neuromuscular blocking agents
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on Nov 10, 2012 Says :
on Jul 21, 2012 Says :
great presentation with well organized ppts.
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Slide 1 :
Neuromuscular blocking agents (muscle relaxants) Dr.Shraddha Naik (Bahulekar) Assistant Prof,KIMS,Karad.
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Classification Muscle Relaxants are classified as: I)Peripherally acting A.Neuromuscular blocking agents:- Depolarizing muscle relaxants. Non-depolarizing muscle relaxants B.) Directly acting: Dantrolene, Quinine II)Centrally acting Chlorzoxazone,Chlormezanone, Diazepam, Baclofen, Tizanidine, Metaxalone.
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Classification Depolarizing Muscle relaxants: Succinylcholine (short acting) Non-depolarizing Muscle relaxants:
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Role of NMB’s NMB’s are co-administrated with anasthetics in the induction phase to induce muscle paralysis facilitate the surgery, especially intra-abdominal and intra-thoracic surgeries. facilitate endotracheal intubation. Also used in ICU settings in patients requiring prolonged ventilation especially where it is mandatory to reduce the work of breathing.
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Normal neuromuscular transmission
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Scoline-mechanism of action Block transmission by causing prolonged depolarization of endplate at neuromuscular junction. Manifestation by initial series of muscle twitches (fasciculation) followed by flaccid paralysis. It immediately metabolize in plasma by Pseudo-cholinesterase which is synthesized by liver so to prevent its metabolism in plasma it should be given at faster rate. D0se-1-1.5 mg/kg.
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Systemic effects Cardiovascular: Produces muscarinic effects as acetylcholine , therefore causes bradycardia ( but when given high doses causes tachycardia because of stimulation of nicotinic receptors at sympathetic ganglions).Bradycardia is attributed to metabolite of scoline namely succinylmonocholine. Hyperkalemia: Increases the serum pottasium levels by about 0.5mEq/lit. Ventricular fibrillation can occur due to hyperkalemia. CNS: Increases intracranial tension. Eye: Increases intraocular pressure.
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GIT: Increases intra-gastric pressure , salivation, peristalsis. Muscle pains ( myalgia): This is a very common problem in post operative period. These are due to excessive muscle contractions. Malignant hyperthermia Severe Anaphylaxis Masseter Spasm : Sch can cause masseter spasm especially in children & patients susceptible for malignant hyperthermia. Doesnot require reversal rather cholinesterase inhibitors (neostigmine) can prolong the depolarizing block (because these agents also inhibits the pseudocholinesterase)
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Hyperkalemia: Serum K > 5.5 is an absolute contraindication for use of Sch. Head Injury : It increase ICP Newborns and infants: These have extrajunctional receptors which are sensitive to depolarizing agents & Sch can produce severe hyperkalemia by interacting with these receptors. Glaucoma & open eye injuries. Susceptibility to malignant hyperthermia. Contraindications
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Contraindications(contd) Up to 2-3 months after trauma, Up to 6 months after hemiplegia/paraplegia, Up to 1 year after burns. In these conditions the denervated/regenerating nerve develops extra junctional receptors which can produce hyperkalemia. Renal Failure : If associated with hyperkalemia. Diagnosed case of atypical pseudocholinesterase & low pseudocholinesterase. Duchene muscular dystrophy Dystrophia myotonica: Permanent contractures may develop if SCh is given in these patients.
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Contd…… Tetanus. Gullian Barre Syndrome Metabolic Acidosis :Acidosis is associated with hyperkalemia. Prolonged intra abdominal infection can be associated with hyperkalemia. Spinal cord injury.
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Non-depolarizing Muscle relaxants: Mechanism of action: It blocks nicotinic receptors competitively resulting in inhibition of sodium channels and excitatory post-synaptic potential. It binds at the same site at which acetylcholine binds. All NDMR are quarternary ammonium compounds & highly water soluble i.e. hydrophilic. So, they do not cross blood brain barrier & placenta except Gallamine.
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Classification of nondepolarizing neuromuscular blockers according to duration of action
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Differences between Depolarizing & Non-depolarizing block
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Common steroidal compounds Pancuronium(Pavulon) Onset of action 3-5 min. Duration of action -60-90min. It releases noradrenaline & can cause tachycardia & hypertension. Because of this there are increased chances of arrhythmia with halothane. 60%excretion by liver and 40% via kidneys.therefore action is rolonged in hepatic and renal impairment. Produces selective vagal blockade and activation of sympathetic system.
