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252 PART IV Noncoronary Diseases: Diagnosis and Management
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Fig. 25.1 Basic mechanisms of supraventricular tachycardia (SVT). Typical atrial flutter (Aflutter)
is a reentrant circuit around the tricuspid valve in the right atrium. Atrioventricular nodal reentry
tachycardia (AVNRT) is reentry within the atrioventricular node (AVN) and perinodal tissue.
Orthodromic AVNRT is a reentry circuit that traverses down the AVN and up a bypass tract,
leading to a narrow QRS. In antidromic atrioventricular reentry tachycardia (AVRT), conduction is
first down the bypass tract and then up the AVN, leading to a wide QRS complex. Atrial tachycardia
(AT) is an ectopic focus of atrial activity at a faster rate than the sinus node. Atrial fibrillation
(AFib) is several simultaneous wavelets in the atrium with variable conduction through the AVN.
Multifocal atrial tachycardia (MAT) involves at least three distinct ectopic atrial foci. (From Link
MS. Clinical practice: evaluation and initial treatment of supraventricular tachycardia. N Engl J
Med. 2012;367[15]:1438–1448.)
Fig. 25.2 Atrial fibrillation with rapid ventricular response.
CHAPTER 25 Diagnosis and Treatment of Unstable Supraventricular Tachycardia 253
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Fig. 25.3 Typical atrial flutter with variable conduction. Typical negatively deflected flutter waves
are seen in the inferior leads with positive flutter waves in V
be difficult to distinguish from atrioventricular nodal reentry tachycardia; adenosine can be used
to increase the degree of atrioventricular block and unmask the flutter waves.
. 2 : 1 atrial flutter can sometimes
1
occur in different locations within either atrium, are less common,
and are typically observed in patients with prior atrial fibrillation
ablations or cardiac surgeries. The flutter rate is usually around
300 beats/min, with the ventricular rate determined by the degree
of AV node block. Acute atrial flutter presents with a rapid rise
in ventricular rate to about 150 beats/min, consistent with 2 : 1
AV node block. The ventricular rate can be irregular if there are
varying degrees of AV node block. Typical sawtooth-appearing
flutter waves can be seen on the surface ECG.
Atrioventricular nodal reentry tachycardia (AVNRT; Fig. 25.4)
is a reentry circuit within the AV node or perinodal tissue
characterized by a rapid-onset, regular tachycardia with a rate
typically between 150 and 250 beats/min. There are two pathways
within the AV node with different conduction properties. The
difference in conduction allows for a premature atrial contraction
(PAC) or premature ventricular contraction (PVC) to stimulate
conduction down one pathway while the other is refractory. At
the right timing, conduction can then propagate retrograde up
the previously refractory pathway, thereby initiating a continuous
circuit within the AV node. Conduction of the atria (retrograde)
and ventricle (anterograde) occur almost simultaneously in this
setting; this is reflected in an ECG that shows a P wave that is
either buried in the QRS complex or occurs just shortly after it
(pseudo S wave in inferior leads).
Atrioventricular reentry tachycardia (AVRT) is a reentry circuit
involving the AV node and an atrioventricular bypass tract some
distance from the AV node. Like AVNRT, it is precipitated by a
PAC or PVC and is characterized by a rapid onset with a ventricular rate between 150 and 250 beats/min. If conduction occurs
initially down the AV node and then retrograde up the bypass
tract, depolarization of the His-Purkinje system and synchronized
ventricular contraction occur and the QRS complex is narrow
(orthodromic AVRT). A retrograde P wave is typically seen further
after the QRS than in AVNRT. If conduction occurs down the
bypass tract first, there is slow myocyte-to-myocyte ventricular
depolarization with subsequent retrograde conduction through
the AV node, leading to a wide QRS complex on surface ECG
(antidromic AVRT). A prior ECG can be helpful in establishing
the diagnosis, as it may identify preexcitation down a bypass
tract characterized by a short PR interval with a delta wave
(Wolff-Parkinson-White syndrome).
