We often underuse the auscultation and physical examination techniques our predecessors mastered to successfully evaluate the cardiovascular system. Instead, we lean on echocardiography to offset the subtle nuances we fail to recognize.
Before the advent of echocardiography, the only noninvasive tools used to routinely evaluate the cardiovascular system were a thorough physical examination, electrocardiography, and thoracic radiography. Diagnoses that could not be readily procured from these techniques would ultimately require invasive procedures, such as angiocardiography, to further characterize the underlying disorder. While echocardiography has replaced diagnostic cardiac catheterization in most circumstances, its utility and easy access have also produced an untoward side effect: the cardiovascular physical examination appears to have fallen by the wayside.
We often underuse the auscultation and physical examination techniques our predecessors mastered to successfully evaluate the cardiovascular system. Instead, we lean on echocardiography to offset the subtle nuances we fail to recognize. This holds so true in the medical profession that echocardiography is considered by many to be an extension of the physical examination.1 Nonetheless, cardiac auscultation still provides a cost-effective method of making serial observations, aids in the early detection of critical findings, helps intelligently guide the selection of costly diagnostic tests, and provides a therapeutic value of physical contact between physician and patient.2
In this article, I review the basic concepts and techniques necessary to perform a thorough cardiovascular physical examination. As with any other technique, a systematic approach enables you to effectively perform the examination and not miss a vital clue.
Begin the physical examination by carefully observing the patient from a distance. I frequently do this while recounting the history and current medical complaint. Although often overlooked, the observation period enables you to characterize the pet's general appearance, attitude, and respiratory rate and effort. If you forgo this step, you may not detect subtle changes that owners may have failed to recognize.
Patients with severe, chronic cardiac compromise may exhibit marked weight loss and muscle wasting along the temporal region of the head and along the dorsolumbar aspect of the spine. Other pets may present with abdominal distention or weight gain from ascites subsequent to right-sided heart failure. Reluctance to move in a normally active or nervous patient may signal substantial cardiovascular compromise. Similarly, tachypnea, dyspnea, coughing, or an orthopneic stance with an inability to lie comfortably may be associated with substantial fluid accumulation within or around the lungs.
This step of the physical examination involves a careful inspection of the mucous membranes, eyes, and neck.
Alterations within the oral mucous membranes often do not occur until late in the process of many cardiac diseases, but the appearance of the oral mucosa may yield valuable information when combined with findings from the remainder of the physical examination. Normal mucous membranes are pink and moist with a brisk (one- to two-second) capillary refill time after blanching the gums. Although the capillary refill time is a nonspecific and often crude index of cardiac performance, it may be prolonged in instances of reduced cardiac output.
In addition to estimating the capillary refill time, inspect the mucous membranes for pallor or discoloration. Cyanosis is seen when the deoxygenated hemoglobin concentration exceeds 5 g/dl.3 Cyanotic mucous membranes often signify arterial hypoxemia, as seen with severe pulmonary disease or right-to-left shunting of blood (e.g. tetralogy of Fallot). Cyanosis may also be seen in patients with normal arterial oxygen saturation complicated by decreased perfusion to peripheral vascular beds. Peripheral cyanosis is usually observed in the digits or ear tips of patients with reduced cardiac output, marked arterial vasoconstriction, or vascular obstruction. While peripheral cyanosis is more common in patients afflicted by shock or hypothermia, a common cardiac manifestation is hindlimb footpad cyanosis encountered in cats with aortic thromboembolism. Patients with cyanotic cardiac disease may also display injected mucous membranes subsequent to polycythemia.
Acute blindness may be the first sign of systemic hypertension in a patient. This complication highlights the importance of inspecting the pupillary light responses and ocular fundus in patients with suspected systemic hypertension. Abnormalities that you may see include retinal detachment or hemorrhages, papilledema, or hyphema. Although infrequently recognized today, cats with dilated cardiomyopathy secondary to taurine deficiency may display central retinal degeneration.
Carefully inspect both the thyroid glands and the jugular veins before performing thoracic auscultation. Because of the connection between hyperthyroidism and the cardiovascular system, always palpate for enlarged thyroid glands in cats with suspected heart disease. As a consequence of the concentric hypertrophy and high cardiac output state associated with hyperthyroidism, cats with increased circulating thyroid hormone concentrations may have audible murmurs or gallop sounds.
