Incidence of postacute myocardial infarction complications between alcohol users and nonalcohol users

This ex-post facto study examined the medical records of 66 postacute myocardial infarction (MI) men to compare the incidence of potentially life-threatening complications between alcohol users and nonusers. A statistically significant difference was hypothesized between the two groups in the frequency of 1) arrhythmias, 2) congestive heart failure, and 3) emboli. A one-way analysis-of-variance of the data, however, did not support the hypothesis (p > .05), therefore, the alcohol user did not differ from the nonuser at a statistically significant level. Additional findings, however, suggested that the alcohol-using subject would have a more severe heart attack, be younger at the onset of his MI (mean 58-93 years), and tend to be a more active smoker than the nonuser. The nonuser did have some conduction disturbances at a statistically significant level, but this finding may have been due to deterioration of conduction tissue expected in an older population (nonuser, mean age, 66-74). For future studies, this investigation recommended collection of data during the acute MI period and control of some variables, such as age and risk factors. The nursing profession must recognize regular alcohol use as a potentially dangerous problem for individuals, especially those with coronary artery disease. Postacute MI patients should be observed for signs of left ventricular dysfunction, and taught a discerning use of alcohol to avoid further aggravation of heart disease.

THE INCIDENCE OF POSTACUTE MYOCARDIAL INFARCTION COMPLICATIONS BETWEEN ALCOHOL USERS AND NONALCOHOL USERS by Christine Ann Fregulia A thesis submitted to the faculty of The University of Utah in partial fulfillment of the requirements for the degree of Master of Science College of Nursing The University of Utah December 1978 THE CNIVERSITY OF UTAH GRADUATE SCHOOL SUPERVISORY COMMITTEE APPROVAL of a thesis submitted by Christine Ann Fregulia � I have read this thesis and have found it to d ���yJ"£ D' . Chairman. SupervIsory Committee I have read this thesis and have found it to be of satisfactory quality for a master's degree. II-I?·- Date 7<:>:;: Member. Supcnisory C"mmittee I have read this thesis and have found it to, degree. //-/7- 7J Date e of satisfactory quality fo· / . . THE UNIVERSITY OF UTAH GRADUATE SCHOOL FINAL READING APPROVAL To the Graduate Council of The University of Utah: Frequl i a Chr; sti ne Ann \ have read the thesis of in its final form and have found that (\) its format. citations. and bibliographic style are consistent and acceptable; (2) its illustrative materials including figures. tables. and charts are In place; and (3) the final manuscript is satisfactory to the Supervisory Committee and is ready for submission to the Graduate School. � JU Member. Supervl,ory Committee Approved for the MajOf Department - ') ! Chairman Appru\cd tor the r! Graduate Councii James L. De�n l)i The Dean ciaYtO Graduate School _ ABSTRACT This ex-post facto study examined the medical records of 66 postacute myocardial infarction (MI) men to compare the incidence of potentially life-threatening complications between alcohol users and nonusers. A statistically significant difference was hypothesized between the two groups in the frequency of 1) arrhythmias, gestive heart failure, and 3) emboli. 2) con- A one-way analysis-of-variance of the data, however, did not support the hypothesis (~> .05), there- fore, the alcohol user did not differ from the nonuser at a statistically significant level. Additional findings, however, suggested that the alcohol-using subject would have a more severe heart attack, be younger at the onset of his MI (mean 58-93 years), and tend to be a more active smoker than the nonuser. The nonuser did have some conduction disturbances at a statistically significant level, but this finding may have been due to deterioration of conduction tissue expected in an older population (nonuser, mean age, 66-74). For future studies, this investigation recommended collection of data during the acute MI period and control of some variables, such as age and risk factors. The nursing profession must recognize regular alcohol use as a potentially dangerous problem for individuals, especially those with coronary artery disease. Postacute MI patients should be observed for signs of left ventricular dysfunction, and taught a discerning use of alcohol to avoid further aggravation of heart disease. v ACKNOt4LEDGMENTS My appreciation is extended to my committee chairman and members who helped me develop this thesis, especially Marie Holley, who spent much of her personal time supervising my efforts. The chore of, retrieving medical records was facilitated by Cecilia Thompson, Bill James, and Ed Santiones. Carolyn Bennion, my typist, eased my work and worry through her conscientious efforts. 11m grSteful to Maeona Jacobs and Judy Graff, who offered direction and support during my graduate nursing program. Thanks, too, to Liz Close, who helped me write the early chapters and gain insight and confidence in expressing myself. Finally, 11m especially thankful for the knowing patience and gentle encouragement to "hang in there from my parents, friends, ll and Lord. TABLE OF CONTENTS Page ABSTRACT . . . . iv ACKNOWLEDGMENTS vi LIST OF TABLES ix CHAPTERS I II III IV INTRODUCTION . . . . . . . The Purpose of the Study Hypotheses . . . . . 3 REVIEW OF LITERATURE . . . 4 2 The Nature of Alcohol and Its Physiological Effects on the Heart . . . . . . . . . . The Relationship of Alcohol Ingestion to Alcoholic Cardiomyopathy, Coronary Artery Disease, and Myocardial Infarction . . . . . . . . . . . . . . . . The Complications Following a Myocardial Infarction and Their Occurrence in Alcohol Use . . . . . Mechanical Failure Causes . . . . Electrical Failure Causes . Both or Ei ther . . . . . Arrhythmias . . . . . . . . Congestive Heart Failure Embol i . . . . . . . . . . . ...... . The Role of the Nurse With the Alcohol-Using . ... Patient . . 22 METHODOLOGY 25 . . . . 4 7 13 14 14 14 14 17 20 Samp 1e . . . . . . . . . . . . Definition of Terms .. Method of Data Collection Limitations . . . . . . . . . 25 RESULTS AND FINDINGS. 34 Introduction . . . . 34 28 32 32 The Hypotheses Hypothesis 1 Hypothesis 2 . . . . . Hypothesis 3 Ancillary Findings . . . . . . 41 42 SUMMARY AND RECOMMENDATIONS 47 Implications for Nursing 50 A EXAMPLE OF DATA COLLECTION SHEET . 52 B VARIABLES STUDIED . . . . . . . . 54 C CODING USED FOR SPECIFIC VARIABLES . 57 D SIGNIFICANT VARIABLES STUDIED BETWEEN ALCOHOL USERS AND NONUSERS 60 v 34 34 39 APPENDICES REFERENCES . 63 VITA . . . 68 vi;; LIST OF TABLES Table 1. 2. 3. 4. 5. 6. 7. Page Means, Standard Deviations (SO), and Associated F-Ratios Obtained by a One-Way Analysis-of-Variance of Alcohol Users and Nonusers Using the Demographic and Medical History Data Pertaining to the Postacute MI Subjects (!i = 66) . . . . . . . . . . . . . . . . . . . . . . . . . 27 Means, Standard Deviations (SO), and Associated F-Ratios in One-Way Analysis-of-Variance Data Comparing-Postacute Myocardial Infarction Arrhythmias Among Alcohol Users (li = 47) and Nonusers (~ = 19) . . . . . . . . . . . . . . 35 Means, Standard Deviations (SO), and Associated F-Ratios in One-Way Ana1ysis-of-Variance Data Comparing-Postacute Myocardial Infarction Arrhythmias Among Alcohol Users (~ : 47) and Nonusers (~ = 19) . . . . . . . . . . . . 36 Means, Standard Deviations (SO), and Associated F-Ratios in a One-Way Analysis-of-Variance of Data Comparing Postacute MI Congestive Heart Failure and Emboli Among Alcohol Users (~= 47) and Nonusers (~ = 19) . . . . . 40 The Significant Positive and Negative Correlations Found Between Increased Age and the Other Variables from Pearson Product-Moment Correlation. . . . . . . . . . 43 Means, Standard Deviations (SO), and Associated F-Ratios Obtained by a One-Way Analysis-of-Variance Between Alcohol Users (N = 36), Former Users (N = 11, and Nonusers C~L = 19) -: . . . . . . . . . . . -. . . . . . . . 45 The Absolute and Relative (%) Frequencies of Significant Variables Studied Between Alcohol Users and Nonusers . 61 CHAPTER I INTRODUCTION Alcohol, the leading abused substance in the United States, is consumed by 100 million Americans annually. Alcoholic beverages such as beer, wine, and distilled spirits, are highly advertised and readily available products, in spite of increasing evidence of their potentially harmful psychological, physiological, and socioeconomic effects. Chronic or excessive ingestion of alcohol can lead to a dependence on alcohol, known as alcoholism. Ranked fourth in the nation's health problems, alcoholism is associated with each of the three leading diseases: (1) cardiovascular disease, (2) cancer, and (3) mental illness (Burgess, 1973; Keller, 1974; Burkhalter, 1975). This current study evolved from this nurse-investigator's concern for cardiovascular patients, who had suffered an acute myocardial infarction (MI) or heart attack, and had a known history of chronic alcohol abuse. Initially, it was wondered whether or not the chronic alcohol user and/or regular user would have more difficulty in recovering from the acute MI. That is, might the alcohol user with the addi- tional trauma of a heart attack have a greater risk of complication and possible death? In light of alcohol IS questionable deleterious effects on the heart, including structural changes of the myocardium and diminished left ventricular function, this investigator determined 2 that the study of the life-threatening complications following an acute MI in the known alcohol-user would be invaluable to the coronary care nurse. In addition to being attentive to the individual needs of the post-MI patient, the CCU (Coronary Care Unit) nurse attempts to prevent life-threatening conditions. Through her constant vigilance, facilitated by monitoring equipment and her assessment skills, the CCU nurse should intelligently evaluate changes in the health continuum of the MI patient and intervene appropriately. If this study were to identify risk characteristics of the alcohol user who has had aMI, the information would assist the CCU nurse in the anticipation and control of these complications. The life-threatening complications selected were limited to those potentially amenable to nursing intervention: mias, emboli. (2) congestive heart failure, and (1) Major arrhyth- (3) systemic and pulmonary Each of these sequelae will be discussed in the review of literature. High mortality complications, such as cardiogenic shock and cardiac rupture, were considered as additional items and were excluded because of their poor response to current medical regimen. The Purpose of the Study The purpose of this study is to examine the frequency and type of potentially lethal postmyocardial infarction (post-MI) complications of regular alcohol users compared to nonusers. In turn, any relevant information obtained may assist the CCU nurse in the assessment and care of the alcohol-using cardiac patient. Faye 3 Abdellah (1972) advocates the nurse's awareness of various disease entities, when she states the role of the CCU nurse is: to identify new content areas and scientific knowledge in relation to the care of all kinds of cardiovascular patients. (p. 49) If high risk cardiac patients are identified, the effectiveness of available therapy for post-MI complications may be enhanced. Thus, if alcohol users are more susceptible to life-threatening sequelae following a heart attack than nonusers, detection and intervention early in the disease process may prevent further deterioration and death (Kleiger, Martin, Miller, & Oliver, 1975). Hypotheses The hypotheses for this study are: 1. There will be a significant difference between alco- hol users and nonusers in the incidence of life-threatening postacute myocardial infarction arrhythmias. 