ABSTRACT
Hypokalaemia, a side-effect of these diuretics, predisposes to arrhythmias during sotalol therapy
Normalize potassium levels before starting sotalol in patients already taking these diuretics. When starting these diuretics in patients already taking sotalol, monitor potassium levels every 4-6 weeks until stable
BETA-BLOCKERS – SOTALOL
IVABRADINE Risk of arrhythmias Additive effect; ivabradine slows the sinus node
Monitor ECG closely
BETA-BLOCKERS
BETA-BLOCKERS ALCOHOL Acute alcohol ingestion may ≠ hypotensive effect. Chronic moderate/heavy drinking ↓ hypotensive effect
Additive hypotensive effect. Mechanism of opposite effect with chronic intake is uncertain
Monitor BP closely as unpredictable responses can occur. Advise patients to drink only in moderation and to avoid large variations in the amount of alcohol drunk
BETA-BLOCKERS ANAESTHETICS – GENERAL Risk of severe hypotensive episodes during induction of anaesthesia (including patients using timolol eye drops)
Most general anaesthetics are myocardial depressants and vasodilators, so additive ↓ BP may occur
Monitor BP closely, especially during induction of anaesthesia
BETA-BLOCKERS ANAESTHETICS – LOCAL
Remember that ≠ BP can occur when epinephrine-containing local anaesthetics are used with patients on beta-blockers ➣ Sympathomimetics, below BETA-BLOCKERS BUPIVACAINE Risk of bupivacaine toxicity Beta-blockers, particularly
propranolol, inhibit hepatic microsomal metabolism of bupivacaine
Watch for bupivacaine toxicity – monitor ECG and BP
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Mechanism Precautions
↓ intravenous lidocaine 2. Risk of lidocaine toxicity due to ≠ plasma concentrations of lidocaine, particularly with propranolol and nadolol 3. ≠ plasma concentrations of propranolol and possibly some other beta-blockers
1. Additive negative inotropic and chronotropic effects 2. Uncertain, but possibly a combination of beta-blocker-induced reduction in hepatic blood flow (due to ↓ cardiac output) and inhibition of metabolism of lidocaine 3. Attributed to inhibition of metabolism by lidocaine
1. Monitor PR, BP and ECG closely; watch for development of heart failure when intravenous lidocaine is administered to patients on betablockers 2. Watch for lidocaine toxicity 3. Be aware. Regional anaesthetics should be used cautiously in patients with bradycardia. Betablockers could cause dangerous hypertension due to stimulation of alpha-receptors if epinephrine is used with local anaesthetic
BETA-BLOCKERS ANALGESICS
BETA-BLOCKERS NSAIDS – INDOMETACIN, PIROXICAM, POSSIBLY IBUPROFEN, NAPROXEN
↓ hypotensive efficacy of betablockers. There does not seem to be this effect with other NSAIDs
Additive toxic effects on kidney, and sodium and water, retention by NSAIDs. NSAIDs can raise BP by inhibiting renal synthesis of vasodilating prostaglandins. It is uncertain why this effect is specific to these NSAIDs
Watch for ↓ response to betablockers
METOPROLOL VALDECOXIB Risk of ≠ hypotensive efficacy of metoprolol
Metoprolol is metabolized by CYP2D6, which is inhibited by valdecoxib
Monitor BP at least weekly until stable. Warn patients to report symptoms of hypotension (light-headedness, dizziness on standing, etc.)
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CARDIOVASCULAR DRUGS BETA-BLOCKERS Other beta-blockers
of timolol eye drops 2. ≠ plasma concentrations of esmolol when morphine is added 3. ≠ plasma concentrations of metoprolol and propranolol when dextropropoxyphene is added
1. Methadone inhibits CYP2D6, which metabolizes these betablockers 2. Unknown 3. ↓ hepatic clearance of metoprolol and propanolol
1. Monitor BP at least weekly until stable 2. Monitor BP closely 3. Monitor BP at least weekly until stable. Warn patients to report symptoms of hypotension (lightheadedness, dizziness on standing, etc.)
