Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3736_Библиотеки_им_академика_М_И_Перельмана
.pdf
13 Introduction toElectrophysiology Devices
https://t.me/medicina_free
137
One of the most common problems with a
permanent pacemaker or ICD is either a lead
fracture or a break in the insulation of the wire.
The lead impedance (measured in ohms) will
provide information on the integrity of a lead.
An abrupt or greater than 30% change in the lead
impedance is concerning. If a lead itself fractures, the impedance or resistance will go up. If
the insulation is broken, the impedance or resistance will go down. This also can result in premature battery depletion and oversensing. If a
lead problem is suspected based on the device
interrogation, the next step is to obtain a chest
x-ray, both anterior posterior and lateral [4]. If
there is an abrupt rise or fall in the impedance on
the RV lead in patient with history of complete
heart block or who is dependent on their device,
the patient may need to be hospitalized to manage this issue. Lead fractures can also manifest
themselves as loss of capture, oversensing, and
undersensing.
Loss of capture means that a pacemaker spike
can be seen on the monitor, but no depolarization
of the heart occurs (Fig.13.5). If you are evaluating a patient with a temporary transvenous pacemaker, the rst step is to check all the connections.
Then you can turn the milliamps on the device
console slowly to see if this changes. Consider
ordering a chest x-ray at this point to check lead
position. Acute causes of failure to capture
include lead dislodgement or malposition, which
can be more common with temporary pacemakers or in the immediate post-operative period
after implantation of a permanent device.
Premature battery depletion is another cause of
loss of capture. Depending on the indication for
the device, the patient may need to be admitted
for expedited generator change. Other causes
include battery at end of life of device, lead fracture, insulation breach, brosis where the lead is
implanted, as well as metabolic derangements
[7].
Undersensing means there is a failure to sense
the intrinsic activity. Pacing spikes will be seen
where they should not be present on telemetry or
an EKG.Commonly, pacemaker spikes may be
seen within intrinsic QRS complexes. To correct
this, the fence or sensitivity needs to be lowered
so that the device appropriately senses chamber
depolarization. The lead may need to be replaced
if programming changes do not correct the
problem.
Fig. 13.5 Loss of capture in a dual chamber pacemaker secondary to end of life. There are no QRS waveforms seen
after any pacemaker spikes
138
https://t.me/medicina_free
J. A. Dietrich
Oversensing means there is inappropriate
detection of a signal that is not intrinsic activity.
There is a lack of pacing activity when there
should be spikes on telemetry or EKG.To correct
this, the fence needs to be raised so that background noise is not detected by the device as
chamber depolarization. In emergency settings,
the device sensitivity can be set to least sensitive
(highest mV level) or asynchronous, where pacing occurs at a xed rate and sensing is disabled
by utilizing the magnet. The lead may need to be
replaced if programming changings do not correct the problem.
One of the other issues encountered on a
device interrogation maybe called lead noise.
This essentially means there is an issue interfering with the device’s ability to sense the intrinsic
activity. This can be due to lead fracture or insulation breach, oversensing, interactions between
leads, or electromagnetic interference from external source. If the noise is on a RV lead in an ICD,
there would be concern that the device could provide inappropriate shocks to the patient as it
thinks the noise is VF.There are some algorithms
on ICDs which can differentiate lead noise from
VT/VF and withhold detection if there is lead
noise noted on the RV lead.
There may be times when the debrillator
function of an ICD should be turned off urgently
or a programmer is not available. This could
occur if a patient is having recurrent inappropriate shocks or if a patient is at end of life. Placing
a magnet overtop of the ICD will suspend any
arrhythmia therapies but will not interfere with
the pacing programing of a debrillator if it is
needed [5].
Clinical Pearls
• CRT has leads in right and left ventricle to
resynchronize the “squeeze”.
• CRT should have a high percentage of biven-
tricular pacing to get maximal benet.
• RV apical pacing appears as LBBB on EKG,
while biventricular pacing may have a more
RBBB morphology.
