MI

MYOCARDIAL INFARCTION A Case Study Presented to The Faculty of the College of Nursing Our Lady of Fatima University In Partial Fulfillment of the Requirements for the Degree of Bachelor in Science in Nursing By Natividad, Michelle L. Oclos, Jonalyn A. Pascual, Eduardo Jr. A. Pineda, Wilson T. Planas, Ma. Bhernavette R. Quibod, Rosie Mae P. Ragsac, Elsie U. Ramos, Mary Rose B. Reston, Cindy L. Reyes, Labli Julyet F. Rodriguez Fhrance Benjamin G. Sagabaen Ralph Klein R. Samilin, Richelle L. Sampilo, Alexander B. September 2007 TABLE OF CONTENTS  Introduction  Patient’s Profile  Anatomy and Physiology of the Heart  Pathophysiology  Lab Data Results  Drug Study  Medical Management  Nursing Care Plan  Discharge Summary I. INTRODUCTION Diagram of a myocardial infarction (2) of the tip of the anterior wall of the heart (an apical infarct) after occlusion (1) of a branch of the left coronary artery (LCA, right coronary artery = RCA). Myocardial Infarction (MI) Acute myocardial infarction (AMI or MI), more commonly known as a heart attack, is a medical condition that occurs when the blood supply to a part of the heart is interrupted. The resulting ischemia or oxygen shortage causes damage and potential death of heart tissue. It is a medical emergency, and the leading cause of death for both men and women all over the world. Important risk factors are a previous history of vascular disease such as atherosclerotic coronary heart disease and/or angina, a previous heart attack or stroke, any previous episodes of abnormal heart rhythms or syncope, older age—especially men over 40 and women over 50, smoking, excessive alcohol consumption, the abuse of certain illicit drugs, high triglyceride levels, high LDL ("Lowdensity lipoprotein") and low HDL ("High density lipoprotein"), diabetes, high blood pressure, obesity, and chronically high levels of stress in certain persons. The term myocardial infarction is derived from myocardium (the heart muscle) and infarction (tissue death due to oxygen starvation). The phrase "heart attack" is sometimes used incorrectly to describe sudden cardiac death, which may or may not be the result of acute myocardial infarction. Classical symptoms of acute myocardial infarction include chest pain (typically radiating to the left arm), shortness of breath, nausea, vomiting, palpitations, sweating, and anxiety or a feeling of impending doom. Patients frequently feel suddenly ill. Women often experience different symptoms from men. The most common symptoms of MI in women include shortness of breath, weakness, and fatigue. Approximately one third of all myocardial infarctions are silent, without chest pain or other symptoms. Immediate treatment for suspected acute myocardial infarction includes oxygen, aspirin, glyceryl trinitrate and pain relief, usually morphine sulfate. The patient will receive a number of diagnostic tests, such as an electrocardiogram (ECG, EKG), a chest X-ray and blood tests to detect elevated creatine kinase or troponin levels (these are chemical markers released by damaged tissues, especially the myocardium). Further treatment may include either medications to break down blood clots that block the blood flow to the heart, or mechanically restoring the flow by dilatation or bypass surgery of the blocked coronary artery. Coronary care unit admission allows rapid and safe treatment of complications such as abnormal heart rhythms. The pathogenesis can include:  Occlusive intracoronary thrombus - a thrombus overlying an ulcerated or fissured stenotic plaque causes 90% of transmural acute myocardial infarctions.  Vasospasm - with or without coronary atherosclerosis and possible association with platelet aggregation.  Emboli - from left sided mural thrombosis, vegetative endocarditis, or paradoxic emboli from the right side of heart through a patent foramen ovale. The gross morphologic appearance of a myocardial infarction can vary. Patterns include:  Transmural infarct - involving the entire thickness of the left ventricular wall from endocardium to epicardium, usually the anterior free wall and posterior free wall and septum with extension into the RV wall in 15-30%. Isolated infarcts of RV and right atrium are extremely rare.  Subendocardial infarct - multifocal areas of necrosis confined to the inner 1/3-1/2 of the left ventricular wall. These do not show the same evolution of changes seen in a transmural MI. Gross morphologic changes evolve over time as follows: Time from Onset 18 - 24 Hours 24 - 72 Hours 3 - 7 Days 10 - 21 Days 7 weeks Gross Morphologic Finding Pallor of myocardium Pallor with some hyperemia Hyperemic border with central yellowing Maximally yellow and soft with vascular margins White fibrosis Microscopic morphologic changes evolve over time as follows: Time from Onset 1 - 3 Hours 2 - 3 Hours 4 - 12 Hours 18 - 24 Hours 24 - 72 Hours 3 - 7 Days 10 - 21 Days 7 Weeks Microscopic Morphologic Finding Wavy myocardial fibers Staining defect with tetrazolium or basic fuchsin dye Coagulation necrosis with loss of cross striations, contraction bands, edema, hemorrhage, and early neutrophilic infiltrate Continuing coagulation necrosis, pyknosis of nuclei, and marginal contraction bands Total loss of nuclei and striations along with heavy neutrophilic infiltrate Macrophage and mononuclear infiltration begin, fibrovascular response begins Fibrovascular response with prominent granulation tissue Fibrosis The above gross and microscopic changes over time can vary. In general, a larger infarct will evolve through these changes more slowly than a small infarct. Clinical complications of myocardial infarction will depend upon the size and location of the infarction, as well as pre-existing myocardial damage. Complications can include:          Arrhythmias and conduction defects, with possible "sudden death" Extension of infarction, or re-infarction Congestive heart failure (pulmonary