Showing posts with label Pulmonology. Show all posts
Showing posts with label Pulmonology. Show all posts

07 February 2012

Acute Respiratory Failure Ppts



Acute Hypoxemic Respiratory Failure: Respiratory failure is nearly any condition that affects breathing function or the lungs themselves and can result in failure of the lungs to function properly.

Acute Respiratory Failure
by Cindy Kin
Acute%20Resp%20Failure.ppt

Respiratory  Failure
by Dr.  Sat Sharma
critical_care/165137-165138-167981-168117.ppt

Acute  Respiratory Distress Syndrome: Just the FACTTs
by Wayne  Strauss MD PhD
https://www.eventbuilder.com/files/providence/60576/File/strauss-10-15-08.ppt

Noninvasive  mechanical ventilation in hypoxemic respiratory  failure
by Akın  KAYA
1506/LDMC6BTMRHSIYLO.ppt

Hypercapnic  Respiratory Failure
by Erik  van Lunteren, M.D.
Hypercapnic%20Respiratory%20Failure.ppt

Acute  Respiratory Failure
by Yoon  Jung Oh,M.D.
http://wwwold.ajou.ac.kr/~pulmo/Acute%20Respiratory%20Failure.ppt

Respiratory  Failure
http://basic.shsmu.edu.cn/jpkc/rjnk/3/ppt/32.ppt

Positioning in  ARDS
By Lindsay Peña
Trauma_Intranet/Trauma_Conference

Focus  on Respiratory Failure
RespiratoryFailure.ppt

Key messages from the British Thoracic Society Emergency Oxygen Guideline
Clinical%20Information/Emergency%20Oxygen

Early  Detection and Interventions in Respiratory  Failure
by Dr  Nigam Prakash Narain
Conference_abstracts/

The Role  of Steroids in ARDS A  review of the evidence
Alex%20Yartsev%20-%20The%20Role%20of%20Steroids%20in%20ARDS.ppt

Acute  Respiratory Failure: Recognition and Early Intervention
by Carrie  Samiec, D.O.
http://2011rapidresponse.files.wordpress.com/2011/02/acuterespfailure.ppt

Pulmonary Pathophysiology
http://clt.astate.edu/mgilmore/pathophysiology/Pulmonary%20Pathophysiology%202.ppt

Review of Pathophysiology and Ventilator Management
Review%20of%20ventilator%20management.ppt

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29 January 2012

Pleuritis Ppts and latest 20 articles




Tuberculous Pleural Effusion
by Maggie Davis  Hovda, MD
http://www.med.unc.edu/medicine/web/8.11.08%20Davis-Hovda.%20TB%20pleurisy.ppt

Drug  Induced Pleural Effusions
by Andrea  Honeycutt
http://www.med.unc.edu/medicine/web/4.16.08%20Honeycutt.ppt

Pleural  Effusions 
by Andrew  Smitherman
https://medicine.med.unc.edu/education/internal-medicine-residency-program/files/ppt/5.27.09%20Smitherman.Pleural%20effusions.ppt

Contagious Caprine Pleuropneumonia
http://www.cfsph.iastate.edu/DiseaseInfo/ppt/ContagiousCaprinePleuropneumonia.ppt

Systemic  Lupus Erythematosus (SLE)
by Heidi  Roppelt, MD
https://cbase.som.sunysb.edu/cbase/faculty/uploads/SLE%20CTD%20course%202010.ppt

Thorax &  Lungs
by Dr. Gregory  Casey
http://virtualhumanembryo.lsuhsc.edu/hs2412/Lectures/Greg%27slectures/LecIII_Thorax_and_LungsFall2011_post_.ppt

Diseases of the Pleura
by J. Tavares,MD,FACP,FCCP,FAASM
http://www.medicine.nevada.edu/residency/lasvegas/internalmed/documents/Diseasesofthepleura.ppt

Systemic Lupus Erythematosus
http://mailer.fsu.edu/~pgilmer/glp_website/pptfall2004/ppt2004gr4.ppt


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19 November 2011

Acute Respiratory Failure, Respiratory Failure Vent Support, Respiratory Failure and ARDS ppts



Acute respiratory failure - A physiologic approach
By: Robert Paine, M.D
http://www.med.umich.edu/lrc/students/m2/respiratory/resources/Paine-AcuteRespiratoryFailureSlides.ppt

Acute Respiratory Failure
By: Cindy Kin
http://scalpel.stanford.edu/ICU/presentations/Acute%20Resp%20Failure.ppt

Critical Care Board Review
By: Sachin B. Patel, M.D.
http://www.med.unc.edu/medicine/web/6.9.08%20Patel%20Crit%20Care%20Board%20Rev

Respiratory Failure Vent Support
http://faculty.msugf.edu/caykob/Documents/RC%20171..ENT%20SUPPORT.ppt

Respiratory Failure and ARDS
By: Nancy Jenkins
http://www.austincc.edu/nursmods/cec/cec_lev4/rnsg_2432/documents/RESP09.PPT

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31 August 2011

Lung Examination Presentations



Lung Examination
by Arcot J. Chandrasekhar, M.D.
http://www.meddean.luc.edu/lumen/MedEd/MEDICINE/PULMONAR/pdself/lungabnormal.ppt

Pneumonia
by Ken Lyn-Kew, M.D.
http://www9.georgetown.edu/faculty/wheltosa/Pneumonia.ppt

Lung Cancer Screening
by Caryn Gee Morse, MD
http://intmedweb.wfubmc.edu/download/lungca.ppt

Lung Abscess
http://wwwappskc.lonestar.edu/programs/respcare/Missy%27s%20website/Cardiopulmonary%20Disease/Chapter_016.ppt

Physical Examination of the Chest
http://occonline.occ.cccd.edu/online/dfarrell/Physical%20Examination.ppt

Introduction to Respiratory Therapy
http://faculty.mdc.edu/pslocum/RET%201024%20Mod%204.2%20Assessment%20-%20Inspection.ppt

Interstitial Lung Diseases
By Joaquim S.Tavares, MD, FCCP, FAASM
http://www.medicine.nevada.edu/residency/lasvegas/internalmed/documents/pulmonaryboardreviewworkshop-1.ppt

Pediatric Pneumonia
by Pisespong Patamasucon, M.D
http://www.medicine.nevada.edu/residency/lasvegas/pediatrics/documents/PediatricPneumonia.Sept08version.ppt

Treatment of Langerhans Cell Histiocytosis
by Tanya Wildes
http://hematology.wustl.edu/conferences/presentations/Wildes20050923.ppt

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13 February 2010

Lower Respiratory Tract Infections



Lower Respiratory Tract Infections
By: Divya Ahuja, M.D.

Lower respiratory infections: anatomic classification
* Tracheitis; bronchitis; tracheobronchitis
* Bronchiolitis
* Bronchopneumonia
* Segmental pneumonia
* Lobar pneumonia
* Interstitial pneumonia

Case #1
* 40-year-old man
* no underlying lung disease
* 7-day history of mild shortness of breath with exertion, and a productive cough.
* Temperature = 37°C, pulse 84 beats/min, and his respiratory rate 17 breaths per minute.
* no rales are heard; scattered wheezes are heard in the lung bases.

Acute bronchitis (“chest cold”)
* Usually of viral etiology(influenza, rhinovirus, parainfluenza, RSV, human metapneumovirus)
* A common cause for overuse of antibiotics
* Bacteria implicated are
o Bordetella pertussis (whooping cough)
o Mycoplasma pneumoniae
o Chlamydia pneumoniae

Acute bronchitis
* Similar to URIs but more prolonged
* Cough persists > 5 days (upto 40 days)
* 40% will have reduction in pulmonary function
* Main differential includes
o Asthma/ bronchiolitis
o Bronchiectasis
o Chronic bronchitis (cough and sputum for 3 months during 2 years

Acute Bronchitis

* Cough in the absence of fever, tachycardia, and tachypnea suggests bronchitis, rather than pneumonia
* Antimicrobial agents are not recommended in most cases of acute bronchitis
* Antimicrobial therapy is indicated when a treatable pathogen is identified (influenza, Bordetella pertussis )

Acute exacerbations of chronic bronchitis

* Chronic bronchitis is associated with cigarette smoking and COPD
* Extent to which specific bacterial pathogens explain exacerbations is controversial.
* However, repeated bacterial infections (especially H. influenzae) contribute to deterioration of lung function.

