Respiratory Pharmacology

Adrenergics

Receptors

• Adrenergics:– Beta 1 (heart, when stimulated cause contraction, increased HR)---

Isoperternal, Epinephrine– Beta 2 (lungs, when stimulated cause dilation)----Albuterol/Xopenex– Alpha 1 (blood vessels/brain/kidney, when stimulated cause vessel

constriction)—Racemic Epinephrine– Alpha 2 (Sphincters, GI tract, inhibits insulin release; stimulation causes

constriction)

Stimulated by neurotransmitter Epinephrine/ norepinephrine

*Stimulation of a receptor= agonist*Blocking of a receptor = antagonist

Receptors

• Cholinergic:– Nicotinic (found in the CNS and the peripheral nervous system. The

neuromuscular receptors are found in the neuromuscular junctions of somatic muscles; stimulation of these receptors causes muscular contraction)

• Blocked with Nicotinic acetylcholine receptors can be blocked by curare; used for anesthesia and mechainical ventilation– Muscarinic (found primarily in lung; G-protein-coupled receptors that activate

other ionic channels via a second messenger cascade. sub types; M1-M5)

– responds to the binding neurotransmitter acetylcholine

Airway Receptors

• Adrenergic receptors

– Also known as sympathetic and sympathomimetic

receptors

– Sympatholytics = block response

– Stimulated by epinephrine or norepinephrine

– Antiadrenergic drugs block receptors for

norepinephrine or epinephrine (usually to slow the

heart rate or decrease blood pressure)

Airway Receptors

• Cholinergic receptors

– Also known as parasympathetic or

parasympathomimetic receptors

– Stimulated by acetylcholine

– Blocked by ant-cholingergics

– In airway anti-musacarinic (anti-cholinergic) = bronchodilation

– Anti-nicotinics= neuromuscular paralysis

ACh• Airway smooth-muscle cells are innervated by

postganglionic parasympathetic nerves. Acetylcholine (ACh) release from these nerves triggers the contraction of airway smooth muscles. This activity is predominantly mediated by smooth-muscle M3 receptors, but activation of postsynaptic M2 receptors is also likely to contribute to this response/ ACh also leads to the activation of pre-junctional M2 muscarinic Ach receptor (mAChR) autoreceptors, which mediate the inhibition of ACh release

• M2 receptive for cholinersterase (we block all M receptors, so also the “good” M2)

Adrenergic Receptors

• The adrenergic receptors which subserve the responses of the sympathetic nervous system have been divided into two discrete subtypes: alpha adrenergic receptors (alpha receptors) and beta adrenergic receptors (beta receptors).

Adrenergic Receptors• The mechanism of adrenergic receptors. Adrenaline

or noradrenaline are receptor ligands to either α1, α2 or β-adrenergic receptors.

• Blood vessels: α1 couples to Gq, which results in increased intracellular Ca2+ which results in smooth muscle contraction. α2, on the other hand, couples to Gi, which causes a decrease of cAMP activity, resulting in e.g. smooth muscle contraction.

• Heart/Lung: β receptors couple to Gs, and increases intracellular cAMP activity, resulting in e.g. heart muscle contraction, smooth muscle relaxation and glycogenolysis.

Beta Receptors• Beta Receptors Beta receptors have been further subdivided

into beta1 and beta2 receptors.

• beta3 and beta4 receptors have recently been isolated, cloned and characterized. The beta3 receptor may be involved in regulating the metabolism of fatty acids. This receptor could be the site of antiobesity drugs in the future. The functions of the beta4 receptor remain to be discovered.

• The classification of beta receptors is based on the interaction of a series of drugs with these receptors.

Beta Receptors

• Beta Receptor Systems• Most tissues express multiple receptors.

However, the receptor mainly utilized by the sympathetic nervous system to affect myocardial function in the normal heart is the beta1 receptor; while in vascular and nonvascular smooth muscle it is the beta2 receptor.

