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The Alveolararterial gradient (Aa gradient), is a measure of the difference between the
alveolar concentration (A) of oxygen and the arterial (a) concentration of oxygen. It is used
in diagnosing the source of hypoxemia .
The equation for calculating the Aa gradient is:

A-a gradient = PAO2 - PaO2

Where: FiO2 is fraction of inspired oxygen.
PAO2 = alveolar PO2 (calculated from the alveolar gas equation)
PAO2 = ( FiO2 * (Patm=760 - PH2O=47)) - (PaCO2 / 0.8)
PaO2 = arterial PO2 (measured in arterial blood)
On room air ( FiO2=0.21, or 21% ), at sea level ( Patm=760mmHg , P H2O=47 mmHg) assuming
100% humidity in the alveoli, a simplified version of the equation is:
Disorders that can cause hypoxemia can be broken down into 4 categories:
Hypoventilation,Decrease in inspired oxygen,Shunting,and V/Q mismatch. By ABG analysis
and A-a gradient calculation one can determine wether administering 100% oxygen leads to
improvement, and one can determine the specifiv type of hypoxemia plaguing a particular
The characteristics of each category of hypoxemia are as follows:
1)Hypoventilation presents with an elevated PaCO2 with a normal A-a gradient
2)Low inspired Oxygen presents with a normal PaCO2 and normal A-a gradient
3)Shunting presents with a normal PaCO2 and elevated A-a gradient that doesn not correct with
administration of 100% oxygen
4)V/Q mismatch presents with a normal PaCO2 and elevated A-a gradient that does correct with
100% oxygen.
A normal A-a gradient is <15 in a young person. Values increase with age, but an A-a gradient >30
is considered elevated regardless of age.
Increased A-a Gradient
1. V/Q Mismatch
1. Congestive Heart Failure
2. Adult Respiratory Distress Syndrome (ARDS)
3. Pneumonia
4. Atelectasis
5. Exacerbation of Bronchial asthma
2. Pulmonary shunt
1. Pulmonary Embolism
2. Patent Foramen Ovale
3. Atrial Septal Defect
3. Alveolar hypoventilation
1. Interstitial Lung Disease
2. Normal A-a Gradient
1. Hypoventilation
1. Neuromuscular disorders
2. Central nervous system disorder
2. Low inspired FIO2 (e.g. high altitude)

Normal values of ABG

Normal Respiratory Rate: 12-22/min

pH 7.35-7.45 ...[H+] 36-44 nmol/L Normal DLCO : 80-120%

PCO2 33-45 mm Hg ... 4.4-5.9 kPa
PO2 75-105 mm Hg ... 10.0-14.0 kPa
Important Definitions in Pulmonology:

Tidal volume: volume of air moved during normal respiration.

Total lung capacity: vol of air in lungs after maximal inspiration.
Vital capacity: maximum volume of air that can be exhaled after maximal inspiration.
Residual volume: volume of air remaining at the end of maximum exhalation.
Compliance: reflects ease with which ventilatory work may be performed--function of
tissue elasticity. Normal compliance is > 100 ml/cm. Compliance is normally used to guide
increases in PEEP .Compliance= Tidal volume (volume of normal expiration and inspiration) /
(Peak inspiratory pressure (obtained from ventilator) - PEEP)
Ventialation is defined as the product of the respiratory rate nd the tidal volume(should be
6ml/kg).Respiratory alkalosis results from hyperventilation(due to washing out CO2).In
mechanically ventilated patients with respiratory alkalosis in the setting of an appropriate
tidal volume,the respiratory rate should be lowered.Reductions in tidal volume can trigger
an increased ventilatory rate,potentially exacerbating the situation.
its common after surgery in smokers. Bronchoscopy needs to be done to remove mucus
Plug.Pt prestns with tachycardia, tachypnea, low grade fever. Once Bronchopscopy is done,
cxr is repeatd and coughing is encouraged.
Beware that GERD presents with Asthma-like symptoms occuring only at night and not
during the day (look for history of obesity,worse condition after meals and lying
down,medication,heartburn,water brash,chronic cough and hoarseness ...) so advise such
patient to adopt anti-GERD lifestyle and receive a trial of PPI.A 24hr PH recording is the
most specific test for acidic gastroesophageal reflux.It is usually employed to diagnose the
cause of chest pain or supra-esophageal complications of GERD in patients with negative
Wegner's granulomatosis ( granulomatois+polyangiitis) is defined clinically as the triad of
systemic vasculitis of small and medium sized arteries with peak incidence among
caucasians 30-50 years of age,upper and lower airway granulomatous
inflammation(bloody/purulent nasal discharge,oral ulcers,and sinusitis,dyspnea,cough and
hemoptysis),and glomerulonephritis( rapidly progressive-microscopic hemturia and red
blood cell casts).Systemic symptoms like fever,weight loss,fatigue,Nasal Cartilage
Destruction and vasculitic cutaneous lesions(tender nodules,palpable purpura,ulcerations)are
common .Diagnosis is made by c-ANCA positivity and tissue biopsy.Treatment involves
high dose corticosteroids and cytotoxic agents.
A non-productive cough is observed in 5-20% of patients receiving ACEI. It is caused by an
accumulation of kinins,and possible by the activation of the arachidonic acid
pathway.Simple discontinuation of the drug should precede any diagnostic testing in patients
with chronic dry cough who are taking ACEI.
ARDS most often develops in the clinical settings of sepsis(most
common),pneumonia,aspiration,toxic ingestions,trauma, and/or burns.The pathophysiology
of ARDS involves release of inflammatory mediators as a result of local or distant tissue
injury.These mediators cause alveolar damage,increased alveolar capillary permeability,and
leakage of proteinaceous fluid into the alveoli.
Clinically, this leads to the acute onset of tacypnea,tachycardia,fever,and dyspnea.ABG reveals
hypoxemia and CXR reveals bilateral alveolar infiltrates.The differential diagnosis for hypxemia
and bilateral infiltrates on CXR also includes cardiogenic pulmonary edema.An important
diagnostic tool for differentiating ARDS from cardiogenic pulmonary edema is measurment of the
pulmonary capillary wedge pressure(PCWP).
A PCWP <18mmHg suggests ARDS, while a value >18mmHg suggests cardiogenic pulmonary
edema(impaired left ventricular function).In ARDS: acute onset of respiratory distress in the setting

