1. Can hypertension be
an emergency
by
Hossam Ahmed
Mowafi

2. Hypertensive Crisis

3. Systemic hypertension

4. It is estimated that 50 million persons in the
United States have systemic
, hypertension
.many of whom are inadequately treated

5. Between 1% and 2% of the 50 million have
primary hypertension that
progresses to a crisis phase
accounting for more than 50% of all cases
.of hypertensive crisis

6. Uncontrolled or suboptimally controlled
hypertension
causes high rates of mortality from
,premature cardiac, vascular
. and renal disease

7. In most instances, end-organ damage
occurs after
decades
.of elevated blood pressure

8. Hypertensive crisis

9. In rare instances, hypertension may become acutely
life threatening. This emergency situation, occurs
when an
abrupt, marked increase in blood pressure
“relative to the patient's baseline” causes
acute or rapidly progressing end-organ
damage.

10. Unless promptly recognized and treated,
hypertensive crisis can lead to
cardiovascular, renal,
and
central nervous system
complications and
death.
Effective and prompt anti-hypertensive treatment
improves the prognosis.

11. Hypertensive crisis can manifest
de novo,
but most patients have a history of
chronically elevated blood pressure that
has been
poorly controlled or untreated.

12. Public health campaigns
aimed at educating and treating patients
with hypertension have
markedly decreased
. the incidence of hypertensive crisis

13. Nevertheless, it continues to represent a
large portion of
.emergency department visits

14. Because the cardiovascular system is
, imminently threatened
cardiologists
are called on to provide expert management
of these emergencies, and patients with
severe elevations in blood pressure often
. go to a cardiologist for initial care

15. The cardiologist must be able to differentiate
an
emergency from urgency or a
pseudoemergency;
understand the underlying pathophysio-
logic mechanisms, potential
complications, and treatment
options;
and
guide the evaluation.

16. Overzealous treatment can cause severe
morbidity and even death. A working
knowledge of the
pharmacologic characteristics
and
side effects of the various
.therapeutic agents is essential

17. Classification

18. Hypertensive crisis traditionally has
been classified as
,emergency or urgency
depending on the presence of
acute or progressive
. end-organ damage

19. , This distinction
, although not absolute
aids in formulating an effective and
.safe treatment plan

20. Hypertensive emergencies include
conditions characterized by
rapid decompensation of vital organ
function caused by inappropriate
. elevations in blood pressure

21. Treatment requires
immediate reduction
in blood pressure and parenteral
medication, usually in an intensive care
.unit
Delay may cause
.irreversible organ damage and death

22. Several clinical syndromes can manifest as
.hypertensive emergencies

23. Accelerated or
malignant hypertension
and
hypertensive encephalopathy
are the prototypical hypertensive
emergencies.

24. Accelerated or malignant hypertension is a
systemic disease characterized by:.
• An extreme elevation in blood pressure (mean
arterial blood pressure [MAP] greater than 120
mm Hg).
• Bilateral retinal hemorrhage.
• Exudates.
• Papilledema.
This hypertensive emergency demands
emergency treatment and close follow-up
care.

25. HYPERTENSIVE EMERGENCIES 16
– In general, diastolic blood pressure exceeds 120 mm
Hg.
– Malignant hypertension with papilledema.
– Hypertensive encephalopathy.
– Severe hypertension in the setting of stroke.
– Subarachnoid hemorrhage.
– Head trauma

26. – Acute aortic dissection.
– Hypertension and left ventricular failure.
– Hypertension and myocardial ischemia and infarction.
– Hypertension after coronary artery bypass operation.
– Pheochromocytoma crisis.
– Food or drug interactions with monoamine oxidase
inhibitors.

27. – Cocaine abuse.
– Rebound hypertension after sudden drug withdrawal
(clonidine).
– Idiosyncratic drug reactions (atropine).
– Eclampsia.

28. Exceptions include cardiovascular dysfunction
in which low blood pressure may represent an
emergency.

29. "Considered emergencies when associated with
end-organ damage;
otherwise treated as urgencies.

