HY Pulmonary PaPh Assessment 6
Gas Exchange
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Hypoxemia:
o Decreased oxygen tension in circulating blood compared to normal
A-a gradient
o Difference between Alveolar (A) and arterial (a) partial pressures of oxygen
o Normally less than 25mmHg
o Normal A-a can be calculated: (Age +4 / 4)
Causes of Hypoxemia
Normal A-a gradient
Decreased PIO2
Hypoventilation
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Widened A-a gradient
Diffusion limitation
R to L shunt
V/Q mismatch**Most common
PACO2=K x VCO2 / VA
o As ventilation increases carbon dioxide decreases
o As ventilation decreases carbon dioxide increases
 More carbon dioxide means respiratory acidosis (carbonic anhydrase)
o As carbon dioxide increases, alveolar oxygen decreases (less ventilation, less oxygen)
PAO2=PI02-(PCO2/0.8)
o PIO2= 0.21 (760mmHg-47mmHg), usually 150mmHg
o 0.8 comes from VCO2 production/VO2 consumption (200/250=0.8)
 Known as respiratory quotient
Shunts
o Bypass lungs
o 5% of blood is shunted from arterial to venous system normally
o Anything that causes a defect in ventilation area would cause a functional shunt
o Adding 100% oxygen does not improve this condition
o QS/QT
VA/Q
o High = oxygen not getting to blood (too much VA not enough Q)
o Low = blood not getting oxygen (too little VA, plenty of Q)
Oxygen Transport
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Lungs, blood, heart involved in oxygen transport
Oxygen distribution equation
o DO2 (ml/min)=CO (L/min) x CaO2 (ml/dl) x 10 dl/L
 CO is usually 5L/min (HR x SV ; 72 bpm x 70 ml)
 Increases in cardiac output increases DO2 linearly
 PaO2does not increase DO2 linearly (due to Hb sat. curve)
 Hb content increases DO2 linearly
 CaO2=[1.39 x Hb (g/dl) x Hb Sat. %] + [0.003 PaO2]
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 Normally 165
 Normally 15g of Hb in 1 dl of blood
 15g x 1.39=20.85g/dl
 Note: The 1.39 is at 100% hemoglobin saturation
Normally adult consumes 250 ml O2/min
VO2 (ml O2/min) = CO(L/min) x [CaO2-CvO2]x 10 (dl/L)
 This equation calculates the consumption of oxygen in the body
 CvO2=1.39 x Hb x SvO2 +(.003 x PvO2)
Figure 1. Hb Sat. Curve (KNOW THIS)
Curve shifts to Rdeceased affinity for oxygen
COPD
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Chronic bronchitis is a disease of airways, not alveoli
o 3 months in 2 years of excessive coughing with copious sputum production
o Increased reid index
Emphysema is a disease of alveoli and small airways
Bronchiectasis=necrotizing infection of bronchi leading to dilation of airways
COPD definition: disease state characterized by airflow limitation that is not completely
reversible
o Major mechanism of hypoxemia in COPD patients is a V/Q mismatch445
Allergic Bronchopulmonary asperigillosis
o Criteria:
o 1)asthma, 2)immediate cutaneous rx. To a. fumigates, 3)IgG ab to A. fumigates,
4)IgE>1000ng/ml, 5) Increased IgE Ab to A. fumigates
o Type III hypersensitivity
Nocturnal asthma
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Decline of catecholamines/cortisol at night (thus decreased b-2 activity) leads to
nocturnal asthma
o Tx.
o Tx. With albuterol or salmoterol
o PEFR worse at night due to this, best at 4pm worst at 4am
Methacholine challenge w/ no asthma signs can rule out asthma (High NPV)
Drug induced asthma triad
o Aspirin
o Nasal polyps
o Asthma
Restrictive Lung Disease
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Can be due to loss of lung, pleura, chest wall, or NMJ abnormalities
Respiratory failure=hypoxemia in absence of hypercapnia
Ventilatory failure= hypercapnia
Hypercapnia develops from
o Increase in dead space
o Decrease in minute ventilation
o Increase in carbon dioxide poisoning
Give oxygen to hypercapnic patients!
o Three reasons why carbon dioxide goes up after giving oxygen
o Haldane effect
o Worsening V/Q mismatch ** main cause
o PCO2 inversely related to ventilation
o Pt. with COPDgiven 40% oxygen and CO2 goes up, should we cut oxygen? NO Keep on
oxygen and increase until at least 88% sat. Keep on mechanical vent.
