Recent Publications by CFE Educators

Respiratory bronchiolitis-associated interstitial lung disease is a distinct clinical syndrome found in current or former cigarette smokers. The disease often is confused with other interstitial lung diseases, especially idiopathic pulmonary fibrosis. The clinical presentation resembles those of patients with other interstitial lung diseases--cough and dyspnea, with coarse rales on physical examination. Diffuse fine reticulonodular interstitial opacities are found on chest radiograph, usually with normal-appearing lung volumes. Bronchial wall thickening, prominence of peribronchovascular interstitium, small regular and irregular opacities, and small peripheral ring shadows are distinctive features. Pulmonary function testing may be normal but usually demonstrates mild to moderate restriction and normal or slightly reduced diffusing capacity. A mixed obstructive-restrictive pattern is common. Respiratory bronchiolitis-associated interstitial lung disease is characterized histologically by an inflammatory process involving the membranous and respiratory bronchioles. The pathologic findings are dominated by the finding of tan-brown pigmented macrophages within respiratory bronchioles and neighboring alveolar ducts and alveoli. The pulmonary parenchyma away from the airway usually is normal or may demonstrate mild hyperinflation. The clinical course and prognosis of respiratory bronchiolitis-associated interstitial lung disease are unknown. Most patients respond favorably to corticosteroids, with documented improvement in lung function and chest radiographs. Smoking appears to play a role in the pathogenesis, so smoking cessation is important in the resolution of this syndrome.

Many of the diseases associated with bronchiolitis may produce varying degrees of both histologic manifestations--i.e., proliferative and constrictive bronchiolitis. The factors responsible for producing one pattern or the other are not known. It therefore is important that one consider both the etiologic and histologic classification when attempting to identify a case of bronchiolitis. In some instances, it appears that proliferative bronchiolitis, the more common variety, is an "early" lesion that may completely or partially resolve. Constrictive bronchiolitis is a rare finding and may be the final outcome of persistent and severe proliferative bronchiolitis. Most often, constrictive bronchiolitis appears to be a separate process dependent on the type, extent, and severity of the initial insult.

OBJECTIVES

This study was designed to test the hypothesis that active compression-decompression cardiopulmonary resuscitation increases transmitral flow and end-decompression left ventricular volume over levels achieved with standard manual cardiopulmonary resuscitation.

BACKGROUND

Recently, cardiopulmonary resuscitation incorporating active compression and decompression of the chest has been demonstrated to improve hemodynamic status in a canine model and in humans after cardiac arrest.

METHODS

The active compression-decompression device was applied midsternum in five consecutive patients and results compared sequentially (in random order) with those of standard manual cardiopulmonary resuscitation. Both techniques were performed at 80 compressions/min with a 1.5- to 2-in. (3.8 to 5.1 cm) compression depth and a 50% duty cycle. Transesophageal echocardiographic data obtained in each patient included the velocity-time integral of transmitral pulsed Doppler recordings and two-dimensional images of the left ventricle in the long-axis view. Planimetric volume measurements of the left ventricle were obtained at both end-compression and end-decompression.

RESULTS

No difference was observed in end-compression volume between the two techniques (p = 0.81). Increased end-decompression volume (active compression-decompression technique 81.3 +/- 12.5 vs. standard technique 69.4 +/- 10.8, p 0.05), stroke volume (active compression-decompression technique 32.6 +/- 6.8 vs. standard technique 17.6 +/- 5.2, p 0.05) and velocity-time integral of transmitral flow (active compression-decompression technique 15.8 +/- 4.3 vs. standard technique 7.8 +/- 2.3, p 0.05) were found in the active compression-decompression group. The transmitral velocity-time integral was highly correlated with left ventricular stroke volume (r = 0.90).

CONCLUSIONS

Improved transmitral flow, end-decompression left ventricular volume and stroke volume are seen with active compression-decompression resuscitation, suggesting a biphasic cardiothoracic cycle of flow. Active decompression of the chest appears to be a beneficial adjunct to standard cardiopulmonary resuscitation.

