Chapter 6, cont… (Page 2)

Is the patient adequately oxygenated?

Fig. 6­4. Effects of carbon monoxide on oxygen dissociation curve. ([Redrawn from Roughton, F.J.W., and Darling, R.C.: Am. J. Physiol. 141:17­31, 1944.] and reproduced with permission from Comroe, J.H., Jr.: Physiology of respiration, 2nd edition. Copyright 1974 by Year Book Medical Publishers, Inc., Chicago.)

Arterial blood gas measurement may or may not be helpful when carbon monoxide poisoning is suspected, depending on what is actually measured. All blood gas instruments measure PO₂, and from this measurement the SaO₂ can be estimated, but it is always better to measure the SaO₂. This measurement is obtained with an instrument called a CO­Oximeter.^*

An estimate of SaO₂, based on a standard oxygen dissociation curve, will be incorrect if carbon monoxide is present in any excess. It is important to always know what was measured when blood gas results are reported. The PaO₂ is unaffected by carbon monoxide and may be normal in the presence of carbon monoxide poisoning. It is the SaO₂ that is always reduced from excess carbon monoxide. Thus if the SaO₂ is estimated from the arterial PO₂, it may be falsely reported as normal. The clue to a diagnosis of carbon monoxide poisoning (without direct measurement of %HbCO) is a measured SaO₂ inappropriately low for the PaO₂, e.g., a PaO₂ of 80 mm Hg and a SaO₂ of 50%. The definitive diagnosis of carbon monoxide poisoning is made by measuring %HbCO directly, a measurement that can also be done with some CO-Oximeters.

EFFECTS OF CARBON MONOXIDE EXPOSURE

People breathing carbon monoxide­free air will have a percent carboxyhemoglobin (%HbCO) of less than 2%. Exposure to heavy downtown traffic for 8 hours can produce %HbCO between 3% and 5%, and heavy cigarette smokers may have up to 10% HbCO. Although these levels should not produce symptoms in otherwise healthy people, they can have long­term harmful effects in some groups. For example:

a. Chronic lung disease patients show decreased exercise tolerance at approximately 4% HbCO.

b. Excess HbCO results in an increase in coronary artery blood flow to compensate for the decreased oxygen content; in the presence of fixed coronary artery obstruction, this increase may not occur. The result can be a decrease in the aerobic capacity of the myocardium and, in severe eases, actual anaerobic metabolism. This effect has been shown to occur at levels of 5% to 8% HbCO.

c. There is a decrease in the threshold for ventricular fibrillation, which may relate to the sudden death of smokers with coronary artery disease, and there is a possible role for carbon monoxide in the initiation or the acceleration of atherosclerosis itself.

d. Finally, the low birth weight seen in the newborns of mothers who smoke is probably caused by chronic maternal carboxyhemoglobinemia.

Automobile exhaust in closed spaces and fires are the most common causes of acute carbon monoxide poisoning. In treating fire victims, it is important not to let the presence of burns or smoke inhalation hide the less obvious but more immediate danger of carbon monoxide poisoning. There are other sources of carbon monoxide poisoning; malfunctioning fireplaces, wood stoves, and space heaters, as well as charcoal grills or hibachis that are used in closed spaces.

When they are conscious, victims of carbon monoxide poisoning initially have headache; in more severe cases, lethargy or coma can be the initial symptoms. Shortness of breath is not a typical symptom of carbon monoxide poisoning. There is a rough correlation of the symptoms with the level of HbCO (Table 6­1). Any patient complaining of a chronic headache, especially during the winter months, should: (1) be asked if anyone else in the home is having headaches; (2) be asked about the use of space heaters and charcoal fires; and (3) have his %HbCO level measured, a measurement that can be done on venous blood. An alternative to HbCO analysis is the measurement of PaO₂ and SaO₂.

The physical examination is usually not helpful in assessing carbon monoxide poisoning other than in assessing alertness. "Cherry­red coloration" in carbon monoxide poisoning is usually not present. Because the PaO₂ is not reduced, the patients do not hyperventilate and do not appear dyspneic. The chest x­ray film is often normal, and the arterial blood gas values suggest the diagnosis only if measured SaO₂ is inappropriately low for the PaO₂. To make the diagnosis of carbon monoxide poisoning, it must first be suspected; then laboratory confirmation must be obtained. Failure to consider this diagnosis can result in a preventable tragedy.

The treatment of carbon monoxide poisoning is based on the fact that high oxygen pressures compete with carbon monoxide for the Fe++ binding site of hemoglobin and thus speed the dissociation of HbCO and the excretion of carbon monoxide. Treatment is discussed further in Chapter 9.

METHEMOGLOBINEMIA AND SULFHEMOGLOBINEMIA

Aside from carbon monoxide, other factors can affect the affinity of hemoglobin for oxygen. Methemoglobin (metHb) occurs when the Fe⁺⁺ of hemoglobin is oxidized to Fe⁺⁺⁺; oxidized hemoglobin is then unable to carry oxygen. Normally, about 1.5% of hemoglobin is in the oxidized state; an amount greater than 1.5% defines a state of methemoglobinemia.