2. There will be a significant difference between alco- hol users and nonusers in the incidence of postacute myocardial infarction congestive heart failure. 3. There will be a significant difference between alco- hol users and nonusers in the incidence of reported postacute myocardial infarction systemic and pulmonary emboli. CHAPTER II REVIEW OF LITERATURE The research on alcohol and its use has been extensive, especially since the National Institute on Alcohol Abuse and Alcoholism (NIAAA) has funded several multidisciplinary projects. Due to the large quantity of literature, therefore, this survey is limited to recent sources. The four general areas reviewed pertain to: nature and physiological effects of alcohol; (1) The (2) the relationship of alcohol ingestion to alcoholic cardiomyopathy, coronary artery disease (CAD), and myocardial infarction (MI); and (3) MI complications; (4) the role of the nurse with the alcohol-using patient. Since the physiological effects of alcohol are complex and interrelated, this investigator will briefly overview alcohol itself. This background information will help clarify the discussion to follow on alcohol and the cardiovascular system. The Nature of Alcohol and Its Physiological Effects on the Heart Alcohol, also termed ethyl alcohol and ethanol, is derived from the fermentation, or decomposition through the action of microorganisms, of grains and fruits (Fort, 1973). The reaction of a sub- ject to the ingestion of alcohol has a psychological component in that the effect depends upon the subject's underlying personality and what he expects the drink will do for him. 5 However, general physiological response is detenmined by: (1) Types of alcohol, tion, and (2) rate of consumption, (3) rate of absorp- (4) the body weight, tolerance, and blood alcohol level (Fort, 1973). Alcoholic beverages differ in the amount (percentage) of alcohol they contain. In order to raise the blood alcohol level to 0.03%, one could drink either one and one-half ounces of whiskey, five and one-half ounces of wine, or two bottles of beer (Hoff, 1974). A 0.10% concentration is considered to be the legally drunk level. When consumed, alcohol is absorbed into the bloodstream within five minutes and the concentration peaks within one-half to two hours (Wintrobe, Thorne, Adams, Braunwald, Isselbacher, &Petersdorf, 1974). Alcohol, with the enzyme alcohol dehydrogenase, converts to acetylaldehyde in the liver, then enters into (and is speculated to disrupt) some metabolic pathways. Significant effects of alcohol metabolism include the enhancement of the breakdown of carbohydrates and fats, which results, respectively, in hyperglycemia and hyperlipidemia. Initially, alcohol will depress the antidiuretic hormone (ADH), causing diuresis, but not, as once believed, enough to dehydrate the patient. From malnutrition, a condition that actually exists with only a small percentage of alcoholics, and malabsorption of nutrients from alcohol IS alteration of normal digestive processes, important electrolytes and minerals are lost. These include calcium, phosphorous, magnesium, and potassium (Worthington, 1977). Hypomagnesia is a common side effect of pro- longed, heavy alcohol use and is characterized by irritability of skeletal and cardiac muscle. As well as influencing the signs and 6 symptoms seen in alcohol withdrawal, a loss of magnesium is speculated to cause the fibrosis associated with alcoholic cardiomyopathy. This process of fibrosis in the myocardium involves the replacement of healthy contracting tissue with nonfunctional tissue. Thus, the pump- ing muscle of the heart becomes stiffer and less able to eject blood efficiently and effectively. Alcohol has been mistaken as a cardiac stimulant, since it initially increases the heart rate, blood preSSIJre, and cardiac output of the normal heart. However, cardiac catheterization measuring pressures within the atria and ventricles, disputes the stimulant tenet by showing both elevated left ventricular end diastolic pressure (LVEDP) and myocardial oxygen consumption (MV0 2 ) after the ingestion of alcohol. These findings indicate that the ability of the myocardium to contract is decreased due to the depressed cardiac muscle function (Regan, 1972; Hurst, Logue, Schlant, &Wenger, 1974; French, 1976; Stutts, 1977). Normally, the unaffected ventricle will expand to accept a larger venous return then contract forcefully to meet the body's demand for more oxygenated blood. Law. This phenomenon is referred to as Frank-Starling's In the heart exposed to large amounts 9f alcohol, the myocardium is unable to compensate through altering the stroke volume for increased energy needs, and thus becomes a less effective pump. In the past, alcohol was utilized as a vasodilator for peripheral or cardiovascular circulation insufficiencies, such as frostbite or angina. This practice has been questioned. Although one of the deriva- tives of ethanol metabolism, acetylaldehyde, was found to dilate peripheral blood vessels, alcohol itself was reported to be a potent 7 vasoconstrictor (Knott &Beard, 1976). For this reason, as well as the accelerated heart rate associated with alcohol use, the use of alcohol in ischemic vascular diseases is questionable and deserves further study. The Relationship of Alcohol Ingestion to Alcoholic Cardiomyopathy, Coronary Artery Disease, and Myocardial Infarction The cardiac patient was thought to benefit from the occasional use of alcohol, since it was believed to reduce tension, relieve chest pain, improve circulation, and thus enhance his general well-being. Recent studies, however, demonstrate that alcohol could be toxic to the heart muscle (Hurst, et al., 1974; Wintrobe, et al., 1974; Perloff &Whereat, 1976; Regan, Ettinger, Hoider, Ahmed, Oldewartel, & Lyons, 1977). Regan (1972) found that after prolonged (approximately ten years), heavy drinking, an individual could develop alcoholic cardiomyopathy. In this disease of the myocardium, the cellular damage leads to fibrosis and dilatation of the ventricles, diminished heart pump performance, and is manifested by signs and symptoms of congestive heart failure, palpitations, and premature contractions (Hurst, et al., 1974; Knott &Beard, 1976; Chung, 1977). The exact contribution of alcohol to this congestive type cardiomyopathy is uncertain. Perloff and Whereat (1976) offer several speculations, one being that the heart lacks the enzyme, alcohol dehydrogenase, to convert alcohol to its end products. When the liver is unable to break down massive amounts of ethanol through its enzyme systems, the heart muscle could be directly exposed to alcohol IS toxic 8 effects. Postmortem histological studies of the heart of the chronic alcohol abuser show mitochondrial structural damage, destruction of the myofibers, edema, necroses, fibrotic areas, and deposits of glycogen and lipids (Hurst, et al., 1974; Talbott, 1975; Chung, 1977). With injury to the mitochondria, the Ilpowerhouse" of the cell, the energy source, ATP (adenine triphosphate), is less available for the work of myocardial contraction. Alcohol's derivative, acetylaldehyde, is considered to be a myocardial irritant, as well (Hurst, et al., 1974; Perloff & Whereat, 1976; Regan, et al., 1977). The release of the cardiac catecholamine norepinepherine, which occurs with the presence of acetylaldehyde in the blood, may be toxic to the myocardium, as well as a stimulant. On the other hand, the dissipation of norepinepherine and the subsequent loss of its sympathetic action may also contribute to pathological changes in the cardiac muscle (Hurst, et al., 1974). The previously mentioned suggestions as tO,the possible causes for alcoholic cardiomyopathy, illustrate that the association of alcohol and congestive cardiomyopathy is still a speculative field of research. Although etiologies of cardiomyopathy include viral infec- tions, nutriti-onal deficiencies, toxic substances, and metabolic disturbances, current experimental research supports the view that alcohol has a direct effect on cardiac muscle disease and its consequent myocardial dysfunction. The signs and symptoms associated with the early stages of alcohol-related cardiomyopathy include dyspnea on exertion and tachyarrhythmias with ventricular ectopic beats. As the disease progresses, 9 signs of moderate to severe heart failure, that is dilatation, hypertrophy, cardiomegaly, and pulmonary congestion may appear, then advance to pulmonary edema (Hurst, et al., 1974; Chung, 1977). is reversible if the person stops drinking. This condition In the later stages of the disease, however, abstinence will be ineffective (Regan, et al., 1977). Because of the evidence of damage to the myocardium with chronic alcohol ingestion, this researcher expects the chronic alcohol user to have more postacute MI complications. Another issue under consideration is the role alcohol may have in precipitating coronary artery disease and serving as a risk factor for a myocardial infarction. At one time, alcohol was suggested by leading authorities to be one of the risk factors in the atherosclerotic process of coronary artery disease (CAD) (Wilhemson, Widel & Tibblin, 1973; Hurst, et al., 1974; Myrhed, 1974; Lifsic, 1976; Smith, 1977). However, postmortem studies of alcoholics revealed a decreased incidence of the characteristic plaque formation and Coronary artery occlusion (Regan, Wu, Weisse, Moschos, Ahmed &Lyons, 1975; Regan, et al., 1977; Burch &Giles, 1977). The Framingham Heart Study cited the lower incidence of CAD with an individual who consumed