Transcript Respiratory Pharmacology Week 4

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 Subtype
Heart
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 nerveending 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 short
Epinephrine
Adrenaline Cl
Alpha
Beta1
Beta2
SVN: 1% solution
(1:100), 0.25 – 0.5
ml, qid
MDI: 0.2 mg/puff, puffs
as ordered
Onset: 3 – 5
minutes
Peak: 5 – 20
minutes
Duration: 1 – 3 hours
Racemic
Epinephrine
(airway
swelling)
Micro-Nefrin,
AsthmaNefrin
Alpha
Beta1
Beta2
SVN: 2.25% solution,
0.25 – 0.5 ml, qid
Isoproterenol
Isuprel
Beta1
Beta2
SVN: 0.5% solution
(1:200), 0.25 – 0.5
ml, qid
Bronkosol
Beta2
SVN: 1% solution,
0.25 – 0.5 ml, qid
Onset: 3 – 5
minutes
Peak: 5 – 20
minutes
Duration: 0.5 – 2
hours
Onset: 2 – 5
minutes
Peak: 5 – 30
minutes
Duration: 0.5 – 2
hours
Onset: 1 – 6
minutes
Peak: 15 – 60
minutes
Duration: 1 – 3
hours
(not given as a
bronchodilator
usually, used to
stop bleeding,
primary cardiac
stimulator)
(not used as a
bronchodilator
any longer)
Isoetharine
(weak, rarely
used)
Short Acting Bronchodilators
Albuterol
(asthma COPD,
pulmonary e
Proventil,
Ventolin,
Pro-air
Beta2
SVN: 0.5% solution,
0.5ml,
2.5MG with 3ml NS tid, qid
MDI: 90 µg/puff, 2 puffs,
tid, qid
Onset: 15 minutes
Peak: 30 – 60
minutes
Duration: 5 – 8 hours
Levalbuterol
Xopenex
Beta2
SVN: 0.63 mg/3 ml, tid
1.25 mg/3 ml, tid
0.31mg
MDI 45 ug/puff, 2 puffs
tid/qid
Onset: 15 minutes
Peak: 30 – 60
minutes
Duration: 5 – 8 hours
• PAGE 98 CH 6
• Responsible for dose, onset, peak, duration,
names for:
– Albuterol
– Xopenex
– Racemic Epi
– ALL LABAs
Short Acting Bronchodilators
Terbutaline
Brethaire
Beta2
MDI: 200 µg/puff, 2 puffs,
q4 – 6 hours
Tab: 2.5 or 5 mg, q6
hours
Onset: 5 – 30
minutes
Peak: 30 – 60
minutes
Duration: 3 – 6 hours
Maxair
Beta2
MDI: 200 µg/puff, 2 puffs,
q4 – 6 hours
Onset: 5 minutes
Peak: 30 minutes
Duration: 5 hours
Beta2
SVN: 0.2% solution,
1.25 ml, bid – qid
MDI: 370 µg/puff, 2 puffs,
q8 hours
Onset: 3 – 4 minutes
Peak: 30 – 60
minutes
Duration: 5 – 8 hours
(used now as a
anti contraction
med to prevent
early delivery)
Pirbuterol
(automatic
MDI
actuation)
Bitolterol
Tornalate
Long Acting Bronchodilators
Salmeterol
Serevent
Beta2
DPI: 50 µg/blister,
twice daily
Onset: 20 minutes
Peak: 3 – 5 hours
Duration: 12 hours
Foradil
Beta2
DPI: 12 µg/inhalation,
twice daily
Onset: 15 minutes
Peak: 30 – 60 minutes
Duration: 12 hours
Brovana
Beta2
SVN: 15 µg/2 ml unit
dose, twice daily
Onset: 15 minutes
Peak: 30 – 60 minutes
Duration: 12 hours
(combined
with Flovent
to make
Advair)
Formoterol
(combined
with
pulmicort to
make
symbicort)
Arformoterol
(has a short
acting
component)
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
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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
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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 Salbuterol 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 Salbuterol 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 (Ralbuterol). 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 Ralbuterol 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
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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
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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 shortacting inhaled Beta 2 agonists.
2. Dosage: (MDI version D/C’d after 9-16-03)
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- DPI: 1 inhalation (50mcg) twice daily, 12 hours apart
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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.