Philip R. Fox, DVM, MSc, DACVIM/ECVIM (Cardiology), ACVECC
Vincent Astor Chair in Comparative Medicine, Caspary Institute, The Animal Medical Center, New York, NY, USA
The history and physical examination form the cornerstone for diagnosis and management of cardiopulmonary disease. This information represents the "glue" which binds together subjective aspects of patient evaluation with technical details from diagnostic tests. An insightful history coupled with a thorough and detailed examination is a prerequisite for accurate diagnosis, assessment of treatment efficacy, and optimal outcome.
What the History Accomplishes
A good history uncovers the body system or disease process associated with clinical signs and client complaint. The history solicits information intended to: 1) distinguish between cardiac and pulmonary disease, 2) establish a diagnosis, 3) determine the frequency and extent of clinical impairment, 4) assess response (or lack of response) to therapy, 5) detect other medical conditions, and 6) establish a doctor-client relationship.
Taking the History
The history comprises a complete and comprehensive set of well planned questions. The owner is asked to relate their observations and concerns. This offers a glimpse of the clients' emotional state, health care experience, intelligence, and provides information about the clinical condition. It also gives the client the satisfaction of being heard. The pet owner will not often volunteer all relevant information due to incomplete observation of clinical signs, incorrect description of signs through misinterpretation, emotional status, and a sometimes, a sense of denial that serious illness is present. The clinician then directs the client using well planned questions to evaluate relevant clinical observations: 1) onset of signs, their related chronology, and severity; 2) precipitating factors; and 3) response (or lack of response) to therapy.
Congenital heart disorders may be implied if siblings, dam or sire have been effected with known cardiovascular disease. Results from diagnostic procedures (radiographs, ECG's, echocardiograms, clinical pathology) performed at other veterinary practices are important to evaluate. When drugs have already been prescribed, knowledge of doses, compliance and therapeutic response can offer valuable insights.
Signalment (age, breed and gender). Many congenital and some acquired diseases have certain predilections regarding age, breed and gender.
Dyspnea, exercise intolerance, syncope, coughing, and cyanosis are common to both cardiac and respiratory disease.
Dyspnea. Acute dyspnea suggests pulmonary edema, pneumonia, airway obstruction, pneumothorax, or pulmonary thromboembolism. Chronic, progressive dyspnea may occur with right-sided heart failure, pericardial or bronchial disease, pleural effusions, progressive anemia, or pulmonary neoplasia. Inspiratory dyspnea suggests upper airway obstruction; expiratory dyspnea suggests lower airway obstruction, parenchymal lung disease, heart failure, chronic obstructive lung disease, and other conditions. Paroxysmal dyspnea can accompany brady- or tachyarrhythmias, especially if accompanied by episodic weakness or syncope. A history indicating that dyspnea diminished or resolved following cardiac drugs suggests heart failure.
Cough. Most coughs sound alike and more than one etiology may coexist. Cardiogenic pulmonary edema in dogs results from left-heart volume overload (mitral regurgitation, endocardiosis) or dilated cardiomyopathy. Coughing from acute pulmonary edema is usually less than a few days duration and progresses rapidly in severity. The cough is generally soft, mild, and accompanies exertional dyspnea. Chronic pulmonary congestion may cause mild intermittent coughing and nocturnal dyspnea or cough. Fulminant edema yields small quantities of frothy, pink-tinged foam from the mouth or nares. In dogs impingement of the left main stem bronchus by a left atrium enlarged by chronic mitral regurgitation contributes to chronic coughing. Cats appear not to cough, even when severe pulmonary edema is present.
Large airway disease causes chronic paroxysmal coughing characterized as harsh, resonant, dry, and "goose honking" in nature. Coughing may persist for years, is paroxysmal, and elicited by excitement. Dogs with collapsed trachea usually have normal exercise capacity between coughing episodes.
Weakness and exercise intolerance. When caused by decompensated heart failure, lack of exercise ability, lethargy, or fatigue results. Additional causes include obstruction to ventricular outflow, cardiac tamponade, arrhythmias, anemia, systemic and metabolic diseases, hypotension, and respiratory disease.
Syncope. This results from transient loss of consciousness from inadequate cerebral blood flow. It occurs most commonly in coughing, excited, small breed dogs with chronic, severe mitral regurgitation, whose paroxysmal coughing is immediately followed by transient collapse (cough syncope). Syncope may occur with severe subaortic stenosis, pulmonary valve stenosis, hypertrophic obstructive cardiomyopathy, pulmonary hypertension, right-to-left cardiac shunts (tetralogy of Fallot, PDA), tachy- or bradyarrhythmias (e.g., complete AV block) and conduction abnormalities such as sick sinus syndrome.
