Monitoring of Respiration and Circulation

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  1. Introduction to monitoring of respiration and circulation - Blom - Biomedical Engineering
  2. Monitoring of Respiration and Circulation
  3. In this issue
  4. Citation Manager Formats

The author's goal is to provide a survey of the field, a review of the necessary fundamentals on which deeper study can be based, and an overview of possible search terms.

Introduction to monitoring of respiration and circulation - Blom - Biomedical Engineering

The early chapters of Monitoring of Respiration and Circulation provide an overview of the fundamentals of the respiratory and circulatory systems, and modeling. The intermediate chapters describe important clinical measurement methods and the information they provide about patients, including approaches, possibilities, limitations, and accuracies. Next, the book discusses state-of-the-art therapeutic instruments and supporting systems, such as infusion drips and pumps, heart-lung machines, and pacemakers.

If we model both lungs together as one perfect sphere, what would the lung surface area be? And what would the lung surface be if this one perfect 6-l sphere were densely packed with 8,, small perfect spheres? Generations 1 through 16 are called the conductive zone; they mainly serve as airways that transport gas to and from generations 17 through 23, the respiratory zone, where oxygen and carbon dioxide exchange takes place between the air in the lung and the blood in the small-diameter blood vessels that surround the alveoli.

The air ducts of generation 0 the trachea through generation 11 are surrounded by cartilaginous rings, which prevent their collapse. Higher generation ducts are so compliant that they collapse are compressed when the pressure outside a duct becomes larger than the inside pressure, i. The transmural pressure is defined as the pressure inside the tube minus the pressure outside the tube. In an infinitely compliant tube, the transmural pressure cannot become negative; the outside pressure would just close the tube. Normally, the transmural pressure can become slightly negative before the tube is fully closed.

Surfactant, intrapleural pressure The lung tissue is elastic, and the lung by itself would—like a balloon—tend to decrease its volume. Since the fluid in the space between both pleurae cannot expand, this elastic force is in turn propagated to the thorax. The thorax, however, is also elastic and also tends to preserve its shape and its volume. The generations of the bronchial tree. Generations 1 to 16 transport gas. Gas exchange takes place in generations 17 to If, somehow, a perforation causes the intrapleural space to become connected to the outside air, it loses its underpressure and both lung and thorax will assume their resting volume.

This condition is known as pneumothorax. We will now be more specific and study the origin of the intrapleural pressure in detail. Let us start with a model for a single alveolus. The alveolus contains air and we can think of it as being surrounded by liquid, since its surface consists of a thin layer of cells with an embedded network of tiny capillaries. This prompts the analogy of an alveolus with an air bubble in water.

The surface tension acts to compress the air inside the bubble and thus produces an overpressure in the bubble relative to the hydrostatic pressure in the fluid. This overpressure causes an opposing force. A stable air bubble requires an equilibrium between both forces. As a thought experiment, we split the air bubble into two equal parts Figure 1.

Two forces determine the volume of a gas bubble under water. Surface tension acts at the gas-liquid interface and attempts to decrease the volume. The result is an over-pressure inside the bubble, which resists the volume decrease. It indicates that high pressures will exist in small bubbles. The lung, however, consists of alveoli of unequal sizes. Since alveoli are mutually interconnected via airways, the pressure difference would cause airflow. This flow would go from the higher pressure the smaller bubble to the lower pressure the larger bubble , causing the smaller bubble to empty itself into the larger one and thus cease to exist.

This is clearly not the case in a healthy lung. That even the smallest alveoli of a healthy lung can remain in existence is due to a liquid called surfactant, a product of the alveolar cells, which covers the inside of the alveoli in a mono-molecular layer. The effect is that alveoli of different radii can coexist peacefully. For an alveolus with a radius of 0. Thus 1 The units mm Hg and cm H2O are still very much in use in the medical community, the first especially for circulatory pressures and the second for respiratory pressures. We will use these units too.

Whether that model is accurate enough to represent the new situation is still to be tested, a process called model validation. Because of the surfactant, there is an approximately linear relation between the radius of an alveolus and its surface tension. For reference, the surface tension values for soap and water are given as well. Macroscopically, this is the situation with the whole lung which is kept open by the underpressure in the intrapleural space. In the context of lung mechanics, a balloon is often taken as a model for the lung.

