It is generally accepted that alcohol impairs haemodynamic physiology in normal subjects. Alcohol is also thought to have a detrimental effect in shock states. However, most research has concentrated on haemorrhagic shock, whereas in cardiac tamponade, the pathophysiology of shock is very different. Although some studies have mentioned alcohol as a negative factor in patients with cardiac tamponade, none have adequately assessed its effect. In a clinical study of 50 patients who presented to Groote Schuur Hospital Trauma Unit with acute cardiac tamponade due to penetrating chest injury, those who were intoxicated fared the same as their sober counterparts. Although more patients in the intoxicated group were "moribund" or "in extremis" on admission, this did not lead to a higher overall mortality. Haemodynamic parameters and results of special investigations in the two groups were also similar. These findings suggested that intoxicated patients with cardiogenic shock, specifically acute cardiac tamponade, behaved differently from intoxicated patients with haemorrhagic shock. However, the multitude of variables and the stress involved in treating patients with life-threatening acute conditions, makes studies such as this difficult. Because of these limitations, an animal model of acute cardiac tamponade was developed, so that actions of alcohol on haemodynamic physiology could be studied in a controlled environment. Fourteen young pigs were randomly assigned to receive either 30% alcohol or tap-water via a gastrostomy. The former resulted in blood alcohol levels which were compatible with moderate to severe intoxication. Cardiac tamponade was then induced by instilling warmed plasmalyte-8 into the pericardia! sac using a pressure-cycled system. Despite the fact that animals in the tamponade/alcohol group were more hypotensive, and reflex increase in heart rate was inhibited, cardiac output was similar in the two groups. The actions of alcohol in isolation were also studied in eight sham-operated pigs. The only noticeable effect in this instance were higher pulmonary artery wedge pressures in the sham/non-alcohol group. In other words, cardiac performance in both the tamponade/alcohol and sham/alcohol groups was at least equal to, or even better than that in animals that did not receive alcohol. It would seem therefore, that alcohol does not have a negative effect on haemodynamic physiology of acute cardiac tamponade. Theoretically, alcohol may "protect" patients with acute cardiac tamponade by decreasing peripheral vascular resistance and "afterload". It is also possible that inhibitory actions on the respiratory centre may prevent hyperpnoea or tachypnoea, and thereby diminish competitive filling of the right and left ventricles. However, further studies of cardiac function in intoxicated subjects with tamponade using more sophisticated techniques are necessary, before mechanisms will become apparent. In practice, an aggressive approach should be adopted towards moribund patients with penetrating chest injuries; if they have acute cardiac tamponade and are intoxicated, their prognosis is not necessarily dismal. This is of particular relevance in Cape Town, where both alcohol abuse and assault are endemic. As for a therapeutic effect of alcohol, these studies do not support its use for pharmacological manipulation of cardiac tamponade.

Pacemaker-lead-associated right ventricular perforation is a life-threatening complication. Acute perforation usually presents within 24 hours. Patients with lead perforation are often asymptomatic but fatal complications like hemopericardium, leading to cardiac tamponade and death, are reported. Diagnosis is based on chest x-ray, computed tomography (CT) scan, and echocardiography. The management of the lead perforation is based on clinical presentation. Extraction is avoided in cases of chronic asymptomatic lead perforations because of the associated complications. Urgent intervention is needed in hemodynamically unstable patients with pericardial effusion or cardiac tamponade physiology.

Submitted by Divisão de Documentação/BC Biblioteca Central (ddbc@ufam.edu.br) on 2018-04-11T12:40:06Z No. of bitstreams: 2 Dissertação_Antonio Araujo.pdf: 3932538 bytes, checksum: 332c2dd4e1e40b884f495ce9cf7a0233 (MD5) license_rdf: 0 bytes, checksum: d41d8cd98f00b204e9800998ecf8427e (MD5) / Approved for entry into archive by Divisão de Documentação/BC Biblioteca Central (ddbc@ufam.edu.br) on 2018-04-11T12:40:21Z (GMT) No. of bitstreams: 2 Dissertação_Antonio Araujo.pdf: 3932538 bytes, checksum: 332c2dd4e1e40b884f495ce9cf7a0233 (MD5) license_rdf: 0 bytes, checksum: d41d8cd98f00b204e9800998ecf8427e (MD5) / Made available in DSpace on 2018-04-11T12:40:21Z (GMT). No. of bitstreams: 2 Dissertação_Antonio Araujo.pdf: 3932538 bytes, checksum: 332c2dd4e1e40b884f495ce9cf7a0233 (MD5) license_rdf: 0 bytes, checksum: d41d8cd98f00b204e9800998ecf8427e (MD5) Previous issue