This document discusses the management of hypertensive emergencies. It begins by defining hypertensive emergencies as sudden increases in blood pressure associated with end organ damage, versus urgencies which are severe elevations without damage. It then discusses the pathophysiology, symptoms, examination findings, and management of various hypertensive crises including those involving the brain, heart, vasculature, kidneys, and pregnancy. It provides guidelines on drug therapy and goals for lowering blood pressure in different situations, as well as considerations for perioperative and intraoperative hypertension.

1. MANAGEMENT OF
HYPERTENSIVE EMERGENCIES
PRESENTOR:DR DEEPTI
MODERATOR-DR HRICHA

2. Introduction
• Hypertension is one of the leading causes of the global burden of disease.
• Hypertension doubles the risk of cardiovascular diseases, including
coronary heart disease (CHD), ischemic and hemorrhagic stroke, renal
failure, and peripheral arterial disease
• Worldwide, hypertension may affect as many as 1 billion people and be
responsible for ~7.1 million deaths per year
• HTN is No 1 modifiable risk factor for CVD.

3. JNC guidelines

4. Acute Hypertensive Crises
●Hypertensive emergencies, sudden increase in systolic and
diastolic blood pressure associated with end organ damage of
the CNS, heart & or kidneys.
●Hypertensive urgencies, severely elevated BP without acute
end-organ damage.

5. ●Pathophysiology:
●Abrupt ↑ in systemic vascular resistance (humoral
vasoconstrictors)
●Severe elevations of BP→endothelial injury →fibrinoid
necrosis of the arterioles →deposition of platelets and
fibrin → breakdown of the normal autoregulatory
function.
●Resulting ischemia →release of vasoactive substances

6. Hypertensive Crises
●Neurologic – Ischemic & Hmg stroke, head
trauma, HTN encephalopathy
●Cardiac- acute coronary syndrome , acute heart
failure
●Vascular – acute aortic dissection
●Renal – acute renal failure
●Pregnancy- Eclampsia
●Sympathetic overactivity- pheochromocytoma ,
withdrawal of drugs likeclonidine/b-blockers

7. Symptoms of HMOD
Headache,confusion,seizure,unresponsiveness
Blurry vision
Nausea & vomiting
Chest pain
Shortness of breath
Severe anxiety
Thirst, polyuria, nocturia, haematuria
Cold extremities

8. Examination of HMOD
• Neurological examination and cognitive status
• Fundoscopic examination for hypertensive retinopathy(hard exudates,
cotton wool spots & papilloedema is indicates severe
(grade2/3)hypertensive retinopathy)
• Palpation and auscultation of heart and carotid arteries
• Kidney palpation for renal enlargement (PCOD)
• Auscultation of heart & renal arteries for murmurs or bruits indicative
of aortic coarctation/ renovascular hypertension
• Comparison of radial with femoral pulse: to detect R-F delay in aortic
coarctation

10. Management of Hypertensive crises
●Hospital Care (urgencies), ICU care (emergencies)
●Invasive BP monitoring for emergencies
●Lower the BP + stabilize and reverse the damage to target
organs
●Sodium restriction and diuretics if fluid overload
●Parenteral anti-hypertensives (emergencies),
oral/parenteral (urgencies)

11. DRUGS DOSE ONSET
min
DOA
min
ADVERSE
EFFECT
ROLE
Clevidipine 1-2mg/hr iv infusion
Max dose-21mg/hr
or 100ml per 24hr
d/t lipid load
Delivered in lipid
emulsion
2-4 5-15 AF, lipid
formulation
contain
allergen(egg,
soya)
HTN EMR
Enalaprilat 1.25- 5mg every 6hr
iv
15-30 6-
>12h
r
Headache,dizzin
ess,ppt fall in
pressure in high
renin states
Acute LVF
Avoid in
pregnancy,
derranged kft
Fenoldopam 0.1mcg/kg/min
Max-1.6mcg/kg/min
5-10 30-
60
Tacycardia,head
ache,flushing
HTN EMR
Avoid-glaucoma,
raised ICP
Hydralazine 10-20mg iv/im(max
im-40mg)
iv-10-
20
1-
>4hr
Sudden ppt
drop in
BP,tachycardia,a
ggravation of
angina,flushing,
headache
In general
avoided-d/t
prolong &
unpredictable
hypotension

