Angina (FL Autonomous Practice INITIAL Differential Diagnosis)

Angina is the term we use for chest pain of cardiac origin. When someone says, "I am having angina," we automatically assume it is all about the heart. We further make the mental leap that ischemia, an inadequate supply of oxygen rich blood to tissues in the body, is at the heart of the pain.

This is not always the case. The term angina is not exclusive to any specific bodily organ, nor is a sensation of chest tightness or pain limited to the heart alone. Even those symptoms which are directly related to cardiac distress can be experienced in diverse ways other than one stereotyped image of angina. This means that descriptions which nicely fit into our concept of pain of cardiac origin may have nothing to do with the heart at all.

This course seeks to expand awareness of alternative causes of angina and will review the types of pathologies which may cause this feeling. We will look at various means to distinguish between them; and then discuss methods which may be employed to treat this pain in the neck, and chest, when it does relate to cardiac distress. So, deep breath and hang on tight as we discover some of the hidden meanings that rest behind the term, “angina”.

Angina, and the “anginal equivalents”, are seen in clients by health professionals much too frequently. The occurrence of distressing discomfort and constrictive pain characteristic of angina spasms may originate from many different conditions. Some causes require prompt medical attention (e.g. tearing of the aortic blood vessel, ischemic heart attack, or pulmonary embolism), while other sources of angina type pain may allow more time for accurate diagnosis and establishment of a treatment regimen (e.g. gallbladder attacks, esophageal spasm, pericarditis, panic attacks, etc.).

The term angina does not mean heart. Angina is a descriptive word focused on the sensation being experienced, regardless of its source. The word angina can, and is, applied to a wide range of conditions which manifest in a painful intermittent strangling sensation reminiscent of suffocative constriction or anoxic spasms. Differentiating between causes of angina type sensations can be complex and taxing, and we will discuss some of the more common disease processes that are observed in conjunction with the sensation of angina and those individually unique variant symptoms which are being referred to in recent literature as anginal equivalents.

In its most common medical use, the term angina is automatically associated with the chest discomfort accompanying a decrease in the supply of oxygenated blood flow to the heart muscle in relation to oxygen demand. The reason for this association is frankly, prevalence. According to the American Heart Association Heart Disease and Stroke Statistics - 2016 Update, more than eight million Americans experienced angina related directly to cardiovascular disease.³

Angina related to cardiac injury or disease effects around 9.8 million Americans each year, with approximately 500,000 new cases of angina occurring annually. ⁴

While cardiac ischemia related chest pain is both life-threatening and prevalent, other causes of angina type pain are frequently encountered by health professionals as well.

Cardiac and non-cardiac disorders can cause angina. It is therefore important to have an awareness of possible alternative causes of anginal sensations, as well as to be able to differentiate serious, imminently life-threatening conditions from sources of discomfort that are still serious yet less emergent. It should also be emphasized that factors and conditions not directly related to the heart itself can increase myocardial oxygen demand and present credibly as angina pectoris.

Non-cardiac imposters that produce angina and can blur and confuse an initial diagnosis include disease processes such as anemia, fever, hypoxia, thyrotoxicosis (extreme hyperthyroidism), aortic stenosis, sympathomimetic drug effects, general anxiety disorder/ panic attack, or cocaine use. The following is a listing of some non-cardiac causes of angina type chest pain.

Cardiac or cardiac associated chest pain can by itself have many different etiologies other than coronary artery disease. One example is in aortic valve disease where the aortic orifice is obstructed to some degree in its function. This occurrence can readily increase systolic pressure and result in a deficit in the level of myocardial oxygenation. The end result of such an aortic valve disease is often heart hypertrophy with a chronic increase in myocardial oxygen demand, and chest pain.

Another cardiac related origin of chest pain can be seen in mitral valve prolapse where valvular function is compromised by an overabundance of mitral valve leaflet tissue. The result to that person is an increased opportunity to experience chest pain related to oxygen deficit.

Idiopathic hypertrophic sub-aortic stenosis (IHSS) is another example of an unexpected angina producer. IHSS is a type of gross obstruction of the left ventricular outflow tract originating from a hypertrophied heart septum, not uncommon in a congestive heart. The increase in muscle mass that accompanies congestive heart failure produces an increased oxygen demand at the same time that a hyper-contractile state exists. This leads to a resultant overall decrease in blood volume flow, and the experience of constrictive chest pain, angina.

