LETTERS TO THE EDITOR
649
The Cardiac Cycle To the Editor: In his review article, “Central Venous Pressure Monitoring: Clinical Insights Beyond the Numbers,“’ Mark’s attention to precise definitions and morphological details of waveforms prompts me to offer a brief resume of the cardiac cycle and an alternate, more traditional viewpoint on the division of the cardiac cycle into systole and diastole, and also a correction to his Fig 2. The mechanical cycle of the ventricle consists of four periods: (1) Isovolumic ventricular contraction. Following electrical excitation of the ventricular myocardium, manifest by the QRS complex, there is an electromechanical time delay of 50 to 60 milliseconds until individual fibers begin to shorten. The duration of the QRS represents the temporal dispersion of excitation, and there is a similar dispersion for the onset of contraction among myocardial fibers. Nevertheless, whatever degree of contraction is needed to raise interventricular pressure higher than that in the atrium will result in movement of the atvio-ventricular valvular (mitral/tricuspid) leaflets toward closure. Coaptation of the leaflets’ edges, ballooning of the pressurized leaflets, and tensing of the chordal apparatus are the principal generators of the first heart sound, particularly the mid- and high-frequency components. With the AV valve closed, but the semilunar valve (aortic/pulmonic) not yet open, ventricular volume remains unchanged; hence, the period is isovolumic, provided that the AV valve is competent. However, as contraction proceeds, increasing tension in the ventricular wall does force the left ventricle (LV) to transform from an elongated or pear shape to a more spherical shape with concomitant shortening of the long axis from apex to base. While this diminishing distance from apex to base has been known as “descent of the base,” this description is inaccurate, because it is the apex that moves upward toward the less mobile base. The base of the heart includes all four cardiac valves, which lie nearly in a single plane, adjacent to one another, and comprise a unified structure bound together by the heart’s fibrous skeleton. As such, the base is tethered by the great vessels and is not capable of great movement. With the heart literally suspended from the great vessels, the decreasing distance from base to apex results from movement of the apex toward the base, including a torsional component, a result of the spiral configuration of the ventricular fibers as they course around the chamber of the LV. A forceful impact of the apex against the anterior chest wall results. Ventricular pressure continues to rise rapidly, the slope of which (dP/dt) is often regarded as an index of contractility, until pressure exceeds that in the great vessel, thereby opening the semilunar valve, the event that terminates isovolumic contraction as ejection commences. (2) Ventricular ejection. The increase of interventricular pressure above that in the great vessel creates a small pressure gradient, normally only several mm Hg, which is sufficient to effect ejection. However, it is the physical movement of blood through the semilunar valve that opens the leaflets. Blood velocity, hence the rate of volumetric ejection accelerates to a peak, thereafter declining as ventricular contraction is less able to maintain ejection due to mechanics of myofibrillar shortening and gross geometry of a spherical chamber. Although myofibrillar mechanics are beyond the scope of the present synopsis, the geometrical relation between circumference and volume are readily appreciated. Myofibrillar length determines ventricular circumference (C), which is linearly proportional to diameter (D), as C = ITD. However, a given change in diameter has a greater effect on the volume (V) of a sphere the larger the diameter:
V+R3+D3
D where R = 2
Taking the derivative for the rate of change of volume with respect to diameter yields: dV ,ir s=2DZ
or
dV=tD2dD
Equation 2 shows that the rate of change of a spherical volume with respect to a changing diameter (dV/dD) is related to the square of the diameter; hence, the volumetric effect of a change in diameter is greater at larger diameters. Therefore, as ejection proceeds and ventricular volume diminishes, it becomes progressively more difficult for the contracting myofibrils to increase or even maintain the rate of ejection. The maximum rate of ejection is reached when the foregoing geometrical considerations overwhelm myofibrillar mechanics, and thereafter the rate of ejection declines. However, before transvalvular flow returns to zero, the inertia of blood will maintain some forward flow while the myofibrils begin the active biochemical process of relaxation; this brief interval is the protodiastolic period of Wiggers, which ends with closure of the semilunar valve.
