management of hypertensive crisis

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


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.


Classification of Blood Pressure for AdultsClassification of Blood Pressure for Adults


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


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


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.


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


Common clinical manifestations of end organ damage Common clinical manifestations of end organ damage in hypertensive emergencyin hypertensive emergency

Damage


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


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


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


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


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”


Physical examination…Physical examination…


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


Workup...Workup...


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.


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


Sodium nitroprussideSodium nitroprussidePotent short acting arterial and venous dilator

(reduces pre- and afterload)

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.


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


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


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.


50mg/100ml

DosageDosage


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.


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)


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”.

.


Special scenariosSpecial scenarios


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 .


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


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.



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.


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).


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


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 .


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


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).


Withdrawal of centrally acting anti HTN drugs (clonidine)

Pheochromocytoma

Cocaine intoxication

Abuse of sympathomimetics

Post operative Hypertension

Oral drugs for HTN urgenciesOral drugs for HTN urgencies


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


Lifestyle modifications to manage hypertensionLifestyle modifications to manage hypertension


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


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.


ReferencesReferences

Harrison’s Principles of Internal Medicine 18th edition

Joint National Committee on prevention, detection, evaluation

and treatment of high blood pressure. Seventh Report.


Thank youThank you


management of hypertensive crisis

Health & Medicine