This is a 5 year old male with a history of fever and coughing. His temperature has been up to 40 degrees C (104 degrees F). He has been ill for three days. He has vomited 8 times today and 4 times yesterday. He is also weak and oral intake has been poor. His past medical history and family history are unremarkable.
Exam: VS T39.0, P140, R50, BP 100/70, oxygen saturation 93% in room air, height and weight 50th percentile. He is drowsy, in moderately severe respiratory distress, and mildly toxic in appearance. His eyes are clear but sunken. His TMs are normal. His oral mucosa is sticky. His neck is supple without adenopathy. Cardiac exam demonstrates tachycardia without murmurs. Lungs reveal coarse breath sounds without wheezing. Moderate retractions are present with obvious tachypnea. Abdomen is soft and non-tender. His color and perfusion are good. His neurologic exam is intact except for the fact that he is slightly weak.
A chest radiograph shows a right middle lobe infiltrate. A CBC is remarkable for a WBC of 28.5 with 15% bands, 65% segs, 15% lymphs, 5% monos. A chemistry panel shows Na 136, K3.6, Cl 100, bicarb 17, glucose 100. A blood culture is also drawn. An arterial blood gas obtained with the patient breathing room air shows pH 7.35, pCO2 33, pO2 80, BE -7, HCO3 16, O2sat 93%. He is placed on 6 L oxygen by mask, an IV fluid infusion is begun, and antibiotics are administered. His oxygen saturation increases to 100% while breathing supplemental oxygen.
A normal blood gas should be memorized using single values rather than a range: pH 7.40, pCO2 40, pO2 100, BE 0, HCO3 24. Our patient's arterial blood gas (ABG) shows that the partial pressure of oxygen (pO2) is slightly low, but satisfactory. Once supplementary oxygen is administered, his oxygenation improves as demonstrated by a rise in oxygen saturation. His ABG also shows that he has a metabolic acidosis (high negative base excess-BE and low bicarbonate). He has partial respiratory compensation since his low pCO2 partially offsets the metabolic acidosis.
An arterial blood gas (ABG) measures three components: pH, pCO2, pO2. All the other numbers on a blood gas are calculated. The bicarbonate (HCO3) value is calculated based on the measured pH and the measured pCO2, using the Henderson-Hasselbalch equation. The base excess (BE) is calculated using a similar equation. The oxygen saturation is calculated based on the assumption that normal adult hemoglobin (HgbA) is the dominant hemoglobin in the sample (using the oxygen hemoglobin dissociation curve).
The pH measures the net circulating acid/base level. The pH can be affected by ventilation and by metabolic factors. Although the Henderson-Hasselbalch equation relates the pH, pCO2 and the HCO3 (bicarbonate, bicarb for short) values, suggesting that the three are in a dynamic equilibrium, it is easiest to interpret a blood gas based on the assumption that pCO2 and HCO3 are independent contributors to the pH. As the bicarb goes up, the pH goes up (less acidic, more alkaline). As the pCO2 goes up, the pH goes down (more acidic). The pCO2 determines the respiratory component of the pH, while the bicarb determines the metabolic component of the pH. The pCO2 and the bicarb contribute to the acidosis in opposite directions.
Even though we learned in chemistry that a pH of 7.0 is neutral, this is not the same for biological systems. The human body functions best at a pH of 7.40. Human proteins, hence cellular function, have reduced bioactivity at a pH outside of this value. Anything less than 7.40 is an acidosis. Anything above 7.40 is an alkalosis.
Table 1 below lists several ABG examples to help us. The interpretation of blood gases should be done in conjunction with the patient's clinical status.
