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Terms in this set (164)

• RR? >20 Tachypnic
• O2 Sat? < 90 is Hypoxic
• PaO2? <60 is Hypoxic
• Pulsus Paradoxus? An abnormally large decrease in systolic pressure and pulse wave amplitude during inspiration.
• General appearance? Respiratory distress, cyanotic, posturing (Tripod??), obese, body habitus, malnutrition, Thin Middle/Old aged Man with pursed lips? (COPD)
• Inspection? Retractions, accessory muscle of respirations being used? Effort of breathing, paradoxical breathing pattern of chest and abdomen
• Are they able to speak in full sentences? The inability represents obstruction of airway or neuromuscular weakness
• Ask the patient to dorsiflex the wrist with the arms outstretched and spread fingers if a flapping tremor (asterexis) is present could be a sign of CO2 retention (or liver disease)
• Muscle wasting and weakness is a sign of cachexia due to malignancy
• Hoarseness may be due to recurrent laryngeal nerve palsy associated with carcinoma of the lung usually left sided, or laryngeal carcinoma. MCC however is laryngitis
• Nasal Polyps? Common in asthmatics
• Engorged bogey turbinates? Common in allergic conditions
• JVD? Elevated JVP may be caused by Right sided HF, Pneumothorax, COPD and Cardiac Tamponade
• AP diameter? Increased AP diameter in COPD
• Chest/Thoracic Expansion? Asymmetry if pleural effusion or PTX
• Palpation?
o First palpate the accessory muscles or respiration in the neck- SCM and scalene (assist in elevating the rib cage); hypertrophy and contraction indicate increased resp. effort!!
o Trachea should be palpated and should lie in the midline of the neck- a deviated trachea may suggest a collapsed lung (PTX),
o Neck masses should be noted
o Thoracic expansion- place hands on posterior lower chest with thumbs touching and fingers spread apart; thumbs should slightly separate during inspiration and fingers should spread symmetrically
o Fremitus= a slight vibration felt best with the ulnar side of the hand while the patient speaks (say "99") Fremitus is increased in areas of consolidation!!! Decreased in pleural effusions and ptx
o Crepitus? Rice Crispies?? Sign of pneumomediastinum
o Tactile Fremitus? Increased Vibration with consolidation and Decreased with PTX, Pleural effusion
• Percussion?
o Resonance is Normal!!!
o Hyper-resonance is seen in COPD, PTX
o Dullness in consolidation, lung mass, and pleural effusion
• Auscultation?
o Clear to auscultation B/l is Normal! Equal air entry bilaterally
o Normal breath sounds are vesicular and bronchial!! Bronchial breath sounds are heard over the central/bronchial airways and are louder and coarser. Vesicular breath sounds are heard over the periphery and base of the lungs and are much softer than bronchial.
o Bronchial breath sounds in the periphery→Abnormal bronchial breath sounds and may be caused by consolidation
o Consolidation is when normal air filled spaces in the lungs are filled with fluid or tissue!
o Diminished Breath Sounds? PTX, Pleural effusions
o Inspiratory Wheezing is called Stridor? Acute epiglottitis, FB aspiration, Croup
o Expiratory Wheezing? Asthma, COPD, CHF
o Egophony? Abnormal if spoken "ee" sounds like "aa" which is heard in consolidation
o Whispered Pectoriloquy? Increased transmission of vocal sounds with consolidation
o Extra pulmonary sounds?
• Crackles= can be coarse rattles or fine Velcro like sounds; Coarse crackles are often caused by mucus or consolidation in the airways; Fine crackles are produced during inspiration by the opening of collapsed alveoli and most commonly heard over the bases and are heard in pulmonary edema and interstitial fibrosis, (sometimes heard in healthy older adults during deep inspiration)
• Wheezes= higher pitched sounds; when heard locally suggest large airway obstruction; the wheezing of asthma and CHF patients is lower in pitch and heard over the all lung fields; localized wheezing can be heard in PE, tumor obstruction, & FB.
• Rub= a pleural sound that is caused by inflamed pleural spaces rubbing together. May be heard in patients with pleural effusion. The sound can be described as two pieces of leather rubbing together against each other. A crunching sound can be heard with patients w/pneumomediastinum.
• Absent lung sounds→ PTX, obstruction, hydrothorax, or hemothorax
• Extremities? Cold, cyanotic, edema, clubbing?
Signs and Symptoms: Wheezing, dyspnea, cough, sputum production, fever, allergic symptoms (shiners, enlarged nasal turbinates, post nasal drip), tripoding, chest tightness, diaphoresis, and altered level of consciousness.
Samter's Triad= Asthma, ASA sensitivity, and nasal polyps

Precipitating Factors: Smoking is the most common stimulus, pollution, weather, exercise, allergens, respiratory infection, stress

PE: Tachypnic, tachycardia, cyanosis, pursed lips, use of accessory muscles (SCM, Scalenes, Pectoralis minor), wheezing, prolongation of expiratory phase, hyperinflation of lungs

Dx: Respiratory Alkalosis in ABGs because hyperventilating, CXR may be normal or may show signs of an infection like pneumonia, Spirometry will show an obstructive pattern (FEV1:FVC ratio <70%) and will show an increase in FEV1 by 12% with the bronchoprovocation test

