Chapter i,II,III

Southern Luzon State University College of Allied Medicine Lucban, Quezon

CASE STUDY MYOCARDIAL INFARCTION

Presented to:

Mrs. Lorna Quevedo COAM- Clinical Instructor

PRESENTED BY:

Cuevas, Deanne M. Group 5 BSN IV-B

2010

CHAPTER I A.

OBJECTIVES A.1 GENERAL OBJECTIVES After providing care to the client and conducting a careful and thorough study of the client’s condition, the student will be able to gain knowledge, develop skills and enhance attitude in rendering quality nursing care in actual situation to the patient with diagnosis of MYOCARDIAL INFARCTION. A.2 SPECIFIC OBJECTIVES 1.

Define what Myocardial Infarction is.

2.

Enumerate the clinical manifestations shown by the client.

3.

Trace the pathophysiology of the disease condition.

4.

Establish a therapeutic nurse-patient relationship.

5.

Determine the client’s status through: a.

General and Demographic data

b.

Present History of the Illness

c.

Family Health History

d.

Personal and Social History

e.

Physical Assessment

6. Analyze laboratory results and correlate it with the client’s present condition and manifestations. 7. Familiarize self with the diagnostic procedures done to the patient in determining the present illness. 8. Identify and understand the importance of pharmacological interventions to the patient’s present condition. 9. Render quality nursing care through implementation of nursing care plan. 10. Evaluate the effectiveness of the nursing care plan and medical management.

B. INTRODUCTION The world today is far different from what our ancestors were used to. Today, several innovations and technology emerges creating a new and modern culture far beyond what we know before. This change is accompanied by changes in lifestyle and living of people thus, making us more susceptible to illness brought by our lifestyle. One of these diseases is Myocardial Infarction. Myocardial infarction is a major cause of death and disability worldwide. Coronary atherosclerosis is a chronic disease with stable and unstable periods. During unstable periods with activated inflammation in the vascular wall, patients may develop a myocardial infarction. Myocardial infarction may be a minor event in a lifelong chronic disease, it may even go undetected, but it may also be a major catastrophic event leading to sudden death or severe hemodynamic deterioration. A myocardial infarction may be the first manifestation of coronary artery disease, or it may occur, repeatedly, in patients with established disease. Information on myocardial infarction attack rates can provide useful data regarding the burden of coronary artery disease within and across populations, especially if standardized data are collected in a manner that demonstrates the distinction between incident and recurrent events. From the epidemiological point of view, the incidence of myocardial infarction in a population can be used as a proxy for the prevalence of coronary artery disease in that population. Furthermore, the term myocardial infarction has major psychological and legal implications for the individual and society. It is an indicator of one of the leading health problems in the world, and it is an outcome measure in clinical trials and observational studies. With these perspectives, myocardial infarction may be defined from a number of different clinical, characteristics.

electrocardiographic,

biochemical,

imaging,

and

pathological

CHAPTER II REVIEW OF THE RELATED LITERATURE The term "myocardial infarction" focuses on the heart muscle, which is called the myocardium, and the changes that occur in it due to the sudden deprivation of circulating blood. This is usually caused by arteriosclerosis with narrowing of the coronary arteries, the culminating event being a thrombosis (clot). The main change is death (necrosis) of myocardial tissue. The word "infarction" comes from the Latin "infarcire" meaning "to plug up or cram." It refers to the clogging of the artery, which is frequently initiated by cholesterol piling up on the inner wall of the blood vessels that distribute blood to the heart muscle. Myocardial infarction reflects cell death of cardiac myocytes caused by ischemia, which is the result of a perfusion imbalance between supply and demand. Ischemia in a clinical setting most often can be identified from the patient’s history and from the ECG. Possible ischemic symptoms include various combinations of chest, upper extremity, jaw, or epigastric discomfort with exertion or at rest. The discomfort associated with acute myocardial infarction usually lasts at least 20 min. Often, the discomfort is diffuse, not localized, not positional, not affected by movement of the region, and it may be accompanied by dyspnea, diaphoresis, nausea, or syncope. These symptoms are not specific to myocardial ischemia and can be misdiagnosed and thus attributed to gastrointestinal, neurological, pulmonary, or musculoskeletal disorders. Myocardial infarction may occur with atypical symptoms, or even without symptoms, being detected only by ECG, biomarker elevations, or cardiac imaging. The following prevalence estimates are for people age 18 and older from a survey in 2005: •

Among whites only, 12.0% have heart disease, 6.6% have CHD, 21.0% have hypertension and 2.3% have had a stroke.

•

Among blacks, 10.2% have heart disease, 6.2% have CHD, 31.2% have hypertension and 3.4% have had a stroke.

•

Among Hispanics or Latinos, 8.3% have heart disease, 5.9% have CHD, 20.3% have hypertension and 2.2% have had a stroke.

•

Among Asians, 6.7% have heart disease, 3.8% have CHD, 19.4% have hypertension and 2.0% have had a stroke.

•

Among Native Hawaiians or other Pacific Islanders, 22.4% have hypertension (other prevalence estimates considered unreliable).

