1. DR.RISHIKESAN K.V
SPECIALIST PHYSICIAN
VENNIYIL MEDICAL CENTRE SHARJAH
ACUTE PRESSURE
SYNDROMES
FROM THREAT TO THERAPY
GIVING ACUTE HYPERTENSION THE HYPER ATTENTION IT
DESERVES

2. HTN AFFECTS AT LEAST 1 BILLION
INDIVIDUALS

4. DEFINITIONS
Hypertensive crisis, is somewhat of a generic term and
most clinicians break this into 2 categories.
The first category is referred to as hypertensive
emergency. This is a severe elevation of BP, defined as
>180/120 mm Hg, and it is complicated by target-organ
dysfunction or damage.
Hypertensive urgency means there is a severe elevation
in BP but target-organ function remains intact.
In terms of severity, pts. who have HE are in worse
condition than those who have hypertensive urgency.

7. HYPERTENSIVE CRISES – OTHER TERMS
ACCELARATED HYPERTENSION
BP is elevated progressively, at fast pace, with retinal
hemorrhage and exudates (Grade III Keith-Wagner-
Barker retinopathy ).
MALIGNANT HYPERTENSION
Severe elevation BP accompanied with papilledema
which may be accompanied by encephalopathy or
nephropathy.
In addition to Grade IV Keith-Wagner-Barker
retinopathy.

9. TARGET ORGAN DAMAGE / DYSFUNCTION
HE includes
Hypertensive encephalopathy,
ICH, AMI, acute LVD with pul. edema,
UA, Dissecting aortic aneurysm,
In women who are pregnant, eclampsia.
In terms of hypertensive urgency, this is
stage II HTN, which may present with
severe headache; shortness of breath; epitasis, or
nosebleed; or severe anxiety.

10. HOW COMMON IT IS ? IT IS COMMON
Most of these patients :
• are generally known to have hypertension
• are oftentimes noncompliant with treatment
• or have been inadequately treated for their
hypertension.
• Patients who have had hypertension for 5, 10, or
15 years and have never been well controlled are
at high risk for these disorders.

12. EPIDEMIOLOGY
How common is this disorder?
These numbers are are somewhat suspect. It probably is
underreported.
Something on the order of 3% of the patients presenting ED
have hypertensive crisis ie on an annual basis, perhaps 2 to 6
out of 100,000 patients coming through EDs
Of 500,000 American patients per year who have this
disorder, about 25% present to the medical section of the ED,
and among these, cerebral infarction may occur in up to a
quarter, along with other catastrophes like encephalopathy
and ICH.

17. URGENCY VS. EMERGENCY
In terms of presentation, there are some differences
between HU and HE, but it is not hugely different.
People who present with HE tend to be slightly older.
Men slightly less commonly have HU; it is fairly equal
for emergency.
If you look at the SBP, it's important to note that the
BP is the same on average: 210 mm Hg.
In those in whom it is unknown whether they had
hypertension in the past, urgency is a little more
common than emergency.

22. PRESENTATION
We look at the 2 columns on
the right, headache is slightly
more common for pts. Who
have HU compared with HE.
Epistaxis is more common.
Chest pain, Dyspnoea, is
more common for emergency.
Psychomotor agitation is
more common with urgency,
and neurological deficit with
emergency.

23. RISK FACTORS
The risk factors for
developing hypertensive
crises.
Having a h/o CRF, a history
of heart failure, known
elevations in SBP and DBP--
all of these are basically risk
factors for the development
of HE.
When taking a history, you
probably would want to ask
about these things.

25. PATHOGENESIS
The pathogenesis of elevations in BP is multifactorial;
There is increases in mechanical stress and vascular wall damage which results in
increase in vascular permeability,.
There is cell proliferation and activation of the coagulation cascade. The
endothelial cell surface lining of the vascular compartment is damaged, and
when this is damaged, this leads to endothelial cell dysfunction, which further
promotes vasoconstriction and platelet aggregation. There is the release of
various vasoconstrictors with this situation.
There is activation of the RAAS. Angiotensin II is a very potent vasoconstricting
substance, but in addition, it increases the elaboration of cytokines such as IL-6 and
NF-kappaB, which is a pro-inflammatory factor.
There is white blood cell (WBC) adhesion, as well as proliferation of vascular
smooth muscle cells. NADPH, which generates reactive oxygen species, is also
increased
There is a reduction of NO, which is a protective substance, that leads to vasodilation
and inhibition of platelet aggregation, and again, this leads to this inflammatory factor.
So this is not a simple situation. There is not a single drug per se that attacks
all of these potential targets within the cascade of hypertensive emergency.

