Biology Review – Normal Physiology of the Heart - The heart is a four-chambered pump. The two upper chambers are the right and left atria (plural for atrium), and the two lower chambers are the right and left ventricles. The period from the end of one heart contraction to the end of the next contraction is called the cardiac cycle. This cycle consists of a period of relaxation, called diastole, followed by a period of contraction called systole. Blood returning from the body enters the right atrium, moves to the right ventricle where it is pumped to the lungs via the pulmonary arteries to exchange carbon dioxide for fresh oxygen, returns from the lungs to the left atrium by the pulmonary veins, is then pumped from the left atrium to the left ventricle, and is pumped back out to the body via the aorta. Cardiac output is the quantity of blood pumped by the left ventricle into the aorta each minute, and venous return is the quantity of blood flowing from the veins into the right atrium each minute.

The A-V (atrial-ventricular) valves prevent backflow of blood from the ventricles to the atria during systole, and the semi-lunar valves prevent backflow from the aorta and pulmonary arteries into the ventricles during diastole. The mitral valve is between the left atrium and the left ventricle of the heart; it is composed of two cusps, anterior and posterior. It is also known as the bicuspid valve. The tricuspid valve guards the opening between the right atrium and the right ventricle; it has three points, or cusps.

Chronic heart valve disease (endocardiosis) is common in many aging dogs. The valve leaflets and the cords (chordae tendinae) holding them in place gradually degenerate and become thickened and distorted with age. Furthermore, lumps (nodules) develop on the valve leaflets, and chemical changes take place that make the valves less flexible (fibrosis). All heart valves can be affected to some extent, but the mitral valve, in the left (high-pressure) side of the heart is most frequently and seriously affected. When this valve loses its flexibility, it starts to leak (valve insufficiency or regurgitation). Initially, mild mitral valve insufficiency causes no distress to the animal, but a heart murmur may be heard. Later, as the leak becomes more pronounced, and the heart becomes overstretched by heart failure, the leakage is accentuated. Further serious complications can include a flail valve, rupture of chordae tendineae and even rupture of the overstretched left atrium, together with heart rhythm disturbances which can cause dramatic flooding of the lungs, collapse or sudden death.

Mitral Valve Disease in Cavaliers - Peter GG Darke, BVSc, PhD, DVR, DVC, MRCVS, wrote that a statistical analysis of the clinical database at the University of Edinburgh showed that Cavaliers shared a predisposition to mitral valve disease with Chihuahuas, Pekingese, miniature and toy Poodles, Lhasa Apsos, and surprisingly for an athletic breed, Whippets. However, whereas some of these other breeds averaged about 6 or 7 times the prevalence that might be expected in the ‘average’ dog, * NOTE Dr. Darke’s exact words: "Cavaliers showed about 21 TIMES as much mitral insufficiency as typical ‘normal’ dogs. These data were derived mainly from a first-opinion fee-paying clinic, and might therefore be taken as reasonably representative of the population at large." In Sweden, studies suggest on the population level that Cavaliers develop chronic valvular disease early in life and that age of onset of mitral regurgitation predicts the age of death due to congestive heart failure.

Differentiating Heart Disease and Heart Failure - Heart murmurs, arrhythmias (abnormal rhythms) and other cardiac abnormalities provide evidence for heart disease. Individuals with these signs will not show heart failure until these disease states are severe. Many forms of heart disease may not warrant therapy; however, all forms of heart failure require therapeutic intervention. Suggestions for therapeutic intervention will be in the next issue of "Quotes", to be published in March, 1999.

Heart failure (HF) is the state wherein the heart fails to meet the metabolic demands of the tissues. Therefore cardiac output is insufficient to meet the needs of the tissues. This usually occurs in the face of elevated left ventricular

pressures at end diastole.

HF may occur in conditions where the heart is producing a normal cardiac output, but the metabolic needs of the tissues are increased, such as in hyperthyroidism or anemia, and so cardiac output fails to meet their needs. Thus, it may occur in conditions where the strength of the heart muscle appears normal.

However, most conditions that result in heart failure occur a result of a markedly weakened left ventricle or right ventricle or both.

Congestive heart failure (CHF) occurs when left ventricular pressure at end diastole is elevated. This results in elevated pulmonary venous pressures and pulmonary edema. CHF occurs when the volume of blood presented to the heart is in excess of the heart's capacity to move it along. Consequently, fluid builds up behind the heart. If the inability to move the volume of blood forward is due to a left heart problem, then pulmonary venous congestion develops and later pulmonary edema. Subsequently this can lead to pleural effusion (effusion is the escape of fluid into a part) and abdominal effusion. If the abnormality lies in the right heart or the pulmonary arteries, wherein they limit the ability to move blood forward, then congestion occurs behind the right heart (causing pleural effusion and/or build up of fluid in the abdomen). Many but not all cases of heart failure also have congestive heart failure. Therefore, it is frequently useful to look for evidence of congestion to suggest the presence of heart failure.

