2. A 52-year-old man presented to the
emergency department with
worsening occipital headache
Confusion
12 hours
numbness and weakness involving the right
side of his body
blurry vision.
Past medical history
Hypertension
hyperlipidemia..
3. On physical examination
Blood pressure was 213/134 mm Hg.
Confused.
Papilledema was seen on fundoscopic examination.
motor weakness (4/5) in the right upper extremity.
4. Laboratory studies revealed
following:
serum potassium, 3.1 mEq/L;
blood urea nitrogen, 36 mg/dL; and
serum creatinine, 2.5 mg/dL (baseline creatinine, 1.5
mg/dL).
Electrocardiogram revealed left ventricular hypertrophy by
voltage criteria and nonspecific ST-T wave abnormalities in
the lateral leads.
Computed tomography scan of the head without contrast
revealed diffuse bilateral white matter changes consistent
with hypertensive encephalopathy
5. Although not specifically addressed in the JNC 7
report, patients with a systolic BP > 179 mm Hg or a
diastolic BP > 109 mm Hg are usually considered to be
having a “hypertensive crisis”.
Crises
Emergency Urgency
6. The term malignant hypertension has been used to
describe a syndrome characterized by elevated BP
accompanied by encephalopathy or acute
nephropathy. This term, however, has been removed
from National and International Blood Pressure
Control guidelines and is best referred to as a
hypertensive emergency.
CHEST / 13 1/6/ JUNE, 2007
7. Left with 2 terms
Hypertensive Emergency
Hypertensive Urgency
8. Hypertensive emergency (crisis)
severe elevation in blood pressure (> 180/120 mm Hg)
complicated by evidence of impending or progressive target organ
dysfunction.
Target organ dysfunction (Acute) include Emergency not defined
by a
coronary ischemia,
specific number, but
disordered cerebral function,
rather by evidence of
cerebrovascular events,
acute dysfunction in
intracerebral or subarachnoid hemorrhage or
hypertensive encephalopathy. (cerebral edema)
cardiovascular,
pulmonary edema, and
neurologic, or renal
systems
renal failure.
The rate of change in blood pressure
Dept. of Health and Human Services, National Institutes of Health,
Can Fam Physician 2011;57:1137-41 National Heart, Lung, and Blood Institute; 2004. NIH Publication No.
04–5230.
11. Hypertensive urgency,
severe elevation in blood pressure without progressive
target organ dysfunction (>160/110)
Examples
upper levels of stage II hypertension associated with
severe headache,
shortness of breath,
epistaxis, or
severe anxiety.
The Seventh Report of the Joint National Committee on
Prevention,Detection,Evaluation, and Treatment of High Blood
12. Pathophysiology
Check
Activation of Coagulation cascade and
standing
pro-inflammatory mediators BP
Underlying Precipitating
Hypertension Factor
13. Index case
The patient was admitted to the intensive care unit
and started on intravenous nitroprusside.
Blood pressure decreased to 190/100 mm Hg over the
first 3 hours and neurologic symptoms resolved within
5 hours.
He was switched to his usual oral regimen on the third
day of hospital admission and was discharged home on
the fifth day with controlled blood pressure
14. Management of Urgency
Oral antihypertensive agents in an outpatient or
observational setting
low doses
incremental doses
Avoid excessive reduction in elderly, patients with
PAD/CVD/intracranial disease
The initial goal is to reduce blood pressure to 160/110 mm Hg
over several hours to days using conventional oral therapy
(24-48 hrs)
Mean arterial pressure should be reduced by no more
than 25% within the first 24 hours using conventional oral
therapy.
15. Captopril
ACE inhibitor
onset of action 15 to 30 minutes
maximum drop in blood pressure 30 and 90 minutes
25-mg oral dose initially, followed by incremental doses of 50 to 100
mg 90 to 120 minutes later
Significant adverse effects include cough, hypotension,
hyperkalemia, angioedema, and renal failure (especially in
patients with bilateral renal artery stenosis, in whom it should be
avoided).
