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StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-.
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Last Update: July 30, 2023 .
Cardiac muscle also called the myocardium, is one of three major categories of muscles found within the human body, along with smooth muscle and skeletal muscle. Cardiac muscle, like skeletal muscle, is made up of sarcomeres that allow for contractility. However, unlike skeletal muscle, cardiac muscle is under involuntary control.
The heart is made up of three layers—pericardium, myocardium, and endocardium. The endocardium is not cardiac muscle and is comprised of simple squamous epithelial cells and forms the inner lining of the heart chambers and valves. The pericardium is a fibrous sac surrounding the heart, consisting of the epicardium, pericardial space, parietal pericardium, and fibrous pericardium.[1]
The cardiac muscle is responsible for the contractility of the heart and, therefore, the pumping action. The cardiac muscle must contract with enough force and enough blood to supply the metabolic demands of the entire body. This concept is termed cardiac output and is defined as heart rate x stroke volume, which is determined by the contractile forces of the cardiac muscle and the frequency at which they are activated. With a change in metabolic demand comes a change in the contractility of the heart.
Cardiac muscle cells (cardiomyocytes) are striated, branched, contain many mitochondria, and are under involuntary control. Each myocyte contains a single, centrally located nucleus surrounded by a cell membrane known as the sarcolemma. The sarcolemma of cardiac muscle cells contains voltage-gated calcium channels, specialized ion channels that skeletal muscle does not possess.
Cardiac muscle cells contain branched fibers connected via intercalated discs that contain gap junctions and desmosomes. These interconnections allow the cardiomyocytes to contract together synchronously to enable the heart to work as a pump.[2]
Gap junctions between adjacent cardiomyocytes allow for the propagation of coordinated action potentials from one cell to the next in a phenomenon known as electrical coupling.[3] Cardiac desmosomes are intercellular structures that anchor cardiac muscle fibers together and are vital in maintaining the structural integrity of the heart.[4]
The functional unit of cardiomyocyte contraction is the sarcomere, which consists of thick (myosin) and thin (actin) filaments, the interactions between which form the basis of the sliding filament theory.[5]
The sarcolemma is the cardiomyocyte plasma membrane containing transverse tubules (t-tubules). These t-tubules are highly branched invaginations of the cardiomyocyte sarcolemma that function in excitation-contraction coupling (ECC), action potential initiation and regulation, maintaining the resting membrane potential, and signal transduction. T-tubules regulate the cardiac ECC by concentrating voltage-gated L-type calcium channels and positioning them in close proximity to calcium sense and release channels, ryanodine receptors (RyRs), at the junctional membrane of the sarcoplasmic reticulum.[6]
The development of the heart occurs in various stages. During embryogenesis, the formation of the primitive streak follows the invagination of epiblast cells, indicating the start of gastrulation. Gastrulation divides the embryonic plate, which originally contained two layers between the yolk sac and amniotic cavity, into three germ layers; ecto-, meso-, and endoderm. The mesoderm is situated between the ectoderm and endoderm layers and, during development, spreads laterally and cranially, forming different structures, particularly the heart.[7]
The myocardium begins developing during the second week of gestation in the dorsal mesocardium. After three weeks post-fertilization, the primitive heart begins to develop as a straight tube changing its configuration as time proceeds. This entails folding of the tube, giving rise to bulges that become analogous to the adult heart; truncus arteriosus develops into the aorta and pulmonary artery, bulbus cordis develops into smooth left and right ventricles, primitive ventricle into trabeculated LV/RV, primitive atrium into trabeculated atria and the sinus venosus which develops into the right atrium (sinus venarum) and coronary sinus.[8]
Around the fourth week of development, the heart undergoes a cardiac looping process that establishes the heart's left-sided orientation. This is performed with the help of cilia, a motile structure, and dynein, a protein.[9] If these factors fail to function correctly, dextrocardia will occur, which places the heart on the right side of the chest. This cardiac anomaly is typically seen in Kartagener Syndrome and primary ciliary dyskinesia (PCD).[10]
Further developmental changes occur as the heart is shaped into its proper configuration. The heart begins as a single chamber, but four separate chambers are created through the growth of various septa. The muscular ventricular septum originates from the bottom of the ventricle, with a membranous septum forming shortly after, joining with the aortic-pulmonary septum as its twists down and fuses. The endocardial cushions also appear at this time and separate the left and right atria and ventricles. Any structural changes or defects in these processes can lead to congenital heart disorders.
