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HYPERTENSION IN THE ED Treat now, later or never? 2012 Dr Peter Jordan Registrar Teaching Northern ED Case 1 58-year-old man c/o left temporal headache – Gradual onset, mod severity No history of hypertension BP 146/96 mm Hg – Mildly tender L) temporal area otherwise NAD Case 2 71-year-old woman sent in by her LMO who noted an elevated BP 190/100. Triage BP 190/110 mm Hg. Asymptomatic ?Ix/ Treatment Case 3 0600 - 96-year-old woman from home presents in pulmonary oedema. ? pMHx - diltiazem 240 and frusemide 80/40 Resus - BP 220/130 mm Hg, RR 28 sitting in a tripod position. BP treatment required Background Physicians definitions of HT are generally not useful in ED Overtreatment may convert patients from a stable, asymptomatic, hypertensive state to an unstable, symptomatic, normotensive or hypotensive state. Historically, nifedipine was used routinely for hypertensive states, urgencies and emergencies,.. Grossman E, et al..Should a moratorium be placed on sublingual nifedipine capsules given for hypertensive emergencies and pseudoemergencies? JAMA. 1996;276(16):1328-1331. (Review) BP Screening 25% to 75% of patients with elevated systolic or diastolic BP in the ED remain hypertensive at follow-up. Central Questions When Treating Hypertension In The ED Are ED measurements of blood pressure accurate in determining if the patient is truly hypertensive? Is there any evidence that the patient’s current blood pressure is contributing to the acute condition? Is there any evidence that the patient’s current blood pressure is contributing to active end-organ damage? How aggressively should the patient’s blood pressure be managed? What is the appropriate disposition and follow-up? Evidence Hoekstra J, Qureshi A. Management of hypertension and hypertensive emergencies in the emergency department: the EMCREGinternational consensus recommendations. Ann Emerg Med. 2008;51(3):S1-S38. (Consensus guideline) National Guidelines Clearinghouse (www.guidelines.gov) = 400 guidelines for the management of hypertension - focus on chronic disease and do not address immediate evaluation and management in any depth Chobanian AV, Bakris GL, Black HR, et al. Seventh report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. Hypertension. 2003;42(6):12061252. (Report) “Patients with marked BP elevations and acute target organ damage (eg, encephalopathy, myocardial infarction, unstable angina, pulmonary oedema, eclampsia, stroke, head trauma, life-threatening arterial bleeding, or aortic dissection) require hospitalization and parenteral drug therapy. Patients with markedly elevated BP but without acute targetorgan damage usually do not require hospitalization, but they should receive immediate combination oral antihypertensive therapy. They should be carefully evaluated and monitored for hypertension-induced heart and kidney damage and for identifiable causes of hypertension.” Only 1 guideline (ACEP) specifically directed at ED management of hypertension. ACEP Clinical policy: critical issues in the evaluation and management of adult patients with asymptomatic hypertension in the emergency department. Ann Emerg Med. 2006;47(3):237-249. (Clinical policy) End-organ effects: Stroke (29%) Pulmonary oedema (23%) encephalopathy (18%) congestive heart failure (15%) Acute Coronary Syndrome (13%) Prospective studies of triage vital signs show 20 - 28% hypertensive (140 syst or 90 diast) - 6% having an SBP > 180 or Diastolic > 110mm Hg Essential hypertension (90%) progresses in varying degrees through interactions among the cardiovascular, renal, and central nervous systems. Cardiac remodeling then occurs secondary to increased afterload. Secondary HT (approx 10%)- primary aldosteronism, Cushing syndrome, pheochromocytoma, renovascular Hypertensive emergencies or urgencies generally occur after an abrupt increase in systemic vascular resistance, resulting in endothelial injury, fibrin deposition, and arteriolar necrosis. Differential Diagnosis Of Hypertension In The ED Acutely Dangerous Less Acute Stroke Obstructive uropathy Aortic dissection Hyperthyroidism/hyperparathy Drug intoxication: cocaine, amphetamine, monoamine oxidase inhibitor Drug withdrawal: antihypertensives, alcohol, other sedative hypnotics Renal failure Pheochromocytoma or other tumor Thyroid storm roidism Sleep apnea Cushing syndrome Primary hyperaldosteronism Renovascular hypertension Essential hypertension Causes of secondary hypertension need to be specifically identified because their treatments differ substantially from the treatment of essential hypertension. CVA - BP is permitted to remain elevated for cerebral protection (consensus) Aortic Dissection - BP is aggressively controlled to avoid rupture or propagation Key Questions Have you ever been told you have high blood pressure? Concern(s)? Do you have any chest pain? Do you have any shortness of breath? Are you on any medications, or are you using any recreational drugs or herbal medicines? Have you recently stopped taking any medications or recreational drugs or herbal medicines? Have you had any focal weakness, slurring of speech, numbness, or clumsiness? Do you snore or wake up during sleep? Do you feel tired throughout the day? Have you had high blood pressure in the past that has not responded to multiple medications? Clonidine etc Examination Systematic/ Complete Vital signs Cardiovascular Fundoscopy Cognitive state/ focal neurology Thyroid/ reflexes Toxidromes Abdominal aorta/ Peripheral pulses Investigations Should be tailored to the individual patient FBE – rarely useful K+ low in 45% of patients with primary hyperaldosteronism ECG - specific, but not very sensitive Cornell criteria: Sum of R wave in aVL and S wave in V3, >2.8 mV in men or >2.0 mV in women = best predictor of future cardiovascular mortality. Investigations (cont.d) Urinalysis - Renovascular hypertension, nephrotic syndrome, nephritic syndrome, preeclampsia Pregnancy test - Possible preeclampsia; (avoid ACEIs) LVH Treatment - Asymptomatic Patients With BP Less Than 180/110 mm Hg ED BP readings—especially persistently high ones—are good indicators of chronic HT If BP < 180/110 mm Hg - Follow-up with LMO 1 wk to 1 month Asymptomatic patients with BP >180/110 and a History of Hypertension on Antihypertensive Medications Non compliant – restart Compliant – adjust meds – preferably in consultation with LMO Asymptomatic Patients with BP over 180/110 and No History of Hypertension Commence antihypertensive medication if they cannot see a primary care provider the next day The choice of initial agent is multifactorial Antihypertensive options Agent Starting Dose Indications Negatives ACEIs e.g. Lisinopril 5-10mg daily CCF, DM, Post MI Renal artery stenosis, dehydration, hyperkalaemia Angiotensin receptor blockers (eg Irbesartan) 75-150mg daily As per ACEI – if intolerant of or in addition to See above β-Blockers (eg, metoprolol) 25-50 mg bd 25-50 mg bd Patients with coronary artery disease; longterm management of CHF; rate control; hyperthyroidism Not a good monotherapy; heart block; bradycardia; sick sinus syndrome; bronchospasm; decompensated CHF Agent Start dose Indications Negatives Calcium channel Blockers (eg. diltiazem) 180-240 mg daily Rate control or coronary artery disease in patients who cannot take βblockers Not a good monotherapy, oedema; may lower heart rate works well with other agents Gout, hypokalemia, Hypercalcemia, Diminishing effectiveness as GFR decreases; electrolyte disturbances; Thiazide 12.5 mg daily diuretics (eg. hydrochlorothiazid e) Hypertensive Emergencies Cerebral infarction or haemorrhage Acute pulmonary oedema Hypertensive encephalopathy acute CHF aortic dissection (Pre Eclampsia) CVA - Ischaemic Treatment guidelines based on expert opinion: BP> 220/120 suggests IV Rx (SNP) Thrombolysis cut-off 185/110 – many titrate to just below but monitor tightly No increase in adverse events CVA - Haemorrhagic Classic tightrope – Adequate Perfusion pressure v increasing haemorrhage No prospective or efficacy data – 1. If SBP is > 200 mm Hg or MAP is > 150 mm Hg, consider aggressive reduction of BP with continuous IV infusion, with BP monitoring every 5 minutes. 2. If SBP is > 180 mm Hg or MAP is > 130 mm Hg and there is evidence for or suspicion of elevated intracranial pressure, consider monitoring intracranial pressure and reducing BP using intermittent or continuous IV medications to keep cerebral perfusion pressure > 60-80 mm Hg. 3. If SBP is > 180 mm Hg or MAP is > 130 mm Hg and there is no evidence for or suspicion of elevated intracranial pressure, consider a modest reduction of BP (eg, MAP of 110 mm Hg or target BP of 160/90 mm Hg) using intermittent or continuous IV medications; clinically re-examine the patient every 15 minutes. APO Mortality inversely proportional to BP levels (during Tx) Mortality Proportional to hypotension, renal failure, cardiacischaemia and arrhythmia Evidence positive for CPAP, weakly positive for GTN and neutral/ mixed for Frusemide in severe APO only Hypertensive Encephalopathy Sx - headache, seizures, visual disturbances, nausea, vomiting. Diagnosis made only after other potential hypertensive emergencies are excluded Nitroprusside – avoid - decreased systemic pressure and preserved intracranial perfusion pressures (Consensus) goal = 20% to25% reduction in MAP or Diastolic BP 100 to 110. Aortic Dissection Standard Tx: titratable IV B-blocker (eg, Esmolol/ metoprolol), and nitroprusside for BP control. Second line – Calcium channel blockers Theory = reducing the force of left ventricular contractions enhances laminar flow and lessen stress on the aortic wall. Turbulent flow is increased by using a vasodilator alone. Target pressure is the lowest pressure tolerated by the patient: (100 to 120 systolic ) Beware B Blocker if acute AI Sympathetic Crisis BDZs and Vasodilators Theoretical risk of unopposed alpha activation but evidence suggests nil harm and reduced incidence AMI. Unstable Angina/NSTEMI Nitroglycerin can be used to control both symptoms and BP Other therapies are more likely to have a beneficial effect on outcomes. oralb-blockers < 24/24. ACEIs and/ or angiotensin receptor blockers If HT and LVF or APO < 24/24. Renal Failure If low GFR - treatment of hypertension should involve an ACE inhibitor, especially for patients on hemodialysis Cr and K need close monitoring initially Pre Eclampsia/ Eclampsia Many common drugs contraindicated because of the potential for toxic effects on the fetus Goal is a reduction in SBP to 140 and DBP of 90 Classic therapy hydralazine/ Mg – beware precipitous drops in BP Case 1 conclusion 58 YO - headache Headache responded to Ibuprofen, Paracetamol and metoclopramide. CRP <10. HT was being followed by his LMO , so no further investigations or Mx for BP was undertaken. Case 2: 96-year-old woman incidental finding BP 190/110 ECG - normal sinus rhythm Creatinine 80 / K+ 4.1 mEq/L After discussion with her LMO lisinopril and hydrochlorothiazide combination prescribed and review in 5 days arranged. Case 3 96-year-old woman – APO hypertensive 210/130 Chest Auscultation - Basal creps Med reg requested BNP level (elevated). CXR - Pulmonary oedema. Mx: GTN infusion /CPAP/ Frusemide 40 mg IV . BP eased to 175/110 mm Hg – Weaned off GTN infusion in ED and ward admitted