16.pdf

The human heart is composed of two pumps: the right heart: which receives blood from the peripheral tissues and pumps it through the lungs the left heart: which receives oxygenated blood from the lungs and pumps it back to the peripheral tissues. Each pump is composed of an atrium and a ventricle...

The human heart is composed of two pumps: the right heart: which receives blood from the peripheral tissues and pumps it through the lungs the left heart: which receives oxygenated blood from the lungs and pumps it back to the peripheral tissues. Each pump is composed of an atrium and a ventricle. The atria function as conduits and primer pumps that fill the ventricles with blood. The ventricles contract and impart high pressure to the blood, which is responsible for propelling it through the circulation. PHYSIOLOGY OF CARDIAC MUSCLE There are three major types of cardiac muscle: atrial muscle, ventricular muscle, and specialized excitatory and conductive muscle fibers cardiac muscle is striated and have actin and myosin filaments that interdigitate and slide along each other during contraction. Cardiac muscle has intercalated discs between cardiac muscle cells that have very low electrical resistance, allowing an action potential to travel rapidly between cardiac muscle cells. The cardiac muscle is a syncytium of many heart muscle cells in which the action potential spreads rapidly from cell to cell. The atrioventricular (A-V) junction slowly conducts impulses from the atria to the ventricles. In normal patients this is an exclusive pathway because the atrial syncytium and ventricular syncytium are normally insulated from one another by fibrous tissue. Action Potentials in Cardiac Muscle The resting membrane potential of cardiac muscle is about −85 to −95 millivolts and the action potential is 105 millivolts. the membranes remain depolarized for 0.2 second in the atria and for 0.3 second in the ventricles, this is called Plateau. Slow Entry of Sodium and Calcium Ions Into the Cardiac Muscle Cells Is One of the Causes of the Action Potential Plateau. The action potential of cardiac muscle initiate by entry of sodium through fast sodium channels, which remain open for only a few ten thousandths of a second and make initial spike of the action potential. cardiac muscle also has unique slow calcium channels, or calcium- sodium channels. Calcium and sodium ions flow through the slow channels into the cell after the initial spike of the action potential, and they maintain the plateau. Calcium that enters the cell through these channels also promotes cardiac muscle contraction. Another Cause of the Plateau of the Action Potential Is a Decrease in the Permeability of Cardiac Muscle Cells to Potassium Ions. The decrease in cardiac potassium permeability also prevents return of the membrane potential in cardiac muscle. When the slow calcium-sodium channels close after 0.2 to 0.3 second, the potassium permeability increases rapidly. Potassium ions thus exit the cardiac myocytes, and membrane potential returns to its resting level. Diffusion of Calcium Into the Myofibrils Promotes Muscle Contraction. The action potential spreads into each cardiac muscle fiber along the transverse (T) tubules, causing the longitudinal sarcoplasmic tubules to release calcium ions into the sarcoplasm. These calcium ions catalyze the chemical reactions that promote the sliding of the actin and myosin filaments along one another to cause muscle contraction. There are another means of calcium entry into the sarcoplasm in cardiac muscle. The T tubules of cardiac muscles have 25 times as great a volume as those in skeletal muscle volume. These T tubules contain large amounts of calcium that are released during the action potential. In addition, the T tubules open directly into the extracellular fluid in cardiac muscle, so their calcium content highly depends on the extracellular calcium concentration. At the end of the plateau of the action potential, the influx of calcium ions into the muscle fiber abruptly stops, and calcium is pumped back into the sarcoplasmic reticulum and T tubules. Thus, the contraction ends. The Spread of the Action Potential in the Heart Initiates Each Heartbeat. Each beat of the heart begins with a spontaneous Action potential that is initiated in the sinus node of the right atrium near the opening of the superior vena cava. The action potential travels through both atria and the A-V node and bundle into the ventricles. A delay of about 0.13 second occurs in the A-V node and bundle, which allows the atria to contract before the ventricles contract. Electrocardiogram The electrocardiogram is a recording of the voltage generated by the heart from the surface of the body during each heartbeat. The P wave is caused by spread of depolarization across the atria, which causes atrial contraction. The QRS waves appear as a result of ventricular depolarization about 0.16 second after the onset of the P wave, initiating ventricular contraction. The ventricular T wave is caused by repolarization of the ventricle. The Atria Function as Primer Pumps for the Ventricles About 80 percent of ventricular filling occurs during diastole before contraction of the atria. contraction of the atria causes the remaining 20 percent of ventricular filling. contraction of the atria increase the ventricular pumping effectiveness as much as 20 percent When the atria fail to function properly, little difficulty is encountered unless a person exercises, and then shortness of breath and other symptoms of heart failure may occur. The Ventricles Fill With Blood During Diastole The following events occur just before and during diastole: During systole, the A-V valves are closed, and the atria fill with blood. At the beginning of diastole is the period of isovolumic relaxation, caused by ventricular relaxation. When ventricular pressure decreases below that of the atria, the A-V valves open. During diastole the higher pressure in the atria pushes blood into the ventricles. The period of rapid filling of the ventricles occurs during the first third of diastole and provides most of the ventricular filling. At the middle third of diastole blood flow to the ventricles continuouslyl. Atrial contraction occurs during the last third of diastole and contributes about 20 percent of the filling of the ventricle. This contraction is commonly known as the “atrial kick.” Outflow of Blood From the Ventricles Occurs During Systole. The following events occur during systole: At the beginning of systole, ventricular contraction occurs, the A-V valves close, and pressure begins to build up in the ventricle. No outflow of blood occurs during this period of ventricular contraction (the period of isovolumic or Isometric contraction). isovolumic means “the same volume” and refers to the ventricular volume. Isometric means increasing in cardiac muscle tension but no shortening of the muscle fibers. When the left ventricular pressure exceeds the aortic pressure of about 80 mm Hg and the right ventricular pressure exceeds the pulmonary artery pressure of 8 mm Hg, the aortic and pulmonary valves open and Ventricular outflow occurs, called the period of ejection. 70% of ejection occurs during the first third of this period (period of rapid ejection). 30% of ejection occurs during the later two third of this period (the period of slow ejection) At the end of diastole, the volume of each ventricle is 110 to 120 milliliters; this volume is called the end-diastolic volume. The stroke volume, which has a value of about 70 milliliters, is the amount of blood ejected with each beat. The end-systolic volume is the remaining volume in the ventricle at the end of systole and measures about 40 to 50 milliliters. The ejection fraction is calculated by dividing the stroke volume by the end-diastolic volume; it has a value of about 60 percent. The stroke volume of the heart can be doubled by increasing the end- diastolic volume and decreasing the end-systolic volume.