HYPERTENSIVE EMERGENCIES

Sulaiman Usaid G.
MBChB V
Facilatator: Dr Jack T.
 OUTLINE

• Case presentation
• Definitions
• Epidemiology
• Etiology/pathophysiology
• Approach to mgt
• Workup
• Treatment
 case presentation
Demographics
• Name: Mulindwa Robert
• Age: 30y
• Sex: male
• Tribe: muganda
• Religion: christian
• Occupation:blacksmith
• Address: mayirikiti, Mityana
• Marital status: single
• DOA: 30/7/2021
• Presenting complaint:
– Generalized body swelling 2/52
• History of presting complaint
– M.R was relatively well 2 weeks prior to admission when he developed generalized body
swelling of gradual onset, started as early morning facial puffiness subsiding as day progresses
– Later progressed to involve the feet and then the abdomen
– It was associated with passing out frothy urine, occasionally tea colored, reduced urinary
frequency and painful urination
– Abdominal pain; localized in the epigastrium & lower abdomen, nause, vomiting, diarrhoea,
heartburn + fevers were reported
– Also reported hx of chest pain, exertional dyspnoea, shortness of breath while flat and air
hunger at night
• Review of system:
– CNS: pt reports hx of bluring of vision, other senses intact, no LOC, seizures or
evidence of FND.
– Other systems unremarkable
• Medical hx:
– Index admission, sero –ve for HIV, no hx chronic illness/ medication, no allergies
• Surgical hx: unremarkable
• Social hx: +ve hx of chronic alcohol consumption and ciggarate smooking
with (7.5 pack years)
• Family hx: -ve hx familial disesese
• Summary:
• M.R a 30year old male presented with 2/52 hx of gen body
swelling associated with frothy tea colored urine, decreased
urinary frequency, dysuria, fever and abdominal pain. This was
also associated with chest pain, exertional dyspnoea,
orthopnoea and PND.
• Patient is a chronic alcoholic and ciggarate smooker.
• O/E
– Young man, sick looking, unkempt, afebrile, with moderate pallor, no
jaundice, dry mucus membrane, facial puffiness, hypo-pigmented
skin lesions, bilateral pitting oedema
– Vitals: BP; 222/137 mmHg, PR: 85 b/min, SPO2: 97%, RR: 18b/min
– P/A: Mild tenderness, soft, epigastric + suprapubic tenderness, no
organomegalies, bowel sounds heard.
– Other systems unremarkable
• Impression: A 30yr/M with
– Malignant hypertension
– ? CKD complicated by
• Aneamia
• Uremic gastritis
– r/o heart failure
• Investigations
– Urinalysis: showed protein ++++
– CBC: hb (low) 9.0g/dL, neutrophils (low): 7.7x10ᶟµL, RDW(high); 61.4 fL
– Abdominal ultrasound: showed features of renal paranchyma disease, transudative ascitis
– Fundoscopy, electrolytes, RFTs, LFTs, CXR were ordered, however not done.
• Treatment
– IV lasix 80mg b.d *5/7
– Tabs carvedilol 12.5mg b.d *1/52
– Tabs methyldopa 250mg 8hrly * 2/52
– Tabs calcivita 1T o.d * 2/52
– Tabs cacitriol 0.25mcg o.d* 2/52
– Oral morphine 5mls 6hrly * 2/52
– Tabs bisacodyl 10mg o.d * 2/52
– Caps omeprazole 20mg o.d * 2/52
– Patient linked with social workers for socio economic support
British HTN society
 Definitions
• Hypertensive emergency(crisis);
– Defined as severe elevation of BP>(180/120mmHg) coupled with
evidence of impending or progressive end organ damage
• HTN urgency:
– Urgency is defined as severely elevated BP (ie, systolic BP >180 mm
Hg or diastolic BP >120 mm Hg) with no evidence of target organ
damage.
• Resistant HTN
– This is failure to reach goal BP in patients who adhering to full doses
of an appropriate 3 drug regimen that includes a diuretic.
 Other Terminology
• Accelerated HTN
– defined as a recent significant increase over baseline BP that is
associated with target organ damage. This is usually seen as vascular
damage on funduscopic examination, such as flame-shaped
hemorrhages or soft exudates, but without papilledema.
• malignant HTN
– MHT as a group of disorders with out of range elevation in blood
pressure with the concomitant damage of at least two different
target organs + papilloedem
 Epidemiology
• With progress in anti-hypertensive treatment – decrease in the lifetime incidence of
HTN emergencies from 7% to 1% in the USA.
• Hypertensive crisis more common among elderly.
• HTN related problems amount for 25% of all patient visits to emergency department,
33% of these are HTN emergencies
• Morbidity and mortality depend on the extent of end-organ damage on presentation
and the degree to which BP is controlled subsequently. BP control may prevent
progression to end-organ impairment.
• The 1-year survival rate associated with this condition has increased from only 20%
(prior to 1950) to a survival rate of more than 90% with appropriate medical treatment.
• Nonetheless, despite its relative rarity, the number of US emergency department (ED)
visits for hypertensive emergency and the rate per million adult ED visits increased
more than two-fold between 2006 and 2013. [4]
 Etiology
Most common
- most have history of poor treatment/compliance, or an abrupt discontinuation of
their medication
- rapid unexplained rise in BP in patient with chronic essential HTN
- Drug withdrawal eg benzos, alcohol