12. Nicardipin
e
5-15mg/hr iv
infusion
Max-30mg/hr
5-15 1.5-
>4hr
Local
phlebitis,edema,flushi
ng headache
HTN
EMR(+pregna
ncy)
avoid in HF
NTG 5-100mcg/min iv
infusion
2-5 5-10 methHB,tolerance,
reflex tachy,hypoxemia
Adjunct drug
in ACS
Nitroprussi
de
0.25-10mcg/kg/min
iv infusion
max:10mcg/kg/min
in <10min
0.5-1 1-10 Cyanide/thiocynate
toxicity, inc.ICP,dec.
CBF/coronary blood
flow, m/s spasm
Avoid in
CAD/CVA,
kidney & liver
failure,inc.ICP
Esmolol Load-500mcg/kg in
1min
25/50mcg/kg/min
infusion
1-2 10-30 bronchospas,bradycar
dia,t1/2 inc. in anemia
Periop HTN
Avoid-
decomp. HF
Labetolol Bolus-20mg iv
f/b 20-89mgiv bolus
every 10min
Max-300mg
Inf-0.5-2mg/min
5-10 2-4hrs Bronchospasm,paresth
esia,heart block
Aovid—
decomp.HF
/reactive
airway

13. Metoprolol 1-25-5mg iv ,f/b
2.5-5mg iv every 3-
6hr
20min 5-8hr role in MI,
periop
HTN(avoid in
decomp.HF)
Phentolamine 5-15mg iv bolus
every 5-15 min
1-2min 10-30 Tachyarryth
mia,flushing
role in
adrenergic
crisis like
pheochromo
cytoma,
cocaine
overdose

16. Acute coronary syndrome
• Pref. drugs-IV beta blockers(lobet/esmolol) with
vasodilator(NTG), ACEI
• Trea if SBP>160 7/or DBP>100
• Reduce BP by 20-30% of baseline
• Thrombolytics C/I if BP>185/100

17. Acute heart failure
• Pts with acute left ventricular dysfunction & acute
pul.edema receive loop diuretics
• Vasodilator like NTG/sod.nitroprusside help reduce
afterload
• The goal of these therapies is to ameliorate vol.excess
& improve pul.edema(mostly seen with 10-15%
reduction of BP)
• Note- drugs that inc. cardiac work(hydralazine) or
acutely decrease cardiac contractility( lobet) should be
avoided

18. Acute aortic dissection
• It is of 2 types:
-Type A-sx management
-Type B- medical management
• The mgt involves rapid SBP lowering to 100-
120mmhg in 20min to reduce aortic shearing forces
• Combination of beta blocker+vasodilator to reduce
force of ventricular contraction(lobet/esmolol+ NTG)

19. Acute ischaemic stroke
• If BP is high it can cause haemorrghagic transformation
of infarct/cerebral edema, but if CPP is low it can cause
ischaemic penumbra
• So intervene if SBP>220/DBP>120/MAP>145 mm Hg
• Agent of choice: lobet, clevididpine ,nicardipine
• For thrombolysis , BP<185/110

20. Acute haemorrhagic stroke
• Drug of choice:nicardipine,esmolol,lobet.
• Avoid-SNP,hydralazine
• Intracerebral-
a)Raised ICP-maintain SBP<180 for 1st 24 hrs
b)Normal ICP-maintain SBP<160 for 1st 24hrs
• Subarachnoid-maintain SBP<160 till aneurysm
treated/cerebral vasospasm occurs.

21. Hypertensive encephalopathy
• Goal is to reduce MAP by 20% over next 8hrs
• Drug of choice:clevidipine,lobet
• Avoid drugs like SNP(raise ICP)
• Avoid drugs like reserpine ,methyldopa which
have adverse effect on CNS

22. Renal emergencies
• Pathophysiology include: increased vascular
resistance, activation of RAAS &
hyperparathyroidism
• Goal is to prevent further renal damage by
maintaining adequate blood flow
• SNP,lobet are useful
• Short term dialysis may be required

23. Adrenergic crises
• Alpha blockage-
• Prazocin:2.5 mg bd/tds-max 20mg
• Doxazocin: 1-2 mg OD
• Terazocin: 1-5 mg OD
• Beta blockage:
• Propranolol-10mg qid

