Pulmonary Pathophysiology

Pulmonary Pathophysiology

Suggested HW: Complete the end of chapter questions for:CH 11-30ANSWERS TO THESE QUESTIONS FOUND ON EVOLVE WEBSITE

EXAM WILL PARTLY COME FROM THESE CHAPTER QUESTIONS

Educational ObjectivesList the etiology and risk factors, clinical manifestations, pathological changes, and diagnostic results for:BronchitisPulmonary emphysemaAsthmaBronchiectasisPulmonary infectionsAcute respiratory distress syndrome (ARDS)Interstitial lung disease (ILD)Lung cancerPulmonary Vascular DisordersNeuromuscular DisordersPleural Diseases (including pneumothorax)

Educational ObjectivesDifferentiate and define obstructive pulmonary disease and restrictive pulmonary disease

Classification of Pulmonary DisordersObstructive disease Causes a decrease in the rate of airflow in the conducting airwaysRestrictive disease Causes a decrease in the volume of lung, especially the inspiratory capacity and vital capacity

Obstructive Diseases

Airway ObstructionEnlarged submucosal glandHyperinflated alveoliMucus PlugInflammation of epithelium

Chronic Obstructive Pulmonary DiseaseA group of disorders characterized by progressive limitations in predominantly expiratory airflow that are partially reversible by bronchodilator or anti-inflammatory therapy

Risk Factors for COPD

Salla disease 1 of 40 Finnish heritage disease characterized by early physical impairment and mental retardationHypocomplementemic urticarial vasculitis a form of vasculitis that causes hives and/or red patches due to the swelling of the small blood vesselsAlpha 1 Antichymotrypsin an inhibits the activity of enzymes called proteases, this activity protects some tissues, such as the lower respiratory tract 8

DefinitionsFVC Forced vital capacity: the determination of the vital capacity from a maximally forced expiratory effort FEV1 Volume that has been exhaled at the end of the first second of forced expirationPEF The highest forced expiratory flow measured with a peak flow meter MVV Maximal voluntary ventilation: volume of air expired in a specified period during repetitive maximal effortMIP: Maximum inspiration (IC), used to assess diaphragm strength

IC inspiratory capacity9

Forced Vital CapacityVital capacity is the maximum amount of air a person can expel from the lungs after a maximum inspiration. It is equal to the inspiratory reserve volume plus VT plus the expiratory reserve volume.A person's vital capacity can be measured by a spirometer In combination with other physiological measurements, the vital capacity can help make a diagnosis of underlying lung disease. The unit that is used to determine this vital capacity is the millilitre (mL).A normal adult has a vital capacity between 3 and 5 litres. Predicted normal values for VC depend on age, sex, height, weight and ethnicity

Overall Classification of Pulmonary DisordersObstructive Disease (COPD)Causes a decrease in the rate of airflow in the conducting airways, causes an increase in residual volume due to air trappingFEV1 , FVC , FEV1/FVC < 70% of predicted, TLC > 120% of predicted,

RV > 120% of predicted, MMV , DLCO < 80% of predicted, PEF

Overall Classification of Pulmonary DisordersIn obstructive lung disease, the FEV1 is reduced due to obstruction to air escape. Thus, the FEV1/FVC ratio will be reduced. More specifically, the diagnosis of COPD is made when the FEV1/FVC ratio is less than 70%.The Global Initiative for Obstructive Lung Disease (GOLD) criteria also require that values are after bronchodilator medication has been given to make the diagnosisDx: Pre-post bronchodilator testing with Spriomtery testing. In Emphysema/Bronchitis small change less than 5%; Asthma typically changes >12% or 200 mL

Overall Classification of Pulmonary DisordersRestrictive Disease (everything besides COPD)Causes a decrease in the volume of lung, especially the inspiratory capacity and vital capacityFEV1 , FVC , FEV1/FVC or normal, TLC < 80% of predicted,

RV < 80% of predicted, MVV , DLCO > 120-140% of predicted,

PEF normal or increased

Overall Classification of Pulmonary DisordersIn restrictive lung disease, the FEV1 and FVC are equally reduced due to fibrosis or other lung pathology (not obstructive pathology). Thus, the FEV1/FVC ratio should be approximately normal, or even increased due to an increased FEV1 value (because of the decreased compliance associated with the presence of fibrosis in some pathological conditions).

Spirogram

Spirogram Capacities and VolumesTLC Total lung capacity: the volume in the lungs at maximal inflation RV Residual volume: the volume of air remaining in the lungs after a maximal exhalation ERV Expiratory reserve volume: the maximal volume of air that can be exhaled from the end-expiratory positionIRV Inspiratory reserve volume: the maximal volume that can be inhaled from the end-inspiratory level

Spirogram Capacities and VolumesIC Inspiratory capacity: the sum of IRV and TV IVC Inspiratory vital capacity: the maximum volume of air inhaled from the point of maximum expiration VC Vital capacity: the volume equal to TLC RVVT Tidal volume: that volume of air moved into or out of the lungs during quiet breathing FRC Functional residual capacity: the volume in the lungs at the end-expiratory position RV/TLC% Residual volume expressed as percent of TLC

FEV1/FVC ratioThe FEV1/FVC ratio, also called Tiffeneau index, is a calculated ratio used in the diagnosis of obstructive and restrictive lung diseaseIt represents the proportion of the forced vital capacity exhaled in the first secondNormal values are approximately 80% of predictedPredicted normal values are calculated based on age, sex, height, weight and ethnicity, sometimes smoking A derived value of FEV1% is FEV1% predicted, which is defined as FEV1% of the patient divided by the average FEV1% in the population for any person of similar age, sex and body composition.

DLCODLCO test is performed by having the test subject blow out all of the air that they can to reach residual volume.The person then takes a full vital capacity inhalation of a test gas mixture that contains a small amount of carbon monoxide (usually 0.3%) and some helium or other non-absorbed tracer gas. The test gas is held in the lung for about 10 seconds and then is exhaled from the lung. The first part of the expired gas is discarded and the next portion which represents gas from the alveoli is collected.By analyzing the concentrations of carbon monoxide and helium in the inspired gas and in the exhaled gas, it is possible to calculate how much carbon monoxide was taken up during the breath hold, and what the partial pressure of carbon monoxide was during the breath hold. This method is known as the single-breath diffusing capacity test.

Diffusing Capacity of the lung for carbon monoxide19

DLCOValues between 75% and 125% of average diffusion capacity in the healthy population are considered normal.The diffusing capacity (DLCO) is a test of the integrity of the alveolar-capillary surface area for gas transfer. It may be reduced in disorders that damage the alveolar walls (septa) such as emphysema, which leads to a loss of effective surface area. The DLCO is also reduced in disorders that thicken or damage the alveolar walls such as pulmonary fibrosis. Lung Volumes and DLCo

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Chronic Obstructive Pulmonary DiseaseMay be preventable and treatable. Disease state characterized by airflow limitation that is not fully responsive to bronchodilator therapy. The airflow limitation is progressive and associated with an abnormal inflammatory response of the airway.Primary cause is cigarette smokingA significant response to the bronchodilator is considered by an increase in the FEV1 by 12% AND an increase in VC by 200 mL.

Therapy at Each Stage of COPD

EpidemiologySome 16 Million Americans are affectedCOPD is the 3rd leading cause of death in the U.S.COPD caused 726,000 hospitalizations in 2000Total health expenditure of $32.1 Billion in 2000Most common form of COPD is Chronic Bronchitis

Risk Factors for COPDCigarette smoking/passive smokingPollutionOccupational exposure to dust and fumesRecurrent lung infectionsHereditary factorsAllergiesSocioeconomic factorsAlcohol ingestionAge

Chronic Obstructive Pulmonary DiseaseSmoking#1 cause of COPDIncreased mucous productionInhibition of mucociliary clearanceToxicity of inhaled gases and particulatesBronchospasmDecrease in macrophage activityDisruption of the alveolar wall and capillary endothelium

General Manifestations of COPDSmall airways ( < 2mm) are most susceptible to airway obstruction in COPDDiagnosed by PFT, clinical signs and symptomsEarly to middle manifestations of COPD include:Changes in pulmonary function testingShortness of breath with exertionChanges in CXRIncreases in sputum productionCoughRecurrent pulmonary infectionsWheezingLate manifestations of COPD include:Accessory muscle usageEdema from Cor PulmonaleMental status changes from chronic hypoxia/hypercapneaClubbing of fingersBarrel Chest or Increased A-P Diameter

Chronic Obstructive Pulmonary Disease ystic Fibrosis ronchitis Chronic sthma ronchiectasis mphysema ronchiolitis

Emphysema

What is Emphysema?Loss of elastic recoil This loss of recoil leads to an increased compliance and inability to expel gas out of the alveoliLeading to trapped air in the lungAlveoli cluster together forming blebsUnderstanding COPDEmphysema

What is Emphysema ContDamage occurs to the tiny airways in the lungs called bronchioles. Bronchioles are joined to alveoli, tiny grape-like clusters of sacs in the lungs where oxygen from the air is exchanged for carbon dioxide from the body. The elastic properties of the lung reside in the tissue around the alveoli

Because the lungs lose elasticity they become less able to contract.

This prevents the alveoli from deflating completely, and the person has difficulty exhaling.

Emphysema ContHence, the next breath is started with more air in the lungs. The trapped "old" air takes up space, so the alveoli are unable to fill with enough fresh air to supply the body with needed oxygen.

Pulmonary EmphysemaCentrilobular emphysemaAbnormal weakening and enlargement of the respiratory bronchioles in the proximal portion of the acinusPrimary changes occur in upper lobesHigh correlation with smoking

Pulmonary EmphysemaBullous emphysemaChanges seen at both respiratory bronchiole and alveolar levelsProminent bullae formation (air spaces greater than 1 cm in diameter)

Emphysema ContA person with emphysema may feel short of breath during exertion and, as the disease progresses, even while at rest. Emphysema is one of several irreversible lung diseases that diminish the ability to exhale. This group of diseases is called chronic obstructive pulmonary disease (COPD). The two major diseases in this category are emphysema and chronic bronchitis, which often develop together.

Accessory muscle use

EmphysemaTypically, symptoms of emphysema appear only after 30 to 50 percent of lung tissue is lost. Emphysema rates are highest for men age 65 and older. More people in the Midwest have emphysema than in any other region in the country. Emphysema is an irreversible disease that can be slowed but not reversed or stopped.

