-inhaled corticosteroids

-inhaled long-acting B-2 agonists

-Methylxanthines

-Leukotriene modifiers

-short-acting B-2 agonist

-atnicholinergics

-systemic corticosteroids

MOST EFFICIENT

minimizes systemic AE

technique is important for optimal results and avoidance of AEs

poor technique can cause oropharyngeal accumulation such as:

-decreased effectiveness (less meds to airway), mouth or throat irritation, hoarseness, local infxns (candidia)

Inhalation

-short-acting-MOST effective for reversing acute airway obstruction caused by bronchoconstriction; onset begins in less than 5 min; lasts 4-6 hrs; better bronchodilation that theophylline or anticholinergics

-long-acting-up to 12 hours of bronchodilator actions; for chronic asthma, for add on therapy for asthma not controlled on low to med dose of inhaled corticosteroids; shouldn't be used as monotherapy (could increase mortality)

short acting B2 agonist

50:50 mixture of R(active) & S (adverse effects)isomers 

Dosage: PO liquid/tab, MDI, neb solution

MDI: 2 puffs every 4- h

short-acting B2 agonists

pure R isomer; less AE of tachycardia

Pirbuterol (Maxair)

Terbutaline (Brethaire)

long-acting B2 agonist

partial agonist with onset of about 30 m (DON'T use with quick relief); BID

long acting B2 agonist

full agonist, quicker onset

inhaled corticosteroids and long-acting B2-agonists

Fluticasone/Salmeterol (Advair diskus)

Budesonide/formoterol (Symbicort)

-used to suppress inflammatory cell activation and function-decrease airway inflammation

-prevention of microvascular leakage-decrease airway edema

-decrease mucous production and secretion

-up-regulate B2 receptors-increase response to B2 agonist

-effects begin in a few hrs

-maximal effects take greater than 2 weeks or regular tx

-BID dosing

AE typically to oropharyngeal deposition of drug: oral candiasis (decrease risk by using a spaser and rinsing mouth), dysphonia/hoarseness, systemic AE's uncommon

-Fluticasone (Flovent)

-Budesonide (Pulmicort)

-more AE, reserved for refractory symptoms, injectable, little to no benefit over PO (although PO is preferred)

-AE-HPA suppression, weight gain, F/E abnl, psychiatric disturbance, immunosuppresion, impaired wond healing

-LT control-qday or every other day with attempts to decrease dosage; LT therapy should be tapered

-Burst therapy- give for short period of time to regain control of symptoms, clinical reponse in 4-12 h; helps to avoid LT AE, don't req extensive tapering if in use for short period of time 

-Prednisone (Sterapred), methylprednisolone (Medrol), dexamethasone (Decadron)

Montelukast (Singulair)-doesn't inhibit CYP 450, but is a CYP 450 substrate

-Zifurkulast (Accolate)-some CYP 450 inhibition

-MoA-inhibition of 5-lipoxygenase 

-e.g. Zileuton (Zyflow)-don't commonly use due to AE, DI, and dosing; hepatotoxicity (LFTs), inhibition of CYP450, 4 daily doses 

MoA: inhib the effects of Ach on muscarinc receptors in the airway

AE: blurred vision, dry mouth, urinary retention, constipation

-use with B2 agonists in moderate to severe asthma exacerbations and COPD

-drugs: Ipratropium (Atrovent)-onset 30 min and lasts 4-8 h, MDI and nebulizer

-Tiotropium (Spiriva)-DPI 

-alternative tx for asthma and COPD

-Theophylline-loading dose then qday 

-MoA: anti-inflammatory and immunomodulating

-narrow TI req bloodwork 

non-linear kinetics

DI: CYP 450 substrate

AE: HA, irritability, N/V, arrhythmias, seizures

-O2 therapy for hypxemia during exacerbations (CAUTION: COPD pts rely on mild hypoxemia for resp drive)

-bronchodilators, corticosteroids, methylxanthines (2nd/3rd line)

