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Anesthesiology:
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Mechanisms of Hypotension and Bradycardia during Regional Anesthesia in the Sitting Position

Liguori, Gregory A. M.D.*; Kahn, Richard L. M.D.; Gordon, Michael A. M.D.; Urban, Michael K. M.D., Ph.D.

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To the Editor:—
We would like to commend Drs. Campagna and Carter for their informative review 1 on the Bezold-Jarisch reflex and mechanisms of heart rate and blood pressure regulation. It is clear from their exhaustive report that these mechanisms are complex, interactive, and, as yet, not fully understood.
We disagree, however, with the authors’ interpretation of previously proposed mechanisms of hypotension and bradycardia during shoulder surgery in the sitting position under peripheral nerve blockade. They state that others have attributed these cardiac events to “peripheral vasodilation from the sitting position” as well as “venous pooling in the setting of peripheral nerve blockade.” However, the mechanism D’Alessio et al.2 proposed to account for activation of the Bezold-Jarisch reflex is in fact “venous blood pooling (induced by the sitting position), and a heightened cardiac contractile state (induced by the β-adrenergic effects of epinephrine).”
During anesthesia under interscalene block, the resulting blockade of sympathetic innervation to the upper extremity results in vasodilation only in that arm with minimal, if any, systemic hemodynamic effects. The venous pooling is more likely related to the sitting position rather than the peripheral nerve blockade. There is evidence that during tilt table testing, positive responders have an associated decrease in left ventricular volume due to lower extremity venous pooling. 3 It is reasonable to assume some degree of venous pooling in the beach chair position as well.
We believe that the important activating events are central volume depletion and vigorous cardiac contractions. Jacobsen et al.4 evaluated central volume depletion diagnosed echocardiographically secondary to epidural anesthesia and found a relationship with acute bradycardia. Contrary to the current authors’ assertion, the studies by Liu et al.5 and Davrath et al.6 did in fact reveal that patients with a positive tilt response had a decrease in left ventricular volumes, although modest in nature. These reports lend support to the hypothesis that some degree of central volume depletion is involved in this reflex.
We believe that the relative contribution of the central volume depletion to the degree of fractional shortening is the key to activation of reflex slowing. For example, a vigorously contracting, moderately empty ventricle may be as prone to slowing as a normally contracting, severely depleted one. To our knowledge, this has not been formally evaluated, but it may explain some of the contradictions in various published studies.
The reference the current authors cite for “no evidence of increased contractility in response to concentrations of epinephrine seen in local anesthetic mixtures for nerve block”7 actually refers to epidural, not peripheral neural, blockade. Furthermore, that study shows that epinephrine causes complex dose-dependent effects on cardiac output, stroke volume, and vascular resistance in the described situations, making actual determinations of contractility difficult to predict. During shoulder surgery in the sitting position under interscalene block, there are other sources of exogenous epinephrine, in addition to that added to the local anesthetic. These sources include subcutaneous infiltration by the surgeons, and epinephrine added to the irrigating solution used for arthroscopy. This additional epinephrine is likely absorbed during the case and may, as in Bonica et al.’ s study, 7 affect hemodynamic variables.
Finally, the authors cite a case as evidence that the mechanism involved is not the Bezold-Jarisch reflex. A variety of potential causes of the hypotension and bradycardia are observed in this patient, including local anesthetic toxicity, preexisting cardiac pathology, or reflex events. Without additional information, this case offers no insight into the mechanisms of hypotension and bradycardia in this setting.
“Taken as a whole,” we believe that the literature does support the mechanism of the Bezold-Jarisch reflex in this clinical scenario. It certainly is not conclusive, and further clinical studies must be performed before making definitive statements.
Gregory A. Liguori, M.D.*
Richard L. Kahn, M.D.
Michael A. Gordon, M.D.
Michael K. Urban, M.D., Ph.D.
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References

1. Campagna JA, Carter C: Clinical relevance of the Bezold-Jarisch reflex. A nesthesiology 2003; 98: 1250–60

2. D’Alessio JG, Weller RS, Rosenblum M: Activation of the Bezold-Jarisch reflex in the sitting position for shoulder arthroscopy using interscalene block. Anesth Analg 1995; 80: 1158–62

3. Shalev Y, Gal R, Tchou PJ, Anderson AJ, Avitall B, Akhtar M, Jazayeri MR: Echocardiographic demonstration of decreased left ventricular dimensions and vigorous myocardial contractions during syncope induced by head-up tilt. J Am Coll Cardiol 1991; 18: 746–51

4. Jacobsen J, Sofelt S, Brocks V, Fernandes A, Warberg J, Secher N: Reduced left ventricular diameters at onset of bradycardia during epidural anaesthesia. Acta Anaesthesiol Scand 1992; 36: 831–6

5. Liu JE, Hahn RT, Stein KM, Markowitz SM, Okin PM, Devereux RB, Lerman BB: Left ventricular geometry and function preceding neurally mediated syncope. Circulation 2000; 101: 777–83

6. Davrath LR, Gottshall RW, Tucker A, Sadeh WZ, Lukasen GJ, Downes TR, Coonts CC: The heart is not necessarily empty at syncope. Aviat Space Environ Med 1999; 70: 213–9

7. Bonica JJ, Akamatsu TJ, Berges PU, Morikawa K, Kennedy WF: Circulatory effects of peridural block: II. Effects of epinephrine A nesthesiology 1971; 34: 514–22

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