CausesGenerally, lungs become damaged because of reactions to irritants entering the airways and alveoli. Researchers continue to investigate the factors that may make some people more susceptible to emphysema than others. But there are some clear causes for emphysema:Cigarette smoking Alpha-1 antitrypsin deficiency

Other CauseAlpha-1 Antitrypsin Deficiency

People who a deficiency of a protein called alpha-1 antitrypsin (AAT) are at a higher risk of developing severe emphysema. Alpha-1 antitrypsin deficiency (AAT deficiency) is an inherited condition and occurs in varying degrees

AATAAT is thought to protect against some of the damage caused by macrophages. In AAT deficiency-related emphysema, the walls of the bronchial tubes and the alveoli are both damaged, often leading to severe disease. About 2 out of every 1,000 people have an alpha-1 antitrypsin deficiency. People who smoke and have AAT deficiency are almost certain to develop emphysema.

CausesCigarette smoking is the major cause of emphysema. When exposed to cigarette smoke, the air sacs of the lungs produce defensive cells, called macrophages, which "eat" the inhaled particles. But macrophages are stimulated to release materials which can destroy the proteins that let the lungs expand and contract, called elastin and collagen.

Cigarette smoke also damages the cilia, tiny hair-like projections in the bronchi that "sweep" foreign bodies and bacteria out of the lungs

Symptoms The first sign of emphysema is shortness of breath during exertion.Eventually, this shortness of breath occurs while at rest. As the disease progresses, the following symptoms which are related to one of the other major lung diseases also caused by smoking - bronchitis - may occur:

Difficulty breathing (dyspnea)Coughing (with or without sputum) Wheezing (this can also be caused by emphysema itself) Excess mucus production A bluish tint to the skin (cyanosis) HypoxemiaTachycardiaPolycythemia

More SymptomsClubbed fingers (chronic hypoxia)Right Heart FailureStained yellow fingers, teeth

DiagnosisHistory And Physical Examination

Smoking history (calculate pack years, # packs smoked times # years smoked)Working environment- breathing in any harmful chemicals?A physical examination will include an examination of your chest and breathing patterns; prolonged expiratory timesNasal flaring, accessory muscle usage (due to loss of diaphragm recoil from air trapping)

Diagnosis ContinuedX-Ray and/or CT of the ChestChest x-rays are a very useful tool to evaluate anatomy of the lung. In emphysema, there is evidence of increased air in the chest and destruction of some of the lung tissue. Bronchitis can be suspected on a chest x-ray by presence of thickening of the tissue around the large airways (bronchi). Chest x-rays are also useful as screening for lung cancer and heart disease.Computerized axial tomography or CAT scans indicate lung anatomy in greater detail. In some cases, this information is needed to fully evaluate lung disease.

Routine lung function tests can help define the kind and amount of damage to the lungs. The following tests can identify various stages of emphysema:

Spirometry measures breathing capacity. A common measure of breathing capacity is the forced expiratory volume in one second (FEV1), or the amount of air that can be forced out of the lungs in one second. This is a common way to determine the amount of airway obstruction. Lung Function Tests

Lung Function TestsFrequently, your physician will ask that spirometry and body plethysmography be repeated after administration of an inhaled bronchodilator

This test will help your physician determine if there is an asthmatic component present

Lung Volumes measures the amount of air in the lungs. This increases markedly in emphysema.

Lung Function TestsDiffusing Capacity measures the ability of the lung to transfer the gases from the air to the blood and vice versa. Decrease in diffusing capacity allow fairly accurate estimation of amount of emphysema. Body Plethysmography is a rapid way of evaluating both degree and type of obstruction and lung volumes. It is a useful adjunct to understanding the mechanism of airway obstruction - e.g., asthma vs emphysema. Arterial blood gases (ABG) analyzes blood from an artery for amounts of carbon dioxide and oxygen. This test is often used in more advanced stages of emphysema to help determine if a person needs supplemental oxygen.

Lung Function Tests

Arterial Blood GasPatients with emphysema have chronic CO2 retention due to the inability to expel gas. Their blood reflects higher levels of CO2 than normal people; CO2 is acidic in nature.

Over time their body compensates for this higher CO2 by creating more buffer in the blood in the form of HCO3- from the kidneys.

Emphysema Diagnosis ContTests For Alpha-1 Antitrypsin DeficiencyThe symptoms of alpha-1 antitrypsin deficiency-related emphysema tend to appear between the ages of 30 and 40. The symptoms and diagnostic tests are basically the same in any kind of emphysema except that, in this disease, emphysematous changes are greatest in the lower lung. However, if AAT deficiency is suspected, a special blood test can confirm the diagnosis.

Treatment for EmphysemaThere is no cure for emphysema. The goal of treatment is to slow the development of disabling symptoms. The most important step to take is to stop smoking.Treatments for emphysema caused by smoking include medication, breathing retraining, and surgery.People with inherited emphysema due to alpha-1 antitrypsin deficiency can receive alpha 1-proteinase inhibitor (A1PI), which slows lung tissue destruction.

Breathing TechniquesDiaphragmatic Breathing

The diaphragm is a major muscle used in breathing and is located beneath the lowest two ribs. At rest, the diaphragm muscle is bell shaped. During inspiration, it lowers and flattens out.Optimizing the use of the diaphragm is beneficial because it pulls air into the lower lobes of the lungs where more gas exchange takes place. Not only is the diaphragm the most efficient of all respiratory muscles, but using it tends to be very relaxing and calming.Along with our diaphragm, we use intercostal and abdominal muscles in the work of breathing. The intercostals (muscles between the ribs) pull to lift the rib cage up and out. This causes the lungs to open in all directions and air can be pulled down the airways. To exhale, the muscles that have been pulling relax and air is forced out.The diaphragm tenses, pulling air in; and relaxes, letting the spring of the ribs push the air out again.

Breathing TechniquesDiaphragmatic Breathing

Pursed Lip Breathing

How:Breathe in through your nose. Purse lips slightly as if to whistle. Breathe out slowly through pursed lips. Do not force the air out. Pursed Lip Exercise

Medications UsedMedications To Treat EmphysemaEmphysema cannot be cured and, except for oxygen, does not reverse with any medication. However, emphysema is frequently associated with bronchitis and asthma and the symptoms associated with these processes often can be alleviated with medication (hence, you can see the value of pulmonary function and other tests designed to discover if there is asthmatic component present:Bronchodilator medication Corticosteroids Supplemental oxygen

Bronchodilator MedicationBronchodilator medication may be prescribed for airway tightness. Bronchodilators react similar to norepinephrine through the sympathetic nervous system The most commonly prescribed bronchodilators are beta2 agonists, the anti-cholinergic drug ipatropium bromide, and theophylline.Anti-cholinergics block musacaric receptors which normally respond to acetylcholine and cause bronchoconstriction

Medications Used

Medications UsedCorticosteroidsThe potent anti-inflammatory medications known as corticosteroids - commonly called steroids - may be used to help lessen the inflammation that often accompanies emphysema. These may be taken by mouth or inhaled.

Oxygen Due to the chronic state of increased CO2 in the blood (hypercapnia), the patient has adapted a breathing regulation in the brain that responds to changes in O2 and not CO2 like most peopleIf you give a patient with COPD more than 30% oxygen they will slow their breathingGive low flow oxygen at 2 LPM by NCOr high flow oxygen with a venturi mask at 22-30%What Would Happen If The World Lost Oxygen For 5 Seconds?Home Oxygen Therapy, What To Expect

Surgical Interventions

Surgical treatments for emphysema remain experimental and are not covered by insurance. Most people with emphysema are not candidates for surgery.Two types of surgery for people with emphysema are:

Lung ReductionLung Transplantation

History of lung volume reduction surgery

Lung Reduction

A surgical procedure called lung reduction may improve symptoms for people with certain types of emphysema. During the procedure, part of the lung is cut out, giving healthy lung tissue more room to expand. Lung reduction may eliminate the need for supplemental oxygen and make it much easier for the person to breathe. Early studies show that it reduces the volume of the over-inflated lungs. This improves the ability of the lung and chest wall to spring back during exhalation. This more-elastic lung appears to be the biggest reason that emphysema sufferers experience relief.

ConclusionEmphysema is a chronic disease that takes years to progress; usually as a result of heavy cigarette smoking but also can be caused by inherited Alpha-1 antitrypsin deficiencyIt destroys the stability of the alveoli and bronchioles leaving them over compliant This leads to air trapping and an accumulation of CO2 and decrease in O2The air trapping leads to dyspneaDiagnose with symptoms, ABG, CXR, PFT and historyTreatment consists of stop smoking, medications and lung reduction surgery or transplant

Cystic Fibrosis(Mucoviscidosis)

Cystic FibrosisHereditary DiseaseMost common lethal genetic disease among Caucasian AmericansAffects 30,000 persons in the U.S.Mean life expectancy +/-(5 years) 38 yrs.Caused by a genetic mutation of the gene coding for a large protein that controls the movement of chloride ions through the cell membrane.Movement of chloride is vital to the proper production and regulation of secretions in the lungs, pancreas, sweat glands and others.

IntroductionCF is an inherited disease of your mucus and sweat glandsIt affects mostly the lungs, pancreas, liver, intestines, sinuses and sex organsAn abnormal gene causes mucus to become extra thick and stickyThis gene makes a protein that controls the movement of salt and water not work properly (retaining salt=thick secretions)This leads to mucus plugs

Introduction ContinuedMucus plugs lead to collapsed lungs (atlectasis)Increased mucus in the lungs also allows for more bacterial growth which leads to frequent pneumoniaConstant infections lead to inflammation in the lung

Introduction ContinuedCystic fibrosis is the most common cause of chronic genetic lung disease in children and young adults, and the most common fatal hereditary disorder affecting Caucasians in the US. CF is a multi-system disorder of exocrine glands causing the formation of a thick mucus substance that affects the lungs, intestines, pancreas, and liver. The standard test for diagnosis is a sweat test which evaluates the level of chloride excreted by the body.