Beta Receptors

Tissue Receptor SubtypeHeart beta1

Adipose tissue beta1beta3?

Vascular Smooth Muscle beta2

Airway Smooth Muscle beta2

Kindney-Renin release from JG cells beta1

Beta Blockers• Beta Blockers used as anti arrthymia agents for A-fib,

A-flutter• beta-adrenergic antagonists, beta-adrenoreceptor

antagonists or beta antagonists, are a class of drugs used for various indications. They are particularly for the management of cardiac arrhythmias, cardioprotection after myocardial infarction and hypertension

Ex: Labetalol, Esmolol. Metoprolol…

Airway Receptors

• Cholinergic receptors

– Muscarinic drugs stimulate acetylcholine

receptors specifically at parasympathetic nerve-

ending sites

– Anticholinergic drugs block receptors for

acetylcholine

How Bronchodilators Work

• Receptor sites

– Alpha sites – cause vasoconstriction and

vasopressor effects, increasing blood pressure

– Beta1 sites – cause increase in heart rate and

myocardial contractility

How Bronchodilators Work

• Receptor sites

– Beta2 sites – cause relaxation of bronchial

smooth muscle, stimulate mucociliary activity,

and have mild inhibitory effects on inflammatory

mediator release

Autonomic System

• We give drugs that:• 1. increase sympathetic nervous system response (increase

BP/HR/bronchodilate)• 2. drugs that increase the parasympathetic response (induce

bronchoconstriction, slow heart, increase muscle contraction)• 3. drugs that block the sympathetic nervous system response

(decrease HR/BP)• 4. drugs that block the parasympathetic response (prevent

bronchoconstriction)

Autonomic System• Sympathetic nervous system: fight or flight. Half of ANS

system• Parasympathetic nervous system: rest and digest, other half

of ANS system• Sympathetic agonist: simulate fight/flight• Parasympathetic agonist: simulate rest/digest• Antagonists block response• Sympathetic agonist have similar response as

parasympathetic antagonist

Sympathomimetic

• Mimic, imitate, increase sympathetic nervous system response.

• Sympathetic agonists• Albuterol, Xopenex, Racemic Epinephrine,

Serevent, Brovona, Foradil• Most cardiac stimulators

Sympatholytic

• Decrease the sympathetic nervous system response. Block or decrease sympathetic nervous system response

• Sympathetic antagonists• Drugs that block beta receptors to decrease

heart rate/BP• Contraindicated with Asthma/COPD

Parasympathomimetic

• Mimic, imitate, increase parasymoathetic nervous system response

• Parasympathetic agonists• Methocholine (induces bronchoconstriction)• Medications to slow heart/BP

Parasympatholytics

• Block parasympathetic response• Parasympathetic antagonist• Example: Atrovent (block AcH), Atropine

(increase HR), Spiriva

Autonomic Nervous System• You DO NOT control ANS (automatic)• ANS controls functions of organs

automatically, many drugs that affect the ANS affect many organs causing side effects (such as Albuterol/Xopenex)

• ANS drugs affect: Heart, blood vessels, pancreas, ureters, bladder, eyes, pupils, lungs, salivary glands

Autonomic Nervous System

• Do not confuse ANS with the PNS and the CNS

• Central nervous system• Brain and spinal cord• Neurons end on other neurons

• Peripheral Nervous System– Outside of the skull and spinal cord– Neurons end on organs and muscle (non smooth

muscle)

Autonomic Nervous System

• Do not confuse the ANS with the Voluntary nervous system– Voluntary means willing– You DO control your voluntary nervous system– You control your skeletal muscles to move your

body (includes the diaphragm)

Sympathomimetics• Substances that mimic effects of the

sympathetic nervous system

• Part of the autonomic nervous system (not under conscious control)

• Activated by “fight or flight” response

Sympathomimetics• Neurotransmitters include:

– Epinephrine – http://www.youtube.com/watch?v=-gUC7ZQTp34

– Norepinephrine– Catecholmines– Dopamine

• Fight or Flight response allows for:– Bursts of energy– Increased heart rate– Increased blood to brain– Increased Oxygen through

BRONCHODILATION

Sympathomimetics• Sympathomimetic drugs given by

aerosol to the lungs MIMIC fight or flight neurotransmitters and cause DIRECT bronchodilation

• Examples of Sympathomimic bronchodilators:– Fast Acting: Albuterol, Xopenex, Racemic

Epinephrine– Long Acting: Serevent, Brovona

Sympathomimetics• Sympathomimetic drugs bind to Beta 2 receptor sites on

bronchial smooth muscle cells producing an adrenergic agonist response

1. Once attached to a β2 receptor in bronchial smooth muscle the drug then attaches to the intracellular

Gs protien which stimulates adenly cyclase to form cAMP from ATP which then decreases Ca2+↓ and Myosin resulting in SM relaxation .

2. Also activate β receptors on mast cell mb. , thus used in prophylaxis of allergic asthma .

Sympathomimetics• Sympathomimetic drugs can enter

the blood stream and also stimulate Beta 1 receptors increasing systemic side effects such as increased HR

• These drugs are given for patients with reversible airflow obstruction such as Asthma and COPD

Parasympatholytic• Substances that reduce the activity of

the parasympathetic nervous system• The PNS is part of the ANS and is often

referred as the rest and digest phase.

• The primary neurotransmitter in this phase is:– Acetycholine (Ach)

Parasympatholytic• The Ach response causes:

– Decrease in HR– Decrease in BP– Skeletal muscle contraction– Bronchial smooth muscle constriction

• Ach causes: M3 muscarinic receptor reaction in blood vessels, as well as the lungs causing bronchoconstriction.

• Drugs that are parasympatholytic BLOCK M3 response and thus indirectly allow for bronchodilation

Parasympatholytic• Examples of Parasympatholytics

bronchodilators:– Fast Acting: Atrovent/Atropine– Long Acting: Spiriva– Parasymptholytic bronchodilators are referred

to as anticholinergics, they are Ach antagonists– Ach enters bronchial smooth muscle cells

through muscanaric receptors– Atrovent works by blocking all M receptors

resulting in the formation of Cyclic guanosine monophosphate

Parasympatholytic• cGMP inhibits constriction and mucus production• cGMP acts as a secondary messenger much like cAMP but

instead of converting ATP, cGMP prevents neurotransmitters from entering the bronchial smooth muscle cell

• Unlike sympathometic bronchodilators, Atrovent/Spiriva do not cross the blood brain barrier and thus have essentially no systemic side effects (both are derivatives of Atropine, but are quaternary amines)

• Slower bronchodilator effects and less intense than adrenergics

How Bronchodilators Work

• Adrenergic bronchodilators

– ATP converts to cyclic 3’5’-adenosine

monophosphate (cAMP)

– cAMP produces bronchodilation

How Bronchodilators Work

• Anticholinergic agents

– Parasympathetic stimulation of the muscarinic

sites leads to production of guanosine

triphosphate (GTP)

– GTP converts to cyclic guanosine monophosphate

(cGMP)

– http://www.youtube.com/watch?v=g_H5PWlr3lk

How Bronchodilators Work

• Anticholinergic agents

– Anticholinergic agents block the parasympathetic

stimulation at the muscarinic site

How Bronchodilators Work

• Xanthines

– In the presence of phosphodiesterase, cAMP

denatures to form GMP

– Xanthines inhibit the action of

phosphodiesterase, prolonging bronchodilation

Adrenergic Bronchodilators

• Short acting bronchodilators

– Includes catecholamines

– Indicated for relief of acute reversible airflow

obstruction

– Also known as “rescue” bronchodilators

– Primary drugs Albuterol and Xopenex

Adrenergic Bronchodilators

• Short acting bronchodilators

– Rapid onset (3-5 minutes)

