Dr. Matthew Bogard, Iowa doctor - CARDIOMEGALY

Dr. Matthew Bogard, Iowa doctor - CARDIOMEGALY

I.          BACKGROUND. Cardiomegaly is a physical enlargement of the heart. This is a physical finding, often the result of other diseases, and is almost always abnormal. Heart size is easily, rapidly, and most commonly determined radiographically on chest x-ray by the cardiothoracic ratio (CTR). This is the sum of the distances from the body midline (a vertical line through the spinous processes) to the furthest left and right heart borders, which is then divided by the widest thoracic diameter measured horizontally between the inner surfaces of the ribs. The CTR is normally 050 to 055 in adults and up to 06 in infants and children. The heart may therefore appear falsely enlarged due to abnormalities of the chest wall, or to radiographic technique.

II.        PATHOPHYSIOLOGY

A.        Etiology. Ventricular aneurysm and pericardial effusion can enlarge the cardiac silhouette. However, most cardiac enlargement is due to pressure overload and muscle hypertrophy of one or more chambers of the heart, volume overload with dilation of cardiac chambers, or cardiomyopathy. As such, cardiomegaly is usually the result of other cardiovascular disorders (hypertension, ischemic or valvular heart disease, familial structural abnormalities) but can also be caused by systemic diseases (anemia, viral or rickettsial infections, bite or sting toxins, medications, anabolic steroids [Ahlgrim], hyperthyroidism, hypothyroidism, hyperparathyroidism, acromegaly [SCHWARZ] , diabetes, autoimmune and infiltrative (amyloid) diseases, and metastases). In many cases, particularly with left ventricular hypertrophy, cardiomegaly is reversible with treatment of the underlying cause.

B.        Epidemiology. Cardiomegaly can be an incidental finding when discovered early in the disease process. It can occur in children and young adults as a result of rheumatic heart disease, infections, or familial cardiomyopathies, where the presenting symptom may be sudden death from arrhythmias, often brought on by physical exertion, as in sports. Left ventricular mass is increased in obese adolescents (1). Due to the higher prevalence of ischemia and hypertension, most cases are in older adults.

III.       EVALUATION

A.        History. Past medical history may include congestive heart failure, coronary disease, hypertension, rheumatic fever, and systemic diseases. Family history may reveal hypertension, hyperlipidemia, or sudden death. Social history might include alcohol or substance abuse or an exposure to a cardiac toxin. System review could include fatigue, dizziness, dyspnea, angina, cough, edema, nocturia, and loss of weight with cardiac cachexia, as well as symptoms more specific to any systemic underlying disease.

B.        Physical examination

1.         Cardiac. Examination may note a chest deformity causing apparent cardiomegaly. Inspection may note a visible heave lateral to the midclavicular line. Palpation of the point of maximal impulse (PMI) below the fifth intercostal space and lateral to the midclavicular line is highly specific for left ventricular enlargement, in the absence of chest wall abnormalities. The PMI may be diffuse (2–3 cm) and may be weak in dilated cardiomyopathy, or it may be hyperdynamic in increased sympathetic states. The PMI may be nonpalpable with pericardial effusion. Peripheral pulses may be weak and pulsus alternans detectable with decreased left ventricular function. If the PMI cannot be appreciated by palpation, the location of the left border of the heart can be ascertained by dullness to percussion. Dullness beyond the midclavicular line and fifth intercostal space is abnormal. Heart murmurs of abnormal valves responsible for the cardiomegaly may be auscultated, as well as the regurgitant murmurs resulting from dilated chambers. Diminished heart sounds or friction rubs may be noted with pericardial disease. S₃ and S₄ gallops may be heard with heart failure resulting from the cardiomegaly. Arrhythmias are common with cardiomegaly. Hypertension, as a cause of cardiomegaly, may be present.

2.         Extracardiac. Examination findings may relate to the underlying causes of cardiomegaly (e.g., autoimmune, infectious, and endocrine diseases, and alcoholism). The typical extracardiac findings of heart failure (cough, dyspnea, rales, wheezes, edema, hepatojugular reflux, jugular venous distension) resulting from the cardiomegaly may also be present.

C.        Testing. Cardiomegaly is detectable by chest x-ray, electrocardiogram (ECG), and echocardiography. Serologic testing primarily identifies systemic causative disorders, and B-type natriuretic peptide increases with ventricular wall stretch (2).

1.         A standard upright posterior-anterior chest x-ray with the 10th rib visible at full inspiration in a nonrotated position without chest deformity is useful for determining the CTR. However, 20% of echocardiogram-confirmed cases of cardiomegaly are not seen on chest x-ray (2). Determination of specific chamber enlargement by x-ray is most reliable with the left atrium, where enlargement projects it posteriorly and superiorly, resulting in increased cardiac density centrally, displacement of the left main bronchus superiorly giving it a more horizontal take-off, and a more readily visible, and curved, left atrial appendage. These findings are significant, because left atrial enlargement is associated with a poor prognosis and was the only identified independent predictor of mortality in a cohort of patients with ischemic cardiomyopathy (3).

