HYPERTENSIVE
EMERGENCIES
BY
NAGASAI ROMPICHERLA
A&E DEPARTMENT
ALL AMERICAN INSTITUTE OF
MEDICAL SCIENCES
Contents
Definitions
Etiology
Clinical Features
Approach to Acute Management
Diagnostics
Treatment
Prognosis
Summary
References
Definitions
Hypertensive crisis or acute severe hypertension: an acute increase in systolic
pressure ≥ 180 mm Hg and/or diastolic blood pressure ≥ 120 mm Hg
Hypertensive urgency: hypertensive crisis that is either asymptomatic or with
isolated nonspecific symptoms (e.g., headache, dizziness, or epistaxis) without signs
of organ damage
Hypertensive emergency: hypertensive crisis with signs of end-organ damage,
mainly in the cardiovascular, central nervous, and renal systems.
Etiology
Drug-related
• Nonadherence to antihypertensives Drugs that may exacerbate hypertension (e.g.,
monoamine oxidase inhibitors (MAOIs), and tricyclic antidepressants (TCAs)., NSAIDS,
cocaine, amphetamines, ecstasy, stimulant diet pills)
Consumption of foods rich in tyramine (e.g., wine, chocolate, aged
cheese, cured meat) during therapeutic use of MAOIs
Pheochromocytoma, hyperthyroidism
Acute and rapidly progressive renal disorders
Collagen vascular diseases (e.g., SLE)
Eclampsia/Pre-eclampsia
Head trauma, spinal cord disorders
Clinical Features
Hypertensive urgency
 Asymptomatic or isolated, nonspecific symptoms (e.g., headache, dizziness, or epistaxis)
Hypertensive emergency
 Signs and symptoms of end-organ dysfunction
 Cardiac
 Heart failure exacerbation, pulmonary edema: dyspnea, crackles on examination
 Myocardial infarction: chest pain, diaphoresis
 Aortic dissection: chest pain, asymmetric pulses
 Neurologic
 Hypertensive encephalopathy: headache, vomiting, confusion, seizure, blurry vision, papilledema
 Ischemic or hemorrhagic stroke: focal neurological deficits, altered mental status
 Renal: Acute hypertensive nephrosclerosis (formerly malignant nephrosclerosis)
 Acute kidney injury (azotemia and/or oliguria, edema) and microhematuri
Ophthalmic
Acute hypertensive retinopathy: blurry vision, decrease in visual acuity, retinal flame hemorrhages, papilledema
Other
Microangiopathic hemolytic anemia: fatigue, pallor
Clinical Features
Approach to Acute Management
1. Confirm blood pressure manually and on bilateral upper extremities.
2. Determine if there are signs of end-organ damage.
a. Focused history/physical (RED FLAGS: Dyspnea, Chest pain, Altered mental status, Focal neurologic symptoms)
b. Select screening tests
3. For hypertensive emergencies
a. ABCDE approach
b. Admit patients (ideally to ICU).
c. Lower the blood pressure acutely using IV agents and aim for targets based on the affected end-organs (see "Treatment" below).
d. Evaluate and treat underlying disorders.
4. For hypertensive urgency
a. Select, reinstitute, or modify oral antihypertensive therapy
b. In patients with a new diagnosis, evaluate for secondary causes of hypertension.
c. Arrange follow-up, monitoring, and counseling.
Diagnostics
Evaluate for signs of end-organ damage
 Laboratory studies
 CBC: signs of microangiopathic hemolytic anemia
 U&E: altered electrolytes and/or elevated creatinine and urea, which suggest kidney failure
 BNP: elevated in heart failure
 Troponin: elevated in myocardialischemia
 Urinalysis: signs of glomerular injury (e.g., proteinuria, hematuria)
 ECG: left ventricular hypertrophy , signs of cardiac ischemia (e.g., ST depressions or elevations)
 Chest x-ray: cardiomegaly, pulmonary edema
Diagnostics
Additional evaluation to consider
 Urine pregnancy test
 Toxicology screen
 CT chest with IV contrast if chest pain is concerning for aortic dissection
 Consider Transthoracic echocardiography if clinical features suggest pulmonary edema
 Consider CT head if neurological symptoms are present.
Treatment – Urgency
 Outpatient treatment is recommended.
 Move patient to a quiet room for 30 minutes.
 First diagnosis of hypertension, consider evaluation for secondary hypertension
 Reinstitute or increase the dosage of existing oral antihypertensive therapy or consider a rapid-acting oral antihypertensive
agent prior to discharge:
 Clonidine
 Captopril
 Labetalol
 Prazosin
 Monitor the patient for a few hours to ensure BP is improving.
