Functions of the Heart

Functions of the Heart

Both sides of the heart contract at the same time, and eject equal volumes of blood. However, pressure is lower in the right atrium and ventricle than in the left atrium and ventricle. In atrial systole, the cardiac cycle begins. In a resting adult, this lasts for about 100 ms.

Atrial Systole

There are three steps to atrial systole, as follows:

■■ As the atria contract, rising pressure pushes blood into the ventricles, through the right and left atrioventricular (AV) valves.

■■ As atrial systole begins, the ventricles are filled to about 70% of their capacity, because of passive blood flow at the end of the previous cardiac cycle. The atria contract, and increasing atrial pressure provides the other 30%, pushing blood through the AV valves. Therefore, atrial systole basically “fills up” the ventricles to 100%.

■■ As atrial systole ends, the ventricles contain the maximum amount of blood they will hold in this cardiac cycle, which is known as the ­end-diastolic volume or EDV. This volume is about 130 ml, or 4.4 ounces, in a resting adult who is standing.

Ventricular Systole

Ventricular systole begins after atrial systole, and lasts about 270 ms in an adult who is resting. Pressures in the ventricles rise to become greater than the atrial pressures, and the AV valves are forced to close. There are also three steps to ventricular systole:

■■ Early in ventricular systole, the ventricles con-tract but blood flow has not occurred. The pressures care not yet enough to force the semilunar valves to open, or to push blood into the pulmo-nary or aortic trunks. At this time, the ventricles contract isometrically, generating tension and increased pressure, yet blood does not flow out. This is called isovolumetric contraction, in which all heart valves are closed. The ventricular volume does not change, but ventricular pres-sure is increasing.

■■ When ventricular pressure exceeds the pressure in the arterial trunks, the semilunar valves open. Blood flows into the pulmonary and aortic trunks, which is the beginning of ventricular ejection. The ventricles then contract isotonically, mean-ing their muscle cells shorten and there is a near constant production of tension. When a peak is reached, ventricular pressure gradually reduces, near the end of ventricular systole. The right ven-tricle also experiences isovolumetric contraction and ventricular ejection, yet pressure in the right ventricle and pulmonary trunk are significantly lower. The amount of blood ejected by each ven-tricle during contraction, 70 to 80 mL of blood, is the stroke volume of the heart. At rest, this is about 60% of the end-diastolic volume. This percentage is called the ejection fraction, and is varied based on the different demands placed on the heart.

■■As ventricular systole is ending, pressures inthe ventricles quickly fall. Blood in the aorta and ­pulmonary trunk begin to flow back to the ventricles, closing the semilunar valves. When backflow starts, pressure reduces in the aorta.Once the semilunar valves are closed, pressure increases again, and the elastic walls of the arteries recoil. This short pressure increase causes a “valley” in the pressure tracing, known as a dicrotic notch. Blood remaining in the ventricle when its ­semilunar valve closes is called the end-systolic volume or ESV. At rest, this volume is 50 mL, which is about 40% of the end-diastolic volume.

Ventricular Diastole

Ventricular diastole lasts for about 430 ms in the cur-rent cardiac cycle, yet continues through atrial systole in the next cycle. There are two steps in ventricular diastole:

■■ During this period, all heart valves are closed, and the myocardium is relaxing. Ventricular pressures are still higher than that of the atria, and blood can-not flow into the ventricles. This is called isovol-umetric relaxation. Pressure in the ventriclesdrops quickly since elasticity of the heart’s connec-tive tissue and cardiac skeleton help the ventricles to re-expand toward resting dimensions.

■■ When ventricular pressures reduce to below atrial pressures, the AV valves are forced open. Blood flows from the atria into the ventricles, meaning that all these chambers are in diastole. However, ventricular pressures continually reduce as the ventricles expand. Pressures in the ventricles are so much less than the pressure in the major veins that blood moves quickly through the relaxed atria, through the AV valves, and into the ventricles. This is a passive mechanism, and is the main method of ventricular filling. Before the cardiac cycle ends, the ventricles become almost 75% full.

Overall, atrial systole does not contribute greatly to ventricular volume. This means that people with severe atrial damage often survive. However, dam-age to one or both ventricles, can cause the heart to be unable to pump blood through the peripheral organs and tissues. This is the condition known as heart failure. Blood flow through the heart and its­physiology are shown in FIGURE 18-7.