a of a predisposing condition,PaO2/FiO2 ratio<200,bilateral infiltrates on CXR and a normal

PCWP.( Pulmonary arterial pressure is variable in patients with ARDS, and pulmonary HTN
occurs in 25% secondary to hypoxic vasoconstriction and destruction of lung parenchyma).
ARDS causes hypoxemia refractory to high inspired oxygen concentrations.Adequate
oxygenation in ARDS often requires positive end expiratory pressure(PEEP) delivered via
mechanical ventialtion;thus,preventing alveolar collapse at the end of expiration.Increasing FiO2 is
contraindicated due to the risk of oxygen toxicity and the goal of managing all ventialted patients
should be to keep FiO2 below 40% at all times.Do not increase tidal volume (>6ml/kg) as it might
lead to barotrauma and do not increase respiratory rate even if it washes out CO2 since in ARDS the
focus is on managing hypoxemia and not hypercapnia.
Summary: In ARDS,mechanical ventilation with low tidal volumes and PEEP can improve
oxygenation.Potential complications of PEEP include barotrauma,tension pneumothorax,
alveolar damage and hypotension.

CHF exacerbation ( look for risk factors as uncrontrolled HTN,smoking, Coronary artery
disease,COPD,...)can cause tchypnea as left ventricular dysfucntion allows fluid to pool in
the lungs,causing a pleural effusion and hypoxemia due to reduced ventialtion.Tachypnea
causes hypocapnia and respiratory alkalosis. Exam typically shows signs of fluid
overload,S3and S4 gallops,cardiomegaly and bibasilar crackles in the lungs(due to pleural
effusions from CHF).More specific testing for CHF would inculde assessment of the B-type
natriuretic peptide(BNP) and the pulmonary capillary wedge pressure.
In COPD exacerbation, examination typically shows widespread bilateral wheezes and
ABG findings include respiratory acidosis and hypoxia.
The most common cause of pulmonary complications in patients with systemic sclerosis is
interstitial fibrosis.
Cor pulomnale is a term of right sided heart failure most commonly due to pulmonary
disease.Signs of right sided heart failure inculde:jugular venous distension,right sided
S3,right ventricular heave,hepatomegaly,ascites and dependant edema.A chest radiograph
may reveal a prominent right ventricle and pulmonary artery,in addition to any lung disease
that can be visualized.
Pulmonary emboli classically presents with sudden onset pleuritic chest pain( pain
worsened on inspiration),cough,dyspnea,and hemoptysis.PE may arise from the right
heart,pelvic veins,or upper extremity veins,the deep veins of the lower extremities are the
most frequent source.Lower extremity deep vein thrombosis is divided into two categories:
proximal vein thrombosis(above the knee and includes iliac/femoral/popliteal veins)-Calf
vein thrombosis.Proximal deep veins account for more than 90% of acute Pes.Patients have
Hypoxemia and respiratory alkalosis(low PaCO2) with a widended A-a gradient.Chest
CT shows wedge-shaped infarction known as Hamptons Hump ( pathognomonic
feature). Lung cancer would show a rounded mass on CT.
Pneumothroax typically presents with acute onset pleuritic chest pain and dyspnea when it
is symptomatic.Physical Examination reveals hyperreasonance to percussion,diminished
tactile and vocal fremitus,and decreased or absent breath sounds in the affected area.
Pulmonary embolism should be suspected in all patients at risk for deep vein
thrombosis(DVT)(prolonged immobility, OCP use, obesity,s moking, recent abdominal or
orthopedic surgery/ trauma, occult malignancy and other hypercoagulable conditions
including sickle cell trait and Factor V Leinden Deficiency-most common
hypercoagulability and thromboses predisposing factor) who present with acute onset
tachypnea,dyspnea,and chest pain(pleuritic in nature).Pulmonary Angiography is Gold
Standard but the most commonly used and the diagnostic chest of choice is Helical CT of
the chest ( V/Q test could be used sometimes when contrast angiography is contraindicated
as in renal failure patients."Mismatched perfusion defect" which means an area of
perfusion defect without ventilation defect,is characteristic but it is found in <50% of the
patients).A negative D-Dimer is very helpful in excluding the diagnosis of pulmoary venous

