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_5537_Библиотеки_им_академика_М_И_Перельмана.pdf
agents should be used with caution as patients with significant AS do not
have the ability to augment their cardiac output to compensate for a significant drop in blood pressure.
Ultimately, severe symptomatic AS is treated surgically through valve
replacement. The operative mortality varies significantly depending on
age and co-morbidities. For those patients deemed high risk, percutaneous
valvuloplasty represents a less invasive approach to temporarily improve
symptoms; however, no mortality benefit has been demonstrated with this
technique.
Mitral Stenosis (MS)
Mitral stenosis is a narrowing of the mitral valve opening that impedes
blood flow from the left atrium to the left ventricle during diastole.
Etiology
The most common cause of mitral stenosis is rheumatic heart disease.
After the initial episode of rheumatic fever, a latency period of 20–40
years occurs until the onset of symptoms. Given the widespread use
of antibiotics in the United States, the incidence has decreased significantly over time. However, it still poses a significant problem in developing countries.
Rarer causes of MS include malignant carcinoid, congenital MS, and
collagen vascular diseases, such as systemic lupus erythematosis and
rheumatoid arthritis.
History and Physical
Unless the degree of stenosis is severe, patients are asymptomatic at
rest. Certain clinical situations which increase the heart rate such as
pregnancy, exercise, hyperthyroidism, rapid atrial fibrillation, and fever
can all lead to reduction in ventricular filling time during diastole. This
leads to diminished cardiac output and causes a decline in functional
224
M. Harrison and L. Duvall
capacity, dyspnea, orthopnea, and fatigue. Elevated left atrial pressure
predisposes patients to the development of atrial fibrillation, and pulmonary edema.
Cardiac examination for MS is best conducted with the patient in the
left lateral decubitus position with the stethoscope applied to the cardiac
apex. An accentuated S1 and variable S2 is followed by an opening snap
with an accompanying diastolic, low-pitched, rumbling murmur. Other
physical findings are related to the degree of heart failure (i.e. elevated
JVP, peripheral edema) and the presence of atrial fibrillation (irregular
heart beat).
Diagnosis and Testing
Initially, echocardiography is the diagnostic study of choice to assess for
the presence of mitral stenosis. Echocardiography can identify the severity
and etiology of MS as well as morphologic features of the valve, subvalvular structures, and pulmonary hypertension. On occasion, cardiac
catheterization is indicated to determine the severity of MS and pulmonary
pressures, when clinical and echocardiographic assessments are discordant.
ECG is an insensitive method to detect MS, but may reveal atrial fibrillation, left atrial enlargement and/or right ventricular hypertrophy. On
CXR, patients with advanced disease often demonstrate left atrial or pulmonary artery enlargement and pulmonary congestion.
Treatment
Medical therapy for MS is directed at decreasing the heart rate, reducing
CHF symptoms (most frequently with diuretics), and decreasing the risk
of thromboembolism. Rate control, especially in patients with atrial fibrillation often requires the use of beta blockers, calcium channel blockers,
and/or digoxin. Systemic anticoagulation for patients with mitral stenosis
and ongoing atrial fibrillation is indicated indefinitely. For patients in
sinus rhythm, the severity of MS and the degree of left atrial enlargement
is often considered in the decision to anticoagulate.
225
Valvular Heart Disease
Aortic Regurgitation (AR)
Aortic regurgitation may result from intrinsic abnormalities of the aortic
valve, the ascending aorta, or both. Typically, AR worsens over an extended
period of time, but acute onset AR does occur and often in a dramatic
fashion.
Etiology
Congenital bicuspid aortic valves, rheumatic heart disease, and collagen
vascular diseases are predisposing valvular conditions that can lead to
progressive AR. Senile valvular changes, which are almost always
accompanied by AS, can also lead to regurgitation. One of the important
causes of acute AR is infective endocarditis.
Entities that primarily affect the aortic root distal to the valve can
cause dilation and produce regurgitation. These include aortic dissection,
Marfans disease, thoracic aneurysms, and syphilis aortitis.
History and Physical
Aortic regurgitation presents variably depending on the underlying etiology and natural history. Acute AR typically presents with tachycardia
and severe dyspnea from pulmonary edema. A brief diastolic murmur is
sometimes auscultated. In acute AR, patients should be evaluated for
acute aortic dissection and/or endocarditis.
In those with chronic disease, the degree of symptoms is dependent
on the amount of left ventricular compensation. Those who have
advanced disease describe shortness of breath with exertion and fatigue.
On physical exam, classic features of chronic AR include a widened
pulse pressure (often > 100 mmHg), diastolic decrescendo murmur at the
upper sternal border, and an Austin-Flint murmur which is a low-pitched
diastolic murmur at the apex. Water-hammer pulses, uvular bouncing,
femoral bruits and pulsations in the nail beds (Quinckes pulse) can also
be appreciated.