Just like with a balloon, we can learn more about the volume-pressure relationship of a lung if we slowly increase the volume of an isolated lung and keep track of the resulting pressure. We can also determine the volume-pressure relationship of an isolated thorax. In fact, the combined curve can be measured in a cooperative patient, who must not breathe during the test and keep the glottis open, by slowly adding volume to the lung. Point A in Figure 1. Point B is the resting volume of the combination of lung and thorax, which exists at the end of a normal expiration.

This volume is called the functional residual capacity, FRC see Section 1. Pressure-volume relationships of lung V1, thorax Vth and the combination of both Vtot. The volume scale has markers at 1—l intervals. Volume A is the resting volume of the thorax. The smaller volume B is the resting volume of the lung-thorax combination. We could also apply a pressure and measure the resulting volume.

Redraw the figure with pressure as the independent variable. This is true for all lungs.

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The latter is greatly reduced and thus the compliance increased by surfactant. A small compliance indicates a stiff lung, a large compliance a compliant lung. Normal values of the compliances of the lung and of the thorax are both around 0. The lung-thorax compliance is the compliance of lung and thorax combined. Breathing causes volume changes of the thorax. An inspiration is caused by muscle action which creates an addition to the thorax volume and can thus be represented by shifting the curve of the thorax volume to the right, whereas a forced expiration shifts it to the left.

As a result, the combination curve also shifts. A linearized representation is given in Figure 1. It shows that on inspiration the resting curve shifts downward. This shift can be interpreted as either a volume change where the pressure change is zero the chest expansion or a pressure change at the same volume due to muscle action.

We can write these relationships as 1. Linearized pressure-volume relationship of lung-thorax combination. Then the above formulas tell us that 1. The lung volume is thus 1. Derive the expression for the lung volume when both compliances are not equal. Note that this question can be rephrased as: How can Clung-thorax be computed if Clung and Cthrox are given.

There are thus two ways to change the volume of the lung, through Palv and through Pmuscle. When the airways are open and breathing is slow, the pressure drop due to the airways resistance can be neglected and the pressure Palv in the lung will be approximately zero. A change of Pmuscle will directly cause a volume change 1. Total cross-sectional area of each airway generation.

The resistance to flow is mainly concentrated in generations 0 to about The friction between gas and airway walls causes an opposition to the flow, which is called the airway resistance R see Section 2. Airway resistance depends upon the type of flow laminar or turbulent and on the cross sections of the tubes through which the gas flows. Numerous small airways in parallel provide less resistance to a certain flow F than one large airway with an equivalent cross section see Section 4.

As a result of the tremendous branching of the airways and the rapid increase of the total cross-sectional area at higher generations Figure 1. Because the airways distend as the lung becomes larger, the airway resistance decreases as lung volume increases. The simplest lung mechanics model consists of only airway resistance R and lungthorax compliance C Figure 1. The simplest lung mechanics model consists of airway resistance R and lungthorax compliance C. We apply a flow F during some time, resulting in a lung volume V, and then make the flow F zero again. The dynamic compliance Cdyn is the straight line, which forms the long axis of the approximately elliptic curve.

The area enclosed by the curve of Figure 1. There may also be imposed work of breathing if resistance R is artificially increased, e. The dynamic compliance Cdyn is the major axis of the ellipse. The respiratory muscles Spontaneous respiration is an active process, in which contractions of respiratory muscles cause a volume change of the thorax and thus a volume change of the lung. When breathing normally, only inspiration is active. The ribs are elastically connected through cartilaginous joints to the vertebrae of the spine and to the sternum at the front of the chest.

When a group of intercostal muscles the muscles between the ribs contract, they force the ribs apart and thus lift the rib cage as a total, increasing its volume; this is called chest breathing. The diaphragm, a large muscular plate- or dome-like structure that separates thorax and abdomen, contracts as well, which also increases the volume of the thoracic space; this is called abdominal breathing.

Both volume changes are about ml in an adult, combining into a tidal volume the volume of one breath of about ml. Exhalation is normally a passive process; the respiratory muscles relax and, due to the elasticity compliance of both lung and thorax and gravity forces, when erect , lung and thorax reassume their resting volume. Exhalation can be speeded by another group of intercostal muscles, whose effect is to forcefully reduce the thorax volume.

