• Work exposures?
• Baseline Pulmonary function- does it occur at rest??
• Associated symptoms? Dizziness, chest pain, wheezing, fever, syncope, cough, weight loss, chills, trauma, edema, orthopnea, Paroxsymal nocturnal dyspnea,
• Productive vs dry; how much sputum? What color sputum? Timing of cough?
• Nocturnal Cough? Asthma, CHF, and GERD
o Hemoptysis? MCC in U.S is acute bronchitis, The most common worldwide is Tb!
• Massive amounts >500 mL of blood is considered an Emergency! Common causes include lung cancer, lung cavities, Tb, Pulm hemorrhage, and bronchiectasis
• Always distinguish epitstaxis from hemoptysis!
o Dyspnea? If SOB is acute and not accompanied by CP think PTX, PE, pulmonary edema, and Pleural effusion; If SOB is chronic think of conditions such as COPD, pulmonary fibrosis, PHTN, and neuromuscular diseases
• Sx? Recent sx, May be PE, atelectasis, infection
• Meds? Bleomycin can cause Pulmonary Fibrosis, Amiodarone, Beta Blockers can cause Asthma or COPD exacerbation, ACE-I (dry hacking cough), Immunosuppressants
• Family Hx? Alpha 1 Anti-trypsin Deficiency looks like COPD, Cystic Fibrosis, Asthma
• Social Hx? Smoking?? Pack years. Recent Travel (TB)? Contact exposures, Work exposures (silica, asbestosis, coal), pets (birds), Allergies, Geographical location (Histoplasmosis is Mississppi Ohio River Valley & Coccidiomyocosis is California Arizona Valley), Spelunking (Cave diving)?
• 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
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
o Resonance is Normal!!!
o Hyper-resonance is seen in COPD, PTX
o Dullness in consolidation, lung mass, and pleural effusion
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
Effective inhaler usage
Avoid smoking or 2nd hand smoke
Avoid known allergens- vacuum, clean air filer, no carpets
Influenza and PSV23 Vaccinations recommended
For the treatment of asthma or COPD
Albuterol (Proair, proventil, ventolin)
Short-acting Beta-2 agonists or SABAs
Inhaled adrenergic agonists with beta-2 activity are the drugs of choice for mild asthma—(in patients showing only occasional, intermittent symptoms).
Direct-acting beta-2 agonists are potent bronchodilators that relax airway smooth muscle.
1. Quick-Relief: Most clinically useful beta-2 agonists have a rapid onset of action (5 to 30 minutes) and provide relief for four to six hours. They are used for symptomatic treatment of bronchospasm, providing quick relief of acute bronchoconstriction.
Adverse effects, (tachycardia, hyperglycemia, hypokalemia, & hypomagnesemia) are minimized with dosing via inhalation versus systemic routes.
ADRs: Paradoxical bronchospasm, hypokalemia, hypomagnesemia, in high doses.
In well-controlled asthma, SABA use should be infrequent (less than 2 times a week)
Tolerance (tachyphylaxis from receptor down-regulation) can occur with regular use.
All patients with asthma should be prescribed a quick relief inhaler and regularly assessed for appropriate inhaler technique. ("Show & Tell")
Beclomethasone (Beclonase AQ QVAR) for Asthma, COPD and Allergic rhinitis
Budesonide (Pulmicort, and Rhinocort) is for Asthma, COPS and Allergic rhinitis
Fluticasone (flonase and flovent) is for Allergic Rhinitis, Asthma, and COPD
Mometasone (Nasonex, asmanex) is for Allergic rhinitis and Asthma
Triamcinolone (Nasacort AQ) is for Allergic rhinitis
Actions on lung:
ICS do not directly affect the airway smooth muscle.
ICS therapy directly targets underlying airway inflammation by decreasing the inflammatory cascade (eosinophils, macrophages, and T lymphocytes), reversing mucosal edema, decreasing the permeability of capillaries, and inhibiting the release of inflammatory leukotrienes.
After several months of regular use, ICS reduce the hyper-responsiveness of the airway smooth muscle to a variety of bronchoconstrictor stimuli, such as allergens, irritants, cold air, and exercise.
*rinse mouth after steroid use
A pulmonary hamartoma is a benign neoplasm composed of cartilage, connective tissue, muscle, fat, and bone. It is one of the commonest benign tumours of the lung, and accounts for ~8% of all lung neoplasms and 6% of solitary pulmonary nodules.
