- Email: [email protected]
Sarcoidosis: The Significance of an Acinar Pattern on Chest Roentgenogram
tipped catheter was placed in the pulmonary artery for pressure monitoring as a guide to fluid therapy. Postmortem examination revealed a large antemortem thrombus surrounding the catheter tip (Fig 3). The narrowed portion in the middle of the thrombus suggested that this area was compressed during life, perhaps by the pulmonary conus. If this were true and considering that the catheter was withdrawn 8-10 cm just prior to death, the distal tip of the thrombus would have protruded through the pulmonic valve into the main ^pulmonary artery during life. Since the main pulmonary artery normally has a diameter in vivo of about 20-30 mm,3 and since the thrombus diameter at its distal end was about 14 mm, the thrombus must have obstructed at least 50 percent of the main pulmonary artery. Despite the failure to recognize thrombus formation prior to death, in retrospect there were several observations that should have suggested obstruction of the pulmonary vasculature superimposed on extensive pulmonary parenchymal disease. (1) The pressure tracings early after placement indicated that only intermittent patency of the catheter was present after flushing with saline solution (Fig 1). (2) The falling systemic blood pressure and urine output, as well as the development of a metabolic acidosis (probably secondary to lactic acidosis, although not confirmed) were probably related to a decrease in cardiac output. (3) The development of hypercapnea while minute ventilation was maintained constant on the respirator, was an indication either of an increase in deadspace ventilation, which is characteristic of pulmonary artery occlusion,4 or an increase in COz production. Since the metabolic state of the patient was stable, the latter explanation is unlikely. Although hyperventilation frequently occurs following pulmonary vascular occlusion, it could not in this patient because minute ventilation was fixed by the respirator. (4) The widening of the inspired-arterial oxygen difference is also consistent with pulmonary vascular obstruction. (5) The shift in the electrical axis of the ECG from ~30 to +90° was further evidence consistent with massive pulmonary vascular obstruction with right ventricular strain. Although results of premortem coagulation screening tests were normal, disseminated intravascular coagulation was present on pathologic examination. This may have been an important factor in the genesis of the rapid thrombus formation occurring about the catheter tip, although it is not clear whether the disseminated intravascular coagulation state initiated the formation of the thrombus, or whether the thrombus, by decreasing cardiac output with resultant tissue hypoxia, was responsible for the disseminated intravascular coagulation state. The occurrence of massive and rapid thrombus formation about this type of catheter is most unusual and has not previously been reported. Of 70 patients with acute myocardial infarction in whom the catheter was used by Swan et al,1 only two had significant thrombus formation occur about the catheter tip. Both were associated with catheter placement for longer than 48 hours. The thrombus formation in our case with resultant pulmonary vascular obstruction was an important, if not the primary, cause of the patient's death. This complication is rare, but because of its potential life threatening 684 SAHN, SCHWARZ, LAKSHMINARAYAN
effects, the catheter should probably be removed when consistendy damped pressure tracings are observed in association with hemodynamic or pulmonary function abnormalities that would be consistent with pulmonary vascular occlusion, ie, acute cor pulmonale, shock, increased deadspace ventilation (causing hypercapnea using volume ventilators), and increasing hypoxemia with afixedinspired oxygen concentration. REFERENCES
1 Swan HJC, Ganz W, Forrester J, et al: Catheterization of the heart in man with use of a flow-directed balloon-tipped catheter. N Engl J Med 283:447-451, 1970 2 Petty TL, Ashbaugh DG: The adult respiratory distress syndrome. Chest 60:233-239, 1971 3 Dotter CT, Steinberg I: The angiocardiographic measurement of the normal great vessels. Radiology 52:353-357, 1949 4 Severinghaus, JW, Stupfel M: Alveolar dead space as an index of distribution of blood flow in pulmonary capillaries. J Appl Physiol 10:335-348, 1957
Sarcoidosis: The Significance of an Acinar Pattern on Chest Roentgenogram* Steven A. Sahn, M.D.,•• Marvin I. Schwarz, M.D., F.C.C.P.t and S. Lakshminarayan, M.D.%
A young black woman presented with dyspnea on exertion and a productive cough* The chest roentgenogram showed predominance of an acinar rosette pattern without hilar adenopathy. Lung biopsy showed multiple noncaseating granulomata in the interstitium, compatible with the diagnosis of sarcoidosis, with alveoli filled with mononuclear cells. The term alveolar sarcoidosis Is a radiologic diagnosis based on certain proposed criteria for acinar filling. Supported by pathologic correlation, it appears that the acinar radiographic pattern may represent a secondary nonspecific response of the lung to the primary interstitial injury.
