Cardiac A&P Review - BMH/Tele

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Cardiac A&P Review - BMH/Tele

  1. 1. Cardiovascular Review Natalie Bermudez, RN, BSN, MS Clinical Educator for Cardiac Telemetry Telemetry Course
  2. 2. The Human Heart <ul><li>Layers (3) </li></ul><ul><li>Atria (2) </li></ul><ul><li>Ventricles (2) </li></ul><ul><li>Valves (4) </li></ul><ul><li>Veins </li></ul><ul><li>Arteries </li></ul>
  3. 3. Layers of the Heart <ul><li>Pericardium </li></ul><ul><li>2) Myocardium </li></ul><ul><li>3) Endocardium </li></ul>
  4. 4. The Pericardium <ul><li>Double-walled serous sac surrounding the heart </li></ul><ul><li>Strengthened externally by a tough fibrous connective tissue layer </li></ul>
  5. 5. The Pericardium: Three Layers <ul><li>Fibrous pericardium (outer) </li></ul><ul><ul><li>Pericardiophrenic ligament </li></ul></ul><ul><ul><ul><li>Blends with the outer fibrous layer or adventitia of all the great vessels except the IVC </li></ul></ul></ul><ul><ul><li>Sternopericardial ligaments </li></ul></ul><ul><ul><ul><li>Keeps heart in its place; attaches to the sternum </li></ul></ul></ul>
  6. 6. The Pericardium: Three Layers <ul><li>Parietal Pericardium </li></ul><ul><ul><li>Lines the inner surface of the fibrous pericardium </li></ul></ul><ul><li>Visceral Pericardium </li></ul><ul><ul><li>Aka epicardium </li></ul></ul><ul><ul><li>Serous fluid secreted by these cells forms a thin lubricating film in the pericardial cavity that provides a friction-free environment for the beating heart </li></ul></ul>
  7. 7. Cardiac Tamponade <ul><li>It is a potentially fatal condition that occurs when fluid rapidly accumulates in the pericardial cavity as a result of trauma, aortic aneurysm, or cardiac surgery. </li></ul><ul><li>The increased fluid causes external compression of the heart, which decreases venous return and CO. </li></ul>
  8. 8. The Myocardium <ul><li>P Cells </li></ul><ul><li>Pacemaker cells </li></ul><ul><ul><li>Responsible for generation of action potentials </li></ul></ul><ul><ul><li>electrical activity </li></ul></ul><ul><li>Cardiomyocytes </li></ul><ul><li>Myocardial Cells </li></ul><ul><ul><li>Contractile cells that generate force </li></ul></ul><ul><ul><li>Mechanical activity </li></ul></ul>
  9. 9. Myocardial Cardiac Cell Types <ul><li>Fibroblasts </li></ul><ul><li>Cells residing in the extracellular mix </li></ul><ul><li>Endotehlial & Smooth Muscle Cells </li></ul><ul><li>Cells found in the blood vessels </li></ul>
  10. 10. Atria & Ventricles <ul><li>Right Atrium </li></ul><ul><li>Left Atrium </li></ul><ul><li>Right Ventricle </li></ul><ul><li>Left Ventricle </li></ul>
  11. 11. Heart Valves <ul><li>Right: </li></ul><ul><li>Tricuspid </li></ul><ul><li>Pulmonic </li></ul><ul><li>Left: </li></ul><ul><li>Bicuspid (Mitral) </li></ul><ul><li>Aortic </li></ul>
  12. 12. Valvular Structures <ul><li>Leaflets </li></ul><ul><li>AV Valves </li></ul><ul><li>(2 or 3) </li></ul><ul><li>Semilunar (3) </li></ul>
  13. 13. Additional Valvular Structures <ul><li>Help to keep A-V valves closed during ventricular systole </li></ul>
  14. 14. Blood Vessels <ul><li>Aorta (A & D) </li></ul><ul><li>SVC </li></ul><ul><li>IVC </li></ul><ul><li>Pulmonary Artery </li></ul><ul><li>Pulmonary Vein </li></ul>
  15. 15. Coronary Arteries Anterior View
  16. 16. Coronary Arteries Posterior View
  17. 18. Coronary Blood Flow <ul><li>Coronary filling occurs during ventricular Diastole </li></ul>
