depolarization of the ventricles is approximately 225 ms. membrane potentials and ion movement in cardiac conductive cells action potentials are considerably different between conductive and contractive cardiomyocytes. while sodium na+ and potassium k+ ions play essential roles, calcium ions ca2+ are also critical for both types of cell. unlike skeletal muscles and neurons, cardiac conductive cells do not have a stable resting potential. conductive cells contain a series of sodium ion channels that allow a normal and slow influx of sodium ions that causes the membrane potential to rise slowly from an initial value of −60 mv up to about –40 mv. the resulting movement of sodium ions creates spontaneous depolarization (or prepotential depolarization). at this point, calcium channels open and ca2+ enters the cell, further depolarizing it at a more rapid rate until it reaches a value of approximately +5 mv. at this point, the calcium ion channels close and potassium channels open, allowing outflux of k+ and resulting in repolarization. when the membrane potential reaches approximately −60 mv, the k+ channels close and na+ channels open, and the prepotential phase begins again. this process gives the autorhythmicity to cardiac muscle. 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; there is no resting potential. 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, although they are capable of doing so, but rather wait for an impulse to reach them. contractile cells demonstrate a much more stable resting phase than conductive cells at approximately −80 mv for cells in the atria and −90 mv for cells in the ventricles. 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. this rapid influx of positively charged ions raises the membrane potential to approximately +30 mv, at which point the sodium channels close. the rapid depolarization period typically lasts 3–5 ms. depolarization is followed by the plateau phase, in which membrane potential declines relatively slowly. this is due in large part to the opening of the slow ca2+ channels, allowing ca2+ to enter the cell while few k+ channels are open, allowing k+ to exit the cell. the relatively long plateau phase lasts approximately 175 ms. once the membrane potential reaches approximately zero, the ca2+ channels close and k+ channels open, allowing k+ to exit the cell. 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 250 and 300 ms. the absolute refractory period for cardiac contractile muscle lasts approximately 200 ms, and the relative refractory period lasts approximately 50 ms, for a total of 250 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. (a) there is long plateau phase due to the influx of calcium ions. the extended refractory period allows the cell to fully contract before another electrical event can occur.(b) the action potential for heart muscle is compared to that of skeletal muscle. 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. calcium ions also combine with the regulatory protein troponin in the troponin complex. both roles enabling the myocardium to function properly. approximately 20 percent of the calcium required for contraction is supplied by the influx of ca2+ during the plateau phase. the remaining ca2+ for contraction is released from storage in the sarcoplasmic reticulum. comparative rates of conduction system firing 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 80–100 times per minute. although each component of the conduction system is capable of generating its own impulse, the rate progressively slows 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. cardiac cycle main article: cardiac cycle cardiac cycle shown against ecg the period of time that begins with contraction of the atria and ends with ventricular relaxation is known as the cardiac cycle. the period of contraction that the heart undergoes while it pumps blood into circulation is called systole. the period of relaxation that occurs as the chambers fill with blood is called diastole. both the atria and ventricles undergo systole and diastole, and it is essential that these components be carefully regulated and coordinated to ensure blood is pumped efficiently to the body. the cardiac cycle as correlated to the ecg pressures and flow fluids, move from regions of high pressure to regions of lower pressure. accordingly, when the heart chambers are relaxed (diastole), blood will flow into the atria from the higher pressure of the veins. as blood flows into the atria, the pressure will rise, so the blood will initially move passively from the atria into the ventricles. when the action potential triggers the muscles in the atria to contract (atrial systole), the pressure within the atria rises further, pumping blood into the ventricles. during ventricular systole, pressure rises in the ventricles, pumping blood into the pulmonary trunk from the right ventricle and into the aorta from the left ventricle. phases of the cardiac cycle at the beginning of the cardiac cycle, both the atria and ventricles are relaxed (diastole). blood is flowing into the right atrium from the superior and