management of hypertensive crisis
TRANSCRIPT
Management of Hypertensive crisisManagement of Hypertensive crisis
By Gelaye M.
Hypertensive crisis 1
Ambo UniversityDepartment of medicine
July 2016
OutlinesOutlines Introduction
Etiology
Pathophysiology
Clinical Evaluation
Work up
Management
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Introduction Introduction
Clinically, Hypertension may be defined as level of blood pressure at
which the institution of therapy reduces blood pressure–related morbidity
and mortality.
Current clinical criteria for defining hypertension generally are based on the
average of two or more seated blood pressure readings during each of two
or more outpatient visits
Although approximately 60 million Americans have hypertension, only 1%
develop hypertensive crises.
Any disorder that causes hypertension can give rise to a hypertensive crisis,
but the most common cause is poorly controlled essential hypertension.
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Classification of Blood Pressure for AdultsClassification of Blood Pressure for Adults
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Mechanism of hypertensionMechanism of hypertension
Cardiac output and peripheral resistance are the two determinants of arterial pressure
Cardiac output is determined by stroke volume and heart rate; stroke volume is related to myocardial contractility and to the size of the vascular compartment.
Peripheral resistance is determined by functional and anatomic changes in small arteries (lumen diameter 100–400 m) and arterioles
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Hypertensive CrisisHypertensive Crisis
It is a clinical syndrome that is associated abrupt, marked
increase in blood pressure “relative to the patient's
baseline” causes acute or rapidly progressing end-organ
damage.
It includes
Hypertensive Urgency
Hypertensive Emergency
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Hypertensive UrgenciesHypertensive Urgencies
Hypertensive urgency is acute severe elevation in blood
pressure (>180/120 mmHg) without evidence of end organ
damage
Usually due to under-controlled HTN.
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Hypertensive EmergenciesHypertensive Emergencies
A severe elevation in blood pressure (usually >180/120
mmHg) complicated by impending or progressive target
organ dysfunction involving neurological, cardiac or renal
systems”
Require lowering of BP within 1 hour to decrease morbidity
Not determined by a BP level, but rather the imminent
compromise of vital organ function
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Common clinical manifestations of end organ damage Common clinical manifestations of end organ damage in hypertensive emergencyin hypertensive emergency
Damage
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Heart - CHF, MI, angina
Kidneys - acute kidney injury, microscopic hematuria
CNS - encephalopathy, intracranial hemorrhage, Grade 3-4 retinopathy
Vasculature - aortic dissection, eclampsia
Etiology Etiology Most common causes:
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
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
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PathophysiologyPathophysiology 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
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Hypertensive crisis 12Joseph varon et al.Critical care 2008
Clinical EvaluationClinical EvaluationHistory 1) focus on presence of Sx of end-organ dysfunction(eod) 2) any identifiable etiology Hypertension Hx
last known normal BP prior diagnoses + Rx dietary and social factors
Medication Steroid use Estrogens Sympathomimetics MAO inhibitors
Social history smoking, alcohol illicit drugs (cocaine, stimulants)
Family history early HPT in family members cardiovascular and cerebrovascular disease Diabetes Pheochromocytoma
Pregnant? Hypertensive crisis 13
Clinical EvaluationClinical Evaluation......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 syndromeHypertensive crisis 14
Clinical EvaluationClinical Evaluation......Physical Examination: Confirm elevated BP
Proper position, appropriate cuff size
Supine and standing and both arms
Asses – EOD present Fundoscopy examination
Cardiovascular examination
Neurological examination
Neck
Pulmonary
Renal
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Physical Examination...:fundoscopyPhysical Examination...:fundoscopy
Hypertensive Retinopathy Fundoscopy used to be considered a
definitive tool in diagnosing HTN
encephalopathy
useful in recognizing acute EOD as in
HTN encephalopathy, but the absence
of retinal exudates, hemorrhages, or
papilledema does not exclude the
diagnoses.
