1. Hypertensive
Urgency/Emergency
Dr. Sudhir Deo
House Officer
GPEM, BPKIHS

2. JNC 7 Classification Of HTN

3. Evaluation Of Patient’s with HTN
Evaluation of hypertensive patients has three objectives:
(1) to assess lifestyle and identify other cardiovascular
risk factors or associated disorders that may affect
prognosis and guide treatment
(2) to reveal identifiable causes of high BP
(3) to assess the presence or absence of target organ
damage

4. Cardiovascular risk factors
Major Risk Factors
Hypertension*
Age (older than 55 years for men, 65 years for women)†
Diabetes mellitus*
Elevated LDL (or total) cholesterol, or low HDL cholesterol*
Estimated GFR <60 mL/min
Family history of premature CVD (men <55 years of age or
women <65 years of age)
Microalbuminuria
Obesity* (BMI >30 kg/m2)
Physical inactivity
Tobacco usage, particularly cigarettes

5. Identifiable causes of hypertension
Chronic kidney disease
Cushing’s syndrome and other glucocorticoid excess states
including chronic steroid therapy
Drug induced or drug related (see table 18)
Obstructive uropathy
Pheochromocytoma
Primary aldosteronism and other mineralocorticoid excess
states
Renovascular hypertension
Sleep apnea
Thyroid or parathyroid disease

6. Target Organ Damage
Heart
LVH
Angina/prior MI
Prior coronary revascularization
Heart failure
Brain
Stroke or transient ischemic attack
Dementia
CKD
Peripheral arterial disease
Retinopathy
Placenta
Eclampsia

7. Approach to All Patients With HTN
Look for:
• LOC and orientation
• Respiratory status
• For neurological deficits
 Hemiparesis, slurred speech
• Baseline
Temperature, HR, RR, BP
• Maintain continuous monitoring of BP and HR
• BP should not only be measured in both the supine position
and the standing position (assess volume depletion), but it
should also be measured in both arms (a significant difference
may suggest aortic dissection).

8. •Assess for changes in cardiac rhythm if patient is on a monitor
•Monitor I&O
SaO2 via pulse oximetry if available
For associated symptoms
Visual disturbance, chest pain, peripheral edema, hematuria

9. Drug use in Hypertension

13. Combination drugs

14. REF: JNC -7 (THE 7TH REPORT OF JOINT NATIONAL COMMITTEE ON PREVENTION,
DETECTION, EVALUATION AND TREATMENT OF HIGH BLOOD PRESSURE) PAGE 27, 28,29

15. HTN URGENCY

16. Severe elevations in BP (DBP≥120-130mmhg) without evidence
progressive target organ dysfunction
Examples:
Severe uncomplicated essential hypertension
Severe uncomplicated secondary hypertension
Postoperative hypertension
Drug-induced hypertension
Rebound hypertension (i.e., sudden withdrawal of clonidine)
Cessation of prior antihypertensive therapy
Severe hypertensive crises related to anxiety, panic attacks or pain

17. TREATMENT OF HTN URGENCY:
Goals: Lower mean arterial pressure to goal or near goal within several hours.
Oral medications can be used.
MAP=(2xDP)+SP/3
Lower mean arterial pressure by 20- 25% or diastolic pressure to <100 to 110
mmHg within 30–60 minutes. excessive falls in pressure that may precipitate
renal, cerebral, or coronary ischemia.
Agents that reliably cause an immediate fall in BP include
captopril(25-50 mg), central sympatholytics(clonidine0.1–0.2
mg), labetalol(200–400 mg), and amlodipine(2.5–5 mg)
•Initiation of therapy with two oral agents is appropriate to lower BP
to an intermediate target over 24 to 72 hours
•Appropriate follow-upwithin 3 days.

19. HTN EMERGENCY

20. Hypertensive Emergencies
Severe elevations in BP (>180/120 mmHg)
Complicated by evidence of impending or progressive target
organ dysfunction.
Require immediate BP reduction (not necessarily to normal) to
prevent or limit target organ damage.
Examples
hypertensive encephalopathy
Intracerebral hemorrhage,
acute MI
acute left ventricular failure with pulmonary edema
unstable angina
dissecting aortic aneurysm,
eclampsia

21. Initial Evaluation of Patients with a Hypertensive
Emergency
History
• Prior diagnosis and treatment of hypertension
• Intake of pressor agents: street drugs, sympathomimetics
• Symptoms suggesting an acute end-organ involvement
• chest pain –myocardial infarction, thoracic aortic
dissection
• back pain –thoracic aortic dissection
• dyspnea–acute pulmonary edema
• neurological symptoms-hypertensive encephalopathy

