Drug manual

First-line treatment for regular narrow-complex tachycardia when vagal manoeuvres have failed. Acts by blocking the AV node for a few seconds, making it both therapeutic for reentry involving the node and diagnostic for arrhythmias that do not — atrial flutter and atrial tachycardia are unmasked when the ventricular response is slowed. The half-life of a few seconds means both the effect and side effects are over before one can regret it, but requires that the injection be given rapidly followed by a flush.

Multi-channel blocker for oral and intravenous use with properties from classes I–IV. Extensive tissue distribution and a half-life measured in weeks — initiation and discontinuation have consequences for months.

First-line treatment for symptomatic bradycardia, but only when the bradycardia is vagally mediated or located in the sinus node or AV node. Atropine blocks muscarinic receptors and thereby removes parasympathetic braking — if there is no such brake to remove, nothing happens, which is the entire explanation for why the drug is ineffective in infranodal block. The effect comes within one minute and fades over an hour or so, making it a bridge to pacing rather than a treatment.

Na⁺/K⁺-ATPase inhibitor with positive inotropy and vagal AV-node slowing. Rate control fails under adrenergic stress — making it a poor choice for the active patient and a reasonable one for the bedridden.

A potent sodium channel blocker with marked efficacy on atrial arrhythmias in structurally normal hearts. The CAST trial showed increased mortality after myocardial infarction — that boundary remains the most important fact in the drug's history.

The only drug that reduces heart rate without affecting contractility, blood pressure, or conduction — it inhibits the funny current (If) that drives spontaneous depolarisation of the sinus node and does nothing else. It therefore works only in sinus rhythm: in atrial fibrillation the rate control sits in the AV node and ivabradine is ineffective. Its place in treatment is the symptomatic patient with HFrEF who remains above 70 beats per minute despite maximally tolerated beta-blockade, where SHIFT demonstrated reduced risk of heart failure hospitalisation.

The most β₁-selective of the routinely used beta-blockers, with documented mortality benefit in heart failure from CIBIS-II. Bioavailability is close to 90 % and elimination is equally shared between liver and kidney, giving a predictable dose–effect relationship without the CYP2D6-dependent variability that makes metoprolol response unpredictable. The half-life of 10–12 hours is sufficient for once-daily dosing.

The beta-blocker to choose when reversibility matters. With a half-life of 9 minutes and the effect gone 20–30 minutes after the infusion ends, it is useful in patients where beta-blockade is desirable but risky — impending heart failure, obstructive lung disease, uncertain haemodynamics.

A cornerstone drug for hypertension and stable angina, and the easiest calcium channel blocker to use: once-daily dosing, a half-life of almost two days, and no dose adjustment in renal impairment. Unlike verapamil and diltiazem, amlodipine has no clinically significant negative inotropic effect and can therefore be used in heart failure with reduced ejection fraction when blood pressure or angina requires it. The slow onset makes the drug unsuitable for acute blood pressure reduction.

Ultra-short-acting dihydropyridine broken down by esterases in blood and tissue — the half-life is 5 minutes and the effect can be steered minute by minute. Selective for smooth muscle in the vessel wall: lowers systemic vascular resistance without affecting contractility, conduction, or filling pressure.

The intermediate form among calcium channel blockers: slows the AV node like verapamil but with less negative inotropy and more vasodilation, and causes less constipation. The cardiac oral formulations were withdrawn from the Swedish market in 2025 — only a rectal ointment remains registered — so oral and intravenous diltiazem require a named-patient licence. Verapamil or a beta-blocker is therefore the practical first choice for rate control in this setting.

A highly vascular-selective dihydropyridine given as a modified-release tablet once daily for hypertension and stable angina. The selectivity for vascular smooth muscle means felodipine lacks the nodal effects of verapamil and diltiazem — no bradycardia, no AV block, and no clinically significant negative inotropy, making it combinable with beta-blockers. The price of pure vasodilatation is dependent oedema, which is dose-related and the most common reason for discontinuation.

Prodrug hydrolysed to candesartan during absorption that binds the AT₁-receptor tightly and slowly reversibly — hence the even effect over 24 hours with once-daily dosing. The ARB that together with valsartan has documented mortality benefit in heart failure (CHARM), and the first choice when an ACE inhibitor must be switched due to cough. The target dose in heart failure is 32 mg — four times the usual hypertension dose.

Prodrug hydrolysed to enalaprilat. Reduces mortality in heart failure with reduced ejection fraction — the effect is dose-dependent, and underdosing is more often than adverse effects the reason for absent benefit.

