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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5537_Библиотеки_им_академика_М_И_Перельмана.pdf
should be doubled until a diuresis occurs. Addition of a thiazide diuretic
can be an effective way to block sodium reabsorption at other sites of the
nephron. Delivering loop diuretics as a continuous intravenous infusion
avoids rebound tubular sodium reabsorption and produces a steady diuresis. On occasion, it may be necessary to measure cardiac filling pressures
and resting hemodynamics in those instances where doubt exists as to a
patient’s true volume status and cardiac output. Addition of a vasodilator
or inotrope may be indicated in cases of a reduced cardiac output to
increase both renal perfusion and GFR.
An alternative way to reduce congestion is to mechanically remove
fluid. Ultrafiltration uses a pressure gradient across a semipermeable
membrane to remove fluid. The composition of this fluid contains more
sodium than that produced by loop diuretics. Although clinical experience
with this device is limited, in one study ultrafiltrated patients spent fewer
days in hospital and required repeat heart failure hospitalizations less
often than patients receiving loop diuretics.
13
Current barriers to widespread use of ultrafiltration include its more invasive nature, need for vascular access, telemetry or intensive care unit monitoring and cost.
Vasodilators
Vasodilators are effective drugs for treating acute decompensated heart
failure, because they quickly improve the loading conditions on the heart.
They act by relaxing vascular smooth muscle cells and in so doing reduce
systemic vascular resistance and increase venous capacitance. By lowering both afterload and preload, vasodilators reduce ventricular volumes,
myocardial wall stress and oxygen demand. The efficiency of cardiac contraction improves and cardiac output increases. Vasodilators also decrease
the severity of mitral regurgitation, when present, and further lower pulmonary capillary pressure. Unlike diuretics, vasodilators may decrease
neurohormonal stimulation. They are usually reserved for patients who
have more pronounced symptoms upon presentation or persistent symptoms in spite of treatment with intravenous diuretics. Vasodilators work
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G. Sayer and S. Pinney
particularly well in patients with significant hypertension. They should be
used cautiously in patients with a reduced blood pressure and are contraindicated in cardiogenic shock.
Currently, three vasodilators are used for the treatment of acute heart
failure: nitroglycerin, sodium nitroprusside and nesiritide. Nitroglycerin
produces vascular relaxation by first being converted to nitric oxide,
which in turn signals cyclic guanosine monophosphate (cGMP) production. It is primarily a venodilator, but is often used in patients with acute
coronary syndromes because of its ability to dilate coronary arteries. Its
use may be limited by headache, hypotension and tachyphylaxis. When it
is employed to treat heart failure, much higher doses than those used in
treating myocardial ischemia are required. Sodium nitroprusside works
through a similar mechanism as nitroglycerin, but is a more potent arterial
dilator. As a result, it is more likely to produce hypotension and it should
be administered only in an intensive care unit with continuous arterial blood
pressure monitoring. Nitroprusside may worsen myocardial ischemia by
producing coronary steal and reflex tachycardia. Prolonged infusion may
result in thiocyanate toxicity, particularly in patients with impaired renal
function. Nesiritide is a recombinant form of B-type natriuretic peptide
which lowers pulmonary capillary wedge pressure more quickly than
nitroglycerin while alleviating dyspnea to a similar degree.
14
It has a
longer half-life than nitroglycerin or nitroprusside and requires minimal,
if any, dose titration. Its primary side effect is hypotension, which can be
mitigated by omitting an initial bolus.
Inotropes
Inotropes enhance cardiac contractility by promoting actin–myosin bridging in myocardial cells. Dobutamine and dopamine work through beta-1
receptors, stimulating the production of cyclic adenosine monophosphate
(cAMP) and increasing intracellular calcium. Milrinone is a phosphodiesterase-3 inhibitor that prevents breakdown of cAMP. In addition to its
myocardial effects, milrinone produces vascular smooth muscle cell
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Acute Decompensated Heart Failure
relaxation and vasodilation. As opposed to the catecholamines, milrinone
leaves the beta-receptor unoccupied and allows for concomitant therapy
with a beta-blocker. This approach may be particularly useful when transitioning hospitalized patients off inotropes to chronic medical therapy.
Inotropes should be reserved for patients with poor peripheral perfusion
where augmenting cardiac output is required to restore an adequate circulation and relieve symptoms.
All inotropes possess significant side effects. They elevate the heart
rate, promote tachyarrhythmias and, in the case of milrinone, produce
hypotension. Increases in the heart rate and contractility increase
myocardial oxygen demand and may worsen ischemia. As in chronic
heart failure, routine inotrope use increases mortality and is strongly
discouraged.
