The cardiac cycle is defined as a sequence of alternating contraction and relaxation of the atria and ventricles in order to pump blood throughout the body. It starts at the beginning of one heartbeat and ends at the beginning of another. The process begins as early as the 4th gestational week when the heart first begins contracting.
Each cardiac cycle has a diastolic phase (also called diastole) where the heart chamber is in a state of relaxation and fills with blood that receives from the veins and a systolic phase (also called systole) where the heart chambers are contracting and pumps the blood towards the periphery via the arteries. Both the atria and the ventricles undergo alternating states of systole and diastole. In other words, when the atria are in diastole, the ventricles are in systole and vice versa.
|Atrial diastole||Atria passively filling
Atrioventricular valves open
|Atrial systole||Action potential from the sinuatrial node (SAN)
Synchronous atrial contraction
Active filling of ventricles
|Ventricular diastole||First third of the diastolic phase (early ventricular diastole): ventricular rapid inflow
Middle third of the diastolic phase (late ventricular diastole): passive inflow or diastasis
Last third of the diastolic phase (atrial diastole): ventricular filling due to atrial contraction (20%)
|Ventricular systole||Isovolumetric contraction – atrioventricular and semilunar valves are closed
Semilunar valve opens
Emptying of the ventricle
This article will discuss the phases of the cardiac cycle and the underlying physiological principles that govern the process. There will be a brief review of the conducting system of the heart, as well as discussion of the disorders that affect the cardiac cycle.
- Conducting system of the heart
- Cardiac cycle phases
- Wiggers Diagram
- Frank-Starling mechanism
- Disorders affecting the cardiac cycle
Conducting system of the heart
Myocardiocytes are unique cells found in the heart that are able to independently generate and spread electrical activity from one cell to another. They are able to communicate through gap junctions (points of permeability) at the intercalated discs (where cell walls meet). The communication is so efficient that the cells form a syncytium where ions can freely and rapidly flow from one cell to another. As a result of this network, the heart muscles undergo almost simultaneous contraction.
There is an area of sub-specialized cells known as the sinuatrial node (SA node). This area is located near the opening of the superior vena cava on the superior lateral wall of the right atrium. The SA node is able to contract faster than the rest of the heart tissue and as a result, it sets the pace of cardiac contraction. Therefore it is referred to as the pacemaker of the heart. The SA node is able to spread its impulse to the rest of the right and left atria through preferential conductive pathways.
There is a secondary area of concentrated conductive tissue known as the atrioventricular node (AV node) that is located medial and posterior to the tricuspid valve. Like the SA node, the AV node also has autonomous properties and is able to generate an action potential. However, these cells are slower than those in the SA node and as a result, they act in response to activity from the SA node. There are preferential internodal pathways that exist for more efficient transmission of the impulse to the AV node.
The AV node is connected to a network of fibers that run down the interventricular septum then through the walls of the ventricles. The initial segment of this pathway is called the bundle of His. The bundle of his then bifurcates into the left and right bundle branches. The left bundle branch also gives of left posterior branches, which carries impulses to the posterior aspect of the left ventricle. Both the left and right bundle branches give off numerous branches known as Purkinje fibers that supply the ventricular myocardium.
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Cardiac cycle phases
The events of the cardiac cycle, start with a spontaneous action potential in the sinus node as we described previously. This stimulus causes a series of events in the atria and the ventricles. All these events are “organized” in two phases:
- diastole (when the heart fills with blood)
- and systole (when the heart pumps the blood)
During these two phases, many different events are observed and we will describe them in the following paragraphs.
Atrial diastole is the very first event of the cardiac cycle. It occurs some milliseconds before the electrical signal from the SA node arrives at the atria. The atria function as conduits that facilitate the passage of blood into the ipsilateral ventricle. They also act as primers to pump residual blood into the ventricles. During atrial diastole, blood enters the right atrium through the superior and inferior vena cava and the left atrium via the pulmonary veins. In the early part of this phase, the atrioventricular valves are closed and blood pools in the atria.
There comes a point when the pressure in the atrium is greater than the pressure in the ventricle of the same side. This pressure difference results in the opening of the atrioventricular valves, allowing blood to flow into the ventricle.
The autonomous sinuatrial node initiates an action potential that is propagated throughout the atrial myocardium. The electrical depolarization results in simultaneous contraction of the atria, thus forcing any residual blood from the upper chambers into the lower chambers of the heart. The atrial contraction causes a further increase in atrial pressures.
