2. HYPERTENSIVE EMERGENCY
BP elevation is associated with ongoing
neurological, myocardial, hematological or renal TARGET
ORGAN DISEASE (TOD)
HYPERTENSIVE URGENCY
- potential for TOD is great & likely to occur if BP is not
controlled.
- occurs on chronic stable complication
7. MANIFESTATIONS OF TARGET ORGAN DISEASE
LARGE VESSELS Aneurysmal dilations ,
atherosclerosis
Aortic dissection
CARDIAC Acute - pulm edema , MI
Chronic - LVH , CAD
CEREBROVASCULAR Intracerebral bleed, TIA, seizures,
mental
status change, stroke
RENAL Hematuria, azotemia, Cr>1.5,
proteinuria
8. INITIAL EVALUATION
Cardinal points in history-
- TOD symptoms (most imp)
- prior Htn
- Medical Renal Disease
- medicine with compliance
- cocaine, amphetamine
-Usually occurs on background of essential hypertn.
Imp secondary causes- renovascular(fibromuscular
dysplasia/atheresclerosis)
-chronic GN/reflux nephropathy/analgesic
nephropathy
9. SYMPTOMS OF HYPERTENSIVE
CRISIS
MC is - headache (usually worse in morning)
- visual (scotoma, diplopia, hemianopia, blindness)
- neuro (focal deficits, stroke, TIA, somnolence)
- ischemic chest pain
- renal (polyuria, nocturia, hematuria)
- back pain (aortic aneurysm)
- nausea ,vomiting
- wt loss.
10. Threshold BP
There is no specific BP where hypertensive emergencies
occur
But, organ dysfunction is rare with diastolic BPs < 130 mm
Hg
Rate of increase may be more important
Hence, encephalopathy will occur at lower BPs in pregnancy
and in children
11. Initial Evaluation
Focused history
History of hypertension?
How well is hypertension controlled?
What antihypertensives?
Adherence to antihypertensive regimen?
Last dose of antihypertensive?
13. Initial Evaluation
Confirm BP in both arms
Use appropriate sized BP cuff
Cuff that is too small
Falsely elevate BP measurements in obese patients
14. Initial Evaluation
Assess for end-organ damage
Vascular Disease
Assess pulses in all extremities
Auscultate over renal arteries for bruits
Cardiopulmonary
Listen for rales
Murmurs or gallops
15. Initial Evaluation
Neurologic Exam
Hypertensive Encephalopathy - mental status changes, nausea,
vomiting, seizures
Lateralizing signs uncommon and suggest cerebrovascular
accident
Retinal Exam
Lost art
Keith-Wagener-Barker Classification
16. Keith-Wagener-Barker Classification
Grade 1
Mild narrowing of the arterioles
“Copper Wire”
Grade 2
Moderate narrowing - Copper wire and AV nicking
Changes associated with long standing essential hypertension
20. Keith-Wagener-Barker Classification
Grade 3
Severe Narrowing - Silver wire changes, hemorrhage, cotton
wool spots, hard exudates
Grade 4
Grade 3 + Papilledema
Grade 3 and 4 highly correlated with progression to end organ
damage and decreased survival
24. Lab Testing
Aortic Dissection?
Suspect with severe tearing chest pain, unequal pulses, widened
mediastinum
Contrast Chest CT Scan or MRI
Pulmonary Edema/CHF
Transthoracic Echocardiogram
25. Management
ED considerations
- Many HPT pts – only small number will require emergent treatment
- Primary goal of EP?
The pts – syptoms of EOD and require immediate iv parenteral therapy.
VS
The pt with acutely elev BP(SBP>200 or DBP>120) without EOD
symptoms, who require initiation of medical therapy and close follow
up as outpatient /inpatient
Remember - “treat the patient and not the number”
26. Treatment
ED Care - general principles
1. Consider context of elevated BP (pain, anxiety)
2. Screen for EOD (Hx/workup)
- Pts without evidence of EOD – d/c + f/up
- Pts with EOD – require ICU admission and rapid but gradual
lowering of BP - using IV meds.
27. BP should not be lowered to normal levels
- Rapid reduction in BP – below the autoregulatory range results
in reduction in organ blood flow – risk of ischemia and infarction
- General rule – the MAP should be lowered by no more than
20% - 1st hour
remains stable - BP lowered to 160/110 in next 2-6hrs
- BP goals best achieved by a continuous infusion of a short-
acting, titratable,
- parenteral anti-HPT agent, along with constant intensive
patient monitoring
33. “IDEAL IV ANTI-
HYPERTENSIVE”
Lower the BP without compromising blood flow to critical
organs
Vasodilators generally considered 1st , because they
preserve organ blood flow in the face of reduced perfusion
and also tend to increase CO.
