Chapter 29 - Cardiology

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  • Chapter 29 - Cardiology

    1. 1. Cardiology Chapter 28
    2. 2. Cardiovascular Disease <ul><li>Incidence </li></ul><ul><li>Morbidity and mortality </li></ul><ul><li>Risk factors </li></ul><ul><li>Prevention strategies </li></ul>
    3. 3. Heart Anatomy <ul><li>Muscular pump consisting of four chambers: </li></ul><ul><ul><li>Two atria </li></ul></ul><ul><ul><li>Two ventricles </li></ul></ul><ul><li>Cone-shaped, approximately the size of a closed fist </li></ul>
    4. 4. Heart Anatomy <ul><li>Located in the mediastinum of the thoracic cavity </li></ul><ul><ul><li>2/3 of heart's mass lies left of midline of sternum </li></ul></ul>
    5. 5. Pericardium <ul><li>Fibrous outer layer, thin inner layer that surrounds the heart </li></ul><ul><li>Cavity between the two layers contains pericardial fluid </li></ul><ul><ul><li>Reduces friction as heart moves within pericardial sac </li></ul></ul>
    6. 6. Coronary Vessels <ul><li>Seven large veins normally carry blood to the heart: </li></ul><ul><ul><li>Four pulmonary veins carry blood from the lungs to the left atrium </li></ul></ul><ul><ul><li>Superior and inferior vena cavae carry blood from the body to the right atrium </li></ul></ul><ul><li>Coronary sinus carries blood from the walls of the heart to the right atrium </li></ul>
    7. 7. Coronary Vessels <ul><li>Two arteries exit the heart: </li></ul><ul><ul><li>Aorta carries blood from left ventricle to body </li></ul></ul><ul><ul><li>Pulmonary trunk carries blood from right ventricle to lungs </li></ul></ul><ul><ul><li>Right and left coronary arteries exit aorta and supply heart muscle with oxygen and nutrients </li></ul></ul>
    8. 8. Heart Chambers and Valves <ul><li>Right and left chambers are separated by a septum </li></ul><ul><ul><li>Interatrial septum separates the right and left atria </li></ul></ul><ul><ul><li>Interventricular septum separates the two ventricles </li></ul></ul>
    9. 9. Atrioventricular Valves <ul><li>Allow blood to flow from atria into ventricles </li></ul><ul><li>Prevent blood from flowing back to the atria </li></ul><ul><li>Tricuspid valve </li></ul><ul><ul><li>Located between the right atrium and right ventricle </li></ul></ul><ul><li>Mitral (bicuspid) valve </li></ul><ul><ul><li>Located between the left atrium and left ventricle </li></ul></ul>
    10. 10. Semilunar Valves <ul><li>Aortic and pulmonary semilunar valves </li></ul><ul><ul><li>Meet in center of artery to block blood flow </li></ul></ul><ul><ul><li>Blood flowing out of ventricles pushes against each valve, forcing it open </li></ul></ul><ul><ul><li>Blood flowing back from aorta or pulmonary trunk toward ventricles causes valves to close </li></ul></ul>
    11. 11. Peripheral Circulation <ul><li>Flow of blood: </li></ul><ul><ul><li>Ventricles </li></ul></ul><ul><ul><li>Arteries </li></ul></ul><ul><ul><li>Arterioles </li></ul></ul><ul><ul><li>Capillaries </li></ul></ul><ul><ul><li>Venous system </li></ul></ul>
    12. 12. The Capillary Network <ul><li>Blood is supplied to each capillary network by arterioles </li></ul><ul><li>Blood flows through network into venules </li></ul><ul><ul><li>Flow is regulated by smooth muscle cells (precapillary sphincters) </li></ul></ul><ul><li>Major function is exchange of nutrients and waste products </li></ul>
    13. 13. Arteries and Veins <ul><li>Three layers of elastic tissue comprise all blood vessel walls (except capillaries and venules): </li></ul><ul><ul><li>Tunica intima (inner layer) </li></ul></ul><ul><ul><li>Tunica media (middle layer) </li></ul></ul><ul><ul><li>Tunica adventitia (outer layer) </li></ul></ul>
    14. 14. Types of Arteries <ul><li>Conducting arteries </li></ul><ul><ul><li>(Large elastic arteries) </li></ul></ul><ul><li>Distributing arteries </li></ul><ul><ul><li>(Small to medium-sized arteries) </li></ul></ul><ul><li>Arterioles </li></ul><ul><ul><li>(Smallest arteries) </li></ul></ul>
    15. 15. Venules <ul><li>Similar in structure to capillaries </li></ul><ul><li>Collect blood from capillaries and transport blood to small veins </li></ul><ul><li>Nutrient exchange occurs across the walls of venules </li></ul>
    16. 16. Veins <ul><li>Walls are a continuous layer of smooth muscle cells </li></ul><ul><li>Medium-sized and large veins </li></ul><ul><ul><li>Carry blood to venous trunks and then to the heart </li></ul></ul><ul><li>Large veins </li></ul><ul><ul><li>Have valves that allow blood to flow to but not from the heart </li></ul></ul><ul><ul><li>Prevents backflow of blood, especially in dependent tissues </li></ul></ul>
    17. 17. Arteriovenous Anastomoses (AV shunts) <ul><li>Allow blood to flow from arteries to veins without passing through capillaries </li></ul><ul><li>Natural AV shunts occur in the sole of the foot and nail beds where they regulate body temperature </li></ul><ul><li>Pathological shunts may result from injury or tumors </li></ul>
    18. 18. Coronary Arteries <ul><li>Exclusive suppliers of arterial blood to the heart muscle </li></ul><ul><ul><li>Left coronary artery carries about 85% of the blood supply to the myocardium </li></ul></ul><ul><ul><li>Right coronary artery carries the remainder </li></ul></ul><ul><li>Originate just above the aortic valve where the aorta exits the heart </li></ul>
    19. 19. Left Coronary Artery <ul><li>Subdivides into left anterior descending and circumflex arteries </li></ul><ul><ul><li>Left anterior descending (LAD) supplies: </li></ul></ul><ul><ul><ul><li>Anterior wall of left ventricle </li></ul></ul></ul><ul><ul><ul><li>Interventricular septum </li></ul></ul></ul><ul><ul><li>Circumflex supplies: </li></ul></ul><ul><ul><ul><li>Lateral and posterior portions of left ventricle </li></ul></ul></ul><ul><ul><ul><li>Part of right ventricle </li></ul></ul></ul>
    20. 20. Coronary Arteries <ul><li>Right coronary artery and the left anterior descending artery supply: </li></ul><ul><ul><li>Most of the right atrium and ventricle </li></ul></ul><ul><ul><li>Inferior aspect of the left ventricle </li></ul></ul><ul><li>Anastomoses between arterioles of coronary arteries provide collateral circulation </li></ul>
    21. 21. Coronary Capillaries <ul><li>Permit exchange of nutrients and metabolic wastes </li></ul><ul><li>Merge to form coronary veins </li></ul><ul><li>Deliver most of the blood to the coronary sinus, which empties directly into right atrium </li></ul><ul><li>Coronary sinus </li></ul><ul><ul><li>Major vein draining myocardium </li></ul></ul>
    22. 22. Physiology <ul><li>The heart can be thought of as two pumps in one: </li></ul><ul><ul><li>A low-pressure pump (right atrium and right ventricle) supplying pulmonary vasculature </li></ul></ul><ul><ul><li>A high-pressure pump (left atrium and left ventricle) supplying systemic vasculature </li></ul></ul>
    23. 23. Blood Flow Through Heart <ul><li>Blood enters right atrium from systemic circulation via the inferior and superior vena cavae and from the heart via the coronary sinus </li></ul><ul><li>Blood passes into the right ventricle </li></ul><ul><li>Ventricles push blood against tricuspid and semilunar valves </li></ul><ul><li>Blood enters pulmonary trunk </li></ul>
    24. 24. Blood Flow Through Heart <ul><li>Pulmonary arteries carry blood to lungs </li></ul><ul><ul><li>Carbon dioxide is released </li></ul></ul><ul><ul><li>Oxygen is picked up </li></ul></ul><ul><li>Blood enters left atrium through pulmonary veins </li></ul><ul><li>Left atrium contracts and fills ventricles </li></ul><ul><li>Blood enters aorta and is distributed throughout body </li></ul>
    25. 25. Cardiac Cycle <ul><li>Systole </li></ul><ul><ul><li>Atrial </li></ul></ul><ul><ul><li>Ventricular </li></ul></ul><ul><li>Diastole </li></ul><ul><ul><li>Atrial </li></ul></ul><ul><ul><li>Ventricular </li></ul></ul>
    26. 26. Heart Action During Atrial Systole
    27. 27. Heart Action During Ventricular Systole
    28. 28. Cardiac Output <ul><li>Stroke volume </li></ul><ul><li>Heart rate </li></ul><ul><li>Contractility </li></ul><ul><li>Starling's law </li></ul>
    29. 29. Nervous System Control of the Heart <ul><li>Extrinsic control by parasympathetic and sympathetic nerves of autonomic nervous system is a major factor influencing: </li></ul><ul><ul><li>Heart rate </li></ul></ul><ul><ul><li>Conductivity </li></ul></ul><ul><ul><li>Contractility </li></ul></ul>
    30. 30. Nervous System Control of the Heart <ul><li>Atria supplied with many sympathetic and parasympathetic nerve fibers </li></ul><ul><li>Ventricles supplied mainly by sympathetic nerves </li></ul>
    31. 31. Sympathetic Control <ul><li>Postganglionic sympathetic fibers release norepinephrine </li></ul><ul><ul><li>Inotropic effect on myocardium </li></ul></ul><ul><ul><li>Dromotropic effect on myocardium </li></ul></ul><ul><ul><li>Chronotropic effect on myocardium </li></ul></ul>
    32. 32. Sympathetic Control <ul><li>Sympathetic stimulation of the heart causes dilation of coronary blood vessels along with the constriction of peripheral vessels </li></ul><ul><ul><li>Ensures that increased oxygen demands of the heart are met by an increase in blood and oxygen supply </li></ul></ul>
    33. 33. Sympathetic Control <ul><li>Cardiac effects of norepinephrine result from stimulation of alpha and beta adrenergic receptors </li></ul><ul><li>Strong sympathetic stimulation of the heart may significantly increase heart rate </li></ul>
    34. 34. Parasympathetic Control <ul><li>Parasympathetic innervation of the heart is through the vagus nerve </li></ul><ul><ul><li>Has a continuous inhibitory influence on the heart primarily by decreasing heart rate and, to a lesser extent, contractility </li></ul></ul>
    35. 35. Hormonal Regulation of the Heart <ul><li>Sympathetic impulses are transmitted to the adrenal medulla at the same time they are transmitted to all blood vessels </li></ul><ul><ul><li>Cause adrenal medulla to secrete epinephrine and norepinephrine </li></ul></ul>
    36. 36. Epinephrine <ul><li>Epinephrine has essentially the same effect on cardiac muscles as norepinephrine, increasing the rate and force of contraction </li></ul><ul><li>Epinephrine also causes: </li></ul><ul><ul><li>Constriction of blood vessels in the skin, kidneys, GI tract, and other viscera </li></ul></ul><ul><ul><li>Dilation of skeletal and coronary vessels </li></ul></ul>
    37. 37. Norepinephrine <ul><li>Causes constriction of peripheral blood vessels in most areas of the body </li></ul><ul><li>Stimulates cardiac muscle </li></ul>
    38. 38. Role of Electrolytes <ul><li>Myocardial cells are bathed in an electrolyte solution </li></ul><ul><li>Major electrolytes that influence cardiac function: </li></ul><ul><ul><li>Calcium </li></ul></ul><ul><ul><li>Potassium </li></ul></ul><ul><ul><li>Sodium </li></ul></ul><ul><li>Magnesium also plays an important role </li></ul>
    39. 39. Electrophysiology of the Heart <ul><li>Two basic groups of cells within the myocardium: </li></ul><ul><ul><li>Specialized cells of the electrical conduction system </li></ul></ul><ul><ul><ul><li>Responsible for the formation and conduction of electric current </li></ul></ul></ul><ul><ul><li>Working myocardial cells </li></ul></ul><ul><ul><ul><li>Possess the property of contractility </li></ul></ul></ul>
    40. 40. Electrical Activity of Cardiac Cells <ul><li>Ions are charged particles that are electrically positive or negative, depending on their ability to accept or donate electrons </li></ul><ul><ul><li>Cations </li></ul></ul><ul><ul><li>Anions </li></ul></ul>
    41. 41. Electrical Activity of Cardiac Cells <ul><li>Electrically charged particles may be thought of as small magnets </li></ul><ul><ul><li>Require energy to push them apart if they have opposite charges </li></ul></ul><ul><ul><li>Require energy to push them together if they have like electrical charges </li></ul></ul>
    42. 42. Membrane Potentials <ul><li>The electrical magnetic-like attraction gives separated particles of opposite charges potential energy </li></ul><ul><ul><li>Establishes a membrane potential between the inside and the outside of the cell </li></ul></ul><ul><ul><li>Electrical charge between the inside and outside of cells is expressed in millivolts (mV) </li></ul></ul>
    43. 43. Resting Membrane Potential <ul><li>When the cell is in its “resting” state, the electrical charge difference is called a resting membrane potential (RMP) </li></ul><ul><ul><li>The inside of the cell is negative compared with the outside of the cell membrane </li></ul></ul>
    44. 44. Resting Membrane Potential <ul><li>RMP is primarily established by the difference between the intracellular potassium ion level and the extracellular potassium ion level </li></ul>
    45. 45. Depolarization <ul><li>Sodium is a positively charged ion on the outside of the cell </li></ul><ul><ul><li>Has a chemical and electrical gradient </li></ul></ul><ul><ul><li>Tends to cause it to move intracellularly </li></ul></ul>Sodium channels remain closed in resting cell membrane.
