Every cell in the body needs a constant supply of oxygen to produce energy to grow, repair or replace itself and to maintain normal vital functions.
Every cell in the body needs a constant supply of oxygen to produce energy to grow, repair or replace itself and to maintain normal vital functions. The respiratory system is the body's link to its supply of oxygen. It includes the diaphragm and chest muscles, the nose and mouth, the pharynx and trachea, the bronchial tree and the lungs. The bloodstream, heart and brain are also involved. The bloodstream takes oxygen from the lungs to the rest of the body and returns carbon dioxide to them to be removed. The heart creates the force to move the blood at the right speed and pressure throughout the body. The smooth functioning of the entire system is directed by the brain and the autonomic nervous system.
Air containing oxygen enters the body through the nose and mouth. From there it passes through the pharynx on its way to the trachea. The trachea divides into two main bronchi upon reaching the lungs. One bronchus serves the right lung and the other serves the left lung. The bronchi subdivide several times into smaller bronchi, which then divide into smaller and smaller branches called bronchioles. After many subdivisions, the bronchioles end at the alveolar ducts. At the end of each alveolar duct are clusters of alveoli. The oxygen transferred through the system is finally transferred to the bloodstream at the alveoli. Blood vessels from the pulmonary arterial system accompany the bronchi and bronchioles. These blood vessels also branch into smaller and smaller units ending with capillaries, which are in direct contact with each alveolus. Gas exchange occurs through this alveolar-capillary membrane as oxygen moves into and carbon dioxide moves out of the bloodstream (perfusion). In the blood, oxygen is transported in two forms: dissolved in plasma (which is measured by PO2) and bound to hemoglobin (measured by SpO2). The amount of oxygen bound to hemoglobin is much larger than the amount dissolved in plasma. The "matching" of ventilation and perfusion is important to proper lung function. It does no good to ventilate an alveolus that is not being perfused (alveolar dead space) or to perfuse an alveolus that is not being ventilated because of atelectasis. In the normal lung, ventilation and perfusion are not evenly matched (known as V/Q mismatch) and this worsens with lung disease and dorsal or lateral recumbencies. Both ventilation and perfusion increase toward the dependant regions of the lung, but since blood is heavier than lung parenchyma, perfusion increases at a faster rate than ventilation. Vasodilation or vasoconstriction, caused by disease or anesthetic drugs, enhances V/Q mismatching and hypoxemia. From an anesthetic point of view, alveolar ventilation is very important because this will control the amount of volatile or gaseous anesthetic agent that can diffuse into the bloodstream. Any increase in alveolar ventilation will increase anesthetic uptake into the pulmonary blood.
The movement of air into and out of the lungs is called ventilation. The contraction of the inspiratory muscles, mainly the diaphragm, causes the chest cavity to expand, creating negative pressure. This is inspiration. During maximal inspiration, the diaphragm forces the abdominal ventrally and caudally. The external intercostal muscles are also involved. These muscles contract and raise the ribs during inspiration, increasing the diameter of the chest cavity.
Normal expiration is a passive process resulting from the natural recoil or elasticity of the expanded lung and chest wall. However, when breathing is rapid, the internal intercostal muscles and the abdominal muscles contract to help force air out of the lungs more fully and quickly. At the end of inspiration, the elasticity of the lung causes it to return to its smaller interbreath size. The ability to do this is called elastic recoil. The volume of air remaining in the lung at the end of a normal breath (the end expiratory lung volume) is the functional residual capacity (FRC). FRC is composed of the expiratory reserve volume and the residual volume. On expiration, there is still air left in the lungs, if there weren't, all of the alveoli would collapse. FRC decreases slightly in supine and lateral recumbency compared to prone. FRC is diminished with small airway diseases. At FRC the alveoli in the non-dependant lung sections is larger than those in the dependant regions because of gravity and the weight of the lung. Alveoli in the dependant regions are squashed and compressed by the weight of the overlying lung tissue. In lateral or dorsal positions the dependant alveoli are also compressed by the weight of the mediastinal structures and by the weight of the abdominal contents pressing against the diaphragm. In patients with large abdominal masses or excessive bloating (GDV) the problem becomes especially significant.
