what does s4 signify? what cardiac findings will you expect to find in a hypertensive?
Essentials of the Diagnosis of Middle Failure
Am Fam Physician. 2000 Mar 1;61(5):1319-1328.
Article Sections
- Abstract
- History
- Physical Examination
- Laboratory Findings
- Diagnostic Tests
- Systolic vs. Diastolic Dysfunction
- References
Although heart failure is a common clinical syndrome, especially in the elderly, its diagnosis is often missed. A detailed clinical history is crucial and should address not but current signs and symptoms of heart failure but also signs and symptoms that point to a specific cause of the syndrome, such as coronary artery disease, hypertension or valvular heart disease. It is important to make up one's mind whether the patient has had a previous cardiac upshot, in particular a myocardial infarction. The physical examination should include Valsalva's maneuver, a test that is highly specific and sensitive for the detection of left ventricular systolic and diastolic dysfunction in patients with heart failure. An electrocardiograph and a chest radiograph should as well exist obtained. Ii-dimensional echocardiography of the heart helps differentiate systolic from diastolic dysfunction. Coronary angiography is indicated in patients with heart failure and anginal chest pain and should be strongly considered in patients with an electrocardiogram suggestive of ischemia or myocardial infarction.
Heart failure affects an estimated 4.9 million Americans,1 or 1 percent of adults fifty to lx years of age and 10 percent of adults in their 80s.2 Each twelvemonth, most 400,000 new cases of centre failure are diagnosed in the United States.1 This clinical syndrome is the virtually frequent cause of hospitalizations in the elderly and is responsible for 5 to ten percentage of all infirmary admissions.1 Centre failure causes or contributes to approximately 250,000 deaths every year.three
The clinical syndrome of heart failure manifests when cellular respiration becomes impaired considering the heart cannot pump enough claret to support the metabolic demands of the body, or when normal cellular respiration tin just exist maintained with an elevated left ventricular filling force per unit area.4
The Framingham,v Duke6 and Boston7 criteria were established before noninvasive techniques for assessing systolic and diastolic dysfunction became widely available. The three sets of criteria were designed to assist in the diagnosis of heart failure. The Boston criteria (Table 1)8 take been shown to have the highest combined sensitivity (50 percent) and specificity (78 percent ). All of these criteria are most helpful in diagnosing advanced or severe heart failure, a status that occurs in 20 to xl per centum of patients with a decreased ejection fraction.9
Table 1.
Boston Criteria for Diagnosing Heart Failure
| Criterion | Point value* |
|---|---|
| Category I: history | |
| Remainder dyspnea | 4 |
| Orthopnea | 4 |
| Paroxysmal nocturnal dyspnea | 3 |
| Dyspnea while walking on level area | ii |
| Dyspnea while climbing | 1 |
| Category II: physical examination | |
| Middle rate abnormality (1 point if 91 to 110 beats per minute; ii points if more than 110 beats per minute) | 1 or two |
| Jugular venous elevation (2 points if greater than half dozen cm HtwoO; three points if greater than 6 cm H2O plus hepatomegaly or edema) | 2 or iii |
| Lung crackles (i point if basilar; two points if more than basilar) | 1 or ii |
| Wheezing | three |
| Third center sound | 3 |
| Category 3: chest radiography | |
| Alveolar pulmonary edema | 4 |
| Interstitial pulmonary edema | 3 |
| Bilateral pleural effusion | 3 |
| Cardiothoracic ratio greater than 0.50 | 3 |
| Upper zone period redistribution | 2 |
Early diagnosis of heart failure is essential for successfully addressing underlying diseases or causes and, in some patients, preventing further myocardial dysfunction and clinical deterioration. However, initial diagnosis may be difficult considering the presentations of heart failure tin change from no symptoms to pulmonary edema with cardiogenic shock. It is estimated that eye failure is correctly diagnosed initially in only l per centum of affected patients.10,11 A systematic approach tin can ameliorate overall accuracy in diagnosing this status.
