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Hypertensive Crisis.ppt
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- 2. Outline of thislecture: What is Heart Hypertensive Crisis? Epidemiology. Classification of Hypertensive Crisis. Causes of Hypertensive Crisis Clinical presentation of Hypertensive Crisis Managment of Hypertensive Crisis Jwan Ali AlSofi
- 3. What is HypertensiveCrisis? •The term hypertensive crisis is defined as a severe elevation in blood pressure (BP), generally considered to be a diastolic blood pressure greater than 120 mm Hg Jwan Ali AlSofi
- 4. What is HypertensiveCrisis? •This disorder can be further classified as hypertensive urgency or hypertensive emergency when there is evidence of acutely progressive end-organ damage. •If these disorders are not treated promptly, a high rate of morbidity and mortality will occur the 5-year mortality for patients with a history of hypertensive crisis is 26% Jwan Ali AlSofi
- 5. Epidemiology • Approximately 1%of hypertensive pts. may develop hypertensive crises during their lifetime. • Annual incidence of hypertensive emergencies being 1-2 cases/1,00,000 pts. • Higher rates have been reported in African Americans, low socioeconomic people, in developing countries. • Incidence in men 2 times higher than in women Epidemiology Jwan Ali AlSofi
- 6. BLOOD PRESSURE –CLASSIFICATION (for adults >= 18 years old) DIAS. PRESSURE (mmHg) SYS. PRESSURE (mmHg) CATEGORY <80 <120 OPTIMAL <85 <130 NORMAL 85-89 130-139 HIGH NORMAL(PRE HT): HYPERTENSION 90-99 140-159 STAGE 1 (MILD) 100-109 160-179 STAGE 2 (MODERATE) >=110 >=180 STAGE 3 (SEVERE) Jwan Ali AlSofi
- 7. Definitions of hypertensivecrisis:- • Hypertensive emergencies:- are defined as severe elevations in BP (>180/120 mm Hg) associated with evidence of new or worsening target organ damage. • Hypertensive urgencies:- are situations associated with severe BP elevation (>180/120 mm Hg) in otherwise stable patients without acute or impending change in target organ damage or dysfunction. • Accelerated hypertension (aka malignant hypertension):- A severe increase in blood pressure to 180/120 mmHg or higher (and often over 220/120 mmHg) with signs of retinal haemorrhage and/or papilloedema (grade 3-4). It is usually associated with new or progressive target organ damage. Jwan Ali AlSofi
- 8. Definition of HTN-emergency:- JwanAli AlSofi
- 9. Classification of HypertensiveCrisis Jwan Ali AlSofi
- 10. • Renovascular Disease •Pheochromocytoma 1. Non-adherence to anti-HTN medications (most common) 2. Hyperaldosteronism 3. Anti-hypertensive withdrawal syndromes 4. Head injuries and CNS trauma 5. Post-op hypertension 6. Drug-induced hypertension Causes of hypertensive emergencies ? Jwan Ali AlSofi
- 11. • As withhypertensive emergencies ,severe BP elevations may result from inadequate control or poor adherence to current antihypertensive drug regimens. • Another cause for patients reaching hypertensive urgency is previous inaccurate BP measurements that underestimate or do not detect increased BP at all (e.g. poor patient technique for self‐monitoring). Causes of hypertensive Urgencies ? Jwan Ali AlSofi
- 12. Causes Hypertensive Urgencies Drugs: •Non-Narcotic Analgesics : - Non-steroidal anti-inflammatory agents including aspirin - Selective COX-2 inhibitors • Sympathomimetic agents: - Decongestants - Diet pills - Cocaine • Stimulants: -Methylphenidate, amphetamine. Causes of hypertensive Urgencies ? Jwan Ali AlSofi
