MEDICINE 2 – [PULMO]: WORKSHOP AY 20-21

Roland M. Panaligan, MD; Patrick Gerard L. Moral, MD; Ma. Piedad R. Natividad, MD 18 FEB 21

TABLE OF CONTENTS B. CHEST RADIOGRAPH

I. CASE 1 .................................................................................. 1
A. INITIAL IMPRESSION ....................................................... 1
B. CHEST RADIOGRAPH ..................................................... 1
C. ABG RESULTS AND INTERPRETATION ......................... 1
D. IS THE PATIENT HYPOXEMIC? ....................................... 2
E. MECHANISM OF HYPOXEMIA......................................... 2
II. CASE 2 .................................................................................. 3
A. PE FINDINGS ................................................................... 3
B. INITIAL IMPRESSION ....................................................... 3
C. CHEST RADIOGRAPH ..................................................... 3
D. ABG RESULTS AND INTERPRETATION ......................... 4
E. IS THE PATIENT HYPOXEMIC? ....................................... 4
F. MECHANISM OF HYPOXEMIA......................................... 4

MUST KNOW BOOK PREVIOUS TRANS

  
Notes from Dr. Panaligan, Dr. Natividad, and Dr. Moral are color-coded as
follows, please be guided accordingly.

I. CASE 1
79M, smoker, came in because of dyspnea. There was use of
accessory muscles of respiration during the physical Figure 1. Chest radiograph: Are there signs of hyperinflation?
examination. BP 120/80; CR 90/min; RR 14/min. Question: Given the CXR above, are there signs of
hyperinflation?
A. INITIAL IMPRESSION
● Abdomen
Question: What is your initial impression? → Low-set diaphragm (at T11)
a) PTB → Diaphragm with a flat contour
b) ECOPD ■ We cannot see the dome where we measure the
c) ECOPD, CAP perpendicular line; almost flat, probably not going to give
d) PE you any measurement
● Thoracic Cage
● PTB → Widened ICS
→ Usually presents as chronic cough and weight loss ■ Good to compare it with previous CXR to see if there is
→ Rarely would it have an acute presentation like this unless you widening
are thinking of complications of related to the PTB (ex.: ● Mediastinum/Midline Structures
pneumothorax because of the parenchymal issues) → Tubular or slender or narrow heart (expected in patients with
→ Not Doc’s first consideration, placed last; TB may not present hyperinflation or emphysema)
dyspnea as the main manifestation ■ Apex beat not at MCL
● ECOPD ● Lung
→ Important additional data: Smoker → Lung parenchyma is very dark except for the left upper lobe
■ Think possibly of COPD ■ Connotes hyperaeration and one can correlate this with the
● ECOPD, CAP – Initial impression flattening of the diaphragm
→ It can also be an acute exacerbation.
→ Usually, exacerbations are caused by infections, whether it be C. ABG RESULTS AND INTERPRETATION
viral or bacterial so pneumonia would also be possible.
● PE
→ Dyspnea
→ 79M
■ Cancer may be there
■ Prostatic issues can be there

Figure 2. ABG results

● pH: 7.33 (Low) → Acidosis
● pCO2 mmHg: 63 (High); opposite of pH → Respiratory

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QUILING
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● HCO3 mEq/L:29(High); moves in the SAME direction with pCO2 = 0.56