edema) Cardiogenic shock Pericarditis Mural thrombosis, with possible embolization Myocardial wall rupture, with possible tamponade Papillary muscle rupture, with possible valvular insufficiency Ventricular aneurysm formation Sudden death is defined as death occurring within an hour of onset of symptoms. Such an occurrence often complicates ischemic heart disease. Such patients tend to have severe coronary atherosclerosis (>75% lumenal narrowing). Often, a complication such as coronary thrombosis or plaque hemorrhage or rupture has occurred. The mechanism of death is usually an arrhythmia. Risk factors for atherosclerosis are generally risk factors for myocardial infarction:        Older age Male gender Cigarette smoking Hypercholesterolemia (more accurately hyperlipoproteinemia, especially high low density lipoprotein and low high density lipoprotein) Diabetes (with or without insulin resistance) High blood pressure Obesity (defined by a body mass index of more than 30 kg/m², or alternatively by waist circumference or waist-hip ratio). Many of these risk factors are modifiable, so many heart attacks can be prevented by maintaining a healthier lifestyle. Physical activity, for example, is associated with a lower risk profile. Non-modifiable risk factors include age, gender, and family history of an early heart attack (before the age of 60), which is thought of as reflecting a genetic predisposition. Socioeconomic factors such as a shorter education and lower income (particularly in women), and living with a partner may also contribute to the risk of MI. To understand epidemiological study results, it's important to note that many factors associated with MI mediate their risk via other factors. For example, the effect of education is partially based on its effect on income and marital status. Women who use combined oral contraceptive pills have a modestly increased risk of myocardial infarction, especially in the presence of other risk factors, such as smoking. Inflammation is known to be an important step in the process of atherosclerotic plaque formation. C-reactive protein (CRP) is a sensitive but non-specific marker for inflammation. Elevated CRP blood levels, especially measured with high sensitivity assays, can predict the risk of MI, as well as stroke and development of diabetes. Moreover, some drugs for MI might also reduce CRP levels. The use of high sensitivity CRP assays as a means of screening the general population is advised against, but it may be used optionally at the physician's discretion, in patients who already present with other risk factors or known coronary artery disease. Whether CRP plays a direct role in atherosclerosis remains uncertain. Inflammation in periodontal disease may be linked coronary heart disease, and since periodontitis is very common, this could have great consequences for public health. Serological studies measuring antibody levels against typical periodontitis-causing bacteria found that such antibodies were more present in subjects with coronary heart disease. Periodontitis tends to increase blood levels of CRP, fibrinogen and cytokines; thus, periodontitis may mediate its effect on MI risk via other risk factors. Preclinical research suggests that periodontal bacteria can promote aggregation of platelets and promote the formation of foam cells. A role for specific periodontal bacteria has been suggested but remains to be established. Baldness, hair greying, a diagonal earlobe crease and possibly other skin features are independent risk factors for MI. Their role remains controversial; a common denominator of these signs and the risk of MI is supposed, possibly genetic. Symptoms: Rough diagram of pain zones in myocardial infarction (dark red = most typical area, light red = other possible areas, view of the chest). Back view The onset of symptoms in myocardial infarction (MI) is usually gradual, over several minutes, and rarely instantaneous. Chest pain is the most common symptom of acute myocardial infarction and is often described as a sensation of tightness, pressure, or squeezing. Chest pain due to ischemia (a lack of blood and hence oxygen supply) of the heart muscle is termed angina pectoris. Pain radiates most often to the left arm, but may also radiate to the lower jaw, neck, right arm, back, and epigastrium, where it may mimic heartburn. Any group of symptoms compatible with a sudden interruption of the blood flow to the heart are called an acute coronary syndrome. Other conditions such as aortic dissection or pulmonary embolism may present with chest pain and must be considered in the differential diagnosis. Shortness of breath (dyspnea) occurs when the damage to the heart limits the output of the left ventricle, causing left ventricular failure and consequent pulmonary edema. Other symptoms include diaphoresis (an excessive form of sweating), weakness, lightheadedness, nausea, vomiting, and palpitations. Loss of consciousness and even sudden death can occur in myocardial infarctions. Women often experience markedly different symptoms than men. The most common symptoms of MI in women include dyspnea, weakness, and fatigue. Fatigue, sleep disturbances, and dyspnea have been reported as frequently occurring symptoms which may manifest as long as one month before the actual clinically manifested ischemic event. In women, chest pain may be less predictive of coronary ischemia than in men. Approximately half of all MI patients have experienced warning symptoms such as chest pain prior to the infarction. Approximately one fourth of all myocardial infarctions are silent, without chest pain or other symptoms. These cases can be discovered later on electrocardiograms or at autopsy without a prior history of related complaints. A silent course is more common in the elderly, in patients with diabetes mellitus and after heart transplantation, probably because the donor heart is not connected to nerves of the host. In diabetics, differences in pain threshold, autonomic neuropathy, and psychological factors have been cited as possible explanations for the lack of symptoms. What causes a myocardial infarction?  