Epidemiology and Demographics of ST Elevation MI Myocardial infarction is a common presentation of ischemic heart disease. The World Heart Organization (WHO) estimated in 2002 that, 12.6 percent of deaths worldwide were from ischemic heart disease. Ischemic heart disease is the leading cause of death in developed countries, but third to AIDS and lower respiratory infections in developing countries. Although it is difficult to ascertain the true incidence of ST elevation myocardial infarction (STEMI), according to studies, a conservative estimate is that approximately 500,000 patients suffer STEMI each year. The incidence of STEMI has decreased over time. In an observational study of 5,832 patients spanning from 1975 to 1997, the incidence of STEMI decreased from 171/100,000 to 101/100,000. Risk Factors for ST Elevation Myocardial Infarction Important ST elevation myocardial infarction risk factors are a previous history of vascular disease such as atherosclerotic coronary heart disease and/or angina, a previous heart attack or stroke, advanced age, smoking, the abuse of certain illicit drugs such as cocaine, high LDL ("Low-density lipoprotein") and low HDL ("High density lipoprotein"), diabetes, high blood pressure, obesity and family history of coronary artery disease. Other risk factors for STEMI mirror those for coronary artery disease (CAD) and include diabetes mellitus, cerebrovascular disease manifested by stroke or transient ischemic attack, peripheral arterial disease, aortic atherosclerosis and aneurysm, age (male ≥45 years old, female ≥55 years old), family history of premature CAD (MI or sudden death before age 55 in a first-degree male relative or before age 65 in a firstdegree female relative), tobacco abuse, hypertension and hyperlipidemia. The mortality among patients who suffer STEMI has progressively declined in recent years. From 1975 to 1997, one observational study reported that the in-hospital mortality decreased from 24% to 14%. In the Global Registry of Acute Coronary Events (GRACE), a multinational cohort study that includes 16,814 patients with STEMI were enrolled and followed up in 113 hospitals in 14 countries between 1999 and 2006, inhospital mortality declined from 8.4% in 1999 to 4.6% in 2005. The reason for this decline in mortality is likely multifactorial and includes, but is certainly not limited to, decline in symptom onset-to-presentation time, more widespread

use of primary PCI, improvements in time to reperfusion (door-to-needle and door-toballoon times and improved medical therapy, including increases in the use of evidencebased therapies such as aspirin beta blockers, clopidogrel, statins and angiotension converting enzyme inhibitors or angiotensin receptor blockers. Triggers of ST Elevation Myocardial Infarction A trigger is an activity or environmental condition that produces short-term physiological changes that may lead directly to onset of STEMI. ST elevation myocardial infarction triggers include physical exertion, psychological stress, sexual activity, diurnal (daily) variations in cortisol and platelet aggregation and circannual (yearly) variations in lipids and infectious etiologies, exposure to pollution and or particulate matter, cocaine and ingestion of a recent fatty meal. Frequency United States MI is a leading cause of morbidity and mortality in the United States. Approximately 1.3 million cases of nonfatal MI are reported each year, for an annual incidence rate of approximately 600 cases per 100,000 people. The proportion of patients diagnosed with NSTEMI compared with STEMI has progressively increased. International Cardiovascular diseases account for 12 million deaths annually worldwide. MI continues to be a significant problem in industrialized countries and is becoming an increasingly significant problem in developing countries. Mortality/Morbidity Approximately 500,000-700,000 deaths are caused by ischemic heart disease annually in the United States. One third of patients who experience STEMI die within 24 hours of the onset of ischemia, and many of the survivors experience significant morbidity. For many patients, the first manifestation of coronary artery disease is sudden death likely from malignant ventricular dysrhythmia. •

More than one half of deaths occur in the prehospital setting.

•

In-hospital fatalities account for 10% of all deaths. An additional 10% of deaths occur in the first year postinfarction.

•

A steady decline has occurred in the mortality rate from STEMI over the last several decades. This appears to be due to a combination of a fall in the incidence of MI (replaced in part by an increase in the incidence of unstable angina) and a reduction in the case-fatality rate once an MI has occurred.

Sex A male predilection exists in persons aged 40-70 years. Evidence exists that women more often have MIs without atypical symptoms. The atypical presentation in women might explain the sometimes delayed diagnosis of MIs in women. In persons older than 70 years, no sex predilection exists. Age MI most frequently occurs in persons older than 45 years. Certain subpopulations younger than 45 years are at risk, particularly cocaine users, persons with type 1 diabetes mellitus, patients with hypercholesterolemia, and those with a positive family history for early coronary disease. A positive family history includes any first-degree male relative aged 45 years or younger or any first-degree female relative aged 55 years or younger who experienced a myocardial infarction. In younger patients, the diagnosis may be hampered if a high index of suspicion is not maintained.

CLINICAL History The history is critical in making the diagnosis of MI and sometimes may provide the only clues that lead to the diagnosis in the initial phases of the patient presentation. •

Chest pain, usually across the anterior pericardium is typically described as tightness, pressure, or squeezing.

•

Pain may radiate to the jaw, neck, arms, back, and epigastrium. The left arm is more frequently affected; however, a patient may experience pain in both arms.

•

Dyspnea, which may accompany chest pain or occur as an isolated complaint, indicates poor ventricular compliance in the setting of acute ischemia. Dyspnea may be the patient's anginal equivalent, and, in an elderly person or a patient with diabetes, it may be the only complaint.

•

Nausea, abdominal pain, or both often are present in infarcts involving the inferior or posterior wall.

•

Anxiety

•

Lightheadedness with or without syncope

•

Cough

•

Nausea with or without vomiting

•

Diaphoresis

•

Wheezing

•

Elderly patients and those with diabetes may have particularly subtle presentations and may complain of fatigue, syncope, or weakness. The elderly may also present with only altered mental status. Those with preexisting altered mental status or dementia may have no recollection of recent symptoms and may have no complaints whatsoever.

