Unilateral pulmonary edema complicating acute myocardial infarction

Unilateral pulmonary edema complicating acute myocardial infarction

182 BRIEF REPORTS Unilateral PulmonaryEdema ComplicatingAcute MyocardialInfarction ANDRE KEREN, MD DAN TZIVONI, MD SHMUEL GOllLlEB, MD JESAIA BENHOR...

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Unilateral PulmonaryEdema ComplicatingAcute MyocardialInfarction ANDRE KEREN, MD DAN TZIVONI, MD SHMUEL GOllLlEB, MD JESAIA BENHORIN, MD SHLDMO STERN, MD


nilateral pulmonary edemais a rare clinical condition that is usually associatedwith rapid reexpansion of the lung after drainageof pneumo- or hydrothorax.1 Pulmonary edema may be unilateral also during leftsided heart failure, when it occurs in patients with congenital or acquired l-sided pulmonary perfusion defect. Rarely, left-sided heart failure may manifest as unilateral pulmonary edema in the absenceof previous lung injury. 2.3In previous reports,the cardiac origin of the unilateral pulmonary opacity was retrospectively supportedby clearing of the lung after diuretic therapy2or autopsyfinding of unilateral lung congestion.3We describea patient with unilateral pulmonary edema and absenceof associatedlung pathology in whom hemodynamic monitoring, instituted shortly after hospitalization, proved the cardiac origin of the pulmonary processand served as a useful guideline for proper therapy. From the Heiden Department of Cardiology, Bikur Cholim Hospital, P.O.B. 492, and Hebrew University-Hadassah Medical School, Jerusalem 91002, Israel. Manuscript received April 12, 1985; revised manuscript received June 4,198s. accepted June 7, 1985.

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performed on the day ot admlsslon lung and clear left lung fields.

A 95-year-oldwoman without a remarkablehistory was hospitalized with the diagnosisof acute anterior wall myocardial infarction and cardiogenic shock. Examination revealed a fully consciouspatient with regular pulseof 130 beats/min, bloodpressureof 90/75 mm Hg, 40 breaths/min and signsof central cyanosis (Pa02 at room air 52 mm Hg). There was jugular venousengorgement,hepatomegalyand slight peripheral edema.On auscultation,signsof mitral regurgitation and crackles over the right chest were found. Chest radiogram revealed cardiomegaly, calcified mitral valve anulus and unilaieral, right-sided pulmonary opacities (Fig. 1). The initial diagnosisof the pulmonary findings included bronchopneumoniaand pulmonary embolism. However, there were no clinical signsof infection, the gram stainsof the sputumwere negative,and a lung perfusion scanwas not consistent with a diagnosisof pulmonary embolus.Hemodynamic measurementsperformed shortly after admission showed:mean right atria1pressure,14mm Hg; pulmonary artery pressure,50/35 mm Hg (mean 42); mean pulmonary capillary wedge pressure,34 mm Hg; cardiac index, 1.6 Iiters/min/m2; and systemic and pulmonary vascuIar resistances,2,200 and 266 dynes s cmo5,respectively. The measurementsindicated the presence of biventricular failure, pulmonary hyperfension and low cardiac output. After institution of mechanical ventilation, infusion of dopamine and Iater nitroprussideand diuretic drugs,her clinical condition gradually improved. During the next 2 daysbacteriologic examination of the sputum yielded negative results and the chest radiogram showed a clear left lung field and progressivelesseningof right lung congestion; the unilateral appearanceof lung opacities remained unaltered by frequent changesin the position of the patient in the bed.She wasextuhated3 days after admission.At that time the chestroentgenogram showed clear lung fields and hemodynamic measurements showednorma pressuresexceptfor the pulmonary capillary wedgepressureof 16mm Hg. The cardiac index increasedto 2.3 Iiters/min/m2 and Pa02at room air was 90 mm Hg. CIinicaI improvement ensuedand mobilization was started.Six dayslater chest pain recurred, ventricular fibrillation developedand the patient died. The characteristicradiographicappearanceof pulmonary edemais a symmetric “butterfly-shaped” density involving both lungs. If a pulmonary infiltrate is unilateral, the diagnosisof an inflammatory, thromboembolic atelectatic or neoplastic processrather than pulmonary congestionis usually made, even in patients in whom acuteleft heart failure is prone to develop.2 However, the rare occurrence of left-sided heart failure, manifesting itself as unilateral pulmonary edema,was alreadyrecognizedin early radiologic published reports4+5; we are aware of 12 clinical or pathologic reports of this condition.2-6In 11 of the 12 previously published cases,the unilateral edema involved the right lung, as it did in our patient. In patients prone to having acute left-sided heart failure who show persistent right lung opacities,the


differential diagnosis of the pulmonary findings should include unilateral pulmonary edema. The information provided by hemodynamic monitoring will supplement the clinical and laboratory data and will help to reach a correct diagnosis.

