Signs Of Cardiac Tamponade Research Articles

Protocolo diagnóstico y diagnóstico diferencial del taponamiento cardiaco

Cardiac tamponade is a medical emergency caused by compression of the heart due to pericardial effusion. This fluid accumulation in the intrapericardial space raises the pressure surrounding the heart to the point where cardiac filling is altered. This syndrome is understood as a continuum and its manifestations range from a slight increase in intrapericardial pressure with minimal repercussion on cardiac function to severe hemodynamic compromise that may even be fatal. The severity of tamponade depends on speed of fluid accumulation. The clinical diagnosis is essential. Signs of cardiac tamponade are: low cardiac output and elevated jugular venous pressure, as well as reactive vasoconstriction and tachycardia. Often physical diagnosis should be completed with other diagnostic tests as electrocardiography, chest radiography and echocardiography. This imaging technique is an important tool for evaluating patients with cardiac tamponade. Echocardiography allows to confirm the presence, location, distribution and size of the pericardial effusion, as well as to assess its hemodynamic consequences and the need for pericardiocentesis. Cardiac magnetic resonance imaging (CMR) and computed tomography (CT) are other imaging modalities which may help accurate diagnosis.

Acute Pericarditis Secondary to Hydatid Cyst Rupture

A 37-year-old man, a construction worker, presented to the emergency department with chest pain. He was a smoker with no other relevant clinical history, with the exception of a liver hydatidosis treated successfully by surgery 20 years before. The pain was substernal, started at rest, had a relatively rapid onset, and worsened by lying down and with deep breathing. There was no history of recent respiratory tract infection or fever. On arrival, the vital parameters were normal. At physical examination, a friction rub was audible, and no signs of cardiac tamponade were present. The ECG showed diffuse ST-segment elevation with upward concavity (Figure 1). Chest radiography revealed a mild enlargement of the cardiac silhouette. Hemogram, creatine kinase, and troponins were normal; erythrocyte sedimentation rates were markedly increased (80 mm/h). The diagnosis of acute pericarditis was made, and treatment with nonsteroidal anti-inflammatory drugs was initiated. Figure 1. Twelve-lead ECG. Diffuse ST-segment elevation with upward concavity is seen. Two-dimensional echocardiography detected moderate pericardial effusion …

Cardiac tamponade following heart surgery

This article explores cardiac tamponade in postoperative cardiac patients and highlights the role and responsibilities bestowed upon the cardiac nurse in assessing, preventing, recognising and managing this situation. Cardiac tamponade is the compression of the heart that occurs when blood builds up in the space between the myocardium and the pericardium. In this condition, blood collects in the pericardium and mediastinum; this can prevent the ventricles from expanding fully. Excess pressure from the fluid prevents the heart from functioning normally. The signs of cardiac tamponade and cardiogenic shock are discussed, as are the urgent treatments they require. The cardiac nurse requires specialist skills and knowledge in managing surgical patients postoperatively. A thorough assessment, observation, early detection and quick intervention can mean the difference between life and death for patients who suffer cardiac tamponade following cardiac surgery. The standards of care suggested throughout this article are based on local practice in association with national and European guidelines.

Very late erosion of amplatzer septal occluder device presenting as pericardial pain and effusion 8 years after placement

We report the case of a very late erosion of an Amplatzer septal occluder (ASO) device more than 8 years after implant, presenting without signs of cardiac tamponade. To date, this case represents the longest period between ASO device implantation and clinical presentation following erosion. The overall rate of device erosion remains low, and the majority reported so far has occurred early, but clinicians should remain alert to the possibility of very late erosion in patients with ASO devices.