common roentgenographic features of pulmonary Thesarcoidosis have been well described. Lymph 1-3
node enlargement, disseminated miliary densities, localized infiltrates andfibroticchanges, alone or in combination, are the more typical findings. Although it is a granulomatous disease of the interstitium, there is a form of sarcoidosis that produces an acinar roentgenographic pattern. However, histopathologic correlation of this form of sarcoidosis with roentgenography has not been reported. We have recently observed a young black •From the University of Colorado Medical Center, Denver. ••Instructor, Department of Medicine, Division of Piilmonary Disease. tChief, Pulmonary Diseases, General Rose Memorial Hospital and Assistant Professor of Medicine, Division of Pulmonary Disease. ^Assistant Professor of Medicine, Division of Pulmonary Diseases. Reprint requests: Dr. Sahn, 4200 East Ninth, Denver 80220
CHEST, 65: 6, JUNE, 1974
Table 2—Arterial Blood Gas Measurement
FIGURE 1. Closeup view of chest radiograph showing fine acinar rosette pattern of infiltrate.
woman with progressive dyspnea and a radiograph demonstrating a pattern of predominantly diffuse acinar filling without hilar adenopathy. Lung biopsy was compatible with the diagnosis of sarcoidosis. The case represents an unusual roentgenographs presentation of sarcoidosis: the acinar rosette pattern. It also supports the concept that parenchymal pulmonary sarcoidosis is a disease of the interstitium and that the acinar filling most likely represents a reaction of the lung to the primary injury. CASE R E P O R T
A 26-year-old black woman was admitted to the hospital with the chief complaint of dyspnea on exertion and productive cough of one month's duration. At that time she noticed the onset of substernal pain, dyspnea on exertion and a lowgrade temperature. The dyspnea progressed and became present at rest. This was associated with a 5.42 kg weight loss. She denied any history of skin rash, arthralgias, visual disturbance or polyuria. The physical examination of the chest revealed decreased bilateral expansion, dullness to percussion, increase in fremitus and medium rales at the bases, implying air space consolidation. The remainder of the physical examination, including slit-lamp examination of the
Data
Date
Supplemental 0 2
Po2
Pco2
pH
10/12/72
2 liters/min nasal
56
35
7.41
10/27/72
room air prednisone 60 mg 6 days
65
40
7.45
eyes, disclosed no abnormalities. Laboratory examination revealed a hematocrit of 43 percent and a leukocyte count of 5,100/mm3, with a normal differential. Urinalysis was normal. The serum calcium value was 9.4 mg percent, and the serum phosphorus level was 4.3 mg percent. Results of protein electrophoresis, blood sugar, serum creatinine and liver function tests were normal. Laboratory studies of a 24-hour urine collection for calcium were normal. Results of examination of sputa for pathogenic bacteria, including acid-fast bacilli and fungi, were negative. Periodic acid-Schiff (PAS) stain of the sputum was negative. The chest roentgenogram revealed a bilateral, diffuse acinar rosette pattern without hilar adenopathy (Fig 1). Pulmonary function studies on admission showed a moderate to severe restrictive ventilatory defect (see Table 1). Arterial blood gas measurements breathing 2 liters/min of oxygen via nasal prongs revealed an oxygen tension (P02) of 56 mm Hg, a arterial carbon dioxide pressure (PCO2) of 35 mm Hg and a pH of 7.41 (Table2). An open lung biopsy was performed on the sixth hospital day. The histologic sections revealed multiple interstitial and peribronchiolar noncaseating granulomas composed of multinucleated giant cells, with peripherally arranged nuclei, lymphocytes, fibroblasts and epithelioid cells (Fig 2). Asteroid bodies were noted in several giant cells. The alveoli in the region of the granulomata were filled with mononuclear cells without evidence of granuloma formation. The alveolar lining cells were normal and the walls were of normal thickness (Fig 3). Special staining of the lung tissue with Ziehl-Neelsen, PAS and methenamine silver revealed no abnormalities. She was treated with prednisone, 60 mg daily, and after six days of therapy showed significant improvement in arterial oxygenation and pulmonary function (Table 1, 2). However, she continued to have dyspnea with mild exertion. DISCUSSION