2.         The ECG is almost always abnormal with cardiomegaly, although the changes are often nonspecific. The voltage amplitude is often increased or the axis shifted. Atrial and ventricular arrhythmias are common, with atrial fibrillation occurring in 25% of patients with cardiomyopathy [HANCOCK]. Because lead V₁ is directly over the atria, this lead can best indicate atrial enlargement. A diphasic P wave in V₁ indicates atrial hypertrophy. In right atrial hypertrophy, the initial half of the wave is the largest segment. If the second half of the diphasic P wave in lead V₁ is larger or wider, there is left atrial hypertrophy. As lead V₅ is over the left ventricle, a tall R wave in V₅ indicates left ventricular hypertrophy. There may be ischemic changes noted on the ECG in cardiomegaly as well.

3.         Echocardiography is the test of choice for a definitive diagnosis of cardiac enlargement. It can also yield useful information about systolic and diastolic function, wall hypertrophy, ischemic areas, aneurysms, pericardial effusion, and the heart valves.[PEWSNER]

D.        Genetics. There are familial dilated as well as obstructive cardiomyopathies and a familial right atrial enlargement. Studies have indicated that the presence of certain gene alleles can modify the risk of cardiac hypertrophy (5). Many autoimmune and endocrine causes of cardiomegaly are known to be familial.

IV.       DIAGNOSIS

A.        Differential diagnosis. The differential diagnosis of cardiomegaly consists mainly in distinguishing true from factitious cardiomegaly due to suboptimal chest x-ray technique. Here the most important factor is an adequate inspiration revealing the 10th rib. Otherwise, the heart appears larger and more globular toward the left. Anterior-posterior films and portable chest x-rays, shot closer than the standard upright view, also falsely enlarge the heart. Supine views preclude adequate inspiration. Trunk rotation, scoliosis, and pectus excavatum can cause apparent cardiomegaly.

B.        Clinical manifestations. An enlarged heart is less efficient in providing adequate blood flow to the body and itself. Therefore, clinical manifestations of cardiomegaly are primarily those of heart failure (e.g., dyspnea, dizziness, fatigue). Additional symptoms are arrhythmia, angina, and sudden death. Other manifestations are signs and symptoms particular to the specific disease causing the cardiomegaly.

References

Damias PG, Tritos NA. Increased left ventricular mass in obese adolescents. Eur Heart J 2005;26(2):201–202.

Sutter M, Diereks DB. New insights into decompensated heart failure. Emerg Med 2005:18–25.

Sabharwal N, Cemin R, Rajan K, et al. Usefulness of left atrial volume as a predictor of mortality in patients with ischemic cardiomyopathy. Am J Cardiol 2004;94(6):760–763.

Wenger NK, Abelman WH, Roberts WC. Cardiomyopathy and specific heart muscle disease. In: Hurst JW, ed. The heart, arteries, and veins, 7th ed. New York, NY: McGraw-Hill, 1990:1278–1347.

Dursanoglu D. ACE polymorphism in healthy young subjects. Acta Cardiol 2005;60(2): 153–158.

Schwarz, E., Jammula, P., Gupta, R., & Rosanio, S. (2006). A case and review of acromegaly-induced cardiomyopathy and the relationship between growth hormone and heart failure: cause or cure or neither or both?. Journal Of Cardiovascular Pharmacology And Therapeutics, 11(4), 232-244

Pewsner, D., Jüni, P., Egger, M., Battaglia, M., Sundström, J., & Bachmann, L. (2007). Accuracy of electrocardiography in diagnosis of left ventricular hypertrophy in arterial hypertension: systematic review. BMJ (Clinical Research Ed.), 335(7622), 711.

Hancock, E., Deal, B., Mirvis, D., Okin, P., Kligfield, P., Gettes, L., & ... Wellens, H. (2009). AHA/ACCF/HRS recommendations for the standardization and interpretation of the electrocardiogram: part V: electrocardiogram changes associated with cardiac chamber hypertrophy: a scientific statement from the American Heart Association Electrocardiography and Arrhythmias Committee, Council on Clinical Cardiology; the American College of Cardiology Foundation; and the Heart Rhythm Society. Endorsed by the International Society for Computerized Electrocardiology. Journal Of The American College Of Cardiology, 53(11), 992-1002.

Ahlgrim, C., & Guglin, M. (2009). Anabolics and cardiomyopathy in a bodybuilder: case report and literature review. Journal Of Cardiac Failure, 15(6), 496-500.

Originally Published in:  Bogard, Matthew.  “Cardiomegaly.”  Taylor’s 10-Minute Diagnosis Manual.  Editors: Paulman, P., Paulman, A., Harrison, J.  Lippincott, Williams, & Williams.

*** Dr. Matthew Bogard is an emergency medicine doctor primarily at the Lucas County Health Center in Chariton, Iowa. Presently, he is Board Certified in Family Medicine by the National Board of Physicians and Surgeons and the American Academy of Family Physicians.