Upon completion of this course, you will be able to:

• Identify the basic elements of blood gas studies.
• Explain how the results are analyzed, and how that information is used in health care.
• List and discuss the range of blood gas values that are considered "normal" and "abnormal".
• Identify blood gas analyzers and explain their function.

Arterial blood gas analysis has become an essential skill for all healthcare practitioners. It provides important information with regard to adequacy of ventilation, oxygen delivery to the tissues and acid–base balance. Although each patient’s clinical presentation will be judged individually, situations that warrant analysis of a blood gas sample include respiratory compromise, post-cardiorespiratory arrest, evaluation of interventions such as oxygen therapy, respiratory support and as a baseline before surgery.

Assessment of arterial blood gas has been the gold standard for determining carbon dioxide and oxygen levels. Interpretation of acid-base disturbances is an essential skill for critical care nurses. Understanding acid-base disturbances is essential in the care of the critically ill patient. Through a systematic evaluation of patient symptoms and arterial blood gas values, patient care can be improved. In addition, blood gases are the most common and one of the most important laboratory values performed in the neonatal intensive care unit.

In this course we will review Blood Gas Basics, all the aspects of gas exchange and Acid-Base Balance, including O2 transport, ventilation, control of respiration, and a generalized summary - animals utilize O2 and produce CO2 + heat = occurs in the mitochondria - for cellular respiration to occur, must be a steady supply of O2 and CO2 must be steadily removed. There will be some overlap since the topics are all intertwined.

Close relationship between interdependence of plants and animals e.g. plants produce O2 as a result of photosynthesis (however, can only occur during daylight) and the interconnectedness between the physical, chemical and biological aspects to life (e.g. O2 level in water, ice and atmosphere - "circle of life".

Note: balance of atmospheric gases, the needs of both animal & plants is in some way delicate & can be disturbed/disrupted via man's activities i.e. think about the environmental contaminants assignment. However, first we should review some basics of Respiration:

Arterial blood gases:
Measurement of the pH level and the oxygen and carbon dioxide concentrations in arterial blood; important in diagnosis of many respiratory diseases

Alternative meaning:
Arterial blood gas A test which analyses arterial blood for oxygen, carbon dioxide and bicarbonate content in addition to blood pH.

Used to test the effectiveness of respiration.

Acronym: ABG

pH: <chemistry> The symbol relating the hydrogen ion concentration or activity of a solution to that of a given standard solution.

Numerically the pH is approximately equal to the negative logarithm of hydrogen ion concentration expressed in molarity. PH 7 is neutral, above 7 is alkaline and below is acidic.

What are Blood Gases?

There are two broad components to the blood gas panel: respiratory and metabolic. The values reported are as follows:

• pH--This is a logarithmic expression of hydrogen ion concentration--the acidity or alkalinity of the blood. The normal human arterial pH is 7.4. Any pH below this is acid, and any pH above it is alkaline.
• There is a narrow range of pH values (7.35 to 7.45) that the human body and its complicated system of enzyme-supported system operates within. pH values below 7.0 and above 7.6 are incompatible with life.
• HCO3--This value is derived through the blood gas analyzer's manipulation of the Henderson-Hasslebach Equation. An uncompensated decrease in the HCO3 value causes a decline in pH. An increased HCO3 results in alkalinization of the blood. Either condition can be life threatening. Decreased HCO3 is often the result of kidney or other major organ failure or uncontrolled diabetes. Increased HCO3 is more rare and is usually the result of inappropriate administration of certain drugs such as some kinds of diuretics or an excess of NaHCO3.
• PCO2--This value is measured directly by the CO2 electrode. An increased PCO2 is often the result of acute, chronic or impending respiratory failure, whereas a decreased PCO2 is the result of hyperventilation stimulated by a metabolic acidosis or hysteria and severe anxiety reactions. The normal arterial PCO2 is 40 mmHg.
• PO2--The partial pressure of oxygen in the blood is measured directly by a polarographic O2 electrode. The normal acceptable range is roughly between 85 and 100. An increased PO2 is usually the result of excessive oxygen administration that needs to be adjusted downwards on such results. A decreased PO2 is often the result of any number of respiratory or cardiopulmonary problems.

