CONTENTS

• Background
  • Use the MAP
  • Pathophysiology of malignant hypertension
• (1) Is there a known cause of the HTN?
• (2) Is this actually a hypertensive emergency?
• (3) Re-evaluation for an underlying cause of the HTN.
• (4) Control Bp with IV antihypertensive agents.
  • Nicardipine
  • Clevidipine
  • IV Labetalol
  • (Medications to avoid)
• (5) Transition to oral antihypertensives.
  • Calcium channel blockers
  • PO Labetalol
  • ACEi & ARBs
• Podcast
• Questions & discussion
• Pitfalls

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Preamble: Use the MAP

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Before getting started, it will be useful to define our preferred measurement of blood pressure: the mean arterial pressure (MAP). The MAP is the average arterial pressure, which can be estimated as follows:

MAP = [2(diastolic Bp) + Systolic Bp]/3

There are several reasons that MAP is the preferred measurement of blood pressure, as follows:

reason #1: MAP is what the automated Bp cuff is actually measuring

• Automated oscillometric Bp cuffs measure the MAP directly (whereas the systolic and diastolic Bp are estimated using proprietary algorithms).
• This could make the MAP the most accurate measurement.

reason #2: MAP may be most closely related to the risk of hypertensive emergency

• We tend to focus on the systolic blood pressure (“she had a systolic of 250!!”). However, the risk of hypertensive emergency seems overall be more closely related to the diastolic pressure than the systolic pressure.
• MAP is probably the single parameter most closely related to the risk of hypertensive emergency.

reason #3: MAP is preferred in guiding therapy

• The dosing of any antihypertensive drug can be titrated only against a single variable. The best way to titrate antihypertensive drugs in a logical fashion is to target a specific MAP.
• Trying to titrate an antihypertensive infusion against systolic and diastolic blood pressure simultaneously is often impossible and confusing (for example, what happens if the systolic target is reached but not the diastolic?).

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pathophysiology of malignant hypertension

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what is malignant hypertension?

• When chronic hypertension is not treated, it may eventually reach a tipping point where the hypertension itself is causing progressive microvascular damage. This leads to a vicious spiral that, if untreated, will progress to death.
• The term “malignant hypertension” is somewhat outdated (classically this was defined based on the presence of extreme hypertension and hypertensive retinopathy – which was often lethal before the advent of antihypertensives). Nonetheless, as a general concept this remains useful.
  • Malignant hypertension is the “purest” form of primary hypertensive emergency.

pathophysiology of malignant hypertension

• The vicious spiral is shown above. The core of this spiral is that hypertension causes microcirculatory damage that impairs renal perfusion, leading to activation of the renin-angiotensin system (RAS). RAS activation, in turn, causes vasoconstriction – which leads to worsening hypertension.
• Clinical implications of this pathophysiology include the following:
  • (#1) The primary pathophysiological problem is excessive vasoconstriction. Thus, the optimal treatment may include a vasodilator (most often a calcium channel blocker). Alternatively, use of a beta-blocker will not address this underlying problem.
  • (#2) Patients are sometimes intravascularly volume depleted (due to sodium excretion in the kidney that is triggered by the hypertension). When vasoconstriction is treated, this may unmask underlying volume depletion – which is best treated with IV crystalloid administration.

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(1) Is there a known cause of the HTN?

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secondary hypertension

• Secondary hypertension is used here to refer to hypertension which is a result of some other primary process. In most cases, the primary process will be more obvious clinically, dominating the initial clinical presentation (e.g. aortic dissection, sympathetic crashing acute pulmonary edema, cocaine intoxication).
• Treatment will vary widely, depending on the specific context. This will be covered in other chapters regarding these individual conditions. For example:
  • Preeclampsia 📖
  • Sympathetic crashing acute pulmonary edema 📖
  • Ischemic stroke 📖
  • Intracranial hemorrhage 📖
  • Subarachnoid hemorrhage 📖
  • Sympathomimetic intoxication 📖
  • Pain 📖
• ⚠️ Please note that the remainder of this chapter doesn't apply to secondary hypertension.

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(2) Is this actually a hypertensive emergency?

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two criteria are required to diagnose hypertensive emergency:

(a) severe hypertension:

• Usually a MAP of at least >135 mm is needed to cause a hypertensive emergency.(34670853)
• However, this may vary considerably depending on the patient's baseline Bp. The relative change in blood pressure from baseline is more important than its absolute value. Hypertensive emergency can occur at lower MAPs in previously normotensive patients who have acute hypertension (e.g., pregnant women with preeclampsia).(26674757) Alternatively, patients with chronic hypertension may have extremely elevated Bp without hypertensive emergency.

