The Cardiac Cycle Clive M. Baumgarten, Ph.D. OBJECTIVES: 1. Describe periods comprising cardiac cycle and events within each period 2. Describe the temporal relationships between pressure, blood flow, ventricular volume, the venous pulse, heart sounds and the electrocardiogram 3. Describe the temporal differences between right and left heart events 4. Describe venous A-, C-, and V-waves and pulmonary capillary wedge pressure 5. Describe changes in the arterial pulse as the pressure wave moves from the aorta to the femoral artery 6. Describe heart sounds and their basis I. EVENTS OF THE CARDIAC CYCLE A. The cardiac cycle represents one cycle of electrical and mechanical activity of the heart. The cycle is divided into periods primarily based on the activity of the left ventricle. 1. Atrial Systole 110 msec 2. Isovolumetric Ventricular Contraction 60 msec 3. Rapid Ventricular Ejection 120 msec 4. Reduced Ventricular Ejection 170 msec 5. Isovolumetric Ventricular Relaxation 90 msec 6. Rapid Ventricular Filling 120 msec 7. Reduced Ventricular Filling or Diastasis 160 msec Approximate durations are listed for a HR of 72 bpm. The major effect of HR is to alter the duration of diastasis; increasing HR decreases diastasis. The duration of systole is also inversely related to HR. However, changes in the duration of systole are much less pronounced than changes in diastasis. B. Temporal relationships between physiological variables including the ECG, mechanical activity, pressure in the chambers of the heart, aorta and veins, and cardiac sounds are considered for the cardiac cycle in the Wiggers diagram.
II. GENERAL RELATIONSHIPS BETWEEN ELECTRICAL AND MECHANICAL ACTIVITY A. Atrial electrical activity begins with the P-wave and ends during the QRS complex. Because the SA node is on the right side, RA events preceded LA events. Ventricular electrical activity begins with the Q-wave and ends at the end of the T-wave. B. Contraction lags behind the corresponding electrical events by 20-50 msec. For the ventricle, mechanical relaxation is complete just after full repolarization. For the atria, relaxation occurs as much as 40 msec after repolarization. The atrial action potential is much shorter in duration than the ventricular action potential, although the contractions are nearly equal in duration. C. The exact relationships between electrical and mechanical activity depend on heart rate. With increasing heart rate, APD shortens more than the duration of contraction. III. VENTRICULAR SYSTOLE A. Isovolumetric Contraction 1. Isovolumetric contraction begins after the onset of the QRS-wave. Its beginning is marked by the first increase of ventricular pressure following the completion of atrial contraction. This is often approximated by the peak of the R-wave. 2. At the end of diastasis, the AV valves are tensed and nearly closed. They are fully closed immediately by the pressure increased caused by isovolumetric contraction. The aortic and pulmonic values are closed throughout this period. 3. Ventricular pressure rises rapidly, and ventricular volume remains constant. No blood is ejected. 4. Closure of AV valves corresponds to the first heart sound, S1. B. Rapid Ventricular Ejection 1. When ventricular pressure exceeds that in the aorta and in the pulmonary artery, the semilunar valves open marking the beginning of rapid ejection. 2. There is a rapid blood flow from LV to aorta (and RV to pulmonary artery). The peak of aortic flow precedes the peak of ventricular pressure. By the time ventricular pressure reaches it peak, aortic flow has decreased to about 70% of its maximum value. 3. Ventricular volume decreases sharply. Approximately 60% of the SV is ejected. 4. Atrial pressure falls below central venous pressure, and atrial filling begins. 5. The onset of the T-wave marks the end of rapid ventricular ejection.
