Structure and Function for the Management of Heart Disease
World Small Animal Veterinary Association World Congress Proceedings, 2003
Robert L. Hamlin, DVM, PhD, DACVIM (Cardiology/Internal Medicine)
Columbus, OH, USA

This session will discuss features of structure and function essential to the diagnosis of, and the selection of drugs to treat, heart diseases in dogs and cats. The diseases of importance are: mitral regurgitation, dilated cardiomyopathy, and arrhythmic cardiomyopathy in dogs, hypertrophic cardiomyopathy and systemic arterial hypertension in cats. The function of importance are: heart rate, conduction through the heart, force of contraction, interference to ejection of blood into and through the arterial tree, myocardial energetics, myocardial compliance.

Heart rate is determined by the rate of discharge of the SA node at the junction of the right atrium and cranial vena cava. Heart rate may be measured by counting the number of heart beats, femoral arterial pulsations, or P waves in an electrocardiogram (ECG) for 6 minute, and multiplying the number by 10. For normal animals, the SA node discharges (expressed in beats/minute) according to the table below:

During sleep

During Examination

During Excitement


45 to 60

90 to 120

180 to 240



140 to 210


Heart rates slows when increasing parasympathetic (vagal) tone produces acetylcholine (ACH) which binds to muscarinic cholinergic receptors, it speeds when increasing sympathetic tone produces norepinephrine (NE) which binds to the beta-1 (B1) adrenergic receptors; parasympatholytic drugs (e.g., atropine, glycopyrrolate) speed heart rate and sympatholytic drugs (e.g., propranolol, atenolol) slow heart rate. Digitalis glycosides (e.g., digoxin) and calcium channel blockers (e.g., diltiazem) also slow heart rate. Pain, fever, excitement, hypotension, and hyperthyroidism speed heart rate; sleep, tranquility, and hypothermia slow heart rate. Interestingly, within a species heart rates do not depend upon the size of the dog or cat, but among species heart rates do vary inversely with size.

Typically a healthy, quiet or sleeping dog has a respiratory sinus arrhythmia (RSA), in which heart rate speeds during inspiration (due to reduction in vagal tone) and slows during expiration (due to increase in vagal tone). Dogs that have difficulty breathing may have an exaggerated RSA due to vigorous irradiations from the medullary respiratory centers to the juxtaposed cardioregulatory centers; animals with heart failure have high heart rates and reduced RSA due to reduced vagal tone. Cats do not have nearly so marked RSA.

Conduction of the wave of depolarization originating in the SA node may be studied best by electrocardiography. Conduction through the atria determines the duration of the P wave, conduction from atria to ventricles determines the PQ (PR) interval, and conduction through the ventricles determines the QRS duration. The "weakest link" for conduction is usually through the AV node and is identified by lengthening of the PQ interval to > 140 ms in dogs or > 80 ms in cats. Occasionally the AV node does not conduct at all and the ventricular rate falls precipitously, necessitating installation of a pacemaker.

Force of contraction of any chamber--of greatest concern is that of the left ventricle--is determined by the volume of blood within the chamber [the end diastolic volume (EDV or preaload)] just before it contracts, by the velocity with which the contractile units cycle (myocardial contractility), and the interference to ejection (afterload or peak wall tension). Afterload may be estimated by multiplying systemic arterial pressure times preload and dividing by wall thickness. If afterload is constant, the greater the preload and the greater velocity of cycling, the greater the force of contraction. The preload is determined by the blood volume (a balance between water drunk and urine made), the ability of systemic veins to store blood (venous capacitance), the force with which the atrium "kicks" blood into the ventricle, and the stiffness of the ventricular wall. Myocardial contractility is increased when heart rate speeds, under the influence of norepinephrine, or when animals are given positive inotropes (e.g., digitalis, milrinone). Cats with hypertrophic cardiomyopathy have thick, stiff ventricles, their preload is low, therefore the force of ventricular contraction is low. The ventricular muscle fibers of dogs with dilated cardiomyopathy have a reduced rate of cycling (i.e., myocardial contractility is reduced), therefore the force of ventricular contraction is reduced.