Fundoscopy findings
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Retinopathy...Retinopathy... HTN Retinopathy (Keith-Wagner)•Grade I
– Mild arteriolar narrowing and sclerosis•Grade II
– Definite focal narrowing and AV nicking
– Moderate to marked sclerosis of the arterioles
•Grade III– Retinal haemorrhages, exudates and
cotton wool spots•Grade IV
– Severe grade III and papilledema– “presence of stage III and IV lesions –
implies failure of the CNS vascular autoregulation and makes the Dx of Malignant HPT definitive”
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Physical examination…Physical examination…
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WorkupWorkup Lab studies:
Electrolytes, urea and creatinine
FBC and smear
Urinalysis – dipstix + microscopy Imaging studies
CXR (chest pain or SOB)
Head CT/MRI brain (abn neurology)
Chest CT/TEE/Aortic angio (Aortic dissection) Other Tests
ECG
toxicology screen and
pregnancy test
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Workup...Workup...
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ManagementManagement Normalization of BP is usually not recommended
Sudden fall in BP may cause acute hypoperfusion of vital organs and
results in myocardial ischemia or infarction, hemiplegia,or acute renal
failure.
Older patients with long lasting hypertension and preclinical organ
involvement(LVH, atherosclerosis and arteriolar remodelling) are at risk of
these complications as the lower limit of autoregulation shifted to right.
Two questions that should be considered in all patients with hypertensive
crises are at what rate and to what extent should the blood pressure be
lowered.
The answers depend on whether it is a hypertensive emergency or urgency.
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Hypertensive emergenciesHypertensive emergencies
GOAL :reduce MAP by no more than 20-25%, DBP to 100-110mm Hg
within few minutes to 2 hours.
More aggressive and rapid BP reduction (Acute Pulmonary
edema ,Aortic dissection)
More slowly for acute cerebrovascular damages with monitoring of
neurological status.
Constant infusion of intravenous agents required (no intermittent IV
boluses/oral/sublingual drugs- drastic BP fall).
Ideal drug : Fast acting Easily titratableRapidly reversible and safe
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Sodium nitroprussideSodium nitroprussidePotent short acting arterial and venous dilator
(reduces pre- and after- load)
Rapid onset of action.(seconds)
Continuous intra-arterial BP monitoring required.
Infusion chamber and tubing to be covered.
intracranial pressure (caution in intracerebral hemorrhage)
Induces coronary steal (non selective coronary vasodilation)
Increases mortality in pts with acute MI. (NEJM,1982)
Thiocyanate toxicity (nausea,vomiting,lactic acidosis and altered mental status)
Usually rare, seen in pts with renal ,hepatic dysfunction.
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FenoldopamFenoldopam
A peripheral dopamine-1 receptor antagonist (DA1)
10 –fold more potent than dopamine as a renal vasodilator.
Antihypertensive effect by combined natriuretic and vasodilatory
effect (esp. intrarenal arteries)
Agent of choice in hypertensive emergencies assosciated with
renal dysfunction.
Adv effects – hypotension ,hypokalemia
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NicardipineNicardipine
Second generation DHP CCB.
Strong cerebral and coronary vasodilation.
Onset of action 5-15 min, Duration being 2-6 hrs.
Increases both stroke volume and coronary blood flow with a favourable
effect on myocardial oxygen balance.
CAD with Systolic HF. C/I in Aortic stenosis.
Dosage independent of weight.
Infusion rate of 5mg/h – 2.5 mg/h increments every 5 min –max being 15
mg/h.
IV Nicardipine maintained BP in Treatment range > IV Labetalol
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ClevidipineClevidipine Third generation, intravenous, dihydropyridine calcium channel antagonist.
FDA approval (2008)
Ultra short half life of about 1 min.
Potent arterial vasodilation (no effect on venous capacitance, myocardial contractility)*
No significant adverse effect on heart rate’.
Injectable emulsion.
99.9% bound to protein.
