Week 3 - Pulmonary Function & Disease

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Week 3 - Pulmonary Function & Disease
2013-07-23 22:22:48

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  1. Goblet cells
    • secrete mucous to trap particles in the lower airway
    • ~100 mL of mucous daily
    • chronic bronchitis >200 mL a day
  2. Two types of alveoli & fxn
    • Type I: provide structure
    • Type II: make surfactant
  3. Perfusion
    movement of blood into and out of the capillary beds of the lungs to body organs and tissues
  4. Dorsal Respiratory Group (DRG)
    • mostly in control when relaxing, when not paying attention, when sleeping
    • receives signals from chemoreceptors from the periphery
    • any changes in O2 or CO2 or pH will send signals to this group to either pick up or slow down breathing
  5. Ventral Respiratory Group (VRG)
    • inspiration and expiration
    • takes over when exercising, when need increased ventilatory response
  6. Pneumotaxic center
    • inspiration
    • activated to limit some volume of air moving in and out
    • pain, anxiety, strong emotions regulate pattern
    • one in the upper pons that rhythmically inhibits inspiration.
  7. apneustic center
    • decreases amt of breathing (for prolonged breathing) when O2 requirements become elevated
    • promotes inspiration by stimulation of neurons in medulla oblongata
    • the neurons in the brain stem controlling normal respiration.
  8. Chemoreceptors
    • in carotids, aorta, and stretch receptors in lungs which are sensing things constantly to send signals to the DRG (such as changes in O2 or CO2)
    • Peripheral and central receptors
  9. Peripheral chemoreceptors
    • carotid and aortic bodies
    • 3 different types: 
    • -1) Irritant (respond to noxious stimuli)
    • -2) Stretch (increased or decreased lung volumes)
    • -3) j-receptors (increases in pressure of capillaries that surround lungs 
    • Sensitive to PaO2 in bloodstream (if drops, turns up)
    • -->then send back to DRG
  10. Central chemoreceptors
    • Near the respiratory center, closer to brain
    • Sense changes in pH in CSF
    • Sensitive to PaCO2 (when this rises, N~40, these receptors input to chemosensitive center (which directly communicate w/ DRG about changes)
    • PaCO2 changes pH (H+)
  11. surfactant
    • lowers alveolar surface tension
    • 2 groups:
    • -hydrophobic (repels water to keep alveoli lubricated and open for gas exchange)
    • -hydrophilic (inhibit pathogens)
    • This is why newborns are at risk for respiratory problems when born prematurely b/c don't have surfactant until about 36 days into gestation.
  12. Boyle's Law
    • Volume and pressure are inversely related: as V increases, P decreases
    • With inspiration, volume increases and pressure decreases (more atm pressure); ACTIVE process
    • With expiration, volume decreases and pressure increases (Passive recoil process)
  13. V/Q mismatch
    • Ventilation (V): 4L air/min
    • Perfusion (Q): 5L blood/min
    • Actual is 4/5 = 0.8
    • Low: decreased ventilation but normal perfusion -> hypoxemia (not enough O2 in blood)
  14. shunting
    • inadequate ventilation of adequately perfused lung
    • Can happen because of:
    • Atelectasis: collapse of lung tissue
    • pulmonary edema (alveoli fills w/ fluid)
    • pneumonia (exudate)
  15. alveolar dead space
    • space in alveoli occupied by air that does not participate in oxygen–carbon dioxide exchange
    • adequate ventilation with poor perfusion
    • pulmonary embolus (blood clot travels and lodges it in pulmonary artery)
    • No space for O2 to go
  16. Oxygen saturation
    • measures binding of O2 to Hb
    • 97% of O2 is transported to cells bound to Hb
  17. Hypercapnia
    • increased CO2 
    • caused by alveolar hypoventilation
    • caused by:
    • -respiratory acidosis (pH < 7.35) 
    • -depression of respiratory center from drugs (morphine) -> most common!
