Exam 2 Notes Cardiac Function 1 2nd half missed 1st half Cardiac Cell Structure Intercalated disks with desmosomes Small discrete cells Gap junctions syncytium Many mitochondria SR and t tubules Striated carefully aligned for cross bridge cycling Figure 13 9 Cardiac Muscle Cells Electrical sinsissium electrical continuity Shared intracellular space by gap junction held by desmosome Cross bridge cycle taking place btwn thin and thick filaments Length Tension passive in vitro in life active in vevo inside a person cross bridge cycling total sum of the 2 pg 340 390 there is a certain optimal length that allows you to generate the most force Fig 13 10 Cardiac Conduction System SA node pacemaker AV node secondary pacemaker Electrical Activity of the Heart E of Ca 130 mV E of Na 60 mV E of K 94 mV Implications of this Pacemaker game The area that depolarizes most rapidly drives the rest L Channels Slow initial depolarization caused by closing of K channels Next funny channels open Allow Na to enter causing depolarization Only open briefly This depolarization opens two types of Ca channels T type channels open briefly before inactivating L type channels then open finishing depolarization Ionic Bases of the Autorhythmic Cell Action Potential See the Cardiac Cycle on CD Ionic Bases of the Contractile Cell Action Potential Ventricular action potential Duration for complete contraction of the cardiac pump Long AP with long refractory period to prevent fibrillation random uncoordinated muscle twitches o AED defibrillates stops electrical activity in heart and hopefully pacemaker cells are healthy enough to resume electrical activity Autonomic Input to the Heart Figure 13 23 vagus nerve bearing down vaguling out don t cut vagus it tells lungs to stop breathing goes into shock SABP sinoatrial node AV node bundle of piss Terminology Inotropic response strength of beat or Chronotropic response speed of beat o Tachycardia o Bradycardia Funny channels open in response to hyperpolerization or repolarization Normally VG Na channels open in response to depolarization Important Concepts Mechanism of Muscle contraction CD Length Tension Curve Starling s law See Fig 12 18 See http moon ouhsc edu dthompso namics ltprops htm Cardiac muscle cell structure function relationships Heart structure s Ionic bases of Vm and APs in SA node and ventricular muscle cells Heart and cardiac muscle structure Structure Function relationships Ion channels Funny L and T type channels GION during AP on SA node and ventricular muscle cells Signal Transduction pathways for ACh parasympathetic muscarinic on SA node b1 on SA node and on Ventricular muscles Tables 13 1 13 2 and Figures related to above Effects of Sympathetic Activity on SA Nodal Cells Fig 13 24a need to know this Effects of Parasympathetic Activity on SA Nodal Cells Fig 13 24b Effects of Parasympathetic Activity on Heart Rate Effects of Sympathetic Activity on Ventricular Contractility Fig 13 26 1 increase of calcium 2 3 cross bridges generate faster 4 reuptake of Ca rapid relaxation 1st Lecture After Exam Cardiac Function 2 look at cardiovasc CD Extracellular recording records differences in polarity between a pair of electrodes Intracellular recording measures actual membrane potentials don t need to memorize just need to know they have PQRST P wave atrial depolarization vent Depolarization atrial muscles depolarization vent Repolarization AV nodal delay QRS complex T wave PQ segment QT segment TQ interval ventricular diastole ventricular systole AP on ventricular muscle cells Abnormal HRs Sinus rhythm rhythm generated by SA node Abnormal Heart Rates Tachycardia fast Bradycardia slow 3rd Degree Heart Block Loss of conduction through AV node P wave independent of QRS complex Atrial and ventricular contractions are independent Extrasystole Extra contraction PAC premature atrial contraction PVC premature ventricular contraction Ventricular Fibrillation Defibrillation depolarize everything and hopefully sino atrial node takes over Loss of coordination of electrical activity o Atrial fibrillation weakness o Ventricular fibrillation death within minutes Terminology End Systolic Volume ESV in ml End Diastolic Volume EDV in ml Stroke Volume SV in ml beat SV EDV ESV Stroke Volume page 383 Atrial stroke vol what fills ventricles Relaxing expanding sucking blood out of veins Stroke V Y axis ventricular pressure mmHg X axis ventricular Volume mL Things to place on P V Loop Systole Diastole o Atrial Ventricular Ejection Filling Location of mitral and aortic valves opening closing Elements of ECG DP and SP Opening closing of SA node ion channels Opening closing of ventricular ion channels EDV ESV SV HR preload afterload Starling s Law of the Heart Increased EDV or myocardial fiber length results in increased strength of contraction and thus increased SV As the ventricle fills with more blood it responds by forming more cross bridges and generating more tension due to the inherent property of cardiac muscle Physical Basis for Starling s Law The more you fill the ventricle the more force you need to generate in the muscle to put enough pressure to open the aortic valve and eject the blood Laplace s Law P 2T r o P pressure in ventricle or aorta at ejection o T myocardial tension required to generate that tension o r radius of ventricle at beginning of systole Digitalis or b Blockers decrease HR but increase strength why starling s law Problem Go to the Left Ventricular PV curve and re draw it after sympathetic stimulation n diastolic vol would increase n systolic vol would decrease b c generating more force want stroke vol to get bigger pressure would go up how greater vol flow rate or constrict vessles want greater flow rate be able to know the effects of increasing or decreasing anything on this table know this Fig 13 8 Graph isovolumetric portion QRS at QRS atrial pressure is below pressure in ventricle the AV valve snaps shut 1st heart sound ventricular vol doesn t change until the pressure exceeds pressure in aorta force drawing blood into ventricle is the relaxation of ventricle be able to label everything you did on vent Vol graph Regulation of Blood Flow Would rather 120 80 than 160 120 because it takes a lot more energy to maintain 160 120 even though they both have the same flow rate What determines pressure in the system Resistance of vessels o Constriction increases P and R o Measured as Total Peripheral Resistance TPR o To increase flow increase pressure on