Spinal anaesthesia is a commonly used neuraxial technique that provides <br />profound analgesia and muscle relaxation, particularly for lower abdominal, <br />pelvic, and lower limb surgeries.<br />However, one of its most significant physiological effects is its impact on <br />haemodynamic stability, particularly blood pressure regulation. Hypotension <br />following spinal anaesthesia is a common occurrence due to sympathetic <br />blockade, decreased systemic vascular resistance (SVR), and reduced <br />cardiac output. This review provides a detailed exploration of the <br />physiological mechanisms, risk factors, assessment methods, prevention <br />strategies, and management protocols for blood pressure fluctuations postspinal anaesthesia. Additionally, multiple case studies and clinical guidelines <br />are included to provide practical insights into best practices for monitoring <br />and intervention.<br />1. Introduction<br />Spinal anaesthesia (SA) is a regional anaesthesia technique in which a local <br />anaesthetic is injected into the subarachnoid space at the L3-L4 or L4-L5 <br />interspace, resulting in sensory, motor, and autonomic blockade. It is widely <br />used due to its rapid onset, effective analgesia, lower risk of deep sedation, <br />and reduced systemic opioid requirements.<br />However, spinal anaesthesia has significant effects on blood pressure <br />regulation, and the extent of these effects depends on:<br />Level of blockade (higher levels cause more haemodynamic disturbances).<br />Patient factors (age, comorbidities, volume status).<br />Anaesthetic drug choice and dose.<br />Why is blood pressure assessment important after spinal anaesthesia?<br />Preventing severe hypotension that can lead to myocardial ischemia and <br />organ<br />hypoperfusion.<br />Identifying patients at risk of cardiovascular collapse.<br />Optimizing fluid and vasopressor management.<br />Key complications related to blood pressure changes include:<br />1. Hypotension (most common), which can lead to cerebral and myocardial<br />hypoperfusion.<br />2. Bradycardia, often seen in higher-level spinal blocks.<br />3. Severe cardiovascular instability in patients with pre-existing hypertension, <br />sepsis, or cardiac dysfunction.<br />2. Physiological Mechanisms of Blood Pressure Changes After <br />Spinal Anaesthesia<br />2.1 Sympathetic Blockade and Vasodilation<br />The primary cause of hypotension after spinal anaesthesia is sympathetic <br />blockade. The blockade of preganglionic sympathetic fibers (T1-L2) results in:<br />1. Loss of vascular tone (arterial and venous dilation →↓ SVR).<br />2. Reduced venous return (preload)→↓ stroke volume→↓ cardiac output.<br />3. Bradycardia (if cardiac sympathetic fibers at T1-T4 are affected).<br />Effects by spinal blockade level:<br />Above T5: Profound hypotension and bradycardia due to high sympathetic <br />blockade.<br />T6-T10: Moderate vasodilation and BP reduction.<br />Below T10: Minimal haemodynamic impact.<br />2.2 Effects on Cardiac Output and Stroke Volume<br />Spinal anaesthesia leads to:<br />Decreased preload due to venous pooling.<br />Decreased afterload due to vasodilation.<br />Variable cardiac output depending on patient's volume status and <br />compensatory mechanisms.<br />2.3 Baroreceptor and Hormonal Response<br />Baroreceptors (carotid sinus, aortic arch) attempt to compensate by <br />increasing sympathetic outflow, which is blocked by spinal anaesthesia.<br />Renin-angiotensin-aldosterone system (RAAS) is activated, but delayed <br />compensation limits its effectiveness in acute BP drops.