- Email: [email protected]
Physical Examination of the Pulmonary System
RESPIRATORY MEDICINE AND SURGERY
0195-5616/00 $15.00 + .00
PHYSICAL EXAMINATION OF THE PULMONARY SYSTEM Robert L. Hamlin, DVM, PhD
The term physical examination means various things to various persons, but for the purpose of this review, it refers to the process by which information is gained about a patient by inspection, palpation, percussion, and auscultation. History and anamnesis, as important as they are, are not included. Clinically meaningful decisions about most common pulmonary disorders may be made with information gained by the physical examination alone. To glean optimal information from the physical examination, the examiner must have as much interest in, and experience at, performing the examination as he or she does in techniques requiring more expensive, elaborate, and glamorous methods. The other aspects of the examination are enormously valuable to confirm inferences made by the physical examination, and they clearly add a profound dimension of security for the examiner. Many examiners use the stethoscope as neck jewelry rather than as a device for diagnosis, and many veterinary students receive little training in methods of auscultation and interpretation of lung sounds. Percussion is even more contentious and requires even more training and experience to be useful. This review describes how diagnoses of certain common pulmonary disorders (e.g., pleural effusion, pneumothorax, pulmonary edema, asthma, pulmonary fibrosis) may be made by means of the physical examination. The physical examination is based on understanding the origin and transmission of vesicular breath sounds, crackles, wheezes, brassy versus subtle coughs, and notes of percussion (Table 1}.4• 5 These features are discussed in veterinary patients, all of whom share the following physiFrom the Department of Veterinary Biosciences, The Ohio State University, College of Veterinary Medicine, Columbus, Ohio
VETERINARY CLINICS OF NORTH AMERICA: SMALL ANIMAL PRACTICE VOLUME 30 • NUMBER 6 • NOVEMBER 2000
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Table 1. PHYSICAL EXAMINATION FINDINGS FOR COMMON RESPIRATORY DISORDERS IN DOGS AND CATS Respiratory Rate
Respiratory Effort
Phase of Respiratory Difficulty
Asthma
Increased
Increased
Expiratory
Chronic bronchitis Pulmonary fibrosis Pleural effusion Pneumothorax Pneumonia Pulmonary edema Tracheal collapse
Increased Increased Increased Increased Increased
Increased Increased Increased Increased Increased Increased
Expiratory Inspiratory Inspiratory Inspiratory
-
-
-
-
Inspiratory (if extrathoracic tracheal collapse)
Percussion
May be hyperresonant
-
-
Dull Hyper-resonant May be dull May be dull
-
Auscultation
Cough
Wheezes and crackles
Hacking, if present
Crackles Loud crackles Distant Distant Loud crackles Loud crackles May hear a snap
Hacking Hacking Uncommon Uncommon Soft, half-hearted Half-hearted "Honking," high pitched
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cal findings: shortness of breath (predominantly due to tachypnea rather than hyperpnea), cyanosis, and reluctance to lie down; therefore, these findings are not repeated for each patient. It is important to note that the physical findings shared by most pulmonary diseases are also shared by most of the important heart diseases (e.g., mitral regurgitation, dilated cardiomyopathy, heartworm disease). COUGH
Everyone knows what a cough is, but it is important to differentiate a hacking (or honking) cough that sounds like it is coming from the throat from a half-hearted cough that sounds like it is coming from deep within the thorax. Hacking coughs are almost always caused by injury to large airways (e.g., trachea, mainstem bronchi). For example, hacking coughs are heard with tracheal collapse, tracheobronchitis, or compression of the left mainstem bronchus as might be caused by an enlarged left atrium due to mitral regurgitation. The half-hearted cough usually arises from injury to pulmonary parenchyma such as occurs with edema or pneumonia. Of course, everyone knows that these are general rules to which there are frequent exceptions manifested by individual patients. TACHYPNEA VERSUS HYPERPNEA
Dyspnea is a subjective term that describes a human experience of "air hunger." Labored breathing, the condition we recognize in our veterinary patients, may be a manifestation of increased rate of respiration (tachypnea) or increased depth of respiration (hyperpnea). As is the case with different types of cough, there are exceptions, but tachypnea most often arises from a stiff injured lung or thoracic wall, and hyperpnea arises from derangement of blood gases (i.e., high carbon dioxide, low oxygen, low pH). Although almost all healthy and quiet dogs, cats, and human beings breathe fewer than 20 times per minute, most veterinary patients examined in a rather unfamiliar environment breathe at a rate proportional to their level of excitement. I usually instruct clients to watch their pets breathe late at night when the pet is sleeping or resting and the house is quiet. At a short distance from the pet, watch the thorax and abdomen move in and out, count the number of breaths for 15 seconds, and multiply the number by 4 to obtain the respiratory rate per minute. (If the number the client gives you is not divisible by 4, do not trust the number.) If the lung is edematous, fibrotic, or otherwise stiff, the degree of tachypnea is proportional to the severity of the disease. If there is blood gas derangement, however, the patient usually does not breathe more rapidly but does breathe more deeply than normal. This hyperpnea is typical in pets with metabolic acidosis or in pets with elevated partial pressure of carbon dioxide. Whereas tachypnea can be documented by respiratory rate, the veterinarian must search
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for secondary signs of hyperpnea. That is because the depth of respiration is commonly measured as tidal volume, or the volume of air taken in during a normal quiet inspiration. It is difficult to determine if a pet's tidal volume has increased by 50%, although it is quite simple to determine if the respiratory rate has increased by even 25%. Signs of hyperpnea may be bulging of the eyes, muscular shaking during inspiration, sucking in of the skin covering the thoracic inlet, tensing of the "strap" muscles of the neck, reluctance to lie down, standing with thoracic limbs abducted, or unusual flaring of the nostrils. To document this, you can produce respiratory acidosis by holding your breath for 15 seconds. Then count the number of breaths for the 15 seconds after you resume breathing. You can see that you breathe more deeply but no more rapidly than before you held your breath. VESICULAR BREATH SOUNDS
