Can the respiratory quotient be calculated from a formula or must it be measured directly?

Can the respiratory quotient be calculated from a formula or must it be measured directly?

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I found the following question on the Respiratory quotient:

A normal human diet has a Respiratory quotient (RQ) of approximately 0.85. Given that pure oxidation of fatty acids has a Respiratory quotient (RQ) of 0.7 and pure oxidation of carbohydrates has Respiratory quotient (RQ) of 1, can one determine the fraction between the amount of oxygen used for aerobic respiration of the fat and the amount used for aerobic respiration of the carbohydrates?

My solution:

$$ ext{glucose} + ce{O_2} + ext{fat} + x , ce{O_2 ightarrow} ce{CO_2} + 0.7x , ce{CO_2} , + ce{H2O}$$

Note that I haven't balanced the equation excepted for $ce{O_2}$ and $ce{CO_2}$ where I added coefficients based on the given RQ. This equation gives $$ ext{RC}_{total}=frac{1+0.7x}{1+x} = 0.85$$

Hence $1+0.7x=0.85(1+x)$, which gives $x=1$, so the amount of oxygen used for Aerobic respiration of the fat and the amount used for Aerobic respiration of the carbohydrates is equal.

Is this correct?

Controlled Atmosphere Technology

A.K. Thompson , D. Bishop , in Reference Module in Food Science , 2016

Respiratory Quotient

Respiratory quotient is the measure of moles CO 2 evolved to moles O2 absorbed in plant cells. It is 1 when the substrate is carbohydrate but lower for lipids and proteins. Burton (1952) measured RQ in potatoes stored at 10°C in 5–7 kPa CO2 for up to 14 weeks. The increased CO2 reduced both O2 uptake and CO2 output by about 25–30%, but the RQ was unaffected and remained close to 1. Wollin et al. (1985) discussed the possibility that RQ may be used to calculate the lowest O2 level that can be tolerated in fruit storage to be incorporated in an automated CA system. Yearsley et al. (1996) considered that the fermentation threshold RQ represented the safest estimate of the true lower O2 limit for optimizing storage atmospheres.


The respiratory quotient (RQ) is calculated from the ratio:

RQ = CO2 produced / O2 consumed

In this calculation, the CO2 and O2 must be given in the same units, and in quantities proportional to the number of molecules. Acceptable inputs would be either moles, or else volumes of gas at standard temperature and pressure (time units may be included, but they cancel out since they must be the same in numerator and denominator).

The range of respiratory coefficients for organisms in metabolic balance usually ranges from 1.0 (representing the value expected for pure carbohydrate oxidation) to

0.7 (the value expected for pure fat oxidation). See BMR for a discussion of how these numbers are derived. A mixed diet of fat and carbohydrate results in an average value between these numbers. An RQ may rise above 1.0 for an organism burning carbohydrate to produce or "lay down" fat (for example, a bear preparing for hibernation).

RQ value corresponds to a caloric value for each liter (L) of CO2 produced. If O2 consumption numbers are available, they are usually used directly, since they are more direct and reliable estimates of energy production.

RQ as measured includes a contribution from the energy produced from protein. However, due to the complexity of the various ways in which different amino acids can be metabolized, no single RQ can be assigned to the oxidation of protein in the diet.

Growth Kinetics

Ghasem D. Najafpour , . Ghasem Najafpour , in Biochemical Engineering and Biotechnology , 2007

Example 6

The respiratory quotient (RQ) is often used to estimate metabolic stoichiometry. Using quasi-steady-state and by definition of RQ, develop a system of two linear equations with two unknowns by solving a matrix under the following conditions: the coefficient of the matrix with yeast growth (γ = 4.14), ammonia (γN = 0) and glucose (γS = 4.0), where the evolution of CO2 and biosynthesis are very small (σ = 0.095). Calculate the stoichiometric coefficient for RQ = 1.0 for the above biological processes:

Can the respiratory quotient be calculated from a formula or must it be measured directly? - Biology

There are several methods of analyzing metabolic control of an organism. In humans, levels of glucose, thyroid hormones and thyroid-stimulating hormone, insulin, glucagon, oxygen, and carbon dioxide can all be measured in the blood. Because these hormones and substrates have a predictable effect on metabolism, they can be used as indicators of metabolic function. They can also be used as indicators of disorders, as in the case of blood glucose or thyroid-stimulating hormone.


The MCAT does not expect you to know what levels are healthy for any of these indicators, but can easily pose data interpretation questions related to them.

Respirometry allows accurate measurement of the respiratory quotient, which differs depending on the fuels being used by the organism. The respiratory quotient (RQ) can be measured experimentally, and can be calculated as:


for the complete combustion of a given fuel source. The respiratory quotient for carbohydrates is around 1.0, while the respiratory quotient for lipids is around 0.7. In resting individuals, the respiratory quotient is generally around 0.8, indicating that both fat and glucose are consumed. The respiratory quotient changes under conditions of high stress, starvation, and exercise as predicted by the action of different hormones.

Calorimeters can measure basal metabolic rate (BMR) based on heat exchange with the environment. Human calorimetry makes use of large insulated chambers with specialized heat sinks to determine energy expenditure. Because of the isolationist nature of testing and the expense of creating a calorimetry chamber, other measures of BMR are preferred. Because of previous experimentation, BMR can be estimated based on age, weight, height, and gender.