When the first roentgenogram was obtained from our patient one month after the onset of symptoms, an acinar rosette pattern without hilar adenopathy was observed. The absence of hilar nodes with this pattern is unusual but has been observed by others. 4 The patient was treated with corticosteroids resulting in a good clinical response within one week, with a decrease in cough and an
Table 1—Pulmonary Function Studies
Date
Steroid Rx
TLC Liters (% Predicted)
RV Liters (% Predicted)
DLco (ml/ mm Hg/Min) SB (% Predicted)
FVC Liters (% Predicted)
FEVi Liters (% Predicted)
MMEF Liters/M in (% Predicted)
1.76 (44)
1.76 (53)
2.83 (75)
2.54 (44)
0.82 (46)
13.8 (50)
3.37 (84)
2.69 (80)
2.63 (69)
3.91 (68)
0.54 (30)
7.9 (29)
10/16/72 none Admission prednisone 12/19/72 20 mg CHEST, 65: 6, JUNE, 1974
SARCOIDOSIS: ACINAR PATTERN ON ROENTGENOGRAM 685
FIGURE 2 . Note multiple interstitial and peribronchiolar granulomas with giant cells (hematoxylin & eosin stain; original magnification: X 125).
improvement of her dyspnea. Her Po 2 increased from 56 mm Hg on 2 liters/min of oxygen via nasal prongs, to 65 mm Hg breathing ambient air (Table 2). There was marked clearing of findings on the chest roentgenogram and by 21 days after the initial radiograph no abnormalities could be noted. Pulmonary function studies showed a progressive increase in vital capacity but a concomitant decrease in the single breath diffusing capacity for carbon monoxide. There was also a steady decrease in residual volume over the observation period. These data, despite the now normal chest roentgenogram, suggested that significant pulmonary disease was present in spite of high-dosage corticosteroid therapy. Siltzbach5 found that 14 of 123 patients with intrathoracic lesions due to sarcoidosis had conglomerate pneumonic consolidation of an acinar character on their first roentgenogram. Ellis and Ren thai 6 found nodular pulmonary densities in 36 percent of 135 cases, with
approximately three-fourths of those representing acinar lesions. Although this roentgenographic appearance occurs in fewer than 20 percent of patients with sarcoid, the frequency of the disease makes the acinar roentgenographic pattern not uncommon. 5 However, the acinar rosette pattern of pulrr*onary sarcoid appears to be rare, and histopathologic correlation has not been documented. Ziskind et al7 have emphasized the importance of recognition of the acinar pattern and have divided this pattern into rosettes (lobular consolidations) and stippling (sublobular consolidations). In the majority of acinar-filling diseases the roentgenographic shadows are confluent, and individual acinar units cannot be identified easily. This has certainly been the pattern in previously reported cases of "alveolar" sarcoidosis. The present case is unusual in that distinct acinar shadows of both types are easily observed. The lung biopsy demonstrated that the acinar rosette pattern seen on the chest roentgenogram was most likely caused by alveolar filling with mononuclear cells and not by the noncaseating granulomas, which were situated in the interstitium of the lung. These mononuclear cells presumably represent a response to the interstitial granulomatous reaction and are totally nonspecific.7 Whether these cells are hematogenous in origin or are a result of desquamation of alveolar lining cells is unclear. Sarcoidosis is a disease of the pulmonary interstitium, and the term "alveolar" sarcoid is a roentgenographic diagnosis based on certain proposed criteria. Supported by pathologic correlation, it appears that the acinar radiographic pattern may represent a secondary nonspecific response of the lung to the primary interstitial injury and not intra-alveolar granulomas. However, since sarcoidosis is a disease of unknown etiology with certain immunologic abnormalities, further immunohistologic studies of lung tissue might clarify the role of these mononuclear cells in the alveoli. REFERENCES
1 Bernstein S, Sussman M: Thoracic manifestations of sarcoidosis. Radiology 44:37-43, 1945 2 Garland LH: Pulmonary sarcoidosis: The early roentgen
3 (a, left). Note mononuclear-filled alveoli with normal alveolar walls (hematoxylin & eosin stain; original magnification: X 125). (b) Higher magnification of alveolous filled with mononuclear cells (hematoxylin & eosin stain; original magnification: X 500).