ABG-A is a normal blood gas in room air. ABG-B (pH 7.20, pCO2 60, pO2 70, bicarb 24, BE -3) shows a patient with acute respiratory failure. The pH is less than 7.40 which means that the patient has an acidosis. The pCO2 is very high so this is the respiratory component which contributes to the acidosis. The bicarb is normal (equivalent to saying that the base excess is 0). This is called a respiratory acidosis. The pCO2 is indicative of the minute ventilation, in other words, the amount of total air that is moved in and out of the lungs per unit time. The minute ventilation can be increased by increasing the respiratory rate or increasing the tidal volume or both. As the minute ventilation increases, the pCO2 will decrease. A high pCO2 signifies a decreased minute ventilation. Thus, in general, pCO2 = ventilation. A very high pCO2 in conjunction with a low pO2 (hypoxia) suggests acute respiratory failure. This patient is likely to be lethargic, with a poor respiratory effort. This patient requires prompt positive pressure ventilation by bag-mask ventilation and eventual tracheal intubation and mechanical ventilation.
If this patient is allowed to remain hypoxemic without any intervention, ABG-C (pH 7.04, pCO2 60, pO2 70, bicarb 16, BE -13) will result. Because the tissues are hypoxic for a prolonged period, they shift to anaerobic metabolism and generate lactic acid. Since bicarb is the dominant cellular and extracellular buffer, the bicarb will decline as metabolic acid levels increase. This ABG shows a worsening of the acidosis since both the respiratory and metabolic components are contributing to the acidosis.
ABG-D (pH 7.31, pCO2 60, pO2 80, bicarb 30, BE +4) shows a low pH, hence an acidosis. The pCO2 is high which causes an acidosis, so this is a respiratory acidosis. In chronic lung disease, such as in infants with bronchopulmonary dysplasia or adults with chronic emphysema, air exchange is chronically poor, thus pCO2 is chronically high. The kidneys sense the acidosis, and compensate by retaining bicarbonate to partially raise the pH. This is called metabolic (as opposed to respiratory) compensation. This does not occur acutely which is why ABG-B (acute respiratory failure) shows no metabolic compensation. Note that with the pCO2 of 60, and a normal bicarb (24), the pH is 7.22, but with the same pCO2 and a higher bicarb (30), the pH is closer to 7.40. ABG-D can be described as a respiratory acidosis with metabolic compensation.
Look at ABG-D again: pH 7.31, pCO2 60, pO2 80, bicarb 30, BE +4. Why couldn't we call this a metabolic alkalosis with secondary respiratory compensation? Because the pH is less than 7.40, this is an acidosis, not an alkalosis. Thus, since the metabolic factor should cause an alkalosis, but the pH shows an acidosis, this must be a respiratory acidosis, with secondary metabolic compensation.
ABG-E (pH 7.26, pCO2 34, pO2 100, bicarb 15, BE -11) is a patient with renal failure who requires hemodialysis every other day. Because his kidneys cannot excrete acid, he has a chronic metabolic acidosis (bicarb 15, BE -11). To compensate for this, the brain senses the acidosis and the brain's respiratory center stimulates the respiratory rate to cause a tachypnea, which increases the minute ventilation to increase the pH. ABG-E can be described as a metabolic acidosis with partial respiratory compensation. Why can't we call this a respiratory alkalosis with secondary metabolic compensation? Because the pH is less than 7.40, this is an acidosis, not an alkalosis. Thus, since the respiratory factor should cause an alkalosis, but the pH shows an acidosis, this must be a metabolic acidosis, with secondary respiratory compensation.
ABG-E, could also be seen in a dehydrated patient. The dehydration causes a metabolic acidosis, which causes some secondary tachypnea (respiratory compensation). The same thing occurs in diabetic ketoacidosis. But since the degree of acidosis is generally more severe, the degree of tachypnea is generally more exaggerated (Kussmaul respirations).
So far we have seen an example of: 1) a respiratory acidosis with metabolic compensation, and 2) a metabolic acidosis with respiratory compensation. Is it clinically possible to see other combinations? Specifically, could the following scenarios be possible: 3) a respiratory alkalosis with metabolic compensation and 4) a metabolic alkalosis with respiratory compensation.