History
- Abstract
- History
- Concrete Test
- Laboratory Findings
- Diagnostic Tests
- Systolic vs. Diastolic Dysfunction
- References
The beginning step in diagnosing heart failure is to obtain a consummate clinical history. The patient should be questioned about dyspnea, cough, nocturia, generalized fatigue and other signs and symptoms of heart failure.
Dyspnea, a cardinal symptom of a failing heart, often progresses from dyspnea on exertion to orthopnea, paroxysmal nocturnal dyspnea and dyspnea on rest. Cough, unremarkably nocturnal and nonproductive, may back-trail dyspnea and often occurs in similar settings (i.east., on exertion or when the patient is supine).
Nocturia, also a frequent sign of heart failure, occurs secondary to increased renal perfusion when the patient is supine.12 Generalized fatigue (caused by the low perfusion state) and peripheral edema with inability to clothing usual footwear are frequent complaints.
As heart failure progresses, gastrointestinal symptoms (east.g., abdominal bloating, anorexia and fullness in the correct upper quadrant) are occasionally seen. With severe, longstanding heart failure, cardiac cachexia (emaciation resulting from heart disease) may develop secondary to poly peptide-losing enteropathy and increased levels of certain cytokines, such every bit tumor necrosis gene. Cardiac cachexia may mimic the cachexia seen in patients with disseminated cancerous illness.
Confusion and altered mental status may occur because of decreased cerebral perfusion or cardiac cirrhosis. In heart failure, cirrhosis develops secondary to chronic passive congestion of the liver.
The patient should be asked about previous chest hurting or myocardial infarction because coronary artery affliction is responsible for upwards to 75 per centum of cases of center failure with decreased left ventricular function.xiii A history of myocardial infarction has a better combination of sensitivity, specificity and positive and negative predictive value for heart failure compared with other symptoms or aspects of the medical history.xiv
It is important to place a history of hypertension, in that high blood pressure is the second most frequent cause of middle failure. Information about other possible causes of heart failure should also be sought (Tabular array 2).
Tabular array 2.
Causes of Center Failure
| Most common causes |
| Coronary avenue disease |
| Hypertension |
| Valvular heart disease (especially aortic and mitral illness) |
| Other causes |
| Infections: viruses (including man immunodeficiency virus), bacteria, parasites |
| Pericardial diseases |
| Drugs (e.1000., doxorubicin [Adriamycin], cyclophosphamide [Cytoxan], cocaine) |
| Alcohol |
| Connective tissue disease |
| Infiltrative disease (due east.chiliad., amyloidosis, sarcoidosis, hemochromatosis, malignancy) |
| Tachycardia |
| Obstructive cardiomyopathy |
| Neuromuscular disease (e.g., muscular or myotonic dystrophy, Friedreich's ataxia) |
| Metabolic disorders (e.k., glycogen storage disease type ii [Pompe'southward disease] and blazon 5 [McArdle's disease]) |
| Nutritional disorders (due east.g., beriberi, kwashiorkor) |
| Pheochromocytoma |
| Radiations |
| Endomyocardial fibrosis |
| Eosinophilic endomyocardial disease |
| High-output center failure (e.g., intracardiac shunt, atrioventricular fistula, beriberi, pregnancy, Paget's disease, hyperthyroidism, anemia) |
| Peripartum cardiomyopathy |
| Dilated idiopathic cardiomyopathy |
Once heart failure is suspected, the functional class of the patient should be adamant. The New York Eye Association (NYHA) functional classification of congestive center failure is presented in Table iii.15
TABLE three.
New York Heart Association Functional Nomenclature of Congestive Centre Failure
The rightsholder did non grant rights to reproduce this item in electronic media. For the missing detail, see the original print version of this publication.
Physical Examination
- Abstract
- History
- Physical Examination
- Laboratory Findings
- Diagnostic Tests
- Systolic vs. Diastolic Dysfunction
- References
A complete concrete examination is the 2d component in the diagnosis of centre failure. The patient'southward full general appearance should be assessed for evidence of resting dyspnea, cyanosis and cachexia.
