scholarly journals Sinus Arrest and Bradycardia Induced by Carotid Baroreceptor Reflex Activation during Rotational Angiography: A Case Report

Author(s):  
Atsuhiro Kojima ◽  
Isako Saga ◽  
Hideaki Kanki ◽  
Miho Negishi ◽  
Takashi Iwama
2013 ◽  
Vol 8 (4) ◽  
pp. 125-128
Author(s):  
Lou Mastrine ◽  
Sameer Chada ◽  
Evbu Enakpene ◽  
Gerald Hollander

1999 ◽  
Vol 86 (1) ◽  
pp. 285-293 ◽  
Author(s):  
Stephen S. Blevins ◽  
Martha J. Connolly ◽  
Drew E. Carlson

The roles of the carotid arterial baroreceptor reflex and of vagally mediated mechanisms during positive end-expiratory pressure (PEEP) were determined in pentobarbital-anesthetized dogs with isolated carotid sinuses. Spontaneously breathing dogs were placed on PEEP (5–10 cmH2O) with the carotid sinus pressure set to the systemic arterial pressure (with feedback) or to a constant pressure (no feedback). Right atrial volume was measured with a conductance catheter. With carotid baroreceptor feedback before bilateral cervical vagotomy, total peripheral resistance increased ( P < 0.01) and mean arterial pressure decreased (−9.8 ± 4.3 mmHg) in response to PEEP. With no feedback after vagotomy, mean arterial pressure decreased to a greater extent (−45 ± 6 mmHg, P < 0.01), and total peripheral resistance decreased ( P < 0.05) in response to PEEP. In contrast, cardiac index decreased similarly during PEEP ( P < 0.01) for all baroreceptor and vagal inputs. This response comprised a decrease in the passive phase of right ventricular filling ( P< 0.01) that was not matched by the estimated increase in active right atrial output. Although the carotid baroreceptor reflex and vagally mediated mechanisms elicit vasoconstriction to compensate for the effects of PEEP on the arterial pressure, these processes fail to defend cardiac output because of the profound effect of PEEP on the passive filling of the right ventricle.


1985 ◽  
Vol 3 (4) ◽  
pp. 408
Author(s):  
H Becker ◽  
Th Unger ◽  
M A Petty ◽  
D Ganten ◽  
R E Lang

2014 ◽  
Vol 2014 ◽  
pp. 1-4 ◽  
Author(s):  
Ravi K. Thimmisetty ◽  
Janardhana Rao Gorthi ◽  
Mahmoud Abu Hazeem

We present a case of sinus node arrest leading to symptomatic junctional bradycardia from oral phenytoin toxicity, which is a rare presentation. Our patient had no prior cardiac history and was on phenytoin therapy for seizure disorder. Although bradycardia is more commonly associated with intravenous phenytoin and there were few case reports of bradycardia with oral phenytoin reported, the literature is limited. In this case report, we also reviewed the pathophysiology of phenytoin-induced cardiac toxicity.


1985 ◽  
Vol 54 (6) ◽  
pp. 1498-1512 ◽  
Author(s):  
G. L. Gebber ◽  
S. M. Barman

