Hypertensive Crisis


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jane    on Jul 27, 2009 Says :

Thanks a lot, doctor.Your presentation on Hypertensive Crisis helped me a immensely in my college project.what a wonderful thesis it is!thanks again.
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1 : Hypertensive Crisis Ahmed Magdy, MD, FACC, FSCAI National Heart Institute, Cairo January 2008
2 : Hypertensive crisis An ER physician is having trouble controlling his BP. During a shift, it rockets sky-high. He helps himself to various sample drugs from the back room. Beta blockers, calcium blockers, ACE inhibitors -- nothing works for long. It doesn't help that he's under great financial stress and is working many extra shifts.One day he faints on the job, and the nurses ask his friend the internist to come see him. The internist notices retinal hemorrhages and a blood pressure of 240 over 130, and hears a story suggesting stress-responsive hypertension.When asked about his stresses, the ER doc pours out an angry history of charge cards and overdue bills via a wife who shops too much.The internist calls the wife. "Your husband's blood pressure is very sensitive to stress, and your spending is a major factor," he says. "If you can't live on a reasonable budget, he'll be dead in six months!"The wife arrives at the hospital in tears. Running to the stretcher on which her husband lies, she gasps, "Oh, honey. I'm so sorry. The doctor said you only have six months to live!"
3 : BP Levelto consider crisis? If the diastolic BP is > 120-130 mm Hg. (however) Child with acute glomerulonephritis may present with encephalopathy while his BP is only 150/100 mm Hg.
4 : Blood Pressure Level Lady in the third trimester with protienuria and edema can develop convulsions due to eclampsia at a level of 160/110 mm Hg. Asymptomatic patient may refuse hospitalization for BP of 240/140 mm Hg with no grave sequel.
5 : Hypertensive CrisisHypertensive Urgency No end organ damage BP can be lowered over 24-48 hrs, may be managed as outpatient
6 : Severe hypertension associated with end organ damage Hypertensive encephalopathy Subarachnoid/Intracerebral hemorrhage Acute pulmonary edema Dissecting aneurysm Angina Or endanger the pregnant lady or baby in eclampsia Hypertensive Crisis Hypertensive Emergency
7 : Hypertensive Crisis Other Terms:Accelerated Hypertension BP is elevated progressively, at fast pace, with retinal hemorrhage and exudates (Grade III Keith-Wagner-Barker retinopathy ).
8 : Hypertensive CrisisMalignant Hypertension Severe elevation BP accompanied with papilledema which may be accompanied by encephalopathy or nephropathy. In addition to Grade IV Keith-Wagner-Barker retinopathy.
9 : Papilledema
10 :
11 : Epidemiology hypertensive crisis incidence Recently, came down to < 1 % of hypertensive patients, due to better management. Common in the black & elderly patients. Previous history of HTN and treatment.
12 : Epidemiology of Hypertensive crises Formed 1/4 of the medical urgencies and emergencies presenting during 12 months to ER Hypertensive urgencies constituted 76 % of the hypertensive crises while emergencies were 24%. Zampaglione et al, Hypertension 1996; 27(1)144-147
13 : Epidemiology End organ damage in hypertensive emergencies Cerebral infarct (24%) Acute pulmonary edema (23%) Hypertensive encephalopathy (16%) Cerebral hemorrhage (4.5%)
14 : EpidemiologyAge, Diastolic BP and History Of HTN in Hypertensive Crisis Zampaglione et al, Hypertension 1996; 27(1)144-147
15 :
16 : Pathogenesis increased level of circulating norepinephrine, angiotensin II and ADH Increase in systemic VR
17 : Pathogenesis endothelial damage more VC and ischemia of the end organs, more ischemia Sheer stress of high pressure Vasoactive substances
18 : Cerebral auto regulation Ability of the brain vascular system to adjust itself, to avoid the harmful effects of elevated BP
19 : Cerebral auto regulation Gets disturbed if BP goes down more than 20-25% from the resting level. Reduce the mean BP of patients in hypertensive crisis by no more than 20-25% Gifford RW Jr. Hypertension 1983; 5(Suppl.III):17-20.
20 : Causes and Precipitating Factors of Hypertensive Crises Unidentified cause (the most common ) Abrupt increase in BP in patients with chronic HTN without demonstrable precipitating factors Drug Withdrawal Usually centrally acting drugs (Clonidine) However, it can occur with most antihypertensive drugs.
21 : Causes and Precipitating Factors of Hypertensive Crises - Renal dysfunction or abnormalities Acute glomerulonephritis, parenchymal renal disease, Reno vascular HTN, renin secreting tumors. -CNS abnormalities Head injuries, intracranial mass, intracerebral or subarachenoid hemorrhage. Autonomic hyperactivity in various spinal cord syndromes.
