AUGUST 2022 | VOLUME 24 | ISSUE 8

Emergency Medicine Practice Evidence-Based Education • Practical Application

CLINICAL CHALLENGES:
• What are the signs and symptoms
of acute valvular emergencies?
• What physical examination
findings differentiate valvular
emergencies?
• What diagnostic testing should
you use to diagnose valvular
emergencies?

Authors
Adam Sigal, MD
Associate Program Director, Emergency
Medicine Residency; Research Director,
Department of Emergency Medicine, Reading
Hospital, West Reading, PA

Stephanie Costa, MD
Department of Emergency Medicine, Reading
Hospital, West Reading, PA

Peer Reviewers Managing Acute Cardiac

Abbas Husain, MD
Associate Program Director, Associate
Professor of Emergency Medicine, Northwell
Health, New Hyde Park, NY
Evan Leibner, MD
Assistant Professor of Emergency Medicine,
Department of Emergency Medicine; Icahn
School of Medicine at Mount Sinai; Attending
Physician, Emergency Medicine and Cardiac
ICU; Director of Simulation Institute for Critical
Care Medicine, The Mount Sinai Hospital; New
York, NY
Prior to beginning this activity, see “CME
Information” on page 2.
Valvular Emergencies in the
Emergency Department
n Abstract
Valvular heart disease is becoming more prevalent as the United
States’ population ages, with aortic and mitral valves most
commonly affected. Complications, including syncope, heart
failure, dyspnea, and chest pain, can arise from slow progression
of stenosis and regurgitation, though acute regurgitation from
an ischemic or traumatic event can be life-threatening. Patients
with valvular disease may present with cardiogenic shock, and
vasoactive agent treatment will depend on determination of the
valvular etiology. This issue reviews aortic and mitral valvular
disease as potential causes of a patient’s emergency department
presentation, including history, diagnostic testing, and physical
examination findings that can help guide treatment.

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This issue is eligible for CME credit. See page 2. EBMEDICINE.NET

 CME Information
Date of Original Release: August 1, 2022. Date of most recent review: July 10, 2022. Termination date: August 1, 2025.
Accreditation: EB Medicine is accredited by the Accreditation Council for Continuing Medical Education (ACCME) to provide continuing
medical education for physicians.
Credit Designation: EB Medicine designates this enduring material for a maximum of 4 AMA PRA Category 1 CreditsTM. Physicians should claim
only the credit commensurate with the extent of their participation in the activity.
Specialty CME: Not applicable. For more information, call Customer Service at 678-366-7933.
ACEP Accreditation: Emergency Medicine Practice is approved by the American College of Emergency Physicians for 48 hours of ACEP Category I
credit per annual subscription.
AAFP Accreditation: The AAFP has reviewed Emergency Medicine Practice, and deemed it acceptable for AAFP credit. Term of approval is from
07/01/2022 to 06/30/2023. Physicians should claim only the credit commensurate with the extent of their participation in the activity. This session, Man-
aging Acute Cardiac Valve Emergencies in the Emergency Department, is approved for 4.0 enduring material AAFP Prescribed credits.
AOA Accreditation: Emergency Medicine Practice is eligible for 4 Category 2-A or 2-B credit hours per issue by the American Osteopathic Association.
Needs Assessment: The need for this educational activity was determined by a practice gap analysis; a survey of medical staff, including the editorial
board of this publication; review of morbidity and mortality data from the CDC, AHA, NCHS, and ACEP; and evaluation responses from prior educa-
tional activities for emergency physicians.
Target Audience: This enduring material is designed for emergency medicine physicians, physician assistants, nurse practitioners, and residents.
Goals: Upon completion of this activity, you should be able to: (1) identify areas in practice that require modification to be consistent with current
evidence in order to improve competence and performance; (2) develop strategies to accurately diagnose and treat both common and critical ED pre-
sentations; and (3) demonstrate informed medical decision-making based on the strongest clinical evidence.
CME Objectives: Upon completion of this activity, you should be able to: (1) describe the etiologies of common cardiac valve diseases, including aortic ste-
nosis, mitral stenosis, aortic regurgitation, and mitral regurgitation; (2) list the diagnostic studies required, based on patient history and physical examination;
and (3) determine treatment of valvular emergencies based on staging and patient needs.
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that is outside Food and Drug Administration approved labeling. Information presented as part of this activity is intended solely as continuing medical
education and is not intended to promote off-label use of any pharmaceutical product.
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financial relationships based on each individual's role(s). Please find disclosure information for this activity below:
Planners Faculty
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• Andy Jagoda, MD (Editor-in-Chief): • Stephanie Costa, MD (Author): Nothing to Disclose
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 Case Presentations
A 65-year-old woman with a history of coronary artery disease presents complaining of chest pain
and sudden onset of feeling short of breath…
• The patient had presented to the ED the week before with chest pain and was discharged after normal
serial cardiac troponins and serial ECGs, and an unremarkable chest radiograph. The patient reports
CASE 1

that 1 week ago, she ran out of her aspirin and clopidogrel.
• As you enter the room, you note the patient has an increased work of breathing. Vital signs are: heart
rate, 105 beats/min; blood pressure, 100/75 mm Hg; respiratory rate, 28 breaths/min; temperature,
37.4°C; and oxygen saturation, 89% on room air.
• Your exam is concerning for new-onset heart failure with pulmonary congestion and jugular venous
distention. When you auscultate a new cardiac murmur, you are concerned about an ischemia-induced
valvulopathy. You consider what would be the best way to manage this patient….

An 85-year-old woman is brought in by EMS after a syncopal event...

• The patient reports that she was reading a book in her house when she lost consciousness, and her
family called for help.
CASE 2

• On exam, the woman is resting quietly on the stretcher with no complaints. Her vital signs are: heart
rate, 75 beats/min; blood pressure, 155/85 mm Hg; respiratory rate, 18 breaths/min; temperature,
37.4°C; and oxygen saturation, 96% on room air.
• Your physical exam is significant for a harsh holosystolic murmur in the second right intercostal space.
• You wonder whether aortic valve disease is the cause of her syncope, and what therapeutic
interventions are needed at this time . . .

A 22-year-old man complaining of chest pain is brought in by EMS from the scene of a motor vehicle
accident…
• The patient is speaking, but he is clearly in distress.
CASE 3

• He is diaphoretic, and his vital signs are: heart rate, 115 beats/min; blood pressure, 85/50 mm Hg;
respiratory rate, 18 breaths/min; temperature, 37°C; and oxygen saturation, 96% on room air.
• You move him quickly to the resuscitation room, where a chest x-ray shows a widened mediastinum.
You hear a diastolic murmur on cardiac auscultation.
• You consider how best to correlate the radiologic and physical exam findings . . .

n Introduction This issue of Emergency Medicine Practice

Cardiac valvular disease is an important consideration
on the differential diagnosis for complaints of chest
discomfort, dyspnea, and syncope. The 2000 United
States’ census reported that the overall prevalence of
valve diseases was 2.5%, with an overrepresentation
in the elderly population.1 As the United States’ pop-
ulation ages, there are increases in mitral and aortic
valve disease, with men having a higher prevalence
of aortic stenosis.1 Nonetheless, with women’s longer
life expectancy, the prevalence of aortic stenosis may
be greater in women due to a potential sample bias.2
Singh et al showed that men and women are more
likely to have trace mitral regurgitation and tricuspid
regurgitation rather than severe mitral/tricuspid regur-
gitation.3 Both sexes also showed a low prevalence
of aortic regurgitation across all age groups; however,
the severity of regurgitation increased with age.3
Other comorbid conditions observed with specific
valve diseases include congestive heart failure and
myocardial infarction.
discusses pathologies related primarily to the aortic
valve and mitral valve. The tricuspid and pulmonic
valves will be briefly mentioned, as pathologies
affecting these valves infrequently result in acute
presentations to the emergency department (ED).
However, their pathology can compound dysfunction
and disease in the presence of aortic and mitral
disease. Recognition of underlying valvular disease
resulting in acute presentations will aid in directed
treatment and proper disposition of patients.
n Critical Appraisal of the Literature
Literature for this review was obtained by searching
PubMed, using the search terms: aortic regurgita-
tion, ARISTOTLE Trial, epidemiology of valvular
disease, fluid management in cardiac valvular disease,
fluid resuscitation in cardiac valvular disease, mitral
stenosis AND valvular emergencies, mitral steno-
sis presentation, prehospital chest pain, prosthetic

AUGUST 2022 • www.ebmedicine.net 3 © 2022 EB MEDICINE. ALL RIGHTS RESERVED.