Epidemiology: Patients usually present in the 4th and 5th decades of life and is very uncommon in children. There is a recognised male predilection ( M:F being ~2-3:1). Most lesions are diagnosed incidentally.
Clinical presentation: Pulmonary hamartomas are usually asymptomatic and found incidentally when imaging the chest for other reasons. It can occasionally present with haemoptysis, bronchial obstruction and cough (especially endobronchial types) 6.
Pathology: Hamartomas may be chondromatous or leiomyomatous (the former being more common) or a mixture. They are unencapsulated, lobulated tumours with connective tissue septa.
As with any hamartoma it is composed of tissues that normally constitute in the lung and bronchi. The tissue elements, although mature, are disorganized. On rare occasion, they contain principally fatty tissue, in which case they are called lipomatous hamartomas or endobronchial lipomas.
Location:The vast majority of pulmonary hamartomas are located peripherally within the lungs (> 90%), with endobronchial hamartomas representing only 1.4-10% of such lesions 10-11.
Typically, hamartomas manifest incidentally as solitary nodules in the periphery of the lung.
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
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
CT or PET scan
- Anterior Mediastinal Mass DDX- The 5 Ts→ thymoma, teratoma, thyroid tumor, terrible lymphoma, mesenchymal tumors (lipoma, and fibroma)
- Middle Mediastinal Mass- primary tumors of structures in this location: trachea, esophagus, aortic arch, and great vessels, PA and LN
- Posterior Mediastinal Mass- Neurogenic Mass like schwannomas, neurofibroma, neuroblastoma, ganglioneuroblastoma, ganglioneuroma
• Primarily found in the appendix, small bowel, rectum, bronchi, esophagus, stomach, colon, ovary, biliary tract, or pancreas
• Age most patients <40 yo
• Carcinoid syndrome symptoms - flushing, diarrhea, bronchospasm, hypotension.
- Symptoms are caused by action of serotonin, bradykinin, histamine produced by tumors arising from neuroendocrine cells.
• Labs: Elevated 24 hour urine 5-HIAA in pts with diarrhea or malabsorption
• Secrete a variety of biogenic amines, especially serotonin
• Carcinoid Syndrome
- Facial flushing
• Dx- CXR and CT scan
• Treatment- Surgical resection if the tumor is localized
• Chemotherapy for pts with unresectable or recurrent carcinoid tumors
• Control of clinical manifestations
• Diphenoxylate w/ atropine (Lomotil) for diarrhea
• H1 and H2 receptor agonists (ie benadryl + ranitidine) for flushing
• Bronchodilators (albuterol) for bronchospasm
• 1. Injury from a specific exposure
- Asbestos, Amiodarone, Moldy hay, Auto-immune-mediated disorder (RA) or unknown (IPF)
• 2. Immunopathologic response of lung to irritants causes an initial inflammation that heals by scar tissue formation
- Lung responds by imperfect repairing with increased interstitial tissue replacing normal capillaries, alveoli, & healthy interstitium
• 3. Extensive disruption of alveolar tissue, loss of functional alveoli
• 4. If irritant/disease is persistent, a chronic phase of disorder is seen causing disruption of pulmonary function & gas exchange
• 5. Larger airway can be involved in inflammatory process, leading to broncholitis obliterans & an organizing pneumonia (BOOP)
The lung is naturally exposed to repetitive injury from a variety of exogenous and endogenous stimuli.
Several local & systemic factors (e.g., fibroblasts, circulating fibrocytes, chemokines, growth factors, & clotting factors) contribute to tissue healing & functional recovery.
Dysregulation of this intricate network through genetic predisposition, autoimmune conditions, or superimposed diseases can lead to aberrant wound healing with the result of pulmonary fibrosis. Alternatively, excessive injury to lung may overwhelm even intact reparative mechanisms and lead to pulmonary fibrosis.
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
• 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
• 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)
• 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.
• 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
• 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)
• 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
• 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
Turkey handler's disease
Laboratory worker's hypersensitivity pneumonitis
Epoxy resin lung- epoxy resin fumes inhalation
• 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
• 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.
• 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
• 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
• Most common ILD in USA
• Highest incidence in African Americans & Northern Europeans
• Women > Men
• 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
• Elevated ESR & hypercalcemia (5% of pts)
• Angiotensin-converting enzyme levels (ACE) are elevated in 40-80% of patients with active disease
bilateral hilar adenopathy
• 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.
• 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
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
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)
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)
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
Fever, chills,productive cough, tachypnea, tachycardia, dyspnea, pleuritic CP (pain on inspiration)
Elderly, DM, and infants may have atypical symptoms
Rales, Rhonci, Dullness to percussion, Increased Tactile Fremitus, Positive egophony/broncophony/whispered pectoriloquy.
