Muscle relaxants depolarizing blockers

L C. Rapacuronium is a skeletal muscle relaxant that works by competing with ACh for receptors at the postjunctional membrane. Nicotine and succinylcholine also act at the end plate receptors but cause depolarization. Hexamethonium is a ganglion blocker that has essentially no activity at the end plate receptors, and scopolamine blocks cholinergic muscarinic receptors and thus does not act at the end plate receptors. 

Muscle contraction responses to different patterns of nerve stimulation used in monitoring skeletal muscle relaxation. The alterations produced by a nondepolarizing blocker and depolarizing and desensitizing blockade by succinylcholine are shown. In the train of four (TOF) pattern, four stimuli are applied at 2 Hz. The TOF ratio (TOF-R) is calculated from the strength of the fourth contraction divided by that of the first. In the double burst pattern, three stimuli are applied at 50 Hz, followed by a 700 ms rest period and then repeated. In the posttetanic potentiation pattern, several seconds of 50 Hz stimulation are applied, followed by several seconds of rest and then by single stimuli at a slow rate (eg, 0.5 Hz). The number of detectable posttetanic twitches is the posttetanic count (PTC)., first posttetanic contraction. 

BETA-BLOCKERS NON-DEPOLARIZING 1. Modest t in efficacy of muscle relaxants, particularly with propanolol 2. Risk of 1 BP with atracurium and alcuronium 1 and 2. Uncertain 1. Watch for prolonged muscular paralysis after muscle relaxants 2. Monitor BP at least weekly until stable... 

CALCIUM CHANNEL BLOCKERS NON-DEPOLARIZING t effect of non-depolarising muscle relaxants with parenteral calcium channel blockers the effect is less certain with oral therapy. In two cohort studies, vecuronium requirements were halved in patients on diltiazem. Nimodipine does not seem to share this interaction Uncertain postulated that ACh release at the synapse is calcium dependent 1 calcium concentrations at the nerve ending may 1 ACh release, which in turn prolongs the nerve blockade Monitor nerve blockade carefully in patients on calcium channel blockers, particularly near to the end of surgery, when muscle relaxation may be prolonged and difficult to reverse... 

Muscle relaxants Non-depolarizing neuromuscular blockers Short-lasting muscle paralysis Pancuronium, atracurium... 

Atracurium - muscle relaxant (non-depolarizing neuromuscular blocker) adjunct to... 

Explain the action of depolarizing blockers in skeletal muscle relaxation. 

Figure 27-2. Drug interactions with the ACh receptor on the skeietal muscle end plate. Top ACh, the normal agonist, opens the sodium channel. Bottom left Nondepolarizing blockers bind to the receptor to prevent opening of the channel. Bottom right Succinylcholine causes initial depolarization (fasciculation) and then persistent depolarization of the channel, which leads to muscle relaxation. (Reproduced, with permission, from Katzung BG [editor] Basic Clinical Pharmacology, 8th ed. McGraw-Hill, 2001.)...

All three classes also inhibit depolarization-induced contraction of venous smooth muscle in vitro. However, venous relaxation does not substantially contribute to the hemodynamic actions of Ca2+ channel blockers. 

Drugs of this group are calcium channel blockers that inhibit slow transmembrane calcium ion flow in the cell of the conductive system of the heart during depolarization, which causes a slowing of atrioventricular conductivity and increased effective refractive period of atrioventricular ganglia, which eventually leads to the relaxation of smooth muscle of heart musculature and restores normal sinus rhythm during supraventricular tachycardias. 

Voltage-sensitive Ca + channels (L-type or slow channels) mediate the entry of extracellular Ca + into smooth muscle and cardiac myocytes and sinoatrial (SA) and atrioventricular (AV) nodal cells in response to electrical depolarization. In both smooth muscle and cardiac myocytes, Ca + is a trigger for contraction, albeit by different mechanisms. Ca +-channel antagonists, also called Ca -entry blockers, inhibit Ca + channel function. In vascular smooth muscle, this leads to relaxation, especially in arterial beds. These drugs also may produce negative inotropic and chronotropic effects in the heart. 

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