A respiratory alkalosis could only be caused by increasing the minute ventilation. Clinically, this would have to be done by hyperventilating. Since metabolic compensation does not occur acutely, one would have to hyperventilate for a long time for metabolic compensation to occur. This would not be a realistic clinical condition. However, in a patient on a mechanical ventilator set such that the patient is deliberately hyperventilated for a prolonged period, the kidneys may sense the alkalosis and thus, excrete bicarb to partially compensate for this. An ABG example of this would be pH 7.41, pCO2 35, pO2 100, bicarb 22, BE -2. This would be an unusual case of a respiratory alkalosis with metabolic compensation.
The last possibility is a metabolic alkalosis with respiratory compensation. This is even less likely clinically. How can a patient develop a metabolic alkalosis? There are only a few possibilities: 1) The patient would have to take a drug which excretes chloride or retains bicarbonate. 2) The patient would have to consume excess amount of alkaline substances, such chronic antacid use. 3) The patient would have to be a chronic vomiter (e.g., bulimia nervosa) since chronic vomiting results in excessive hydrochloric acid loss. Do such patients develop respiratory compensation? To do this, they must hypoventilate!! This is possible, but not likely. This clinical situation is unlikely.
How do venous and capillary blood gasses differ from an arterial blood gas? Looking at the three blood gas measurements: 1) The venous bicarb and the arterial bicarb are roughly the same. 2) The venous pCO2 is slightly higher than the arterial pCO2 because additional CO2 is picked up from the tissues, but the difference between the two is rather small. 3) The venous pO2 is substantially lower than the arterial pO2.
Since only the pCO2 and the bicarb contribute to the pH, the venous pH and the arterial pH are roughly the same. A venous or a capillary blood gas very closely approximates the arterial pH, pCO2 and bicarb (or BE), under ideal conditions with well perfused tissues, but they do not approximate the arterial pO2. All that can be said about a venous pO2 is that it is lower than the arterial pO2. All that can be said about a capillary pO2 is that it lies somewhere between the venous pO2 and the arterial pO2. Fortunately, pulse oximetry accurately reflects the arterial pO2. Therefore, a venous blood gas or capillary blood gas done in conjunction with a pulse oximeter measurement, should accurately reflect the arterial blood gas as long as the capillary source is well perfused. Often, no blood gas is needed at all. The bicarb value can be obtained by ordering a standard set of electrolytes, the pO2 can be accurately estimated using a pulse oximeter, and the pCO2 can be clinically estimated using auscultation by listening for the degree of air exchange.
The arterial pO2 is frequently described as the paO2 to denote that this is an arterial sample, as opposed to a venous or capillary pO2. Blood gases and pulse oximeters can be occasionally fooled so it is important to know when these tests provide us with misleading information. It is important to understand the difference between the pO2, the oxygen saturation (often called SO2 or SaO2), the oxygen content and the oxygen delivery rate.
The pO2 represents the partial pressure of oxygen or the gas tension. This concept is difficult to visualize, but it can best be thought of as the force that the oxygen particles exert on the side of an enclosed container. Gases travel rapidly, so that the partial pressures of gases tend to be identical in samples that are next to each other for at least 5 seconds. Gas pressure or gas tension is measured in mmHg or Torr, which are exactly the same thing. The atmospheric pressure at sea level is 760 mmHg (or Torr) and the atmosphere contains 21% oxygen. Thus the pO2 that we breathe in is 160.