FIGURE
684 SAHN, SCHWARZ, LAKSHMINARAYAN
CHEST, 65: 6, JUNE, 1974
findings. Radiology 48:333-354, 1947 3 Meisels E: The course of Besnier-Boeck's disease of the lungs in serial roentgenograms. Am J Roentgenol Radium Ther Nucl Med 44:564-567, 1940 4 Greenspan RH: Chronic disseminated alveolar diseases of the lung. Semin Roentgenol 2:77-97, 1967 5 Siltzbach LE: Pulmonary sarcoidosis. Am J Surg 89:556568, 1955 6 Ellis K, Renthal C: Pulmonary sarcoidosis: Roentgenologic observations on course of disease. Amol J Roentgenol Radium Ther Nucl Med 88:1070-1083, 1962 7 Ziskind MM, Weill H, Buechner HA, et al: Recognition of distinctive radiologic patterns in diffuse pulmonary disease. Arch Intern Med 114:108-112, 1964 8 Liebow AA: personal communication
DESCRIPTION OF TRACINGS
The tracings reproduced in Figures 1 and 2 are rhythm strips from a monitor lead recorded in a 72-yearold man, suspected of having "sick sinus node" syndrome. The patient was on no medication, had no evidence of cardiac or respiratory failure, and had normal serum potassium levels. Figure 1A shows atrial tachycardia, with a rate of 200/min. Slight variations in the length of the P-R intervals are present on close observation. The QRS complexes are narrow and of normal configuration. The basic ventricular rate is 65/min. On several occasions, however, as shown in the middle portion of this rhythm strip, longer pauses appear, reducing abruptly the rate to 33/min, one-half of the basic frequency. Figure IB shows two examples of the same arrhythmia, in which the longer pauses are interrupted by ventricular escape beats. These beats are not followed by a compensatory pause and disrupt the basic QRS rhythm. The interval between the end of the ventricular escape beats and the onset of the next normal QRS complex is similar to the basic R-R interval. Figure 2, recorded with a different monitor lead, displays the same ventricular rate as in Figure 1. The atrial rate, however, is now 250/min.
Exit Block Around a Junctional Pacemaker* M. Mirowski, M.D., F.C.C.P., A. G. Antonopoulos, M.D., and Morton M. Mower, M.D.
An arrhythmia displaying the phenomenon of exit block around a junctional pacemaker in a patient with atrial tachycardia and complete A-V block at the junctional level is described. The importance of the exit block concept for a rational interpretation of cardiac arrhythmias is discussed.
INTERPRETATION AND DISCUSSION
Because the basic ventricular rate (65/min) was approximately one-third of the atrial rate (200/min), the arrhythmia displayed in Figure 1A was initially interpreted as atrial tachycardia with 3:1 block. The longer pauses between the QRS complexes were explained by increase in the degree of A-V block to 6:1. It seemed strange, however, that no other intermediate degrees of block, such as 4:1 or 5:1, were noted on the numerous rhythm strips recorded. An alternative possibility of complete A-V block with junctional pacemaker driving the ventricles at a rate of 65/min was therefore considered. The longer pauses, which were double the basic R-R interval, could then be explained by the phenomenon of exit block around the junctional pacemaker. Additional observations supported this second interpretation. Although the slightly different lengths of the PR intervals noted in Figure 1A already suggested complete dissociation between the atria and the ventricles, this was confirmed when increases in atrial rate up to 250/min (Fig 2) did not alter the basic ventricular rate, which remained at 65/min.
