Heart failure occurs when the heart is unable to pump the blood that it receives. We will limit our discussion to left ventricular failure.
There are four basic causes of heart failure: 1) excessive work, 2) decrease in the quantity of contractile units (eg., myocardial ischemia), and 3) decrease in the quality of contractile units (eg., myocardiopathy). Excessive work can be divided into increased afterload (the pressure against which the left ventricle must pump) or increased preload (the volume of blood delivered to the left ventricle). Examples of afterload lesions include systemic hypertension, aortic stenosis and coarctation of the aorta. Examples of preload lesions include diseases which cause overcirculation (anemia, thyrotoxicosis, pregnancy, cardiac shunts), and valvular incompetence.
Patients who present with radiographic evidence of left heart failure may present with shortness of breath. On physical exam, the signs of left heart failure include a third heart sound, jugular venous distention and rales.
The earliest finding of left heart failure on the chest radiograph is equalization or cephalization of the pulmonary vessels. Normally, the vessels in the lung bases are larger and more numerous than the vessels in the lung apices. This is due to gravitational effects and the fact there is a larger volume of lung in the bases. When the heart begins to fail, the end-diastolic pressure increases. This increased pressure is transmitted to the pulmonary veins and capillaries. When the increased pressure exceeds the atmospheric pressure in the alveoli, fluid leaks out of the vessels. Fluid initially leaks into the interstitium. Before this is radiographically apparent, it causes the blood vessels in the bases to constrict. Since the pressure in the vessels is higher in the lung bases than in the apices (due to gravity), the lung bases are affected first. Thus, blood is preferentially "shunted" to the upper lungs giving the radiographic appearance of cephalization.
If the pressure in the vessels continues to rise, the fluid in the interstitium will become radiographically evident as interstitial edema. You may see bronchial wall thickening as the fluid collects in the peribronchial interstitium. The vessels become less will-defined as fluid collects in the perivascular interstitium. Fluid also collects in the interlobular septa. This is radiographically evident as "Kerley" lines. The most noticeable are the Kerley B lines (B=bases). These are short thin lines which extend to and are perpendicular to the pleura.
As the pressure in the vessels continues to rise, fluid will then leak into the alveoli, resulting in alveolar edema. This is manifested radiographically as bilateral symmetric perihilar, coalescent opacities. The vessel become indistinguishable and the bronchi may become visible as branching air-containing structures (air bronchograms).
The radiographic findings of heart failure correlate with the left atrial pressure (as measured by the mean pulmonary wedge pressure, or swan pressure reading). Cephalization of the pulmonary vessels occurs at a wedge pressure of 12 - 19 mm Hg, interstitial edema occurs at a wedge pressure of 20 -25 mm Hg, and alveolar edema occurs at wedge pressures greater than 25 mm Hg.
 C01 |
- Normal |
 C02 |
- Grade I PVH |
 C03 |
- Normal |
 C04 |
- Grade II PVH |
 C05 |
- Grade III PVH |