In spite of many protective mechanisms in place in the lungs, including FRC, small airway and alveolar collapse (atelectasis) still occurs in the normal animal. Atelectasis is especially prominent in the dependant lung regions when an animal is recumbent. Intermittent deep positive pressure breaths in the anesthetized patient can help minimize small airway and alveolar collapse. The use of positive end expiratory pressure (PEEP) has been proven to help as well. PEEP increases airway pressure and FRC to help keep small airways and alveoli open. PEEP valves are commercially available (in 5, 10, and 15 cm H2O) and can be added to the anesthesia machine for this purpose. Unfortunately, once atelectasis has occurred, it is very difficult to open the closed alveoli. Applying excessive pressure in an attempt to open alveoli (as in the case of attempting to re-inflate a packed off lung during a thoracotomy) tends only to damage the already working tissue (barotrauma) before re-inflation takes place. Re-inflation is a slow, delicate process and will happen on its own in healthy tissue over time or once recumbency or insult changes.
The degree of stiffness or compliance of the lung tissue affects the amount of pressure needed to increase or decrease the volume of the lung. With increasing stiffness, the lung becomes less able to return to its normal size during expiration. Virtually all diseases cause the compliance of the lungs to decrease.
The amount of airflow resistance can also affect lung volumes. Resistance is the degree of ease in which air can pass through the airways. It is determined by the number, length and diameter of the airways. An animal with a high degree of resistance may not be able to exhale fully, thus some air becomes trapped in the lungs.
Ventilation is the process by which gas in closed spaces is renewed or exchanged. As it applies to the lungs, it is a process of exchanging the gas in the airways and alveoli with gas from the environment. Breathing provides for ventilation and oxygenation.
Tidal volume is the volume of gas passing into and out of the lungs in one normal respiratory cycle. Normal tidal volume for mammals is 10-20 ml/kg. Minute volume is used to describe the amount of gas moved per minute and is approximately 150-250 ml/kg/minute. Minute volume = tidal volume x respiratory rate. It is alveolar ventilation that is important for gas exchange however. Tidal volume is used to ventilate not only the alveoli, but also the airways leading to the alveoli. Because there is little or no diffusion of oxygen and carbon dioxide through the membranes of the airways, they comprise what is known as dead space ventilation. The other part of dead space is made up of alveoli with diminished capillary perfusion. Ventilating these alveoli is ineffective and will do nothing to improve blood gases. The non-perfused alveoli and the airways are known as physiologic dead spaces. Therefore tidal volume has a dead space component and an alveolar component. Dead space ventilation is about 30-40% of tidal volume and minute volume in a normal patient breathing a normal tidal volume. Dead space ventilation has a purpose. It assists in humidifying and tempering inhaled air and it cools the body as in panting. Panting is predominantly dead space ventilation. During panting, the respiratory frequency increases and the tidal volume decreases, so that alveolar ventilation remains approximately constant. This is the reason that when animals under anesthesia pant, they very often wake up. They are not effectively ventilating their alveoli and exchanging gas well. Often times these patients will be hypercarbic because they are not able to effectively reduce their carbon dioxide levels. Slower, deeper breaths are usually more efficient. Certain pieces of anesthesia equipment can add to the anatomical dead space of a patient by "extending" their airways. Endotracheal tubes that are too long and extend far beyond the patient's nose would be an example. Adding this dead space presents a further challenge to patients trying to effectively ventilate.
Monitoring ventilation on patients under anesthesia can be done a number of ways. Ventilation is assessed in terms of rate, rhythm, and tidal volume. First of all, a good look at the patient's chest excursions should be done to evaluate for quality and effort. Auscultation of the lungs should be performed prior to sedating or anesthetizing any patient. Normal lung sounds should be heard on both sides of the chest. Any abnormal sounds should be investigated prior to moving forward with anesthesia as anesthetic drugs can depress respiration and ventilation and may worsen existing problems.
