Lutembacher Syndrome 

Updated: Dec 15, 2020
Author: Kamran Riaz, MD; Chief Editor: Yasmine S Ali, MD, MSCI, FACC, FACP 



Lutembacher syndrome is defined as a combination of mitral stenosis and a left-to-right shunt at the atrial level. Typically, the left-to-right shunt is an atrial septal defect (ASD) of the ostium secundum variety. Both these defects, ASD and mitral stenosis, can be either congenital or acquired.

The definition of Lutembacher syndrome has undergone many changes. The earliest description in medical literature is found in a letter written by anatomist Johann Friedrich Meckel to Albrecht von Haller in 1750.[1, 2] In 1916, Lutembacher described his first case of this syndrome, involving a 61-year-old woman, and he attributed the mitral valvular lesion to congenital mitral stenosis.[1, 3] Because the mitral stenosis was, in fact, rheumatic in etiology, the syndrome was defined eventually as a combination of congenital ASD and acquired, frequently rheumatic, mitral stenosis.

Thus, causes of mitral stenosis include the following:

  • Mitral stenosis, often but not always rheumatic in origin[4]

  • Congenital mitral stenosis (very rare)

  • ASD, either congenital or iatrogenic

In the current era of mitral valvuloplasty for acquired mitral stenosis, however, residual iatrogenic ASD secondary to transseptal puncture is more common than congenital ASD, as is the combination of ASD and mitral stenosis.[3] Although this syndrome is generally defined as mitral stenosis in combination with ASD, some have argued to define the syndrome as a combination of ASD and any mitral valve lesion, ie, mitral stenosis, mitral insufficiency, or mixed lesion. Currently, any combination of ASD, congenital or iatrogenic, and mitral stenosis, congenital or acquired, is referred as Lutembacher syndrome.


Mitral stenosis can be either congenital, as initially described, or acquired in origin, often due to rheumatic mitral valve disease. Isolated mitral stenosis is now known to be a rare congenital disorder, and many cases of mitral stenosis initially thought to be congenital were, in fact, caused by rheumatic mitral valve disease.

Similarly, understanding of the etiology of atrial septal defect (ASD) as associated with Lutembacher syndrome has evolved over time. Initially, high left atrial pressure due to mitral stenosis was thought to stretch open the patent foramen ovale (PFO), causing left-to-right shunt and providing another outlet for the left atrium. Now ASD in this syndrome, like mitral stenosis, is recognized as being either congenital or acquired, as already described.

Acquired ASD is almost always iatrogenic, either intentional or as a complication of a percutaneous interventional procedure. The incidence of left-to-right atrial shunt following mitral valvuloplasty is estimated at 11-12%. Although most of these ASDs are small and hemodynamically insignificant, some can be large enough to have hemodynamic consequences, especially in patients who develop restenosis of the mitral valve.

The hemodynamic effects of this syndrome are a result of the interplay between the relative effects of ASD and mitral stenosis. In its initial description, the ASD was typically large in Lutembacher syndrome, thus providing another route for blood flow. Iatrogenic ASDs tend to be smaller but still may be hemodynamically significant. The direction of blood flow is determined largely by the compliance of left and right ventricles. Normally, the right ventricle is more compliant than the left ventricle.

As a result, in the presence of mitral stenosis, blood flows to the right atrium through the ASD instead of going backward into the pulmonary veins, thus avoiding pulmonary congestion. This happens at the cost of progressive dilatation and, ultimately, failure of the right ventricle and reduced blood flow to the left ventricle. Development of Eisenmenger syndrome or irreversible pulmonary vascular disease is very uncommon in the presence of large ASD and high left atrial pressure because of mitral stenosis.

The term reverse Lutembacher syndrome is sometimes used to describe those rare cases in which a predominant right-to-left shunt develops owing to development of severe tricuspid stenosis.


United States statistics

The true incidence of Lutembacher syndrome is not clearly known. Although mitral stenosis is encountered in 4% of patients with an atrial septal defect (ASD), congenital mitral stenosis itself is very rare, accounting for only 0.6% of congenital heart disease cases at autopsy. The incidence of ASD in patients with mitral stenosis is 0.6-0.7%. In one US study, the combination was found in 5 of 25,000 autopsies. The syndrome was diagnosed more frequently in the past for the following reasons:

  • Without echocardiography, the combination of mid diastolic murmur, actually due to increased blood flow across the tricuspid valve, and systolic murmur of ASD led to a mistaken diagnosis of Lutembacher syndrome.

