HTN Hypertension

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					       HTN: Chapter 83

Marx: Rosen's Emergency Medicine:
Concepts and Clinical Practice, 6th
               ed.
                                    Perspective

 Perspective
     Medical management of hypertension has reduced stroke mortality by 50% on an age-
      adjusted basis
     Probably partially responsible for the decline in mortality from coronary artery
      disease.
     Although approximately 75% of patients with chronically elevated BP are aware of
      their disease
          as few as one half to one quarter of these patients are adequately treated.
   Anxiety and pain often cause transient hypertension, but evaluation of the patient for
    evidence of acute end-organ ischemia is important.

   Even if the patient's BP does remain elevated without end-organ damage, urgent treatment
    is rarely beneficial, and an appropriate referral for long-term management should be made.
                   Principles of Disease

 Definition
     In adults, a systolic pressure less than 140 mm Hg and a diastolic pressure
      less than 90 mm Hg are considered normal.
     Prehypertension
          If the systolic pressure is between 140 and 159 mm Hg or if the diastolic pressure
           is between 90 and 95 mm Hg, the term prehypertension is now applied.
              reflecting that the lifetime incidence of hypertension in these individuals is
                twice that of individuals in the “normal” range.[2]
     Hypertension
          The patient with a systolic pressure of 160 mm Hg or greater or a diastolic
           pressure over 95 mm Hg is considered to be hypertensive.
   Even isolated systolic hypertension in elderly patients is a significant risk factor for
    cardiovascular disease, especially when combined with other risk factors.
   In older patients, an elevated pulse pressure (determined by subtracting diastolic from
    systolic pressure) is an equally significant risk factor for stroke and MI.
   A single elevated BP does not necessarily mean that the patient has hypertension.
    This is especially true in children.[9] BP measurement should be repeated after the
    patient is in a reclining position for at least 10 minutes and should be checked in both
    arms.
      If the second reading is also elevated or close to the hypertensive range, the

        patient should be advised of the potential for hypertension and referred for
        follow-up.
                          Pathophysiology

 Essential hypertension.
       No specific cause of essential hypertension has been identified, although many
        factors, including heredity, age, race, obesity, and the amount of dietary sodium, may
        contribute to the elevated BP
 Two major theories exist:
       (1) hypertension results from alterations in the contractile properties of
        smooth muscle in arterial walls
       (2) alterations of arterial smooth muscle are a response to chronically
        elevated BP resulting from a primary failure of normal autoregulatory
        mechanisms.
               Renin, Angiotensin, and
                    Aldosterone
 Renin
         An enzyme produced by the kidney that splits off angiotensin I from a plasma
         globulin precursor.[11] Angiotensin I is converted by an enzyme in the lung to produce
         angiotensin II. Angiotensin II is a potent vasoconstrictor and also stimulates
         aldosterone production in the adrenal gland.


 ACE inhibitors or angiotensin blockers are clearly the drugs of choice in
  hypertensive patients with diabetes or decreased left ventricular function, or
  both.
                           Renal Disease

 All types of renal disease have been associated with hypertension
 Renovascular hypertension results from the overproduction of renin secondary
  to reduced blood flow through the stenotic renal artery. The increased levels of
  renin lead to activation of the angiotensin pathway and resultant hypertension.
 Another vascular lesion associated with arterial stenosis and hypertension is
  fibromuscular dysplasia of the renal arteries. This disease is predominant in
  young white women, and flank bruits are often present.
 Up to 70% of patients with chronic pyelonephritis have elevated BP.
                            Arterial Disease

 Coarctation of the aorta
        An important cause of secondary hypertension, and early surgical
        intervention can greatly improve the patient's prognosis.
            triad of upper extremity hypertension, a systolic murmur best heard over the
             back, and delayed femoral pulses should alert the examiner to the diagnosis of
             coarctation.
 Loss of elasticity in the larger arteries associated with the aging process
  produces systolic hypertension as well as elevations in pulse pressure.
 The current literature strongly suggests that isolated systolic
  hypertension is associated with an increased risk of stroke, heart disease,
  and renal failure and should be treated.
      Thyroid and Parathyroid
              Disease
 In thyroid storm, patients are usually
  hypertensive and tachycardic and β-blockade
  is a mainstay of the acute management.
                    Pheochromocytoma

 Pheochromocytomas are responsible for less than 1% of cases of hypertension.
 The characteristic feature of pheochromocytoma is paroxysms of hypertension
  associated with palpitations, tachycardia, malaise, apprehension, and sweating.
 These episodes may be related to physical and emotional stress, eating, position,
  or even micturition.
       Because of the episodic nature of this syndrome, the patient is often dismissed, and a
        diagnosis of hyperventilation syndrome or anxiety attack is made.
 The diagnosis is confirmed with elevated urinary levels of catecholamines,
  metanephrines, and vanillylmandelic acid.
 Treatment consists of α-blockade to control hypertension and subsequent β-
  blockade for the control of cardiac dysrhythmias.
              Emergency Department
                  Presentation
 Hypertension is seen in the emergency department in the following four
  general ways:
    
        1. “Hypertensive emergency” or “hypertensive crisis” with acute end-
        organ ischemia
    
        2. “Hypertensive urgency,” a historical term related to arbitrarily elevated
        BP with nonspecific symptoms
    