226
M. Harrison and L. Duvall
Diagnosis and Testing
Similar to other valvular lesions, the ECG and CXR are often nonspecific.
A transthoracic echocardiogram (TTE) is indicated to assess the severity
of AR, left ventricular size and function, dimension of aortic root, leaflet
morphology and evidence of endocarditis. On the basis of TTE findings,
transesophageal echocardiography can be used to clarify the presence of
vegetation on the valve or aortic dissection. Depending on the clinical scenario and institution, MRI/CT can also be utilized to evaluate the aorta
when dissection is suspected.
Treatment
Aortic valve surgery is indicated for patients with increased left ventricular size, reduced LV function, or symptomatic aortic regurgitation. Medical
therapy plays a limited role. Vasodilators (i.e. ACE inhibitors, Hydralazine,
peripherally acting calcium channel blockers) can be used to improve
hemodynamics. Patients who present in decompensated heart failure
require diuretics to relieve pulmonary congestion. Appropriate antibiotics
are indicated when endocarditis is present.
Mitral Regurgitation (MR)
The mitral valve is a complex anatomic structure composed of an annulus, two leaflets and a subvalvular apparatus (chordate tendineae and papillary muscles). Disruption of any one of these components can lead to
mitral regurgitation.
Etiology
Mitral regurgitation etiologies can be organized into six major categories:
(a) Degenerative, which is a primary pathology of the valve itself (i.e.
mitral valve prolapse); (b) Dilated cardiomyopathy, where regurgitation
results from widening of the left ventricle and dilation of the mitral valve
227
Valvular Heart Disease
annulus; (c) Ischemic, syndromes in which ischemia or infarction of papillary muscles disrupt mitral valve functioning; (d) Rheumatic, which is
often associated with concomitant MS; (e) Infective endocarditis, that
destroys the leaflet tissue; and (e) Other, including congenital anomalies
of the valve (i.e. cleft) and hypertrophic cardiomyopathy with obstruction.
History and Physical
Similar to other valvular disease, MR will present variably based on the
natural history of the underlying pathology. Acute MR will present with
significant shortness of breath from pulmonary edema. In the chronic setting, mitral regurgitation can be asymptomatic for years. As the disease
progresses, patients report dyspnea with exertion, palpitations (often from
atrial fibrillation) and other symptoms of heart failure.
On examination, a systolic murmur can be heard best at the apex with
radiation to the axilla. The murmur is often but not always holosystolic.
Crackles on lung exam, lower extremity edema, elevated JVP, and auscultation of an extra heart sound, can identify patients with concomitant
heart failure.
Diagnosis and Testing
All patients with suspected significant MR should undergo an ECG (to
assess for the presence of LVH, left atrial enlargement, and atrial fibrillation) and CXR (for inspection of cardiac size and degree of pulmonary
edema). Confirmatory echocardiography evaluates the degree and etiology of regurgitation. On occasion a right and left heart catheterization is
indicated to further elucidate the severity, and cause of MR as well as
measure pulmonary artery pressures.
Treatment
Severe acute mitral regurgitation often requires stabilization in an intensive
care setting with aggressive afterload reduction through IV nitroprusside
228
M. Harrison and L. Duvall
and on occasion, an intraortic balloon pump. Diuretics are usually needed
to relieve pulmonary congestion. In stable patients, oral vasodilators such
as ACE inhibitors, angiotension receptor blockers, or hydralazine can
achieve the desired effect. Depending on the natural history and etiology
of MR, patients may benefit from surgical repair or replacement of the
valve. Indications for surgery include the presence of symptoms, a reduced
ejection fraction, LV dilatation, pulmonary hypertension, or atrial fibrillation. When technically feasible, mitral valve repair is preferred.
References
1. Bonow RO, Carabello BA, Kanu C, et al. (2006) ACC/AHA 2006
guidelines for the management of patients with valvular heart disease:
A report of the American College of Cardiology/American Heart
Association Task Force on Practice Guidelines (writing committee to
revise the 1998 Guidelines for the Management of Patients With
Valvular Heart Disease): developed in collaboration with the Society
of Cardiovascular Anesthesiologists: endorsed by the Society for
Cardiovascular Angiography and Interventions and the Society of
Thoracic Surgeons. Circulation 114: e84–e231.
2. Maganti K, Rigolin VH, Sarano ME, et al. (2010) Valvular heart dis-
ease: Diagnosis and management. Mayo Clin Proc 85: 483–500.
3. Braunwald E, Bonow RO. (2012) Braunwald’s Heart Disease:
A Textbook of Cardiovascular Medicine. Saunders; Philadelphia,
pp. xxiv, 1961. p.