Atrial fibrillation with conduction down an accessory pathway
(Fig. 25.5) is of concern, as it can lead to ventricular fibrillation.
Rapid irregular depolarization of wavelets within the atrium
can conduct directly down the bypass tract into the ventricle
without protection by the AV node, leading to a wide complex
irregular tachycardia with a ventricular rate that can be greater
than 250 beats/min.
Atrial tachycardia (Fig. 25.6) involves an ectopic atrial pace-
maker that can overtake the rate of the sinus node. These
tachycardias are more likely to occur under a state of sympathetic
activation and thus are more common in the ICU. Atrial tachycardia is characterized by an acute-onset, regular tachycardia
with a ventricular rate generally less than 220 beats/min. There
is often a slow increase in rate (warm up) over the first 5 to 10
seconds. Atrial tachycardia is also characterized by frequent short
bursts. The ECG is characterized by a regular ventricular rate
and a P wave morphology distinct from the P wave in sinus
rhythm that depends on the anatomic origin of the ectopic atrial
ac tivity.
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Fig. 25.4 Typical atrioventricular nodal reentry tachycardia. Regular narrow complex tachycardia
with pseudo–S wave pattern seen in inferior leads and retrograde P wave seen shortly after the
QRS in lead V1.
Fig. 25.5 Preexcited atrial fibrillation characterized by a bizarre, wide complex irregular
tachycardia.
CHAPTER 25 Diagnosis and Treatment of Unstable Supraventricular Tachycardia 255
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Fig. 25.6 Atrial tachycardia with 2 : 1 atrioventricular block. Note the P waves in lead III that do
not appear to be sinus P waves. The 2 : 1 atrioventricular pattern is most clearly seen in lead V1.
Multifocal atrial tachycardia (MAT) involves the presence of
multiple ectopic atrial pacemakers with a faster rate than the
sinus node. The ECG shows an irregular ventricular rhythm
with at least three distinct P wave morphologies and variable
PR intervals. MAT is associated with severe pulmonary disease,
often during an acute exacerbation. Thus MAT is not uncommon
in the ICU.
THERAPY
The therapy for SVT outlined is largely consistent with the 2015
American Heart Association (AHA) Advanced Cardiac Life
Support (ACLS)4 guidelines and the 2015 American College of
Cardiology (ACC)/AHA/Heart Rhythm Society (HRS) SVT
guidelines.5 Patients with SVT should be initially evaluated for
hemodynamic instability. This includes assessment of blood
pressure, cardiopulmonary status, mental status, and peripheral
perfusion by physical examination.
If it is clear that the SVT is causing hemodynamic instability,
it should be immediately treated with synchronized DCCV,
regardless of the exact rhythm. Adequate sedation should be
provided during the procedure if tolerated hemodynamically.
Pads should be placed on the chest with the heart between the
pads. The initial voltage of cardioversion depends on the suspected
arrhythmia based on QRS width and regularity of the tachyarrhythmia. Cardioversion can be repeated at a higher voltage if
initially unsuccessful. A second set of pads may be applied to
the patient’s chest to increase the voltage, especially for patients
with a large body habitus. Repeated recurrence of SVT should
prompt consideration for the use of an antiarrhythmic drug
(AAD) and consultation with an electrophysiologist.
For patients who have a regular tachycardia that causes
symptoms but are hemodynamically stable, vagal maneuvers
should be performed to temporarily block AV node conduction.
Vagal maneuvers include carotid massage, having the patient
bear down, and application of ice-cold water to the face. Performed appropriately, vagal maneuvers can terminate AV
node–dependent reentrant arrhythmias (AVNRT, AVRT) in up
to 20% of patients.6 A modified Valsalva maneuver with transition
from a sitting to supine position with passive leg raise after
Valsalva strain was shown to improve the success rate for cardioversion to about 43% in the REVERT trial.7 For SVT due to
enhanced automaticity or due to non-AV node–dependent
reentrant arrhythmias (atrial fibrillation, atrial tachycardia, atrial
flutter, MAT), vagal maneuvers may temporarily block AV node
conduction to unmask atrial activity. This can be useful diagnostically, especially during 2 : 1 atrial flutter when typical flutter waves
may not be easily discerned without increasing the degree of AV
node block.