valve thrombosis, pulmonary valve regurgitation,
tricuspid valve stenosis, tricuspid valve pathology,
and TTE cost. Searches were filtered by English
language articles published within the last 10 years.
We searched for clinical trials, meta-analyses, reviews,
and systematic reviews. Literature was also obtained
by searching Google Scholar for prehospital manage-
ment of cardiogenic shock. Selected studies from the
bibliographies and references of the papers initially
searched were also obtained, if the initial clinical trial
was relevant.
n Etiology and Pathophysiology
Aortic Valve Disease
Aortic stenosis results from degeneration,
calcification, or rheumatic heart disease.4,5 Aortic
stenosis can be secondary to a bicuspid aortic
valve, which is a less common etiology of aortic
regurgitation. When patients are diagnosed with a
bicuspid valve, they also need to be screened for an
aortic aneurysm. Illustrations of valve pathologies can
be seen in Figure 1.
Aortic stenosis is associated with other valvular
pathologies. Aortic stenosis causes ventricular
remodeling and subsequent mitral valve disease in
most cases, and tricuspid disease if the underlying
aortic stenosis pathology is rheumatic in origin. Aortic
Figure 1. Aortic Valve Pathology
Abbreviations: LCA, left coronary artery; RCA, right coronary artery.
Used with permission of Elsevier Science & Technology Journals. From The Practice of Clinical Echocardiography. Catherine Otto, Ed. Nikolaus Jander,
Jan Minners. Sixth edition. 2021. Permission conveyed through Copyright Clearance Center, Inc.
AUGUST 2022 • www.ebmedicine.net
regurgitation is commonly observed with aortic
stenosis. Mitral regurgitation is commonly seen as
a concomitant valve disease, due to the left-sided
heart changes that take place in the setting of aortic
stenosis. When rheumatic heart disease is primary,
mitral stenosis can accompany aortic stenosis.
Aortic regurgitation may be due to an aortic root
malfunction (as in bicuspid aortic valve), root dilation
from congenital syndromes such as Marfan syndrome,
and leaflet lesions due to current or prior disease pro-
cesses.2,6 Because chronic aortic regurgitation patho-
physiology results in left ventricular enlargement with
increased compliance, cardiac output is maintained
through increased stroke volume.4
Mitral Valve Disease
Mitral stenosis can be due to rheumatic disease,
aging, or radiation damage to valve leaflets.
Rheumatic disease causes commissural fusion
in young patients, and calcified leaflets with
commissural fusion in older patients. The commissural
fusion is generally not appreciated in non–rheumatic
mitral stenosis.7 Calcified valves are common causes
of mitral stenosis in the aging population and as
secondary valvular pathology, especially in aortic
stenosis.2 Leaflet disease can then be compounded
by chordal disease, including fusion and shortening,
all impeding flow. Patients from areas endemic for
4 ©2022 EB MEDICINE
rheumatic heart disease or patients of advanced age
should be screened for valvular dysfunction.
Patients can have acute or chronic presentations
of mitral regurgitation. Acute presentations result
from chordal rupture, infection, or ischemia leading
to papillary muscle rupture. Chronic presentations
can be caused by mitral valve prolapse, rheumatic
disease, endocarditis, dilated cardiomyopathy,
posterior wall myocardial infarction, or other structural
defects that affect the mitral valve. Mitral valve
prolapse is a potential etiology of mitral regurgitation,
with acute presentation involving atrial fibrillation
or chordal rupture, leading to acute onset of
regurgitation. More insidious complications of mitral
valve prolapse with mitral regurgitation are natural
progressions of disease and infective endocarditis.6
Important to note is that left ventricular outflow tract
obstructions can pull mitral valve leaflets, leading
to mitral regurgitation, and can be an important
component in hypotensive patients who have a
history of recent mitral or aortic valve surgery not
responsive to inotropes.8 Over time, the chronic
mitral regurgitation leads to left-sided heart overload.
Tricuspid and Pulmonary Valve Disease
Tricuspid valve disease is uncommon, but important
to understand, as this can indicate left-sided valve
pathology.9 Organic etiologies of tricuspid disease
are due to leaflet pathology or damage.10 Tricuspid
valve stenosis is most often due to congenital
defects, masses, or rheumatic disease. Tricuspid
valve regurgitation etiologies include congenital
defects, endocarditis, medication, radiation exposure,
cardiac device placement, and trauma. Additional
etiologies include pulmonary hypertension, tricuspid
valve prolapse, and acute right ventricle dilation. For
example, a pulmonary embolus could potentially
cause this valvular condition if right ventricular
pathology developed.
Because pulmonary valvular disease is even more
uncommon than tricuspid disease, it will be briefly
mentioned here only for completeness. Pulmonary
valve stenosis is usually secondary to congenital
conditions, and will improve with age.6 Pulmonary
valve regurgitation is due to pulmonary hypertension
or post-surgical or post-infectious etiologies, and is
appreciated with a diastolic murmur on examination.
n Differential Diagnosis
With valvular heart disease, patients often present
with dyspnea or shock, but they can also present with
signs and symptoms similar to myocardial infarction,
heart failure, and many other disease states. Some
symptoms of acutely decompensated valvular
disease include altered mental status and signs of
heart failure with cardiogenic shock, including poor
peripheral perfusion, pulmonary congestion, and
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oliguria. Therefore, the differential diagnosis for this
symptomatology includes some of the most common
cardiac and pulmonary causes of dyspnea, including
acute coronary syndromes (ACS), pulmonary
embolism, tamponade, chronic obstructive pulmonary
disease (COPD), pneumonia, or pneumothorax.
Nonetheless, as common diagnoses become less
likely based on the history, physical examination, and
ancillary testing, valvular pathology becomes more
important to consider.
n Prehospital Care
Prehospital providers are experienced in triaging
patients with chest pain and shortness of breath.
According to the National Model EMS [emergency
medical services] Clinical Guidelines, EMS providers
recognize certain presentations, such as chest pain,
shortness of breath, and diaphoresis as concerning
for ACS; however, atypical presentations of chest
pain are not specifically addressed in the national
guidelines.11 EMS personnel should obtain a past
medical history (such as prior myocardial infarction
or percutaneous coronary intervention and
hyperlipidemia) and a medication list, especially
indicating aspirin use, to help direct the differential
diagnosis and potentially treat the patient en route
to the hospital. However, atypical presentations such
as no history of prior coronary revascularization and
subtle electrocardiogram (ECG) findings may lead to
an initial misdiagnosis in the prehospital setting.12
Therefore, a history of prior cardiac surgery or cardiac
valve replacement should alert providers to atypical
ACS. Another clue to a potential underlying valvular
disorder may be symptoms of heart failure or COPD
without a prior history of that disease. Any history
obtained or examination findings that could indicate
valvular disease should be teased out.
In the presence of a shock state, priority is given
to rapid evaluation and stabilization of the patient,
including obtaining vital signs; assessing the airway,
respiratory status, and breathing; obtaining an ECG
and monitoring for arrhythmias; blood glucose
check, and obtaining intravenous (IV) access. In the
shock state, the guidelines recommend initiating IV
crystalloid fluids and vasoactive medications, with
the caveat that if the patient deteriorates or develops
rales after fluid administration, consider cardiogenic
shock and stop IV fluid administration.11
In the evaluation of syncope, EMS are recom-
mended to take a full history of events that preceded
the loss of postural tone and consciousness. Key
aspects of the history that EMS should obtain include
preceding events such as exertion, involuntary move-
ments, body position, and any prodromal symptoms
such as lightheadedness. The guidelines state that
examinations should include neurologic, pulmonary,
abdominal, and cardiovascular, including vital signs,
5 © 2022 EB MEDICINE. ALL RIGHTS RESERVED.
cardiac monitoring, and 12-lead ECG.11 There are
details given based on recognition and treatment of
arrhythmias. The guidelines stress that syncope can
be caused directly by aortic stenosis, among other
cardiovascular pathology.11
For any patient presenting with chest pain,
dyspnea, systemic congestion, pulmonary congestion,
or poor perfusion, initial steps performed by EMS
include obtaining a full set of vital signs, a 12-lead
ECG, and initial management of symptoms or vital
sign abnormalities.13 EMS should initiate noninvasive
ventilation, diuretics, and/or nitrates for pulmonary
edema, fluid overload, and elevated blood pressure,
respectively.13 However, keeping valvular disease on
the differential is important, as common prehospital
interventions, such as IV crystalloid fluids or nitrates,
may be detrimental to patient stability and survival.
n Emergency Department Evaluation
History
There are a few key pieces of information that would
indicate not only whether the etiology was potentially
valvular in nature, but also which valve may be the
primary culprit.
Aortic Stenosis
Presentations of syncope, heart failure, and angina
occur once the aortic stenosis is severe; otherwise,
a murmur may be the only suggestion of aortic
stenotic disease. The patient may not present with
chest pain, making a good physical examination
and high suspicion highly important. Patients may
also present with cardiac ischemic-like events,
either postexertional or postprocedural. In a study
by Lumley et al, aortic stenosis patients were
found to be at risk for ischemic events due to
the inability to compensate for increased cardiac
demand requirements.14 Therefore, events due to
aortic stenosis may present after exertion or while
undergoing anesthesia, due to vasodilation.
Aortic Regurgitation
The acute presentation of aortic regurgitation, in
which compensatory changes to the left ventricle and
left atrium have not had time to occur, usually exhibit
pulmonary edema and cardiovascular collapse with
apparent hypotension, poor peripheral perfusion,
and altered mental status. The acute presentation is
usually due to the heart being unable to compensate
for large-volume insults, with rapid deterioration,
most likely due to endocarditis.15 Chronic aortic
regurgitation can become acute in the setting of
ischemia and in endocarditis, affecting the leaflets
or chordal rupture. Chronic aortic regurgitation is
less dramatic, as the left heart has already adapted,
often exhibiting widened pulse pressure. In aortic
regurgitation, additional symptoms such as constant
AUGUST 2022 • www.ebmedicine.net
shortness of breath with worsening valvular disease,
palpitations, and tachycardia can be appreciated.16
However, the tachycardia will be present only initially,
until decompensation and shock develop.
Mitral Stenosis
Patients presenting to the ED with acute
decompensation of mitral stenosis can have dyspnea
and sometimes hemoptysis. The sudden rise in left
atrial pressures can cause rupture of the bronchial
veins, causing mild to severe hemoptysis. Patients
with mitral stenosis can quickly decompensate in
the setting of increased flow or tachycardia, due
to low functional reserve.12,17 Atrial fibrillation
with resulting tachycardia then leads to dyspnea.
Tachycardia impedes diastolic filling, also worsening
overall stability. According to a study by Kato et al,
symptomatic mitral stenosis was associated with atrial
fibrillation, chronic lung diseases, low stroke volume,
and higher transvalvular gradients.18 Therefore, even
if patients have an underlying pathology, such as a
chronic lung condition, they still need to be evaluated
for potential valve dysfunction causing their acute
symptoms. It is important to note that the differential
diagnosis for mitral stenosis includes obstructive
structures such as myxoma and clots, and cor
triatriatum should be assessed in patients presenting
with dyspnea.
Mitral Regurgitation
Presenting symptoms of mitral regurgitation may
include dyspnea with rales on lung auscultation
secondary to pulmonary edema or cardiogenic shock.
There may or may not be a murmur appreciated, due
to a rapid rate of pressure equalization. Chronic mitral
regurgitation may present with dyspnea, especially
with exertion, fatigue, and palpitations.
Tricuspid Disease
Patients with tricuspid disease may present with
right heart failure stigmata, such as hepatomegaly,
edema, or ascites. However, with the discussion
of the etiologies above, more evaluation should
be performed to determine whether there is an
underlying infectious disorder or primary valve
disease. Some symptoms associated with pulmonary
valve stenosis such as exertional dyspnea, can lead
to signs of right-sided heart failure on examination.
Severe disease may progress to episodes of syncope
and angina. Presenting symptoms of pulmonary valve
regurgitation include dyspnea, signs of right heart
failure on examination, fatigue, and angina.
6 ©2022 EB MEDICINE
Physical Examination sign), and the systolic murmur over the femoral artery
The examination findings in valvular disease (Duroziez sign).20,21 Acute aortic regurgitation, how-
vary, depending on the acuteness of the disease ever, often presents with obvious decompensation
process. In patients with acute valve failure, with signs of cardiogenic shock: pulmonary edema,
chamber accommodation to an increase in volume hypotension, pallor, peripheral edema, and altered
and pressure has not had time to occur, and mental status. Extremity blood pressure differences
the constellation of signs resembles acute heart may indicate aortic dissection as the etiology for
failure. Conversely, chronic valve disease allows acute aortic regurgitation.21
for compensation and the development of well-
recognized murmurs and extracardiac findings. Mitral Stenosis
A summary of physical examination findings in On auscultation of the heart apex, the mitral stenosis
aortic stenosis, aortic regurgitation, mitral stenosis, murmur is characterized as a mid-late diastolic
and mitral regurgitation is presented in Table 1. murmur with an opening snap. Pulmonary edema
on lung auscultation, atrial fibrillation on cardiac
Aortic Stenosis auscultation, or signs of right heart congestion can
Auscultatory findings may provide valuable clues to also be found on examination. Long-standing mitral
the involved valve. A late-peaking systolic murmur at stenosis may lead to pulmonary hypertension, in
the right upper sternal border can be heard in aortic which key signs of right heart failure, including edema
stenosis.6,19 A diminished and delayed carotid up- and ascites, would be observed. Patients may also
stroke may also be observed (parvus et tardus). have concomitant tricuspid regurgitation in the
setting of severe mitral stenosis.
Aortic Regurgitation
The examination of a patient with chronic aortic re- Mitral Regurgitation
gurgitation, in which the left ventricle and left atrium The murmur appreciated in mitral regurgitation is
have adjusted to changes in volume and pressure, a blowing systolic murmur, best heard in the left
may have many classic findings. The murmur associ- infrascapular and axilla regions if the anterior leaflet
ated with aortic regurgitation is an early diastolic is affected, or anteriorly in the thorax if the posterior
murmur, with notable tachycardia. Murmur duration leaflet is affected.19,22 If the aortic regurgitation is
indicates regurgitation severity. Systolic pulsations of secondary to mitral valve prolapse, the murmur will
the uvula (Müller sign) and head-bobbing with heart- be late in systole.22 On the extracardiac examination,
beats (Musset sign) may be the first signs observed. large jugular venous pulsations (V waves) may be
Other observed changes in chronic aortic regurgita- appreciated secondary to the increased right-sided
tion include water-hammer pulses (Corrigan pulse) filling pressures.23
with abrupt filling and collapse, very apparent systolic
and diastolic sounds over the femoral artery (Traube
n Diagnostic Testing
Laboratory Testing
Depending on the presentation, ED testing includes
Table 1. Potential Physical Examination cardiac enzymes, brain natriuretic peptide (BNP),
Findings in Valvular Disease electrolytes, blood urea nitrogen/creatinine ratio
Valve Pathology Murmur Other Examination (BUN/CR), a complete blood cell count, and
Findings coagulation profile.
Aortic stenosis Late-peaking systolic After the S2 heart In addition to laboratory testing, ECG, chest
murmur, right sound, “tardus” is x-ray, and bedside ultrasound testing should be con-
sternal border present, indicating sidered when valvular pathology is suspected. With
severe aortic stenosis
practice, most emergency clinicians should be able
Aortic regurgitation Early diastolic Tachycardia, blood to use bedside ultrasound to assist in assessing the
murmur pressure differences
in extremities if aortic
probability of the diseases in the differential diagno-
regurgitation is due to sis. Table 2, page 8, summarizes the diagnostic test-
dissection ing findings of the valvular pathologies seen on ECG,
Mitral stenosis Mid-late diastolic Atrial fibrillation, signs chest x-ray, and bedside ultrasound.
murmur at apex of heart failure, other
valve murmurs, Electrocardiogram
pulmonary edema
• Aortic stenosis: ECG findings include left
Mitral regurgitation Blowing systolic If mitral valve prolapse ventricular hypertrophy and the underlying
murmur, axilla present, murmur may
disease causing the valvular dysfunction.
occur later in systole
• Aortic regurgitation: ECG findings may be sec-
www.ebmedicine.net ondary to the underlying disorder (ie, if a myocar-