Case # 2

* 54 year male, chronic cough x 1 year. no hemoptysis. Denies fevers, shakes, chills. No sick contacts

Bronchiectasis
* Abnormal dilatation of bronchi with chronic productive cough.
* Can be clue to cystic fibrosis in younger patients (associated with S. aureus and Pseudomonas species)
* Uncommon associations: immunodeficiency disorders, dyskinetic cilia syndrome

Case # 3
* 54 year old male
* Flu like illness 2 weeks ago
* 5 day history of chills, fever, difficulty breathing, right sided pleuritic chest pain, cough and yellow sputum

Pneumonia
* 6th leading cause of death in U.S.A.
* About 3 million cases per year; > 500,000 hospital admissions
* About 50% of cases and the majority of deaths are due to bacteria
* Precise diagnosis is usually desirable but difficult to obtain

Acute pneumonia

* History
* Symptoms-cough, sputum, fever, malaise
* Clinical setting-community acquired, nosocomial
* Defects in host defense- HIV, neutropenia
* Possible exposures

Organisms in community acquired pneumonia

Organisms:
S pneumoniae
H influenzae
o P aeruginosa
o S aureus
o Atypicals
+ Chlamydia, Legionella
+ Mycoplasma, Bordetella

Pneumonia (2)
* Streptococcus pneumoniae the most common cause of community-acquired pneumonia requiring hospitalization
* Haemophilus influenzae and Moraxella catarrhalis are increasing in frequency
* Legionella species and Chlamydia pneumoniae have emerged
* Pneumocystis carinii (HIV disease)

Pneumonia: pathogenesis
* Endogenous vs. exogenous (inhalation)
* Bronchogenous vs. lymphohematogenous
* “Pulmonary clearance”: mucociliary blanket, alveolar macrophages
* Factors that impair pulmonary clearance: viral URI; smoking; alcohol; uremia; bronchial obstruction; 100% oxygen; others

“Typical” versus “atypical” pneumonia

* “Typical” (virulent bacteria): abrupt onset; productive cough with purulent sputum; pleuritic chest pain; impressive physical findings; leukocytosis or leukopenia
* “Atypical” (viral, Mycoplasma pneumoniae, others): gradual onset, nonproductive cough; substernal chest pain; unimpressive physical exam; white blood count normal

Typical versus atypical pneumonia

Classic pneumococcal pneumonia

* Antecedent upper respiratory infection
* Sudden onset with single violent chill, then fever
* Pleuritic chest pain
* Signs of lobar consolidation on exam
* If untreated, terminates gradually by “lysis” or suddenly by “crisis”

Atypical pneumococcal pneumonia

* Caught early: signs of consolidation may be absent
* Elderly: fever, classic history may be absent
* COPD: CXR and physical findings are distorted
* Ethanolism: blunted history; prostration, leukopenia
* Epilepsy: lack of history; fever and tachycardia may be attributed to seizures; anaerobes may co-exist
* Recurrent pneumonia: In same area, suggests obstruction or bronchiectasis

Some current problems with pneumococcal disease

* Failure of antibiotic therapy to improve survival during first 3 days
* Vaccine efficacy and distribution
* Resistance to penicillin G
* Overwhelming sepsis in asplenic persons
* Need for developing better diagnostic techniques

Group A streptococcal pneumonia

* Rare, except during influenza epidemics
* Large empyema (“pus in the chest”) is characteristic

Hemophilus influenzae pneumonia

* 2% to 18% of community-acquired pneumonias;
* Predisposition: underlying lung disease, alcoholism, recent URI, advanced age
* Often a patchy segmental pneumonia or bronchopneumonia
* Virtually-diagnostic Gram’s stain: small, pleomorphic gram-negative coccobacilli

Moraxella catarrhalis pneumonia

* AKA: Neisseria catarrhalis; Branhamella catarrhalis
* A large gram-negative diplococcus
* Causes pneumonia and bronchitis especially in persons with chronic lung disease
* Often a patchy bronchopneumonia

Mycoplasma pneumoniae pneumonia

* The classic “primary atypical pneumonia”
* Typically occurs in younger adults, often the parents of young children
* Subtle presentation
* Favors lower lobes
* Pleural effusion may occur (up to 20%)

Some nonrespiratory manifestations of Mycoplasma pneumoniae pneumonia

* Myringitis (sometimes bullous)
* Hemolytic anemia
* Arthritis, arthralgias, myalgias
* Pericarditis, myocarditis
* Hepatitis (mild)
* Erythema multiforme, other rashes
* Meningitis, meningoencephalitis, neuropathy

Chlamydia pneumoniae pneumonia

* Accounts for <5% of community-acquired pneumonias
* C. pneumoniae more commonly causes pharyngitis and hoarseness
* Bronchitis is often insidious
* Pneumonia usually mild and localized but difficult to eradicate

Legionella pneumophila pneumonia

* Up to 23% of community-acquired pneumonias but with wide geographic distribution
* L. pneumophila is not part of the normal flora; a true inhalation disorder
* CXR: patchy or nodular infiltrates that may progress rapidly; up to 50% are bilateral

Legionella pneumophila pneumonia (2)

* Relative bradycardia in 65%
* Neurologic findings in 26%
* Gram’s stain may show purulence without a predominant microorganism
* Laboratory: may have hyponatremia; elevations of AST (SGOT), alkaline phosphatase, and bilirubin; proteinuria, hematuria, and renal failure

Treatment

* S. pneumoniae resistance is increasing
* Options are cephalosporins, amox/clvulanic acid, macrolides, doxycycline, a respiratory fluoroquinolone
* All atypicals are covered by the macrolides , doxycycline and the fuoroquinolones
* Judge the severity to see if outpatient treatment will suffice

Aspiration (“mouth flora”) pneumonia

* usually presents as a subacute illness in patients with some combination of alcoholism, malnutrition, homelessness, and poor dentition
* sputum often has foul odor
* Necrotizing pneumonia; lung abscess(es) with air-fluid levels; empyema

Pneumonia: some clues
* Tularemia: rabbits and hares; ticks and fleas; inhalation (e.g., after mowing over carcasses)
* Psittacosis: birds
* Plague: ground squirrels, chipmunks, rabbits, prairie dogs, rats
* Legionnaire’s disease: contaminated aerosols (air coolers; hospital water supplies)
* Histoplasmosis: dust from soil enriched with bird or bat droppings; Mississippi and Ohio River valleys
* Coccidiodomycosis: southern California (esp.. San Joachin Valley); southwest Texas, Arizona, N Mexico
* Pneumocystis carinii: HIV risk factors
* Relative bradycardia: viral infection; Mycoplasma pneumoniae; Psittacosis; Tularemia; Legionella
* Q fever (Coxiella burnetii): goats, cattle, sheep
* Meliodosis: travel to S.E. Asia, East Indies, Australia, Guam, South or Central America
* Brucellosis: cattle; goats; pigs; abattoir works and veterinarians
* Anthrax: cattle, swine, horses; goat hair, wool, or hides

Pneumococcal pneumonia: Predisposing factors
* Sickle cell disease
* Asplenia
* IgG disorders: agammaglobulinemia, myeloma, chronic lymphocytic leukemia
* Nephrotic syndrome
* Cirrhosis
* Alcoholism

Case # 4
* RA 57 year Caucasian male
* Cough , dyspnea, diarrhea for weeks
* No response to cephalexin
* CT sinuses - normal
* Progressive malaise and presented to ER
* pO2 on 100% NRB- 90, Creatinine 1.8, WBC: 12
* CXR-read as normal, HIV positive

Pneumonia in AIDS patients
* When in doubt, respiratory isolation for Tb
* S. pneumoniae is the number 1 cause
* Investigations
o Obtain sputum for gram stain and culture
o Other serology and antigen testing as indicated (histoplasma, cryptococcus, PCP, coccidio, etc.
o AFB stain if indicated(sensitivity with 3 specimens is about 60%)

PCP: Diagnosis (Imaging)
Chest x ray: PCP pneumonia with bilateral, diffuse granular opacities.
Credit: L, Huang, MD, HIV InSite