Vesicular breath sounds are produced by air traveling through the bronchopulmonary tree during inspiration and expiration. 2' 3, 6, 7 For airflow to produce sound, it must travel at a high enough velocity to change its laminar flow pattern and become turbulent or to shed vortexes (swirls of air). It is the disturbed flow that causes the bronchopulmonary tubes to oscillate at sufficient magnitude (>15 dB) and frequency (>60 Hz) to be heard on the torso as sound. The prime factor in the generation of vesicular breath sounds is the velocity of airflow. Because the velocity of a gas flowing is equal to the total flow divided by the cross-sectional area of the tubes through which the flow moves, it is important to know where the cross-sectional areas are smallest, because flow through those regions is most likely to be disturbed and to produce the vesicular breath sounds. Individually, the small airways (e.g., bronchioles, respiratory bronchioles, alveolar ducts) are minute (far < 1 mm in diameter). Taken together, however, the hundreds of thousands of these small airways constitute an enormous cross-sectional area through which air flows. Because of their enormous cross-sectional area, the velocity of air flowing through them is much too slow for the flow to be turbulent or for vortexes to develop, and no vesicular breath sound is made by air flowing into or out of the small airways. Taken singly, the large airways (e.g., trachea and mainstem, lobar, and lobular bronchi) are relatively large; however, because there are so few of them, the total cross-sectional area is less than .005 of the total cross-sectional area of the small airways, and vesicular breath sounds are made as air tumbles through the larger airways. In general, the larger airways are located in the neck and the middle of the thorax, and the smaller airways are located in the periphery of the lung just under the thoracic wall. Although vesicular sounds are made in the larger airways and thus may be heard best by listening (auscultating) over the area where they are made, these sounds are transmitted primarily in the direction that the air flows. This is different from true sound, which is transmitted
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centrifugally; as a result, breath sounds are termed pseudosounds. True sound is made when you snap your fingers, and the sound can be heard uniformly in all directions from your fingers. An example of pseudosound occurs when you stand in front of and blow on the rotating blades of a fan. The sound (pseudosound) can be heard mainly at the front of the fan and not behind it, that is, this pseudosound travels mainly in the direction the air is blown by the fan. The tracheal vesicular breath sounds may be heard clearly during inspiration and expiration, when auscultating over the trachea, because that is closest to where the sound is made. If you place your stethoscope over the diaphragmatic (basilar) lobes of lung the inspiratory vesicular breath sound heard is softer than that over the trachea. This is because the sound made by air tumbling through the trachea is being transmitted to the lung, in the direction the air is flowing and because the sound is attenuated by the distance between the tracheal and basilar lobes. During expiration, there is either no sound or only a soft expiratory vesicular breath sound heard over the diaphragmatic lobes. This occurs because the sound is made in the trachea and is blown out of the thorax rather than being "sucked" into the thorax. Place your stethoscope chest piece in front of your mouth and breathe through your wide-open mouth and you hear only a soft inspiratory sound but a much louder expiratory sound. The sound, actually pseudosound, is produced by air tumbling through your trachea or other large airways, and that sound is sucked into the lung during inspiration so that it is heard only slightly during inspiration. During expiration, the sound is still made in the large airways, but is blown out of the mouth. The intensities of even normal vesicular breath sounds vary greatly among the species, breeds, ages, and tidal volumes; as a result, to know what "normal" is requires an enormous commitment to auscultating hundreds of normal individuals. The following cases are meant to serve as practical examples of common situations encountered in daily veterinary practice. Pleural Effusion and Pneumothorax
Our first patients are a cat with pleural effusion and a dog with pneumothorax. Remember that they share (with all the patients to follow) the clinical signs of dyspnea, cyanosis, and reluctance to lie down. When auscultating over the trachea, normal tracheal, vesicular breath sounds are heard. When auscultating over the basilar lobes, however, the vesicular breath sounds are extremely difficult to hear. Why would this be if the sounds are made within the trachea and heard quite normally over the trachea? Remember that the vesicular breath sounds heard over the basilar lobes are actually made in the large airways, and are transmitted into the parenchyma of the lungs as air flows in that direction. The fact that these breath sounds are not heard on the thoracic wall over the lung may indicate that the sounds are either reflected or
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attenuated in their path from the lung to the thoracic wall. Reflection of sound occurs when sound traveling through one medium (e.g., an airway) reaches a much denser medium (e.g., pleural effusion). Instead of the sound traveling from the lung to the thoracic wall, it is reflected by the dense pleural effusion. The sound heard on the other side of the air-fluid boundary is attenuated greatly because of the reflection of much of the acoustic energy. Conversely, if a pneumothorax were present, the sound on the other side of the pneumothorax would be greatly attenuated, because sound does not travel well through relatively rare air. Remember that you can detect a train coming much earlier if you put your ear to the rail than if you try to listen through the air. Pleural effusion and pneumothorax thus would result in the absence or great attenuation of the inspiratory vesicular breath sounds heard normally over the thoracic wall. So how can you differentiate between attenuation of sound due to either pleural effusion or pneumothorax? A mere thump on (i.e., percuss) the thoracic wall is sufficient. When percussing on a dense water-filled structure like your forehead, you hear a dull note. I cannot tell you what a dull note is, but when you listen to the note of percussion produced when you thump on your forehead, you know instantly what a dull note is. When percussing over an air-filled structure such as a pneumothorax, you hear a hyper-resonant note of percussion. I cannot tell you what a hyper-resonant note of percussion sounds like, but when you percuss over a gas-filled stomach (which you can produce by gulping a can of cola), you know instantly what a hyper-resonant note of percussion is. An interesting rule-of-thumb is that you should always put a needle into the thorax when there is an absence of inspiratory vesicular breath sounds. In the first instance, you may drain pleural fluid. In the second instance, you may evacuate pneumothorax. The exception to this rule may be if the liver is herniated through the diaphragm into the thoracic cavity. In such a case, the breath sounds are attenuated and the note of percussion is dull, but little benefit would accrue from performing a thoracentesis. Pulmonary Edema or Exudate (Pneumonia)