- 13. Causes Hypertensive Urgencies •Lifestyle: - High salt diet, excessive alcohol use. • Comorbid Conditions: - Thyroid storm, trauma, renovascular disease, acute ischemic stroke or adrenal dysfunction Causes of hypertensive Urgencies ? Jwan Ali AlSofi
- 14. Clinical Presentation ofHC Emergency • Characterized by severe increase in systolic and/or diastolic blood pressure associated with signs or symptoms of acute end-organ damage. • Usually, SBP > 180 mm Hg - DBP > 120 mm Hg • Requires an immediate BP reduction in few minutes - hours. • Requires an ICU care & IV drugs Urgency • Elevated BP ( usually systolic > 180 mmHg &/or diastolic > 120 mmHg ) but without evidence of end-organ damage. • Usually asymptomatic; severe headache, shortness of breath, epistaxis, severe anxiety. • Adequate treatment of these conditions, a BP lowering within 24-48 hrs by administration of oral drugs. • ICU admission is usually not required • Controlled by oral medications. Jwan Ali AlSofi
- 15. Clinical Presentation ofHC Emergency • Rarely develop in patients without a previous history of hypertension • occur in patients with pheochromocytoma or renal vascular disease • CNS:- • Cerebral infarctions, • HTN Encephalopathy • intracranial or subarachnoid hemorrhage. • Heart:- • acute heart failure (HF) and pulmonary edema • acute myocardial infarction, • unstable angina. • Acute dissection, • Eclampsia . Urgency • Not all patient present with same symptoms • 90% of patients had a history of hypertension • Headache (42%) and dizziness (30%). • visual changes, • chest discomfort, • nausea, • epistaxis, • Fatigue • psychomotor agitation. Jwan Ali AlSofi
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- 17. • Single organdamage in approximately 83%. • Two organ damage found in 14%,multiorgan damage in 3 % pts. Most common clinical presentations : - cerebral infarction (24%) - pulmonary oedema (22%) - HTN encephalopathy (16%) - Cong. HF (12%) •Less common presentations – - IC hemorrhage, - Aortic dissection Acute End-organ Damage (Complication of HC). Jwan Ali AlSofi
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- 19. ACUTE END ORGANDAMAGE- CNS 1. Neurological – -normal: increase in BP cerebral arterioles vasoconstrict cerebral blood flow (CBF) remains constant -hypertensive emergency: loss of autoregulation ability (decomp.) dialation of cerebral vessel exsessive cerebral blood flow+ leakage from cappilaries RESAULT: 1. Hypertensive encephalopathy- 3RD MOST COMMON (16.3%) 2. Cerebral vascular accident/cerebral infarction – MOST COMMON (24.5%) 1. Subarachnoid hemorrhage 2. Intracranial hemorrhage 3. Retinopathy Keith-Wagner- GRADES 3 AND 4. 4. Eclampsia Jwan Ali AlSofi
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- 21. HYPERTENSION CRISIS- RETINA Retinalhemmorhages (grade 3)- ACCELERATED HT Pappiledema (grade 4)- MALIGNANT HT Jwan Ali AlSofi
- 22. Hypertensive Encephalopathy • Isa presentation of hypertensive emergency • Our brains are under tight control. With severe rises in BP, autoregulation fails and leads to cerebral edema. • Hypertensive encephalopathy is defined as the presence of signs or symptoms of cerebral edema secondary to severe and/or sudden rises in BP. It’s characterized by: • Severe Hypertension with 1+ of: 1. Seizures 2. Lethargy 3. Cortical Blindness 4. Coma • It is a diagnosis of exclusion Jwan Ali AlSofi
- 23. Of note, thereis little evidence to suggest that headache alone is a sign of a hypertensive emergency, however, in combination with visual changes, lethargy, seizures or altered mental status it may be an indication of hypertensive encephalopathy.
