Dynamics of Neuraxial Blocks in
Obstetrics and Gynaecology

Neuraxial block techniques: 
Nowadays, anaesthestists and obstetricians believe that neuraxial anaesthesia is safer than general anaesthesia due to less maternal morbidity and mortality risks related to the difficult airway problem.
Neuraxial anaesthesia includes spinal, epidural, and combined spinal-epidural blocks.
One-shot spinal anaesthesia in obstetrics and gynaecology is given by the anaesthetist while the patient is in the sitting or the lateral decubitus position. The procedure is carried out with a sterile field and the identification of anatomic landmarks. The approach to reach the subarachnoid space is either the midline or the paramedian one.
Epidural anaesthesia is a more difficult technique, but offers greater flexibility than spinal anaesthesia in extent and duration. The potential for continuation of postoperative analgesia with narcotics or local anaesthetics has dramatically increased the popularity of epidural anaesthesia.
The advantages of spinal anaesthesia over epidural anaesthesia include its simplicity, rapidity of onset, reliability, predictability, reproducibility, safety for both the mother and newborn and the reciprocal psychological bonding between them, added to its cost-effectiveness.
The combined spinal-epidural anaesthetic technique combines the benefits of the reliabity of intrathecal block, with the flexibility of epidural block regarding  extent and duration. It may be done by the double segment or the single segment needle through needle approach.

Haemodynamics of neuraxial blocks:
The most common serious side-effects of neuraxial blocks are bradycardia and hypotension due to reflex cardiovascular depression.  This has been termed the vasovagal syncope, the Bezold-Jarisch reflex and the neuroendocrinal syncope. Many case reports have discussed the extremes of these terms in the form of cardiac arrest fatalities during neuraxial blockade.  An overall incidence of 7 cases of cardiac arrest for every 10.000 spinal anaesthetics were reported (1,2) , versus one case for every 10.000 epiduarl anaesthetics (3). A review of literature from the 1930s to the 1950s on maternal mortality during Caesarean section under spinal anaesthesia reported sudden cardiac arrests following sudden bradycardia in many cases when heart rate was recorded (4,5). In a study including 20.000 spinal anaesthetics, cardiac arrests were reported in young patients less than 30 years of age (6).  A closed claims analysis reported 14 cardiac arrests out of 900 spinal anaesthetics during 1978-1986 in young healthy patients undergoing minor surgical procedures (3).

Perioperative Haemodynamic Mechanisms:

(A) Neuraxial anaesthesia:
A responsible mechanism for cardiac arrest during neuraxial anaesthesia needs an investigation of a possible respiratory, cerebral or circulatory origin.

A possible respiratory mechanism:
A respiratory etiology for cardiac arrest during neuraxial anaesthesia may be considered because most of such patients receive a sedative cover that may be accused for inadequate ventilation. However, sensory levels up to T4 do not lead to hypoventilation, but are rather associated with hyperventilation (7, 8).  Before the widespread use of pulse oximetry, it was argued that oversedation played a key role in cardiac arrests during spinal anaesthesia, till many authors recorded settings of 95-100% oxygen saturation  at the time of such arrests (9-11).  Many studies concerning side-effects of spinal anaesthesia, failed to find a link between sedation and cardiac arrest or to document a primary respiratory etiology for these arrests (1, 2, 12).  However, for safety, one should consider that oversedation may increase the risk of bradycardia (3) and the patient may not be able to communicate symptoms of early warning of a vasovagal attack (13).

Spinal anaesthesia has been recently accused to have direct effect on the suppression of consciousness as some studies have observed that patients appear drowsy after spinal anaesthesia despite the lack of sedative medication (14, 15). In fact, greater sedation has been observed with high spinal blocks (14, 15). The possible mechanisms include the rostral spread of local  anaesthetic  agents, or a reduction in the function of the reticular activating system caused by an interruption of afferent inputs. The clinical message is that patients undergoing spinal anaesthesia have a reduced requirement for pharmacological sedatives (16). Again, the prophylactic administration of oxygen during spinal anaesthesia may be another useful clinical message, because hypoxemia may occur with high block causing central hypoventilation or a reduction in cardiac output with a shunt effect. Pulse oximetry is helpful and end-tidal carbon dioxide monitoring may be useful with side-stream capnography even in un-intubated patients.