    • -diseases or trauma to CNS
    • -Spinal cord disruption
    • -diseases of respiratory muscles
    • -Chest injury
    • -Large airway obstruction
    • -emphysema
  18. Hypoxemia
    • Reduced O2 (PaO2) in BLOOD (vs. in tissue in hypoxia)
    • causes respiratory alkalosis (pH >7.45)
    • Caused by:
    • -shunting
    • -alveolar dead space
    • -hypOventilation
    • -thickened alveolar capillary membrane
    • -intercardiac defects
  19. Pneumothorax
    • presence of air or gas in pleural space
    • destroys negative pressure
    • 2 types:
    • open: air is drawn in during inspiration and forced back out during expiration
    • TENSION: serious!! can happen in minutes = death; one way valve permitting air in, but not out. Pushes heart and trachea to -> too much pressure on heart to beat
  20. Pleural effusion
    • presence of fluid in the pleural space
    • migration of fluids from vascular space
    • transudate (from vasculature and more watery)
    • exudate (thicker icky stuff, with WBCs and plasma proteins) 
    • empyema (pus)
    • *Must drain!*
  21. Pneumonia
    • infection of lower respiratory tract
    • risk factors: advanced age, lung disease, alcoholism, intubation, malnutrition, smoking, nursing home resident, impaired swallowing
    • aspiration of oropharyngeal secretions
    • inhalation of microorganisms
    • symptoms: cough, fever, chills, dyspnea (SOB)
    • Evaluation: Chest X-ray, Complete blood count (CBC), sputum culture
  22. aspiration
    swallowing food into the lungs
  23. Community acquired pneumonia (CAP)
    • Things that may cause CAP: 
    • Streptococcus pneumoniae
    • Mycoplasma pneumoniae
    • Influenza
    • Respiratory Syncytial Virus
  24. hospital acquired pneumonia (HAP)
    • Contributors:
    • Pseudomonas aeruginosa
    • Klebsiella pneumoniae
    • Staphylococcus aureus
    • Escherichia coli
    • Ventilator Associated Pneumonia (VAP) - usually worse in small hospitals
  25. Tuberculosis (TB)
    • A chronic granulomatous infection caused by Mycobacterium tuberculosis. 
    • -Granulomas form when the immune system attempts to wall off substances that it perceives as foreign but is unable to eliminate it. Collection of macrophages.
    • Leading cause of death from a curable infectious disease 
    • Transmitted by airborne droplets (must wear fitted N95 mask)
    • Usually first introduced into the lungs but can affect other parts of the body
    • Risk factors: crowded living conditions, Immunocompromised, substance abuse, homelessness
    • Can remain dormant (may never become active), but still treated. 
    • S/S: weight loss, night sweats, hemoptysis (coughing up blood)
    • *Patient will always be on more than one drug -> 4 drugs (except in dormant and b/c 1 creates resistance): INH, RIF, Pyrazinamide, & Ethambutol
    • -> Isoniazid (INH), rifampin (RIF), PZA, EMB
    • Induction and maintenance stages of treatment
  26. Mycobacterials
    acid-fast bacilli (TB) that hold a stain even after washed with acid (has outer waxy coat that protects them from disinfectants), and slow growing
  27. Isoniazid (INH)
    • First-line med for prevention and treatment of TB (tablet, syrup, and injectable forms)
    • Action: causes cell disruption; bactericidal
    • ADME: metabolized in liver
    • SE: GI distress, hepatitis (inflammation of liver)
    • Daily use of ETOH increases risk of liver toxicity!
    • Can be combined w/ Rifampin - Rifamate
  28. Rifampin (RIF)
    • Action: Broad-spectrum bactericidal; blocks RNA
    • ADME: well absorbed orally, widely distributed, lipid soluble so can reach intracellular bacteria
    • Metabolized in liver
    • SE: GI distress, flu-like symptoms
    • *Reddish/orange-brown discoloration of body fluids; will stain contact lenses
    • *No ETOH!
    • Can be combined w/ INH as drug - Rifamate
  29. Pyrazinamide
    • Treats TB (usually in combination w/ other drugs)
    • Action: Bacteriostatic or bactericidal depending on dose
    • ADME: Need to maintain water at 2500mL/day; metabolized in liver
    • SE: can cause jaundice
    • Can be combined with INH and RIF -> Rifater
  30. Ethambutol
    • Treats TB (usually in combination)
    • Action: Bacteriostatic; only effective against dividing mycobacteria
    • ADME: metabolized in liver
    • SEoptic and peripheral neuritis (damage to nerves), decreased ability to see red and green, elevated uric acid levels
  31. Streptomycin
    • Action: aminoglycoside, bactericidal
    • ADME: poorly absorbed in GI tract, so given IM
    • SE: ototoxicity (damage to eye nerves) and nephrotoxicity, peripheral neuritis
    • Need to monitor peak and trough levels (to ensure adequate dosing)
    • Second-line drug b/c more toxic and doesn't treat as well (don't see this drug much anymore)
  32. Pulmonary Embolism (PE)
    • Embolus with infarction:
    • --embolus: any detached, traveling intravascular mass (s, l, or gas) carried by circulation and capable of clogging arterial capillary beds
    • --infarction: tissue death (necrosis) caused by a local lack of oxygen, due to an obstruction of the tissue's blood supply
    • --> this causes death or a portion of lung tissue
    • Embolus w/o infarction: no permanent lung injury
    • Massive occlusion
    • Multiple pulmonary emboli: scattered, can be recurrent
    • S/S: chest pain, dyspnea, hemoptysis, fainting, cardiac arrest, tachycardia, fever.