1. Conduction System

Strands and clumps of specialized cardiac muscle con-tain only a few myofibrils and are located throughout the heart. These areas initiate and distribute impulses through the myocardium, comprising the cardiacconduction system, which coordinates the cardiaccycle (FIGURE 18-8). This system is also known as the conducting system or nodal system and includes the sinoatrial (S-A) node, atrioventricular (A-V) node, and conducting cells, which are found in intermodalpathways that distribute contractile stimuli to atrialmuscle cells.

Depolarization and contraction of cardiac muscle are intrinsic and do not depend on the nervous system. The heart can continue to beat in rhythm even when all nerve connections are severed. However, a normal healthy heart has many autonomic nerve fibers able to alter its rhythm. Noncontractile cardiac cells are specialized to initiate and then distribute impulses in the heart, keeping its depolarization and contraction orderly and in sequence.

A stable resting membrane potential is main-tained in uninsulated contractile cardiac cells. How-ever, the cardiac pacemaker cells have an unstable resting potential. These autorhythmic cells continu-ously depolarize and move slowly toward threshold. Their spontaneously changing membrane potentials are called prepotentials, or pacemaker potentials. These potentials initiate action potentials, which spread through the heart and trigger contractions.

In pacemaker cells, the three parts of an action potential are pacemaker potential, depolarization, and repolarization. Cardiac pacemaker cells exist in the S-A node, A-V node, atrioventricular (A-V) bundle, right and left bundle branches, and Purkinje fibers. Impulses pass across the heart in this order, beginning with the S-A node and ending with the Purkinje fibers.

S-A Node

The sinoatrial node (S-A node) is a small crescent-shaped mass of specialized tissue just beneath the epicardium, in the right atrium. It is located near the opening of the superior vena cava, with fibers continu-ous with those of the atrial syncytium. The S-A node’s cells can reach threshold on their own, initiating impulses through the myocardium, stimulating con-traction of cardiac muscle fibers. Its rhythmic activity occurs 70 to 80 times per minute in a normal adult. Because it generates the heart’s rhythmic contractions, it is often referred to as the pacemaker. No other part of the conduction system has a faster depolarization rate than the S-A node. The path of a cardiac impulse travels from the S-A node into the atrial syncytium. The atria begin to contract almost simultaneously. The characteristic rhythm of the S-A node is called the sinus rhythm, which determines heart rate.

A-V Node

The impulse passes along junctional fibers of the conduction system to a mass of specialized tissue called the atrioventricular node (A-V node), located in the inferior interatrial septum, beneath the endocardium. The A-V node provides the only normal conduction pathway between the atrial and ventricular syncytia. Impulses are slightly delayed for 0.1 second because of the small diameter of the junctional fibers. The atria therefore have more time to contract and empty all their blood into the ventri-cles before ventricular contraction occurs. Impulse conduction is slower in the A-V node than in other parts of the conduction system. Damage to the A-V node is referred to as heart block.

A-V Bundle

When the cardiac impulse reaches the distal A-V node, it passes into a large A-V bundle, or bundle ofHis, entering the upper part of the interventricular septum . The atria and ventricles are not connectedby gap junctions even though they meet each other. The only electrical connection between them is the A-V bundle.

Right and Left Bundle Branches

The A-V bundle soon splits into the right and left bun-dle branches. These branches move along the interven-tricular septum toward the apex of the heart.

Purkinje Fibers

Nearly halfway down the septum, the right and left bundle branches spread into enlarged Purkinjefibers, extending into the papillary muscles. Thefibers consist of long strands of barrel-shaped cells with only a few myofibrils, which continue to the heart’s apex, curving around the ventricles and pass-ing over their lateral walls. They complete the pathway through the interventricular septum. The Purkinje fibers have numerous small branches that become continuous with cardiac muscle fibers and irregular whorls. Superiorly, the Purkinje fibers turn into the ventricular walls. Purkinje fiber stimulation causes the ventricular walls to contract in a twisting motion to force blood into the aorta and pulmonary trunk. The Purkinje fibers are also referred to as the subendocar-dial conducting network.