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 dial infarction resulted in the regurgitation). Left
ventricular hypertrophy may be appreciated with
severe disease.
• Mitral stenosis: Indications of mitral stenosis
may be found on ECG. Patients may present with
signs of atrial fibrillation because the stenosis
causes increased left atrial pressure and dilation.
• Mitral regurgitation: ECG findings may be
unremarkable or may show the underlying
pathology of the valvular regurgitation. In chronic
mitral regurgitation, the ECG may show left atrial
enlargement.
Chest X-Ray
• Aortic stenosis: Chest x-ray may show pulmonary
edema.
• Aortic regurgitation: Chest x-ray may show pul-
monary edema or the underlying disease process,
such as an aortic dissection with a wide medias-
tinum. Dilated aortic structures and left ventricle
may also be observed.
• Mitral stenosis: Chest x-ray may show pulmonary
edema, a large left atrium, and/or pulmonary
arterial hypertension.
• Mitral regurgitation: Chest x-ray may show
pulmonary edema, and unilateral pulmonary
edema may be appreciated if a pulmonary vein is
favored during the valve dysfunction.
Bedside Ultrasound
• Aortic stenosis: If the aortic stenosis is secondary
to rheumatic heart disease, thickened cusps with
commissural fusion may be visible on ultrasound;
however, rheumatic disease affects many valves,
and concomitant mitral valve disease may be
observed. Formal Doppler echocardiography is
required to diagnose and stage aortic stenosis.
• Aortic regurgitation: Left ventricular dilation may
be visualized if regurgitation has been a chronic
condition; color-flow Doppler can demonstrate
the regurgitant flow. Transthoracic echocardiogra-
phy (TTE) should be able to characterize the valvu-
lar disease, with transesophageal echocardiogra-
phy (TEE) reserved for more thorough testing.
• Mitral stenosis: A large left atrium may be
visualized; however, a TEE may be needed
to visualize the valve more clearly. Pulmonary
hypertension is a marker of severity in mitral
stenosis, but a formal echocardiogram may
be needed to diagnose. Other conditions,
such as atrial fibrillation, anemia, infection,
and pregnancy, can alter the symptom onset
irrespective of valve area/previous staging.
• Mitral regurgitation: Patients may show left-
sided heart dilation if chronic disease is present,
flail leaflet or abnormal leaflet movement, or
ruptured papillary muscle. TEE is recommended
for inconclusive TTE study results.24
Echocardiography
Many valvular pathologies require echocardiography
for accurate description of the valve involved, the
predominance of a stenotic or regurgitant pathology,
and the grading of severity. Point-of-care bedside
ultrasound evaluations provide new approaches to
rapid diagnosis of many valve emergencies and have
facilitated diagnostic efficiency and management.
Bedside cardiac ultrasound can visualize a pericardial
effusion, wall motion abnormalities, and major valve
abnormalities or masses. Other applications include
evaluating inferior vena cava collapsibility, which
can predict fluid responsiveness (especially in shock
states), and gross ventricular function, which can give
insight into the need for inotropes and the degree of
fluid resuscitation that may be tolerated. Even during
advanced cardiovascular life support (ACLS) and
return of spontaneous circulation (ROSC), detection
of asystole, pulseless electrical activity, and abnormal
ventricular motion after ROSC may serve to guide
continuation of therapy and further management.25
TTE is the gold standard for initial evaluation
of valvular heart disease; more-advanced imaging
includes TEE and cardiac magnetic resonance
imaging. TTE is also the choice for surveillance
of asymptomatic valvular heart disease.7 Overall,
echocardiography is low in cost, and TTE requires
only the ultrasound machine and appropriate probe.
TTE can give insight into the ejection fraction of the

Table 2. Diagnostic Testing Findings, Per Valvular Pathology

Murmur Pathology Electrocardiogram Chest X-Ray Bedside Ultrasound
Aortic stenosis Left ventricular hypertrophy Pulmonary edema Thickened valves (possible)
Aortic regurgitation Left ventricular hypertrophy Pulmonary edema, possible wide Left ventricle dilation (possible)
mediastinum
Mitral stenosis Atrial fibrillation Pulmonary edema, pulmonary Left atrium enlargement (possible)
hypertension
Mitral regurgitation Underlying pathology Pulmonary edema, potentially Left heart dilation or leaflet movement
unilateral abnormality (possible)

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heart, the size of the structures, presence of effusion,
and right heart strain. Nonetheless, TTE may not be
able to visualize the structures needed for a diagnosis
or may yield an inconclusive study, and a TEE may
be needed.26 TEE is more invasive, and carries risks,
such as bleeding or damage to the esophagus. TEE
involves more extensive preparation, and patients
generally require sedation, telemetry, monitoring by
an additional specialist while under sedation, and
recovery time from the sedation.
Figures 2, 3, 4, and 5 present TEE and TTE
images of aortic stenosis, atrial regurgitation, mitral
stenosis, and mitral regurgitation.

