This is a comprehensive approach to a hypertensive patient presenting to the emergency department.
Discussing:-
- Hypertensive emergency
- Hypertensive Urgency
- Hypertensive Crisis
- Hypertensive encephalopathy and retinopathy
- Accelerated Hypertension
- Malignant hypertension
2. Outline of this lecture:
What is Heart Hypertensive Crisis?
Epidemiology.
Classification of Hypertensive Crisis.
Causes of Hypertensive Crisis
Clinical presentation of Hypertensive
Crisis
Managment of Hypertensive Crisis
Jwan Ali AlSofi
3. What is Hypertensive Crisis?
•The term hypertensive crisis is defined as a
severe elevation in blood pressure (BP),
generally considered to be a diastolic
blood pressure greater than 120 mm Hg
Jwan Ali AlSofi
4. What is Hypertensive Crisis?
•This disorder can be further classified as
hypertensive urgency or hypertensive
emergency when there is evidence of
acutely progressive end-organ damage.
•If these disorders are not treated promptly,
a high rate of morbidity and mortality will
occur the 5-year mortality for patients with
a history of hypertensive crisis is 26%
Jwan Ali AlSofi
5. Epidemiology
• Approximately 1% of hypertensive pts. may develop
hypertensive crises during their lifetime.
• Annual incidence of hypertensive emergencies being
1-2 cases/1,00,000 pts.
• Higher rates have been reported in African Americans, low
socioeconomic people, in developing countries.
• Incidence in men 2 times higher than in women
Epidemiology
Jwan Ali AlSofi
7. Definitions of hypertensive crisis:-
• Hypertensive emergencies:- are defined as severe
elevations in BP (>180/120 mm Hg) associated with
evidence of new or worsening target organ damage.
• Hypertensive urgencies:- are situations associated with
severe BP elevation (>180/120 mm Hg) in otherwise stable
patients without acute or impending change in target
organ damage or dysfunction.
• Accelerated hypertension (aka malignant hypertension):- A
severe increase in blood pressure to 180/120 mmHg or
higher (and often over 220/120 mmHg) with signs of
retinal haemorrhage and/or papilloedema (grade 3-4). It is
usually associated with new or progressive target organ
damage.
Jwan Ali AlSofi
10. • Renovascular Disease
• Pheochromocytoma
1. Non-adherence to anti-HTN medications (most
common)
2. Hyperaldosteronism
3. Anti-hypertensive withdrawal syndromes
4. Head injuries and CNS trauma
5. Post-op hypertension
6. Drug-induced hypertension
Causes of hypertensive emergencies ?
Jwan Ali AlSofi
11. • As with hypertensive emergencies ,severe BP
elevations may result from inadequate control or poor
adherence to current antihypertensive drug regimens.
• Another cause for patients reaching hypertensive
urgency is previous inaccurate BP measurements that
underestimate or do not detect increased BP at all
(e.g. poor patient technique for self‐monitoring).
Causes of hypertensive Urgencies ?
Jwan Ali AlSofi
13. Causes Hypertensive Urgencies
• Lifestyle:
- High salt diet, excessive alcohol use.
• Comorbid Conditions:
- Thyroid storm, trauma, renovascular disease, acute
ischemic stroke or adrenal dysfunction
Causes of hypertensive Urgencies ?
Jwan Ali AlSofi
14. Clinical Presentation of HC
Emergency
• Characterized by severe increase in
systolic and/or diastolic blood pressure
associated with signs or symptoms of
acute end-organ damage.
• Usually, SBP > 180 mm Hg - DBP >
120 mm Hg
• Requires an immediate BP reduction in
few minutes - hours.
• Requires an ICU care & IV drugs
Urgency
• Elevated BP ( usually systolic > 180
mmHg &/or diastolic > 120 mmHg ) but
without evidence of end-organ
damage.
• Usually asymptomatic; severe
headache, shortness of breath,
epistaxis, severe anxiety.
• Adequate treatment of these conditions,
a BP lowering within 24-48 hrs by
administration of oral drugs.
• ICU admission is usually not required
• Controlled by oral medications.
Jwan Ali AlSofi
15. Clinical Presentation of HC
Emergency
• Rarely develop in patients without a
previous history of hypertension
• occur in patients with
pheochromocytoma or renal vascular
disease
• CNS:-
• Cerebral infarctions,
• HTN Encephalopathy
• intracranial or subarachnoid hemorrhage.
• Heart:-
• acute heart failure (HF) and pulmonary
edema
• acute myocardial infarction,
• unstable angina.
• Acute dissection,
• Eclampsia .
Urgency
• Not all patient present with
same symptoms
• 90% of patients had a history
of hypertension
• Headache (42%) and dizziness
(30%).