Our third and fourth patients are dogs just as dsypneic, cyanotic, and reluctant to lie down as the first two patients. Normal tracheal vesicular breath sounds are heard. But when listening over the basilar lobes, much louder than expected inspiratory breath sounds as well as higher pitched expiratory vesicular breath sounds are heard. The reason why the expiratory vesicular sounds are much louder than expected is because the expiratory sounds are normally soft to absent. Vesicular breath sounds that are louder than expected are termed bronchial or bronchovesicular breath sounds; however, they are still made in the large airways and are transmitted (but with less decrement) over the basilar
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lobes. So, what might decrease the decrement of sounds through the thorax from the large airways to the regions over the basilar lobes? The answer is a dense pathway, and a dense pathway may be a liquid-filled lung, a lung filled with edema (as is the case with heart failure), or exudate (as is the case with pneumonia). 1 You might question, "Why are sounds louder with a wet and dense lung than with pleural effusion?" The answer is simple. If the parenchyma of the lung is wet and dense, sounds are transmitted better than normally through the dense walls. If the sound meets an air-water interface, the sound is attenuated. The higher pitched sounds of edema and pneumonia result from the pulmonary parenchyma being wet, heavy, and stiff. Stiff structures tend to resonate at higher frequencies than flaccid structures. Try striking a balloon that is taut (i.e., stiff) and another balloon that is flaccid. You notice that the taut balloon oscillates for a much shorter duration and at a higher frequency than the flaccid balloon. Can you differentiate between the bronchovesicular breath sounds of edema and those of pneumonia? Unfortunately not. Because both lungs may be equally dense, they transmit sound equally well. Of course, differentiation may be made by the "company the vesicular breath sound keeps." If one dog is a Doberman Pinscher with dilated cardiomyopathy and the other is a young German Shepherd puppy with a high fever and leukocytosis, it is likely that the Doberman Pinscher has edema and the German Shepherd has pneumonia. Animals with pleural effusion, pulmonary edema, and pneumonia all have relatively dense thoracic contents; as a result, a relatively dull note or percussion is elicited. Because this dullness may be quite subtle, it is much more difficult to identify a dull note than the hyper-resonant note of pneumothorax. CRACKLES AND WHEEZES: ADVENTITIOUS BREATH SOUNDS
The precise origins of crackles (also called rales) and wheezes (also called sibilant rhonchi) are obscure. Wheezes are almost always loudest during expiration, whereas crackles are almost always loudest during inspiration but are also heard during expiration. Adventitious breath sounds are not caused by air flowing through airways but probably occur as a result of airways being "scrunched" closed or, if already closed, "popping" open. To mimic the sound of pulmonary crackles, place the chest piece of your stethoscope over an unwrapped loaf of bread and squeeze the load of bread. The tiny pockets (alveoli) made within the bread as the carbon dioxide is released just before baking "scrunch" closed as the loaf is squeezed, and crackles are produced. For an airway to close, at least three features must be present. First, airways must be collapsible. Because large airways are normally supported by rather rigid cartilaginous rings, rhonchi do not usually arise from larger airways because they cannot collapse. Conversely,
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because small airways are not supported by rigid cartilaginous structures, they can close, and their closure probably produces rhonchi. Second, for an airway to close, it must be rather small to start with. This would require less compression before it actually closes. An airway would be small when the lung is closest to residual volume, and an airway would be smaller than usual if the lung were wet and heavy so that it would tend to "settle" within the thorax. This would tend to compress airways at the bottom of the lung and to overexpand airways at the top of the lung. (Think of how the rings of a Slinky are closer together at the bottom than at the top.) Rhonchi would thus be expected when auscultating the bottom portions of the thorax. Third, for an airway to close, the pressure on the outside must be greater than the pressure on the inside. This can only occur if the equal pressure point, that is, the position along the airways where the pressures inside and outside the airway are equal, is situated upstream from a collapsible portion of the airway. Because the equal pressure point is normally located in a noncollapsible region of the lung, rhonchi would not be expected. With small airway diseases (e.g., chronic bronchitis, asthma, emphysema, edema), the equal pressure point is located in the small airways upstream from collapsible small airways; as a result, airways downstream from the equal pressure point collapse, producing endexpiratory rhonchi. Once collapsed at end expiration, they pop open during mid-inspiration. In general, the more severe the disease is, the earlier in expiration and inspiration the rhonchi may be heard. Our fifth patient has pulmonary edema, and our sixth patient has pneumonia. In both instances, the lungs are wet and heavy, they settle down in the thorax, and the airways at the bottom of the lung are small. Because these patients have dense regions within their lungs, bronchovesicular breath sounds are heard from regions of the thorax over the affected lobes. In addition, end-expiratory and mid-inspiratory crackles are heard. Our