16.
17.
18. Nicardipine
Calcium channel blocker
oral dose is 30 mg,
Repeated every 8 hours until the target blood pressure is
achieved.
Onset of action is ½ to 2 hours.
Common adverse reactions include palpitations, flushing,
headache, and dizziness
Am Heart J 1995;129:917–23
19. Labetalol
has mixed α1- and β-adrenergic blocking
properties(1:7)
onset of action within 1 to 2 hours
Starting dose is 200 mg orally, which can be
repeated every 3 to 4 hours
Common side effects include nausea and dizziness.
20. Clonidine
central sympatholytic (α2-adrenergic receptor agonist) agent
onset of action within 15 to 30 minutes
peak effect within 2 to 4 hours
oral regimen is a 0.1 to 0.2 mg loading dose followed by 0.05 to 0.1
mg every hour until target blood pressure is achieved, up to a
maximum dose of 0.7 mg.
Common side effects include sedation, dry mouth, and orthostatic
hypotension.
Beware of “withdrawl”
21. calcium channel blocker
Peak effect within 10 to 20 minutes.
Short-acting nifedipine is not approved by the US FDA
(unpredictable drops in blood pressure and associated risk
of stroke)
In 1995, an ad hoc panel convened by the National
Heart,Lung, and Blood Institute concluded that “short-
acting nifedipine should be used with great caution (if at all),
especially at higher doses, in the treatment of hypertension.”
22. Treatment of hypertensive
emergency
Use parenteral drugs
Continuous monitoring of blood pressure.
Reduce the mean arterial pressure by 10% during the first hour and an additional 15% within the
next 2 to 3 hours
JNC VII
Reduce mean arterial BP by no more than 25 per-cent (within minutes to 1 hour),
then if stable, to 160/100–110 mmHg within the next 2–6 hours.
If tolerated further gradual reductions toward a normal BP can be implemented in the next 24–48 hours
More rapid reduction in blood pressure may result in cardiac or renal or cerebrovascular hypo-
perfusion.
altered autoregulation curve
Pressure natriuresis may cause volume depletion in patients with hypertensive emergency, and
administering vasodilator medications to these patients can lead to precipitous drops in blood
pressure. Patients with volume depletion should receive intravenous (IV) saline to restore
intravascular volume and shut off the renin-angiotensin-aldosterone system.
Elliot WJ. Clinical features and management of selected hypertensive
emergencies. J Clin Hypertens (Greenwich)
2004;6:587–92
23. Exceptions to treatment of
Emergency
Aortic dissection
Pulmonary edema
Stroke
Patient requiring thrombolysis
24. Hypertension in the setting of an intracerebral bleed
Treat only when blood pressure is more than 180/ 105
mm Hg.(or 200/110)
MBP should be maintained <130 mm Hg
Ischemic stroke,
Observe first 1 to 2 hours to determine if it spontaneously
decrease s
Only a persistently MAP>130 mm Hg or a SBP> 220 mm Hg
or DBP >120, should be carefully treated.
Mean arterial pressure should be lowered by 15% to 20% (10-
15% JNC VII) over 24 hrs
Bring BP <185/110 for thrombolysis. Maintain at <180/105
Labetelol,Sodium Nitroprusside , nicardipine, enalipritat
used
American Heart association recommendation
Adams HP Jr, Adams RJ, Brott T, et al. Guidelines for the early management of patients with ischemic stroke: a scien-tific
statement from the Stroke Council of the American Stroke Association. Stroke 2003; 34:1056 –1083
The European Stroke Initiative Executive Committee andthe EUSI Writing Committee. European Stroke
Initiativerecommendations for stroke management: update 2003.Cerebrovasc Dis 2003; 16:311–337
25. Acute aortic dissection,
IV β-blocker (eg, labetalol or esmolol) followed by a
vasodilating agent, classically IV nitroprusside.
lower the SBP to a goal of < 120 mm Hg within 20
minutes (MAP <80).
