Hypertensive CrisisHypertensive Crisis

Sofiya Lypovetska MD PhD

Ternopil state medical university

SCOPE of the PROBLEMSCOPE of the PROBLEM Hypertension is an increasingly important medical and

public health issue.

The prevalence of hypertension increases with advancing age to the point where more than half of people aged 60 to 69 years old and approximately three-fourths of those aged 70 years and older are affected

Data from observational studies involving more than 1 million individuals have indicated that death from both ischemic heart disease and stroke increases progressively and linearly from BP levels

Definitions and classification Definitions and classification of blood pressure levels (mmHg) of blood pressure levels (mmHg)

Factors influencing prognosisFactors influencing prognosis

Factors influencing prognosisFactors influencing prognosis

High/Very high risk subjectsHigh/Very high risk subjects

Blood pressure measurement

Position statement: Ambulatory and home BP measurement

JNC –VII GuidelinesJNC –VII Guidelines

Patient characteristics associated with resistant hypertension

Secondary causes of resistant hypertension

Medication that can interfere with blood pressure control

Conditions favouring use of some antihypertensive drugs versus others

Compelling and possible contraindications to use of antihypertensive drugs

Hypertensive CrisisHypertensive Crisis

Definitions- Is This : A Crisis?

An Emergency?

An Urgency?…

Clinical PresentationsTreatments

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 Keith-Wagener-Baker retinopathy

“malignant HPT”– describe those individuals with group 4 KWB

retinopathy changes + papilledema

DefinitionsDefinitionsHypertensive CrisisHypertensive Crisis

Hypertensive Emergency………1-2 hours– Rapid / progressive end organ damage

Hypertensive Urgency………….24-48 hrs– Inc. BP without evidence of end organ damage

Uncontrolled Hypertension……..1 week– Do not require acute intervention

Shayne PH - Ann Emerg Med - 01-APR-2003; 41(4): 513-29

Hypertensive EmergencyHypertensive Emergency

Hypertensive encephalopathy Intracerebral bleed Acute MI Acute CHF with pulm edema Unstable angina Aortic dissection Eclampsia

Tx: parenteral agent

BP >180/120 with evidence of target organ dysfunction

Cerebrovascular Hypertensive Cerebrovascular Hypertensive EmergenciesEmergencies

Cerebral Infarct Intracerebral Hemorrhage Cerebral Edema

Hypertensive Encephalopathy

Cerebral Perfusion PressureCerebral Perfusion Pressure

Cerebral blood flow a function of CPP

Autoreg. Fails at 25% of MAP

ICP CPP – Vulnerable to MAP

CBF = blood flow; CPP = cerebral perfusion pressure; ICP = intracranial pressure; MAP = mean arterial pressure;TCA = total circulatory arrest.

Hypertensive Encephalopathy

Pathophysiology:

- Loss of Cerebral Autoregulation of blood flow resulting in hyperperfusion of the brain, loss of integrity of the blood brain barrier, and vascular necrosis.

- Loss of Autoregulation occurs at a constant cerebral blood flow of above MAP 150 to 160 mmHg.

- Acute Onset- Reversible

Hypertensive Encephalopathy

Symptoms: Headache, Nausea/Vomiting, Lethargy, Confusion, Lateralizing neurological symptoms that are not often in an anatomical distribution.

Signs: Papilledema, Retinal Hemorrhages Decreased level of consciousness, Coma Focal neurological findings

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

HPT Encephalopathy

Not adequately treated – cerebral heamorrhage, coma and death.

BUT with proper treatment – completely reversible

Clinical diagnoses (exclusion)

Management of Hypertensive Encephalopathy

Reduce Mean Arterial Pressure (MAP) by 20 to 25% (T.397) and do not exceed this within first 30 to 60 min.

Rosen recommends reduction of 30 to 40% (R.1759) MAP= 1/3(SBP-DBP) + DBP Treatment Reduces vasospasm that occurs at these

high pressures Avoid excessive BP reduction to prevent

hypoperfusion of the brain and further cerebral ischemia

Hypertensive EncephalopathyHypertensive Encephalopathy

Cerebral overperfusion– MAP overwhelms autoregulation– Vasodilation and Inc. Perm.– Cerebral Edema

Hemorrhage, Coma, DeathTx: Nipride, Fenoldopam,

Labatalol, Nicardipine

Hemorrhagic CVAHemorrhagic CVAcausescauses

Hypertensive Vascular DiseaseArteriovenous Anomalies (AVM)Arterial AneurysmsTumorsTrauma

Hemorrhagic CVA Management

Hemorrhagic CVA’s commonly results in a profound reactive rise in blood pressure

Management is CONTROVERSIAL. Subarachnoid Hemorrhage: oral nimodipine

(nimotop) 60mg po q 4 hours to reverse vasospasm.

Nicardipine: 2mg IV boluses followed by an IV infusion of 4 to 15 mg/hr is used by some to treat Subarachnoid Hemorrhage.

Ischemic CVAIschemic CVA

Pathophysiology:

Elevated Blood Pressure can be the cause of the central nervous system event, OR, it may be a normal physiologic response (Cushing’s Reflex)

Ischemic CVA Management

Favors lowering MAP (mean arterial pressure) by 20%.

Recommends IV Labetalol in small doses of 5mg increments IF Diastolic Blood Pressure is higher than 140 mmHg.