T
he phenomenon of exit block is defined as a failure of normally elaborated impulses to capture the surrounding myocardium. The block can follow the pattern of progressive delay in conduction (type 1) or occur without warning (type 2). Conceptually, this conduction disorder can interfere with the function of any cardiac pacemaker, including artificial pulse generators. The occurrence of exit block around an A-V junctional focus is, however, not well documented in the literature, the review of which revealed only two relevant references.1'2 Because of the significance of the exit block concept for a rational interpretation of some cardiac arrhythmias, we thought it worthwhile to report this recently observed case. °From the Department of Medicine, Sinai Hospital of Baltimore, and the Departments of Pediatrics and Medicine, The Johns Hopkins University School of Medicine, Baltimore. Reprint requests: Dr. Mirowskiy Sinai Hospital, Baltimore 21215
LL
B t -4» X
I
I
4t t
4t I
^
1
1
i t FIGURE 1A. Atrial tachycardia of 200/min, with complete A-V block. Junctional pacemaker (arrows) is driving heart at rate of 65/min. Longer pauses reflect phenomenon of exit block around junctional pacemaker (open arrows). For further details see text. (B) Two examples of same arrhythmia. Escape ventricular ectopic beats interrupt long pauses and reset junctional pacemaker (arrows). For further details see text.
CHEST, 65: 6, JUNE, 1974
EXIT BLOCK AROUND JUNCTIONAL PACEMAKER 687
effects, the catheter should probably be removed when consistendy damped pressure tracings are observed in association with hemodynamic or pulmonary function abnormalities that would be consistent with pulmonary vascular occlusion, ie, acute cor pulmonale, shock, increased deadspace ventilation (causing hypercapnea using volume ventilators), and increasing hypoxemia with afixedinspired oxygen concentration. REFERENCES
1 Swan HJC, Ganz W, Forrester J, et al: Catheterization of the heart in man with use of a flow-directed balloon-tipped catheter. N Engl J Med 283:447-451, 1970 2 Petty TL, Ashbaugh DG: The adult respiratory distress syndrome. Chest 60:233-239, 1971 3 Dotter CT, Steinberg I: The angiocardiographic measurement of the normal great vessels. Radiology 52:353-357, 1949 4 Severinghaus, JW, Stupfel M: Alveolar dead space as an index of distribution of blood flow in pulmonary capillaries. J Appl Physiol 10:335-348, 1957
Sarcoidosis: The Significance of an Acinar Pattern on Chest Roentgenogram* Steven A. Sahn, M.D.,•• Marvin I. Schwarz, M.D., F.C.C.P.t and S. Lakshminarayan, M.D.%
A young black woman presented with dyspnea on exertion and a productive cough* The chest roentgenogram showed predominance of an acinar rosette pattern without hilar adenopathy. Lung biopsy showed multiple noncaseating granulomata in the interstitium, compatible with the diagnosis of sarcoidosis, with alveoli filled with mononuclear cells. The term alveolar sarcoidosis Is a radiologic diagnosis based on certain proposed criteria for acinar filling. Supported by pathologic correlation, it appears that the acinar radiographic pattern may represent a secondary nonspecific response of the lung to the primary interstitial injury.
common roentgenographic features of pulmonary Thesarcoidosis have been well described. Lymph 1-3
node enlargement, disseminated miliary densities, localized infiltrates andfibroticchanges, alone or in combination, are the more typical findings. Although it is a granulomatous disease of the interstitium, there is a form of sarcoidosis that produces an acinar roentgenographic pattern. However, histopathologic correlation of this form of sarcoidosis with roentgenography has not been reported. We have recently observed a young black •From the University of Colorado Medical Center, Denver. ••Instructor, Department of Medicine, Division of Piilmonary Disease. tChief, Pulmonary Diseases, General Rose Memorial Hospital and Assistant Professor of Medicine, Division of Pulmonary Disease. ^Assistant Professor of Medicine, Division of Pulmonary Diseases. Reprint requests: Dr. Sahn, 4200 East Ninth, Denver 80220
CHEST, 65: 6, JUNE, 1974
Table 2—Arterial Blood Gas Measurement
FIGURE 1. Closeup view of chest radiograph showing fine acinar rosette pattern of infiltrate.