Inspecting the neck for jugular venous distention or abnormal pulsation enables you to crudely estimate systemic venous pressures. Normally, the jugular veins are not distended and collapse quickly after manual compression. Pulsations do not normally traverse greater than one-third the height of the neck in a standing animal. Jugular venous distention or abnormal pulsation may signify right-sided heart failure subsequent to tricuspid insufficiency, dilated cardiomyopathy, pericardial effusion or cardiac tamponade, or constrictive pericarditis. Additional causes may include atrioventricular dissociation, cranial vena caval obstruction, or hypervolemia. Hepatojugular reflux (identifying jugular venous distention while applying steady, firm pressure to the abdomen) is suggestive of right ventricular systolic or diastolic dysfunction, tricuspid valve disease, or pericardial disease.
Although cardiac auscultation is often the focus when you examine the chest, thoracic palpation and respiratory evaluation are important as well.
Be sure to examine the chest for rib or sternal deformities. Record the pet's inspiratory and expiratory respiratory pattern, including the frequency, regularity, depth, and effort required. Pulmonary auscultation—to detect fluid lines, rhonchi, and wheezes or crackles and rales—usually precedes cardiac auscultation.
Next, identify the location and intensity of the cardiac impulse, and document palpable thrills (vibrations). While the strongest cardiac impulse, or apical beat, is usually identified over the left apex of the heart, the location may be displaced and the strength diminished by any condition that alters the position of the heart, including cardiomegaly, pleural or pericardial effusions, intracavitary masses, or thoracic or pericardial herniations. The location of the apical beat is often a good place to begin cardiac auscultation.
When performed appropriately, cardiac auscultation can yield tremendous insight into diagnosing cardiovascular disease. Important considerations when performing this technique include using a familiar and comfortable stethoscope, auscultating in a quiet environment, having a thorough understanding of the physiologic and pathologic genesis of cardiac sounds, and, finally, using a combination of practice and patience. Using pediatric stethoscopes for cats and small dogs tends to be based on clinician preference. I use an adult stethoscope for dogs and cats, reserving a pediatric stethoscope for small exotic-animal species.
Since its invention by René Théophile Hyacinthe Laënnec in 1816, the stethoscope has become the almost universal sign of a physician or veterinarian. The modern, binaural stethoscope commonly has a single- or double-tube system composed of 1 /8-in internal diameter tubing connected to a combination bell and diaphragm. The bell of the stethoscope, lightly applied to the patient to form an airtight seal, accentuates low frequency sounds, and the diaphragm detects high frequency sounds.
Listen for three things during auscultation—heart sounds, heart murmurs, and cardiac arrhythmias.
Heart sounds are relatively brief, auditory vibrations that can be characterized by their intensity (loudness), frequency (pitch), and quality (timbre).2 The basic heart sounds identified in veterinary patients include the first, second, third, and fourth heart sounds (S1, S2, S3, and S4, respectively). While we identify heart sounds and cardiac murmurs on a daily basis (see the boxed text titled "Standardize your auscultation technique" ), we often fail to recall what physiological and pathophysiological events account for these vital pieces of information.
Normal, transient heart sounds. The normal transient sounds that we recognize include the high-frequency S1 and S2. While these sounds are not produced by simple atrioventricular or semilunar valve cusp closure, we can consider that S1 and S2 coincide with mitral and tricuspid valve closure and aortic and pulmonic valve closure, respectively. Therefore, the association between mitral valve closure and S1 produces the loudest audible component of S1 over the left apical region of the heart (the location of the mitral valve). Similarly, with an understanding that S2 is associated with aortic and pulmonic valve closure and the sudden deceleration of blood, we most commonly hear S2 loudest at the left heart base (the location of the pulmonic and aortic valves). Recognizing that S1 is loudest at the left apex and S2 is loudest at the left heart base will help you localize cardiac murmurs, no matter the chest conformation. Furthermore, S1 and S2 mark the beginning and end of systole, respectively, providing a framework around which to recognize and categorize the other audible transient heart sounds and murmurs (Figure 1).
Figure 1. Electrical events precede mechanical events, so there is a delay between the electrocardiographic deflections and the individual heart sounds with which they are associated. In this schematic (A), atrial depolarization is associated with S4, ventricular depolarization with S1, ventricular repolarization with S2, and the period of early rapid ventricular filling with S3. In regard to cardiac auscultation, systole is defined as the period between S1 and S2, while diastole is the period between S2 and S1. Two of the most commonly encountered murmurs include the systolic plateau (regurgitant) and systolic crescendo-decrescendo (ejection) murmurs (B). Diastolic decrescendo murmurs typically signify aortic insufficiency, while continuous murmurs are most often identified with a left-to-right shunting patent ductus arteriosus (C).
