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Lung Ventilation: Natural and Mechanical 

Lung Ventilation: Natural and Mechanical
Lung Ventilation: Natural and Mechanical

Yuan Lei

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date: 27 October 2021

3.1 Introduction

This chapter describes the processes of respiration and lung ventilation. It focuses on the issues directly related to mechanical ventilation, especially its pneumatic process. It touches just briefly on general respiratory anatomy and physiology; please refer to relevant text or reference books for more details.

3.2 An overview of respiration

3.2.1 Anatomy of the respiratory system

The respiratory system refers to the six functional parts required to complete the vital process of gas exchange: the airway, lungs, chest wall, respiratory muscles, phrenic nerve, and respiratory centre. These parts can be divided roughly into two groups: (a) the anatomic foundation for gas exchange, and (b) the driving force and regulation of that gas exchange (Fig. 3.1).

Fig. 3.1 Six key parts of the respiratory system.

Fig. 3.1 Six key parts of the respiratory system.


The airway, also known as the pulmonary airway or respiratory tract, refers to those parts of the respiratory system through which air flows, beginning at the nose and mouth, and ending at the alveoli (Fig. 3.2). As these names imply, the airway is the gas passageway between the atmosphere and alveoli. It is not involved in gas exchange between the alveoli and blood.

The airway consists of the upper airway and the lower airway. Typically, we think of the upper airway as including the nose, nasal cavity, mouth, pharynx, and larynx. The lower airway includes everything from the trachea to the small bronchioles.

The airway poses resistance to gas flow in both directions. Airway resistance is one of the most important properties in lung mechanics. Several respiratory diseases, such as asthma, upper airway obstruction, and bronchospasm, result from abnormally high airway resistance.

The airway normally contains a certain amount of gas, which is always an inevitable part of tidal volume. This volume is called dead space or anatomical dead space because the volume is not involved in gas exchange. We need to pay particular attention to dead space, particularly when the tidal volume is tiny.


Humans have two lungs located in the rib cage. They are sponge-like organs. The trachea divides into two main stem bronchi for the respective lungs. Each main stem bronchus then branches into smaller and smaller bronchi like a tree. The tiniest branch is called a bronchiole. At the end of each bronchiole is a cluster of tiny air sacs called alveoli.

Each alveolus has a mesh of tiny blood vessels called capillaries. The very thin walls of the alveoli and bronchioles provide a moist, extremely thin, and large surface for gas exchange to occur. The gradients of partial pressure of O2 and CO2 drive the gases to diffuse (Fig. 3.3). Inhaled O2 diffuses from the alveoli into the capillaries, while CO2 from the blood diffuses into the alveoli. The waste CO2 in the alveoli is then expired through lung ventilation.

Fig. 3.3 Gas exchange at alveolar wall.

Fig. 3.3 Gas exchange at alveolar wall.

Because energy demand for all living cells and tissues is continuous, respiration must also be continuous. For an individual cell as well as for the whole body, death is inevitable if respiration stops for a certain length of time.

The lungs and the chest wall are elastic. During quiet breathing, inspiration is an active process, meaning that contraction of respiratory muscles, especially the diaphragm, causes the total lung volume to increase from when the lungs were in their resting position. Expiration is normally a passive process, meaning that the inspiratory muscles relax, and the loaded elastic recoil force of the chest wall and lungs brings the lungs back to their resting position. This is similar to a stretched rubber band retracting when the applied force is removed. The elasticity of the lungs and chest wall is the basis of lung compliance, which is another key property of respiratory mechanics. The elasticity may be higher than normal (causing ‘stiff lungs’, as in patients with acute respiratory distress syndrome (ARDS)), or lower than normal (causing ‘soft lungs’, as in patients with chronic obstructive pulmonary disease (COPD)). In the case of pneumothorax, the elasticity causes the affected lung to collapse partially or completely.

The effectiveness of alveolar gas exchange is determined by: (a) the total area and thickness of the diffusion membrane, (b) alveolar ventilation, and (c) pulmonary capillary circulation. We will discuss these further in section 3.2.2.

Chest wall

The chest or thorax is a part of the human trunk between the neck and the abdomen (Fig. 3.4). The chest wall is made up of bones and muscles. The bones (primarily ribs, sternum, and vertebrae) form a protective cage for the internal structures of the thorax. The main muscles of the chest wall are the external and internal intercostals. The contraction of external intercostals enlarge the thoracic cavity by drawing the ribs together and elevating the rib cage, while the internal intercostals decrease the dimensions of the thoracic cavity.

