The most frequently encountered adverse event during spinal anesthesia is a drop in blood pressure. This effect is notably more pronounced in individuals who have a background of chronic hypertension [1]. While antihypertensive therapies aim to stabilize blood pressure, their diverse cardiovascular actions can lead to varying hemodynamic consequences, particularly in the early stages following administration of spinal anesthesia [2]. A comprehensive understanding of these pharmacologic agents allows anesthesiologists to better predict and manage perioperative hemodynamic fluctuations.

Both spinal and general anesthetic agents typically diminish sympathetic nervous system activity, which plays a key role in cardiovascular stability. Consequently, under anesthesia, the body increasingly relies on the renin–angiotensin system (RAS) to sustain blood pressure levels. Pharmacologic agents such as angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs), which inhibit RAS function, impair this compensatory mechanism. As a result, patients on these medications are more likely to experience intraoperative hypotension and may require the administration of inotropes to restore hemodynamic balance [3].

Extensive research has explored the impact of various antihypertensive medications in both general and spinal anesthetic contexts. Particular attention has been given to the perioperative continuation of beta-blockers and calcium channel blockers, with data supporting their use on the day of surgery for both types of anesthesia [4-6]. However, the question of whether ACE inhibitors should be continued during the perioperative period in patients receiving spinal anesthesia remains unresolved, as existing studies present conflicting outcomes [7-9]. Whether to maintain therapy with RAS inhibitors, such as ACE inhibitors and ARBs, during surgery continues to be a subject of clinical debate. This investigation seeks to evaluate the influence of ARBs on intraoperative blood pressure and heart rate in patients undergoing surgery with spinal anesthesia who have continued these medications on the day of the procedure.

A total of 100 patients scheduled for surgical procedures under spinal anesthesia were enrolled. Participants were divided into two cohorts: Group N, comprising 50 normotensive individuals, and Group H, including 50 hypertensive patients maintained on monotherapy with ARBs.

Inclusion Criteria: Participants with a confirmed diagnosis of essential hypertension who had been receiving ARB therapy for a minimum duration of one month were considered eligible. Only those scheduled for elective operations under spinal anesthesia were included.

Exclusion Criteria: Subjects with concurrent medical conditions such as diabetes mellitus, ischemic heart disease, other cardiovascular disorders, marked volume depletion, pregnancy, or systemic infection were excluded.

Procedure details: At the preoperative assessment clinic, following written informed consent, comprehensive medical histories were collected, detailing the use of antihypertensive agents, treatment duration, existing comorbidities, and concurrent pharmacotherapy.

Upon arrival in the operating room, patients received a preloading dose of Ringer’s lactate solution at a volume of 10 mL/kg. Standard monitoring protocols were employed, encompassing continuous electrocardiography, pulse oximetry, pulse rate monitoring, and automated non-invasive blood pressure (NIBP) measurement. Baseline values were documented after fluid administration during the rest phase.

Spinal anesthesia was administered using strict aseptic techniques at the L3–L4 interspace. Upon confirming free cerebrospinal fluid flow, 3 mL of 0.5% hyperbaric bupivacaine was injected over a 10-second interval. Patients were then positioned supine, and NIBP and heart rate were monitored every 2 minutes for the initial 10 minutes and subsequently at 5-minute intervals until completion of surgery—specifically at 2, 4, 6, 8-, 10-, 15-, and 20-minutes post-anesthesia.

Hypotension was defined as a drop in mean arterial pressure (MAP) exceeding 30% from the baseline within a 20-minute observation window. An event was considered clinically relevant if it necessitated intervention with intravenous fluids or vasopressor agents within the same timeframe [1]. When hypotension occurred, it was managed with 6 mg of intravenous mephentermine per dose, along with 5 mL/kg of intravenous fluids until both MAP and systolic blood pressure surpassed the critical thresholds. The timing and total dosage of rescue medications were recorded.

Bradycardia, characterized by a heart rate below 50 beats per minute that was unresponsive to fluid therapy, was treated with an intravenous bolus of 0.6 mg atropine. Ringer’s lactate infusion was maintained throughout the surgical procedure, and the total intraoperative fluid volume was documented. The administration of all therapeutic agents was at the discretion of the attending anesthesiologist.