Presence of infiltrated on CXR
CBC (~WBC> 15,000), CMP, Sputum Gram stain and culture
Admission Criteria- CURB 65
Uremia (BUN>20 mg/dL)
Respiratory Rate (>30 min); Hypoxemia O2 sat < 90%
BP low (<90 sys <60 dias)
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)
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 should begin to improve within 48-72 hrs on antibiotics if notor worsening they need to follow up
Supportive care- antipyretics, fluids
• Lung abscess is a necrotizing lung infection characterized by a pus-filled cavitary lesion
• Symptoms are persistent cough, fever, sweats, and weight loss
• Alcoholic and stroke patients, the same risk factors as in aspiration pneumonia
• Patients with very poor dentition; Peridontal disease
Pathogens- Mixed anaerobes and aerobes most commonly seen
Other conditions may lead to lung abscess development:
• Necrotizing bacterial pneumonias caused by S. Aureus, Klebsiella Pneum, or other gram - bacilli
• A result of bronchial obstruction caused by tumors, FB, or bronchial stenosis
• Pulmonary tuberculosis, fungal infection, or actinomyocosis often leads to cavity formation
• In the immunocompromised host, Nocardia and other opportunistic infections may also produce cavitations
• Primarily with CXR
• Anaerobic coverage with a Beta-Lactem or beta-lactemase inhibitor, Clindamycin
Inflammation of the bronchi due to URI
Generally caused by a virus- the usual viral causes include Influenza A, Influenza B, Adenovirus. Parainfluenza, Coronavirus 1-3, rhinovirus, RSV.
Other pathogens, although less common include, Strep. Pneumo, M Catarrhalis, H Influenzae, Mycoplasma Pneumonia, Chlamydia Pneumonia, and Bordetella Pertussis.
Cough lasting >5 days which may be productive. Cough should only last up to 3 weeks
Cold symptoms of nasal discharge, sore throat
Fever is an unusual sign in patients with acute bronchitis and suggest the presence of influenza or pneumonia.
PE: Signs of consolidation should not be present! But wheezing may be heard due to bronchospasms. Vital signs should be normal.
DX: Mostly based on Hx and PE
TX: Treat symptomatically unless you suspect bacterial cause.
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
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
Depends on age, health status
Infants and young children
Lower respiratory tract infection (LRTI)
Older children (and adults)
Upper respiratory tract infection, or
Comorbid bacterial infection
Age < 12 months with LRTI, Winter Season, known RSV circulation
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
Prevention of transmission
Respiratory or fluid support
Hospitalization and respiratory support in infants with LRTI, bronchiolitis, pneumonia and O2 saturation< 90%
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
Respiratory illness most commonly caused by Parainfluenza Virus (type 1 is the MC). May be caused by other virus such as influenza, measles, RSV.
The infection causes the larynx (voice box) to become swollen and the trachea (windpipe) to become blocked, and may affect the tubes in the lungs (bronchi). It is sometimes called laryngo-tracheo-bronchitis
Characterized by cough, hoarseness, inspiratory stridor ("seal bark/cough"). Slower onset. Moderate fever
Patient looks well, non toxic, and able to swallow
Most frequent in the fall and winter and seen in 3-36 months of age.
Is clinical, Imaging A/P chest or neck X-Ray shows "steeple sign." Note that this Xray finding can be seen in different phases of normal breathing in children.
Treatment depends on severity; May include Humidified O2, antipyretic, nebulizer racemic epinephrine, dexamtheasone and fluids.
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.
* Accentuated S2*
Left parasternal lift
Pan systolic murmur of tricuspid regurgitation, diastolic murmur of PR, right ventricular S3 and S4.
Signs of right sided heart failure
Lung sounds are usually normal
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.
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
b. Interstitial Lung Disease
c. Sleep Disordered breathing
4. Pulmonary HTN due to chronic thrombotic and or embolic disease (CTEPH)
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!!
*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.
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
-Elevation of hydrostatic pressure (as in CHF)
-Decreased plasma oncotic pressure (as in Cirrhosis, and Nephrotic syndrome)
- Increased Capillary permeability (as in Neoplasm or Infection)
-symptoms of the underlying disease
-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
-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.
Malignancy (usually lung, breast or lymphoma), infection, trauma, connective tissue disorder, PE, Uremia, Asbestosis, Pancreatitis, Hemothorax, Post CABG.