BETA-BLOCKERS ANTACIDS CONTAINING MAGNESIUM AND ALUMINIUM
≠ bioavailability of metoprolol and ↓ bioavailability of atenolol, which may produce mild variation in the response to metoprolol and atenolol
Variations in absorption of the respective beta-blockers
Clinical significance may be minimal but be aware; monitor BP at least weekly until stable when initiating antacid therapy. Warn patients to report symptoms of hypotension (light-headedness, dizziness on standing, etc.)
BETA-BLOCKERS ANTIARRHYTHMICS – AMIODARONE, DISOPYRAMIDE, FLECAINIDE, MEXILETINE, PROCAINAMIDE, PROPAFENONE
Risk of bradycardia (occasionally severe), ↓ BP and heart failure. A single case report has described bradycardia when timolol eye drops were given to a patient on flecainide. Also, ≠ plasma levels of propranolol and metoprolol
Additive negative inotropic and chronotropic effects. In addition, high-dose amiodarone is associated with ≠ plasma levels of metoprolol due to inhibition of CYP2D. Also, mexiletine is known to inhibit CYP1A2-mediated metabolism of propanolol. Lastly, propafenone is extensively metabolized by CYP2D6 enzymes and interferes with the metabolism of propranolol and metoprolol
Monitor PR, BP and ECG closely, especially when loading patients on beta-blockers with antiarrhythmics; watch for the development of heart failure. ↓ doses of beta-blocker accordingly, especially when coadministering propafenone with metoprolol or propanolol
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Mechanism Precautions
are halved by 1 g doses of ampicillin (but not smaller doses)
Uncertain Monitor BP closely during initiation of therapy with ampicillin
BETA-BLOCKERS RIFAMPICIN ↓ plasma concentrations and efficacy of bisoprolol, carvedilol, celiprolol, metoprolol and propanolol
Rifampicin induces hepatic enzymes (e.g. CYP2C19), which ≠ metabolism of the beta-blockers; in addition, it may also ≠ P-gp expression
Monitor PR and BP; watch for poor response to beta-blockers
BETA-BLOCKERS ANTICANCER AND IMMUNOMODULATING DRUGS
BETA-BLOCKERS CYTOTOXICS Imatinib may cause an ≠ in plasma concentrations of metoprolol, propanolol and timolol, with a risk of toxic effects
Imatinib is a potent inhibitor of CYP2D6 isoenzymes, which metabolize beta-blockers
Monitor for clinical efficacy and toxicity of beta-adrenergic blockers
ACEBUTOLOL, ATENOLOL, BETAXOLOL, BISOPROLOL, METOPROLOL, PROPANOLOL
CICLOSPORIN ≠ risk of hyperkalaemia Beta-blockers cause an efflux of potassium from cells, and sideeffect has been observed during ciclosporin therapy
CARVEDILOL CICLOSPORIN Possible ≠ in plasma concentrations of ciclosporin
Carvedilol is metabolized primarily by CYP2D6 and CYP2D9, with a minor contribution from CYP3A4
Usually a dose reduction (20%) of ciclosporin is required
BETA-BLOCKERS CORTICOSTEROIDS ↓ efficacy of beta-blockers Mineralocorticoids cause ≠ BP as a result of sodium and water retention
Watch for poor response to beta-blockers
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CARDIOVASCULAR DRUGS BETA-BLOCKERS Other beta-blockers
Additive hypotensive effect. Aldesleukin causes ↓ vascular resistance and ≠ capillary permeability
Monitor BP at least weekly until stable
BETA-BLOCKERS ANTIDEPRESSANTS
BETA-BLOCKERS LITHIUM Report of episode of ≠ lithium levels in elderly patient after starting low-dose propanolol. However, propanolol is often used to treat lithium-induced tremor without problems
Mechanism uncertain at present, but propanolol seems to ↓ lithium clearance
Monitor lithium levels when starting propanolol therapy in elderly people
BETA-BLOCKERS MAOIs ≠ hypotensive effect Additive hypotensive effect. Postural ↓ BP is a common side-effect of MAOIs
Monitor BP at least weekly until stable. Warn patients to report symptoms of hypotension (light-headedness, dizziness on standing, etc.)