A possible cerebral mechanism:
There is some evidence in early literature that cerebral hypoxia might occur during spinal anaesthesia in some patients (17, 18).  Again, high epidural anaesthesia in monkeys was shown to decrease arterial BP by 47%, resulting in a 35% decrease of CBF (19).  
Cerebral complications may be attributed to a disturbance in cerebral oxygen balance, between oxygen supply to the brain and oxygen demand (20). Spinal anaesthesia producing a significant decrease of mean arterial pressure (MAP) and cerebral perfusion pressure (CPP) was associated with a significant decrease of jugular bulb oxygen saturation (SjbO2), jugular bulb oxygen content (CjbO2) and a concomitant increase in arterio- jugular oxygen content difference (Ca-jO2) in ten patients undergoing transuretheral resection of the prostate (TURP) and eight of them developed TURP syndrome (21). 
SjbO2  ≤ 50% has been considered as a critical low threshold for an imbalance between oxygen supply and demand to the brain (22-24).  Recently, Atallah et al  (25) proved that following spinal anaesthesia and during TURP, some patients developed impaired cerebral oxygenation.  An editorial has appraised this finding and advised further studies to demonstrate impaired cerebral oxygenation in patients undergoing surgery under spinal anaesthesia in which irrigating fluid is not used, to prove that impaired cerebral oxygenation is unrelated to fluid absorption (26).
Although impaired cerebral oxygenation seems not to be a primary etiology for fatal spinal anaesthesia (27), we suggest that a disturbance in cerebral oxygen balance might be a precipitating factor for the occurrence of cardiac arrest in specific surgical situations during spinal anaesthesia, which should not be ignored.

A possible circulatory mechanism:

A circulatory etiology for cardiac arrest during spinal anaesthesia is directly or indirectly related to the blockade of sympathetic afferents (28, 29).  The cardiovascular responses to spinal anaesthesia are almost entirely due to the fact that the local anaesthetic injected into the subdural space not only blocks somatic sensory and motor fibers, but also produces preganglionic sympathetic denervation. Somatic levels are determined by pinprick, which tests the extent of block of the pain conducting fibers segmentaly innervating areas of the skin and the absence of pain to pinprick is a sign of analgesia. It should be emphasized that levels of sympathetic block are not synonymous with somatic levels as assessed by pinprick, but they are two to six segments higher. So, a patient with T4 sensory block may have completely blocked cardiac accelerator fibers that originate from T1 to T4 and such blockade can result in a variety of bradyarrhythmias (30). Skin discrimination of temperature may be used as a clinical correlate of the level of sympathetic denervation during regional anaesthesia.
A more important effect of sympathetic inhibition during spinal or epidural anaesthesia is a significant decrease in venous return due to dilatation of resistance and capacitance vessels (31).  Reductions of the right atrial pressure of 36% and 53% have been reported after low and high spinal blocks respectively (8). High sympathetic blockade caused more hypotension due to dilatation of splanchnic vessels and decrease of catecholamine release by the adrenal medulla.  An exaggerated decrease in central venous pressure up to 66% took place when spinal block was associated with blood loss of 10ml/kg (7).
It is clear that a circulatory etiology underlies the occurrence of severe bradycardia and asystoly, given the blockade of sympathetic afferents and the profound decrease in venous return associated with higher levels of spinal sympathetic blockade (16).
The cardiac sympathetic outflow emerges from C5 to T5 levels, with the main supply to the ventricles from T1 to T4.  A significant part of the chronotropic and inotropic control of the heart and its oxygen demand is mediated through the upper four thoracic spinal segments.  The major determinant of heart rate is the balance between sympathetic and parasympathetic systems with the latter predominating. A high thoracic sympathetic blockade covering the cardiac segments T1-T4 produces significant reduction in heart rate.  However, high sympathetic blockade may leave some cardiac sympathetic activity intact, since sympathetic responses to hypercarbia are not totally suppressed by T1 to T5 blockade (32). 
Decreases in preload after spinal anaesthesia initiate reflexes that cause severe bradycardia. Mackey et al (11) have suggested three working reflexes: (a) the pacemaker stretch reflex: the rate of firing of the pacemaker cells within the myocardium is proportional to the degree of stretch.  Decreased venous return results in decreased stretch and a slower heart rate. (b) low pressure baroreceptors in the right atrium and vena cava when stimulated may cause bradycardia. It is known that arterial baroreceptor activation secondary to increases in BP, decreases sympathetic outflow and increases parasympathetic activity leading to vasodilation and bradycardia and that with a decrease in BP, arterial baroreceptor activity ceases.  However, with progressive hypovolaemia, there may be a paradoxical recurrence of baroreceptor discharge, the so-called “collapse firing” (13). (c) the Bezold-Jarisch reflex: mechanoreceptors in the left ventricle when stimulated may cause bradycardia. The Bezold-Jarisch reflex includes reactions triggered by cardiac mechanoreceptor activation and it has been used to describe perioperative bradycardia with hypotension (11, 33).  Some unmylenated afferent pathways from the inferoposterior wall of the left ventricle pass via the glossopharyngeal and vagus nerves to the brain stem and may respond to decreased venous return due to relative hypovolaemia by bradycardia.  This bradycardia is a protective reflex that prevents the heart from contracting when relatively empty (34).
Although reflex cardiovascular depression with vasodilation and bradycardia is usually triggered by reduced venous return, it can be also triggered through affective stimuli as pain or fear initiating the famous vasovagal mechanism (13).  So, the vasovagal reflex is probably mediated in part via afferent nerves from the heart, but also via various non-cardiac baroreceptors which may become paradoxically active by stimulating the limbic sympatho-inhibitory centers (13).
True vasovagal reactions have been described associated with anxiety and pain of venepuncture (35-38).  Case reports noted a history of fainting as well as the added influence of orthostatic stress from the sitting position used for spinal needle insertion leading to vasovagal asystoly (39). In such patients, a detailed history may provide a pattern to the syncopal attacks and its precipitating factors (13).  Oral sedatives and/or anticholinergics and topically applied local anaesthetic cream at venepuncture site can prevent asystole (38). To decrease the incidence of vasovagal syncope the lateral position for spinal anaesthesia may be preferable to the sitting position (40).
One should observe that reflex cardiovascular depression with vasodilation and bradycardia has been variously termed vasovagal syncope, Bezold-Jarisch reflex and neurocardiogenic syncope with loss of consciousness caused by reduced arterial pressure and blood supply to the brain mediated through neural mechanisms rather than primary cardiac dysfunction.  However, the trigger may be central from psychic stress or pain, or may be initiated peripherally by a reduction in venous return. The Bezold-Jarisch reflex overlaps the vasovagal syncope as it became a term which includes reactions triggered by cardiac mechanoreceptors and describes perioperative bradycardia with hypotension (11, 33, 41).

(B) Haemorrhage:
Obstetric haemorrhage is a leading cause of maternal death, and the most common contributor to serious obstetric morbidities (42). In the latest report from the United Kingdom “Why Mothers Die 2000-2002”, obstetric haemorrhage was the second most common direct cause of death (43).
Vasovagal reactions from peripheral stimuli may occur when there is a decrease in venous return, from either hypovolaemia or a redistribution of blood volume. Hypovolaemic hypotensive patients sometimes presented with a slow heart rate (44). During progressive withdrawal of venous blood, blood pressure was initially maintained by vasoconstriction. With continuing blood loss, there might be a sudden fall in blood pressure, heart rate and peripheral resistance (45). Barcroft and colleagues found that the incidence of ‘fainting’ increased as blood loss increased, from 4% after loss of 440 ml to 50% after loss of 1000-1200 ml. (46). An important later clinical finding was that, in cases where haemorrhage presented with relative bradycardia, transfusion alone would reliably increase the heart rate. (47, 48)
This pattern of cardiovascular change in response to haemorrhage is unfamiliar, as sustained tachycardia is mediated via a withdrawal of afferent input from the arterial baroreceptors (49). This is probably because most hypovolaemic patients respond with a tachycardia, whereas the bradycardic response is noted in a minority only. If the pattern of hypovolaemia presenting with bradycardia is not recognized, some patients may be treated inadequately or inappropriately (49).