Alterations of the normal, transient heart sounds. The intensity of S1 primarily depends on the position of the larger anterior mitral valve leaflet at the onset of ventricular systole.2 A more intense S1 is present when the valve is deeply recessed into the left ventricle and may be auscultated in patients with fast heart rates, short P-R intervals, or high sympathetic tone. Additional contributing factors may include anemia, systemic hypertension, or thinness.3 Because of acoustic dampening, obese patients, patients with pericardial or pleural effusion, or patients with space-occupying lesions such as tumors or hernias may display a muted or less distinctive S1. Myocardial failure, a prolonged P-R interval, premature mitral valve closure, various cardiac arrhythmias (including atrial fibrillation), or shock may also reduce the intensity of S1.2,3
Occasionally, the mitral and tricuspid valves will close asynchronously, enabling you to detect a split S1. This finding may occur in normal large-breed dogs, may be associated with marked intraventricular conduction delays (i.e. bundle branch blocks, artificial pacemakers, or ventricular arrhythmias), or may be heard in patients with mitral or tricuspid valve stenosis.3 More commonly, S2 may be split into two audible components. Normally during inspiration, the aortic component of S2 precedes the pulmonic component because of the variations in the pulmonary vascular bed capacitance and an inspiratory increase in right ventricular volume.2 So splitting of S2 may rarely be heard in normal dogs with large fluctuations of intrapleural pressure.4 More often, pathologic splitting of S2 is encountered when the pulmonic component is delayed because of prolonged right ventricular ejection in cases of pulmonary hypertension, atrial or ventricular septal defects, pulmonic stenosis, or right bundle branch block.
Abnormal, transient heart sounds. While S1 and S2 represent the normal transient sounds audible in dogs and cats, we may also identify abnormal transient heart sounds such as S3 and S4. Because of their low frequency, these sounds are usually best heard with the bell of the stethoscope and often impart a galloping sound to the heart. Although this triple cadence is often referred to as a gallop rhythm, it does not represent an abnormality within the heart's conduction system or origin of the cardiac impulse. Instead, S3 and S4 gallops are most often associated with myocardial hypertrophy or elevated filling pressures.
An S3 gallop, also known as a ventricular gallop or protodiastolic gallop, is associated with the termination of the early, rapid ventricular filling phase of diastole.4 While this sound may be recognized in normal horses or cows, an audible S3 in dogs and cats is generally associated with the ventricular dilatation or eccentric hypertrophy recognized in dilated cardiomyopathy, atrioventricular valve insufficiency, or substantial left-to-right shunting lesions. An S3 gallop is heard best over the left apex and should be listened for carefully with the bell of the stethoscope as it may be the only auscultatory abnormality in patients with dilated cardiomyopathy.
S4 gallop sounds, also known as atrial gallops or presystolic gallops, are often heard when an augmented atrial contraction is required to fill a stiff, concentrically hypertrophied ventricle. Similar to the low-frequency S3 gallop, this presystolic gallop is detected most readily with the bell of the stethoscope. S4 gallops may be the only auscultatory abnormality in patients with hypertrophic cardiomyopathy, systemic hypertension, and hyperthyroidism, or they may be recognized in cases of semilunar valve stenosis. In cats with rapid heart rates, it may be difficult to determine whether the gallop sound is an S3, an S4, or a summation of an S3 and S4. Nonetheless, the most important aspect is detection of the gallop sound, followed by an appropriate work-up.
While normal and abnormal heart sounds represent brief, transient auscultatory events, heart murmurs are prolonged auditory vibrations produced when blood flows turbulently through abnormal communications between the cardiac chambers or through stenotic or insufficient heart valves. They also occur subsequent to alterations in blood viscosity (e.g. anemia) or vessel diameter (the larger the vessel, the more likely blood flow is turbulent).
Figure 2. Characterizing Heart Murmurs
Heart murmurs are characterized by their timing and duration within the cardiac cycle, intensity (loudness), frequency (pitch), configuration (shape), and location and direction of radiation.2 An overview of their characterization is presented in Figure 2.
Table 1. Heart Murmur Classification
Left basilar systolic murmurs. There are five types of left basilar systolic murmurs—innocent murmurs, physiologic murmurs, and murmurs caused by subvalvular aortic stenosis, pulmonic stenosis, and atrial septal defects.
