Studies of pulmonary function
Pulmonary function tests (PFTs) are rarely indicated in preparation for anes-thesia, though they can tell us whether a patient with severe lung disease has been optimally prepared. Pulmonary restrictive and obstructive diseases worry us. Short of treating infection, we cannot do much about restrictive disease; how-ever, it can co-exist with obstructive bronchospasm, which is common and can be treated with bronchodilators. Of the many pulmonary function studies, we pay particular attention to forced vital capacity (FVC). FVC values below 15 mL/kg give rise to great concern. How much the patient can exhale in 1 second (FEV1), and whether this can be improved by bronchodilators determines obstructive disease.
Typically, PFT results are reported as “% of predicted,” based on popula-tion studies that consider the patient’s height, age, and gender. We accept values of at least 80% predicted as normal. With obstructive disease, the patient exper-iences airway closure during exhalation, measured as a low FEV1 (Table 10.1). With advanced disease and air trapping, the FVC might also decline, though not as much as the FEV1, thus the hallmark of obstructive disease is a reduced ratio of FEV1 to FVC. With age, this ratio declines as well (to perhaps 0.7), so again we look at the percentage predicted. Flow volume loops (Fig. 10.4) can also be helpful.
When we call for an analysis of arterial blood gases (ABG), we are really asking about the function of two organs: lungs and kidneys. An ABG reports the partial pressures of oxygen and carbon dioxide in arterial blood, both clearly related to lung function, but also provides the pH and bicarbonate concentration, which tells us something about how the kidneys are handling non-volatile acids and bases.
In the laboratory, the ABG values are corrected to 37 °C. This facilitates interpret-ation of data because of the complexities introduced by temperature changes: in addition to a direct effect on pH, both the dissociation constants and solubility of gases are temperature dependent. For example, a PaCO2 of 40 mmHg at 37 °C, will drop to 25 mmHg when temperature falls 10 degrees. The total carbon dioxide con-tent stays the same, but the distribution of the components of the CO2–carbonic acid–bicarbonate complex has changed (see below). Thus, if not corrected in the laboratory, a drop in temperature from 37 °C to 27 °C would raise the reported pH of the blood sample from 7.4 to about 7.54.
The lab reports the partial pressure of oxygen in arterial blood as PaO2 in mmHg, and the saturation of arterial hemoglobin with oxygen as % SaO2. Most ABG ana-lyzers calculate the SaO2 based on a standard, adult oxyhemoglobin dissociation curve. When there is doubt regarding the actual saturation, e.g., in the patient with suspected carbon monoxide inhalation, we must order co-oximetry, which analyzes the transmission of several wavelengths of light, the better to distinguish reduced from oxygenated hemoglobin, as well as met- and carboxyhemoglobins. Please observe the convention of writing SaO2 for the laboratory calculation of arterial hemoglobin saturation, SpO2 for the estimation of this value by pulse oximetry, and specify SaO2 by co-oximetry if available. These values are rarely, if ever, identical but usually agree within a percent or so.
Carbon dioxide in blood affects the pH because CO2 in an aqueous medium (i.e. blood) will form carbonic acid, which dissociates into bicarbonate and hydrogen ions:
CO2+ H2O ↔ H2CO3↔ H++ HCO−3
We often describe this relationship with Henderson Hasselbalch’s5 equation:
where pKa= the dissociation constant for carbonic acid (∼6.1), that is, the pH at which 50% of the weak carbonic acid is ionized into equal amounts of HCO−3 and H2CO3 (for which PCO2× 0.03 is substituted). Thus the ratio of bicarbonate to PCO2 determines pH, not their individual concentrations.
From this equation, we see that if we add carbon dioxide, the pH drops (res-piratory acidosis). The interaction of CO2 with water will lead to the generation of carbonic acid, which will lower the pH while increasing bicarbonate, without which the pH would be even lower. Slowly (over 1–2 days), the kidneys retain extra bicarbonate to further offset the acidosis, although never completely correcting it. When faced with an ABG demonstrating respiratory acidosis (decreased pH and increased PCO2), we can use the 1–2–4–6 Rule of Ten (see Table 10.2), which simply says that the indicated acute or chronic respiratory disturbance will cause the bicarbonate to change. If that change did not take place or is exaggerated, we need to look for metabolic explanations.
The addition of acids, e.g., keto acids in diabetes, will also lower the pH. From Henderson Hasselbalch’s equation, we predict that the addition of hydrogen ions (lower pH) will cause the bicarbonate to gobble up some of the H+ (lowering the concentration of HCO−3), leading to the generation of more carbonic acid, which can then dissociate into CO2 and water. The CO2 gas can be exhaled, thus reducing the effect of having added hydrogen ions.