A study was made of 170 neurons of the lateral tegmental field (LTF) of the cat medulla with spontaneous activity temporally related to the 2- to 6-Hz slow wave in inferior cardiac postganglionic sympathetic nerve discharge (as demonstrated with spike-triggered averaging). LTF neurons were excited by the iontophoresis of L-glutamate, and an inflection on the rising phase of their action potentials was observed. Thus, the site of extracellular unit recording presumably was in the region of the cell body. The lag between LTF unit spike occurrence and the peak of the 2- to 6-Hz slow wave in sympathetic nerve discharge (SND) was unchanged when blood pressure and, thus, baroreceptor nerve activity were lowered to a level at which the phase relationship between the slow wave and the cardiac cycle was disrupted. Thus, the discharges of LTF neurons apparently were more closely associated with those of elements of "efferent" brain stem networks controlling SND than with those of interneurons in the afferent limb of the baroreceptor reflex arc. LTF neurons with sympathetic nerve- and cardiac-related activity were classified into three types depending on their responses to elevated carotid sinus pressure (i.e., baroreceptor reflex activation). Of the 82 neurons tested, 33 were inhibited, 16 were excited, and 33 were unaffected by baroreceptor reflex activation. Using data collected in this and previous studies from our laboratory, we compared the firing times of neurons in the LTF, rostral ventrolateral medulla, and medullary raphe nuclei relative to the peak of the sympathetic nerve slow wave. LTF neurons that were inhibited by baroreceptor reflex activation are presumed to subserve a sympathoexcitatory function. These neurons fired significantly earlier during the sympathetic nerve slow wave than their counterparts in the rostral ventrolateral medulla and medullary raphe nuclei. LTF neurons classified as sympathoinhibitory (i.e., excited by baroreceptor reflex activation) fired significantly earlier than their counterparts in the medullary raphe nuclei. These data raise the possibility that LTF neurons are closer (at least in a temporal sense) to the region of origin of the 2- to 6-Hz component of SND than are ventrolateral medullary and raphe neurons. The firing times of sympathoexcitatory and sympathoinhibitory LTF neurons were not significantly different. These data are discussed relative to potential mechanisms involved in generating SND. Microstimulation of the second thoracic spinal segment was used to determine whether the axons of LTF neurons with sympathetic nerve-related activity projected to this level.(ABSTRACT TRUNCATED AT 400 WORDS)


1990 ◽  
Vol 64 (3) ◽  
pp. 1019-1032 ◽  
Author(s):  
S. M. Barman

1. Spike-triggered averaging was used to identify 104 hypothalamic (HYP) neurons whose spontaneous or L-glutamate-induced action potentials were synchronized to inferior cardiac postganglionic-sympathetic nerve discharge (SND) in 39 pentobarbital sodium-anesthetized cats. Neurons were located primarily in the lateral hypothalamus but also in the posterior, dorsal, ventromedial, and anterior hypothalamus, as well as in the paraventricular region. Most neurons tested (41/60) were classified as sympathoexcitatory (SE) because their firing rate decreased during baroreceptor reflex activation. Because the firing rate of 15 neurons increased during the pressor response produced by aortic obstruction, they were classified as sympathoinhibitory (SI). The firing rate of the other four neurons tested was unaffected by baroreceptor reflex activation. 2. Microstimulation of the medullary lateral tegmental field (LTF; stereotaxic plane P10.5-P12, 2.3-3 mm lateral to the midline) antidromically activated 11 of 58 HYP neurons with sympathetic nerve-related activity, including seven SE neurons and one SI neuron. Antidromic mapping was used to trace the axonal trajectories of HYP neurons that were activated by LTF microstimulation. The results of these experiments suggested that the axons of eight of these neurons branched or terminated in the LTF. The data obtained from another series of experiments were consistent with the view that these HYP neurons excited LTF-SE neurons. LTF-SE neurons were synaptically activated by electrical stimulation of the posterior or lateral hypothalamus. This stimulus also increased SND. The modal onset latency (36 +/- 7.2 ms, mean +/- SE) of synaptic activation of LTF-SE neurons was similar to the onset latency (38 +/- 6.8 ms) of antidromic activation of HYP neurons by LTF microstimulation. These data support the view that LTF-SE neurons are involved in mediating HYP influences on SND. 3. Rostral ventrolateral medullary (RVLM)-SE neurons, including those whose axons projected to the thoracic intermediolateral nucleus (IML), also appear to be involved in mediating HYP-stimulus-induced increases in SND. HYP stimulation synaptically activated these neurons with a modal onset latency of 36 +/- 9.6 ms. Microstimulation of the region containing RVLM-SE neurons antidromically activated 16 of 60 HYP neurons with sympathetic nerve-related activity. The nine neurons tested were classified as SE. antidromic mapping revealed that RVLM microstimulation activated the main axon rather than an axonal branch or terminal of 9 of 12 of these HYP neurons. 4. Microstimulation of the mesencephalic periaqueductal gray (PAG) at stereotaxic planes A2-A3.5 antidromically activated 30 of 61 HYP neurons with sympathetic nerve-related activity, including 13 SE neurons and three SI neurons.(ABSTRACT TRUNCATED AT 400 WORDS)


2008 ◽  
Vol 55 (1) ◽  
pp. 114
Author(s):  
Jae Gyok Song ◽  
Kang Ryu ◽  
Seok-Kon Kim

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