Link for the technical aspects of how the equipment works:

http://www.bloodgas.org/e77b74d4-ae83-4626-ab9d-e747b1b7c492.W5Doc?track=tech

   Arterial Blood Gases

How does it work?

The pH, PO2 and pCO2 of the sample are measured with specific electrodes. By equilibrating the sample against different CO2, mixtures the bicarbonate concentration is calculated.

What does it tell us?

Arterial blood gas analysis is the gold standard for assessing respiratory function. The gas exchange capability of the lung can be directly measured.
The three main measurements made by the blood gas analyzer are used together to obtain a detailed picture of the state of the respiratory system.

Oxygen: the PaO2 is the standard for measuring blood oxygenation. Decreases in PaO2 are due to hypoventilation, inspiration of hypoxic gas mixtures or impairment of gas exchange. Further information can be gained when the inspired oxygen level is changed from 21% to 100% and the PaO2 re-measured.

Carbon dioxide: PaCO2 is set by the balance between CO2 production and CO2 elimination. During anesthesia, CO2 production is fairly constant so the arterial level is determined by elimination. If the lungs are healthy the etCO2 is a good substitute for PaCO2 but in pulmonary dysfunction the difference between them increases which is useful diagnostically.

HCO3-, base excess, anion gap, pH: These all measure different aspects of acid-base balance. Patients with metabolic diseases may have acid-base disturbances and blood gas analysis can be used to monitor and treat them.

A blood gas analyzer is not a routine piece of monitoring equipment. Interpretation of the results requires knowledge of pulmonary and renal physiology, and because the arterial sample has to be transported to the machine for analysis there is a delay in obtaining the results. However, a blood gas analyzer is invaluable for critical care patients, pulmonary research and advanced procedures such as cardiopulmonary bypass and transplantation.

   The Basics of Blood Gases

With most lab blood work there are two types of tests that are in some way time-dependent: stat tests, which must be done as quickly as possible and routine tests. If there were such a thing as "super stat," blood gas tests would fall into that category.

The values obtained represent a mere moment in time for the patient, and although trends and stabilization of blood gas values can be obtained, more often than not the results are worthless later if changes in treatment are contemplated based on their values. Such therapeutic changes often involve critical, life-saving and time-dependent interventions such as adjustment upwards or downwards of oxygen, carbon dioxide and pH values. There is no time to waste in a critical situation.

Most blood samples can be collected routinely, on rounds, and kept and transported at room temperature until they are analyzed. Temperature does not affect their results. This is not true for arterial blood gases. As a living tissue, blood collected for this panel degrades rapidly unless kept in an ice/water bath until analyzed if any delay at all is expected in performing the analysis. And at the moment of analysis, the sample must be re-warmed to body temperature for an accurate result as the partial pressure of oxygen and CO2 decreases at lower temperatures and increases at higher ones. The most accurate reflection of these numbers lies in analyzing the sample at the proper temperature and correcting the values for the patient's actual body temperature if the patient is either hypothermic or febrile.

   Sample Collection

Most blood labs are performed on tourniqueted venous blood drawn from a superficial vein that is easily palpated and often even visually apparent. Today, lab technologists use a special needle and a Vacutainer containing an appropriate anticoagulant, other substance or nothing at all, depending on the test. Such tubes are identified by a color-coded cap that is never removed. This makes for unparalleled safety and protection from needlesticks and accidental exposure to bloodborne pathogens.

Arterial blood gases, as their name implies, must be drawn from an artery with a free-flowing, unimpeded flow of blood coursing through it. This procedure is known as an arterial stick and is usually performed on a palpable radial artery. If this site is unavailable, the brachial artery must be used. If no upper limb artery can be used, the next most favored site is one of the femoral arteries.

