What is the difference between nodal cells and conducting cells

Since the left ventricle is much larger than the right, the left bundle branch is also considerably larger than the right. Portions of the right bundle branch are found in the moderator band and supply the right papillary muscles. Because of this connection, each papillary muscle receives the impulse at approximately the same time, so they begin to contract simultaneously just prior to the remainder of the myocardial contractile cells of the ventricles.

This is believed to allow tension to develop on the chordae tendineae prior to right ventricular contraction. There is no corresponding moderator band on the left.

Both bundle branches descend and reach the apex of the heart where they connect with the Purkinje fibers see image above, step 4. This passage takes approximately 25 ms. The Purkinje fibers are additional myocardial conductive fibers that spread the impulse to the myocardial contractile cells in the ventricles. They extend throughout the myocardium from the apex of the heart toward the atrioventricular septum and the base of the heart.

The Purkinje fibers have a fast inherent conduction rate, and the electrical impulse reaches all of the ventricular muscle cells in about 75 ms see image above, step 5. Since the electrical stimulus begins at the apex, the contraction also begins at the apex and travels toward the base of the heart, similar to squeezing a tube of toothpaste from the bottom.

This allows the blood to be pumped out of the ventricles and into the aorta and pulmonary trunk. The total time elapsed from the initiation of the impulse in the SA node until depolarization of the ventricles is approximately ms. Action potentials are considerably different between cardiac conductive cells and cardiac contractive cells. Unlike skeletal muscles and neurons, cardiac conductive cells do not have a stable resting potential.

The resulting movement of sodium ions creates spontaneous depolarization or prepotential depolarization. This phenomenon explains the autorhythmicity properties of cardiac muscle Figure 4. Figure 4. The prepotential is due to a slow influx of sodium ions until the threshold is reached followed by a rapid depolarization and repolarization.

The prepotential accounts for the membrane reaching threshold and initiates the spontaneous depolarization and contraction of the cell.

Note the lack of a resting potential. There is a distinctly different electrical pattern involving the contractile cells. In this case, there is a rapid depolarization, followed by a plateau phase and then repolarization. This phenomenon accounts for the long refractory periods required for the cardiac muscle cells to pump blood effectively before they are capable of firing for a second time.

These cardiac myocytes normally do not initiate their own electrical potential, although they are capable of doing so, but rather wait for an impulse to reach them. Despite this initial difference, the other components of their action potentials are virtually identical. In both cases, when stimulated by an action potential, voltage-gated channels rapidly open, beginning the positive-feedback mechanism of depolarization.

The rapid depolarization period typically lasts 3—5 ms. Depolarization is followed by the plateau phase, in which membrane potential declines relatively slowly.

The relatively long plateau phase lasts approximately ms. The repolarization lasts approximately 75 ms. At this point, membrane potential drops until it reaches resting levels once more and the cycle repeats. The entire event lasts between and ms Figure 5. Figure 5. The extended refractory period allows the cell to fully contract before another electrical event can occur.

The absolute refractory period for cardiac contractile muscle lasts approximately ms, and the relative refractory period lasts approximately 50 ms, for a total of ms.

This extended period is critical, since the heart muscle must contract to pump blood effectively and the contraction must follow the electrical events.

Without extended refractory periods, premature contractions would occur in the heart and would not be compatible with life. Calcium ions play two critical roles in the physiology of cardiac muscle. Their influx through slow calcium channels accounts for the prolonged plateau phase and absolute refractory period that enable cardiac muscle to function properly. Calcium ions also combine with the regulatory protein troponin in the troponin-tropomyosin complex; this complex removes the inhibition that prevents the heads of the myosin molecules from forming cross bridges with the active sites on actin that provide the power stroke of contraction.

This mechanism is virtually identical to that of skeletal muscle. The pattern of prepotential or spontaneous depolarization, followed by rapid depolarization and repolarization just described, are seen in the SA node and a few other conductive cells in the heart. Since the SA node is the pacemaker, it reaches threshold faster than any other component of the conduction system.

It will initiate the impulses spreading to the other conducting cells. The SA node, without nervous or endocrine control, would initiate a heart impulse approximately 80— times per minute. Although each component of the conduction system is capable of generating its own impulse, the rate progressively slows as you proceed from the SA node to the Purkinje fibers. Without the SA node, the AV node would generate a heart rate of 40—60 beats per minute.