  • The prevalence of both rheumatic heart disease and mitral stenosis was higher in western developed countries before the antibiotic era. With the decline in the frequency of rheumatic fever, the prevalence of mitral stenosis has decreased and so has diagnosis of the syndrome. A history of rheumatic fever is frequently absent.

  • Even though ASD may be underdiagnosed in the United States, the combination of ASD and mitral stenosis may not be evident on physical examination and for that reason is best confirmed by echocardiography.

International statistics

Although the exact prevalence of Lutembacher syndrome is not known, it is probably higher in areas where rheumatic heart disease is still common.

Race-, sex-, and age-related demographics

No data are available regarding racial distribution of the condition.

Lutembacher syndrome is more common in females than males. Part of the reason is the higher incidence of both congenital ASD and rheumatic mitral stenosis in females.

This syndrome can present at any age. Cases have been diagnosed in the seventh decade of life. Lutembacher's original case was a 61-year-old woman who had been pregnant 7 times. In the current era of balloon mitral valvuloplasty and development of ASD, the age of presentation may change.


The overall prognosis is good for Lutembacher syndrome, especially in patients diagnosed early and without pulmonary hypertension. Patients with this condition have lived into their ninth decade without developing any cardiac symptoms, and women have had multiple pregnancies without complications.


No definite data are available regarding morbidity and mortality. Boths are related to the relative severity of the individual lesions.


Complications may include the following:

  • Pulmoary hypertension and right-sided heart failure

  • Atrial arrhythmias

  • Pulmonary congestion

  • Subacute bacterial endocarditis (SBE_

Patient Education

Educate patients regarding the basic anatomic defects and physiological consequences of Lutembacher syndrome.

Heart failure education should include the following:

  • Low-salt diet

  • Daily weighing

  • Early warning signs of worsening right or left heart failure

Educate patients regarding the role of bacterial endocarditis prophylaxis.




Patients may remain asymptomatic for many years. Symptoms are mainly due to the atrial septal defect (ASD), and signs and symptoms vary according to the size of the ASD. With a large ASD, symptoms of pulmonary congestion, typical of isolated mitral stenosis, do not appear until late in the course of the disease. Conversely, these symptoms may appear early if the patient has an associated small ASD or develops pulmonary hypertension for other reasons. Patients with large ASD and moderate-to-severe mitral stenosis have signs and symptoms due mainly to right ventricular overload and right-sided heart failure, while patients with a small ASD and moderate-to-severe mitral stenosis have signs and symptoms of pulmonary congestion typical of mitral stenosis. Note the following:

  • The patient may or may not have a history of rheumatic fever.

  • Fatigue and reduced exercise tolerance result from decreased systemic blood flow. The presence of mitral stenosis and left-to-right blood flow in diastole through the ASD reduces the forward flow of blood into the left ventricle, thereby reducing systemic blood flow and leading to fatigue and poor exercise tolerance.

  • Palpitations are a common presenting symptom. Because of the augmented left-to-right shunt caused by higher left atrial pressure and mitral stenosis, both atria are dilated. This predisposes patients to atrial arrhythmias; atrial fibrillation is very common.

  • Weight gain, ankle edema, right upper quadrant pain, and ascites are seen more commonly in patients with large ASD. Such symptoms are manifestations of the development of right-sided heart failure. A chronically increased left-to-right blood flow at the atrial level can eventually lead to right-sided heart failure.

  • Paroxysmal nocturnal dyspnea, orthopnea, and hemoptysis are signs of pulmonary venous congestion. Such symptoms are caused by mitral stenosis and are seen less frequently in Lutembacher syndrome than in isolated mitral stenosis. They are more common in patients with small ASD and are probably more common in patients who develop reverse Lutembacher syndrome. In some patients with large pulmonary blood flow due to a large left-to-right shunt, orthopnea can develop because of decreased compliance of the lungs.

Physical Examination

Physical examination reveals signs due to the atrial septal defect (ASD) and mitral stenosis, which are modified because of the presence of both lesions in the same patient.