30. Hypertensive encephalopathy causes
, headache, irritability
and
altered state of consciousness
from a sudden marked increase in blood
. pressure

31. Hypertensive encephalopathy occurs when
cerebral edema is induced by
markedly elevated blood pressures
that overwhelm the
auto-regulatory capabilities
. of the brain

32. This condition tends to affect a person with
previously normal blood pressure who has
. a rapid rise in blood pressure

33. Persons with
chronic hypertension
are relatively
resistant
to encephalopathy because their
autoregulatory systems have
adapted to
.the chronically elevated blood pressure

34. When persons with
chronic hypertension do have
encephalopathy, it is usually in the setting
of markedly elevated blood pressure
diastolic blood pressures higher
. than 150 mm Hg

35. Mental status reverts to normal with the
. lowering of blood pressure

36. Hypertensive urgencies
manifest as marked elevations in blood
pressure
diastolic blood pressure higher than
120mm Hg
without
evidence of acute or progressive target
organ damage and minimal or no
. symptoms

37. .The risk for tissue damage is not immediate

38. Blood pressure can be lowered
. over a period of hours to days
Patients usually can be treated with oral
.medication, often as outpatients

39. Pseudoemergencies
must be differentiated from true
hypertensive emergencies because the
treatments
. differ markedly

40. The increase in blood pressure in a
pseudoemergency is caused by
massive sympathetic outflow
as the result of
pain, hypoxia, hypercarbia,
hypoglycemia, anxiety, or the
. postictal state
Treatment is directed at the underlying
.cause

41. HYPERTENSIVE URGENCIES
Diastolic blood pressure exceeds 120 mm Hg, but
patients have no symptoms, and there are no
signs of tissue damage

42. Clinical presentation.
If an emergency is suspected, appropriate
arrangements for ICU admission
and parenteral treatment are made without
waiting
for the results of further tests.

43. – Chest pain.
– shortness of breath.
– Headache.
– Blurred vision.
– signs of altered mental status.
– Focal neurologic signs.
– Grade III or IV retinopathy.
– Rales.
– Gallop.
– Pulse deficits.

44. – Chest pain.
– shortness of breath.
– Headache.
– Blurred vision.
– signs of altered mental status.
– Focal neurologic signs.
– Grade III or IV retinopathy.
– Rales,
– Gallop.
– Pulse deficits.
all point toward an emergency.

45. Severe hypertension in the presence of
chronic organ damage
without associated symptoms does not
. constitute an emergency
Pseudoemergencies must be ruled
.out

46. Signs and symptoms.
The following history is elicited from patients
withincreased
blood pressure.

47. – Nausea.
– Vomiting, weight loss.
– Anorexia.
– Shortness of breath, chest pain.
– Headache.
– Blurred vision.
– Abdominal pain.
– Patients with accelerated or malignant hypertension
often have oliguria.

48. Chronology of symptoms
. is important

49. . History of hypertension
Most patients with accelerated or malignant
hypertension have an underlying history of
,chronic essential hypertension
although
a significant percentage of patients
have secondary forms of
. hypertension
A search for correctable causes is
.indicated

50. :Concurrent medications may include
– Cardiac medications.
– Antihypertensive agents.
– Oral contraceptives.
– Diuretics.
– Psychotropic agents.
– Monoamine oxi-dase inhibitors.
– Ephedrine.
– Over-the-counter cold remedies.

51. Use of recreational drugs,
cocaine, amphetamines.

52. Smoking history. Smokers are at increased
risk for progression to malignant
hypertension.

53. Physical findings

54. . Vital signs
Blood pressure is measured in both upper
. and lower extremities

55. Severe hypertension is confirmed with two
blood pressure measurements separated
. by 15 to 30 minutes

56. No absolute level of blood pressure
differentiates an emergency
from an
.urgency

57. The distinction is based on a thorough
. clinical evaluation

58. Optic fundi are examined for signs of
retinopathy, including exudates,
hemorrhages, or papilledema.

59. The CNS is examined for
– Mental status.
– Focal neurologic signs.
– Patients with hypertensive encephalopathy
may manifest focal neurologic signs,
confusion, or seizure activity.