BLOOD Pressure level AND Centre Rate
The patient's blood force per unit area and heart charge per unit should be recorded. High, normal or depression claret pressure may be present. The prognosis is worse for patients who present with a systolic blood pressure of less than xc to 100 mm Hg when non receiving medication (angiotensin-converting enzyme [ACE] inhibitors, beta blockers or duretics).16 Tachycardia may be a sign of eye failure, especially in the decompensated land. The heart rate increases as ane of the compensatory means of maintaining adequate cardiac output. A decrease in the resting middle charge per unit with medical therapy can be used as a surrogate marker for treatment efficacy. A weak, thready pulse and pulsus alternans are associated with decreased left ventricular function. The patient should as well be monitored for evidence of periodic breathing (Cheyne-Stokes respiration).
JUGULAR VENOUS DISTENTION
Jugular venous distention is assessed while the patient is supine with the upper body at a 45-degree angle from the horizontal plane. The elevation of the waveform of the internal jugular venous pulsation determines the height of the venous distention. An imaginary horizontal line (parallel to the floor) is then drawn from this level to above the sternal angle. A peak of more than 4 to five cm from the sternal angle to this imaginary line is consistent with elevated venous force per unit area (Figure one).
FIGURE one.
Assessment of jugular venous distention.
Elevated jugular venous pressure is a specific (90 pct) but not sensitive (30 pct) sign of elevated left ventricular filling. The reproducibility of the jugular venous distention cess is depression.17
POINT OF MAXIMAL IMPULSE
The point of maximal impulse of the left ventricle is normally located in the midclavicular line at the 5th intercostal space. With the patient in a sitting position, the physician uses fingertips to identify this point. Cardiomegaly usually displaces the cardiac impulse laterally and down.
At times, the point of maximal impulse may exist difficult to locate and therefore loses sensitivity (66 percent). Yet the location of this point remains a specific indicator (96 pct) for evaluating the size of the heart.14
3rd AND FOURTH HEART SOUNDS
A double apical impulse can represent an auscultated third middle sound (Siii). But as with the displaced betoken of maximal impulse, a 3rd heart sound is not sensitive (24 percent) for heart failure, but information technology is highly specific (99 per centum).xiv Patients with center failure and left ventricular hypertrophy can as well have a fourth middle sound (Due south4). The physician should be alert for murmurs, which can provide information about the cause of eye disease and too aid in the selection of therapy.
PULMONARY Test
Concrete test of the lungs may reveal rales and pleural effusions. Despite the presence of pulmonary congestion, rales can be absent considering of increased lymphatic drainage and compensatory changes in the perivascular structures that accept occurred over time. Wheezing may be the sole manifestation of pulmonary congestion. Ofttimes, asthma is erroneously diagnosed in patients who actually have heart failure.
LIVER SIZE AND HEPATOJUGULAR REFLUX
The key component of the intestinal test is the evaluation of liver size. Hepatomegaly may occur because of right-sided heart failure and venous congestion.
The hepatojugular reflux tin be a useful examination in patients with right-sided heart failure. This test should be performed while the patient is lying down with the upper torso at a 45-degree angle from the horizontal aeroplane. The patient keeps the mouth open and breathes ordinarily to forestall Valsalva's maneuver, which can give a false-positive test. Moderate pressure is then practical over the middle of the abdomen for 30 to 60 seconds. Hepatojugular reflux occurs if the summit of the neck veins increases by at least iii cm and the increase is maintained throughout the compression flow.18
LOWER EXTREMITY EDEMA
Lower extremity edema, a common sign of heart failure, is usually detected when the extracellular book exceeds 5 L. The edema may exist accompanied by stasis dermatitis, an oft chronic, normally eczematous condition characterized by edema, hyperpigmentation and, commonly, ulceration.
VALSALVA'S MANEUVER
Valsalva'south maneuver is rarely used in the evaluation of patients with heart failure. Yet this test is unproblematic to perform and carries one of the all-time combinations of specificity (91 percentage) and sensitivity (69 percent) for the detection of left ventricular systolic and diastolic dysfunction in patients with eye failure.xix,20
Valsalva's maneuver is performed with the blood force per unit area cuff inflated 15 mm Hg over the systolic blood pressure. While the medico auscultates over the brachial artery, the patient is asked to perform a forced expiratory attempt confronting a airtight airway (the Valsalva'due south maneuver).
