The left ventricle is considered an integral part of the cardiovascular system. It is thought off as a pump that supplies blood to the body, and when injured or forced to change, disease symptoms can ensue. This article will explore some of the finite details of the left ventricle as well as the larger picture of the function, pathophysiology and clinical significance of left ventricular function.
Cardiac failure is among the leading causes of death. It correlates with changes in the architecture of the ventricular wall such as ventricular dilation and mural thinning. Alterations in various components of the myocardium precede these ventricular changes such as focal myocyte loss and fibrotic replacement, as well as hypertrophic myocyte activity leading to larger muscle wall thickness. These myocardial changes lead to a decrease in the ability of the individual myocytes to contract with sufficient speed and force to maintain normal cardiac output.
Cardiac tissue is only found in the heart and nowhere else in the body. It is an involuntary, striated muscle, that is highly coordinated with a single nucleus, many mitochondria and possesses an extensive cardiac capillary network. Myocytes are the individual muscle cells that are organized into sarcomeres and interconnected via intercalated discs. The interconnections allow the cardiac myofibrils to contract together in a fluid synchronized fashion to enable the heart to work as a pump. The primary function of the left ventricle muscle is to pump blood which physiologically is dependent upon an increasing concentration of calcium and sodium within the cytosol of the muscle triggering muscle contraction. The basic unit of contraction in the myocyte is the sarcomere which is bound to the T-tubule system on both ends. The T-tubules are part of the sarcolemma where L-type calcium channels are contained and become more numerous around the sarcoplasmic reticulum of the cell, and its calcium release channels known ryanodine receptors. The amount of calcium transiently determines the contractility of the heart. The heart contracts as a unit to carry out its role of supplying oxygen and nutrients throughout the body while simultaneously delivering waste products to organs for filtration and excretion. When the left ventricle faces with a physiological or pathological increase in cardiac demand, such as increases in preload or afterload, it changes to better meet these new needs. These changes can include cardiac remodeling via induvial myocyte hypertrophy, or fibroblast proliferation leading to fibrosis, vascularization, or even cell death.
From conception, the cells from the primary cardiac crescent form bilaterally within the embryonic disc and migrate to the cervical region where they form the primary heart tube. There are subsequent divisions and contributions from the bulbus cordis developing into the right ventricle and the primitive ventricle from the primary cardiac crescent forming the left ventricle. During subsequent weeks, the primitive heart folds into an "s" shape which places the chambers and major vessels into alignment and shape, mirroring that of the adult heart. The partitioning of the atria and ventricles by the interatrial, interventricular and the atrioventricular septum proceed, and the formation of the semilunar valves follow.
The left ventricle is also subject to genetic defects, one example being hypoplastic left heart syndrome. This condition is a congenital condition where an underdeveloped left ventricle results from several malformations during fetal developments, such as situations where the mitral or aortic valves are not formed or are very small, or the ascending portion of the aorta is underdeveloped or is too small. Depending on how many structures are affected coincides with the degree of severity of this defect. The ultimate result is underdevelopment of the left side of the heart that is unable to pump blood out to the rest of the body. Most newborns affected with this will have an atrial septal defect, and medication is given to help the foramen ovale remain patent as well as help lower their blood pressure and remove excess fluid. A large patent ductus arteriosus can be present which supplies blood to the systemic circulation. Later in life, the newborn will need surgery to help increase blood flow to the body and bypass the poorly functioning left side of the heart, which means that the right heart becomes the main pumping chamber to the body.
The left ventricle connects to the rest of the body through its intrinsic function of supplying all of the organs with nutrition and oxygen in the blood, which it pumps with every heartbeat. If the left ventricle is damaged or undergoes pathological change over time, this may lead to a decrease in its ability to pump blood out to the rest of the body. This failure would result in all other organs receiving impaired blood flow and therefore decreased nutrients and oxygen. A person might experience syncopal episodes due to lack of blood flow to the brain, or their kidneys might start to release the hormone renin due to the decrease of blood supply reaching their receptors in the afferent arterioles. The decreased cardiac output can also lead to catecholamine release which can cause an increased heart rate, as well as vasoconstriction, causing certain vessels to constrict and others to dilate, increasing blood supply to vital organs such as the brain. If the left side of the heart should become strained blood can back up into the lungs and cause fluid overload in the pulmonary alveoli due to increases in hydrostatic pressure, thus leading to pulmonary edema. This edema can lead to pulmonary pathologies such as pulmonary hypertension and over time lead to right heart strain and cause right heart damage leading to right heart fluid overload. The fluid will again build up and back up, this time into the vena cava and can cause liver pathologies and cause portal hypertension.