a minimum of an ounce of IIhard" liquor daily (Stason, Neff, Meittenen, &Jick, 1976). In research comparing the frequency of nonfatal myocardial infarction between heavy drinkers (greater than six ounces of ethanol per day) and nondrinkers, Stason, et ale (1976) found that the abstainers had the higher incidence. other words, chronic alcohol users were less likely to have an MI. In 10 This finding, however, does not exempt the alcohol user from a heart attack (MI). Barboriak (1977) and others cautioned against the alcohol user assuming a false sense of security. The presence of other risk factors such as smoking, hypertension, and obesity, may make him a candidate for coronary artery d.isease (CAD). CAD, the common precursor of a myocardial infarction, is the process whereby lipid plaques form in the lining of the coronary artery wall, then gradually calcify and narrow the lumen of the vessel. Again, most of the current evidence challenges earlier thinking and studies which suggested a causal relationship between alcohol and CAD. Some studies imply that ethanol actually protects the user from atherosclerosis. Barboriak (1977) established that alcoholics have a high plasma level of alpha density lipoproteins (HDL), which are a combination of lipids and over 50 percent protein. vascular walls. These lipoproteins did not tend to adhere to the By contrast, subjects with coronary artery disease had a hyperlipidemia which consisted of lesser density lipoproteins (very low density lipoproteins, VLDL), which have an atherogenic effect. The Tecumseh Heart Study found a similar inverse relationship between alcohol users and the incidence of coronary artery disease (CAD). However, a group of former drinkers was noted to have a greater evidence of CAD than the current drinkers or nondrinkers. The ra- tionale for this finding was not conclusive, but suggested as causes: Aging, poor health, and possibly some unknown physiological effect from the cessation of regular alcohol use (Keller, 1974). A Swedish project examined the relationship between alcohol consumption and some known risk factors for coronary artery disease. 11 The sample consisted of male monozygote and dizygote twins, who differed in drinking patterns. Some were categorized into a high alcohol (consumption) group (HAG) and others into a low alcohol group (LAG). The HAG had a significant association with heavy smoking, hypertension, and elevated serum levels of glucose and uric acid. No meaningful difference was noted between the groups in weight or levels of serum lipids. However, despite the lack of evidence of excessive CAD or cardiomyopathy in the heavy alcohol group, the HAG did show signs of increased heart volume, palpitations, and an elevated heart rate (Myrhed, 1974). Although recent studies dispute the concept that alcohol was a precipitating factor in CAD, alcohol use in the presence of coronary artery disease is harmful, not a panacea as popularly believed. A glass of wine with dinner or an alcoholic beverage to ease tensions and minimize the chance of chest pain were at one time practices considered therapeutic for some cardiac patients (Lucia, 1971). results challenge these practices. Research The word, however, has not con- vinced many health professionals and consumers. Knott and Beard (1976) stated that unfortunately the use and abuse of the beverage alcohol is so plagued by emotionalism and personal prejudice that investigation and clinical judgments have been compromised. (Knott &Beard, 1976, p. 346) Although alcohol eases the perception of pain with angina pectoris, it does not reverse the ischemia of myocardial tissue that triggered the angina (Orlando, Aronow, Cassidy, & Prakash, 1976). This finding was verified by showing that the ST segment of an electrocardiogram 12 (ECG) taken during an angina attack remained depressed after ethanol consumption. (An ECG tracing with a ST segment depression of 1 mm. or more from a normal baseline is interpreted as myocardial ischemia during stress testing.) Furthermore, Horwitz (1975) cautioned against the cardiac patient resuming physical activity once ingested alcohol has relieved chest pain, since the additional exercise could lead to a MI. If an individual with CAD insists on drinking alcohol, Horwitz advised moderation in usage, as well as resting for two hours after a drink with a meal. This practice would hopefully prevent the masking of ischemia from the combined physiological demands of digestion and exercise. As previously discussed, the alcohol user is subject to myocardial infarction, the disease process where viable heart muscle necroses, usually after blockage of a coronary artery from atherosclerosis (Cheitlin, McAllister &de Castro, 1975). Ischemia, the lack of oxygenated blood, of 20 or more minutes heralds irreversible damage; greater than 60 minutes results in cell death (Meltzer & Dunning, 1972; Sobel, 1974). Regan, et al. (1974) investigated the incidence of MIls in alcoholics without evidence of coronary artery disease. Reganls re- search attributed these atypical MIls to "concentric periarterial fibrosis ll surrounding the coronary artery. This condition restricts the coronary blood flow necessary to meet the oxygen needs of the myocardium. Although a less common phenomenon, an individual can suffer a MI from the imbalance of too little a blood supply available 13 to meet an increased oxygen demand~ Normally, the resting heart re- moves 65 percent of the oxygen from the blood as it flows through the coronary arteries of the heart muscle. Additional oxygen cannot be taken from the blood, with an increased workload, for 65 percent is the maximum portion extracted (Cheitlin, et al., 1975). Therefore, the amount of blood pumped through the coronary arteries must increase to improve the oxygen supply. Thus, although atherosclerotic occlu- sive disease is not evident, an alcohol user may have a MI from constriction of the coronary arteries, secondary to fibrosis of areas of the heart muscle. The preceding discussion reviewed the physiological effects of alcohol on the cardiovascular system, illustrating that alcohol in itself is not a risk factor in CAD, but, nevertheless, can be harmful to the person with ischemic heart disease. The literature suggests metabolic changes and myocardial damage with chronic alcohol use which may lead to atypical MIls and/or a congestive type of cardiomyopathy. This investigator reasons that the regular alcohol user, having experienced a MI, may be more susceptible to post-MI complications. The remainder of this section reviews the post-MI complications under study. and what role alcohol has in eliciting them. The Complications Following a Myocardial Infarction and Their Occurrence in Alcohol Use The complications of a myocardial infarction (MI) are well documented. This is primarily due to the intensive surveillance of cardiac patients since the advent of coronary care units in the early 14 1960's (Meltzer & Dunning, 1972). White (1971) categorizes the potentially lethal post-MI complications under the following two etiologies, mechanical failure and electrical failure: Mechanical Failure Causes (1) (2) (3) (4) Pulmonary edema Congestive heart failure Cardiogenic shock Rupture of the myocardium (a) ventricle (b) interventricular septum (c) papillary muscle Electrical Failure Causes Arrhythmias, all types (a) supraventricular tachyarrhythmias (b) ventricular ectopic arrhythmias (c) bradycardia and systole Both or Either (1) (2) Thromboembolic phenomenon Peripheral origin (White, 1971, p. 6) The focus of the current study is to address those serious post-MI complications responsive to nursing intervention: mias, (2) congestive heart failure, and (1) Major arrhyth- (3) emboli. Arrhythmias Arrhythmia is the term used to categorize a type of cardiac depolarization that differs from the regular rhythm of 60-100 beats 15 per minute initiated by the sinus node, which is known as normal sinus rhythm (Andreoli, Hunn, Zipes, &Wallace, 1968). Changes in rhythm occur from a variety of causes, such as neurohormonal and chemical influences, which may have no adverse effect on the normal heart. However, in the damaged heart, arrhythmias represent serious problems because they alter coronary blood flow. For instance, premature ven- tricular contractions (PVC's) concurrent with a MI indicate an irritable heart muscle and may trigger ventricular fibrillation. Ventricular fibrillation, along with rapid ventricular tachycardia and ventricular systole, are lethal arrhythmias if not treated immediately. They are associated with sudden cessation of cardiac output and blood pressure. Consequently, there is no circulation of oxygenated blood to the vital organs of the body. neurons in the brain will die within four minutes. Without oxygen, Control centers of basic life functions will stop operating; death will ensue. Interestingly, Regan, et al. (1977) and Chung (1977) credit a high number of sudden deaths in young men to lethal arrhythmias from heavy and frequent drinking of alcohol, a characteristic drinking pattern with the young American male. Bigger (1974) cited that 90 percent of the MI patients who are admitted into the CCU experience arrhythmias. The etiology may be either the decreased blood supply from a coronary occlusion leading to elevated lactate levels from anaerobic metabolism, the loss of intracellular potassium into the extracellular fluid, the stimulation of the autonomic nervous system, or from a combination of these. For 16 instance, the sympathetic nervous system normally responds to the diminished cardiac output (the amount of blood pumped per minute) following a myocardial infarction by activating compensatory mechanisms; that is, an increased heart rate and peripheral vasoconstriction. This excitation can lead to tachyarrhythmias and ectopic beats. On the other hand, vagal stimulation, due to parasympathetic activity secondary from pain, may cause a bradycardia. This slow rate often leads to ventricular fibrillation in the first few hours after the onset of an acute myocardial infarction (AMI), from an ectopic beat stimulated by the hypoxic state of the myocardium or the bradyarrhythmias. Another concern in the postacute MI patients' status is the presence of conduction defects. These will be included along with major arrhythmias in the data collection. Conduction defects, are delays in the transmission of electrical impulses through the structures innervating the heart. The dan- gerous blocks include the Mobitz type II, complete heart block, and right bundle branch block (RBBB). A Mobitz type II, which involves a delay in the conduction between the atria and ventricles, can progress to a complete heart block, where there is a dissociation