ACUTE TX: Short acting Beta 2 agonists like Albuterol inhaled; Anti-cholinergic like Ipratroprium (Atrovent) given in a metered dose inhaler; COMBIVENT is the combination of the two medications.
IV or PO glucocorticoids if necessary
Magnesium 2-4 gm IV over 10-20 minutes can be given in an emergency. Mg inhibits calcium channel mediated smooth muscle activity/contractions

Long term treatment:
Mild persistent asthma should be treated with a Controller medication such as Low dose inhaled glucocorticoid (Pulmicort)
Moderate to Severe Persistant asthma should be treated with an inhaled glucocorticoid plus a long acting beta 2 agonist; Symbicort, Advair, or Dulera

Patient Education:
Effective inhaler usage
Avoid smoking or 2nd hand smoke
Avoid known allergens- vacuum, clean air filer, no carpets
Influenza and PSV23 Vaccinations recommended
Leading cause of cancer death, accounting for ¼ of deaths in both men and women
• Peak incidence ~55-65 yo
• Cigarette smoking is the most important risk factor 87% of lung cancer pts

Presentation on CXR:
• Small cell and Epidermoid are usually central masses
• Adenocarcinoma and Large Cell are usually peripheral masses

Clinical manifestations of Lung Cancer- usually never detected when asymptomatic
• Unintentional Weight loss, anorexia, and fever
• Central endobronchial tumor- cough, hemoptysis, wheeze, stridor, dyspnea, pneumonitis
• Peripheral lesions- pain, cough, dyspnea, symptoms of lung abscess resulting from cavitation
• Mets spread- tracheal obstruction, dysphagia, hoarseness, Horner's syndrome, SVC syndrome, pleural effusion, pericardial effusion, respiratory failure
Horner's syndrome= pancoast's tumor- ptosis (lid lag), miosis (pupil constriction), and anhydrosis
SVC syndrome= obstruction of venous return to SVC causes distension of neck veins, edema of face and upper extremities and cyanosis
Pericardial effusion- flask shape appearance in CXR
Pleural effusion- elevated hemi-diaphragm and blunted costophrenic angles

Diagnosis:
Bronchoscopy with fine needle aspiration or CT guided biopsy.
• Radiographic features suggesting malignancy
- Absence of a benign pattern of calcification in detected lesion
- A nodule or mass that is growing
- A nodule with a spiculated or lobulated border
- A larger lesion > 8 mm is suspicious (>3 cm is considered malignant unless proven otherwise)
- A cavitary lesion that is thick walled

• CXR findings
- Adenocarcinoma- Commonly produces small peripheral masses
- Large cell tumors- Produce large peripheral masses
-Small cell presents typically centrally
- Squamous cell/Epidermoid- Commonly produces a hilar mass, mediastinal widening, and cavitation
- Mesothelioma- Presents with pleural thickening
- Bronchioalveolar cell carcinoma- Pneumonia like appearance

Staging:
CT or PET scan
Impairment in lung physiology:
• Gas exchange is impaired due to V/Q mismatching, shunt, & decreased diffusion across abnormal interstitium.
• Work of breathing markedly increased because of decreased lung compliance.
- If initiating injury or abnormal repair from injury is not stopped, progressive tissue damage can lead to worsening impairment & death

HPI:
• Pay specific attention to duration and progressive of illness
• Obtain a lifelong occupational hx and hobbies
• Inquire about exposures to inhaled agents, medications, family hx
• Cigarette smoking is a risk factor for several ILD's including IPF, PLCH, Goodpasture's syndrome & respiratory bronchioliitis

Symptoms: chronic symptoms more common
• Exertional dyspnea (most common complaint)
• Cough-non -productive
• Constitutional- Fatigue/Weakness/Loss of appetite/Weight loss

PE findings:
• Can be normal or range from bilateral fine-inspiratory crackles more prominent at bases, wheezing, rhonchi, or decreased BS.
• Findings may include clubbing of nails, tachypnea, tachycardia, & skin changes associated with any associated connective tissue disease (CTD)

CXR:
• Usually important role in establishing Dx.
• Obtain previous CXR to ascertain disease progression
• Infiltrates in lower lung zones provide clue to presence & have "ground-glass" appearance in early stage of disease, & nodular, linear, honeycombed appearance in later stages (honey combing is indicative of advanced fibrosis)
• Upper-lung-zone predominance of nodular opacities is noted in several ILDs, including PLCH, sarcoidosis, chronic hypersensitivity pneumonitis and silicosis.