LE-ERS
650
TO THE EDITOR
(3) Isovolumic ventricular relaxation. With the semilunar valve just closed, ventricular relaxation continues without any change in volume and interventricular pressure decreases toward that in the atrium. However, the atrium continues to fill as it did during ventricular ejection, and atria1 pressure continues to increase, thereby continuing to trace the ascending limb of the v-wave. When interventricular pressure decreases below the pressure in the atrium the AV valve is urged to open, thereby ending the ascent of the v-wave and beginning the y-descent. Thus, the peak of the v-wave is virtually coincident with opening of the AV valve and the end of this isovolumic period. Because Mark has proposed to define the end of systole coincident with opening of the AV valve (a definition to be discussed later), the vertical boundary between systole and diastole in his Fig 2 should ideally intersect the peak of the v-wave. Mark’s Fig 2 erroneously shows the vertical boundary line falling beyond the peak of the v-wave, on the early y-descent. However, real-life catheter systems introduce transmission delays, hence the relation seen on the oscilloscopic monitor or chart recorder would show the peak of the v-wave slightly delayed with respect to the actual instant of AV valvular opening and also the instantaneous electrocardiogram (ECG) trace. (4) Ventricular diastolic filling. With atria1 pressure at a peak, opening of the AV valve permits a rapid rate of flow into the ventricle, and the height of this flow rate is coincident with the third heart sound or its abnormal counterpart, the “ventricular gallop.” Then follows a period of slower ventricular filling. Last, atria1 contraction causes a return to more rapid filling, the height of which coincides with the fourth heart sound or its abnormal counter-part, the so-called “atria1 gallop,“ although this sound is indeed generated within the ventricle. Thus, three segments of ventricular filling can be identified at slow or normal heart rates, ie, (1) early rapid filling, (2) slow filling, and (3) atria1 contraction. At increasing heart rates the cycle length shortens, principally at the expense of the diastolic period of slow ventricular filling and at a heart rate of 105 to 110 beats/min the third and fourth heart sounds will coincide and summatc.’ Having reviewed the cardiac cycle, we are now prepared to evaluate Mark’s proposal that diastole be redefined to designate only that portion of the cardiac cycle between AV valvular opening and closing, namely the period of ventricular filling and, therefore, relegate isovolumic relaxation to systole. Although we do not object to redefinitions based on newer knowledge and changing concepts, we see no compelling virtue to the redefinition proposed by Mark, and encounter several distinct problems created by it. First, it is conceptually more orderly to associate ventricular contraction with systole and relaxation with diastole. Furthermore, recent knowledge has recognized myofibrillar relaxation as an active process, hence the new terminology of diastolic function and designation of abnormal relaxation as diastolic dysfunction. Mark’s proposed redefinition would place isovolumic relaxation into systole and create a contradiction of terminology and thought without providing a counterbalancing benefit. Second, and particularly pertinent to the anesthesiologist using an esophageal stethoscope, the second heart sound would no longer signal the end of systole and the beginning of diastole under Mark’s redefinition, which includes isovolumic relaxation into the systolic interval. Furthermore, regurgitation through the semilunar valve, ie, pulmonic insufficiency 01 aortic insufficiency, eliminates truly isovolumic relaxation and results in ventricular filling, albeit retrograde. The corresponding murmur can commence immediately after the second sound. Under Mark’s proposed redefinition, such retrograde filling would commence during the systolic period, an unhappy notion, and the murmurs of aortic and pulmonic regurgitation would begin in the systolic period and continue into diastole. A great deal of descriptive and simple terminology would need to be revised. Third, Mark’s proposed definition that “diastole extends from mitral (tricuspid) valve opening until mitral (tricuspid) focus on the aortic (pulmonic) valve closure” seems arbitrarily focused on the AV valve. One could, with equal justification, valve and take systole as the period between semilunar valve opening and closing, which is the period of ejection. Neither focus is acceptable, for they both ignore the isovolumic periods. The period of isovolumic contraction provides important indices of myocardial contractility and systolic function, and is appropriately a systolic interval. Similarly. isovolumic relaxation is gaining increasing importance as a reflection of diastolic function. In conclusion, the traditional, time-tested designation of systole and diastole remain the most useful and virtuous. Both systole and diastole have two subdivisions-an isovolumic period followed by a period of changing volume. The image is conceptually simple and clean. while also being the most useful to all subdisciplines of medical research and practice concerned with hemodynamics.
Joseph Grayzel, ML, Englewood, NJ
REFERENCES I. Mark JB: Centralvenous
2. Grayzel 20:1053-1062.
J: Gallop 1959
pressure monitoring. J Cardiothorac Vast Anesth 5:163-173, 1991 rhythm of the heart. II. Quadruple rhythm and its relation to summation
and augmented
gallops.
