Chapter 1 Diseases of the Cardiovascular System
The cardiovascular system plays an important role in maintaining homeostasis throughout the body. It performs this function by regulating the flow of blood through miles of vessels and capillaries. It is in the capillaries that vital nutrients are transported into the body cells and removal of waste materials from the cells occurs.
To understand cardiovascular disease, one must first study the anatomy and physiology of the cardiovascular system (refer to an anatomy and physiology text for a detailed description). Simply stated, the cardiovascular system is composed of a pump (the heart) and pipes (the vessels). The pump circulates fluid (blood) through the vessels where it delivers its content to the cells and removes waste products. This system is a “closed” system—that is, change in one portion of the system affects the other portions of the system.
At the center of the cardiovascular system is the heart, a four-chambered pump designed to contract, pumping blood to all parts of the body. Specialized cardiac muscle cells located in the sinoatrial (SA) node generate electrical impulses that spread, through a specialized conduction system, resulting in simultaneous contraction of the cardiac muscle cells. This contraction pushes blood into the arterial vessels and returns blood to the heart from the veins. This electrical activity can be measured as it moves across the surface of the body, using an electrocardiograph (Fig. 1-1). The electrocardiographic instrument measures the electrical activity generated by the heart by the placement of electrodes at specific points on the body surface. Each mechanical contraction of the heart is preceded by an electrical wave front that stimulates heart muscle contraction. This electrical wave front begins at the SA node and travels to the muscle cells of the ventricle through the cardiac conduction system. These wave fronts are recorded as the electrocardiogram (ECG). Figure 1-2 shows a normal ECG of a dog. Figure 1-3 represents the normal pathway for electrical conduction through the heart.
Figure 1-1 Using an electrocardiograph.
(From Edwards NJ: Bolton’s handbook of canine and feline electrocardiography, ed 2, Philadelphia, 1987, WB Saunders, by permission.)
Figure 1-2 Normal electrocardiogram of a dog.
(From Edwards NJ: ECG manual for the veterinary technician, Philadelphia, 1993, WB Saunders, by permission.)
(From McBride DF: Learning veterinary terminology, ed 2, St Louis, 2002, Mosby, by permission.)
Many cardiac diseases involve a failure of this pump to function properly. Congestive heart failure, cardiomyopathy, valvular disease, and congenital malformations can all affect the pumping efficiency of the heart, and ultimately the function of the entire body.
Connected to the pump are a series of vessels. Arteries carry oxygenated blood at high pressure (the systolic blood pressure) to arterioles and onto capillaries where exchange of nutrients and gases occurs. Blood then moves into venules, through veins, and is returned to the right side of the heart. Arteries are capable of dilation and constriction, routing blood to areas where it is needed and away from those areas not in need. Constriction serves to increase blood pressure, and dilation serves to decrease it.
Vascular diseases affect the flow of blood through the body and, ultimately, its return to the heart. If the volume of blood returning to the heart is abnormal, the heart will compensate by altering the rate of contraction, the strength of contraction, or both to return homeostasis to the circulatory system.
When the blood returning to the heart cannot be pumped out at a rate matching the body’s need, heart failure occurs. Many causes for heart failure exist, and the disease is often difficult to explain. The clinical signs of the disease and treatment regimens depend on individual animal diagnosis and evaluation. The veterinarian must determine whether the failure is the result of myocardial dysfunction (pump failure) or circulatory failure (lack of circulating fluid volume).
Heart failure is termed congestive heart failure when the failing heart allows fluid congestion and edema to accumulate in the body. Most heart failure will become “congestive” as the pump progressively fails.
Dilated cardiomyopathy (DCM) is one of the most common acquired cardiovascular diseases of dogs. It is primarily a disease of older, male large and giant breed dogs such as Scottish deerhounds, Dobermans, boxers, Irish wolfhounds, St. Bernards, Newfoundlands, Afghans, and Old English sheepdogs. The disease has also been seen in English and American cocker spaniels. It is rare in dogs weighing less than 12 kg.
The pathology of the disease involves dilation of all chambers of the heart. This dilation (caused by weak, thin, and flabby cardiac muscle) results in a decreased cardiac output and an increase in cardiac afterload (blood left in the heart in diastole). The cause of this disease is unknown, although viral, nutritional, immune-mediated, and genetic causes have been proposed. DCM results in impaired systolic function of the ventricles and, therefore, decreased stroke volume (the volume of blood ejected from the heart with each contraction). The effect on the animal is one of low-output circulatory failure, exhibited by weakness, exercise intolerance, syncope, or shock.
Dogs with DCM frequently experience development of atrial fibrillation, which further contributes to a decrease in cardiac output. Signs of atrial fibrillation include rapid, irregular heart rhythms or sudden death.
In the uncommon canine disease hypertrophic cardiomyopathy (HCM), the left ventricular muscle hypertrophies, decreasing the filling capacity of the ventricle and often blocking the outflow of blood during systole. The cause appears to be heritable.
