Anatomic and physiologic dead space

Last updated: February 23, 2023

Anatomic and physiologic dead space

Cardiothoracic Disease

Cardiothoracic Disease

Respiratory system anatomy and physiology
Lung volumes and capacities
Anatomic and physiologic dead space
Ventilation
Alveolar gas equation
Compliance of lungs and chest wall
Combined pressure-volume curves for the lung and chest wall
Alveolar surface tension and surfactant
Airflow, pressure, and resistance
Breathing cycle
Breathing control
Pulmonary chemoreceptors and mechanoreceptors
Ideal (general) gas law
Boyle's law
Dalton's law
Henry's law
Fick's laws of diffusion
Graham's law
Diffusion-limited and perfusion-limited gas exchange
Hypoxia
Oxygen binding capacity and oxygen content
Oxygen-hemoglobin dissociation curve
Erythropoietin
Carbon dioxide transport in blood
Regulation of pulmonary blood flow
Zones of pulmonary blood flow
Pulmonary shunts
Ventilation-perfusion ratios and V/Q mismatch
Pulmonary changes during exercise
Pulmonary changes at high altitude and altitude sickness
Diffuse parenchymal lung disease: Clinical
Restrictive lung diseases: Pathology review
Restrictive lung diseases
Idiopathic pulmonary fibrosis
Sarcoidosis
Lung cancer: Clinical
Lung cancer and mesothelioma: Pathology review
Mesothelioma
Cardiovascular system anatomy and physiology
Lymphatic system anatomy and physiology
Cardiac cycle
Normal heart sounds
Abnormal heart sounds
Blood pressure, blood flow, and resistance
Resistance to blood flow
Laminar flow and Reynolds number
Compliance of blood vessels
Pressures in the cardiovascular system
Physiological changes during exercise
Cardiovascular changes during hemorrhage
Cardiovascular changes during postural change
Measuring cardiac output (Fick principle)
Cardiac and vascular function curves
Altering cardiac and vascular function curves
Stroke volume, ejection fraction, and cardiac output
Frank-Starling relationship
Pressure-volume loops
Changes in pressure-volume loops
Cardiac work
Cardiac preload
Cardiac afterload
Law of Laplace
Baroreceptors
Renin-angiotensin-aldosterone system
Chemoreceptors
Cardiac conduction system
Action potentials in pacemaker cells
Action potentials in myocytes
Cardiac conduction velocity
Excitability and refractory periods
Cardiac excitation-contraction coupling
Cardiac contractility
Cerebral circulation
Coronary circulation
Control of blood flow circulation
Microcirculation and Starling forces
Cardiomyopathies: Clinical
Cardiomyopathies: Pathology review
Hypertrophic cardiomyopathy
Dilated cardiomyopathy
Restrictive cardiomyopathy
Sleep apnea
Apnea of prematurity
Aortic aneurysms and dissections: Clinical
Aortic dissections and aneurysms: Pathology review
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Marfan syndrome
Peripheral vascular disease: Clinical
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Vasculitis: Pathology review
Vasculitis
Kawasaki disease
Behcet's disease
Nutcracker syndrome
Superior mesenteric artery syndrome
Subclavian steal syndrome
Coronary steal syndrome
Lymphedema
ECG basics
ECG normal sinus rhythm
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ECG QRS transition
ECG cardiac hypertrophy and enlargement
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Heart blocks: Pathology review
Premature ventricular contraction
Premature atrial contraction
Atrial fibrillation
Atrial flutter
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Wolff-Parkinson-White syndrome
Atrioventricular block
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Long QT syndrome and Torsade de pointes
Ventricular tachycardia
Brugada syndrome
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Class II antiarrhythmics: Beta blockers
Class III antiarrhythmics: Potassium channel blockers
Class IV antiarrhythmics: Calcium channel blockers and others
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Adrenergic antagonists: Presynaptic
cGMP mediated smooth muscle vasodilators
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Heart failure: Clinical
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Cor pulmonale
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Pulmonary edema
Anatomy of the coronary circulation
Asthma: Clinical
Obstructive lung diseases: Pathology review
Asthma
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Alpha 1-antitrypsin deficiency
Bronchodilators: Beta 2-agonists and muscarinic antagonists
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Non-corticosteroid immunosuppressants and immunotherapies
Cystic fibrosis: Pathology review
Cystic fibrosis
Bronchiectasis
Anatomy of the heart
Anatomy clinical correlates: Heart
Cardiac muscle histology
Marfan syndrome
Ehlers-Danlos syndrome
Arteriole, venule and capillary histology
Cardiac muscle histology
Artery and vein histology
Trachea and bronchi histology
Bronchioles and alveoli histology
Nasal cavity and larynx histology
Coarctation of the aorta
Mitral valve disease
Pulmonary valve disease
Tricuspid valve disease
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Ventricular arrhythmias: Pathology review
Supraventricular arrhythmias: Pathology review
Coronary artery disease: Clinical
Atherosclerosis and arteriosclerosis: Pathology review
Coronary artery disease: Pathology review
Arterial disease
Angina pectoris
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Myocardial infarction
Prinzmetal angina
Coronary steal syndrome

Transcript

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The main job of the lungs is gas exchange, pulling oxygen into the body and getting rid of carbon dioxide.

