Po2 and pco2 relationship quiz

Easy blood gas quiz with answers, by Lawrence Martin, MD

po2 and pco2 relationship quiz

An arterial blood gas (ABG) measures three components: pH, pCO2, pO2. . It is important to understand the difference between the pO2, the oxygen saturation. Get an answer for 'What is the relationship between hemoglobin and Po2? How do temperature, H+, Pco2, and BPG influence the affinity of Hb for O2?' and find. Adv Exp Med Biol. ; Relationship between alveolar-arterial PO2 and PCO2 differences and the contact time in the lung capillary. Mochizuki.

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. 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: 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: 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 BEunder 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 SaO2the 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. Thus the pO2 that we breathe in is 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 mmHg. If one sends a sample of coffee to the blood gas lab, the blood gas machine should measure a pO2 of Normal pO2 in arterial blood is only 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 beit 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. Substituting coffee for blood, is like removing all the RBCs and letting plasma alone flow though the body.

ABG (Arterial Blood Gas) | Lab Tests | GLOWM

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 pressurebut 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.

If the patient breathes supplemental oxygen, the inspired pO2 increases to mmHg, mmHg or higher depending on how much oxygen is inhaled. Oxygen saturation SaO2 is a measurement of the percentage of oxygen binding sites that contain oxygen. 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.

po2 and pco2 relationship quiz

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. 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.

po2 and pco2 relationship quiz

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.

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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.

Lung compliance is also reduced due to increased blood volume and a combination of alveolar collapse and airway closing in the lung basis [ 3 ]. The effects of obesity on total lung capacity TLC and vital capacity VC are modest, whereas functional residual capacity FRC and particularly expiratory reserve volume ERV may be severely decreased [ 14 — 6 ].

An observational study of 37 morbidly obese patients showed that massive weight loss following bariatric surgery was associated with a significant improvement of ERV [ 7 ].

The effects of various patterns of obesity on pulmonary function have been studied. It has also been suggested that waist-to-hip ratio WHRrather than BMI, explains a large part of the variance in pulmonary gas exchange [ 910 ]. Current literature is scarce about the possible relationship between various levels of obesity and pulmonary gas exchange.

If increasing levels of extreme obesity have detrimental effects on pulmonary gas exchange, this might have prognostic and therapeutic implications. We aimed to investigate how various measures of overall and abdominal obesity are related to arterial blood gases and pulmonary function in a population of morbidly obese patients with normal lung function. The study design, methods, and population have been described in detail [ 11 ]. After exclusion of 47 subjects who declined to participate or who had heavy comorbidities, subjects were found potentially eligible for either lifestyle intervention or bariatric surgery.

The remaining subjects were defined as having normal lung function and were included in the analysis. All participants gave informed written consent before enrolment. Data Source and Measurements All subjects were examined by a physician. Demographic data and medical history, including smoking habits recorded as pack-yearsand use of bronchodilators were recorded. Height, weight, neck circumference NCwaist circumference WCand hip circumference HC were measured with subjects in an upright position wearing light clothes and no shoes.

NC was measured at the cricoid cartilage and WC at the level midway between the lowest rib margin and the iliac crest. The sampling was carried out by either a physician AMG or two experienced nurses. For analyses we used an ABL Radiometer Copenhagen, Denmark calibrated in accordance with the manufacturer's specifications. Lung function measurements included dynamic spirometry, static lung volumes, and gas diffusion capacity. All tests were carried out by two experienced nurses according to the guidelines recommended by the ATS-ERS task force [ 15 — 17 ] and with subjects sitting in an upright position wearing a nose clip.

These reference values have been derived from studies of healthy, non-smoking adults of European descent [ 13 ].