Testing to determine the cause of intermittent weakness or syncope usually includes and electrocardiogram (ECG)(obtained while resting, during exercise, and/or after exercise or a vagal maneuver), a complete blood count (CBC) serum biochemical analysis (including electrolytes and glucose), neurologic examination, thoracic radiographs, heartworm testing, and echocardiography. Other studies to rule out neuromuscular or neurologic disease may also be valuable. Intermittent cardiac arrythmias not apparent on resting ECG may be uncovered by 24-hour ambulatory ECG (Holter monitor), event monitoring, or in-hospital continuous ECG monitoring.

Signs of heart disease in dogs may be present even if the animal is not in a state of heart failure. Objective signs of heart disease include cardiac murmurs, rhythm disturbances, jugular pulsations and cardiac enlargement. Other clinical signs that can result from heart disease include syncope, excessively weak or strong arterial pulses, cough or respiratory difficulty, exercise intolerance and cyanosis. Further evaluation using thoracic radiography, electrocardiography, echocardiography and sometimes other tests is usually indicated when signs suggestive of cardiovascular disease are present.

The clinical signs of heart failure relate to high venous pressure behind the heart (congestive signs) or inadequate blood flow out of the heart (low output signs). Congestive signs secondary to right-sided heart failure stem from systemic venous hypertension and its sequelae; congestion behind the left side of the heart results in pulmonary venous hypertension and edema. Chronic left-sided congestive heart failure may facilitate the development of right-sided heart failure if pulmonary arterial pressure rises secondary to pulmonary venous hypertension. Low output signs from right ventricular failure are similar to the low output signs of left ventricular failure because the left heart can pump only what it receives from the right heart. Biventricular failure develops in some animals.

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Signs and symptoms of syncope in dogs and cats.

Cardiac output often becomes inadequate in animals with heart disease or heart failure, especially in association with activity. Reduced exercise tolerance and tiring can result from impaired skeletal muscle perfusion during exercise and the vascular and metabolic changes that result over time. Episodes of exertional weakness or collapse can relate to these changes or to an acute decrease in cardiac output caused by arrhythmias.

Syncope in dogs and cats is an abrupt and transient loss of consciousness and postural tone caused by insufficient delivery of oxygen or glucose to the brain. As such, syncope is not a diagnosis itself but a sign of underlying disease. Various cardiac and non-cardiac abnormalities can cause syncope in dogs and cats as well as intermittent weakness. Syncope can be confused with episodes of intermittent weakness or seizures. A careful description of the animal’s behavior or activity before the collapse event, during the event itself, and after the collapse, as well as a drug history, helps the clinician differentiate among syncopal attacks, episodic weakness, and true seizures.

Dogs and cats syncope is often associated with exertion or excitement. The actual event may be characterized by rear limb weakness or sudden collapse, lateral recumbency, stiffening of the forelimbs and opisthotonos, and micturition. Vocalization is common; however, tonic-clonic motion, facial fits, and defecation are not. An aura (which often occurs before seizure activity), postictal dementia, and neurologic deficits are generally not seen in dogs and cats with cardiovascular syncope.

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Dogs and cats cough

Congestive heart failure in dogs is often manifested by coughing, tachypnea and dyspnea. These signs also occur in association with the pulmonary vascular disease and pneumonitis of heartworm disease in both dogs and cats. Noncardiac conditions including diseases of the upper and lower airways, pulmonary parenchyma (including noncardiogenic pulmonary edema), pulmonary vasculature, and plural space, as well as certain nonrespiratory conditions, also can cause cough, tachypnea and dyspnea.

The cough accompanying left-sided heart failure in dogs is often soft and moist but sometimes sounds like gagging. In contrast, cough is an unusual sign of pulmonary edema in cats. Tachypnea progressing to dyspnea occurs in both species. Pleural and pericardial effusions occasionally are associated with coughing as well. Mainstem bronchus compression caused by severe left atrial enlargement can stimulate a cough (often described as dry or hacking) in dogs with chronic mitral insufficiency, even in the absence of pulmonary edema or congestion. A heartbase tumor or other mass that impinges on an airway can also mechanically stimulate coughing.

When respiratory signs are caused by heart disease, other evidence such as generalized cardiomegaly, left atrial enlargement, pulmonary venous congestion, lung infiltrates that resolve with diuretic therapy, and/or a positive heartworm test are usually present. Thorough physical examination, thoracic radiographs, an echocardiogram if possible, and an ECG facilitate differentiation of cardiac from noncardiac causes of cough and other respiratory signs.

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Physical evaluation of the animal with suspected heart disease includes observation (e.g., attitude, posture, body condition, level of anxiety, respiratory pattern) and a general physical examination. The cardiovascular examination itself consists of evaluating the peripheral circulation (mucous membranes), systemic veins (especially the jugular veins), systemic arterial pulses (usually the femoral arteries), and the precordium (left and right chest wall over the heart) :palpating or percussing for abnormal fluid accumulation (e.g., ascites, subcutaneous edema, pleural effusion); and auscultating the heart and lungs. Proficiency in the cardiovascular examination requires practice. But these skills are important for accurate patient assessment and monitoring.