60. Heart
and lungs are examined for presence of
edema, S3, or S4.
Vascular system
is examined for pulses and bruits.

61. Patients with chronic hypertension
usually progress
to an accelerated or malignant phase or
have severe blood pressure elevations
and progressive end-organ damage and
. aortic dissection

62. A thorough search
for secondary causes and precipitants is
indicated in the evaluation of all patients
. with hypertensive crisis

63. Between 20% and 56% of patients have an
identifiable underlying
cause, compared with less than 5% of those
.with uncomplicated hypertension

64. CONDITIONS THAT MAY
PRECIPITATE A HYPERTENSIVE
CRISIS
– Essential hypertension.
– Renovascular hypertension.
– Parenchymal renal diseases.
– Drug-induced causes.
– Head injuries.
– Central nervous system events.
– Vasculitis Collagen vascular disease.

65. HYPERTENSIVE CRISIS
A common situation is that a patient has
been.
– Inadequately treated.
– Has been noncompliant with a medical
regimen.

66. Risk factors for progression to
hypertensive crisis include.
– Male sex.
– Black race.
– Cigarette smoking.
– Tobacco abuse.
– Oral contraceptive use.
– Low socioeco-nomic status.

67. Unlike essential hypertension, the incidence
of which increases with age, the
peak incidence
of hypertensive crisis occurs among persons
40 to 50 years old.

68. Underlying diseases that can precipitate
hypertensive crisis include
– Renal parenchymal disease.
– Renovascular hypertension.
– Collagen vascular disease.
– Pheochromocytoma.
– Vasculitis.
– Preeclampsia.
– Burns
– Head trauma.

69. A number of medications can cause marked
elevations in systemic blood pressure.
The most common offenders are
– Oral contraceptives.
– Sympathomimetic agents.
– Cold remedies.
– Nonsteroidal antiinflammatory drugs.
– Cocaine.
– Tricyclic antidepressants.
– Mono-amine oxidase inhibitors.

70. In rare instances, a hypertensive crisis is the
first manifestation of disease. These
patients tend to have secondary forms of
hypertension, most commonly:
– Renovascular.
– Renal parenchymal disease.
– Reaction to medications.

71. Left ventricular failure or pulmonary
. edema

72. Elevated blood pressure poses an
enormous workload on a failing heart.
Even patients with normal systolic function
can have pulmonary edema in the setting
of markedly elevated blood pressures
.afterload mismatch

73. Hypertensive crisis associated with
. hypercatecholaminemia

74. A hypercatecholamine state can cause
severe
elevations in blood pressure that threaten
tissue function and necessitate
. parenteral treatment

75. Hypercatecholamine commonly are induced
by the
exaggerated effects of medication
, drugs
or
. food-drug interactions

76. . Postoperative hypertension

77. Severe hypertension can
complicate
the postoperative course after coronary and
. peripheral vascular procedures
The elevated pressure threatens suture
. lines and promotes excessive bleeding

78. Pathophysiology

79. Pathophysiology
Although the exact pathophysiologic
mechanism is unknown, it is believed that
hypertensive emergencies are triggered
by an abrupt increase in systemic vascular
resistance caused by increases in
circulating vasoconsictors,
norepinephrine,
angiotensin II.

80. The resulting increase in
blood pressure
leads to
:Arteriolar fibrinoid necrosis characterized by
– Endothelial damage.
– Fibrin deposition.
– Loss of autoregulatory function.

81. Ischemia and dysfunction in the target organ
cause further release of vasoactive
substances, producing
– A cycle of increasing SVR.
– Elevated systemic blood pressure.
– Decreased cardiac output.
– Vascular injury.
– Tissue damage.

82. An alternative explanation is that elevated blood
pressure complicates a
Primary
disease process and
. accelerates tissue injury
The specific organ system affected defines the
hypertensive crisis
– Aortic dissection.
– Acute left ventricular failure.
– Stroke.

83. Autoregulation

84. The kidney, brain, and heart all possess
autoregulatory mechanisms that maintain
blood flow at
near constant
levels despite fluctuations in blood pressure.

