hypertensive crisis

Views:
 
Category: Education
     
 

Presentation Description

No description available.

Comments

Presentation Transcript

PowerPoint Presentation:

Dr Maged Abulmagd,MD,EDIC Consultant intensivist,EBGH Hypertensive Crisis

Hypertensive Crisis :

Hypertensive Crisis Hypertensive Urgency SBP >180 or DBP>110 w/o TOD Hypertensive Emergency SBP >180 or DBP>110 (esp >120) +TODs: Brain: Hypertensive encephalopathy/edema, ICH, ischemic stroke,posterior leukoencephalopathy. Retina: Grade IV retinopathy (papilledema) CVS: ACS, Acute pulmonary edema, CHF, Aortic dissection Kidneys: accelerated nephrosclerosis, nephritic syndrome Pregnancy: HELLP, Ecclampsia

PowerPoint Presentation:

Decision-making. 1- Should the blood pressure be lowered? 2- Should the blood pressure be lowered acutely? 3- How much should the blood pressure be lowered? 4- Which medication should be used to lower the blood pressure?

PowerPoint Presentation:

What Constitutes a Hypertensive Emergency?

PowerPoint Presentation:

Urgency Rapid reduction in BP >>>> significant morbidity; organ hypoperfusion Ischemia Infarction Lower gradually over 24 – 48 hours Oral medications pressure induced natriuresis>>> volume repleting

PowerPoint Presentation:

Emergency Reduce DBP by 10 – 15%, or to ~ 110 mm Hg over 30 – 60 minutes Aortic Dissection Rapid lowering over 5 – 10 minutes SBP < 120 and MAP < 80

PowerPoint Presentation:

Threshold BP There is no specific BP where hypertensive emergencies occur Organ dysfunction is rare with diastolic BPs < 130 mm Hg Rate of increase may be more important, encephalopathy will occur at lower BPs in pregnancy and in children

PowerPoint Presentation:

Pathophysiology Sudden increase in Systemic Vascular Resistance BP Mechanical Stress with endothelial injury, increased permeability, Coag/Plt activation, fibrin deposition Fibrinoid necrosis Ischemia Activation of RAA Proinflammatory cytokines

PowerPoint Presentation:

Vaughan and Delanty Lancet 2000; 356:411

Case:

Case A 19-year-old man presents to ED with episodic headaches that resolved spontaneously. In the last week, the headaches have become much more severe and frequent, occurring almost daily, and are accompanied by throbbing chest pain, sweating, dizziness and palpitations.

Case:

Case On arrival in ED, the pt is complaining of a severe headache, BP is 235/135 mm Hg, HR 90. He has profuse sweating and is complaining of dizziness and chest pain. ECG shows non-specific ST depressions.

Question :

Question Define hypertensive urgency and hypertension emergency. What are some clinical findings associated with hypertensive emergenices?

PowerPoint Presentation:

Question What is the most common complaint in hypertensive emergency? Neurologic defect Gross Hematuria Chest pain Headache Epistaxis

PowerPoint Presentation:

Clinical Presentation Frequency of signs and symptoms Chest Pain 27% Dyspnea 22% Neuro defect 21% Interestingly…. Headache was only 3% and epistaxis was 0% in this study

Clinical Findings:

Clinical Findings Of predisposing disease Thyrotoxicosis/Thyroid storm, Hypothyroidism/Myxedema, goiter HPT: hypercalcemia (psychosis, constipation,cataract, nephrocalcinosis, N-DI, dystrophic calcifications of soft tissue (X-ray) Cushing’s: Cushinoid Conn’s: hypokalemic metabolic alkalosis Pheochromocytoma: perspiration, palpitation, pain (chest, AP), labile pressure (+/- orthostatic hypotension), pallor RAS: Renal bruits OSA/Pickwikian Syndrome: day time somnolence, apnea attacks Pregnancy: HELLP, Ecclampsia (edema, protienuria, sz)

Clinical Findings:

Clinical Findings Of Complications/TOD Brain: meningism, FND, delirium, decreased LOC, seizures, coma. Retina: blurred vision, papilledema (IV) +/- cotton wool exudate, flame shape hg, AV nipping and silver wiring (G I-III in chronic Htn). CVS: chest pain, ACS (MR, ECG, trop), CHF, pulse/BP bi limbs deficit (AD). Kidneys: active sediment, proteinuria, hematuria, tubular casts.

