Diagnostic Tests for Cardiomegaly
Cardiomegaly Tests: Book Excerpts
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Cardiomegaly Diagnosis: Book Excerpts
Diagnostic Tests for Cardiomegaly: Online Medical Books
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CARDIOMEGALY:
DIAGNOSTIC WORKUP
(Algorithmic Diagnosis of Symptoms and Signs)
A CBC, sedimentation rate, ANA, chemistry panel, VDRL test, thyroid profile, EKG, and chest x-ray should be done on all patients. An echocardiogram will be helpful in diagnosing valvular disease, myocardiopathies, congestive heart failure, and pericardial effusion. If congestive heart failure is suspected, venous pressure and circulation time can be measured, and one should do pulmonary function studies. If there is fever, then one would want to do a streptozyme test, ASO titer, and serial blood cultures. If there is hypertension, a hypertensive workup may be indicated
. Patients with cyanosis need a workup for congenital heart disease, which will probably include cardiac catheterization and angiocardiography.
Most prudent physicians will refer the patient with cardiomegaly to a cardiologist before pursuing this extensive diagnostic workup.
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Source: Algorithmic Diagnosis of Symptoms and Signs, 2003
Cardiomegaly:
Physical examination
(The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter)
The typical signs of CHF are usually noted on examination. A decreased arterial pulse with narrowed pulse pressure is common. Cyanosis is rare. Significant cardiac enlargement should be evident on physical examination. Examples of these finding include the following:
A. Lung sounds. Rales or pleural effusion with dullness to percussion and decreased breath sounds may be indicative of left ventricular failure.
B. Heart sounds. Gallops, soft heart sounds, and regurgitant heart murmurs are nonspecific findings of advanced CHF. Alterations in S1 or S2, specific murmurs, (e.g., a Valsalva-enhanced systolic murmur in hypertrophic obstructive cardiomyopathy), and muffled sounds with pericardial effusion, all indicate specific underlying pathology.
C. Cardiac pulsations or point of maximal impulse (PMI). Visible pulsations seen lateral to the midclavicular line signify cardiac enlargement unless is found a thoracic deformity or congenital absence of the pericardium.
D. Apical beat or PMI. The apical beat, or PMI, which is typically palpable in only 40% of cases, is highly dependent on body habitus. Use the flat of the hand to palpate the PMI. Time the pulsations using the carotid pulse or auscultated heart sounds. The left lateral decubitus position increases the palpability of both normal and pathologic apical beats.
A PMI within or superior to the fifth intercostal space is normal. Left ventricular enlargement displaces the PMI laterally and downward. A PMI lateral to the midclavicular line or more than 10 cm lateral to the midsternal line is a sensitive but nonspecific indicator of left ventricular enlargement. An apical impulse of more than 3 cm diameter is an accurate sign of left ventricular enlargement.
With moderate or severe left ventricular hypertrophy, the outward systolic thrust persists throughout ejection, often lasting up to the second heart sound. In patients with volume overload or sympathetic stimulation, the left ventricular impulse is brisker and larger than normal but is hypokinetic in patients with reduced stroke volume (e.g., acute myocardial infarction or dilated cardiomyopathy). Large left ventricular aneurysms are palpable above and medial to the apex beat. Thoracic deformities—particularly scoliosis and pectus excavatum—can laterally displace a normal heart.
E. Percussion. In the absence of an apical beat, as in patients with pericardial effusion or with dilated cardiomyopathy and a markedly displaced, hypokinetic apical beat, the left border of the heart can be outlined by means of percussion. Percussed dullness in the left fifth intercostal space more than 10.5 cm from the midsternal line is sensitive and specific for cardiomegaly (3).
Testing
A. Radiographs. The cardiothoracic ratio is quick to measure and relatively reliable as an indicator of cardiomegaly on an adequate, upright, posterior–anterior chest film. Watch for rotation and adequate inspiration: the diaphragm should be lowered to at least the posterior portion of the ninth rib. Calculate the ratio by first measuring the transverse cardiac diameter horizontally through the widest part of the cardiac silhouette. Divide this by the chest diameter measured at the widest part between the inner surface of the ribs. A ratio of 0.5 to 0.55 or less can be considered within the limits of normal for an adult. Ratios of up to 0.6 are normal in children and infants. Fluid accumulation in the pericardium causes distention, enlarging the cardiac silhouette and overlapping and obscuring the hilar vessels. In CHF, the vessels become congested and appear more prominent than normal. Also, the epicardial fat line (radiolucent stripe) on the lateral chest film between the anterior surface of the heart and the retrosternal mediastinal fat should be no more than 1 to 2 mm. Widening beyond this is a reliable indicator of pericardial effusion.
B. Sonography. An echocardiogram is generally considered the standard in assessing cardiac dimensions. With evidence of cardiomegaly on physical examination, an echocardiogram is appropriate if clinically useful in the patient’s care.
C. ECG. The ECG is almost invariably abnormal in true cardiomegaly. Common findings are premature ventricular contractions, atrial fibrillation, atrioventricular and intraventricular conduction abnormalities, and nonspecific ST segment and T-wave changes. Left ventricular hypertrophy and atrial enlargement can be diagnosed by morphology and voltage, but the ECG is rarely diagnostic of a specific underlying cause. Pericarditis causes ST elevation with flat or concave ST segments. Pseudoinfarction patterns are seen in hypertrophic obstructive cardiomyopathy (4).