Endovascular Stenting of the Ascending Aorta for Type A Aortic Dissections in Patients at High Risk for Open Surgery

Open repair is the gold standard for type A aortic dissection (TAAD). Endovascular option has been proposed in very limited and selected TAAD patients. We report our experience with endovascular TAAD repair. Inclusion criteria were: (1) entry tear in the ascending aorta; (2) proximal landing zone of at least 2cm; (3) distance between entry tear and brachio-cephalic trunk of at least 0.5cm; (4) no signs of cardiac tamponade or severe aortic regurgitation and (5) no signs of aortic branches ischaemia. Patients with cardiac revascularisation from ascending aorta were excluded. From April 2009 to June 2012, 37 patients with TAAD were admitted to our hospital. As many as 28 underwent surgical repair and 9 were considered at high surgical risk in a multidisciplinary meeting. Four met our inclusion criteria for an endovascular approach. Two of them had previous ascending aortic repair for TAAD and one had aortic valve replacement. Technical success was achieved in 100% of the patients. No mortality was registered during a median follow-up of 15 months (range 4-39 months), no migration of the graft and complete false lumen thrombosis of the ascending aorta in three patients. Endovascular treatment of TAAD is challenging but feasible in a selected subset of patients. Further research remains mandatory.

Intracoronary thrombus in an infant with Kawasaki disease and giant coronary aneurysm

A previously healthy 5-month-old girl presented to ouremergency department with history of fever for 2 weeks,skin rash, red and cracked lips and bilateral redness of theeyes appeared 4 days after fever started. On physicalexamination, the general condition was stable includinggood peripheral perfusion. There was no lymphadenopathy.Chest and abdominal examinations were unremarkable.Electrocardiography, apart from mild sinus tachycardia(HR 110 bpm), was normal with no sign of myocardialischaemia or hypertrophy. Chest X-ray showed cardiomeg-aly. Her blood investigation results were as follows: WBC16.2 9 100/lL (neutrophils 36.7%), normal haemoglobinand platelets 1356 9 100/lL. The kidney function and liverfunction tests were normal. Troponin-T 27 lg/L (lab nor-mal value 14 lg/L) and CKMB 42 lg/L (lab normal value25 lg/L). The diagnosis of Kawasaki disease (KD) wasestablished according to the combination of the clinicalpicture and blood investigations. Echocardiogram wasperformed and showed severe dilatation of left anteriordescending coronary artery with giant fusiform aneurysm(Fig. 1) and intracoronary thrombus (Fig. 2). Additionally,normal myocardial function and moderate pericardialeffusion with no sign of cardiac tamponade. Despite thelate presentation, immunoglobulin infusion was startedcombined with heparin, warfarin and low-dose aspirin. Itwas planned after two days to discontinue heparin. Anelective cardiac computerized tomography (CT) with con-trast injection was performed and shows giant aneurysmaldilatation of right coronary artery (RCA; Fig. 3). A repeatedechocardiography, directed on the RCA, confirms the CTfinding (Fig. 4). The critical evaluation of the initial echo-cardiography examination revealed that the RCA aneurysmwas there from the start but was missed as it is very adjacentto and almost as large as right atrium.Kawasaki disease is also known as mucocutaneouslymph node syndrome. Its diagnosis is usually done throughcombination of certain clinical criteria. One of the mostserious complications of KD is dilatation and fatal aneu-rysms or rupture of coronary arteries in untreated patients.The initial echocardiographic study always evaluates theexistence of coronary artery aneurysms. In the presence of aproximal aneurysm, further coronary artery evaluation isusually performed through CT or magnetic resonancetomography combined with contrast injection and/or car-diac catheterization and angiography.Myocardial ischaemia due to thromboembolism is also awell-reported complication. The guidelines for treatment of

POSTOPERATIVE PERICARDIAL EFFUSION SYNDROME

Objective: Today, despite many recent improvements in intraoperative management and postoperative care, late pericardial effusions remain an important cause of morbidity after cardiac surgery. Because of widespread use of chronic anticoagulation and increased complexity of operations, the incidence of effusion may be higher. Thus we need to update the information on the symptoms, risk factors, diagnostic methods and treatment of Postoperative pericardial effusion syndrome. Patients and methods: A cross-sectional and prospective study of all patients admitted to hospital because of pericardial effusion after open heart surgery from 1/2010 to 9/2012. Study the clinical characteristics, paraclinicals, evaluate the results of treatment of pericardial effusion after open heart surgery. Results: Symptoms of pericardial effusion are nonspecific. Some patients with pericardial effusion report minimal problems. In the present study, few patients have the classic presentation of tamponade. Echocardiography is the diagnostic accuracy pericardial effusion after open heart surgery. This treatment mainly is pericardial drainage with 100%. Conclusion: Pericardial effusion is a common complication after open-heart surgery, symptoms of pericardial effusion are nonspecific to diagnostic method is echocardiographic surveillance.patients can be treated with internal medicine if has no tamponade and less fliuds. Pericardial drainage is absolute only in patients with pericardial effusion with signs of cardiac tamponade or pericardial many of effusion.