Until now, we've been discussing metabolism on a very small scale, but metabolic controls are also involved in maintaining body mass (weight loss or gain). Body mass is primarily determined by several factors, including water, carbohydrates, proteins, and lipids, while nucleic acids do not contribute significantly to its maintenance. The overall mass of carbohydrates and proteins tends to be stable over time, although it can be modified slightly by periods of prolonged starvation or by significant muscle-building activities. Water is very quickly adjusted by the endocrine system and the kidneys therefore, it does not factor into our discussion of obesity and weight regulation. Water is the primary source of frequent minor weight fluctuations because it is subject to rapid adjustment. Therefore, lipids, stored in adipocytes, are the primary factor in the gradual change of body mass over time.

An individual who is maintaining his weight consumes the same amount of energy that is spent on average each day. If energy consumed is greater than energy expenditure over a significant period of time, then fat stores begin to accumulate. The opposite is also seen. If an energy deficit exists where calories consumed are less than calories burned, then a decrease in weight is observed. As individuals increase in mass, basal metabolic rate (the amount of energy required for one sedentary day) also increases. Thus, a caloric excess will cause an increase in body mass until equilibrium is reached between the new basal metabolic rate and the existing intake. In weight loss the reverse trend is seen.

This effect does have a threshold that differs between individuals. Small adjustments in intake, even over a prolonged period of time, are partially or fully compensated by changes in energy expenditure. Similarly, a small increase or decrease in activity level will be compensated by changes in hunger. Deliberate alterations of body mass require alterations above this threshold level, which is higher in negative energy balance than in positive energy balance&mdashin other words, larger changes must be made to lose weight than to gain it.

Diet (energy intake) and exercise (energy expenditure), genetics, socioeconomic status, and geography all play key roles in weight control. As described earlier, hormonal control by thyroid hormones, cortisol, epinephrine, glucagon, and insulin is critical to the integration of metabolism. In addition, there are hormones that control hunger and satiety, including ghrelin, orexin, and leptin. Have you ever wondered why, even if you don't feel hungry, when you walk into your favorite restaurant you're suddenly ravenous? This is the job of ghrelin and orexin. Ghrelin is secreted by the stomach in response to signals of an impending meal. Sight, sound, taste, and especially smell all act as signals for its release. Ghrelin increases appetite and also stimulates secretion of orexin. Orexin further increases appetite, and is involved in alertness and the sleep–wake cycle. Hypoglycemia is also a trigger for orexin release. Leptin is a hormone secreted by fat cells that decreases appetite by suppressing orexin production. Genetic variations in the leptin molecule and its receptors have been implicated in obesity a knockout mouse unable to produce leptin is shown on the left in Figure 12.11. These messengers and receptors are the target of current research for now, questions regarding body mass modifications on the MCAT mostly come down to food and exercise.

Figure 12.11. Leptin Knockout Mouse (left) Compared to Normal Mouse (right)

Motivation, a psychological concept discussed in Chapter 5 of MCAT Behavioral Sciences Review, is often linked with physiological drives and signaling pathways. The hypothalamus, which produces orexin and responds to leptin and ghrelin, is responsible for regulating hunger, thirst, and libido.

MCAT Concept Check 12.7:

Before you move on, assess your understanding of the material with these questions.

1. How is the respiratory quotient expected to change when a person transitions from resting to brief exercise?

2. True or False: Body mass can be predicted by the leptin receptor phenotype and caloric intake alone.

3. True or False: It is easier to gain weight than to lose weight.

4. If you were designing a study to assess metabolism, which measurement method would you choose? Defend your answer.

Respiratory exchange ratio

The ratio is determined by comparing exhaled gases to room air. Measuring this ratio can be used for estimating the respiratory quotient (RQ), an indicator of which fuel (e.g. carbohydrate or fat) is being metabolized to supply the body with energy. Using RER to estimate RQ is only accurate during rest and mild to moderate aerobic exercise without the accumulation of lactate. The loss of accuracy during more intense anaerobic exercise is among others due to factors including the bicarbonate buffer system. The body tries to compensate for the accumulation of lactate and minimize the acidification of the blood by expelling more CO2 through the respiratory system. [3]

An RER near 0.7 indicates that fat is the predominant fuel source, a value of 1.0 is indicative of carbohydrate being the predominant fuel source, and a value between 0.7 and 1.0 suggests a mix of both fat and carbohydrate. [4] In general a mixed diet corresponds with an RER of approximately 0.8. [5] The RER can also exceed 1.0 during intense exercise. A value above 1.0 cannot be attributed to the substrate metabolism, but rather to the aforementioned factors regarding bicarbonate buffering. [3]

Calculation of RER is commonly done in conjunction with exercise tests such as the VO2 max test. This can be used as an indicator that the participants are nearing exhaustion and the limits of their cardio-respiratory system. An RER greater than or equal to 1.0 is often used as a secondary endpoint criterion of a VO2 max test. [3]

Document maximal effort – RER

The respiratory quotient and the RER are both calculated as the ratio of the volume of carbon dioxide (CO2) produced to the volume of oxygen (O2) used, or VCO2/VO2. The respiratory quotient, which typically ranges between 0.7 and 1.0, is an indicator of metabolic fuel or substrate use in tissues it must be calculated under resting or steady-state exercise conditions. A ratio of 0.7 is indicative of mixed fat use, whereas a ratio of 1.0 indicates the exclusive use of carbohydrates.33 Thus, during low- intensity, steady-state exercise, the respiratory quotient and the RER are typically between 0.80 and 0.88, when fatty acids are the primary fuel.

