Mechanical Activity of Heart

6.4.1 Cardiac Cycle and Wiggers Diagram

Cardiac cycle refers to the cardiac events that occur from the beginning of one heartbeat to the beginning of the next. Each cycle is initiated by spontaneous generated action potential in the sinus node.

Fig. 6.3 Wiggers diagram showing the eight phases in a cardiac cycle

heartbeat and includes systole (isovolumetric contraction, ejection), diastole (isovolumetric relaxation and filling), and then back to systole. The cardiac cycle is divided into the following various stages and events (Fig. 6.3).

6.4.1.1 Isovolumetric Contraction

It is the first phase of ventricular systole in the cardiac cycle lasting for 0.05 s. Isometric contraction is characterized by increase in tension, without any change in the length of muscle fibers. Immediately after atrial systole, at the onset of ventricular contraction, the pressure in the lumen is essen­tially equal to that in the atria and the AV valves have floated almost into opposition. As soon as ventricular pressure exceeds atrial pressure, the AV valves close. Semilunar valves are already closed, and the ventricles contract as closed chambers, in such a way that there is no change in the volume of ventricular chambers or in the length of muscle fibers. The ventricles contract around the contained blood, which is incompressible. During isometric contraction, only the tension in the ventricular muscle increases, and as a result of this increased tension in the ventricular musculature, the pressure inside the ventricles increases significantly. This marks the end of diastole and the beginning of systole.

The QRS complex denotes ventricular depolarization and follows the P wave by a time interval (PR interval) necessary for the impulse to traverse the conduction system and reach the ventricular muscle cells. At the time of the peak of the R wave in the ECG, ventricular contraction begins. At the beginning of this phase, the closure of atrioventricular valves occurs producing the first heart sound.

6.4.1.2 Maximum Ejection

The period of maximum ejection begins with the opening of the semilunar valves and lasts until the peak of the arterial pressure curve. About 75% of the blood ejected during sys­tole flows during this period and flows into the aorta, and pulmonary artery exceeds runoff into the peripheral arteries, causing the pressure to rise. During this period of systole, aortic pressure is exceeded by left ventricular pressure and the blood is accelerated to a peak velocity of 1-2 m/s.

6.4.1.3 Reduced Ejection

As peripheral runoff reaches equilibrium with ventricular ejection into the great arteries, the pressure curve reaches a maximum. This is the beginning of the reduced ejection phase, and blood runoff begins to exceed the ejection rate, causing the pressures to decrease. The pressure in the ventricles exceeds that in the great vessels throughout the systole. However, the pressure within the ventricle only exceeds that in the great vessels during the first half of systole when most of the blood is ejected. During the last half of systole, pressure in the great vessels exceeds that in the ventricle even though blood is still flowing out of the ventri­cle. This paradox occurs because of the reduced momentum and kinetic energy of the blood as it leaves the ventricle.

6.4.1.4 Protodiastole

This marks the beginning of ventricular relaxation and is a point on the ventricular pressure curve that is often difficult to identify. Due to the ejection of blood, the pressure in the ventricle continues to fall below that in the aorta and pulmo­nary artery. A brief retrograde flow occurs, closing the semi­lunar valves. This marks the end of protodiastole and the beginning of the next phase. Protodiastole is the first stage of ventricular diastole, and the duration of this period is 0.04 s. Thus, protodiastole denotes the end of systole and beginning of diastole. The semilunar valves close during this phase producing the second heart sound.

6.4.1.5 IsovolumetricRelaxation

This marks the end of ventricular systole and the beginning of the diastole. The short period of reversal of blood flow in the great vessels as the ventricles relax closes the semilunar valves and produces the incisura or dicrotic notch on the pressure wave in the great vessels. The semilunar valves keep blood from leaking back into the ventricles as the ventricular pressure drops to very low values. Since the ventricles are closed chambers, myocardial relaxation results in a steep fall in intraventricular pressure but no alteration in ventricular volume. This phase, with a rapid decrease in ventricular pressure and no blood flowing into or out of the ventricles, is isovolumetric relaxation. The aortic and pulmo­nary artery pressures decline during diastole as blood flows through the tissues. Isometric relaxation is characterized by decrease in tension without any change in the length of muscle fibers and is also called as isovolumetric relaxation. During isometric relaxation period, once again all the heart valves are closed. During this phase, both the ventricles relax as closed chambers without any change in volume. Intraven­tricular pressure decreases during this period, and the phase lasts for about 0.08 s. The T wave signifies repolarization in the ventricular muscles and relaxation of the ventricular chambers.