Blockage: The most common cause of an MI is fatty deposits (plaque) inside one or more of the coronary arteries. The disease that causes fatty deposits to narrow arteries in your heart and elsewhere in the body is called atherosclerosis. Atherosclerosis is also called "hardening of the arteries". The fatty deposits may cause your blood vessels to become too narrow, which can cause an MI. However, most MIs happen when a blood clot forms on the rough fatty deposits in a coronary artery, blocking it even more. Spasm: Sometimes a coronary artery can spasm (suddenly tighten) and cause blood flow to be cut off to part of the heart muscle. Most people with coronary artery spasms have fatty deposits as well. It is not known what causes most coronary artery spasms. Some things are known to cause coronary artery spasms, such as cocaine use. Other causes: Other conditions, such as certain heart valve problems, can cause blood clots that may lead to an MI. Sudden and severe (very bad) stress can trigger a heart attack as well. Talk to your caregiver if you have questions about what caused your MI.   II. PATIENT’S PROFILE Patient’s Name: Saguil, Marcelo Age: 34 y/o, Male Address: Talibo St. San Pasual Obando Bulacan Date Admitted: May 29, 2007 Present Working Diagnosis: ACS, MI killips 1 Attending Physician: Dra. Priscila Fortuna / Dr. Orly Deduyo Chief Complaint: Chest Pain History of Present Illness: This is the case of MS, 34 y/o, who came in with the chief complaint of chest pain which started about 3 days prior to admission, characterized as moderate in intensity lasting for about a minute precipitated by physical activity relieved by rest. No other associated signs or symptoms noted like fever, blurring of vision, loss of consciousness, nausea and vomiting. No medication was taken and no consultation was done. Few hours prior to admission, patient still with the above symptoms, associated with difficulty in breathing, consulted a private clinic and was given Vitamin B complex (Neurobion) and was referred to our institution for further evaluation and management and was subsequently admitted. Past Medical History: (-) history of hypertension (-) history of previous hospitalization (-) history of blood transfusion (-) known allergies to foods or drugs (-) history of accidents or injuries (-) known history of diabetes mellitus Family History: Patient denies any heredofamilial disease like hypertension, DM, heart disease, lung disease, cardio vascular disease and cancer and pulmonary tuberculosis. Personal and Social History: Patient is a smoker (22 and  pack years) and an alcoholic beverage drinker. He has food preference like fatty foods and has no regular exercise. Review of System: General: Skin: (-) chills (-) lesion (-) headache (-) fever (-) weight loss (-) rashes (-) hyperpigmentation HEENT: (-) blurring of vision (-) eye pain (-) chest pain (-) palpitation (-) tinnitus (-) diplopia (-) DOB (-) PND Respiratory: (-) hemoptysis Cardio: (-) chest pain (-) shortness of breath (-) orthopnea (-) easy fatigability GIT: (-) constipation (-) abdominal pain GUT: (-) dysuria (-) hematuria MS: Hema: Endo: (-) cramps (-) numbness (-) myalgia (-) joint pain (-) pallor (-) palpitation (-) frequency (-) urgency (-) incontinence (-) diarrhea (-) hematochezia (-) melena (-) easy bruising (-) polyuria (-) bleeding tendencies (-) polyphagia (-) tremor (-) polydipsia (-) hot/cold intolerance Physical Examination: General Survey: Patient is conscious, responded to question, ambulatory, medium built, wellnourished, and not in distress and with the following vital signs: BP = 130/100 mmHg CR = 66bpm RR = 24cpm T = 36.8 0C HEENT: Patient has pink palpebral conjunctiva, anicteric sclerae, no naso-aural discharge, no neck vein engorgement, no tonsilo-pharyngeal congestion, no cervicolymphadenopathy, no carotid bruit noted, (+) neck vein engorgement. Chest and Lungs: Patient has symmetrical chest expansion, no intercostals retractions, no crackles and wheezes noted. Heart: Patient has a dynamic precordium, apex beat at 6 th ICS, LMCL, no heaves, lift, or thrills, normal heart sounds, normal rate, regular rhythm, no murmurs noted. Abdomen: Patient has flabby abdomen, soft with normoactive bowel sounds, non-tender, no bruit, liver, spleen and kidneys are not palpable. Extremities: Patient has grossly normal extremities, with full and equal pulses, no cyanosis, and no edema. Neuro exam: Patient is awake, responsive to question Cranial Nerves: Unremarkable Motor: Right upper extremities = 5/5 Right lower extremities = 5/5 Left upper extremities = 5/5 Left lower extremities = 5/5 Sensory: Both right upper and lower extremities = 100% Both upper and lower extremities = 100% DTR: unremarkable (-) meningial signs (-) Babinsky sign Course in the Ward: On admission, patient still with chest pain, with the following vital signs BP = 130/100 mmHg, CR = 66bpm, RR = 24cpm, Temp. 36.8 0C. He was ordered NPO. Foley catheter was inserted. CBC was done to know if the patient has infection which revealed normal. CBG was done to have a baseline blood sugar which revealed increased (CBG = 139). Urinalysis was done to know if the patient has UTI hematuria (RBC = 0-2) Pyuria (0-2). Mucus thread, blood, and a few protein. Lipid profile was requested to determine liver function. BUN and Creatinine were requested to asses the kidney function which revealed a normal result. PT and PTT were requested to assess blood parameters which revealed an INR 1.01 and activity of 98.02%. Serum electrolytes were done to know if there is an electrolyte imbalance. ECG was done to assess electrical activities of the heart. Chest X-ray was also requested which revealed heart that