What is the pO2 in a cup of coffee? As the coffee sits on the table, its gas content rapidly equilibrates with the environment so the pO2 in the liquid coffee is 160 mmHg. If one sends a sample of coffee to the blood gas lab, the blood gas machine should measure a pO2 of 160. Normal pO2 in arterial blood is only 100 mmHg. If I replaced my blood with coffee, my brain and other tissues would not be happy since although the pO2 of the coffee may be 160, it does not contain much oxygen. Blood holds a lot of oxygen which is why we need blood. One ml of coffee contains only a few oxygen molecules, while one ml of blood contains many, many more oxygen molecules. Each hemoglobin molecule has four oxygen binding sites. Blood contains red blood cells and plasma. RBCs hold a lot of oxygen while the plasma contains only minute amounts of oxygen. The pO2 of RBCs is the same as the pO2 of the plasma, yet the oxygen content of the plasma is minute, compared to the oxygen content of RBCs. Substituting coffee for blood, is like removing all the RBCs and letting plasma alone flow though the body. This is the difference between pO2 and oxygen content. While many fluids may have reasonably good pO2s, only blood has a satisfactory oxygen content. The pO2 of a fluid sample is a measurement of its oxygen gas tension (or pressure), but it is not a measurement of oxygen content.
An oxygen saturation measurement can only be done on blood, as opposed to a pO2 which can be done on coffee or any fluid. The pO2 and the SaO2 are related to each other by the oxygen hemoglobin dissociation curve, which students learn in physiology. This curve plots the oxygen saturation (in %) on the vertical axis and pO2 on the horizontal axis. The oxygen saturation % steadily increases as the pO2 increases up to about a pO2 of 100 mmHg at which point the oxygen saturation is 99% to 100% (i.e., all the hemoglobin oxygen binding sites contain oxygen). If the patient breathes supplemental oxygen, the inspired pO2 increases to 200 mmHg, 400 mmHg or higher depending on how much oxygen is inhaled. Thus, a patient breathing supplemental oxygen may have a pO2 as high as 400 mmHg, but his oxygen saturation is still 100%, since it can't get any higher than this. So the typical appearance of an oxygen hemoglobin dissociation curve, has a steep rise at pO2s below 100 mmHg, at which point it becomes a plateau since the oxygen saturation cannot increase above 100%.
Oxygen saturation (SaO2) is a measurement of the percentage of oxygen binding sites that contain oxygen. If all the oxygen binding sites contain oxygen, then the oxygen saturation is 100%. An oxygen saturation measurement can only be done on blood, as opposed to a pO2 which can be done on coffee or any fluid. The pO2 and the SaO2 are related to each other by the oxygen hemoglobin dissociation curve, which students learn in physiology. This curve plots the oxygen saturation (in %) on the vertical axis and pO2 on the horizontal access. The oxygen saturation % steadily increases as the pO2 increases up to about a pO2 nearing 90 to 100 mmHg at which point the oxygen saturation is 99% to 100% (i.e., all the hemoglobin oxygen binding sites contain oxygen). If the patient breathes supplemental oxygen, the inspired pO2 increases to 200 mmHg, 400 mmHg or higher depending on how much oxygen is inhaled. Thus, a patient breathing supplemental oxygen may have a pO2 as high as 400 mmHg, but his oxygen saturation is still 100% (it can't get any higher than this). So the typical appearance of an oxygen hemoglobin dissociation curve, has a steep rise at pO2s below 100 mmHg, at which point it becomes a plateau since the oxygen saturation cannot increase above 100%.
Oxygen saturation can be measured continuously and non-invasively by pulse oximetry. Pulse oximetry uses light absorption through a pulsing capillary bed usually in a toe or finger, but it will also pick up in the nose, ear, palm, side of the foot, etc. The probe looks red, but it actually uses two light sources; one is red and the other is invisible infrared. Absorption using these two wave lengths measures oxygen saturation for hemoglobin A. Pulse oximetry will not measure the oxygen saturation correctly for other hemoglobins such as methemoglobin or carboxyhemoglobin. However, for sickle hemoglobin or fetal hemoglobin, the measurement is nearly as accurate as for hemoglobin A. Oxygen saturation can be measured by co-oximetry but this requires a blood sample Co-oximetry is capable of determining the true oxygen saturation for methemoglobin and carboxyhemoglobin. If the true oxygen saturation is known, then the pO2 can be estimated or calculated using the oxygen hemoglobin dissociation curve assuming that the patient is circulating hemoglobin A (which is not always the case).