Figure 2. Echocardiogram of Aortic Figure 4. Echocardiogram of Mitral

Stenosis Stenosis

Apical long axis view, with color Doppler. Left ventricle (LV) apex
faces toward the top of the image (11-12 o’clock). The entire LV is
seen. Preserved function. Color box is centered over LV outflow, with
aortic valve very calcified leaflets with reduced opening.
Image courtesy of Andrey Koretsky, RDCS.
www.ebmedicine.net
Parasternal long axis view. Right ventricle is at the top. Interventricular
septum and left ventricle (LV) below it (LV facing 9 o’clock). Very
thick anterior mitral valve has a classic “hockey stick” appearance in
diastole when it opens (arrow). Left atrium is dilated, probably due to
mitral stenosis.
Image courtesy of Andrey Koretsky, RDCS.
www.ebmedicine.net

Figure 3. Echocardiogram of Aortic Figure 5. Echocardiogram of Mitral

Regurgitation Regurgitation

Color Doppler view of the aortic valve. Highly mosaic color flow origi- Four-chamber view with color Doppler. Left ventricle apex is facing down
nates at the aortic valve, filling back into the left ventricle in diastole. This 6 o’clock. Left atrium is at the top of image. Color box is centered at the
suggests severe aortic insufficiency with poor aortic leaflets coaptation. left atrium–mitral valve–left ventricle.
Image courtesy of Andrey Koretsky, RDCS. Image courtesy of Andrey Koretsky, RDCS.
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n Treatment
Treatment depends on the underlying valvular
abnormality and the staging and severity with which
the patient presents.
Aortic Stenosis
Multiple interventions for aortic stenosis are
available, including medications, mechanical
support, and surgical repair. Medications include
vasoactive medications, diuretics, and vasodilators.
Nitroprusside can be used to improve cardiac index
in cardiogenic shock in order to bridge the patient to
oral vasodilators or valve replacement.27,28 However,
nitroprusside should be used only for patients with
left ventricular dysfunction.28
There is much debate on the role of vasodilator
therapy in aortic stenosis. Jentzer et al noted that
vasodilators and diuretics need to be used with cau-
tion and give specific guidelines, as demonstrated in
Figure 6.29 Another source notes that, because aortic
stenosis can be considered a preload-dependent
condition, vasodilators will decrease preload and
possibly worsen cardiogenic instability.23 Even with
risks for hypotension and worsening stability, in the
correct patient, vasodilators may help. According to
Shah et al, vasodilators (such as nitroprusside) given
to patients with heart failure without severe shock
aided in afterload reduction to allow for better stroke
volumes.30 With inotropic support and diuretic use
based on the patient’s hemodynamic requirements,
vasodilators may prove beneficial.
Other medications appropriate in the presence
of cardiogenic shock include norepinephrine
and inotropic agents such as milrinone and
dobutamine.27,30 Phenylephrine or vasopressin
have also been recommended for patients with
aortic stenosis who are in cardiogenic shock.31 Atrial
arrhythmias, such as atrial fibrillation, are poorly
tolerated in this population. Therefore, it is important
to treat atrial arrhythmias, as optimal atrial function is
needed to maintain ventricular function.23
Other appropriate interventions include mechani-
cal support, such as intra-aortic balloon pump and
extracorporeal membrane oxygenation (ECMO).

Figure 6. Aortic Stenosis Interventions, from Jentzer et al29

Decompensated aortic stenosis

Treat reversible causes

Cardioversion if new atrial fibrillation

Hypotensive/shock Normotensive Hypertensive

• Consider IVF bolus
l 3-4 mL/kg (25 mL)
l Repeat if no evidence of pulmonary
congestion
• Initiate norepinephrine
l Goal MAP >65 mm Hg
• Early PAC placement
l Identify shock subtype
l Evaluate CI and SVO2
• Inotrope if low CI/SVO2
l Dobutamine > epinephrine
l Restore adequate perfusion
• Consider MCS and/or BAV
l IABP or Impella®
l ECMO if severe shock
• NIPPV if needed
l Caution during intubation
• Inpatient TAVI evaluation
l Palliative care consultation
• Initiate diuresis • Initiate diuresis
l IV furosemide bolus +/- may l IV furosemide bolus
consider furosemide infusion • Consider vasodilators
l Avoid aggressive diuresis l Initiate at low dose
• NIPPV if needed l Nitroprusside, clevidipine, or
• Caution with vasodilators nitroglycerin
l Initiate at low dose • NIPPV if needed
l Consider nitroprusside or • Outpatient evaluation for SAVR or TAVI
nitroglycerin, titrated slowly
• Inotrope if hypoperfusion
l Low-dose dobutamine or milrinone
• Inpatient vs outpatient evaluation for
SAVR or TAVI

Abbreviations: BAV, balloon aortic valvuloplasty; CI, cardiac index; ECMO, extracorporeal membrane oxygenation; IABP, intra-aortic balloon pump;
IV, intravenous; IVF, intravenous fluid; NIPPV, noninvasive positive-pressure ventilation; MAP, mean arterial pressure; MCS, mechanical circulatory
support; PAC, pulmonary artery catheter; SAVR, surgical aortic valve replacement; SVO2, mixed venous oxygen saturation; TAVI, transcatheter aortic
valve implantation.
Reproduced from The Journal of Intensive Care Medicine. Jacob C. Jentzer, Bradley Ternus, Mackram Eleid, et al. Structural heart disease emergencies.
Copyright 2021, © SAGE Publications. Used with permission.

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Catheter interventions, such as balloon valvuloplasty
and transcatheter aortic valve replacement (TAVR),27
are also potential treatments. Percutaneous balloon
valvuloplasty cannot be employed in patients with
bicuspid valves or moderate to severe aortic regurgi-
tation.23 Rarely, balloon valvuloplasty can cause acute
aortic regurgitation, necessitating either emergent
transcatheter or surgical valve replacement,32 so the
best surgical option may be TAVR or surgical valve
replacement. Emergency clinicians must manage car-
diogenic shock as soon as possible, as shock duration
is potentially proportionally related to mortality.27
The decision on surgical repair is based on mul-
tiple variables, including maximum velocity across the
valve, mean systolic pressure gradient between the
left ventricle and aorta, ejection fraction, and clinical
testing.7 The variable clinical presentations and treat-
ment considerations are outlined in Figure 7. Surgical
or transcatheter valve replacement can be considered
for many patients; however, patients in stage C aortic
stenosis who demonstrate decreased blood pressure
and exercise capacity on exercise treadmill, rapid pro-
gression of symptoms, BNP >3 times the normal limit,
or maximal velocity ≥5 m/sec with low surgical risk
should be considered for surgical valve replacement.7
Patients with persistently decreased left ventricle
ejection fraction on serial examinations or stage B
patients undergoing other cardiac surgery should also
have a surgical valve replacement.7
Patients need an aortic valve replacement if they
are symptomatic, have decreased exercise tolerance,
have decreased heart function, or if they are having
another cardiac surgery.7 The decision between
surgical versus transcatheter valve replacement is

Figure 7. Aortic Stenosis Staging and Treatment7

Aortic stenosis

Stage A Stage B Stage C Stage D

Asymptomatic, due Asymptomatic, Due to leaflet Asymptomatic and Due to Symptomatic Severe leaflet
to congenital valve progressive calcifications, severe disease severe leaflet and severe calcification,
abnormality or disease fibrosis, or calcification, disease fibrosis, or
sclerosis rheumatic fibrosis, or congenital
disease congenital stenosis (D1)
stenosis

Normal
hemodynamics May have early
LV diastolic C1 C2 D1 D2 D3
dysfunction

SAVR if other LV diastolic LVEF <50%, LV diastolic LV diastolic Increased LV

cardiac surgery dysfunction, systolic dysfunction, dysfunction, wall thickness
occurring LVH and dysfunction LVH, LVH, LVEF with small
normal LVEF; pulmonary <50%; LV chamber
may have HTN; symptoms of and low SV,
symptoms symptoms on HF, angina, restrictive
with exercise exertion syncope filling, LVEF
testing ≥50%;
symptoms of
HF, angina,
syncope

SAVR AVR AVR AVR AVR

Abbreviations: AVR, aortic valve replacement; HF, heart failure; HTN, hypertension; LV, left ventricle; LVEF, left ventricle ejection fraction; LVH, left
ventricle hypertrophy; SV, stroke volume; SAVR, surgical aortic valve replacement.

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based on the age of the patient, anticoagulation
risk, surgical risk, and overall health of the patient.
Surgical aortic valve replacement is recommended
for patients with severe symptoms or reduced left
ventricular ejection fraction. Mechanical valves are
recommended for younger patients (<50 years), and
mechanical or bioprosthetic valves are recommended
for those aged 50 to 65 years. Bioprosthetic valves
are recommended for patients aged >65 years
or patients who are unable to tolerate vitamin K
antagonists. Transcatheter aortic valve implantation
is recommended for the high-surgical-risk patient
population and patients with limited life expectancy.7
In updated approvals and clinical evidence with
limited data, TAVR is now available to patients with
any surgical risk, including low-risk patients and
younger patients.33
Aortic Regurgitation
Interventions for aortic regurgitation are based on
the staging of the disease, as outlined in Figure 8.
Acute unstable aortic regurgitation requires emergent
surgical intervention, where medical therapy serves as
a temporizing measure while preparing the operating
room. If the patient has mild aortic regurgitation or
severe aortic regurgitation but is stable, medical
therapy and further evaluation with echocardiography
can be attempted. However, with conservative
management, the natural history of this pathology
leads to heart failure and need for valvular surgery.
If the ejection fraction declines, patients need to be
transitioned from medical to surgical therapy.16
Medical therapy is based on afterload reduction
with vasodilators, as well as use of inotropes and
volume management.23 Beta blockers are contraindi-
cated, since an elevated heart rate is a compensatory
mechanism.29 Appropriate medical therapy includes
norepinephrine and inotropic agents, with intervention
being either surgical or catheter-based.27 Inotropic
agents for a patient in cardiogenic shock include milri-
none and dobutamine30 or dopamine.31 Temporizing
measures, such as intra-aortic balloon pumps, ECMO,
and LVAD, worsen aortic regurgitation and should
not be used.23 Intra-aortic balloon pump use was also
noted to be contraindicated by Stout et al.15
Additionally, with an increased risk for
endocarditis, patients with aortic regurgitation need
antibiotic prophylaxis.16 For patients with acute
severe aortic regurgitation who are in situations
requiring anesthesia, low diastolic pressures and

Figure 8. Aortic Regurgitation Staging and Treatment7

Aortic regurgitation

Stage A Stage B Stage C Stage D

Due to valve Mild valve Asymptomatic and Due to calcified Severe disease Due to calcified
abnormalities calcification, severe disease valve, BAV, with exertional valve, BAV, dilated
including BAV, rheumatic dilated aortic symptoms of aortic sinuses,
valve sclerosis, sequelae, dilated sinuses, rheumatic dyspnea, angina, rheumatic disease,
aortic disease, or aortic sinuses, disease, IE or HF IE
rheumatic disease history of IE

No hemodynamic Normal If moderate C1: Normal C2: AVR if Normal AVR

concerns or systolic disease LVEF with Decreased progressive LVEF, mild
symptoms function and another mild- LVEF, disease, to severe LV
without cardiac moderate abnormal low surgical dysfunction,
symptoms surgery LV dilation systolic risk, or other moderate to
occurring, function, cardiac severe LV
consider AVR severe LV surgery dilation
dilation occurring

Abbreviations: AVR, aortic valve replacement; BAV, balloon aortic valvuloplasty; HF, heart failure; LV, left ventricle; IE, infective endocarditis; LVEF, left
ventricle ejection fraction; SAVR, surgical aortic valve replacement.