Fig. 3.4 Anatomic structure of the chest wall and the organs inside.

Fig. 3.4 Anatomic structure of the chest wall and the organs inside.

There are three subdivisions inside the thorax. The two lateral subdivisions hold the lungs. Between the lungs is the mediastinum, which contains the heart, the great vessels, parts of the trachea and oesophagus, and other structures.

The lung surface and the inner wall of the chest cage are actually not attached directly to each other. Instead, the lung literally floats in the thoracic cavity, surrounded by a very thin layer of pleural fluid. This potential space is called the pleural cavity. The cavity normally contains a small amount of serous liquid for lubrication of lung movement during breathing. Although normally the pleural cavity is a potential space, under abnormal conditions it can contain a large amount of air (pneumothorax) or liquid (pleural effusion). If so, the affected lung collapses partially or totally, preventing it from performing its function.

The thorax contains several vital soft organs, including the heart, lungs, and large blood vessels. A high positive end-expiratory pressure (PEEP) to expand the lungs compresses the neighbouring organs, and disturbs haemodynamics to a certain extent.

As we mentioned earlier, lung compliance is a key property of a pulmonary system. It is the measurement of elasticity of the lungs and chest wall together. Sometimes respiratory compliance is used to indicate the total or sum of lung compliance and chest wall compliance.

The chest and abdomen are separated by the soft diaphragm, which permits thoracic pressure to be easily transmitted to the abdomen, and vice versa. For this reason, a high PEEP can lead to high abdominal tension. On the other hand, a high abdominal tension can decrease respiratory compliance.

Respiratory muscles

The contraction and relaxation of respiratory muscles increases or decreases the volume of the thoracic cavity, resulting in corresponding changes in alveolar pressure. Air is sucked into the lungs when alveolar pressure is lower than ambient pressure. Gas is pushed out of the lungs when alveolar pressure is higher than ambient pressure.

During inspiration

The principal muscles involved in inspiration are the diaphragm and the external intercostal muscles. The thoracic cavity is enlarged in two ways: (a) contraction of the diaphragm increases the vertical dimensions of the thoracic cavity, or (b) contraction of the external intercostal muscle increases the width of the thoracic cavity. During intensive breathing, accessory respiratory muscles also participate in inspiration. Typical accessory muscles are the sternocleidomastoid and the scalene muscles.

During expiration

During peaceful breathing, expiration is a passive process. When the inspiratory muscles relax, the elastic recoil force of lungs and chest wall brings the lung volume to its resting position, generating a positive alveolar pressure. The resultant pressure gradient pushes out a certain amount of the gas inside the lungs. When expiration is active, the abdominal muscles and the internal and innermost intercostal muscles help expel the gas.

Alternating contraction and relaxation of respiratory muscles provide the ultimate driving force for lung ventilation. If the muscle activities are weakened or suppressed by disease, fatigue, general anaesthesia, or trauma, lung ventilation deteriorates. In this case, mechanical ventilation is indicated.

The activation of accessory respiratory muscles is a strong indication of respiratory distress or ‘air hunger’.

Respiratory nerves

The diaphragm is innervated by the left and right phrenic nerves, which arise from the cervical spinal cord (C3–C5) in humans. Innervation of respiratory intercostal and abdominal muscles comes from the thoracolumbar spinal cord, T1–T11 and T7–L2, respectively.

Drawing on this fact, Swedish ventilator manufacturer Maquet developed a technical feature called NAVA (neurally adjusted ventilatory assist). Neurally adjusted ventilatory assist uses a special catheter sensor positioned at the lower oesophagus to detect phrenic nerve impulses. The detected signals in turn are used to guide the ventilator operation.

Spinal cord injury at C4 or higher can disrupt nerve impulses from the brain to the phrenic nerve. Such injuries can paralyse the diaphragm, requiring the injured person to be on a ventilator. A spinal cord injury below C5 does not involve the phrenic nerve; thus, a person with such an injury can still breathe despite possible paralysis of the lower limbs.

Respiratory centre

The respiratory centre refers to a group of nerve cells in the medulla oblongata and pons of the brain that: (a) receive sensory signals about the level of O2, CO2, and pH in the blood and cerebrospinal fluid; (b) determine whether and how to change the breathing pattern; and (c) send the signals to the respiratory muscles to execute this change in breathing pattern.