thromboembolism in low- risk patient; however, a positive D-Dimer is far from diagnostic
and must be followed by more specific studies.Pleural effusions associated with pulmonary
embolism are usually small and almost always exudative.
In order to differentiate the effusion as exudate or transudate, the classic Light Criteria
classify an exudate as having at least one of the following:
1) Pleural fluid protein/serum protein ratio>0.5
2)Pleural fluid LDH/serum LDH ratio>0.6
3)Pleural fluid LDH > 2/3 of the upper limit of normal for serum LDH.( Exudative>200IU/ml
and Transudative<200IU/ml)
Exudates are caused by increased capillary permeability(infections,autoimmune disease and
neoplasm) while transudates are caused by increased hydrostatic(as CHF) or decreased oncotic
pressure( as in liver failure).Exudates has more protein content than transudates.
***Pleural effusion in Congestive Heart Failure are typically bilateral,symmetrical,and caused by increased
intravascular hydrostatic pressure( in hypoalbuminemia effucsion is due to decreased intravascular oncotic
pressure).Effusions are transudative with few RBCs and WBCs and a glucose concentration equal to that of serum.
Malignancy in lungs or pleural space can cause turbid or bloody exudates with lymphocte predominance of the WBC
fraction and many RBCs and variable glucose concentration depending on the tumor burden but approximates serum
value in early effusions. Aspiration pneumonia will initially cause an exudate due to chemical pneumonitis which can
progress into pulmonary abscess and empyema if left untreated.***

Parapneumonic effusion usually occur from pneumonia.The fluid may be sterile in the intial
stages and resolve with antibiotic therapy;however, in few cases the patient will ontinue to
have elevated temperatures,pleuritic chest pain, and dyspnea.CT scan will identify the fluid
collection.The fluid may be aspirated to determine if empyema has set in.The aspirated fluid
should always be analyzed for protein content,gram stain,cell count,cytology(to rule out
malignancy),and glucose levels( low in RA,TB,Empyema,Malignancy, and Esophageal
rupture).When PH of pleural fluid is <7.2 or Glucose Content <60mg/dl or Positive
Gram Stain=>Drain the infected pleural space with a chest tube( in other words
thoracostomy indication).
Low glucose concentration in exudative effusions is due to the high metabolic activity of
leukocytes within the pleural fluid.(<30mg/dl suggest empyema/rheumatic effusion- 3050mg/dl indicates an effusion due to malignancy/lupus/TB/esophageal rupture)
Management of suspected Pulmonary Embolism:

Acute DVT should be treated with a combination of warfarin and heparin for the first 5 days.After 5
days, the heparin may be discontinued if the patient's INR is theraputic.Warfarin should be
continued for at least 6 months in most patients with a first time clot.A progressing clot in a patient
with a sub-theraputic INR requires bridging heparin until the INR is theraputic.
A massive PE can cause RV dilatation and failure that results in
hypotension,tahycardia,syncope,and shortness of breath.Hemodynamic instability is an absolute
indication, and RV strain a relative indication, for thrombolytics in the setting of PE.

Causes of Pleural Effusion(V.V.IMP):



Heart Failure


Nephrotic Syndrome

Paraneumonic Effusions(pneumonia)

Liver Disease


Pulmonary Embolism

Pulmonary Embolism


Collagen Vascular Disease(RA,SLE)

Drug induced

A pleural effusion presentswith abscence of lung sounds and dullness to percussion at the involved
lung base(s). Undiagnosed pleural effusion is best evaluated with thoracocentesis,except in patients
with clear-cut evidence of CHF where a trial of diuretics is warranted.
Pulmonary Hypertension:
It is defined as a mean pulmonary arterial pressure>25mmHg at rest or 30mmHg with excercise.It is
seen following the narrowing of the precapillary vessels, the loss of the pulmonary capillary bed,or
passive backpressure from the post capillary vessels from any cause. It can be classified as follows:
1. Pulmonary hypertension asscociated with disorders of the respiratory system,hypoxemia,or
2. Pulomnary hypertension due to pulmonary venous hypertension(Left Vtricular Heart
disease,Mitral valve disease or pulmonary veno-occlusive disease).
3. Pulmonary hypertension following chronic thromboembolic disease.
4. Pulmonary arterial hypertension(1ry pulmonary hypertension,Hypertension associated with
5. Pulmonary hypertension due to disorders directly affecting the pulmonary
vasculature(pulmonary capillary hemangiomatosis).
Clinical Features are the same regardless of the underlying cause.It includes Dyspnea,weakness,and
fatigue( early complaints), which may be followed by chest pain,hemoptysis,syncope,or hoarseness(
due to compression of recurrent laryngeal nerve).RVF develops late in the disease and manifests
with RV heave,JVD,tender hepatomegaly,ascites,edema..CXR would show enlargement of the
pulmonary arteries with rapid tapering of the dital vessels(pruning) and enlargement of the right
ventricle.An EKG may show right axis deviation,which is secondary to right ventricular strain and
hypertophy ue to pulmonary hypertension.Untreated pulmonary hypertension would eventually lead
to Cor-pulmonale.
Germ cell tumors typically affect young patients especially males and display aggressive
biologic behavior.Nonseminomatous germ cell tumors typically produce both alpha-feto
protein(AFP) and human chorionic gonadotropin(B-HCG) as tumor markers.
Newer antipneumoccoccal quinolones,like levofloxacin or moxifloxacin, are the drugs of
first choice for inpatient treatment of CAP. For outpatient therapy,either azithromycin or
doxycycline( when macrolide resistance is suspected) can be used.
TMP/SMX is best inital treatment for and prophylaxis against pneumocystis
pneumonia(PCP).If there is toxicity, switch to clindamycin+primaquine or pentamidine.
Vancomycin is used for suspected methicillin resistant staphylococcus infection.This is often
seen in nosocomial pnemonia patients.
Clindamycin is used if there is a suspicion for aspiration pneumonia like in patients who had
a recent stroke,history of unconsciousness(heavy alcohol user),recent sedation for
Goodpasture's Disease affects the lungs causing couh,dyspnea,and hemoptysis and the
kidneys causing nephritic range proteinuria(<1.5g/day),acute renal failure,and dysmorphic
red cells/red cell casts on urinalysis. Systemic symptoms are uncommon. Diagnosis is made
by renal biopsy showing linear IgG antibodies to alpha-3 chain of type IV collagen which is
a protein expressed strongly on the glomerular and alveolar basement membrane.DLCO is

Glucocorticoids cause neutrophilia by increasing the bone marrow release and mobilizing
the marginated neutophil pool.Eosinophils and lymphocytes are decreased.
Recurrent pneumonia in the same anatomic location is a red flag for lung
cancer.Furthermore,smoking is the primary risk factor for bronchogenic carcinoma. When
lung cancer is suspected,CT scan of the chest is warranted. Bronchoscopic or Ct guided
biopsy may then be performed depending on whether the lesion has a peribronchial or
peripheral location.
Patients with HIV have a 10% per year risk of experiencing reactivation of tuberculosis
which manifests wth fever,night sweats,weight loss,fatigue,pleuritic chest pain,chronic
cough and hemoptysis.CXR findings classically include an apical cavitary lesion.
M.tuberculosis preferentially reactivates in the apices of the lungs because it is an aerobic
organism, and the oxygen tension is highest in this segment of the lungs.
A neoplasm in the pulmonary apex at the thoracic inlet can compress the inferior portion of
the brachial plexus(invasion of the 8th cervical and first thoracic nerves) resulting in shoulder
pain radiating in an ulnar distribution.this is known as Pancoast syndrome.
Aortic arch aneurysm would demonstrate a fusiform dilation of the ascending aorta and
arch,which project to the left within the chest.
Legionella pneumophila is an intracellular gram negative organism commonly spread by
cooling towers and water supplies.Travel-associated infection is well
documented.Symtpoms suggestive of legionnaire's disease include cough,fever>39C,GI
symptoma,and confusion.Diagnosis is confirmed by urine antigen testing or culture on
charcoal agar.Treatment with azithromycin or levofloxacin is appropriate.

Allergic Bronchopulmonar Aspergillosis

ABPA is characterized by transient recurrent pulmonary infiltrates, peripheral eosinophilia,
asthma and immediate wheel and flare reaction to Aspergilus fumigatus and presence of
antibodies in serum against Aspergillus fumigatus. Other characteristics are history of
Brownish plug in the sputum and high IgE levels. Glucocorticoids are used to treat it.
Whenever an Asthmatic pt is suspected of having ABPA, skin testing with Aspergillos
antibody is first diagnostic step, if its negative ABPA is ruled out. If positive serum
precipitants agianst Aspergillus and IgE levels are checked. ABPA is excluded if IgE is
<1000, or if serum precipitants against Aspergilus are absent. DDX1: JOB SYND, a
recurrenct bacterial infection and markedly elevated IgE. Infections are due to Staph and are
SKIN infections. Neutrophils exihibit impaired chemotaxis. Other feaatures are eczema,
asthma, allergic rhinitis. Tx is antibiotics. DDX2: Wiskot Aldrich, X-link, Triad of
eczema,thrombocytopenia, pyogenic recurent infections. IgA & IgE are high while IgM is
low, DDX3:Chronic Eosinophilic Pneumonia , is the mc eosinophilic pneumonia in US. Pts
presents with systemic signs of fever, malaise, anorexia, weight loss. Eosinophils >40% is
suggestive of this dis. Tx is Glococorticoid. DDX4: Churg-Strauss is a multisystem vasulitic
disorder of unknown etiology hat affects skin,kidney, CNS, lungs, GI and heart. There is
asthma, , fever, marked Eosinophilia. Tx is glucocorticoids.

Aspergilloma can grow in the apex of the lung but does not cause arm pain.The patient may
present with hempotysis,fever,weight loss, and a chronic cough. The mass is usually mobile
and moves with position.The diagnosis is made by finding hyphae in the
specimen.Aspergillosis can also be seen in immunocompromised patients;however,the chest
xray typically shows a solid mass surrounded by a radiolucent crescent(crescent
sign,Monod's Sign).A mobile cavitary mass in the lung, which presents with intermittent
hemoptysis is usually indicative of aspergilloma.
Cryptogenic organizing pneumonia causes dry cough and systemic symptoms that last for
months.Chest radiography demonstrates Bilateral Ground Glass infiltrates.
Gram negative bacilli (GNB)accounts for <2% of CAP,but account for most of the
nosocomial infection and have high mortality rates. Some of the common gram-negative
bacteria(GNB) causing pneumonia are E.coli(non-capsulated),Klebsiella