Figure 3. The areas of favored projection for murmurs on the left side of the chest include the left basilar region (1 & 2), the left apical region (3), and the left parasternal region (4). Murmurs arising from the pulmonary valve in dogs are generally loudest at the third intercostal space (1). Aortic valve lesions are usually most audible between the third and fourth intercostal spaces just below the shoulder line (2), while mitral valve murmurs have a point of maximal intensity at the fifth intercostal space near the costochondral junction (3). Another important area for auscultation in cats is the left parasternal region (4). Heart murmurs associated with tricuspid valve disease in dogs are usually loudest at the right fourth intercostal space near the costochondral junction (5). Similar to the left parasternal region, the right parasternal region (6) must be carefully examined in cats to detect dynamic outflow tract murmurs.
Left apical systolic murmurs. The most common cardiac auscultatory abnormality in middle-aged to older small-breed dogs is a variable-intensity, left apical, systolic, plateau-shaped murmur of mitral insufficiency. These murmurs vary in intensity from grade I to VI, depending on the severity of insufficiency, the left ventricular to left atrial pressure gradient, the radiation characteristics of the insufficient jet, and the presence or absence of comorbid conditions (e.g. pericardial or pleural effusion, obesity, abnormal chest conformation). Soft, grade I/VI mitral insufficiency murmurs are usually early systolic to midsystolic and fail to obscure either S1 or S2. Louder, grade IV to V/VI mitral insufficiency murmurs are often harsh and mixed-frequency, radiate widely to the right thorax (making documentation of tricuspid insufficiency difficult), and encompass all of systole.
Chronic degenerative valvular disease is the most common cause of mitral insufficiency, although diseases that produce eccentric hypertrophy or dilatation of the mitral valve annulus (e.g. dilated cardiomyopathy, left-to-right patent ductus arteriosus, ventricular septal defect) or alterations of the mitral valve apparatus (e.g. mitral valve dysplasia, valvular endocarditis, systolic anterior motion of the mitral valve) are also associated with mitral insufficiency. Therefore, a left apical, systolic, plateau-shaped murmur is suggestive of mitral insufficiency although it is not diagnostic of the underlying disease process.
Standardize your auscultation technique
Right-sided systolic murmurs. Right-sided systolic murmurs are often due to tricuspid insufficiency or ventricular septal defects.
Parasternal murmurs. Cats with mitral valve dysplasia or left ventricular concentric hypertrophy (e.g. hypertrophic cardiomyopathy, hyperthyroidism, systemic hypertension) may have a left ventricular outflow tract obstruction in which the anterior mitral valve leaflet is pushed, pulled, or sucked into the outflow tract. This phenomenon is often accompanied by mitral insufficiency and high-velocity, turbulent blood flow through the left ventricular outflow tract, producing a harsh, left apical or sternal, systolic murmur that intensifies with increasing heart rates and contractility. Heart murmurs associated with dynamic right ventricular outflow tract obstruction display similar characteristics and can often only be differentiated through Doppler echocardiography.
Diastolic murmurs. Diastolic murmurs are often due to aortic insufficiency or mitral stenosis.
Continuous murmurs. Residual patency of the ductus arteriosus results in high-velocity, turbulent blood flow entering the pulmonary artery from the descending aorta throughout both systole and diastole. So the characteristic murmur of a patent ductus arteriosus is a variable-intensity, left basilar (axillary), continuous murmur that peaks in intensity near S2. The diastolic run-off associated with this abnormal communication will commonly produce bounding femoral pulses. Patent ductus arteriosus murmurs may range in intensity from grade I to grade VI, depending on the size of the lesion, the aortic to pulmonary arterial pressure gradient, and the radiation characteristics of the turbulent blood flow. In cases of a balanced or a right-to-left patent ductus arteriosus, the murmur may be absent with a split S2.
Although uncommon, other potential causes of continuous heart murmurs include aorticopulmonary windows, pulmonary arteriovenous fistulas, coronary arteriovenous fistulas, and abnormal communications between the coronary vasculature and right atrium.
Disturbances in the normal cardiac rhythm are commonly detected in dogs and cats during physical examination. Single premature supraventricular or ventricular complexes followed by a pause in the rhythm or paroxysms of tachycardia that terminate abruptly may be detected in a variety of cardiac or systemic disease conditions. The fast, irregular rhythm associated with atrial fibrillation often indicates marked underlying myocardial or valvular disease, whereas a slow, regular rhythm may suggest conduction system disease (e.g. atrioventricular block), electrolyte imbalances (e.g. hyperkalemia), or alterations in the autonomic nervous system. Although electrocardiography is required for definitive diagnosis of the rhythm disturbance, physical examination often provides the premise for performing an electrocardiographic examination.