(High) → N.V. = 0.75- 0.8
→ One is compensating for the other ● The a/A ratio of the patient is only 0.56 which is lower than the
→ Partially compensated respiratory acidosis normal values, hence the patient is hypoxemic
● Correlating ABG result of partially compensated respiratory ● AaDO2 = pAO2 - paO2
acidosis with the chest x-ray = 177.93 - 100
→ There is presence of air trapping, which places the diaphragm = 77.93 or 78
at a disadvantage; the ventilatory process is impaired hence → N.V. <15 for age up to 30 years old; for age >30 years old. Add
the patient retains CO2 3 for every decade above 30
→ Chronic process (at least more than 3 days) because the → So for the 79 y/o patient the
kidneys are already compensating and pH is not that low, ■ Expected AaDO2 = 15 + (3 x 5 decades)
considering the CO2 is high, hence compatible with the = 15 + 15
diagnosis of COPD which is a chronic condition = 30
→ Note: PTB can also be a differential diagnosis since there is ● The AaDO2 of the patient is 70 which is widened or increased,
presence of left upper lobe infiltration and patient manifest with hence the patient is hypoxemic
dyspnea, but still COPD is the most likely cause ● Out of all the parameters used, the AaDO2 is the most reliable,
since the age is not a big factor (also easy to remember).
Although the P/F ratio is also accurate, but you need to modify it
based on the age. Other parameters can be affected by the age
as well as the amount of O2 being given.
● Take note that other parameters are also important for certain
conditions
→ ARDS: make use of P/F ratio to classify disease severity
E. MECHANISM OF HYPOXEMIA

Figure 3. ABG Flowchart.

● This is the ABG flowchart, you can use to trace and identify the
patient’s condition
Table 1. Case 1 ABG Result
Parameters N.V. Actual Values
P(A-a)O2 mmHg 25-65 78
aA ratio 0.75-0.8 0.56
PF ratio 250-350 278 Figure 4. Algorithm on the Approach to a Patient with Hypoxemia
Desired FiO2 22-26 0.26
• The figure is lifted from the 17th edition of Harrison’s
● These values above can be derived from a formula and are • Dr Panaligan: It is important for us to understand where the
included in the indices of hypoxemia hypoxemia is coming from or the mechanism of the hypoxemia.
● Use these values to answer the question: Is the patient • First, we look at the partial pressure of your CO2. Is it
hypoxemic? increased or decreased?
D. IS THE PATIENT HYPOXEMIC? • If it is increased, we go on the left side and it is caused by
hypoventilation.
● P/F ratio = PaO2/FiO2
● P/F ratio = 100/0.36 • The second parameter we look into is the alveolar-arterial O2
= 277.7 gradient. Is it widened/increased?
● Expected P/F is 400 for age <60 years old but since patient is 79 → If it is not, then the mechanism is the hypoventilation alone.
years old, we need to calculate: Then, it might be due to a decrease in respiratory drive or
→ Expected PF = 400 - [ (years above 60) x5] due to a neuromuscular disease.
= 400 - (19 x 5) → If it is widened/increased, then there is hypoventilation plus
= 400 - 95 another mechanisms surrounding it.
= 305 • So, how do we know the other mechanism?
● P/F ratio of the patient is only 277.7 which is lower than the → We challenge the patient with O2 correction.
expected P/F hence the patient is hypoxemic → O2 challenge - giving the patient 100% of FiO2. This can be
done if the patient is ventilated or intubated, then this can be
easily done by adjusting the amount of FiO2 being given to
● pAO2 = 713 x FiO2 - pCO2 / 0.8 the patient.
= (713 x 0.36) - 63/ 0.8 • If there is O2 correction, we have a V/Q mismatch.
= 256.68 - 78.75 → Common entities implicated are airway diseases (asthma,
= 177.93 COPD), interstitial lung disease, alveolar disease, and
● a/A = paO2 / pAO2 pulmonary vascular disease.
= 100/177.93 • If there is no O2 correction, then we think of shunting.
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→ Common causes are alveolar collapse (atelectasis), intra- ● CAP