•

As many as half of MIs are clinically silent in that they do not cause the classic symptoms described above and consequently go unrecognized by the patient. A high index of suspicion should be maintained for MI especially when evaluating women, patients with diabetes, older patients, patients with dementia, and those with a history of heart failure. Patients with a permanent pacemaker in place may confound recognition of STEMI by 12-lead ECG due to the presence of paced ventricular contractions.

Physical Examination The physical examination can often be unremarkable. •

Patients with ongoing symptoms usually lie quietly in bed and appear pale and diaphoretic.

•

Hypertension may precipitate MI, or it may reflect elevated catecholamine levels due to anxiety, pain, or exogenous sympathomimetics.

•

Hypotension may indicate ventricular dysfunction due to ischemia. Hypotension in the setting of MI usually indicates a large infarct secondary to either decreased global cardiac contractility or a right ventricular infarct.

•

Acute valvular dysfunction may be present. Valvular dysfunction usually results from infarction that involves the papillary muscle. Mitral regurgitation due to papillary muscle ischemia or necrosis may be present.

•

Rales may represent congestive heart failure.

•

Neck vein distention may represent pump failure. With right ventricular failure, cannon jugular venous a waves may be noted.

•

Third heart sound (S3) may be present.

•

A fourth heart sound is a common finding in patients with poor ventricular compliance that is due to preexisting heart disease or hypertension.

•

Dysrhythmias may present as an irregular heartbeat or pulse.

•

Low-grade fever is not uncommon.

Causes The most frequent cause of myocardial infarction (MI) is rupture of an atherosclerotic plaque within a coronary artery with subsequent arterial spasm and thrombus formation. Other causes include the following: •

Coronary artery vasospasm

•

Ventricular hypertrophy

•

Hypoxia due to carbon monoxide poisoning or acute pulmonary disorders

•

Coronary artery emboli, secondary to cholesterol, air, or the products of sepsis

•

Cocaine, amphetamines, and ephedrine

•

Arteritis

•

Coronary anomalies, including aneurysms of the coronary arteries

•

Increased afterload or inotropic effects, which increase the demand on the myocardium

•

Aortic dissection, with retrograde involvement of the coronary arteries

•

Although rare, pediatric coronary artery disease may be seen with Marfan syndrome, Kawasaki disease, Takayasu arteritis, progeria, and cystic medial necrosis

Killip Classification The Killip classification is a system used in individuals with an acute myocardial infarction (heart attack), in order to risk stratify them. Individuals with a low Killip class are less likely to die within the first 30 days after their myocardial infarction than individuals with a high Killip class. The study was a case series with unblinded, unobjective outcomes, not adjusted for confounding factors, nor validated in an independent set of patients. The setting was the coronary care unit of a university hospital in the USA. 250 patients were included in the study (aged 28 to 94; mean 64, 72% male) with a myocardial infarction. Patients with a cardiac arrest prior to admission were excluded. Patients were ranked by Killip class in the following way:

•

Killip class I includes individuals with no clinical signs of heart failure.

•

Killip class II includes individuals with rales or crackles in the lungs, an S3 gallop, and elevated jugular venous pressure.

•

Killip class III describes individuals with frank acute pulmonary edema.

•

Killip class IV describes individuals in cardiogenic shock or hypotension (measured as systolic blood pressure lower than 90 mmHg), and evidence of peripheral vasoconstriction (oliguria, cyanosis or sweating).

Conclusions The numbers below were accurate in 1967. Nowadays, they have diminished by 30 to 50% in every class. Within a 95% confidence interval the patient outcome was as follows: •

Killip class I: 81/250 patients; 32% (27–38%). Mortality rate was found to be at 6%.

•

Killip class II: 96/250 patients; 38% (32–44%). Mortality rate was found to be at 17%.

•

Killip class III: 26/250 patients; 10% (6.6–14%). Mortality rate was found to be at 38%.

•

Killip class IV: 47/250 patients; 19% (14–24%). Mortality rate was found to be at 81%. The Killip-Kimball classification has played a fundamental role in classic

cardiology, having been used as a stratifying criterion for many other studies. Worsening Killip class has been found to be independently associated with increasing mortality in several studies. Killip class 1 and no evidence of hypotension or bradycardia, in patients presenting with acute coronary syndrome, should be considered for immediate IV beta blockade.

A.

ANATOMY & PHYSIOLOGY

SIZE, FORM AND LOCATION OF THE HEART The adult heart is shaped like a blunt cone and is approximately the size of a closed fist. It is larger in physically active adults than in less active but otherwise healthy adults, and it generally decreases in size after approximately age 65, especially in those who are not physically active. •

APEX- blunt, rounded point of the cone

•

BASE- larger, flat part at the opposite end of the cone

The heart is located at in the thoracic cavity between the two pleural cavities, which surround the lungs. The heart lies obliquely in the mediastinum, with its base directed posteriorly and slightly superiorly and the apex directed anteriorly and slightly inferiorly. The apex is also directed to the left so that approximately two-thirds of the heart’s mass lies to the left of the midline of the sternum. The base of the heart is located deep to the sternum and extends to the level of the second intercostal space. The apex is located deep to the left fifth intercostal space, approximately 7-9cm. to the

left of the sternum near the midclavicular line, which is perpendicular line that extends down from the middle of the clavicle. ANATOMY OF THE HEART The heart is the muscular organ of the circulatory system that constantly pumps blood throughout the body. Approximately the size of a clenched fist, the heart is composed of cardiac muscle tissue that is very strong and able to contract and relax rhythmically throughout a person's lifetime. The heart has four separate compartments or chambers: •