34. Profile of an ideal IV
antihypertensive
Preserves GFR and renal blood flow
Few or no drug reactions
Little or no potential for exacerbation of co-morbid conditions
Rapid onset and offset of action
Minimal hypotension “overshoot”
Minimal need for continuous BP monitoring and frequent dose
titration
No acute tolerance
Ease of use and convenience
Safe and no toxic metabolites
Multiple formulations for short and long term use
Minimal symphathetic activation
35. Sodium Nitroprusside
MoA:
Direct smooth muscle dilator (art + ven)
Nitric oxide compound
Potent preload and afterload reducer
Causes cerebral vasodilation
Ultra short acting
Immediate onset - DoA : 10min
Dose:
0.1-0.5mcg/kg/min IV infusion
titrate to desired effect
rates>10mcg/kg/min – cyanide toxicity
36. Adverse affects/Precautions:
Cyanide and thiocyanate toxicity (pts with liver/renal
dysfunction)
Can cause precipitous drop in BP (hypotensive effects
unpredictable)
Ideally Art.line with continuous BP monitoring
Causes significant reflex tachycardia ( incr Oxygen demand)
(angina/aortic dissection/cerebral oedema)
Nausea and vomiting
Increased ICP
Drug of choice:
Perioperative HPT
Cocaine toxicity
Aortic dissection(combination)
Neurologic syndromes
37. Nitroglycerin
MoA:
Potent vasodilator (nitric oxide compound)
Primary affects the venous system, decrease preload
Decreases coronary vasospasm
Dose: cont infusion
start 5mcg/min, incr by 5mcg/min
every 3-5min to 20mcg/min
If NO Response
increase by 10mcg/min every 3-5min,up
200mcg/min
Onset : 2-5min/DoA : 5-10min
38. Adverse effects/precautions:
Constant monitoring is essential
Tolerance from uninterrupted use (12hr withdrawal)
Headache, tachycardia, flushing
Contra ind:
Concurrent use with PDE-5 inhibitors - causes significant
hypotension
Head trauma/cerebral haemorrhage
Severe anaemia
Drug of choice:
Acute HF
ACS
39. Nicardipine
Ca channel blocker – selective arterial vasodilator
Onset: 1-5min
DoA: 15-30min
Dose: start 5mg/hr IV infusion, titrate every 15min to max 15mg/hr.
Advantages:
Cause cerebral and coronary vasodilatation
Precautions: can worsen/cause HF
liver failure
can exacerbate renal insuff.
Ideal for CNS emergencies
40. Fenoldapam
MoA:
Peripheral dopamine agonist
(high vs low doses)
causes selective neuro
vasodilatation
mesenteric vasodilatation
increases renal blood flow and
sodium excretion
Onset – <5min, but more gentle,
lasts for 30min (titratable, predictable
and stable)
Standard BP monitoring is sufficient,
no toxic metabolites
Dosing:
Start at 0.1-0.3mcg/kg/min IV
infusion
May be increased in
increments of 0.05-
0.1mcg/kg/min every 15min,
until target BP reached
Precautions:
Pts with glaucoma or intraocular
hypertension
Dose related tachycardia can
occur – angina
Close BP monitoring
Close K monitoring
Caution with raised ICP
Drug of choice
Renal insuffiency
Strokes ( combination with
nicardipine)
41. Hydralazine
MoA:
Decreases systemic resistance by direct vasodilation of
arterioles
Dose:
5-20mg IV bolus or 10-40mg IM repeat every 4-6hrs
“old school”
used too much
boluses takes 20min to work
not titratable
Adverse effects/Precautions
tachycardia, flushing, headache
sodium and water retention
increased ICP
adjust dose in severe renal dysfunction
response may be delayed and unpredictable
Still drug of choice in pregnancy(Eclampsia), but B-blocker/Labetalol
42. Enalaprilat
The active component of Enalapril (hydrolyzed in liver and kidney)
MoA:
ACE inhibitor
Dose:
0.625-2.5mg every 6hr IV
Not titratable
Onset – within 30 min + long half life
Adverse effects/Precautions
Contra-indicated – volume depletion, renal vascular disease
Prolonged ½ life
43. Labetalol
MoA:
selective alpha blocker – will reduce vascular smooth m. resistance
non-selective Beta blocker – decrease cardiac inotropic and
myocardial O2 consumption, will prevent reflex tachycardia
Dose:
Bolus: effect in 5-10min,max effect at 20min. (DoA: 2-6hrs)
1st dose 20mg then every 10-20min
2nd dose 40mg, 3rd dose 80mg.
