What is the goal of glaucoma treatment?

The goal is to reduce intraocular pressure in order to delay or prevent progression of optic nerve damage and visual field loss.

What are the first-line drugs for glaucoma?

Prostaglandin analogues are frequently used as first-line therapy because of their effectiveness in reducing intraocular pressure and their simple dosing schedule.

When should topical beta-blockers be used?

Topical beta-blockers may be used as an alternative or add-on therapy, but require caution in patients with asthma, COPD, bradycardia, atrioventricular block or heart failure.

What are the main adverse effects of glaucoma eye drops?

Adverse effects may include conjunctival hyperaemia, ocular irritation, iris pigmentation changes, eyelash growth, dry eye, local allergy and systemic effects depending on the pharmacological class.

Should glaucoma treatment be continued long term?

Yes. In most cases, treatment is chronic and should be used regularly, with ophthalmological follow-up to assess intraocular pressure, the optic nerve and the visual field.

When should more than one drug be combined?

Combination therapy may be required when target intraocular pressure is not achieved with monotherapy or when there is progression despite appropriate treatment.

When should laser or surgery be considered?

Laser or surgery should be considered when pressure control is insufficient, disease progression occurs, topical therapy is not tolerated or there is significant difficulty with adherence.

Why is adherence to eye drops important?

Treatment adherence is essential because interruption or irregular use of eye drops may lead to increased intraocular pressure and irreversible progression of visual loss.

Glaucoma medications: drugs and mechanisms

Medical treatment of glaucoma is based on reducing intraocular pressure (IOP) as the main therapeutic goal, currently achieved mainly through modulation of aqueous humour dynamics. Options include drugs that reduce aqueous humour production, such as carbonic anhydrase inhibitors, beta-blockers and alpha-agonists, and agents that increase trabecular or uveoscleral outflow, such as prostaglandin analogues, cholinergic agonists and combined agents, as well as fixed combinations that improve adherence and help achieve lower pressure targets.
This table provides a comparative summary of the main pharmacological classes used in open-angle glaucoma, including their mechanisms of action, relevant adverse effects, preferred indications and key clinical safety notes.

Podcast transcript

Initial assessment (ECG)

Patient with tachycardia and suspected atrial fibrillation. The first step is to confirm the diagnosis with a 12-lead ECG. Once AF is confirmed, define the treatment strategy, starting with the identification of reversible secondary causes.

Reversible secondary causes

Screen for electrolyte or acid–base disturbances, pericarditis, myocarditis, hyperthyroidism, sepsis, anaemia, gastrointestinal bleeding, hypothermia, or drug toxicity. Also consider decompensated heart failure, acute coronary syndrome, and hypovolaemia. If any cause is identified, treat the underlying condition.

Hemodynamic stability and red flags

If no reversible cause is found, the therapeutic decision centres on rhythm vs rate control. First, assess hemodynamic stability. Instability presents with systolic BP < 90 mmHg associated with altered mental status, chest pain, dyspnoea, or presyncope/syncope. Other red flags include acute ischaemia with ST-segment changes, elevated cardiac biomarkers, or decompensated heart failure.

Accessory pathway and specialist support

If the patient is hemodynamically unstable, request specialist support. Do the same when an accessory pathway is suspected—e.g., wide, bizarre, or polymorphic QRS complexes; history of Wolff–Parkinson–White; or a delta wave on prior ECGs.

Treatment strategy: rhythm vs rate

In stable patients, choose between rhythm and rate control. Rate control is generally favoured in patients >65 years, with hypertension, without heart failure, those preferring this approach, refractory to prior antiarrhythmics, or minimally symptomatic. Rhythm control can be considered when significant symptoms persist despite adequate rate control.

Cardioversion and episode duration

The decision to perform pharmacological or electrical cardioversion depends on AF duration. If <48 hours, cardioversion can be considered directly. If >48 hours or unknown, a minimum of 3 weeks of effective anticoagulation is required, or alternatively, a transoesophageal echocardiogram to exclude intracardiac thrombus. Recent stroke/TIA, peripheral thromboembolism, mechanical valve, or rheumatic heart disease contraindicate immediate cardioversion without prior anticoagulation.

