Post-induction Hypotension: Tension(s) Beyond the Induction Agent!

Sir, Kiran et al.,1 recently publish an interesting study, having compared the hemodynamic profile of etomidate with that of propofol-phenylephrine combination, for inducing general anesthesia in an adult cardiac surgical patient population. Aligned with the valuable proposition of compensating for the propofol-associated systematic vascular resistance (SVR) reduction with phenylephrine, the authors outline a comparable incidence of post-induction hypotension with etomidate and propofol-phenylephrine combination.1 That being said, in addition to the lack of substantiation of research findings with the corresponding SVR values, there exist other pertinent aspects mandating elucidation.1-5 To begin with, the sample size in the index investigation, happens to be based on the data emanating from a pathophysiological study by Abou Arab et al.2 Of note however, the patients in this study demonstrated preserved the left ventricle (LV) ejection fraction, in contrast to the Kiran et al.1 study involving a wider spectrum of LV dysfunction. As an extension of the same, it is believed that concurrent LV diastolic dysfunction ought to have been accounted for. In addition, the authors should have clarified whether all their study participants manifested a normal sinus rhythm.1 Meanwhile Abou Arab et al.2 executed caution to formally exclude patients with pre-existing atrial fibrillation (AF), the detrimental hemodynamic consequences of de novo AF at anesthetic induction, can also not be undermined.3 Emphasizing upon the predilection to post-hypotension in American Society of Anesthesiologists Physical Status (ASAPS) class III-IV patients (as was the case in the Kiran et al.1 study), a systematic review by Chen et al.4 concurrently highlights the role of reduced baseline blood volume. Out of a total of 12 included studies, a couple of studies in the systematic review focusing this aspect, attributed the contextual odds ratio; 95% confidence interval of 1.16; 1.00–1.34 and 1.17; 1.09–1.26, to stroke volume variation and inferior vena cava ultrasonography, respectively.4 In this regard, the account of preoperative diuretics can indeed be difficult to overlook wherein the ASA-PS III-IV cardiac patients, are much at the same time, often on preoperative angiotensin converting enzyme inhibitor or angiotensin receptor blockers.1,4 Moreover, the heterogeneous subset within a small sample size of 90 patients, ranging from coronary artery disease to stenotic and regurgitant valvular heart disease patients, necessitates a closer look. Given every fifth patient happened to be suffering from severe stenosis of the mitral valve, the right heart can have its’ own distinct part to play.1 With a consensus article by Arora et al.5 labeling induction of general anesthesia as the most hemodynamically crucial phase for a vulnerable right ventricle (RV), the narration of the degree of RV dysfunction alongside pulmonary hypertension could have offered further useful insights.1 Finally, it is humbly suggested that such research endeavors would be served well with an objective uniform endpoint of anesthetic induction, potentially the Bispectral index monitoring. Herein, administering titrated doses of the induction agents till the loss of response to verbal command, likely, renders the matter subjective, particularly when the complex trinity of dose, depth (anesthetic), and deleterious effects like hypotension, are being evaluated in close conjunction to one another.1 Financial support and sponsorship Nil. Conflicts of interest There are no conflicts of interest.