  18. 19. Coronary Blood Flow <ul><li>An increase in heart rate shortens diastole and can decrease myocardial perfusion </li></ul>
  19. 20. Coronary Blood Flow <ul><li>RCA Blood Supply: </li></ul><ul><li>(a) Originates behind the right coronary cusp of the aortic valve </li></ul><ul><li>(b) Supplies </li></ul><ul><li>Right atrium and Right ventricle </li></ul><ul><li>SA Node and AV node </li></ul><ul><li>Inferior-posterior wall of the LV </li></ul><ul><li>(in 90% of hearts) </li></ul><ul><li>Inferior-posterior third of the intraventricular septum </li></ul>
  20. 21. Coronary Blood Flow <ul><li>LCA Blood Supply: </li></ul><ul><li>Divides into the Anterior Descending Artery & Circumflex Artery </li></ul><ul><li>Left atrium </li></ul><ul><li>Most of the left ventricle </li></ul><ul><li>Most of the intraventricular septum </li></ul>
  21. 22. Coronary Blood Flow <ul><li>Cardiac veins lie superficially to the arteries </li></ul><ul><li>The largest vein, the coronary sinus empties into to the right atrium </li></ul>
  22. 23. Coronary Blood Flow <ul><li>Most of the major cardiac veins empty into the coronary sinus </li></ul><ul><li>However, the anterior cardiac veins empty into the right atrium </li></ul>
  23. 24. Pumping Action of the Heart <ul><li>Diastole: </li></ul><ul><li>Atrial Contraction </li></ul><ul><li>(ventricular muscle relaxation) </li></ul><ul><li>Pressure Greater in the Atria </li></ul><ul><li>A-V Valves Open </li></ul><ul><li>Ventricles Fill </li></ul>
  24. 25. Pumping Action of the Heart <ul><li>Atrial Contraction -> 10% to 20% left ventricular filling </li></ul><ul><li>Pulmonary Veins passively fill left ventricle while mitral valve is open </li></ul>
  25. 26. Pumping Action of the Heart <ul><li>In elevated heart rates Atrial Contraction -> 40% left ventricular filling </li></ul><ul><li>A.K.A. Atrial Kick </li></ul>
  26. 27. Pumping Action of the Heart <ul><li>End-Diastolic Volume (EDV) </li></ul><ul><li>Amount of blood in ventricular volume right before systole occurs </li></ul><ul><li>Left Ventricular EDV is approximately 120 ml </li></ul>
  27. 28. Aortic Valve Opens Aortic Valve Closes S 1 S 2 AV Valve Closes AV Valve Opens
  28. 29. Pumping Action of the Heart <ul><li>Ventricular Contraction </li></ul><ul><li>Systole: </li></ul><ul><li>(relaxation of atrial muscles) </li></ul><ul><li>Pressure Greater in Ventricles than Aortic & Pulmonic Blood Vessels </li></ul><ul><li>Aortic & Pulmonic Valves Open </li></ul><ul><li>Blood Ejected into Vessels </li></ul>
  29. 30. Pumping Action of the Heart <ul><li>Stroke Volume </li></ul><ul><li>The amount of blood ejected by the left or right ventricle at each heartbeat. </li></ul><ul><li>The amount varies with age, sex, and exercise but averages 60 to 80 ml. </li></ul><ul><li>EDV = LVEDV - LVESV </li></ul><ul><li>(Taber’s Medical On-line Dictionary) </li></ul>
  30. 31. Pumping Action of the Heart <ul><li>Cardiac Output </li></ul><ul><li>The amount of blood discharged from the left or right ventricle per minute. </li></ul><ul><li>(Taber’s Medical On-line Dictionary) </li></ul>
  31. 33. Pumping Action of the Heart <ul><li>Ejection Fraction </li></ul><ul><li>The percentage of the blood emptied from the ventricle during systole </li></ul><ul><li>The left ventricular ejection fraction averages 60% to 70% in healthy hearts </li></ul><ul><li>(Taber’s Medical On-line Dictionary) </li></ul><ul><li>Normal LV EF = 50% to 75% </li></ul><ul><li>EF = Ventricular EDV/EDV x 100 </li></ul>