Mucous membrane color should be assessed regularly. The tongue and gums should be pink. Any change in color, especially blue or purple tingeing can indicate hypoxemia.
Respirometers can be used to measure tidal volume and minute volume. Expired gas passes through oblique slits, which creates circular gas flow in a chamber, causing rotation of a double-vaned rotor. The rotor is coupled via a set of linkage gears to a display indicator dial and needle. Accumulated minute volume is recorded and each breath's tidal volume can be viewed. The respirometer measures volume in one direction only. Flow can be calculated by averaging recorded volumes over time. Owing to inertia in the system it tends to overestimate higher volumes and underestimate lower volumes.
Apnea or respiratory monitors detect the movement of gas through the proximal end of the endotracheal tube. They provide no information on tidal volume or the physiologic state of the patient. They can be falsely activated by pressure on the chest or abdomen of the patient or by cardiac oscillations that cause gas movement in the trachea.
Pulse oximetry is a simple non-invasive method of monitoring the percentage of hemoglobin which is saturated with oxygen. The pulse oximeter consists of a probe attached to the patient (usually lingually in veterinary medicine although many other sites work well) which is linked to a computerized unit. The unit displays the percentage of hemoglobin saturated with oxygen together with an audible signal for each pulse beat, a calculated heart rate and in some models, a graphical display of the blood flow past the probe. An oximeter detects hypoxia before the patient becomes clinically cyanotic. A source of light originates from the probe at two wavelengths. The light is partly absorbed by hemoglobin, by amounts which differ depending on whether it is saturated or desaturated with oxygen. By calculating the absorption at the two wavelengths the processor can compute the proportion of hemoglobin which is oxygenated (SpO2). The oximeter is dependant on a pulsatile flow and produces a graph of the quality of the flow. Any reduction in pulsatile flow produced by vasoconstriction, hypovolemia, severe hypotension, hypothermia, and some cardiac arrythmias will result in an inadequate signal for analysis. Sometimes moving the probe to a new location will work. The probe can cause constriction of the vessels beneath it over time. Bright ambient light can affect the signal as well. Pulse oximetry cannot differentiate between different forms of hemoglobin. Movement artifact is a problem for the pulse oximeter. This comes mostly into play during recovery when patients begin shivering or gaining control of their tongues. The oxygen saturation should always be above 95%. Slight changes over time may just mean the probe needs to be repositioned, but the overall patient should be assessed for de-saturation. Sudden steady decreases, especially during thoracic surgery or in the critical patient, should be investigated immediately and supportive measures taken. Usually this means instituting positive pressure ventilation immediately while the cause is determined and rectified.