- 24. ACUTE END ORGANDAMAGE- CVS 2. Cardiovascular - Myocardial ischemia/infarction – 4TH (12%). - Acute left ventricular dysfunction - Acute pulmonary edema – 2ND MOST COMMON (22.5% ) - Aortic dissection Jwan Ali AlSofi
- 25. ACUTE END ORGANDAMAGE- Renal 3. RENAL ARTERIOSCLEROSIS, FIBRINOID NECROSIS overall impairment of renal protective autoregulation mechanisms! RESAULT: - Worsening renal function - Acute renal failure/insufficiency (↑BP) - Hematuria + red blood cell (RBC) cast formation - Proteinuria. 4. Microangiopathic hemolytic anemia Jwan Ali AlSofi
- 26. MALIGNANT HYPERTENSION - Isa HYPERTENSIVE EMERGENCY!!! - Leading to an acute end organ damage - Less than 1% of ht patients develop the malignant phase - Avarage age of diagnosis is 40 - Men>women Jwan Ali AlSofi
- 27. MALIGNANT HYPERTENSION- PATHOPHYSIOLOGY BP =PVR*CO(SV*HR) Rateat which MAP rises more important than absolute rise Acute rise in BP Failure of vasoconstriction Endothelial by autoregulation damage FIBRINOID Activates coag. and Deposition. of proteins/ NECROSIS inflammation fibrinogen in vessel wall - RAAS plays an important role in initiating and perpetuating BP rise by causing vasoconstriction and fluid retention. - THIS CYCLE MUST BE STOPPED IN ORDER TO PREVENT FURTHER VASCULAR INJURY AND TISSUE ISCHEMIA! Jwan Ali AlSofi
- 28. MANAGEMENT OF HC JwanAli AlSofi
- 29. • The treatmentof hypertensive crises must balance preventing further end-organ damage while maintaining tissue perfusion. • The initial goal for blood pressure reduction is not to obtain a normal blood pressure. • Rapid and aggressive reductions in blood pressure can actually induce cerebral, myocardial, or renal ischemia or infarction if the blood pressure falls below the range at which tissue perfusion can be maintained by autoregulation. MANAGEMENT History Examination Assessment Treatment Jwan Ali AlSofi
- 30. • Duration anddegree of pre existing hypertension • Details of antihypertensive therapy • Compliance with medications • Use of the over counter drugs • History of recent operations. History Examination Assessment Treatment HISTORY Jwan Ali AlSofi
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- 32. CLINICAL SYMPTOMS C.V: • palpitations, •arrhythmias, • chest pain, • dyspnea, • pul. Edema. BRAIN: • headaches, • nausea, vomiting, • blindness, • seizures, • coma KIDNEY: • oliguria, • hematuria, • proteinuria, • electrolyte imbalance, • uremia, • azothemia EYE: • flashes, • scotoma GENERAL: • sweating, • pallor, • flushes, • tinnitus, • epitaxis, • fear of death Jwan Ali AlSofi
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- 34. Lab tests &investigations may be required:- - CBC, - ECG, - urinalysis, - renal function - Echo. - consider head imaging if neurological symptoms are present ASSESMEN with INVESTIGATION Jwan Ali AlSofi
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- 37. Clinical Presentation ofHC Emergency • rarely develop in patients without a previous history of hypertension • occur in patients with pheochromocytoma or renal vascular disease • Cerebral infarctions, encephalopathy and intracranial or subarachnoid hemorrhage. • acute heart failure (HF) and pulmonary edema and acute myocardial infarction, unstable angina. Acute dissection, eclampsia. Urgency • headache (42%) and dizziness (30%). Other symptoms include visual changes, chest discomfort, nausea, epistaxis, fatigue, and psychomotor agitation. • Not all patient present with same symptoms • 90% of patients had a history of hypertension Jwan Ali AlSofi