As with carboxyhemoglobin (HbCO), each one percent increase of metHb means 1% less oxyhemoglobin (HbO₂). In addition, metHb strengthens the affinity of normal hemoglobin (Fe⁺⁺) for oxygen. Thus, as with HbCO, metHb causes hypoxia in two ways: (1) it reduces the amount of oxygen that hemoglobin can bind at the pulmonary capillary, causing a reduction in arterial oxygen content; and (2) it causes the hemoglobin that does bind with oxygen to hold the oxygen more tightly so that it is less available at the tissue level. This last effect represents a leftward shift of the oxygen dissociation curve since, for a given PaO₂, oxygen is more tightly bound to hemoglobin than when metHb is not present.

In contrast to HbCO, metHb causes profound cyanosis because of the color of oxidized hemoglobin. Patients with only 1.5 gm% metHb (10% metHb with a hemoglobin content of 15 gm%) will appear cyanotic, but they may not be particularly hypoxic or symptomatic. (By contrast, cyanosis from hypoxemia requires at least 5 gm% of desaturated hemoglobin in the systemic capillaries.)

Although methemoglobinemia can occur as an inherited defect, in adults it most commonly occurs as an idiosyncratic reaction to certain oxidant drugs, particularly nitrites and sulfonamides. Several drugs that have been implicated in causing methemoglobinemia are listed in Table 6­2.

Treatment of methemoglobinemia depends on its severity; in mild to moderate eases, e.g. %metHb less than 30%, use of supplemental oxygen and removal of the offending drug may be all that are necessary. The oxidized hemoglobin will convert to normal over a period of I to 3 days. In severe or symptomatic eases for which a quick conversion is necessary, the drug of choice is methylene blue.

Methylene blue acts as a reducing agent, converting Fe⁺⁺⁺ to Fe⁺⁺ so that hemoglobin can again carry oxygen. The dose is 1 mg/kg intravenously over a 5­minute period.

Sulfhemoglobin (SuHb) is produced when a sulfur atom is incorporated into the hemoglobin molecule; like metHb, SuHb occurs most commonly as a drug reaction and results in a deep bluish skin color. Unlike metHb, SuHb is not reversible and does not respond to methylene blue. Also in contrast to metHb, SuHb causes a rightward shift of the oxygen dissociation curve, thus ameliorating the arterial hypoxemia. In the presence of excess SuHb, oxygenated hemoglobin gives up its oxygen more readily at the tissue level.

CAUSES OF REDUCED SaO₂

Except for patients whose primary problem is anemia, all cases of hypoxemia manifest a reduction in SaO₂ (see Causes of Hypoxia, p. 113) . Causes of reduced SaO₂ are listed in Table 6­3; this table should be compared and contrasted with Table 5­1 .

Included in Table 6­3 are two categories that require further explanation. Abnormal hemoglobin refers to a hemoglobin molecule composed of an amino acid sequence that differs from the normal sequence. These hemoglobinopathies are inherited defects. Several abnormal hemoglobins are known to cause a rightward shift of the oxygen dissociation curve, resulting in arterial desaturation. (Some abnormal hemoglobins result in a leftward shift, which increases arterial saturation for a given PaO₂­)

Plasma factors refer to those physical and biochemical changes that may shift the oxygen dissociation curve to the right: increased 2,3­diphosphoglycerate (DPG), increased body temperature, and acid pH (see Fig. 6­3).

As noted in Chapter 5, unless the alveolar air­pulmonary capillary interface is altered, changes in hemoglobin should not affect PaO₂. For this reason SaO₂ must always be measured if its value is to be used for clinical purpose. Treatment based on only a calculated SaO₂ may be misdirected.

OXYGEN DELIVERY

Knowing just the oxygen content of a patient's blood may not be sufficient to assess the adequacy of oxygenation. Low or inadequate cardiac output may impair oxygen delivery, which is the total cardiac output (QT) times arterial oxygen content (CaO₂):

Oxygen delivery = QT x CaO₂ (Eqn 6-2)

For example, assuming a normal QT and a normal CaO₂:

Oxygen delivery = 5000 ml/min x 20 ml O₂/100 ml blood = 1000 ml O₂/min

Patients in shock can have a normal CaO₂ but still suffer severe hypoxia because of decreased cardiac output and inadequate oxygen delivery. In such patients CaO₂ measurement is not sufficient to assess adequacy of oxygenation, and cardiac output or other measurements must be obtained.

Normal resting cardiac output ranges between 4 and 7 L/min, and a normal CaO₂ between 16 and 20 ml O₂/100 ml blood. Hence, normal oxygen delivery for a given individual may range between 640^* and 1400^** ml O₂/min.

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