alveolar filling (pneumonia, pulmonary edema), intracardiac → Is the triad present? Fever, Cough, Dyspnea?
shunt, and vascular shunt within lungs. ■ NO. Patient only presents with cough and dyspnea but
• Going back to the top of the algorithm. What if PaCO2 is not don’t forget to look at the patient’s age! So all of these may
increased? We then go to the second parameter. We look at the not be present all the time
alveolar-arterial gradient/difference. → Due to the presence of crackles although there is no
→ If it is not widened or increased, it probably due to low consolidation, this will still be my first consideration
inspired PO2 wherein you are in a high altitude area or ● ECOPD
probably the basic FiO2 is low/decreased. → Patient is 60 years old, there are signs of airway obstruction
→ If it is widened or increased, we proceed again with O2 (wheezing)
correction. ● PTB
• Case 1’s mechanism of hypoxemia → Rarely seen as a cause for respiratory failure or even
→ Patient’s PaCO2 is 68. PaCO2 is increased. Initial respiratory distress not unless there are complications
mechanism is hypoventilation. ● Pulmonary Embolism
→ P(A-a)O2 mmHg is 78 which is increased. → A massive embolism may impair the oxygenation process (O2
saturation of 70%)
→ Is low PO2 correctable with O2? We need to give an FiO2
→ However, usually if it’s massive patient should be hypotensive
of 100%, the patient was only given an FiO2 of 36%. Is it
and tachycardic
safe to say that, in terms of O2 correction, we really
■ Patient is not hypotensive (BP 130/80 mmHg)
challenged this patient? No, this is not the ideal condition
for O2 correction. Is there a quick and easy trick to eyeball Question: Differentiate the Respiratory Failure
if there is O2 correction? ● TYPE 1 (PURE OXYGENATION FAILURE)
→ For eyeballing if the O2 is corrected, here is an example, → Cyanosis is present but patient is awake and cooperative
the FiO2 of room air is 21% so we multiply this by 5 and → Tx: NON-INVASIVE VENTILATION OR INTUBATION
the PaO2 of a normal person is 100. (FiO2 x 5 = PaO2) In ■ See if oxygenation improves
our patient, his FiO2 is 36% multiply this by 5 we get 180 ● TYPE 2 (VENTILATORY FAILURE ± HYPOXEMIA)
but, his PaO2 is only 100 so there a portion of the → Even without ABG, if you see the ventilatory muscles are
oxygen in your alveoli not moving towards you already tired
capillaries. So there is still some gas exchange issue → Tx: VENTILATION
going on. ● Our patient has Type 2 Respiratory Failure and our main
→ Ideally we challenge by giving a 100% FiO2. But in this differentials are CAP or ECOPD
patient maybe he is used to having a high O2, if we give
him 100% FiO2 we remove his hypoxic drive and this C. CHEST RADIOGRAPH
might stop him from breathing. So what we can do here is
compute using his nasal FiO2 and maintain the “sats”.
→ There is no correction of his PO2 so we might be thinking
of a shunt. Probable causes are flooded intra-alveolar
filling because of pneumonia or pulmonary edema. These
will be the common causes of why patients are having
hypoxemia.
II. CASE 2
A 60 year old male rushed to the emergency room because of a 3-
day history of dyspnea, increased cough, and sputum
production. He had BP 130/80 mmHg, HR 110 regular, RR 32 cpm,
T 36.6C, O2 saturation 70% at room air. He had supraclavicular
retractions, paradoxical breathing, and peripheral cyanosis, rhonchi,
and wheezes on both lung fields. He was intubated and hooked to
the mechanical ventilator with the following set-up: TV 400, RR 12
(with actual RR of 25), FiO2 of 50%. CXR was done one day ago.