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- 39. MALIGNANT HYPERTENSION- THERAPY -general - HOSPITALIZATION - RELAXATION (NON STRESSED ENV.) SCREEN FOR END ORGAN DAMAGE INITIAL AIMS: 1. CORRECTION OF MEDICAL COMPLICATION 2. REDUCTION OF MAP BY 20-25% IN THE 1ST HOUR 3. REDUCTION OF DIASTOLIC PRESSURE TO 13 OVER MINUTES TO HOURS HOURS=110 mmHg (BUT NOT BELOW <95 mmHg – IN ORDER NOT TO CAUSE CEREBRAL HYPOPERFUSION) BP should be reduced - immediately- - gradually (Specifically) DRUGS should be used i.v Jwan Ali AlSofi
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- 41. Hypertensive Emergency THERAPY –IV DRUGS Jwan Ali AlSofi
- 42. Hypertensive Emergency THERAPY –IV DRUGS cont. 2 MAIN CLASSES OF DRUGS: 1.Vasodilators: Nitroprusside Nitroglycerine Nicardipine Hydralazine Enalapril Fenoldopam 2. Adrenergic inhibitors Labetalol (a+b blocker) Esmolol (b-1 selective blocker) Phentolamine (a1 blocker) Jwan Ali AlSofi
- 43. Hypertensive Emergency THERAPY –SPECIFIC DRUGS 1. NITROPRUSSIDE : - 1ST CHOICE FOR HT CRISIS! - ONSET 30 SEC FOR FEW MIN VEINS + ARTERIES DECREASE PRELOAD = USED IN ACUTE MI! SIDE EFFECT: THIOCYANIDE TOXICITY, METHEMOLOBINEMIA, HYPOTHYRODISM 2. NITROGLYCERIN: - Coronary vasodilator - Direct venodilator (variable arterial effects) SIDE EFFECT: headaches and tachycardia ,Methemoglobinemia 3. LABETALOL: Combined alpha & beta blocker Beta blockade blunts reflex tachycardia from alpha blockade Myocardial depression Caution in patients with reactive airway disease Jwan Ali AlSofi
- 44. Hypertensive Emergency – THERAPY– SPECIFIC DRUGS 4. FENOLDOPAM : (DOPAMIN AGONIST) Short acting (30 MIN) Rapid elimination upon discontinuation No dosing adjustment for pre-existing renal or hepatic impairment Increases renal blood flow and maintains GFR 5. HYDRALAZINE (oral): - Strict arteriole vasodialator -3rd 4th option in HT crisis. Jwan Ali AlSofi
- 45. Hypertensive Emergency THERAPY: SPECIFICRECOMMENDATION FOR DIFFERENT CLINICAL FORMS (exmamples) 1. Hypertensive encephalopathy Preferred medications : Labetalol Nicardipine Esmolol Medications to avoid : Nitroprusside (was used in the past- caused ICP ) Hydralazine Treatment guidelines: Reduce mean arterial pressure (MAP) 25% over 8 hours. Jwan Ali AlSofi
- 46. Hypertensive EmergencyTHERAPY: SPECIFIC RECOMMENDATIONFOR DIFFERENT CLINICAL FORMS (exmamples) 2. Aortic dissection – Immediate redn. In BP and mainly shear stress (change in BP with change in time) is essential to limit the extension of damage as surgery is being considered. Preferred medications Labetalol Nicardipine Nitroprusside (with beta-blocker) Esmolol Morphine sulfate Medications to avoid Avoid beta-blockers if there is aortic valvular regurgitation or suspected cardiac tamponade, HYDRALAZINE (increase shear stress) Treatment guidelines: Maintain SBP <110 mm Hg, unless signs of end-organ hypoperfusion are present. +Narcotic analgesics TIME TO ACHIEVE: 20 MINUTES!!!!! Jwan Ali AlSofi
- 47. Hypertensive Emergency THERAPY: SPECIFICRECOMMENDATION FOR DIFFERENT CLINICAL FORMS (exmamples) 3. Preeclampsia/eclampsia Preferred medications Hydralazine Labetalol Nifedipine Medications to avoid Nitroprusside Angiotensin-converting enzyme inhibitors Esmolol Treatment guidelines: In women with eclampsia or preeclampsia, SBP should be <160 mm Hg and DBP <110 mm Hg in the prepartum and intrapartum periods. If the platelet count is <100,000 cells mm3 BP should be maintained below 150/100 mm Hg. Patients with eclampsia or preeclampsia should also be treated with IV magnesium sulfate to avoid seizures Jwan Ali AlSofi