 Discharge and ensure close follow-up with an outpatient provider / clinic
 Recommend a Sodium restriction diet
Treatment -
Emergency
General principles
 ABCDE assessment
 Admission and immediate initiation of
intravenous antihypertensive therapy
 Continuous cardiac monitoring
 Consider intra-arterial blood pressure
monitoring.
 Identify and treat any contributing
comorbidities (e.g., chronic renal failure).
 IV fluids if signs of volume depletion
 Monitor U&E every 6 hours.
Treatment - Emergency
Consider the following factors when choosing intravenous antihypertensive drugs:
 Desired rate of decrease in blood pressure
 End-organ system affected
 Underlying disorder
 Presence or absence of comorbidities (e.g., heart failure, COPD)
 Pharmacokinetics and adverse effects of the agent
The drugs most commonly used to treat hypertensive emergencies are nitroprusside (carries a
risk of cyanide toxicity), labetalol, and nicardipine.
Treatment - Emergency
Intravenous antihypertensives:
 Calcium channel blockers
 Nicardipine
 Clevidipine
 Nitric-oxide dependent vasodilators
 Sodium nitroprusside
 Nitroglycerin
 Direct arterial vasodilators:
 Hydralazine (The response to and duration of action of IV hydralazine can be unpredictable. It should, therefore, be used with caution.)
 Antiadrenergic drugs
 Selective beta-1 antagonist: esmolol
 Nonselective beta blocker with alpha-1 antagonism: labetalol
 Nonselective alpha antagonist: phentolamine
 D1 agonist
 Fenoldopam ACE inhibitor: enalaprilat
Treatment - Emergency
Mean arterial pressure should not be lowered by more than 25% within the first hour, except in special cases.
Reducing the blood pressure too rapidly can lead to hypoperfusion and ischemia in certain organs (e.g., brain,
kidney, heart).
Calculation:
 MAP = cardiac output (CO) × total peripheral resistance (TPR)
 MAP = ⅓ systolic (SP) + ⅔ diastolic (DP) = (SP + 2 x DP)/3
 MAP = DP + 1/3(SP – DP)
Treatment - Emergency
General goal
 Reduce BP by max. 25% within the first hour to prevent coronary insufficiency and to ensure adequate cerebral perfusion press
 Reduce BP to ∼ 160/100–110 mm Hg over the next 2–6 hours.
 Reduce BP to patients baseline over 24–48 hours.
Special cases
Indications for the rapid lowering of systolic BP (usually to < 140 mm Hg) in the first hour of treatment include severe
 aortic dissection,
 pre-eclampsia or eclampsia
 pheochromocytoma with hypertensive crisis.
Hypertension in Jamaica
 If left untreated, hypertensive emergencies are associated with a 1-year mortality ra
of > 80% and a median survival of 10–11 months.
 One in 3 Jamaicans are hypertensive – 35.8% women and 31.7% men, according to
the Jamaica Health and Lifestyle Survey for 2016/17.
 Four out of every 10 people with the disease are unaware of their status – 60% men
and 26% women.
 At the same time, more and more Jamaicans aged 15 to 74 years old are developing
hypertension.
Summary
 Hypertensive crises refer to acute increases in blood pressure (generally defined as
≥ 180/120 mm Hg) that cause or increase the risk of end-organ damage
 They can be due to primary hypertension or precipitated by underlying conditions
 Management consists of rapidly identifying end-organ damage with patient history
physical examination, and focused testing.
 Emergency requires admission and IV anti-hypertensives .
 Urgency requires rapid follow-up and oral anti-hypertensives.
References
 Amboss Clinic Resource, www.Amboss.com, https://www.amboss.com/us/knowledge/Hypertensive_crises/
(Accessed September 2, 2021)
 Whelton, PK, Carey, RM et al. 2017 ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ASH/ASPC/NMA/PCNA Guideline
for the Prevention, Detection, Evaluation, and Management of High Blood Pressure in Adults. Hypertension.
2017
 Shantsila A, Lip GYH. Malignant Hypertension Revisited—Does This Still Exist?. American Journal of
Hypertension. 2017
 Varon J, Marik PE. Clinical review: the management of hypertensive crises. Crit Care. 2003; 7 (5): p.374-384.
 Peixoto AJ. Acute Severe Hypertension. N Engl J Med. 2019; 381 (19): p.1843-1852. doi: 10.1056/nejmcp1901117
Hypertensive Crisibjknvfklncrukbchbns.pptx

Hypertensive Crisibjknvfklncrukbchbns.pptx

  • 1.