Pneumoniae(encapsulated),Pseudomonas(encapsulated-seen in cystic
fibrosis,neutropenia,advanced AIDS,bronchiectasis,and ICU
pneumonias),Proteus,Enterobacter,Serratia marcescens and Acinetobacter.GNB pneumonias
are rare in healthy individuals and usually occur in infants,elderly,alcoholics and
immunocompromised host especially with neutropenia. The usual pathophysiological
mechanism is colonization of the oropharynx,followed by micro aspiration of upper airway
Friedlander's pneumonia or Klebsiella pneumonia most frequently affect upper lobe and
produce Currant Jelly-like sputum with tissue necrosis and early abscess formation and a
fulminant course.Klebsiella is one of the most common organisms responsible for
pneumonia in alcoholics ( grows as mucoid colonies).
Carcinoid tumors are usually centrally located and easily visible with bronchoscope.They
may present with a cough and recurrent hemoptysis.The tumors are slow growing and have
the best prognosis of all lung cancers.
Chronic Bronchitis is characterized by a chronic productive cough for at least 3 months
over 2 consecutive years and not attributed to other causes.It occurs following prolonged
exposure of the tracheobronchial tree to nonspecific irritants and is characterized by
hypersecretion of mucus and structural changes in the tracheobronchial tree,The prescence
of a chronic productive cough,prominent bronchovascular marking,mild flattening of the
diaphragm and normal DLCO is suggestive of chronic bronchitis rather than emphysema in
this patient.Patients with predominant chronic bronchitis are also called Blue Bloaters as
they generally have a stocky build with a chronic productive cough,recurrent or persistent
signs of right heart failure, and profound oxygen desaturation.
Acute Bronchitis is a common cause of blood tinged sputum and is usually viral in
etiology.In afebrile patient with new onset blood-tinged sputum without significant signs of
more serious disease,observation and close clinical follow up is the best treatment strategy.
Emphysema is a pathologic diagnosis characterized by permenant and destructive
enlargement of airspaces distal to the terminal bronchioles with loss of normal
artitecture.Patients are generally thin with severe dyspnea(Pink Puffers),and have
hyperinflation of the chest,decreased vascuar markings,decreased DLCO( due to destruction
of alveoli),and moderate oxygen desaturation.Panacinar emphysema is typical for alpha-1antitrypsin deficiency, whereas centriacinar emphysema is more characteristic of COPD.
The development of clubbing and sudden onset joint arthropathy in a chronic smoker is
suggestive of Hypertrophic PulmonaryOsteoarthropathy.This condition is often
associated with lung cancer, and therefore a CXR is indicated to rule out malignancy and/or
other lung pathology(TB, bronchiectasis, or emphysema).
The kidney compensates for respiratory alkalosis by preferentially excreting bicarbonate in
the urine( low bicarbonate excretion and high H+ secretion in acidosis).( in ventilated
patients, ventialtion=tidal volumexRR...and according to this equation u evaluate hypo and
Acidosis accompanied by hypercarbia and a normal/elevated serum bicarbonate is
diagnostic of a respiratory acidosis.Hypoventialtion is a major cause of respiratory acidosis
and may occur in post-ictal state( in post ictal state the lactic acidosis from prolonged and
forceful skeletal muscle activity will manifest as metabolic acidosis with decreased HCO3).
Peak Airway Pressure=Resistive Pressure+Elastic Pressure+PEEP
Peak Airway Pressure is the maximum pressure during the respiratory cycle.
Elastic(Plateau)Pressure(calculates Lung Compliance) is the pressure at the end of an
inspiratory hold maneuver.It is the the product of the lung's elastance and the volume of gas
delivered.(Elastic recoil is inverseley proportional to lung compliance,i.e: a decrease in compliance
as in pulmonary fibrosis is accompanied by increase in the elastic pressure)
Resistive (Peak) Pressure measures total airway resistance which takes into account the
resistance of the ventialtor circuit,endotracheal tube,and the patient's airways(in mechanically
ventilated patients).( it's impossible to calculate upper airway resistance when a patient has an
endotracheal tube in place because the tube bypasses the upper airway)

