When first alerted to a patient presenting in crisis, the goal of the initial examination is to rapidly identify any imminently life-threatening problems via a streamlined, efficient, clinical examination.
When first alerted to a patient presenting in crisis, the goal of the initial examination is to rapidly identify any imminently life-threatening problems via a streamlined, efficient, clinical examination. Evaluation of the cardiovascular and respiratory systems is a high priority, both because these systems need to function well to maintain life and also because in many of these patients it is cardiopulmonary dysfunction that is causing the crisis. Although initial assessment must also include evaluation of the central nervous system, abdominal palpation and body temperature, most of this lecture will focus on examination of the cardiopulmonary system. For any patient, the initial survey of each major body system is abbreviated such that the clinical signs that yield the most important information are examined first. Stabilization measures should be initiated for any major problems prior to the remainder of the full physical evaluation.
A very brief history should be obtained at presentation, focusing on the owner's chief complaint. Does the information suggest the patient is at high risk? Preliminary physical exam focuses on the basics: Can the patient draw a breath? Does it look sick or dehydrated? Any gross abnormalities of vital signs? What is the level of consciousness (LOC) - is the patient depressed or agitated? Can it walk? Next, a more focused exam concentrates attention on the organ system referred to in the owner complaint and other high-risk possibilities. Are there skin wounds, active bleeding, is the abdomen distended or painful?
Vital signs provide very useful information. Hypothermia may be due to environmental causes or severe illness (including heart failure and in cats, septic shock). Occasionally animals with respiratory difficulty will have hyperthermia; this is usually due to obstruction of upper airways causing resistance to breathing and the extra muscular effort required to pull or push gas past the obstruction generates excess heat. These patients should receive assistance in cooling.
The heart rate should be assessed. A quietly resting or sleeping dog will have a heart rate between 40 and 90 BPM; this is inappropriately slow in an alert dog presented to a veterinary clinic. If the dog does appear depressed or obtunded, a heart rate > 120 BPM is considered tachycardia. Most cats presented to a clinic in health or disease have high heart rates (> 180 BPM). Persistent tachycardia (> 220 BPM) in quiet cats is normal in some but may indicate that underlying pathology is present and driving the heart rate high. Relative bradycardia (< 160 BPM) is the most common serious rhythm disturbance in sick cats and is routinely accompanied by hypothermia, often an ominous sign.
Pulse character should be determined: is it normal, hyperkinetic, thready, or weak? The most common conditions that change the clinical hemodynamic parameters are hypovolemia, anemia, sepsis/inflammatory response syndrome and abnormal cardiac function. Familiarity with how each condition in isolation affects the clinical hemodynamic parameters facilitates identification of the patient with multiple causes of abnormal perfusion. Most animals with abnormal perfusion have some component of hypovolemia so recognizing uncomplicated hypovolemia is the rational starting point. In uncomplicated hypovolemia, mucous membrane color, capillary refill time (CRT) and vigor, pulse profile (height and width), heart rate, and cardiac auscultation provide the means of intravascular volume assessment. Pulses (femoral and metatarsal) should be carefully palpated to allow assessment of their height (to estimate pulse pressure) and their width i.e., the length of time the pulse lasts. Assessing the height and width of the pulse together allows an estimation of pulse volume and a perceptive clinician can generate a mental image of the pulse profile (Figure 1). One should develop an awareness of the normal variation in pulse profile. A normovolemic animal that is stressed or painful will have slightly higher and narrower pulse profile than a resting animal.
Figure 1: Normal pulse profile
In the compensatory stages of hypovolemia dogs will develop a moderate tachycardia of 130-160 beats per minute. The increased heart rate and contractility, reduced blood volume, and stiffer arterial tree produces a pulse that is narrower and higher than normal (Figure 2). This pulse profile is often referred to as "bounding" or "snappy" but these terms often serve to confuse rather than clarify. In compensatory hypovolemia metatarsal pulses should still be palpable. Mucous membranes should be pink to pinker than normal with a rapid CRT of less than one second duration. As hypovolemia becomes more severe, the duration of the pulse narrows disproportionately in excess of any reduction in amplitude and the pulse quality becomes 'thready' (Figure 3).