In critically ill patients requiring frequent samples, physicians often insert an arterial line that simplifies the procedure immeasurably. The blood must be drawn through a needle (or directly into a syringe if an a-line is available) into a heparinized (wet or dry lithium) syringe. A milliliter or less of blood is required to perform the procedure using most modern blood gas analyzers. Any air bubble left in the hub or top of the syringe must be carefully and gently expelled and the needle capped using the safety coverlet supplied with most arterial blood gas sampling kits. The syringe is then placed in a plastic bag containing crushed ice and immediately transported for analysis.

   Blood Gas Analyzers

To save time in the transport and analysis of blood samples on critically ill patients, many blood gas operations are housed in or near intensive care units as well as in or near the operating or recovery room. Because of the immediate life-threatening nature of blood gas abnormalities and the need to correct them rapidly on an objective and rational basis, blood gas labs should be equipped with a minimum of two analyzers in case one goes down due to routine maintenance or through some unforeseen malfunction or equipment failure. There can be no excuse for not being able to provide blood gas analysis rapidly and accurately on site at all times. Failure to do so can result in a potentially avoidable patient death.

Modern blood gas analyzers are electronic marvels compared to the methods used for this purpose 20 years ago. On attaching the sample syringe to the cuvette, they automatically draw the sample into a heated sampling chamber with miniaturized electrodes that quickly and accurately (if properly calibrated) measure pH, PCO2 and PO2 values. Based on these three measured values, these units automatically calculate HCO3, total CO2, percent oxygen saturation and O2 content, which is based on entry of the patient's measured hemoglobin values.

A companion to such units, known as a co-oximeter, directly measures percent oxygen saturation and hemoglobin, and then accurately calculates oxygen content and carboxyhemoglobin, a value that reflects the degree of carbon monoxide in the blood in smoke inhalation victims.

In addition to arterial sampling, critical care specialists often order blood gas panels in blood drawn through a central venous line since PO2 and O2 content values of this blood, when compared against arterial PO2 and O2 content, enable an estimate of cardiac output, another valuable service performed by blood gas testing. Such samples are often collected and run from patients undergoing cardiac catheterization and the results must be returned while the patient is still on the table.

The primary function of the respiratory system is to supply the body with oxygen while removing carbon dioxide. Other important functions include vocalization and assisting in regulating plasma pH.

"Respiration" is actually several distinct processes:

• Ventilation - movement of air into/out of the lungs
• External Respiration - gas exchange between blood and the air-filled chambers of the lungs
• Transport of gases between the lungs and the rest of the body tissues
• Internal Respiration - gas exchange between systemic blood and the tissue cells.
• Cellular Respiration - the mitochondrial process in which oxygen is utilized during ATP synthesis. (Note that this type of cellular respiration is often referred to as "aerobic respiration" as opposed to "anaerobic respiration," where ATP synthesis occurs without oxygen.)

Functions of the respiratory system include:

• Oxygen intake
• Expulsion of carbon dioxide
• Sound/voice production
• Regulation of plasma pH.
• Removal/destruction of airborne pathogens and toxins.

Anatomical structures of the respiratory system include: nose, nasal cavity, pharynx, larynx, trachea, bronchi, bronchioles, and alveoli. We can divide these structures into conducting zones and respiratory zones.

Conducting zones transport, cleanse, warm and humidify incoming air. They are not involved in gas exchange. The conducting portions include the nose, nasal cavity, pharynx, larynx, trachea, all bronchi, and all bronchioles except for the respiratory bronchioles.

The respiratory zones function in gas exchange. They include respiratory bronchioles and alveoli.

   Nasal Cavity

The nasal cavity contains olfactory epithelium (which is involved in?) as well as pseudo-stratified columnar ciliated epithelium with goblet cells, a.k.a. respiratory epithelium.