Other causes
- Renal parenchymal disease (80% of secondary causes)
- Reno vascular disease eg Atherosclerosis, reanal artery stenosis
- Endocrine eg Pheochromocytoma, conn dse
- Coarctation of the aorta
- Preeclampsia/Eclampsia
- Medications
 Pathophysiology
• Failure of normal autoregulation + abrupt rise in SVR
• Increase in SVR due to release of humoral vasoconstrictors from the stressed vessel
wall.
• Endothelium plays a central role in BP homeostasis via substances such as Nitric
oxide and prostacyclin
• Increased pressure starts a cycle of
- endothelial damage
- local activation of clotting cascade
- fibrinoid necrosis of small vessels
- release of more vasoconstrictors
• Process leads to progressive increase in resistance and further endothelial
dysfunction
 PATHOPHYSIOLOGY
• BP=CO * TPR
• Rate at which MAP rises more important than absolute rise.

Acute rise in BP Failure of vasoconstriction Endothelial

by autoregulation damage

FIBRINOID Activates coagn and Depsn. of proteins/

NECROSIS inflammation fibrinogen in vessel wall

 RAAS plays an important role in initiating and perpetuating BP rise by causing vasoconstriction and
fluid retention.
 CENTRAL NERVOUS SYSTEM
• The CNS is affected as the elevated BP overwhelms the normal cerebral
autoregulation.
• Under normal circumstances, with an increase in BP, cerebral arterioles
vasoconstrict and cerebral blood flow (CBF) remains constant.
• During a hypertensive emergency, the elevated BP overwhelms arteriolar control
over vasoconstriction and autoregulation of cerebral blood flow
• This results in transudate leak across capillaries and continued arteriolar damage.
• Subsequent fibrinoid necrosis causes normal autoregulatory mechanisms to fail,
leading to clinically apparent papilledema, the clinical picture of malignant
hypertension.
• The end result of loss of autoregulation is hypertensive encephalopathy, CVA,
cerebral infarctionsubarachnoid hemorrhage, and/or intracranial hemorrhage.
 CARDIOVASCULAR SYSTEM
• The cardiovascular system is affected as increased cardiac
workload leads to acute left ventricular dysfunction; this is
accompanied by myocardial ischemia/infarction,acute
pulmonary edema, and/or aortic dissection.
 RENAL SYSTEM
• The renal system is impaired when high BP leads to
arteriosclerosis, fibrinoid necrosis, and an overall impairment
of renal protective autoregulation mechanisms.
• The end result is acute renal failure/insufficiency,
• This may manifest as worsening renal function, hematuria, red
blood cell (RBC) cast formation, and/or proteinuria.
 Pregnancy
• In pregnant patients, acute hypertensive crisis usually results
from underlying hypertensive disease or severe preeclampsia
and can lead to maternal stroke, cardiopulmonary
decompensation, fetal decompensation caused by reduced
uterine perfusion, abruption, and stillbirth.
• Preeclampsia may also be complicated by pulmonary edema
 Hypertensive Retinopathy
• Fundoscopy used in diagnosing HTN retinopathy
• but the absence of the Fundoscopy findings like retinal
exudates, haemorrhages, or papilledema does not exclude the
diagnosis.
 HTN Retinopathy - Fundoscopy
• Keith-Wagener classification
