Hypertensive Emergencies and Urgencies

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Chapter: Essential pharmacology : Antihypertensive Drugs

Systolic BP > 180 or diastolic BP > 120 mm Hg with evidence of active end organ damage is labelled ‘hypertensive emergency’, while the same elevation of BP without signs of endorgan damage is termed ‘hypertensive urgency’.



Systolic BP > 180 or diastolic BP > 120 mm Hg with evidence of active end organ damage is labelled ‘hypertensive emergency’, while the same elevation of BP without signs of endorgan damage is termed ‘hypertensive urgency’.


Controlled reduction of BP over minutes (in emergencies) or hours (in urgencies) is required to counter threat to organ function and life in:


·      Cerebrovascular accident (haemorrhage) or head injury with high BP.


·      Hypertensive encephalopathy.


·      Hypertensive acute LVF and pulmonary edema.


·      Unstable angina or MI with raised BP.


·      Dissecting aortic aneurysm.


·      Acute renal failure with raised BP.


·      Eclampsia.


·      Hypertensive episodes in pheochromocytoma, cheese reaction or clonidine withdrawal.


Nifedipine (10 mg soft geletine cap) orally every ½–1 hr was widely employed for rapid BP reduction in urgencies. This practice has now been discarded because of inability to control rate and degree of fall in BP as well as serious adverse consequences/mortality. Other rapidly acting oral drugs like captopril (25 mg) or clonidine (100 μg) every 1–2 hours have also been found unsatisfactory. Parenteral drugs with controllable action are now used. Mean BP should be lowered by no more than 25% over minutes or a few hours and then gradually to not lower than 160/100 mmHg. Drugs employed are:


1. Sodium Nitroprusside 

Because of predictable, instantaneous, titratable and balanced arteriovenous vasodilatory action which persists without tolerance till infused, nitroprusside (20–300 μg/min) is the drug of choice for most hypertensive emergencies. However, it needs an infusion pump and constant monitoring, but is the most effective drug.


2. Glyceryl Trinitrate 

Given by i.v. infusion (5–20 μg/min) GTN also acts within 2–5 min and has brief titratable action. Its predominant venodilator action makes it particularly suitable for lowering BP after cardiac surgery and in acute LVF, MI, unstable angina. Tolerance starts developing after 18–24 hours of continuous infusion.


3. Diazoxide 

Given as fractional i.v. bolus doses—BP once lowered remains so for > 6 hours; constant monitoring is not required.


4. Hydralazine 

10–20 mg i.m. or slow i.v. injection; acts in 20–30 min and keeps BP low for 4–8 hours. It has been especially used in eclampsia. It is to be avoided in patients with myocardial ischaemia or aortic dissection.


5. Esmolol 

This β blocker given as 0.5 mg/kg bolus followed by slow i.v. injection (50–200 μg/kg/min) acts in 1–2 min; action lasts for 10–20 min. It is particularly useful when cardiac contractility and work is to be reduced, such as in aortic dissection (nitroprusside may be given concurrently) and during/after anaesthesia. The BP lowering action is weaker. Excess bradycardia is to be guarded.


6. Phentolamine 

This α1 + α2 blocker is the drug of choice for hyperadrenergic states—hypertensive episodes in pheochromocytoma, cheese reaction, clonidine withdrawal. Injected i.v. (5–10 mg) it acts in 2 min and action lasts 5–15 min. Tachycardia and myocardial ischaemia may complicate its use. A β blocker may be added.


7. Labetalol 

Injected i.v., it is an alternative to α + β blockers for lowering BP in pheochromocytoma, etc. but has only weak α blocking action. It has been used to lower BP in MI, unstable angina, eclampsia also. Concomitant CHF and asthma preclude its use.


8. Furosemide 

(20–80 mg oral or i.v.) It may be given as an adjunct with any of the above drugs if there is volume overload (acute LVF, pulmonary edema, CHF) or cerebral edema (in encephalopathy), but should be avoided when patient may be hypovolemic due to pressure induced natriuresis (especially in eclampsia, pheochromocytoma).

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