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Abstracts and Test 2

This abstract discusses the regulation of pacemaker cells in frog hearts, heart block, the conducting system, and strategies for prolonging the survival of in vitro organs. It also covers the cardiac cycle, heart murmurs, blood composition, and the prevention of action potential conduction. Additionally, it explores factors that control cardiac output, such as heart rate, stroke volume, and afterload.

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Abstracts and Test 2

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  1. Abstracts and Test 2 • Earning up to 5 points for Test # 2 based on topics of Frog Heart Lab: • Regulation of pacemaker cells by temperature, hormones, neurotransmitters, antagonists • Heart block: 1st, 2nd, and 3rd degree • The conducting system • Strategies for prolonging survival of in vitro organs Cardiac Cycle Animation

  2. 1QQ #24 for 10:30Write each letter and circle the letter of correct statements. • Heart murmurs are caused by the closure of heart valves. • The first heart sound is produced by the closure of the atrioventricular valves. • Blood is about 65% plasma. • Pacemaker cells produce action potentials that last about 200-300 milliseconds. • Chordae tendonae and papillary muscles prevent eversion of the semilunar valves.

  3. 1QQ #24 for 11:30Write each letter and circle the letter of correct statements. • The buffy coat is thicker in a person with an infection. • The first heart sound is produced by the closure of the atrioventricular valves. • Blood is about 45% plasma. • Pacemaker cells produce action potentials that last about 200-300 milliseconds. • The tricuspid valve is situated between the right ventricle and the pulmonary artery.

  4. S 8 F=Q=ΔP/R Flow = Pressure gradient/Resistance from Ohm’s Law (V=IR) R = 8Lη/πr4 R = 8Lη/πr4 Q=ΔP πr48LηPoiseulle’s equation Double radius … 16x flow Half radius….1/16th flow

  5. S 1 Cardiac Output = Heart Rate X Stroke VolumeWhat regulatesheart rate?CO = HR x SV5L/min = 72 beat/min x 70 ml/beat What regulatesStroke Volume? The Cardiac Cycle animation

  6. S 4 Figure 12.11 S 5 SA node cells do not have stable resting membrane potential, spontaneously produce AP, are Pacemaker cells

  7. S 15 Figure 12.22 Intrinsic Rate = 100 beat/min 2 effects of Parasymp:hyperpolarization &slower depolarization

  8. S 6 NE EPI ACh mAChR Beta-adrenergic receptors Effect of atropine Effect of “Beta blockers” Recall: CO = HR x SV

  9. S 7 What prevents the AP from being conducted from ventricles to atria? Fibrous connective tissue between atria and ventricles prevents the conduction of action potential. Only route is via AV node, bundle of His, bundle branches, Purkinje fibers, and to ventriclular myofibers.

  10. S 8 “Sis-toe-lee” 1st Heart Sound = Closure of Atrioventricular (AV) valves at beginning of Ventricular Systole “die-ass-toe-lee” 2nd Heart Sound = Closure of Semilunar valves at beginning of Ventricular Diastole

  11. Systolic Diastolic S 9 Figure 12.20 Atrial Fibrillation Ejection Fraction = SV/EDV Stroke Volume Ventricular Fibrillation & Defibrillation Animation

  12. S 10 Events are same for Cardiac Cycle for Right Side of Heart; only difference is lower systolic pressures in right atrium and right ventricle.

  13. S 1 CO = HR x SV5L/min = 72 beat/min x 70 ml/beat 35L/min = ? beat/min x ? ml/beat 3 So far, we’ve dealt with the factors that control Cardiac Output by changing heart rate. 2 + sympathetic 1 - parasympathetic The Cardiac Cycle animation

  14. S 2 Figure 12.20 Stroke Volume Animation

  15. S 3 Frank-Starling Law of the Heart Does not depend on hormones or nerves Assures that the heart adjusts its output based on VENOUS RETURN Ventricular Function Curve Ways to enhance Venous Return:1) muscle contractions2) “respiratory pump”3) venoconstriction FS LoH = SV is proportional to EDV ↑VR→ ↑EDV → ↑SV

  16. Respiratory pump Mechanical pump for bedridden patients Muscle pump

  17. S 4 Fig. 09.21 Length-tension “curve” for Cardiac muscle High EDV Low EDV Overinflation of ventricles leads to less effective pumping

  18. S 5 Overinflation of ventricles results in reduction in stroke volume Treatments? …..diuretics

  19. S 6 NE from Symp postganglionics & EPI from Adrenal medulla Contractility Increase Ejection Fraction Note: cardiac myofibers NOT innervated by parasympathetic division

  20. S 7 3 Effects of SympatheticStimulation 1: Increase rate of contraction 2: Increase peak tension 3: Decrease twitch duration Why should the contraction be shorter?

  21. S 8 Summary: Control of Stroke Volume • End diastolic volume (preload) • Contractility (strength of ventricular contraction due to adrenergic stimulation) • Pressure in arteries that must be overcome = Afterload FS LoH

  22. Afterload is analogous to trying to pump more air into a tire that is already fully inflated (heart contracting to overcome diastolic pressure.) S 9 High blood pressure increases the workload of the heart….. Cardiac hypertrophy….increase chance of irregular conduction of AP through heart Hypertrophic cardiomyopathy

  23. S 11 CO = HR x SV5L/min = 72 beat/min x 70 ml/beat 35L/min = ? beat/min x ? ml/beat Factors that control Cardiac Output by changing heart rate and stroke volume. Afterload (MAP) VR and EDV (FSLoH) + sympathetic Contractility (catecholamines) - parasympathetic

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