2. BP ≥ 180/120 mmHgHTN Crisis
HTN
Emergency
HTN
Urgency
BP ≥ 180/120 mmHg
+
Target organ damage
BP ≥ 180/120 mmHg
+
NO organ damage
3. • Acute head injury or trauma
• Generalized neurologic symptoms: agitation, delirium, stupor,
seizures, or visual disturbances
• Symptoms of ischemic or hemorrhagic stroke
• Fresh flame hemorrhages, exudates (cotton-wool spots), or
papilledema
• Nausea and vomiting: increased intracranial pressure
• Chest discomfort: myocardial ischemia or aortic dissection
• Acute, severe back pain: aortic dissection
• Dyspnea: pulmonary edema
• Pregnancy, as such patients with severe hypertension could have
preeclampsia or develop eclampsia
• Use of cocaine, amphetamines, phencyclidine, MAOIs, or recent
discontinuation of Clonidine or other sympatholytic agents
8. Renal
• Acute hypertensive nephrosclerosis
• Fenoldopam
• Withdrawal of anti-HTN
• Ingestion of Cocaine/MDMA
• Phentolamine
• Pheochromocytoma
• Phenoxybenzamine+Propranolol
• Eclamspia
• Methyldopa/Hydralazine/Labetalol
Sympathetic over activity
Pregnancy
9. Urgency
Target MAP reduction 25-30% over 2-4 hours
160/100 mmHg as soon as possible
Usual targets in long-run
Clonidine/Captopril
+
Amlodipine/Chlorthalidone
Editor's Notes
In patients with ischemic stroke, the perfusion pressure distal to the obstructed vessel is low, and the distal vessels are dilated. Because of impaired cerebral autoregulation, blood flow in these dilated vessels is thought to be dependent upon the systemic blood pressure.
The arterial blood pressure is usually elevated in patients with an acute stroke. This may be due to chronic hypertension, an acute sympathetic response, or other stroke-mediated mechanisms [53]. In many cases, however, the acutely elevated blood pressure is necessary to maintain brain perfusion in borderline ischemic areas
Severe elevations in blood pressure may worsen ICH by representing a continued force for bleeding, causing hemorrhage expansion
the signs and symptoms of hypertensive encephalopathy (eg, headache, confusion, nausea, vomiting) usually abate after the blood pressure is lowered
The goal of these therapies is amelioration of volume excess and heart failure and improvement in pulmonary edema
reduce myocardial oxygen consumption, to reduce the underlying coronary ischemia, and to improve prognosis
An intravenous beta blocker is given first to reduce the heart rate below 60 beats per minute and the shear stress on the aortic wall
Administer esmolol (250 to 500 mcg/kg IV loading dose, then infuse at 25 to 50 mcg/kg/minute; titrate to maximum dose of 300 mcg/kg/minute) or labetalol (20 mg IV initially, followed by either 20 to 80 mg IV boluses every 10 minutes to a maximal dose of 300 mg, or an infusion of 0.5 to 2 mg/minute IV). If beta blockers are not tolerated, alternatives are verapamil, diltiazem, or nicardipine.Once heart rate is consistently <60 BPM, give vasodilator therapy. IF the systolic blood pressure remains above 120 mmHg, initiate nitroprusside infusion (0.25 to 0.5 mcg/kg/minute titrated to a maximum of 10 mcg/kg/minute) or nicardipine infusion (2.5 to 5 mg/hour titrated to a maximum of 15 mg/hour). Vasodilator therapy (eg, nitroprusside, nicardipine) should not be used without first controlling heart rate with beta blockade.
microscopic hematuria and an elevated serum creatinine.
Antihypertensive therapy leads to worsening kidney function. the reduction in kidney function may be reversed with long-term blood pressure control
clonidine, propranolol, or other beta blockers- start the anti-HTN again. If not controlled, short acting IV anti HTN is needed
An alpha-adrenergic blocker is given 10 to 14 days preoperatively to normalize blood pressure and expand the contracted blood volume
Phenoxybenzamine is an irreversible, long-acting, nonspecific alpha-adrenergic blocking agent
After adequate alpha-adrenergic blockade has been achieved, beta-adrenergic blockade is initiated, which typically occurs two to three days preoperatively. The beta-adrenergic blocker should never be started first, because blockade of vasodilatory peripheral beta-adrenergic receptors with unopposed alpha-adrenergic receptor stimulation can lead to a further elevation in blood pressure.
Unless a beta blocker was recently withdrawn, administration of a beta blocker alone is contraindicated in these settings since inhibition of beta receptor-induced vasodilation can result in unopposed alpha-adrenergic vasoconstriction and a further rise in blood pressure
This suggestion stems from and seeks to balance two major concerns. These include:
●The risk of adverse events (eg, stroke, acute kidney injury, or myocardial infarction) that may occur if the blood pressure is lowered too rapidly or to a level below the ability for autoregulation to maintain adequate tissue perfusion [8,14,15].
●The potential risk of imminent cardiovascular events that may result from severe hypertension if the blood pressure is not quickly and sufficiently reduced. In patients visiting an emergency department for severe hypertension, potential legal ramifications partially motivate lowering the blood pressure in a short period of time
There is no proven benefit from rapid reduction of blood pressure in patients with severe asymptomatic hypertension [2,7,11,12,14,16], and most such patients who present in the ambulatory setting can be managed as outpatients.
Esmolol is a cardioselective beta blocker
Labetalol is an alpha and a beta blocker
avoided in patients with asthma, chronic obstructive lung disease, heart failure, bradycardia, or greater than first-degree heart block