The functioning of the respiratory centre is critical to proper respiration. In most ventilated patients, the respiratory centre is intact, that is, an active patient has a normal respiratory response to changes in blood O2, CO2, and pH. A normal respiratory centre is required for several newer ventilator features, such as the proportional assist ventilation (PAV) mode, tube resistance compensation (TRC, or automatic tube compensation (ATC)), and NAVA. Nevertheless, the respiratory centre may not function properly in neurological or neurosurgical patients.

3.2.2 Physiology of respiration

Two essential questions about respiration

Why is respiration necessary?

All living cells need an energy supply to survive and execute their physiological functions. Energy is produced in the cells through the biochemical process of metabolism (Fig. 3.5). The metabolic chemical process consumes oxygen (O2) and glucose, and produces water, carbon dioxide (CO2), and adenosine triphosphate (ATP), which is the major ‘currency’ of energy in the body.

Fig. 3.5 Diagram of metabolic process.

Fig. 3.5 Diagram of metabolic process.

Metabolism is a continuous process, continuously consuming O2 and producing CO2. To keep local O2 and CO2 concentrations within proper ranges, new O2 must be continuously brought to the cells and the waste CO2 removed. This is the task of respiration.

What is respiration?

In short, respiration is the process of transporting O2 from atmospheric air to the cells within tissues, and transporting CO2 from the cells to the air. In general, respiration has three major parts: gas exchange in the lungs, blood circulation, and gas exchange in tissues and cells (Fig. 3.6).

Fig. 3.6 Diagram of the entire respiration process.

Fig. 3.6 Diagram of the entire respiration process.

Oxygen and CO2 are transported in blood as it circulates. If the blood supply to a tissue is drastically reduced or even stopped, the local O2 concentration falls, and the CO2 concentration rises rapidly. The tissue will die if the normal blood supply does not resume quickly. A typical example is a heart infarct.

Gas transport

Oxygen and CO2 are transported in three ways: (1) gas diffusion, (2) lung ventilation, and (3) blood circulation.

Gas diffusion

Gas diffusion is a natural process in which gas molecules move from an area of high concentration to a neighbouring area of low concentration. The two areas share a common diffusion membrane. Such gas diffusion takes place mainly in three areas: (a) alveolar walls, (b) blood capillary walls, and (c) tissues and cell membranes.

The speed of gas diffusion depends on: (a) the difference in gas molecular concentrations, (b) properties of the diffusion membrane, including its total area and thickness, and (c) the solubility and molecular weight of the gas involved. Carbon dioxide diffuses 20 times as fast as O2.

Blood transport of O2 and CO2

Oxygen is transported in two ways within the blood. Red blood cells or erythrocytes carry 97% of all O2 molecules in chemical combination with haemoglobin. The remaining 3% are dissolved in plasma.

Haemoglobin (Hb), a globular protein, is the primary vehicle for O2 transport in blood. At the alveolar capillary where the O2 concentration is high, O2 binds readily to the haemoglobin present. At tissue blood capillaries where the O2 concentration is low, the haemoglobin releases the O2 into the tissue. The oxygen-haemoglobin dissociation curve is used to express the relationship between the O2 concentration and whether the haemoglobin is acquiring or releasing O2 molecules.

CO2 is transported in blood in three ways. Most CO2 molecules are transported in the form of bicarbonate ions (HCO3-), about 10% are bound to haemoglobin and plasma proteins, and the remaining 5% are dissolved in plasma.

Lung ventilation

Lung ventilation is an essential part of respiration, responsible for the gas exchange between alveoli and the atmospheric air. It involves regularly replacing stale gases in the lungs with fresh gases from the atmosphere.

A simple physical model can help us better understand lung ventilation (Fig. 3.7). A suitable one is a modified pair of fireplace bellows with ‘extendable thoracic walls,’ an ‘airway,’ and a ‘total lung volume.’ A spring is added between the two handles of the bellow to mimic ‘elastic recoil force’. Another modification is that the model does not have a one-way valve, so the air enters and exits exclusively through the nozzle.

Fig. 3.7 The airway-lung-chest wall assembly can be mimicked by modified fireplace bellows.

Fig. 3.7 The airway-lung-chest wall assembly can be mimicked by modified fireplace bellows.

The respiratory system always has two opposite forces, one for lung expansion and the other for lung retraction. The lung volume is determined by the balance of the two forces. The lungs are inflated if the expansion force is greater than the retraction force, and they are deflated if the opposite occurs. The lung volume is unchanged if both forces are equal. At the end of expiration, the lung volume is stable at the resting position. This volume is called the functional residual capacity (FRC) (Fig. 3.8). FRC is critical for alveolar gas exchange.