If the AV node were blocked, the atrioventricular bundle would fire at a rate of approximately 30—40 impulses per minute. The bundle branches would have an inherent rate of 20—30 impulses per minute, and the Purkinje fibers would fire at 15—20 impulses per minute. While a few exceptionally trained aerobic athletes demonstrate resting heart rates in the range of 30—40 beats per minute the lowest recorded figure is 28 beats per minute for Miguel Indurain, a cyclist , for most individuals, rates lower than 50 beats per minute would indicate a condition called bradycardia.

Depending upon the specific individual, as rates fall much below this level, the heart would be unable to maintain adequate flow of blood to vital tissues, initially resulting in decreasing loss of function across the systems, unconsciousness, and ultimately death.

Figure 6. In a lead ECG, six electrodes are placed on the chest, and four electrodes are placed on the limbs. By careful placement of surface electrodes on the body, it is possible to record the complex, compound electrical signal of the heart. This tracing of the electrical signal is the electrocardiogram ECG , also commonly abbreviated EKG K coming kardiology, from the German term for cardiology.

Careful analysis of the ECG reveals a detailed picture of both normal and abnormal heart function, and is an indispensable clinical diagnostic tool. The standard electrocardiograph the instrument that generates an ECG uses 3, 5, or 12 leads. The greater the number of leads an electrocardiograph uses, the more information the ECG provides. A normal ECG tracing is presented in Figure 7. Each component, segment, and interval is labeled and corresponds to important electrical events, demonstrating the relationship between these events and contraction in the heart.

The small P wave represents the depolarization of the atria. The atria begin contracting approximately 25 ms after the start of the P wave. The large QRS complex represents the depolarization of the ventricles, which requires a much stronger electrical signal because of the larger size of the ventricular cardiac muscle.

The ventricles begin to contract as the QRS reaches the peak of the R wave. Lastly, the T wave represents the repolarization of the ventricles. Figure 7. The major segments and intervals of an ECG tracing are indicated in the image below. Segments are defined as the regions between two waves. Intervals include one segment plus one or more waves. The PR interval is more clinically relevant, as it measures the duration from the beginning of atrial depolarization the P wave to the initiation of the QRS complex.

Since the Q wave may be difficult to view in some tracings, the measurement is often extended to the R that is more easily visible. Should there be a delay in passage of the impulse from the SA node to the AV node, it would be visible in the PR interval. Figure 8 correlates events of heart contraction to the corresponding segments and intervals of an ECG.

Figure 8. This diagram correlates an ECG tracing with the electrical and mechanical events of a heart contraction. This impulse spreads from its initiation in the SA node throughout the atria through specialized internodal pathways , to the atrial myocardial contractile cells and the atrioventricular node. The internodal pathways consist of three bands anterior, middle, and posterior that lead directly from the SA node to the next node in the conduction system, the atrioventricular node see [link].

The impulse takes approximately 50 ms milliseconds to travel between these two nodes. The relative importance of this pathway has been debated since the impulse would reach the atrioventricular node simply following the cell-by-cell pathway through the contractile cells of the myocardium in the atria.

Regardless of the pathway, as the impulse reaches the atrioventricular septum, the connective tissue of the cardiac skeleton prevents the impulse from spreading into the myocardial cells in the ventricles except at the atrioventricular node. The electrical event, the wave of depolarization, is the trigger for muscular contraction. The wave of depolarization begins in the right atrium, and the impulse spreads across the superior portions of both atria and then down through the contractile cells.

The contractile cells then begin contraction from the superior to the inferior portions of the atria, efficiently pumping blood into the ventricles. The atrioventricular AV node is a second clump of specialized myocardial conductive cells, located in the inferior portion of the right atrium within the atrioventricular septum.

The septum prevents the impulse from spreading directly to the ventricles without passing through the AV node. There is a critical pause before the AV node depolarizes and transmits the impulse to the atrioventricular bundle see [link] , step 3. This delay in transmission is partially attributable to the small diameter of the cells of the node, which slow the impulse.

Also, conduction between nodal cells is less efficient than between conducting cells. These factors mean that it takes the impulse approximately ms to pass through the node. This pause is critical to heart function, as it allows the atrial cardiomyocytes to complete their contraction that pumps blood into the ventricles before the impulse is transmitted to the cells of the ventricle itself.