For patients who do not respond to vagal maneuvers, adenosine
should be administered. Adenosine is a short-acting endogenous
nucleotide that blocks AV node conduction for a few seconds.
Its half-life is very short, as it is metabolized by red blood cells;
the drug should be administered rapidly via a large-bore IV and
flushed with saline. Like vagal maneuvers, adenosine is useful
therapeutically and diagnostically, as it can terminate AV node–
dependent reentry SVT or unmask atrial activity with increased
AV node block. Caution should be taken in administering the
drug to patients with significant reactive airway disease, as it
can cause bronchospasm. Patients who have undergone heart
transplantation are particularly sensitive to adenosine and should
receive a smaller dose. Adenosine can precipitate atrial fibrillation
in up to 10% to 15% of patients after administration.
of consequence with antidromic AVRT, as conversion to atrial
fibrillation in this setting can cause rapid conduction down the
atrioventricular bypass tract and lead to hemodynamic instability.
8
This is
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In addition to adenosine, β-blockers and nondihydropyridine
calcium channel blockers (diltiazem, verapamil) can also be used
to block the AV node and suppress node-dependent reentrant
tachycardias. Caution should be exercised with the use of these
agents in a critically ill patient given a longer half-life and more
potently negative inotropic effects than adenosine. AV nodal
blockers are also effective in controlling the ventricular rate of
atrial tachyarrhythmias.
An AAD can be administered to cardiovert patients with
SVT, to facilitate DCCV, or to promote maintenance of sinus
rhythm. The most commonly used AAD used in the acute setting
by intensivists is the class III drug amiodarone. The drug has
properties of all the major classes in the Vaughan Williams–Singh
antiarrhythmic classification and is less likely to be proarrhythmogenic than other AADs. Amiodarone is frequently used to
control the rate of atrial fibrillation and to prevent recurrence
after spontaneous or DC cardioversion. Use of amiodarone long
term should be limited given its toxicities (thyroid, pulmonary,
liver, skin). Other AADs may be used in consultation with and
electrophysiologist depending on the clinical scenario.
Unlike most other SVTs, preexcited atrial fibrillation
frequently causes hemodynamic instability. Vagal maneuvers,
adenosine, or other nodal-blocking agents should not be used
as they have no effect on the conduction of the bypass tract.
Prompt DCCV or administration of procainamide or ibutilide
are reasonable initial management options, with subsequent
consideration of accessory pathway ablation. Procainamide
is a class Ia antiarrhythmic that blocks sodium channels; it
causes decreased conduction velocity manifested on the ECG
with a widening of the QRS complex. It works primarily by
modifying the accessory pathway conduction and decreasing
the degree of preexcitation. Ibutilide is an intravenous class
III antiarrhythmic that terminates preexcited atrial fibrillation
by cardioverting it to sinus rhythm. It can cause potent QTc
prolongation; thus pads should be placed on the patient’s chest
and potassium and magnesium levels should not be low. Ibutilide
should be avoided if the patient has significant hypokalemia or
hypomagnesemia.
After conversion of SVT to sinus rhythm or after achievement
of hemodynamic stability, attention should shift to potential
precipitating causes of SVT and ongoing arrhythmia management.
Consultation with an electrophysiologist should be considered,
especially for AV node reentrant arrhythmias, accessory pathways,
or atrial flutter, as these arrhythmias are readily amenable to
ablation. Ablation should be performed when the patient is
hemodynamically stable and the underlying factors predisposing
to SVT have been addressed.
The full reference list for this chapter is available at
ExpertConsult.com.
CHAPTER 25 Diagnosis and Treatment of Unstable Supraventricular Tachycardia 256.e1
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REFERENCES
1. Link MS. Clinical practice. Evaluation and initial treatment of
supraventricular tachycardia. N Engl J Med.
2012;367(15):1438–1448.
