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12. 6. 2012.


About the size of a fist and located in the center of the thoracic cavity, the heart is the primary pump that circulates blood through the entire vascular system. As shown in the figure below, the heart has two atria that act as receving chambers and two ventricles acting as pumping units. It is enclosed in a tough membranous sac called the pericardium. The thin cavity between the pericardium and the heart is filled with pericardial fluid, which is necessary to reduce friction between the sac and the beating heart.

Blood flow through the heart

The heart is sometimes considered to be two separate pumps, with the right side of the heart pumping deoxygenated blood to the lungs through the pulmonary circulation and the left side of the heart pumping oxygenated blood to all other tissues in the body through the systemic circulation. Blood that has circulated through the body, delivering oxygen and nutrients and picking up waste products, returns to the heart through the great veins – the superior vena cava and inferior vena cava – to the right atrium. This chamber receives all the deoxygenated blood from the systemic circulation.

From the right atrium, blood passes through the tricuspid valve into the right ventricle. This chamber pumps the blood through  the pulmonary valve into the pulmonary artery, which carries the blood to the lungs. Thus, the right side of the heart is known as the pulmonary side, sending the blood that has circulated throughout the body into the lungs for reoxygenation.
After blood is oxygenated in the lungs, it is transported back to the heart through the pulmonary veins. All freshly oxygenated blood is received from the pulmonary veins by the left atrium. From the left atrium, the blood passes through the mitral valve into the left ventricle. Blood leaves the left ventricle by passing through the aortic valve into the aorta and is distributed to the systemic circulation. The left side of the heart’s known as the systemic side. It receives the oxygenated blood from the lungs and then sends it out to supply all other body tissues.


Cardiac muscle is collectively called the myocardium, or myocardial muscle. Myocardial thickness at various locations in the heart varies according to the amount of stress placed on it. The left ventricle is the most powerful of the four heart chambers. This chamber must contract to generate sufficient pressure to pump blood through the entire body. When a person is sitting or standing, the left ventricle must contract with enough force to overcome the effect of gravity, which tends to pool blood in the lower extremities.
The left ventricle must generate a considerable amount of force to pump blood to the systemic circulation, and this is reflected by the greater thickness of its muscular wall compared with that of the other heart chambers. This hypertrophy is the result of the pressure placed on the left ventricle at rest or under normal conditions of moderate activity. With more vigorous exercise – particularly intense aerobic activity, during which the working muscles’ need for blood increases considerably – the demand on the left ventricle to deliver blood to exercising muscle is high. In response to both intense aerobic and resistance training, the left ventricle will hypertrophy. In contrast to the positive adaptations that occur as a result of physical training, cardiac muscle also hypertrophies as a result of diseases, such as high blood pressure or valvular heart disease. In response to either training or disease, over time the left ventricle adapts by increasing its size and pumping capacity, similar to the way skeletal muscle adapts to physical training. However, the mechanisms for adaptation and cardiac performance with disease are different from those observed with aerobic training.
Although striated in appearance, the myocardium differs from skeletal muscle in several important ways. First, cardiac muscle fibers are anatomically interconnected end to end by dark-staining regions called intercalated disks. These disks have desmosomes, which are structures that anchor the individual cells together so that they do not pull apart during contraction, and gap junctions, which allow rapid transmission of the action potentials that signal the heart to contract as one unit. Secondly, the myocardial fibers are rather homogenous in contrast to the mosaic of fiber types in skeletal muscle. The myocardium contains only one fiber type, thought to be similar to type I fibers in skeletal muscle in that it is highly oxidative, is highly capillarized, and has a large number of mitochondria.
In addition to these differences, the mechanism of muscle contraction also differs between skeletal and cardiac muscle. Cardiac muscle contraction occurs by “calcium-induced calcium release”. The action potential spreads rapidly along the myocardial sarcolemma from cell to cell via gap junctions, and also to the inside of cell through the T-tubules. Upon stimulation, calcium enters the cell by the dihydropyridine receptor in the T-tubules. Unlike what happens in skeletal muscle, the amount of calcium that enters the cell is not sufficient to directly cause the cardiac muscle to contract; but it serves as a trigger to another type of receptor, called the ryanodine receptor, to release calcium from the sarcoplasmic reticulum. Figure below also summarizes and differences between cardiac and skeletal muscle.

The myocardium, just like skeletal muscle, must have a blood supply to deliver oxygen and nutrients and remove waste products. Although blood courses through each chamber or the heart, little nourishment comes from this blood supply. The primary blood supply to the heart is provided by the right and left coronary arteries, which arise from the base of the aorta and encircle the outside of the myocardium. 

The right coronary artery supplies the right side of the heart, dividing into two primary branches, the marginal artery and the posterior interventricular artery. The left coronary artery, also referred to as the left main coronary artery, also divides into two major branches, the circumflex artery and the anterior descending artery. The posterior interventricular artery and the anterior descending artery merge, or anastomose, in the lower posterior area of the heart, as does the circumflex. These arteries are very susceptible to atherosclerosis, or narrowing by the accumulation of plaque and inflammation, leading to coronary artery disease. Anomalies – shortenings, blockages, or misdirections – sometimes occur in the coronary arteries, and such congenital abnormalities are a common cause of sudden death in athletes.
The ability of the myocardium to contract as a single unit depends on initiation and propagation of an electrical signal through the heart, the cardiac contraction system.