Fig. 3.8 Functional residual capacity (FRC), tidal volume, and dead space.

Fig. 3.8 Functional residual capacity (FRC), tidal volume, and dead space.

Te: expiratory time: Ti; inspiratory time: VT; tidal volume.

During natural inspiration, the contraction of respiratory muscles (mainly the diaphragm) increases the chest volume, generating a temporary negative alveolar pressure (Palv). Air is sucked into the lungs, and is mixed with the gases present there. This inhaled gas volume is called the inspiratory tidal volume. During inspiration the elastic recoil force (shown as the stretched spring) is loaded.

During expiration, the respiratory muscles relax, and the elastic recoil force pulls the chest and lungs back to their resting position, generating a temporary positive Palv. A certain amount of gas is pushed out of the lungs. This expelled gas volume is called expiratory tidal volume. A breath must include both an inspiratory action and an expiratory action. Inspiratory and expiratory tidal volumes are roughly equal.

The tidal volume of every breath contains two parts. The part that participates in alveolar gas exchange is alveolar tidal volume. The other part that does not participate in the gas exchange is (anatomical) dead space. Dead space volume is always moved in or out first.

Dead space is inevitable. Do not forget it when setting and interpreting tidal volume or minute volume. During mechanical ventilation, the dead space usually increases due to the presence of the artificial airway. The effective alveolar ventilation is determined by the difference between the tidal volume and the total dead space. If the tidal volume is very close to, or equal to, the dead space volume, the alveolar ventilation is (nearly) zero, i.e. CO2 removal is (nearly) zero. This unwanted situation is known as dead space ventilation.

Note that after every breath, only a part of the alveolar gas is replaced.

In addition to defining ventilation in terms of a single breath, we can also define it over a minute interval (Fig. 3.9). When we talk about minute ventilation or minute volume, we need to define a few common respiratory terms:

  • Respiratory rate: The number of breaths occurring per minute;

  • Minute volume: The sum of the tidal volume (inspiratory or expiratory) of all breaths occurring per minute;

  • Alveolar ventilation: The sum of the alveolar tidal volume (inspiratory or expiratory) of all breaths occurring per minute.

Fig. 3.9 The relationship between minute volume, tidal volume, rate, and dead space.

Fig. 3.9 The relationship between minute volume, tidal volume, rate, and dead space.

The relationship can be expressed with a simple equation:

A l v e o l a r   m i n u t e   v o l u m e = R a t e × ( T i d a l   v o l u m e D e a d   s p a c e )

Regulation of respiration

Even under normal conditions, a human’s energy demand varies widely. Think about how much energy you need during sleep compared to during physical exercise. Biochemically these activities differ greatly in metabolic rate, O2 consumption, and CO2 production. There is no such thing as a normal value for energy demand.

On the other hand, it is physiologically important to maintain the arterial partial pressure of oxygen and carbon dioxide (PaO2, PaCO2), and pH within relatively narrow normal ranges even when energy demand changes. This is achieved through a control mechanism that automatically and precisely adapts the breathing pattern (i.e. rate and depth of breathing) to the current levels of PaO2, PaCO2, and pH. To a limited extent, we can freely change our breathing pattern.

This control mechanism uses a three-part sequence:

  1. a. Central and peripheral chemoreceptors detect the current O2, CO2, and pH in the blood and cerebrospinal fluid.

  2. b. The controller (respiratory centre) at the medulla and pons receives signals from the receptors, decides how to respond, and then sends the instruction to the effectors.

  3. c. The effectors (respiratory muscles) execute the commands received.

The mechanism responds to changes in PaCO2, PaO2, and arterial pH. Of these, PaCO2 is the primary stimulant. As Fig. 3.10 shows, increased PaCO2 results in sharply increased alveolar ventilation, and vice versa. In this manner, all three stimulants are normally maintained within their normal ranges even when O2 consumption and/or CO2 production changes drastically.

Fig. 3.10 Effect of increased arterial PCO2 and decreased arterial pH on the rate of alveolar ventilation.

Fig. 3.10 Effect of increased arterial PCO2 and decreased arterial pH on the rate of alveolar ventilation.

Reprinted with permission from Textbook of Medical Physiology, 8th edition, Guyton A.C., p447. Copyright (1990) with permission from Harcourt College Publishers and Elsevier Inc.

In most ventilated patients, this respiratory control mechanism remains intact. The mechanism plays a key role in respiratory distress syndrome, patient-ventilator asynchrony, and weaning. It may be abnormal in some neurological and neurosurgical patients.