woman with progressive dyspnea and a radiograph demonstrating a pattern of predominantly diffuse acinar filling without hilar adenopathy. Lung biopsy was compatible with the diagnosis of sarcoidosis. The case represents an unusual roentgenographs presentation of sarcoidosis: the acinar rosette pattern. It also supports the concept that parenchymal pulmonary sarcoidosis is a disease of the interstitium and that the acinar filling most likely represents a reaction of the lung to the primary injury. CASE R E P O R T
A 26-year-old black woman was admitted to the hospital with the chief complaint of dyspnea on exertion and productive cough of one month's duration. At that time she noticed the onset of substernal pain, dyspnea on exertion and a lowgrade temperature. The dyspnea progressed and became present at rest. This was associated with a 5.42 kg weight loss. She denied any history of skin rash, arthralgias, visual disturbance or polyuria. The physical examination of the chest revealed decreased bilateral expansion, dullness to percussion, increase in fremitus and medium rales at the bases, implying air space consolidation. The remainder of the physical examination, including slit-lamp examination of the
Data
Date
Supplemental 0 2
Po2
Pco2
pH
10/12/72
2 liters/min nasal
56
35
7.41
10/27/72
room air prednisone 60 mg 6 days
65
40
7.45
eyes, disclosed no abnormalities. Laboratory examination revealed a hematocrit of 43 percent and a leukocyte count of 5,100/mm3, with a normal differential. Urinalysis was normal. The serum calcium value was 9.4 mg percent, and the serum phosphorus level was 4.3 mg percent. Results of protein electrophoresis, blood sugar, serum creatinine and liver function tests were normal. Laboratory studies of a 24-hour urine collection for calcium were normal. Results of examination of sputa for pathogenic bacteria, including acid-fast bacilli and fungi, were negative. Periodic acid-Schiff (PAS) stain of the sputum was negative. The chest roentgenogram revealed a bilateral, diffuse acinar rosette pattern without hilar adenopathy (Fig 1). Pulmonary function studies on admission showed a moderate to severe restrictive ventilatory defect (see Table 1). Arterial blood gas measurements breathing 2 liters/min of oxygen via nasal prongs revealed an oxygen tension (P02) of 56 mm Hg, a arterial carbon dioxide pressure (PCO2) of 35 mm Hg and a pH of 7.41 (Table2). An open lung biopsy was performed on the sixth hospital day. The histologic sections revealed multiple interstitial and peribronchiolar noncaseating granulomas composed of multinucleated giant cells, with peripherally arranged nuclei, lymphocytes, fibroblasts and epithelioid cells (Fig 2). Asteroid bodies were noted in several giant cells. The alveoli in the region of the granulomata were filled with mononuclear cells without evidence of granuloma formation. The alveolar lining cells were normal and the walls were of normal thickness (Fig 3). Special staining of the lung tissue with Ziehl-Neelsen, PAS and methenamine silver revealed no abnormalities. She was treated with prednisone, 60 mg daily, and after six days of therapy showed significant improvement in arterial oxygenation and pulmonary function (Table 1, 2). However, she continued to have dyspnea with mild exertion. DISCUSSION
When the first roentgenogram was obtained from our patient one month after the onset of symptoms, an acinar rosette pattern without hilar adenopathy was observed. The absence of hilar nodes with this pattern is unusual but has been observed by others. 4 The patient was treated with corticosteroids resulting in a good clinical response within one week, with a decrease in cough and an
Table 1—Pulmonary Function Studies
Date
Steroid Rx
TLC Liters (% Predicted)
RV Liters (% Predicted)
DLco (ml/ mm Hg/Min) SB (% Predicted)
FVC Liters (% Predicted)
FEVi Liters (% Predicted)
MMEF Liters/M in (% Predicted)
1.76 (44)
1.76 (53)
2.83 (75)
2.54 (44)
0.82 (46)
13.8 (50)
3.37 (84)
2.69 (80)
2.63 (69)
3.91 (68)
0.54 (30)
7.9 (29)
10/16/72 none Admission prednisone 12/19/72 20 mg CHEST, 65: 6, JUNE, 1974
SARCOIDOSIS: ACINAR PATTERN ON ROENTGENOGRAM 685
FIGURE 2 . Note multiple interstitial and peribronchiolar granulomas with giant cells (hematoxylin & eosin stain; original magnification: X 125).
