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Richard Dionne MD CCFP-EM Assistant Professor Emergency Medicine – University of Ottawa Associate Medical Director – Regional Paramedic Program for Eastern Ontario Special Thanks : Dr Jason Frank April 1 st , 2010. Severe Hypertension in the ED (Back to Basics 2010). Goals & Objectives.

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severe hypertension in the ed back to basics 2010

Richard Dionne MD CCFP-EM

Assistant Professor Emergency Medicine – University of Ottawa

Associate Medical Director – Regional Paramedic Program for Eastern Ontario

Special Thanks : Dr Jason Frank

April 1st, 2010

Severe Hypertension in the ED(Back to Basics 2010)

goals objectives
Goals & Objectives
  • Differentiate malignant hypertension from secondary causes
  • Understand the principles of managing hypertension and the risks associated
  • Differentiate and identify the target-organ damage causes by hypertension emergencies
definition
Definition
  • Essential hypertension
      • > 140 systolic / > 90 diastolic
  • BP = CO X PVR
      • Blood Pressure = Cardiac Output X Vascular Resistance
  • Autoregulation phenomenon overwhelmed
      • Rapid rate rise in MAP : Mean Arterial Pressure

MAP = 1/3 Systolic + 2/3 Diastolic

      • Vascular endothelial stress injury pattern
causes
Causes
  • Severe uncontrolled Hypertension :
      • > 180 systolic / > 120 diastolic
  • Hypertensive Emergency (Malignant):
      • Acute target organ damage / effect
  • Hypertensive Urgencies:
      • At risk of short term end organ effect
differential diagnosis
Differential Diagnosis
  • Primary Hypertension
      • Long standing, uncontrolled, drug withdrawal
  • Secondary Hypertension

A- Increased cardiac output

      • Renal failure with fluid overload
      • Acute renal disease
      • Hyperaldosteronism

B-Increased vascular resistance

      • Renovascular hypertension
      • Pheochromocytoma
      • Drugs (sympathomimetics, MOA,etc.)
      • Cerebrovascular (CVA, ICH, SAH)
renin angiotensin aldosterone
Renin-Angiotensin-Aldosterone
  • Renin produced by the kidneys stimulates the formation of angiotensin II, a potent vasoconstrictor.
      • DDX: Renal Artery Stenosis
  • In turn promotes aldosterone release and consequently the retention of Na+ & water.
  • Both increase in vascular resistance and intravascular volume will increase blood pressure.
hyperaldosteronism
Hyperaldosteronism
  • Na+ retention, water retention, increased CO
  • Hypernatremia & Hypokalemia typical
  • Primary:
    • Adrenal adenoma / hyperplasia
  • Secondary:
    • Cushing’s, exogenous mineralocorticoids
pheochromocytoma
Pheochromocytoma
  • Tumour in the adrenal gland (medulla)
    • Increase in catecholamines (epi, norepi)
  • Paroxysmal : HTN, HA, palpitations, diaphoresis, anxiety ... Not panic attacks!
  • Dx: urine metanephrines & vandillymandelic acid
break down
Break Down
  • Malignant Hypertension & Emergencies
  • Hypertensive Urgencies
  • Severe Uncontrolled Hypertension
malignant hypertension
Malignant Hypertension
  • 1% of patient with primary hypertension will go on to have an accelerated malignant phase

Severe Hypertension + End-organ damage

    • Denotes an elevated blood pressure with the presence of papilledema on fundoscopy
      • Grade 3: vascular injury with possible hemorrhages, cotton-wool spots, arterio-venous “nicking”
end organ damage
End-organ damage
  • CNS:
    • Hypertensive encephalopathy / CVA
  • CVS:
    • Cardiac ischemia / Pulmonary edema / Aortic dissection
  • Renal: ARF
  • Heme:microangiopathichemolyticanemia
clinical evaluation
Clinical Evaluation
  • Focus on “End-organ compromise”:
      • Headache, Chest pain, Dyspnea,Visual disturbance, Change in mental status / confusion.
      • Potential drug interactions, compliance to RX, etc.
      • Examination: BP both arms with appropriate size cuff, fundoscopy, cardiac & neurological .
      • Work-up: CBC, Lytes, renal function, ECG, urine & CXR.
        • May need CT-head / urine tox screen, etc.
r egulation brain vasculature
Regulation Brain Vasculature
  • Normal individual:
      • Adapts with cerebral vasoconstriction if BP rises, and vasodilation if BP drops...
      • Adaptation to a wide range of MAP changes
  • Chronic Hypertensive:
      • Cannot adapt as well, so a rapid drop in BP will cause drop in cerebral perfusion pressure, therefore a risk of cerebral ischemia ...
      • Caution with lowering the BP too fast !!!
management
Management

Goal

1- Decrease MAP 15-20% within 1 hour

2- Further reduction towards 160/100 mmHg within the following 6 hours

3-Gradual reduction to normal range over the next 24 hrs if the patient is stable

treatment
Treatment
  • Vasodilators:
    • Nitroprusside:
      • 0,25 – 10 ug/kg/min perfusion IV
      • Vasodilator: decrease in MAP, afterload, preload & renal blood flow.
  • Adrenergic inhibitors:
    • Labetolol:
      • 20 – 80 mg IV q 10 min, then infusion prn
      • Beta-blocker with an alpha blocking property, reduces PVR with no reflex tachycardia...
hypertensive urgencies
Hypertensive Urgencies
  • Severe elevation in blood pressure that is not causing end-organ damage...

Goal

    • Control within 24hrs
    • Consider if Diastolic BP > 115 – 130
    • Oral regiment may be all that is needed
      • Captopril : 6.25 – 25 mg q 6h
      • Clonidine: 0,1 – 0,2 mg q 12 – 24 h
      • Labetolol : 100 – 200 mg q 12 h
severe uncontrolled hypertension
Severe Uncontrolled Hypertension

Classification

Stage 1:SBP 120-139 / DBP 80-89

  • “prehypertension”

Stage 2: > 160 / 100

  • Categorize according to risk profile...

Treatment regiment:

  • Diuretics: older patients & African Americans
  • ACE inhibitors: comorbidity, diabetes, etc.
  • Beta-Blockers: cardiovascular disease, Hx: MI & angina
follow up
Follow-up
  • Hypertensive Emergency & Malignant crisis:
      • Admission & IV start of treatment required
      • Needs ICU & monitoring
  • Hypertensive urgencies & Uncontrolled severe hypertension:
      • Oral treament started in ER vs early outpatient , but mandatory close follow-up with primary care MD
conclusion
Conclusion
  • Measure blood pressure appropriately
  • Most patient do not require emergent treatment for their hypertension in the ED
  • Severe hypertension = evaluate for end-organ effects
  • Rapid recognition & lowering of BP in hypertensive emergencies
  • Careful of over treating & risk of cerebral ischemia