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Clinical and Experimental Evaluation of Sympatho-Vagal Interaction: Power Spectral Analysis of Heart Rate and Arterial Pressure Variabilities
Published in Irving H. Zucker, Joseph P. Gilmore, Reflex Control of the Circulation, 2020
Alberto Malliani, Massimo Pagani, Federico Lombardi, Sergio Cerutti
Reflex bradycardia accompanying rises in arterial pressure has traditionally been considered the result of the stimulation of a restricted reflexogenic area (Heymans and Neil, 1958). More recently, it became appreciated (Sagawa, 1983) that multiple baroreceptors send neural signals to various levels of the central nervous system and through multiple-efferent pathways to a variety of effector organs. However, such a multiinput-multioutput and multilevel regulatory mechanism has never been interpreted to depend also on the interplay of reflexes of opposite signs.
Paroxysmal Autonomic Syncope
Published in David Robertson, Italo Biaggioni, Disorders of the Autonomic Nervous System, 2019
Ronald G. Victor, C.M.T. Jost, R. L. Converse, Tage N. Jacobsen
Activation of the sympathetic nervous system, with reflex vasoconstriction and tachycardia, is a major compensatory adjustment during many hypotensive states (Bedford and Jackson, 1916; Vatner, 1974; Abboud, 1985). In addition, the sudden withdrawal of sympathetic drive can be a primary cause of acute, episodic hypotension with reflex bradycardia and peripheral vasodilation, which are seemingly paradoxical autonomic responses in the setting of hypotension (Wallin and Sündlof, 1982; Scherrer et al., 1990). Such sympathoinhibition appears to cause several clinical syndromes which collectively can be termed “paroxysmal autonomic syncope”. Paroxysmal hypotension with inappropriately normal or frankly decreased heart rate and peripheral vascular resistance is well known to be the haemodynamic basis of emotional fainting (Lewis, 1932; Murray et al., 1961; Glick and Yu, 1963). However, it is much less well appreciated that the same type of vasovagal, or vasodepressor, reaction also may contribute importantly to the morbidity and mortality of cardiovascular emergencies such as acute myocardial infarction and haemorrhagic shock.
Vasoconstrictors: Chemistry, Mode of Action, and Dosage
Published in Marwali Harahap, Adel R. Abadir, Anesthesia and Analgesia in Dermatologic Surgery, 2019
β-blocking agents, as expected, block the β-receptor activity of epinephrine, resulting in unopposed α-receptor activity (24). This may result in severe hypertension and reflex bradycardia (10). A study of 114 patients given from 1 to 9 mL of lidocaine with epinephrine (1:100,000) resulted in no adverse reactions and no significant changes in blood pressure (25). They concluded that discontinuation of β-blockers is not routinely necessary if small amounts of epinephrine are to be used in dermatologic surgery.
Descriptions and outcomes of cardiac evaluations in pediatric patients hospitalized for asthma
Published in Journal of Asthma, 2020
Raymond Parlar-Chun, Kokila Kakarala, Mani Singh
There is limited epidemiological data on respiratory causes of syncope compared to cardiac syncope or vasovagal syncope. Katz reported on a series of cases in asthmatic children where asthma and persistent cough caused transient syncopal episodes. These patients typically returned to baseline within ten seconds with a negative pathological workup and no EEG or EKG abnormalities. Asthma was the source of cough in these patients and syncope was thought to be the result of transient cerebral hypoxia resulting from cough induced increases in intrapleural pressure, decreased venous return, decreased right ventricle output, decreased left ventricle filling, and decreased cardiac output (16). There have also been reported cases of inhaler syncope caused by reflex bradycardia and asystole produced by the use of asthma inhalers (17). In our 6 syncopal patients, one episode was result of cardiac syncope with a new diagnosis of hypertrophic cardiomyopathy. The other five could be plausibly explained by vasovagal, cough, or inhaler syncope causes.
Acquired methemoglobinemia after hydroxocobalamin administration in a patient with burns and inhalation injury
Published in Clinical Toxicology, 2018
Alisha Z. Jiwani, Vikhyat S. Bebarta, Leopoldo C. Cancio
Serial arterial blood gases and co-oximetry (ABGs) demonstrated a persistently elevated lactate (7–8 mmol/L) despite large-volume resuscitation within the first 12 hours. Consequently, the patient received 5 g IV hydroxocobalamin over 15 minutes for possible cyanide toxicity at postburn hour 19. The patient immediately became hypertensive (SBP >220 mmHg) with reflex bradycardia (30 bpm). Concern for possible intracranial hypertension prompted administration of 3% hypertonic saline at 80 ml/h, and 500 mcg of IV nicardipine to maintain SBP <180 mmHg. The SpO2 decreased from 100% to 91% while on 40% FiO2. SpO2 then dropped to and remained at 74–80% despite an increase in FiO2 to 100%. One hour after hydroxocobalamin administration, ABG on 100% FiO2 showed pH 7.20, PCO2 46.5, PO2 355.3, bicarbonate 17.5, base excess −10.2, estimated arterial oxygen saturation (SaO2) 98%, measured oxyhemoglobin by cooximetry (OxyHb) 94.1%, lactate 5.51 mmol/L, and MetHb 4.10%. Head computed tomography scan revealed no intracranial abnormalities, and hypertonic saline infusion was discontinued. Continuous renal replacement therapy (veno-venous hemofiltration) was initiated for refractory acidosis and hyperkalemia (K 5.05 mmol/L) at postburn hour 21.
A randomized open label, parallel-group study to evaluate the hemodynamic effects of Cafedrine/Theodrenaline vs Noradrenaline in the treatment of intraoperative hypotension after induction of general anesthesia: the “HERO” study design and rationale
Published in Current Medical Research and Opinion, 2023
Benjamin Vojnar, Götz Geldner, Susanne Huljic-Lankinen, Melanie Murst, Thomas Keller, Stephan Weber, Christine Gaik, Tilo Koch, Andreas Weyland, Peter Kranke, Sascha Kreuer, Daniel Chappell, Leopold Eberhart
While both medicinal products effectively increase blood pressure, pharmacologic properties suggest a more pronounced increase of cardiac output in response to C/T when compared to NA. Cafedrine/Theodrenaline has been shown to effectively increase the MAP by combined effects on preload, contractility, and afterload, while heart rate is mostly unaffected14. Increase of cardiac index (CI) and MAP seem to be more pronounced in women15. Noradrenaline has potent alpha-adrenergic and slight beta-adrenergic effects resulting in potent vasoconstriction and less potent inotropy. The increase in blood pressure may cause reflex bradycardia16,17. To date, no direct comparison between the two medicinal products is available.