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General Anesthetic Management of a Patient With Hypertrophic Cardiomyopathy for Oral Surgery: Did Digitalis Contribute to Bradycardia?
Aiji Sato(Boku) DDS, PhD,
 Maki Morita DDS,
 MinHye So MD,
 Tetsuya Tamura MD, PhD,
 Fumiaki Sano MD,
 Yasuyuki Shibuya DDS, PhD,
 Jun Harada MD, PhD, and
 Kazuya Sobue MD, PhD
Article Category: Case Report
Volume/Issue: Volume 65: Issue 3
Online Publication Date: Jan 01, 2018
DOI: 10.2344/anpr-65-03-12
Page Range: 192 – 196

-controlled infusion). The SVV during this time was 5%, with CI of 1.5 L/min/m 2 and SV of 30 mL/beat. We were concerned with administering phenylephrine due to possible reflex bradycardia, as vagal nerve blockade with atropine was ineffective. Circulatory management was therefore provided with dopamine started and maintained at 3 mcg/kg/min. This improved the patient's heart rate to 50 beats/min, blood pressure to 100 mm Hg systolic, SVV 9%, CI to 3.0 L/min/m 2 , and SV to 60 mL/beat within 10 minutes of administration ( Table 2 ). Before the end of the surgery, we administered

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; Arrows indicate the timing each medication was administered. Ephedrine was given at 8 mg/bolus, phenylephrine at 0.05 mg/bolus, and dopamine at 2 μg/kg/min.
Naohiro Ohshita,
 Shoko Gamoh,
 Masahiko Kanazumi,
 Masahiro Nakajima,
 Yoshihiro Momota, and
 Yasuo M. Tsutsumi

Arrows indicate the timing each medication was administered. Ephedrine was given at 8 mg/bolus, phenylephrine at 0.05 mg/bolus, and dopamine at 2 μg/kg/min.

; Figure 4. Catecholamine synthesis. The molecular structure of catecholamines includes a catechol and an amine. During their termination, each of these moieties is a target for a specific enzyme, ie, catechol-O-methyltransferase (COMT) and monoamine oxidase (MAO). Catecholamine synthesis proceeds in a stepwise fashion, each step driven by a specific enzyme leading to a molecular change indicated by the asterisks. In the adrenal medulla the final step in the pathway results in the synthesis of epinephrine. Sympathetic neurons do not contain the methylating enzyme and therefore cannot synthesize epinephrine. All 3 neurotransmitters are found throughout the brain, but neurons within the basal ganglia release dopamine because they lack dopamine hydroxylase.
Daniel E. Becker

Figure 4. Catecholamine synthesis. The molecular structure of catecholamines includes a catechol and an amine. During their termination, each of these moieties is a target for a specific enzyme, ie, catechol-O-methyltransferase (COMT) and monoamine oxidase (MAO). Catecholamine synthesis proceeds in a stepwise fashion, each step driven by a specific enzyme leading to a molecular change indicated by the asterisks. In the adrenal medulla the final step in the pathway results in the synthesis of epinephrine. Sympathetic neurons do not contain the methylating enzyme and therefore cannot synthesize epinephrine. All 3 neurotransmitters are found throughout the brain, but neurons within the basal ganglia release dopamine because they lack dopamine hydroxylase.

; Preoperative 12-lead electrocardiogram. Sinus bradycardia (heart rate 44 beats/min) and negative T wave (II, III, aVF, V3–6) were observed.
Aiji Sato(Boku),
 Maki Morita,
 MinHye So,
 Tetsuya Tamura,
 Fumiaki Sano,
 Yasuyuki Shibuya,
 Jun Harada, and
 Kazuya Sobue

Preoperative 12-lead electrocardiogram. Sinus bradycardia (heart rate 44 beats/min) and negative T wave (II, III, aVF, V3–6) were observed.

Figure 1; Pathophysiology of nausea and vomiting. Vomiting is caused by noxious stimulation of the vomiting center directly or indirectly via 1 or more of 4 additional sites: the gastrointestinal (GI) tract, the vestibular system, the chemoreceptor trigger zone, and higher centers in the cortex and thalamus. Once receptors are activated, neural pathways lead to the vomiting center, where emesis is initiated. Neural traffic originating in the GI tract travels along afferent fibers of cranial nerves IX (glossopharyngeal) and X (vagal). Antiemetic targets for drug interventions are predicated on their ability to block the illustrated receptor sites. Receptors illustrated along with their conventional ligands are as follows: H1 histamine, M1 acetylcholine, 5-HT3 serotonin, DA2 dopamine, NK1 (neurokinin) substance P, and mu/kappa opioids. Transmitter mediators in the cerebral cortex and thalamus are poorly understood, although cortical cannabinoid (CB1) pathways have been characterized.
Daniel E. Becker
Figure 1
Figure 1

Pathophysiology of nausea and vomiting. Vomiting is caused by noxious stimulation of the vomiting center directly or indirectly via 1 or more of 4 additional sites: the gastrointestinal (GI) tract, the vestibular system, the chemoreceptor trigger zone, and higher centers in the cortex and thalamus. Once receptors are activated, neural pathways lead to the vomiting center, where emesis is initiated. Neural traffic originating in the GI tract travels along afferent fibers of cranial nerves IX (glossopharyngeal) and X (vagal). Antiemetic targets for drug interventions are predicated on their ability to block the illustrated receptor sites. Receptors illustrated along with their conventional ligands are as follows: H1 histamine, M1 acetylcholine, 5-HT3 serotonin, DA2 dopamine, NK1 (neurokinin) substance P, and mu/kappa opioids. Transmitter mediators in the cerebral cortex and thalamus are poorly understood, although cortical cannabinoid (CB1) pathways have been characterized.