(C)Compression of inferior vena cava during pregnancy:
In late pregnancy some women suffer an acute circulatory collapse, severe enough to mimic haemorrhagic shock, in the supine position (50, 51). The cause was identified as compression of the inferior vena cava by the gravid uterus, reducing venous return and right atrial pressure. (47) Further reports of this phenomenon noted that sudden bradycardia occurred in some cases, (45, 47) and Lees and co-workers linked this ‘supine hypotensive syndrome of pregnancy’ with vasovagal fainting. (47)
Holmes reviewed the literature from the 1930s to the 1950s on maternal mortality during Caesarean section with spinal anaesthesia. Problems occurred soon after the patient was moved into the supine position, as the sympathetic block developed. Sudden bradycardia was found in cases when heart rate was recorded (4, 5). Holmes suggested that unappreciated compression of the vena cava was the likely cause, rather than other possibilities such as respiratory insufficiency (4, 5). The risk is present even without the sympathetic block induced by regional anaesthesia: a patient with severe pre-operative supine hypotension died after induction of general anaesthesia (52). These life-threatening reactions are now rare since the introduction of lateral tilt during Caesarean section. (53, 54)

So, it is clear that this haemodynamic response may occur during regional anaesthesia, haemorrhage or supine inferior vena cava compression of pregnancy; these factors are additive when combined. In these circumstances hypotension may be more severe than that caused by bradycardia alone, because of unappreciated vasodilation. The identification of a minority of patients who demonstrate vasovagal responses during regional anaesthesia, haemorrhage, or inferior vena cava compression, might suggest that these individuals are qualitatively different. Development of testing by the tilt table and lower body negative pressure devices gave the hope of distinguishing “normal” from “abnormal” individuals (55, 56). However, such simple division of the population into two groups, prone or not prone to vasovagal syncope, was not confirmed as syncope occurred in asymptomatic subjects, and some patients with a clinical history of the syncope did not show syncopes on testing (55, 56).

Hypovolaemia and the standing position may be counted as ‘natural’ stresses which the circulatory reflexes are designed to counteract, but head-up tilt and neuraxial block affect the integrated cardiovascular response to reduced venous return. During head-up tilt the leg muscles do not contract and therefore the ‘muscle pump’ that augments venous return is inactive, so that vasovagal reactions can occur in subjects who do not give a clinical history. (57) Epidural anaesthesia inhibits not only the muscle pump but also the compensatory veno-and arterioconstriction.

It may be concluded that there is no true separation between normal and abnormal, but  there is a range of individual susceptibility to vasovagal reactions from those who may have life threatening problems during their daily life (58) to those who do not response to provocative testing. A patient may show syncope in some circumstances but not in others. A practical approach in clinical practice is to separate patients on the basis of whether or not they have a history of syncopy episodes. Regional anaesthesia should be avoided in patients with a history of vasovagal syncopy.