of rate and timing between atrial and ventricular contractions, leading to decreased cardiac output, and possible failure or fibrillation. bundle branch block indicates severe myocardial damage. Right RBBB occurs with the blockage of the left anterior descending coronary artery, the main supplier of oxygenated blood to the left ventricle and the interventricular septum, where important conduction pathways lie. The 17 mortality rate for MI patients with bundle branch blocks is 50 percent greater than without a block. In alcoholic cardiomyopathy, the associated dilatation of the ventricles and suspected stretching of the conduction pathways can lead to an asynchronous contractions of the atria and ventricles. The ventricles are then deprived of additional blood they would normally receive from the atrial contraction. Bundle branch blocks, along with the tachyarrythllli as and PVC IS, are seen wi th alcohol ic cardi omyopathy (Chung, 1977). In summary, the causes of the arrhythmias and conduction defects seen in alcohol use may be due to metabolic disturbances from the loss of nutrients, the loss of electrolytes vital for the electrophysiology of conduction or the process of muscle contraction, the direct toxic effects of alcoholic beverages and/or their additives, and from structural changes evident at the cellular level and more pronounced in the late stages of alcoholic cardiomyopathy. Again, it must be emphasized that arrhythmias and conduction defects in the presence of cardiac disease are potential precursors of dangerous complications, because they can drastically alter cardiac output, and, in turn, diminish oxygenated coronary blood flow to the heart muscle (White, 1971). The arrhythmias credited to acute and chronic alcohol use suggested that alcohol users experiencing an acute MI may be inclined to have more life threatening arrhythmias. Congestive Heart Failure Heart failure results when the heart muscle is unable to pump an adequate amount of blood (Guyton, 1976). The congestion evolves 18 from the backup of blood in the circulatory tree, leading to varying degrees of pulmonary and/or systemic congestion depending upon the ventricle(s) affected. This investigation, however, is more specifi- cally concerned with the failure of the left ventricle, the chamber which ejects the blood into the systemic circulation. The left ventri- cle is the general site of most confirmed MIls, since it is more muscular and vascularized than the right ventricle. Left ventricular failure is manifested by varying degrees of pulmonary congestion. When the pulmonary artery pressure is so elevated that it forces fluid to leak from the bloodstream into the pulmonary tree, if not remedied, acute respiratory distress and possible death may result. After a myocardial infarction, the heart functions at 70 percent of its normal capacity, that is, the cardiac output (CO), is decreased by almost a third. Guyton (1976) plotted changes that take place in cardiac output after an MI. In short, there is an immediate fall in CO, but compensatory mechanisms quickly return the CO to near normal within 30 seconds, through sympathetic stimulation and an increased peripheral resistance to raise the amount of venous return to the right side of the heart. Due to this increased volume of blood flowing into the heart, cardiac output is improved, but right atrial pressure is elevated. If the heart must respond to a workload beyond maintaining baseline body activities at rest, the heart will fail. In an ineffective decompensated state, the impaired left ventricle cannot eject enough blood to maintain the CO, nor handle the increased venous return. Likewise, with the necrosis and injury to the 19 myocardium after a MI, a portion of the left ventricular wall may lose enough contractile tissue to become dyskinetic or akinetic, and further hamper pump performance. In an alcoholic patient, diminished left ventricular function limits an individual's ability to respond to the increased oxygen demands of exercise and stress (Knott &Beard, 1976). studies, Based on recent Smith (1977) commented that although alcoholic cardiomyo- pathy cannot be diagnosed in all drinking cardiac patients, some degree of cardiac injury should be assumed with alcohol use. In alcoholic cardiomyopathy, the left ventricle becomes a poor pump. Mitochondrial damage leads to the ventricle dilating to compensate and create enough force to expel blood from the chamber. An analogy of this concept of compensatory dilatation might be the stretching of a rubber band and the greater force it yields when it rebounds. With an expanded left ventricle, a larger stroke volume would be ejected. However, if this condition persists, a point is reached where dilatation becomes ineffective. The heart muscle is stretched beyond the limit where it can contract forcefully and characteristically becomes enlarged and flabby (Chung, 1977). Some blood remains in the chamber, this added volume increases the pressure already present from the congestion of blood following a poor contraction. The La Place Law illustrates the normal relationship of tension and stretched muscle in the ventricle. The La Place equation, T = P·r , demonstrates that when the chamber's radius(r) increases 2 with dilatation, the tension(T) within the ventricular wall must rise 20 to maintain a given pressure (P) to propel the blood from the ventricle (Hurst, et al., 1974). The energy required to maintain the tension within the contracting myofibers (actin and myosin protein filaments), increases the amount of oxygen needed for myocardial cells, that is, the mycoardia1 oxygen consumption (MV0 2 ). Therefore, even in the resting state in the subject with alcoholic cardiomyopathy, the existing need for more oxygen in an already stressed ventricle, enhances the opportunity for congestive heart failure. The tendency toward poor cardiac reserve following an acute MI and evidenced in cases of alcoholic cardiomyopathy, suggest that the MI patient's chances for congestive heart failure, may be aggravated by regular alcohol use. Emboli An embolus is some type of matter floating in the bloodstream, after being introduced from another site. In a myocardial infarction, an emob1us results from a thrombus thrown off from the atria or ventricles (a mural thrombus), or from a clot usually dislodged from the deep veins of the lower extremities. The evolvement of a thrombus differs from the coagulation process and, in turn, determines the type of medical regimen used (Sherry, 1974). An arterial thrombus forms at the site of an atherosclerotic or endocardial lesion. Platelets adhere to these sites, then fibrin material sets in (Mustard, 1974). A somewhat different process, coagulation, results from the accumulation of clotting factors where there is constriction of the blood vessel or stasis of blood from inactivity, such as, that which occurs in the lower extremities after prolonged bed rest. 21 In this instance, a clot dislodged from the deep veins of the pelvis or legs can eventually occlude a pulmonary artery and cause extensive damage of lung tissue. A pulmonary embolus is potentially lethal if a large portion of necrotic lung tissue is unavailable for perfusion. On the other hand, systemic emboli, which usually result from mural thrombi being propelled from the left side of the heart into the circulation, often go undetected because their manifestations are not as dramatic as those of respiratory distress associated with a pulmonary embolus. For instance, signs observed when a systemic embolus travels to the brain, may range from subtle to quite obvious neurological changes. In alcoholic cardiomyopathy, there is a high incidence (80%) of mural endocardial thrombi, secondary to material forming over fibrosed myocardium, or possibly from clotting in the stagnated blood of grossly dilated ventricles (Regan, et al., 1977). Prior to the review of literature, this investigator had a contrasting view, that the chronic alcohol user would be less susceptible to clot formation. This impression rose from the investigator's knowledge of changes in cell formation and the disruption of the clotting mechanism in liver disease, that are seen with the chronic ingestion of large amounts of alcohol. However, researchers have cited that gross liver disease usually does not occur along with alcoholic cardiomyopathy, and are unable to explain this situation (Regan, 1972; Hurst, et al., 1974). Reasoning from current literature that a certain degree of myocardial damage follows chronic alcohol use, this investigator 22 suspects that there will be a greater incidence of systemic emboli in the alcohol using MI patient, than in the nonuser. As for pulmonary emboli, this researcher has little evidence from literature to suggest a relationship, but speculates that the alcohol user with poor cardiac reserve may be more prone to pulmonary emboli during the convalescent period, since physical activity may not be tolerated as well. That is, prolonged bed rest and minimal exercise can enhance clotting in the peripheral vessels. In conclusion, this investigator reasoned that in light of the cardiac muscle damage and metabolic changes reported with alcohol use, the alcohol user with the additional myocardial injury of a MI may have a greater incidence of life-threatening arrhythmias, congestive heart failure, and systemic and pulmonary emboli, than the nonuser. Current literature supports alcohol's toxicity inthe myocardium and its harmful effect on a person with ischemic heart disease. How- ever, there has been little research on what effect regular alcohol use may have on the acute MI patient. Based on recent literature, alcohol apparently causes arrhythmias and leads to left ventricular dysfunction in acute and chronic use. Likewise, the suspected myo- cardial injury and lowered exercise tolerance with chronic alcohol use, provides the setting for the formation of emboli. The Role of the Nurse With the Alcohol-Using Patient The implications for cardiac nursing are especially significant, if a MI patient's complications are aggravated by regular alcohol use. The CCU nurse could expect a higher incidence of tachyarrhythmias 23 and ventricular ectopics in the known alcohol user, and thus be prepared to initiate the prescribed antiarrhythmic drugs. However, if the patient has already ingested alcohol or is acutely intoxicated, the nurse must be mindful of particular drug incompatabilities with ethanol, such as the antabuse-like hypersensitivity reaction between alcohol and edecrin or certain antibiotics, anticoagulent depression, the additive effect with sedatives and tranquilizers, or the increased sensitivity to digoxin (Horwitz, 1975; Carroll &Becker, 1976; Smith, 