Delayed management of penetrating cardiac injury – Less urgency, more options

A 34 year old male sustained a stab injury to his left parasternal edge at the 4th intercostal space. Following a delay of 48 h, he presented to his local secondary hospital. At the time of admission he had a blood pressure of 73/38 mmHg – no other clinical signs of cardiac tamponade – and this normalised with intravenous fluids. Basic x-rays were performed and computed tomography (CT) of his chest was undertaken. This demonstrated a haemopericardium with left sided haemothorax (Fig. 1). Following, the patient was urgently transferred to our Level 1 Trauma Unit. On arrival, vitals were normal. Arterial blood gas results were pH 7.44, lactate 0.4 mmol/L and base excess 7.3 mmol/L. Electrocardiogram demonstrated T wave flattening at lead 3 and ST elevation at V3. Retrospective analysis of his chest X-rays from the secondary hospital revealed straightening of the left heart border, highly suspicious of haemopericardium. Transthoracic echocardiography was also performed and confirmed pericardial effusion. Troponin was elevated at 1.1 mg/L. The patient was taken to the operating theatre. A pericardial window was initially performed which demonstrated

Technology in medicine

“What are the cardinal signs of cardiac tamponade?” I often begin my student supervisions with a clinical question, and this day was no exception. “Just a second,” a student said. Without hesitation, he reached into his pocket, extracted his phone, and did a rapid search on the topic. “Raised jugular venous pressure, hypotension, and muffled heart …

Tuberculous pericarditis : experience in a community hospital

Tuberculosis is a major public health problem worldwide. In Butantan district of Sao Paulo city, the average incidence over the last 7 years was 47.7 new cases/100,000 inhabitants. Tuberculous pericarditis is a serious form of extrapulmonary tuberculosis in which diagnosis is often difficult. Diagnosis needs to be reached fast and accurately once tuberculous pericarditis has high morbimortality rates if untreated. We report the experience of a community hospital on tuberculous pericarditis with emphasis on the clinical presentation and diagnosticprocedures. From 2003 to 2010, 59 patients were diagnosed with pericarditis, 6 (10.16%) of which had tuberculous pericarditis. Demographic, clinical, imaging, laboratorial, microbiological and histological data were reviewed. There were 4 female (66.7%) and 2 male (33.3%) patients. Age ranged from 17 to 62 years(median= 25.5). One patient (17%) had HIV co-infection. Five patients (83.3%) had cardiac tamponade on Echocardiogram. Histopathology was confirmatory in 4 cases (66.7%) while cultures were positive in 2 cases (33.3%). Four patients (66.7%) had definite and 2 (33.3%) had probable diagnosis of tuberculous pericarditis. One patient (17%) died during admission. Reuter´s diagnostic index was ≥6 in 5 patients (83.3%). We concluded that the clinical picture, Reuter´s diagnostic index, signs of cardiac tamponade on Echocardiogram and the pericardium biopsy were the most important features for the diagnosis of tuberculous pericarditis.

Successful drainage of a traumatic haemopericardium with pericardiocentesis through an intercostal approach

A case of traumatic haemopericardium, sustained after blunt thoracic trauma, is described in a paediatric patient that was successfully drained by needle pericardiocentesis under 2D-echocardiographic guidance, via an intercostal approach, in the Children's Intensive Care Unit. The patient was haemodynamically unstable with obvious signs of cardiac tamponade. Drainage of the haemopericardium resulted in immediate improvement in haemodynamics. There was no re-accumulation of the haemopericardium. There were no complications as a result of the pericardiocentesis. No further surgical intervention was required.