  32. 34. Pumping Action of the Heart <ul><li>Cardiac Output is determined by: </li></ul><ul><li>Preload </li></ul><ul><li>Contractility </li></ul><ul><li>Afterload </li></ul><ul><li>Heart Rate </li></ul><ul><li>(Core Curriculum for Progressive Care Nurses, p. 138) </li></ul>
  33. 35. Pumping Action of the Heart <ul><li>Preload </li></ul><ul><li>Stretching of the muscle fibers in the ventricle. Results from blood volume in the ventricles at diastole (EDV). </li></ul><ul><li>(Comerford & Mayer, 2007, p. 15) </li></ul><ul><li>… Refers to the degree of stretch of the cardiac muscle fibers at the end of diastole </li></ul><ul><li>(Smeltzer et al, 2008, p. 786) </li></ul>
  34. 36. Frank-Starling Mechanism <ul><li>Preload is described by the </li></ul><ul><li>Frank-Starling Mechanism </li></ul><ul><li>A.K.A. </li></ul><ul><li>Frank-Starling Law of the Heart </li></ul><ul><li>or </li></ul><ul><li>Starling’s Law </li></ul>
  35. 37. Frank-Starling Mechanism <ul><li>In the intact heart, this means that the force of contractions will increase as the heart is filled with more blood and is a direct consequence of the effect of an increasing load on a single muscle fiber. </li></ul>
  36. 38. Frank-Starling Mechanism <ul><li>The Rubber Band Effect </li></ul><ul><li>The farther a rubber band is stretched, the farther it will go!! </li></ul>
  37. 39. Preload <ul><li>Increased Preload Occurs With: </li></ul><ul><li>Increased circulating volume </li></ul><ul><li>Venous constriction (decreases venous pooling and increases venous return to the heart) </li></ul><ul><li>Drugs: Vasoconstrictors </li></ul>
  38. 40. Preload <ul><li>Decreased Preload Occurs With: </li></ul><ul><li>Hypovolemia </li></ul><ul><li>Mitral stenosis </li></ul><ul><li>Drugs: Vasodilators </li></ul><ul><li>Cardiac Tamponade </li></ul><ul><li>Constrictive Pericarditis </li></ul>
  39. 41. Pumping Action of the Heart <ul><li>Contractility </li></ul><ul><li>Refers to the inherent ability of the myocardium to contract normally </li></ul><ul><li>It is directly influenced by preload </li></ul><ul><li>The greater the stretch, the more forceful the contraction </li></ul><ul><li>(Comerford & Mayer, 2007, p. 15) </li></ul>
  40. 42. Contractility <ul><li>Increased Contractility Occurs With: </li></ul><ul><li>Drugs: Positive inotropic agents </li></ul><ul><ul><li>digoxin, milrinone, epinephrine, dobutamine </li></ul></ul><ul><li>Increased heart rate </li></ul><ul><ul><li>Bowditch’s phenomenon </li></ul></ul><ul><li>Sympathetic stimulation </li></ul><ul><ul><li>via ß 1 -receptors </li></ul></ul>
  41. 43. Contractility <ul><li>Decreased Contractility Occurs With: </li></ul><ul><li>Drugs: Negative inotropic agents </li></ul><ul><ul><li>Type 1A antiarrhythmics, ß-Blockers, CCBs, barbituates </li></ul></ul><ul><li>Hypoxia </li></ul><ul><li>Hypercapnia </li></ul><ul><li>Myocardial ischemia </li></ul><ul><li>Metabolic acidosis </li></ul>
  42. 44. Pumping Action of the Heart <ul><li>Afterload </li></ul><ul><li>Refers to the pressure that the ventricular muscles must generate to overcome the higher pressure of the aorta to the blood out of the heart </li></ul><ul><li>(Comerford & Mayer, 2007, p. 15) </li></ul>
