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Transcript
1. Cardiac Physiology 2. Circulatory System Review Components Heart Blood vessels Blood 3. Fig. 9-1, p. 242 4. Fig. 9-2b, p. 243 5. Right and Left Ventricles Both pump same volumes at same time Pulmonary Low pressure Low resistance Systemic High pressure High resistance 6. Heart Wall Inner layer Endothelium Middle layer Myocardium Cardiac muscle Interlacing bundles spiraling around heart Outer layer Visceral pericardium 7. http://www.dkimages.com/discover/previews/740/76722. JPG 8. Cardiac Muscle Tissue Striated Sarcomeres Thick and thin filaments like skeletal muscle T-tubules No lateral sacs/triads Mitochondria Myoglobin Intercalcalated discs Desmosome Gap junction 9. Fig. 9-5, p. 246 10. Functional Syncytia Atria – functional syncytium Ventricles – functional synctium Atrial cells do no connect with ventricular cells ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ Atria and ventricles separated by nonconducting layer of fibrous connective tissue Atrial depolarization and contraction separate from ventricular depolarization and contraction Conduction system provides synchronization 11. Electrical Activity Contractile cells Autorhythmic cells Initiate and conduct AP Don’t “rest” Pacemaker potential 12. Fig. 9-6, p. 247 13. Locations Sinoatrial node Atrioventricular node Bundle of His (atrioventricular bundle) Left and right bundle branches Purkinje fibers 14. Fig. 9-7, p. 247 15. Fig. 9-8ab, p. 248 16. Fig. 9-8cd, p. 248 17. Coordination Atrial excitation/contraction needs to be finished before ventricular contraction takes place Each chamber must contract as a unit Each pair of atria and each pair of ventricles should contract simultaneously 18. Fig. 9-9, p. 250 19. Action Potential of Cardiac Cells Resting potential = -90mV Threshold = -70mV 20. Fig. 9-10, p. 251 21. Fig. 9-11, p. 251 22. Refractory Period 250msec Prevents tetanus 23. Electrocardiography ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ Composite of all APs generated by nodal and contractile cells 24. Fig. 9-13a, p. 253 25. Fig. 9-13b, p. 253 26. Fig. 9-14, p. 254 27. EKG - Intervals PQ interval (PR) Start of atrial excitation to start of ventricular excitation ST segment Depolarization of entire ventricular myocardium QT interval Start of ventricular depolarization through repolarization 28. 29. http://www.anaesthesiauk.com/article.aspx? articleid=100685 30. http://www.anaesthesiauk.com/article.aspx? articleid=100685 31. 32. http://www.frca.co.uk/images_main/resourc es/ECG/ECGresource27.jpg http://www.anaesthesiauk.com/article.aspx? articleid=100685 33. http://library.med.utah.edu/kw/ecg/mml/ec g_v_fib.html 34. Mechanical Physiology Systole Period of contraction Diastole Period of relaxation Cardiac cycle Atrial systole + atrial diastole + ventricular systole + ventricular diastole Heart beat ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ 35. Summary Blood flows from region of higher pressure to region of lower pressure Pressure changes due to alternating contraction and relaxation of myocardium Pressure changes control opening and closing of valves 36. Early Ventricular Diastole - Fig. 9-16, pg. 256 EKG – Atria AV valves SL valves Ventricular volume Ventricular pressure 37. Late Ventricular Diastole - Fig. 9-16, pg. 256 EKG – Atria AV valves SL valves Ventricular volume Ventricular pressure 38. End of Ventricular Diastole Ventricle at maximum volume End-diastolic volume (EDV) ~135ml 39. Ventricular Excitation EKG – QRS complex Onset of ventricular systole Increased ventricular contraction of AV valves closing 40. Isovolumetric Contraction - Fig. 9-16, pg. 256 EKG – Atria in AV valves SL valves Ventricular volume Ventricular pressure 41. Ventricular Ejection - Fig. 9-16, pg. 256 EKG – Atria in AV valves SL valves Ventricular volume Ventricular pressure 42. End of Ventricular Systole End-systolic volume ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ Amount of blood remaining in ventricle at end of systole (ESV) ~65ml Stroke volume Amount of blood pumped out of each ventricle during each contraction (SV) SV = EDV - ESV 43. Isovolumetric Relaxation - Fig. 9-16, pg. 256 EKG – Atria in AV valves SL valves Ventricular volume Ventricular pressure 44. Fig. 9-16, pg. 256 45. Fig. 9-16, pg. 256 46. Fig. 9-16, pg. 256 47. Fig. 9-16, pg. 256 48. Fig. 9-16, pg. 256 49. Cardiac Output Cardiac output (CO) CO = HR x SV ~5 liters/minute Cardiac reserve 50. Regulation of Cardiac Output Heart rate (HR) Stroke volume (SV) 51. Regulation of Stroke Volume Stroke volume is difference between EDV and end systolic volume (ESV) SV = EDV -ESV Typically ~60% of blood in ventricle is pumped out when ventricle contracts Factors affecting SV Preload Contractility Afterload 52. Preload Degree of stretch of heart muscle ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ Resting cardiac muscles cells are less than optimum length Increased venous return Increased ED Increased SV 53. Frank-Starling Law - Fig. 9-20, pg. 262 54. Contractility - Fig. 9-22, pg. 263 Strength of contraction given any EDV Increased contractility leads to increased ejection fraction Due to increased Ca2+ 55. Afterload Back pressure exerted by arterial blood 80mmHg/8mmHg Not usually a major determinant of stroke volume 56. Control of Stroke Volume Intrinsic control Venous return Increased return results in increased SV Extrinsic control Degree of sympathetic stimulation Increased epinephrine and norepinephrine results in increased calcium influx and greater cross-bridge cycling Shifts Starling curve to left Also enhances venous return 57. Fig. 9-22, pg. 263 58. http://www.thiemeconnect.com/bilder/srccm/200103/srm00083.01 59. Heart Rate Intrinsic rate set by SA node Autonomic influences Parasympathetic Atrium SA node AV node Sparse in ventricles Sympathetic All of the above + rich innervation of the ventricles 60. ANS Influence on Heart Rate Parasympathetic ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ Decrease rate of depolarization of SA Increases AV delay Little effect of ventricular contraction Sympathetic Increase rate of depolarization of SA Decrease AV delay Speed transmission of AP through conduction pathway Increased contractile strength 61. Fig. 9-18, pg. 260 62. Fig. 9-19, pg. 261 63. Table 9-3, pg. 260 64. Heart Failure Inability of cardiac output to meet demands for oxygen/nutrient delivery and removal of wastes Decrease in contractility 65. Fig. 9-24, pg. 264 66. Compensatory Mechanisms Sympathetic stimulation Increased salt and water retention by the kidneys Decompensated heart failure Cardiac muscle cells stretched Congestive heart failure Backup of blood in venous system 67. Fig. 9-24, pg. 264 68. Heart Failure Causes Damage to heart muscle Prolonged pumping against elevated BP 69. Coronary Artery Disease (CAD) Coronary Circulation Endothelium impermeable Myocardium too thick for diffusion Receives blood during diastole Blood flow adjusted to match heart’s requirements CAD Pathology in coronary arteries Insufficient flow in times of need ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ Myocardium too thick for diffusion Receives blood during diastole Blood flow adjusted to match heart’s requirements CAD Pathology in coronary arteries Insufficient flow in times of need 70. CAD Myocardial ischemia/myocardial infarction Vascular spasm Cold, exertion, anxiety Atherosclerotic plaques Thromoboembolism 71. Atherosclerosis Plaque Under vessel lining Lipid core Smooth muscle Connective tissue Formation Injury Inflammatory resonse Cholesterol, free radicals, high blood pressure, homocysteine, bacteria, viruses 72. Atherosclerosis Accumulation of low-density lipoprotein (LDL) Endothelial cells release chemicals that attract monocytes Macrophages phagocytize LDL Smooth muscle forms atheromas 73. Atherosclerosis Plaque bulges into lumen of vessel Damaged vessels unable to dilate normally Plaque inhibits diffusion – fibroblasts Ca2+ deposited into plaque 74. Fig. 9-25a, p. 266 75. Complications Angina pectoris Myocardial infarction Thromboembolism Thrombus Embolus 76. Fig. 9-26ab, p. 267 77. Fig. 9-27, p. 268 78. Table 9-4, p. 269 ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________ ____________________________