METOPROLOL SSRIs ≠ plasma concentrations of metoprolol
SSRIs inhibit metabolism of metoprolol (paroxetine, fluoxetine, sertraline, fluvoxamine via CYP2D6, and (es)citalopram via mechanism uncertain at present)
Monitor PR and BP at least weekly; watch for metoprolol toxicity, in particular loss of its cardioselectivity
PROPANOLOL, TIMOLOL SSRIs ≠ plasma concentrations and efficacy of propranolol and timolol
Fluvoxamine inhibits CYP1A2-, CYP2C19-and CYP2D6-mediated metabolism of propranolol. Fluoxetine inhibits CYP2C19-and CYP2D6-mediated metabolism of propanolol and timolol. Paroxetine and sertraline inhibit CYP2D6mediated metabolism of propanolol and timolol and can impair conduction through the AV node
Monitor PR and BP at least weekly. Warn patients to report symptoms of hypotension (light-headedness, dizziness on standing, etc.). Watch for propanolol toxicity
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Mechanism Precautions
CLOMIPRAMINE
with amitriptyline and clomipramine
These TCAs inhibit CYP2D6mediated metabolism of betablockers
Monitor BP at least weekly until stable. Warn patients to report symptoms of hypotension (light-headedness, dizziness on standing, etc.)
LABETALOL, PROPANOLOL
IMIPRAMINE ≠ imipramine levels with labetalol and propanolol
Uncertain at present. Postulated that imipramine metabolism ↓ by competition at CYP2D6 and CYP2C8
Monitor plasma levels of imipramine when initiating beta-blocker therapy
PROPANOLOL MAPROTILINE Cases of ≠ plasma levels of maprotiline with propanolol
Uncertain at present. Postulated that maprotiline metabolism ↓ by alterations in hepatic blood flow
Monitor plasma levels of maprotiline when initiating beta-blocker therapy
BETA-BLOCKERS VENLAFAXINE ≠ plasma concentrations and efficacy of metoprolol, propranolol and timolol
Venlafaxine inhibits CYP2D6mediated metabolism of metoprolol, propanolol and timolol
Monitor PR and BP at least weekly; watch for metoprolol toxicity (in particular, loss of its cardioselectivity) and propanolol toxicity
BETA-BLOCKERS ANTIDIABETIC DRUGS
BETA-BLOCKERS ANTIDIABETIC DRUGS Beta-blockers may mask the symptoms and signs of hypoglycaemia. They also ↓ insulin sensitivity; however, beta-blockers that also have vasodilating properties (carvedilol, celiprolol, labetalol, nebivolol) seem to ≠ sensitivity to insulin
↓ glucose tolerance and interfere with the metabolic and autonomic responses to hypoglycaemia
Warn patients about masking of signs of hypoglycaemia. Vasodilating beta-blockers are preferred in patients with diabetes, and all betablockers should be avoided in those having frequent hypoglycaemic attacks. Monitor capillary blood glucose levels closely, especially during initiation of therapy ➣ For signs and symptoms of hypoglycaemia, see Clinical Features of Some Adverse Drug Interactions, Hypoglycaemia
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CARDIOVASCULAR DRUGS BETA-BLOCKERS Other beta-blockers
propanolol or timolol eye drops
These beta-blockers inhibit the rebound in blood glucose that occurs as a response to a fall in blood glucose levels
Cardio-selective beta-blockers are preferred, and all beta-blockers should be avoided in those having frequent hypoglycaemic attacks. Monitor capillary blood glucose levels closely, especially during initiation of therapy ➣ For signs and symptoms of hypoglycaemia, see Clinical Features of Some Adverse Drug Interactions, Hypoglycaemia
BETA-BLOCKERS ANTIDIARRHOEALS – KAOLIN
Possibly ↓ levels of atenolol, propanolol and sotalol
↓ absorption Separate doses by at least 2 hours
BETA-BLOCKERS ANTIEPILEPTICS
BETA-BLOCKERS BARBITURATES Regular barbiturate use may ≠ elimination of those beta-blockers metabolized by the liver (metoprolol, propanolol, timolol)
