154 terms

Pulmonary Clin Med

Developmental "cut-off" for respiratory distress syndrome
24 weeks
Typical pulmonary artery pressure
The two sets of respiratory centers & what they control
Medullary: Controls resting breathing
Pontine: Controls laboured breathing
What are the three pulmonary "West zones"?
Zone 1: Apical lobes-Seldom perfused
Zone 2: ABOVE≈ 3cm above the heart. Blood flows in pulses. Perfused at Systole, not at Diastole.
Zone 3 Perfused throughout the cardiac cycle.
What is V/Q? What is the ideal V/Q value?
V/Q= Ventilation : Perfusion ratio. It is the ratio of air delivered to alveoli : blood delivered to alveoli;
1 L of blood holds ≈ same amount of O2 found in 1 of air, so V/Q = 1
Name and define the two V/Q mismatches
Shunt: An area with no ventilation (V/Q = 0)
Dead space: An area with no perfusion (V/Q is "undefined," approaching infinity)
When do pulmonary shunts occur? How does a shunt respond to O2 therapy?
Occur in pneumonia or in areas around pulmonary effusions filled with fluid.
Shunts have poor or absent response to O2 therapy
When do dead spaces occur? How does a dead space respond to O2 therapy?
Occur in areas of limited or absent arterial perfusion. Dead spaces have poor or absent response to O2 therapy
How do normal lungs accommodate to Ventilation-Perfusion mismatches?
During local or regional hypoxia, vasoconstriction is triggered. This directs blood away to healthier parts of the lung, where ventilation & perfusion are matched.
Name the four types of pulmonary testing
DLCO (Diffusion of the Lung to CO)
Body Plethysmography
Bronchial Challenge
What does DLCO measure, and how is it accomplished?
-DLCO measures the extent to which O2 passes from the alveoli into the blood;
-Involves measuring the Pp difference between inspired and expired CO.
Four limitations of pulmonary function testing
Calibration, Coaching, Care of Equip, Cognizance of poor results
The most reliable & available pulmonary test
The two lung volumes that are NOT amenable to direct spirometry?
The two criteria for performing spirometry
Known/suspected lung Dz;
Pt at risk for pulmonary Dz undergoing general anesthesia
Lung volumes altered in obstructive lung diseases
Increased: RV [X 2.5!]
Decreased: IRV & ERV
Net: Increase by ≈20%
Lung volumes altered in restrictive lung diseases
Decreased: IRV, ERV, RV, TV
Net: Decrease ≈25%
The three most significant indicators of pulmonary health in spirometry
These three remain: FVC, FEV1, FEV1/VC-
and the greatest of these is FEV1/VC
If FEV1/VC is LOW, suspect . . .
Obstructive lung dz
Why is FEV1/VC a much better measure of obstruction than FEV1 alone?
FEV1 by itself doesn't take into account small lung volumes or hemi-pleurectomy
How do you distinguish between Restrictive and Obstructive lung dz using the 3 main spirometry values?
Restrictive: FVC=low, FEV1=low, FEV1/VC=HIGH;
Obstructive: FVC=low, FEV1=VERY LOW, FEV1/VC=low
WHY does FEV1/VC INCREASE ijn Restrictive lung dz?
Fibrous scar tissue rebounds faster than less collagenated, healthy tissue
The three levels of Obstructive Lung Disease & FEV1/VC ranges
Mild: 60-69%
Moderate: 46-59%
Severe: <45%
Three asthma Indicators in spirometry
Albuterol Improvement:
FEV1 or FVC>12%
VC: >10% inhaled improvement vs exhaled improvement
Portion of a Flow Volume curve that is altered by forced expiration
Effort-dependent (peak portion)
Portion of Flow Volume curve that is altered in lung disease, & how it changes
Effort-independent (bottom portion);
Restrictive: Effort Independent (peak) remains high, but Effort-Dependent is more narrow than NORMAL;
Obstructive: Both peak height and loop width are reduced
What DLCO measures
(Diffusion of the Lung to Carbon Monoxide)
-Measures the RATE of diffusion of CO into the blood from the alveoli
-The rate of CO diffusion is a reflection of Alveolar SURFACE AREA
Main applications of DLCO
1. Diagnose & confirm Interstitial Lung disease
2. Confirm Emphysema (known by spirometry)
Affectors of DLCO
Anything that alters lung perfusion or gas uptake:
Cardiac Output, Hct, Pulmonary HTN
Body Plethysmography
Measures Functional Residual Capacity
Spirometry "Challengers"
Methacholine, SO2, Allergens
Methacholine challenge effect
REDUCES FEV1 by 205 in Asthmatics.