is enlarged, left ventricular vascular markings are accentuated.CPK-MB revealed a level of 54.7. Troponin-T is negative. Patient was given Aspirin 325 gm tab OD as an antithrombolytic. Pantoprazole (Pantoloc) 40 mg tab OD as a proto pump inhibitor. Morphine 2.5 mg as an analgesic. Isosorbide dinitrate (Isoket) as an anti-angina. Ramipril (Tritace) an ACE inhibitor. Lactulose (Duphalac) a laxative. Later that day Metropolol tartrate (Betaloc) a betablocker and Clodripogel (Plavix) a thrombolytic were started. Vital signs monitored every hour. First hospital day, patient still with chest pain not associated with DOB, BP = 160/100 mmHg. Isosorbide dinitrate (Isoket) was increased. Medications continued. Second hospital day, patient condition still persisted, patient was transferred to the care of a cardiologist. Isosorbide mononitrate (Imdur) was started. Other medications were continued. III. ANATOMY AND PHYSIOLOGY OF THE HEART Location of the Heart The heart is located in the chest between the lungs behind the sternum and above the diaphragm. It is surrounded by the pericardium. Its size is about that of a fist, and its weight is about 250-300 g. Its center is located about 1.5 cm to the left of the midsagittal plane. Located above the heart are the great vessels: the superior and inferior vena cava, the pulmonary artery and vein, as well as the aorta. The aortic arch lies behind the heart. The esophagus and the spine lie further behind the heart. An overall view is given in Figure 1 (Williams and Warwick, 1989). Fig. 1. Location of the heart in the thorax. It is bounded by the diaphragm, lungs, esophagus, descending aorta, and sternum. Fig. 2. The anatomy of the heart and associated vessels. Anatomy of the Heart The walls of the heart are composed of cardiac muscle, called myocardium. It also has striations similar to skeletal muscle. It consists of four compartments: the right and left atria and ventricles. The heart is oriented so that the anterior aspect is the right ventricle while the posterior aspect shows the left atrium (see Figure 2). The atria form one unit and the ventricles another. This has special importance to the electric function of the heart, which will be discussed later. The left ventricular free wall and the septum are much thicker than the right ventricular wall. This is logical since the left ventricle pumps blood to the systemic circulation, where the pressure is considerably higher than for the pulmonary circulation, which arises from right ventricular outflow. The cardiac muscle fibers are oriented spirally (see Figure 3) and are divided into four groups: Two groups of fibers wind around the outside of both ventricles. Beneath these fibers a third group winds around both ventricles. Beneath these fibers a fourth group winds only around the left ventricle. The fact that cardiac muscle cells are oriented more tangentially than radially, and that the resistivity of the muscle is lower in the direction of the fiber has importance in electrocardiography and magnetocardiography. The heart has four valves. Between the right atrium and ventricle lies the tricuspid valve, and between the left atrium and ventricle is the mitral valve. The pulmonary valve lies between the right ventricle and the pulmonary artery, while the aortic valve lies in the outflow tract of the left ventricle (controlling flow to the aorta). The blood returns from the systemic circulation to the right atrium and from there goes through the tricuspid valve to the right ventricle. It is ejected from the right ventricle through the pulmonary valve to the lungs. Oxygenated blood returns from the lungs to the left atrium, and from there through the mitral valve to the left ventricle. Finally blood is pumped through the aortic valve to the aorta and the systemic circulation.. Fig. 3. Orientation of cardiac muscle fibers. Cardiac Muscle Cell In the heart muscle cell, or myocyte, electric activation takes place by means of the same mechanism as in the nerve cell - that is, from the inflow of sodium ions across the cell membrane. The amplitude of the action potential is also similar, being about 100 mV for both nerve and muscle. The duration of the cardiac muscle impulse is, however, two orders of magnitude longer than that in either nerve cell or skeletal muscle. A plateau phase follows cardiac depolarization, and thereafter repolarization takes place. As in the nerve cell, repolarization is a consequence of the outflow of potassium ions. The duration of the action impulse is about 300 ms, as shown in Figure 4 (Netter, 1971). Associated with the electric activation of cardiac muscle cell is its mechanical contraction, which occurs a little later. For the sake of comparison, Figure 5 illustrates the electric activity and mechanical contraction of frog sartorius muscle, frog cardiac muscle, and smooth muscle from the rat uterus (Ruch and Patton, 1982). An important distinction between cardiac muscle tissue and skeletal muscle is that in cardiac muscle, activation can propagate from one cell to another in any direction. As a result, the activation wavefronts are of rather complex shape. The only exception is the boundary between the atria and ventricles, which the activation wave normally cannot cross except along a special conduction system, since a nonconducting barrier of fibrous tissue is present.. DEPOLARIZATION REPOLARIZATION RESTORATION OF IONIC BALANCE Fig. 4. Electrophysiology of the cardiac muscle cell. Fig.5. Electric and mechanical activity in (A) frog sartorius muscle cell, (B) frog cardiac muscle cell, and (C) rat uterus wall smooth muscle cell. In each section the upper curve shows the transmembrane voltage behavior, whereas the lower one describes the mechanical contraction associated with it. The Conduction System of the Heart Located in the right atrium at the superior vena cava is the sinus node (sinoatrial or SA node) which