When present, pulmonary hypertension can result in anginal symptoms. This can occur first by dilation of the pulmonary arteries, or secondly by the varying degree of right ventricular ischemia which results from pulmonary hypertension.

Angina pectoris is a clinical syndrome that is the result of an imbalance between the oxygen demand present in heart tissue and an insufficient supply of oxygen carrying blood due to changes in the coronary arteries supplying the heart itself. This imbalance, or oxygen starvation, results in myocardial ischemia. The supply of oxygenated blood can be impaired for a variety of reasons. These range from actual blood flow blockage due to coronary atherosclerosis or coronary spasm to reduction of available supply due to such things as hypotension and anemia. Vascular processes such as preload, afterload, and heart rate affect the demand side of the equation. Preload is the volume of blood waiting to be pumped by the heart, or from another angle, it is the resident pressure that distends the ventricle prior to ventricular contraction. Afterload is the resistance against which the left ventricle of the heart must push the blood that is being pumped.

Angina pectoris is itself broken into categories in order to better describe the qualities and conditions of the term.

Stable angina: chest pain occurs when the myocardial oxygen demand exceeds the ability of a coronary artery to supply oxygenated blood to the heart muscle itself. As a person exercises, myocardial work increases and is accompanied by an increase in myocardial oxygen demand. Normal coronary arteries dilate in response to this demand and coronary blood flow increases.

Stable angina is found frequently in an individual with a fixed obstruction in their coronary vessels, such as is often seen in coronary artery disease. This fixed disease condition limits the blood flow in a consistent manner as it flows through the diseased artery regardless of tissue demand requirements. The result is a consistently reproducible oxygen deficit during activities such as exercise which increase myocardial oxygen demand. For even though demand has increased the oxygen supply remains fixed, resulting in chest pain secondary to mounting ischemia. With rest, myocardial oxygen demand again falls within the limit of supply and the pain is relieved as the deficit decreases. Therefore, these triggers initiating “stable angina” occur when the heart is working harder than usual such as when exercising, doing yard work, experiencing emotional stress, eating a large meal, or going out into cold weather. The pain associated with stable angina usually goes away after a few minutes of rest or after taking a medication for angina. Often these attacks last from one to five minutes.⁶

Because stable angina occurs in a repetitive pattern it is sometimes referred to as chronic stable angina or brief myocardial ischemia. A diagnostic history of this type of chest pain is characterized by the presence of; the same precipitating factors, repetition in quality or duration, and/or a consistent response to the same modes of treatment such as rest or use of nitroglycerin. As a general rule for diagnosis the angina pattern of presentation should remain unchanged for at least one month.

Unstable angina, in contrast, implies a precipitous and critical reduction in coronary artery blood flow. Key factors that relate to the potential for diminution in coronary blood flow should be considered for diagnosis of unstable angina. Be aware, unstable angina can occur at any time, even when a person is at rest. It may ensue with or without physical exertion, and it should always be treated as an emergency.⁷

Coronary blood flow is reduced by the known presence of pre-existing arterial plaque, especially plaque rich in foam cells (lipid macrophages). Plaque composed of these cells may be easily fractured or dislodged. This easily dislodged plaque may result in a debris fragment that partially occludes a coronary artery. Such non-occlusive, partial blockages may be identified on angiography and coronary angioscopy. This type of occurrence is the presumed etiology for the majority of the individuals who present with unstable angina.⁸

Prinzmetal’s variant angina, also known by the newer term vasospastic angina, is a focal spasm of a coronary artery that can occur at rest. Spasm of the arteries supplying oxygenated blood to the heart muscle can be caused by adrenergic input, hyperventilation, emotional stress, cold stimuli, or street drugs such as cocaine. Coronary artery vasospasm may also explain transient ischemia associated with microcirculatory angina, in which only the small intramural branches of coronary vessels constrict and lead to pain, while the larger epicardial supply arteries remain unaffected.