15
Transition Home
Hospitalization for acute heart failure offers a “teachable moment” for clinicians to instruct patients about living with heart failure. Spending adequate time teaching patients and their families about triggers of heart
failure, prognosis, importance of compliance, and identifying signs and
symptoms of clinical worsening can often reduce the need for subsequent
hospitalization. Prior to going home, all patients should receive written
discharge instructions that address:
• Dietary restrictions;
• Activity level;
• Discharge medications;
• Followup appointments;
• Daily weight monitoring;
• What to do if symptoms worsen.
Clinicians should ensure that patients have achieved euvolemia
and are receiving optimal doses of ACE/ARB and beta-blockers. The
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G. Sayer and S. Pinney
ventricular rate of atrial fibrillation should be controlled. Whenever
possible, hospitalized heart failure patients should be referred to an
outpatient disease management team. Taking the time to complete
these steps in accordance with clinical practice guidelines will ensure
a safe, high-quality discharge.
Conclusion
Treating acute heart failure patients remains a clinical challenge. Current
therapies effectively improve symptoms, but have uncertain effects on
mortality. Applying the evidence-based approaches outlined above and
summarized in Fig. 2 should help improve outcomes for these complex
patients.
217
Acute Decompensated Heart Failure
failure. D = diuretic therapy or mechanical volume removel; V = vasodilator therapy; I =
inotropic therapy (Reprinted, with permission, from Ref. 17.)
References
1. Lloyd-Jones D, Adams R, Carnethon M, et al. (2009) Heart disease
and stroke statistics — 2009 update: A report from the American
Heart Association Statistics Committee and Stroke Statistics
Subcommittee. Circulation 119: 480–486.
2. Krumholz HM, Parent EM, Tu N, et al. (1997) Readmission after
hospitalization for congestive heart failure among Medicare beneficiaries. Arch Intern Med 157: 99–104.
3. Goldberg RJ, Ciampa J, Lessard D, et al. (2007) Long-term survival
after heart failure: A contemporary population-based perspective. Arch
Intern Med 167: 490–496.
4. Stevenson LW. (1999) Tailored therapy to hemodynamic goals for
advanced heart failure. Eur J Heart Fail 1: 251–257.
5. Gheorghiade M, Zannad F, Sopko G, et al. (2005) Acute heart failure
syndromes: Current state and framework for future research.
Circulation 112: 3958–3968.
6. Peacock WFt, De Marco T, Fonarow GC, et al. (2008) Cardiac troponin
and outcome in acute heart failure. N Engl J Med 358: 2117–2126.
7. Fonarow GC, Abraham WT, Albert NM, et al. (2008) Factors identified as precipitating hospital admissions for heart failure and clinical
outcomes: Findings from OPTIMIZE-HF. Arch Intern Med 168:
847–854.
8. Maisel AS, Krishnaswamy P, Nowak RM, et al. (2002) Rapid measurement of B-type natriuretic peptide in the emergency diagnosis of
heart failure. N Engl J Med 347: 161–167.
9. Fonarow GC, Abraham WT, Albert NM, et al. (2007) Influence of a
performance-improvement initiative on quality of care for patients
hospitalized with heart failure: Results of the Organized Program to
Initiate Lifesaving Treatment in Hospitalized Patients with Heart
Failure (OPTIMIZE-HF). Arch Intern Med 167: 1493–1502.
10. Gheorghiade M, Pang PS. (2009) Acute heart failure syndromes. J Am
Coll Cardiol 53: 557–573.
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11. Fonarow GC, Adams KF, Jr., Abraham WT, et al. (2005) Risk stratification for in-hospital mortality in acutely decompensated heart failure: Classification and regression tree analysis. JAMA 293: 572–580.
12. Levy WC, Mozaffarian D, Linker DT, et al. (2006) The Seattle Heart
Failure Model: Prediction of survival in heart failure. Circulation 113:
1424–1433.
13. Costanzo MR, Guglin ME, Saltzberg MT, et al. (2007) Ultrafiltration
versus intravenous diuretics for patients hospitalized for acute decompensated heart failure. J Am Coll Cardiol 49: 675–683.
14. Publication Committee for the VMAC Investigators (Vasodilatation
in the Management of Acute CHF). (2002) Intravenous nesiritide vs
nitroglycerin for treatment of decompensated congestive heart failure:
A randomized controlled trial. JAMA 287: 1531–1540.
15. Cuffe MS, Califf RM, Adams KF, Jr., et al. (2002) Short-term intravenous milrinone for acute exacerbation of chronic heart failure: A
randomized controlled trial. JAMA 287: 1541–1547.