Cystic FibrosisChloride levels in sweat is elevated due to lack of normal removal, as a result CF patients are vulnerable to dehydration. A sweat chloride test is used for the diagnosis of the disease (> 60mEq/L in infants and > 80 in adults)Pancreatic insufficiency reduces the number of digestive enzymes. These patients experience malnutrition, diarrhea, vitamin deficiency and undigested fat in the stool.

Diagnosis

The sweat chloride test is performed to determine the amount of chloride that is excreted in sweat from the body during a certain period of time. The test may be performed on infants to determine if cystic fibrosis is present. Children with cystic fibrosis have increased sodium and chloride concentrations in their sweat. Normal Sweat 18 mEq/L Positive Test 60 mEq/L

Often the first sign of CF begins after birth, the mother kisses the baby and they taste salty.Poor feeding occurs from blocked bile ducts (bile released from pancreas helps digest food)

Diagnosis

Diagnosis

DiagnosisCystic Fibrosis: Early Intervention

Genetic Carrier Testing More than 10 million Americans are symptomless carriers of the defective CF gene. This blood test can help detect carriers, who could pass CF onto their children. To have cystic fibrosis, a child must inherit one copy of the defective CF gene from each parent.Each time two carriers of the CF gene have a child, the chances are:25% (1 in 4) the child will have CF;50% (1 in 2) the child will carry the CF gene but not have CF; and25% (1 in 4) the child will not carry the gene and not have CF

Diagnosis

Diagnosis Continued

Diagnosis ContinuedDetailed medical history is obtained (CF is Hereditary)Chest X-RAY to show scarring from frequent inflammationSinus X-RAY Pulmonary Function Test (CF is a COPD); used only with individuals old enough to comply > 8years old usuallySputum Cultures to determine certain bacteria growthBlood tests to find abnormal CF gene

Symptoms

Ileus blockage or disruption75

SymptomsIncreased WOB from plugged airways and air trappingTenacious SecretionsFrequent productive coughFrequent bouts of bronchitis and pneumoniaDehydration and malnutrition despite huge appetite; failure to thriveInfertility (mostly in men)Ongoing diarrhea and stomach pain

Cystic Fibrosis

Finger Clubbing

Cystic Fibrosis

Radiologic Findings:Translucent (dark) lung fieldsDepressed or flattened diaphragmsRight ventricular enlargementAreas of atelectasis and fibrosis Occasionally:Abscess formationPneumothorax

CF leads toSinusitis: the sinuses have mucus build up leading to headaches, ear and equilibrium problems.

Bronchiectasis: damaged lungs become overly stretched and retain secretions and gas.

Pancreatitis: Leads to inability to digest food, leading to bowel obstruction and sepsis.

Liver Disease, Diabetes, Gallstones and low bone density from lack of Vitamin D.

CF leads to Respiratory failureThe mucus plugs the airways causing collapse of the alveoli and increased WOBIncreased PaCO2, decreased PaO2 and eventual death if not treated.Infections lead to inflamed and damaged lung liningBlocked pancreas leads to vitamin deficienciesThere is no cure for CF only treatments; average life span is 38 years

Treatments for CFChest physiotherapy (CPT) is the traditional means of airway clearance in CF. It uses postural drainage in various positions, percussion, vibration, deep breathing, and coughing to loosen and move secretions out of the lungs. The treatment time including an aerosol before is about 45 minutes. Done so by using manual percussion with hand, pneumatic precursor with device or by Vest.

Cystic Fibrosis Physical Therapy of Toddler

Treatment for CFChest Physical Therapy:Using the Vest or manual precursor. Helps loosen secretions with percusion

Treatment ContinuedPEP is a technique that uses a hand held device which can be used with a nebulizer attached. It has a restricted orifice. When exhaled into, this creates pressure in the lungs. This pressure allows air to enter behind areas of mucus obstruction and keeps the airways open during exhalation. As you exhale, mucus moves towards the larger airways, so it can be more easily coughed up with the huff technique. PEP can be taught to children as young as 5 years, and can be passively given to infants via a mask. The treatment time is about 20 minutes.

AcapellaAcapella Choice

PEP Device

Treatment ContinuedVibratory Positive Expiratory Pressure (Flutter, Acapella) Vibratory positive expiratory pressure is a hand held device. Exhaling into this device results in oscillations of pressure and airflow which vibrate the airway walls (loosening mucus), helps hold the airway open (which allows air to get behind secretions and keeps the airways open during exhalation). It speeds up airflow helping mucus move up to the larger airways where it can be more easily coughed up. Vibratory PEP can be taught to children as young as 2 years old by mask, and to ages 5 and up via mouthpiece. Treatment time is about 20 minutes.

Treatment ContinuedIntrapulmonary Percussive Ventilation. The IPV is a pneumatic (air driven) device thatdelivers both continuous airway pressure and minibursts of air. At the same time the IPV delivers adense aerosol. The combination allows air to enter behind mucus blockage, and vibration to dislodge mucus from the airway walls so it can be more easily coughed up.IPV

Treatment ContinuedActive Cycle of BreathingActive cycle of breathing is a series of breathing techniques, consisting of thoracic expansion exercises (deep breathing), breathing control (using the diaphragm), and the forced expiration technique (huff). These breathing cycles are performed in various positions of drainage similar to CPT positions but without the percussion. This can be taught at about the age of 8 years. Treatment time, including an aerosol before, is about 45 minutes.

TreatmentsAutogenic Drainage is a breathing technique which involves 3 phases of breathing levels:

Phase One is the unsticking phase which is inhalation and exhalation of small amounts of air. Phase Two is the collection phase where medium sized breaths are inhaled and exhaled. Phase Three is the evacuation phase where large amounts of air are inhaled and exhaled.

Treatments Hand Held Nebulizers are used in conjunction with PEP, IPV, CPT and breathing techniques

The nebulizer will nebulize medications that bronchodilate and help break up mucus

Antibiotics can also be used in a nebulizer

Medications UsedAntibiotics: Tobramycin and Azithromycin to fight bacterial infection. Given by aerosol in nebulizer or by IVAnti-Inflammatory Drugs: Steroids given inhaled or by IV; also Ibuprofen is givenBronchodilators: Albuterol/Xopenex given to relax smooth muscleMucolytics: Given with bronchodilators to break up thick secretions. Main one is Dornase Alfa (Pulmozyne) made specifically for CF patients

More TreatmentsOxygen Therapy at low concentrations.Lung Transplantation; depends on severity of illness and health of participateNutritional therapy; oral pancreatic enzymes to digest fats and proteins and absorb vitamins. Vitamin supplements of A, D, E and KFeeding tube at night (G-Tube)Enemas and stomach meds to control acid

ConclusionCF is a deadly hereditary disease that is treatable but not curableCF causes abnormally thick mucus which blocks bile ducts and plugs up the lung and sinusMay lead to respiratory failure, malnutrition and frequent occurrences of pneumoniaTreatment includes methods to remove and thin mucus and medications to treat digestive problems, and infections

Chronic Bronchitis

Chronic BronchitisPresence of cough and sputum production for three or more months in two successive yearsEtiologySmokingAir pollutionChronic infectionsChronic Bronchitis Symptoms

Chronic Bronchitis14 million Americans are affectedMost common causes are smoking/pollutionRepeated lung infections, especially in childhood increase riskCommon pathogens include Haemophilus influenzae and Streptococcus pneumoniaeGastroesophageal reflux disease (GERD) can lead to pneumonias from aspiration of stomach contents

Chronic Bronchitis PathophysiologyMost changes in the lungs occur in the conducting airwaysAirway changes occur from:Chronic inflammation and swellingExcessive mucus production and accumulationPartial or total mucus pluggingHyperinflation of alveoliSmooth muscle constriction of airways

Chronic Bronchitis Pathophysiology

Changes in mucus glandsIncrease in number of mucus secreting glands; goblet cells increase, causing decrease in ciliated columnar cells; submucosal glands hypertrophySmooth muscle hypertrophy in bronchial airwaysDiminished airway radius

Chronic Bronchitis PathophysiologyIncrease in sputum productionAccumulation of secretions Loss of ciliated cellsImpairment of mucociliary escalatorDecreased flow rates, VC, FVC, FEV1, MVVIncreased RV, FRC, TLC

Chronic Bronchitis

Radiologic FindingsHyperinflation of the LungsFlattened Hemidiaphram Peripheral Pulmonary Vasculature may be ProminentPulmonary Vascular EngorgementLong and narrow heart (pulled down by the diaphragms)Enlarged heart

Chronic Bronchitis

Chronic Bronchitis Clinical FindingsTypical appearance is of the Blue BloaterStocky buildCyanoticIncreased A-P diameterJugular vein distensionEdema

Chronic Bronchitis Clinical FindingsCoughSmokers coughMorning coughContinual coughSputum productionVolume increases slowly leading to abnormal production but typically less than a cup/dayThick, gray, mucoid in natureMucopurulent infections leading to yellow or green sputum

Chronic Bronchitis Clinical Findings Increase in respiratory rateStimulation of peripheral chemoreceptors secondary to hypoxemia and chronic CO2 retentionDecrease in lung complianceAnxietyIncrease in heart rateDyspnea, especially on exertionUse of accessory musclesBS: rhonchi, crackles, wheezing and decreased BSBreath Sounds

Chronic Bronchitis Clinical Findings Pursed lip breathingIncrease in A-P diameter of the chest (barrel chest) secondary to hyperinflationClubbingIncreased sputum productionABG resultsFully compensated pH unless in an acute exacerbationIncrease in PaCO2Decrease in PaO2

CXR Interpretation for COPDChest x-ray interpretation --COPD and Emphysema

Pink Puffer Vs. Blue BloaterA "pink puffer" is a person where emphysema is the primary underlying pathology. As you recall, emphysema results from destruction of the airways distal to the terminal bronchiole--which also includes the gradual destruction of the pulmonary capillary bed and thus decreased inability to oxygenate the blood. So, not only is there less surface area for gas exchange, there is also less vascular bed for gas exchange--but less ventilation-perfusion mismatch than blue bloaters. The body then has to compensate by hyperventilation (the "puffer" part).

Pink Puffer Vs. Blue BloaterPink Puffers:Their arterial blood gases (ABGs) actually are relatively normal because of this compensatory hyperventilation. Eventually, because of the low cardiac output, people afflicted with this disease develop muscle wasting and weight loss. They actually have less hypoxemia (compared to blue bloaters) and appear to have a "pink" complexion and hence "pink puffer". Some of the pink appearance may also be due to the work (use of neck and chest muscles) these folks put into just drawing a breath.