The Physical Examination
Examination of the cardiopulmonary system involves 1) extern al patient inspection at rest and during activity to assess respiratory effort and rate; 2) assessment of the nares, oropharynx, and larynx for obstruction; 3) palpation of the neck for tracheal conformity and masses; 4) observation of the external jugular veins for abnormal distension or pulsations; 5) palpation of the femoral arterial pulses for strength, regularity and contour (normal, hypokinetic, hyperkinetic, etc.); 6) palpation of the precordium for cardiac apex beat (location, strength of pulsation, point of maximal impulse) and thrills (vibratory sensations which are palpable manifestations of loud, harsh, low frequency murmurs); 7 thoracic percussion; and 8) heart and lung auscultation.
The most effective instruments are made of plastic tubing 10 to 12 inches (25-30 cm) long with an internal diameter of 1/8 inch (3mm). They should be connected to large, comfortable ear pieces that fit tightly. The bell is applied with light pressure and collects low frequency sounds (e.g., 3rd and 4th heart sounds, diastolic murmurs of mitral and tricuspid origin). The diaphragm is applied with firm pressure and collects high frequency sounds best (e.g., 1st and 2nd heart sounds, systolic clicks, high pitched murmurs). Electronic stethoscopes are also available.
General Principles of Auscultation
Auscultate in a quiet room. The animal should be relaxed, standing or comfortably positioned, not panting, barking or purring. Palpate the left and right precordium to detect the presence of thrills (vibrations) and determine the cardiac apex beat. Assess heart rate. Simultaneously palpate the femoral arterial pulse (a peripheral pulse occurs just after the 1st heart sound). Pulse deficits suggest an arrhythmia. Vagal maneuvers may slow the heart rate during tachycardia.
Develop a systematic approach beginning at the left apex where the 1st heart sound is normally loudest, then inching forward, then dorsally. Take note of various factors that effect loudness of heart sounds and murmurs. Increased loudness: a thin chest, sympathetic stimulation, thyrotoxicosis, and anemia. Decreased loudness: include obesity, pericardial/pleural effusions, intrathoracic masses, pneumothorax, abdominal herniation into the chest or pericardium, and myocardial failure.
Principal areas of cardiac auscultation include: 1) Pulmonic area- left 2nd to 4th ICS just above the sternum (cat--2nd to 3rd ICS about 1/3 distance from the sternum to the vertebrae); 2) Aortic area--left 4th ICS at the CCJ (cat--left 2-3ICS, just dorsal to the pulmonic area); apex: 3) Mitral area--left 5th ICS at the CC (may be left 5th to 6th ICS and more sternal in cats); 4) Tricuspid area--right 3rd to 5th ICS at the CC (cat--right 4th or 5th ICS toward the sternum). Auscultation should not be limited to these sites only.
Utilize selective listening. Focus on one part of the cardiac cycle at a time. Listen separately to the 1st heart sound (S1), then the 2nd heart sound (S2), the systolic interval, then the diastolic interval. Determine the intensity, quality, and splitting of each sound. The systolic and diastolic intervals should then be listened to for additional heart sounds or murmurs.
The cardiac cycle consists of two periods: A) contraction (systole) when the heart ejects blood, and B) relaxation (diastole) when the heart chambers fill. Ventricular systole follows closure of mitral and tricuspid valves (related to the 1st heart sound, S1). When ventricular pressure increases and exceeds aortic and pulmonic pressure, aortic and pulmonic valves open, causing rapid ejection of blood. Later in systole, ventricular pressure falls, ejection is reduced and ultimately ceases. Ventricular diastole follows closure of aortic and pulmonic valves (related to the second heart sound, S2). Following the early diastolic filling phase, atrial contraction occurs, contributing up to 20-25% of ventricular filling.
The initial heart sounds occur at the beginning of ventricular systole (S1, the 1st heart sound). The 2nd heart sound, S2, occurs at the end of ventricular systole. The period between S1 and S2 is represents ventricular systole; the interval following S2 and up until the following S1 represents ventricular diastole.
Heart Sounds and Murmurs
These are characterized according to: 1) Location--i.e., the valve area where murmur is heard best (point of maximal intensity). 2) Intensity or loudness--loudness of murmurs can be graded on a 1 to 6 scale as follows: I/VI--heard after only intense concentration; II/VI--heard immediately, but faint; III/VI--moderately loud; IV/VI--quite loud but without a palpable thrill; V/VI--loud with a precordial thrill, VI/VI--loudest murmur with a thrill; audible without a stethoscope. 3) Timing--occurring during systole, diastole, or both. 4) Frequency--the number of sound waves cycles/second generated by a vibrating body determines the pitch, a subjective sensation indicating whether a tone is high, low or medium on a musical scale. High frequency sounds indicate a greater number of wave cycles/second and are best heard with the diaphragm applied firmly. A low frequency indicates fewer wave cycles/second and are best heard with the bell placed lightly on the skin. 5) Quality--e.g., blowing, harsh, rough, musical. Murmurs often have identifiable shape to their sound: crescendo/decrescendo (diamond-shaped), decrescendo, crescendo, plateau. Murmurs can be described as ejection (i.e., diamond-shaped), regurgitant (i.e., plateau) or continuous based on phonocardiographic description. 6) Duration--length of time the sound is heard. 7) Radiation--other locations murmur is heard.