The addition of many acids will increase the anion gap. Recognizing there must always be electroneutrality, if we add up all the cations (Na+ , K+ , Ca2+ , Mg2+ ), they must equal all the anions (HCO−3, Cl− , PO34− , SO34− , proteins, organic acids). Since we do not routinely measure the proteins and organic acids, these become the “anion gap,” the difference between cations and anions.6 We simplify all this math by only counting sodium, chloride, and bicarbonate and accepting as normal an anion gap of 12 mEq/L +/− 4 mEq/L thus,
Anion gap = Na+− (Cl−+ HCO−3)
Were it not for buffers in blood and tissue, any change in hydrogen ion concentra-tion would cause large swings of pH. The buffers in blood (primarily hemoglobin) avidly sop up hydrogen ions, mitigating shifts in pH; therefore, a severely anemic patient will experience greater shifts in pH than a patient with normal hemoglobin values. When buffering proves insufficient and correcting a low cardiac output fails to help, we must treat a serious metabolic acidosis with the titration of bicar-bonate. We calculate the initial dose7 as
which should not fully correct the acidemia. We then look at repeated blood gas values presenting pH, bicarbonate, and PCO2, realizing that the addition of bicarbonate will increase the pH while also liberating CO2,which must (if possible) be exhaled.
A normal room air8 arterial blood gas in a nonpregnant9 patient should look something like:
pH 7.35−7.45, PCO2 35−45 mmHg, PO2 75−100 mmHg,
HCO−3 22−26 mmol/L.
Other values include methemoglobin (met Hb) <2%, carboxyhemoglobin (CO Hb) <3%, and base excess −2 to 2 mEq/L.
When the laboratory reports abnormal results, we ask several questions:
(i)Is the PO2 OK? Apply alveolar air equation.
(ii) Is the pH OK? If not, is there a metabolic or respiratory disturbance with or without compensation or is it a mixed disturbance? (See Table 10.3.)
Case 1: A PACU nurse calls because a post-operative patient has a low SpO2, whichdid not normalize by giving the patient oxygen by face mask.
(i) SpO2 of 90% on FiO2 of 0.5.
The alveolar air equation estimates (presuming – probably falsely – a normal arterial CO2 of 40 mmHg) an alveolar oxygen tension of 306 mmHg (0.50 × (760–47) – (40/0.8)). A SpO2 of 90% corresponds to a PaO2 of approximately 60 mmHg. Thus there is a large A-a difference.
(ii) ABG: pH 7.28, PCO2 55 mmHg, PO2 60 mmHg, HCO−3 26 mmol/L.
The measured PaO2 corresponds (miraculously exactly) with the estimated PaO2 using the SpO2 data. The elevated PaCO2 of 55 mmHg indicates hypoven-tilation, which would explain the low PaO2.
Step 1: The pH of 7.28 indicates acidemia.
Step 2: The elevated arterial carbon dioxide tension implies a respiratory source.
Step 3: The CO2is increased (55 – 40=15 mmHg). The pH fall of 0.12 (7.40 – 7.28)is consistent with an acute respiratory acidosis (0.08 per 10 mmHg rise in the CO2). In confirmation, according to Table 10.2, an acute elevation of PCO2 by 15 mmHg should be associated with a rise of bicarbonate of 1.5 mEq/L.
The patient’s bicarbonate confirms our suspicion that we are dealing with an acute, i.e., so far uncompensated, respiratory acidemia.
We must now determine whether obstruction (is the airway patent? Do bandages impede ventilation?), weakness (is there a muscle relaxant hangover?), or central depression (effects of narcotics?) can explain the hypoventilation. Therapy will depend on what we find.
Case 2: The ambulance brings a trauma patient to the Emergency Department.The patient has a fractured hip. As a routine, a nurse applies a face mask deliv-ering 50% oxygen. SpO2 is 100%. An ABG reveals: pH 7.23, PCO2 25 mmHg, PO2 250 mmHg, HCO3− 12 mmol/L.
We welcome the SpO2 of 100% but realize that the patient can still have a ventilation/perfusion abnormality. However, the PaO2 of 250 mmHg confirms a small A-a difference (PAO2= 0.5 × (760−47) − 25/0.8 = 325 mmHg).
Step 1: The pH of 7.23 shows acidemia.
Step 2: The low PaCO2and HCO−3describe a metabolic source (with significanthyperventilation).
Step 3: The respiratory response is appropriate (PCO2≈25≈(1.5×12)+8 mmHg).
We follow up with additional studies, such as electrolyte levels to calculate the anion gap, to identify the cause of the patient’s trouble (Table 10.4).
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