Summary

This document provides a detailed explanation of the cardiac cycle. It explores the phases of the cycle, the role of heart valves, and the associated electrocardiogram (ECG) and phonocardiogram (PCG) measurements. Useful for understanding cardiovascular physiology.

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CARDIAC CYCLE & HEART SOUNDS MEHMET OZANSOY, Ph.D. Dept. of Physiology  The cardiac events that occur from the beginning of one heartbeat to the beginning of the next are called the cardiac cycle.  Each cycle is initiated by spontaneous generation of an action potential in the sinus node ...

CARDIAC CYCLE & HEART SOUNDS MEHMET OZANSOY, Ph.D. Dept. of Physiology  The cardiac events that occur from the beginning of one heartbeat to the beginning of the next are called the cardiac cycle.  Each cycle is initiated by spontaneous generation of an action potential in the sinus node  The closing and opening of the cardiac valves define four phases of the cardiac cycle  The cardiac pump is of the two-stroke variety.  Like a pump with a reciprocating piston, the heart alternates between a filling phase and an emptying phase. Diastole and Systole  The cardiac cycle consists of a period of relaxation called diastole, during which the heart fills with blood  Followed by a period of contraction called systole Electrocardiogram and the Cardiac Cycle  The P wave is caused by spread of depolarization through the atria, and this is followed by atrial contraction, which causes a slight rise in the atrial pressure curve immediately after the electrocardiographic P wave.  About 0.16 second after the onset of the P wave, the QRS waves appear as a result of electrical depolarization of the ventricles, which initiates contraction of the ventricles and causes the ventricular pressure to begin rising  The QRS complex begins slightly before the onset of ventricular systole  The ventricular T wave in the electrocardiogram.  This represents the stage of repolarization of the ventricles when the ventricular muscle fibers begin to relax.  Therefore, the T wave occurs slightly before the end of ventricular contraction Pressure Changes in the Atria: The a, c, and v Waves  The a wave is caused by atrial contraction.  Ordinarily, the right atrial pressure increases 4 to 6 mm Hg during atrial contraction, and the left atrial pressure increases about 7 to 8 mm Hg  The c wave occurs when the ventricles begin to contract;  It is caused partly by  slight backflow of blood into the atria at the onset of ventricular contraction but mainly  by bulging of the A-V valves backward toward the atria because of increasing pressure in the ventricles  The v wave occurs toward the end of ventricular contraction;  It results from slow flow of blood into the atria from the veins while the A-V valves are closed during ventricular contraction.  Then, when ventricular contraction is over, the A-V valves open, allowing this stored atrial blood to flow rapidly into the ventricles and causing the v wave to disappear Period of Rapid Filling of the Ventricles  During ventricular systole, large amounts of blood accumulate in the right and left atria because of the closed AV valves.  As soon as systole is over and the ventricular pressures fall again to their low diastolic values, the moderately increased pressures that have developed in the atria during ventricular systole immediately push the A-V valves open and allow blood to flow rapidly into the ventricles Emptying of the Ventricles During Systole  Immediately after ventricular contraction begins, the ventricular pressure rises abruptly causing the A-V valves to close.  Then an additional 0.02 to 0.03 second is required for the ventricle to build up sufficient pressure to push the semilunar (aortic and pulmonary) valves open against the pressures in the aorta and pulmonary artery  During this period, contraction is occurring in the ventricles, but there is no emptying.  This is called the period of isovolumic or isometric contraction, meaning that tension is increasing in the muscle but little or no shortening of the muscle fibers is occurring Period of Ejection  When the left ventricular pressure rises slightly above 80 mm Hg (and the right ventricular pressure slightly above 80 mm Hg), the ventricular pressures push the semilunar valves open.  Immediately, blood begins to pour out of the ventricles, with about 70 per cent of the blood emptying occurring during the first third of the period of ejection and the remaining 30 per cent emptying during the next two thirds.  