Circulation
649
The Cardiac Cycle To the Editor: In his review article, “Central Venous Pressure Monitoring: Clinical Insights Beyond the Numbers,“’ Mark’s attention to precise definitions and morphological details of waveforms prompts me to offer a brief resume of the cardiac cycle and an alternate, more traditional viewpoint on the division of the cardiac cycle into systole and diastole, and also a correction to his Fig 2. The mechanical cycle of the ventricle consists of four periods: (1) Isovolumic ventricular contraction. Following electrical excitation of the ventricular myocardium, manifest by the QRS complex, there is an electromechanical time delay of 50 to 60 milliseconds until individual fibers begin to shorten. The duration of the QRS represents the temporal dispersion of excitation, and there is a similar dispersion for the onset of contraction among myocardial fibers. Nevertheless, whatever degree of contraction is needed to raise interventricular pressure higher than that in the atrium will result in movement of the atvio-ventricular valvular (mitral/tricuspid) leaflets toward closure. Coaptation of the leaflets’ edges, ballooning of the pressurized leaflets, and tensing of the chordal apparatus are the principal generators of the first heart sound, particularly the mid- and high-frequency components. With the AV valve closed, but the semilunar valve (aortic/pulmonic) not yet open, ventricular volume remains unchanged; hence, the period is isovolumic, provided that the AV valve is competent. However, as contraction proceeds, increasing tension in the ventricular wall does force the left ventricle (LV) to transform from an elongated or pear shape to a more spherical shape with concomitant shortening of the long axis from apex to base. While this diminishing distance from apex to base has been known as “descent of the base,” this description is inaccurate, because it is the apex that moves upward toward the less mobile base. The base of the heart includes all four cardiac valves, which lie nearly in a single plane, adjacent to one another, and comprise a unified structure bound together by the heart’s fibrous skeleton. As such, the base is tethered by the great vessels and is not capable of great movement. With the heart literally suspended from the great vessels, the decreasing distance from base to apex results from movement of the apex toward the base, including a torsional component, a result of the spiral configuration of the ventricular fibers as they course around the chamber of the LV. A forceful impact of the apex against the anterior chest wall results. Ventricular pressure continues to rise rapidly, the slope of which (dP/dt) is often regarded as an index of contractility, until pressure exceeds that in the great vessel, thereby opening the semilunar valve, the event that terminates isovolumic contraction as ejection commences. (2) Ventricular ejection. The increase of interventricular pressure above that in the great vessel creates a small pressure gradient, normally only several mm Hg, which is sufficient to effect ejection. However, it is the physical movement of blood through the semilunar valve that opens the leaflets. Blood velocity, hence the rate of volumetric ejection accelerates to a peak, thereafter declining as ventricular contraction is less able to maintain ejection due to mechanics of myofibrillar shortening and gross geometry of a spherical chamber. Although myofibrillar mechanics are beyond the scope of the present synopsis, the geometrical relation between circumference and volume are readily appreciated. Myofibrillar length determines ventricular circumference (C), which is linearly proportional to diameter (D), as C = ITD. However, a given change in diameter has a greater effect on the volume (V) of a sphere the larger the diameter:
V+R3+D3
D where R = 2
Taking the derivative for the rate of change of volume with respect to diameter yields: dV ,ir s=2DZ
or
dV=tD2dD
Equation 2 shows that the rate of change of a spherical volume with respect to a changing diameter (dV/dD) is related to the square of the diameter; hence, the volumetric effect of a change in diameter is greater at larger diameters. Therefore, as ejection proceeds and ventricular volume diminishes, it becomes progressively more difficult for the contracting myofibrils to increase or even maintain the rate of ejection. The maximum rate of ejection is reached when the foregoing geometrical considerations overwhelm myofibrillar mechanics, and thereafter the rate of ejection declines. However, before transvalvular flow returns to zero, the inertia of blood will maintain some forward flow while the myofibrils begin the active biochemical process of relaxation; this brief interval is the protodiastolic period of Wiggers, which ends with closure of the semilunar valve.
