HYPERTENSIVE EMERGENCIES by yurtgc548

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									Hypertensive Emergencies




     Trevor Langhan PGY-3
      November 10, 2005
Objectives

   Discuss cases of hypertension in ED
   How to lower BP and when not to do it
   How low is too low? Or too fast?
Receptor sites

        alpha-receptor             beta-receptor
   Vasoconstriction           vasodilation (b2)
   iris dilation              cardioacceleration (b1)
   intestinal relaxation      intestinal relaxation
   intestinal sphincter        (b2)
    contraction                uterus relaxation(b2)
   bladder sphincter          bronchodilation (b2)
    contraction
quiz
Nitroprusside

             PRO                                CON
   Vasodilator                      Increase ICP
   Direct effect on smooth          Metabolized to thiocyanate
                                      by KD
    muscle
                                        cyanide can build up
   Dose related BP reduction
                                        ARF and prolonged use
   Drug of choice for most HTN
                                        Avoid in pregnancy
    emergencies
                                     Must be IV
   Rapid onset
                                        Unstable in UV light
   Short duration                      Must be wrapped

                                     Supine to prevent orthostasis
                                     S/E due to decreased BP and
                                      vasodilation
Fenoldopam

             PRO                               CON
   Peripheral dopamine agonist      Tachycardia, flushing and
   Improves renal function           h/a may occur
   Rapid action
   Does not cross blood brain
    barrier
   Hypotension less often
nitroglycerin

             PRO                            CON
   Vasodilating agent            Limit to pts with cardiac
      venous                      ischemia or pulmonary
   Decreases LVEDP                edema
   Reduces BP by decreasing      Hypotension with pts who
    preload and CO                 have RV dysfunction
   Sublingual or IV
hydralazine

              PRO                               CON
   Direct arterial vasodilator      Reflex tachycardia
   Historically used ++ in PIH      May provoke angina
    and eclampsia                    Flushing, n/v, h/a
                                     Chronic use results in lupus
                                      like syndrome
Beta-blockers - labetalol

              PRO                                CON
   Selective alpha1 and non-          IV use has deep orthostasis
    selective beta blocker             Supine post admin x 2-3
   IV or oral                          hours
   No reflex tachycardia              No effect on renal or
   Less uncontrolled drops in          cerebral blood flow
    BP                                 Contraindicated:
   May not need ICU                      Heart block

   Good for aortic dissection or         CHF

    cardiac ischemia                      Asthma

                                          pheo
Beta-blockers - esmolol

              PRO                        CON
   Ultra short acting         Thrombophlebitis
   Selective beta1            Tissue necrosis
   Little BP effects          Contraindicated:
   Good for reflex tachy         Heart block

                                  CHF

                                  Asthma

                                  Pheo

                                  cocaine
alpha-blockers - phentolamine

             PRO                            CON
   Alpha-blocker                 Reflex tachycardia
   Use in catecholamine HTN
    crisis:
      Pheo

      MAOI crisis

      cocaine
nicardipine

              PRO                          CON
   IV CCB                      Caution in poor LV fxn
   Titratable                  Liver metabolism
   Less negative inotropy      H/a, flushing, tachycardia
   Less tachycardia
   Mostly vasodilator
   Safe in pregnancy
Enalaprilat/enalipril

             PRO                                CON
   IV ace-I                         Not dose related
   Infrequent hypotension           May precipitate ischemia if
   Increasing evidence for use       MAP drop too steep
    in cardiac                       Angioedema
      Remodeling                    Cough
                                     ARF
                                     Toxic in 1st trimester
quiz - fin
Hypertension

 What is normal BP?
       SBP < 140
       DBP < 90
 What is hypertension?
       SBP >160
       DBP >100
 Anything in between GRAY.
Hypertension

 Possible cardiovascular causes of increased BP:
    Loss of vessel elasticity with age
    Coarctation of aorta
       Delayed femoral pulses
       Hypertensive upper extremities
       Bruit in upper back
Hypertension

 Endocrine causes for elevated BP:
    Pheo
    Excess steroids
       Often iatrogenic
       Cushings
          Look for hypokalemia
          Volume overload from Na retention
Hypertension

 Other causes include:
    Withdrawal of sedative drugs
       EtOH, benzo
    Tyramine toxicity in MAO-I patients
    Aortic dissection
    Sympathomimmetic drug intoxication
    Withdrawal of clonidine or beta blocking agents
    Reno-vascular disease
    Renin-angiotensin system abnormality
Hypertension

 HTN will present to the ED in a variety of ways:
    1. Hypertensive crisis/emergency
    2. Hypertensive urgency
    3. Mild hypertension without EOD
    4. Transient hypertension
Malignant hypertension

