Pharmacology and Anaesthesia
Anaesthetic agents
Inhaled agents are compared by MAC, the concentration abolishing movement to a standard stimulus in half of patients; potency is inversely related to MAC. Induction agents differ in haemodynamics: propofol causes vasodilatation and hypotension, ketamine preserves blood pressure and is useful in hypovolaemia, etomidate is stable but suppresses adrenal steroidogenesis, and thiopentone is the classic choice when intracranial pressure must be controlled.
Muscle relaxants
Suxamethonium is depolarising and rapid; it causes hyperkalaemia (dangerous after burns, denervation or prolonged immobility beyond 24–48 hours), triggers malignant hyperthermia (treated with dantrolene 2.5 mg/kg) and reveals pseudocholinesterase deficiency as prolonged apnoea. Non-depolarising agents are reversed with neostigmine plus an antimuscarinic, or rocuronium with sugammadex.
Local anaesthetics
These are weak bases; onset depends on pKa relative to tissue pH, so inflamed acidic tissue slows onset. Maximum doses for lidocaine are about 3 mg/kg plain and 7 mg/kg with adrenaline; bupivacaine is limited to 2 mg/kg because of cardiotoxicity. Local anaesthetic systemic toxicity is treated with intravenous 20% lipid emulsion.
Perioperative drugs
NSAIDs impair renal function and platelet aggregation and may delay bone healing. Warfarin is reversed with vitamin K and prothrombin complex; heparin with protamine; dabigatran with idarucizumab.
Rule of thumb: the closer a local anaesthetic's pKa is to body pH, the greater the uncharged fraction and the faster the block - which is why infection and acidosis slow it down.