As the intensity of the exercise increases and carbohydrates become the dominant or primary fuel, the respiratory quotient and the RER increase to between 0.9 and 1.0. Because the respiratory quotient reflects tissue substrate use, it cannot exceed 1.0. By contrast, the RER, which reflects the respiratory exchange of CO2 and O2, commonly exceeds 1.0 during strenuous exercise. During non–steady-state, strenuous exercise, the volume of CO2 production rises as a result of hyperventilation and the increased buffering of blood lactic acid derived from skeletal muscles thus, the RER no longer reflects substrate usage but rather high ventilation rates and blood lactate levels.

Because RER reproducibly increases during exercise, it is considered a parameter that can document maximal effort. Issekutz,33 who was the first to propose the use of RER as a criterion for VO2max, noted that it must exceed 1.15. A higher value may suggest a more accurate assessment of VO2max. The 1.15 value appears to be reasonable, although not all persons are able to achieve it. Studies have noted values of 1.00, 1.05, 1.10, and 1.13 as criterion for maximal performance but at present, no clear consensus has been reached.

Difference between Respiratory Exchange Ratio (RER) and Respiratory Quotient (RQ)

Respiratory Exchange Ratio (RER) and Respiratory Quotient (RQ) are two terms that no everyone may be familiar with, but may have heard in the context of sports, fitness, or physiology, which is a part of human biology. Each human body, and in fact every living being, partakes in Respiratory Exchange Ratio (RER) and Respiratory Quotient (RQ), irrespective of whether or not they are aware of it.

The confusion between the two terms is quite common, as not only do they sound similar but are also interrelated. This dynamic is further complicated by the fact that when resting, they are in fact the same.

As its name suggests, RER, short for Respiratory Exchange Ratio is a ratio that aims to measure the amount of carbon dioxide (CO2) produced in comparison to the amount of oxygen (O2) used. Humans in general tend to inhale more oxygen than the carbon dioxide they exhale. Hence, the ratio is useful to measure the difference, which can be indicative of physical health.

As its name suggests, RER, short for Respiratory Exchange Ratio is a ratio that aims to measure the amount of carbon dioxide (CO2) produced in comparison to the amount of oxygen (O2) used. Humans in general tend to inhale more oxygen than the carbon dioxide they exhale. Hence, the ratio is useful to measure the difference, which can be indicative of physical health.

The ratio is typically measured by comparing the room air with the gases that are exhaled to find the difference. The ratio once calculated can then be quite useful for determining the Respiratory Quotient (RQ).

The Respiratory Quotient (RQ), also known as respiratory coefficient, is a number that is quite useful to calculate the basal metabolic rate (BMR). The respiratory quotient (RQ) is calculated by the formula: RQ = CO2 eliminated / O2 consumed. These days it is quite common to use an apparatus called respirometer to calculate the RQ.

This is why the two are often confused, like the RER, the RQ also measures the amount of carbon dioxide (CO2) produced in comparison to the amount of oxygen (O2) used. However, while the RER calculates it as a ratio, RQ calculates it as a quotient, i.e. a number. While at first glance the two might seem the same, however, there are certain differences between the two. The RER is the ratio, dividing which one will get the RQ, which in turn is used in calculations of basal metabolic rate (BMR) when it is estimated from carbon dioxide production. Hence, it can be said that the RER can be used to calculate the RQ, which is used to calculate BMR.

Another additional difference between the two is amongst the applications of the two figures. As the RER calculates the amount of oxygen utilized by the body, in comparison to the amount of carbon dioxide expended, the RER will fluctuate depending on the amount activity. A person sitting still will have a lower ratio, as compared to someone exercising intensely, who will ideally expel larger amounts of carbon dioxide, hence resulting in a higher ratio.

Both RER and RQ also fluctuate depending on the type of substance that is being used as fuel by the body, i.e. fats, carbohydrates, protein, etc. will all yield in different ratios and quotients, which can then be used to gauge a person’s health and body composition and improve accordingly.

While, RQ can be used for dieting and fitness, the primary application of RQ is in cases of chronic obstructive pulmonary disease. Here the patients need to spend a lot of energy on respiration. By figuring out which foods result in the most RQ, the RQ can be driven down, hence resulting in conservation of energy that would have otherwise be spent on respiratory effort. This energy can then be utilized somewhere else. A RQ closer to 1 typically means more carbohydrate is being burned and a value closer to 0.7 typically means fat is being burned.

Comparison between Respiratory Exchange Ratio (RER) and Respiratory Quotient (RQ):

How to Measure Energy Expenditure (With Diagram)

Total energy expenditure per unit time is called the metabolic rate. It can be measured directly or indirectly as in the case of calorific value of foods. In the direct method for the measurement of energy expenditure for individuals, the Atwater calorimeter is used which consists of a chamber in which a person could live and work for several days allowing at the same time the measurement of his total output of heat.

The energy expenditure thus measured can be related to net energy intake which is the energy in food, minus the energy lost in urine and faeces. Atwater’s experiments, measuring energy intake and energy output, lasted a number of days and he was able to demonstrate consistently a fair amount of agreement between the input and the output.

Although nobody uses the human calorimeter these days on account of the difficulties of technique, Atwater’s experiment was the first of its kind which demonstrated that the human body behaved like any engine running on combustion of fuels, thus taking the wind out of the sails of the theory of living matter possessing vital spirits.