1. Explain the major differences between cardiac and skeletal muscle fibers.

2. Describe aerobic respiration and its effects on the heart.

3. Identify the locations of cardiac pacemaker cells.

4. Why is it important for impulses from the atria to be delayed at the A-V node before they pass into the ventricles?

Electrocardiogram

An electrocardiogram (ECG) is used to record electri-cal changes in the myocardium during the cardiac cycle, using a machine known as an ­electrocardiograph. An ECG provides information about coronary circula-tion. As action potentials stimulate cardiac muscle fiber contraction, a specific pattern appears—it is not the same as individual action potentials. Because body flu-ids conduct electrical currents, these electrical changes can be detected on the body’s surface. Nodes are placed on the skin and connected by wires to the electrocar-diograph. Typically, 12 leads or electrodes are used that respond to weak electrical changes by moving a pen or stylus on a moving strip of paper. The movements cor-respond to myocardial electrical changes. The regular movement of the paper allows the distance between the pen movements to record the time between phases of the cardiac cycle.

Three of the electrodes are bipolar leads. They measure voltage differences between both arms or between one arm and one leg. Nine of the electrodes are unipolar leads. The total of 12 leads provides a complete picture of the electrical activity of the heart.

A normal electrocardiographic pattern includes several waves or deflections during each cardiac cycle. In between, muscle fibers remain polarized, and the pen does not move except for indicating the baseline reading (FIGURE 18-9). As the S-A node triggers an impulse, the atrial fibers depolarize to produce a recordable electrical change. The first pen movement produces a P wave that shows the depolarization of the atrial fibers leading to atrial contraction. The P wave lasts about 0.08 seconds.

As the impulse reaches ventricular fibers, they quickly depolarize, showing a greater electrical change because of the thicker ventricular walls. When the change ends, the resulting mark is called the QRS com-plex, consisting of a Q, R, and S waves that correspondto the depolarization of ventricular fibers before ven-tricular contraction. The QRS complex has an intri-cate shape because there is a constant change in the paths of depolarization waves through the ventricular walls. The QRS complex also takes about 0.08 seconds.

As the ventricles repolarize, a T wave is pro-duced and recorded. Atrial repolarization is missing from the pattern because atrial fibers repolarize at the same time the ventricular fibers are depolarizing. The T wave lasts about 0.16 seconds. Because repolariza-tion is slower than depolarization, the T wave appears more spread out, with a lower amplitude height than the QRS complex. It is often obscured by the larger QRS wave being recorded simultaneously.

Electrocardiographic patterns are used to assess the heart’s conduction of impulses. The P-Q interval is the time period between the P wave and the QRS complex and can indicate impulse transmission times between the S-A node and A-V node to indicate isch-emia or other conditions that affect the A-V conduc-tion pathways. Damage to the A-V bundle can extend the QRS complex, showing a different recording on an ECG. The P-Q interval takes about 0.16 seconds and is also referred to as the P-R interval if the Q portion is not visible. The P-R interval includes atrial depolariza-tion, contraction, and the passage of the depolarization wave through the remainder of the conduction system.

The S-T segment occurs when the action poten-tials of the ventricular myocytes are in their plateau phases. At this tie, all the ventricular myocardium is depolarized. The Q-T interval lasts about 0.38 ­seconds. It is the period from the start of ventricular depolar-ization through ventricular repolarization.

Speed of Conduction

From the time the S-A node generates an impulse until depolarization of the final ventricular muscle cells takes only 220 ms in a healthy heart. After the ventricular depolarization wave, ventricular contrac-tion is nearly immediate. The motion of contraction starts at the heart apex, moves toward the atria, and follows the excitation wave’s direction through the ventricle walls. Some contained blood is ejected supe-riorly into the large arteries that leave the ventricles.

Various speeds of spontaneous depolarization also exist. The heart normally beats 75 times per ­minute because of the actions of the S-A node. If the S-A node was not there, the A-V node would depolarize approximately 50 times per minute. If the A-V node was not providing input, the A-V bundle and remain-der of the conduction system would depolarize only approximately 30 times per minute, even though their conduction speed is extremely rapid.

Without the conduction system, cardiac impulses would travel very slowly. Instead of moving several meters per second in most areas, they would move only 0.3 to 0.5 meters per second. This would reduce the effectiveness of the heart’s pumping action because it would allow certain muscle fibers to contract a long time before others.

Parasympathetic and Sympathetic Innervation

When the body requires more blood, such as during exercise, the heart rate increases to pump more blood to the body. Parasympathetic fibers that innervate the heart arise from neurons in the medulla oblongata of the brain. Many of these fibers branch out to the S-A and A-V nodes. Nerve impulses reach nerve fiber end-ings, secreting acetylcholine, decreasing S-A and A-V node activity, and decreasing heart rate.

