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Terms in this set (42)

...Cardiocytes are joined end to end by thick connections called intercalated (in-TUR-ka-LAY-ted) discs. With the right histological stain, these appear as dark lines thicker than the striations. An intercalated disc is a complex steplike structure with three distinctive features not found in skeletal muscle:

Interdigitating folds. The plasma membrane at the end of the cell is folded somewhat like the bottom of an egg carton. The folds of adjoining cells interlock with each other and increase the surface area of intercellular contact.

Mechanical junctions. The cells are tightly joined by two types of mechanical junctions: the fascia adherens and desmosomes. The fascia adherens21 (FASH-ee-ah ad-HEER-enz) is the most extensive. It is a broad band in which the actin of the thin myofilaments is anchored to the plasma membrane and each cell is linked to the next via transmembrane proteins. The fascia adherens is interrupted here and there by desmosomes. Described in more detail on p. 167, desmosomes are patches of mechanical linkage between cells. They prevent the contracting cardiocytes from pulling apart.

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Electrical junctions. The intercalated discs also contain gap junctions, which form channels that allow ions to flow from the cytoplasm of one cardiocyte directly into the next (see p. 167). They enable each cardiocyte to electrically stimulate its neighbors. Thus, the entire myocardium of the two atria behaves almost like a single cell, as does the entire myocardium of the two ventricles. This unified action is essential for the effective pumping of a heart chamber.

Skeletal muscle contains satellite cells that can divide and replace dead muscle fibers to some extent. Cardiac muscle lacks these, however, so the repair of damaged cardiac muscle is almost entirely by fibrosis (scarring). A limited capacity for myocardial mitosis and regeneration was discovered in 2001, raising hope that it might one day be clinically enhanced to repair hearts damaged by myocardial infarction.
...Even though the heart has its own pacemaker, it does receive both sympathetic and parasympathetic nerves that modify the heart rate and contraction strength. Sympathetic stimulation can raise the heart rate to as high as 230 bpm, and parasympathetic stimulation can slow it to as low as 20 bpm or even stop the heart for a few seconds.

The sympathetic pathway to the heart originates in the lower cervical to upper thoracic segments of the spinal cord. Preganglionic nerve fibers extend from there to the adjacent sympathetic chain ganglia, and some of them ascend to the cervical ganglia. Postganglionic fibers arise in the cervical ganglia, pass through a cardiac plexus in the mediastinum (see fig. 15.4, p. 566), and continue by way of cardiac nerves to the heart. These fibers terminate in the SA and AV nodes and in the atrial and ventricular myocardium, as well as in the aorta, pulmonary trunk, and coronary arteries. Sympathetic stimulation increases the heart rate and contraction strength and dilates the coronary arteries to increase myocardial blood flow.

The parasympathetic pathway begins with nuclei of the vagus nerves in the medulla oblongata. Preganglionic fibers extend through the vagus nerves to the cardiac plexus, where they mingle with the sympathetic fibers, and continue to the heart by way of the cardiac nerves (see fig. 15.7, p. 570). They synapse with postganglionic neurons in the epicardial surface and within the heart wall. Postganglionic fibers from the right vagus nerve lead mainly to the SA node and those from the left vagus lead mainly to the AV node, but each has some fibers that cross over to the other target cells. There is little or no parasympathetic innervation of the myocardium. Parasympathetic stimulation reduces the heart rate. Autonomic effects on heart rate and contraction strength are described in more detail later in this chapter.

From the foregoing description, you can see that the cardiac nerves from the plexus to the heart contain both sympathetic and parasympathetic efferent fibers. They also carry sensory (afferent) fibers from the heart to the CNS. Those fibers are important in cardiovascular reflexes and the transmission of pain signals from the heart.

The atrioventricular (AV) bundle, or bundle of His22 (pronounced "hiss"), is the pathway by which signals leave the AV node. The bundle soon forks into right and left bundle branches, which enter the interventricular septum and descend toward the apex.