A normal response would exist an initial rise in systolic claret pressure at the onset of straining (phase I) with Korotkoff's sounds heard (Figure 2). While the maneuver is maintained (phase Ii), a decrease in the claret pressure occurs with loss of Korotkoff'southward sounds. Release of the maneuver (phase III) is followed by an overshoot of blood pressure and the reappearance of heart sounds (stage IV). Abnormal responses occurring in patients with eye failure are maintenance of beats throughout Valsalva's maneuver (foursquare moving ridge) or lack of reappearance of Korotkoff's sounds after release of the maneuver (absent-minded overshoot).
FIGURE 2.
Arterial claret pressure response and Korotkoff's sounds during Valsalva'south maneuver. (A) Sinusoidal response in normal patient. (B) Absent overshoot in patient with heart failure. (C) Square wave response in patient with heart failure. The ruddy lines bespeak when Korotkoff'southward sounds are heard. (BP = claret force per unit area)
DIAGNOSTIC CHALLENGES
Diagnosing center failure in elderly patients may be particularly challenging because of the atypical presentations in this age group. Anorexia, generalized weakness and fatigue are often the predominant symptoms of heart failure in geriatric patients. Mental disturbances and anxiety are also common.
When older persons get symptomatic on exertion, they decrease their level of activity to the point of condign relatively asymptomatic. A wheel of symptoms on exertion and consequent decrease in activeness often continues equally the illness progresses, until the patient finally becomes symptomatic at rest (i.e., NYHA class IV).
The physical findings in older patients with middle failure may be difficult to interpret accurately. Resting tachycardia is uncommon, and pulse profile abnormalities are hard to assess secondary to peripheral arteriosclerotic changes. At times, auscultatory findings on the lung examination are singular considering of concomitant pulmonary disease.21
Laboratory Findings
- Abstruse
- History
- Physical Examination
- Laboratory Findings
- Diagnostic Tests
- Systolic vs. Diastolic Dysfunction
- References
Most patients with center failure accept normal electrolyte levels. However, extended use of kaliuretic diuretics tin lead to hypokalemia, and the use of potassium-sparing diuretics and ACE inhibitors may consequence in hyperkalemia. Claret urea nitrogen and creatinine levels may become elevated, reflecting prerenal azotemia. Hyponatremia may exist present in patients with avant-garde middle failure.
When the liver becomes congested, serum transaminase and bilirubin levels may get elevated, and jaundice may be present. With chronic congestive hepatomegaly, cardiac cirrhosis may occur and cause hypoalbuminemia, hypoglycemia and an increased prothrombin time.
The prognosis is worse in patients with hyponatremia or abnormalities secondary to congested hepatomegaly.
Anemia may contribute to worsening middle failure. When severe, anemia may fifty-fifty crusade eye failure.
In all patients with newly diagnosed heart failure, thyroid function tests should be performed to dominion out hypothyroidism or hyperthyroidism.
It may soon be possible to routinely obtain serum measurements of two plasma enzymes secreted by the overloaded centre. Plasma atrial natriuretic peptide is secreted in response to increased intra-atrial pressure level, and brain natriuretic peptide (BNP) is secreted by the declining ventricle. Levels of these enzymes, but specifically BNP, are elevated in patients with dyspnea resulting from heart failure. In one written report, elevated BNP levels had more than than a 90 percent specificity and sensitivity for center failure.22
Diagnostic Tests
- Abstract
- History
- Physical Examination
- Laboratory Findings
- Diagnostic Tests
- Systolic vs. Diastolic Dysfunction
- References
ELECTROCARDIOGRAPHY
An electrocardiogram (ECG) should exist obtained in all patients who present with middle failure. No specific ECG feature is indicative of heart failure, just atrial and ventricular arrhythmias are common findings. For example, atrial fibrillation is present in 25 percent of patients with cardiomyopathy, especially elderly patients with advanced center failure.23 The prognosis is worse for patients with atrial fibrillation, atrial or ventricular tachycardia, or left parcel co-operative cake.16,24
Low voltage on the ECG in association with conduction disturbances may advise the presence of amyloidosis.