Arterial pulse

  • Small volume

  • Rhythm regular or irregular: Atrial fibrillation is the most common arrhythmia

Jugular venous pulse

  • Distended jugular veins, even in the absence of right heart failure

  • Large a waves when sinus rhythm is present

  • Increased right ventricular pressure a more important determinant than equalization of atrial pressures in increasing jugular venous pressure

Precordial examination

  • Left parasternal lift, caused by transmitted right ventricular and pulmonary artery impulse, is common.

  • Left ventricular impulse is unimpressive, owing to reduced filling of the left ventricle secondary to mitral stenosis.

  • A tapping apex impulse due to the palpable, loud first heart sound of mitral stenosis may be present.

  • A diastolic thrill at the apex is unusual.

Heart sounds

A loud first heart sound, opening snap, and a mitral early-to-mid diastolic murmur are the classic auscultatory findings of mitral stenosis and are variably present.

  • Reduced transmitral pressure gradient resulting from decompression of the left atrium through the ASD and displacement of the left ventricular apex due to a large right ventricle attenuate these classic findings of mitral stenosis.

  • Development of pulmonary hypertension and, consequently, an increase in right atrial and left atrial pressures may increase transmitral pressure gradient and bring out these auscultatory findings, but this phenomenon is canceled by further dilatation of the right ventricle, thus obscuring the left ventricular apex.

The second heart sound (S2) may be widely split for 2 reasons. Increased right heart flow of ASD can result in late closure of the pulmonary component of the S2, and decreased left ventricular and aortic flow, secondary to mitral stenosis and ASD, can cause early closure of the aortic component of S2.

Additional heart sounds and murmurs

Third and fourth heart sounds of right ventricular origin may be audible at the left sternal border and are louder with inspiration.

Systolic murmurs are due to the following:

  • ASD along the upper left parasternal area - Typically a flow murmur due to increased flow across the pulmonic valve

  • Tricuspid regurgitation along the lower left parasternal area - Due to the displaced tricuspid valve secondary to right ventricular dilatation; common

  • Holosystolic murmur at the left parasternal area due to tricuspid regurgitation - Usually increases with inspiration (Carvallo sign), which differentiates it from ASD and mitral regurgitation

Mid-diastolic murmurs are due to the following:

  • Increased flow across the tricuspid valve due to ASD or accompanying tricuspid stenosis, best heard at left lower sternal border or at apex for reasons already mentioned

  • Mitral stenosis, best heard with stethoscope bell at apex after exercise and with patient in left lateral position

Continuous murmur in the lower right sternal area is due to continuous shunting of blood across a small ASD in the presence of severe mitral stenosis. This is an unusual finding on physical examination.


Ascites and hepatomegaly may be noted in the presence of right heart failure.


Ankle edema may be present in the presence of right-sided heart failure.





Imaging Studies

Chest radiography

Chest radiographs of patients with Lutembacher syndrome may include the following findings:

  • Pulmonary plethora due to left-to-right shunt

  • Mild left atrial enlargement

  • Right ventricular enlargement

  • Pulmonary artery enlargement

  • Mitral valve calcification late in life

  • Pulmonary vascular congestion and marked left atrial enlargement in cases of severe mitral stenosis and small ASD


Transthoracic (TTE) or transesophageal echocardiography (TEE) findings during various stages of the disease may show features outlined below.[3]

Two-dimensional echocardiography

  • Large left atrium

  • Large right atrium and ventricle

  • Enlarged pulmonary artery

  • Atrial septal defect (ASD)

  • Stenotic mitral valve

See the following images.

Lutembacher Syndrome. This is a two-dimensional tr Lutembacher Syndrome. This is a two-dimensional transesophageal echocardiogram during diastole in a 74-year-old woman who presented with signs of right-sided heart failure. Note the thickened, narrowed, and calcified mitral valve apparatus and doming of the anterior leaflet of the mitral valve.