6. Eddy currents keep the semilunar valve leaflets away from the arterial walls. They prevent the leaflets from blocking the coronary ostia which are located within the Sinuses of Valsalva behind the left and right aortic valve leaflets. C. Reduced Ventricular Ejection 1. Ejection of blood is slower, and ventricular volume decreases at a slower rate. The muscle fibers have come close to their minimum length. Repolarization during the T-wave signals that contraction is ending. 2. Ventricular and aortic pressure begin to fall from their peak values. Aortic pressure falls because runoff of blood to the peripheral vasculature is greater than blood flow from the ventricle to the aorta. 3. Aortic pressure very slightly exceeds ventricular pressure during most of this period. Ejection continues at a slow rate despite the reversed pressure gradient because of the momentum of blood. The energy available for ejection is the sum of the potential energy (pressure gradient) and kinetic energy (momentum). 4. Atrial pressure remains below central venous pressure, and atrial filling continues. IV. VENTRICULAR DIASTOLE A. Isovolumetric Relaxation 1. As contraction ends, left ventricular pressure falls below aortic pressure, and the aortic valve closes. The pulmonic valve closes slightly after the aortic valve. This delay is increased by inspiration and decreased by expiration. Since ventricular pressure remains higher than atrial pressure, the AV-valves remain closed. 2. Semilunar valve closure occurs because of both the pressure gradient and eddy currents. At the beginning of this period, before closure of the values are complete, there is there is a very slight retrograde flow. This appears as a brief negative aortic flow in the Wiggers diagram. 3. During isovolumetric relaxation, ventricular pressure falls rapidly, and ventricular volume is constant since all values are closed. 4. Closure of the semilunar valves corresponds to the second heart sound, S2. 5. Following closure of the aortic valve, aortic pressure increases a second time in the absence of flow into the aorta. This creates the dicrotic notch or incisura in the aortic pressure trace. The second pressure increase is caused, in part, by elastic recoil of the aortic valve and aorta. The pressure wave passing down the arterial tree is reflected at branch points. Reflections propagate upstream and also cause aortic pressure after the dicrotic notch. 6. Isovolumetric relaxation occurs after completion of the T-wave.
B. Rapid Ventricular Filling 1. Isovolumetric relaxation ends when ventricular pressure falls below atrial pressure, the AV valves open, and rapid ventricular refilling begins. In the Wiggers diagram, the left ventricular and atrial pressure are shown with mitral value opening. 2. Relaxation of the ventricle assists refilling by sucking blood into the ventricle. 3. Blood flow from the aorta to the peripheral arteries continues and aortic pressure falls towards its diastolic level. 4. Rapid blood flow into the ventricle and/or rapid relaxation of the muscle sets up vibrations giving the third heart sound, S3, which occurs near start of this period. C. Diastasis 1. Ventricular filling continues at a slower rate. The point of transition from rapid filling to diastasis is somewhat arbitrary. 2. The duration of diastasis is inversely proportional to heart rate. Increasing heart rate markedly decreases the time for ventricular refilling (both diastasis and rapid refilling). At HR > 100 bpm, refilling is incomplete. D. Atrial Systole 1. Atrial contraction follows the P-wave near the end of diastasis. 2. Atrial systole increases intra-atrial pressure by ~5 mm Hg owing to atrial ejection of blood. This contributes up to 20% of ventricular filling at high HR but only 5% at slow HR, and ventricular volume and pressure rise corresponding amounts. 3. Atrial systole causes the A-wave in the atrial and central venous pressure traces. 4. After atrial contraction is completed, blood flow back towards the atria from the ventricles starts to close the AV-valves. 5. At slow HR, the effect of atrial systole on ventricular pressure (atrial kick) is obvious in recordings of ventricular pressure. At high heart rates, the contribution fuses with the rapid increase in ventricular pressure and volume (i.e, atrial systole occurs during rapid ventricular filling; diastasis is virtually eliminated). Absence of a clear step in ventricular pressure does not mean that atrial contraction is unimportant at high heart rates. To the contrary, atrial contraction is quite important and makes a significant contribution to ventricular filling at high heart rates because the time for passive refilling is reduced. 6. The QRS complex marks the end of atrial systole.
V. COMPARISON OF LEFT AND RIGHT HEART Critical differences in timing of right and left heart events can be summarized from the following observation: Isovolumetric contraction and relaxation of the right heart occur total within the corresponding periods for the left heart. This results from the physiology of electrical conduction and differences in pressures. Differences include: A. RA contraction occurs before LA contraction because the SAN is in the RA. B. LV contraction starts before RV contraction, and the mitral valve closes before the tricuspid valve. The RV lags because the right bundle branch of the His- Purkinje system is longer and, hence, conduction time is greater. C. LV ejection starts last and ends first. (1) Pulmonic valve opens before the aortic valve because it takes longer to develop the higher pressure needed on the left side. (2) LV ejection ends before RV ejection because high aortic pressure induces valve closure first. D. Mitral valve opens after tricuspid. More time is needed for the higher pressure on the left side to fall.