The left ventricle functions to pump oxygenated blood from the lungs out to the body. Decreased function of the left ventricle, therefore, impairs tissue oxygenation. With the advancement of medicine and technology, researchers can delve deeper into the physiological aspects of what causes the cardiac muscle to contract and use that information to manage patients with therapeutic techniques that decrease their morbidity and mortality and to continue their activities of daily living.
The function of the left ventricle is the result of three measures: the end-diastolic left ventricular chamber size, the left ventricular performance related to left ventricular ejection fraction (LVEF), and third by the index of muscle performance relative to the mean velocity of circumferential fiber shortening (MVCFc). All of these indices of measurements are preload and afterload dependent and therefore can influence relative inotropic sensitivity.
Medications now exist that help left the ventricular function in two manners, myocyte contractile performance, and electrophysiological variables. These medications are therapeutic for those who suffer from chronic left ventricular dysfunction. One example is digoxin which has a direct effect on the contractile function and the electrophysiological properties of the cardiac myocyte. Therapy can normalize action potential characteristics and result in improved left ventricular pump function in the setting of left ventricular failure.
The left ventricle pumps blood at higher pressures compared to the rest of the other heart chambers, as it faces a much higher workload and mechanical afterload. In comparison to that of the right ventricle, the free wall of the left ventricle is much thicker. As stated earlier, myocyte contraction is dependent upon an influx of calcium through L type calcium channels phosphorylation. The influx of calcium triggers the contraction of the cardiac myocyte and through the excitation-contraction coupling, the whole heart contracts.
The electrophysiology behind the left ventricle starts at the sinoatrial (SA) node which initiates an action potential. This action potential is carried across and down the atria until it reaches the atrioventricular (AV) node. The AV node delays the electrical current by about 100ms before further transmitting the impulse to the atrioventricular bundle known as the "bundle of His." The electrical impulse then travels down the right and left bundle branches to the Purkinje fibers. It is from here that it finally reaches the contractile fibers of the right and left ventricle causing the contraction to start from the apex of the heart, which then progresses upwards.
Heart disease can manifest in different ways and affect left ventricular heart function such as ECG abnormalities, palpitations, wall motion abnormalities, or a change in chamber geometry. It is essential to know the signs and symptoms, understand the next steps to take, and identify any abnormal results for proper diagnosis and management. The steps to measure the performance of cardiac tissue should not be minimized. However, practical steps must be taken to gain valuable information in the least invasive manners first while assessing and monitoring patients.
A common example is heart failure. Heart failure is a clinical diagnosis that can be the result of a multitude of different structural and functional cardiac disorders that affect intrinsic myocardial contractility. It is largely a clinical diagnosis and is characterized by the inability of the ventricle to fill with blood or eject blood properly. A patient might exhibit systolic as well as diastolic dysfunction, and present with dyspnea, fatigue, and fluid retention. Testing through stress testing and echocardiograms are noninvasive diagnostic exam methods used to assess for cardiac lesions and monitor myocardial functionality and may reveal chamber size abnormalities, wall motion abnormalities as well as improper valve function. It has been shown that stress echocardiography in combination with various stressors can detect significant coronary stenosis ranging from 80 to 90% in accuracy, making it a powerful prognostic tool in those with chronic coronary artery disease.
An important diagnostic tool in heart failure is left ventricular ejection fraction (LVEF). It is a load-dependent test and indicator of left ventricular performance. The fraction percentage identifies the different categories of heart failure: preserved ejection fraction greater than or equal to 50%, mid-range left ventricular ejection fraction 41 to 49%, and reduced ejection fraction less than or equal to 40%. This differentiation between the preserved, midrange and reduced LVEF is important for continued quality of care performance and measurement in heart failure patients.
The circumferential fiber shortening is another measurement that can aid in determining ventricular pump performance as a direct relation to muscle function. It is an index of myocardial performance relative to wall stress. There exists an inverse linear relationship between end-systolic wall stress and the velocity of circumferential fiber shortening, the index of which is a sensitive measure of the cardiac contractile state independent of preload and accounting for afterload.
Tissue Doppler is another noninvasive method of testing the systolic and diastolic function and performance of the left ventricle. It is used to assess for changes in the myocardium due to strain, twists, rotations that are distinct from previous tests.
Left ventricular heart failure can result from a variety of pathologies such as ischemia, excessive peripheral demands, high output failure, volume overload, pressure, and volume overload and primary muscle disease. Four determinants of left ventricular performance are an intrinsic decrease in muscle contractility, increase in systemic afterload causing decreased cardiac output, preload is increased and can back up into the lungs causing pulmonary congestion, and increased heart rate associated with an increased sympathetic tone.
