Side Bar 1. They briefly disrupt the heart's autorhythmic beating. It feels like your heart "skips a beat. If they become more regular a health professional should be consulted to determine a cause. Long QT Syndrome is a defect of the electrical system in which the heart's electrical cells take longer than normal to recover after each heartbeat.
Long QT Syndrome can be inherited or acquired after taking certain medications, or caused by a combination of medications. Persons with Long QT Syndrome may be susceptible to ventricular fibrillation rapid, chaotic quivering of ventricles. During ventricular fibrillation, the blood pressure falls to zero, and the person falls unconscious.
An immediate, life-saving shock defibrillation must be delivered to the heart to restore a normal rhythm. What is a Heart Block? If the electrical impulses from the upper atria chambers of the heart are not properly transmitted to the lower ventricular chambers, the condition is known as a heart block.
Different types of heart block may require different treatments, depending on exactly which part of the conduction system is faulty. Other symptoms such as fatigue, lightheadedness, or fainting may develop. In some cases a permanent pacemaker is the primary treatment. What is Sick Sinus Syndrome Sick sinus syndrome is a cluster of symptoms that indicate the heart's natural pacemaker, the SA node, is not functioning properly. The heart rate can switch back and forth between a slow bradycardia to fast tachycardia heartbeat.
The condition may not be diagnosed until it has advanced, usually with age. The muscle relaxes as the calcium level drops, calcium unbinds from the troponin, and tropomyosin recovers the actin bindings sites. EKG reflects the overall spread of electrical activity during the cardiac cycle and is measurable because the electrical activity of many of the cells are synchronized during the cycle.
The current technique of recording the EKG employs Einthoven's triangle which is an imaginary triangle that surrounds the heart with its corners at the right and left arms and the left leg. These correspond to places where electrodes are placed.
Pairs of electrodes leads are compared and are given Roman numeral designations with one designating a positive electrode and the other a negative electrode. P wave Upward deflection associated with atrial depolarization. QRS complex Upward and downward deflections associated with ventricular depolarization corresponds with phase 0 of the ventricular contractile cells.
T wave Upward deflection associated with ventricular repolarization phase 3. It is important to remember that the EKG represents the patterns of action potentials in populations of contractile cells and not that of an individual cell. Certain intervals and segments of the ECG can provide important information about the function of the heart:.
P-Q interval - gives an estimate of the time of conduction through the AV node. Q-T interval - gives an estimate of the time the ventricles are contracting. T-Q interval - gives an estimate of the time the ventricles are relaxing. R-R interval - is the time between heartbeats. Dividing 60 by this time gives the heart rate. Examples of Abnormal Electrical Activity. Sinus Tachycardia - Abnormally fast resting heart rate.
Sinus Bradycardia - Abnormally slow resting heart rate. Altered conduction through the AV node :. Shows an increased P-Q interval. Conduction through AV node does not occur at all. Ventricular contraction occurs independent of stimulation from the AV node.
However, the rate is very slow times per minute because it is determined by the rate of bundle of His fiber discharge. Stimuli outside of normal conduction pathway may cause an extra contraction called extrasystole. In the atrium it is called a premature atrial contraction PAC. In the ventricle it is called a premature ventricular contraction PVC. Fibrillation occurs when the cardiac muscle no longer displays synchronous depolarization.
Atrial fibrillation is lack of synchronized depolarization of atria and is not life threatening. Ventricular fibrillation is lack of synchronized depolarization of ventricles and is incompatible with life. The cardiac cycle can be further divided into:. Ventricular Filling During early-to-late diastole, the pressure of blood in the veins drives blood through the atria into the ventricles.
AV valves are opened and semilunar valves are closed. Late in diastole atria contract and drive more blood into the ventricles. Isovolumetric Contraction At the beginning of systole, ventricles are contracting but the amount of blood in the ventricles remains the same.
This is due to the fact that pressure exerted on the blood closes the AV valves but is not yet high enough to force the semilunar valves to open.