RISK FACTORS:

Vagotonia:
Patients with vagotonia are at increased risk of cardiac arrest during spinal anaesthesia (59). Vagotonia denotes strong resting vagal tone (i.e. the athlete heart syndrome) and describes the clinical situation of resting bradycardia or first degree atrioventricular block that is present in 7% of the population (60). Therefore, in vagotonic patients cardiac arrest can occur when procedures that increase vagal activity are  performed (10,30,60-62). It can be strongly stated that patients with a baseline heart rate < 60 beats/min are at increased risk of asystoly during spinal anaesthesia (29, 59). Carpenter et al (12) reported that such patients are associated with five fold increase in the risk of cardiac arrest during spinal anaesthesia.
Spinal anaesthesia has been associated with progression of first-degree to second degree heart block (60, 63), or with onset of sick sinus syndrome (64). In such situations, complete heart block and cardiac arrest may simply represent the most severe vagaly induced bradyarrhythmia associated with spinal anaesthesia (65).

High sensory level block:

Patients with sensory level block above T6 during spinal anaesthesia are at increased risk of cardiac arrest. In this situation, cardiac accelerator fibers that originate from T1 to T4 may be completely blocked (30).  Although, block height cannot be precisely controlled with single shot spinal anaesthesia, important factors during spinal bock as drug dose, rate of administration and its baricity together with patient positioning are under the control of the anaesthetist (66).

Age and ASA Physical Status:

Young patients have strong vagal tone and those < 50 years of age are at increased risk of cardiac arrest during spinal anaesthesia (67). Carpenter et al (12) reported that ASA physical status I young patients have three-fold increased risk of developing moderate bradycardia of < 50beats/min during spinal anaesthesia.  The most important factor implicated in complications was dermatomal block to T5 - T6 or higher. Bradycardia was more likely in young age, ASA I patients, while hypotension was more frequent in the elderly.
Beta-adrenergic blockade:
Patients under current therapy of B-blockers are at increased risk of developing cardiac arrest during spinal anaesthesia (12).
Pollard (68) has recently summarized the risk factors for bradycardia < 50 beats/min during spinal anaesthesia in the form of baseline heart rate < 60 beats/min, ASA physical status I, age < 50 years, sensory level block above T6, prolonged P-R interval and the use of B-blocking drugs.
Pollard (68)  holds the opinion that the presence of a single risk factor out of these six, does not make it certain that a patient will experience severe bradycardia or cardiac arrest. However, when two or more of these six factors are present, the patient may be considered at high-risk for bradycardia and cardiac arrest during spinal anaesthesia.  
It needs to be remembered that often two or more of these risk factors are present in patients who receive spinal or epidural anaesthesia for labour or Cesarean delivery.  However, epidural anaesthesia is associated with far lower incidence of cardiac arrest compared to spinal anaesthesia (2).  It is known that the slower onset of epidural anaesthesia and the incremental dosing may allow time for compensatory mechanisms to counteract the decrease in preload.  Again, the physiologic changes associated with pregnancy as a decreased parasympathetic tone play a key role of a weaker vagal tone that decreases the risk of cardiac arrest during spinal or epidural anaesthesia. Note that lateral tilting to avoid inferior vena cava compression is a must. Neglect of such a simple manoeuvre after induction of spinal or general anaesthesia leads to sudden bradycardia and may be asystole (69). Such acute circulatory collapse is similar to haemorrhagic shock. This is because problems occurred soon after the patient was moved into the supine position as the sympathetic block developed. 

Management:

Proper selection of patient and operation:

It is strongly addressed that it should be appropriate to reconsider the use of spinal anaesthesia for a patient with vagotonia.  Similarly, it may be prudent not to use spinal anaesthesia when significant blood loss or the use of vasodilators is anticipated, because the vasodilatation caused by spinal anaesthesia can make resuscitation ineffective.

