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What are heart sounds?

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Where is the heart located in the human body?

In humans, the heart is situated between the two lungs and slightly to the left of center, behind the breastbone. It rests on the diaphragm, the muscular partition between the chest and the abdominal cavity.

What is the heart wall made up of?

The heart consists of several layers of a tough muscular wall, the myocardium. A thin layer of tissue, the pericardium, covers the outside, and another layer, the endocardium, lines the inside.

What causes the heart to beat?

The pumping of the heart, or the heartbeat, is caused by alternating contractions and relaxations of the myocardium. These contractions are stimulated by electrical impulses from a natural pacemaker, the sinoatrial, or S-A, node located in the muscle of the right atrium.

The rhythmic noises accompanying the heartbeat are called heart sounds. The two distinct sounds are heard, a low, slightly prolonged “lub” (first sound) occurring at the beginning of ventricular contraction or systole and a sharper, higher-pitched “dup” (second sound), caused by the closure of aortic and pulmonary valves at the end of systole.

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heart , organ that serves as a pump to circulate the blood . It may be a straight tube, as in spiders and annelid worms, or a somewhat more elaborate structure with one or more receiving chambers (atria) and a main pumping chamber (ventricle), as in mollusks. In fishes the heart is a folded tube, with three or four enlarged areas that correspond to the chambers in the mammalian heart. In animals with lungs —amphibians, reptiles, birds, and mammals—the heart shows various stages of evolution from a single to a double pump that circulates blood (1) to the lungs and (2) to the body as a whole.

In humans and other mammals and in birds , the heart is a four-chambered double pump that is the centre of the circulatory system . In humans it is situated between the two lungs and slightly to the left of centre, behind the breastbone; it rests on the diaphragm , the muscular partition between the chest and the abdominal cavity .

The heart consists of several layers of a tough muscular wall, the myocardium . A thin layer of tissue , the pericardium , covers the outside, and another layer, the endocardium , lines the inside. The heart cavity is divided down the middle into a right and a left heart, which in turn are subdivided into two chambers . The upper chamber is called an atrium (or auricle), and the lower chamber is called a ventricle . The two atria act as receiving chambers for blood entering the heart; the more muscular ventricles pump the blood out of the heart.

The heart, although a single organ, can be considered as two pumps that propel blood through two different circuits. The right atrium receives venous blood from the head , chest, and arms via the large vein called the superior vena cava and receives blood from the abdomen , pelvic region, and legs via the inferior vena cava. Blood then passes through the tricuspid valve to the right ventricle, which propels it through the pulmonary artery to the lungs . In the lungs venous blood comes in contact with inhaled air, picks up oxygen , and loses carbon dioxide . Oxygenated blood is returned to the left atrium through the pulmonary veins. Valves in the heart allow blood to flow in one direction only and help maintain the pressure required to pump the blood.

The low-pressure circuit from the heart (right atrium and right ventricle), through the lungs, and back to the heart (left atrium) constitutes the pulmonary circulation . Passage of blood through the left atrium, bicuspid valve, left ventricle, aorta , tissues of the body, and back to the right atrium constitutes the systemic circulation . Blood pressure is greatest in the left ventricle and in the aorta and its arterial branches. Pressure is reduced in the capillaries (vessels of minute diameter) and is reduced further in the veins returning blood to the right atrium.

The pumping of the heart, or the heartbeat , is caused by alternating contractions and relaxations of the myocardium. These contractions are stimulated by electrical impulses from a natural pacemaker, the sinoatrial , or S-A, node located in the muscle of the right atrium . An impulse from the S-A node causes the two atria to contract, forcing blood into the ventricles. Contraction of the ventricles is controlled by impulses from the atrioventricular , or A-V, node located at the junction of the two atria. Following contraction, the ventricles relax, and pressure within them falls. Blood again flows into the atria, and an impulse from the S-A starts the cycle over again. This process is called the cardiac cycle . The period of relaxation is called diastole . The period of contraction is called systole . Diastole is the longer of the two phases so that the heart can rest between contractions . In general, the rate of heartbeat varies inversely with the size of the animal . In elephants it averages 25 beats per minute, in canaries about 1,000. In humans the rate diminishes progressively from birth (when it averages 130) to adolescence but increases slightly in old age; the average adult rate is 70 beats at rest. The rate increases temporarily during exercise , emotional excitement, and fever and decreases during sleep . Rhythmic pulsation felt on the chest, coinciding with heartbeat, is called the apex beat. It is caused by pressure exerted on the chest wall at the outset of systole by the rounded and hardened ventricular wall.

The rhythmic noises accompanying heartbeat are called heart sounds . Normally, two distinct sounds are heard through the stethoscope : a low, slightly prolonged “lub” (first sound) occurring at the beginning of ventricular contraction, or systole, and produced by closure of the mitral and tricuspid valves, and a sharper, higher-pitched “dup” (second sound), caused by closure of aortic and pulmonary valves at the end of systole. Occasionally audible in normal hearts is a third soft, low-pitched sound coinciding with early diastole and thought to be produced by vibrations of the ventricular wall. A fourth sound, also occurring during diastole, is revealed by graphic methods but is usually inaudible in normal subjects; it is believed to be the result of atrial contraction and the impact of blood, expelled from the atria, against the ventricular wall.

Heart “murmurs” may be readily heard by a physician as soft swishing or hissing sounds that follow the normal sounds of heart action. Murmurs may indicate that blood is leaking through an imperfectly closed valve and may signal the presence of a serious heart problem. Coronary heart disease , in which an inadequate supply of oxygen-rich blood is delivered to the myocardium owing to the narrowing or blockage of a coronary artery by fatty plaques, is a leading cause of death worldwide.

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• J Cardiovasc Dev Dis

What Is the Heart? Anatomy, Function, Pathophysiology, and Misconceptions

Gerald d. buckberg.

1 Department of Cardiothoracic Surgery, David Geffen School of Medicine at UCLA, 10833 Le Conte Avenue, Room 62-258 CHS, P.O. Box 951741, Los Angeles, CA 90095-1741, USA

Navin C. Nanda

2 Division of Cardiovascular Diseases, University of Alabama at Birmingham, 1900 University Boulevard, Birmingham, AL 35233, USA; ude.bau@adnan

Christopher Nguyen

3 Cedars-Sinai Medical Center, 8700 Beverly Blvd. PACT, Suite 800, Los Angeles, CA 90048, USA; [email protected]

Mladen J. Kocica

4 UC Clinical Centre of Serbia, Clinic for Cardiac Surgery, 8th Kosta Todorovic St., 11000 Belgrade, Serbia

Associated Data

Cardiac dynamics are traditionally linked to a left ventricle, right ventricle, and septum morphology, a topography that differs from the heart’s five-century-old anatomic description of containing a helix and circumferential wrap architectural configuration. Torrent Guasp’s helical ventricular myocardial band (HVMB) defines this anatomy and its structure, and explains why the heart’s six dynamic actions of narrowing, shortening, lengthening, widening, twisting, and uncoiling happen. The described structural findings will raise questions about deductions guiding “accepted cardiac mechanics”, and their functional aspects will challenge and overturn them. These suppositions include the LV, RV, and septum description, timing of mitral valve opening, isovolumic relaxation period, reasons for torsion/twisting, untwisting, reasons for longitudinal and circumferential strain, echocardiographic sub segmentation, resynchronization, RV function dynamics, diastolic dysfunction’s cause, and unrecognized septum impairment. Torrent Guasp’s revolutionary contributions may alter future understanding of the diagnosis and treatment of cardiac disease.

1. Introduction

The current approach to understanding cardiac dynamics relies upon movements that adhere to the conventional topographical separation of cardiac muscle into the left ventricle, right ventricle, and septum. Functional analyses have addressed them independently, and this approach has resulted in many suppositions that this report will define and question.

Alternatively, cardiac muscle mass is formed by the helix and surrounding circumferential wrap described by Lower in the 1600s [ 1 ], Senac in the 1700s [ 2 ], Krehl in the 1800s [ 3 ], Mall in the 1900s [ 4 ], and more recently by Torrent Guasp [ 5 ]. The integrated function of this wrap and helical architectural configuration explains the heart’s mechanical actions [ 6 , 7 , 8 ].

For example, the left ventricular free wall and septum are usually discussed separately, yet both are formed by the same muscle ( Figure 1 ) and their function cannot be separated unless isolated focal lesions exist. For this reason, the anterior descending and posterior descending coronary arteries are simply vascular highways perched upon the top or bottom of the helical muscle forming the septum and its adjacent LV free wall.

( a ) Helical ventricular myocardial band unfolding. Upper left—intact heart. Upper right—circumferential or basal loop unfolding its right segment. Second layer—further circumferential or basal loop unfolding of its left segment and showing inner helix. Third layer—helix unfolding to display descending segment (DS) after ascending segment (AS) is separated. The entire basal loop (containing RS and LS) is also shown. Bottom layer—HMVB unraveled to display its rope-like model appearance. Longitudinal fibers only exist within the two papillary muscles; ( b ) unfolding of HVMB model. Upper left—intact heart. Upper right—circumferential wrap or basal loop with transverse fibers and the inner helix. Lower right—unfolded helix showing the oblique fibers of the inner descending helical arm that is separated from the outer ascending helical arm. Lower right—outer ascending helical arm. Marker arrow points to the left anterior descending artery pathway that bisects the helical muscles forming septum and left ventricular free wall. Reproduced form the references [ 6 , 8 ] with Publisher’s permission.

Treating disease requires restoration of normality, so decisions must be based upon an understanding of anatomic normality. The heart’s functional counterpart involves only six movements; narrowing, shortening, lengthening, widening, twisting, and uncoiling. The helical ventricular myocardial band model of Torrent Guasp [ 5 ] appears in the two classical anatomy texts of Clemente [ 9 , 10 ], and Moore and Dally [ 11 ] and its mechanics explain each motion [ 6 , 8 , 12 ].

This knowledge answers the query about the heart by explaining the only valid definition of heart structure involves describing a mechanical architecture whose motion can account for all dynamic cardiac movements. Misconceptions happen without it. For example, rather than focusing upon cardiac compression, the pivotal role of twisting for mechanical proficiency must be understood [ 13 ]. Twisting occurs because the helical cardiac design allows the natural 15% muscle fiber shortening to create a 60% ejection fraction [ 13 ], but this truth is not generally appreciated.

The background behind this misunderstanding started 2200 years ago when Erasistratus (280 BC), then Galen (180 AD) and subsequently Borelli (1600s) [ 14 ] described twisting, which causes blood to have an ebb and flow motion. But William Harvey, who uncovered the circulation in 1628, also introduced a compression and dilating action (mimicking a clenched and open fist) [ 15 ], an action that changed Galen’s ebb and flow hypothesis. His supporters deemed Galen’s concept incorrect, and Harvey’s approach has prevailed for 400 years—gaining further support from two-dimensional imaging (ventriculogram and echo) studies. The newer three-dimensional imaging tools (MRI and speckle tracking) provide the spatial resolution that allowed re-emergence of the clockwise and counterclockwise twisting rotations Erasistratus described 2200 years ago.

The capacity to understand the dynamics of the surrounding wrap and helix is a very different approach from using deductions to explain many ‘accepted cardiac mechanical relationships’. This tactic will lead to questioning of many ‘state of the art’ concepts. They include heart anatomy as LV, RV, and septum, timing of mitral valve opening, the isovolumic relaxation period, structural reasons for torsion/twisting, the term untwisting, structural reasons for circumferential and longitudinal strain, echocardiographic cardiac sub segmentation, resynchronization, RV function dynamics, and diastolic dysfunction’s cause and its unrecognized septum involvement.

2. Topographical versus Structural Heart

A heart with two ventricles, separated by a midline muscular septum defines its classic morphologic description. Despite correct topography, no functional insight is provided to define what these three structures do. A different structural guideline has existed for 500 years, whereby heart architecture contains a helix formed by right- and left-handed fibers and a surrounding circumferential wrap [ 1 , 2 , 3 , 5 , 16 ]. This anatomy preceded Torrent Guasp’s identifying the interweaving architecture by unraveling its muscle bundle formation to solve the Gordian Knot of anatomy [ 5 ] ( Figure 2 ). His novel description of a helical ventricular myocardial band (HVMB) [ 17 ] identifies a vortex at the tip of the apex, which is formed by the overlapping of coiled helical arms. Yet when uncoiled, the entire heart’s rope-like configuration becomes revealed ( Supplementary Video S1 ).

Apical view of heart muscle showing the fibers clockwise and counterclockwise spiral formation. Images display common anatomy from Lower in 1669 ( left ), and Torrent Guasp in 1970 ( right ). Reproduced form the reference [ 17 ] with Publisher’s permission.

Torrent Guasp’s macroscopic anatomic pattern ( Figure 1 ), whereby the transverse muscle at the base of the heart (circumferential wrap) turns downward to form an inner descending arm of the helix, which creates an apex by turning upward to form an outer ascending helical arm that ends at the aortic root. Grant [ 18 ], Lev and Simkins [ 19 ], and Anderson [ 20 ] questioned his macroscopic findings because of concerns about the validity of his dissection planes in cadaver tissue. Our analysis of the 1971 functional studies by Armour and Randall [ 21 ] also questioned the proper site for posterior papillary muscle, but their correct location is now displayed in subsequent HVMB dissections. The only basic element needed to uncover the mechanical reasons for the living heart motions is a valid structure/function relationship comprehension.

Controversy and Criticism: MacIver, Anderson’s colleague, recently proposed a report to put “an end to unique myocardial band” approach, because its presence cannot be defined by two- dimensional histology [ 22 , 23 ]. Our report is a counterforce to this conclusion, since mechanically explaining cardiac function is the only hallmark for determining the creditability of structure. MacIver questions whether abrupt helical changes occur in a wrapped myocardium by using CT images, thereby taking a position that countermands their presence during gestation, with ongoing helical persistence during adulthood ( Figure 3 ). His argument that a circumferential (horizontal) wrap exists in the septum would functionally erase the twisting motion, which is the most powerful force of cardiac efficiency. It would introduce a wedge that shall impair motion between the gliding helical arms, as shown in Supplementary Video S2 and Figure 4 . Moreover, adult DT-MRI images from the same laboratory that generated the prior gestation studies ( Figure 3 ), further documents that circumferential fibers are absent in the septum [ 24 ]. MacIver believes thinking twisting is only a minor contributor to stroke volume, thereby presenting a pathophysiology concept that vastly differs from current functional knowledge showing septal twisting is responsible for 80% of right ventricular output [ 25 ], and loss of left ventricular twisting is the earliest sign of heart failure [ 26 ]. Conversely, the mechanics of the myocardial band completely describes this pathophysiology during health and disease.

Human myocardial fibrillogenesis: ( a ) 1 and 2 show DT-MRI during the myocardial fibrillogenesis (gradual increase in number and spatial helical arrangement) of the ventricular myocardial fibers in human embryo at 10 and 14 weeks, respectively; ( b ) DT-MRI in adult heart showing helical right handed helix (red), left handed helix (green/yellow) and blue circumferential or horizontal fibers with zero helix. Note absent circumferential fibers in septum. Reproduced form the references [ 8 , 24 ] with Publisher’s permission.

Doppler longitudinal strain imaging of septum (right and left sides) in apical four-chamber view. Longitudinal strain marked by red (right) and green (left) circles, showing deformation in opposite directions on right and left septum sides—relative to baseline zero value. Timing shows LV first and RV second. SR, Strain rate; AVC, aortic valve closure; RV, right ventricle; LV, left ventricle. Reproduced form the reference [ 38 ] with Publisher’s permission.

