Hypertensive emergency: Difference between revisions

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==Diagnosis==
''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>


* End-organ damage 2/2 increased BP (generally >180/120, usually > 220/130)
===Etiology===
* Brain - Encephelopathy, seizure, ICH, ischemic stroke
*Idiopathic
* Eyes - Retinal hemorrhage, exudate, papilledema
*[[Sympathomimetic]] drug use
* CV - MI, CHF/LV failure/pulm edema, aortic dissection
*[[Preeclampsia]]
* Renal - Acute failure, hematuria, proteinuria
*Acute [[glomerulonephritis]]
* Ancillary Tests
* Chemistry - assess renal failure
* UA - Assess renal failure, glomerulo nephritis, preeclampsia
* Troponin
* CXR - Evidenceo failure, dissection
* ECG


==Etiology==
===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
*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


* Idiopathic
==Differential Diagnosis==
* Sympathomimetic drug use
{{Hypertension DDX}}
* Preeclampsia
* Acute glomerulonephritis


Treatment
==Evaluation==
===Workup===
''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>
*CBC with peripheral smear- assess for microangiopathic hemolytic anemia
*Chem 8 - assess renal failure and possible secondary causes
*[[Troponin|Cardiac enzymes]]
*[[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.


* Goal: Lower diastolic pressure to 105mmHg within 2-6 hours
===Diagnosis===
* Maximum initial fall in BP should not exceed 25% of presenting value
*Must have evidence of end-organ dysfunction
* Be careful of lowering BP in pts with CVA!
**''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''


Drug Dose Mechanism Pros Cons Notes
==Management==
Nitroprusside 0.25-8µg/kg/min
'''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]]


(start at 0.25)
===By Drug===
{| class="wikitable"
|-
| '''Drug'''
| '''Dose'''
| '''Mechanism'''
| '''Pros'''
| '''Cons'''
| '''Notes'''
|-
| [[Nitroprusside]]
|


Arterial and veno-dilator 1. Very effective  
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
2. Immediate onset/offset


1. Cyanide Toxicity
|
1. Cyanide Toxicity


2. Coronary steal?
2. Coronary steal?


3. Incr HR
3. Increased HR


1. Avoid in liver/renal failure
|
1. Avoid in liver/renal failure


2. Avoid with incr ICP
2. Avoid with increased ICP


3. Avoid in pregnancy
3. Avoid in pregnancy


|-
Nitgroglycerin 5-100 µg/min Veno>arteriodilation 1. Rapid on/offset  
| [[Nitroglycerin]]
| Start 5-100 mcg/min
| Veno>arteriodilation
|
1. Rapid on/offset


2. Increases coronary flow
2. Increases coronary flow


Causes Tachycardia Drug of choice in pts w/ cardiac ischemia,
| Causes tachycardia
|
Drug of choice in patients with cardiac ischemia,


LV dysfunction, and pulm edema
LV dysfunction, or pulmonary edema


|-
Labetalol 20-80mg IV bolus q10min OR
| [[Labetalol]]
|
20-80mg IV bolus q10 min '''OR'''


0.5-2mg/min IV
0.5-2 mg/min IV infusion or


Beta>alpha blocker 1. No change in HR, cerebral flow
200mg to 400mg PO BID


| Beta>α-blocker
|
1. No change in HR, cerebral flow
2. Rapid onset
2. Rapid onset


Avoid in COPD, CHF
|
 
Avoid in COPD, CHF and heart block
heart block
 
1. Consider in ACS


|
1. Consider in ACS
2. Consider in ischemic CVA
2. Consider in ischemic CVA


|-
 
| [[Esmolol]]
|
Esmolol 250-500 µg/kg/min;
Load 250-500 mcg/kg over 2min


may repeat bolus after
Infuse 50 mcg/kg/min over 4min


5min or incr to 300µg/min
- if ineffective repeat load, increase infusion rate by &nbsp;50mcg/kg/min up to 300mcg/kg/min