    46. 46. Depolarization <ul><li>Depolarization (electrical conduction) takes place when sodium rushes into the cell, making it more positive on the inside compared with the outside </li></ul>
    47. 47. Depolarization Depolarization of cell membrane causes sodium channels to open.
    48. 48. Diffusion Through Ion Channels <ul><li>The cell membrane is: </li></ul><ul><ul><li>Relatively permeable to potassium </li></ul></ul><ul><ul><li>Somewhat less permeable to calcium chloride </li></ul></ul><ul><ul><li>Minimally permeable to sodium </li></ul></ul>
    49. 49. Diffusion Through Ion Channels <ul><li>The cell membrane appears to have individual protein-lined channels that allow passage of a specific ion or group of ions </li></ul><ul><li>Permeability is influenced by: </li></ul><ul><ul><li>Their electrical charge </li></ul></ul><ul><ul><li>Their size </li></ul></ul><ul><ul><li>The proteins that open and close the channels (gating proteins) </li></ul></ul>
    50. 50. Sodium-Potassium Pump <ul><li>Actively pumps sodium ions out of the cell and potassium ions in </li></ul><ul><li>Normally transports three sodium ions out for every two potassium ions taken in </li></ul><ul><li>Returns the cell to its resting state </li></ul>
    51. 51. Sodium-potassium Exchange Pump
    52. 52. Channels <ul><li>In cardiac muscle, sodium and calcium ions can enter the cell through two separate channel systems in the cell membrane: </li></ul><ul><ul><li>Fast channels </li></ul></ul><ul><ul><li>Slow channels </li></ul></ul>
    53. 53. Channels <ul><li>Fast channels are sensitive to small changes in membrane potential </li></ul><ul><ul><li>As the cell drifts toward threshold level (the point at which a cell depolarizes), fast sodium channels open </li></ul></ul><ul><ul><li>Results in a rush of sodium ions intracellularly and in very rapid depolarization </li></ul></ul><ul><li>Slow channel selectively permeable to calcium and, to a lesser extent, sodium </li></ul>
    54. 54. Action Potential <ul><li>Rapid depolarization creates a local area of current known as the action potential </li></ul><ul><li>After one patch of membrane is depolarized, the electrical charge spreads along the cell surface, opening more channels </li></ul>
    55. 55. Action Potential <ul><li>The cardiac action potential can be divided into 5 phases (phases 0 through 4) </li></ul><ul><li>Phase 0 (rapid depolarization phase) </li></ul><ul><li>Phase 1 (early rapid depolarization phase) </li></ul><ul><li>Phase 2 (plateau phase) </li></ul><ul><li>Phase 3 (terminal phase of rapid repolarization) </li></ul><ul><li>Phase 4 </li></ul>
    56. 56. Action Potential of Myocardial Cells
    57. 57. Propagation of Action Potential <ul><li>An action potential at any point on the cell membrane acts as a stimulus to adjacent regions of the cell membrane </li></ul><ul><ul><li>The excitation process, once started, is spread along the length of the cell and on to the next </li></ul></ul><ul><ul><li>A stimulus strong enough to cause a cell to reach threshold and depolarize (action potential) starts a cascade of depolarization from one cell to another </li></ul></ul><ul><ul><ul><li>All-or-none principle </li></ul></ul></ul>
    58. 58. Absolute Refractory Period <ul><li>During the absolute refractory period, the cardiac muscle cell is completely insensitive to further stimulation </li></ul><ul><li>The refractory period of the ventricles is of about the same duration as that of the action potential </li></ul>
    59. 59. Relative Refractory Period <ul><li>During the relative refractory period, the muscle cell is more difficult than normal to excite, but it can still be stimulated </li></ul>
    60. 60. Electrical Conduction System <ul><li>Sinoatrial node (SA node) </li></ul><ul><li>Atrioventricular (AV) junction </li></ul><ul><ul><li>AV node </li></ul></ul><ul><ul><li>Bundle of His </li></ul></ul><ul><li>His-Purkinje system </li></ul><ul><ul><li>Bundle branches </li></ul></ul><ul><ul><ul><li>Right </li></ul></ul></ul><ul><ul><ul><li>Left anterior fascicle </li></ul></ul></ul><ul><ul><ul><li>Left posterior fascicle </li></ul></ul></ul>
    61. 61. Characteristics of Myocardial Cells <ul><li>Automaticity </li></ul><ul><li>Excitability </li></ul><ul><li>Conductivity </li></ul><ul><li>Contractility </li></ul>
    62. 62. Intrinsic Rates <ul><li>SA node (60 to 100/min) </li></ul><ul><li>AV junctional tissue (40 to 60/min) </li></ul><ul><li>Ventricles--bundle branches and Purkinje fibers (20 to 40/min) </li></ul>
    63. 63. Ectopic Electrical Impulse Formation <ul><li>An ectopic beat results when pacemaker function is assumed for one beat by cells other than those in SA node </li></ul><ul><ul><li>Sometimes called premature beats because they occur early in diastole before the SA node is normally scheduled to discharge </li></ul></ul>
    64. 64. Ectopic Electrical Impulse Formation <ul><li>Depending on the location of the ectopic focus, the premature beats may be of: </li></ul><ul><ul><li>Atrial origin--premature atrial complexes (PACs) </li></ul></ul><ul><ul><li>Junctional origin--premature junctional complexes (PJCs) </li></ul></ul><ul><ul><li>Ventricular origin--premature ventricular complexes (PVCs) </li></ul></ul>
    65. 65. Ectopic Electrical Impulse Formation <ul><li>Two basic mechanisms by which ectopic electrical impulses can be generated in the heart: </li></ul><ul><ul><li>Enhanced automaticity </li></ul></ul><ul><ul><li>Reentry </li></ul></ul>
    66. 66. Enhanced Automaticity <ul><li>Caused by an acceleration in depolarization </li></ul><ul><li>Commonly results from an abnormally high leakage of sodium ions into the cells </li></ul><ul><ul><li>Causes the cells to reach threshold prematurely </li></ul></ul><ul><ul><li>As a result, the rate of electrical impulse formation in potential pacemakers increases beyond their inherent rate </li></ul></ul><ul><li>Responsible for dysrhythmias in Purkinje fibers and other myocardial cells </li></ul>
    67. 67. Enhanced Automaticity <ul><li>May occur secondary to: </li></ul><ul><ul><li>Excess catecholamines (i.e., norepinephrine, epinephrine) </li></ul></ul><ul><ul><li>Digitalis toxicity </li></ul></ul><ul><ul><li>Hypoxia </li></ul></ul><ul><ul><li>Hypercapnia </li></ul></ul><ul><ul><li>Myocardial ischemia or Infarction </li></ul></ul><ul><ul><li>Increased venous return (preload) </li></ul></ul><ul><ul><li>Hypokalemia or other electrolyte abnormalities </li></ul></ul><ul><ul><li>Atropine administration </li></ul></ul>
    68. 68. Reentry <ul><li>The reactivation of myocardial tissue for the second or subsequent time by the same impulse </li></ul><ul><li>Occurs when the progression of an electrical impulse is delayed, blocked, or both in one or more segments of the heart's electrical conduction system </li></ul>
    69. 69. Reentry Conduction through A) normal and B) severely depressed Purkinje fibers.
    70. 70. Reentry <ul><li>Reentry dysrhythmias can occur in the SA node, atria, AV junction, bundle branches, or Purkinje fibers </li></ul>
    71. 71. Delayed Impulses <ul><li>Common causes of delayed or blocked electrical impulses: </li></ul><ul><ul><li>Myocardial ischemia </li></ul></ul><ul><ul><li>Certain drugs </li></ul></ul><ul><ul><li>Hyperkalemia </li></ul></ul>
    72. 72. Chief Complaint <ul><li>Cardiovascular disease may present with a variety of symptoms </li></ul><ul><li>Common chief complaints include: </li></ul><ul><ul><li>Chest pain or discomfort, including shoulder, arm, neck, or jaw pain or discomfort </li></ul></ul><ul><ul><li>Dyspnea </li></ul></ul><ul><ul><li>Syncope </li></ul></ul><ul><ul><li>Abnormal heart beat or palpitations </li></ul></ul>
    73. 73. Chest Pain or Discomfort <ul><li>Most common chief complaint of patients with myocardial infarction </li></ul><ul><li>Many causes of chest pain are unrelated to cardiac disease </li></ul><ul><ul><li>Pulmonary embolus </li></ul></ul><ul><ul><li>Pleurisy </li></ul></ul><ul><ul><li>Reflux esophagitis </li></ul></ul><ul><li>A history of chest pain is important </li></ul><ul><ul><li>Use the OPQRST method (or a similar method) to obtain information when possible </li></ul></ul>
    74. 74. Dyspnea <ul><li>Often associated with myocardial infarction </li></ul><ul><li>Primary symptom of pulmonary congestion caused by heart failure </li></ul><ul><li>Common causes of dyspnea that may be unrelated to heart disease include: </li></ul><ul><ul><li>Chronic obstructive pulmonary disease </li></ul></ul><ul><ul><li>Respiratory infection </li></ul></ul><ul><ul><li>Pulmonary embolus </li></ul></ul><ul><ul><li>Asthma </li></ul></ul>
    75. 75. Dyspnea <ul><li>Historical factors important in differentiating breathing difficulties: </li></ul><ul><ul><li>Duration and circumstances of onset of dyspnea </li></ul></ul><ul><ul><li>Anything that aggravates or relieves the dyspnea, including medications </li></ul></ul><ul><ul><li>Previous episodes </li></ul></ul><ul><ul><li>Associated symptoms </li></ul></ul><ul><ul><li>Orthopnea </li></ul></ul><ul><ul><li>Prior cardiac problems </li></ul></ul>
    76. 76. Syncope <ul><li>Caused by a sudden decrease in cerebral perfusion </li></ul><ul><li>Cardiac causes of syncope result from events that decrease cardiac output </li></ul><ul><ul><li>The most common cardiac disorders associated with syncope are dysrhythmias </li></ul></ul>
    77. 77. Syncope <ul><li>Other causes of syncope in the medical patient include: </li></ul><ul><ul><li>Stroke </li></ul></ul><ul><ul><li>Drug or alcohol intoxication </li></ul></ul><ul><ul><li>Aortic stenosis </li></ul></ul><ul><ul><li>Pulmonary embolism </li></ul></ul><ul><ul><li>Hypoglycemia </li></ul></ul>
    78. 78. Syncope--History <ul><li>Pre-syncope aura (nausea, weakness, lightheadedness) </li></ul><ul><li>Circumstances of occurrence </li></ul><ul><ul><li>Patient's position before the event </li></ul></ul><ul><ul><li>Severe pain </li></ul></ul><ul><ul><li>Emotional stress </li></ul></ul><ul><li>Duration of syncopal episode </li></ul><ul><li>Symptoms before syncopal episode (palpitation, seizure, incontinence) </li></ul><ul><li>Other associated symptoms </li></ul><ul><li>Previous episodes of syncope </li></ul>
    79. 79. Palpitations <ul><li>Palpitations are sometimes a normal occurrence but may also indicate a serious dysrhythmia </li></ul>
    80. 80. Palpitations <ul><li>Important information to obtain includes: </li></ul><ul><ul><li>Pulse rate (if obtained) </li></ul></ul><ul><ul><li>Regular versus irregular rhythm (if obtained) </li></ul></ul><ul><ul><li>Circumstances of occurrence </li></ul></ul><ul><ul><li>Duration </li></ul></ul><ul><ul><li>Associated symptoms (chest pain, diaphoresis, syncope, confusion, dyspnea) </li></ul></ul><ul><ul><li>Previous episodes, frequency </li></ul></ul><ul><ul><li>Medications (drug stimulant or alcohol use) </li></ul></ul>
    81. 81. Significant Past Medical History <ul><li>Is the patient taking prescription medications, particularly cardiac medications? </li></ul><ul><li>Is the patient being treated for any other illness? </li></ul>
    82. 82. Significant Past Medical History <ul><li>Has the patient ever had any of the following? </li></ul><ul><ul><li>Myocardial infarction or episodes of angina pectoris </li></ul></ul><ul><ul><li>Coronary artery bypass procedure or angioplasty </li></ul></ul><ul><ul><li>Implanted pacemaker or ICD </li></ul></ul><ul><ul><li>Heart failure </li></ul></ul><ul><ul><li>Hypertension </li></ul></ul><ul><ul><li>Diabetes </li></ul></ul><ul><ul><li>Chronic lung disease </li></ul></ul>
    83. 83. Significant Past Medical History <ul><li>Does the patient have any allergies? </li></ul><ul><li>Are there any other associated risk factors for a cardiac event? </li></ul><ul><li>Does the patient have an implanted pacemaker or implantable cardioverter-defibrillator (ICD)? </li></ul>