The cardioacceleratory center of the medulla oblon-gata projects to sympathetic preganglionic neurons in levels T1 to T5 of the spinal cord. These neurons synapse­ with postganglionic neurons located in the cervical and upper thoracic sympathetic trunk. Post-ganglionic fibers then run through the cardiac plexus to the heart, innervating the S-A and A-V nodes as well as the heart muscle and coronary arteries. The cardioinhibitory center sends impulses to the para-sympathetic dorsal vagus nucleus, also in the medulla oblongata. This sends inhibitory impulses to the heart via vagus nerve branches.

Continual parasympathetic fiber activity can increase or decrease heart rate, working in opposing fashion. Increased parasympathetic impulses slow down the heart rate while decreased parasympathetic impulses raise the heart rate. Sympathetic fibers reach the heart structures and nodes, and their ends secrete norepinephrine in response to nerve impulses that increase myocardial contraction rates and forces. Basi-cally, the sympathetic nervous system is described as “accelerating” heart rate, whereas the parasympathetic nervous system is described as “decelerating” heart rate.

Effects of the sympathetic and parasympathetic nerve fibers are balanced by baroreceptor reflexes that involve the brain’s cardiac control center. Sensory impulses are received and relayed between the brain and heart. Baroreceptors detect changes in blood pres-sure. Cerebral or hypothalamic impulses also influence the cardiac control center, as do temperature changes and certain ions.

Ions

The most important ions that influence heart action are potassium and calcium. Excess extracellular potassium ions or hyperkalemia decrease contraction rates and forces, whereas deficient extracellular potassium ions or hypokalemia may cause a potentially life-threatening abnormal heart rhythm or arrhythmia. Excess extracel-lular calcium ions, a condition called hypercalcemia, can cause the heart to contract for an abnormally long time, whereas deficient extracellular calcium ions, known as hypocalcemia, depress heart action.

1. Describe how an ECG records electrical heart activities.

2. Define what is occurring during the P-R interval, QRS complex, and the T wave on an ECG.

3. Contrast the cardioacceleratory and cardioinhibitory centers.

2. Heart Sounds

A heartbeat makes a characteristic double thumping sound when heard through a stethoscope, because of vibrations of the heart tissues related to the valves closing. The first thumping sound occurs during ­ventricular contraction when the A-V valves close and indicates when ventricular pressure rises above atrial pressure. This is the beginning of ventricular systole. The first sound is usually the loudest, longest,and most resonant heart sound. The second sound occurs during ventricular relaxation when the pulmo-nary and aortic or semilunar valves close. This is the beginning of ventricular relaxation or diastole, and the sound is shorter and sharper than the first. The two heart sounds are often described as “lub-dup,” “pause,” “lub-dup,” “pause,” and so on.

The mitral valve closes just before the tricus-pid valve. Also, the aortic semilunar valve usually closes just before the pulmonary valve. Auscultating the four specific regions of the thorax distinguishes each individual valve sound. The four points are not directly superficial to the valves because the sounds take various paths to reach the chest wall. However, these points help to define the four corners of a nor-mal heart. By understanding a normal heart’s location and size, one can more easily recognize a disease and/ or enlarged heart.

The four points of auscultation used to hear each individual valve sound are as follows:

■■ Aortic valve: second intercostal space at the right sternal margin

■■ Pulmonary valve: second intercostal space at the left sternal margin

■■ Mitral valve: over the heart apex, in the fifth inter costal space, in line with the middle of the clavicle

■■ Tricuspid valve: usually heard in the right sternal margin of the fifth intercostal space

3. Cardiac Cycle

One cardiac cycle causes pressure in the heart cham-bers to rise and fall and valves to open and close. The sequence of contraction of the heart chambers is both atria, followed by both ventricles. Early during diastole, pressure in the ventricles is low, causing the A-V valves to open and the ventricles to fill with blood. Nearly 70%

of returning blood enters the ventricles before contrac-tion. As the atria contract, the remaining 30% is pushed into the ventricles. As the ventricles contract, ventricu-lar pressure rises. When it exceeds atrial pressure, the A-V valves close and papillary muscles contract, pre-venting the cusps of the A-V valves from bulging into the atria excessively. During ventricular contraction, the A-V valves are closed and atrial pressure is low. Blood flows into the atria while the ventricles are contracting, so the atria are prepared for the next cardiac cycle.

