Drug Therapy Protocols

Inhibits NMDA receptors and activates GABA-A receptors in the CNS at sub-anaesthetic doses, producing rapid analgesic effect without loss of consciousness. At prehospital doses, does not cause general anaesthesia.

Inhibits prostaglandin synthesis centrally via COX pathways and activates descending serotonergic pathways. Antipyretic action via hypothalamic temperature regulation. Unlike NSAIDs, lacks peripheral anti-inflammatory effect.

Binds to mu (μ), kappa (κ) and delta (δ) opioid receptors in the CNS and periphery, producing analgesia, sedation, euphoria, and respiratory depression. Reduces pain perception and affective response to pain.

Potent selective mu (μ) opioid receptor agonist. 100× more potent than morphine. Rapid onset due to high lipid solubility. Short duration of action. Causes analgesia, sedation, euphoria, respiratory depression.

Selective β2-adrenoceptor agonist. Stimulates β2 receptors in bronchial smooth muscle, activating adenylyl cyclase → increased cAMP → bronchodilation. Also stimulates Na+/K+ ATPase (can cause hypokalaemia at high doses). Minimal β1 cardiac effects at therapeutic doses.

Competitive antagonist of muscarinic (ACh) receptors in bronchial smooth muscle. Reduces bronchoconstriction and secretions by blocking parasympathetic tone. Slower onset than salbutamol — used as adjunct. Promotes mucociliary tone.

Supplemental oxygen increases alveolar partial pressure of O2 (PAO2), increasing haemoglobin saturation and arterial oxygen content (CaO2). Corrects hypoxaemia. At high concentrations, can cause free radical injury (oxygen toxicity) and in COPD patients, may suppress hypoxic respiratory drive.

Irreversibly inhibits cyclo-oxygenase (COX-1 and COX-2), preventing thromboxane A2 synthesis in platelets. This reduces platelet aggregation for the platelet's lifespan (~7–10 days). Also has analgesic and antipyretic properties via prostaglandin inhibition.

Releases nitric oxide (NO) in vascular smooth muscle → activates guanylyl cyclase → increased cGMP → smooth muscle relaxation and vasodilation. Predominantly venodilation, reducing preload. At higher doses, dilates coronary arteries and reduces afterload. Decreases myocardial O2 demand.

Multi-channel blocker: primarily blocks K+ channels (prolongs action potential and refractory period), also blocks Na+ and Ca2+ channels and has β-blocking properties. Slows conduction and decreases automaticity. Used for shock-refractory VF/pVT.

Irreversibly blocks ADP-binding P2Y12 receptors on platelets, inhibiting ADP-mediated platelet aggregation. Prodrug — requires hepatic conversion to active metabolite. Used alongside aspirin for dual antiplatelet therapy in ACS.

Positive allosteric modulator of GABA-A receptors. Binds to benzodiazepine site → increases frequency of Cl⁻ channel opening → hyperpolarisation of neurons → CNS depression. Produces anxiolysis, sedation, muscle relaxation, retrograde amnesia, and anticonvulsant effects.

Competitive antagonist at mu (μ), kappa (κ) and delta (δ) opioid receptors, rapidly reversing opioid-induced respiratory depression, sedation and analgesia. Shorter duration than many opioids — re-sedation may occur ("renarcotisation"). Does not produce analgesia.

D2 receptor antagonist (dopamine blocker). Also blocks alpha-adrenergic, muscarinic, and histamine receptors. Produces sedation, anti-nausea, and antipsychotic effects. Used prehospitally for severe behavioural disturbance and acute agitation.

Blocks serotonin (5-HT3) receptors peripherally in the gut and centrally in the chemoreceptor trigger zone (CTZ) and vomiting centre. Reduces afferent vagal stimulation from gut and central emetic signals. No antidopaminergic effects (no extrapyramidal side effects at standard doses).

Reversibly inhibits COX-1 and COX-2 enzymes, reducing prostaglandin synthesis. Anti-inflammatory, analgesic and antipyretic. Unlike aspirin, effect is reversible on platelets. Peripheral and central action.

Pure glucose (dextrose) absorbed rapidly from the GI tract and buccal mucosa into the bloodstream. Principal energy source for cells — especially CNS neurons which are entirely dependent on glucose. Corrects hypoglycaemia by raising blood glucose levels.

IV glucose directly raises blood glucose levels when oral route is unavailable (unconscious patient, unable to swallow). 10% solution (100 mg/mL) provides glucose substrate for cellular metabolism. Faster and more reliable than oral glucose in altered conscious patients.

Endogenous pancreatic hormone. Activates hepatic glycogenolysis and gluconeogenesis → raises blood glucose. Also has positive inotropic and chronotropic effects via cAMP. Used when IV access unavailable for hypoglycaemia, and as an antidote in beta-blocker/calcium channel blocker overdose.

Acts on alpha-1 (vasoconstriction → increases SVR and coronary perfusion pressure), beta-1 (increases HR and contractility), and beta-2 (bronchodilation) adrenoceptors. In cardiac arrest: increases aortic diastolic pressure and myocardial perfusion. In anaphylaxis: reverses vasodilation, bronchospasm and angioedema.

Competitive antagonist of acetylcholine at muscarinic receptors. Blocks parasympathetic (vagal) tone, increasing heart rate via SA node. Also dries secretions, dilates pupils, relaxes smooth muscle. Used for bradycardia with haemodynamic compromise and organophosphate poisoning.

Physiological calcium antagonist and membrane stabiliser. Reduces acetylcholine release at neuromuscular junction. Decreases myometrial tone (tococolysis). Blocks NMDA receptors (anticonvulsant). Widens T-wave and prolongs refractory period (antiarrhythmic). Acts on smooth muscle bronchodilation.

Binds glucocorticoid receptors → decreases synthesis of inflammatory mediators (prostaglandins, leukotrienes, cytokines). Reduces capillary permeability, inflammation and immune response. Slow onset (4–6 hours for full anti-inflammatory effect) — adjunct to adrenaline in anaphylaxis. Also replaces cortisol in adrenal insufficiency.

Potent synthetic glucocorticoid (25–30× more potent than hydrocortisone). Binds glucocorticoid receptors, powerfully suppresses inflammation and immune response. In croup: reduces subglottic oedema and stridor. Minimal mineralocorticoid activity.

Selective antagonist of peripheral H1 histamine receptors. Non-sedating — minimal CNS penetration. Blocks histamine-mediated vasodilation, bronchoconstriction, urticaria and pruritus. Used as adjunct in mild–moderate allergic reactions. Not effective in anaphylaxis — adrenaline is required.

Beta-lactam antibiotic that inhibits bacterial cell wall synthesis by binding penicillin-binding proteins (PBPs), leading to cell lysis and death. Broad-spectrum including gram-positive and gram-negative organisms. Excellent CSF penetration — used for meningococcal septicaemia prehospitally.

Binds cyanide ions with high affinity to form cyanocobalamin (non-toxic), which is excreted in urine. Restores mitochondrial cytochrome oxidase function and cellular respiration. Direct antidote — superior to other treatments. Turns body fluids red/brown (benign side effect).

Binds antithrombin III, potentiating inhibition of factor Xa and thrombin. Prevents fibrin clot formation and extension. More predictable pharmacokinetics than unfractionated heparin. Used in ACS to prevent coronary re-thrombosis.