16. Konstam MA, Gheorghiade M, Burnett JC, Jr., et al. (2007) Effects of
oral tolvaptan in patients hospitalized for worsening heart failure: The
EVEREST Outcome Trial. JAMA 297: 1319–1331.
17. Yancy CW. (2008) Vasodilator therapy for decompensated heart
failure. J Am Coll Cardiol 52: 208–210.
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Valvular Heart Disease
Mark Harrison†and Lane Duvall *
Key Pearls
• With the aging of the US population, the four major types of
valvular heart disease (aortic stenosis, aortic regurgitation, mitral
stenosis and mitral regurgitation) will continue to increase in prevalence. Transthoracic echocardiography plays a key role in making
the diagnosis.
• In patients with severe symptomatic aortic stenosis, (as manifested by
syncope, shortness of breath, or angina), surgical valve replacement is
the best current treatment option.
• Mitral stenosis is usually caused by rheumatic heart disease and ther-
apy is targeted towards reducing CHF symptoms and decreasing the
risk of thromboembolism.
• Aortic regurgitation presents variably, depending on the underlying
etiology and natural history.
• Mitral regurgitation is caused by a wide number of entities. Medical
therapy is centered around relieving pulmonary congestion, but when
patients become symptomatic, they may benefit from surgical repair
or replacement of the valve.
221
*Mount Sinai Medical Center, New York, NY, USA.
†
The Hudson Valley Heart Center, Poughkeepsie, NY, USA.
21
Chapter
Introduction
Valvular heart disease includes a group of congenital or acquired conditions
characterized by abnormal valvular function (stenosis, regurgitation, or both)
which can cause significant morbidity and mortality.
1–2
While the exact
prevalence is unknown, estimates have identified up to 5 million Americans
affected, with the number expected to increase as the population ages.
3–4
Transthoracic echocardiography plays a key role in making the diagnosis.
5–6
Aortic Stenosis (AS)
A normal trileaflet aortic valve allows for unobstructed flow between the
left ventricle and the aorta. Under certain pathologic circumstances, aortic stenosis develops, in which the valve can narrow and prevent complete
opening, impeding normal blood flow.
Etiology
In the United States, the most common cause of AS is progressive calcification and degeneration of the valve occurring with age. “Senile” AS usually presents in the seventh through ninth decade of life. Worldwide,
rheumatic fever can be a cause of AS, presenting in the third through fifth
decade of life, and usually accompanied by mitral valve disease. Due to
recurrent inflammation, the valve progressively narrows through fibrous
contracture and fusion of adjacent cusps. Finally, a congenital cause of AS
occurs in patients with a bicuspid aortic valve, consisting of two cusps
instead of three. Occurring in 1–2% of people, bicuspid aortic valves are
especially prone to the formation of calcium deposits and bicuspid AS
usually presents in the 40s and 50s.
History and Physical
Symptoms of aortic stenosis tend to develop gradually. Ultimately,
patients with progressive disease experience the classic triad of chest pain,
syncope, and congestive heart failure (CHF).
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M. Harrison and L. Duvall
In patients with angina, the five-year mortality rate is 50%. Syncope
can be attributed to poor cardiac output, decreased cerebral blood flow, or
cardiac arrhythmias. After a syncopal event, the median survival is three
years. Finally, for individuals with symptoms of CHF, the prognosis is
extremely poor, with a two-year mortality of 50% if the valve is not
replaced. Symptoms of heart failure may occur from a combination of
systolic dysfunction, diastolic dysfunction, or both.
On examination, patients with aortic stenosis typically have a harsh
systolic crescendo-decrescendo murmur heard at the right upper sternal
border which radiates to both carotids. Advanced disease is suggested by
a diminished S2, late peaking murmur, and weak and delayed carotid
pulses.
Diagnosis and Testing
The standard evaluation for patients with suspected AS includes an ECG,
chest X-ray (CXR) and an echocardiogram. In advanced aortic stenosis,
the 12-lead ECG will often reveal left ventricular hypertrophy; however,
it is not present in all patients. On CXR, cardiomegaly and calcification of
the aorta and aortic valve support the diagnosis of AS.
Ultimately, echocardiography can confirm the clinical diagnosis of
aortic stenosis. Beyond assessing the degree and severity of valve narrowing, echo provides additional information on ventricular size, systolic
and diastolic function, valve leaflet number, valve morphology, and the
degree of calcification. Cardiac catheterization can be used for hemodynamic confirmation of severity if needed.
Treatment
The initial management of patients with significant AS presenting with
congestive heart failure includes monitoring, supportive oxygen, intravenous access, and diuretics. For patients with angina, measures should be
taken to relieve the chest discomfort, which may include administration of
oxygen, nitrates, and beta blockers. Importantly, blood pressure lowering
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Valvular Heart Disease