 CO2 increases upon giving oxygen due to Haldane effect, and respiratory muscle
fatigue
Hypoxemia of ILD due to V/Q mismatch
Type II pneumocytes increase in ILD
Ground glass appearance on CXR
Increased lymphocytes=sarcoidosis, Increased PMN’s=pneumonia
Normal BAL: 90% macrophages, 10% lymphocytes, <1% PMNs
Increased thickness and decreased surface area cause a decrease in DLCO!!!
40 y/o sandblaster, FEV<80%, DLCO less than 80% what was involved? Silicosis
o What does this predispose to ? TB
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ARDS
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TNF-alpha, IL-1: Inflammation, Coagulation, Tissue Repair
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ARDS characterized by acute decrease in lung compliance
High grade systemic inflammation in ARDS
Treatment w/ Mechanical Ventilator’ in ARDS, 6-8c, decrease in tidal volume prevents further
damage and decreased mortality
Increase PEEP to improve oxygenation in ARDS
Non-survivors have increased pro-inflammatory cytokines
o Patients have a huge shunt area once alveoli are collapsed
o PEEP allows to break shunt
o MODS can develop
Pleural Effusions
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Visceral pleura: cells are loose
Parietal pleura: cells are tight
Normal content of pleural fluid: colorless, protein<1.5g, 1500 cells/ml
Pleural fluid moves from parietal pleuravisceral pleura where it is reabsorbed
o Hydrostatic pressure gradient
o (Pc-Ppl) - (pic-pipl)
Only parietal pleura has lymphatic openings
Increased hydrostatic pressureheart failuretransudate
Decreased pleural pressureatelectasistransudate
Decreased oncotic pressure of plasmalow albumintransudate
Increased oncotic pressure of pleural fluidinflammationexudate
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pH, glucose, cell count etc. do not effect difference between transudate and exudates
KNOW THIS FOR TEST
KNOW FOR TEST
Know the differences between exudates and transudates
Protein>0.5 and LDH > 0.6 are indicative of an exudates (ratio’s of fluid/serum
amounts), also >60mg/dL cholesterol
Most frequent cause of pleural effusion is heart failure
Increased permeability (Slide 14)
o Increased production of fluid due to increased inflamed area (infection, inflammation,
cancer) causes increased vascular permeability and increased protein concentration in
pleural effusion
o KNOW FOR TEST
Etiology of Pleural Effusion (Slide 17)
o Heart failure is the leading cause, KNOW THIS
o Know what is present in pleural fluid (remember must have >10mm on lateral decubitus
film to perform!)
 Especially: Color, total protein, LDH, cholesterol, and WBC count
o Know lymphocytic exudates in pleura
 Most likely cause: Tuberculosis or cancer
 Rule in TB with acid fast bacteria stain
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<1000cell/ml=transudate
>5k=chronic exudates (TB, cancer)
>10K=inflammation (pneumo, pancreatitis, pulmonary infarction)
>50K = parapneumonic effusions only
Pneumonia
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Aspiration=bacteria
Inhalation=atical pneumonia, viruses, etc.
Test questions (from Dr. Muthiah):
1. What determines outcome in patients with pneumonia? Host response
2. Bronchial breath sounds are a sign of consolidation. THIS IS ON TEST.
3. ARDS can be is frequently a complication of pneumonia.
4. Resolution of pneumonia if right antibiotic is started, first thing that gets better is
oxygenation (respiratory rate decreases). Radiologic resolution of pneumonia lags behind
clinical resolution of pneumonia (especially if patient has other lung disease)
5. Patient detioriates rapidly is most likely due to MRSA (strain USA-300) and also produces a
Panton-valentine-leukocydin toxin which destroys neutrophils
6. Drug of choice for MRSA? Vancomycin.
A. Know: Age, social habits, occupation, geography, co-morbidities, are all risk factors for CAP.
Don’t memorize the specifics just the general categories. Resolution happens usually within 6-8
weeks
DVT/PE
II. Test Question: (Slide 2),KNOW FOR TEST
A. 25 year old man studying for the bar exam the last two weeks is confined to a chair 20 hours
per day. Now at Methodist hospital ER, he has developed right sided pleuretic chest pain.