Safe in pts with renal, hepatic dysfunction.
C/I –allergies to soy products, eggs and egg products, defective lipid metabolism.
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50mg/100ml
DosageDosage
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An IV infusion at 1–2 mg/hour is recommended for initiation and
should be titrated by doubling the dose every 90 seconds.
As the blood pressure approaches goal, the infusion rate should
be increased in smaller increments and titrated less frequently.
The maximum infusion rate for Cleviprex is 32 mg/hour.
Most patients in clinical trials were treated with doses of
16 mg/hour or less.
No more than 1000 mL (or an average of 21 mg/hour) of
Cleviprex infusion is recommended per 24 hours.
LabetalolLabetalol
Combined selective 1 adrenergic and non selective β adrenergic receptor
blocker (1:7).
Hypotensive effect – in 2-5 min after IV admin.
Maintains cardiac output (unlike other BB).
Reduces SVR, but does not decrease PBF.
Cerebral,renal,coronary blood flow maintained.
Less placental transfer can be used in pregnancy induced HTN emergency.
Metabolised by liver.
Oral/IV.
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EsmololEsmolol
Ultrashort acting cardioselective β adrenergic blocking agent.
Ideal β blocker in critical cases.Useful in severe postoperative HTN.
Onset of action is within 60 sec
Duration of action being 10-20min.
Rapid hydrolysis of ester linkages by RBC esterases(metabolism),
not dependent on renal or hepatic function.
0.5 to 1mg/kg loading dose over 1min,followed by an infusion -
50ug/kg/min.(max 300ug/kg/min)
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Not to useNot to useSublingual NifedipineSublingual Nifedipine
Drug is poorly soluble, not absorbed through buccal mucosa
Sudden uncontrolled and severe reductions in BP,may precipitate
cerebral, renal and myocardial ischemic events.
Lack of clinical documentation attesting to a benefit from its use.
The Cardiorenal Advisory Committee of the FDA has concluded
“that the practice of administering SL/oral nifedipine should be
abandoned because this agent is not safe nor efficacious”.
.
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Special scenariosSpecial scenarios
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Myocardial ischemia/infarctionMyocardial ischemia/infarction may be assosciated with HTN at presentation
(usually in a previously HTN pt).
High BP exacerbated by pain and agitation.
IV Nitrates reducing systemic vascular
resistances,LVpreload, improves coronary perfusion.
B blockers may contribute to a fall in BP (reduces myocardial
O2 consumption)
BP control mandatory before thrombolysis (BP<180/100
mmHg). Hypertensive crisis 32
Acute Cardiogenic Pulmonary EdemaAcute Cardiogenic Pulmonary Edema
Ventilation
Reduction of LV preload and afterload.
IV nitrate, loop diuretics.
Others – urapidil, nicardipine,sodium nitroprusside.
Bolus 12.5-25 mg (50 mg),infusion 5-40mg/h onset 3-6
min,duration 4-6 hr .
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Aortic DissectionAortic Dissection
Most dramatic and rapid fatal complication in HTN emergencies.
Acute BP reduction reduces shear forces on damaged aorta.
Aim of treatment to reduce SBP as rapidly as possible down to 100-
110 mmHg, simultaneously control tachycardia resulting form the
sympathetic activation.
B blocker + vasodilator to be given
Esmolol + nitroprusside would be a better combination.
Hydralazine is C/I
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Ischemic strokeIschemic stroke
BP elevations can occur in previously hypertensive and in
normotensive pts.
BP declines to pre stroke values within 3-4 days after an
ischemic stroke.
Severe HTN Rx controversial issue.
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Shift to right in case of chronic HTN
AHA recommendationAHA recommendation
Threshold for treatment BP > 220/120 mmHg
Target BP should be a 10-15% lowering of BP.
Raised ICP – MAP<130 (1st 24hrs)
No raised ICP – MAP<110
IV Labetalol or Nicardipine .
IV tPA (if to be given) BP <185/110mm Hg.
