Isolated Bradycardia During Aneurysmal Clipping: Rebleed or Trigeminocardiac Reflex?

The most common cause of nontraumatic subarachnoid hemorrhage is the rupture of intracranial aneurysm. After initial bleed, the risk of rebleeding is highest in the early postictal period and this rebleed is strongly associated with poor neurological outcome. The major goal of anesthesia in these surgeries is to prevent the rebleed. If rebleeding occurs prior to the craniotomy, it results in the acute rise of intracranial pressure and usually presents as bradycardia and hypertension (Cushing’s reflex). Here we reported a case where rebleeding presented unusually as isolated bradycardia without associated hypertension and was mistaken as trigeminocardiac reflex. The surgeon was informed about the event and they planned to proceed. After craniotomy, despite all the efforts the brain was persistently tight and surgery could not be completed. Postoperative scan showed rebleeding and the patient died after a few days in ICU.We highlighted in this case report the fact that isolated transient bradycardia may also be the presentation of rebleed with closed cranial vault. It is not always necessary to see all the features of Cushing’s traid in every patient. If bradycardia occurs before the craniotomy, the surgeon should be notified, the severity of bleed should be assessed, and further management should be planned according to the severity of bleed.

The Effectiveness of Low-dose Dexmedetomidine Infusion in Sedative Flexible Bronchoscopy: A Retrospective Analysis

Background and objectives: Flexible bronchoscopy has been widely used for diagnosis and intervention, while various drugs are used for sedation during bronchoscopy. We examined two regular standardized sedation options (with or without dexmedetomidine) regularly used in our regional hospital. The aim was to assess the efficacy and safety of dexmedetomidine on conscious sedation under bronchoscopy. Materials and Methods: A retrospective chart review was conducted from April 2017 to March 2018. All patients undergoing flexible bronchoscopy with moderate sedation were enrolled. Patients having received dexmedetomidine-propofol-fentanyl were defined as group D, and those having received midazolam-propofol-fentanyl were defined as group M. The primary outcome was a safety profile during the procedure, including the incidence of procedural interference by patient cough or movement, transient hypoxemia, and hypotension. The secondary outcome was measured by the recovery profile (awake and ambulation time). Results: Thirty-five patients in group D and thirty-three in group M were collected in this retrospective study. All patients underwent the procedure successfully. Group D showed higher safety with fewer procedural interference incidences by cough or body movement than Group M (3.3% versus 36.3%, p < 0.001) and minor respiratory adverse effects. Patients in group D showed faster recovery in a shorter ambulation time than group M (24.9 ± 9.7 versus 31.5 ± 11.9, p = 0.02). In group D, bronchoscopist satisfaction to sedation was higher than group M (p = 0.01). More transient bradycardia episodes were noted in patients receiving dexmedetomidine (p < 0.05), but all recovered without atropine intervention. Overall post-procedural adverse events and satisfaction were comparable in the two groups. Conclusions: The co-administration of dexmedetomidine met the safety and recovery demands of flexible bronchoscopy. Compared to the conventional midazolam-propofol-fentanyl regimen, the application of dexmedetomidine improved sedative effectiveness with less procedural interruptions, shorter time to ambulation and higher bronchoscopist satisfaction.

Pelvic vein embolisation of gonadal and internal iliac veins can be performed safely and with good technical results in an ambulatory vein clinic, under local anaesthetic alone – Results from two years' experience

Objectives Pelvic vein embolisation is increasing in venous practice for the treatment of conditions associated with pelvic venous reflux. In July 2014, we introduced a local anaesthetic “walk-in walk-out” pelvic vein embolisation service situated in a vein clinic, remote from a hospital. Methods Prospective audit of all patients undergoing pelvic vein embolisation for pelvic venous reflux. All patients had serum urea and electrolytes tested before procedure. Embolisation coils used were interlock embolisation coils (Boston Scientific, USA) as they can be repositioned after deployment and before release. We noted (1) complications during or post-procedure (2) successful abolition of pelvic venous reflux on transvaginal duplex scanning (3) number of veins (territories) treated and number of coils used. Results In 24 months, 121 patients underwent pelvic vein embolisation. Three males were excluded as transvaginal duplex scanning was impossible and six females excluded due to lack of complete data. None of these nine had any complications. Of 112 females analysed, mean age 45 years (24–71), 104 were for leg varices, 48 vulval varices and 20 for pelvic congestion syndrome (some had more than one indication). There were no deaths or serious complications to 30 days. Two procedures were abandoned, one completed subsequently and one was technically successful on review. One more had transient bradycardia and one had a coil removed by snare during the procedure. The mean number of venous territories treated was 2.9 and a mean of 3.3 coils was used per territory. Conclusion Pelvic vein embolisation under local anaesthetic is safe and technically effective in a remote out-patient facility outside of a hospital.