Barbiturates induce CYP1A2-, CYP2C9-and CYP2C19-mediated metabolism of propanolol
Monitor BP at least weekly until stable and watch for ≠ BP
BETA-BLOCKERS PHENYTOIN Phenytoin may ↓ propanolol levels Phenytoin induces CYP1A2-and CYP2C19-mediated metabolism of propanolol
Monitor BP at least weekly until stable and watch for ≠ BP
BETA-BLOCKERS ANTIGOUT DRUGS – SULFINPYRAZONE
Antihypertensive effects of oxprenolol ↓ by sulfinpyrazone
Unknown Monitor PR and BP closely; consider starting an alternative beta-blocker
BETA-BLOCKERS ANTIHYPERTENSIVES AND HEART FAILURE DRUGS
BETA-BLOCKERS ACE INHIBITORS, ADRENERGIC NEURONE BLOCKERS, ANGIOTENSIN II RECEPTOR ANTAGONISTS
≠ hypotensive effect Additive hypotensive effect; may be used therapeutically
Monitor BP at least weekly until stable. Warn patients to report symptoms of hypotension (light-headedness, dizziness on standing, etc.)
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Mechanism Precautions risk
prazosin and terazosin
Additive hypotensive effect; may be used therapeutically. Betablockers prevent the ability to mount a tachycardia in response to ↓ BP; this ≠ the risk of firstdose ↓ BP when starting alphablockers in patients already on beta-blockers
Monitor BP at least weekly until stable; watch for first-dose ↓ BP. Warn patients to report symptoms of hypotension (light-headedness, dizziness on standing, etc.)
BETA-BLOCKERS CENTRALLY ACTING ANTIHYPERTENSIVES
Risk of withdrawal ≠ BP (rebound ≠ BP) with clonidine and possibly moxonidine
Withdrawal of clonidine, and possibly moxonidine, is associated with ≠ circulating catecholamines; beta-blockers, especially noncardioselective ones, allow the catecholamines to exert an unopposed alpha-receptor action (vasoconstriction)
Do not withdraw clonidine or moxonidine while a patient is taking beta-blockers. Withdraw betablockers several days before slowly withdrawing clonidine and moxonidine
BETA-BLOCKERS VASODILATOR ANTIHYPERTENSIVES
≠ hypotensive effect Additive hypotensive effect with diazoxide, hydralazine, minoxidil and sodium nitroprusside. In addition, hydralazine may ≠ the bioavailability of beta-blockers with a high first-pass metabolism (e.g. propanolol and metoprolol), possibly due to alterations in hepatic blood flow or inhibited hepatic metabolism
Monitor BP closely
BETA-BLOCKERS ANTIMALARIALS
METOPROLOL ARTEMETHER/ LUMEFANTRINE
≠ risk of toxicity Uncertain Avoid co-administration
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CARDIOVASCULAR DRUGS BETA-BLOCKERS Other beta-blockers
Mefloquine can cause cardiac conduction disorders, e.g. bradycardia. Additive bradycardic effect. Single case report of cardiac arrest with co-administration of mefloquine and propanolol, possibly caused by Q-T prolongation
Monitor PR closely
BETA-BLOCKERS QUININE Risk of ≠ plasma concentrations and effects of labetalol, metoprolol and propranolol; ≠ systemic effects of timolol eye drops
Quinine inhibits CYP2D6, which metabolizes these beta-blockers
Monitor BP at least weekly until stable
BETA-BLOCKERS ANTIPARKINSON’S DRUGS – LEVODOPA
≠ hypotensive effect Additive hypotensive effect; however, overall, adding betablockers to levodopa can be beneficial (e.g. by reducing the risk of dopamine-mediated risk of arrhythmias)
Monitor BP at least weekly until stable
BETA-BLOCKERS ANTIPSYCHOTICS
BETA-BLOCKERS ANTIPSYCHOTICS ≠ hypotensive effect Dose-related ↓ BP (due to vasodilatation) is a side-effect of most antipsychotics, particularly the phenothiazines
Monitor BP at least weekly until stable, especially during initiation of treatment. Warn patients to report symptoms of hypotension (light-headedness, dizziness on standing, etc.)