Rhythm control: drugs and exclusions

If rhythm control is chosen and no exclusion criteria are present (second/third-degree AV block, prolonged QT, hypokalaemia, pregnancy, or severe renal/hepatic impairment), antiarrhythmics such as amiodarone, flecainide, propafenone, or sotalol may be used. In structural, ischaemic, or valvular heart disease, or with LV hypertrophy, avoid flecainide and propafenone; prefer amiodarone or sotalol. In heart failure, amiodarone is usually the drug of choice.

Rate control: LVEF-dependent

When opting for rate control, selection depends on left-ventricular ejection fraction. If LVEF <40%, use low-dose beta-blockers (e.g., metoprolol) and consider adding digoxin. With preserved LVEF, beta-blockers, non-dihydropyridine calcium-channel blockers (diltiazem or verapamil), or digoxin can be used alone or in combination.

Chronic anticoagulation

After initial control, start maintenance therapy (rhythm or rate) according to the chosen strategy. In all cases, assess thromboembolic risk and the need for long-term anticoagulation based on the CHA₂DS₂-VASc score.

Shared decision-making and follow-up

Therapy should be individualised, considering symptoms, comorbidities, contraindications, and the patient’s informed preference. Ensure an appropriate follow-up plan after discharge.

Clinical cases

Clinical cases — Atrial fibrillation

Case 1 — Recent-onset AF, stable patient

Male, 45, no relevant history, palpitations for 12 hours. ECG: atrial fibrillation, HR 140 bpm, no signs of ischaemia. BP 125/75 mmHg, no dyspnoea, no HF. No prior anticoagulation. What is the most appropriate next step?

Start anticoagulation for 3 weeks and only then consider cardioversion
Start aspirin 150–300 mg/day
Immediate cardioversion (electrical or pharmacological), followed by anticoagulation according to CHA₂DS₂-VASc
Rate control only with IV diltiazem

Show answer

c) Immediate cardioversion (<48 h), followed by an anticoagulation decision according to thromboembolic risk. Rationale: In AF of <48 h duration and a stable patient, it is acceptable to cardiovert without prior anticoagulation; ensure post-cardioversion anticoagulation according to CHA₂DS₂-VASc and bleeding risk. A 3-week delay is required when duration is >48 h or unknown.

Case 2 — AF with pre-excitation (suspected accessory pathway)

Female, 28, rapid irregular palpitations; ECG: irregular tachyarrhythmia with variable wide QRS; prior records show a delta wave. Haemodynamically stable. What is the best initial therapeutic option?

IV adenosine bolus
IV diltiazem
IV amiodarone loading
IV procainamide (or electrical cardioversion if the patient deteriorates)

Show answer

d) IV procainamide (or immediate electrical cardioversion if unstable).
Rationale: In AF with an accessory pathway, avoid AV-node blockers (adenosine, verapamil/diltiazem, digoxin and, in many protocols, IV amiodarone) due to the risk of facilitating conduction via the pathway and degeneration to VF. Agents that slow conduction in the accessory pathway (e.g., procainamide or ibutilide) are preferred; if instability occurs, perform immediate electrical cardioversion.

Case 3 — AF >48 h/unknown duration: pre-cardioversion strategy

Male, 72, with hypertension and diabetes (CHA₂DS₂-VASc = 3), intermittent palpitations for “several days,” no precise record. ECG: AF, HR 110 bpm; stable. What is the correct approach before elective cardioversion?

Immediate cardioversion without anticoagulation because he is haemodynamically stable
Start a DOAC and maintain effective anticoagulation for ≥3 weeks before cardioversion (or TOE to exclude thrombus and cardiovert earlier)
Start aspirin monotherapy for 3 weeks
Prophylactic heparin for 24 h and then cardioversion

Show answer

b) Effective anticoagulation for ≥3 weeks (or a TOE-guided strategy).
Rationale: With duration >48 h or unknown, cardioversion requires anticoagulation for ≥3 weeks, or a strategy using trans-oesophageal echocardiography to exclude thrombus before cardioversion. Continue post-cardioversion anticoagulation according to CHA₂DS₂-VASc.

FAQ

Frequently Asked Questions about Atrial Fibrillation (AF) in Acute Care

1) How is AF diagnosed in the emergency setting?

Diagnosis is confirmed with a 12-lead ECG, showing disorganised atrial activity (no clear P waves) and irregularly irregular RR intervals. In an irregular tachyarrhythmia with a wide QRS, suspect an accessory pathway until proven otherwise.

2) What are the signs of haemodynamic instability?