85. Because the brain is encased in a definit
space and because it maximally extracts
, oxygen at baseline
it is most vulnerable when its autoregulatory
. systems fail

86. Excess blood flow results in
– Cerebral edema.
– Elevated intracranial pressure.
– Ischemia.

87. Cerebral blood flow normally is maintained
at a near-constant level despite variations
.in cerebral perfusion pressure

88. An elevated MAP causes an
increase
in CPP, whereas a decreasing MAP causes
decreased
CPP. Despite changes in CPP, cerebral
autoregulatory mechanisms maintain CBF; as
MAP
rises, vasoconstriction
occurs, and as MAP
.decreases, vasodilatation occurs
.CPP: Eerebral perfusion pressure

89. This system has upper and lower limits beyond
.which CBF can no longer be controlled

90. When CPP decreases below the lower limits
of autoregulation,
brain hypoxia ensues, and symptoms of
hypoperfusion manifest:
– Headache.
– Nausea.
– Dizziness.
– Altered sensorium.
– Lethargy.

91. If unconnected or extreme,
this may ultimately cause infarction.

92. When MAP exceeds
autoregulatory capabilities,
hyperperfusion
occurs, leading to an increase in ICP,
cerebral edema, and progressive organ
dysfunction.

93. Most persons with normal blood pressure
maintain autoregulation of MAP between
, 50 and 150 mm Hg
. although this is highly variable

94. These values generally increase among
.patients with chronic hypertension

95. These patients consequently may have
cerebral hypoperfusion at an MAP that is
. considered normal

96. – Elderly persons.
– Cerebrovascular accidents.
– Subarachnoid hemorrhage.
– Hypertensive encephalopathy.
– Accelerated or malignant hypertension
have altered autoregulation.

97. Treatment must be tempered by the fact
that
overzealous blood pressure reduction
can lead to permanent neurologic
. damage

98. – Cerebrovascular accidents.
– Blindness-piaralysis.
– Coma.
– MI.
– Death
have been reported sequences of
aggressive blood pressure
reduction.

99. Prognosis

100. The prognosis of a patient who has
undergone hypertensive crisis and not
been treated
is
poor.

101. Before the introduction of effective
antihypertensive agents,
more than 90%
of patients with accelerated malignant
hypertension died within
1 year
of diagnosis.

102. Modern pharmacotherapy and the
availability of dialysis have substantially
, increased survival rates
with studies reporting survival rates of
more than 70%
.at 5-year follow-up

103. Laboratory examination and diagnostic
. testing

104. The diagnostic evaluation must be brief
because
. time to treatment is crucial
Diagnostic imaging if clinically indicated can
be performed after treatment has been
.instituted

105. Azotemia and hemolysis
indicate
an emergency.

106. Blood chemistries to rule out uremia.

107. Urinalysis to look for
– Proteinuria.
– Hematuria.
– casts.
Hematuria and moderate to severe proteinuria
indicate an emergency.

108. Finger-stick glucose test can rule out
hypoglycemia
as a cause of changes
in
mental status.

109. Ischemic changes on the
electrocardiogram indicate
an emergency.

110. Pulmonary edema on chest
radiography indicates an
emergency.

111. Computed tomography may be
needed in the setting of a possible
cerebrovascular accident.

112. Therapy

113. The presence of acute or rapidly progressive
end-organ damage, not the absolute blood
pressure reading, determines
whether
the situation is an emergency or urgency.

114. This determination dictates the type
of treatment
– Parenteral.
– Oral.
– ICU.
– Ward.
– outpatient.

115. For example, a blood pressure of
120/80 mm Hg
may represent a hypertensive
emergency
for a patient with aortic dissection, whereas
a blood pressure of 200/120 mm Hg for a
person with
asymptomatic chronic hypertension
usually does not necessitate emergency
therapy.

116. The appropriate diagnostic evaluation and
therapeutic
plan also are dictated by the specific
disease.

117. For example, the specific pharmacologic
regimen for a
pregnant woman
with preeclampsia differs from that for an
elderly man who has had a stroke.

118. Regardless of drug regimen, the
goal of treatment
is
– Break the cycle of increasing blood pressure.
– Preserve cardiac output.
– Renal blood flow.
– Limit end-organ damage.