Stage I- arteriolar sclerosis with thickening, irregularity and tortuosity
Stage II -AV nipping or compression
Stage III -Flame shaped haemorrhages and cotton wool spots
Stage IV -Papilledema
• “presence of stage III and IV lesions – implies failure of the CNS vascular
auto-regulation”
 HTN Retinopathy
• ..
HTN retinopathy
• The most common clinical presentations of hypertensive
emergencies are cerebral infarction (24.5%), pulmonary edema
(22.5%), hypertensive encephalopathy (16.3%), and congestive
heart failure (12%).
• Other clinical presentations associated with hypertensive
emergencies include intracranial hemorrhage, aortic
dissection, and eclampsia, as well as acute myocardial
infarction, and retinal and renal involvement.
APPROACH TO MANAGEMENT
 Approach con’t
History • Assertain etiology:
• Focus on symptoms of acute end organ • Medications: esp hypertensive
damage
drugs/their compliance, usage of
• CNS: confusion, seizures, irritability, focal
neurological deficits, coma, evidence of illicit drugs
intracranial hemmorrhage on CT • Family hx, lifestyle
• CVS: chest pain, dyspnea, fatigue, • Comorbidities
features of HF
• Renal: heamaturia, evidence of AKI
• Ophalmoologic: visual changes, retinal
hemorrhage and papilledema
 Approach con’t
Physcal evaluation
• Use an approach based on organ systems to identify signs of
end-organ damage
• Full CNS, CVS exam + lung auscultaion for crackles.
• BP measurement on both arms
• Check for abdominal masses and bruits.
• Fundoscopy
 Investigations
• Labs • Imaging / others
– Urinalysis – CXR /Aortic angiography
– Blood urea, creatinine and – Head CT
electrolytes – Renal ultrasound:
– CBC – Renal angiography
– Blood glucose – Echocardiogram/ 12-lead ECG: to
– Urinary catecholamines detect or quantify left ventricular
– pregnancy test, and endocrine hypertrophy
testing may be obtained, as needed.
– Serum and HDL cholesterol
 Treatment
Guidelines recommendations (The 2017 American College of Cardiology/American Heart
Association)
• Admit adults with a hypertensive emergency to an ICU for continuous monitoring of BP
and target organ damage, as well as for parenteral administration of an appropriate
medication.
• For adults with a compelling condition (ie, aortic dissection, severe preeclampsia or
eclampsia, or pheochromocytoma crisis), lower SBP to below 140 mm Hg during the first
hour and to below 120 mm Hg in aortic dissection.
• For adults without a compelling condition, reduce the SBP to a maximum of 25% within
the first hour; then, if the patient is clinically stable, lower the BP to 160/100 -110 mm
Hg over the next 2-6 hours, and then cautiously to normal over the following 24-48
hours.
 VASODILATORS
DRUG DOSAGE ONSET/DUR ADV.EFFE
Nitroprusside 0.25-10mcg/kg/min Instant/1-2min. Thiocyanate,cyanide
poisoning
Nitroglycerine 5-100mcg/min 1-5min/3-5min Flushing,headache,met
hemoglobin
Nicardipine 5-15mg/hr 5-10min/1-4hr Tachycardia,flushing.heada
che
Hydralazine 10-20mg 5-15min/3-8hr Flushing,tachy,caution in
CVA
Enalapril 10-40mg IM,1.25- 20-30min/6hr Hypotension,vomiting,hype
5MG1Vq6hr rkalemia
Fenoldopam 0.1-0.3mcg/kg/min 5min/10-15min Flushing,headache,tachy
 ADRENERGIC INHIBITORS