The connective tissue that underlies the respiratory epithelium is quite vascular. This helps warm the inspired air. There are also a good number of mucous glands, Together with the goblet cells; they secrete the mucus that will help trap any pathogens or particulate matter within the air. The mucus also contains lysozyme and IgA antibodies. In the nasal cavity, there are 3 bony projections on each lateral wall. These are the nasal conchae (#'s 3,5,and 7 in the frontal section below).

The nasal conchae act to increase the surface area exposed to the air. They also make the air flow turbulent, which makes it slow down. These factors increase our ability to filter the inspired air.

The nasal cavity is surrounded by a ring of paranasal sinuses located in the frontal, sphenoid, ethmoid, and maxillary bones. These sinuses assist in the warming and humidification of inspired air.

   

From the nasal cavity, we travel into the pharynx. There are 3 regions of the pharynx: nasopharynx, oropharynx, and laryngopharynx. The nasopharynx is lined by respiratory epithelium and contains the pharyngeal tonsils. The oropharynx is lined by stratified squamous epithelium (because it is also a passageway for food/drink) and contains the palatine tonsils. The laryngopharynx is also lined by stratified squamous epithelium (it is also a common pathway) and extends to the larynx - where the respiratory and digestive paths diverge.

Take a look at these sagittal sections and see what respiratory structures you can identify.

    Larynx

The larynx connects the laryngopharynx superiorly and the trachea inferiorly.

The larynx has a base framework of 9 cartilages connected by membranes and ligaments. There are 8 pieces of hyaline cartilage: the thyroid, cricoid, and the 3 sets of small paired cartilages. The 9th piece of cartilage, the epiglottis, is composed of elastic cartilage. The lumen of the larynx is lined by both stratified squamous epithelium (above the vocal cords) and respiratory epithelium (below the vocal cords). Lying underneath the laryngeal mucosa are the vocal ligaments which function in voice production. Air expelled through the larynx causes vibration of the vocal cords and results in sound production. The length and tension of the vocal cords are regulated by the state of contraction of the intrinsic laryngeal muscles. The vocal ligaments and overlying mucosa are referred to as the vocal folds or true vocal cords. Lying just superior to them is a similar pair of mucosal folds called the vestibular folds, or false vocal cords, which play no role in voice production.

The opening to the larynx is called the glottis and it is protected by the elastic epiglottis. During swallowing, the epiglottis is pulled downward and covers the glottis, thus preventing food/drink from passing into the larynx and trachea.

    Trachea

The trachea extends from the larynx to the mediastinum and ends by dividing into 2 primary bronchi. The trachea is reinforced by 16-20 C-shaped rings of cartilage. These rings prevent collapse of the trachea during inspiration. The lack of cartilage in the back of these rings allows for expansion of the esophagus during swallowing. The 2 ends of the cartilage C are connected by the trachealis muscle which is involved in coughing. The trachea is, not surprisingly, lined by respiratory epithelium. At the point where the trachea divides into the 2 primary bronchi, the last tracheal cartilage ring is expanded and a spar of cartilage extends posteriorly. This spar of cartilage is known as the carina and its mucosal lining is extremely sensitive to foreign matter.

Take a look at this cross-section of a trachea.

    Bronchial Tree

Each primary bronchus runs obliquely before plunging into the hilus of the lung on its own side. Within the lungs, the primary bronchi divide into the secondary bronchi. Each secondary bronchus supplies one lobe of the lung. Since there are 2 lobes on the left and 3 on the right, there are 3 secondary bronchi on the right and 2 on the left. The secondary bronchi will divide into tertiary bronchi and then quaternary bronchi and so on until about 23 branchings have occurred. As these branchings occur, what's happening to total cross-sectional area?

As the conducting tubes become smaller and smaller...

• The cartilage support changes. It goes from rings in the trachea to plates in the bronchi to none in the bronchioles. The cartilage must be absent by the time we get into the respiratory zone. It is not easy for gases to diffuse through a mass of hyaline cartilage.
• The epithelia changes. It goes from respiratory epithelium to simple columnar to simple cuboidal. Eventually, in the respiratory zone we will have simple squamous, which will facilitate diffusion.
• The amount of cilia and goblet cells decrease.
• The amount of smooth muscle increases. This will allow us to regulate the passage of air into certain areas of the lungs.

Passages with diameters of less than 1mm are bronchioles. Bronchioles lack cartilage. There are 2 types that we'll be concerned with: terminal bronchioles and respiratory bronchioles.

    Alveoli

The respiratory zone is defined by the presence of thin-walled air sacs known as alveoli. Sporadic alveoli begin to appear in the respiratory bronchioles. Hence the respiratory bronchioles are the initial structures in the respiratory zone. The last bronchioles without alveoli are known as terminal bronchioles and are at the end of the conducting zone. Respiratory bronchioles lead into alveolar ducts which terminate in clusters of alveoli called alveolar sacs.

Alveoli are made of simple squamous epithelium consisting of 2 cell types: Type I and Type II alveolar cells.

Type I alveolar cells are extremely thin and occupy most of the alveolar surface area. Their external surfaces are cobwebbed with capillaries. Both the thinness and the "sheet" of capillaries around them make these alveolar cells ideal participants in the diffusion of gases. Also note the elastic fibers surrounding the alveoli. Their importance will become apparent soon.

The basement membranes of the alveolar I cells and the capillary endothelium are actually fused together. Thus the exchange surface (a.k.a. the respiratory membrane) consists of the alveolar I cell membrane, the endothelial cell membrane, and the fused basement membranes.

Scattered amongst the Type I alveolar cells are the Type II alveolar cells. Their primary function is the secretion of a chemical known as surfactant (more on it later). Crawling on and about both the Type I and Type II cells are the alveolar macrophages (dust cells) that deal with any foreign matter.

Lung Gross Anatomy

Let's now briefly discuss the gross anatomy of the lungs. The lungs occupy the entire thoracic cavity except for the mediastinum. The anterior, lateral, and posterior surfaces are all adjacent to the ribcage. The apex of each lung is just inferior to the clavicle and each base is superior to the diaphragm. On the medial surface is the hilus where the primary bronchi enter and the blood vessels and nerves enter/exit. The left lung is smaller than the right and has an indentation where the heart normally sits. The left lung is divided into 2 lobes whereas the right is divided into 3. The pulmonary arteries bring deoxygenated blood (for gas exchange) to the lungs while the bronchial arteries bring oxygenated blood (to supply oxygen for the structural tissue). The lungs are drained by the pulmonary veins.

The lungs are associated with a double-layered membrane - the pleurae. The parietal pleura covers the chest wall and the superior diaphragm. The visceral pleura covers the external lung surface. The pleurae produce fluid that fills the slit-like cavity between them. The pleural fluid helps affix the lungs to the chest wall and causes the lungs to move when the thorax does.

Pressure

Recall that blood flowed due to the pressure gradient created by ventricular systole. Air flow will also be governed by pressure gradients. Let's now discuss some important pressures.

• Atmospheric Pressure (Patm) - pressure exerted by the air surrounding the body. At sea level it’s equal to 760mmHg. For our purposes, we'll assume it to be constant and assign it a value of 0mmHg.
• Intrapulmonary Pressure (Palv) - pressure exerted by the air within the alveoli. It rises and falls during inspiration and expiration but it always equalizes with atmospheric pressure.
• Intrapleural Pressure (Pip) - pressure within the pleural cavity. It is always lower than both atmopsheric pressure and intrapulmonary pressure.

Before we discuss the mechanics of inspiration & expiration, let's deal with the importance of the intrapleural pressure. The lungs are an elastic tissue and as such, they have a tendency to recoil - i.e., they want to collapse. The fact that the pressure in the pleural space is lower than the pressure within the alveoli prevents collapse. Because a pressure gradient exists between the alveolar pressure and pleural pressure, air tries to flow from the alveoli into the pleural space. It cannot, but by exerting force against the walls of the alveoli, it counteracts the tendency of the lungs to recoil.

