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Intracardiac

Isoproterenol may also be used in cardiac arrest. It is often adrninistered as an iv or intracardiac bolus along with sustained external cardiac massage to circulate the dmg and stimulate the SA pacemaker to resume automaticity (86). [Pg.120]

Parenteral drug administration means the giving of a drug by the subcutaneous (SC), intramuscular (IM), intravenous (IV), or intradermal route (Fig. 2-5). Other routes of parenteral administration that may be used by the primary care provider are intralesional (into a lesion), intra-arterial (into an artery), intracardiac (into the heart), and intra-articular (into a joint), hi some instances, intra-arterial dragp are administered by a nurse. However, administration is not by direct arterial injection but by means of a catheter that has been placed in an artery. [Pg.20]

Hoffman D, Gong G, PinchukL, and Sisto D. Safety and intracardiac function of a silicone-pol)oirethane elastomer designed for vascular use. Clin Mater, 1993, 13, 95-110. [Pg.251]

In initial ICC studies, animals were treated with MDA or MDMA using the protocol described by Ricaurte et al. (1985). Adult Sprague-Dawley rats (150 to 200 g) reeeived subcutaneous injections of racemic MDA or MDMA every 12 hours for 4 days. Each dose was equivalent to 20 mg/kg of the free base. The rats were sacrificed by intracardiac aldehyde perfusion 2 weeks after the final dose. In order to study subacute effects for evidence of degeneration, additional rats received MDA every 12 hours for 2 days and were sacrificed 24 hours after the last injection. Additional experimental details are described elsewhere (O Heam et al. 1986 O Heam et al. 1988). A series of animals treated identically and in parallel were analyzed for changes in 5-HT levels and density of uptake sites using paroxetine binding (Yeh et al. 1986 Battaglia et al. 1987). [Pg.278]

Oscillating intracardiac mass on valve or supporting structures, in the path of regurgitant, or on implanted material in the absence of an alternative anatomic explanation, or Abscess, or... [Pg.1094]

Microorganisms demonstrated by culture or histologic examination of a vegetation that has embolized, or an intracardiac abscess specimen, or... [Pg.1094]

Pathologic lesions vegetation or intracardiac abscess confirmed by histologic examination showing active endocarditis Clinical criteria ... [Pg.1094]

A single intracardiac dose of 40 ig/g body weight lead acetate induced a 25-fold increase in mitosis of mouse liver cells 5 hours after injection (Choie and Richter 1978). Results were mixed for various manifestations of genotoxicity or cell cycle disruptions in several experiments with lead acetate in mammals (Bruce and Heddle 1979 Deknudt and Gerber 1979 Deknudt et al. 1977 Jacquet and Tachon 1981 Jacquet et al. 1977 Muro and Goyer 1969 Tachi et al. 1985 Willems et al. 1982). [Pg.304]

Radionuclide angiocardiography is used to measure ejection fraction (EF), regional ventricular performance, cardiac output, ventricular volumes, valvular regurgitation, asynchrony or wall motion abnormalities, and intracardiac shunts. [Pg.146]

The need for a rapid onset of action (and/or clearance) usually requires that an IV route be used, although at a certain stage of cardiopulmonary resuscitation (for example), the need for an even more rapid effect may require the use of an intracardiac injection. The required site of action may influence the choice of route of administration (e.g., certain radiopaque dyes are given intraarterially near the site being evaluated streptokinase is sometimes injected experimentally into the... [Pg.449]

Intraventricular administration - In cardiac resuscitation, injection may be made into the ventricular cavity do not inject into the myocardium. Replace the IV needle with a suitable intracardiac needle. [Pg.17]

Parenteral therapy The dangers of parenteral use of quinidine are increased in the presence of AV block or absence of atrial activity. Administration is more hazardous in patients with extensive myocardial damage. Use of quinidine in digitalis-induced cardiac arrhythmia is extremely dangerous because the cardiac glycoside may already have caused serious impairment of intracardiac conduction system. Too rapid IV administration of as little as 200 mg may precipitate a fall of 40 to 50 mm Hg in arterial pressure. [Pg.425]

THIETHYLPERAZINE Do not use IV (may cause severe hypotension). Use of this drug has not been studied following intracardiac or intracranial surgery. [Pg.978]

II.b.2.1. Prokinetic agents. Cisapride cisapride treatment can be demonstrated to improve sphincter and motor function and to improve modestly the symptoms of heartburn. However, it is relatively ineffective in severe disease, and adverse effects of impaired intracardiac electrical conduction causing ventricular tachyarrhythmias have resulted in its withdrawal from general use. [Pg.621]

Some of the dosage formulations available for protein pharmaceuticals are listed in Table 5.7. An examination of Table 5.7 reveals that no protein drug up until this time has been formulated for oral administration. Most protein drugs are administered by means of injection (parenteral administration). Parenteral administration includes intravenous, intra-arterial, intracardiac, intraspinal or intrathecal, intramuscular, intrasynovial, intracuta-neous or intradermal, subcutaneous injections, and injection directly into a dermal lesion (e.g., a wart). The parenteral route of administration requires a much higher standard of purity and sterility than oral administration. It also may require trained... [Pg.118]

Intracardiac, Intraspinai or Intrathecal, Intramuscular, Intrasynoviai, Intracutaneous or Intradermal, Subcutaneous powders to be reconstituted into solution enzymes, hormones, vaccines... [Pg.119]

In this case, each of the drugs the patient was taking was individually capable of slowing intracardiac conduction in a concentration-dependent manner. Death occurred as a result of their additive effect amplified by the decision to give each one as a single nighttime dose. That decision substantially increased the peak concentration of each drug and consequently resulted in a fatal arrhythmia. [Pg.34]