Breast RADIOGRAPHY
Chest radiographs tin can be helpful in the diagnosis of heart failure. Cardiomegaly is ordinarily manifested past the presence of an increased cardiothoracic ratio (greater than 0.50) on a posteroanterior view. However, patients with predominantly diastolic dysfunction may accept normal center size, one of the distinguishing markers of diastolic versus systolic dysfunction. Right ventricular enlargement is suggested by the loss of gratuitous infinite betwixt the cardiac silhouette and the sternum on a lateral view.
Signs of increased pulmonary venous pressure seen on chest radiographs may progress from redistribution of claret flow from the bases of the lungs to the apices to linear densities reflecting interstitial edema (Kerley'south lines) to a hazy advent full-bodied generally around the hila of the mediastinum and presenting a butterfly pattern.
Chest radiographs are too helpful in detecting pleural effusion secondary to heart failure.
ECHOCARDIOGRAPHY
Transthoracic two-dimensional echocardiography with Doppler period studies is highly recommended for all patients with heart failure.25 This exam helps in the assessment of left ventricular size, mass and function.
The ejection fraction can be calculated by several methods, including visual estimation, which has good correlation with ejection fractions obtained by angiography26 or radionuclide cineangiography.27 Regional wall motion and valvular integrity can also be evaluated.
Transesophageal echocardiography offers college quality images than transthoracic studies. However, this technique is invasive and is best reserved for apply when the quality of the 2-dimensional echocardiogram is unacceptable.
ANGIOGRAPHY
Radionuclide angiography is another non-invasive method for assessing systolic and diastolic part. This imaging technique is used when ii-dimensional echocardiography is not diagnostic considering adequate images could not exist obtained or the findings do non agree with the clinical picture. Radionuclide angiography provides a reliable and quantitative measurement of the left ventricular ejection fraction and the regional wall movement. However, ectopic action and atrial fibrillation adversely touch the accuracy of its measurements.28
Left ventricular angiography tin be used to assess the ejection fraction, the left ventricular volume and the severity of valvular regurgitation or stenosis. In addition, detailed measurements of ventricular filling pressures and indices of left ventricular diastolic relaxation rate can be helpful in confirming diastolic dysfunction.
OTHER TECHNIQUES
Magnetic resonance imaging (MRI)29 and ultrafast or cinematics computed tomography (CT)30 can measure out the ejection fraction and assess regional wall motion. Yet, assessment of cardiac function using these studies is simply performed in a express number of centers, and the superiority of the studies to echocardiography and angiography has non been proved.
Sometimes coronary artery illness must be excluded as a causal cistron in patients with heart failure. Cardiac catheterization and coronary angiography should be strongly considered in all patients with heart failure and angina who are candidates for interventional procedures. In patients with known coronary artery affliction and heart failure but no angina, coronary arteriography or noninvasive testing (i.e., a thallium stress test or stress echocardiogram), followed past coronary arteriography in those patients with ischemia, should be considered. The intensity of the search for ischemic heart illness in patients with center disease depends on the patient's probability of having coronary artery affliction.
If imaging techniques cannot confirm the cause of cardiac dysfunction, an endomyocardial biopsy may provide important data in patients receiving cardiotoxic drugs and in patients suspected of having infectious (i.e., astute or chronic viral myocarditis), genetic or systemic diseases with possible cardiac involvement.25 However, the diagnostic yield of this procedure is typically less than 10 percentage.31
Systolic vs. Diastolic Dysfunction
- Abstruse
- History
- Concrete Examination
- Laboratory Findings
- Diagnostic Tests
- Systolic vs. Diastolic Dysfunction
- References
As many as 40 pct of patients with clinical heart failure take diastolic dysfunction with normal systolic part.32 In addition, many patients with systolic dysfunction have elements of diastolic dysfunction. With systolic dysfunction, the pumping ability of the ventricle is impaired. With diastolic dysfunction, ventricular filling is defective.