2. Annane D, Sébille V, Duboc D, et al. Incidence and prognosis of
sustained arrhythmias in critically ill patients. Am J Respir Crit
Care Med. 2008;178(1):20–25.
3. Marill KA, Wolfram S, Desouza IS, et al. Adenosine for widecomplex tachycardia: efficacy and safety. Crit Care Med.
2009;37(9):2512–2518.
4. Editorial Board. 2015 American Heart Association Guidelines
Update for Cardiopulmonary Resuscitation and Emergency
Cardiovascular Care. Circulation. 2015;132:S313–S314.
5. Page RL, Joglar JA, Caldwell MA, et al. 2015 ACC/AHA/HRS
Guideline for the Management of Adult Patients With
Supraventricular Tachycardia: A Report of the American College
of Cardiology/American Heart Association Task Force on Clinical
Practice Guidelines and the Heart Rhythm Society. J Am Coll
Cardiol. 2016;67(13):e27–e115.
6. Smith GD, Fry MM, Taylor D, Morgans A, Cantwell K.
Effectiveness of the Valsalva Manoeuvre for reversion of
supraventricular tachycardia. Cochrane Database Syst Rev.
2015;(2):CD009502.
7. Appelboam A, Reuben A, Mann C, et al. REVERT trial
collaborators.. Postural modification to the standard Valsalva
manoeuvre for emergency treatment of supraventricular
tachycardias (REVERT): a randomised controlled trial. Lancet.
2015;386(10005):1747–1753.
8. Strickberger SA, Man KC, Daoud EG, et al. Adenosine-induced
atrial arrhythmia: a prospective analysis. Ann Intern Med.
1997;127(6):417–422. Erratum in: Ann Intern Med 1998 Mar
15;128(6):511.
OUTLINE
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Acute Aortic Regurgitation, 257
Etiology, 257
Pathophysiology, 258
Clinical Presentation, 259
Diagnosis, 259
Treatment, 261
Aortic Stenosis, 262
Etiology, 262
Treatment, 262
Post–Transcatheter Aortic Valve Replacement Aortic
Regurgitation, 263
Post–Left Ventricular Assist Device Aortic Regurgitation,
264
Acute Mitral Regurgitation, 264
Etiology, 264
Pathophysiology, 265
Clinical Presentation, 265
26
Acute Presentations of
Valvular Heart Disease
Ruth Hsiao, Daniel Blanchard, Barry Greenberg
Diagnosis, 265
Treatment, 267
Ischemic Mitral Regurgitation, 268
Acute Prosthetic Valve Dysfunction, 269
Etiology and Clinical Presentation, 269
Diagnosis, 270
Treatment, 271
Congestive Heart Failure, 271
Prosthetic Valve Endocarditis, 271
Prosthetic Valve Thrombosis, 272
Tricuspid Regurgitation, 272
Etiology, 272
Clinical Presentation, 273
Diagnosis, 273
Treatment, 274
Conclusion, 274
Acute deterioration in valvular function represents a tremendous
challenge to the practicing clinician. The presentation of valvular
emergencies is usually dramatic; a thorough knowledge of predisposing etiologies, hemodynamic abnormalities, and therapeutic
modalities is essential to making appropriate management decisions. Despite an increasing population of patients with prosthetic
valves, a resurgence of rheumatic fever, and the continued rise in
intravenous drug use–associated infective endocarditis, the overall
incidence of valvular emergencies in cardiac intensive care unit
(CICU) settings is low. However, the consequences of a missed
diagnosis or a delay in therapy can be devastating. Therefore, an
important guideline is to always entertain the possibility of acute
valvular dysfunction in a patient presenting with hemodynamic
instability or acute congestive heart failure.
This review focuses primarily on acute dysfunction of the
aortic and mitral valves leading to severe regurgitation and aortic
valves leading to acute stenosis. The unique valvular complications
associated with prosthetic valves and acute tricuspid regurgitation
will also be discussed. Finally, valvular complications associated
with mechanical assist devices will be addressed.