Macroscopic analysis has the limitations of not addressing the microscopic display of the nests of layers and lamellae within individual myocytes that interact with cardiac ejection and filling. LeGrice found sarcomeres clustered in 1–12 groups within their connective tissue netting [ 27 , 28 ]. While microscopic relationships are correct, they must also coordinate with the heart’s macroscopic geometric form to fulfill Sallin’s [ 13 ] fundamental form/function relationship. This need is emphasized in clinical heart failure where the normal conical heart shape develops a spherical configuration [ 29 ]. This geometric change transforms the fiber direction of helical arms into a more transverse architectural fiber orientation which impairs LV systolic and diastolic function [ 13 ].

The conceptual understanding of macroscopic cardiac structure is straight forward because only three components need be known. There is a circumferential wrap of transverse fibers that surrounds both ventricles—called a basal loop—which compresses and rotates the global heart, and predominantly forms the RV free wall [ 25 ]. The second is the muscular helix that resides within an apical loop nestled within its surrounding circumferential wrap [ 30 ]. Its two oblique fiber arms cross each other at 60° angles [ 31 ], with the inner helical coil descending from base to apex, and outer helical coil ascending from apex to base. The same helix forms the septum and part of the LV free wall, whose movements are shortening, lengthening and twisting.

Simplicity underlies the solution to the structure function relationship, since its three structural components (the wrap and two helical arms) produce the heart’s six readily apparent dynamic movements of narrowing, shortening, lengthening, widening, twisting, and uncoiling [ 6 , 7 , 8 ]. This interaction precisely follows Keith’s 1918 Harvean Lecture comment “no theory of function is true unless it explains each detail of structure” [ 32 ].

Functional balance exists between the structural wrap and helix, as the wrap causes counterclockwise motion before ejection, the helix produces twisting, and the wrap triggers clockwise recoil during post ejection interval that includes the isovolumic period [ 6 ].

State-of-the-art imaging reports do not recognize this dynamic balance because they do not address the fundamental role of the surrounding wrap [ 33 , 34 , 35 ]. This gap keynotes the hiatus between deduction and anatomic knowledge, especially since this large circumferential wrap muscle mass highlights the framework structural contributions of William Harvey [ 15 ], Krehl [ 3 ], Mall [ 4 ], Robb [ 16 ], and Torrent Guasp [ 5 ].

Echo motion recordings amplify the circumferential basal loop’s presence by documenting cardiac lengthening during the pre-ejection isovolumic interval [ 6 ], while MRI imaging authenticates its global counterclockwise rotation [ 36 , 37 ]. The circumferential wrap’s large muscle mass predominates, and thus overcomes the shortening and clockwise rotation expected from the ongoing subendocardial muscle contraction. A common analogy explains such domination, as one could imagine a train heading south at 60 miles per hour, while its first car houses a runner who speeds northward toward the back car at 6 miles per hour; the power of the southern train always wins, as does the wrap over the helix.

The anatomy documenting the location of the outer circumferential wrap becomes evident from echo studies showing the smooth reciprocal movement (in different directions) between the contracting inner and outer helical arms ( Supplementary Video S2 ). Interposing a transverse band of compressing muscle between these gliding surfaces would interrupt this motion, as well as impair the smooth positive and negative septum strain displacement on longitudinal strain recordings ( Figure 4 ).

Macroscopic interlocking of structure and function is aided by the comparison of their dynamic clockwise and counterclockwise helical motions in Supplementary Video S2 , with their anatomic configuration in post mortem CT images ( Figure 5 ).

Computerized Ttomography of cardiac short axis, at mid ventricle level, following air insufflation to separate collagen scaffold netting. Plane between the two septum muscle mass rims reflects the echogenic line in septum, and Supplementary Video S4 records motion between these post mortem rims. Reproduced form the reference [ 39 ] with Publisher’s permission.

The plane identifying the mid ventricular overlapping between helical arms ( Supplementary Video S2 ) extends from apex to base and is called the hyperechogenic zone. It is 1 cm wide in low fidelity tracings, narrows to 3 mm in higher fidelity recordings, and shrinks to 100 μm [ 12 ] following higher fidelity echo examination [ 39 , 40 , 41 ] ( Figure 6 ). The smooth and efficient muscle movements, on either side of it, suggest this zone reflects is a glide path for helical arm motions. The working heart is a precursor for this zone’s presence, since it disappears when cardioplegia arrests the heart [ 12 ].

( a ) Mid-septal hyperechogenic line shown in low and high-resolution echocardiogram; ( b ) septum high-resolution ultrasound image at transducer frequency (12 MHz), displaying its bilayer line with inner dimension structure of 100 to 150 μm. Working septum muscle fibers display different directionality on either side of septum line. This disappears, as does the echogenic line—when cardioplegia (cardiac arrest) stops contractile function. Reproduced form the reference [ 8 ] with Publisher’s permission.

These dynamic findings differ from conclusions made from post mortem DT-MRI observations that suggest circumferential fibers exist within the septum mid myocardium due to observations of zero helix angles [ 42 ]. Yet physiologic testing exposes uncertainty about the anatomic validity of DT-MRI findings, because the 100 micron thick echogenic zone disappears following cardioplegia, yet the dead heart septum MRI studies describe a circumferential muscle that occupies half of its muscle mass [ 43 , 44 ].

3. How Three Structural Components Cause Normal Functional Dynamics

The most powerful or dominant muscle amongst these three architectural components governs the direction of movement, and their contraction takes place at different timing intervals [ 45 ]. For example, the wrap narrows and stretches the ventricle during the pre-ejection isovolumic phase, as it overcomes the simultaneously contracting inner descending helix that should make the ventricle shorten [ 6 , 7 ].

Conversely, shortening during ejection emphasizes the dominance of the inner descending helical arm. The ventricle twists as the base rotates clockwise and apex turns counterclockwise from the torque of the outer ascending helical arm’s longer lever radius [ 46 ]. The outer helical coil cannot produce shortening because its longitudinal strain signal is positive (showing elongation) ( Figure 4 ). Despite this, both helical arms exert dominance during twisting because the inner descending coil causes shortening (generating twice the longitudinal strain) [ 47 ] while the outer ascending helical coil makes the apex turn counterclockwise [ 46 ]. Our imaging tools provide insight into this action via the echogenic septal line ( Figure 6 ) as the echo beam suggests their fiber orientation pathways by passing along or across the ascending and descending muscle masses [ 12 ].

The wrap [ 6 , 7 ] causes clockwise global recoil during the post ejection isovolumic phase, as it springs backward to reverse its pre-ejection counterclockwise motion [ 37 , 48 , 49 ]. The helix is not involved in this component of recoil because its outer ascending arm is still contracting—but the dominant circumferential wrap’s clockwise motion overturns its counterclockwise motion. Simultaneously, the ventricle lengthens from straightening of the contracting outer ascending helical coil that starts when the dominant inner descending helix contraction stops ( Figure 7 ) [ 7 ].

Upper left shows intact heart containing a basal loop (circumferential wrap with right (RS) and left (LS) segments) and helix (dark color) with descending (DS) and ascending (AS) segments. Lower left—diastole without contraction. Lower middle—displays shows torsion (twisting) with stronger contraction of descending helical arm (tighter coils), and stretching of ascending helical arm. Lower right—recoil with global clockwise rotation; note lengthening due to ongoing contraction of ascending helical arm. Upper drawing—cobra shows similar elongation from its contracting muscle. Reproduced form the reference [ 17 ] with Publisher’s permission.

Global longitudinal strain measurements match those recorded by sonomicrometry [ 6 ] and the observed septum motion in opposite directions reflects the reciprocal fiber orientation of its helical muscles ( Figure 4 ). The outer ascending helical arm starts contracting ~60 ms later than the earlier inner descending helical arm, followed by a ~90 ms timing gap that earmarks the difference between the end of shortening of the inner (descending) arm, followed by the end of outer (ascending) helical arm shortening [ 45 ]. This timing hiatus between the end of contraction in the inner and outer helical arms provides a mechanical contradiction (i.e., presence of contraction) to suggestions that repolarization starts earlier in ascending than descending helical arms [ 50 ].

4. Mitral Valve Opening

Mitral valve opening (MVO) is a term reflecting the Doppler based echocardiographic recording of initial transmitral inflow into the left ventricle. This passage coincides with left ventricular pressure falling below atrial pressure, and the most rapid anterior mitral leaflet motion [ 51 ]. Its designation is universal and the term MVO appears in text books and journal reports ( Figure 8 ). Yet physical separation of the mitral leaflets is the only valid MVO requirement. Lee in 1990 [ 52 ] called MVO “the mitral valve artifact that correlates with the E point in the mitral echogram, but is unrelated to actual mitral valve opening”, and others have also questioned its validity [ 53 , 54 ].

Physiologic observations in all texts and medical journals, showing mitral valve opening (MVO) when LV pressure falls below left atrial pressure, and that the isovolumic relaxation phase exists between aortic valve closure and MVO. Reproduced form the reference [ 6 ] with Publisher’s permission.

MRI recordings quantify leaflet separation, and Supplementary Video S3 documents that mitral valve leaflets detach from each other at the end of systole—with an open aortic valve. Abrupt loss of leaflet coaptation begins when recoil starts, ~27 ms before aortic valve closure [ 55 ], coinciding with negative dP/dt or deceleration of left ventricular pressure. Such MVO documentation exposes an enormous discrepancy between reality versus what has been deduced. The uncoiling process causes MVO, and introduces the muscular action that may trigger diastolic dysfunction.

The functional dynamics of the wrap and helix establishes the mechanical insight to explain why MVO occurs during systole. This geometric process focuses upon the architectural interaction between the mobile ventricle that uncoils—and the mitral annulus that is fixed. The circumferential wrap causes clockwise recoiling, which rotates the helix that contains the papillary muscles that connect with the mitral leaflets and annulus. Their counterclockwise rotation during ejection allows them to close the fixed annulus by a leaflet flap, and this ‘trap door’ re-opens—as they spring backward during recoil to produce MVO ( Supplementary Video S2 ). The dynamics of papillary motion are shown in Supplementary Video S4 . Figure 9 a,b anatomically displays them at rest and during motion. The 1911 report of Mall [ 4 ], a renowned anatomist, demonstrates their clockwise and counterclockwise ventricular movements during twisting and uncoiling.

( a ) Mitral valve apparatus composed of fixed annulus and mobile leaflets, chordae tendineae, papillary muscles, and ventricular wall; ( b ) Mall’s 1911 report showing how apical counterclockwise rotation of the apex shuts the valve during torsion—by bringing spiral papillary muscles together. Mitral valve inflow area opens during from its clockwise rotation during recoil. Reproduced form the reference [ 56 ] with Publisher’s permission.

MVO can only happen when helix’s inner descending contraction has ended, an action that permits initiation of outer ascending helix arm lengthening ( Supplementary Video S3 ) as quantified by Karwatowski [ 57 ]. These cohesive actions of recoiling (by the wrap) and elongation (by the outer helix arm) reinforce why mechanical factors play such a vital role in mitral leaflet separation.

Our understanding of diastolic dysfunction is enhanced by a fuller understanding of MVO—since uncoiling cannot begin while torsion is ongoing. Ventricular recoil begins at the inception of negative dP/dt, so that this measurement may become a signpost to determine when unwinding starts. If MVO timing is normal, the hiatus or time gap between the end of the inner and outer helix contraction is ~90 ms—and its disruption will impair uncoiling [ 6 , 7 , 58 ]. Prolonged torsion narrows this gap, so that thinking about the mechanical reasons for MVO may spawn some of the new treatments that will be subsequently considered [ 56 ].

Finally, the traditional identification of MVO is incorrect, so that the physiological term “mitral valve inflow” (MVI) should replace it. MVO is due to anatomic changes that carry vast physiologic implications—as we suspect recoiling will become the centerpiece behind understanding diastolic dysfunction.

5. Isovolumic Relaxation Time

Isovolumic relaxation time (IVRT) joins MVO in being a universally accepted term ( Figure 8 ). It signifies that part of the cardiac cycle between aortic valve closure and MVO, where the ventricle relaxes (diastole) without lengthening, and ventricular volume is unaltered. Wiggers described it in 1923 [ 59 , 60 ], as does today’s Stedman Medical Dictionary [ 60 ].

The ventricle is isovolumic, yet the other three components reflect deductions that are incorrect. First, the MVO during clockwise recoil is caused by the wrap—initiating when LV negative dP/pt starts, rather than when a LV pressure falls below left atrial pressure. Second, the entire ventricle does not relax—ongoing strain measurements and sonomicrometer crystal recordings confirm outer ascending helical arm contraction [ 6 ]. Finally, it produces lengthening that is quantified by MRI ( Supplementary Video S3 ), two-dimensional echo [ 6 ], and longitudinal strain recordings [ 38 ]. This elongation movement may mirror how a cobra develops an erectile stance before striking [ 17 ].

Rademakers described the impact of the post ejection isovolumic interval on ventricular filling when he defined a dissociation between untwisting and filling, whereby 50–60% of recoil occurs during this isovolumic interval [ 61 ]. He reasoned that this motion may promote the suction that explains the explosive LV filling that follows the falling LV pressure below left atrial pressure, and wondered if unwinding released the potential energy stored in elastic elements during prior systolic deformation [ 61 ].

The interdependence of torsion and recoiling is a vital interaction because torsion must stop before unwinding can start. The post ejection isovolumic time frame interval is ~90 ms ( Figure 10 ), but diastolic dysfunction may develop when protracted inner descending helix contraction widens this timing gap to >100 ms as seen during aortic stenosis, hypertension, and ischemia [ 58 , 62 , 63 , 64 ].

Left ventricular contraction sequence by anterior LV sonomicrometer crystals. Blue shading shows pre ejection isovolumic interval, yellow shading shows post ejection recoil. Note (a) ascending helical arm does not contract during pre-ejection, but contracts during recoil; (b) negative dP/dt is yardstick for starting recoil, and marks when inner helical arm stops contracting. Reproduced form the reference [ 6 ] with Publisher’s permission.

Current thoughts about recoil during isovolumic relaxation imply that the epicardium governs the clockwise rotation of the LV apex, suggesting that it reverses torsion’s apical counterclockwise rotation [ 61 , 65 ]. The dynamics of functional anatomy challenges this conclusion, since the epicardium (outer ascending helical muscle) is still contracting ( Figure 10 ). Instead, the circumferential wrap causes clockwise rotation, as outlined previously for mitral valve opening. The term ‘isovolumic relaxation interval’ is incorrect because the ascending helix is still contracting, it should be renamed the ‘post ejection isovolumic period’.

This revision has historic precedence, as Wiggers can now join Harvey (who described compression versus twisting) and Vesalius (who described apex moving toward the base versus its natural base to apex motion) as being astounding titans that were not perfect.

6. Twisting or Torsion

There is agreement that the spiral architecture of LV muscle fibers produces LV systolic wringing or twisting during ejection by producing differential rotation of the LV base (clockwise) and apex (counterclockwise). This is called torsion by expressing its rotational angle, along the LV longitudinal axis. The responsible muscular mechanisms have important functional implications, yet these have only been deduced.

Taber’s bioengineering model has been accepted [ 66 ], as it introduces a helical architecture containing a single layer composed of obliquely aligned muscle fibers embedded in an isotropic matrix [ 65 ]. Torsion is described as being developed “within each helix arm”—epicardial fiber contraction rotates the apex counterclockwise and base clockwise, whereas subendocardial fiber contraction rotates them in the opposite directions. Geometric mechanisms differ, as torsion develops “between the helix arms” with the entire inner descending arm rotating the base clockwise, and the entire outer ascending arm rotating the apex counterclockwise ( Figure 11 ).