Positive End Expiratory Pressure(PEEP) is calculated with the end expiratory hold maneuver.
(alveolar end-expiratory pressure=atmospheric pressure increases in obstructive lung disease due
to inability of alveoli to empty completely).
Respiratory muscle strength is determined by measuring the patint's negative inspiratory
Chest CT is indicated in cases of hemoptysis where PE,mass lesions, bronchiectasis or
vascular malformations are suspected.If diagnosis is unclear and in cases of recurrent
hemoptysis, Bonchoscopy is indicated.
An enlarged left atrium in mitral stenosis( look for history of rheumatic fever-immigrant...)
can cause a persistent cough and elevation of the left main stem bronchus(and phrenic
Histoplasma capsulatum(Histoplasmosis) is a common and usually asymptomatic
infection in endemic areas like Mississippi and Ohio River valleys and Central America.It is
usually found in soil with a high concentration of bird or bat guano droppings.the infection
is contracted by inhalation of the spores or mycelial fragments.Less than 5% of infected
people develop the symptomatic disease.The extent of disease is determined by the amount
of exposure and immunity of the host.Symptomatic lunginfection is mostlycharaerized by
self-limiting fever,chills,and a non-productive cough.A chest xray may show patchy lobar or
multinodular lobar infiltrates.Chronic cavitary pulmonary histoplasmosis is a progressive
fatal form of histoplasmosis that usually develops in older COPD patients.Disseminated
histoplasmosis is seen in immunocompromised adults and young children.Occasionally,
mediastinal lymph node enlargement occurs as a result of a lymphagenous reaction to
Postnasal drip of nasal secretions can cause irritation and initiation of the cough reflex.H1
histamine receptor antagonists (like chlorpheniramine) decrease nasal inflammation and post
nasal drip in patients with allergic rhinitis(there would be a background of environmental
allergies and diagnosis is made based on history and physical exam).
New clubbing in patients with COPD often indicates the development of lung cancer.
(Pulmonary HTN and hypoxemia due to congenital heart disease often result in clubbing
but those of COPD are rarely associated with digital clubbing)
Airway disease is the most common cause of both mild and massive hemoptysis.Chronic
Bronchitis is a frequent cause of mild hemoptysis in patients with significant smoking
history.(Note: thrombocytopenia may present with hemoptysis if the platelet count is
markedly decreased-look for signs of bleeding as epistaxis or petechiae)
Allergic Rhinitis
Dark puffy eyelids is called allergic shiners. The red crease over the nose causes constant
rubbing, called allergic salute. Tx is avoidance and decongestants. ****If rhinitis is not clear
if its allergic or infectious, then next step is Nasal cytology. Demonstration of neutrophils in
nasal secretions suggests infectious cause. Predominant of Eosinophils suggest allergic
cause. Other cause of nasal eosinophilia include Nasal Polyposis (Aspirin sensitivity).
Aspirin Sensitivity Syndrome(V.IMP) (clues to diagnosis include aspirin
ingestion,persistent nasal blockage,and episodes of bronchoconstriction)is believed to be
pseudo-allergic reaction.It results from aspirin-induced prostaglandin/leukotriene
misbalance in susceptible individuals which triggers bronchoconstriction and polyp
formation.Treatment includes avoidance of NSAIDs and the use of leukotriene receptor
antagonists(drug of choice).
Recurrent bacterial infections in an adult patient may indicate humoral immunity
defect.Quantitative measurement of serum immunoglobulin levels helps to establish the
Theophylline toxicity usually manifests as CNS stimulation(headache,insomnia),GIT
disturbances(nausea,vomiting),and cardiac toxicity(arrythmia).The mechanisms responsible
for the toxicity may include phosphodiesterase inhibition,adenosine antagonism,and
stimulation of epinephrine release.
Lung consolidation causes bronchial breath sounds which are loud(assuming patent

airways otherwise decreased sounds),dullness to percussion,increased

fremitus,bronchophony,egophony,and whispered pectoriloquy on physical exam.Bronchial
breath sounds have a full expiratory phase.
On CXR, a pneumothorax would be evident as a radiolucent(black) region of
extrapulmonary air.
Bronchopleural fistula is a possible cause of empyema.It typically occurs following
surgical procedures involving the bronchi,such as a pneumonectomy,but may also result in
patients with recurrent pneumothoraces or as a sequela of infection.On CXR, it would
appear as air in the pleural space.
Asbestos exposure increases the risk of malignancy,pulmonary fibrosis and pleural
plaques.In terms of malignancies,both bronchogenic carcinoma and mesothelima are linked
to asbestos exposure,with bronchogenic carcinoma being the more common cancer in these
patients(Mesothelioma affects the pleura).
Bronchiectasis presents with cough,mucopurulent sputum,and hemoptysis that often
responds to antibiotics.CXR is frequently abnormal but not sufficient for diagnosis of
bronchiectasis.High resolution CT scan is the definitive test for diagnosis.
Inhaled antimuscarinic agents such as ipratropium are the mainstay of symptom
management in COPD.These anti-cholinergic medications may be combined with shot
acting beta-adrenergic agonists for greater symptom relief.
Right mainstem bronchus intubation is a relatively common complication of endotracheal
intubation.It causes asymmetric breath sounds immediately after intubation and s fixed by
withdrawal of the tube. Needle thoracostomy may be performed in patients with a life
threatening tension pneumothorax.Chest tube may be used for
pneumothorax,hemothorax,empyema or malignant effusion requiring drainage.
Short acting beta adrenergic agonists administered 20mins before excercise are the first line
treatment for isolated excercise induced asthma(long acting Beta agonists may be used in
children or athletes who engage in athletic activities throughout the day).The inciting trigger
in excercise-induced asthma is rapid ventilation of cold dry air.
Malignancy is the most common cause of SVC Syndrome (Dyspnea,venous
congestion,swelling of head-neck-arms).Lung cancer( particulariy small cell lung cancer)
and NHL are often implicated.Other possible causes include fibrosing
mediastinitis(secondary to hisoplasmosis or TB infection) or thrombosis secondary to
indwelling central venous devices.When the history and physical examination are suggestive
CXR is warranted.Abnormalities on CXR warrant follow-up with chest CT and histology to
determine the tumor type and to guide therapy.
Blood in the chest,if not evacuated,can get infected.The majority of patients will present
with a low-grade fever,dyspnea, and chest pain.Surgery is required to remove the clotted
blood and fibrinous peel(decortication).If empyema is of recent onset it can be removed by
fibrinolytic therapy.Both steptokinase and urokinase have been used.However, if patient
with recent trauma, fibrinolytic therapy is contraindicated and do not have much success
when empyema is loculated and has a thick rim around it.
Tension pneumothorax leads to compression of the mediastinum and impaired right
ventricular filling,hence the hypotension,tachycardia,and absent left-sided breath sounds.
All patients with suspected bacterial pneumonia should have a CXR done first and
antibiotics should be administered as soon as possible without waiting for sputum gram stain
or cultures.
Indicators of a severe asthma attack include normal to increased PCO2 values(indicates CO2
retention becuase of severe airway obstruction-air trapping and/or respiratory muscle
fatigue),speech difficulty,diaphoresis,altered sensorium,cyanosis,and silent lungs.
Patients with impaired consciousness,advanced dementia,and other neurologic disorders are
predisposed to aspiration pneumonia due to impaired epiglottic function.
Nasal eosinophilia is characteristic for allergic rhinitis,although this finding is not
specific.Other causes of nasal eosinophilia include nasal polyposis(including aspirin
sensitivity) and non-allergic rhinitis with eosinophilia.Nasal eosinophilia is absent in