improvement of her dyspnea. Her Po 2 increased from 56 mm Hg on 2 liters/min of oxygen via nasal prongs, to 65 mm Hg breathing ambient air (Table 2). There was marked clearing of findings on the chest roentgenogram and by 21 days after the initial radiograph no abnormalities could be noted. Pulmonary function studies showed a progressive increase in vital capacity but a concomitant decrease in the single breath diffusing capacity for carbon monoxide. There was also a steady decrease in residual volume over the observation period. These data, despite the now normal chest roentgenogram, suggested that significant pulmonary disease was present in spite of high-dosage corticosteroid therapy. Siltzbach5 found that 14 of 123 patients with intrathoracic lesions due to sarcoidosis had conglomerate pneumonic consolidation of an acinar character on their first roentgenogram. Ellis and Ren thai 6 found nodular pulmonary densities in 36 percent of 135 cases, with
approximately three-fourths of those representing acinar lesions. Although this roentgenographic appearance occurs in fewer than 20 percent of patients with sarcoid, the frequency of the disease makes the acinar roentgenographic pattern not uncommon. 5 However, the acinar rosette pattern of pulrr*onary sarcoid appears to be rare, and histopathologic correlation has not been documented. Ziskind et al7 have emphasized the importance of recognition of the acinar pattern and have divided this pattern into rosettes (lobular consolidations) and stippling (sublobular consolidations). In the majority of acinar-filling diseases the roentgenographic shadows are confluent, and individual acinar units cannot be identified easily. This has certainly been the pattern in previously reported cases of "alveolar" sarcoidosis. The present case is unusual in that distinct acinar shadows of both types are easily observed. The lung biopsy demonstrated that the acinar rosette pattern seen on the chest roentgenogram was most likely caused by alveolar filling with mononuclear cells and not by the noncaseating granulomas, which were situated in the interstitium of the lung. These mononuclear cells presumably represent a response to the interstitial granulomatous reaction and are totally nonspecific.7 Whether these cells are hematogenous in origin or are a result of desquamation of alveolar lining cells is unclear. Sarcoidosis is a disease of the pulmonary interstitium, and the term "alveolar" sarcoid is a roentgenographic diagnosis based on certain proposed criteria. Supported by pathologic correlation, it appears that the acinar radiographic pattern may represent a secondary nonspecific response of the lung to the primary interstitial injury and not intra-alveolar granulomas. However, since sarcoidosis is a disease of unknown etiology with certain immunologic abnormalities, further immunohistologic studies of lung tissue might clarify the role of these mononuclear cells in the alveoli. REFERENCES
1 Bernstein S, Sussman M: Thoracic manifestations of sarcoidosis. Radiology 44:37-43, 1945 2 Garland LH: Pulmonary sarcoidosis: The early roentgen
3 (a, left). Note mononuclear-filled alveoli with normal alveolar walls (hematoxylin & eosin stain; original magnification: X 125). (b) Higher magnification of alveolous filled with mononuclear cells (hematoxylin & eosin stain; original magnification: X 500).