Foreign Material Reaction to BioGlue® as a Possible Cause of Cardiac Tamponade

We describe the case of a 65-year-old female patient who underwent aortic valve reconstruction for aortic valve stenosis. During the operation, repair of a left ventricular laceration produced by a left ventricular vent was necessary. BioGlue® (CryoLife, Atlanta, GA, USA) and pledgeted sutures were used for repair. Pericardial effusion with signs of cardiac tamponade developed five months later. The patient was treated successfully by the removal of all foreign material and part of the BioGlue®. Microbiological findings were sterile. Histology showed a chronic granulomatous inflammatory response suggesting a foreign material reaction to BioGlue® as the cause of the effusion. Though all visible material was removed, the risk of pericardial effusion still persists as part of the BioGlue® remained within the ventricular wall.

Porridge-like tuberculous cardiac tamponade: treatment difficulties in the Horn of Africa

A 16-year-old boy was hospitalized for fever, chest pain, and cardiovascular collapse. Transthoracic echocardiography revealed a 30-mm circumferential echogenic "porridge-like" pericardial effusion with signs of cardiac tamponade. Tuberculosis (TB) was suspected because of its prevalence in Djibouti. Emergency pericardiocentesis was attempted, but only 10 ml of pericardial fluid was obtained. Subxiphoid pericardiotomy and drainage were then performed, and pericardial fibrinous pockets were surgically collapsed. Antituberculosis chemotherapy was given, and the pericardial effusion progressively disappeared without corticosteroids. The diagnosis of TB was subsequently confirmed by cultures of the pericardial fluid. A pericardial biopsy was normal. After 3 months of follow-up, there was no sign of constrictive pericarditis. Pericardiocentesis may fail in cases of advanced-stage fibrinous TB pericardial effusion. Thus, pericardiotomy with complete open draining is the only lifesaving procedure.

A case of right atrial tumor diagnosed by cardiac computed tomography

A 60-year-old woman was admitted with chief complaints of dyspnea for the previous 3 weeks. Transthoracic echocardiography (TTE) showed the amount of pericardial effusion and signs of cardiac tamponade. However, a tumor was not detected by TTE in any view. Multidetector computed tomography (MDCT) showed that the tumor protruded into the right atrium, invading to the outside of the heart. Transesophageal echocardiography (TEE) also showed the mobile tumor in the right atrium. In conclusion, this report may demonstrate that MDCT and TEE are required as complementary methods in the detection of cardiac tumors.

Three-dimensional imaging of intrapericardial adhesions within a large pericardial effusion

A 59-year-old man presented with fever and cough. An examination revealed jugular venous distention, pulsus paradoxus of 15 mmHg, bibasilar pulmonary rales and diminished heart sounds. A chest x-ray showed cardiomegaly and a right lower lobe infiltrate. Two-dimensional transthoracic echocardiography (Figure 1) demonstrated a large pericardial effusion (EFF) with signs of cardiac tamponade. Multiple intrapericardial strands (arrowheads) were seen within the pericardial fluid. Three-dimensional transthoracic echocardiography (Figure 2) provided additional information regarding the size, thickness and extent of the strands. Three-dimensional imaging revealed the strands to be an extensive network of intrapericardial adhesions (arrowheads) extending from the visceral pericardium to the thickened parietal pericardium (PER). Right heart catheterization was performed and demonstrated a right atrial pressure of 19/14 mmHg, right ventricular pressure of 36/16 mmHg and mean pulmonary capillary wedge pressure of 15 mmHg. Following echocardiographic-guided removal of 1700 mL of exudative fluid, right atrial pressure fell to 8/2 mmHg. Pericardial fluid stains and cultures were negative. The patient improved after the institution of antibiotics for pneumonia. Figure 1 Figure 2

Periportal edema and ascites: computed tomographic signs of traumatic cardiac tamponade

Multislice spiral computed tomography (MSCT) is becoming an increasingly common choice for evaluation of patients with suspected multiple trauma. Here, we present a trauma patient presenting with hypotension. Pericardial fluid and ascites in Morrison pouch were found via focused assessment with sonography for trauma. After pericardiocentesis, MSCT showed pericardiac fluid, periportal low attenuation, and peritoneal ascites. She received pericardiotomy and laparatomy. Numerous blood clots were evacuated from the pericardial space, but no intra-abdominal injury was found. The findings indicate the importance of computed tomographic (CT) signs of cardiac tamponade in avoiding negative laparatomy in patients with trauma (Fig. 1).

