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Exam 2 NotesCardiac Function 1 (2nd half, missed 1st half)Cardiac Cell Structure- Small discrete cells- Intercalated disks with desmosomes- Gap junctions = syncytium- Many mitochondria- SR and t tubules- Striated- carefully aligned for cross bridge cyclingFigure 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 filamentsLength – Tension passive- in vitro (in life)active- in vevo (inside a person), cross bridge cyclingtotal- sum of the 2pg. 340 & 390there is a certain optimal length that allows you to generate the most forceFig 13.10: Cardiac Conduction SystemSA node- pacemaker; AV node- secondary pacemakerElectrical 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•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 depolarizationIonic Bases of the Autorhythmic Cell Action Potential L ChannelsSee 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 activityAutonomic 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 pissTerminology- Inotropic response: strength of beat + or -- Chronotropic response: speed of beato Tachycardia (+)o Bradycardia (-)Funny channels- open in response to hyperpolerization or repolarizationNormally VG Na channels open in response to depolarizationImportant 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 musclesTables 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 RateEffects of Sympathetic Activity on Ventricular Contractility: Fig 13.26 1. increase of calcium2.3. cross bridges generate faster4. reuptake of Ca- rapid relaxation1st Lecture After ExamCardiac Function 2- look at cardiovasc. CD!!!!Extracellular recording-records differences in polarity between a pair of electrodesIntracellular recording- measures actual membrane potentials*don’t need to memorize, just need to know they have PQRSTP wave - atrial depolarizationQRS complex- vent. Depolarization (atrial muscles depolarization)T wave - vent. RepolarizationPQ segment - AV nodal delayQT segment- ventricular systole (AP on ventricular muscle cells)TQ interval- ventricular diastoleAbnormal HRs“Sinus rhythm” = rhythm generated by SA nodeAbnormal Heart Rates:- Tachycardia- fast- Bradycardia- slow3rd Degree Heart Block - Loss of conduction through AV node- P wave independent of QRS complex- Atrial and ventricular contractions are independentExtrasystole - Extra contraction- PAC = premature atrial contraction- PVC = premature ventricular contractionVentricular Fibrillation - Defibrillation- depolarize everything and hopefully sino atrial node takes over- Loss of coordination of electrical activityo Atrial fibrillation - weaknesso Ventricular fibrillation - death within minutesTerminology- End Systolic Volume (ESV in ml) - End Diastolic Volume (EDV in ml))- Stroke Volume (SV in ml/beat)- SV = EDV – ESVStroke Volume: page 383 - Atrial stroke vol- what fills ventricles? Relaxingexpandingsucking blood out of veinsY axis- ventricular pressure (mmHg)X axis- ventricular Volume (mL)Things to place on P – V Loop - Systole & Diastoleo 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, afterloadStarling’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/ro P = pressure in ventricle or aorta at ejectiono T = myocardial tension required to generate that tensiono r = radius of ventricle at beginning of systoleDigitalis 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 rateStroke V**be able to know the effects of increasing or decreasing anything on this table**know thisFig 13.8 Graphisovolumetric portion- QRSat QRS atrial pressure is below pressure in ventricle the AV valve snaps shut 1st heart soundventricular vol doesn’t change until the pressure exceeds pressure in aortaforce drawing blood into ventricle is the relaxation of ventricle**be able to label everything you did on vent. Vol. graphRegulation of Blood FlowWould

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UMD BSCI 440 - Exam 2 Notes

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