The active metabolite of enalapril, given directly intravenously. Rarely used in hypertensive crisis: onset is slow, duration 8–24 hours, and the effect varies widely between individuals because it is governed by plasma volume and renin activity.

Inhibits the Na⁺/Cl⁻ cotransporter in the distal tubule and is the most commonly used thiazide diuretic for hypertension. The key point is that the dose–response curve for blood pressure flattens already at 2,5 mg, while the adverse effect curves for potassium, sodium, urate, and glucose continue to rise — higher doses therefore purchase side effects without blood pressure benefit. The antihypertensive effect is partly vasodilatory and persists after the initial volume reduction has normalised.

Inhibits the Na⁺/K⁺/2Cl⁻ transporter in the loop of Henle. The dose–response relationship is a threshold curve, not a line: below the threshold nothing happens, and in renal failure the threshold dose must be raised to achieve any effect at all.

The only antihypertensive that increases renal perfusion while blood pressure falls. A selective D1 agonist without alpha or beta effects, with onset within minutes and duration under one hour — theoretically attractive in hypertensive crisis with renal involvement, but without documented hard-endpoint benefit.

Direct-acting arteriolar vasodilator with no effect on the venous circulation. The rapid afterload reduction triggers reflex sympathetic activation, making the drug unsuitable as first-line treatment in hypertensive crisis — but useful in pre-eclampsia and as afterload relief in combination with a nitrate and beta-blocker.

Non-selective alpha-blocker with onset within minutes and duration under half an hour. A niche drug: catecholamine-induced hypertensive crisis — phaeochromocytoma, cocaine and amphetamine intoxication, MAO inhibitor crisis — and local treatment of skin necrosis after noradrenaline extravasation.

The only drug that reverses all components of anaphylaxis, and the cornerstone of cardiac arrest treatment. The most clinically dangerous property is not pharmacological but practical: two concentrations with a tenfold difference are used in the same setting.

Pure inotropy when the problem is the pump and not vascular tone. Strong β₁ effect with marked β₂ effect means that stroke volume increases while systemic vascular resistance falls at low doses — good in the cold, hypoperfused patient with an acceptable blood pressure, less so when blood pressure is already low. The dose threshold lies around 5 μg/kg/min: below that vasodilation predominates, above it the vascular effect shifts toward constriction.

Pharmacological pacemaker. Potent β₁-stimulation produces marked chronotropy and inotropy, while equally potent β₂-stimulation dilates the vessels — completely without alpha effect. The result is that heart rate rises while systemic vascular resistance and diastolic blood pressure fall, so the drug raises rate but not pressure. Used where rate itself is the problem: bradycardia while awaiting pacing, bradycardia-dependent torsades de pointes, and electrical storm in Brugada syndrome.

High-intensity statin with a long half-life, allowing it to be taken at any time of day unlike simvastatin. Muscle complaints are frequently reported but rarely confirmed in blinded re-challenge.

Inhibits intestinal cholesterol uptake via NPC1L1 and reduces LDL by an additional 20–25 % on top of a statin, independently of the statin dose. The first step when the statin is maximised and the LDL target is still not reached — a fixed dose of 10 mg, no titration, essentially no interactions, and an adverse effect profile barely distinguishable from placebo. IMPROVE-IT showed that the additional LDL lowering also translates into fewer cardiovascular events, making ezetimibe the first non-statin drug with outcome data.

Direct-acting factor Xa inhibitor with fixed dosing and no routine monitoring. Lower risk of intracranial haemorrhage than warfarin — but the short half-life means a missed dose has consequences within hours.

The only DOAC that directly inhibits thrombin and the only one with a specific, rapidly acting antidote — idarucizumab achieves complete reversal within minutes, which weighs heavily in patients who may need emergency surgery. The price is that approximately 80 % of absorbed drug is eliminated renally, so renal function governs treatment entirely. Dyspepsia affects one in ten patients and is the most common reason for discontinuation in clinical practice.

The workhorse anticoagulant in hospital practice: subcutaneous dosing once daily, predictable effect, and no need for routine monitoring, allowing home administration. The difference between the prophylactic dose and the therapeutic dose is fourfold and is expressed in IU — confusing the two is the most common dosing error. Unlike unfractionated heparin, dalteparin is eliminated renally, so at eGFR below 30 ml/min the effect accumulates and the dose must be adjusted or the drug changed.

