Hypertensive Crisis Sofiya Lypovetska MD PhD Ternopil state medical university.
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Transcript of Hypertensive 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)
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)
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