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					HYPERTENSIVE
EMERGENCIES

 Igbokwe Uchenna. B
    (M.B.Ch.B, Ife)
Outline
 Terminology
 Categories
 Etiology/Pathophysiology
 History/Physical
 Workup
 Treatment
 Conclusion
              Case Scenarios
 An 85 yo male with h/o HTN, chronic renal insufficiency
  presents for a routine physical, found to have BP of
  230/130mmHg, and grade 2 hypertensive retinopathy.


 A 62 yo female with no significant PMH presents to the ER
  with headache, found to have BP 210/110mmHg and
  papilledema.


 A 76 yo female is brought to the ER by the family due to
  altered mental status. BP is 240/110 mmHg with no focal
  neuro findings.
Terminologies (hypertensive crisis)
 Systolic blood pressure >220 and diastolic >120mmHg.


 -HYPERTENSIVE EMERGENCY: is severe hypertension
  with acute impairment of an organ system. In these
  conditions, the blood pressure (BP) should be lowered
  aggressively over minutes to hours.

 -HYPERTENSIVE URGENCY: the BP is a potential risk
  but has not yet caused acute end-organ damage. These
  patients require BP control over several days to weeks.
Terminologies (hypertensive crisis)

 -ACCELERATED HYPERTENSION: recent
  significant increase over baseline blood pressure,
  with vascular damage on fundoscopic
  examination, such as flame-shaped hemorrhages
  or soft exudates, but without papilledema.


 -Presence of papilledema indicates MALIGNANT
  HYPERTENSION.
                             ETIOLOGY
   Essential hypertension : Inadequate blood pressure control and noncompliance are common
    precipitants
   Renovascular
   Eclampsia/pre-eclampsia
   Acute glomerulonephritis
   Pheochromocytoma
   Anti-hypertensive withdrawal syndromes
   Head injuries and CNS trauma
   Renin-secreting tumors
   Drug-induced hypertension
   Post-op hypertension
   Coarctation of aorta
        PATHOPHYSIOLOGY
 NORMAL                  AUTOREGULATION
 AUTOREGULATION          FAILURE
                           RISE IN BP
   RISE IN BP


                           FAILURE OF
                           VASOCONSTRICTION
   ARTERIAL AND
   ARTERIOLAR
   CONSTRICTION
                            ENDOTHELIAL DAMAGE
                            (due to shear stress on the
                            wall)
Normal flow.(flow=P/r)
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 auto-regulation                         damage




    FIBRINOID               Activates coagn and                  Depsn. 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.

    Cycle of ischemia, platelet deposition and further autoregulatory failure with release
     of vasoactive substances
Categories
    CENTRAL NERVOUS SYSTEM
   During a hypertensive emergency, the elevated BP overwhelms
    arteriolar control over vasoconstriction and autoregulation of CBF.

   This results in transudate leak across capillaries and continued
    arteriolar damage.

   Subsequent fibrinoid necrosis leads to clinically apparent
    papilledema, the sine qua non of malignant hypertension.

   The end result of loss of autoregulation is hypertensive
    encephalopathy.
CENTRAL NERVOUS SYSTEM

 Hypertensive encephalopathy
 ???Cerebral vascular accident/cerebral
  infarction
 Subarachnoid hemorrhage
 Intracerebral hemorrhage
 CARDIOVASCULAR SYSTEM

 Myocardial ischemia/infarction
 Acute left ventricular dysfunction
 Acute pulmonary edema
 Aortic dissection
          RENAL SYSTEM
 Affected when high BP leads to arteriosclerosis,
  fibrinoid necrosis, and an overall impairment of
  renal protective autoregulation mechanisms.

 This may manifest as;
         RENAL SYSTEM
 Worsening renal function
 Acute renal failure
 Hematuria
 Red blood cell (RBC) cast formation, and/or
  proteinuria.
Pregnancy asso. emergencies
? Etiology...alteration in immune response resulting
  from abnormal trophoblastic invasion

 Eclampsia


 Preeclampsia


 HELLP
Catecholamine-Induced
States
 Pheochromocytoma,


 Sympathomimetic use (cocaine, phenylephrine),


 Antihypertensive withdrawal (clonidine),


 MAOI and TCA interactions (sympathomimetic
  drugs or foods containing tyramine)
Others
 Bleeding (epitaxis, haemoptysis,
  metorrhagia, intra-op bleeding e.t.c)

 Retinopathy
         EPIDEMIOLOGY
 In Nigeria: About 10% of population have
  hypertension, 1/3 are aware, 1/3 on tx and
  1/3 compliant.
 The unaware and non-compliant are @risk
  of developing hypertensive emergencies.