The anticoagulant to choose when the ability to reverse rapidly matters: the half-life is one to two hours, the effect can be measured in real time with APTT, and it can be neutralised completely with protamine within minutes. This is why unfractionated heparin is the first choice in severe renal failure, in the bleeding-prone patient, and when surgery or thrombolysis may become necessary at short notice. The disadvantages are continuous infusion, an unpredictable dose–response relationship due to binding to plasma proteins, and the risk of heparin-induced thrombocytopenia.

Irreversibly acetylates COX-1, eliminating thromboxane synthesis in platelets for their entire lifespan. This is why a low once-daily dose is sufficient, and why the effect persists for 7–10 days after discontinuation.

Fibrin-specific plasminogen activator that dissolves fresh thrombus and is the standard thrombolytic for ischaemic stroke and haemodynamically significant pulmonary embolism. The dosing regimens differ entirely between indications — stroke is weight-based, pulmonary embolism and myocardial infarction use a fixed 100 mg — and confusing them is the most common serious error. The short half-life means the effect cannot be reversed once the dose is given.

Monoclonal antibody fragment that binds dabigatran with approximately 300 times higher affinity than dabigatran binds to thrombin — in practice it never lets go. The effect is immediate and complete: unbound dabigatran in plasma falls by over 99 per cent directly after the infusion. The specificity is also the limitation — it does nothing at all against apixaban, rivaroxaban, edoxaban, warfarin, or heparin.

An SGLT2 inhibitor whose clinical importance extends well beyond the diabetes indication. DAPA-HF demonstrated reduced cardiovascular death and worsening heart failure with reduced ejection fraction, DELIVER showed equivalent benefit with preserved and mildly reduced EF, and DAPA-CKD demonstrated slowed renal function decline and reduced mortality in chronic kidney disease with albuminuria, with or without diabetes. The dose is the same — 10 mg once daily — for all indications, making this drug unusually straightforward to manage.

A diabetes drug now used mostly for reasons other than glucose control. Empagliflozin reduced cardiovascular death in type 2 diabetes in EMPA-REG OUTCOME, reduced heart failure events regardless of ejection fraction in EMPEROR-Reduced and EMPEROR-Preserved, and slowed renal function decline down to eGFR 20 in EMPA-KIDNEY. The glucose-lowering effect diminishes as eGFR falls, but the cardiorenal effect persists — which is the entire point of the drug.

Two entirely different drugs in the same ampoule. In severe hypoglycaemia, 1 mg intramuscularly is the treatment that a family member can give when the patient cannot swallow and intravenous access is unavailable — the effect arrives within ten minutes through hepatic glycogenolysis. In beta-blocker intoxication, glucagon is instead an inotrope that bypasses the blocked beta receptor, and the doses are five to ten times higher. Never confuse the two indications.

The first-line treatment for severe hypoglycaemia in a patient who cannot swallow and in whom intravenous access is available. The effect arrives within a minute but is also short-lived — the bolus reverses unconsciousness but does not treat the cause. What determines management is the underlying aetiology: long-acting insulin and in particular sulphonylurea require follow-up infusion and hours of monitoring, whereas a missed meal in a type 1 diabetic can be managed with a sandwich.

The mealtime insulin in Swedish healthcare and simultaneously the insulin used for intravenous infusion in diabetic ketoacidosis and hyperosmolar hyperglycaemic state. Subcutaneously it has an onset within 10–20 minutes and a duration of 3–5 hours; intravenously the half-life is a few minutes, which makes the infusion fully controllable but also means the effect ceases within minutes if the drip stops. Always clearly distinguish the subcutaneous from the intravenous regimen — they have no dose relationship.

The basal insulin that covers the basal insulin requirement between meals and overnight, with a largely flat profile over 24 hours and therefore a lower risk of nocturnal hypoglycaemia than NPH insulin. It is titrated against fasting glucose and nothing else — the morning fasting value drives the evening dose. Available in two strengths, 100 units/ml and 300 units/ml, and the two are not the same medicine even though both are dosed in units.

First-line agent for osteoporosis and the best-documented fracture-preventing treatment in primary care. Efficacy for vertebral and hip fractures is well established, but depends on the patient's ability to follow the administration instructions and on adequate calcium and vitamin D status. After five years, treatment should be reviewed and is often paused.

