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48 Cards in this Set

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Chronic Dyspnea
1. Progressive COPD
2. Pulmonary Fibrosis, other ILD
3. Large pleural effusion
4. Severe Anemia
5. CHF
PFTs and Anemia
Normal PFTs, except for a low diffusion (dec. DLCO)
FVC = 85%P
FEV1 = 85%P
FEV1/FVC = 85%P
TLC = 95%P
RV = 95%P
DLCO = 45%P
How is dyspnea related to COPD?
1) Prolonged expiratory time (I:E = 1:4 or longer)

2) Reduced thoracic excursion?
3) Hyperresonant to percussion
4) Dec. breath sounds +/-wheezing
5) ABG - May be hypoxic, hypercapnic
How is dyspnea related to Pulmonary fibrosis?
1) Normal I:E ratio
2) Normal percussion
3) Breath sounds: crackles (velcro rales)
4) Extremities often have clubbing, may have cyanosis, 5)If there is long-standing fibrosis associated with pulmonary hypertension, they may have edema.
6) ABG - May be hypoxic, hypercapnic (IPF, UIP)
How is dyspnea related to Pleural Effusion?
1) Reduced thoracic excursion on side of effusion
2) Dullness to percussion over fluid
3) Absent vocal (tactile) fremitus
4) Absent breath sounds (but may have bronchial breath sounds &/or crackles above the level of the fluid
5) ABG - May be hypoxic
How is dyspnea related to CHF (pulmonary edema)?
1) Normal thoracic excursion
2) Normal percussion (unless there is a related pleural effusion as well)
3) Breath sounds: crackles (different sound than the crackles of pulmonary fibrosis) and may be wheezing
4) May have third heart sound
5) Extremities: no clubbing, +edema
6) ABG - May be hypoxic
ABGs w/ UIP?
ABG - May be hypoxic, hypercapnic (IPF, UIP)
A White CXR might indicate what conditions?
Pulmonary fibrosis or other 1) ILD
2) Large pleural effusion
3) Congestive heart failure
Restrictive PFTs associated with ILD (particularly UIP/IPF)
FVC = 55% predicted
FEV1 = 55% predicted
FEV1/FVC = 90%
TLC = 65% predicted
RV = 50% predicted
DLCO = 45% predicted
Obstructive PFTs with low DLCO = COPD
FVC = 70% predicted
FEV1 = 50% predicted
FEV1/FVC = 55%
TLC = 130% predicted
RV = 130% predicted
DLCO = 45% predicted
Obstructive PFTs with normal DLCO = Asthma
FVC = 70% predicted
FEV1 = 50% predicted
FEV1/FVC = 55%
TLC = 130% predicted
RV = 130% predicted
DLCO = 95% predicted
5 Common Conditions in the Differential Diagnosis of Acute Dyspnea
1) Community acquired pneumonia
2) Spontaneous pneumothorax
3) Pulmonary edema
4) Pulmonary embolus
5) Acute asthma exacerbation
ABG: pH=7.48, PaCO2=30, PaO2=50 (RA)
You calculate his PAO2 to be 113

What is his A-a gradient and is it normal or increased?
ABG: pH=7.48, PaCO2=30, PaO2=50 (RA)
You calculate his PAO2 to be 113

PAO2 – PaO2 = A-a gradient
113 – 50 = 63
Normal = 3-16
What are two conditions associated with a normal A-a gradient?
1) Alveolar hypoventilation (such as patient who has had a large stroke or overdosed on drugs)

2)Low inspired FIO2
On CXR, what do alveolar infiltrates with air bronchograms suggest?
Consolidation
--> (pneumonia, partial atelectasis, pulmonary infarct, etc.)
6 Clues in History for Pneumonia
Cough (often with purulent sputum)
Fever +/- rigors
Dyspnea (particularly with exertion)
Pleuritic chest pain
May have viral prodrome
?Exposure to ill contacts
4 Clues on exam for Pneumonia
1) Often has high fever
2) Focal crackles, bronchophony, egophony, pectoriloquy
3) Focal increased vocal fremitus
4) Focal dullness to percussion
4 Clues on laboratory for Pneumonia
May have high fever
Elevated WBC
Hypoxemia with increased A-a gradient
Focal alveolar infiltrates with air bronchograms
2 Clues in History for Pneumothorax + 3 Risk Factors
1. Severe pleuritic chest pain
2. sudden onset of dyspnea (exact time)

Risk factors:
1) Tall and slender (Marfan’s syndrome)
2) Certain infections (Pneumocystis carinii pneumonia – PCP)
3) Chest trauma (stabbing)
5 Clues on Exam for R-sided pneumothorax
1) R-sided bronchial or absent breath sounds
2) No vocal fremitus on right
3) Hyper-resonant to percussion on right
4) May have chest asymmetry (R>L)
5) Possible crepitation of neck
4 Clues in History for CHF
1)Dyspnea significantly worse with lying flat (feeling of “drowning” - orthopnea)
2) May have cough with pink frothy sputum
3) Often with a PMH of heart disease
4) Could occur after eating a large salt load (a bag of potato chips)
3 Clues on exam for CHF
1) Diffuse fine crackles
2) May have extra heart sounds (+S3)
3) May have wheezes
4 Clues in History for Pleural Effusion + 3 Risk Factors
1) Sudden onset of dyspnea (exact time)
2) Pleuritic chest pain
3) Hemoptysis
4) Low-grade fever

Risk factors
1) Stasis: obese/diabetic/congestive heart failure/pregnant, recent long trip
2) Venous injury: lower extremity surgery, trauma, burns
3) Hypercoagulable: h/o cancer, smoker, oral contraceptive pills, inherited / acquired deficiency
7 Clues on Exam for PE
1) May be normal
2) Usually tachycardic (regular-sinus)
3) May have low-grade fever
4) May have crackles, bronchophony, egophony, pectoriloquy
5) May have focal increased vocal fremitus
6) May have focal dullness to percussion
7) <50% have swollen, red, painful lower extremity
Clues on Laboratory in PE
1) CBC: often normal, ABG: increased A-a
2) EKG: sinus tachycardia, S1 Q3 T3
3) CXR: maybe normal or plate-like atelectasis, Hampton’s hump, Westermark sign
4) V/Q scan: segmental defects in perfusion
5) CT chest (PE protocol): may have filling defect
6) LE dopplers (next step – no risk)
7)Pulmonary angiogram
2 ways to manage PE
1) Anticoagulation with heparin or
2)Low-molecular weight heparin while awaiting studies
Describe the CXR in patient with pulmonary embolus
CXR in patient with pulmonary embolus is often normal.
When even THINKING about PE what should you do?
When even THINKING about PE, you must anticoagulate (unless there is a contraindication) while awaiting further studies.
4 Clues in History for Asthma
1) May be acute, but often has episodic dyspnea increasing over days, +wheezing, often with cough, +/- fevers

2) PMH/FH of allergies and/or asthma
3) Environmental triggers: fumes, chemicals, allergens, hairspray, etc.
4) Dyspnea, cough, & wheezing may be improved with bronchodilators
4 Clues on Exam for Asthma
1) May have diffuse expiratory wheezes
2) May have minimal air movement (bad sign)
3) Often tachycardic
4) Prefers sitting position (increased dyspnea with leaning back or lying flat)
Clues on Laboratory for Asthma Exacerbation
1) CBC and ABG often normal
2) ABG may have high pH and low PaCO2
3) CXR: normal or hyperinflated
4) Peak expiratory flow rate: low
Two ways to manage Asthma exacerbation
1) Bronchodilators: albuterol and ipratropium
2) Systemic corticosteroids
Respiratory Rate
Bradypnea: rate less than ? per minute
Tachypnea: rate greater than ? per minute
Respiratory Rate
Bradypnea: rate less than 8 per minute
Tachypnea: rate greater than 25 per minute
Different patterns of breathing
-Sleep apnea
-Cheyne strokes
-Pursed lip breathing
-Orthopnoea: Short of breath in supine position, gets some relief by sitting or standing up.
What causes central cyanosis?
1)Results from pulmonary dysfunction, the mucous membrane of conjunctiva and tongue are bluish.

2) If there was chronic hypoxemia and secondary erythrocytosis, you can detect the conjunctival and scleral vessels to be full, tortuous and bluish.
What is clubbing?
In clubbing, there is widening of the AP and lateral diameter of terminal portion of fingers and toes giving the appearance of clubbing.
The angle between the nail and skin is greater than 180.
The periungual skin is stretched and shiny.
There is fluctuation of the nail bed.
One can feel the posterior edge of the nail.
When do you observe clubbing?
Intrathoracic malignancy: Primary or secondary (lung, pleural, mediastinal)
Suppurative lung disease: (lung abscess, bronchiectasis, empyema)
Diffuse interstitial fibrosis: Alveolar capillary block syndrome
In association with other systemic disorders
In what disorders do you see weight loss?
Emaciation cachectic
Malignancy
Tuberculosis
What characteristics describe increased effort of breathing?
Person appears uncomfortable. Breathing seems voluntary.
Accessory muscles are in use, expiratory muscles are active and expiration is not passive any more.
The degree of negative pleural pressure is high.
The respiratory rate is increased.
You would see tracheal deviation in what type of disorders?
-->Any deviation of the mediastinum is abnormal

Lateral shift: The mediastinum can be either pulled or pushed away from the lesion
1) Pull: Loss of lung volume (Atelectasis, fibrosis, agenesis, surgical resection, pleural fibrosis)

2) Push: Space occupying lesions (pleural effusion, pneumothorax, large mass lesions)
3) Mediastinal masses and thyroid tumors
Percussion: in what conditions would you hear dullness, hyperresonance?
Dullness
Decreased resonance is noted with pleural effusion and all other lung diseases
The dullness is flat and the finger is painful to percussion with pleural effusion

Hyper resonance: Increased resonance can be noted either due to lung distention as seen in asthma, emphysema, bullous disease or due to Pneumothorax
Breath sounds: in what conditions would they be diminished or absent? Increase?
Intensity of breath sounds, in general, is a good index of ventilation of the underlying lung.
Breath sounds are markedly decreased in emphysema.
Symmetry: If there is asymmetry in intensity, the side where there is decreased intensity is abnormal.
Any form of pleural or pulmonary disease can give rise to decreased intensity.
Harsh or increased: If the intensity increases there is more ventilation and vice versa.
In what locations is Bronchial breathing abnormal? In what disease would you hear low pitched BB and what disease would you hear high pitched?
Bronchial breathing anywhere other than over the trachea, right clavicle or right inter-scapular space is abnormal.
In consolidation, the bronchial breathing is low pitched and sticky and is termed tubular type of bronchial breathing.
In cavitary disease, it is high pitched and hollow and is called cavernous breathing. You can simulate this sound by blowing over an empty coke bottle.
1) What are rhonchi?
2) What condistions would you assoc. with rhonchi that are: diffus or localized, during inspiration or expiration?
Rhonchi are long continuous adventitious sounds, generated by obstruction to airways.

When detected, note whether it is generalized or localized, during inspiration or expiration, and the pitch.

Diffused rhonchi would suggest a disease with generalized airway obstruction like asthma or COPD.

Localized rhonchi suggests obstruction of any etiology e.g., tumor, foreign body or mucous. Mucous secretions will disappear with coughing, so would the rhonchus.

Expiratory rhonchi implies obstruction to intrathoracic airways.

Asthmatics can also have inspiratory rhonchi while it is uncommon in COPD.
Describe pleural rub
Normal parietal and visceral pleura glide smoothly during respiration.

If the pleura is roughened due to any reason, a scratching, grating sound, related to respiration is heard.

You can hear the sound by compressing harder with the stethoscope and making the patient take deep breaths.

It is localized and can be palpable.
Distinguish when you would hear fine, medium, and coarse crackles
Crackles are interrupted adventitious sounds

Crackles heard only at the end of inspiration are called fine crackles.

When the surfactant is depleted, the alveoli collapse. Air enters the alveoli at the end of inspiration.

This sound is generated as the alveoli pop open from it's collapsed state.

When the crackles are heard at the end of inspiration and the beginning of expiration the fluid or secretions are probably in respiratory bronchioles: medium crackles.

If the crackles are heard throughout it implies the secretions are in bronchi: coarse crackles.
When would tactile fremitus be increased? Decreased?
Decreased: A quantitative decrease in voice transmission could be due to any other form of lung or pleural disease.
Qualitative alteration:
A qualitative alteration of voice transmission is noted over consolidation and along the upper margin of pleural effusion: Egophony
The sound is like a nasal twang or goat bleating.
Hemoptysis
DDx
Airways
-Bronchitis
-Bronchiectasis
-Bronchogenic carcinoma


Pulmonary vasculature
-Left ventricular failure
-Mitral stenosis
-Pulmonary embolism
-Arteriovenous malformation


Pulmonary parenchyma
-Pneumonia
-Abscess
-Tuberculosis
-Aspergilloma
-Parasites, e.g., paragonimiasis, ascariasis, hookworm, strongyloidiasis
-Goodpasture's syndrome
-Wegener's granulomatosis
-SLE
-Crack cocaine inhalation
-Idiopathic pulmonary hemosiderosis
-Leukemia


Iatrogenic
-Transbronchial lung biopsy
-Anticoagulation
-Pulmonary artery rupture by PA line