Information

Amount of air in lungs after death


Do lungs keep the same amount of air they had at the moment of an animal's death? I'm curious mainly about humans and the theoretical situation of someone dying while holding his breath.


  • The lung volumes that can be measured using a spirometer include tidal volume (TV), expiratory reserve volume (ERV), and inspiratory reserve volume (IRV).
  • Residual volume (RV) is a lung volume representing the amount of air left in the lungs after a forced exhalation this volume cannot be measured, only calculated.
  • The lung capacities that can be calculated include vital capacity (ERV+TV+IRV), inspiratory capacity (TV+IRV), functional residual capacity (ERV+RV), and total lung capacity (RV+ERV+TV+IRV).
  • tidal volume: the amount of air breathed in or out during normal respiration
  • residual volume: the volume of unexpended air that remains in the lungs following maximum expiration
  • spirometry: the measurement of the volume of air that a person can move into and out of the lungs

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, gender, 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 (see Figure 1 and Table 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).

Figure 1. Human lung volumes and capacities are shown. The total lung capacity of the adult male is six liters. Tidal volume is the volume of air inhaled in a single, normal breath. Inspiratory capacity is the amount of air taken in during a deep breath, and residual volume is the amount of air left in the lungs after forceful respiration.

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.

Practice Questions

The inspiratory reserve volume measures the ________.

  1. amount of air remaining in the lung after a maximal exhalation
  2. amount of air that the lung holds
  3. amount of air the can be further exhaled after a normal breath
  4. amount of air that can be further inhaled after a normal breath

Of the following, which does not explain why the partial pressure of oxygen is lower in the lung than in the external air?

  1. Air in the lung is humidified therefore, water vapor pressure alters the pressure.
  2. Carbon dioxide mixes with oxygen.
  3. Lungs exert a pressure on the air to reduce the oxygen pressure.
  4. Oxygen is moved into the blood and is headed to the tissues.

The total lung capacity is calculated using which of the following formulas?

  1. residual volume + expiratory reserve volume + tidal volume + inspiratory reserve volume
  2. residual volume + tidal volume + inspiratory reserve volume
  3. residual volume + expiratory reserve volume + inspiratory reserve volume
  4. expiratory reserve volume + tidal volume + inspiratory reserve volume

residual volume + expiratory reserve volume + tidal volume + inspiratory reserve volume

Careers in ScienCE

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.

Respiratory therapists use various tests to evaluate patients. For example, they test lung capacity by having patients breathe into an instrument that measures the volume and flow of oxygen when they inhale and exhale. Respiratory therapists also may take blood samples and use a blood gas analyzer to test oxygen and carbon dioxide levels.

Respiratory therapists also perform chest physiotherapy on patients to remove mucus from their lungs and make it easier for them to breathe. Removing mucus is necessary for patients suffering from lung diseases, such as cystic fibrosis, and it involves the therapist vibrating the patient’s rib cage, often by tapping the patient’s chest and encouraging him or her to cough. Respiratory therapists may connect patients who cannot breathe on their own to ventilators that deliver oxygen to the lungs. Therapists insert a tube in the patient’s windpipe (trachea) and connect the tube to ventilator equipment. They set up and monitor the equipment to ensure that the patient is receiving the correct amount of oxygen at the correct rate.

Respiratory therapists who work in home care teach patients and their families to use ventilators and other life-support systems in their homes. During these visits, they may inspect and clean equipment, check the home for environmental hazards, and ensure that patients know how to use their medications. Therapists also make emergency home visits when necessary.

In some hospitals, respiratory therapists are involved in related areas, such as diagnosing breathing problems for people with sleep apnea and counseling people on how to stop smoking.

In Summary: Breathing Capacity

The lungs can hold a large volume of air, but they are not usually filled to maximal capacity. Lung volume measurements include tidal volume, expiratory reserve volume, inspiratory reserve volume, and residual volume. The sum of these equals the total lung capacity.


Respiratory Volumes and Capacities

Respiratory volume is the term used for various volumes of air moved by or associated with the lungs at a given point in the respiratory cycle. There are four major types of respiratory volumes: tidal, residual, inspiratory reserve, and expiratory reserve (Figure 4).

Figure 4. These two graphs show (a) respiratory volumes and (b) the combination of volumes that results in respiratory capacity.

Tidal volume (TV) is the amount of air that normally enters the lungs during quiet breathing, which is about 500 milliliters. Expiratory reserve volume (ERV) is the amount of air you can forcefully exhale past a normal tidal expiration, up to 1200 milliliters for men. Inspiratory reserve volume (IRV) is produced by a deep inhalation, past a tidal inspiration. This is the extra volume that can be brought into the lungs during a forced inspiration. Residual volume (RV) is the air left in the lungs if you exhale as much air as possible. The residual volume makes breathing easier by preventing the alveoli from collapsing. Respiratory volume is dependent on a variety of factors, and measuring the different types of respiratory volumes can provide important clues about a person’s respiratory health (see Table 1).

Table 1. Pulmonary Function Testing
Pulmonary Function Test Instrument Measures Function
Spirometry Spirometer Forced vital capacity (FVC) Volume of air that is exhaled after maximum inhalation
Forced expiratory volume (FEV) Volume of air exhaled in one breath
Forced expiratory flow, 25–75 Air flow in the middle of exhalation
Peak expiratory flow (PEF) Rate of exhalation
Maximum voluntary ventilation (MVV) Volume of air that an be inspired and expired in 1 minute
Slow vital capacity (SVC) Volume of air that can be slowly exhaled after inhaling past the tidal volume
Total lung capacity (TLC) Volume of air in the lungs after maximum inhalation
Functional residual capacity (FRC) Volume of air left in the lungs after normal expiration
Residual volume (RV) Volume of air in the lungs after maximum exhalation
Total lung capacity (TLC) Maximum volume of air that the lungs can hold
Expiratory reserve volume (ERV) The volume of air that can be exhaled beyond normal exhalation
Gas diffusion Blood gas analyzer Arterial blood gases Concentration of oxygen and carbon dioxide in the blood

Respiratory capacity is the combination of two or more selected volumes, which further describes the amount of air in the lungs during a given time. For example, total lung capacity (TLC) is the sum of all of the lung volumes (TV, ERV, IRV, and RV), which represents the total amount of air a person can hold in the lungs after a forceful inhalation. TLC is about 6000 mL air for men, and about 4200 mL for women. Vital capacity (VC) is the amount of air a person can move into or out of his or her lungs, and is the sum of all of the volumes except residual volume (TV, ERV, and IRV), which is between 4000 and 5000 milliliters. Inspiratory capacity (IC) is the maximum amount of air that can be inhaled past a normal tidal expiration, is the sum of the tidal volume and inspiratory reserve volume. On the other hand, the functional residual capacity (FRC) is the amount of air that remains in the lung after a normal tidal expiration it is the sum of expiratory reserve volume and residual volume.