- 48. Hypertensive Emergency THERAPY: SPECIFICRECOMMENDATION FOR DIFFERENT CLINICAL FORMS (exmamples) 4. CARDIAC CRISIS L.V FAILURE AND PUL. EDEMA Preferred medications Nitroglycerin Enalaprilat Nitroprusside Treatment guidelines: Treatment with vasodilators (in addition to diuretics) for SBP ≥140 mm Hg. IV or sublingual nitroglycerin is the preferred agent BP CONTROL IS SECONDARY to the primary problem - open the infarct related artery and treat pain, diurese and oxygenate those in pulmonary edema Jwan Ali AlSofi
- 49. Hypertensive Emergency THERAPY: SPECIFICRECOMMENDATION FOR DIFFERENT CLINICAL FORMS (exmamples) 4. RENAL INSUFFICENCY: Goal is to prevent further renal damage by maintaining adequate blood flow. Preferred medications: Nitroprusside Jwan Ali AlSofi
- 50. Hypertensive Emergency- PROGNOSIS Median survivalduration:144 months for all patients presenting to ED with hypertensive emergency. 5 yr survival rate :74%. Jwan Ali AlSofi
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- 52. TREATMENT OF HYPERTENSIVEEMERGENCY 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 MANAGEMENT Jwan Ali AlSofi
- 53. Target of BPin HYPERTENSIVE EMERGENCY Jwan Ali AlSofi
- 54. TREATMENT OF HYPERTENSIVEEMERGENCY 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 TREATMENT OF HYPERTENSIVE EMERGENCY Jwan Ali AlSofi
- 55. TREATMENT OF HYPERTENSIVEEMERGENCY 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 TREATMENT OF HYPERTENSIVE EMERGENCY Jwan Ali AlSofi
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- 59. GOAL • Overall Goalof Management: reduce SBP by ~ 25% over 24‐48 hours. • More conservative BP lowering reduces the risk of potential adverse effects (i.e. perfusion complications worsening incidence of MI, stroke, and death) associated with more aggressive BP lowering if the blood pressure falls below the range at which tissue perfusion can be maintained by autoregulation . • All treatment strategies should consider the patient’s comorbidities and risk of adverse events. • Treated by oral medications not IV. TREATMENT OF HYPERTENSIVE URGENCY Jwan Ali AlSofi
- 60. TREATMENT OF HYPERTENSIVEURGENCY GOAL • Overall Goal of Management: reduce SBP by ~ 25% over 24‐48 hours. • More conservative BP lowering reduces the risk of potential adverse effects (i.e. perfusion complications worsening incidence of MI, stroke, and death) associated with more aggressive BP lowering if the blood pressure falls below the range at which tissue perfusion can be maintained by autoregulation . • All treatment strategies should consider the patient’s comorbidities and risk of adverse events. MANAGEMENT Jwan Ali AlSofi
- 61. Take-Home Points Fundoscopyand urine dip are key in the assessment of the severely hypertensive patient who you are working up for a possible hypertensive emergency Keep a high index of suspicion for hypertensive encephalopathy in the severely hypertensive and altered or comatose patient with or without seizures or cortical blindness Treat the patient and not the number Jwan Ali AlSofi
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Editor's Notes
- #29 Hypertensive crisis
- #37 Diagnosis and management of a hypertensive crisis. Colors correspond to Class of Recommendation in Table 1. *Use drug(s) specified in Table 19. †If other comorbidities are present, select a drug specified in Table 20. BP indicates blood pressure; DBP, diastolic blood pressure; ICU, intensive care unit; and SBP, systolic blood pressure.
- #57 Management of hypertension in patients with acute ICH. Colors correspond to Class of Recommendation in Table 1. BP indicates blood pressure; ICH, intracerebral hemorrhage; IV, intravenous; and SBP, systolic blood pressure.
- #58 Management of hypertension in patients with acute ischemic stroke. Colors correspond to Class of Recommendation in Table 1. BP indicates blood pressure; DBP, diastolic blood pressure; IV, intravenous; and SBP, systolic blood pressure.