The two indirect methods for measure­ment of energy expenditure in individuals commonly used are:

1. The Benedict-Roth Spirometer Method:

This is a closed-circuit breathing apparatus which is filled with oxygen and has a capacity of about 6 litres. Oxygen is contained in a metal drum which floats on a water seal. The person whose O2 consumption is to be measured breathes in oxygen through an in­spiratory valve and breathes out into the drum through an expiratory valve and a soda-lime canister, so that the CO2 produced is absorbed.

As the O2 is used up, the drum sinks and its movement is recorded on a moving paper mounted on a kymograph from this, the rate of oxygen consumption can be read. The apparatus is accurate and simple to use. It has the disadvantage that it can be used only when the person is at rest or doing very light exercise.

2. Douglas Bag Method:

This is a canvas or plastic bag with a variable capacity, usually 100, 200 or 300 litres. The subject breathes through a mouth piece which contains inspiratory and expiratory valves. Room air is breathed in, but breathing out is into the Douglas bag so that all the expired air is collected in it.

The bag is then emptied through a gas meter and a sample of the expired air is taken for analysis of O2 and CO2 content from which the rates of oxygen utilization and CO2 production can be calculated. This method has the advantage that both O2 consumption and CO2 production can be measured at varying grades of activity or muscular exercise.

Respiratory Quotient:

The respiratory quotient (RQ) measures the ratio of the volume of carbon dioxide (Vc) produced by an individual to the volume of oxygen consumed (Vo).

This is represented by the following equation:

This quotient is useful because the volumes of CO2 and O2 produced depend on which fuel source is being metabolized. Measuring RQ is a convenient way to gain information about the source of energy which a person is using.

We can then compare the metabolism of a person under different environmental conditions by simply comparing RQ for various foods:


Four equations are taught briefly in medical school but are grossly under-emphasized in importance and are therefore invariably forgotten in later years, when they are most needed. The reasons why these highly important equations are ‘under taught’ in medical school are several:

  • a crowded curriculum that must make room for immunology and cell biology
  • the teachers may have little or no clinical experience with respiratory patients, and therefore can’t possibly know how important these equations are in the everyday practice of medicine
  • misguided leadership of curriculum committees that may feel every subject deserves equal balance, and thus leave it up to the student to ‘learn it all’ without anyone guiding them as to what is really important in the care of patients. (For example, one hour on surfactant may be equally weighted with one hour on gas exchange, which may be OK for training Ph.D.’s but is misguided for training physicians).

These four equations express relationships that are extremely important in clinical practice. They are the:

  • PCO2 equation
  • Henderson-Hasselbalch equation
  • Alveolar Gas equation, and
  • Oxygen Content equation.

Emphasis should be placed on understanding the simple qualitative relationships expressed by these equations. Each equation can be clinically applied in the assessment of abnormal oxygenation, ventilation, or acid-base balance. For example, variables in the PCO2 equation, and not any bedside observations, define the common terms hyperventilation and hypoventilation and explain why a dyspneic, tachypneic patient may be retaining CO2. Ignorance of this and other relationships expressed in the four equations is reflected in some common diagnostic and therapeutic mistakes.


There is disparity between the physiology we teach and expect medical students to learn and the physiology that medical residents and practicing physicians seem to know and understand. This disparity is perhaps best exemplified by four simple equations important in understanding cardiopulmonary and renal disorders (Table I). These equations are seldom emphasized beyond medical school, yet not appreciating the physiology behind them can (and often does) lead to clinical errors.

Intensive care units have contributed to the weakening knowledge of physiology among primary care physicians. Today, the more profound physiologic derangements are usually managed in ICUs by organ-specific specialists these derangements (e.g., shock, pulmonary edema, acute ventilatory failure, acute renal failure) are literally outside the care of most physicians and surgeons. Not all serious physiologic problems are handled in ICUs however, and the need for understanding basic physiology – in the office, on the general medical wards – remains paramount.

The four equations in this paper (Table I, below) are important clinically not so much for the numbers they generate as for their qualitative relationships. All four equations can be abbreviated to simpler terms that are adequate for most clinical purposes.

  1. not enough total ventilation (as may occur from central nervous system depression or respiratory muscle weakness) or
  2. too much of the total ventilation ending up as dead space ventilation (as may occur in severe chronic obstructive pulmonary disease, or from rapid, shallow breathing) or
  3. some combination of 1) and 2).

Excess CO2 production is omitted as a specific cause of hypercapnia because it is never a problem for the normal respiratory system unimpeded by a resistive load. During submaximal exercise, for example, where CO2 production is increased, PaCO2 stays in the normal range because VA rises proportional to the rise in VCO2. With extremes of exercise (beyond anaerobic threshold) PaCO2 falls as compensation for the developing lactic acidosis. 2 In health PaCO2 may be reduced but is never elevated.

An important clinical corollary of the PaCO2 equation is that we cannot reliably assess the adequacy of alveolar ventilation – and hence PaCO2 – at the bedside. Although VE can be easily measured with a handheld spirometer (as tidal volume times respiratory rate), there is no way to know the amount of VE going to dead space or the patient’s rate of CO2 production. A common mistake is to assume that because a patient is breathing fast, hard and/or deep he or she must be “hyperventilating.” Not so, of course.