• Magnet over a pacemaker asynchronously
paces at a preprogrammed rate.
• Magnet over an ICD suspends any arrhythmia
therapies but does not affect the pacing
function.
• Oversensing = underpacing; undersensing =
overpacing.
References
1. Weachter R. Leadless cardiac pacemaker therapy.
An overview for the hospitalist. Am J Hosp Med.
2018;2(3):2018.016. https://doi.org/10.24150/
ajhm/2018.016.
2. Kenny T.The nuts and bolts of cardiac pacing. WileyBlackwell; 2005.
3. Wang P. Pacemakers. 2022. American College of
Cardiology Self-Assessment Program. www.acc.org.
4. Kusumoto F, Schoenfeld M, Barrett C, Edgerton J,
Ellenbogen K, Gold M, Goldschlager N, Hamilton R,
Joglar J, Kim R, Lee R, Marine J, McLeod C, Oken
K, Patton K, Pellegrini C, Selzman K, Thompson
A, Varosy P. 2018 ACC/AHA/HRS guideline on the
evaluation and management of patients with bradycardia and cardiac conduction delay. J Am Coll Cardiol.
2019;74(7):e51–e156. https://doi.org/10.1016/j.
jacc.2018.10.044.
5. Chen J. Implantable cardioverter-debrillator. 2022.
American College of Cardiology Self-Assessment
Program. www.acc.org.
6. Al-Khatib S, Stevenson W, Ackerman M, Bryant W,
Callans D, Curtis A, Deal B, Dickeld T, Field M,
Fonarow G, Gillis A, Granger C, Hammill S, Hlatky
M, Joglar J, Kay G, Matlock D, Myerburg R, Page
R. 2017 AHA/ACC/HRS guideline for management
of patient with ventricular arrhythmias and the prevention of sudden cardiac death. J Am Coll Cardiol.
2018;72(14):e91–e220. https://doi.org/10.1016/j.
jacc.2017.10.054.
7. Sabbagh E, Abdelfattah T, Karim M, Farah A, Grubb
B, Karim S.Causes of failure to capture in pacemakers and implantable cardioverter-debrillators. J Innov
Card Rhythm Manag. 2020;11(2):4013–7.
Cardioversion
https://t.me/medicina_free
LoraRaines
14
Cardioversion refers to the restoration of sinus
rhythm, either by electrical cardioversion
(DCCV) or pharmacologic cardioversion. Direct
current cardioversion is performed by delivering
an electrical shock that is synchronized with the
QRS to avoid inducing ventricular brillation.
Pharmacologic cardioversion is performed by
administering an antiarrhythmic agent for the
purpose of restoring sinus rhythm. Patients
should be adequately anticoagulated prior to proceeding with either electric or pharmacologic
cardioversion and should continue oral anticoagulation (OAC) for at least 4weeks post cardioversion [1].
Electrical Cardioversion
For patients undergoing electrical cardioversion,
electrodes are placed in an anteroposterior location. The patient is then sedated, and once they
are no longer conscious, a synchronized electrical shock is delivered in an attempt to restore normal sinus rhythm. The primary risk associated
with a cardioversion is stroke. Depending on
whether or not a patient has been adequately anticoagulated, a TEE may be performed just prior to
the cardioversion to rule out a LAA thrombus. In
some cases, a CT scan may be performed to rule
out LAA thrombus.
Pharmacologic Cardioversion
Certain antiarrhythmics may be used to try to
convert a patient to sinus rhythm. Some of the
most common drugs used are high dose ecainide
or propafenone and ibutilide [1, 2]. Pharmacologic
cardioversion should be performed in the hospital
during continuous telemetry monitoring [1].
For patients receiving Ibutilide, the major risk
is QT prolongation and development of polymorphic VT.ECG monitoring should be continuous
and should be continued for ≥4 hours after
administration [2].
