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The Vascular System Lecture 11

This lecture discusses the factors influencing stroke volume, including preload, contractility, and afterload. It also covers the regulation of heart rate and the chemical and reflex mechanisms that affect the heart. Congestive heart failure, congenital heart defects, and coronary artery disease are also discussed.

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The Vascular System Lecture 11

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  1. The Vascular System Lecture 11

  2. Regulation of Stroke Volume • SV = end diastolic volume (EDV) minus end systolic volume (ESV) • EDV = amount of blood collected in a ventricle during diastole • ESV = amount of blood remaining in a ventricle after contraction

  3. Factors Affecting Stroke Volume • Preload – amount ventricles are stretched by contained blood • Contractility – cardiac cell contractile force due to factors other than EDV • Afterload – back pressureexerted by blood in the large arteries leaving the heart

  4. Frank-Starling Law of the Heart • Preload, or degree of stretch, of cardiac muscle cells before they contract is the critical factor controlling stroke volume • Slow heartbeat and exercise increase venous return to the heart, increasing SV • Blood loss and extremely rapid heartbeat decrease SV

  5. Extrinsic Factors Influencing Stroke Volume • Contractility is the increase in contractile strength, independent of stretch and EDV • Increase in contractility comes from: • Increased sympathetic stimuli • Certain hormones • Ca2+ and some drugs

  6. Extrinsic Factors Influencing Stroke Volume • Agents/factors that decrease contractility include: • Acidosis • Increased extracellular K+ • Calcium channel blockers Chapter 18, Cardiovascular System

  7. Contractility and Norepinephrine • Sympathetic stimulation releases norepinephrine and initiates a cyclic AMP second-messenger system Figure 18.22

  8. Regulation of Heart Rate • Positive chronotropic factors increase heart rate • Caffeine • Negative chronotropic factors decrease heart rate • Sedatives Chapter 18, Cardiovascular System

  9. Regulation of Heart Rate: Autonomic Nervous System • Sympathetic nervous system (SNS) stimulation is activated by stress, anxiety, excitement, or exercise • Parasympathetic nervous system (PNS) stimulation is mediated by acetylcholine and opposes the SNS • PNS dominates the autonomic stimulation, slowing heart rate and causing vagal tone • If the Vagus Nerve was cut, the heart would lose its tone. Thus, increasing the heart rate by 25 beats per minute.

  10. Atrial (Bainbridge) Reflex • Atrial (Bainbridge) reflex – a sympathetic reflex initiated by increased blood in the atria • Causes stimulation of the SA node • Stimulates baroreceptors in the atria, causing increased SNS stimulation

  11. Chemical Regulation of the Heart • The hormonesepinephrine and thyroxineincrease heart rate • Intra- and extracellular ion concentrations must be maintained for normal heart function

  12. Factors Involved in Regulation of Cardiac Output Figure 18.23

  13. Congestive Heart Failure (CHF) • Congestive heart failure (CHF) is caused by: • Coronary atherosclerosis • Persistent high blood pressure • Multiple myocardial infarcts • Dilated cardiomyopathy (DCM) – main pumping chambers of the heart are dilated and contract poorly

  14. Developmental Aspects of the Heart Figure 18.24

  15. Developmental Aspects of the Heart • Fetal heart structures that bypass pulmonary circulation • Foramen ovale connects the two atria • Ductus arteriosusconnects pulmonary trunk and the aorta

  16. Examples of Congenital Heart Defects Figure 18.25

  17. Age-Related Changes Affecting the Heart • Sclerosis and thickening of valve flaps • Decline in cardiac reserve • Fibrosis of cardiac muscle • Atherosclerosis

  18. Congestive Heart Failure • Causes of CHF • coronary artery disease, hypertension, MI, valve disorders, congenital defects • Left side heart failure • less effective pump so more blood remains in ventricle • heart is overstretched & even more blood remains • blood backs up into lungs as pulmonary edema • suffocation & lack of oxygen to the tissues • Right side failure • fluid builds up in tissues as peripheral edema Chapter 18, Cardiovascular System

  19. Coronary Artery Disease • Heart muscle receiving insufficient blood supply • narrowing of vessels---atherosclerosis, artery spasm or clot • atherosclerosis--smooth muscle & fatty deposits in walls of arteries • Treatment • drugs, bypass graft, angioplasty, stent

  20. Clinical Problems • MI = myocardial infarction • death of area of heart muscle from lack of O2 • replaced with scar tissue • results depend on size & location of damage • Blood clot • use clot dissolving drugs streptokinase & heparin • balloon angioplasty • Angina pectoris • heart pain from ischemia (lack of blood flow and oxygen ) of cardiac muscle

  21. By-pass Graft

  22. Percutaneous Transluminal Coronary Angioplasty Chapter 18, Cardiovascular System

  23. Arteries and Veins Anotomy Chapter 18, Cardiovascular System

  24. Exchange b/w blood of capillary and tissue fluid

  25. Systemic circulation

  26. Systemic veins

  27. Head and Neck veins and arteries

  28. Chapter 18, Cardiovascular System

  29. Fetal Circulation

  30. Hormones that affect blood pressure Chapter 18, Cardiovascular System

  31. The Renin-Angiotensin mechanism

  32. Nervous mechanism that regulate blood pressure Chapter 18, Cardiovascular System

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