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IC bleedIC bleed
To prevent rebleeding and reduce edema formation.
BP >180/105 mmHg ,may benefit from gradual 20-25%
reduction in BP.
Nimodipine, a dihydropyridine calcium blocker,is effective
(antagonist effects on cerebro vasospasm).
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Hypertensive EncephalopathyHypertensive Encephalopathy
Potential lethal complication of severe or abrupt BP
elevation.
Previously HTN/normotensive pts.
Acute glomerular nephropathy, Eclampsia, TTP,
Pheochormocytoma, Erythropoietin administration,
immunosupressive drugs
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Hypertensive Encephalopathy…Hypertensive Encephalopathy…
Cerebral ischemia resulting from arteriolar spasm*.
Severe headache, vomiting, visual disturbances,
confusion, focal or generalized seizures.
Fundoscopic examination(key role)
Mean BP should be reduced by 20% within first hour.
IV sodium nitroprusside is DOC (rapid onset of action)
IV labetalol,nicardipine,hydralazine .
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EclampsiaEclampsiaHypertension complicates 12% pregnancies, 18% maternal deaths.
Volume expansion,MgSo4 for seizure prophylaxis.
MgSo4 4-6 g in 100ml 5%D over 15- 20 min - 1-2g/h infusion (hourly DTR,urine output).
Antihypertensive therapy (to prevent complications in mother).
SBP :155-160 mmHg,DBP>105mm Hg.(initiation of Rx)
ICH is a devastating complication.
Methyl dopa,Hydralazine DOC,
Others being IV labetalol,nicardipine.
Avoid sublingual or oral nifedipine.
Nitroprusside,ACEI – C/I
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HTN emergencies due to catecholamine HTN emergencies due to catecholamine excessexcessAbrupt increase in alpha adrenergic tone.
IV labetalol
Pheochromocytoma crisis (IV alpha blocker phentolamine)
followed by B blocker(for tachycardia or VPCs).
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Withdrawal of centrally acting anti HTN drugs (clonidine)
Pheochromocytoma
Cocaine intoxication
Abuse of sympathomimetics
Post operative Hypertension
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Oral drugs for HTN urgenciesOral drugs for HTN urgencies
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Management…Management…
Lifestyle Interventions These interventions should address overall cardiovascular disease risk.
Impact of lifestyle interventions on blood pressure is more pronounced
in persons with hypertension
Dietary modifications that effectively lower blood pressure are:
weight loss,
reduced NaCl intake,
increased potassium intake,
moderation of alcohol consumption, and
an overall healthy dietary pattern
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Lifestyle modifications to manage hypertensionLifestyle modifications to manage hypertension
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PrognosisPrognosis The prognosis of a patient who has undergone hypertensive crisis and not been
treated is poor.
Before the introduction of effective antihypertensive agents, more than 90%
of patients with accelerated malignant hypertension died within 1 year of
diagnosis.
Modern pharmacotherapy and the availability of dialysis have substantially
increased survival rates, with studies reporting survival rates of more than
70% at 5-year follow-up
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Discharge/follow-up plansDischarge/follow-up plans A normal blood pressure should not be the discharge goal of patients admitted with
hypertensive emergencies.
Aiming for a diastolic blood pressure of 100–110 at discharge may be reasonable.
Patient education is critical in helping to prevent future hypertensive crises and in
managing blood pressure in general.
Stressing compliance with diet, weight reduction if necessary, avoidance of illicit
drugs and other substances (i.e., sympathomimetics), and adherence to
antihypertensive therapy is important.
Scheduling a 2-week follow up with a primary care physician should be
coordinated at the time of discharge.
Patients should be instructed to call their doctor or return to seek medical attention
if any acute symptoms return or appear.
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ReferencesReferences
Harrison’s Principles of Internal Medicine 18th edition
Joint National Committee on prevention, detection, evaluation
and treatment of high blood pressure. Seventh Report.
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Thank youThank you
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