Ventricular diastolic role depends on the pressure-to-book relationship in the left ventricle. Decreased compliance of the left ventricular wall leads to a higher pressure for a given diastolic book. The end upshot is dumb ventricular filling, inappropriately elevated left atrial and pulmonary venous pressure, and decreased ability to increase stoke volume. These dysfunctions lead to the clinical syndrome of center failure.
Findings suggestive of diastolic dysfunction on the two-dimensional echocardiogram are left ventricular hypertrophy, a dilated left atrium, a normal or nearly normal ejection fraction and reversal of the normal design of menstruation velocity (measured past Doppler flow studies) beyond the mitral valve (Figures 3 and 4).
FIGURE 3.
2-dimensional echocardiogram showing a four-chambers view of the middle in a patient with systolic dysfunction. Annotation dilated LV. (LV = left ventricle; RV = right ventricle; RA = right atrium; LA = left atrium)
Effigy 4.
Two-dimensional echocardiogram showing a four-chambers view of the heart in a patient with diastolic dysfunction. Note the normal LV size with hypertrophy.
Differentiating between systolic and diastolic dysfunction is essential because their long-term treatments are different33 (Table 434 and Effigy 5). The treatments of choice in patients with systolic dysfunction are ACE inhibitors, digoxin, diuretics and beta blockers. In patients with diastolic dysfunction, the cornerstones of treatment depend on the underlying cause. Beta blockers and calcium aqueduct blockers are frequently used when diastolic dysfunction is secondary to ischemia or hypertension.
TABLE 4.
Clues for Differentiating Between Systolic and Diastolic Dysfunction in Patients with Heart Failure
| Clues from the evaluation | Systolic dysfunction | Diastolic dysfunction | |
|---|---|---|---|
| History | |||
| Hypertension | 20 | XXX | |
| Coronary artery affliction* | XXX | X | |
| Diabetes mellitus | XXX | XX | |
| Valvular heart affliction* | XXX | — | |
| Physical examination | |||
| Third heard audio (Sthree) gallop* | XXX | X | |
| Fourth heart sound (S4) gallop* | 10 | Xxx | |
| Rales | Xx | XX | |
| Jugular venous distention | Twenty | X | |
| Edema | Xx | Ten | |
| Displaced bespeak of maximal impulse* | Twenty | — | |
| Mitral regurgitation* | XXX | X | |
| Chest radiograph | |||
| Cardiomegaly* | Thirty | X | |
| Pulmonary congestion | XXX | Xxx | |
| Electrocardiogram | |||
| Q moving ridge | XX | X | |
| Left ventricular hypertrophy* | X | 30 | |
| Echocardiogram | |||
| Decreased ejection fraction* | Xxx | — | |
| Dilated left ventricle* | 20 | — | |
| Left ventricle hypertrophy* | X | Thirty | |
Treatment of Diastolic or Systolic Dysfunction
FIGURE 5.
Suggested algorithm for the treatment of diastolic or systolic dysfunction. (ACE = angiotensin-converting enzyme; NYHA = New York Heart Association; IV = intravenous.)
The history, physical exam, ECG and chest radiographs provide some clues that can be helpful in differentiating systolic and diastolic dysfunction. For instance, predominantly systolic dysfunction is suggested past a history of myocardial infarction and younger patient age, a displaced point of maximal impulse and an South3 gallop on the physical exam, the presence of Q waves on the ECG and the finding of cardiomegaly on the breast radiograph. In dissimilarity, diastolic dysfunction is suggested past a history of hypertension and older patient age, a sustained signal of maximal impulse and an Siv gallop on the physical exam, left ventricular hypertrophy on the ECG and a normal-sized eye on the breast radiograph.36 However, the findings tin overlap considerably, and echocardiography of the heart is usually necessary.
To see the full article, log in or buy access.
REFERENCES
show all references
1. Heart and stroke statistical update. Dallas: American Heart Association, 1997. ...
2. Kannel WB, Belanger AJ. Epidemiology of center failure. Am Middle J. 1991;121(three pt one):951–7.
iii. Centre failure: evaluation and care of patients with left ventricular systolic dysfunction Rockville, Doctor: US Dept of Health and Human being Services, Public Health Service, Agency for Health Care Policy and Research, 1994; AHCPR publication no. 94-0612.