Lab studies:
• ANA & RA factor at low titers are observed in some IPF pts without a connective tissue disorder.
• Specific serum antibodies can confirm exposure to relevant antigens in hypersensitivity pneumonitis

ILD dx:
• Histological exam usually necessary for diagnosis
- Most infiltrative disease require High Resolution CT scan guided needle Bx or open lung Bx. for Dx.
- Transbronchial biopsy via bronchoscopy (only in cases where a small tissue may suffice to make Dx)

Management:
• Remove exposure of pulmonary irritants
• Prevent destruction of lung tissue by inhibiting inflammatory reaction within the lung
• Relieve symptoms of these disease processes
• Glucocorticoids can be highly effective for eosinophilic pneumonias, COP, hypersensitivity pneumonitis (HP), radiation pneumonitis & drug induced ILD/ Prednisone at 0.5-1.0 mg/kg qd is commonly given for 4-12 weeks, followed by a gradual tapering dose.
o Glucocorticoids are typically not beneficial for IPF.
• Smoking cessation
• Oxygen for patients with significant hypoxemia (PaO2 < 55 mmHg)
Vaccinations are important (yearly influenza and pneumoccocus vaccines)

*Lung Transplant for young patients with end-stage ILD's should be considered
Hypersensitivity Pneumonitiis: AKA extrinsic allergic alveolitis

• Inflammatory lung disorder caused by repeated inhalation of an organic agent in a susceptible individual.
• Usually organic antigens, particularly thermophilic actinomycetes

Antigens:
• Thermophilic bacteria-Moldy hay, sugar cane, compost
• Other bacteria-contaminated water, wood dust, fertilizer, paprika dust
• Fungi-moldy cork, contaminated wood dust, barley, maple logs
• Animal proteins-bird droppings, animal urine, bovine & porcine pituitary powder
• Chemically altered human proteins (albumin)-toluene diisocyanate
• Phthalic anhydride-heated epoxy resin

Types of Hypersensitivity Pneumonitis:
Farmer's lung- hay dust and mold spores
Bagassosis- moldy molasses (bagasse)
Bird Fancier's Disease- bird droppings
Mushroom worker's disease- basidiospores
Pigeon breeder's lung- bird droppings
Duck fever
Turkey handler's disease
Laboratory worker's hypersensitivity pneumonitis
Epoxy resin lung- epoxy resin fumes inhalation


History:
• Occupational history & history of possible exposures & relationship to symptoms important
• Symptoms of dyspnea, coughing, & fever abate when affected person leaves environment where offending antigen is located.
• Suspect in patients with respiratory symptoms that worsen in certain environments such as returning to work after a weekend or vacation

Physical Exam:
• Nonspecific
• May reveal rales in lung fields
• Cyanosis in advanced cases

• CXR- Nonspecific changes in interstitial structures; pleural changes or hilar adenopathy rare
• Chest CT scans typically show ground glass opacification in acute and subacute forms that are consistent with HP,
• In some cases lung biopsy (transbronchial or open lung) may be required to confirm Dx.

Treatment:
• Avoidance of offending antigen is essential
• Systemic corticosteroids may be required in subacute or chronic HP
• Chronic form may be partially irreversible at time of Dx.
• Prednisone 1(mg/kg)/d for 7-14 d, followed by tapering schedule over 2-6 weeks to lowest possible dose
• Pts with acute form usually recover without glucocorticoids
• Idiopathic multisystem (lung, skin, eyes, peripheral nerves, liver, kidney, heart, other tissues) inflammatory disorder that commonly involves lungs
• Systemic granulomatous disease of unknown etiology

Pathophysiology:
• Affected organs with accumulation of lymphocytes & mononuclear phagocytes, noncaseating epitheliod granulomas, & derangement's of normal tissue architecture
• Mononuclear cells, mostly T-helper lymphocytes & mononuclear phagocytes, accumulate in affected organs followed by formation of granulomas

Epidemiology:
• Most common ILD in USA
• Highest incidence in African Americans & Northern Europeans
• Women > Men

Clinical manifestations:
• May be asymptomatic & discovered on routine CXR as bilateral hilar adenopathy & right paratracheal lymphadenopathy
• Constitutional Systems- Fever, Malaise, Dyspnea
• Symptoms related to skin, eyes, peripheral nerves, liver, kidney, or heart.
• Nervous system: May involve CNS, cranial, peripheral nerves
• Heart: May involve LV wall or conduction system, causing disturbances of rhythm &/or contractility
• Eye: Uveitis in approximately 25%; may progress to blindness
• BM & Spleen-Mild anemia; thrombocytopenia may occur
• Liver-Involved on biopsy in 60 to 90%; rarely important clinically
• Kidney-May have parenchymal disease or more commonly nephrolithiasis 2nd to abnormalities of Ca++ metabolism
• Lymph nodes-Intrathoracic & peripheral LN's may be enlarged
• Skin-25% will have skin involvement including erythema nodosum, plaques, maculopapular eruptions, subcutaneous nodules & blue-purple shiny lesions on face, fingers & knees


Labs:
• Elevated ESR & hypercalcemia (5% of pts)
• Angiotensin-converting enzyme levels (ACE) are elevated in 40-80% of patients with active disease

CXR:
bilateral hilar adenopathy

Treatment:
• Many cases remit spontaneously & do not require treatment
• Major morbidity & mortality related to progressive respiratory dysfunction in association with severe ILD
• Eye involvement (including blindness) is most common extra-pulmonary complication
• Ophthalmologic examination is indicated in all patients because ocular findings (iridocyclitis, uveitis, conjunctivitis, & keratopathy) are found in > 25% of documented cases.

Treatment:
• Corticosteroids when Rx required
Initial therapy should consist of prednisolone 30-60 mg/day or its equivalent. Alternate day therapy can be used during the maintenance phase
• Severe symptoms -(dyspnea or CP), hypercalcemia, ocular, CNS, cardiac involvement, or progressive pulmonary disease.
• Patients with progressive disease refractory to corticosteroids may be treated with methotrexate or azathioprine (Imuran)
RAPID SEQUENCE INTUBATION
Rapid sequence intubation is defined as the simultaneous administration of a powerful sedative (induction) agent and a paralytic agent to facilitate intubation and decrease the risk of aspiration.
Although a detailed discussion of RSI is beyond the scope of this chapter, the basic steps are reviewed below. These can be recalled as the six P‟s.
1. Preparation - prepare all equipment, personnel, and medications
2. Pre-oxygenation - patient breathing 100% oxygen for 3-5 minutes or asking the patient to take 4-8 full breaths on 100% oxygen will wash out the nitrogen in the lungs, and prolong the time available for intubation before desaturation occurs.
3. Pretreatment - pretreatment with medications such as atropine in children, defasciculating doses of a non-depolarizing muscle relaxant prior to the administration of succinycholine, and lidocaine in the setting of head injury is considered optional, given the lack of evidence for their benefit
4. Paralysis with induction - administration of a sedative agent (e.g. ketamine, propofol, etomidate) followed rapidly by the administration of a muscle relaxant (e.g. succinylcholine or rocuronium)
5. Place the tube with proof - intubate the patient, and confirm tube placement with end-tidal capnometry
6. Post-intubation management - chest x-ray, analgesia and sedation, further resuscitation
Relative contraindications to rapid sequence intubation include:
• €anticipated difficult airway, especially difficult bag-valve mask ventilation. In this situation, an ―awake‖ intubation with the patient maintaining respirations is preferred
• €inadequate familiarity and comfort with the technique
• €unnecessary (e.g. the patient in cardiac arrest or near-arrest)
COPD: Progressive Inflammatory Airway Ds

Chronic Bronchitis= Excessive mucus production with airway obstruction and hyperplasia of mucus producing glands; "Blue Bloaters"; presence of a productive cough on most days for at least 3 months; Inflammatory response leads to fibrosis

Emphysema= Destruction and enlargement of air spaces distal to the terminal bronchioles without obvious fibrosis. This causes an abnormal alveoli with limited gas exchange capacity; "Pink Puffers"

I. Etiology: smoking, air pollution and occupational exposures


II. Symptoms: Chronic Cough, DOE or decreased exercise intolerance, increased sputum production, wheezing, frequent chest infections, altered lever of consciousness


III. PE: Increased AP diameter (barrel chest commonly seen in emphysema), decreased breath sounds, hyper-resonance to percussion, prolonged expiration, cyanosis, pursed lips, tripod, cachexia


IV. Dx:

a. Obtain spirometry (<FEV1, <FEV1: FVC), & CXR (showing flat diaphragms, hyperlucency due to destruction of lung tissue and trapped, increase in retrosternal air space due to hyperinflation), and a baseline ECG. Heart can appear more vertical in shape.

b. Hypercapnia and Hypoxemia (PaCo2:PaO2 known as the 50:50 club)

c. Consider alpha 1 anti-trypsin deficiency testing in pt <45 yo

d. Chronic Respiratory Acidosis due to increased levels of CO2


V. Tx:

a. Acute Tx= Oxygen to O2 sat >90% and COMBIVENT

b. Maintenance Tx: An inhaled glucocorticoid plus a long acting beta 2 agonist; Breo Ellipta, Symbicort, Advair, or Dulera


VI. Patient Education:

a. Smoking Cessation!

b. Yearly Influenza and a PSV23 vaccine because respiratory infections are the primary cause of COPD

c. Pulmonary Rehabilitation increases functional capacity and quality of life
Pneumonia: Infection of the lung parenchyma (alveoli)

Typical Pathogens
Most common cause of CAP is Streptococcus pneumoniae (rust colored sputum, abrupt onset chills, pleuritic CP)

2nd MC CAP is Haemophilus Influenzae

Aspiration pneumonia? Mixed anaerobes and aerobes

Alcoholics commonly get Kiebsiella Pneumonia

Cystic Fibrosis patient commonly get Pseudomonas Aeurginosa

COPD and Smokers commonly get H. Influenzae

IVDA commonly get Staph Aureus

Viruses are more common in children < 5yo (RSV, Influenza, Parainfluenza, Adenovirus)

Atypical Pathogens:
Mycoplasma Pneumonia MC atypical and is more common in patients <40 yo; sometimes the patients have an associated rash, HA, malaise, non-productive cough, low grade fever, bullous myringitis (inflamed TM)

Legionella species- Patients with recent stay in a convention, cruise or hotel; Relative bradycardia, GI symptoms, confusion/AMS, lethargy. May have hyponatremia (SIADH)

Bordetella Pertussis- Cough >2 weeks with whoop or post-tussive vomiting

HIV/AIDs patients- M. Tuberculosis, Pneumocystitis Jiroveci, or CMV

Chlamydia Pneumonia patients have a stoccato cough, seen in infants primarily.

Anthrax- widening of the mediastinum

Exposure to birds? Chlamydia Psittaci

Travel to desert or SW California/Arizona? Coccidiodmycosis

Spelunking or Travel to the Midwest Ohio/Mississippi? Histoplasmosis

Presentation:
Fever, chills,productive cough, tachypnea, tachycardia, dyspnea, pleuritic CP (pain on inspiration)
Elderly, DM, and infants may have atypical symptoms

PE:
Rales, Rhonci, Dullness to percussion, Increased Tactile Fremitus, Positive egophony/broncophony/whispered pectoriloquy.