Related Terms

  • Vital capacity – The volume of air that a person can forcibly exhale following maximum, forced inspiration.
  • Minute ventilation – The volume of air that is breathed in and out within a minute.
  • Inspiratory Capacity – The maximum amount of air that can be taken into the lungs following natural exhalation.
  • Tidal volume – The amount of air that is inhaled an exhaled naturally and without force.

1. Which of the following is true of obstructive lung diseases?
A. The residual volume is no different from normal
B. The diseases don’t allow for full expansion of the lungs
C. The residual volume is lower than normal
D. The residual volume is higher than normal

2. What is the average amount of residual volume in healthy lungs?
A. Two liters
B. One liter
C. Three liters
D. Six liters

3. Why is it that we can’t empty out our lungs?
A. Due to the amount of nitrogen contained in the air
B. Due to air pollution
C. The lungs would collapse and not be able to inflate again
D. Helium can’t leave the lungs


Alveolar Air: Composition and Effects | Respiration | Humans | Biology

In this article we will discuss about:- 1. Definition of Alveolar Air 2. Method of Collecting Alveolar Air 3. Composition 4. Partial Pressure of Gases 5. Tension of Gases 6. Method of Measurement 7. Effects 8. Factors 9. Alveolar PO2 and Venous Admixture.

Definition of Alveolar Air:

Alveolar air represents the air located in the respi­ratory part of the lungs which takes part in gas ex­change with the blood in the pulmonary capillaries. Alveolar air, therefore, is a physiological quantity and does not represent the air located strictly in the anatomical alveoli.

It measures about 3000 ml and is the most important part of the air in the respiratory system since it is primarily responsible for oxygenation of venous blood and unloading the venous blood of adequate quantities of CO2. With a tidal volume of 500 ml about 350 ml of oxygen-rich atmospheric air mixes with the alveolar air to replenish the oxygen lost from alveolar air by absorption with the venous blood.

Method of Collecting Alveolar Air:

i. Haldane and Priestley’s Method (Fig. 8.19):

A tube, about 1.22 m (4 feet) long, is taken. It is fitted with a mouthpiece at one end. A side tube is attached very near to the mouthpiece and is attached to a sampling tube. Through the mouthpiece, the subject makes forcible expiration twice-at first (1) after normal inspiration and then (2) after normal expiration.

This is nec­essary because the alveolar air varies slightly in com­position in different phases of respiration. Through the sampling tube, two samples of air are drawn in from the last part of the expired air, while the subject closes the mouthpiece with his tongue at the end of expiration.

ii. Otis-Rahn Method (Fig. 8.20):

A second method of automatic collection of alveolar air has been described by Otis and Rahn method and is shown in the diagram (Fig. 8.20). During inspiration the end expiratory air of the previous expiration from the neighbourhood is drawn into the balloon by movement of the expiratory value.

During expiration the balloon is compressed so that no dead space air may contaminate the alveolar air collected into the balloon.

iii. Method of Analysis of Alveolar Air:

The classical method is to analyse alveolar air with Llyod’s modification of Haldane’s gas-analysis apparatus, which is used for analysis of respiratory gases. A measured quantity of air is admitted in the apparatus and its volume is accurately noted. The gas is then passed over caustic potash solution and its volume is noted again.

The diminution in volume is due to absorption of CO2 and from the difference between the original reading and the second reading the percentage of CO2 in the alveolar air may be calculated. The gas is now passed through alkaline pyrogallol solution which absorbs oxygen. From the reduction in volume the percentage of O2 in the alveolar air can be calculated.

Composition of Alveolar Air:

The composition of inspired air, normal expired air and alveolar air and also the tension of different gases are shown in the Table 8.2.

The increase in the percentage of nitrogen in the expired air is not real but relative. This is be­cause the volume of the expired air is slightly less than that of inspired air, which is caused by the fact that the amount of CO2 evolved is less than the amount of oxygen absorbed. Consequently, in the percentage composition, nitrogen shows a relative rise.

Further the composition of expired air varies depending on metabolic activity so that the composition of the alveolar air is kept as constant as possible.

Partial Pressure of Gases in Inspired Air Expired Air and Alveolar Air:

In a gas mixture, the pressure exerted by a particular gas is directly proportional to the percentage composition of the same gas in the mixture. Supposing in a mixture, oxygen constitutes 20% then oxygen will exert 20% (i.e., one fifth) of the total pressure. The Table 8.3 shows the partial pressures of the various gases.

It will be noted that the alveolar air differs in composition from that of the inspired (atmospheric) air.

The reasons for this difference are:

i. Only a part of the alveolar air is replaced by inspired air .

ii. There is continuous absorption of O2 from the alveolar air by pulmonary venous blood – the alveolar air, therefore, is poorer in oxygen.

iii. CO2 is added continuously to the alveolar air by the pulmonary venous blood- the alveolar air, therefore, is richer in CO2.

iv. The inspired air is dry but gets saturated with water vapour during its passage through the respiratory tract. Since some of the space in the alveoli is now occupied by water vapour, the space available for other gases is diminished.

It has been noted that part of the expired air (‘dead space’ air) is atmospheric air rich in O2 and poor in CO2. As expiration progresses the expired air becomes a mixture of ‘dead space’ air and alveolar air and that the last part of the expired air is pure alveolar air. The expired air, therefore, is richer in O2 but poorer in CO2 as compared to alveolar air.

Method of Collection of Expired Air:

Expired air is collected in a Douglas bag (Fig. 8.14) over a certain period of time. The sample of air is taken out from the side tube and analysed with the help of Llyod’s modification of Haldane gas analysis apparatus.

Tension of Gases in the Alveolar Air:

In the steady state the total tension of gases including water vapour in the alveoli is equal to the ambient barometric pressure. At sea-level the barometric pressure is 760 mmHg. The alveolar air is saturated with water vapour which exerts a tension of 47 mmHg at body temperature irrespective of the barometric pressure.