Name for Sleep study
Polysomnography (makes sense, eh?)
Sleep study tells . . .
Sleep stage, Respiratory responses, Limb movements, O2 sat
Most common URIs
1. Viral: Flu A/B, Rhino-, Corona-, RSV, Adeno-
2. Bacterial: Strep pyogenes, Strep pneu, HiB, Moraxella
Pulmonary Ix Workup sequence
Distinguishing Viral vs Bacterial RIs
Viral: Diverse S/s, less severe;
Bacterial: Circumscribed, more severe
Strep throat S/s
Sore throat, fever, Tonsillar exudate (pus),Cervical/Submaxillary Adenopathy
NB: NO rhinorrhea, conjunctivitis, cough
Centor score system
For Strep Dx, FATEL-->
Fever >100
Absent cough
Tender nodes
Less than 15 yrs
Strep Dx
Rapid An test (clinical std)
Throat culture (much better sensitivity)
Strep Tx
-Pen V 10D (too many resistant!)
-Amoxy or Augmentin 6D
-Erythromycin for PCN allergy
Return to school 24 hr after 1st dose
Acute bronchitis S/s
Productive cough
Purulent sputum
But-- no fever, chills or Crackles [these indicate pneumonia]
Acute bronchitis etiology
Viral or bacterial infection, especially in COPD & Asthmatics
DDX: Bronchitis v Pneumonia
Infiltrates (Exudate)
Elevated WBC
When to Rx in Acute Bronchitis, & Drugs
Culture results
Significant prior COPD
Rx: Augmentin, Levo or Azithro
The 'Flu antivirals & when valuable
Must be 1st 48 hrs of exposure (@ first S/s)
U.S. flu mortality
40K/yr in US
Signs and symptoms common to 'flu
Fever/chill, headache, cough, myalgia.
The 1st three together have high specificity.
Signs and symptoms absent in 'flu
NO: abnormal CXR, WBC-cytosis
Rapid Influenza screening test sensitivity & specificity
Sensitivity: ≈70%
Specificity: "very high"
Three phases of pertussis & associated signs/symptoms
Catarrhal: Malaise, mild cough, conjunctivals
Paroxysmal: Severe cough/stridor, may have post-tussive emesis (1-6 weeks)
Convalescent: Slow (2-3 weeks) recovery
Pertussis findings & treatment
S/s: Paroxysmal coughing w/ stridor
Tx: Erythromycin, Azithromycin, or TMP-SMX [Bactrim]
The four most common pneumonia signs
-Cough w/ purulent sputum or hemoptysis
-Crackles or pleuritic chest pain
-Dyspnea & SOB
Pneumonia risk progresion
CA <CA + comorbid <HA <Immunocompromised
CAP pathogens
Strep pneumoniae, HiB, Moraxella, Chlamydia, Mycoplasma, Legionella (last three "atypicals")
HA-PNA pathogens
MRSA, Pseudomonas (vent), Klebsiella
Local pulmonary/systemic mycosis
Coccidiodes immitis
U.S. Endemic Mycoses
Coccidiodes, Histoplasma (obligate parasite), Blastomyces, Aspergillis & Rhizopus
Fungal lung infection pharmacotherapy
Fluconazole or Amphotericin B
When should you resect pulmonary granulomas/spherules?