1. Pleuretic pain is sharp well localized to the lateral area of chest increasing with cough
(inflamed pleura rub against other pleura)
2. Afebrile, HR=122, RR=32, D-Dimer =2200 ng/ml, CXR is clear
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3. Diagnosis is pulmonary embolism most likely from deep venous thrombosis
B. Which of the following statements are true regarding pulmonary thromboembolism? (this is
on our test)
1. Pathognomonic EKG finding of S1Q3T3 is seen only in a minority of patients.
a) KNOW THIS FOR TEST
III. Factor V leiden mutation (KNOW FOR TEST)
A. Factor V activates protein C which is a natural anticoagulant
IV. Protein C/S, antithrombin III deficiencies
V. Prothrombin G20210A deficiency
VI. Estrogen use, hormonal changes, malignancy, and thrombocytosis can cause a hypercoaguable state
(Slide 14)
A. KNOW ABOUT ESTROGEN USE AND DVT FOR TEST
VII. Impaired gas exchange
A. Most likely due to V/Q mismatch (#1 cause of hypoxemia in patients), KNOW FOR TEST
VIII. Compensation by the circulation KNOW FOR TEST, (Slide 20)
A. Vasodilation of uninvolved vasculature
1. Decrease the increase in pulmonary vascular resistance
2. Improves V/Q ratio
3. Improves overall oxygenation
IX. (Age +4) / 4 is normal A-a gradient for a person
1. Note A-a gradient may be normal in pulmonary embolisms
X. Chest Radiography PE (Slide 29)
A. Usually they are normal, KNOW FOR TEST
B. Pleural effusions are pretty small when present with pulmonary embolism
XI. Westermark’s Sign (Slide 34), KNOW FOR TEST
A. No vascular markings in R.lung because of a massive PE that cutoff circulation in the r.
pulmonary artery
XII. Recap (Slide 59)
A. More than 90% of emboli come from lower extremities
B. Normal perfusion scan excludes PE
If scan is normal or d-dimer is <500 the possibility of DVT is extremely low. Applicable in low clinical
probability settings. KNOW FOR TEST
XIII. Fat Embolism (Slide 74), KNOW FOR TEST
A. Farmer who falls of tractor, tractor runs over long bones (which is associated with fat emboli)
and goes to lungs and causing a triad of:
1. Mental status change
2. Thrombocytopenia
3. Petechiae in chest and neck
4. Diagnosis is fat embolism, KNOW FOR TEST
COPD
Test Questions: (From Dr. Muthiah)
1. Photomicrograph of emphysema asking you to ID emphysema
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Normal
Emphysema
2. Case scenario asking physician who has COPD, descriptive statements about chronic bronhicits
vs. emphysema (both have obstructive patterns, emphysema has out of proportion decrease in
DLCO differentiates chronic bronchitis from emphysema)
3. Treatments that prolong life in COPD: Smoking cessation and oxygen therapy
a. Management of stable COPD includes all of the following except?
i. Oral systemic glucocorticoids in patients with mild COPD, KNOW FOR TEST
b. Used short & long acting bronchodilators, anti-cholinergic bronchodilators can also be
used
c. Long term management with oxygen therapy (at least 15-24 hours a day), KNOW FOR
TEST
d. PaO2 less than 55 is an indication for oxygen therapy
e. Characterized by abnormal enlargement of airspaces distal to terminal bronchioles
i. Centri-lobular
1. Most common due to cigarette smoking
ii. Pan-Acinar
1. Most common due to alpha-1-antitrypsin def.
iii. Centrilobular emphysema is most common, KNOW FOR TEST
f. Major site of airflow limitation is the small conducting airways (<2mm in diameter),
KNOW FOR TEST.
4. In asthma there is predominately CD4 T lymphocytes, in COPD there is predominately CD8 Tlymphocytes. KNOW FOR TEST.
a. Production of sputum for 3 months in 2 consecutive years is the clinical definition of
chronic bronchitis. KNOW FOR TEST
b. DLCO is reduced in COPD patients with emphysema (it is normal in chronic bronchitis,
and asthma!), KNOW FOR TEST
c. TB has caseating granuloma’s (will be on assessment 7), KNOW FOR TEST
5. Pulmonary embolism (Slide 63)
a. Most common is a normal chest radiograph, KNOW FOR TEST
b. Features of benignity, KNOW FOR TEST
i. Well defined nodules
ii. No assosciated lymph node or mediastinal masses
iii. No satellite lesions
iv. Calcified nodules
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HY Pulmonary PaPh Assessment 6
6. Types of Benign Calcification (Slide 70)
a. Dense calcification and popcorn calcifications
b. Lamellar calcification
c. KNOW FOR TEST
7. Features of malignancy (Slide 72)
a. Lymph node spread
b. Spiculated nodules
c. Pressence of cavitation
d. Non-calcified nodules
e. Larger nodules
f. KNOW FOR TEST
8. Slide 57 is on our test, KNOW FOR EXAM.
9. Know anatomy of lung for the exam
10. Two questions will be on our test from this picture
A. Westermark’s sign (complete lack of vasculature in one of lungs), KNOW FOR TEST, Slide 66
(see below figure)
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