Prinzmetal angina is relatively rare, most often affecting people less than 50 years old and has fewer risk factors for heart disease, unless they are smokers. Low levels of the element magnesium are thought to play a role in coronary vasospasm and more individuals of Japanese descent than Caucasian suffer from this form of angina.⁸

Symptoms of Prinzmetal angina often share these characteristics:^8,9

• Chest pain tends to be located under the breast bone
• Pain described more as discomfort with tightness, pressure, squeezing, or crushing sensation with discomfort radiating to the neck, jaw, arm, or shoulder
• Pain has a gradual onset, lasts from 5 to 15 minutes, and gradually fades
• Nitroglycerin is often successful relieving the pain
• An episode may be accompanied by nausea, sweating, dyspnea, dizziness, or the feeling of palpitations

The causes of coronary spasms are not exactly known and theories related to problems with the thin lining of the blood vessels’ endothelium and the chemical produced by the vessel epithelial lining called nitric oxide is being researched. The presence of nitric oxide widens the blood vessel diameter allowing blood to easily flow. When there is a reduction in this chemical a coronary spasm may occur. Levels of this artery widening chemical are higher when estrogen levels are also high at specific stages of the women’s menstrual cycle and interestingly women have a lesser incidence of Prinzmetal angina. Smokers on the other hand tend to have a lower level of nitric oxide in their blood vessels than nonsmokers and also a higher incidence of experiencing vasospastic angina.

Other research studies suggest the following:^9,10

• Atherosclerosis or other conditions producing partial vasoconstriction create a reduced threshold for exceeding myocardial demand leading to reactive spasms in the coronary arteries.
• Stimulation in the nervous system (brain and spinal cord) or muscle tissue from chemical triggers involved in making the arteries narrow and widen could contribute to coronary spasms. Some known triggers of spasm in susceptible individuals include exposure to or elevation in chemicals associated with; tobacco or cocaine use, hyperventilation, acetylcholine, ergonovine, histamine, and serotonin.
• The presence of inflammation or oxidative stress in coronary arteries resulting in hyperstimulation leading to coronary vasospasm.

A heightened platelet tendency to activate and adhere can affect a coronary artery leading to progressive narrowing until the resultant stenosis is sufficiently severe to produce pain even at rest. This mechanism is sometimes observed following balloon angioplasty, stent placement or other revascularization procedures when restenosis is observed. The gradual re-narrowing of restenosis happens most often between 3 to 12 months after revascularization procedures such as stent placement. Typically, recurrent angina is a primary indication, however an acute myocardial infarction may occur in around 10 percent of restenosis patients.¹¹

Patients with a history of acute coronary syndrome often times have recurrent transient reduction in coronary blood supply due to vasoconstriction and thrombus formation at the site of an atherosclerotic plaque rupture. This is due to episodic platelet aggregation and complex interactions among the vascular wall, atherogenic lipoproteins, platelets, and leukocytes.¹²

Evidence suggests that chronic low-grade inflammation plays an important role in atherogenesis and thrombogenesis. While experts are not yet sure exactly what role inflammation of the blood vessels takes in atherosclerotic build up evidence does show it inflammation as the initiating event in many heart attacks and strokes.¹³ Inflammatory markers, such as C-reactive protein and amyloid A, have proven to be predictive of mortality and future cardiac events in unstable coronary syndromes.

Coronary Inflammation

Angina may also be classified as either typical or atypical. Typical angina has a gradual onset and is brought on by predictable precipitating factors such as exercise, shoveling snow, or chasing down a taxi.

Be aware that typical angina and stable angina are not the same thing. Stable angina – a.k.a. angina pectoris brought about by decreased blood supply to the heart muscle has a gradual initiation, consistent symptoms, and tapered relief with rest. In typical angina, observation into the pattern of response to a causative event is the key. Physical exertion or intense emotional stress tends to be the consistent initiator of typical angina. Attacks of classic substernal chest discomfort tend to accompany typical angina which will characteristically last between three to five minutes and rarely exceed 30 minutes. Either rest or use of nitroglycerin works to end an episode. If an angina attack persists for 30 minutes or longer, particularly if this is a deviation to the typical presentation for this individual, it is wise to rule out a myocardial infarction.

Typical angina as a general rule responds well to sublingual nitroglycerin. Most people with typical angina can predict fairly accurately when their angina will occur, that is in response to what provocation, as well as the manner in which it will progress or resolve. This sort of forecast is greatly helpful during diagnostic work-ups, allowing the use of a 12-lead ECG to document changes.