Abdominal palpation and ballottement are important in assessing right-sided cardiac dysfunction and in evaluating cardiac manifestations of systemic disease. Pericardial diseases and disorders of the right side of the heart or caudal vena cava may increase systemic venous pressures and produce hepatomegaly or ascites. Hepatojugular reflux suggests elevated central venous pressure in which the right side of the heart is unable to accommodate any additional venous return.
Be sure to carefully palpate the kidneys of older cats with heart murmurs because of the relationship between renal disease, systemic hypertension, and the development of left ventricular concentric hypertrophy or outflow tract obstructions.
Palpating the femoral pulses and extremities may help you detect rhythm disturbances, regional or generalized perfusion deficits, and occlusion of peripheral veins or lymphatics.3 A common misconception is that the strength and quality of the femoral pulse are merely determined by the systolic performance of the heart. Instead, the pulse amplitude and character have many determinants, including forward stroke volume, rate of ejection, distensibility of the vascular bed, systemic vascular resistance, and the pulse pressure (the difference between the systolic and diastolic arterial pressures).3
Weak pulses may be identified in cases of myocardial failure in which the left ventricle ejects a small stroke volume, the peripheral vascular resistance is high, and the pulse pressure is narrow.3 The combination of a weak and late to rise femoral pulse (pulsus parvus et tardus) and a left basilar, systolic, crescendo-decrescendo murmur is suggestive of moderate to severe subaortic stenosis. Widening of the pulse pressure subsequent to diastolic run-off in dogs with patent ductus arteriosus produces a bounding, or water-hammer, pulse. Other conditions associated with diastolic run-off and bounding pulses include aortic insufficiency and peripheral arteriovenous fistulas. Because systemic hypertension tends to represent an increase in both the systolic and diastolic arterial pressures, the femoral pulse amplitude and character remain normal. A palpable reduction in the femoral pulse quality during inspiration (pulsus paradoxus) is most commonly detected in patients with pericardial effusion and cardiac tamponade.
The absence of palpable femoral pulses, coolness of the affected limbs, muscular rigidity and pain, and pallor of the footpads or nails are suggestive of vascular obstruction.3 Systemic thromboembolism in cats is commonly associated with myocardial disease, while dogs may develop vascular obstruction subsequent to bacterial endocarditis or any condition that promotes hypercoagulability (e.g. hyperadrenocorticism, protein losing nephropathy, immune-mediated hemolytic anemia).
Good physical examination skills and an understanding of the pathophysiology associated with cardiac disease are vital to maintaining the health and well-being of our patients. A physical examination can provide an intelligent guide for recommending advanced diagnostic techniques, is a cost-effective method of making serial observations, and aids in the early detection of critical findings. Although electrocardiography, radiography, and echocardiography are required to confirm the disease process, assess its severity, and rule out concurrent cardiac conditions, these diagnostic modalities will never supplant the utility of observation, inspection, palpation, and cardiac auscultation.
Barret J. Bulmer, DVM, MS, DACVIM (cardiology)
Department of Clinical Sciences
College of Veterinary Medicine
Kansas State University
Manhattan, KS 66506
1. Oh JK, Seward JB, Tajik AJ. Overview. In: The echo manual. 2nd Ed. Philadelphia, Pa: Lippincott Williams & Wilkins, 1999;1-5.
2. Braunwald E. Physical examination of the heart and circulation. In: Zipes DP, Libby P, Bonow RO, et al, eds. Braunwald's heart disease: a textbook of cardiovascular medicine. 7th Ed. Philadelphia, Pa: Elsevier Saunders, 2005;77-106.
3. Sisson DD, Ettinger SJ. The physical examination. In: Fox PR, Sisson DD, Moise NS, eds. Textbook of canine and feline cardiology: principles and clinical practice. 2nd Ed. Philadelphia, Pa: WB Saunders Co, 1999;46-64.
4. Detweiler DK, Patterson DF. Abnormal heart sounds and murmurs of the dog. J Small Anim Pract 1967;8:193-205.
5. Lehmkuhl LB, Ware WA, Bonagura JD. Mitral stenosis in 15 dogs. J Vet Intern Med 1994;8:2-17.
The author would like to thank Mal Hoover for her assistance with Figure 3.