Contents of Section A
Intern's Credo. .
15 Laws of Hospital Practice
10 Laws of Outpatient Practice
5 Rules for Lab Tests
6 Medical Truisms
10 Medical Cliches
1 Useful Mnemonic
15 Once-Difficult Diagnoses
8 Bedrock Lab Tests
10 Rules for Reading Chest X-rays
15 Rules on Oxygen Therapy
6 Signs of Obvious Breathing
10 Occupational Hazards for Physicians
***************************************** INTERN'S CREDO There's no admission like no admission. Anonymous *****************************************
THE HOUSE OFFICER'S 10 LAWS OF OUTPATIENT
15 ONCE-DIFFICULT DIAGNOSES
In the 19th and part of the 20th century, astute clinicians argued interminably over the following diagnoses. The reason? There was no readily available or convenient method by which to test their clinical observations. How we do it today (in parentheses) seems so simple!
pneumonia vs. no pneumonia (chest x-ray)
hypo- vs. hyper- glycemia (blood sugar measurement)
low vs. high PaCO2 (blood gas measurement)
low vs. normal PaO2 (blood gas measurement)
hypothyroidism vs. euthyroid state (thyroid function tests)
euthyroid state vs. hyperthyroidism (thyroid function tests)
low vs. high serum potassium (serum electrolytes)
big spleen vs. normal spleen (ultrasound; CT scan)
big kidneys vs. normal kidneys (ultrasound; CT scan)
big liver vs. normal liver (ultrasound; CT scan)
acidosis vs. alkalosis (blood gases and serum electrolytes)
increased intracranial pressure vs. normal ICP (CT scan, LP)
seizures vs. pseudo seizures (EEG)
myocardial infarction vs. no MI (EKG, enzymes, echocardiogram)
cardiogenic shock vs. septic shock (Swan-Ganz catheterization)
And the difficult diagnoses today? Each of the following diagnostic considerations often leads to several tests, which are just as often inconclusive or difficult to interpret.
pulmonary embolism (most difficult of the common diagnoses)
cause of non-essential hypertension
chronic fatigue syndrome
any condition of viral etiology
8 BEDROCK LAB TESTS
A few tests are universally available and enormously useful. The better a house officer understands these "bedrock" lab tests, and their underlying science, the better care he or she can give patients. As a minimum, any house officer in the primary care fields should be comfortable with interpreting these tests, i.e., should be able to understand the data and apply it to the patient. Sadly, although each test is predicated on time-honored science and physiology, they are not emphasized in medical school teaching. It would behoove any curriculum to instill in students a true understanding of these tests. They are listed alphabetically.
Arterial blood gases (pH, PaO2, PaCO2, SaO2)
Chest x-ray (PA and lateral)
Complete blood count (hematocrit, WBC, differential, platelet
Serum electrolytes, BUN and blood glucose
Sputum analysis (Wright's stain, Gram's stain)
1. PO2 , SaO2 , CaO2 are all related but different.
The house officer who understands the difference between
PaO2, the partial pressure of oxygen in the arterial blood, is determined solely by the pressure of inhaled oxygen pressure (the PIO2), the PaCO2, and the architecture of the lungs. The most common physiologic disturbance of lung architecture is ventilation-perfusion (V-Q) abnormality; less commonly, there can be diffusion block or anatomic right to left shunts. If the lungs are normal, then PaO2 is affected only by the alveolar PO2, which in turn is determined by the fraction of inspired oxygen, the barometric pressure and the PaCO2 (see Four Most Important Equations in this book in Section H or at http://www.lakesidepress.com/pulmonary/papers/eq/eq1.html").
PaO2 is a major determinant of SaO2, and the relationship is the familiar sigmoid-shaped oxygen dissociation curve. SaO2 is simply the percentage of available binding sites on hemoglobin that are bound with oxygen in arterial blood. The O2 dissociation curve (and hence the SaO2 for a given PaO2) is affected by PaCO2, body temperature, pH and other factors. However, SaO2 unaffected by the content of hemoglobin, so anemia does not affect SaO2.
CaO2 is arterial oxygen content. Unlike either PaO2 or SaO2, the value of CaO2 directly reflects the total number of oxygen molecules in arterial blood, both bound and unbound to hemoglobin. CaO2 depends on the hemoglobin content, SaO2, and the amount of dissolved oxygen. Units for CaO2 are ml oxygen/100 ml blood (see Four Most Important Equations in Section H).
2. PaO2 is a sensitive and non-specific indicator of the lungs'
ability to exchange gases with the atmosphere.
In patients breathing ambient or "room" air (FIO2 = .21), a decreased PaO2 indicates impairment in the gas exchange properties of the lungs, usually signifying V-Q imbalance. PaO2 is a very sensitive indicator of gas exchange impairment; it can be reduced from virtually any parenchymal lung problem, including asthma, chronic obstructive pulmonary disease, and atelectasis that doesn't show up on a chest x-ray.