The same substance is used for four entirely different indications with doses differing up to a hundredfold — antidiuretic substitution in central diabetes insipidus, symptom relief in nocturia and nocturnal enuresis, and haemostatic release of von Willebrand factor and factor VIII. Selectivity for the V2 receptor means it lacks the vasoconstrictive effect of vasopressin. The danger is not the drug itself but the fluid the patient drinks with it.

Aminopenicillin that covers Haemophilus influenzae in addition to pneumococci — and it is that difference from phenoxymethylpenicillin that determines its use. Amoxicillin is therefore not first-line for uncomplicated acute otitis media — that role belongs to phenoxymethylpenicillin — but for treatment failure, recurrent otitis, otitis with concurrent purulent conjunctivitis, and as a suspension alternative in pneumonia in young children. Oral bioavailability is substantially better than phenoxymethylpenicillin and is not affected by food.

First-line treatment for community-acquired pneumonia and erysipelas, and the foundation of the narrow-spectrum antibiotic tradition. Pneumococci, streptococci, and most oral anaerobes remain sensitive, and the resistance situation is favourable compared to almost all other countries. Time-dependent killing means that the dosing interval matters more than the size of any individual dose — four doses are preferable to two large ones.

Broad coverage of pneumococci, Haemophilus, meningococci, and most Enterobacterales, with good CNS penetration — making this the standard choice for community-acquired bacterial meningitis and severe sepsis of unknown origin. The price is ecological: cephalosporins are one of the strongest drivers of Clostridioides difficile and ESBL-producing enteric bacteria, and should therefore be stepped down to a narrower alternative as soon as culture results allow.

The tetracycline that covers both respiratory pathogens and the intracellular organisms that beta-lactams miss — Mycoplasma pneumoniae, Chlamydophila, and Borrelia. Near-complete oral absorption and a long half-life make once-daily dosing possible. It is the standard choice in pneumonia in penicillin-allergic patients and in atypical pneumonia, but the age limit of 8 years and pregnancy significantly restrict use.

The beta-lactamase-stable penicillin and accordingly the first-line choice for skin and soft tissue infections where Staphylococcus aureus is the likely pathogen — wound infection, abscess, furuncle, mastitis, and infected eczema. Absorption is destroyed by food, making the timing of administration a genuine treatment variable and not a formality. The most clinically important adverse effect is delayed: cholestatic liver injury can present several weeks after the course has ended.

The first-choice oral penicillin for the most common respiratory and skin infections in outpatient care, and one of the reasons Sweden maintains a favourable resistance situation. The spectrum covers group A streptococci and pneumococci but not Haemophilus influenzae or staphylococci. Dosing differs substantially between indications — tonsillitis and acute otitis media are treated with different doses and durations, and this is a common source of error in practice.

Formoterol is the only long-acting β₂-agonist with onset within a few minutes, and that property is precisely what makes the combination useful both as maintenance and as reliever therapy. The product can therefore be prescribed in two entirely different ways: as a fixed dose morning and evening with a separate SABA as needed, or as maintenance-and-reliever therapy in the same inhaler. The two regimens must never be confused — this is the most common prescribing error with this drug.

First-line treatment for allergic rhinoconjunctivitis and chronic urticaria — one tablet daily, available without prescription, with good effect on itching, sneezing, and rhinorrhoea but weaker on nasal congestion. The critical difference from clemastine and promethazine is that cetirizine penetrates the blood-brain barrier poorly, but it is not entirely free of sedation: a distinct minority of patients become drowsy, and this should be asked about in professional drivers. Renal function governs the dose.

Betapred is a distinctive formulation: the soluble tablet allows a child with croup or a patient with an allergic reaction to receive a full steroid dose without an injection, and the long biological duration means a single dose suffices. Potency is approximately 25 times that of hydrocortisone and mineralocorticoid effect is absent, making it suitable in cerebral oedema and cord compression where sodium retention is undesirable. The effect is not immediate — it requires hours and never replaces adrenaline in anaphylaxis.

Endogenous cortisol in pharmaceutical form and accordingly the first choice when the intention is substitution rather than immunosuppression. Unlike prednisolone, betamethasone, and dexamethasone, hydrocortisone has a clinically meaningful mineralocorticoid effect, which is the entire point in adrenocortical insufficiency — and the short duration allows the daily dose to be distributed to mimic the physiological cortisol pattern. Keep the three dose levels distinct: substitution, stress dose, and crisis.