4. Colucci W, Braunwald E. Pathophysiology of center failure. In: Braunwald E, ed. Heart disease: a textbook of cardiovascular medicine. 5th ed. Philadelphia: Saunders, 1997:394–420.
v. McKee PA, Castelli WP, McNamara PM, Kannel WB. The natural history of congestive centre failure: the Framingham study. N Engl J Med. 1971;285:1441–6.
6. Harlan WR, Oberman A, Grimm R, Rosati RA. Chronic congestive heart failure in coronary artery disease: clinical criteria. Ann Intern Med. 1977;86:133–8.
seven. Carlson KJ, Lee DC, Goroll AH, Leahy Grand, Johnson RA. An analysis of physicians' reasons for prescribing long-term digitalis therapy in outpatients. J Chron Dis. 1985;38:733–9.
8. Marantz PR, Tobin JN, Wassertheil-Smoller S, Steingart RM, Wexler JP, Budner Northward, et al. The relationship betwixt left ventricular systolic office and congestive heart failure diagnosed by clinical criteria. Circulation. 1988;77:607–12.
ix. Redfield MM. Diagnosis and evaluation of heart failure. In: Murphy J, ed. Mayo Clinic cardiology review. Armonk, N.Y.: Futura, 1997:597–611.
x. Remmes J, Miettinen H, Reunanen A, Pyorala K. Validity of clinical diagnosis of heart failure in primary health care. Eur Centre J. 1991;12:315–21.
11. Wheeldon NM, MacDonald TM, Flucker CJ, McKendrick Advertizing, McDevitt DG, Struthers Advertisement. Echocardiography in chronic heart failure in the community. Q J Med. 1993;86:17–23.
12. Braunwald Eastward, Grossman W. Clinical aspects of eye failure. In: Braunwald Due east, ed. Heart disease: a textbook of cardiovascular medicine. 5th ed. Philadelphia: Saunders, 1997:445–lxx.
13. Studies of left ventricular dysfunction (SOLVD)—rationale, pattern and methods: two trials that evaluate the effect of enalapril in patients with reduced ejection fraction. Am J Cardiol. 1990;66:315–22 [Published erratum in Am J Cardiol. 1990;66:1026]
fourteen. Davie AP, Francis CM, Caruana 50, Sutherland GR, McMurray JJ. Assessing diagnosis in heart failure: which features are whatsoever apply? Q J Med. 1997;90:335–9.
fifteen. Criteria Commission, New York Center Clan. Dieases of the centre and blood vessels. Classification and criteria for diagnosis. 6th ed. Boston: Little, Brown, 1964:114.
16. Cleland JG, Dargie HJ, Ford I. Mortality in centre failure: clinical variables of prognostic value. Br Heart J. 1987;58:572–82.
17. Stevenson LW, Perloff JK. The express reliability of the physical signs for estimating hemodynamics in chronic center failure. JAMA. 1989;261:884–viii.
eighteen. Ducas J, Magder Southward, McGregor M. Validity of hepatojugular reflux as a clinical test for congestive heart failure. Am J Cardiol. 1983;52:1299–303.
19. Zema MJ, Masters AP, Margouleff D. Dyspnea: the center or the lungs? Differentiation at bedside by use of the elementary Valsalva maneuver. Chest. 1984;85:59–64.
20. Zema MJ, Restivo B, Sos T, Sniderman KW, Kline Southward. Left ventricular dysfunction—bedside Valsalva manoeuvre. Br Eye J. 1980;44:560–9.
21. Tresch DD. The clinical diagnosis of eye failure in older patients. J Am Geriatr Soc. 1997;45:1128–33.
22. Davis M, Espiner Eastward, Richards G, Billings J, Town I, Neill A, et al. Plasma brain natriuretic peptide in assessment of acute dyspnoea. Lancet. 1994;343:440–4.