(b) target organ damage, such as:

• Acute kidney injury (often with microscopic hematuria).
• Myocardial ischemia (type-II myocardial ischemia).
  • This should be a true myocardial infarction, not solely an elevated troponin.📖
• Pulmonary edema.
• Hypertensive encephalopathy (e.g., visual disturbance, seizure, delirium). In situations where this is unclear, the presence of increased optic nerve sheath diameter on ultrasonography might support the diagnosis of hypertensive encephalopathy with increased intracranial pressure.
• 🔑 Epistaxis, proteinuria, chronic renal failure, or headache don't qualify as target organ damage.(34670853)

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“hypertensive urgency” (asymptomatic uncontrolled hypertension)

• “Hypertensive urgency” is a term that has been used to refer to patients with severely elevated blood pressure (e.g., >~180/120) who do not have target organ damage. However, this is a misnomer because there is no “urgent” need to reduce the blood pressure, specifically:
  • (1) There is NO need for referral to the emergency department.
  • (2) There is NO need for hospital admission.
  • (3) There is definitely NO need for ICU admission!
  • If there is any doubt about this, please see the the AHA/ACC guidelines reproduced below.(29133354) Aggressive reduction in blood pressure is more likely to cause harm than benefit in this clinical context.
• It would probably be ideal to eliminate the term “hypertensive urgency” and replace it with the term “asymptomatic uncontrolled hypertension” (which would discourage over-reacting to this condition).(34670853)
• If a patient with hypertensive urgency is encountered in the outpatient context, it might be reasonable to start them on a low dose of a chronic oral antihypertensive agent with a relatively benign side-effect profile (e.g., amlodipine). It might also be wise to arrange close follow-up with their primary care provider for management of their blood pressure. Obtaining adequate follow-up and ambulatory blood pressure measurement is probably more important than the immediate patient management. This is not a critical care topic, so it's beyond the scope of this book.

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(3) Re-evaluate for any underlying disease process causing HTN

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causes of severe hypertension include:

• Nonadherence with antihypertensive medications (especially clonidine withdrawal).
• Physiologic stimuli:
  • Volume overload.
  • Hypercapnia, or nonadherence with CPAP or BiPAP therapy for sleep disordered breathing.
  • Pain.
  • Anxiety, agitation.
  • Urinary obstruction.
• Medications:
  • Sympathomimetics (e.g., cocaine, over-the-counter decongestants).
  • Calcineurin inhibitors (cyclosporine, tacrolimus).
  • Erythropoietin.
  • Steroid.
  • NSAIDs.
  • Metoclopramide.
  • Anti-angiogenic medications.
  • Monoamine oxidase inhibitors with high dietary tyramine intake.
• Withdrawal:
  • Alcohol or benzodiazepine withdrawal.
  • Clonidine or tizanidine withdrawal.
• Stroke (e.g., ischemic stroke, intracranial hemorrhage, subarachnoid hemorrhage).
• SCAPE (sympathetic crashing acute pulmonary edema).
• Aortic dissection.
• Preeclampsia.
• Endocrinopathy:
  • Pheochromocytoma.
  • Hyperaldosteronism.
  • Cushing's syndrome.
  • Hyperthyroidism.
• Renal:
  • Scleroderma renal crisis.
  • Acute glomerulonephritis.
  • Renal artery stenosis.
• Dysautonomia:
  • GBS (Guillain-Barre syndrome).
  • Autonomic dysreflexia following spinal cord injury. 📖

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evaluation may include:

physical examination

• Repeat blood pressure measurement: Initial Bp measurement in the emergency department is often transiently elevated (possibly reflective of a “white coat hypertension” phenomenon). Simply allowing the patient to rest quietly and repeating the blood pressure will often lead to a substantial reduction.(34670853)
• POCUS:
  • Assessment of volume status.
  • Evaluation for ultrasonographic papilledema and/or increased optic nerve sheath diameter.

history

• Baseline Bp?  (Ask patient & review any electronic records.)
• History of hypertension?
  • Antihypertensive regimen?
  • Compliance with regimen?
  • Any prior episodes of hypertensive emergency?
• Home medications, especially any recent changes? (Including over the counter decongestants.)
• Symptoms (including chest discomfort, dyspnea, weakness, visual disturbance, headache)?
• Illicit drug use? (31279421)

labs

• Chemistries.
  • ? Acute kidney injury.
• Complete blood count.
  • ? Schistocytes (implies true hypertensive emergency).
• Troponin (only if EKG/clinical evidence to support MI).
• Urinalysis.
• Urine toxicology screen may be considered.
• Pregnancy evaluation as appropriate.

other studies

• EKG.
• Non-contrast head CT, if presentation is worrisome for possible intracranial hemorrhage.