Lung volumes We have already encountered some names for different lung volumes. Pulmonary medicine employs the following terminology for different volumes Figure 1. This volume is realized at the end of a maximum inspiration. Other terms that are in use: The remaining part of the minute volume about 1. The rigid segments models b for inspiration; d for expiration show the directions of the forces of both muscle groups.

This zone is called the anatomical dead space normally about ml. In a healthy subject the right ventricle of the heart pumps all the blood through the lung; the alveolar perfusion is then equal to the cardiac output. If some of the blood takes a path that bypasses the lung, we have shunt flow, due to the shunt, some of the blood cannot acquire oxygen and release carbon dioxide.

The respiratory quotient is the ratio of carbon dioxide produced and oxygen consumed; a normal value is 0. Partial pressures Respiratory air is usually composed of different gases. At the left, the different lung volumes are indicated. The right part shows a time trace of lung volume as the patient breathes quietly, inhales fully up to the maximum inspiratory level, then exhales fully down to the maximum expiratory level. The sum of the partial pressures of all gases equals, of course, the total pressure of the gas mix. Similarly, the partial volume of one gas within a certain volume is defined as the volume which this single gas would have, keeping the pressure unchanged, if all other gases were removed.

The fraction of a gas in a mixture of gases is equal to its partial pressure divided by the total pressure or, equivalently, to its partial volume divided by the total volume. The concentration, expressed as a percentage, is times the fraction. These four terms therefore carry the same information for gases.

As an example, let us compute the partial pressure of oxygen in atmospheric air. It states that 1. This includes many of the gases that play a role in respiration, such as oxygen, nitrogen, and carbon dioxide. Water vapor partial pressures at various temperatures. But since water vapor is not an ideal gas, we need to take special measures, especially when we consider expiratory gas, which is water vapor saturated.

One way is to physically remove all water vapor; this will leave ideal gases only anesthetic vapors, if present, have concentrations of at most a few percent. Another way is to numerically correct for the partial pressure of water vapor. That compensation is necessary is shown in Table 1. What is even more important is what happens when a water vapor saturated gas mixture cools off. Since at lower temperatures the saturated water vapor partial pressure is less, some of the water vapor must turn into water.

This explains why condensation will always take place in the expiratory tubing of ventilators. The condensed water will collect at the lowest point in the tubing and may, if excessive, cause expiration to become more difficult see PEEP, Section 8. In respiratory gas composition measurements, one always needs to specify volume, pressure, temperature and water vapor content. In order to compare measurements, certain standard conditions are introduced. The following terms are often encountered: One also speaks of partial pressures of blood gases. When a gas is brought into contact with a liquid e.

When equilibrium has been reached—which may take some time, depending upon the solubility of the gas—the partial pressure of the gas dissolved in the liquid is by definition equal to the partial pressure of the remaining gas. Since alveolar gas and blood are so closely in contact, the partial pressures of oxygen and carbon dioxide in the blood leaving the pulmonary circulation will only differ slightly from the partial pressures in the alveolar gas. Let us consider the values for oxygen. The alveolar gas concentrations, which can be measured at the end of expiration, show that some oxygen has disappeared.

The O2 partial pressure in the expiratory gas is higher than that of the alveolar gas due to mixing with the dead space O2. Partial gas pressures in mm Hg throughout the respiratory and circulatory systems. In some tissues, such as hard-working muscles, the oxygen partial pressure can go down to zero, with a concomitant increase in carbon dioxide partial pressure. The arterial blood O2 partial pressure is therefore almost as high as the alveolar O2 partial pressure.

The tissues extract oxygen, which is reflected in the O2 partial pressures of the tissues and of the venous blood. Dead space The conductive zone of the airways, generations 1 through about 16, has a transport function only; it lacks capillaries and does not participate in gas exchange. Its volume is called the anatomical dead space. At the end of inspiration, this space has been filled with gas, but this gas is exhaled unchanged; its O2 and CO2 concentrations will be the same as those in the inspired gas. In a breathing system, device dead space is minimized by transporting inspiratory and expiratory gases through separate tubes.