Chest x ray: PCP pneumonia with bilateral perihilar opacities, interstitial prominence, hyperlucent cystic lesions. Credit: HIV Web Study, www.hivwebstudy. org, © 2006 University of Washington

PCP
* PCP is a SUBACUTE pneumonia, CD4 usually <200
* Dyspnea, dry cough, chest discomfort
* In 30% patients
o CD4 > 200
o CXR normal
* TMP/SMX and steroids if hypoxic

Tuberculosis in HIV patients
* Occurs at any CD4 count
* Primary TB
o Occurs especially in people with advanced HIV infection
o Comprises about 1/3 of TB cases in HIV patients
* Reactivation of latent TB
o More likely in HIV-infected patients
o 7-10% annual risk in HIV-infected patients with positive tuberculin skin test (TST)
+ In HIV uninfected, 5-10% lifetime risk
* Patients with TB have HIV viral loads and faster progression of HIV

Case # 5
* 45 year female
* Intubated in the ICU for 7 days
* Now has worsening fever, leukocytosis and increased oxygen requirement

Nosocomial pneumonia
* Role of oropharyngeal colonization, especially of gram-negative rods (Pseudomonas, acinetobacter, etc.) : by end of one week, 45% of ICU patients are colonized; pneumonia develops in 23% of colonized patients versus 3.3% of non-colonized patients
* Risk factors to colonization: more advanced illness, longer duration in the hospital, antibiotics, intubation, azotemia, underlying pulmonary disease

Case # 6
* 23 year male, acute leukemia and bone marrow transplant
* Is severely neutropenic due to chemotherapy

Cavitary pneumonia
* Tuberculosis
Actinomyces
Nocardia
Klebsiella
Staphylococcus aureus
Anaerobic organisms
* Fungal infection Histoplasmosis
Coccidiomycosis, aspergillus

Complications of pneumonia
* Pleuropulmonary: lung abscess; adult respiratory distress syndrome (ARDS); pleural effusion; empyema; bronchopleural fistula; bronchiectasis; fibrosis; slow resolution
* Extrapulmonary: meningitis; brain abscess; endocarditis; pericarditis; arthritis; osteomyelitis

Lung Abscess
* Lung abscesses are usually caused by mouth flora(viridans strep, anaerobes, etc.)
* They need prolonged courses of antibiotics
* Options are the clindamycin, amox/clavulanic acid, pip/tazo, carbapenems

Pneumonia: Summary
* 6th leading cause of death and most common nosocomial infection causing death
* Precise diagnosis desirable but all-too-often not obtained
* Bronchoalveolar lavage and endobronchial sampling are now standard in nosocomial or difficult to diagnose pneumonia


Lower Respiratory Tract Infections.ppt

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16 July 2009

Chest Trauma



Chest Trauma
by:Kent J. Blanke, D.O., FACOS
Introduction
Thoracic Trauma
Penetrating Chest Injuries
* Majority are stab wounds or gunshot wounds (GSW)
* Lower mortality rates--less likely to include multiorgan injury
* 85% of penetrating chest wounds can be treated with tube thoracostomy and supportive measures
Penetrating Chest Trauma
* Wounds that enter or exit inferior to the nipple or the posterior tip of scapula may perforate the dome of the diaphragm.
* Any penetrating wound such as this should be considered to have an abdominal component until proven otherwise.

Penetrating Chest Trauma: Treatment
* ATLS protocol: A,B,C,D,E’s
* Emergency management
o Needle thoracentesis
o Tube thoracostomy
o Subxiphoid pericardotomy
o Video assisted thoracic surgery (VATS)

Work-up of Penetrating Chest Trauma
* Physical examination
o Look, Listen, Feel
o Contusions, diminished or absent breath sounds, SQ emphysema can readily be found
* CXR- best, least expensive and fastest initial evaluation
* Ultrasound-may soon replace CXR as initial radiographic study in chest trauma
* Angiography- to look for great vessel injuries
* CT Scan: for better evaluation of chest wall and parenchyma
* Transesophogeal Echocardiography

Penetrating Chest Injuries
* Operative intervention required for:
o Massive or persistent bleeding
o Massive air leak
o Tracheobronchial injuries
o Esophageal perforation
o Cardiac or great vessel injuries
o Post-traumatic empyema
* Wounds that enter or exit inferior to the nipple or the posterior tip of scapula may perforate the dome or the diaphragm.
* Any penetrating wound such as this should be considered to have an abdominal component until proven otherwise.

Penetrating Chest Trauma:Indications for Mechanical Ventilation
Intrapulmonary Foreign Bodies
* Bullets, fragments: indications for removal
Intrapulmonary Foreign Bodies
Pulmonary Parenchymal Laceration
High Velocity Missile Injuries
Blunt Chest Trauma
Categories of chest wall injuries
* Open pneumothorax
* Contusion and Hematoma
* Sternal fractures
* Scapular fractures
* Flail chest
* Intercostal vessel injury
Categories of Intra-thoracic Injuries
* Pulmonary
o Pneumothorax, hemothorax
o Pulmonary contusion
o Pulmonary laceration
* Vascular
o Great vessel disruption (Ao dissection, pulmonary vasculature)
* Cardiac
o Blunt Cardiac Injury, Penetrating injury

Work-up of Blunt Chest Trauma
* Physical examination
o Look, Listen, Feel
o Contusions, diminished or absent breath sounds, SQ emphysema can readily be found
* CXR- best, least expensive and fastest initial evaluation
* Ultrasound-may soon replace CXR as initial radiographic study in chest trauma
* Angiography- to look for great vessel injuries
* CT Scan: for better evaluation of chest wall and parenchyma
* Transesophogeal Echocardiography

Categories of chest wall injuries
* Contusion and hematoma

Categories of chest wall injuries
* Open pneumothorax
* Pneumothorax
Operative Intervention for Hemothorax
* As noted previously
* Hemothorax: massive = initial drainage more than 1,000 cc or
* Continuous bleeding of 200 cc/hr for 2 hrs

Fractured Ribs: Chest Wall Trauma
Blunt Cardiac Injury
Categories of chest wall injuries
* Sternal fractures
Categories of chest wall injuries
* Scapular fractures
* Flail chest
Pulmonary Contusion
Intra-thoracic Trauma: Pulmonary Contusion
Intra-thoracic Trauma: Great Vessel and Mediastinal Trauma
* Aorta
* Pulmonary vessels
* Tracheobronchial lacerations
* Esophageal lacerations

Intra-thoracic Trauma: Great Vessel and Mediastinal Trauma—Work-up
* Plain CXR to identify thoracic aorta injuries
* Look for air in the mediastinum
* Persistent airleak should cue into:
o Bronchopulmonary or tracheobronchial injury
* Mediastinitis, tube feedings in chest tube or saliva in chest tube should cue into:
o Esophageal injury
* Bronchoscopy
* Esophagoscopy
* CT
* Serial CXR

Initial CXR of Concern

Indications for Angiography
* Lateral deviation of the NGT in esophagus
* Widened mediastinum (>8cm)
* Loss of visualization of the aortic knob
* Hematoma of the Left cervical pleura (pleural cap)
* Depressed left main stem bronchus
* Rt lateral deviation of the trachea
* Widened mediastinum (>8cm)
* Forward displacement of the trachea on the lateral CXR
* Fx of the 1st or 2nd rib
* Massive chest trauma w/ multiple rib fx
* Fx or dislocation of the thoracic spine
* Major deceleration injury
Complete Aortogram

Chest Trauma.ppt

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Radiographic Findings in Blunt Chest Trauma



Soft Tissue Radiographic Findings in Blunt Chest Trauma
By:Jonathan Yarris MSIV

Trauma
* Trauma is the leading cause of death in patients < 40 years
* 4th leading COD overall
* 80% of trauma is due to blunt mechanisms

Blunt Chest Trauma (BCT)
* Seen in about ½ of blunt trauma cases
* ~20% of trauma deaths attributable to BCT
* Etiology: typically deceleration injury
* Radiographic evaluation should begin immediately after initial trauma team assessment