More on Pulmonary Edema – When the left side of the heart fails without the right side failing as well, blood continues to be pumped into the lungs by the normal right heart, while it is not pumped adequately out of the lungs by the left heart. As a result, the mean (average) pulmonary pressure rises while the mean systemic pressure falls because of shift of large volumes of blood from the systemic circulation into the pulmonary (lung) circulation. As the volume of blood in the lungs increases, the pulmonary vessels enlarge, and once the pulmonary capillary pressure rises above a critical point, fluid begins to filter out of the capillaries into the interstitial spaces and alveoli (air sacs in the lungs where exchange of oxygen and carbon dioxide occurs), resulting in pulmonary edema. With the abnormal accumulation of fluid, the dog may show signs of shortness of breath and open-mouth breathing, and may stand or assume a sitting position with the elbows held away from the chest only, in preference to lying down. Unless the congestion with serous fluid and blood is checked, the normal respiratory gaseous exchange of oxygen and carbon dioxide is cut off, and the dog is literally drowning. If a decision has been made to not treat the dog for whatever reason, it is much kinder to make a decision to euthanize than to let the dog die a "natural death".

Myocardial oxygen consumption - Myocardial oxygen consumption (MVO2) refers to the amount of oxygen consumed (required) by the heart muscle for a contraction. Afterload refers to the resistance the left ventricle encounters as it tries to eject blood. Afterload is only conceptual and cannot be measured directly. Preload refers to the stretching of the myocardial cells in a chamber during diastole, prior to the onset of contraction. This is the priming process of the pump. Preload is measured as the end-diastolic volume or end-diastolic pressure. Therefore, preload is equal to venous return plus the residual volume left in the cardiac chamber after the last contraction.

• Dyspnea (difficulty breathing, even at rest) /wheeze/cough/orthopnea (ability to breathe only in the upright position) - due to pulmonary edema or pleural effusion. Owners will probably find this very disturbing. Coughing is usually dry and wheezy, but it may appear that the dog is trying to ‘bring something up’. Cough may occur due to mitral valve insufficiency with left atrial enlargement and compression of the left main-stem bronchus; this may often occur in the absence of heart failure. Many dogs with heart failure may not cough, whereas dyspnea, wheezes and sometimes orthopnea are common historical findings. Some dogs will cough with relatively mild edema and others only cough with severe pulmonary edema. It appears that the speed with which the pulmonary edema develops may play a role in determining when or if cough is to develop. With severe heart failure, pink frothy liquid may be coughed up as the fluid in the lungs spills into the airways and windpipe. This is very serious; indicating life-threatening heart failure.

• The dog slows down in eating or does not complete a normal portion. Weight loss may also occur in the terminal stages of heart failure.

• Syncope (sudden loss of strength or fainting) /lethargy - due to reduced cerebral perfusion (passage of blood through an organ). This may not be noticed unless the animal does reasonably strenuous exercise.

• Weakness/reduced stamina - due to reduced skeletal muscle perfusion.
• Abdominal distention - due to ascites (abnormal accumulation of fluid in the abdominal cavity) and/or
• Hepatomegaly (enlargement of the liver) or splenomegaly (enlargement of the spleen).

Physical examination findings may include:

• slow capillary refill time (> 2 sec) – your vet can check this by pressing on the dog’s gum and seeing how long it takes for the colour to return to normal
• pale or cyanosed (bluish discolouration showing lack of oxygen) mucous membranes
• dry or tacky (sticky) mucous membranes
• cool extremities or reduced rectal temperature
• jugular venous distention (neck veins are stretched out) or positive hepato-jugular reflux test (a test the vet will do)
• dyspnea (laboured or difficult breathing), cough, harsh lung sounds, wheezes, or crackles on auscultation
• thrill on precordial palpation (a tremor which can be felt on the chest wall in the area over the heart)
• enlarged heart, spleen, or liver
• abdominal effusion
• abnormal fluid accumulated in the intercellular spaces, felt under the skin
• weak femoral arterial pulse
• pulse deficits (present when the pulse rate is less than the heart rate) with irregular cardiac rhythm
• muffled heart sounds, gallop rhythms, heart murmurs, or arrhythmias may be detected on cardiac auscultation

• Chest x-rays are useful to show:

• Heart enlargement: as the MVD progresses, the heart tends to increase in size. X-rays are very useful for charting the progression.
• Fluid in the lungs (pulmonary edema): X-rays are the best means of identifying fluid in the lungs.
• Other chest problems: coughing and breathlessness may be caused by other conditions apart from MVD. Many lung diseases will produce changes on X-rays which can be identified and distinguished from heart problems.

