**Table 4.**

 *Vasopressors used for prevention and treatment of spinal/epidural anesthesia-induced hypotension.* *Cardiac Arrest Following Central Neuraxial Block DOI: http://dx.doi.org/10.5772/intechopen.106600*

also be done simultaneously as bradycardia may be the manifestation of reduced preload. The possibility of cephalad spread of hyperbaric local anesthetic and hemodynamic effects must be anticipated. When the level of the sensory block is higher than or at T6, there can be pooling of 20% circulating blood volume in the hepato-splanchnic region and this volume can be mobilized by the use of vasopressors [76]. A transcutaneous pacemaker should be used if bradycardia is not responding [77].

**Treatment of hypotension:** Incidence of hypotension during spinal is 47% [47]. Systolic blood pressure less than 80% of the baseline value should be treated [68]. Mean arterial pressure should be targeted more than systolic blood pressure. When the same level of dermatomal block is achieved following epidural and spinal anesthesia, the incidence of hypotension is similar, although the onset of hypotension may be slower with epidural anesthesia [3].

20 degrees head low position, co-loading with colloids or crystalloids (around 1000 ml) and vasopressors are used for treatment. Ephedrine is used when there is bradycardia and hypotension [66]. Phenylephrine 100 mcg is used for the treatment of hypotension (100 mcg bolus or 10 mg ampoule in 100 ml saline—100 mcg/ml, i.e., 1 ml/min drip-rate). Phenylephrine can reduce the level of spinal and produce hypertensive crises when administered with atropine [40]. Reflex bradycardia due to hypertension usually limits hypertensive crises. Noradrenaline can also be used instead of phenylephrine with less risk of bradycardia. A combination of caffedrine (covalently linked norephedrine and theophylline) having an inotropic effect and theodrenaline (covalently linked noradrenaline and theophylline) having vasoconstricting effect is used in Germany. The combination has early-onset and long-lasting hypertensive effects [70, 71]. Additional evidence is awaited (**Table 4**).

**Treatment of cardiac arrest:** Vasodilatation during spinal anesthesia can make resuscitation refractory [3]. Epinephrine is to be administered after CA to maintain coronary perfusion pressure of 15–20 mm of Hg. Rosenberg has recommended 0.01–0.1 mg/kg adrenaline for the treatment of refractory bradycardia but once CA develops one mg of adrenaline must be administered. Spinal anesthesia blocks nerves going to the adrenal glands. Their suppression results in a reduction in circulating levels of noradrenaline and adrenaline during the stress of CA and is an important reason for refractory CA [78]. Adrenaline is not having a vagolytic effect and its use does not preclude the use of other drugs [1]. Veno-arterial ECMO can be used if ROSC is not restored. It may be difficult to find out the cause of cardiac arrest. 12 lead ECG, Troponin test, S. tryptase and 2D Echo would be helpful to diagnose myocardial infarction, anaphylaxis, embolism and hypovolemia. Veno-arterial ECMO may be helpful during this period [79].

After the restoration of circulation, myocardial stunning may need vasopressor support for prolonged period. Refractory cardiac failure may need to leave ventricular assist device [27].

Summary of treatment of bradycardia and cardiac arrest:

	- a.Atropine 0.4–0.6 mg, IV, b. Ephedrine 25–50 mg, c. Epinephrine 0.2–0.3 mg.

#### **Figure 3.**

*Treatment of cardiac arrest under spinal/epidural block. \*LAST—Local anesthetic systemic toxicity, \*\*Be careful if arrest is within 30 minutes after block as there is risk of higher spread of local anesthetic. \*\*\*ROSC— Restoration of spontaneous circulation.*

Reposition the patient and stop surgical stimulus.

