Transcript HYPERTENSIVE EMERGENCIES Louis Muller 11 March 2009

HYPERTENSIVE
EMERGENCIES
Louis Muller
11 March 2009
Content
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Introduction
Definitions
Prevalence/morbidity/mortality
Etiology & pathophysiology
Diagnosis
Causes
Differential diagnoses
Workup
Management
Treatment
Pharmacology IV Anti-hypertensives
References
Introduction
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Hypertension(HPT) very common Western soc.
50 mil. US – affected (world - approx. 1 billion people)
Despite awareness + treatment still 30% adults unaware
40% known with HTN - not on treatment
60% on treatment BP not controlled to <140/90 mm Hg
• New data – shown incr. lifetime risk of HPT
- incr. risk of CVS complications with “normal”
BP levels
Classification
• Joint National Committee (JNC – 7) introduced
a new classification system for HTN – 2004
• Normal – SBP<120 and DBP<80
• Prehypertension – SBP 120-139 or DBP 80-89
• Stage I hypertension – SBP 140-159 or DBP
90-99
• Stage II hypertension – SBP >160 or DBP
>100
• Stage II HPT further divided into:
– Hypertensive urgency
– Hypertensive emergency
Other Terminology
• Severely elevated BP (JNC VII)
• Defined as BP > 180/120
• “accelerated HPT”
– term used to describe individuals with chronic
hypertension with associated group 3 KeithWagener-Baker retinopathy
• “malignant HPT”
– describe those individuals with group 4 KWB
retinopathy changes + papilledema
Definitions
• HPT emergency(crisis): Is characterized by a
severe elevation in BP, complicated by evidence
of impending or progressive target/end organ
dysfunction
VS
• HPT urgency: is a severe elevation in BP
without progressive target organ dysfunction
NB – these definitions do not specify absolute
BP levels
Conditions constituting evidence
of EOD
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Hypertensive encephalopathy
Intracerebral heamorrhage
Stroke
Head trauma
Ischemic heart disease (most common)
– AMI
– Acute LVF with P/oedema
– Unstable angina
• Aortic dissection
• Eclampsia
• Life threatening arterial bleed
Prevalence/ morbidity/
mortality
Prevalence:
- With progress in anti-hypertensive Rx – decrease in the lifetime
incidence of HPT emergencies from 7% to 1%
- Hypertensive crisis more common among elderly and black patients
- Studies – HPT related problems amount for 25% of all pt visits to
medical section of ED. 33% of these - HTN emergencies.
Morbidity/mortality
- Dependent on the extent of EOD on presentation and the degree to
which BP is controlled subsequently.
- 1year survival rate has increased from 20% to more than 90% with
appropriate treatment.
- 10-year survival rate approaches 70% with approp treatment
- 1-year and 5-year mortality rate - following untreated HPT
emergency are 70 to 90% and 100% respectively
Etiology
• Most common
- rapid unexplained rise in BP in pt with chronic essential HPT
- most have history of poor treatment/compliance or an abrupt discont
of their meds
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Other causes
Renal parenchymal disease (80% of sec.causes)
Systemic disorders with renal involvement (SLE)
Renovascular disease (Atheroscleroses/fibromuscular dysplasia)
Endocrine ( phaeochromocytoma/cushing syndrome)
Drugs (cocaine/amphetam/clonidine withdrawal/diet pills)
CNS (trauma or spinal cord disorders – Guillain-Barre
Coarctation of the aorta
Preeclampsia/Eclampsia
Postop. HPT
Pathophysiology
• Not well understood
• Failure of normal autoregulation + abrupt rise in SVR
• Increase in SVR due to release of humoral
vasoconstrictors from the stressed vessel wall.
• Endothelium plays a central role in BP homeostasis via
substances as Nitric oxide and prostacyclin
• Increased pressure starts a cycle of
- endothelial damage
- local activation of clotting cascade
- fibrinoid necrosis of small vessels
- release of more vasoconstrictors
• Process leads to progressive increase in resistance and
further endothelial dysfunction
Pathophysiology
• Single organ inv. in approximately 83%
• Two organ inv found in 14%
• Multiorgan involvement found in 3% of pts
• Most common clinical presentations
- cerebral infarction(24%)
- pulmonary oedema (22%)
- HPT encephalopathy(16%)
- Cong. HF (12%)
• Less common presentations – IC hemorrhage, aortic
dissection and eclampsia
Case example - HPT
Encephalopathy
• 52yr male presents to ED
• worsening headache and confusion, numbness and
weakness involving right side of body, blurry vision over
past 12 hrs
• PMx: HPT, bilateral artery stenosis, cocaine abuse,
hyperlipidemia.
