Vital Capacity - an overview (2023)

The vital capacity (VC) is defined as the total volume of air that can be displaced from the lungs by maximal expiratory effort.

From: Handbook of Clinical Neurology, 2013

Related terms:

  • Respiratory Failure
  • Lung Volumes
  • Functional Residual Capacity
  • Thoracic Wall
  • Respiratory Muscle
  • Forced Expiratory Volume
  • Forced Vital Capacity
  • Residual Volume
  • Total Lung Capacity
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Pulmonary Function Testing : Physiologic and Technical Principles

V. Courtney Broaddus MD, in Murray & Nadel's Textbook of Respiratory Medicine, 2022

Vital Capacity and Other Static Lung Volumes

The measurement of VC requires the subject to inhale as deeply as possible and then to exhale fully, taking as much time as required.Figure 31.2 illustrates the subdivisions of lung volume.20 The measurement can also be obtained by adding two of its components: theexpiratory reserve volume (ERV), obtained by having the subject exhale maximally from the resting end-tidal level; and theinspiratory capacity (IC), obtained by having the subject inspire fully from the resting end-tidal level. The sum of these two measurements yields the “combined VC”; as long as the resting end-tidal lung volume is the same for the two component maneuvers, the combined VC and the VC are equal. In patients with severe airflow obstruction, the combined VC appears to be larger than the VC, suggesting the presence of poorly ventilated regions of lungs, or so-called trapped gas. This result probably reflects increased transmural pressure, which tends to cause airway closure during a large portion of the single maneuver—but only in the portion near RV during the combined VC maneuver.

A similar inference can be made by comparing the “slow VC” (performed without regard to time) and FVC, or by comparing inspired VC (maximal volume inhaled from RV to TLC) with the expired VC maneuver just described. Except for those subdivisions involving RV, each of the defined volumes can be recorded and measured by simple spirometry. The RV can be measured only by indirect methods (e.g., nitrogen [N2] washout, helium (He) dilution, or body plethysmography).Figure 31.2 illustrates the fact that VC can be decreased in two different ways: by a decrease in TLC or by an increase in RV. Only by measuring RV and TLC can these two causes be differentiated.

Control of Ventilation and Respiratory Muscles

Theodoros Vassilakopoulos, in Clinical Respiratory Medicine (Fourth Edition), 2012

Vital Capacity

Vital capacity (VC) is easily measured with spirometry; decreases in VC point to respiratory muscle weakness. The VC averages approximately 50mL/kg in normal adults. VC changes are not specific, however, and decreases may result from both inspiratory and expiratory muscle weakness and may be associated with restrictive lung and chest wall diseases. A marked fall (of greater than 30%) in VC in the supine compared with that in the erect posture (which in the normal person is 5% to 10%) is associated with severe bilateral diaphragmatic weakness.

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(Video) Lung Function - Lung Volumes and Capacities

Pulmonary Function Testing

Grant C. Fowler MD, in Pfenninger and Fowler's Procedures for Primary Care, 2020

Vital Capacity

80%–120% of predicted valueNormal
70%–79% of predicted valueMild reduction
50%–69% of predicted valueModerate reduction
<50% of predicted valueSevere reduction

Again, restrictive lung disease is characterized by reduced vital capacity and relatively normal airflow rates. If obstruction is present (see below), the reduction in vital capacity may only be reported as “probably secondary to obstruction” if the severity of the reduced vital capacity and that of the obstructive findings are approximately equal. In comparing vital capacities obtained at different times (including those obtained before and after bronchodilator administration), the expiratory time must be considered and compared. The raw curves should also be compared.

Perioperative Management

Kimberly M. Hamilton, Gregory R. Trost, in Benzel's Spine Surgery, 2-Volume Set (Fourth Edition), 2017

Pulmonary Function Testing and Spirometry.

The vital capacity (VC) is the maximum volume expired after a maximum inspiration. VC is decreased in restrictive disease but is usually normal in obstructive disease. A VC that is less than 50% of predicted indicates severe disease. The forced expiratory volume is the maximum volume expired after a maximum inspiration. Forced expiratory volume equals VC in restrictive disease but is less than VC in obstructive disease. Patients undergoing head and neck or spine surgeries with unexplained dyspnea or pulmonary symptoms should undergo preoperative pulmonary function tests. Spirometry can assist in identifying high-risk patients and procedures. Patients with forced expiratory volume or forced vital capacity measured less than 70% of expected are at higher risk for postoperative pulmonary complications.60

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Pulmonary Function Testing : Interpretation and Applications