Hypotension (SBP < 90 mmHg), altered mental status, chest pain/ischaemia, severe dyspnoea or decompensated heart failure. In these cases, prioritise electrical cardioversion and specialist support.

3) When should I choose rhythm control versus rate control?

In stable patients, rate control is generally preferred (e.g., age > 65 years, comorbidities, mild symptoms). Rhythm control is appropriate when significant symptoms persist despite adequate rate control, in recent-onset AF, or when rapid functional recovery is desired.

4) How does AF duration guide cardioversion?

If duration is < 48 hours, immediate cardioversion can be considered. If > 48 hours or unknown, it requires effective anticoagulation for ≥ 3 weeks or a TOE-guided strategy to exclude thrombus before cardioversion.

5) Who should receive anticoagulation and for how long?

Decide based on the CHA₂DS₂-VASc score. After cardioversion, maintain anticoagulation for at least 4 weeks and, long-term, according to thromboembolic and bleeding risk. Aspirin does not replace anticoagulation in AF.

6) What should be avoided if an accessory pathway (pre-excited AF) is suspected?

Avoid drugs that block only the AV node (e.g., adenosine, verapamil/diltiazem, digoxin). Prefer agents acting on the accessory pathway (e.g., procainamide) or electrical cardioversion if unstable.

7) How do I choose rate-contr

References

Authorship and updates

Author(s): Elvira Teles Sampaio (MD)