FIGURE
684 SAHN, SCHWARZ, LAKSHMINARAYAN
CHEST, 65: 6, JUNE, 1974
findings. Radiology 48:333-354, 1947 3 Meisels E: The course of Besnier-Boeck's disease of the lungs in serial roentgenograms. Am J Roentgenol Radium Ther Nucl Med 44:564-567, 1940 4 Greenspan RH: Chronic disseminated alveolar diseases of the lung. Semin Roentgenol 2:77-97, 1967 5 Siltzbach LE: Pulmonary sarcoidosis. Am J Surg 89:556568, 1955 6 Ellis K, Renthal C: Pulmonary sarcoidosis: Roentgenologic observations on course of disease. Amol J Roentgenol Radium Ther Nucl Med 88:1070-1083, 1962 7 Ziskind MM, Weill H, Buechner HA, et al: Recognition of distinctive radiologic patterns in diffuse pulmonary disease. Arch Intern Med 114:108-112, 1964 8 Liebow AA: personal communication
DESCRIPTION OF TRACINGS
The tracings reproduced in Figures 1 and 2 are rhythm strips from a monitor lead recorded in a 72-yearold man, suspected of having "sick sinus node" syndrome. The patient was on no medication, had no evidence of cardiac or respiratory failure, and had normal serum potassium levels. Figure 1A shows atrial tachycardia, with a rate of 200/min. Slight variations in the length of the P-R intervals are present on close observation. The QRS complexes are narrow and of normal configuration. The basic ventricular rate is 65/min. On several occasions, however, as shown in the middle portion of this rhythm strip, longer pauses appear, reducing abruptly the rate to 33/min, one-half of the basic frequency. Figure IB shows two examples of the same arrhythmia, in which the longer pauses are interrupted by ventricular escape beats. These beats are not followed by a compensatory pause and disrupt the basic QRS rhythm. The interval between the end of the ventricular escape beats and the onset of the next normal QRS complex is similar to the basic R-R interval. Figure 2, recorded with a different monitor lead, displays the same ventricular rate as in Figure 1. The atrial rate, however, is now 250/min.
Exit Block Around a Junctional Pacemaker* M. Mirowski, M.D., F.C.C.P., A. G. Antonopoulos, M.D., and Morton M. Mower, M.D.
An arrhythmia displaying the phenomenon of exit block around a junctional pacemaker in a patient with atrial tachycardia and complete A-V block at the junctional level is described. The importance of the exit block concept for a rational interpretation of cardiac arrhythmias is discussed.
INTERPRETATION AND DISCUSSION
Because the basic ventricular rate (65/min) was approximately one-third of the atrial rate (200/min), the arrhythmia displayed in Figure 1A was initially interpreted as atrial tachycardia with 3:1 block. The longer pauses between the QRS complexes were explained by increase in the degree of A-V block to 6:1. It seemed strange, however, that no other intermediate degrees of block, such as 4:1 or 5:1, were noted on the numerous rhythm strips recorded. An alternative possibility of complete A-V block with junctional pacemaker driving the ventricles at a rate of 65/min was therefore considered. The longer pauses, which were double the basic R-R interval, could then be explained by the phenomenon of exit block around the junctional pacemaker. Additional observations supported this second interpretation. Although the slightly different lengths of the PR intervals noted in Figure 1A already suggested complete dissociation between the atria and the ventricles, this was confirmed when increases in atrial rate up to 250/min (Fig 2) did not alter the basic ventricular rate, which remained at 65/min.
T
he phenomenon of exit block is defined as a failure of normally elaborated impulses to capture the surrounding myocardium. The block can follow the pattern of progressive delay in conduction (type 1) or occur without warning (type 2). Conceptually, this conduction disorder can interfere with the function of any cardiac pacemaker, including artificial pulse generators. The occurrence of exit block around an A-V junctional focus is, however, not well documented in the literature, the review of which revealed only two relevant references.1'2 Because of the significance of the exit block concept for a rational interpretation of some cardiac arrhythmias, we thought it worthwhile to report this recently observed case. °From the Department of Medicine, Sinai Hospital of Baltimore, and the Departments of Pediatrics and Medicine, The Johns Hopkins University School of Medicine, Baltimore. Reprint requests: Dr. Mirowskiy Sinai Hospital, Baltimore 21215
LL
B t -4» X
I
I
4t t
4t I
^
1
1
i t FIGURE 1A. Atrial tachycardia of 200/min, with complete A-V block. Junctional pacemaker (arrows) is driving heart at rate of 65/min. Longer pauses reflect phenomenon of exit block around junctional pacemaker (open arrows). For further details see text. (B) Two examples of same arrhythmia. Escape ventricular ectopic beats interrupt long pauses and reset junctional pacemaker (arrows). For further details see text.
CHEST, 65: 6, JUNE, 1974
EXIT BLOCK AROUND JUNCTIONAL PACEMAKER 687