Diagnostic assessment
The significance of cardiomegaly is determined by the underlying pathology. The most common presenting conditions to consider are listed in Table 7.1.
References
1. Frishman WH. Cardiomegaly on chest x-ray: prognostic implications from a ten-year cohort study of elderly subjects: a report from the Bronx Longitudinal Aging Study. Am Heart J 1992;124:1026–1030.
2. Craddock LD. Cardiac enlargement and the cardiomyopathies. In: Friedman HH, ed. Problem oriented medical diagnosis, 5th ed. Boston: Little, Brown and Company, 1991:67–71.
3. Heckerling PS. Accuracy of precordial percussion in detecting cardiomegaly. Am J Med 1991;91:328–334.
4. Kamiyama N. Electrocardiographic features differentiating dilated cardiomyopathy from hypertrophic cardiomyopathy. J Cardiol 1997;30:301–306.
» READ BOOK EXCERPT ONLINE »
Source: The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter, 2000
Cardiomegaly/Congestive Heart Failure:
Diagnostic Approach
(Field Guide to Bedside Diagnosis)
The Framingham criteria for congestive heart failure are a good reference point. Major criteria include paroxysmal nocturnal dyspnea, rales, cardiomegaly, acute pulmonary edema, third heart sound, jugular pressure greater than 16 cm, and positive abdominojugular reflex. Minor criteria include edema, night cough, dyspnea on exertion, hepatomegaly, pleural effusion, and pulse rate slower than 120. Functional limitation is most often classified using the New York Heart Association (NYHA) system: Class I—symptoms of heart failure only at levels of exertion that would limit normal individuals; Class II—symptoms of heart failure with ordinary exertion; Class III—symptoms of heart failure with less than ordinary exertion; Class IV—symptoms of heart failure at rest.
History is key in CHF. Findings due to excess fluid accumulation include dyspnea, edema, hepatic congestion, and ascites. Findings due to reduced cardiac output include weakness and fatigue, more pronounced with exertion. Acute and subacute CHF produce primarily shortness of breath with exertion or at rest. Other common symptoms include orthopnea, paroxysmal nocturnal dyspnea, and right upper quadrant discomfort due to hepatic congestion in right heart failure.
Decreased cardiac output is counterbalanced by increased sympathetic activity, manifest as sinus tachycardia, diaphoresis, and peripheral vasoconstriction (cool and cyanotic extremities due to decreased perfusion and increased oxygen extraction). A prominent dicrotic notch may be felt in severe left ventricular dysfunction, as the compensitory increase in total peripheral resistence and corresponding reduced aortic compliance accentuate the aortic valve closure. Pulsus alternans (alternating strong and weak pulse beats) is uncommon but pathognomonic of advanced heart failure. Volume overload is manifest as pulmonary congestion (rales), peripheral edema, and elevated jugular venous pressure. The medulla controls the respiratory rate based on pCO 2. The length of the Cheyne-Stokes cycle is proportional to the circulatory delay from the alveoli to the arterioles (r = 0.80).
Systolic heart failure is marked by decreased cardiac output, with manifestations such as weakness, fatigue, and decreased exercise tolerance. Mitral regurgitation, especially when acute, augments early diastolic inflow and may produce an S3 with normal systolic function. Diastolic heart failure is associated with reduced ventricular compliance and increased filling pressures with manifestations of dyspnea and rales.
Findings suggesting left ventricular hypertrophy include a sustained forceful apical thrust, a double apical impulse, an apical impulse larger than 3 cm, and a fourth heart sound on auscultation. Left ventricular enlargement will cause the apical impulse (PMI) to be displaced downward and to the left. Right ventricular hypertrophy will cause a sustained right parasternal lift. It is seen with pulmonary hypertension, pulmonic stenosis, and volume overload with tricuspid regurgitation or atrial septal defect. Right ventricular failure is recognized by edema, jugular venous distension, and abdominojugular reflex.
Key findings on physical examination:
Rales Increased interstitial fluid/pressure causes alveoli to pop open. Pulmonary venous capacitance increases in chronic heart failure, and rales may be absent.
Third heart sound (S3) Ventricular vibration occurs during rapid inflow of blood in early diastole when the long-axis expansion limit is reached, due to reduced LV compliance or increased filling pressure. S3 is a low-pitched sound over the apex, and yield is doubled in the 45 degree left lateral decubitus position. JVD and S3 are independent on multivariate analysis.
JVD The IJ is a right atrial manometer. High JVD (present .45 deg) has a LR 4.1 that CVP is .10 cm. Low JVD (present ,30 deg) has a LR 3.4 that CVP is ,5 cm.
Abdominojugular reflux Apply abdominal pressure for 10 sec. A positive AJR is a 4 cm or greater drop in JVP after release, due to decreased RV compliance or increased LVEDP.
Edema With renin-angiotensin-aldosterone activation, pulmonary and peripheral fluid accumulates. After the extracellular fluid is in excess of about five liters, symmetric, dependent, and pitting peripheral edema develops.
Valsava response The normal response is for BP to rise .15 mm Hg during valsalva, but to fall before 10 seconds passes. When valsalva is released, the BP rises again .15 mm over the resting threshold. In CHF, an abnormal response can consist of absent phase 4 overshoot or a square wave in phase 2.
» READ BOOK EXCERPT ONLINE »
Source: Field Guide to Bedside Diagnosis, 2007
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