23. Wenger NK, Abelman WH, Roberts WC. Cardiomyopathy and specific heart muscle illness. In: Hurst JW, ed. The heart, arteries and veins. 7th ed. New York: McGraw-Colina, 1990:1278–1347.
24. Middlekauff HR, Stevenson WG, Stevenson LW. Prognostic significance of atrial fibrillation in avant-garde middle failure. A study of 390 patients. Apportionment. 1991;84:twoscore–8.
25. Guidelines for the evaluation and management of eye failure. Written report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Commission on Evaluation and Management of Centre Failure). J Am Coll Cardiol. 1995;26:1376–98.
26. Mueller 10, Stauffer JC, Jaussi A, Goy JJ, Kappenberger L. Subjective visual echocardiographic approximate of left ventricular ejection fractions equally an alternative to conventional echocardiographic methods: comparing with contrast angiography. Clin Cardiol. 1991;xiv:898–902.
27. Amico AF, Lichtenberg GS, Reisner SA, Rock CK, Schwartz RG, Meltzer RS. Superiority of visual versus computerized echocardiographic estimation of radionuclide left ventricular ejection fraction. Am Heart J. 1989;118:1259–65.
28. Rumberger JA, Behrenbeck T, Bell MR, Breem JF, Johnston DL, Holmes DR, et al. Determination of ventricular ejection fraction: a comparison of available imaging methods. The Cardiovascular Imaging Working Grouping. Mayo Clin Proc. 1997;72:860–70.
29. Stratemeier EJ, Thompson R, Brady TJ, Miller SW, Saini S, Wisner GL, et al. Ejection fraction determination by MR imaging: comparison with left ventricular angiography. Radiology. 1986;158:775–7.
30. Rumberger JA, Sheedy PF, Breen JF. Use of ultrafast (cine) x-ray computed tomography in cardiac and cardiovascular imaging. In: Giuliani ER, Gersh BJ, McGoom MD, Hayes DL, Schaff HV, eds. Mayo Dispensary do of cardiology. 3d ed. St. Louis: Mosby, 1996:303–24.
31. Chow LC, Dittrich HC, Shabetai R. Endomyocardial biopsy in patients with unexplained congestive heart failure. Ann Intern Med. 1988;109:535–9.
32. Soufer R, Wohlgelernter D, Vita NA, Amuchestegui K, Sostman HD, Berger HJ, et al. Intact systolic left ventricular office in clinical congestive heart failure. Am J Cardiol. 1984;55:1032–6.
33. Coodley E. Newer drug therapy for congestive eye failure. Curvation Intern Med. 1999;159:1177–83.
34. Young JB. Assessment of centre failure. In: Brauwnwald E. Atlas of heart illness. Vol 4. Philadelphia: Current Medicine, 1995:vii.i–7.two.
35. Pitt B, Zannad F, Remme WJ, Cody R, Castaigne A, Perez A, et al. The effect of spironolactone on morbidity and mortality in patients with astringent heart failure. North Engl J Med. 1999;341:809–17.
36. Goldsmith SR, Dick C. Differentiating systolic from diastolic heart failure: pathophysiologic and therapeutic considerations. Am J Med. 1993;95:645–55.
This article is 1 in a serial adult in collaboration with the American Heart Clan. Guest editor of the series is Rodman D. Starke, M.D., Senior Vice President of Scientific discipline and Medicine, American Center Association, Dallas.
Copyright © 2000 by the American University of Family Physicians.
This content is owned by the AAFP. A person viewing information technology online may brand one printout of the material and may employ that printout just for his or her personal, non-commercial reference. This textile may not otherwise be downloaded, copied, printed, stored, transmitted or reproduced in whatsoever medium, whether now known or afterwards invented, except every bit authorized in writing past the AAFP. Contact afpserv@aafp.org for copyright questions and/or permission requests.
Nearly RECENT Outcome
Mar 2022
Admission the latest effect of American Family Physician
Read the Event
E-mail Alerts
Don't miss a single issue. Sign up for the costless AFP email table of contents.
Sign Up At present
Source: https://www.aafp.org/afp/2000/0301/p1319.html