The first third is called the period of rapid ejection, and the last two thirds, the period of slow ejection. Period of Isovolumic (Isometric) Relaxation  At the end of systole, ventricular relaxation begins suddenly, allowing both the right and left intraventricular pressures to decrease rapidly.  The elevated pressures in the distended large arteries that have just been filled with blood from the contracted ventricles immediately push blood back toward the ventricles, which snaps the aortic and pulmonary valves closed  For another 0.03 to 0.06 second, the ventricular muscle continues to relax, even though the ventricular volume does not change, giving rise to the period of isovolumic or isometric relaxation.  During this period, the intraventricular pressures decrease rapidly back to their low diastolic levels.  Then the A-V valves open to begin a new cycle of ventricular pumping  During diastole, normal filling of the ventricles increases the volume of each ventricle to about 110 to 120 milliliters.  This volume is called the end-diastolic volume.  Then, as the ventricles empty during systole, the volume decreases about 70 milliliters, which is called the stroke volume output.  The remaining volume in each ventricle, about 40 to 50 milliliters, is called the end-systolic volume.  The fraction of the end-diastolic volume that is ejected is called the ejection fraction— usually equal to about 60 per cent. Function of the Valves  The A-V valves (the tricuspid and mitral valves) prevent backflow of blood from the ventricles to the atria during systole  The semilunar valves (the aortic and pulmonary artery valves) prevent backflow from the aorta and pulmonary arteries into the ventricles during diastole  These valves close and open passively.  That is, they close when a backward pressure gradient pushes blood backward, and they open when a forward pressure gradient forces blood in the forward direction. PressureVolume Loop  Phase 1, the inflow phase, includes segments AB and BC.  Phase 2, isovolumetric contraction, includes segment CD.  Phase 3, the outflow phase, includes segments DE and EF.  Phase 4, isovolumetric relaxation, includes segment FA.  Segments CDEF represent systole, whereas segments FABC represent diastole. Function of the Papillary Muscles  Papillary muscles attach to the vanes of the A-V valves by the chordae tendineae.  The papillary muscles contract when the ventricular walls contract  They pull the vanes of the valves inward toward the ventricles to prevent their bulging too far backward toward the atria during ventricular contraction Aortic and Pulmonary Artery Valves  The aortic and pulmonary artery semilunar valves function quite differently from the A-V valves.  First, the high pressures in the arteries at the end of systole cause the semilunar valves to snap to the closed position, in contrast to the much softer closure of the A-V valves.  Second, because of smaller openings, the velocity of blood ejection through the aortic and pulmonary valves is far greater than that through the much larger A-V valves  Because of the rapid closure and rapid ejection, the edges of the aortic and pulmonary valves are subjected to much greater mechanical abrasion than are the A-V valves.  Finally, the A-V valves are supported by the chordae tendineae, which is not true for the semilunar valves Heart Sounds  When listening to the heart with a stethoscope, one does not hear the opening of the valves because this is a relatively slow process that normally makes no noise.  However, when the valves close, the vanes of the valves and the surrounding fluids vibrate under the influence of sudden pressure changes, giving off sound that travels in all directions through the chest  When the ventricles contract, one first hears a sound caused by closure of the A-V valves.  The vibration is low in pitch and relatively long-lasting and is known as the first heart sound  When the aortic and pulmonary valves close at the end of systole, one hears a rapid snap because these valves close rapidly, and the surroundings vibrate for a short period.  This sound is called the second heart sound.  The duration of each of the heart sounds is slightly more than 0.10 second—the first sound about 0.14 second, and the second about 0.11 second.  The reason for the shorter second sound is that the semilunar valves are more taut than the A-V valves, so that they vibrate for a shorter time than do the A-V valves. Third Heart Sound  Occasionally a weak, rumbling third heart sound is heard at the beginning of the middle third of diastole.  A logical but unproved explanation of this sound is oscillation of blood back and forth between the walls of the ventricles initiated by inrushing blood from the atria Atrial Heart Sound (Fourth Heart Sound)  An atrial heart sound can sometimes be recorded in the phonocardiogram, but it can almost never be heard with a stethoscope because of its weakness and very low frequency—usually 20 cycles/sec or less.  