ACUTE AORTIC REGURGITATION
Etiology
Aortic regurgitation occurs as a result of either dilation of the
aortic root and annulus or disruption of the valve leaflets. The
most common etiologies of acute aortic regurgitation are infective endocarditis and aortic dissection.1 Infective endocarditis is
more likely to occur in a congenitally abnormal or rheumatically
involved valve; it results in acute aortic regurgitation through
a process of endothelial damage, development of nonbacterial
thrombotic vegetation, adherence of circulating organisms to
the vegetation, proliferation of infection within the vegetation,
and progressive valve destruction.
tion is complicated by some degree of aortic regurgitation in
approximately 50% of cases.
regurgitation by direct extension of the dissection to the base of
the aortic valve leaflets, dilation of the sinuses with incomplete
coaptation of the leaflets at the center of the valve, involvement
of a valve commissure leading to inadequate leaflet support, and/
or prolapse of the dissection flap across the aortic valve into
2
Acute, type A, aortic dissec-
3,4
Aortic dissection can lead to aortic
257
CHAPTER 26 Acute Presentations of Valvular Heart Disease 257.e1
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Keywords
acute valvular heart disease
acute heart failure
acute valve regurgitation
acute valve stenosis
acute valve dysfunction
acute prosthetic valve dysfunction
258 PART IV Noncoronary Diseases: Diagnosis and Management
160
LV volume (mm/m
)
Acute
LV pressure (mm Hg)
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BOX 26.1 Etiologies of Acute
Aortic Regurgitation
Infective endocarditis
Aortic dissection—predisposing and associated conditions
Hypertension
Marfan syndrome
Congenital bicuspid aortic valve
Coarctation of aorta
Ehler-Danlos syndrome
Turner syndrome
Chest trauma
Rupture of a myxomatous valve
Systemic connective tissue disorders
Ankylosing spondylitis
Systemic lupus erythematosus
Granulomatous diseases
Tertiary syphilis
Giant cell arteritis
Takayasu arteritis
the left ventricular outflow tract in diastole, impeding leaflet
closure. Other etiologies of acute aortic regurgitation are listed
in Box 26.1.
40
30
20
10
0
Fig. 26.1 Diastolic pressure-volume relationships in the left
ventricle. Acute regurgitation is sudden volume loading of the left
ventricle without the benefit of adaptive ventricular remodeling.
It results in the left ventricle functioning on the steep portion of
the normal curve (dotted line). Chronic regurgitation is volume
loading in the presence of a remodeled ventricle. It shifts the
curve to the left and allows normalization of left ventricular (LV)
filling pressure at significantly increased LV volumes. Hypertrophy
(e.g., aortic stenosis) shifts the curve to the right and results in a
noncompliant ventricle that is highly dependent on atrial booster
pump function for LV filling. (From Hall RJ, Julian DG. Diseases of
the Cardiac Valves. New York: Churchill Livingstone, 1989; 291.)
Hypertrophy
Normal
200406080 100 140120
regurgitation
Chronic
regurgitation
2
Pathophysiology
The presentation of acute, severe aortic regurgitation differs
significantly from that of chronic aortic regurgitation owing to
the dramatic hemodynamic changes that occur when the
unadapted left ventricle (LV) is suddenly required to augment
total stroke volume in order to maintain normal forward flow
while simultaneously being exposed to a substantial increase in
volume overload. The basic function of the heart is to maintain
cardiac output commensurate with body demands. In the normal
setting, it does so while operating on the flat portion of the
curvilinear LV diastolic pressure-volume relationship and filling
pressures remain low. Cardiac output is the product of heart
rate and forward stroke volume. Forward stroke volume is the
total stroke volume minus the regurgitant volume. Under normal
circumstances, the latter is negligible so that total and forward
stroke volumes are synonymous.