Ventricular Ejection During the remainder of systole, the pressure of blood in the ventricles is strong enough to open the semilunar valves and blood is ejected from the ventricles into the pulmonary trunk and aorta. When the pressure in the ventricles declines to that below that of the aorta and pulmonary trunk the semilunar valves close and systole ends. Isovolumetric Relaxation On the onset of diastole, the ventricular muscles begin to relax but pressure on the AV valves is still enough to keep them closed.
With the semilunar and AV valves closed at the same time, the volume of blood in the ventricles remains the same as the pressure drops. Once the pressure has dropped low enough the AV valves open and the cycle begins again. Atrial and Ventricular Pressure. By convention pressure is measured in mm of mercury and is relative to atmospheric pressure mm Hg which is taken as zero e. Atrial contraction is associated with a small and short-lived rise in pressure associated with atrial contraction.
Ventricular pressure stays low in early diastole but there is a small abrupt rise in late diastole due to atrial contraction forcing blood into the ventricles. A much larger increase in pressure occurs as systole begins with ventricular contraction. During early diastolic, pressure falls to near zero. During the remainder of diastole the pressure slowly rises as the ventricles fill with blood.
Aortic Pressure. During diastole aortic pressure shows a gradual decline. The minimum pressure is diastolic pressure. During phase 2 with the onset of systole, aortic pressure continues to fall. During phase 3 with ventricular ejection, aortic pressure rises rapidly. This group of cells is self-excitable and able to depolarize to threshold and fire action potentials on their own, a feature called autorhythmicity; they do this at set intervals which determine heart rate.
If embryonic heart cells are separated into a Petri dish and kept alive, each is capable of generating its own electrical impulse followed by contraction. When two independently beating embryonic cardiac muscle cells are placed together, the cell with the higher inherent rate sets the pace, and the impulse spreads from the faster to the slower cell to trigger a contraction.
As more cells are joined together, the fastest cell continues to assume control of the rate. A fully developed adult heart maintains the capability of generating its own electrical impulse, triggered by the fastest cells, as part of the cardiac conduction system. The components of the cardiac conduction system include the sinoatrial node, the atrioventricular node, the atrioventricular bundle, the atrioventricular bundle branches, and the Purkinje cells Figure Normal cardiac rhythm is established by the sinoatrial SA node , a specialized clump of myocardial conducting cells located in the superior and posterior walls of the right atrium in close proximity to the orifice of the superior vena cava.
The SA node has the highest inherent rate of depolarization and is known as the pacemaker of the heart. It initiates the sinus rhythm , or normal electrical pattern followed by contraction of the heart. 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 Figure 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.
Figure 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 cardiac skeleton 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 Figure 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 Figure 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 Figure Since the electrical stimulus begins at the apex, the contraction also begins at the apex and travels superiorly 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 contractial cells. Unlike skeletal muscles and neurons, cardiac conductive cells do not have a stable resting potential. The resulting movement of sodium ions creates a spontaneous depolarization or prepotential depolarization and brings the cell to threshold.
This phenomenon explains the autorhythmicity properties of cardiac muscle Figure 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.
Electrical Signal Flow - Conduction Pathway. Click here for an animation on the cardiac cycle of the heart. Click here for even more practice questions. Heart Sounds.
Cardiac Output CO and Reserve. Cardiac output CO is the amount of blood ejected by the left ventricle into the aorta per minute. Stroke Volume SV is the amount of blood pumped out by a ventricle with each beat.
Cardiac Reserve - Cardiac reserve is the difference between resting and maximal CO - ratio between the maximum cardiac output a person can achieve and the cardiac output at rest. Normally the figure is four to five times the resting output. Preload Stretch - Frank - Starling law - the greater the stretch on cardiac fibers just before they contract draws myosin fibers closer together increases their force of contraction, the more blood is ejected from the ventricle the heart is filled during diastole the greater the force of contraction.
Contractility - strength of a contraction at any give preload. Substances that increase contractility positive inotropic agents include hormones glucagons, thyroxine , catecholemines epinephrine and norepinephrine , drugs digitalis and increased calcium concentration in the extracellular fluid. Afterload - the pressure in the large arteries leaving the heart that must be overcome before the aortic semilunar valve can open. Increased afterload results in decreased stroke volume.
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