The oxygen content is determined by the oxygen saturation percentage and the hemoglobin concentration. A patient with a hemoglobin of 14 has twice as much oxygen per ml of blood compared to a patient with a hemoglobin of 7, assuming that they both have 100% oxygen saturations. Similarly, the visual presence of cyanosis is dependent upon the concentration of desaturated (blue) hemoglobin. Thus, a patient with a hemoglobin of 7 at 80% saturation has a deoxygenated hemoglobin concentration of 1.4. This patient will visually appear to be just as blue (though paler) as a patient with a hemoglobin of 14 at 90% saturation, since this latter person also has a deoxygenated hemoglobin concentration of 1.4. Additionally, a patient with a hemoglobin of 14 at 80% saturation will look more cyanotic than a patient with a hemoglobin of 7 at 80% saturation. In this comparison, the more cyanotic patient is doing better with a higher oxygen content and oxygen delivery.
The hematocrit is the percentage of the blood that contains RBCs. The hematocrit is directly proportional to the hemoglobin concentration. The hematocrit (in percent) is roughly three times the hemoglobin concentration (in gm per dl). Chronically hypoxic patients can survive by raising their hematocrit as a compensation maneuver. Chronic hypoxia stimulates erythropoietin which stimulates RBC production raising the hematocrit. Thus, a patient with a normal hemoglobin of 12 (hematocrit 36) and an oxygen saturation of 100%, has the same oxygen content as a patient with an oxygen saturation of 80% and a hemoglobin of 15 (hematocrit 45). The former patient looks pink, while the latter patient looks blue.
The last factor is the oxygen delivery rate. This is determined by the oxygen content and the cardiac output. Conceptually, imagine a patient with a weak heart and only half the cardiac output of a normal patient with signs of congestive heart failure. If pulmonary edema were not present, and such a patient had an oxygen saturation of 100%, their hemoglobin would have to be twice as high as another patient with a normal cardiac output to achieve the same oxygen delivery rate. This might be better understood by measuring a patient's venous blood gas. In room air, a normal arterial pO2 would be 100 mmHg, and the venous pO2 would be about 75 mmHg. However, if a patient had a very low cardiac output, the arterial pO2 might still be 100 mmHg, but the venous pO2 might be 50 mmHg. This occurs because the cardiac output is so low, that much more oxygen is extracted from the RBCs as they pass through the capillaries.
Pulse oximetry can be fooled by conditions with abnormal hemoglobin color. The major condition in this category is carbon monoxide (CO) poisoning. CO poisoning results in the formation of carboxyhemoglobin. Carboxyhemoglobin does not carry oxygen. It is really a hemoglobin molecule with all oxygen carrying sites occupied by CO. The CO has such a high affinity for hemoglobin, that oxygen cannot displace it. Consider carboxyhemoglobin totally useless in oxygen transport. CO poisoning results from CO exposure, most commonly exposure to fuel combustion (fuel burning heaters, stoves, automobile exhaust, etc.), so it most commonly occurs during cold periods where people are in closed quarters to conserve the heat originating from fuel combustion. Symptoms include headache, nausea, vomiting and weakness. The patient is classically described as cherry red, but in reality, they appear to be pink, which lowers the clinician's suspicion for hypoxia. Thus, these symptoms are commonly attributed to viral flu-like illnesses. If a patient has a carboxyhemoglobin level of 25%, and their hemoglobin is 12, this means that they effectively have a hemoglobin of only 9 (since 25% of their hemoglobin is useless). If the carboxyhemoglobin level is 25%, then the maximum oxygen saturation that can be attained is 75%. However, the pulse oximeter will read 100% because the color of carboxyhemoglobin is bright red, which is what the pulse oximeter reads. Thus, pulse oximetry measurements are fooled by CO poisoning. The arterial blood gas is not usually helpful either. Since the ABG measures oxygen gas tension (pO2) and not oxygen content or true oxygen saturation, the oxygen gas tension (pO2) will be normal. The only abnormality on an ABG may be metabolic acidosis, which is a consequence of inadequate oxygen delivery to the peripheral tissues, resulting an anaerobic metabolism and lactic acid production. If CO poisoning is suspected, one must order a CO level or a test called co-oximetry. Co-oximetry is done routinely in some blood gas analyzers, but most do not, so this must be specifically ordered. Co-oximetry is capable of measuring the true oxygen saturation percentage and the percentage of nonfunctional hemoglobins such as carboxyhemoglobin and methemoglobin. The treatment for CO poisoning is oxygen, but if the CO level is very high, or if the victim is pregnant, hyperbaric oxygen is indicated to more effectively displace the CO from the hemoglobin.