consists of specialized muscle cells. The sinoatrial node in humans is in the shape of a crescent and is about 15 mm long and 5 mm wide (see Figure 6). The SA nodal cells are self-excitatory, pacemaker cells. They generate an action potential at the rate of about 70 per minute. From the sinus node, activation propagates throughout the atria, but cannot propagate directly across the boundary between atria and ventricles, as noted above. The atrioventricular node (AV node) is located at the boundary between the atria and ventricles; it has an intrinsic frequency of about 50 pulses/min. However, if the AV node is triggered with a higher pulse frequency, it follows this higher frequency. In a normal heart, the AV node provides the only conducting path from the atria to the ventricles. Thus, under normal conditions, the latter can be excited only by pulses that propagate through it. Propagation from the AV node to the ventricles is provided by a specialized conduction system. Proximally, this system is composed of a common bundle, called the bundle of His (named after German physician Wilhelm His, Jr., 1863-1934). More distally, it separates into two bundle branches propagating along each side of the septum, constituting the right and left bundle branches. (The left bundle subsequently divides into an anterior and posterior branch.) Even more distally the bundles ramify into Purkinje fibers (named after Jan Evangelista Purkinje (Czech; 1787-1869)) that diverge to the inner sides of the ventricular walls. Propagation along the conduction system takes place at a relatively high speed once it is within the ventricular region, but prior to this (through the AV node) the velocity is extremely slow. From the inner side of the ventricular wall, the many activation sites cause the formation of a wave front which propagates through the ventricular mass toward the outer wall. This process results from cell-to-cell activation. After each ventricular muscle region has depolarized, repolarization occurs. Repolarization is not a propagating phenomenon, and because the duration of the action impulse is much shorter at the epicardium (the outer side of the cardiac muscle) than at the endocardium (the inner side of the cardiac muscle), the termination of activity appears as if it were propagating from epicardium toward the endocardium. Fig. 6. The conduction system of the heart. Because the intrinsic rate of the sinus node is the greatest, it sets the activation frequency of the whole heart. If the connection from the atria to the AV node fails, the AV node adopts its intrinsic frequency. If the conduction system fails at the bundle of His, the ventricles will beat at the rate determined by their own region that has the highest intrinsic frequency. The waveforms of action impulse observed in different specialized cardiac tissue are shown in Figure 7. Fig. 7. Electrophysiology of the heart.The different waveforms for each of the specialized cells found in the heart are shown. The latency shown approximates that normally found in the healthy heart. A classical study of the propagation of excitation in human heart was made by Durrer and his co-workers (Durrer et al., 1970). They isolated the heart from a subject who had died of various cerebral conditions and who had no previous history of cardiac diseases. The heart was removed within 30 min post mortem and was perfused. As many as 870 electrodes were placed into the cardiac muscle; the electric activity was then recorded by a tape recorder and played back at a lower speed by the ECG writer; thus the effective paper speed was 960 mm/s, giving a time resolution better than 1 ms. Figure 8 is redrawn from these experimental data. The ventricles are shown with the anterior wall of the left and partly that of the right ventricle opened. The isochronic surfaces show clearly that ventricular activation starts from the inner wall of the left ventricle and proceeds radially toward the epicardium. In the terminal part of ventricular activation, the excitation wavefront proceeds more tangentially. This phenomenon and its effects on electrocardiogram and magnetocardiogram signals are discussed in greater detail later. Fig. 8. Isochronic surfaces of the ventricular activation. (From Durrer et al., 1970.) IV. PATHOPHYSIOLOGY Causes:  Coronary Atherosclerotic Heart Disease  Coronary Thrombosis/Embolism  Decreased Blood Flow w/ Shock and/or Hemorrhage  Direct Trauma Myocardial Ischemia  Myocardial O2 Supply  Cellular Hypoxia  Cardiac Output  Myocardial Contractility Altered Cell Membrane Int.  Arterial Pressure Baroreceptor Stimulation Sympathetic Receptor Stimulation  Peripheral Vasoconstriction  Afterload  Myocardial Contractility  Heart Rate  Diastolic Filling  Myocardial Tissue Perfusion  Myocardial O2 Demand V. LAB DATA RESULTS A. Diagnostic Exams 1. Chest X-Ray Heart is enlarge, L ventricular markings are accentuated. Impression: Cardiomegaly with pulmonary and congestive changes. 2. ECG Anterior wall MI with D5 V1 – V3 Disposition: Currently admitted B. Laboratory Exams B.1 Blood Lipids EXAMINATION Cholesterol Triglycerides HDL CHOL LDL CHOL B.2 Hematology EXAMINATION WBC Lymphocytes Hemoglobin Hematocrit RBC Platelet Neutrophil Monocytes B.3 Clinical Chemistry EXAMINATION Creatinine Sodium Potassium Calcium Chloride RESULT 73.1 138 3.6 1.15 101 NORMAL VALUE 44 – 97 mmol/L 135 – 145 meq/L 3.50 – 5.0 meq/L 2.15 – 2.5 mmol/L 97 – 107 mmol/L RESULT 10.3 0.22 147 0.43 5.18 217 0.73 0.05 NORMAL VALUE 4.5 – 11 0.25 – 0.35 120 – 150 0.37 – 0.47 4.0 – 5.4 200 – 400 0.40 – 0.75 0.01 – 0.10 RESULT 6.52 mmol/L 0.80 mmol/L 0.68 mmol/L 5.47 mmol/L NORMAL VALUE 3.88 – 6.72 0.56 – 1.69 0.85 – 1.95 1.70 – 4.52 VI. DRUG STUDY DRUG NAME & DOSAGE Generic Name: RAMIPRIL Brand Name: Altace DOSAGE: 10mg PO DRUG CLASS DRUG ACTION INDICATIONS  Treatment of hypertension alone or in combination with thiazide-type diuretics  Treatment