Transcript 01. hypertensive

Hypertensive Crisis
Sofiya Lypovetska MD PhD
Ternopil state medical university
SCOPE of the PROBLEM

Hypertension is an increasingly important
medical and public health issue.
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The prevalence of hypertension increases
with advancing age to the point where more
than half of people aged 60 to 69 years old
and approximately three-fourths of those
aged 70 years and older are affected
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Data from observational studies involving
more than 1 million individuals have indicated
that death from both ischemic heart disease
and stroke increases progressively and
linearly from BP levels
Definitions and classification
of blood pressure levels (mmHg)
Factors influencing prognosis
Factors influencing prognosis
High/Very high risk subjects
Blood pressure measurement
Position statement: Ambulatory and home BP measurement
JNC –VII Guidelines
Patient characteristics associated
with resistant hypertension
Secondary causes of resistant hypertension
Medication that can interfere
with blood pressure control
Conditions favouring use of some antihypertensive drugs versus others
Compelling and possible contraindications to use of antihypertensive drugs
Hypertensive Crisis
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Definitions- Is This : A Crisis?
An Emergency?
An Urgency?…
Clinical Presentations
 Treatments
Other Terminology
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Severely elevated BP (JNC VII)
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Defined as BP > 180/120
“accelerated HPT”
– term used to describe individuals with chronic
hypertension with associated group 3 KeithWagener-Baker retinopathy
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“malignant HPT”
– describe those individuals with group 4 KWB
retinopathy changes + papilledema
Definitions
Hypertensive Crisis
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Hypertensive Emergency………1-2 hours
– Rapid / progressive end organ damage
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Hypertensive Urgency………….24-48 hrs
– Inc. BP without evidence of end organ damage
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Uncontrolled Hypertension……..1 week
– Do not require acute intervention
Shayne PH - Ann Emerg Med - 01-APR-2003; 41(4): 513-29
Hypertensive Emergency
BP >180/120 with evidence of target organ dysfunction
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Hypertensive encephalopathy
Intracerebral bleed
Acute MI
Acute CHF with pulm edema
Unstable angina
Aortic dissection
Eclampsia
Tx: parenteral agent
Cerebrovascular Hypertensive
Emergencies
Cerebral Infarct
Intracerebral Hemorrhage
Hypertensive Encephalopathy
Cerebral Edema
Cerebral Perfusion Pressure