Pink Puffer Vs. Blue BloaterA "blue bloater" is a person where the primary underlying lung pathology is chronic bronchitis. Just a reminder, chronic bronchitis is caused by excessive mucus production with airway obstruction resulting from hyperplasia of mucus-producing glands, goblet cell metaplasia, and chronic inflammation around bronchi. Unlike emphysema, the pulmonary capillary bed is undamaged. Instead, the body responds to the increased obstruction by decreasing ventilation and increasing cardiac output.

Pink Puffer Vs. Blue BloaterThere is a dreadful ventilation to perfusion mismatch leading to hypoxemia and polycythemia. In addition, they also have increased carbon dioxide retention (hypercapnia). Because of increasing obstruction, their residual lung volume gradually increases (the "bloating" part). They are hypoxemic/cyanotic because they actually have worse hypoxemia than pink puffers and this manifests as bluish lips and faces--the "blue" part.

Pink Puffer Vs. Blue Bloater

Asthma

Watch an Asthma Attack

AsthmaA disease of the airway characterized by an increased responsiveness of the trachea and bronchi to various stimuli and is manifested by widespread narrowing of the airways that change in severity either spontaneously or as a result of treatment (ATS)

AsthmaAirway constriction may be partially or completely reversible either spontaneously or with treatmentAffects more than 15 million AmericansRecognized more than 2000 years agoMore than 5,000 die per year - Teen dies of asthmaThe most common chronic illness of childhoodMay develop in adulthood with increased mortalityMay disappear at puberty

AsthmaAllergic or Extrinsic AsthmaResults from an antigen-antibody reaction on mast cells causing a release of histamine, bradykinins, and other chemicalsIdiopathic or Intrinsic AsthmaCannot be linked to a specific antigenResults from an imbalance of the autonomic nervous systemNon-specific AsthmaResults from an unknown cause, possibly viral, emotional, or exercise

AsthmaFrom your text page 189:Occupational Sensitizers (box 12-1)Seen predominantly in adults, more than 300 substances contribute to it.Sensitive work environments include:FarmingAgriculturalPaintingCleaning workPlastic manufacturing

Immunologic Mechanism (from your text, page 188)When exposed to specific antigens, lymphoid tissue forms specific IgE antibodiesThe IgE antibodies attach themselves to surface of mast cells in the bronchial wallRe-exposure to the same antigen creates antigen-antibody reaction on the surface of the mast cell, causes mast cell to degranulate and release chemical mediators:HistamineEosinophil/neutrophil chemotactic factorsLeukotrienesProstglandins and platelet activating factorAllergies

Mast Cell Degranulation

Exposed to antigen, form antibodies, attach to mast cellsRe-exposure to antigen causes the degranulation of mast cell and release of inflammatory cells

Mast Cell Degranulation

Following an Asthma attack; the patient will have congestion and increased sputum production for several days

Inflammatory cell release (page 189)Release of chemical mediators from mast cell stimulates parasympathetic nerve endings in the bronchial airways leading to reflex bronchoconstriction and mucous hyper-secretionThe mediators also increase permeability of capillaries causing dilation of blood vessels and tissue edema

Early vs. late response (after steroids and bronchodilators have worn off)

Mast Cell inhibitors for asthma treatmentCromolyn sodium (Intal) and nedocromil (Tilade) are used to prevent allergic symptoms like runny nose, itchy eyes, and asthma. The response is not as potent as that of corticosteroid inhalers.How mast cell inhibitors workThese drugs prevent the release of histamine and other chemicals from mast cells that cause asthma symptoms when you come into contact with an allergen (for example, pollen). The drug is not effective until four to seven days after you begin taking it.Who should Use itPatients with extrinsic asthma, with known allergiesFrequent dosing is necessary, since the effects last only six to eight hours. Mast cell inhibitors are available as a liquid to be used with a nebulizer, a capsule that is placed in a device that releases the capsule powder to inhale, and handheld inhalers

Intal and Tilade

Both drugs are used only for prophylaxis of asthma, not for treatment of the acute exacerbation or for the symptomatic patient

Anti- LeukotriensDo not prevent mast cell degranulation, as do Intal and TiladeThey stop the inflammatory mediators once the mast cells is degranulated Leukotrienes are proinflammatory mediators with special significance in asthma. Released by numerous cell types, particularly after exposure to allergens, leukotrienes cause a potent contraction of bronchial smooth muscle, resulting in reduced airway caliber. Further, they cause plasma to leak from the vessels, resulting in edema, and enhance the secretion of mucus

Anti-leukotriene drugs

ORAL ONLY. First drug of this type (Nov 1996) is the leukotriene-receptor antagonist Zafirlukast [Accolate], 20 mg bid. The 2nd approved anti-leukotriene (Jan 1997) is the leukotriene-synthesis inhibitor Zileuton [Zyflo], with a 600 mg QID dosage schedule. Both are approved only for asthma, and for patients 12 years or older. The 3rd approved anti-leukotriene, Montelukast (Singulair), 10 mg qd, is also approved for ages 6-14 in a 5 mg QD dose. All anti-leukotrienes have some bronchodilator as well as anti-inflammatory activity.

AsthmaEtiologyHeredity one or more parents with diseaseAllergies, especially if onset between ages five and fifteenInhaled irritantsPollenDust mitesGrassesPollutionAnimal danderChemicals

The Role of Heredity in Asthma

Heredity.To some extent, asthma seems to run in families. People whose brothers, sisters or parents have asthma are more likely to develop the illness themselves.Atopy.A person is said to have atopy (or to be atopic) when he or she is prone to have allergies. For reasons that are not fully known, some people seem to inherit a tendency to develop allergies. This is not to say that a parent can pass on a specific type of allergy to a child. In other words, it doesn't mean that if your mother is allergic to bananas, you will be too. But you may develop allergies to something else, like pollen or mold. In addition, several factors must be present for asthma symptoms to develop:Specific genesmust be acquired from parents. Exposure to allergensor triggers to which you have a genetically programmed response. Environmental factorssuch as quality of air, exposure to irritants, behavioral factors such as smoking, etc.

Asthma Risk Factors (page 190)Obesity: Certain mediators such as leptins may have an effect on airway function that can lead to development of asthmaGender: Males up to 14, have a higher prevalence, due to possible lung size of boys vs. girls, after 14, girls have a higher prevalence Infections: upper viral infections and bacterial infections contribute to asthma. Commonly seen in children after RSV, parainfluenza, rhinovirus.Exercise induced: heat loss, water loss, increased osmolority increase inflammatory release

Asthma Risk Factors (page 190)Outdoor/indoor air pollution: increases in asthma incidences occur in heavily polluted areas. Smoke, gas fumes, biomass fuels for heating, molds and cockroach droppings contribute to asthma Drugs/foods/preservatives: Aspirin sensitivity, and other non-steroidals (NSAIDS), beta-blocking agents to treat hypertension and tachycardia, tartazine (food coloring), and preservatives for restaurant foodGERD: regurgitation and aspiration, may lead to asthma or exacerbate it

Asthma Risk Factors (page 190)Emotional Distress: psychological factors can induce tachypnea and stress the lung contributing to asthma exacerbationPerimenstrual asthma: symptoms worsen 2-3 days before menstruation

Allergy Test Skin test - numerous known substances are placed on the skin, reactions are noted and allergens are then determined

Allergy TestBesides the skin allergy test they also do blood tests. The RAST test measures the levels of the allergy antibody IgE that is produced when your blood is mixed with a series of allergensin a laboratory.

CausesSubstances that cause allergies(allergens) such as dust mites, pollens, molds, pet dander, and even cockroach droppings. In many people with asthma, the same substances that cause allergy symptoms can also trigger an asthma episode. These allergens may be things that you inhale, such as pollen or dust, or things that you eat, such as shellfish. It is best to avoid or limit your exposure to known allergens in order to prevent asthma symptoms. Irritants in the air, including smoke from cigarettes, wood fires, or charcoal grills. Also, strong fumes or odors like household sprays, paint, gasoline, perfumes, and scented soaps. Although people are not actually allergic to these particles, they can aggravate inflamed, sensitive airways. Today most people are aware that smoking can lead to cancer and heart disease. Smoking is also a risk factor for asthma in children, and a common trigger of asthma symptoms for all ages

CausesRespiratory infections such as colds, flu, sore throats, and sinus infections. These are the number one asthma trigger in childrenGERD: Gastric esophageal reflux disease, stomach acid can be aspirated and inflame the airwayExercise and other activities that make you breathe harder. Exerciseespecially in cold airis a frequent asthma trigger. A form of asthma called exercise-induced asthma is triggered by physical activity. Symptoms of this kind of asthma may not appear until after several minutes of sustained exercise. (When symptoms appear sooner than this, it usually means that the person needs to adjust his or her treatment.) The kind of physical activities that can bring on asthma symptoms include not only exercise, but also laughing, crying, holding one's breath, and hyperventilating (rapid, shallow breathing). The symptoms of exercise-induced asthma usually go away within a few hours Exercise Induced Asthma Attack

More CausesWeather such as dry wind, cold air, or sudden changes in weather can sometimes bring on an asthma episode.Expressing strong emotions like anger, fear or excitement. When you experience strong emotions, your breathing changes -- even if you dont have asthma. When a person with asthma laughs, yells, or cries hard, natural airway changes may cause wheezing or other asthma symptoms.Some medicationslike aspirin can also be related toepisodes in adults who are sensitive to aspirin. Irritants in the environment can also bring on an asthma episode. These irritants may include paint fumes, smog, aerosol sprays and even perfume.