An oral dose of ecainide or propafenone can
be used to try to restore sinus rhythm. Because
conversion to sinus rhythm may be associated
with bradycardia due to sinus node or AV node
dysfunction, the initial conversion trial should be
performed in a monitored setting with continuous
ECG/telemetry [1, 2].
Recommendation forPrevention
ofThromboembolism [3]
L. Raines (*)
Wellstar Health System, Marietta, GA, USA
e-mail: Lora.Raines@wellstar.org
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023
R. Musialowski, K. Allshouse (eds.), Cardiovascular Manual for the Advanced Practice Provider,
https://doi.org/10.1007/978-3-031-35819-7_14
• For patients with AF or Autter of 48 hours
duration or longer (or if duration unknown),
anticoagulation with warfarin (INR 2–3), a
139
140
https://t.me/medicina_free
L. Raines
factor Xa inhibitor, or a direct thrombin inhibitor is recommended for at least 3 weeks
before and at least 4 weeks after cardioversion, regardless of CHA2DS2VASc score or
method (electrical or pharmacologic) (Class
I).
• For patients with AF or Autter of more than
48hours duration (or unknown duration) that
requires immediate cardioversion due to
hemodynamic instability, anticoagulation
should be started as soon as possible and continued for at least 4weeks after DCCV unless
contraindicated (Class I).
• After DCCV for AF of any duration, decision
on long-term OAC should be based on risk of
both thromboembolism and bleeding (Class
I).
• If AF/Autter duration less than 48 hours with
CHA2DS2VASc≥2in men and≥3in women,
administration of heparin, factor Xa inhibitor,
or direct thrombin inhibitor is reasonable as
soon as possible before cardioversion, followed by long-term therapy (Class IIa).
• For patients with AF/AFL duration 48 hours
or longer (or unknown) who have not been
anticoagulated for the preceding 3weeks, it is
reasonable to perform a TEE before cardioversion and proceed with cardioversion if no
LA/LAA thrombus is identied, provided that
anticoagulation is started before the TEE and
maintained for at least 4weeks after cardioversion (Class IIa).
• In patients with AF/AFL of less than 48hours
duration with CHA2DS2VASc=0in men and
1in women, initiation of IV heparin, factor Xa
inhibitor, or direct thrombin inhibitor vs no
anticoagulation therapy may be considered
before DCCV, without need for postcardioversion anticoagulation.
Clinical Pearls
• Patients can be converted with electricity or
medications.
• If a patient is in an atrial arrhythmia > 48
hours, they should have an atrial thrombus
ruled out prior to elective cardioversion of any
kind.
• Any patient post cardioversion should be anticoagulated for at least 4 weeks after
conversion.
• CHA2DS2VASc score is used to evaluate
patient’s stroke risk.
References
1. January CT, Wann LS, Alpert JS, Calkins H, Cigarroa
JE, Cleveland JC Jr, Conti JB, Ellinor PT, Ezekowitz
MD, Field ME, Murray KT, Sacco RL, Stevenson
WG, Tchou PJ, Tracy CM, Yancy CW, American
College of Cardiology/American Heart Association
Task Force on Practice Guidelines. 2014 AHA/ACC/
HRS guideline for the management of patients with
atrial brillation. J Am Coll Cardiol. 2014;64(21):e1.
2. Baltazar RF.Basic and bedside electrocardiography.
Philadelphia: Wolters Kluwer; 2009.
3. January CT, Wann LS, Calkins H, Chen LY, Cigarroa
JE, Cleveland JC Jr, Ellinor PT, Ezekowitz MD, Field
ME, Furie KL, Heidenreich PA, Murray KT, Shea JB,
Tracy CM, Yancy CW. 2019 AHA/ACC/HRS focused
update of the 2014 AHA/ACC/HRS guideline for the
management of patients with atrial brillation. J Am
Coll Cardiol. 2019;74(1):104–32.
Cardiac Syncope
https://t.me/medicina_free
KristaAllshouse andRichardMusialowski
15
Introduction andPathophysiology
Cardiovascular syncope is described as a sudden
loss of consciousness with loss of postural tone.