A house officer was called to the bedside of an elderly woman patient late at night. She was in hospital for evaluation of a pelvic mass. The patient was noted to be anxious and complaining of shortness of breath her lung fields were clear to auscultation and vital signs were normal except for slight tachycardia and respiratory rate of 30/minute. A nurse commented that the patient “gets like this every night.” The physician ordered a benzodiazepine drug for what he described as “hyperventilation and anxiety.” Thirty minutes later the patient’s breathing slowed considerably and she became cyanotic, whereupon she was transferred to the ICU.

Although nothing in the PCO2 equation directly relates respiratory rate or depth of breathing to PaCO2, physicians commonly (and mistakenly) use these observations to assess a patient’s PaCO2. The error in this case was to assume the patient was hyperventilating (because she was breathing fast) and could tolerate the sedative in fact she was hypoventilating – her PaCO2 was elevated (as will be explained further under Equation 2).

Hypercapnia represents a failure of the respiratory system in some aspect and therefore a state of severe organ system impairment. In addition to this clinical fact there are three physiologic reasons why elevated PaCO2 is potentially dangerous. First, as PaCO2 increases, unless HCO3 – also increases by the same degree pH will fall (see Equation 2). Second, as PaCO2 increases PAO2 (and hence PaO2) will fall unless inspired oxygen is supplemented (see Equation 3). Third, the higher the PaCO2, the less defended is the patient against any further decline in alveolar ventilation.

This last point is graphically illustrated by plotting PaCO2 against alveolar ventilation Figure 1. The higher the PaCO2 is to begin with, the more it will rise for any given decrement in alveolar ventilation. For example a decrease in alveolar ventilation of one L/minute (as may occur from anesthesia, sedation, congestive heart failure, etc.) will increase a baseline PaCO2 of 30 mm Hg to 36.3 mm Hg when VCO2 is 200 ml/min the same one L/min decline in VA will raise a baseline PCO2 of 60 mm Hg to 92 mm Hg Figure 1). Whereas the hyperventilating or normally- ventilating patient can almost always tolerate sedating drugs (without clinically important hypoventilation), even a small amount of sedative may be dangerous in the hypercapnic patient.

TABLE II: pH and Hydrogen Ion Concentration Top
Blood pH [H + ] (nM/L) % Change from normal
7.00 100 + 150
7.10 80 + 100
7.30 50 + 25
7.40 40
7.52 30 – 25
7.70 20 – 50
8.00 10 – 75

Unfortunately, the logarithmic nature of pH and the fact that acid-base disorders involve simultaneous changes in three biochemical variables and in the function of two organ systems (renal and respiratory), have all combined to made acid-base a difficult subject for many clinicians. In the 1970s nomograms incorporating the H-H variables and compensation bands for the four primary acid-base disorders were introduced as aids to determining a patient’s acid-base status. 3-8 While nomograms can be helpful if readily available and properly used, there is much to be gained by simply knowing the relationship among the three H-H variables and the type of changes expected with each disorder. In this regard the following items of clinical importance bear emphasis.

a) If any of the three H-H variables is truly abnormal the patient has an acid-base disturbance without exception. Thus any patient with an abnormal HCO3 – or PaCO2, not just abnormal pH, has an acid-base disorder. Most hospitalized patients have at least one bicarbonate measurement as part of routine serum electrolytes this is usually called the ‘CO2‘ or ‘total CO2‘ when measured in venous blood. (Total CO2 includes bicarbonate and the CO2 contributed by dissolved carbon dioxide, the latter 1.2 mEq/L when PaCO2 is 40 mm Hg. For this reason, and because bicarbonate concentration is slightly higher in venous than in arterial blood, total CO2 runs a few mEq/L higher than the bicarbonate value calculated using the H-H equation.) If total CO2 is truly abnormal the patient has an acid-base disorder. In Case 1 there were two sets of electrolyte measurements on the patient’s chart when the sedative was ordered both showed total CO2 elevated at 34 mEq/L. The patient had been taking a diuretic so it was probably assumed that her elevated total CO2 reflected a mild metabolic alkalosis. More likely, however, it represented chronic respiratory acidosis with renal compensation. When she arrived to the ICU her arterial blood gas showed pH 7.07, PaCO2 83 mm Hg, PaO2 55 mm Hg (breathing supplemental oxygen), HCO3 – 23 mEq/L, values that reflected a worsening of previously- unrecognized respiratory acidosis plus a new metabolic acidosis (lactic acidosis from decreased organ perfusion). The patient’s long smoking history and the physical findings suggested chronic obstructive lung disease (later confirmed by pulmonary function tests). Her anxiety prior to MICU transfer was related to worsening acidosis and dyspnea.

e) Compensatory changes for acute respiratory acidosis 11 and alkalosis, 12 and metabolic acidosis 13,14 and alkalosis, 15,16 occur in a predictable fashion, making it relatively easy to spot the presence of a mixed disorder in many situations. 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.g., respiratory alkalosis and metabolic acidosis in a septic patient. Although pH can end up in the normal range (7.35-7.45) in single disorders of a mild degree when fully compensated, a truly normal pH with abnormal HCO3 – and PaCO2 should make one think of two or more primary acid-base disorders. Similarly, a high pH in a case of acidosis or a low pH in a case of alkalosis signifies two or more primary disorders.

f) Maximal respiratory compensation for a metabolic disorder takes about 12-24 hours and maximal renal compensation for a respiratory disorder takes up to several days. As a rule of thumb, in maximally compensated metabolic acidosis the last two digits of the pH approximate the PaCO2. 17 For example, a patient with a disease causing uncomplicated metabolic acidosis over 24 hours’ duration, whose pH is 7.25, should have a PaCO2 equal or close to 25 mm Hg. In metabolic alkalosis respiratory compensation is more variable and there is no simple relationship by which to predict the final PaCO2. 16