Almost never (severe hemoptysis)-- mortality is 25%
Allergic bronchopulmonary aspergilliosis signs and symptoms
-Severe asthma symptoms
-Elevated IgE & eosinophils
-Hypersensitivity to spores/hyphae;
What a POS Mantoux means
You've made ABs to mycobacteria in the LOWER lobes. Hopefully, you developed delayed hypersensitivity and your cell-mediated immunity killed all but the mycobacteria in your UPPER lobes
Signs and symptoms of primary TB seen in most patients
None- primary TB is usually asymptomatic. Reactivation TB presents with the commonly named symptoms (fever/chills, productive cough with hemoptysis, pleuritic chest pain, weight loss)
Signs and symptoms of reactivated TB
Weight loss, night sweats, productive cough (may show purulence & hemotypsis), pleuritic chest pain
Four common TB CXR findings
Cavitating pneumonia
Calcified nodules
Hilar effusion or lymphadenopathy
Upper lobe atelactasis (collapse)
How do you diagnose activeTB?
POS Mantoux AND POS CXR or Acid Fast staining
Active TB Rx regimens
9 mo Tx: Rifampin & Isoniazid (INH)
6 mo Tx: Rifampin & Isoniazid (INH) & Pyrazanamide
NB: IF Resistant strain or recurrent pt: ADD Ethambutol or Streptomycin
How do you diagnose latent TB?
Positive Mantoux only
When do you treat latent TB?
-Anyone <35;
-Recent intimate exposure
-If >15 mm Mantoux induration
-Previous NEG Mantoux & now converted POS
Latent TB pharmacotherapy regimen
9 mo Isonizid (INH)
Lung abscess etiology & diagnosis
Drinkers pass out, oral bacteria make way into lungs;
Look for poor dentition, purulent cough and halitosis-- Confirm with CXR or bronchoscopy
Why is lung CA often well-progressed before identified?
There is no sensory innervation of the lungs, so patient may be asymptomatic until tumor mass interferes with pulmonary function
Lung CA signs and symptoms
Cough, Hemoptysis, Dyspnea. Metastatic S/s: Invasion of neighboring tissue, Distant neoplasia, paraneoplastic syndromes (eg, Cushing's or Phaeochromocytoma)
Indications of local invasion by lung tumors
Cardiac tamponade, dysphagia, bronchial occlusion
The mathematics of mutation: What is the statistical impact of smoking? Of asbestos exposure?
Smoking (Benzpyrene) multiplier: 9X
Asbestos multiplier: 5X
Both smoking/asbestos: 50X
The two broad classes of lung CA
Small cell, Non-small cell
Etiology of SCLC [Small Cell Lung Cancer]
Arise from neuroendocrine cells.
Lung CA diagnostic tools
Chest film (poor)
CT (better): allows visualizing lymph nodes in area
Bronchoscopy (variable success)
The prognostic assumption that must always be made with small cell lung cancer.
SCLC is always assumed to be malignant.
Lung cancer staging using TNM classification of CA
1: Tumor confined to the lung, no evidence of node involvement or metastasis.
2: Tumor confined to the lung, Hylar lymph node involvement, but no metastasis.
3a. Tumor confined to the lung, Hylar and ipsilateral mediastinal adenopathy but no metastasis
3b: Tumor may be invading adjacent structures, w/ hilar & contralateral mediastinal adenopathy
4: Distant metastasis
When to deny resection of small cell lung cancer.
1. If class 3B or 4;
2. If FEV1 is already low & you predict it will be reduced by ANOTHER 20% (to below 800 ml) as a result of surgery.
Treatment of NSCLC [non-small cell lung cancer]
1. Resection preferred- if you're sure you'll get it all
2. Radiation- provides symptomatic relief, no increased survival
3. Chemo: almost useless in NSCLC
Treatment of SCLC (small cell lung cancer]
1. Assume malignant at discovery
2. Chemotherapy (Methotrexate or Etoposide)
3. Radiation to primary site
4. Surgery is controversial, only used for limited disease
Lung CA survival & recurrence at 5 yrs by stage
Stage 1: 50% @ 5 yr
Stage 2: 30% @ 5 yr
Stage 3: 15% @ 5 yr
Small Cell: If recurs, won't respond to radiation a 2nd time.