    84. 84. Physical Examination <ul><li>The “classic presentation” of myocardial infarction is pain or discomfort beneath the sternum that lasts more than 30 minutes </li></ul><ul><li>Associated signs and symptoms: </li></ul><ul><ul><li>Apprehension </li></ul></ul><ul><ul><li>Diaphoresis </li></ul></ul><ul><ul><li>Dyspnea </li></ul></ul><ul><ul><li>Nausea and vomiting </li></ul></ul><ul><ul><li>Sense of impending doom </li></ul></ul><ul><li>Presentation may also be atypical </li></ul><ul><ul><li>A thorough medical history and physical examination is important </li></ul></ul>
    85. 85. Initial Assessment <ul><li>Level of consciousness </li></ul><ul><li>Respirations </li></ul><ul><li>Pulse (rate, regularity) </li></ul><ul><li>Blood pressure </li></ul>
    86. 86. Physical Examination <ul><li>“Look-listen-feel” approach </li></ul>
    87. 87. Look <ul><li>Skin color, capillary refill, skin moisture </li></ul><ul><ul><li>Indications of adequate hemoglobin oxygenation (pulse oximetry) </li></ul></ul><ul><ul><li>Indications of cardiac function (peripheral perfusion) </li></ul></ul><ul><li>Jugular vein distention (JVD) </li></ul><ul><ul><li>Should be evaluated with the patient's head elevated at 45 degrees </li></ul></ul><ul><ul><li>May be difficult to assess in obese patients </li></ul></ul>
    88. 88. Look <ul><li>Peripheral and presacral edema </li></ul><ul><ul><li>Caused by chronic back-pressure in systemic venous circulation </li></ul></ul><ul><ul><li>Most obvious in dependent areas (ankles and sacral region in bedridden patients) </li></ul></ul><ul><ul><li>May be: </li></ul></ul><ul><ul><ul><li>Nonpitting--minimal or no depression of tissue after removal of finger pressure </li></ul></ul></ul><ul><ul><ul><li>Pitting--depression of tissue remains after removal of finger pressure </li></ul></ul></ul>
    89. 89. Look <ul><li>Additional indicators of cardiac disease </li></ul><ul><ul><li>Nitroglycerin patch </li></ul></ul><ul><ul><li>Midsternal scar from coronary surgery </li></ul></ul><ul><ul><li>Implanted pacemaker or automatic implantable cardioverter-defibrillator (left upper chest; abdominal wall) </li></ul></ul><ul><ul><li>Medic alert information </li></ul></ul>
    90. 90. Listen <ul><li>Lung sounds </li></ul><ul><ul><li>Assess for equality </li></ul></ul><ul><ul><li>Assess for adventitious sounds that may indicate pulmonary congestion or edema </li></ul></ul><ul><li>Heart sounds </li></ul>
    91. 91. Heart Sounds <ul><li>May be auscultated for: </li></ul><ul><ul><li>Frequency (pitch) </li></ul></ul><ul><ul><li>Intensity (loudness) </li></ul></ul><ul><ul><li>Duration </li></ul></ul><ul><ul><li>Timing in the cardiac cycle </li></ul></ul>
    92. 92. Auscultating Heart Sounds
    93. 93. Heart Sounds <ul><li>Aortic </li></ul><ul><ul><li>Second intercostal space to the right of the sternum </li></ul></ul><ul><li>Pulmonic </li></ul><ul><ul><li>Second intercostal space to the left of the sternum </li></ul></ul>
    94. 94. Heart Sounds <ul><li>Tricuspid </li></ul><ul><ul><li>Fifth left intercostal space close to the sternal border </li></ul></ul><ul><li>Mitral </li></ul><ul><ul><li>Fifth intercostal space just medial to the left midclavicular line </li></ul></ul><ul><ul><li>Directly over the left ventricle </li></ul></ul><ul><ul><li>Sometimes called the apical area or apex </li></ul></ul>
    95. 95. S1 <ul><li>The lub of the lub-dub sound produced by the heart </li></ul><ul><ul><li>Occurs as the mitral and tricuspid valves close </li></ul></ul><ul><ul><li>Marks the beginning of ventricular systole </li></ul></ul><ul><li>Best heard with the diaphragm of the stethoscope at the apex of the heart (fifth intercostal space) </li></ul>
    96. 96. S2 <ul><li>The dub of the lub-dub sound </li></ul><ul><ul><li>Occurs as the aortic and pulmonic valves close </li></ul></ul><ul><ul><li>Marks the end of ventricular systole </li></ul></ul><ul><li>Best heard with the diaphragm of the stethoscope at the second intercostal space to the right and left of the sternum (aortic and pulmonic areas) </li></ul>
    97. 97. S3 <ul><li>An extra heart sound associated with rapid ventricular filling </li></ul><ul><li>Common in children, athletes, and young adults </li></ul><ul><li>The presence of a third heart sound is considered abnormal in persons over age 30 </li></ul><ul><li>Best heard at the apex with the bell of the stethoscope </li></ul>
    98. 98. S3 <ul><li>Sounds like Ken-Tuck-Y with the emphasis on Tuck </li></ul><ul><ul><li>Ken = S1, Tuck = S2, Y = S3 </li></ul></ul><ul><li>May be a warning sign of impending congestive heart failure </li></ul>
    99. 99. S4 <ul><li>Thought to be due to the last of ventricular filling, tensing of the atrioventricular valves, and atrial contraction </li></ul><ul><li>Heard just before S1 </li></ul><ul><li>Best heard at the apex with the bell of the stethoscope </li></ul><ul><li>Sounds like Ten-nes-see with the emphasis on Ten </li></ul><ul><ul><li>Ten = S4, Nes = S1, See = S2 </li></ul></ul>
    100. 100. Feel <ul><li>Peripheral or presacral edema </li></ul><ul><li>Pulse </li></ul><ul><ul><li>Rate </li></ul></ul><ul><ul><li>Regularity </li></ul></ul><ul><ul><li>Equality </li></ul></ul><ul><ul><li>Pulse deficit </li></ul></ul><ul><ul><li>Pulsus paradoxus </li></ul></ul><ul><ul><li>Pulsus alternans </li></ul></ul>
    101. 101. Point of Maximal Impulse (PMI) <ul><li>Apical impulse </li></ul><ul><ul><li>Visible and palpable force produced by the contraction of the left ventricle </li></ul></ul><ul><li>Pulse deficits can be noted by palpating or auscultating the apical impulse and the carotid pulse simultaneously </li></ul>
    102. 102. Feel <ul><li>Skin </li></ul><ul><ul><li>Diaphoretic pale skin is an indicator of peripheral vasoconstriction and sympathetic stimulation </li></ul></ul><ul><ul><li>Cyanosis is an indicator of poor oxygenation </li></ul></ul><ul><ul><li>Fever is usually an indicator of infection </li></ul></ul>
    103. 103. ECG Monitoring <ul><li>The ECG is a graphic representation of the heart's electrical activity generated by depolarization and repolarization of the atria and ventricles </li></ul>
    104. 104. ECG Monitoring <ul><li>Valuable diagnostic tool for identifying cardiac abnormalities including: </li></ul><ul><ul><li>Abnormal heart rates and rhythms </li></ul></ul><ul><ul><li>Abnormal conduction pathways </li></ul></ul><ul><ul><li>Hypertrophy or atrophy of portions of the heart </li></ul></ul><ul><ul><li>Approximate location of ischemic or infarcted cardiac muscle </li></ul></ul>
    105. 105. ECG Monitoring <ul><li>The ECG tracing is only a reflection of the heart's electrical activity </li></ul><ul><li>It does not provide information regarding mechanical events such as force of contraction or blood pressure </li></ul>
    106. 106. ECG Monitoring <ul><li>The summation of all the action potentials transmitted through the heart during the cardiac cycle can be measured on the surface of the body </li></ul><ul><ul><li>This measurement is obtained by applying electrodes on the body's surface connected to an ECG machine </li></ul></ul><ul><ul><li>Voltage changes are fed to the machine, amplified, and displayed visually on the oscilloscope, graphically on ECG paper, or both </li></ul></ul>
    107. 107. Voltage <ul><li>Voltage may be: </li></ul><ul><ul><li>Positive--seen as an upward deflection on the ECG tracing </li></ul></ul><ul><ul><li>Negative--seen as a downward deflection on the ECG tracing </li></ul></ul><ul><ul><li>Isoelectric--no electrical current detected </li></ul></ul><ul><ul><ul><li>Seen as a straight baseline on the ECG </li></ul></ul></ul>
    108. 108. ECG Leads <ul><li>An ECG lead consists of two surface electrodes of opposite polarity </li></ul><ul><ul><li>Bipolar lead </li></ul></ul><ul><ul><ul><li>Two electrodes of opposite polarity </li></ul></ul></ul><ul><ul><li>Unipolar lead </li></ul></ul><ul><ul><ul><li>Single positive electrode and reference point </li></ul></ul></ul>
    109. 109. Leads <ul><li>Bipolar leads constitute the standard limb leads (I through III) </li></ul><ul><li>Unipolar leads make up the: </li></ul><ul><ul><li>Augmented limb leads (aVR, aVL, and aVF) </li></ul></ul><ul><ul><li>Precordial leads (V1 through V6) </li></ul></ul><ul><li>Each lead assesses electrical activity from a different angle </li></ul>
    110. 110. Lead Comparison Unipolar Chest lead V1-V6 Unipolar Limb lead aVR, aVL, aVF Bipolar Limb lead I, II, III
    111. 111. Leads and Cardiac Surfaces Lateral wall V5, V6, I, aVL Anterior wall V3, V4 Septum V1, V2 Inferior wall II, III, aVF Cardiac Surface Viewed Lead
    112. 112. Waveforms <ul><li>The various leads produce different ECG tracings </li></ul><ul><ul><li>If the wave of depolarization moves toward a positive electrode, ECG shows an upward deflection </li></ul></ul><ul><ul><li>If the wave moves away from a positive electrode, a negative deflection appears on the ECG </li></ul></ul>
    113. 113. Rule of Electrical Flow
    114. 114. Standard Limb Leads <ul><li>Record the difference in electrical potential between the left arm, the right arm, and the left leg electrodes </li></ul><ul><li>Represent the axes (the average direction of the heart’s electrical activity) of the standard limb leads </li></ul>
    115. 115. Axis <ul><li>If the axes are moved so that they cross a common midpoint without changing their orientation, they form three intersecting lines of reference </li></ul><ul><ul><li>Triaxial reference system </li></ul></ul>
    116. 116. Axis <ul><li>Lead I is a lateral (leftward) lead </li></ul><ul><ul><li>Assesses the heart's electrical activity from a vantage point defined as 0 degrees on a circle divided into an upper negative 180 degrees and a lower positive 180 degrees </li></ul></ul>
    117. 117. Axis <ul><li>Leads II and III are inferior leads </li></ul><ul><ul><li>Assess the heart's electrical activity from vantage points of +60 degrees and +120 degrees, respectively </li></ul></ul>
    118. 118. Bipolar Lead Placement <ul><li>The electrodes of the three bipolar leads are placed on the following areas of the body: </li></ul>Left arm Left leg III Right arm Left leg II Right arm Left arm I Negative Electrode Positive Electrode Lead
    119. 119. Augmented Limb Leads <ul><li>Use the same set of electrodes as the standard limb leads </li></ul><ul><li>Record the difference in electrical potential between the respective extremity lead sites and a reference point with zero electrical potential at the center of the electrical field of the heart </li></ul>
    120. 120. Augmented Limb Leads <ul><li>The axis of each lead is formed by the line from the electrode site (on the right arm, left arm, or left leg) to the center of the heart </li></ul>
    121. 121. Augmented Limb Leads <ul><li>The aVR, aVL, and aVF leads intersect at different angles than the standard limb leads and produce three other intersecting lines of reference </li></ul><ul><ul><li>With the standard limb leads, these leads make up the hexaxial reference system </li></ul></ul>
    122. 122. Augmented Limb Leads <ul><li>Measure an axis between the two bipolar leads by electronically combining the negative electrodes </li></ul>
    123. 123. Lead aVR <ul><li>Distant recording electrode </li></ul><ul><li>Looks down at heart from right shoulder </li></ul>
    124. 124. Lead aVL <ul><li>Acts as a lateral lead </li></ul><ul><li>Records the heart's electrical activity from a vantage point that looks down from the left shoulder (-30 degrees) </li></ul>
    125. 125. Lead aVF <ul><li>Acts as an inferior lead </li></ul><ul><li>Records the heart's electrical activity from a vantage point that looks up from the left lower extremity (+90 degrees) </li></ul>
    126. 126. Limb Leads Combined electrical vantage points. Leads II, III, aV F = inferior leads; I, aV L = lateral leads.
