Acute Rupture of the Pulmonic Valve by a Balloon-tipped Catheter Producing a Musical Diastolic Murmur

How this increased permeability occurs is unclear, although there are several hypotheses. Chronic alveolar hypoxia or anoxia has been proposed as a cause. 0.£ this increased permeability.' Warren et al" concluded from their studies that hypoxia had a direct effect on alveolar capillary membrane permeability. However, careful evaluation of their data is not consistent with alterations in membrane permeability; rather, since the hypoxia produced increased lymph flow with a decreased protein content, elevated pulmonary vascular hydrostatic forces, such as might occur secondary to nonuniform hypoxic pulmonary vasoconstriction, could be implicated as the cause of the increased lung lymph flow. Additionally, it has been suggested that the pulmonary capillaries might be somehow damaged by long-term alveolar collapse, and the application of a highly negative intrapleural pressure might "stretch" endothelial pores, leading to an increased permeability pulmonary edema.t-! However, there is no evidence in the literature to substantiate this hypothesis. No explanation is available for the presence of an exudative pleural effusion in this patient. There was no evidence for pancreatitis, acute infection, tumor, pulmonary embolus or collagen vascular disease, either clinically or at postmortem examination. Regrettably, this effusion must be classified as idiopathic. In summary, we presented a case of reexpansion pulmonary edema. Physiologic measurements obtained at the time of injury disclosed a normal pulmonary capillary wedge pressure and an edema fluid-serum protein ratio of 0.85. We believe that reexpansion pulmonary edema should be included in the list of causes for a diffuse pulmonary capillary leak syndrome. REFERENCES

1 Riesman D. Albuminous expectoration following thoracentesis. Am J Med Sci 1906; 123: 620-30 2 Ziskind MM, Weill H, George RA. Acute pulmonary edema following the treatment of spontaneous pneumothorax with excessive negative pressure. ARRD 1965; 92:632-36 3 Miller WC, Toon R, Palat H, Lacroix J. Experimental pulmonary edema following re-expansion of pneumothorax. ARRD 1974; 108:664-66 4 Mahajan VK, Simon M, Huber R. Re-expansion pulmonary edema. Chest, 1979; 75: 192-94 5 Sherman S, Ravikrishnan KP. Unilateral pulmonary edema following re-expansion of pneumothorax of brief duration. Chest 1980; 77 :714 6 Humphreys RL, Berne AS. Rapid re-expansion of pneumothorax: a cause of unilateral pulmonary edema. Radiology 1970; 96:509-12 7 Carlson RW, Schaeffer RC, Michaels SG, Wei! MH. Pulmonary edema fluid: spectrum of features in 37 patients. Circulation 1979; 60: 1161-69 8 Pavlin JP, Cheney FW. Unilateral pulmonary edema in rabbits after re-expansion of collapsed lung. JAP: Resp, Environ, Exercise Physiol 1979; 46:31-35 9 Warren MF, Peterson DK, Drinker CK. The effects of heightened negative pressure in the chest, together with further experiment upon anoxia in increasing the How of lung lymph. Am J Physiol 1942; 137:641-48

CHEST, 81: 2, FEBRUARY, 1982

Acute Rupture of the Pulmonic Valve by a Balloon-tipped Catheter Producing a Musical Diastolic Murmur· Keith M. Lindgren, M.D.; Kathleen McShane, M.D.; and WiUiam C. Roberts, M.D., F.C.C.P.

Attention is called to tbe development of severe pulmonic-valve regurgitation during withdnwal of a balloon-tipped catheter tbat bad been in place for six days. The resulting pulmonic regurgitation produced a loud (grade 5/6), musical di_oUe murmur recorded by phonocardiogram at the time of its initial production. Autopsy disclosed a noninfected tear in one of the three pulmonic valve cusps. of the major pulmonary arteries with Catheterization a How-directed balloon-tipped catheter for hemo-

dynamic measurement has gained wide usage in critically ill patients. Although relatively infrequent when certain guidelines for insertion and withdrawal are followed, 1 numerous complications of the technique have been described. Recognition of the complications requires close clinical observation. This report describes the sudden appearance of a loud musical diastolic murmur during withdrawal of a Swan-Ganz catheter across the pulmonic valve with autopsy confirmation of a tear in a pulmonic valve cusp. CASE REPORT