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tachycardia can precipitate ischemia.15 Therefore,
carefully consider the effects of anesthetic or sedation
agents in these patients when preparing for airway
management with endotracheal intubation. In
patients with chronic aortic regurgitation, indications
for intervention include severity of disease, stage
D, or stage C with ejection fraction ≤55% or if the
patient is undergoing another cardiac surgery.7
Mitral Stenosis
There are medical and surgical options for treat-
ment of mitral stenosis. Interventions are based on
the staging of the disease, as outlined in Figure 9.
Appropriate medical intervention includes vasopres-
sors (eg, norepinephrine) and inotropic agents (eg,
milrinone and dobutamine).27,30 It is also reasonable
to consider phenylephrine or vasopressin for vasoac-
tive management in cardiogenic shock.31 Diuretics and
beta blockers may also be helpful,17,23,34 but atenolol
should not be used in pregnant patients.17 The selec-
tive pacemaker inhibitor, ivabradine, at 5 mg twice
daily, has been proposed as another medication op-
tion because it affects only the heart rate,35 and can be
used either with or in place of a beta blocker if heart
rate control is not achieved.35,36 Even on an outpatient
basis, this medication was shown to reduce symptoms
associated with mitral stenosis.35
Arrhythmias need to be controlled. Rhythm con-
trol is preferred in valvular etiology, and anticoagula-
tion should be started unless the atrial fibrillation can
be cardioverted safely (ie, arrhythmia for <48 hours
duration). The antiarrhythmic of choice in this case,
especially for rheumatic mitral stenosis, is amioda-
rone.37 If needed, amiodarone with cardioversion can
be used for maintaining sinus rhythm.36
Vitamin K or non–vitamin K antagonists are
appropriate for anticoagulating patients with valvular
heart disease and atrial fibrillation, except for
those with rheumatic heart disease or mechanical
valve replacements.7 For patients with rheumatic
heart disease and/or mechanical valves with atrial
fibrillation, vitamin K antagonist anticoagulation
needs to be used.7
Other management options for mitral stenosis
include ECMO, balloon valvuloplasty, and
transcatheter valve implantation. Percutaneous
balloon valvuloplasty is the preferred intervention due
to less risk in all patients except the elderly, in whom
valve replacement is the intervention of choice.17
Patients with rheumatic mitral stenosis require
percutaneous mitral balloon commissurotomy once
stage D is reached, but the valve is still pliable. Surgery

Figure 9. Mitral Stenosis Staging and Treatment7

Mitral stenosis

Stage A Stage B Stage C Stage D

At risk, where Rheumatic changes, Asymptomatic, Rheumatic changes, Severe disease with Rheumatic changes,
valve has mild commissural fusion, severe disease commissural exertional symptoms commissural
doming in diastole doming of valve fusion, doming or decreased fusion, doming
during diastole of valve during exercise tolerance of valve during
diastole, decreased diastole, decreased
valve area valve area

Normal Mild to Severe LA If pliable valve Severe LA If valve is pliable If good surgical
hemodynamic moderate LA enlargement, and increased enlargement, or poor surgical candidate with
function; enlargement; elevated pulmonary artery elevated candidate with nonpliable valve
asymptomatic asymptomatic pulmonary systolic pressure pulmonary severe HF, with severe HF,
artery systolic or new atrial artery systolic percutaneous valve repair,
pressure fibrillation, consider pressure mitral balloon commissurotomy,
percutaneous commissurotomy or replacement
mitral balloon are options
commissurotomy

Abbreviations: HF, heart failure; LA, left atrium.

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is recommended when patients are stage D with
severe symptoms, have a nonpliable valve, and are
good surgical candidates.7 Intervention differs in non–
rheumatic mitral stenosis, as these patients are generally
older than the rheumatic disease mitral stenosis patient.
Any intervention is considered only in the severely
symptomatic patient due to the valve calcification and
expected comorbidities of these patients.7
Disposition depends on patient stability, underly-
ing pathology, and need for further evaluation. If a
patient with mitral stenosis develops atrial fibrillation,
a more extensive workup will be needed for under-
lying disease assessment and treatment.36 Also, if
patient stability allows discharge, patient risk factors
need to be considered prior to discharge. Interest-
ingly, increased mortality was associated with inac-
tivity, left ventricular ejection fraction <50%, higher
transmitral gradient, and higher right ventricular
systolic pressures, but mortality was not connected
with valvular symptoms.18
Mitral Regurgitation
Interventions for mitral regurgitation are based on
the staging of the disease, as outlined in Figure
10. Primary mitral regurgitation requires surgery,
whereas secondary mitral regurgitation is treated
medically or with other devices before surgery should
be considered.22 Medical therapy includes inotropic
agents such as milrinone or dobutamine23,27,29 and
vasodilators, such as nitroprusside.27 However,
norepinephrine or dopamine may also be considered
in cardiogenic shock.31 Hypertension results in higher
afterload and worsening of the valvular dysfunction;
therefore, blood pressure needs to be controlled.29
Other interventions include intra-aortic balloon
pump, left ventricular assist device, ECMO, and
mitral valve clip placement.27 In patients with mitral
regurgitation, surgery is indicated in stage C2 and D,
unless the patient is a poor surgical candidate.7
A key point to remember is that acute myocardial
infarction can cause papillary ischemia, leading
to acute mitral regurgitation.27 If the area of
infarction is revascularized, this may treat the mitral
regurgitation.27,30 Reperfusion therapy is indicated

Figure 10. Mitral Regurgitation Staging and Treatment7

Mitral regurgitation

Stage A Stage B Stage C Stage D

Mild MVP with valve
thickening and leaflet
movement restriction
Asymptomatic; valve
disease due to moderate
to severe prolapse,
rheumatic changes, or
history of IE
Asymptomatic; due
to severe prolapse,
loss of coaptation,
flail leaflet, rheumatic
changes, history of IE, or
thickened leaflets
Severe disease, with
symptoms on exertion
or decreased exercise
tolerance
Loss of coaptation, flail
leaflet due to rheumatic
changes, history of IE, or
thickened leaflets due to
severe prolapse

Normal Mild LA Moderate to C1: Normal LVEF C2: Decreased Moderate to

hemodynamics and enlargement severe LA LVEF severe LA
asymptomatic enlargement with enlargement with
LV enlargement, LV enlargement,
pulmonary HTN pulmonary HTN

Valve repair or Valve surgery or Consider valve

replacement repair for rheumatic
options valve disease are
options. Consider
transcatheter repair,
if high surgical risk
surgery or
transcatheter repair
if high surgical risk

Abbreviations: HTN, hypertension; IE, infective endocarditis; LA, left atrium; LV, left ventricle; LVEF, left ventricular ejection fraction; MVP, mitral
valve prolapse.