    127. 127. Modified Lead Recording <ul><li>Limb lead placement can be altered to mimic the precordial leads (V1 through V6) </li></ul><ul><ul><li>Called modified chest leads and become MCL1 through MCL6 </li></ul></ul><ul><li>These leads may help: </li></ul><ul><ul><li>Distinguish between supraventricular tachycardia with aberration and ventricular tachycardia </li></ul></ul><ul><ul><li>Diagnose conduction blocks in the bundle branches </li></ul></ul>
    128. 128. MCL1 <ul><li>Positive electrode is placed in the V1 position (in the fourth intercostal space, just to the right of the patient’s sternum) </li></ul><ul><li>Negative electrode is placed anteriorly, just below the lateral end of the left clavicle </li></ul>
    129. 129. MCL6 <ul><li>Positive electrode is placed on the left midaxillary line at the level of the fifth intercostal space (as for lead V6) </li></ul><ul><li>Negative electrode is placed anteriorly, just below the left shoulder </li></ul>
    130. 130. Routine ECG Monitoring <ul><li>Usually obtained in lead II or MCL1 </li></ul><ul><ul><li>Best leads to monitor for dysrhythmias because of their ability to visualize P waves </li></ul></ul>
    131. 131. Single-Lead ECG Monitoring <ul><li>Information that can be gathered from a single monitoring lead: </li></ul><ul><ul><li>Heart rate </li></ul></ul><ul><ul><li>Regularity of heart beat </li></ul></ul><ul><ul><li>Length of conduction in different parts of the heart </li></ul></ul><ul><li>Limitations </li></ul><ul><ul><li>May fail to reveal various abnormalities (particularly ST-segment changes that signal myocardial injury or infarction) </li></ul></ul>
    132. 132. 12-Lead ECG Monitoring <ul><li>Obtained through 10 electrodes: </li></ul><ul><ul><li>Four limb leads (right arm, right leg, left arm, left leg) </li></ul></ul><ul><ul><ul><li>Provide readings of leads I, II, and III, and aVF, aVL, and aVR </li></ul></ul></ul><ul><ul><li>Six chest leads (V1 through V6) </li></ul></ul>
    133. 133. 12-Lead ECG Monitoring <ul><li>Each lead views the left ventricle from the position of its positive electrode </li></ul>
    134. 134. 12-lead ECG Monitoring <ul><li>Can be used to help: </li></ul><ul><ul><li>Identify ST and T-wave changes relative to myocardial ischemia, injury, and infarction </li></ul></ul><ul><ul><li>Identify VT in wide-complex tachycardia </li></ul></ul><ul><ul><li>Determine electrical axis and the presence of fascicular blocks </li></ul></ul><ul><ul><li>Determine the presence and location of bundle branch blocks </li></ul></ul>
    135. 135. Precordial Leads <ul><li>The six precordial leads used in 12-lead (and 9-lead) ECG monitoring are projected through the anterior chest wall toward the patient's back (the negative end of each chest lead) </li></ul><ul><ul><li>These positive leads are placed on the chest in reference to the thoracic landmarks </li></ul></ul><ul><ul><li>Record the heart's electrical activity in the transverse or horizontal plane </li></ul></ul>
    136. 136. Precordial Leads <ul><li>Leads V1 and V2 are septal leads </li></ul><ul><li>V2 through V4 are anterior leads </li></ul><ul><li>V4 through V6 are lateral precordial leads </li></ul>
    137. 137. Application of Monitoring Electrodes <ul><li>Electrodes are pre-gelled, stick-on disks that can easily be applied to the chest wall </li></ul><ul><li>When applying electrodes: </li></ul><ul><ul><li>Cleanse the area with alcohol to remove dirt and body oil </li></ul></ul><ul><ul><li>Use the inner surfaces of the arms and legs when attaching electrodes to extremities </li></ul></ul>
    138. 138. Application of Monitoring Electrodes <ul><li>When applying electrodes: </li></ul><ul><ul><li>Trim excess body hair (if necessary) before placing the electrodes </li></ul></ul><ul><ul><li>Attach the electrodes to the prepared site </li></ul></ul><ul><ul><li>Attach the ECG cables to electrodes </li></ul></ul><ul><ul><li>Turn on the ECG monitor and obtain a baseline tracing </li></ul></ul>
    139. 139. Monitoring Electrodes <ul><li>If the signal is poor, recheck the cable connections and electrode contact with the patient's skin </li></ul><ul><li>Other causes of a poor signal include: </li></ul><ul><ul><li>Excessive body hair </li></ul></ul><ul><ul><li>Dried conductive gel </li></ul></ul><ul><ul><li>Poor electrode placement </li></ul></ul><ul><ul><li>Diaphoresis </li></ul></ul>
    140. 140. 12-lead Electrode Application Locate the jugular notch. Palpate for the angle of Louis. Follow the angle of Louis to patient’s right until it articulates with second rib. Locate the second intercostal space (immediately below second rib). From the second intercostal space, the third and fourth intercostal spaces can be found. V1 is positioned in the fourth intercostal space just to the right of sternum. From V1 position, find corresponding intercostal space on left of sternum.
    141. 141. 12-lead Electrode Application Place V2 electrode in fourth intercostal space just to left of sternum. From V2 position, locate fifth intercostal space and follow it to midclavicular line. Position the V4 electrode in fifth intercostal space in midclavicular line. Position V3 halfway between V2 and V4. V5 is positioned in anterior axillary line, level with V4. Position V6 in midaxillary line, level with V4.
    142. 142. 9-Lead from a 3-Lead <ul><li>To obtain a 9-lead reading from a standard 3-lead monitor, enable the machine’s diagnostic setting (if available) </li></ul><ul><li>Run leads I, II, and III </li></ul><ul><ul><li>Obtain a representative sample of each lead and label it </li></ul></ul>
    143. 143. 9-Lead from a 3-Lead <ul><li>Leave the monitor in lead III (the negative electrode at the left shoulder) and move the left leg cable (the red lead wire) to each of the MCL positions (from V1 to V6) to obtain a readout </li></ul><ul><li>Label each sample </li></ul>
    144. 144. Nine-lead ECG read-out
    145. 145. ECG Graph Paper <ul><li>ECG graph paper is standardized to allow comparative analysis of an ECG wave </li></ul><ul><li>Divided into squares 1 mm in height and width </li></ul><ul><ul><li>Further divided by darker lines every fifth square, both vertically and horizontally </li></ul></ul><ul><ul><li>Each large square is 5 mm high and 5 mm wide </li></ul></ul>
    146. 146. ECG Graph Paper <ul><li>As the graph paper moves past the stylus of the ECG machine, it measures time and amplitude </li></ul><ul><li>Time is measured on the horizontal plane (side to side) </li></ul><ul><li>When the ECG is recorded at the standard paper speed of 25 mm/sec: </li></ul><ul><ul><li>Each small square equals 1 mm (0.04 second) </li></ul></ul><ul><ul><li>Each large square (the dark vertical lines) equals 5 mm (0.20 second) </li></ul></ul>
    147. 147. ECG Graph Paper <ul><li>Amplitude is measured on the vertical axis (top to bottom) of the graph paper </li></ul><ul><li>Each small square of the graph paper equals 0.1 mV </li></ul><ul><li>Each large square (five small squares) equals 0.5 mV </li></ul>
    148. 148. ECG Graph Paper
    149. 149. Calibration <ul><li>The sensitivity of the 12-lead ECG machine is standardized </li></ul><ul><li>When properly calibrated, a 1-mV electrical signal produces a 10-mm deflection (two large squares) on the ECG tracing </li></ul>
    150. 150. Time Interval Markings <ul><li>Denoted by short vertical lines on the ECG graph paper </li></ul><ul><li>At standard speed, the distance between each short vertical line is 75 mm (3 seconds) </li></ul>
    151. 151. Relationship of ECG to Electrical Activity <ul><li>Each waveform represents the conduction of an electrical impulse through a specific part of the heart </li></ul><ul><li>All waveforms begin and end at the isoelectric line </li></ul><ul><ul><li>The isoelectric line represents the absence of electrical activity in cardiac tissue </li></ul></ul>
    152. 152. Relationship of ECG to Electrical Activity <ul><li>A deflection above the baseline is positive </li></ul><ul><ul><li>Indicates electrical flow toward positive electrode </li></ul></ul><ul><li>A deflection below the baseline is negative </li></ul><ul><ul><li>Indicates electrical flow away from positive electrode </li></ul></ul>
    153. 153. Relationship of ECG to Electrical Activity <ul><li>The normal ECG consists of a P wave, a QRS complex, and a T wave </li></ul><ul><li>Other components that should be evaluated: </li></ul><ul><ul><li>PR interval </li></ul></ul><ul><ul><li>ST segment </li></ul></ul><ul><ul><li>QT interval </li></ul></ul><ul><li>The combination of these waves represents a single heartbeat or one complete cardiac cycle </li></ul>
    154. 154. P Wave <ul><li>First positive (upward) deflection on ECG </li></ul><ul><li>Represents atrial depolarization </li></ul><ul><li>Usually rounded and precedes the QRS complex </li></ul><ul><ul><li>Begins with first positive deflection from baseline </li></ul></ul><ul><ul><li>Ends at point where wave returns to baseline </li></ul></ul>
    155. 155. P Wave <ul><li>Duration normally 0.10 second or less </li></ul><ul><li>Amplitude normally 0.5 to 2.5 mm </li></ul><ul><li>Usually followed by a QRS complex unless conduction disturbances are present </li></ul>
    156. 156. PR Interval <ul><li>Represents the time it takes for an electrical impulse to be conducted through the atria and the AV node up to the instant of ventricular depolarization </li></ul><ul><ul><li>Measured from the beginning of the P wave to the beginning of the next deflection on the baseline (the onset of the QRS complex) </li></ul></ul><ul><li>Normal is 0.12 to 0.20 second </li></ul>
    157. 157. PR Interval <ul><li>A normal PR interval indicates that the electrical impulse has been conducted through the atria, AV node, and bundle of His normally and without delay </li></ul>
    158. 158. QRS Complex <ul><li>Generally composed of three individual waves: the Q, R, and S waves </li></ul><ul><li>Begins at the point where the first wave of the complex deviates from the baseline </li></ul><ul><li>Ends where the last wave of the complex begins to flatten at, above, or below the baseline </li></ul>
    159. 159. QRS Complex <ul><li>Direction of the QRS complex may be: </li></ul><ul><ul><li>Predominantly positive (upright) </li></ul></ul><ul><ul><li>Predominantly negative (inverted) </li></ul></ul><ul><ul><li>Biphasic (partly positive, partly negative) </li></ul></ul>
    160. 160. QRS Complex <ul><li>The normal QRS complex is narrow and sharply pointed </li></ul><ul><li>Duration is generally 0.08 to 0.10 second or less </li></ul><ul><li>Amplitude normally varies from less than 5 mm to more than 15 mm </li></ul>
    161. 161. Q Wave <ul><li>The first negative (downward) deflection of the QRS complex on the ECG </li></ul><ul><ul><li>May not be present in all leads </li></ul></ul><ul><li>Represents depolarization of the interventricular septum </li></ul>
    162. 162. R Wave <ul><li>First positive deflection after the P wave </li></ul><ul><ul><li>Subsequent positive deflections in the QRS complex that extend above the baseline and that are taller than the first R wave are called R prime (R’), R double prime (R’’), and so on </li></ul></ul>
    163. 163. S Wave <ul><li>Negative deflection that follows the R wave </li></ul><ul><ul><li>Subsequent negative deflections are called S prime (S’), S double prime (S”), and so on </li></ul></ul><ul><li>R and S waves represent the sum of electrical forces resulting from depolarization of the right and left ventricles </li></ul>
    164. 164. QRS Complex <ul><li>Follows the P wave </li></ul><ul><li>Marks the approximate beginning of mechanical systole of the ventricles, which continues through the onset of the T wave </li></ul><ul><li>Represents ventricular depolarization </li></ul><ul><ul><li>Conduction of an electrical impulse from the AV node through the bundle of His, Purkinje fibers, and the right and left bundle branches </li></ul></ul>
    165. 165. QRS Complex
    166. 166. ST Segment <ul><li>Represents the early phase of repolarization of the right and left ventricles </li></ul><ul><li>Immediately follows the QRS complex and ends with the onset of the T wave </li></ul>
    167. 167. ST Segment <ul><li>The point at which the ST segment “takes off” from the QRS complex is called the J point </li></ul>
    168. 168. ST Segment <ul><li>The position of the ST segment is commonly judged as normal or abnormal using the baseline of the PR or TP interval as a reference </li></ul><ul><ul><li>ST segment elevation </li></ul></ul><ul><ul><li>ST segment depression </li></ul></ul>
    169. 169. ST Segment <ul><li>Abnormal ST segments may be seen in: </li></ul><ul><ul><li>Infarction </li></ul></ul><ul><ul><li>Ischemia </li></ul></ul><ul><ul><li>Pericarditis </li></ul></ul><ul><ul><li>After digitalis administration </li></ul></ul><ul><ul><li>Other disease states </li></ul></ul>
    170. 170. T Wave <ul><li>Represents repolarization of ventricular myocardial cells </li></ul><ul><li>Occurs during the last part of ventricular systole </li></ul><ul><li>May be above or below the isoelectric line and is usually slightly rounded and slightly asymmetrical </li></ul>
    171. 171. T Wave <ul><li>Deep and symmetrically inverted T waves may suggest cardiac ischemia </li></ul><ul><li>A T wave elevated more than half the height of the QRS complex (peaked T wave) may indicate a new onset of myocardial ischemia or hyperkalemia </li></ul>