(T. 398)

HPT Retinopathy

AV crossing changes

HPT retinopathy

HPT retinopathy

Cardiovascular Hypertensive Cardiovascular Hypertensive EmergenciesEmergencies

AorticDissection

CongestiveHeart Failure

Acute MI

Congestive Heart FailureCongestive Heart Failure

Pathophysiology:

Increased Afterload with decreased Cardiac Output

CHF / Pulmonary Edema

Symptoms: Shortness of Breath, Cough, Chest Pain

Lower Extremity Swelling

Signs: Jugular Venous Distension, Rales, S3 Gallop

Hepatomegaly, Pedal Edema

CHF / Pulmonary Edema

Treatment:Treatment:– DiureticsDiuretics– NitroglycerinNitroglycerin– VasodilatorsVasodilators– DigitalisDigitalis– Beta-adrenoceptor agonistsBeta-adrenoceptor agonists– Other positive inotropic agentsOther positive inotropic agents

Acute Coronary SyndromeAcute Coronary Syndrome

Pathophysiology: - Increased

afterload, cardiac workload, and myocardial oxygen demand

- Decreased coronary artery blood flow

Acute Coronary Syndrome / Acute MI

Symptoms: Chest Pain, Nausea / Vomiting, Diaphoresis, Shortness of Breath

Signs: Congestive Heart Failure Signs, S4 Gallop (due to decreased ventricular compliance) Few physical findings in many patients Clinical History is very Important

Acute Coronary Syndrome/Acute MI

- Immediate Blood Pressure reduction is indicated to prevent Myocardial Damage

- No specific Defined BP target

Management:

Nitroglycerin IV or Sublingual - Beta Blockers (Esmolol, Lopressor) - Nitroglycerin is Drug of Choice

Aortic DissectionAortic Dissection

Pathophysiology:- Atherosclerotic Vascular

Disease, Chronic Hypertension, increased shearing force on the thoracic aorta, leading to intimal tear.

- 50% begin in ascending aorta

- 30% at aortic arch- 20% in descending aorta

Dissection of Thoracic Aorta

Symptoms:- Chest pain radiating to the back (classic presentation)- Neurological Symptoms (carotid artery dissection)- Angina (coronary artery dissection)- Shortness of breath (aortic insufficiency, cardiac tamponade)

Signs:- Differential Blood Pressure (in UE)- Bruit (interscapular)- Neurological Deficits- Acute Cardiac Tamponade (rare)

Dissection of Thoracic Aorta

Optimal Blood Pressure in these patients is undefined and must be tailored for each patient, however,

SBP of 120-130mmHg may be a intial starting point. (T.408)

Acute Renal Failure

Pathophysiology:

- Hypertensive Glomerulonephropathy, Acute Tubular Necrosis

- Worsening renal function in the setting of severe hypertension with elevation of BUN/CR, proteinuria, or the presence of red cells and red cell casts in the urine.

Acute Renal Failure

Symptoms:- Many times there are few actual symptoms- Facial or Peripheral Edema due to fluid overload

or proteinuria may be present, shortness of breath

Signs: - Few findings unless edematous- Pulmonary Edema

Acute Renal Failure

Management:

- Nitroprusside is agent of choice - Dialysis (as needed)- Lasix to enhance Sodium excretion; Also

recommends Nitroprusside or Nifedipine - Nitroglycerin is also a good agent in this setting

since it is hepatically metabolized and gastrointestinally excreted.

Preeclampsia / EclampsiaPreeclampsia / Eclampsia

Pathophysiology:

- Systemic arterial vasoconstriction (including placental, leading to decreased uterine blood flow).

- Defined as SBP = 140/90 mmHg or greater, OR a 20 mmHg rise in SBP or 10 mmHg rise in DBP from baseline and evidence of HELLP Syndrome

Preeclampsia / EclampsiaPreeclampsia / EclampsiaSymptoms: lower extremity swelling, headache,

confusion, seizures, coma

Signs: edema, hyperreflexia, elevation of blood pressure related to baseline BP prior to pregnancy (elevation may be mild 125/75)

Management:

IV Magnesium Sulfate, Hydralazine.- May also use nifedipine or labetalol Delivery of

Fetus is definitive treatment of pre-eclampsia

Treatment of acute severe hypertension in preeclampsiaTreatment of acute severe hypertension in preeclampsia

Pheochromocytoma

Pathophysiology:- Alpha and Beta stimulation of

the cardiovascular system due to adrenergic excess states

Symptoms: Episodic Headaches, flushing,

tremor, diaphoresis, diarrhea, hyperactivity, and palpitations

Signs: Tachycardia, tachypnea, tremor,

hyperdynamic state (high output CHF)

Pheochromocytoma

Management:

- Alpha Blocker FIRST, followed by a Beta Blocker

- Phentolamine (alpha) + Esmolol (beta)- Labetalol IV (combined alpha and beta

blockade)

Pharmacologic AgentsPharmacologic AgentsHypertensive EmergenciesHypertensive Emergencies

Rapid Onset Rapid Maximal effect Rapid offset Ease of Titration

Parenteral Agents

Parenteral drugs for treatment of hypertensive emergenciesParenteral drugs for treatment of hypertensive emergencies

Oral Regimens for Treatment of Hypertensive

Urgency in the ED - Clonidine: 0.1 to 0.2mg PO, repeat 0.1mg q hour

to desired BP reduction or max of 0.7mg.- Labetalol: 200 to 400mg PO, repeat every 2 to 3

hours- Captopril: 25mg PO- Losartan: 50mg PO

Key ConceptsKey Concepts Acute End-organ damage determines hypertensive

emergency Be familiar with the agents of choice in specific

emergencies Goal for most is careful reduction of MAP by 20-25%

over minutes to hours– DBP not less than 100 to 110– Except: Pregnancy, Dissection, MI,

Patients without acute end-organ ischemia rarely require urgent intervention

Thank You!