Per the CDC, 1 in 4 people die of heart disease each year in the United States and is the leading cause of death in both men and women. Heart failure is still a challenge to many health care providers and is associated with higher rates of readmissions and increased morbidity and mortality. Based on the pathophysiology’s mentioned above, the treatment will vary. The primary goals of management are to improve prognosis and reduce morbidity and mortality with appropriate therapies. If the patient is admitted to the hospital, an additional goal would be to reduce rates of readmission as well as the length of stay. Additionally, other comorbidities that could enhance cardiac dysfunction should be addressed and managed appropriately.
|||Capasso JM,Fitzpatrick D,Anversa P, Cellular mechanisms of ventricular failure: myocyte kinetics and geometry with age. The American journal of physiology. 1992 Jun; [PubMed PMID: 1621835]|
|||Winslow RL,Scollan DF,Holmes A,Yung CK,Zhang J,Jafri MS, Electrophysiological modeling of cardiac ventricular function: from cell to organ. Annual review of biomedical engineering. 2000; [PubMed PMID: 11701509]|
|||Torrealba N,Aranguiz P,Alonso C,Rothermel BA,Lavandero S, Mitochondria in Structural and Functional Cardiac Remodeling. Advances in experimental medicine and biology. 2017; [PubMed PMID: 28551793]|
|||Anderson RH,Webb S,Brown NA,Lamers W,Moorman A, Development of the heart: (3) formation of the ventricular outflow tracts, arterial valves, and intrapericardial arterial trunks. Heart (British Cardiac Society). 2003 Sep; [PubMed PMID: 12923046]|
|||Loar RW,Burkhart HM,Taggart NW, Septum primum atrial septal defect in an infant with hypoplastic left heart syndrome. The heart surgery forum. 2014 Aug; [PubMed PMID: 25179980]|
|||Sandor GG, Echocardiographic Tests of Left Ventricular Function in Pediatric Cardiology: Are We Searching for the Holy Grail? The Canadian journal of cardiology. 2016 Oct; [PubMed PMID: 26922289]|
|||McMahon WS,Holzgrefe HH,Walker JD,Mukherjee R,Arthur SR,Cavallo MJ,Child MJ,Spinale FG, Cellular basis for improved left ventricular pump function after digoxin therapy in experimental left ventricular failure. Journal of the American College of Cardiology. 1996 Aug; [PubMed PMID: 8800131]|
|||Kondo RP,Dederko DA,Teutsch C,Chrast J,Catalucci D,Chien KR,Giles WR, Comparison of contraction and calcium handling between right and left ventricular myocytes from adult mouse heart: a role for repolarization waveform. The Journal of physiology. 2006 Feb 15; [PubMed PMID: 16357014]|
|||Oberman R,Bhardwaj A, Physiology, Cardiac 2019 Jan; [PubMed PMID: 30252345]|
|||Marwick TH, Stress echocardiography. Heart (British Cardiac Society). 2003 Jan; [PubMed PMID: 12482809]|
|||Yancy CW,Jessup M,Bozkurt B,Butler J,Casey DE Jr,Drazner MH,Fonarow GC,Geraci SA,Horwich T,Januzzi JL,Johnson MR,Kasper EK,Levy WC,Masoudi FA,McBride PE,McMurray JJ,Mitchell JE,Peterson PN,Riegel B,Sam F,Stevenson LW,Tang WH,Tsai EJ,Wilkoff BL, 2013 ACCF/AHA guideline for the management of heart failure: executive summary: a report of the American College of Cardiology Foundation/American Heart Association Task Force on practice guidelines. Circulation. 2013 Oct 15; [PubMed PMID: 23741057]|
|||Ponikowski P,Voors AA,Anker SD,Bueno H,Cleland JGF,Coats AJS,Falk V,González-Juanatey JR,Harjola VP,Jankowska EA,Jessup M,Linde C,Nihoyannopoulos P,Parissis JT,Pieske B,Riley JP,Rosano GMC,Ruilope LM,Ruschitzka F,Rutten FH,van der Meer P, 2016 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure: The Task Force for the diagnosis and treatment of acute and chronic heart failure of the European Society of Cardiology (ESC)Developed with the special contribution of the Heart Failure Association (HFA) of the ESC. European heart journal. 2016 Jul 14; [PubMed PMID: 27206819]|
|||Ruschhaupt DG,Sodt PC,Hutcheon NA,Arcilla RA, Estimation of circumferential fiber shortening velocity by echocardiography. Journal of the American College of Cardiology. 1983 Jul; [PubMed PMID: 6853920]|
|||Parmley WW, Pathophysiology of congestive heart failure. The American journal of cardiology. 1985 Jul 10; [PubMed PMID: 4014051]|
|||Inamdar AA,Inamdar AC, Heart Failure: Diagnosis, Management and Utilization. Journal of clinical medicine. 2016 Jun 29; [PubMed PMID: 27367736]|
|||Tamargo J,López-Sendón J, Novel therapeutic targets for the treatment of heart failure. Nature reviews. Drug discovery. 2011 Jun 24; [PubMed PMID: 21701502]|