8 Phases Of Cardiac Cycle

Cardiac Cycle

A cardiac cycle is defined as the steps involving the conversion of deoxygenated claret to oxygenated blood in the lungs and pumping information technology past the heart to the body through the aorta [40].

From: Healthcare Data Analytics and Management , 2019

Anatomical photo representations for cardiac imaging training

I. Lakshmi , in Image Processing for Automated Diagnosis of Cardiac Diseases, 2021

3.ane.2 The cardiac cycle and electrical activation

The cardiac cycle is a series of electrical and mechanical events that occur during the phases of heart relaxation (diastole) and contraction (systole). The ventricular diastolic stage involves blood flow from the atria to the ventricles, and the ventricular systole includes blood menses from the ventricles to the pulmonary artery and the aorta. Cardiac systole is the myocardial cells' mechanical response to an electrochemical stimulus originating from the sinoatrial (SA) node. By acting every bit a pacemaker it controls the cardiac cycle. The electric activity originating from the SA node propagates through the centre's fibrous skeleton (showtime the atrial mass, and then the AV node) and the subsequent depolarization moving ridge from superlative to bottom of the center triggers the mechanical activation (cf. Refs. [ii, 3]). The conduction of the electrical activity through the fibrous skeleton tin be seen on an electrocardiogram (ECG), as shown in Fig. 3.three.

During each heartbeat, the ECG recording represents the electrophysiological activity and is obtained using electrodes mounted on the skin. In the aforementioned effigy the conduction at the atria is shown as the P-wave and the PR interval corresponding to the delay in the AV node follows. The propagation of electric activity across the ventricular myocardium creates the QRS complex, and the T-wave is known as ventricular repolarization (relaxation of the muscles). In imaging devices, the ECG signal is often widely used as a gating signal to capture heart images at unlike phases of the middle bike.

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Biofluid Dynamics in Homo Organs

Ali Ostadfar PhD , in Biofluid Mechanics, 2016

four.1.2 The Cardiac Bicycle

The cardiac cycle describes the sequence of electrical and mechanical events that occurs with every heartbeat. The normal elapsing of a cardiac cycle for a heart rate of 75 beats/minutes is 0.8 seconds [iii],

(4.i) $Duration of cardiac cycle (seconds / beats) = \frac{lx (seconds / minutes)}{Centre rate (beats / minutes)}$

The cardiac bicycle may exist divided into phases in any number of methods, for example four phases [ane,3] or 7 phases [2]. In the four phases method, the opening and closing of the center valves explains this method of the cardiac cycle. These phases are [i,iii]:

▪: Phase I: Filling period—the inlet valve is opened to fill up the ventricle and the outlet valve is airtight. The volume of claret in the ventricle increases from about 45 mL (from previous cycle) to about 115 mL.
▪: Phase Ii: Period of isovolumetric contraction—both valves are closed, blood volume is constant only the blood pressure increases to about 80 mmHg.
▪: Phase III: Period of ejection—the outlet valve of the ventricle is opened and the inlet is closed and due to more than wrinkle, the blood pressure level rises.
▪: Phase IV: Menstruum of isovolumetric relaxation—both valves are airtight and intraventricular pressure decreases without any blood volume changes.

The flow of relaxation is called diastole in which the ventricle fills with blood and the menstruum of ventricle wrinkle is called systole. Fig. 4.4 shows the cardiac wheel events for the left pump of the heart for two consummate cycles. This effigy illustrates the pressure–volume of the events. The top three curves illustrate the force per unit area changes in the left pump of heart including the aorta, left ventricle and left atrium. The 4th curve from the top denotes the volume changes in the left ventricle, the fifth one is electrocardiogram bend and the sixth bend denotes phonocardiogram (PCG; heart sound).

Electrocardiogram (ECG) of cardiac cycle: The ECG is a full general clinical device used to measure the electrical activity of the center. This device records the modest extracellular signals which are produced by the move of cardiac action potential through the transmembrane ion channels in the myocytes. This cardiac potential can be measured past microelectrodes. Scientific experiments take proved that a membrane potential is almost −ninety mV for a resting ventricular myocyte. The ECG is recorded past an arrangement of electrodes at precise locations on the trunk surface. The electrodes are located on each leg and arm, and half-dozen electrodes are located on the chest to obtain a standard ECG. Fig. iv.5 shows a standard ECG and its waves (P, QRS and T). Repeating waves denote the sequence of depolarization and repolarization of the atrium and ventricles.

