Hypertensive Emergency

Plan to spend at least 30-60 minutes preparing for this talk by using the Interactive Board for Learning/Preparing and clicking through the graphics animations to become familiar with the flow and content of the talk. Print out copies of the Learner’s Handout so learners can take notes as you expand on the pathophysiology and management. The first page of the handout is a blank schematic that learners can fill in as you go through the presentation.

The anticipated time to deliver this talk is about 15-20 min without cases and 30-35 min with cases. It can also be divided into two separate talks. The recommended break down for this would be to complete objectives 1-3 in the first session (10-15 min), then objective 4 and the interactive cases in the subsequent session (15-20 min).

Begin with reviewing the objectives for the session. We recommend progressing in order, though this gives you the flexibility of doing more focused teaching. All clickable elements are indicated by a cursor icon.

Objective 1 – Define Hypertensive emergency

Hypertensive emergency is defined as systolic blood pressure (SBP) greater than 180 or diastolic blood pressure (DBP) greater than 120 and the presence of end organ dysfunction. The presence of end organ dysfunction differentiates hypertensive emergency from hypertensive urgency (or uncontrolled severe hypertension). Of note, the rate of BP rise is more important than the actual BP. Patients with chronically elevated BPs can tolerate severe hypertension exceeding > 180/120 without signs of end organ damage. A previously normotensive patient can develop end organ damage at a BP < 180/120.²

Objective 2 – End Organ Failure

Click on each organ system to reveal the corresponding manifestation of hypertensive emergency. End organ damage can broadly be classified as neurologic, cardiovascular, and renal emergencies:

• Neurologic emergencies consist of three primary manifestations: 1) hypertensive encephalopathy, 2) intraparenchymal or subarachnoid hemorrhage, 3) acute ischemic stroke.

• • Hypertensive encephalopathy is often a diagnosis of exclusion that is confirmed retrospectively when symptoms improve after BP is lowered. Presents insidiously with non-focal symptoms of headache, confusion, nausea, vomiting, and/or seizures related to cerebral edema. MRI may show vasogenic edema in the white matter of the parieto-occipital regions, a finding consistent with posterior reversible encephalopathy syndrome (PRES).^2,3
  • Papilledema may be present of physical exam from intracranial hypertension. It can occur with or without concurrent hypertensive encephalopathy.
  • Both intraparenchymal hemorrhage and ischemic stroke can present with focal neurologic deficits and are differentiated from one another by neuroimaging. Subarachnoid hemorrhage presents with severe headache.
• Cardiovascular emergencies include: 1) acute left ventricular failure and pulmonary edema, 2) acute coronary syndrome, and 3) aortic dissection.
  • Aortic dissection should be suspected in a patient with sudden onset severe chest that radiates to the neck or to the back. Sign of an ascending aortic dissection (type A) may include a blood pressure differential between upper extremities, neurologic deficits, elevated troponin and ischemic changes on EKG. A descending aortic dissection (type B) may present with an elevated Cr and diminished pedal pulses.
• Renal emergencies include rapidly progressive renal failure, as evidenced by rapidly rising serum creatinine, decreased urine output, and microscopic hematuria.
• Other comorbidities associated with hypertensive emergencies include 1) eclampsia, 2) pheochromocytoma crisis, 3) ingestion of sympathomimetic agents (cocaine, amphetamines).
  • Eclampsia presents with generalized, tonic-clonic seizures or coma in pregnant women typically beyond 20 weeks gestation.
  • Thrombotic microangiopathies (TMAs) can also occur. 
  • Pheochromocytoma classically presents with paroxysmal headache, sweating, tachycardia, and hypertension. Pheochromocytoma crisis involves severe hypertension, hyperthermia, mental status changes and other organ dysfunction.²
  • Ingestion of sympathomimetic agents presents similarly to pheochromocytoma crisis with additional history of ingestion or positive urine drug screen.² Of note, other medications such as VEGF inhibitors can also cause hypertension that can lead to hypertensive emergency.

Objective 3 – Treatment goals of hypertensive emergency versus hypertensive urgency

The overall treatment goal for hypertensive emergency is to prevent irreversible end-organ damage. It is not to normalize BP. Dropping blood pressure too quickly can be dangerous due to autoregulation of the vascular beds in the brain: vascular beds supplying the brain become habituated to higher blood pressures and acute drop can cause hypoperfusion and ischemic injury.