A 59-year-old man was admitted to Washington Adventist Hospital with recurrent acute myocardial infarction complicated by severe congestive heart failure. Physical examination and phonocardiogram documented a late systolic crescendo murmur and prominent third and fourth heart sounds. No diastolic murmur was heard or recorded. On the fourth hospital day, a No. 6 double lumen, balloontipped catheter (Edwards, Swan-Ganz) was inserted and advanced to the pulmonary wedge position under pressure monitoring. No difficulty was encountered. With the balloon deflated, sampling was done on pullback from pulmonary trunk, to right ventricle, right atrium and superior vena cava to exclude a ventricular septal defect. The catheter was again advanced with the balloon inHated and with pressures monitored to wedge position. Chest roentgenogram confirmed the location of the catheter in the pulmonary artery to the right lower lobe. The right-sided pressures (in mm Hg) were: right atrial mean, 18; right ventricular, 60/22; pulmonary arterial 60/30; and pulmonary arterial wedge mean, 30, with V waves of 40. Auscultatory findings were unchanged. After nitroprusside infusion, the pulmonary arterial wedge mean pressure fell to 22 mm Hg and the pulmonary arterial pressure to 45/20 mm Hg. Six days after the balloon-tipped °From the Department of Cardiology, Washington Adventist Hospital, Takoma Park, Md, and the Pathology Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda. Reprint requests: Dr. Lindgren, 7600 Carroll Avenue, Takoma Pat'k, Maryland 20012

ACUTE RUPTURE OF PULMONIC VALVE 251

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At autopsy, a tear was present in one of the three pulmonic valve CllSPS (Fig 3) . No inflammatory cells or microorganisms were observed in the pulmonic valve cusps. The other three cardiac valves were normal, The heart weighed 420 g, and both acute and healed left ventricular myocardial infarcts were present. The posteromedial papillary muscle was severely scarred. The kidneys contained many abscesses with gram-negative organisms. COMMENTS

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1. On withdrawal of catheter from pulmonary trunk

into right ventricle, diamond-shaped diastolic murmur (DM) is abruptly transformed into very intense musical murmur, generally decrescendo. LSB left sternal border.

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catheter had been inserted, an early diastolic crescendodecrescendo grade 2/6 murmur was heard along the left sternal border . On the assumption that the catheter induced pulmonic regurgitation, the catheter was removed with the balloon deflated while recording a phonocardiogram from the third left intercostal space. As the catheter was withdrawn, the diastolic murmur became consistently grade 4 to .5/6 in intensity with pure frequency (100 cycles/sec) and a honking musical character (Fig 1 and 2) . The patient experienced no immediate untoward effects. Six days after the balloon-tipped catheter had been removed, he developed Escherichia coli septicemia. The congestive heart Iallur« worsened. and four days later he died.

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1111 1111 1111111111 1111 11 11 1111111 11111 1111 111 11111111111 II I1 I 1IIII1 I'IGUIIE 2. Persistent diastolic murmur (DM) following removal of pulmonary artery catheter. Murmur very intense (associated with palpable thrill) along left sternal border, with musical characteristic: ie, pure frequency with demonstrable harmonics. Most intense vibrations approximately 100 cycles/psec, with harmonic of lesser intensity at twice this frequency producing visual image of murmur within murmur. Murmur begins with rapid crescendo after pulmonic closure and prolonged decrescendo, ending abruptly with onset of atrial systole as marked by 5•. Systole relatively quiet. Murmur varies little during inspiration [inspir} and expiration (expir}; CAR carotid arterial tracing; ECG lead 2, and LSB left sternal border.

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252 LINDGREN, McSHANE, ROBERTS

