Normal Heart Sounds

With the aid of a stethoscope you can hear the characteristic sounds of the normal heartbeat, typically described as a "lub-dub." These sounds are produced by the closure of the heart valves. The first heart sound or "lub" results from closure of the tricuspid and mitral valves. It is a rather low-pitched and a relatively long sound which, as indicated in, represents the beginning of ventricular systole.

The second heart sound, or "dub," marks the beginning of ventricular diastole. It is produced by closure of the aortic and pulmonary (pulmonic) semilunar vanes when the intraventricular pressure begins to fall. This "dub" sound is typically heard as a sharp snap because the semilunar valves tend to close much more rapidly than the AV valves. Because diastole occupies more time than systole, a brief pause occurs after the second heart sound when the heart is beating at a normal rate. Therefore, the pattern that one hears is one of: "lub-dub" pause, "lub-dub" pause, and so on.

Cardiac output as a function of stroke volume and heart rate

Let us concentrate now on the work that is performed by the beating heart. The volume of blood pumped by one ventricle during one beat is called the stroke volume.

Because cardiac work performance is typically related to a fixed time interval (i.e., one minute), it is possible to calculate the cardiac output by simply multiplying the stroke volume by the number of times the ventricles beat per minute. Thus, the cardiac output represents that volume of blood pumped by one ventricle in one minute. For example, in a resting adult the heart might beat 72 times per minute and pump about 70 ml of blood with each ventricular contraction. This being the case,

Cardiac output = stroke volume x heart rate (number of ventricular contractions/min)

= 70 ml/stroke x 72 strokes/min

= 5040 ml/min (5.04 litres/min)

Although the cardiac output for the resting adult heart is ordinarily on the order of 5 to 6 litres per minute, during strenuous exercise the heart may increase its output four or five times. Simple multiplication demonstrates that under such conditions the heart may pump as much as 20 to 30 litres of blood per minute. Even more amazingly, the heart of a well-trained athlete can increase its output up to seven times.

The maximum percentage that the cardiac output can be increased above normal is defined as the cardiac reserve. Therefore, if during exercise the output can increase to a maximum of five times normal, the cardiac reserve is 400%. From the previous equation, it should be clear that cardiac output varies as a function of either stroke volume or heart rate. Let us examine just how these two important variables are regulated.

Stroke volume, or the volume of blood pumped by one ventricle during one contraction, has a direct effect upon cardiac output. Although the ventricles do not eject all of their blood when they contract, the more forcefully they contract, the greater the volume of blood ejected. Moreover, the volume of blood returned to the heart via the great veins varies from time to time. Thus, stroke volume is regulated mainly by venous return and by sympathetic stimulation.

The volume of blood delivered to the heart by the great veins, the venous return, together with subsequent stretching of the cardiac muscle, is perhaps the most important determinant of cardiac output. The greater the volume of blood returned to the heart via the veins, the greater the volume of blood pumped by the heart. This relationship, known as Starling's law of the heart, permits the heart to pump all of the blood returned to it within physiological limits. As additional quantities of blood fill the chambers of the heart, cardiac muscle cells are stretched to a greater extent and subsequently contract with a greater force. Thus, increased quantities of blood are pumped into the arteries. Increasing the stroke volume in this manner can raise the normal output of 5 litres per min to a maximum output of approximately 14 litres per minute.

When the venous return is even greater, the heart is able to keep pace with the excessive volume only through sympathetic stimulation, leading to an increased heart rate and force of contraction. The release of noradrenaline by sympathetic nerve fibres not only increases heart rate but also increases the force of cardiac muscle contraction. This increased force of contraction is distinct from that which is brought about by an increased blood volume, as mentioned previously. adrenaline, a hormone released by the adrenal medulla, has a similar effect on cardiac muscle. Thus, when the force of contraction increases, the stroke volume increases, and this in turn leads to an increase in cardiac output.

The heart is innervated by both components of the autonomic nervous system. Parasympathetic fibres decrease heart rate, whereas sympathetic fibres increase heart rate. Parasympathetic innervation originates in the cardiac inhibitory centre in the medulla oblongata of the brain stem and is conveyed to the heart by way of the vagus nerve (Cranial Nerve X).

Both the SA and AV nodes are richly supplied with vagal fibres. There is a minor distribution of vagal fibres to muscle of the atria and ventricles. When these parasympathetic fibres are stimulated they release acetylcholine, which slows the heart rate.

Normally, the parasympathetic innervation represents the dominant neural influence on the heart.

Maximal stimulation of vagal fibres can actually lead to a complete cessation of ventricular contraction. This can result from either a block in impulse transmission through the AV junctional fibres or complete inhibition of rhythmic signal generation by the SA node. Even with continued parasympathetic stimulation, the ventricles will begin to beat (10 to 40 beats per minute) after a short interval (typically 5 to 10 seconds). This phenomenon is called ventricular escape and is the result of new rhythmic impulses being generated in an abnormal site, for example, the AV bundle.