With extreme stimulation by the SA node, the AV node can transmit impulses maximally at per minute. This establishes the typical maximum heart rate in a healthy young individual. Damaged hearts or those stimulated by drugs can contract at higher rates, but at these rates, the heart can no longer effectively pump blood. Arising from the AV node, the atrioventricular bundle , or bundle of His , proceeds through the interventricular septum before dividing into two atrioventricular bundle branches , commonly called the left and right bundle branches.

The left bundle branch has two fascicles. The left bundle branch supplies the left ventricle, and the right bundle branch the right ventricle. Since the left ventricle is much larger than the right, the left bundle branch is also considerably larger than the right.

Portions of the right bundle branch are found in the moderator band and supply the right papillary muscles. Because of this connection, each papillary muscle receives the impulse at approximately the same time, so they begin to contract simultaneously just prior to the remainder of the myocardial contractile cells of the ventricles.

This is believed to allow tension to develop on the chordae tendineae prior to right ventricular contraction. There is no corresponding moderator band on the left. Both bundle branches descend and reach the apex of the heart where they connect with the Purkinje fibers see [link] , step 4.

This passage takes approximately 25 ms. The Purkinje fibers are additional myocardial conductive fibers that spread the impulse to the myocardial contractile cells in the ventricles.

They extend throughout the myocardium from the apex of the heart toward the atrioventricular septum and the base of the heart. The Purkinje fibers have a fast inherent conduction rate, and the electrical impulse reaches all of the ventricular muscle cells in about 75 ms see [link] , step 5.

Since the electrical stimulus begins at the apex, the contraction also begins at the apex and travels toward the base of the heart, similar to squeezing a tube of toothpaste from the bottom. This allows the blood to be pumped out of the ventricles and into the aorta and pulmonary trunk. The total time elapsed from the initiation of the impulse in the SA node until depolarization of the ventricles is approximately ms.

Action potentials are considerably different between cardiac conductive cells and cardiac contractive cells. Unlike skeletal muscles and neurons, cardiac conductive cells do not have a stable resting potential.

The resulting movement of sodium ions creates spontaneous depolarization or prepotential depolarization. This phenomenon explains the autorhythmicity properties of cardiac muscle [link]. Membrane Potentials and Ion Movement in Cardiac Contractile Cells There is a distinctly different electrical pattern involving the contractile cells. In this case, there is a rapid depolarization, followed by a plateau phase and then repolarization. This phenomenon accounts for the long refractory periods required for the cardiac muscle cells to pump blood effectively before they are capable of firing for a second time.

These cardiac myocytes normally do not initiate their own electrical potential but rather wait for an impulse to reach them. Despite this initial difference, the other components of their action potentials are virtually identical. In both cases, when stimulated by an action potential, voltage-gated channels rapidly open, beginning the positive-feedback mechanism of depolarization.

The rapid depolarization period typically lasts 3—5 ms. Depolarization is followed by the plateau phase, in which membrane potential declines relatively slowly. The relatively long plateau phase lasts approximately ms. The repolarization lasts approximately 75 ms. At this point, membrane potential drops until it reaches resting levels once more and the cycle repeats. The entire event lasts between and ms [link]. The absolute refractory period for cardiac contractile muscle lasts approximately ms, and the relative refractory period lasts approximately 50 ms, for a total of ms.

This extended period is critical, since the heart muscle must contract to pump blood effectively and the contraction must follow the electrical events. Without extended refractory periods, premature contractions would occur in the heart and would not be compatible with life.

Calcium Ions Calcium ions play two critical roles in the physiology of cardiac muscle. Their influx through slow calcium channels accounts for the prolonged plateau phase and absolute refractory period that enable cardiac muscle to function properly. Calcium ions also combine with the regulatory protein troponin in the troponin-tropomyosin complex; this complex removes the inhibition that prevents the heads of the myosin molecules from forming cross bridges with the active sites on actin that provide the power stroke of contraction.

This mechanism is virtually identical to that of skeletal muscle. The pattern of prepotential or spontaneous depolarization, followed by rapid depolarization and repolarization just described, are seen in the SA node and a few other conductive cells in the heart.