First (S1) and second (S2) heart sounds--S1 heralds the onset of ventricular systole. S1 is caused by closure of the mitral (M1) and tricuspid (T1) valves. It is a high frequency sound heard best with the diaphragm at the apex where it is slightly louder, longer and lower pitched than S2. Pathologic splitting of S1 is rare. Occasional causes include right bundle branch block and PVC's. S2 indicates the termination of systole and is classically related to closure of the aortic (A2) and pulmonic (P2) valves; Aortic valve closure normally precedes the pulmonic valve because systemic pressure exceeds pulmonary pressure and this forces the aortic valve to close earlier than the pulmonic valve. S2 is normally louder at the left cardiac base, shorter and more highly pitched than S1. Normal or physiological splitting of S2 occur If both components of S2 are separately distinguishable. This is normally heard on inspiration where a decrease in intrathoracic pressure increases right heart venus return, prolonging right ventricular systole and delaying P2 closure. High heart rates in dogs and cats make detection of physiological spitting difficult. Causes of abnormal S2 splitting include 1) "fixed" (persistent) splitting due to delay in pulmonary closure from right heart lesions or diseases. The split widens during inspiration and may narrow with expiration. Causes of delayed pulmonic closure include pulmonic stenosis, heartworm disease, RBBB, LV ectopic beats. Causes of early aortic closure include shortened LV mechanical systole due to severe MR or VSD [L to R], normotensive ASD; 2) reversed ("paradoxic") splitting where the split increases during expiration and decreases with inspiration. Causes of delayed aortic closure include LBBB, RV ectopic beats, prolonged LV mechanical systole (LBBB, AS, systemic hypertension, severe AI, PDA.
Third (S3) and fourth (S4) heart sounds--These are referred to as gallop sounds. S3 is associated with early (proto) diastolic rapid ventricular filling. Low frequency, it is heard best with the bell. Causes include 1) high cardiac output states (anemia, hyperthyroidism, large left-to-right shunts [e.g., PDA, VSD), 2) rapid ventricular filling (MR, TR, AI), and 3) myocardial failure. S4 is associated with active ventricular filling during late diastole and follows atrial contraction just before S1. Like S3 it is a low frequency sound in relation to decreased ventricular compliance and is called an atrial or presystolic gallop. Causes of right-sided S4 include pulmonary hypertension, cardiomyopathy and PS; causes of left-sided S4 include systemic hypertension, AS, and HCM. Isolated S4 may be related to 2 o or 3o degree AV block.
Ejection sounds and clicks--Systolic high-pitched sounds heard best with the diaphragm. Early systolic clicks usually coincide with full opening of semilunar valves while mid systolic clicks can be associated with mitral valve prolapse.
Differential diagnosis of cardiac disease is often based upon the timing and location of murmurs. Systolic murmurs heard loudest at the left base include SAS, PS, and ASD; Tetralogy of Fallot may be heard at the left base and right sternal border. Mitral regurgitation is loudest at the left apex. Systolic murmurs heard loudest over the right chest (2nd-4th ICS) can include SAS. Tricuspid regurgitation and VSDs are heard loudest at the 3rd-5th ICS. Diastolic murmurs associated with aortic/pulmonary insufficiency are heard over the related valve regions. Continuous ("machinery") murmur associated with PDA may be focal and heard over the left cranioventral chest.
1. Atkins CE. Evaluation of cough in dogs with mitral valve insufficiency. The Compendium.1994; 16: 1547-1552
2. Sisson D, Ettinger SJ. The Physical Examination. In Fox PR, Sisson DD, Moise NS (eds): Textbook of Canine and Feline Cardiology Principles and Clinical Practice
3. Fox PR. The History. In Fox PR, Sisson DD, Moise NS (eds): Textbook of Canine and Feline Cardiology Principles and Clinical Practice. 2nd Ed, WB Saunders, Philadelphia, 1999, p 41
4. Piirilä P, Sovijärvi ARA. Crackles: recording, analysis, and clinical significance. Eur Respir J 1995; 8: 2139-2148