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if the mitral regurgitation is due to an ST-elevation
myocardial infarction (STEMI).23
With respect to management of the whole
patient, it is important to note that anesthesia in
patients with acute mitral regurgitation can lead to
cardiopulmonary collapse.15
Cardiogenic Shock
As discussed in the preceding sections, patients with
valvular diseases can present in cardiogenic shock.
The basics of treatment in these patients include
increasing cardiac output and treating the
underlying etiology, such as arrhythmias and
myocardial infarctions. Inotropes suggested for
cardiogenic shock are milrinone and dobutamine;
dobutamine is preferred for its shorter half-life
compared to milrinone.30 Both agents can cause
arrhythmias and hypotension, but the quicker
elimination of dobutamine is preferred in the event
of ectopy or hypotension.3 In refractory cases,
the addition of vasopressin or norepinephrine are
considerations; norepinephrine may be associated
with fewer arrhythmias.31 Inotropes for patients with
hypotension and concomitant heart failure include
norepinephrine, dobutamine, or dopamine.38
Vasodilators are often contraindicated in cardiogenic
shock, though in hypertensive patients with severe
impaired contractility, vasodilators (eg, nitroglycerin,
nesiritide, and nitroprusside) may decrease afterload
and thus improve cardiac output. Rapid clinical
deterioration may necessitate urgent surgical
intervention.27 See Table 3 for a summary of
vasoactive medications used for cardiogenic shock
in patients with valvulopathy.
Because definitive management requires
intervention, early consultation with cardiothoracic
surgery and interventional cardiology is important
in the ED, with disposition to a critical care setting,
Table 3. Vasoactive Medications for Cardiogenic Shock in Valvulopathy31
Medication Usual Dosing Range
Norepinephrine 0.04-1 mcg/kg/min
Epinephrine 0.01-2 mcg/kg/min
Vasopressin 0.03 units/min
Phenylephrine 0.1-0.3 mcg/kg/min
Dopamine 5-10 mcg/kg/min
>10 mcg/kg/min
Dobutamine 2.5-20 mcg/kg/min
Milrinone 0.125-0.75 mcg/kg/min
Abbreviations: CO, cardiac output; PCWP, pulmonary capillary wedge pressure; SVR, systemic vascular resistance.
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such as a pulmonary or cardiac critical care unit. This
multidisciplinary approach is supported by growing
evidence for cardiogenic shock teams, which are
gaining recognition as improving patient survival.39
n Special Populations
Patients With Prosthetic Valves
Patients who have had valve replacements pose a
unique challenge in management due to their risk for
clot formation and need for anticoagulation.40 Factors
to consider when evaluating clot risk in patients with
valve replacements include the endothelium at the
suture zone of the valve, and the hemodynamics,
such as low cardiac output and blood flow through
the valve.41 Also important to note is that not all
valves are affected to the same degree; tricuspid
valves are more likely to clot than left-sided valves,
and mitral valves are more likely to clot than aortic
valves.41 With artificial valves, the natural resistance
to clot formation provided by the endothelium is
no longer present, triggering a cascade of protein
absorption and adhesion of blood components, with
activation of complement and thrombin.42 In addition
to the valve surface causing pathology, turbulent flow
allows for platelet adhesion,42 increasing thrombotic
risk. There may also be an obstructive pathology due
to vegetation or clot.41
Mechanical valve complications are primarily
related to thrombosis, whereas bioprosthetic
valve complications are usually due to stenosis or
regurgitation.43 In patients with prosthetic valves,
severe obstruction presents as heart failure, whereas
a partial obstruction presents with dyspnea, and a
nonobstructive thrombus may be found incidentally.41
These may be detected with bedside ultrasound
by noting valve movement or directly visualizing a
thrombus.41 The thrombus may not be visualized in
Hemodynamic Effect
Vasopressors
↑CO; ↑↑SVR; ↑PCWP
↑↑CO; ↑SVR; ↑PCWP
↓CO; ↑SVR; ↑PCWP
↓CO; ↑SVR; ↑PCWP
↑CO
↑CO; ↑SVR
Inotropic Agents
↑↑CO; ↓↔SVR; ↓↔PCWP
↑↑CO; ↓↓SVR; ↓↓PCWP
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the heart; however, the patient may be presenting
with signs and symptoms of systemic embolization.42
If a patient with a valve replacement presents
with a new murmur and symptoms of heart failure,
an urgent TTE or TEE is needed.43 TTE can be used
preoperatively and postoperatively; however, TEE is
frequently used if TTE is indeterminate or in aortic
and mitral valve procedures.44 When considering the
presence of prosthetic valve regurgitation, expect
bioprosthetic valves to produce central regurgitation
and mechanical valves to result in paravalvular
regurgitation.43 In prosthetic tricuspid regurgitation
bedside ultrasound, dilation of right heart structures
and flat interventricular septum may be visualized.
However, if tricuspid regurgitation is suspected,
additional TEE would be required.42
Of note, with increased aortic bioprosthetic
valve use and breakdown over the years, patients
may present with stenosis, but they would need a
full workup to determine the underlying etiology
of valve failure.45 An option for patients with a
failing bioprosthetic valve may be a valve-in-valve
implantation; Dvir et al showed a 1-year survival rate
of 83.2% with this intervention.45
Because prosthetic valves are prone to thrombus
formation, vitamin K antagonists are the medica-
tion of choice for anticoagulation in these patients.7
In a study by Eikelboom et al examining the use
of dabigatran versus warfarin for mechanical heart
valves, dabigatran was associated with an increased
risk for thromboembolic events and bleeding, result-
ing in early study termination. The study concluded
that with no benefit and notable risk, dabigatran was
not an acceptable alternative to warfarin in patients
with mechanical valves.46 With respect to antiplatelet
use, these medications are clinically indicated for ACS
prevention after valve replacement.42
If a clot is found in a patient with a prosthetic
valve, surgery or fibrinolysis are the 2 management
options. If a thrombus is in a left-sided prosthetic
valve or is large or mobile, surgery is the treatment of
choice. Fibrinolysis is less preferred due to embolic
potential.41 With a small (≤5 mm) or nonobstructive
thrombus, heparin, aspirin plus warfarin, or fibrinolysis
can be used, depending on the clinical situation.41
With respect to degeneration of bioprosthetic valves,
transcatheter mitral valve replacement showed
promising outcomes in one study.47
Disposition depends on patient stability,
complications of the valve, and the degree of valvular
failure. These patients most likely need formal
echocardiography and consult to cardiology.
Pregnant Patients
Pregnancy causes physiological strain, especially with
respect to cardiovascular function. Pregnancy can
exacerbate mitral stenosis, which may be suspected
if the patient has a history of rheumatic heart disease,
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because a larger blood volume and increased heart
rate must now pass through the narrowed valve
diameter, resulting in increased pressure back into
the left atria.48,49 Symptoms of this include pulmonary
edema, dyspnea, decreased exertional tolerance,
orthopnea, and paroxysmal nocturnal dyspnea.48
Most importantly, mitral stenosis and increased left
atrial pressures can lead to atrial arrhythmia. Chest
x-ray may show vascular congestion, while a TTE may
show abnormalities in leaflet movement and flow.48,49
Treatment for this patient population is
metoprolol to aid directly in cardiac function, and
subcutaneous heparin if atrial fibrillation is present.
If the patient is in heart failure, vasodilators such as
nitroglycerin or nitroprusside, loop diuretics, digoxin,
and beta blockers can be considered, based on the
individual clinical situation and vital signs.48 If the
patient progresses to cardiogenic shock, the inotrope
of choice is dobutamine or milrinone.48 Even though
morbidity with mitral stenosis during pregnancy
is high, mortality is rare.49 This morbidity and
mortality phenomenon is similar to pregnant patients
with aortic stenosis.49 However, there are fetal
complications in 20% of pregnancies, which include
slowed intrauterine growth and premature delivery.17
Lastly, it is important to note that hypertensive
emergencies may mimic valvular diseases in that
hypertension can cause pulmonary edema, chest
pain, and dyspnea.48
n Controversies and Cutting Edge
The 2020 ACC/AHA Guideline for the Management
of Valvular Heart Disease summarized the
limitations of the evidence upon which many current
recommendations are based and delineates areas in
which further research should concentrate.7 Evidence
from observational studies still contributes too much
of the data upon which current guidelines are based.7
Prospective randomized controlled trials are required
to base recommendations on higher-order evidence.7
For emergency clinicians caring for patients
with known or suspected valvular disease, there are
2 practice areas that may be impacted by further
research: First is whether direct oral anticoagulants
have a role in antithrombotic therapy post prosthetic
valve replacement.7 Second, it is important to
define the optimal medication regimens targeting
hypertension and valvular dysfunction to prevent or
slow the rate of disease progression.7
16 ©2022 EB MEDICINE
 Case Conclusions
For the 65-year-old woman with a history of coronary artery disease who presented complaining of
chest pain and the sudden onset of feeling short of breath…
CASE 1

You obtained an ECG, which showed T-wave inversions. You ordered an emergent TTE and placed a
consult from cardiology. The ultrasound sonographer called you to the bedside to report a possible
papillary muscle rupture, causing mitral regurgitation, and you called interventional cardiology for further
management of the patient.

For the 85-year-old woman who was brought in by EMS for a syncopal event...
CASE 2

You ordered basic blood work, ECG, and screened for possible underlying infectious etiology of the
syncope. With no acute abnormalities found on initial evaluation, you ordered a TTE in the ED. The
valvular area was significantly narrowed, concerning for severe aortic stenosis, and you placed a consult to
cardiology to discuss possible valve replacement.

For the young man who was in a car accident and was “not looking good…”
CASE 3

With a wide mediastinum on chest x-ray, you started IV crystalloid fluid resuscitation and a norepinephrine
infusion for inotropic support. You obtained a stat CTA, which confirmed
5 theRecommendations
diagnosis of aortic dissection.
Cardiothoracic surgery evaluated the patient and took the patient emergently TotoApply
the operating room.
in Practice

n Summary
Cardiac valvular emergencies can present in a variety
of ways, including common cardiac and pulmonary
complaints. These disease states can present with
pulmonary edema, syncope, dyspnea, and even
cardiogenic shock. Treatment and interventions
for valvular diseases differ from more common
diagnoses and even between the different valve
diseases. Emergency clinicians must keep the valvular
diseases on the differential diagnosis, understanding
physical examination findings and diagnostic testing
that may indicate underlying valve conditions, and
appreciating how to manage cardiogenic shock and
its treatments.
Aortic stenosis can present with a systolic murmur
and pulmonary edema. Treatments include inotropes,
vasodilators, and diuretics. However, it is important
to note that aortic stenosis is considered preload-
dependent, so medication interventions need to be
used with caution. Aortic regurgitation can be due to
many different etiologies, but acute aortic regurgita-
tion is a surgical emergency. Procedural and surgical
interventions depend on which valve is diseased, but
these will be determined by cardiology.
For mitral stenosis, a diastolic murmur and pul-
monary edema may be noted. Underlying arrhythmias
need to be treated. Diuretics, beta blockers, and
vasoactive medications can be used, as needed, with
caution. In patients with mitral regurgitation, a mur-
mur may or may not be noted and pulmonary edema
may also be seen on chest x-ray and point-of-care
ultrasound. Treatments usually include vasodilators
and inotropes, as needed.
5 Recommendations
To Apply in Practice
5 Things
5 That Will
Recommendations
ChangeToYour
ApplyPractice
in Practice
1. In patients with acute-onset cardiogenic
shock, consider a valvular emergency.
2. Consider an early echocardiographic
evaluation in patients with suspected cardiac
valve disease.
3. Valvular regurgitation is treated with
vasodilators and diuretics to reduce afterload,
making forward blood flow easier for the
heart.
4. Caution should be exercised in treating aortic
stenosis with inotropes or vasodilators, as this
pathology relies on low heart rate to facilitate
ventricular filling.29
5. Vasoconstrictors and beta blockers can be
helpful in managing mitral stenosis.29
Special thanks to Tyler Nghiem, DO, for his review of
this content. Dr. Nghiem does not report any relevant
financial relationships with ineligible companies.

