高血压危象（英文版）课件

Click to edit Master title style,Click to edit Master text styles,Second level,Third level,Fourth level,Fifth level,Click to edit Master title style,Click to edit Master text styles,Second level,Third level,Fourth level,Fifth level,*,Click to edit Master title style,Click to edit Master text styles,Second level,Third level,Fourth level,Fifth level,*,单击此处编辑母版标题样式,单击此处编辑母版文本样式,第二级,第三级,第四级,第五级,*,高血压危象（英文版） PPT,高血压危象（英文版） PPT,1,SCOPE 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,SCOPE of the PROBLEMHypertensi,2,高血压危象（英文版）课件,3,Definitions and classification,of blood pressure levels (mmHg),Definitions and classification,4,Factors influencing prognosis,Factors influencing prognosis,5,Factors influencing prognosis,Factors influencing prognosis,6,大家学习辛苦了，还是要坚持,继续保持安静,大家学习辛苦了，还是要坚持继续保持安静,7,高血压危象（英文版）课件,8,High/Very high risk subjects,High/Very high risk subjects,9,Blood pressure measurement,Blood pressure measurement,10,Position statement: Ambulatory and home BP measurement,Position statement: Ambulatory,11,JNC VII Guidelines,JNC VII Guidelines,12,高血压危象（英文版）课件,13,Patient characteristics associated,with resistant hypertension,Patient characteristics associ,14,Secondary causes of resistant hypertension,Secondary causes of resistant,15,Medication that can interfere,with blood pressure control,Medication that can interfere,16,Conditions favouring use of some antihypertensive drugs versus others,Conditions favouring use of so,17,Compelling and possible contraindications to use of antihypertensive drugs,Compelling and possible contra,18,Hypertensive Crisis,Definitions- Is This : A Crisis?,An Emergency?,An,Urgency?,Clinical Presentations,Treatments,Hypertensive CrisisDefinitions,19,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,Other TerminologySeverely elev,20,Definitions,Hypertensive 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,DefinitionsHypertensive Crisi,21,Hypertensive 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,Hypertensive EmergencyHyperte,22,Cerebrovascular Hypertensive Emergencies,Cerebral Infarct,Intracerebral Hemorrhage,Cerebral Edema,Hypertensive Encephalopathy,Cerebrovascular Hypertensive E,23,Cerebral 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.,Cerebral Perfusion PressureCer,24,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 EncephalopathyPat,25,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 EncephalopathySym,26,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,Hypertensive encephalopathyCli,27,HPT Encephalopathy,Not adequately treated cerebral heamorrhage, coma and death.,BUT with proper treatment ,completely,reversible,Clinical diagnoses (exclusion),HPT EncephalopathyNot adequate,28,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,Management of Hypertensive Enc,29,Hypertensive Encephalopathy,Cerebral overperfusion,MAP overwhelms autoregulation,Vasodilation and Inc. Perm.,Cerebral Edema,Hemorrhage, Coma, Death,Tx: Nipride, Fenoldopam,Labatalol, Nicardipine,Hypertensive EncephalopathyCer,30,Hemorrhagic CVAcauses,Hypertensive Vascular,Disease,Arteriovenous,Anomalies (AVM),Arterial Aneurysms,Tumors,Trauma,Hemorrhagic CVAcausesHyperten,31,Hemorrhagic CVA Management,Hemorrhagic CVAs 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.,Hemorrhagic CVA ManagementHemo,32,Ischemic CVA,Pathophysiology,:,Elevated Blood Pressure can be the cause of the central nervous system event, OR, it may be a normal physiologic response (Cushings Reflex),Ischemic CVAPathophysiology:,33,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),Ischemic CVA Management,34,HPT Retinopathy,HPT Retinopathy,35,AV crossing changes,AV crossing changes,36,HPT retinopathy,HPT retinopathy,37,HPT retinopathy,HPT retinopathy,38,Cardiovascular Hypertensive Emergencies,Aortic,Dissection,Congestive,Heart Failure,Acute MI,Cardiovascular Hypertensive Em,39,Congestive Heart Failure,Pathophysiology,:,Increased Afterload with decreased Cardiac Output,Congestive Heart FailurePathop,40,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 EdemaSymptoms:,41,CHF / Pulmonary Edema,Treatment:,Diuretics,Nitroglycerin,Vasodilators,Digitalis,Beta-adrenoceptor agonists,Other positive inotropic agents,CHF / Pulmonary EdemaTreatment,42,Acute Coronary Syndrome,Pathophysiology,:,-,Increased,afterload, cardiac workload, and myocardial oxygen demand,-,Decreased,coronary artery blood flow,Acute Coronary SyndromePathoph,43,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 / Ac,44,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,Acute Coronary Syndrome/Acute,45,Aortic 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,Aortic DissectionPathophysiolo,46,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,47,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),Dissection of Thoracic Aorta,48,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 FailurePathophysio,49,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 FailureSymptoms:,50,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.,Acute Renal FailureManagement:,51,Preeclampsia / 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 / EclampsiaPathop,52,Preeclampsia / Eclampsia,Symptoms,: 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,Preeclampsia / EclampsiaSympto,53,Treatment of acute severe hypertension in preeclampsia,Treatment of acute severe hype,54,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),PheochromocytomaPathophysiolog,55,Pheochromocytoma,Management,:,Alpha Blocker,FIRST, followed by a Beta Blocker,Phentolamine (alpha) + Esmolol (beta),Labetalol IV (combined alpha and beta blockade),PheochromocytomaManagement:,56,Pharmacologic Agents,Hypertensive Emergencies,Rapid Onset,Rapid Maximal effect,Rapid offset,Ease of Titration,Parenteral Agents,Pharmacologic AgentsHypertens,57,Parenteral drugs for treatment of hypertensive emergencies,Parenteral drugs for treatment,58,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,Oral Regimens for Treatm,59,Key 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,Key ConceptsAcute End-organ d,60,