V. Courtney Broaddus MD, in Murray & Nadel's Textbook of Respiratory Medicine, 2022

Obstructive Ventilatory Defect

Obstruction to airflow is characterized by a decrease in FEV1/FVC, reduced FEV1, normal (or reduced) FVC, normal (or reduced)vital capacity (VC), and a decrease in measures that may reflect small airway disease (Table 32.2). It is also characterized by an upward concavity in the expiratory flow-volume curve (also described as curvilinear) (Fig. 32.2). Supplementary data supporting airflow obstruction include increasedresidual volume (RV), RV/total lung capacity (TLC) ratio andairway resistance (Raw), uneven distribution of ventilation, and significant reversibility of airflow obstruction, with or without decreased diffusing capacity. Examples of diseases that manifest with airflow obstruction are shown ineTable 32.1.

eTable 32.1. Examples of Diseases Resulting in the Major Pulmonary Function Test Patterns



Bronchial asthma

Acute bronchitis



Cystic fibrosis

Alpha1-antitrypsin deficiency

Bronchiolitis obliterans

Associated with connective tissue disease

After allogeneic hematopoietic stem-cell transplantation

After lung transplantation

Drug toxicity



Interstitial lung disease

Idiopathic pulmonary fibrosis

Nonspecific interstitial pneumonitis



Eosinophilic pneumonia



Congestive heart failure

Drugs (amiodarone, methotrexate, nitrofurantoin)






Ankylosing spondylitis

Respiratory muscle weakness

Guillain-Barré syndrome

Amyotrophic lateral sclerosis

Muscular dystrophy

Myasthenia gravis

Diaphragmatic paralysis


Pleural disease (rheumatoid arthritis, asbestosis, fibrothorax)

Lung resection


Cystic fibrosis


Pulmonary Langerhans cell histiocytosis


Hypersensitivity pneumonitis

Congestive heart failure

(Video) Respiratory | Spirometry: Lung Volumes & Capacities


Sue Ann Sisto PT, MA, PhD, Kim Ratner PT, BS, in Spinal Cord Injuries: Management and Rehabilitation, 2009

Vital Capacity

VC is the maximal volume of gas that can be expelled from the lungs after a maximal inhalation or a full breath. An incentive spirometer is used to obtain this measurement (Figure 6-9, A). If the patient has a tracheostomy tube in place or has difficulty channeling air out of his mouth as opposed to his nose, assistance may be given to block the tracheostomy tube or close the nose shut while he exhales. Nose clips are also available that will gently pinch off the nose to avoid nasal air leakage when mouth expiration is required (Figure 6-9, B). It is important to note the patient's position and whether he is wearing an abdominal binder when testing VC. To get an accurate physiological measure, it is best to first measure the patient without the abdominal binder. Then another measure may be taken with the binder to determine if there is any improvement.

The resting position of the diaphragm is higher in supine position than it is in a short sit position (SSP); therefore patients with SCI will tend to have a higher VC in the supine position. The supine position allows for greater potential excursion of the diaphragm. In the SSP, the diaphragm is lower due to gravity (unless an abdominal binder is worn) and therefore has a small potential excursion distance. To ensure a good test, the clinician needs to provide active forceful coaching until three acceptable maneuvers are obtained. An acceptable maneuver is defined as a quick and forceful start with no coughing, especially during the first second, no early termination of expiration, no variable flows, and good reproducibility and consistency of effort.9

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Chronic Obstructive Pulmonary Disease

Howard J. Miller MD, in Anesthesia Secrets (Fourth Edition), 2011

(Video) Spirometry, Lung Volumes & Capacities, Restrictive & Obstructive Diseases, Animation.

11 How do general anesthesia and surgery affect pulmonary mechanics?

Vital capacity is reduced by 25% to 50%, and residual volume increases by 13% following many general anesthetics and surgical procedures. Upper abdominal incisions and thoracotomy affect pulmonary mechanics the greatest, followed by lower abdominal incisions and sternotomy. Expiratory reserve volume decreases by 25% after lower abdominal surgery and 60% after upper abdominal and thoracic surgery. Tidal volume decreases 20%, and pulmonary compliance and functional residual capacity decrease 33%. Atelectasis, hypoventilation, hypoxemia, and pulmonary infection may result. Many of these changes require a minimum of 1 to 2 weeks to resolve.

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Pulmonary Vascular Abnormalities

Claire L. Shovlin PhD, James E. Jackson MBBS, in Murray and Nadel's Textbook of Respiratory Medicine (Sixth Edition), 2016

Pulmonary Function.

Vital capacity is generally normal.68-72 There is no airflow obstruction unless a second pathology such as asthma or COPD is present.68,77 With large R-L shunts (>20%), the carbon monoxide diffusing capacity (DlCO) is often moderately reduced (71% to 78%),68,71 but in the majority of patients with less R-L shunting, DlCO is equal to or greater than 90% of predicted (interquartile range, 76% to 100%).72 Patients with the lowest DlCO values generally have widespread and small vascular malformations.