This clinical presentation may be caused by
tachycardia, bradycardia, and hypotension.
Syncopal events are common, occurring 3% in
men and 3.5% in women over a lifetime according to the Cleveland Clinic [1]. These events
become more common as individuals age. There
are many causes, some of which are more concerning. Cardiac syncope is the most concerning
etiology as it carries a 1-year mortality rate of
20–40%. The high risk of patient mortality occurs
within 1–6 months after an event especially in
patients with structural heart disease. Thorough
evaluation for the underlying cause of a syncopal
event is essential for risk stratication and prognosis. Cardiac etiologies may be divided into
electrical and obstructive. Electrical causes
include bradycardic or tachycardic arrhythmias.
Obstructive causes include HCM, valvular disease, tamponade, and pulmonary embolus (PE)
(see Table15.1).
K. Allshouse (*)
Atrium Health, Levine Childrens’ Congenital Heart
Center, Charlotte, NC, USA
e-mail: Krista.Allshouse@atriumhealth.org
R. Musialowski
Sanger Heart and Vascular Institute, Atrium Health,
Charlotte, NC, USA
e-mail: Richard.Musialowski@atriumhealth.org
Table 15.1 Cardiac causes of syncope
Electrical Structural
VT/Torsades
VF
Bradycardia: SSS-sinus arrest,
conversion pause, marked sinus brady
Heart block
Tachycardia: SVT, WPW with atrial b
Inherited channelopathy-LQTS,
Brugada, CPVT
Adapted from chart Recognizing Life-Threatening Causes
of Syncope. Cardiology Clinics. Vol. 31, Issue 1, P51–66.
Feb. 1, 2013
HCM
AS
MS
Atrial
myxoma
Tamponade
Pulmonary
HTN
PE
Symptoms
Cardiac syncope often occurs suddenly, without
preceding symptoms. It is often associated with
true loss of consciousness, and the patient often
incurs traumatic injury from the loss of postural
tone. Some patients may experience chest pain,
shortness of breath, palpitations, or dizziness
before a syncopal episode. Syncope often has
prodromal symptoms including sweating, nausea, or near loss of consciousness. Symptoms
prior to the event are important to ascertain, as
cardioinhibitory syncope allows the patient to sit
or lay down before they lose consciousness (see
cardioinhibitory below). The presence of these
prodromal symptoms often suggests an etiology
other than high risk cardiac syncope.
Most acute syncope evaluations are completed
on an inpatient basis if the patient has underlying
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023
R. Musialowski, K. Allshouse (eds.), Cardiovascular Manual for the Advanced Practice Provider,
https://doi.org/10.1007/978-3-031-35819-7_15
141
142
https://t.me/medicina_free
K. Allshouse and R. Musialowski
cardiac disease or if the event appears to be high
risk (i.e., resulting in injury). The etiology of
more than half of syncopal events may be discerned from the history alone. Detailed historytaking is critical to guide additional testing. It is
imperative to be aware of “red ags” indicating
more concerning symptoms including syncope
related to exercise (either during or after), syncope without preceding symptoms or with resultant signicant injury. Traumatic facial injuries
are highly suggestive of cardiac syncope. Seizurelike activity and loss of bowl or bladder control
are also concerning but less common with cardiac syncope. These symptoms more commonly
lead to a diagnosis of seizure disorder. Seizures
may occur in severe syncope of any etiology due
to hypoperfusion of the brain.
It is critical to obtain a specic, detailed history regarding the syncopal episode. The events
preceding the syncopal event should be discussed.
This includes symptoms, relation to activity, how
the patient looked to others, any resultant injury,
and how quickly the patient recovered. The
patient’s last conscious recollection before the
event and the rst memory afterward is very
important to determining the diagnosis. Ask about
any similar symptoms in the past.
The patient’s medical history should be
reviewed including medical problems, daily
medications, over the counter meds/supplements,
and any new medications recently started.