Cont. infusion: 0.5 – 2mg/min – titrate to response,max 300mg total
dose
Difficult to titrate due to very wide dose range
Advantages:
smooth onset
Transition to oral Rx easy (dose equivalent)
Improve cerebral blood flow – stroke pt
No need for ICU/Arterial line
44. Adverse effects/precautions
Relative CI – Heart failure, heart block, Asthma (bronchoconstriction)
Vomiting, scalp tingling
Impaired hepatic function
Elderly patients
Contraindicated in HPT secondary to Cocaine
use/Phaeochromocytoma
(B-blocker effect outway the alpha effect, thus unapposed alpha
constriction)
Drug of choice:
Aortic dissection
Hypertensive emergencies
45. Esmolol
MoA:
highly selective beta
blocker
Dose: (titratable)
bolus: 250-500mcg/kg IV
over 1-3min
infusion: 50-
100mcg/kg/min
may repeat bolus after
5min or increase
infusion rate to
300mcg/kg/min
Onset 1-2min / short acting
Adverse effect/Precautions
Hypotension common
nausea
Asthma
1st degree AV block
heart failure
Contraindications
Sinus bradycardia
Heart block
Cardiogenic shock
Bronchial asthma
Uncompensated CF
Pregnancy
Drug of choice:
Aortic dissection ( with
nitrate)
46. Phentolamine
MoA:
alpha adrenergic
receptor blocker
Dose:
load 5-20mg IV every
5min or
infusion 0.2-0.5mg/min
Onset 1-2min
Adverse
effect/precautions
tachycardia
flushing/headache
MI
cerebrovascular spasm
Contra-indications
renal impairment
Concurrent use with PDE-5 inhibito
coronary or cerebral arterioscleros
Drug of choice
Cocaine associated HPT crisis
Pheochromocytoma HPT crisis
48. Neurological
emergencies
Acute Ischemic stroke
often loss of cerebral auto-regulation
ischemic region more prone to hypoperfusion
thus BP reduction not recommended
unless SBP>220 or DBP>120
UNLESS planning fibrinolysis – SBP<185 & DBP< 110
Drug of choice:
Labetalol
Nicardipine
Sodium Nitroprusside
49. Neurological
emergencies
Acute ICH/SAH
Treatment based on clinical/radiographic evidence of raised ICP
Raised ICP – MAP<130 (1st 24hrs)
No raised ICP – MAP<110
Drug of choice:
Sodium Nitroprusside
Labetalol
Nicardipine
50. Cardiovascular
emergencies
ACS
treat if SBP>160 and/or DBP>100
Reduce MAP by 20 -30% of baseline
nitrates should be given till symptoms subside or until
DBP<100
Drug of choice:
Nitroglycerine
Labetalol
Nicardipine
51. CVS emergencies
Acute HF (pulmonary edema)
treat with vasodilator (additional to diuretics)
Sodium Nitroprusside in conjunction with morphine,
oxygen and loop diuretic
Enalaprilat also an option
52. CVS emergencies
Aortic dissection
anti-hypertensive Rx is aimed at reducing the shear
stress on aortic wall (BP and Pulse)
immediate lowering of BP – lifesaving
maintain SBP<110, unless signs of end organ
hypoperfusion
preferred Rx is combination of Morphine, B-blocker and
vasodilator
Nitroprusside + Labetalol
53. Other disorders
Cocaine toxicity/pheochromocytoma
Hpt and tachycardia rarely require specific Rx
Alpha adrenergic blockers – preferred
B – blockers can be added, but only after alpha
blockade.
Drug of choice
Phentolamine
Labetalol
Diazepam
54. Other disorders
Pre-eclampsia/Eclampsia
Goal SBP<160 and DBP<110 in pre-and- intrapartum
periods.
Platelets < 100 000, BP should be maintained < 150/100
IV Magnesium to prevent seizures
Drug of choice:
Methyldopa
Hydralazine
55. Other disorders
Perioperative hypertension
target BP to within 20% of baseline, except if potential for
life threatening arterial bleeding
typically related to catecholamine surge post-op.
Drug of choice :
B-blocker
Labetalol