6.4.1.6 Rapid Filling

Beginning with the opening of the AV valves, ventricular volume increases as blood that has accumulated in the atria under increasing pressure flows quickly into the relaxed ventricle. The blood volume in each atrium is slightly greater than that of the corresponding ventricle, thus providing a reservoir of blood sufficient to fill the ventricle completely for each beat. The end of this phase is not clearly distinguish­able as it merges with the next. At the transition between this and the following phase, the usually inaudible third heart sound (S3) may be recorded on a phonocardiogram. When atrioventricular valves open, there is a sudden rush of the accumulated atrial blood into the ventricles. About 70% of ventricular filling takes place during this phase, which lasts for 0.11 s.

6.4.1.7 Reduced Filling (Diastasis)

This is a period of slower filling of the cardiac chambers during which blood continues to flow into both atria and ventricles as into a common chamber. It is terminated by the onset of atrial systole. Following the sudden rush of blood, the ventricular filling becomes slow. About 20% of filling occurs in this phase, and this phase lasts for 0.19 s.

6.4.1.8 Atrial Systole

After slow filling phase, the atria contract and pump a small quantity of blood into ventricles and about 10% of ventricular filling takes place. Flow of additional amount of blood into ventricle due to atrial systole is referred to as atrial kick. In the normal heart, the initial impulse for a heartbeat arises within the SA node and quickly spreads to the two atria. The atrial wall muscles are basically arranged in a circular fashion such that the volume of blood within the atria decreases with each contraction. The ventricles are relaxed when the atria contract and blood enters the ventricle due to the pressure gradient. Atrial contraction produces only a small increase in ventricular volume and pressure. This phase ends at the onset of ventricular isovolumetric contraction, completing the car­diac cycle.

The duration of the cardiac cycle is the reciprocal of the heart rate:

For example, for a heart rate of 75 beats/min, the cardiac cycle lasts for 0.8 s.

6.4.1.8.1 PressureChanges

Atrial pressure rises during atrial systole and continues to rise during isovolumetric ventricular contraction as the AV valves bulge into the atria (Fig. 6.3). The pressure drops quickly as the AV valves are forced down by the contracting ventricular muscle, then rises as blood flows into the atria, and finally rises as the AV valves open early in diastole. By lowering atrial capacity, the AV valves’ return to their relaxed configuration also contributes to this pressure increase. Three distinct waves (a, c, and v) are produced in the record of jugular pressure as a result of the transmission of atrial pressure changes to the great veins. The “a” wave is due to atrial systole. Some blood regurgitates into the great veins when the atria contract. In addition, venous inflow stops, and the resultant rise in venous pressure contributes to this wave. During atrial contraction, the right atrial pres­sure normally rises by 4-6 mmHg, and the left atrial pressure increases about 7-8 mmHg; it is caused partly by slight backflow of blood into the atria at the onset of ventricular contraction but mainly by the c wave that occurs when the ventricles begin to contract bulging of the AV valves back­ward toward the atria because of increasing pressure in the ventricles.

The “c” wave is the transmitted manifestation of the rise in atrial pressure produced by the bulging of the tricuspid valve into the atria during isovolumetric ventricular contraction.

The slow flow of blood from the veins into the atria during ventricular contraction causes the “v” wave, which appears at the end of ventricular contraction. Then, as ventricular con­traction is over, the AV valves open, allowing this stored atrial blood to flow rapidly into the ventricles and causing the “v” wave to disappear.

6.4.2 Heart Sounds

Cardiac sounds are the sounds produced by mechanical activities of heart during each cardiac cycle. They are classi­fied as either transients or murmurs. The transients are of brief duration and are named as the first, second, third, and fourth heart sounds. Murmurs refer to prolonged groups of vibrations that occur during normally silent intervals of the cardiac cycle.

The first heart sound (S1) is associated with the closure of the AV valves (the mitral and tricuspid valves). The actual closure of these valves does not produce this sound; the valve leaflets are so light and thin that their closing would be almost silent. However, there is a momentary backflow of blood from the ventricles to the atria at the beginning of ventricular systole. When this backflow of blood is brought to a sudden stop against the closing valves, brief vibrations are created in the blood and in the cardiac walls. These vibrations create the first heart sound. The other factors that contribute to the first heart sound are vibrations generated within the contracting ventricular myocardium, opening of the semilunar valves, and vibrations generated within the wall of the aorta and pulmonary artery as blood is ejected into the arteries at the onset of systole. The first heart sound is longer and has lower frequency than the second heart sound. The first heart sound is usually best heard over the cardiac apex.

