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Epinephrine cardiac arrest

Sinus bradycardia. An abnormally low sinoatrial impulse rate (<60/min) can be raised by parasympatholytics. The quaternary ipratropium is preferable to atropine, because it lacks CNS penetrability (p. 107). Sympathomimet-ics also exert a positive chronotropic action they have the disadvantage of increasing myocardial excitability (and automaticity) and, thus, promoting ectopic impulse generation (tendency to extrasystolic beats). In cardiac arrest epinephrine can be used to reinitiate heart beat... [Pg.134]

Catecholamines such as isoproterenol and epinephrine have been used in the temporary emergency management of complete heart block and cardiac arrest. Epinephrine may be useful in cardiac arrest in part by redistributing blood flow during cardiopulmonary resuscitation to coronaries and to the brain. However, electronic pacemakers are both safer and more effective in heart block and should be inserted as soon as possible if there is any indication of continued high-degree block. [Pg.190]

Epinephrine is administered by a variety of different routes in anaphylaxis, except for the oral route, which is not feasible because of rapid inactivation of epinephrine in the gastrointestinal tract by catechol-O-methyltransferase and monoamine oxidase [9]. The initial intramuscular epinephrine doses of 0.3-0.5 mg currently recommended for adults with anaphylaxis are low compared with the doses required for resuscitation following cardiac arrest [1, 2,4,18]. [Pg.214]

M (7/12 ventricular fibrillation after epinephrine challenge, 1/12 cardiac arrest)... [Pg.28]

Despite these potential advantages, clinical experience with vasopressin is limited and comparative trials with epinephrine have produced mixed results. Overall, these studies suggest that vasopressin is effective as part of ACLS after cardiac arrest, but its superiority to epinephrine remains questionable. [Pg.92]

Cardiostimulation. By stimulating Pi-receptors, hence activation of ade-nylatcyclase (Ad-cyclase) and cAMP production, catecholamines augment all heart functions, including systolic force (positive inotropism), velocity of shortening (p. clinotropism), sinoatrial rate (p. chronotropism), conduction velocity (p. dromotropism), and excitability (p. bathmotropism). In pacemaker fibers, diastolic depolarization is hastened, so that the firing threshold for the action potential is reached sooner (positive chronotropic effect, B). The cardiostim-ulant effect of p-sympathomimetics such as epinephrine is exploited in the treatment of cardiac arrest Use of p-sympathomimetics in heart failure carries the risk of cardiac arrhythmias. [Pg.84]

Sniffing aerosols of fluorochlorinated hydrocarbons has caused sudden death from cardiac arrest probably due to cardiac arrhythmias from sensitization of the myocardium to epinephrine. ... [Pg.225]

Cardiac arrhythmias have been provoked in a number of species. Inhalation of 3 5 00-6100 ppm by dogs for 5 minutes caused ventricular fibrillation and cardiac arrest after injection of epinephrine. The minimal concentration that elicited cardiac arrhythmias in the anesthetized monkey was 50,000ppm. ... [Pg.698]

Epinephrine (adrenaline) should be given every 3-5 min whilst the patient remains in cardiac arrest, immediately if the patient has an initially non-shockable rhythm (asystole or pulseless electrical activity) but delayed until before the third shock for shockable rhythms. Continued administration of epinephrine (adrenaline), cardiac massage, and DC shock may be required for several cycles. [Pg.508]

The cornerstone of therapy for ventricular fibrillation is electrical deflbrillation. In the acute setting, defibrination is first-line therapy. Intravenous bretylium can occasionally contribute to conversion, but this is infrequent. In the management of out-of-hospital cardiac arrest, high-dose epinephrine (5 mg intravenously) improves the rate of successful resuscitation in patients with asystole, but not in those with ventricular fibrillation, when compared with the standard dose of 1 mg. Vasopressin (40 U intravenously) may more effective than 1 mg intravenous epinephrine in out-of-hospital patients with ventricular fibrillation that is resistant to electrical defibrillation. The OPTIC smdy (see Connolly et al., 2006) showed that amiodarone plus jS-blocker is superior than sotalol or jS-blocker alone for reducing ICD shocks in patients with reduced left ventricular function and history of sustained VT, VF, or cardiac arrest. [Pg.605]

Gueugniaud PY, Mols P, Goldstein P, Pham E, Dnhien PY, Deweerdt C et al. A comparison of repeated high doses and repeated standard doses of epinephrine for cardiac arrest ontside the hospital. Enropean Epinephrine Stndy Gronp. N Engl J Med 1998 339 1595-601. [Pg.606]

Vasoconstriction induced by local application of a-sympathomimetics can be employed in infiltration anesthesia (p.204) or for nasal decongestion (naphazoline, tetra-hydrozoline, xylometazoline p.94, 336, 338). Systemically administered epinephrine is important in the treatment of anaphylactic shock and cardiac arrest. [Pg.88]

Q3 Patients who suffer a cardiac arrest are usually given epinephrine (adrenaline) and external cardiac massage. If necessary, atropine is also administered. Explain the pharmacological actions of epinephrine and atropine on the heart. [Pg.49]

Intravenous. A double cuff is applied to the arm, inflated above arterial pressure after elevating the limb to drain the venous system, and the veins filled with local anaesthetic, e.g. 0.5-1% lidocaine without adrenaline (epinephrine). The arm is anaesthetised in 6-8 min, and the effect lasts for up to 40 min if the cuff remains inflated. The cuff must not be deflated for at least 20 minutes. The technique is useful in providing anaesthesia for the treatment of injuries speedily and conveniently, and many patients can leave hospital soon after the procedure. The technique must be meticulously conducted, for if the full dose of local anaesthetic is accidentally suddenly released into the general circulation severe toxicity and even cardiac arrest may result. Bupivacaine is no longer used for intravenous regional anaesthesia as cardiac arrest caused by it is particularly resistant to treatment. Patients should be fasted and someone skilled in resuscitation must be present. [Pg.360]

Weaver WD, Fahrenbruch CE, Johnson DD, Hallstrom AP, Cobb LA, Copass MK. Effect of epinephrine and lidocaine therapy on outcome after cardiac arrest due to ventricular fibrillation. Circulation 1990 82(6) 2027-34. [Pg.2058]

The treatment of cardiac arrest should follow the American Heart Association guidelines for Advance Cardiac Life Support. After three shocks, epinephrine or vasopression are administered. If this fails, then antiarrhythmics are given to facilitate the conversion and maintenance of NSR. [Pg.10]

Catecholamines are sympathomimetic drugs. Dopamine and norepinephrine are used as vasopressors (antihypotensives). Epinephrine is used as a vasoconstrictor, cardiac stimulant, or bronchodilator to counter allergic reaction, anesthesia, and cardiac arrest. It is also an antiglaucoma agent. [Pg.487]


See other pages where Epinephrine cardiac arrest is mentioned: [Pg.40]    [Pg.113]    [Pg.128]    [Pg.130]    [Pg.153]    [Pg.185]    [Pg.204]    [Pg.239]    [Pg.709]    [Pg.16]    [Pg.148]    [Pg.121]    [Pg.232]    [Pg.14]    [Pg.148]    [Pg.279]    [Pg.317]    [Pg.75]    [Pg.912]    [Pg.550]    [Pg.550]    [Pg.121]    [Pg.9]    [Pg.121]    [Pg.175]    [Pg.175]    [Pg.175]    [Pg.175]    [Pg.176]   
See also in sourсe #XX -- [ Pg.14 ]




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