seventh patient has severe pulmonary fibrosis and chronic bronchitis. The pulmonary parenchyma is shrunken and gnarled. As the lungs become smaller toward end expiration, the already shrunken and gnarled lungs become even more compressed. As they become more compressed, they generate exceptionally loud and "ugly" crackles much like you might hear if you placed your stethoscope chest piece over a loaf of bread wrapped in wax paper and squeezed the loaf of bread. Of course, when the lung re-expands during inspiration, the collapsed airways pop open, and even louder crackles are produced. Most crackles of edema or pneumonia are relatively soft and higher pitched, whereas crackles of fibrosis are relatively loud and coarse. Finally, our eighth patient has asthma. Asthma is caused by abnormal constriction of bronchioles or bronchiolar smooth muscle that leads to compression of small airways primarily during the end of expiration. Bronchoconstriction can be caused by an allergic reaction or by a bronchoconstrictory reflex initiated by distention of pulmonary veins as might result from left-sided heart disease. When airways made smaller
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by bronchoconstriction close during end expiration, the sibilant rhonchi are termed wheezes or sometimes whistles rather than crackles. Of course, you should expect wheezes to become softer or to disappear in response to bronchodilators. DIFFERENTIATION BETWEEN LUNG DISEASE AND HEART DISEASE
Specific lung diseases may be inferred from the physical examination and most often may be confirmed by radiography. Lung disease may be differentiated from heart disease by other features of the physical examination, however. Of course, errors of diagnosis may be made even with the most elaborate diagnostic methods; however, inferences may be made about whether the patient is ill primarily because of lung disease rather than heart disease by means of other features of the physical examination. Animals with long-standing cyanosis, with the rare exception of those with congenital heart diseases possessing rightto-left shunts (e.g., tetralogy of Fallot), most likely are ill due to lung disease rather than heart disease. Cyanosis is caused most often when regions of the lung are ventilated poorly but are perfused either normally or less poorly. When cyanosis is present due to heart disease, it usually indicates severe heart disease, and the patient is either likely to die soon or to be made better by aggressive therapy. As a result, the cyanosis is short-lived. With severe pulmonary fibrosis and bronchitis, however, the systemic arterial desaturation develops slowly and remains despite therapy; as a result, the cyanosis is long-lived. Whereas edema may be treated, the shrunken and gnarled lung of fibrosis and chronic bronchitis always remains shrunken and gnarled. Most dogs symptomatic from heart disease have rapid heart rates detected by auscultation and palpation of femoral pulses. This results from abnormal baroreceptor function and activation of the sympathoadrenal system. On the contrary, animals ill from lung disease usually expend great ventilatory efforts to expand the chronically stiff lungs. The increased efforts of ventilation arise from increased activity of the medullary ventilatory centers juxtaposed to which are the cardioregulatory centers. The increased irradiation from the ventilatory centers to the cardioregulatory centers produce a pronounced respiratory sinus arrhythmia (i.e., heart rate speeds during inspiration and slows during expiration). Animals ill from lung disease thus have relatively slow heart rates with pronounced respiratory sinus arrhythmias rather than the relatively diminished sinus arrhythmia resulting from constantly reduced vagal efferent traffic. Finally, animals with long-standing stiff lungs or with long-standing obstructive lesions fatigue their muscles of ventilation. This may be observed by palpation, but is better detected by thoracic radiography as pulmonary retractions. With retractions, the thoracic wall over the diaphragmatic lobes may actually be sucked inward during inspiration.
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This occurs, of course, because pleural pressure must be abnormally negative to ventilate the stiff lungs. The increased negative pleural pressure is achieved by great increased effort (tension) from muscles of ventilation. This increased tension may result in fatigue of muscles of ventilation and in decreased muscular blood flow, that is, a tense muscle tends to compress the intramuscular blood vessels, to increase vascular resistance to blood flow, to decrease muscular blood flow, and therefore to produce oxygen debt. This oxygen debt leads to depletion of adenosine triphosphate stores, which weakens the muscles of ventilation further, activates genes to produce muscular hypertrophy, and produces heave hues in horses and some dogs. Fatigue of muscles of ventilation seems to be greater in those muscles covering the basilar (diaphragmatic) lobes than in the apical lobes for two reasons. First, the muscles of ventilation over the apical lobes are "assisted" by the abduction of the thoracic limbs and possibly by the strap muscles in the neck. The muscles of ventilation covering the diaphragmatic lobes have no "help." Second, the radius of curvature of the thorax is greater in the basilar regions than in the apical regions; thus, according to the law of LaPlace, the muscles over the region with the greatest radius of curvature must generate more tension to produce comparable pleural pressure compared with muscles over the region of least radius of curvature. Not only may pulmonary retractions be well visualized on the dorsoventral thoracic radiograph, but the retractions may be identified by palpation. Place your right hand on the right hemithorax and your left hand on the left hemithorax so that your fingertips lay in the respective axillae and your thumbs "try" to meet over the dorsum. During inspiration as the thorax expands, the fingers move apart, but the thumbs may either stay still or actually move together. The physical examination of the thorax requires great experience and extensive training; however, it is extraordinarily helpful in arriving at a diagnosis, it is inexpensive to perform, it requires no special equipment save a stethoscope, it is repeatable, and, most of all, it is rewarding and fun. As mentioned earlier, if he or she spends as much time learning the techniques of physical examination as learning various imaging techniques, the veterinarian may be quite surprised at how easily most information required to make a difference in the outcome of the patient can be acquired.