During the early stages of ventricular diastole, both the atrioventricular and semilunar valves are closed. During this phase, there is no change in the amount of blood in the ventricle, but there is a precipitous fall in the intraventricular pressure. This is known as isovolumetric relaxation.
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Eventually, the ventricular pressure becomes less than the atrial pressure, and the atrioventricular valves open. This results in filling of the ventricles with blood, which is often referred to as the rapid filling of the ventricles. It accounts for most of the blood that is in the ventricle before it contracts. A small volume of blood flows directly into the ventricles from the venae cavae. Towards the end of ventricular diastole, any residual blood in the atria is pumped into the ventricle. The total volume of blood present in the ventricle at the end of diastole is called the end-diastolic volume or preload.
Ventricular systole refers to the period of contraction of the ventricles. The electrical impulse arrives at the atrioventricular node (AV node) shortly after the atria are depolarized. There is a small delay at the AV node, which allows the atria to complete contracting before the ventricles are depolarized. The action potential passes to the AV node, down the bundle of His, and subsequently to the left and right bundle branches (conductive fibers that travel through the interventricular septum and branches to supply the ventricles). These fibers carry the electrical impulses through their respective ventricular territories, leading to ventricular contraction.
As the ventricle begins to contract, the pressure exceeds that of the corresponding atrium, resulting in the closure of the atrioventricular valves. At the same time, the pressure is not sufficient to open the semilunar valves. Therefore, the ventricles are in a state of isovolumetric contraction – as there is no change in the overall volume (end-diastolic volume) in the ventricle.
As the ventricular pressure exceeds the pressure in the outflow tract, the semilunar valves open, allowing blood to leave the ventricle. This is the ejection phase of the cardiac cycle. The amount of blood left in the ventricle at the end of systole is known as the end-systolic volume (afterload, between 40 – 50 ml of blood). The amount of blood actually ejected from the ventricle is known as the stroke volume output. The ratio of the stroke volume output to the end-diastolic volume is called the ejection fraction and usually amounts to around 60%.
The ventricles re-enter in a state of isovolumetric relaxation and the atria continue to fill. The process starts over and continues to repeat for as long as the individual is alive.
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The American-born physiologist Dr. Carl J Wiggers has provided many health care students over the past 100 years with a unique tool to understand the cardiac cycle. The Wiggers diagram highlights the relationship between pressure and volume over time, along with the electrical activity of the heart. The diagram uses the left chambers of the heart to demonstrate:
- Aortic pressure
- Atrial pressure
- Ventricular pressure
- Ventricular volume
- Electrocardiogram (ECG)
- Phonocardiogram (heart sounds)
The aortic pressure graph shows the change in pressure within the aorta throughout the cardiac cycle. The graph has a moderate incline followed by a notch, then a smaller incline. The graph ends with a gradual decline before starting over.
The increase in ventricular pressure during systole causes the aortic valve to open. The pressure generated in the ventricle is then transmitted to the aorta. The walls of the aorta are able to dilate due to their high elasticity in order to accommodate the sudden, dramatic increase in pressure. These pressure changes are represented by the first and largest wave on the aortic pressure graph.
At the end of systole, the left ventricle stops contracting but the aorta maintains relatively higher pressures. The sudden change in the pressure gradient results in a small backflow of blood into the left ventricle just before the aortic valves close. This is represented on the aortic pressure graph by a sharp decline or ‘incisura’ and then a sharp increase. The aortic pressure then gradually decreases throughout ventricular diastole until it reaches its resting pressure.
This graph is similar to the pressure relationship between the right ventricle and the pulmonary artery. The main difference is that the pressure is significantly lower.
The atrial pressure wave shows the change in the atrial pressure during systole and diastole. There are three significant pressure changes represented by the letters a, v, and c. The pressure change generated as the atria fill with blood is represented by the ‘v’ wave towards the end of the atrial pressure wave. There is a slight decline in the atrial pressure that corresponds with the opening of the atrioventricular valve. This is followed by the ‘a’ wave which represents the contraction of the atria. The ‘a’ wave is followed by a downward slope as the atrioventricular valves close. This is followed by another increase labeled as the ‘c’ wave. This represents bulging of the atrioventricular valves into the atria during ventricular contraction.
Ventricular pressure and volume
The pressure and volume changes that occur in the ventricle is represented on two separate curves. However, they are best interpreted together. The ventricular pressure curve has two waves – an initial small wave followed by a return to the baseline pressure, then a significantly larger wave. The ventricular volume curve, however, has a mixture of sudden and gradual slopes and inclines throughout its cycle.
Consider the start of the ventricular volume curve at the beginning of diastole. Here, there is a residual volume of about 50 mL of blood left in the ventricle. At this point, the pressure curve is on a sharp decline during isovolumetric relaxation. Once the ventricular pressure is less than the atrial pressure, the atrioventricular valve opens. There is a rapid increase in the ventricular volume followed by a slow gradual increase (in-keeping with the passive filling phase). During this time, the ventricular pressure remains unchanged as the chamber is able to accommodate the increasing volume.
The first increase in the ventricular pressure occurs as the atria contract to pump residual blood into the ventricle. This increase doesn’t last for a long time and the ventricular pressure soon returns to baseline. At this time more blood is being pumped into the ventricle, bringing it to its end-diastolic or preload volume. At the beginning of systole, the atrioventricular valves are closed and the ventricle is in isovolumetric contraction. So there is a sharp increase in pressure but the volume remains the same. Once the ventricular pressure overcomes the aortic pressure, the aortic valves open and there is a sudden fall in ventricular volume. As the volume decreases, the ventricular pressure begins to fall as well. Eventually, the ventricle stops contracting, re-enters the diastolic phase, and begins isovolumetric relaxation.
Electrocardiogram (ECG or EKG)
The electrocardiogram is a graphical representation of the electrical activity across the heart. It is comprised of a series of waves that represent depolarization and troughs that represent repolarization. If you need a refresher on the basic principles of the ECG, please refer to other articles on Kenhub that covers this material.
There is a lag between the depolarization of the myocardiocytes and the actual contraction of the muscles. As a result, the waves of the ECG will precede the waves of the pressure curves (which are caused by actual contraction of the heart muscle). The ‘P’ wave which represents atrial depolarization precedes the ‘a’ wave of the atrial pressure graph. The ‘QRS’ complex represents ventricular depolarization, which causes the ventricles to contract. The large wave of the ventricular pressure graph begins shortly after the ‘QRS’ wave. The ‘T’ wave of the ECG represents a time of ventricular repolarization and subsequent relaxation. Therefore, this wave starts toward the end of systole.
Phonocardiogram (heart sounds)
The phonocardiogram represents the heart sounds throughout the cardiac cycle. These heart sounds are which are appreciated during auscultation represent the effects of the heart valves as they close. They are commonly referred to as the “lub” and “dub” sounds.
The first heart sound or S1 or the “lub” sound is caused by the closure of the atrioventricular valves. This occurs at the beginning of ventricular systole. It can be graphically represented at the point after the first ventricular pressure wave. This coincides with the ‘a’ wave of the atrial pressure wave, and the ‘R’ wave of the ECG.
The second heart sound or S2 or the “dub” sound is caused by the closure of the semilunar valves. This occurs at the beginning of diastole, during the isovolumetric relaxation phase. It coincides with the ‘incisura’ of the aortic pressure curve and the terminal end of the ‘T’ wave of the ECG.
It is not abnormal to hear a third heart sound or S3 at times. This is usually caused by a sudden rush of blood into the ventricles from the atria. It is, therefore, most commonly a mid-diastolic sound that occurs after S2.
The heart has a remarkable capacity to accommodate an increased volume of blood coming into the heart. In fact, increasing the end-diastolic volume also results in an increase in cardiac output. This principle has been described by two renowned physiologists, and therefore referred to as the Frank-Starling mechanism of the heart. The underlying principle is that the heart will pump all the blood that returns to it by way of the veins, within physiological limits.
When there is an increase in ventricular preload, the ventricle is distended and by extension, the myocardiocytes are also stretched. This distension brings the actin and myosin components of the muscle fiber to a more optimal degree. Consequently, the muscle fibers will contract with a greater force in order to pump the extra blood. Note, however, that this principle is only valid up to an optimal point. Any further distension beyond that point will dissociate the actin-myosin complex, making it difficult for a contraction to occur.
Disorders affecting the cardiac cycle
The cardiac cycle is a highly coordinated process that keeps blood moving throughout the body. It is heavily dependent on tight choreography of events and any disruption of these events can be detrimental. Some of these problems can occur acutely (electrolyte imbalances) or may take years to develop (heart failure).
Electrolytes are important ions found both within cells and in the extracellular fluid. They are particularly important in generating and propagating action potentials. One particularly important ion as it pertains to activation of muscle action potentials is potassium (K+). Potassium ions are important in altering the cells’ resting membrane potential. Significant increase or decrease in the amount of these ions in the extracellular fluid (hyperkalemia and hypokalemia) can be fatal.
A build-up of potassium ions in the blood is referred to as hyperkalemia. The presence of more potassium ions outside the cells changes the electrical gradient across the cell membrane. As a result, the cell membrane becomes less negative and is initially more easily excitable. However, as the potassium concentration increases more, fewer sodium ion channels are recruited during depolarization. This results in a decline in the influx of sodium ions into the muscle cells and consequently a slower generation of action potential and eventually a reduction in the conduction of the impulse. Hyperkalemia can also cause AV nodal block, which impairs the passage of the depolarization wave to the ventricles.
Hyperkalemia is most detrimental when it develops over a short period of time. While some patients may remain asymptomatic, others may complain of chest pain, shortness of breath, muscle paralysis, and palpitations. There are classic signs on the ECG tracing that are highly suggestive of hyperkalemia:
- The T waves become tall and peaked because of the sudden repolarization
- The P wave widens and becomes flattened due to paralysis of the atria
- The PR interval widens due to a delay in the conduction from the SAN to the AVN
- The QRS complex becomes wider and may eventually blend with the T wave. This results from the AV nodal block.
Essentially, the heart becomes flaccid, dilated, and slow. This decreased contractility results in a decrease in the forward movement of blood, which can be fatal.
A significant fall in the number of potassium ions in the blood is referred to as hypokalemia. Hypokalemia has the opposite effect on the membrane potential than hyperkalemia. The decrease in extracellular potassium causes the cellular membrane to become more negative, resulting in an increase in the electrical gradient across the membrane. While this makes it more difficult for other cells to depolarize, an increased electrical gradient causes faster depolarization of myocardiocytes. This effect is most profound at the Purkinje fibers, which are most sensitive to changes in potassium concentration.
The increased excitability at points other than the pacemaker site predisposes the heart to develop ectopic heartbeats. These may lead to uncoordinated contraction of the ventricles and varying types of ventricular arrhythmias.
Additionally, a dramatic fall in the serum potassium level can also cause inhibition of some potassium ion channels. This impairs the transportation of potassium from the intracellular to the extracellular space. Consequently, ventricular repolarization is impaired and the cell may become depolarized prematurely. This can cause reentrant rhythms and other arrhythmias to occur. These repolarization abnormalities can be appreciated on ECG as:
- Flattening and inversion of the T wave
- More prominent U waves
- Depression of the ST segment
- Prolonged QT intervals
The rapid, irregular heart is no longer effective in propelling blood forward through the circulatory system.
Heart failure is a syndrome that refers to the inability of the heart to move blood forward through the circulatory system. This is often the common final pathway of many different forms of heart failure. Heart failure may occur as a result of reduced contractility of the ventricles or increased resistance to blood flow. Both these factors are the hallmark features of systolic dysfunction. On the other hand, the ventricles may not relax properly or the walls may be too stiff, thus impairing cardiac filling. These features are typical of diastolic dysfunction.
Heart failure can be further subdivided into right and left heart failure depending on the symptoms and signs present. Patients with left heart failure often have a history of chronic, uncontrolled (or poorly controlled) systemic hypertension, valvular insufficiency, or dilated cardiomyopathy. Patients may experience:
- Shortness of breath
- Paroxysmal nocturnal dyspnea
- Coughing with or without rusty sputum
In contrast, patients with right heart failure may have a history of pulmonary hypertension, tricuspid insufficiency, pulmonary stenosis, or left heart failure (referred to as left to right heart failure). In the absence of left heart failure, symptoms of right heart failure include:
- Peripheral edema
- Sacral edema
- Weight loss (cardiac cachexia)
Although there are many compensatory mechanisms that mitigate the progression of heart failure, the process – once it has begun – cannot be reversed. Patients may continue to compensate for the impaired cardiac function; they may still have acute decompensation following illness or noncompliance with medication or dietary restriction.
Cardiac cycle: want to learn more about it?
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