22 : Causes and Precipitating Factors of Hypertensive Crises Causes related to increased catecholamine production: Pheochromocytoma, cocaine, MAO inhibitors and tyramine ingestion, other drug-induced causes (NSAID, steroids, tricyclic antidepressants, sympathomimetics such as amphetamines and ephedrine, ergot alkaloids)
23 : Causes and Precipitating Factors of Hypertensive CrisesMiscellaneous causes Eclampsia, peri-operative HTN (especially open heart surgery), severe body burns, disseminated vasculitis, progressive systemic sclerosis, SLE
24 : Symptoms Hypertensive urgencies Headache (22%) epistaxis (17 %) faintness psychomotor agitation (10 %). Hypertensive emergencies Chest pain (27%) , dyspnea (22%) , neurological deficit (21%)
25 :
26 : Recognition of Hypertensive Emergency
27 : Ask about mental status changes, chest pain, SOB Obtain all vital signs Determine the reason for admission Ask about the patient’s BP over the last 24 hrs Approach in stepsfigure out if this is an urgency or an emergency!
28 : When you get there…Chart check New medications? BP meds held? PMHx – CHF, CAD, Renal artery stenosis, Renal failure? Check most recent labs – Cr, K, Na
29 : When you get to the bedside VS- Measure the bp again in BOTH ARMS HEENT- jvd, thyromegaly, fundoscopic exam LUNGS- Crackles CV- New murmur, S3, S4, tachycardia ABD- Renal or aortic bruits EXT- Edema Neuro- Brief mental status exam, gross motor exam
30 : Laboratory Tests Urine for proteinuria, gross or microscopic hematuria and casts. BUN and creatinine, lytes CBC, Thrombocytopenea, ESR. Cardiac enzymes if angina
31 : Investigation EKG X Ray for dissection, HF Echocardiography CT if encephalopathy
32 : If you determine a hypertensive urgency (no evidence of end organ damage)… Aggressive therapy, rapid reduction can induce cerebral or myocardial ischemia Goal BP, safe level in 6 hrs, 160/110 over 12-24 hrs with conventional oral therapy Identify the cause and give appropriate TTT. can give extra or double dose of what the patient is already on. Patients can be sent home.
33 : Hypertensive Urgency… Most Oral Agents Can be Used Meds (use short acting agents that you can titrate quickly) ACE-I Captopril 12.5 mg po, 25 mg PO, repeat as required 15-30 minutes (caution if Aortic Stenosis or renal artery stenosis) Felodipine, 5 mg po Lopressor , 25 mg po (watch hr) Hydralazine 10 mg po Nifedipine 10-20 mg PO repeat after 30 minutes 15-30 minutes Cautions: Rapid, uncontrolled reduction in BP may precipitate circulatory collapse in patients with aortic stenosis
34 : Management of HTN Emergencies (signs of end organ damage )Do NOT waste time! Admission to a CCU Hemodynamic monitoring (ECG, central venous pressure and arterial line). Ensuring proper ventilation, free air way, control of seizures and adequate urinary output are important.
35 : Management of Hypertensive Emergency BP should be immediately and promptly reduced parentrally. Don’t wait for lab. Results. The mean BP should be lowered by approximately 25 % Reduce the diastolic BP to 100-110 mm Hg over a period of several hours ( 8 to 12 hrs).
36 : Rate of lowering of the blood pressure Acute Dissection of The aorta 15-30 min Acute pulmonary edema 15-30 min Hypertensive Encephalopathy 2-3 hours Acute cerebral infarction or intracranial bleeding. 6-12 hours
37 : Immediate reduction of the BP can be obtained with the following drugs Sodium Nitroprusside. Nitroglycerine can be added if there is acute coronary insufficiency. Loop diuretic + Nitroglycerine + Sodium Nitroprusside are effective if pulmonary edema is present.