The heart receives its sympathetic innervation from nerves originating in the medulla (cardiac accelerating centre) and upper thoracic spinal cord. These reach the myocardium via several nerves sometimes referred to as the accelerator nerves. Sympathetic fibres innervate SA and AV nodal tissue as well as cardiac muscle cells themselves. When stimulated, the sympathetic fibres release noradrenaline, which leads not only to an increase in heart rate, but to an increase in the strength of ventricular and atrial contraction as well. The heart rate may nearly triple, and the strength of contraction may nearly double, under the influence of maximal sympathetic stimulation.

Various parts of the circulatory system relay messages (e.g., regarding blood pressure) to the cardiac centres, which respond by sending messages to the heart via the vagus nerves. In this manner the cardiac centres are responsible for maintaining a balance between the inhibitory effects of the parasympathetic nerves and the stimulatory effects of the sympathetic nerves. When the parasympathetic messages decrease, the sympathetic nerves are able to function in an unopposed manner and thereby increase the heart rate. For example, severance of vagal nerve fibres results in an increased heart rate.

Under conditions of stress, adrenaline and noradrenaline are released from the tissues of the adrenal medulla into the general circulation. Each of these hormones produces an increase in heart rate.

Elevation of the body temperature markedly increases the heart rate. This most probably results from an increased permeability of cardiac muscle-cell plasma membranes to the passage of various ions, thereby causing an accelerated generation of rhythmic action potentials. During fever, for example, it is not uncommon for the individual to experience a heart rate in excess of 100 beats per minute. Lowering of the body temperature, or hypothermia, is accompanied by a reduction in heart rate. This latter observation is taken advantage of clinically, for example, when the patient's temperature is deliberately lowered during heart surgery.

The effects of calcium, potassium, and sodium on action potentials and membrane potentials is discussed in the pages on fluid and electrolyte balance. In addition the importance of calcium ions and their role in cardiac muscle contraction was indicated earlier in these pages. It should be apparent then that the concentrations of these particular ions within the extracellular environment may have a significant influence on cardiac function. Ordinarily the concentrations of these ions are kept within appropriate limits and thus do not affect the heart adversely. However, in instances where their concentration becomes excessive or deficient, cardiac function may be seriously affected.

An excess of potassium ions in the extracellular environment markedly reduces the heart rate as well as the strength of contraction. On the other hand, spastic contraction of the heart results from the presence of excess calcium ions. This typically results from the direct effects of calcium ions upon the contractile process of cardiac muscle. A marked reduction in the calcium ion concentration has effects similar to those observed with high potassium levels.

Excessive levels of sodium ions result in depression of cardiac function, which is thought to stem from their competition with calcium ions at some critical site during the contractile process. At the other extreme, a deficiency of sodium ions in the extracellular environment leads to the development of a potentially lethal condition called cardiac fibrillation. In this situation, the cardiac muscle contracts at an extremely high rate and in an uncoordinated fashion such that little or no blood is actually pumped by the heart.

The heart rate is also influenced by the sex and the age of an individual. In adult females the heart rate is typically 70 to 80 beats per minute. In adult males it is somewhat slower, approximately 70 beats per minute. The infant heart beats about 120 times per minute, and that of a child about 77 times per minute. Although the adult heart beats approximately 72 times per minute, its rate does slow somewhat with advancing age.

The heart of a trained athlete will actually undergo enlargement (up to 50% in extreme cases) and increase its pumping efficiency. Even under resting conditions, such a heart is capable of pumping more than 20 litres of blood per minute without the assistance of sympathetic stimulation. Thus, the heart (and pulse) rate of the trained athlete at rest is frequently less than 50 beats per minute. Moreover, in the athlete this resting heart rate increases less during exercise than in the untrained individual.

Conditions sometimes develop in which the volume of venous return to the heart is markedly reduced (e.g., during haemorrhage), and cardiac output is significantly decreased. A diseased heart is simply not able to pump all of the blood delivered to it--a condition called cardiac failure. Furthermore, since the right and left halves of the heart really represent two distinct and separate pumps, either may fail independently of the other. Any condition that impairs the ability of the heart to pump blood can lead to the onset of cardiac failure. Cardiac valvular disease, congenital malformations of the heart, reduced coronary blood flow, and hypertension are but a few of the causes of cardiac failure.

The waves of depolarisation that spread through the heart during each cardiac cycle generate electrical currents, which in turn spread through the interstitial fluid and onto the body's surface. Recording electrodes, placed on the surface of the body on opposite sides of the heart, are used to detect such electrical potentials. These signals are then transmitted to an electrocardiograph, which amplifies and records the electrical activity. The record that results from this procedure is termed an electrocardiogram (ECG, or EKG). If desired, the output of the electrocardiograph may also be tape recorded.

The electrical currents produced as the atrial muscle cells depolarise prior to contraction lead to the generation of the P wave.

This is followed by the QRS complex and results from currents generated as the ventricles depolarise prior to their contraction.

Hence, both the P wave and the QRS complex represent depolarisation waves.

Subsequent to ventricular contraction, the ventricles repolarise, and the electrical currents that are produced generate the T wave. Therefore, the T wave is one of repolarisation and typically occurs 0.25 to 0.35 second following ventricular depolarisation.

The interval between the beginning of the P wave and the beginning of the QRS complex is designated by the PQ interval. Repolarisation of the atria is also masked by the QRS complex.

Since the Q wave is often absent, it is also termed the PR interval and represents the duration of time (normally about 0.16 second) between the onset of atrial contraction and the onset of ventricular contraction.

In patients with heart disease, scarred or inflamed tissue may lead to a lengthening of the PR interval because more time is required for the depolarisation wave to spread through the atrial myocardium and the AV node.

The time required for the generation of the QRS complex is termed the QRS duration and represents the amount of time needed for ventricular depolarisation.

The QT interval extends from the beginning of the QRS complex to the end of the T wave and represents the time required for ventricular contraction and repolarisation.

Typically, the normal QT interval lasts for approximately 0.35 second. The ST interval represents the time required for the ventricles to repolarise and extends from the S wave to the termination of the T wave.

In the general population, individuals with normal hearts may have either very rapid or very slow heart rates. However, in many instances such extremes may be indicative of very serious cardiac disorders.

Tachycardia (from tachy, fast, and cardia, heart) refers to a fast heart rate, typically designated as more than 100 beats per minute. The picture below indicates what an electrocardiogram obtained from an individual with tachycardia would look like.

Ventricular fibrillation, on the other hand, is a life-threatening condition because no blood is pumped into the arteries. Approximately one out of every four persons dies in ventricular fibrillation. There are several causes of this condition, including electrical shock, inadequate oxygen supply to the myocardium, heart attacks, trauma, and the effects of certain drugs. A heart in ventricular fibrillation is unable to restore its normal rhythm by itself.

The heart can be defibrillated by applying a brief but strong electrical current to the chest wall. This stimulates depolarisation of all the cardiac muscle fibres simultaneously, so that all contractions momentarily cease. If the SA node then begins to function, normal cardiac rhythm may be re-established.

When the transmission of an action potential becomes delayed or blocked at some point in the conduction system, a condition known as heart block ensues. Sinoatrial block is a rare condition in which the impulse generated in the SA node is prevented from entering the atrial muscle. The ventricles may acquire a new rhythm, usually from the AV node, and continue to beat, although at a slower pace.

Conditions that decrease or completely block the transmission of an impulse through the atrio-ventricular bundle result in what is termed atrioventricular heart block. If transmission is not completely interrupted, the condition is known as incomplete heart block.

Several conditions may either block or lead to a significant delay in the rate of conduction through the AV bundle and these include:

(1) lack of adequate blood supply (ischemia) to AV nodal fibres, which may be the result of coronary artery insufficiency;

(2) presence of scar tissue, which may lead to compression of the AV bundle;

(3) inflammatory processes involving the AV bundle or the AV node;

(4) excessive stimulation of vagus nerve (CN X) fibres.

Two forms of heart block, first-degree and second-degree, are of the incomplete type.

Ordinarily, the time interval between the initiation of the P wave and the initiation of the QRS complex is approximately 0.16 second. This interval (PR interval) may vary somewhat with the heart rate. However, if it exceeds 0.20 second in an individual with a normal heart rate, the person is considered to have first-degree heart block.

Second-degree heart block is a condition in which some atrial impulses reach the ventricles while others do not. This typically occurs when the PR interval is between 0.25 and 0.45 second. As a result the atria may beat two or three times before the ventricles do. This type of heart block yields a characteristic ECG pattern wherein QRS complexes may be "dropped" following some of the P waves. If every other QRS complex is dropped, the heart is said to have a 2:1 rhythm with regard to atrial beats and ventricular beats, respectively. It is not uncommon for individuals with second-degree heart block to develop 3: 2 or even 3:1 rhythms. Lastly, should a block occur within one of the Purkinje bundles (right or left bundle branch block), the ventricles may not contract synchronously. In this instance an impulse may spread through one ventricle more rapidly than through the other. The resulting ECG pattern would exhibit an abnormally long QRS complex.

Should the conditions leading to delayed conduction in the AV node or AV bundle become very severe, a total block of impulses travelling from the atria to the ventricles may occur. This is considered as complete AV heart block, or third-degree heart block. The atria continue to beat at their normal rate or even at an accelerated rate (sometimes as high as 100 times per minute). The ventricles also beat, but much slower than normal (typically about 40 beats per minute). In this form of heart block the ventricles beat independent of the atria and utilise impulses generated by the AV node as their pacemaker. They have, in a sense, escaped from their normal atrial control.

Some individuals exhibit a special form of third-degree heart block in which the total block occurs periodically. In such cases the ventricles stop beating for approximately three to five seconds, the brain is deprived of blood, and the person typically faints. Subsequently, as a result of ventricular "escape," blood flow to the brain resumes and the individual recovers from the faint. Patients who suffer from periodic fainting spells as a result of this form of heart block are said to exhibit the Stokes-Adams syndrome.

Artificial pacemakers are frequently implanted in individuals with severe heart-block syndromes. Such a procedure involves the implantation of the pacemaker beneath the skin and connection of its electrodes to the heart. The pacemaker serves as an external source of continuous, rhythmic impulses to drive the heart at a normal rate and with a normal rhythm.