Why Does My Asthma Act Up at Night?For reasons we don't fully understand, uncontrolled asthma -- with its underlying inflammation -- often acts up at night. It probably has to do with natural body rhythms and changes in your bodys hormones, as well as the fact that some symptoms appear hours after you come in contact with a trigger. Also during sleep you release less norepinephrine (adrenaline) which acts as your bodies natural bronchodilator

A Tragic Asthma Attack Story

Asthma PathophysiologyAirway InflammationAcute Phase Response triggered by activation of mast cells and the release of intracellular mediatorsBronchospasmIncrease in secretionsMucosal edemaSignificant reduction in airflow

Asthma PathophysiologyAirway InflammationSubacute phaseContinuous inflammatory patternSignificant airflow limitationCan continue for days to weeks

Asthma PathophysiologyAirway InflammationChronic inflammationPresent between episodes of exacerbationControlled by corticosteroids, mast cell modifiers, or leukotriene modifiers

Asthma PathophysiologyAirway HyperresponsivenessUsually most evident in acute phaseIncreased sensitivity to both specific and non-specific causesRelease of immunoglobulin E (IgE) mediators into the cellular tissue causing bronchoconstriciton of the smooth muscle of the airway, degranulation of mast cells releasing histamines, leukotrienes, certain interleukins, prostaglandins and othersTreated with beta2 agonists

Asthma Pathophysiology

Degranulation of the mast cell

Smooth muscle contraction

Mucous accumulation

Mucous plugging

Hyperinflation of alveoli

Asthma ClassificationClassifications of AsthmaMild intermittent asthmaSymptoms < 2/week or < 2 times/month at nightLittle effect on day to day activitiesExpiratory flow 80% of predicted

Asthma ClassificationClassifications of AsthmaMild Persistent AsthmaSymptoms > 2/week but less than 1/day; < 2 times/month at nightExacerbations may affect activityExpiratory flow 80% of predicted

Asthma ClassificationClassifications of AsthmaModerate persistent asthmaSymptoms daily; > 1/week at nightLimitations 2/week; may last daysExpiratory flow > 60% but < 80% of predicted

Asthma ClassificationClassifications of AsthmaSevere persistent asthmaSymptoms continually with frequent symptoms at nightFrequent exacerbations which limit activityExpiratory flow < 60% of predicted

Asthma Pulmonary Function ResultsMay have normal results when asymptomaticAirway obstructionDecrease in FEV1Decrease in FEV1/FVC ratioDemonstrate reversibility of obstruction following bronchodilator administration ( in FEV1 of at least 12% and an increase in VC of 200mL or more)Decrease in expiratory flow rates: peak flows are used to monitor asthmatic events in the home.

Asthma Pulmonary Function ResultsBronchoprovocation TestingAdministration of MethacholineCauses decrease in FEV1 by 20% or more in hyperresponsive airwaysDiagnostic test used in the evaluation of suspected asthma. The methacholine challenge is also used for research purposes to study airway hyperreactivity. Under special circumstances it plays a role in the clinical arena. Cold-air exercise tests are another example of a bronchoprovocation test.A bronchoprovocation test might be ordered in the evaluation of suspected asthma. It is not considered a routine test. Usually, the patient describes subtle symptoms suggestive of asthma. Spirometry and other pulmonary function testing are entirely normal.

MethacholineMethacholine (Provocholine) is a synthetic choline ester that acts as a non-selective muscarinic receptor agonist in the parasympathetic nervous system

Using a Peak FlowA Peak Flow device is a assessment tool used to measure the effectiveness of fast acting bronchodilators.Given during the attack, before and after treatmentsIt is a handheld device that the patient exhales forcibly on; as the airway opens and improves, the value increases

Peak Flow ContinuedPeak Flow Meter Demo

Asthma Action Plan

Asthma Clinical Findings

Asthma Clinical FindingsAuscultation episodic wheezingAbsence of wheezing does not preclude asthmaNot all wheezing is asthmaBreath sounds may get worse but patient could be improving Shortness of breathTachypneaTachycardiaUse of accessory musclesPursed-lip breathingAnxietyHypoxia Altered LOCFull ArrestBS wheezes, crackles, rhonchi, decreased BS

Asthma Clinical FindingsBlood Gas Results In mild to moderate episode: pH PCO2 HCO3 slightly PaO2In moderate to severe episode:pH PCO2 HCO3 slightly PaO2

Status AsthmaticusA severe asthma attack not responsive to bronchodilatorsTypically requires intubation and mechanical ventilation due to respiratory failureTypically, patients present a few days after the onset of a viral respiratory illness, following exposure to a potent allergen or irritant, or after exercise in a cold environment. Frequently, patients have underused or have been under prescribed anti-inflammatory therapy. Illicit drug use may play a role in poor adherence to anti-inflammatory therapy. Patients report chest tightness, rapidly progressive shortness of breath, dry cough, and wheezing and may have increased their beta-agonist intake (either inhaled or nebulized) to as often as every few minutes.

Early and Late Asthmatic ResponseLate response is usually more severe and longer lasting.

Mosby items and derived items 2009 by Mosby, Inc., an affiliate of Elsevier Inc. 158PharmacotherapyCorticosteroidsMost effective mediation in treatment of asthmaReduces symptoms and mortalityUse of inhaled steroids for long-term treatment preferredUse spacer and rinse mouth to eliminate or minimize side effectsLong-term use of oral steroids should be restricted to patients with asthma refractory to other treatment.Short-term oral steroid use during exacerbation reduces severity, duration, and mortality.

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Mosby items and derived items 2009 by Mosby, Inc., an affiliate of Elsevier Inc. 159PharmacotherapyInhaled Corticosteroids (page 194)Beclomethasone (QVAR); 40 or 80 ug/puff BIDFlunisolide (Aerobid); 250 ug/puff; BIDFluticosone (Flovent); 44, 110, or 220 ug/puff, BIDBudesonide (Pulmicort); SVN 0.25 or 0.5 mg, BIDMomestone furoate (Asmanex twisthaler) DPI 220 ug QD

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Mosby items and derived items 2009 by Mosby, Inc., an affiliate of Elsevier Inc. 160PharmacotherapySystemic Steroids Corticosteroids (page 194)Prednisone (short term use following an acute attack) usually 3-5 days, BID

Methylpredinsone (Solu-Medrol); Typically an IV potent systemic steroid, given during and after acute attacks

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HHN DeliveryDelivery of the a small volume nebulizer takes practice and in fact the way the medication is delivered to a patient can dictate the hazards. Below is a link of the proper way to give a nebulizer treatment, granted it is from another RT program, I think it shows the proper components of neb delivery

You Tube- Neb Delivery

MDI DeliveryDelivering an MDI to a patient takes some practice. Below are three videos, one for an MDI using a closed mouth technique, one showing an open mouth technique and one showing an MDI with a holding chamber (Aerochamber). You should encourage MDI use with a holding chamber

1. You Tube- closed mouth

2. You Tube- open mouth

3. You Tube- holding chamber

Mosby items and derived items 2009 by Mosby, Inc., an affiliate of Elsevier Inc. 163Pharmacotherapy (cont.)Cromolyn (NSAID) non-steroidal anti-inflammatory drugProtective against allergens, cold air, exercise Administered prophylactically, CANNOT be used during an acute asthma attackOf limited use in adults Drug of choice for atopic children with asthma

Nedocromil (NSAID)Similar to Cromolyn, it is 410 times more potent in preventing acute allergic bronchospasm.

NSAID - Nonsteroidal antiinflammatory drug 163

Mosby items and derived items 2009 by Mosby, Inc., an affiliate of Elsevier Inc. 164Pharmacotherapy (cont.)DOSAGES AND FREQUENCIES:

Cromolyn (NSAID)SVN 20 mg QIDMDI 2 puffs 800 ug QID

Nedocromil (NSAID)Similar to Cromolyn, it is 410 times more potent in preventing acute allergic bronchospasm.MDI only, 2 puffs 1.75 mg/puff QID

NSAID - Nonsteroidal antiinflammatory drug 164

Mosby items and derived items 2009 by Mosby, Inc., an affiliate of Elsevier Inc. 165Pharmacotherapy (cont.)Leukotriene inhibitorsLeukotrienes mediate inflammation and bronchospasms. Modestly effective to control mild to moderate asthmaAccolate, Singular, ZyfloInhaled steroids remain the anti-inflammatory drug of choice for the treatment of asthma.

Methyxanthines (use is controversial)Oral or IV use if admitted for acute asthma attackTheophylline

NSAIDs have not been found to be more effective then steroids

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Mosby items and derived items 2009 by Mosby, Inc., an affiliate of Elsevier Inc. 166Pharmacotherapy (cont.)2-Adrenergic agonists Short ActingMost rapid and effective bronchodilator Drug of choice for exercise-induced asthma and emergency relief of bronchospasmsShould be used PRNImproves symptoms not underlying inflammationRegular use may worsen asthma control and increase risk of death.Albuterol (Proventil, Ventolin); SVN UD 0.5% Soln, or 2.5 mg (0.5 ml) give TID, QID, Q4, Q6 or PRNLevalbuterol (Xopenex), SVN 0.31, 0.63, or 1.25 mg

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Mosby items and derived items 2009 by Mosby, Inc., an affiliate of Elsevier Inc. 167Pharmacotherapy (cont.)2-Adrenergic agonists Short Acting

Albuterol MDI = Pro Air/ Ventolin 90 ug: 2 puffs TID/QID

Xopenex MDI = Xopenex HFA 45 ug/puff x 2 puffs Q4-6

Combivent: MDI of Albuterol and AtroventDuoNeb: SVN of Albuterol and Atrovent

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Mosby items and derived items 2009 by Mosby, Inc., an affiliate of Elsevier Inc. 168Pharmacotherapy (cont.)2-Adrenergic agonists Ultra Short Acting

Epinephrine (Epinephrine Mist, Primatene mist): SVN 1% soln (1:100), 0.25-0.5 ml QID; MDI 0.22 mg/puff

Racemic Epinephrine; (Micronephrine, Nephrone); SVN 2.25% soln, 0.25-0.5 ml QID

Last about 90 minutes, Racemic has a strong Beta and Alpha response, used for upper airway swelling

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Mosby items and derived items 2009 by Mosby, Inc., an affiliate of Elsevier Inc. 169Pharmacotherapy (cont.)2-Adrenergic agonists Long Acting and Combination drugsSalmeterol (Serevent); DPI 50 ug/inhalation; 50 ug BID

Formoterol (Foradil) DPI, 12 ug, BID

Arformoterol (Brovona) SVN 15 ug/2ml, BID (some fast acting response)