Similarly, methemoglobinemia is a condition in which there are high circulating levels of methemoglobin which does not carry oxygen. The major difference is that methemoglobin is brown in color. Patients with methemoglobinemia are classically "ashen gray" in color. Their pulse oximetry value will read LOW, so this condition does not fool the pulse oximeter as it does in CO poisoning. Another clue is that when supplemental oxygen is given to the patient, the pulse oximetry reading does not change. It will still be low. When an arterial blood gas is drawn, the blood appears to be a chocolate brown color which is quite eye opening. A simple bedside test can be done by taking a drop of the patient's blood on a filter paper or gauze. Get another drop of blood from a normal person (either your or your fellow residents and medical students). Blow oxygen over the surface of these two blood spots. The normal blood will become red or stay red, while the methemoglobinemia patient's blood will stay the same color (brown or dark) since the methemoglobin will not carry oxygen. This illustrates the fact that the oxygen gas tension (pO2) does not reflect the degree of oxygen carrying capacity. Co-oximetry or a methemoglobin level can be ordered to measure the severity of the methemoglobinemia, but the pulse oximeter will be able to estimate it also. Most symptomatic methemoglobinemia occurs in infants with diarrhea. The cause is usually idiopathic, but the ingestion of nitrites is one of the known causes. The condition is usually self-limited and resolves gradually with IV fluid hydration. IV methylene blue can be given for severe cases. Oxygen supplementation is somewhat helpful and PRBC transfusion can be used to increase the oxygen carrying capacity in severe cases.
The two common elements of CO poisoning and methemoglobinemia is that the pO2 does not identify the condition. You can think of carboxyhemoglobin and methemoglobin as useless hemoglobin, just like the coffee in the cup example. Coffee (or water) is capable of carrying oxygen, but very little. Just because the pO2 of the coffee or carboxyhemoglobin or methemoglobin is 150 Torr, this does not mean that it is carrying much oxygen at all. CO poisoning is a harder diagnosis to make, because the pulse oximeter reads falsely normal. A typical ABG in CO poisoning or methemoglobinemia patients is pH 7.26, pCO2 34, pO2 100, bicarb 15, BE -11, if the patient is breathing room air. If the patient is breathing supplemental oxygen, then the ABG will be pH 7.26, pCO2 34, pO2 400, bicarb 15, BE -11 (i.e., just the pO2 goes up), although this does not change the oxygen saturation much. Although the blood gas machine will calculate that the oxygen saturation is 100%, remember that the ABG machine did not measure this, but rather it calculates this based on the assumption that the sample contains normal hemoglobin (which is not the case if the patient has CO poisoning or methemoglobinemia). The paradox is that the ABG slip will indicate that the oxygen saturation is 100%, while the co-oximetry report will indicate that the oxygen saturation is very low (e.g., 70%).
In summary, CO poisoning has a low true oxygen saturation, red color, 100% oxygen saturation on pulse oximetry (which is false), and normal pO2 on ABG. Methemoglobinemia has a low true oxygen saturation, brown color, low oxygen saturation on pulse oximetry, and normal pO2 on ABG.
