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Pulmonary Clin Med

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Developmental "cut-off" for RDS
24 weeks
Typical Pulmonary A pressure
20/8
Two sets of respiratory centers & their fx's
Medullary: Control resting breathing
Pontine: Control laboured breathing
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.
Ventilation:Perfusion ratio & Ideal value
Ratio of Air delivered to alveoli to Blood delivered to alveoli;
1 L of blood holds ≈ O2 in 1 of air, so V/Q = 1
Ventilation Perfusion 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 Shunts occur? Response to O2 therapy?
Occur in Pneumonia or area around pulmonary effusions filled w/ fluid.
Poor or absent response to O2 therapy
When do Dead Spaces occur? Response to O2 therapy?
Occur in areas of limited or absent arterial perfusion. Again, no 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 four types of pulmonary testing
Spirometry
DLCO (Diffusion of the Lung to CO)
Body Plethysmography
Bronchial Challenge
What does DLCO measure, and how is it accomplished?
-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 PFT (Pulmonary Function Testing)
FOUR C's
Calibration, Coaching, Care of Equip, Cognizance of poor results
Most reliable & available pulmonary test
Spirometry
What two lung volumes are not amenable to direct spirometry?
TLC & RV
Two criteria for performing spirometry
Known/suspected lung Dz;
Pt at risk for pulmonary Dz undergoing general anesthesia
Lung volumes altered in Obstructive lung dz's
Increased: RV [X 2.5!]
Decreased: IRV & ERV
Net: Increase by ≈20%
Lung volumes altered in Restrictive lung dz's
Decreased: IRV, ERV, RV, TV
Net: Decrease ≈25%
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
Three levels of Obstructive Lung Dz & FEV1/VC ranges
Mild: 60-69%
Moderate: 46-59%
Severe: <45%
Asthma Indicators
Albuterol Improvement:
FEV1 or FVC>12%
VC: >10% Inhaled improvement vs Exhaled improvement
Portion of Flow Volume curve that is altered by forced expiration
Effort-dependent (peak portion)
Portion of Flow Volume curve that is altered in lung dz, & 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
CC-S/s-Eti-Epi-Pathophys-DDx-Dx-Tx-F/u
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
Exudate/swelling
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
DOE/SOB
But-- no fever, chills or Crackles [these indicate pneumonia]
Acute bronchitis etiology
Viral or bacterial infection, especially in COPD & Asthmatics
DDX: Bronchitis v Pneumonia
PN:
Fever/chills
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
AmANTADINE, RimANTADINE, OseltAMIVIR, ZanAMIVIR
Must be 1st 48 hrs of exposure (@ first S/s)
U.S. flu mortality
40K/yr in US
Flu S/s
Fever/chill, headache, cough, myalgia.
The 1st three together have high specificity.
Absent in flu
NO: abnormal CXR, WBC-cytosis
Rapid Influenza screen values
Sensitivity: ≈70%
Specificity: "very high"
Three phases of pertussis
Catarrhal: Malaise, mild cough, conjunctivals
Paroxysmal: Severe cough/stridor, may have post-tussive emesis (1-6 wk)
Convalescent: Slow (2-3 wk) recovery
Pertussis findings & Tx
S/s: Paroxysmal coughing w/ stridor
Lymphocytosis
Tx: Erythromycin, Azithromycin, or TMP-SMX [Bactrim]
Pneumonia S/s tetrad
Fever/chill
Cough w/ purulent sputum or hemoptysis
Crackles or pleuritic chest pain
dyspnea & SOB
TWO IS ENOUGH TO REQUIRE CULTURE & CXR
Pneumonia risk progresion
CA <CA + comorbid <HA <Immunocompromised
Pneumonia test sensitivity & specificity
Bronchoscopy: ≈50% ea
Lung biopsy: 50% & >90%
But biopsy too invasive unless already in there
CAPn pathogens
Strep pneu, HiB, Moraxella, Chlamydia, Mycoplasma, Legionella (last three "atypicals")
HA-Pn pathogens
MRSA, Pseudomonas (vent), Klebsiella
Local pulmonary/systemic mycosis
Coccidiodes immitis
U.S. Endemic Mycoses
Coccidiodes, Histoplasma (obligate parasite), Blastomyces, also Aspergillis & Rhizopus
Fungal lung Ix tx
Fluconazole or Amphotericin B
When should you resect pulmonary granulomas/spherules
Almost never (severe hemoptysis)-- mortality is 25%
Aspergilliosis S/s & Tx
Severe asthma S/s
Elevated IgE, eosinophils
Hypersensitivity to spores/hyphae;
Tx: Prednisone
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
S/s of Primary TB
USUALLY asymptomatic,
may have Reactivation S/s
S/s of Reactivated TB
Wt loss, night sweats, productive cough (may show purulence & hemotypsis), pleuritic chest pain
TB CXR
Cavitating pneumonia
Calcified nodules
Hilar effusion or lymphadenopathy
Upper lobe atelactasis (collapse)
How do you Dx ACTIVE TB
POS Mantoux AND POS CXR or Acid Fast
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 Dx LATENT TB?
Positive Mantoux only
When do you Tx LATENT TB?
Anyone <35;
Recent intimate exposure
HIV POS
If >15 mm Mantoux induration
Previous NEG Mantoux & now converted POS
LATENT TB Rx regimens
9 mo Isonizid (INH)
Lung Abscess Etiology & Dx
Drinkers pass out, oral bacteria make way into lungs;
Look for poor dentition, purulent cough and halitosis-- Confirm w/ CXR or bronchoscopy
Why is lung CA often well-progressed before identified?
No sensory innervation in lungs, so may be asymptomatic until tumor mass interferes w/ pulmonary fx
Lung CA S/s
Cough, Hemoptysis, Dyspnea, Metastatic S/s: Invasion of neighbouring tissue, Distant neoplasia, Paraneoplastic syndromes (eg, Cushing's or Phaeo)
Indications of local invasion by lung tumors
Cardiac tamponade, Dysphagia, Bronchial occlusion
The mathematics of mutation: Smoking & Asbestos
Smoking (Benzpyrene) multiplier: 9X
Asbestos multiplier: 5X
Both smoking/asbestos: 50X
Two classes of lung CA
Small cell, Non-small cell
Etiology of SCLC [that is, Small Cell Lung Cancer]
Arise from neuroendocrine cells. [wow...I didn't know that...]
Lung CA Dx tools
Chest film (poor)
CT (better): bonus is seeing lymph nodes in area
Bronchoscopy (Good- if you find the tumor)
The Small Cell Assumption you must make
Assume it's malignant. Always.
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 CA
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), you must call it off.
Tx of NSCLC (Non-Small Cell Lung CA)
1. Resection- if you're sure you'll get it all
2. Radiation- Symptomatic relief, no increased survival
3. Chemo: Almost useless in Non-Small Cell CA
Tx of SCLC (Small Cell Lung CA)
1. Assume malignant at discovery
2. Chemotherapy (Methotrexate or Etoposide)
3. Radiation to primary site
4. Surgery is controversial, only used for limited dz
Lung CA Survival & Recurrence
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 w/ low malignancy, usually in GI;
28% occur in Respiratory sys
Carcinoid S/s
Catecholamine effects: Flushing, Palpitations, Diarrhea, Wheezing, Abdominal cramps;
Resp effects IF pulmonary site: Cough, Hemoptysis, Recurrent PN, Airway obstruction
Carcinoid Dx
1. 24-hr Urine for Hydroxyindole Acetic Acid (5-HIAA, a serotonin metabolite)
2. Serotonin (plasma)
3. Biopsy
Carcinoid Tx
Resection
Ablation by laser
Octreotide
Lung nodules
Measure 3-6 cm, show on CXR, & entirely within lung.
20% malignant
Four management strategies for COPD
1. O2 if PaO2< 55 torr
2. Mucous clearing (Guaifenisin)
3. Exercise!
4. Surgery- lung volume reduction is last resort
Chronic Bronchitis Dx criteria & Pathophys
Dx: Productive cough at least 3 mo for @ least two yrs;
Path: Hypertrophy & hyperplasia of mucous glands in bronchial mucosa, (often w/ submucosal inflammation)
Lab Values & CXR in Chronic Bronchitis
Labs NORMAL
CXR will only show other comorbidities (eg, emphysema)
Chronic bronchitis Tx
Quit Smoking!
Mucous clearance (Guaifenisin)
If active Ix (which you should assume) Azithromycin, 5d
COPD/Chronic hypoxemia progression
Hypoxic pulmonary vasoconstriction -->
R-CHF--> Increased JVP, Peripheral edema, Hepatic congestion
COPD & BMI
You want 'em LARGE- Thin COPD's have exaggerated inflammatory response
Why COPDs may develop Pneumothorax
Dead space--> Bullae--> Pneumothorax if "pop"
Bronchiectasis def & etiology
IRREVERSIBLE dilation of the medium & large bronchi caused by DESTRUCTION OF ELASTIC TISSUE in the airway.
Usual causes include: PYOGENIC Ix, CF, or Kartagener's syndrome (AR causes defect in respiratory cilia), Aspergilliosis
Bronchiectasis S/s
Chronic productive cough
Recurrent LRI
Hemoptysis
Crackles
Bronchiectasis on CXR
Hyperinflation (Crowd mediastinum & chest wall);
Cysts & saccules
Dilated peripheral airways on Hi Res CT
Bronchiectasis Tx
Mucous clearance (Guaifenisin)
Postural drainage
Hydration (thins mucus)
Inhaled Tobramycin or Cipro (Pseudomonas)
CF 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;
CF cellular pathology
CFTR (Cystic Fibrosis Transmembrane Conductance Regulator) Cl channel defect
CF Dx
"Sweat Chloride test" (Pilocarpine iontophoresis) >60 mmol/L
CF Tx
1. Pancreatic enzyme replacement;
2. High calorie/fat soluble Vitamin diet;
3. Mucous clearance (chest vibrator);
4. DNAse inhaler to digest DNA "dumped" by pathogen in thickened mucus.
CF Lung Transplantation requirement
Make it a double--
Both lungs re invariably Ix'd. You'd kill your pt when immune suppressants were started if you didn't take both.
This D/o is a Type 1 HS response to allergens in a pulmonary setting
Asthma
That atopic triad we all know and love...
Asthma, Allergic rhinitis & Atopic dermatitis [eczema, eh?]
The Asthma S/s triad
Coughing, Wheezing & Dyspnea
Two values that are EPISODICALLY reduced in asthma
FEV1 & PEFR (Peak Expiratory Flow Rate)
What the heck is PEFR & how's it 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 tests
1. PFT (including FEFR)
2. Metacholine challenge: Reduces FEV1 to <80%
3. CXR: MAY show hyperinflation
Asthma Tx progression- by CLASS
1. Inhaled SHORT-TERM ß-blocker for rescue;
2. Inhaled Corticosteroids (prophylaxis);
3. Inhaled LONG-TERM ß-blocker;
4. Inhaled Hi-dose CS
5. Chromomes or Interleukin modifiers
6. Anti-IgE antibody
Asthma Tx progression- by Rx
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 re ceptor antagonist]
5. OmalizumAB [mast cell IgG antagonist]
6. Systemic CS- last resort
Acute Asthma attack S/s
HELP!
Hyperventilation
Elevated PaCO2
Level of Consciousness changes (ALOC)
Pulsus paradoxus
ILD PFT results
ALL volumes decline
Most valuable Dx'c tools for ILD
1. PHx & PE;
2. PFT
3. CXR
Histological damage in ILD
Injury-> Inflammation -> Disordered repair (Pseudostratified epithelium replaces squamous layer [METAPLASIA])-> Pulmonary fibrosis (SCARRING!)
ILD major causes
1. Pneumoconiosis: Silicosis, Anthracosis, asbestosis;
2. Hypersensitivity [pigeons & bats, moldy hay]
3. Rx's/toxins [Amiodarone & Flecainide]
4. Sarcoidosis & Collagen Vascular Disease
ILD S/s
CCCGGH
**Crackles
Clubbing
Cyanosis
"Ground Glass" EVEN distribution, BOTH LUNGS
Honeycombing
ILD Pathognomic finding & Specificity
"Honeycomb" lung w/ cross-hatching & nodules on HR CT;
85-90% Specifric
ILD spirometry & 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%
ILD Tx
None effective;
Prednisone or Prednisolone to suppress inflammation (only little to start)
Non-Silicosis Interstitial Lung Dz (NSILD) differences from ILD
MORE inflammatory- better response to Corticosteroids;
Associated w/ AIs" SLE, RA, Polymyositis, BOOP (Bronchiolitis obliterans organizing PN)
Sarcoidosis pathonogmic finding
LYMPHATIC dz that spreads to form Non-caseating Granulomas. May appear in ANY organ, but 94% of pts 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
Venography
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;
D-C-3:
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
PE Tx
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
P-HTN Tx
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
Pneumothorax;
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