With these data in view it is possible to calculate tension of O2 and CO2 in the alveolar air provided the percentage composition of these gases in the alveolar air is known according to the ‘law of partial pressure’. Which states that the tension of a particular gas in a gas mixture is proportional to its percentage composition.

Thus in atmosphere the pressure of O2 is roughly 1/5 th of 1 atmosphere = 153 mm Hg approximately. The atmospheric air, however, is dry. In calculation of tension of gases in the alveolar air, the pressure of water vapour (47 mm Hg) is to be deducted from the total pressure of gases in the alveoli which amounts to 760 mm Hg at sea-level.

Similarly tension of CO2 in the alveolar air is 5.5% of 713 = 39.2 mm Hg or 40 mm Hg (approx.). Of the 4 gases present in alveoli (O2 + CO2 + N2 + H2O vapour) the N2 and H2O vapour are neither taken into the blood stream nor added to alveolar air and as such the sum of partial pressure of these gases is constant in the alveoli.

This of course, means that the sum of partial pressure of O2 and CO2 is constant in the alveoli under steady state of metabolism and amounts roughly to 140 mm Hg at sea-level. A subject, therefore, can alter the PO2 of his alveolar air only at the expense of this alveolar PCO2 which is rather limited because the alveolar PCO2 cannot be reduced from normal 40 mm Hg to below 24 mm Hg.

Method of Measurement of Alveolar and Arterial PCO2:

Diffusion of CO2 is so rapid that alveolar PCO2 is always equal to arterial PCO2. Arterial PCO2 can be measured by direct electrochemical method using a CO2 sensitive electrode through an arterial puncture needle.

Indirect bloodless method has also been evolved by Campbell et, a and gives reliable result. An anaesthetic bag is filled with about 1 litre of O2 and the subject breaths and re-breaths into this bag for 1½ minutes. During this period there occurs an almost perfect ‘lung bag’ equilibrium so that the PCO2 of the bag air is almost equal to PCO2 of the alveolar air.

However to get an accurate result, the subject takes rest for at least 2 minutes and then re-breaths into the bag once again for 20 seconds during which period there occurs fine adjustment between the mixed venous PCO2 (PvCO2) and the bag air.

Recirculation of the blood and consequent higher PCO2 value is avoided by keeping the second rebreathing period limited to 20 seconds. After the end of the experiment the gas in the bag is analysed and its PCO2 is calculated. This is equal to mixed venous PCO2. The arterial PCO2 is always 6 mmHg lower than the venous PCO2.

Effects of Alveolar Air:

i. Effect of Voluntary Hyperpnoea on Alveolar Air:

Hyperpnoea flushes out the alveoli with air so that the CO2 content and CO2 tension of the alveolar air and so of the arterial blood is diminished. This causes depression of respiration and may lead to temporary apnoea. During the depressed respiratory phase CO2 builds up again till the alveolar PCO2 attains its normal value and breathing is resumed. The alveolar PO2 rises in the early phase when the PCO2 is depressed but this has no effect on arterial saturation, which is normally 95% saturated.

ii. Effects of Voluntary Apnoea on Alveolar Air:

After normal inspiration breath can be held for 30 to 50 seconds. This is normal ‘breath-holding time’.

During breath -holding time the percentage of CO2 and PCO2 in the alveolar air gradually rises and the percentage of O2 and PO2 in the alveolar air gradually falls.

At the breaking point the O2 content of the alveolar air is about 8% (PO2=57 mm Hg) and its CO2 content is about 7% (PCO2 = 50 mm Hg). It will be noted that during apnoea there occurs a more significant fall in percentage and tension of oxygen in the alveolar air than rise of CO2 content and tension.

This is due to different shape of the dissociation curves of the two gases, so that removal of a given quantity of oxygen from blood will cause a more significant fall in oxygen tension than elevation of CO2 tension when the same volume of C2 is added.

Further CO2 being highly soluble most of it gets dissolved in body fluids and less is available for elevation of alveolar PCO2. Here the two stimuli of O2 lack and CO2 excess interact with each other in stimulation of respiration.

Inhalation of O2 before voluntary apnoea will prolong the breath-holding time by 15 to 20 seconds.

i. Absence of O2 lack stimulus during breath-holding period.

ii. The sensitivity of respiratory centre to CO2 excess is less in the absence of oxygen lack.

Voluntary hyper-apnoea before breath holding will wash off CO2 from the alveolar air and the breath- holding time will be increased considerably so that the subject may develop cyanosis due to O2 lack before the alveolar PCO2 rises sufficiently to stimulate the respiration. This shows that CO2 excess plays a more significant role in stimulating respiration than oxygen lack.

If a gas mixture with CO2 and O2 in quantities similar to that at the termination of the breath-holding time is re-breathed by a person at the time of breaking point he can hold his breath for a further period in spite of diminished oxygen and elevated CO2 in the lungs. This indicates other factors besides O2 lack and CO2 excess play an important role in precipitation respiratory movement.

During the period of apnoea a larger volume of O2 is removed than the volume of CO2 added to the lungs. This causes a sense of discomfort and distress. Further, holding the chest in a fixed position stimulates afferents from the respiratory muscles which are obviated by the re-breathing experiment cited above. The afferent stimuli originating in the chest muscles, therefore, constitute the third important factor in determining the breaking point after breath-holding.

iii. Effects of High Altitude on Alveolar Oxygen:

At high altitude the barometric pressure falls and so the tension of gases in the inspired air and also in the alveolar air falls. Water vapour exerts a tension of 47 mmHg at all altitudes and CO2 is continuously exerted from the body into the respiratory alveoli. As a result of this adverse combination, the PO2 of the alveolar air falls at high altitude. Further the fall of alveolar PO2 is disproportionately low because of extremely low O2 tension of tissues, O2 is absorbed very quickly from the alveoli.

The formula for calculating alveolar PO2 at different altitudes is:

Alveolar PO2 = PB – PCO2 – 47 / 5 – PO2 loss (PO2 loss is the oxygen pressure decrease caused by oxygen uptake into the blood and the value 47 is the vapour pressure of water.)