1977). Furthermore, in congestive heart failure, the CCU nurse1s prediction that the alcohol user would have a heart compromised to some degree, would make her aware of signs and symptoms of failure. Likewise, she could foresee problems with fluid and electrolyte balance, and would plan to monitor the patient's intake and output, weight, and serum electrolytes. The nurse must consider the effects of alcohol when observing for and treating emboli. In the care of the uncomplicated MI patient, the practitioner supervises the prophylactic regimen, which may consist of anticoagulation with heparin and coumadin, early and progressive physical activity, and the questionable use of elastic stockings. In the alcohol user, especially if alcoholic cardiomyopathy is diagnosed, she may have to modify her approach. Considering the depres- sive effect of alcohol on anticoagulants, the nurse must check prothrombin times regularly to insure that therapeutic doses were given (Carroll & Becker, 1976). In alcoholic cardiomyopathy, strict 24 abstinence from alcohol and prolonged bed rest are usually prescribed. However, inactivity predisposes the MI patient to thrombus formation. With this in mind, if the patient shows signs of poor tolerance to exercise, the nurse modifies the alcohol user1s rehabilitative plan accordingly, to insure minimal activity at a slower progression. Finally, it is hoped that the CCU nurse and medical personnel will assume a more objective attitude toward alcohol use and critically analyze its benefits and potential hazards, then incorporate their knowledge into their health teaching so that the cardiac patient uses alcohol discriminately. CHAPTER III METHODOLOGY This investigator conducted an ex-post facto descriptive study of the medical records for data on the incidence of postacute myocardial infarction complications in alcohol users. approved by the hospital IS This endeavor was Chief of Medical Records and the Univer- sity's Human Subjects' Committee with the stipulation that the names of the patients and the hospital under study would not be disclosed. Sample Patients with the diagnosis of an acute myocardial infarction (MI), who were treated in the coronary care unit (CCU) from January, 1976, through December, 1977, inclusively, were considered as subjects in this retrospective search. A 24-month period was selected to equalize the effect of seasonal changes on the incidence of complications. This researcher then reviewed the hospital records to identify those individuals clearly indicating alcohol use or nonuse. Patients' records without documentation of alcohol use or abstinence were not included in the study, since those patients could not be assumed to be abstinent. A preliminary computer readout of the total number of subjects identified approximately 130 acute MI patients during the two-year period. Hagland and Schuckit (1977) estimated that 47 per- cent of hospital admissions were for alcohol-related problems. 26 Therefore, this investigator planned to match an equal number of alcohol users and nonusers (approximately 50 subjects per group), in age, sex, MI site, and the severity of the MI. The extensiveness of myocardial infarction would be measured by the number of days of chest pain and Ki11up's classification of severity (Hurst, 1974). The limited number of subjects available, however, did not permit this approach. After omitting patients whose records were not available (many having been sent to another facility), or lacked documentation of an acute MI or alcohol habits, this investigator obtained a total of 66 subjects. Of the 66 male subjects, 47 (71.2%) were alcohol users: 36 or 54.5%, of these were current drinkers and 11, or 16.7%, were former drinkers. Nineteen, or 28.8%, were nonusers. Of the total subjects, 16.7% were described as former drinkers, that is, previous alcohol users who had not consumed alcohol regularly for one year or longer. These men were included in the alcohol-user group because of the myocardial changes suggested with alcohol consumption. A comparison of the two groups, that is alcohol users and alcohol nonusers, with regard to demographic data and medical history prior to hospitalization is presented in Table 1. Although the intent was to match subjects in each group with regard to this type of data, it was not possible due to the small sample of postacute MI subjects available during the designated time period. Examination of Table 1 clearly shows that the alcohol using groups were younger (mean age = 58.93) than the nonuser group (mean age = 66.74) resulting in statis- tically significant differences between the groups relative to age (F = 5.391, P < .001). 27 Table 1 Means, Standard Deviations (SO), and Associated F-Ratios Obtained by a One-Way Analysis-of-Variance of Alcohol Users and Nonusers Using the Demographic and Medical History Data Pertaining to the Postacute MI Subjects (~: 66) Alcohol Variables Age (No. of years) Marital Status"" Employment Status"" MI Location"" No. of Chest Pain Days Severity of MI~ Previous No. of MI's CPK Peak (lab values) SGOT Peak (lab values) LOH Peak (Lab values) Expired No. of CCU Days Present Smoker"""" ?ast Smoker*"'" Heredi ty* Serum Cholesterol Cardiac Disease* Respiratory Disease"" C'IA ** DVi** Pulmonary Embo1us** QJD** Gout/Arthritis"""" Cancer*"" Su rgery ITrauma *"" Anem; a ** Cardiomega1y*"" l.1urmur* Ga 11 op'" Ra 1es" JVO"'" Peripheral Edema~ I\bnorma 1 Pctass i um ;NL 35-.:lS) Abnom.a 1 Gl ucose ,: ~l L 100 /~q) NOTE: 58.8298 3.5172 1.3261 3.8222 2.0652 2.6170 .7021 568.000 160.8696 490.1923 .2444 5.6596 .8205 .5333 1.8929 145.2222 3.9630 4.4667 .0425 .0426 .0213 .0851 .1915 .0638 .3904 1.1064 .3617 1.0638 2.3404 .9362 .2553 .1702 10.7872 ~bbreviations e.. = <".05. 11.9370 .9864 .5983 2.9870 1.7989 1. 0120 1.1405 496.2290 119.9145 184.1762 .4346 3.4533 .3888 .5164 2.2000 139.1831 .8077 1.6847 .2040 .2040 .1459 .2821 .3977 .2471 .5224 3.1084 .4857 1.4204 2.0566 .6726 .4408 .3799 19.2206 31.6809 78.4901 Alcohol Nonuser ,1"1 :: 19) Mean SO 66.7363 13.9198 3.4286 .9376 1.2632 .5620 3.2105 3.0107 1.8421 1.5371 1. 6667 1. 0847 .6842 .7493 448.7857 319.2605 164.2500 134.4232 455.4545 289.6585 .0526 .2294 6.5789 2.588 .4372 .2353 .4577 .2667 2.5317 2.1333 54.0000 106.0000 1.2401 3.9167 4.0000 .3746 .1579 .0000 .0000 .0000 .0000 .3153 .1053 .4776 .3158 .2294 .0526 .4956 .3684 3.1530 1.0526 .4776 .3158 T• ~211 2.0088 1.8421 2.0073 .6070 .5789 .3153 .1053 .3684 .4956 6.4737 15.8197 42.5842 defined in Appendix S Appendix C ,.. .. /es :: l/No " I) 'IOTE: Users (N :: 41) Mean SO 107.7487 F-Ratio 5.391 .079 .154 .558 .230 11 .036 .004 .6i3 .006 .194 3.291 1.094 24.874 2.240 .105 1.343 .019 .072 2.594 .319 Level Of Si 9 ni fica nc e £l..'::' .001 ~IS NS NS e...::.. . 001 ~S NS NS NS NS NS e..,::. •001 NS NS 'is NS NS NS :lS .401 NS .065 1.175 .029 .040 .004 .122 .668 .805 4.027 1.818 3.076 .749 NS .213 NS NS rlS NS NS NS NS e...:. .01 NS NS NS NS 28 The mode of the ages was 58 years with a third of the sample over 70 years of age. results. However, two subjects may have distorted the One, a 34 year-old alcohol user had few post-MI complica- tions except for congestive failure and cardiomegaly. The other sub- ject was a 97 year-old man, a nonuser, who experienced some complications which may have been age-related or due to medications taken prior to admission. The two extr~les in ages of the subjects obviously influence the relationships among the variables and will be discussed with the ancillary findings. The alcohol users were also more frequently tobacco smokers than the nonalcohol users (f = 24.874, ~ < .001). In addition, there are differences between the groups relative to the severity of their myocardial infarctions. The alcohol users tended to experience much more severe MIls than did the nonusers (E = 11.036, £ < .001). The groups studied were comparable with regard to the remaining demographic and medical history data shown on Table 1. The frequencies of occur- rences of each item for each group are included in Appendix D. Definition of Terms Several authors referred to the difficulty of conducting a reliable and replicable research on alcohol use, due to the complexity of its psychosocial and physiological effects, the ambiguity of terms used to define the degrees of alcohol consumption (alcoholic, alcohol abuser, heavy drinker, problem drinker, etc.), and the reluctance of subjects to admit to the degree of their alcohol use (Freed, 1976). The criteria for identification of the extent of alcohol consumption must not be limited to What, or how much, the subject ingests. 29 Additional data from the overall assessment of the patient during history taking and the physical exam would provide a more specific picture of the effect of alcohol upon the individual. This investiga- tor depended upon the physician's assessment and systematic documentation of a data base of information for the identification of alcohol users and nonusers (Weed, 1971). Usually, a comment on a patient's drinking habits was available in the record's social or medical history. At the facility under study, the notations on alcohol use were frequently brief, lacked clarity, and hidden within a lengthy narrative. (Likewise, an informal survey of nursing kardexes and histories used in this facility and other local hospitals, revealed little, if any, information on the cardiac patient's alcohol usage.) Descrip- tions of alcohol use ranged from behaviors such as IIdrank barrels a day up to 1952,11 to vague comments such as IIremote alcohol use." Obviously, the bias of the interviewer, the method of questioning, and the reliability of the respondent influence the validity of the interpretations of the extent of alcohol use. Freed (1976) pointed out the difficulty in obtaining a IIhomogenous group in studying drinking patterns. II Therefore, for the purpose of lending some homogeneity to this current study, this researcher used the following definitions: 1. Alcohol user refers to the person who ingested ethanol on a daily or weekly basis in the form of wine, beer, or hard liquor. Alcohol use was established by hospital records indicating quantities of regularity and/or 30 a history of alcohol ingestion, described as social drinker, moderate drinker, heavy drinker, or practicing alcoholic. 2. Former user refers to the subject who had a his- tory of drinking alcoholic beverages on a daily or weekly basis, but had no reported alcohol consumption for one year or more. A former (alcohol) user was identified in the medical records by description, clearly indicating termination of regular alcohol use at least one year prior to his admission. 3. Alcohol nonuser refers to the individual who either - abstained from alcohol ingestion or drank small amounts on a few special occasions, rather than on a weekly or monthly basis. Nonuse will be determined by clear state- ments in the hospital record, such as, abstinence or only a glass of wine at Christmas or at a wedding. 4. Myocardial infarction refers to the process of necrosing cardiac tissue, documented by two of the three following conditions: (1) History, (2) elevated cardiac enzymes, and/or '(3) electrocardiogram (ECG) changes compatible with tissue death and injury such as ST segment or T wave changes, or the presence of Q waves. 5. Postacute myocardial infarction (post-MI) in- cludes that time period directly after the onset of an infarction which, for this study, will be the interim of the patient's stay in the coronary care unit (CCU). That 31 is, the data collection includes the time period from the subject's admission to that of his transfer from the CCU. 6. Complications refers to the previously discussed post-MI sequelae: a. Arrhythmias are changes in heart rate and rhythm from normal sinus rhythm, which are potentially harmful in a diseased heart, since cardiac output is reduced; b. Congestive heart failure (CHF) is the retro- grade f10w of blood into the lungs and/or the circulatory tree due to inadequate pumping of the heart muscle. CHF is evidenced by signs and symptoms of pulmonary congestion and/or systemic congestion, depending on which side of the heart is damaged; c. Emboli are matter floating in the bloodstream such as clots or fat globules, which occlude a blood vessel and cause tissue ischemia or death. Pu1monary emboli originate in the circulatory system, usually the deep veins of the extremities, and may obstruct a pulmonary artery or arteriole causing acute dyspnea. A systemic embolus usually breaks off from mural thrombus adhering to a chamber wall in the left side of the heart, then may block off a systemic artery such as the brachial or cerebral arteries, leading to signs of hypoxia or aroxia of the affected organ or limb. 32 Method of Data Collection According to the established criteria in the definitions, the medical records were coded and sorted into two main groups: users (former and current), and nonusers. alcohol Information was collected in a narrative fornl on the subject's cardiac and health history, the incidence of postacute MI complications during his stay in the CCU, and, finally, the outcome of the MI. of the data collection sheet. See Appendix A for an example The variables selected for study were coded and processed by a computer. See Appendix B for a list of variables and an explanation of the coding system used. The usual standard of measure was the frequency that a variable occurred. How- ever, additional measures of a degree or type of a variable such as arrhythmias, were qualitatively coded for further clarification. The types of disease, signs, and symptoms selected were those most commonly recorded for the individuals under study as shown in Appendix C. Limitations This nurse investigator is aware of the following limitations: 1. The inconsistency within the-medical field defin- ing the degrees of alcohol use; 2. The possibility of incorrect information docu- mented in the medical records; 3. The inability to verify the data in the records; 4. The difficulty of isolating alcohol as a causal factor in the frequency of MI complications in human 33 subjects due to the influence of internal and external environmental factors such as past illnesses and risk factors; 5. The lack of control of prophylactic measures and medical regimen, i.e., medications, which could have aggravated complications; 6. The limited collection of pertinent data, such as frequencies of complications, due to the deaths of 18.2 percent of the subjects. This researcher attempted to rectify some of the limitations by adhering to the definitions described for the respective groups and by documenting significant data, verbatim. CHAPTER IV RESULTS AND FINDINGS Introduction The data were analyzed at the University of Utah Computer Center (UUCC) using a Univac 1108 computer. The Statistical Package for the Social Sciences (SPSS) was used to calculate the descriptive statistics and analysis-of-variance obtained. The University of Utah Computer Center library program FACTOR 300 was also utilized in a regression analysis. at the ~~ The confidence levels were previously established .05 level. This chapter will address the findings related to the research hypotheses and then discuss significant ancillary findings. The Hypotheses Hypothesis 1 Hypothesis 1 proposed a statistically significant difference between alcohol users and nonusers ln the incidence of life threatening postacute myocardial infarction (MI) arrhythmias. The basic tenet was that alcohol users would experience more arrhythmia problems than post MI subjects who were nonusers. Table 2 presents the find- ings from the one-way analysis-of-variance used to test the hypothesis. It clearly shows by the generally low I-ratios that, for most of the arrhythmias recorded in the subjects' medical records, there was not 35 Table 2 Means, Standard Deviations (SO), and Associated F-Ratios Obtained by a One-Way Ana1ysis-of-Variance of A1cohol Users and Nonusers Using the Demographic and Medica1 History Data Pertaining to the Postacute MI Subjects (~ : 66) Type of Arrhythmia S.B. Days AlcOhOl Users = 47) Mean SO --rl!. Alcohol Nonuser Mean- SO F-Ratio Level of Significance (N :z19) .2340 .5976 .4737 1. 1239 1.270 NS S. B. Frequency .5957 1 .3778 .7368 1. 5218 .134 NS S. T. Days .5532 1.0386 .3158 .6710 .845 NS S.T. Frequency .9362 1 .5798 .6316 1.3421 .546 NS PAC Days (No. ) PAC Frequency .3191 .9804 .1579 .3746 .482 NS .3830 .9902 .3684 .9551 .003 NS .1489 .7512 .3158 .3765 .401 NS .1489 .5890 .2105 .9177 .011 NS AF Days (No. ) AF FreqlJency .2979 1.1212 .3158 1.3765 .003 NS .2340 .8133 .2105 .9177 .011 NS SVT Days .0851 .2821 .0000 .0000 .2553 .3961 .0000 .0000 1.1277 1.4981 1.1579 1.0679 .006 NS 1.21281.2672 1.4737 1.3068 .564 NS (No. ) (No. ) Atrial Fl. Days (No. ) Atrial Fl. Frequency (rlo. ) SVT Frequency PVC Days Ulo.) PVC Frequency 'IT Days .2766 .4979 .3158 .5824 . 076 NS VT Frequency .2766 .4979 .4211 .8377 .752 NS Days : ~lo. ) VF Frequency .0851 .2821 .0000 .0000 .1915 .7113 .0000 .0000 (No. ) 'IF NOTE: Abbreviations are explained in Appendix B. 36 Table 3 Means, Standard Deviations (SO), and Associated F-Ratios in One-Way Analysis-of-Variance Data Comparing Postacute r1yocardia1 Infarction Arrhythmias Amonq Alcohol Users (~= 47) and Nonusers (R = 19) Type of Conduction Disturbances 10 AV Block Days Alcohol Users (~ .. 41) Mean Alcohol Nonusers (1" 19) SO Mean SO 3.7158 F-Ratio E. .1915 .5763 1. 1579 l oAV Block Frequency .4255 1.1748 .4211 1.2612 .000 20 AV .0851 .3508 .1053 .3153 .047 NS NS (No.) 3.066 Level of Significance* < .05 NS Block Days (No. ) 20 AV 8lock Frequency .1702 .7015 .2105 .6306 .047 30 AV alack Oays .2340 .8133 .1053 .3153 .446 ~S 3°,d, V Block Frequency .3830 1.0745 .1579 .5015 .761 NS RBBB Days (No.) RBBS Frequency .1277 .4942 1.2532 3.9135 3.891 .3191 1.0238 .4211 1. 2612 .117 .1064 .7293 .6842 2.0562 2.875 .0851 .5835 .4211 1.2612 2.202 (No. ) BBB Days No. ) BBB Frequency 1< .2 < .05 E.. < .05 NS .E. .05 tiS 37 a statistically significant difference in the frequency or number of However, in Table 3, significant findings were arrhythmic days noted. obtained with regard to: (f = 3.891, £ < .05); blocks (LBBB) (f = 2.875, (1) Days of right bundle branch blocks (RBBB) (2) number of days which left bundle branch £ < .05); and number of days reported with first degree atrial ventricular (AV) block (f = 3.066, £ < .05). Con- trary to what was expected, the nonusers of alcohol experienced significantly more difficulty relative to these conduction disturbances. Two subjects with histories of prior myocardial infarctions had 9 and 15 days of RBBB, respectively. RBBB is a common occurrence following an acute MI, especially when there is evidence of occlusion of the left anterior descending (LAD) coronary artery. Extensive LAD block- age was verified in one of the subjects at an autopsy. The bundle branch block described in alcoholic cardiomyopathy may indicate that RBBB would only be evident in cases of long-term chronic alcohol abuse. A comparative study of different degrees and lengths of time of alcohol consumption and the incidence of postacute MI arrhythmias and conduction defects might be more descriptive. Right bundle branch block (RBBB) may have existed prior to the subject's MI, since individuals with MIls or cardiac disease, evident prior to the current study, were not excluded. Likewise, left bundle branch block (LBBB), which leads to the delayed stimulation of the left ventricle, has been found to exist before a heart attack in 85 percent of acute MI patients (Fowler, 1976). The use of past medical records limits investigation of the possibility of prior existence of some arrhythmias. First degree AV block, which is the 38 delayed conduction of an electrical impulse between the atria and ventricles beyond the normal two-tenth second PR interval, may have been associated with the use of cardiogenic drugs, such as digoxin, which is known to prolong the atrioventricular conduction time. Finally, the presence of these conduction defects in the nonusers who were generally an older group (mean age = 66.74), may be indicative of some degeneration of conductive tissue related to the aging process. The data suggest that the two groups were comparable with regard to experiencing other types of arrhythmias. The data in Table 3 also shows that in spite of the increased incidence of conductive defects, the nonusers experienced more normal sinus rhythm than did the alcohol users (~ = 3.738, J: < .05). The increased incidence of normal sinus rhythm (NSR) in the nonuser, that is, the absence of arrhythmias, could indicate less chemical and structural changes following a heart attack in the individual who does not consume alcoholic beverages on a regular basis. Generally, however, the analysis of the data obtained from the hospital records did not support Hypothesis 1. It may be premature to conclude that the alcohol users were more advantaged with regard to post-MI arrhythmias and conduction disturbances without first considering the mortality data for each group. Eight subjects in the alcohol-using group, as well as three former users, died during the immediate postacute MI period. one subject, who had not used alcohol, expired. However, only These deaths, soon after the onset of an MI, tended to distort the number and frequency 39 of complications recorded, e.g., arrhythmias, congestive heart failure, and embolism. The short time period involved for observation and ac- curate documentation reduced the potential for