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Mosby items and derived items 2009 by Mosby, Inc., an affiliate of Elsevier Inc. 170Pharmacotherapy (cont.)2-Adrenergic agonists Long Acting and Combination drugsAdvair (fluticosone and Serevent); DPI; 3 doses; 500/50, 250/50 and 100/50; the fluctuating dose is the steroidAlso comes in a MDI

Symbicort (Pulmicort and Foradil); MDI 80 and 160 ugDULERA mometasone furoate and a long acting beta2-agonist medicine (LABA) called formoterol fumarateArcapta (indacaterol maleate inhalation powder)

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Mosby items and derived items 2009 by Mosby, Inc., an affiliate of Elsevier Inc. 171Pharmacotherapy (cont.)AnticholinergicsCan be used as adjunct to first-line bronchodilators if there is an inadequate responseHas an additive affect to 2-agonists

Blocks musacarenic receptors (Acetycholine)

Ipatropium Bromide (Atrovent); SVN 0.5 mg, 0.02% solutionMDI 18 ug/puff; dose TID, Q6

Tiotropium (Spiriva), used through a handi-haler, QD

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Mosby items and derived items 2009 by Mosby, Inc., an affiliate of Elsevier Inc. 172Asthma and Environmental ControlRecognized relationship between asthma and allergy 7585% asthma patients react to inhaled allergens

Environmental control is aimed at reducing exposure to allergens.Avoid outdoor allergens by remaining inside, windows closed, AC onIndoor allergens are combated byAir purifiers and no petsDust mites: airtight covers on bed and pillow, no carpets in bedroom, chemical agents to kill mites

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Mosby items and derived items 2009 by Mosby, Inc., an affiliate of Elsevier Inc. 173Special Considerations in Asthma Management (cont.)Nocturnal asthma Present in two-thirds of poorly controlled asthmaticsMay be due to diurnal decrease in airway tone or gastric refluxTreatment should include:Steroid treatment targeted to relieve night symptomsSustained release theophylline New long-acting 2-agonistsAntacids for reflux

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Mosby items and derived items 2009 by Mosby, Inc., an affiliate of Elsevier Inc. 174Special Considerations in Asthma Management (cont.)Aspirin sensitivity5% of adult asthmatics will have severe, life-threatening asthma attacks after taking NSAIDs.All asthmatics should avoid; suggest Tylenol use.

Asthma during pregnancyA third of asthmatics have worse control at this time.Much higher fetal risk associated with uncontrolled asthma than that of asthma medicationsTheophyllines, 2-agonists, and steroids can be used without significant risk of fetal abnormalities.

NSAIDs nonsteroidal antiinflammatory drugs such as aspirin174

Mosby items and derived items 2009 by Mosby, Inc., an affiliate of Elsevier Inc. 175Special Considerations in Asthma Management (cont.)Sinusitis may cause asthma exacerbation.CT of sinuses will diagnosis problem.Treat: 23 weeks antibiotics, nasal decongestants, and nasal inhaled steroids

SurgeryAsthmatics at higher risk for respiratory complicationsArrest during induction Hypoxemia with/without hypercarbiaImpaired cough, atelectasis, pneumoniaOptimize lung function preoperatively. Use steroids during procedure.

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ReviewEmphysema:Low expiratory flows (FVC, FEV1 less than 80%), FEV1/FVC less than 70%Decreased DLCOIncreased Lung VolumesMain cause smoking, also caused by genetic alpha anti-trypson disorder, environmental Chronic hypercapnia, hypoxemia, barrel chest, clubbing of fingers, hyperinflated lungs on CXR (hyperlucent with flattened diaphragms), accessory muscle use, SOB at rest...Damage occurs primarily in upper lobesPersistent irritants overwhelm lungs natural macrophage and neutrophil removal, causing loss of elastin creating bullae

ReviewEmphysema:Treatments include breathing exercises, diaphragmatic breathing, pursed lip breathing; low supplemental oxygen less than 30% to avoid knocking out hypoxic drive; bronchodilators, and steroids. Bronchial hygiene, Possible lung transplant, smoking cessationIncreased pressure in alveoli causes: decreased VA, increased VD/VT, decreased in PaO2, PAO2, CaO2, SaO2, increase in A-a gradient, CO2, HbGet frequent pneumonia, bronchitis

ReviewCystic FibrosisHeredity basedDisease of tenacious mucus, blocks bile ducts, lungs and sinuses.

Bronchiectasis

BronchiectasisAn Amazing Story

BronchiectasisBronchiectasis is characterized by chronic dilation and distortion of one or more bronchi as a result of extensive inflammation and destruction of the bronchial wall cartilage, blood vessels, elastic tissue, and smooth muscle componentsCan affect one or both lungsCommonly limited to a lobe or segmentMost frequently found in the lower lobesThe smaller bronchi, with less supporting cartilage are predominantly affected

Bronchiectasis

BronchiectasisThree forms or anatomic varieties of bronchiectasis have been described:

Varicose or fusiformCylindrical or tubularSaccular or cystic

BronchiectasisEtiologyNot as common today because of increased use of antibiotics for lower respiratory infectionsMay be acquired or congenital but not thoroughly understoodAcquired bronchiectasis is thought to occur by repeated and prolonged respiratory infections, bronchial obstruction from a foreign body, tumor or enlarged hilar lymph nodesPeople with cystic fibrosis have a much higher incidence of bronchiectasis due to the chronic airway obstruction

BronchiectasisEtiologyCongenital BronchiectasisKartageners Syndrome responsible for 20% of all bronchiectasis. Consists of a triad of Bronchiectasis, dextracardia (heart on right side of chest), and pansinusitusHypogammaglobulinemia: An inherited immune deficiency disorder that leaves the lung vulnerable to infection

BronchiectasisFusiform or VaricoseBronchial walls are dilated and constricted in an irregular fashion similar to varicose veins ultimately ending in a distorted bulbous shape ending in nonfunctional respiratory unitsEvidence of bronchitis or bronchiolitis often present

Bronchiectasis

BronchiectasisCylindricalBronchial walls dilated with regular outlines.Least severe form

Bronchiectasis

BronchiectasisSaccularComplete destruction of bronchial wallsNormal tissue replaced by fibrous tissueMost severe form with poorest prognosis

Bronchiectasis

BronchiectasisPathophysiologyLoss of ciliated epithelium and respiratory unitsChronic inflammationSloughing of mucosa with ulceration and possible abscess formationReduced volume of distal lung and adjacent lung secondary to scarring and bronchial obstructionExcessive production of sputum (greater than 1 cup/day) Sputum is foul-smelling and hemoptysis is commonHyperinflation of alveoliAtelectasis, consolidation and parenchymal fibrosis

BronchiectasisRadiologic FindingsBronchograms have been largely replaced by thin slice CT imagery May show multiple cystsMay show cor pulmonale

Bronchiectasis

BronchiectasisPFT Findings

FVC , FEV1 , FLOWS , VC , FRC , TLC

Bronchiectasis is obstructive in nature when in a non acute phaseWhen in an acute phase, can be restrictive due to bronchial filling and subsequent alveolar atelectasis and collapse

Bronchiectasis Clinical FindingsChronic loose cough exacerbated by change of positionRecurrent infectionsIncreased sputum production: tri-layer sputumTop layer thin, frothyMiddle layer mucopurulentBottom layer opaque, mucopurulent or purulent with mucus plugs, foul-smelling

Bronchiectasis Clinical FindingsHalitosis (bad breath)HemoptysisSevere V/Q abnormalitiesClubbingBS- rhonchi, crackles, diminished

Bronchiolitis

Sick with Bronchiolitis

BronchiolitisAlso called pneumonitisCaused primarily by the respiratory syncytial virus (RSV)RSV is the most common viral respiratory pathogen seen in infancy and early childhood but can be acquired at any ageOutbreaks are usually seasonal in fall and winterMost children under 6 months of age require hospitalization.Spread by aerosol/droplets from coughs and sneezesBronchiolitis BoyBaby with Bronchiolitis and seconday complications

Old Treatment for RSV- RibavirinRibavirin (Virazole) is an anti-viral drug indicated for severe RSV infection. Ribavirin is active against a number of DNA and RNA viruses. It is a member of the nucleoside antimetabolite drugs that interfere with duplication of viral genetic material. Ribavirin is active against influenzas, flaviviruses and agents of many viral hemorrhagic fevers.Side effects:Teratogenic effectsAnemiaRSV - what is it?RSV preventions

----- Meeting Notes (11/12/13 08:11) -----Teratogenic - the causing of embryo or fetal malformations

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BronchiolitisPathophysiology Inflammation and swelling of the peripheral airwaysExcessive airway and nasal secretionsSloughing of necrotic airway epitheliumPartial airway obstruction and alveolar hyperinflationComplete airway obstruction and atelectasisConsolidation

BronchiolitisDiagnosis made by:Obtaining a nasal swab or nasopharyngeal aspirateImmunofluorescense stainingResults available within 2-6 hoursX-ray results show streaky peribronchial opacities associated with air trapping, hyperinflation, and lobar pneumonic consolidation

Bronchiolitis

Clinical ManifestationsExcessive nasal, oral and bronchial secretionsBS: wheezes, crackles, rhonchi, expiratory gruntingIncreased RR, HR, BP, COApneaIntercostal/Substernal retractionsCyanosisNasal flaring

Percussive Vest Therapy

Vest Percussion Therapy

Pulmonary Infections

Pulmonary InfectionsInfections occur more frequently in the respiratory tract than in any other organ, yet this might be anticipated when one considers the heavy and constant environmental exposure to which the lung is subjected by breathing. Although most of these infections are in the upper airways, various types of microbial agents also injure the lung. In the upper airways, viral infections predominate.