References 1. Donnerberg R Druzgalski C, Hamlin RL, et al: Sound transfer function of the congested
canine lung. British Journal of Diseases of the Chest 1:23-31, 1980 2. Forgacs P: The functional basis of pulmonary sounds. Chest 73:399-405, 1978 3. Loudon R, Murphy RL, Jr: Lung sounds. Am Rev Respir Dis 130:663--673, 1984 4. Roudebush P, Ryan J: Breath sound terminology in the veterinary literature. JAVMA 194:1415-1417, 1989 5. Roudebush P: Lung sounds. JAVMA 181:122-126, 1982
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6. Shykoff BE, Ploysongsang Y, Chang HK: Airflow and normal lung sounds. Am Rev Respir Dis 137:872-876, 1988 7. Stoneman SA, Parker R, Jones A: Correlation of breath sounds with diagnoses of lung dysfunction: Experimental observations. Proc Inst Mech Eng [H] 203:151-158, 1989
Address reprint requests to Robert L. Hamlin, DVM, PhD, DACVIM Department of Veterinary Biosciences The Ohio State University College of Veterinary Medicine 1900 Coffey Road Columbus, OH 43210 e-mail: [email protected]
0195-5616/00 $15.00 + .00
PHYSICAL EXAMINATION OF THE PULMONARY SYSTEM Robert L. Hamlin, DVM, PhD
The term physical examination means various things to various persons, but for the purpose of this review, it refers to the process by which information is gained about a patient by inspection, palpation, percussion, and auscultation. History and anamnesis, as important as they are, are not included. Clinically meaningful decisions about most common pulmonary disorders may be made with information gained by the physical examination alone. To glean optimal information from the physical examination, the examiner must have as much interest in, and experience at, performing the examination as he or she does in techniques requiring more expensive, elaborate, and glamorous methods. The other aspects of the examination are enormously valuable to confirm inferences made by the physical examination, and they clearly add a profound dimension of security for the examiner. Many examiners use the stethoscope as neck jewelry rather than as a device for diagnosis, and many veterinary students receive little training in methods of auscultation and interpretation of lung sounds. Percussion is even more contentious and requires even more training and experience to be useful. This review describes how diagnoses of certain common pulmonary disorders (e.g., pleural effusion, pneumothorax, pulmonary edema, asthma, pulmonary fibrosis) may be made by means of the physical examination. The physical examination is based on understanding the origin and transmission of vesicular breath sounds, crackles, wheezes, brassy versus subtle coughs, and notes of percussion (Table 1}.4• 5 These features are discussed in veterinary patients, all of whom share the following physiFrom the Department of Veterinary Biosciences, The Ohio State University, College of Veterinary Medicine, Columbus, Ohio
VETERINARY CLINICS OF NORTH AMERICA: SMALL ANIMAL PRACTICE VOLUME 30 • NUMBER 6 • NOVEMBER 2000
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Table 1. PHYSICAL EXAMINATION FINDINGS FOR COMMON RESPIRATORY DISORDERS IN DOGS AND CATS Respiratory Rate
Respiratory Effort
Phase of Respiratory Difficulty
Asthma
Increased
Increased
Expiratory
Chronic bronchitis Pulmonary fibrosis Pleural effusion Pneumothorax Pneumonia Pulmonary edema Tracheal collapse
Increased Increased Increased Increased Increased
Increased Increased Increased Increased Increased Increased
Expiratory Inspiratory Inspiratory Inspiratory
-
-
-
-
Inspiratory (if extrathoracic tracheal collapse)
Percussion
May be hyperresonant
-
-
Dull Hyper-resonant May be dull May be dull
-
Auscultation
Cough
Wheezes and crackles
Hacking, if present
Crackles Loud crackles Distant Distant Loud crackles Loud crackles May hear a snap
Hacking Hacking Uncommon Uncommon Soft, half-hearted Half-hearted "Honking," high pitched
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cal findings: shortness of breath (predominantly due to tachypnea rather than hyperpnea), cyanosis, and reluctance to lie down; therefore, these findings are not repeated for each patient. It is important to note that the physical findings shared by most pulmonary diseases are also shared by most of the important heart diseases (e.g., mitral regurgitation, dilated cardiomyopathy, heartworm disease). COUGH
Everyone knows what a cough is, but it is important to differentiate a hacking (or honking) cough that sounds like it is coming from the throat from a half-hearted cough that sounds like it is coming from deep within the thorax. Hacking coughs are almost always caused by injury to large airways (e.g., trachea, mainstem bronchi). For example, hacking coughs are heard with tracheal collapse, tracheobronchitis, or compression of the left mainstem bronchus as might be caused by an enlarged left atrium due to mitral regurgitation. The half-hearted cough usually arises from injury to pulmonary parenchyma such as occurs with edema or pneumonia. Of course, everyone knows that these are general rules to which there are frequent exceptions manifested by individual patients. TACHYPNEA VERSUS HYPERPNEA
Dyspnea is a subjective term that describes a human experience of "air hunger." Labored breathing, the condition we recognize in our veterinary patients, may be a manifestation of increased rate of respiration (tachypnea) or increased depth of respiration (hyperpnea). As is the case with different types of cough, there are exceptions, but tachypnea most often arises from a stiff injured lung or thoracic wall, and hyperpnea arises from derangement of blood gases (i.e., high carbon dioxide, low oxygen, low pH). Although almost all healthy and quiet dogs, cats, and human beings breathe fewer than 20 times per minute, most veterinary patients examined in a rather unfamiliar environment breathe at a rate proportional to their level of excitement. I usually instruct clients to watch their pets breathe late at night when the pet is sleeping or resting and the house is quiet. At a short distance from the pet, watch the thorax and abdomen move in and out, count the number of breaths for 15 seconds, and multiply the number by 4 to obtain the respiratory rate per minute. (If the number the client gives you is not divisible by 4, do not trust the number.) If the lung is edematous, fibrotic, or otherwise stiff, the degree of tachypnea is proportional to the severity of the disease. If there is blood gas derangement, however, the patient usually does not breathe more rapidly but does breathe more deeply than normal. This hyperpnea is typical in pets with metabolic acidosis or in pets with elevated partial pressure of carbon dioxide. Whereas tachypnea can be documented by respiratory rate, the veterinarian must search