AUGUST 2022 • www.ebmedicine.net 17 © 2022 EB MEDICINE. ALL RIGHTS RESERVED.

 Risk Management Pitfalls for Cardiac Valve Emergencies
1. “This patient has frequent COPD
exacerbations.” Do not fail to include valvular
pathology in the differential diagnosis. Patients
can have diverse pathology, which can present
similarly to their chronic conditions. Therefore, it
is important to avoid prematurely anchoring on a
diagnosis.
2. “Order aspirin and consult cardiology in the
morning for his chest pain.” ACS pathology can
have an underlying etiology of valvular pathology.
It is important to get consultants involved early to
ensure that the patient receives a comprehensive
workup to avoid missing valvular disease.
3. “The patient had a TAVR last year, so his
symptoms couldn't be due to heart valves.”
Valve pathology does not evolve on its own. The
heart is a complex pump that relies on the whole
structure to function properly. Therefore, more
than 1 valve can be diseased from underlying
pathology or structural changes over time from
the initial valve disease.
4. “I never asked the past medical history.” A
full history should be taken to assess for risk
factors that would move valvular pathology up in
the differential diagnosis. Examples of historical
risk factors include if a patient came from a
developing country where rheumatic disease is
prevalent, the patient was born with a bicuspid
aortic valve, or if the patient recently had a
myocardial infarction.
5. “The inpatient service can treat the atrial
fibrillation.” It is important to manage the
patient’s vital signs and symptoms, especially
during an acute event, to optimize cardiac
functioning. Nonetheless, in certain valve
diseases, abnormal vital signs are a compensatory
mechanism and should not be treated. Atrial
fibrillation should be treated.
AUGUST 2022 • www.ebmedicine.net
6. “The patient crashed when we intubated him.”
Anesthesia can acutely worsen a cardiac event
due to the vasodilation that is associated with
anesthetics. Any use of anesthetics should be
carefully considered for timing and preparedness.
Pressors and any adjunctive therapies should be
prepared prior to using anesthetics.
7. “I think it’s the aortic valve that’s causing all
the problems.” Many interventions are driven
by formal echocardiographic measurements,
and these measurements may be needed for
an official diagnosis. For appropriate staging,
patients will need to have additional studies
beyond the initial bedside TTE performed by the
emergency clinician.
8. “Her blood pressure was mildly elevated, so
I ordered furosemide.” If a patient is relying
on preload for continued cardiac function, do
not give medications that would decrease the
preload. The desire to treat other symptoms, such
as blood pressure or pulmonary edema, needs
to be weighed carefully with how the heart is
compensating to function.
9. “I gave phenylephrine to support her
pressures.” Cardiogenic shock is not a peripheral
vascular issue. Therefore, if the patient needs an
inotropic agent or needs a decrease in afterload,
choose agents based on the correction of the
pathophysiology.
10. “I’ll call cardiothoracic surgery! This patient
needs surgery NOW.” Different valvular diseases
require different interventions, based on staging.
Patients may need medical therapy, optimization,
or surgery. This is best determined by definitive
testing and cardiology evaluation. Be sure to get
your consultants involved early.
18 ©2022 EB MEDICINE
n References
Evidence-based medicine requires a critical appraisal
of the literature based upon study methodology
and number of subjects. Not all references are
equally robust. The findings of a large, prospective,
randomized, and blinded trial should carry more
weight than a case report.
To help the reader judge the strength of each
reference, pertinent information about the study,
such as the type of study and the number of patients
in the study is included in bold type following the
references, where available. The most informative
references cited in this paper, as determined by
the authors, are noted by an asterisk (*) next to the
number of the reference.
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6. Helms AS, Bach DS. Heart valve disease. Prim Care Clin Office
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7.* Otto CM, Nishimura RA, Bonow RO, et al. 2020 ACC/AHA
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10. Tabata N, Sinning J-M, Kaikita K, et al. Current status and future
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11. NASEMSO Medical Directors Council. National model EMS
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13. Mebazaa A, Tolppanen H, Mueller C, et al. Acute heart failure
and cariogenic shock: a multidisciplinary practical guidance.
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14. Lumley M, Williams R, Asrress KN, et al. Coronary physiology
during exercise and vasodilation in the healthy heart and in
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severe aortic stenosis. J Am Coll Cardiol. 2016;68(7):688-697.
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17. Chandrashekhar Y, Westaby S, Narula J. Mitral stenosis. Lancet.
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19. Bonow RO, Carabello BA, Chatterjee K, et al. ACC/AHA 2006
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20. Lindman BR, Bonow RO, Otto CM. Aortic valve disease. In: Zipes
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Textbook of Cardiovascular Medicine. 11th edition. Philadelphia,
PA: Elsevier; 2019:1389-1414. (Textbook chapter)
21. Akinseye OA, Pathak A, Ibebuogu UN. Aortic valve regurgita-
tion: a comprehensive review. Curr Probl Cardiol. 2018;43:315-
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22. O’Gara PT, Grayburn PA, Badhwar V, et al. 2017 ACC expert
consensus decision pathway on the management of mitral
regurgitation. J Am Coll Cardiol. 2017;70:2421-2449. (Expert
consensus)
23.* Maheshwari V, Barr B, Srivastava M. Acute valvular heart dis-
ease. Cardiol Clin. 2018;36:115-127. (Review)
DOI: 10.1016/j.ccl.2017.08.006
24. Zoghbi WA, Adams D, Bonow RO, et al. Recommendations for
noninvasive evaluation of native valvular regurgitation: a report
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nance. J Am Soc Echocardiogr. 2017;30(4):303-371. (Guidelines)
25. Levitov A, Frankel HL, Blaivas M, et al. Guidelines for the appro-
priate use of bedside general and cardiac ultrasonography in
the evaluation of critically ill patients- part II: cardiac ultrasonog-
raphy. Crit Care Med. 2016;44:1206-1227. (Guidelines)
26. Omerovic S, Jain A. Echocardiogram. StatPearls [Internet]. Trea-
sure Island, FL: StatPearls Publishing; 2021. (Review article)
27.* Akodad M, Schurtz G, Adda J, et al. Management of valvu-
lopathies with acute severe heart failure and cardiogenic shock.
Arch Cardiovasc Dis. 2019;112:773-780. (Review)
DOI: 10.1016/j.acvd.2019.06.009
28. Khot UN, Novaro GM, Popović ZB, et al. Nitroprusside in
critically ill patients with left ventricular dysfunction and aortic
stenosis. N Engl J Med. 2003;348(18):1756-1763. (Prospective;
25 patients)
29. Jentzer JC, Ternus B, Eleid M, et al. Structural heart disease
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lytical review)
30. Shah P, Cowger JA. Cardiogenic shock. Crit Care Clin.
2014;30:391-412. (Review)
31.* van Diepen S, Katz JN, Albert NM, et al. Contemporary man-
agement of cardiogenic shock: a scientific statement from the
American Heart Association. Circulation. 2017;136(16):e232-
e268. (AHA Scientific Statement)
DOI: 10.1016/j.ccc.2014.03.001
32. Dall’Ara G, Saia F, Moretti C, et al. Incidence, treatment, and
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34. Harb SC, Griffin BP. Mitral valve disease: a comprehensive
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fingertips on our new mobile app
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n CME Questions
Current subscribers receive CME credit
absolutely free by completing the
following test. Each issue includes 4 AMA
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issue, scan the QR code below with your
smartphone or visit www.ebmedicine.net/E0822
1. What is a differentiating factor between
rheumatic and nonrheumatic mitral stenosis?
a. Multivalvular involvement
b. Heart size
c. Commissural fusion
d. Calcification
2. In mitral regurgitation, which etiology is
considered a chronic cause?
a. Chordal rupture
b. Papillary muscle rupture
c. Ischemia
d. Endocarditis
3. In aortic regurgitation, which is NOT a
potential examination finding?
a. Late-peaking systolic murmur
b. Tachycardia
c. Pulmonary edema on chest x-ray
d. Wide mediastinum on chest x-ray
4. In mitral regurgitation, what murmur may be
appreciated on examination?
a. Early diastolic murmur
b. Blowing systolic murmur
c. Mid-late diastolic murmur
d. Mid-systolic click
AUGUST 2022 • www.ebmedicine.net
5. In mitral regurgitation, which ultrasound
finding may indicate a chronic disease finding?
a. Free papillary muscle movement
b. Normal atrial size
c. Left atrial enlargement
d. Isolated cardiac wall hypokinesis
6. In aortic stenosis, what intervention cannot be
used in bicuspid aortic stenosis?
a. Surgical valvular replacement
b. Percutaneous balloon valvuloplasty
c. Transcutaneous valvular replacement
d. Extracorporeal membrane oxygenation
(ECMO)
7. In acute aortic regurgitation, where the
patient is unstable, which is the correct
intervention?
a. Medical therapy with vasodilators
b. Stress test
c. Transesophgeal echocardiography (TEE)
d. Emergent surgical intervention
8. In aortic regurgitation, which SHOULD be used
in management?
a. Beta blockers
b. Ventricular assist devices
c. Intra-aortic balloon pumps
d. Vasoactive agents
9. In mitral stenosis, which strategy should
be considered first, when managing atrial
