ damage and they are not indication for acute BP reduction'' | |||
==Management== | |||
'''High blood pressure without end organ damage is NOT hypertensive emergency (see [[asymptomatic hypertension]])''' | |||
*Goal: Lower mean arterial or systolic pressure by no more than 10-20% in the first hour<ref>Elliott WJ. Clinical features in the management of selected hypertensive emergencies. Prog Cardiovasc Dis. 2006;48(5):316-325. doi:10.1016/j.pcad.2006.02.004</ref> | |||
**Then lower by an additional 5-15% over the next 23 hours for no more than 25% in the first 24 hours | |||
**Exception is [[aortic dissection]] which requires rapid reduction to systolic BP to 100-120 mmHg | |||
*Be careful of lowering BP in patients with [[CVA]] | |||
===By Drug=== | |||
{| class="wikitable" | |||
|- | |||
| '''Drug''' | |||
| '''Dose''' | |||
| '''Mechanism''' | |||
| '''Pros''' | |||
| '''Cons''' | |||
| '''Notes''' | |||
|- | |- | ||
| Nitroprusside | | [[Nitroprusside]] | ||
| | | | ||
0. | |||
0.3-0.5 mcg/kg/min IV initial infusion | |||
Increase by 0.5 mcg/kg/min up to 2mcg/kg/min | |||
| Arterial > venodilator | |||
| Arterial | | | ||
| | |||
1. Very effective | 1. Very effective | ||
2. Immediate onset/offset | 2. Immediate onset/offset | ||
| | |||
| | |||
1. Cyanide Toxicity | 1. Cyanide Toxicity | ||
2. Coronary steal? | 2. Coronary steal? | ||
3. | 3. Increased HR | ||
| | |||
| | |||
1. Avoid in liver/renal failure | 1. Avoid in liver/renal failure | ||
2. Avoid with | 2. Avoid with increased ICP | ||
3. Avoid in pregnancy | 3. Avoid in pregnancy | ||
|- | |- | ||
| | | [[Nitroglycerin]] | ||
| 5-100 | | Start 5-100 mcg/min | ||
| Veno>arteriodilation | | Veno>arteriodilation | ||
| | | | ||
1. Rapid on/offset | 1. Rapid on/offset | ||
2. Increases coronary flow | 2. Increases coronary flow | ||
LV dysfunction, or | | Causes tachycardia | ||
| | |||
Drug of choice in patients with cardiac ischemia, | |||
LV dysfunction, or pulmonary edema | |||
|- | |- | ||
| Labetalol | | [[Labetalol]] | ||
| | | | ||
20-80mg IV bolus | 20-80mg IV bolus q10 min '''OR''' | ||
0.5- | 0.5-2 mg/min IV infusion or | ||
| Beta> | |||
| | 200mg to 400mg PO BID | ||
| Beta>α-blocker | |||
| | |||
1. No change in HR, cerebral flow | 1. No change in HR, cerebral flow | ||
2. Rapid onset | |||
| | |||
| | Avoid in COPD, CHF and heart block | ||
Avoid in COPD, CHF | |||
| | |||
| | |||
1. Consider in ACS | 1. Consider in ACS | ||
2. Consider in ischemic CVA | |||
|- | |- | ||
| Esmolol | | [[Esmolol]] | ||
| | | | ||
250-500 | Load 250-500 mcg/kg over 2min | ||
Infuse 50 mcg/kg/min over 4min | |||
- if ineffective repeat load, increase infusion rate by 50mcg/kg/min up to 300mcg/kg/min | |||
| Beta selective | | Beta selective | ||
| | | Rapid on/offset | ||
| | | | ||
Avoid in COPD, CHF | Avoid in COPD, CHF | ||
bradycardia | bradycardia | ||
| | |||
| | |||
Consider in ACS | Consider in ACS | ||
|- | |- | ||
| Nicardipine | | [[Nicardipine]] | ||
| | | | ||
| Decreases PVR<br /><br /> | Start 5mg/h | ||
If ineffective after 15min increased in 2.5mg/hr interval up to 15mg/hr | |||
| Decreases PVR<br/><br/> | |||
| Good for intracranial pathology | | Good for intracranial pathology | ||
| Slower onset/offset | | Slower onset/offset | ||
| Avoid in CHF, ACS | | Avoid in CHF, ACS | ||
|- | |- | ||
| | | [[Phentolamine]] | ||
| 5- | | | ||
5-15mg IV bolus q5-15min '''OR''' | |||
0.2-0.5mg/min IV infusion | |||