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for secondary signs of hyperpnea. That is because the depth of respiration is commonly measured as tidal volume, or the volume of air taken in during a normal quiet inspiration. It is difficult to determine if a pet's tidal volume has increased by 50%, although it is quite simple to determine if the respiratory rate has increased by even 25%. Signs of hyperpnea may be bulging of the eyes, muscular shaking during inspiration, sucking in of the skin covering the thoracic inlet, tensing of the "strap" muscles of the neck, reluctance to lie down, standing with thoracic limbs abducted, or unusual flaring of the nostrils. To document this, you can produce respiratory acidosis by holding your breath for 15 seconds. Then count the number of breaths for the 15 seconds after you resume breathing. You can see that you breathe more deeply but no more rapidly than before you held your breath. VESICULAR BREATH SOUNDS
Vesicular breath sounds are produced by air traveling through the bronchopulmonary tree during inspiration and expiration. 2' 3, 6, 7 For airflow to produce sound, it must travel at a high enough velocity to change its laminar flow pattern and become turbulent or to shed vortexes (swirls of air). It is the disturbed flow that causes the bronchopulmonary tubes to oscillate at sufficient magnitude (>15 dB) and frequency (>60 Hz) to be heard on the torso as sound. The prime factor in the generation of vesicular breath sounds is the velocity of airflow. Because the velocity of a gas flowing is equal to the total flow divided by the cross-sectional area of the tubes through which the flow moves, it is important to know where the cross-sectional areas are smallest, because flow through those regions is most likely to be disturbed and to produce the vesicular breath sounds. Individually, the small airways (e.g., bronchioles, respiratory bronchioles, alveolar ducts) are minute (far < 1 mm in diameter). Taken together, however, the hundreds of thousands of these small airways constitute an enormous cross-sectional area through which air flows. Because of their enormous cross-sectional area, the velocity of air flowing through them is much too slow for the flow to be turbulent or for vortexes to develop, and no vesicular breath sound is made by air flowing into or out of the small airways. Taken singly, the large airways (e.g., trachea and mainstem, lobar, and lobular bronchi) are relatively large; however, because there are so few of them, the total cross-sectional area is less than .005 of the total cross-sectional area of the small airways, and vesicular breath sounds are made as air tumbles through the larger airways. In general, the larger airways are located in the neck and the middle of the thorax, and the smaller airways are located in the periphery of the lung just under the thoracic wall. Although vesicular sounds are made in the larger airways and thus may be heard best by listening (auscultating) over the area where they are made, these sounds are transmitted primarily in the direction that the air flows. This is different from true sound, which is transmitted
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centrifugally; as a result, breath sounds are termed pseudosounds. True sound is made when you snap your fingers, and the sound can be heard uniformly in all directions from your fingers. An example of pseudosound occurs when you stand in front of and blow on the rotating blades of a fan. The sound (pseudosound) can be heard mainly at the front of the fan and not behind it, that is, this pseudosound travels mainly in the direction the air is blown by the fan. The tracheal vesicular breath sounds may be heard clearly during inspiration and expiration, when auscultating over the trachea, because that is closest to where the sound is made. If you place your stethoscope over the diaphragmatic (basilar) lobes of lung the inspiratory vesicular breath sound heard is softer than that over the trachea. This is because the sound made by air tumbling through the trachea is being transmitted to the lung, in the direction the air is flowing and because the sound is attenuated by the distance between the tracheal and basilar lobes. During expiration, there is either no sound or only a soft expiratory vesicular breath sound heard over the diaphragmatic lobes. This occurs because the sound is made in the trachea and is blown out of the thorax rather than being "sucked" into the thorax. Place your stethoscope chest piece in front of your mouth and breathe through your wide-open mouth and you hear only a soft inspiratory sound but a much louder expiratory sound. The sound, actually pseudosound, is produced by air tumbling through your trachea or other large airways, and that sound is sucked into the lung during inspiration so that it is heard only slightly during inspiration. During expiration, the sound is still made in the large airways, but is blown out of the mouth. The intensities of even normal vesicular breath sounds vary greatly among the species, breeds, ages, and tidal volumes; as a result, to know what "normal" is requires an enormous commitment to auscultating hundreds of normal individuals. The following cases are meant to serve as practical examples of common situations encountered in daily veterinary practice. Pleural Effusion and Pneumothorax
Our first patients are a cat with pleural effusion and a dog with pneumothorax. Remember that they share (with all the patients to follow) the clinical signs of dyspnea, cyanosis, and reluctance to lie down. When auscultating over the trachea, normal tracheal, vesicular breath sounds are heard. When auscultating over the basilar lobes, however, the vesicular breath sounds are extremely difficult to hear. Why would this be if the sounds are made within the trachea and heard quite normally over the trachea? Remember that the vesicular breath sounds heard over the basilar lobes are actually made in the large airways, and are transmitted into the parenchyma of the lungs as air flows in that direction. The fact that these breath sounds are not heard on the thoracic wall over the lung may indicate that the sounds are either reflected or
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attenuated in their path from the lung to the thoracic wall. Reflection of sound occurs when sound traveling through one medium (e.g., an airway) reaches a much denser medium (e.g., pleural effusion). Instead of the sound traveling from the lung to the thoracic wall, it is reflected by the dense pleural effusion. The sound heard on the other side of the air-fluid boundary is attenuated greatly because of the reflection of much of the acoustic energy. Conversely, if a pneumothorax were present, the sound on the other side of the pneumothorax would be greatly attenuated, because sound does not travel well through relatively rare air. Remember that you can detect a train coming much earlier if you put your ear to the rail than if you try to listen through the air. Pleural effusion and pneumothorax thus would result in the absence or great attenuation of the inspiratory vesicular breath sounds heard normally over the thoracic wall. So how can you differentiate between attenuation of sound due to either pleural effusion or pneumothorax? A mere thump on (i.e., percuss) the thoracic wall is sufficient. When percussing on a dense water-filled structure like your forehead, you hear a dull note. I cannot tell you what a dull note is, but when you listen to the note of percussion produced when you thump on your forehead, you know instantly what a dull note is. When percussing over an air-filled structure such as a pneumothorax, you hear a hyper-resonant note of percussion. I cannot tell you what a hyper-resonant note of percussion sounds like, but when you percuss over a gas-filled stomach (which you can produce by gulping a can of cola), you know instantly what a hyper-resonant note of percussion is. An interesting rule-of-thumb is that you should always put a needle into the thorax when there is an absence of inspiratory vesicular breath sounds. In the first instance, you may drain pleural fluid. In the second instance, you may evacuate pneumothorax. The exception to this rule may be if the liver is herniated through the diaphragm into the thoracic cavity. In such a case, the breath sounds are attenuated and the note of percussion is dull, but little benefit would accrue from performing a thoracentesis. Pulmonary Edema or Exudate (Pneumonia)