    • Evaluation: chest Xray, ultrasound of legs, VQ scan
  33. Pulmonary Hypertension (PH)
    • High BP in pulmonary (lung) circulation
    • Normally a low pressure system: 15/8 mmHg
    • Causes: idiopathic (unknown), drug induced, HIV, respiratory disease, chronic pulmonary embolus
    • *Chronic PH is cor pulmonale: failure of R-side of heart brought on by long-term high BP in pulmonary arteries and R ventricle of heart.
    • S/S: dyspnea, chest pain, fatigue, tachypnea
    • Evaluation: Echocardiogram, Right heart catheterization
  34. Lung cancer
    • Arise from epithelium of the respiratory tract
    • Most common cause of death in the US
    • Risk factors: smoking, genetic abnormalities
    • 2 categories:
    • -Non-small cell lung cancer (NSCLC): Squamous cell carcinoma (80%, cough, hemoptysis); Adenocarcinoma (chest pain, SOB); large cell carcinoma
    • -neuroendocrine tumors: small cell carcinomas (rapid growth, worst prognosis, endocrine malfunction); typical and atypical carcinoid (cough, weight loss, hemoptysis)
    • Evaluation: chest Xray, Chest CT, Biopsy, bronchoscpy
  35. Cystic Fibrosis (CF)
    • Increased production and altered properties of mucous from excess Na absorption and defective Cl ion transport
    • Persistent cough or wheeze, recurrent pneumonia, pneumothorax, hemoptysis, cor pulmonale
    • Evaluation: sweat chloride test - putting an electrode and pad on skin to stimulate and measure the weight and amt of salt on the pad.
    • Such thick secretions that it's difficult to breath and promotes breeding ground for bacteria b/c not being cleared.
  36. Sudden Infant Death Syndrome (SIDS)
    • Unknown cause (idiopathic)
    • Increases in 2nd month of life and peaks at 3-4 months
    • Risk factors: winter months, respiratory infections, Sibling of prior SIDS victim, Cigarette smoke exposure, prone sitting, poverty
    • Put babies on back (facedown may decrease respiratory drive)
  37. What disease does Restrictive Lung Disease include?
    • Aspiration
    • Atelectasis
    • Bronchiectasis (widening/destruction of airways/lung tissue)
    • Bronchiolitis (swelling of airway w/ mucous buildup)
    • Pulmonary fibrosis
    • Pulmonary Edema
    • Acute Respiratory Distress Syndrome (ARDS)
    • RDS of Newborn (RDS)
  38. Atelectasis
    • collapse of lung tissue
    • Compression: external pressure from tumor or fluid
    • Absorption: hypOventilated alveoli
    • Surfactant impairment: decreased production and inactivation
    • *90% of pts administered a general anesthetic will have this! 
    • *Nurse can encourage spirometer and deep breathing; promote coughing with splinting (pillow over abdomen) to open alveoli
  39. Pulmonary Edema
    • Abnormal buildup of fluid in air sacs of lungs, leading to SOB
    • Most common cause is L-side heart failure
    • Capillary injury and inflammation 
    • Symptoms: DIB (Difficulty in breathing), pink/frothy sputum, Crackles (Rales)
    • *Versus: pulmonary effusion, which is fluid in pleural space - around lung [not alveoli]).
  40. Acute respiratory distress syndrome (ARDS)
    • A sudden, progressive form of respiratory failure marked by:
    • -noncardiogenic pulmonary edema (caused by various disorders in which factors other than elevated pulmonary capillary pressure are responsible for protein and fluid accumulation in the alveoli)
    • -refractory hypoxemia (cannot be corrected by giving pt extra O2 to breathe)
    • -decreased lung compliance
    • -diffuse pulmonary infiltrates
    • Mortality: 50-70% and 70-90% in sepsis with ARDS
    • Direct risk factors: pulmonary contusion, gastric aspiration, inhalation of toxic agents, pulmonary infection, near drowning
    • Indirect risk factors: sepsis, multiple transfusions, multiple trauma, burns
    • Pathogenesis: Phase I (24-48 hrs)-III (2-3 wks)
    • Clinical manifestations: dyspnea, tachypnea, cough, restlessness
    • Chest X-ray: bilateral infiltrates "white out"
  41. Respiratory distress syndrome of newborns (RDS)
    • premature infants
    • decreases significantly after 36 weeks gestation
    • more common in boys
    • Symptoms: progressive hypoxemia and dyspnea, central cyanosis
    • Caused by underdeveloped and small alveoli; also surfactant deficiency
  42. Obstructive Lung Disease
    • Airway obstruction worse with expiration
    • 3 Diseases:
    • Asthma
    • Chronic Obstructive Pulmonary Disease (COPD)
    • --Chronic Bronchitis and Emphysema
    • **Versus restrictive lung disease (everything becomes stiff)
  43. Autonomic Nervous System
    • Sympathetic: stimulation causes bronchodilation and decreased secretions
    • --fight or flight, increased HR, epinephrine
    • Parasympathetic: vagus nerve stimulation releases ACh by mechanical means (dust, pollen, air pollution) which can initiate bronchoconstriction and increased secretion of mucous.
    • --rest and digest; decreased HR, pupillary constriction
    • --PNS primary control of smooth muscle tone and sympathetic tone
  44. Asthma
    • chronic inflammatory disorder 
    • familial disorder
    • occurs in people of all ages
    • Risk: air pollution, tobacco smoke, urban environment, gastroesophageal reflux disease (GERD), obesity
    • Hyper-responsiveness of airway, edema of respiratory mucosa, excessive sputum prod.
    • Disease of airway, NOT alveoli.
    • Inflammation usually begins w/ mast cell and eosinophil activation 
    • *Airway obstruction -> airway trapping -> CO2 retention -> respiratory acidosis -> status asthmaticus (severe asthma attacks) -> respiratory failure
    • Clinical manefestations: dyspnea, wheezing, nonproductive cough, prolonged expiration, tachycardia (fast heart rate), tachypnea (fast respiration), accessory muscle use, allergic salute and shiners, chest tightness, nocturnal awakenings
  45. Bronchodilation
    Beta2 receptors on lung (Beta1 receptors on heart for vasodilation) mediate this
  46. Bronchoconstriction
    • Histamine 
    • --found in mast cells 
    • --released in response to allergens and some drugs (i.e. morphine)
  47. Metered-dose inhalers (MDI)
    • 1-2 puffs of aerosol soln inhaled 
    • requires respiration/hand coordination
    • Only ~10% reaches lungs, 80% oropharynx
    • Propellants (a compressed inert gas that dispenses the contents of an aerosol container when the pressure is released): Hydrofluoroalkane (HFA)
  48. Dry powder inhalers (DPI)/diskus
    • ~20% of drug to lungs
    • No propellant: put mouth to disk and suck in -> no coordination
    • Breath activated/micropowder directly inhaled
  49. Nebulizer
    • Fine mist
    • requires machine
    • Best option: high doses of medication possible
    • --given slower (over ~5 mins), and as airways open, greater penetration 
    • Usually reserved for children and adults w/ exacerbation and inhalers not working
  50. Beta 2 Agonists
    • Used to treat as asthma
    • Mechanism of action: relaxes bronchiolar smooth muscle
    • --inhaled/oral
    • --Fast relief, and used for long-term maintenance
    • --warning: if dose high, can cause systemic effects
  51. Albuterol
    • Used to prevent and treat wheezing, shortness of breath, coughing, and chest tightness caused by lung diseases such as asthma and chronic obstructive pulmonary disease (COPD) 
    • Short-acting Beta 2 Agonist (SABA)
    • Onset: 5-30 minutes
    • No anti-inflammatory capabilities
    • Adverse: hyperglycemia (pts with diabetes mellitus, DM only), tremor/nervousness/possible cardiac dysrhythmias (in oral)
    • Long-acting (not first-line drug) and may increase risk of asthma-related death is not used properly
  52. Step-wise approach to Asthma
    • 1) Mild: SABA - if used more than 2x/wk, consider step 2.