In acute, severe aortic regurgitation, the large regurgitant
volume imposed on the unprepared LV markedly reduces forward
stroke volume and shifts the LV diastolic pressure–volume
relationship to the steep ascending portion of the curve. Because
the LV and its surrounding pericardium have limited distensibility,
acute increases in LV end-diastolic volume due to regurgitant
flow result in an abrupt rise in LV end-diastolic pressure (LVEDP)
(Fig. 26.1). This leads to a rapid increase in the ventriculoatrial
gradient, which can cause the mitral valve to close prematurely
before the onset of the next systole. This is beneficial in that the
high LVEDP is not transmitted to the pulmonary venous system
and it offers a degree of protection against the development of
pulmonary edema. However, protection owing to premature
mitral valve closure can be lost if a further rise in the ventriculoatrial gradient reopens the mitral valve in late diastole, leading
to diastolic mitral regurgitation. Systolic mitral regurgitation
can also manifest from the persistent ventriculoatrial gradient
as a result of extension of the high LVEDP level to the isovolumic
contraction period during early systole, causing mitral valve
opening. This mitral regurgitation is usually effective in lowering
the LVEDP and the left atrium (LA) essentially serves as a reservoir
for blood that has regurgitated from the aorta to the LV. However,
left atrial pressure may rise further, leading to pulmonary edema.
5
Coronary ischemia can complicate acute aortic regurgitation
as a reduction in diastolic coronary flow leads to a decrease in
myocardial perfusion, while elevated LVEDP and tachycardia
increase myocardial oxygen demand. Diastolic coronary flow
may be reduced by a reduction in diastolic blood pressure in
the aorta, elevation of diastolic pressures in the LV, and by the
adverse effects of regurgitant flow on forward flow into the
coronary vessels owing to the Venturi effect. The supply-demand
mismatch that develops in the setting of acute aortic regurgitation
is worsened further if obstructive coronary lesions are present
or when aortic dissection impairs coronary flow.
6
To further complicate the picture, reflex sympathetic activation,
in response to a reduction in cardiac output and systemic blood
pressure, produces tachycardia and increases systemic vascular
resistance (SVR). This rise in SVR further worsens regurgitant
flow and impedes ejection of blood from the LV to the aorta so
that a rise in aortic systolic pressure is inhibited. In some cases,
the LV and aortic diastolic pressures are equalized. As opposed
to chronic aortic regurgitation, aortic diastolic pressure usually
does not fall significantly in the acute setting for two reasons:
(1) the rapid increase in LVEDP reduces the driving gradient
between the aorta and LV and (2) peripheral runoff is limited
by an increase in SVR.
7,8
CHAPTER 26 Acute Presentations of Valvular Heart Disease 259
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Clinical Presentation
The clinical features of aortic regurgitation are profoundly
different in the acute compared to the chronic setting. These
differences include the presence of markedly elevated LVEDP
and absence of a wide pulse pressure in patients with acute severe
aortic regurgitation. Because compensatory structural changes
in the LV develop gradually over time, the presentation of an
additional volume load imposed by acute aortic regurgitation
on the unprepared LV may lead to the rapid onset of severe
congestive heart failure or cardiogenic shock.
9,10
Detection of
aortic regurgitation can be difficult in the acute setting; it is
often misdiagnosed as another acute condition, such as sepsis,
pneumonia, or nonvalvular heart disease.
5
Patients with acute aortic regurgitation typically present
with severe dyspnea, weakness, or hypotension. They are often
tachycardic. The LV impulse may be normal in both location
and duration. Owing to early mitral valve closure from the
rapid elevation of LVEDP and consequent reversal of pressures
between the LV and LA in late diastole, the first heart sound is
often soft or inaudible. Occasionally, mitral valve closure may
be heard during diastole and accompanied by diastolic mitral
regurgitation.
11,12
The Austin-Flint murmur, which is thought
to represent turbulent flow from the LA to the LV because of
partial mitral valve closure from the aortic insufficiency jet, is
either absent or brief and ceases when LV pressure exceeds LA
pressure in diastole.