Our third and fourth patients are dogs just as dsypneic, cyanotic, and reluctant to lie down as the first two patients. Normal tracheal vesicular breath sounds are heard. But when listening over the basilar lobes, much louder than expected inspiratory breath sounds as well as higher pitched expiratory vesicular breath sounds are heard. The reason why the expiratory vesicular sounds are much louder than expected is because the expiratory sounds are normally soft to absent. Vesicular breath sounds that are louder than expected are termed bronchial or bronchovesicular breath sounds; however, they are still made in the large airways and are transmitted (but with less decrement) over the basilar
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lobes. So, what might decrease the decrement of sounds through the thorax from the large airways to the regions over the basilar lobes? The answer is a dense pathway, and a dense pathway may be a liquid-filled lung, a lung filled with edema (as is the case with heart failure), or exudate (as is the case with pneumonia). 1 You might question, "Why are sounds louder with a wet and dense lung than with pleural effusion?" The answer is simple. If the parenchyma of the lung is wet and dense, sounds are transmitted better than normally through the dense walls. If the sound meets an air-water interface, the sound is attenuated. The higher pitched sounds of edema and pneumonia result from the pulmonary parenchyma being wet, heavy, and stiff. Stiff structures tend to resonate at higher frequencies than flaccid structures. Try striking a balloon that is taut (i.e., stiff) and another balloon that is flaccid. You notice that the taut balloon oscillates for a much shorter duration and at a higher frequency than the flaccid balloon. Can you differentiate between the bronchovesicular breath sounds of edema and those of pneumonia? Unfortunately not. Because both lungs may be equally dense, they transmit sound equally well. Of course, differentiation may be made by the "company the vesicular breath sound keeps." If one dog is a Doberman Pinscher with dilated cardiomyopathy and the other is a young German Shepherd puppy with a high fever and leukocytosis, it is likely that the Doberman Pinscher has edema and the German Shepherd has pneumonia. Animals with pleural effusion, pulmonary edema, and pneumonia all have relatively dense thoracic contents; as a result, a relatively dull note or percussion is elicited. Because this dullness may be quite subtle, it is much more difficult to identify a dull note than the hyper-resonant note of pneumothorax. CRACKLES AND WHEEZES: ADVENTITIOUS BREATH SOUNDS
The precise origins of crackles (also called rales) and wheezes (also called sibilant rhonchi) are obscure. Wheezes are almost always loudest during expiration, whereas crackles are almost always loudest during inspiration but are also heard during expiration. Adventitious breath sounds are not caused by air flowing through airways but probably occur as a result of airways being "scrunched" closed or, if already closed, "popping" open. To mimic the sound of pulmonary crackles, place the chest piece of your stethoscope over an unwrapped loaf of bread and squeeze the load of bread. The tiny pockets (alveoli) made within the bread as the carbon dioxide is released just before baking "scrunch" closed as the loaf is squeezed, and crackles are produced. For an airway to close, at least three features must be present. First, airways must be collapsible. Because large airways are normally supported by rather rigid cartilaginous rings, rhonchi do not usually arise from larger airways because they cannot collapse. Conversely,
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because small airways are not supported by rigid cartilaginous structures, they can close, and their closure probably produces rhonchi. Second, for an airway to close, it must be rather small to start with. This would require less compression before it actually closes. An airway would be small when the lung is closest to residual volume, and an airway would be smaller than usual if the lung were wet and heavy so that it would tend to "settle" within the thorax. This would tend to compress airways at the bottom of the lung and to overexpand airways at the top of the lung. (Think of how the rings of a Slinky are closer together at the bottom than at the top.) Rhonchi would thus be expected when auscultating the bottom portions of the thorax. Third, for an airway to close, the pressure on the outside must be greater than the pressure on the inside. This can only occur if the equal pressure point, that is, the position along the airways where the pressures inside and outside the airway are equal, is situated upstream from a collapsible portion of the airway. Because the equal pressure point is normally located in a noncollapsible region of the lung, rhonchi would not be expected. With small airway diseases (e.g., chronic bronchitis, asthma, emphysema, edema), the equal pressure point is located in the small airways upstream from collapsible small airways; as a result, airways downstream from the equal pressure point collapse, producing endexpiratory rhonchi. Once collapsed at end expiration, they pop open during mid-inspiration. In general, the more severe the disease is, the earlier in expiration and inspiration the rhonchi may be heard. Our fifth patient has pulmonary edema, and our sixth patient has pneumonia. In both instances, the lungs are wet and heavy, they settle down in the thorax, and the airways at the bottom of the lung are small. Because these patients have dense regions within their lungs, bronchovesicular breath sounds are heard from regions of the thorax over the affected lobes. In addition, end-expiratory and mid-inspiratory crackles are heard. Our seventh patient has severe pulmonary fibrosis and chronic bronchitis. The pulmonary parenchyma is shrunken and gnarled. As the lungs become smaller toward end expiration, the already shrunken and gnarled lungs become even more compressed. As they become more compressed, they generate exceptionally loud and "ugly" crackles much like you might hear if you placed your stethoscope chest piece over a loaf of bread wrapped in wax paper and squeezed the loaf of bread. Of course, when the lung re-expands during inspiration, the collapsed airways pop open, and even louder crackles are produced. Most crackles of edema or pneumonia are relatively soft and higher pitched, whereas crackles of fibrosis are relatively loud and coarse. Finally, our eighth patient has asthma. Asthma is caused by abnormal constriction of bronchioles or bronchiolar smooth muscle that leads to compression of small airways primarily during the end of expiration. Bronchoconstriction can be caused by an allergic reaction or by a bronchoconstrictory reflex initiated by distention of pulmonary veins as might result from left-sided heart disease. When airways made smaller