In the dogs, S1 is usually more intense than S2, whereas the opposite is true for horses under basal conditions. Fur­thermore, a marked beat-to-beat variation in the intensity of S1 is usual in horses. Numerous extracardiac and cardiac factors influence the intensity of S1 and other sounds. The most common reasons for decreased intensity of S1 are obesity, pericardial or pleural effusions, hypervolemia, pro­nounced first-degree AV block, diaphragmatic hernia, perito­neal pericardial diaphragmatic hernia, and barrel conformation of the thorax. Intensity of S1 is increased in animals during periods of excitement and immediately after exercise. More vigorous closing and tensing of the AV valves related to increased sympathetic activity probably account for increased intensity of S1 under these circumstances. Other common reasons for increased intensity of S1 are deep tho­rax, anemia, fever, hypertension, and chronic mitral valve disease.

6.4.1.9 Splitting of First Heart Sound

Split of heart sound is a rare event in all species. Split of S1 is determined by a delayed closure of one of the AV valves. It can be occasionally heard in animals with severe right or left bundle branch block.

6.4.1.10 Second Heart Sound

The second heart sound (S2) is associated with closure of the aortic valve on the left side of the heart and the pulmonic valve on the right side of the heart. The pulmonic component of S2 normally follows the aortic component. However, they are usually heard as a single sound. S2 is a shorter higher pitched sound than S1. It is usually briefer, sharper, and higher pitched than the first heart sound. The second heart sound is caused by the echo that occurs as the valves sud­denly close, stopping the brief backflow of blood into the ventricles. The aortic and pulmonic valve closure is normally simultaneous. Under certain conditions, however, the two valves close at slightly different times, and the second heart sound is heard as two distinct sounds in quick succession; this condition is called a split-second heart sound.

Decreased intensity of S2 is observed in pericardial and pleural effusion, diaphragmatic and peritoneal pericardial diaphragmatic hernia, thoracic masses, myocardial failure, and severe chronic mitral valve degeneration. The most com­mon causes of increased intensity of S2 are fever, anemia, pulmonary hypertension, and hyperthyroidism.

6.4.1.10.1 Splitting of Second Sound

Splitting of S2 occurs when the semilunar valves close out of phase. The split of S2 is difficult to auscultate in dogs and cats due to the short interval between A2 and P2, while it is a common auscultatory finding in horses. The most common reason for splitting of S2 is delayed closure of the pulmonic valve, and for this reason, it is usually best heard over the pulmonic area of auscultation. Splitting of S2 can be physio­logic or pathologic. Physiologic splitting of S2 is a respiratory-related phenomenon appearing during inspiration and disappearing during expiration. During inspiration, increased venous return to the right side of the heart occurs as a consequence of decreased intrathoracic pressure. The resultant lengthening of right ventricular ejection time causes the pulmonic valve to close later. Simultaneously, the act of inspiration hinders venous return to the left side of the heart, and this in turn abbreviates left ventricular ejection time and causes the aortic valve to close earlier. During expiration, right ventricular ejection time returns to normal and left ventricular ejection time lengthens to handle the increased amount of blood delivered to the lungs during the preceding inspiration. Therefore, S2 becomes a single sound. Respiratory-related splitting of S2 is detectable in some nor­mal dogs, particularly if the heart rate is slow and pronounced sinus arrhythmia is present. Splitting of S2 is detectable by auscultation in most normal horses, and it tends to be fixed rather than vary with respiration. Pathologic splitting of S2 is a characteristic of certain cardiac abnormalities such as pul­monary hypertension, pulmonic stenosis, right bundle branch block, and interatrial septal defect in dogs. Pathologic split tends to be fixed differently from physiologic one.

6.4.1.11 Third Heart Sound

Third heart sound (S3) occurs early in diastole near the end of rapid ventricular filling. It is associated with sudden tensing of the chordae tendineae, deceleration of the filling wave of blood, and vibrations arising in the walls of the ventricles. Although S3 is detectable in PCGs of apparently normal dogs, it is rarely audible due to low-frequency sounds. How­ever, the third heart sound can be easily recognized in dogs afflicted with myocardial disease such as dilated cardiomy­opathy. In these patients, the presence of S3 may be the only auscultatory abnormality and is generated by increased myocardial stiffness and elevated filling pressure. An audible S3 may also be present in cats with end-stage cardiomyopa­thy. Occasionally, S3 is more intense than either of the two major heart sounds, S1 and S2. The third sound is readily audible in many apparently normal horses. The sound is quite intense and clicking in some horses; in others, it is soft and dull. As in dogs, S3 in horses with congestive heart failure is frequently very intense.