Before the late 1980s, feline DCM was one of the most frequent cardiac diseases reported in cats. After the association of the disease with taurine deficiency, additional taurine was added to commercial diets, and the incidence of the disease significantly decreased. The pathologic condition is similar to DCM in dogs. Evidence has been found of a genetic predisposition to DCM in cats fed taurine-deficient diets.
HCM in cats is similar to the disease in dogs, with left ventricular hypertrophy being the predominant pathology. Neutered male cats between the ages of 1 and 16 years have been found to be most at risk. The cause of the disease may be related to abnormal myocardial myosin or calcium transport within the muscles of the heart.
Thrombus formation is a common and serious complication of myocardial disease in the cat. It is estimated that between 10% and 20% of cats with HCM will experience development of thrombi in the left side of the heart, which may dislodge and become trapped elsewhere in the arterial system. Cats appear to have inherently high platelet reactivity, making clot formation a more likely sequel to endothelial damage and sluggish blood flow occurring with myocardial disease. Approximately 90% of these emboli lodge as “saddle thrombi” in the distal aortic trifurcation, resulting in hind-limb pain and paresis. Rarely will a thrombus lodge at other arterial sites such as the renal artery, the coronary arteries, the cerebral arteries, or the mesenteric artery.
The goal of treatment is to dissolve the thrombus and restore perfusion to the area. Several drugs have been tried with varying results. Tissue plasminogen activator (tPA) has shown some success, but it is expensive. Heparin has also been used with some success. Low-dose aspirin therapy can be used prophylactically in cats with myocardial disease.
While malformations of the heart and great vessels represent a small cause of clinical heart disease, it is important to identify them in newly acquired pets or those to be used for breeding. Technicians should be encouraged to use their stethoscopes to routinely listen to the heart. With practice, subtle changes will become noticeable, allowing the technician to note abnormalities in the patient’s record.
Many malformations have a genetic basis. Breed predilections for congenital heart disease are listed in Table 1-1. The diagnostic approach for congenital heart disease should include a good history, with special attention paid to breed, sex, and age of the patient. Clinical signs of congenital heart failure include failure to grow, dyspnea, weakness, syncope, cyanosis, seizures, and sudden death; however, many animals with congenital malformations may be asymptomatic.
|Boxer||SAS, PS, ASD|
|Bull terrier||MVD, AS|
|Chow chow||PS, CTD|
|Cocker spaniel||PDA, PS|
|English bulldog||PS, VSD, TOF|
|English springer spaniel||PDA, VSD|
|German shepherd||SAS, PDA, TVD, MVD|
|German shorthaired pointer||SAS|
|Golden retriever||SAS, TVD, MVD|
|Great Dane||TVD, MVD, SAS|
|Labrador retriever||TVD, PDA, PS|
|Newfoundland||SAS, MVD, PS|
|Samoyed||PS, SAS, ASD|
|West Highland white terrier||PS, VSD|
AS, Aortic stenosis; ASD, atrial septal defect; CTD, cor triatriatum dexter; MVD, mitral valve dysplasia; PDA, patent ductus arteriosus; PPDH, peritoneopericardial diaphragmatic hernia; PS, pulmonic stenosis; SAS, subaortic stenosis; TOF, tetralogy of Fallot; TVD, tricuspid valve dysplasia; VSD, ventricular septal defect.
From Oyama MA, Sisson DD, Thomas WP, Bonagura JD: Congenital heart disease. In Ettinger SJ, Feldman EC, editors: Textbook of veterinary internal medicine, ed 6, vol 2, St Louis, 2005, Saunders.
Most cases of congenital abnormalities are identified during the first visit to the veterinarian after the pet has been purchased. On examination, a loud murmur often accompanied by a precordial thrill (a vibration of the chest wall) may be heard. With some defects, the clinician may observe pulse abnormalities, cyanosis, jugular pulses, or abdominal distension. Laboratory test results may all be normal. Whereas radiographs may suggest cardiac disease in some animals, echocardiography can provide an accurate diagnosis of the defect.
Causes of congenital heart disease include genetic, environmental, infectious, nutritional, and drug-related factors. More is understood of the genetic factors than the other causes. Studies suggest the defects are polygenetic in nature and that they might be difficult to eliminate entirely from a specific breed.
Failure of the ductus arteriosus to close after parturition results in blood shunting from the systemic circulation to the pulmonary artery. Normally the ductus carries blood from the pulmonary artery to the aorta during fetal development. The increase in oxygen tension in the blood at birth results in closure of the path in the first 12 to 14 hours of life. If the ductus remains open, blood will hyperperfuse the lung and the left side of the heart will become volume overloaded (Fig. 1-4). The resulting cardiac murmur is often referred to as a “machinery murmur”; this type of murmur is heard best over the main pulmonary artery high on the left base.
Figure 1-4 Circulation in a dog with a large left-to-right shunting patent ductus arteriosus. The shunt results in pulmonary overcirculation and left ventricular volume overload. Ao, aorta; LA, left atrium; LV, left ventricle; PA, pulmonary artery; RA, right atrium; RV, right ventricle.
(From Kittleson MD, Kienle RD: Small animal cardiovascular medicine, St Louis, 1998, Mosby.)