-anticholinergics-inhaled produces bronchodilation by inhibiting cholinergic receptors in the bronchial smooth muscle, decrease mucus production

-antimicrobials-if greater than 2 of increased dyspnea, sputum volume, and sputum purulence; empiric therapy for most common organisms (H. influenza, M. catarrhalis, S. pneumoniae) 

-Macrolide-Azithromycin (Zithromax) or Clarithhromycin (Biaxin)

-2nd or 3rd G Cephalosporin

-doxycycline

if drug R pneumococcus, P. aeruginosa

-FQ with pseudomonal and pneumococcal activity (respiratory FQ)

-Levofloxacin (Levaquin)

-Moxifloxacin (Avelox)

-Gatifloxacin (Tequin)

Strep. pneumoniae

found in URT and can colonize into pts with chronic pts

7-10 d mostly 

except azithromycin and levaquin 5 d

-if in hospital, antimicrobials 7-10 d, unless blood culture then 14 d after blood culture negative

-refer to PH center

-tx primary HTN

-Vasodilators: CCBs, prostacyclin analogs, endothelin antag

-anticoagulants

-drugs to increase CO

-drugs to decrease volume overload

relax vascular smooth muscle and dilate the arteriole to alleviate the pulm vasoconstriction and prolong life

AE: constipation, dizzy, HA, fatigue, HoTN

-Epoprostenol (Flolan)

-potent, short-acting vasodilator and inhibitor of platelet aggregation

-continuous IV infusion (ambulatory pump), increase exercise tolerance/capacity, quality of life, hemodynamic status, and LT survival rate

AE-CV/lung, CP, palpitations, flushing, tachycardia, HoTN, arrythmia, dyspnea, GI:N/V/D, abd pain, CNS: dizzy, HA, anxiety 

-prevent thrombosis

-Warfarin (Coumadin)-vit K antag

-+ hemodynamic effects in RV failure and PH

-Digoxin (Lanoxin, Digitek)

-MoA: inhin of ATPase pump, lead to increase in intracellular Ca (increase contractility)

AE: arrhythmias, heart blocks, visual disturbances, HA, Gi upset, others

DI: CYP 450 substrate, other meds that effect HR or contractility, others 

MoA-blocks endothelin receptors on vascualr endothelium and smooth muscle, prevent vasoconstriction

AE: HA, anemia, increase LFTs, flushing HoTN, palpitations

-mgmt and prevention of volume overload

-Loop: Furosemide (Lasix)

-PDE inhib-inhibit phosphodiesterase 5 in smooth muscle of pulm vasculature-causes relaxation

AE: HA, GI upset, flushing, dizzy, abnl vision, mylagia, increased LFTs, hematologic abnl

-DI: CYP 450 substrate, CYP 450 1A2 inhibitor; nitrates=HoTN, alpha blockers

-Sildenafil (Revatio, Viagra)

tx of hypoxemic respiratory failure:

pulm edema 

loop: Lasix

Nitrates: NTG-decrease myocardial demand

-analgesics: Morphine-anxiolytic effects and vasodilation

Inotropes: Dobutamine-+contractility and vasodilation

-bronchodilators: Albuterol (Proventil)

-Anticholinergics (Ipratropium)

-Corticosteroids-use early to accelerate recovery 

-initial resuscitation-maintain CV and renal function/perfusion; IVF

-cx

-antibiotic therapy-empirical (against all likely pathogens that could penetrate into the presumed source of sepsis); reassess daily, combo therapy for suspected pseudomonas and neutropenic pts; eliminate non-essential therapy with C&S results; tx for 7-10 d (dependent on pt)

-may need vasopressors for septic shock-induced HoTN

-inotropes-to maintain cardiac function (if dysfunction signs are present)

-recombinant human activated protein C: Drotregcogin alfa (Xiaris) 

-MoA: inhib of factors Va and VIIIa-limits thrombotic events; probable blockade of inflammatory responses involved in sepsis

-AE: bleeding, immune rxn (Ab production)