In a diseased lung it can happen that certain parts of the lung are not perfused by the pulmonary circulation, although they are ventilated. These non-perfused parts of the lung are also dead space. The total dead space—anatomic plus non-perfused lung volumes—is called the physiological dead space. A significant dead space leads to respiratory problems, because wasted effort is expended to inhale and exhale the dead space gas volume. In a completely healthy person the physiological dead space is, of course, equal to the anatomical dead space.

Instruments can also contribute to dead space, when the instrument is connected to the trachea by a hose or tube in which gas moves back and forth. Consider what would happen when you would breathe through a long vacuum cleaner hose, whose volume is larger than your vital capacity. Due to the large volume of the hose, the oxygen-poor and carbon dioxide-rich gas that is exhaled in one breath remains in the tube and will be re-inhaled in the next breath; the exhaled carbon dioxide cannot be purged to the outside air, and the outside air cannot replenish the consumed oxygen, however strenuous the breathing.

For this reason, the dead space volume of connecting tubes or hoses must be as small as possible. But a short tube is impractical and a narrow tube would normally introduce too much resistance to the gas flow see Section 2.

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A good solution exists; it is based on our recognition that dead space exists only in tubes with a back-and-forth flow. If two tubes are used, an inspiratory and an expiratory tube, and if unidirectional valves ensure that the flow in these tubes is unidirectional, the tubes will not add to the dead space volume. The two tubes come together in what is called a Y-piece or Tpiece Figure 1. The volume of the common leg of the Y-piece, in which the flow is bidirectional, can be made sufficiently small.

To show the effect of instrument dead space, assume that the patient breathes through an extra piece of tubing of length 10 cm and diameter 3 cm. Calculate the volume of this tube. Assuming a normal adult dead space value of ml, what percentage have we added to it? And assuming a neonatal dead space value of 20 ml, what percentage have we added?

Change in oxygen a and carbon dioxide b partial pressures in capillary blood as the blood flows through the lung capillary bed. In normal lungs, diffusion is rapid enough to reach equilibrium. Thus, only about one quarter of the oxygen that we inspire is taken up by the blood, and an approximately equal volume is returned as carbon dioxide.

Another difference between the inspired and expired gases is that the latter is fully saturated with water vapor, whereas the former usually contains only little of it. Diffusion through the surface takes place from a high to a low concentration. Instead of concentrations, we can also consider partial pressures. Since the total lung surface area is unknown, the parameter that characterizes the transport of a gas through the lung membrane is its diffusion capacity D, now redefined as the mass flow rate of that gas through the membrane divided by the partial pressure difference of the gas across the membrane.

Monitoring of Respiration and Circulation

It is also proportional to the gas solubility and inversely proportional to the square root of the molecular weight of the gas. Some gases may therefore pass the same membrane easily oxygen, carbon dioxide, carbon monoxide ; other gases may pass only with difficulty nitrogen or hardly at all helium. For oxygen, diffusion across the alveolar membrane is rapid; for carbon dioxide, it is even about 20 times faster Figure 1. In rest, red blood cells remain in the lung capillaries for about 0.

During exercise, the cardiac output is larger and the time available for oxygenation is reduced. As long as exercise is moderate, however, diffusion of both O2 and CO2 is essentially complete in the normal lung. When surgery is finished and the use of N2O discontinued, it will rapidly leave the blood and fill up the alveoli. The latter normally means that some of the total alveolar surface area is not ventilated or that some of the area is not perfused.

In the expression ventilation-perfusion ratio, alveolar ventilation stands for the volume of gas that is transported into and out of the lungs each minute, and alveolar perfusion stands for the volume of blood that perfuses the alveoli per minute. A normal value of this ratio is between 0.

The value of the ventilation-perfusion ratio is often used as a measure for the adequacy of gas transport across the lung membrane. If a part of the lung is blocked to ventilation but the perfusion is normal, the ratio decreases. This is a sign of shunt flow: If a part of the lung is normally ventilated but not perfused, the ratio increases. This is a sign of physiological dead space: The value of the ventilationperfusion ratio is thus an indication whether significant shunt flow or physiological dead space is present. In extreme cases such as the following, however, the value of the ventilationperfusion ratio may lead to a false conclusion Figure 1.