3.2.3 Respiratory failure

In summary, respiration is a mechanism to maintain PaO2 and PaCO2 within their normal ranges even when energy demand fluctuates.

Respiratory failure refers to the syndrome where the respiratory system fails to maintain PaO2 or PaCO2 within normal ranges, that is PaO2 = 80–100 mmHg and PaCO2 = 35–45 mmHg (Table 3.1). Respiratory failure can occur due to severe functional impairment of the airway, lungs, chest wall, respiratory centre, respiratory nerves, and respiratory muscles for a variety of clinical reasons.

Table 3.1 Definition of normal and abnormal pH, PaO2, and PaCO2

Below normal

Normal ranges

Above normal

  • pH < 7.35

  • Acidosis

pH 7.35–7.45

  • pH > 7.45

  • Alkalosis

  • PaO2 < 80 mmHg

  • Hypoxaemia

PaO2 80–100 mmHg

  • PaO2 > 100 mmHg

  • Hyperoxaemia

  • PaCO2 < 35 mmHg

  • Hypocapnia

PaCO2 35–45 mmHg

  • PaCO2 > 45 mmHg

  • Hypercapnia

At this point, it is necessary to introduce two key terms. Hypoxia means that PaO2 is below 80 mmHg, while hypercapnia means that PaCO2 is above 45 mmHg.

Respiratory failure can be classified roughly into two types, type 1 and type 2.

Type 1 respiratory failure is also known as hypoxic respiratory failure or lung failure. Its primary feature is abnormally low PaO2 (<60 mmHg) but nearly normal PaCO2. Type 1 respiratory failure is typically caused by inadequate oxygenation when blood passes through the lungs due to: (a) ventilation/perfusion mismatch, (b) arteriovenous shunt, or (c) gas diffusion impairment.

Type 2 respiratory failure is also known as hypercapnic respiratory failure or pump failure. Its primary feature is abnormally high PaCO2 (>50 mmHg) and abnormally low PaO2 (<60 mmHg). Type 2 respiratory failure is typically caused by inadequate lung ventilation due to: (a) excessive airway resistance, (b) decreased respiratory drive, (c) respiratory muscle fatigue or failure, or (d) abnormal status of the lungs and chest wall.

The clinical signs of respiratory failure include tachypnoea, tachycardia, cyanosis, sweating, intercostal retractions, grunting, and nose flaring. Pulse oximetry and blood gas analysis can help diagnose respiratory failure. Note that these clinical signs are non-specific.

For simplicity, we can think of the pathophysiologic process of respiratory failure as having several steps (Fig. 3.11):

  1. a. The underlying diseases lead to deterioration in the efficiency and effectiveness of respiratory function.

  2. b. PaO2 tends to decrease and/or PaCO2 tends to increase.

  3. c. The patient strengthens their breathing efforts with the intention to maintain normal PaO2 and/or PaCO2.

  4. d. Increased breathing efforts further increase the energy demand.

Fig. 3.11 Respiratory failure is a downward spiral.

Fig. 3.11 Respiratory failure is a downward spiral.

If the patient can maintain normal PaO2 and PaCO2 with these intensified breathing efforts, the compensation is successful. If not, however, respiratory failure is inevitable.

Depending on the underlying diseases, both types of respiratory failure can be acute, with symptoms occurring rapidly; as in near drowning, asthma attack, respiratory arrest, drug overdose, upper airway obstruction, or chest and lung injury. Respiratory failure can also be progressive (chronic), as in emphysema, chronic bronchitis, or neuromuscular disease. For purposes of clinical treatment, it is important to differentiate between types 1 and 2, as shown in Table 3.2.

Table 3.2 Summary of respiratory failure


Type 1 respiratory failure

Type 2 respiratory failure

Other names

  • Hypoxic respiratory failure

  • Lung failure

  • Hypercapnic respiratory failure

  • Pump failure

Main feature

Hypoxia and normal PaCO2

Hypercapnia and hypoxia

Typical causes

  • Ventilation/perfusion mismatch

  • Arteriovenous shunt

  • Gas diffusion impairment

  • Excessive airway resistance

  • Decreased ventilator drive

  • Respiratory muscle fatigue or failure

  • Abnormal status of the lungs and chest wall

The treatment of respiratory failure typically involves: (a) oxygen therapy, (b) ventilatory support with a ventilator system or a continuous positive airway pressure (CPAP) system, (c) treatment of the underlying cause, and (d) other supporting measures, such as administration of fluids and nutrition. Acute respiratory failure is usually treated in an intensive care unit, while chronic respiratory failure is usually treated at home or in a long-term care facility.