• Exam:
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BP 213/134
confused, papilledema on fundoscopy
Mild motor weakness (4/5) right arm
Lab studies rased creatinine
ECG – LVH
CT Brain – diffuse bilateral white matter changes – HPT
encephalopathy
Case example – HPT
Encephalopathy
• Mx
– admitted ICU
– started on IV Nitroprusside
– BP decreased to 190/100 mmHg over first
3hrs
• Outcome:
– Neurology symptoms resolved within 5hrs
– he was switched to his usual oral regimen on
3rd day in hospital
– discharged day 5 – controlled BP
Hypertensive encephalopathy
• Clinical manifestation of cerebral edema
and microhemorrhages seen with
dysfunction of cerebral autoregulation
• Defined as an acute organic brain
syndrome or delirium in the setting of
severe hypertension
HTN Encephalopathy
• Symptoms
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Severe headache
Nausea and vomiting
Visual disturbances
Confusion
focal or generalized
weakness
• Signs
– Disorientation
– Focal neurologic
defects
– Focal or generalized
seizures
– nystagmus
HPT Encephalopathy
• Not adequately treated – cerebral
heamorrhage, coma and death.
• BUT with proper treatment – completely
reversible
• Clinical diagnoses (exclusion)
Hypertensive Retinopathy
• Fundoscopy used to be considered a
definitive tool in diagnosing HTN
encephalopathy
• NOW – still usefull in recognizing acute
EOD as in HTN encephalopathy, but the
absence of retinal exudates, hemorrhages,
or papilledema does not exclude the
diagnoses.
• Fundoscopy findings
HPT Retinopathy Fundoscopy
• Keith-Wagener classification
– Stage I arteriolar sclerosis with thickening, irregularity
and tortuosity
– Stage II AV dipping or compression
– Stage III Flame shaped haemorrhages and cotton
wool spots
– Stage IV Papilledema
• “presence of stage III and IV lesions – implies
failure of the CNS vascular autoregulation and
makes the Dx of Malignant HPT definitive”
HPT Retinopathy
AV crossing changes
HPT retinopathy
HPT retinopathy
PanOptic ophtalmoscope
Diagnosis
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History
1) focus on presence of Sx of end-organ dysfunction(eod)
2) any identifiable etiology
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Hypertension Hx
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Medication
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smoking, alcohol
illicit drugs (cocaine, stimulants)
Family history
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Steroid use
Estrogens
Sympathomimetics
MAO inhibitors
Social history
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last known normal BP
prior diagnoses + Rx
dietary and social factors
early HPT in family members
cardiovascular and cerebrovascular disease
Diabetes
Pheochromocytoma
Pregnant?
Diagnoses
• History (cont)
• Symptom spesific Hx – suggesting EOD
• CVS Hx
– previous MI/angina/arrhythmias
– chest pain/SOB/Sx of CF/claudication/flank or
back pain
• Neurologic Hx
– prior strokes, neuro dysfunction
– visual changes, blurriness, loss of visual fields, severe headaches,
nausea and vomiting, change in mental status
• Renal Hx
– Underlying renal disease (RF)
– Acute onset changes in renal frequency (anuria/oliguria)
• Endocrine Hx
– diabetes, thyroid dysfunction, Cushing’s syndrome
Diagnoses
Examination
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Confirm elevated BP
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Proper position, appropriate cuff size
Supine and standing and both arms
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Asses – EOD present
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Fundoscopy
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Chronic HPT will have findings
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Acute changes
new retinal bleeds
Superficial/flame shaped
Deep/punctuate
exudates
hard/cotton wool spots
papilledema
Neck
Enlarged thryoid, carotid bruit, jugular venous distention
CVS
Enlarged heart, S3, asymmetric pulses, arrhythmias
Pulmonary
Signs of LV dysfunction ( crackles, rhonchi)
Renal
Renal bruit, abdominal masses
Neurologic
Level of consciousness, evidence of stroke, any focal signs
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Workup
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Lab studies
Electrolytes, urea and creatinine
FBC and smear
Urinalysis – dipstix + microscopy
Optional - tox screen
- BHCG
- Endocrine testing
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Imaging studies
CXR (chest pain or SOB)
Head CT/MRI brain (abn neurology)
Chest CT/TEE/Aortic angio (Aortic dissection)
• Other Tests
- ECG
Management
• ED considerations
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Many HPT pts – only small number will require emergent treatment
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Primary goal of EP?
The pts – syptoms of EOD and require immediate iv parenteral therapy.