6.4.1.12 Fourth Heart Sound

The fourth or atrial sound is generated by vibration of cardiac structures associated with atrial contraction. Although the fourth heart sound is seldom heard in dogs, it can be recognized in normal giant breeds. Fourth heart sound is common in apparently normal horses. In many animals, S4 indicates pronounced first degree AV block. A longer AV conduction time allows for completion of the sequence of events leading to its generation. S4 is generated by transient closing and tensing of the AV valves. Pathologic S4 is present in animals with myocardial disease characterized by diastolic dysfunction such as hypertrophic cardiomyopathy, wherein there is an increased volume of blood in the atria at the onset of their contraction which induces a more energetic atrial contraction, and S4 might become audible. Other conditions associated with the presence of a detectable S4 are advanced second-degree and third-degree AV block.

6.4.1.13 Gallop Rhythm

Gallop rhythm occurs during tachycardia when S3 and S4 merge into a single heart sound. This rhythm is so called because the sequence of S1 and S2 and fusion of S3 and S4 resemble the sound of a galloping horse. As the period of diastole shortens with an increase in heart rate, atrial systole becomes superimposed upon the rapid filling phase of the ventricles. In small animals, the presence of a gallop rhythm is associated with significant myocardial failure. In cats, gallop rhythms are present in animals with hypertrophic cardiomyopathy or hyperthyroidism.

6.4.1.14 Other Systolic Sounds

Two “extra” sounds sometimes occur between S1 and S2. One of these, the ejection sound or ejection click, is an accentuation of the terminal component of S1. It often coexists with abnormalities that cause dilation of either the aorta or the pulmonary artery of the dog but is common in normal horses and in young small animals. The other extra systolic sound is the systolic click, which is often intermit­tent. Systolic click is a common finding in the early stages of chronic mitral valve disease in dogs. The origin of the sys­tolic click is caused by the tensing of redundant chordate tendineae and rapid deceleration of blood against the mitral valve leaflets at maximum prolapse into the left atrium. The sound is usually midsystolic, but the timing can vary and can be closer to S1 or S2.

6.4.2 Cardiac Murmurs

A murmur is a prolonged series of auditory vibrations emanating from the heart or blood vessels that may occur at different times during the cardiac cycle. Turbulence in flowing blood is the major source of murmurs, and the turbulent blood flow may be caused due to (1) morphology alteration in heart valves (insufficiency or stenosis), (2) abnor­mal communication between the two sides of the heart and/or great vessels (interatrial septal defect, interventricular septal defect, or patent ductus arteriosus), (3) increased blood flow velocity through a normal valve orifice or vessel, and (4) changes to the blood viscosity, such as in severe anemia.

Murmurs are generally classified based on the following criteria: location, quality, timing, radiation, and intensity. The point of maximum intensity (PMI) of a cardiac murmur is usually located over the turbulence site and gives an indica­tion of the origin of the murmur. The cause of murmurs can be further classified from their timing within the cardiac cycle. Murmurs occur during systole, during diastole, or during both systole and diastole. The frequency or pitch of a murmur may also aid diagnosis of the underlying cause. The direction in which a murmur radiates over the body surface also helps in localizing the site of origin. The inten­sity of murmurs is most commonly graded on a 1-6 scale, with a grade 1 murmur being the softest and a grade 6 the loudest. The heart murmur may be palpated as a precordial thrill in animals with a grade 5 or grade 6.

Functional (Physiological) Systolic Murmurs

Soft systolic murmurs are common in puppies, kittens, and horses having apparently normal valve orifices and great arteries. Turbulent blood flow stemming from increased blood velocity is of prime importance in the generation of these innocent murmurs. Severe anemia can also cause a functional systolic murmur by changed blood viscosity. A functional murmur is usually of low intensity (grade 1-3) and is composed of mid- or high-frequency sounds. The murmur is usually timed to early systole and ends early or in the middle of systole. The intensity of the murmur may vary with the heart rate and respiration.

Innocent Diastolic Murmurs

It is usual to find soft diastolic murmurs in apparently normal horses less than 5 years of age. These are high pitched and very brief in duration. They occur immediately after S2, and their cause is unknown.