A. PE FINDINGS
Question: Is the patient in respiratory failure? Figure 5. Chest Radiograph

● YES, because the patient presents with paradoxical breathing Question: Based on the CXR above, what is causing the
which is a sign of diaphragm fatigue Acute Respiratory Failure?
● Other findings that point out to RESPIRATORY FAILURE ● Abdomen
→ Central cyanosis → Right costophrenic sulcus is blunted
→ Alteration in sensorium ■ There may be 200 mL of fluid
● Findings that point out to RESPIRATORY DISTRESS → Right hemidiaphragm is flat
→ Supraclavicular retractions ● Thoracic cage
→ Use of accessory muscles for respiration → No fractures
→ Peripheral cyanosis → No narrowing of the intercostal spaces
→ Tripod position ● Mediastinum
Question: What management will you do for a patient in → Trachea is deviated to the right
Acute Respiratory Failure? → However it is affected by the positioning of the patient; the
● Give supplemental oxygen and intubate patient clavicles are not aligned
→ Cardiac border: apex is in the midclavicular line so there is no
B. INITIAL IMPRESSION cardiomegaly
● Lung lesions
Question: What is your initial impression?
→ Air bronchograms in the right lower lung field
● RULE OUT COVID FIRST! → Can signify consolidation
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● Based on the chest x-ray, the most likely cause is pneumonia → Check if AaDO2 is increased
→ Might be a middle lobe pneumonia ■ Increased AaDO2 – consider hypoventilation + another
→ Can see some hyperaeration → there might be some mechanism
underlying obstructive lung disease too → Check if low PO2 is correctable with O2
→ There might be tuberculosis, but is not the cause of the ■ Multiply the value of FiO2 to 5
respiratory failure of the patient − 50 x 5 = 250
■ Compare the value (250) to the actual pO2 which is 110
D. ABG RESULTS AND INTERPRETATION
only
● ABG result: at 50% FiO2 ■ If it is correctable – the pO2 value should be more or less
Table 2. Case 2 ABG results the same with the computed value
Parameters N.V. Actual values ■ For this patient, the low pO2 is not correctable with O2
pH 7.35-7.45 7.25 because the pO2 (110) is lower than the computed value
pCO2 mmHg 35-45 75 (250) – Shunt could be considered
pO2 mmHg 80-100 110 − Most likely: Intra-alveolar filling (Pneumonia)
HCO3 mEq/L 22-28 29 ● History, PE, chest radiograph are all compatible with the ABG
O2 sat % 90-100 99 findings and mechanism of hypoxemia
BE mEq/L -2 - +2 -4 → Hx: Cough, sputum production in an elderly patient
FiO2 20-100 0.50 → Chest X-Ray: signs of consolidation
P9A-a)O2 mmHg 25-65 → Patient is hypoxemic
aA ratio 0.75-0.8 → Mechanism: not correctable by O2 – Shunt – flooding of alveoli
– secondary to Pneumonia
PF ratio 250-350
Desired FiO2 22-26 END OF TRANSCRIPT
● Interpretation: Partially compensated respiratory acidosis
REFERENCES
→ Low pH: acidosis
→ High pCO2: respiratory Panaligan, R (2021). Chest X-ray and ABG [PowerPoint Presentation]. Manila,
→ High HCO3: partially compensated Philippines: Faculty of Medicine and Surgery, University of Santo
Tomas. MED 2
E. IS THE PATIENT HYPOXEMIC?
● P/F Ratio
→ Calculate the P/F Ratio
P/F Ratio = pO2/FiO2
= 110/0.50
= 220
→ Calculate the Expected P/F ratio of the patient:
Expected P/F Ratio = 400 – (years above 60) x 5)
= 400 – (0x5)
= 400
→ The computed P/F Ratio of 220 is lower than the expected P/F
Ratio of 400 – Patient is HYPOXEMIC
● a/A Ratio
→ Calculate the a/A Ratio
a/A Ratio = pO2/alveolar O2
CTTO: Medical Memes for Sleep Deprived Kids
= 110/alveolar O2
■ Computing for alveolar O2 (pAO2)
pAO2= 713x FiO2-pCO2/0.8
= (713x 0.50)- 75/0.8
= 356.5-93.75
=262.75
→ a/A Ratio= pO2/alveolar O2
= 110/262
= 0.41
→ The computed a/A ratio of 0.41 is lower than the expected
value of 0.75 – patient it HYPOXEMIC
● AaDO2 (Aa gradient/difference)
→ Calculate the AaDO2
AaDO2 = pAO2 – paO2
= 262.75 – 110
= 152.75
→ The expected AaDO2 is 15 + 3 (3) = 24
■ Normal value is <15 for age up to 30 years old
■ For age above 30 years old, add 3 for every decade above
30 years old
→ There is a large difference on the calculated AaDO2 (152.75)
and the expected AaDO2 (24) – patient is HYPOXEMIC
● Based on the 3 parameter, the patient is hypoxemic and there is
evidence of gas-exchange dysfunction.
F. MECHANISM OF HYPOXEMIA
● Mechanism of Hypoxemia (Refer to the algorithm)
→ Check if PaCO2 is increased
■ Increased PaCO2 – possible hypoventilation
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APPENDIX