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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
Management
• The EP must be capable of:
- Appropriately evaluating pts with an elevated BP
- Correctly classify the HPT
- Determine the aggressiveness and timing of
therapeutic interventions
- Making disposition decisions
Remember - “treat the patient and not the
number”
Treatment
• Prehospital care
- Address the manifestations of a HPT
emergency eg.chest pain or HF
- Reduction of BP not indicated in
prehospital setting
- Rapid lowering of BP can critically
decrease end-organ perfusion
Treatment
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ED Care - general principles
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Consider context of elevated BP (pain, anxiety)
Screen for EOD (Hx/workup)
- Pts without evidence of EOD – d/c + f/up
Misconception - never d/c patient from ED with elevated BP ?
- oral nifedipine – NOT indicated and may be dangerous!
- Pts with EOD – require ICU admission and rapid but gradual lowering of BP -
using IV meds.
BP should not be lowered to normal levels
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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
NB Exceptions
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BP goals best achieved by a continuous infusion of a short-acting, titratable,
parenteral anti-HPT agent, along with constant intensive patient monitoring
Treatment
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Medication options
1. Oral antihypertensives
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Chronic hypertensive
Hypertensive urgency
2. IV antihypertensives
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Hypertensive emergency
Pharmacology – IV anti-HPT
1. Vasodilators
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Sodium nitroprusside
Nitroglycerin
Nicardipine
Fenoldapam
Hydralazine
Enalapril
2. Adrenergic inhibitors
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Labetalol
Esmolol
Phentolamine
“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.
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
Sodium Nitroprusside
(Hypoten L)
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MoA:
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Direct smooth muscle dilator (art + ven)
Nitric oxide compound
Potent preload and afterload reducer
Causes cerebral vasodilation
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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
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Adverse affects/Precautions:
– Cyanide and thiocyanate toxicity (pts with liver/renal dysfunction)
Max dose, max 10min
– 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
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Drug of choice:
– Perioperative HPT
– Cocaine toxicity
– Aortic dissection(combination)
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Neurologic syndromes
Nitroglycerin
(Nitrocine / Isoket / Tridal)
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MoA:
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Potent vasodilator (nitric oxide compound)
Primary affects the venous system, decrease preload (CO + BP)
Decreases coronary vasospasm
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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
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Adverse effects/precautions:
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Contra ind:
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Constant monitoring is essential
Tolerance from uninterrupted use (12hr withdrawal)
Headache, tachycardia, flushing
Concurrent use with PDE-5 inhibitors - causes significant hypotension
Head trauma/cerebral haemorrhage
Severe anaemia
Drug of choice:
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Acute HF
ACS
Nicardipine
(Nimodipine – Nimotop)
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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 and
liver failure
can exacerbate renal insuff.
• Ideal for CNS emergencies
• Not available SA
Fenoldapam
(Carlopam)
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New (not available SA)
MoA:
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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:
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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
Max infusion rate – 1.6mcg/kg/min
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
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Renal insuffiency
Strokes ( combination with nicardipine)
Hydralazine
(Apresoline)
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Dose:
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used too much
boluses takes 20min to work
not titratable
Adverse effects/Precautions
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5-20mg IV bolus or 10-40mg IM repeat every 4-6hrs
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Decreases systemic resistance by direct vasodilation of arterioles
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 and
Fenoldapam are also safe options
Only available PO, Dihydralazine discontinued
Enalaprilat
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The active component of Enalapril (hydrolyzed in liver and kidney)
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MoA:
– ACE inhibitor
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Dose:
– 0.625-2.5mg every 6hr IV
– Not titratable
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Onset – within 30 min + long half life
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Adverse effects/Precautions
– Contra-indicated – volume depletion, renal vascular disease
– Prolonged ½ life
• Expensive, not available SA
Labetalol
(Trandate)
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MoA:
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selective alpha blocker – will reduce vascular smooth m. resistance
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non-selective Beta blocker – decrease cardiac inotropy and miocard O2 consumption, will prevent reflex
tachycardia
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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.
