Anesthesia induction-related hypotension is not uncommon and is still challenging for anesthesiologists to predict, despite advanced monitoring techniques. In current anesthesia practices, approximately 20-30% of patients develop hypotension during and after anesthesia induction. In large observational studies, the relationship between intraoperative hypotension and adverse cardiac, renal, and cerebral outcomes has been reported. Approximately one-third of intraoperative hypotension episodes occur during and after the induction of anesthesia, and most can be prevented if foreseeable. Therefore, we need quick and easy markers to predict patients at risk of hypotension to achieve the stable induction of anesthesia.~Many studies have used noninvasive and invasive monitoring techniques for the preoperative prediction of hypotension after anesthesia induction.~However, most studies evaluate the cardiovascular system with parameters that determine the preload and fluid responsiveness to predict the risk of post-induction hypotension, though the arterial system and its interaction with the ventricle are ignored.The heart and the arterial system are both anatomically and functionally interconnected and do not act independently. The major determinant of cardiovascular system performance and cardiac energetics is ventriculoarterial coupling (VAC). Ea is an indicator of cardiac afterload and arterial tone and can be calculated by the ratio of the end-systolic pressure (ESP) and stroke volume (SV) obtained from arterial wave analysis.Ea provides information about the ESP/SV relationship and dynamic afterload and gives the clinician the opportunity to evaluate VAC indirectly. We hypothesized that Ea values before anesthesia induction could predict post-induction hypotension. To test our hypothesis, we aimed to investigate the reliability of the Ea value, which was monitored preoperatively using the pressure analytical recording method (PRAM) to predict the risk of hypotension that may occur after anesthesia induction.
Hypotension is very common during and after anesthesia induction. A prolonged fasting period, a patient's underlying comorbidities, a sympathetic blockade by anesthetic agents, vasodilation, a reduction in preload, and cardiac contractility can cause post-induction hypotension.1,2 The relationship of even short-term hypotension with myocardial damage, renal injury, and stroke has been shown in many studies; therefore, it is very important to provide stable anesthesia induction.3 In current anesthesia practice, we can only intervene when hypotension occurs. If we can identify patients who may experience hypotension during anesthesia induction before it occurs, we can prevent possible postoperative organ dysfunctions by reducing the duration and depth of hypotension with prophylactic fluid and vasopressor administration. We hypothesized that arterial elastance (Ea) values before anesthesia induction could predict post-induction hypotension. To test our hypothesis, we aimed to investigate the reliability of the Ea value, which was monitored preoperatively using the pressure analytical recording method (PRAM) to predict the risk of hypotension that may occur after anesthesia induction.