 Mortality/Morbidity: Depends on the
  extent of end-organ damage on
  presentation and the degree to which BP is
  controlled subsequently.
         EPIDEMIOLOGY
 Race: Blacks have a higher incidence of
  hypertensive emergencies than Caucasians.

 Sex: Males are at greater risk of
  hypertensive emergencies than females.

 Age: Most commonly in middle-aged
  people.
         EPIDEMIOLOGY
A five-year review of hypertension-related
admissions in UNTH, Enugu:

 64% = males and 36% = females
 Case fatality = 42.9%
 Mean age at death = 54.8 +/- 15.8 years
 45% of deaths occurred during acute
  hypertensive crises.
                  HISTORY
 Focus on circumstances surrounding
 hypertension & etiology :
 -Medications: esp. hypertensive drugs/their compliance,
  Illicit drugs
  -Duration of hypertension
  -Duration of current symptoms
  -Date of LMP
  -Other medical problems: prior hypertension,
  thyrotoxicosis, Cushing’s, SLE, Renal
                HISTORY
 Focus on complications :

 CNS: headaches, blurred vision, wt.loss, nausea,
  vomiting, weakness, fatigue, confusion and
  mental status changes.

 CVS: symptoms of CHF, angina, dissection


 Renal: hematuria, oliguria.
                       PHYSICAL
   Vital signs
     – BP in both supine position and the standing position
     – BP should also be measured in both arms (significant diff may
        suggest aortic dissection).
     – Pulse symmetry

   Fundoscopy
     – New retinal hemorrhages, exudates, or papilledema

   CNS
     – Level of consciousness
     – Visual fields
     – Focal neurologic signs
                           Physical
   Cardiovascular - Evaluate for the presence of heart failure.
     – Jugular venous distension
     – Crackles
     – Peripheral edema
     – extra heart sounds

   Abdomen - Abdominal masses or bruits
         DIFFERENTIALS

Acute Coronary Syndrome     Stroke, Hemorrhagic
CHF, pulmonary edema        Stroke, Ischemic
Aneurysm, Abdominal         Subarachnoid Hemorrhage
Anxiety                     SLE
Cushing Syndrome            Brain tumour
Delirium Tremens            Head injury
Encephalitis                Steroid use
Glomerulonephritis, Acute   Sympathomimetic drugs
Headache, Cluster           Acute vasculitis
Headache, Migraine          Serotonin syndrome
Headache, Tension
                           Work-up
Laboratory Studies
 E/Cr/U to evaluate for renal impairment
 CBC and smear to exclude microangiopathic anemia


   Urinalysis
     – Dipstick urinalysis (UA) to detect hematuria or proteinuria
     – Microscopic UA to detect RBCs or RBC casts (renal impairment)

   Other studies
     – Toxicology screen
     – Pregnancy test
     – Endocrine testing
     – Cardiac enzymes
                          Work-up
Imaging Studies
   Chest radiography is indicated in patients with chest pain or shortness
    of breath.
     – Cardiac enlargement
     – Pulmonary edema
     – Widened mediastinum

   Chest CT scan,

   Transesophageal echocardiography, or

   Aortic angiography in cases where aortic dissection is suspected.
                         Work-up
   Head CT and/or brain MRI are indicated in patients with abnormal
    neurologic examinations or clinical concern for the following:

     – Intracranial bleeding
     – Cerebral edema
     – Cerebral infarction



   Electrocardiography (ECG) to assess for evidence of myocardial
    ischemia or left ventricular hypertrophy
                    TREATMENT
   Weigh benefits of decreasing BP against risks of decreasing end-
    organ perfusion. Important steps include:

    -Appropriately evaluating patients with an elevated BP

    -Correctly classifying the hypertension

    -Determining aggressiveness of therapy



   An important point to remember in the management of the patient
    with any degree of BP elevation is to "treat the patient and not the
    number."
                    Treatment
 Initial considerations:
   – Place patient who is not in distress in a quiet room and
     reevaluate after an initial interview. BP may fall below
     critical levels after relaxation without specific treatment.