Fluid support:
Hypotension following spinal anaesthesia for Caesarean section is a common and troublesome complication, both from the maternal and fetal points of view. Methods to prevent hypotension include mechanical means such  as leg wrapping,  anti-thromboembolic stockings, patient positioning, and fluid administration (70).
Although one might assume that maintaining preload during spinal or epidural anaesthesia is a uniform practice of anaesthetists, the literature demonstrates otherwise as many cases with cardiac arrest occurred in settings without volume preloading (71).
With decrease of venous return due to hypovolaemia or a redistribution of blood volume, blood pressure is initially maintained by vasoconstriction.  During progressive and continuing decrease in venous return, there may be a sudden fall in blood pressure, heart rate and peripheral resistance(40). An important clinical finding in cases where haemorrhage presented with relative bradycardia is that transfusion alone could reliably increase the heart rate (72).
In a review of the efficacy of increasing central blood volume on the incidence of bradycardia and hypotension after spinal anaesthesia, Pamela et al (71) observed that crystalloid preload was inconsistent in prevention, whereas colloid preload decreased but did not abolish the incidence of bradycardia and hypotension. Restoration of venous return is always urgent as spontaneous recovery from asystole may occur if this is achieved (39).  A simple maneouvre as leg elevation if possible should not be ignored (3).
Preload is rapidly redistrubted, and may induce atrial natriuretic peptide secretion, resulting in peripheral vasodilation followed by an increased rate of excretion of the preloaded fluid (73).
A more rational approach during elective Caesarean section might be to apply rapid fluid loading (Coloading) at the time that the local anaesthetic block is starting to take effect. This might maximize intravenous volume expansion during vasodilation from the sympathetic blockade, and limit fluid redistribution and excretion (70). In an original recent study, Mirt and Vesna(74) compared the use of 12ml/kg Lactated Ringer (LR) solution within 20 min before spinal anaesthesia versus within 20 min starting immediately after spinal anaesthesia.  In the first group of patients, the cardiac output (CO) increased by 20% after the infusion and returned to baseline value 30 min after spinal block.  In the second group, CO increased after spinal block and was still 11.3% above the baseline 30 min after the spinal block. They (74) concluded that the decrease in CO after spinal anaesthesia can be prevented by the infusion of LR solution, with CO reaching the highest value while the infusion is running.

Pharmacological Support:
Inspite of emphasizing the importance of volume loading and prompt replacement of fluid loss during spinal anaesthesia, decreases in preload can occur so quickly with altering the patient position, releasing a tourniquet or similar  events that there may not be enough time to give sufficient fluid volumes over several minutes.  Here, the administration of pharmacological drug support may be appropriate.  In such situations or when bradycardia is the presenting sign, atropine may decrease the incidence of cardiac arrest during spinal anaesthesia (1, 75). Brown et al (75) advised vigilance of the anaesthetist and the willingness to utilize iv atropine (0.4 – 0.6mg), ephedrine (25-50mg) and epinephrine (0.2– 0.3mg) in stepwise escalation of therapy when bradycardia develops following spinal analgesia.  Successful resuscitation was carried out in all settings where atropine was typically used as the first line of therapy (62, 65, 75).  Atropine may not be the best single agent if bradycardia is accompanied by vasodilatation as hypotension may persist after the relief of bradycardia by atropine (76). 
It may be useful to note that the report of Caplan et al (3) postulated that prophylactic treatment of patients with heart rates less than 60 beats per minute with vagolytic agents before spinal analgesia may be an effective prophylactic strategy.
The report of Mackey et al (11) describing asystoly during spinal anaesthesia described the “event” as a sudden decrease in heart rate, although often a gradual decline during stable anaesthesia had preceeded this.  Bradycardia was reversed by atropine in all subjects, but ephedrine, epinephrine and external cardiac massage were also needed in some cases.  
It should be clear that bradycardia with heart rate of 50 beats / min is consistent with cardiac sympathetic nerve inhibition associated wit mid-thoracic block level (66). However, the development of sudden bradycardia over a few heart beats and the potential for the reversal of bradycardia by postural changes that increase venous return, can only be explained by a vasovagal reaction (66).
When bradycardia is profound or a full cardiac arrest occurs after spinal anaesthesia, the early administration of epinephrine is crucial.  The vasodilatation caused by spinal anaesthesia can make cardiopulmonary resuscitation ineffective.  Successful resuscitation requires a coronary perfusion pressure gradient of 15 to 20 mmHg and during spinal anaesthesia this may require epinephrine 0.01 to 0.1 mg/kg (77).  
It is important to consider that if hypotension persists after adequate doses of ephedrine or epinephrine, an alpha-agonist like phenylephrine should be given. It is only in this situation that selective alpha-agonists have therapeutic place, because these agonists if given to a patient with bradycardia, heart rate may be reduced further if baroreceptor function remains active (78).
A standard sequence using atropine, ephedrine and then epinephrine to treat bradycardia during spinal anaesthesia has been advocated (71).  But, although flexibility is necessary, Kinsella and Tuckey (13) have recently suggested that ephedrine, due to its cardiac and vascular actions, is the most logical choice for a single agent to treat profound bradycardia during regional anaesthesia, given the lack of vasoconstrictor effect of atropine and the potential for heart rate reduction with alpha-agonists.  As mentioned before, with the occurrence of asystole or persistent severe bradycardia, epinephrine should be used early.