Four women with a chronic respiratory illness characterized by chronic cough, dyspnea, mild to severe physiologic abnormalities, relatively normal chest radiographs, and lack of response to bronchodilators or prednisone were identified and prospectively evaluated. Constrictive bronchiolitis, defined as concentric narrowing of the bronchiolar lumen, mural scarring, smooth muscle hyperplasia, and mucus stasis, was the major histologic finding on open lung biopsy in all cases. Each presented with an illness clinically distinct from asthma, connective tissue disorders, occupational or environmental lung disease, bronchiectasis, diffuse panbronchiolitis, cystic fibrosis, and emphysema. None of the patients smoked cigarettes. None had clinical evidence of a recent viral lower respiratory tract infection. The physical examinations were normal except for rales heard on chest examination in two patients. Chest radiographs showed increased bronchovascular markings in three patients. Lung function was normal in one patient, two of the patients had a reduced diffusing capacity associated with moderate hypoxemia and an obstructive ventilatory defect, and one patient exhibited a mixture of restrictive and obstructive defects. None have experienced significant progression of their disease over 1 to 5 yr of follow-up. However, complete return to normal function did not occur. We hypothesize that patients with the constellation of findings described represent a distinct and definable clinicopathologic entity and further clarifies the spectrum of "small airways disease." Establishing the diagnosis appears important for prognostic and possibly therapeutic reasons.

The interstitial lung diseases encompass a wide array of inflammatory and fibrotic processes that produce a significant amount of morbidity in the elderly. Diagnosis usually requires a systematic approach and often requires lung biopsy. Treatment typically involves the use of immunosuppressive dosages of corticosteroids or cytotoxic agents. The use of these medications in the elderly demands meticulous, close follow-up because side-effects can be substantial.

Because of the better resolution of higher frequency transducers and the proximity of the coronary arteries to the esophageal window, TEE is emerging as a valuable method for evaluation of coronary artery disease. TEE allows imaging of the proximal coronary arteries, measurement of coronary flow reserve, identification of coronary artery anomalies, and observation of wall motion during transesophageal atrial pacing. The application of TEE in evaluation of coronary artery disease will continue to grow as technology improves.

The superior imaging capabilities of TEE have rapidly thrust this technique into the mainstream of noninvasive cardiology. However, the semi-invasive nature of this procedure requires specialized training on the part of the echocardiographer and adaptations of the traditional echocardiographic laboratory. These requirements will become even more evident as this technique is employed increasingly for interventional studies such as transesophageal atrial pacing and pharmacologic stress. TEE has proved efficacious and safe, even in critically ill patients, and its applications continue to expand. Following an article on anatomy, encompassing single and biplane orientation, the remainder of this monograph addresses the established as well as the emerging applications of TEE.

Many echocardiographic signs of severe MR are clearly demonstrated, particularly when both TEE and TTE are used. When these signs are assiduously sought, the recognition of severe MR should pose little problem. Part of the confusion concerning MR and the grading of its severity comes from the fact that the hemodynamic consequences of a given degree of MR vary widely from one individual to another. A regurgitant volume of 50 mL might prove incapacitating to one patient while seeming inconsequential in a second patient. A regurgitant fraction of 50% is poorly tolerated in some patients and asymptomatic in others. Similarly, a regurgitant orifice 0.5 cm2 has unpredictable consequences to the organism, and, in fact, this orifice may vary considerably in size depending on hemodynamic conditions. Thus, a universal definition of the severity of MR is lacking, and there is no agreement on the units with which to quantitate it. The net effect of this confusion is not an inability to recognize severe MR but frustration in differentiating moderate MR from severe MR. We believe that precise quantitation of MR will occur when comprehensive pharmacologic interventions with either TEE or surface echocardiographic monitoring are performed to define the severity of MR by its range of responses to these agents. We have had some success with Doppler measurement of the response of pulmonary artery pressure to dynamic exercise. Patients with normal pulmonary artery pressure at rest tend to show exaggerated rises in pulmonary pressure when MR is clinically important and has resulted in left ventricular dysfunction. Anticipated progress notwithstanding, competently performed TEE is the method of choice for recognizing severe MR.