recordings of lengthy periods (days and frequencies) of complications. Hypothesis 2 Hypothesis 2 proposed a significant difference in the incidence of postacute myocardia 1 infarct i on congest i ve hea rt fa i 1ure between alcohol users and nonusers. The findings relevant to the test of this hypothesis are shown in Table 4. The incidence of con- gestive heart failure is slightly greater among the alcohol-using group although the difference is not statistically significant (£ = 1.506, £ > .05). Therefore, the analysis of data obtained does not support the hypothesis at a statistically significant level. These findings somewhat conflict with the changes in left ventricular function suggested in the literature (Hurst, et al, 1974; Regal, et al; 1977). The left ventricular dysfunction cited in the research studies has been observed following the ingestion of ethanol in normal subjects, as well as in chronic alcohol abusers who regularly consume excessive amounts of alcohol to the extent of causing physiological or behavioral changes. Twenty-eight percent of the alcohol users in this study were reported in the medical records to be alcoholics or alcohol abusers. The remainder apparently consumed alcohol regularly, but-in varying amounts. Thus, the alcohol consumption may not be of a sufficient amount to lead to structural changes in the Table 4 Means, Standard Deviations, and Associated F-ratios in a One-Way Analysis of Variance of Data Comparing Postacute MI-Congestive Heart Failure and Emboli Among Alcohol Users (~ = 47) and Nonusers (~= 19) Alcohol Users Nonusers F-Ratio Mean SD Mean SD Congestive Heart Failure .8511 .8335 .5789 .7685 1.506 Emboli .2340 .7861 .0526 .2294 .970 Level of Significance ~ a 41 myocardium. Likewise, even if mild degrees of cardiomyopathy do exist with regular alcohol use, diminished cardiac output may be compensated by physiological neurohormonal responses and thus not necessarily lead to signs of congestive failure. Interestingly, a significant difference between groups was noted in the existence of rales (I = 4.027, Q < .05). Rales usually reflect a mild degree of congestive heart failure, but may also be a sign of pulmonary congestion secondary to pneumonia or pulmonary fibrosis. Rales, the crackling sound auscultated usually over the lung bases, is indicative of fluid having seeped into the alveoli from the bloodstream. However, as previously mentioned, no significant difference was found between the two groups in the reported cases of congestive heart failure. The reason for the existence of rales not being interpreted as a sign of congestive heart failure may have evolved from the physician1s uncertainty of the etiology of the rales, since other respiratory conditions may manifest this sign. Hypothesis 3 Hypothesis 3 proposed a statistically significant difference in the incidence of reported postacute MI systemic and/or pulmonary emboli between alcohol users and nonusers. No significant difference was evident between alcohol users and nonusers in the occurrence of recorded pulmonary and/or systemic emboli as reflected in the findings of Table 4 (~= 1.506, £> cases of reported emboli. .05). The nonuser group did not have any Only three subjects, alcohol users, had documented pulmonary emboli. Usually, the incidence of emboli is : I i . i 42 approximately 8 percent following an MI. This percentage includes patients in their convalescent period outside of the coronary care unit (CCU). Of the total sample of this study, the 5 percent in- cidence of emboli may not only reflect a shorter period of observation due to the high mortality rate within the alcohol-using group and the average 5-6 day CCU stay, but also the effects of prophylactic anticoagulants and early physical activity, which are incorporated into the medical regimen of the patient to diminish clot formation. A larger sample observed over a longer convalescent period may be revealing. Likewise, as previously mentioned in relation to conges- tive heart failure, the unknown range of alcohol consumption within the alcohol users may bias the results. Ancillary Findings With regard to the sex variability of the sample, all the subjects were men. Therefore, the results of this study may be generaliz- able only to men. As previously mentioned, the index of age of the subjects were significantly different between the two groups ([ = 5.391, ~ < .001). Unfortunately, the ages of two subjects, each in different groups (one, 34 years of age, an alcohol user, the other, 97 years old, a nonuser), may have skewed the results relative to the total sample, so that findings may not be representative of postacute MI men. Table 5 depicts the significant position and negative relationship between the ages of the subjects and some other variables under study. tions obtained seemed reasonable for advancing age. The correla- 43 Ta b1e 5 The Significant Positive and Negative Correlations Found Between Increased Age and the Other Variables From Pearson ProductMoment Correlation Variables Nonuser S.B. Days lOAV Block Days RBBB Days Normal Sinus Rhythm Employment Status Alcoholism - Alcohol Abuse Murmurs Obesity lOAV Block Frequency Present Smoker CVA Documented Stress *.e. % <.05. Correlation (r) 0.28 0.28 0.28 0.28 0.28 -0.28 -0.28 0.33 -0.33 0.34 -0.34 0.37 -0.40 Level of Significance* .E < .05 E.< E. < £< £ < £< £< Q< Q< £< Q< Q< Q. < .05 .05 .05 .05 .05 .05 .01 .01 .01 .01 .01 .01 44 Additional data analysis divided the sample into three groups of subjects, yielding the following: users, and 19 nonusers. 36 alcohol users, 11 former Table 6 contains statistics reflecting significant differences in cigarette smoking and severity of the MI between the nonusers and both the regular alcohol users and former users. Of the total 66 subjects in Table 6, active smokers were well represented in the alcohol users and former users ([ = 13.976, p < .0004). The nonusers were significantly different from the other two groups. Positive correlations were found between present smokers and respiratory diseases (r (~= 0.45, ~ < = 0.36, .01). p < .01) and alcoholism/alcohol abuse Previous research has supported the relation- ship between smoking and chronic obstructive pulmonary disease, which was the most frequently appearing respiratory problem in the sample. The suggested relationship between alcohol use and smoking has been observed in other studies (Myrhed, 1974; Keller, 1974). An impressive finding was the significant difference in the incidence and degree of MI severity among the three groups ([ p = 5.433, = .007) shown in Table 6. As previously mentioned, severity of MI was determined by Killup's classification signs reflecting varying degrees of circulatory failure. Among the three groups, the nonusers again were significantly different from the alcohol users and former users, who appeared to have more severe myocardial injury than the nonuser. The alcohol user and former user demonstrated an increased evidence of left ventricular dysfunction ranging from signs of 45 Table 6 Means, Standard Deviations (SD), and Associated F-Ratios Obtained By a One-VJay Analysis-of-Variance Between Alcohol Users (N = 36), Former Users (N = 11), and-Nonusers (N ::: 19) - Mean Level of Significance* SD F-Ratio .8910 .6250 .2353 .3408 .5175 .4372 13.976 .e. <.0004 Severi ty of t~I User (N = 36) 2.6111 Former-User (N = 11 ) 2.6364 1.6667 Nonuser (~ = 17) 1.0220 1 .0269 1 .0847 5.433 .e. <.007 Variable Present Smoker User (N = 31) Former User (N = 8) Nonuser (~ = 17) *.e. ::: <.05 46 moderate pulmonary and/or systemic congestion to irreversible cardiogeni c shoc k. CHAPTER V SUMMARY AND RECOMMENDATIONS This study compared the incidence of postacute myocardial infarction (MI) complications between alcohol-using and nonalcoholusing men ranging in age from 34 to 97 years. The hypotheses proposed a significant difference between these two groups in the incidence of: (1) Postacute MI potentially life-threatening arrhythmias, gestive heart failure, and jected (£ > (3) emboli. (2) con- The three hypotheses were re- .05), following a one-way analysis-of-variance. In other words, although the investigator assumed that the alcohol user would be more susceptible to problems, no significant differences were found between alcohol users and nonusers in the frequency of arrhythmias, congestive heart failure, and systemic and/or pulmonary emboli. Ancillary findings, however; did reveal a statistically significant difference when the total subjects were studied in three groups: alcohol users, former alcohol users, and nonusers. The findings sug- gested that the current alcohol user and former user were more likely to be active tobacco smokers, to be younger at the onset of their MI, and to experience more extensive left ventricular dysfunction, that is, a more severe MI, than the nonuser. As discussed in an earlier chapter, several limitations in the study influenced the results. Briefly, these limitations were: 48 1. The inconsistency within the medical field defin- ing the degrees of alcohol use; 2. The possibility of incorrect information docu- mented in the medical records; 3. The inability to verify the data in the records; 4. The difficulty of isolating alcohol as a causal factor in the frequency of MI complications in human subjects due to the influence of internal and external environmental factors such as past illnesses and risk factors; 5. The lack of control of prophylactic measures and medical regimen, i.e., medications, which could have aggravated complications; 6. The limited collection of pertinent data, such as frequencies of complications, due to the deaths of 18.2 percent of the subjects. In addition to the above limitations, two subjects with extreme years of age for this study's sample may have skewed the results. One man, 34 years old, an alcohol user; and the other, a less complicated 97 year-old, nonuser, may have distorted some of the relationships studied. Further investigation of the effect of alcohol consumption in patients with cardiovascular problems, will require clearer definitions of alcohol use. Quantitative descriptions of the amount and duration of use, evidence of physiological and psychological harm, as well as 49 the type of alcoholic beverage ingested, would provide more interpretive information. A study conducted from the onset of the subjects' hospitalization would diminish some of the difficulties of data collection, such as having to search through lengthy narrative and then interpret the data, which inherently involves some investigator bias. The investi- gator could dictate a data collection tool with specific definitions of variables to be studied. Collecting data during the subject's MI, rather than ex-post facto, would then facilitate