Torsion. The bioengineering approach (upper left) shows it develops ‘within each helix’; epicardial (outer) muscle has counterclockwise apex and clockwise base rotation, while endocardial (inner) muscle has clockwise apex and counterclockwise base rotation to reflect these reciprocal actions in each helical arm. The right image shows the suggested inner and outer cones occupied by the inner and outer helix. The lower images are anatomic: torsion develops ‘between helices’ as the entire inner descending helix rotates clockwise, and entire outer ascending helix rotates counterclockwise. Reproduced form the reference [ 8 ] with Publisher’s permission.

Evidence for this structural explanation is supported by architectural and imaging studies. The anatomically unfolded heart reflects an uncoiled rope ( Figure 1 ) that, when re-folded, contains a helix composed of the 60° overlapping of inner and outer spiral coils that aim at either the apex (inner helical arm) or base (outer helical arm). Septum strain recordings confirm deformation in different longitudinal directions [ 12 , 38 ], and high frequency echo tracings record the smooth transition of functionally overlapping fibers ( Supplementary Video S2 ) which pass along or across its mid septal echogenic line [ 12 ].

Downward shortening of both helical coils cannot cause torsion, because the systolic septum longitudinal strain shows the positive deformation (elongation) of the outer ascending helical arm ( Figure 4 )—a motion that continues during recoil, evident by sono micrometer ( Figure 10 ) and by MRI evaluation ( Supplementary Video S3 ). Interactions between torsion and recoil are independent of torsion’s peak value, because prolonged torsion introduces a twist-based retardation of the unwinding required to develop suction.

Torsion and recoil affect ventricular performance in a way that relates to the contractile patterns of the inner descending and outer ascending helical arms. Torsion ends when the inner descending helical arm stops contracting—since uncoiling cannot begin until that happens. This recoil interval includes the post ejection isovolumic phase and first-third of diastole [ 67 ]. Prolonged torsion delays the recoil’s starting—becoming a precursor for development of diastolic dysfunction. This interdependence between torsion and recoil emphasizes why diastolic dysfunction cannot be thought to exist in a patient whose ejection fraction is considered normal and healthy.

7. Untwisting

Untwisting during recoil represents the antonym for twisting during ejection. This traditional term is used to describe the clockwise rotation of the apex that counteracts its counter-clockwise motion during twisting for ejection [ 55 ]. Yet the physical designations of these actions differ; “twisting” mirrors rotating the upper fist clockwise and the lower one counterclockwise, to confirm reciprocal left and right handed helical muscle rotations shown by MRI and echocardiogram. However, the MRI does not record the expected ‘untwisting counterpoint’ of apical clockwise and basal counterclockwise rotation. Instead, a global clockwise rotation exists during recoil [ 48 ]. It is caused by a dominant circumferential wrap that overpowers the outer ascending helical arm’s ongoing systolic counterclockwise motion.

Each muscle must return to its starting point, so these anatomic reasons do not counteract the recoil that helix and wrap muscles must develop. Instead, functional aspects of the HVMB explain why recoil’s expected global clockwise and counterclockwise ‘untwisting’ cannot occur. The term ‘untwisting’ should be changed into ‘uncoiling, recoiling, or unwinding’ to capture recoil’s inception point since it may evolve future diastolic dysfunction treatments.

8. Longitudinal and Circumferential Strain

Strain measurements define muscle deformation relative to original length by addressing “shortening in circumferential or longitudinal dimensions or thickening in radial dimensions”, but they do not define why deformation happens or what it means. For example, two-thirds of strain is circumferential and only one-third longitudinal, so that it is considered a more robust tool [ 40 , 68 ], especially because some believe the predominant muscle fiber orientation is followed [ 69 ].

The functional importance of deformation is linked to its muscular cause. Longitudinal strain reflects coiling downward of the oblique helical spiral fibers to generate the normal ~60% ejection fraction [ 13 ]. Conversely, short axis shortening arises from predominantly circumferential fiber deformation, but only a ~30% ejection fraction is yielded [ 13 ]. These fiber angulation changes have powerful implications, because impaired systolic contractile strength develops when the ventricle becomes spherical and the helical muscle fibers develop a more transverse orientation [ 13 ].

Longitudinal strain quantifies ventricular shortening, and was thought to reflect how the apical part pulls the ventricular base downward [ 70 ]. The helix and wrap architectural configuration application defines a different sequence, since longitudinal strain reflects how the spiral coil of the inner descending helical arm sequentially shortens due to its base-to-apex contraction—a trajectory that follows the human excitation studies showing that upper septum activation precedes apical stimulation. [ 71 , 72 , 73 ]. Longitudinal muscles “for pulling” do not exist in the ventricle ( Figure 1 ) (except for thin papillary muscles), so that “pulling down” deductions contradict natural motion dynamics [ 70 ].

Two factors explain why circumferential deformation produces ventricular compression or cardiac narrowing. The first is short axis shortening of the wrap or basal loop’s transverse fibers. The second is transverse shortening produced by thickening of the contracting inner helix’s descending arm. Their individual contributions cannot be determined because they are superimposed within the LV free wall. Conversely, the septum does not contain a circumferential wrap so that its longitudinal strain measurement is possible ( Figure 4 ).

Longitudinal strain reflects deformation of helical spiral fibers, and is measured by recording mitral annulus excursion toward the apex (or MAPSE mitral annular plane systolic excursion) [ 74 ]. Figure 6 shows the dominance of the spiral inner descending helical segment in producing longitudinal strain during systole.

Impaired longitudinal strain is an early finding in dilated hearts [ 75 ] and develops when the ventricular shape becomes spherical. This geometric change makes the natural oblique fibers develop a more transverse configuration [ 75 , 76 ] that disrupts their twisting capacity ( Figure 12 ). This concept’s functional validity is confirmed by the consistent return the cardiac twisting when the failing heart’s spherical shape becomes rebuilt into its natural elliptical shape [ 77 ].

Helical fiber orientation (yellow arrows) in normal ventricle (above) with reciprocal 60° angulation and a conical shape. Spherical heart (below) shows a more transverse pattern with 45° or less angulation, mirroring the failing dilated heart. Reproduced form the reference [ 56 ] with Publisher’s permission.

The surrounding basal loop fibers provide a short axis supporting restraint [ 78 ] that follows ventricular longitudinal strain limitation. For example, circumferential strain is augmented when intraoperative septum damage causes RV longitudinal systolic dysfunction [ 79 ]; the LV follows a similar sequence [ 69 ]. Conversely, increased ventricular sphericity follows loss of this circumferential restraint [ 78 ].

Worsened longitudinal systolic strain exists when relaxation is altered during diastolic dysfunction [ 80 ]. The query “is it only diastolic dysfunction?” arose after this coincidence was observed in hypertensive patients with diastolic dysfunction [ 81 ]. The differential function of the inner descending and outer ascending helical arms answers this mechanical question [ 58 ], as described in the upcoming section on diastolic dysfunction.

9. Regional Function versus HVMB

Regional echo based structure function analysis is linked to perfusion related changes [ 82 ]. Regional deformation (grading shortening and thickening) is aligned with the perfusion territories of 17 echo segments that are based within three circular rings of the basal, mid, and apical ventricle [ 82 ]. This arbitrary selection of transmural muscle (with comparable mass) into echo based LV sub-segmentation provides useful information about regional perfusion, yet except for segment 17 that shows absent apical deformation, this topographical approach does not record the performance dynamics forthcoming from HVMB analysis [ 45 ].

A similar arbitrary concept guides how readers are taught to understand the architecture of the helical muscles in the LV elliptical shape. They are considered to exist within overlapping cones, with “state of the art” reports [ 65 ] showing the inner cone describes endocardial muscle, and outer cone identifying epicardial muscle [ 65 , 83 ].

This designation is incorrect because the outer ascending helical arm forms different parts of the endocardium. An example of this unsuitability is that helical muscle overlap is absent in the septum muscle endocardium below the aortic valve [ 7 ]. Velocity vector imaging studies confirm this during the pre-ejection isovolumic phase, since the upper septum bulges like an aneurysm because contraction of outer ascending helix has not yet started [ 7 , 12 ] ( Figure 13 ). The outer ascending helix also forms the endocardium in the posterior LV wall where helical overlap is absent. Validity of descriptions of the heart’s architecture is only possible by following the sheaths within muscle planes of its helical arms and circumferential wrap.

( a ) Pre wall ejection motion from velocity vector imaging (VVI) is correlated with cardiac anatomy. The upper septum bulges into the right ventricle (upper right); ( b ) The helical architecture demonstrates absence of helical overlap in region beneath the aortic valve. Its endocardium is formed by the outer, ascending left handed helical arm that does not contract during this interval. Reproduced form the reference [ 8 ] with Publisher’s permission.

10. Resynchronization

Excitation contraction coupling provides the infrastructure behind how twist develops during each HVMB contraction. This process requires the natural flow of electrical impulse from the conduction system into the responsible myocytes. Insight into the HVMB anatomy and interventricular conduction relationship is gained by reviewing the evolution of clinical ‘resynchronization’ therapy (CRT). ‘Synchrony’ is the traditional term used to characterize the coordinated contraction of the LV, RV and septum—observed from two-dimensional echo or ventriculography. They record harmonized “all at once“ movement—mimicking the making of a fist with all fingers squeezing in unison in patients with a normal narrow QRS interval. Conversely, a wide QRS interval defines delayed regional electrical activation, and is associated with uncoordinated contraction that may produce septum bulging or billowing, mitral regurgitation, and raise LV volume.

‘Resynchronization’ is achieved by simultaneously pacing the LV and RV with the aim of restoring ‘synchrony’, but its portended treatment goals are only sometimes met [ 84 ]. For example, ~30% of patients do not respond [ 84 ], LV volume is not reduced in 40% [ 85 ], recovery of twisting is inconsistent [ 83 , 86 ], and late survival [ 87 ] increases only 0.85 years in comparison to optimal pharmacologic therapy. A suggested way to solve this dilemma is to search for a better site for LV pacing [ 85 ], but the validity of the ‘resynchronization concept’ must also be examined.

This change in thinking may be important because normal cardiac motion is not ‘synchronous’. Instead it is a ‘sequential’ motion that evolves when the electrical impulse traverses the natural conduction system and its collagenous cardiac netting matrix to stimulate individual muscle fibers. The clenched fist that is traditionally used to define contractility does not reflect an ‘all at once’ motion. Instead, it represents the ‘chronological closing’ of the little finger, ring finger, middle, and then index fingers, as they create the whirling motion which mirrors the normal heart’s natural twisting movement. Such coordinated torsion develops because the electrical propagation velocity is 10× faster (at 3 m/s) through the natural His-Purkinje fiber conduction system, than via direct ventricular muscle stimulation (at 0.3 m/s) [ 88 ]. Wiggers in 1925 described the functional dilemma of asynergic ventricular muscle motions that follow synchronous single electrical excitation [ 89 ]. His observation had no impact, because this form of stimulation persists to remain the unchanged stalwart of conventional pacing.

Twisting was recently evaluated by recording HVMB motions following either isolated (direct) ventricular, or biventricular stimulation (CRT), and torsion was inconsistent [ 90 ]. Conversely, pacing of the His-Purkinje system [ 91 ] returns the sequential activation responsible for twisting to restore natural torsion. The clash between these pacing avenues highlights that a limitation of CRT is that it reflects the two-dimensional approach of isolated site excitation which can only gain compression. In contrast, natural conduction excites the inbuilt conduction circuits which unfold the three-dimensional approach that returns cardiac twisting.

CRT provides mechanical, but not physiological improvements. For example, a wide QRS interval delays septum activation, so that the earlier LV free wall contraction will make it billow or bulge. The resultant ventricular stretching will tether the posterior papillary muscle (adjacent to septum) connected to the mitral leaflet, and produce mitral regurgitation from poor leaflet coaptation. CRT returns the septum to its midline position to offset papillary muscle tethering and remedy mitral regurgitation—but it does not consistently restore cardiac twisting. Conversely, His-Purkinje pacing rebuilds normal conduction by shortening the QRS interval [ 92 ]. It generates a sequential heart beat that permits the natural twisting motion to resume [ 93 ]. Awareness of these differences may hasten interest in evolving of His-bundle pacing approaches.

11. Right Ventricular Function

Right ventricular failure is difficult to manage because its underlying mechanisms are uncertain. Decision dilemmas follow such incomplete functional knowledge. For example, the RV is considered a passive chamber because early functional recovery follows its exclusion by the Glenn (superior vena cava to pulmonary artery) or Fontan (pulmonary artery to right atrium) procedures [ 94 , 95 ]. Yet this conclusion is contradicted by the ~40% mortality that develops in patients that occlude a right coronary artery containing large septal branches [ 96 ].

RV cardiac function is determined by myocardial fiber orientation ( Figure 14 ). A thin circumferential wrap containing predominantly transverse muscle fibers forms its free wall. Their contraction produces compression via a bellows action that accounts for 20–30% of ejection fraction [ 13 , 97 ]. Conversely, only helical fibers construct its thicker midwall septum, and these oblique fibers [ 98 ] generate the twisting action responsible for 80% of RV global function, making the septum “the functional lion of the RV” [ 25 , 99 ].

Right ventricular fiber pattern and HVMB, where the circumferential wrap or basal loop causes compression and narrowing, and the underlying helix with oblique fibers at 60° angles causes shortening and lengthening. Reproduced form the reference [ 8 ] with Publisher’s permission.

Investigative studies document the dynamics of RV’s compression and twisting movements. For example, unaltered RV function follows RV free wall exclusion by cauterization, patch replacement [ 100 , 101 ] or its regional ventricular fibrillation [ 102 ] if the septum is intact. Yet RV failure follows septal injury when pulmonary hypertension co-exists [ 103 ]. This functional distinction between helix and wrap has not influenced the guidelines of the American Society of Echocardiography and European Association of CV Imaging that recommend measuring 2D STE-RV free wall strain, but do not identify that it accounts for only 30% of RV performance [ 82 ]. This functional discrepancy explains outcomes following a report that limited RV free wall ventriculotomy, aiming to avoid late RV failure [ 104 ]. It was not successful because of RV free wall’s minor effect on right heart performance.

The interplay becomes especially clear following cardiac surgery, where postoperative RV performance remains unimpaired, despite almost 50% of patients developing paradoxical septum motion [ 105 ]. But this compensatory circumferential wrap compression can only be effective when pulmonary vascular resistance (PVR) is low; RV failure develops if septum twisting is lost when PVR is increased [ 103 ]. This explains why the Glenn and Fontan procedures are contraindicated if PVR is high, since they exclude the septum, whose role is to the generate the twisting needed to counteract high afterload.

Tricuspid annular plane systolic excursion (TAPSE) quantifies the extent and rate of helically induced longitudinal strain [ 25 ] by documenting how ventricular shortening by the coiling helix will bring the base closer to the apex. The RV and LV chambers are thought to be topographically separate, but they share a common HVMB architecture, so that the twisting behind TAPSE in the RV reflects MAPSE in the LV. Vascular resistance is the counterforce to twisting and influences decision-making when right heart failure is caused by impaired septum function. If pulmonary pressure is high, treatment with vasodilator drugs (amrinone, milrinone) may be preferable to vasoconstrictor agents (epinephrine, dopamine) that would accentuate the afterload confronting the poorly contracting septum.

The interface between RV helical and circumferential muscle interaction is further clarified from RV function examination following either conventional or catheter based aortic valve replacement (AVR). Longitudinal and circumferential strain is unaltered in catheter based AVR that does not use cardioplegia. In contrast, the use of cardioplegia during surgical SVR results in the commonplace finding of septal damage [ 105 ]. This injury had an associated 50% reduction in TAPSE (the helix), which resulted in a 60% increase of compensatory circumferential strain (the wrap) [ 79 ].

