Harrison 20 edition based hypertension crisis with latest guidelines

1. HYPERTENSIVE CRISES
Presenter: Awatif Bashir MD (PGY1, IM)
Moderator: Semir Abdi MD (Internist)

2. OUTLINE OF PRESENTATION
oIntroduction
oEpidemiology
oEtiology
oClassification
oClinical Picture
oDiagnosis
oManagement

3. HYPERTENSIVE CRISES
oDefinition: These are acute, severe elevations in blood
pressure that may or may not be associated with end
organ damage or dysfunction.
oBP Values:
oSBP: >180 mmHg
oDBP: >120 mmHg
oThese can be one of two subsets:
oHypertensive Urgency
oHypertensive Emergency

4. HYPERTENSIVE CRISES
oHypertensive Urgency: Severe elevations in Blood
pressure without any evidence of end-organ
damage
oHypertensive Urgency: Severe elevations in Blood
pressure with any evidence of end-organ damage

5. EPIDEMIOLOGY
oApproximately 1% of hypertensive patients may
develop a HTN crises in their lifetime.
oAnnual Incidence: 1-2100,000 patients
oIncidence is higher in African Americans, low
SES and in developing countries.
oTwice as common in men.

7. RISK FACTORS
oThere is no single predisposing factor identified to be
associated with these conditions.
oThe most common ones are:
oPoorly controlled HTN
oReno-vascular disease
oCerebro-Vascular Disease
oLow Socioeconomic status
oSubstance or alcohol abuse
oCigarette smoking
oOral Contraceptive Use

9. PATHOPHYSIOLOGY
oThe underlying mechanism is still not fully understood.
oThe transition from mild hypertension or normo-tension to
a hypertensive crisis usually is precipitated by an event
that leads to an abrupt increase in blood pressure.
oThese may include:
oCessation of hypertensive medications with potential
rebound effects
oconsumption of illicit drugs
osevere pain
oseveral clinical syndromes

10. PATHOPHYSIOLOGY
oIn most hypertensive crises, the initial rise in blood pressure is
secondary to increased systemic vascular resistance.
oThe rise in systemic vascular resistance is believed to be caused
by humoral vasoconstrictors With the increase in blood pressure,
mechanical stress on the arteriolar wall leads to endothelial
damage and fibrinous necrosis of the arterioles, this in
turn leads to loss of auto-regulatory mechanisms, ischemia, and
acute end-organ damage, which prompts further release of
vasoconstrictors, thereby initiating a vicious circle

11. PATHOPHYSIOLOGY
oIt is also linked to 4 distinct mechanisms:
oVascular damage:
oDue to mechanical stress and vascular damage.
oRAAS Activation:
oCausing vasoconstriction and Expression of inflammatory cytokines
oOxidative stress:
oDue to increase in production of reactive oxygen species
oEndothelial Dysfunction:
oDue to excessive vasoconstriction and coagulation cascade activation

12. HYPERTENSIVE EMERGENCIES
oHypertensive Encephalopathy
oAcute Pulmonary Edema
oAcute Myocardial Infraction Angina
oAcute Renal Failure
oPost-Operative HTN
oAcute Aortic Dissection
oEclampsia
oMalignant Hypertension

13. CLINICAL PRESENTATION
Hypertensive Urgency:
oMostly Completely Asymptomatic
oCan Present with:
• Headaches
• Nausea
• Epistaxis
• Severe Anxiety
oSigns
• Elevated BP

14. CLINICAL PRESENTATION
Hypertensive Emergency:
oDepends on the End-Organ Affected:
• Chest Pain
• Acute Myocardial Infraction
• Myocardial IschemiaAngina
• Back Pain
• Thoracic Aortic Dissection
• Dyspnea
• Acute Pulmonary Edema
• Altered Mentation of FND
• Hypertensive Encephalopathy
• Cerebrovascular Event

16. CLINICAL APPROACH
1. Complete History Taking
2. Physical Examination
3. Investigate for Underlying Organ Damage
4. Management

17. HISTORY TAKING
• Current Sx like headache, blurred vision, chest pain, back
pain, dyspnea, etc.
• Any associated symptom
• Co-morbid conditions
• Duration of HTN and Medication Control, Compliance,
Abrupt cessation
• Any Illicit Drug use, Smoking, or Alcohol consumption
• Any Other medication ex. MOA, SSRI
• Any recent head trauma

18. PHYSICAL EXAM
• Full and Thorough examination is needed
• Vital Signs Specially BP (both setting and standing), if
peripheral pulses are reduced take lower limb BP as well
• General: signs of dehydration (natriuresis occurs in response to
rapid BP rise)
• CVS: murmurs (aortic insufficiency or ischemic MR). S3 gallop,
peripheral edema, raised JVP
• Respiratory: Basal Crackles, Tachypnea
• Neuro: Altered mental status, FND
• Funduscopic: Cotton wool exudates, Hemorrhage, Papilledema

19. WORKUP OF PATIENTS
Work-up should be done to check for damaged organs and
includes:
• Complete blood count
• Urinalysis (Proteinuria and Hematuria)
• Creatinine and BUN
• Cardiac Bio-markers
• Urine Toxicology
• RBS
• Liver Function Test
• Serum Electrolytes
• ECG
• Echocardiogram
• Chest Radiography
• Non-Contrast Head CT
• Contrast Induced Chest CT
or Transesophageal Echo

20. MANAGEMENT
o1st ask yourself these 3 question:
ois there any end organ damage?
oYes: Manage HTN Emergency
oNo: Manage HTN Urgency
oHow Quickly should BP be reduced?
oWhat is the BP Target during that time period?
oHow should that Goal be Achieved?