Exercise habits and tolerance should be ascertained. Social history is important regarding
smoking, vaping, or use of illicit or synthetic
drugs. Family history should be obtained including any history of sudden cardiac death (SCD)
before age 50, unexplained motor vehicle accidents, SIDS deaths or drownings, ICDs/PPMs,
and seizure disorders.
Physical Exam
A full cardiovascular exam is warranted to evaluate potential causes of syncope. Patients with a
cardiac etiology of syncope may have structural
ndings such as a systolic murmur of valvular
dysfunction or hypertrophic cardiomyopathy
(HCM). Vital signs including BP and HR may
show abnormalities, including orthostatic
changes. Abnormal extra heart sounds (S3, S4) or
displaced impulses may be noted.
Diagnostics
EKG is the rst test that should be performed
with syncope. This may show evidence of ischemia, abnormalities in conduction, including
signs of block, arrhythmia, or QT interval
prolongation.
Transthoracic echocardiography should be
completed to assess for structural disease if any
abnormalities are found on physical exam.
Echocardiography can assess for valvular abnormalities, HCM, abnormal coronary origins in
young adults, and evaluate for decreased LV
function. Risk of death with low EF and syncope
is high (see Ventricular Tachycardia, VT). If the
etiology of syncope appears to be non-cardiac by
history, echocardiography is not required.
Other tests may be done based upon the ndings of the initial workup. If no structural disease
is found, a patient can have ambulatory monitoring such as event or looping monitors.
Subcutaneous loop recorders may be implanted
for suspicious or recurrent events.
Syncope can occur in a patient with a previously implanted pacemaker. Interrogation of the
device is important to determine the potential
cause including device malfunction and exact
rhythm during the syncopal event. Think of an
implanted pacemaker as a continuous monitor of
the cardiac rhythm. Representatives of the device
manufacturers are always available for
assistance.
Stress testing may be done to rule out exerciseinduced arrhythmias and ischemia if the event
occurred with activity. If underlying coronary
artery disease or congestive heart failure is suspected, a cardiac catheterization may be warranted. An electrophysiology study may be
needed to test the patient’s conduction system
and evaluate for ventricular arrhythmias.
15 Cardiac Syncope
https://t.me/medicina_free
143
Management
If patient has structural disease, management
will be guided by specic disease type. Referral
to a cardiac specialist should be considered. A
patient with signicant HCM and syncope will
likely need medical treatment and potential
ICD.Syncope with a reduced EF and structural
heart disease must be treated as potential VT and
EP evaluation and ICD should be considered. If
a valvular or coronary anomaly is found, surgery
may be the treatment recommendation. If the
patient has ischemia on EKG or stress testing,
cardiac catheterization may be needed for evaluation and ultimate treatment. Symptomatic bradycardia is a common cause of sudden,
unprovoked syncope. If the EKG shows conduction abnormalities, pacemaker implantation may
be needed (see bradycardia). If the EKG shows
QT segment abnormalities suggestive of a channelopathy, further testing may be needed (see
Chap. 11). There are other unusual etiologies
that may require specialized management including pulmonary hypertension, cardiac tamponade, and PE.
Another common type of syncope is neurocardiogenic. This is an umbrella term describing
various types of syncope including reex syncope, vasodepressor syncope, postural syncope,
and autonomic dysfunction. This may be
described as the “common faint” and occurs in a
patient with a normal heart. Prodromal symptoms occur more slowly with preceding symptoms of lightheadedness, blurry/blackened
vision, mufed hearing, sweating, and nausea.
Patients tend to be pale, bradycardic, and sweaty
immediately prior to and after an episode.
Recovery of mentation is usually quick when
supine. The mechanism is not well understood
but is thought to involve dysfunction of the autonomic nervous system, orthostatic intolerance,
and intravascular volume depletion.