Color flow and Doppler imaging

This imaging modality confirms the presence and evaluates the severity of ASD, mitral stenosis and mitral regurgitation, tricuspid regurgitation, and pulmonary pressure (see the images below).[5]

Lutembacher Syndrome. This color-flow imaging of a Lutembacher Syndrome. This color-flow imaging of a 74-year-old woman who presented with signs of right-sided heart failure on transthoracic echocardiogram (TTE) demonstrates an anteriorly directed jet of moderate mitral regurgitation.
Lutembacher Syndrome. This color-flow imaging (sub Lutembacher Syndrome. This color-flow imaging (subcostal view) on transthoracic echocardiogram shows the left-to-right shunt across the atrial septum of a 74-year-old woman who presented with signs of right-sided heart failure.
Lutembacher Syndrome. This is a color-flow image d Lutembacher Syndrome. This is a color-flow image during transesophageal echocardiography at the mitral valve level of a 74-year-old woman who presented with signs of right-sided heart failure. Note the anteriorly directed jet of moderate-to-severe mitral regurgitation during systole.
Lutembacher Syndrome. This color-flow imaging duri Lutembacher Syndrome. This color-flow imaging during transesophageal echocardiography shows blood flow across the atrial septum in a 74-year-old woman who presented with signs of right-sided heart failure.
Lutembacher Syndrome. These are Doppler measuremen Lutembacher Syndrome. These are Doppler measurements at the mitral inflow level of a 74-year-old woman who presented with signs of right-sided heart failure. Note the reduced E-A slope and a peak transmitral velocity giving rise to a peak transmitral gradient of 21 mmHg.
Lutembacher Syndrome. Doppler measurement across t Lutembacher Syndrome. Doppler measurement across the atrial septum reveals a peak velocity of 4 m/s of a 74-year-old woman who presented with signs of right-sided heart failure.

Doppler pressure half-time method

This technique usually overestimates the mitral valve area. Because of the presence of ASD, the transmitral pressure gradient is generally lower than expected for the degree of the mitral stenosis, thereby falsely underestimating the pressure half-time and overestimating the mitral valve area. On the other hand, planimetry and the Doppler continuity equation method should give an accurate assessment of the mitral valve area in Lutembacher syndrome.[6]

Transesophageal echocardiography

TEE be required to differentiate between the patent foramen ovale from the ASD and to fully delineate the anatomy.

Other Tests

Other tests in the workup of mitral stenosis may include those outlined below.



  • Sinus rhythm

  • Atrial fibrillation

P wave morphology

  • Tall, broad, or bifid in lead II with a deep negative force in V1 suggesting biatrial enlargement

  • Isolated left atrial abnormality more indicative of a more severe mitral stenosis with small atrial septal defect (ASD)

QRS morphology and axis

  • Right-axis deviation

  • Complete or incomplete right bundle-branch block or right ventricular hypertrophy


Cardiac catherization

Cardiac catheterization is not performed routinely to confirm the diagnosis of Lutembacher syndrome. It can be used, however, to evaluate the severity of the atrial septal defect, detect reversible pulmonary hypertension, measure the mitral valve area by the Gorlin formula, and evaluate the presence of coronary artery disease in high-risk patients.



Medical Care

Diuretics may be used for symptomatic relief of right-sided heart failure. 

Digoxin, beta blockers, and calcium channel blockers are used mainly for rate control of atrial arrhythmias, whereas amiodarone and sotalol are used not only for rate control but also for conversion into and maintenance of normal sinus rhythm.

Patients with Lutembacher syndrome who have undergone complete repair with prosthetic material or a device need subacute bacterial endocarditis (SBE) prophylaxis for the first 6 months after the repair procedure. In addition, patients with previous history of endocarditis warrant SBE prophylaxis.

Diet and activity

Patients should adhere to a low-sodium diet. Activity should be as tolerated by the patient.


Consultation with a cardiothoracic surgeon or interventional cardiologist may be indicated.

Surgical Care

Until relatively recently, surgery was the only definite curative treatment available for Lutembacher syndrome and involved closure of the atrial septal defect (ASD) and mitral commissurotomy or mitral valve replacement.[7]

Percutaneous closure of ASD and mitral balloon valvuloplasty[8, 9, 10, 11, 12] ​

Percutaneous closure of the ASD with a clamshell device and mitral valvuloplasty provides a nonsurgical approach to correct these defects. Although mitral valvuloplasty has been performed for several decades, percutaneous closure of an ASD with a device represents a still-developing technology.

As already described, mitral valvuloplasty alone can be complicated by development of ASD secondary to transseptal puncture performed as a part of the procedure.