1, 1966


2. Richman

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Usefulnessof Atrioventricular Nodal WenckebachPeriodicityin Predicting Sinus NodalEntranceBlock DuringAtrial Pacing PAUL WANG, MD JAMES A. REIFFEL, MD JOHN ZIMMERMAN, MD FRANK LIVELLI, Jr,, MD JERRY GLIKLICH, MD KEVIN FERRICK, MD J. THOMAS BIGGER, Jr., MD PATRICIA NOETHUNG, RN


inus nodal (SN) dysfunction and atrioventricular (AV) nodal dysfunction frequently coexist.1-4 Both nodes are depressed by vagal stimuli, have similar cellular electrophysiology, and are often coinvolved by disease. Moreover, prolongation of SN conduction time and AV nodal conduction (AH interval) often occur together.*J AV nodal conduction can be assessed rapidly during clinical electrophysiologic testing. The resting AH interval is easily measured on His bundle electrograms, and the AV nodal response to pacing as determined by the longest paced cycle length (PCL) causing AV nodal Wenckebach periodicity during incremental atria1 overdrive pacing (normal 500 ms or less] is also easily and quickly determined. However, assessment of SN conduction time is more tedious. Although resting SN conduction time can be quickly determined when SN electrograms are directly recorded, it usually is determined indirectly from atria1 premature stimulation. Moreover, because SN conduction during pacing is usually invisible on intracardiac recordings, assessing the SN conduction response to pacing must always be indirect. This is done by determining the PCL at which the SN recovery times after overdrive From the Arrhythmia Control Unit, Division of Cardiology, Department of Medicine, Columbia University, New York, New York. This study was supported in part by U.S. Public Health Service Grants HLl.2738 and RR00645, National Institutes of Health, Bethesda, Maryland. Manuscript received May 6, 1985; revised manuscript received June 24, 1985, accepted June 25, 1985.






N Engl

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4. Nessa CB, Rigler edema.


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6. Wirtzfeld A. Unliloteral



3. Bahl OP, Oliver GC, Rockoff SD, Parker EM. Localized unilateral pulmonary edema: an unusual presentation of left heart failure. Chest 1971;


GD, Woodruff

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A, Lutilsky

fiche Manifestation 1973;62:961-965.

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pacing are consistently the longest-termed peak paced cycle length.5 PCLs shorter than peak PCL are associated with SN entrance block. Because peak PCL is a calculated number that cannot be determined until the results of multiple 230~second pacing runs (interspersed with 130 seconds of rest] are known, it is timeconsuming. In normal subjects, peak PCL is always 600 ms or less, but in patients with SN dysfunction it can be at any PCL from sinus cycle length to 400 ms (the shortest PCL usually tested). Because each PCL must be tested in patients being evaluated for SN dysfunction, it usually takes 15 to 30 minutes to acquire the data needed to correctly determine peak PCL in such patients and another 5 to 10 minutes to make the measurements. However, it can take less than 3 minutes to effectively determine the longest PCL producing AV nodal Wenckebach (PCL/AV) periodicity, both in normal subjects and in patients with AV nodal dysfunction,6 using lo- to l&second periods of incremental pacing over the same range of PCLs used for peak PCL. If a prolonged peak PCL and a prolonged PCL/AV Wenckebach periodicity were related, as prolonged resting SN conduction time and AH intervals often are, testing time could be shortened and patient tolerance of electrophysiologic testing could be improved. If a peak PCL-PCL/AV Wenckebach relation exists, knowing the PCL/AV Wenckebach [email protected] (quickly obtained) may allow peak PCL to be rapidly estimated. The estimated peak PCL could then allow the actual peak PCL to be quickly determined, because only 3 paced cycle lengths may have to be tested. Because the maximal sinus recovery time obtained in patients is almost always obtained at the peak PCL or at an adjacent PCL, an estimate of peak PCL would also shorten the time required to determine the maximal sinus recovery time. To assess if a relation does exist between peak PCL and PCL/AV Wenckebach periodicity in patients with SN or AV nodal disease-a relation without which peak PCL could not be quickly estimated-we assessed the records of 309 patients studied electrophysiologically for SN and AV nodal function. Each patient underwent atria1 pacing in the fasting, nonsedated, unmedicated state for 30 seconds at PCLs from sinus cycle length to 400 ms, 3 to 4 times each, with PCL decrements of 100 ms. Two hundred seventeen patients had normal peak PCL (600 to 400 ms) and normal PCL/AV Wenckebach [email protected] (500 or 400 ms) [Ta-