## **Treatment of local anesthetic systemic toxicity (LAST)**:

LAST needs a special mention. Seizures should be suppressed immediately to reduce oxygen consumption, and prevent hypoxia and hypercarbia. Administration of a benzodiazepine (midazolam 1 to 2 mg I.V.) is preferred. If ventilation is inadequate, suxamethonium is administered and the airway is secured. The management of ventricular arrhythmias and CA as a result of LAST is different than other CA scenarios and may require prolonged effort [50]. Amiodarone and defibrillation are used for the treatment of ventricular fibrillation. Lignocaine should not be used. Based on animal studies, the bolus dose of epinephrine is to be reduced to ≤1 mcg/ kg IV to avoid arrhythmogenic effects. The optimal dose of epinephrine is unknown. *Cardiac Arrest Following Central Neuraxial Block DOI: http://dx.doi.org/10.5772/intechopen.106600*

#### **Figure 4.**

*Treatment of cardiac arrest due to local anesthetic systemic toxicity (LAST). \*Do not use vasopressin. \*\*Do not use lignocaine/procainamide to treat ventricular fibrillation. \*\*\* A bolus can be repeated once or twice and infusion rate should be doubled for persistent cardiovascular instability. An infusion should be continued for at least 10 minutes after achieving hemodynamic stability. Maximum dose is approximately 12 ml/kg. # ECMO— Extracarporeal membrane oxygenator, ##ECHO—echocardiolography.*

Vasopressin should not be used as it can lead to pulmonary hemorrhage. Administer 20% lipid emulsion along with advanced cardiac life support or when neurotoxicity is evident. 1.5 mL/kg bolus followed by infusion at 0.25 ml/kg/minute IV (for patient**≤**70 kg) and 100 ml I.V., followed by the infusion of 200 to 250 ml I.V. over 15 to 20 minutes (for patient **>**70 kg). A bolus can be repeated once or twice and the infusion rate should be doubled for persistent cardiovascular instability. An infusion should be continued for at least 10 minutes after achieving hemodynamic stability. The maximum dose is approximately 12 ml/kg. Lipid emulsion improves cardiac conduction, contractility, and coronary perfusion by drawing the lipid-soluble local anesthetic out of the cardiac tissue (**Figure 4**).

Propofol should not be used as a substitute for 20 percent intralipid. Cardiopulmonary bypass may be necessary to allow time for the local anesthetic to diffuse from cardiac receptors if advanced cardiac life support and intralipid emulsion are not effective and may be lifesaving [37].

Evolution in the knowledge of the pathophysiology of CNB, better availability of monitoring devices, safer local anesthetic agents and treatment, and now the outcome in the last two decades are better. Institution of timely treatment leads to recovery of patients without any sequelae [1].

Unfortunately, the fact remains that despite timely treatment death may result [9].

CNB is used frequently all over the world and the number of patients developing CA is reported in the current literature. The detailed analysis of these cases will help to prevent catastrophes in the future.

## **6. When to anticipate cardiac arrest?**

Unexpected CA may be observed in ASA grade I patients during spinal anesthesia [1]. Although the common belief is that CA usually occurs within the first 20–30 minutes, [32]; however, this is not true. Cardiac arrest has been reported within 12 to 72 minutes of spinal anesthesia and 180 min after epidural due to the residual sympathetic block [2, 5, 20, 35]. Lesser et al., while using automatic record keeping systems, observed that the mean interval to develop unexpected CA after the administration of spinal anesthesia was 58 minutes [53]. This finding is worrisome since after a short duration of surgical procedures, the situation can arise in the postoperative recovery room or ward when the situation might be worse. Close monitoring should be continued in the postoperative period [21].

Sudden bradycardia and CA may develop in a patient under vigilance with normal vital parameters. It is yet a mystery. Brown et al. reported sudden loss of consciousness and CA during patient chatting with the anesthesiologist [76]. These situations are often attributed as the consequence of mismanagement of the spinal technique and not due to an intrinsic risk of the technique itself [32].

Vigilance will not prevent the episodes of catastrophe but will help to provide timely treatment effectively and uneventful recovery of the patient.