Figure 2: Moderate Hypovolemia
The increases in heart rate seen in dogs with hypovolemia are surprisingly independent of body weight such that severe hypovolemia results in a heart rate of 180-220 in most dogs. Heart rates in excess of this should raise suspicions of a primary arrhythmia rather than just a sinus tachycardia in response to hypovolemia. Heart sounds are often very quiet due to the severe hypovolemia (as are heart murmurs that will become apparent during volume loading!). Mucous membranes have little or no red coloration (white, muddy, or grey), and CRT is prolonged or absent. With severe hypovolemia and in animals with anaphylaxis, severe sepsis, or septic shock the femoral pulses become both narrow and low-amplitude: both systolic and diastolic pressures fall and the difference between them is very small. This produces a weak femoral pulse (Figure 4) and metatarsal pulses should not be palpable.
Figure 3: Thready pulse
Detection and characterization of these variations is essential to monitor patients over time, and nursing staff should be trained to recognize these pulse types. The ability to estimate intravascular volume status using clinical signs becomes invaluable when assessing the response to acute volume replacement. In general, during successful volume replacement perfusion parameters will gradually and predictably return to normal through the same stages in reverse. This enables the clinician to rapidly detect an inadequate response to volume resuscitation and pursue the underlying cause.
Figure 4: Weak pulse
Mucus membrane color gives information about perfusion, hemoglobin concentration, and saturation. Pale mucus membranes may indicate anemia, hypoxemia from lung disease, or hypovolemia. Cyanotic mucus membranes most often suggest airway obstruction or loss of lung volume due to pleural effusion. A combination of pallor and cyanosis (gray) suggests both poor perfusion and hypoxemia. Brown mucus membranes suggest the presence of methemoglobin, most often seen in companion animals following acetaminophen intoxication.
Capillary refill time is obtained by squeezing the blood out of a tissue bed and observing how rapidly the color returns to baseline. This is most conveniently (and accurately) obtained by blanching the mucus membranes over the maxilla above the gum line. A normal animal should have pink mucous membranes with a vigorous capillary refill that takes 1-1¾ seconds. Animals with poor circulation shut down the blood flow to their skin (including mucus membranes of the mouth), so the color becomes paler and it takes longer to return to baseline after releasing digital compression. Many animals with poor circulation also have positional changes in their CRT: it may be normal when the head is held at the same level as their heart, then color becomes pale and CRT prolonged when the head is elevated up high. Animals with sepsis syndrome cannot turn off the blood supply to their skin even when they might desperately need to do so. In these patients their skin and mucus membranes are over-perfused, yielding a deep red color to the gums and a brisk CRT. Do not confuse the gum line hyperemia of animals with dental disease with the uniform hyperemia of the oral cavity in animals with sepsis syndrome.
Palpation of the precordial cardiac impulse often yields much useful information. The location and nature of the impulse may provide information about cardiac enlargement (dilatation or hypertrophy). Loud murmurs may also produce precordial thrills (palpable vibrations on the chest wall at the point of maximal intensity of the murmur), which are useful in localizing the source of the murmur. The cardiac rhythm can be assessed as well as the compressibility of the thorax (cats).