3.3 Mechanical ventilation

3.3.1 What is mechanical ventilation?

Today, mechanical ventilation is the principal therapy used to treat severe respiratory failure caused by a serious disease or injury of any of the six key parts of respiratory system (i.e. the lungs, chest wall, airway, respiratory centre, respiratory nerves, and respiratory muscles).

If applied appropriately, this therapy effectively assists, supports, or replaces compromised natural lung ventilation, artificially satisfying the vital demands of respiration. This gives the clinician valuable time to treat the underlying diseases and improve the general condition of the patient.

In most cases, mechanical ventilation therapy is temporary, lasting several hours, days, or weeks. The therapy should be terminated as soon as the patient can breathe adequately on their own. The only exception is the patient with permanently damaged pulmonary function, who may be ventilator dependent for their entire life.

Is there a limit to what mechanical ventilation can accomplish?

This is a critical but seldom asked question. The answer is yes. Mechanical ventilation depends entirely on the residual functioning of the patient’s injured lungs. When the functionality of a patient’s lungs falls below a certain threshold, mechanical ventilation cannot help. In this case, ECMO (extracorporeal membrane oxygenation) should be used.

3.3.2 Three operating principles

As we noted in Chapter 1, mechanical ventilation can be realized with one of three principles: intermittent positive pressure ventilation (IPPV), intermittent negative pressure ventilation (INPV), and high-frequency ventilation (HFV). Let’s take a close look at each of these operating principles.

Intermittent positive pressure ventilation (IPPV)

With the IPPV principle, the patient’s respiratory system is integrated into the ventilator system. A positive pressure is applied intermittently to the patient’s airway. When the airway pressure is temporarily higher than the alveolar pressure, fresh gas is pushed into the lungs, the process of inspiration. When the airway pressure is lower than alveolar pressure, the gas is expelled out of the lungs, the process of expiration. Both inspiration and expiration are regulated by the operator’s settings. Fig. 3.12 shows a typical pressure waveform in IPPV.

Fig. 3.12 Pressure waveform in intermittent positive pressure ventilation (IPPV).

Fig. 3.12 Pressure waveform in intermittent positive pressure ventilation (IPPV).

IPPV is the common principle of most modern ventilators, whether invasive or non-invasive. Some popular IPPV ventilator models are shown in Fig 3.13.

Fig. 3.13 Some popular ICU ventilators based on the intermittent positive pressure ventilation (IPPV) principle.

Fig. 3.13 Some popular ICU ventilators based on the intermittent positive pressure ventilation (IPPV) principle.

Intermittent negative pressure ventilation (INPV)

With the INPV principle, the ventilated patient’s mouth and nose are open to the atmosphere so that gas can move in or out when alveolar pressure changes relative to atmospheric pressure. During inspiration, a negative pressure is applied to the surface of the chest wall, temporarily reducing the alveolar pressure. Fresh air is now sucked into the lungs. During expiration, the applied negative pressure is removed. The elastic recoil force temporarily generates a positive alveolar pressure, squeezing the stale gas out of the lungs. The driving pressure changes opposite to the way it does in IPPV. Fig. 3.14 shows a typical pressure waveform in INPV.

Fig. 3.14 Pressure waveform in intermittent negative pressure ventilation (INPV).

Fig. 3.14 Pressure waveform in intermittent negative pressure ventilation (INPV).

Two common ventilator designs are based on INPV (Fig. 3.15). The first is the famous iron lung, where a patient’s body, except for the head, is placed in a sealed gas container with rigid walls. A negative pressure is generated intermittently inside the container, resulting in inspiration and expiration. Different variations of the iron lung were developed during the 1920s and 1930s. They were used widely during the polio outbreaks in the 1940s and 1950s. The second type is the cuirass ventilator, in which a rigid shell or cuirass fits over the thoracic area only. An intermittent negative pressure is applied locally to change the thoracic volume.

Fig. 3.15 a) An iron lung, b) A cuirass ventilator.

Fig. 3.15 a) An iron lung, b) A cuirass ventilator.

(a) Poumon artificiel, Wikimedia Commons, accessed 6 October 2016, This image is in the public domain and thus free of any copyright restrictions. This media comes from the Centers for Disease Control and Prevention’s Public Health Image Library.

Today, INPV ventilators are used primarily for non-invasive ventilatory assistance.