| α-blocker | |||
| | |||
| | | | ||
| | | Used for catecholamine-induced hypertension | ||
| Used for catecholamine-induced | |||
|- | |- | ||
| | | [[Enalaprilat]] | ||
| 1.25mg over 5min q6hr | | Bolus 1.25mg over 5min q6hr, titrate at 30min intervals to max of 5mg q6hr | ||
| Decreases HR, SV, systemic arterial pressure | | Decreases HR, SV, systemic arterial pressure | ||
| Does not impair cerebral flow | | Does not impair cerebral flow | ||
| Variable response | | Variable response | ||
| | | | ||
1. Used in | 1. Used in patients at risk for cerebral hypotension, CHF | ||
2. Avoid in pregnancy | 2. Avoid in pregnancy | ||
|- | |||
| [[Clonidine]] | |||
| | |||
0.1 - 0.3 mg PO q12 scheduled; For hypertensive emergency, 0.2 mg x1, then 0.1 mg q1 hr PRN, max 0.6 mg total | |||
| α-2 agonist, BP effects within 30-60 min after PO dose | |||
| | |||
| | |||
| Reduced CNS sympathetic flow, decreasing SVR, HR, BP; no renal blood flow changes; tolerance/tachyphylaxis develop quickly | |||
|- | |||
| [[Hydralazine]] | |||
| | |||
10 - 20 mg slow IV/IM bolus q4-6 hr PRN, max 40 mg/dose | |||
| Peripheral vasodilator, with fall in BP beginning within 30 min, lasting 2-4 hrs | |||
| | |||
| | |||
| Decrease in DBP > SBP; has increased HR, stroke volume and cardiac outpt; preferential vasodilation > venodilation | |||
|} | |} | ||
==Disease | ===By Disease=== | ||
=== | ====[[Aortic Dissection]]==== | ||
=== | *Rapidly reduce sys BP to 100-120; HR 60-80 within 20min | ||
* | *Adequate analgesia will decrease sympathetic drive and assist with BP and HR control | ||
* | *Avoid volume depletion | ||
*Prevent reflex tachycardia | |||
**Labetalol alone | |||
**Nitroprusside or nicardipine AFTER metoprolol or esmolol | |||
====[[Pulmonary Edema]]==== | |||
*Reduce BP by 20-30% | |||
*Promote diuresis AFTER vasodilation | |||
====[[ACS]]==== | |||
*No more than 20-30% reduction for SBP >160 | |||
*Consider NTG, beta-blocker | |||
=== | ====[[Cocaine]]/[[Amphetamine]] Toxicitiy==== | ||
* | |||
* | *[[Benzos]] | ||
** | *Mixed α + B blockade | ||
**Phentolamine '''OR''' nitroprusside AND β-blocker | |||
====[[Renal Failure]]==== | |||
*Reduce BP by no more than 20% | |||
*Avoid nitroprusside (renal metabolism) | |||
*Labetalol or nicardipine | |||
=== | ====[[Eclampsia]]/[[Pre-eclampsia]]==== | ||
*Goal BP <160/110 | |||
* | *Labetalol or nicardipine | ||
*Magnesium | *Magnesium | ||
=== | ====[[Hypertensive emergency]]==== | ||
* | *Decrease MAP by 15-20% | ||
* | **Avoid overly aggressive lowering | ||
**Phentolamine | *[[Nicardipine]] or [[labetalol]] | ||
====[[CVA]]==== | |||
*[[SAH]] | |||
**See [[Subarachnoid Hemorrhage (SAH)]] | |||
*[[ICH]] | |||
*See [[ICH#Guidelines|current guidelines]] for best practice | |||
**[[Labetalol]] or [[Nicardipine]] or [[Esmolol]] | |||
*[[Stroke (Main)|Ischemic]] | |||
**If thrombolytic treatment is planned then goal systolic blood pressure 185 mm Hg and diastolic blood pressure 110 mm Hg<ref>Acute Stroke Practice Guidelines for Inpatient Management of Ischemic | |||
Stroke and Transient Ischemic Attack (TIA) https://www.heart.org/idc/groups/heart-public/@wcm/@private/@hcm/documents/downloadable/ucm_309996.pdf</ref> | |||
**If no thrombolytics then consider blood pressure control if SBP >220 mmHg or DBP >120 mmgHg | |||
**[[Labetalol]] or [[Nicardipine]] are both effective and safe | |||
====[[Pheochromocytoma]]==== | |||
*Phentolamine '''OR''' (nitroprusside AND β-blocker) | |||