Approach to Trauma Radiographs
* Initial exclusion of life threatening injuries
* Followed by search for less critical injuries
* Life threatening Injuries:
Pneumothorax
Deep Sulcus Sign
Tension Pneumothorax
Tension PTX
Pulmonary Contusion
Laceration
Laceration with Pneumatocele
Hematoma
Pulmonary hematoma
Pneumatocele
Pulmonary Contusion with pneumatocele
Blunt Cardiac Injury (BCI)
Hemopericardium
Great Vessel Injury
Thoracic Aorta Injury
Intimal Flap with double lumen
Airway Injury
* Tracheobronchial tears are uncommon
* Leads to persistent PTX
* Specific Symptom: persistent PTX after chest tube placement
* Finding: “Fallen Lung Sign”, pneumomediastinum, pneumopericardium, sub cut. Emphysema
* ET Tube balloon inflation >2.8cm implies tracheal rupture
Pneumomediastinum
* Etiology: alveolar, tracheobronchial or esophageal rupture
* Most common cause: alveolar rupture due to sudden increased intra-alveolar pressure (Macklin Effect) with air tracking centrally
* Findings:
o Air outlining mediastinal soft tissues and parietal pleura.
o Continuous diaphragm sign
Pneumomediastinum
Pneumopericardium with tamponade
Esophageal Injury
Other
* Skeletal injuries:
* Diaphragm injuries:

Radiographic Findings in Blunt Chest Trauma.ppt

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Lung Examination: Abnormal



Lung Examination: Abnormal
By:Arcot J. Chandrasekhar, M.D.

Illustrative Pathological problems
* Consolidation
* Atelectasis
* Pleural effusion
* Pneumothorax
* Mass
* Diffuse lung disease

Steps
* General Examination
* Mediastinal position
* Chest expansion
* Lung resonance
* Breath sounds
* Adventitious sounds
* Voice transmission
* Respiratory rate
* Pattern of breathing
* Cyanosis
* Clubbing
* Weight
* Cough
* Hospital setting
* Effort of ventilation
* Shape of thorax

Respiratory Rate
* Bradypnea: rate less than 8 per minute
* Tachypnea: rate greater than 25 per minute

Pattern of Breathing
* Kussmals
* Sleep apnea
* Cheyne strokes
* Pursed lip breathing
* Orthopnoea: Short of breath in supine position, gets some relief by sitting or standing up.

Sleep apnea syndrome
Central Cyanosis
Corpulmonale
Clubbing
Significance: Clubbing Observed In:
* Intrathoracic malignancy: Primary or secondary (lung, pleural, mediastinal)
* Suppurative lung disease: (lung abscess, bronchiectasis, empyema)
* Diffuse interstitial fibrosis: Alveolar capillary block syndrome
* In association with other systemic disorders
Effort of Ventilation
* Person appears uncomfortable. Breathing seems voluntary.
* Accessory muscles are in use, expiratory muscles are active and expiration is not passive any more.
* The degree of negative pleural pressure is high.
* The respiratory rate is increased.

Resting Size and Shape of Thorax
* Barrel chest
* Kyphosis
* Scoliosis
* Pectus excavatum
* Gibbus
Barrel Chest
AP Diameter = Transverse Diameter
Tracheal Position: Mediastinum
Chest Expansion
Percussion: Decreased or Increased Resonance is Abnormal
* Dullness
* Hyper resonance
* Traube's space

Breath Sounds: Diminished or Absent
* Intensity of breath sounds, in general, is a good index of ventilation of the underlying lung.
* Breath sounds are markedly decreased in emphysema.
* Symmetry: If there is asymmetry in intensity, the side where there is decreased intensity is abnormal.
* Any form of pleural or pulmonary disease can give rise to decreased intensity.
* Harsh or increased: If the intensity increases there is more ventilation and vice versa.
* Bronchial breathing anywhere other than over the trachea, right clavicle or right inter-scapular space is abnormal.
* In consolidation, the bronchial breathing is low pitched and sticky and is termed tubular type of bronchial breathing.
* In cavitary disease, it is high pitched and hollow and is called cavernous breathing. You can simulate this sound by blowing over an empty coke bottle.

Bronchial breathing
Rhonchi
Pleural Rub
Crackles
Voice Transmission (tactile fremitus, vocal resonance)
* Asymmetrical voice transmission points to disease on one side.
* Increased:
* Decreased
* Qualitative alteration:
Voice Transmission
Bronchophony
Whispering Pectoroliquy
Normal whisper
Egophony

Lung Examination: Abnormal.ppt

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Thoracic Trauma



Thoracic Trauma

Dave Lloyd, MD
Introduction to Thoracic Injury
* Vital Structures
* 25% of MVC deaths are due to thoracic trauma
* Abdominal injuries are common with chest trauma.
* Prevention Focus

Anatomy and Physiology of the Thorax
* Thoracic Skeleton
* Diaphragm
* Associated Musculature
* Physiology of Respiration
* Trachea, Bronchi & Lungs
* Mediastinum
* Heart
* Contraction Cycle
* Great Vessels
* Esophagus
* Blunt Trauma
* Penetrating Trauma
Pathophysiology of Thoracic Trauma
Injuries Associated with Penetrating Thoracic Trauma
* Closed pneumothorax
* Open pneumothorax (including sucking chest wound)
* Tension pneumothorax
* Pneumomediastinum
* Hemothorax
* Hemopneumothorax
* Laceration of vascular structures
* Tracheobronchial tree lacerations
* Esophageal lacerations
* Penetrating cardiac injuries
* Pericardial tamponade
* Spinal cord injuries
* Diaphragm trauma
* Intra-abdominal penetration with associated organ injury

Pathophysiology of Thoracic Trauma Chest Wall Injuries
* Contusion
* Rib Fractures
* Sternal Fracture & Dislocation
* Flail Chest
* Simple Pneumothorax
* Open Pneumothorax
* Tension Pneumothorax
* Dyspnea
* Progressive ventilation/perfusion mismatch
* Hypoxemia
* Hyperinflation of injured side of chest
* Hyperresonance of injured side of chest
* Diminished then absent breath sounds on injured side
* Cyanosis
* Diaphoresis
* AMS
* JVD
* Hypotension
* Hypovolemia
* Tracheal Shifting
* Hemothorax
* Blunt or penetrating chest trauma
* Shock
* Dull to percussion over injured side
* Pulmonary Contusion
* Myocardial Contusion
* Bruising of chest wall
* Tachycardia and/or irregular rhythm
* Retrosternal pain similar to MI
* Associated injuries
* Chest pain unrelieved by oxygen
* Pericardial Tamponade
* Dyspnea
* Possible cyanosis
* Beck’s Triad
* Weak, thready pulse
* Shock
* Kussmaul’s sign
* Pulsus Paradoxus
* Electrical Alterans
* PEA
* Myocardial Aneurysm or Rupture
* Traumatic Aneurysm or Aortic Rupture
* Other Vascular Injuries
* Traumatic Esophageal Rupture
* Tracheobronchial Injury
* Traumatic Asphyxia
* Scene Size-up
* Initial Assessment
* Rapid Trauma Assessment
* Ongoing Assessment
* Ensure ABC’s
* Anticipate Myocardial Compromise
* Shock Management
* Rib Fractures
* Sternoclavicular Dislocation
* Flail Chest
* Open Pneumothorax
* Tension Pneumothorax
* Hemothorax
* Myocardial Contusion
* Pericardial Tamponade
* Aortic Aneurysm
* Tracheobronchial Injury
* Traumatic Asphyxia

Thoracic Trauma.ppt

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Artificial Airways



Artificial Airways

Definition
* A tube or tube-like device that is inserted through the nose, mouth, or into the trachea to provide an opening for ventilation

Types of Artificial Airways
* Oropharyngeal airways
* Nasopharyngeal tubes
* Orotracheal tubes
* Nasotracheal tubes
* Tracheostomy tubes
* Esophageal obturator airway
* Cricothyroid tubes

Indications for Artificial Airways
* Relief of airway obstruction -guarantees the patency of upper airway regardless of soft tissue obstruction.
* Protecting or maintaining an airway N. have 4 main airway protect. reflexes 1. Pharyngeal reflex - 9th & 10th cranial nerves gag and swallowing
* Reflexes (cont’d) 2.Laryngeal -vagovagal reflex - will cause laryngospasm 3.Tracheal -vagovagal reflex - cough when a foreign body or irritation in trachea 4.Carinal -cough with irritation of carina
* Facilitation of tracheobronchial clearance
- mobilization of secretions from the trachea requires either an adequate cough or direct suctioning of the trachea
* Facilitation of artificial ventilation
- ventilation with a mask should on be used for short periods d/t gastric insufflation

