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80 Cards in this Set

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  • Back
  • 3rd side (hint)
Alveolar Gas Equation
Gas Equation
Causes of Hypoxemia
-Alveolar hypoventilation
-Reduced partial pressure 02 (PiO2)
-Ventilation perfusion (V/Q) mismatch
-Diffusion abnormality
Draw algorithm for determining cause of hypoxemia
See Pathophysiology for the Boards and Wards p. 90
Causes of PCO2 change
-V/Q mismatch
Restrictive diseases (hint available)
Pleural disease
Alveolar filling disease
Interstitial disease
Neuromuscular disease
Thoracic cage abnormality
Difference between restriction and obstruction
Restriction: Can't fully inhale

Obstruction: Can't fully exhale
Factors that affect DLCO
-Ability to get CO to alveolus (ventilation)
-Ability of blood stream to pick up CO (perfusion)
-Ability of RBC to pick up CO (hemoglobin)
Obstructive lung disease with normal DLCO
-Upper airway obstruction
Why might a TLC (total lung capacity) measured by plethmysography be higher than one measured by helium
"Helium may not reach all areas of the lung. It will thus be diluted in a smaller volume of lung than actually exists."

(from syllabus p. 73 by J. Unterborn)
Causes of obstructive lung disease (Hint available)
-Foreign body/upper airway problem
-Chronic bronchitis/bronchiectasis
-Small airways (ie bronchiolitis)
Obstructive lung disease with reduced DLCO
Restrictive lung disease with normal DLCO
-Pleural disease
-Neuromuscular disease
-Thoracic cage abnormality (Chest wall disease)
Restrictive lung disease with reduced DLCO
-Alveolar filling disease
-Intersticial disease
Respiratory muscles: Two major physiologic principles governing function: Explanation
1. Length-tension (the longer the muscle prior to contraction, the stronger the contraction)
2. Force-velocity (the faster a muscle contracts, the smaller the force)
Respiratory muscles: Two major physiologic principles governing function: Examples of dysfunction
1. Length-tension. (In COPD, the diaphragm, scaleni, and sternomastoids are shortened already. Little tension can be generated.)

2. Force-velocity (High activity/severe obstruction --> increased velocity --> less force)
Definitions of muscle fatigue and weakness
Fatigue: Decline of ability to generate force

Weakness: Inability to exert force to the degree expected given general physical fitness
What is the progression of ARDS (acute respiratory distress syndrome)
1. Acute Lung Injury
2. Increased Permeability
3. Increased Lung Water (Interstitial/Alveolar)
4. Reduced Compliance


4. Increased shunt leading to hypoxemia
What are the parameters measured in mechanical ventilation and why?
1. PEEP (positive end-expiratory pressure - to maintain maximal recruitment of alveolar units)
2. mean airway pressure (to promote recruitment and predictor of hemodynamic effects)
3. plateau pressure (best predictor of alveolar overdistention)
Why are low tidal volumes preferred over high tidal volumes in mechanical ventilation? What are the cautions associated with low tidal volumes?
High tidal volumes --> overstretched alveoli --> volutrauma (2ndary lung injury)

Cautions: low tidal volume --> hypercapnia and atelectasis
What are three reasons that PEEP (positive end-expiratory pressure) is important?
1. Prevents alveolar collapse
2. Recruits more lung units
3. Increases FRC (functional residual capacity)
4. Redistributes fluid in the alveoli
What are the causes of increased airways resistance in asthma and what is primarily responsible for these changes?
Inflammation leads to:

1)excess airway secretions
2)abnormal smooth muscle contraction
3)thickening of the airway wall
What cells infiltrate the airway wall in asthma?
1) eosinophils
2) Th2 cells
3) Mast cells
What are the stages of inflammation in an asthma attack and what are their time durations?
1) Early phase - starts within minutes of exposure, maximal at 30 minutes, subsides in 1-2 hours
2) Late phase - 4-6 hours after exposure, maximal at
What are the stages of inflammation in an asthma attack and what happens in them?
1) Early phase - Mast cells release histamines
2) Recruited inflammatory cells and other mediators.
Difference between inflammatory responses in asthma and COPD
Asthma: CD4+ lymphocytes and eosinophils

COPD: CD8+ lymphocytes, neutrophils and macrophages
Mild intermittent asthma: Definition and treatment
Def: less than 2 days per week and/or less than 2 nights per month

Tx: No daily medication needed. Systemic corticoids recommended for severe exacerbations.
Mild persistent asthma: Definition and treatment
Def: More than 2 days per week but less than once per day and/or more than 2 nights per month.

Tx: Low dose inhaled corticosteroids.
Moderate persistent asthma: Definition and treatment
Definition: Daily symptoms plus more than 1 night per week

Tx: Low to medium dose inhaled corticosteroids AND long-acting inhaled beta2-agonists
Severe persistent asthma: Definition and treatment
Definition: Continual symptoms during the day and frequent symptoms at night

Tx: High dose inhaled corticosteroids AND long-acting inhaled beta2-agonists AND (as needed) corticosteroid tablets
Asthma: Common symptoms
-Dyspnea at rest/with exertion
-Cough (exacerbated frequently by deep inspiration or laughing)
-Chest tightness/pain
-Exercise intolerance
-Hyperventilation syndrome
Pathogenesis of COPD
1. Chronic inflammation + Imbalance between proteinases and anti-proteinases + oxidant stress + time
2. Destruction and remodeling of alveolar units
3. Lack of elastic recoil & expiratory airway collapse
Basic treatment of COPD (hint available)
1. Smoking cessation
2. Inhaled bronchodilators (beta2-agonists, anticholinergics)
3. Systemic bronchodilators (theophylline)
4. Systemic corticosteroids (acute only)
5. Immunization
6. Nutrition
7. Oxygen
8. Pulmonary rehab
8 treatment measures
Define cor pulmonale
Right ventricular hypertrophy resulting from pulmonary circulation system
Mechanisms of pleural effusions
1. Increased hydrostatic forces (CHF --> increased pulmonary venous pressure)
2. Reduced plasma oncotic pressure (hypoproteinemia)
3. Reduced mean intra-pleural pressure (respiration atelectasis)
4. Disruption of mesothelium and capillary walls (inflammation/tumors)
5. Lymphatics (destruction/hypoplasia/obstruction)
6. Transdiaphragmatic flow (ascites)
6 in total
Treatment of pleural effusions (transudate versus exudate)
Transudate: Treat underlying problem.
Exudate: Further diagnostic tests
Pleural effusions: How to distinguish transudate from exudate
Exudate if presence of at least one:

-pleural fluid protein: serum protein ratio > 0.5
-pleural fluid lactate dehydrogenase: serum LDH ratio > 0.6
Pleural effusions: Symptoms and signs
Sx: 1) Dyspnea 2) Chest pain

Si: 1) Reduced excursion over the effusion 2) dullness to percussion 3) diminished/absent breath sounds over the effusion
Definition: CFTR
Transmembrane conductance Regulator
Function of CFTR and result of its absence
cAMP-dependent Cl transport into lumen of organs

Absence: Very viscous secretions
Pathogenesis of cystic fibrosis (hint available)
1. CFTR incompetence
2. Increased viscosity of secretions
3. Airflow obstruction AND Colonization by P. aeruginosa, H. flu, or S. aureus
4. Chronic inflammation (lumen destruction)
5. Destruction of airways and bronchiectasis
6. Expiratory flow limitation
6 steps
Treatment of cystic fibrosis/bronchiectasis
1. Antibiotics
2. Inhaled mucolytics
3. Bronchodilators (may worsen if loss of airway tone by making airway floppy)
4. Physical maneuvers for clearing functions
Common features of interstitial lung diseases
-Exertional dyspnea
-Bilateral diffuse infiltrates on CXR
-“Restrictive” physiology (decreased lung volumes) with abnormalities in gas exchange at rest or with exercise.
-Immunocompetent host; absence of infection or neoplasm
-Varying degrees of inflammation and fibrosis on histopathology
General picture: Restrictive PFTs
1. Shift in pressure volume curve to the right
2. Reduction in:
a. TLC
b. VC (due to fall in compliance)
c. RV
3. Classic obstruction absent
Signs, symptoms, and treatment: IPF (Idiopathic Pulmonary Fibrosis)
1. Interstitial infiltrates/honeycomb lung (end stage)
2. Restriction on PFTs

1. Dyspnea
2. Dry cough
3. Gradual weight loss
4. Fatigue
5. Clubbing (enlargement of the fingertips or sometimes the toes)

Tx: Anti-inflammatory
Signs, symptoms, and treatment: Sarcoidosis
1) Non-caseating granulomas involving at least 2 organs
2) Bi-basilar end-inspiratory crackles
3) Restriction on PFTs

1) Uveitis
2) Cough (non-productive)
3) Dyspnea
4) Weakness, fatigue, weight loss

Tx: Corticosteroids
Signs, symptoms, and treatment: Hypersensitivity Pneumonitis
AKA Farmer's/Pigeon Breeder's/Mushroom Picker's Lung

1) Honeycomb lung
2) Restriction on PFTs

1) Fever, chills, malaise
2) Chest tightness
3) Dyspnea

1) Allergen avoidance
2) Corticosteroids
How do you distinguish between acute, subacute hypersensitivity pneumonitis
Acute: More severe, shorter duration

Subacute: Less severe, longer duration
Definition: Occupational Asthma
Occupational asthma includes only those individuals whose asthma is attributable to the work place and to no other outside exposure
Most common manifestation of asbestosis
Pleural plaques
All manifestations of asbestosis
Pleural manifestations (pleural plaques, benign asbestos pleural effusion, mesothelioma)

Lung parenchymal involvement (asbestosis, lung cancer)
Silicosis: clinical presentation
Sx: Usually none, or dyspnea and non-productive cough.