Dx:
Presence of infiltrated on CXR
CBC (~WBC> 15,000), CMP, Sputum Gram stain and culture
Mycoplasma serology

Admission Criteria- CURB 65
Confusion
Uremia (BUN>20 mg/dL)
Respiratory Rate (>30 min); Hypoxemia O2 sat < 90%
BP low (<90 sys <60 dias)
Age >65

Tx:
Outpatient with no Co-Morbidities or risk of drug resistance:
Macrolide (azithromycin, erythromycin), or
Doxycycline if not pregnant and at high risk for QT prolongation

Outpatient with Co-Morbidities, use of antibiotics within the last 3 months or other drug resistance risk factors:
Respiratory Fluoroquinolone (Levofloxacin 750 mg), or
A beta-lactem like high dose Amoxicillin, Augmentin, Ceftriaxone PLUS a Macrolide (or Doxycycline if at high risk for QT prolongation)

Inpatient, not ICU:
Respiratory Fluoroquinolone, or
A Beta Lactem PLUS Macrolide (doxycycline)

Inpatient ICU
Antipneumococcal Beta-Lactem (cefotaxime, ceftriaxone, ampicillin-sulbactem (unasyn)) PLUS Azythromycin, or
Antipneumococcal Beta-Lactem (cefotaxime, ceftriaxone, ampicillin-sulbactem (unasyn)) PLUS Respiratory Fluoroquinolone (Levofloxacin 750 mg), or
For PCN allergic patients, a respiratory fluoroquinolone PLUS aztreonam

Pseudomonas patients consider zosyn, plus levofloxacin

CA-MRSA infection add Vancomycin or Linezolid

Mycoplasma Pneumonia with a Macrolide

Patient Education:
Patient should begin to improve within 48-72 hrs on antibiotics if notor worsening they need to follow up
Supportive care- antipyretics, fluids
Causes acute respiratory tract illness in persons of all ages
Almost all children are infected by 2 yo, reinfection common
Most common cause of lower respiratory tract infection (LRTI)
The clinical manifestations vary with age, health status, and whether the infection is primary or secondary.
November - April, peak in January-February

Transmission:
Direct contact
Primarily by inoculation of nasopharyngeal or ocular mucous membranes with virus-containing secretions or fomites
Large aerosol droplets
RSV can survive several hours on hands, fomites
Hand washing - important in prevention
Incubation - 4 to 6 days (range 2 to 8 days)
Immunity - infection does not provide immunity

Clinical manifestations:
Depends on age, health status
Infants and young children
Lower respiratory tract infection (LRTI)
Bronchiolitis
Pneumonia
Older children (and adults)
Upper respiratory tract infection, or
Tracheobronchitis
Comorbid bacterial infection

Diagnosis:
Clinical
Age < 12 months with LRTI, Winter Season, known RSV circulation
Laboratory
Analysis of respiratory secretions
Nasal wash - best yield
Nasopharyngeal swab or throat swab - adequate
Rapid assays - 90% sensitivity and specificity
PCR assay - FDA approved, detect multiple respiratory pathogens; alternative to culture; confirming the Rapid Assays

Management:
Self-limited disease
Hand washing
Prevention of transmission
Supportive care
Respiratory or fluid support
Hospitalization and respiratory support in infants with LRTI, bronchiolitis, pneumonia and O2 saturation< 90%

Pharmacotherapy:
No bronchodilators (no proven long term outcome improvement)
No corticosteroids (no proven efficacy)
Exception to this: bronchodilators and corticosteroids may be more effective in older children and adults, and must be used in patients with asthma
Ribavirin (Anti-HCV) not indicated in children with RSV
Acute respiratory illness caused by Influenza A or B that mainly occurs in the winter.

Transmission:
Acquisition via large particle droplets requires close contact with an infected individual.
Typical incubation period is 1-4 days (average 2 days)

Presentation:
Influenza characteristically begins with abrupt onset of fever, HA, myalgia and malaise.
These symptoms are accompanied by symptoms of respiratory infection such as nonproductive cough, sore throat, and nasal discharge.
Fever usually ranges from 100.4 to 104 F but can get up to 106 F.
GI symptoms such as vomiting, diarrhea, are usually part of influenza in children but not common in adults.

PE:
Mild LAD may be present
Patient may appear hot and flushed
Oropharyngeal erythematous

Dx:
Leukocytes may be elevated but may not be early on.
Rapid Antigen Tests: Immunoassays that can identify influenza A or B viral nucleoprotein antigens in respiratory specimens. Results are qualitative (+/-)
**Testing only indicated if onset of symptoms is between 24-48 hrs!! Viral shedding peaks between 24-48 hrs of illness and then rapidly declines. Little or no replicable load can be detected around 5 to 10 days in immunocompetent hosts.
Nucleic Acid Testing: Reverse-transcriptase polymerase chain reaction (PCR) is the most sensitive test for influenza. Yields results relatively fast and differentiates between Influenza A or B.

Tx:
Two classes of medications are available to treat influenza
1. Neuraminidase Inhibitors: Oseltamivir (Tami-flu, for patients over 2 weeks old), Zanamivir (for patients >7 yo and not for patients with chronic respiratory disease), and Peramivir (used IV for patients >18 yo who have been ill for under 2 days). These antivirals prevent the release of irons from the host cell. They are active against Influenza A and B!!
2. Adamantanes: Amantadine and Rimantadine are used to treat Influenza A; High levels of resistance and no longer used to treat influenza.
AKA whooping cough
A highly contagious respiratory illness caused by the bacteria Bordetella Pertussis
Incubation period is between 7 to 10 days

Presentation: Three phases
Catarrhal Phase- Lasting one to two weeks and characterized by nonspecific cold symptoms (generalized malaise, rhinorrhea, and mild cough). Diagnostic test are more accurate at this phase, however clinical suspicion rarely lead to pertussis due to nonspecific symptoms
Paroxysmal Phase- Begins during the second week and has the hallmark paroxysmal cough. A series of severe, vigorous coughs that occur during a single expiration. Following this a vigorous inspiration causes a "whooping" sound. Posttussive syncope or emesis is common.
Convalescent Phase- characterized by a general reduction in the frequency and severity of cough. It usually lasts one to two weeks but may be prolonged.

The total duration of all three phases is typically about three months.

Adolescents and Adults clinical manifestations of pertussis are often less severe than in infants and in children. Prolonged cough may be the only symptom in this community. Other symptoms of sputum production, sweating, coryza, and sore throat may also occur.

Prior infection or immunization attenuates the illness but neither confers lifelong immunity.

Diagnosis:
Lymphocytosis
Culture is necessary for diagnosis. Specimen must be collected by swab or aspiration from ciliated respiratory epithelium of the posterior nasopharynx where B. pertussis resides.
For patients with < 2 weeks of cough PCR is the diagnostic test of choice
For patients with >4 weeks of cough, only serology is useful.

Treatment:
Most individuals clear the infection without antibiotic treatment within 6 weeks.
Azithromycin 500 mg Day one, and then 250 mg BID days 2-5; plus Clarithromycin 500 mg BID x 7 Days.
or
Bactrim One DS Tab BID x 14 days
Reduction of O2 content in the blood.
PaO2 < 60 mmHg or O2 sat < 90%

Signs include tachypnea, alkalemia, cyanosis, agitation, and somnolence.

3 Mechanisms of Hypoxemia:
1. Diffusion Abnormalities- Alveolar membrane abnormalities or a reduction in the number of alveoli resulting in a reduction of surface area for gas exchange; i.e. fibrotic lung disease. Usually only evident during exercise. Normal blood spends 0.75 seconds in the pulmonary capillaries, if their is an abnormality in diffusion may need more time for diffusion and hypoxemia occurs
2. V/Q mismatch-
A) R to L shunting occurs when blood goes from right side of the heart to the left without opportunity for gas exchange. This R-to-L shunting can be anatomical or physiologic. Shunting occurs with perfusion without ventilation. This is the MCC of hypoxic respiratory failure in critically ill patients!! Causes of shunting are pneumonia, pulmonary edema, atelectasis, pulmonary hemorrhage, CHF.
B) Dead space ventilation causes include PE and low cardiac output
3. Hypoventilation: characterized by elevated CO2 and low O2. Causes a respiratory acidosis because CO2 is acidic. Gas exchange worsens during sleep resulting in morning HA, impaired sleep quality, fatigue, daytime somnolence, mental confusion. Causes include brainstem injury, trauma, infarction, depressant drugs like opiates, spinal cord trauma or tumor, nerve root injury, Nervous system trauma or motor neuron disease, respiratory muscle fatigue or malnutrition, airway obstruction or decreased chest wall compliance.

Treatment: Increase FiO2 (fraction of inspired air)
Mean pulmonary arterial pressure (PAP) >25 mmHg at rest!
High blood pressure in the pulmonary arteries causing the heart to work harder. This causes people to have trouble breathing and feel tired.

Signs and Symptoms:
Dyspnea with exertion, fatigue, weakness, angina, syncope, and edema.

PE findings:
* Accentuated S2*
Left parasternal lift
Pan systolic murmur of tricuspid regurgitation, diastolic murmur of PR, right ventricular S3 and S4.
Cyanosis
Signs of right sided heart failure
Lung sounds are usually normal

EKG:
Demonstrates signs of RVH such as tall right precordial R waves, right axis deviation (lead 1 QRS down and AVF QRS up) and right ventricular strain in V1 and lead 2.
Possible RBBB

CXR:
Right Ventricular hypertrophy will show as a prominent right heart border
Prominent pulmonary arteries on radiograph.

Classification of PHTN:
1. Pulmonary arterial hypertension (PAP >25 mmHg and PCWP <15 mmHg)
a. Idiopathic (iPAH)
b. Familial (fPAH)
c. Connective tissue disorder
d. Congenital systemic-to-pulmonary shunts
e. Portal HTN
f. Drugs and Toxins
g. HIV infection
2. Pulmonary HTN with Left Ventricular Disease (PAP<25 mmHg and PCWP >15 mmHg)
a. Left sided valvular heart disease
b. Left sided or ventricular heart disease
3. Pulmonary HTN with Lung Disease/ and or Hypoxemia
a. COPD
b. Interstitial Lung Disease
c. Sleep Disordered breathing
4. Pulmonary HTN due to chronic thrombotic and or embolic disease (CTEPH)

Dx:
Blood test, HIV test, Abdominal Ultrasound, Exercise Capacity with a 6 Min Walk Test/stress echo
**Right heart catheterization with vasoreactivity is the GOLD STANDARD of Dx!!