the gathering of accurate information. In this current study, many variables were included to correlate possible contributory factors, which could lead to postacute MI complications. In future studies, some of the variables should be controlled, such as age limits and deleted, if insignificant to the nature of the study, such as cardiac serum enzyme values; or, described, such as the specific location of rales. In this way, perti- nent and relevant data could be obtained. In the Coronary Care Unit, hemodynamic monitoring could indicate the degree of left ventricular failure through such measurements as cardiac output or arterial blood pressures reflecting left ventricular and diastolic pressure (LVEDP). This invasive iechnique would provide additional and more accurate data. Further recommendations for study include investigation into the roles of magnesium or vitamin deficiencies in arrhythmia or left ventricular dysfunction, or what additional cardiogenic drugs may have an untoward effect with alcohol use. 50 Implications for Nursing With the regular alcohol user, the Coronary Care Unit (CCU) nurse must be watchful for signs and symptoms of left ventricular failure, such as tachyarrhythmias and basilar rales. The fact that 23 percent of the alcohol users expired in this current study, however, should alert the CCU nurse that the alcohol user is a high mortality risk. To facilitate the CCU nurse's vigilance, he/she must recognize the need to identify the alcohol-using habits of postacute MI patients and clearly document this behavior. In addition, a caring, noncondemning attitude is imperative to facilitate nursing care to alcohol users. Nursing literature cited that a nurse's attitudes toward alcohol consumption may influence her delivery of care (Cornish &Miller, 1976; Reed, 1976). Many nurses have perceived alcoholics, for instance, as dependent and irresponsible individuals. Heineman's study showed a change in nurses' negative perceptions through additional learning about alcohol's physiological and psychosocial effects. These experiences enhanced nurses' under- standing of and effectiveness in working with alcoholics (Heineman, 1974). Hopefully, further education will help the health care professional to acquire more informed attitudes about the potentially serious implications of alcohol for their patients, especially since 47 percent of hospital admissions are for an alcohol-related problem (Haglund &Schuckit, 1977). In turn, the cardiac consumer may avoid the detrimental effects of alcohol if nursing assumes the special role in 51 health maintenance to become involved in recognizing alcohol-related problems and teaching about the discriminate use of alcohol. APPENDIX A EXAMPLE OF DATA COLLECTION SHEET 53 NAME 5.5. No. Code No. Age: Admission Date Occupation: Marital Status: Alcohol Use: Risk Factors: Past Hi story: Past/Current Medications: Physical Exam Findings (On Admission) Laboratory Results (On Admission) ECG Chest X-Ray Blood Work CCU Course DOS #1: (Date) DOS #2 (Date) DOS #3 (Date) DOS #4 (Date) (CCU Course included comments and data on significant physiological and psychological changes) (DOS - Day of stay) APPENDIX B VARIABLES STUDIED 55 Variables Studied V 1, V 1, V 2, V 3, V 4, V 5, V 6, V 7, V 8, V 9, V10, V11, V12, V13, V14, V15, V16, V17, V18, V19, V20, V21, V22, V23, V24, V25, V26, V27, V28, V29, V30, V31, V32, V33, V34, V35, V36, V37, V38, V39, V40, V41, V42, V43, V44, ID Number/ Age/ User/ Former User/ Non-User/ Marital Status/ Employment Status] MI Location/ No. of Chest Pain Days/ Severity of MI/ Previous No. of MIls/ CPK Peak/ SGOT Peak/ LDH Peak/ Expi red/. No. of CCU Days/ Present Smoker/ Past Smoker/ Age/ Sex/ Heredity/ Diabetes Mellitus/ Serum Cholesterol/ Hypertension/ Obesity/ Personality Type/ Sedentary Life Style/ Documented Stress/ Cardiac/ Respiratory/ Ulcers/ HH REF ESO/ Etohism/ Arterial Insufficiency/ Renal Fai1ure/ CVA/ DVT/ PEl DJD/ Gout ArthJ Cancer/ Surg Tra/ Anemia/ Cardiomeg/ Murmer/ V45, V46, V47, V48, V49, V50, V5l, V52, V53, V54, V55, V56, V57, V58, V59, V60, V61, V62, V63, V64, V65, V66, V67, V68, V69, V70, V7l, V72, V73, V74, V75, V76, V77, V78, V79, V80, V8l, V82, V83, V84, V85, V86, V87, GallpJ Rales/ JVD/ Pedemaj JH Reflux/ ABnl K ABnl Glue Normal Sinus Rhythm/ SB Days/ SB Freq/ ST Days/ ST Freq/ PAC Days/ PAC Freq/ AFL Days/ AFL Freq/ AF Days/ AF Freq/ SVT Days/ SVT Freq/ PVC Days/ PVC Freq/ VT Days/ VT Freq/ VF Days/ VF Freq/ One AV Days/ One AV Freq/ Two AV Days/ Two AV Freq/ Three AV Days/ Three AV Freq/ RBBB Days/ RBBB Freq/ lBBB Days/ LBBB Freq/ CHF/ Emboli/ Rupture/ Card Shoc/ Pericardial Friction Rub/ Extens/ Pneumon/ 56 Explanation of Abbreviations V 11-13 V 28 V 29 V 31 V 35 V 36 V 37 V 38 V 39 V 41 V 43 V 47 V 48 V 49 V 50 V 51 V 53 V 55 V 57 V 59 V 61 V 63 V 65 V 67 V 69 V 71-76 V 77-78 V 79-80 V 81 V 84 V 86 V 87 Cardiac enzymes peak blood levels during CCU stay Cardiac diseases found in sample Respiratory diseases found in sample Hiatal hernia: reflux esophagitis Cerebral vascular accident Deep vein thrombosis Pulmonary embolus Degenerative joint disease I Gout; arthritis Surgery; traumatic injuries Cardiomegaly Jugular venous distention Periateral Edema Hepato-jugular reflex Abnormal K (Potassium) Abnormal (blood) glucose Sinus bradycardia Sinus tachycardia Premature atrial contraction Atrial Flutter Atrial fibrillation Supraventricular tachycardia Premature ventricular contraction Ventricular tachycardia Ventricular fibrillation Atrio-ventricu1ar Right bundle branch block Left bundle branch block Congestive heart failure Cardiogenic shock Extension of the MI Pneumonia APPENDIX C CODING USED FOR SPECIFIC VARIABLES 58 1 - Yes o- No Marital Status o - Single 1 - Divorced 2 - Separated 3 - Widowed 4 - Married Employment Status o - Unemployed 1 - Retired 2 - Employed MI Location o - Unknown (ST Change Undeterminate) 1 - Lateral 2 - Inferior (Diaphragmatic) 3 - Inferior - Lateral 4 - Posterior 5 - Posterior - Lateral 6 - Anterior 7 - Anterior - Lateral 8 - Anterior - Inferior 9 - Anterior - Posterior 10 - Septal 11 - Septal - Anterior Severity (Killups Classification) 1 - Class I - No Complications 2 - Class II - Mild Congestion 3 - Class III - Pulmonary Edema 4 - Class IV - Cardiogenic Shock Personality Type 1 - B 2 - A =1 =2 Sedentary Life Style 1 - Yes - 1 o - No (Exercises regularly) - Cardiac Disease 1 - Valvular 2 - Arrhythmias 3 - Congestive Heart Failure (CHF) 4 - Coronary Artery Disease (CAD) 5 - CHF and CAD 6 - Coronary Artery Bypass Graft 7 CAD with Arrhythmias Respiratory Diseases 1 - Chronic Bronchitis 2 - Silicosis 3 - Chronic Asthma 4 - Chronic Obstructive Pulminary Disease 5 - COPD and Bronchitis 6 - Pulminary Fibrosis, 7 - Pulminary Fibrosis, COPD and Brochitis 8 - COPO and Chronic Asthma Murmur 1 - Diastolic 2 - Systol ic 3 - Holosystolic 4 - Systolic and Diastolic 5 - Systoli.c and Holystolic 6 - Systolic, Holosystolic, Gallop Diastolic 3 - S3 4 - S4 5 - S3 and S4 (Summation Gallop) Rales 1 - Basilar 2 - Present at more than onehalf way up from bases 59 Arrhythmias Frequency 1 - Rare 2 - Occasional/Intermittent 3 - Frequent 4 - Persistent/Continuous CHF 1 - Mild to moderate 2 - Severe (Pulmonary Edema) Emboli 1 - Thrombus 2 - Systemic 3 - Pulmonary APPENDIX D SIGNIFICANT VARIABLES STUDIED BETWEEN ALCOHOL USERS AND NONUSERS 61 Table 7 The Absolute and Relative U~) Frequencies of Significant Variables Studied Between Alcohol Users and Nonusers Variables "arita] Status Divorced SeparHe!l I 3 5.3 2 Itidowed 1 3 "4arr; ed 22 5.2 5.2 15.7 6.3 <16.a 5.1 3.G 2 ')'7 6 31 5.2 63.1 31.5 4 37 24 1 1. , 4.7 Emelo~ent Status Uneflployed Retired E.:no loyed Not recorded 3 2S IS 1 [nformation on Present ~I MI !.ocat1an Unknown (no st. address) Lateral Inferior [nferior - Lateral Anterior Anterior - Latera I ,).nteriar -Inferior Septa I Anterior 1thers :Iumoer 'Jf Chest ?lin Da;ts (no pa, n reeorde<1l , 6.3 53.1 38.2 2 26.3 5.2 22 3 5 3 31. 5 46.8 6.3 10.5 17 15.7 10.5 10.5 4 8.5 21 44.7 10 21.2 5 10.5 12 :I 2 2 63.2 15.7 10.5 10.5 12.1 15.2 3.0 4.5 4 33 ~3 6 50 19.7 7 10.6 13.6 ~ ~, .5 11 16.7 :9 8 13 17 27.7 43.3 12. ~ 10.5 3 15 3 ~ :;.7 .1.5 .'1['5 11 23.4 : _..1 ;4 29.3 ~ 22 ~6.3 11 23.4 32 68.1 17 .. 4.5 42.1 is.7 ;;<.pireo .~'" 1.5 42.* 10.5 3 :0 34 26 6 51. 5 52.5 5.2 :.3 ;2 ;8.2 Zit,2 .\.8.5 .12.1 :Jro iac :nzymes !! > .05) of 1.5 oW.7 55.3 34.0 1:J.6 '10. 36A 5 21 25 16 .... ,.." 6.1 56.1 13.5 i 28 3 3 10 2 6.3 14..9 ''''e'lious '1umoer of 6 S.5 ~ Severitz of MI .(111uPS \..Iassification) I (na compl ications) 2 ',orese!1(;e of I'a 1es ) 3 ,Pu lrnonary Edema) 4. rCaroiogemc ShOCk) :10C "'ecorOe!l 1 12 Jal::s ~ _7 of ~iSK Factors 'resent ,moker ,: Ooc iJmen teo ) :l3S t smOker : Documentl!<l) '\oe' ..10 Sex --:"'a leI 10 7 :0.5 Hi 52.5 36.3 32 21. 1 21.1 36 12 54.5 18.:: 95.5 66 ! CO.::! 13 ~"esence g 4. 4 19 45 100 ~f ;:'ami 1" "E!!I1oers "lcn riistorv or ':dI'd 1 ac :: i sease ~ereditv ;No. 10 9 4 ·2 - J j doetes :rQ I ~ster':) j '" 200 ~ypertens i on ; >90 ~ ";g) :l iast:l j J:es i tj -",:)11 26.3 42.1 21.2 '] 20 16 ~6 ~ ld.1 : 9.1 l1g) 1S 3.5 42.6 3.+.:1 42.1 12 53.2 3.2 13 r'j./ 23 23 .l2* .1 42. J ~ I 62 Table 7--Continued Users (N • 472 Absolute Relative Variables \:tl Nonusers I~ 11 191 Absolute Relative (:;1 Total Absolute 'N . ~gl Relative Persona I i t~ t~ee (Document I 5 A a 10.6 9.1 i.5 <) Sedentarl Life Stlle Exercise Sedentary Unknown 6.3 Stress (OoclJll4lnted) 18 38.2 Cardfac Dfsease CAD Others Not recorded 19 40.4 Resefratorl Di seases CO PO COPO (Bronchitis) 4 21.1 41 15.1 12.8 10.6 Otl1er~ 4.5 9.1 5.2 10.6 5.2 22 33.3 28 4 ea) - 27 42.4 16.6 40.3 7 5 10.6 7.6 « (< lea) 10.5 1iot ,.ec;orded 6.0 - 50 75.8 Past Illnesses \.E > .OS S ig,ns and S~2toms Card f alHt941y Murmur Systolic All others Galio!) S3 54 S3 & S4 (SlJII1IIation 17 36.2 5 31.5 2.3 34.3 13 6 27.7 12.3 4- 21.1 21.1 17 25.8 ~ 2. 49 a 5.2 ~2.1 2 31 3 47 55.3 19.1 47 35 53 5.2 10 25.6 17 10.5 14 15 2 1 23 Jugular venous distentfon :JUO) Per; phera 1 Edema Hepato·Jugular Reflex Abnormal PotaSSium (Serum) (.E.;> .J5) Abnorma I 51 ucese (serum) l.e .05) 26 9 12 a 2 El ectrocardiograenic Flndings ~ormal sinus rhythm (Not recordea) Arrhythm ias (p. >. 36.9 .1.3 3.5 26.3 9 5.7 15.2 1J. 6 86.4 aS) Except for '1entric1J iar fi bri 114 t1 on (frequency) 2 4.3 Conductf on defects (~ > .:)5) Except for Rig"t bundle orane" b 1ocl< 1 6.3 2 3 g 15 !'lot recordea :o"gestive Heart Failure :"Ii 1d to mooer! te Severe ~ot recoroed :moo1us Systemic Pulmonary 4.5 6.3 G4l1oo) Races Basi lar :"One na I f way up chest 1 17 11 36.2 23 .~ 6.3 4.5 1.5 5.2 5.2 26.3 15.7 1.. 5 1 1.5 50 90.9 22 14 33. J 21 ~ 2 1 1.5 (~) REFERENCES 64 Abdellah, F. G. The nursing role in the coronary care system. In L. E. Meltzer &A. J. 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