Consequences of cardiac arrest during central neural block:

Despite well-conducted CPR efforts, high mortality rates (26%) were observed in two French reviews by AUROY et al. [15, 16]. Reports during 2001 revealed that 89% of patients had neurological damage or death [30]. The use of atropine with vasopressors resulting in successful resuscitation with minimal or no neurological damage is reported later on in many studies [9, 29, 53]. Caplan pointed out that those patients in whom epinephrine was used after 8 minutes of CA had a worse prognosis [7]. Ayuroy et al. reported that epinephrine was used in less than half of the patients with severe bradycardia and the mortality rate was 25% [48]. If the patient develops CA, prolonged resuscitation efforts may be needed, especially if a high sympathetic blockade is present and also for the treatment of LAST [32, 37].

Evolution in the knowledge of the pathophysiology of CNB, better availability of monitoring devices, safer local anesthetic agents and early treatment, and now the outcome have improved a lot in the last two decades [5, 6, 8]. After restoration of circulation, myocardial stunning may need vasopressor support or left ventricular assist device for refractory cardiac failure [27].

*Cardiac Arrest Following Central Neuraxial Block DOI: http://dx.doi.org/10.5772/intechopen.106600*

Patient with CA within 20 minutes after spinal has a better prognosis than delayed CA (more than 40 minutes), in which resuscitation is difficult due to blood loss during surgery, postural changes, and surgical procedures like cementing [16]. One should believe and intervene immediately if any detectable abnormalities are seen. Disbelief and insecurity are common patterns in this situation and may influence the outcome [32]. Therefore, the knowledge of the physiologic changes caused by CNB and its complications, proper patient selection, respecting the contraindications of the procedure, adequate monitoring, and constant vigilance are important deciding factors for outcome [8].

Anesthesiologists would face medicolegal problems following such incidents. It is necessary to maintain the proper documentation (preferably electronic medical record systems) of the preoperative status of patients, discussion during informed consent, details of technique, monitoring, perioperative events, consultation, and treatment. Anesthesiologists may be called upon long after the event and proper records will be very helpful to defend. Electronic medical record systems, reporting the adverse events to the national board, and finding out risk factors in a specific group of patients will help to improve patient safety in the future.

## **7. Discussion**

Anesthesiologists are facing problems as well as challenges and have raised queries long ago about unexpected cardiac arrest during CNB which are yet to be answered. Future research is needed in these directions [32].

When CNB is administered, physiological changes are almost always present. It is not clear why do some individuals have these severe complications while the majority of others do not? Efforts to identify the definitive risk population in the preoperative period are needed. Hypovolemia is difficult to diagnose as well as assess clinically during perioperative period and therefore to treat up to the mark. Perioperative treatment of hypovolemia is essential, although it might not be the key factor in preventing hemodynamic instability during CNB [63]. It seems additional knowledge regarding the effect of reduced venous return, vasodilatation, and several reflexes mediated by intrinsic and/or neural mechanisms is needed. Are we missing any links?

We still do not understand what the definitive cause of sudden onset CA is during CNB when vital parameters in immediate pre-arrest period are normal. What happens during the period immediately preceding the cardiac arrest? Is automatic record keeping the answer? Unfortunately, information about this is inadequate and not provided by authors even while reporting an account of their cases recorded by automated anesthesia record keepers [53]. Finding out this information would be difficult without continuous invasive arterial blood pressure monitoring [32]. We need to find out whether this mystery can be solved by using advanced noninvasive hemodynamic monitors such as echocardiography, biomedical impedance, and inferior vena cava dimensions during the perioperative period.

One more dilemma is regarding the dosages of atropine. Whether we should use a higher dose of Atropine (1 mg) to treat bradycardia during CNB as recommended treating other bradyarrhythmias as per AHA 2020 guidelines? Should we use atropine during treatment of cardiac arrest following spinal anesthesia as there is no parasympatholytic action to adrenaline [1]. Atropine is not included in the treatment of asystole as per AHA 2019 guidelines [80].