<br />3. Blood Pressure Assessment Methods<br />3.1 Non-Invasive Blood Pressure (NIBP) Monitoring<br />Oscillometric method (most common).<br />Every 1-2 minutes in the first 15 minutes post-SA, then every 5 minutes.<br />3.2 Invasive Blood Pressure (IBP) Monitoring<br />Continuous real-time BP monitoring for high-risk patients (cardiac disease, <br />major<br />vascular surgeries).<br />More sensitive to rapid haemodynamic shifts than NIBP.<br />3.3 Heart Rate and ECG Monitoring<br />Bradycardia (HR <50 bpm) is a sign of severe hypotension.<br />ECG abnormalities (e.g., ischemic changes in high-risk patients).<br />3.4 Perfusion Index (PI) Monitoring<br />A non-invasive marker of sympathetic activity suppression and vasodilation.<br />4. Risk Factors for Blood Pressure Instability<br />4.1 Patient-Related Risk Factors<br />Elderly patients (>65 years): Reduced compensatory response.<br />Hypertension: BP fluctuations are exaggerated in these patients.<br />Cardiac disease: Risk of ischemia, arrhythmias, and heart failure <br />exacerbation.<br />Hypovolemia: Exacerbates BP drops.<br />4.2 Procedural Factors<br />High spinal block (T5 or above).<br />Excessive local anaesthetic dose.<br />Rapid injection of spinal anaesthetic.<br />4.3 Drug-Related Factors<br />Bupivacaine: Longer duration, more pronounced hypotension.<br />Lidocaine: Shorter duration, milder BP effects.<br />Opioid additives (fentanyl, morphine): Can potentiate hypotension.<br />5. Prevention and Management of Blood Pressure Changes<br />5.1 Preventive Strategies<br />1. Preloading with IV Fluids<br />Crystalloids (Ringer's lactate, normal saline) - 10-15 mL/kg before SA.<br />Colloids (Hetastarch, Gelatin solutions) - More effective, but risks include<br />coagulopathy.<br />2. Vasopressor Use<br />Phenylephrine (50-100 mcg IV bolus) - First-line treatment; direct <br />vasoconstriction.<br />Ephedrine (5-10 mg IV) - Increases cardiac output and BP; used in <br />bradycardia.<br />3. Positioning Adjustments<br />Trendelenburg position - Increases venous return.<br />Left lateral tilt (pregnant patients) - Relieves aortocaval compression.<br />4. Drug Selection Adjustments<br />Lower doses of local anaesthetic in elderly or hypovolemic patients.<br />Epinephrine (0.2 mg) addition to spinal anaesthetic for BP stabilization.<br />6. Case Studies<br />Case Study 1: Severe Hypotension in an Elderly Patient<br />Patient: 72-year-old male with hypertension undergoing total knee <br />replacement.<br />Spinal Anaesthesia: 2.5 mL of 0.5% bupivacaine + 25 mcg fentanyl.<br />BP Trend: 140/80 80/50 mmHg in 10 minutes.<br />Management:<br />✔ Phenylephrine 100 mcg IV → BP improved to 100/65 mmHg.<br />✔ 500 mL RL fluid bolus.<br />✔ Ephedrine 6 mg IV for persistent bradycardia.<br />Outcome: BP stabilized to 120/75 mmHg. Surgery continued safely.<br />7. Conclusion<br />Blood pressure assessment after spinal anaesthesia is essential due to its <br />profound haemodynamic effects. Hypotension is the most common <br />complication due to sympathetic blockade and decreased cardiac output. <br />Risk assessment, early fluid administration, vasopressor use, and patient <br />positioning adjustments are crucial in managing haemodynamic stability.<br />8. References<br />1. Carpenter RL, Caplan RA, Brown DL, et al. (1992). Incidence and risk <br />factors for side effects of spinal anesthesia. Anesthesiology, 76(6), 906-916.<br />2. Morgan GE, Mikhail MS, Murray MJ. (2020). Clinical Anesthesiology. <br />McGraw Hill.<br />3. Butterworth JF, Mackey DC, Wasnick JD. (2018). Morgan & Mikhail's <br />Clinical Anesthesiology, 6th Edition. McGraw-Hill<br /><br />م.محمد خضير عباس<br /><br />Al-Mustaqbal University is the first university in Iraq