Treatment:
*iPAH will usually have a positive vasoreactivity response and then can be given calcium channel blockers long-term

• Diuretics for right ventricular failure.
• Oxygen if hypoxemic.
• Avoid pregnancy
- the hemodynamic changes pregnancy induces are dangerous in PAH, and some PAH drugs are teratogenic.
• Get regular aerobic exercise (may need medical supervision).
• Influenza and pneumococcal vaccinations.
• If Idiopathic PAH, consider anticoagulation with warfarin.
• Refer the patient to a pulmonologist specializing in PAH for treatment
- The disease severity and the patient's symptoms will determine treatment (PO ambrisentan/sildenafil vs INH ilioprost vs continuous IV epoprostenol or SC treprostinil vasodilator treatments)
Occurs when a collection of fluid occurs in the potential space between the parietal and visceral pleuras.

Pathophysiology:
1. Increased pleural fluid formation is the MCC
- Elevation of hydrostatic pressure
- Decreased plasma oncotic pressure
- Increased capillary permeability
2. Decreased pleural fluid absorption
- lymphatic obstruction
-elevation of systemic venous pressure resulting in impaired lymph drainage
3. Both

Transudative Effusions:
-Elevation of hydrostatic pressure (as in CHF)
-Decreased plasma oncotic pressure (as in Cirrhosis, and Nephrotic syndrome)

Exudative Effusions:
- Increased Capillary permeability (as in Neoplasm or Infection)

Symptoms:
-dyspnea
-nonproductive cough
-pleuritic pain
-symptoms of the underlying disease

PE:
-diminished or absent breath sounds
-reduced tactile fremitus
-dullness to percussion
-asymmetric thoracic expansion, with lagging expansion on the affected side

CXR: plain film is diagnostic imaging method of choice
-Blunting of the costophragmatic angle
-Free pleural fluid gravitates toward the dependent portion of the lung
-A lateral decubitus film (obtained with the patient lying on their side, effusion side down, with a cross table shoot through technique) can visualise small amounts of fluid layering against the dependent parietal pleura.
- Mediastinal shift can occur away from the side of the pleural effusions

Treatment-
-Thoracocentesis diagnostic and potentially therapeutic
Fluid is evaluated for total protein, glucose, WBC count, LDH, pH, bacteria, gram stain, AFB, cultures, and cytology
*Limit fluid removal to 1000 to 1500 mL at a time due to possibility of pulmonary edema in expanded lung.
Current Acute Tx Anticoagulants for PE:
• Unfractionated Heparin - Lab Monitor PTT and Route is IV
• LMWH- No lab monitoring and given SC route
o Dalteparin
o Enoxaparin
o Tinzaparin
• Factor Xa Inhibitor- No lab monitoring and given SC route
o Fondaparinux
• Direct thrombin inhibitor- No lab monitoring and given PO route
o Rivaroxaban

Anticoagulation:
*It is the mainstay of treatment for PE by preventing recurrent PE's
• Initiate early- LMWH or Fondaparinux is preferred over Unfractionated heparin or Rivaroxaban
• Warfarin should be started the same day
• Overlap heparin and warfarin for at least 5 days and only stop heparin once the INR is 2.0-3.0 for at least 24 hrs

Advanced VTE treatment for Massive PE patients (i.e. saddle embolus):
• Anticoagulation + Systemic Thrombolysis with TPA IV 100mg x 2 hours
o Make sure there are no CI for tPA
• Anticoagulation + Catheter-based reperfusion for PE
• Anticoagulation + Surgical embolectomy
• IVC Filter for patients for anticoagulation therapy (tPA) or for recurrent PE

Current Long-Term Oral Anticoagulation Options in PE (cannot be used in pregnancy):
*Vitamin K Antagonist (VKA):
Warfarin (Coumadin) -
Cheap & well studied
Must be monitored with PT/INR (multiple food and drug interactions, Narrow therapeutic index, genetic variation in metabolism)
Delayed onset (must start/overlap with parenteral anticoagulant)
Reversal with vitamin K is slow (may require FFP if severe bleeding)

*Factor Xa Inhibitor:
Rivaroxaban (Xarelto)-
Expensive and not well studied yet (recent FDA approval)
Fixed dose and does not require laboratory monitoring
Lower bleeding risk than coumadin
Quick onset (may be used immediately for acute PE)
Short half-life
No antidote for reversal, but discontinuing drug may be enough to control bleeding
Not for use in patients with a creatinine clearance <30 mL/min or significant hepatic impairment

*Direct Thrombin Inhibitor:
•Dabigatran (Pradaxa) -
•Recently FDA approved for treating deep vein thrombosis (DVT) and pulmonary embolism (PE) in patients who have been treated with a parenteral anticoagulant for five to 10 days (even though this drug has a rapid onset).
• Expensive and not well studied yet (recent FDA approval)
• Fixed dose and does not require laboratory monitoring
• Not for use in patients with a creatinine clearance <30 mL/min
•Pregnancy Category C
• Short half-life
• No antidote for reversal, but discontinuing drug may be enough to control bleeding