119. Neurologic emergencies

120. Patients with neurologic findings and severe
hypertension present a
particular challenge.

121. Neurologic emergencies can result from
hypertensive emergencies or may
themselves cause
markedly elevated
blood pressures, which may exacerbate
neurologic damage.

122. The key differentiating point is that
neurologic alterations caused by elevated
blood pressure are reversed when blood
pressure is controlled, whereas primary
neurologic disorders
are not.

123. The insidious progression of symptoms in
hypertensive encephalopathy aids in
differentiating hypertensive
encephalopathy from cerebrovascular
accidents, which usually
manifest abruptly.

124. Nevertheless, the diagnosis is one of
exclusion because other hypertensive
emergencies.
– Cerebrovascular accident.
– Subarachnoid hemorrhage.
– Intraparenchymal bleeding.
– Primary seizure disorder.
Share many symptoms and signs.

125. Evaluation often
necessitates further diagnostic imaging,
such as CT, and consultation with a
neurologist.

126. Hypertensive emergencies

127. The goal of therapy is immediate, controlled
reduction in blood pressure.
toxic side effects of antihypertensive
agents must be understood and
anticipated.

128. Patients are
treated in an ICU, where clinical
status and vital signs can
be constantly monitored with the aid of an
arterial line.

129. Attention is focused on the status of
airway, breathing, and circulation
(ABCs). Ancillary measures such as
intubation and dialysis are
instituted if necessary.

130. Blood pressure is reduced in a
controlled, predictable manner.

131. The lower limit of autoregulation among
persons with normal blood pressure
and those with hypertension is
approximately
25% of MAP.

132. It is recommended that blood pressure
initially be reduced by no more than 25%
of MAP over minutes to hours and that
further reductions occur
over days to weeks
to
allow the autoregulatory mechanisms
to reset.

133. Exceptions include.
– Aortic dissection.
– Left ventricular failure.
– Pulmonary edema.
which demand more aggressive blood
pressure reduction to limit tissue damage.

134. Specific antihypertensive therapy is tailored
to the underlying disease
as
aortic dissection
angina

135. Diagnosis and treatment are reassessed if
the clinical condition,
especially neurologic status,
deteriorates
with reduction of blood pressure.

136. Medical therapy.

137. A number of parenteral antihypertensive
medications are available to manage
hypertensive emergencies.

138. The specific clinical scenario dictates the
agents used.

139. Characteristics of an ideal agent
include
– Rapid onset.
– Cessation of action.
– A predictable dose-response curve
– Minimal side effects.

140. Patients with hypertensive
emergencies have
– Excessive elevations in SVR.
– Decreased cardiac output.
– Decreased renal blood flow.
– Volume depletion.

141. The most useful agents are vasodilating
agents such as
nitroprusside.
Diuretics and beta-blockers are
avoided
unless the patient has
– Aortic dissection.
– MI.
– Pulmonary edema.

142. For hypertensive encephalopathy,
cerebrovascular accidents,
or other conditions in which mental status
must be monitored, agents that have
prominent CNS side effects
as sedation
are avoided.

143. For conditions associated with
elevated ICP, such as
– Cerebrovascular accident.
– Subarachnoid hemorrhage.
– Hypertensive encephalopathy.
Agents that directly increase CBF
are avoided.

144. The agent selected has the most favorable
hemodynamic and side effect profile on
the basis of the specific hypertensive
emergency.

145. The drug of choice for most hypertensive
crises is
sodium nitroprusside.
Effective alternatives include
labetalol
in certain circumstances,
nitroglycerin or hydralazine
may be preferred.

146. Sodium nitroprusside is the drug of choice
for most hypertensive emergencies.

147. – The favorable hemodynamic profile.
– Rapid onset.
– Rapid cessation of action of sodium
nitroprusside.
Make it the preferred parenteral
agent for most emergencies.

148. A potent, direct vascular smooth muscle
relaxant, sodium nitroprusside decreases
afterload and preload
by
dilating arterioles
and
increasing venous capacitance.

149. Hemodynamic effects include a
decrease in
– MAP.
– Afterload
– Preload
an increase or no change in
– Cardiac output
– Increased
– Renal blood flow
– Glomerular filtration rate.

150. Although the direct action of sodium
nitroprusside on the cerebral vasculature
may cause increased cerebral perfusion,
this is
counteracted by
a potent effect on MAP.

151. Most patients with neurologic crisis who
need blood pressure control tolerate
sodium nitroprusside without a worsening
of neurologic status.

152. However, the possibility of an increase in
ICP and further clinical deterioration
despite a decrease in MAP must be
kept in mind
as a potential side effect in patients with
severely increased ICP.

153. Administration.

154. Sodium nitroprusside must be administered
by means of
constant intravenous infusion
in an intensive care setting
with
constant monitoring of arterial blood
pressure.

155. It has a rapid onset of action, and its effect
ceases
within 1 to 5 minutes
of cessation of infusion.

156. Side effects.

157. Red blood cells and muscle cells
Metabolize
sodium nitroprusside to
cyanide
which is converted to
thiocyanate
in the liver and excreted in the urine.

158. Thiocyanate levels rise in patients with
renal insufficiency,
and cyanide accumulates in patients
with
hepatic disease.

159. Signs of thiocyanate toxicity include
- Nausea. -Vomiting.
- Headache. - Fatigue.
- Delirium. - Muscle spasms.
- Tinnitus - Seizures.

160. Monitoring for signs and symptoms of
toxicity and maintaining thiocyanate levels
less than 12 mg/dL
allow safe use of sodium nitroprusside.

161. Labetalol
is useful in most hypertensive crises. The
main disadvantage is its relatively
long duration of action.

162. Labetalol is an
alpha-blocker
and
Nonselective beta-blocker with partial B2
agonist activity.

163. When given through continuous intravenous
infusion, the relative beta- to alpha-
blocking
Effect
of labetalol is 7 : 1.

164. The hemodynamic effects of labetalol include
decrease in
– SVE.
– MAP.
– Heart rate.
a decrease or no change in
– Cardiac output.

165. Labetalol has little direct effect on cerebral
vasculature,
does not increase ICP
and is considered by some to be the
drug of choice
in situations characterized by markedly
elevated ICP.

166. Labetalol begins to lower blood pressure
within 5 minutes,
and its effects can last
1 to 3 hours after cessation of the
infusion.

167. Contraindications.

168. Labetalol is contraindicated for
patients with
– Congestive heart failure.
– Bradycardia.
– Heart block more than first degree.
– Reactive airway disease.

169. Nitroglycerin is considered the drug
of choice for managing
hypertension in the setting of
– Myocardial ischemia.
– Acute MI.
– Pulmonary edema.
– After coronary artery bypass grafting.

170. The role of intravenous nitroglycerin
therapy is limited to hypertension
complicating
– Myocardial ischemia.
– MI.
– Congestive heart failure.

171. Nitroglycerin is primarily a venodilator and
has modest effects on afterload
at high doses.

172. The decrease in preload and afterload
decreases
myocardial oxygen demand.

173. Nitroglycerin also
– Dilates the epicardial coronary arteries.
– Inhibits vasospasm.
– Favorably redistributes blood flow to the
endocardium.

174. Nitroglycerin directly increases CBF and is
not used in situations characterized
by high ICP.

175. Fenoldopam
Is a selective peripheral dopamine-1-
receptor agonist approved for
the management of severe hypertension.
Fenoldopam is an arterial vasodilator with
a rapid onset of action and a relatively
short half-life when administered
intravenously.

176. It may be of particular benefit
in patients with
renal insufficiency
as it has been shown to improve renal
perfusion.

177. Fenoldopam may cause a reflex
tachycardia,
which can be blunted by the
concomitant use of a beta-blocker.

178. Fenoldopam is contraindicated in
patients with
glaucoma
because it can increase intraocular
pressure.

179. Hydralazine
The role of intravenous hydralazine is
limited to the treatment of pregnant
women with
preeclampsia.

180. Hydralazine is a direct arterial vasodilator
with no effect on venous capacitance. It
crosses the uteroplacental barrier but has
minimal effects on the fetus.