– Rapidly metabolized, resulting in short duration

of action (3-8 hours)

– Common side effects: increased HR, trembling,

nervousness

– If HR increases by 20+ stop treatment

Adrenergic Bronchodilators

• Long acting bronchodilators

– Indicated for maintenance bronchodilation and

control of bronchospasm

– Used to control nocturnal symptoms

– Slower onset

– Long duration of action, generally 12 hours

– Include Serevent, Brovona, Foradil

Catecholamines Ultra shortEpinephrine(not given as a bronchodilator usually, used to stop bleeding, primary cardiac stimulator)

Adrenaline Cl AlphaBeta1Beta2

SVN: 1% solution (1:100), 0.25 – 0.5 ml, qidMDI: 0.2 mg/puff, puffs as ordered

Onset: 3 – 5 minutesPeak: 5 – 20 minutesDuration: 1 – 3 hours

Racemic Epinephrine(airway swelling)

Micro-Nefrin,Asthma-Nefrin

AlphaBeta1Beta2

SVN: 2.25% solution, 0.25 – 0.5 ml, qid

Onset: 3 – 5 minutesPeak: 5 – 20 minutesDuration: 0.5 – 2 hours

Isoproterenol(not used as a bronchodilator any longer)

Isuprel Beta1Beta2

SVN: 0.5% solution (1:200), 0.25 – 0.5 ml, qid

Onset: 2 – 5 minutesPeak: 5 – 30 minutesDuration: 0.5 – 2 hours

Isoetharine(weak, rarely used)

Bronkosol Beta2 SVN: 1% solution, 0.25 – 0.5 ml, qid

Onset: 1 – 6 minutesPeak: 15 – 60 minutesDuration: 1 – 3 hours

Short Acting BronchodilatorsAlbuterol(asthma COPD, pulmonary e

Proventil,Ventolin, Pro-air

Beta2 SVN: 0.5% solution, 0.5ml,2.5MG with 3ml NS tid, qidMDI: 90 µg/puff, 2 puffs, tid, qid

Onset: 15 minutesPeak: 30 – 60 minutesDuration: 5 – 8 hours

Levalbuterol Xopenex Beta2 SVN: 0.63 mg/3 ml, tid 1.25 mg/3 ml, tid 0.31mgMDI 45 ug/puff, 2 puffs tid/qid

Onset: 15 minutesPeak: 30 – 60 minutesDuration: 5 – 8 hours

• PAGE 98 CH 6• Responsible for dose, onset, peak, duration,

names for:– Albuterol– Xopenex– Racemic Epi– ALL LABAs

Short Acting BronchodilatorsTerbutaline

(used now as a anti contraction med to prevent early delivery)

Brethaire Beta2 MDI: 200 µg/puff, 2 puffs, q4 – 6 hoursTab: 2.5 or 5 mg, q6 hours

Onset: 5 – 30 minutesPeak: 30 – 60 minutesDuration: 3 – 6 hours

Pirbuterol Maxair

(automatic MDI actuation)

Beta2 MDI: 200 µg/puff, 2 puffs, q4 – 6 hours

Onset: 5 minutesPeak: 30 minutesDuration: 5 hours

Bitolterol Tornalate Beta2 SVN: 0.2% solution, 1.25 ml, bid – qidMDI: 370 µg/puff, 2 puffs, q8 hours

Onset: 3 – 4 minutesPeak: 30 – 60 minutesDuration: 5 – 8 hours

Long Acting BronchodilatorsSalmeterol

(combined with Flovent to make Advair)

Serevent Beta2 DPI: 50 µg/blister, twice daily

Onset: 20 minutesPeak: 3 – 5 hoursDuration: 12 hours

Formoterol

(combined with pulmicort to make symbicort)

Foradil Beta2 DPI: 12 µg/inhalation, twice daily

Onset: 15 minutesPeak: 30 – 60 minutesDuration: 12 hours

Arformoterol

(has a short acting component)

Brovana Beta2 SVN: 15 µg/2 ml unit dose, twice daily

Onset: 15 minutesPeak: 30 – 60 minutesDuration: 12 hours

Adrenergic Bronchodilators

• Primary drug given for acute and chronic

bronchospasm

• Used frequently for all sorts of conditions.