RV failure sometimes develops in heart failure patients with high PVR following implantation of a left ventricular assist device (LVAD). Ventricular decompression by LVAD changes cardiac geometry by collapsing the LV. This maneuver bows the septum toward the left side, making its helical fibers more transverse and dysfunctional [ 56 ]. RV failure ensues, but can be quickly resolved by diminishing the extent LV decompression in order to mechanically restore the septum’s midline position as it re-establishes its natural geometry [ 106 ].

12. Diastolic Dysfunction

Diastolic dysfunction is characterized by how impaired ventricular relaxation and increased wall stiffness can limit LV filling in ~50% of patients with heart failure, despite their having normal ejection fraction [ 107 ]. Nishimura’s [ 67 ] classic 1997 overview emphasized empirical treatment, because of absent clear-cut pathophysiologic concepts—a limitation that still prevails. Historian David McCullough observed a similar conundrum in politics, stating “it is like trying to repair an engine that you do not know how to take apart”.

Normal ventricles receive 70% of their filling during the first third of diastole, but uncertainty exists about why this happens. Uncoiling via apical clockwise rotation influences early filling, but this motion begins in the last half of systole and extends to the first third of diastole [ 67 ]. Despite its acknowledgment [ 67 , 108 ], calling this interval “passive” rapid ventricular filling introduces a vis a tergo mechanism with reliance upon an intraventricular pressure gradient (IVPG) that promotes blood movement toward the apex [ 108 , 109 ].

The alternate mechanism is “active” ventricular suction to aspirate atrial blood, using peak negative dP/dt and the time constant of relaxation (tau) as measurement indexes [ 67 ]. Understanding the energy conversion process needed for either active recoil [ 110 ] or via a muscular mechanism [ 109 , 111 ] has been its missing component. The HVMB structure function relationship identifies this answer.

There is clear-cut understanding of how ventricular pressure increases during filling of a stiff ventricular wall, yet this “compliance mechanism” is absent during normal rapid ventricular filling, where ventricular pressure falls as volume increases [ 112 ]. “Diastolic suction” explains this process, as it draws ventricular blood from the atrial reservoir [ 113 , 114 , 115 , 116 ] to create a negative diastolic pressure. Brecher documented this negativity from recordings of the heart withdrawing blood from a lower reservoir [ 114 ].

The current term “passive rapid ventricular filling” parallels the prior controversy between twisting or compression for ejection. Background exists, as Galen, in 180 AD described “the overlying heart, at each diastole, robs the vena cava by violence of a quantity of blood”. Wiggers, in 1921, rejected a vis a fronte ventricular filling [ 117 ], and Roberts, in 1979, described “suction” by finding the left atrium had invaginated into the left ventricle through the mitral valve [ 118 ] during a post mortem exam after terminal hypovolemic hemorrhage.

Concepts about elastic recoil or systolic ventricular filling are best tested by evaluating the integration of form and performance. Van Dalen’s elegant series of observations [ 26 , 119 , 120 , 121 , 122 ] clarified the echo based dynamics of “untwisting”, but he ascribed these motions to oblique muscles. He reasoned that repolarized epicardial fibers (outer helical arm) actively untwisted to move clockwise, since endocardial fibers (inner helical arm) were reported to be still depolarized [ 50 ]. His focus upon “untwisting” as a new diastolic dysfunction treatment goal is an important consideration (as described below), but his suggested mechanism cannot occur. The helix is not involved in post ejection isovolumic phase recoil, because unwinding is caused by the basal loop whose contraction has stopped [ 6 ]. Conversely, the ascending segment (epicardium) is still contracting (depolarized) during the isovolumic interval, so that its persistent counter-clockwise motion would oppose the prevailing clockwise movement ( Figure 10 ) [ 6 , 33 , 41 ].

Torrent Guasp’s geometric contributions are central to our structure/function approach, but his “systolic ventricular filling” concept [ 109 ] uses only form to deduce function. He ascribes it to ongoing contraction of the ascending (outer helical) arm. HVMB dynamic analysis certifies that its post ejection isovolumic phase shortening has stopped before rapid filling begins ( Figure 10 ). Consequently, its elastic recoil causes the explosive ventricular filling that follows its springing back into its starting position. As stated, uncoiling may reflect how stored potential energy during ejection [ 61 ] is released during this unwinding process that creates a centrifugal force for aspiration of atrial blood.

The interdependence of torsion and recoil are fundamental concepts behind understanding how HVMB clarifies why diastolic dysfunction develops. The central theme is that recoil cannot start until torsion ends. The recoil process causes the predominance of ventricular filling in the healthy heart, yet 50% of this unwinding exists during the pre-filling phase, reaching 60% after catecholamine infusion [ 61 , 123 ]. The remainder of recoil happens during rapid filling and is due to uncoiling of the outer ascending helical arm [ 6 ].

The time-frame between the end of contraction of the inner descending and then, of the outer ascending helix arms, creates a “temporal hiatus” ( Figure 10 ), and this “time gap” becomes the centerpiece for understanding the HVMB muscular actions that are responsible for diastolic dysfunction. Curtailment of recoil will restrict suction and by narrowing of this temporal hiatus. Consequently, a vis a tergo mechanism must be used to cause ventricular filling by raising the compensatory factor of atrial pressure. Pressure related enhancement of filling is normal after atrial contraction at the end of diastole, but lung congestion may follow its presence during early diastole.

Disruption of the HVMB dynamics responsible for the interface between torsion and recoil creates diastolic dysfunction in several ways, because prolonged systole during torsion will encroach upon the aforementioned “temporal hiatus” during aortic stenosis [ 62 ], hypertrophic cardiomyopathy, ischemia [ 64 ], impaired sarcolemmal calcium flux efficiency [ 124 ], and age-related calcium turnover [ 124 ]. Its genesis is that unwinding cannot start until the prolonged inner descending helix arm contraction has ended.

Most importantly, thoughts of diastolic dysfunction that focus upon an isolated relaxation disorder must be reexamined, since each patient shows combined systolic and diastolic abnormalities [ 125 ]. These alterations involve impaired ventricular twisting and longitudinal deformation (strain) patterns [ 81 ] that delay untwisting to reduce suction and impair early diastolic filling [ 126 ]. Restricted helical systolic function is evident by reduced longitudinal strain, despite normal ejection fraction. This corresponds to how the prolonged torsion in patients with aortic stenosis can compromise their uncoiling process [ 62 ].

Mechanism related treatments can reverse diastolic dysfunction, since aortic valve replacement allows regression of LV hypertrophy with resulting return of twisting and recoil to normal [ 127 ]. Post ischemic diastolic dysfunction is reversed when sodium hydrogen ion inhibitors limit calcium accumulation within the inner helix. Their avoidance of prolonged contraction restores the natural time gap between the end of inner and then outer helix shortening to allow the recovery of the suction that accentuates ventricular filling [ 58 ].

The LV free wall and septum are formed by the same HVMB muscle mass ( Figure 1 and Figure 15 ) and this association confirms why diastolic dysfunction after routine cardiac surgery is clinically important. Diastolic and septum dysfunction are similar, but this conclusion has not yet been appreciated. It is well known that septum dysfunction is commonplace after cardiac surgery, as 43% of 3292 patients [ 105 ] develop septal paradoxical motion (lesser damage was not reported). Impaired myocardial protection causes this injury, but this damage can be avoided [ 128 ], as undamaged hearts show improved longitudinal helical deformation [ 129 ].

Figure 1 anatomy modification with “simulated left anterior descending artery” that is a vascular highway that bisects the helix, which constructs the septum and the LV free wall. Anatomy (above), and how (below) LV free wall is on vessel’s left side, and septum (which is three-dimensionally deeper) is on right side.

Diastolic dysfunction, its sequel, develops in 44% to 75% of patients undergoing coronary grafting or aortic valve procedures [ 130 , 131 , 132 ]. This incidence mirrors the frequency of septum damage [ 105 ] and both entities may disappear in 6–12 months [ 133 , 134 ]. Conventional consideration has not recognized the similarity between septum damage and diastolic dysfunction, because heart anatomy had been viewed topographically (LV, RV, septum), yet their coincidence is apparent and becomes predictable when the HVMB is used to recognize their commonality.

13. Conclusions

This rethinking of the core cardiology values started after learning of the contributions of Francisco Torrent Guasp. His studies exposed the simple design of cardiac architecture by showing that the HVMB contains a helix and a circumferential wrap. These two structures create the functional mechanics behind cardiac motion and thus define ‘what the heart is’. Application of this foothold knowledge reveals that many ‘accepted’ cardiac events are based upon deductions drawn from presumed myocardial structure, rather than from its natural configuration. Torrent Guasp’s revolutionary contribution opens the door toward an exciting future for the understanding, diagnosis, and treatment of cardiac disease.

Supplementary Materials

The following are available online:

Video S1 ( http://www.mdpi.com/2308-3425/5/2/33/s1 ): Francisco Torrent Guasp doing cardiac dissection to unravel the HVMB;

Video S2 ( http://www.mdpi.com/2308-3425/5/2/33/s2 ): MRI of Mitral Valve Opening. Note MVO occurs while the aortic valve is open, and its inception is just as the septum begins to elongate. Recoil begins as the mitral valve opens, an event that accompanies the beginning of clockwise ventricular rotation evident on next MRI video; Reproduced form the reference [ 6 ] with Publisher’s permission;

Video S3 ( http://www.mdpi.com/2308-3425/5/2/33/s3 ): Short axis apex MRI that displays cardiac rotation and papillary muscle motion. Note the counterclockwise rotation during torsion, and closeness of papillary muscles. Clockwise motion is associated with a widening or the distance between papillary muscles. They attach to the mitral leaflets and leaflet separation (mitral opening) accompanies the clockwise ventricular motion during recoil;

Video S4 ( http://www.mdpi.com/2308-3425/5/2/33/s4 ): Short axis high resolution echocardiographic view of torsion and recoil in normal heart. The inner and outer mobile arms correspond to how they are portrayed in the Figure 5 post mortem MRI images. Note (a) the smoothness of these superimposed reciprocal movements, as the inner helical arm rotates clockwise, and outer helical arm rotates counterclockwise during torsion development and (b) how the inner and outer coils spring back to their starting position during recoil.

Author Contributions

G.D.B. wrote the paper; G.D.B. and M.J.K. made substantial contributions to conception, drafting, and revision of the article, giving final approval of the version to be submitted; N.C.N. and C.N. made contributions to drafting and revision of the article, giving final approval of the version to be submitted.

Conflicts of Interest

Buckberg consults with Helical Heart Company LLC ( www.helicalheart.com ), which makes a spatial heart model of helical ventricular myocardial band anatomic configuration. The other authors declare no conflict of interest.

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Heart Definition

The heart is a muscular organ that pumps blood throughout the body. It is located in the middle cavity of the chest, between the lungs. In most people, the heart is located on the left side of the chest, beneath the breastbone.

The heart is composed of smooth muscle. It has four chambers which contract in a specific order, allowing the human heart to pump blood from the body to the lungs and back again with high efficiency. The heart also contains “pacemaker” cells which fire nerve impulses at regular intervals, prompting the heart muscle to contract.

This animation shows the functioning of this extraordinarily complex pump in action. As you read this article, try scrolling back up and seeing if you can spot the chambers, valves, and blood vessels we’re discussing in action:

The heart is one of the most vital and delicate organs in the body. If it does not function properly, all other organs – including the brain – begin to die from lack of oxygen within just a few minutes. As of 2009, the most common cause of death in the world was heart disease.

Most heart disease occurs as a result of age or lifestyle. Cholesterol can build up in the arteries as a person gets older, and this is more likely for people who have diets high in saturated fat and cholesterol. Rarely, however, heart disease can also occur due to a virus or bacterium that infects the heart or its protective tissues.

Scientists have had some success replicating the heart’s pumping action with artificial pumps, but these pumps can be rejected by the body, and they break down over time.

The four-chambered heart found in mammals and birds is more efficient than the one, two, or three-chambered hearts found in some other animals. It is thought that warm-blooded animals need highly efficient circulation to satisfy their cells’ high demand for oxygen. This is especially true of humans, whose huge brains require a near-constant supply of oxygen to function!

Function of the Heart

The heart pumps blood through our immense and complicated circulatory systems at high pressure. It is a truly impressive feat of engineering, as it must circulate about five liters of blood through a full 1,000 miles worth of blood vessels each minute! We will talk more about how the heart accomplishes this remarkable task under the “Heart Structure” section below.

The pumping action of the heart allows the movement of many substances between organs in the body, including nutrients, waste products, and hormones and other chemical messengers. However, arguably the most important substance it circulates is oxygen.

Oxygen is required for animal cells to perform cellular respiration. Without oxygen, cells cannot break down food to produce ATP, the cellular currency of energy. Soon, none of their energy-dependent processes can function. Without its energy-dependent processes, a cell dies.

Neural tissues, including the brain, are particularly sensitive to oxygen deprivation. Neural tissues maintain a special cellular chemistry which must be constantly maintained through the consumption of lots and lots of energy. If ATP production stops, neural cells can begin to die within minutes.

For this reason, the body has taken many special measures to protect the heart. It is located below the strongest part of the ribcage and cushioned between the lungs. It is also surrounded by a protective membrane called the pericardium, which is filled with additional cushioning fluid.

Heart Structure

The heart’s unique design allows it to accomplish the incredible task of circulating blood through the human body. Here we will review its essential components, and how and why blood passes through them.

Layers of the Heart Wall

The heart has three layers of tissue, each of which serve a slightly different purpose. These are:

• The Epicardium . The epicardium is also sometimes considered a part of the protective pericardial membrane around the heart. It helps to keep the heart lubricated and protected.
• The Myocardium . The myocardium is the muscle of the heart. You can remember this because the root word “myo” comes from “muscle,” while “cardium” comes from “heart.” The myocardium is an incredibly strong muscle that makes up most of the heart. It is responsible for pumping blood throughout the body.
• The Endocardium . The endocardium is a thin, protective layer on the inside of the heart. It is made of smooth, slippery endothelial cells, which prevent blood from sticking to the inside of the heart and forming deadly blood clots.

Chambers of the Heart

The heart has four chambers, which are designed to pump blood from the body to the lungs and back again with extremely high efficiency. Here we’ll see what the four chambers are, and how they do their jobs:

• The Right Atrium . The right and left atria are the smaller chambers of the heart, and they have thinner, less muscular walls. This is because they only receive blood from the veins – they don’t have to pump it back out through the whole circulatory system! The right atrium only has to receive blood from the body’s veins and pump it into the left ventricle, where the real pumping action starts.
• The Right Ventricle . The ventricles are larger chambers with stronger, thicker walls. They are responsible for pumping blood to the organs at high pressures. There are two ventricles because there are two circuits blood needs to be pumped through – the pulmonary circuit, where blood receives oxygen from the lungs, and the body circuit, where oxygen-filled blood travels to the rest of the body. Maintaining these two separate circuits with two separate ventricles is much more efficient than simply pumping blood to the lungs and allowing it to flow to the rest of the body from there. With two ventricles, the heart can generate twice the force, and deliver oxygen to our cells much faster. The right ventricle is the one attacked to the pulmonary circuit. It pumps blood through the pulmonary artery and to the lungs, where the blood fills with oxygen, at high pressure. The blood then returns to…
• The left atrium receives oxygenated blood from the pulmonary veins. It pumps this blood into the left ventricle, which…
• The left ventricle pumps blood throughout the rest of the body.

After the blood has circulated through the body and the oxygen has been exchange for carbon dioxide waste from the body’s cells, the blood re-enters the right atrium and the process begins again.

In most people, this whole circulatory path only takes about a minute to complete!

Valves of the Heart

You may be wondering how the heart ensures that blood flows in the right direction between these chambers and blood vessels. You may also have heard of “heart valves” referred to in a medical context.

Heart valves are just that – biological valves that only allow blood to flow through the heart in one direction, ensuring that all the blood gets to where it needs to be.

Here is a list of the most important valves in the heart, and an explanation of why they are important:

• The Tricuspid Valve . The tricuspid valve is what is called an “atrioventricular” valve. As you might guess by the name, it ensures that blood only flows from the atrium to the ventricle – not the other way around. These atrioventricular valves have to stand up to very high pressures to ensure that no blood gets through, as the ventricle contracts quite powerfully to squeeze blood out. The tricuspid valve is the valve that ensures that blood in the right ventricle goes into the pulmonary artery and reaches the lungs, instead of being pushed back into the right atrium.
• The Pulmonary Valve . The pulmonary valve is what is called a semilunar valve. Semilunar valves are found in arteries leaving the heart. Their role is to prevent blood from flowing backwards from the arteries into the heart’s chambers. This is important because the ventricles “suck” blood in from the atria by expanding after they have expelled blood into the arteries. Without properly functioning semilunar valves, blood can flow back into the ventricle instead of going to the rest of the body. This drastically decreases the efficiency with which the heart can move oxygenated blood through the body. The pulmonary valve lies in between the pulmonary artery and the left ventricle, where it ensures that blood pumped into the pulmonary artery continues to the lungs instead of returning to the heart.
• The Mitral Valve . The mitral valve is the other atrioventricular valve. This one lies between the left atrium and the left ventricle. It prevents blood from flowing back from the ventricle into the atrium, ensuring that that blood is pumped to the rest of the body instead! The mitral valve lies at the opening of the aorta, which is the largest blood vessel in the body. The aorta is the central artery from which all other arteries fill. It is thicker than a garden hose, extends all the way from our hearts down to our pelvis, where it splits in two to become the femoral artery of each leg.
• The Aortic Valve . As you might have guessed, the aorta needs a semilunar valve just like the pulmonary artery does. The aortic valve prevents blood from flowing backwards from the aorta into the left ventricle as the left ventricle “sucks” in oxygenated blood from the left atrium.

Many people have minor irregularities with these valves, such as mitral valve prolapse, which make their hearts less efficient or more prone to experiencing problems. People with minor valve issues can often lead a normal, healthy life.

However, total failure of any of these valves can be catastrophic for the heart and for blood flow. That’s why people with conditions like mitral valve prolapse are often turned down by the military and other programs that involve conditions which can be very taxing for the heart.

The Sinoatrial Node

The sinoatrial node is another very important part of the heart. It is a group of cells in the wall of the right atrium of the heart – and it is what keeps the heart pumping!

The cells in the sinoatrial node produce small electrical impulses in a regular rhythm. These impulses are what drive the contractions of the four chambers of the heart.

Artificial pacemakers replicate the action of the sinoatrial node by making similar electrical impulses for people whose sinoatrial node isn’t functioning properly. However, healthy people have a natural pacemaker built right into the heart!

Moore, K. L., Agur, A. M., & Dalley, A. F. (2018). Clinically oriented anatomy. Philadelphia: Wolters Kluwer. Heart. (n.d.). Retrieved July 08, 2017, from http://www.innerbody.com/image/card01.html (n.d.). Retrieved July 08, 2017, from https://training.seer.cancer.gov/anatomy/cardiovascular/heart/structure.html Blood Vessels. (2017, May 19). Retrieved July 08, 2017, from https://www.fi.edu/heart/blood-vessels

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Human heart: Anatomy, function & facts

The human heart is an organ that pumps blood throughout the body via the circulatory system.

Additional resources

The human heart is an organ that pumps blood throughout the body via the vessels of the circulatory system , supplying oxygen and nutrients to the tissues and removing carbon dioxide and other wastes. 

"The tissues of the body need a constant supply of nutrition in order to be active," said Dr. Lawrence Phillips, a cardiologist at NYU Langone Medical Center in New York. "If [the heart] is not able to supply blood to the organs and tissues, they'll die."

The human heart is located in the center of the chest - slightly to the left of the sternum (breastbone). It sits between your lungs and is encased in a double-walled sac called the pericardium, according to the Texas Heart Institute . The pericardium serves to protect the heart and anchor it inside the chest. Pericardial fluid acts as a lubricant between the outer layer, the parietal pericardium, and the inner layer, the serous pericardium. The fluid lubricates the heart during contractions and movements of the lungs and diaphragm .

Related: Heart of the Matter: 7 Things to Know About Your Ticker

What does the human heart look like?

In humans, the heart is roughly the size of a large fist and weighs between about 10 and 12 ounces (280 and 340 grams) in men, and between 8 and 10 ounces (230 and 280 grams) in women, according to Henry Gray's " Anatomy of the Human Body ." 

The physiology of the heart basically comes down to "structure, electricity and plumbing," Phillips told Live Science.

The human heart has four chambers: two upper chambers (the atria) and two lower ones (the ventricles), according to the National Institutes of Health . The right atrium and right ventricle together make up the "right heart," and the left atrium and left ventricle make up the "left heart." A wall of muscle called the septum separates the two sides of the heart.

Related: Spaceflight and long-distance swimming shrink the heart

The heart's outer wall consists of three layers. The outermost wall layer, or epicardium, forms the inner wall of the pericardium. The middle layer, or myocardium, contains the muscle that contracts the heart. The inner layer, or endocardium, lines the heart chambers, according to the British Heart Foundation .

Connecting the upper and lower chambers of the heart are the atrioventricular (AV) valves — made up of the tricuspid valve and the mitral valve. The pulmonary semi-lunar valve separates the right ventricle from the pulmonary artery, and the aortic valve separates the left ventricle from the aorta. The heartstrings, or chordae tendinae, anchor the valves to heart muscles.

• Related; What is heart rate variability

How does the human heart work?

The heart circulates blood through two pathways: the pulmonary circuit and the systemic circuit.

In the pulmonary circuit, deoxygenated blood leaves the right ventricle of the heart via the pulmonary artery and travels to the lungs; then the oxygenated blood returns through the pulmonary vein to the left atrium of the heart, according to the journal Biomedical Sciences .

In the systemic circuit, oxygenated blood leaves the heart and travels through the left ventricle to the aorta, and from there enters the arteries and capillaries where it supplies the body's tissues with oxygen. Deoxygenated blood returns through veins to the venae cavae, re-entering the heart's right atrium.

Of course, the heart is also a muscle, so it needs a fresh supply of oxygen and nutrients, too, Phillips said.

"After the blood leaves the heart through the aortic valve, two sets of arteries bring oxygenated blood to feed the heart muscle," he said. The left main coronary artery, on one side of the aorta, branches into the left anterior descending artery and the left circumflex artery. The right coronary artery branches out on the right side of the aorta.

Blockage of any of these arteries can cause a heart attack , or damage to the heart muscle, Phillips said. A heart attack is distinct from cardiac arrest, which is a sudden loss of heart function that usually occurs as a result of electrical disturbances of the heart rhythm. A heart attack can lead to cardiac arrest, but the latter can also be caused by other problems, he said.

Related: Do other animals get heart attacks?

The heart contains electrical "pacemaker" cells, which cause it to contract — producing a heartbeat.

"Each cell has the ability to be the 'band leader' and [to] have everyone follow," Phillips said. In people with an irregular heartbeat, or atrial fibrillation, every cell tries to be the band leader, he said, which causes them to beat out of sync with one another.

A healthy heart contraction happens in five stages. In the first stage (early diastole), the heart is relaxed. Then the atrium contracts (atrial systole) to push blood into the ventricle. Next, the ventricles start contracting without changing volume. Then the ventricles continue contracting while empty. Finally, the ventricles stop contracting and relax. Then the cycle repeats. Valves prevent backflow, keeping the blood flowing in one direction through the heart.

By the end of the day, your heart will have beaten around 100,000 times (around 60 to 80 beats per minute). This will pump around 1.5 gallons (around 6.8 liters) of blood per minute through the 60,000 miles (around 97,000 kilometers) of blood vessels that are in the human body , according to the Cleveland Clinic . 

Can humans get heartworm?

Heartworm is a disease that affects pets - predominantly dogs - resulting in heart failure and organ damage, according to the U.S. Food and Drug Administration (FDA). The disease is caused by a parasitic worm - called Dirofilaria immitis - which enters the pet's body from an infected mosquito bite. Humans, however, are not a natural host for the parasites - the heartworm larvae often die before reaching adulthood - therefore cases in people are very rare. A review published in 2005 in the journal Veterinary Parasitology found that between 1941 and 2005, there had been 81 reported cases of heartworm in humans. 

• The National Institutes of Health has  information about heart and vascular diseases .
• The American Heart Association has tips about  how to keep your heart healthy .

This article was updated on Oct. 22, 2021 by Live Science staff writer Scott Dutfield. 

Follow Tanya Lewis on  Twitter . Follow us @livescience , Facebook & Google+ .

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• Biology Article

Human Heart

The heart is a muscular organ that is situated in the front of the chest. It pumps blood all through the body in a process called circulation. Apart from the heart, the blood vessels and blood as a unit constitute the cardiovascular system.

Table of Contents

• Introduction
• Functions of the Human Heart

Types of Circulation

Pericardium, structure of the heart wall, chambers of the heart, blood vessels, facts about human heart.

• Important Questions about the Human Heart
• Practise Labelling the Human Heart Diagram

Introduction to the Human Heart

The human heart is one of the most important organs responsible for sustaining life. It is a muscular organ with four chambers. The size of the heart is the size of about a clenched fist.

The human heart functions throughout a person’s lifespan and is one of the most robust and hardest working muscles in the human body.

Besides humans, most other animals also possess a heart that pumps blood throughout their bodies. Even invertebrates such as grasshoppers possess a heart like pumping organ, though they do not function the same way a human heart does.

Also Refer:  Human Circulatory System

Position of Heart in Human Body

The human heart is located between the lungs in the thoracic cavity, slightly towards the left of the sternum (breastbone). It is derived from the embryonic mesodermal germ layer.

The Function of Heart

The function of the heart in any organism is to maintain a constant flow of blood throughout the body. This replenishes oxygen and circulates nutrients among the cells and tissues.

Following are the main functions of the heart:

• One of the primary functions of the human heart is to pump blood throughout the body.
• Blood delivers oxygen, hormones, glucose and other components to various parts of the body, including the human heart.
• The heart also ensures that adequate blood pressure is maintained in the body

There are two types of circulation within the body, namely pulmonary circulation and systemic circulation.

Pulmonary circulation (blue) and Systemic circulation (red)

• Pulmonary circulation is a portion of circulation responsible for carrying deoxygenated blood away from the heart , to the lungs and then bringing oxygenated blood back to the heart.
• Systemic circulation is another portion of circulation where the oxygenated blood is pumped from the heart to every organ and tissue in the body, and deoxygenated blood comes back again to the heart.

Now, the heart itself is a muscle and therefore, it needs a constant supply of oxygenated blood. This is where another type of circulation comes into play, the coronary circulation.

• Coronary circulation is an essential portion of the circulation, where oxygenated blood is supplied to the heart. This is important as the heart is responsible for supplying blood throughout the body.
• Moreover, organs like the brain need a steady flow of fresh, oxygenated blood to ensure functionality.

In a nutshell, the circulatory system plays a vital role in supplying oxygen, and nutrients and removing carbon dioxide and other wastes from the body. Let us gain a deeper insight into the various anatomical  structures of the heart:

Structure of the Human Heart

The human heart is about the size of a human fist and is divided into four chambers, namely two ventricles and two atria . The ventricles are the chambers that pump blood and the atrium are the chambers that receive blood. Among these both the right atrium and ventricle make up the “right heart,” and the left atrium and ventricle make up the “left heart.”  The structure of the heart also houses the biggest artery in the body – the aorta .

The right and the left region of the heart are separated by a wall of muscle called the septum. The right ventricle pumps the blood to the lungs for re-oxygenation through the pulmonary arteries. The right semilunar valves close and prevent the blood from flowing back into the heart. Then, the oxygenated blood is received by the left atrium from the lungs via the pulmonary veins.  Read on to explore more about the structure of the heart.

External Structure of Heart

One of the very first structures which can be observed when the external structure of the heart is viewed is the pericardium.

The human heart is situated to the left of the chest and is enclosed within a fluid-filled cavity described as the pericardial cavity. The walls and lining of the pericardial cavity are made up of a membrane known as the pericardium.

The pericardium is a fibre membrane found as an external covering around the heart. It protects the heart by producing a serous fluid, which serves to lubricate the heart and prevent friction between the surrounding organs. Apart from the lubrication, the pericardium also helps by holding the heart in its position and by maintaining a hollow space for the heart to expand itself when it is full. The pericardium has two exclusive layers—

• Visceral Layer:  It  directly covers the outside of the heart.
• Parietal Layer: It  forms a sac around the outer region of the heart that contains the fluid in the pericardial cavity.

The heart wall is made up of 3 layers, namely:

• Epicardium – Epicardium is the outermost layer of the heart. It is composed of a thin-layered membrane that serves to lubricate and protect the outer section.
• Myocardium – This is a layer of muscle tissue and it constitutes the middle layer wall of the heart. It contributes to the thickness and is responsible for the pumping action.
• Endocardium – It is the innermost layer that lines the inner heart chambers and covers the heart valves. Furthermore, it prevents the blood from sticking to the inner walls, thereby preventing potentially fatal blood clots.

Internal Structure of Heart

The internal structure of the heart is rather intricate with several chambers and valves that control the flow of blood.

Vertebrate hearts can be classified based on the number of chambers present. For instance, most fish have two chambers, and reptiles and amphibians have three chambers. Avian and mammalian hearts consists of four chambers. Humans are mammals; hence, we have four chambers, namely:

• Left atrium
• Right atrium
• Left ventricle
• Right ventricle

Atria are thin and have less muscular walls and are smaller than ventricles. These are the blood-receiving chambers that are fed by the large veins.

Ventricles are larger and more muscular chambers responsible for pumping and pushing blood out into circulation. These are connected to larger arteries that deliver blood for circulation.

The right ventricle and right atrium are comparatively smaller than the left chambers. The walls consist of fewer muscles compared to the left portion, and the size difference is based on their functions. The blood originating from the right side flows through the pulmonary circulation, while blood arising from the left chambers is pumped throughout the body.

In organisms with closed circulatory systems, the blood flows within vessels of varying sizes. All vertebrates, including humans, possess this type of circulation. The external structure of the heart has many blood vessels that form a network, with other major vessels emerging from within the structure. The blood vessels typically comprise the following:

• Veins supply deoxygenated blood to the heart via inferior and superior vena cava, and it eventually drains into the right atrium.
• Capillaries are tiny, tube-like vessels which form a network between the arteries to veins.
• Arteries are muscular-walled tubes mainly involved in supplying oxygenated blood away from the heart to all other parts of the body. Aorta is the largest of the arteries and it branches off into various smaller arteries throughout the body.

Also Refer: Difference between Arteries and Veins

Valves are flaps of fibrous tissues located in the cardiac chambers between the veins. They ensure that the blood flows in a single direction (unidirectional). Flaps also prevent the blood from flowing backwards. Based on their function, valves are of two types:

• Atrioventricular valves are between ventricles and atria. The valve between the right ventricle and right atrium is the tricuspid valve, and the one which is found between the left ventricle and left atrium is known as the mitral valve.
• Semilunar valves are located between the left ventricle and the aorta. It is also found between the pulmonary artery and the right ventricle.

Also Read: Blood and its Composition

• The heart pumps around 6,000-7,500 litres of blood in a day throughout the body.
• The heart is situated at the centre of the chest and points slightly towards the left.
• On average, the heart beats about 100,000 times a day, i.e., around 3 billion beats in a lifetime.
• The average male heart weighs around 280 to 340 grams (10 to 12 ounces). In females, it weighs around 230 to 280 grams (8 to 10 ounces).
• An adult’s heart beats about 60 to 100 times per minute, and a newborn baby’s heart beats at a faster pace than an adult which is about 90 to 190 beats per minute.

Also Refer:  Heart Health

To know more about the human heart structure and function, or any other related concepts such as arteries and veins, the internal structure of the heart, and the external structure of the heart,  e xplore BYJU’S Biology. Also, learn an  easy diagram of the heart, concepts and relevant questions for the human heart for Class 10  by downloading BYJU’S – The Learning App.

More to Explore:

• Heart Diseases
• Hepatic Portal System

Frequently Asked Questions

1. what is pulmonary circulation explain..

Pulmonary circulation is a type of blood circulation responsible for carrying deoxygenated blood away from the heart, and to the lungs, where it is oxygenated. The system then brings oxygenated blood back to the heart to be pumped throughout the body.

2. Define systemic circulation.

In systemic circulation, the heart pumps the oxygenated blood through the arteries to every organ and tissue in the body, and then back again to the heart through a system of veins.

3. Elaborate on coronary circulation and its significance.

The heart is a muscle, and it needs a constant supply of oxygenated blood to survive and work effectively. This is where coronary circulation fulfils this function through a network of arteries and veins in the heart. The coronary arteries supply oxygenated blood to the heart, and the cardiac veins drain the blood once it has been deoxygenated by the tissues of the heart.

4. Briefly explain the structure of the human heart.

The human heart is divided into four chambers, namely two ventricles and two atria. The ventricles are the chambers that pump blood and atrium are the chambers that receive the blood. Among which, the right atrium and ventricle make up the “right portion of the heart”, and the left atrium and ventricle make up the “left portion of the heart.”

5. Name the chambers of the heart.

6. what is pericardium explain its function..

The pericardium is a fibrous membrane that envelops the heart. It also serves a protective function by producing a serous fluid, which lubricates the heart and prevents friction between the surrounding organs. Furthermore, the pericardium also holds the heart in its position and provides a hollow space for the heart to expand and contract.

7. Explain the three layers of the heart wall.

• Epicardium – This is the outermost layer of the heart. It is composed of a thin layer of membrane that protects and lubricates the outer section.
• Myocardium – This is a layer of muscle tissue that constitutes the middle layer wall of the heart. It is responsible for the heart’s “pumping” action.
• Endocardium – The innermost layer that lines the inner heart chambers and covers the heart valves. Prevents blood from sticking, thereby avoiding the formation of fatal blood clots.

8. Explain the three major blood vessels of the human body.

The  blood vessels comprise:

• Veins – It supplies deoxygenated blood to the heart via inferior and superior vena cava, eventually draining into the right atrium.
• Capillaries – They are minuscule, tube-like vessels which form a network between the arteries and veins.
• Arteries – These are muscular-walled tubes responsible for supplying oxygenated blood away from the heart to all other parts of the body.

9. What is the function of the heart valves? Provide examples of various valves.

Valves are flaps of tissues that are present in cardiac chambers between the veins. They prevent the backflow of blood. Examples include the atrioventricular valves, tricuspid valves, mitral valves and the semilunar valves.

10. What is meant by myocardial infarction?

Myocardial infarction is a serious medical condition where the blood flow to the heart is reduced or entirely stopped. This causes oxygen deprivation in the heart muscles, and prolonged deprivation can cause tissues to die.

Label the Heart Diagram below:

Practice your understanding of the heart structure. Drag and drop the correct labels to the boxes with the matching, highlighted structures.

Instructions to use:

• Hover the mouse over one of the empty boxes.
• One part in the image gets highlighted.
• Identify the highlighted part and drag and drop the correct label into the same box.
• After finishing all the labelling, check your answers.
• Semilunar valve
• Pulmonary artery
• Pulmonary vein

Put your understanding of this concept to test by answering a few MCQs. Click ‘Start Quiz’ to begin!

Select the correct answer and click on the “Finish” button Check your score and answers at the end of the quiz

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The Anatomy of the Heart, Its Structures, and Functions

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• Cell Biology
• Weather & Climate
• B.A., Biology, Emory University
• A.S., Nursing, Chattahoochee Technical College

The heart is the organ that helps supply blood and oxygen to all parts of the body. It is divided by a partition (or septum) into two halves. The halves are, in turn, divided into four chambers. The heart is situated within the chest cavity and surrounded by a fluid-filled sac called the pericardium. This amazing muscle produces electrical impulses that cause the heart to contract, pumping blood throughout the body. The heart and the circulatory system together form the cardiovascular system.

Heart Anatomy

The heart is made up of four chambers:

• Atria : Upper two chambers of the heart.
• Ventricles : Lower two chambers of the heart.

The heart wall consists of three layers:

• Epicardium : The outer layer of the wall of the heart.
• Myocardium : The muscular middle layer of the wall of the heart.
• Endocardium : The inner layer of the heart.

Cardiac Conduction

Cardiac conduction is the rate at which the heart conducts electrical impulses. Heart nodes and nerve fibers play an important role in causing the heart to contract.

• Atrioventricular Bundle : A bundle of fibers that carry cardiac impulses.
• Atrioventricular Node : A section of nodal tissue that delays and relays cardiac impulses.
• Purkinje Fibers : Fiber branches that extend from the atrioventricular bundle.
• Sinoatrial Nod e: A section of nodal tissue that sets the rate of contraction for the heart.

Cardiac Cycle

The Cardiac cycle is the sequence of events that occurs when the heart beats. Below are the two phases of the cardiac cycle:

• Diastole phase : The heart ventricles are relaxed and the heart fills with blood.
• Systole phase : The ventricles contract and pump blood to the arteries.

Heart valves are flap-like structures that allow blood to flow in one direction. Below are the four valves of the heart:

• Aortic valve : Prevents the backflow of blood as it is pumped from the left ventricle to the aorta.
• Mitral valve : Prevents the backflow of blood as it is pumped from the left atrium to the left ventricle.
• Pulmonary valve : Prevents the backflow of blood as it is pumped from the right ventricle to the pulmonary artery .
• Tricuspid valve : Prevents the backflow of blood as it is pumped from the right atrium to the right ventricle.

Blood Vessels

Blood vessels are intricate networks of hollow tubes that transport blood throughout the entire body. The following are some of the blood vessels associated with the heart:

• Aorta : The largest artery in the body, of which most major arteries branch off from.
• Brachiocephalic artery : Carries oxygenated blood from the aorta to the head, neck, and arm regions of the body.
• Carotid arteries : Supply oxygenated blood to the head and neck regions of the body.
• Common iliac arteries: Carry oxygenated blood from the abdominal aorta to the legs and feet.
• Coronary arteries : Carry oxygenated and nutrient-filled blood to the heart muscle.
• Pulmonary artery : Carries deoxygenated blood from the right ventricle to the lungs.
• Subclavian arteries : Supply oxygenated blood to the arms.
• Brachiocephalic veins : Two large veins that join to form the superior vena cava.
• Common iliac veins : Veins that join to form the inferior vena cava.
• Pulmonary veins : Transport oxygenated blood from the lungs to the heart.
• Venae cavae : Transport de-oxygenated blood from various regions of the body to the heart.
• The Cardiac Cycle
• The Function of the Heart Ventricles
• Circulatory System: Pulmonary and Systemic Circuits
• How the Main Pulmonary Artery Delivers Blood to the Lungs
• Anatomy of the Heart: Valves
• Types of Cells in the Human Body
• 4 Steps of Cardiac Conduction
• Atria of the Heart Function
• Anatomy of the Heart: Aorta
• Heart Nodes and Electrical Conduction
• Superior and Inferior Venae Cavae
• Evolution of the Human Heart’s Four Chambers
• Coronary Arteries and Heart Disease
• The 3 Layers of the Heart Wall
• Anatomy of the Heart: Pericardium
• Artery Structure, Function, and Disease

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The human heart

Find out more about the human heart – the main organ of your circulatory system – and its essential role in the body.

What is the heart?

The heart is one of the most important organs in the human body. It is a powerful fist-sized muscle that pumps blood around the body through a network of blood vessels – together, the heart and blood vessels make up the body’s cardiovascular system.

Our hearts beat on average 72 times every minute – over 100,000 times per day. Each minute, vital materials are circulated in our blood and waste products are removed. Each minute counts in helping our body function.

• Download a fun poster to help children learn more about the heart   (2.2MB PDF)

What side is the heart located?

The heart is located in the front of the chest, just behind and slightly left of the breastbone, and between the left and right lungs. Because the heart sits more in the left side of the chest, the left lung is slightly smaller to make room. The ribcage protects the heart.

Heart anatomy

The heart muscle consists of walls, chambers, valves, blood vessels and an electrical conduction system. The entire heart is surrounded by a protective sac called the pericardium that produces fluid to lubricate the heart and protect it from rubbing against other organs.

The heart walls

The heart walls are the muscles that contract and relax to pump blood around the body. There is a layer of muscular tissue (septum) that divides the heart walls into the left and right sides.

The heart walls have three layers: endocardium (inner layer), myocardium (muscular middle layer) and epicardium (protective outer layer that makes up one layer of the pericardium).

The heart chambers

The heart is divided into four chambers: two on the right (right atrium and right ventricle) and two on the left (left atrium and left ventricle). The atria are the upper chambers, and the ventricles are the lower chambers.

• Right atrium: The right atrium receives oxygen-poor blood from the veins and pumps it to the right ventricle.
• Right ventricle: The right ventricle receives the oxygen-poor blood from the right atrium and pumps it to the lungs through the pulmonary arteries, where the blood is loaded with oxygen.
• Left atrium: The left atrium receives the oxygen-rich blood from the lungs through the pulmonary veins and pumps it to the left ventricle.
• Left ventricle: The left ventricle receives the oxygen-rich blood from the left atrium and pumps it to the rest of the body through the aorta. The left ventricle is slightly larger than the right ventricle and is the strongest chamber of the heart. The contractions by the left ventricle are what create blood pressure.

The heart chambers receive oxygen-poor blood from the veins and pump oxygen-rich blood around the body.

Heart valves

The heart has four valves that act like doors to each of its chambers.

• Tricuspid valve: The tricuspid valve lies between the right atrium and right ventricle.
• Mitral valve: The mitral valve lies between the left atrium and left ventricle.
• Aortic valve: The aortic valve lies between the left ventricle and the aorta, the main artery that carries oxygen-rich blood to the body.
• Pulmonic valve: The pulmonic valve lies between the right ventricle and the pulmonary arteries, the arteries that carry oxygen-poor blood to the lungs to be loaded with oxygen.

The valves open and close to allow blood to flow through the heart, and they keep the blood moving in the correct direction by opening only one way and only when they need to. The valves have flaps that open and close once during each heartbeat.

The heart valves open and close to control the flow of blood through the heart chambers.

Blood vessels

The heart pumps blood through three main types of blood vessels: arteries, veins and capillaries.

• Arteries: Arteries carry oxygen-rich blood from the heart throughout the body. They begin with the aorta, the large artery leaving the heart, and branch several times, becoming smaller and smaller as they carry blood further away from the heart to the organs.
• Veins: Veins carry oxygen-poor blood from the body back to the heart, where it can be pumped to the lungs to be loaded up with oxygen again. Veins become larger and larger as they get closer to the heart.
• Capillaries: Capillaries are the small blood vessels that connect the arteries and veins and through which the body exchanges oxygen-rich blood with oxygen-poor blood. Their thin walls allow oxygen, nutrients and waste products like carbon dioxide to pass to and from the cells of the organs.

The heart requires a supply of oxygen and nutrients to function properly, but it does not receive any nourishment from the blood that it pumps through its chambers. Instead, it receives its own supply of oxygen-rich blood through the coronary arteries, a network of arteries that run along the surface of the heart. In coronary artery disease, fatty plaque builds up in the coronary arteries and prevents the heart from getting the oxygen-rich blood it needs.

Electrical conduction system

The heart has an electrical conduction system that powers the pumping of the heart, which in turn keeps blood circulating through the body. This system includes two nodes and a specialised network of electrical bundles and fibres.

• Sinoatrial (SA) node: This small bundle of specialised cells located in the right atrium is known as the heart’s natural pacemaker. It sends the signals that make the heart beat and sets the rate and rhythm of the heartbeat.
• Atrioventricular (AV) node: This cluster of cells is located in the centre of the heart, between the atria and ventricles. It carries electrical signals from the heart’s upper chambers to its lower ones.
• His-Purkinje network: This pathway of fibres sends the electrical impulse to the walls of the ventricles, causing them to contract and pump blood out.

The electrical conduction system of the heart triggers its beating.

Heart function

The main function of the heart is to pump oxygen- and nutrient-rich blood around the body. This circulation of blood around the body results in the continuous exchange of oxygen-rich blood with oxygen-poor blood, providing all systems of the body with the oxygen and nutrients they need to function properly.

The heart works with other bodily systems to control heart rate and blood pressure .

How does the heart beat?

Heartbeats are triggered by the electrical impulses that travel through the electrical conduction system of the heart. They occur when the heart contracts and relaxes. The four chambers of the heart work together, alternately contracting and relaxing, to pump blood through the heart. When the ventricles contract, blood is forced into the blood vessels going to the lungs and body. When the ventricles relax, they are filled with blood coming from the atria.

The electrical impulses start in the SA node, located in the right atrium. This electrical activity spreads through the walls of the atria, causing them to contract.

The AV node, located between the atria and ventricles, slows this electrical activity before it enters the ventricles, giving the atria time to contract before the ventricles do.

The electrical activity then passes through the His-Purkinje network to the walls of the ventricles, causing them to contract. This contraction pumps blood out to the lungs and body.

The SA node fires another electrical impulse, and the cycle begins again.

How does the heart work with other organs

The heart works with other systems in the body to control the heart rate, blood pressure and other body functions. The primary systems are the nervous system and endocrine system.

• Nervous system: The nervous system originates in the brain. It controls movements, thoughts and other body systems and processes. The nervous system helps control the heart rate by sending signals that tell the heart when to beat faster or slower, such as during times of stress or rest.
• Endocrine system: The endocrine system is made up of glands that create and release hormones that control nearly all the processes in the body. These hormones tell the blood vessels to constrict or relax, which affects blood pressure . Hormones from the thyroid gland can also tell the heart to beat faster or slower.

Problems with these body systems can affect the heart and lead to cardiovascular disease . For example, diabetes is an endocrine disorder that develops when not enough of the hormone insulin is made, or when insulin in the body does not work as it should. Diabetes is a major risk factor for cardiovascular disease, and it can also cause damage to the nervous system.

Conditions that may affect the human heart

Conditions that affect the heart are among the most common type of disorder. In fact, cardiovascular disease (CVD) is the world’s leading cause of death and disability. CVD refers to all the diseases of the heart and circulation, including the following.

• Atrial fibrillation : Atrial fibrillation is a common, irregular heartbeat condition that is linked to one in three strokes.
• Coronary heart disease : Also known as coronary artery disease, coronary heart disease is a common condition where the major blood vessels to the heart (coronary arteries) become blocked and narrowed, restricting the flow of oxygen-rich blood to the heart.
• Diabetes : Diabetes is a condition in which the body cannot maintain healthy blood glucose levels. People living with diabetes are over twice as likely to develop CVD as the general population.
• Heart attack : A heart attack occurs when the heart is deprived of oxygen due to a blocked artery, and it can lead to death if not treated immediately. It is also known as myocardial infarction.
• Heart failure : Heart failure is when the heart does not work as well as it should in pumping blood and oxygen around the body. Heart failure preserved ejection fraction (HFpEF), a “stiff” type of heart failure where the heart cannot relax properly, is the most common type.
• Stroke : Stroke occurs when the blood supply to the brain is suddenly cut off, such as by a blood clot blocking an artery to the brain. It is a leading cause of disability globally.