Audible heart sounds include transient sounds (those of brief duration) and murmurs (longer duration sounds). The first heart sound (S1) is caused by closing and tensing of the left and right AV valves (mitral and tricuspid valves) at the onset of systole. The intensity of Sl depends on a variety of factors, including the PR interval of the electrocardiogram (which determines the position of the AV valves prior to ventricular contraction), cardiac contractility, how full the ventricle are before they contract (ventricular preload), and the condition of the lungs and chest wall, and where one listens on the chest. Remember that the intensity of sound decreases with the square of the distance from the source, so it is important to listen to all areas of the thorax if one is to hear soft murmurs that generally do not radiate (transmit) well. S1 is normally longer, louder, and lower pitched than S2 (the second heart sound). S2 is caused by the closing and tensing of the left and right semilunar valves (aortic and pulmonic valves) at the end of ventricular ejection, when the pressure in the right and left ventricles falls below that of the pulmonary artery and aorta, respectively. Normal blood flow across all of the valves (e.g., from the left atrium into the left ventricle across the mitral valve during diastole, and from the left ventricle into the aorta across the aortic valve during systole) early in diastole) is laminar (undisturbed flow) and therefore silent. S2 is shorter and higher pitched than Sl, and although it is not as loud, it will appear louder when one listens at the heart base because of the proximity of the aortic and pulmonic valves to the stethoscope. The intensity of S2 is also influenced by a variety of factors, most importantly the diastolic pressure in the aorta and pulmonary artery (thus a loud or "cracking" pulmonary component of S2 might be associated with pulmonary hypertension). Sl and S2 are normal sounds audible in all dogs and cats. The cadence of Sl and S2 ("lub dup") changes in different situations, becoming more difficult to sort out at extremely high heart rates (> 250) since the normally much longer period of diastole shortens disproportionately with increasing heart rate. When in doubt about which is S1 or S2, it is helpful to palpate the arterial pulse while auscultating, since Sl occurs just before (nearly simultaneously with) the upstroke of the peripheral pulse. Along with the third and fourth heart sounds (S3 and S4, early and late diastolic sounds considered pathologic findings caused by an excessively stiff (noncompliant) ventricle in dogs and cats) and a variety of "clicks" and other brief sounds occasionally heard in dogs and cats, S1 and S2 are classified as transient sounds.
Heart murmurs are prolonged sounds, generally caused by the formation of turbulent blood flow within the heart or great vessels. Whether or not turbulence forms is a function of several physiologic variables, including the velocity of the blood flow, the size of the chamber or vessel, and the viscosity of the blood (highly dependent on the packed call volume). Murmurs often radiate in the direction of turbulent blood flow (e.g., the murmur of aortic stenosis is heard best at the left heart base, over the aortic valve, but it is also heard well at the right heart base, since the aortic arch crosses to the right hemithorax high up under the right foreleg, at the heart base), although other factors, such as the acoustical coupling (the 2 structures to transmit sound between them) of the cardiovascular structure generating the sound to the chest wall at a particular location, may also play an important role. A description of a murmur should include its anatomic location (point of maximal intensity), timing (when it occurs with respect to the cardiac cycle), intensity (loudness), pitch (frequency), and quality (the "shape" of the murmur when recorded on paper). The most common murmurs auscultated in animals in crisis include a long murmur superimposed over S1 in dogs with mitral valve disease, and murmurs between S1 and S2 in cats with hypertrophic cardiomyopathy.
What is the respiratory pattern and rate? Tachypnea and hyperpnea often indicate a need to increase minute ventilation in response to cardiopulmonary or systemic disease. Fast shallow respirations are a common mechanism to increase minute ventilation in the face of lungs made stiff by edema. Deep respirations often suggest that the patient needs to increase minute ventilation with normal lungs, for example as a method to compensate for metabolic acidosis. Abdominal breathing (active contraction of the abdominal muscles to increase the strength of exhalation) is often associated with air trapping due to asthma (in cats), large airway collapse (dogs), or pleural effusion (dogs and cats).
The term dyspnea refers to the experience of distress secondary to respiratory disease. In man it is most often associated with increased resistance to airflow but may also be caused by anything leading to clinically significant hypoxemia or hypercapnia (especially if acute). Like pain, its presence is inferred from facial expressions and behavioral signs of distress. Dyspnea is a true medical emergency; our goal is to relieve it within minutes of presentation. In contrast, the terms labored breathing or increased respiratory effort refer to the physical manifestations of increased work of breathing. This may be objectively measured, but most of the time is inferred from subjective appraisal of physical signs. Whereas an animal with dyspnea is having a crisis, an animal with labored breathing may be very well adapted to its condition and be free from distress. Where a given patient lies on this spectrum must be inferred from their behavior. In general, as an animal approaches dyspnea it must focus more and more conscious effort on the act of breathing. Animals that are interactive and engaged with their environment usually still have OK physiological reserves; those that appear withdrawn and focused on the act of breathing are heading toward respiratory arrest. A notable exception to this generalization is the puppy. Juvenile dogs will often remain active, alert, and hungry even with advanced respiratory failure and may go straight to the brink of death before showing compelling behavioral signs of distress.