The discomfort or pain associated with typical angina is usually located in the sub or retrosternal area of the anterior chest. Do not expect the client to be able to pinpoint the exact location. Vagueness in relation to describing the source of the discomfort is in fact typical of this form of angina, yet often you may observe a clenching of the fist over the sternal region. This is known as Levine’s Sign, and is a useful diagnostic observation.¹⁴

In typical angina, the discomfort experienced is frequently transmitted to the left shoulder and radiates down one or both arms. It may also radiate to the throat, neck and jaw. On questioning the client regarding the quality of their feelings it is best to avoid using the actual word pain. Talking only about pain tends to lead people away from other descriptive terms and very well may cause the person not to mention or describe any other feelings that they are having such as heaviness, crushing, burning, or squeezing sensations.

Atypical angina, or angina equivalents, are so-named as they can manifest in unusual and at times bizarre fashions, often unique to that individual experiencing them. Equivalent sensations may be reported to the health professional as dyspnea, syncope with exertion, or epigastric sensations such as nausea and indigestion that occur even during rest periods while exercising.

Variant angina known as Prinzmetal’s angina is a form of atypical constrictive chest pain that falls into the category of unstable angina, and is most frequently caused by a focal spasm of a normal coronary artery or by a spasm superimposed on a fixed lesion. It tends to be cyclic and occurs at rest without relation to effort. Often, yet not always, it is associated with ST segment elevation on the electrocardiogram (ECG).⁹

Equivalent angina encompasses the many forms of cardiac induced chest pain that do not present as expected. They may manifest as dyspnea, belching, fatigue or even faintness. This form of angina is often found in women who are experiencing an acute cardiac event. Do not neglect persistent symptoms just because they are not what might be expected in a middle aged, overweight, beer drinking, cigar smoking man.

The classic description of chest pain from ischemia related cardiac sensations is most commonly seen in the male, middle aged population among those with risk factors for a coronary artery disease such as atherosclerosis. However, amongst the female population of all ages, clients with diabetes and in the elderly a large number of anginal events are described as different or atypical sensations.

Anginal equivalents are frequently not “noticed” (e.g. are “silent”) or are not regarded as potentially serious indicators of cardiac risk by those experiencing them. Wearable ECG monitors and other equipment have revealed that more than 75 percent of ischemic episodes during regular daily activities go ignored or unnoticed.¹⁶ This suggests that our preconceptions of what angina should look like must change to avoid misdiagnosing those whose presenting symptoms differ from our classically trained expectations.

The following are two commonly used classification tools for describing angina. Chances are good that you will see one or both of these tools in active use in your local area of practice.

Prompt diagnosis of cardiac ischemic angina combines the results of a person’s history and their physical presentation. The following are the most common signs and symptoms of an acute episode of cardiac ischemic angina.

Generally speaking, the first thing an emergency room visit with angina will bring is a search for a myocardial infarction. It is well known that angina does not always signal myocardial infarction (MI), yet due to the immediate threat to life that such an emergent event causes, suspicion of a heart attack always takes precedence when the cause of angina symptoms is unknown.

In many instances, ischemic angina of cardiac origin can be readily ruled out by history, physical examination findings, and basic laboratory panels. A complete blood count and electrolyte panels with BUN, creatinine, and glucose levels provide quick assistance for isolating infectious or metabolic origins of chest pain. Such lab results, as well as chest x-ray findings are usually normal in those individuals with true angina pectoris. Chest x-rays may also show evidence of cardiomegaly in those who have had a previous MI, ischemic cardiomyopathy, pericardial effusion, or are experiencing acute pulmonary edema.

A cardiac stress test is a tool the physician may utilize to determine if the heart is getting the blood it needs under external stress, even if the patient has no signs of a problem when the heart is “at rest”. When a patient has arthritis or another medical condition that prevents the patient from exercising during a stress test the physician may give a medication which makes the heart work hard, as it would during exercise. This is called a pharmacological stress test.

On a less urgent event note, graded exercise stress testing is the most widely used diagnostic test for the evaluation of patients presenting with chest pain. In those who have an established stable angina pectoris, it also can provide prognostic information about the extent of disease. Exercise stress testing has the ability to be performed alone or in conjunction with echocardiography and myocardial perfusion scintigraphy studies. For detection of cardiac ischemic processes stress echocardiography has shown an overall sensitivity of 68 percent with a specificity of 77 percent.¹⁹ While exercise stress testing alone generally has a somewhat lower diagnostic sensitivity, it is less expensive and therefore a reasonable choice in certain circumstances.