If the intrapleural pressure in the lungs rises (say due to a stab wound that opens the pleural cavity to the atmosphere and allows atmospheric and intrapleural pressure to equalize), the pressure gradient between alveoli and pleural space is abolished and the lungs collapse. This is known as pneumothorax. The difference between the pleural and alveolar pressures is known as transpulmonary pressure and is obviously quite important. Also, realize that because the lungs are each surrounded by their own pleural membrane, collapse of one does not necessarily affect the other.

Pressure Volume Relationships

Before we delve any further, let's examine some basic relationships between volume and pressure. Boyle's Law states that pressure varies indirectly with volume. In other words, as volume decreases, pressure increases; and as volume increases, pressure decreases. This is due to the fact that pressure is caused by collisions of gas particles with the walls of the container (i.e., pressure equals force divided by area). If the volume increases, there will be fewer collisions with the container walls and the pressure will drop.

Inspiration and Expiration

Inspiration begins with the contraction of the diaphragm and the external intercostals.

Compare the diaphragm at rest with the diaphragm contracting.

Contraction of the diaphragm causes thoracic volume to increase which causes lung volume to increase. This causes alveolar pressure to decrease. Now intrapulmonary pressure is less than atmospheric pressure and we have a pressure gradient. Air then flows in until the pressures are equalized. Remember - throughout the inspiration intrapleural pressure also changes so that it is always lower than intrapulmonary pressure. During forced inspiration (e.g., during exercise), other muscles (scalenes, sternocleidomastoids, and pectoralis minor) can come into play to create a larger change in thoracic volume and thus a larger pressure gradient.

Unlike normal inspiration which is an active process, normal expiration is a passive process due to the elasticity of the lungs and the relaxation of the inspiratory muscles. As the elastic lungs recoil and the inspiratory muscles relax, the thoracic volume decreases which yields a decrease in lung volume which yields an increase in lung pressure. Now the gradient has been reversed and air flows outward.

Forced expiration, on the other hand, is active and involves muscle contraction so as to create a larger pressure gradient. Such muscles include: external and internal obliques, transversus and rectus abdominus, internal intercostals, and latissimus dorsi.

Take a look at this diagram depicting a single respiratory cycle.

Airway Resistance

Let's now switch topics and look at another similarity between air flow and blood flow. Air flow is not only directly proportional to the pressure gradient, it's also indirectly proportional to airway resistance. Airway resistance is due primarily to the diameter of the conducting tubes. For example, increased parasympathetic activity would cause a decrease in bronchiole diameter and thus an increase in airway resistance. Increased sympathetic activity would have the opposite effect. Other chemicals also exert effects; histamine can cause bronchoconstriction and thus greatly increase resistance. During asthma, bronchioles constrict - yielding a decrease in air flow

Local accumulations of mucus, infectious materials or solid tumors are also sources of airway resistance.

Surfactants and Compliance

Let's return to something we briefly mentioned earlier: the production of surfactant by type II alveolar cells. Water molecules have a fantastic attraction for other water molecules. Water lines the surface of our alveoli. Because of the tendency for water molecules to hydrogen bond with and interact with other water molecules, there is a tendency for alveoli to collapse. Luckily, our type II cells produce surfactant. Surfactant is a detergent-like molecule that will interfere with the cohesion of water. This lowers the surface tension within the alveoli and helps prevent their collapse. Surfactant production does not normally occur until 34wks of gestation. Thus a premature baby is at risk of neonatal respiratory distress syndrome and will have much difficulty expanding her immature lungs.

Surfactant acts to increase the compliance of the lungs - the ease with which they expand. The higher the lung compliance, the more efficient the ventilation. Another factor that affects compliance is fibrosis. If inelastic scar tissue forms within the lungs, their compliance will decrease.