Prolonged Washout Period for Avoiding Azilsartan-Induced Refractory Hypotension During General Anesthesia for a Patient With Renal Impairment
Takayuki Hojo DDS, PhD,
 Yukifumi Kimura DDS, PhD,
 Keiji Hashimoto DDS,
 Takahito Teshirogi DDS, and
 Toshiaki Fujisawa DDS, PhD
Article Category: Case Report
Volume/Issue: Volume 68: Issue 4
Online Publication Date: Dec 15, 2021
DOI: 10.2344/anpr-68-02-08
Page Range: 220 – 223

.5%, oxygen 1 L/min and room air 2 L/min, plus a continuous remifentanil infusion 0.1 μg/kg/min. Profound hypotension of 48/31 (37) mm Hg with a heart rate of 83 bpm ensued 1 minute after intubation. Blood pressure remained low at 53/35 (39) mm Hg for ∼23 minutes after intubation despite repeated intravenous boluses of ephedrine (total dose 8 mg) and phenylephrine (total dose 1.2 mg). Meanwhile, the patient's heart rate remained stable at 81 bpm. Because of the patient's inadequate response to the previous vasopressors, a continuous dopamine infusion of 2 to 3 μg/kg/min was

Anesthetic Management of a Patient With Restless Legs Syndrome: A Case Report
Naohiro Ohshita DDS, PhD,
 Koji Yamagata PhD,
 Akio Himejima DDS, PhD,
 Kazuhiro Kaneda DDS, PhD,
 Teruyuki Yasutome DDS, PhD,
 Yoshiko Matsuda DDS, PhD,
 Yasuo M. Tsutsumi MD, PhD, and
 Yoshihiro Momota DDS, PhD
Article Category: Case Report
Volume/Issue: Volume 67: Issue 4
Online Publication Date: Dec 31, 2020
DOI: 10.2344/anpr-67-02-10
Page Range: 226 – 229

pramipexole (a dopamine agonist) after magnetic resonance imaging of her brain confirming no structural abnormalities. DISCUSSION RLS is a chronic neurological sensory disorder, first described in 1685, that interferes with rest and sleep. 1 – 3 The prevalence of RLS is typically low in Asian countries and approximately 1 to 4% in Japan. It has a higher prevalence in women versus men. Early-onset RLS has a peak incidence at 20 to 40 years of age, and a prevalence of 1.9% among children aged 8 to 11 years. 1 The onset of suspected RLS symptoms

Psychotropic Drugs: Implications For Dental Practice
Daniel E. Becker DDS
Article Category: Research Article
Volume/Issue: Volume 55: Issue 3
Online Publication Date: Jan 01, 2008
DOI: 10.2344/0003-3006-55.3.89
Page Range: 89 – 99

. Psychiatric illnesses are believed to result in part from biochemical derangements within the limbic structures. Much of this reasoning is based on known pharmacological actions of several psychotropic drug classes. For example, the efficacy of antipsychotic medications is attributed to inhibiting the actions of dopamine, and the psychoses are therefore believed to be attributable in some manner to excess dopamine transmission. This reasoning is hardly scientific and merely reflects our current futility in comprehending psychiatric illnesses. Psychotropic drugs are

Office-based General Anesthesia for a Patient With a History of Neuroleptic Malignant Syndrome
Zakaria S. Messieha DDS
Article Category: Case Report
Volume/Issue: Volume 70: Issue 1
Online Publication Date: Mar 28, 2023
DOI: 10.2344/anpr-69-04-01
Page Range: 20 – 24

of NMS ranges from 0.2% to 3.2% of psychiatric inpatients. While NMS is rare, it can be life threatening if unrecognized and not managed properly. 3 The pathogenesis of NMS is currently unknown. However, the 2 main postulated theories to explain NMS include central dopamine receptor blockade 6 or muscle defect. 7 , 8 Drugs that act to antagonize dopamine D2 receptors are usually found in most NMS cases, and a sudden decrease in central dopaminergic activity due to D2 blockade explains many of NMS's clinical features. Central dopamine receptor blockade

Nausea, Vomiting, and Hiccups: A Review of Mechanisms and Treatment
Daniel E. Becker DDS
Article Category: Research Article
Volume/Issue: Volume 57: Issue 4
Online Publication Date: Jan 01, 2010
DOI: 10.2344/0003-3006-57.4.150
Page Range: 150 – 157

dopamine, NK 1 (neurokinin) substance P, and mu/kappa opioids. Transmitter mediators in the cerebral cortex and thalamus are poorly understood, although cortical cannabinoid (CB 1 ) pathways have been characterized. Figure 1. Pathophysiology of nausea and vomiting. Vomiting is caused by noxious stimulation of the vomiting center directly or indirectly via 1 or more of 4 additional sites: the gastrointestinal (GI) tract, the vestibular system, the chemoreceptor trigger zone, and higher centers in the cortex and thalamus. Once receptors are activated