Respiratory Quotient

The respiratory quotient (or RQ or respiratory coefficient), is a dimensionless number used in calculations of basal metabolic rate (BMR) when estimated from carbon dioxide production. It is calculated from the ratio of carbon dioxide produced by the body to oxygen consumed by the body. Such measurements, like measurements of oxygen uptake, are forms of indirect calorimetry. It is measured using a respirometer. The Respiratory Quotient value indicates which macronutrients are being metabolized, as different energy pathways are used for fats, carbohydrates, and proteins. A value of 0.7 indicates that lipids are being metabolized, 0.8 for proteins, and 1.0 for carbohydrates. The approximate respiratory quotient of a mixed diet is 0.8. Some of the other factors that may affect the respiratory quotient are energy balance, circulating insulin, and insulin sensitivity.

Carbohydrates: The respiratory quotient for carbohydrate metabolism can be demonstrated by the chemical equation for oxidation of glucose:

C6H12O6 + 6 O2 ? 6 CO2+ 6 H2O

Because the gas exchange in this reaction is equal, the respiratory quotient for carbohydrates is: RQ = 6 CO2 / 6 O2 = 1.0

Fats: The chemical composition of fats differs from that of carbohydrates in that fats contain considerably fewer oxygen atoms in proportion to atoms of carbon and hydrogen. The substrate utilization of palmitic acid is:

C16H32O2 + 23 O2 ? 16 CO2 + 16 H2O

Thus, the RQ for palmitic acid is approximately 0.7. RQ = 16 CO2 / 23 O2 = 0.696

Proteins: The respiratory quotient for protein metabolism can be demonstrated by the chemical equation for oxidation of albumin:

C72H112N18O22S + 77 O2 ? 63 CO2 + 38 H2O + SO3 + 9 CO(NH2)2

The RQ for protein is approximately 0.8. RQ = 63 CO2/ 77O2 = 0.8

Due to the complexity of the various ways in which different amino acids can be metabolized, no single RQ can be assigned to the oxidation of protein in the diet however, 0.8 is a frequently utilized estimate.

Practical applications of the respiratory quotient can be found in severe cases of chronic obstructive pulmonary disease, in which patients spend a significant amount of energy on respiratory effort. By increasing the proportion of fats in the diet, the respiratory quotient is driven down, causing a relative decrease in the amount of CO2 produced. This reduces the respiratory burden to eliminate CO2, thereby reducing the amount of energy spent on respirations.

Respiratory Quotient can be used as an indicator of over or underfeeding. Underfeeding, which forces the body to utilize fat stores, will lower the respiratory quotient while overfeeding, which causes lipogenesis, will increase it. Underfeeding is marked by a respiratory quotient below 0.85, while a respiratory quotient greater than 1.0 indicates overfeeding. This is particularly important in patients with compromised respiratory systems, as an increased respiratory quotient significantly corresponds to increased respiratory rate and decreased tidal volume, placing compromised patients at a significant risk.

Because of its role in metabolism, respiratory quotient can be used in analysis of liver function and diagnosis of liver disease. In patients suffering from liver cirrhosis, non-protein respiratory quotient (npRQ) values act as good indicators in the prediction of overall survival rate. Patients having a npRQ < 0.85 show considerably lower survival rates as compared to patients with a npRQ > 0.85.A decrease in npRQ corresponds to a decrease in glycogen storage by the liver. Similar research indicates that non-alcoholic fatty liver diseases are also accompanied by a low respiratory quotient value, and the non protein respiratory quotient value was a good indication of disease severity.

30.2 Gas Exchange Across Respiratory Surfaces

In this section, you will explore the following questions:

  • What are the names and descriptions of lung volumes and capacities?
  • How does gas pressure influence the movement of gases into and out of the body?

Connection for AP ® Courses

The information in this section about lung volumes and capacities is outside the scope for AP ® . However, the content about the movement of gases across the membranes of alveoli is an important application of the principles of diffusion that we explored in the chapter on passive transport. In addition, gas exchange provides the oxygen needed for aerobic cellular respiration and for the removal of carbon dioxide produced as a metabolic waste product.

Gas movement into or out of the lungs is dependent on the pressure of the gas. Because the air we breathe is a mixture of several gases, including N, O2 and CO2, the amount of each gas is measured by its partial pressure. As you remember from our earlier exploration of diffusion, molecules move from an area of higher concentration to lower concentration, or, in the case of gases, from higher partial pressure (measured in mmHg) to lower partial pressure. In other words, O2 and CO2 move with their concentration gradients. Because both gases are small, nonpolar molecules, they freely travel across the phospholipid bilayer of the plasma cell membrane.

Information presented and the examples highlighted in the section support concepts outlined in Big Idea 2 of the AP ® Biology Curriculum Framework. The AP ® Learning Objectives listed in the Curriculum Framework provide a transparent foundation for the AP ® Biology course, an inquiry-based laboratory experience, instructional activities, and AP ® exam questions. A learning objective merges required content with one or more of the seven science practices.