Hazards of Artificial Airways
* Infection d/t bypassing the normal defense mechanisms that prevent bacterial contamination
* Ineffective cough maneuver
* Impaired verbal communication
* Loss of personal dignity

Oropharyngeal Airway
* Device designed for insertion along the tongue until the teeth &/or gingiva limit the insertion
* Lies between the posterior pharynx and the tongue and pushes the tongue forward
* Will activate the gag reflex, should use on unconscious patient
* Correct sizing of airway is imperative

Hazards of Oropharyngeal Airway
* If too small, may not displace tongue or may cause tongue to obstruct airway or may aspirated
* It too large, may cause epiglottis impaction
* Roof of mouth may be lacerated upon insertion
* Aspiration from intact gag reflex

Nasopharyngeal Airway
* Located so that it can provide a clear path for gas flow into the pharynx
* Is a soft rubber catheter
* Can be tolerated by the conscious patient
* Useful for patient with a soft tissue obstruction who have jaw injury or spasm of jaw muscles
* Proper sizing and insertion

Orotracheal Airway
* Used in conditions of, or leading to respiratory failure
* Usually the method of choice in emergencies that do not involve trauma to the mouth or mandible
* Oral route in usually easiest
* Accomplished by using a laryngoscope to directly visualize the trachea

Nasotracheal Airway
* More difficult route than oral
* Requires a longer and more flexible tracheal tube
* Insert through nose by touch and when in oropharynx use larynoscope and forceps (can perform “blind”)
* Usually N. T. tube is better tolerated by patient than oral

Tracheostomy Tube
* Tracheostomy is performed through the anterior tracheal wall either by the open method or percutaneous method
* Performed usually to prevent or treat long-term respiratory failure
* Decreases anatomic deadspace by 50%

Complications and Hazards of Tracheostomies
* Postsurgical bleeding
* Infection
* Mediastinal emphysema
* Pneumothorax
* Subcutaneous emphysema
* Stoma collapse (should not be moved or changed first 36 hours)

Esophageal Obturator Airway (EOA)
* Place in the esophagus to prevent stomach contents from entering the lungs while the patient is being artificially ventilated
* Cuff must be passed beyond carina before inflated
* Inflated cuff with 35 cc air
* Mask must fit tightly to ensure ventilation

Pharyngealtracheal Lumen Airway (PTL)
* Double-lumen airway combining an EOA and an endotracheal tube
* Designed to be inserted blindly
* Has an oropharyngeal cuff and a cuff that can seal off either the trachea or the esophagus

Other Specialized ET Tubes
* Rae Tube, directs the airway connection away from the surgical field
* Endotrol Tube, controls the distal tip for intubation
* Hi-Lo Jet Tube, for high freq. jet ventilation
* Laser Flex Tube, reflects a diffused beam if comes in contact with tube
* Endobronchial Tubes

Artificial Airways.ppt

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Thoracic Trauma



Thoracic Trauma
By:EMS Professions
Temple College

Thoracic Trauma
* Second leading cause of trauma deaths after head injury
* Cause of about 10-20% of all trauma deaths
* Many deaths due to thoracic trauma are preventable
* Prevention Strategies
* Mechanisms of Injury
* Anatomical Injuries


What structures may be involved with each injury?
* Often result in:
o Hypoxia
o Hypercarbia
o Acidosis
* Ventilation & Respiration Review
* General Pathophysiology
* Initial exam directed toward life threatening:
o Injuries
o Conditions
* Assessment Findings

Specific Injuries
Rib Fracture
* Management
Sternal Fracture
* Management
Flail Chest
* Management
Simple Pneumothorax
* Management
Open Pneumothorax
* Management
Tension Pneumothorax
* Management
Hemothorax
* Management
Pulmonary Contusion
* Management
Cardiovascular Trauma
Myocardial Contusion
* Management
Pericardial Tamponade
* Management
Traumatic Aortic Dissection/Rupture
* Management
Traumatic Asphyxia
* Management
Diaphragmatic Rupture
* Management
Diaphragmatic Penetration
Esophageal Injury
* Management
Tracheobronchial Rupture
* Management
Pitfalls to Avoid

Thoracic Trauma.ppt

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10 July 2009

Respiratory System



Respiratory System

Respiration
* Process of air exchange
* Oxygen is obtained and carbon dioxide is eliminated
* Gas exchange occurs in the alveoli

Four parts of respiration
* Ventilation – movement of air between the atmosphere and alveoli
* Perfusion – blood flow through the lungs
* Diffusion – oxygen and carbon dioxide are transferred between alveoli and blood
* Regulation – respiratory muscles and nervous system

Respiratory Tract
* Nose, pharynx, larynx, trachea, bronchi
* Series of tubes that function as airway passages
* Filter, warm and humidify incoming air

Epiglottis
Heimlich Maneuver
Heimlich Maneuver - Infant
Trachea
Cilia - Smokers
Lungs
Bronchi
Alveoli
Surfactant
Lack of Surfactant
Nervous System Role
Disorders of Respiratory System
Drugs for Asthma and Broncho-constrictive Disorders
Asthma
* Airway disorder characterized by
o Hyper-reactivity to various stimuli - trigger
o Broncho-constriction
o Inflammation
Clinical Manifestations - Asthma
Precipitating Factors - Triggers
Pathophysiology
Drug to Treat Asthma
Quick Relief
Teaching
Long Term Control
Mild Persistent Asthma
Moderate Persistent Asthma
Corticosteroids
Action of Corticosteroids
When to call MD or go to ED
Emergency Treatment
Intermediate Acting Corticosteroid
Methylprednisone
Diagnostics
Peak Flow Meter
Hyper-inflated Lungs in Asthma
COPD - Chronic Bronchitis
COPD - Emphysema
COPD - Clinical Manifestations
Side Effects - Complications
Leukotriene Modifiers
Montelukast
Mast Cell Stabilizer
Toxicity of Drugs
Bronchodilator Overdose
Theophylline Overdose
Antihistamines and Allergic Disorders
Histamines
Action
Types of Allergic Reactions
Allergic Rhinitis
Allergic Dermatitis
Urticaria
Allergic Drug Reactions
Anaphylaxis – Life-threatening allergy
Emergency Treatment
Antihistamines
Use with Caution
H1 receptor antagonists
Management of common cold
Cold Remedies
Cough
Cough Remedies
Antitussive Drugs
Expectorants
Anti-histamines
Mucolytic Drugs
Nasal Sprays

Respiratory System.ppt

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Drugs Affecting Respiratory System



Drugs Affecting Respiratory System
By:Jan Bazner-Chandler MSN, CNS, RN, CPNP

Common Cold
* Most cold are caused by viral infections
o Rhinovirus
o Influenza
* Virus invade the mucosa of the upper respiratory tract, nose, pharynx and larynx which leads to the upper respiratory system.
* Signs and symptoms: excessive mucous production leads to sore throat, coughing, upset stomach.
* Treatment: reduce symptoms
* Note: antibiotics do not help viral infections

Echinacea
* Herbal Therapy
* Has been shown in clinical trials to reduce cold symptoms and recovery time when taken early in the illness.
* Adverse effects: dermatitis, upset stomach, dizziness, headache, and unpleasant taste.

Antihistamines
* Action: act directly on histamine receptor sites H1 blockers.
* Used as an inflammatory mediator for allergic disorders, allergic rhinitis (hay fever and mold, and dust allergies), anaphylaxis, angioedema, insect bites and urticaria (itching).

Antihistamines
* Antihistamines associated with sedation (CNS)
* Non-sedating antihistamines

Antihistamines: sedating
* Classification: H1 antihistamine
o chlorphenramine (Chlor-Trimeton)
o dephenhydramine (Benadryl)
diphenhydramine

* Trade name: Benadryl
* One of the oldest anti-histamines
* Action: Antagonizes the effects of histamine at the H1 receptor sites.
* Adverse Effects: Significant CNS depressant: drowsiness, dizziness, hypotension, dry mouth.
o Onset: immediate to 60 minutes
o Peak: 1-4 hours
o Duration: 4-8 hours

Non-sedating Antihistamine
* The drugs were developed to eliminate the unwanted adverse effects; mainly sedation.
* Action: Works peripherally (do not cross the blood brain barrier) to block the actions of histamine.

loratadine
* Generic name: loratadine
* Trade name: Claritin
* Action: blocks peripheral effects of histamine released during allergic reactions.
* Therapeutic Effects: decreased symptoms of allergic reactions (nasal stuffiness, red swollen eyes)
o Onset within 1-3 hours
o Peak within 8-12 hours
o Duration: > 24 hours

cetirizine
* Trade name: Zyrtec
* Therapeutic classification: allergy, cold, and cough remedies, antihistamine
* Action: Antagonizes the effects of histamine at H1-receptor sites; anticholinergic effects are minimal.
o Onset: 30 minutes
o Peak: 4-8 hours
o Duration: 24 hours

Decongestants
* Nasal congestion is due to excessive nasal secretions and inflamed and swollen nasal mucosa.
o Three types of decongestants
+ adrenergic
+ anticholinergic
+ corticosteroids

Route of administration

* Orally to produce systemic effect
* Inhaled: directly to lungs with some systemic effects
* Nasally: local with some systemic effects

Nasal Drugs

* Adrenergic Drugs: topical application directly into the nares provides a very potent decongestive effect.
* Main side effect: rebound effect (after a few days of use if discontinued can have rebound congestion).

Adrenergic Nasal Drugs
* Afrin
* Neo-Synephrine
* Sinex

Intranasal Steroids
* Often used prophylactically to prevent nasal congestion in patients with chronic upper respiratory tract infections.
* Action: aimed at the anti-inflammatory response
* Trade names
o Nasacort
o Flonase
o Nasalide

Drugs to Treat Coughs
* Antitussives
o Opioid
o Non-opioid
* Expectorants

Antitussive Drugs
* Opioid drugs all have antitussive effects
* Codeine is the only opioid used as a cough medicine
* Action: suppress the cough reflex through direct action on the cough center in the CNS (medulla).
* Adverse effects: CNS and respiratory depression and addictive potential

Antitussive Drugs
* Non opioid
* Generic: dextromethorphan
* Trade names:
o Vicks Formula 44
o Robitussin DM
o Safe, non-addicting and does not cause CNS or respiratory depression.

Expectorants
* Aid in the coughing up and spitting out of the excess mucous that has accumulated in the respiratory tract by breaking down and thinning the secretions.
* Action:
o Loosening and thinning the respiratory tract secretions
o Direct stimulation of the secretory glands in the respiratory tract.
* Guaifenesin is the only drug currently available.
* Trade names: Robitussin, Humibid, Guiatuss
* Therapeutic effect: relief of respiratory congestion and cough suppression

Bronchodilators and Other Respiratory Drugs
Lungs
* Right side has 3 lobes
* Left side 2 lobes
* Contains the lower respiratory structures

Bronchi
* Definition: The bronchi are small air passages, composed of hyaline cartilage, that extend from the trachea to the bronchioles. There are two bronchi in the human body that branch off from the trachea. The bronchi are lined with mucous membranes that secrete mucus and cilia that sweep the mucus and particles up and out of the airways.

Alveoli
* Have a very thin membrane that allows rapid diffusion of oxygen and carbon dioxide between capillary blood and alveolar air spaces.
* Lined with surfactant to prevent alveolar collapse.

Surfactant
* Essential fluid that lines the alveoli and smallest bronchioles.
* Reduces surface tension of the lung allowing the oxygen and carbon dioxide across the membrane.

Lack of Surfactant
Nervous System Role
* Nervous system regulates the rate and depth of respirations.
* Medulla oblongata is the respiratory control system of the brain.
* Cough reflex is stimulated by nervous system.

Diseases of Respiratory System
* Upper respiratory tract: colds, rhinitis, hay fever
* Lower respiratory tract: asthma, emphysema and chronic bronchitis
o All involve obstruction of airflow through the airways.

Bronchial Asthma

* Recurrent and reversible shortness of breath that occurs when the bronchi and bronchioles become narrow as a result of bronchospasm, inflammation, and edema of the bronchial mucosa, and the production of viscid (sticky) mucous.

Allergic Asthma

* Caused by hypersensitivity to an allergen or allergens in the environment.
o Allergen is substance that elicits an allergic reaction.
o Antigen: Substance (usually a protein) that causes the formation of an antibody and reacts with the antibody.
o Antibody: Immunoglobulins produced by Lymphocytes in response to bacteria, viruses, or other antigen substances. (IgE)

Stepwise Therapy for Management of Asthma
* Step 1: mild intermittent
Treatment of mild intermittent Asthma
* Quick relief:
o Short-acting inhaled B2 agonists
+ Albuterol or Proventil

Albuterol (short acting bronchodilator)
* Therapeutic classification: bronchodilators
* Pharmacologic classification: adrenergic
* Indications: Used as a bronchodilator in the management of reversible airway obstruction.
* Action: Binds to beta 2-adrenergic receptors in airway smooth muscle.
* Therapeutic effects: bronchodilator

Albuterol
* Adverse effects:
o Nervousness, restlessness, tremor, headache, insomnia
o Cardiovascular: chest pain, palpitations, angina, hypertension, tachycardia

Albuterol
* Inhaled:
o Onset 15 to 30 minutes
o Peak: 2-3 hours
o Duration: 8 hours

Inhaler
Albuterol INH - Nebulizer
Teaching
* May give up to 3 treatments at 20 minute intervals
* If taking more than one inhaled medications take 5 minutes apart
* Encourage fluid intake
* Signs and symptoms of respiratory distress
* If no relief need to call PMD or go to ED

Mild Persistent Asthma
* Step 2:
o Short acting inhaled B2 agonist prn
+ Proventil (albuterol)
+ Xopenex (levoalbuterol)
o Low dose inhaled corticosteroids (beclomethasone, fluticasone, triamcinolone
+ Pulmicort, Flovent, Azmacort
o Cromolyn (particularly in children)

cromolyn
* Classification: Mast cell stabilizer
* Trade name: Intal, NasalCrom
* Indications: adjunct in the prophylaxis (long-term control) of allergic disorders including rhinitis and asthma
* Action: prevents the release of histamine and slow-reacting substance of anaphylaxis (SRS-A) from sensitized mast cells.
* Route: inhalation, solution for nebulization or nasal solution.

Inhaled Corticosteroids
* Generic name: fluticasone
* Trade name: Flovent
* Action: potent locally acting anti-inflammatory and immune modifier.
* Therapeutic effects:
o Decrease frequency of asthma attacks
o Prevention of pulmonary damage associated with chronic asthma.

Inhaled Corticosteroids
* Adverse reactions and side effects:
o EENT: hoarseness, oropharyngeal fungal infections
o Dry mouth, esophageal candidia.

Client Teaching
* Take medication as directed.
* Do not discontinue without consulting MD
* When using corticosteroids and bronchodilators use bronchodilators first and follow 5 minutes later with corticosteroids.
* Rinse and spit after inhalation therapy to prevent oral fungal infections.
* Use a tight fitting mask in infant / small child

Oral Thrush
Moderate Persistent Asthma
Antileukotriene Drugs
Severe Persistent Asthma
Corticosteroids
Prednisone
Exercise Induced Asthma
Chronic Bronchitis
COPD
Moderate COPD
Treatment of COPD
Salmeterol

Drugs Affecting Respiratory System.ppt

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27 May 2009

Asthma



ASTHMA
By:Rochelle M. Nolte, MD
CDR USPHS, Family Medicine

Objectives
* At the conclusion of the presentation, participants should be able to:
o ID signs and symptoms consistent with asthma and allergic rhinitis
o Differentiate the various severities of asthma
o Summarize an appropriate treatment regimen for asthma of various severities

Allergic Rhinitis
* Symptoms: sneezing, itching, rhinorrhea, and congestion
* Nasal smear with >10% eosinophils suggestive
* Dx can be confirmed by allergen-specific Ig-E
* Classification
* Affects 15%-50% of world-wide population
* Affects 40 million people in the US
* Prevalence increasing
* Associated with asthma

Management of Allergic Rhinitis
* Identification of allergens
* Avoid or minimize exposure to allergens
* Patient education
* Pharmacotherapy
* Allergen Immunotherapy

Definition of Asthma
* Chronic inflammatory disorder of the airways in which many cells and cellular elements play a role. In susceptible individuals, this inflammation causes recurrent episodes of wheezing, breathlessness, chest tightness, and coughing, particularly at night or in the early morning. These episodes are associated with widespread but variable airflow obstruction that is reversible either spontaneously, or with treatment.

