Category Archives: Intensive Coronary Care Unit

Nursing Staff of The Coronary Care Unit

coronary_care-unit-11   

Nursing Staff of The Coronary Care Unit

A coronary care unit (CCU) is a specially designed aad equipped facility staffed by highly skilled per­sonnel who provide optimum care for patients with smpected or confirmed acute myocardial infarction. Many institutions have expanded the function of the CCU by admitting patients with other cardiac emer­pen:.ies to the unit. Included in this latter group are puients with acute pulmonary edema, major arrhyth­mias unrelated to myocardial infarction, and those roquiring pacemakers.

The success of the coronary care system depends above all on the competence of the nurse members of the CCU team. As noted, unless nurses are ade­quately trained for their role and are delegated authority to make and carry out therapeutic decisions based on their own observations and judgment, coro­nary care is merely a token gesture.

For optimum effectiveness a CCU should maintain a ratio of one professional nurse for every two or three patients at all times. Thus a four- to six-bed unit requires two nurses per shift-or a total nursing staff of at least 10 or 12 professional nurses for full coverage (including relief during illness, vacations, and days oil). This high quota of nurses may be unrealistic for many hospitals. In this circumstance, licensed practical nurses can be employed to assume some of tile lesser duties of tile professional nurse. However, it is essential that at least one professional nurse be present in the CCU at all limcs, the responsi­bility of the unit must never be delegated to a licensed practical nurse, even for a few minutes. This is not to say that highly motivated practical nurses cannot provide valuable assistance in patient carc, but it does mean that duties and responsibilities ol’coronary care nursing are so encompassing that none but specially trained professional nurses should undertake them. When practical nurses are included as members ofthe CCU team, they should participate in relevant por­tions of the training program offered to professional nurses.

Nursing in a coronary care unit (CCU) requires skills, knowledge, and judgment beyond that which can be acquired in a basic nursing school curriculum. Consequently, additional training is necessary to prepare nurses (even those with extensive general duty experience) for their specialized role in the (‘CU. Before describing the details of this instruc­tional program, it is pertinent to consider some of the most important qualifications (personal and profes­sional) for coronary care nursing.

 SELECTION OF NURSES FOR THE CCU

Despite hospital staffing problems, CCU nurses must be deliberately selected for their role rather than accepted merely because of their availability or willingness to work in the unit; under no circum­stances should nurses be forced or persuaded to work in a CCU against their desire. The underlying pur­pose of the selection process is to ensure that the members of the nursing staff are all well qualified and able to work together as a team in providing quality nursing care. In view of the time, effort, and cost involved in preparing CCU nurses for the responsi­bilities they will be asked to assume, it is important for prospective candidates to decide at the onset if they are qualified and suited for coronary care nursing. To this end, it is useful for the nursing director to establish a list of basic requirements for those who contemplate working in a CCU. This practice mini­mizes misconceptions about CCU nursing and re­duces undue turnover; it also results in a stable, smoothly functioning unit. The following personal and professional qualifications should be included among the selection criteria for CCU nurses.

 Personal Qualifications

Emotional Stability

It must be recognized that patients admitted to a CCU are usually seriously ill and that the death rate among them is substantially higher than in other divisions of a hospital. The prospective CCU nurse should evaluate tier personal reactions to working in this potentially depressing setting and make certain that she can cope with it. Also to be considered is whether making decisions instantly and assuming serious responsibility-inherent elements in coro­nary care nursing-are likely to produce adverse emotional effects. To be weighed and balanced against these emotional challenges is the sense of accomplish­ment and satisfaction that CCU nurses derive from saving lives through their own efforts-an experience that is probably unique in the nursing profession.

Social Maturity

Because intensive coronary care is a team effort, an ability to work closely with others is an essential attribute for CCU nurses. It is understandable that in a small, confined area like a CCU, where team members are together constantly, frictions may de­velop easily, particularly during stressful situations. Unless mature interpersonal relationships are maintained, the team’s effectiveness is greatly weakened and the quality of care diminished. In addition to working collaboratively with fellow nurses, CCU nurses must also maintain a secure, interdependent relationship with the physician mem­bers of the team. Unfortunately, some physicians are still unaccustomed to delegating authority to nurses, and problems may arise because of this. It is not ancommon, for example, for CCU nurses to become more proficient in interpreting arrhythmias than some physicians, thus challenging the physician’s status and judgment. It takes considerable discretion and a -ature approach for nurses to handle these situations.

 Motivation

Although usually an exciting experience, coronary :are nursing can become dull and routine if the nurse Lacks enthusiasm for her work and the motivation to Learn continually. The nurse should appreciate that nursing in a CCU is meant to be an ongoing learning experience-something to look forward to and enjoy. The degree of enthusiasm of the nursing staff corre­lates well with the quality of care offered. In fact, one of the most revealing characteristics of a superior CCU is a highly enthusiastic nursing staff.

 Integrity

The importance of honesty in a CCU cannot be overemphasized. Errors are bound to occur at one . time or another because actions often must be taken instantly and usual safeguards are bypassed. If the errors are recognized and reported immediately, corrective measures can be instituted. Thus total Integrity on the part of all CCU personnel is manda­tory. Those who cover up their mistakes or are fearful to admit them are ill-suited to work in a CCU.

Dependable Attendance

Nurses who are frequently ill or who are unable to comply regularly with the CCU time schedule for other reasons are poor candidates for coronary care nursing. Recognizing that the proper function of a CCU depends on an adequate nursing staff at all times, it is understandable that any absence or lateness can create a serious problem. This is particularly true in small coronary units where there is a invited number of nurses available as replacements.

Employment Commitment

In view of the time required to prepare CCU nurses (and for them to acquire enough experience to assumefull responsibilities), it is only reasonable that candi­dates agree to remain employed for at least one year, unless some unforeseen circumstance arises. Lesser periods of employment weaken the stability of the CCU team and are defeating for all concerned.

 Age

As a general rule, relatively recent graduates of basic nursing programs are the most adaptablee and make the best adjustment to the demands required of CCU nurses. However, older nurses with excellent qualifications need not be excluded from CCU nursing solely because of their age. Indeed, the older nurse is often a distinct asset to the CCU staff, particularly if she is flexible and adapts relatively easily to the setting.

 Professional Qualifications

Nursing School Record

All CCU nurses must be graduates of an accredited school of nursing, preferably a baccalaureate pro­gram. It is clear that a high ability to learn is an important requisite for nurses selected to work in a CCU. The specialized training program for CCU nurses includes many new concepts and skills which must be mastered quickly. Therefore nurses whose academic record in nursing school indicates a high level of intelligence and superior learning ability are apt to be the best candidates for coronary care nursing.

 Dedication to Bedside Nursing

Because coronary care nursing is concerned almost entirely with direct patient care, it is essential that CCU nurses be dedicated to bedside nursing care and enjoy the nurse-patient relationship inherent in this role. Unless a nurse has a keen interest in direct patient care, working in a CCU is ill-advised. In fact, nurses who are more interested in the medical than the nursing aspects of coronary care are not apt to be the best candidates to work in a CCU.

 Previous Nursing Experience

A particularly valuable asset for prospective CCU nurses is at least six months prior experience in caring for acutely ill medical patients in other settings. This background provides a foundation for the added duties and responsibilities of specialized coronary nursing.

 

NEXT : PREPARATION OF THE CCU NURSE

 Reference :

Lawrence E. Meltzer,MD ; Rose Pinneo,RN,MS ; J. Roderick Kitchell,D (Fourth Edition). “Intensive   Coronary Care a Manual for Nurses”, by Robert J. Brady Company, Bowie, Maryland 20715.

Acute Myocardial Infarction

miAcute Myocardial Infarction

 

When there is profound and sustained ischemic to a portion of the myocardium the cells deprived of oxygen cannot survive, and local death of tissue (necrosis) develops in the involved Area. This de­structive process is termed acute myocardial  infarc­tion. The event that produces this irreversible tissue damage (infarction) is often called a coronary throm­bosis, a coronary occlusion, a coronary, or a heart attack. These latter terms are used synonymously in clinical practice to describe what properly should be designated acute myocardial infarction.

With few exceptions acute myocardial infarction results from advanced atherosclerosis of the coronary arteries. The final insult of progressive coronary atherosclerosis usually occurs when one of the main coronary arteries or its branches becomes occluded. Although the narrowing process is gradual, the obstruction takes place suddenly in most instances. The exact reason that a coronary artery blocks off at a certain moment is not fully under­stood, but three main causes have been incriminated: 1) a clot may develop on the roughened surface of an atherosclerotic plaque and occlude the lumen of the artery; 2) the atherosclerotic lesions may irritate the underlying arterial wall, causing bleeding beneath the plaque (subintimal hemorrhage), which dislodges the plaque and obstructs the artery, 3) a piece of a large plaque may break off and block a small distal artery. Although all of these mechanisms offer a logical explanation for the suddenness of the event, it is now clear that none oftlicni can account foral/ myocardial infarctions. Autopsy studies have shown, for in­stance, that acute myocardial infarction can occur even though the coronary arteries have no clots and are not completely obstructed. In these latter in­stances, it is presumed that at a particular moment the heart is faced with an enormous oxygen demand (e.g., during intense physical activity, such as shoveling snow) which cannot be met by the available blood supply through partially narrowed arteries. In effect, even though the coronary arteries are not completely obstructed, the persistent myocardial demand for oxygen simply overwhelms the limited supply and tissue necrosis develops because of’ this relative oxygen deprivation. Another possibility is that coro­nary artery spasm may be superimposed on existing coronary artery disease, causing a partially narrowed vessel to close completely during the transient spasm. (Although this is an attractive concept, the role of coronary artery spasm in acute myocardial infarction has not been determined as yet.)

The site of an infarction depends fundamentally on which coronary artery (or arteries) is blocked. When the left coronary artery or its branches are occluded, the infarction involves primarily the anterior wall of the left ventricle and is called an anterior infarction. Occlusion of the right coronary artery results in infarction of the inferior (diaphragmatic) wall of the left ventricle—an inferior infarction. Very often more than one area of the left ventricle is damaged by the ischemic process; in these cases more specific terms are used to describe the location of the infarct. For example, if the infarction involves both the anterior and lateral walls of the left ventricle, it is termed an anterolateral infarction. Similarly, dam­age to the anterior wall of the left ventricle and to the interventricular septum is called an anteroseptal infarction.

Myocardial infarction involving the right ventricle alone is very rare because this chamber receives a relatively greater proportion of blood for its (smaller) muscle mass than the left ventricle, and also has less oxygen requirements. However, right ventricular in­farction is not uncommon in conjunction with inferior myocardial infarction. This relationship is under­standable since the right ventricle and the inferior wall of the left ventricle share a common blood supply through the right coronary artery. Nevertheless, the frequency of these combined infarctions was not appreciated until the recent introduction of radio­nuclide methods for the diagnosis of acute myocardial infarction (as described in the next chapter). With these (and other) means it has been shown that at least 25% of patients with acute inferior myocardial infarc­tion also have some evidence of right ventricular damage.

The extent of an infarction is determined first by the size of the vessel obstructed and second by the capacity of the collateral circulation to bring addi-. tional blood to the oxygen-deprived areas. If there is widespread myocardial necrosis extending through and through the entire ventricular wall (from the endocardium to the pericardium), the infarction is termed transinural (Figure 1.7A). Lesser degrees of damage which do not involve the full thickness of the ventricular wall are categorized as nontransmural infarctions (Figure 1.713). Other descriptive terms for nontransmural infarctions are intramural and sub­endocardial infarctions.

In the early stages of acute myocardial infarction there are, at least in concept, three zones of tissue damage (Figure 1.8). The first zone consists of necrotic myocardial tissue that has been irreversibly destroyed by prolonged deprivation of oxygen. Sur­rounding this dead tissue is a second zone (zone of injury) in which the myocardial cells, although injured and jeopardized, may still survive if adequate circu­lation to the area is restored. Zone 3, called the zone of ischemic, represents cells that have not received adequate oxygen but can be expected to recover unless the ischemic process worsens. In effect, the ultimate size of an infarction may depend on the fate of the zones of injury and ischemic. (These latter zones are not actually distinct or separate areas as the foregoing description suggests. Instead, they appear histologically as a combined outer zone surrounding the central zone of necrosis. This outer zone is diffuse and consists of patchy areas of necrotic, injured and ischemic tissues, merging with normal myocardium. Because of its in-between location and status, this peripheral zone is usually described as the border zone or twilight zone.)

Once the coronary circulation is interrupted and a myocardial infarction occurs, a series of events follows which places life and death in balance. This book is concerned with these events and describes a concept of specialized care, known as intensive coronary care, designed to lower the death rate from acute myocardial infarction.

Stable and Variant Angina Pectoris

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Stable and Variant Angina Pectoris

Classic angina pectoris, as described above, be­haves in a predictable and reproducible manner: it is brought on by physical activity or emotional stress, which increases myocardial oxygen demands, and is relieved promptly by rest, which decreases oxygen requirements. This established pain pattern is called stable angina pectoris. It is associated with fixed narrowing of the coronary arteries, resulting from advanced atherosclerosis. Coronary arteriograms usually show at least 75% narrowing of one or more of the arteries; most often, two or three vessels are involved.

Angina pectoris may also result from coronary artery spasm. The arterial spasm reduces coronary blood flow sufficiently to produce ischemic artery disease. Coronary artery spasm may be manifested clinically in several ways, but its most typical form is described as variant angina, or Prinzmetal’s angina. The pain pattern of variant angina differs greatly from stable angina; indeed, it is almost the opposite in many of its characteristics. The main feature of variant angina is that the pain occurs with rest and not with activity. In fact, patients with variant angina do not develop chest pain or characteristic clectrocardio-: graphic signs of ischemia even during exercise testing. Also, the pain has an unusual cyclic pattern, often awakening the patient each night at about the same time. Furthermore, the electrocardiographic changes that accompany variant angina are entirely different than those associated with stable angina. The cause of coronary artery spasm is still unknown, but it is related somehow to abnormal con­traction of the smooth muscles in the walls of arteries.

Although variant angina is very uncommon com­pared to stable angina, it has commanded increasing attention in recent years. Part of this interest can be attributed to a new class of drugs, called calcium antagonists or calcium blocking agents, that have proved very effective in inhibiting or releasing coro­nary spasm and relieving variant angina. Much more important is that these drugs also seem to benefit certain patients with fixed coronary artery obstruc­tion. This implies that coronary spasm may con­tribute to the classic anginal syndrome even when the dominant cause of ischemia is advanced coronary atherosclerosis. However, the mechanism of action of these drugs in controlling stable angina is not known with certainty, but the very fact that calcium antagonists are effective for this purpose has caused a reevaluation of the causes and treatment of ischemic heart disease. Clinical research now in progress is likely to produce many new concepts about an old disease.

 

Intermediate Coronary Syndrome (Unstable Angina)

The term intermediate coronary syndrome has been used to characterize a clinical state that lies between stable angina pectoris and acute myocardial infarction. The syndrome has several different pat­terns, which accounts for the variety of names given to this condition in the past. Among the older (but still used) terms are: impending myocardial infarction, preinfarction angina, crescendo angina, accelerated angina, and acute coronary insufficiency. At present the preferred term is unstable angina, connoting that the common feature of the syndrome is its clinical instability.

Unstable angina may occur as the initial symptom of CHID or, more often, as a sudden worsening of stable angina. The chest pain, instead of lasting briefly as with stable angina, usually persists for 10­20 minutes or longer. It develops with increasing frequency and is provoked by less effort, often occurring at rest. Nitroglycerin provides incomplete or no relief in most cases of unstable angina. Electro­cardiographic signs of ischemic are common but without definite evidence of acute myocardial infarc­tion.

The mechanism of unstable angina is not entirely clear but progressive narrowing of the coronary arteries probably plays a major role, especially in patients with stable angina previously. In any case, unstable angina is more serious than stable angina since frequently it is an immediate forerunner of acute myocardial infarction.

The diagnosis of unstable angina implies, theo­retically, that despite prolonged ischemic adequate oxygenation was restored before actual myocardial destruction occurred. However from a clinical stand­point it is often difficult to rule out the possibility that small areas of the myocardium were in fact injured or destroyed during the ischemic episodes. For this reason and because of the changing and unpredictable course of the condition, patients with unstable angina are admitted to a coronary care unit, at least until the diagnosis of acute myocardial infarction has been excluded.

 

 

NEXT : Acute Myocardial Infarction

Diagnosis of ANGINA PECTORIS

Diagnosis of Angina Pectoris

ro-angina-pectorisThe most important diagnostic evidence of angina pectoris is the patient’s history. If the chest pain is central in location, brief in duration, oppressive in quality and related to effort, the diagnosis of angina pectoris is virtually assured; no other confirmation is necessary. Physical examination and electrocardio­grams at rest are normal in the majority of patients and seldom contribute directly to the diagnosis. When the chest pain pattern is suspicious but not entirely characteristic of angina, several diagnostic tests may be performed to determine if the pain is ischemic in origin.

 

Exercise (Stress) Testing. The simplest and most widely used diagnostic method is the exercise, or stress, test. It consists of recording an electrocardio­gram during progressively strenuous exercise when the oxygen demands of the myocardium increase greatly and electrocardiographic signs of myocardial ischemia are most likely to appear. The exercise is performed by riding a stationary bicycle or walking on a treadmill while the heart rate, blood pressure and electrocardiogram are monitored continuously. The test starts with low level exercise and builds up in stages until a target heart rate (based on the patient’s age) is achieved. In patients with significant ob­structive disease of the coronary arteries a point is soon reached where myocardial oxygen demand exceeds oxygen supply and, as a consequence, elec­trocardiographic signs of myocardial ischemia ap­pear. Although chest pain may develop during exer­cise, a positive stress test is defined only on the basis of characteristic electrocardiographic changes of ischemia, not the presence or absence of angina. One of the main limitations of stress testing is that many elderly or sedentary patients are unable to exercise sufficiently to achieve the target heart rate; the test must often be terminated prematurely in this group because of fatigue, leg weakness or shortness of breath.

 

Radionuclide Studies. In recent years various nuclear scanning techniques have assumed an in­creasingly useful role in the diagnosis and assessment of CHD. One of these methods, known as radio­nuclide angiography, provides indirect information about myocardial blood flow and is used in combi­nation with exercise testing to confirm the diagnosis of angina pectoris. The test is based on the fact that myocardial ischemia, in addition to producing typical electrocardiographic signs, also causes abnormalities in contraction of segments (regions) of the left vcn­tricle. These transient abnormalities in regional ventricular wall motion with exercise can be detected by nuclear scanning of the heart. The procedure involves the intravenous injection of a radioactive isotope at the peak exercise period and then sequen­tially recording ventricular wall motion with a nuclear camera. With significant coronary artery disease blood flow to the region supplied by the involved vessel is reduced, as reflected by the abnormal contractile pattern of that portion of the ventricle. Radionuclide angiography has greater diagnostic accuracy than customary stress testing alone, but it is much more costly.

 

Coronary Arteriography. The most definitive method for the diagnosis of coronary obstructive disease is coronari, arteriography. In fact it serves as the standard of accuracy for the comparison of all other tests used in the diagnosis of CHD. As men­tioned previously, coronary arteriography permits visualization of the coronary arteries (with a radio­paque dye) and thereby defines the precise number of arteries involved, the extent of narrowing in each vessel, and the degree of collateral circulation. This anatomic description of the disease process is par­ticularly important in evaluating patients for coronary bypass surgery.

In addition to coronary arteriography, cardiac catherization and ventriculography are also per­formed as part of a complete study. Cardiac cathe­terization involves the introduction of catheters into the cardiac chambers and great vessels in order to measure pressures and oxygen concentrations in each of these sites. These data are essential for patients in whom coronary surgery is contemplated. Ventricu­lography is used to assess ventricular pumping func­tion and to detect regional wall abnormalities. The technique consists of injecting a radiopaque dye through a catheter placed in the left ventricle and recording motion pictures of ventricular motion. This latter information is similar, but more precise, than that obtained by radionuclide studies. The main disadvantage of coronary arteriography (and the other components of the test) is that heart catheteri­zation is an invasive procedure not entirely without risk, and requires expensive hospitalization.

NEXT : Stable and Variant Angina Pectoris

CHD : Angina Pectoris

Angina Pectoris

angina-pectorisThe classic indication of impaired circulation to the myocardium is a distinctive type of chest pain called angina pectoris. The pain signifies insufficient oxy­genation (ischcmia) of the myocardium; it occurs when the oxygen demands of the myocardium exceed the capacity of the coronary circulation to supply oxygen. In other words, angina represents a signal from the heart, indicating that the myocardium is not receiving sufficient oxygen to meet its needs at the moment. Because angina pectoris is usually the key to the diagnosis of CHD, it is essential to understand its clinical features.

 

Site of Pain. The pain of myocardial ischemia is located most often directly under the center of the breastbone. It may radiate from this substernal location to both sides of the chest, the left or right arm, the neck, the jaws, or the shoulders and upper back. In some instances the pain occurs only at these latter sites without a substernal component; this pattern, however, is much less common than central chest pain.

 

Quality of Pain. The discomfort is usually de­scribed as pressure, tightness, or constriction within the chest. Some patients place a clenched fist against the sternum in attempting to characterize the tight, constricting nature of the sensation. Although angina generally lasts for only a few minutes (as described below), the pain is steady and is not influenced by breathing, breath-holding, or change in body position. This constancy of the pain is a characteristic aspect of angina and is often more significant than other descriptive qualities (e. g., burning, pressure, or ” indi­gestion”).

 

Occurrence of Pain. Any situation that increases the myocardial demand for oxygen is capable of producing angina. In general, oxygen demand is determined by the amount of work the heart performs. As would be anticipated on this basis, the pain is usually brought on by physical effort which increases the heart rate and work and, in turn, myocardial oxygen requirements. Certain activities are espe­cially prone to precipitate angina: walking uphill or against the wind, hurrying after meals, unaccustomed exercise. Conversely, angina is relieved by rest. As soon as physical activity stops the oxygen demand falls promptly and as a consequence the pain sub­sides. This relationship (activity — pain, rest — dis­appearance of pain) is typical of transient myocardial ischemia and distinguishes angina of effort from other nonischemic causes of chest pain in which this pattern does not occur. In addition to physical exertion, sudden emotional stress (e.g., anger, fear, or even the excitement of watching a football game) may induce an anginal episode. The mechanism is the same as with angina of effort: the workload of the heart is transiently increased beyond the ability of coronary circulation to satisfy the additional demands. In all, any physical or emotional stress that produces a sudden increase in the heart rate or elevation in blood pressure may induce angina.

 

Duration of Pain. Angina is characteristically of brief duration, lasting usually from 1-5 minutes before abating with rest. Occasionally the pain may last for more than 5 minutes, particularly if the stimulus for the attack persists. The cessation of pain indicates that the myocardial demand for oxygen has been met and that the oxygen deficit was only transient and not destructive to the myocardium. If the pain does not subside within minutes after rest, myocardial damage may be suspected.

Relief of Pain. Another distinctive feature of angina is the prompt relief of pain that follows the use of nitroglycerin. Failure of nitroglycerin, admin­istered sublingually, to terminate ischemic pain is unusual and is cause for suspicion that the attack is not due to angina of effort. Nitroglycerin (and other nitrates) acts by dilating the coronary vessels, thus increasing the blood flow and oxygen supply to the myocardium. At the same time, nitrates lower the blood pressure and thereby reduce the workload of the heart by diminishing pumping resistance.

 

 

 

Next : The Diagnosis of Angina Pectoris

THE CLINICAL SPECTRUM OF CORONARY ATHEROSCLEROSIS

heart-angiogram-sd3453-ga1THE CLINICAL SPECTRUM OF CORONARY ATHEROSCLEROSIS

 

Asymptomatic Coronary Atherosclerosis

If the degree of arterial obstruction is moderate and does not significantly reduce the blood supply to the myocardium, the disease may never be suspected by the patient or the physician. Results of autopsy studies among persons dying of other causes indicate that this is a common situation. In fact, practically all men in the United States have evidence of coronary atherosclerosis by age 50; it is only the degree of involvement that varies.

Even if the coronary arteries are grossly narrowed by intimal plaques, it still does not follow that the disease will be clinically evident or produce symp­toms. This paradox can be explained partly by the fact that as the coronary arteries gradually narrow small branches of these vessels may enlarge or new branches may form in order to bring more blood to the myocardium. This additional blood supply, called collateral circulation, is of great importance in determining the clinical effects of coronary athero­sclerosis since this network of vessels is often sub­stantial enough to maintain an adequate blood supply to portions of the myocardium despite the presence of advanced atherosclerosis in a major vessel. It is the total blood supply to the myocardium rather than the state of the main coronary arteries that determines whether the disease will be symptomatic. It is important to realize there is no definite correlation between the extent of coronary artery disease and symptoms. In fact, about 30% of patients who die of CHD experience ence no symptoms of the disease before the fatal event.

 

Symptomatic Coronary Disease

Coronary heart disease, by definition, implies that the myocardium is affected by inadequate coronary blood flow. The symptoms of CHD are due to myocardial oxygen deprivation and are manifested in progressive order of severity by three main clinical patterns: angina pectoris, intermediate coronary syn­drome (unstable angina), and acute myocardial in- farction. Each of these syndromes is described separately in the following pages.

 

Next : ANGINA PECTORIS

CAUSES OF CORONARY HEART DISEASE

 (Coronary Heart Disease – Chapter 2)

 coronary-disease

CAUSES OF CORONARY HEART DISEASE

 

An unrelenting search has been in progress for more than 50 years attempting to ascertain why and how the coronary arteries are affected by athero­sclerosis. The question has never been answered, and the cause of coronary atherosclerosis remains un­known. However, one fundamental fact has emerged: a combination of several factors is undoubtedly involved in the development of CHD; no single mechanism can be held responsible in its own right. According to this concept, all of the following factors (called risk factors) may contribute to the formation and progression of coronary atherosclerosis.

 

 

1. Sex and Age

CHD is distinctly more prevalent in men than in women. Indeed, during the child-bearing years women are seemingly protected from CHD unless they have many other risk factors (e.g., hypertension and diabetes). After the menopause, however, the incidence of CHD in females rises rapidly and equals the male rate thereafter. In contrast, symptomatic CHD may occur in men as young as 30 years (or even younger). This sex-age discrepancy suggests that hormonal influences may be important in the disease process.The incidence of CHD increases greatly with age in both sexes. For example, a man in his fifties has four times the risk of a heart attack as a man in his thirties. The fact, however, that young persons may develop CHD makes it clear that coronary atherosclerosis is not simply a disease of aging.

 

2. Diet, Cholesterol, and Lipoproteins

Several epidemiologic studies have demonstrated that the incidence of premature CHD (i.e., coronary disease occurring before the age of 60) can be correlated with the different dietary patterns of var­ious societies. Specifically, in affluent countries (as the United States), where animal fats constitute a large percentage of the total diet, the frequency of CHD is very high; and in poorer countries, where animal fat intake is much less, the incidence of the disease is low. The gross disparity in the amount of animal fat eaten (e.g., eggs, butter, cream, milk, and fatty meats) in different parts of the world is believed to account for the fact that “normal” serum choles­terol levels in the United States may be 200-240 mg%, whereas in those countries in which CHD is un­common the comparable levels are only 100-120 mg%. Further evidence in support of the danger of high-fat diets is the reported decrease in the number of deaths from CHD during World War 11 in those countries where animal fats became scarce, followed by a prompt increase in the death rate after the war ended, when the economy improved and fats again became available. From data of this type many re­searchers have concluded that overeating of animal fats (also called saturated fats) is a prime factor in the etiology of CHD.

More specific information about the danger of high serum cholesterol levels has been obtained from the Framingham Heart Study. In this study more than 5000 men and women in the town of Framingham, Massachusetts, have been examined at regular inter­vals for more than 25 years to determine which factors contribute to the development of CHD. The results indicate that the risk of a heart attack is at least three times greater in men with serum cholesterol levels of more than 240 mg% than it is in those with levels of less than 200 mg%.

Although serum cholesterol has received the most attention, other serum lipids (e.g., triglycerides) and substances that transport lipids in the blood (lipo­proteins) are also recognized as important risk factors for CHD in their own right. It has been shown, for example, that elevated serum triglyceride levels (above 200 mg%) are associated with an increased incidence of CHD even though serum cholesterol levels may be normal or only slightly elevated. In other words, cholesterol and triglyceride levels are not necessarily related and a high concentration of either lipid may indicate an increased risk of CHD. Elevated triglyceride levels, unlike elevated choles­terol levels, are usually induced by the ingestion of carbohydrates (rather than saturated fats) and are commonly associated with diabetes or abnormal glucose tolerance.

Cholesterol and triglycerides, as lipids, are insol­uble in plasma and are carried in the blood in combination with a group of proteins, called lipo­proteins, that are soluble. Lipoproteins can be sepa­rated into three main classes: low-density lipopro­teins (LDLs), very low-density lipoproteins (VLDLs), and high-density lipoproteins (HDLs). About two-thirds of the cholesterol in the blood is carried by LDLs while HDLs carry less than one-third. (VLDLs are involved primarily in the transport of triglycerides and carry only small amounts of cholesterol.) Epidemiologic studies have revealed that the higher the concentration of LDH cholesterol, the greater the risk of CHD. On the other hand, there is an inverse association between HDL cholesterol and the incidence of CHD. This means that the higher the percentage of HDL cholesterol (of the total scrim cholesterol), the lower the risk of CHD. In fact this latter relationship appears so definite that HDL cholesterol actually seems to protect against CHD.

 

 

* Consequently, prediction of risk of CHD can be enhanced substantially by measuring HDL and LDL cholesterol in conjunction with the total serum choles­terol levels.

 

3. Hypertension

High blood pressure is thought to predispose to CHD by accelerating the rate of atherosclerosis and by increasing the oxygen demands of the myocar­dium. In the Framingham Heart Study it was ob­served that blood pressures in excess of 160/95 were associated with a fivefold increase in the incidence of CHD compared with normal pressures. Thus from a statistical standpoint hypertension appears to be one of the most serious risk factors.