Big Idea 2 Biological systems utilize free energy and molecular building blocks to grow, to reproduce, and to maintain dynamic homeostasis.
Enduring Understanding 2.B Growth, reproduction and dynamic homeostasis require that cell create and maintain internal environments that are different form their external environment.
Essential Knowledge 2.B.2 Growth and dynamic homeostasis are maintained by the constant movement of molecules across membranes.
Science Practice 1.4 The student can use representations and models to analyze situations or solve problems qualitatively and quantitatively.
Science Practice 1.1 The student can create representations and models of natural or man-made phenomena and systems in the domain.
Science Practice 7.2 The student can connect concepts in and across domain(s) to generalize or extrapolate in and/or across enduring understandings and/or big ideas.
Learning Objective 2.12 The student is able to use representations and models to analyze situations or solve problems qualitatively and quantitatively to investigate whether dynamic homeostasis is maintained by the movement of molecules across membranes.

The structure of the lung maximizes its surface area to increase gas diffusion. Because of the enormous number of alveoli (approximately 300 million in each human lung), the surface area of the lung is very large (75 m 2 ). Having such a large surface area increases the amount of gas that can diffuse into and out of the lungs.

Basic Principles of Gas Exchange

Gas exchange during respiration occurs primarily through diffusion. Diffusion is a process in which transport is driven by a concentration gradient. Gas molecules move from a region of high concentration to a region of low concentration. Blood that is low in oxygen concentration and high in carbon dioxide concentration undergoes gas exchange with air in the lungs. The air in the lungs has a higher concentration of oxygen than that of oxygen-depleted blood and a lower concentration of carbon dioxide. This concentration gradient allows for gas exchange during respiration.

Partial pressure is a measure of the concentration of the individual components in a mixture of gases. The total pressure exerted by the mixture is the sum of the partial pressures of the components in the mixture. The rate of diffusion of a gas is proportional to its partial pressure within the total gas mixture. This concept is discussed further in detail below.

Lung Volumes and Capacities

Different animals have different lung capacities based on their activities. Cheetahs have evolved a much higher lung capacity than humans it helps provide oxygen to all the muscles in the body and allows them to run very fast. Elephants also have a high lung capacity. In this case, it is not because they run fast but because they have a large body and must be able to take up oxygen in accordance with their body size.

Human lung size is determined by genetics, sex, and height. At maximal capacity, an average lung can hold almost six liters of air, but lungs do not usually operate at maximal capacity. Air in the lungs is measured in terms of lung volumes and lung capacities (Figure 30.12 and Table 30.1). Volume measures the amount of air for one function (such as inhalation or exhalation). Capacity is any two or more volumes (for example, how much can be inhaled from the end of a maximal exhalation).

The volume in the lung can be divided into four units: tidal volume, expiratory reserve volume, inspiratory reserve volume, and residual volume. Tidal volume (TV) measures the amount of air that is inspired and expired during a normal breath. On average, this volume is around one-half liter, which is a little less than the capacity of a 20-ounce drink bottle. The expiratory reserve volume (ERV) is the additional amount of air that can be exhaled after a normal exhalation. It is the reserve amount that can be exhaled beyond what is normal. Conversely, the inspiratory reserve volume (IRV) is the additional amount of air that can be inhaled after a normal inhalation. The residual volume (RV) is the amount of air that is left after expiratory reserve volume is exhaled. The lungs are never completely empty: There is always some air left in the lungs after a maximal exhalation. If this residual volume did not exist and the lungs emptied completely, the lung tissues would stick together and the energy necessary to re-inflate the lung could be too great to overcome. Therefore, there is always some air remaining in the lungs. Residual volume is also important for preventing large fluctuations in respiratory gases (O2 and CO2). The residual volume is the only lung volume that cannot be measured directly because it is impossible to completely empty the lung of air. This volume can only be calculated rather than measured.

Capacities are measurements of two or more volumes. The vital capacity (VC) measures the maximum amount of air that can be inhaled or exhaled during a respiratory cycle. It is the sum of the expiratory reserve volume, tidal volume, and inspiratory reserve volume. The inspiratory capacity (IC) is the amount of air that can be inhaled after the end of a normal expiration. It is, therefore, the sum of the tidal volume and inspiratory reserve volume. The functional residual capacity (FRC) includes the expiratory reserve volume and the residual volume. The FRC measures the amount of additional air that can be exhaled after a normal exhalation. Lastly, the total lung capacity (TLC) is a measurement of the total amount of air that the lung can hold. It is the sum of the residual volume, expiratory reserve volume, tidal volume, and inspiratory reserve volume.

Lung volumes are measured by a technique called spirometry. An important measurement taken during spirometry is the forced expiratory volume (FEV), which measures how much air can be forced out of the lung over a specific period, usually one second (FEV1). In addition, the forced vital capacity (FVC), which is the total amount of air that can be forcibly exhaled, is measured. The ratio of these values (FEV1/FVC ratio) is used to diagnose lung diseases including asthma, emphysema, and fibrosis. If the FEV1/FVC ratio is high, the lungs are not compliant (meaning they are stiff and unable to bend properly), and the patient most likely has lung fibrosis. Patients exhale most of the lung volume very quickly. Conversely, when the FEV1/FVC ratio is low, there is resistance in the lung that is characteristic of asthma. In this instance, it is hard for the patient to get the air out of his or her lungs, and it takes a long time to reach the maximal exhalation volume. In either case, breathing is difficult and complications arise.