LE-ERS
650
TO THE EDITOR
(3) Isovolumic ventricular relaxation. With the semilunar valve just closed, ventricular relaxation continues without any change in volume and interventricular pressure decreases toward that in the atrium. However, the atrium continues to fill as it did during ventricular ejection, and atria1 pressure continues to increase, thereby continuing to trace the ascending limb of the v-wave. When interventricular pressure decreases below the pressure in the atrium the AV valve is urged to open, thereby ending the ascent of the v-wave and beginning the y-descent. Thus, the peak of the v-wave is virtually coincident with opening of the AV valve and the end of this isovolumic period. Because Mark has proposed to define the end of systole coincident with opening of the AV valve (a definition to be discussed later), the vertical boundary between systole and diastole in his Fig 2 should ideally intersect the peak of the v-wave. Mark’s Fig 2 erroneously shows the vertical boundary line falling beyond the peak of the v-wave, on the early y-descent. However, real-life catheter systems introduce transmission delays, hence the relation seen on the oscilloscopic monitor or chart recorder would show the peak of the v-wave slightly delayed with respect to the actual instant of AV valvular opening and also the instantaneous electrocardiogram (ECG) trace. (4) Ventricular diastolic filling. With atria1 pressure at a peak, opening of the AV valve permits a rapid rate of flow into the ventricle, and the height of this flow rate is coincident with the third heart sound or its abnormal counterpart, the “ventricular gallop.” Then follows a period of slower ventricular filling. Last, atria1 contraction causes a return to more rapid filling, the height of which coincides with the fourth heart sound or its abnormal counter-part, the so-called “atria1 gallop,“ although this sound is indeed generated within the ventricle. Thus, three segments of ventricular filling can be identified at slow or normal heart rates, ie, (1) early rapid filling, (2) slow filling, and (3) atria1 contraction. At increasing heart rates the cycle length shortens, principally at the expense of the diastolic period of slow ventricular filling and at a heart rate of 105 to 110 beats/min the third and fourth heart sounds will coincide and summatc.’ Having reviewed the cardiac cycle, we are now prepared to evaluate Mark’s proposal that diastole be redefined to designate only that portion of the cardiac cycle between AV valvular opening and closing, namely the period of ventricular filling and, therefore, relegate isovolumic relaxation to systole. Although we do not object to redefinitions based on newer knowledge and changing concepts, we see no compelling virtue to the redefinition proposed by Mark, and encounter several distinct problems created by it. First, it is conceptually more orderly to associate ventricular contraction with systole and relaxation with diastole. Furthermore, recent knowledge has recognized myofibrillar relaxation as an active process, hence the new terminology of diastolic function and designation of abnormal relaxation as diastolic dysfunction. Mark’s proposed redefinition would place isovolumic relaxation into systole and create a contradiction of terminology and thought without providing a counterbalancing benefit. Second, and particularly pertinent to the anesthesiologist using an esophageal stethoscope, the second heart sound would no longer signal the end of systole and the beginning of diastole under Mark’s redefinition, which includes isovolumic relaxation into the systolic interval. Furthermore, regurgitation through the semilunar valve, ie, pulmonic insufficiency 01 aortic insufficiency, eliminates truly isovolumic relaxation and results in ventricular filling, albeit retrograde. The corresponding murmur can commence immediately after the second sound. Under Mark’s proposed redefinition, such retrograde filling would commence during the systolic period, an unhappy notion, and the murmurs of aortic and pulmonic regurgitation would begin in the systolic period and continue into diastole. A great deal of descriptive and simple terminology would need to be revised. Third, Mark’s proposed definition that “diastole extends from mitral (tricuspid) valve opening until mitral (tricuspid) focus on the aortic (pulmonic) valve closure” seems arbitrarily focused on the AV valve. One could, with equal justification, valve and take systole as the period between semilunar valve opening and closing, which is the period of ejection. Neither focus is acceptable, for they both ignore the isovolumic periods. The period of isovolumic contraction provides important indices of myocardial contractility and systolic function, and is appropriately a systolic interval. Similarly. isovolumic relaxation is gaining increasing importance as a reflection of diastolic function. In conclusion, the traditional, time-tested designation of systole and diastole remain the most useful and virtuous. Both systole and diastole have two subdivisions-an isovolumic period followed by a period of changing volume. The image is conceptually simple and clean. while also being the most useful to all subdisciplines of medical research and practice concerned with hemodynamics.
Joseph Grayzel, ML, Englewood, NJ
REFERENCES I. Mark JB: Centralvenous
2. Grayzel 20:1053-1062.
J: Gallop 1959
pressure monitoring. J Cardiothorac Vast Anesth 5:163-173, 1991 rhythm of the heart. II. Quadruple rhythm and its relation to summation
and augmented
gallops.
Circulation