of CHF in stable patients in the first few days after MI  To decrease the risk of MI, stroke, death from CV disease in patients at risk for developing CAD ADVERSE EFFECTS  CV: Tachycardia, angina pectoris, MI, Reynaud’s Syndrome, CHF, hypotension in salt or volume-depleted patients,syncope  Rash,pemphigoid like reaction, pruritus, photosensitivity, erythema multiforme, StevenJohnson syndrome  GI: Gastric irritation, aphtous ulcers, dysgeusia, cholestatic jaundice, hepatocellular injury, anorexia, constipation  GU: Protenuria, renal failure, oliguria  Neutropenia, agranulocytosis  Cough, malaise, dry mouth, angioedema NURSING RESPONSIBILITIES  History: Allergy to Ramipril, impaired renal function, CHF, salt or volume depletion  Physical: Skin color,lesions, turgor, T, P, BP, peripheral perfusion, mucous membranes, bowel sounds, liver evaluation tests, CBC and differential Antihypertensive Ace inhibitor Ramipril blocks ACE from converting angiotensin I to angiotensin II,a powerful vasoconstrictor, leading to decreased BP, decreased aldosterone secretion, a small increase in serum potassium levels & sodium & fluid loss; increased prostaglandin synthesis also may be involved in the antihypertensive action. DRUG NAME & DOSAGE Generic Name: LACTULOSE ( laxative ) Brand Name: Chronulac, Constilac, Constulose, Duphalac, Lactulax (CAN) Laxilose (CAN) DOSAGE: 20ml PO DRUG CLASS DRUG ACTION INDICATIONS ADVERSE EFFECTS NURSING RESPONSIBILITIES  GI: Transient flatulence, distention, intestinal cramps, belching, diarrhea, nausea  Acid-base imbalances  History: Allergy to lactulose, lowgalactose diet, diabetes, lactation, pregnancy  Physical: Abdominal examination, bowel sounds, serum electrolytes, serum ammonia levels Laxative The drug passes  Treatment of unchanged into the constipation colon where bacteria  Prevention & break it down to treatment of organic acids that portal-systemic increase the osmotic encephalopathy pressure in the colon & slightly acidify the colonic contents, resulting in an increase in stool water content, stool softening, laxative action. DRUG NAME & DOSAGE DRUG CLASS DRUG ACTION INDICATIONS ADVERSE EFFECTS  Pharyngitis, erythematous rash, fever, sore throat, laryngospasm  Dizziness, vertigo, tinnitus, fatigue, emotional depression, paresthesias, sleep disturbances, hallucinations,memo ry loss  CHF, cardiac arrythmias, peripheral vascular insufficiency, CVA, claudication, pulmonary edema, hypotension  Rash, pruritus, sweating, dry skin  Eye irritation, dry eyes, conjunctivitis, blurred vision  Gastric pain, flatulence, constipation, diarrhea, nausea NURSING RESPONSIBILITIES  History: Sinus Bradycardia ( HR < 45 beats/min ), second or third degree heart block ( PR interval > 0.24sec ), cardiogenic shock, CHF, systolic BP <100mmHg; diabetes or thyrotoxicosis; asthma or COPD; lactation,  Physical: Weight, skin condition, neurologic status, renal & thyroid function tests, blood & urine glucose Generic Name: Beta1-selective METROPOLOL adrenergic TARTRATE blocker antihypertensive Brand Name: Loppressor Injection DOSAGE: Competitively  Hypertension, blocks betaalone or with adrenergic receptors other drugs, in the heart and especially juxtaglomerular diuretics apparatus,  Immediate-release decreasing the tablets & influence of the injection: sympathetic Prevention of nervous system on reinfarction in these tissues & the MI patients who excitability of the are heart, decreasing hemodynamicall cardiac output & the y stable or within release of rennin, & 3-10 days of the lowering BP; acts in acute MI the CNS to reduce  Treatment of sympathetic outflow angina pectoris & vasoconstrictor tone. DRUG NAME & DOSAGE Generic Name: CLOPIDOGREL Brand Name: Plavix DOSAGE: 75 mg DRUG CLASS DRUG ACTION INDICATIONS  Treatment of patients at risk for ischemic events—recent MI, recent ischemic stroke, peripheral artery disease  Treatment of patients with acute coronary syndrome ADVERSE EFFECTS NURSING RESPONSIBILITIES  Headaches, dizziness, weakness, syncope, flushing  Hypertension, edema  Rash, pruritus  Nausea, GI distress, constipation, diarrhea, GI bleed  Increased bleeding risk  History: Allergy to clopidogrel, pregnancy, lactation, bleeding disorders, recent surgery, hepatic impairment, peptic ulcer  Physical: Skin color, T, lesions; orientation, reflexes, affect; P, BP, orthostatic BP, baseline ECG, peripheral perfusion; R, adventitious sounds ADP receptor antagonist Antiplatelet Inhibits platelet aggregation by blocking ADP receptors on platelets, preventing clumping of platelets. DRUG NAME & DOSAGE Generic Name: ISOSORBIDE MONONITRATE Brand Name: Imdur, ISMO, Isotrate ER, Monoket DOSAGE: 20 mg bid PO DRUG CLASS DRUG ACTION INDICATIONS  Prevention of angina pectoris ADVERSE EFFECTS  Headache, apprehension, restlessness, weakness, vertigo, dizziness, faintness  Tachycardia, retrosternal discomfort, palpitations, hypotension, syncope, collapse, orthostatic hypotension, angina, rebound hypertension, atrial fibrillation, postural hypotension  Rash, exfoliative dermatitis, cutaneous vasodilation with flushing  Nausea, vomiting, incontinence, diarrhea  Muscle twitching, pallor, cold sweat NURSING RESPONSIBILITIES  Allergy to nitrates, severe anemia, GI hypermobility, head trauma, cerebral hemorrhage, hypertrophic cardiomyopathy  Skin color, T, lesions; orientation, reflexes, affect, P, BP, orthostatic BP, baseline ECG, peripheral perfusion; R, adventitious sounds; liver evaluation, normal output; CBC, Hgb Antianginal Nitrate Vasodilator Relaxes vascular smooth muscle with a resultant decrease in venous return & decrease in arterial BP, which reduces left ventricular workload & decreases myocardial oxygen consumption VII. MEDICAL MANAGEMENT A heart attack is a medical emergency which demands both immediate attention and activation of the emergency medical services. The ultimate goal of the management in the acute phase of the disease