Cardiac conduction system

Cardiac muscle has the unique ability to generate its own electrical signal, called spontaneous rhytmicity, which allows it to contract without any external stimulation. The contraction is rhythmical, in part because of the anatomical coupling of the conduction cells through gap junctions. With neither neural nor hormonal stimulation, the intrinsic heart rate(HR) averages – 100 beats (contractions) per minute. This resting heart rate of about 100 beats/min can be observed in patients who have undergone cardiac transplant surgery, because their transplanted hearts lack neural innervation.
Figure below illustrates the four main components of the cardiac conduction system:
  • Sinoatrial(SA) node
  • Atrioventricular(AV) node
  • AV bundle(bundle of His)
  • Purkinje fibers.

The impulse for normal heart contractions is initiated in the sinoatrial(SA) node, a group of specialized cardiac muscle fibers located in the upper posterior wall of the right atrium. These specialized cells spontaneously depolarize at a faster rate than other myocardial muscle cells because they are especially leaky to sodium. Because this tissue generates the electrical impulse, typically at a frequency of about 100 beats/min – the fastest intrinsic firing rate – the SA node is known as the heart’s pacemaker, and the rhythm it establishes is called the sinus rhythm. The electrical impulse generated by the SA node spreads through both atria and reaches the atrioventricular(AV) node, located iin the right atrial wall near the center of the heart. As the electrical impulse spreads through the atria, they are signaled to contract.

The AV node conducts the electrical impulse from the atria into the ventricles. The impulse is delayed by about 0.13s as it passes through the AV node, and then it enters the AV bundle. This delay allows blood from the atria to completely empty into the ventricles to maximize ventricular filling before the ventricles contract. While most blood moves passively from the atria to the ventricles, active contraction of the atria(sometimes called the “atrial kick”) completes the process. The AV bundle travels along the ventricular septum and then sends right and left bundle branches into both ventricles. These branches send the impulse toward the apex of the heart and then outward. Each bundle branch subdivides into many smaller ones that spread throughout the entire ventricular wall. These terminal branches of the AV bundle are the Purkinje fibers. They transmit the impulse through the ventricles approximately six times faster than through the rest of the cardiac conduction system. This rapid conduction allows all parts of the ventricle to contract at virtually the same time.
Occasionally, chronic problems develop within the cardiac conduction system, hampering its ability to maintain appropriate sinus rhythm throughout the heart. In such cases, an artificial pacemaker can be surgically installed. This small, battery-operated electrical stimulator, usually implanted under the skin, has tiny electrodes attached to the right ventricle. An electrical stimulator is useful, for example, to treat a condition called AV block. With this disorder, the SA node creates an impulse, but the impulse is blocked at the AV node and cannot reach the ventricles, resulting in the heart rate’s being controlled by the intrinsic firing rate of the pacemaker cells in the ventricles(closer to 40 beats/min). The artificial pacemaker takes over the role of the disabled AV node, supplying the needed impulse and thus controlling ventricular contraction.

Extrinsic control of heart activity

Although the heart initiates its own electrical impulses(intrinsic control), both the rate and effect can be altered. Under normal conditions, this is accomplished primarily through three extrinsic systems:

The parasympathetic system, a branch of the autonomic nervous system, originates centrally in a region of the brain stem called the medulla oblongata and reaches the heart through the vagus nerve(cranial nerve X). The vagus nerve carries impulses to the SA and AV nodes, and when stimulated releases acetylcholine, which causes hyperpolarization of the conduction cells. The result is a decrease in a heart rate. At rest, parasympathetic system activity predominates and the heart is said to have “vagal tone”. Recall that, in the absence of vagal tone, intrinsic heart rate would be approximately 100 beats/min. The vagus nerve has a depressant effect on the heart: it slows impulse generation and conduction and thus decreases the heart rate. Maximal vagal stimulation can decrease the heart rate to as low as 20 to 30 beats/min. The vagus nerve also decreases the force of cardiac muscle contraction.
The sympathetic nervous system, the other branch of the autonomic system, has opposite effects. Sympathetic stimulation increases the rate of impulse generation and conduction speed, and thus heart rate. Maximal sympathetic stimulation allows the heart rate to increase up to 250 beats/min. Sympathetic input also increases the contraction force of the ventricles. The sympathetic system predominates during times of physical or emotional stress, when the heart rate is greater than 100 beats/min. The parasympathetic system dominates when heart rate is less than 100. Thus, when exercise begins, or if exercise is at a low intensity, heart rate first increases due to withdrawal of vagal tone, with further increases if necessary due to sympathetic activation, as shown in the figure below.

The third extrinsic influence, the endocrine system, exerts its effect through two hormones released by the adrenal medulla: norepinephrine and epinephrine. These hormones are also known as catecholamines. Like norepinephrine that serves as the major neurotransmitter in the sympathetic nervous system, norepinephrine and epinephrine stimulate the heart, increasing its rate and contractility. In fact, release of these hormones from the adrenal medulla is triggered by sympathetic stimulation during times of stress, and their actions prolong the sympathetic response.
Normal resting heart rate(RHR) typically varies between 60 and 100 beats/min. With extended periods of endurance training(months to years), the RHR can decrease to 35 beats/min or less. A RHR as low as 28 beats/min has been observed in a world class, long-distance runner. These lower training-induced RHRs are postulated to result from increased parasympathetic stimulation(vagal tone), with reduced sympathetic activity playing a lesser role.

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