The main underlying cause of CVD is atherosclerosis – the build-up of fatty plaques on the walls of the arteries. These plaques are made up of fat, cholesterol, calcium and other substances. Over time, the plaques harden, narrowing the opening of the arteries and restricting blood flow. These atherosclerotic plaques can break, forming a thrombus (blood clot) that can further limit, or even block the flow of blood throughout the body.

How to keep the heart healthy

There are several factors that can impact the health of the heart and increase the risk of heart conditions . Positive lifestyle changes to help keep the heart healthy include the following.

• Eat a nutritious diet that includes a variety of colourful fruit and vegetables , as well as wholegrains and protein .
• Limit intake of processed foods. It’s important to check the nutrition labels of these foods and limit their intake, as they can contain high amounts of saturated fat , trans fat, LDL cholesterol , salt and sugar.
• Avoid soft drinks and other sugary drinks; stay well-hydrated with water instead.
• Choose healthier sources of fat , such as nuts, seeds, avocado and salmon.
• Make regular exercise or physical activity part of your daily routine. Experts recommend at least 30 minutes of moderate-intensity physical activity on most days of the week. Exercise sessions do not need to be done in one block – even small amounts of activity can help.
• Maintain a healthy weight by eating a balanced, nutritious diet and exercising regularly .
• Limit intake of alcohol . Excessive amounts of alcohol can increase the levels of some fats in the blood, reduce the levels of “good” (HDL) cholesterol and increase blood pressure . These can all increase the risk of CVD.
• Quit smoking . Smoking significantly increases the risk of CVD. Both first-hand smoking and long-term exposure to second-hand smoke can damage the arteries that supply blood to the heart and body.

How is HRI protecting the human heart?

HRI conducts groundbreaking research across a broad range of heart-related topics, in our mission to reduce the number of people who die from diseases affecting the heart and to offer a better life for those already suffering from heart disease by developing new treatments and medical devices.

Our Cardiovascular-protective Signalling and Drug Discovery Group is investigating how to repurpose existing drugs for next-generation therapies for heart disease and CVDs.

Our Clinical Research Group is conducting research to detect the earliest signs of heart and blood vessel damage with a view to preventing serious complications later in life due to CVDs such as congenital heart disease .

Our Heart Rhythm and Stroke Prevention Group is investigating strategies to screen for the heart condition atrial fibrillation in the general population, to prevent associated stroke .

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Essay on Human Heart: Location and structure (With Diagram)

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In this essay we will discuss about:- 1. Location of Human Heart 2. Weight of Human Heart 3. Structure 4. Heart Beat 5. Heart Rate 6. Cardiac Output 7. Pulse 8. Cardiac Cycle 9. Heart Sounds 10. Auto Rhythmicity of Heart Beat 11. Electrocardiogram.

• Essay on the Electrocardiogram

Essay # 1. Location of Human Heart:

Human heart is located between the lungs in the thoracic cavity.

Pericardium (Protective Covering):

It is a 2-layered sac consisting of outer parietal pericardium and inner visceral pericardium attached to the heart. In between the two layers, a space, the pericardial cavity is present which is filled with a pericardial fluid. The pericardium protects the heart from shocks and mechanical injuries and also allows free movements of the heart.

Essay # 2. Weight of Human Heart:

An average adult heart is about 12 cm. Its weight varies in males from 280-340 g (average 300 g) and in females from 230-280 g (average 250 g).

Weight of the heart is said to be about 0.45% of body weight in males and 0.40% in females. Adult weight is achieved between 17-20 years.The heart is a hollow, fibro muscular organ of a somewhat conical or pyramidal form with upper broad part, the base and lower narrow, the apex. The apex is slightly directed to the left.

Essay # 3. Structure of Human Heart:

External Structure:

Human heart is four chambered, consisting of two atria and two ventricles.

(i) Grooves (Sulci):

The left and right atria are separated externally by a shallow vertical interatrial groove. The atria are demarcated externally from the ventricles by an oblique groove called atrioventricular sulcus. There are present coronary sulcus, anterior inter ­ventricular sulcus and posterior inter ventricular sulcus. These have coronary arteries, through which the heart receives blood.

(ii) Atria (sing, atrium):

As stated earlier, there are left and right atria which have thin walls. The left atrium is smaller than the right atrium. The right atrium is a roughly quadran­gular chamber. Each atrium has an appendage called an auricle (L auris- ear), so named because its shape resembles a dog’s ear. The auricle increases the atrium’s surface area. The superior vena cava, inferior vena cava and coronary sinus open into the right atrium.

(a) The superior vena cava carries blood from the body’s upper region,

(b) The inferior vena cava is larger than the superior and carries blood from the lower body’s region,

(c) The coronary sinus carries the majority of blood from the heart itself. The coronary veins open into the coronary sinus. The right atrium receives deoxygenated blood. The left atrium is less in volume than that of right atrium but it has thicker walls. The left atrium is roughly cuboidal. It projects as the left auricle towards the left side.

(d) The left atrium receives oxygenated blood from the lungs through two pairs of pulmonary veins.

(iii) Ventricles:

There are present left and right ventricles with thick walls. The wall of the right ventricle is thinner than that of the left ventricle. The left ventricle is longer and narrower than the right ventricle. The walls of the left ventricle are about three times thicker than the right ventricle.

(iv) Pulmonary Trunk and Aorta:

The pulmonary trunk arises from the right ventricle. It divides into left and right pulmonary arteries that carry deoxygenated blood to the lungs. The aorta arises from the left ventricle. It is divisible into the ascending aorta, arch of aorta and descending aorta.

The right and left coronary arteries arise from the ascending aorta. The arch of the aorta (also called aortic arch) gives rise to the brachiocephalic artery (Innominate artery), left common carotid artery and left subclavian artery. The descend­ing aorta runs through the thorax and abdomen and hence it is divisible into thoracic and abdominal parts.

The pulmonary trunk is connected with the aorta by the ligamentum arteriosum that represents the remnant of an embryonic connection between the pulmonary trunk and aorta. In embryo the ligamentum arteriosum is called ductus arteriosus. Coronary arteries arise from the ascending aorta and supply blood to the heart.

Internal Structure:

The internal structure of the heart can be better studied by dissect­ing it from the ventral side.

The two thin walled atria are separated from each other by the interatrial septum. The right atrium receives the openings of superior vena cava, inferior vena cava and coronary sinus. The opening of inferior vena cava is guarded by Eustachian valve.

The opening of the coronary sinus has coronary or Thebasian valve. In the right atrium adjoin­ing the interatrial septum, an oval depression, the fossa ovalis is present. It marks the position of an opening, the foramen ovale, between the two atria in the foetus, but in the adult it persists only as a depression. The left artrium receives four openings of pulmonary veins.

(ii) Bicuspid and Tricuspid Valves:

The artrioventricular opening between the left atrium and the left ventricle is guarded by the bicuspid valve, also called mitral valve (having two flaps). The right atrio-ventricular opening is guarded by the tricuspid valve, as it has three flaps.

Attached to the flaps of the bicuspid and tricuspid valves are special fibrous cords, the chordae tendineae, which are joined to the other ends with the special muscles of the ventricular wall, the papillary muscles. The chordae tendineae prevent the bicuspid and tricuspid valves from collapsing back into the atria during powerful ventricular contractions.

The chordae tendineae can be seen extending from the valves to the columnae carneae, which are the muscular ridges or projections on the walls of the ventricles. The columnae carneae divide the cavity of the ventricles into smaller spaces, known as fissures. The walls of the ventricles are thicker than the atria. The thickest portion of the human heart is the wall of the left ventricle.

(iv) Semilunar valves:

As stated in the external structure, the pulmonary trunk and aorta arise from the right and left ventricles respectively. At the base of the pulmonary trunk and aorta are located three half-moon shaped pockets known as pulmonary semilunar valves and aortic semilunar valves respectively. These valves allow the free and forward flow of blood, but prevent any backward flow.

Thus the valves of the heart are:

(a) Bicuspid valve,

(b) Tricuspid valve,

(c) Aortic semilunar valves and

(d) Pulmonary semilunar valves.

Histologically, the heart has an outermost smooth coelomic epithelium— the visceral pericardium, the middle thick muscular layer— the myocardium, composed of cardiac muscle fibres and the innermost layer, the endothelium consisting of simple squamous epithelial cells.

The heart collects blood through both the atria and then distributes it through the ventricles. The action of heart includes contractions and relaxations of the atria and ven­tricles. A contraction of the heart is called a systole and its relaxation a diastole. The atria and ventricles contract alternately.

The contraction of heart (systole) and the relaxation of heart (diastole) constitute the heart beat. The contraction of atria is initiated and activated by the sinoatrial node (SA Node— pace maker; Fig. 18.10) which spreads waves of contraction across the walls of the atria via muscle fibres at regular intervals.

When the wave of contraction originating from the sinoatrial node reaches the atrio­ventricular node (AV Node— pace setter), the latter is stimulated and excitatory impulses are rapidly transmitted from it to all parts of the ventricles via bundle of His and Purkinje’s fibres.

These impulses stimulate the ventricles to contract simultaneously. The ventricles force blood through long system of arteries and hence must exert great pressure on the blood.

Essay # 4. Heart Beat:

What is heart beat? Heart beat is the rhythmic contraction and relaxation of the heart. Each heart beat includes one systole (contraction phase) and one diastole (relaxation phase) of the heart to distribute and receive blood to and from the body. The heart of a healthy person beats 72 times per minute (average).

Beating is an inherent capacity of the heart. The heart of a resting human being pumps about 5 litres of blood per minute. This means that a quantity of blood equal to the total amount contained in the body passes through the heart each minute. During exercise both the number of beats per minute and the amount of blood pumped per beat are greatly increased.

The heart beat is of two types: neurogenic and myogenic. The neurogenic heart beat is initiated by a nerve impulse coming from a nerve ganglion (mass of nerve cells) situated near the heart. It is present in the heart of some annelids and most arthropods. The myogenic heart beat is initiated by a patch of modified heart muscle itself. It is found in hearts of molluscs and vertebrates including human beings.

Origin of heart beat (Fig. 18.10):

The mammalian heart is myogenic (myomuscle, genic originating from). It means the heart beat originates from a muscle, (however, it is regulated by the nerves). The heart beat originates from the sinoatrial node (SA Node)— pace maker, which lies in the wall of the right atrium near the opening of the superior vena cava.

The SA node is a mass of neuromuscular tissue. Sometimes, the SA-node may become damaged or defective. So the heart does not function properly. This can be remedied by the surgical grafting of an artificial pace maker in the chest of the patient. The artificial pace maker stimulates the heart at regular intervals to maintain its beat.

Conduction of heart beat (Fig. 18.10):

Another mass of neuromuscular tissue, the atrio-ventricular node (AV node) is situated in the wall of the right atrium. The AV node picks up the wave of contraction propagated by SA node. A mass of specialized fibres, the bundle of His, originates from the AV node. The bundle of His divides into two branches, one going to each ventricle.

Within the mycocardium of the ventricles the branches of bundle of His divide into a net work of fine fibres called the Purkinje fibres. The bundle of His and the Purkinje fibres convey impulse of contraction from the AV node to the myocardium of the ventricles. Regulation of heart beat (= Regulation of Cardiac Activity).

The rate of heart beat is regulated by two mechanisms:

(i) Neural Regulation (Fig. 18.11):

The cardiac centre lies in the medulla oblongata of the brain. The cardiac centre is formed of cardio-inhibitor and cardio-accelerator parts. The former decreases the rate of heart beat and the latter accelerates it. The cardio-inhibitor is connected with the heart through vagus nerve (it carries parasympathetic nerve fibres) and cardio accelerator through sympathetic nerve fibres.

Sensory fibres extend from the recep­tors present in the superior vena cava, aorta and carotid sinuses to the cardiovascular centre in the medulla oblongata. The impulses received from the aorta and carotid sinuses decrease the heart rate, whereas the impulses from the vena cava increase the heart rate.

(ii) Hormonal Regulation:

Adrenaline (epinephrine) and noradrenaline (norepineph­rine) hormones are secreted by the medulla of the adrenal glands. Noradrenaline accelerates the heart beat under normal conditions while adrenaline does this function at the time of emergency. These hormones directly influence the SA node.

Thyroxine hormone secreted by thyroid gland increases oxidative metabolism of the body cells. This requires more oxygen and thus indirectly increases heart beat.

Essay # 5. Heart Rate :

Human heart beats about 72 times per minute in an adult person at rest. This is called heart rate of that person. The heart rate increases during exercise, fever, fear and anger. Because smaller animals have the higher metabolic rate, their heart rate is higher than larger animals. An elephant has normal heart rate of about 25 per minute whereas mouse has a normal heart rate of several hundred per minute.

Essay # 6. Cardiac Output (Heart Output):

The amount of blood pumped by heart per minute is called sraidiae output or heart output. Heart of a normal person beats 72 times per minute and pumps out about 70 mL of blood per beat. Thus the cardiac output is 72 x 70 or 5040 mL per minute i.e., about 5 litres per minute which is equivalent to the total body blood volume (about 5.5 litres).

Essay # 7. Pulse:

Pulse is the rhythmic contraction and relaxation in the aorta and its main arteries. Thus pulse is a wave of increase which passes through arteries as the left ventricle pumps its blood into the aorta. Pulse is a regular jerk of an artery. Therefore, it is also called arterial pulse.

The pulse rate is exactly the same as the heart rate because an artery pulses every time the heart beats. Pulse is usually taken on the radial artery in the wrist but it can be taken on any artery that flows near enough to the surface of the body to be felt.

The factors which affect the pulse rate are as follows:

(i) The pulse rate in children is more rapid than in adults,

(ii) The pulse rate is more rapid in the female than in the male,

(iii) When the person is standing up the pulse rate is more rapid than when he/she is lying down,

(iv) When any strong emotion is experienced the pulse rate is increased, for example, anger, excitement, fear, etc. (v) Any exercise increases the rate of the pulse.

Essay # 8. Cardiac Cycle (Fig. 18.12 & 18.13):

The cardiac cycle consists of one heart beat or one cycle of contraction and relaxation of the car­diac muscle. During a heartbeat there is contraction and relaxation of atria and ventricles. The contrac­tion phase is called the systole while the relaxation phase is called the diastole. When either the atria and ventricles are in diastolic or relaxed phase, this is referred to as a joint diastole.

During this phase, the blood flows from the superior and inferior venae cavae into the atria and from the atria to the respec­tive ventricles through auriculo ventricular valves. But there is no flow of blood from the ventricles to the aorta and pulmonary trunk as the semilunar valves remain closed.

The successive stages of the cardiac cycle are briefly described below.

(a) Atrial Systole:

The atria contract due to a wave of contraction, stimulated by the SA node. The blood is forced into the ventricles as the bicuspid and tricuspid valves are open.

(b) Beginning of Ventricular Systole:

The ventricles begin to contract due to a wave of contraction, stimulated by the AV node. The bicuspid and tricuspid valves close immedi­ately producing part of the first heart sound.

(c) Complete Ventricular Systole:

When the ventricles complete their contraction, the blood flows into the pulmonary trunk and aorta as the semilunar valves open.

(d) Beginning of Ventricular diastole:

The ventricles relax and the semilunar valves are closed. This causes the second heart sound.

(e) Complete Ventricular Diastole:

The tricuspid and bicuspid valves open when the pressure in the ventricles falls and blood flows from the atria into the ventricles. Contraction of the heart does not cause this blood flow. It is due to the fact that the pressure within the relaxed ventricles is less than that in the atria and veins. The duration of a cardiac cycle is 0.8 sec.

Essay # 9. Heart Sounds:

The beating heart produces characteristic sounds which can be heard by placing the ear against the chest or by using stethoscope (an instrument which magnifies sounds and conducts them to ear). In a normal person, two sounds are produced per heart beat.