DRUG DOSAGE ONSET/DUR ADV.EFF

Labetalol 20-80mg iv bolus every 5-10min/3-6hrs Heart block,ortho
10 min,2mg.min iv hypotension.avoid-heart
(a+b blocker) failure,asthma
infusion
Esmolol 200-500 mcg/kg/min for 1-2min/10-20min Hypotension,avoid-heart
4min,then 150- failure,asthma
(b-1 selective
300mcg/kg/min
blocker)
Phentolamine 5-15mg iv 1-2min/3-10min Tachycardia,flushing,heada
che
(a1 blocker)
 Neurological emergencies
• Hypertensive encephalopathy
– In hypertensive encephalopathy, the treatment guidelines are to
reduce the MAP 25% over 8 hours.
– Labetalol, nicardipine, esmolol are the preferred medications;
nitroprusside and hydralazine used with caution
 Neurological emergencies
• Acute Ischemic stroke
– For acute ischemic stroke, the preferred medications are labetalol and
nicardipine.
– Withhold antihypertensive medications unless the SBP is above 220 mm Hg or
the DBP is over 120 mm Hg, UNLESS the patient is eligible for IV tissue
plasminogen activator (tPA); then, the goal is a gradual reduction of BP with a
goal SBP of less than 185 mm Hg and a DBP below 110 mm Hg before
initiating thrombolitic therapy.
– After initiating drug therapy but before administering tPA, the SBP should be
maintained at less than 180 mm Hg and the DBP below 105 mm Hg for 24
hours.
 Neurological emergencies
• Acute Intra-cerebral haemorrhage
– For acute intracerebral hemorrhage, the preferred medications are
labetalol, nicardipine, and esmolol; avoid nitroprusside and hydralazine
or use with caution
– The treatment is based on clinical/radiographic evidence of increased
intracranial pressure (ICP). If there are signs of increased ICP, maintain
the MAP just below 130 mm Hg (or SBP < 180 mm Hg) for the first 24
hours after onset.
– In patients without increased ICP, maintain the MAP below 110 mm Hg
(or SBP < 160 mm Hg) for the first 24 hours after symptom onset.
 Neurological emergencies
• Subarachnoid hemorrhage
– In subarachnoid hemorrhage, nicardipine, labetalol, and esmolol are
also the preferred agents; again, nitroprusside and hydralazine should
be avoided.
– Maintain the SBP below 160 mm Hg until the aneurysm is treated or
cerebral vasospasm occurs.
– Although oral nimodipine is used to prevent delayed ischemic
neurologic deficits, it is NOT indicated for treating acute
hypertension.
 Cardiovascular emergencies
• Aortic dissection
– Beta blockers are the recommended antihypertensive agents in
patients with hypertension and thoracic aortic disease.
– In aortic dissection, the preferred medications are labetalol,
nicardipine, nitroprusside (with beta-blocker), esmolol, and morphine
sulfate
– However, avoid beta-blockers if there is aortic valvular regurgitation
or suspected cardiac tamponade
 CVS emergencies
• Acute coronary syndrome
– For acute coronary syndrome, beta blockers and nitroglycerin are the
preferred drugs.
– Treatment is indicated if the SBP is above 160 mm Hg and/or the DBP
is over 100 mm Hg. Reduce the BP by 20%-30% of baseline.
– Note that thrombolytics are contraindicated if the BP is above
185/100 mm Hg.
 CVS emergencies
• Acute heart failure
– In acute heart failure, the preferred medications are IV nitroglycerin
or sublingual nitroglycerin and IV enalaprilat. Treat with vasodilators
(in addition to diuretics) for a SBP of 140 mm Hg.
– In hypertensive adults with preserved ejection fraction and
symptoms of volume overload, prescribe diuretics to control BP.
– For those with persistent hypertension after management of volume
overload, prescribe ACEIs or ARBs and beta blockers titrated to
achieve an SBP below 130 mm Hg.
 Preeclampsia/eclampsia

• The preferred medications are hydralazine, labetalol, and

nicardipine. Avoid enalapril
• In women with eclampsia or preeclampsia, the SBP should
lowered to below 140 mm Hg during the first hour.
• If the platelet count is less than 100,000 cells mm3, the BP
should be maintained below 150/100 mm Hg.
• Patients with eclampsia or preeclampsia should also be treated
with IV magnesium sulfate to avoid seizures
 Renal emergency
• Renal insufficiency/CKD: are a cause and effect of high BP. Goal
is to prevent further renal damage by maintaining adequate
blood flow.
• Nicardipine, labetalol, hydralazine, nitroglycerine are effective,
avoid IV nitropruside.
 Cocaine toxicity/pheochromocytoma

• Diazepam, phentolamine, and nitroglycerin/nitroprusside are the preferred

drugs.
• Hypertension and tachycardia from cocaine toxicity rarely require specific
treatment. Alpha-adrenergic antagonists (phentolamine) are the preferred
agents for cocaine-associated acute coronary syndromes.
• Pheochromocytoma treatment guidelines are similar to that of cocaine
toxicity. The ACC/AHA recommends lowering the SBP to below 140 mm Hg
during the first hour, with phentolamine IV bolus dose of 5 mg.
• Additional bolus doses may be given every 10 minutes as needed to achieve
target BP. Only after alpha blockade can beta blockers be added for BP control
 REFERENCE
• Harrison’s principles of internal medicine 19th edition.
• Davidson’s principles and practice of medicine 22nd edition.
• www.medscape.com