Cardiac cycle is the term referring to all of the events that occurs from the beginning of one heartbeat to the beginning of the next. The frequency of the cardiac cycle is the heart rate. The time taken to complete one cardiac cycle is 0.8 sec and is called cardiac cycle time.
Some events of cardiac cycle are as follows:
1. Mechanical Changes
2. Pressure Changes
3. Volume Changes
4. Electrical Changes
5. Phonocardiogram
Event # 1. Mechanical Changes:
I. Atrial Events:
i. Atrial systole (0.1s)
ii. Atrial diastole (0.7s)
Atrial systole initiates the cycle, because of presence of pacemaker SA node and is followed by atrial diastole. At the end of diastole, the atrial systole returns, and the cycle goes on.
II. Ventricular Events:
a. Ventricular Systole (0.3s):
i. Isovolumetric contraction phase
ii. Rapid ejection
iii. Reduced ejection
b. Ventricular Diastole (0.5s):
i. Protodiastole
ii. Isovolumetric relaxation
iii. First rapid filling
iv. Diastasis
v. Second rapid filling
At the end of atrial systole, ventricular systole (0.3s) starts. This is followed by ventricular diastole (0.5s). At the end of diastole, the ventricular systole repeats, and the cycle goes on like this.
Description:
Cardiac cycle begins with the atrial systole. During this period, the atria contract and expel their contents into the ventricles. The LA being away from the SA node, contract a little after the RA. But practically their contractions are simultaneous.
After atrial systole, comes atrial diastole. During this period, the atria relax and receive blood from the great veins. RA from vena cavae, and LA from pulmonary veins.
Ventricular systole commences at the end of atrial systole. This is because the impulse originating in the SA node after passing through the atria, will travel down the junctional tissues and enter the ventricles resulting in contraction. Systoles of atria and ventricles will never overlap.
At the end of ventricular systole, the first heart sound occurs. It is caused by sudden closure of AV valves due to sharp rise in intraventricular pressure. The semilunar valves open a little later, because, until the intraventricular pressure goes above that in the aorta and pulmonary artery, SL valves will not open.
Thus, at the beginning of ventricular systole, there is a brief period during which both the valves are closed and the ventricles are contracting as closed cavities. No blood passes out and hence, no shortening of the muscle will occur. This period is called isovolumetric contraction phase (0.05s).
At the end of this period, SL valves open and ejection phase starts (0.25s). During this phase, blood is expelled from the ventricles, from LV to systemic aorta and from RV to pulmonary artery. In the first part of this period (0.11s), the outflow is very rapid. Hence, this is known as rapid ejection phase. In the last part, (0.14s) the rate of outflow slows down. Hence, this is called reduced ejection phase. Here, the ventricular systole ends and the diastole start.
As soon as the ventricles relax, the intraventricular pressure starts falling. The blood column in the aorta and pulmonary trunk try to roll back towards ventricles, but are stopped by the sharp closure of SL valves. This produces the second heart sound. The second sound occurs at the end of ventricular systole. But this statement is not exact, because, till the falling of intraventricular pressure goes below the intra- aortic pressure, the SL valves will not close.
Consequently, there will be short interval between the onset of diastole and the closure of SL valves. This is called protodiastolic phase (0.04s).
Although the SL valves have closed, yet the AV valves are still not open. Because the falling intraventricular pressure takes a little time to go below that of atria, so that the AV valves may open. So, there will be a brief interval during which both the valves remain closed and ventricles are relaxing as closed cavities. Since no blood enters the ventricles there will be no lengthening of cardiac muscle fibers. This phase is called as isovolumetric relaxation phase (0.05s).
At the end of isometric relaxation phase, the AV valves open. Blood rushes into the ventricles and ventricular filling begins. The first part of this phase is known as the first rapid filling phase (0.11s). Because, as soon as the AV valves open, blood accumulating so long in the atria rushes into the ventricles.
The steep fall of the intraventricular pressure during the isometric relaxation phase, makes the inflow all the more intense. Although the duration is less, yet the largest part of ventricular filling takes place during it. The rapid rush of blood produces a third heart sound.