Potent NSAID with good effect in musculoskeletal and postoperative pain, but with the most unfavourable cardiovascular profile in the class — the increase in risk for myocardial infarction, stroke, and heart failure resembles that of selective COX-2 inhibitors and is seen already at doses below 100 mg/day and with short treatment duration. Oral diclofenac therefore requires a prescription in Sweden since 1 June 2020, while topical formulations remain non-prescription because systemic exposure is low.

The first-line NSAID in Sweden and the one with the least cardiovascular risk at a low dose. A short half-life of around 2 hours means the effect arrives and resolves quickly, which is an advantage: the drug suits as-needed use and can be discontinued with rapid recovery of renal function and platelet function. The short duration is also why three to four doses per day are required for continuous pain.

The only anaesthetic that both sedates and stabilises the circulation — the indirect sympathetic stimulation makes ketamine the first choice for induction in the bleeding, septic, or otherwise preload-dependent patient, and the bronchodilation makes it valuable in life-threatening asthma. Respiratory drive and laryngeal reflexes are largely preserved, which is an explanation but never a guarantee. The key practical distinction is between the three dose levels: analgesia, procedural sedation, and induction are different drugs in the same ampoule.

The benzodiazepine with two faces. As a single dose in seizures it is fast and reliable — high lipid solubility gives onset within a couple of minutes intravenously, and the rectal solution works when no intravenous access is available. As standing treatment it is something entirely different: the parent compound has a half-life of one to two days and the active metabolite desmethyldiazepam up to four, so the concentration continues to rise for a week after initiation. That long tail is simultaneously the point in withdrawal treatment, where it provides a smooth self-tapering.

A tricyclic antidepressant that is rarely used for depression in contemporary practice — its role today is neuropathic pain and prophylaxis for migraine and chronic tension-type headache, at doses well below the antidepressant range. The effect on pain occurs already at 10–50 mg and depends on noradrenergic and sodium-channel-mediated modulation, not on antidepressant action. What limits treatment is anticholinergic side effects, and what makes the drug dangerous is cardiotoxicity in overdose.

The most selective of the SSRIs and one of the best tolerated for depression and generalised anxiety disorder. What governs dosing is not efficacy but the heart: a dose-dependent QT prolongation was identified, and the maximum dose has since been capped at 20 mg for adults and 10 mg for patients over 65 years. In the elderly, hyponatraemia is the adverse effect most often causing discontinuation.

The most widely used dopamine antagonist in acute agitation and delirium in Swedish emergency departments and wards, with rapid onset and minimal anticholinergic burden. The drug has two entirely different dosing worlds: a few milligrams in acute psychotic agitation in younger patients, and tenths of a milligram in delirium in the elderly, where the lowest effective dose for the shortest possible time is the whole principle. What governs safety is the QT interval and extrapyramidal adverse effects.

The same mechanism as pregabalin — binding to the α2δ subunit of voltage-gated calcium channels — but with a critical difference in kinetics: absorption occurs via a saturable amino acid transporter in the gut, so bioavailability falls as the dose rises and the dose–concentration relationship is non-linear. Hence the wide dose range and three-times-daily regimen. Used in peripheral neuropathic pain and as adjunctive treatment in focal epilepsy. Excreted unchanged renally, making renal function the single most important dosing variable.

First-line urate-lowering treatment for gout, with the goal of titrating upward until serum urate is stably below 360 μmol/l — not setting a fixed dose and leaving it. Treatment is lifelong, and the first months require flare prophylaxis because falling urate levels themselves trigger attacks. Two features make this drug dangerous: the hypersensitivity syndrome and the combination with azathioprine.

First-line intervention in hyperkalaemia with ECG changes: calcium restores the margin between resting membrane potential and threshold potential and protects the myocardium against arrhythmia within minutes — but does not lower potassium by a tenth of a millimole. Insulin-glucose, beta-agonists, and dialysis must be started in parallel, otherwise the arrhythmia risk returns when the calcium effect wanes after half an hour. Calcium gluconate contains approximately one third as much elemental calcium per ml as calcium chloride, and that confusion is the most common dosing error in acute calcium treatment.

Potassium deficiency is corrected slowly because extracellular potassium is only two per cent of the body's total potassium store — the plasma value indicates the starting point, not the magnitude of the deficit. Rate, not daily dose, is what determines safety: peripherally 10 mmol per hour, in a central vein up to 20 mmol per hour, and at most 40 mmol per hour in life-threatening hypokalaemia under continuous ECG monitoring. Hypokalaemia that refuses to rise despite adequate replacement is almost always caused by concurrent hypomagnesaemia, and magnesium must then be given first.