4. • Severe hypertension is also known as Hypertensive Crisis
Described as acute elevation of BP to a level that has the
potential to cause end organ damage.
• Rare in children
• But a potential life threatening medical emergency so as
to avoid serious long term sequelae from end organ
damage with timely and appropriate intervention
• The most commonly damaged organs are,
- CNS
- Heart
- Eyes
- Kidneys
11. Hypertensive crisis is predominantly associated with
the vasoconstrictive action ofangiotensin.
Angiotensin II
facilitates nor-epinephrine release and inhibits reuptake
and
potentiates vascular responsiveness tonor-epinephrine.
1
PATHOPHYSIOLOGY
VASOCONSTRICTION
12. Severe hypertension induces changes in renal arterioles leading to,
1
endothelial damage,
platelet and fibrin deposition, and
thromboxane release.
This cascades into
vasoconstriction,
ischemia,
Myointimal proliferation, and
decompensation of autoregulatory mechanisms, resulting in
hypoperfusion to the:
• heart,
• kidney, and
• brain.
13. ETIOLOGY
Newborn
- Renal artery and venous thrombosis
- Coarctation of the aorta
- Congenital nephrotic syndrome
- Mydriatics
- Theophylline overdose
- Caffeine overdose
14. Infancy to 12 years
- Renal parenchymal disease
- Renovascular disease
- Coarctation of the aorta
- Malignancy
- Endocrine
(conn’s disease,cushings)
Adolescents
-Essential hypertension
-Renal parenchymal disease
-Substance abuse
-Renovascular disease
16. INVESTIGATIONS
• Diagnostic testing limited to basic evaluation
• Focus should be on lowering pressure
• Needs evaluation for end organ damage
(emergency v/s urgency )
HISTORY
• s/o end organ damage
• past h/o hypertension
• Drug history
17. Recheck BP
look for evidence of neurologic dysfunction and heart failure
Volume status
Funduscopy - hemorrhage, papilledema, or infarcts.
Any discrepancy in upper and lower extremity BPmeasurements.
Abdominal bruit -renovascular cause of hypertension
Any abdominal mass ?
Wilms tumor,pheochromocytoma,neuroblastoma
23. Sodium nitroprusside
• DOC
• Metabolises to NO , Arteriolar and venous dilator
• Onset 0.5-2 minutes , duration 3-5 min
• Should be scheilded from light to prevent degradation
• Manily used in CCF with HTN
• S/E Cyanide toxicity , tachyphylaxis
24. Hydralazine
• Direct arteriolar dilator
• Onset 5-15 min, duration 3-8hrs
• Iv/im/oral
• Dosenot affect coronary or venous smooth muscle
• Affect arteriolar smooth muscle and stimulate sympathetic nervous
system , tachycardia increased renin activity and sodium retention
25. Labetalol
• Alpha- beta adrenergic blocker
• Causes vasodilation without significant altering in cardiac output
• Onset 5-10 min , and duration 3-6 hrs
• Blocking ratio of iv 1:7, and oral 1:3
• avoided in asthma , a/c LVF , heartblock
26. Esmolol
• Cardio selective beta blocker
• Particularly useful after the repair of Congenital Heart disease and
presence of tachycardia
• Causes CCF, bradycardia , bronchospasm
• Well suited in multi organ failure, b/c metabolised by intracytoplasmic
red cell esterase
27. Fenoldopam
• First available peripheral dopamine receptor agonist
• Vasodilation in renal and splanchnic vessels , with less effect in
coronary and cerebral circulation
• Maintains or increase in renal perfusion , short term increase in urine
output and creatine clearance
• Reflex tachycardia and tachyphylaxis
28. Nicardipine
• Dihydropyridine ca channel blocker
• Arteriolar vasodilator with prompt hypotensive effect
• Onset of action and efficacy compared to nitroprusside
• Selective vasodilation of the cerebral and coronary vasculature ,
useful in MI but should be avoided in raised ICT and head trauma
29.
30. MANAGEMENT IN SPECIFIC SETTINGS
Fluid overload Rapid acting diuretic( furosemide )
Renal parenchymal disease ACE inhibitors
Coarctaion of aorta Beta blockers
Preoperative mx of catecholamine secreting tumors preoperative volume expansion +phentolamine
End stage renal disease on dialysis Daily ultrafiltration
A/C ICH or stroke Nicardipine / Labetalol
CCF / A/c pulmonary edema Sodium nitroprusside / Nitroglycerine
A/c renal failure Nicardipine/ Clevidipine /fenoldopam
A/C aortic dissection Esmolol
Perioperative hypertension Nitroprusside
Sympathetic crisis /catecholamine toxicity Phentolamine / Clevidipine / fenoldopam
31. GENERAL GUIDELINES FOR MANAGEMENT
• IV Infusion of nitroprusside(0.3-.8 microg/kg/min) or labetalol
• Gradual reduction of BP is planned
• after calculating the observed and desired (95th percentile )
32. Severe HTN
Assessment for target organ dysfunction AND
Etiology of HTN
target organ dysfunction
Hypertensive
emergency
• Hypertensive
urgency
Reduce target BP 25% by 6-8 hrs and
subsequent reduction in 24-48hrs
Oral antihypertensive
Complete etiological workup
Management of etiology
Change to long acting oral or parenteral antihyperetensives
yes no
33. • IV infusion is not an option , particularly in hypertensive urgencies
iv/im bolus administration of hydralazine or diazoxide
• If Setting up an iv infusion is delayed , oral nifedipine should be
administered (.1-.25mg/kg)
• 2 IV accesses are maintained ( one =drug,other + IVF )
34. • MONITORING
• Blood pressure monitoring
Invasive monitoring q5min OR
non invasive monitoring q15min
• Level of sensorium , pupillary reflex, visual acuity
35. • If target BP reached
• Oral medications can be added
• Enteral antihypertensive drugs is instituted with in 6-12 hours of
parenteral therapy , and later gradually withdrawn over the next 12-
24 hours