  43. 45. Afterload <ul><li>Increased Afterload Occurs With: </li></ul><ul><li>Aortic stenosis </li></ul><ul><li>Peripheral arteriolar vasoconstriction </li></ul><ul><li>Hypertension </li></ul><ul><li>Polycythemia </li></ul><ul><li>Drugs: Arterial vasoconstrictors </li></ul>
  44. 46. Afterload <ul><li>Decreased Afterload Occurs With: </li></ul><ul><li>Hypovolemia </li></ul><ul><li>Sepsis </li></ul><ul><li>Drugs: Arterial vasodilators </li></ul>
  45. 47. Heart Rate <ul><li>Influenced By Many Factors: </li></ul><ul><li>Blood volume status </li></ul><ul><li>Sympathetic & Parasympathetic Tone </li></ul><ul><li>Drugs </li></ul><ul><li>Temperature </li></ul><ul><li>Respiration </li></ul><ul><li>Dysrhythmias </li></ul><ul><li>Peripheral Vascular Tone </li></ul><ul><li>Emotions </li></ul><ul><li>Metabolic Status (includes hyperthyroidism) </li></ul>
  46. 48. Heart Rate <ul><li>Determinant of Myocardial O 2 Supply & Demand: </li></ul><ul><li>Increased heart rates increase myocardial oxygen demand </li></ul><ul><li>Fast heart rates (> 150 bpm) decrease diastolic coronary blood flow (shorter diastole) </li></ul>
  47. 49. Ventricular Function Curve
  48. 51. Pumping Action of the Heart <ul><li>Systemic Vascular Resistance </li></ul><ul><li>Also affects cardiac output… </li></ul><ul><li>The resistance against which the left ventricle must pump to move blood throughout systemic circulation </li></ul><ul><li>(Comerford & Mayer, 2007, p.13) </li></ul>
  49. 52. Pumping Action of the Heart <ul><li>Systemic Vascular Resistance </li></ul><ul><li>Can be affected by: </li></ul><ul><li>Tone and diameter of the blood vessels </li></ul><ul><li>Viscosity of the blood </li></ul><ul><li>Resistance from the inner lining of the blood vessels </li></ul><ul><li>(Comerford & Mayer, 2007, p.13) </li></ul>
  50. 53. Pumping Action of the Heart <ul><li>Systemic Vascular Resistance </li></ul><ul><li>SVR has an inverse relationship to CO </li></ul><ul><li>If SVR decreases, CO increases </li></ul><ul><li>If SVR increases, CO decreases </li></ul><ul><li>SVR = mean arterial pressure – central venous pressure x 80 </li></ul><ul><li>cardiac output </li></ul><ul><li>(Comerford & Mayer, 2007) </li></ul>
  51. 54. Pumping Action of the Heart <ul><li>Systemic Vascular Resistance </li></ul><ul><li>Conditions that cause an increase in SVR: </li></ul><ul><li>Hypothermia </li></ul><ul><li>Hypovolemia </li></ul><ul><li>Pheochromocytoma </li></ul><ul><li>Stress response </li></ul><ul><li>Syndromes of low CO </li></ul>
  52. 55. Pumping Action of the Heart <ul><li>Systemic Vascular Resistance </li></ul><ul><li>Conditions that cause a decrease in SVR: </li></ul><ul><li>Anaphylactic and neurogenic shock </li></ul><ul><li>Anemia </li></ul><ul><li>Cirrhosis </li></ul><ul><li>Vasodilation </li></ul>
  53. 56. Blood Vessels <ul><li>About 60,000 miles of arteries, aterioles, capillaries, venules, and veins keep blood circulating to and from every functioning cell in the body! </li></ul><ul><li>There is approximately 5 liters of total circulating blood volume in the adult body </li></ul>
  54. 57. Blood Vessels <ul><li>Five Types: </li></ul><ul><li>Arteries </li></ul><ul><li>Arterioles </li></ul><ul><li>Capillaries </li></ul><ul><li>Venules </li></ul><ul><li>Veins </li></ul>
  55. 58. Arteries <ul><li>Strong, compliant elastic-walled vessels that branch off the aorta, carry blood away from the heart, and distribute it to capillary beds throughout the body </li></ul><ul><li>A high-pressure circuit </li></ul><ul><li>Able to stretch during systole and recoil during diastole because of the elastic fibers in the arterial walls </li></ul>
