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Vasoplegic syndrome after cardiac surgery: Better the devil you know!

A sound risk stratification almost always constitutes the primary step towards effective management of any postoperative complication. One such representative example is the domain of vasoplegic syndrome (VS) following cardiac surgery. Ever since the first description of VS by Gomes et al, VS in cardiac surgery was conceptualized as a clinical condition inexorably linked to exposure to an extracorporeal circuit. The subsequent studies demonstrating VS in patients undergoing off‐ pump coronary artery bypass surgery unveiled the multifactorial aetiology of the syndrome, resulting in an increased emphasis on outlining the risk factors of cardiac‐surgery associated VS. VS is a relatively common postoperative haemodynamic complication in cardiac surgical setting, with a reported incidence ranging from 9 to 40%. It is peculiarly characterized by a low systemic vascular resistance, normal to high cardiac index and meagre response to volume therapy. Such a scenario often mandates prolonged postoperative infusions of potent vasopressors to circumvent the deleterious effects of compromised end organ perfusion. In addition to an extended intensive care unit (ICU) stay, patients with VS demonstrate almost three times the operative mortality. However, the predisposition to the syndrome remains debatable till date. The literature with respect to the perioperative factors associated with VS has been largely limited to retrospective and prospective studies with inconclusive evidence regarding specific predictors. However, the recent meta‐analysis published this year, accumulated the available evidence in the form of a systematic evaluation of the risk factors in interrogation. The pioneer meta‐analysis meticulously outlined the risk of VS with the various perioperative factors under evaluation (Table 1). The range of factors associated with an elevated risk of VS, were consistent with the literature. It was noteworthy that the preoperative angiotensin‐ converting enzyme inhibitor therapy did not account for an increased risk of VS in the analysis, contrary to the conventional notion. In addition, preoperative β‐blocker therapy demonstrated a protective tendency for VS. The authors attributed the finding to a frequent administration of β‐blockers in hypertensive patients. A closer look at the meta‐analysis reveals certain important caveats. Despite a preliminary search yielding 109 studies, only 10 studies could be included as the others did not compare the patient characteristics with respect to the development of VS. Moreover, the peculiarity of a meta‐analysis, wherein the pooled sample size increases at the expense of an augmented diversity, was clearly apparent in the present analysis considering that the working definition of VS was heterogeneous amongst the studies. The cut‐offs of mean arterial pressure employed in various studies were less than 50, 60, 65, and 70mmHg and the cardiac index cut‐offs ranged from more than 2.2, 2.5, and 3.5 L/minute/m. Lastly, many untouched aspects like effect of preoperative European system for cardiac risk evaluation (Euro SCORE), New York heart association (NYHA) functional status, smoking, other drugs (diuretics, calcium channel blockers, amiodarone, etc), intraoperative core temperature and haematocrit on VS, limits the horizon. To conclude, VS continues to be a challenging postoperative complication following major cardiac surgery and implies a poorer prognosis. Using the commonly employed cut‐off of MAP less than 60 to 65mmHg and CI more than 2.2 to 2.5 L/minute/m to standardize the definition of VS and stratifying the syndrome according to the vasopressor dose requirements will allow for better characterization and more accurate predictors of the syndrome in future studies, aimed at combatting this persistent perioperative problem, as it is aptly said: “To be forewarned is to be forearmed, and half the victory.”