inferior venae cavae and the coronary sinus. blood flows into the left atrium from the four pulmonary veins. the two atrioventricular valves, the tricuspid and mitral valves, are both open, so blood flows unimpeded from the atria and into the ventricles. approximately 70–80 percent of ventricular filling occurs by this method. the two semilunar valves, the pulmonary and aortic valves, are closed, preventing backflow of blood into the right and left ventricles from the pulmonary trunk on the right and the aorta on the left. atrial systole and diastole contraction of the atria follows depolarization, represented by the p wave of the ecg. as the atrial muscles contract from the superior portion of the atria toward the atrioventricular septum, pressure rises within the atria and blood is pumped into the ventricles through the open atrioventricular (tricuspid, and mitral or bicuspid) valves. at the start of atrial systole, the ventricles are normally filled with approximately 70–80 percent of their capacity due to inflow during diastole. atrial contraction, also referred to as the "atrial kick," contributes the remaining 20–30 percent of filling. atrial systole lasts approximately 100 ms and ends prior to ventricular systole, as the atrial muscle returns to diastole. ventricular systole ventricular systole follows the depolarization of the ventricles and is represented by the qrs complex in the ecg. it may be conveniently divided into two phases, lasting a total of 270 ms. at the end of atrial systole and just prior to ventricular contraction, the ventricles contain approximately 130 ml blood in a resting adult in a standing position. this volume is known as the end diastolic volume (edv) or preload. initially, as the muscles in the ventricle contract, the pressure of the blood within the chamber rises, but it is not yet high enough to open the semilunar (pulmonary and aortic) valves and be ejected from the heart. however, blood pressure quickly rises above that of the atria that are now relaxed and in diastole. this increase in pressure causes blood to flow back toward the atria, closing the tricuspid and mitral valves. since blood is not being ejected from the ventricles at this early stage, the volume of blood within the chamber remains constant. consequently, this initial phase of ventricular systole is known as isovolumic contraction, also called isovolumetric contraction. in the second phase of ventricular systole, the ventricular ejection phase, the contraction of the ventricular muscle has raised the pressure within the ventricle to the point that it is greater than the pressures in the pulmonary trunk and the aorta. blood is pumped from the heart, pushing open the pulmonary and aortic semilunar valves. pressure generated by the left ventricle will be appreciably greater than the pressure generated by the right ventricle, since the existing pressure in the aorta will be so much higher. nevertheless, both ventricles pump the same amount of blood. this quantity is referred to as stroke volume. stroke volume will normally be in the range of 70–80 ml. since ventricular systole began with an edv of approximately 130 ml of blood, this means that there is still 50–60 ml of blood remaining in the ventricle following contraction. this volume of blood is known as the end systolic volume (esv). ventricular diastole ventricular relaxation, or diastole, follows repolarization of the ventricles and is represented by the t wave of the ecg. it too is divided into two distinct phases and lasts approximately 430 ms. during the early phase of ventricular diastole, as the ventricular muscle relaxes, pressure on the remaining blood within the ventricle begins to fall. when pressure within the ventricles drops below pressure in both the pulmonary trunk and aorta, blood flows back toward the heart, producing the dicrotic notch (small dip) seen in blood pressure tracings. the semilunar valves close to prevent backflow into the heart. since the atrioventricular valves remain closed at this point, there is no change in the volume of blood in the ventricle, so the early phase of ventricular diastole is called the isovolumic ventricular relaxation phase, also called isovolumetric ventricular relaxation phase. in the second phase of ventricular diastole, called late ventricular diastole, as the ventricular muscle relaxes, pressure on the blood within the ventricles drops even further. eventually, it drops below the pressure in the atria. when this occurs, blood flows from the atria into the ventricles, pushing open the tricuspid and mitral valves. as pressure drops within the ventricles, blood flows from the major veins into the relaxed atria and from there into the ventricles. both chambers are in diastole, the atrioventricular valves are open, and the semilunar valves remain closed. the cardiac cycle is complete. heart sounds main article: heart sounds one of the simplest methods of assessing the heart's condition is to listen to it using a stethoscope. in a healthy heart, there are only two audible heart sounds, called s1 and s2. the first heart sound s1, is the sound created