  56. 59. Arterial Baroreceptors <ul><li>These are receptors that are sensitive to arterial wall stretching </li></ul><ul><li>Located in the aortic arch and near the carotid sinuses </li></ul><ul><li>Responsible for modulation of vascular resistance and heart rate in order to maintain appropriate BP </li></ul><ul><li>Keep MAP constant </li></ul>
  57. 60. Arterial Baroreceptors <ul><li>Vasomotor Center: </li></ul><ul><li>In high blood pressures, the aortic arch and carotid sinus stretch </li></ul><ul><li>When stretching is sensed, a message is sent via the vagus nerve (aortic arch) and the glossopharyngeal nerve (carotid sinus) </li></ul>
  58. 61. Arterial Baroreceptors <ul><li>Inhibition of SNS outflow to the peripheral blood vessels & Stimulates the PNS </li></ul><ul><li>Blood Pressure Decrease by: </li></ul><ul><ul><li>Vasodilation of peripheral vessels </li></ul></ul><ul><ul><li>Decrease in HR & contractility </li></ul></ul><ul><ul><li>Decrease SVR </li></ul></ul>
  59. 62. Arterial Baroreceptors <ul><li>Responsible for short-term adjustment of BP </li></ul><ul><li>Respond to abrupt fluctuations in BP (postural changes) </li></ul><ul><li>Less effective in long-term regulation of BP </li></ul><ul><ul><li>Reset or become insensitive when subjected to prolonged elevated BP </li></ul></ul>
  60. 63. Arterial Baroreceptors <ul><li>In low blood pressures: </li></ul><ul><li>SNS is stimulated & PNS is inhibited </li></ul><ul><li>Blood Pressure Increased by: </li></ul><ul><ul><li>Increased HR & Contractility </li></ul></ul><ul><ul><li>Peripheral Arterial & Venous Constriction </li></ul></ul><ul><ul><ul><li>Preserves blood flow to the brain & heart </li></ul></ul></ul>
  61. 64. Arterioles <ul><li>Control systemic vascular resistance and thus arterial pressure </li></ul><ul><li>Lead directly into capillaries </li></ul><ul><li>Have strong smooth muscle walls innervated by the ANS </li></ul>
  62. 65. Arterioles <ul><li>Autonomic Nervous System </li></ul><ul><li>Adrenergic (Stimulatory) System </li></ul><ul><ul><li>2 Neurotransmitters </li></ul></ul><ul><ul><ul><li>Epinephrine: stimulates β -receptors which increases heart rate and contractility and causes arteriolar vasodilation </li></ul></ul></ul><ul><ul><ul><li>Norepinephrine: stimulates α -receptors which results in vasoconstriction </li></ul></ul></ul>
  63. 66. Arterioles <ul><li>Autonomic Nervous System </li></ul><ul><li>Cholinergic (Inhibitory) System </li></ul><ul><ul><li>1 Neurotransmitter </li></ul></ul><ul><ul><ul><li>Acetylcholine: Decreases heart rate; releases nitric oxide causing vasodilation </li></ul></ul></ul>
  64. 67. Capillaries <ul><li>Microscopic </li></ul><ul><li>Walls are composed of only a single layer of endothelial cells </li></ul>
  65. 68. Capillaries <ul><li>Capillary pressure is extremely low to allow for exchange of nutrients, oxygen, and carbon dioxide with body cells </li></ul>
  66. 69. Sphincters <ul><li>At the ends of the arterioles and beginning of capillaries </li></ul><ul><li>Dilate to permit blood flow </li></ul><ul><li>Constrict to increase blood pressure </li></ul><ul><li>Close to shunt blood </li></ul>
  67. 70. Venules <ul><li>Gather blood from capillaries </li></ul><ul><li>Walls are thinner than those of arterioles </li></ul>