Cardio-pulmonary resuscitation:
Severe bradycardia (<40 beats/min) if persistent inspite of pharmacological therapy should be managed like asystoly by cardiopulmonary resuscitation comprising its usual principles of basic and advanced life support. Successful use of thump pacing for asystoly during regional anaesthesia has been described (79).  However, once persisting cardiac arrest occurs, external cardiac massage must be started to ensure circulation of drugs and perfusion of vital organs. Prompt treatment with epinephrine has been emphasized as crucial for successful recovery (5, 55, 63).

Recent Trends:
Selective Spinal Anaesthesia:
Selective spinal anaesthesia (SSA) has been defined as “the practice of employing minimal doses of intrathecal agents so that only the nerve roots supplying a specific area and only the modalities that require to be anaesthetized are affected”. Dorsal column and motor functions are essentially preserved with selective spinal anaesthesia. (80) 
Selective spinal anaesthesia has opened up the possibility of providing “walk in - walk out” spinal anaesthesia with a real possibility of fast-tracking outpatients through the recovery process, with the feasibility of bypassing the recovery room. (81) According to many authors, SSA is a “low-dose, low-volume, low-flow” technique (81).
Although spinal anaesthesia competes with the newer general anaesthetics for ambulatory surgery, the discharge times are longer, and this is a significant point of difference between the two techniques.  In an effort to make spinal anaesthesia successfully selective and optimally efficient for ambulatory surgery, smaller doses or mini-doses of local anaesthetics are used because complete return of sensation to pinprick remains the rate-limiting step to early discharge (82). The addition of a small dose of intrathecal opioid overcomes the potential risk of inadequate block associated with small dose local anaesthesia (82, 83). Intrathecal opioids act synergistically with intrathecal local anaesthetics to enhance subtherapeutic doses of local anaesthetics that, as a sole drug, may not provide an adequate block. (82)  The dose of spinal lidocaine can be reduced from 75 mg to 10 mg without compromising intraoperative conditions. (80, 82)  As the dose of local anaesthetic is progressively reduced, there are beneficial effects in terms of a more stable hemodynamic profile, as well as preservation of spinal cord function with selective blockade of the spinothalamic column (82). Vaghadia et al (82) showed that a combination of 25 mg of lidocaine and 25 µg of fentanyl produces sufficient anaesthesia for brief laparoscopic procedures, with patients meeting discharge criteria at 122 min.

Examples of techniques of SSA
For spinal-narcotic-based labour:
Spinal-narcotic based labour is a technique known as “walking spinal”. Once normal delivery is initiated, spinal analgesia is carried out by 25G spinal needle at the L2-3 level using 25mg fentanyl and 0.25 mg morphine added to 2 ml saline. This is a very effective approach to normal labour without disrupting its normal course. It is associated with minimal headache, retention of urine or itching. However, delayed respiratory depression mandates cancellation of the use of the hydrophilic morphine and to use the lipophylic fentanyl alone. Again, for combined spinal epidural analgesia, fentanyl 50 mg, morphine 0.25 mg, and epinephrine 0.2 mg added to 2 ml saline are injected intrathecally. This gives profound analgesia for normal labour without motor impairment. If Caesarean section is decided adequate volumes of 2% lidocaine can be injected through the epidural catheter. However, intrathecal morphine should be noted for its respiratory depressant effect.

