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Query: UMLS:C0020440 (hypercapnia)
 7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Simultaneous recording of activity in the vagal and sympathetic supplies to the heart has revealed that in reflexly and centrally evoked activity these two "antagonists" do not necessarily change action reciprocally. Coactivation occurs in chemoreceptor reflexes and related reactions, upon stretching of the sinoatrial nodal region of the right atrium and when certain hypothalamic regions are stimulated. The objective of the present work was to assay the physiological importance of coactivation of the two potentially antagonistic cardiac nerves in anesthetized dogs. Output from the heart was monitored by recording volume flow in the thoracic aorta just below the aortic arch; cardiac contractility was measured as left ventricular dp/dt. Tape recordings of vagus and sympathetic nerve activity during chemoreceptor and baroreceptor reflexes, during reciprocal and nonreciprocal changes produced by hypothalamic stimulation, and during hypoxia and hypercapnia were used to trigger stimulators feeding a stimulus per action potential to cardiac vagus and sympathetic nerves after central connections were cut. The vagus stimulation alone produced a decrease in aortic blood flow; stimulation of the sympathetic nerve alone resulted in increased aortic blood flow. Simultaneous stimulation of vagus and sympathetic, however, produced an even greater cardiac output (measured by aortic blood flow). Intermediate degrees of heart rate and strength of myocardial contraction were maintained in coactivation. Obviously, an association of increased vagus and sympathetic actions, which can be effected reflexly or by action of higher centers, is of physiological benefit. In control reactions that relate cardiac function to body need, both reciprocal and synergistic actions (coactivation) of cardiac nerves are used.
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PMID:Functional significance of coactivation of vagal and sympathetic cardiac nerves. 695 59

Vocal cord paralysis can produce extrathoracic airway obstruction with severe respiratory failure, post-surgical traumatism being the most frequent. Definitive treatment can require aritenoidectomy. For emergency treatment tracheal intubation of tracheotomy are frequently needed. We report a patient with acute post-surgical upper airway obstruction successfully treated with CPAP application through nasal mask. A 29 year-old female showed stridor and retraction of the supraclavicular, intercostal and epigastric region following an uncomplicated tracheal extubation immediately after surgery (radical thyroidectomy with nodal dissection). Pulsosaturometry showed O2 desaturation despite high flow O2 administration. She received intravenous steroids and O2 through intermittent positive pressure by nasal mask (manual resuscitator) increasing SpO2 to 90%. Laringoscopy showed both vocal cords fixed at medium line. CPAP through a nasal mask was initiated with a 5 cm H2O pressure and high FIO2. Immediately afterwards, dyspnea, stridor, supraclavicular retraction and respiratory accessory muscles use disappeared. Heart rate decreased (120 to 92 x min.) and SpO2 increased to 99%. Arterial blood gases did not show hypercapnia. Dyspnea and physical signs of upper airway obstruction appeared immediately after interrupting CPAP application, with a marked decrease in SpO2. So the mask was reinstalled keeping the same pressure level during 18 hs. The procedure was well tolerated. There were no local or hemodynamic complications. CPAP was progressively discontinued.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Treatment of respiratory insufficiency secondary to vocal cord bilateral paralysis with continuous positive pressure]. 785 91

The autonomic consequences of seizures can be severe. Death can follow from autonomic overactivity that causes a parasympathetically mediated bradyarrhythmia. We studied the cardiovascular consequences of unilateral and bilateral stimulation of the distal segments of transected vagus nerve in rats anesthetized with urethane. The range of stimulation rates tested is comparable to the firing rates observed in vagus nerve during seizures. There was a consistent inverse relation between stimulus rate and heart rate with nodal block appearing at 5-10 Hz and minimum HR levels (cardiac standstill) occurring at 50 Hz. Cardiac standstill could last many seconds. Blood pressure during VNS was maintained during lower frequency VNS, but collapsed at frequencies > or =20 Hz to dramatically impair ventricular filling. Recovery of heart rate and blood pressure after VNS was rapid. In the presence of sympathetic co-activation (pharmacological or hypercapnia and/or hypoxia), mean arterial pressure was better maintained and there was much better ventricular filling, but cardiac performance was worse (e.g. ejection fraction derived from echocardiography). The combination of sympathetic and parasympathetic overactivity was sometimes associated with prolonged (> or =20 s) apneic periods during VNS. We conclude that an abrupt increase in parasympathetic activity on the order of 5 times the background of parasympathetic tone can produce transient bradyarrhythmias, and increases on the order of 20 times can produce cardiac standstill, sometimes accompanied by apnea. Our findings suggest that parasympathetically mediated bradyarrhythmia must be accompanied by airway obstruction to sustain parasympathetic overactivity and produce hypoxia to ultimately cause death.
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PMID:Vagus nerve stimulation-induced bradyarrhythmias in rats. 1965 41