is to salvage as much myocardium as possible and prevent further complications. As time passes, the risk of damage to the heart muscle increases; hence the phrase that in myocardial infarction, "time is muscle," and time wasted is muscle lost. The treatments itself may have complications. If attempts to restore the blood flow are initiated after a critical period of only a few hours, the result is reperfusion injury instead of amelioration. Other treatment modalities may also cause complications; the use of antithrombotics for example carries an increased risk of bleeding. First line Oxygen, aspirin, glyceryl trinitrate (nitroglycerin) and analgesia (usually morphine, hence the popular mnemonic MONA, morphine, oxygen, nitro, aspirin) are administered as soon as possible. In many areas, first responders can be trained to administer these prior to arrival at the hospital. Morphine is the preferred pain relief drug due to its ability to dilate blood vessels, which aids in blood flow to the heart as well as its pain relief properties. Of the first line agents, only aspirin has been proven to decrease mortality. Once the diagnosis of myocardial infarction is confirmed, other pharmacologic agents are often given. These include beta blockers, anticoagulation (typically with heparin), and possibly additional antiplatelet agents such as clopidogrel. These agents are typically not started until the patient is evaluated by an emergency room physician or under the direction of a cardiologist. These agents can be used regardless of the reperfusion strategy that is to be employed. While these agents can decrease mortality in the setting of an acute myocardial infarction, they can lead to complications and potentially death if used in the wrong setting. Reperfusion The concept of reperfusion has become so central to the modern treatment of acute myocardial infarction, that we are said to be in the reperfusion era. Patients who present with suspected acute myocardial infarction and ST segment elevation (STEMI) or new bundle branch block on the 12 lead ECG are presumed to have an occlusive thrombosis in an epicardial coronary artery. They are therefore candidates for immediate reperfusion, either with thrombolytic therapy, percutaneous coronary intervention (PCI) or when these therapies are unsuccessful, bypass surgery. Individuals without ST segment elevation are presumed to be experiencing either unstable angina (UA) or non-ST segment elevation myocardial infarction (NSTEMI). They receive many of the same initial therapies and are often stabilized with antiplatelet drugs and anticoagulated. If their condition remains (hemodynamically) stable, they can be offered either late coronary angiography with subsequent restoration of blood flow (revascularization), or non-invasive stress testing to determine if there is significant ischemia that would benefit from revascularization. If hemodynamic instability develops in individuals with NSTEMIs, they may undergo urgent coronary angiography and subsequent revascularization. The use of thrombolytic agents is contraindicated in this patient subset, however. The basis for this distinction in treatment regimens is that ST segment elevations on an ECG are typically due to complete occlusion of a coronary artery. On the other hand, in NSTEMIs there is typically a sudden narrowing of a coronary artery with preserved (but diminished) flow to the distal myocardium. Anticoagulation and antiplatelet agents are given to prevent the narrowed artery from occluding. At least 10% of patients with STEMI don't develop myocardial necrosis (as evidenced by a rise in cardiac markers) and subsequent q waves on EKG after reperfusion therapy. Such a successful restoration of flow to the infarct-related artery during an acute myocardial infarction is known as "aborting" the myocardial infarction. If treated within the hour, about 25% of STEMIs can be aborted Coronary artery bypass surgery during mobilization (freeing) of the right coronary artery from its surrounding tissue, adipose tissue (yellow). The tube visible at the bottom is the aortic cannula (returns blood from the HLM). The tube above it (obscured by the surgeon on the right) is the venous cannula (receives blood from the body). The patient's heart is stopped and the aorta is cross-clamped. The patient's head (not seen) is at the bottom. Despite the guidelines, emergency bypass surgery for the treatment of an acute myocardial infarction (MI) is less common then PCI or medical management. In an analysis of patients in the U.S. National Registry of Myocardial Infarction (NRMI) from January 1995 to May 2004, the percentage of patients with cardiogenic shock treated with primary PCI rose from 27.4% to 54.4%, while the increase in CABG treatment was only from 2.1% to 3.2%. Emergency coronary artery bypass graft surgery (CABG) is usually undertaken to simultaneously treat a mechanical complication, such as a ruptured papillary muscle, or a ventricular septal defect, with ensueing cardiogenic shock. In uncomplicated MI, the mortality rate can be high when the surgery is performed immediately following the infarction. If this option is entertained, the patient should be stabilized prior to surgery, with supportive interventions such as the use of an intra-aortic balloon pump. In patients developing cardiogenic shock after a myocardial infarction, both PCI and CABG are satisfactory treatment options, with similar survival rates. Coronary artery bypass surgery involves an artery or vein from the patient being implanted to bypass narrowings or occlusions on the coronary arteries. Several arteries and veins can be used, however internal mammary artery grafts have demonstrated significantly better long-term patency rates than great saphenous vein grafts. In patients with two or more coronary arteries affected, bypass surgery is associated with higher long-term survival rates