Carcinoid tumors etiology
Neuroendocrine tumors with low malignancy, usually in GI;
28% occur in respiratory system
Carcinoid signs and symptoms
Catecholamine effects: Flushing, Palpitations, Diarrhea, Wheezing, Abdominal cramps;
Respiratory effects occur only if pulmonary site, and include: Cough, Hemoptysis, Recurrent PNA, Airway obstruction
Carcinoid diagnosis
1. 24-hr Urine for Hydroxyindole Acetic Acid (5-HIAA, a serotonin metabolite)
2. Serotonin (plasma)
3. Biopsy
Carcinoid treatment
Ablation by laser
Appearance on CXR and CT of lung nodules. Frequency of malignancy.
Measure 3-6 cm and reside entirely within lung.
20% malignant
Four management strategies for COPD
1. O2 if PaO2< 55 torr
2. Mucous clearing (Guaifenisin & hydration)
3. Exercise!
4. Surgery- lung volume reduction is last resort
Pathogenesis and diagnostic criteria of chronic bronchitis
Pathogenesis: Hypertrophy & hyperplasia of mucous glands in bronchial mucosa, (often with submucosal inflammation)
Diagnostic criteria: Productive cough of at least 3 months duration for @ least two consecutive years.
Lab Values & CXR in chronic bronchitis
CXR will only show other comorbidities (eg, emphysema)
Chronic bronchitis treatment
Quit Smoking!
Mucous clearance (Guaifenisin and hydration)
If active infection exists (which you should not assume) Azithromycin, 5d
COPD/Chronic hypoxemia progression
Hypoxic pulmonary vasoconstriction -->
R-CHF--> Increased JVP, Peripheral edema, Hepatic congestion
You want 'em LARGE- Thin COPD's have exaggerated inflammatory response
Why COPD patients may develop pneumothorax
Dead space--> Bullae--> Pneumothorax develops if bullae burst
Bronchiectasis definition and etiology
IRREVERSIBLE dilation of the medium & large bronchi caused by DESTRUCTION OF ELASTIC TISSUE in the airway.
Usual causes include: PYOGENIC infectiion, cystic fibrosis, Kartagener's syndrome, Aspergilliosis
Bronchiectasis clinical presentation
Chronic productive cough
Recurrent lower respiratory infections
Bronchiectasis appearance on CXR
Hyperinflation (crowding of mediastinum & chest wall);
Cysts & saccules
Dilated peripheral airways on high resolution CT
Bronchiectasis treatment
Mucous clearance (Guaifenisin & hydration)
Postural drainage
Inhaled Tobramycin or Ciprofloxacin (for Pseudomonas)
Cystic fibrosis Genetics
1 in 25 Europeans carriers;
1 in 2500 European livebirths, 1/3500 in U.S.;
One 3 bp deletion accounts for 50%-- but 1500 mutations exist;
Cystic fibrosis cellular pathology
CFTR (Cystic Fibrosis Transmembrane Conductance Regulator) Cl channel defect
Cystic fibrosis diagnosis
"Sweat Chloride test" (Pilocarpine iontophoresis) >60 mmol/L
Cystic fibrosis treatment
1. Pancreatic enzyme replacement;
2. High calorie/fat soluble vitamin diet;
3. Mucous clearance (chest vibrator);
4. DNAse inhaler to digest DNA deposited by pathogens in thickened mucus.
Cystic fibrosis lung transplantation requirement
Remove both lungs.
Both lungs are invariably infected. You'd kill your patient when immune suppressants were started if you didn't take both lungs.
