Pao2 paco2 relationship quizzes


metHb– methemoglobin, PaCO2 – arterial PCO2 in mm Hg, PACO2– alveolar PCO2 in mm Hg. PaO2– arterial PO2 in mm Hg, PAO2– alveolar PO2 in mm Hg These four equations express relationships that are extremely important in clinical .. lung disease (later confirmed by pulmonary function tests). (PaCO2); the difference can be greater in severely hypoperfused patients Arterial of oxygen (PaO2) and using this value in additional .. Subscribers may take individual CE tests online and get real-time scores at CompendiumVet. com. The important relationship to keep in mind when caring for patients: PaCO2 ~ VCO2 / i.e., Alveolar PO2 = the pressure of oxygen inhaled minus the PaCO2.

Why couldn't we call this a metabolic alkalosis with secondary respiratory compensation? Because the pH is less than 7. 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.

Because his kidneys cannot excrete acid, he has a chronic metabolic acidosis bicarb 15, BE 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? 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: Is it clinically possible to see other combinations? Specifically, could the following scenarios be possible: 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. 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.

Respiratory Equations/ A-a gradient VQ mismatch nonsense | MCQ Quiz | Synap

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.

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

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. 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.

Respiratory Equations/ A-a gradient VQ mismatch nonsense

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. 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. The primary event leads to a large change in pH larger arrows.

Each primary disorder may be caused by a variety of specific clinical conditions see text. Each primary acid-base disorder arises from one or more specific clinical conditions, e. For example, a patient with obvious metabolic acidosis from uremia could present with a high pH due to a concomitant metabolic alkalosis which may not be as clinically obvious. Acidemia low pH and alkalemia high pH are terms reserved for derangements in blood pH only.

ABG interpretation

This terminology helps separate diagnosable and treatable clinical disorders from derangements in acid-base that exist only because of the primary disorder. For example, single acid-base disorders do not lead to normal pH.

Two or more disorders can be manifested by normal pH when they are opposing, e. Although pH can end up in the normal range 7. Similarly, a high pH in a case of acidosis or a low pH in a case of alkalosis signifies two or more primary disorders.

As a rule of thumb, in maximally compensated metabolic acidosis the last two digits of the pH approximate the PaCO2. In metabolic alkalosis respiratory compensation is more variable and there is no simple relationship by which to predict the final PaCO2. A year-old woman presented to the emergency room with mild diabetic ketoacidosis DKA and dyspnea; arterial pH was 7.

Her breathing difficulty was attributed to Kussmaul-type respirations characteristic of DKA. Judging her DKA non-critical, the admitting physician placed her on a general medical ward and began appropriate treatment with insulin and fluids.

Four hours later she appeared more dyspneic; repeat blood gas showed pH 7. She was transferred to MICU where she was noted to be wheezing; bronchodilator therapy was begun.