• Even hyperkalemia (although you need >20

mg in 15 minutes)

Adrenergic Bronchodilators

• Adverse effects

– Bronchospasm (some patients have allergic

reaction)

– Dizziness

– Tachycardia

Adrenergic Bronchodilators

• Adverse effects

– Nausea (common with almost all drugs)

– Worsening ventilation/perfusion ratio

– Tachyphylaxis

Albuterol Sulfate• Albuterol is used to prevent and treat wheezing, difficulty

breathing and chest tightness caused by lung diseases such as asthma and chronic obstructive pulmonary disease (COPD; a group of diseases that affect the lungs and airways). Albuterol inhalation aerosol is also used to prevent breathing difficulties during exercise. Albuterol is in a class of medications called bronchodilators. It works by relaxing and opening air passages to the lungs to make breathing easier.

Albuterol• Albuterol comes as a tablet, extended-release (long-acting) tablet, and a

syrup to take by mouth and as an aerosol, a solution (liquid), and a powder-filled capsule to inhale by mouth. The solution is inhaled using a nebulizer, and the powder-filled capsules are inhaled using a special dry powder inhaler. Albuterol tablets and syrup are usually taken three or four times a day, and extended-release tablets are usually taken twice a day. For the treatment or prevention of asthma symptoms, the oral inhalation is usually used every 4 to 6 hours as needed. For the prevention of bronchospasm during exercise, the oral inhalation is used 15 minutes before exercise. The nebulized solution is used three or four times a day. Albuterol is often mixed with other drugs specifically Atrovent when given to COPD patients

Albuterol• Generic Name: Albuterol• Trade Name: Proventil, Ventolin, Salbuterol (International name)• Classification: Fast acting front door bronchodilator, Beta- 2 Adrenergic Sympathomimetic

Bronchodilator• Purpose: Relaxation of the bronchial smooth muscle resulting in bronchodilation, Quick onset

time within 15 minutes, peak effect 30-60 minutes and lasts 5-8 hours• How it works: Stimulates intracellular production of cyclic 3’5’- AMP which causes dilation of

bronchial smooth muscle, promotes bronchodilation via the neurotransmitter norepinephrine, which is similar to epinephrine (Adrenaline).

• Receptor Sites: Beta 1 (Cardiac smooth muscle stimulation) +1, Beta 2 (Bronchial smooth muscle stimulation) + 4, Alpha (Vasoconstriction) 0

• Delivery Device: Primarily as an Aerosol for RT’s lasts 10-15 minutes, MDI (metered dose inhaler), Liquid syrup or as a tablet

• Doses: Unit Dose and most common is 2.5 mg mixed with 2.5 ml of saline given TID, QID, Q4, or Q6. As an MDI given with the same frequency but usually with 2 to 4 puffs using a spacer.

Xopenex• XOPENEX is a short-acting beta-agonist used to treat and prevent

bronchospasm in children and adults. Medicines like XOPENEX, called bronchodilators, relax the tightened muscles around the airways in the lungs when bronchospasm occurs allowing the airways to open. Similar to Albuterol but believed to have less cardiac effects with a longer duration, making it the ideal choice for front line fast acting bronchodilation except that the drug is relatively new and costly. There is two ways of giving the drug, aerosol and MDI. The MDI is relatively new (2006) and is called XOPENEX HFA™ (levalbuterol tartrate) Inhalation Aerosol is a short-acting beta-agonist and has been approved by the FDA for the treatment or prevention of bronchospasm in patients 4 years of age and older. By subtracting the (S)-isomer from racemic albuterol, it differs from Albuterol.

Xopenex• Generic Name: Levalbuterol• Trade Name: Xopenex, Chemical name: Racemic Albuterol• Classification: Fast acting front door bronchodilator, Beta- 2 Adrenergic Sympathomimetic

Bronchodilator• Purpose: Relaxation of the bronchial smooth muscle resulting in bronchodilation, Quick onset

time within 1-5 minutes, peak effect 30-60 minutes and lasts 6-8 hours• How it works: Stimulates intracellular production of cyclic 3’5’- AMP which leads to activation

of protein kinase A, which inhibits phospholylation of myosin and lowers intracellular ionic calcium concentrations resulting in relaxation of all the airways (trachea, bronchi and bronchioles).

• Receptor Sites: Beta 1 (Cardiac smooth muscle stimulation) +1, Beta 2 (Bronchial smooth muscle stimulation) + 4, Alpha (Vasoconstriction) 0

• Delivery Device: Primarily as an Aerosol for RT’s lasts 10-15 minutes, MDI (metered dose inhaler)

• Doses: 0.31mg/3mL (Infants), 0.63mg/3mL (Children, Adults) & 1.25mg/3mL (Adults) unit dose vials

Albuterol vs Xopenex

• No conclusive evidence to show Xopenex is superior

• Xopenex is only slightly different in its chemical structure having one less R-isomer

• http://www.5min.com/Video/Asthma-Meds---Xopenex-vs-Albuterol-9547

Is Xopenex Better than Albuterol

• It’s not completely clear. When Xopenex was first developed, animal studies suggested that S-albuterol caused inflammation in the lungs, which could possibly worsen asthma. It was also thought that as more racemic albuterol (mixture of the R and S-albuterol isomers) was taken, the S-albuterol isomer would accumulate within the lungs and result in contraction of the smooth muscles around the lungs, thereby worsening asthma symptoms. Xopenex was therefore expected to work better at treating asthma symptoms than racemic albuterol.

Is Xopenex Better than Albuterol• Early studies did show that Xopenex was better at treating

asthma than albuterol, since less Xopenex was needed to achieve control of asthma symptoms than comparable amounts of albuterol. Since Xopenex is the active half of albuterol, one would expect that half the dose of Xopenex would be equivalent to twice the dose of albuterol; however, these studies suggested that only one-fourth of the dose of albuterol was needed to achieve the same result when using Xopenex. This was thought to be due to the lack of the S-albuterol isomer in Xopenex, which was working against the R-albuterol isomer.

Is Xopenex Better than Albuterol• Recent data on Xopenex, however, along with an overview of

all of the available data, suggests that Xopenex is no better at treating asthma than would be expected. The dose of Xopenex required to achieve the same result of treating asthma does appear to be approximately one-half, which is what is expected since it contains the active isomer (R-albuterol). The S-albuterol isomer appears to be inert, meaning that it does not act for or against the treatment of asthma symptoms.

Is Xopenex Better than Albuterol• Albuterol is well-known to cause certain side effects, including

muscle tremors, jitteriness, palpitations and increased heart rate. Early studies on Xopenex suggested that because far less medicine was needed to achieve the same benefit as albuterol, fewer side effects would occur. In addition, it was initially thought that the S-albuterol isomer was primarily responsible for many of the albuterol side effects, and therefore Xopenex, which does not contain the S-albuterol isomer, would cause few side effects.

Is Xopenex Better than Albuterol• Recent studies suggest, however, that the side effects of

Xopenex are equivalent to albuterol, since it is actually the R-albuterol isomer that is responsible for the albuterol side effects. The S-albuterol isomer is inert, meaning is does not contribute to side effects. The package insert for Xopenex states that the rate of the above mentioned side effects are similar for equivalent doses of Xopenex and albuterol.