Special considerations:
Patients who require long-term treatment with LMWH
Pregnant patients
Cancer patients
• Exposures
- Mining
- Milling
- Manufacture of asbestos products
- Shipbuilding & other construction trades-pipefitting, boilermaking
- Manufacturing of safety garments, filler for plastic material & friction materials (brake & clutch linings)
• Many houses / offices still contain building materials with asbestos, particularly insulation, so care must be taken when doing remodeling or reconstruction
• Along with work exposures in these areas bystander exposure(e.g., spouse )can be responsible for some asbestos related lung diseases

Asbestos fibers:
• Asbestos fiber becomes coated with iron & calcium
• Often referred to as a "ferruginous body" as seen here with an iron stain

Asbestos:
• Range of respiratory diseases have been associated with asbestos exposure
• Asbestosis can develop after 10 years of exposure & no specific therapy is available

Major Health Effects from Asbestos Exposure:
• Pulmonary Fibrosis(Asbestosis)
- Diffuse interstitial fibrosing disease of lung
- Related to intensity & duration of exposure usually requiring > 10 years of moderate to severe exposure
- PFT's show restrictive pattern & reduced diffusing capacity for CO(DLCO) on PFT
• Pleural changes
- Plaques, effusions, & mesothelioma
• Cancers of respiratory tract, pleura, & peritoneum
- Bronchogenic carcinoma
- Mesothelioma
• Lung Cancer
- Some risk with asbestos exposure alone; but smoking & asbestos together greatly increase risk.

Fibrous pleural plaque:
• Pleural plaques indicate that asbestos exposure has occurred, but they are typically not symptomatic
• Seen here on pleural side of diaphragmatic leaves are several tan-white pleural plaques.
• Gross lesion typical for pneumoconioses, & asbestosis in particular

Asbestosis:
• CXR shows bilateral calcified pleural plaques consistent with asbestos-related pleural disease.
• Poorly defined linear & reticular abnormalities are seen in lower lobes bilaterally.
Pleural Plaque from


Asbestos and cancer:
• Excess frequency of lung cancer occurs 15 to 20 years after first asbestos exposure
• More commonly predisposes to bronchogenic carcinomas, increasing risk by a factor of 5
• Smoking increases lung cancer risk by a factor of 10
• Smokers with a history of asbestos exposure have a risk 50 fold greater likelihood of for developing bronchogenic lung cancer.
• Smoking increases risk of lung CA after asbestos exposure but does not alter risk of mesotheliomas which peaks 30 to 35 years after initial exposure
• Lung cancer is clearly associated with asbestos exposure, but does not typically present for at least 15 years post exposure.
• Lung cancer risk increases multiplicatively with cigarette smoking


Treatment:- Chronic interstitial lung diseases(e.g., asbestosis, CWP) not responsive to glucocorticosteroids
• Results from chronic exposure to inhaled silica particles.
• Occurs in mining, stone cutting, abrasive industries(e.g., stone, clay, glass & cement manufacturing), foundry work, blasting, tunneling, quarrying & farming

Pathophysiology:
• Exposure to free silica(crystalline quartz) induces a fibrogenic response when macrophages ingest crystals & secrete cytokines
• Result is production of many scattered nodular foci of collagen deposition in lung
• Acute & Chronic Forms

Silica Crystals in Lung:
• Bright white crystals of varying sizes
Acute silicosis:
• Heavy exposure over a relatively brief time period(as little as 10 months) can cause acute"
• Can be severe and progressive resulting rapidly fatal pulmonary fibrosis
• Whole lung lavage may be of some therapeutic benefit

Simple silicosis:
• Results from longer-term exposure
• Associated with small rounded opacities in upper lobes of lungs
• Calcification of hilar LN's can give characteristic "eggshell"appearance
• CXR commonly shows upper lung zone-predominant abnormalities characterized by multiple small nodular opacities in central lung tissue.

Chronic silicosis:
• Longer-term, less intense exposures associated with upper lobe fibrosis & hilar adenopathy > 15 years after exposure
• Fibrosis is nodular & may lead to pulmonary restriction & airflow obstruction
• Degree of exposure to silica & length of exposure determine amount of silicotic nodule formation & degree of restrictive lung disease
• CXR in a patient with silicosis shows variably sized, poorly defined nodules (arrows) predominating in upper lobes

Complicated silicosis:
• Progressive nodular fibrosis can result in masses > 1 cm in diameter
• When such masses become very large, term progressive massive fibrosis is used to describe condition
• Multiple silicotic nodules that have become confluent resulting in severe restrictive lung disease

Silicosis and increased risk of TB:
• Due to impaired cell- mediated immunity silicosis patients are at increased risk of TB, atypical mycobacterial infections & fungal infections
• Associate with higher than normal risk for TB(2- to 30-fold more often than coworkers without silicosis) & pts with chronic silicosis & positive PPD warrant anti-tuberculosis treatment

Silicone and increased risk of cancer:
• Silicosis increases risk for lung CA only about 2-fold (risk is increased when combined with exposure to tobacco smoke, diesel exhaust, or radon gas)

• Treatment: Supportive (there are no proven therapies)