patients with infectious causes(demonstration of neutrophils) and vasomotor rhinitis.

Bronchogenic cysts are usually found in the middle mediastinum( which also includes
tracheal tumors/pericardial cysts/lymphoma and LN enlargement, and aoritc arch
aneurysms).Thmoma is usually found in the anterior mediastinum.All neurogenic
tumors(meningocele,enteric cysts,lymphomas,diaphragmatic hernias,esophageal tumors,and
aortic aneurysms) are located in the posterior mediastinum.
Inhaled albuterol and systemic steroids are appropriate treatments for acute asthma
attacks.Patients on high doses of Beta 2 Agonists may develop hypokalemia(by driving
potassium into cells),which may present with muscle weakness,arrhythmias and EKG
abnormalities.Other common side effects of beta 2 agonists include tremor,palpitations and
Secondary pneumothorax should be suspected in COPD patients presenting with
catastrophic worsening of their respiratory symptoms and is usually due to dilated alveolar
blebs that rupture air into the pleural space.Patients with pneumothorax typically present
with acute onset of chest pain and shortness of breath.On the affected side,breath sounds are
markedly reduced and the chest is hyperresonant to percussion.
Bronchoalveolar lavage(BAL) is most useful in the evaluation of suspected malignancy
and opportunistic infection.BAL is ?90% sensitive and specific for PCP.BAL is of less
diagnostic utility in evaluating other forms of interstitial lung disease such as
IPF,sarcoidosis,and connective tissue disease.
Blastomycosis is a pulmonary fungal infection endemic to the Great Lakes,and Mississppi
and Ohio River basins.Systemic Blastomycosis may cause skin and bone lesions in addition
to pulmonary manifestations.Broad-based budding yeast grown from the sputum confirm the
diagnosis.Itraconazole or amphotericin B may be used to treat symptomatic disease.
Coccidiodomycosis is a fungal infection of the lungs that can cause fever,cough,and night
sweats.Extrapulmonary manifestations may involve the skin,meninges,and skeleton.It is
endemic to the southwestern US.

In patient presenting with sudden onset of severe shortness of breath-stridor and harsh
respiratory sounds from the trachea, upper airway obstruction should be immediately ruled
out. ( Laryngeal edema is a common cause-look for history of food allergies and urticaria)
Bird Fancier's Lung is a form of hypersensitivity pneumonitis caused by repeated
inhalation of an inciting antigen which leads to alveolar inflammation.Common responsible
antigens inculde aerosolized bird droppings and molds associated with farming(farmer's
lung). A history of antigen exposure is highly suggestive.Acute episodes may present with
cough,breathlessness,fever and malaise that occur 4-6 hours after exposure.With chronic
exposure patients may develop pulmonary fibrosis and a restrictive pattern on lung
spirometry.Classic radiographic findings include ground glass opacity or haziness of the
lower lung fields.Best treatment is avoidance of antigen exposure.Continued exposure risks
disease progression.
Obesity hypoventialtion Syndrome is defined by severe obesity greater than 150% of ideal
bodyweight and alveolar hypoventialtion during wakefulness.ABG will demonstrate

hypercapnia,hypoxemia and respiratory acidosis as a consequence of decreased lung