As ventricular pressure exceeds pulmonary trunk and aorta pressure, the pulmonary and aortic valves open. Blood is ejected from the ventricles into these arteries, and ventricular pressure drops. When it is lower than in the aorta and pulmonary trunk, the semilunar valves close. When ventricular pressure is lower than atrial pressure, the A-V valves open and the ventricles begin to refill.

Cardiac muscle fibers are similar in function to skeletal muscle fibers but are connected in branched networks. If any part of the network is stimulated, impulses are sent throughout the heart, and it con-tracts as a single unit. A functional syncytium is a mass of merging cells that function as a unit. There are two of these structures in the heart, one in the atrial walls and one in the ventricular walls. A small area of the right atrial floor is the only part of the heart’s muscle fibers not separated by the fibrous cardiac skeleton­. Here, the atrial syncytium and the ventric-ular ­syncytium are connected by cardiac conduction system fibers.

4. Cardiac Output

Heart action determines the amount of blood enter-ing the arterial system with each ventricular contrac-tion. Stroke volume is defined as the volume of blood discharged from the ventricle with each contraction. An average adult male’s stroke volume is relatively constant, at about 70 mL. The movements and forces that are generated during contractions of the heart are referred to as cardiodynamics. The cardiac output is defined as the volume discharged from the ven-tricle per minute. It is calculated by multiplying the stroke volume by the heart rate, in beats per minute.So, if the stroke volume is 70 mL and heart rate is 75 beats per minute, the cardiac output is 5,250 mL per ­minute. Blood pressure varies with cardiac output and increases or decreases based on similar changes in stroke volume or heart rate. If the heart is seriously weakened or blood volume decreases greatly, stroke volume declines, and cardiac output is maintained by increasing contractility and heart rate.

The average adult cardiac output is calculated as follows:

Cardiac output increases when stroke volume increases, when the heart beats faster, or both. It decreases when one or both of these factors decrease.

Remember that stroke volume represents the dif-ference between end-diastolic volume and end-systolic volume. End-diastolic volume is the amount of blood that collects in a ventricle during diastole. End-systolicvolume is the amount of blood that remains in a ventri-cle after it has already contracted. End-diastolic volume is normally 120 mL, and end-systolic volume is nor-mally 50 mL. Therefore, the difference between them is 120 mL minus 50 mL, which equals 70 mL. FIGURE 18-10 summarizes the factors affecting cardiac output.

Preload

The three most important things to remember about the regulation of stroke volume are preload, contrac-tility, and afterload. Preload is the degree the heart muscle can stretch just before contraction. It is directly proportional to the end-diastolic volume, and affects how the muscle cells are able to produce tension. When sarcomere length increases past resting length, the force that is produced during systole increases. The amount of preload and degree of myocardial stretch-ing changes with demands placed upon the heart. In ventricular systole, there is little developed power in the cardiac muscle cells. The amount of blood in the ventricle after contraction or end-systolic volume, is relatively high since there is only a short amount of muscle cell contraction.

With exercise, venous return is increased, and there is more blood flowing into the heart. The end-­ diastolic volume increases, and there is more stretch-ing of the myocardium. When the ­sarcomeres are close to their optimal lengths, ventricular muscle cells are able to contract better, producing stronger­ contractions. They become shorter, and more blood can be pumped out of the heart. Preload controls­ stroke volume, and in normal conditions the higher the preload,­ the higher the stroke volume. The ­relationship between the preload and stroke volume­ is called the Frank-Starling lawof the heart . Resting cardiac cells are usually shorter than their optimal length, so stretching can cause significant increases in contractile force. The most important factor concerning preload is venous return, which is the amount of blood returning to the heart and distend-ing its ventricles. The atrial reflex or Bainbridge reflex concerns adjustments made to heart rate as a response to increases in venous return.

Contractility

Contractility is the contractile strength achieved at acertain muscle length. Extrinsic factors increasing contractility of the heart muscle can also enhance stroke volume. Greater contractility results in more blood being ejected from the heart, which increases stroke volume and lowers end-systolic volume. Con-tractility is increased when sympathetic stimulation is increased. Various substances also affect contrac-tility. Positive inotropic agents are substances that increase contractility and include epinephrine, glucagon, thyroxine,­ digitalis, and extracellular calcium ions. Negative inotropic agents decrease contractil-ity and include excessive hydrogen ions, increased ­extracellular potassium levels, and calcium channel blockers.