There occurs a light fall in alveolar PCO2 due to hyperventilation but this cannot compensate for O2 deficit at high altitude. The Table 8.4 gives alveolar PCO2 and PO2 at different altitudes along with barometric pressure (PB) and percentage saturation of arterial blood with oxygen.

It may be noted that an altitude of 15 km or 50,000 feet the barometric pressure is only 87 mmHg. This therefore, is the total pressure of gases and water vapour in the alveoli, the latter accounts for 47 mm Hg leading only (87 – 47) = 40 mm Hg for O2, N2 and CO2. Since PCO2 is 24 mm Hg, only 16 mm Hg of pressure is distributed between N2 and O2 present in the ratio of approximately 4:1.

That being so on theoretical ground, one would expect that the alveolar PO2 at this altitude would be about 3 mm Hg. But due to increased uptake of O2 by grossly anoxic tissues at this altitude the alveolar PO2 falls to 1 mm Hg only. Even if pure O2 is inhaled and all the N2 in the alveoli is replaced by it – the PO2 in alveoli would be increased to 16 mm Hg only. Oxygen, therefore, must be administered under pressure to sustain life at this altitude.

Factors Controlling Alveolar PCO2:

Two important factors are:

Metabolic rate, i.e., production of CO2 in the body. The higher metabolic rate the greater will be the PACO2.

2. Alveolar Ventilation:

The greater the alveolar ventilation the lower will be the PACO2 and the higher will be PAO2.

Alveolar PO2 and Venous Admixture:

There is normally a difference between pulmonary capillary PO2 (Pco2) and arterial PO2. Alveolar PO2 which normally is in near equilibrium with pulmonary end-capillary PO2 therefore, is higher than arterial PO2.

The difference is explained by the fact that under normal conditions some blood passes from the venous side to the arterial side avoiding the lungs and without being exposed to alveolar O2. For example, the Thebesian veins draining directly into the left heart, the bronchpulmonary anastomosis already mentioned.

It has been estimated that about 6% of venous blood pumped by the right heart by-passes the lungs altogether and thus reduces the PO2 of the pulmonary venous blood. This is called shunt effect and by definition it is anatomical shunt-contributing to venous admixture.

Physiological Shunt:

Even under physiological conditions the millions of alveoli of the lungs are not adequately ventilated and some of them may be completely non-ventilated. Blood flowing through the non-ventilated alveoli will not be oxygenated at all and so will contribute to venous admixture effect. Similarly venous blood flowing through poorly ventilated alveoli will not be adequately oxygenated and thus will produce the same effect as noted above.

It is possible that both hypoventilated and hyperventilated alveoli may be present in the same lung but because of the fact that normally ventilated alveoli can effect almost complete saturation of haemoglobin with oxygen – the defective oxygenation of venous blood perfused through hypoventilated alveoli cannot be compensated by perfusion of hyperventilated alveoli. From quantitative aspect, therefore, physiological shunt is larger than anatomical shunt. It is the commonest cause of hypoxia in respiratory diseases.

The concept of anatomical and physiological shunts is analogous to the concept of anatomical and physi­ological dead space. Normally alveolar ventilation is about 4 litres/minute and about 5 litres of blood (cardiac output) is per­fused through the alveoli per minute. The average ventilation/perfusion ratio for the whole lungs, therefore, is 4/5 or 0.8.

Increase in physiological dead space is due to absence or diminution of blood flow through well-ventilated alveoli – the condition, therefore, is attended with increase in ventilation/perfusion ratio. The reverse is true in increase in ‘shunt’ or venous admixture effect when the ratio of ventilation to perfusion is decreased.


Avian Respiration

Birds have evolved a respiratory system that enables them to fly. Flying is a high-energy process and requires a lot of oxygen. Furthermore, many birds fly in high altitudes where the concentration of oxygen in low. How did birds evolve a respiratory system that is so unique?

Decades of research by paleontologists have shown that birds evolved from therapods, meat-eating dinosaurs (Figure 20.14). In fact, fossil evidence shows that meat-eating dinosaurs that lived more than 100 million years ago had a similar flow-through respiratory system with lungs and air sacs. Archaeopteryx and Xiaotingia , for example, were flying dinosaurs and are believed to be early precursors of birds.

Figure 20.14.
(a) Birds have a flow-through respiratory system in which air flows unidirectionally from the posterior sacs into the lungs, then into the anterior air sacs. The air sacs connect to openings in hollow bones. (b) Dinosaurs, from which birds descended, have similar hollow bones and are believed to have had a similar respiratory system. (credit b: modification of work by Zina Deretsky, National Science Foundation)

Most of us consider that dinosaurs are extinct. However, modern birds are descendants of avian dinosaurs. The respiratory system of modern birds has been evolving for hundreds of millions of years.

All mammals have lungs that are the main organs for breathing. Lung capacity has evolved to support the animal’s activities. During inhalation, the lungs expand with air, and oxygen diffuses across the lung’s surface and enters the bloodstream. During exhalation, the lungs expel air and lung volume decreases. In the next few sections, the process of human breathing will be explained.


Practical Work for Learning

Class practical

A spirometer is the standard equipment used to measure the capacity of the human lungs. There are several versions of this laboratory apparatus available, but all consist of a chamber (of capacity approximately 6 dm 3 ) suspended freely over water and counterbalanced so that gas passed in or drawn out makes the chamber rise or fall. You can make a permanent record of the movements of the chamber either by attaching a pen to it and allowing it to write on a drum revolving slowly (kymograph) or by attaching a motion sensor which will convert movement into electronic signals that are then interpreted by your datalogging software.

These notes explain the working of a spirometer, so that students are aware of the apparatus and how it works. The notes include some of the hazards and risk control measures required for safe operation of the apparatus. We have also provided some example traces for your students to analyse and interpret. You could use these even if you do not have access to a spirometer, or if you feel it is too complicated to set up.

There are some hand-held versions of spirometers available – small devices that measure air flow and calculate volume electronically. For example, Philip Harris offer a ‘pocket spirometer’ at around £140 which can be used outside the laboratory for collecting data in the field, and PASCO produce a datalogging spirometer (Pasport Spirometer) for which you would need the Data Studio software, but it produces instant traces on screen.

Lesson organisation

Students should use a spirometer only under the direct supervision of a teacher. Never carry out an investigation on a human subject if you are not being supervised.

Apparatus and Chemicals

For the class – set up by technician/ teacher:

Spirometer and carbosorb
Disinfectant

Oxygen cylinder (optional for short investigations – see Notes 2 and 5 below)

Kymograph
or Motion sensor and datalogging software

Health & Safety and Technical notes

Student health: Give careful consideration to the selection of subjects – it may be helpful to know medical histories. Participation in school sports teams is usually a good indication of fitness.

1 Carbosorb/ sodalime: Refer to Hazcard 91 for more information about soda line and Carbosorb. Wear eye protection when handling these carbon dioxide absorbing chemicals they are corrosive although safer to use than sodium hydroxide. For spirometers use granules of the size 5 to 10 mesh (similar to aquarium gravel) rather than 8 to 14 mesh (which has lumps similar in size to demerara sugar).

Ensure that the valve in the tubing connected to the spirometer is positioned so that air is always exhaled through the soda lime/ Carbosorb to avoid inhalation of any soda lime/ Carbosorb dust. Reduce this risk further by placing a small layer of polymer wool (as used in aquarium filters) at the inflow and outflow of the carbon dioxide absorbent chamber. Carbosorb (from VWR (see Suppliers)) has been treated with an indicator dye that changes colour (from pale brown to greyish white) to show when no more carbon dioxide can be absorbed. Indicating soda lime should be stored in a dark place to prevent colour fading. If there is any doubt about its condition, test a small sample with carbon dioxide to see if there is any further colour change.

2 Oxygen from cylinders: Oxygen forms explosive compounds with many oils and greases, so such lubricants should not be put on the connectors or regulators of oxygen cylinders or on the tubing connectors to spirometers. Use water or soap solutions only if you need to ease any of the connections between the apparatus and corrugated tubes. The risks of using ordinary oxygen compared with medical oxygen are insignificant.

3 Cleaning the spirometer: Disinfect the mouthpiece after each person has used it. Use a fresh solution of Milton and disinfect for 30 minutes, then rinse in water. Milton leaves no unpleasant aftertaste. If you need to disinfect more quickly, ethanol will disinfect in 5 minutes, but leaves an unpleasant taste. It is best to have several clean mouthpieces available during each lesson, or use disposal mouthpieces where possible. At the end of each lesson, disinfect the T-piece and the internal surfaces of the corrugated tubes connecting the T-piece to the spirometer. (Hang these up to drain first.) Ethanol is preferable for this as it will evaporate more readily from the tubing crevices.

4 Exercise and safety: Spirometers should not be used to investigate breathing during vigorous exercise: most resistance to breathing will be noticed when ventilation rate and amplitude are elevated, and exercising while attached to a spirometer can be stressful. Make sure that students are appropriately dressed (and wearing appropriate footwear) for any exercise undertaken as part of an investigation. Also, make sure that any apparatus used, for example, steps or blocks, are sturdy, well-built and anchored.

5 The spirometer: Do not use home-made spirometers. Supervise students using the spirometer closely at all times. Any investigations involving re-breathed air require particular vigilance on the part of the teacher. If any resistance to breathing is felt by the subject, end the investigation immediately.

With a spirometer filled with oxygen and carbon dioxide absorbed, the maximum time a student should use the spirometer is 5 minutes. Useful results can usually be obtained within 2-3 minutes. Without carbon dioxide accumulation, normal regulation of breathing does not occur and lack of oxygen will produce no visible signs of distress, until the participant becomes unconscious. There is no danger of the subject losing consciousness if more than half of the oxygen remains in the spirometer. For investigation of breathing after exercise, or breathing over an extended time, it is essential to use a spirometer filled with oxygen.

With a spirometer filled with air and carbon dioxide not absorbed, the maximum time a student should use the spirometer is 1 minute. Only a fifth of atmospheric air is oxygen and as the carbon dioxide level rises, the subject will experience a feeling of suffocation, feel short of breath and breathe faster and deeper. Brief the students that they may remove the mouthpiece and end the investigation themselves without being prompeted if they feel any distress! If the spirometer is filled with oxygen instead, there is no danger of lack of oxygen, but the subject will still show the symptoms of stimulated breathing.

With a spirometer filled with air and carbon dioxide absorbed, the maximum time a student should use the spirometer is 1 minute. As in the first case, the subject will feel no ill effects until unconsciousness sets in. There should be little danger if the experiment is run for under a minute, but the teacher should monitor the time and the subject closely – observing the student writing while using the spirometer enables a constant check to be made for impaired alertness at the onset of oxygen shortage.

6 Student health: Give careful consideration to the selection of subjects – it may be helpful to know medical histories. Participation in school sports teams is usually a good indication of fitness.

Ethical issues

Using a student as a subject for an investigation raises ethical issues. Any student involved should read the attached Acting as a subject for an investigation briefing and consent sheet (52 KB) and sign to say they are happy to take part.

Procedure

SAFETY:
Take care handling Carbosorb/ soda lime.
Follow all safety directions for working with oxygen cylinders.
Check the spirometer has been set up correctly and ensure that readings are taken for only the time periods indicated in Note 5.
Ensure students using the spirometer are supervised at all times.
Disinfect the spirometer mouthpieces as directed (Note 3) and disinfect the spirometer at the end of the lesson.

Preparation - setting up the spirometer

a Fill the canister with a chemical for absorbing carbon dioxide, suchy as Carbosorb ® or self-indicating soda-lime granules (Note 1).


b Check for leaks by filling the spirometer with air, closing all the taps and loading the lid of the chamber with a 200 g mass. If the chamber does not move during five minutes, there are no serious leaks.

c If using a kymograph, check that the pen writes on the drum throughout a complete revolution of the drum, and that the pen is towards the top of the recording chart paper with the chamber full of air/ oxygen. If using a motion sensor, make sure that the sensor and datalogging software are appropriately connected and you know how to collect the data.

d Calibrate the spirometer as follows:

i Empty all the air out of the chamber. If using a kymograph, make sure that the pen makes a mark on the lower part of the drum.

ii Let a specific volume of air into the spirometer chamber (say 500 cm 3 ). Record the position of the chamber by making a mark on the kymograph.

iii Do this again, letting in the same volume of air each time, until the chamber has risen as high as possible.

e When you have finished calibrating, flush the spirometer with oxygen four times and leave it full, with the taps closed (Note 2).