181. It is usually administered in boluses
of 10 to 20 mg and has a long
duration of action.
– Hydralazine decreases SVR.
– Induces compensatory tachycardia.
– Increases ICP.

182. It can exacerbate angina and is
contraindicated in the care of
patients with
– Ongoing coronary ischemia.
– Aortic dissection.
– Increased ICP.

183. Management of specific emergencies

184. Accelerated or malignant
hypertension

185. In the acute phase, the pharmacologic agent
of choice is sodium nitroprusside.
Labetalol is an effective alternative.

186. Because patients usually have marked
elevations of SVR and volume depletion,
diuretics are contraindicated.

187. Hypertensive encephalopathy

188. The treatment of choice is sodium
nitroprusside or labetalol.
Agents that depress the sensorium or
increase ICP are avoided.

189. Most patients with hypertensive
encephalopathy
improve within hours
of blood pressure reduction

190. If there is no improvement despite a
decrease in blood pressure, the
diagnosis must be reconsidered.

191. Neurologic complications include
– Cerebrovascular accident.
– Embolie stroke.
– Intraparenchymal hemorrhage.
– Subarachnoid hemorrhage.

192. Extreme caution
Must be exercised when lowering even
markedly elevated blood pressures in the
setting of a cerebrovascular accident.

193. Elevated ICP caused by cerebral edema or
intraparenchymal hemorrhage increases
the MAP needed to adequately perfuse
the brain
CPP = MAP - ICP.

194. Subarachnoid hemorrhage is characterized
by intense vasospasm at and adjacent to
the site of rupture. Reduction of blood
pressure in these circumstances
may cause
global
or in the case of subarachnoid hemorrhage
focal hypoperfusion.

195. Markedly elevated blood pressures,
however, may increase risk for
rebleeding in subarachnoid hemorrhage or
extend a hemorrhagic infarct.

196. Lesions that are potentially surgically
correctable such as sub-arachnoid
hemorrhage and neoplasms must be
identified.

197. Management of markedly elevated blood
pressure in the setting of cerebrovascular
accident or subarachnoid hemorrhage is
tempered by
concerns about further reducing
blood flow to underperfused areas
of the brain.

198. The following
guidelines are suggested.

199. When blood pressure is less than 180/105
mm Hg,
no treatment is recommended.

200. When blood pressure is 180/105 to 230/120
mm Hg for longer than 60 minutes,
treatment is started.

201. When treatment is indicated, it must be
closely monitored, often with direct ICP
monitor.

202. Target blood pressures are
160/100 to 175/110 mm Hg for patients who
had normal blood pressure and
180/110 to 185/120 mm Hg for persons with
chronic hypertension.

203. The drug of choice is labetalol or sodium
nitroprusside.

204. Nimodipine
A calcium channel blocker with modest
antihypertensive effect, has been
beneficial in the management of
subarachnoid hemorrhage.

205. If blood pressure remains higher than
desired despite use of nimodipine, therapy
sodium nitroprusside or labetalol
may be considered.

206. Agents that directly increase CPP and
therefore ICP are avoided.

207. Aortic dissection is an emergency.

208. Blood pressure must be lowered
immediately.

209. Patients with type A dissection have a
mortality rate of 1% per hour in the first 48
hours
unless medical therapy
is instituted and the patient is referred for
emergency surgical intervention.

210. Antihypertensive therapy is the treatment of
choice for type B dissection.

211. Labetalol or the combination of sodium
nitroprusside with a beta-blocker is the
treatment of choice.

212. Aggressive blood pressure reduction is
indicated even for patients with normal
blood pressure because
shear force and afterload
must be reduced to limit tissue damage.

213. A reasonable goal is a MAP of
approximately 70 mm Hg.

214. Drugs that decrease afterload and
induce compensatory tachycardia
are contraindicated.

215. Left ventricular failure or
pulmonary edema.

216. Treatment is best accomplished with sodium
nitroprusside and small doses of diuretics.

217. Nitroglycerin is an effective alternative,
especially if ischemia is present.

218. Sodium nitroprusside and nitroglycerin often
are used concomitantly.

219. Beta-Blockers and calcium channel blockers
must be avoided in the decompensated
state.

220. Myocardial ischemia.

221. Blood pressure reduction with nitrates and
beta-blockers is the treatment of choice.

222. Sodium nitroprusside is added if further
blood pressure reduction is required.
Reperfusion and antithrombotic
therapy are the mainstays of management
of acute MI and unstable angina.