Asthma
Asthma Triggers
* Allergens
* Pharmacologic agents (ASA, beta-blockers)
* Physical triggers (exercise, cold air)
* Physiologic factors

Diagnostic Testing
* Peak expiratory flow (PEF)
* Spirometry
* Methacholine challenge
* Diagnostic trial of anti-inflammatory medication (preferably corticosteroids) or an inhaled bronchodilator

Goals of Asthma Treatment
* Control chronic and nocturnal symptoms
* Maintain normal activity, including exercise
* Prevent acute episodes of asthma
* Minimize ER visits and hospitalizations
* Minimize need for reliever medications
* Maintain near-normal pulmonary function
* Avoid adverse effects of asthma medications

Treatment of Asthma
Written Action Plans
* Written action plans for patients to follow during exacerbations have been shown to:
o (Cochrane review of 25 studies)
o Decrease emergency department visits
o Decrease hospitalizations
o Improve lung function
o Decrease mortality in patients presenting with an acute asthma exacerbation
o NAEPP recommends a written action plan*







Pharmacotherapy

* Long-acting beta2-agonists (LABA)
o Beta2-receptors are the predominant receptors in bronchial smooth muscle
o Stimulate ATP-cAMP which leads to relaxation of bronchial smooth muscle and inhibition of release of mediators of immediate hypersensitivity
o Inhibits release of mast cell mediators such as histamine, leukotrienes, and prostaglandin-D2
o Beta1-receptors are predominant receptors in heart, but up to 10-50% can be beta2-receptors

Pharmacotherapy
* Long-acting beta2-agonists (LABA)
* Albuterol
* Inhaled Corticosteroids
* Mast cell stabilizers (cromolyn/nedocromil)
* Leukotriene receptor antagonists
* Theophylline

Various severities of asthma
* Step-wise pharmacotherapy treatment program for varying severities of asthma
* Patient fits into the highest category that they meet one of the criteria for

Mild Intermittent Asthma
Moderate Persistent Asthma
Severe Persistent Asthma

Pharmacotherapy for Adults and Children Over the Age of 5 Years
* Step 1 to 4
Pharmacotherapy for Infants and Young Children (<5 years)
* Step 1to 4
Acute Exacerbations
* Beneficial
* Likely to be beneficial
Exercise-induced Bronchospasm
* Evaluate for underlying asthma and treat
* SABA are best pre-treatment
* Mast cell stabilizers less effective than SABA
* Anticholinergics less effective than mast cell stabilizers
* SABA + mast cell stabilizer not better than SABA alone

Questions &Answers

ASTHMA.ppt

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14 May 2009

Learning Respiratory Physiology



Learning Respiratory Physiology

4 THINGS TO KNOW
* Ventilation
* Lung Volumes & Capacities
* Blood Gases
* Lung Gas Pressures & Flows

Functional anatomy
Alveolar ventilation
Increased Alveolar Dead Space
Pulmonary Embolism Model
Occurs in All Lung Diseases
Negative intrapleural pressure
Chest & lung trauma
Incorrect spirometry
Correct spirometry
Lung volumes & capacities
Direct spirometry
FEV1/FVC
Normal posture change
Respiratory diseases
Airflow limitation
Dynamic Compression
LARGE AIRWAYS
Thick Wall – High Raw
LARGE AIRWAYS
Non-Collapsible Components
Maintain Flow during FVC
SMALL AIRWAYS
Thin Wall – Low Raw
Small Airways
Airway Disease-More Collapsible
More Airflow Limitation-Dynamic
Compression of Airways
Collapsible Components of Airways
Spirometric Diagnosis

Learning Respiratory Physiology.ppt

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Smoking Cessation- Role of a Physician



“Effect on Smoking quit rate of telling patients their lung age: the step 2 quit randomised controlled trial”
Article Review by : Pooja Singhal, MD

Structure
Background

* Currently 23% Men and 19% women in USA smoke
* Cigarette smoking was estimated to be responsible for nearly 5 million premature deaths worldwide in 2000
* In the United States (US), cigarette smoking is the major preventable cause of disease, and is estimated to result in more than 400,000 deaths annually.
* The most important causes of smoking-related mortality include atherosclerotic cardiovascular disease, lung cancer, and chronic obstructive pulmonary disease (COPD)
* The incidence of a MI has increased six-fold in women and threefold in men who smoke at least 20 cigarettes per day compared to subjects who never smoked
* In the United States alone, the health consequences and productivity losses associated with smoking are estimated to cost in excess of 90 billion dollars every year

Smoking Cessation- Role of a Physician

* 70% smokers see a physician each year
* Advice from physician leads to a spontaneous quit rate of 2-4%
* Pharmacological vs. Behavorial Approach
* Pharmacological- Bupropion, Nicotine replacement therapy, and varenicline
* Behavorial – counseling and motivational interviewing
* Pt.s willing to quit -5 A’s – Ask, Assess, Advise, Assist and Arrange
* Pts unwilling to quit- 5 R’s- Relevance, Rewards, Roadblocks, and Repetition

Whether the biomarkers like Cotinine or tests like Spirometry can promote Smoking cessation?
Research so far – Role of Biomarkers in Smoking cessation?


Research Study
* Hypothesis- Telling smokers their “lung age” would lead to successful smoking cessation, especially in those with most damage.
* Design- Randomized controlled trial
* Setting- 5 general practices in Hertfordshire, England
* Participants- 561 current smokers aged over 35, control 281, intervention 280

Exclusion Criteria:
* Patients on home Oxygen
* Hx of lung cancer
* Silicosis
* TB
* Asbestosis
* Pneumonectomy

Table 2 Baseline characteristics of groups. Figures are means (SDs) unless stated otherwise
Instruments used to confirm baseline comparability of groups
* St. George’s respiratory questionnaire- self administered under supervision and to measure the impact of respiratory diseases (asthma and COPD) on an individual’s life.
* Prochaska’s stages of change questions in relation to smoking
Instruments and Test
* MicroLab 3500 Spirometers- newly purchased
* Saliva samples for Cotinine testing with documentation of people on nicotine replacement therapy
Men Lung age=2.87 x height (in inches)–(31.25 x observed FEV1 (litres)–39.375
Women Lung age=3.56 x height (in inches)–(40 x observed FEV1 (litres)–77.28
Lung age calculation formula developed
by Morris and Temple5
Lung Age - The age of the average healthy individual who would perform similar to them on spirometry.

Intervention vs. control group
* If the lung age was equal to or less than the individual’s chronological age, he or she was informed test result was normal
* Lung age> chronological age – lung age in years given
* Control group – no results given – told them they would be reinvited for a second test after 12 months to see if there had been any change in lung fxn
* 4 weeks – After reviewing the results with checking quality of the spirometry tracing, written results were sent to both control and intervention group
* Control group – FEV1 with no further explanation
* Intervention group – Lung age

Communication to the patients (Intervention group)
* Results after Spirometry given immediately in the form of lung age
* Visual aid (graphs)
* Verbal Counseling - How lung function normally reduces gradually with age and that smoking can damage lungs as if they are aging more rapidly than normal.
* Personalized letter

Results
* Follow-up was 89%
* Quit rates at 12 months in the intervention and control groups, respectively, were 13.6% and 6.4%
* Difference -7.2%, P=0.005, 95% confidence interval 2.2% to 12.1%
* NNT( number needed to treat) = 14
* People with worse spirometric lung age were no more likely to have quit than those with normal lung age in either group.
* Cost per successful quitter was estimated at £280 (€366, $556).
* A new diagnosis of obstructive lung disease was made in 17% in the intervention group and 14% in the control group.