    172. 172. QT Interval <ul><li>The period from the beginning of ventricular depolarization (onset of the QRS complex) until the end of ventricular repolarization, or the end of the T wave </li></ul>
    173. 173. QT Interval <ul><li>From the peak of the T wave onward, the conduction system is in a relative refractory period in which premature impulses may depolarize the heart while it is vulnerable </li></ul>
    174. 174. Artifact <ul><li>A series of deflections on the ECG display or tracing produced by factors other than the heart's electrical activity </li></ul><ul><li>Common causes of artifact: </li></ul><ul><ul><li>Improper grounding of the ECG machine </li></ul></ul><ul><ul><li>Patient movement </li></ul></ul><ul><ul><li>Loss of electrode contact with the patient's skin </li></ul></ul><ul><ul><li>Patient shivering or tremors </li></ul></ul><ul><ul><li>External chest compressions </li></ul></ul>
    175. 175. Artifact - Muscle Tremors
    176. 176. Artifact - AC (60 cycle) Interference
    177. 177. Artifact – Loose Electrode
    178. 178. Artifact - Biotelemetry
    179. 179. Rhythm Analysis <ul><li>Five questions that must be asked to determine the presence or potential for life-threatening rhythm disturbances: </li></ul><ul><ul><li>Is the patient sick? </li></ul></ul><ul><ul><li>What is the heart rate? </li></ul></ul><ul><ul><li>Are there normal-looking QRS complexes? </li></ul></ul><ul><ul><li>Are there normal-looking P waves? </li></ul></ul><ul><ul><li>What is the relationship between P waves and QRS complexes? </li></ul></ul>
    180. 180. Step 1: Analyze the QRS Complex <ul><li>Analyze the QRS complex for regularity and width </li></ul><ul><li>Supraventricular QRS complexes are less than or equal to 0.10 second wide </li></ul>
    181. 181. Normal QRS Complexes
    182. 182. Step 1: Analyze the QRS Complex <ul><li>Complexes that are equal to or greater than 0.12 second wide indicate either: </li></ul><ul><ul><li>A conduction abnormality in the ventricles </li></ul></ul><ul><ul><li>A focus that originates in the ventricles and is abnormal </li></ul></ul>
    183. 183. Analyzing the QRS Complex <ul><li>When evaluating an abnormal QRS width, identify the lead with the widest QRS complex because part of the QRS complex may be blended with the baseline in some leads </li></ul>
    184. 184. Abnormal QRS Complexes
    185. 185. Abnormal QRS Complexes
    186. 186. Abnormal QRS Complexes
    187. 187. Step 2: Analyze the P Waves <ul><li>Are P waves present? </li></ul><ul><li>Are the P waves regular? </li></ul><ul><li>Is there one P wave for each QRS complex, and is there a QRS complex following each P wave? </li></ul><ul><li>Are they upright or inverted? </li></ul><ul><li>Do they all look alike? </li></ul>
    188. 188. Normal P Waves
    189. 189. Step 3: Analyze the Rate <ul><li>If the rate is below 60, it is considered a bradycardia </li></ul><ul><li>If the rate is equal to or greater than 100, it is considered a tachycardia </li></ul>
    190. 190. Heart Rate Rulers <ul><li>Available from a number of manufacturers </li></ul><ul><li>Reasonably accurate if the rhythm is regular </li></ul><ul><ul><li>A mechanical device or tool should not be solely relied on to determine heart rate since one may not be readily available </li></ul></ul>
    191. 191. Heart Rate Calculator Ruler
    192. 192. Triplicate Method <ul><li>Requires memorizing two sets of numbers: 300-150-100 and 75-60-50 </li></ul>
    193. 193. R-R Method 1 <ul><li>Measure the distance in seconds between the peaks of two consecutive R waves </li></ul><ul><li>Divide this number into 60 to obtain heart rate </li></ul>
    194. 194. R-R Method 2 <ul><li>Count the large squares between the peaks of two consecutive R waves </li></ul><ul><li>Divide this number into 300 to obtain the heart rate </li></ul>
    195. 195. R-R Method 3 <ul><li>Count the small squares between the peaks of two consecutive R waves </li></ul><ul><li>Divide this number into 1500 to obtain the heart rate </li></ul>
    196. 196. Six-Second Method <ul><li>Least accurate method of determining heart rate </li></ul><ul><ul><li>May be used to quickly obtain an approximate rate in regular and irregular rhythms </li></ul></ul><ul><li>Count number of QRS complexes in a 6-second interval and multiply number by 10 </li></ul>
    197. 197. Step 4: Analyze the Rhythm <ul><li>To analyze ventricular rhythm, compare R-R intervals systematically from left to right </li></ul><ul><li>If distances between the R waves are equal or vary by less than 0.16 sec, rhythm is regular </li></ul><ul><li>If the shortest and longest R-R intervals vary by more than 0.16 second, the rhythm is “irregular” </li></ul>
    198. 198. Determining the Rhythm
    199. 199. Regular Rhythm
    200. 200. Step 4: Analyze the Rhythm <ul><li>Regularly irregular rhythm - patterned irregularity or “group beating“ </li></ul>
    201. 201. Step 4: Analyze the Rhythm <ul><li>Occasionally irregular--only one or two R-R intervals are unequal to the others </li></ul>
    202. 202. Step 4: Analyze the Rhythm <ul><li>Irregularly irregular--totally irregular; no relationship between R-R intervals </li></ul>
    203. 203. Step 5: Analyze the PR Interval <ul><li>Indicates the time it takes for an electrical impulse to be conducted through the atria and AV node </li></ul><ul><li>Should be constant across the ECG tracing </li></ul>
    204. 204. Step 5: Analyze the PR Interval <ul><li>Prolonged PR interval </li></ul><ul><ul><li>Indicates a delay in the conduction of the impulse through the AV node or bundle of His and is called an AV block </li></ul></ul><ul><li>Short PR interval </li></ul><ul><ul><li>Indicates that the impulse progressed from the atria to the ventricles through pathways other than the AV node </li></ul></ul>
    205. 205. Normal PR Intervals
    206. 206. Normal PR Intervals
    207. 207. Abnormal PR Intervals
    208. 208. Abnormal PR Intervals
    209. 209. Causes of Cardiac Dysrhythmias <ul><li>Myocardial ischemia or necrosis </li></ul><ul><li>Autonomic nervous system imbalance </li></ul><ul><li>Distention of heart chambers </li></ul><ul><li>Acid-base abnormalities </li></ul><ul><li>Hypoxemia </li></ul><ul><li>Electrolyte imbalance </li></ul><ul><li>Drug effects or toxicity </li></ul><ul><li>Electrical injury </li></ul><ul><li>Hypothermia </li></ul><ul><li>CNS injury </li></ul>
    210. 210. Classification of Dysrhythmias <ul><li>Can be based on a number of factors including: </li></ul><ul><ul><li>Changes in automaticity versus disturbances in conduction </li></ul></ul><ul><ul><li>Cardiac arrest (lethal) rhythms and non-cardiac arrest (non-lethal) rhythms </li></ul></ul><ul><ul><li>Site of origin </li></ul></ul>
    211. 211. Dysrhythmias Originating in the SA Node <ul><li>Sinus bradycardia </li></ul><ul><li>Sinus tachycardia </li></ul><ul><li>Sinus dysrhythmia </li></ul><ul><li>Sinus arrest </li></ul>
    212. 212. Dysrhythmias Originating in the Atria <ul><li>Wandering pacemaker </li></ul><ul><li>Premature atrial complex (PAC) </li></ul><ul><li>Paroxysmal supraventricular tachycardia (PSVT) </li></ul><ul><li>Atrial flutter </li></ul><ul><li>Atrial fibrillation </li></ul>
    213. 213. Dysrhythmias Originating in the AV Node <ul><li>Premature junctional complex (PJC) </li></ul><ul><li>Junctional escape complexes or rhythms </li></ul><ul><li>Accelerated junctional rhythm </li></ul>
    214. 214. Dysrhythmias Originating in the Ventricles <ul><li>Ventricular escape complexes or rhythm </li></ul><ul><li>Premature ventricular complex (PVC) </li></ul><ul><li>Ventricular tachycardia (VT) </li></ul><ul><li>Ventricular fibrillation (VF) </li></ul><ul><li>Asystole </li></ul><ul><li>Artificial pacemaker rhythm </li></ul>
    215. 215. Disorders of Conduction <ul><li>AV blocks </li></ul><ul><ul><li>First-degree AV block </li></ul></ul><ul><ul><li>Second-degree AV block Type I </li></ul></ul><ul><ul><li>Second-degree AV block Type II </li></ul></ul><ul><ul><li>Third-degree AV block </li></ul></ul><ul><li>Disturbances of ventricular conduction </li></ul><ul><li>Pulseless electrical activity (PEA) </li></ul><ul><li>Preexcitation syndrome: Wolff-Parkinson-White (WPW) syndrome </li></ul>
    216. 216. Treatment Guidelines <ul><li>First, treat the patient, not the monitor </li></ul><ul><li>Algorithms for cardiac arrest presume that the condition under discussion continually persists, that the patient remains in cardiac arrest, and that CPR is always performed </li></ul><ul><li>Apply different interventions whenever appropriate indications exist </li></ul>
    217. 217. Treatment Guidelines <ul><li>Adequate airway, ventilation, oxygenation, chest compression, and defibrillation are more important than administration of medications and take precedence over initiating an IV line or administering pharmacological agents </li></ul>
    218. 218. Treatment Guidelines <ul><li>Several medications can be administered via the endotracheal tube </li></ul><ul><ul><li>Use an endotracheal dose 2 to 2.5 times the intravenous dose for adults </li></ul></ul><ul><li>With a few exceptions, IV meds should always be administered rapidly in bolus method </li></ul><ul><ul><li>After each IV medication, give a 20- to 30-mL bolus of IV fluid and immediately elevate the extremity </li></ul></ul><ul><li>Last, treat the patient, not the monitor </li></ul>
    219. 219. Dysrhythmias Originating in the SA Node <ul><li>Most sinus dysrhythmias result from increases or decreases in vagal tone </li></ul><ul><li>The SA node generally receives sufficient inhibitory parasympathetic impulses from the vagus nerve to keep the heart rate well below the intrinsic discharge rate of the pacemaker cells </li></ul><ul><ul><li>If vagal discharge increases, the heart rate becomes bradycardic </li></ul></ul><ul><ul><li>If vagal discharge decreases, sympathetic stimulation results in sinus tachycardia </li></ul></ul>
    220. 220. Dysrhythmias Originating in the SA Node <ul><li>ECG features common to all SA node dysrhythmias: </li></ul><ul><ul><li>Normal duration of QRS complex (in the absence of bundle branch block) </li></ul></ul><ul><ul><li>Upright P waves in lead II </li></ul></ul><ul><ul><li>Similar appearance of all P waves </li></ul></ul><ul><ul><li>Normal duration of PR interval (in the absence of AV block) </li></ul></ul>
    221. 221. Sinus Rhythm
    222. 222. Sinus Bradycardia <ul><li>Results from slowing of the pacemaker rate of the SA node </li></ul><ul><li>Causes </li></ul><ul><li>ECG characteristics </li></ul><ul><li>Clinical significance </li></ul><ul><li>Management </li></ul>
    223. 223. Sinus Bradycardia
    224. 224. Sinus Tachycardia <ul><li>Results from an increase in the rate of sinus node discharge </li></ul><ul><li>Causes </li></ul><ul><li>ECG characteristics </li></ul><ul><li>Clinical significance </li></ul><ul><li>Management </li></ul>
    225. 225. Sinus Tachycardia
    226. 226. Sinus Dysrhythmia <ul><li>Present when the difference between the longest and shortest R-R intervals is greater than 0.16 second </li></ul><ul><li>Causes </li></ul><ul><li>ECG characteristics </li></ul><ul><li>Clinical significance </li></ul><ul><li>Management </li></ul>
    227. 227. Sinus Dysrhythmia
    228. 228. Sinus Arrest <ul><li>Results from a marked depression in SA node automaticity </li></ul><ul><ul><li>Failure of the sinus node causes short periods of cardiac standstill until lower-level pacemakers discharge (escape beats) or the sinus node resumes its normal function </li></ul></ul><ul><li>Causes </li></ul><ul><li>ECG characteristics </li></ul><ul><li>Clinical significance </li></ul><ul><li>Management </li></ul>
    229. 229. Sinus Arrest
    230. 230. Dysrhythmias Originating in the Atria <ul><li>May originate in the tissues of the atria or in the internodal pathways </li></ul><ul><li>Common causes of atrial dysrhythmias: </li></ul><ul><ul><li>Ischemia </li></ul></ul><ul><ul><li>Hypoxia </li></ul></ul><ul><ul><li>Atrial dilation caused by: </li></ul></ul><ul><ul><ul><li>Congestive heart failure </li></ul></ul></ul><ul><ul><ul><li>Mitral valve abnormalities </li></ul></ul></ul><ul><ul><ul><li>Increased pulmonary artery pressures </li></ul></ul></ul>
    231. 231. Dysrhythmias Originating in the Atria <ul><li>ECG features common to all atrial dysrhythmias (provided there is no ventricular conduction disturbance): </li></ul><ul><ul><li>Normal QRS complexes </li></ul></ul><ul><ul><li>P waves (if present) that differ in appearance from sinus P waves </li></ul></ul><ul><ul><li>Abnormal, shortened, or prolonged PR intervals </li></ul></ul>
    232. 232. Wandering Atrial Pacemaker <ul><li>The passive transfer of pacemaker sites from the sinus node to other latent pacemaker sites in the atria and AV junction </li></ul><ul><li>The shift in the site is usually transient, back and forth along the SA node, atria, and AV junction </li></ul><ul><li>Causes </li></ul><ul><li>ECG characteristics </li></ul>
    233. 233. Wandering Atrial Pacemaker
    234. 234. Multifocal Atrial Tachycardia <ul><li>A variant of wandering atrial pacemaker </li></ul><ul><ul><li>Resembles wandering pacemaker but is frequently associated with rates in the 120 to 150 per minute range (always considered pathological) </li></ul></ul><ul><li>Most often found in patients with severe COPD and may respond to treatment of this underlying disorder </li></ul><ul><li>ECG characteristics </li></ul><ul><li>Clinical significance </li></ul><ul><li>Management </li></ul>