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Acute Neuromuscular Respiratory Failure in Myasthenia Gravis and Guillain-Barré Syndrome

Osman Samil Kozak, Eelco F.M. Wijdicks, in Critical Care Medicine (Third Edition), 2008


Vital capacity (VC), the volume of exhaled air after maximal inspiration, normally is 60 to 70 mL/kg and in normal persons is determined primarily by the size of the thorax and lungs. Reduction of VC to 30 mL/kg is associated with weak cough, accumulation of oropharyngeal secretions, atelectasis, and hypoxemia. Another measure of respiratory muscle strength is the ability to generate negative pressure with inspiratory effort. In normal persons, respiratory muscles cause pleural and alveolar pressures to change by approximately 3 cm H2O during the breathing cycle. Maximal pressure generation can be determined by blocking the upper airway and recording mouth pressure changes during inspiratory effort. Maximal negative inspiratory pressures (NIPs) generated by adults average −114 cm H2O in young men and −67 cm H2O in young women (normal, exceeding −70 cm H2O). Forced expiratory pressures average 160 cm H2O in young men and 95 cm H2O in young women (normal, greater than 100 cm H2O). This means that the respiratory muscles are capable of generating more than 30 times the amount of force necessary for tidal breathing.4 NIP measures the strength of the diaphragm and other muscles of inspiration and reflects the ability to maintain normal lung expansion and avoid atelectasis. Positive expiratory force (PEF) measures strength of the muscles of expiration, and correlates with strength of cough and ability to clear secretions from the airway3 (Box 65-1).

(Video) Lung Volumes and Capacities

A simple bedside test, asking patients to count to 20 without the need of an additional respiration, may identify early weakness.

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Physiology and Testing of Respiratory Muscles

Theodoros Vassilakopoulos, Charis Roussos, in Clinical Respiratory Medicine (Third Edition), 2008

Testing Respiratory Muscle Function

Muscles have two functions: to develop force and to shorten. In the respiratory system, force is usually estimated as pressure and shortening as lung volume change. Thus, quantitative characterization of the respiratory muscles usually relies on measurements of volumes and pressures.

Vital Capacity

Vital capacity (VC) is an easily obtained measurement with spirometry, which, when decreased, points to respiratory muscle weakness. The VC averages approximately 50 mL/kg in normal adults. However, VC is not specific and may be decreased because of both inspiratory and expiratory muscle weakness and restrictive lung and chest wall diseases. A marked fall (>30%) in VC in the supine compared with the erect posture (which in the normal individual is 5–10%) is associated with severe bilateral diaphragmatic weakness.

Maximal Static Mouth Pressures

Measurement of the maximum static inspiratory (PI,max) or expiratory (PE,max) pressure that a subject can generate at the mouth is a simple way to estimate inspiratory and expiratory muscle strength. These are measured at the side port of a mouthpiece that is occluded at the distal end. A small leak is incorporated to prevent glottic closure and buccal muscle use during inspiratory or expiratory maneuvers. The inspiratory and expiratory pressure must be maintained, ideally for at least 1.5 sec, so that the maximum pressure sustained for 1 sec can be recorded (Figure 8-3). The pressure measured during these maneuvers (Pmo) reflects the pressure developed by the respiratory muscles (Pmus), plus the passive elastic recoil pressure of the respiratory system including the lung and chest wall (Prs) (Figure 8-4). At FRC, Prs is 0 so that Pmo represents Pmus. However, at residual volume (RV), where PI,max is usually measured, Prs may be as much as 30 cm H2O, and thus makes a significant contribution PI,max of up to 30% (or more if Pmus is decreased). Similarly, PE,max is measured at total lung capacity (TLC), where Prs can be up to 40 cm H2O. Clinical measures and normal values of PI,max and PE,max do not conventionally subtract the elastic recoil of the respiratory system. Normal values are available for adults, children, and the elderly. The tests are easy to perform and are well tolerated. However, the measurements exhibit significant between-subject and within-subject variability, as well as learning effect (values obtained improve as subjects become accustomed to the maneuvers). The normal ranges are wide, so that values in the lower quarter of the normal range are compatible both with normal strength and with mild or moderate weakness. However, a PI,max of −80 cm H2O usually excludes clinically important inspiratory muscle weakness. Values less negative than this are difficult to interpret, and more detailed studies are required. A normal PE,max with a low PI,max suggests isolated diaphragmatic weakness.

Transdiaphragmatic Pressure

When inspiratory muscle weakness is confirmed, the next diagnostic step is to unravel whether this is due to diaphragmatic weakness, because the diaphragm is the most important inspiratory muscle. This is accomplished by the measurement of maximum transdiaphragmatic pressure (Pdi,max). Pdi,max is the difference between gastric pressure (reflecting abdominal pressure) and esophageal pressure (reflecting intrapleural pressure) on a maximum inspiratory effort after the insertion of appropriate balloon catheters in the esophagus and the stomach, respectively.