Outcome
* Primary outcome- cessation of smoking by salivary cotinine testing 12 mos after recruitment
* Secondary outcomes –
* Changes in daily consumption of cigarettes
* Identification of new diagnoses of COPD
Limitations
* Outcome data limited to point-prevalence abstinence.
* The study does not compare the effect of patient counseling with visual/graphical communication of lung age. The study compares FeV1 with lung age which points to the fact that patients tend to understand simpler terms and images than complicated parameters like FeV1.
* The additional verbal and graphical interaction given to the intervention group as compared to minimal interaction given to the control may have biased the outcome.
* The study included a very select population from a distinct geographic area of UK.
* Practical application of the Lung age formula in the clinics.

The Lung Age calculator
Conclusion

* Informing smokers of their lung age significantly improved the likelihood of them quitting smoking, but the mechanism by which this intervention achieves its effect is unclear.

Discussion
* The results only support the conclusion that for smokers over 35 yrs who undergo spirometry, communication about lung age is a more effective motivator for tobacco cessation than uninterpreted spirometry measurements.
* Decision- wait for a trial comparing the potential benefit for smoking cessation of spirometry testing using lung age feedback vs no spirometry testing? Or adopt this method?
References

Smoking quit rate.ppt

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Incentive Spirometry



Incentive Spirometry

I. S. Introduction
* Also called SMI (sustained maximal inspiration)
* Involves the use of a device that encourages a patient to make larger-than-normal inspiratory effort and establish a breathing incentive
* Involves pt. mentally and physically and is less expensive and usually as effective as IPPB
* I. S. devices let the patient see their own progress
* Results in the generation of increased negative transpulmonary pressures increased Vt for the primary purpose of opening and stabilizing atelectatic areas of the lung against recurrent atelectasis
* Prevention of postoperative complications
- primary purpose is to help open closed alveoli, facilitate the cough reflex, help mobilize secretions, and prevent hyperventilation.

* Preoperative “cleanup”, which strengthens pulmonary muscles, increases voluntary ventilation, improves “bronchial toilet”
* Psychological support


Contraindications for I. S.
* Uncooperative or physically disabled pt.
* Patient with mental or CNS disorders
* Patients that are physically unable to generate large enough Vt (10-15 ml/kg)

Hazards and Complications of I.S.
* Hyperventilation may occur if SMI is performed too rapidly, without rest periods between deep breaths, which may lead to dizziness, light-headedness, a tingling sensation in the extremities, and possible muscle tremors
* Barotrauma in pt. with emphysematous blebs
* Pulmonary embolism from decrease Ppl

Procedure for I. S.

* Determine baseline volume expectations
* If post-op, set realistic, achievable goals initially and increase level by 200 ml until pt. reaches desired Vt
* Make sure pt. understands proper use of device
* Stress importance of achieving goals and coughing to clear secretions
* Splint surgical incisions
* Noseclips can be used to better facilitate a deep breath
* Asses pt., incl. V.S. and chest auscultation
* Explain and demonstrate
* Proper technique includes having pt. inspire slowly and deeply from FRC
* At the end of max. inspir. have pt. do breath hold for 5 sec.
* Repeat 6 - 10 times or as prescribed
* Instruct proper cough
* Reassess pt.

Incentive Spirometry.ppt

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The Respiratory System and Spirometry



The Respiratory System & Spirometry

* Identify parts of the respiratory system
* Examine histology of the: Trachea, Lung
* Examine the operation of the lung model
* Biopac L012-Lung-1: Spirometry
o Measure lung volumes and capacities

Respiratory System Structure
* Conduction zone: pathway for pulmonary ventilation
* Respiratory zone: membrane for gas exchange external respiration
* Clinically, two parts:
o Upper respiratory tract
o Lower respiratory tract
Histology reflects the different functions of the different parts of the system
Position in respiratory pathway determines cell type
* non-keratinized stratified squamous
* pseudostratified ciliated columnar
* cuboidal ciliated
* simple squamous / Type I Alveolar cells

Pseudostratified Columnar Epithelium
Lamina Propria
Hyaline Cartilage
mucosa
Submucosa
seudostratified epithelium = lamina propria
ucous glands
mooth muscle
artilage
Gross Section Through Lung
Smoker’s Lungs
Non-smoker
Small Bronchiole
Lung Tissue slide
Respiratory Bronchiole
Alveolar Duct
Alveoli
Alveolar Sac
Capillaries in Alveolar Wall
Spirometry
SPIROMETRY – RESPIRATORY VOLUMES AND CAPACITIES

Total Lung Capacity = Inspiratory Reserve Volume (IRV) + Tidal Volume (TV) + Expiratory Reserve Volume (ERV) + Residual Volume (RV)
Vital Capacity = Inspiratory Reserve Volume (IRV) + Tidal Volume (TV) + Expiratory Reserve Volume (ERV)
Inspiratory Capacity = Inspiratory Reserve Volume (IRV) + Tidal Volume (TV)
Functional Residual Capacity = Expiratory Reserve Volume (ERV) + Residual Volume (RV)

Spirometry – Calibration
Insert the calibration syringe/filter assembly into the side of the airflow transducer labeled "Inlet."
Inlet
Wait for 8 seconds of no air flow Inlet
Experimental Treatments

The Respiratory System & Spirometry.ppt

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Spirometry



Spirometry

Respiration
* External respiration – Gas exchange between blood and alveoli
* Internal respiration – Gas exchange between blood and tissue cells

Pulmonary Ventilation
* Inspiration – Diaphragm and intercostals muscles contract resulting in increased volume and decreased pressure in the thoracic cavity; air rushes in
* Expiration – Diaphragm and intercostals muscles relax resulting in decreased volume and increased pressure in the thoracic cavity; air pushed out

Respiratory Volumes
* Tidal volume - normal amount of air inhales or exhaled
* Inspiratory reserve volume amount of air that can be forcefully inhaled after normal inhalation
* Expiratory reserve volume – amount of air that can be forcefully exhaled after normal exhalation
* Vital capacity – maximum amount of air that can be exhaled after maximum inhalation
* Residual volume – amount of air that can be exhaled after maximum inhalation

Factors altering normal function
* Diseases
* Disorders
* Pollutants in the environment
* Trauma

Spirometry.ppt

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10 May 2009

Respiratory Distress in Newborn



Respiratory Distress in Newborn
Presentation lecture by:Leena Mane and Rhea Mane


Case study:

* A male infant weighing 3000 g (6 lb 10 oz) is born at 36 weeks' gestation, with normal Apgar scores and an unremarkable initial examination. At 48 hours of age he is noted to have dusky episodes while feeding, and does not feed well. On repeat examination the child is tachypneic, with subcostal retractions. Lung sounds are clear and there is no heart murmur.

What Next ?
Tests & labs…

* Pulse oximetry on room air is 82%.
* Arterial blood gases on 100% oxygen show a pCO2 of 26 mm Hg (N 27-40), a pO2 of 66 mm Hg (N 83-108),
* blood pH of 7.50 mg/dL (N 7.35-7.45), and a base excess of -2 mmol/L (N -10 to -2).
* Hemoglobin- 22.0g/dl (N13.0- 20.0)
* Hematocrit- 66 % (N 42- 66)
* WBC- 19,000/mm3 (N9000-30,000)
* Blood cultures- Pending.
* Chest X-ray- Increased vascular marking, Large thymus.


Most likely diagnosis
* 1- Transient tachypnea of newborn
* 2- Congenital heart disease
* 3- Hyaline membrane disease
* 4- Neonatal sepsis
* 5- Hyperviscosity syndrome

Transient Tachypnea of Newborn
* Most common cause of respiratory distress.
* 40% cases.
* Residual fluid in fetal lung tissues.
* Risk factors- maternal asthma, c- section, male sex, macrosomia, maternal diabetes

TTN

* Tachypnea immediately after birth or within two hours, with other predictable signs of respiratory distress.
* Symptoms can last few hours to two days.
* Chest radiography shows diffuse parenchymal infiltrates, a “ wet silhouette” around heart, or intralobar fluid accumulation

X-ray
Fluid in the fissure
Respiratory Distress Syndrome
RDS
Meconium Aspiration Syndrome
Infections
Other causes-
Congenital Heart disease
Hyperoxia Test
Treatment
Transient Tachypnea of Newborn
Respiratory distress Syndrome
Meconium Aspiration Syndrome
Algorithm
Evaluation
Treatment

Respiratory Distress in Newborn.ppt

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