fibrillation?
a. Valvular replacement
b. TEE evaluation
c. Rhythm control
d. Cardiac magnetic resonance imaging
10. In mitral stenosis, atrial fibrillation needs to be
managed with anticoagulation. In which case
would the patient NOT be placed on a non-
vitamin K antagonist?
a. Rheumatic valvular disease
b. Advanced age
c. Multivalvular disease
d. None of the above
21 © 2022 EB MEDICINE. ALL RIGHTS RESERVED.
The Emergency Medicine Practice Editorial Board
EDITOR-IN-CHIEF
Andy Jagoda, MD, FACEP
Professor and Chair Emeritus,
Department of Emergency
Medicine; Director, Center for
Emergency Medicine Education
and Research, Icahn School of
Medicine at Mount Sinai, New
York, NY
ASSOCIATE EDITOR-IN-CHIEF
Kaushal Shah, MD, FACEP
Assistant Dean of Academic
Advising, Vice Chair of Education,
Professor of Clinical Emergency
Medicine, Department of
Emergency Medicine, Weill Cornell
School of Medicine, New York, NY
EDITORIAL BOARD
Saadia Akhtar, MD, FACEP
Associate Professor, Department
of Emergency Medicine, Associate
Dean for Graduate Medical
Education, Program Director,
Emergency Medicine Residency,
Mount Sinai Beth Israel, New York,
NY
William J. Brady, MD
Professor of Emergency Medicine
and Medicine; Medical Director,
Emergency Management, UVA
Medical Center; Operational
Medical Director, Albemarle
County Fire Rescue, Charlottesville,
VA
Calvin A. Brown III, MD
Director of Physician Compliance,
Credentialing and Urgent
Care Services, Department of
Emergency Medicine, Brigham and
Women's Hospital, Boston, MA
Peter DeBlieux, MD
Professor of Clinical Medicine,
Louisiana State University School of
Medicine; Chief Experience Officer,
University Medical Center, New
Orleans, LA
Deborah Diercks, MD, MS,
FACEP, FACC
Professor and Chair, Department
of Emergency Medicine, University
of Texas Southwestern Medical
Center, Dallas, TX
Daniel J. Egan, MD
Harvard Affiliated Emergency
Medicine Residency, Massachusetts
General Hospital/Brigham and
Women's Hospital, Boston, MA
AUGUST 2022 • www.ebmedicine.net
Marie-Carmelle Elie, MD
Associate Professor, Department
of Emergency Medicine & Critical
Care Medicine, University of Florida
College of Medicine, Gainesville,
FL
Nicholas Genes, MD, PhD
Clinical Assistant Professor,
Ronald O. Perelman Department
of Emergency Medicine, NYU
Grossman School of Medicine,
New York, NY
Michael A. Gibbs, MD, FACEP
Professor and Chair, Department
of Emergency Medicine, Carolinas
Medical Center, University of North
Carolina School of Medicine,
Chapel Hill, NC
Steven A. Godwin, MD, FACEP
Professor and Chair, Department
of Emergency Medicine, Assistant
Dean, Simulation Education,
University of Florida COM-
Jacksonville, Jacksonville, FL
Joseph Habboushe, MD MBA
Assistant Professor of Clinical
Emergency Medicine, Department
of Emergency Medicine, Weill
Cornell School of Medicine, New
York, NY; Co-founder and CEO,
MDCalc
Eric Legome, MD
Chair, Emergency Medicine, Mount
Sinai West & Mount Sinai St.
Luke's; Vice Chair, Academic Affairs
for Emergency Medicine, Mount
Sinai Health System, Icahn School
of Medicine at Mount Sinai, New
York, NY
Keith A. Marill, MD, MS
Associate Professor, Department
of Emergency Medicine, Harvard
Medical School, Massachusetts
General Hospital, Boston, MA
Angela M. Mills, MD, FACEP
Professor and Chair, Department
of Emergency Medicine, Columbia
University Vagelos College of
Physicians & Surgeons, New York,
NY
Charles V. Pollack Jr., MA, MD,
FACEP, FAAEM, FAHA, FACC,
FESC
Clinician-Scientist, Department of
Emergency Medicine, University
of Mississippi School of Medicine,
Jackson MS
22
Ali S. Raja, MD, MBA, MPH RESEARCH EDITORS
Executive Vice Chair, Emergency
Aimee Mishler, PharmD, BCPS
Medicine, Massachusetts General
Emergency Medicine Pharmacist,
Hospital; Professor of Emergency
Program Director, PGY2 EM
Medicine and Radiology, Harvard
Pharmacy Residency, Valleywise
Medical School, Boston, MA
Health, Phoenix, AZ
Robert L. Rogers, MD, FACEP,
Joseph D. Toscano, MD
FAAEM, FACP
Chief, Department of Emergency
Assistant Professor of Emergency
Medicine, San Ramon Regional
Medicine, The University of
Medical Center, San Ramon, CA
Maryland School of Medicine,
Baltimore, MD
INTERNATIONAL EDITORS
Alfred Sacchetti, MD, FACEP Peter Cameron, MD
Assistant Clinical Professor, Academic Director, The Alfred
Department of Emergency Emergency and Trauma Centre,
Medicine, Thomas Jefferson Monash University, Melbourne,
University, Philadelphia, PA Australia
Robert Schiller, MD Andrea Duca, MD
Chair, Department of Family Attending Emergency Physician,
Medicine, Beth Israel Medical Ospedale Papa Giovanni XXIII,
Center; Senior Faculty, Family Bergamo, Italy
Medicine and Community Health,
Icahn School of Medicine at Mount
Suzanne Y.G. Peeters, MD
Sinai, New York, NY
Attending Emergency Physician,
Flevo Teaching Hospital, Almere,
Scott Silvers, MD, FACEP The Netherlands
Associate Professor of Emergency
Medicine, Chair of Facilities and
Edgardo Menendez, MD, FIFEM
Planning, Mayo Clinic, Jacksonville,
Professor in Medicine and
FL
Emergency Medicine; Director of
EM, Churruca Hospital of Buenos
Corey M. Slovis, MD, FACP, Aires University, Buenos Aires,
FACEP Argentina
Professor and Chair Emeritus,
Department of Emergency
Dhanadol Rojanasarntikul, MD
Medicine, Vanderbilt University
Attending Physician, Emergency
Medical Center, Nashville, TN
Medicine, King Chulalongkorn
Memorial Hospital; Faculty
Ron M. Walls, MD of Medicine, Chulalongkorn
Professor and COO, Department University, Thailand
of Emergency Medicine, Brigham
and Women's Hospital, Harvard
Stephen H. Thomas, MD, MPH
Medical School, Boston, MA
Professor & Chair, Emergency
Medicine, Hamad Medical Corp.,
CRITICAL CARE EDITORS Weill Cornell Medical College,
Qatar; Emergency Physician-in-
William A. Knight IV, MD, FACEP,
Chief, Hamad General Hospital,
FNCS
Doha, Qatar
Associate Professor of Emergency
Medicine and Neurosurgery,
Medical Director, EM Advanced Edin Zelihic, MD
Practice Provider Program; Head, Department of Emergency
Associate Medical Director, Medicine, Leopoldina Hospital,
Neuroscience ICU, University of Schweinfurt, Germany
Cincinnati, Cincinnati, OH
Scott D. Weingart, MD, FCCM
Professor of Emergency Medicine;
Chief, EM Critical Care, Stony
Brook Medicine, Stony Brook, NY
©2022 EB MEDICINE
 Points & Pearls
QUICK READ
AUGUST 2022 | VOLUME 24 | ISSUE 8
Points
• Cardiac valvular disease is an important consider-
ation on the differential diagnosis for complaints
of chest discomfort, dyspnea, and syncope.
• Comorbid conditions include congestive heart
failure and myocardial infarction.
• Aortic stenosis results from degeneration,
calcification, or rheumatic heart disease.4,5
• Aortic stenosis causes ventricular remodeling and
subsequent mitral valve disease.
• Events due to aortic stenosis may present after
exertion or while undergoing anesthesia.
• Medications for aortic stenosis include vasoactive
medications, diuretics, and vasodilators.
• Mitral stenosis can be due to rheumatic disease,
aging, or radiation damage to valve leaflets.
• Patients of advanced age or from areas endemic
for rheumatic heart disease should be screened
for valvular dysfunction.
• Mitral stenosis is associated with atrial fibrillation,
chronic lung disease, low stroke volume, and
higher trans valvular gradients.18
• Physical examination findings can vary in valve
disease; a summary of physical examination
findings can be seen in Table 1.
• Diagnostic testing for valvular disorders includes
ECG, chest x-ray, and bedside ultrasound. Table
2 summarizes the diagnostic testing findings that
may be seen in each valvular pathology.
• Echocardiography, both TTE and TEE, are
required to accurately diagnose and grade the
severity of the valvular pathology. To view im-
ages of TEE images of the 4 valvular pathologies
discussed, see Figures 2, 3, 4, and 5.
• Arrhythmias need to be controlled; rhythm
control is preferred in valvular etiology, and
anticoagulation should be started.
• For patients with atrial fibrillation and rheumatic
heart disease and/or mechanical valves, vitamin
K antagonist anticoagulation should be used.
• Patients with aortic regurgitation should be given
antibiotic prophylaxis.16
• Mechanical valve complications are primarily
AUGUST 2022 • www.ebmedicine.net
Managing Acute Cardiac
Valvular Emergencies in the
Emergency Department
Pearls
• Presentations of severe aortic stenosis include
syncope, heart failure, and angina, but a
murmur may be the only sign.
• Acute aortic regurgitation usually exhibits
pulmonary edema and cardiovascular collapse
with hypertension, poor peripheral perfusion,
and altered mental status.
• Acute decompensation due to mitral stenosis
can present with dyspnea and hemoptysis.
• Presenting symptoms of mitral regurgitation
may include dyspnea with rales secondary to
pulmonary edema or cardiogenic shock.
• Cardiogenic shock must be managed as
quickly as possible, as shock duration is
proportionally related to mortality.27
• Treatment for cardiogenic shock includes
increasing cardiac output and treating the
underlying etiology. See Table 3 for dosing
and hemodynamic effects of vasoactive
medications for cardiogenic shock.31
• Acute unstable aortic regurgitation requires
emergent surgical intervention.
• Hypertensive emergencies may mimic valvular
diseases, with pulmonary edema, chest pain,
and dyspnea.47
related to thrombosis; bioprosthetic valve
complications are usually due to stenosis or
regurgitation.42
• Severe prosthetic valve obstruction presents
as heart failure; partial obstruction presents as
dyspnea.40
• Vitamin K antagonists are the medication of choice
for anticoagulation in patients with prosthetic
valves.7
• Pregnancy can exacerbate mitral stenosis.
Symptoms include pulmonary edema, dyspnea,
decreased exertional tolerance, orthopnea, and
paroxysmal nocturnal dyspnea.47
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