Capnography measures the carbon dioxide concentration in expired gas. It provides a non-invasive means of measuring arterial carbon dioxide pressure (PaCO2). At the end of expiration, assuming there is no rebreathing, the airway and the lungs are filled with carbon dioxide free gases. Carbon dioxide diffuses into the alveoli and equilibrates with the end-alveolar capillary blood. As the patient exhales, a carbon dioxide sensor at the end of the endotracheal tube (if there is one) will detect no carbon dioxide as the initial gas sampled will be the dead space gas. As exhalation continues, carbon dioxide concentration rises gradually and reaches a peak as the carbon dioxide rich gas from the alveoli make their way to the sensor. At the end of exhalation, the carbon dioxide concentration decreases to zero (base line) as the patient commences inhalation of the carbon dioxide free gases. The number given on the capnograph is called the end tidal CO2 (ETCO2). The ETCO2 value is approximately 5-10 mm Hg less than the PaCO2 of the patient with normal pulmonary function. The evolution of the carbon dioxide from the alveoli to the sensor during exhalation, and inhalation of carbon dioxide free gases during inspiration gives the characteristic shape to the carbon dioxide curve on the capnograph and which is identical in every animal. Any deviation from this identical shape should be investigated to determine a physiological or pathological cause producing the abnormality. A report of inspired carbon dioxide (graph not returning to baseline-zero) on the monitor means rebreathing of CO2 is occurring and can indicate equipment problems such as expired soda sorb or a malfunction in the valves of the anesthetic machine. Excessive dead space can also be a cause. Abnormal shapes on the capnograph can be caused by a number of things and can be interpreted if normal wave physiology is understood. The beginning of exhalation should be the baseline. The upswing represents the variable emptying of alveoli (airway disease will flatten out the slope). The plateau reflects alveolar gas. The down slope represents inspiration. Rebreathing will make the down slope less steep. If there is no waveform, it means the patient is apnic for some reason. If the baseline is increased it represents rebreathing malfunction. An increased plateau is representative of hypoventilation or increased rate of carbon dioxide production. A decreased plateau to a new stable level indicates hyperventilation, hypothermia, airway leaks, tachypnea, or a calibration error. An abrupt drop to zero means an airway obstruction, disconnect, apnea or cardiac arrest. An unstable, fluctuating plateau represents patient "bucking" the ventilator. Normal CO2 is 35-45 mm Hg. Low CO2 can indicate over ventilation or very poor perfusion. High carbon dioxide (hypercarbia) can indicate hypo-ventilation, airway disease or obstruction or anesthetic machine malfunction.
Capnography is easy to use and non-invasive. It provides a continuous measurement of end tidal carbon dioxide. It provides information on the adequacy of ventilation, airway obstruction, disconnection from the breathing system and severe circulatory problems. It is also a useful tool in an arrest situation to help determine the adequacy of CPR. Expense may limit use in practice.
Blood gases are the gold standard method of monitoring ventilation. The analysis of carbon dioxide and oxygen tensions in an arterial blood sample provides very useful information on pulmonary function. Most analyzers also provide acid-base status and some electrolyte values as well. There are now many different bedside portable blood gas units available, although expense will limit their availability in general practice.
Blood gas samples are drawn from an artery, either directly or through an arterial catheter into a heparinized syringe. Care must be taken to make sure that the sample is not exposed to room air or drawn into a syringe with excessive heparin in it as this can affect results. Most blood gas analyzers will measure or calculate PaO2, PaCO2, pH, BE, HCO3-, k+, Na+, and perhaps other electrolytes.
In animals breathing room air and with normal lung function, PaO2 should be 80-85 mm Hg. Numbers below this can indicate hypoxemia. Increases in inspired oxygen lead to increases in PaO2. As a general rule, PaO2 should be 5 times the inspired oxygen concentration. Therefore, an animal on 100% oxygen should have a PaO2 of greater than 500 mm Hg. To evaluate blood gas results for ventilation effectiveness first look at the pH to determine acid/base status. Normal pH should be 7.35-7.45. Results are considered acidotic if the pH is less than 7.35 or alkalotic if the pH is greater than 7.45. Next look at the PaCO2. Remember normal is considered to be 35-45 mmHg. If pH is less than 7.35 and PaCO2 is greater than 45-50 mm Hg it is indicative of a respiratory acidosis and the patient is under ventilating or not being ventilated adequately. If the pH is alkalotic, and the PaCO2 is low, it is indicative of a respiratory alkalosis and the patient is hyper, or over ventilating. It can help to think of CO2 as an acid. Therefore, if there is a lot of it (result is high) than the pH should indicate acidosis, and vice versa.