date: 2017-11-08 / JUSTIFICATION: Few studies comment on how fatal heart injuries are implicated in the causes of death and its relation to death mechanisms, such as cardiac exsanguination and tamponade. OBJECTIVES: (1) To verify the frequency of fatal cardiac trauma in the city of Manaus, Amazon, Brazil, between November 2015 and October 2016; (2) to clarify the mechanisms of trauma and death in addition to cases which have or have not received prior hospital treatment, as well as the injuries associated with cardiac trauma. METHODS: This is a retrospective, observational, cross-sectional study which reviewed the necropsy reports of individuals whose causa mortis was cardiac trauma admitted to the city’s Medico-legal Institute (IML) between November 2015 and October 2016, whose death cause was cardiac trauma. RESULTS: During the study period, of the 2,330 necropsies performed at the IML, 138 deaths were caused by cardiac trauma, corresponding to index of 5.98%. Males accounted for 92% of these cases, whereas females corresponded to 8% of them. Median age was 27 years for men and 30 years for women. Regarding the mechanisms of injury used, gunshots accounted for 62.3% and stab wounds for 29.7%. With respect to injury morphology, 47.8 and 42% of the individuals presented perforating and transfixing lesions, respectively. Causa mortis was cardiac exsanguination in 81.9% of cases and cardiac tamponade in 29%. On-site death was described in 86.2% of the cases, and the median time between trauma and death was 50 minutes. The ventricles were the most common site of cardiac injury. Single lesions were observed in 43.5% of the cases, whereas multiple lesions were found in 20.3%. Hemothorax was identified in 90.6% of the individuals. Only 23 (16.7%) of the patients were taken to the Emergency Room (ER); Of these, six (26.2%) were not submitted to thoracotomy for the treatment of the lesions, being the diagnosis made post mortem in the IML. Of the 300 associated injuries, the lung was affected unilaterally in 57% of the cases and bilaterally in 43% of them. CONCLUSIONS: The fatal cardiac trauma represents an index of 5.98% in the city of Manaus. Most patients die on site, usually due to exsanguination, with puncture and transfixing lesions caused by firearms, and especially in cases of on-site death, with lung injury and associated hemothorax. About a quarter of patients who reach the emergency room are not diagnosed with cardiac trauma to justify a thoracotomy. / JUSTIFICATIVA: Poucos estudos comentam a maneira como os ferimentos cardíacos fatais estão implicados nas causas de óbitos e sua relação com os mecanismos de morte, tais como a exsanguinação e o tamponamento cardíaco. OBJETIVOS: (1) Verificar o índice de trauma cardíaco fatal na cidade de Manaus, no período de novembro de 2015 a outubro de 2016; (2) esclarecer os mecanismos de trauma e de morte, além dos casos que receberam ou não tratamento hospitalar prévio, assim como as lesões associadas ao trauma cardíaco. METODOLOGIA: Trata-se de um estudo retrospectivo, observacional, transversal, que revisou os laudos de necrópsias dos indivíduos admitidos no Instituo Médico Legal (IML) entre novembro de 2015 e outubro de 2016, cuja causa mortis tenha sido o trauma cardíaco. RESULTADOS: No período do estudo, foram analisados 138 óbitos por trauma cardíaco dentre 2.306 necrópsias realizadas no IML, correspondendo a um índice de 5,98%. O sexo masculino foi afetado em 92% dos casos, enquanto as mulheres, em 8%. A mediana de idade foi de 27 para os homens e de 30 anos para as mulheres. A arma de fogo foi o mecanismo de trauma em 62,3% e a arma branca em 29,7%. Quanto à morfologia das lesões, 47,8% e 42% dos indivíduos apresentavam lesões perfurantes e transfixantes, respectivamente. O mecanismo de morte foi a exsanguinação em 81,9% dos casos, enquanto o tamponamento em 29%. O óbito no local foi descrito em 86,2% dos casos e a mediana de tempo entre o trauma e o óbito foi de 50 minutos. O local anatômico de lesão cardíaca mais comum foram os ventrículos. Em 43,5% dos casos, as lesões eram únicas, ao passo que em 20,3% eram múltiplas. O hemotórax foi descrito em 90,6%. Apenas 23 (16,7%) dos doentes foram removidos até o pronto-socorro. Destes, seis (26,2%) não foram submetidos à toracotomia para o tratamento das lesões, sendo o diagnóstico realizado post mortem no IML. Das 300 lesões associadas, o pulmão foi acometido em 57% unilateralmente e 43% bilateralmente. CONCLUSÕES: O trauma cardíaco fatal representou um índice de 5,98% na cidade de Manaus. A maioria dos doentes morre na cena do trauma, geralmente devido à exsanguinação, com lesões perfurativas e transfixantes por arma de fogo, principalmente nos casos de óbito na cena do trauma, geralmente com lesão pulmonar e hemotórax associado. Cerca de um quarto dos pacientes que chega ao pronto-socorro e evolui ao óbito, não é diagnosticado com trauma cardíaco para justificar uma toracotomia.