Assume one lung whose ventilation is normal, but whose perfusion is zero. There is no gas exchange in this lung. In the other lung, the ventilation is blocked but the perfusion is normal. Since the ventilation-perfusion ratio is just one number that characterizes both lungs together, its computation follows from a ventilation of half the normal value only one lung is ventilated divided by a perfusion half its normal value only one lung is perfused. Although the ratio is perfectly normal, we have a situation that is not compatible with life. In a less extreme case, one lung is correctly ventilated and perfused, whereas both gas flow and blood flow to the other lung are blocked.

Here, too, we find a normal ventilation-perfusion value. This is not a lifethreatening situation people do survive after removal of one lung , but it is clear that the ventilationperfusion ratio does not tell the whole story and must be used in combination with other information. How does the ventilation-perfusion ratio change if a patient is accidentally ventilated by a tube into one of the two main bronchi rather than in the trachea? How does the ventilation-perfusion ratio change if a patient is accidentally ventilated by a tube into the esophagus rather than in the trachea?

How does the ventilation-perfusion ratio change in case of pulmonary embolism a full or partial obstruction of the flow in the pulmonary artery? The ventilation-perfusion ratio, which is normally 0. Some pathophysiologies Pathologies of the lung mechanics can be classified as either obstructive or restrictive. Obstructive diseases are characterized by an increase of the airway resistance, which can be found in, e.

Obstructions make it difficult to inhale and exhale. Patients with obstructive diseases require much effort just to breathe. Asthma is an allergy of the airways, which results in inflammation and an increase in tone of the bronchial smooth muscles that control the diameter of the airways. In an acute asthma attack, bronchospasm decreases the diameters of the airways even more.

Due to the smooth muscle contractions, gas may become trapped in parts of the lung behind closed airways. Extra respiratory effort is required to transport the respiratory gas through the extra-narrow passages, and the resulting extra-high intra-thoracic pressure may close off collapsible airway passages and thus lead to exaggerated airway collapse see Section 2. To minimize collapse, a patient with acute asthma will breathe at high lung volumes, inspiring close to total lung capacity see Section 6. Emphysema is characterized by destruction of alveolar walls, resulting in dilation of the alveolar spaces and a very compliant lung.

The lung is kept chronically hyperinflated. This has two effects: The high lung volume, however, flattens the curvature of the diaphragm, making its force less efficiently employed. Restrictive diseases are characterized by a decrease in useful lung volume VC , often accompanied by a decrease in total lung capacity TLC. An example is pulmonary fibrosis, where the lungs are abnormally stiff. Very large drops in intrapleural pressure are required to inflate the lungs, so deep breaths are difficult.

Patients tend to breathe shallowly and rapidly. Restrictions can also be due to rigidity of the chest wall or to muscle weakness or paralysis. The valves of the heart ensure that blood flows in one direction. In between arteries and veins we find a very large number of tiny peripheral vessels that bring the blood into close proximity of all the cells.

Each of the two pumps, the left and the right heart, consists of two chambers, called the atrium and the ventricle Figure 1. The ventricles are high power pumps that, when they contract, generate enough pressure to force the blood through the small peripheral blood vessels. The atria have much less power; it is their function to pump blood into the ventricles, where the real work is done. Between each atrium and the corresponding ventricle we find a one-way valve, which prevents blood from flowing backward. Valves are also found where the blood leaves the ventricles.

Note that there is no valve where the blood enters the atrium; such a valve is not necessary because when the atrium contracts, the ventricle is fully relaxed and, through an easily opened valve between atrium and ventricle, is easily filled with blood. Blood transport The right heart pumps blood from the systemic veins through the pulmonary circulation toward the left heart, where an adequate filling pressure for the left atrium must be provided. The left heart pumps the blood from the pulmonary circulation into the aorta, from where it is further distributed to the organ tissues.

Arteries branch into successively smaller vessels. The smallest vessels are the capillaries. The vein collects the blood again. The volume of blood ejected by each cardiac contraction is called the stroke volume 70 ml at rest. At rest the heart rate is about 70 beats per minute.

Since the total blood volume is about 5 l, the average circulation time of the blood is about 1 min. The right and the left heart contract at the same times and in the same rhythm, so the stroke volumes of left and right heart must be the same on average. The large arteries that leave the ventricles successively branch into ever smaller vessels Figure 1.

Gas exchange takes place in the smallest vessels, the capillaries. Another branching network at the venous side returns the blood to a vein. Thus, the blood that is provided by one artery is usually collected by a single vein: This is a general rule: The liver, however, has two major blood supplies, the liver artery and the portal vein Figure 1. Can you think of a reason why the intestine and the liver are connected in series? The pulmonary arterial system transports the blood to the lung.

It also buffers the pulsatile pressure output of the right heart to a more constant pressure. The pulmonary peripheral circulation consists of those small blood vessels that surround the alveoli of the lung; this is where oxygen is picked up by the blood and carbon dioxide released. The pulmonary venous system collects the oxygen-enriched blood from the pulmonary peripheral circulation, returning it to the left heart.

The systemic arterial system distributes the oxygenated blood to the various organs; it also buffers the pulsatile pressure of the left heart to a more constant pressure. The systemic peripheral circulation provides oxygen to the interstitial fluid surrounding all cells and collects excess carbon dioxide. The systemic venous system collects the oxygen-poor blood that has traversed the organs to return it to the right heart and the lung for renewed oxygenation.

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It also functions as a pool where variations in total blood volume are taken up. The volume of blood at the venous side of the systemic circulation ml is much larger than that of the arterial side ml , and the compliance of the veins is much larger than that of the arteries. The vascular beds of most organs lie between one major artery and one major vein.

The liver is an exception. This means that the veins can store large volumes of blood at low pressures. In fact, the endothelial cells, which line the capillaries, normally block only the passage of blood cells and large protein molecules. Fluids and small molecules freely pass between blood and the interstitial space. Moreover, fluid is added to the circulation from the intestines and removed from the circulation—together with superfluous electrolytes and waste products— via the kidneys. Yet, although the circulation is essentially open for fluids, a number of control processes operate to stabilize the filling of the circulatory system to about 5 or 6 l in adults.

Shock is especially threatening; at an arterial pressure lower than about 50 mm Hg the oxygen supply to the brain is inadequate. The subject faints and must be helped immediately. If the shock persists for longer than a few minutes, it becomes lethal. Differences between the systemic and the pulmonary circulation. We mention only a few. Regulation of the regional blood flow to the various organs tunes itself to the oxygen requirements of those organs through the contraction of the muscles that control the diameters of the arterioles which feed the organs.

The venous volumes adapt to variations in the flows of blood offered to them, thus keeping pressures within narrow bounds. Other control systems regulate arterial blood pressures, protecting the vessel walls from stressfully high tensions, yet ensuring adequate perfusion of the various tissues.

Another set of control systems see Section 1. When these break down, one speaks of ventilationperfusion mismatch. Blood; blood gases; hemoglobin; hematocrit Blood is a fluid—this fluid is called plasma—in which we find three types of free-floating cells: The major function of platelets also called thrombocytes is in the repair of damaged blood vessels, where they direct fibrinogen, one of the proteins that is found in the blood, to form a mesh of fibers that repairs the wound.

The major function of the white cells also called leukocytes is to find and destroy foreign material that has made its way into the blood or the tissues. The red blood cells, also called erythrocytes, are the most numerous. In fact, fully one-third of all the cells of the human body are erythrocytes. Their major function is oxygen transport. The oxygen dissociation curve. This is a so-called equilibrium reaction, because the reaction can proceed in either direction: When the oxygen partial pressure in the blood is low in the systemic peripheral circulation, where the cells consume oxygen, effectively removing it from the blood , oxyhemoglobin is converted back into hemoglobin.

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This mechanism keeps the O2 partial pressure in the peripheral blood almost constant 40 to 50 mm Hg , although in hard-working muscles it can drop to almost zero. A rough calculation shows that after 4 passages through the tissues, all oxygen would have been consumed if oxygen uptake from the lung would stop.

Since the blood circulates in about 1 min, this indicates an oxygen reserve in the order of 4 min. The figure also indicates that raising the PO2 above 80 or mm Hg will hardly increase the oxygen content dissolved plus bound oxygen of the blood. Thus, ventilating a patient with a gas containing a high oxygen percentage normally makes no sense.