6.4.2.1 Clinical Correlations

6.4.2.1.1 SystolicMurmurs

Systolic murmurs (between S1 and S2) occur as blood regurgitates through incompetent AV valves, or as blood is pumped through the semilunar valves or through a ventricu­lar septal defect.

Aortic stenosis: A stenotic valve refers to a narrowed, stiff, valve that does not open completely, and hence the blood must be forced through the constricted opening at tremen­dous velocity, resulting in turbulence that produces an abnormal whistling sound. Subaortic stenosis is the most common form of congenital heart disease in dogs. How­ever, aortic or subaortic stenosis is unusual in horses, and in cats the aortic stenosis is usually a consequence of hyper­trophic cardiomyopathy. The principal hemodynamic con­sequence of aortic stenosis is an increased resistance to left ventricular outflow, with a proportional elevation of left ventricular systolic pressure if flow remains constant. Aor­tic stenosis usually causes a systolic murmur with the intensity of the murmur increasing until mid-ventricular systole and then decreasing during the remainder of ven­tricular systole. Its intensity and quality are dependent on the severity of stenosis, ranging from a soft low-intensity murmur to very loud murmurs of harsh quality.

Pulmonic stenosis: The characteristics of pulmonic stenosis are very similar to aortic stenosis, and it may be very difficult to distinguish murmurs caused by pulmonic ste­nosis from those caused by aortic stenosis in dogs and cats using auscultation. The murmur is systolic, and the inten­sity depends on the severity of stenosis, ranging from a soft low-intensity murmur to very loud murmurs of harsh quality. Right ventricular ejection time may be prolonged with more severe forms of pulmonic stenosis, and splitting of S2 may be present. Pulmonic stenosis is a common congenital lesion in dogs but is less common in cats and is extremely rare in horses.

Mitral insufficiency: A valve having edges that do not fit together properly and hence cannot close completely is referred to as an insufficient or incompetent valve. Turbu­lence is produced when blood flows backward through the insufficient valve and collides with blood moving in the opposite direction, creating a swishing or gurgling murmur.

Mitral insufficiency or regurgitation may be primary (i.e., caused by an abnormal mitral valve) or secondary (i.e., caused by left ventricular dilatation that leads to separa­tion of the mitral valve leaflets). Primary mitral insuffi­ciency is the cause of most systolic murmurs in middle­aged to old dogs and horses, and it occurs as a conse­quence of chronic progressive lesions of primarily the AV valves, referred to as myxomatous valve disease. It is also the most common cause of congestive heart failure in dogs and horses. Primary mitral insufficiency is uncommon in cats, but it may, like aortic stenosis, develop as a conse­quence of hypertrophic cardiomyopathy. The sound begins as a soft apical systolic murmur on the left side of the thorax and may be intermittent and sometimes audible only during inspiration. With further progression, the sound becomes more intense, and harsher in quality, and may radiate over to the right side of the thorax.

Tricuspid insufficiency: The characteristics of the systolic murmur of tricuspid insufficiency are very similar to mitral insufficiency. The intensity of the murmur may increase during inspiration and decrease during expiration. Generally, the intensity of tricuspid regurgitation murmurs is lower than that of mitral valve insufficiency murmurs. Conditions associated with increased right ventricular pressure, such as pulmonary arterial hypertension, can cause louder tricuspid insufficiency murmurs.

Interventricular septal defect: The systolic murmur associated with interventricular septal defect (VSD), which is the most common congenital heart defect in cats and horses wherein the murmur is generated as blood flows from the left ventricle into the right ventricle. This murmur tends to be of uniform intensity throughout its course and is usually high pitched and blowing.

Interatrial septal defect: Interatrial defect occurs as a con­genital anomaly, wherein the blood flows from the left atrium to the right atrium during atrial systole (i.e., during late ventricular diastole), thereby increasing the stroke volume of the right ventricle and causing relative pul­monic stenosis. Therefore, this systolic murmur is caused by relative pulmonic stenosis rather than by blood flow through the defect itself.

Tetralogy of Fallot: Tetralogy of Fallot is a rare congenital disease in dogs, but comparatively more common in cats and horses. The murmur associated with tetralogy of Fallot is primarily caused by the pulmonic stenosis. It is a shunting defect, wherein there is usually no resistance to flow between the left and right ventricles. Hence, the blood flows to the right and left circulations proportional to systemic and pulmonary resistances. The pulmonic stenosis in tetralogy may be so severe that resistance to flow through the pulmonic valve is greater than systemic vascular resistance. Consequently, a significant amount of blood flows from the right ventricle, through the ventricu­lar septal defect, and out the aorta. The intensity and character of the murmur depend on pulmonic stenosis characteristics.