   Malignant hypertension: Term no-longer used
   Prognosis of this d/o has changed much since first
    introduced in 1928
   1-2/100 000 people in developed countries
   1 year survival has increased
      <22% in 1939 – 90 % in recent series

   Only age and renal function at presentation are
    independent markers of prognosis
Hypertensive Emergency

 Also called hypertensive crisis
 Elevated blood pressure
    signs of acute damage to target organs
       Brain
       Eyes
       Heart
       kidneys
Hypertensive Emergency

 Malignant hypertension
       Hypertensive encephalopathy
       Microangiopathic hemolytic anemia
       Acute renal failure
 Eclampsia/preeclampsia
 Aortic dissection
 HTN in setting of:
       MI
       Left ventricular failure
       Bleeding
       Thrombolytic therapy
Hypertensive Urgency

 Blood pressure elevation is an imminent risk for
  target-organ damage
 No acute end organ damage but risk is high if BP
  elevation continues
 Relative increase in BP more important than specific
  numbers
•Hypertensive Emergency

   Rosen’s states:
      True medical emergencies

      Immediate reduction of BP in 1 hour
Pathophysiology

 Mild to moderate increase in BP leads to initial
  vasoconstriction
 “autoregulation”
    Maintains perfusion at relatively stable level
    Prevents increased pressure from being
     transmitted downstream to smaller vessels
 As BP further increases, autoregulation fails
 Elevated BP disrupts vasc endothelium, causing
  narrowing
Pathophysiology

 Chronic increase in BP causes arteriolar hypertrophy
 Will decrease the amount of pressure passed on to
  more distal vessels
    Chronically hypertense people need diastolic BP’s
     >130 for symptoms
    Normotensive people can have hypertensive crisis
     at DBP > 100
Case 1

 45 y male c/o 12 hour history of SOBOE, mild chest
  heaviness
 Vomiting, drowsy
 Bi-frontal headache
 Blurred vision both eyes
 BP 240/150, HR 102, RR 16, sats 95%
Case 1

 PMHx: ? HTN, was on a “water pill” many years ago.
  No DM, no CAD, generally healthy
 Labs normal, except Creat: 150
 Inx? DDx? Mgnt?
Hypertensive Emergency
Hypertensive Emergency
Hypertensive Encephalopathy

 Cerebral edema:
    breakthrough hyper-perfusion from severe and
     sudden increase BP
    BP has exceeded the capacity of autoregulation
    vessels that can’t accommodate the pressure
    leakage and edema (fibrinoid necrosis)
 Autoregulation must be considered during treatment
    Hypertrophied vessels can’t vasodilate
    caution with lowering blood pressure
    Avoid relative hypoperfusion
Hypertensive Encephalopathy

 True medical emergency
 Is an acute presentation, but reversible
 Progression of untreated cerebral edema leads to
  coma and death
 Admission and invasive BP monitoring is the
  recommended mainstay of therapy
Hypertensive Encephalopathy

 Test:
    1) BP 140/90
          What is MAP?        Approx- 110

          What is goal MAP    Goal – 85

    2) BP 240/140
                               Approx – 175
          What is MAP?
                               Goal - 130
          What is goal MAP?
Hypertensive Encephalopathy

 First hour goals:
    Reduce MAP by 25%
    Keeping DBP > 110 mmHg
 Goal at 4-6 hours:
    Reduction to pt’s normal BP
 What agents?
    Nitroprusside - titratable, easy off, potential
     toxicity
    labetalol – alpha and beta blocker
Case 2

 67 y female known CAD, DM, smoker, atrial fib.
 Presents with c/o weakness left side
 BP 160/100, HR 94, RR 14, sats 99%
 O/E left facial droop, markedly weak left upper/lower
  extremity
 EKG: a fib, nil acute
 Chest exam unremarkable
Case 2

 Management?
 How do you treat her elevated BP?
Stroke syndromes

 Most patients with this presentation are ischemic
  strokes (85%) not hemorrhagic
 Likely don’t have acutely elevated BP
 May have mild to moderate BP elevation
 ***CAUTION***
    lowering BP as watershed area sensitive to
     hypoperfusion
    Lowering BP may worsen ischemic brain injury
Stroke syndromes

 Rarely stoke with grossly elevated DBP > 140

 But a contraindication to tPA is a BP >185/110
    Patients receiving reperfusion therapy may require
     a lowering of BP

 Titrate labetalol slowly to achieve decrease in MAP by
  a max of 20%
Stroke syndromes