38 : MEDS- Choose IV over PO Nitroprusside IV, 0.25 mcg/kg/min Dilates arterioles and veins Most effective iv drug for hypertensive emergency Acts within seconds Continuous bp monitoring required CAUTION: metabolizes to Cyanide?cyanide or thiocyanate toxicity (MS change, lactic acidosis)? give smallest dose possible
39 : Hypertensive Emergency Nitroglycerin , IV: 5 mcg/min Greater venodilation than arteriolar dilation Most useful in pts with CAD or S/P CABG Onset of action is 2-5 minutes Duration of action is 5-10 minutes Headache and tachycardia –side effects
40 : Hypertensive emergencyNicardipine CCB Give IV, start at 5 mg/hr?15 mg.hr Major limit: longer t1/2 so can’t titrate quickly
41 : Hypertensive EmergencyLabetalol BB and alpha blocker Rapid onset of action (less than 5 min) Only BB useful in Rx hypertensive emergencies Great for pts with CAD, b/c keeps hr low too Avoid in CHF, Bradycardia, Asthma
42 : Hypertensive Emergency Hydralazine - 10 mg IV bolus, Used intramuscularly in hypertensive urgencies. Direct arterolar vasodilator, no effect on venous circulation, Fall in bp within 10-30 minutes and last 2-4 hrs - Has a cerebral vasodilator effect (not indicated in crisis with cerebral accidents). Precaution with dissecting aneurysm and BB should be given concurrently to minimize reflex sympathetic stimulation Hypotensive response is less predictable, tachycardia Primarily, use in eclampsia
43 : Hypertensive EmergencyEnalapril IV prep of ACE Inhibitor Response is variable (probably b/c these pts have variable plasma renin activity) Contraindicated in pregnancy Start at 1.25 mg iv and up to 5 mg iv q 6 hrs Onset of action: 15 minutes, peak effect 4 hrs Duration of action: 12-24 hours
44 : ` Fenoldopam Selective dopamine agonist. Have oral and parenteral routes. Peripheral vasodilator (Stimulating dopamine adrenergic receptors). Diuretic & natruretic effects. No evidence of rebound after cessation of the infusion.
45 : Urapidil As effective as Sodium Nitroprusside in controlling blood pressure in hypertensive crisis Urapidil has a lower incidence of adverse effect.
46 : Immediate reduction of the BP according to condition aortic dissection Sodium Nitroprusside and beta blocker eclampsia: hydralazine is the drug of choice, labetalol, and calcium antagonists are alternative drugs to use. Pheochromocytoma crisis: alpha blocker phentolamine is given. Labetalol or sodium nitroprusside + beta blockers are alternate therapy.
47 :
48 : HYPERTENSIVE EMERGENCIESHypertensive encephalopathy The pathogenesis is cerebral edema, petechial hemorrhages and micro infarctions Presentation: Severe headache, nausea, vomiting, visual disturbances and cloudy memory. BP is usually > 250/150 mm Hg.
49 : Hypertensive encephalopathy (cont.) There is history of HTN, not treated, stopped or reduced treatment. Symptoms develop over 48-72 hours. Examination of the optic fundi may show exudative retinopathy.
50 : Hypertensive encephalopathy: (cont.) The drug of choice is sodium nitroprusside BP should be reduced gradually over 2-3 hours down to 140-150 mm Hg systolic or 90-110 mm Hg diastolic The maximum drop is 25% of the mean arterial blood pressure. Alternately diazoxide or labetalol hydrochloride can be given IV in small doses.
51 : Subarachenoid Hemorrhage: Reduction of BP is of no benefit. If the Blood pressure is very high it ought to be reduced by 20-25%. Sodium nitroprusside over 6-12 hours. B P should not be lowered < 170-180/100 mm Hg.
52 : Cardiac ComplicationsAcute LV failure Sodium nitroprusside is the favorable drug. No need for cardiac inotropic drugs. Furosamide should be administrated by IV route. ACE inhibitors orally will help when the intravenous sodium nitroprusside is discontinued Nitroglycerine IV is more effective in decreasing the preload.
53 : Acute Coronary Syndromes Unstable angina, MI may be associated with severe rise of blood pressure. Nitroglycerine increase the blood flow distal to the stenosed artery while sodium nitroprusside decreased the flow (Steal phenomenon).
54 : Acute Aortic Dissection: Prompt and rapid lowering of the blood pressure is mandatory (Sodium Nitroprusside). Systolic BP should be lowered to between 120-100 mm Hg within 15- to 30 minutes. Lower levels can be attempted provided the urine output is maintained.
55 : Acute Aortic Dissection (cont.) Drugs which decrease the sheering force on the aortic intima are thought to be better (Beta blockers & Trimethaphan). Oral beta-blockers are the best for maintenance of the blood pressure after control of the acute phase.
56 : Hypercatecholaminemia Pheochromocytoma. Food interaction with MAOI. Withdrawal of clonidine hydrochloride. Ingestion or injection of sympathomimitic agents including cocaine.
57 : Hypercatecholaminemia (cont.) Oral therapy is enough for most of these urgencies. Prazosin hydrochlodide is the drug of choice. In Clonidine withdrawal, hypertension can be corrected by readministration of Clonidine in around one hour. Bolus of phentolamine or sodium nitroprusside will be effective if parenteral route is indicated.
58 : Peri-operative Hypertension Drugs are given parenterally. Methyldopa is useful in these situations (sedation). Surgery on the arteries or CABG may require sodium nitroprusside parenteraly adjusted continuously to avoid leak of sutures with high pressure and thrombosis with low pressure.

 

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