Cardiopulmonary bypass in pregnancy.

Cardiac surgery carried out on cardiopulmonary bypass (CPB) in a pregnant woman is associated with poor neonatal outcomes although maternal outcomes are similar to cardiac surgery in non‑pregnant women. Most adverse maternal and fetal outcomes from cardiac surgery during pregnancy are attributed to effects of CPB. The CPB is associated with utero‑placental hypoperfusion due to a number of factors, which may translate into low fetal cardiac output, hypoxia and even death. Better maternal and fetal outcomes may be achieved by early pre‑operative optimization of maternal cardiovascular status, use of perioperative fetal monitoring, optimization of CPB, delivery of a viable fetus before the operation and scheduling cardiac surgery on an elective basis during the second trimester.

Surgical retrieval of embolised atrial septal occluder device from pulmonary artery: pathophysiology and role of the intraoperative transoesophageal echocardiography.

Atrial septal defect is usually closed in the cardiac catheterisation laboratory using atrial septal occluder (ASO) device. One of the complications associated with the procedure is embolisation of the device into the pulmonary artery. We are reporting two cases wherein the pulmonary embolisation of ASO device occurred during the procedure in one patient and in the early post-procedure period in another; both were retrieved surgically. We are also describing the haemodynamic consequences of this complication and the role of intraoperative transoesophageal echocardiography during surgical retrieval of the device.

Inflammatory Response to Cardiac Surgery and Strategies to Overcome it.

A general activation of the immune system is observed during any operative procedure as a physiological response to the surgical trauma. Cardiopulmonary bypass may directly activate the inflammatory response by three distinct mechanisms: direct 'contact activation' of the immune system following exposure of blood to the foreign surfaces, ischaemia-reperfusion injury to vital organs and systemic endotoxaemia resulting from gut translocation of endotoxin. The inflammatory response depends upon recruitment and activation of inflammatory cells. The cellular immune response, in particular polymorphonuclear cell-endothelial adhesion, leads to widespread endothelial damage and dysfunction. Increased oxygen derived free radical activity represents a risk for myocardial and pulmonary complications. The clinical consequences of the stress response vary from a mild generalised transient response, termed the 'systemic inflammatory response syndrome,' to life threatening organ dysfunction. The introduction of the 'off-pump' coronary artery bypass graft surgery has now made it possible to differentiate the influence of cardiopulmonary bypass and surgical access on different modalities of the immune response. 'Off-pump' cardiac surgery has been found to trigger inflammatory response, lesser than 'on-pump' cardiac surgery. Researches are directed towards understanding this complex interplay of humoral and cellular mediators and develop strategies to limit the resultant organ dysfunction. Current literature on the various mediators of this inflammatory response, the role of surgical stress, the pathogenesis of the organ damage and strategies to limit / overcome this response are reviewed.

A comparative study of release of interleukin-6 and tumour necrosis factor during normothermic and hypothermic cardiopulmonary bypass.

The institution of cardiopulmonary bypass generates many pro-inflammatory cytokines and several clinical variables, including temperature, have been shown to influence cytokine release during and after cardiopulmonary bypass. The release of tumour necrosis factor and interleukin-6 are the best predictors of post-cardiopulmonary bypass related morbidity. Their release during normothermic and hypothermic cardiopulmonary bypass and the correlation with clinical parameters of organ injury was studied. This prospective study was carried out in 52 adult patients, scheduled for cardiac surgery, exposed to normothermic and 27 to hypothermic cardiopulmonary bypass. Samples for estimation of tumour necrosis factor and interleukin-6 were collected preoperatively, 1 hour and 24 hours post cardiopulmonary bypass and analysed by ELISA. Haemodynamic parameters and respiratory parameters were noted and lung injury scores calculated. Interleukin-6 levels were raised in both the groups at 1 hour and 24 hours post cardiopulmonary bypass and the response was higher in the normothermic group. Tumour necrosis factor response was, however, similar in both the groups, with a rise at 1 hour returning back to baseline by 24 hours post cardiopulmonary bypass. The normothermic group had a better respiratory index in the postoperative period, early extubation was possible, had better clinical haemodynamics, a shorter cardiopulmonary bypass time and had reduced requirement of defibrillation after the release of aortic cross clamp. We conclude that the release of interleukin-6 was thermo-dependant but did not correlate with the clinical signs of organ injury. Tumour necrosis factor levels were significantly raised after the cardiopulmonary bypass but the rise was not thermo-dependant.