Purkinje23 (pur-KIN-jee) fibers are nervelike processes that arise from the lower end of the bundle branches and turn upward to spread throughout the ventricular myocardium. Purkinje fibers distribute the electrical excitation to the cardiocytes of the ventricles. They form a more elaborate network in the left ventricle than in the right.

Once the Purkinje fibers have delivered the electrical signal to their limits, the cardiocytes themselves perpetuate it by passing ions from cell to cell through their gap junction
...Firing of the SA node excites atrial cardiocytes and stimulates the two atria to contract almost simultaneously. The signal travels at a speed of about 1 m/sec through the atrial myocardium and reaches the AV node in about 50 msec. In the AV node, the signal slows down to about 0.05 m/sec, partly because the cardiocytes here are thinner, but more importantly because they have fewer gap junctions over which the signal can be transmitted. This delays the signal at the AV node for about 100 msec—like highway traffic slowing down at a small town. This delay is essential because it gives the ventricles time to fill with blood before they begin to contract.

The ventricular myocardium has a conduction speed of only 0.3 to 0.5 m/sec. If this were the only route of travel for the excitatory signal, some cardiocytes would be stimulated much sooner than others. Ventricular contraction would not be synchronized and the pumping effectiveness of the ventricles would be severely compromised. But signals travel through the AV bundle and Purkinje fibers at a speed of 4 m/sec, the fastest in the conduction system. Consequently, the entire ventricular myocardium depolarizes within 200 msec after the SA node fires, causing the ventricles to contract in near unison.

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Signals reach the papillary muscles before the rest of the myocardium. Thus, these muscles contract and begin taking up slack in the tendinous cords an instant before ventricular contraction causes blood to surge against the AV valves. Ventricular systole begins at the apex of the heart, which is first to be stimulated, and progresses upward—pushing the blood upward toward the semilunar valves. Because of the spiral arrangement of ventricular cardiocytes, the ventricles twist slightly as they contract, like someone wringing out a towel.
...Apnea21 (AP-nee-uh)

Temporary cessation of breathing (one or more skipped breaths)

Dyspnea22 (DISP-nee-uh)

Labored, gasping breathing; shortness of breath

Hyperpnea23 (HY-purp-NEE-uh)

Increased rate and depth of breathing in response to exercise, pain, or other conditions

Hyperventilation

Increased pulmonary ventilation in excess of metabolic demand, frequently associated with anxiety; expels CO2 faster than it is produced, thus lowering the blood CO2 concentration and raising the blood pH

Hypoventilation24

Reduced pulmonary ventilation; leads to an increase in blood CO2 concentration if ventilation is insufficient to expel CO2 as fast as it is produced

Kussmaul25 respiration

Deep, rapid breathing often induced by acidosis; seen in diabetes mellitus

Orthopnea26 (or-thop-NEE-uh)

Dyspnea that occurs when a person is lying down or in any position other than standing or sitting erect; seen in heart failure, asthma, emphysema, and other conditions

Respiratory arrest

Permanent cessation of breathing (unless there is medical intervention)

Tachypnea27 (tack-ip-NEE-uh)

Accelerated respiration

Other variations in pulmonary ventilation serve the purposes of speaking, expressing emotion (laughing, crying), yawning, hiccuping, expelling noxious fumes, coughing, sneezing, and expelling abdominal contents. Coughing is induced by irritants in the lower respiratory tract. To cough, we close the glottis and contract the muscles of expiration, producing high pressure in the lower respiratory tract. We then suddenly open the glottis and release an explosive burst of air at speeds over 900 km/h (600 mi./h). This drives mucus and foreign matter toward the pharynx and mouth. Sneezing is triggered by irritants in the nasal cavity. Its mechanism is similar to coughing except that the glottis is continually open, the soft palate and tongue block the flow of air while thoracic pressure builds, and then the soft palate is depressed to direct part of the airstream through the nose. These actions are coordinated by coughing and sneezing centers in the medulla oblongata.