   – Consider the context of the elevated BP (e.g, severe pain)

   – Screen for end-organ damage- admit and rapidiy lower of
     BP using iv meds which depend on the end-organ system
     damaged.

   – Patients without evidence of end-organ effects may be
     discharged with follow–up.
DRUGS
 Once the diagnosis of hypertension is made and end-
  organ damage confirmed, the BP should be lowered by
  about 25% of the mean arterial pressure.

 There are 2 main classes of drugs:


   -Vasodilators

   -Adrenergic inhibitors
                 VASODILATORS
    DRUG         DOSAGE          ONSET/DU          ADV.EFFE

Nitroprusside    0.25-           Instant/1-2min.   Thiocyanate,cya
                 10mcg/kg/min                      nide poisoning
Nitroglycerine   5-100mcg/min    1-5min/3-5min     Flushing,headac
                                                   he,methemoglobi
                                                   n
Nicardipine      5-15mg/hr       5-10min/1-4hr     Tachycardia,flushin
                                                   g.avoid-heart
                                                   failure
Hydralazine      10-20mg         5-15min/3-8hr     Flushing,tachy,avoi
                                                   d-A.diss,MI
Enalapril        10-40mg         20-30min/6hr      Hypotension,renal
                 IM,1.25-                          failure,hyperkalemi
                 5MG1Vq6hr                         a

Fenoldopam       0.1-            5min/10-15min     Flushing,headache
                 0.3mcg/kg/min                     ,tachy
                 ADRENERGIC INHIBITORS

DRUG              DOSAGE            ONSET/DU          ADV.EFF
                                    R
Labetalol         20-80mgiv bolus   5-10min/3-6hrs    Heart block,ortho
                  every 10                            hypotension.avoid-
(a+b blocker)                                         heart
                  min,2mg.min iv
                                                      failure,asthma
                  infusion
Esmolol           200-500           1-2min/10-20min   Hypotension,avoid-
                  mcg/kg/min for                      heart
(b-1 selective                                        failure,asthma
                  4min,then 150-
blocker)          300mcg/kg/min
Phentolamine      5-15mg iv         1-2min/3-10min    Tachycardia,flushin
                                                      g,headache
(a1 blocker)
ORAL DRUGS
DRUG                DOSAGE              ONSET/DU            ADV. EFF.
                                        RATION
CAPTOPRIL           6.25-25MG q 6hrs.   15-30min/6 hrs.     Hypotension in
(ACE inhibitor)                                             high renin states


CLONIDINE           0.1-0.2 mg hrly,    30-60min/6-12hrs.   Sedation,bradycard
(a2 agonist-        Upto max 0.8mg in                       ia,dry mouth
centrally acting)   24hrs.

LABETALOL           100-200mg q 12hrs 30-120min/8-12hrs     Heart failure,heart
                                                            block,bronchospas
                                                            m
Specific treatment
             Hypertensive
            Encephalopathy
 Goal is to reduce MAP by 25% over 8hours.

 Labetalol, fenoldopam are drugs of
  choice.

 Avoid Nitroprusside (used in past)is a
  powerful arteriloar dilator, so a rise in ICP
  may occur
Intracerebral Hemorrhage
 Labetalol,Esmolol,Nicardipine agents of
  choice.
 Avoid Nitroprusside,Hydralazine


 Raised ICP, maintain MAP just below 130
  mm Hg (or SBP <180 mm Hg) for first 24
  hours.
 No raised ICP, maintain MAP <110 mm Hg
  (or SBP <160 mm Hg) for first 24 hours.
SAH
– Nicardipine,Labetalol,Esmolol agents of choice


– Avoid Nitroprusside,Hydralazine


– Maintain SBP <160 mm Hg until the aneurysm is
  treated or cerebral vasospasm occurs.

– Oral nimodipine is used to prevent delayed
  ischemic neurological deficits, but it is NOT
  indicated for treating acute hypertension.
Acute Ischemic Stroke
 High BP can cause hemorrhagic transformation of
  infarct ,cerebral edema.
 But, if CPP is low, ischemic penumbra may occur.


 Intervene if SBP>220 or DBP>120 or
  MAP>145mmHg(unless asso. end-organ damage
  is due to BP).
 For thrombolysis, BP<185/110.