PowerPoint Presentation:

Hypertensive Emergency/Urgency: Differential Diagnosis Untreated or suboptimally treated essential hypertension (most common) Renal parenchymal disease Including microvascular thrombosis TTP, HUS, vasculitis, acute glomerulonephritis Renal vascular disease (Renal artery stenosis) Pregnancy Induced Hypertension/Pre-eclampsia/Eclampsa Endocrine: Pheochromocytoma (or exogenous catecholamines) Cushing’s syndrome Renin-secreting tumors

PowerPoint Presentation:

Drugs Sympathomimetic consumption/overdose Cocaine Amphetamines PCP Witdrawal from antihypertensive Rx MAOI interactions

PowerPoint Presentation:

Others Autonomic hyper-reactivity Guillan-Barre Autonomic dysreflexia Porphyria Elevated ICP

PowerPoint Presentation:

Investigations Book for history and physical examination Need for resuscitation (LOC, arrhythmias, pulmonary edema, seizures, tearing chest pain, etc) History of HTN (and detailed history of Rx, compliance and course of care as available), drug use, pregnancy (and pregnancy hx), systemic vascular disease, etc.

Investigations:

Investigations Previous difficulty managing BP, or flares of symptoms (pheo can’t be that rare if we’ve seen 2 cases within a year) Medications including OTC and recreational drugs

PowerPoint Presentation:

Investigations, continued Physical exam: Vital signs… HR as well as BP, to guide therapy Arterial line, particularly if IV medications are used Neuro (LOC/encephalopathy, seizures, focal deficits) Cardiovascular (heart failure, volume status, arrhythmias) Respiratory (pulmonary edema) Abdominal exam Systolic/diastolic bruits, palpable aneurysm masses occupying the entire epigastrium and invading the liver and aorta (hey, you never know)

PowerPoint Presentation:

Investigations, continued CBC ( Hemolytic anemia) ‘Lytes, renal indices (renal failure as cause or consequence of hypertension) Β-hcg If Hx unclear, urine for cocaine or amphetamine metabolites

PowerPoint Presentation:

Investigations, continued Chest X-ray (pulmonary edema) ECG ( Myocardial ischemia or clues to chronicity, such chamber enlargement and strain patterns.) Echocardiogram (systolic/diastolic function, hypertrophy, chamber size)

PowerPoint Presentation:

Investigations, continued CT Brain: intracranial hemorrhage, tumor, posterior leukoencephalopathy CT Abdomen/Pelvis If contrast is possible (renal failure), this can be used to assess renal arteries as well as look at adrenals and extra-adrenal masses CT Chest if aortic dissection is a concern

PowerPoint Presentation:

Investigations, continued CT Brain: intracranial hemorrhage, tumor, posterior leukoencephalopathy CT Abdomen/Pelvis If contrast is possible (renal failure), this can be used to assess renal arteries as well as look at adrenals and extra-adrenal masses CT Chest if aortic dissection is a concern

PowerPoint Presentation:

Here it is: Internal medicine-type stuff Plasma renin and aldosterone Urine metanephrines (24-hr collection) Serum metanephrines would be nice, if you could find a lab that would do them in a timely fashion

PowerPoint Presentation:

CVA’s Ischemic CVA Protective physiologic response to maintain CPP Impaired auto-regulation Some evidence for induced HTN Treat if: Thrombolysis (SBP/DBP < 185/110) End organ damage SBP > 220, DBP >120 (critical point at which sphincter tone becomes unbearable)

PowerPoint Presentation:

Cerebral Autoregulation

PowerPoint Presentation:

CVA’s Hemorrhagic CVA Controversial No evidence HTN leads to increased size of ICH, but there is an association Evidence suggests lowering BP rapidly leads to increased mortality Maintain SBP < 200, DBP < 130 Lowering MAP ~ 15% does not seem to reduce CBP

Profile of an ideal IV antihypertensive:

Profile of an ideal IV antihypertensive Preserves GFR and renal blood flow Few or no drug reactions Little or no potential for exacerbation of co-morbid conditions Rapid onset and offset of action Minimal hypotension “overshoot” Minimal need for continuous BP monitoring and frequent dose titration No acute tolerance Ease of use and convenience Safe and no toxic metabolites Multiple formulations for short and long term use Minimal symphathetic activation

PowerPoint Presentation:

Pharmacodynamics of antihypertensive drugs Drug Route Dosage Onset Duration Nitroprusside i.v. infusion 0.25-10 mcg/kg/min Immediate 1-2 min Labetalol i.v. bolus i.v. infusion 10-20 mg up to 80 mg every 10 minutes 0.5-2 mg/min 3-5 min 3-6 h Nitroglycerin i.v. infusion 5-300 mcg/min 1-2 min 1-3 min Nicardipine i.v. infusion 5-15 mg/h 5-10 min 15-40 min Fenoldapam i.v. infusion 0.1-1.6 mcg/kg/min 15 min 30-60 min Esmolol i.v. loading i.v. infusion 1 mg/kg for 1 min 150-300 mcg/kg/min 1-2 min 20-30 min Phentolamine i.v. bolus 5-10 mg every 10 min 1-2 min 10-30 min Enalaprilat i.v. bolus 0.625-1.25 every 6h 10-15 min 6-8 h Hydralazine i.v. bolus 5-20 mg 10-30 min 3-6 h

Case Based Presentation: Hypertension in the ICU:

Case Based Presentation: Hypertension in the ICU

PowerPoint Presentation:

Nitroprusside The prototype of a short-acting easy-to-titrate arteriolar and venous vasodilator. Most common adverse effect is hypotension which can be treated by reducing dosage and administering fluids if needed (lasts 1-2 min) Other adverse effects include reflex tachycardia and cyanide/thiocyanate toxicity

PowerPoint Presentation:

Nitroprusside Nitroprusside is metabolized through combination with hemoglobin to produce cyanomethemoglobin . A mitochondrial enzyme in the liver (rhodanase), catalyzes the reaction of cyanide with thiosulphate to produce thiocyanate Thyocyanate is then excreted in the urine So hepatic insufficiency leads to cyanide accumulation whereas renal insufficiency leads to thiocyanate accumulation

PowerPoint Presentation:

Nitroprusside Cyanide toxicity manifests as lactic acidosis, confusion, and hemodynamic instability. Other signs include abdominal pain, delirium, headache, nausea, muscle spasms and restlessness. Cyanide toxicity is best prevented by avoiding large doses (>3mcg/kg/min) of nitroprusside for greater than 72h, especially in patients with hepatic or renal dysfunction. Maximal doses of 10 mcg/kg/min should not be administered for more than 10 minutes

PowerPoint Presentation:

Labetalol A non-selective β-blocker with associated α-blocking activity, in a 7 to 1 ratio in i.v. formulation. Reduces peripheral vascular resitance with mild reduction in heart rate while maintaining cardiac output. Contraindicated in reactive airway disease or second to third degree heart block. Should be used with caution in patients with second to thir degree heart block.

PowerPoint Presentation:

The ratio of relative potency alpha: beta adrenoceptor antagonism after intravenous labetalol was approximately 1:7, whereas in the same subjects after oral labetalol the ratio was approximately 1:3 Labetalol

PowerPoint Presentation:

Nitroglycerin A venous and coronary artery dilator. Can dilate systemic arteries at higher doses. Indicated in patients with acute coronary syndromes; has also been used in perioperative hypertension. Side effects include headache, nausea, bradycardia, hypotension, and methemoglobinemia. Prlonged use may cause tachyphylaxis.