• visual changes,
• chest discomfort,
• nausea,
• epistaxis,
• Fatigue
• psychomotor agitation.
Jwan Ali AlSofi
17. • Single organ damage in approximately 83%.
• Two organ damage found in 14%,multiorgan damage
in 3 % pts.
Most common clinical presentations :
- cerebral infarction (24%)
- pulmonary oedema (22%)
- HTN encephalopathy (16%)
- Cong. HF (12%)
•Less common presentations –
- IC hemorrhage,
- Aortic dissection
Acute End-organ Damage
(Complication of HC).
Jwan Ali AlSofi
22. Hypertensive Encephalopathy
• Is a presentation of hypertensive emergency
• Our brains are under tight control. With severe rises in BP,
autoregulation fails and leads to cerebral edema.
• Hypertensive encephalopathy is defined as the presence of
signs or symptoms of cerebral edema secondary to severe
and/or sudden rises in BP. It’s characterized by:
• Severe Hypertension with 1+ of:
1. Seizures
2. Lethargy
3. Cortical Blindness
4. Coma
• It is a diagnosis of exclusion
Jwan Ali AlSofi
23. Of note, there is little evidence to
suggest that headache alone is a sign
of a hypertensive emergency, however,
in combination with visual changes,
lethargy, seizures or altered mental
status it may be an indication of
hypertensive encephalopathy.
24. ACUTE END ORGAN DAMAGE- CVS
2. Cardiovascular
- Myocardial ischemia/infarction – 4TH (12%).
- Acute left ventricular dysfunction
- Acute pulmonary edema – 2ND MOST COMMON
(22.5% )
- Aortic dissection
Jwan Ali AlSofi
25. ACUTE END ORGAN DAMAGE- Renal
3. RENAL
ARTERIOSCLEROSIS, FIBRINOID NECROSIS overall
impairment of renal protective autoregulation mechanisms!
RESAULT:
- Worsening renal function - Acute renal failure/insufficiency (↑BP)
- Hematuria + red blood cell (RBC) cast formation
- Proteinuria.
4. Microangiopathic hemolytic anemia
Jwan Ali AlSofi
26. MALIGNANT HYPERTENSION
- Is a HYPERTENSIVE EMERGENCY!!!
- Leading to an acute end organ damage
- Less than 1% of ht patients develop the
malignant phase
- Avarage age of diagnosis is 40
- Men>women
Jwan Ali AlSofi
27. MALIGNANT HYPERTENSION-
PATHOPHYSIOLOGY
BP =PVR*CO(SV*HR)
Rate at which MAP rises more important than absolute rise
Acute rise in BP Failure of vasoconstriction Endothelial
by autoregulation damage
FIBRINOID Activates coag. and Deposition. of proteins/
NECROSIS inflammation fibrinogen in vessel
wall
- RAAS plays an important role in initiating and perpetuating BP rise by causing
vasoconstriction and fluid retention.
- THIS CYCLE MUST BE STOPPED IN ORDER TO PREVENT FURTHER VASCULAR
INJURY AND TISSUE ISCHEMIA!
Jwan Ali AlSofi
29. • The treatment of hypertensive crises must balance
preventing further end-organ damage while
maintaining tissue perfusion.
• The initial goal for blood pressure reduction is not to
obtain a normal blood pressure.
• Rapid and aggressive reductions in blood pressure can
actually induce cerebral, myocardial, or renal
ischemia or infarction if the blood pressure falls below
the range at which tissue perfusion can be maintained
by autoregulation.
MANAGEMENT
History Examination Assessment Treatment
Jwan Ali AlSofi
30. • Duration and degree of pre existing hypertension
• Details of antihypertensive therapy
• Compliance with medications
• Use of the over counter drugs
• History of recent operations.
History Examination Assessment Treatment
HISTORY
Jwan Ali AlSofi
34. Lab tests & investigations may be required:-
- CBC,
- ECG,
- urinalysis,
- renal function
- Echo.
- consider head imaging if neurological symptoms
are present
ASSESMEN with INVESTIGATION
Jwan Ali AlSofi
37. Clinical Presentation of HC
Emergency
• rarely develop in patients
without a previous history of
hypertension
• occur in patients with
pheochromocytoma or renal
vascular disease
• Cerebral infarctions,
encephalopathy and
intracranial or subarachnoid
hemorrhage.
• acute heart failure (HF) and
pulmonary edema and acute
myocardial infarction, unstable
angina. Acute dissection,
eclampsia.
Urgency
• headache (42%) and
dizziness (30%). Other
symptoms include visual
changes, chest discomfort,
nausea, epistaxis, fatigue,
and psychomotor agitation.