Respiratory Therapist

Respiratory therapists or respiratory practitioners evaluate and treat patients with lung and cardiovascular diseases. They work as part of a medical team to develop treatment plans for patients. Respiratory therapists may treat premature babies with underdeveloped lungs, patients with chronic conditions such as asthma, or older patients suffering from lung disease such as emphysema and chronic obstructive pulmonary disease (COPD). They may operate advanced equipment such as compressed gas delivery systems, ventilators, blood gas analyzers, and resuscitators. Specialized programs to become a respiratory therapist generally lead to a bachelor’s degree with a respiratory therapist specialty. Because of a growing aging population, career opportunities as a respiratory therapist are expected to remain strong.

Gas Pressure and Respiration

The respiratory process can be better understood by examining the properties of gases. Gases move freely, but gas particles are constantly hitting the walls of their vessel, thereby producing gas pressure.

Air is a mixture of gases, primarily nitrogen (N2 78.6 percent), oxygen (O2 20.9 percent), water vapor (H2O 0.5 percent), and carbon dioxide (CO2 0.04 percent). Each gas component of that mixture exerts a pressure. The pressure for an individual gas in the mixture is the partial pressure of that gas. Approximately 21 percent of atmospheric gas is oxygen. Carbon dioxide, however, is found in relatively small amounts, 0.04 percent. The partial pressure for oxygen is much greater than that of carbon dioxide. The partial pressure of any gas can be calculated by:

Patm, the atmospheric pressure, is the sum of all of the partial pressures of the atmospheric gases added together,

× (percent content in mixture).

The pressure of the atmosphere at sea level is 760 mm Hg. Therefore, the partial pressure of oxygen is:

At high altitudes, Patm decreases but concentration does not change the partial pressure decrease is due to the reduction in Patm.

When the air mixture reaches the lung, it has been humidified. The pressure of the water vapor in the lung does not change the pressure of the air, but it must be included in the partial pressure equation. For this calculation, the water pressure (47 mm Hg) is subtracted from the atmospheric pressure:

and the partial pressure of oxygen is:

These pressures determine the gas exchange, or the flow of gas, in the system. Oxygen and carbon dioxide will flow according to their pressure gradient from high to low. Therefore, understanding the partial pressure of each gas will aid in understanding how gases move in the respiratory system.

Gas Exchange across the Alveoli

In the body, oxygen is used by cells of the body’s tissues and carbon dioxide is produced as a waste product. The ratio of carbon dioxide production to oxygen consumption is the respiratory quotient (RQ). RQ varies between 0.7 and 1.0. If just glucose were used to fuel the body, the RQ would equal one. One mole of carbon dioxide would be produced for every mole of oxygen consumed. Glucose, however, is not the only fuel for the body. Protein and fat are also used as fuels for the body. Because of this, less carbon dioxide is produced than oxygen is consumed and the RQ is, on average, about 0.7 for fat and about 0.8 for protein.

The RQ is used to calculate the partial pressure of oxygen in the alveolar spaces within the lung, the alveolar P O 2 Above, the partial pressure of oxygen in the lungs was calculated to be 150 mm Hg. However, lungs never fully deflate with an exhalation therefore, the inspired air mixes with this residual air and lowers the partial pressure of oxygen within the alveoli. This means that there is a lower concentration of oxygen in the lungs than is found in the air outside the body. Knowing the RQ, the partial pressure of oxygen in the alveoli can be calculated:

With an RQ of 0.8 and a P CO 2 in the alveoli of 40 mm Hg, the alveolar P O 2 is equal to:

Notice that this pressure is less than the external air. Therefore, the oxygen will flow from the inspired air in the lung ( P O 2 = 150 mm Hg) into the bloodstream ( P O 2 = 100 mm Hg) (Figure 30.13).

In the lungs, oxygen diffuses out of the alveoli and into the capillaries surrounding the alveoli. Oxygen (about 98 percent) binds reversibly to the respiratory pigment hemoglobin found in red blood cells (RBCs). RBCs carry oxygen to the tissues where oxygen dissociates from the hemoglobin and diffuses into the cells of the tissues. More specifically, alveolar P O 2 is higher in the alveoli ( P ALVO 2 = 100 mm Hg) than blood P O 2 (40 mm Hg) in the capillaries. Because this pressure gradient exists, oxygen diffuses down its pressure gradient, moving out of the alveoli and entering the blood of the capillaries where O2 binds to hemoglobin. At the same time, alveolar P CO 2 is lower P ALVO 2 = 40 mm Hg than blood P CO 2 = (45 mm Hg). CO2 diffuses down its pressure gradient, moving out of the capillaries and entering the alveoli.

Oxygen and carbon dioxide move independently of each other they diffuse down their own pressure gradients. As blood leaves the lungs through the pulmonary veins, the venous P O 2 = 100 mm Hg, whereas the venous P CO 2 = 40 mm Hg. As blood enters the systemic capillaries, the blood will lose oxygen and gain carbon dioxide because of the pressure difference of the tissues and blood. In systemic capillaries, P O 2 = 100 mm Hg, but in the tissue cells, P O 2 = 40 mm Hg. This pressure gradient drives the diffusion of oxygen out of the capillaries and into the tissue cells. At the same time, blood P CO 2 = 40 mm Hg and systemic tissue P CO 2 = 45 mm Hg. The pressure gradient drives CO2 out of tissue cells and into the capillaries. The blood returning to the lungs through the pulmonary arteries has a venous P O 2 = 40 mm Hg and a P CO 2 = 45 mm Hg. The blood enters the lung capillaries where the process of exchanging gases between the capillaries and alveoli begins again (Figure 30.13).


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