Statistical Methods: Descriptive statistics were used to analyze baseline characteristics. One-way ANOVA was applied to assess intra-group variability of systolic blood pressure (SBP), diastolic blood pressure (DBP), MAP, and heart rate across time points. Post hoc analysis was conducted to identify time intervals demonstrating the most significant deviations from baseline values. For intergroup comparisons at each time point, unpaired t-tests were employed. A p-value of ≤0.05 was deemed statistically significant, and values >0.05 were interpreted as not significant.

In the present study, baseline characteristics of the participants in both normotensive (Group N) and hypertensive (Group H) cohorts are detailed in Table 1. The groups were comparable in terms of gender distribution, while Group H participants were notably older and had higher body weights. As expected, baseline systolic blood pressure (SBP), diastolic blood pressure (DBP), and mean arterial pressure (MAP) were significantly elevated in the hypertensive group. Additionally, baseline heart rate (HR) was marginally higher in Group H compared to Group N.

Table 1: Baseline profile of study participants

The incidence of hemodynamic alterations following spinal anesthesia is summarized in Table 2. A greater proportion of patients in the hypertensive group experienced a ≥30% decline in both SBP and MAP post-anesthesia, and these differences were statistically significant. While the decline in DBP was also more common in Group H, the intergroup difference did not reach statistical significance. The need for vasopressor support was higher in the hypertensive cohort, though this difference approached but did not achieve statistical significance. Fluid administration volumes were similar across groups, and the occurrences of bradycardia and the subsequent requirement for atropine were identical in both groups.

Table 2: Occurrence of hypotension, bradycardia, IV fluid usage, rescue medication use

A marked decrease in SBP was more prominent in Group H, with 22 patients experiencing a reduction of ≥30% from baseline, compared to 10 in Group N—a difference with significant statistical relevance. This was interpreted by the attending anesthesiologist as clinically significant, prompting the use of mephentermine as a vasopressor. Although 30% DBP reductions were recorded in 7 and 12 participants in Groups N and H respectively, these were not used as criteria for intervention.

The necessity for vasopressor therapy was seen in 10participants from Group N and 20 from Group H. However, of the 22 Group H patients showing a notable SBP drop, only 19 received rescue medication, as the other threeretained SBP values above 100 mmHg despite the percentage decrease. This variability in vasopressor administration, based on absolute SBP thresholds rather than relative changes, resulted in the between-group difference being statistically non-significant. This may imply that, although hypotension was more frequent in hypertensive individuals on ARBs who continued medication on the day of spinal anesthesia, the overall requirement for hemodynamic correction was not markedly greater compared to normotensive counterparts.

During the initial 20 minutes post-anesthesia, no significant change in DBP was observed between the groups. Baseline DBP values were approximately 7 mmHg lower in Group N, and this disparity remained evident across all time intervals, with Group H consistently showing higher DBP readings. Notably, statistical significance was reached at the 2-, 6-, 8-, and 10-minute marks, although these findings lacked clinical importance and did not necessitate intervention.

Following spinal anesthesia, HR declined up to the 10-minute mark in Group N and to the 6-minute mark in Group H, after which it began to rise gradually in both groups but remained below baseline levels. The earlier and more pronounced HR elevation in Group B might be attributed to the inverse relationship between BP and HR [10], whereby the greater hypotensive response triggered a compensatory increase in HR.

While spinal anesthesia-induced hypotension is a well-recognized physiological consequence, it is frequently mischaracterized as a complication. A distinction must be made between predictable physiological effects and adverse events that pose potential harm. Rooke et al. [11] observed that blood pressure reductions were more significant in older adults and those with cardiovascular pathology, with systemic vascular resistance falling by approximately 25% and cardiac output by 10%.

Singla et al. [12] identified several independent predictors of early intraoperative hypotension, including age, female gender, obesity (BMI ≥30 kg/m²), hypertension history, diabetes, anemia, baseline hemodynamic parameters, and the extent of the neural blockade (T6 level or higher). In our study, Group B participants were, on average, about a decade older than those in Group A, potentially contributing to the more substantial MAP reductions observed in this group.

Earlier studies by Samad et al. [5], Sear et al. [6], and Hohne et al. [9] have highlighted the hypotensive risk posed by RAS inhibitors in the context of both general and spinal anesthesia. These authors warned that a reduction in BP by 25% may compromise perfusion in critical vascular territories such as the heart and brain. Sear et al. [6] also noted that while laryngoscopic responses were unaffected in patients with mild-to-moderate hypertension, hypotensive episodes were exaggerated in those on ACE inhibitors. Similarly, Coriat et al. [13] documented a higher incidence of post-induction hypotension in individuals on chronic ACE inhibitor therapy.