ATRIUM - upper chamber on each side of the heart -receives and collects the blood coming to the heart. -atrium then delivers blood to the ventricle

•

VENTRICLE- powerful lower chamber -pumps blood away from the heart through powerful, rhythmic contractions. The human heart is actually two pumps in one. The right side receives oxygen-

poor blood from the various regions of the body and delivers it to the lungs. In the lungs, oxygen is absorbed in the blood. The left side of the heart receives the oxygen-rich blood from the lungs and delivers it to the rest of the body. a) Coronary Arteries- network of blood vessels that carry oxygen- and nutrient-rich blood to the cardiac muscle tissue. The blood leaving the left ventricle exits through the aorta, the body’s main artery. Two coronary arteries, referred to as the "left" and "right" coronary arteries, emerge from the beginning of the aorta, near the top of the heart. • left main coronary- initial segment of the left coronary artery -approximately the width of a soda straw and is less than an inch long. -branches into two slightly smaller arteries: the left anterior descending coronary artery and the left circumflex coronary artery. The left anterior descending coronary artery is embedded in the surface of the front side of the heart.

The left circumflex coronary artery circles around the left side of the heart and is embedded in the surface of the back of the heart. Just like branches on a tree, the coronary arteries branch into progressively smaller vessels. The larger vessels travel along the surface of the heart; however, the smaller branches penetrate the heart muscle. The smallest branches, called capillaries, are so narrow that the red blood cells must travel in single file. In the capillaries, the red blood cells provide oxygen and nutrients to the cardiac muscle tissue and bond with carbon dioxide and other metabolic waste products, taking them away from the heart for disposal through the lungs, kidneys and liver. When cholesterol plaque accumulates to the point of blocking the flow of blood through a coronary artery, the cardiac muscle tissue fed by the coronary artery beyond the point of the blockage is deprived of oxygen and nutrients. This area of cardiac muscle tissue ceases to function properly. The condition when a coronary artery becomes blocked causing damage to the cardiac muscle tissue it serves is called a myocardial infarction or heart attack. b) Superior Vena Cava- one of the two main veins bringing de-oxygenated blood from the body to the heart. Veins from the head and upper body feed into the superior vena cava, which empties into the right atrium of the heart. c) Inferior Vena Cava- one of the two main veins bringing de-oxygenated blood from the body to the heart. Veins from the legs and lower torso feed into the inferior vena cava, which empties into the right atrium of the heart. d) Aorta- largest single blood vessel in the body. It is approximately the diameter of your thumb. This vessel carries oxygen-rich blood from the left ventricle to the various parts of the body. e) Pulmonary Artery- vessel transporting de-oxygenated blood from the right ventricle to the lungs. A common misconception is that all arteries carry oxygenrich blood. It is more appropriate to classify arteries as vessels carrying blood away from the heart. f) Pulmonary Vein- vessel transporting oxygen-rich blood from the lungs to the left atrium. A common misconception is that all veins carry de-oxygenated blood. It is more appropriate to classify veins as vessels carrying blood to the heart. g) Right Atrium- receives de-oxygenated blood from the body through the superior vena cava (head and upper body) and inferior vena cava (legs and lower torso).

h) Right Ventricle- receives de-oxygenated blood as the right atrium contracts. i) Left Atrium- receives oxygenated blood from the lungs through the pulmonary vein. j) Left Ventricle- receives oxygenated blood as the left atrium contracts. k) Papillary Muscles- attach to the lower portion of the interior wall of the ventricles. They connect to the chordae tendineae, which attach to the tricuspid valve in the right ventricle and the mitral valve in the left ventricle. The contraction of the papillary muscles opens these valves. When the papillary muscles relax, the valves close. l) Chordae Tendineae- are tendons linking the papillary muscles to the tricuspid valve in the right ventricle and the mitral valve in the left ventricle. As the papillary muscles contract and relax, the chordae tendineae transmit the resulting increase and decrease in tension to the respective valves, causing them to open and close. The chordae tendineae are string-like in appearance and are sometimes referred to as "heart strings." m) Tricuspid Valve- separates the right atrium from the right ventricle. It opens to allow the de-oxygenated blood collected in the right atrium to flow into the right ventricle. It closes as the right ventricle contracts, preventing blood from returning to the right atrium; thereby, forcing it to exit through the pulmonary valve into the pulmonary artery. n) Mitral Value- the left atrium from the left ventricle. It opens to allow the oxygenated blood collected in the left atrium to flow into the left ventricle. It closes as the left ventricle contracts, preventing blood from returning to the left atrium; thereby, forcing it to exit through the aortic valve into the aorta. o) Pulmonary Valve- separates the right ventricle from the pulmonary artery. As the ventricles contract, it opens to allow the de-oxygenated blood collected in the right ventricle to flow to the lungs. It closes as the ventricles relax, preventing blood from returning to the heart. p) Aortic Valve- separates the left ventricle from the aorta. As the ventricles contract, it opens to allow the oxygenated blood collected in the left ventricle to flow throughout the body. It closes as the ventricles relax, preventing blood from returning to the heart.

q) Heart Wall The heart wall is divided into three layers: •

Epicardium- describes the outer layer of heart tissue (from Greek; epi- outer, cardium heart). When considered as a part of the pericardium, it is the inner layer, or visceral pericardium.Its largest constituent is connective tissue and functions as a protective layer. The visceral pericardium apparently produces the pericardial fluid, which lubricates motion between the inner and outer layers of the pericardium.During ventricular contraction, the wave of depolarization moves from endocardial to epicardial surface.