Key tenets of treatment for hypertensive emergency include admission to the ICU, use of IV antihypertensives for rapid titration, and removal of exacerbating factors (i.e., pain). This is in contrast to hypertensive urgency which can generally be managed as an outpatient with reinitiation or uptitration of oral medications.¹

• In general, the goal is to lower SBP by max 25% in 1 hour, then to 160/110 over the next 2-6 hours, then to normal over the next 24-48 hours.¹

• Exceptions to the general treatment goals include treatment of aortic dissection, severe pre-eclampsia or eclampsia, pheochromocytoma crisis, or acute ischemic stroke.

• In presence of aortic dissection, eclampsia, pheochromocytoma crisis: reduce SBP to <140 in first hour and to <120 in aortic dissection ASAP within 20 minutes²
  • For aortic dissection the goal reduction in HR is to 60 bpm, people should typically be maxed on β blocker (esmolol) then add nitroprusside
• In presence of acute ischemic stroke: permissive hypertension if BP <220/110, if greater than 220/110, reduce by 15% in first 24h. Unless patient is a candidate for tPA, then BP must be reduced to <185/110 prior to administration of tPA.

Objective 4: Medications used in the treatment of hypertensive emergency

Medications used to treat hypertensive emergency can be separated into two overarching types: vasodilators and adrenergic inhibitors. Understanding the mechanism of action of individual antihypertensives is important for deciding which medication is appropriate to use for the various clinical presentations of hypertensive emergency.

• Vasodilators include arterial/arteriolar only (nicardipine and hydralazine), mixed arterial and venous (nitroprusside, fenoldapam), and venous only (nitroglycerin).
  • Arterial/arteriolar.
    • Hydralazine works through an unclear mechanism but causes reflexive increase in sympathetic activity leading to increased cardiac workload and myocyte demand, therefore it is relatively contraindicated in ACS. It also leads to increased intracranial pressure and should be used cautiously in acute stroke. BP drops less predictability to hydralazine compared to other agents and generally is not a first line agent for acute treatment in most patients.^1,4
    • Nicardipine is a calcium channel blocker and helps to prevent vasospasm; it is the preferred agent for use in acute ischemic stroke.
    • Both nicardipine and hydralazine can be used in pregnancy.
  • Mixed vasodilators decrease preload and afterload and can be used in almost all hypertensive emergency scenarios except pregnancy.
    • Nitroprusside is a fast-acting nitrate. It should be used with caution in acute ischemic stroke as it can increase intracranial pressure or affect platelet function; AKI given risk of cyanide toxicity.^4,5 Tachyphyalxis can occur with prolonged use.¹
    • Fenoldapam is a dopamine agonist  that causes renal artery vasodilation and can be particularly helpful with acute renal failure.² It can also lead to an increase in intracranial pressure and intra-ocular pressure.^1,4
  • Venous vasodilators, such as nitroglycerin, are particularly beneficial with ACS and acute LV failure with pulmonary edema as they decrease preload thereby reducing cardiac wall stress and ischemia, as well as reducing hydrostatic pressure in the pulmonary venous system. However, it has less antihypertensive effect than other antihypertensive agents listed and tachyphylaxis occurs with prolonged use.
• Adrenergic antagonists – as a brief review, a1 adrenergic receptors are on the peripheral arterioles and cause vasoconstriction. B1 receptors are on the heart and increase HR and contractility. B2 receptors in the circulatory system also acts on the heart to increase HR and contractility and dilate peripheral arterioles.
  • Phentolamine is an a1 antagonist that is used to treat hypertensive emergencies from catecholamine excess such as pheochromocytoma crisis, ingestion of sympathomimetics (cocaine, amphetamines), clonidine withdrawal.
  • Labetalol is a combination a1/b antagonists that is safe in pregnancy, reduces preload and is a negative chronotropic agent. Therefore, it can be used in eclampsia, in hypertensive ACS to reduce wall stress and improve ischemia, and in aortic dissection to minimize shear stress on the aortic wall. It is contraindicated in RV infarction which is preload dependent.
  • Esmolol is a pure b1 antagonist that can be used in combination with a vasodilator to treat aortic dissection, again by reducing wall stress and by preventing rebound tachycardia.¹

Cases – After the completion of the talk, review the practice cases.