HYPERTENSIVE EMERGENCIES by YLQnN65G

VIEWS: 12 PAGES: 29

									JOACQUIM A.O
   ILEOYE S.A
                   OUTLINE
 INTRODUCTION
 DEFINITION OF TERMS
 SPECIFIC EXAMPLES
      ACUTE LEFT HEART FAILURE/ACUTE PULMONARY
       OEDEMA
      MALIGNANT HYPERTENSION
      DISSECTING AORTA
              INTRODUCTION
 Hypertensive emergencies are life threatening
 complications that emerge as a result of hypertension
 and require prompt medical attention.
           Definition of terms
 Hypertension: persistently elevated blood pressure
 above 140mmHg for systolic and 90mmHg for
 diastolic.

 Emergency: sudden crisis requiring prompt action.
 ACUTE LEFT
HEART FAILURE
          PATHOPHYSIOLOGY
 Hypertension    increased peripheral vascular
 resistance       increased left ventricular load left
 ventricular hypertrophy increased left diastolic
 pressure increased pressure in the left atrium,
 pulmonary veins and capillaries.

 When the hydrostatic pressure exceeds the oncotic
 pressure in the capillaries fluid moves onto the
 alveolar
               PRECIPITANTS
 Infections
 Poor drug compliance
      CLINICAL PRESENTATION
 Symptoms:
    Sudden onset of breathlessness
    Preceding hx of orthopnea, PND, non-compliace with
     HT drugs
    Wheezes.
    Fever
    Cough productive of frothy sputum
       CLINICAL PRESENTATION
 Signs:
    Dypsnoea at rest
    Tachypnoea
    Agitated and distressed
    Sweaty
    Cyanosed
    Pale
    Tachycardia
    Elevated Bp
    Diplaced apex beat
    S3 heart sound
    Bibasal fine crepitations
                MANAGEMENT
   Place the px in cardiac or sitting position
   Ensure the airways are patent
   Ensure px is breathing
   Administer intranasal oxygen high dose 4-6L/min of 40-
    60%
   Reduce preload with vasodilators like nitroprusside or
    nitroglycerine
   Furosemide for the pulmonary oedema
   Reduce afterload with ACE inhibitors
   ionotropes like digoxin
   Treat the precipitant
   axiolytics
              MANAGEMENT
 Important investigations include:
    Chest x-ray
    Blood glucose
    FBC
    Electrolyte urea and creatinine
    DIFFERENTIAL DIAGNOSIS
 Acute asthmatic attack
 Acute exacerbation of COPD
 Pneumothorax
 Pulmonary embolus
 DKA
  AORTIC
DISSECTION
           PATHOPHYSIOLOGY
 A breach in the integrity of the aortic wall allows
  arterial blood to burst into the media of the aorta
  which is then split into two layers creating a false
  lumen along side the true lumen.
 Bleeding from the vasa vasorum which the ruptures
  into the true lumen
 DeBakey and coworkers classified it into 3 types
 Stanford classified it into 2 types
OTHER AETIOLOGICAL FACTORS
 Hypertension 80% of cases
 Aortic coarctation
 Collagen disorders
 Previous aortic surgery
 Pregnancy
 Trauma
 iatrogenic
      CLINICAL PRESENTATION
 The presentations of aortic dissection and its variants
  are the consequences of intimal tear, dissecting
  hematoma, occlusion of involved arteries, and
  compression of adjacent tissues.
 Severe tearing chest pain
 syncope, dyspnea, and weakness
 Collapse/shock
 Paraplegia
 Acute abdomen
      CLINICAL PRESENTATION
Signs:
 Asymmetry of brachial, carotid or femoral pulses.
 Bounding pulse
 hypertension or hypotension
 a diastolic murmur often radiating along the right
  sternal border.
 Hemopericardium and cardiac tamponade may
  complicate a type A lesion with retrograde dissection
                MANAGEMENT
 Important investigations
    X-ray :broadening of the upper mediastinum and
     distortion of the aortic knuckle,left sided pleural
     effusion
    ECHO: aortic regurg,dilated aortic root, flap of the
     dissection
    ECG
    CT
    MRI
                 MANAGEMENT
 monitoring hemodynamics and urine output
 Unless hypotension is present, therapy should be aimed at
    reducing cardiac contractility and systemic arterial
    pressure, and thereby shear stress
   Pain control
   Anti-hypertensives (labetalol)
   sodium nitroprusside infusion to lower systolic blood
    pressure to 120 mmHg
   The calcium channel antagonists, verapamil and diltiazem,
    may be
   used intravenously if nitroprusside or labetalol cannot be
    employed.
                MANAGEMENT
 Emergent or urgent surgical correction is the preferred
  treatment for ascending aortic dissections (type A) and
  complicated type B dissections
 Surgery involves excision of the intimal flap, obliteration of
  the false lumen, and placement of an interposition graft
 Long-term therapy for patients with aortic dissection (with
  or without surgery) consists of the control of hypertension
  and reduction of cardiac contractility with the use of beta
  blockers plus other antihypertensive agents such as ACE
  inhibitors or calcium antagonists
MALIGNANT
HYPERTENSION
                 DEFINITION
 Abnormally elevated Bp (usually diastolic blood
 pressure greater than 130 mmHg) associated with
 rapidly progressive end organ damage such as grade 3
 or 4 retinopathy, renal dysfunction and/or
 hypertensive encephalopathy
           PATHOPHYSIOLOGY
 The pathogenesis of malignant hypertension
 However, at least two independent processes—dilation
  of cerebral arteries and generalized arteriolar fibrinoid
  necrosis—contribute to the associated signs and
  symptoms
 Accelerated microvascular damage with necrosis in the
  walls of small arteries and arterioles and by
  intravascular thrombosis.
 unless treated, it may lead to death from progressive
  renal failure, heart failure, aortic dissection or stroke
      CLINICAL PRESENTATION
may present with:
 severe headaches
 visual disturbances
 fits
 transient loss of consciousness
 Oliguria
 symptoms of heart failure
     CLINICAL PRESENTATION
Signs:
 High Bp
 Signs of heart failure
 Fundoscopy: grade 3 or 4 retinopathy
                 MANAGEMENT
 The initial aims of therapy should be (1) correction of
  medical complications, and (2) reduction of diastolic
  pressure by one-third, but not to a level less than 95
  mmHg.

 Important investigations:
    Chest x-ray
    ECHO
    Renal ultrasound
    Urinalysis
    Urea, electrolyte and creatinine
                MANAGEMENT
 it is unwise to reduce the blood pressure too rapidly since
  this may lead to cerebral, renal, retinal or myocardial
  infarction, and the blood pressure response to therapy
  must be carefully monitored, preferably in a high-
  dependency unit. In most cases, the aim is to reduce the
  diastolic blood pressure to 100-110 mmHg over 24-48 hours.
  (150/90 mmHg)

 Nitroprusside Continuous IV 0.25 g/kg per min 1 min 1–2
  min 2–5 min No
 Nitroglycerin Continuous IV 5 g/min
 Hydralazine IV, IM 5–10 mg
 Labetalol IV 20–80 mg
CONCLUSION
THANK YOU

								
To top