Patients may complain of dizziness while
upright, tingling of the ears, nose, ngers, nausea, headaches, fatigue, atypical sharp stabbing
chest pain, and palpitations. It can be worse in the
heat, during menses or with febrile illness.
Postural Orthostatic Tachycardia Syndrome,
POTS, is a subset of this condition where the
heart rate increases 30 beats per minute within 10
minutes of upright posture during a TILT table
test without the blood pressure drop of orthostatic hypotension. TILT table testing has limited
utility and should be considered only if the history of POTS is unclear.
Management of this constellation of symptoms consists of intense oral hydration, salt supplementation, lower extremity exercises (the
Dallas protocol), and compression sleeves for the
calves. Some patient symptoms improve with
medications such as udrocortisone, a mineralocorticoid or midodrine, a vasoconstrictor (alpha
adrenergic agonist). Some patients may also have
improvement with taking selective serotonin
reuptake inhibitors, regulating their menstrual
cycle (OCPs), and other therapies. Many centers
now have multidisciplinary Dysautonomia
Clinics for difcult cases. Difcult to manage
patients may have concomitant collagen vascular
disease or signicant spinal injury.
Patients with high risk and unexplained syncopal events may not be allowed to drive for
6 months (state dependent) following the event
unless underlying cause is corrected.
Clinical Pearls
• Facial or other severe trauma after syncope is
suggestive of a cardiac cause.
• Syncope with structural heart disease or car-
diomyopathy is high risk and ventricular
tachycardia must be considered.
• Prodromal symptoms often suggest a non-
cardiac cause of syncope.
• The clinical history is important to determine
the etiology of syncope.
Further Reading
1. Dick M. Clinical cardiac electrophysiology in the
young. 2nd ed. NewYork: Springer; 2006/2015.
2. Eagle KA, Balinga RR. Practical cardiology.
Evaluation and treatment of common cardiovascular
disorders. Philadelphia, PA: Lippincott, Williams and
Wilkins; 2013.
Part IV
https://t.me/medicina_free
Structural/Valvular Heart Disease
AnneBooke MichaelRinaldi
ElisabethA.Powell LarryWatts
RickMusialowski
Introduction
The heart valves have very important and specic functions which will be
further discussed in this chapter. These valves are instrumental in creating
cardiac output as described in Chap. 2. The bedside description of the cardiac
cycle is dened by the opening and closing of the valves during ventricular
systole and diastole. The heart sounds (S1 and S2) heard during physical
examination are the closure of the atrioventricular and semilunar valves,
respectively. This synchronized series of valve open and closure allows
proper movement of blood oxygenating the tissues with each cardiac
contraction.
Pathologic changes of the valves result in very specic disease states with
corresponding physical examination ndings. These pathologies may be
described as stenotic or regurgitant. As the leaets degenerate due to age and
other etiologies, the structure of the leaets and/or supportive apparatus will
change. Depending on the valve and underlying etiology of the changes, the
leaets will develop reduced mobility (stenosis) and restrict the forward
movement of blood. The leaets may become incompetent and allow blood
to reverse course back to the cardiac chamber just exited (regurgitant). Often,
there is a combination of both pathologies.
A. Booke · M. Rinaldi
Interventional and Structural Heart Cardiology, Atrium Health/Sanger Heart and
Vascular Institute, Charlotte, NC, USA
e-mail: Anne.Booke@atriumhealth.org
L. Watts · R. Musialowski
Atrium Health/Sanger Heart and Vascular Institute, Charlotte, NC, USA
e-mail: Michael.Rinaldi@atriumhealth.org; Larry.Watts@atriumhealth.org;
Richard.musialowski@atriumhealth.org
E. A. Powell
Banner University Medical Center, Tucson, AZ, USA
e-mail: elisabeth.powell@bannerhealth.com
146
https://t.me/medicina_free
These different disease states cause a diverse spectrum of symptoms and
physical ndings. Stenotic pathology of the aortic and pulmonic valves
produces a crescendo/decrescendo murmur due to rapidly changing pressure
and volume of blood ow during ventricular systole. This murmur will radiate according to the path of blood ow after passing over the stenotic valve
leaets. Incompetence of mitral and tricuspid valves results in a holosystolic
blowing murmur as blood ows back into the atria at a xed pressure and
volume. Radiation of these murmurs also follows the direction of the turbulent blood ow. These systolic murmurs are noted between S1 and S2.