1. Restrictive lung disease: Restrictive diseases are characterized by pulmonary changes that reduce lung compliance and make the lungs more difficult to inflate. At the same time, the underlying disorder typically compromises the oxygenating capacity of the lung. Arterial hypoxemia and lung inflammation or edema are direct respiratory stimulants and provoke an increase in desired minute alveolar ventilation. Thus, when severe, the animal is faced with the need to increase ventilation with lungs that are increasingly stiff and difficult to inflate. The archetypical pattern that results from this combination is breathing at a relatively fast rate and small tidal volume. Clinically, the animal develops an increased frequency with rapid shallow inspirations. As inspiration becomes more difficult (or fatigue develops with acute illness), one of the first behavioral changes is a reluctance to lie in lateral recumbency. As difficulties progress, the dog may have trouble remaining in sternal recumbency for prolonged periods and position changes become more frequent. Finally it may be difficult to lie down for any significant period and the dog will prefer to sit or stand, even in the face of exhaustion. During this progression, the dog begins to extend the head and neck and recruit accessory muscles of inspiration, including the scalenes and the sternomastoids. The forelimbs are abducted as breathing difficulty becomes greater. The head may bob up and down with respiratory effort. If the elastic recoil of the lung is sufficient, exhalation may be completely passive. If there is excessive air trapping from airway collapse, or if passive recoil of the lung does not provide sufficient emptying the dog may exhale actively (contraction of intercostal muscles) and may recruit accessory muscles of expiration (abdominal muscles).
2. In contrast to what is seen with airway obstruction or pleural space disease, hypoxemia from lung disease typically causes more pallor than cyanosis, yielding a pale-to-grey color of the mucus membranes. If the underlying cause is rapidly progressing the animal may develop fatigue of the respiratory muscles quickly and go on to develop hypoventilation (respiratory failure).
3. Any disorder that increases in the water content of the lung tissue will reduce its compliance by increasing the opening pressure required to inflate pulmonary exchange units. This occurs with all forms of edema (heart failure, injury) and inflammation (pneumonia). As edema develops, regions of the lung will lose ventilation and venous admixture increases. Because the lungs are relatively stiff, the prototypical pattern will be relatively shallow breaths at a relatively high frequency. As these disorders tend to develop rapidly, respiratory fatigue may develop quickly and hasten death in the absence of ventilatory support.
4. Pleural space disease: The introduction of air or fluid (blood, pus, or edema fluid) into the pleural space produces characteristic changes in respiration. The thoracic girth is normally maintained by the opposing forces of lung (which wants to collapse) and rib cage (which wants to spring outward). Separation of the two with a layer of air or fluid in the pleural space produces a reduction in lung volume and an increase in thoracic girth. As lung volume falls exchange units are lost as the reduction in volume becomes sufficient to favor small airway collapse, leading to hypoxemia due to venous admixture and if severe, hypoventilation. At the same time this is occurring the total intrathoracic volume is growing, flattening the diaphragm (placing it at a mechanical disadvantage) and shifting external intercostal muscle function towards exhalation. As the problem progresses, inspiratory efforts increase and accessory muscles of inspiration may be recruited. Expiratory efforts increase as small airway collapse produces air trapping and a need to forcefully push air out of the lungs.
All normal lung sounds are generated by turbulent airflow in the trachea and larger airways, as flow in small airways is slow and laminar and generates no audible sound. The origin of canine breath sounds has been investigated using a hollow airway cast instrumented with an intraluminal microphone introduced into different-sized airways ranging from 2 – 19 mm diameter and subjected to a range of airflows. This work supports an intrapulmonic source of breath sounds: most inspiratory sound is produced within lobar and subsegmental airways (down to diameters of 5 – 8 mm), and most expiratory sound originates in the trachea and large bronchi.
The sound heard at the chest wall is the final product of its generation within the airways and subsequent modification as it passes through the structures of the chest. As sound travels from its source in the larger airways, it passes through lung parenchyma, the pulmonary pleura, the pleural space, the chest wall pleura, the muscle, bone and skin of the chest wall. The sound must then bridge the gap between skin and stethoscope – a gap usually filled with hair in veterinary patients. The sound is further modified acoustically by the stethoscope and how it fits the wearer's ear canals.