 What if on CT it is an ICH?
 Little data about acute BP lowering in ICH
 Many centers lower MAP 20%
    May be a negative thing to do
    CPP depends on BP in setting of increased ICP
    Most ICHs have elevations of ICP
 If lowering is done, use an agent that dose not
  vasodilate
    Avoid nitrates
    Labetolol is best (ACE-I have some benefit)
Case 3
   55 year male known LV dysfunction (EF 30%)
   Chronic HTN
   On low dose lasix and daily asa, metoprolol
   Was off his low Na+ diet over all-inclusive vacation to
    Mexico
   Weighs 8 pounds more than usual
   Legs swollen
   HR 95, BP 190/120, sats 89%, RR 25
Case 3
   Chronic pulmonary edema results in increased PVR
    and HTN
   Acute decompensation in setting of CHF can have
    marked increase in BP due to catecholamines
Case 3
   Standard treatment of CHF:
      Morphine

      Oxygen

      Nitrates (nitroprusside better than NTG)

      lasix

   Improving evidence for use of ACE-I in setting of
    acute LV dysfunction and CHF
   Be on lookout for stroke syndrome as result of
    acutely lowered BP in someone chronically HTN
Case 4

 32 y female awaiting “sweatgland” surgery from
  plastics for hyperhydrosis, c/o H/A, palpitations
 BP 170/90, HR 150 sinus, RR 18
 Otherwise healthy
 Treatment:
    Nitroprusside if emergency
    Phentolamine – 1-5 mg IV boluses (alpha-block)
       Followed by beta-blockade
Case 4

   Pheochromocytoma
   Rare tumor – 0.2% of pts with essential HTN
   Episodic H/A, tachycardia, sweating, HTN
   Tumor secreting norepinephrine and epinephrine
   Diagnosis:
      Radiographic
      measurement of urinary and plasma levels of
       catecholamines and metabolites
Case 5 Hypertension in pregnancy

 25 y G2P1, LMP 6 months ago
 When do you treat HTN in pregnancy?
    SBP > 160
    Treat to goal of 140-155
    5-10% of all pregnancies
 Any acute DBP elevation >100 is a true HTN
  emergency
 Eclampsia and preeclampsia may occur without
  extreme elevation of BP
 Treatment:
    Prevention and control of seizures
    Early obs consult
   Ecclampsia Dx:
      Elevated BP in late 2
                             nd or 3rd trimester

         SBP > 140, DBP >90

         Elevated urine proteins

         Pedal edema

   No mortality benefit treating SBP 140-170
   Expert consensus that SBP > 160 need treatment
   Methyldopa, CCB, acute episodes with lobetolol or
    hydralazine
   Eclampsia seizure risk peaks during delivery and 24-
    48 hours after – prevention of seizures with
    prophylaxis recommended
Case 6

 33 year male stock broker. Snorted a “couple of rails”
  of cocaine ½ hour ago.
 Presents with crushing retrosternal chest pain,
  diaphoresis and H/A
 BP 190/100, HR 130, RR 28, sats 96%
 EKG ST segment elevation V1-V3
 Nurse asks “what do you want to give?”
Case 6

 Beta blocker contraindicated
    Beta antagonism will decrease heart rate, but will
     also block B2 receptors
    Will have unopposed alpha agonism by cocaine
     toxicity – dangerous HTN crisis
    Need alpha blockade first
    Like pheo can use phentolamine, some sources
     say hydralazine
    benzo dosing to decrease BP, HR and battle
     sympathetic tone of cocaine
Case 7

 55 year male smoker, HTN, DM, unstable angina
  getting worse.
 Shoveling snow and developed left RSCP that
  radiated to his jaw.
 HR 120, BP 190/90, RR 19, sats 99%
 EKG obvious ant/lateral infarct
 How do you treat his pressure?
Case 7

 Agents of choice in HTN during ACS
    Immediate lowering of BP indicated to prevent
     myocardial damage
    Also lower BP if pt to undergo reperfusion tx
       NTG agent of choice
       Beta block
       ACE-I (shown improvement in mortality)
       CCB (if BB is contraindicated)
 Contraindicated agents include:
    Hydralazine – reflex tachycardia
    Nitroprusside – reflex tachycardia
Key concepts

 Presence of acute target organ damage determines
  HTN crisis
 All pts with persistent elevation of BP should be
  investigated for EOD
 ER doc should be familiar with indications and
  contraindications of meds to treat HTN crisis
 Goal of treat is relative decrease in MAP of 25% in
  first hour, DBP should not fall <110 mmHg
 Pts without EOD rarely require urgent management
  of HTN

								
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