4. Hurst JW, Fuster V, Walsh RA, et al. (2011) Hurst’s the Heart.
McGraw-Hill Medical; New York, p. 2 v. (xxix, 2444, I–2480 p.).
5. Otto CM, Schwaegler RG, Freeman RV. (2011) Echocardiography
Review Guide: Companion to the Textbook of Clinical
Echocardiography. Saunders, Philadelphia, PA, p. p.
6. Otto CM, Pearlman AS. (1995) Textbook of Clinical Echocardiography.
W.B. Saunders, Philadelphia: p. xiv, 404 p.
229
Valvular Heart Disease
This page intentionally left blankThis page intentionally left blank
Atrial Fibrillation and Flutter
Kabir Bhasin* and Jonathan L. Halperin*
Key Pearls
• Atrial fibrillation (AF) is the most common sustained arrhythmia and
is associated with considerable morbidity and increased mortality.
Atrial flutter is less common.
• Immediate cardioversion is indicated when AF causes hemodynamic
instability manifested as angina, acute heart failure or shock.
• Rate control can usually be achieved by administering beta-blockers or
nondihydropyridine calcium channel blockers (diltiazem or verapamil)
to slow conduction across the AV node. Digitalis or amiodarone may
used for this purpose in patients with heart failure.
• Anticoagulant therapy is the most effective stroke prevention strategy
and should be employed whenever the risk of thromboembolism
exceeds the risk of bleeding.
• Catheter ablation is the most effective way to achieve sustained main-
tenance of sinus rhythm, but as an invasive procedure it carries risks
that must be considered in case selection.
231
*Mount Sinai Medical Center, New York, NY, USA.
22
Chapter
Introduction
Atrial fibrillation (AF) is a sustained supraventricular arrhythmia in which
normal atrial electrical activity is replaced by multiple, rapid, irregular
areas of depolarization throughout the atria. Atrial flutter is a more organized form of rapid atrial depolarization. Both result in loss of organized
atrial contraction and variable, often rapid, ventricular depolarization.
Clinical manifestations result from impaired hemodynamics secondary to
loss of atrioventricular synchrony, progressive ventricular dysfunction
due to tachycardia, and increased risk for ischemic events due to
embolism of a thrombus arising from stasis in the left atrium.
Epidemiology
AF is the most common sustained arrhythmia, affecting over 2 million
individuals in the United States. The overall prevalence is 1%, higher in
men and increasing with age from 0.1% among adults under 55 years old
to 9% of those over 80.
1
The incidence of AF also increases with age,
accruing to an estimated lifetime risk of approximately one in four.
2
Atrial
AF and atrial flutter may cause symptoms of palpitation, fatigue, and
impaired exercise tolerance and are associated with higher rates of mortality. The risk of stroke is approximately fivefold greater than that for
otherwise comparable patients in sinus rhythm, and is most pronounced in
those over age 75 and in those with certain comorbid conditions. Several
observational studies have demonstrated that AF nearly doubles the risk
of premature death.
3
Etiologies and Associated Conditions
Although there are several competing theories on the mechanism of AF, its
initiation and maintenance depend on two conditions: (1) an electrical trigger (a manifestation of increased excitability) necessary for initiating the
arrhythmia and (2) an abnormal myocardial substrate, typically involving
232
K. Bhasin and J. L. Halperin
atrial fibrosis and electrical remodeling with or without dilation, allowing
for re-entrant circuits.
3
Many, if not all, of the etiologic and predisposing
factors contribute to one or both of these conditions. AF typically originates in the left atrium near the ostia of the four pulmonary veins. Typical
atrial flutter involves a large re-entrant circuit in the right atrium, usually
in the region of the tricuspid isthmus.
Clinical Findings
History and Physical Examination
In the evaluation of patients with AF or atrial flutter, the clinical history
should:
• Characterize the pattern of arrhythmia as paroxysmal or persistent;
• Define the impact of associated symptoms;
• Identify possible etiologies and predisposing factors;
• Estimate the risk of thromboembolism and response to previous
treatment.
Symptoms may include palpitation, fatigue, dyspnea, or reduced exercise capacity. Many patients are asymptomatic, with the arrhythmia
identified incidentally.
Physical examination may confirm the diagnosis and identify contributory causes (e.g. hyperthyroidism) or consequences (e.g. heart failure or
shock). Apulse deficit (the difference between the apical heart rate and the
peripheral pulse rate) provides information about the adequacy of rate
control and ventricular function. Auscultation may demonstrate associated
valvular disease, heart failure, or pulmonary disease.
Electrocardiogram
Diagnosis is based on the ECG demonstrating disorganized atrial electrical
activity in the form of fibrillatory waves or the more organized rapid pattern of atrial flutter and the absence of P waves. The ventricular response
233
Atrial Fibrillation and Flutter