Stress echocardiography testing can be very useful in the evaluation of segmental wall motion during exercise. Visualization of the cardiac structure makes it possible to detect changes in the regional wall movements that tend to occur during myocardial ischemia. Experience has shown that during ischemia, normal myocardium becomes hyperdynamic in response to stresses such as exercise, while affected ischemic segments become hypokinetic or akinetic. Stress echocardiography also has the benefit of allowing simultaneous evaluation of left ventricular function, cardiac dimensions, and visualization of any valvular disease affects. It is especially useful in patients with baseline ECG abnormalities and those with systolic murmurs suggestive of aortic stenosis or hypertrophic cardiomyopathy. Most useful of all perhaps is its help in the localization of ischemia and evaluation of its severity.

Thallium-201 (TI-201) and technetium-99m sestamibi (Tc-99m) are the most frequently used myocardial perfusion scintigraphy (imaging) tests. These tests are widely available and very useful in individuals with unstable chest pain and baseline ECG abnormalities to localize the region of ischemic changes, and as prognostic indicators.

During the imaging scan, a camera takes pictures of the heart after a special test medicine (radioactive tracer) is given through an IV. The tracer travels through the blood and into the heart muscle. As the tracer moves through the heart muscle, areas that have good blood flow absorb the tracer. Areas that do not absorb tracer may not be getting enough blood or may have been damaged by a heart attack.

In essence this type of testing is used to:

• Assess the amount of blood reaching the heart muscle.
• To identify areas of heart muscle lacking an adequate blood supply as a result of a heart attack.
• To identify blocked coronary arteries and evaluate the effectiveness of coronary bypass grafts of angioplasty.

Contrary to the belief of many in the health professions electrocardiography (EKG or ECG) is not absolutely definitive when attempting to determine the cause of acute angina. In fact, about 50 percent of patients experiencing angina specifically related to an ischemic cardiac process have normal findings on a resting ECG.⁴

Information obtained from an ECG is very helpful as it can provide evidence of prior MI, intraventricular conduction delay, various degrees of atrioventricular block, arrhythmias, or ST-T wave changes. The point is simply not to dismiss chest pain in the presence of a normal ECG, as evidenced by those patients with known coronary artery disease who have been documented as showing pseudonormalization of a resting ECG, even during active monitoring of chest pain.

Cardiac catheterization is an invasive procedure that involves aspects of both diagnosis and the potential for treating some types of ischemic cardiac disorders. Catheterization assesses angina by taking a close look at coronary hemodynamics. A cardiac cath (cardiac angiography) is usually performed in a special area under local anesthesia and sterile conditions. A flexible catheter is introduced into the heart via an artery and/or vein located in the groin or arm and advanced into the target area. Dye is injected through the catheter into the coronary arteries and/or heart's chambers, while an x-ray is taken and recorded on film. This procedure allows the physician to visualize the coronary arteries, as well as the function of the heart and its valves. Indications for cardiac catheterization include the following:

• Confirm or exclude coronary atherosclerosis
• Assess the feasibility of surgical correction of lesions
• Detect valvular disease
• Evaluate left ventricular hemodynamics
• Assess for congenital cardiac anomalies
• Confirm the presence of tumors, cardiomyopathies or anomalous coronary arteries

Angina pectoris is a result of an imbalance between the oxygen supply to the heart and the demand. When the demand for oxygen is greater than the supply, chest pain occurs. The pain is caused by an insufficient supply of blood to the heart causing a temporary ischemia of the myocardium (inadequate oxygen for the myocardium to meet its metabolic needs). The coronary arteries are unable to provide enough oxygen carrying blood to meet the oxygen requirements of the heart muscle.

Dramatic life style changes often accompany the onset of angina in a person’s life. Treatment options for angina, particularly angina that is cardiac ischemic in origin, play an important role in the dialog between clients and health professionals. We will discuss five methods for increasing the supply of needed oxygen to the muscle of the heart itself.

The first, increasing the concentrations of oxygen present in the carrying medium, is mostly of aid on an acute basis. There are a small number of angina sufferers who use oxygen routinely as part of their individual treatment regimen. Oxygen administration is certainly a valid complementary treatment for the most difficult cases of angina associated with ischemia whether it is of cardiac or non-cardiac origin.

The second method of increasing oxygen flow to the heart muscle is by use of medications whose purpose is to increase availability of flow by the carrying medium. In one manner of speaking the goal of pharmacologic intervention here is to convert unstable angina into stable, predictable angina. The following are medications commonly used in the treatment of angina.