 

4. Cigarette Smoking

There is firm statistical evidence to indicate that heavy cigarette smokers have a higher incidence of CHD than nonsmokers. In the Framingham Study, the risk of a heart attack was nearly twice as great in cigarette smokers. However, the risk was associated primarily with middle-aged men and was less im­pressive in older men and in women. Curiously, cigar and pipe smokers are at no greater risk than non­smokers, presumably because they do not inhale. The manner in which cigarette smoking affects the coro­nary arteries is not understood. The suggestion that nicotine may cause sufficient constriction of the arteries to reduce coronary blood flow has not been confirmed. On the other hand, nicotine increases the work of the heart (by increasing the heart rate and blood pressure) and could produce a relative oxygen deficiency. Moreover, cigarette smoking is associated with elevated carbon monoxide levels in the blood, which may also interfere with myocardial oxygena­tion. Regardless of its mechanism of action, cigarette smoking is generally considered among the most serious risk factors for premature CHD.

 

5. Heredity

A familial pattern of CHD has long been recog­nized, but the degree of risk is still uncertain (because family histories are unreliable in many instances). However, our own experience suggests that heredity ranks among the highest risk factors, particularly when CHD occurs during the fourth or fifth decade of life. In these latter cases it is commonly found that a man’s father, grandfather, and brothers often devel­oped CHD at about the same age. It has been postulated (but not proven) that the physical structure of the coronary arteries and the rate of atherosclerosis may be genetically determined.

 

6. Diabetes

CHD develops more frequently and at all earlier age among diabetic patients than among non-diabetics. Even when diabetes is mild or well con­trolled the risk of CHD remains substantially greater. These facts along with data indicating that other

metabolic diseases (e.g., gout) are associated with a high incidence of Cl 11) suggest that a biochemical disturbance may be central to the underlying disease process.

 

7. Sedentary Life

Lack of physical activity has been incriminated as a risk factor in CHD, but the evidence for this belief is still inconclusive. Several studies have revealed, for example, that CHD occurs more frequently in seden­tary workers (e.g., postal clerks) than in those whose occupations demand substantial physical activity (e.g., mail carriers); yet many observers have ques­tioned the significance of these findings, noting that there were so many other variables between the two groups that physical inactivity should not be singled out as a risk factor in its own right. Although there is good reason to believe that exercise may benefit the myocardium, it remains to be seen if’ physical activity (or inactivity) affects coronary arteries and influences atherosclerosis.

 

8. Obesity

Insurance company statistics suggest that obesity predisposes to fatal CHD, but (as with physical inactivity) the issue is by no means settled. In fact in the Framingham Study moderate obesity by itself was not associated with an increased incidence of CHD. However, overweight persons are especially prone to hypertension, diabetes, and elevated lipid levels, and it may be that the risk of obesity lies with these secondary effects. In any case obesity is classified as a risk factor even though its mechanism of action is uncertain.

 

9. Emotional Stress

Epidemiologic studies have consistently shown a markedly higher increase of CHD in industrialized (civilized) countries than in primitive, less-demanding societies. Many believe that this gross disparity is a reflection or a direct result of emotional stress imposed by modern, fast-paced styles of life. For this reason CHD is considered by some to be a disease of “overcivilization.” According to this the­ory, civilized mail has developed chronic anxiety in attempting to cope with rapidly changing socioeco­nomic and sociocultural forces, and this tension in some way promotes atherosclerosis. In principle, this is an attractive concept since it has been demon­strated that anxiety is often accompanied by a distinct rise in serum cholesterol, which could favor the devel­opment of atherosclerotic plaques. Moreover, stress is known to accelerate Wood coagulation, allowing small clots to form within the coronary arteries. Nevertheless, the relationship between emotional stress and CHD has been difficult to prove, partic­ularly since there are no available methods to actually measure degrees of stress. Some research studies in fact have cast doubt on the importance of stress as a risk factor. For example, one large investigation involving telephone company employees showed that the incidence of CHD was actually less common among high-level executives (who presumably func­tion under great stress) than it was among workers who installed or repaired equipment. Further study will be needed to determine the significance of emotional stress as a risk factor.

 

10. Behavioral Patterns

Attempts have been made to correlate CHD with certain personality traits and behavioral patterns. The coronary-prone person—called a type A per­sonality—is said to be one who is aggressive, am­bitious, highly competitive, and, most of all, possessed with a profound sense of the urgency of time. Those with this type behavioral pattern reportedly have significantly higher cholesterol levels and an in­creased incidence of CHD than their counterparts (type B personalities), in whom these particular characteristics are not as apparent. This interesting observation requires confirmation, but many now accept type A behavior as a distinct risk factor.

 

Summary of Risk Factors

It is essential to point out that there is no definite evidence that any of the risk factors just described actually cause CHD. All that can be said is that individuals with multiple risk factors are high-risk candidates for CHD; conversely, the absence of these factors predicts little likelihood of developing the disease. For example, a man with hypertension and a high serum cholesterol level who is a heavy cigarette smoker may have ten times the risk of sustaining a heart attack than a person with none of these factors. In other terms, there is a statistical association between risk factors and CHD but, on the other hand, no proof that these risk factors in themselves are the direct cause of coronary atherosclerosis.