Sniff Pressures

A sniff is a short, sharp voluntary inspiratory maneuver performed through one or both unoccluded nostrils. It achieves rapid, fully coordinated recruitment of the diaphragm and other inspiratory muscles. The nose acts as a Starling resistor, so that nasal flow is low and largely independent of the driving pressure that is the esophageal pressure. Pdi measured during a sniff (Pdi,sn,max) reflects diaphragm strength, and Pes reflects the integrated pressure of the inspiratory muscles on the lungs (Figure 8-5). Pressures measured in the mouth, nasopharynx, or one nostril give a clinically useful approximation to esophageal pressure during sniffs without the need to insert esophageal balloons, especially in the absence of significant obstructive airway disease. To be useful as a test of respiratory muscle strength, sniffs need to be maximal, which is relatively easy for most willing subjects, but may require some practice. The nasal sniff pressure is the easiest measurement for the subject. Pressure is measured by wedging a catheter in one nostril by use of foam, rubber bungs, or dental impression molding (Figure 8-6). The subject sniffs through the contralateral unobstructed nostril. There is a wide range of normal values, reflecting the wide range of normal muscle strength in different individuals. In clinical practice, Pdi,sn,max values greater than 100 cm H2O in males and 80 cm H2O in females are unlikely to be associated with clinically significant diaphragm weakness. Values of maximal sniff esophageal or nasal pressure numerically greater than 70 cm H2O (males) or 60 cm H2O (females) are also unlikely to be associated with significant inspiratory muscle weakness. However, these reflect the integrated pressure of all the inspiratory muscles, and it is possible that there could be a degree of weakness of one or more of these muscle groups that would not be detected at this level. In chronic obstructive pulmonary disease, nasal sniff pressure tends to underestimate sniff esophageal pressure because of dampened pressure transmission from the alveoli to the upper airway but can complement PI,max in excluding weakness clinically.

Electrophysiologic Testing

The next diagnostic step consists of determining whether weakness is due to muscle, nerve, or neuromuscular transmission impairment. This requires the measurement of Pdi in response to bilateral supramaximal phrenic nerve electrical or magnetic stimulation, with concurrent recording of the elicited electromyogram (EMG) of the diaphragm (called the compound muscle action potential, CMAP) with either surface or esophageal electrodes (Figure 8-7). If the phrenic nerve is stimulated, the diaphragm contracts. This contraction is called a twitch. If the stimulus is intense enough, all phrenic fibers are activated synchronously giving reproducible results. The intensity of the twitch increases with the frequency of stimulation. If multiple impulses stimulate the phrenic nerve, the contractions summate to cause a tetanic contraction. Thus, if both phrenic nerves are stimulated with various frequencies (1, 10, 20, 50, and 100 Hz) at the same lung volume with closed airway (to prevent entry of air and thus changes in lung volume and initial length of the diaphragm), the isometric force-frequency curve of the diaphragm is obtained (Figure 8-8). (It should be noted that the usual rate of motor nerve discharge during voluntary muscle contraction in humans is between 5 and 15 Hz, and, because of the steep shape of the force-frequency curve in this range, small alterations in the discharge rate cause significant changes in the force produced. Maximum voluntary contractions, such as the PI,max are achieved with discharge rates higher than 50 Hz, but cannot be sustained for long. Stimulation of the phrenic nerve with high frequencies is technically difficult to achieve (because of displacement of the stimulating electrode by local contraction of the scalene muscles and movement of the arm and shoulder because of activation of the brachial plexus). Therefore, the transdiaphragmatic pressure developed in response to single supramaximal phrenic nerve stimulations at 1 Hz, called the twitch Pdi, is commonly measured.

Although technically demanding, this approach has the great advantage of being independent of patient effort/motivation. This also allows for the measurement of phrenic nerve conduction time or phrenic latency (i.e., the time between the onset of the stimulus and the onset of CMAP [Mwave] on the diaphragmatic EMG) (Figure 8-7, B). A prolonged conduction time suggests nerve involvement.

However, electrophysiologic testing also has shortcomings. Although the conduction time or latency is prolonged in neuropathies that are predominantly demyelinating, it may be preserved in neuropathies that are predominantly axonal despite substantial diaphragm weakness. Moreover, when the preceding technique is used, it is important that costimulation of the brachial plexus be avoided, otherwise the action potential recorded from surface electrodes may originate from muscles other than the diaphragm. This problem is compounded if the phrenic nerve is stimulated by use of a magnetic technique. Classically, an axonal neuropathy is characterized by the finding of preserved latencies with diminished CMAP. Lack of CMAP after nerve stimulation is an indication of paralysis with the lesion located proximal to or at the neuromuscular junction. Decreased twitch Pdi in the face of normal CMAP is characteristic of contractile dysfunction that resides within the muscle.

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