Cerebral blood flow a
function of CPP
 Autoreg. Fails at 25%
of MAP
 ICP
CPP
– Vulnerable to
MAP
CBF = blood flow; CPP = cerebral perfusion pressure;
ICP = intracranial pressure; MAP = mean arterial pressure;
TCA = total circulatory arrest.
Hypertensive Encephalopathy
Pathophysiology:
- Loss of Cerebral Autoregulation of blood flow
resulting in hyperperfusion of the brain, loss of
integrity of the blood brain barrier, and vascular
necrosis.
- Loss of Autoregulation occurs at a constant
cerebral blood flow of above MAP 150 to 160
mmHg.
- Acute Onset
- Reversible
Hypertensive Encephalopathy
Symptoms:
Headache, Nausea/Vomiting, Lethargy,
Confusion, Lateralizing neurological symptoms
that are not often in an anatomical distribution.
Signs:
Papilledema, Retinal Hemorrhages
Decreased level of consciousness, Coma
Focal neurological findings
Hypertensive
encephalopathy
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Clinical manifestation of cerebral edema
and microhemorrhages seen with
dysfunction of cerebral autoregulation
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Defined as an acute organic brain syndrome
or delirium in the setting of severe
hypertension
HPT Encephalopathy
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Not adequately treated – cerebral
heamorrhage, coma and death.
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BUT with proper treatment – completely
reversible
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Clinical diagnoses (exclusion)
Management of Hypertensive
Encephalopathy
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Reduce Mean Arterial Pressure (MAP) by 20 to
25% (T.397) and do not exceed this within first 30
to 60 min.
Rosen recommends reduction of 30 to 40%
(R.1759)
MAP= 1/3(SBP-DBP) + DBP
Treatment Reduces vasospasm that occurs at these
high pressures
Avoid excessive BP reduction to prevent
hypoperfusion of the brain and further cerebral
ischemia
Hypertensive Encephalopathy
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Cerebral overperfusion
– MAP overwhelms autoregulation
– Vasodilation and Inc. Perm.
– Cerebral Edema
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Hemorrhage, Coma, Death
 Tx: Nipride, Fenoldopam,
Labatalol, Nicardipine
Hemorrhagic CVA
causes
 Hypertensive
Vascular
Disease
 Arteriovenous
Anomalies (AVM)
 Arterial Aneurysms
 Tumors
 Trauma
Hemorrhagic CVA
Management
Hemorrhagic CVA’s commonly results in a
profound reactive rise in blood pressure
 Management is CONTROVERSIAL.
 Subarachnoid Hemorrhage: oral nimodipine
(nimotop) 60mg po q 4 hours to reverse
vasospasm.
 Nicardipine: 2mg IV boluses followed by an IV
infusion of 4 to 15 mg/hr is used by some to treat
Subarachnoid Hemorrhage.
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Ischemic CVA
Pathophysiology:
Elevated Blood
Pressure can be the
cause of the central
nervous system event,
OR, it may be a
normal physiologic
response (Cushing’s
Reflex)
Ischemic CVA Management
Favors lowering MAP (mean arterial
pressure) by 20%.
Recommends IV Labetalol in small doses of
5mg increments IF Diastolic Blood
Pressure is higher than 140 mmHg.
(T. 398)
HPT Retinopathy
AV crossing changes
HPT retinopathy
HPT retinopathy
Cardiovascular Hypertensive
Emergencies
Aortic
Dissection
Congestive
Heart Failure
Acute MI
Congestive Heart Failure
Pathophysiology:
Increased
Afterload with
decreased
Cardiac Output
CHF / Pulmonary Edema
Symptoms:
Shortness of Breath, Cough, Chest Pain
Lower Extremity Swelling
Signs:
Jugular Venous Distension, Rales, S3 Gallop
Hepatomegaly, Pedal Edema
CHF / Pulmonary Edema
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Treatment:
– Diuretics
– Nitroglycerin
– Vasodilators
– Digitalis
– Beta-adrenoceptor agonists
– Other positive inotropic agents
Acute Coronary Syndrome
Pathophysiology:
- Increased
afterload, cardiac
workload, and
myocardial oxygen
demand
- Decreased
coronary artery
blood flow
Acute Coronary Syndrome /
Acute MI
Symptoms:
Chest Pain, Nausea / Vomiting, Diaphoresis,
Shortness of Breath
Signs:
Congestive Heart Failure Signs,
S4 Gallop
(due to decreased ventricular compliance)
Few physical findings in many patients
Clinical History is very Important
Acute Coronary Syndrome/
Acute MI
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Immediate Blood Pressure reduction is
indicated to prevent Myocardial Damage
No specific Defined BP target
Management:
Nitroglycerin IV or Sublingual
- Beta Blockers (Esmolol, Lopressor)
- Nitroglycerin is Drug of Choice
Aortic Dissection
Pathophysiology:
- Atherosclerotic Vascular
Disease, Chronic
Hypertension, increased
shearing force on the
thoracic aorta, leading to
intimal tear.
- 50% begin in ascending
aorta
- 30% at aortic arch
- 20% in descending aorta
Dissection of Thoracic Aorta
Symptoms:
-
Chest pain radiating to the back (classic presentation)
Neurological Symptoms (carotid artery dissection)
Angina (coronary artery dissection)
Shortness of breath (aortic insufficiency, cardiac tamponade)
Signs:
- Differential Blood Pressure (in UE)
- Bruit (interscapular)
- Neurological Deficits
- Acute Cardiac Tamponade (rare)
Dissection of Thoracic Aorta
Optimal Blood Pressure in these
patients is undefined and must be
tailored for each patient, however,
SBP of 120-130mmHg may be a
intial starting point. (T.408)
Acute Renal Failure
Pathophysiology:
-
Hypertensive Glomerulonephropathy,
Acute Tubular Necrosis
- Worsening renal function in the setting of severe
hypertension with elevation of BUN/CR,
proteinuria, or the presence of red cells and red
cell casts in the urine.
Acute Renal Failure
Symptoms:
- Many times there are few actual symptoms
- Facial or Peripheral Edema due to fluid overload
or proteinuria may be present, shortness of breath
Signs:
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Few findings unless edematous
Pulmonary Edema
Acute Renal Failure
Management:
Nitroprusside is agent of choice
Dialysis (as needed)
Lasix to enhance Sodium excretion; Also
recommends Nitroprusside or Nifedipine
- Nitroglycerin is also a good agent in this setting
since it is hepatically metabolized and
gastrointestinally excreted.
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Preeclampsia / Eclampsia
Pathophysiology:
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Systemic arterial vasoconstriction
(including placental, leading to
decreased uterine blood flow).
Defined as SBP = 140/90 mmHg or
greater, OR a 20 mmHg rise in SBP
or
10 mmHg rise in DBP from
baseline and evidence of HELLP
Syndrome
Preeclampsia / Eclampsia
Symptoms: lower extremity swelling,
headache, confusion, seizures, coma
Signs: edema, hyperreflexia, elevation of
blood pressure related to baseline BP prior
to pregnancy (elevation may be mild
125/75)
Management:
IV Magnesium Sulfate, Hydralazine.
- May also use nifedipine or labetalol
Delivery of Fetus is definitive treatment of
pre-eclampsia
Treatment of acute severe hypertension in preeclampsia
Pheochromocytoma
Pathophysiology:
- Alpha and Beta stimulation of
the cardiovascular system due
to adrenergic excess states
Symptoms:
Episodic Headaches, flushing,
tremor, diaphoresis, diarrhea,
hyperactivity, and palpitations
Signs:
Tachycardia, tachypnea, tremor,
hyperdynamic state (high
output CHF)
Pheochromocytoma
Management:
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Alpha Blocker FIRST, followed by a Beta
Blocker
Phentolamine (alpha) + Esmolol (beta)
Labetalol IV (combined alpha and beta
blockade)
Pharmacologic Agents
Hypertensive Emergencies
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Rapid Onset
 Rapid Maximal effect
 Rapid offset
 Ease of Titration
Parenteral Agents
Parenteral drugs for treatment of hypertensive emergencies
Oral Regimens for Treatment
of Hypertensive
Urgency in the ED
Clonidine: 0.1 to 0.2mg PO, repeat 0.1mg q hour
to desired BP reduction or max of 0.7mg.
- Labetalol: 200 to 400mg PO, repeat every 2 to 3
hours
- Captopril: 25mg PO
- Losartan: 50mg PO
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Key Concepts
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Acute End-organ damage determines hypertensive
emergency
 Be familiar with the agents of choice in specific
emergencies
 Goal for most is careful reduction of MAP by 2025% over minutes to hours
– DBP not less than 100 to 110
– Except: Pregnancy, Dissection, MI,
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Patients without acute end-organ
ischemia rarely require urgent
intervention
Thank You!