• ECGs – a recording of electrical activity of the heart – this is most useful when there are changes in the heart rhythm.

• Blood tests – these do not usually help to diagnose heart problems, but they can identify other causes of fainting or collapse. Blood tests may also be needed to check kidney function before some types of heart treatment.

• Ultrasound scans – depending on how much is already known about whether your dog has MVD. Echo scans can actually demonstrate the thickened mitral valve leaflets of MVD. A harmless beam of ultra-high frequency sound is directed at the beating heart, and produces moving black and white pictures of the heart chambers. The images produced show dilation of the heart chambers and abnormal movement of mitral valve leaflets. The most sophisticated ultrasound machines can also demonstrate the leaking of the valves, showing the direction and speed of blood flow in colour.

Explanations - Compensatory Measures that Occur in Heart Failure –

Reading this section will be helpful to better understanding of treatment measures in the next issue. The body tries to compensate with measures that occur in response to a fall in cardiac output. In the short-term, these compensatory mechanisms are beneficial and help to restore the fluid volume and blood pressure. They are life-saving in cases with transient circulatory collapse, such as hemorrhage, but become maladaptive when stimulated by chronic conditions, such as heart disease. These measures include:

1. Increase in sympathetic tone - resulting in:

• increase in heart rate to maintain cardiac output
• increase in arterial vasomotor tone (increasing peripheral arterial resistance or afterload) to maintain blood pressure
• increase in venomotor tone to increase venous return which increases preload
• release renin from kidney elaborates angiotensin II and aldosterone which increase vasomotor tone (increasing afterload) and increase venous vasomotor tone (increasing preload) and increase sodium and water retention (also increases preload)
• increase contractility (how heart muscle contracts)
• promote arrhythmias (abnormal rhythms)
• increase MVO2 (myocardial oxygen demand)

1. Circulatory changes:

• Chemicals cause non-essential blood vessels to shut down, to conserve blood flow for vital organs such as the brain and the heart itself, rather than the skin, which causes pale mucous membranes, slow capillary refill time, and cool extremities
• Reducing flow to the gastrointestinal tract, which can affect absorption and produce ischemic bowel with ulceration and hemorrhage
• Since the left ventricle is pumping less blood forward to the body, the kidneys become relatively starved of blood supply. The reaction is to retain fluid and sodium (the kidneys are assuming the body has become dehydrated). The excess retained fluid can contribute to the edema.

1. Increased thirst - causing fluid overload (increasing preload).
2. Increased arginine vasopressin (ADH) resulting in:

• increased arterial vasomotor tone (increasing afterload)
• increased fluid retention - fluid overload (increasing preload)

Comments: The net effect of these compensatory measures usually has deleterious effects on cardiac performance chronically.

Cardiovascular Disease, Veterinary Heart Institute, Principles of Heart Disease, http://www.vetheart.com/diseases.html.

Darke, Peter GG, BVSc, PhD, DVR, DVC, MRCVS, "Mitral Valve Disease in Cavalier King Charles Spaniels", presentation to The Cavalier King Charles Spaniel Club, Saturday 2 November 1996.

Fuentes, Virginia Luis, Royal (Dick) School of Veterinary Studies, University of Edinburgh, "The Diagnosis and Treatment of Mitral Valve Disease in Cavaliers", presentation to The Cavalier King Charles Spaniel Club, Saturday 2 November 1996.

Kvart, Clarence, DVM, PhD and Jens Häggström, DVM, Phd, Faculty of veterinary medicine, Uppsala, Sweden. Occurrence and consequences of chronic valvular disease in Cavalier King Charles Spaniels, presentation to The Cavalier King Charles Spaniel Club, Saturday 2 November 1996.

O’Grady, Dr. Michael, Cardiology Concepts, Therapy of Heart Failure, http://www.ovcnet.uoguelph.ca/ClinStudies/Courses/Public/Cardiology/Concepts/.

Disclaimer: Your veterinarian is the most qualified person to answer all of the questions you have about your pet's health. Nothing in this article should be construed as medical advice regarding any individual animal’s condition.