Cardiomegaly/Congestive Heart Failure
Differential Overview
❑ Congestive heart failure
❑ Hypertensive left ventricular hypertrophy
❑ Anterior myocardial ischemia
❑ Athlete’s heart
❑ Mitral regurgitation
❑ Aortic stenosis
❑ High output
❑ Hypertrophic obstructive cardiomyopathy
❑ Pulmonary hypertension
❑ Cor pulmonale
❑ Dilated cardiomyopathy
❑ Endocarditis
❑ Pericardial effusion
❑ Left ventricular aneurysm
❑ Mitral stenosis
❑ Amyloidosis
Diagnostic Approach
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.
Clinical Findings
Congestive heart failure Signs of left or right heart failure such as symmetric bibasilar rales, edema, and a third heart sound are present.
Hypertensive left ventricular hypertrophy The PMI is discrete, brisk, and brief. A fourth heart sound is prominent. Blood pressure control is usually suboptimal.
Anterior myocardial ischemia Classic exertional angina indicates ischemic heart disease. A systolic bulge in the left third and fourth interspace that is medial to the PMI occurs transiently during episodes of chest pain and corresponds to anterior dyskinesia.
Athlete’s heart Isometric training, such as weight lifting, will produce the greatest degree of enlargement although enlargement can also be seen in persons with expanded aerobic capacity.
Mitral regurgitation The PMI is diffuse, rolling, and displaced downward to the left. There will be a holosystolic murmur at the apex, radiating toward the axilla. Atrial fibrillation is often present with severe mitral regurgitation.
Aortic stenosis A crescendo-decrescendo murmur is loudest at the upper right sternal border, radiating into the carotids.
High output A systolic flow murmur will be detected. Causes include hyperthyroidism, anemia, pregnancy, arteriovenous fistula, and Paget disease.
Hypertrophic obstructive cardiomyopathy An aortic outflow murmur changes dramatically in loudness with changes in position (intensifying with standing).
Pulmonary hypertension This is marked by a right parasternal lift and accentuated P2.
Cor pulmonale Vasodilation, large volume pulses, warm extremities, and throbbing fingers are signs. The cardiac apex may be hidden by the expanded lung volume. Causes include massive or recurrent pulmonary embolism, primary pulmonary hypertension, or emphysema.
Dilated cardiomyopathy The PMI is diffuse, displaced, and sluggish.
Endocarditis Valvular damage with acute regurgitation (aortic or mitral), fever, myocarditis, and anemia all contribute to the heart failure. Clues include underlying valvular heart disease with a change in character or intensity of the murmur and embolic stigmata such as splinter hemorrhages, Osler nodes, and conjunctival or retinal petechiae (Roth spots).
Pericardial effusion The heart sounds are muffled. There may be a pericardial friction rub or chest pain that is partially relieved by sitting forward. Signs of hemodynamic compromise (pericardial tamponade) include hypotension, jugular venous distension with Kussmaul sign (filling on inspiration), and pulsus paradoxus. Uremia, hypothyroidism, lupus, or acute myocardial infarction are frequent underlying causes.
Left ventricular aneurysm A systolic bulge is palpable, similar to anterior ischemia, but presents continuously. There is a history of prior anterior myocardial infarction.
Mitral stenosis The PMI is normally located, but the impulse is snapping in quality. There is a right ventricular lift. A low-pitched apical diastolic murmur can be heard with the bell of the stethoscope. A malar flush, cold blue fingers, and small volume pulses are other features.
Amyloidosis Suspect in a patient with a chronic inflammatory condition, or when proteinuria or organomegaly is present.
Pictures
Book Source Details
- Book Title: Field Guide to Bedside Diagnosis
- Author(s): David S. Smith
- Year of Publication: 2007
- Copyright Details: Field Guide to Bedside Diagnosis, Copyright © 2007 Lippincott Williams & Wilkins.
Other Book Chapters Related to Heart symptoms
Read excerpts from these other book chapters related to Heart symptoms:
Medical Books Excerpts
- Cardiomegaly
- "The 10-Minute Diagnosis Manual: Symptoms and Signs in the Time-Limited Encounter" (2000)
- [ read ]
Copyright Details: Field Guide to Bedside Diagnosis, Copyright © 2008 Williams & Wilkins.
More About Causes of Heart symptoms
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More About This Book:
Title: Field Guide to Bedside Diagnosis
Authors: David S. Smith
Publisher: Lippincott Williams & Wilkins
Copyright: 2007
ISBN: 0-78178-165-5
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