26. PATHOGENESIS

27. Vasoactive
substances Vasoa
ctive
substa
nces
Sheer stress of
high pressure

29. UNCONTROLLED HYPERTENSION
• Hypertensive emergencies encompass a spectrum of
clinical presentations in which uncontrolled BPs lead to
progressive or impending EOD. In these conditions, the BP
should be lowered aggressively over minutes to hours.
With the advent of anti hypertensives, the incidence of
hypertensive emergencies has declined from 7% to
approximately 1% of patients with hypertension .
• In addition, 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.

33. ADAPTIVE VASCULAR CHANGES
• A PATIENT WITH CHRONIC HTN IS LIKELY TO
HAVE ADAPTIVE VASCULAR CHANGES WHICH
PROTECT END ORGANS.
• CONVERSELY PTS. WITH NO H/o HTN LACK
THESE PROTECTIONS AND MAY DEVELOP A HE
AT A SURPRISINGLY LOW BP (FOR EG. ACUTE
GLOMERULONEPHRITIS, ECLAMPSIA IN
PREGNANACY

34. TREAT THE PATIENT AND NOT THE NUMBER
• The fundamental principle in determining the
necessary ED care of the hypertensive patient is
the presence or absence of end-organ dysfunction.
Many patients present to the ED with elevated BPs;
however, only a small proportion of patients will
require emergency treatment.
• An important point to remember in the management
of the patient with any degree of BP elevation is to
"treat the patient and not the number."

36. IF YOU DETERMINE A HU ( NO EVIDENCE OF END
ORGAN DAMAGE )
• Rapid reduction can induce cerebral or myocardial
ischemia
• Goal BP, safe level in 6 hrs, 160/110 over 12-24 hrs with
conventional oral therapy
• Identify the cause and give appropriate TTT.
• can give extra or double dose of what the patient is
already on.
• Patients can be sent home.
• Oral agents may be used in hypertensive urgency, but
they are discouraged in hypertensive emergency.

38. HYPERTENSIVE EMERGENCIES
• Admission to a CCU
• Hemodynamic monitoring (ECG, CVP and arterial line).
• Ensuring proper ventilation, free air way, control of seizures and
adequate urinary output are important
• The initial goal is to lower the arterial BP by no more than 25%
within an hour after the patient is seen and then, if the patient is
stable, to titrate the BP to the range of 160/100-110 mm Hg
diastolic within the next 2 to 6 hours.
• We do not want to lower the BP in the first 5 minutes.
• Avoid excessive reduction, because this can precipitate
changes in blood flow to vital organs, such as the kidney, brain,
or coronary arteries

39. WHY NOT ENTERAL OR INTRAMUSCULAR
Oral absorption or absorption through other routes, is
not dependable in this situation.
Someone having HE probably does not have normal
blood flow to the gut nor the skin; the same would be
true for the muscles.
Pts. with HE are volume depleted. They are pumping
blood at the kidney at an accelerated rate, meaning
high RBF, and essentially pts. are salt and water
depleted secondary to having very high renal blood
flow.

41. NEUROLOGIC EMERGENCIES
Rapid BP reduction is indicated in HTNVE
encephalopathy, acute ischemic stroke, acute
ICH,SAH.
In hypertensive encephalopathy, the treatment
guidelines are to reduce the MAP 25% over 8 hours.
Labetalol, Nicardipine , Esmolol are the preferred
medications;
However, Nitroprusside and Hydralazine should be
avoided

46. • What you see here is a so-
called U- or J-shaped curve:
for DBPs >105 and <70 mm
Hg, the 90-day death rate is
higher, whereas if the
diastolic is in the range of 70
to 105 mm Hg, you have the
lowest death rate. For SBP
there is a very similar
relationship: having a
systolic >220 mm Hg is bad,
but having a systolic in the
range of 155 to 220 mm Hg
gives you the best outcome.
HTN IS NOT BAD
IN AIS

47. ACUTE ISCHAEMIC STROKE

48. ICH AND SAH
• PREFERRED MEDICATIONS ARE
• LABETALOL,NICARDIPINE AND ESMOLOL
• IN CASE OF INCREASED ICP
• MAINTAIN MAP < 130 mmHg or SBP < 180mmHg FOR THE FIRST 24 HOURS
• IF NORMAL ICP MAP <130mmHg OR SBP<160mmHg
SAH
PREFERRED AGENTS ARE AGAIN
LABETALOL, NICARDIPNE AND ESMOLOL.
MAINTAIN SYS.BP <160 mmHg UNTIL THE ANEURYSM IS
TREATED OR
CEREBRAL VASOSPASM OCCURS