Depolarization of the left and right atrium muscle is reflected by the P wave and during this event the atrioventricular (AV) valve is open up and ventricle will exist filled with blood. The QRS denotes depolarization of ventricular muscle and it appears 0.16 seconds after the P wave, during this event, due to ventricle contraction, the ventricular pressure rises rapidly. The T wave reflects depolarization of both ventricles and they begin to relax [iii,4], see Fig. 4.iv.

Ordinarily, ECGs are recorded on paper with a vertical calibration of 1 mV/cm and a speed of 25 mm/seconds. In a normal record of ECG, a QRS follows each P wave. The shape of the ECG shows the heart function and it can reveal some centre problems, such every bit [2]:

▪: atrial flutter,
▪: atrial fibrillation,
▪: first-degree AV block,
▪: second-degree AV cake,
▪: tertiary-caste AV block,
▪: premature ventricular complex,
▪: ventricular tachycardia and
▪: ventricular fibrillation.

In the atrial pressure level graph of Fig. iv.4, there are three minor pressure level rises, a, c and v. The a wave occurs because of atrial contraction, the c wave occurs when the ventricles begin to contract, and the v wave occurs near to the end of ventricle contraction [1].

PCG of cardiac wheel: The opening and closing of the heart valves during the cardiac bike produces sounds and these sounds are recorded by a phonocardiograph. There are two major sounds (S ₁ and S ₂) and 2 other sounds (Southward ₃ and S ₄). The sound of S ₁ (sound of "lub") is for the closure of the AV valves (mitral and tricuspid valves), S ₂ (audio of "dub") is for the aortic and pulmonary valves, Southward _iii is a normal sound for children but for adults information technology is considered as a problem due to ventricular dilation and S ₄ is abnormal sound during atrium wrinkle due to changes in ventricle tissues. Come across Fig. four.4 for the location of these sounds in cardiac wheel.

The frequency range of heart sound is between x and 500 Hz with low intensity [v]. Heart murmurs are abnormal heart sounds and they are produced because of turbulent flow of blood in the centre. Simply a few heart problems produce abnormal noise, such as:

▪: regurgitation or back menstruum due to heart valve problems (mitral or aortic valves);
▪: stenosis or abnormal narrowing in mitral or aortic valves and
▪: other murmurs, such as patent ductus arteriosus, the ductus arteriosus fails to close in infants after nascency.

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Introduction

Lambros S. Athanasiou , ... Lampros K. Michalis , in Atherosclerotic Plaque Characterization Methods Based on Coronary Imaging, 2017

1.1.2 The Cardiac Wheel

The cardiac cycle includes two phases: diastole and systole ( Fig. ane.4). In the diastole phase, blood returns to the heart from the superior and interior vena cava and flows into the right atrium. The force per unit area in the right atrium increases as claret flows into it. When the pressure of the right atrium exceeds the force per unit area of the right ventricle, the tricuspid valve opens passively assuasive blood to catamenia into the correct ventricle. At the same time, the oxygenated blood returning from the lungs flows into the left atrium. Every bit left atrial pressure increases, the mitral valve opens and blood flows into the left ventricle.

In the systole phase, blood is forced to flow from the two atria into their respective ventricles as the atrial muscles contract due to the depolarization of the atria. There is a period chosen isovolumetric wrinkle during which the ventricles contract but the pulmonary and aortic valves are closed every bit the ventricles do non have enough strength to open them. The atrioventricular valves also remain closed during the isovolumetric contraction period. The semilunar valves open when the ventricular muscle contracts and generates claret pressure within the ventricle higher than inside the arterial tree. When the eye musculus relaxes the diastole stage begins again.

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The eye

David A. Rubenstein , ... Mary D. Frame , in Biofluid Mechanics (Third Edition), 2022

5.iii The cardiac bicycle

The cardiac cycle describes all of the events that occur during 1 heartbeat and during the latent time until the next heartbeat. It makes the most sense to describe these events starting from the initiation of an action potential within the SA node (run across Section 5.two). The cardiac bike consists of two phases: diastole and systole. Cardiac myocytes do non contract during diastole, and this is when the majority of blood fills the heart chambers. During systole, the myocytes contract and squirt blood from the detail chamber either into other center chambers or into the vascular system. This textbook and many other resources use the terms systole and diastole interchangeably with ventricular systole and ventricular diastole. The contraction cycle of the atria can be described past their ain systolic and diastolic pattern, however, the ventricular bike is much more meaning for the functionality of the heart and is typically the 1 referenced during normal word.

To depict the cardiac bicycle, the aortic pressure, the left ventricular pressure, the left atrial pressure, the left ventricular volume, and the ECG are overlaid onto ane figure that is plotted against time (Fig. 5.10; a like effigy can exist drawn for the right side of the middle, with pressure values that are approximately i-sixth of the value compared with the left side of the eye). Recall that the ECG P moving ridge is associated with atrial depolarization. During this time, the mitral valve is open and the left atrium forces the remaining blood into the left ventricle, effectively priming the left ventricles for contraction. This priming action occurs because during much of left ventricular diastole (and left atrial diastole), the left atrial pressure is higher than the left ventricular pressure, which suggests that the mitral valve is open. Any blood that enters the left atria from the venous pulmonary circulation passes directly into the left ventricles. Hence, one can notice a steady ascent in ventricular volume during the diastolic portion of the cardiac cycle. During atrial systole, x to 20 mL of claret is forced into the ventricles, which acts to expand the ventricular muscle mass. This expansion causes an initial elastic recoil response, in add-on to the ventricle muscle contraction, to aid in moving claret through the cardiovascular system. Note again that although we are discussing the left side of the heart, the same pattern is observed on the right side of centre (eastward.one thousand., during ventricular diastole, blood passes from the right atria direct into the correct ventricles).

Upon the onset of the QRS complex, there is a rapid increase in ventricular pressure because of ventricle contraction. This is associated with the closing of the mitral valve and isovolumic contraction of the ventricle. The left ventricle contracts for a short amount of time without losing book considering both the mitral valve and the aortic valve are airtight and we assume that the compressibility of blood is negligible. As the QRS complex ends, the aortic valve opens (as a outcome of the left ventricle pressure surpassing the aortic pressure) and the left ventricle ejects blood into the systemic circulation. The duration of ventricle wrinkle is termed systole. The volume of blood in the ventricles reduces from approximately 120 mL to approximately 45 mL, which is termed the residual ventricular volume or finish-systolic volume. The difference between the terminate-diastolic volume and the end-systolic volume is referred to every bit the stroke volume. During systole, the T wave is recorded, and this is when the ventricles begin to relax. At this fourth dimension, the vascular pressure (due east.thou., aortic) is however lower than the ventricular pressure, so that blood continues to be ejected out of the eye for a few milliseconds. Toward the cease of the T wave, the aortic valve closes (because the left ventricular force per unit area drops below the aortic pressure) and the ventricle enters the isovolumic relaxation phase, which marks the get-go of ventricular diastole. Afterwards a few milliseconds, the pressure in the ventricles returns to approximately ane mmHg and the mitral valve opens again. At this point, diastole continues until the ventricles begin to contract and the mitral valve closes in one case again. As mentioned earlier, during the entire period of diastole, even though the left atrium is non contracting, the left ventricle is filling with blood. In fact, approximately 75% of the blood that enters the atrium passes directly into the ventricle without the aid of atrial contraction. During atrial contraction, the remaining blood volume enters the ventricles. Annotation that the word was for the left side of the heart, which is shown in Fig. 5.10. A similar give-and-take for the correct side of the centre could be conducted, merely the pressure level would be reduced compared with the left side of the heart and the volumes are subtly unlike, although the stroke book is largely the same.

The force per unit area in the atria remains fairly abiding (and low) during the entire cardiac cycle. However, three major changes occur within the atrial pressure level waveform, and they are denoted as the a (atrial contraction), c (ventricular contraction), and v (venous filling) waves. The a wave is associated with atrial contraction and occurs immediately after the P moving ridge of the ECG. During the a wave, both atria experience an increment in pressure of virtually vi to seven mmHg, with the left atrium experiencing a slightly higher force per unit area increase than the correct atrium. The c moving ridge corresponds to the first of ventricular contraction and occurs immediately after the QRS circuitous of the ECG. This is caused primarily past the increased ventricular pressure level acting on the AV valves. In improver, at the commencement of systole, at that place is a pocket-sized amount of blood backflow into the atria considering the valves have not yet fully closed. Combined, these two changes induce an increase in atrial pressure level. The v wave represents a steady increase in atrial pressure that occurs during ventricular contraction, which is acquired by venous claret from the systemic or pulmonary circuits entering the atria. When the AV valves reopen, this increased pressure aids in claret motion straight into the ventricles without atrial contraction.

Fig. 5.10 depicts the cardiac wheel for the left ventricle, left atrium, and aorta. The aortic force per unit area curve is what is estimated when a patient has his or her blood pressure taken, or more accurately, the maximum aortic pressure and the pressure level at which the aortic valve opens. At the point that the aortic valve opens, the pressure level in the aorta increases because of blood being forced into the vascular system from the left ventricle. At peak systole, the claret pressure in the aorta reaches approximately 120 mmHg nether normal healthy man developed conditions. At the point that the aortic valve closes, the pressure in the aorta is approximately 100 mmHg. At the time of valve closure, the pressure increases by approximately 5 to ten mmHg every bit a effect of aortic rubberband recoil and claret passing from the apex of the aortic arch back toward to the aortic valve. The backflow of blood occurs considering the left ventricular pressure has dropped below the aortic pressure, and then the pressure level slope favors blood moving downwardly the aortic arch toward both the abdominal aorta and the aortic valve (e.g., the dissimilar sides of the curvation). The slight rise in the aortic pressure is termed the dicrotic notch. The following rise in aortic pressure is referred to as the dicrotic moving ridge. So, as a result of the viscoelastic recoil of the aorta, there is a slow, merely continual, subtract in aortic pressure level during diastole. At the end of diastole and the isovolumic contraction stage, the aortic pressure is approximately 80 mmHg. Once the left ventricular pressure surpasses this, the aortic valve opens and the pressure increases again to approximately 120 mmHg.

An additional interesting betoken is the audio that the heart makes during the cardiac cycle. A physician tin heed to these sounds with a stethoscope. These sounds are caused by first the closure of the AV valves and then the closure of the semilunar valves. The sounds are generated by the valve vibrations during the closing process. As mentioned previously, the AV valves tin bulge into the atrium and the semilunar valves can burl into the ventricles immediately subsequently closure. This is caused by an increase and a reversal in the force per unit area slope beyond the leaflets. With respect to the AV valves, the papillary muscles and the tendons that attach to the valves (the chordate tendineae) experience recoil, inducing valve leaflet vibration. The semilunar valves are highly elastic and experience recoil because of the pressure divergence. This elastic recoil generates an audible audio.

As we know, the middle beats approximately 72 beats per minute for an average human. Comparing between other animals, one tin see that center rate is inversely proportional to trunk mass (Fig. 5.11). Many models can be used to draw this human relationship, some of which account for if the beast is warm-blooded or cold-blooded, what the daytime activity of the fauna is, and how the animal developed from an evolutionary standpoint. For this textbook, it is important to proceed in mind that, in full general, animals with a lower mass volition accept a college centre rate compared with animals with a larger mass.

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Normal Cardiac Physiology and Ventricular Office

B.D. Hoit , in Reference Module in Biomedical Sciences, 2014

The Cardiac Bike

The cardiac cycle describes pressure level, book, and flow phenomena in the ventricles as a function of time. This bicycle is similar for both the left and right ventricles, although in that location are differences in timing, which stem from differences in the depolarization sequence and the levels of pressure in the pulmonary and systemic circulations. For simplicity, the cardiac cycle for the left heart during one trounce has been described ( Figure x).

The QRS circuitous on the surface ECG represents ventricular depolarization. Contraction (systole) begins after an approximately 50 ms delay and results in closure of the mitral valve. The left ventricle contracts isovolumetrically until the ventricular pressure exceeds the systemic pressure, which opens the aortic valve and results in ventricular ejection. Bulging of the mitral valve into the left atrium during isovolumetric contraction causes a slight increase in left atrial pressure (c moving ridge). Shortly afterwards ejection begins, the active state of ventricular myocardium declines and ventricular pressure begins to decrease. Left atrial pressure level rises during ventricular systole (5 wave) every bit claret returns to the left atrium by means of the pulmonary veins. The aortic valve closes when left ventricular pressure falls below aortic force per unit area, and momentum briefly maintains frontwards flow despite greater aortic than left ventricular pressure. Ventricular pressure then declines exponentially during isovolumetric relaxation, when both the aortic and mitral valves are airtight. This begins the ventricular diastole. When ventricular pressure declines beneath left atrial pressure, the mitral valve opens and ventricular filling begins. Initially, ventricular filling is very rapid because of the relatively large pressure level slope betwixt the atrium and ventricle. Ventricular pressure continues to decrease later mitral valve opening considering of connected ventricular relaxation; its subsequent increase (and the decrease in atrial force per unit area) slows ventricular filling. Specially at low end-systolic volumes, early on rapid ventricular filling can be facilitated past ventricular suction produced past elastic recoil. Ventricular filling slows during diastasis, when atrial and ventricular pressures and volumes increase vary gradually. Atrial depolarization is followed past atrial contraction, increased atrial pressure level (a wave), and a 2nd, late rapid-filling phase. A subsequent ventricular depolarization completes the bicycle.