2-Cork Mnemonic Gives left right differences in timing of valve motion VI. VENOUS PRESSURE A. Venous Pulse A Measure of Right Atrial Pressure Cervical neck veins communicate with the right atrium without intervening valves. Consequently, alterations in RAP are transmitted to the neck veins and are easily distinguished on physical examination. The morphology of left and right atrial and central venous pressure traces are quite similar. The major waves are represented in recordings from each, and the same terminology is applied. 1. A-wave a. Venous pressure slowly increases during diastasis as RA volume and pressure slowly increase. b. The maxima of the A-wave is caused by atrial systole. 2. C-wave a. A second maxima closely follows the A-wave. Venous pressure rises during isovolumetric contraction period reaching a maxima early in the rapid ejection period. b. The C-wave is caused by the bulging of the tricuspid valve into the right atria due to right ventricular contraction. It was named erroneously because it was initially thought that it was an 'artifact' of carotid artery pulsation and /or of gross cardiac movement during systole. 3. V-wave a. Venous pressure reaches a minima at the end of the rapid ejection period. It rises to a peak at the end of isovolumetric relaxation, and then falls. b. The V-wave reflects blood flow from the great veins into the right atria increasing RAP (rising phase) and from RA to RV decreasing RA pressure during rapid ventricular filling (falling phase). On physical examination, A and C-waves merge. Thus, findings are often expressed in terms of A and V-waves only.
B. Pulmonary Capillary Wedge Pressure A Measure of Left Atrial Pressure Information on left atrial pressure is often obtained in clinical situations as Pulmonary Capillary Wedge Pressure. A catheter is placed into a peripheral vein and is advanced through the superior vena cava, right atrium, right ventricle, and pulmonary artery until it wedges in the distal portion of the pulmonary arterial bed. Since there are no valves between the left atrium and the pulmonary capillaries, the contours of pulmonary wedge pressure directly reflect LAP, although the numerical values are slightly different. A, C, and V-waves correspond to the morphology of the venous pulse. On left side, the mitral valve bulges into the left atria because of LV contraction. VIII. ARTERIAL PRESSURE The pressure pulse generated by LV contraction moves down the arterial tree with a high velocity, ~5 m/sec. Its velocity increases in the periphery as vessel compliance decreases. In contrast, the velocity of blood flow is only ~0.1m/sec. High frequency components of the pressure pulse are damped by vessel walls. The pressure pulse is partially reflected at branch points, and the reflected wave adds to the pressure. Result: systolic and pulse pressures are higher in femoral a. and abdominal aorta than in thoracic aorta! Mean pressure decreases distally from heart and controls flow.
VIII. HEART SOUNDS Auscultation of the heart means ascertaining its condition by listening to its sounds with a stethoscope. The vibrations (sounds) are brief, low frequencies (30-250 Hz), and low amplitude. Vibrations are caused by disturbances in flow; normally, flow through open valves is silent. A phonocardiogram is a record of electronically amplified sounds. It significantly extends the range of detectable frequencies. A. First Heart Sound (S1) - 'lubb' S1 occurs during isovolumetric contraction and results from the sudden tension and recoil of the AV valves and adjacent structures. Although normally fused (i.e., heard as one sound), the mitral valve closes before the tricuspid. The sounds may be split (i.e., heard as two sounds) on inspiration. B. Second Heart Sound (S2) - 'dup' S2 occurs on closure of the semilunar valves at onset of isovolumetric relaxation. This initiates vibrations in the column of blood and tensed vessel walls. S2 is higher in pitch, shorter in duration, and lower in intensity than S1; it is described as a snapping sound. Inspiration causes splitting of S2. Inspiration: 1. Decreases intrathoracic pressure 2. Increases RV end-diastolic volume 3. Increase RV stroke volume and ejection time Thus, the pulmonic valve closure is delayed relative to the aortic valve.
C. Third Heart Sound (S3) S3 is caused by blood vibrating the ventricular walls as it passively flows from atria to ventricle during the rapid phase of ventricular refilling. It is a very soft, low-pitch, muffled sound. S3 is physiologically normal in young individuals. When it returns, it often reflects decreased compliance of the ventricular wall (e.g., in congestive failure). D. Fourth Heart Sound (S4) S4 is caused by rapid filling of the ventricle during atrial systole. It occurs at the peak of atrial contraction, immediately before S1. It is always inaudible in normal adults. IX. REFERENCES A. Koeppen, B.M. and Stanton, B.A. Berne & Levy Physiology, 6th Ed., 2008. pp. 321-325. B. Costanzo, L.S., Physiology, 3rd Ed., Saunders, 2006, Chapter 4, pp. 148-151. 8-Cardiac Cycle-2009.doc 8/28/2008