24. Pheochromocytoma
• Adrenal medulla tumor causing excess secretion of
catecholamine
• Test of diagnosis:24hr urine
metanephrine/VMA/catechols,CT,MRI
• In a hypertensive crisis with a pheochromocytoma,
intravenous phentolamine provides the optimal blockade of
catecholamine-induced vasoconstriction as a non-selective
alpha-receptor blocker which may be given as an initial test
dose of 1 mg followed by repeat 5 mg boluses or
continuous infusion at 0.5-1 mg/minute f/b beta blockade-
propanolol/lobet/esmolol

25. Hypertension in Pregnancy
HTN in pregnancy is defined as BP measurements of SBP ≥ 140 &/ DBP ≥ 90 mmHg.
It includes :
1.Pre-existing/Chronic HTN: precedes pregnancy / develops before 20 wks of
gestation, & persists for >6 weeks post-partum
2.Gestational HTN: develops >20 wks of gestation, without significant proteinuria &
usually resolves within 6 wks postpartum.
3.Preeclampsia is gestational HTN with significant proteinuria (>0.3 g/24 h or ≥30
mg/mmol). It is usually accompanied by headache, visual disturbances, abdominal pain.
4.Eclampsia is occurrence of seizures in a patient with preeclampsia.
5.Preeclampsia superimposed on Pre-existing HTN
Investigations include –urine analysis , a urine protein dipstick test showing >1+
warrants evaluation of ACR with values of ≥30mg/mmol being abnormal.
-CBC, hematocrit, liver enzymes, serum creat./urea
-Additional tests - USG of the kidneys and adrenals and USG-doppler of the uterine
arteries.

26. Management of PIH
1.Methyldopa is recommended for women whose HTN is 1st diagnosed during
pregnancy , CCBs (nifedipine), Labetalol can also be used.
2.In Mild HTN, T/t initiated if the BP is ≥ 140/90 mmHg along with gestational HTN or
subclinical HMOD or in any patient with BP≥150/95mmHg. ABP target of<140/90mmHg
has been suggested.
3. Severe HTN i.e BP ≥160/110 mmHg is a medical emergency. It needs immediate
hospitalization and T/t initiated with IV labetolol, CCB or oral methyldopa.
- IV NTG is the DOC in severe HTN with pulmonary edema.
- IV MgSO4 is the DOC both for prevention and treatment of seizures (eclampsia).
- IV hydralazine can be used but is not currently available in India.
- In some cases of eclampsia, anti-HTN treatment fails to control HTN and the only
means of controlling HTN would be to induce delivery.
4.CI drugs in pregnancy - ACEIs, ARBs & sodium nitroprusside (d/t risk of fetal cyanide
toxicity).
- Use of low dose diuretics is discouraged, since pre-eclampsia is a volume-depleted
state.

28. PERIOPERATIVE HYPERTENSION
• It occurs in 25% of hypertensive patient’s that
undergo sx.
• Most important cause of periop HTN is cessation of
antihypertensive on arrival to hospital in a known
HTN
• Common predictors of perioperative hypertension
are previous history of hypertension, especially a
DBP>110 mm Hg, and the type of surgery
• Importance:
– Increased risk of cardiovascular events
– Increased post-operative morbidity and mortality
– Association with end-organ damage

29. Effects of Peri-operative hypertension
●CVS effects:
●Increased BP→ ↑ afterload & myocardial O2 demand →
myocardial O2 supply and demand imbalance.
●Hypertrophied myocardium → decreased compliance →
Abn. diastolic filling.Diastolic dysfunction esp. apparent during stress,
important during surgery & acute recovery interval
● CNS effects:
●Increased risk of stroke
●Impaired cerebral autoregulation(imp. in neuro SX pt.)
● Effects on renal function
●Effective control of BP prevents renal dysfunction
●Intraop.urine output monitoring for assessment of
perioperative renal function

30. Preoperative evaluation
❖Determine adequacy of blood pressure control
❖Review pharmacology of drugs being administered
❖Evaluate for evidence of end organ damage
❖Continue drugs used for control of blood pressure
•The magnitude of blood pressure decreases during
anesthesia is greater in hypertensive than in
normotensive patients.

31. ●Preoperative history and examination
●End-organ damage
●Associated cardiovascular pathology
●Current anti hypertensive medications
● To be continued during perioperative period
● Special care regarding β-blockers and
clonidine(rebound HTN)
●Patients with preoperative HTN, more likely to
develop intra-operative hypotension. (ACE
inhibitors)

32. ●Preoperative ACE inhibitors & AT-1 antagonists:
●Refractory /exaggerated hypotension
●As long as euvolumia, no hypotension
●Pts. with preoperative BP elevations; exaggerated
intraoperative BP fluctuations & ECG evidence of
ischemia.
●Preop. Control of BP; ↓tendency to perioperative
ischemia.