        3. Mild hypertension without end-organ ischemia
    
        4. Transient hypertension related to anxiety or the primary complaint
      CLINICAL PRESENTATION OF
     HYPERTENSIVE EMERGENCIES

 BP is usually markedly elevated and there is
  evidence of acute dysfunction in the
  cardiovascular, neurologic, or renal organ
  system. These conditions are true medical
  emergencies and mandate reduction of BP
  within 1 hour.
         Hypertensive Encephalopathy

 Throughout the normal range of BP, cerebral blood flow is maintained by
  fluctuations in the vascular tone of the cerebral resistance vessels known as
  autoregulation.
 Hypertensive encephalopathy is an uncommon syndrome resulting from an
  abrupt, sustained rise of BP that exceeds the limits of cerebral autoregulation of
  the small resistance arteries in the brain.
 Hypertensive encephalopathy
         (1) acute in onset
        (2) reversible.
         Patients present with severe headaches, vomiting, drowsiness, and confusion.
 Hypertensive encephalopathy is a true medical emergency; untreated patients
  develop increasing coma, and death may ensue within a few hours. The rapid
  measured reduction of BP is mandatory. The standard treatment regimen is
  intravenous (IV) nitroprusside with a careful reduction of the MAP by 25% or to
  a minimum diastolic pressure of 110 mm Hg over an hour.
               Malignant Hypertension

 Malignant (accelerated) hypertension is severe hypertension associated
  with evidence of acute and progressive damage to end organs.
       The diastolic BP is usually greater than 130 mm Hg.
 Patients with malignant hypertension appear ill and often present with
  complaints of severe headache, blurred vision, dyspnea, and chest pain
  or with symptoms of uremia.
 In addition to elevated BP, these patients must demonstrate evidence of
  acute end-organ damage as a result of the hypertension.
 Malignant hypertension is treated by the judicious lowering of MAP by
  25% of pretreatment levels over the initial minutes to hours, then toward
  a target of 160/100 over 2 to 6 hours
                 Stroke Syndromes

 In most of these patients, elevated BP is the physiologic
  response to the stroke itself and is not the immediate cause
 Some have recommended careful antihypertensive treatment
  for patients with persistent, extreme elevations of BP after a
  stroke (e.g., diastolic pressure >140 or MAP >130 mm Hg),
  but data are lacking.
 If BP reduction is pursued in these patients, labetalol is the
  agent of choice.
              Pulmonary Edema

 Most patients with congestive heart failure have
  some degree of increased peripheral vascular
  resistance (PVR) and resultant hypertension; this is
  a normal response.
 With standard treatment of pulmonary edema,
  including morphine, nitrates, oxygen, ACE
  inhibitors, and furosemide, catecholamine levels
  fall and BP returns rapidly toward normal.
                  Pregnancy

 Any acute elevation of the diastolic BP
  above 100 mm Hg in the pregnant patient
  represents a true hypertensive emergency.
 Although it may cause tachycardia and
  hypotension, the antihypertensive agent of
  choice in preeclampsia has classically been
  IV hydralazine.
             Aortic Dissection

 The goals of medical therapy are to lower the
  BP to a systolic level of 100 to 120 mm Hg
  and to reduce the ejection force of the heart.
 The combined α/β-blocker labetalol has been
  used successfully
      MANAGEMENT OF HYPERTENSIVE
            EMERGENCIES

 Vasodilators
     Sodium Nitroprusside
       Nitroprusside (Nipride, Nitropress) is a powerful
        vasodilator, with a direct effect on the smooth muscle
        of both resistance and capacitance vessels.
       Cyanide is an intermediate metabolite, but cyanide
        toxicity is extremely rare
                           Vasodilators

 Nitroglycerin
     Nitroglycerin is a vasodilating agent that acts
      predominantly on the venous system, decreasing left
      ventricular end-diastolic pressure.
 Hydralazine
     Hydralazine (Apresoline) is a direct arteriolar vasodilator that was widely
      used in the past for the treatment of hypertensive emergencies of pregnancy.
     The usual starting dose of hydralazine is 5 mg IV, with repeated doses of 5
      to 10 mg every 20 minutes as needed to keep the diastolic pressure below
      110 mm Hg
                    β-Blockers

 Labetalol
     Labetalol (Trandate, Normodyne) is a selective
      α1-blocker and nonselective β-blocker with a
      ratio of α/β-blockade between 1:3 and 1:7.
     Labetalol lowers BP by blockade of the α1-
      receptors in vascular smooth muscle and the
      cardiac β-receptors.
                 α-Blockers

 Phentolamine (Regitine) is an α-blocking
  agent used for the management of
  catecholamine-induced hypertensive crises
  (e.g., pheochromocytoma, MAOI crisis,
  cocaine overdose).
 Nicardipine
     Nicardipine (Cardene) is a parenteral dihydropyridine
      calcium channel blocker that has become very popular in
      the treatment of postoperative hypertension.
     Nicardipine is administered as an infusion beginning at 5
      mg/hr, increasing the infusion rate every 15 minutes until
      the desired reduction of BP has been achieved, to a
      maximum dose of 15 mg/hr.
        Enalaprilat and Enalapril

 Enalaprilat (Vasotec) is a parenteral active
  metabolite of the ACE inhibitor enalapril.
 The acute dose is 0.625 to 5 mg administered
  as a single bolus.
        Osteopathic Considerations

 Sub-occipital release
     Normalizes the parasympathetics
 Rib raising
     Normalizes the sympathetics