High-frequency ventilation (HFV)

Both IPPV and INPV are regarded as ‘conventional’, because the tidal volume and respiratory rate are similar to physiological ones.

The third principle of mechanical ventilation is high-frequency ventilation. HFV uses a much higher respiratory rate (150 b/min or higher) than we see with the other types (Fig. 3.16). The tidal volume is much smaller than the physiological range, often smaller than dead space.

Fig. 3.16 During high-frequency ventilation (HFV), positive pressure or positive-negative pressure is applied to the airway opening at a very high rate.

Fig. 3.16 During high-frequency ventilation (HFV), positive pressure or positive-negative pressure is applied to the airway opening at a very high rate.

The mechanisms of gas transport and exchange in HFV are very different from IPPV and INPV, and are not well understood.

Due to the differences in deployed technologies, respiratory rate, ranges of pressure swings, and baseline pressure, HFV has evolved into five forms: (a) high-frequency positive pressure ventilation (HFPPV), (b) high-frequency jet ventilation (HFJV), (c) high-frequency flow interruption (HFFI), (d) high-frequency percussive ventilation (HFPV), and (e) high-frequency oscillatory ventilation (HFOV). HFJV and HFOV are the commonly used forms.

Clinically HFV is often applied in neonates. Sometimes it is also used to treat patients with ARDS, especially those who require very high positive airway pressures. HFV can be combined with conventional IPPV as well as surfactant therapy. Fig. 3.17 shows a typical high-frequency ventilator.

Fig. 3.17 3000A high-frequency oscillatory ventilator from CareFusion.

Fig. 3.17 3000A high-frequency oscillatory ventilator from CareFusion.

Image of 3100A Ventilator © 2014, CareFusion Corporation; Used with permission.

Of all the three principles, IPPV currently dominates. Unless otherwise specified, the term ‘mechanical ventilator’ in this book refers to a ventilator based on the IPPV principle.

3.3.3 IPPV pneumatic process

To recap, the objective of mechanical ventilation is to restore or maintain adequate lung ventilation by using artificial means to intermittently change lung volume. Mechanical ventilation requires a ventilator system, which will be described in depth in Chapters 4 and 5.

Pneumatically, a ventilator system can be regarded as having two pressure areas connected by an airway (Fig. 3.18). The pressure on the device side is called the airway opening pressure (Pao), and the pressure on the lung side is called the alveolar pressure (Palv). Both Pao and Palv fluctuate regularly during mechanical ventilation. If the ventilated patient is passive, Pao is actively changed, while Palv follows. If the patient is active, both Pao and Palv can change actively.

Fig. 3.18 A ventilator system has two pressure areas that are connected by an airway.

Fig. 3.18 A ventilator system has two pressure areas that are connected by an airway.

It is necessary to mention that a patient’s lungs are a dead-end structure. During inspiration, alveolar pressure rises as more and more gas enters the lungs. In a pressure-based breath, inspiratory flow drops to zero if Pao and Palv are equal at any level.

Under normal conditions of mechanical ventilation, at any time point Pao, Palv, and lung volume are determined by these forces (Fig. 3.19):

Fig. 3.19 The forces to inflate and deflate the lungs.

Fig. 3.19 The forces to inflate and deflate the lungs.

  • The inherent force to keep the lungs open, including that contributed by the chest wall, pleural negative pressure, and surfactant;

  • The inherent force to retract the lungs, mainly the elastic recoil force of the lungs and chest wall;

  • The external force to inflate the lungs, including contraction of inspiratory muscles and the application of a positive Pao;

  • Additional recoil force, which is generated when the lungs and chest wall are stretched. This is the force to pull the lung and chest wall back to the resting position. This situation is comparable to a stretched rubber band. Whenever the stretching force is removed, the recoil force causes the band to retract.

The lungs at their resting position

The lungs are at their resting position typically at the end of an adequate expiration. This is a static state with zero airway flow, because the inherent forces to open and retract the lungs are equal and there is no externally applied force. Note that in this position, the lungs are not totally empty, but instead contain a volume of gas known as the FRC. The FRC is physiologically important. Some lung diseases can cause FRC to abnormally increase (e.g. COPD) or decrease (e.g. ARDS).

The lungs at their inflated position

The inflated position of the lungs represents another static state with zero airway flow. Here the forces to inflate the lungs and the forces to deflate the lungs are equal. The lungs are at their inflated position in these two cases: (a) at the end of an adequate inspiration in a pressure-based breath, and (b) at the end of inspiration in a volume breath with inspiratory pause.