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diagnostic/therapeutic management of any obvious causes of hypertension

Before initiation of antihypertensives, consider some simple interventions which may be highly effective in reducing the blood pressure. Overlooking these factors may eventually lead to overshoot hypotension. For example, if pain is driving the hypertension but you initiate therapy with antihypertensives first, when the pain eventually resolves the patient may develop overshoot hypotension.

interventions that may rapidly reduce the blood pressure:

• Pain: Treat with appropriate analgesia.
• Agitation: Treat with antipsychotics or dexmedetomidine.
• Volume overload: Treat with diuresis or dialysis.
• Drug withdrawal: Treat appropriately, for example:
  • Alcohol withdrawal: Phenobarbital.
  • Clonidine/tizanidine withdrawal: Restart therapy.
• Urinary retention: Foley catheter.

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(4) Control Bp with IV antihypertensives

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blood pressure goal?

• There isn't solid evidence behind this. The following approach seems reasonable & consistent with guidelines: (29133354, 30165588)
  • (#1) The initial goal is to decrease the MAP by ~20% within 1-2 hours.
  • (#2) If this reduction is tolerated, then decrease the MAP to ~125 mm (~160/110 mm) over the next 2-6 hours.
  • (#3) The blood pressure may subsequently be gradually decreased further over a period of days, as clinically tolerated.
• Bp targets may need to be individualized. Consider what the patient's baseline pressure is, and how rapid the increase in pressure was.
  • Chronic severe hypertension: A more gradual approach to lowering the Bp may be wise.
  • Acute development of hypertension: More rapid reduction of Bp makes sense.
• 💡 Whenever possible, try to clearly define the baseline Bp (e.g., obtain multiple Bp readings in both arms before starting antihypertensives). Lack of a definite baseline Bp leads to uncertainty regarding all downstream Bp targets.

IV antihypertensives can be divided into three groups: 

• (1) Truly titratable agents
  • Duration of action is <<30 minutes.
  • The drug must be given as a continuous infusion. It is fairly easy to titrate.
  • Examples: Clevidipine, nitroglycerine, esmolol.
• (2) Quasi-titratable agents
  • Duration of action is <1-2 hours.
  • The drug is generally given as a continuous infusion, but it's a bit sluggish to titrate. Care is required to avoid medication accumulation, which may cause hypotension.
  • Examples: Nicardipine, diltiazem.
• (3) Bolus agents
  • Duration of action is >1-2 hours
  • The most sensible way to give the drug is via intermittent bolus doses. If an infusion is used, it will tend to accumulate and be difficult to titrate.
  • Examples: Labetalol, metoprolol.

preferred IV antihypertensive infusion

• Calcium channel infusions are usually the best agents. Most patients have excessive vasoconstriction, a physiologic problem which is corrected by calcium channel blockers.
  • Clevidipine might be the best agent, if available.
  • Nicardipine is an excellent choice, if clevidipine isn't available.

is an arterial line needed?

• There is no solid data on this.
• Indications for an arterial line might include:
  • Very labile blood pressures.
  • Profound hypertension (too high to be real?).
  • Clinical deterioration despite noninvasive management.
• An arterial line is probably unnecessary in most cases of hypertensive emergency, for the following reasons.
  • The pain of arterial line insertion can exacerbate hypertension.
  • No prospective evidence exists to show that this procedure is beneficial or necessary.
  • Bp targets are arbitrary and poorly defined. It's illogical to tightly chase after an arbitrary target.

if the blood pressure plummets, evaluate for hypovolemia and volume resuscitate if necessary

• Patients often have a combination of:
  • (1) Excessive vasoconstriction, which is driving their hypertension.
  • (2) Hypovolemia due to the diuretic effect of hypertension (“pressure diuresis”).
• When treated with vasodilation, these patients may develop hypotension (due to unmasking of their hypovolemia). Overall this may lead to wide fluctuations in blood pressure, which is difficult to control. Stabilizing these patients requires addressing both problems:
  • (1) Control excessive vasoconstriction with a vasodilator.
  • (2) Control hypovolemia with volume administration.