•

Myocardium- muscular middle layer of the wall of the heart. Composed of spontaneously contracting cardiac muscle fibers which allow the heart to contract. Stimulates heart contractions to pump blood from the ventricles and relaxes the heart to allow the artria to receive blood. The walls of the heart are largely made from myocardium, which is a special kind of muscle tissue. This muscle is so constructed that it is able to perform the 60 to 70 contractions which the healthy adult human heart undergoes every minute. It is the muscular tissue responsible for the contraction of the heart

•

Endocardium- innermost layer of tissue that lines the chambers of the heart. Its cells are embryologically and biologically similar to the endothelial cells that line blood vessels.

B.

OVERVIEW OF THE DISEASE Myocardial infarction (MI) or acute myocardial infarction (AMI), commonly known as a heart attack, is the interruption of blood supply to part of the heart, causing some heart cells to die. This is most commonly due to occlusion (blockage) of a coronary artery following the rupture of a vulnerable atherosclerotic plaque, which is an unstable collection of lipids (fatty acids) and white blood cells (especially macrophages) in the wall of an artery. The resulting ischemia (restriction in blood supply) and oxygen shortage, if left untreated for a sufficient period of time, can cause damage or death (infarction) of heart muscle tissue (myocardium). Classification There are two basic types of acute myocardial infarction: •

Transmural: associated with atherosclerosis involving major coronary artery. It can be subclassified into anterior, posterior, or inferior. Transmural infarcts extend through the whole thickness of the heart muscle and are usually a result of complete occlusion of the area's blood supply.

•

Subendocardial: involves small area in the subendocardial wall of the left ventricle, ventricular septum, or papillary muscles. Subendocardial infarcts are thought to be a result of locally decreased blood supply, possibly from a narrowing of the coronary arteries. The subendocardial area is farthest from the heart's blood supply and is more susceptible to this type of pathology. Clinically, myocardial infarction is further subclassified into ST elevation

MI versus non ST elevation MI based on ECG changes. Signs and Symptoms Not all people who have heart attacks experience the same symptoms or experience them to the same degree. Many heart attacks aren't as dramatic as the ones you've seen on TV. Some people have no symptoms at all. Still, the more signs and symptoms you have, the greater the likelihood that you may be having a heart attack. Common heart attack symptoms include: 

Pressure, a feeling of fullness or a squeezing pain in the center of your

chest that lasts for more than a few minutes 

Pain extending beyond your chest to your shoulder, arm, back, or even to

your teeth and jaw



Increasing episodes of chest pain



Prolonged pain in the upper abdomen



Shortness of breath



Sweating



Impending sense of doom



Fainting



Nausea and vomiting

Additional, or different, heart attack symptoms in women may include: 

Abdominal pain or heartburn



Clammy skin



Lightheadedness or dizziness



Unusual or unexplained fatigue

Causes

A heart attack occurs when one or more of the arteries supplying your heart with oxygen-rich blood (coronary arteries) become blocked. Over time, a coronary artery can become narrowed from the buildup of cholesterol. This buildup — collectively known as plaques — in arteries throughout the body is called atherosclerosis. During a heart attack, one of these plaques can rupture and a blood clot forms on the site of the rupture. If the clot is large enough, it can block the flow of blood through the artery. When your coronary arteries have narrowed due to atherosclerosis, the condition is known as coronary artery disease. Coronary artery disease is the major underlying cause of heart attacks. An uncommon cause of a heart attack is a spasm of a coronary artery that shuts down blood flow to part of the heart muscle. A heart attack is the end of a process that typically evolves over several hours. With each passing minute, more heart tissue is deprived of blood and deteriorates or dies. However, if blood flow can be restored in time, damage to the heart can be limited or prevented. Risk Factors

Certain

factors

contribute

to

the

unwanted

buildup

of

fatty

deposits

(atherosclerosis) that narrow arteries throughout your body, including arteries to your heart. You can improve or eliminate many of these risk factors to reduce your chances of having a first or second heart attack.

Heart attack risk factors include:

•

Age. Men who are 45 or older and women who are 55 or older are more likely to have a heart attack than younger men and women.

•

Tobacco. Smoking and long-term exposure to secondhand smoke damage the interior walls of arteries — including arteries to your heart — allowing deposits of cholesterol and other substances to collect and slow blood flow. Smoking also increases the risk of deadly blood clots forming and causing a heart attack.

•

Diabetes. Diabetes is the inability of your body to adequately produce or respond to insulin properly. Insulin, a hormone secreted by your pancreas, allows your body to use glucose, which is a form of sugar from foods. Diabetes can occur in childhood, but it appears more often in middle age and among overweight people. Diabetes greatly increases your risk of a heart attack.

•

High blood pressure. Over time, high blood pressure can damage arteries that feed your heart by accelerating atherosclerosis. The risk of high blood pressure increases as you age, but the main culprits for most people are eating a diet too high in salt and being overweight. High blood pressure can also be an inherited problem.