22. Physical examination
• Blood pressure –both upper limbs
• Fundoscopy
• Cardiopulmonary status
AR, MR , signs of CHF
• Neurologic status
level of consciousness, focal sigh of ischemia
• Body fluid volume assessment
• Peripheral pulses

23. Laboratory evaluation
Hematocrit and blood smear (microangiopathic hemolysis)
Urine analysis
Automated chemistry: creatinine, glucose, electrolytes
Electrocardiogram
Chest radiograph (if heart failure or aortic dissection is
suspected)
CT brain in patients with neurological symptoms
CT chest or MRI in patients with unequal pulses/ an enlarged
mediasternum

24. Clinical Characteristics HTN Emergency
Blood pressure: usually >140 mm Hg diastolic
Fundoscopic findings :
accelerated HT -grade 3 retinopathy ( haemorrhages,
exudates)
malignant HT -grade 4 retinopathy (papillodema)
Neurologic status: headache, confusion, somnolence,
stupor, vision loss, focal deficits, seizures, coma
Renal status: oliguria, azotemia high levels of nitrogen-
containing compounds
Gastrointestinal status: nausea, vomiting

25. HTN EMERGENCY TREATMENT
GOALS:
Almost all hypertensive emergencies are caused or
exacerbated by intense systemic vasoconstriction,
often with profound blood volume reduction
goal of therapy is to reduce vasoconstriction while
maintaining adequate perfusion of target organs

26. Treatment:
 All HTN Emergencies should be admitted and treated in
ICU/CCU
 The initial goal of therapy in hypertensive emergencies is to
reduce mean arterial BP by no more than 25 percent
(within minutes to 1 hour)
 If clinical is stable, reduce BP to 160/100–110 mmHg
within the next 2–6 hours
 Further gradual reductions toward a normal BP can be
implemented in the next 24–48 hours.

27. Exceptions
• acute stroke in evolution (for which no BP
lowering is generally recommended)
• The American Heart Association recommends
• Treatment with intravenous labetalol or nicardipine
Started when BP values are above 220/120mmHg
The target BP should be a 10–15% lowering of BP

28. DRUGS FOR HTN EMERGENCY
• Nitroprusside — a rapidly acting arteriolar and venous dilator, given as an
intravenous infusion. Initial dose: 0.25 to 0.5 mcg/kg per min; maximum
dose: 8 to 10 mcg/kg per min which should be continued for no more
than 10 minutes.
• Nitroglycerin — a rapidly acting venous and, to a lesser degree, arteriolar
dilator, given as an intravenous infusion. Initial dose: 5 mcg/min;
maximum dose: 100 mcg/min.
• Labetalol — an alpha- and ß-adrenergic blocker, given as an intravenous
bolus or infusion. Bolus: 20 mg initially, followed by 20 to 80 mg every 10
minutes to a total dose of 300 mg. Infusion: 0.5 to 2 mg/min.
• Nicardipine — a calcium channel blocker, given as an intravenous
infusion. Initial dose: 5 mg/h; maximum dose: 15 mg/h.
• Clevidipine — a calcium channel blocker. Initial dose: 1 mg/hour;
maximum dose: 16 mg/hour .

29. DRUGS FOR HTN EMERGENCY
• Fenoldopam — a peripheral dopamine-1 receptor agonist, given as an
intravenous infusion. Initial dose: 0.1 mcg/kg per min; the dose is titrated
at 15 min intervals, depending upon the blood pressure response.
• Hydralazine — an arteriolar dilator, given as an intravenous bolus. Initial
dose: 10 mg given every 20 to 30 minutes; maximum dose: 20 mg.
• Propranolol — a ß-adrenergic blocker, given as an intravenous infusion
and then followed by oral therapy. Dose: 1 to 10 mg load, followed by 3
mg/h.
• Phentolamine — an alpha-adrenergic blocker, given as an intravenous
bolus. Dose: 5 to 10 mg every 5 to 15 minutes.
• Enalaprilat — an angiotensin converting enzyme inhibitor, given as an
intravenous bolus. Dose: 1.25 mg every six hours.

30. Drugs In HTN Emergency

35. Drugs of choice and relative contraindications for hypertensive emergencies

37. References
• JNC VII Seventh report of Prevention,
Detection, Evaluation, and Treatment of
High Blood Pressure
• Manual of Hypertension of the European
Society of Hypertension 2008