Incompetence of the aortic and pulmonic valves produces diastolic murmurs
as the high pressure of the great vessels pushes blood back in the ventricles
during ventricular diastole. These sounds occur after the second heart sound
(S2) and are decrescendo in nature due to a runoff of great vessel pressure.
Diastolic sounds of the mitral and tricuspid valves are rare and difcult to
auscultate.
The management of valve disease is dependent on the valve and specic
pathology. This chapter will review the cardiac valves with relevant examples
of regurgitant and stenotic physiology. This is a rapidly advancing eld with
changes in management of valvular heart disease ever evolving. Surgical
intervention with replacement and repair has an important role. Catheter
based interventions are rapidly developing with less associated morbidity and
mortality. Collaborative patient management using structural heart teams,
advanced cardiovascular imaging, and therapeutic discussions are critical for
best practice management.
Structural/Valvular Heart Disease
General Information About Valve Disease
In evaluating patients with known or suspected valvular disease, transthoracic
echocardiography (TTE) is the primary test for assessment of the valve anatomy, etiology, concurrent valve disease, ventricular function, and associated
abnormalities such as aortic dilatation. For stenotic valves, key measurements
include the maximum velocity, mean gradient, and valve area. For regurgitant
valves, key measurements include the regurgitant orice area, regurgitant
volume, and regurgitant fraction as determined by Doppler readings.
Assessment of pulmonary systolic pressures along with RV size and function
is also important. When indicated, additional testing is obtained, including
but not limited to chest X-ray, stress testing, transesophageal echocardiography TEE, CT heart, cardiac MRI, and cardiac catheterization for measurement of hemodynamics.
The American College of Cardiology (ACC) and American Heart
Association (AHA) Indications for surveillance echocardiogram vary depending on stage of valvular disease and patient symptomatology. At a minimum,
patients should be seen for yearly examination. Additionally, patients should
report changes in their symptoms and a physical exam should be performed
at each visit with echo performed if there are changes in exam. The purpose
of follow-up is to prevent consequences of valvular heart disease, including
alterations of ventricular function and pulmonary circulation, and to determine when referral is indicated for consideration of intervention (Fig.1).
Adapted from (6)
Structural/Valvular Heart Disease
https://t.me/medicina_free
Every 1-2 y
(moderate severity)
Mitral Regurgitation
Mitral Stenosis
Every 3-5 y
)
2
Every 3-5 y
(MV area >1.5 cm
(mild severity)
Every 6-12 mo
Every 1-2 y
Dilating LV: more frequently
)
2
)
2
Every year
(MV area <1.0 cm
(MV area 1.0-1.5 cm
147
Every 1-2 y
Every 3-5 y
(mild severity)
Aortic Regurgitation
max 2.0-2.9 m/s)
Aortic Stenosis
Every 3-5 y
(mild severity; V
Every 1-2 y
Stage
Progressive
(Stage B)
(moderate severity)
Every 6-12 mo
Dilating LV: more frequently
max 3.0-3.9 m/s)
max >4 m/s)
Every 6-12 mo
(V
(moderate severity; V
Severe asymptomatic
(Stage C1)
Fig. 1 Type of valve lesion. (Adapted from Otto CM, Nishimura RA, Bonow RO, Carabello BA, Erwin JP III, Gentile F. 2020 ACC/AHA Guideline for the management of
patients with valvular heart disease: a report of the American College of Cardiology/American Heart Association Joint Committee on clinical practice guidelines. J Am Coll
Cardiol. 2021;77(4):e25–e197)
Соседние файлы в папке Библиотека им академика М.И. Перельмана