  • 2.
    Contents Definitions Etiology Clinical Features Approach toAcute Management Diagnostics Treatment Prognosis Summary References
  • 3.
    Definitions Hypertensive crisis oracute severe hypertension: an acute increase in systolic pressure ≥ 180 mm Hg and/or diastolic blood pressure ≥ 120 mm Hg Hypertensive urgency: hypertensive crisis that is either asymptomatic or with isolated nonspecific symptoms (e.g., headache, dizziness, or epistaxis) without signs of organ damage Hypertensive emergency: hypertensive crisis with signs of end-organ damage, mainly in the cardiovascular, central nervous, and renal systems.
  • 4.
    Etiology Drug-related • Nonadherence toantihypertensives Drugs that may exacerbate hypertension (e.g., monoamine oxidase inhibitors (MAOIs), and tricyclic antidepressants (TCAs)., NSAIDS, cocaine, amphetamines, ecstasy, stimulant diet pills) Consumption of foods rich in tyramine (e.g., wine, chocolate, aged cheese, cured meat) during therapeutic use of MAOIs Pheochromocytoma, hyperthyroidism Acute and rapidly progressive renal disorders Collagen vascular diseases (e.g., SLE) Eclampsia/Pre-eclampsia Head trauma, spinal cord disorders
  • 5.
    Clinical Features Hypertensive urgency Asymptomatic or isolated, nonspecific symptoms (e.g., headache, dizziness, or epistaxis) Hypertensive emergency  Signs and symptoms of end-organ dysfunction  Cardiac  Heart failure exacerbation, pulmonary edema: dyspnea, crackles on examination  Myocardial infarction: chest pain, diaphoresis  Aortic dissection: chest pain, asymmetric pulses  Neurologic  Hypertensive encephalopathy: headache, vomiting, confusion, seizure, blurry vision, papilledema  Ischemic or hemorrhagic stroke: focal neurological deficits, altered mental status
  • 6.
     Renal: Acutehypertensive nephrosclerosis (formerly malignant nephrosclerosis)  Acute kidney injury (azotemia and/or oliguria, edema) and microhematuri Ophthalmic Acute hypertensive retinopathy: blurry vision, decrease in visual acuity, retinal flame hemorrhages, papilledema Other Microangiopathic hemolytic anemia: fatigue, pallor
  • 7.
  • 8.
    Approach to AcuteManagement 1. Confirm blood pressure manually and on bilateral upper extremities. 2. Determine if there are signs of end-organ damage. a. Focused history/physical (RED FLAGS: Dyspnea, Chest pain, Altered mental status, Focal neurologic symptoms) b. Select screening tests 3. For hypertensive emergencies a. ABCDE approach b. Admit patients (ideally to ICU). c. Lower the blood pressure acutely using IV agents and aim for targets based on the affected end-organs (see "Treatment" below). d. Evaluate and treat underlying disorders. 4. For hypertensive urgency a. Select, reinstitute, or modify oral antihypertensive therapy b. In patients with a new diagnosis, evaluate for secondary causes of hypertension. c. Arrange follow-up, monitoring, and counseling.
  • 9.
    Diagnostics Evaluate for signsof end-organ damage  Laboratory studies  CBC: signs of microangiopathic hemolytic anemia  U&E: altered electrolytes and/or elevated creatinine and urea, which suggest kidney failure  BNP: elevated in heart failure  Troponin: elevated in myocardialischemia  Urinalysis: signs of glomerular injury (e.g., proteinuria, hematuria)  ECG: left ventricular hypertrophy , signs of cardiac ischemia (e.g., ST depressions or elevations)  Chest x-ray: cardiomegaly, pulmonary edema
  • 10.
    Diagnostics Additional evaluation toconsider  Urine pregnancy test  Toxicology screen  CT chest with IV contrast if chest pain is concerning for aortic dissection  Consider Transthoracic echocardiography if clinical features suggest pulmonary edema  Consider CT head if neurological symptoms are present.
  • 11.
    Treatment – Urgency Outpatient treatment is recommended.  Move patient to a quiet room for 30 minutes.  First diagnosis of hypertension, consider evaluation for secondary hypertension  Reinstitute or increase the dosage of existing oral antihypertensive therapy or consider a rapid-acting oral antihypertensive agent prior to discharge:  Clonidine  Captopril  Labetalol  Prazosin  Monitor the patient for a few hours to ensure BP is improving.  Discharge and ensure close follow-up with an outpatient provider / clinic  Recommend a Sodium restriction diet
  • 12.
