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LETTERS TO THE EDITOR

Cardiac Arrest During Spinal Anesthesia

Department of Anesthesia, Green Lane Hospital, Auckland, New Zealand

To the Editor:

Pollard is to be commended on his article (1) about the serious problem of cardiac arrests during spinal anesthesia (SA). One possible fundamental mechanism for these cardiac arrests, sudden vasodilation in muscle beds above and below the level of the block leading to severe loss of afterload, could have been added.

Studies involving syncope were mentioned by Pollard (1). These studies are important because there are distinct similarities between other forms of syncope and the phenomena seen with cardiac arrest under SA. These include sudden bradycardia, involvement of cardiac receptors, the concept of loss of preload being a fundamental trigger to the sequence, and, of course, the essence of speed (this is a fast response). Furthermore, studies of "non-SA" syncope may provide insights about cardiac arrest under SA. In particular these studies strongly suggest that decreased afterload is a fundamental mechanism of "non-SA" syncope.

Fifty-five years ago, venesection (to the point of syncope) was shown to lead to progressive hypotension accompanied by rising heart rate (HR) and increased peripheral resistance. Before syncope, however, HR decreased suddenly, as did peripheral resistance (2). Others showed that this vasodilation occurs in arterial vessels to skeletal muscles and activates in <10 s (3). Another study showed that susceptible individuals who are provoked into syncope experience serious hypotension even with HR supported by internal cardiac pacing (4). Severe vasodilation, distinct from bradycardia, is clearly involved in this syncope.

Vasoconstriction above the block level is a significant compensation mechanism for the "partial sympathetic blockade" of SA (5). In addition, arterial vessels in the block region are not maximally dilated (5). If under SA, reduced venous return induces cardiac receptors into causing sudden bradycardia (which is what Pollard rightly suggests), is it not possible that the important other mechanism of "normal" human vasovagal responses is activated as well? Could profound additional arterial vasodilation be occurring rapidly in the block area and in previously constricted vessels above the block?

If pathophysiologic arterial vasodilation is operative, this suggests management of hypotension and bradycardia in the context of SA involves early administration of intravascular fluids and/or vasoactive drugs that are vasoconstrictors, such as ephedrine, as opposed to reliance on atropine. If SA leads to cardiac arrest, full epinephrine resuscitation doses would be logical and critical.

References

1. Pollard JB. Cardiac arrest during spinal anesthesia: common mechanisms and strategies for prevention. Anesth Analg 2001; 92: 252–6.[Free Full Text]
2. Barcroft H, Edholm OG, McMichael J, Sharpey-Schafer EP. Post hemorrhagic fainting: study by cardiac output and forearm flow. Lancet 1944; 15: 489–91.
3. Wallin BG, Sundlof G. Sympathetic outflow to muscles during vasovagal syncope. J Auton Nerv Syst 1982; 6: 287–91.[Web of Science][Medline]
4. Sra JS, Jazayeri MR, Avitall B, et al. Comparison of cardiac pacing with drug therapy in the treatment of neurocardiogenic (vasovagal) syncope with bradycardia or asystole. N Engl J Med 1993; 328: 1085–90.[Abstract/Free Full Text]
5. Cousins MJ, Bridenbaugh PO. Neural blockade in clinical anesthesia and management of pain. 2nd edition. Philadelphia: Lippincott Williams & Wilkins; 1988, pp 230–1.

Response

Palo Alto Health Care System, Palo Alto, CA

In Response:

I am thankful that Dr. Cooper emphasized that vasoconstriction above the block level is an important compensatory mechanism during central neuraxial blockade and that vasodilation can trigger cardiac arrest. As stated in the article (1), decreases in afterload can contribute to these arrests and there are at least five cases in which bradycardia or cardiac arrest during epidural anesthesia were associated with initiating sodium nitroprusside (2). In two of these cases, pulmonary artery pressures were noted to decrease just before the onset of bradycardia. Vasodilation worsens hypovolemia and can predispose these patients to cardiac arrest.

If pathophysiologic arterial vasodilation is operative, then the use of epinephrine could be an ideal treatment. Evidence that epinephrine alone may be insufficient to treat bradycardia or full arrest during extensive sympathetic blockade comes from the observation that there have been at least seven patients who have developed severe bradycardia or cardiac arrest during epidural anesthesia while an epinephrine infusion was administered (2,3). Liguori and Sharrock (2) offered two explanations for this. One is that the increase in contractility resulting from epinephrine may contribute to reflex slowing attributed to the Bezold-Jarish reflex. Alternatively, because epinephrine has no effect on the vagal response, these failures provide additional evidence for the importance of the vagal limb in these arrests.

Good outcomes after severe bradycardia and cardiac arrest during spinal anesthesia have been reported when both atropine and a vasopressor have been used to treat these events (4–6). Both epinephrine and atropine (in addition to transcutaneous pacing) are widely recommended to treat asystole.

Ideally, many of these arrests can be avoided by administering sufficient volumes of IV fluids to avoid severe hypovolemia and an overwhelming vagal response. However, when acute vasodilatation, swift blood loss, or other causes rapidly decrease preload with a profound vagal response, all potentially useful treatments should be considered. The rapid infusion of fluids, the administration of atropine, and the use of a vasopressor are all appropriate interventions in this setting.

References

1. Pollard JB. Cardiac arrest during spinal anesthesia: Common mechanisms and strategies for prevention. Anesth Analg 2001; 92: 252–6.
2. Ligouri G, Sharrock N. Asystole and severe bradycardia during epidural anesthesia in orthopedic patients. Anesthesiology 1997; 86: 250–7.[Web of Science][Medline]
3. Heidegger T, Kreienbuhl G. Unsuccessful resuscitation under hypotensive epidural anesthesia during elective hip arthroplasty. Anesth Analg 1998; 86: 847–9.[Medline]
4. Brown DL, Carpenter RL, Moore DC, et al. Cardiac arrest During Spinal Anesthesia III (letter). Anesthesiology 1988; 68: 971–2.
5. Geffin B, Shapiro L. Sinus bradycardia and asystole during spinal and epidural anesthesia: a report of 13 cases. J Clin Anesth 1998; 10: 278–85.[Web of Science][Medline]
6. Lovstad RZ, Granhus G, Hetland S. Bradycardia and asystolic arrest during spinal anesthesia: a report of five cases. Acta Anaesthesiol Scand 2000; 44: 48–52.[Web of Science][Medline]

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a colleague Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Cooper, J. Articles by Pollard, J. Search for Related Content PubMed PubMed Citation Articles by Cooper, J. Articles by Pollard, J.