Respiratory difficulty (dyspnea) usually causes the animal to appear anxious. Increased respiratory effort, flared nostrils, and often a rapid rate of breathing are evident. Increased depth of respiration (hyperpnea) frequently results from hypoxemia, hypercarbia, or acidosis. Pulmonary edema (as well as other pulmonary infiltrates) increases lung stiffness; rapid and shallow breathing (tachypnea) results as an attempt to minimize the work of breathing. An increased respiratory rate is an early indicator of pulmonary edema in the absence of primary lung disease. Large-volume pleural effusion or other pleural space disease (e.g., pneumothorax) generally causes exaggerated respiratory motions as an effort to expand the collapsed lungs. It is important to note whether the respiratory difficulty is exaggerated during a particular phase of respiration. Prolonged, labored inspiration is usually associated with lower airway obstruction or pulmonary infiltrative disease (including edema).

Animals with severely compromised ventilation may may refuse to lie down; they stand or sit with elbows abducted to allow maximal rib expansion, and they resist being positioned in lateral or dorsal recumbency (orthopnea). Cats with dypnea often crouch in a sternal position with elbows abducted. Open-mouth breathing is usually a sign of severe respiratory distress in cats. The increased respiratory rate associated with excitement, fever, fear or pain can usually be differentiated from dyspnea by careful observation and physical examination.

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Mucous membrane color and capillary refill time (CRT) are used to estimate the adequacy of peripheral perfusion. Normally the oral membranes are assessed; however, caudal mucous membranes (prepuce or vagina) also can be evaluated. The color of the caudal membranes should be compared with that of the oral membranes in polycythemic cats and dogs regardless of whether a cardiac murmur is detected. If the oral membranes are pigmented, the ocular conjunctiva can be evaluated. The CRT is assessed by applying digital pressure to blanch the membrane; color should return within 2 seconds. Slower refill times occur from dehydration and other causes of decreased cardiac output because of high peripheral vasoconstriction.

However, the CRT is normal in anemic animals unless hypoperfusion is also present; the CRT can be difficult to assess in severely anemic animals because of the lack of color contrast. Petechiae in the mucous membranes may be noticed in dogs and cats with platelet disorders. In addition, oral and ocular membranes are often the sites where icterus (jaundice) is first detected. A yellowish cast to these membranes should prompt further evaluation for hemolysis or hepatobiliary disease.

System venous and right heart filling pressures are reflected at the jugular veins in dogs and cats. These veins should not be distended when the animal is standing with its head in a normal position (jaw parallel to the floor). Persistent jugular vein distention occurs in association with right-sided congestive heart failure (because of high right heart filling pressure), external compression of the cranial vena cava, or jugular vein or cranial vena cava thrombosis.

Also abnormal are jugular pulsations extending higher than one third of the way up the neck from the thoracic inlet. Sometimes the carotid pulse wave is transmitted through adjacent soft tissues, mimicking a jugular pulse from carotid transmission, the jugular vein is occluded lightly below the area of the visible pulse. If the pulse disappears, it is a true jugular pulsation; if the pulse continues, it is being transmitted from the carotid artery.

Jugular pulse waves are related to atrial contraction and filling. Visible pulsations occur in dogs and cats with tricuspid insufficiency (after the first heart sound, during ventricular contraction), conditions causing a stiff and hypertrophied right ventricle (just before the first heart sound, during atrial contraction), or arrhythmias that cause the atria to contract against closed atriaventricular (AV) valves (so-called cannon A waves).

Impaired right ventricular filling, reduced pulmonary blood flow, or tricuspid regurgitation can cause a positive hepatojugular reflux even in the absence of jugular distention or pulsations at rest. To test for this reflux, firm pressure is applied to the cranial abdomen while the animal stands quietly. This transiently increases venous return. Jugular distention that persists while abdominal pressure is applied constitutes a positive (abnormal) test; normal dogs and cats have little to no change in the jugular vein.