Gas Exchange

Now let's discuss the actual exchange of gases within the lungs. Factors that can influence the diffusion of O2 and CO2 across the respiratory membrane include:

• Partial pressures of O2 and CO2
• Thickness & surface area of the respiratory membrane
• Solubility of O2 and CO2
• Temperature

Partial pressure simply refers to the pressure of one specific gas in a mixture of gases (such as atmospheric air). O2 and CO2 move down their partial pressure gradients during gas exchange. The Po2 of systemic venous blood and pulmonary arterial blood is 40mmHg while the Po2 of alveolar air is an almost constant 100mmHg. This means that O2 will flow from the alveolus across the respiratory membrane and down its partial pressure gradient into the pulmonary capillaries. The Pco2 of systemic venous blood and pulmonary arterial blood is 46mmHg while the Pco2 of alveolar air is 40mmHg. This means that CO2 will flow across the respiratory membrane and down its partial pressure gradient from the pulmonary capillaries into the alveoli. Now let's examine exchange in systemic tissues. Pulmonary venous and systemic arterial blood has a Po2 of 100mmHg while the intracellular Po2 is typically 40mmHg at most. (Intracellular Po2 is kept low because O2 is continually being used in the ATP-generating processes of cellular respiration.) O2 will thus leave the capillaries and diffuse into the tissues. Pulmonary venous and systemic arterial blood has a Pco2 of 40mmHg and a Pco2 of at least 46mmHg. Thus CO2 will leave the tissues and enter the capillaries.

Take a look at this diagram depicting gas exchange.

Even though the partial pressure gradient for CO2 is not as large as the gradient for O2, relatively equal amounts of the gases are exchanged because CO2 is much more soluble in plasma and alveolar fluid than O2.

An increase in temperature increases the kinetic energy and thus the movement of gases within the alveoli. This will result in an increased rate of gas exchange.

In healthy lungs, the respiratory membrane (alveolar membrane + endothelial membrane + fused basement membranes) is 0.5-1.0um thick and gases diffuse through it with ease. In pneumonia, the thickness of the RM increases due to mucus build-up. This decreases the efficiency of the diffusion. In pulmonary edema, fluid builds up between the alveolar membrane and endothelial membrane. This would also decrease gas exchange.

The surface area of healthy lungs is enormous - 300 million alveoli! In emphysema, the surface area decreases, which of course impacts gas exchange.

    Oxygen Transport

Let's now examine the means by which O2 and CO2 are transported within the blood. 1.5% of transported O2 is dissolved within the plasma. The other 98.5% is bound to the hemoglobin in the RBCs. Each Hb can bind up to 4 molecules of O2 and this binding is quite reversible. Hb containing bound O2 is oxyhemoglobin while Hb w/o bound O2 is deoxyhemoglobin.

Look at this reversible equation that shows the loading and unloading of oxygen by hemoglobin:

HHb + O2 <- -> HbO2 + H+

In the lungs, this reaction would proceed as written from left to right as hemoglobin picks up oxygen. It proceeds in this direction because the concentration of free oxygen is so high. In the tissues, it would proceed in the opposite direction as hemoglobin unloads oxygen. It proceeds in this direction in the tissues, because the concentration of free oxygen is low.

When inadequate amounts of oxygen reach the tissue it is known as hypoxia. Without oxygen, cells are unable to perform cellular respiration and produce ATP. Without ATP, cell death is inevitable.

Carbon monoxide has a greater affinity for Hb than O2 does.Why is this so bad?

O2 binding is cooperative. The binding of the 1st O2 molecule facilitates the binding of the 2nd which facilitates the binding of the 3rd which facilitates the binding of the 4th. In other words, as the loading of O2 proceeds, the affinity of Hb for O2 increases. If the Hb has 4 O2 molecules bound to it, it is saturated. If it has less than 4, it is unsaturated.

Hb is almost completely saturated at a Po2 of 70mmHg. At the tissu