This sound occurs when the atria contract, and presumably, it is caused by the inrush of blood into the ventricles, which initiates vibrations similar to those of the third heart sound. Auscultation of Normal Heart Sounds  Listening to the sounds of the body, usually with the aid of a stethoscope, is called auscultation  Although the sounds from all the valves can be heard from all these areas, the cardiologist distinguishes the sounds from the different valves by a process of elimination.  That is, he or she moves the stethoscope from one area to another, noting the loudness of the sounds in different areas and gradually picking out the sound components from each valve  The aortic area is upward along the aorta because of sound transmission up the aorta  The pulmonic area is upward along the pulmonary artery.  The tricuspid area is over the right ventricle  The mitral area is over the apex of the left ventricle, which is the portion of the heart nearest the surface of the chest Rheumatic Valvular Lesions  By far the greatest number of valvular lesions results from rheumatic fever.  Rheumatic fever is an autoimmune disease in which the heart valves are likely to be damaged or destroyed.  It is usually initiated by streptococcal toxin  The sequence of events almost always begins with a preliminary streptococcal infection caused specifically by group A hemolytic streptococci.  These bacteria initially cause a sore throat, scarlet fever, or middle ear infection.  But the streptococci also release several different proteins against which the person’s reticuloendothelial system produces antibodies.  The antibodies react not only with the streptococcal protein but also with other protein tissues of the body, often causing severe immunologic damage.  These reactions continue to take place as long as the antibodies persist in the blood—1 year or more  Rheumatic fever causes damage especially in certain susceptible areas, such as the heart valves.  The degree of heart valve damage is directly correlated with the concentration and persistence of the antibodies.  Because the mitral valve receives more trauma during valvular action than any of the other valves, it is the one most often seriously damaged, and the aortic valve is second most frequently damaged  A valve in which the leaflets adhere to one another so extensively that blood cannot flow through it normally is said to be stenosed.  Conversely, when the valve edges are so destroyed by scar tissue that they cannot close as the ventricles contract, regurgitation (backflow) of blood occurs when the valve should be closed Systolic Murmur of Aortic Stenosis  In aortic stenosis, blood is ejected from the left ventricle through only a small fibrous opening of the aortic valve.  Thus, a nozzle effect is created during systole, with blood jetting at tremendous velocity through the small opening of the valve.  The turbulent blood impinging against the aortic walls causes intense vibration, and a loud murmur Diastolic Murmur of Aortic Regurgitation  In aortic regurgitation, no abnormal sound is heard during systole, but during diastole, blood flows backward from the high-pressure aorta into the left ventricle, causing a “blowing” murmur of relatively high pitch  This murmur results from turbulence of blood jetting backward into the blood already in the low-pressure diastolic left ventricle. Systolic Murmur of Mitral Regurgitation  In mitral regurgitation, blood flows backward through the mitral valve into the left atrium during systole.  This also causes a high-frequency “blowing”  It is transmitted most strongly into the left atrium.  However, the left atrium is so deep within the chest that it is difficult to hear this sound directly over the atrium.  As a result, the sound of mitral regurgitation is transmitted to the chest wall mainly through the left ventricle to the apex of the heart Diastolic Murmur of Mitral Stenosis  In mitral stenosis, blood passes with difficulty through the stenosed mitral valve from the left atrium into the left ventricle, and because the pressure in the left atrium seldom rises above 30 mm Hg, a large pressure differential forcing blood from the left atrium into the left ventricle does not develop.  Consequently, the abnormal sounds heard in mitral stenosis are usually weak and of very low frequency, so that most of the sound spectrum is below the low-frequency end of human hearing

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