Valve closure and rapid-filling phases are audible with a stethoscope placed on the chest and can be recorded phonocardiographically after electronic distension. The offset heart sound, resulting from cardiohemic vibrations with closure of the AV (mitral, tricuspid) valves, heralds ventricular systole. The second centre sound, shorter and composed of higher frequencies than the first, is associated with closure of the semilunar valves (aortic and pulmonic) at the end of ventricular ejection. 3rd and quaternary heart sounds are low-frequency vibrations caused past early rapid filling and late diastolic atrial contractile filling, respectively. These sounds can be heard in normal children, just in adults they normally indicate disease.

An alternative time-contained representation of the cardiac bike is obtained past plotting instantaneous ventricular pressure and volume (Figure 11). During ventricular filling, pressure and volume increase nonlinearly (phase I). The instantaneous gradient of the pressure–volume (P-V) curve during filling (dP/dV) is diastolic stiffness, and its inverse (dV/dP) is compliance. Thus, every bit bedchamber book increases, the ventricle becomes stiffer. In a normal ventricle, operative compliance is loftier, because the ventricle operates on the flat portion of its diastolic P-V curve. During isovolumetric wrinkle (stage Ii) pressure increases and book remains constant. During ejection (phase Iii) pressure rises and falls until the minimum ventricular size is attained. The maximum ratio of force per unit area to volume (maximal active chamber stiffness or elastance) normally occurs at the end of ejection. Isovolumetric relaxation follows (phase 4), and when left ventricular pressure falls beneath left atrial force per unit area, ventricular filling begins. Thus, end-diastole is at the lower right-mitt corner of the loop, and terminate systole is at the upper left corner of the loop. Left ventricular P-V diagrams can illustrate the effects of changing preload, afterload, and inotropic country in the intact ventricle (run across the following).

A P-5 loop can also be described for atrial events (Hoit et al., 1994). During ventricular ejection, descent of the ventricular base lowers atrial pressure level and thus assists in atrial filling. Filling of the atria from the veins results in a v wave on the atrial and venous force per unit area tracing. When the mitral and tricuspid valves open, blood stored in the atria empties into the ventricles. Atrial contraction denoted by an a wave on the atrial force per unit area tracing actively assists ventricular filling. The resultant atrial P-V diagram has a figure-of-viii configuration with a clockwise V loop, representing passive filling and emptying of the atria and a counterclockwise A loop, representing active atrial contraction. Thus, the atria function equally a reservoir and conduit for venous flow (during ventricular systole and diastole, respectively), and as a booster pump for ventricular filling late in diastole.

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Computational Modelling of Cardiac Biomechanics

Emiliano Votta , Alberto Redaelli , in Modelling Methodology for Physiology and Medicine (2d Edition), 2014

20.seven.iii Heart Valve–Blood Interaction

During the cardiac bicycle, middle valves open and close due to their interaction with blood. The most accurate style to account for it is FSI modelling. However, the latter is even more challenging than ventricle FSI modelling, due to the abrupt nature of valve transient closure and opening. It is also due to leaflets' coaptation, which implies the apply of very fine fluid meshes and of small-scale time steps in the numerical solution of the trouble, thus leading to excessive computational expense. As a result, FSI modelling is commonly adopted only in arcadian models characterized by simple geometries and nonphysiological parameter ranges (eastward.g., blood majority modulus and Reynolds number), although Chandran and Vigmostad lately proposed the preliminary results of their in-dwelling house FSI algorithm allowing for patient-specific simulations with physiologic Reynolds numbers, realistic fabric properties, and highly resolved grids [35]. With this exception, in advanced patient-specific models it is usual to account for claret pressure simply by applying time-dependent distributed pressure loads on the leaflets surfaces.

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Biological Electrical Potentials: Their Display and Recording

P.D. Davis BSc CPhys MIstP MIPSM , ... G.N.C. Kenny BSc (Hons) Physician FRCA , in Basic Physics and Measurement in Amazement (Fourth Edition), 1995

ECG

During a cardiac cycle a wave of depolarization passes from the atrial pacemaker cells over the atrium and down the AV bundle to spread through the ventricular myocardial syncytium. Potentials from the heart are transmitted through the tissues and can exist detected by electrodes to give an ECG recording. These potentials are attentuated equally the indicate passes through the tissues. Hence the size of the ECG signal detected is only one to 2 mV instead of the original potential of about 90 mV mentioned in a higher place. The larger the bulk of the cardiac muscle through which the waves of depolarization pass, the larger the potential detected at the surface, so there is a big QRS complex from the depolarization wave in the ventricles and a smaller P wave from the atria.

The actual appearance of the ECG depends on the position of the electrodes relative to the heart (Fig. 15.ii). Because the atrial bespeak spreads outwards, the P wave is usually positive regardless of the electrode position. Nonetheless, in the example of the ventricles the wave of depolarization travels downwards and to the left, and so the QRS complexes vary in appearance according to the electrode position. With an oesophageal electrode positioned close behind the atria of the heart a specially clear ECG signal of the P waves is obtainable. The fourth dimension intervals in the complexes are important. For example, a PR interval of over 200 ms indicates delayed conduction from the atria.

Because other muscles requite rise to potentials prior to contaction, the patient must relax and brand no movement during the recording.

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Contractile function and eye failure

E. Donal , ... A. Manrique , in Advanced Cardiac Imaging, 2015

12.ii Echocardiographic approach to the LV contractility

During a cardiac wheel, the LV wall shortens, thickens, and twists along the long axis. Shortening and thickening can be quantified past measuring regional strains. Strain or myocardial deformation from developing forces is expressed as either the fractional or the percent modify from the original dimension [ 17,18]. Positive radial strains represent wall thickening (radial deformation), whereas negative strains represent segment shortening (east.g., circumferential shortening, longitudinal shortening, and fiber shortening) [14].

3 perpendicular axes orienting the global geometry of the LV ascertain the local cardiac coordinate system: radial, circumferential, and longitudinal.

Echocardiographic techniques like tissue Doppler imaging take excellent temporal resolution (± 4 ms) and could be used for the assessment of myocardial deformations [14] (see Chapter 2).

The base and apex of the LV rotate in opposite directions. Twist defines the base to apex gradient in the rotation angle along the longitudinal axis of the LV and is expressed in degrees per centimeter [9,23]. Torsion and twist are equivalent terms. Torsion tin can also be expressed equally the centric gradient in the rotation angle multiplied by the average of the outer radii in apical and basal cross-sectional planes, thereby representing the shear deformation angle on the epicardial surface (unit of measurement degrees or radians) [23]. This normalization can be used as a method for comparing torsion for different sizes of LV. When the apex-to-base of operations deviation in LV rotation is not normalized, the absolute difference (also in degrees or radians) is stated as the net LV twist angle [24].

Speckle-tracking echocardiography (STE) has emerged every bit an culling technique [25] (see Chapter two). The robustness and the clinical applicability of that technique are nowadays merely validated for the assessment of global longitudinal strain [26,27]. When considering regional longitudinal strains, there are inaccuracies according to the software used. Longitudinal LV mechanics, which are predominantly governed past the subendocardial region, are the well-nigh vulnerable component of LV mechanics and therefore most sensitive to the presence of myocardial disease. The start of them is the ischemic etiology that volition affect first the subendocardium. The mid-myocardial and epicardial function may remain relatively unaffected or weakly bear upon in patients with HF and preserved LV EF. Circumferential strain and twist may remain normal or bear witness exaggerated compensation for preserving LV systolic functioning. Increase in cardiac muscle stiffness, all the same, may cause progressive delay in LV untwisting. Loss of early diastolic longitudinal relaxation and delayed untwisting attenuate LV diastolic operation, producing elevation in LV filling pressures and a phase of predominant diastolic dysfunction, although the LV EF may remain normal. The diagnostic of these HF with preserved ejection that most affect the subendocardium could be very hard and might require submaximal exercise stress echocardiographies [28]. It has not been proposed in past recommendation, but that could change [29].

On the other hand, an astute transmural insult (like a myocardial infarction) or progression of affliction results in concomitant mid-myocardial and subepicardial dysfunction, leading to a reduction in LV circumferential and twist mechanics and a reduction in LV EF. Assessment of myocardial function, therefore, can be tailored per the clinical goals. The detection of contradistinct longitudinal function alone may suffice if the overall goal of analysis is to detect the presence of early myocardial illness. Further label of radial strains, circumferential strains, and torsional part provides assessment of the transmural illness burden and provides pathophysiologic insight into the mechanism of LV dysfunction [30]. For example, the pathophysiologic process such every bit radiations that affects both the pericardium and the subendocardial region may produce attenuation of both longitudinal (start) and circumferential (afterwards) LV function [31]. Several studies have reported the strain values in patients with systolic HF (Tabular array 12.1), HF with preserved LV EF, and hypertrophied cardiomyopathies. The data proposed in Table 12.1 are rather convergent; however, these measurements of LV systolic longitudinal strains are not used or proposed in guidelines such as in those for HF with preserved LV EF.

Table 12.i. Principal studies published in the field of heart failure with depressed LV ejection fraction

Report	n	Population	Stop-point	Follow-upwardly duration	GLS prognostic value	LV EF in the population (calendar month)
Bertini et al. [32]	1060	Ischemic cardiomyopathies	Death, cardiovascular hospitalization	31 months	− 11.v%	Median = 34(25–58)
Mignot et al. [33]	147	Heart failure	idem	> 12-months	− 7%	Mean = 29.9 ± 8.ix
Donal et al. [34]	140	Heart failure	idem	38 months	− 8%	Mean = 30 ± 9%
Nahum et al. [35]	125	Heart failure	idem	viii.eight ± 6	− 9%	Hateful = 31 ± ten%
Lacoviello et al. [36]	308	Heart failure	et idem + maligant arrhythmias	26 ± 13
Cho et al. [37]	201	Heart failure	Cardiac death + cardiovascular hospitalization	39 ± 17	Not available − 10.7% for hateful circumferential strain	Mean = 34 ± xiii%

GLS, global longitudinal strain.

Equally a rule of pollex, a global longitudinal strain less than − 17% is an independent parameter of severity of the cardiomyopathy [33]. In HF with preserved LV EF, the prognostic cutting-off that is well-nigh frequently reported is − xvi% [38].

In more complex cardiomyopathies like those induced past anthracyclins, it seems that as presently as the global longitudinal strain is less than − 19%, physicians accept to advisedly monitor the patients. Studies are ongoing to know whether defended treatments similar ACE-inhibitor and B-blockers should be introduced [26].

Although strain data are valuable in patients with systolic HF, the indication for an ICD or a biventricular pace maker remains dependent upon the caste of LV dysfunction every bit determined by the LV EF (Figures 12.1 and 12.2). The LV EF should exist measured, co-ordinate to recommendations using the upmost four- and two-chamber views using the Simpson method. The M way should non be used especially in hearts having a spherical remodeling.

In the present and fifty-fifty more in the very near future, real-fourth dimension 3D echocardiography (RT3DE) should improve the robustness and reproducibility of the echo information [39–41]. Information technology is not yet available everywhere (see Chapter 2). Notwithstanding, improvements in transducer are required for the actual transfer of the 3D approach in clinical practise. Feasibility remains lower than for the 2d approach [42,43]. It has been demonstrated that in patients in whom serial examinations are obtained, the 3D echocardiographic approach is the most reliable [39,44].

Other approaches are bachelor (Figures 12.ane–12.four) [25,45]. Pulse tissue Doppler is the about relevant and is a way for assessing LV longitudinal systolic function too as MAPSE.

In improver to these measurements (LV EF required, global longitudinal strain, or pulse tissue Doppler), ane must measure the LV stroke volume (Doppler and volumetric approaches) for estimating the cardiac output and finally the efficacy of this LV contractility to eject enough blood in the arterial tree (Figure 12.5).

Also, as already mentioned, stress tests might be required to wait for contractile reserve, in detail. Without going into much detail in regard to the technique, dobutamine could be used, but submaximal practice stress echocardiography is probably the ideal approach to test the systolic response and the diastolic response of the failing heart. In HF with preserved ejection, the absence of systolic and diastolic reserve has already been mentioned. In ischemic heart disease, it has to be tested; sometimes, one is "surprised" to find that without any astute ischemia, the practise unmasks a dynamic functional mitral regurgitation that might be very useful for understanding the symptoms and is maybe the all-time handling of a patient with systolic HF [46].

In addition to the assessment of viability or contractile reserve, information technology might be necessary to look for myocardial ischemia. The techniques are the same every bit in a non-failing centre, being nonetheless aware of the risk of maximal dobutamine stress exam in patients with a failing heart (gamble of ventricular arrhythmia, in particular).

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The Electrocardiogram—A Brief Background

Leif Sörnmo , Pablo Laguna , in Bioelectrical Betoken Processing in Cardiac and Neurological Applications, 2005

half-dozen.vi.v High-Resolution ECG

For many years the estimation of resting ECGs was based on measurements derived from waves whose amplitude were at least several tens of microvolts; waves with smaller amplitudes were ignored since these were almost e'er acquired by noise. This limitation was, however, removed with the advent of the high-resolution ECG with which it became possible to detect signals on the society of i µ V thanks to point averaging techniques (therefore, these signals are sometimes denoted "micropotentials"). The high-resolution ECG has helped unlock novel information and has demonstrated that point processing for the purpose of racket reduction is a clinically viable technique. The acquisition procedure is usually the aforementioned as for the resting ECG, except that the signal is recorded over an extended time menstruum and then that a sufficiently low noise level is attained, i.e., sufficiently many heartbeats must exist bachelor for averaging.

In contrast to the averaging of evoked potentials, where information is available on when the external stimulus is elicited, the time reference ("fiducial betoken") must be determined from each individual heartbeat before ensemble averaging can be performed. The fiducial point must be accurate, otherwise depression-amplitude, high-frequency components of the ECG will be distorted by smearing (cf. Section iv.iii.6 on the furnishings of latency shifts). The high-resolution ECG rests on the assumption that the point to be estimated has a fixed beat-to-beat morphology, whereas betoken averaging during exercise must exist able to runway ho-hum changes in morphology. Since the highresolution ECG is often expected to incorporate loftier-frequency components, the sampling charge per unit is at least 1 kHz (a lower sampling charge per unit is sufficient in the other, higher up-mentioned ECG applications).

Several subintervals of the cardiac bike have received special attention in high-resolution ECG assay, and low-level signals take been considered in connectedness with

•: the package of His which depolarizes during the PR segment, i.e., an interval which in the resting ECG is considered silent [44, 45,
•: the terminal part of the QRS complex and the ST segment where late potentials may exist present [46–48],
•: intra-QRS potentials [49–51], and
•: the P wave [52–54].

Of these four applications, the analysis of late potentials has received the almost widespread clinical attention. Late potentials may be constitute in patients with myocardial infarction where ventricular depolarization tin can terminate many milliseconds subsequently the end of the QRS circuitous (Figure half-dozen.twenty). This prolongation is due to delayed and fragmented depolarization of the cells in the myocardium which surround the expressionless region (scarred tissue) caused by infarction; the conduction capability of the adjoining cells is severely impaired by infarction. Many studies have demonstrated the importance of belatedly potentials when, for example, identifying postinfarct patients at high risk of future life-threatening arrhythmias [55].

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Adaptive Reorientation of Myofiber Orientation in a Model of Biventricular Cardiac Mechanics

Marieke Pluijmert , ... Peter H.Chiliad. Bovendeerd , in Biomechanics of Living Organs, 2017

Remodeling of myofiber orientation

During simulation of the cardiac cycle, the myofiber orientation ${\vec{e}}_{f, 0}$ in the unloaded country changes into the actual myofiber orientation ${\vec{e}}_{f}$ , due to deformation of the tissue. In addition, remodeling of the extracellular matrix in response to load-induced damage and regular collagen turnover is considered to cause a structural modify of the myofiber orientation ${\vec{due east}}_{f, 0}$ in the unloaded state. The conceptual model of this procedure of remodeling of myofiber orientation is explained in item in Fig. 2. To describe remodeling induced changes, nosotros used the model by Kroon et al. (2009b), in which myofiber orientation changes according to the post-obit development equation:

(8) $\begin{array}{l} \frac{\partial {\vec{e}}_{f, 0}}{\partial t} = \frac{1}{κ} ({\vec{e}}_{f}^{*} - {\vec{e}}_{f, 0}) \end{array}$

with κ representing the adaptation time constant, which was ready to 4 times the cardiac cycle time. ${\vec{e}}_{f}^{*}$ is the actual myofiber orientation in the deformed tissue, corrected for rigid torso rotation:

(9) $\begin{array}{l} {\vec{e}}_{f} = \frac{F \cdot {\vec{e}}_{f, 0}}{λ_{f}} = \frac{R \cdot U \cdot {\vec{e}}_{f, 0}}{λ_{f}} = R \cdot {\vec{e}}_{f}^{*}; λ_{f} = | U \cdot {\vec{e}}_{f, 0} | \end{array}$

with λ _f the myofiber stretch ratio and F the deformation gradient tensor that consists of the actual deformation U and a rigid body rotation R . Rigid body rotations are non taken into account for accommodation, considering they cannot be sensed by the tissue. Myofiber reorientation only occurs if the unloaded fiber management ${\vec{e}}_{f, 0}$ does not coincide with any of the master strain directions (eigenvectors of U ), that is, in case of fiber cross-fiber shear. On the endo- and epicardial surfaces, the myofiber vector resulting from Eq. (8) was modified by projecting information technology onto the surface to ensure that myofibers practise not stick out of these surfaces.

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