    235. 235. Premature Atrial Complex <ul><li>A single electrical impulse originating in the atria, outside the sinus node </li></ul><ul><li>PACs may originate from a single ectopic pacemaker site or from multiple sites in the atria </li></ul><ul><li>Probably results from enhanced automaticity or a reentry mechanism </li></ul><ul><li>Causes </li></ul><ul><li>ECG characteristics </li></ul><ul><li>Clinical significance </li></ul><ul><li>Management </li></ul>
    236. 236. PACs
    237. 237. SVT and PSVT <ul><li>Supraventricular tachycardias (SVTs) include: </li></ul><ul><ul><li>Paroxysmal supraventricular tachycardia (PSVT) </li></ul></ul><ul><ul><li>Nonparoxysmal atrial tachycardia </li></ul></ul><ul><ul><li>Multifocal atrial tachycardia </li></ul></ul><ul><ul><li>Junctional tachycardia </li></ul></ul><ul><ul><li>Atrial flutter </li></ul></ul><ul><ul><li>Atrial fibrillation </li></ul></ul><ul><li>PSVT </li></ul><ul><ul><li>A supraventricular tachycardia that begins abruptly </li></ul></ul>
    238. 238. SVT and PSVT <ul><li>Can originate in the atria (paroxysmal atrial tachycardia [PAT]) or AV junction (paroxysmal junctional tachycardia [PJT]) </li></ul><ul><li>Results from rapid atrial or junctional depolarization that overrides the SA node </li></ul><ul><li>Causes </li></ul><ul><li>ECG characteristics </li></ul><ul><li>Clinical significance </li></ul><ul><li>Management </li></ul>
    239. 239. PSVT
    240. 240. Atrial Flutter <ul><li>Usually the result of a rapid atrial reentry focus </li></ul><ul><li>Causes </li></ul><ul><li>ECG characteristics </li></ul><ul><li>Clinical significance </li></ul><ul><li>Management </li></ul>
    241. 241. Atrial Flutter
    242. 242. Atrial Fibrillation <ul><li>Results from multiple areas of reentry within the atria or ectopic atrial pacemakers outside the SA node </li></ul><ul><li>Electrical activity results in chaotic impulses too numerous for all to be conducted by the AV node through the ventricles </li></ul><ul><ul><li>AV conduction is random </li></ul></ul><ul><ul><li>Ventricular response is irregular but usually rapid unless the patient is on medication (e.g., digoxin) to slow the ventricular rate </li></ul></ul>
    243. 243. Atrial Fibrillation <ul><li>Etiology </li></ul><ul><li>ECG characteristics </li></ul><ul><li>Clinical significance </li></ul><ul><li>Management </li></ul>
    244. 244. Atrial Fibrillation
    245. 245. Dysrhythmias of the AV Junction <ul><li>When the SA node and the atria cannot generate the electrical impulses needed to begin depolarization, the AV node or the area surrounding the AV node may assume the role of the secondary pacemaker </li></ul>
    246. 246. Dysrhythmias of the AV Junction <ul><li>May occur because of: </li></ul><ul><ul><li>Hypoxia </li></ul></ul><ul><ul><li>Ischemia </li></ul></ul><ul><ul><li>Myocardial infarction </li></ul></ul><ul><ul><li>Drug toxicity </li></ul></ul><ul><li>Usually a benign dysrhythmia, but must be assessed to determine the patient's tolerance of the rhythm disturbance </li></ul>
    247. 247. Premature Junctional Complex <ul><li>Results from a single electrical impulse originating in the AV junction, which occurs before the next expected sinus impulse </li></ul><ul><li>Causes </li></ul><ul><li>ECG characteristics </li></ul><ul><li>Clinical significance </li></ul><ul><li>Management </li></ul>
    248. 248. PJCs
    249. 249. Junctional Escape Complex or Rhythm <ul><li>An isolated impulse or rhythm (series of impulses) </li></ul><ul><li>Results when rate of primary pacemaker (usually the SA node) falls below that of AV junction </li></ul><ul><li>Causes </li></ul><ul><li>ECG characteristics </li></ul><ul><li>Clinical significance </li></ul><ul><li>Management </li></ul>
    250. 250. Junctional Escape Complex or Rhythm
    251. 251. Accelerated Junctional Rhythm <ul><li>Results from increased automaticity of the AV junction, causing it to discharge faster than its intrinsic rate (40 to 60 beats per minute), overriding the primary (SA node) pacemaker </li></ul><ul><li>Causes </li></ul><ul><li>ECG characteristics </li></ul><ul><li>Clinical significance </li></ul><ul><li>Management </li></ul>
    252. 252. Accelerated Junctional Rhythm
    253. 253. Dysrhythmias Originating in the Ventricles <ul><li>Ventricular rhythms are usually considered life threatening </li></ul><ul><li>Generally result from failure of the atria, AV junction, or both, to initiate an electrical impulse </li></ul>
    254. 254. Dysrhythmias Originating in the Ventricles <ul><li>Are secondary to enhanced automaticity or reentry phenomena in the ventricles </li></ul><ul><ul><li>May lead to PVCs, VT, and even VF </li></ul></ul><ul><li>Often associated with myocardial ischemia or infarction </li></ul><ul><li>Least efficient pacemaker of the heart </li></ul>
    255. 255. Ventricular Escape Complexes or Rhythms <ul><li>An isolated impulse or rhythm (series of complexes) </li></ul><ul><ul><li>Also known as idioventricular rhythm </li></ul></ul><ul><li>Results when impulses from higher pacemakers fail to fire or to reach the ventricles or when the rate of discharge of higher pacemakers falls to less than that of the ventricles </li></ul><ul><li>Serves as a compensatory mechanism to prevent cardiac standstill </li></ul>
    256. 256. Ventricular Escape Complexes or Rhythms <ul><li>Causes </li></ul><ul><li>ECG characteristics </li></ul><ul><li>Clinical significance </li></ul><ul><li>Management </li></ul>
    257. 257. Ventricular Escape Rhythm
    258. 258. “ Dying Heart” or Agonal Rhythm
    259. 259. Premature Ventricular Complexes <ul><li>A single ectopic impulse arising from an irritable focus in either ventricle (bundle branches, Purkinje fibers, or ventricular muscle) </li></ul><ul><li>Occurs earlier than the next expected sinus beat </li></ul><ul><li>A common dysrhythmia that can occur with any underlying cardiac rhythm </li></ul><ul><li>Results from enhanced automaticity or a reentry mechanism </li></ul>
    260. 260. PVCs
    261. 261. Compensatory Pause <ul><li>Confirmed by measuring the interval between the R wave before the PVC and the R wave after it </li></ul><ul><li>If the pause is compensatory, the distance equals at least twice the R-R interval of the underlying rhythm </li></ul><ul><li>Interpolated PVC </li></ul><ul><ul><li>A PVC that falls between two sinus beats without interrupting the rhythm </li></ul></ul>
    262. 262. Interpolated PVC
    263. 263. Unifocal and Multifocal PVCs <ul><li>Unifocal PVCs originate from a single site within the ventricles and look alike </li></ul><ul><li>Multifocal PVCs originate from different ventricular sites and have varying shapes and sizes </li></ul>
    264. 264. Unifocal & Multifocal PVCs
    265. 265. Fusion Beats <ul><li>PVCs that occur at the same time as ventricular activation by the underlying rhythm can cause ventricular depolarization to occur simultaneously in two directions </li></ul><ul><li>This fusion beat results in a QRS complex that has the characteristics of the PVC and the QRS complex of the underlying rhythm </li></ul>
    266. 266. Fusion beat with PVC
    267. 267. Grouped Beating <ul><li>PVCs frequently occur in patterns of grouped beating: </li></ul><ul><ul><li>Bigeminy occurs when every other complex is a PVC </li></ul></ul><ul><ul><li>Trigeminy occurs when every third complex is a PVC </li></ul></ul><ul><ul><li>Quadrigeminy occurs when every fourth complex is a PVC </li></ul></ul>
    268. 268. Ventricular Bigeminy & Trigeminy
    269. 269. PVCs <ul><li>Consecutive PVCs that are not separated by a complex of the underlying rhythm can also occur on the ECG: </li></ul><ul><li>Couplets are two PVCs in a row </li></ul><ul><li>Three or more sequential PVCs at a rate of 100 per minute or more = a run of VT </li></ul><ul><li>R-on-T phenomenon </li></ul>
    270. 270. R-on-T Phenomenon
    271. 271. PVCs--Causes <ul><li>Occur in healthy individuals without apparent cause and are usually of no significance </li></ul><ul><li>Pathological PVCs are usually a result of: </li></ul><ul><ul><li>Myocardial ischemia </li></ul></ul><ul><ul><li>Hypoxia </li></ul></ul><ul><ul><li>Acid-base and electrolyte imbalance </li></ul></ul><ul><ul><li>Hypokalemia </li></ul></ul><ul><ul><li>Congestive heart failure </li></ul></ul><ul><ul><li>Increased catecholamine and sympathetic tone (as in emotional stress) </li></ul></ul><ul><ul><li>Ingestion of stimulants (alcohol, caffeine, tobacco) </li></ul></ul><ul><ul><li>Drug toxicity </li></ul></ul><ul><ul><li>Sympathomimetic drugs </li></ul></ul>
    272. 272. PVCs <ul><li>ECG characteristics </li></ul><ul><li>Clinical significance </li></ul><ul><li>Management </li></ul>
    273. 273. Ventricular Tachycardia <ul><li>A dysrhythmia defined by three or more consecutive ventricular complexes occurring at a rate of more than 100 beats per minute, which overrides the primary pacemaker </li></ul><ul><li>Generally starts suddenly, triggered by a PVC </li></ul><ul><li>During VT, the atria and ventricles are asynchronous </li></ul><ul><li>If the rhythm disturbance is sustained, the patient's condition may become unstable, possibly leading to unconsciousness and occasionally even to loss of a perfusing pulse </li></ul>
    274. 274. Ventricular Tachycardia <ul><li>Causes </li></ul><ul><li>ECG characteristics </li></ul><ul><li>Clinical significance </li></ul><ul><li>Management </li></ul>
    275. 275. Monomorphic VT
    276. 276. Torsade de Pointes <ul><li>Causes </li></ul><ul><li>ECG characteristics </li></ul><ul><li>Clinical significance </li></ul><ul><li>Management </li></ul>
    277. 277. Torsade de Pointes
    278. 278. 12-Lead Strategies for Wide-Complex Tachycardias <ul><li>Assess leads I, II, III, MCL1 (V1), and MCL6 (V6) to determine axis deviation </li></ul><ul><ul><li>If the QRS complex is negative in leads I, II, and III (extreme right axis deviation or “no-man’s land”) and positive in MCL1 (V1), the rhythm indicates VT </li></ul></ul><ul><ul><li>If this criterion is not met, proceed to step two </li></ul></ul>
    279. 279. Criteria for VT
    280. 280. 12-Lead Strategies for Wide-Complex Tachycardias <ul><li>If extreme right axis deviation is not present, assess the QRS deflection in MCL1 (V1) and MCL6 (V6) </li></ul><ul><ul><li>Regardless of the QRS deflection in leads I, II, and III, positive QRS deflections with either a single peak, a taller left “rabbit ear,” or an RS complex with a fat r wave or slurred s wave in MCL1 (V1) indicates VT </li></ul></ul><ul><ul><li>A negative QS complex, a negative rS complex, or any wide Q wave in MCL6 (V6) also indicates VT </li></ul></ul>
    281. 281. Note “rabbit ear”
    282. 282. 12-Lead Strategies for Wide-Complex Tachycardias <ul><li>If right axis deviation is present (negative QRS complex in lead I; positive QRS complex in leads II and III) and the QRS complex is negative in MCL1 (V1), it indicates VT </li></ul>
    283. 283. Right axis deviation and a downward MCLI indicates VT
    284. 284. 12-Lead Strategies for Wide-Complex Tachycardias <ul><li>If all precordial leads (V leads) are either positive or negative (precordial concordance), it indicates VT </li></ul>
    285. 285. VT-Concordance
    286. 286. 12-Lead Strategies for Wide-Complex Tachycardias <ul><li>If the RS interval is greater than 0.10 second in any V lead (increased ventricular activation time), it indicates VT </li></ul>
    287. 287. VT (RS interval is .16 sec)
    288. 288. Ventricular Fibrillation <ul><li>A chaotic ventricular rhythm that results in quivering ventricular movements and pulselessness </li></ul><ul><li>Causes </li></ul><ul><li>ECG characteristics </li></ul><ul><li>Clinical significance </li></ul><ul><li>Management </li></ul>
    289. 289. Ventricular Fibrillation
    290. 290. Coarse and Fine VF
    291. 291. Ventricular Asystole <ul><li>Refers to absence of all ventricular activity </li></ul><ul><li>Causes </li></ul><ul><li>ECG characteristics </li></ul><ul><li>Clinical significance </li></ul><ul><li>Management </li></ul>
    292. 292. Ventricular Asystole
    293. 293. Artificial Pacemaker Rhythms <ul><li>Artificial pacemakers generate a rhythm by regular electrical stimulation of the heart through an electrode implanted in the heart </li></ul><ul><ul><li>Fixed rate or asynchronous pacemakers </li></ul></ul><ul><ul><li>Demand pacemakers </li></ul></ul><ul><ul><li>Atrial synchronous ventricular pacemakers </li></ul></ul><ul><ul><li>AV sequential pacemakers </li></ul></ul><ul><ul><li>Rate-responsive pacemakers </li></ul></ul><ul><li>Clinical significance </li></ul><ul><li>Management </li></ul>
    294. 294. Artificial Pacemaker Rhythms
    295. 295. Potential Causes of Pacemaker Malfunction <ul><li>Battery failure </li></ul><ul><li>Runaway pacemaker </li></ul><ul><li>Failure of the sensing device in demand pacemaker </li></ul><ul><li>Failure to capture </li></ul>
    296. 296. Heart Blocks <ul><li>Partial delays or complete interruptions in cardiac electrical conduction </li></ul><ul><li>Can occur anywhere in the atria, between the SA node and the AV node, or in the ventricles between the AV node and the Purkinje fibers </li></ul><ul><li>May be caused by pathology in the conduction system or by a physiological block, as occurs in atrial fibrillation or atrial flutter </li></ul>
    297. 297. Heart Blocks — Causes <ul><li>AV junctional ischemia </li></ul><ul><li>AV junctional necrosis </li></ul><ul><li>Degenerative disease of the conduction system </li></ul><ul><li>Electrolyte imbalances (e.g., hyperkalemia) </li></ul><ul><li>Drug toxicity, especially with digitalis </li></ul>
