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Developmental "cut-off" for RDS

24 weeks

Typical Pulmonary A pressure


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

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)

Calibration, Coaching, Care of Equip, Cognizance of poor results

Most reliable & available pulmonary test


What two lung volumes are not amenable to direct spirometry?


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


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

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
Tx: Erythromycin, Azithromycin, or TMP-SMX [Bactrim]

Pneumonia S/s tetrad

Cough w/ purulent sputum or hemoptysis
Crackles or pleuritic chest pain
dyspnea & SOB

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


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
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

Ablation by laser

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

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


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

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


"Sweat Chloride test" (Pilocarpine iontophoresis) >60 mmol/L


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


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

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


"Ground Glass" EVEN distribution, BOTH LUNGS

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%


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

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

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