(to be Continued…….THE CLINICAL SPECTRUM OF
CORONARY ATHEROSCLEROSIS)

Coronary Heart Disease-1

Coronary Heart Disease

(Chapter 1)

jantungWhen the incredible complexity of the human system is considered along with the vast number of possible sources of illness and death, it seems incongruous that the life of so many depends finally on the health of two small arteries; but the fact is undeniable. Disease of the coronary arteries has become the single greatest threat to life in industrialized countries throughout the world. In the United States, for example, more than 650,000 deaths a year—or one-third of all deaths—are directly attributable to this one disease.
As the sole blood supply to the heart musculature (myocardium), the coronary arteries assume extreme importance. Any significant interference with blood flow through these vessels can impair the entire function of the myocardium, with dire consequences including sudden death. Before describing the clinical aspects of coronary disease it is pertinent first to consider the coronary arteries and the basic disease process that affects them.

THE CORONARY ARTERIES

The two coronary arteries, the left and right, arise from the aorta just above the aortic valve. The left coronary artery then divides into two large branches: the left anterior descending artery and the left circumflex artery.
Each artery supplies a different area of the heart. Briefly, the left anterior descending artery supplies most of the anterior wall of the left ventricle, the anterior portion of the interventricular septum, as well as the anterior wall of the right ventricle. The left circumflex artery supplies the lateral aspect of the left ventricle and the left atrium. The right coronary artery supplies the right atrium and the right ventricle, along with the posterior portions of the left ventricle and interventricular septum. The arteries lie on the outer surface of the ventricles and give offininierous branches that penetrate all parts of the heart. The terminal branches of the arteries have many interconnections, forming an extensive vascular network throughout the myocardium.
The function of the coronary arteries is to bring oxygen-carrying blood to the myocardium, oxygen being an essential ingredient in producing the energy the heart requires to contract. As a pump that works incessantly (contracting more than 100,000 times a day), the myocardium has very great oxygen needs. This constant demand call be met only by an adequate coronary blood flow. Indeed, 250 cc of blood per minute—or 36,000 liters per day—pass through the coronary arteries to oxygenate the myocardium under normal conditions. The oxygen demands of the myocardium increase greatly with exercise or emotional stress. Since the heart utilizes nearly all of its available oxygen supply even with normal activity and has a very limited oxygen reserve, these additional needs can only be satisfied by an increase in coronary blood flow.

CORONARY ATHEROSCLEROSIS
The primary disease affecting the coronary arteries is atherosclerosis, a process in which fatty substances (particularly cholesterol) deposit as plaques along the inner lining of the vessels and narrow the passages. If the narrowing reaches a stage where the blood flow through the arteries is insufficient to meet the oxygen demands of the myocardium, then coronary heart disease (CHID) is said to exist.
Coronary atherosclerosis usually develops gradually over a period of years. However, the process begins at an early age so that by adulthood most men (and women, to a lesser degree) have some evidence of atherosclerosis in the coronary arteries. Autopsy studies have shown, for example, that among young American soldiers (average age of 22 years) killed in action during the Korean war nearly 80% had definite signs of coronary atherosclerosis. It is essential to realize, however, that the critical determinant of coronary heart disease is not the mere presence of atherosclerosis but rather the extent of arterial narrowing and the reduction in blood flow the lesions produce. Atherosclerosis can be categorized into four grades according to the degree of arterial obstruction. Grade I atherosclerosis indicates that the diameter (lurnen) of the artery is reduced by no more than 25%; grade 2 represents a 50% reduction, grade 3 a 75% reduction, and grade 4 complete (100%) obstruction of the vessel . An obstruction of at least 75% is necessary to produce a significant reduction in coronary blood flow; lesser degrees of narrowing can usually be tolerated without affecting myocardial function. Obstruction may occur in any (or all) of the coronary arteries, but involvement of the left anterior descending artery is particularly dangerous. This vessel supplies a much larger portion of the total myocardial mass than the right coronary and left circumflex arteries and therefore has the greatest blood flow. Even more serious is obstruction of the left main coronary artery. Significant narrowing of this short (2 cm) vessel causes a reduction in blood flow through both the left anterior descending and left circumflex arteries and therefore compromises the blood supply to nearly all of the left ventricle. Fortunately, obstruction of the left main coronary artery is the least common lesion of the coronary circulation, occurring in only 5-10% of patients with symptoms of CHD.
The site and extent of arterial narrowing call be determined by means of coronary aneriograplv, a technique that permits the arteries to be visualized by x-rays. The procedure involves the insertion of a catheter into the root of the aorta (by way of a peripheral artery) and the injection of a radiopaque dye through the openings (ostia) of the two coronary arteries. As the dye is being injected a rapid series of x-ray films or photographs (cineangiograms) are taken to outline the entire arterial tree; significant lesions can readily be detected in this way.

 

to be continued…..”CAUSES OF CORONARY HEART DISEASE“.