The primary function of cardiac muscle is to pump blood into circulation by generating sufficient force. The mechanism behind each coordinated contraction involves the cardiac muscle and electrical impulses. These contractile functions of the heart require ATP, which can be obtained through various substrates, including fatty acids, carbohydrates, proteins, and ketones. Aerobic production is the core utilization process; however, the heart may use anaerobic processes in a limited capacity.[11]
The cardiac action potential lasts approximately 200 ms and is divided into 5 phases: (4) resting, (0) upstroke, (1) early repolarization, (2) plateau, and (3) final repolarization.
Approximate resting membrane potential (RMP): -90 mV
Phase 4 - RMP due to activity of the Na/K ATPase pump. The exchange of three sodium ions out for two potassium ions in maintains the negative intracellular potential.
Phase 0 - depolarization to approximately +52 mv due to sodium influx via fast sodium channelsPhase 1 - partial repolarization due to the closure of fast sodium channels and efflux of potassium and chloride
Phase 2 - plateau phase maintained by the influx of calcium. Potassium efflux also occurs.Phase 3 - repolarization back to RMP due to potassium efflux and closure of sodium and calcium channels
The generation of a cardiac action potential is involuntary and proceeds via a process known as excitation-contraction coupling (ECC). Action potentials travel along the sarcolemma and into the t-tubules to depolarize the membrane. Voltage-sensitive dihydropyridine (DHP) receptors on t-tubules allow calcium influx into the cell via L-type (long-lasting) calcium channels during the plateau phase (phase 2) of the action potential. This increased intracellular calcium concentration triggers the sarcoplasmic reticulum to release more calcium through the ryanodine receptor, known as calcium-induced calcium-released.[12]
The released calcium attaches to troponin C, causing tropomyosin to detach from the myosin-binding sites on actin. Actin and myosin then form a cross-bridge, and contraction occurs. Cross bridges last as long as calcium is attached to troponin.[13]
Lusitropy is the term used to define the relaxation of the myocardium following ECC. Lusitropy is mediated by the SERCA (sarco-endoplasmic reticulum calcium-ATPase) pump, which sequesters calcium into the sarcoplasmic reticulum, allowing calcium to be removed from troponin-C and returning the myocardium to its relaxed state.[14]
Unlike the cardiac muscle cells, the pacemaker cells' action potential is divided into 3 phases instead of 5, as phases 1 and 2 are absent. Pacemaker cells are comprised of sinoatrial (SA) and atrioventricular (AV) nodes, which are known to fire spontaneously, sending electrical activity throughout the heart, and do not require stimulation to initiate their action.
This autorhythmicity transpires because of funny current channels, which allow sodium ions to leak continuously into the cell (Phase 4), slowly raising the membrane potential until a certain threshold is reached, causing depolarization of the cell. This subsequently opens calcium channels causing calcium ions to enter the cell, further raising the membrane potential (Phase 0). After a positive membrane potential is sensed, potassium channels open, causing an outward flow of ions, returning the membrane potential to its resting potential (Phase 3).[15]
Many clinical tests are utilized to evaluate the function of cardiac muscle. This list discusses high-yield clinical testing and is not meant to be exhaustive.
Echocardiogram: an ultrasound of the heart routinely used to identify cardiac abnormalities. An echocardiogram can assess valvular abnormalities, masses, pericardial disease, congenital abnormalities, and pulmonary hypertension. An echo is also routinely utilized to assess cardiac muscle function and is useful in diagnosing congestive heart failure and cardiomyopathies. An echocardiogram can be performed as a transthoracic echocardiogram (TTE) or a transesophageal echocardiogram (TEE).
TTE: a non-invasive test that utilizes an echocardiography probe placed on the chest wall.TEE: a specialized probe with an ultrasound transducer at the tip passed into the patient's esophagus, allowing for a posterior view of the heart.
Echocardiogram reports are detailed and offer essential information regarding the heart's function. Echo reports typically include:
