Hypertensive Crisis.ppt

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

1. HYPERTENSIVE
CRISIS
JWAN ALI AHMED ALSOFI

2. Outline of this lecture:
What is Heart Hypertensive Crisis?
Epidemiology.
Classification of Hypertensive Crisis.
Causes of Hypertensive Crisis
Clinical presentation of Hypertensive
Crisis
Managmentof 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
emergencywhen 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% ofhypertensive 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
socioeconomicpeople, in developing countries.
•Incidence in men 2 times higher than in women
Epidemiology
Jwan Ali AlSofi

6. BLOOD PRESSURE –CLASSIFICATION
(for adults >= 18 years old)
DIAS.
PRESSURE
(mmHg)
SYS.
PRESSURE
(mmHg)
CATEGORY
<80<120
OPTIMAL
<85<130
NORMAL
85-89130-139
HIGH NORMAL(PRE
HT):
HYPERTENSION
90-99140-159
STAGE 1 (MILD)
100-109160-179
STAGE 2 (MODERATE)
>=110>=180
STAGE 3 (SEVERE)
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 withoutacute or impending change in target
organ damage or dysfunction.
•Accelerated hypertension (akamalignant hypertension):-A
severe increase in blood pressure to 180/120mmHg or
higher (and often over 220/120mmHg)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

8. Definition of HTN-emergency:-
Jwan Ali AlSofi

9. Classification of Hypertensive Crisis
Jwan Ali AlSofi

10. •RenovascularDisease
•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 measurementsthat
underestimate or do not detect increased BP at all
(e.g. poor patient technique for self‐monitoring).
Causes of hypertensive Urgencies?
Jwan Ali AlSofi

12. Causes Hypertensive Urgencies
Drugs:
•Non-NarcoticAnalgesics :
-Non-steroidal anti-inflammatory agents including
aspirin
-Selective COX-2 inhibitors
•Sympathomimeticagents:
-Decongestants
-Diet pills
-Cocaine
•Stimulants:
-Methylphenidate, amphetamine.
Causes of hypertensive Urgencies?
Jwan Ali AlSofi

13. Causes Hypertensive Urgencies
•Lifestyle:
-High salt diet, excessive alcohol use.
•ComorbidConditions:
-Thyroid storm, trauma, renovasculardisease, 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 withsigns or symptoms of
acuteend-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 >120mmHg ) but
withoutevidence 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 hrsby
administration of oral drugs.
•ICU admission is usually notrequired
•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
pheochromocytomaor 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

16. ACUTE PROGRESSIVE
END-ORGAN DAMAGE

17. •Singleorgan damagein approximately 83%.
•Twoorgan damagefound 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
-Eclampsia
Acute End-organ Damage
(Complication of HC).
Jwan Ali AlSofi

18. Jwan Ali AlSofi

19. ACUTE END ORGAN DAMAGE -CNS
1. Neurological –
-normal: increase in BP cerebral arterioles vasoconstrict cerebral blood flow
(CBF) remains constant
-hypertensive emergency: loss of autoregulation ability (decomp.) dialationof
cerebral vessel exsessivecerebral blood flow+ leakage from cappilaries
RESAULT:
1.Hypertensive encephalopathy-3
RD
MOST COMMON (16.3%)
2.Cerebral vascular accident/cerebral infarction –
MOST COMMON (24.5%)
1.Subarachnoid hemorrhage
2.Intracranial hemorrhage
3.Retinopathy Keith-Wagner-GRADES 3 AND 4.
4.Eclampsia
Jwan Ali AlSofi

20. Hypertensive retinopathy:-
Acute/severe
hypertensive
retinopathy
Jwan Ali AlSofi

21. HYPERTENSION CRISIS -RETINA
Retinal hemmorhages(grade 3)-
ACCELERATED HT
Pappiledema(grade 4)-
MALIGNANT HT
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 edemasecondary 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 adiagnosis 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 –4
TH
(12%).
-Acute left ventricular dysfunction
-Acute pulmonary edema –2
ND
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. Microangiopathichemolytic anemia
Jwan Ali AlSofi

26. MALIGNANT HYPERTENSION
-Is a HYPERTENSIVE EMERGENCY !!!
-Leading to an acute end organ damage
-Less than 1% of htpatients develop the
malignant phase
-Avarageage of diagnosis is 40
-Men>womenJwan 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

28. MANAGEMENT OF HC
Jwan Ali AlSofi

29. •The treatment of hypertensive crises must balance
preventing further end-organ damagewhile
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 TreatmentJwan 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

31. EXAMINATION
Jwan Ali AlSofi

32. CLINICAL SYMPTOMS
C.V:
•palpitations,
•arrhythmias,
•chest pain,
•dyspnea,
•pul. Edema.
BRAIN:
•headaches,
•nausea,
vomiting,
•blindness,
•seizures,
•coma
KIDNEY:
•oliguria,
•hematuria,
•proteinuria,
•electrolyte
imbalance,
•uremia,
•azothemia
EYE:
•flashes,
•scotoma
GENERAL:
•sweating,
•pallor,
•flushes,
•tinnitus,
•epitaxis,
•fear of death
Jwan Ali AlSofi

33. 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

35. Jwan Ali AlSofi

36. Jwan Ali AlSofi

37. Clinical Presentation of HC
Emergency
•rarely develop in patients
without a previous history of
hypertension
•occur in patients with
pheochromocytomaor 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

38. TREATMENT OF HYPERTENSIVE
EMERGENCY

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 1
ST
HOUR
3. REDUCTION OF DIASTOLIC PRESSURE TO 1\3 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

40. Jwan Ali AlSofi

41. Hypertensive Emergency
THERAPY –IV DRUGS
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+bblocker)
Esmolol(b-1 selective blocker)
Phentolamine(a1 blocker)
Jwan Ali AlSofi

43. Hypertensive Emergency
THERAPY –SPECIFIC DRUGS
1. NITROPRUSSIDE :
-1
ST
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
-3
rd
\4
th
option in HT crisis.
Jwan Ali AlSofi

45. Hypertensive EmergencyTHERAPY:
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

50. Hypertensive Emergency-
PROGNOSIS
Median survival duration:144 months
for all patients presenting to ED with hypertensive
emergency.
5 yr survival rate:74%.
Jwan Ali AlSofi

51. Jwan Ali AlSofi

52. TREATMENT OF HYPERTENSIVE EMERGENCY
GOAL
•reduceMAPbynomorethan20-25%,DBPto100-
110mmHgwithinfewminutesto2hours.
•MoreaggressiveandrapidBPreduction(Acute
Pulmonaryedema,Aorticdissection)
•Moreslowlyforacutecerebrovasculardamageswith
monitoringofneurologicalstatus.
•Constantinfusionofintravenousagentsrequired
MANAGEMENT
Jwan Ali AlSofi

53. Target of BP in HYPERTENSIVE EMERGENCY
Jwan Ali AlSofi

54. TREATMENT OF HYPERTENSIVE EMERGENCY
GOAL
•reduceMAPbynomorethan20-25%,DBPto100-
110mmHgwithinfewminutesto2hours.
•MoreaggressiveandrapidBPreduction(Acute
Pulmonaryedema,Aorticdissection)
•Moreslowlyforacutecerebrovasculardamageswith
monitoringofneurologicalstatus.
•Constantinfusionofintravenousagentsrequired
TREATMENT OF HYPERTENSIVE EMERGENCY
Jwan Ali AlSofi

55. TREATMENT OF HYPERTENSIVE EMERGENCY
GOAL
•reduceMAPbynomorethan20-25%,DBPto100-
110mmHgwithinfewminutesto2hours.
•MoreaggressiveandrapidBPreduction(Acute
Pulmonaryedema,Aorticdissection)
•Moreslowlyforacutecerebrovasculardamageswith
monitoringofneurologicalstatus.
•Constantinfusionofintravenousagentsrequired
TREATMENT OF HYPERTENSIVE EMERGENCY
Jwan Ali AlSofi

56. Jwan Ali AlSofi

57. Jwan Ali AlSofi

58. TREATMENT OF HYPERTENSIVE
URGENCY

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
Fundoscopyand 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

62. Jwan Ali AlSofi