Heart Physiology PDF

Heart Physiology Dr Sakineh Shafia TEXTBOOK OF MEDICAL PHYSIOLOGY GUYTON & HALL 14TH EDITION What you will learn about heart physiology in this term? Functional physiology of the Heart Chambers Valves Myocardial Physiology Cardiac Cycle Intrinsic Conduction System...

Heart Physiology Dr Sakineh Shafia TEXTBOOK OF MEDICAL PHYSIOLOGY GUYTON & HALL 14TH EDITION What you will learn about heart physiology in this term? Functional physiology of the Heart Chambers Valves Myocardial Physiology Cardiac Cycle Intrinsic Conduction System Cardiac Output Controls & EKG The heart is placed in the chest slightly inclined to the left and is surrounded by a two-layer sac called the pericardium, which protects the heart and holds it in place. The Function of the Pericardium: Protects and anchors the heart Prevents overfilling of the heart with blood Allows for the heart to work in a relatively friction-free environment 4 The heart is a part of the circulatory system which produces the proper pumping force for blood movement. The heart moves blood through the vascular system. The movement of blood starts from the left heart, through the arterial system , and returns to the right heart through the venous system The heart consists of multiple layers,.including the inner endocardium, myocardium, and more outward epicardium and pericardium layers The heart consists of two kind chamber pump: composed of atrium and ventricle. This picture shows that the left heart wall is thicker than the right heart 10 The heart, is actually two separate pumps, a right heart that pumps blood through the lungs and a left heart that pumps blood through the systemic circulation that provides blood flow to the other organs and tissues of the body Each atrium is a weak primer pump for the ventricle, helping to move blood into the ventricle. The ventricles then supply the main pumping force that propels the blood either (1) through the pulmonary circulation by the right ventricle or (2) through the systemic circulation by the left ventricle. PHYSIOLOGY OF CARDIAC MUSCLE The heart is composed of three major types of cardiac muscle: atrial muscle ventricular muscle, specialized excitatory and conductive muscle fibers. The atrial and ventricular types of muscle contract in much the same way as skeletal muscle, except that the duration of contraction is much longer. The specialized excitatory and conductive fibers of the heart, however, contract feebly because they contain few contractile fibrils; instead, they exhibit automatic rhythmical electrical discharge in the form of action potentials or conduction of the action potentials through the heart, providing an excitatory system that Controls the rhythmical beating of the heart cardiac muscle is striated in the same manner as in skeletal muscle. cardiac muscle has typical myofibrils that contain actin and myosin filaments almost identical to those found in skeletal muscle; these filaments lie side by side and slide during contraction in the same manner as occurs in skeletal muscle. In other ways, cardiac muscle is quite different from skeletal muscle. Cardiac muscle anatomy the cardiac muscle histology, demonstrating cardiac muscle fibers arranged in a latticework, with the fibers dividing, recombining, and then spreading  Functional anatomy of the heart cardiac muscle Heart Muscle Characteristics Striated Short branched cells Uninucleate Intercalated discs T-tubules larger Cardiac Muscle Is a Syncytium. The dark areas crossing the cardiac muscle fibers are called intercalated discs; they are actually cell membranes that separate individual cardiac muscle cells from one another. At each intercalated disc, the cell membranes fuse with one another to form permeable communicating junctions (gap junctions) that allow rapid diffusion of ions. In intercalated discs ions move with ease in the intracellular fluid along the longitudinal axes of the cardiac muscle fibers so that action potentials travel easily from one cardiac muscle cell to the next, past the intercalated discs. Thus, cardiac muscle is a syncytium of many heart muscle cells in which the cardiac cells are so interconnected that when one cell becomes excited, the action potential rapidly spreads to all of them. The heart actually is composed of two syncytia; the atrial syncytium, which constitutes the walls of the two atria; and the ventricular syncytium, which constitutes the walls of the two ventricles. The atria are separated from the ventricles by fibrous tissue that surrounds the atrioventricular (A-V) valvular openings between the atria and ventricles. Normally, potentials are not conducted from the atrial syncytium into the ventricular syncytium directly through this fibrous tissue. Instead, they are only conducted by way of a specialized conductive system called the A-V bundle, a bundle of conductive fibers several millimeters in diameter. ACTION POTENTIALS IN CARDIAC MUSCLE The action potential recorded in a ventricular muscle fiber, averages about 105 millivolts, which means that the intracellular potential rises from a very negative value between beats, about -85 millivolts, to a slightly positive value, about +20 millivolts, during each beat. After the initial spike, the membrane remains depolarized for about 0.2 second, exhibiting a plateau, followed at the end of the plateau by abrupt repolarization. The action potential is caused by opening of 3 types of channels: (1) The same voltage activated fast sodium channels  (2) L-type calcium channels (slow calcium channels), which are also called calcium-sodium channels. (3) The voltage potassium channels 26 27 The presence of this plateau in the action potential causes ventricular contraction to last as much as 15 times longer in cardiac muscle than in skeletal muscle. What Causes the Long Action Potential and Plateau in Cardiac Muscle? the action potential of skeletal muscle is caused almost entirely by the sudden opening of large numbers of fast sodium channels. At the end of this closure, repolarization occurs, and the action potential is over within about another thousandth of a second. immediately after the onset of the action potential, the permeability of the cardiac muscle membrane for K ions decreases about fivefold, permeability of the cardiac muscle membrane for Ca-Na ions increases This decreased K permeability may result from the excess calcium influx through the calcium channels. When the slow calcium-sodium channels do close at the end of 0.2 to 0.3 second, and the membrane permeability for potassium ions also increases rapidly. This rapid loss of potassium from the fiber immediately returns the membrane potential to its resting level, thus ending the action potential. THE CARDIAC ACTION POTENTIAL 33 The latent period between excitation and development of tension in a skeletal muscle includes the time needed to release Ca++ from sarcoplasmic reticulum, move tropomyosin, and cycle the cross-bridges.  Muscle twitch: A twitch is a single contraction/relaxation cycle Contraction as the result of a single stimulus – Latent period: Lasting only ~5 ms – Tension is developed:40 ms – Relaxation:50 ms 36 37 Velocity of Signal Conduction in Cardiac Muscle. The velocity of conduction in both atrial and ventricular muscle fibers is : about 0.3 to 0.5 m/sec, or about 1/250 the velocity in nerve fibers and about 1/10 the velocity in skeletal muscle fibers. The velocity of conduction in the specialized heart conductive system—in the Purkinje fibers—is as high as 4 m/sec Refractory Period of Cardiac Muscle. Cardiac muscle, like all excitable tissue, is refractory to restimulation during the action potential.  REFRACTORY PERIODS Skeletal Muscle Cardiac Muscle 40 41 The normal refractory period of the ventricle is 0.25 to 0.30 second, which is about the duration of the prolonged plateau action potential. There is an additional relative refractory period of about 0.05 second during which the muscle is more difficult to excite than normal but can be excited by a very strong excitatory signal. Excitation-contraction coupling— function of calcium ions and the transverse tubules The term excitation-contraction coupling refers to the mechanism whereby the action potential causes the myofibrils of muscle to contract. Excitation-Contraction Coupling 1.Starts with CICR (Ca2+ induced Ca2+ release) 2. AP spreads along sarcolemma T-tubules contain voltage gated L-type Ca2+ channels which open upon depolarization 3.Ca2+ entrance into myocardial cell and opens RyR (ryanodine receptors) Ca2+ 4.release channels release of Ca2+ from SR causes a Ca2+ “spark” 5.6. Ca2+ produce actin & myosin intraction Relaxation 7. Ca2+ is transported out of the cell by a Na+/Ca2+ exchanger (NCX) 8.Ca2+ is transported back into the SR and As ICF Ca2+ levels drop, interactions between myosin/actin are stopped Without the calcium from the T tubules, the strength of cardiac muscle contraction would be reduced considerably because the sarcoplasmic reticulum of cardiac muscle is less well developed than that of skeletal muscle and does not store enough calcium to provide full contraction. The T tubules of cardiac muscle, have a diameter five times as great as that of the skeletal muscle tubules Also, inside the T tubules is a large quantity of mucopolysaccharides that are electronegatively charged and bind an abundant store of calcium ions, keeping them available for diffusion to the interior of the cardiac muscle The strength of contraction of cardiac muscle depends to a great extent on the concentration of calcium ions in the extracellular fluids. In fact, a heart placed in a calcium free solution will quickly stop beating. Cardiac glycosides from Digitalis digitoxin purpurea Highly toxic in large dosage: destroys all Na+/K+ pumps In low dosage: partial block of Na+ removal from myocardial cells 50 Duration of Contraction. Cardiac muscle begins to contract a few milliseconds after the and continues to contract until a few milliseconds after the action potential ends. Therefore, the duration of contraction of cardiac muscle is mainly a function of the duration of the action potential, including the plateau— about 0.2 second in atrial muscle and 0.3 second in ventricular muscle. CARDIAC CYCLE events that occur from the beginning of one heartbeat to the beginning of the next are called the cardiac cycle. Each cycle is initiated by the spontaneous generation of an action potential in the sinus node, This node is located in the superior lateral wall of the right atrium near the opening of the superior vena cava, and the action potential travels from here rapidly through both atria and then through the A-V bundle into the ventricles. Diastole and