3. FIO2 is the same at all altitudes.
The percentage of individual gases in air (oxygen, nitrogen, etc.) doesn't change with altitude, but the atmospheric (or barometric) pressure does. FIO2, the fraction of inspired oxygen in the air, is thus 21% (or .21) throughout the breathable atmosphere. PaO2 declines with altitude because the inspired oxygen pressure declines with altitude (inspired oxygen pressure is fraction of oxygen times the atmospheric pressure). Average barometric pressure at sea level is 760 mm Hg; it has been measured at 253 mm Hg on the top of Mt. Everest.
4. Normal PaO2 decreases with age.
A patient over age 70 may have a normal PaO2 around 70-80 mm Hg, at sea level. A useful rule of thumb is normal PaO2 at sea level (in mm Hg) = 100 minus the number of years over age 40.
5. Oxygen from the wall outlet is always 100%.
As oxygen leaves the outlet the FIO2 at that point is 100%. However, unless the patient is connected to a ventilator, or has a tight-fitting face mask, the appliance used to deliver oxygen to the face will always result in an inhaled FIO2. less than 100%.
6. The body does not store oxygen.
Athletes who inhale a few minutes of oxygen, and then return to the playing field, are not benefitted in any physiologic way. If a patient needs supplemental oxygen it should be for a specific physiologic need, e.g., hypoxemia during sleep or exercise, or even continuously (24 hours a day) as in some patients with severe, chronic lung disease.
7. Supplemental O2 is an FIO2 > 21%.
Supplemental oxygen means an FIO2 greater than the 21% oxygen in room (ambient) air. When you give supplemental oxygen you are raising the patient's inhaled FIO2 to something over 21%; the highest FIO2 possible is 100%. To give more oxygen requires a hyperbaric chamber, an expensive piece of equipment found in relatively few hospitals.
8. Supplemental oxygen is a drug.
Like any other drug, it has indications, contra-indications, and side effects. Unlike the situation with most drugs, there are also easily measurable "levels" of oxygen (either PaO2 with a blood gas measurement or SaO2 with a pulse oximeter).
9. Supplemental oxygen is the most commonly prescribed drug
An estimated 1/4 to 1/3 of all patients admitted to a hospital will receive supplemental oxygen at some point. It is the only prescription drug in common use on all inpatient services (except perhaps Psychiatry).
10. A reduced PaO2 is a non-specific finding.
It can occur from any parenchymal lung problem, and only signifies a disturbance of gas exchange (usually due to V/Q imbalance). A low PaO2 should not be used to make any particular diagnosis, including pulmonary embolism.
11. A normal PaO2 and Alveolar-arterial PO2 difference (A-a
gradient) do not rule out pulmonary embolism.
About 5% of confirmed cases of PE manifest a normal A-a gradient.
12. High FIO2 doesn't affect COPD hypoxic drive.
The reason a high FIO2 may raise PaCO2 in a patient with COPD is not because the extra oxygen cuts off the hypoxic drive. Modest rise in PaCO2 occurs mainly because the extra oxygen alters V/Q relationships within the lungs, creating more physiologic dead space.
13. A given liter flow rate of nasal O2 does not = any specific
The oft-quoted rule that 2 l/min =an FIO2 of 24%, 3 l/min = 28%, etc., is an illusion, based on nothing experimental or scientific. The actual FIO2 with nasal oxygen depends on the patient's breathing rate and tidal volume, i.e., the amount of room air inhaled through the mouth and nose that mixes with the supplemental oxygen.
14. Face masks cannot deliver 100% oxygen unless there is a
So-called non-rebreather face masks can deliver an FIO2 up to around 80%. It is a mistake to label a patient with any loose-fitting face mask as receiving an "FIO2 of 100%." (Again, 100% oxygen can only be delivered with a ventilator or tight-fitting face mask.)
15. Oxygen masks migrate.
Face masks are useful for delivering a precise FIO2 (e.g., "venturi" type masks) and a high FIO2 (e.g., non-rebreathing masks), but outside of the ICU or ER (where the patient can be closely watched) masks tend to migrate - either to the patient's forehead, around the neck, to the bed sheets or the floor. For oxygen therapy, use a nasal cannula whenever feasible; it is more apt to deliver oxygen to the patient continuously.
6 SIGNS OF OBVIOUS BREATHING
If a patient's breathing is obvious on initial contact (for example, when you first see the patient on walking into the room) it is abnormal. Normal breathing at rest is simply not obvious; one has to look very closely for chest movement to appreciate breathing. Six signs that may make someone's breathing obvious to the observer - all abnormal - are listed below.
10 Occupational Hazards for Physicians
Practicing in the United States
(Other countries may present different infectious disease risks; hazards are listed alphabetically)
END OF SECTION A