The strength and regularity of the peripheral arterial pressure waves and the pulse rate are assessed by palpation of the femoral or other peripheral arteries. Subjective evaluation of pulse strength is based on the difference between the systolic and diastolic arterial pressures (pulse pressure). When the difference is wide, the pulse feels strong on palpation; abnormally strong pulses are termed hyperkinetic. When the pressure difference is small, the pulse feels weak (hypokinetic). If the rise to maximum systolic arterial pressure is prolonged, as in animals with severe subaortic stenosis, the pulse also feels weak (pulsus parvus et tardus). Both femoral pulses should be palpated and compared; absence of pulse or a weaker pulse on one side may be caused by thromboembolism. Femoral pulses can be difficult to palpate in cats, even when normal. Often an elusive pulse can be found by gently working a fingertip toward the cat’s femur in the area of the femoral triangle, where the femoral artery enters the leg between the dorsomedial thigh muscles.
The femoral arterial pulse rate should be evaluated simultaneously with the direct heart rate, whick is obtained by chest wall palpation or auscultation. Fewer femoral pulses than heartbeats constitute a pulse deficit. Various cardiac arrhythmias indulce pulse deficits by causing the heart to beat before adequate ventricular filling has occured. Consequently, minimal or even no blood is ejected for those beats, and a palpable pulse is absent. Other arterial pulse variations occur occasionally. Alternately weak then strong pulsations can result from severe myocardial failure (pulsus alternans) or from a normal heartbeat alternating with a premature beat (bigeminy), which causes reduced ventricular filling and ejection. An exaggerated decrease in systolic arterial pressure during inspiration occurs with cardiac tamponade; a weak arterial pulse strength (pulsus paradoxus) may be detected during inspiration in such a case.

The precordium in pets is palpated by placing the palm and fingers of each hand on the corresponding side of the animal’s chest wall over the heart. Normally, the strongest impulse is felt during systole over the area of the left apex (located at approximately the left fifth intercostal space near the costochondral junction). Cardiomegaly or a space-occupying mass within the chest can shift the precordial impulse to an abnormal location. Decreased intensity of the precordial impulse can be caused by obesity, weak cardiac contractions, pericardial effusion, intrathoracic masses, pleural effusion, or pneumothorax.



The precordial impulse should be stronger on the left chest wall than on the right. A stronger right precordial impulse can result from right ventricular hypertrophy or displacement of the heart into the right hemithorax by a mass lesion, lung atelectasis, or chest deformity. Very loud cardiac murmurs cause palpable vibrations on the chest wall known as a precordial thrill. This feels like a buzzing sensation on the hand. A precordial thrill is usually localized to the area of maximal intensity of the murmur.

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Right-sided congestive heart failure promotes abnormal fluid accumulation within body cavities or, usually less noticeably, in the subcutis of dependant areas. Palpation and ballotement of the abdomen, palpation of dependant areas, and percussion of the chest in the standing animal are used to detect effusions and subcutaneous edema. Fluid accumulation secondary to right-sided heart failure is usually accompanied by abnormal jugular vein distention and/or pulsations, unless the animal’s circulating blood volume has been decreased by diuretic use or other cause. Hepatomegaly and/or splenomegaly may also be noted in cats and dogs with right-sided heart failure.

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Thoracic auscultation in dogs and cats is used to identify normal heart sounds, determine the presence or absence of abnormal sounds, assess heart rhythm and rate, and evaluate pulmonary sounds. Heart sounds are created by turbulent blood flow and associated vibrations in adjacent tissue during the cardiac cycle. Although many of these sounds are too low in frequency and/or intensity to be audible, others can be heard with the stethoscope or even palpated. Heart sounds are classified as transient sounds (those of short duration) and cardiac murmurs (longer sounds occurring during a normally silent part of the cardiac cycle). Cardiac murmurs and transient sounds are described using general characteristics of sound: frequency (pitch), amplitude of vibrations (intensity/loudness), duration, and quality (timbre); the timbre is affected by the physical characteristics of the vibrating structures. Because many heart sounds are difficult to hear, cooperation of the animal and a quiet room are important during auscultation.
If possible, the animal should be standing so that the heart is in its normal position. Panting in dogs is discouraged by holding the animal’s mouth shut. Respiratory noise can be decreased further by placing a finger over one or both nostrils for a short time. Purring in cats may be stopped by holding a finger over one or both nostrils, waving an alcohol-soaked cotton ball near the cat’s nose, or turning on a water faucet near the animal. Various other artifacts can interfere with auscultation, including respiratory clicks, air movement sounds, shivering, muscle twitching, hair rubbing against the stethoscope (crackling sounds), gastrointestinal sounds and extraneous room noises.

The traditional stethoscope has both a stiff, flat diaphragm and a bell on the chest piece. The diaphragm, when applied firmly to the chest wall, allows better auscultation of higher frequency heart sounds than those of low frequency. The bell, applied lightly to the chest wall, facilitates auscultation of lower frequency sounds. Some stethoscopes have a single-sided chest piece that is designed to function as a diaphragm when used with firm pressure and as a bell when used with light pressure. Ideally the stethoscope should have short double tubing and comfortable eartips. The binaural eartubes should be angled rostrally to align with the examine’s ear canals.

Both sides of the chest should be carefully auscultated, with special attention paid to the valve areas. The stethoscope is moved gradually to all areas of the chest. The examiner should concentrate on the various heart sounds, correlating them to the events of the cardiac cycle, and listen for any abnormal sounds in systole and diastole successively. The normal heart sounds are used as a framework for timing abnormal sounds. The point of maximal intensity (PMI) of any abnormal sounds should be located. The examiner should focus on cardiac auscultation separately from pulmonary auscultation because full assimilation of sounds from both systems simultaneously is unlikely.

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