 Labetalol, Nicardipine-agents of choice.
Aortic dissection
 Labetalol,Nicardipine,Nitroprusside (with beta-
  blocker),Esmolol,Morphine sulfate

 Use narcotic analgesics + beta blockers +
  vasodilators .

 Ca blockers for beta blockers if there is aortic
  regurgitation or cardiac tamponade.

 Maintain SBP <110 mm Hg.
Acute coronary syndrome
 Preferred medications; Beta-blockers,
  Nitroglycerin

 Treat if SBP >160 mmHg and/or DBP>100mm Hg.


 Reduce BP by 20-30% of baseline.


 Thrombolytics are contraindicated if BP is
  >185/100 mm Hg.
Acute LVF / Pulm oedema
 Preferred medications
  – Nitroglycerin
  – Enalaprilat


 Treatment with vasodilators (in addition to
  diuretics) for SBP ≥140 mm Hg.

 IV or sublingual nitroglycerin is the
  preferred agent.
Renal insufficiency
 Goal is to prevent further renal damage by
  maintaining adequate blood flow.

 Nitroprusside effective.
Cocaine
toxicity/pheochromocytoma
 Use Diazepam, Phentolamine,
  Nitroglycerin/nitroprusside

 Avoid Beta blockers prior to phentolamine
  administration.

 Beta-blockers can be added for BP control
  only after alpha-blockade.
Preeclampsia/eclampsia
 Use Hydralazine, Labetalol, Nifedipine
 Avoid Nitroprusside, ACE inhibitors,
  Esmolol

 SBP <160 mm Hg and DBP <110 mm Hg
 Platelet ct <100,000 cells mm3 BP should
  be maintained below 150/100 mm Hg.

 IV magnesium sulfate to avoid seizures.
Discharge
 When BP is controlled and evidence of end
  organ damage resolved.

 BP not required to return to normal before
  discharge

 Initial clinic appointment= 1week
                     FOLLOW-UP
    The Joint National Committee on High Blood Pressure has published a
     series of recommendations for appropriate follow-up, assuming no
     end-organ damage.

      -For a systolic BP 140-159 mm Hg/diastolic 90-99 mm Hg, confirm BP
      within 2 months.
    -For systolic BP 160-179 mm Hg/diastolic 100-109 mm Hg, evaluate
      within a month.
    - For systolic BP 180-209 mm Hg/diastolic 110-119 mm Hg, evaluate
      within a week.

     For systolic BP greater than 210 mm Hg/diastolic greater than 120
     mm Hg, evaluate immediately.
                  Prevention
 Good long-term control of hypertension is the best
  method for prevention of acute hypertensive
  emergencies.

 Patient education and close follow-up care in patients who
  have had a hypertensive crisis are essential to prevent
  recurrent hypertensive emergencies.



 Proper use of antihypertensive medications is the major
  tool in avoiding development of hypertensive
  emergencies.
           Patient Education
 Patients need continuing education about
  antihypertensive medications and complications arising
  from inadequate BP control.



 Dangers of uncontrolled hypertension, including
  associated serious morbidity and death, must be
  emphasized.



 Education and maintenance of BP control are important
  to help prevent further complications.
             PROGNOSIS
 Median survival duration is 144 months for
  all patients presenting to ED with
  hypertensive emergency.

 -5 yr survival rate is 74%.
                CONCLUSION
 Though evidence about effectiveness of antihypertensive
    agents in people with hypertensive emergencies is weak,

 emphasis of management lies on early detection of specific
    ongoing end organ damage,

 as well as perfectly working the thin line between arrest or even
    reversal of the damage,

   and further end organ compromise which results from over-
    aggressive BP control.
So,……….
 An 85 yo male with h/o HTN, chronic renal insufficiency
  presents for a routine physical, found to have BP of
  230/130mmHg, and grade 2 hypertensive retinopathy.-
  ACCELERATED HYPERTENSION

 A 62 yo female with no significant PMH presents to the ER
  with headache, found to have BP 210/110mmHg and
  papilledema. -MALIGNANT HYPERTENSION

 A 76 yo female is brought to the ER by the family due to
  altered mental status.BP is 240/110 mmHg with no focal
  neuro findings. –HYPERTENSIVE EMERGENCY
Thank you

				
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