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Cont. infusion: 0.5 – 2mg/min – titrate to response,max 300mg total dose
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Difficult to titrate due to very wide dose range
Advantages:
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smooth onset
– Transition to oral Rx easy (dose equivalent)
– Improve cerebral bloodflow – stroke pt
– No need for ICU/Arterial line
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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
Esmolol
(Brevibloc)
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MoA:
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Dose: (titratable)
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Sinus bradycardia
Heart block
Cardiogenic shock
Bronchial asthma
Uncompensated CF
pregnancy
Drug of choice:
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Hypotension common
nausea
Asthma
1st degree AV block
heart failure
Contraindications
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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
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highly selective beta blocker
Aortic dissection ( with nitrate)
Not availalble anymore
Phentolamine
(Regitine)
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MoA:
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Dose:
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renal impairment
Concurrent use with PDE-5 inhibitors
coronary or cerebral arteriosclerosis
Drug of choice
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tachycardia
flushing/headache
MI
cerebrovascular spasm
Contra-indications
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load 5-20mg IV every 5min or
infusion 0.2-0.5mg/min
Onset 1-2min
Adverse effect/precautions
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alpha adrenergic receptor blocker
Cocaine associated HPT crisis
Pheochromocytoma HPT crisis
Not available in SA anymore
Neurological emergencies
• Hypertensive encephalopathy
– reduce MAP by 25% or diastole to 100mmHg
over 8 hrs
– If neurology worsens, suspend Rx
– Drug of choice:
• Sodium nitroprusside
• Labetalol
Neurological emergencies
• Acute Ischemic stroke
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often loss of cerebral autoregulation
ischemic region more prone to hypoperfusion
thus BP reduction not recommended
unless SBP>220 or DBP>120
UNLESS planning fibrinolysis – SBP<185
and DBP< 110
– Drug of choice:
• Labetalol
• Nicardipine
• Sodium Nitroprusside
Neurological emergencies
• Acutes 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
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
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
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
Other disorders
• Cocaine toxicity/pheochromocytoma
– Hpt and tachycardia rarely require spesific Rx
– Alpha adrenergic blockers – preferred
– B – blockers can be added, but only after
alpha blockade.
– Drug of choice
• Phentolamine
• Labetalol
• Diazepam
Other disorders
• Pre-eclampsia/Eclampsia
– Goal SBP<160 and DBP<110 in pre-andintrapartum periods.
– Platelets < 100 000, BP should be
maintained < 150/100
– IV Magnesium to prevent seizures
– Drug of choice:
• Methyldopa
• Hydralazine
Other disorders
• Perioperative hypertension
– target BP to within 20% of baseline, except if
potential for life threatening arterial bleeding
– typically related to catecholamine surge postop.
– Drug of choice:
• B-blocker
• Labetalol
Local
• Tygerberg
– F1(medical outpatients)
• Nitroglycerine
– Cardiology ICU
• Nitroglycerine
– Renal unit
• Labetalol
– Obstetrics
• Labetalol
• Hydralazine
Local
• Grootte Schuur (C15)
– Nitroglycerine (Tridal)
• Victoria
– Nitroglycerine (Tridal/Nitrocine)
– Labetalol
– Can get Sodium nitroprusside
Summary
• HPT crisis - serious condition - associated with
EOD, if left untreated
• High mortality - untreated
• Main causes – non-compliance and poorly
controlled chronic hypertension.
• Urgency vs emergency
• Treatment should be tailored to the individual’s
condition
• HPT urgency – initial goal max 25% drop in MAP
in first 3 hours
• Precipitous drop just as bad – good continuous
monitoring essential
References
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Joint National Committee on prevention, detection, evaluation and treatment of
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Kitiyakara C, Guzman NJ. Malignant hypertension and hypertensive
emergencies.J Am Soc Nephrol 1998;9:135
Vaidya CK, Ouellette JR. Hypertensive Urgency and Emergency. Hospital
Physician March 2007; 43-50
Vidt D. Hypertensive Crises: emergencies and urgencies. The Cleveland clinic
disease management project. 12 Jan 2006. Available at
www.clevelandclinicmeded.com/diseasemanagement/nephrology/crises/crises.htm
McCowan C. Hypertensive Emergencies. Available at
www.emedicine.medscape.com/emergencymedicine/cardiovascular. Updated Jan
26, 2009
Hollander JE. Cocaine intoxication and hypertension. Ann Emerg Med. Mar
2008;51:S18-20
Characteristics and management op patients presenting to the emergency
department with hypertensive urgency. J.Clin Hypertens. 8:2006;12-18
Peck TE, Hill SA, Williams M.Pharmacology for anaesthesia and intensive care. 3rd
Edition.Chapters 15 & 16,p246-269.
AggarwalMD, Khan IA. Hypertensive Crisis: Hypertensive emergencies and
Urgencies.Cardiology Clinics 24:2006;135-146
Flanigan JS.Vitberg D.Hypertensive Emergency and Severe Hypertension: What
to Treat, Who to Treat, and How to Treat. Med Clin N Am 90:2006;439-451