21. NO END ORGAN DAMAGE - URGENCY
How Quickly Should BP be Reduced?
oThe cut-off of lowering BP time is controversial and decision
should be taken considering individual risk factors for
patients.
oHowever, Generally: BP should be reduced gradually over
the period of hours to days, to avoid causing ischemic
injury and tissue hypo-perfusion to vital organs.
What is the Target BP in that Period?
oShort-Term Goal: lower BP to <160<100mmHg in first few
hours provided that MAP shouldn’t be lowered more then
25% over first 24 hours

22. NO END ORGAN DAMAGE - URGENCY
How should that goal be achieved?
oPreviously the preferred agent was Sublingual or Oral
Nefidipine
oThat is no longer recommended due to propensity to cause
Severe Rebound Hypotension and Organ Ischemia.
oCurrent preferred agents Include:
oCaptopril
oClonidine
oLabetalol

24. NO END ORGAN DAMAGE - URGENCY
In the case of not requiring rapid BP reduction, BP should be
reduced over the period of days with specific considerations
 Pre-Exisitng Hypertension (Options are:)
 Re-administer previous medication
 Increase the dose of previous medication or add another agent
 Add diuretic and adjust sodium intake for patient
 Un-Treated Hypertension:
 Gradually reduce BP using one of previously mentioned agents.
 Evaluate patient's HTN and start new individualized Anti-HTN
treatment regimen, considering risk factors, duration of treatment
and adverse effects

25. END ORGAN DAMAGE - EMERGENCY
oOverall Approach: choice of drug, BP goal, and
outcome varies based on specific emergency faced
oGenerally: MAP should be lowered 10-20% in the
first hour and subsequent 5-15% over next 23
hours.
oTime Frame: <180120mmHg over first hour
o <160110mmHg over next 23 hours

26. END ORGAN DAMAGE - EMERGENCY
oExceptions to that rule are certain conditions:
1. Acute Ischemic Stroke: BP isn’t lowered unless
>185110mmHg if ptn is candidate for reperfusion and
>220120mmHg if ptn are not candidates for reperfusion
2. Acute Aortic Dissection: SBP should be rapidly
lowered to target of 100-120mmHg within 20 minutes
to reduce the shearing force of the aorta
3. Intracerebral Hemorrhage: goal of HTN management
in these patient’s is variable and individualized case
dependant

27. END ORGAN DAMAGE - EMERGENCY
oChoice of medication is dependent on the type of
emergency encountered.
oDuring the first 8-24 hours, BP control should be obtained
via Parenteral Drugs.
oAfter that period patients should be switched to oral
agents with tapering of parenteral agents

28. END ORGAN DAMAGE - EMERGENCY
oManagement Specific Emergencies should be undertaken
as well as BP Control
oEx:
otPa for Ischemic Stroke Patients
oRevascularization for Acute MI patients
oDialysis for ESRD patients
oManagement Protocol for Acute Heart Failure
oSurgery for Acute Aortic Dissection

29. HYPERTENSIVE EMERGENCIES
oNeurologic Emergencies
oIschemic or Hemorrhagic Stroke
oHead Injury
oHypertensive Encephalopathy
oCardiac Emergencies
oAcute Heart Failure
oAcute Coronary Syndrome
oVascular Emergencies
oAcute Aortic Dissection
oPost Op Hypertension

30. HYPERTENSIVE EMERGENCIES
oRenal Emergencies
oAcute Hypertensive Nephroscelerosis
oSympathetic Over activity
oAntihypertensive Withdrawal
oSerotonin Syndrome
oMalignant Hypertension
oPheochromocytoma
oSevere Autonomic Dysfunction Ex. Guillian Barre
Syndrome
oPregnancy Emergencies
oEclampsia

33. FOLLOW UP - URGENCY
1. Observe patient for few hours at hospital to make
Ascertain BP Stably improving and that patients
remains Asymptomatic
2. Send Home with close monitoring for one week
explaining signs of end organ damage
3. Over next weeks to months frequent follow up with
dose adjustment of antihypertensive drugs should be
commenced to achieve desired pressure goals for
individual patients

34. FOLLOW UP - EMERGENCY
1. Since Secondary causes are more common in HTN
emergencies, patients should be evaluated and
treated for secondary causes if present
2. Ensure high quality out-patient follow up and for
presenting problems (ex. Dialysis for patients with
ESRD)
3. Recurrence and 2nd admission rate is high due to
inadequate follow up

35. THANK YOU FOR LISTENING
ANY QUESTIONS?