Investigation – resting breathing rate and vital capacity

f The subject should be rested and sitting down, with a nose-clip in place. With the two-way tap closed and the mouthpiece connected to the outside atmosphere, insert the mouthpiece into the subject’s mouth and allow the subject to breathe steadily (normally) until they are accustomed to the apparatus.

g If you are using a kymograph, set the speed at 1 mm s –1 .

h When ready to proceed, at the end of an outward breath, turn the two-way tap to connect the subject to the spirometer chamber. This must be done at the end of an outward breath so that the first movement of the spirometer lid will be downwards.

i After recording normal breathing for a minute or so, ask the subject to breathe in as deeply as possible, and then resume normal breathing.

j After a few more breaths, ask the subject to breathe out as far as possible, and then to resume normal breathing for a minute or so.

k Dispose of or clean the mouthpiece used by the subject (Note 3).

l Find the mass of the subject in kilograms.

Investigation – oxygen consumption

m Use a subject who has not eaten for at least two hours before the investigation, and who has been resting for 30 minutes – preferably lying down. With the two-way tap closed, and the mouthpiece connected to the outside atmosphere, put the nose-clip on the subject and the mouthpiece in their mouth, and allow them to breathe until they are accustomed to the apparatus.

n At the end of an outward breath, open the two-way tap and begin recording tidal breathing. Record for five minutes.

o Ask the subject to perform some vigorous exercise for about 5 minutes – walking up and down a flight of stairs or stepping on and off a low, stable bench (Note 4).

p While the subject is exercising, recharge the spirometer with oxygen and have the nose-clip and mouthpiece ready so they can record their breathing as soon as the exercise is over. Remember to start the record at the end of an outward breath.

Teaching notes

Interpreting the trace

The depth of breathing is determined by measuring the vertical movement of the pen (or motion sensor) from one peak to the next trough on the trace and comparing this with the initial volume calibration.


The rate of breathing (breaths per minute) may be determined with reference to the time scale. From a kymograph trace, you would need to know the speed of rotation of the drum (in mm s – 1 ) to calculate the horizontal displacement equivalent to 10 or 60 seconds.

Our normal resting breathing moves only a small percentage of the air contained in our lungs. The lungs are highly elastic and can move significantly more air when we take exercise than we normally move at rest.

  • The volume of air that a human breathes into and out of their lungs while at rest is called the tidal volume. This is a relatively small volume of air (around 500 cm 3 ) and provides enough oxygen for a human’s resting needs.
  • The maximum amount of air that may be inspired, above tidal inspiration, is called the inspiratory reserve volume. The typical adult value is 2 to 3.2 dm 3 .
  • The maximum amount of air that can be breathed out, above tidal expiration is called the expiratory reserve volume. The typical adult value is 0.75 dm 3 to 1 dm 3 .
  • The vital capacity is the sum of all three of these volumes.

Tidal volume, inspiratory reserve volume and expiratory reserve volume can all be calculated from the trace made by the spirometer in the above procedure.


Even in dead mammals, the lungs are never completely empty of air. The air that we cannot expel from the lungs, even with the hardest effort of expiration, is called the residual volume. The typical adult value is around 1.2 dm 3 .

Estimate the total lung capacity by multiplying the expiratory reserve volume by six. Typical adult human value is around 5.5 to 6 dm 3 . Then calculate the residual volume by subtracting the vital capacity.

Under the slightly unusual circumstances of the investigation, the subject may be breathing abnormally. If the subject is breathing ‘high up’ or ‘low down’ in the lungs, calculated values of vital and total lung capacity may appear unnaturally large or small.

A normal inspiration brings the tidal volume of air into the lungs, where it mingles with the air already there. However, not all of the air in the tidal volume is available for gas exchange. Some of the tidal inspiration never reaches the alveoli, but remains in the trachea and other tubes in the system. The lining of most of the bronchial trees is unavailable for gas exchange, and is known as the ‘dead space’. The dead space of a subject’s lungs is roughly in proportion to their total body mass. A mass of 0.45 kg is roughly equivalent to 1 cm 3 of dead space.

Using the spirometer to investigate cellular respiration and metabolic activity

The amount of oxygen consumed is found by comparing the lowest point of a trace at the start of a time period with the lowest point of the same trace at the end of this period. Compare this vertical distance with the initial volume calibration.

If a line drawn through all the peaks of a trace in any one period is straight, this shows that the subject consumed oxygen at a constant rate.


Oxygen consumption gives a measure of metabolic rate. Humans can release approximately 20.18kJ of available energy for every dm3 of oxygen consumed. The calculation for resting metabolic rate is:

resting metabolic rate (kJ h -1 ) = 20.18 x oxygen consumption per hour (dm 3 )

This is not the basal metabolic rate, as the subject is likely to have eaten in the last 12-18 hours and is still absorbing food from the gut, and is also sitting rather than lying down. The attached spreadsheet (15 KB) might make it easier to calculate the metabolic rate for the traces given on the student sheet (1.0 MB) .

If the exercise is anything more than very light, the subject will incur an oxygen debt, and therefore oxygen uptake during or immediately after exercise will not give an accurate picture of energy usage during exercise.

A subject who has just finished some vigorous exercise usually feels hot. The expired air may be at a higher temperature than previously which would affect the volume of the gas in the spirometer. Measure the temperature of the air in the spirometer on both occasions to make sure this is not the case. If it differs considerably, make a correction when calculating the volume of oxygen. (Use the formula derived from Boyle’s Law).


Contents

Signs and symptoms of spontaneous subcutaneous emphysema vary based on the cause, but it is often associated with swelling of the neck and chest pain, and may also involve sore throat, neck pain, difficulty swallowing, wheezing and difficulty breathing. [5] Chest X-rays may show air in the mediastinum, the middle of the chest cavity. [5] A significant case of subcutaneous emphysema is easy to detect by touching the overlying skin it feels like tissue paper or Rice Krispies. [8] Touching the bubbles causes them to move and sometimes make a crackling noise. [9] The air bubbles, which are painless and feel like small nodules to the touch, may burst when the skin above them is palpated. [9] The tissues surrounding SCE are usually swollen. When large amounts of air leak into the tissues, the face can swell considerably. [8] In cases of subcutaneous emphysema around the neck, there may be a feeling of fullness in the neck, and the sound of the voice may change. [10] If SCE is particularly extreme around the neck and chest, the swelling can interfere with breathing. The air can travel to many parts of the body, including the abdomen and limbs, because there are no separations in the fatty tissue in the skin to prevent the air from moving. [11]

Trauma Edit

Conditions that cause subcutaneous emphysema may result from both blunt and penetrating trauma [5] SCE is often the result of a stabbing or gunshot wound. [12] Subcutaneous emphysema is often found in car accident victims because of the force of the crash.

