European Journal of Cardiovascular Medicine

Spinal anesthesia (SA), or subarachnoid block (SAB), remains a cornerstone of anesthetic practice for surgeries below the umbilicus, prized for its efficacy, reliability, and favorable safety profile. It provides excellent surgical conditions, profound analgesia, and avoids the potential complications of general anesthesia, such as airway manipulation and postoperative nausea and vomiting. Despite these advantages, hemodynamic instability is its most frequent and consequential drawback, with hypotension and bradycardia representing the primary manifestations of this instability [1].

 

The physiological basis for this phenomenon is well-understood. The administration of local anesthetic into the cerebrospinal fluid produces a sympathetic blockade, which typically extends to a higher dermatomal level than the sensory blockade. This leads to a decrease in systemic vascular resistance (SVR) through the vasodilation of arterioles and, crucially, a reduction in venous return to the heart due to pooling of blood in the capacitant venous system [2]. The resultant decrease in cardiac output precipitates a fall in arterial blood pressure. The body's natural compensatory mechanisms, such as tachycardia and increased contractility, are often blunted by the unopposed parasympathetic activity and the potential blockade of cardiac accelerator fibers (T1-T4) [3].

 

While all patients are susceptible, those with a pre-existing history of hypertension are considered particularly vulnerable. Chronic hypertension induces structural and functional adaptations in the cardiovascular system. There is a chronic increase in sympathetic tone and a restructuring of the arterial walls, leading to reduced vascular compliance [4]. Furthermore, to maintain perfusion pressures against stiffened arteries, a relative central redistribution of blood volume occurs [5]. Spinal anesthesia disrupts this precarious equilibrium. The sympathetic blockade abruptly removes the tonic vasoconstriction, causing a more dramatic fall in SVR in hypertensive patients compared to normotensive individuals with more compliant vessels. Concurrently, the loss of venous tone exacerbates the reduction in preload, to which hypertensive patients are less able to mount an effective compensatory response [6]. Consequently, a similar level of neural blockade can induce a disproportionately greater decrease in blood pressure in hypertensive patients [1, 7].

 

The clinical implications of this exaggerated hypotensive response are significant. Pronounced or prolonged hypotension can lead to critical reductions in end-organ perfusion, potentially causing myocardial ischemia, renal dysfunction, or cerebral hypoperfusion, especially in a patient population that may already have compromised vascular reserve [8]. Therefore, the preservation of hemodynamic stability is a paramount concern for anesthesiologists.

 

Although the increased risk in hypertensive patients is a widely accepted tenet, the extant literature presents a nuanced picture. Studies such as the one by Gebrargs et al. [1] strongly support this view, reporting a significantly higher incidence of hypotension in controlled hypertensives. However, other investigations, like the one by Acar NS et al. [7], have observed that while absolute blood pressure values differ, the pattern of change post-SAB might be similar. Furthermore, the impact of different antihypertensive regimens adds another layer of complexity, with some studies suggesting that the type of medication may influence the hemodynamic response [9].

 

This ongoing discourse underscores the need for continued, focused research in this area. A clear and precise understanding of the hemodynamic differences between these patient populations is essential for optimizing perioperative management. This study was, therefore, designed as a prospective, observational comparison to rigorously evaluate and compare the hemodynamic parameters—specifically the incidence, magnitude, and timing of hypotension and bradycardia—following spinal anesthesia between medically controlled hypertensive and normotensive patients undergoing elective infraumbilical surgery. The findings aim to provide robust data to guide clinical vigilance and prophylactic strategies, ultimately enhancing patient safety.

Study Design and Setting A prospective, observational study was conducted over one year after obtaining institutional ethical clearance. A total of 100 patients, scheduled for elective surgery below the umbilicus under spinal anesthesia, were enrolled. Written informed consent was obtained from all participants. Inclusion Criteria Patients aged 40-65 years, of American Society of Anesthesiologists (ASA) physical status I and II, with a Body Mass Index (BMI) <30 kg/m² Exclusion Criteria Pregnant women; patients on ACE inhibitors or ARBs; patients with diabetes mellitus, known cardiac, renal disease, or coagulopathy; patients refusing or with contraindications to regional anesthesia; and those with uncontrolled hypertension. Study Groups Patients were divided into two groups: • Group H (Hypertensive, n=50): Patients with a known history of hypertension on regular antihypertensive medication (excluding ACEIs/ARBs, which were withheld as per exclusion criteria). • Group N (Normotensive, n=50): Patients with baseline blood pressure <140/90 mm Hg and no history of antihypertensive drug use. Anesthetic Technique All antihypertensive medications were continued on the day of surgery. A pre-anesthetic check was performed one day prior. On the day of surgery, an intravenous line was secured, and preloading was done with 10 ml/kg of isotonic saline over 20 minutes. Standard monitoring (ECG, NIBP, SpO₂) was initiated. Under aseptic conditions, spinal anesthesia was performed in the sitting position at the L3-L4 interspace using a 25-gauge Quincke spinal needle, injecting 3.5 ml of 0.5% hyperbaric bupivacaine. The patient was immediately placed supine, and surgery commenced after achieving an adequate sensory block (T6 level). Data Collection Baseline hemodynamic parameters (SBP, DBP, MAP, HR) were recorded in the premedication room. Measurements were repeated after fluid preloading and subsequently at 1, 3, 5, 10, 20, 30, 40, 50, and 60 minutes after the administration of spinal anesthesia. Hypotension was defined as a fall in SBP of more than 25% from the baseline value and was treated with intravenous boluses of ephedrine 6 mg. Bradycardia was defined as a heart rate of less than 50 beats per minute and treated with intravenous atropine 0.6 mg. Statistical Analysis Data were analyzed using SPSS version 25.0. Continuous variables were expressed as mean ± standard deviation and compared using Student's t-test. Categorical data (incidence of hypotension/bradycardia) were expressed as numbers (%) and compared using the Chi-square test. A p-value of <0.05 was considered statistically significant.