This disorder is a Type 1 hypersensitivity response to allergens in a pulmonary setting
The atopic triad
Asthma, allergic rhinitis & atopic dermatitis
The Asthma presentation triad
Coughing, Wheezing & Dyspnea
Two values that are episodically reduced in asthma
FEV1 & PEFR (Peak Expiratory Flow Rate)
PEFR and how it is measured.
Peak Expiratory Flow Rate;
Measured using a Wright Peak Flow Meter
PEFR (L/min) ≈ [Height (cm) - 80] x 5
How are PEFR results interpreted?
"Green:" 80-100% expected
"Yellow:" 50-80%
"Red:" <50%
G: Smile, Y: Watch, R: Think about another med
Three asthma diagnostic tests
1. PFT (including FEFR)
2. Metacholine challenge: Reduces FEV1 to <80%
3. CXR: MAY show hyperinflation
Asthma treatment progression- by medication class
1. Inhaled short-term ß agonist for rescue;
2. Inhaled low-dose corticosteroids (prophylaxis);
3. Inhaled long-term ß agonist;
4. Inhaled high-dose corticosteroid
5. Mast cell stabilizer or interleukin modifiers
6. Anti-IgE antibody
Asthma treatment progression- by medication name
AL-BE-SA-CRO-OMA (I'll Be Sacral, Oma)
1. Albuterol or Metaproterenol
2. Beclomethasone or Fluticasone
3. Salmeterol (dry powder inhaler)
4. Cromolyn [mast cell inhibitor] or Monteleukast [leukotriene receptor antagonist]
5. Omalizum-AB [mast cell IgG antagonist]
6. Systemic CS- last resort
Acute asthma attack signs and symptoms
Elevated PaCO2
Level of consciousness changes (ALOC)
Pulsus paradoxus
Interstitial lung disease PFT results
ALL volumes decline
Most valuable diagnostic tools for interstitial lung disease
1. PHx & PE;
2. PFT
3. CXR
Histological damage in interstitial lung disease
Injury-> Inflammation -> Disordered repair (Pseudostratified epithelium replaces squamous layer [METAPLASIA])-> Pulmonary fibrosis (SCARRING!)
Interstitial lung disease major etiologies
1. Pneumoconiosis: Silicosis, Anthracosis, asbestosis;
2. Hypersensitivity [pigeons & bats, moldy hay]
3. Prescription drugs/toxins [Amiodarone & Flecainide]
4. Sarcoidosis & Collagen Vascular Disease
Interstitial lung disease signs and symptoms
"Ground Glass" on CXR [should be even distribution in both lungs]
Interstitial lung disease pathognomic finding and its specificity
"Honeycomb" lung with cross-hatching & nodules on HR CT;
85-90% specific
Interstitial lung disease spirometry and lung test findings
1. DLCO Decreases persistently. This is the most sensitive test.
2. O2 desaturates 15 Torr on exercise
3. Lung volumes & flow rates decrease
4. FEF increases 25-75%
Interstitial lung disease treatment
None is effective in reversing the disease.
Prednisone or Prednisolone may be used to suppress inflammation (only little to start)
Differences between non-silicosis interstitial lung disease (NSILD) and ILD
NSILD is more inflammatory- has better response to corticosteroids;
Associated with autoimmune disorders: SLE, RA, Polymyositis, BOOP (Bronchiolitis obliterans organizing PN)
Sarcoidosis pathonogmic finding
Lymphatic disease that spreads to form non-caseating granulomas. May appear in ANY organ, but 94% of patients have in lungs (73% Lymph nodes, 32% Skin, 21% Eyes...)
