Overview of The Myocyte The myocyte is composed of various protein filaments that comprise the contractile apparatus of the cardiac cell. Myofibrils, a collection of individual sarcomeres, enable contraction and relaxation of the myocyte. The sarcomere is the chief contractile unit of the cell. It is made up of two main proteins, myosin (thick filament) and actin (thin filament), as well as two regulatory proteins, tropomyosin and troponin. In order for the myocyte to contract and shorten it must receive a stimulus allowing myosin and actin to interact. This stimulus comes from the depolarization of the cardiac cell membrane (sarcolemma) at the cell surface. The sarcolemma is composed of a hydrophobic phospholipid membrane that prevents
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There are three main types of electrical tissue in the myocardium: ventricle & atria, SA & AV node (pacemaker cells) and Purkinje fibers. Each type of cell differs in the composition of ion channels in the membrane, which influences the action potential and transmission of electrical stimulus. There are 4 phases of the action potential. During phase 0, activation of voltage-gated fast sodium channels cause a rapid increase in the intracellular Na+ and change in membrane potential. This leads to opening of L- type Ca++ channels releasing Ca++ into the cell (phase 1). Next, K+ channels open and K+ exits the cell balancing the influx of Ca++ leading to a plateau of the action potential (phase 2). As more K+ channels open (phase 3), L-Type Ca+ channels begin to close and the membrane potential returns to its resting state (phase 4). The number of fast sodium channels differs in each cell type: purkinje fibers>atrial/ventricle>SA/AV nodal cells. This helps explain the difference in the speed of depolarization and conduction in each of these …show more content…
Stroke volume is the difference in ventricular end diastolic volume (EDV) and end systolic volume (ESV). Some of the factors that influence SV and thus CO include contractility, preload and afterload. Afterload is the resistance felt by the ventricle during systole. An increase in afterload when preload and contractility are constant will result in a decrease in SV and subsequent decrease in CO. Preload is the passive stretch of sarcomeres in the myocyte before systole, also known as the end diastolic length of the sarcomere. It is the amount of volume in the ventricle immediately before systole otherwise known as end diastolic volume. Simply, preload is analogous to venous return. As venous return increases, the EDV increases leading to a larger stretch in the sarcomere. In a normal compliant ventricle, the increased stretch of the sarcomere leads to a greater force of contraction. This is referred to as the Frank-Starling mechanism. This mechanism also known as the length-tension relationship, states that the force or tension of the myocyte will increase as the sarcomere is stretched. Although not completely understood, the increase in force due to sarcomere stretch is thought to be a result of increased myosin-actin interaction and myofilament sensitivity to calcium. As the sarcomere is lengthened, the distance between the thin and thick filaments
There are three main types of electrical tissue in the myocardium: ventricle & atria, SA & AV node (pacemaker cells) and Purkinje fibers. Each type of cell differs in the composition of ion channels in the membrane, which influences the action potential and transmission of electrical stimulus. There are 4 phases of the action potential. During phase 0, activation of voltage-gated fast sodium channels cause a rapid increase in the intracellular Na+ and change in membrane potential. This leads to opening of L- type Ca++ channels releasing Ca++ into the cell (phase 1). Next, K+ channels open and K+ exits the cell balancing the influx of Ca++ leading to a plateau of the action potential (phase 2). As more K+ channels open (phase 3), L-Type Ca+ channels begin to close and the membrane potential returns to its resting state (phase 4). The number of fast sodium channels differs in each cell type: purkinje fibers>atrial/ventricle>SA/AV nodal cells. This helps explain the difference in the speed of depolarization and conduction in each of these …show more content…
Stroke volume is the difference in ventricular end diastolic volume (EDV) and end systolic volume (ESV). Some of the factors that influence SV and thus CO include contractility, preload and afterload. Afterload is the resistance felt by the ventricle during systole. An increase in afterload when preload and contractility are constant will result in a decrease in SV and subsequent decrease in CO. Preload is the passive stretch of sarcomeres in the myocyte before systole, also known as the end diastolic length of the sarcomere. It is the amount of volume in the ventricle immediately before systole otherwise known as end diastolic volume. Simply, preload is analogous to venous return. As venous return increases, the EDV increases leading to a larger stretch in the sarcomere. In a normal compliant ventricle, the increased stretch of the sarcomere leads to a greater force of contraction. This is referred to as the Frank-Starling mechanism. This mechanism also known as the length-tension relationship, states that the force or tension of the myocyte will increase as the sarcomere is stretched. Although not completely understood, the increase in force due to sarcomere stretch is thought to be a result of increased myosin-actin interaction and myofilament sensitivity to calcium. As the sarcomere is lengthened, the distance between the thin and thick filaments