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nicardipine

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advantages & general comments 💊

• Excellent therapy for most patients with primary hypertensive emergency. Nicardipine is usually the workhorse agent in hospitals that don't have clevidipine.

drawbacks & contraindications

• Contraindications:
  • Cirrhosis (cleared by the liver).
• Drawbacks:
  • Longish half-life may give the infusion a tendency to accumulate and cause hypotension. This may be avoided by cutting the infusion back once the target blood pressure is reached (see “dose” section below).
  • May promote volume overload (nicardipine is often provided in a relatively dilute form that may cause substantial volume administration).
  • May cause headache, reflex tachycardia.

onset & duration

• Onset ~5-15 minutes.
• Efficacy lasts ~1 hour.
• Half-life: 2-4 hours.

dose

• Start at 5 mg/hr.
• If Bp is above target, increase by 2.5 mg/hr every 15-30 min, to a maximum rate of 15 mg/hour.
• When Bp reaches target, reduce the infusion to 3-5 mg/hr to prevent accumulation.
• If Bp falls below target, decrease infusion to 2.5 mg/hr or stop entirely.
  • If the blood pressure falls substantially below target, stop the infusion entirely.

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clevidipine

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advantages & general comments 💊

• Clevidipine is similar to nicardipine, but it has a shorter half-life which allows it to be a truly titratable agent.
  • Clevidipine has been shown to be more successful than nicardipine at achieving tight blood pressure control.(18806012) It's easier to use than nicardipine, with a lower risk of overshoot hypotension.
• Clevidipine is cleared by ester hydrolysis within the blood (so its clearance isn't affected by hepatic or renal dysfunction).(Vincent 2023)
• Clevidipine is provided in a milky lipid emulsion (similar to propofol).

drawbacks & contraindications

• Contraindications:
  • Hyperlipidemia, lipoid nephrosis, or acute pancreatitis.
• Drawbacks
  • Unavailable at many hospitals due to cost/acquisition barriers.
  • May cause reflex tachycardia, headache.

onset & duration

• Onset in ~3 minutes.
• Lasts ~10 minutes.

dose

• Start at 1-2 mg/hour
• Double every 2 minutes until Bp begins approaching target, then titrate by smaller increments every 5-10 minutes.
• Dose range is 1-32 mg/hour.

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IV labetalol

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general comments 💊

• Labetalol is a reasonable agent in most situations, especially if you're trying to drop the Bp by only a moderate amount (e.g., 10-30 mm). For severe hypertension, labetalol is less effective than nicardipine.(21707983)
• ⚠️ The problem with labetalol for hypertensive emergency is that labetalol often doesn't address the underlying physiological problem. The primary driver of most hypertensive emergencies is excessive afterload (vasoconstriction). However, labetalol works predominantly as a beta-blocker (with negative inotropic and negative chronotropic effects). Beta-blocking someone with excessive afterload could theoretically reduce the cardiac output and thereby promote systemic hypoperfusion.

drawbacks & contraindications

• Contraindications:
  • Bradycardia.
  • Heart block or sick sinus syndrome.
  • Cardiogenic pulmonary edema.
  • Asthma exacerbation.
  • Acute cocaine/sympathomimetic intoxication.
• Drawbacks:
  • Can cause bradycardia.
  • Nonselective beta-blocker, so it may cause hyperkalemia.
  • High doses may cause fetal bradycardia (>800 mg per day)(30165588)

onset & duration

• Onset in 5-10 minutes.(30165588)
• Lasts 3-6 hours.(30165588)

dose

• (#1) Start with sequential pushes of 20mg, 40mg, 80mg, 80mg, 80mg (q15 min PRN).
  • Escalating boluses of labetalol can be useful to achieve rapid control of severe hypertension at the bedside if this is needed (e.g. acute Bp spike which requires immediate control).
  • If a total dose of 300mg doesn’t work, switch to another agent.
  • Individual responses vary.
• (#2) Once Bp controlled, may use intermittent boluses to keep the blood pressure in range (e.g. 10-20 mg IV q10 minutes PRN).
  • The optimal bolus dose will vary between patients. This may be determined empirically as described above in #1. The goal of the bolus dose is to drop the Bp effectively, but not excessively.
  • The blood pressure must be monitored carefully, with repeat PRN doses used as necessary (figure below).
• Labetalol lasts ~2-4 hours, so it doesn't make sense to give it as a continuous infusion (a continuous infusion will gradually accumulate and eventually cause overshoot hypotension).