•

High blood cholesterol or triglyceride levels. Cholesterol is a major part of the deposits that can narrow arteries throughout your body, including those that supply your heart. A high level of the wrong kind of cholesterol in your blood increases your risk of a heart attack. Low-density lipoprotein (LDL) cholesterol (the "bad" cholesterol) is most likely to narrow arteries. A high LDL level is undesirable and is often a result of a diet high in saturated fats and cholesterol. A high level of triglycerides, a type of blood fat related to your diet, also is undesirable. However, a high level of high-density lipoprotein (HDL) cholesterol (the "good" cholesterol), which helps the body clean up excess cholesterol, is desirable and lowers your risk of heart attack.

•

Family history of heart attack. If your siblings, parents or grandparents have had heart attacks, you may be at risk, too. Your family may have a genetic condition that raises unwanted blood cholesterol levels. High blood pressure also can run in families.

•

Lack of physical activity. An inactive lifestyle contributes to high blood cholesterol levels and obesity. People who get regular aerobic exercise have better cardiovascular fitness, which decreases their overall risk of heart attack. Exercise is also beneficial in lowering high blood pressure.

•

Obesity. Obese people have a high proportion of body fat (a body mass index of 30 or higher). Obesity raises the risk of heart disease because it's associated with high blood cholesterol levels, high blood pressure and diabetes.

•

Stress. You may respond to stress in ways that can increase your risk of a heart attack. If you're under stress, you may overeat or smoke from nervous tension. Too much stress, as well as anger, can also raise your blood pressure.

•

Illegal drug use. Using stimulant drugs, such as cocaine or amphetamines, can trigger a spasm of your heart muscle that causes a heart attack.

Test and Diagnosis •

Electrocardiogram (ECG). This is the first test done to diagnose a heart attack. It's often done while you are being asked questions about your symptoms. This test records the electrical activity of your heart via electrodes attached to your skin. Impulses are recorded as "waves" displayed on a monitor or printed on paper. Because injured heart muscle doesn't conduct electrical impulses normally, the ECG may show that a heart attack has occurred or is in progress.

•

Blood tests. Certain heart enzymes slowly leak out into your blood if your heart has been damaged by a heart attack. Emergency room doctors will take samples of your blood to test for the presence of these enzymes.

Additional tests

•

Chest X-ray. An X-ray image of your chest allows your doctor to check the size and shape of your heart and its blood vessels.

•

Echocardiogram. This test uses sound waves to produce an image of your heart. During an echocardiogram, sound waves are directed at your heart from a transducer, a wand-like device, held on your chest. The sound waves bounce off your heart and are reflected back through your chest wall and processed electronically to provide video images of your heart. An echocardiogram can help identify whether an area of your heart has been damaged by a heart attack and isn't pumping normally or at peak capacity.

•

Nuclear scan. This test helps identify blood flow problems to your heart. Small amounts of radioactive material are injected into your bloodstream. Special cameras can detect the radioactive material as it flows through your heart and lungs. Areas of reduced blood flow to the heart muscle — through which less of the radioactive material flows — appear as dark spots on the scan.

•

Coronary catheterization (angiogram). This test can show if your coronary arteries are narrowed or blocked. A liquid dye is injected into the arteries of your heart through a long, thin tube (catheter) that's fed through an artery, usually in your leg, to the arteries in your heart. As the dye fills your arteries, the arteries become visible on X-ray, revealing areas of blockage. Additionally, while the catheter is in position, your doctor may treat the blockage by performing an angioplasty, also known as coronary artery balloon dilation, balloon angioplasty and percutaneous coronary intervention. Angioplasty uses tiny balloons threaded through a blood vessel and into a coronary artery to widen the blocked area. In most cases, a mesh tube (stent) is also placed inside the artery to hold it open more widely and prevent re-narrowing in the future.

•

Exercise stress test. In the days or weeks following your heart attack, you may also undergo a stress test. Stress tests measure how your heart and blood vessels respond to exertion. You may walk on a treadmill or pedal a stationary bike while attached to an ECG machine. Or you may receive a drug intravenously that stimulates your heart similar to exercise.

Stress tests help doctors decide the best long-term treatment for you. If your doctor also wants to see images of your heart while you're exercising, he or she may order a nuclear stress test, which is similar to an exercise stress test, but uses an injected dye and special imaging techniques.

•

Cardiac computerized tomography (CT) or magnetic resonance imaging (MRI). These tests can be used to diagnose heart problems, including the extent

of damage from heart attacks. In a cardiac CT scan, you lie on a table inside a doughnut-shaped machine. An X-ray tube inside the machine rotates around your body and collects images of your heart and chest. In a cardiac MRI, you lie on a table inside a long tube-like machine that produces a magnetic field. The magnetic field aligns atomic particles in some of your cells. When radio waves are broadcast toward these aligned particles, they produce signals that vary according to the type of tissue they are. The signals create images of your heart.

Complications

Heart attack complications are often related to the damage done to the heart during a heart attack. This damage can lead to the following conditions:

•

Abnormal heart rhythms (arrhythmias). If your heart muscle is damaged from a heart attack, electrical "short circuits" can develop resulting in abnormal heart rhythms, some of which can be serious, even fatal.

•

Heart failure. The amount of damaged tissue in your heart may be so great that the remaining heart muscle can't do an adequate job of pumping blood out of your heart. This decreases blood flow to tissues and organs throughout your body and may produce shortness of breath, fatigue, and swelling in your ankles and feet. Heart failure may be a temporary problem that goes away after your heart, which has been stunned by a heart attack, recovers over a few days to weeks. However, it can also be a chronic condition resulting from extensive and permanent damage to your heart following your heart attack.