6.4.2.1.2 DiastolicMurmurs

Murmurs heard after S2 are designated as diastolic murmurs, are extremely rare in dogs and cats, and are not uncommon in horses.

Mitral or tricuspid stenosis: Although pathology of the AV valves is virtually nonexistent in domestic animals, lesions such as interatrial septal defect, mitral insufficiency, or tricuspid insufficiency can result in an increased rate of blood flow through the appropriate AV valve during early diastole in domestic animals leading to diastolic rumble or early diastolic murmur.

Pulmonic insufficiency: Diastolic murmurs due to pulmonic insufficiency are rare in animals in spite of the fact that mild-to-moderate pulmonic insufficiency is very common in all species. The murmur of pulmonic insufficiency tends to be soft and blowing. Occasionally, dilatation of the pulmonary artery with attendant incompetence of the pulmonic valve resulting from pulmonary hypertension is the cause of a diastolic murmur in the dog. Likewise, a diastolic murmur of pulmonic insufficiency sometimes appears after surgical correction of pulmonic stenosis.

Aortic insufficiency: Like pulmonic insufficiency, mild aor­tic insufficiency is common in dogs, while moderate-to- severe insufficiency is comparably uncommon in dogs and cats. They are common in old horses and mostly occur as “noisy,” high pitched with a blend of a wide range of vibration frequencies. It occurs either as a consequence of myxomatous lesions or, less commonly, due to bacte­rial endocarditis, or as a consequence of congenital aortic stenosis.

Continuous murmurs: Patent ductus arteriosus (PDA) is one of the most common congenital conditions in dogs; it occurs in cats and horses, but less commonly than in dogs. In PDA, the fundamental pathophysiologic event is shunting of blood through the patent duct. The flow direction is usually from the left (aorta) to the right (pul­monic artery) side because of the pressure gradient, but with larger ducts, which are uncommon, the flow ceases or can even be from the right to the left side (reversed PDA).

Turbulence in blood flowing through the PDA is respon­sible for generating the murmur. Since the abnormal blood flow is continuous during systole and diastole, the murmur is likewise continuous during systole and diastole. The intensity of the murmur increases during systole, attains a peak at the time of S2, and decreases during diastole. The murmur of PDA is frequently referred to as a “machinery” murmur. The murmur is audible over the left hemithorax region at the aortic and pulmonary valve areas.

6.4.3 Cardiac Output

Cardiac output refers to the amount of blood pumped from each ventricle. Usually, it refers to left ventricular output through aorta.

Normal cardiac output for dogs and cats is 100-200 mL/ kg/min and 120 mL/kg/min, respectively. Cardiac output can be expressed in three ways:

• Stroke volume

• Minute volume

• Cardiac index

Stroke volume is the amount of blood pumped out by each ventricle during each beat. The output of the right and left ventricle per beat is approximately equal. Normal value of stroke volume is 70 mL (60 to 80 mL) when the heart rate is normal (72/minute).

Minute volume refers to the amount of blood pumped out by each ventricle in 1 min. It is the product of stroke volume and heart rate. It can be expressed as stroke volume ? heart rate. The normal value of minute volume is 5 L/ventricle/ min.

Cardiac index is defined as the amount of blood pumped out per ventricle/minute/square meter of the body surface area. In an adult with an average body surface area of 1.734 square meter and a normal minute volume of 5 L/ min, the normal value of the cardiac index is 2.8 ± 0.3 L/ square meter of body surface area/min.

Ejection Jraction is the fraction of end diastolic volume that is ejected out by each ventricle. Normal ejection fraction is 60-65%.

Cardiac reserve is defined as the maximum amount of blood that can be pumped out by heart above the normal value. Cardiac reserve plays an important role in increasing the cardiac output during the conditions like exercise. Cardiac reserve is usually expressed in percentage. In a normal young healthy adult, the cardiac reserve is 300-400%. In old age, it is about 200-250%. It increases to 500-600% in athletes. In cardiac diseases, the cardiac reserve is minimum or nil.

The functionalities of the heart related to rate, contractile strength, conduction velocity, excitability, and relaxation rate can be described by the following terms:

Chronotropic effect—influence on heart rate Inotropic effect—influence on contractile strength Dromotropic effect—influence on conduction velocity Bathmotropic effect—influence on excitability of heart Lusitropy effect—rate of myocardial relaxation

6.4.4.1 Physiological Variations in Cardiac Output

Age: Cardiac output is lesser in young animals as compared to adults because of reduced blood volume. Cardiac index is more in young animals because of reduced body surface area compared to adults.

Sex: Cardiac output is less in female animals than in males because of decreased blood volume. Cardiac index is more in females than males due to reduced body surface area.

Diurnal variation: Cardiac output is low in early morning and increases in daytime. Increase in temperature above 30 °C raises cardiac output.

Stress: Stress increases cardiac output about 50-100% through the release of catecholamines, which increase the heart rate and force of contraction.

Feeding: During the first 1 h after taking feed, cardiac output increases.

Exercise: Cardiac output increases during exercise as a result of increase in heart rate and force of contraction.

High altitude: In high altitude, the cardiac output increases due to the increased secretion of adrenaline, which is stimulated by hypoxia.

Pregnancy: Cardiac output increases by 40% during later stages of pregnancy.

6.4.4.2 Methods of Cardiac Output Measurement The following four methods are currently in use for measur­ing an animal’s cardiac output:

1. Transthoracic or esophageal echocardiography is an invasive method which utilizes high-frequency sound waves (ultrasound) aimed at the heart or aorta and records the echoes reflected from the various structures. A shift in the sound-wave frequency occurs when the waves are reflected from a moving object and the magnitude of shift can be used to calculate blood flow velocity. This technique involves insertion of a flexible probe into midthoracic part of esophagus. A pulse-wave ultrasonic Doppler transducer is fixed at the tip of the probe. This transducer calculates the velocity of blood flow in descending aorta. The diameter of aorta is determined by echocardiography. Cardiac output is calculated by using the values of velocity of blood flow and diameter of aorta. Multiplying the integration of a velocity-time curve from the ascending aorta by the cross-sectional area of the aorta and the heart rate gives an estimate of cardiac output. The advantage of this technique is that the cardiac output can be measured continuously and it can be used during car­diac surgery.

2. Indicator dilution technique: It is used frequently in animal research and in a few clinical situations. A known quantity of indicator is injected into a large sys­temic vein or, preferably, into the right atrium. This passes rapidly through the right side of the heart, then through the blood vessels of the lungs, through the left side of the heart, and, finally, into the systemic arterial system. The indicator may be a dye (e.g., indocyanine green), radio­isotope, ion (e.g., lithium), or a thermal mass (e.g., cold saline). When a known quantity of the indicator is injected into an unknown volume and the diluted indicator’s con­centration is measured by a detector situated in the flow of blood, the cardiac output can be calculated. The concen­tration of the dye is recorded as the dye passes through one of the peripheral arteries, giving a curve. The cardiac output can be determined using the following formula:

The results obtained through this technique are accurate. The major disadvantage of this technique is that it is an invasive method involving injection of marker substance. The ultrasound velocity dilution method is an adaptation of the indicator dilution technique but requires an arterio­venous loop, which is only practical in anesthetized animals. However, it is a relatively noninvasive technique adaptable to mammals under 250 kg.

3. Fick method: Fick method is also the oldest, being first described by Adolph Fick in 1870, and involves the appli­cation of the law of conservation of mass. Fick method of determining cardiac output involves the measurement of animal’s oxygen consumption as well as the oxygen con­tent of arterial and venous blood.

Cardiacoutput=

Oxygenconsumption (mL∕ min)

Oxygencontentofarterialblood—Oxygencontentofvenousblood The Fick principle states that the amount of a substance taken up by an organ (or by the whole body) per unit of time is equal to the arterial level of the substance minus the venous level (A-V difference) times the blood flow. This principle can be used to determine cardiac output by measuring the amount of O₂ consumed by the body in a given period and dividing this value by the A-V difference across the lungs. Because systemic arterial blood has the same O₂ content in all parts of the body, the arterial O₂ content can be measured in a sample obtained from any convenient artery. A sample of venous blood in the pul­monary artery is obtained by means of a cardiac catheter. The procedure is generally benign. Catheters are inserted through the right atrium and ventricle into the small branches of the pulmonary artery.