Are cardiac arrests reported long after spinal/epidural anesthesia has been administered, really due to the anesthetic technique? How to establish the cause effect relationship is a real challenge. CA is reported in postoperative period as late as 72 minutes after epidural anesthesia [5, 20]. What is the adequate timing for sending the patient back to the ward? Guidelines are not uniform and definitive. Is it enough to wait till the recovery of motor and sensory blocks? Sympathetic block outlasts motor block. Is it justified to send the patient inward when he is moving lower limbs or should we wait till the patient voids urine spontaneously? We have to find out userfriendly device to assess sympathetic block.

## **8. Summary and conclusions**

Without any question, central neuraxial blocks are safe and are indispensable techniques in the practice of modern anesthesia. However, safety should not be taken for granted. Although the development of bradycardia is predictable, one should not forget that the possibility of acute evolution to CA is real. The severity of CA increases because ASA grade I young patients may be affected by undergoing elective surgeries unexpectedly.

The definitive etiology of CA following CNB is still not known and seems to be multifactorial. Sympathetic blockade producing a reduction in preload seems to be the founding stone and parasympathetic over activity, the final common pathway of the etiology of CA. Abrupt changes in patient position, intraoperative blood loss, use of vasodilators, release of tourniquet, etc., can trigger the effects resulting from reduced preload contributing to CA, particularly in elderly patients. Patients treated with beta-blockers, the "vagotonic" patients, and patients undergoing hip surgery are more likely to develop CA. Proper selection of patients and type of anesthesia, and adequate monitoring and constant vigilance are essential for early diagnosis, treatment, and successful outcome following CA. CNB technique has to be modified (unilateral spinal, CSE, or continuous spinal) along with invasive monitoring if these blocks are be administered in critical patients having compromised cardiac function. Atropine premedication would be useful in vagotonic patients. Preloading with colloids or co-loading with colloids or crystalloids, vasopressors, head low position may be helpful in preventing and treating hypotension. Early use of adrenaline for treating severe bradycardia, if atropine is not effective reduces the chances of CA and increases the chances of successful revival without subsequent morbidity. A better understanding of the physiologic changes caused by CNB and its complications, availability of safe local anesthetic drugs, and monitoring devices contribute to a successful outcome after CA and complete recovery of the patient. Sympathetic blockade causes significant vasodilatation, which might make CPR difficult, and long-duration CPR may be necessary. Effective and aggressive treatment is necessary to improve the prognosis following CA. ECMO, left ventricular assist device, non-invasive monitors such as abdominal USG (for the size of inferior vena cava), and echocardiography can be useful diagnostic tools if cardiac failure is persistent or CA is refractory. A high index of suspicion and respecting the contraindications of the spinal and epidural block are equally important. Continuous vigilance during and after the procedure till complete recovery after spinal and epidural is essential as unexpected CA can occur at any time during this period.

Electronic medical records and a national registry of cases of CA following central neuraxial block will enable to conduct the research and better understanding of risk factors and etiology of unexpected CA. With the popularity of spinal anesthesia and the reported frequency of these arrests, the potential impact of these interventions on further improving the safety of spinal anesthesia could be substantial.

*Cardiac Arrest Following Central Neuraxial Block DOI: http://dx.doi.org/10.5772/intechopen.106600*

## **Author details**

Sadhana S. Kulkarni1 \* and Savani S. Futane2

1 MGM Medical College Aurangabad, Constituent Unit of MGMIHS, Navi Mumbai, Maharashtra, India

2 Maharashtra Postgraduate Institute of Medical Education and Research, Nashik, Maharashtra, India

\*Address all correspondence to: kulkarnisadhana@yahoo.com

© 2022 The Author(s). Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Section 6