Afterload

Afterload is the back-pressure exerted by the arterialblood on the aortic and pulmonary valves. The ventri-cles must overcome this pressure to eject blood. This pressure is about 80 mm Hg in the aorta and about 10 mm Hg in the pulmonary trunk. When a person is healthy, afterload is relatively constant, but in hyper-tensive people, afterload reduces the ventricles’ ability to eject blood. As a result, the heart retains more blood after systole, which increases end-systolic volume and decreases stroke volume.

Cardiac reserve is the difference between the­resting and maximal cardiac output. It is usually four to five times the resting cardiac output in a nonathletic person. This resting output is 20 to 25 litersper­ minute­. However, in a trained athlete, cardiac output may reach seven times the resting cardiac output, which is 35 liters per minute.

5. Regulation of Heart Rate

Stroke volume is fairly consistent in a healthy heart and cardiovascular system. Regulation of heart rate includes homeostatic mechanisms such as autonomic, chemical, hormonal, and other forms of regulation.

Autonomic Tone

The heart, like other organs that have dual innerva-tion, has a resting autonomic tone. Both divisions of the ANS are usually active at a steady pace. Ace-tylcholine and norepinephrine are released at the nodes, and into the .myocardium. Because of this, if the vagus nerves are cut, the heart rate increases. Sympathetic blocking agents (such as beta-­blockers) decrease heart rate. When a healthy person is at rest, parasympathetic effects dominate. When there is no autonomic innervation, the heart rate is established by the pacemaker cells of the SA node. The heart then beats between 80 and 100 times per minute. However, an average adult heart at rest, with normal innerva-tion, beats between 70 and 80 times per minute. This is because of activity in the parasympathetic­ nerves that innervate the SA node. The heart rate becomes even slower if parasympathetic activity increases. Oppositely, heart rate increases when parasympa-thetic activity decreases, or when sympathetic acti-vation occurs. The ANS uses dual innervation and autonomic tone adjustments to delicately adjust car-diovascular function, meeting the demands of other body systems.

When the right atrial walls stretch, the stretch receptors trigger a reflexive increase in the heart rate, via the stimulation of sympathetic activity. Therefore, when venous return to the heart increases, the heart rate also increases, as well as cardiac output. Venous return also directly affects the nodal cells. When there is an increase in venous return, the atria receive more blood, and atrial walls stretch. The stretched SA node cells result in faster depolarization, and increased heart rate.

Chemical Regulation

Heart rate is also influenced by many chemicals, especially when they are present in very high or very low amounts. Hormones and ions are ­implicated here. Hormones include epinephrine and thyroxine­. During sympathetic activation, epinephrine is liberated by the adrenal medulla. This hormone produces equivalent cardiac effects to those from norepinephrine­ when it is released by the sympa-thetic nerves. The heart rate and contractility are both enhanced. Thyroxine from the thyroid gland increases production of body heat as well as meta-bolic rate. In large amounts, the heart rate increases and remains sustained. Thyroxine acts directly on the heart while enhancing effects of both epi-nephrine and norepinephrine. Intracellular and extracellular ions, in normal levels, also maintain normal heart function. When plasma electrolytes are out of ­balance, the heart may be affected to a severe degree.

Other Types of Regulation

Heart rate is also influenced by age, body temperature, exercise, and gender. The resting heart rate of infants is highest, at 140 to 160 beats per minute, but gradu-ally declines throughout life. Women have an average heart rate that is higher than men’s. In women, this is 72 to 80 beats per minute and in men, 64 to 72 beats per minute. Via the sympathetic nervous system, exercise raises the heart rate and increases systemic blood pressure. In a physically fit adult, resting heart rate is usually much lower than in people who are out of shape. By enhancing the metabolic rate of cardiac cells, heat increases heart rate. For example, a high fever often makes you feel as if your heart is pounding rapidly. This is similar to the effects of extreme exer-cise, because the muscles are generating large amounts of heat. Oppositely, the heart rate is directly decreased by cold temperatures.

1. What causes the sounds of the heart?

2. What is a cardiac cycle?

3. Name the factors that affect cardiac output.

4. Differentiate between autonomic, chemical, and hormonal regulation of heart rate.

5. What are common causes of tachycardia?