BIOL 2002C 1st Edition Lecture 6 Outline of Last Lecture I Blood Outline of Current Lecture I Blood Typing II Start of Chapter 20 Current Lecture 1ROUTE OF BLOOD THROUGH THE HEART 9 Relate the flow of blood through the heart naming the chambers valves and vessels in the correct order Fig 20 10 Superior inferior vena cava coronary sinus right atrium tricuspid valve right ventricle pulmonary valve pulmonary trunk pulmonary arteries lungs gas exchange pulmonary veins lef atrium bicuspid valve lef ventricle aortic valve aorta body circulation coronary arteries 11 Explain why knowing the heart s location is important For CPR Define the following Pericarditis inflammation of serous pericardium which results in less serous fluid so more friction when the heart beats Cardiac tamponade can be result of pericarditis it is when excessive inflammatory fluid fills the pericardial cavity the fluid compresses the heart and makes it hard to beat Myocardial infarction commonly know as a heart attack it is a result of a stop in the delivery of oxygen ischemia which causes tissue damage and eventual tissue death These notes represent a detailed interpretation of the professor s lecture GradeBuddy is best used as a supplement to your own notes not as a substitute Angina pectoris a decrease in the blood flow causes chest pain it is damaging to heart tissue the link to aerobic respiration Nitroglycerin is used to treat it because it is a vasodilator 20 5 HISTOLOGY 12 Relate the structural and functional characteristics of cardiac muscle cells Fig 20 12 Myofibrils composed of myofilaments Myofilaments actin thin filament and myosin thick filament Intercalated discs Desmosomes hold the cardiac cells together and anchor them Gap junctions allow ions to pass from cell to cell T tubules surround myofibrils extension of the sarcolemma allowing action potentials to enter the interior of the cell SR sarcoplasmic reticulum contains calcium and is a form of smooth endoplasmic reticulum Nucleus control center contains DNA determines what proteins will be made Mitochondria makes lots of ATP aerobically 13 Compare and contrast cardiac muscle vs skeletal muscle Cardiac Muscle Skeletal Muscle Basic cellular structure Small and branched Long and unbranched Energy requirements usage Uses fatty acids Stored as glycogen All or none law Entire organ contracts or not at all A muscle fiber contracts completely or not at all Refractory period Longer refractory period Shorter refractory period 14 Explain the structure and function of the conducting system of the heart What is the proper sequence of the structures involved and the time and set heart rate of each Fig 20 13 These are in proper order a Sinoatrial SA node in upper R atrium 70 80 bpm pacemaker of the heart actual normal heart rate is between 72 75 b Atrioventricular AV node in lower R atrium 40 60 bpm 0 04 seconds from the SA to AV node c AV bundle of His 30 bpm delay is 0 11 seconds total delay now is 0 15 which gives time for the atria to contract d Right and left bundle branches 30 bpm spreads very fast e Purkinje fibers in ventricular walls 30 bpm spreads very fast 20 6 ELECTRICAL PROPERTIES 16 Explain what is meant by the autorhythmicity of cardiac muscle and relate it to the pacemaker potential Describe what happens during the pacemaker potential depolarization action potential and repolarization Fig 20 15 Only 1 of the total cardiac fibers are autorhythmic able to depolarize on their own The rest are called contractile fibers respond to depolarization through gap junctions a Pacemaker potential Prepotential unstable resting membrane potential in autorhythmic cells K permeability is unstable in autorhythmic cells so K movement is reduced resulting in proportionately more Na moving into the cell This makes the membrane potential less negative and it drifs toward the threshold of 40mV b Depolarization action potential When the membrane potential reaches 40mV fast Ca 2 channels open and Ca 2 rushes in from outside the cell This Ca 2 influx causes further depolarization and generation of an action potential c Repolarization Ca 2 channels close K voltage gated channels open and K moves out of cell Ca 2 is actively pumped out of the cell Na K pump works to restore resting concentrations Define ectopic focus and predict the consequences for the heart s pumping effectiveness if numerous ectopic foci in the ventricles produce action potentials at the same time 17A Any part of the heart other than the SA nodes that create a heart beat Common causes include malfunctioning SA node blockage of conduction pathways drugs inflammation ischemia irregularities of Calcium and Potassium concentrations How does the depolarization spread from autorhythmic heart cells to contractile cells Through gap junctions 17B Describe in detail the processes of depolarization early repolarization plateau and final repolarization in contractile cells Fig 20 14 a Depolarization Na and Ca 2 ions move into contractile cells from autorhythmic cells through gap junctions These ions cause a voltage change in contractile cells which opens fast voltage gated Na channels so Na rushes in from outside the cell These channels close quickly but cause depolarization from 90mV to 30mV and therefore cause the action potential b Early Repolarization Plateau Some voltage gated K channels open causing early repolarization Slow voltage gated Ca 2 channels have also opened so Ca 2 enters from outside the cell This Ca 2 triggers the release of additional Ca 2 from the sarcoplasmic reticulum 20 from outside 80 from SR 2 This Ca keeps the membrane depolarized for a longer period of time about 200msec c Repolarization Ca 2 channels close and many voltage gated K channels open so K leaves cell This causes the membrane potential to become more negative Ca 2 ions are also pumped back into the SR and out of the cell In summary How do these events cause cardiac muscle contraction The wave of depolarization produced in the contractile cells spreads down the T tubules and causes the SR to release Ca 2 into the sarcoplasm Excitation contraction coupling occurs just like in skeletal muscle contraction with Ca binding to troponin causing exposure of binding sites on actin cross bridge pulling of myofilaments power stroke and contraction The influx of Ca 2 through slow Ca 2 channels also contributes to and prolongs this process In summary How does the contraction spread Action potentials spread from autorhythmic to contractile