More recently, percutaneous transcatheter treatment with Accura balloon valvuloplasty and Amplatzer septal occluder device closure has been used for successful management of an 18 year old with congenital ASD and acquired rheumatic mitral stenosis.[13]

Indications for surgery or percutaneous intervention include the following:

  • ASD with a Qp/Qs ratio of more than 1.5

  • Moderate-to-severe mitral stenosis

  • Any degree of pulmonary hypertension, except individuals with irreversible pulmonary hypertension (Eisenmenger syndrome, see below)

Surgery is now performed early rather than late because the rates of heart failure and cardiac arrhythmia increase with age. Patients with pulmonary hypertension should demonstrate reversibility of pulmonary vascular resistance prior to surgical (or percutaneous) correction of ASD. Patients with pulmonary hypertension and irreversibly increased pulmonary vascular resistance (ie, Eisenmenger physiology) invariably develop progressive right-sided heart failure after ASD closure and die.

The symptoms of Lutembacher syndrome depend upon the size of the atrial septal defect, severity of mitral stenosis, compliance of the right ventricle, and pulmonary artery hypertension. Khanna et al reported on a patient with Lutembacher syndrome who had severe pulmonary hypertension and underwent successful surgical repair.[14]

Long-Term Monitoring

Follow-up care of patients with Lutembacher syndrome includes subacute bacterial endocarditis prophylaxis and surveillance for worsening signs or symptoms of heart failure. Periodic echocardiograms are indicated to assess the severity of mitral stenosis and the magnitude of left-to-right shunt and pulmonary artery pressure.

Periodic assessment of the following:

  • Blood urea nitrogen (BUN) levels

  • Creatinine levels

  • Serum electrolyte levels in patients taking diuretics



Guidelines Summary

The European Society of Cardiology (ESC) updated their 2010 guidelines on the management of adult congenital heart disease (ACHD) in 2020.[15, 16]  Class I and III recommendations regarding ACHD and atrial septal defect (ASD) are outlined below.

Refer CHD patients with documented arrhythmias or at high risk for postprocedural arrhythmias (eg, atrial septal defect [ASD] closure at older age) considered for percutaneous or surgical (re)interventions to a center with a multidisciplinary team with expertise in these interventions and in invasive treatment of arrhythmias.

ASD (native and residual)

ASD closure is recommended regardless of symptoms in those with evidence of right ventricular (RV) volume overload without pulmonary artery hypertension (PAH) (no noninvasive signs of pulmonary arterial pressure [PAP] elevation or invasive proof of pulmonary vascular resistance [PVR] < 3 Wood units [WU] in case of such signs) or left ventricular (LV) disease.

Device closure is recommended as the method of choice for secundum ASD closure when technically suitable. In seniors not candidates for device closure, carefully weigh the surgical risk against the potential benefit of ASD closure.

In patients with noninvasive signs of PAP elevation, invasive PVR measurement is required. In patients with LV disease, perform balloon testing, and carefully weigh the benefit of eliminating left-to-right (LR) shunt against the potential negative impact of ASD closure on outcome due to an increase in filling pressure (when considering closure, fenestrated closure, and no closure).

ASD closure is not recommended in those with Eisenmenger physiology, those with PAH and PVR ≥5 WU despite targeted PAH treatment, or exercise desaturation.



Medication Summary

The goals of pharmacotherapy are to reduce morbidity and to prevent complications.


Class Summary

These agents inhibit sodium and chloride reabsorption. They are used to treat right-sided heart failure.

Furosemide (Lasix)

Increases excretion of water by interfering with chloride-binding cotransport system, which inhibits sodium and chloride reabsorption in ascending loop of Henle and distal renal tubule. Dose must be individualized to patient. Depending on response, administer at increments of 20-40 mg, no sooner than 6-8 h after previous dose, until desired diuresis occurs. When treating infants, titrate with 1-mg/kg/dose increments until satisfactory effect achieved.

Cardiac glycosides

Class Summary

These agents are used to treat atrial arrhythmias. They have both direct and indirect effects.

Digoxin (Lanoxin)

Cardiac glycoside with direct inotropic effects in addition to indirect effects on cardiovascular system. Acts directly on cardiac muscle, increasing myocardial systolic contractions. Indirect actions result in increased carotid sinus nerve activity and enhanced sympathetic withdrawal for any given increase in mean arterial pressure.

Antibiotics, prophylactic

Class Summary

These agents provide prophylaxis for subacute bacterial endocarditis (SBE). Patients with Lutembacher syndrome are at high risk for SBE owing to associated mitral stenosis.