56. ACUTE CARDIOPULMONARY COMPROMISE

58. NICARDIPINE
• Nicardipine is good because
• It doesn't depend on renal function or in terms of
liver function for its excretion . It can be given as an
IV bolus or constant infusion, and so it is very useful
• Dose: 5–15 mg/ hr IV .Onset 5–10 min Duration13–
30 min, may exceed 4 hr
• AE :Tachycardia, headache, flushing, local phlebitis
• Indication : Most HE except acute heart failure;
• Caution: coronary ischemia

60. FENOLDOPAM
• Fenoldopam mesylate
• Dose 0.1–0.3 µg/kg/min as IV infusion. onset of action <5
min . Duration 30 min .
• AE: Tachycardia, headache, nausea, flushing
• Indication Most HEs; Caution with glaucoma
• Fenoldopam, I think, is a very expensive alternative drug for
the treatment of hypertensive urgency; again, it must be
given by constant infusion.
• There were reportedly advantages in terms of preserving
renal function

61. SNP
Sodium nitroprusside is a very quick-acting , quick
both in terms of onset and offset.
It is good for many situations, but it requires very
careful monitoring, usually within arterial lines, to make
sure that you are measuring the true BP.
The drug should not be used in pts. who have renal
insufficiency because the metabolic pathway for SNP
leads to -CN, and -CN, of course, is very toxic.
So in pts. with renal insufficiency, avoid this drug

64. • NOTE THAT DIURETICS
ARE GENERALLY
AVOIDED IN HTNVE
EMERGENCIES AS MANY
PTS.ARE HYPOVOLEMIC
DUE TO PRESSURE
INDUCED NATRIURESIS.
• EXCEPTIONS ARE
PATIENTS WITH HEART
FAILURE AND OR
PULMONARY EDEMA
DIURETICS

65. BETABLOCKERS , ALPHA BLOCKERS
• The adrenergic inhibitors include the beta-blockers labetalol and esmolol and
the alpha-blocker phentolamine
• Labetalol is useful in terms of being both an IV bolus with a constant infusion
and then potentially a follow-up oral therapy
• Esmolol, of course, is ultra-short-acting. It is very useful in critical care
situations in surgery, but certainly not a very useful long-term drug. Adverse
effects apply for all beta-blockers in patients who have bronchospastic
disease, and please note, this means asthma patients, not chronic obstructive
pulmonary disease (COPD) patients.
• And lastly, phentolamine is a very special-use drug. It specifically blocks the
alpha receptor and is particularly useful in situations such as
pheochromocytoma, in which the secretion of catecholamines such as
epinephrine and norepinephrine are responsible for severe swings in
hypertension. This drug is only given IV and is actually somewhat difficult to
find.

66. IV labetalol and hydralazine are considered first-line Rx
for the management of acute-onset, severe
hypertension in pregnant and postpartum women.
Second line alternatives to consider include labetalol or
nicardipine by infusion pump .SNP should be reserved
for extreme emergencies and used for the shortest
amount of time possible because of concerns about
cyanide and thiocyanate toxicity and increased ICP
with potential worsening of cerebral edema in the
mother

67. THAT IS NOT A GOOD IDEA ……….

68. S/L NIFEDIPINE
There are studies for captopril, nifedipine, and prazosin given
orally.
These drugs should be avoided. Even though the stuff is
out there, it is not really a good idea, especially for
nifedipine We had several disasters with sublingual
administration of nifedipine.
You poke a hole in the capsule for the immediate-release
nifedipine and you squirt it under the tongue.
We had several patients who developed severe
hypotension and had to be given IV fluids and pressors to
get their BP back.

71. CLEVIDIPINE
Clevidipine, an intravenous CCB, was approved by the
FDA in August 2008 for the management of acute,
severe hypertension .
A 3rd generation DHP CCB that inhibits L-type calcium
channels . A short half life of 1 to 2 minutes, a quick
onset of action of 2 to 4 min. and a short duration of
action of 5 to 15 min.
Clevidipine lowers SVR , it has greater effects on
arterial vasodilatation

75. CLEVIPREX
The antihypertensive efficacy of intravenous clevidipine
was compared with a placebo in cardiac surgery patients
in 2 randomized, double-blind multicenter studies.
• These studies showed that clevidipine was effective in
the treatment of both acute preoperative and
postoperative hypertension.
• The antihypertensive efficacy of clevidipine was also
compared with the efficacies of nitroprusside,
nitroglycerin, and nicardipine.
• Overall the blood pressure control was similar among
the 4 treatments.

76. CLEVIDIPINE