Beta selective 1. Rapid on/offset Avoid in COPD, CHF
| Beta selective
| Rapid on/offset
|
Avoid in COPD, CHF


bradycardia
bradycardia


Consider in ACS
|
Consider in ACS


|-
Nicardipine   5-15mg/h Decreases PVR Good for intracranial pathology Slower onset/offset Avoid in CHF, ACS
| [[Nicardipine]]
Hydralazine 5-10mg IV bolus, max dose 20mg OR 0.5-1mg/min IV infusion Arteriolar vasodilator Rarely causes hypotension Avoid in CAD Primarily used in pregancy
|
Phentolamine 5-10mg IV bolus q5-15min OR
Start 5mg/h


0.2-5mg/min IV infusion
If ineffective after 15min increased in 2.5mg/hr interval up to 15mg/hr


Alpha blocker Used for catecholamine-induced HTN
| Decreases PVR<br/><br/>
Enalapril 1.25mg over 5min q6hr Decreases HR, SV, systemic arterial pressure Does not impair cerebral flow Variable response 1. Used in pts at risk for cerebral hypotension, CHF
| Good for intracranial pathology
| Slower onset/offset
| Avoid in CHF, ACS
|-
| [[Phentolamine]]
|
5-15mg IV bolus q5-15min '''OR'''


2. Avoid in pregnancy
0.2-0.5mg/min IV infusion


| α-blocker
Disease Specific
|
|
| 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


HTN Encephalopathy
2. Avoid in pregnancy
 
    Controlled redxn of BP over 1h; never < 110 diastolic
 
          Labetolol, nicardipine, fenoldopam; nitroprusside of diastolic > 140
 
 
Stroke
 
    10-15% reduction of MAP; diastolic not < 110
 
    lower to 185/110 in ischemic stroke to meet t-PA criteria
 
          Labetolol, nicardipine, nitroprusside as above
 


Acute Aortic Dissection
|-
| [[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


    Rapid redxn of BP, systolic bp 100-120; HR 60-80 within 20mins
| 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


    Prevent reflex tachycardia


          Nitroprusside, fenoldopam, nicardipine with metoprolol or esmolol; labetolol alone
|-
| [[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


ACS and Pulmonary Edema


    Nitroglycerin
|}


===By Disease===


Eslampsia/Pre-eclampsia
====[[Aortic Dissection]]====


    Labetolol, nicardipine or IV hydralazine
*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


    Magnesium
====[[Pulmonary Edema]]====
*Reduce BP by 20-30%
*Promote diuresis AFTER vasodilation


====[[ACS]]====


Cocaine and Amphetamine Toxicitiy
*No more than 20-30% reduction for SBP >160
*Consider NTG, beta-blocker


    BDZs
====[[Cocaine]]/[[Amphetamine]] Toxicitiy====


    Mixed alpha + B blockade: phentolamine or nitroprusside plus beta blocker
*[[Benzos]]
*Mixed α + B blockade
**Phentolamine '''OR''' nitroprusside AND β-blocker


====[[Renal Failure]]====


Pheochromocytoma
*Reduce BP by no more than 20%
*Avoid nitroprusside (renal metabolism)
*Labetalol or nicardipine


    Phentolamine or nitroprusside plus beta blocker
====[[Eclampsia]]/[[Pre-eclampsia]]====


*Goal BP <160/110
*Labetalol or nicardipine
*Magnesium


ARF
====[[Hypertensive emergency]]====
*Decrease MAP by 15-20%
**Avoid overly aggressive lowering
*[[Nicardipine]] or [[labetalol]]


    Fenoldopam, nicardipine; nitroprusside risk cyanide toxicity (renal metabolism)
====[[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


Source
====[[Pheochromocytoma]]====
*Phentolamine '''OR''' (nitroprusside AND β-blocker)


Adapted from Bessen, Bresler (ACEP '09), UpToDate
==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:Cards]]
[[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

Prehospital

Clinical Features

End-Organ Dysfunction[3]

Differential Diagnosis

Hypertension

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

CVA

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

References

  1. 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
  2. Cienki JJ, DeLuca LA. Agreement between emergency medical services and expert blood pressure measurements. J. Emerg Med. 2012;43(1):64-68.
  3. Levy PD. Hypertensive Emergencies — On the Cutting Edge. EMCREG - International. 2011. 19-26.
  4. 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.
  5. 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
  6. 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