    298. 298. Heart Blocks – Classifications <ul><li>Conduction blocks may be classified by several characteristics: </li></ul><ul><ul><li>Site of block (e.g., left bundle branch block) </li></ul></ul><ul><ul><li>Degree of block (e.g., second-degree AV block) </li></ul></ul><ul><ul><li>Category of AV conduction disturbances (e.g., Type I) </li></ul></ul>
    299. 299. First-Degree AV Block <ul><li>Not a true block but rather a delay in conduction, usually at the level of the AV node </li></ul><ul><li>Not considered a rhythm in itself because it is usually superimposed on another rhythm </li></ul><ul><li>Underlying rhythm also must be identified </li></ul><ul><li>Etiology </li></ul><ul><li>ECG characteristics </li></ul><ul><li>Clinical significance </li></ul><ul><li>Management </li></ul>
    300. 300. First-degree AV Block
    301. 301. Identifying Heart Blocks
    302. 302. Second-Degree AV Block Type I (Wenckebach) <ul><li>An intermittent block that usually occurs at the level of the AV node </li></ul><ul><li>Conduction delay progressively increases from beat to beat until conduction to the ventricle is blocked </li></ul><ul><ul><li>Produces a characteristic cyclical pattern in which the PR intervals get progressively longer until a P wave occurs that is not followed by a QRS complex </li></ul></ul><ul><li>Clinical significance </li></ul><ul><li>Management </li></ul>
    303. 303. Second-degree AV block, type I
    304. 304. Second-Degree AV Block Type II <ul><li>An intermittent block that occasionally occurs when atrial impulses are not conducted to the ventricles </li></ul><ul><li>Characterized by consecutive P waves being conducted with a constant PR interval before a dropped beat </li></ul>
    305. 305. Second-Degree AV Block Type II <ul><li>Usually occurs in a regular sequence with the conduction ratios (P waves to QRS complexes) such as 2:1, 3:2, and 4:3 </li></ul>
    306. 306. Second-degree AV block, type II
    307. 307. 3:2 AV block & 4:3 AV Block
    308. 308. Second-Degree AV Block Type II <ul><li>Usually occurs below the bundle of His </li></ul><ul><li>When at least two consecutive impulses (atrial P waves) fail to be conducted to the ventricles, the AV block is called a high-grade AV block </li></ul>
    309. 309. 3:1 high-grade AV Block
    310. 310. Second-Degree AV Block Type II <ul><li>Clinically malignant high-grade AV blocks and those with a more favorable prognosis are distinguished by the underlying atrial and ventricular rates </li></ul><ul><li>Clinical significance </li></ul><ul><li>Management </li></ul>
    311. 311. Third-Degree Heart Block <ul><li>Results from complete electrical block at or below the AV node (infranodal) </li></ul><ul><li>SA node serves as the pacemaker for the atria, and an ectopic focus serves as a pacemaker in the ventricles </li></ul><ul><li>P waves and QRS complexes occur rhythmically, but the rhythms are unrelated to each other (AV dissociation) </li></ul>
    312. 312. Third-Degree AV Block <ul><li>Etiology </li></ul><ul><li>ECG characteristics </li></ul><ul><li>Clinical significance </li></ul><ul><li>Management </li></ul>
    313. 313. Third-degree AV Block
    314. 314. Ventricular Conduction Disturbances
    315. 315. Bundle Branch Blocks and Hemiblocks <ul><li>Are delays or interruptions in the transmission of electrical impulses that occur below the bifurcation of the bundle of His </li></ul>
    316. 316. Bundle Branch Blocks and Hemiblocks <ul><li>Common causes of bundle branch block: </li></ul><ul><ul><li>Ischemic heart disease </li></ul></ul><ul><ul><li>Acute heart failure </li></ul></ul><ul><ul><li>Acute myocardial infarction </li></ul></ul><ul><ul><li>Hyperkalemia </li></ul></ul><ul><ul><li>Trauma </li></ul></ul><ul><ul><li>Cardiomyopathy </li></ul></ul><ul><ul><li>Aortic stenosis </li></ul></ul><ul><ul><li>Infection </li></ul></ul>
    317. 317. Bundle Branch Anatomy <ul><li>Bundle of His begins at the AV node and divides to form the left and right bundle branches </li></ul><ul><ul><li>Right bundle branch continues toward the apex and spreads throughout right ventricle </li></ul></ul><ul><ul><li>Left bundle branch subdivides into the anterior and posterior fascicles and spreads throughout the left ventricle </li></ul></ul><ul><li>Conduction of electrical impulses through the Purkinje fibers stimulates the ventricles to contract </li></ul>
    318. 318. Bundle Branch Anatomy <ul><li>Major divisions of ventricular conduction system and possible sites of block and the conduction deficits that may be produced </li></ul>
    319. 319. Bundle Branch Anatomy <ul><li>With normal conduction, the first part of the ventricle to be stimulated is the left side of the septum </li></ul><ul><li>The electrical impulse then traverses the septum to stimulate the other side </li></ul><ul><li>Shortly after that, the left and right ventricles are simultaneously stimulated </li></ul>
    320. 320. Normal Ventricular Activation
    321. 321. Bundle Branch Block <ul><li>Common ECG Findings </li></ul><ul><ul><li>When an electrical impulse is blocked from passing through either the right or left bundle branch, one ventricle depolarizes and contracts before the other </li></ul></ul><ul><ul><li>Because ventricular activation is no longer simultaneous, the QRS complex widens </li></ul></ul><ul><ul><ul><li>Often with a slurred or notched appearance known as “rabbit ears” </li></ul></ul></ul><ul><li>Hallmark of bundle branch block is a QRS complex that is equal to or greater than 0.12 second </li></ul>
    322. 322. Bundle Branch Block <ul><li>Two criteria for bundle branch block recognition: </li></ul><ul><ul><li>A QRS complex equal to or greater than 0.12 second </li></ul></ul><ul><ul><li>QRS complexes produced by supraventricular activity </li></ul></ul>
    323. 323. Bundle Branch Block <ul><li>Best identified by monitoring leads MCL1 and MCL6 (or by monitoring V1 and V6 with a 12-lead machine) </li></ul><ul><ul><li>These leads permit the easiest differentiation of the right and left bundle branch blocks </li></ul></ul><ul><li>Normal conduction </li></ul><ul><ul><li>During normal conduction, MCL1 is predominantly negative, and the QRS complex is usually 0.08 to 0.10 wide </li></ul></ul>
    324. 324. Right Bundle Branch Block <ul><li>In right bundle branch block, the left bundle branch performs normally, activating the left side of the heart before the right </li></ul><ul><li>ECG characteristics </li></ul><ul><ul><li>Initial negative deflection (S wave) </li></ul></ul><ul><ul><li>RSR-prime pattern </li></ul></ul><ul><ul><li>QRS (or in this case, RSR) duration at least 0.12 second </li></ul></ul>
    325. 325. Right Bundle Branch Block
    326. 326. Left Bundle Branch Block <ul><li>In left bundle branch block, the fibers that usually fire the interventricular septum are blocked </li></ul><ul><ul><li>This alters normal septal activation and sends it in the opposite direction </li></ul></ul><ul><li>ECG characteristics: </li></ul><ul><ul><li>Initial Q wave in MCL1 </li></ul></ul><ul><ul><li>R wave in MCL1 </li></ul></ul><ul><ul><li>Deep, wide S wave (QS pattern) </li></ul></ul><ul><ul><li>QRS duration at least 0.12 second </li></ul></ul>
    327. 327. Left Bundle Branch Block
    328. 328. Left vs. Right BBB <ul><li>Find J point of QRS complex </li></ul><ul><li>Draw line back into QRS complex </li></ul><ul><li>Fill in triangle created </li></ul><ul><li>Note direction triangle points </li></ul>
    329. 329. Anterior Hemiblock <ul><li>Occurs more frequently than posterior hemiblock </li></ul><ul><li>The anterior fascicle of the left bundle branch is a longer and thinner structure, and its blood supply comes primarily from the left anterior descending (LAD) coronary artery </li></ul><ul><li>Anterior hemiblock is characterized by left axis deviation in a patient who has a supraventricular rhythm </li></ul>
    330. 330. Anterior Hemiblock <ul><li>Other ECG findings associated with an anterior hemiblock include: </li></ul><ul><ul><li>A normal QRS complex (less than 0.12 second) or a right bundle branch block </li></ul></ul><ul><ul><li>A small Q wave followed by a tall R wave in lead I </li></ul></ul><ul><ul><li>A small R wave followed by a deep S wave in lead III </li></ul></ul><ul><li>These patients are at high risk of developing complete heart block </li></ul>
    331. 331. Anterior Hemiblock Showing 1 Block of 3 Fascicles
    332. 332. Posterior Hemiblock <ul><li>Identified by right axis deviation with a normal QRS complex or a right bundle branch block </li></ul><ul><li>Other ECG findings that indicate the presence of a posterior hemiblock: </li></ul><ul><ul><li>A small R wave followed by a deep S wave in lead I </li></ul></ul><ul><ul><li>A small Q wave followed by a tall R wave in lead III </li></ul></ul>
    333. 333. Posterior Hemiblock Showing 2 of 3 Fascicles Blocked
    334. 334. Bifascicular Block <ul><li>Blockage of two out of three pathways for ventricular conduction </li></ul><ul><li>Occurs in the presence of right bundle branch block with anterior or posterior hemiblock, and in left bundle branch block </li></ul><ul><li>Compromises myocardial contractility and cardiac output </li></ul><ul><li>Patients may develop complete heart block suddenly and without warning </li></ul>
    335. 335. Multi-Lead Determination of Axis and Hemiblocks <ul><li>Identifying axis can be useful in determining the presence of hemiblocks </li></ul><ul><li>Best evaluated by looking at the QRS complexes in leads I, II, and III </li></ul>
    336. 336. Multi-Lead Determination of Axis and Hemiblocks <ul><li>Axis is considered: </li></ul><ul><ul><li>Normal when the QRS deflection is positive (upright) in all bipolar leads </li></ul></ul><ul><ul><li>Physiologic left (which may be normal in some patients) when the QRS deflection is: </li></ul></ul><ul><ul><ul><li>Positive in leads I and II </li></ul></ul></ul><ul><ul><ul><li>Negative (inverted) in lead III </li></ul></ul></ul><ul><ul><li>Pathological left when the QRS deflection is: </li></ul></ul><ul><ul><ul><li>Positive in lead I </li></ul></ul></ul><ul><ul><ul><li>Negative in leads II and III (indicating an anterior hemiblock) </li></ul></ul></ul>
    337. 337. Multi-Lead Determination of Axis and Hemiblocks <ul><li>Right axis when the QRS deflection is: </li></ul><ul><ul><li>Negative in lead I, negative or positive in lead II </li></ul></ul><ul><ul><li>Positive in lead III (pathologic in any adult) </li></ul></ul><ul><ul><li>Indicative of a posterior hemiblock </li></ul></ul><ul><li>Extreme right (“no man’s land”) when the QRS deflection is negative in all three leads (indicating the rhythm is ventricular in origin) </li></ul><ul><li>Management </li></ul>
    338. 338. Pulseless Electrical Activity <ul><li>Pulseless electrical activity (PEA) is the absence of a detectable pulse and the presence of some type of electrical activity other than VT or VF </li></ul><ul><li>Prognosis for PEA invariably is poor unless an underlying cause can be identified and corrected </li></ul><ul><li>The highest priority of care is to maintain circulation for the patient with basic and advanced life support techniques while searching for a correctable cause </li></ul>
    339. 339. Pulseless Electrical Activity <ul><li>Correctable causes: </li></ul><ul><ul><li>Cardiac tamponade </li></ul></ul><ul><ul><li>Tension pneumothorax </li></ul></ul><ul><ul><li>Hypoxemia </li></ul></ul><ul><ul><li>Acidosis </li></ul></ul><ul><ul><li>Hyperkalemia </li></ul></ul><ul><ul><li>Hypothermia </li></ul></ul><ul><ul><li>Drug overdoses </li></ul></ul><ul><li>Management </li></ul><ul><li>Less correctable causes: </li></ul><ul><ul><li>Massive myocardial damage from infarction </li></ul></ul><ul><ul><li>Prolonged ischemia during resuscitation </li></ul></ul><ul><ul><li>Profound hypovolemia </li></ul></ul><ul><ul><li>Massive pulmonary embolism </li></ul></ul><ul><ul><li>Patients in profound shock of any type </li></ul></ul>
    340. 340. Various PEA rhythms as seen in lead II
    341. 341. Preexcitation Syndromes <ul><li>Preexcitation syndrome (anomalous or accelerated AV conduction) is a clinical condition associated with an abnormal conduction pathway between the atria and ventricles that bypasses the AV node and/or bundle of His </li></ul><ul><ul><li>Allows the electrical impulses to initiate depolarization of the ventricles earlier than usual </li></ul></ul><ul><ul><li>Premature ventricular activation may occur through one of several accessory pathways </li></ul></ul><ul><li>Most common preexcitation syndrome is Wolff-Parkinson-White (WPW) syndrome </li></ul>
    342. 342. Wolff-Parkinson-White Syndrome <ul><li>Description </li></ul><ul><li>Etiology </li></ul><ul><li>P waves: Normal </li></ul><ul><li>Rate: Normal unless associated with rapid supraventricular tachycardia </li></ul><ul><li>Rhythm: Regular </li></ul><ul><li>PR interval: Usually less than 0.12 second, since the normal delay at the AV node does not occur </li></ul>
    343. 343. Wolff-Parkinson-White Syndrome <ul><li>Three characteristic ECG findings in WPW: </li></ul><ul><ul><li>A short PR interval </li></ul></ul><ul><ul><li>A delta wave </li></ul></ul><ul><ul><li>QRS widening </li></ul></ul><ul><li>Clinical significance </li></ul><ul><li>Management </li></ul>
