Rupture or laceration of the aorta is a more common result of nonpenetrating traumatic injury than is generally appreciated. Approximately 15 per cent of individuals with traumatic rupture survive temporarily. If the lesion is promptly diagnosed appropriate surgical treatment may be life-saving. Diagnosis may be difficult and at times the rupture may remain clinically silent for variable periods. The natural course from aortic rupture to false aneurysm formation with secondary rupture of the aneurysm may be brief or extend over many years. Surgical treatment of a false aneurysm that has remained stable for a prolonged period has been successful, but in some instances conservative management may be the treatment of choice.

Nonpenetrating Traumatic Injury of the Aorta

Knowledge about the role of the right ventricle in health and disease historically has lagged behind that of the left ventricle. Less muscular, restricted in its role to pumping blood through a single organ, and less frequently or obviously involved than the left ventricle in diseases of epidemic proportions such as myocardial ischemia, cardiomyopathy, or valvulopathy, the right ventricle has generally been considered a mere bystander, a victim of pathological processes affecting the cardiovascular system. Consequently, comparatively little attention has been devoted to how right ventricular dysfunction may be best detected and measured, what specific molecular and cellular mechanisms contribute to maintenance or failure of normal right ventricular function, how right ventricular dysfunction evolves structurally and functionally, or what interventions might best preserve right ventricular function. Nevertheless, even the proportionately limited information related to right ventricular function, its impairment in various disease states, and its impact on the outcome of those diseases suggests that the right ventricle is an important contributor and that further understanding of these issues is of pivotal importance.

For this reason, the National Heart, Lung, and Blood Institute convened a working group charged with delineating in broad terms the current base of scientific and medical understanding about the right ventricle and identifying avenues of investigation likely to meaningfully advance knowledge in a clinically useful direction. The following summary represents the presentations and discussions of this working group.

The right ventricle is affected by and contributes to a number of disease processes, including perhaps most notably pulmonary hypertension caused by a variety of lung or pulmonary vascular diseases (cor pulmonale). Other diseases affect the right ventricle in different ways, including global, left ventricular–, or right ventricular–specific cardiomyopathy; right ventricular ischemia or infarction; pulmonary or tricuspid valvular heart disease; and left-to-right shunts.

The right ventricle pumps the same …

Right Ventricular Function and Failure Report of a National Heart, Lung, and Blood Institute Working Group on Cellular and Molecular Mechanisms of Right Heart Failure

Interstudy reproducibility of right ventricular volumes, function, and mass with cardiovascular magnetic resonance

1. 1. All normal human hearts have essentially the same number of myocardial fibers and myocardial nuclei. During physiologic growth the number of myocardial fibers remains constant; the fibers enlarge, but their length-to-width ratio remains constant (harmonic growth). The number of capillaries increases with growth, with one capillary per four fibers in the infant and one capillary per fiber in the adult. However, the width of the spaces of the capillary net is essentially the same for all age groups. The number of fibers and nuclei is roughly the same for the right ventricle as the left; the left ventricle is heavier than the right because its fibers are thicker. There are fewer layers of fibers in the right ventricle than in the left. It follows from this that the inner surface area of the right ventricle must be greater than for the left. 2. 2. The average weight of the normal heart in man is about 300 gm. Through athletic exertion it can attain a weight of 500 gm. This increase is due to an extension of physiologic growth, with the fibers increasing in length and width but not increasing in number. The growth results in a larger than normal mobilizable blood volume. 3. 3. As a result of pathologic demands for increased heart work as, for example, in hypertension, the “critical” heart weight of 500 gm. is exceeded. Increases in heart weight above the “critical” level are due to increase in the number of fibers with little further thickening. There is also an increase in capillaries, with the ratio of one capillary per fiber maintained. The coronary insufficiency that occurs with advanced hypertrophy is not principally due to a failure of capillary supply but to the fact that with hypertrophy the growth of the coronary arteries and coronary ostia is retarded and atherosclerotic lesions of the coronary system become more frequent. 4. 4. As a result of the coronary insufficiency a dilatation takes place. However, the Z-band to Z-band distance (i.e., the length of sarcomeres) of myocardial fibers in dilated hearts is the same as for normal hearts. In addition to longitudinal growth of the muscle fibers in dilatation there are also structural alterations in the myocardium with rearrangements of the architectural relationship among the muscle fibers. Therefore, dilatation as encountered in man is not characterized by overstretched fibers. This is true of dilatation whether due to coronary sclerosis, myocarditis or excessive hypertrophy. It is called “structural dilatation” as opposed to the “functional dilatation” of the acutely overloaded heart. There is an increased residual ventricular volume in the dilated heart, but it is not mobilizable. 5. 5. Structural dilatation is the morphologic substrate of the decompensated heart. The cross section area of muscle capable of contracting is too small for the increased volume of the ventricle. Cardiac insufficiency results, not from overstretching of the fibers or inadequate oxygen consumption per fiber length in the Starling sense, but for strictly mechanical reasons. The unit muscle weight may produce a normal amount of energy liberated on contraction but it is no longer adequate to expel a normal stroke volume from a ventricle of these dimensions. In other words, the essence of myocardial failure is the discrepancy between the amount of energy necessary to expel a stroke volume and the amount of energy available. In these studies it has been shown that in most clinical cardiac disorders with heart failure the discrepancy can be adduced from changes in the quantitative morphology of the heart.

Heart failure from the point of view of quantitative anatomy.

Six patients with acute myocardial infarction presented with hemodynamic evidence of predominant right ventricular failure, characterized by a mean right atrial pressure averaging 20.2 mm Hg and left ventricular filling pressure averaging 16.3 mm Hg. Autopsy in two cases revealed extensive involvement of the right as well as the left ventricle. Clinically the patients usually had evidence of diaphragmatic wall infarction, distended neck veins, hypotension and heart block. Pressure contours and mean pressure often showed no significant change as the catheter was advanced from the right atrium to the pulmonary artery. Shock in three patients was effectively treated with plasma volume expansion, to increase further right-sided pressure, or the administration of sodium nitroprusside, to reduce left-sided filling pressure. It is suggested that when right ventricular infarction accompanies left ventricular infarction, a unique clinical and hemodynamic syndrome occurs because the ability of the right ventricle to maintain adequate left ventricular filling is impaired. Recognition of this syndrome is vital if appropriate therapy is to be instituted.

Right ventricular infarction. Clinical and hemodynamic features.

The absence of conspicuous increments of venous pressure after severe damage to the right ventricle of the dog, with a discussion of the relation between clinical congestive failure and heart disease

William A. Jeffers

Papers

The absence of conspicuous increments of venous pressure after severe damage to the right ventricle of the dog, with a discussion of the relation between clinical congestive failure and heart disease