1 / 60

Hypertensive Crisis

Hypertensive Crisis. Sofiya Lypovetska MD PhD Ternopil state medical university. SCOPE of the PROBLEM. Hypertension is an increasingly important medical and public health issue.

phoebe
Download Presentation

Hypertensive Crisis

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript

  1. Hypertensive Crisis Sofiya Lypovetska MD PhD Ternopil state medical university

  2. SCOPE of the PROBLEM Hypertension is an increasingly important medical and publichealth issue. The prevalence of hypertension increases withadvancing age to the point where more than half of peopleaged 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 bothischemic heart disease and stroke increases progressively andlinearly from BP levels

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

  4. Factors influencing prognosis

  5. Factors influencing prognosis

  6. High/Very high risk subjects

  7. Blood pressure measurement

  8. Position statement: Ambulatory and home BP measurement

  9. JNC –VII Guidelines

  10. Patient characteristics associated with resistant hypertension

  11. Secondary causes of resistant hypertension

  12. Medication that can interfere with blood pressure control

  13. Conditions favouring use of some antihypertensive drugs versus others

  14. Compelling and possible contraindications to use of antihypertensive drugs

  15. Hypertensive Crisis Definitions- Is This : A Crisis? An Emergency? An Urgency?… Clinical Presentations Treatments

  16. 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

  17. DefinitionsHypertensive 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

  18. Hypertensive Emergency • Hypertensive encephalopathy • Intracerebral bleed • Acute MI • Acute CHF with pulm edema • Unstable angina • Aortic dissection • Eclampsia BP >180/120 with evidence of target organ dysfunction Tx: parenteral agent

  19. Cerebrovascular Hypertensive Emergencies Cerebral Infarct Intracerebral Hemorrhage Cerebral Edema Hypertensive Encephalopathy

  20. 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 = cerebralperfusion pressure; ICP = intracranial pressure; MAP =mean arterial pressure; TCA = total circulatory arrest.

  21. 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

  22. 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

  23. 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

  24. HPT Encephalopathy Not adequately treated – cerebral heamorrhage, coma and death. BUT with proper treatment – completelyreversible Clinical diagnoses (exclusion)

  25. 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

  26. Hypertensive Encephalopathy Cerebral overperfusion MAP overwhelms autoregulation Vasodilation and Inc. Perm. Cerebral Edema Hemorrhage, Coma, Death Tx: Nipride, Fenoldopam, Labatalol, Nicardipine

  27. Hemorrhagic CVAcauses Hypertensive Vascular Disease Arteriovenous Anomalies (AVM) Arterial Aneurysms Tumors Trauma

  28. 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.

  29. Ischemic 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)

  30. 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)

  31. HPT Retinopathy

  32. AV crossing changes

  33. HPT retinopathy

  34. HPT retinopathy

  35. Cardiovascular Hypertensive Emergencies Aortic Dissection Congestive Heart Failure Acute MI

  36. Congestive Heart Failure Pathophysiology: Increased Afterload with decreased Cardiac Output

  37. CHF / Pulmonary Edema Symptoms: Shortness of Breath, Cough, Chest Pain Lower Extremity Swelling Signs: Jugular Venous Distension, Rales, S3 Gallop Hepatomegaly, Pedal Edema

  38. CHF / Pulmonary Edema Treatment: Diuretics Nitroglycerin Vasodilators Digitalis Beta-adrenoceptor agonists Other positive inotropic agents

  39. Acute Coronary Syndrome Pathophysiology: - Increased afterload, cardiac workload, and myocardial oxygen demand - Decreased coronary artery blood flow

  40. 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

  41. 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

  42. 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

  43. 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)

  44. 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)

  45. 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.

  46. 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

  47. 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.

More Related