compliance.Weight loss,ventilator support,oxygen therapy, and progestins(a respiratory
stimulant) are all potential therapies for these patients.
Non-Invasive testing is critical in the work-up of DVT. For patients at moderate to high
risk,compression U/S is used to detrmine the need for anitcoagulation(contrat venography
when U/S results are unquivocal).In patients at low risk,the D-Dimer level should be
checked .If negative,no anticoagulation is necessary.If elevated,compression U/S is used to
determine the need for anticoagulation.
Choriocarcinoma is a metastatic form of gestational trophoblastic may occur after
molar pregnancy o normal gestation,and the lungs are the most frequent site of metastatic
spread.Suspect choriocarcinoma in any postpartum woman with pulmonary symptoms and
multiple nodules on CXR.An elevated B-hCG helps to confirm the diagnosis.
Hepatopulmonary Syndrome:it is a triad of cirrhotic liver disease,hypoxia,and worsening
of shortness of beath upon sitting upright(orthodeoxia).It is presumed to be from
vasodilatory substances that are not cleared by the diseased liver.This leads to abnormal
pulmonaryvascular dilation and right to left shunting.It is confirmed by contrast
echocardiography.Technetium labeled albumin as a perfusin study can also be diagnostic.
before and after administration of a bronchodialator (Beta-2 agonist). Significant
improvement in FEV1 after bronchodialator indicates reversibility of destruction, which is
more consistant with Asthma. ****Mast cell stabalizers (Sodium Cromolyn) are doc for pts
who have other allergic disorders, so give this to a boy who started to have night time cough
and wheeze with hx of allergic rhinitis.**** Exercise induces Asthma (not to be confused
with post excercise asthma) presnts with chest discomfort, wheezing cough, breathlessness,
fatigue and abdominal discomfort. Beta Agonist and Mast cell stabalizers (Sodium
Cromolyn) are the best tx for these pts. **** When an asthmatic pt presents with
Subcutaneous Emphysema, which is face becomes all swollen and palpation reveals
crepitans all over face and neck, then the first thing to do is to do Cxr to rule out
Penumothorax. Once that is rules out just observe the pt, it needs no tx.****Inhaled
corticosteriods are indicartd in pt with persistent asthma symptoms. The agents are
beclomethasone. In adults SE of low-dose drug are limited to are Dysphonia and Thrush. In
high-dose systemic toxicity may occur. ****Its a common illness in childhood. 10% of
children come ro ED with un-remitting asthma (continues wheezing despite tx with
neubelizers and een steriods). This is called Acute Status Asthmaticus. Of these pts 10%
require MECHANICAL VENTILATION, however hospitalization is mandatory. If on
auscultation there is no air entry bilateraly, the child has 'silent chest' or absent air entry and
continues to desaturate despite Prednisone therapy, therefor the best option is mechanical
ventilation and hospitalization.*****For pt who have asthma accompanied with other
allergic disorders, mast cell stabilizers like Sodium Cromolyn are the agent of choice.
*****1st neubelizers, 2nd IV steroids, 3rd mech ventilax.Normal PCO2 is one of the
indicators of a severe attack. During an attack, pt is tachpneac so he hyperventilates which
should cause decrease in PCO2. So if PCO2 seems to be normal that means the obstruction
is getting worst or respiratory muscel are getting too tired. Other signs of severity are broken
speech, diaphoresis, cyanosis, altered sensorium and "silent lung". Inhaled corticosteriods
improve long term quality of life in Asthmatics. Initial hypertensive therapy for pt with
asthma is Hydrochlorothiazide.***To differentiate b/w Asthma and COPD (Emphysema)
the best test is a bronchodialator response test. , its conducted by measuring FEV1 .

The leading cause of cancer death in the United States. Risk factors include
tobacco smoke (except for bronchoalveolar carcinoma) and radon or asbestos exposure.
Types are as follows:
Small cell lung cancer (SCLC):Highly correlated with cigarette exposure.Has a central
location.Has a neuroendocrine origin; associated with paraneoplastic syndromes.
Metastases are often found on presentation in intrathoracic and extrathoracic
sites such as brain, liver, and bone.
Non-small cell lung cancer (NSCLC ) : Represents a group of cancers,with the most
common types being adenocarcinoma, squamous cell carcinoma(SCC), and large cell
carcinoma. These cancers are less likely than SCLC to metastasize at an early stage.
Adenocarcinoma:The most common lung cancer; has a peripheral location.Includes
bronchoalveolar carcinoma, which is associated with multiple nodules, interstitial
infiltration, and prolific sputum productionbut is not associated with smoking.
SCC: Has a central location; 98% are seen in smokers.
Large cell/neuroendocrine carcinomas: Least common; associated with a poor
Presents with cough, hemoptysis, dyspnea, wheezing, pneumonia, chest pain, weight loss,
and possible abnormalities on respiratory examination (crackles, atelectasis).
Other findings include the following:
Horner's syndrome (miosis, ptosis, anhidrosis)... patients with Pancoast's tumor at the apex
of the lung.

Flow Volume Loops Interpretation (V.IMP)

Laryngeal Edema

Flow volume loops diagrams express airflow in different lung diseases and give the relationship
between flow rates compared with lung volumes.On the Vertical(Y) Flow Rate is expressed and On
the Horizontal(X) axis Volume is expressed( it increases to the left).The shape of the loop can
characterize the type and distribution of airway obstruction.
When comparing Normal flow volume loop with one of Restrictive lung disease, the restrictive lung
disease alters the loop by shifting to the right of the x-axis which means a reduction in lung
On the other hand,obstructive lung disease alters the shape of the loop by causing a reduction of
airflow( alteration on the y-axis).
Now in case of fixed airway obstruction(tracheal stenosis /laryngeal edema which occurs after
prolonged intubation) the flow of the loop is is flattened on the top and the bottom. In dynamic
extrathoracic airway obstruction( as in vocal cord paralysis), the obstruction occurs mostly with
inspiration while expiration is mostly normal.This effect causes the flow volume loop to be
flattened only on bottom( the inspiration flow curve will be a straight line almost along the
horizontal axis while there is an expiratory curve).