Chest trauma, a major cause of subcutaneous emphysema, can cause air to enter the skin of the chest wall from the neck or lung. [9] When the pleural membranes are punctured, as occurs in penetrating trauma of the chest, air may travel from the lung to the muscles and subcutaneous tissue of the chest wall. [9] When the alveoli of the lung are ruptured, as occurs in pulmonary laceration, air may travel beneath the visceral pleura (the membrane lining the lung), to the hilum of the lung, up to the trachea, to the neck and then to the chest wall. [9] The condition may also occur when a fractured rib punctures a lung [9] in fact, 27% of patients who have rib fractures also have subcutaneous emphysema. [11] Rib fractures may tear the parietal pleura, the membrane lining the inside of chest wall, allowing air to escape into the subcutaneous tissues. [13]

Subcutaneous emphysema is frequently found in pneumothorax (air outside of the lung in the chest cavity) [14] [15] and may also result from air in the mediastinum, pneumopericardium (air in the pericardial cavity around the heart). [16] A tension pneumothorax, in which air builds up in the pleural cavity and exerts pressure on the organs within the chest, makes it more likely that air will enter the subcutaneous tissues through pleura torn by a broken rib. [13] When subcutaneous emphysema results from pneumothorax, air may enter tissues including those of the face, neck, chest, armpits, or abdomen. [1]

Pneumomediastinum can result from a number of events. For example, foreign body aspiration, in which someone inhales an object, can cause pneumomediastinum (and lead to subcutaneous emphysema) by puncturing the airways or by increasing the pressure in the affected lung(s) enough to cause them to burst. [17]

Subcutaneous emphysema of the chest wall is commonly among the first signs to appear that barotrauma, damage caused by excessive pressure, has occurred, [1] [18] and it is an indication that the lung was subjected to significant barotrauma. [19] Thus the phenomenon may occur in diving injuries. [5] [20]

Trauma to parts of the respiratory system other than the lungs, such as rupture of a bronchial tube, may also cause subcutaneous emphysema. [13] Air may travel upward to the neck from a pneumomediastinum that results from a bronchial rupture, or downward from a torn trachea or larynx into the soft tissues of the chest. [13] It may also occur with fractures of the facial bones, neoplasms, during asthma attacks, when the Heimlich maneuver is used, and during childbirth. [5]

Injury with pneumatic tools, those that are driven by air, is also known to cause subcutaneous emphysema, even in extremities (the arms and legs). [21] It can also occur as a result of rupture of the esophagus when it does, it is usually as a late sign. [22]

Medical treatment Edit

Subcutaneous emphysema is a common result of certain types of surgery for example it is not unusual in chest surgery. [8] It may also occur from surgery around the esophagus, and is particularly likely in prolonged surgery. [7] Other potential causes are positive pressure ventilation for any reason and by any technique, in which its occurrence is frequently unexpected. It may also occur as a result of oral surgery, [23] laparoscopy, [7] and cricothyrotomy. In a pneumonectomy, in which an entire lung is removed, the remaining bronchial stump may leak air, a rare but very serious condition that leads to progressive subcutaneous emphysema. [8] Air can leak out of the pleural space through an incision made for a thoracotomy to cause subcutaneous emphysema. [8] On infrequent occasions, the condition can result from dental surgery, usually due to use of high-speed tools that are air driven. [24] These cases result in usually painless swelling of the face and neck, with an immediate onset, the crepitus (crunching sound) typical of subcutaneous emphysema, and often with subcutaneous air visible on X-ray. [24]

One of the main causes of subcutaneous emphysema, along with pneumothorax, is an improperly functioning chest tube. [2] Thus subcutaneous emphysema is often a sign that something is wrong with a chest tube it may be clogged, clamped, or out of place. [2] The tube may need to be replaced, or, when large amounts of air are leaking, a new tube may be added. [2]

Since mechanical ventilation can worsen a pneumothorax, it can force air into the tissues when subcutaneous emphysema occurs in a ventilated patient, it is an indication that the ventilation may have caused a pneumothorax. [2] It is not unusual for subcutaneous emphysema to result from positive pressure ventilation. [25] Another possible cause is a ruptured trachea. [2] The trachea may be injured by tracheostomy or tracheal intubation in cases of tracheal injury, large amounts of air can enter the subcutaneous space. [2] An endotracheal tube can puncture the trachea or bronchi and cause subcutaneous emphysema. [12]

Infection Edit

Air can be trapped under the skin in necrotizing infections such as gangrene, occurring as a late sign in gas gangrene, [2] of which it is the hallmark sign. Subcutaneous emphysema is also considered a hallmark of fournier gangrene. [26] Symptoms of subcutaneous emphysema can result when infectious organisms produce gas by fermentation. When emphysema occurs due to infection, signs that the infection is systemic, i.e. that it has spread beyond the initial location, are also present. [9] [21]

Air is able to travel to the soft tissues of the neck from the mediastinum and the retroperitoneum (the space behind the abdominal cavity) because these areas are connected by fascial planes. [4] From the punctured lungs or airways, the air travels up the perivascular sheaths and into the mediastinum, from which it can enter the subcutaneous tissues. [17]

Spontaneous subcutaneous emphysema is thought to result from increased pressures in the lung that cause alveoli to rupture. [5] In spontaneous subcutaneous emphysema, air travels from the ruptured alveoli into the interstitium and along the blood vessels of the lung, into the mediastinum and from there into the tissues of the neck or head. [5]

Significant cases of subcutaneous emphysema are easy to diagnose because of the characteristic signs of the condition. [1] In some cases, the signs are subtle, making diagnosis more difficult. [13] Medical imaging is used to diagnose the condition or confirm a diagnosis made using clinical signs. On a chest radiograph, subcutaneous emphysema may be seen as radiolucent striations in the pattern expected from the pectoralis major muscle group. Air in the subcutaneous tissues may interfere with radiography of the chest, potentially obscuring serious conditions such as pneumothorax. [18] It can also reduce the effectiveness of chest ultrasound. [27] On the other hand, since subcutaneous emphysema may become apparent in chest X-rays before a pneumothorax does, its presence may be used to infer that of the latter injury. [13] Subcutaneous emphysema can also be seen in CT scans, with the air pockets appearing as dark areas. CT scanning is so sensitive that it commonly makes it possible to find the exact spot from which air is entering the soft tissues. [13] In 1994, M.T. Macklin and C.C. Macklin published further insights into the pathophysiology of spontaneous Macklin's Syndrome occurring from a severe asthmatic attack.