•

Heart rupture. Areas of heart muscle weakened by a heart attack can rupture, leaving a hole in part of the heart. This rupture is often fatal.

•

Valve problems. Heart valves damaged during a heart attack may develop severe, life-threatening leakage problems.

Treatment

Medications With each passing minute after a heart attack, more heart tissue loses oxygen and deteriorates or dies. The main way to prevent heart damage is to restore blood flow quickly.

Medications given to treat a heart attack include:

•

Aspirin. You may be given aspirin by emergency medical personnel soon after they arrive or as soon as you get to the hospital. Aspirin reduces blood clotting, thus helping maintain blood flow through a narrowed artery.

•

Thrombolytics. These drugs, also called clotbusters, help dissolve a blood clot that's blocking blood flow to your heart. The earlier you receive a thrombolytic drug following a heart attack, the greater the chance you will survive and lessen the damage to your heart.

•

Superaspirins. Doctors in the emergency room may give you other drugs that are somewhat similar to aspirin to help prevent new clots from forming. These include medications such as clopidogrel (Plavix) and others called platelet IIb/IIIa receptor blockers.

•

Other blood-thinning medications. You'll likely be given other medications, such as heparin, to make your blood less "sticky" and less likely to form more dangerous clots. Heparin is given intravenously or by an injection under your skin and is usually used during the first few days after a heart attack.

•

Pain relievers. If your chest pain or associated pain is great, you may receive a pain reliever, such as morphine, to reduce your discomfort.

•

Nitroglycerin. This medication, used to treat chest pain (angina), temporarily opens arterial blood vessels, improving blood flow to and from your heart.

•

Beta blockers. These medications help relax your heart muscle, slow your heartbeat and decrease blood pressure making your heart's job easier. Beta blockers can limit the amount of heart muscle damage and prevent future heart attacks.

•

Cholesterol-lowering medications. Examples include statins, niacin, fibrates and bile acid sequestrants. These drugs help lower levels of unwanted blood cholesterol and may be helpful if given soon after a heart attack to improve survival.

Surgical and other procedures • Coronary angioplasty and stenting. Emergency angioplasty opens blocked coronary arteries, letting blood flow more freely to your heart. Doctors insert a long, thin tube (catheter) that's passed through an artery, usually in your leg, to a blocked artery in your heart. This catheter is equipped with a special balloon tip. Once in position, the balloon tip is briefly inflated to open up a blocked coronary artery. At the same time, a metal mesh stent may be inserted into the artery to keep it open long term, restoring blood flow to the heart. Depending on your condition, your doctor may opt to place a stent coated with a slow-releasing medication to help keep your artery open. Coronary angioplasty is done at the same time as a coronary catheterization (angiogram), a procedure that doctors do first to locate narrowed arteries to the heart. When getting an angioplasty for heart attack treatment, the sooner the better to limit the damage to your heart. •

Coronary artery bypass surgery. In rare cases, doctors may perform emergency bypass surgery at the time of a heart attack. Usually, your doctor may suggest that you have bypass surgery after your heart has had time to recover from your heart attack. Bypass surgery involves sewing veins or arteries in place at a site beyond a blocked or narrowed coronary artery (bypassing the narrowed section), restoring blood flow to the heart. Once blood flow to your heart is restored and your condition is stable following your heart attack, you may be hospitalized for observation. Visitors are usually limited to family members and close friends.

Prognosis The prognosis for patients with myocardial infarction varies greatly, depending on the patient, the condition itself and the given treatment. Using simple variables which are immediately available in the emergency room, patients with a higher risk of adverse outcome can be identified. For example, one study found that 0.4% of patients with a low risk profile had died after 90 days, whereas the mortality rate in high risk patients was 21.1%.

Prevention It's never too late to take steps to prevent a heart attack - even if you've already had one. Taking medications can reduce your risk of a second heart attack and help your damaged heart function better. Lifestyle factors also play a critical role in heart attack prevention and recovery.

Lifestyle changes In addition to medications, the same lifestyle changes that can help you recover from a heart attack can also help prevent future heart attacks. These include: •

Smoking cessation

•

Controlling certain conditions, such as high blood pressure, high cholesterol and diabetes

•

Staying physically active

•

Eating healthy foods

•

Maintaining a healthy weight

•

Reducing and managing stress

CHAPTER III CASE STUDY PROPER

A. GENERAL DATA Name

:

Lorenzo Mendoza

Address

:

Sariaya, Quezon

Birthday

:

March 2, 1945

Birth place

:

Sariaya, Quezon

Age/Sex

:

64 y/o

Religion

:

Roman Catholic

Civil Status

:

Married

Occupation

:

none

Mother

:

Zoraida Cruz

Father

:

Leonardo Mendoza

Admission Date

:

December 2, 2009 10:15am

Admitting Physician

:

Dra. Luce

Case Number

:

09120563

Chief Complaint

:

chest pain PTA

Admitting Diagnosis

:

Unstable Angina

Final Diagnosis

:

Acute Myocardial Infarction

B. HISTORY OF PRESENT ILLNESS Two months prior the admission the patient felt chest pain. He ignored the pain thinking that it will be gone later on. One week prior to admission, the patient felt chest pain that is severe. The pain scale is 8. It is now radiating to his left arm. He also experienced difficulty of breathing. Thus, his family decided to bring him to the hospital in Sariaya, Quezon. The doctor assessed the patient and was referred to the Quezon Medical Center.