    344. 344. WPW <ul><li>(A) Usual appearance of WPW syndrome in leads where QRS complex is predominantly upright </li></ul><ul><li>(B) Appearance of WPW syndrome with QRS complex predominantly negative </li></ul>
    345. 345. Pathophysiology of Atherosclerosis
    346. 346. Atherosclerosis <ul><li>A disease process characterized by progressive narrowing of the lumen of medium and large arteries (e.g., the aorta and its branches, cerebral arteries, coronary arteries) </li></ul><ul><li>Results in the development of thick, hard atherosclerotic plaque called atheromas or atheromatous lesions which are most commonly found in areas of turbulent blood flow </li></ul><ul><li>Major risk factors </li></ul>
    347. 347. Atherosclerosis — Effects <ul><li>Two major effects on blood vessels: </li></ul><ul><ul><li>The disease disrupts the intimal surface, causing a loss of vessel elasticity and an increase in thrombogenesis </li></ul></ul><ul><ul><li>The atheroma reduces the diameter of the vessel lumen and thus decreases the blood supply to tissues </li></ul></ul>
    348. 348. Angina Pectoris <ul><li>A symptom of myocardial ischemia </li></ul><ul><li>Literally means “choking pain in the chest” </li></ul><ul><li>Caused by an imbalance between myocardial oxygen supply and demand </li></ul><ul><li>Results in an accumulation of lactic acid and carbon dioxide in ischemic tissues of the myocardium </li></ul><ul><ul><li>These metabolites irritate nerve endings that produce anginal pain </li></ul></ul>
    349. 349. Angina Pectoris <ul><li>Most common cause is atherosclerotic disease of the coronary arteries </li></ul><ul><li>A temporary occlusion caused by spasm of a coronary artery with or without atherosclerosis (Prinzmetal's angina) can also cause angina pectoris </li></ul><ul><li>Precipitating events </li></ul>
    350. 350. Stable Angina <ul><li>Usually precipitated by physical exertion or emotional stress </li></ul><ul><li>Pain typically lasts 1 to 5 minutes but may last as long as 15 minutes </li></ul><ul><li>Relieved by rest, nitroglycerin, or oxygen </li></ul><ul><li>“ Attacks” are usually similar in nature and are always relieved by the same mode of therapy </li></ul>
    351. 351. Unstable Angina <ul><li>Also called preinfarction angina </li></ul><ul><li>Denotes an anginal pattern that has changed in its ease of onset, frequency, intensity, duration, or quality </li></ul><ul><li>Includes any “new-onset” anginal chest pain </li></ul><ul><li>May occur during periods of light exercise or at rest </li></ul><ul><li>Pain usually lasts 10 minutes or more </li></ul><ul><li>Less promptly relieved with cessation of activity or nitroglycerin than the stable anginal pattern </li></ul>
    352. 352. Angina Pectoris <ul><li>Pain is usually described as a pressure, squeezing, heaviness, or tightness in the chest </li></ul><ul><ul><li>30% of patients feel pain only in the chest </li></ul></ul><ul><ul><li>Others describe the pain as radiating to the shoulders, arms, neck, and jaw and through to the back </li></ul></ul><ul><li>Associated signs and symptoms: </li></ul><ul><ul><li>Anxiety </li></ul></ul><ul><ul><li>Shortness of breath </li></ul></ul><ul><ul><li>Nausea or vomiting </li></ul></ul><ul><ul><li>Diaphoresis </li></ul></ul><ul><li>Management </li></ul>
    353. 353. Myocardial Infarction <ul><li>Occurs when there is a sudden and total occlusion or near-occlusion of blood flowing through an affected coronary artery to an area of heart muscle </li></ul><ul><li>Results in ischemia, injury, and necrosis of the area of myocardium distal to the occlusion </li></ul><ul><li>Most often associated with atherosclerotic heart disease (ASHD) </li></ul><ul><li>Precipitating events </li></ul>
    354. 354. Types and Locations of Infarcts <ul><li>Infarction develops distally to the occluded artery </li></ul><ul><li>Size of the infarct determined by: </li></ul><ul><ul><li>Metabolic needs of the tissue supplied solely or predominantly by the occluded vessel </li></ul></ul><ul><ul><li>Presence of collateral circulation </li></ul></ul><ul><ul><li>Duration of time until flow is reestablished </li></ul></ul>
    355. 355. Types and Locations of Infarcts <ul><li>Emergency care is directed at: </li></ul><ul><ul><li>Increasing oxygen supply by administering supplemental oxygen </li></ul></ul><ul><ul><li>Decreasing the metabolic needs and in providing collateral circulation </li></ul></ul><ul><ul><li>Reestablishing perfusion to the ischemic myocardium as quickly as possible after the onset of symptoms </li></ul></ul>
    356. 356. Types and Locations of Infarcts <ul><li>Most AMIs involve the left ventricle or interventricular septum, which is supplied by either of the two major coronary arteries </li></ul><ul><ul><li>Some patients sustain damage to the right ventricle </li></ul></ul>
    357. 357. Types and Locations of Infarcts <ul><li>Anterior, lateral, or septal wall infarction is usually the result of left coronary artery occlusion </li></ul><ul><li>Inferior wall infarction (of the inferior-posterior wall of the left ventricle) is usually the result of right coronary artery occlusion </li></ul>
    358. 358. Myocardial Infarction <ul><li>Infarction can be classified into one of three ischemic syndromes based on the rupture of an unstable plaque in an epicardial artery: </li></ul><ul><ul><li>Unstable angina </li></ul></ul><ul><ul><li>Non-ST-elevation myocardial infarction </li></ul></ul><ul><ul><li>ST-elevation myocardial infarction </li></ul></ul>
    359. 359. Infarction <ul><li>Unstable Angina </li></ul><ul><ul><li>The early thrombus has not completely obstructed coronary flow </li></ul></ul><ul><ul><li>Causes an intermittent ischemic episode that may eventually result in complete occlusion and AMI </li></ul></ul><ul><li>Non-ST-elevation MI </li></ul><ul><ul><li>Evident only with ST-segment depression or T-wave abnormalities </li></ul></ul>
    360. 360. Infarction <ul><li>ST-elevation MI </li></ul><ul><ul><li>Formerly called Q-wave MI </li></ul></ul><ul><ul><ul><li>Diagnosed by development of abnormal Q waves </li></ul></ul></ul><ul><ul><ul><li>Pathologic Q waves </li></ul></ul></ul><ul><ul><ul><ul><li>Greater than 5 mm in depth or greater than .04 sec in duration in two or more contiguous leads </li></ul></ul></ul></ul>
    361. 361. Death of Myocardium <ul><li>When blood flow to the myocardium ceases, cells switch from aerobic to anaerobic metabolism </li></ul><ul><ul><li>This contributes to produce ischemic pain (angina) </li></ul></ul><ul><li>As cells lose their ability to maintain their electrochemical gradients, they begin to swell and depolarize </li></ul><ul><li>If collateral flow and reperfusion are inadequate, much of the muscle distal to the occlusion dies </li></ul>
    362. 362. Area of Infarction
    363. 363. Myocardial Infarction <ul><li>Deaths secondary to myocardial infarction usually result from: </li></ul><ul><ul><li>Lethal dysrhythmias </li></ul></ul><ul><ul><ul><li>VT </li></ul></ul></ul><ul><ul><ul><li>VF </li></ul></ul></ul><ul><ul><ul><li>Cardiac standstill </li></ul></ul></ul><ul><ul><li>Pump failure </li></ul></ul><ul><ul><ul><li>Cardiogenic shock </li></ul></ul></ul><ul><ul><ul><li>CHF </li></ul></ul></ul><ul><ul><li>Myocardial tissue rupture </li></ul></ul><ul><ul><ul><li>Rupture of the ventricle, septum, or papillary muscle </li></ul></ul></ul>
    364. 364. Myocardial Infarction -Signs and Symptoms <ul><li>Pain is similar to anginal pain and may radiate to the arms, neck, jaw, or back </li></ul><ul><li>Dyspnea </li></ul><ul><li>Anxiety </li></ul><ul><li>Agitation </li></ul><ul><li>Sense of impending doom </li></ul><ul><li>Nausea and vomiting </li></ul><ul><li>Diaphoresis </li></ul><ul><li>Cyanosis </li></ul><ul><li>Palpitations </li></ul>
    365. 365. Myocardial Infarction -Signs and Symptoms <ul><li>Chest pain associated with AMI is often constant and is not altered or alleviated by nitroglycerin or other cardiac medications, rest, changes in body position, or breathing patterns </li></ul><ul><ul><li>Onset of pain in over half of all patients with AMI occurs during rest </li></ul></ul><ul><ul><li>Most patients have experienced warning anginal pain (preinfarction angina) hours or days before the attack </li></ul></ul>
    366. 366. Myocardial Infarction -Common ECG Findings <ul><li>A damaged heart muscle is unable to contract effectively and remains in a constant depolarized state </li></ul><ul><ul><li>The flow of current between the pathologically depolarized and normally repolarized areas produce abnormal ST-segment elevation on the ECG </li></ul></ul><ul><ul><li>ST-segment elevation greater than 0.1 mV in at least two contiguous ECG leads suggests AMI </li></ul></ul><ul><li>Management </li></ul>
    367. 367. ST-segment Elevation Likely With Acute Injury
    368. 368. ST-Elevation & Infarct Location Right Right ventricle V4R, V5R, V6R Left Lateral wall I, aVL, V5, V6 Left Anterior wall (most lethal) V3, V4 Left Septal wall V1, V2 Right Inferior wall (most common) II, III, aVF Coronary Artery Involved Location of Infarction Lead
    369. 369. Multi-lead Assessment of the Heart
    370. 370. Left Ventricular Failure (LVF) and Pulmonary Edema <ul><li>LVF occurs when the left ventricle fails to function as an effective forward pump, causing a back-pressure of blood into the pulmonary circulation </li></ul>
    371. 371. LVF and Pulmonary Edema <ul><li>May be caused by a variety of forms of heart disease including ischemic, valvular, and hypertensive heart disease </li></ul><ul><li>Untreated, significant LVF culminates in pulmonary edema </li></ul>
    372. 372. LVF <ul><li>Signs and symptoms </li></ul><ul><ul><li>Severe respiratory distress </li></ul></ul><ul><ul><li>Severe apprehension, agitation, confusion </li></ul></ul><ul><ul><li>Cyanosis (if severe) </li></ul></ul><ul><ul><li>Diaphoresis </li></ul></ul><ul><ul><li>Adventitious lung sounds </li></ul></ul><ul><ul><li>JVD </li></ul></ul><ul><ul><li>Abnormal vital signs </li></ul></ul><ul><li>Management </li></ul>
    373. 373. Right Ventricular Failure (RVF) <ul><li>Occurs when the right ventricle fails as an effective forward pump, causing back-pressure of blood into the systemic venous circulation </li></ul>
    374. 374. Right Ventricular Failure (RVF) <ul><li>Can result from: </li></ul><ul><ul><li>Chronic hypertension (in which LVF usually precedes RVF) </li></ul></ul><ul><ul><li>COPD </li></ul></ul><ul><ul><li>Pulmonary embolism </li></ul></ul><ul><ul><li>Valvular heart disease </li></ul></ul><ul><ul><li>Right ventricular infarction </li></ul></ul><ul><li>RVF most commonly results from LVF </li></ul>
    375. 375. RVF <ul><li>Signs and symptoms </li></ul><ul><ul><li>Tachycardia </li></ul></ul><ul><ul><li>Venous congestion </li></ul></ul><ul><ul><ul><li>Engorged liver, spleen, or both </li></ul></ul></ul><ul><ul><ul><li>Venous distention; distention and pulsations of the neck veins </li></ul></ul></ul><ul><ul><li>Peripheral edema </li></ul></ul><ul><ul><li>Fluid accumulation in serous cavities </li></ul></ul><ul><ul><li>History--common signs and symptoms of acute right-sided heart failure include chest pain, hypotension, and distended neck veins </li></ul></ul><ul><li>Management </li></ul>
    376. 376. Cardiogenic Shock <ul><li>The most extreme form of pump failure </li></ul><ul><li>Occurs when left ventricular function is so compromised that the heart cannot meet the metabolic needs of the body </li></ul><ul><li>Usually caused by extensive myocardial infarction, often involving more than 40% of the left ventricle, or by diffuse ischemia </li></ul><ul><li>Signs and symptoms </li></ul><ul><li>Management </li></ul>
    377. 377. Cardiac Tamponade <ul><li>Impaired diastolic filling of the heart caused by increased intrapericardial pressure and volume </li></ul><ul><ul><li>As the volume of pericardial fluid encroaches on the capacity of the atria and ventricles to fill adequately, ventricular filling is mechanically limited and stoke volume is decreased </li></ul></ul><ul><li>Causes </li></ul><ul><li>Signs and symptoms </li></ul><ul><li>Management </li></ul>
    378. 378. Thoracic and Abdominal Aortic Aneurysms <ul><li>Aneurysm is a nonspecific term meaning “dilation of a vessel” </li></ul><ul><li>May result from: </li></ul><ul><ul><li>Atherosclerotic disease (most common) </li></ul></ul><ul><ul><li>Infectious disease (primarily syphilis) </li></ul></ul><ul><ul><li>Traumatic injury </li></ul></ul><ul><ul><li>Certain genetic disorders (e.g., Marfan's syndrome) </li></ul></ul>
    379. 379. Thoracic and Abdominal Aortic Aneurysms <ul><li>Signs and symptoms of a leaking or ruptured AAA </li></ul><ul><li>Management </li></ul>
    380. 380. Branches of Aorta
    381. 381. Pathogenesis of Dissecting Aneurysms <ul><li>A) Medial and intimal degeneration in anotic wall </li></ul><ul><li>(B) Hemodynamic forces produce tear </li></ul><ul><li>(C) Dissecting hematoma propagated by pulse wave </li></ul>
    382. 382. Acute Arterial Occlusion <ul><li>A sudden blockage of arterial flow most commonly caused by: </li></ul><ul><ul><li>Trauma </li></ul></ul><ul><ul><li>Embolus </li></ul></ul><ul><ul><li>Thrombosis </li></ul></ul><ul><li>Severity of the ischemic episode depends on: </li></ul><ul><ul><li>Site of occlusion </li></ul></ul><ul><ul><li>Quality of collateral circulation around the blockage </li></ul></ul>
    383. 383. Acute Arterial Occlusion <ul><li>Signs and symptoms </li></ul><ul><ul><li>Pain in

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