pericardial decompression syndrome ( pds ) is an unexpected clinical scenario with an incidence less than 5% in all surgically or percutaneously managed pericardial tamponade patients , . pericardial decompression syndrome is defined as paradoxical hemodynamic instability , left ventricular ( lv ) or bi ventricular systolic dysfunction and pulmonary edema after pericardial fluid drainage , , . the aim of this manuscript was to describe a case with cardiac tamponade in whom acute biventricular heart failure and pulmonary edema developed after surgical creation of a pericardial window , and to discuss this case in light of the literature . raising awareness of pds may help its diagnosis and management of this potentially devastating but reversible complication after cardiac surgery . a 43-year - old woman , had an operation for mitral valve disease 3 weeks ago , after discharged from the hospital , was admitted to our cardiovascular surgery department with a 3  days history of worsening dyspnea , tachycardia , and palpitation . physical examination revealed heart rate was 110 beats per minute ( chronic atrial fibrillation ) , blood pressure was 110/76  mmhg , and respiratory rate was 25 breaths per minute , and jugular venous distension was noted . she was further investigated with a transthoracic echocardiogram , which confirmed the presence of large quantity of pericardial fluid ( 35  mm in the posterior wall , 25  mm in the anterior wall ) with partial compression of the right ventricle ( fig . 1 ) and good systolic function of the left ventricle ( ejection fraction was 60% ) . the prothrombin time was prolonged due to warfarin usage and fresh frozen plasma and vitamin k intravenously was applied slowly . after acceptable levels of inr achieved , an emergent rapid drainage of the pleural and pericardial cavity with left anterior mini thoracotomy was carried out . after creation of pericardio - pleural window , by excising a large piece of pericardium anterior to the phrenic nerve , more than 1000  ml of serosanguineous fluid were quickly removed from the pericardial space during the procedure , and both right atrium and pulmonary capillary wedge pressures ( pcwp ) transiently dropped to near - normal values . the chest was closed as per routine , two chest tubes was placed , one in the pericardial cavity and the other in the left pleural cavity . after the decompression of the heart patient was transferred to intensive care unit and monitored , during the following hours of the decompression , the patient s condition deteriorated . overt pulmonary edema developed within hours , bilateral rales were audible on physical examination , and pcwp increased to 28  mm  hg . a chest x - ray performed at that time showed bilateral pulmonary edema ( fig . 2 ) . intravenous dobutamine , nitroglycerin , norepinephrine and furosemide therapy was initiated for hemodynamic support and pulmonary edema . on the second day of intensive care unit ( icu ) , a transthoracic echocardiogram repeated , very little pericardial effusion without hemodynamic compromise , but systolic dysfunction of both ventricles , global diffuse hypokinesia , 1520% lvef was found . high - dose inotropic support with dobutamine and diuretics was continued , continuous positive airway pressure ( cpap ) therapy was used for her respiratory distress at times . during follow up she was progressively weaned off inotropes , ejection fraction raised to 35% on control tte . two weeks later , she was discharged from the hospital on the therapy of beta blockers , digoxin , warfarin , and furosemide . at discharge , repeated tte showed normal lv and rv function , lv ejection fraction was 50% , and normally functioning prosthetic mitral valve . acute cardiac failure is a very unusual complication after removal of pericardial effusion for cardiac tamponade . we describe a case with a normal lv systolic function at baseline who developed transient biventricular heart failure immediately after the pericardial window drainage . this syndrome was first described by vandyke et al . in 1983 and angouras et al . proposed the use of the term  pericardial decompression syndrome  ,   to gain wider recognition of this potentially fatal complication . the incidence of this rare complication was reported to be 4.8% ( 5 of 104 patients with pericardial effusion who underwent surgical subxiphoid pericardiostomy ) by angouras et al . , . pathologies which affects myocardial performance such as malignant myocardial infiltration or chemotherapy induced cardiomyopathy may be considered causative factors , . yet , in the majority of cases there is no obvious cause for the development of paradoxical ventricular dysfunction after decompression , as observed in our case . various hypotheses have been raised to explain the pathophysiology of this phenomenon , but a single pathway has not yet been elucidated . possible mechanisms implicated in the post - pericardial decompression syndrome are : a rapid drainage of a large pericardial effusion , could lead to a disproportionate increase in right ventricular ( rv ) end - diastolic volume compared with left ventricular ( lv ) end - diastolic volume . this interventricular volume mismatch in the presence of vasoconstriction due to high catecholamine levels could lead to an increase in lv end - diastolic pressure and transient lv dysfunction for the previously diseased heart , . an acute increase in  wall stress  due to the acute distension of the cardiac chambers secondary to increased venous return at high filling pressures , combined with a negative pressure in the pericardial cavity immediately after large volume pericardiocentesis may be another mechanism , . in our patient , both ventricles were hypokinetic and cvp returned to a high following the transient decrease during evacuation of effusion ; this supports that these mechanisms might be responsible for the cardiac failure however we can not rule out other proposed mechanisms that might have lead to cardiac failure . myocardial stunning due to mismatch of oxygen supply for the acutely increased wall stress in myocardium might have resulted . tamponade resulted in a disproportionately greater decrease of the coronary blood flow , but any occult dysfunction may be masked by the reduction in chamber sizes and associated tachycardia , , . the autonomic nerve system is also likely to have influenced the cardiac function before and after pericardiocentesis . wolfe and edelman   argued in a case report that the removal of the stimulus for sympathetic outflow ( the drainage of pericardial effusion ) might well lead to the unmasking of left ventricular dysfunction , which was obscured due to the high catecholamine levels producing transient tachycardia and inotropic effect . many literature articles support , post pericardial drainage low cardiac output syndrome can complicate any method of surgical pericardial drainage even in patients with apparently normal myocardium and preoperative hemodynamic status , . therefore , these patients require close postoperative monitoring for the first 24  h , preferably in the icu , and aggressive heart failure treatments should be managed if low cardiac output develops . in conclusion , despite the multiple etiologies of pericardial effusions and preexisting heart conditions in the previously reported cases , it is likely that the mechanism underlying such hemodynamic derangement is rapid evacuation of a large volume of pericardial effusion . we recommend gradual removal of pericardial effusion under hemodynamic monitoring , especially in patient with postcardiotomy tamponade . ethics committee approval was received for this study from the the institutional ethics committee of siyami ersek hospital . this research did not receive any specific grant from funding agencies in the public , commercial , or not - for - profit sectors .
highlightspericardial decompression syndrome is an unexpected clinical scenario with an incidence less than 5% in all surgically or percutaneously managed pericardial tamponade patients.yet , in the majority of cases there is no obvious cause for the development of paradoxical ventricular dysfunction after decompression.close postoperative monitoring for the first 24  h , preferably in the icu , and aggressive heart failure treatments should be managed even if low cardiac output develops.we recommend gradual removal of pericardial effusion under hemodynamic monitoring , especially in patient with postcardiotomy tamponade .