4. Pressure Recording Analytical Method (PRAM)

Arterial pressure-wave contour analysis by a dedicated monitor is an old method that has recently been commercialized, but its accuracy in animals has yet to be determined. It can be used for cardiac output measurement in anesthetized animals (such as dog and swine) with a clinically stable hemodynamic status. It is a pulse contour method, wherein stroke volume and other hemodynamic parameters are estimated from the analysis of the arterial pulse waveform. The technique is based on the principle that the arterial blood pressure waveform is a result of interaction between the systolic ejection volume and the physical characteristics of the systemic vascular system (aortic impedance, vascular compliance, and peripheral arterial resistance). The monitor provides a beat-by-beat assessment of cardiac output from the arterial pressure wave. In addition to the cardiac output, heart rate, systolic, diastolic, and mean arterial pressures, pulse pressure and its variation and stroke volume and its variation are also continuously provided by the monitor. It is minimally invasive as it only requires the insertion of a regular, non-dedicated arterial catheter and does not need calibra­tion prior to clinical use. However, due to the requirement to identify the dicrotic notch at each beat, the analytical method for pressure recording has some drawbacks. The calculations are erroneous, and the cardiac output measurements could be artifactual if the monitor is unable to accurately identify the dicrotic notch at each beat. Clinically, in the awake animal, the transthoracic ultra­sound method is the most feasible, while the lithium dilution and pulmonary artery thermodilution techniques are being utilized in anesthetized patients.

6.4.4.3 Factors Influencing Cardiac Output

Cardiac output is determined by four factors: venous return, force of contraction, heart rate, and peripheral resistance.

6.4.4.3.1 Venous Return

Venous return is the amount of blood which is returned to the heart from different parts of the body. When it increases, the ventricular filling and cardiac output are increased. Thus, cardiac output is directly proportional to venous return.

6.4.4.3.2 Force of Contraction

Cardiac output is directly proportional to the contraction force. Force of contraction depends upon preload and afterload. Preload refers to the force of stretching of the cardiac muscle fibers at the end of diastole, just before con­traction. It is due to the increase in ventricular pressure caused by filling of blood during diastole. Stretching of muscle fibers increases their length, which increases the contraction force and cardiac output. Afterload is the force against which ventricles must contract and eject the blood, and the force is determined by the arterial pressure. At the end of isometric contraction period, semilunar valves are opened and blood is ejected into the aorta and pulmonary artery. Hence, the pressure increases in these two vessels. Now, the ventricles have to work against this pressure for further ejection. Thus, the afterload for right ventricular pressure is determined by pressure in pulmonary artery and the afterload for left ventricle is determined by aortic pressure. Force of contraction of heart and cardiac output is inversely propor­tional to afterload.

6.4.4.3.3 Heart Rate

Cardiac output is directly proportional to heart rate. The resting heart rate of an animal is related to its metabolic rate and body size (Table 6.1).

• The heart rates can remarkably increase from 100 in rest­ing state to 300 beats per minute in greyhounds, and from 30 to 150 bpm in camels, and similarly in equine cardiac outputs may rise to 250-450 L/min.

• During drought hibernation, the heart rate of the Nile crocodile (Crocodylus niloticus) can decrease to 2 beats per minute.

Table 6.1 Heart rate in different species

6.4.4.3.4 Peripheral Resistance

Peripheral resistance refers to the resistance offered to the flow of blood at the peripheral blood vessels against which the heart has to pump the blood. Hence, the cardiac output is inversely proportional to peripheral resistance.

Birds have evolved a high-performance efficiently func­tioning cardiovascular system to meet the rigorous demands of running, flying, swimming, or diving in a variety of extreme environments. Sustained increased-level activities in these environments possess severe demands on the cardio­vascular system to provide adequate delivery of oxygen to working vascular beds and for efficient removal of metabolic products. Furthermore, birds being endothermic, the cardio­vascular system has a major role in conserving or removing body heat.

Birds have larger hearts, bigger stroke volumes, lower heart rates, and higher cardiac output than mammals of corresponding body mass, which contribute to the high aero­bic energy input needed to sustain flapping flight. Similar to the vascular changes occurring during flight, swimming is associated with changes in regional vascular perfusion with myocardium and active leg musculature blood flow increas­ing by 30% and 300%, respectively. These perfusion changes are quite evident in the aquatic birds that engage in surface swimming and submerged or diving swimming. The phases of the cardiovascular response to a voluntary dive include an initial tachycardia during the immediate predive followed by a diving bradycardia. After surfacing, there is usually a post­dive tachycardia which aids in loading and replenishing oxygen stores and eliminating carbon dioxide. For example, during an emperor penguin’s 16-min dive, its heart rate may decrease to 6 beats per minute over 5 min during the dive, with a minimum of 3 bpm. Tufted ducks ’ surface swimming at maximal sustainable speeds is aided with a 70% increase in cardiac output from 276 to 466 mL/min.

6.5