Normally, during an inhale - the diaphragm and chest muscles contract to pull open the chest and that sucks in air like a vacuum cleaner, and then during an exhale - the muscles relax, allowing the lungs to spring back to their normal size pushing that air out.

But as it turns out, not all the air that we breathe in, ends up participating in gas exchange.

As we inhale, air enters the nasal cavity or the oral cavity and travels down the trachea and then splits into the two mainstem bronchi and enters the two lungs.

Within the lungs, the bronchi divide into progressively smaller and smaller bronchioles until air gets down to tiny thin-walled air-sacs called alveoli which are surrounded by tiny capillaries. This is the site of gas exchange.

So, the part of the respiratory tree prior to these alveoli, starting from the nose, or the mouth, right up to the tiny terminal tiny bronchioles without these alveoli, merely acts to conduct or transport air to the alveoli. This part is known as the conducting zone and it does not take part in gas exchange.

The volume of air contained in this conducting zone is known as anatomic dead space.

‘Dead’ sounds kind of ominous but it basically reflects the fact that this air is as good as dead to the body, because you can’t extract oxygen from it.

Anatomic’ means that this dead space is inbuilt within the anatomy of the respiratory system and doesn’t really change; no matter what we do, we cannot ever use this air for gas exchange.

Alright, so now let’s simplify all this—so this ball represents all the alveoli, and this portion represents all of the conducting zone, in other words the anatomic dead space. So how much air is part of this anatomic dead space?

A normal person, when breathing quietly without any active effort, takes in about 500 ml or half a liter of air - this is the tidal volume, represented by these three blocks.

Almost a third of this tidal volume or about 150 ml is trapped in this anatomic dead space, and the remaining 350 mL or so is used for gas exchange.

OK so let’s go way back to when an infant is born, at this point there’s no air inside the lungs, so the alveolar air sacs are completely collapsed.

As the baby takes its first breath, new oxygenated air rushes in through the respiratory tree and inflates the alveoli, but about a third of the air is left in the anatomic dead space, shown in orange, but we’ll keep it half purple since it’s still oxygenated air.

Those purple blocks then participate in gas exchange, converting them to old deoxygenated air, shown in green.

As the baby starts to exhale air for the first time, this dead space air which did not participate in gas exchange is the first to be exhaled out, and the conducting zone gets filled with air from the alveoli which has already taken part in gas exchange and given its oxygen to the body.

During the next inhalation, it’s this old green deoxygenated air that re-enters the alveoli first, and it’s joined by fresh oxygenated purple air from the new tidal volume.

The dead space gets filled with fresh air that has just been breathed in.

This goes on for every subsequent breath cycle throughout the life of the person.

So to summarize, if you sample the dead space air after a person has just inhaled, then the dead space air would be fresh air from the environment, and if you sample the air sample of air from the dead space after a person has just exhaled, then the air would be from the alveoli.

So to gauge how effectively gas exchange is taking place in the lungs, it’s important to time it just right, and take an air sample from the dead space at the end of exhalation.

Now, so far, we’ve been assuming that the air that manages to reach the alveoli is able to participate in gas exchange. Unfortunately, that’s not always the case.

Some alveoli may have an inadequate blood supply, so when these alveoli get filled with air fresh purple air, they are well-ventilated, but not well perfused. This is known as a ventilation-perfusion defect.

In this situation, the oxygen in the purple air doesn’t functionally make its way into the blood, so some of this air also ends up being dead space air, but this time we call it alveolar dead space, and together we call these the physiologic dead space.

The term ‘physiologic’ refers to all the air that is physiologically inaccessible to the body due to anatomic and functional reasons.

Okay so now that one block of accessible fresh purple air gets exchanged, and then this gets exhaled, we can actually now use some fancy equations to calculate the volume of physiological dead space of the exhaled air, which we’ll say is V sub D for dead space, but first there are a couple important assumptions.

First, we assume that there’s no CO2 in the environment air, the actual figure is about 0.04%, so zero is not too far off the mark, and remember that this is the purple boxes here since that air came from the environment but was never exchanged.

Assumption number two is that none of the CO2 was contributed from the dead space, so based on assumptions 1 and 2, the purple and orange blocks have zero CO2.

That leads to the third assumption, all the CO2 in exhaled air comes only from functioning alveoli, i.e. this last green block.

Now, if the tidal volume is VT , the volume of air trapped in the physiological dead space is VD , and the volume of air present in the functioning alveoli is VA. From this, it’s pretty clear that

				VT = VD + VA

Let’s label the concentration of CO2 in the tidal volume as CT and the concentration of CO2 in the alveolar air as CA .

Now, if you take a volume in mL and multiply by the concentration in say mg / ml, then you end up with the total amount of that something M, in this case in mg.

Now, that means that the total amount of CO2 in the alveoli is the volume VA times the concentration, CA.

CA X VA

Sources

  1. "Medical Physiology" Elsevier (2016)
  2. "Physiology" Elsevier (2017)
  3. "Human Anatomy & Physiology" Pearson (2018)
  4. "Principles of Anatomy and Physiology" Wiley (2014)
  5. "Relationship between the humidity and temperature of inspired gas and the function of the airway mucosa" Critical Care Medicine (1996)
  6. "An Algebraic Solution to Dead Space Determination According to Fowler's Graphical Method" Computers and Biomedical Research (1999)