Although data on ARBs in the setting of spinal anesthesia are limited, our study did not demonstrate any statistically significant impairment in hemodynamic stability necessitating intervention in this patient population. An exception occurred in the control group, where one case of persistent hypotension post-anesthesia led to cancellation of the surgical procedure. This presentation, consistent with vasoplegic syndrome, is a recognized phenomenon with RAS-inhibiting agents under general anesthesia, though seldom reported with spinal techniques.

This study provided a real-world perspective on hemodynamic trajectories following spinal anesthesia, guided solely by the clinical judgment of the anesthesiologist. Parameters were selected based on prior literature to ensure patient safety was not compromised. Nevertheless, the relatively small sample size and the potential for undiagnosed comorbid cardiovascular or systemic conditions remain key limitations of this study.

Within the initial 20 minutes after administration of spinal anesthesia, individuals who had continued angiotensin II receptor antagonists on the day of surgery demonstrated a comparatively greater frequency of hypotensive episodes than their normotensive counterparts. Nonetheless, these declines in blood pressure were successfully managed with appropriate interventions, and no major adverse outcomes were observed. A compensatory rise in heart rate was noted, likely mediated through activation of baroreceptor reflex pathways. It remains essential for anesthesiologists to anticipate potential hemodynamic fluctuations in such patients and to be adequately equipped to address any complications that may arise.

1. Hartmann B, Junger A, Klasen J, Benson M, Jost A, Banzhaf A, et al. The incidence and risk factors for hypotension after spinal anesthesia induction: An analysis with automated data collection. Anesth Analg. 2002; 94:1521–9.
2. Saddler JM. Anesthesia and Hypertension—Update in Anesthesia. Issue 2, Article 3. UK: Royal Devon and Exeter Hospital; 1992.
3. Shear T, Greenberg S. Vasoplegic syndrome and renin-angiotensin system antagonists. J Anesth Patient Saf Found. 2012; 27:18.
4. Kaimar P, Sanji N, Upadya M, Mohammed KR. A comparison of hypotension and bradycardia following spinal anesthesia in patients on calcium channel blockers and β-blockers. Indian J Pharmacol. 2012; 44:193–6.
5. Samad K, Khan F, Azam I. Hemodynamic effects of anesthetic induction in patients treated on beta and calcium channel blockers. Middle East J Anesthesiol. 2008; 19:1111–28.
6. Sear JW, Jewkes C, Tellez JC, Foex P. Does the choice of antihypertensive therapy influence hemodynamic responses to induction, laryngoscopy and intubation? Br J Anaesth. 1994; 73:303–8.
7. Dinakar KR, Sanji N, Ravishankar RB, Vidya HK, Shashikala GH. Comparative study of variations in blood pressure and heart rate among normotensive patients and hypertensive patients receiving angiotensin receptor blockers during surgery under spinal anesthesia. Natl J Physiol Pharm Pharmacol 2018;8(12):1581-1586
8. Cozanitis DA. The importance of inhibiting angiotensin convertase inhibitor treatment before spinal anesthesia—a controlled case report. Anesthesiol Reanim. 2004; 29:16–8.
9. Hohne C, Meier L, Boemke W, Kaczmarczyk G. Angiotensin convertase inhibitor inhibitors do not exaggerate the blood pressure decrease in the early phase of spinal anesthesia. Acta Anaesthesiol Scand. 2003; 47:891–6.
10. Barrett KE, Barman SN, Boitano S, Brooks HL, editors. Cardiovascular regulatory mechanisms. In: Ganong’s Review of Medical Physiology. 24th ed. New Delhi: McGraw-Hill; 2012. p. 589–92.
11. Rooke GA, Freund PR, Jacobson AF. Hemodynamic response and change in organ blood volume during spinal anesthesia in elderly men with cardiac disease. Anesth Analg. 1997; 85:99.
12. Singla D, Kathuria S, Singh A, Kaul T, Gupta S, Mamta. Risk factors for development of early hypotension during spinal anesthesia. J Anesth Clin Pharmacol. 2006; 22:387–93.
13. Coriat P, Richer C, Douraki T, Gomez C, Hendricks K, Giudicelli JF, et al. Influence of chronic angiotensin converting enzyme inhibition on anesthetic induction. Anesthesiology. 1994; 81:299–307.