• Not all patient present with
same symptoms
• 90% of patients had a
history of hypertension
Jwan Ali AlSofi
39. MALIGNANT HYPERTENSION-
THERAPY - general
- HOSPITALIZATION
- RELAXATION (NON STRESSED ENV.)
SCREEN FOR END ORGAN DAMAGE
INITIAL AIMS:
1. CORRECTION OF MEDICAL COMPLICATION
2. REDUCTION OF MAP BY 20-25% IN THE 1ST HOUR
3. REDUCTION OF DIASTOLIC PRESSURE TO 13 OVER MINUTES
TO HOURS HOURS=110 mmHg (BUT NOT BELOW <95 mmHg –
IN ORDER NOT TO CAUSE CEREBRAL HYPOPERFUSION)
BP should be reduced
- immediately-
- gradually
(Specifically)
DRUGS should be used i.v
Jwan Ali AlSofi
42. Hypertensive Emergency
THERAPY – IV DRUGS cont.
2 MAIN CLASSES OF DRUGS:
1.Vasodilators:
Nitroprusside
Nitroglycerine
Nicardipine
Hydralazine
Enalapril
Fenoldopam
2. Adrenergic inhibitors
Labetalol (a+b blocker)
Esmolol (b-1 selective blocker)
Phentolamine (a1 blocker)
Jwan Ali AlSofi
43. Hypertensive Emergency
THERAPY – SPECIFIC DRUGS
1. NITROPRUSSIDE :
- 1ST CHOICE FOR HT CRISIS!
- ONSET 30 SEC FOR FEW MIN
VEINS + ARTERIES
DECREASE PRELOAD = USED IN ACUTE MI!
SIDE EFFECT: THIOCYANIDE TOXICITY, METHEMOLOBINEMIA,
HYPOTHYRODISM
2. NITROGLYCERIN:
- Coronary vasodilator
- Direct venodilator (variable arterial effects)
SIDE EFFECT: headaches and tachycardia ,Methemoglobinemia
3. LABETALOL:
Combined alpha & beta blocker
Beta blockade blunts reflex tachycardia from alpha blockade
Myocardial depression
Caution in patients with reactive airway disease
Jwan Ali AlSofi
44. Hypertensive Emergency –
THERAPY – SPECIFIC DRUGS
4. FENOLDOPAM : (DOPAMIN AGONIST)
Short acting (30 MIN)
Rapid elimination upon discontinuation
No dosing adjustment for pre-existing renal or hepatic impairment
Increases renal blood flow and maintains GFR
5. HYDRALAZINE (oral):
- Strict arteriole vasodialator
-3rd 4th option in HT crisis.
Jwan Ali AlSofi
45. Hypertensive Emergency THERAPY:
SPECIFIC RECOMMENDATION FOR DIFFERENT
CLINICAL FORMS (exmamples)
1. Hypertensive encephalopathy
Preferred medications :
Labetalol
Nicardipine
Esmolol
Medications to avoid :
Nitroprusside (was used in the past- caused ICP )
Hydralazine
Treatment guidelines: Reduce mean arterial pressure (MAP) 25% over 8
hours.
Jwan Ali AlSofi
46. Hypertensive EmergencyTHERAPY:
SPECIFIC RECOMMENDATION FOR DIFFERENT
CLINICAL FORMS (exmamples)
2. Aortic dissection –
Immediate redn. In BP and mainly shear stress (change in BP with change in time)
is essential to limit the extension of damage as surgery is being considered.
Preferred medications
Labetalol
Nicardipine
Nitroprusside (with beta-blocker)
Esmolol
Morphine sulfate
Medications to avoid
Avoid beta-blockers if there is aortic valvular regurgitation or suspected
cardiac tamponade, HYDRALAZINE (increase shear stress)
Treatment guidelines: Maintain SBP <110 mm Hg, unless signs of end-organ
hypoperfusion are present.
+Narcotic analgesics
TIME TO ACHIEVE: 20 MINUTES!!!!!
Jwan Ali AlSofi
47. Hypertensive Emergency THERAPY:
SPECIFIC RECOMMENDATION FOR DIFFERENT
CLINICAL FORMS (exmamples)
3. Preeclampsia/eclampsia
Preferred medications
Hydralazine
Labetalol
Nifedipine
Medications to avoid
Nitroprusside
Angiotensin-converting enzyme inhibitors
Esmolol
Treatment guidelines: In women with eclampsia or preeclampsia, SBP should
be <160 mm Hg and DBP <110 mm Hg in the prepartum and intrapartum
periods. If the platelet count is <100,000 cells mm3 BP should be
maintained below 150/100 mm Hg. Patients with eclampsia or
preeclampsia should also be treated with IV magnesium sulfate to
avoid seizures
Jwan Ali AlSofi
48. Hypertensive Emergency THERAPY:
SPECIFIC RECOMMENDATION FOR DIFFERENT
CLINICAL FORMS (exmamples)
4. CARDIAC CRISIS
L.V FAILURE AND PUL. EDEMA
Preferred medications
Nitroglycerin
Enalaprilat
Nitroprusside
Treatment guidelines: Treatment with vasodilators (in addition to diuretics) for SBP
≥140 mm Hg. IV or sublingual nitroglycerin is the preferred agent
BP CONTROL IS SECONDARY to the primary problem - open the infarct
related artery and treat pain, diurese and oxygenate those in pulmonary
edema
Jwan Ali AlSofi
49. Hypertensive Emergency THERAPY:
SPECIFIC RECOMMENDATION FOR DIFFERENT
CLINICAL FORMS (exmamples)
4. RENAL INSUFFICENCY:
Goal is to prevent further renal damage by
maintaining adequate blood flow.