The third choice for promoting increased oxygen flow to the tissue of the heart is that of revascularization procedures. These invasive procedures have the goal of opening partially occluded blood vessels, or replacing completely blocked vessels. Coronary Artery Bypass Graft surgery (CABG) is a surgical procedure that involves the removal of a portion of healthy blood vessel, such as a vein from the leg or the internal mammary artery (located in the chest) and using it to bypass the blockage(s) that are present in the coronary arteries.

Another revascularization procedure is Directional Coronary Atherectomy (DCA). This is the insertion of a specialized catheter into a compromised coronary artery, similar to an angioplasty, except that plaque is mechanically removed in order to decrease vessel blockage.

Still another revascularization procedure is balloon angioplasty with or without the placement of stents to hold open a diseased cardiac artery.

Balloon Angioplasty

An angioplasty is a procedure performed on patients with blocked or clogged coronary arteries. The technique is similar to a cardiac catheterization except that a special catheter with a small balloon is inserted into the blockage and inflated in order to compress the plaque and open the artery. The uninflated balloon catheter is advanced to the area of blockage. The balloon is then inflated and deflated several times until the blockage is compressed and the artery is widened. When using a stent, a fine wire mesh that is designed to expand and hold open the lumen of an artery is placed using a special catheter. These stents are springy, durable bundles which help provide renewed blood flow to ischemic tissue. Often angioplasty and stent placement occurs during the same procedure, though either can certainly be done on its own. These procedures have proven effective in the revascularization of ischemic cardiac tissues.

A fourth option is that of TMR.⁴ Transmyocardial laser revascularization, is available for clients with persistent angina who are considered inoperable or poor risks for the more traditional revascularization procedures. In this procedure, a surgeon exposes the muscle of the heart, and using a special high energy computerized CO2 laser, creates between twenty and forty, one-millimeter wide channels (think of the width of a pin head) in the muscle of the left heart ventricle. Body responses to these perforations close the outside of the channels, yet the unique characteristics of the cardiac muscle allow the channels inside to remain open, providing new blood flow to ischemic tissue.

The mechanism by which this works is not completely understood even by those specialists who perform TMR. Evidence that has been gathered suggests that coronary blood flow is improved however, and it may be that the procedure promotes angiogenesis, the growth of new, very small, blood vessels that contribute to improved oxygenation of the heart.

A fifth and somewhat exciting option increasingly available for achieving improved oxygenation to the myocardium in cardiac ischemic angina sufferers is that of Enhanced External Counter pulsation (EECP). EECP is a noninvasive treatment using carefully timed, sequential inflations of pressure cuffs placed onto the client’s calves, thighs and buttocks. Inflation and deflation of these cuffs is timed to the patient's ECG, and the effectiveness is observed by noninvasive arterial pressure waveform monitoring.

The overall hemodynamic effect of EECP compressions is to 1) provide diastolic augmentation and thus increase coronary perfusion pressure; to 2) unload systolic cardiac workload volumes and therefore decrease myocardial oxygen demand; and to 3) increase venous return and subsequently, cardiac output. This sequence of pressure shifts works to displace the pressure of flowing blood backwards into the coronary arteries during heart diastole, when the cardiac tissue is in a state of relaxation and resistance to back pressure in the coronary arteries is at its lowest point.

Remarkably, coronary collateral vessel development appears to be stimulated by this noninvasive increase in artery perfusion pressures, and with time a noticeable increase in perfusion capacities can be seen in both the new and pre-existing coronary arteries. Currently this therapy is gaining favor as an exciting adjunct to traditional treatment of cardiac ischemic related angina, and investigation is being done concerning EECP’s strong potential for treating other severe cardiac pathologies.²⁰

Angina is the strangling, compressive discomfort common to a wide spectrum of disease processes. It may be the first visible sign of a disease warranting emergency attention, including but not limited to anoxia and ischemia of the heart muscle. Angina must always be carefully investigated to identify the underlying cause. Awareness of both typical angina, and anginal equivalent symptoms, must be present to aid in the prompt recognition of cardiac ischemic angina and allow timely intervention to restore adequate oxygenation to tissues in distress. By our awareness of what angina is and the alert observations we make, we as health care workers can begin to get a firmer grip on this terrible pain in the neck, and chest, that angina is to us all.

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