Slowed intracardiac conduction (similar to that induced by Type II antiarrhythmics and tricyclic antidepressants)... [Pg.89]

This agent is not sedating, has a low incidence of anticholinergic adverse effects, does not cause weight gain, has no effects on intracardiac conduction, and has no significant safety risk beyond seizures in overdoses. [Pg.123]

The cardiovascular effects of TCAs have also been well documented, and the mechanisms underlying these effects elucidated by in vitro and in vivo animal studies (335). Because the effects of TCAs on intracardiac conduction are concentration dependent and occur at levels above the upper therapeutic threshold, TDM can help avoid iatrogenic cardiotoxicity. [Pg.140]

Nausea Usually transient and dose-related. May improve with dose reduction or symptomatic measures (e.g., food, antacids, addition of drugs that block 5-HT 3 receptors, such as cisapride). There has been increasing concern about using cisapride in combination with antidepressants that can substantially inhibit CYP 3A3/4 (i.e., fluvoxamine, nefazodone). The reason is that high levels of cisapride can cause arrhythmias as a result of delayed intracardiac conduction. [Pg.149]

Nefazodone, like the SSRIs and venlafaxine, has negligible effect on Na ion fast channels and therefore does not slow intracardiac conduction. As a result, during clinical trials development, patients survived drug overdoses exceeding 11,200 mg without the need for any intervention beyond observation and routine nursing care (146, 451). One nonstudy patient who took 2,000 to 3,000 mg of nefazodone with methocarbamol and alcohol experienced a seizure (type not documented) but otherwise recovered uneventfully. [Pg.150]

As with most data for reboxetine, this information primarily comes from summary papers rather than primary sources (473, 474). With this caveat, the adverse-effect profile of reboxetine is consistent with its pharmacology as an NSRI. Thus, it is similar to that of desipramine and maprotiline but without the risk of serious CNS (i.e., seizures, delirium) or cardiac (i.e., conduction disturbances) toxicity. The most common adverse effects of reboxetine are dry mouth, constipation, urinary hesitancy, increased sweating, insomnia, tachycardia, and vertigo. Whereas the first three adverse effects are commonly called anticholinergic, they are well known to occur with sympathomimetic drugs as well. In other words, these effects can be either the result of decreased cholinergic tone or increased sympathetic tone, although they tend to be more severe with the former than the latter. In contrast to TCAs, reboxetine does not directly interfere with intracardiac conduction. The tachycardia produced by reboxetine, however, can be associated with occasional atrial or ventricular ectopic beats in elderly patients. [Pg.152]

Vohra J, Burrows G, Hunt D, et al. The effects of toxic and therapeutic doses of tricyclic antidepressant drugs on intracardiac conduction. EurJ Cardiol 1975 3 219-227. [Pg.162]

Slowing of intracardiac conduction, which can lead to heart blocks, arrhythmias, and sudden death (138)... [Pg.280]

Inhibition of Na fast channels, which can inhibit electrically excitable membranes and produce intracardiac conduction delays ( 137)... [Pg.280]

Decreased venous return to the heart and the resulting reduction of intracardiac volume are important beneficial hemodynamic effects of nitrate. Arterial pressure also decreases. Decreased intraventricular pressure and left ventricular volume are associated with decreased wall tension (Laplace relation) and decreased myocardial oxygen requirement. In rare instances, a paradoxical increase in myocardial oxygen demand may occur as a result of excessive reflex tachycardia and increased contractility. [Pg.258]

A previously healthy 34-year-old woman who underwent ovulation induction with leuprorelin acetate and FSH developed abdominal ascites due to OHSS, followed by acute aphasia and right hemiparesis (76). The stroke was caused by a large intracardiac thrombus. [Pg.490]

Worrell GA, Wijdicks EF, Eggers SD, Phan T, Damario MA, Mullany CJ. Ovarian hyperstimulation syndrome with ischemic stroke due to an intracardiac thrombus. Neurology 2001 57(7) 1342 1. [Pg.493]

Earlier studies (ref. 440-442) with ordinary air microbubbles (without any synthetic surfactant coating) have already shown that echocardiographic contrast produced by microbubbles is useful in the qualitative analysis of blood flow and valvular regurgitation. In addition, quantitative studies (ref. 440) have shown a correlation between individual contrast trajectories on M-mode echocardiography and invasive velocity measurements in human beings. Meltzer et al. (ref. 441) have shown that velocities derived from the slopes of contrast trajectories seen on M-mode echocardiography correlate with simultaneous velocities obtained by Doppler techniques. (This correlation is expected because both measures represent the same projection of the microbubble velocity vector, that is, in the direction of the sound beam.) More detailed studies (ref. 442) confirmed that microbubble velocity obtained from either Doppler echocardiography or M-mode contrast trajectory slope analysis correlates well with actual (Doppler-measured) red blood cell velocity. Thus, these early studies have shown that microbubbles travel with intracardiac velocities similar to those of red blood cells. [Pg.149]


See other pages where Intracardiac is mentioned: [Pg.671]    [Pg.9]    [Pg.107]    [Pg.415]    [Pg.282]    [Pg.30]    [Pg.1422]    [Pg.382]    [Pg.139]    [Pg.256]    [Pg.1422]    [Pg.9]    [Pg.140]    [Pg.146]    [Pg.282]    [Pg.2]    [Pg.51]    [Pg.63]    [Pg.1159]    [Pg.293]   
See also in sourсe #XX -- [ Pg.9 ]




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Intracardiac electrogram

Intracardiac ultrasound

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