In the next phase, the rate of filling slows down. The ventricles are already full to a large extent and ventricular pressure slowly rises. Consequently, the rate of inflow from the atria will be gradually slower. This phase is called diastasis or slow filling phase (0.16s). Although this is the longest phase of ventricular diastole, the amount of filling during this phase is minimum.
Then comes the last phase of ventricular diastole which corresponds to atrial systole. Due to atrial contraction, blood rushes into the ventricles rapidly and this is called second rapid filling phase (0.1s). The rapid rush of blood produces a fourth heart sound. Here the ventricular diastole ends. Again the ventricular systole starts and the cycle repeats.
Characteristics:
i. Quiescent Period:
Period when all chambers are at rest and filling. 70% of ventricular filling occurs during this period. The AV valves are open, the semilunar valves are closed.
ii. Atrial Systole:
Pushes the last 30% of blood into the ventricle.
Event # 2. Pressure Changes:
I. Atrial Pressure Changes:
During atrial systole, atrial pressure rises (‘a’ wave). During atrial diastole, since the AV valves bulge into the atrial cavity in isometric contraction period of ventricle, intra-atrial pressure rises (‘c’ wave).
Then pressure falls during rapid ejection period of ventricles due to three reasons:
a. Atrial relaxation continues
b. As the ventricular muscle shortens, the AV ring is pulled down, so that atrial cavity enlarges
c. Due to reduction of ventricular volume, mediastinal pressure falls. Owing to this negative pressure, the thin walled atria dilate and atrial pressure falls.
In the later part of ventricular systole, intra-atrial pressure slowly rises (‘v’ wave) due to accumulation of blood in the atria as a result of venous filling, and AV valves remaining closed. This rise slowly continues until AV valves open.
During isovolumetric relaxation phase, AV ring rises up and is an additional cause for pressure rising.
As soon as the AV valves open, atrial blood rushes into the ventricles, so that intra-atrial pressure decreases. This fall continues till about middle of ventricular diastole.
As the ventricles fill up during diastasis, intra-atrial pressure slowly rises. After this atrial pressure comes down again.
II. Ventricular Pressure Changes:
a. During Ventricular Systole:
i. In the Isometric Contraction Phase:
Intraventricular pressure rises.
ii. In the Rapid Ejection Phase:
For a short period, force of contraction is more than the rate of outflow intraventricular pressure rises. Then, gradually equalize: horizontal plateau at the summit.
iii. In the Reduced Ejection Phase:
Force of contraction is less than the rate of outflow ― intraventricular pressure decreases.
b. During Ventricular Diastole:
i. In the Protodiastolic Phase:
Intraventricular pressure decreases.
ii. In the Isovolumetric Relaxation Phase:
Ventricles are relaxing as closed cavities—intraventricular pressure decreases.
iii. In the First Rapid Filling Phase:
Rate of relaxation is more than filling intraventricular pressure decreases slowly to some extent.
iv. In Diastasis:
Ventricles are no more relaxing, blood accumulates in it intraventricular pressure rises slowly.
v. In Second Rapid Filling Phase:
Intraventricular pressure rises.
III. Aortic Pressure Changes:
During isovolumetric contraction phase of ventricles, a slight rise of aortic pressure is due to bulging of SL valves into the aorta.
With the opening of SL valves, blood enters the aorta and aortic pressure smoothly rises and falls running parallel to intraventricular pressure.
The fall of aortic pressure in reduced ejection phase is due to two causes:
a. Ventricle is contracting less forcibly than before, so that a comparatively less amount blood is entering the aorta now.
b. More blood is running out into the periphery than is entering the aorta from the ventricles.
With the onset of diastole, ventricular pressure sharply falls causing a backward flow of the aortic blood towards ventricles. Owing to this, aortic pressure drops causing the ‘incisura’. The blood column is reflected back by the sudden closure of SL valves, thus causing a sharp rise in the aortic pressure. The aortic pressure then slowly falls due to continuous passage of blood to periphery. The fall continues till ventricles contract again.
Event # 3. Volume Changes:
Ventricular Volume Changes:
The volume changes of ventricles are to some extent the reverse of its pressure changes.
i. During atrial systole, ventricular volume rises due to rapid filling. This rise is maintained during isovolumetric contraction phase of ventricles, because no blood is going out.
ii. During ejection phase, ventricular volume smoothly and continuously falls up to the end of systole.
iii. In isovolumetric relaxation phase, volume remains same, because no blood is entering.
iv. During first rapid filling phase, volume rises.
v. During diastasis, ventricular volume very slowly increases.
The stroke volume is the volume of blood, in milliliters (ml), pumped out of the heart with each beat, 70 ml/beat.
The output per minute is also called as minute volume. End-diastolic volume (EDV) is the amount of blood in the ventricle at the end of diastole. Normal value is about 120 ml.
Ejection fraction (EF) is the portion of end diastolic volume that is pumped out during one systole. EF = SV/EDV = 70/120 × 100 = 60%
End-systolic volume (EDV) is the amount of blood in the ventricle at the end of systole. Normal value is about 50 ml.
Ventricular Pressure-Volume Relationship:
Left ventricular pressure-volume (PV) loops are derived from pressure and volume information found in the cardiac cycle diagram (see left panel of Fig. 6.13). To generate a PV loop for the left ventricle, the left ventricular pressure (LVP) is plotted against left ventricular (LV) volume at multiple time points during a complete cardiac cycle. When this is done, a PV loop is generated (right panel of Fig. 6.13).
To illustrate the pressure-volume relationship for a single cardiac cycle.
The cycle can be divided into four basic phases:
i. Ventricular filling (phase A, diastole)
ii. Isovolumetric contraction (phase B)
iii. Ejection (phase C)
iv. Isovolumetric relaxation (phase D).
Point 1 on the PV loop is the pressure and volume at the end of ventricular filling (diastole), and therefore, represents the end-diastolic pressure and end-diastolic volume (EDV) for the ventricle. As the ventricle begins to contract isovolumetrically (phase B), the LVP increases but the LV volume remains the same, therefore, resulting in a vertical line (all valves are closed). Once LVP exceeds aortic diastolic pressure, the aortic valve opens (point 2) and ejection (phase C) begins.
During this phase the LV volume decreases as LVP increases to a peak value (peak systolic pressure) and then decreases as the ventricle begins to relax. When the aortic valve closes (point 3), ejection ceases and the ventricle relaxes isovolumetrically that is, the LVP falls but the LV volume remains unchanged, therefore the line is vertical (all valves are closed). The LV volume at this time is the end-systolic (i.e. residual) volume (ESV).
When the LVP falls below left atrial pressure, the mitral valve opens (point 4) and the ventricle begins to fill. Initially, the LVP continues to fall as the ventricle fills because the ventricle is still relaxing. However, once the ventricle is fully relaxed, the LVP gradually increases as the LV volume increases. The width of the loop represents the difference between EDV and ESV, which is by definition the stroke volume (SV). The area within the loop is the ventricular stroke work.
The filling phase moves along the end-diastolic pressure-volume relationship (EDPVR), or passive filling curve for the ventricle. The slope of the EDPVR is the reciprocal of ventricular compliance. The maximal pressure that can be developed by the ventricle at any given left ventricular volume is defined by the end-systolic pressure-volume relationship (ESPVR), which represents the inotropic state of the ventricle.
The pressure-volume loop, therefore, cannot cross over the ESPVR, because that relationship defines the maximal pressure that can be generated under a given inotropic state. The end-diastolic and end-systolic pressure-volume relationships are analogous to the passive and total tension curves used to analyze muscle function.
Event # 4. Electrical Changes:
Electrocardiogram:
ECG stands for electrocardiogram and represents the electrophysiology of the heart. Cardiac electrophysiology is the science of the mechanisms, functions, and performance of the electrical activities of specific regions of the heart. The ECG is the recording of the heart’s electrical activity as a graph. The graph can show the heart’s rate and rhythm, it can detect enlargement of the heart, decreased blood flow, or the presence of current or past heart attacks.
i. The P is the atrial depolarization.
ii. QRS is the ventricular depolarization, as well as atrial repolarization.
iii. T is the ventricular repolarization.
Apical Impulse:
During ventricular systole, all the diameters of the heart are reduced, and the base of the heart is pulled down towards the apex. On account of the spiral arrangement of the cardiac muscle fibers, the apex of the heart is rotated anteriorly and to the right, bringing most of the left ventricle to the front.
Due to this movement, as well as the hardening of the ventricular wall during contraction, there is a forward thrust of the apical region against the chest wall. This causes an impulse which is visible and palpable on the chest wall during each contraction and is called the apical impulse. This is felt on the left 5th intercostal space, 1/2 an inch internal to the midclavicular line. Palpation of the apical impulse gives useful clinical information.
Event # 5. Phonocardiogram:
In healthy adults, there are two normal heart sounds often described as a lub and a dub (ordup), that occur in sequence with each heart-beat. These are the first heart sound (SI) and second heart sound (S2). In addition to these normal sounds, other sounds may be present including gallop rhythms S3, S4 and heart murmurs.
In cardiac auscultation, an examiner uses a stethoscope to listen for these sounds, which provide important information about the condition of the heart.
The aortic area, pulmonary area, tricuspid area and mitral area are areas on the surface of the chest where the heart is auscultated.
First Heart Sound:
S1 is a soft, low pitched sound of long duration 0.1- 0. 17. and frequency of 25-45 Hz. Best heard at the apex.
Causes:
1. Sudden closure of AV valves
2. Vibrations set up by the turbulence of blood due to accelerations and decelerations caused by ventricular contractions
3. Vibrations set up in the ventricular muscle fibers as it begins contracting.
S1 is normally slightly split (~0.04 sec) because mitral valve closure precedes tricuspid valve closure, however, this very short time interval cannot normally be heard with a stethoscope so only a single sound is perceived. It coincides with the spike of the QRS complex of the ECG and just precedes the C wave of the atrial pressure curve.
Second Heart Sound:
S2 is shorter, sharper and of slightly higher pitch, best heard at the base, having duration of 0.1-0.14s and a frequency of 50 Hz.
Causes:
1. Sudden closure of SL valves
2. Vibrations set up in the blood columns and in the walls of aorta and pulmonary artery.
S2 is physiologically split because aortic valve closure normally precedes pulmonary valve closure. This splitting is not of fixed duration. S2 splitting changes depending on respiration, body posture and certain pathological conditions. It coincides with the upstroke of the V wave of atrial pressure curve and the end of T wave of ECG.
Third Heart Sound:
S3 is low pitched, and duration of 0.1s occurs in first rapid filling phase, and may represent tensing of the chordae tendinae and the atrioventricular ring, which is the connective tissue supporting the AV valve leaflets. This sound is normal in children, but when heard in adults it is often associated with ventricular dilation.
Fourth Heart Sound:
Is normally not heard, but only seen in phonocardiogram recording. It has a low frequency of 20 Hz and is caused by vibration of the ventricular wall during atrial contraction. This sound is usually associated with a stiffened ventricle (low ventricular compliance), and therefore is heard in patients with ventricular hypertrophy, myocardial ischemia, or in older adults.
Heart Murmurs:
Heart murmurs are generated by turbulent flow of blood, which may occur inside or outside the heart. Murmurs may be physiological (benign) or pathological (abnormal).
Physiologic Murmurs:
Physiologic murmurs also called functional murmurs can occur in the absence of valvular pathology. Very high flow velocities in the aorta can lead to turbulent flow which will result in murmurs during the ejection phase of the cardiac cycle. Examples of this include high cardiac outputs in trained athletes and high output states during anemia. Another example is pregnancy where the increase in cardiac output especially when coupled with anemia can result in physiologic ejection murmurs.
Abnormal Murmurs:
Abnormal murmurs can be caused by stenosis restricting the opening of a heart valve, resulting in turbulence as blood flows through it. Abnormal murmurs may also occur with valvular insufficiency (or regurgitation), which allows backflow of blood when the incompetent valve closes with only partial effectiveness. Different murmurs are audible in different parts of the cardiac cycle, depending on the cause of the murmur.