Preferred medications:
Nitroprusside
Jwan Ali AlSofi
52. TREATMENT OF HYPERTENSIVE EMERGENCY
GOAL
• reduce MAP by no more than 20-25%, DBP to 100-
110mm Hg within few minutes to 2 hours.
• More aggressive and rapid BP reduction (Acute
Pulmonary edema ,Aortic dissection)
• More slowly for acute cerebrovascular damages with
monitoring of neurological status.
• Constant infusion of intravenous agents required
MANAGEMENT
Jwan Ali AlSofi
53. Target of BP in HYPERTENSIVE EMERGENCY
Jwan Ali AlSofi
54. TREATMENT OF HYPERTENSIVE EMERGENCY
GOAL
• reduce MAP by no more than 20-25%, DBP to 100-
110mm Hg within few minutes to 2 hours.
• More aggressive and rapid BP reduction (Acute
Pulmonary edema ,Aortic dissection)
• More slowly for acute cerebrovascular damages with
monitoring of neurological status.
• Constant infusion of intravenous agents required
TREATMENT OF HYPERTENSIVE EMERGENCY
Jwan Ali AlSofi
55. TREATMENT OF HYPERTENSIVE EMERGENCY
GOAL
• reduce MAP by no more than 20-25%, DBP to 100-
110mm Hg within few minutes to 2 hours.
• More aggressive and rapid BP reduction (Acute
Pulmonary edema ,Aortic dissection)
• More slowly for acute cerebrovascular damages with
monitoring of neurological status.
• Constant infusion of intravenous agents required
TREATMENT OF HYPERTENSIVE EMERGENCY
Jwan Ali AlSofi
59. GOAL
• Overall Goal of Management: reduce SBP by ~ 25% over
24‐48 hours.
• More conservative BP lowering reduces the risk of
potential adverse effects (i.e. perfusion complications
worsening incidence of MI, stroke, and death) associated
with more aggressive BP lowering if the blood pressure
falls below the range at which tissue perfusion can be
maintained by autoregulation .
• All treatment strategies should consider the patient’s
comorbidities and risk of adverse events.
• Treated by oral medications not IV.
TREATMENT OF HYPERTENSIVE
URGENCY
Jwan Ali AlSofi
60. TREATMENT OF HYPERTENSIVE URGENCY
GOAL
• Overall Goal of Management: reduce SBP by ~ 25% over
24‐48 hours.
• More conservative BP lowering reduces the risk of
potential adverse effects (i.e. perfusion complications
worsening incidence of MI, stroke, and death) associated
with more aggressive BP lowering if the blood pressure
falls below the range at which tissue perfusion can be
maintained by autoregulation .
• All treatment strategies should consider the patient’s
comorbidities and risk of adverse events.
MANAGEMENT
Jwan Ali AlSofi
61. Take-Home Points
Fundoscopy and urine dip are key in the
assessment of the severely hypertensive
patient who you are working up for a possible
hypertensive emergency
Keep a high index of suspicion for
hypertensive encephalopathy in the severely
hypertensive and altered or comatose patient
with or without seizures or cortical blindness
Treat the patient and not the number
Jwan Ali AlSofi
Diagnosis and management of a hypertensive crisis. Colors correspond to Class of Recommendation in Table 1. *Use drug(s) specified in Table 19. †If other comorbidities are present, select a drug specified in Table 20. BP indicates blood pressure; DBP, diastolic blood pressure; ICU, intensive care unit; and SBP, systolic blood pressure.
Management of hypertension in patients with acute ICH. Colors correspond to Class of Recommendation in Table 1. BP indicates blood pressure; ICH, intracerebral hemorrhage; IV, intravenous; and SBP, systolic blood pressure.
Management of hypertension in patients with acute ischemic stroke. Colors correspond to Class of Recommendation in Table 1. BP indicates blood pressure; DBP, diastolic blood pressure; IV, intravenous; and SBP, systolic blood pressure.