== | ==Disposition== | ||
* | *Admit | ||
**Patients receiving titratable antihypertensive therapies will likely require admission to critical care unit | |||
== | ==See Also== | ||
* | *[[Hypertension (main)]] | ||
*[[Asymptomatic hypertension]] | |||
*[[IV nitroglycerine alternatives]] | |||
== | ==External Links== | ||
*[http://www.emdocs.net/hypertensive-crisis-pearls-and-pitfalls-for-the-ed-physician/ emDocs - Hypertensive Emergency: Pearls and Pitfalls for the ED Physician] | |||
*[https://emcrit.org/ibcc/hypertensive-emergency/ EMCrit - Hypertensive Emergency] | |||
==References== | |||
<references/> | |||
[[Category: | [[Category:Cardiology]] | ||
Latest revision as of 20:09, 17 April 2024
High blood pressure without symptoms is NOT hypertensive emergency (see asymptomatic hypertension)
Background
- Definition: end-organ damage due to hypertension
- Blood pressure is generally >180/120 (usually > 220/130), but presence of end-organ damage defines disease (not absolute blood pressure number)
- 1%-6% of all ED patients will present with severe hypertension, but less than half of those will have target organ damage[1]
Etiology
- Idiopathic
- Sympathomimetic drug use
- Preeclampsia
- Acute glomerulonephritis
Prehospital
- Prehospital BP measurements should be considered reliable[2]
- Acute lowering of BP is not typically recommended
- Focus on ABCs (assess need for intubation or respiratory support)
- Provide care of treatable etiologies
- CHF
- Respiratory failure from pulmonary edema
- Acute pain
Clinical Features
End-Organ Dysfunction[3]
- Acute kidney injury
- Often with microscopic hematuria
- Pulmonary edema
- Type-II myocardial infarction
- Hypertensive encephalopathy
- Visual disturbances
- Seizure
- Delirium
Differential Diagnosis
Hypertension
- Hypertensive emergency
- Stroke
- Sympathetic crashing acute pulmonary edema
- Ischemic stroke
- Intracranial hemorrhage
- Preeclampsia/Eclampsia
- Autonomic dysreflexia
- Scleroderma renal crisis
- Acute glomerulonephritis
- Type- I myocardial infarction
- Volume overload
- Urinary obstruction
- Drug use or overdose (e.g stimulants, especially alcohol, cocaine, or Synthroid)
- Renal Artery Stenosis
- Nephritic and nephrotic syndrome
- Polycystic kidney disease
- Tyramine reaction
- Cushing's syndrome
- Obstructive sleep apnea
- Pheochromocytoma
- Hyperaldosteronism
- Hyperthyroidism
- Anxiety
- Pain
- Oral contraceptive use
Evaluation
Workup
Consider any of the following based on the patient's clinical presentation[4]
- CBC with peripheral smear- assess for microangiopathic hemolytic anemia
- Chem 8 - assess renal failure and possible secondary causes
- Cardiac enzymes
- Urinalysis - Assess renal failure, glomerulonephritis, preeclampsia
- ECG - LVH, ischemia
- Ultrasound - evaluate for aortic dissection, bladder outlet obstruction, or depressed myocardial function
- Fundoscopic Exam - evaluate for hypertensive retinopathy or papilledema
- CXR - evaluate for pulmonary edema or dissection
- CT head - in hypertensive encephalopathy, may not show acute hemorrhage or other acute pathology
- Hypertensive encephalopathy is thought to be secondary to alteration in cerebral auto-regulation leading to posterior reversible encephalopathy syndrome (now called reversible posterior leukoencephalopathy). Most patients will show changes on MRI, although this is not necessarily indicated in the emergency department.