    • 2) Mild persistent: Low-dose inhaler daily 
    • 3) Moderate: Intermediate-dose ICS (inhaled corticosteroid) or low-dose with long-acting beta agonist (LABA); SABA inhaler for acute symptom control.
    • 4) Moderate: Medium dose ICS + LABA inhaler. SABA inhaler for acute symptom control.
    • **LABA is not used until step 3 when other meds given too.. LABA given alone increases risk of death!!**
    • 5) High dose ICS and LABa
    • 6) Addition of oral steroid used daily.
  53. Glucocorticoids
    • Beclomethosone/Flovent
    • Suppression of inflammation by decreasing:
    • -secretions in inflammatory mediators
    • -infiltration of inflammatory cells
    • -edema of airway mucosa
    • Prophylaxis, given on fixed schedule
    • First-line agents for maintenance
    • *Usually "sone" meds are steroids! 
    • Administration: Use spacer, gargle/rinse afterwards (thrush), Best if used with Beta 2 agonist (for better penetration of glucocorticoid)
    • SE: adrenal suppression, bone loss, candidiasis
    • Oral: adrenal suppression w/ long-term use, increase dose in times of stress
  54. Leukotriene Receptor Agonist
    • Zafirlukast/Accolate (Zyflo) 
    • --reduces eosinophil infiltration, mucus prod., airway edema
    • --blocks LT receptors 
    • Prophylaxis (preventative treatment) is best (not a rescue drug and an alternative to inhaler drugs)
    • *most common: Singulair
  55. Mast Cell Stabilizers
    • Cromolyn/Intal, Nedocromil/Tilade
    • Prevents degranulation and release of histamine, mediators
    • Inhibits eosinophils, macrophages, and other inflammatory cells from migrating
    • Prophylaxis only: 15 mins prior to exercise
    • Intranasal for chronic rhinitis (nose)
    • NO bronchodilator action
    • Little systemic effects - very "safe" drug
  56. Methylxanthines
    • Theophylline/Theodur
    • Not first line agent - many side effects
    • Bronchodilator
    • PO/IV/PR: narrow therapeutic range! 5-15 mcg/mL
    • SE: headache, dizziness
    • Toxicity: Seizures, ventricular dysrrhythmias
  57. Chronic Bronchitis
    • Persistent cough w/ sputum prod. for at least 3 months in 2 consecutive years
    • Excessive mucous prod: hyperplasia (increase in #) of goblet cells
    • Increase mucous traps bacteria/viruses and is a breeding ground
    • Mucous plugs lead to air trapping, hyperinflation
    • widening of alveoli (air trapped in alveoli) during exhalation
    • Clinical manifestations:
    • -dyspnea
    • -sputum
    • -fatigue
    • -decreased FEV1 (air isn't coming out as fast)
    • -Increased PCO2 (trapping of CO2)
    • -Polycythemia (increased prod. of RBCs)
    • -Cyanosis (blue bloaters)
    • -Cor pulmonale
  58. Emphysema
    • Abnormal and permanent enlargement of acini and destruction of alveolar walls
    • Loss of elasticity of tissues (recoil), so air is trapped
    • Reduced surfactant production
    • Neutrophil phagocytosis and elastase (enzyme that digests lung tissue) release
    • Clinical manifestations: dyspnea, tachypnea, prolonged expiration, use of accessory muscles
  59. Alpha-1 Antitrypsin Definciency
    • Very rare (<10%)
    • Inherited enzyme disorder in which enzyme trypsin cannot be produced
    • Alpha-1 Antitrypsin normally inhibits the actions of trypsin, which is a proteolytic enzyme that normally protects the lung
  60. Ipratroprium (Atrovent) - COPD medication
    • Blocks muscarinic (relating to parasympathetic effects) receptors in bronchi, blocking ACh receptors and causing bronchodilation 
    • Use with Albuterol for combination SNS/PNS effect
    • Combivent = albuterol + atrovent
  61. Chronic Obstructive Pulmonary Disease (COPD)
    • Caused by noxious particles or gas, most commonly from tobacco smoking, which triggers an abnormal inflammatory response in the lung
    • 2 main forms:
    • Emphysema - Lung damage and inflammation and enlargement of alveoli
    • Chronic Bronchitis - a cough with sputum production on most days for 3 months of a year, for 2 consecutive years; an increased number (hyperplasia) and increased size (hypertrophy) of the goblet cells and mucous glands of the airway
    • *These diseases commonly coexist.