Normal lung and chest wall act as a low-pass filter. As sound travels across the parenchyma, it must traverse hundreds-to-thousands of air:tissue interfaces as it crosses pulmonary exchange units. Whenever energy waves (such as sound or light) pass through an interface between different media, a portion of the energy will be reflected back. In the case of sound, the higher-frequency components are reflected more efficiently. Thus, while sound recorded directly over the trachea remain intense over a broad frequency range (75-1000 Hz), breath sounds over the chest wall are lower in amplitude (quieter) and lower in pitch, with most sound energy contained in frequencies < 400 Hz. The amplitude and frequency range of normal lung sounds varies with respiratory pattern (airflow volume and velocity) and age.9 Large breaths, high velocity airflow from panting, and increasing age all favor increased lung sound amplitude and frequency, and these must be taken into account when interpreting auscultation of a patient.
Lung sounds may be increased or decreased in disease states. Decreased breath sounds may also be normal in small animals breathing quietly (as in the cat!). Pathological causes of reduced breath sounds include respiratory weakness (small breaths) and pleural space disease. The presence of air or fluid within the pleural space uncouples the chest wall from the lung acoustically and can greatly attenuate sound. Pathological causes of increased lung sounds include any disorder that prompts compensatory increases in airflow velocity (increased tidal volume, panting), causes loss of exchange units (reducing the number of air:tissue interfaces), or involves infiltration of the alveolar septa by edema or cells (pneumonia, neoplasia). Loss of exchange units or thickening of the water-dense medium of the lung allows more of high frequency sound to pass through to the surface and lung sounds become both louder (larger amplitude) and 'harsher' (more high frequency components) in quality. The extreme example is seen with complete consolidation of lung tissue around a patent lobar bronchus. In this case, the lung sounds heard over this nonventilated region of lung are loud and may approximate those heard directly over the trachea, and this has sometimes been called "bronchial breathing". If the bronchus is obliterated, the lobe loses its acoustical connection with the airways and lung sounds are diminished over that region. When measured electronically, increased lung sounds are a sensitive indicator of increased pulmonary water content in dogs with experimentally induced pulmonary edema10. This change occurs long before the development of adventitial sounds such as crackles, and skillful clinicians can detect this change before radiographic changes are evident.
Adventitial sounds may be discontinuous (crackles) or continuous (wheezes and rhonchi). Crackles may be further divided into coarse crackles and fine crackles. Coarse crackles are related to mobilization of secretions in the large upper airways and are audible at the mouth. This sound is easily heard without a stethoscope, and referred sounds heard during auscultation may overwhelm other lung sounds. Fine crackles have nothing to do with the presence of intraluminal fluid. They are caused by the explosive opening of small airways and tend to be most intense late in inspiration and it the dependent region of lung; they are difficult to hear at the mouth. Their presence often indicates small airway closure due to the accumulation of cells and/or fluid in the pulmonary interstitium. This closure is particularly prominent during exhalation, when the vacuum applied by the chest wall and diaphragm is minimal and lung volume is small. During inspiration, as the lung expands, the pleural and interstitial pressure become more negative, and when sufficient to overcome the interstitial fluid pressure the airway snaps back open. This produces a short (< 20 msec), high-frequency sound, and when hundreds of airways in a single region of lung open simultaneously, they produce a sound similar to that produced by pulling Velcro™ apart. The distribution and symmetry of fine crackles provides information about the underlying disease process. For example, most animals with cardiogenic pulmonary edema may have bilateral late-inspiratory fine crackles.
Wheezes are longer duration (>80 msec) continuous sounds with a musical (tonal) quality in the range of 100-1000 Hz, and in most instances are related to fluttering of the wall of an airway. Generation of a wheeze commonly indicates the presence of a flow-restricted zone (partial obstruction, bronchospasm) within an airway with downstream flattening of the tube, although in some instances a partial obstruction with vortex creation and vibration of a round airway may be the cause. Wheezes often indicate small airway disease with airway exudates or secretion. Polyphonic wheezing indicates multiple airway involvement. Wheezes may be heard at the mouth.
Rhonchi are repetitions of complex sound waves that have a tonal, snore-like quality typically < 300 Hz and lasting at least 100 msec and are produced by rupture of fluid films formed by airway secretions, and vibration/collapse of large airways. They are audible at the mouth.