Cardiac response to startle stimuli in larval zebrafish: sympathetic and parasympathetic components

Central regulation of cardiac output via the sympathetic and parasympathetic branches of the autonomic nervous system allows the organism to respond to environmental changes. Sudden onset stimuli, startle stimuli, are useful probes to study central regulatory responses to the environment. In mammals, startle stimuli induce a transient bradycardia that habituates with repeated stimulation. Repeated presentation of the stimulus results in tachycardia. In this study, we investigate the behavioral regulation of heart rate in response to sudden stimuli in the zebrafish. Larval zebrafish show a stereotyped heart rate response to mild electrical shock. Naïve fish show a significant increase in interbeat interval that resolves in the 2 s following stimulation. This transient bradycardia decreases on repeated exposure to the stimulus. Following repeated stimulation, the fish become tachycardic within 1 min of stimulation. Both the transient bradycardia and following tachycardia responses are blocked with administration of the ganglionic blocker hexamethonium, demonstrating that these responses are mediated centrally. The transient bradycardia is blocked by the muscarinic antagonist atropine, suggesting that this response is mediated by the parasympathetic system, while the following tachycardia is specifically blocked by the beta-adrenergic antagonist propranolol, suggesting that this response is mediated by the sympathetic nervous system. Together, these results demonstrate that at the larval stage, zebrafish actively regulate cardiac output to changes in their environment using both the parasympathetic and sympathetic branches of the autonomic nervous system, a behavioral response that is markedly similar to that observed in mammals to similar sudden onset stimuli.

Quantitative evaluation of ontogenetic change in heart rate and its autonomic regulation in newborn mice with the use of a noninvasive piezoelectric sensor

A reliable basal heart rate (HR) measurement in freely moving newborn mice was accomplished for the first time by using a novel noninvasive piezoelectric transducer (PZT) sensor. The basal HR was ∼320 beats/min at postnatal day (P)0 and increased with age to ∼690 beats/min at P14. Contribution of autonomic control to HR was then assessed. Sympathetic blockade with metoprolol significantly reduced basal HR at both P6 (−236 ± 23 beats/min; mean ± SE) and P12 (−105 ± 8 beats/min), but atropine was without effect, indicating the predominant tonic adrenergic stimulation and absence of vagal control for basal HR in newborn mice. In contrast to stable basal HR during 5-min recording, HR measured by ECG (ECG-HR) was markedly decreased because of the restraint stress of attaching ECG electrodes, with accompanying freezing behavior. ECG-HR lowered and further decreased gradually during 5 min (slow cardiodeceleration) at P0–P3 and rapidly decreased and gradually recovered within 5 min (transient bradycardia) at P9–P14. The response was not uniform in P4–P8 mice: they showed either of these two patterns or sustained bradycardia (9–29%), and the number of mice that showed transient bradycardia increased with age (30–100%) during the period. Studies with autonomic blockade suggest that the slow cardiodeceleration and transient bradycardia are mediated mainly by withdrawal of adrenergic stimulation and phasic vagal activation, respectively, and the autonomic control of HR response to restraint stress is likely to change from the withdrawal of adrenergic stimulation to the phasic vagal activation at different stages during P4–P8 in individual mice. The PZT sensor may offer excellent opportunities to monitor basal HR of small animals noninvasively.

Development of the ovine fetal cardiovascular defense to hypoxemia towards full term

We tested the hypothesis that fetal cardiovascular responses to hypoxemia change close to full term in relation to the prepartum increase in fetal basal cortisol and investigated, in vivo, the neural and endocrine mechanisms underlying these changes. Fetal heart rate and peripheral hemodynamic responses to 1 h of hypoxemia were studied in 25 chronically instrumented sheep within three narrow gestational age ranges: 125–130 ( n = 13), 135–140 ( n = 6), and >140 ( n = 6) days (full term ∼145 days). Chemoreflex function and plasma concentrations of vasoconstrictor hormones were measured. Reductions in fetal arterial Po2 during hypoxemia were similar at all ages. At 125–130 days, hypoxemia elicited transient bradycardia, femoral vasoconstriction, and increases in plasma concentrations of catecholamines, neuropeptide Y (NPY), AVP, ACTH, and cortisol. Close to full term, in association with the prepartum increase in fetal basal cortisol, there was a developmental increase in the magnitude and persistence of fetal bradycardia and in the magnitude of the femoral constrictor response to hypoxemia. The mechanisms mediating these changes close to full term included increases in the gain of chemoreflex function and in the magnitudes of the fetal NPY and AVP responses to hypoxemia. Data combined irrespective of gestational age revealed significant correlations between fetal basal cortisol and fetal bradycardia, femoral resistance, chemoreflex function, and plasma AVP concentrations. The data show that the fetal cardiovascular defense to hypoxemia changes in pattern and magnitude just before full term because of alterations in the gain of the neural and endocrine mechanisms mediating them, in parallel with the prepartum increase in fetal basal cortisol.