For gynaecologic laparoscopy:
Outpatient laparoscopy for gynaecological surgery, a procedure traditionally performed under general anaesthesia, can be safely performed with selective spinal anaesthesia. Upon arrival in the operating room, routine monitors are applied to the patient (ECG, BP and Spo2).  The SSA technique was described by Stewart et al. (84)  Spinal anaesthesia was administered while the patient was in the sitting position with a midline approach at  the L3-4 or L4-5 level using a 25-gauge needle.  The orifice of the needle was placed cephalad and the spinal solution was injected rapidly.  The 3ml solution consists of 1% lidocaine 10 mg (1ml), sufentanil 10μg (0.2ml) and sterile water (1.8ml).  This is a hypobaric solution with a specific gravity of 1.002 (CSF = 1.0069).  The patient remained sitting for one min, after which she was allowed to lie down, and the operating table was placed in 20-30° reverse trendelenburg position while lithotomy positioning and skin preparation took place, and was kept in this position for 6-8 min to facilitate cephalad spread of the hypobaric solution.  Before insufflation of the abdomen, the table was returned to the horizontal position. Three to four litres of CO2 were insufflated before insertion of trocars.  Anxiety and abdominal or shoulder discomfort were treated with increments of midazolam 1mg and fentanyl 25-50 μg iv, respectively. Supplementary oxygen was administered for oxygen saturation < 93%.  
In this technique, it is clear that synergism between intrathecal opioids and local anaesthetics allows a reduction in the dose of local anaesthetic, and cause less sympathetic block and hypotension, while still maintaining adequate anesthesia (85).

For perineal surgery:

Most anaesthetists know the technique of conventional dose spinal anaesthesia for saddle block to facilitate anorectal or perineal surgery. However, the technique is not used on a wide scale and achieving selectivity for ambulatory spinal anaesthesia by using small dose intrathecal local anaesthetic was recently described (86).
An upper-extremity vein was cannulated for vascular access. No attempt was made to prehydrate the patient before placement of the spinal needle.  The spinal anaesthetic dose was placed with a 25 gauge spinal needle with the patient in the sitting position.  Lidocaine 25mg with fentanyl 25 μg or ropivacaine 4mg with fentanyl 25 μg were used for low spinal injection.
After sitting upright for at least 10 min the patient was placed in the operative position for perineal or rectal surgery. The need for increased iv fluids and/or vasopressor administration was assessed by the anaesthetist.Buckenmaier et al (86) proved that ultra-small dose of ropivacaine 4mg is similar to lidocaine 25 mg in providing acceptable surgical anaesthesia where patient positioning and the local anaesthetic dose were manipulated to achieve isolated selective sacral anaesthesia while attempting to avoid lower extremity weak. 

Key-points:

1. Administration of spinal anaesthesia implies proper patient selection including history of vasovagal attacks, anticipated blood loss, and the use of vasodilators.
2. Psychological and pharmacological preparation to abolish fear and pain, is mandatory.
3. Lateral tilting of caesarean section patients is a must to guard against the supine hypotension syndrome.
4. For proper spinal anaesthesia, proper fluid support is essential perioperatively to optimize venous return.
5. With continuing blood loss,there might be a sudden fall of blood pressure,heart rate and peripheral resistance.
6. In pregnancy; regional  anaesthesia ,haemorrhage and supine aortocaval compression are additive when combined,affecting  the haemodynamics
7. It is crucial to understand the role of drugs used in haemodynamic support including oxygen, vasopressors and inotropes.
8. During spinal anaesthesia, basic and advanced life support is early resorted to, if needed.
9. More use of selective spinal anaesthesia should be encouraged for normal delivery and minor-to-moderate gynaecological day-case surgical procedures.

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