Pulmonary InfectionsPneumonia is the commonest type of lung infection and accounts for 8.5-10% of hospitalizations in the US, as well as for 3% of deaths in the population . PNA is the 4th leading cause of death in the population over 75 yrs. of age, and is a common autopsy finding, often representing the "immediate cause of death." 80% of AIDS patients die of respiratory failure and over 60% of these have a pulmonary infection . Pneumonia has a morphologic spectrum which traditionally includes bronchopneumonia, lobar pneumonia, and interstitial pneumonia. In addition, there is a category of infectious granulomas, due primarily to tuberculosis and a variety of fungi. A Patient's Story

Pulmonary InfectionsBacterial infections typically cause lobar or bronchopneumonia both of which are characterized histologically by neutrophilic intra-alveolar exudates. Viral pneumonias generally manifest as interstitial inflammatory processes, while fungal and mycrobacterial infections are granulomatous. Other infectious lesions are an abscess and empyema (infection of the pleura). Atypical pneumonia is a clinical term applied to patients with an acute febrile respiratory presentation and patchy interstitial infiltrates without alveolar exudates. The most common agents are mycoplasma and legionella. Mycoplasma Pneumonia Rap

Pulmonary InfectionsThe lung is normally a sterile environment. Infection results when there is alteration in normal host defense mechanisms or diminution in the general immune status of an individual, or when an immunocompetent individual is exposed to a virulent organism which overwhelms the host defenses

Entry of Microorganisms

Inhalation Most microbes can be inhaled but in most cases this exposure is without untoward effects on the host. Infection by inhalation depends in some instances on the virulence of the organism i.e. tuberculosis, and in other situations on the dosage of exposure i.e. Histoplasma from bat droppings in caves or the Hantavirus from rodent droppings. Bacteria & viruses are small enough to reside on aerosolized droplets that can be inhaled. Mechanisms which trap particles in the airways are more effective against dry materials than against liquid droplets. The Hantavirus DiseasesHoarder's Hanta VirusYosemite Hanta Virus OutbreakA Patient's Story

Entry of MicroorganismsAspiration Aspiration, particularly at night, is a common event and may include small amounts of the bacterial and fungal flora which resides normally in our mouths. Nocturnal or similar aspiration is not usually a problem as our normal defense mechanisms can eliminate these small dosages. Sometimes, however, these microbes lodge in the upper airways and form larger colonies which when aspirated result in infection.

Pulmonary InfectionsPneumonia Inflammatory process of the lung parenchyma, usually infectious in origin6th leading cause of death in the United States and the most common cause of infection-related mortalityClassifications of PneumoniaCommunity Acquired: AcuteTypical: Streptococcus Pneumoniae, Hemophilus Influenzae, Staphylococcus AureusAtypical: Legionella Pneumophila, Chlamydophila Pneumoniae, Mycoplasma Pneumoniae, Viruses

Streptococcus PneumoniaeGram-positive, A significant human pathogenic bacterium, S. pneumoniae was recognized as a major cause of pneumonia in the late 19th century.The organism causes many types of pneumococcal infections other than pneumonia. These invasive pneumococcal diseases include acute sinusitis, otitis media, meningitis, bacteremia, sepsis, osteomyelitis, septic arthritis, endocarditis, peritonitis, pericarditis, cellulitis, and brain abscessS. pneumoniae is one of the most common causes of bacterial meningitis

Streptococcus PneumoniaeA vaccine against Streptococcus pneumoniae exists, recommended for the elderly or those with chronic lung disease.S. pneumoniae is part of the normal upper respiratory tract flora, but, as with many natural flora, it can become pathogenic under the right conditions (e.g., if the immune system of the host is suppressed). Invasins, such as pneumolysin, an antiphagocytic capsule, various adhesins and immunogenic cell wall components are all major virulence factors.

Hemophilus InfluenzaeGram-negative, rod-shaped bacterium first described in 1892 during an influenza pandemic. it is generally aerobic, but can grow as a facultative anaerobeH. influenzae was mistakenly considered to be the cause of influenza until 1933, when the viral etiology of the flu became apparent. Still, H. influenzae is responsible for a wide range of clinical diseases;A Patient's Story

Hemophilus InfluenzaeMost strains of H. influenzae are opportunistic pathogens; that is, they usually live in their host without causing disease, but cause problems only when other factors (such as a viral infection, reduced immune function or chronically inflamed tissues, e.g. from allergies) create an opportunity.In infants and young children, H. influenzae type b (Hib) causes bacteremia, pneumonia, and acute bacterial meningitis AND EpiglotttisDue to routine use of the Hib conjugate vaccine the incidence of invasive Hib disease has declined

Staphylococcus AureusGram-positive coccal bacterium. It is frequently found as part of the normal skin flora on the skin and nasal passages. It is estimated that 20% of the human population are long-term carriers of S. aureus. S. aureus is the most common species of staphylococci to cause Staph infections. The reasons S. aureus is a successful pathogen are a combination of bacterial immuno-evasive strategies. One of these strategies is the production of carotenoid pigment staphyloxanthin which is responsible for the characteristic golden color of S. aureus colonies. This pigment acts as a virulence factor, primarily being a bacterial antioxidant which helps the microbe evade the hosts immune system in the form of reactive oxygen species which the host uses to kill pathogens

Staphylococcus AureusS. aureus can cause a range of illnesses from minor skin infections, such as pimples, impetigo, boils (furuncles), cellulitis folliculitis, carbuncles, scalded skin syndrome, and abscesses; to life-threatening diseases such as pneumonia, meningitis, osteomyelitis, endocarditis, toxic shock syndrome (TSS), bacteremia, and sepsis. It is still one of the five most common causes of nosocomial infections, often causing postsurgical wound infections. Each year, some 500,000 patients in American hospitals contract a staphylococcal infection.Methicillin-resistant S. aureus, abbreviated MRSA and often pronounced "mer-sa" is one of a number of greatly-feared strains of S. aureus which have become resistant to most antibiotics. MapPimple/BoilMeningitis - Meningoccal

Staphylococcus AureusMRSA strains are most often found associated with institutions such as hospitals, but are becoming increasingly prevalent in community-acquired infections. The treatment of choice for S. aureus infection is Penicillin; in most countries, though, Penicillin resistance is extremely common, and first-line therapy is most commonly a penicillinase-resistant -lactam antibiotic (for example, Oxacillin or Fucloxacillin). Combination therapy with Gentamicin may be used to treat serious infections, such as endocarditis, but its use is controversial because of the high risk of damage to the kidneys. The duration of treatment depends on the site of infection and on severity.

Legionella PneumophilaAerobic, non-spore forming, Gram-negative bacterium the primary human pathogenic bacterium in this group and is the causative agent of Legionellosis or Legionnaires' disease.In humans, L. pneumophila invades and replicates in macrophages. The internalization of the bacteria can be enhanced by the presence of antibody and complement, but is not absolutely required. A pseudopod coils around the bacterium in this unique form of phagocytosisPrimary source of infection = water supplyAzithromycin or Moxifloxacin are the standard treatment

Chlamydophila PneumoniaeC. pneumoniae is a common cause of pneumonia around the world. C. pneumoniae is typically acquired by otherwise healthy people and is a form of community-acquired pneumonia. Because treatment and diagnosis are different from historically recognized causes such as Streptococcus pneumoniae, pneumonia caused by C. pneumoniae is categorized as an "atypical pneumonia.This atypical bacterium commonly causes pharyngitis, bronchitis and atypical pneumonia

Mycoplasma Pneumoniaethe causative agent of human primary atypical pneumonia (PAP) or "walking pneumonia.Mycoplasma pneumoniae is a very small bacteriumAntibiotics with activity against these organisms include certain macrolides (Erythromycin, Azithromycin, Clarithromycin), fluoroquinolones and their derivatives (e.g., Ciprofloxacin, Levofloxacin), and Tetracyclines (e.g., Doxycycline)

Viral PneumoniaViral pneumonia is a pneumonia caused by a virusViruses are one of the two major causes of pneumonia, the other being bacteria; less common causes are fungi and parasites. Viruses are the most common cause of pneumonia in children, while in adults bacteria are a more common cause.Symptoms of viral pneumonia include fever, non-productive cough, runny nose, and systemic symptoms (e.g. myalgia, headache). Different viruses cause different symptoms.

Viral PneumoniaCommon causes of viral pneumonia are:Influenza virus A and BRespiratory syncytial virus (RSV)Human parainfluenza viruses (in children)Rarer viruses that commonly result in pneumonia include:Adenoviruses (in military recruits)MetapneumovirusSevere acute respiratory syndrome virus (SARS, coronavirus) Viruses that primarily cause other diseases, but sometimes cause pneumonia include:Herpes simplex virus (HSV), mainly in newbornsVaricella-zoster virus (VZV) chickenpox, shinglesMeasles virusRubella virusCytomegalovirus (CMV), mainly in people with immune system problems

PneumoniaSixth leading cause of death in the U.S.3 million suffer each year40,000 die each year5 million die each year worldwideCauses includeBacteriaVirusesFungiTuberculosisAnaerobic organismsAspirationInhalation of irritating chemicals

PneumoniaPneumonia or pneumonitis with consolidation is the result of an inflammatory process that primarily affects the gas exchange area of the lung.In response to the inflammation, blood serum and some RBCs from the adjacent capillaries pour into the alveoliLeukocytes move into the infected area to engulf and kill the invading bacteriaIncreased numbers of macrophages appear to remove cellular and bacterial debrisIf all this material fills the alveoli, they are said to be consolidated

PneumoniaPathologic and structural changes associated with pneumonia are:Inflammation of the alveoliAlveolar consolidationAtelectasisPrimarily obstructive in nature

Pneumonia Etiology Inhalation of aerosolized infectious particles aerosol particles generated by coughingAspiration of organisms colonizing the oropharynxOccurs in all individuals, especially during sleepImpairment of the gag reflex allows large volume aspirationDirect inoculation of organisms into the lower airway suction catheters, ET tubes

Pneumonia Etiology Spread of infection to the lungs from adjacent structuresInfrequent source of infectionLiver abscessesSpread of infection to the lungs through the bloodHematogenous dissemination (septic spread)Right-sided bacterial endocarditis

Pneumonia Etiology Reactivation of latent infection, usually resulting from immunosuppression but may occur spontaneouslyThere are four stages of progression in pneumonia:Inflammatory StageRed hepatization stageGrey hepatization stageResolution stage

PneumoniaInflammatory StageInflammatory pulmonary edemaEngorgement of the pulmonary capillariesExudation of serous fluidThis stage is localized to the areas of infection

PneumoniaRed Hepatization StageOnset 24 to 48 Hours Post InfectionAlveolar spaces filled with coagulated exudateFibrinRed blood cellsPolymorphonuclear leukocytesBacteriaRed liver-like appearance of lung tissue

PneumoniaGray Hepatization StageOccurs 4 to 5 days post infectionAlveolar spaces filled with many polymorphonuclear leukocytes and few red blood cellsYellow-gray appearance of lung tissue

PneumoniaResolution StageHealing stageExudate liquefied by enzymes of leukocytesPhagocytes reabsorb the liquidAreas of atelectasis begin to re-inflate

PneumoniaTypes of pneumoniaLobar pneumonia: affects a large and continuous area of the lobe of a lung Bronchial pneumonia: the acute inflammation of the walls of the bronchioles. It is a type of pneumonia characterized by multiple foci of isolated, acute consolidation, affecting one or more pulmonary lobules.