Systole The total duration of the cardiac cycle, including systole and diastole= 0.8 sec/beat. 55 Increasing Heart Rate Decreases Duration of Cardiac Cycle. When heart rate increases, the duration of each cardiac cycle decreases, including the contraction and relaxation phases. The duration of the action potential and systole also decrease. This means that the heart beating very rapidly does not remain relaxed long enough to allow complete filling of the cardiac chambers before the next contraction. In your opinion, a person may faint due to a sharp increase in heart rate? Heart Valves Papillary muscles are attached behind the valve by chorda tendinea 59  Function of the Mitral Valve Prolapse Papillary Muscles 62 HEART VALVES 63 Figure 19.10 Function of the Papillary Muscles. papillary muscles that attach to the vanes of the A-V valves by the chordae tendineae. The papillary muscles contract when the ventricular walls contract they pull the vanes of the valves inward toward the ventricles to prevent their bulging too far backward toward the atria during ventricular contraction. If a chorda tendina becomes ruptured, or if one of the papillary muscles becomes paralyzed due to low blood flow from a myocardial infarction, the valve bulges far backward during ventricular contraction, sometimes so far that it leaks severely and results in severe or even lethal cardiac incapacity. 65  Heart Sounds Heart sounds (lub-dup) are associated with closing of heart valves HEART SOUNDS S1 :occurs as AV valves close and signifies beginning of systole S2 :occurs when aortic valves close at the beginning of ventricular diastole S3: in end of 1/3 the first diastolic S4: in 1/3 end diastolic (atrial contraction) 67  You know that atrial systole is the same time as ventricular diastole atrial systole 1.The Atria Function as Primer Pumps for the Ventricles about 80% of the blood flows directly through the atria into the ventricles, even before the atria contract. (passive stage) 2.Then, atrial contraction usually causes an additional 20% filling of the ventricles.(active stage) Ventricular Diastol has 3 stage: 1. rapid filling: about 80% of the blood flows directly through the atria (the first third of diastole) 2. Diastasis: During the middle third of diastole, only a small amount of blood normally flows into the ventricles. This is blood that continues to empty into the atria from the veins and passes through the atria directly into the ventricles 3. During the last third of diastole, the atria contract and give an additional thrust to the inflow of blood into the ventricles. This mechanism accounts for about 20% of the filling of the ventricles during each heart cycle. Atrial Systole: Passive Active Ventricular Diastole: 1/3 first 1/3 middle 1/3 end 70 The ventricles stiffen with aging or diseases that cause cardiac fibrosis such as high blood pressure or diabetes mellitus. This causes less blood to fill the ventricles in the early portion of diastole and requires more volume or more filling from the later atrial contraction to maintain adequate cardiac output. end-diastolic volume = 120 ml ventricular volume normally increases to about 120 ml, Stork volume= 70 ml end-systolic volume= 50 ml The amount of blood that remains in the ventricle after the previous heartbeat 72 Volume-Pressure Diagram During the Cardiac Cycle; Cardiac Work Output. It is divided into four phases: Phase I: Period of Filling. begins at a ventricular volume of about 50 ml and a diastolic pressure of 2 to 3 mm Hg. As venous blood flows into the ventricle from left atrium the ventricular volume normally increases to about 120 ml, and the diastolic pressure rising to about 5 to 7 mm Hg. Phase II: Period of Isovolumic Contraction. During isovolumic contraction, the volume of the ventricle does not change because all valves are closed. However, the pressure inside the ventricle increases to equal the pressure in the aorta, at a pressure value of about 80 mm Hg, Phase III: Period of Ejection. During ejection, the systolic pressure rises even higher because of still more contraction of the ventricle. At the same time, the volume of the ventricle decreases because the aortic valve has now opened, and blood flows out of the ventricle into the aorta. 76 Phase IV: Period of Isovolumic Relaxation. At the end of the period of ejection ,the aortic valve closes, and the ventricular pressure falls back to the diastolic pressure level. this decrease in intraventricular pressure without any change in volume. Thus, the ventricle returns to its starting point  3 phase 4 phase 2 phase 1 phase 4 phase & 1 phase=Ventricle Diastole= 0.5 second 3 phase & 2 phase =Ventricle Systole= 0.3 second 2 phase=0.03 & 3 phase=0.27 Ventricle Systole= 0.3 sec 4 phase=0.06 & 1 phase=0.44 VentricleDiastole=0.5sec 79 Regulation of stroke volume SV = end diastolic volume (EDV) minus end systolic volume (ESV), SV = EDV-ESV ( 70 ml) EDV = amount of blood collected in a ventricle during diastole= 120 ml ESV = amount of blood remaining in a ventricle after contraction= 50 ml 81 Factors affecting stroke volume Preload – amount ventricles are stretched by contained blood Contractility – cardiac cell contractile force due to factors other than EDV Afterload – back pressure exerted by blood in the large arteries leaving the heart 82 PRELOAD AND AFTERLOAD 83 Figure 18.21