Sarcoidosis S/s
30% pts are symptomatic;
SOB, Cough, Hemoptysis
Sarcoidosis stages
0. Normal
1. Hilar lymphadenopathy
2. Hilar LA + Lung infiltrates
3. Substantial lung infiltrates + fibrosis
4. End stage fibrosis [honeycomb scarring]
Two key Sarcoidosis extra-pulmonary concern
1. Granulomatous Uveitis (red, photophobia --> glaucoma)
2. Hypercalcemia [10-20%] because activated macrophages in the lung and lymph nodes produce calcitriol [vitamin D] independent of PTH -->Cardiomyopathy
Sarcoidosis Tx- Who, When & How
-Stage 3 & 4, OR:
-Cardiac S/s, Uveitis, Hypercalcemia
Tx: Corticosteroids. On-a-yr/off-a-yr
Two ILD's related to vascular disorders
1. Goodpastures: Associated w/ idiopathic alveolar hemorrhage & destruction of the glomerular basement membrane.
2. Wegner's Granulomatosis: Associated w/ vasculitis & autoimmune attack by ANCAs [Anti-Neutrophil Cytoplasmic Antibodies] against small and medium-size blood vessels in the lungs & kidney.
Virchow's Triad & what it most often contributes to
Stasis, Injury & Hypercoagulability;
Appears as DVT and emboli
DVT tests
Doppler US
Impedance Plethysmography
PE epidemiology
120K cases/yr
50% Untreated Symptomatic are fatal
TWO serious problems PE creates
1. Shunt: (no air, lotsa blood), so hypoxia occurs;
2. Blocked pulmonary vessel raises P-BP to over 40 mm Hg (usual 20/8);
NOTE: Shunts don't respond to O2
PE S/s
Dyspnea, Anxiety, Syncope, Chest pain;
DVT, S3 gallop & Crackles are pathognomic when together
The two Pulmonary Embolism tests you must perform
1) D-Dimers: [Positive is 90-95% sensitive]
2) EKG: To rule out MI & check for RBBB
PE Gold Standard
Pulmonary Angiography: Way low risk, Way high value;
BUT: Spiral CT is better
1. Heparin followed by warfarin
2. Thrombolytics (tPA or Streptokinase)
REAL LIFE: DON'T give THROMBOLYTIC- Risks Intercranial hemorrhage
Normal mean Pulmonary Blood Pressure & Pulmonary Hypertension values
Normal is 20/8, so mean is [0.5][20] + 8 = 18 mm of Hg
Pulmonary Hypertension is defined = 25 mm of Hg
Normal causes of P-HTN & why
Ischemic heart dz or LVH/LCHF;
(Left side weak, right backs up)
S/s of RV failure & P-HTN
Pedal edema;
Increased JVP;
S3 (RV "heave")
Diagnosis of pulmonary hypertension
1. Echo;
2. Heart catheterization
3. Pulmonary capillary wedge pressure
4. Spirometry to rule out lung disease mimics
Primary: Warfarin, Vasocilators (CCB or Prostacycline);
Secondary: Tx the underlying Dz & correct hypoxia
Two types of Pleural Effusion
Transudate: Low protein/pus
Exudate: High protein/pus/blood
Causes of transudates
Non-infectious sources of pulmonary hypertension: CHF, Cirrhosis, Renal failure, Hypothyroid
Causes of exudates; Special classes high in blood or fat
PN, Ix, Malignancy, PE;
Hemothorax & chylothorax
Exudate Test values
Protein: >0.5
LDH: >0.6
Also run Glu & pH
Accumulation of air in pleural cavity & sources of air
Sources: Lung, Chest wall, Esophagus, Bacterial metabolism in Ix
Most likely pneumothorax pts
Young, thin men 20-40 yrs. Pleural blebs burst
Pneumothorax Tx (clever, really)
Inject doxycycline-- Irritates pleural membranes, and they fuse during inflammatory response.
Who should get 'flu vaccine?
1) 65 years and over
2) All health care workers
3) Chronic pulmonary morbidities [COPD, Asthma, ILD, also DM]
4) 2nd and 3rd trimester pregnancy
Who should get pneumococcus vaccine?
1. All Chronic pulmonary morbidities (COPD< Asthma, ILD) every 5 yrs until 65
ARDs precipitating causes
Alcohol, Drugs, Trauma, Sepsis, Burns
Allergic bronchopulmonary aspergilliosis treatment
Prednisone plus Itraconazole