1) Egg shell calcifications on CXR
Effect of vascular disease on gas exchange
-Pulm vascular obstruction --> increased Dead Space
-Hypoxemia: related to V/Q mismatch and shunt
Effect of vascular disease on pulmonary function tests
-Either normal or restrictive pattern
-DLCO is normal or reduced
Primary pulmonary hypertension: clinical presentation
1)Young (20-50)
2)Female (2:1)

1)Easy fatigue
2)Exertional dyspnea
3)Dyspnea (especially on exertion)

1) Loud P2
2) Cyanosis
Pulmonary embolus: Risk factors
Virchow's triad (over 90% of cases have at least one):
1) Stasis
2) Inflammation
3) Hypercoagulability
Pulmonary embolus: Clinical presentation
1)Progressive dyspnea
2)Chest pain


1)Multiple thrombi in small to medium sized arteries
Pulmonary hypertension: Treatment
a)Calcium channel blockers
c)Endothelin receptor antagonists
d)Phosphodiesterase 5 inhibitors
2)General measures
Inhaled Delivery of drugs: General advantages
1) Deliver high concentrations of drug to primary site
a. smaller total dose --> fewer systemic side effects
b. faster delivery
2) Large surface area
3) Reproducible absorption kinetics
Bronchodilators - Beta-agonists: Mechanism
Increases cAMP via Beta 2 receptor and increases Ca++ efflux to relax bronchial wall smooth muscle
Bronchodilators - Anti-cholingergics: Mechanism
Blocking of Muscarinic Receptors to block cholinergic bronchoconstiction
Inhaled steroids: Advantage over topical steroids
Fewer systemic effects
Common inhaled steroids
Lung cancer: Usual symptoms
1) Cough
2) Anorexia/weight-loss
3) Dyspnea
4) Hemoptysis
5) Chest pain
Lung cancer: Usual signs
1) Localized wheezing
2) Neurologic (Horner's, vocal cord paralysis, unilateral diaphragm movement)
3) Shoulder pain with ulnar radiation
4) Prescalene/supraclavicular lymphadenopathy
Lung cancer: Risks
1) Smoking
2) Atmospheric pollution
3) Asbestos & other occupational toxins
4) Diffuse Pulmonary Fibrosis
6) HIV
Factors which affect minute ventilation
1) Arterial and CSF PCO2 (+)
2) Voluntary hyperventilation (++)
3) Exercise (++)

1) Sleep
Conditions with impaired response to hypoxia
1) Narcotic addicts
2) Carotid endarterectomy
3) Cyanotic congenital heart disease
4) Altitude native
5) Arnold-Chiari syndrome
Conditions with impaired response to hypercapnia and hypoxia
2) Sleep deprivation
3) Bulbar poliomyelitis
4) Metabolic alkalosis
5) Myxedema
6) Severe Hepatic Failure
7) Bilateral spinothalamic lesions
Conditions with augmented response to hypercapnia and hypoxia
1) Hyperthyroid
2) Salicylism
3) Fever
4) Posthemodialysis
5) Luft’s Syndrome
6) Pregnancy
7) Mild Hepatic Failure
Pathophysiology of Obstructive Sleep Apnea
1) Repetitive episodes of upper airway obstruction
2) Reduction in blood oxygen saturation
3) arousal from sleep
4) symptoms of snoring and sleepiness
5) catecholamine release
Apnea: definition
cessation of airflow for greater than 10 seconds
Hypopnea: definition
reduction of airflow by >50% associated with an arousal or >3% desaturation
Obstructive sleep apnea: Risk factors
-Obesity, neck size >17 “
-Male gender
-Craniofacial abnormalities
-Nasal obstruction/redundant soft palate
-Endocrine abnormalities
-Family History
Obstructive sleep apnea: associated features
-Impotence/loss of libido
-Cognitive Deficits
Sleep deprivation: PFTs
-20% reduction in response to hypoxia and hypercapnia
-Reduced FEV 1
-Reduced FVC
Sleep in COPD
-Delayed onset
-Frequent awakenings
-Nocturnal worsening of hypoxemia
Sleep in restrictive lung disease: chest wall deformity
-Decrease in VC, TV and ERV
-Increase in pulmonary vascular resistance
-Hypercarbia and hypoxemia
-V/Q mismatch
-Rapid shallow breathing
Sleep in restrictive lung disease: pregnancy
-Decrease in FRC and RV
-Increase in V/Q mismatch
-Worse in supine position
Sleep in restrictive lung disease: obesity
-decreased compliance of the thoracic cage
-decreased FRC
-increased V/Q mismatch
Hypoventilation sydromes
Sleep in restrictive lung disease: neuromuscular disorders
-Decrease in : FRC, TV, ERV, -lung compliance
-Increase in: RR
-Pharyngeal and laryngeal muscles involved: increase in OSA
-Hypoventilation, esp in REM
-Hypoxia and hypercarbia