Since the SA node is the pacemaker, it reaches threshold faster than any other component of the conduction system. It will initiate the impulses spreading to the other conducting cells. The SA node, without nervous or endocrine control, would initiate a heart impulse approximately 80— times per minute. Although each component of the conduction system is capable of generating its own impulse, the rate progressively slows as you proceed from the SA node to the Purkinje fibers. Without the SA node, the AV node would generate a heart rate of 40—60 beats per minute.

If the AV node were blocked, the atrioventricular bundle would fire at a rate of approximately 30—40 impulses per minute. The bundle branches would have an inherent rate of 20—30 impulses per minute, and the Purkinje fibers would fire at 15—20 impulses per minute. While a few exceptionally trained aerobic athletes demonstrate resting heart rates in the range of 30—40 beats per minute the lowest recorded figure is 28 beats per minute for Miguel Indurain, a cyclist , for most individuals, rates lower than 50 beats per minute would indicate a condition called bradycardia.

Depending upon the specific individual, as rates fall much below this level, the heart would be unable to maintain adequate flow of blood to vital tissues, initially resulting in decreasing loss of function across the systems, unconsciousness, and ultimately death. By careful placement of surface electrodes on the body, it is possible to record the complex, compound electrical signal of the heart.

This tracing of the electrical signal is the electrocardiogram ECG , also commonly abbreviated EKG K coming kardiology, from the German term for cardiology. Careful analysis of the ECG reveals a detailed picture of both normal and abnormal heart function, and is an indispensable clinical diagnostic tool.

The standard electrocardiograph the instrument that generates an ECG uses 3, 5, or 12 leads. The greater the number of leads an electrocardiograph uses, the more information the ECG provides. A normal ECG tracing is presented in [link].

Each component, segment, and interval is labeled and corresponds to important electrical events, demonstrating the relationship between these events and contraction in the heart. The small P wave represents the depolarization of the atria. The atria begin contracting approximately 25 ms after the start of the P wave. The large QRS complex represents the depolarization of the ventricles, which requires a much stronger electrical signal because of the larger size of the ventricular cardiac muscle.

This is a physiological mechanism allowing sufficient time for the ventricles to empty and refill prior to the next contraction. Absolute refractory period ARP : the cell is completely unexcitable to a new stimulus. Relative refractory period RRP : a greater than normal stimulus will depolarize the cell and cause an action potential. Supranormal period : a hyperexcitable period during which a weaker than normal stimulus will depolarize the cells and cause an action potential.

Cells in this phase are particularly susceptible to arrhythmias when exposed to an inappropriately timed stimulus, which is why one must synchronize the electrical stimulus during cardioversion to prevent inducing ventricular fibrillation. Sequence of depolarization The SA node normally initiates electrical activation. The impulse propagates through atrial tissue to the AV node. There is no direct electrical connection between the atrial and ventricular chambers other than through the AV node, as fibrous tissue surrounds the tricuspid and mitral valves.

AV node allows a very short delay in conduction approximately 0. This pause has two important purposes : Allows the atria time to contract and fully empty prior to ventricular stimulation. Allows the AV node to act as a gatekeeper , limiting the transmission of ventricular stimulation during abnormally rapid atrial rhythms. After crossing the AV node, the impulse spreads into the rapidly conducting bundle of His and through the bundle branches to the Purkinje fibers.

The electrical impulse is distributed throughout the bulk of the ventricular myocyte for precisely timed stimulation and contraction of the ventricles. Excitation-contraction coupling Nature. Contractile proteins Main contractile elements: Myosin : thick filaments with globular heads evenly spaced along their length; contains myosin ATPase.

Actin : smaller molecule thin filaments consisting of two strands arranged as an alpha-helix, woven between myosin filaments. Regulatory elements: Tropomyosin : double helix that lies in the groove between actin filaments. It prevents contraction in the resting state by inhibiting the interaction between myosin heads and actin. Troponin : complex with three subunits that sits at regular intervals along the actin strands.

Troponin T TnT — t ies troponin complex to actin and tropomyosin molecules. Troponin C TnC — binds c alcium ions that regulate contractile process.

The strength of cardiac contraction is proportional to the number of crossbridges formed. Myocyte relaxation As with myocyte contraction, this process is synchronized with the electrical activity of the cell.