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by bronchoconstriction close during end expiration, the sibilant rhonchi are termed wheezes or sometimes whistles rather than crackles. Of course, you should expect wheezes to become softer or to disappear in response to bronchodilators. DIFFERENTIATION BETWEEN LUNG DISEASE AND HEART DISEASE
Specific lung diseases may be inferred from the physical examination and most often may be confirmed by radiography. Lung disease may be differentiated from heart disease by other features of the physical examination, however. Of course, errors of diagnosis may be made even with the most elaborate diagnostic methods; however, inferences may be made about whether the patient is ill primarily because of lung disease rather than heart disease by means of other features of the physical examination. Animals with long-standing cyanosis, with the rare exception of those with congenital heart diseases possessing rightto-left shunts (e.g., tetralogy of Fallot), most likely are ill due to lung disease rather than heart disease. Cyanosis is caused most often when regions of the lung are ventilated poorly but are perfused either normally or less poorly. When cyanosis is present due to heart disease, it usually indicates severe heart disease, and the patient is either likely to die soon or to be made better by aggressive therapy. As a result, the cyanosis is short-lived. With severe pulmonary fibrosis and bronchitis, however, the systemic arterial desaturation develops slowly and remains despite therapy; as a result, the cyanosis is long-lived. Whereas edema may be treated, the shrunken and gnarled lung of fibrosis and chronic bronchitis always remains shrunken and gnarled. Most dogs symptomatic from heart disease have rapid heart rates detected by auscultation and palpation of femoral pulses. This results from abnormal baroreceptor function and activation of the sympathoadrenal system. On the contrary, animals ill from lung disease usually expend great ventilatory efforts to expand the chronically stiff lungs. The increased efforts of ventilation arise from increased activity of the medullary ventilatory centers juxtaposed to which are the cardioregulatory centers. The increased irradiation from the ventilatory centers to the cardioregulatory centers produce a pronounced respiratory sinus arrhythmia (i.e., heart rate speeds during inspiration and slows during expiration). Animals ill from lung disease thus have relatively slow heart rates with pronounced respiratory sinus arrhythmias rather than the relatively diminished sinus arrhythmia resulting from constantly reduced vagal efferent traffic. Finally, animals with long-standing stiff lungs or with long-standing obstructive lesions fatigue their muscles of ventilation. This may be observed by palpation, but is better detected by thoracic radiography as pulmonary retractions. With retractions, the thoracic wall over the diaphragmatic lobes may actually be sucked inward during inspiration.
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This occurs, of course, because pleural pressure must be abnormally negative to ventilate the stiff lungs. The increased negative pleural pressure is achieved by great increased effort (tension) from muscles of ventilation. This increased tension may result in fatigue of muscles of ventilation and in decreased muscular blood flow, that is, a tense muscle tends to compress the intramuscular blood vessels, to increase vascular resistance to blood flow, to decrease muscular blood flow, and therefore to produce oxygen debt. This oxygen debt leads to depletion of adenosine triphosphate stores, which weakens the muscles of ventilation further, activates genes to produce muscular hypertrophy, and produces heave hues in horses and some dogs. Fatigue of muscles of ventilation seems to be greater in those muscles covering the basilar (diaphragmatic) lobes than in the apical lobes for two reasons. First, the muscles of ventilation over the apical lobes are "assisted" by the abduction of the thoracic limbs and possibly by the strap muscles in the neck. The muscles of ventilation covering the diaphragmatic lobes have no "help." Second, the radius of curvature of the thorax is greater in the basilar regions than in the apical regions; thus, according to the law of LaPlace, the muscles over the region with the greatest radius of curvature must generate more tension to produce comparable pleural pressure compared with muscles over the region of least radius of curvature. Not only may pulmonary retractions be well visualized on the dorsoventral thoracic radiograph, but the retractions may be identified by palpation. Place your right hand on the right hemithorax and your left hand on the left hemithorax so that your fingertips lay in the respective axillae and your thumbs "try" to meet over the dorsum. During inspiration as the thorax expands, the fingers move apart, but the thumbs may either stay still or actually move together. The physical examination of the thorax requires great experience and extensive training; however, it is extraordinarily helpful in arriving at a diagnosis, it is inexpensive to perform, it requires no special equipment save a stethoscope, it is repeatable, and, most of all, it is rewarding and fun. As mentioned earlier, if he or she spends as much time learning the techniques of physical examination as learning various imaging techniques, the veterinarian may be quite surprised at how easily most information required to make a difference in the outcome of the patient can be acquired.
References 1. Donnerberg R Druzgalski C, Hamlin RL, et al: Sound transfer function of the congested
canine lung. British Journal of Diseases of the Chest 1:23-31, 1980 2. Forgacs P: The functional basis of pulmonary sounds. Chest 73:399-405, 1978 3. Loudon R, Murphy RL, Jr: Lung sounds. Am Rev Respir Dis 130:663--673, 1984 4. Roudebush P, Ryan J: Breath sound terminology in the veterinary literature. JAVMA 194:1415-1417, 1989 5. Roudebush P: Lung sounds. JAVMA 181:122-126, 1982
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6. Shykoff BE, Ploysongsang Y, Chang HK: Airflow and normal lung sounds. Am Rev Respir Dis 137:872-876, 1988 7. Stoneman SA, Parker R, Jones A: Correlation of breath sounds with diagnoses of lung dysfunction: Experimental observations. Proc Inst Mech Eng [H] 203:151-158, 1989
Address reprint requests to Robert L. Hamlin, DVM, PhD, DACVIM Department of Veterinary Biosciences The Ohio State University College of Veterinary Medicine 1900 Coffey Road Columbus, OH 43210 e-mail: [email protected]