13,14
An accentuated pulmonic closure sound
suggests elevated pulmonary arterial pressure. A third heart sound
(S3) is frequently heard. A fourth heart sound (S4), however,
is usually not present because the mitral valve is either closed
before atrial systole occurs or LVEDP is already so high that
there is little flow to the ventricle during this period. The acute
aortic regurgitation murmur is characteristically short, early,
and of medium pitch, unlike the long, high-pitched murmur
of chronic aortic regurgitation. In tachycardic patients, this
diastolic murmur can easily be overlooked. Edema and weight
gain are not often seen in severe acute aortic insufficiency
because there is inadequate time for substantial secondary salt
and water retention. The extremities may be cool and mottled
owing to both poor cardiac output and elevated SVR. Peripheral
manifestations characteristic of chronic aortic regurgitation, such
as wide pulse pressure and others (e.g., Quincke’s pulse, water
hammer pulse), are uncommon in the acute setting. Clinical
features seen in acute and chronic aortic regurgitation are listed in
Table 26.1.
Diagnosis
The diagnosis of acute aortic regurgitation should be considered
in the differential of any patient presenting with acute pulmonary
edema or circulatory collapse. A history of known valvular disease,
evidence of infective endocarditis, long-standing hypertension,
Marfan syndrome, or chest trauma should make one particularly
suspicious. Initial diagnostic testing in patients suspected of
having acute aortic regurgitation includes an electrocardiogram
(ECG), chest radiograph, blood cultures (if infective endocarditis
is suspected or if the patient has a prosthetic valve), and a
transthoracic echocardiogram (TTE).
TABLE 26.1 Clinical Features of Severe
Aortic Regurgitation
Feature Acute Chronic
Congestive heart
failure
Rhythm Sinus tachycardia Regular rate
Point of maximal
impulse
Pulse pressure Normal Widened
Heart sounds
S
1
S
2
S
3
S
4
Aortic regurgitation
murmur
Cardiac output Decreased Normal
LVEDP Increased Normal
LV size Normal Increased
LV, Left ventricle; LVEDP, left ventricular end-diastolic pressure.
An ECG is required in all patients with pulmonary edema,
primarily to rule out acute myocardial infarction (MI). The ECG
can also be helpful in the patient with acute aortic regurgitation
to identify evidence of myocardial ischemia or injury that results
from the hemodynamic perturbations that adversely affect the
myocardial supply and demand ratio. The ECG in acute aortic
regurgitation may be normal with a left axis deviation. With
early LV volume overload, there can be Q waves in leads I, aVL,
and V3 to V6. As disease progresses, the prominent initial forces
decrease but total QRS amplitude increases.
In the absence of preexisting heart disease, the chest radiograph
generally reveals a normal cardiac silhouette with evidence of
pulmonary edema (Fig. 26.2). A widened aortic root suggests the
presence of dissection. Noninvasive imaging by TTE provides
crucial information regarding the presence, severity, and etiology
of the valve lesion. With severe aortic regurgitation, in addition
to visualizing the regurgitant jet with color Doppler, quantitative
measurements, such as jet or vena contracta (narrowest portion
of regurgitant jet immediately distal to valve orifice) width, can
be obtained (Fig. 26.3, Video 26.1). A jet width greater than 65%
of LV outflow tract and vena contracta greater than 0.6 cm are
consistent with severe aortic regurgitation.5 Continuous wave
Doppler is used to calculate the pressure half-time, which reflects
the equilibration between aortic and LV diastolic pressure. With
acute, severe aortic regurgitation, the rapid equilibration of pressures results in a short pressure half-time of less than 300 msec.15
Other echocardiographic findings supportive of severe aortic
regurgitation include premature closure of the mitral valve,
detected best by M-mode echocardiography and holodiastolic
flow reversal in the descending aorta (Fig. 26.4). Transesophageal
echocardiography (TEE) may be required in individuals in whom
transthoracic echo windows are limited. In addition, TEE has
increased sensitivity for evaluating the underlying etiology of
aortic regurgitation, such as endocarditis (vegetations or aortic
root abscess; Fig. 26.5, Video 26.2) or aortic dissection (dissection
16,17
flap).
Rapid and sudden Insidious
Not hyperdynamic and
nondisplaced
Soft or absent Soft
Soft A2, accentuated P2 Normal P2
Present Absent
Absent Usually absent
Soft, early Holodiastolic
Hyperdynamic and
shifted inferolaterally
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