compared to percutaneous interventions. In patients with single vessel disease, surgery is comparably safe and effective, and may be a treatment option in selected cases. Bypass surgery has higher costs initially, but becomes cost-effective in the long term. A surgical bypass graft is more invasive initially but bears less risk of recurrent procedures (but these may be again minimally invasive). Monitoring for arrhythmias Additional objectives are to prevent life-threatening arrhythmias or conduction disturbances. This requires monitoring in a coronary care unit and protocolised administration of antiarrhythmic agents. Antiarrhythmic agents are typically only given to individuals with life-threatening arrhythmias after a myocardial infarction and not to suppress the ventricular ectopy that is often seen after a myocardial infarction. Rehabilitation Cardiac rehabilitation aims to optimize function and quality of life in those afflicted with a heart disease. This can be with the help of a physician, or in the form of a cardiac rehabilitation program. Physical exercise is an important part of rehabilitation after a myocardial infarction, with beneficial effects on cholesterol levels, blood pressure, weight, stress and mood. Some patients become afraid of exercising because it might trigger another infarct. Patients are stimulated to exercise, and should only avoid certain exerting activities such as shovelling. Local authorities may place limitations on driving motorised vehicles. Some people are afraid to have sex after a heart attack. Most people can resume sexual activities after 3 to 4 weeks. The amount of activity needs to be dosed to the patients possibilities. Secondary prevention The risk of a recurrent myocardial infarction decreases with strict blood pressure management and lifestyle changes, chiefly smoking cessation, regular exercise, a sensible diet for patients with heart disease, and limitation of alcohol intake. Patients are usually commenced on several long-term medications post-MI, with the aim of preventing secondary cardiovascular events such as further myocardial infarctions, congestive heart failure or cerebrovascular accident (CVA). Unless contraindicated, such medications may include:  Antiplatelet drug therapy such as aspirin and/or clopidogrel should be continued to reduce the risk of plaque rupture and recurrent myocardial infarction. Aspirin is first-line, owing to its low cost and comparable efficacy, with clopidogrel  reserved for patients intolerant of aspirin. The combination of clopidogrel and aspirin may further reduce risk of cardiovascular events, however the risk of hemorrhage is increased. Beta blocker therapy such as metoprolol or carvedilol should be commenced. These have been particularly beneficial in high-risk patients such as those with left ventricular dysfunction and/or continuing cardiac ischaemia. β-Blockers decrease mortality and morbidity. They also improve symptoms of cardiac ischemia in NSTEMI. ACE inhibitor therapy should be commenced 24–48 hours post-MI in hemodynamically-stable patients, particularly in patients with a history of MI, diabetes mellitus, hypertension, anterior location of infarct (as assessed by ECG), and/or evidence of left ventricular dysfunction. ACE inhibitors reduce mortality, the development of heart failure, and decrease ventricular remodelling post-MI. Statin therapy has been shown to reduce mortality and morbidity post-MI. The effects of statins may be more than their LDL lowering effects. The general consensus is that statins have plaque stabilization and multiple other ("pleiotropic") effects that may prevent myocardial infarction in addition to their effects on blood lipids. The aldosterone antagonist agent eplerenone has been shown to further reduce risk of cardiovascular death post-MI in patients with heart failure and left ventricular dysfunction, when used in conjunction with standard therapies above.    Omega-3 fatty acids, commonly found in fish, have been shown to reduce mortality postMI. While the mechanism by which these fatty acids decrease mortality is unknown, it has been postulated that the survival benefit is due to electrical stabilization and the prevention of ventricular fibrillation. However, further studies in a high-risk subset have not shown a clear-cut decrease in potentially fatal arrhythmias due to omega-3 fatty acids. VIII. NURSING CARE PLAN Background Knowledge Assessment Subjective: ―Masakit ang dibdib ko,‖ as verbalized by the patient. Diagnosis Acute pain related to biologic injury agents Planning Intervention 1. Quantify the pain using a 1-10 scale (1-least severe and 10most severe). 2. Provide oxygen at 2L/minute. 3. Take Vital Signs 4. Perform EKG look for changes in ST segments. 5. Administer Nitrates or Analgesia. 6. Semi-Fowlers position. Rationale Evaluation Pain related to ischemia of Objective: Ischemia, necrosis, EKG changes, aneurysms, dysrhythmias Temp - 36.8 0C RR – 24cpm PR – 66bpm BP – 130/100 mmHg myocardium Blood flow through Patient expected the coronary arteries to state that pain partially or completely block is relieved ↓ Leads to ischemia(insufficient oxygen in the myocardium) ↓ Prolonged ischemia ↓ Leads to irreversible tissue damage ↓ Infarction (necrosis or cell death) ↓ Acute pain GRAVIDOCARDIO A Case Study Presented to The Faculty of the College of Nursing Our Lady of Fatima University In Partial Fulfillment of the Requirements for the Degree of Bachelor in Science in Nursing By Natividad, Michelle L. Navarro, Rinna F. Oclos, Jonalyn A. Pascual, Eduardo Jr. A. Pineda, Wilson T. Planas, Ma. Bhernavette R. Quibod, Rosie Mae P. Ragsak, Elsie U. Ramos, Mary Rose B. Reston, Cindy L. Reyes, Labli Julyet F. Rodriguez Fhrance Benjamin G. Sagabaen Ralph Klein R. Samilin, Richelle L. Sampilo, Alexander B. Silos, Don Anthony T. Valenzuela, Roslyn C, Visto, Marianne V. Vizcayno, Jamie M. September 2007