Positive pressure ventilation (PPV) is indicated when an animal cannot ventilate adequately on its own. This indication may be defined as one or more of the following: hypercarbia (increased CO2 ,> 60 mm Hg), de-saturation (SpO2 < 95%) in spite of oxygen therapy, hypoxemia (PaO2 of less than 100 mmHg on oxygen) or a low observed or measured minute volume. PPV is always indicated in any surgery requiring an open chest, whenever paralytic neuromuscular blocking drugs are to be used, neuromuscular diseases, chest wall problems, abdominal enlargements, or pulmonary parenchymal disease. Any patient that is to be anesthetized with potentially increased intracranial pressure should be mechanically ventilated. Positive pressure ventilation is of great benefit to many patients but it is not without potential complications. These can be avoided with careful monitoring, attention to detail and a good understanding of the underlying physiological processes. A major contraindication for positive pressure ventilation is a closed pneumothorax, as positive pressure ventilation will make it worse. Positive pressure ventilation can decrease arterial blood pressure and reduce cardiac output especially if airway pressures are consistently more than 10 mm Hg or if circulating blood volume is low. Artificial ventilation decreases pulmonary blood flow, and therefore may lead to ventilation-perfusion abnormalities. Circulatory changes during positive pressure ventilation are caused by prolonged increases in mean airway pressures and decreases in CO2.
Most ventilators used with small animal anesthesia are classified as one of three types. A pressure pre-set ventilator will deliver a tidal volume to a peak pressure pre-set on the ventilator. The advantage of this type of ventilator is that is has a high safety factor because no matter what size patient is attached, the volume delivered to that patient will never exceed the pressure chosen on the ventilator. For instance, if a large dog was the last patient on the ventilator and the next patient is a cat, there is no volume re-set that needs to be done. Tidal volume depends on weight or size of the lungs in healthy patients. These ventilators also compensate for leaks by prolonging inspiratory time because with a leak, the set pressure will not be reached. Changes in the sound of the cycle of the ventilator will indicate problems. Disadvantages are that the volume delivered is variable and will depend on lung compliance, airway resistance, number of functional alveoli and the pressure within the thorax. The pressure setting may need to be increased (increasing tidal volume delivered) during procedures if ventilation becomes inadequate.
Volume cycled ventilators take a minute volume (selected by the operator on the "flow" dial) and divide it up into the number of breaths chosen by adjusting the rate (breaths per minute) knob. Time cycled ventilators have an inspiratory/expiratory (I/E ratio) knob (normal inspiratory time for small animals is about 1.5 seconds) that acts as the rate control. Normally rates of 8-12 bpm are adequate under anesthesia as long as appropriate tidal volumes are selected. Remember that slow, deep breaths are usually more beneficial for alveolar ventilation. These ventilators need to be re-adjusted in between every patient to prevent delivery of excessive volumes inadvertently. Many of these ventilators have an alarm set knob that lets the operator select at which peak inspiratory pressure the alarm sounds. If patients "buck" (begin to breath spontaneously) while being ventilated the alarm may sound, especially if the patient initiates a breath while the ventilator is already delivering a breath adding excess pressure to the system. Tidal volumes are generally calculated as 10-20 ml/kg of lean body weight. Smaller patients will most often do fine with the lower volumes, while larger animals usually need the higher end of the scale. Usually in small animals the peak inspiratory pressure should not exceed 20 cm H2O to prevent damage to the tissues from excessive pressure, but in animals with large abdominal masses, bloating, respiratory disease or compliance issues and in dorsal recumbency, higher pressures may be needed. Overall, whatever it takes to deliver the needed minute volume and adequately ventilate the patient should be done. Ideally, ventilation assessment and adequacy will be determined by monitoring ETCO2 and blood gases. In the absence of these monitors, it is possible to successfully use positive pressure ventilation as long as close attention is paid to peak inspiratory pressure, chest excursions, pulse oximetry, mucous membrane color and blood pressure. Hypotension can be indicative of hypocarbia (low CO2) and over ventilation as CO2 causes sympathetic stimulation and a subsequent rise in arterial blood pressure. Brick red (injected) mucous membranes can be indicative of hypercarbia.
Monitoring the respiratory system function on patients under anesthesia should be a routine part of the overall monitoring plan for each and every patient.
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