PROPANOLOL, TIMOLOL CHLORPROMAZINE, HALOPERIDOL
≠ plasma concentrations and efficacy of both chlorpromazine and propranolol during co-administration
Propanolol and chlorpromazine mutually inhibit each other’s hepatic metabolism. Haloperidol inhibits CYP2D6-mediated metabolism of propanolol and timolol
Watch for toxic effects of chlorpromazine and propranolol; ↓ doses accordingly
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metoprolol, propanolol and timolol
Inhibition of CYP2D6-mediated metabolism of these beta-blockers and CYP2C19-mediated metabolism of propanolol
Use an alternative beta-blocker if possible; if not, monitor closely
BETA-BLOCKERS ANXIOLYTICS AND HYPNOTICS
BETA-BLOCKERS ANXIOLYTICS AND HYPNOTICS
≠ hypotensive effect Additive hypotensive effect; anxiolytics and hypnotics can cause postural ↓ BP
Watch for ↓ BP. Monitor BP at least weekly until stable. Warn patients to report symptoms of hypotension (light-headedness, dizziness on standing, etc.)
BETA-BLOCKERS DIAZEPAM May occasionally cause ≠ sedation during metoprolol and propranolol therapy
Propranolol and metoprolol inhibit the metabolism of diazepam
Warn patients about ≠ sedation
BETA-BLOCKERS BRONCHODILATORS
BETA-BLOCKERS BETA-2 AGONISTS Non-selective beta-blockers (e.g. propanolol) ↓ or prevents the bronchodilator effect of beta-2 agonists
Non-selective beta-blockers antagonize the effect of beta-2 agonists on bronchial smooth muscle
Avoid co-administration
BETA-BLOCKERS THEOPHYLLINE ≠ plasma levels of theophylline with propranolol
Propranolol exerts a dosedependent inhibitory effect on the metabolism of theophylline
Monitor theophylline levels during propranolol co-administration
BETA-BLOCKERS CALCIUM CHANNEL BLOCKERS
BETA-BLOCKERS CALCIUM CHANNEL BLOCKERS
≠ hypotensive effect, bradycardia, conduction defects and heart failure
Additive hypotensive effect; may be used therapeutically
Monitor PR, BP and ECG at least weekly until stable. Warn patients to report symptoms of hypotension (light-headedness, dizziness on standing, etc.)
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CARDIOVASCULAR DRUGS BETA-BLOCKERS Other beta-blockers
beta-blockers
It is uncertain why this severe effect occurs
Monitor PR, BP and ECG at least weekly until stable. Warn patients to report symptoms of hypotension (light-headedness, dizziness on standing, etc.)
BETA-BLOCKERS DILTIAZEM ≠ hypotensive and bradycardic effects: cases of severe bradycardia and AV block when both drugs are administered concurrently in the presence of pre-existing heart failure or conduction abnormalities
Additive effects on conduction; diltiazem causes bradycardia, sinoatrial block and AV block. Also, diltiazem inhibits CYP1A2mediated metabolism of propanolol
Monitor PR, BP and ECG at least weekly until stable. Warn patients to report symptoms of hypotension (light-headedness, dizziness on standing, etc.)
