NEUROMUSCULAR BLOCKING AGENTS

Views:
 
Category: Education
     
 

Presentation Description

No description available.

Comments

Presentation Transcript

NEUROMUSCULAR BLOCKING AGENTS:

DR. RAFIA TABASSUM ANAESTHETIST, DEPT: ANAESTHESIA & SICU, PMCH NAWABSHAH,SIND-PAKISTAN NEUROMUSCULAR BLOCKING AGENTS

QUALITIES OF AN IDEAL NMBA:

QUALITIES OF AN IDEAL NMBA

PowerPoint Presentation:

INDICATIONS TERMINOLOGY

PowerPoint Presentation:

Potency – The potency of a muscle relaxant is described by its effective dose (ED). ED95 and ED50 are the doses of muscle relaxant necessary to suppress the twitch response by 95% (5% twitch height) or 50% (50% twitch height) of baseline (100%) twitch height, respectively. Normally a 2  ED95 dose of a muscle relaxant is injected before an intubation attempt. Onset – Onset describes the interval between injection of the muscle relaxant and development of maximal neuromuscular block. Clinical duration of action (dur25 or dur95) – The clinical duration of action is the interval between injection of the muscle relaxant and recovery of the twitch to 25% or 95% of baseline twitch height (i.e., 75% or 5% twitch suppression). If the surgical conditions require continued relaxation, re-injection of the muscle relaxant becomes necessary at or before 25% recovery.

PowerPoint Presentation:

Recovery index – The recovery index describes the speed of the offset of effect of a muscle relaxant, and is defined as the time taken for recovery from 25% to 75% twitch height. Total duration of action – The total duration of action is described by the interval between injection of the muscle relaxant and recovery of the TOF ratio to 0.9. “Priming” - Two successive injections of a nondepolarizing muscle relaxant can decrease the onset of muscle paralysis. Thus, a small subparalytic (“priming”) dose is injected about 3 minutes before the full intubating dose, it speeds the onset of effect with the subsequent dose.

CLASSIFICATION OF NMBA:

CLASSIFICATION OF NMBA CENTRALLY ACTING PERIPHERALLY ACTING

PowerPoint Presentation:

MECHANISM OF ACTION

PowerPoint Presentation:

SUCCINYLCHOLINE

Succinylcholine-Induced Hyperkalemia:

Succinylcholine-Induced Hyperkalemia Burn injury Massive trauma Severe intraabdominal infection Spinal cord injury Encephalitis Stroke Guillain-Barré syndrome Severe Parkinson's disease Tetanus Prolonged total body immobilization Ruptured cerebral aneurysm Polyneuropathy Closed head injury Hemorrhagic shock with metabolic acidosis Myopathies (eg, Duchenne's dystrophy)

NON DEPOLARIZING NMBA:

NON DEPOLARIZING NMBA T ubocurarine block s autonomic ganglia, thus compromising the ability of the sympathetic nervous system to increase heart contractility and rate in response to hypotension and other intraoperative stresses. P ancuronium (and gallamine) block vagal muscarinic receptors in the sinoatrial node, resulting in tachycardia. A tracurium and mivacurium are capable of triggering histamine release that result in bronchospasm, skin flushing, and hypotension from peripheral vasodilation, particularly at higher doses and rapid injection rates .

INTERACTIONS OF NMBA WITH OTHER DRUGS:

INTERACTIONS OF NMBA WITH OTHER DRUGS Antibiotics Anticonvulsants Antiarrhythmics Cholinesterase inhibitors Dantrolene Inhalational anesthetics Ketamine Local anesthetics Lithium carbonate Magnesium sulfate

RESIDUAL NEUROMUSCULAR BLOCKADE:

RESIDUAL NEUROMUSCULAR BLOCKADE Residual neuromuscular blockade can be defined by inadequate neuromuscular recovery as measured by objective neuromuscular monitoring. Recent opinion suggests a definition of inadequate train of four recovery of less than 0.9 (TOF <0.9)

ADVERSE EFFECTS OF RESIDUAL NEUROMUSCULAR BLOCKADE:

ADVERSE EFFECTS OF RESIDUAL NEUROMUSCULAR BLOCKADE

TREATMENT OF RESIDUAL NEUROMUSCULAR BLOCKADE:

TREATMENT OF RESIDUAL NEUROMUSCULAR BLOCKADE ABC. Rule out other potential causes . Is this really residual neuromuscular blockade? Check nerve stimulator, use a different nerve-muscle combination. Consider giving reversal . In some institutions, it is still not routine for reversal to be used, largely due to concerns of cholinergic symptoms of nausea and bradycardia with cholinesterase inhibition. Wait . Have you given enough time for the reversal to have effect? Is the patient stable enough to tolerate watchful waiting. Consider giving additional reversal. Note however, that if there is already complete inhibition of acetylcholinesterase , giving further neostigmine will not serve any useful purpose. Treat potentiating factors . Many factors prolong neuromuscular blockade, such as inhalational agents, opioids , acidosis, hypothermia, hypercarbia , hypoxia. Consider alternative methods of reversal ( Sugammadex if available)

authorStream Live Help