26. Acute stroke with accelerated htn well within accepted
range but with concomitant noncerebral acute
organ damage .
What next?
Blood pressure should be reduced carefully
beyound the accepted values using emergency
guidelines, with careful monitoring of
neurological status
27. Acute Postoperative Hypertension
early onset, (within 2 h after surgery)
Typically of short duration, (treatment for ≤ 6 hrs)
Complications of APH may include hemorrhagic stroke, cerebral
ischemia,encephalopathy, myocardial ischemia, myocardial
infarction, cardiac arrhythmia, CCF with pulmonary edema,
failure of vascular anastomoses, and bleeding at the surgical site
Most commonly associated with cardiothoracic, vascular, head
and neck, and neurosurgical procedures.
Activation of the sympathetic nervous system, increase in
afterload, increase in SBP and DBP with or without tachycardia
28. Post cardiac surgery, treatment is recommended for a
BP > 140/90 or a MAP of > 105 mm Hg. Other
conditions the goal may vary
Rule out Pain,anxiety, hypothermia with shivering,
hypoxemia, hypercarbia, and bladder distension
Labetalol, esmolol, nicardipine, and clevidipine have
proven effective
30. The Seventh Report of the Joint National Committee
on Prevention,Detection,Evaluation, and Treatment
of High Blood Pressure
31. The current AHA
guidelines recommend the
use of Labetalol or
nicardipine if the SBP is
>220 mm Hg or the DBP is
from 121 to 140
mm Hg, and nitroprusside
for a DBP > 140 mm Hg
The diagnosis and management of hypertensive crises.
Chest 2000
33. 5 patients arrive with identical vital signs: heart rate of 100 beats/min, blood pressure
(BP) of 209/105 mm Hg, respiration rate of 20 breaths/min, and temperature of 36.9oC
Patient A is a 65-year-old man with nausea, Intravenous labetalol, bolus or infusion.Target:
vomiting, and confusion and papilledema Reduce MAP by 20% to 25% over 2 to 8 hours
Nitroglycerin infusion; intravenous
Patient B is a 73-year-old woman with sudden enalaprilat or sublingual captopril.
shortness of breath, pink sputum, and heavy Furosemide will work only after adequate
chest pain and LVH decrease in preload and afterload
Urgent imaging with simultaneous decrease in
Patient C is a 56-year-old man with sharp, BP. Nitroprusside and esmolol infusion;
tearing chest and back pain and diastolic labetalol boluses or infusion.Target: Rapidly
murmer reduce systolic BP to 110 mm Hg if there is
no evidence of hypoperfusion
No treatment.Reduce BP only if it is greater
Patient D is a 64-year-old woman with a 6- than 220/120 mm Hg (embolic) or greater
hour history of right-sided weakness. NCCT than 180/105 mm Hg (hemorrhagic)
no hemorrage. Thrombolysis not
contemplated
Restart the medications she was on (Diuretic
Patient E is a 51-year-old woman with a mild
headache, concerned about her history of and ARB). Ask her to follow up in OPD
hypertension.Poorly compliant. LVH +
Headache and altered level of con-sciousness are the usual manifestations of hyperten-sive encephalopathy.25,26 Focal neurologic findings,especially lateralizing signs, are uncommon in hyper-tensive encephalopathy, being more suggestive of acerebrovascular accident. Subarachnoid hemorrhageshould be considered in patients with a sudden onsetof a severe headache.
Dietary sodium should be reduced tono more than 100 mmol per day (2.4 g of sodi-um).94–
Emergencycharacterized bysevere elevations in BP (>180/120 mmHg) compli-cated by evidence of impending or progressive tar-get organ dysfunction (jnc 7)Examplesinclude hypertensive encephalopathy, intracerebralhemorrhage, acute MI, acute left ventricular failure with pulmonary edema, unstable anginapectoris, dissecting aortic aneurysm, or eclampsiaChronic Target Organ Damage (JNC VII)HeartLVHAngina/prior MIPrior coronary revascularizationHeart failureBrainStroke or transient ischemic attackDementiaCKDPeripheral arterial diseaseRetinopathydecompensation of vital organ functionwhereas in children and pregnantwomen, encephalopathy may develop with a DBP ofonly 100 mm Hg.