C. FAMILY HEALTH HISTORY Lorenzo Mendoza has a family history of Diabetes Mellitus specifically on both his parents. His mother has hypertension and his father died because of a heart attack. D. PAST MEDICAL HISTORY Lorenzo Mendoza was never diagnosed to have any illness previously. His common illnesses were just cough and colds and fever. He was never admitted in the hospital and claims that it was his first time to be confined in the hospital. He also claimed that he has a sedentary and unhealthy lifestyle. E. PSYCHOSOCIAL HISTORY Lorenzo Mendoza is fond of eating fatty foods, drinking alcohol and smoking. Due to his age he also found exercising difficult and very tiring. The patient’s daughter said his father doesn’t have a regular bowel movement. He seldom defecates. Whenever his daughter offers him fruits to help him defecate regularly, he’s just eating a small amount of those and just enjoys himself doing vices and watching television shows. During an ordinary day he usually hangs out with his friends, do some chat and later that day, drinks alcohol or smokes. When he felt that there is something wrong in his body and there is already pain in his chest, his routine changed and decided to eliminate his vices eventually.

F. PHYSICAL EXAMINATION I.

General Survey Lorenzo Mendoza was conscious and coherent, not in respiratory distress

II.

Vital signs DAY 1

DAY 2

DAY 3

DAY 4

DAY 5

DAY 6

DAY 7

DAY 8

TEMPERATURE

36.5°C

37.1°C

36.7°C

36.5°C

36.5°C

36.6°C

36.5°C

36.7°C

RESPIRATORY

32bpm

34bpm

30bpm

32bpm

29bpm

27bpm

25bpm

22bpm

PULSE

78bpm

80bpm

79bpm

75bpm

74bpm

75bpm

74bpm

75bpm

BLOOD PRESSURE

170/110 mmHg

160/100 mmHg

140/90 mmHg

180/120 mmHg

130/90 mmHg

130/90 mmHg

140/90 mmHg

130/90m mHg

III.

Integument

Skin •

The skin is pale and slightly warm to touch. He has a fair skin turgor.

•

The patient has evenly distributed black and white and thick hair.

•

The nails are pale with capillary refill of 2-3 seconds. It has convex

Hair

Nails

curvature and with hard texture. It has intact epidermis. He has long and uncut nails.

IV.

HEENT

Head •

The head is symmetrical with rounded skull contour.

•

Eyebrows are evenly distributed, symmetrically aligned and with good eye

Eyes

movement. •

Eyelashes equally distributed and curled slightly outward.

•

The patient has slightly pinkish conjuctiva. No edema and redness over the lachrymal glands.

•

The pupils are equally reactive to light accommodation and corneal reflex are slightly present.

Ears •

The auricle’s color is same as facial skin with symmetrical in size and shape. It is inline to the outer canthus of the eyes and recoils after it is folded.

•

Cerumen noted on both ears.

•

The nose has the same color as the face.

•

It is symmetrical with nasal septum intact and on midline.

•

There is no redness and swelling noted in the nasal mucosa and no

Nose

discharges noted. Mouth

V.

VI.

VII.

•

The patient has slightly pale lips which is soft and dry texture.

•

The mouth has symmetrical contour.

Neck •

The muscles are equal in size and strength.

•

No scars or palpable mass noted.

•

The thyroid is not visible on inspection.

Thorax and lungs •

The chest is symmetric with skin intact and has uniform temperature.

•

There is clear breath sounds heard on both lung fields upon auscultation.

•

Spine vertically aligned.

•

The patient is in respiratory distress, with elevated RR.

Heart •

The patient has slightly normal rhythm and heart rate is within the normal range.

VIII.

Abdomen •

The patient has soft abdomen upon palpation with no scars noted.

•

Bowel sounds, 9-20 per minute.

•

IX.

Occasional abdominal pain is noted.

Lower Extremities •

The patient has limited range of motion. Large blister noted at left foot.

G. COURSE IN THE WARD

Lorenzo Mendoza is a 64y/o man. He was admitted in QMC’s Medicine Male Cardio Ward on the 2nd day of December 2009, with a chief complaint of chest pain prior to admission. Routine procedures like CBC and urinalysis were done immediately after admission. Dra. Luce as his admitting physician ordered for TPR monitoring every shift. He was hooked with IVF of PNSS 1L x KVO. He was also ordered to have diet as tolerated. The following medications were also ordered: Tramadol 50 mg amp IVP q8 PRN for chest pain and Captopril 250mg 1 tab SL q6 if BP is 140/90mmHG. Exams like ECG, CK-MB, and Prothrombin time were also instructed to be done. On December 3, 2009 the doctor read the ECG result which revealed that there is a poor R-wave progression V1-V3, lateral wall ischemia and LVA by voltage criteria. On December 4, 2009 the result of CK-MB is 142 and was interpreted by Dra. Luce. Same IVF was ordered. On December 5, 2009 Clopidogrel 75mg 4 tabs now then OD, Clexane 0.4 SQ BID, Imidapril 10mg 1 tab OD, Diazepam 5mg 1 tab BID and Aspilet 80mg 1 tab OD were ordered. On December 6, 2009 same IVF was ordered and also Tramadol was given due to severe chest pain. On December 7, same medications was ordered. ECG was repeated. On December 8, 2009 his ECG result was followed up, if vital signs are normal and there is no further complication, possible discharge for the next 2 days.