Force of a weakened ventricular contraction can be improved by restoring preload to normal, by giving positive inotropes, or by decreasing the interference to the flow of blood out of the ventricle. To the contrary injudicious use of diuretics producing volume depletion decrease preload and force of contraction, and negative inotropes such as gaseous anesthetics, decrease contractility and force of contraction.

Interference to the ejection of blood from the left ventricle into and through the arterial tree is comprised of 2 components: impedance, resistance. Both are influenced significantly by the degree of contraction or relaxation of smooth muscle within the walls of the aorta (for impedance) or the systemic arterioles (for resistance). The ventricle ejects blood into the initial portion of the aorta, and the interference the ventricle perceives is due to the stiffness of the aorta. This stiffness accounts for <10% of the effort the ventricle expends. Next, as the ventricle relaxes and the pressure in the aorta slams closed the aortic valve, the elastic recoil of the aorta forces blood through the systemic arterioles. This resistance accounts for approximately 90% of the effort expended by the ventricle. When the ventricle fails, sympathoadrenal and other hormonal mechanisms (e.g., ADH, endothelin) constrict arterial smooth muscle and increase the hindrance to ejection. Thus it is common to administer drugs which relax arterial smooth muscle-so-called afterload reducers (ACE inhibitors)--which than allow even the weakened ventricle to sustain cardiac output.

Myocardial energetics refers to the production of energy to fuel both contraction and relaxation. This energy is stored as ATP, and most of the ATP is produced by mitochondria via a process requiring oxygen in the myocardium. The amount of oxygen in the myocardium is a balance between how much is delivered and how much is used (MV02). The amount delivered depends upon function of the lung, adequate quantities of hemoglobin, and adequate coronary blood flow. Coronary blood flow is determined by the difference in pressure between the aorta (from the coronary arteries arise) and the right atrium (into which the coronary circulation empties), and it is impeded by the heart beating. Each time the heart beats and the tension in the ventricular wall rises, the coronary vessels within the wall are squeezed closed, and coronary circulation and oxygen delivery ceased. The amount of oxygen consumed by the heart (MVO2) is determined by heart rate, myocardial contractility and afterload. Thus when heart rate elevates, both more oxygen is consumed and less is delivered, which may produce a decrease in myocardial oxygen, and diminished fuel (ATP) for both contraction and relaxation of the heart. The importance of modulating heart rate (as with beta blockers, calcium channel blockers and digitalis) cannot be overemphasized.

Myocardial compliance refers to the ease with which the ventricle is filled. It is is opposite of stiffness. Compliance depends upon the physical nature of the wall, for example a chamber surrounded by a fibrotic wall is less compliant than normal myocardium. In addition compliance is determined by the rate with which calcium is resequestered into the sarcoplasmic reticulum. This resequestration requires energy from ATP, thus an energy-deprived heart is stiff. The less compliant the heart either the less it fills and weaker is the force of contraction, or in order to fill it to a normal preload the pressure in the venous portion of the lung must be elevated. This leads to pulmonary congestion and possibly to pulmonary edema, and increase the work of breathing.

The baroreceptors reflex is critical to normal cardiovascular function, and integrates heart rate and afterload. This reflex originates with so-called high pressure baroreceptors located in the aortic and carotid sinuses. These receptors "report" the level of arterial blood pressure to the medulla, over the vagus and glossopharyngeal nerves. The medulla than sends out efferent impulses of the vagus and sympathetic nerves to adjust heart rate and arteriolar tone to achieve a stabile blood pressure. One of the most important "lesions" of heart failure, is that the baroreceptors (laden with sodium-potassium ATPase) report" to the medulla that the blood pressure is too low--even though it is not. Therefore the medulla accelerates heart rate and constricts arteries and arterioles--both destructive forces on an already weakened heart.

These features of cardiovascular structure and function are necessary to understand the origin of signs and symptoms, and the basis of selection of drugs to treat, heart diseases.

Speaker Information
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Robert L. Hamlin, DVM, PhD, DACVIM (Cardiology/Internal Medicine)
Columbus, OH, USA