PowerPoint Presentation:

Nicardipine A dihydropyridine CCB with systemic and coronary vasodilating effects. No negative inotropic or a-v conduction effects. Used in perioperative hypertension and eclampsia/preeclampsia.

PowerPoint Presentation:

Esmolol Short-acting cardioselective β-blocker that can be used in perioperative hypertension and tachycardia. If no other agents are used , a prolonged esmolol infusion is a relatively expensive means of blood pressure control

PowerPoint Presentation:

Phentolamine Periphral α-blocker indicated for management of hypertensive emergencies associated with chatecholamine excess such as pheo, maoi interaction, antihypertensive withdrawal syndrome, and cocaine abuse. Can cause tachycardia, hypotension, vomiting, flushing, and angina.

PowerPoint Presentation:

Enalaprilat The IV formulation and active metabolite of enalapril. Its long duration of action and variable response, do not make it an ideal candidate for hypertensive emergencies. Contraindicated during preganancy, and in renal failure, esp. in renal artery stenosis.

PowerPoint Presentation:

Hydralazine An arteriolar vasodilator. Difficult to use due to its variable magnitude and rate of response. Improves placental blood flow so good for preeclampsia/eclampsia Side effects include tachycardia, and increased CO/myocarial oxygen consumption. Should therefore not be used in aortic dissection or myocardial ischemia.

PowerPoint Presentation:

Rhoney and Peacock. Am J Health-Syst Pharm. 2009; 66:1343-52. Specific Indications

PowerPoint Presentation:

Aortic dissection Goal is to reduce the shear force, and therefore the dP/dt. Goal is an SBP of 100-110 achieved with a beta-blocker and an easily titratable vasodilator if necessary. A vasodilator should not be used alone as this can increase shear force. Labetalol is a good agent as it provides both beta blockade and vasodilatation as one agent.

PowerPoint Presentation:

Preeclampsia/eclampsia Diastolic pressure should be reduced to 90-100 mmHg. Precipitous drops should be avoided as they may compromise placental circulation. Hydralazine and labetalol are the usual agents of choice. Nifedipine can also be used. ACE inhibitors should not be used due to adverse fetal effects.

PowerPoint Presentation:

Perez et al. Cochrane Database of Systematic Reviews 2008, Issue 1. Art. No.: CD003653.

PowerPoint Presentation:

Reversible posterior leukoencephalopathy syndrome A clinical radiographic syndrome of heterogeneous etiologies that are grouped together because of similar findings on neuroimaging studies. It is also often referred to as : Posterior reversible encephalopathy syndrome Reversible posterior cerebral edema syndrome Posterior leukoencephalopathy syndrome Hyperperfusion encephalopathy Brain capillary leak syndrome

PowerPoint Presentation:

RPLS has been described in a number of medical conditions, with hypertensive encephalopathy, eclampsia, and the use of cytotoxic and immunosuppressant drugs being the most common. It appears to be related to disordered cerebral autoregulation and endothelial dysfunction Reversible posterior leukoencephalopathy syndrome

PowerPoint Presentation:

characterized by Headaches Altered consciousness Visual disturbances Seizures Reversible posterior leukoencephalopathy syndrome

PowerPoint Presentation:

A rare tumor of catecholamine-secreting chromaffin cells, 80% to 90% of which are located in the adrenal medulla. 10% to 20% are located extra-adrenal, usually throughout the sympathetic chain in the thorax, abdomen, and pelvis,are referred to as paragangliomas. Pheochromocytoma

PowerPoint Presentation:

A diagnosis of exclusion. Cerebral oedema may be present on a CT scan but haemorrhage or infarction are absent. Immediate blood pressure reduction is mandatory for hypertensive encephalopathy whereas it may worsen neurological deficits in stroke and intracranial haemorrhage Hypertensive Encephalopathy

PowerPoint Presentation:

Acute hypertensive crisis is managed with intravenous nitroprusside or phentolamine Diagnostic tests of choice are 24-hour urine metanephrines and plasma fractionated metanephrines Pheochromocytoma

authorStream Live Help