Which percentage would normally suffice? The oxygen buffering by the oxyhemoglobin is essential. One liter of blood plasma without hgb can contain only 3 ml of O2. One liter of whole blood, with hemoglobin, can contain about ml O2. Oxygen supply to the cells would be far from adequate through only dissolved oxygen. Some of the hemoglobin can be bound to carbon monoxide in the form of carboxyhemoglobin hgbCO , especially in smokers. Moreover, hgbCO is rather stable. As a result, smokers have less hgb available to transport oxygen.

Blood viscosity and maximum oxygen content as functions of hematocrit. The higher the hematocrit, the more hemoglobin and the more oxygen can be carried; this relationship is approximately linear Figure 1. This means that the oxygen transport capacity is higher with a high hematocrit. A high hematocrit means a high viscosity; this relationship is approximately quadratic: Since a higher blood viscosity means an increase in flow resistance see Section 2. In reality, there is an optimum hematocrit value, which ensures best oxygen transport—and this optimum value is the value that we measure in healthy persons.

Using the above relationships, we find 1. Although erythrocytes buffer some CO2, the major mechanism is very different. Carbon dioxide and water form carbonic acid, which partly ionizes 1. If the CO2 partial pressure in the blood rises, the reaction proceeds from left to right, producing more carbonic acid, which splits into a hydrogen ion and a bicarbonate ion. When the hydrogen ion concentration rises, the reaction proceeds to the left, resulting in the production of CO2. This mechanism keeps the CO2 partial pressure in the blood almost constant.

Both too acidic low pH and too alkaline high pH cell environments are prevented by the above equilibrium reaction. Several other chemical reactions modify these basic oxygen and carbon dioxide dissociation processes. Their combined effect is the extra facilitation of oxygen uptake and carbon dioxide release in the lung and oxygen release and carbon dioxide uptake in the tissues.

Although minute volume is increased by a decrease in arterial PO2, this only happens when the decrease is large. Even a slight increase of arterial PCO2, however, is rapidly compensated for.

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During moderate exercise, blood gas concentrations and pH remain unchanged, because ventilation increases in exact proportion to metabolism. During very strenuous exercise, full compensation is no longer possible. Volume-pressure relationships of heart and blood vessels The main difference between arteries and veins is in their compliances and their radii.

As with the vessels of the respiratory system, we notice that a straight-line approximation works well over most of the normal operating range. The slope of the line determines the compliance, and the intersection of the line with the volume axis determines the unstressed volume. Notice that the compliance becomes smaller—the vessel becomes stiffer—at high filling volumes.

It shows that veins are much more compliant than arteries and that they have much larger unstressed volumes. The total blood volume is about 5 l. A volume increase of only 1. The remaining volume of 3. A slower decrease of the blood volume, e. Transmural pressure-diameter curve of a typical artery. The diameter is in arbitrary units. The slope of this curve is related to the compliance: Some properties of various blood vessels.

Stressed volume can be computed as the difference between total volume and unstressed volume. The compliance values are at normal total volumes. The heart receives its inflow from the veins, where pressures are as low as 5 mm Hg, and pumps the blood to the arteries, where systemic mean pressures can be as high as mm Hg. Pressures in the pulmonary left and the systemic right circulation.

The latter is smaller in extent, its outflow pressure is lower about 15 to 30 mm Hg and its pressure fall at the capillaries is less abrupt. The differences between the pressure levels in the pulmonary and the systemic circulation are due to a number of reasons: The blood flow through the organs is ultimately due to the pumping action of the heart, which contracts and expands in a rhythm of about once to three times per second, and to the one-way valves of the heart that ensure that blood flows in one direction only.

The contractile phase of the heart is called systole, and the maximum pressure measured during systole is called the systolic pressure. The relaxation phase of the heart is called diastole, and the minimum pressure measured during diastole is called the diastolic pressure. The blood flow through the organs is controlled by the smooth musculature in the walls of the arterioles, which controls their cross section lumen1 according to the oxygen demands of the organs.

The small radius of the capillaries means that they can be modeled as a pure resistance see Section 2. The term peripheral resistance is used to indicate the total resistance that the flow pumped by the heart meets on its way from ventricle to atrium. Add document to cart. Introduction to monitoring of respiration and circulation - Blom. Monitoring of respiration and circulation Course code: Introduction to monitoring of respiration and circulation Author: Tamara 41 documents uploaded documents sold Send message Follow.

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