The presence of subcutaneous emphysema in a person who appears quite ill and febrile after bout of vomiting followed by left chest pain is very suggestive of the diagnosis of Boerhaave's syndrome, which is a life-threatening emergency caused by rupture of the distal esophagus.

Subcutaneous emphysema can be a complication of CO2 insufflation with laparoscopic surgery. A sudden rise in end-tidal CO2 following the initial rise that occurs with insufflation (first 15-30 min) should raise suspicion of subcutaneous emphysema. [4] Of note, there are no changes in the pulse oximetry or airway pressure in subcutaneous emphysema, unlike in endobronchial intubation, capnothorax, pneumothorax, or CO2 embolism.

Subcutaneous emphysema is usually benign. [1] Most of the time, SCE itself does not need treatment (though the conditions from which it results may) however, if the amount of air is large, it can interfere with breathing and be uncomfortable. [28] It occasionally progresses to a state "Massive Subcutaneous Emphysema" which is quite uncomfortable and requires surgical drainage. When the amount of air pushed out of the airways or lung becomes massive, usually due to positive pressure ventilation, the eyelids swell so much that the patient cannot see. Also the pressure of the air may impede the blood flow to the areolae of the breast and skin of the scrotum or labia. This can lead to necrosis of the skin in these areas. The latter are urgent situations requiring rapid, adequate decompression. [29] [30] [31] Severe cases can compress the trachea and do require treatment. [32]

In severe cases of subcutaneous emphysema, catheters can be placed in the subcutaneous tissue to release the air. [1] Small cuts, or "blow holes", may be made in the skin to release the gas. [16] When subcutaneous emphysema occurs due to pneumothorax, a chest tube is frequently used to control the latter this eliminates the source of the air entering the subcutaneous space. [2] If the volume of subcutaneous air is increasing, it may be that the chest tube is not removing air rapidly enough, so it may be replaced with a larger one. [8] Suction may also be applied to the tube to remove air faster. [8] The progression of the condition can be monitored by marking the boundaries with a special pencil for marking on skin. [32]

Since treatment usually involves dealing with the underlying condition, cases of spontaneous subcutaneous emphysema may require nothing more than bed rest, medication to control pain, and perhaps supplemental oxygen. [5] Breathing oxygen may help the body to absorb the subcutaneous air more quickly. [10]

Air in subcutaneous tissue does not usually pose a lethal threat [4] small amounts of air are reabsorbed by the body. [8] Once the pneumothorax or pneumomediastinum that causes the subcutaneous emphysema is resolved, with or without medical intervention, the subcutaneous emphysema will usually clear. [18] However, spontaneous subcutaneous emphysema can, in rare cases, progress to a life-threatening condition, [5] and subcutaneous emphysema due to mechanical ventilation may induce ventilatory failure. [25]

The first report of subcutaneous emphysema resulting from air in the mediastinum was made in 1850 in a patient who had been coughing violently. [5] In 1900, the first recorded case of spontaneous subcutaneous emphysema was reported in a bugler for the Royal Marines who had had a tooth extracted: playing the instrument had forced air through the hole where the tooth had been and into the tissues of his face. [5] Since then, another case of spontaneous subcutaneous emphysema was reported in a submariner for the US Navy who had had a root canal in the past the increased pressure in the submarine forced air through it and into his face. In recent years a case was reported at the University Hospital of Wales of a young man who had been coughing violently causing a rupture in the esophagus resulting in SE. [5] The cause of spontaneous subcutaneous emphysema was clarified between 1939 and 1944 by Macklin, contributing to the current understanding of the pathophysiology of the condition. [5]


What you have described is an air embolism. Incidences and cases of this happening has been recorded in several different procedures with some like seated posterior fossa surgery with a rate as high as 80%. 1

The variability in amount of air is because of the possible mechanisms by which it can cause death. 1

  1. If a small amount of air is injected it forms micro emboli which can now either cause gradual obstruction to blood flow or spontaneous resorption, which again depends upon rate and volume of air entrained, comorbid conditions causing ventilation-perfusion defect.
  2. A larger amount of air but remaining in venous circulation can cause obstruction of right ventricular outflow tract leading to cardiac arrest.
  3. But when a large amount of air gets trapped on the right side it can increase the pressure in right atrium causing right to left shunting through foramen ovale giving access to arterial circulation.

For the last point its important to know that upto 35% of adults have been reported having undiagnosed patent foramen ovale. 2 As for arterial embolism, experimental procedure on dogs showed injecting 1 to 1 1/4 ml/kg of air in cerebral arterial circulation can cause mortality in 50%. 3 Rukstinant reported ventricular fibrillation on injecting 0.25 ml of air in coronary arteries. 4

Scientific literature on the amount of air for air embolism (venous). A case report in 2001 discussing the volume of air required stated that:

THE morbidity and mortality rates from venous air embolism is determined by the volume of air entrained, the rate of entrainment, and the position and the cardiac status of the patient. As early as 1809, Nysten estimated the lethal dose of air to be 40–50 ml in a small dog and 100–120 ml in a large dog. The exact amount, 7.5 ml/kg, however, was not determined in dogs until 1953 by Oppenheimer et al. In l963, Munson et al. demonstrated a lethal volume of only 0.55 ml/kg in rabbits. The lethal volume of air in an adult human is unknown but is estimated to range from 200 to 300 ml. These numbers are derived from the cases of fatalities reported by Martland, Yeakel, and Flanagan.

This case reported the volume as 200 ml and note Flanagal had reported around the same in 1969.5

Finally, coming to the case air-bubble in syringe. (Because your question also had injecting air in vein, so that was first).

In 2013 nobody (without a malicious intent) would deliberately inject air. Accidental injecting instead of contrast has been reported. Some syringes which come with prefilled air has been asked to expel them during manufacturing prior to packaging to avoid this rare adverse event, although this can be expelled manually prior to injecting by the healthcare personals. 6