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medications to avoid

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nitroprusside is a poor choice in hypertensive emergency for several reasons:

• Nitroprusside can increase the intracranial pressure.
• Nitroprusside can cause cyanide toxicity and lactic acidosis – which may create a confusing picture if the patient deteriorates.
• Nitroprusside tends to cause wide swings in the blood pressure (requiring continuous close attention and meticulous titration).
• Nitroprusside causes coronary vasodilation, which may create a steal phenomenon that causes myocardial ischemia.
• One meta-analysis found that nitroprusside was associated with a higher mortality rate, as compared with clevidipine.(18806012)

intravenous hydralazine should generally be avoided:

• IV hydralazine has an unpredictable effect (sometimes it's minimally effective, sometimes it causes precipitous Bp drop).
• IV hydralazine is impossible to titrate (the duration of action is 2-4 hours).

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(5) Transition to oral antihypertensives

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when to start oral titration

• Start oral antihypertensives after the patient has stabilized and improved on IV antihypertensives for several hours.
• Oral antihypertensives may be gradually up-titrated, with simultaneous weaning off IV antihypertensives.

review the patient's home antihypertensives

• This may provide some clues regarding the dose and number of agents that will be required.
• In some cases, it may be appropriate to resume some or all of the patient's home antihypertensive regimen.

usually preferred agents

• 🏆 Nifedipine extended release 📖
  • Generally a good choice (essentially an oral equivalent of nicardipine).
  • It works rapidly and is effective.
  • The main drawback is that it cannot be crushed for administration via an enteral tube.
• Labetalol 📖
  • Usually a reasonable choice.

occasionally useful agents

• ACEi/ARBs 📖 may be preferred in selected situations:
  • Patients with systolic heart failure.
  • Patients previously on ACEi/ARB.
  • Patients with SCAPE (who are at risk of recurrent episodes of SCAPE).
  • Patients with renal failure on dialysis.
  • Front line therapy for patients with scleroderma renal crisis.
• Clonidine 💉
  • May provide some anxiolysis.
  • Especially useful in patients with incurrent withdrawal.
• Prazosin:
  • May be especially useful in patients with benign prostatic hyperplasia.
  • Pharmacokinetics: Onset in ~2 hrs, duration of action ~12 hours.
  • Dosing: Starting dose 1-2 mg q12 hours, maximal dose 10 mg q12.
• Oral hydralazine 💉

agents to avoid

• 💡 The ideal oral antihypertensive will take effect within a few hours. This allows for a prompt up-titration of oral doses, which allows rapid weaning of the IV antihypertensive agent.
• Amlodipine takes forever to work – this drug is an absolute slug and has no role here.
• Metoprolol drops the heart rate, but is relatively ineffective for controlling blood pressure.

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calcium channel blockers

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advantages & general comments

• These are essentially oral analogues of IV nicardipine or IV clevidipine. Similar to nicardipine or clevidipine, they are widely applicable and generally effective. Nifedipine XR and isradipine are favored here, due to their reasonably fast onset (unlike amlodipine, which takes days to work).
• Nifedipine extended release 💊 is generally an excellent choice. This can be used as a once-daily medication, facilitating transition to the ward and outpatient therapy.
  • (⚠️ Immediate release nifedipine can cause rapid drops in the pressure and shouldn't be used.)
• Isradipine 💊 is very fast-acting, but it has the drawback of being a bit more expensive and less widely available.

drawbacks & contraindications

• Nifedipine XR cannot be crushed and administered via feeding tube.

onset & duration

• Nifedipine XR:
  • Onset within ~2-4 hours.
  • Duration of action ~24 hours.
• Isradipine:
  • Onset within ~2 hours.
  • Duration of action ~10 hours.

dose

• Nifedipine XR:
  • Starting dose is 30-60 mg.
  • Max dose may vary depending on formulation (90 mg daily for Adelat CC, or 120 mg daily Procardia XL).
• Isradipine:
  • Start 2.5 mg q12.
  • Max dose 5 mg q12.

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PO labetalol

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advantages & general comments 💊

• Labetalol is traditionally a preferred oral antihypertensive for hypertensive emergency.
• As an alpha-beta blocker, labetalol is more effective at lowering blood pressure than pure beta-blockers (e.g., metoprolol).
• For patients who respond well to IV labetalol, a transition to oral labetalol makes sense. PRN doses of IV labetalol can be continued after starting oral labetalol for management of breakthrough hypertension. Meanwhile, the dose of oral labetalol may be gradually increased until no additional PRN IV doses are needed.

drawbacks & contraindications

• Contraindications:
  • Bradycardia.
  • Heart block or sick sinus syndrome.
  • Cardiogenic pulmonary edema.
  • Asthma exacerbation.
  • Cocaine/sympathomimetic toxicity.

onset & duration

• Onset in ~2 hours.
• Duration of ~10 hours.

dose

• Start 200 mg q12hr. If no effect is seen following the first dose, an additional dose may be considered after 2-4 hours, followed by a subsequent increase in the maintenance dose.
• Max dose 1,000 mg q12hr.  However, in pregnancy high doses may pose a risk of fetal bradycardia.(30165588)

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ACEi & ARB

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advantages & general comments

• Generally not utilized, for the following reasons:
  • Risk of renal failure.
  • Effects may be widely variable between patients, depending on the patient's level of endogenous activation of their renin/angiotensin/aldosterone system.
• Situations where ACEi/ARB may be useful:
  • (1) Patients with systolic heart failure.
  • (2) Patients previously on ACEi/ARB.
  • (3) Patients with SCAPE, who are at risk of recurrent episodes of SCAPE.
  • (4) Patients with renal failure on dialysis.
  • (5) Front line therapy for patients with scleroderma renal crisis.
• The optimal agent is probably oral captopril, because it has a fast onset and short duration of action (which allows for facile oral titration). Small captopril doses can be initiated cautiously and up-titrated as tolerated. Once the patient has been stabilized on captopril, this may eventually be transitioned to an equivalent dose of lisinopril using a 5:1 conversion (the total daily dose of captopril divided by five will approximate an equivalent lisinopril dose).(8773158) 🌊 Lisinopril is preferred for chronic therapy, since it can be given once daily.

drawbacks & contraindications

• Contraindications:
  • Hyperkalemia.
  • Renal failure (but not chronic ESRD on hemodialysis).
  • Prior intolerance or cough (especially with ACE inhibitors).
• Drawbacks:
  • Can promote renal failure, should be avoided if there is acute kidney injury or other nephrotoxic medications.

onset & duration

• Captopril:
  • Onset in 15-30 minutes.
  • Duration ~6 hours.
• Losartan or Telmisartan:
  • Onset in ~4-6 hours (Telmisartan has faster onset; losartan is slower if administered with food).
  • Duration ~24 hours.

dose 🌊

• Captopril 💊
  • Start 12.5 mg q8hr.
  • Max dose 50 mg q8hr.
• Losartan 💊
  • Start 50 mg daily.
  • Max dose 100 mg daily.
• Telmisartan 💊
  • Start 40 mg daily.
  • Max dose 80 mg daily.

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podcast

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questions & discussion

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To keep this page small and fast, questions & discussion about this post can be found on another page here.

• #1 most common mistake = overdiagnosis of hypertensive emergency among patients with scary high Bp but no target organ damage. This isn't a hypertensive emergency, please don't call the ICU for this. Thanks in advance.
• #2 most common mistake = treating hypertensive emergency too aggressively and dropping the Bp too much and too fast.
• #3 most common mistake = trying to transition from an antihypertensive infusion to an oral agent that takes a long time to have any effect on blood pressure (e.g. amlodipine). This causes patients to be stuck in the ICU on an infusion forever. It's also unpredictable when these drugs take effect, so there is a risk of dose-stacking (i.e. you keep up-titrating oral agents and eventually they all kick in simultaneously, causing hypotension).
• Generally avoid IV hydralazine; this has erratic effects and sometimes bottoms out the blood pressure.
• Don't use IV metoprolol for blood pressure control. Metoprolol isn't very effective for control of blood pressure, but it will slow down the heart rate. That actually makes matters worse, because then you can't use labetalol (since the patient is already bradycardic).

Guide to emoji hyperlinks

• = Link to online calculator.
• = Link to Medscape monograph about a drug.
• = Link to IBCC section about a drug.
• = Link to IBCC section covering that topic.
• = Link to FOAMed site with related information.
• 📄 = Link to open-access journal article.
• = Link to supplemental media.