MYOCARDIAL INFARCTION First Heart Sound due to the coming of the AV valve, slaps at the beginning of ventricular systole

le Second Heart Sound due to the closure of the semi-lunar valve at the beginning of ventricular diastole Murmur can be heard as the blood flows thru a narrowed opening Conduction System - SA node > AV node > left and right bundle branches > Purkinje Fibers Automaticity the ability of the heart to initiate an impulse without external stimulus Excitability the ability of cardiac cells to reach a threshold and respond to a stimulus Conducting Cells make up the specialized conduction system in the heart and are responsible for initiating and spreading the electrical impulse. Contracting Cells make up the walls of atria and ventricles and are responsible for contraction of the chambers. Ischemia temporarily interrupts the blood supply to myocardial tissue but usually doesnt cause ECG changes T wave inversion Injury results from prolonged blood supply interruption causes further cell injury ECG changes elevated ST segment Infarction results when failure of perfusion causes myocardial cell death (necrosis) ECG changes pathologic Q wave SA Node Both Atria Delayed in AV node so that atria has time to contract Picks up speed to Purkinje fibers to the ventricular myocardium Pathophysiology Causes Coronary or Atherosclerotic heart disease Coronary or thrombosis or embolism Decreased blood flow with shock or hemorrhage Direct trauma 3 Is ischemia, injury, infarction MI Causes Myocardial Ischemia Decreased Myocardial Oxygen Supply Increased Cellular Hypoxia Altered Cell Membrane Integrity Decreased Myocardial Contractility Decreased Cardiac Output Decreased Arterial Pressure Stimulation of Baroreceptors Stimulation of Sympathetic Baroreceptors

Increased Peripheral Vasoconstriction Increased Afterload Increased Myocardial Oxygen Demand

Increased Myocardial Contractility

Increased Heartrate Decreased Diastolic Filling Decreased Myocardial Tissue Perfusion

Manifestations of MI Chest pain (crushing, severe, prolonged and not relieved by rest or nitroglycerin) Pain Upper cheek Neck and jaw Gastric

Intracapsular Beneath sternum, radiating to the neck and jaw. Beneath sternum radiating down left arm. Epigastric radiating to neck, jaw and arms Left shoulder, inner aspect of both arm Character: tight, heavy, constricting pain associated with restlessness, cold clammy skin Retrosternal area radiates to shoulder, jaw and left arm and sometimes the pain is in epigastric Factors that relieve the pain of infarction is not relieved by nitroglycerin (a coronary vasodilator) Narrowing of epicardial blood vessels due to atherosclerosis Plaque is the most common cause of MI Total occlusion of the blood vessel of more than 4 to 6 hours results to irreversible myocardial necrosis, but reperfusion can salvage the condition Diagnostic Procedures ECG elevated ST segment (initially ok but later turns convex) T wave inversion (refers ischemia) Pathologic Q wave (develops several hours) Plasma Enzymes Diagnostic Monitoring Requirement for Diagnostic Test Sensitive Specific Early rise Prolonged rise Precise Simple and rapid Cheap Enzyme activities are greater in tissue than in plasma Enzyme clear slowly in blood Creatinine Kinase (CK) comprises 3 isoenzymes in myocardium. CPK (CKMB) increased within 3-12 hours of onset, peak at 24 hours, returns to normal level arter 48072 hours, sensitivity is 95% with very high specificity but not as high as troponin levels. Cardiac enzyme analysis CPK elevation within 4-8 hours of MI onset CPK-MB elevation within 4-8 hours of MI onset LDL elevation within 24-48 hours after MI onset LDH1 elevation within 8-24 hours after MI onset LDH1/LDH2 ration > 1 within 24048 hours after MI onset AST (SGOT) elevation within 8-12 hours after MI onset C-reactive Protein a marker of acute inflammation ESR rises within 3 days and remain elevated for several weeks CBC indicated if anemia is suspected as a precipitant Leukocytosis observed within several hours after MI Troponin not an enzyme but a protein. cTnT known as cardiac troponin T (cardiospecific polypeptide), rises within 3-4 hours after Mi and sustained after 10 days or more cTnT cardiac troponin I Nursing Diagnosis Alteration in comfort related to myocardial ischemia Rate the discomfort, assess the presence of discomfort, provide periods of rest Potential for anxiety Provide information regarding diagnosis, diagnostic procedures Alteration in cardiac output: decreased related Initiate cardiac monitoring Coping potential: ineffective related to diagnosis and fear of dying Encourage verbalization of feelings Monitor physiologic parameters closely Knowledge deficit regarding coronary artery disease Assess knowledge base and learning needs Utilize resources in teaching Nursing Interventions Provide oxygen inhalation at 2 L/min Semifowlers position Administer medications Morphine causes respiratory depression, check RR and HR, relaxes bronchioles and enhances respiration

Nitrates Throbolytic agents Anticoagulants Stool softeners Nitroglycerin causes relaxation Vasodilators Beta-adrenergic blocker Analgesic ACE inhibitors Streptokinase Minimize metabolic demands Provide soft diet Decreased cholesterol, decreased fat Provide rest periods Client teaching: METHOD of discharge planning Medication Environmental sanitation Transfer to lower floor Observe right diet Bed rest 1st 3 days ROM exercise Start dangling of feet at side of bed, if not chest pain sitting out of bed on chair for 30 minutes, if no chest pain ambulation in the room, if no chest pain go to comfort room or toilet, if no chest pain can go outside the room to hallway 3x/day, if no chest pain can go to other places, if no chest pain, can have sexual intercourse If patient can walk 3-4 miles/hour ready to resume SI