Cardiomegaly in a premature neonate after venous umbilical catheterization

Umbilical venous catheters allow rapid central access in neonates, but may be associated with various complications. We present a case of a newborn with pericardial effusion following umbilical venous catheterization. An extremely low birth weight infant was intubated for respiratory distress syndrome and had umbilical venous and arterial lines in place. Massive cardiomegaly was noted on the subsequent chest X-ray. Echocardiography revealed a large pericardial effusion without signs of tamponade. After removing the catheter, the effusion gradually resolved. While pericardial effusion is a well-known complication of percutaneous long central lines, only a few case reports have documented sudden cardiovascular compromise associated with umbilical venous catheters. Pericardial effusion may be asymptomatic and should be suspected in infants with central catheters and progressive cardiomegaly. The prompt removal of catheters and, if signs of cardiac tamponade are present, emergency pericardiocentesis may prove to be life-saving.

QT Prolongation: A Case of Arsenical Pericardial and Pleural Effusion

Arsenic trioxide is an effective treatment for patients with acute promyelocytic leukaemia (APL) who have relapsed from or are refractory to all trans-retinoic acid and anthracycline chemotherapy. Cardiac effects observed include electrocardiographic changes such as QTc prolongation, T-wave abnormalities, torsades de pointes and sudden death. We describe a case of a man, 76 years old, who was admitted to our department for dyspnoea in APL in treatment with arsenic trioxide. Chest radiograph illustrated an enlarged cardiac silhouette and bilateral pleuric effusion and the ECG evidenced QT prolongation. The patient was also submitted to transthoracic echocardiography that revealed moderate pericardial effusion without signs of cardiac tamponade and a normal biventricular function. This condition was considered to be associated with arsenic trioxide polyserosit and the drug therapy was immediately discontinued and steroid drugs started. After 2 weeks of arsenic trioxide therapy suspension there was evidence of complete resolution of pericardial and pleuric effusion and the ECG showed normal QT interval.

Right atrial free wall rupture after blunt chest trauma

We report the case of an 18-year-old man, victim of a car accident, presenting with severe hypotension and signs of cardiac tamponade. Transoesophageal echocardiography was suggestive of right atrial free wall rupture. The patient underwent urgent cardiac surgery for repair of right atrial rupture. The immediate clinical outcome was favourable; the patient is in good general condition at 24-month follow-up. The right atrium is rarely involved in cardiac contusion as compared to the right ventricle or other cardiac structures, owing to its anatomical location and direction of physical forces.

Elevated CA-125 level in acute heart failure due to Toxoplasma gondii perimyocarditis

A 67-year-old Caucasian woman was admitted because of severe dyspnea at rest, left-sided pleuritic chest pain, septic fever (up to 39 °C), generalized lymphadenopathy, and a pericardial effusion, without signs of cardiac tamponade. She had a 5-year history of ischemic heart disease, hypertension and hypercholesterolemia. Three months before the current admission, the patient was hospitalized in our department because of suspectedmyocarditiswith the ejection fraction (LVEF) 35%. However, inflammatory markers were normal: CRP 2.3 mg/L (normal: b3.0 mg/L), fibrinogen 3.2 g/L (normal: b3.5 g/L), leukocytes 5.3×10/L, erythrocyte sedimentation rate 14 mm/h. Serum troponin I (cTnI) was negative. Serologic studies for enteroviruses, influenza and parainfluenza viruses, cytomegalovirus and Epstein–Barr virus were all negative. TSHwas normal and an autoimmune screen was negative. Cardiac catheterization showed no significant (b50%) coronary artery lesions. Takotsubo cardiomyopathy was excluded. On the current admission, her body temperature was 37.2 °C, HR 80/min, respiratory rate 20/min, blood pressure 120/80 mm Hg, and oxygen saturation 96%. Electrocardiography revealed sinus rhythm, low voltage in limb leads, and previously present left bundle branch block. A chest X-ray showed bilateral pleural effusions and an enlarged cardiac silhouette (Fig. 1). Echocardiography disclosed severe