33. Management of perioperative
hypertensive crisis
• The ideal drug for management of hypertensive emergency: rapid
onset of action, a short DOA, rapidly titratable, allow dose
adjustment, have a low incidence of toxicity, be well tolerated &
have few C/I( parenteral antihypertensive agent )
• The goal of therapy is to halt the vascular damage & reverse the
pathological process
• Guidelines by JNC for treating HTN emergencies include reducing
SBP by 10 -15%, up to 25% within 1st hr ,f/b gradual reduction of
BP to 160/110 mmHg over the following 2-6 hours.
• HTN that occurs with tracheal intubation, surgical incision &
emergence from anaesthesia is best treated with CCB,short-acting β-
blockers, vasodilators or ACE inhibitors.
• Postop.hypertension is best managed by correction of precipitating
factors (pain, hypothermia, hypervolemia, hypoxia and hypercarbia).

34. • Unintentional hypotension & associated organ hypoperfusion
can happen with aggressive attempts to lower BP since the
homeostatic mechanisms depend on higher BP for adequate
organ perfusion.
• The alteration b/w overshooting BP & severe hypotensive states
& using vasopressors to get the normotensive levels may
damage end-organs & the vasculature - precise control of BP in
a hypertensive crisis is a challenge
• Chronic HTN shifts cerebral & renal perfusion autoregulation to
a higher level, the brain & kidneys are prone to hypoperfusion
with rapid decrease in blood pressure. So control of blood
pressure to baseline levels should take 24 to 48 hours

35. Intraoperative concerns
●Maintain BP within 20% of the preoperative level
●Stressful intraoperative events:
●Intubation
●Surgical incision
●Emergence from GA and extubation

36. ●Other causes of intra-operative hypertension:
●Inadequate depth of anesthesia
●Pain
●Hypercarbia
●Hypoxemia
●Bladder distension
●Hypervolumia
●Exaggerated response in hypertensive patients
●Increased sympathetic tone
●Decreased intravascularvolume

37. ●Methods to blunt the sympathetic response:
●IV Esmolol (1-2mg/kg, studies with lesser dose
0.4mg/kg)
●IV Lignocaine( 1.5 mg/kg, 90 sec before
intubation/extubation)
●Short acting narcotics (Fentanyl 2-3µg/kg, sufentanil
0.3-0.5µg/kg)
●Increased concentration of inhalational agents
●IV Labetalol (5-20 mg boluses)

38. ●Choice of anesthetic techniques and medications
on the basis of presence of comorbid disease and
type of surgery.
●Hypertensive patients treated with diuretics or
having LVH more susceptible to vasodilatory
effects of inhaled anesthetics & neuraxial blockade

39. Monitoring
●Monitoring in patients with essential hypertension is
influenced by the complexity of the surgery.
●ECG is particularly useful in recognizing the occurrence
of myocardial ischemia during periods of intense painful
stimulation such as laryngoscopy and tracheal
intubation.
●Invasive monitoring with an intra-arterial catheter & a
central venous or pulmonary artery catheter may be useful
if extensive surgery is planned and there is evidence of left
ventricular dysfunction or other significant end-organ
damage.
●TEE is an excellent monitorof left ventricular
function and adequacy of intravascularvolume
replacement

40. Postoperative concerns
●Defined as SBP>190 mm Hg and/or DBP≥100 mm
Hg on two consecutive readings following surgery
●Implications:
●Risk of hemorrhage
●Disruption of vascular or cardiac suture lines
●Cerebral edema
●↑ myocardial wall stress and oxygen consumption→
myocardial ischemia

41. Causes
●Preoperative hypertension
●Withdrawal of antihypertensive medications
●Pain
●Emergence delerium
●Hypoxia
●Hypercarbia
●Hypothermia
●Hypervolumia
●Typeof surgery

42. ●Management:
●Aggressive pain management
●Correction of previously mentioned
causes
●Antihypertensive medications
●Parenteral
●Rapid onset
●Labetalol, hydralazine
●Refractory or profound hypertension
●SNP or NTG