Regulation of Respiration
Start studying relationship between SaO2 and PaO2. CardioPulm PFT & ABG ( lab quiz 1) Health Science Unit 12 Vital Signs: Normal HR, RR, and SpO2. oxygen saturation (SpO2) of PTIs needs to be monitored so that the level of blood . SpO2 levels, no significant difference was found between the groups, with their mean value .. ;28(1), quiz E PMid An arterial blood gas (ABG) measures three components: pH, pCO2, pO2. . 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.
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. Similarly, the visual presence of cyanosis is dependent upon the concentration of desaturated blue hemoglobin.
In this comparison, the more cyanotic patient is doing better with a higher oxygen content and oxygen delivery.
iROCKET Learning Module: Intro to Arterial Blood Gases, Pt. 1
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. 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.
This might be better understood by measuring a patient's venous blood gas. In room air, a normal arterial pO2 would be 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 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.
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. 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 Saturation (SaO2)
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 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. If the patient is breathing supplemental oxygen, then the ABG will be pH 7. Methemoglobinemia has a low true oxygen saturation, brown color, low oxygen saturation on pulse oximetry, and normal pO2 on ABG. There are four heme sites, and hence four oxygen binding sites, per hemoglobin molecule.
Heme sites occupied by oxygen molecules are said to be "saturated" with oxygen. The percentage of all the available heme binding sites saturated with oxygen is the hemoglobin oxygen saturation in arterial blood, the SaO2.
Note that SaO2 alone doesn't reveal how much oxygen is in the blood; for that we also need to know the hemoglobin content. Tissues need a requisite amount of O2 molecules for metabolism. Neither the PaO2 nor the SaO2 provide information on the number of oxygen molecules, i. Note that neither PaO2 nor SaO2 have units that denote any quantity.Oxygen Hemoglobin Dissociation Curve Explained Clearly (Oxyhemoglobin Curve)
This is because CaO2 is the only value that incorporates the hemoglobin content. Oxygen content can be measured directly or calculated by the oxygen content equation introduced in Chapter 2: I have shown the 3 short paragraphs above to dozens of students, interns, residents; almost all will say they understand the differences, no problem.
But, when given questions to test their understanding, they don't show much understanding. So more instruction is needed and, yes, a few problems along the way. Understanding will come from closely reviewing this material AND working on all the problems; do that, and you should be able to teach the subject! PaO2, the partial pressure of oxygen in the plasma phase of arterial blood, is registered by an electrode that senses randomly-moving, dissolved oxygen molecules.
The amount of dissolved oxygen in the plasma phase -- and hence the PaO2 -- is determined by alveolar PO2 and lung architecture only, and is unrelated to anything about hemoglobin.
In this situation a sufficient amount of blood with low venous O2 content can enter the arterial circulation and lead to a reduced PaO2. However, given a normal amount of shunting, neither anemia nor abnormal hemoglobin binding will affect PaO2. Oxygen molecules that pass through the thin alveolar-capillary membrane enter the plasma phase as dissolved free molecules; most of these molecules quickly enter the red blood cell and bind with hemoglobin Figure There is a dynamic equilibrium between the freely dissolved and the hemoglobin-bound oxygen molecules.
However, the more dissolved molecules there are i. Oxygen pressure, saturation and content. Schematic shows cross section of lungs and pulmonary circulation. CO2, nitrogen and other gas molecules are omitted for clarity. PaO2 is always slightly lower than PAO2 because of normal venous admixture, here represented by a connection between the venous and pulmonary circulations. See text for discussion.
Correlation between the levels of SpO2 and PaO2
Thus hemoglobin is like an efficient sponge that soaks up oxygen so more can enter the blood. Hemoglobin continues to soak up oxygen molecules until it becomes saturated with the maximum amount it can hold - an amount that is largely determined by the PaO2.
Of course this whole process is near instantaneous and dynamic; at any given moment a given O2 molecule could be bound or dissolved. However, depending on the PaO2 and other factors, a certain percentage of all O2 molecules will be dissolved and a certain percentage will be bound Figure If there is no interference as from carbon monoxide, for examplethe free O2 molecules bind to these sites with great avidity.
Regulation of Respiration Blood Gas Sensors The first sensor, which has the strongest effect by far on ventilation at sea level is the central chemoreceptor. The neurons responsible are located in the medulla. These are close to, but separate, from the neurons that generate the rhythm of breathing.
Small changes in the partial pressure of carbon dioxide PaCO2 in the systemic arterial blood flowing to the medulla produce pronouced changes in ventilation. The second sensor is the peripheral chemoreceptor, which consists of afferent neurons monitoring the blood in the carotid and aortic bodies.
These are close to the baroreceptors, but entirely separate. By contrast with the central chemoreceptor, the peripheral chemoreceptor has little effect on the breathing of a normal person at rest at sea level.
But in two important circumstances the peripheral chemoreceptor begins to drive breathing. When the partial pressure of oxygen PaO2 falls below about 60 mm Hg. This can occur in various respiratory disorders and at high altitude. With an increase in the hydrogen ion concentration.
This occurs when lactic acid is released into the blood during strenuous exercise. This point, at which ventilation increases markedly, is called the lactate threshold anaerobic threshold.
Oxygen Therapy Oxygen therapy is usually given when PaO2 is below 55 mm Hg, and, although expensive and cumbersome, the oxygen is helpful in COPD when the oxygen falls below this level. But several recent studies have found that patients with less severe COPD are not helped by supplemental oxygen.
However, if a respiratory problem primarily involves a shunt, the PaO2 responds poorly to supplemental oxygen. Think about the effect of the supplemental oxygen on the oxygen content of blood flowing through the ventilated alveoli. Breathing Low Partial Presssures of Oxygen: