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CSU BMS 300 - The Cardiac Cycle to Starling's Law of the Heart

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BMS 300 1st Edition Lecture 28Outline of Last Lecture V. Ec coupling and the sliding filament theory- from LMN to T-SR-the T-SR junction II. DHP receptors: plugIII. RYP recptors: Ca2+ release from SR>Ca2 + realse from SR-The cytoskeleton and its organization in to sarcomeres-Components of the sarcomeres1. Thin filaments>Actin>Trophin (ca2+binding)>Tropomyosin2. Myosin 3. z-lines of actninVI. actomosin bridges and the power stroke-myosin binding to actin-myosin as an ATPase-the power stroke1. ADP Pi leaveVII. Ending recycle -Pumpkin Ca2+in the SRVIII. Rigonmentis Outline of Current Lecture II. Endocardium, myocardium, pericardium 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.A. Myocardium-generates propulsive force on blood in the chambers III. Diastole filling phase IV. Systole myocardial contraction and ejection V. The cardiac cycle and the pressure volume curveB. Diastole (end diastolic volume) C. Systole (isovolumetric contraction, ejection)D. Isovolumetric relaxation VI. Valves of the heart and cardiac system E. What opens and closes valves F. Which valves open and close and when VII. Stroke volume G. End diastolic volume-end systolic volume VIII.Cardiac output ( S.V. x cycles/min) IX. Starlings law of the heart Current LectureRecap of the heart-what we see on the right side we also see on the left side -the resistance of flow from the left is lower then what is on the right -we have a continuous layer of endothelium everywhere in the chambers -mesothelial cells are a kind of epithelium in the cavity that provides a kind of “sac” these are attached by a basal lamina >2 layers >they attach to the wall of the heart >visceral pericardial layer -theres a basal lamina that attaches the mesothelium to the body wall >parietal pericaedial layer **bag filled with fluid pericarditis: the inflammation of the pericardium >pericardial sac fills with fluid -the venous pressures around 3-5mmHg **very dangerous to have fluid in the sav then and increased the pressure Cardiac Cycle/ Pressure volume curve-A: around 50 mm -from points A-B is the diastole period of ventricle filling -B: this increase results because of the atrial myocardium >the contraction (high pressure)>atrial myocardial contraction >end diastolic volume>atrial ventricular valve is closing -from B-C is the isovolumetric contraction -C: the ventricular myocardium is contracting >the aortic valve opens -D: the aortic pressure is greater then the ventricular pressure -the point between D and A is a brief period of isovolumetric relaxation (very short) -the right side is the same thing almost >the pressures are less to open valves>in series (volumes are the same)**when pressures increase the “doors” close and when the ventric pressure is greater the aorticdoor opens There’s a differenceEnd diastolic volume 120mL-End systolic volume 50mL = 70mL stroke volume Cardiac output: the stroke volume x cycles per min >when you exercise the number of cycles per min has to increase Starlings law: increase in end diastolic volume  increase in stroke


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CSU BMS 300 - The Cardiac Cycle to Starling's Law of the Heart

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