Diagnosis
- Must have evidence of end-organ dysfunction
- High blood pressure without symptoms is NOT hypertensive emergency (see asymptomatic hypertension)
- Symptoms such as headache, epistaxis and dizziness are not evidence of acute end-organ damage and they are not indication for acute BP reduction
Management
High blood pressure without end organ damage is NOT hypertensive emergency (see asymptomatic hypertension)
- Goal: Lower mean arterial or systolic pressure by no more than 10-20% in the first hour[5]
- Then lower by an additional 5-15% over the next 23 hours for no more than 25% in the first 24 hours
- Exception is aortic dissection which requires rapid reduction to systolic BP to 100-120 mmHg
- Be careful of lowering BP in patients with CVA
By Drug
| Drug | Dose | Mechanism | Pros | Cons | Notes |
| Nitroprusside |
0.3-0.5 mcg/kg/min IV initial infusion Increase by 0.5 mcg/kg/min up to 2mcg/kg/min
|
Arterial > venodilator |
1. Very effective 2. Immediate onset/offset |
1. Cyanide Toxicity 2. Coronary steal? 3. Increased HR |
1. Avoid in liver/renal failure 2. Avoid with increased ICP 3. Avoid in pregnancy |
| Nitroglycerin | Start 5-100 mcg/min | Veno>arteriodilation |
1. Rapid on/offset 2. Increases coronary flow |
Causes tachycardia |
Drug of choice in patients with cardiac ischemia, LV dysfunction, or pulmonary edema |
| Labetalol |
20-80mg IV bolus q10 min OR 0.5-2 mg/min IV infusion or 200mg to 400mg PO BID |
Beta>α-blocker |
1. No change in HR, cerebral flow 2. Rapid onset |
Avoid in COPD, CHF and heart block |
1. Consider in ACS 2. Consider in ischemic CVA |
| Esmolol |
Load 250-500 mcg/kg over 2min Infuse 50 mcg/kg/min over 4min - if ineffective repeat load, increase infusion rate by 50mcg/kg/min up to 300mcg/kg/min |
Beta selective | Rapid on/offset |
Avoid in COPD, CHF bradycardia |
Consider in ACS |
| Nicardipine |
Start 5mg/h If ineffective after 15min increased in 2.5mg/hr interval up to 15mg/hr |
Decreases PVR |
Good for intracranial pathology | Slower onset/offset | Avoid in CHF, ACS |
| Phentolamine |
5-15mg IV bolus q5-15min OR 0.2-0.5mg/min IV infusion |
α-blocker | Used for catecholamine-induced hypertension | ||
| Enalaprilat | Bolus 1.25mg over 5min q6hr, titrate at 30min intervals to max of 5mg q6hr | Decreases HR, SV, systemic arterial pressure | Does not impair cerebral flow | Variable response |
1. Used in patients at risk for cerebral hypotension, CHF 2. Avoid in pregnancy |
| Clonidine |
0.1 - 0.3 mg PO q12 scheduled; For hypertensive emergency, 0.2 mg x1, then 0.1 mg q1 hr PRN, max 0.6 mg total |
α-2 agonist, BP effects within 30-60 min after PO dose | Reduced CNS sympathetic flow, decreasing SVR, HR, BP; no renal blood flow changes; tolerance/tachyphylaxis develop quickly
| ||
| Hydralazine |
10 - 20 mg slow IV/IM bolus q4-6 hr PRN, max 40 mg/dose |
Peripheral vasodilator, with fall in BP beginning within 30 min, lasting 2-4 hrs | Decrease in DBP > SBP; has increased HR, stroke volume and cardiac outpt; preferential vasodilation > venodilation
|
By Disease
Aortic Dissection
- Rapidly reduce sys BP to 100-120; HR 60-80 within 20min
- Adequate analgesia will decrease sympathetic drive and assist with BP and HR control
- Avoid volume depletion
- Prevent reflex tachycardia
- Labetalol alone
- Nitroprusside or nicardipine AFTER metoprolol or esmolol
Pulmonary Edema
- Reduce BP by 20-30%
- Promote diuresis AFTER vasodilation
ACS
- No more than 20-30% reduction for SBP >160
- Consider NTG, beta-blocker
Cocaine/Amphetamine Toxicitiy
- Benzos
- Mixed α + B blockade
- Phentolamine OR nitroprusside AND β-blocker
Renal Failure
- Reduce BP by no more than 20%
- Avoid nitroprusside (renal metabolism)
- Labetalol or nicardipine
Eclampsia/Pre-eclampsia
- Goal BP <160/110
- Labetalol or nicardipine
- Magnesium
Hypertensive emergency
- Decrease MAP by 15-20%
- Avoid overly aggressive lowering
- Nicardipine or labetalol
CVA
- SAH
- ICH
- See current guidelines for best practice
- Labetalol or Nicardipine or Esmolol
- Ischemic
- If thrombolytic treatment is planned then goal systolic blood pressure 185 mm Hg and diastolic blood pressure 110 mm Hg[6]
- If no thrombolytics then consider blood pressure control if SBP >220 mmHg or DBP >120 mmgHg
- Labetalol or Nicardipine are both effective and safe
Pheochromocytoma
- Phentolamine OR (nitroprusside AND β-blocker)
Disposition
- Admit
- Patients receiving titratable antihypertensive therapies will likely require admission to critical care unit
See Also
External Links
- emDocs - Hypertensive Emergency: Pearls and Pitfalls for the ED Physician
- EMCrit - Hypertensive Emergency
References
- ↑ Chobanian AV, Bakris GL, Black HR, et al. Seventh report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. Hypertension. 2003;42(6):1206-1252. doi:10.1161/01.HYP.0000107251.49515.c2
- ↑ Cienki JJ, DeLuca LA. Agreement between emergency medical services and expert blood pressure measurements. J. Emerg Med. 2012;43(1):64-68.
- ↑ Levy PD. Hypertensive Emergencies — On the Cutting Edge. EMCREG - International. 2011. 19-26.
- ↑ 2013 Practice guidelines for the management of arterial hypertension of the European Society of Hypertension (ESH) and the European Society of Cardiology (ESC): ESH/ESC Task Force for the Management of Arterial Hypertension. J Hypertens. 2013;31(10):1925-1938.
- ↑ Elliott WJ. Clinical features in the management of selected hypertensive emergencies. Prog Cardiovasc Dis. 2006;48(5):316-325. doi:10.1016/j.pcad.2006.02.004
- ↑ Acute Stroke Practice Guidelines for Inpatient Management of Ischemic Stroke and Transient Ischemic Attack (TIA) https://www.heart.org/idc/groups/heart-public/@wcm/@private/@hcm/documents/downloadable/ucm_309996.pdf