PneumoniaClassification of PneumoniaCommunity acquired: acute and chronic Acute: rapid onset of symptomsChronic: slower onset with gradually escalating symptomsHealth care associated pneumonia (HCAP) [previously known as nosocomial infections]Defined as pneumonia occurring in any pt. hospitalized for 2 or more days in the past 90 days in an acute care setting or who, in the past 30 days resided in a LTC or SNF

Pulmonary InfectionsClassifications of PneumoniaVentilator associated pneumonia (VAP)A lower respiratory tract infection that develops more than 48 72 hrs after endotracheal intubation.VAP Busters

PneumoniaCausative agentsGram positive organismsGram negative organismsAtypical organismsAnaerobic bacterial infectionsViral causesOther causes

PneumoniaGram Positive BacteriaStreptococcus pneumoniaeAccounts for 80% of all bacterial pneumoniasFound singly, in pairs, and in short chainsTransmitted by aerosol via cough or sneezeGenerally an acute community acquired organismSputum is usually yellow in color

PneumoniaGram Positive Bacteria (cont)Clostridium difficile (C-diff)Anaerobic spore-forming organisms of drumstick or spindle shapeHospital acquired in patients on antibiotic therapyReplaces normal flora causing severe gastric instability and diarrhea mimicking flu and colitisFast becoming antibiotic resistantHands MUST be washed with soap and water before and after entering patient room

PneumoniaGram Positive Bacteria (cont)Staphylococcus aureusResponsible for Staph infections in humansFound singly, in pairs and in irregular clustersTransmitted by aerosol from a cough or sneeze and via fomitesCommon cause of hospital acquired pneumonia and is becoming extremely resistant to antibiotics thus the abbreviation: MDRSA multiple drug-resistant S. AureusSputum is usually yellow in color and foul smelling

PneumoniaGram Negative BacteriaRod shaped BacilliHaemophilus influenzaeCommon pharyngeal organismInfections most often seen in children between 1 month to 6 yrs of ageAlmost always the cause of acute epiglotitisUsually community acquiredTransmitted via aerosol, contact, fomitesSensitive to cold and does not survive longPicmonic EpiglotitisClinical Symptoms - Stridor,Wheezing and Croup CoughEpiglotitis Explained and Illustrated

PneumoniaGram Negative Bacteria (cont)Klebsiella pneumoniaeAssociated with lobar pneumoniaFound singly, pairs and chainsA normal inhabitant of the GI tractTransmitted by aerosol or fomites especially the hands of healthcare workersUsually a hospital acquired infectionMortality is high because septicemia is a frequent complication

PneumoniaGram Negative Bacteria (cont)Pseudomonas aeruginosaWater loving organismLeading cause of hospital acquired pneumoniaNormally colonizes in the GI tractFrequently found in burns, the respiratory tract of intubated or trached respiratory patients, catheters, respiratory therapy equipmentTransmitted via aerosol or contact with fomitesSputum infected is usually sweet smelling and green

PneumoniaGram Negative Bacteria (cont)Escherichia coli or E.coliNormal GI inhabitantUsually hospital acquired pneumonia

Moraxella catarrhalisNaturally inhabits the pharynxThird most common cause of acute exacerbation of chronic bronchitisUsually hospital acquired

PneumoniaGram Negative Bacteria (cont)Serratia SpeciesVery water loving speciesUsually hospital acquiredLives well on fomites, under sinks, rampant spread in respiratory equipment

Multi Drug Resistant Infections

PneumoniaAtypical OrganismsMycoplasma pneumoniaeCommon cause of mild pneumonia (walking pneumonia)Smaller than bacteria but larger than virusesDescribed as Primary Atypical Pneumonia because the organism escapes ID by standard bacteriologic testsMost frequently seen in people younger than 40Spreads easily where people congregateUsually community acquired

PneumoniaAtypical Organisms (cont)Legionella pneumophilaDiscovered in 1976 during an outbreak of severe pneumonia-like disease at an American Legion conventionGram negative bacillusTransmitted via aerosolThought to have colonized in the AC units of the convention hallCommunity acquired

PneumoniaViral CausesInfluenza VirusSeveral subtypes in which A and B are the most common causes of viral respiratory tract infectionsCommonly occur in epidemicsChildren, young adults and the elderly are most at riskTransmitted via aerosol Survives well in conditions of low moisture and humidityFound also in swine, horses and birds

PneumoniaViral Causes (cont)Respiratory Syncytial Virus (RSV)Member of the paramyxovirus group along with parainfluenza, mumps and rubella virusesMost often seen in children under the age of 6 Transmitted via aerosol and direct contactParainfluenza VirusMember of the paramyxovirus groupType 1 is considered a croup type virus seen in the youngType 2 and 3 present as a severe type of infectionTransmitted via aerosol and direct contact

PneumoniaViral Causes (cont)AdenovirusesMore than 30 subgroupsTransmitted by aerosol Generally seasonal outbreaksCommunity acquired

PneumoniaViral Causes (cont)Severe Acute Respiratory Syndrome (SARS)First reported in China in 2002Newly recognized CoronavirusTransmitted via droplet and aerosol and possibly contaminated objectsIncubation is 2-7 days10-20% require mechanical ventilationCommunity acquired

PneumoniaOther CausesAspiration PneumonitisCaused by aspiration of stomach contentsMajor cause of anaerobic lung infectionsMay progress into ARDSVaricella (chickenpox)Rubella (Measles)RickettsiaeIntracellular parasitesMost well known: Rocky Mountain Spotted Fever

PneumoniaOther CausesYeast pneumonias occur, some of the pathogens include:Candida albicans, Cryptococcus neoformansAspergillus

Fungal InfectionsMost fungi are aerobes thus making lungs prime targetsFungal pathogens include:Histoplasma capsulatumCoccidioides immitisBlastomyces dermatitidis

Tuberculosis

Tuberculosis TodayCDC - TB statistics

Tuberculosis

TB is a chronic bacterial infection that primarily affects the lungs but can involve almost any part of the body

It is one of the oldest diseases known to man and remains one of the most widespread diseases in the world. Chapter 1 - TB

Called consumption, Captain of the men of death and the White plague

10 15 million infected in the U.S.

17,000 new infections per year

WHO estimates that between the years 2000 and 2020 35 million people worldwide will die from TBChapter 2 - TB

TuberculosisCaused by the Mycobacterium tuberculosis organismTransmission from person to person by inhalation of organisms suspended in aerosolized drops of saliva, respiratory secretions, or other fluids

TuberculosisPathophysiologyHighly aerobic organismMultiplies more rapidly in the presence of higher partial pressures of oxygen, especially in lung apicesPrimary TB follows the patients first exposure to the organismUpon inhalation, the bacterium is implanted into the alveoli and begin to multiplyThe initial inflammation causes an influx of macrophages and leukocytes which engulf but do not kill the organism

TuberculosisPathophysiologyThis causes the pulmonary capillary bed to dilate, the interstitium to fill with fluid, and the alveolar epithelium to swell from the edemaThe alveoli become consolidated and at this point the TB skin test becomes positiveIn approx. 2-10 weeks, the lung tissue surrounding the infection slowly produces a protective cell wall around the infection called a tubercle or granuloma

TuberculosisPathophysiologyAfter the formation of the tubercle, the center of the mass breaks down and fills with necrotic tissue. At this point the tubercle is called a caseous lesion or caseous granulomaAs the infection becomes controlled by the immune system or medication, fibrosis and calcification of the lung parenchyma replaces the tubercle.As a result of the fibrosis and calcification, the lung retracts, becomes scarred, and can cause dilation of the bronchi and bronchiectasisChapter 3 - TB

TuberculosisPost primary tuberculosisAlso called secondary or reinfection TBA term used to describe the reactivation of TB months or even years after the initial infection has been controlledTubercle bacilli can remain dormant for decadesAt any time, TB can reactivate; especially in patients with weakened immunity

TuberculosisIf the infection is uncontrolled, cavitation of the tubercle developsIn severe cases a deep tuberculous cavity may rupture and allow air and infected material to flow into the pleural space or the tracheobronchial treePneumothoracies and pleural disease are common complications of TB

Tuberculosis

Granuloma

TuberculosisDiagnostic Testing:CXR may show cavitation or noduleIntradermal (mantoux) skin testing which contains a purified protein derivative (PPD) of the bacillus. An induration of 10mm is positiveAcid-fast stain with sputum culture

TuberculosisRadiologic findingsIncreased opacityCavity formationCalcification & fibrosisPleural effusions

TuberculosisClinical FindingsFatigueFeverNight sweatsWeight lossChronic coughSputum production/hemoptiysis

TuberculosisClinical FindingsAuscultationCracklesWheezesBronchial breath sounds

Tuberculosis/TreatmentKeep isolated in a AIRBORN ISOLATION room, (negative pressure room)The goal of treatment is to cure the infection with drugs that fight the TB bacteria. Treatment of active pulmonary TB will always involve a combination of many drugs (usually four drugs). All of the drugs are continued until lab tests show which medicines work best.The most commonly used drugs include:IsoniazidRifampinPyrazinamideEthambutolOther drugs that may be used to treat TB include:AmikacinEthionamideMoxifloxacinPara-aminosalicylic acidStreptomycinChapter 4 - TB

Restrictive Diseases

AscitesNo explanation needed

Restrictive DiseasesRestrictive diseases generally:Causes a decrease in lung complianceDecrease in lung volumesCan be caused by any alveolar filling lung defectCan be intrinsic or extrinsic

PneumothoraxPresence of air or gas in the pleural space of the thorax creating positive pressure within the pleura

This gas gains entrance into the pleural space in 3 ways:Rupture of bronchus or alveoliClosed PneumothoraxPenetration of chest wallOpen PneumothoraxEsophageal fistula/perfor