BIO 251 1st Edition Lecture 15 Outline of Last Lecture I. Introduction to circulatory system a. Function b. 3 components c. 2 separate loopsII. Structure of heart a. Location b. Heart as dual pumpc. One way blood flowIII. Myocardium a. Structure b. Interconnections IV. Electrical & contractile activity of heart cells a. 2 types myocardial cells b. Autorhythmic cell APc. Contractile cell APd. Molecular basis V. Electrical activity of entire heart a. Autorhythmic regions of heartThese 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.b. Spread of AP in heartc. ElectrocardiogramsOutline of Current Lecture I. Mechanical events in cardiac cycle a. Introduction b. TP interval c. P wave & PQ intervald. QR interval e. RS interval f. ST segment g. Start of T waveh. T wave peak to end of T wave i. TP interval j. Stroke volumek. Sounds II. Cardiac output & control a. Cardiac output b. Control of HRi. Parasympathetic ii. Sympathetic c. Control of SVi. Sympathetic effectsii. Varying length of heart muscle fibersd. Summary III. Nourishing the heart muscle a. Heart muscle doesn’t extract nutrients from blood in chambersb. Coronary circulationIV. ChantV. Top hat questionsVI. ProblemCurrent Lecture-Mechanical events in the cardiac cycle (13.18-13.21, CD cardiac cycle 5-17)oIntroduction -Systole -Contraction & emptying of the chambers-Diastole -Relaxation & filling of chambers -Atria & ventricles go through separate cycles of systole & diastole -Contraction status (being in systole or diastole) determines-Heart chamber pressure which determines-Whether valves are open or closedoTP interval: Ventricular diastole -Atria & ventricles are in diastole (i.e., relaxed)-Blood flows from veins to atria -Ventricular pressure < aortic pressure = aortic valve closed -Atrial pressure > ventricular pressure = AV valve open -Blood flows from atria directly into ventriclesoP wave and PQ interval: late ventricular diastole -Ventricular pressure < aortic pressure = Aortic valve closed -SA node reaches threshold & fires -Atrial Depolarization occurs-Atria contract = atrial systole -Atrial pressure > ventricular pressure = AV valve open -Blood squeezed by atrial contraction from atria into ventricles oQR interval: end of ventricular diastole -Ventricular pressure < aortic pressure = aortic valve closed-Atrial pressure > ventricular pressure = AV valves open -Blood squeezed from atria into ventricles -Electrical impulse enters ventricles from AV node -Ventricles begin to repolarized-R peak is end of ventricular diastole & start of ventricular systoleoRS interval: early ventricular systole -Ventricles being to contract-Atrial pressure < ventricle pressure = AV valves close -Atrial contraction & ventricular filling are completed -Ventricular pressure still not high enough to open aortic valve -End-diastolic volume (EDV)-Volume of blood in ventricles -About 135 ml/ventricle in resting adult -Atria repolarizeoST segment: ventricular systole -Ventricular pressure > atrial pressure = AV valve closed-Ventricular pressure > aortic pressure = aortic valve open -Blood ejected into aorta from ventricles -Atria in diastole & filling w/ blood oStart of T wave: late ventricular systole -Repolarization of ventricles begins oT wave peak to end of T wave: early ventricular diastole -Peak of t wave= end of systole & start of diastole -Ventricles begin to relax -Ventricular pressure < aortic pressure = aortic valve closes -No more blood can leave ventricles -Ventricular pressure > atrial pressure = AV valves closed = no blood can enter ventricles -End systolic volume (ESV)-Remaining volume of blood-~ half of end diastolic volume remains in the ventricles (65ml/ventricle in resting adult) -Atria in diastole & filling w/ blood oTP interval: Ventricular diastole (back where we started) -Atria & ventricles are in diastole (relaxed)-Blood flows from veins into atria -Ventricular pressure < aortic pressure = aortic valve closed -Atrial pressure > ventricular pressure = AV valve open -Blood flows from atria directly into ventriclesoThe stroke volume (SV) -Equal to EDV-ESV = volume of blood pumped by one ventricle per heart beat -Averages ~70 ml/beat when at rest oSounds (13.23) -Classic heart sound description -"lube-dub"-1st sound is turbulent rushing of blood as AV valves are closing -2nd sound is turbulent rushing of blood as aortic & pulmonary valves are closing -Cardiac Output & its Control (CD cardiac output 3-8) oCardiac output-CO is volume of blood pumped by each ventricle/min (NOT volume of blood pumped by whole heart) -CO= heart rate (HR) x stroke volume (SV)-Control of cardiac output is accomplished by controlling HR & SV-At rest for avg individual -HR=70 beats/min-SV= 70 ml/beat (see above)-CO= 70 beats/min x 70 ml/beat = 4900ml/min-b/c total blood volume in a person is 5-5.5 L each 1/2 of heart pumps nearly the whole blood volume each min @ restoControl of Heart Rate (13.24) -Review-SA node sets baseline HR @ 70 beats/min-Parasympathetic can modify baseline rate -Vagus nerve-Primary Parasympathetic nerve to heart -Supplies atrium, especially SA & AV nodes BUT-Has little/no effect on ventricles -Decreases HR by-Decreasing rate of Depolarization in SA node-Increasing AV node delay-Mechanism -Na+ & Ca++ leaks into SA node cells decreased-K+ out increased = membrane potential more negative (13.25b & 13.26) -Sympathetic can modify baseline rate -Sympathetic cardiac nerves supply atria, including SA & AV nodes, also the ventricles -Increases HR by-Increasing rate of Depolarization in SA node -Reducing AV node delay -Speeding up spread of AP through bundles of His & Purkinje fibers-Mechanism -Binding of epi or norepi to beta 1 receptors on pacemakers cells increases rate of Na+ & Ca++ leaks into cell= membrane potential more positive (13.25a & 13.26)oControl of Stroke Volume -Sympathetic effects-Norepi & epi binding beta 1 receptors on contractile cells (13.27) -Increases contractile strength of ventricle cells by -Increasing Ca++ permeability of contractile cells -Increasing Ca++ movement from the SR-Increasing rate of myosin ATPase activity -Increasing rate of pumping Ca++ back into SR-Varying length of heart muscle fibers -Longer fiber