(i) First sound:

This is caused partly by the closure of the bicuspid and tricuspid valves and partly by the contraction of the muscles in the ventricles. The first sound, ‘lubb’ is low pitched, not very loud and of long duration,

(ii) Second sound:

This is caused by the closure of the semilunar valves and marks the end of ventricular systole.

The second sound ‘dup’ is highly pitched, louder, sharper and shorter in duration. The two sounds have been described in words as “lubb dup” and their quality indicates the state of the valves. Damage to the bicuspid or tricuspid valve effects the quality of the first heart sound.

When the semilunar valves are injured, a soft hissing noise “lubb shhh” is heard in place of the second sound. This is called a heart murmur. It may be caused by the syphilis, rheumatic fever or any other disease which injures the semilunar valves and affects their working. Thus, the blood can leak back from the pulmonary trunk and aorta into the ventricles.

Essay # 10. Auto Rhythmicity of Heart Beat:

The automatic rhythmicity of the heart is its ability to contract spontaneously and at a regular rate. As we know, human heart is myogenic (myomuscle, genic originating from), the cardiac impulse normally originates from the SA node (a node of specialized cardiac muscle fibres).

Although the origin of cardiac impulse is myogenic, the rate of its formation and conduction may be changed by the action of nerves.

For example, the sympathetic nerve fibres increase the activity of the SA node to accelerate the heart beat while the vagus 10th cranial nerve (carries parasympathetic nerve fibres) decreases the rate of impulse formation from the SA node and its conduction. Thus vagus cranial nerve decreases the heart beat. AV node, bundle of His and Purkinje fibres together provide auto rhythmicity to the heart.

Essay # 11. Electrocardiogram (ECG) :

ECG is graphic record of the electric current produced by the excitation of the cardiac muscles. The instrument used to record the changes is an electrocardiograph. Waller (1887) first recorded the electrocardiogram but Einthoven (1903) studied ECG in details, therefore, he got Nobel Prize in 1924 for the discovery of ECG. He is also considered “father of the electrocardiography” (the device used).

A normal electro gram (ECG) is composed of a P wave, a QRS wave (complex) and a T wave. The letters are arbitrarily selected and do not stand for any particular words.

1. The P Wave is a small upward wave that represents electrical excitation or the atrial depolarization which leads to contraction of both the atria (atrial contraction). It is caused by the activation of SA node. The impulses of contraction start from the SA node and spread throughout the artia.

2. The QRS Wave (complex) begins after a fraction of second of the P wave. It begins as a small downward deflection (Q) and continues as large upright (R) and triangular wave, ending as downward wave(S) at its base. It represents ventricular de-polarisation (ventricular contraction).

It is caused by the impulses of the contraction from AV node through the bundle of His and Purkinje fibres and the contraction of the ventricular muscles. Thus this wave is due to the spread of electrical impulse through the ventricles.

3. The T Wave is dome-shaped which represents ventricular repolarisation (ven­tricular relaxation). The potential generated by the recovery of the ventricle from the de-polarisation state is called the repolarisation wave. The end of the T-wave marks the end of systole.

Normal P—R interval is < 0.12 to 0.2 sec. Normal QRS complex duration is < 0.10 sec Normal Q—T interval is < 0.42 sec.

Enlargement of the P Wave indicates enlargement of the artia. P—R interval (also called P—Q interval) is the time required for an impulse to travel through the atria and AV node to the remaining conductive tissues. During atherosclerotic heart disease (i.e., formation of plaques and calcification) and rheumatic fever, the P—R interval is lengthened. This is due to the inflammation of atria and AV node.

The enlarged Q and R waves indicate a myocardial infarction (heart attack). The S—T interval represents the time between the end of the spread of impulse through ventricles and its repolarisation. Thus, the S—T segment begins at the end of the S wave and terminates at the beginning of the T wave.

The S—T segment is elevated in acute myocardial infarction and depressed when the heart muscle receives insufficient oxygen. T wave is flat when the heart muscles receive insufficient oxygen as in atherosclerotic heart disease. It may be elevated when the body’s potassium level is increased.

When ECG of a person is to be recorded, four leads (metal electrodes) are attached in the arms and legs. It is done after cleaning and putting a special jelly, which improves electrical conduction. With the help of a rubber suction cup, an additional electrode is placed on the chest.

Now the electrocardiograph is switched on which detects and amplifies the electrical current of the heart and transmits to the recording pen. The latter draws a wavy line that is called the deflection waves (Electrocardiogram). The importance of ECG is that it gives accurate information about the heart. Therefore, ECG is of great diagnostic value in cardiac diseases.

Related Articles:

• Structure of Heart (With Diagram) | Circulatory System | Human Physiology
• Essay on Human Heart: Location, Structure and Other Details (with diagram)

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“How the Heart Works”: Brief Description of the Functions of the Heart Essay

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Introduction

Literature review, works cited.

The heart is arguably the most important organ in human physiology. Its structure and functionality are amazing, to say the least. Through many years of study, scholars and researchers have relentlessly sought out to understand these two aspects of the human heart. As such, this paper shall set out to explore the main functions of the heart about an article published in the magazine “USA today”, titled “How the heart works – descriptions of the various parts of the heart, their functions, and how they work together – Brief Article”.

According to the article, the heart is described as an energetic muscular organ located between the lungs that continuously pumps blood throughout the body via the circulatory system. The heart receives the deoxygenated blood from the body and pumps it to the lungs where the waste (Co2) is removed and gets oxygenated. It is then passed back to the heart where it is discharged to the body yet again.

The human heart is made up of four chambers and several valves which regulate and monitor blood flow within the body. The chambers include; the right atria, right ventricle, left atria and left ventricle. They are strategically located and serve as the pumps through which the blood flows into and out of the heart. Additionally, they are supported by four valves that control the inflow and outflow of the blood towards specific directions by opening and closing systematically. These valves have a set of leaflets that are forced open by the pressure exerted by the blood in motion and are designed specifically to allow a single direction of blood flow.

The heart plays a pivotal role in the circulatory system. Without it, other organs would fail due to a lack of oxygen and other nutrients that are transported throughout the body by the blood. Therefore, the full functionality of the heart is indeed crucial to our survival and existence. The article states that the deoxygenated blood from the veins is received into the heart by the right atrium. This blood is often dark red due to the high amounts of Co2 accumulated from the various tissues and cells within the body. Soon after the atrium fills up, an electrical signal is released causing the heat to beat. In this process, the atria contracts, pushing the blood down to the right ventricle. When this chamber contracts, the venous blood is pumped via the pulmonary valve into the pulmonary artery which directs it into the lungs for the purification process.

In the lungs, the venous blood is cleansed of its Co2 and at the same time gets oxygenated. After this process, it leaves the lungs and flows into the left atrium. At this stage, it is bright red due to a lack of Co2 and a high presence of oxygen. The contraction of the atria forces the blood down to the left ventricle through the mitral valve after which it is pumped to the aorta. The aorta is responsible for the distribution of the blood to the various body tissues.

The article further asserts that for the heart to function accordingly, these four chambers must coordinate efficiently. The contraction of these chambers is triggered by an electrical signal generated by specialized cells within the right atrium known as the sinoatrial node (SA). This is the natural pacemaker that causes the heart to beat through a series of evenly and timely spaced electrical discharges. However, emotional and hormonal factors may lead to an increase of these discharges, therefore, leading to a faster or slower heartbeat.

The electrical impulses move gradually from the right atria through the other chambers and in the process cause the systematic contraction and relaxation of the heart which allows the blood flow. Without such a mechanism, there may arise various complications which may have devastating effects on our health and lives.

This article has provided a very informative and elaborate discussion on the functions of the heart. Conclusively, it is clear that the heart is a very important part of our bodies and functionality, from the article review, the various parts have been highlighted and their functions and contributions discussed. It is therefore crucial that each person take ample precautionary measures to ensure that their heart is at maximum health at all times in order o avoid the dangers that may befall them due to health negligence.

USA Today. “How the heart works – descriptions of the various parts of the heart, their functions, and how they work together – Brief Article”. Society for the Advancement of Education, 1997. Web.

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IvyPanda. (2022, March 13). “How the Heart Works”: Brief Description of the Functions of the Heart. https://ivypanda.com/essays/how-the-heart-works-brief-description-of-the-functions-of-the-heart/

"“How the Heart Works”: Brief Description of the Functions of the Heart." IvyPanda , 13 Mar. 2022, ivypanda.com/essays/how-the-heart-works-brief-description-of-the-functions-of-the-heart/.

IvyPanda . (2022) '“How the Heart Works”: Brief Description of the Functions of the Heart'. 13 March.

IvyPanda . 2022. "“How the Heart Works”: Brief Description of the Functions of the Heart." March 13, 2022. https://ivypanda.com/essays/how-the-heart-works-brief-description-of-the-functions-of-the-heart/.

1. IvyPanda . "“How the Heart Works”: Brief Description of the Functions of the Heart." March 13, 2022. https://ivypanda.com/essays/how-the-heart-works-brief-description-of-the-functions-of-the-heart/.

Bibliography

IvyPanda . "“How the Heart Works”: Brief Description of the Functions of the Heart." March 13, 2022. https://ivypanda.com/essays/how-the-heart-works-brief-description-of-the-functions-of-the-heart/.

Home — Essay Samples — Literature — Romeo and Juliet — The Importance Of The Heart

The Importance of The Heart

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Published: Jun 13, 2024

Words: 600 | Page: 1 | 3 min read

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The physical significance of the heart, the symbolic importance of the heart, the heart's impact on societal dynamics.

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Defendants Acquitted in Panama Papers Money-Laundering Trial

The case focused on the law firm at the heart of the 2016 scandal, in which leaked documents revealed a vast network of offshore tax havens.

By Leila Miller

Reporting from Mexico City

In a striking verdict for a money-laundering case associated with the Panama Papers scandal, a Panamanian judge on Friday acquitted all 28 defendants, among them former employees of the law firm Mossack Fonseca, the source of the leaked documents that set off a worldwide furor in 2016.

The verdict came eight years after a partnership of media outlets published an explosive investigation into 11.5 million documents leaked from the Panama-based firm. The leak exposed the offshore banking industry, prompted international tax investigations and brought down heads of state.

Among the original 29 defendants were the shuttered firm’s co-founders, Jürgen Mossack, 76, and Ramón Fonseca, who died in May at age 71 while awaiting the verdict. In her 339-page ruling, the judge, Baloísa Marquínez, said that the case against Mr. Fonseca was dropped because of his death.

Prosecutors had alleged that Mossack Fonseca had created shell companies with the purpose of hiding money earned in illicit activities, and that the firm failed to act with due diligence and take the necessary care when reviewing its clients.

In a written statement published Friday evening, Panama’s judicial branch said that the judge had found that electronic evidence presented by prosecutors did not meet chain of custody protocols and had suffered from authentication issues. It also said that the judge had not found sufficient evidence to hold the accused responsible.

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Dropping Out Is Biden’s Most Patriotic Option

If he believes that Trump is a unique threat, the choice is clear.

Sign up for The Decision , a newsletter featuring our 2024 election coverage.

Joe Biden says he ran for president in 2020 because of Charlottesville. He says he ran because he saw the threat Donald Trump posed to the country and the threat he posed to democracy. If Biden truly believes that, he needs to end his reelection campaign. Indeed, dropping out could be the most patriotic gesture of his long career in public service, and every senior Democratic official and leader in the country should be pressuring him to act immediately.

Read: A disaster for Joe Biden

Throughout last night’s debate , Trump lied; obfuscated; and made bizarre, unsupported arguments about the economy, foreign policy, abortion, and the January 6 riot. A halfway competent opponent would have capitalized on these many, many errors. But Biden could barely speak coherently. The catastrophe of the incumbent’s performance is almost impossible to capture in words; you have to watch.

According to reporting by The New York Times , the campaign believed that the debate would “provide an opportunity to go on the offensive on issues like immigration and abortion access.” When asked about the latter—Biden’s best issue—he rambled about his worst issue, immigrant crime. You can read for yourself:

There’s many young women who’ve been—including the young woman who was just murdered and he went to the funeral—the idea that she was murdered by an immigrant coming in, they talk about that but here’s the deal, there’s a lot of young women being raped by their in-laws, by their spouses, brothers and sisters, it’s just ridiculous and they can do nothing about, they try to arrest them when they cross state lines.

Before the debate , the president spent a week with a full slate of advisers at Camp David: former Chief of Staff Ron Klain, current Chief of Staff Jeff Zients, White House senior adviser Anita Dunn, and campaign chair Jen O’Malley Dillon. This performance was rehearsed .

It should be the last straw. The president went into this debate as a historically unpopular candidate. At this point in his presidency, a lower percentage of Americans support him than have supported any other president since at least Harry Truman. He’s running behind Democratic candidates for Senate in Arizona, Nevada, Pennsylvania, and Wisconsin .

When the Times ’ Ezra Klein argued in February that Biden should step down , he was shot down by countless White House staff and Democratic leaders who claimed that Biden was up to the challenge of campaigning. And when Biden outperformed expectations at the State of the Union, speculation about his capacity to effectively campaign became more subdued.

But not anymore. Last night, Biden’s advisers were clearly underwhelmed with his performance; during the debate, they began leaking that he had a cold. After the event, when pressed repeatedly by Anderson Cooper on CNN, even Vice President Kamala Harris was forced to concede that the president’s showing had been lackluster. “He’s losing,” one prominent Democratic Party operative, who asked not to be named because of the sensitivity of the issue, told me by direct message. “The campaign said this debate would help him and it did not. Now he has no credible argument for how he’s going to turn the race around by November, especially since the convention is going to be a shit show.”

The problem facing the country is twofold. First, because the primaries are over, Biden would have to voluntarily step aside; there’s no other way for his party to nominate someone else. And second, there’s a first-mover disadvantage at play. No one wants to stick out their neck and end up as the laughingstock of the party—as Representative Dean Phillips of Minnesota did when he briefly challenged Biden for this year’s Democratic nomination. And for those closest to Biden—Jill Biden, Val Biden, Mike Donilon, Ted Kaufman, and all those who joined him at Camp David this week—the question will be whether they can put the needs of their country above their loyalty to the current president.

In their recent book, The Hollow Parties , the political scientists Daniel Schlozman and Sam Rosenfeld discuss the weakening of the Democratic and Republican establishments. In another age, no party apparatus would have allowed an aging, frail Joe Biden to get to this point. I recently asked Schlozman why the Democratic Party hasn’t simply replaced Biden—why Democratic National Committee Chair Jaime Harrison hasn’t called Pennsylvania Governor Josh Shapiro, Michigan Governor Gretchen Whitmer, or any number of other Democrats and tried to whip up support for them as potential replacements for Biden.

As a political scientist, Schlozman hates questions like this, so he answered me somewhat facetiously: He cited “the old joke of ‘Why is Profiles in Courage such a short book?’ ‘Because we don’t see these kinds of behaviors very much.’”

But what’s needed right now is exactly that kind of bravery: uncommon fortitude in the face of atrophied party institutions that have lost the power to prevent the rise of candidates such as Trump, and, more to the point, Biden’s continued presence in the race.

What exactly happens if Biden drops out? Well, there are two options. Either he drops out and endorses another candidate, or he allows the party to decide at the convention. Ideally, he would do the latter, to allow a competitive process to determine his successor as the Democratic nominee.

Either way, I have no illusions that any of this would be orderly. Speeding through a nominating process in a month and a half because the incumbent has decided he’s incapable of victory is going to be chaotic, and the Democrats could end up with a candidate with serious vulnerabilities.

But as Biden showed last night, the party most certainly has a flawed candidate now. The Democrats need to be able to find a nominee who’s actually able to mount a vigorous challenge to Trump and the singular threat he poses to American democracy.