Last review: (16/02/2026) Filipe Cerca, MD

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08/07/2026

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Drug	Class / target	Mechanism / clinical impact	Main adverse effects	Main use	Clinical notes / safety
Prostaglandin analogues / prostamides
Latanoprost	PGF_2α analogue	Increases uveoscleral outflow, reducing intraocular pressure (IOP) by approximately 25–30% with once-daily evening dosing.	Conjunctival hyperaemia, eyelash growth and darkening, iris and eyelid skin pigmentation, mild ocular irritation.	First-line treatment in primary open-angle glaucoma and ocular hypertension, unless contraindicated.	Explain the risk of irreversible cosmetic changes, especially iris colour and eyelid skin pigmentation. Use with caution in patients with previous uveitis, macular oedema or recent ocular surgery.
Travoprost	PGF_2α analogue	Increases uveoscleral outflow; efficacy is similar or slightly superior to latanoprost in some patients.	More marked conjunctival hyperaemia, irritation, iris/eyelid pigmentation and eyelash changes.	First-line alternative when latanoprost is insufficient or poorly tolerated.	Prefer preservative-free formulations in dry eye or ocular surface disease. Monitor pigmentation over time.
Bimatoprost	Prostamide / prostaglandin analogue	Increases uveoscleral and trabecular outflow, with potent IOP reduction.	Frequent conjunctival hyperaemia, pruritus, iris pigmentation, eyelid skin darkening and deepening of the upper eyelid sulcus.	Glaucoma/ocular hypertension when greater IOP reduction is required or after partial failure of other prostaglandin analogues.	Higher risk of periocular cosmetic changes; discuss benefit/risk in younger patients. Avoid in active uveitis or cystoid macular oedema.
Tafluprost (PF)	Preservative-free PGF_2α analogue	Reduces IOP by increasing uveoscleral outflow; similar profile to other prostaglandin analogues, with a preservative-free formulation.	Hyperaemia, irritation, iris and eyelash pigmentation; lower ocular surface toxicity due to absence of preservatives.	Patients with glaucoma and moderate/severe dry eye or intolerance to BAK and other preservatives.	Good option in polymedicated patients and after ocular surgery when the ocular surface is fragile. Continue monitoring pigmentation.
Topical beta-blockers
Timolol	Non-selective beta-blocker	Reduces aqueous humour production, lowering IOP by approximately 20–25% as monotherapy.	Bradycardia, hypotension, bronchospasm, fatigue, depression, erectile dysfunction; mild ocular irritation.	Second-line treatment or add-on therapy in POAG/ocular hypertension, especially when prostaglandin analogues are contraindicated.	Contraindicated in asthma, COPD with bronchospastic component, second- or third-degree AV block and decompensated heart failure. Teach nasolacrimal occlusion to reduce systemic absorption.
Timolol gel 0.1–0.5%	Non-selective beta-blocker, gel formulation	Prolonged release allows once-daily administration with efficacy similar to twice-daily dosing.	Systemic adverse effects similar to timolol solution; transient blurred vision after instillation.	Patients in whom regimen simplification or improved adherence with once-daily dosing is desired.	Despite fewer instillations, the same cardiopulmonary precautions as conventional timolol apply.
Betaxolol	β₁-selective beta-blocker	Reduces aqueous humour production with some cardiac selectivity and lower bronchoconstrictive effect.	Bradycardia, hypotension, fatigue; ocular irritation and stinging after instillation.	Alternative to timolol in patients with mild/stable COPD or increased risk of bronchospasm.	Despite selectivity, it is not free of respiratory risk; avoid in moderate/severe asthma. Monitor heart rate and blood pressure.
Alpha-2 adrenergic agonists
Brimonidine	Selective α₂-adrenergic agonist	Reduces aqueous humour production and increases uveoscleral outflow; lowers IOP by approximately 20–25% as monotherapy.	Frequent follicular allergic conjunctivitis, hyperaemia, dry mouth, fatigue and somnolence.	Second-line or adjunctive therapy in POAG when prostaglandin analogues or beta-blockers are insufficient or poorly tolerated.	Contraindicated in infants under 2 years and not recommended in young children because of the risk of respiratory depression. Monitor for ocular allergy and stop if chronic conjunctivitis develops.
Apraclonidine	α₂-adrenergic agonist	Rapidly reduces aqueous humour production, with strong effect but significant tachyphylaxis.	Allergic conjunctivitis, hyperaemia, skin pallor, dry mouth and headache.	Mainly short-term use: prevention/treatment of post-laser IOP spikes and pharmacological testing in Horner syndrome.	Not recommended as chronic glaucoma therapy because of high rates of tachyphylaxis and allergy. Avoid in young children.
Carbonic anhydrase inhibitors — topical
Dorzolamide	Carbonic anhydrase inhibitor (CAI)	Reduces aqueous humour production by inhibiting carbonic anhydrase in the ciliary body.	Ocular burning/stinging, bitter taste, punctate keratitis and, rarely, sulfonamide-like reactions.	Adjunctive therapy with prostaglandin analogues or beta-blockers when target IOP is not achieved.	Use with caution in patients with Fuchs endothelial dystrophy or very low endothelial cell count because of the risk of corneal oedema.
Brinzolamide	Carbonic anhydrase inhibitor (CAI)	Same mechanism as dorzolamide, with an opalescent suspension and pH closer to tears, improving tolerability in some patients.	Transient blurred vision, mild discomfort, bitter taste; possible sulfonamide reactions.	Topical alternative to dorzolamide as adjunctive therapy or when dorzolamide is poorly tolerated.	Same precautions regarding corneal endothelium and renal function in high-risk patients.
Carbonic anhydrase inhibitors — systemic
Acetazolamide	Systemic CAI, sulfonamide	Systemic carbonic anhydrase inhibition, rapidly reducing aqueous humour production.	Paraesthesia, anorexia, nausea, taste disturbance, polyuria, nephrolithiasis, metabolic acidosis, hypokalaemia and, rarely, severe sulfonamide-like reactions.	Glaucoma crisis and acute situations with very high IOP; bridge therapy before surgery or while topical treatment is being adjusted.	Avoid in significantly reduced eGFR, acidosis, hyponatraemia/hypokalaemia and sulfonamide allergy. Chronic use should be exceptional and requires strict electrolyte monitoring.
Methazolamide	Systemic CAI	Mechanism similar to acetazolamide, with a longer half-life and sometimes better gastrointestinal tolerability.	Similar adverse effects: gastrointestinal symptoms, paraesthesia, acidosis and rare haematological abnormalities.	Alternative to acetazolamide when it is poorly tolerated and systemic CAI therapy remains justified.	The same renal, electrolyte and hypersensitivity contraindications apply. Monitor renal function and electrolytes.
Fixed combinations
Latanoprost + timolol	PGF_2α analogue + beta-blocker	Combines increased uveoscleral outflow from latanoprost with reduced aqueous humour production from timolol, providing additional IOP reduction.	Combined adverse effects: hyperaemia and cosmetic prostaglandin effects plus the risk of systemic beta-blocker effects.	Patients requiring two drugs who are already controlled and tolerant to separate prostaglandin analogue plus beta-blocker therapy.	Reduces the number of instillations and preservative exposure, potentially improving adherence. Maintain beta-blocker contraindications.
Dorzolamide + timolol	Topical CAI + beta-blocker	Combines reduction of aqueous humour production through two complementary mechanisms, allowing greater IOP reduction.	Ocular irritation, bitter taste, risk of corneal oedema from CAI plus systemic beta-blocker effects.	Alternative when prostaglandin analogues are unsuitable or as second-/third-line therapy in refractory IOP.	Useful to simplify multi-drop regimens. Check beta-blocker contraindications and corneal endothelial status.
Brimonidine + timolol	α₂ agonist + beta-blocker	Combines α₂-mediated reduction of aqueous humour production with beta-blockade, with some additional effect on uveoscleral outflow.	Allergic conjunctivitis, dry mouth and sedation from brimonidine plus systemic beta-blocker effects.	Patients with IOP not controlled on monotherapy who tolerate both brimonidine and timolol.	Avoid in young children and in patients with beta-blocker contraindications. Monitor for ocular allergy over time.
Rho-kinase inhibitors (ROCK)
Netarsudil 0.02%	ROCK inhibitor / norepinephrine transporter inhibitor	Increases trabecular outflow, reduces aqueous humour production and may lower episcleral venous pressure, providing additional IOP reduction.	Very frequent conjunctival hyperaemia, punctate conjunctival haemorrhages, asymptomatic corneal verticillata, transient pain or burning.	Adjunctive therapy in glaucoma/ocular hypertension when prostaglandin analogues and classic combinations do not achieve target IOP or are poorly tolerated, where available.	Inform the patient about the high likelihood of hyperaemia. Use with caution in pre-existing corneal disease. Availability may vary by country.