223. Hypertensive crisis associated
with hypercatecholaminemia.

224. The pharmacologic agents of choice include
sodium nitroprusside, labetalol, or calcium
channel blockers.

225. Phentolamine can be useful in cases of
pheochromocytoma.

226. Beta-Blockers must be avoided, because
they can cause a paradoxical increase in
blood pressure because of the effects of
unopposed
alpha-receptor stimulation.

227. Postoperative hypertension.

228. Parenteral treatment with sodium
nitroprusside or labetalol is
preferred.

229. After
coronary bypass grafting,
nitroglycerin is considered the initial drug of
choice.

230. Hypertensive urgencies.

231. Most patients diagnosed with
hypertensive urgency actually
have severe hypertension
and are
not
in any immediate danger of progressing to
hypertensive emergency.

232. They are often persons with chronic
hypertension who are
suboptimally treated or noncompliant.

233. Priority of therapy

234. Hypertensive urgencies usually can be
managed with oral medication without
admission to the hospital.

235. End-organ damage is not imminent, and
blood pressure can be modestly lowered
over a period of hours as long as
adequate follow-up care is ensured.

236. The great danger lies in overtreating these
patients and inciting a hypotensive crisis.

237. Sometimes, placing the patient in a quiet,
calm environment can decrease blood
pressure to a less alarming level.

238. If the blood pressure is still markedly
elevated, reinstitution or enhancement of
prior therapy often is effective.

239. MAP is not decreased more than
15% to 20%.

240. Lower initial doses of antihypertensive
medications are used to treat patients with
cerebrovascular disease or
coronary artery disease who are
taking antihypertensive
drugs or who
are volume depleted.

241. These patients tend to have exaggerated
responses to drug therapy. They also are
especially
vulnerable
to hypotension.

242. Lower doses of medications must be used.
Monitoring for 4 to 6 hours is necessary to
judge treatment effect and look for
complications.

243. Urgent follow-up care is mandatory within 24
hours.

244. Evaluation for secondary causes of
hypertension is indicated.

245. Drug therapy.

246. Oral agents used to manage hypertensive
urgencies.

247. The drugs of choice include
– Captopril.
– Clonidine
– Oral labetalol.

248. Captopril
Considered by some to be the drug of
choice, captopril is the fastest-acting
oral angiotensin-converting
enzyme inhibitor.

249. At small doses, it rarely causes marked
hypotension, although this potential exists
in patients who are markedly volume
depleted or who have renal artery
stenosis.

250. Captopril begins to work within 15 to 30
minutes of ingestion and has a 4- to 6-
hour duration of activity.

251. Caution is advised in the treatment of
patients with marked renal insufficiency or
volume depletion.

252. Clonidine
acts through central alpha-agonist activity.

253. It has been administered in repeated hourly
doses and safely lowers blood pressure
over a period of hours.

254. Untoward effects, include sedation and
rebound hypertension.

255. Clonidine is not administered to anyone with
altered sensorium or who may not
comply
with treatment.

256. Labetalol
“A combined alpha- and beta-blocker”,
labetalol taken orally has a relative beta-
to alpha-blocking effect of approximately
3:1. Dosage begins at 100 mg (taken
orally twice daily) and is titrated to the
desired response.
The onset of action is 30 minutes to 2 hours
after administration; the duration of action
is 8 to 12 hours.

257. Nifedipine.
The use of sublingual nifedipine has
been reported to cause
– Hypotension.
– Syncope.
– Transient ischemic attacks.
– Cerebrovascular accidents.
– Myocardial ischemia.
– Infarction.

258. Sublingual nifedipine
should not be used
in the treatment of patients with
hypertension.

259. ‫دعواتنا جميعا للحبيبة الغالية‬
‫مصـــــــــــــــــــر‬

260. Thank You