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Delayed Rocuronium Onset in a Patient Taking Levetiracetam for Epilepsy: A Case Report
Toru YamamotoDDS, PhD,
Yuhei KoyamaDDS, PhD,
Yutaka TanakaDDS, PhD, and
Kenji SeoDDS, PhD
Article Category: Case Report
Volume/Issue: Volume 71: Issue 2
Online Publication Date: Jul 08, 2024
DOI: 10.2344/23-00018
Page Range: 76 – 80

Many drugs can impact nondepolarizing muscle relaxants (NDMRs), leading to prolonged or enhanced neuromuscular blockade. Long-term use of antiepileptic drugs (AEDs) such as carbamazepine, phenytoin, and valproic acid has been reported to be associated with resistance to both the aminosteroidal (eg, rocuronium, vecuronium) and benzylisoquinolinium (eg, atracurium, cisatracurium) NDMRs. 1–10 Reports on the effects of newer AEDs (eg, lamotrigine, levetiracetam) on rocuronium are scarce and may not be well recognized. Herein, we report a case of delayed

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Figure 1.; Beta lactam structure. Penicillins and cephalosporins contain a beta lactam ring (asterisk) that conveys their antimicrobial action and is the target for microbial resistance.
Daniel E. Becker
<bold>Figure 1</bold> .
Figure 1 .

Beta lactam structure. Penicillins and cephalosporins contain a beta lactam ring (asterisk) that conveys their antimicrobial action and is the target for microbial resistance.

Figure 1; Influences provided by vasodilators. Cardiac output is the principal determinant of systolic pressure while arterial resistance determines diastolic pressure. Venous dilation reduces venous return and subsequent cardiac output, while arterial dilation reduces arterial resistance. This accounts for the value of vasodilation in managing hypertension. In contrast, benefits for managing coronary artery disease (CAD) and congestive heart failure (CHF) relate to reducing stresses on the heart—preload and afterload. Preload (venous return) is a stress factor during diastole, and afterload (arterial resistance) stresses the heart during systole.
Daniel E. Becker
Figure 1
Figure 1

Influences provided by vasodilators. Cardiac output is the principal determinant of systolic pressure while arterial resistance determines diastolic pressure. Venous dilation reduces venous return and subsequent cardiac output, while arterial dilation reduces arterial resistance. This accounts for the value of vasodilation in managing hypertension. In contrast, benefits for managing coronary artery disease (CAD) and congestive heart failure (CHF) relate to reducing stresses on the heart—preload and afterload. Preload (venous return) is a stress factor during diastole, and afterload (arterial resistance) stresses the heart during systole.

; Figure 5. Cardiovascular effects of epinephrine and phenylephrine. Epinephrine increases heart rate (HR) by activating beta-1 receptors in the sinoatrial node, the heart's normal pacemaker. It also activates beta-1 receptors on myocardial cells, increasing their contractility and increasing systolic blood pressure (SBP). However, at low doses such as those provided in local anesthetic formulations, it activates beta-2 receptors on systemic arteries, producing vasodilation. This decline in arterial resistance produces a reduction in diastolic pressure (DBP). The sum of these effects results in little change of mean arterial pressure (MAP). In contrast, phenylephrine activates only alpha receptors, increasing arterial resistance and diastolic pressure. Systolic pressure also rises as the heart compensates for this increase in resistance by increasing its contractility and venoconstriction increases venous return (preload). The net effect is an increase in mean arterial pressure, which is sensed in baroreceptors, and a reflex slowing of heart rate supervenes. (Adapted from Westfall et al.11)
Daniel E. Becker

Figure 5. Cardiovascular effects of epinephrine and phenylephrine. Epinephrine increases heart rate (HR) by activating beta-1 receptors in the sinoatrial node, the heart's normal pacemaker. It also activates beta-1 receptors on myocardial cells, increasing their contractility and increasing systolic blood pressure (SBP). However, at low doses such as those provided in local anesthetic formulations, it activates beta-2 receptors on systemic arteries, producing vasodilation. This decline in arterial resistance produces a reduction in diastolic pressure (DBP). The sum of these effects results in little change of mean arterial pressure (MAP). In contrast, phenylephrine activates only alpha receptors, increasing arterial resistance and diastolic pressure. Systolic pressure also rises as the heart compensates for this increase in resistance by increasing its contractility and venoconstriction increases venous return (preload). The net effect is an increase in mean arterial pressure, which is sensed in baroreceptors, and a reflex slowing of heart rate supervenes. (Adapted from Westfall et al.11)

Figure 4; Norwood operation. This operation is the first stage in the serial surgical treatment. The purpose of this operation is to reduce blood flow resistance from the RV to the A or PA. PDA and the base of the PA are separated from the PA and connected to the A. Blood returns to the PA passes the RV-PA conduit.
Figure 4
Figure 4

Norwood operation.