  62. Allergic Rhinitis
    • Inflammatory disorder of upper/lower airway, eyes
    • -sneezing, rhinorrhea (runny nose), pruritus (itching), nasal congestion
    • -Trigger usually allergen
    • Seasonal: pollen, fungi, etc.
    • Perennial: non-seasonal, indoor allergens
    • Treatment: Oral and intranasal anti-histamines, intranasal glucocorticoids (anti-inflammatory), intranasal Cromlyn Sodium
  63. Non-Allergy Rhinitis
    • Usually viral - not allergy
    • Treatment: sympathomimetics/Decongestants, drops/spray/oral dosing
    • High abuse potential! (People make meth with this)
    • Adverse effects:
    • -rebound congestion (nasal spray only 3-4 days - after that makes it worse!) 
    • -Oral: widespread vasoconstriction (will increase BP esp. in people w/ high BP)
  64. H1 Antagonists (antihistamines)
    • *Histamine made by mast cells and basophils; triggers inflammatory response as part of immune system to foreign pathogens*
    • 2 Generations of H1 blockers:
    • -1st gen: cause sedation (BBB), like Benadryl
    • -2nd gen: non-sedating 
    • Mechanism: Binds to H1 receptors throughout body and block histamine (not release, just effects of it)
  65. Antihistamines
    • Bind to muscarinic (PNS) ACh receptors: anticholinergic effects include dry mouth, urinary retention, blurred vision, tachycardia
    • *caution in pts w/ asthma b/c can dry up secretions and cause buildup of mucous
    • PO/IV 
    • Peripheral effects: reduces itching and pain, blocks mucous secretions
    • SE: dizziness, sedation, incoordination, confusion, fatigue, dry mucous membranes, constipation, palpitations
    • 1st gen: Diphenhydramine (Benadryl)
    • 2nd gen:  Loratidine (Claritin, Zyrtec)
    • Nursing considerations: Anti-cholinergic (blocks ACh in CNS and PNS) effects, use with caution in pts w/ glaucoma, hyperthyroidism (tachycardia)
    • -Sedation: do not take with ETOH, no driving
    • -Not useful for asthma or non-allergic rhinitis
    • *In anaphylaxis, give epinephrine first, then antihistamine later.
  66. Cough
    • Protective reflex that helps clear the airways by explosion expiration
    • Initiated by stimulation of irritant receptors in airway
    • Acute: resolves in 2-3 weeks
    • Chronic: persisting for > 3 weeks, although some 7-8 weeks
  67. Mucokinetic Agents
    • Actions: promote removal of abnormal or excessive secretions; prevent sputum retention
    • Sputum: not the same as saliva! Viscous material from lower respiratory tree; contains mucous
  68. Mucolytic Drugs
    • Prototype: acetylcysteine (Mucomyst) 
    • Action: alters molecular composition of mucous, decreases viscosity
    • Indication: Chronic bronchitis, emphysema, CF
    • Also used for Tylenol overdose
    • ADME: effect w/in 1 min, peak 5-10 mins; unpleasant odor during admin. 
    • SE: N/V, runny nose, throat or lung irritation, sore mouth, stomatitis (mouth), hemoptysis, rash
    • Implications: Give via NG tube; if orally put in juice or on ice and drink fast; Have something to rinse mouth and kill taste; rotten egg smell can induce emesis
  69. Expectorants
    • Prototype: Guaifenesin (Robitussin)
    • -Found in many OTCs
    • -Used to decrease mucous viscosity and surface tension (induces coughing to remove stuff - nonproductive cough into productive one)
    • -Used for colds, bronchitis, sinusitis
  70. Antitussives
    • Primary cough suppressant agents are codeine and dextromethorphan 
    • Prototype: dextromethorphan (Robistussin DM)
    • -may have abuse or euphoric effects
    • Action: affects cough center in medulla, lessens irritation of respiratory tract
    • SE: (minimal) nausea, mild dizziness and drowsiness
    • Nonopioid
    • Opioid: codeine & hydrocodone (anesthetic so you don't cough) 
    • Antihistamines (like Benadryl)
  71. Pulmonary Function Testing (PFT)
    • Test does not diagnose disease but expresses severity
    • -Spirometry
    • -Peak Flow Meter
    • Relationship of lung volumes to ventilatory impairment