  68. 71. Veins <ul><li>Thinner walls than arteries </li></ul><ul><li>Large diameters because of the low blood pressure of venous return to the heart </li></ul>
  69. 72. Veins <ul><li>Valves prevent backflow </li></ul><ul><li>Pooled blood in each valve segment is moved toward the heart by pressure from the moving volume of blood in the previous valve segment </li></ul>
  70. 73. Veins <ul><li>Most veins return blood to the right atrium of the heart </li></ul>
  71. 74. <ul><li>Blood pressure regulation is maintained via vasodilation or vasoconstriction of the arterial vessels </li></ul>
  72. 75. Function of Blood Vessels <ul><li>What is the function of blood vessels??? </li></ul><ul><li>Distribution of blood throughout the body </li></ul><ul><ul><li>Supplies all cells w/ O 2 & nutrients </li></ul></ul><ul><ul><li>Removes metabolic waste & CO 2 </li></ul></ul><ul><li>Provides a conduit for hormones, cells of the immune system, & regulation of body temperature </li></ul><ul><li>FYI – The lymphatic system is a parallel circulatory system that functions to return excess interstitial fluid to the heart </li></ul>
  73. 76. Blood Pressure Regulation <ul><li>Resistance Vessels </li></ul><ul><li>Dilation of arteries (resistance vessels) = decrease in cardiac afterload </li></ul><ul><li>Arteriolar dilators reduce cardiac workload while causing cardiac output and tissue perfusion to increase </li></ul>
  74. 77. Blood Pressure Regulation <ul><li>Capacitance Vessels </li></ul><ul><li>Dilation of veins (capacitance vessels) = reduced force of blood return to the heart thus decreasing preload </li></ul><ul><li>Results in decreased force of ventricular contraction and oxygen consumption, decreased cardiac output and tissue perfusion </li></ul>
  75. 78. Renin-Angiotensin-Aldosterone System <ul><li>Blood Pressure Regulatory Mechanism </li></ul>
  76. 79. R-A-A-S <ul><li>Renin </li></ul><ul><li>a.k.a. angiotensinogenase </li></ul><ul><li>Converts angiotensinogen to angiotensin I </li></ul>
  77. 80. R-A-A-S <ul><li>Angiotensin I </li></ul><ul><li>Has no biological activity </li></ul><ul><li>Exists solely as a precursor to angiotensin II </li></ul>
  78. 81. R-A-A-S <ul><li>Angiotensin II </li></ul><ul><li>Angiotensin I is converted into angiotensin II by the angiotensin-converting enzyme </li></ul><ul><li>Potent vasoconstrictor </li></ul><ul><li>Also acts on the adrenal cortex in releasing aldosterone </li></ul>
  79. 82. R-A-A-S <ul><li>Aldosterone </li></ul><ul><li>Regulates sodium and potassium in the blood – retain sodium & excrete potassium </li></ul><ul><li>Release triggered by increased levels of angiotensin II, ACTH, and potassium </li></ul>
  80. 83. References <ul><li>Comerford, K.C., & Mayer, B.H. (Eds.). (2007). Hemodynamic monitoring made incredibly visual. Ambler, PA: Lippincott, Williams, and Wilkins. </li></ul><ul><li>Donofrio, J., Haworth, K., Schaeffer, L., & Thompson, G. (Eds.). (2005). Cardiovascular care made incredibly easy. Ambler, PA: Lippincott, Williams, and Wilkins. </li></ul><ul><li>Smeltzer et al. (2008). Brunner and suddarth’s textbook of medical-surgical nursing, (11 th ed.). Philadelphia, PA: Lippincott Williams and Wilkins. </li></ul><ul><li>Woods, S. L., Froelicher, E. S., Underhill Motzer, S., & Bridges, E. J. (2005). Cardiac nursing, (5 th ed.). Philadelphia, PA: Lippincott Williams & Wilkins. </li></ul>

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