Htnenchephalopathy is vasodilation, edema, and increased intracranial pres-sure. Clinically, patients present with headache, visual changes, nausea, and vomiting. They might complain of transient and migrating nonfocal neurologic deficits, and might progress to seizures and coma.
Some patients with hypertensive urgencies maybenefit from treatment with an oral, short-actingagent such as captopril, labetalol, or clonidine followed by several hours of observation.The reason for a stepwise reduction in blood pressure is the fact that patients with chronic hypertension have an altered autoregulation curve. Acute normotension would lead to hypoperfusion in these patients. Those with aortic dissection or pulmonary edema are excepted from the rule of gradual blood pressure reduction. In the presence of these diseases, blood pressure must be reduced rapidly to normal values.Patients with hypertensive urgency should have theirBP reduced within 24 to 48 h, whereas patients with
require immediateBP reduction (not necessarily to normal) to pre-vent or limit target organ damage (jnc 7)The initialgoal of therapy in hypertensive emergencies is toreduce mean arterial BP by no more than 25 percent (within minutes to 1 hour), then if stable, to160/100–110 mmHg within the next 2–6 hours.. There are exceptions to the above recommendation—patients with anischemic stroke in which there is no clear evidencefrom clinical trials to support the use of immediate antihypertensive treatment, patients withaortic dissection who should have their SBP lowered to <100 mmHg if tolerated, and patients inwhom BP is lowered to enable the use of thrombolytic agents (see Stroke).return the BP to a level where autoregulation restores normal perfusion pressure to vital organs, not to “nor-mal” BP levels.
Those with aortic dissection or pulmonary edema are excepted from the rule of gradual blood pressure reduction. In the presence of these diseases, blood pressure must be reduced rapidly to normal values.Aortic dissection SBP < 100Pulmonary edema rapid decrease required
SBP ≥180mmHg or DBP ≥105 mmHg usually necessitatestherapy with intravenous agents to prevent intracerebral bleeding (jnc 7)Aortic dissection 75% die in 2 wks without treatment or 75% survive over 5 yrs with treatment. Left ventricular Force of ejection has to be decreased. Only vasodilator will cause tachycardia and propogation of dissectionThe elevated BP is not a manifes-tation of a hypertensive emergency but rather aprotective physiologic response to maintain cerebralperfusion pressure to the vascular territory affectedby ischemia.
Considering the potential for severe toxicity withnitroprusside, this drug should only be used whenother IV antihypertensive agents are not availableand then only in specific clinical circumstances andin patients with normal renal and hepatic function.68The duration of treatment should be as short aspossible, and the infusion rate should not be 2 g/kg/min. An infusion of thiosulfate should be usedin patients receiving higher dosages (4 to 10 g/kg/min) of nitroprusside.7Nitroglycerin reduces BP by reducingpreload and cardiac output; undesirable effects inpatients with compromised cerebral and renal per-fusion Diuretics should beavoided unless specifically indicated for volumeoverload, as occurs in renal parenchymal disease orcoexisting pulmonary edema.
Pulmonary edema also start positive pressure ventilation before furosemide. More rapid decrease is permitted but not very severe decrese. More often decrease should be titrated as per symptomsNitroprusside has a rapid onsetof action, and provides both arterial and venous dilation. Heart rate control with β-blockers must be initiated first to avoid reflex tachycardia that will propagate the dis-section. Alternatively, labetalol, with its a -blocking andβ-blocking properties, is a relatively user-friendly option for controlling heart rate and BP simultaneously.); if a thrombolytic is given, reduce BP to 180/105 mm Hg before treatment and 180/100 mm Hg after treatmen