General notes: medical treatment for glaucoma should be individualised according to glaucoma type, target IOP, age, systemic comorbidities, adherence capacity and ocular tolerability. Prostaglandin analogues are generally first-line; beta-blockers, topical CAIs and α₂ agonists are used as second-line therapy or in fixed combinations when greater IOP reduction is required. Systemic CAIs and apraclonidine are reserved for acute / short-term settings. Across all classes, patient education on instillation technique, nasolacrimal occlusion and adverse effects is essential to optimise efficacy and safety.

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Glaucoma medications: drugs and mechanisms

Initial assessment (ECG)

Reversible secondary causes

Hemodynamic stability and red flags

Accessory pathway and specialist support

Treatment strategy: rhythm vs rate

Cardioversion and episode duration

Rhythm control: drugs and exclusions

Rate control: LVEF-dependent

Chronic anticoagulation

Shared decision-making and follow-up

Clinical cases — Atrial fibrillation

Case 1 — Recent-onset AF, stable patient

Case 2 — AF with pre-excitation (suspected accessory pathway)

Case 3 — AF >48 h/unknown duration: pre-cardioversion strategy

Frequently Asked Questions about Atrial Fibrillation (AF) in Acute Care

1) How is AF diagnosed in the emergency setting?

2) What are the signs of haemodynamic instability?

3) When should I choose rhythm control versus rate control?

4) How does AF duration guide cardioversion?

5) Who should receive anticoagulation and for how long?

6) What should be avoided if an accessory pathway (pre-excited AF) is suspected?

7) How do I choose rate-contr

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Low testosterone levels: differential diagnosis

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Register

Glaucoma medications: drugs and mechanisms

Initial assessment (ECG)

Reversible secondary causes

Hemodynamic stability and red flags

Accessory pathway and specialist support

Treatment strategy: rhythm vs rate

Cardioversion and episode duration

Rhythm control: drugs and exclusions

Rate control: LVEF-dependent

Chronic anticoagulation

Shared decision-making and follow-up

Clinical cases — Atrial fibrillation

Case 1 — Recent-onset AF, stable patient

Case 2 — AF with pre-excitation (suspected accessory pathway)

Case 3 — AF >48 h/unknown duration: pre-cardioversion strategy

Frequently Asked Questions about Atrial Fibrillation (AF) in Acute Care

1) How is AF diagnosed in the emergency setting?

2) What are the signs of haemodynamic instability?

3) When should I choose rhythm control versus rate control?

4) How does AF duration guide cardioversion?

5) Who should receive anticoagulation and for how long?

6) What should be avoided if an accessory pathway (pre-excited AF) is suspected?

7) How do I choose rate-contr

Low testosterone levels: differential diagnosis

Erectile dysfunction: approach to differential diagnosis and treatment

Balanitis: approach to differential diagnosis and treatment

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