Ultra Short Bronchodilator (Racemic Epi)

• Slightly different chemically from epinephrine. Stimulates both alpha and beta adrenergic receptors with a slight preference for the beta2 receptors in the lungs. This results in bronchodilation and a decrease in mucus secretion. It also helps in relieving the subglottic edema associated with croup when administered by inhalation. Croup, or acute laryngotracheobronchitis, is the most common cause of upper airway obstruction in children. Croup produces subglottic edema to varying degrees and affects children between the ages of 6 months and 12 years, with a peak incidence of 2 years of age. The clinical syndrome consists of hoarseness and barky cough, with or without inspiratory stridor. Preceding symptoms often include congestion, runny nose, and fever. Severe cases may present with cyanosis and respiratory distress.

Racemic Epi• Croup is caused by several viruses, of which the most common are

parainfluenza type I and III, respiratory syncytial virus, and influenza. The natural course of the illness includes peaking of symptoms between 24 and 48 hours after the onset of barky cough with expected resolution of all symptoms over a week.

• Current emergency management for moderate to severe croup consists of cool mist therapy, steroids, and/or nebulized racemic epinephrine. The literature on croup has convincingly demonstrated benefit from steroid treatment with respect to improvement of croup scores, decreased need for further therapy, and decreased hospitalization rates

• DECADRON Inhaled/nebulized steroid

Racemic Epi• Generic Name: Racemic Epinephrine• Trade Name: Micronefrin,VapoNefrin• Classification: Alpha-adrenergic Sympathomimetic effect• Purpose: Treats croup, stridor, post extubation, laryngeal tumor or

swelling, bronchiolittis, or any other upper airway edema causing swelling and inflammation.

• How it works: Mucosal vasoconstriction decreases subglottic edema. Bronchodilation, increases heart rate, increases cardiac contractile force.

• Receptor Sites: Strong Alpha effect which causes vasoconstriction, Alpha +4, Beta 2 +2, Beta 1 +2

• Delivery Device: Inhalation only (small-volume nebulizer).

Racemic Epi• Doses: Racemic Epinephrine (2.25%) nebulizer form, Child

under 6 months: 0.25 ml, Child: 0.5 ml, Adolescent: 0.75 ml, usually mixed with 2-3 cc of normal saline.Effect dissipates in 2 hours, Effects last 90 to 120 minutes

• Precautions: Avoid too frequent use due to tachyphylaxis, Observe 2-4 hours after racemic Epinephrine

• Contraindications: Epiglottitis, hypersensitivity to the drug, severe tachyarrhythmias

• Side effects: Headache, angina, palpitations, tachycardia. Use precaution with use with antihistamines or tricyclic antidepressants may cause adverse cardiac effects.

LABA• SEREVENT• Indication: Treatment and prevention of bronchospasm. Serevent • is not intended for the treatment of acute asthma exacerbations or for symptoms

that can be managed with occasional use of short- • acting inhaled Beta 2 agonists. • 2. Dosage: (MDI version D/C’d after 9-16-03)

• - DPI: 1 inhalation (50mcg) twice daily, 12 hours apart

• 3. Onset: 10-20 min • 4. Peaks: 3-4 hours • 5. Duration of action: 12 hours• Typically combined with Flovent to • Make ADVAIR

LABA• Brovana (arformoterol) is a bronchodilator. It works by

relaxing muscles in the airways to improve breathing.• Brovana is used to prevent bronchoconstriction in people with

chronic obstructive pulmonary disease (COPD), including chronic bronchitis and emphysema. Brovana will not treat a bronchospasm attack that has already begun.

LABA• Foradil (formoterol) is a long-acting bronchodilator that relaxes muscles in

the airways to improve breathing.• Foradil is used to prevent bronchospasm in people with reversible

obstructive airways disease, including symptoms of night-time asthma. It is also used in people with chronic obstructive pulmonary disease (COPD) such as emphysema and chronic bronchitis.