BETA-BLOCKERS VERAPAMIL 1. Risk of cardiac arrest when parenteral verapamil is given to patients on beta-blockers 2. Risk of bradycardias when both are given orally
Additive effect. Also, verapamil inhibits CYP1A2-mediated metabolism of propanolol
1. Do not administer intravenous verapamil to patients taking betablockers 2. Monitor ECG and BP carefully when both are given orally
BETA-BLOCKERS CARDIAC GLYCOSIDES
BETA-BLOCKERS DIGOXIN Risk of bradycardia and AV block Additive bradycardia Monitor PR, BP and ECG closely
CARVEDILOL DIGOXIN Carvedilol may ≠ digoxin plasma concentrations, particularly in children
↓ P-gp-mediated renal clearance of digoxin
↓ the dose of digoxin by 25%; watch for signs of digoxin toxicity and monitor digoxin levels
BETA-BLOCKERS COCAINE Risk of hypertensive crisis Cocaine produces both alpha-and beta-adrenergic agonist effects; selective beta-blockade leads to unopposed alpha-agonism (vasoconstriction)
Avoid concurrent use
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Mechanism Precautions
Modafinil is a reversible inhibitor
of CYP2C19 when used in therapeutic doses, and a moderate inducer of CYP1A2 in a concentration-dependent manner
Be aware
BETA-BLOCKERS DRUG DEPENDENCE THERAPIES – BUPROPION
≠ plasma concentrations of metoprolol, propranolol and timolol, with risk of toxic effects
Bupropion and its metabolite hydroxybupropion inhibit CYP2D6
Initiate therapy of these drugs at the lowest effective dose
BETA-BLOCKERS DIURETICS ≠ hypotensive effect Additive hypotensive effect; may be used therapeutically
Monitor BP at least weekly until stable. Warn patients to report symptoms of hypotension (light-headedness, dizziness on standing, etc.)
BETA-BLOCKERS ERGOT DERIVATIVES Three reported cases of arterial vasoconstriction and one of ≠ BP occurred when ergotamine or methysergide was added to propanolol or oxprenolol
Ergotamine can cause peripheral vasospasm, and absence of betaadrenergic activity can ≠ the risk of vasoconstriction
Ergot derivatives and beta-blockers are often co-administered without trouble; however, monitor BP at least weekly until stable (watch for ≠ BP) and warn patients to stop the ergot derivative and seek medical attention if they develop cold, painful feet
PROPANOLOL 5-HT1 AGONISTS – RIZATRIPTAN
Plasma levels of rizatriptan almost doubled during propranolol therapy
Propanolol inhibits the metabolism of rizatriptan
Initiate therapy with 5 mg rizatriptan and do not exceed 10 mg in 24 hours. The manufacturers recommend separating doses by 2 hours, although this has not been borne out by the studies
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CARDIOVASCULAR DRUGS BETA-BLOCKERS Other beta-blockers
propranolol; ≠ systemic effects of timolol eye drops
Cimetidine inhibits CYP2D6, which metabolizes these beta-blockers, and inhibits CYP1A2-and CYP2E1mediated metabolism of propanolol. Ranitidine is a weaker inhibitor of CYP2D6
Monitor BP at least weekly until stable
BETA-BLOCKERS NIZATIDINE ≠ bradycardia when nizatidine is added to atenolol. Other betablockers have not been studied
Uncertain Monitor PR when administering nizatidine to patients on betablockers
BETA-BLOCKERS MUSCLE RELAXANTS
BETA-BLOCKERS NON-DEPOLARIZING 1. Modest ≠ in efficacy of muscle relaxants, particularly with propanolol 2. Risk of ↓ BP with atracurium and alcuronium
1 and 2. Uncertain 1. Watch for prolonged muscular paralysis after muscle relaxants 2. Monitor BP at least weekly until stable
BETA-BLOCKERS SKELETAL – BACLOFEN, TIZANIDINE
≠ hypotensive effect with baclofen or tizanidine. Risk of bradycardia with tizanidine
Additive hypotensive effect. Tizanidine has a negative inotropic and chronotropic effect
Monitor BP at least weekly until stable. Warn patients to report symptoms of hypotension (light-headedness, dizziness on standing, etc.)