Fluid Analysis characteristics:
Pleural to serum protein ratio >0.5
Pleural to serum LDH ratio > 0.6
LDH > 200 IU
Total Protein > 3 g/dL
Spontaneous aka Primary
Secondary (underlying cause such as COPD, Asthma, Cystic Fibrosis, Interstitial lung ds, Infection, Iatrogenic or trauma)
Sudden SOB, sharp CP, Tall male, <40 yo, Smokers
Absence or decreased breath sounds on affected side
and Hyperresonance to percussion
Tactile fremitus will be decreased on affected side
shows visceral pleural lines in CXR
hyperlucency or decreased lung markings
mediastinal shift indicates a tension pneumothorax
O2, Needle aspiration or Chest tube placement
-Pigtail catheter with Heimlich valve or 16 gauge chest tube placement with drainage system.
Malignancy, immobilization, air travel, surgery within 3 months, pre-existing respiratory disease, prior history of Venous thromboembolism, chronic heart disease, stroke.
In women obesity, OCP, pregnancy, HRT, cigarette use, HTN
LE thrombus is MC than UE
Decrease in 50-60% perfusion; Major pathologic effect is V/Q mismatch
Symptoms include dyspnea, tachypnea, pleuritic pain, tachycardia
Leg edema, erythema, tenderness, palpable cord
Syncope or sudden death with massive PE
ABG may be normal or show low CO2 and O2.
Increased A-a gradient
Diagnostic studies for PE:
Pulmonary Angiography* is the gold std.
ABGs, EKGs (S1Q3T3, tachycardia), CXR, Echo, Doppler U/S, cardiac enzymes and Pro-BNP
PERC Criteria to rule out PE
a lage S in lead 1, a Q in lead 3, and an inverted T wave in lead 3.
Sinus Tachycardia is actually the MC EKG finding in a PE.
Westermark's sign= dilation of the pulmonary vasculature proximal to where the embolism is along with collapse of the distal vessels, often with a sharp cut off
Hampton's Hump= pleural based opacities with medial margins that are convexed
Lovely, Meaning Normal CXR
Acute treatment forLow risk patients is Anticoagulation Alone
High risk patients include anticoagulation + lysis/embolectomy
1. start FiO2 low at 28% and slowly increase
2. CPAP for Hypoxemia @ 6-10 cm H20 (good for CHF and Pulmonary Edema)
3. BiPAP for Hypoxemia (ePAP @ 4-6 cm H2O) and Hypercapnia (iPAP @ 8-10 cm H2O)
-Inspiration iPAP < CO2
-Expiration ePAP > O2
*Increase gradually by 2-3 cm H2O
*Max is 20-25 cm H2O
*Remember if iPAP and ePAP are equal than CPAP results not BiPAP.
*Must monitor BP! CPAP and EPAP decreased preload via compression of venous return.
Respiratory arrest, unable to fit mask, uncontrolled vomiting, GI bleeding, Facial Trauma/burns, Airway obstruction, AMS, severe acidosis, pneumothorax, risk of aspiration, epistaxis, pneumomediastinum
Unstable, Pregnancy, Recent upper airway or GI sx, excessive secretions
Complications of N/V:
gastric distension, barotrauma, claustrophobia, pressure necrosis of skin.
- 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 fiber becomes coated with iron & calcium
• Often referred to as a "ferruginous body" as seen here with an iron stain
• 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
• 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
• 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
• 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
• 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
• 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.
• 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
• 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)
Acute, diffuse inflammatory lung injury that leads to increased pulmonary vascular permeability, increased lung weight, and a loss of aerated tissue.
Clinical hallmarks of ARDS are hypoxemia and bilateral radiographic opacities, while the pathological hallmark is diffuse alveolar damage.
Alveolar damage- alveolar edema with or without focal hemorrhage, acute inflammation of the alveolar walls, and hyaline membranes.
Clinical features of ARDS usually appear within 6-72 hrs of an inciting event and worsen rapidly.
-cyanosis or hypoxemia
-respiratory distress is usually evident, including tachycardia, tachypnea, diaphoresis, and use of accessory muscles of respiration.
- cough and CP may also be present
- clinical features of the precipitating event (i.e. sepsis)
bilateral alveolar infiltrates with pulmonary edema
*Cardiogenic pulmonary edema is the primary ddx that needs to be excluded because it is common and can be clinically indistinguishable from ARDS
- absence of S3, S4 gallop, JVD
- A BNP < 100 favors ARDS
High concentration of supplemental O2
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