The patient described is unique for two major reasons: (1) pulmonic valve regurgitation was documented to have been produced by a catheter, and such occurrence has been published, to our knowledge, in only one previous report, and (2) the resulting pulmonic valve regurgitation produced a precordial murmur of unusual character and intensity, both of which were documented by phonocardiogram. Before removal of the catheter, a murmur was heard and recorded which corresponded to the typical murmur of pulmonic regurgitation without pulmonary hypertension ; ie, a crescendo-decrescendo murmur of low-to-moderate frequency and intensity beginning shortly after pulmonic valve closure, After the catheter had been withdrawn, the murmur abruptly changed in character and intensity, becoming a musical or honking murmur which was very intense and palpable. The phonocardiographic representation of this murmur was pure frequency with a first harmonic of less intensity between the fundamental frequency. The murmur reached its peak rapidly and was only slightly decrescendo with an abrupt cessation at the time of atrial systole. The musical character of the murmur in our patient fits the classic description of the murmur produced by a retroverted cusp of the aortic valve." In our patient, it is reasonable to believe that one pulmonic valve cusp retroverted after the catheter had produced a tear. A change in the mechanism generating the murmur from a regurgitant jet to a retroverted cusp accounts for the change in intensity, since the latter mechanism has been known to produce "the loudest murmurs known to medicine."! The abrupt termination of the murmur at atrial systole can be explained by the rise in right ventricular pressure which occurs at this point, often reversing the gradient from pulmonary artery to right ventricle. Musical diastolic murmurs have usually been associated with aortic regurgitation and the high pressure in the left side of the heart. Thus, documentation of a loud, palpable, musical murmur from pulmonic valve regurgitation with only mild elevation of pulmonary pressure supports the fact that the acoustic mechanism of the murmur is more important than the pressure gradient associated with it. In our patient, assuming that the gradient did not change with removal of the catheter, the retroversion of the cusp apparently resulted in increase in intensity of the murmur and its unique characteristics. That the intensity of the musical murmur does not directly parallel the gradient across the valve during the cardiac cycle also can be explained by a valve flap which varies its location in the regurgi-

CHEST, 81: 2, FEBRUARY, 1982

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FIGURE 3. Pulmonic valve at autopsy with probable catheter location and resulting cuspal tear.

tant stream throughout diastole, sometimes actually increasing the diastolic murmur in later diastole. Despite the intensity of the murmur of catheter-induced pulmonic valve rupture in our patient, he appeared to suffer no immediate untoward effects. Similar benign consequences of pulmonic valve regurgitation have been reported by others." In addition, one of the two other reported patients with catheter-induced pulmonary valve rupture survived and apparently is doing well. " The mechanism by which the pulmonic valve cusp in our patient was tom by the catheter is unclear. There is no evidence that the tear was produced at the time of insertion of the catheter, but it must have occurred during the six days that the catheter was in place, since the murmur of pulmonic regurgitation was heard before the catheter was withdrawn. The patient had septicemia, but infective endocarditis clearly was not present at autopsy. Although our patient did have moderate pulmonary arterial hypertension, it is unlikely that the pulmonary arterial diastolic pressure of 30 to 40 mm Hg can cause rupture of a previously normal pulmonic valve cusp. Movement of the catheter while in place can presumably cause cuspal weakening and predispose the cusp to rupture, since others" have reported damage to th e pulmonic valve cusps by indwelling catheters in the form of focal cuspal hemorrhages and endocardial verrucae. However, these specific findings were not documented in this case. REFERENCES

Pape LA, Haffajee CI, Markis JE, et al. Fatal pulmonary

CHEST, 81: 2, FEBRUARY, 1982

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hemorrhage after use of the flow-directed halloon-tipped catheter. Ann Intern Med 1979 ; 90 :344-47 O'Toole JD, Wortzhacher 11, Wearner NE, Jain AC. Pulmonary valve injury and insufficiency during pulmonary artery catheterization. N Engl J Med 1979 ; 30 : 1167-68 Levin HS, Runco V, Wooley CF , Ryan JP. Pulmonic regurgitation following staphylococcal endocarditis. Circula tion 1964; 30 :411-16 ~lcKusick VA, Murray GE, Peeler RG, Webb GN. Musical murmurs. Bull Johns Hopkins Hosp 1955; 97 :136-76 Faruqui A~fA, Silverman ME. Isolated acquired pulmonary valve regurgitation. Br Heart J 1978; 40 : 198-200 Greene JF, Comminger KC. Aseptic thrombotic endocardial vegetations. JAMA 1973 ; 225 :1525-26

Aprindine

In

the Treatment of the

Idiopathic QT Interval Prolongation Syndrome* Larry E. Alves, M.D.;t Edward P. Rose, M.D. ;! and Hiltrud S. Mueller, M.D., F.C .C.P.§

°From the Departments of Medicine, Memorial Hospital, Belleville, Illinois, and St. Louis University School of Medicine, St. Louis, Missouri. tAssistant Clinical Professor of Medicine . §Professor of Medicine, St. Louis University School of Medicine. tCardiologist, Memorial Hospital. Reprint requests: Dr. Mueller, Division of Cardiology , 1325 South Grand Blvd, St. Louis 63104

APRINDINE IN IDIOPATHIC QT INTERVAL PROLONGATION SYNDROME 253