Inspiration is the process to increase lung volume. Typically it begins at the resting position and may or may not end at the inflated position. The process differs in pressure breaths and volume breaths.

In a pressure breath, Pao rises quickly to and stays at a preset level (Fig. 3.20). The pressure gradient is the greatest at the beginning, resulting in the maximum inspiratory flow. Over time, Palv increases as more and more gas enters the lungs. The pressure gradient diminishes, causing a corresponding drop in inspiratory flow. If the inspiration is sufficiently long, the lungs reach the inflated position.

Fig. 3.20 Typical Pao (orange), Palv (dotted white), and airway flow change during a pressure breath (a), and volume breath (b), in a passive patient.

Fig. 3.20 Typical Pao (orange), Palv (dotted white), and airway flow change during a pressure breath (a), and volume breath (b), in a passive patient.

In a volume breath with constant flow, the most common inspiratory flow pattern, the applied positive Pao pushes gas into the lungs at a constant, defined inspiratory flow. The applied Pao must increase steadily to maintain the required pressure gradient. At the end of inspiration, the lungs do not reach their inflated position unless an inspiratory pause is imposed.


Expiration is the process to decrease lung volume. The applied positive Pao drops suddenly to the baseline. The additional recoil force causes the lungs to retract. The pressure gradient (Palv > Pao) pushes the gas out. Over time, Palv and the resultant expiratory flow decrease. The lungs return to their resting position if sufficient expiratory time is allowed. The expiration process is the same in both pressure and volume breaths.

In spontaneously breathing patients

So far, we have discussed the four driving forces, the lung resting and inflated positions, and the inspiration and expiration processes. All of them share the same condition: the patient is passive. In reality, however, many ventilated patients are actively breathing. But the situation is more complicated than that. We know there are two external forces to inflate the lungs, the applied positive Pao and the negative Palv caused by contraction of inspiratory muscles. A similar situation may also be present at expiration, as the contraction of expiratory muscles generates additional positive Palv. This gives us six forces altogether (Table 3.3).

Table 3.3 The six physical forces involved in mechanical ventilation


Lung inflating forces

Lung deflating forces

Lung at resting position (with FRC)

Inherent force to keep the lungs open

Inherent recoil force to retract the lungs

Lung tidal volume change

Applied positive Pao to expand the lungs

Additional recoil force to bring the lungs back to the resting position

Active patients only

Contraction of inspiratory muscles to enlarge the chest cavity and lower Palv

Contraction of expiratory muscles to reduce the chest cavity and raise Palv

Ideally, the patient’s breathing efforts synchronize with the intermittently applied positive Pao for inspiration and expiration. If not, a troubling phenomenon called patient-ventilator asynchrony or ‘patient-ventilator fight’ is inevitable.

3.3.4 Comparison of natural and mechanical ventilation (IPPV)


The ultimate goal of lung ventilation, for both natural and mechanical ventilation, is to alternately increase and decrease the lung volume.

Both natural and mechanical ventilation are realized through the natural pulmonary system, although the functioning of this system is often deteriorated in mechanically ventilated patients. The direction of gas movement during inspiration and expiration is the same for both forms of lung ventilation.

Natural and mechanical expiration are similar. In both cases, the elastic recoil force generates a positive Palv, and the gradient (Palv > Pao) drives the gas out of lungs.


With natural ventilation, gas exchange occurs directly between the human’s lungs and the atmosphere. With mechanical ventilation, the patient’s airway and lungs are integrated into a ventilator system. The patient breathes exclusively through the connected ventilator, isolated from atmospheric air.

With natural inspiration, the contraction of inspiratory muscles generates a negative Palv. The pressure gradient (Palv < Pao) sucks air into the lungs. With mechanical inspiration, a positive Pao is applied, and the pressure gradient (Pao > Palv) pushes the gas into the lungs.

Normally, the FRC is related to the balance of the inherent lung inflation/deflation forces. During mechanical ventilation, a moderate level of PEEP (3–5 cmH2O) is frequently used. It can be regarded as an addition to the inherent force to inflate the lungs, leading to an increased FRC.

With natural ventilation, the respiratory centre automatically and precisely regulates respiratory rate and breath intensity to satisfy current physiological demand. With mechanical ventilation, however, an operator must set the mechanical breath rate and intensity. Ventilator settings often require readjustment to meet the patient’s changing metabolic demands and lung conditions. Actively breathing patients may refuse to accept the imposed ventilation, including the rate, tidal volume, and inspiratory pressure, causing patient-ventilator asynchrony.