This operation is the first stage in the serial surgical treatment. The purpose of this operation is to reduce blood flow resistance from the RV to the A or PA. PDA and the base of the PA are separated from the PA and connected to the A. Blood returns to the PA passes the RV-PA conduit.

Figure 4.; Mechanism of vasopressinergic vs adrenergic vasoconstriction. Vasopressin (V1) receptor activation by vasopressin produces short-term vasoconstriction that increases vascular resistance and mean arterial pressure (MAP).14 V1 receptor agonists are effective in patients with severe hypotension and renin-angiotensin-aldosterone system (RAAS) blockade when conventional adrenergic treatment fails.15
Caitlin M. Waters,
Kristen Pelczar,
Edward C. Adlesic,
Paul J. Schwartz, and
Joseph A. Giovannitti Jr
Figure 4.
Figure 4.

Mechanism of vasopressinergic vs adrenergic vasoconstriction. Vasopressin (V1) receptor activation by vasopressin produces short-term vasoconstriction that increases vascular resistance and mean arterial pressure (MAP). 14 V1 receptor agonists are effective in patients with severe hypotension and renin-angiotensin-aldosterone system (RAAS) blockade when conventional adrenergic treatment fails. 15

Figure 1.; Determinants of arterial blood pressure. The first step for improving blood pressure is to increase venous return (preload). When this proves unsuccessful, contractility must be improved. Arterial resistance and heart rate are rarely primary targets, because they produce a greater impact on myocardial oxygen requirements.
Daniel E Becker and
Daniel A Haas
Figure 1.
Figure 1.

Determinants of arterial blood pressure. The first step for improving blood pressure is to increase venous return (preload). When this proves unsuccessful, contractility must be improved. Arterial resistance and heart rate are rarely primary targets, because they produce a greater impact on myocardial oxygen requirements.

Figure 2.; Muscle Relaxation Monitor. A, NMT module with electrode clips and acceleration detection monitor. B, The acceleration detection monitor attached to the patient’s thumb along with 2 electrodes used to stimulate the ulnar nerve.
Toru Yamamoto,
Yuhei Koyama,
Yutaka Tanaka, and
Kenji Seo
Figure 2.
Figure 2.

Muscle Relaxation Monitor.

A, NMT module with electrode clips and acceleration detection monitor. B, The acceleration detection monitor attached to the patient’s thumb along with 2 electrodes used to stimulate the ulnar nerve.

Figure 1.; Clinical Picture and Chest Radiograph of the Patient. A, Side view of the patient. B, AP chest radiograph demonstrating significant scoliosis and tracheal deviation.
Toru Yamamoto,
Yuhei Koyama,
Yutaka Tanaka, and
Kenji Seo
Figure 1.
Figure 1.

Clinical Picture and Chest Radiograph of the Patient.

A, Side view of the patient. B, AP chest radiograph demonstrating significant scoliosis and tracheal deviation.

Figure 4; Determinants of arterial pressure. Mean arterial pressure (MAP) is the time-weighted average of systolic blood pressure (SBP) and diastolic blood pressure (DBP). The principal determinant of SBP is stroke volume, which is increased by venous return (preload) and contractility. DBP is determined primarily by arterial resistance, which also provides afterload against which the ventricles must work to eject stroke volume (dotted arrow). + indicates positive influence; −, negative influence.
Andrew B. Casabianca and
Daniel E. Becker
Figure 4
Figure 4

Determinants of arterial pressure. Mean arterial pressure (MAP) is the time-weighted average of systolic blood pressure (SBP) and diastolic blood pressure (DBP). The principal determinant of SBP is stroke volume, which is increased by venous return (preload) and contractility. DBP is determined primarily by arterial resistance, which also provides afterload against which the ventricles must work to eject stroke volume (dotted arrow). + indicates positive influence; −, negative influence.