    Treatment - Emergency General principles ABCDE assessment  Admission and immediate initiation of intravenous antihypertensive therapy  Continuous cardiac monitoring  Consider intra-arterial blood pressure monitoring.  Identify and treat any contributing comorbidities (e.g., chronic renal failure).  IV fluids if signs of volume depletion  Monitor U&E every 6 hours.
  • 13.
    Treatment - Emergency Considerthe following factors when choosing intravenous antihypertensive drugs:  Desired rate of decrease in blood pressure  End-organ system affected  Underlying disorder  Presence or absence of comorbidities (e.g., heart failure, COPD)  Pharmacokinetics and adverse effects of the agent The drugs most commonly used to treat hypertensive emergencies are nitroprusside (carries a risk of cyanide toxicity), labetalol, and nicardipine.
  • 15.
    Treatment - Emergency Intravenousantihypertensives:  Calcium channel blockers  Nicardipine  Clevidipine  Nitric-oxide dependent vasodilators  Sodium nitroprusside  Nitroglycerin  Direct arterial vasodilators:  Hydralazine (The response to and duration of action of IV hydralazine can be unpredictable. It should, therefore, be used with caution.)  Antiadrenergic drugs  Selective beta-1 antagonist: esmolol  Nonselective beta blocker with alpha-1 antagonism: labetalol  Nonselective alpha antagonist: phentolamine  D1 agonist  Fenoldopam ACE inhibitor: enalaprilat
  • 18.
    Treatment - Emergency Meanarterial pressure should not be lowered by more than 25% within the first hour, except in special cases. Reducing the blood pressure too rapidly can lead to hypoperfusion and ischemia in certain organs (e.g., brain, kidney, heart). Calculation:  MAP = cardiac output (CO) × total peripheral resistance (TPR)  MAP = ⅓ systolic (SP) + ⅔ diastolic (DP) = (SP + 2 x DP)/3  MAP = DP + 1/3(SP – DP)
  • 19.
    Treatment - Emergency Generalgoal  Reduce BP by max. 25% within the first hour to prevent coronary insufficiency and to ensure adequate cerebral perfusion press  Reduce BP to ∼ 160/100–110 mm Hg over the next 2–6 hours.  Reduce BP to patients baseline over 24–48 hours. Special cases Indications for the rapid lowering of systolic BP (usually to < 140 mm Hg) in the first hour of treatment include severe  aortic dissection,  pre-eclampsia or eclampsia  pheochromocytoma with hypertensive crisis.
  • 20.
    Hypertension in Jamaica If left untreated, hypertensive emergencies are associated with a 1-year mortality ra of > 80% and a median survival of 10–11 months.  One in 3 Jamaicans are hypertensive – 35.8% women and 31.7% men, according to the Jamaica Health and Lifestyle Survey for 2016/17.  Four out of every 10 people with the disease are unaware of their status – 60% men and 26% women.  At the same time, more and more Jamaicans aged 15 to 74 years old are developing hypertension.
  • 21.
    Summary  Hypertensive crisesrefer to acute increases in blood pressure (generally defined as ≥ 180/120 mm Hg) that cause or increase the risk of end-organ damage  They can be due to primary hypertension or precipitated by underlying conditions  Management consists of rapidly identifying end-organ damage with patient history physical examination, and focused testing.  Emergency requires admission and IV anti-hypertensives .  Urgency requires rapid follow-up and oral anti-hypertensives.
  • 22.
    References  Amboss ClinicResource, www.Amboss.com, https://www.amboss.com/us/knowledge/Hypertensive_crises/ (Accessed September 2, 2021)  Whelton, PK, Carey, RM et al. 2017 ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ASH/ASPC/NMA/PCNA Guideline for the Prevention, Detection, Evaluation, and Management of High Blood Pressure in Adults. Hypertension. 2017  Shantsila A, Lip GYH. Malignant Hypertension Revisited—Does This Still Exist?. American Journal of Hypertension. 2017  Varon J, Marik PE. Clinical review: the management of hypertensive crises. Crit Care. 2003; 7 (5): p.374-384.  Peixoto AJ. Acute Severe Hypertension. N Engl J Med. 2019; 381 (19): p.1843-1852. doi: 10.1056/nejmcp1901117

Editor's Notes

  • #5 Nonselective inhibition of monoamine oxidase → ↓ breakdown of epinephrine, norepinephrine, serotonin, and dopamine → ↑ levels of epinephrine, norepinephrine, serotonin, and dopamine Tyramine stimulates the sympathetic nervous system by releasing other neurotransmitters, such as noradrenaline, from vesicles into the synaptic cleft.