Questions
1. Which patient has a higher oxygen content? Patient A with a pO2 of 100 or patient B with a pO2 of 70?
2. ABG pH 7.31, pCO2 60, pO2 80, bicarb 30, BE +4. What is the best description for this ABG considering the concepts of metabolic or respiratory acidosis or alkalosis, and metabolic or respiratory compensation?
3. Describe a possible clinical situation which would yield the ABG in question number 2 above?
4. At what pO2 or oxygen saturation does cyanosis become visible?
5. Write an example of an ABG in a patient with moderately severe diabetic ketoacidosis.
6. In a cardiac arrest victim, you get an ABG which shows pH 6.72, pCO2 55, pO2 200, bicarb 7, BE -25. What can you do to reverse the acidosis?
7. Well oxygenated patients are pink and poorly oxygenated patients are cyanotic. Is there a stage in between these? What is the color of these patients if they aren't pink and they aren't cyanotic? The answer to this question is not found in the above chapter.
8. What condition would give you the following results in an ill appearing patient breathing supplemental oxygen: Pulse oximeter reading 100%, pO2 on ABG 350 Torr, co-oximetry (true oxygen saturation) 65%.
References
1. Blood Gases. In: Jacobs DS, et al (eds). Laboratory Test Handbook, 4th edition. 1996, Hudson (Cleveland): Lexi-Comp Inc, pp. 87-89.
2. Grant BJB, Saltzman AR. Respiratory Functions of the Lung. In: Baum GL, Wolinsky E (eds). Textbook of Pulmonary Disease, fifth edition. 1993, Boston: Little, Brown and Company, pp. 139-218.
Answers to questions
1. This cannot be determined without knowing the hemoglobin or hematocrit of each patient. Patient A could paradoxically have a lower oxygen content if he has a substantially lower hemoglobin (severely anemic) than patient B.
2. This is a respiratory acidosis with metabolic compensation.
3. This patient has bronchopulmonary dysplasia (chronic lung disease) with chronic CO2 retention and metabolic compensation. An alternative answer would be an adult with chronic emphysema. An incorrect answer is acute respiratory failure, because if the respiratory failure were acute, the patient would not have enough time for metabolic compensation and his bicarb would be 24 or lower.
4. Visible cyanosis requires a certain amount of deoxygenated hemoglobin which is why the answer to this question depends on the hemoglobin or hematocrit. Patients with low hematocrits require a lower pO2 for visible cyanosis compared to patients which higher hematocrits. So there is no single answer to this question. For example, a patient with cyanotic congenital heart disease may have a high hemoglobin to compensate. If his chronic oxygen saturation is 80%, he can compensate by having a higher hemoglobin such as a hemoglobin of 16. He will be visibly cyanotic because 20% (100% minus 80% oxygen saturation) of his 16 hemoglobin is desaturated (i.e., 3.2 Hgb is desaturated). For a normal child with a hemoglobin of 13 to have 3.2 desaturated Hgb, this child would have to have 25% (3.2 divided by 13) desaturation (i.e., an oxygen saturation of 75%). Thus, one patient may look bluer at 80% saturation, while another would less blue at 80% because of different hemoglobins.
5. The pH should be low. The bicarb should be low (metabolic acidosis). There should be some respiratory compensation so the pCO2 should be low (hyperventilation or Kussmaul respirations). The pO2 should be fairly normal. So an example might be pH 7.14, pCO2 30, pO2 100, bicarb 10, BE -17.
6. This is a cardiac arrest so the patient is probably intubated. The high pCO2 indicates that the patient is being hypoventilated or the endotracheal tube is not in the trachea. Proper placement of the endotracheal tube should be confirmed. The tidal volume and respiratory rate need to be increased to increase the minute ventilation to decrease the pCO2. Better chest compressions to improve pulmonary blood flow will also facilitate the removal of CO2. The bicarb is low causing a metabolic acidosis. Sodium bicarbonate can be given intravenously to reverse the metabolic acidosis.
7. Their color is pale. Thus pallor can suggest anemia, poor skin perfusion or hypoxia.
8. CO poisoning.