BETA-BLOCKERS NITRATES ≠ hypotensive effect Additive hypotensive effect; may be used therapeutically
Monitor BP at least weekly until stable
BETA-BLOCKERS OESTROGENS ↓ hypotensive effect Oestrogens cause sodium and fluid retention
Monitor BP at least weekly until stable; routine prescription of oestrogens in patients with ≠ BP is not advisable
BETA-BLOCKERS ORLISTAT Case report of severe ≠ BP when orlistat started on a patient on atenolol
Uncertain at present Monitor BP at least weekly until stable
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Mechanism Precautions
PYRIDOSTIGMINE
when neostigmine or physostigmine was given to reverse anaesthesia 2. ↓ effectiveness of neostigmine and pyridostigmine in myasthenia gravis
1. Neostigmine and pyridostigmine cause accumulation of ACh, which may cause additive bradycardia and ↓ BP 2. Beta-blockers are thought to have a depressant effect on the neuromuscular junction and thereby ≠ weakness
1. Monitor PR and BP closely when giving anticholinesterases to reverse anaesthesia to patients on betablockers 2. Monitor the response to neostigmine and pyridostigmine when starting beta-blockers
BETA-BLOCKERS PILOCARPINE ≠ risk of arrhythmias Pilocarpine is a parasympathomimetic and can cause additive bradycardia
Monitor PR and ECG closely
BETA-BLOCKERS PERIPHERAL VASODILATORS – MOXISYLYTE (THYMOXAMINE)
≠ hypotensive effect Additive hypotensive effect Monitor BP at least weekly until stable
BETA-BLOCKERS POTASSIUM CHANNEL ACTIVATORS
≠ hypotensive effect Additive effect Monitor BP at least weekly until stable
BETA-BLOCKERS PROSTAGLANDINS – ALPROSTADIL
≠ hypotensive effect Additive hypotensive effect Monitor BP at least weekly until stable. Warn patients to report symptoms of hypotension (light-headedness, dizziness on standing, etc.)
BETA-BLOCKERS PROTON PUMP INHIBITORS Risk of ≠ plasma concentrations and effects of propranolol
Omeprazole inhibits CYP2D6-and CYP2C19-mediated metabolism of propanolol
Monitor BP at least weekly until stable
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CARDIOVASCULAR DRUGS BETA-BLOCKERS Other beta-blockers
The hypertensive effect of sympathomimetics opposes the hypotensive actions of betablockers
Monitor BP at least weekly until stable; watch for poor response to beta-blockers
BETA-BLOCKERS SYMPATHOMIMETICS – DIRECT
1. Severe ≠ BP and bradycardia with non-cardioselective betablockers (including reports of severe ≠ BP in patients given infiltrations of local anaesthetics containing epinephrine, and one case of a fatal reaction with phenylephrine eye drops) 2. Patients on beta-blockers may respond poorly to epinephrine when given to treat anaphylaxis
1. Unopposed alpha stimulation causes vasoconstriction, which results in a rise in BP. Beta-2 receptors, when stimulated, cause vasodilatation, which counteracts any alpha action; non-selective beta-blockers antagonize beta-2 receptors
1. Monitor BP at least weekly until stable. When using local anaesthetics with epinephrine, use small volumes of low concentrations (such as 1 in 200 000 epinephrine); avoid high concentrations (e.g. 1 in 1000 mixtures) 2. Look for failure of epinephrine therapy and consider using salbutamol or isoprenaline
BETA-BLOCKERS X-RAY CONTRAST SOLUTIONS
Beta-blockers are associated with ≠ risk of anaphylactoid reactions to iodinated X-ray contrast materials
Uncertain, but postulated that beta-receptors have a role in suppressing the release of mediators of anaphylaxis
Consider using low-osmolality contrast media and pretreating with antihistamines and corticosteroids. Stopping beta-blockers a few days before the X-ray is associated with a risk of withdrawal ≠ BP and tachycardia; a risk-benefit assessment must therefore be made