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Vecuronium It is very commonly used relaxant. More cardiovascular stability as compared to pancuronium. Onset of action-3-5min. Duration of action-20-35min. 30%renal excretion,70%hepatic excretion.therefore,dose adjustment required in hepatic and renal impairment.
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Atracurium Onset of action-3-5min. Duration of action20-35min. Elimination by non specific plasma esterases and Hoffmann’s elimination.Therefore safe to be used in patients deranged liver or kidney functions. Laudonosine is the metabolite formed in both the above pathways. Laudonosine is said to cause CNS stimulation and seizures in very large doses(not significant at clinical doses) Produces histamine release.
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Rocuronium 8 times more potent than vecuronium. Because of onset comparable to succinylcholine it is suitable for rapid sequence intubation as an alternative to succinylcholine. Duration of action similar to vecuronium.
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Benzylisoquinoline compounds D- Tubocurare It is named so because it was carried in bamboo tubes & used as arrow poison for hunting by Amazon people. It has highest propensity to release histamine It causes maximum ganglion blockade. Because of ganglion blocking & histamine releasing property it can produce severe hypotension. Due to histamine release it can produce severe bronchospasm.
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Drugs used for reversal of block are cholinesterase inhibitors (anticholinesterases). Reversal should be given only after some evidence of spontaneous recovery appear. Mechanism of Action It inactivate the enzyme acetylcholinesterase which is responsible for break down of actetylcholine, thus increasing the amount of acetylcholine available for competition with non depolarizing agent thereby re-establishing neuromuscular transmission. Anticholinesterases used for reversal are: Neostigmine Pyridostigmine Edrophonium Physostigmine Reversal of blockade
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These agents except physostigmine are quarternary ammonium compounds so they do not cross blood brain barrier. The biggest disadvantage is that these agents also increase the acetylcholine level at muscarinic receptors producing muscarinic side effects like bradycardia, bronchospasm. So, to prevent these muscarinic effects some anti cholinergic like atropine or glycopyrrolate is to be given with cholinesterase inhibitors. Neostigmine : Anticholinergic preferred with it is glycopyrrolate because both have same onset of action (both are slow acting). Edrophonium : Anticholinergic preferred with it is atropine (both fast acting). Pyridostigmine: It is preferred drug for renal failure patients in whom a prolonged stay of muscle relaxant is expected.
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Unreliable signs: Spontaneous eye opening. Protusion of tongue. Arm lift to opposite shoulder. Normal tidal volume breath Normal or near normal vital capacity. Maximum inspiratory pressure <40-50 cm of H2O. Signs of adequate reversal
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Signs of adequate reversal(contd) Reliable signs: Sustained head lift for 5 secs. Sustained leg lift for 5 secs. Sustained hand grip for 5 secs. Sustained tongue depressor test. Normal gag and swallowing reflex. Maximum inspiratory pressure >40-50cm of H2O.
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Inadequate dose of neostigmine. Overdose of inhalational agents/opioids. Renal Failure,Hepatic failure Hypothermia Electrolyte abnormalities (Hypokalemia, Hypocalcemia) Associated neuromuscular diseases. Shock Acid Base abnormalities especially acidosis. It is impossible to reverse a patient with pCO2 more than 50mmHg. Causes of inadequate reversal
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Factors Prolonging the neuromuscular blocakde Neonates Old age Obesity Hepatic disease (both depolarizer & NMDR) Renal disease ( only NDMR) Inhalational agents : Prolong the block by both depolarizers & NDMR. Inhalational agents decrease the requirement of relaxant .The maximum relaxation is by ether followed by desflurane Antibiotics: Both depolarizers & NMDR Aminoglycosides. Tetracyclines.
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Local Anaesthetics : Except procaine local anaesthetics prolong the action by stabilizing post synaptic membrane. Hypothermia : Decreases metabolism of muscle relaxants. Hypocalcemia: Calcium is required for producing action potential. Action of NDMR is enhanced. Hypokalemia : NMDR block is enhanced. Acid base imbalances especially acidosis. Calcium channel blockers Dantrolene Neuromuscular disease Hypermagnesemia.
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Drug interactions These drugs increase the metabolism of NDMR’s and thus reduce the duration of action of these drugs. Phenytoin Carbamazepine Calcium Cholinesterase inhibitors Azathioprine Steroids.
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