Cephalexin (Keflex)

First-generation cephalosporin that inhibits bacterial replication by inhibiting bacterial cell wall synthesis. Bactericidal and effective against rapidly growing organisms forming cell walls.

Resistance occurs by alteration of penicillin-binding proteins. Effective for treatment of infections caused by streptococcal or staphylococcal infection, including penicillinase-producing staphylococci. May use to initiate therapy when streptococcal or staphylococcal infection is suspected.

Used orally when outpatient management is indicated. Primarily active against skin flora, including Staphylococcus aureus.

Amoxicillin (Amoxil, Trimox)

Interferes with synthesis of cell wall mucopeptides during active multiplication, resulting in bactericidal activity against susceptible bacteria. Used as prophylaxis in minor procedures.

Ampicillin (Marcillin, Omnipen)

For prophylaxis in patients undergoing dental, oral, or respiratory tract procedures. Coadministered with gentamicin for prophylaxis in GI or genitourinary procedures.

Clindamycin (Cleocin)

Used in penicillin-allergic patients undergoing dental, oral, or respiratory tract procedures. Useful for treatment against streptococcal and most staphylococcal infections.

Gentamicin (Garamycin)

Aminoglycoside antibiotic for gram-negative coverage. Used in combination with both an agent against gram-positive organisms and one that covers anaerobes. Used in conjunction with ampicillin or vancomycin for prophylaxis in GI or genitourinary procedures.

Vancomycin (Vancocin)

Potent antibiotic directed against gram-positive organisms and active against Enterococcus species. Useful in treatment of septicemia and skin structure infections. Indicated for patients who cannot receive, or have failed to respond to, penicillins and cephalosporins or have infections with resistant staphylococci. Use CrCl to adjust dose in patients diagnosed with renal impairment. Used in conjunction with gentamicin for prophylaxis in patients with penicillin allergy undergoing GI or genitourinary procedures.

Erythromycin (EES, E-Mycin, Eryc)

Used for prophylaxis in patients with penicillin allergy undergoing dental, oral, or respiratory tract procedures.

Cefazolin (Ancef)

First-generation semisynthetic cephalosporins that arrest bacterial cell wall synthesis, inhibiting bacterial growth. Primarily active against skin flora, including Staphylococcus aureus.

Azithromycin (Zithromax)

Macrolide antibiotics which inhibit bacterial growth, possibly by blocking dissociation of peptidyl tRNA from ribosomes, causing RNA-dependent protein synthesis to arrest.

Cefadroxil (Duricef)

First generation semisynthetic cephalosporin that arrests bacterial growth by inhibiting bacterial cell wall synthesis. Bactericidal activity against rapidly growing organisms. Primarily active against skin flora, including Staphylococcus aureus.

Clarithromycin (Biaxin)

Semisynthetic macrolide antibiotic that reversibly binds to P site of 50S ribosomal subunit of susceptible organisms and may inhibit RNA-dependent protein synthesis by stimulating dissociation of peptidyl t-RNA from ribosomes, causing bacterial growth inhibition.


Class Summary

These agents alter the electrophysiologic mechanisms responsible for arrhythmia.

Amiodarone (Cordarone)

May inhibit AV conduction and sinus node function. Prolongs action potential and refractory period in myocardium and inhibits adrenergic stimulation. Prior to administration, control ventricular rate and CHF (if present) with digoxin or calcium channel blockers.

Diltiazem (Cardizem, Dilacor, Tiamate, Tiazac)

During depolarization, inhibits calcium ions from entering slow channels and voltage-sensitive areas of vascular smooth muscle and myocardium.

Verapamil (Calan, Covera, Verelan, Isoptin)

Can diminish PVCs associated with perfusion therapy and decrease risk of ventricular fibrillation and ventricular tachycardia. By interrupting reentry at AV node, can restore normal sinus rhythm in patients with paroxysmal supraventricular tachycardias (PSVT).

Sotalol (Betapace)

Class III anti-arrhythmic agent that blocks potassium channels, prolongs action potential duration (APD), and lengthens QT interval. Noncardiac selective beta-adrenergic blocker.

Esmolol (Brevibloc)

Excellent drug for patients at risk for complications from beta-blockade (particularly those with reactive airway disease, mild-to-moderate LV dysfunction, and/or peripheral vascular disease). Short half-life of 8 min allows for titration to desired effect and quick discontinuation if needed.